TIDE Long Case PRO III Short Notes

~ SHORT NOTES ~

by T.I.D.E team

Together in Delivering Excellence (T.I.D.E)

MEDICAL BASED SURGERY BASED

INDEX MEDICAL PAEDIATRIC PSYCHIATRIC SURGERY O&G ORTHOPAEDIC

2 30 53 59 80 108

“Ya Allah, Kuatkan Ingatan Kami Terhadap Apa Yang Kami Baca Ya Allah, Tutuplah Segala Kesalahan Jawapan Kami Semasa Dalam Peperiksaan Ya Allah, Berikanlah Ilham kpd Kami Untuk Menjawab Sepertimana Yang Pensyarah Kami Mahukan Ya Allah, Kurniakan Pensyarah Yang Baik Hati Dan Pemurah Sebagai Pemeriksa Kami Ya Allah, Kurniakanlah Pesakit Yang Baik Hati Dan Dapat Memberi Kerjasama Kepada Kami Nanti Ya Allah, Semoga Apa Yang Kami Baca Dan Paham Sahaja Yang Ditanya Dalam Peperiksaan Nanti” Aamiin….

Special appreciation to members of “T.I.D.E” Team

Copyright @ 2015 All Rights Reserved Final Year Medical Student (USM)

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Together in Delivering Excellence (T.I.D.E)

MEDICAL Notes

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Together in Delivering Excellence (T.I.D.E) Approach to Chest Pain [IQbaL] HISTORY 1.

2.

3. 4. 5.

Nature of chest pain ( SOCRATES )  Constricting (cardiac ischemic or oesophageal spasm)  Dull, central & crushing, last for 20min (MI)  Radiates to jaw & upper extremities (cardiac cause)  Sharp pleuritic pain that catch on inspiration (pleura or pericardium) & suggest pneumonia, pul. embolism or pericarditis  Sudden substernal tearing & radiate to back ( aortic dissection )

PHYSICAL EXAMINATION 1. 2. 3. 4. 5.

Abnormality of pulse rate and heart sound (cardiac) Crepitation – pneumonia or HF Reduced breath sound in one side – pneumothorax or lung collapsed Tenderness on chest – may causes from MSS however MI can present with chest tenderness GIT origin in normal cardiac and respi system

Pain brought on by food, lying down, hot drinks, or alcohol, and relieved by antacids – GIT causes (eg GERD, PUD, oesophaeal spasm) PMHx – known cardiac dz, HPT, HPL, smoking, FHx can support diagnosis Acute cholecyctitis & pancreatitis can cause pain referred to chest Associated Sx dyspnoea – cardiac ischemia, PE, pneumothorax or pneumonia

INVESTIGATION Basic Ix 1. 12 lead ECG unless non-cardiac causes is confidently being diagnosed eg pneumothorax  ST, QRS, arrhymias, tachy/brady  Pericarditis – widespread concave ST, PR depression 2.

CXR  can confirm respi disorder eg pneumothorax, pneumonia  can provide clues in cardiac dz (widened mediastinum in aortic dissection or a large globular heart in cardiac tamponade)

3.

Echocardiograhy

Laboratory a) Cardiac biomarker – CK-MB, Troponin I & T b) FBC – infection & screen for anaemia c) RFT – baseline d) TFT # some DDx can be excluded/confirmed after basic Hx, PE and these Ix – STEMI, pneumothorax, pneumonia, pericarditis

MANAGEMENT 1) 2)

Management will depends on diagnosis Psychological tx may be helpful in some pt

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Together in Delivering Excellence (T.I.D.E) Diagnostic Approach for Dyspnoea [IQbaL] Diagnostic Hypothesis COPD

Asthma

Pulmonary Etiologies Pulmonary embolism

Pneumonia (CAP, TB, Pneumocystic jiroveci pneumonia)

Intertitial lung disease (ILD)

Clinical Clues History  >20 pack years tobacco   Chronic cough +sputum   Progressive/persistent dyspnea  Exposure to occupational dust/chemical

Test

Treatment

 Spirometry (FEV1/FVC <70%)  Bronchodilator response – largely irreversible  CXR – hyperinflation, bullous changes, pul HPT  ECG – cor pulmonale ( peak P wave @ L2,L3 and AVF )  ABG

 Nebulizer bronchodilator, O2  Antibiotic (H. influenza, Strep pneumonia)  Steroid ( beneficial in acute exacerbation of COAD)

 Wheezing  Assessing for severe asthma and lifethreatening Sx

   

   

 Sudden onset of dyspnea, peuritic chest pain  Hx of cancer  Hx of surgery, immobilization  Estrogen therapy

 Tachypnea, cyanosis  JVP, loud P2, gallop rhythm  Unilateral leg swelling

 D-dimer – exclude PE if normal  CT angiopraphy  Leg Duplex

 Fever, productive cough  Drug injection  High-risk sexual exposures

   

 CXR  FBC, Blood culture  HIV, CD4 (when appropriate)

 Cold, exercise, allergen, pets  symptoms worsening  Fmly Hx (atopic)

Cardiac Etiology

 O2 100%  Morphine + antiemetic  Immediate thrombolysis in massive PE ( bolus alteplase or surgery)  IV Heparin  O2, treat shock  Empirical antibiotic  IV fluid  PRN analgesic

    

CXR - Honeycombing PFT High resolution chest CT Lung biopsy

 Steroid / cyclophosphamide  Tx of underlying Dz

 Chest pain  CAD risk factor

 JVP  S3  crackles

   

ECG Biomakers Stress test Angiography

 “MONA”

 Rheumatic heart disease

 Significant murmurs

Arrhythmias

Anaemia

ABG O2, nebulizer (B-agonist) High dose steroid For severe attack – IV aminophylline, consider ventilation

 Fine basal Crackles  Clubbing  Sx of pul HPT, cor pulmonale & CTD

 Palpitation

Heart failure

Crackles, fever thrush Kaposi sarcoma Skin pop marks Severity – “CURB-65”

PFT Bronchodilator response Methacholine induced CXR – TRO pneumothorax

 Known connective tissue disease (CTD)  Raynaud phenomenon  Occupational exposure – asbestos, silica  Sarcoidosis

ACS

Valvular heart disease

Physical Dec breath sounds, wheezing Clubbing – superimposed bronchogenic CA, chronic infection

 CAD or risk factor  Poorly controlled HPT  PND  Alcohol abuse

 Melaena  Menorrhagia  Rectal bleeding

 Irregular pulse  Variable intensity of S1

   

JVP S3 Crackles Peripheral oedema

   

Pallor, cachexia Pale conjunctiva Thalassemic facies Gum hypertrophy

 Echo  ECG – absent P wave  Holter – paroxysmal AF  Echo – valvular defect, Lt atrial thrombus  TFT

 Identify underlying cause  Cardioversion (electrical or pharmacological)  Control ventricular rate (digoxin)  Antocoagulation – to prevent thromboembolism

 CXR  Echo  BNP

    

 HCT level (low)

Sit pt upright O2 100%, IV access Treat any arrhythmias Monitor ECG Furosemide, dimorphine

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Together in Delivering Excellence (T.I.D.E) Careful Hx-taking is very important 1) Time course  Acute (within min) – life-threatening eg. Acute pul Embolism, MI, pneumothorax, anaphylaxis, FB aspiration, pul. oedema or cardiac temponade  Subacute (hours-days) – AEBA, exacerbation of COPD, pul. oedema.  Chronic (weeks-months) – CCF, COPD, cardiomyopathy, pul. HPT, valvular heart dz, anaemia 2) Severity 3) Associated Sx  Fever - pneumonia, bronchitis, laryngitis, viral causes, sepsis  Fever + cough – community-acquired pneumonia or opportunistic infection in immunocompromised host (need CXR to exclude pneumonia)  Central chest pain – suggest CAD, pul embolism, pneumothorax, FB aspiration  Pleuritic chest pain – suggest pleuritis, pneumonia, pneumothorax  Palpitation – paroxysmal tachyarrhythmias, pul. embolism, valvular heart dz or anxiety attack  Wheezing – Asthma, COPD, pul. oedema, bronchiolitis, FB aspiration  Haemoptysis – exacerbation of bronchiectasis, bronchitis, chest malignancies, tuberculosis, cocaine toxicity  Dysphagia – FB aspiration, tetanus, epiglottitis (+drooling saliva), GERD (+heart burn)  Bone pain – sickle cell anaemia or fat embolism (a/w long bone #) 4) Position  Orthopnea – CCF, COPD  Dyspnea on standing, relieve by supine – pattern foramen ovale 5) Pattern  Appear during working, resolve during period off work – occupational exposure  Seasonal – asthma or reactive airway disease 6) Smoking Hx – COPD, lung Ca, interstitial lung disease

Questions 1.

Common causes of chest pain? ACS, Stable angina, pul embolism, pneumonia, viral pleuritis, GERD, anxiety & panic disorder

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Life threatening chest pain? [PETAAA] PE, Esophageal rupture, Tension pneumothorax, AMI, Angina/ACS, Aortic disection

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Together in Delivering Excellence (T.I.D.E) Acute Coronary Syndrome [Julea] HISTORY NSTEMI/UA : incomplete occlusion, occur at rest STEMI: complete occlusion, not relieved by rest/GTN Chest pain (LORDSANFARO)  Retrosternal/central/left chest  Crushing/pressing/burning in nature  Radiate to jaw/left upper limb  A/w profuse sweating, n&v, sob, palpitation

PHYSICAL EXAMINATION CVS examination Diagnosis of ACS: I. Hx of ischemic type chest pain II. Ecg changes III. Cardiac biomarkers

Atypical sx: fatigue, SOB, epigastric discomfort, n&v Risk fx:  Prev hx of IHD, CVA  DM,HPT,HPL  Smoking, physical inactivity, obese  Family hx of heart dz, stroke DDX chest pain + SOB:  MI  Aortic dissection (sudden severe pain, tearing sensation, radiate to neck,back,abd,leg)  Pulm embolism (period of immobility?)  Pneumothorax (hx of trauma to chest?)  Gerd (burning sensation in chest, sour taste, obesity)  Esophageal rupture (chest pain after vomiting)  Pneumonia (pleuritic chest pain, fever, cough) INVESTIGATION Diagnostic ix: 1. ECG  NSTEMI: ST depression, T inversion  STEMI: ST elevation, T inversion, Q wave 2. Cardiac enzymes: trop T, Trop I, CKMB  NSTEMI:increase enzymes  UA: normal 3. Echocardiography 4. Angiography Supportive ix:  FBC (low hb can precipitate MI)  LFT/BUSE/CREAT  Glucose lvl  Lipid profile  PT/APTT  CXR: cardiomegaly, p.effusion, sign of LV failure  ABG

MANAGEMENT 1. 2. 3. 4. 5. 6. 7. 8.

Assess ABC Bed rest, v/s, continuous ECG monitoring O2 by nasal prong/facemask Analgesic: S/L GTN, IV morphine +antiemetic Pharmacological rx: Antithrombotic(antiplatelet, anticoagulants), B-blockers, nitrates, acei/ARB, statin Non pharmaco: stop smoking, exercise, diet, control HPT, DM, HPL

Specific mx for STEMI: reperfusion therapy thrombolytics ( iv streptokinase) @ PCI if C/I to thrombolytic

MONA Morphine,O2,nitrates(isoket),aspirin

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Together in Delivering Excellence (T.I.D.E) Common/Possible Question in Exam + Answer ECG interpretation !! Advice before discharge: -diet lifestyle, exercise, stop smoking, compliance to meds and f/up Cx of MI:  Cardiac arrhythmia  Heart failure & cardiogenic shock  Thromboembolism (d/t bed rest,cardiac failure)  Cardiac rupture  Pericarditis  Post infarction angina  LV aneurysm  Complex regional pain syndrome (pain at l arm after weeks,months following mi)  Dressler’s syndrome (pericarditis, fever, pericardial effusion)

Indicators of successful reperfusion:  Reduce chest pain  ST segment isoelectric  Restoration of hemodynamic/electrical stability Contraindications for thrombolytics in STEMI:

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Together in Delivering Excellence (T.I.D.E) Congestive Cardiac Failure [Dalilah] HISTORY 1.

Risk factors : CAD, HPT, renal failure, valvular/congenital heart disease, pericardial disease (TB, effusion, tamponade), arrhythmia and anemia

2.

Symptoms of pulmonary edema : Acute breathlessness, orthopnea, PND, dry cough/ coughing with sputum, frothy sputum

3.

Symptoms of right sided heart failure : Lower limb edema, abdominal distension due to ascites

4.

Symptoms of cardiogenic shock : Cool, diaphoretic skin, cyanosis, dyspnea, altered sensorium, reduced urine output

5.

Assess further based on NYHA to get the class of heart failure

PHYSICAL EXAMINATION GENERAL Respiratory distress Decreased alertness ( cardiogenic shock) Tachypneic Tachycardia Cold peripheries, delayed CRT Hypotension Sign of valvular heart lesion Raised JVP Pitting edema SPECIFIC Apex beat shifted to left side ( cardiomegaly ) Gallop rhythm ( pulmonary edema ) Loud P2 ( pulmonary edema) Third and forth heart sound Lung crepitation ( pulmonary edema) Sign of pleural effusion Ascites Tender hepatomegaly

INVESTIGATION 1.

FBP,LFT, BUSE & creatinine, cardiac enzyme, ABG

2.

ECG – Ischaemic changes

3.

Echocardiography – cardiac chamber dimension, systolic n diastolic function, valvular heart disease, cardiomyopathies

4.

Regular BP monitoring or intra-arterial BP monitoring

5.

Urine output (renal perfusion), alertness and conscious level (cerebral perfusion) and general wellbeing

6.

Assessment of venous pressure  CVP (only reflect right ventricular filling pressure)  Pulmonary capillary wedge pressure (PCWP) with Swan-Ganz catheter ; useful in suspected ARDS, exclusion of VSD, associated hypotension requiring treatment with inotrope to guide therapy

MANAGEMENT 1.

Priorities a) Sit pt upright b) Oxygen (35 to 100%) via facemask to maintain PaO2 more than 60 mmHg and SPO2 more than 90% c) Treat underlying arrthymia d) IV canula large bore :  IV morphine (2.5-5 mg) + IV /IM 10 mg metoclopromide  frusemide 40-80mg IV e) Sublingual nitrate if systolic BP > 100 mmHg

2.

Oxygenation

3.

Fluid challenge ( Hartmann’s solution )

4.

Diuretics

5.

Venodilators

6.

Inotropic agent

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Noradrenaline/adrenaline

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Together in Delivering Excellence (T.I.D.E) Details on Management 1. Oxygenation - Increase inspired oxygen to keep SPO2 more than 90% - Mechanical ventilation : if hypercapnia persist despite high flow oxygen (eg NIPPV) - Correct severe metabolic acidosis (pH less than 7.2 ) as it has negative inotropic and proarrthymogenic effect 2.

Fluid challenge ( Hartmann’s solution ) - If invasive hemodynamic monitoring is not available , fluid should be administered in small volumes (100ml ) over 510 min interval with reassessment of BP, heart rate, peripheral perfusion n breath sound. If BP does not responds to fluid (after 500-1000 ml), start vasopressor - If invasive hemodynamic monitoring is available, volume should be administered until a PCWP of 18 mmHg is attained

3.

Diuretics - IV frusemide 40 mg or bumetanide 1 mg at 20 min interval if initial therapeutic response is inadequate

4.

Venodilators - Sublingual nitroglycerin 0.3-0.5 mg up to 3 tabs every 5 min interval - IV nitroglycerin 5-10 microgram/min increased by 5-10 microgram/min every 5 -10 min - IV isoket ( isosorbide dinitrite) 2-10 mg/hr

5.

Inotropic agent - Dopamine 5-10 microgram/kg/min. low dose stimulates systemic vasodilation; high dose stimulates heart rate and contractility - Dobutamine 15-20 microgram/kg/min. acts at beta adrenergic receptor , no alpha adrenergic receptor activity

6.

Noradrenaline/adrenaline - Beta and alpha adrenergic agonist. Increase heart contractility and peripheral vasoconstriction - Noradrenaline : 8 -12 microgram/kg/min - Adrenaline : 0.05 – 0.1 microgram /kg/min

QUESTIONS 1. Medications ( MOA, dose and side effect ) 2.

Chest xray finding Cardiogenic pulmonary edema; cardiomegaly, widened mediastinum, bat wings, upper lobe diversion, kerley A,B,C, blunted costophrenic angle.

3.

PE finding for pulmonary edema

4.

Sign of right heat failure vs left heart failure

ECG findings ( ischaemic changes ST elevation, T inversion, Q wave ), duration and onset. Localization of infarction area. ( sbb associated dengan CAD )

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Together in Delivering Excellence (T.I.D.E) Rheumatic Heart Disease [Ain] HISTORY

PHYSICAL EXAMINATION

- RHD : A chronic heart condition caused by rheumatic fever that can be prevented and controlled. Rheumatic fever is caused by a preceding group A streptococcal (strep) infection. - Multisystem disease affecting connective tissue particularly of the heart, joints, brain, cutaneous and subcutaneous tissues 1. 2. 3. 4. 5. 6. 7. 8. 9.

Age ? - 5-15 yrs school-age children living in closed community (high risk group) Any history of fever or URTI preceeding to the complaint Any joint pain or others ass. symptoms eg.malaise,pallor,fatique ? Which joint affected,nature of the pain,is it migratory or localized? Any skin lesions or rash noted in the body? Any abnormal movement noted? Any swelling anywhere or nodule especially over bony prominence? Assess risk factor – overcrowding,poor sanitation, poverty,poor housing. Any complication symptoms eg.heart failure,atrial fibrillation

#The knees, ankles, elbows, and wrists are the joints most likely to become swollen from rheumatic fever. The pain often migrates from one joint to another.

INVESTIGATION 1. 2. 3. 4. 5.

FBC – anemia,leucocytosis Inflammatory marker – ESR/CRP positive Throats swab for group A streptococcus Anti-streptolysin O titre (ASOT) - elevated Investigations for evidence of carditis • Chest x-ray – cardiomegaly, pulmonary venous congestion • ECG- First degree A-V block, T wave changes, low voltage QRS • Echocardiogram – cardiac dilatation, valve involvement, pericardial effusion

Carditis in RHD : Mitral valve (90 %) : MR –children,adolescent MS – adult,later can get AF as cx. Aortic valve : AR,AS Less common affected : pulmonary, tricuspid MANAGEMENT Principle of management : -

Step I - primary prevention (eradication of streptococci) Step II - anti inflammatory treatment (aspirin,steroids) Step III- supportive management & management of complications Step IV- secondary prevention (prevention of recurrent attacks) Step v – tertiary prevention

1. Bed rest until CRP normal for 2 weeks (maybe by 3 months) 2. Benzylpenicillin 0.6-1.2g IM or Penicillin V 250-500 mg 2-3 times daily for 10 days. (if allergic give erythromycin or azithromycin for 10 days) 3. Analgesia for carditis/arthritis :aspirin 100 mg/kg/d in divided dose (max 8g/d) for 2 day then 70 mg/kg/d for 6 weeks.  if moderate to severe carditis : add prednisolone 4. Immobilize joint in severe arthritis – rest and supportive splinting 5. Treatment of chorea - Haloperidol (0.5 mg/8h) or diazepam 6. Secondary Prevention of Rheumatic Fever- aims to prevent illness or progression of disease once a problem has been identified  Benzathine penicillin G 1 200 000 U every 3 weeks* Intramuscular  Penicillin V 250 mg twice daily Oral # For individuals allergic to penicillin : Erythromycin 250 mg twice daily 7. Tertiary prevention–aims to prevent complications once a disease is established. Reducing symptoms to minimise disability and prevent premature death. Eg.heart valve surgery, medication to manage heart failure eg.diuretics and preventing stroke.

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Together in Delivering Excellence (T.I.D.E) 1. Diagnosis of RHD JONES criteria : evidence of recent strep infection plus 2 major criteria or 1 major criteria + 2 minor

# Exceptions to Jones Criteria -

Chorea alone, if other causes have been excluded Insidious or late-onset carditis with no other explanation Patients with documented RHD or prior rheumatic fever,one major criterion,or of fever,arthralgia or high CRP suggests recurrence

2. Duration of Secondary Rheumatic Fever Prophylaxis    

Fever without carditis - At least 5 y or until age 18 y Rheumatic fever with carditis and heart disease (persistent valval lesion) - At least 10 y since last residual episode and at least until age 40 y,sometimes lifelong prophylaxis Rheumatic fever with carditis & heart disease (no valvar lesion) -10 y or well into adulthood More severe valvular disease,post-valve surgery cases - lifelong

3. Differential diagnosis of acute rheumatic fever based on symptoms

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Together in Delivering Excellence (T.I.D.E) COPD [Rozana] HISTORY

PHYSICAL EXAMINATION

Epidemiology : > 35 yo, 10-20% in over 40s

General : Tachypnoea, use of accessory muscle, wheeze, cyanosis

Chronic bronchitis : defined clinically as cough, sputum production, on most days for 3 months of 2 sucessive years, sx improvise if pt stop smoking

Specific :  sign of airflow limitation and air trapping in advanced stage (barrel chest, loss of cardiac and liver dullness, prolonged expiration, reduced breath soundhyperinflation, reduce expansion)

Emphysema : define histologically as enlarged air spaces distal to terminal bronchioles with destruction of alveolar walls

Cx : cor pulmonale: edema, ↑ JVP, pneumothorax Risk factor : Genes (alpha-1 antitrypsin enzyme deficiency causes panlobular emphysema), Exposure to particles, Tobacco smoke, Organic and inorganic occupational dusts, Indoor air pollution from heating and cooking with biomass in poorly ventilated dwellings, Outdoor air pollution, Lung growth and development, Oxidative stress, Respiratory infections, Socioeconomic status Sx :  

chronic cough, sputum, dyspnoea(interfere daily activities), wheeze, chest tightness extrapulmonary : LOW, cor pulmonale sx

Complication : acute infection +/- infection, polychythaemia, respi failure, cor pulmonale, pneumothorax, lung carcinoma, osteoporosis INVESTIGATION Laboratory : FBC =anemia of chronic disease, PCV ↑(chronic hypoxemia) Others :  Spirometry : post bronchodilator FEV1/FVC ratio < 0.7 = not fully reversible airflow limitation

MANAGEMENT Mx of acute COPD  Controlled oxygen therapy  Nebulized bronchodilators (salbutamol and ipratropium)  Steroids (IV hydrocortisone and oral prednisolone)  Antibiotics, if evidence of infection  Physiotherapy to aid sputum expectoration  If no response  repeat nebulizers and consider iv aminophlline  If no respone 1) Consider nasal intermittent positive pressure ventilation. 2) Consider intubation & ventilation Mx of stable COPD Non pharmaco/ general : smoking cessation, encourage exercise, treat poor nutrition or obesity, influenza and pneumococcal vaccination Pharmaco  Mild (FEV1 50-80% predicted) : antimuscarinic eg. Ipratropium/ B2 agonist inhaled PRN



Peak expiratory flow rate : low





ECG :detect pulmonary HPT ( advanced disease) right atrial and ventricular hypertrophy (cor pulmonale) ABG : PaO2 ↓+/- hypercapnia

Moderate (FEV1 300-49% predicted) : regular anticholinergic eg. Ipratropium or long acting inhaled B2 agonist eg. salmeterol + inhaled corticosteroid eg. beclamethasone



Severe (FEV1 ) : LABA + inhaled steroid, anticholinergic.



Imaging :  Hyperinflation (flattened diaphragm and increased lung volume), large central pulmonary arteries, ↓ peripheral vascular marking, bullae, hyperlucency of lung  Exclude other diagnosis eg. Lung cancer, heart failure, bronchiectasis and TB

Pulmonary HPT : Assess the need of LTOT(long term 02 therapy), treat edema with diuretics

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Together in Delivering Excellence (T.I.D.E)

Pink puffers & blue bloaters (end of a spectrum)  

Pink puffers have ↑ alveolar ventilation, a near normal PAO2 and normal or low PCO2, breathless but not cyanosed, may progressed to type 1 respi failure Blue bloaters have ↓ alveolar ventilation, with low PAO2 and high PACO2, cyanosed but not breathless and may go on to dev. Cor pulmonale

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Together in Delivering Excellence (T.I.D.E) Tuberculosis [Fatin] HISTORY o

o

o

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Epidemiology  Mycobacterium tuberculosis  Transmit through microscopic droplet ( cough, sneeze, speaking) Risk factor  Immunocompromise (DM, chronic dz, HIV, steroid, malnutrition)  Travelling to endemic area  Substance abuse (drug/alcohol)  Contact with TB pt (occupation, family member)  Living in overcrowded area  Prev TB infection S&S  Chronic cough >2w  Blood stained cough  LOW, LOA  Fever, night sweat  SOB, chest pain, pleuritic chest pain  Extra-pulmonary : hematuria (renal), back pain (spine), seizure (meninges) Complication (lymphatohematogenous spread)  Extra-pulmonary TB -bone, brain, liver&kidney, heart  ARDS  Lung failure  Relapse of disease

PHYSICAL EXAMINATION o

General  Cachexic  Fever  Muscle wasting

o

Specific  Lung :  Consolidation =↓chest expansion, dull percussion, bronchial BS, crepitation  Pleura effusion = trachea deviated if massive, ↓chest expansion, stony dull, absent BS, ↓vocal resonance  Lung collapse = trachea deviation ipsilateral mediasternal shift, ↓chest expansion, dull, absent/reduce BS  Other : lymphadenopathy

∆∆ 1) pneumonia 2) lung carcinoma 3) lung abscess 4) fungal infection

INVESTIGATION o

o

Laboratory  FBC –leucocytosis as sign of infection or anaemia due to chronic disease  Sputum direct smear for AFB  Mantoux test- result read after 72H  Sputum c+ sensitivity –3 morning specimen  Sputum cytology- to look for any abnormal cells to suggest malignancy  Blood culture + sensitivity :to detect any microorganism  Broncoscopy - tumour, foreign body, inflammation  Pleura fluid analysis (pleura tapping) Imaging  X-ray :  Primary TB: perihilar and paratracheal lymphadenopathy, patchy area of consolidation, pleura effusion feature  Post 1® TB: consolidation at post segment of upper lobe @ sup segment of lower lobe, tuberculoma at Rt upper lobe, cavitation  Milliary TB : millet seed nodule (1-3mm) evenly distributed

MANAGEMENT Anti-TB therapy  Intensive phase (2M) -> 2EHRZ  Maintainence phase (4M) -> 4HR ST

1 LINE : Rifampicin (R)-hepatitis Isoniazid (H)- hepatitis Pyrazinamide (Z) –joint and ms pain Ethambutol (E)- visual disturbance Streptomycin (S) – ototoxicity DOTS –directly observed therapy short case

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Together in Delivering Excellence (T.I.D.E) Common/Possible Question in Exam + Answer 1)

Screening of high risk group  HIV pt  Immigrant  Person in prison/drug rehab centre  Pt with dm, renal dz, steroid, immune sup drug  Hemato malignancy

2)

Classification of TB  PTB +ve smear : * 2 sputum smear positive AFB * 1 sputum +ve AFB and +ve radiological finding * 1 sputum +ve AFB and +ve culture 

3)

PTB –ve smear : * 3 sputum smear –ve * sputum smear –ve but subsequent culture +ve

TB meningitis Tx   

The duration of anti –tb is longer which for 12 months duration Intensive(2 months) maintenance (10 months) Other drug to give is steroid (6 weeks or longer)

4) Preventive measures Primary intervention  Identification + immediate isolation  Herd immunity-BCG vaccination  Contact tracing of individual who are in close contact with cases  Reduce risk of transmission by using ppe(personal protective equipment), cough etiquette 5)

Why hemoptysis occur? Due to erosion of vessel located in the wall of cavity or rupture of dilated vessel in cavity

6)

Mantoux test

7) Follow up : every 2 months, take CXR and sputum smear AFB 8) Intensive therapy 2 months, then maintenance therapy 4 months but can be extended when : Cavitating lesion in CXR Extrapulmonary TB Immunocompromised pt

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Together in Delivering Excellence (T.I.D.E) Lung Cancer ( Bronchogenic Carcinoma) [Zuraidah] HISTORY

Def : malignancy of the lung arising from the epithelium of the bronchial tree. nd

Prevalence : 2 after prostate ca in men , breast ca in women. Aetiology : smoking, asbestos exposure, radon gas exposure, familial predisposition (genetic), HIV infection, air pollution (pesticide), lung diseases. History : 0 1. Sx related to 1 tumor: cough, dyspnea, hemoptysis, chest pain, postobstructive pneumonia 2.

Sx related to mediastinal spread: - Hoarness of voice with left sided lesion (caused by recurrent laryngeal nerve palsy - Obstructive of svc with right sided tumor or asso lymphadenopathy - Elevation of hemidiaphragm from phrenic nerve palsy - Dysphagia from esophageal obs and pericardial temponade

PHYSICAL EXAMINATION

General - Hoarseness of voice, Cachexic, alopecia (chemo), nicotine staining, cyanosis, clubbing, flaps, cervical l/n, raised JVP + sign of SVC obstruction, leg edema - Vital sign – tachypnea * Horner syndrome (ptosis), paraneoplastic synd ( wasting of small ms of hand) Specific (Respiratory system) Inspection Barrel shaped, mvmnt of chest reduce on affected, use of accessory ms Palpation Trachea deviation, apex beat, chest wall tenderness (mets), inc tactile fremitus Percussion - dullness, liver span enlarged (mets) Auscultate - bronchial bs, rhonchi, rub DDx

3.

Sx related to mets: sites liver, brain, pleural cavity, bone, adrenal glands, contralateral lung & skin

4.

Paraneoplastic synd: - Pain in arm/legs caused by hypertrophic osteoarthropathy - Sx of hypercalcemia caused by scc

5.

Systemic effects: fever, anorexia, low/loa, weakness, profound fatigue INVESTIGATION

Laboratory FBC: WBC raised in concomitant infection ABG: hypoxia with respi acidosis in severe endobronchial obs ESR: > 100 in 1hour Serum sodium, calcium Sputum examination – malignant cell cytology, c+s for any u/l lung infection Lung fx test: FEV1 of 1000ml after planned resection Invasive: pleural fluid cytology, percutaneous transthoracic needle biopsy

Imaging - CXR: 0  1 tumor - hilar mass or coin lesion, rib erosions, raised hemidiaphragm (phrenic nerve palsy), lymphangitis carcinomatosis, any lung collapse 0  if 2 tumor – cannon ball appearance - CT scan TAP: metastasis, staging - Bronchoscopy (+washing & brushing): endobronchial tumor - Bone scan: staging

1. 2. 3. 4. 5.

Pulmonary TB Pneumonia Lung abscess Bronchiectasis Sarcoidosis

MANAGEMENT

Depends on multiplicity factors: 0 It is a 1 or mets lesion Hilar or mediastinal infiltration Chest wall involvement Asso with complication- massive pleural effusion, svc obstruction, collapse-consolidation Phrenic nerve involvement Paraneoplastic syndromes Treatment : 1) Surgery Lobectomy- the most effective type of surgery, even when the lung tumor is very small. A wedge- remove the tumor, surrounded by a margin of normal lung. Segmentectomy- removes the portion of the lung where the cancer developed. Pneumonectomy. If the tumor is close to the center of the chest, remove the entire lung. Radiofrequency ablation- needle inserted into the tumor to destroy the cancer with an electrical current * SCLC is not recommended for surgery d/t aggressive & micromets. Go for chemo 2) Medical – chemotherapy or radiotherapy 3) Treatment for sx such as infection & breasthless 4) Pain management & quality of life 5) Adequate hydration & food intake

16

Together in Delivering Excellence (T.I.D.E) Common/Possible Question in Exam + Answer

1. Cx of lung ca? i. Hemoptysis ii. Acute breathlessness d/t endobronchial narrowing iii. Massive, recurrent hemorrhagic pleural effusin iv. SVC obstruction v. Paraneoplastic syndrome

3. Contraindication for surgery? i. Metastatic carcinoma ii. FEV1 < 15000ml iii. Severe pulmonary hpt iv. Uncontrolled major cardiac arrhythmias v. Co2 retention vi. Myocardial infarction in the past 3 months

2. Aim of staging? To identify candidates for surgical resection, since this approach offers highest potential cure

4. Which tumor respond well to chemo? Small cell lung ca (SCLC), combination of cisplatin & etoposide is the best therapeutic index of ay regime Role for chemo in non small cell ca (NSCLC) suggested that bnefits are small

Notes Types : Small cell lung ca (SCLC) – 20%, rapid growing, strong correlation with smoking, mets rapidly to various organ (liver, brain, bone, git, adrenal glands ), histologically- keratinization Non small cell lung ca (NSCLC) – 80% I. Adenocarcinoma (50%), commonly seen in non smoker, arises from bronchial mucosal glands in the outer, or peripheral area of lungs, histo-gland formation II. Squamous cell carcinomas (30%), aka epidermoid carcinomas, centrally located, cavitary lesion, histo- presence of keratin pearls and has tendency to exfoliate. III. Large cell carcinomas (20%), undifferentiated ca, large peripheral mass on cxr, histo-highly atypical cell with focal necrosis Anatomical Staging -

17

Together in Delivering Excellence (T.I.D.E) Bronchiectasis [Rafidah] HISTORY Definition: Abnormal and permanent dilated airways resulting from Inflamed thickened and irreversibly damage bronchial walls cause mucociliary transport mechanism become impaired and frequent bacterial infection ensues.

Aetiology: 

 

Congenital: cystic fibrosis, Primary ciliary dyskinesia, Kartagener’s syndrome Post-infection: measles, pertussis, Bronchiolitis, pneumonia, HIV, TB Bronchial obstruction: tumour, foreign body Rheumatoid arthritis, IBD Allergic bronchopulmonary aspergillosis

     

Cough with copious purulent sputum Recurrent hemoptysis SOB Intermittent fever and night sweat History of recurrent infection Weight loss



 

PHYSICAL EXAMINATION General: Respiratory distress Finger clubbing Specific: Coarse crackles over affected area, usually basal lung Sign of collapse, fibrosis or pneumonia

S&S

Complication      

Pneumonia Pleural effusion Pneumothorax Hemoptysis Cerebral abscess amyloidosis INVESTIGATION

Laboratory Full blood count – white cell count (infection) Sputum culture Imaging Chest radiograph: cystic shadow, thickened bronchial walls(tramline and ring shadow) High resolution CT scan – thickened, dilated bronchi and cyst at the end bronchioles. Bronchoscopy – to locate site of hemoptysis or exclude obstruction

MANAGEMENT Non surgical: Non pharmacological 1) Postural drainage at least 3 times daily for 10 – 20min Pharmacological 1) Antibiotic: according bacterial sensitivities 2)

Bronchodilator: may be useful in asthma, copd,cf, allergic bronchopulmonary aspergillosis

3)

Corticosteroid: eg. prednisolone

Surgical : resection of the affected lobe

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Together in Delivering Excellence (T.I.D.E) Common/Possible Question in Exam + Answer 1)

What are the major respiratory pathogens in bronchiectasis? Staph. Aureus, pseudomonas aeruginosa, H. influenza, and anerobes

2)

What are the common site for localized disease? Left lower lobe and lingula

3)

What is the indication of surgery in bronchiectasis? Bronchiectasis localized to a single lobe or a segment without clinical, bronchographic, ct evidence of bronchiectasis of bronchitis affecting other parts of the lungs.

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Together in Delivering Excellence (T.I.D.E) Pleural Effusion [Farhan] HISTORY

PHYSICAL EXAMINATION

 Accumulation of fluids in the pleural space  Transudates (<25g/L):  Due to increase venous pressure (CCF, constrictive pericarditis, fluid overload)  Hyponatremia (cirrhosis, nephrotic syndrome, malabsorption)  Hypothyroidism (right pleural effusion)  Meig’s syndrome (benign ovarian tumor, ascites, pleural effusion)

 General examination (look for signs of associated disease):  Malignancy (cachexia, clubbing, lymphadenopathy, mastectomy scar)  Stigmata of CLD (Dupuytren contracture, spider naevi)  Cardiac failure (displaced apex beat, ↓BP, cyanosis, tachycardia)  Hypothyroidism (dry skin, thin hair, cold hands, round puffy face)  SLE (malar rash, discoid rash, oral ulcers, alopecia)  RA (symmetrical joint swelling)

 Exudates (>35g/L):  Increased leakiness of pleural capillaries due to  Infection (pneumonia, tuberculosis)  Ischemia (pulmonary infarction, SLE, rheumatoid arthritis)  Malignancy (bronchogenic ca, malignant mets, lymphoma)

 Chest examination (only apparent if effusion > 300ml):  Inspection: asymmetrical chest movement  Palpation: reduced chest expansion, mediastinal shift, trachea deviation (>1000ml), decreased tactile fremitus,  Percussion: stony dullness  Auscultation: Reduced or absent breath sound, reduced vocal resonance

 Common complaints: dyspnea, cough, pleuritic chest pain.  Ask about associated symptoms e.g. dyspnea with bilateral leg swelling, orthopnea, and PND  CCF; or night sweats, fever, and weight loss  TB  Ask about occupation; might give a clue to illness

INVESTIGATION  CXR (PA):  Blunted costophrenic angle (small effusion)  Clear air fluid level with concave upper border  Air fluid level with flat upper border (presence of pneumothorax)  Lateral decubitus film is useful to detect smaller effusion; layering of an effusion indicates free flowing effusion  Pleural fluid analysis (send for):  Clinical chemistry (protein, glucose, pH, LDH, amylase)  Bacteriology (microscopy & culture, TB culture)  Cytology  Immunology (RF, ANA, complement) – if indicated  Pleural biopsy  If pleural fluid analysis is inconclusive

MANAGEMENT  Transudative effusions are managed by treating underlying causes  If effusion is symptomatic (exudative/transudative) drainage can be done to provide relief  Drain fluid slowly (max 2L/24h)  If drain large amount quickly; it can cause re-expansion pulmonary edema  Pleurodesis (pleural sclerosis)  Talc, tetracycline, bleomycin sulfate, zinc sulfate  Thoracoscopic talc pleurodesis most effective for malignant effusions  S/E: fever, chest pain, nausea  Surgery  Persistent collections and increasing pleural thickness (on ultrasound) requires surgery – pleurectomy

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Together in Delivering Excellence (T.I.D.E)

Light’s criteria To differentiate between transudate and exudate for proteins ranged in between 25 – 35g/L According to Light’s criteria, the fluid is exudate if:  Effusion protein : serum protein ratio > 0.5  Effusion LDH : serum LDH ratio >0.6  Effusion LDH level is greater than 2/3 of the upper limit of serum LDH

Pleural fluid analysis Normal pleural fluid characteristics  Clear ultrafiltrate of plasma that originates from the parietal pleura  A pH of 7.60-7.64  Protein content of less than 2% (1-2 g/dL)  Fewer than 1000 white blood cells (WBCs) per cubic millimeter  Glucose content similar to that of plasma  Lactate dehydrogenase (LDH) less than 50% of plasma Sample Clear, straw-coloured Turbid, yellow Haemorrhagic Clinical chemistry Glucose <3.3mmol/L pH <7.2 LDH ↑ (pleural:serum >0.6) Amylase ↑

Causes Transudate, exudate Empyema, parapneumonic effusion Trauma, malignancy, pulmonary infarction

Empyema, malignancy, TB, RA, SLE Pancreatitis, carcinoma, bacterial pneumonia, oesophageal rupture

Chest drain Safe triangle for chest drain insertion: 1. Lateral border of pectoralis major 2. Anterior border of latissimus dorsi 3. Horizontal line at nipple level

Indication:  Pneumothorax  Malignant pleural effusion, complicated parapneumonic effusion, empyema  Pleural effusion compromising ventilation  Traumatic haemopneumothorax Complication:  Thoracic or abdominal organ injury  Lymphatic drainage  chylothorax  Damage to long thoracic nerve of Bell  winging scapula  Arrhythmia (rare)

21

Together in Delivering Excellence (T.I.D.E) Chronic Kidney Disease (Kidney Damage >3 Months) [Khiru] HISTORY In history: i) Past UTI ii) known BP, DM, FHx iii) Drug hx (NSAIDS, gentamycin, sulphonamides, tetracyclines, vancomycin,amphotericin, cisplatin, ACEi, ARB, methotrexate, heavy metal poisoning) iv) Fatigue, weakness v) Anorexia, vomiting, metallic taste vi) Pruritus vii) Bone pain viii) Dyspnea ix) Ankle swelling Causes        

PHYSICAL EXAMINATION Signs: pallor, yellow skin pigmentation, brown nails, purpura, bruising, excoriation, increase BP,cardiomegaly, pericardial rub, peural effusion, pulmonary or peripheral edema, proximal myopathy

Acute kidney injury DM HPT Glomerulonephritis/ pyelonephritis Polycystic kidney disease Renal vascular disease Analgesic nephropathy (antipyretics, caffeine, NSAIDs) Med

Complication  Electrolyte: hyperk,hypoCa,hyperphosphatemia  Haematological: anemia, bleeding tendency (plt dysfunction)  CVS: cardiac failure, HPT, pericarditis, accelerated atherosclerosis  Neurological: drowsy, seizure, peripheral neuropathy  Metabolic/ endocrine: hyperlipid, renal osteodystrophy  GIT: anorexia, N&V, bleeding  Skin: pruritus, easy bruising

INVESTIGATION 1. Blood: Hb reduced (normochromic normocystic), ESR, Urea & electrolyte (increase urea & creatinine), glucose (DM), reduced calcium, increase phosphate, increase alkaline phosphate (renal osteodystrophy), increase PTH 2. Urine: microscopic culture & sensitivity, dipstick, 24H urinary protein

3. Imaging: renal ultrasound-renal size small, <9cm, but normal or large with CRF in DM, PKD, amyloidosis, myeloma, systemic sclerosis, asymmetric renal vascular disease

MANAGEMENT 1.Refer nephrologist treat reversible causes: relieve obstruction, stop nephrotoxic drugs, deal hypercalcemia & cardiovascular risk. 2.Lifestyle advice. Should exercise, healthy weight & stop smoking. Sodium restriction, moderate protein diet. Potassium restriction only if hyperkalemia; bicarbonate supplements to correct acidosis.

3.HPT. Target BP <140/85 (<130/80 if diabetic or >1g proteinuria/d). In diabetic kidney disease, even with normal BP, treat with ACEi or ARA. 4.CVS: statins & aspirin

4. CXR-cardiomeegaly, pleural effusion, pulmonary edema 5. Bone xray- renal osteodystrophy 6. Renal biopsy- consider if cause is unclear & normal size kidneys

5.Renal bone disease (osteodystrophy): treat if increase hyperparathyroidism. Phosphate rises in CRF, which increase PTH further, & also precipitates in kidney & vasculature. Restrict dietary phosphate. Give binders (calcichew) to bind phosphate in gut to reduce absorption. Vit D (alfacalcidol) & Ca2+ supplements reduce bone disease & hyperparathyroidism 6.Edema. High dose loop diuretics (frusemide) restrict on fluid & sodium intake

7.Restless legs. Clonazepam or gabapentin 8.Prepare for dialysis/ transplantation

22

Together in Delivering Excellence (T.I.D.E) Common/Possible Question in Exam + Answer 1.

Definitions  Azotemia: accumulation of nitrogenous product (chiefly urea) in blood as indicated by raised serum urea & creatinine  Uremia: manifestations of organ dysfunction a/w azotemia  ARF: significant deterioration in renal function occurring over hours or days, clinically manifestation as an abrupt & sustained rise in serum urea & creatinine.  CRF: permanent reduction in GFR (5-25ml/min) sufficient to produce detectable alteration in well-being & organ function. (>3 months)  ESRF: final stage of CRF (GFR<5ml/min) when pt cnt survive w/o transplantation or long term dialysis  Normal GFR:90-120ml/min

2.

Classification of CKD

3.

Indications for dialysis  Acid base imbalance (severe metabolic acidosis pH<7.2 or base excess <10)  Electrolyte imbalance (Resistant hyperK >7mmol/L)  Intoxication (ingestants/toxins-lithium)  Overload (Fluid overload not responsive to diuretics, refractory pulmonary edema, volume overload causing respi distress)  Uremic symptoms (uremic encephalopathy, uremic pericarditis)

4.

Indication for renal biopsy  Unexplained acute renal failure or chronic renal insufficiency  Acute nephritic syndrome  Unexplained proteinuria & hematuria  Previously identified & treated lesions to plan for future therapy  Systemic diseases a/w kidney dysfunction e.g SLE, Foodpasture syndrome, wegener’s granulomatosis t0 confirm extent of renal involvement & to guide management  Suspected transplant rejection, to differentiate it from other causes of acute renal failure  To guide treatment

5.

Renal Osteodystrophy  Skeletal complications of CRF characterized by: i. osteomalacia, osteitis fibrosa (caused by hypocalcemia, hyperphosphatemia & reduced synthesis of 1,25-DHCC) ii. osteoporosis iii. osteosclerosis (increased density at upper & lower ends of vertebra/ ‘jugger jersey’ spine)

6.

Causes of Anemia in CRF  Reduced renal erythropoietin production  Hemolysis & depression of erythropoiesis d/t uremia  GIT bleeding  Marrow fibrosis (osteitis fibrosa of secondary hyperparathyroidism)

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Together in Delivering Excellence (T.I.D.E) Chronic Liver Disease [Sofia] PHYSICAL EXAMINATION

HISTORY A.

Hand: Leukonychia, clubbing, palmar erythema, bruising, asterixis, scratch mark

B.

Face: Jaundice, fetor hepaticus

C.

Chest: Gynecomastia, loss of axillary hair, spider naevi

3. Changes in color of urine and stools

D.

Abdomen: Hepatosplenomegay, ascites, testicular atrophy

4. Social hx: sexual activity and alcohol history

E.

PR exmntn: Stool colour

1. Duration of jaundice 2. Ass symptoms : Dyspepsia , fat intolerance or biliary colic, arthralgia, myalgias, rash, anorexia, abdominal pain, fever, pruritus

5. Complication: bleeding tendency, easily bruising 6. Constitutional hx : LOW or LOA

INVESTIGATION 1.

FBC- low Hb (hemolysis), increased retic count, serum bilirubin, LDH & urobiliogen, decreased plasma

7. Risk factors: Recent travel history, Exposure of patients with jaundice, Parenteral exposures-transfusions, IV abuse, tattoos 8. Occupational history-contact with rats. 9. Exposure to contaminated foods or water. Recent eat shellfish (HAV), any water sport activity, source of water 10. Drug hx: Use or exposure to medication-OTC, physician prescribed, Complementary or alternative medicine-herbal or vitamin preparations or steroids. 11. Family history- hemolytic anemias, congenital hyperbilurbinemias and hepatitis.

haptoglobulin (hemolysis) 2.

FBP- bite cells, blister cells , Heinz bodies

3.

Clotting factor- deranged in liver dz

4.

Liver function tests.

5.

Viral serology for HAV, HBV, HCV

6.

Tumor marker- alpha fetoprotein

7.

Liver biopsy.- in case of hepatocellular carcinoma

8.

ERCP-in case of post hepatic jaundice

9.

Ultrasound – in case of post hepatic jaundice

MANAGEMENT For Viral Hepatitis B: 1. 2.

*basically a lot can be asked, need to rule out other causes 3.

4.

For acute hepatitis mainly supportive mx & monitor HBV markers For chronic  mostly observed unless had high viral load  antiviral: interferon, entecavir, tenofovir. Lamivudine. Response is judged by HBV DNA level, or if HBeAg is present by seroconversion to anti-HBe Pt w chronic hep should had routine lifelong f/up. Fr every 6 month or 1 year check for LFT, alpha-fetoprotein, u/s of liver High risk group shud be screen for HepB and given vaccination

24

Together in Delivering Excellence (T.I.D.E) Causes of jaundice: Prehepatic:  Malaria  Hemolytic anemia: sickle cell anaemia, G6PD deficiency,  Hereditary spherocytosis Intrahepatic:  The viral hepatitis group of infections  Alcoholic liver dz  Leptospirosis  Paracetamol overdose  Primary biliary cirrhosis  Gilbert's syndrome  Liver cancer  Autoimmune hepatitis  Primary sclerosing cholangitis

CAUSES OF HEPATOSPLENOMEGALY  Infection:  Acute viral hepatitis  Infectious mononucleosis  Cytomegalovirus  Rubella  Malaria  Schistosomiasis or filariasis  Haematological disease:  Myeloproliferative disease  Leukaemia  Lymphoma  Pernicious anaemia  Sickle cell anaemia

  

Posthepatic:  Gallstones  Pancreatic Cancer  Gallbladder Cancer Or Bile Duct Cancer  Pancreatitis

    

Thalassaemia Myelofibrosis

Metabolic disease:  Niemann-Pick disease  Gaucher's disease  Hurler's syndrome Chronic liver disease and portal hypertension Amyloidosis Acromegaly Systemic lupus erythematosus Sarcoidosis

Child Pugh score (ABCDE) Parameters Albumin (g/L) Bilirubin (micromol/L) Coagulation (Prothrombin time) Distention (ascites) Encephalopathy

1 point <34 >35 1-3 None none

2 points 34-51 28-35 4-6 Slight 1-2

3 points >51 <28 >6 Moderate 3-4

Grade A: 5-6 Grade B: 7-9 Grade C: >10 *risk of variceal bleeding is higher if score >8 *can also predict mortality: 1 year survival 5 years survival Grade A 84 % 44% Grade C 42% 21%

Hepatic encephalopathy  As liver fails, nitrogenous waste (eg: ammonia) builds up in circulation and passes to the brain, where astrocytes clear it (by process involving the conversion of glutamate to glutamine).  This excess glutamine causes osmotic imbalances and shift fluid into the cell  cerebral edema. Grading: I. Altered mood/behavior, sleep disturbance (eg: reversed sleep pattern) , dyspraxia (pls copy this 5 pointed star), poor arithmetic, no liver flap II. Increased drowsiness, confusion, slurred speech +/- liver flap, inappropriate behavior/personality change (ask family) III. Incoherent, restless, liver flap, stupor but not coma IV. Coma

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Together in Delivering Excellence (T.I.D.E) Approach To Anemia [Baisyatul] HISTORY 1.

2.

3.

4.

5. 6.

Presenting symptoms: Weakness, lethargy, shortness of breath, fatigue, postural dizziness Further history: History of GIT bleed ( hematemesis, PR bleed) Heavy menstrual blood loss Bleeding after tooth extraction Bruising, Heamathrosis Bone pain,Recurrent infection Jaundice Lymph gland swelling (lymphoma) Past medical/surgical history History of gastric surgery/malabsorption Underlying RA, Underlying OA (required NSAIDs), chronic kideney disease History of previous blood transfusion, chemotherapy Social history Strict vegetarian diets (B12 def) Exposure to toxins(benzene) risk of leukemia Alcoholic Family history- thalassemia, sickle cell dzs, colon ca, haemophilia, G6PD Drug history-NSAIDs, anticoagulant

PHYSICAL EXAMINATION General Specific Abdomen -

2.

Peripheral blood film: target cells, tear drop RBCs, poikilocytosis, blast cells, hypersegmented polymorph, pencil cells

3.

Serum iron, serum ferritin, TIBC

4.

Coagulation study: PT, aPTT, INR

5.

Factor assay for factor deficiency

6.

Hb electrophoresis for thalassemia

Surgical scar (gastrectomy, stoma) Hepatosplenomegaly

Lymph node Lymphadenopathy at neck and inguinal Complete examination PR examination Stool occult blood Hematuria

INVESTIGATION Blood investigations: 1. FBC : Hb (low) Total white cell count and differential count leukocytosis (basohilia): CML leukocytosis (eosinophilia): lymphoma lymphocytosis: lymphoma, CLL Platelet count Mean cell volume (MCV) low MCV-microcytic normal MCV-normochromic high MCV-macrocytic Reticulocyte count (reticulocytosis)

Pallor Thalassemic facies Cachexic (malignancy) Pallor of palmar, koilonychia Bruising, scratchmark (pruritus) Conjunctiva pallor, jaundice Angular stomatitis, gum hypertrophy, glossitis

MANAGEMENT 1.

Blood transfusion For actively bleed patient Severe and symptomatic anemia Hb<8

2.

Ferrous sulphate therapy IDA

3.

Nutritional therapy and dietary folate B12 and folate deficiency

4.

Splenectomy Hypersplenism

5.

Bone marrow transplant

6.

Chemotherapy : leukemia

26

Together in Delivering Excellence (T.I.D.E) COMMON QUESTIONS 1.

Anemia classification Morphology Hypochromic microcytic Thalassemia IDA Sideroblastic anemia Causes Blood loss -Trauma -Colon ca -Bleeding oesophageal varices

2.

Lab result Iron deficiency anemia Ferritin: low Iron: low Microcytic hypochromic TIBC: increased

Reference: 1. 2. 3. 4.

Xpress revision short case UM Oxford handbook Student notes medical Medscape

Normochromic normocytic Haemolytic anemia Bone marrow failure Anemia of chronic dzs

Macrocytic B12 deficiency Folate deficiency Alcoholism

Inadequate production -B12 and folate deficiency -Thalassemia, IDA -Leukemia, aplastic anemia -Renal failure

Excessive destruction -G6PD -Haemolytic spherocytosis -AIHA,malaria,sepsis

Thalassemia Ferritin: normal Iron: normal Microcytic hypochromic TIBC: normal

Anemia of chronic disease Ferritin: normal Iron: low Normochromic normocytic TIBC: normal

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Together in Delivering Excellence (T.I.D.E) Systemic Lupus Erythematosus [Aiman] HISTORY Age: 20-40 years old Gender: Female predominat (10x) +ve Family hx

Diagnostic features: (at least 4 features, or 2 features in separate occasion) 1. 2. 3. 4. 5. 6. 7. 8.

Malar rash (spared nasolabial fold) Discoid rash Photosensitivity Oral ulcer (initially painless – unless infected) Arthritis (2 or more, involve peripheral joint) Serositis (pleuritic or pericarditis – chest pain) Renal disorder (persistant proteinuria – frotty urine) Neurological disorder (seizure or psychosis – with absent of offending drugs or metabolic derangement) 9. Haematological disorder (anemia, leucopenia, thrombocytopenia) 10. Immunological (anti dsDNA antibodies, antibody to SM antigen, antiphospholipid antibodies) 11. Antinuclear antibody (ANA)

PHYSICAL EXAMINATION General Examination  Skin : pallor (anemia), petechae (thrombocytopenia), discoid rash, subacute cutaneous erythematosus  Face : butterfly rash, oral ulcer, pale conjunctiva (anemia)  Pitting oedema  generalised oedema  high BP Others  Small joint arthritis (rarely with swelling)  chorea

Differential Diagnosis : Depends on the presentation

Complication:    



HPT – due to renal disorder Thromboembolism and recurrent miscarriage (in +ve of antiphospholipid antibodies) Bleeding tendency (easy bruises) Anemic symptom (SOB, lethargy) HOW and when diagnose + on what medication, how many flare episode INVESTIGATION

Bedside: -urine dipstic : proteinuria Lab: - FBC : anemia, leucopenia, thrombocytopenia – pancytopenia (hemolytic anemia – normocytic normochromic) ESR – raised (CRP normal unless there is serositis/arthritis/infection present) - BUSE : renal function (urea – creatinine), electrolyte imbalance - Urinalysis : RBC, proteinuria, cast on the urine microscopy) Specific: - Identification of autoantibody 1. Antinuclear antibody (ANA) – if negative unlikely to be SLE unless Extractable nuclear antigen is positive (exp: Ro antigen, Sm antigen, La aantigen) 2. Anti dsDNA antibodies (+ve in 20-30%) 3. Antiphphospholipid antibody - C3 C4 level : low in active disease (during flare) - Renal biopsy : in Lupus nephritis - Skin biopsy : deposition of IgG and complement

Discoid skin lesions Erythematous macules Leukemia Nephrotic syndrome

MANAGEMENT 1. Avoid the flare Sunlight exposure (UV light) by using sunblock, clothing 2. Medical therapy Depends on severity: Mild : require analgesic and NSAIDs +troublesome cutaneous and joint symptom : Hydrochloroquine (200400mg/day) Mild-moderate disease : short course of oral corticosteroid (rash, synovitis, serositis) Acute/life-threatening disease : high dose corticosteroid (oral prednisolone 40-60mg/day) or (methylprednisolone 500mg-1g/day) + pulse IV cyclophophomide Then change to other immunosuppressive drug (azathioprine, methotrexate, ciclosporin) for the step down after cyclophosphamide or used with corticosteroid (in renal and cerebral involvement) +antiphospholipid antibody syndrome (thrombosis) : require lifelong warfarin (in recur thrombosis despite on warfarin => target INR 2.5-3.5) Diuretic Anti HPT

28

Together in Delivering Excellence (T.I.D.E) 1.

Definition : chronic, remitting and relapsing multisystem autoimmune disease in which organ and cell undergo damage mediated by tissue-binding autoantibodies and immune complex

2.

Exacerbation or flares usually follows: (all cause apoptosis of cell) o Sun exposure o Viral or bacterial infection (esp: epstein-bar virus) o Sex hormone status(on hormonal therapy, pregnancy-however there is fertility problem in sle patient and no contraindication for pregnancy unless in severe cases) o Oxidative stress o Drugs [hydralazine(anti-HPT), isoniazid(anti-TB), procainamide(anti-arrhythmia)

3.

Immunosuppressive drugs a. Cyclophosphamide(to achieve remission) MOA:cross linking with cell DNA-not specific/SE:myelosuppressive, infertility in male who receive high dose as children b. Ciclosporin MOA:interfere with activity and growth of T celss/SE: nephrotoxic, neurotoxic c. Methotrexate MOA:inhibit Dihydrofolic acid reductase(antifolate), interfere with DNA synthesis specific for S phase/SE: cranial nerve palsy, hepatotoxicity d. Azathioprine(to maintain remission) MOA:purine analogues(affect more to proliferative cells such as T cells and B celss/SE:bone marrow suppression

4.

Exacerbation, complete remission and chronic persistant condition. Early death associated with renal, cerebral or infection. Later age stroke and coronary artery disease become more prominent. Deformity due to joint destruction is rare compare with OA or RA. Increased long term risk to developed lymphoma.

5.

Prolong steroid used side effect. Refer corticosteroid drugs note.

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Together in Delivering Excellence (T.I.D.E)

PAEDIATRIC

Notes

30

Together in Delivering Excellence (T.I.D.E) Acute Exacerbation of Bronchial Asthma (Alliah) HISTORY Definition Chronic airway inflammation leading to increase airway responsiveness leads to recurrent episodes of wheezing,SOB,chest tightness & coughing particularly at night and early morning. Important history  Current sxpattern of sxpresent tx (response & compliancy)  Previous hosp.admission  Typical exacerbation  Precipitating factor  Infection (URTI)  Non-compliance to drug  Home/school environment (allergen:cat,bedsheet,smoking,insects)  Predisposing fctr  Hx of atopy (eczema, allergic rhinitis, conjunctivitis)  Aggravating fctr  Rhinosinusitis  GERD  Sensitive to NSAIDs (esp.aspirin)  Family hx of allergy and asthma  Personal impact to lifestyle  School performance : attendance,academic,co-curiculum  Impact to family  Financial?parents quarrel?  Who take care pt/who send pt to hosp during attack?

PHYSICAL EXAMINATION      

Tachypnea Tachycardia Cough Drowsy Wheezing, rhonchi Prolonged expiratory phase

As attack progress  Cyanosis  Tight chest  Sternal retraction  Agitation  Inability to speak  Tripod sitting position  Diaphoresis  Pulsus paradosus Signs of chronic illness  Barrel chest  Generalized polyphonic expiratory wheeze  Prolonged expiratory phase  Harrison’s sulci  Crepitation (d/t segmental atelectasis)  Reduce liver and cardiac dullness  Eczema/dry skin  Hypertrophied turbinates MANAGEMENT

Complication  Status asthmaticus  Respiratory failure  Pneumothorax  Lung collapse INVESTIGATION

a) Lung function test : PEFR > 5y/o or Spirometry b) Brochodilator reversibility test (improve 10-15% post brochodilator) c) Skin prick test (to aid dx of atopy) d) CXR - particularly to exclude foreign body or chronic chest infection or to exclude complications in severe acute episode

Principle To allow child to lead as normal life as possible by :  Controlling sx  Prevent exacerbation  Optimize pulmonary function  Minimize treatment and side effects Drug Reliever (Short-acting B-agonist ) Controller/preventer : Corticosoteroids, LABA,Combination (Inhaled c/steroid+LABA) , anti-leukotrienes Acute     



Close monitor pulse,color,PEFR,ABG & SpO2 for at least 4H High flow oxygen via face mask Nebulised bronchodilator (salbutamol) Prednisolone 1-2mg/kg body wt orally (max 40mg) If life-threatening features present : - give IV aminophylline 5mg/kg over 20min followed by maintenance infusion then IV hydrocortisone 100mg 6hrly - add Ipratropium bromide 0.25mg to nebulised B-agonist Reassess patient with pulse oximetryresponse to tx

31

Together in Delivering Excellence (T.I.D.E) Common/Possible Question in Exam + Answer Assessment of severity Intermittent

Persistent

Mild

Moderate

Severe

Monitoring (each f/up) 1)

Assessment of asthma control  Interval sx  Frequency & severity of acute exacbtn  Morbidity 2’ asthma  Quality of life  PEFR/FEV1 monitoring

2)

Compliance to asthma therapy  Frequency  Technique

3)

Asthma education  Understanding asthma in childhood  Reemphasize compliance to therapy  Written asthma action plan

   

Daytime sx Nocturnal sx Exercise induced sx Exacerbation affect sleep & activity  PEFR/FEV1

< 1x a week < 1x a month NO NO Normal lung fx > 1x a wk > 2x a mth YES 1x a month >80% Daily > 1x a wk YES > 2x a mth 60-80% Daily Daily Daily > 2x a mth <60%

32

Together in Delivering Excellence (T.I.D.E) Rheumatic Fever [Sofia] HISTORY 1. History of preceded sore throat 2. Risk factor: low socioeconomic status, overcrowding, poor housing, genetic susceptibility 3. Carditis Pericarditis: audible friction rub 4. Arthritis: migratory polyarthritis, large joints usully affected (shoulder, elbow, knee, ankle), a/w fever 5. Syndenham chorea (SC): are involuntary movements, hypotonia, and mild muscular weakness. Chorea can be generalized or unilateral, predominantly involving the face, hands, and arms. Movements are present at rest, aggravated by stress, and usually cease during sleep. interfere with volitional movements and result in a clumsy gait, dropping and spilling, and explosive bursts of dysarthric speech. 6. Erythema marginatum: bright pink macule/ papule that spread outward in circular serpiginous pattern, multiple, appear at trunk / proximal extremities, rarely distal, never on face, non pruritic, painless, blanch on pressure, brought out by warmth 7. Subcutaneous nodules: non pruritic,painless round, firm, freely movable, elbows, wrist, knee, ankle, Achilles tendon, on extensor surface

PHYSICAL EXAMINATION General: Fever, rashes, nodules, involuntary jerky movement, protruding of tongue revealed ‘bag of worm’ CVS: Murmur, pericardial rub, cardiomegaly, sign of cardiac failure Examination of joints involved: red, swollen, warm, synovial aspiration revealed leukocytosis To test for syndenham chorea: pronator sign when raising hand above head, if + pt may pronate 1 or both hand,spoon configuration occur when hand are extended, milking grip elicit by putting ur finger at pt grip hand DDX -

JRA Leukemia SLE INVESTIGATION

1) 2) 3) 4) 5)

FBC- leukocytosis, ESR/CRP – raised, throat swab Anti-streptolysin O titre- >240 Todd U Anti-DNAase B Imaging : ECG, CXR, Echo- to look for carditis Histo: Aschoff bodies in heart (granulomatous structures consisting of fibrinoid change, lymphocytic infiltration, occasional plasma cells, and abnormal macrophages surrounding necrotic centres)

Anitschkow cells are enlarged macrophages found within granulomas (called Aschoff bodies) associated with the disease. Ovoid nucleus and chromatin that is condensed toward the center of the nucleus in a wavy rod-like pattern

MANAGEMENT Aim: to suppress inflammatory response to minimize cardiac damage, provide symptomatic relief, & eradicate pharyngeal infection 1. Bed rest until acute phase protein return normal 2. Anti inflammatory: if no/mild carditis- oral aspirin 80-100mg /kg/day in 4 doses for 4 weeks, taper over 4 weeks If pericarditis/ moderate to severe carditis- oral prednisolone 2mg/ kg/day in 2 divided doses for 4 weeks, taper w addition of aspirin as above 3. Anti failure: diuretics & ACE inhibitors 4. Anti streptococcal therapy: IV C.Penicillin 50 000 U/kg/dose 6H, give oral erythromycin if allergic to penicillin 5. Chorea: control w haloperidol or valproic acid, diazepam Secondary prophylaxis  IM benzathine penicillin every 3 – 4 weeks (<30 kg – 0.6 mega unit, >30kg – 1.2mega unit)  Oral penicillin 250 mg twice daily  If allergic to penicillin give oral erythromycin 250mg twice daily Duration of prophylaxis  Until age of 21 or 5 years after last attack of ARF whichever was longer,  Lifelong if got carditis or valvular involvement * The main symptoms of SC are believed to arise from an imbalance among the dopaminergic system, intrastriatal cholinergic system, and inhibitory gamma-aminobutyric acid (GABA) system. Evidence of this imbalance has been suggested by the successful control of chorea by dopaminergic antagonists and valproic acid, a drug known to enhance GABA levels in the striatum and substantia nigra.

33

Together in Delivering Excellence (T.I.D.E) RHEUMATIC FEVER- d/t delayed immunologic rxtn of group A Beta hemolytic streptococcal infection of pharynx HISTORY 1 Required Criteria and 2 Major Criteria and 0 Minor Criteria 1 Required Criteria and 1 Major Criteria and 2 Minor Criteria Required criteria: Evidence of antecedent Strep infection: ASO / Strep antibodies / Strep group A throat culture / Recent scarlet fever / antideoxyribonuclease B / anti-hyaluronidase Major criteria (CASES)  Carditis  Arthritis  Subcutaneous nodules  Erythema marginatum  Syndenham chorea Minor      

Fever Raised ESR/CRP Arthralgia Prolonged PR Leukocytosis Previous Rheumatic Fever

Evidence of carditis: cardiomegaly, heart failure, pericarditis, tachyC > fever (>10 per celcius), murmur /MR, MS, AR

34

Together in Delivering Excellence (T.I.D.E) Infective Endocarditis [Baisyatul] HISTORY Presenting complain Symptoms of systemic infection ( fever, malaise, anorexia, loss of weight, headache, myalgia, arthralgia) Congestive heart failure ( SOB, orthopnoea, PND, leg swelling) Emboli symptoms ( neurological deficit, haematuria, acute renal failure) Predisposing factor: 50% occur in normal valve (acute IE) Dental procedure Dermatitis IVDU (subacute IE) Prosthetic valve Chronic rheumatic valvular disease Nosocomial infection (IV line) Elderly

INVESTIGATION For diagnosis: DUKE criteria 1. -

Blood investigations FBC (normocytic normochromic anemia, leucocytosis, high ESR and CRP) Blood culture n sensitivity ( 3 samples from different sites)

2. -

Urine FEME Microscopic haematuria

3.

CXR (cardiomegaly)

4.

ECG (prolonged PR interval, regular rhythm)

5.

Echocardiography- transthoracic or transesophageal (to look for vagetations) *transesophageal more sensitive, better for visualizing mitral lesion

PHYSICAL EXAMINATION General examination Thin, poor nutrional status (anorexia) Septic sign ( feverish, tachycardia) Finger clubbing Splinter hemorrhage Osler’s node (tender nodules on finger pulp) Janeway lesion (non tender macule on palms or sole) Pale conjunctiva, subconjuctival petechiae Dental hygiene Specific examination (chest) Changing cardiac murmur Cardiac failure ( gallop rhythm ) Pericardial rub TR/MR Lung crepitations (abdomen) splenomegaly (if emboli and cause abscess formation/ heart failure) Complete examination by Fundoscopy to look for Roth’s spot (central pale area with surrounding) Urine dipstick to look for haematuria (microscopic) MANAGEMENT General management Asses ABC Heart failure management (oxygen, diuretics,monitor input output chart) Antibiotic therapy Duration 2-4 weeks Empirical therapy: benzylpenicillin + gentamicin Adjust according to culture Streptococci (as above) Staphylococci (cloxacillin or vancomycin + gentamicin) Indication for surgery Persistent bacteremia or fever despite optimal antibiotic Extensive valve ring infection Prosthetic valve endocarditis esp staph aureus Recurrent ep of systemic embolism

35

Together in Delivering Excellence (T.I.D.E) COMMON QUESTION 1.

Causes of IE Strep viridans (most common), staph aureus, enterococcus

2.

Diagnostic criteria for IE: DUKE criteria Major criteria:  Positive blood culture Typical organism in 2 separate culture OR Persistently +ve blood culture (>12hour apart)  Evidence of endocardium involved +ve echo ( vegetation, abscess, dehiscence of prosthetic valve) OR New valvular regurgitation (change in murmur not sufficient) Minor criteria:  Predisposing heart condition or IVDU  Fever >38  Vascular or immunological signs  Positive blood culture (that does not meet major criteria)  Positive echo (that does not meet major criteria) How to diagnose: 2 major OR 1 major and 3 minor OR All 5 minor criteria (if no major criteria)

3.

Prophylaxis antibiotic According to AHA guideline, only high risk patient should be considered giving prophylaxis for dental procedure Because the risk associated with adverse effect of antibiotics usually outweighs the benefit of prophylaxis 2008 Cochrane review found there was no evidence prophylaxis antibiotic treatment was either effective or ineffective at preventing IE in at-risk population undergoing invasive dental procedure According to OXFORD handbook~ also explain the same High risk group that need prophylaxis: Prosthetic cardiac valve Congenital heart disease Oral amoxicillin 2g single dose 30-60 minutes before procedure st nd If allergic give 1 or 2 cephalosporin

4.

Classification

-

ACUTE ENDOCARDITIS Sudden onset, progress rapidly(days) Affect normal valve Common organism: Staph. Aureus, GBS

Reference: 1. 2. 3. 4.

Oxford handbook of clinical medicine Express revision short case UM Sarawak handbook Medscape

SUBACUTE ENDOCARDITIS Insidious and progress slowly( weeks to months) Affect abnormal valve Common organism: strep. Viridans, -

PROSTHETIC VALVE ENDOCARDITIS After valve replacement Early PVE occur within 3 months Late PVE occur after 3 months Common organism: strep. Viridans, staph. Aureus, enterococci

36

Together in Delivering Excellence (T.I.D.E) Glomerulonephritis/ Nephrotic Syndrome [Aiman] HISTORY Age: 6-10years old Acute nephritis syndrome: - Oedema-facial puffiness - Hematuria-tea coloured - Oligouria-reduce urine - HPT-headache, burring of vision - Azotemia-fatigue, reduce alertness, confusion(high urea and creatinine) - Post infection AGN: impetigo(24w), pharyngitis (1-2w), cellulitis Rule out other causes: - (Wegener granulomatosis) Sinusitis, nephritis, pulmonary infiltration - (HSP) joint pain, swelling, abdominal pain and purpura - (SLE) arthralgia, malar rash, oral ulcer Complication:  HPT(encephalopathy-seizure)  APO(SOB)  ARF

PHYSICAL EXAMINATION Nephrotic syndrome – clinical syndrome of massive proteinuria - Oedema-generalized swelling (periorbital, scrotal, vulva, leg, ankle swelling and abdominal distension) SOB - Proteinuria-frotty urine Rule out other causes: - Post strep AGN - SLE *after rule out this two causes then we can say it is idiopathic (most common)

Urinalysis -RBC cast-hematuria vs hemoglobinuria

*culture and sensitivity: to detect any growth when UTI is suspected as cause or aggravating factor in both nephron and nephri

Gross proteinuria(>2+) -ve

- Proteinuria:>1gm/m2/d - Early morning(for more concentrated urine) protein creatinine (>3.5mg/mg) - Quantitative urinary protein excretion i)spot protein creat ration ii)24 hr urine protein

Blood investigation *both - FBC-anemia, leukocytosis - BUSE +creatinine – renal f(x) (high urea, high creat)

- Serum cholesterol :hypercholesterolaemia - LFT (se albumin): hypolabuminaemia (<25g/dL)

Post strep: bacteriological and serological: ASOT- >200, increase anti DNAse B, throat and skin swab. Complement:C3 reduce, C4 normal

SLE (for both to rule out) -ANA/anti dsDNA:+ve in SLE Complement: both C3 and C4 reduce

Imaging: ultrasound of kidney Special: renal biopsy

Differential Diagnosis : i) Henoch-schonlein purpura ii) SLE iii) Vasculitis (Wegener granulomatosis) iv) Rapidly progress Glomerulonephritis

Complication:  Hypovolemia (fluid go to rd 3 space)  Primary peritonitis  Thrombosis

INVESTIGATION Urine dipstic - Protein +ve(usually>2+) - Hematuria +ve - Nitrite (positive is evidence of infection)

Nephritic - Altered consciousness level - Oedema but less severe than nephritic th - BP-Hypertension(>90 centile) - Scar at limb

Nephrotic - Leuconychia-due to hypoalbuminimia - Generalized oedema-look at face, limb, genitalia - Distended abdomen with ascites - Patient with generalized oedema with cold peripheries, poor pulse volume, hypotension – hypovolemia - With fever and abdominal tenderness – peritonitis Differential Diagnosis : SLE Post strep AGN

MANAGEMENT Nephrotic chart (fluid intake, Urine output, BP, ddaily weight, urine protein) 1. Fluid restriction (to control oedema + circulatory overload during oliguric phase) -no added salt diet 2. Diuretic : give frusemide 3. Antibiotic: penicillin V x 10/7 4. Look for complication a) HPT - encephalopathy(seizure) *control the BP - heart failure (APO) *oxygen, diuretic, fluid restriction b) ARF (acidosis, uremia, hyperkalemia[cardiac toxicity]hyperphospahtemia, hypocalcimia) *monitor renal function  Follow up fpr 1 yr (3 monthly)  Monitor BP, urinalysis & renal function  Repeat C3 if not normalized during discharge (after 6 wk)  Short term outcome: excellent (mortality <0.5%)  Long term outcome: 1.8% progress to CKD

1. Confirm the diagnosis – fulfill 4 criteria(gross proteinuria, oedema, hypoalbuminimea, hypercholesterolemia) 2. Exclude other causes (SLE, PSAGN) then diagnose as idiopathic 3. Normal protein diet, with adequate calories, no added while oedema 4. Careful assessment of haemodynamic status(hypo vs hypervolemic) -fluid restriction only during chronic oedematous state 5. Penicillin V:during diagnosis and relapse diuretic: no need in steroid responsive 6. Steroid therapy 7. Tx complication a) Hypovolemia: Infuse human albumin(no frusemide) b) Primay peritonitis:penicillin rd and 3 gen cephalosphorin c) Thrombosis: anticoagulant

37

Together in Delivering Excellence (T.I.D.E) COMMON QUESTION 1.

Indication for renal biopsy: a. Steroid resistant nephrotic syndrome (not respond to 4 week treatment of 60mg/m2/day prednisolone) b. Features suggestive non-minimal change NS c. Persistant HPT, renal impairment with or without or gross hematuria d. Severe acute renal failure require dialysis e. Feature suggestive non PSAGN f. Delayed resolution(PAGO): i. Persistant Proteinuria:>6month ii. Azotemia:>3w iii. Gross hematuria:>3w iv. Oliguria:>2w

2.

Steroid therapy: a. To induce remission (rule of 4) i. 4weeks: 60mg/m2/day ii. 4weeks: 40mg/m2/EOD iii. 4month: reduce 25% dose monthly *remission: urine dipstick trace or nil for 3consequtive day b.

In relapse (urine protein >40mg/m2/hr orurine dipsticx >or equal to 2+ for 3 consequtive days) i. 60mg/m2/day until remission ii. 40mg/m2/EOD for 4weeks *if patient has UTI with no gross oedema, steroid therapy is not necessary, treat the infection

c.

Frequent relapse (2 or more relapse in 6 month or 4 or more in 1 year) i. 60mg/m2/day until remission ii. 40mg/m2/EOD for 4weeks iii. Tapered down the dose 2 weekly and keep as low an alternate dose as possible for 6 months. (if relapse during therapy, treat as relapse)

d.

Steroid dependent (2 or more relapse during steroid taper or within 14 days cessation of steroid) i. If non-toxic: reinduce steroid ii. If stroid toxic (short stature, striae, cataract, glaucoma, severe cushingoid features: consider cyclophosphamide therapy 1. For steroid dependent NS with steroid toxicity 2. Counsel parent about effectiveness and SE(leucopenia, gonadal toxicity, hemorrhagic cystitis) 3. Need to monitor FBC and urinalysis 4. Dose:2-3mg/kg/day x 8-12weeks

3. Watch out for adrenal crisis (in long term corticosteroid therapy when they undergone situation of stress)

38

Together in Delivering Excellence (T.I.D.E) Thalassemia [Amy] HISTORY **Autosomal recessive o First presentation – age, pallor/jaundice/FTT  B thal major : 3-6 months  B thal intermedia : later than 18m  Alpha thal intermedia : at birth o Family history – consanguinity, genetic screening done? o Transfusion – pre & post Hb level, condition, no of PC, frequent, transfusion reaction, Hep status  Major : every 3-4 weeks  Intermedia :when symptomatic o Iron chelation therapy (Desferal) – when started o Regular follow up – growth chart, blood level, ferritin level o Any admission d/t complication o Splenectomy done? On Penicillin? o Paediatrics history o Diet history – should avoid high iron diet o Complications  Iron overload : hypothyroidism, DM, CLD(cirrhosis), cardiomyopathy(cardiac haemosiderosis – sterile pericarditis, arrhythmia), Short stature –decreased puberty growth spurt, Delayed puberty  Premature bilirubin stone formation (cholelithiasis)  HypoPTH  Vision & Hearing – Desferrioxamine toxicity o

Social Hx : disease impact on children/family  Academic performance, school missed, able to take part in PJK  Body image, pubertal anxiety  Financial consideration – transport, other cost Understanding of disease, perception, compliance INVESTIGATION 1. FBC MCHC anaemia Leukopenia, Thrombocytopenia – if hypersplenism 2.

Peripheral Blood Film / FBP Microcytic hypochromic RBCs Anisocytosis, poikilocytosis, target cells, fragements(IV haemolysis)

3.

Haemolysis marker Reticulocyte count high LDH elevated

4.

LFT – deranged liver enzyme (cirrhosis), unconjugated bilirubin raise

5.

Hb Electrophoresis Beta thal : HbA2, HbF elevated, decreased hbA Alpha thal : HbA, HbA2, HbF decreased, HbH band in HbH disease

6.

7.

Genotyping Beta thal : point mutation, Alpha thal : deletion mutation

Serum Ferritin Increase – iron overload **iron chelation tx when Se Ferritin >1000mcg/L

PHYSICAL EXAMINATION General Examination o Growth : height, weight-short stature, sexual development o Skin : pallor/jaundice/bronze-iron overload o Thalassemic facies : frontal bossing, prominent maxilla Abdomen o Desferal scar – pigmented, round, no lipodystrophy o Surgical scar – open/lap o Hepatosplenomegaly Chest o Heart failure – displaced apex, murmur, bibasal crept Others o Sign of CLD o Signs of hypothyroidism o Screen visual acuity o Tanner staging

Diagnosis : (Beta thal major/HbE/HbH) , transfusion dependant/not, Clinically thal major/intermedia, ongoing problem&issues

MANAGEMENT Blood transfusion o Thal intermedia or major Chelation Therapy o When Se Ferritin reach >1000mcg/L o Deferoxamine (Desferal) Via slow subcutaneous infusion pumps (6-8h), 6 days a week S/E : ototoxicity, ophthalmotoxicity o

Deferiprone Orally TDS, S/E : agranulocytosis

Splenectomy Indication : increase in red cell transfusion requirement by 50% or more over one year Vaccine :H. Influenzae, Strep Pneumoniae, Neisseria meningitides Prophylaxis : Penicillin Cholecystectomy – if stone present Screening for endocrinopathies o Monitor pubertal development o DM screening – early diagnosis, good control o Thyroid screening – hypothyroidism Ix : Ca/Mg/PO₄ (hypoPTH), TFT, FBS, OGTT, LH/FSH

39

Together in Delivering Excellence (T.I.D.E) 1.

2. Cause of jaundice is thalassemia pt o Aplastic crisis/haemolytic crisis o Gallstone o Infection – Hep B, CMV, EBV o Cirrhosis o Other unrelated causes eg autoimmune, drugs etc 3. Transfusion reaction

40

Together in Delivering Excellence (T.I.D.E) Leukemia [Hidayah] HISTORY Definition Acute leukemia : Heterogenous group of malignant disorder which is characterised by uncontrolled clonal & accumulation of blast cells in the bone marrow & body tissues. Epidemiology  Commonest within 2-10 years (Peak : 3-4 years)  Incidence decreases with age AND rise >40 years.  In children - most common malignant disease (85% ) History 1. Common complaint  Fever  Pallor  Lethargy, malaise  Petechiae or ecchymoses,nosebleed  bone pain, joint pain – refuse to walk,limping gait  CNS disease (mets to CNS) -Headache, vomiting, Abnormal sensorium, Hypothalamic symptom(abn wtgain&hyperphagia)  Testicular swelling 2. Family hx of blood malignancy (leukemia,lymphoma, etc) 3. DDx i. Infection a. Dengue (retro-orbital pain,rashes,myalgia, from dengue area) b. TB (contact with TB pt,night sweats) c. Epstein-barr virus (infectious mononucleosis) hx of sore throat d. OM (fever, bone pain, swelling, redness, focal painful swelling,hx of trauma) e. Rheumatic fever (C-carditis, A-arthritis (polymigratory), S-subcutaneous nodule, E-erythema marginatum, S-sydendham chorea) ii. Non-infectious a. Juvenile rheumatoid arthritis(fever, morning stiffness,rash) b. Haemophilia (bleeding tendency) c. ITP(preceding URTI/viral infection) d. Aplastic anemia (exposure to chloramphenicol, radiation) iii.Malignant disease (Osteosarcoma, Ewing sarcoma) (constitutional sx) iv. Trauma

INVESTIGATION 1. FBC Anemia : normochromic normocytic Thrombocytopenia WBC : normal,leucopenia or leukocytosis 2. Peripheral blood film/smear

3. Bone marrow aspiration (confirm dx) i. Hypercellular ii. Presence of blasts cells iii. Normal haemopoiteic cells are suppressed - FAB classification : presence >30% blasts in bone marrow - WHO classification : presence >20% blasts in marrow 4. Cytochemistry staining Myeloperoxidase (+AML) Periodic acid Schiff (+ALL) Acid phosphatase (+ALL) 1. Immunophenotyping - differentiate T-ALL and B-ALL -Monoclonal antibodies used : AML : CD13, CD33 ALL : B-ALL CD10, CD 19, CD22 T-ALL CD3, CD7 2. Cytogenetics or karyotyping -prognostic value -PCR, FISH, DNA microarrays

MANAGEMENT General 1. Blood & blood product support 2. Insertion of Central venous catheter-better access for chemotherapy, blood products, AB 3. Prevention of vomiting 4. Prophylaxis & treatment of infection 5. Prevention of tumor lysis syndrome 6. Social & psychological support

PHYSICAL EXAMINATION i. ii. iii. iv. v. vi. vii.

Pallor (palm,sole&conjunctiva), bruises Lympadenopathy (cervical, inguinal) Hepatosplenomegaly Painless testicular enlargement CNS involvement (↑ICP –blurring vision,diplopia) Rashes, hess test (dengue) Examination of affected bone (JRA,OM,hemophilia)

Specific 1. Chemotherapy a. Induction : 4-6w initial treatment phase for rapid reduction of leukemic burden b. Consolidation(intensification) c. Maintainance d. CNS prophylaxis : prevent leukemia relapse in CNS (IT methotrexate) 2. Stem cell transplant  Peripheral/bone marrow  Allogenic/autologous

41

Together in Delivering Excellence (T.I.D.E) 1.

Principles of leukaemogenesis



Neoplastic cell is pluripotent cell or early progenitor cell

1. 2. 3.

Dysregulation of cell growth Proliferation of the leukemic clone Blocked of differentiation at an early stage

2.

Causes of Leukemia 1. Hereditary Factors ( Fanconi’s anaemia, Down’s syndrome, Ataxia telangiectasia) 2. Radiation, Chemicals exposure (Benzene, herbicides&pesticides, smoking) & Drugs (alkylating agents,chloramphenicol) 3. Virus related Leukemias (Retrovirus - HTLV 1 & EBV) 4. Pre-existing blood disorders (myelodysplastic disorders,Myelofibrosis, aplastic anaemia, paroxysmal nocturnal haemoglobinuria ,CML)

3.

Prognostic for ALL Age Sex TWBC Chromosomal abn

4.

Good 1-10 Female <50 000 Trisomies (4,10)

Poor <1; >10 Male >50 000 t(9,22)

Complication 1. Tumor lysis syndrome (TLS): massive tumor cell deat with rapid release of intracellular metabolites →exceeds excretory capacity of kidney→ acute renal failure 2. Can occur b4 chemo is started 3. Characteristic i. Hyperuricemia d/t release of intracellular purines ii. Hyperkalaemia d/t tumor cell lysis or renal iii. Hyperphosphatemia lead to tissue damage (renal failure,pruritus,gangrene) iv. Hypocalcemia

5.

Prevention of TLS  Hydration -Double hydration (3000ml/m2/day)  Alkalization of urine (add NaHCO3 into IV fluid, keep urine pH7-7.5)  Allopurinol (10mg/kg/day-max300mg/day)  KIV delay chemotherapy until metabolic status stabilized  Close monitoring electrolyte –BUSE,Ca, PO4, uric acid, creatinine, bicarb  Strict i/o chart

6.

Chemotherapy drugs &side effect

42

Together in Delivering Excellence (T.I.D.E) Haemophilia (Bleeding Disorder) [Hamizah] HISTORY 1.

Sign and symptoms (Bleeding, Bruises) Site of bleeding Frequency Onset (Spontaneous?) or caused by trauma? Does it follow a viral infection (ITP) Is it acute, chronic or recurrent? Associated with rash like petechiae or purpura? -

2. 3. 4. 5.

6. 7.

8.

9.

Joint bleeding signs: tingling, cracking, warmth, psin, stiffness and refusal to use joint. How severe the joint problem. Any symptoms of headache, stiff neck, vomiting, lethargy, irritability suggesting CNS bleed? Any symptoms of hematuria, renal colic?

Any bleeding after immunization, circumcision, epistaxis, hematuria, dental extraction or operation? Past history of requiring blood transfusion. Hx of easy bruising, heavy menses History of concomitant illness eg: chronic inflammatory disorder, liver disease, autoimmune disease, hematologic malignancies and allergic drug reactions. Past hx : Hepatitis, HIV/AIDS, SLE Family history : Consanguineous marriage Bleeding disorder in family Severity of bleeding disease in family Drug history Alcohol Warfarin Steroid NSAIDS Anticonvulsant Complications Symptoms of anaemia & SHOCK

INVESTIGATION Laboratory FBC: Hb (anaemia?), WCC, platelet -

Bleeding time Raised in vWB disease, platelet disorder, on aspirin

-

vWB factor

-

Coagulation profile aPTT prolonged in liver disease, haemophilia, prothrombin time prolonged in liver disease or anticoagulant

-

Assay for Factor 8, factor 9

PHYSICAL EXAMINATION General Pallor Lymphadenopathy Hepatosplenomegaly testicular infiltration (enlargement) Bone tenderness Renal infiltration Skin infiltration (presence of one or more of above suggests leukaemia) Type of bleeding: Bruises: site, size, number, colour Purpura: palpable in HSP Petechiae: sites (buccal mucosa, palate, tongue, retina), no of lesions  indicates platelet or vascular disorder Examine if bleeding occurs in:  Musculoskeletal system (joint) – look for tenderness, pain with movement, decreased range of motion, effusion and warmth.  CNS – look for altered mental state, meningism and abnormal neurological findings.  Genitourinary system – bladder spasm/ distension/ pain and costovertebral angle pain  Retinal examination – to dx intracranial haemorrhage Signs of significant blood loss:  tachycardia  Tachypnea  Hypotension on standing

MANAGEMENT If shock: Resuscitation Lifestyle changes: Avoid violent contact sport Avoid aspirin and NSAIDS that affect platelet function For toddler, safety measures include anticipatory guidance including the use of car seats, seat belt and bike helmets If minor bleeding: pressure and elevation of the part. Desmopressin raises factor 8 levels. If major bleeding: increase factor 8 levels to 50% of normal If life threatening bleeding: need 100% eg: recombinant factor 8. Early appropriate replacement therapy Factor VIII prophylaxis program (aim is to convert severe disease into moderate one. WHO recommendation is Factor VIII 25-40 IU/kg on alternate days a week)

43

Together in Delivering Excellence (T.I.D.E) Common/Possible Question in Exam + Answer 1.

What is hemophilia? Hemophilia is X-linked recessive disorder. Hemophilia A is factor 8 deficiency while hemophilia B(Christmas disease) is factor 9 deficiency.

2.

The common site of bruising: anterior tibia and knee.

3.

Ddx -

Coagulation disorder: Haemophilia A&B, von Williebrand disease Platelet disorder: ITP Vascular cause: Marfan syndrome, SLE Laukaemia

4.

What are the characteristics of abnormal bruising? a. Large bruises that raised and out of proportion to theinjury that caused it b. Unexplained bruises that occur without history of trauma c. Bruises that seems last more than few weeks d. A family histry of bleeding or easy bruising in the family suggest genetic bleeding such as von Williebrand disease and haemophilia. e. Any bruises in an infants who has not started to crawl, cruise or walk f. Bruises in unusual places eg: chest, back, hand, ear, face and buttock. g. Bruises associated with burn, scald, fracture, h. Excessive bleeding after dental procedure or surgery i. Epistaxis that last for longer than 15 minutes after proper tx with direct pressure j. Menstrual periods longer than 7 days or heavy for more than 3 days.

5.

What are primary causes of death in patients with severe haemophilia? The main cause is HIV/AIDS acquired from treatment with contaminated blood product Second is intracranial haemorrhage Other cause: cirrhosis and obstruction of the airways

6.

What are coagulation pathways?

7.

How can synovitis be differentiated from an acute haemarthrosis? The swelling of synovitis does not respond to a single infusion of factor. The joint is less painful than that of acute hemarthrosis and the range of motion is frequently not limited

44

Together in Delivering Excellence (T.I.D.E) Diabetes Mellitus Type 1 (Paeds) [Nur Diana] HISTORY

PHYSICAL EXAMINATION

*Etiology: i) Result from autoimmune destruction of insulinproducing Beta cells (islets) of the pancreas. ii) Can also result from rare inherited defects in mitochondrial genes

   

Assess hydrational status, nutritional well-being Assess vital signs; tachycardia, tachypnea Monitor growth & development; plot growth chart; do developmental assessment after 5 years of onset diabetes- evaluate for complications

*Epidemiology: i) Genetic determinants play a role in the susceptibility to DM1 ii) Siblings/offspring of the patient have a risk of 3-6% to get DM1 iii) identical twin 30-60% at risk to get DM1 *Sign & Symptom: Early  Polyuria  Polydipsia  Polyphagia  Weight loss

   

Late Vomiting Dehydration Abdominal pain Drowsiness

*Cx: i) DKA; may leads to cerebral edema. ii) Dehydration iii) Long term- retinopathy, nephropathy, neuropathy and macrovascular disease. INVESTIGATION

1. 2. 3. 4. 5. 6.

Random blood glucose > 11.1 mmol/L Fasting blood glucose > 7.o mmol/L (no calori intake at least 8 hours) OGTT rarely needed in children Urine dipstick; check for ketone, glucose level Serum TSH; 1x/year- early detection of autoimmune disease. blood lipid profile – hyperlipidemia

**Ix. to look for any complications is ordered accordingly to the patient history and clinical presentation.

MANAGEMENT

A. B. C. D. E. F. G. H. I.

Insulin therapy Home blood glucose monitoring Diet Exercise Education Monitor hba1c Monitor growth and development Screening for celiac disease Refer to diabetes support group

45

Together in Delivering Excellence (T.I.D.E) Frequently asked questions (FAQs) 1.

What is meant by somogyi phenomenon?

It occurs when patient increase evening dose of insulin. Cause nocturnal hypoglycemia. Lead to exaggerated counter-regulatory response and rebound hyperglycemia in the next morning. 2.

How to diagnose DM1? i) Symptoms + random plasma glucose > 11.0 mmol/L ; OR ii) Fasting plasma glucose > 7.0 mmol/L; OR iii) 2-hours post prandial > 11.0 mmol/L during an OGTT.

** (i) or (ii) or (iii) 3.

When should we test for ketone? a) Illness with fever and/or vomiting b) Persistent blood glucose level > 14 mmol/L; in an unwell child, young child, insulin pump users, or patient with history of prior episodes of DKA. c) Persistent polyuria with elevated blood or glucose in urine d) Drowsiness e) Abdominal pain or rapid breathing

46

Together in Delivering Excellence (T.I.D.E) Epilepsy (Recurrent, Unprovoked Seizure) [Khiru] HISTORY -

What pt doing before fits? Duration of fits st 1 episode? Date of last seizure A/w fever? (febrile seizure) Up rolling of eyeball, stiffening of limbs, jerky movement Postictal lethargy/ neurological deficits Urinary incontinence, tongue biting, trauma while falling down Perioral cyanosis How seizure stopped? (spontaneously or by med) If multiple seizure regain consciousness aft each seizure? Total duration? (tro status epilepticus) Family history of epilepsy, dysmorphism, down’s syndrome, frequent abortion Obstetric history (fetal distress, birth trauma, instrumental delivery, neonatal jaundice) Current AED AED history (max dose, efficacy, reason to stop) Previous eeg, mri findings INVESTIGATION nd

Recommend only if 2 afebrile seizure occur 1. FBC 2. RBS 3. BUSE+ calcium+ Mg 4. Lumbar puncture if suspect brain infection 5. Toxicology if suspect drug exposure st 6. EEG recommended after all 1 unprovoked seizure 7. Neuroimaging indication for: persisting postictal deficit, condition of child not returned to baseline within several hours after seizure 8. Anticonvulsant not indicated unless: Neurological deficit in child Unequivocal epilectic activity on eeg Risks of having further seizure unacceptable Brain imaging show structural abnormality

PHYSICAL EXAMINATION -

-

Look for dysmorphism Neurocutaneous sign (cafe au lait, axillary freckles, Lisch nodules, bony lesion, optic glioma, relative, neurofibroma) Complete CNS & developmental examination

MANAGEMENT A) Acute seizure management Rapid cardiopulmonary assessment Put pt in lateral position with head lower than trunk (recovery position) aid drainage of secretion Clear airway & give oxygen via hig flow mask DO NOT restrain seizure movement DO NOT put anything in between teeth Establish IV/ intraosseous assess Diazepam (rectal=0.5mg/kg; iv=0.3mg/kg) max 10mg If seizure persist phenytoin If seizure cont aft >10 mins, consider IV midazolam or phenobarbitone pr sodium valproate (start inotropic support & arrange ICU, secure airway & prepare use mechanical ventilation; titrate phenobarbitone to achieve burst-suppression pattern on EEG)

47

Together in Delivering Excellence (T.I.D.E) Questions 1.

Classification of seizure types Generalized  Tonic-clonic, Abscence (typical, atypical), Myoclonic, Tonic, Clonic, Atonic Focal seizures Epileptic spasms

2.

Principles of antiepileptic drug therapy for epilepsy  Treatment recommended if >2 episodes  Monotherapy as far as possible  Increase dose gradually until epilepsy in controlled OR max dose OR s/e occur nd st nd st  Add on 2 drug if 1 drug failed. Optimize 2 drug, try withdraw 1 drug  Rational combination therapy (combine drug with diff MOA & consider their spectrum of efficacy, drug interactions & adverse effect)  Monitor drug level only to check compliance OR polypharmacy (drug interaction suspected)

3.

Advice for parents  Compliant to med  Treat for 2 years seizure-free period  taper off over 3-6 months  Sudden withdrawal of drug breakthrough seizure  If epilepsy is photosensitive, watch TV in a brightly lit room  Avoid sleep deprivation & alcohol  DO NOT lock bathroom  No cycling in traffic, swimming alone  Inform school

4.

AED & side effects

48

Together in Delivering Excellence (T.I.D.E) Celebral Palsy [Dodi] HISTORY Definition : Disorder of movement and posture d/t non progressive lesion of motor pathways in the developing brain -must be no loss of milestones ACQUIRED previously -mostly diagnosed after 2 y/o( prof salmi - 3 y/o) bcoz before this neuron not complete myelination yet. Risk factor: premature and twin birth S&S: asymmetric gross motor fx,increased ms tone/floppiness, Feeding difficulties ( slow feeding,ganging,vomiting d/t oromotor incoordination),abnormal gait once walking is achieved,generalized windswept deformity d/t contracture and marked ms wasting Hx : -

-

-

Birth hx (antepartum,intrapartum,postpartum) Intrapartum asphyxia : APGAR score- cry spontaneously or not? Dev milestones :  Gross N fine motor, hearing, speech, language, Social, behavior N emotional Any major events like seizures,aspiration -pneumonia(lung infection,mental retardation  Describe it, frequency and interval of free sx Mobilization INVESTIGATION

no definitive laboratory studies for diagnosing cerebral palsy, only studies to rule out other symptom causes, such as metabolic or genetic abnormalities, *Thyroid function studies - Abnormal thyroid function may be related to abnormalities in muscle tone or deep tendon reflexes or to movement disorders. *Lactate and pyruvate levels - Abnormalities may indicate an abnormality of energy metabolism (ie, mitochondrial cytopathy). *Ammonia levels - Elevated ammonia levels may indicate liver dysfunction or urea cycle defect. *Organic and amino acids - Serum quantitative amino acid and urine quantitative organic acid values may reveal inherited metabolic disorders. *Chromosomal analysis - Chromosomal analysis, including karyotype analysis and specific DNA testing may be indicated to rule out a genetic syndrome, if dysmorphic features or abnormalities of various organ systems are present. *Cerebrospinal protein - levels may assist in determining asphyxia in the neonatal period. Protein levels can be elevated, as can the lactate-to-pyruvate ratio. *Imaging :Confirm extent of damage by MRI/CT scan Others:- (EEG) is useful in evaluating severe hypoxic-ischemic injury N diagnosis of seizure disorders - Electromyography (EMG) and nerve conduction studies are helpful when a muscle or nerve disorder is suspected

PHYSICAL EXAMINATION General Inspection Position of the patient Pt is conscious N alert?? (usually pt sleeping) If conscious- I can/cannot build rapport with him/maintain eye contact or not/playing or not with toys Hydrational N nutritional status adequate? No respi distress if presence evidenced by tachypnea,nose flaring,use of accessory muscle N intercostals recession Head appears small but I ‘ll confirm later by plotting head circumference chart Body size is appropariate/inappropriate with age but ill confirm later by plotting growth chart On nasogastric tube( if present) There is minimal movement ? –exmple : at left upper limb,others ______ Abn : fisting of hands,scissoring of legs,flexion of extremities Abn movement-choreoathethoid( not chorea; in Huntington chorea,and syndenham chorea) Wheelchair/stroller- walking difficulties Note any bed sores UMNL : Hypertonia,power at least 3 (cannot be elicited properly as pt do not follow command), hyperreflexia, clonus,babinski positive,no fasciculation

MANAGEMENT Multidisciplinary approach :  Rehabilitation a. Physiotherapy-fx in sitting,standing,walking,gait training,mechanical aid (support,prevention and correction of deformities,assisting wanted movement,controlling involuntary mvmt) b. Occupational therapy-increasing muscular coordination and eye hand coordination (to improve adls) c. Speech therapy-to stimulate language development d. Behavioural therapy 

Orthopaedic mx Tenotomy to correct contractures Tendon transfers to correct deformities from muscle imbalances - Arthrodesing operations  Nutritional needs - Increasing needs d/t involuntary movements,contractures - Poor intake d/t dysfunctional swallowing,inability to chew - Require supplementation  Medication - Control seizures-sodium valproate? - Muscle relexantbeclofe,clonazepam N botox injection - Controlling mvmt - Management of dysf(x) bowel act - Aspiration pneumonia –anti reflux meds-ranitidine -

49

Together in Delivering Excellence (T.I.D.E) 1.

CAUSES OF CP (commonest)  ANTENATAL –Vascular occlusion,cong infection (TORCHES), congenital malf *  INTRAPARTUM-HIE,perinatal asphyxia  POSTPARTUM o Prematurity (PERIVENTRICULAR LEUKOMALACIA) * o Low BW infant* o Kernicterus* o Meningitis* o Head injury- MVA,child abuse* o Stroke* o Symptomatic hypoglycemia

2.

Site of involvement?  *UMN( pyramidal)- spastic  *cerebellum- ataxic hypotonic  *basal ganglia/extrapyramidal tr –dyskinetic

3.

Types of CP

*UMN( pyramidal)- spastic  hemiplegia(UL >LL) o fisting of affected hand o scissoring of LL o pronated forearm  quadriplegia(LL>UL) o a/w hx of HIE o extensor posturing  diplegia(Minimal affected UL) o Scissoring legs o prone in premature infants *cerebellum- ataxic hypotonic  hypotonia,truncal ataxia,dysmetria,gross incoordination  incoordinate mvmt,intention tremor,ataxic gait *basal ganglia/extrapyramidal tr –dyskinetic  frequent involuntary mvmt :chorea,dystonia(proximal lmb),athetosis(distal limb)  floppiness,poor trunk control,delayed motor dvlpmt  intellect relatively unimpaired * both spastic N extrapyramidal types-mixed 4.

Co-morbidites? (Sign N sx)

a) Head  Microcephaly  Seizures  Mental retardation  Developmental delay  Cortical blindness  Hearing prob  Speech d/o  Feeding prob

b) Chest n abdomen  GERD  Hyperactive a/way disease  Recurrent aspiration  Chest deformity  Bronchopneumonia  Constipation

c)others:  Contractures,  Spasticity,  Abnormal movement,  Wearing pampers,  Dislocated hips  Scoliosis

d)DDx : a)with weakness  anterior horn dz (spina bifida, vp shunt)  NMJ (mys.gravis)  peri.neuropathy (charcoat marrie tooth/ HMSN)  duschene muscular atrophy b)w/o weakness  down syndrome  prader willi synd,  ECP

50

Together in Delivering Excellence (T.I.D.E) Down’s syndrome [Amal] HISTORY - Note abt the chief complaint: health/hearing/vision status, developmental delay (Newborn) GI tract : duodenal atresia TOF, p.stenosis-vomiting Anorectal malformation, Hirschprung – no stool CVS : AVSD, VSD, ASD, TOF, PDA CNS : hypotonic, laxity Other: hypothyroid, hip dislocation, cataracts (Childhood) Delay dev milestone, IQ problems, seizures, recurrent URTI, hearing loss, visual impairment, leukemia, hypothyroid Short : myb d/t ht dse, nutritional def d/t feeding problem, coeliac dse, thyroid Under/overweight Atlantoaxial instability – mostly asymptomatic but cn have neck pain, torticollis, limited ROM, gait problem, sensory deficit, hyperreflex, spacticity (Adult) Female :delay menarche. Fertility ok Male: infertile d/t low testosterone - risk for Alzheimer/ dementia Other hx: obstetric hx- maternal age Family hx of down’s

PHYSICAL EXAMINATION SKULL : Flat occiput, bracyµcephaly, large fontanelle, hypoplasia of maxillary EYE : Epichantal folds, upslanting palpebral fissure, brushfiled spots, strabismus, nystagmus, cataracts FACE: Small nose,ear,&mouth. Protruding tongue, , flat nasal bridge, flat facial appearance, hypertelorism, micro&hypodontia, smooth philtrum, thin upper lip NECK : Broad, shot, generous nuchal skin ABDOMEN : Protuberant, umbilical hernia HAND: th Single transverse palmar crease, short 5 finger w clinodactyly, st nd wide space btwn 1 and 2 toes LIMBS: Short extremities, broad hands CNS: Joint hyperflex, hypotonia BEHAVIOUR : Natural spontaneity, cheerful but some are anxious

INVESTIGATION Laboratory :  FBC BMA for leukemia  TSH for hypothyroid  Pap smear every 1-3 yr from first intercourse  Cytogenetic : karyotyping  Echo: for congenital ht dse Radiograph :  Cervical xray to measure atlantodens distance TRO instability at 3 y/o but not indicated in most cases Prenatal screening:  Markers: Low maternal serum alpha fetoprotein, high hCG, low unconjugated estriol  Ultrasound: hypoplastic nasal bone, thick nuchal fold, echogenic bowel, short bone, pyelectasis (dilatation of renal pelvis)  Invasive test: amniocentesis at 14-16 weeks gestation  Chronionic villus sampling 10-13 weeks gestation but risk of contamination, transverse limb deficiency  Percutaneous umbilical blood sampling

MANAGEMENT Medical : -

-

intervention for specific issues : surgical/meds for ht dse, abx for infections, infant stimulation programs, special education, physical/occupational/speech tx goal is for the children to develop to their full potential parent’s support group supportive care balanced diet for appropriate weight follow ups for cardiac/thyroid/hearing/visual assessment dental check-ups at 2 y/o and cont 6 monthly

Surgical : for specific issue etc heart disease

51

Together in Delivering Excellence (T.I.D.E) Common/Possible Question in Exam + Answer

Sx of congenital hypothyroidism : GOOD BABY- decreased activity, Large anterior fontanelle, Poor feeding and weight gain, Small stature or poor growth, Jaundice, Decreased stooling or constipation, Hypotonia, Hoarse cry Hall’s ten cardinal signs of Down Syndrome in neonates Poor moro reflex Hypotonia Flat facial profile Upward-slanting palpebral fissures Simple, small round ears Redundant loose neck skin Single palmar crease Hyperextensible large joints Pelvis radiograph abnormal Hypoplasia of fifth-finger

Fq 85 80 90 80 60 80 45 80 70 60

52

Together in Delivering Excellence (T.I.D.E)

PSYCHIATRIC

Notes

53

Together in Delivering Excellence (T.I.D.E) MDD [Amalina] HISTORY  

F>M, average age onset is 40y/o 50% pt have diurnal variation: severe in morning, less in evening

PHYSICAL EXAMINATION General : Generalized psychomotor retardation. Hand wringing, hair pulling  agitation. Stooped posture, no spontaneous movement, averted gaze. Mood, affect, feeling : May deny depression, but family may complain withdrawal and reduce in xtvt Speech: Reduce rate and volume of speech, respond with single words and delay response to Q’s. Perceptual disturbance: May have psychotic features (delusion/hallucination) If mood incongruent, i.e grandiose + depression, should consider schizo disorder Thought : Negative views, guilt, suicidal

Conditions screening •Substance abuse causing depressed mood (eg. drugs, alcohol, medications) •Medical illness causing depressed mood •Other psychiatric d/o: mania, hypomania, bipolar, schizoaffective, schizophrenia, etc. •Bereavement unless sx persist for >2 months or show marked functional impairment, morbid preoccupation with worthlessness, suicidal ideation, psychotic symptoms, or psychomotor retardation. INVESTIGATION Laboratory 

FBC, LFT/RFT



Adrenal and thyroid function esp in over/underweight



HIV test if homosex, IVDU or high risk pt



Urine toxicology TRO substance abuse



ECG before ECT

DDx :  Medical d/o – mononucleosis esp in adolescent, SLE, adrenal/thyroid disorder  Neurological d/o – Parkinson, dementing illness (Alzheimer), epilepsy, CVA, tumour

MANAGEMENT

Pharmacotx  SSRI – safer, mild S/E : headache, GI disturbance, sex dysfx, rebound anxiety Ex: Citalopram, Fluoxetine  TCA – lethal if overdose. S/E: sedation, weight gain, otostatic hypotension  MAOI – for refractory depression. S/E: otostatic hypotension. hypertensive crisis if w sympatomimetics, serotonin syndrome if with SSRI. Hospitalization:  Risk of suicide, have reduce ability to get food/shelter, need for diagnostic procedure, rapid progressive symptom Psychotx:  Behavior tx, cognitive tx, supportive psychotx, family tx, dynamic psychotx ECT:  If pt unresponsive or unable to tolerate pharmacotx, want rapid reduction of sx  Premed atropine, then GA then muscle relaxant then induce generalized seizure  S/E : Retrograde amnesia

54

Together in Delivering Excellence (T.I.D.E) GOOD prognostic indicators:  Mild episodes  Shorter hospital stay  Absence of psychotic symptom  Stable family  Absence of comorbid psychiatric disorder  Advanced age of onset POOR prognostic indicator :  Coexisting dysthymic disorder  Alcohol and other substance abuse  Anxiety disorder symptom  H/o more than one previous depressive episode  Men generally more chronically impaired than women Treatment: Dose of antidepressant should be raise to max recommended level and maintained for at least 4-5 weeks before consider in unsuccessful. But, if pt improve on low dose, don’t raise unless improvement stop. When pt does not respond to appropriate dose of drug after 2-3 weeks, clinicians may obtain plasma concentration of the drug to check for compliance or pharmacokinetic disposition. Serotonin syndrome: A potentially life-threatening condition resulting from increased CNS serotonergic activity that is usually drug related. Symptoms may include mental status changes, hyperthermia, and autonomic and neuromuscular hyperactivity. Diagnosis is clinical (HUNTER criteria). Treatment is supportive, stop drug and serotonin antagonist cyproheptadine. In most cases, serotonin syndrome manifests within 24 h, and most occur within 6h, of a change in dose or initiation of a drug. Manifestations can range widely in severity. They can be grouped into the following categories:



Mental status alterations: o Anxiety, agitation and restlessness, easy startling, delirium



Autonomic hyperactivity: o Tachycardia, hypertension, hyperthermia, diaphoresis, shivering, vomiting, diarrhea



Neuromuscular hyperactivity: o Tremor, muscle hypertonia or rigidity, myoclonus, hyperreflexia, clonus (including ocular clonus), extensor plantar responses o May be more pronounced in the lower than the upper extremities

Symptoms usually resolve in 24 hr, but symptoms may last longer after use of drugs that have a long half-life or active metabolites (eg, monoamine oxidase inhibitors, SSRIs). MDD Subtype: Melancholic

 

Anhedonia, early morning awakening, psychomotor disturbance, excessive guilt, anorexia. Antidepressant with dual action on serotonergic and noradrenergic receptor

Atypical

 

Hypersomnia, hyperphagia, reactive mood, leaden paralysis, hypersensitivity to interpersonal rejection Effective for MAOI, SSRI, Bupropion

Catatonic



Catalepsy, purposeless motor activity, extreme negativism or mutism, bizarre posture, echolalia

Psychotic

 

Presence of hallucination or delusion Antidepressant + antipsychotic + ECT

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Together in Delivering Excellence (T.I.D.E) Schizophrenia [Hamizah] HISTORY Epidemiology:  Man 20 y.o  Woman 30 y.o  High prevalence in lower socioeconomic grp  Strong association with genetic and substance use Risk factor: 1. Predisposing factor: personality, genetic, environment 2. Precipitating factor: stress, drug 3. Perpuating factor: ongoing stress Criteria of Schizophrenia (DSM V) A.

B. C. D. E. F.

Two (or more) of the following, each present for a significant portion of time during a 1-month period (or less if successfully treated). At least one of these should include 1–3 1. Delusion 2. Hallucination 3. Disorganized speech 4. Grossly disorganized or catatonic behavior 5. Negative symptoms (i.e., diminished emotional expression or avolition) Social/occupational dysfunction Duration of 6 months Schizoaffective and mood disorder exclusion Substance/general mood condition exclusion If there is a history of autism spectrum disorder or other communication disorder of childhood onset, the additional diagnosis of schizophrenia is made only if prominent delusions or hallucinations are also present for at least 1 month (or less if successfully treated).(Global Developmental Delay or Autism Spectrum Disorder)

PHYSICAL EXAMINATION MSE Appearance: Disorganized appearance Speech: Disorganized speech Mood/Affect: Flattened affect Thought: Disorganized thought process -

Loosening of association

-

Thought block

-

Thought content: abnormal, Delusion

-

2.

Blood: FBC, TFT, LFT/RFT (for baseline)



Urine toxicology - to exclude substance



Radiology: CXR



ECG (need to before doing ECT)



Assess support: family, friend, financial, spiritual, belief system

Grandiose

Thought form: Illogical

Insight: Impaired MANAGEMENT 1. Typical

Atypical

pt’s consent) Review old notes/medical report from prev hosp admission

o

judgement

Verify hx from family members and related people (with



Persecutory (Paranoid)

Judgement: Impaired personal and social judgement, normal test

Psychosocial + Spiritual 

o

Cognitive: Intact memory and orientation, impaired attention

Biological 

Reference

Perception: Distorted (Auditory hallucination)

INVESTIGATION

1.

o

2.

Pharmacological : Antipsychotic Haloperidol, Flupentixol MOA: block D2 receptors in limbic and neocortex  reduce dopamine overactivity S/E:  (cortex, limbic) drowsiness, seizure, lethargy  (basal ganglia/ EPS) parkinsonism, dystonia, akithisia  (pituitary gland) hyperprolactinaemia, gynaecomastia, galacctorhea, weight gain Risperidone, Olanzapine MOA: block serotonin receptor & D2 receptor  reduce dopamine and serotonin overactivity S/E:  no EPS  Anti histamine effect eg: allergic, sedation Psychosocial + Spiritual a. Psychoeducation b. Behavioural therapy c. Family therapy d. Group therapy

56

Together in Delivering Excellence (T.I.D.E) 1.

What are the positive and negative symptoms of Schizophrenia Positive symptoms Negative symptoms (5A) Delusion Affective flattening Hallucination Alogia Disorganized behavior Avolition Disorganized speech Anhedonia Attention lacking

2.

How to differentiate between hallucination and pseudo-hallucination ( COINS ) o Conscious o Objective space o Involuntary o No stimulus o Sense organ

3.

Schizophrenia spectrum o Schizophrenia o Schizophreniform o Brief psychotic o Delusional disorder o Schizoaffective

4.

Course of Schizophrenia Prodromal Social withdrawn Psychotic Perceptual disturbance, delusion, disordered thought process/content Residual Flat affect, social withdrawal, odd thinking/behavior

5.

Differential Diagnosis o o o o o o o o o

6.

7.

Medical and neurological disorder Schizophreniform disorder Brief psychotic disorder Mood disorder Schizoaffective disorder Psychotic disorder not otherwise specified Delutional disorder Fastitious disorder and malingering Mental retardation

Prognosis in Schizophrenia Good prognosis Late onset Obvious precipitating factors Acute onset Good premorbid social sexual and work hx Mood disorder symptoms Married Good support system Positive symptoms Female Sex Family history of mood disorder and family history of schizophrenia

Bad prognosis Early onset No precipitating factors Insidious onset Poor premorbid social sexual and work hx Withdrawn, autistic behaviour Single, divorced, widowed Good support system Negative symptoms Female Sex Neurological sign and symptoms History of perinatal trauma No remission in 3 years Many relapse Hx of assaultiveness

Hallucination vs Illusion Hallucination:sensory perception without actual external stimulus eg: auditory, visual, olfactory and tactile

Illusion: Misinterpretation of an existing sensory stimulus

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Together in Delivering Excellence (T.I.D.E) Anxiety Disorder: Panic Disorder + OCD [Julea] Epidemiology:  F>M & more frequently in higher socioeconomic groups Risk factor/causes:  Genetic  Environmental  Biological  Psychosocial fx  Neurotransmitter imbalances(inc NE, dec GABA and serotonin) PANIC DISORDER Panic D with agoraphobia- fear being alone in public place Panic D w/out agoraphobia- specific phobia @ social phobia Panic D:  Recurrent panic attack w/out precipitant with persistent fear of having additional attacks  Intense fear + ≥ 4 : -Palpitation -Sweating -Shaking -SOB -Chest pain -Choking sensation -Nausea -Light headedness -Depersonalization -Fear of losing control -Fear of dying -Numbness or tingling -Chills -Hot flushes st  1 attack may follow period of stress or physical exertion, subsequent attack occur spontaneously  A/w major depression, substance dependence, social and specific phobia, OCD? OCD Obsession: Recurrent & persistent intrusive thought causing marked anxiety & pt attempt to suppress the thought Compulsion: Repetitive behavior in response to obsession, when performed is to relieve anxiety caused by obsession eg Obsessive-Compulsive thoughts:  Fear of being contaminated by germs or dirt  Spending a lot of time washing or cleaning  Excessive focus on religious or moral ideas  Praying excessively or engaging in rituals triggered by religious fear.  Fear of losing or not having things that might need  Accumulating “junk” such as old newspapers or empty food containers.  Order and symmetry: the idea that everything must line up  Ordering or arranging things

DDx Panic Disorder: Rule out other condition before Dx panic D 

Medical conditions: CCF, MI, angina, thyrotoxicosis, temporal lobe epilepsy, multiple sclerosis, COPD



Mental: depressive D, phobia D, OCD, PTSD



Drug: amphetamine, caffeine, nicotine, cocaine, alcohol or opiate withdrawal

Mx for Panic Disorder: Pharmacological: Acute:  Benzodiazepine and SSRI (benzo short course only then tapered dose when SSRI is instituted because benzo can cause dependence) Maintenance:  SSRI (paroxetine and sertraline) Non pharmaco:  Relaxation training  Biofeedback  Cognitive therapy  Insight orientated psychotherapy  Family therapy Mx for specific phobia:  Systemic desensitization  Psychotherapy Mx for social phobia:  SSRI(paroxetine)  Cognitive and behavioural therapy

Management for OCD: Pharmacological:  SSRI Non pharmaco:  Behavioural therapy (exposure & response prevention)

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Together in Delivering Excellence (T.I.D.E)

SURGERY Notes

59

Together in Delivering Excellence (T.I.D.E) Hernia & Scrotal Swelling [Amy] HISTORY Age : young : indirect ,old : direct Gender  Male : inguinoscrotal  Female : femoral RFx :  increased inta-abd pressure (chr cough, chr constipation, BPH)  Weak abd wall (heavy-lifting, grandmultipara, hx of abd surgery (eg, appendisectomy)) Onset, progression, painful/less, reducible/not, Pain may felt – aching/dragging sensation, groin to testis esp while doing exercise Complication  strangulated/obstructed  previously painless->painful  reducible ->non-reducible, I/O symptom – NBO, abd distention/pain

 



  



Diagnosis : side (R/L/bilateral), type (direct/indirect) (Inguinal/Inguionoscrotal) hernia, (obstructed/non) Differential Diagnosis: 1. Inguino/Inguinoscrotal hernia 2. Femoral hernia 3. Inguinal LN 4. Hydrocele (boys)/canal of Nuck(girls) 5. Saphenous varix 6. Undescended testis 7. Lipoma of the cord

PHYSICAL EXAMINATION Standing o Inspection : Lump site – above or below inguinal lig, uni/bilateral, position, enter scrotum, size, skin changes, previous scar o Cough impulse o Palpate : consistency – soft/fluctuant, size, shape, temperature, tenderness, can get above lump, can feel testis, o ask pt to cough + feel for palpable cough impulse o ask pt to reduce lump – reducible/incarcerated Lie supine o Deep ring occlusion test 1. Reduce the hernia 2. Locate deep inguinal ring Find pubic tubercle : umbilicus down to pubic symphysis, st lateral, then 1 bony prominence Find asis Occlude at midpoint of inguinal lig (2cm above) 3. Keep pressure on ring and ask pt to stand up & cough 4. Remained reduced – indirect hernia, bulge out – direct Percussion & Auscultation – ascites, BS **scrotal swelling – translumination test Offer: 1. 2. 3.

Abd exam : scars, masses, ascites, constipation, IO DRE : BPH, impacted stool Respi : COPD

**Scrotal swelling : 1. Hydrocele –1° or 2° 2. Testicular Tumour 3. Epididymal cyst 4. Varicocele INVESTIGATION

1. 2.

Abdominal Xray – IO U/S scrotum

Testicular Tumour Age : young male (25-35 y/o) RFx : undescended testis, trauma Types : Seminoma, Teratoma, Combined, Instestitial Spread : Direct – epididymis, spermatic cord Lymphatic – para-aortic node, Virchow’s node Blood stream – lungs, bones, liver, brain Presentation : painless heaviness lump, dull ache Examination : enlarged testis, mass inseperable from testis, hard, irregular, nodular(teratoma)/ smooth(seminoma), non-tender, not transilluminateable, can get above mass **may present with 2° hydrocele Staging : 1 : testis only, 2 : modes below diaphragm, 3 : nodes above diaphragm, 4: lung or liver mets Tumour marker : LDH, AFP, hCG, LDH Management : orchidectomy + radiotherapy (seminoma) or chemotherapy(teratoma – cisplastin, methotrexate, bleomycin, vincristine)

MANAGEMENT Non-surgical o Reduced intaabdominal pressure – weight loss, change job, tx medical condition – chr cough, chr constipation o Truss : for compression of reducible hernia at deep ring o If obstructed/strangulated : NBM, IV drip, NG tube suction, IV ABx Surgical o Herniotomy/Herniorapphy- indirect hernia o Hernioplasty – direct hernia eg. Lichtenstein **Complication of surgery A. Intra-op : injury to surrounding structure : blood vessels – femoral, inf epigastric artery, bowel or bladder, nerves – ilioinguinal, cord B. Immediate post-op : AUR, haematoma, infection C. Late cx : Recurrence, testicular atrophy, iatrogenic ascend testis

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Together in Delivering Excellence (T.I.D.E) 1.

Boundaries of inguinal canal – 4cm oblique canal about 2cm above inguinal ligament

Roof : Internal oblique, tranversis abdominis ms Anterior : Aponeurosis of external oblique Floor : Inguinal lig, lacunar lig Posterior : Transversalis fascia Content : female – ilioinguinal nerve, round ligament of uterus male – ilioiguinal nerve, spermatic cord – 3 arteries : testicular a., artey to vas deferens, cresmater a. ; 3 nerve : nerve to cremaster, autonomic n. ; 3 structures : vas deferens, lymphatics, pampiform venous plexus

2.

Mid Inguinal Point – mid point between ASIS and pubic symphysis Midpoint of Inguinal Ligament – mid point between ASIS and pubic tubercle

3.

Hesselbach Triangle

M

Course Etiology Neck Reduction Deep ring occlusion test

Indirect Via deep inguinal ring and along the inguinal canal, enter scrotum Patent processus vaginalis Lateral to inf epigastric vessels Narrow, increase risk to strangulate Manually Do not bulge out

L

Direct Via transversalis fascia (Hesselbach’s triangle) don’t enter scrotum Weak abdominal wall/muscle Medial to inf epigastric vessels Broad Automatically Bulge out

61

Together in Delivering Excellence (T.I.D.E) Breast Lump [Nur Nadia] HISTORY

*Hx of lump: site, single/multiple, when/why was it first noticed, painful/painless, overlying skin changes, any increase in size, any nipple changes, nipple discharge, any lump elsewhere. *Estrogen exposure hx: i) Age of menarche ii) Age of menopause iii) Use of hrt> 1 year

PHYSICAL EXAMINATION

*Check list: 1. Breast 2. Nipple 3. Supraclavicular lymph nodes 4. Spinal tap 5. Lung effusion 6. Hepatomegaly

*Any family history of cancer; breast, ovarian, prostate, CRC *Systemic review: LOA, LOW, fever, bone pain, SOB, headache. *Differential diagnosis: A. Painless: carcinoma(elderly, post-menopausal), cyst, fibroadenoma B. Painful: cyst, abscess, fat necrosis, periductal mastitis, galactocele, carcinoma (rare; 10% & advanced) INVESTIGATION *Triple assessment: i) ii)

Clinical examination Imaging: a. Mammography = neodensity/ asymmetric density, microcalcifixation < 0.5mm, stellate lesion with poor outline/ comet sign, architectural distortion b.

Ultrasound = hypoechoeic with/without thick echogenic halo, irregular edges, high central vascularity, microcalcification

c.

Breast MRI = useful for pre-menopausal women with dense breast

iii) Histology:  FNAC  Core biopsy (Trucut/mammotome)  Incisional biopsy  Excisional biopsy

MANAGEMENT *If triple assessments suggest a benign lump, follow-up with physical examination for 1 year to ensure the lump is stable and regress. *If all 3 concordant of malignancy- further staging and treatment. *If 1 or 2 of 3 suggest of malignancy- further workup – excisional biopsy?

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Together in Delivering Excellence (T.I.D.E) Abdominal Mass & Pain [Julea] HISTORY  

Age gender Mass (LORDSANFARO)  location, onset, timing, progression of the mass



Associated symptoms?  Pain (location,nature,radiation,duration, agg and relieving fx)  Solid organs: dull & constant pain  Hollow viscera: colicky pain  Nausea/vomiting  Change of bowel or urinary habit  Flatus/gas  Features of jaundice  Constitutional symptoms e.g. weight loss, sweats, fever, anorexia, pallor  Any blood in the faeces or urine?  Lower urinary tract symptoms



PHYSICAL EXAMINATION General     

Pallor Jaundice Cyanosis: cirrhosis liver with portal hpt Clubbing: cirrhosis, uc, crohn’s Lymphadenopathy

Specific  GIT examination:  Inspection: distension, mass ,umbilicus, scar, pulsations  Palpation: guarding, rigidity, rebound tenderness, mass, organomegaly  Percussion: shifting dullness, fluid thrill  Auscultation: bruit, bowel sound hyperactive, sluggish, absent, normal 

Others: PR, genitalia, hernia orifices

PMH any abdominal procedures-adhesion

INVESTIGATION (Based on ddx)

MANAGEMENT Depends on diagnosis.

Laboratory: 1. FBC: anemia, hyperleukocytosis 2. BUSE 3. LFT Imaging: 1. USG abdomen + pelvis 2. CT abdomen (definitive) 3. Abdominal xray – air fluid level, distended bowel, stones

If abd distension + pain:  pain Mx: NSAIDS opioids, antispasmodic  symptomatic: drugs, ryle’s tube  antibiotics  surgery

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Together in Delivering Excellence (T.I.D.E) Abdominal mass:

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Together in Delivering Excellence (T.I.D.E) Upper GI Bleed [Amal] HISTORY 



Nature of bleed and amount  Hematemesis : fresh/coffee ground  Malena : fresh/stale/iron stool  (gloved finger in water and stirred Malaena black iron  green Causes  ULCERS : epigastric pain may radiate to back (dyspepsia/heartburn) Drugs used? Coffe ground vomit? Melena  VARICES : CLD symptoms? (easy bruising, N&V,LOW, jaundice, dark urine, pale stools, pruritus, impotence) h/o variceal bleedn OGDS?melena? Alcohol? Blood transfusion? High risk behaviour? Hepatitis?  CANCER : early satiety? Dyspepsia? LOA LOW? Bloating?Distension?

  

PHYSICAL EXAMINATION    

General: ill looking, mental status, respi distress Vitals : BP/HR/postural HPT, urine output Peripheral : pallor, CLD stigmata, clammy palm (shock) Abdomen : distension w ascites or organomegaly, dilated veins, c.medusae, palpable liver/spleen, +fluid thrill/shift dull, audible hum DRE Lymph nodes: gastric ca (Troisier’s sign, Virchow’s : Lt supraclvicular fossa ) Trousseau's sign : thrombophlebitis and DVT (nonmets effect of malignancy esp gastric and pancreatic ca)

  

ϪϪ : 1. 2. 3. 4. 5. 6.

Complications Anemia sx? perforated ulcers sx (board like rigidity, abdomen xmove w respiration) shock?

Variceal bleed (portal HPT) Bleeding PUD Acute erosive gastritis Stomach/esophagus ca Malloryweiss tear Bleeding d/o

Comorbidity : elderly, liver/renal dse, IHD, blood d/o INVESTIGATION

Laboratory : 1. FBC – Hb for anaemia. Pancytopenia in hypersplenism 2. BUSE + creat - urea & creat can be high in GI bleed 3. RFT/LFT – tro hepatorenal syndrome(in CLD) and bilirubin and albumin for Child’s score 4. Coagulation profile – coagulopathy in liver dse, also for Child’s score 5. Urease test – H.pylori for PUD 6. GXM 7. Tumour marker – alphafetoprotein (liver) CA 19.9 (gastric) Imaging : 1. OGDS  Diagnostic - to visualise source of bleeding, biopsy, CLO test  Therapeutic- ligation, sclerotherapy, clip, etc 2. Barium meal : initial test for vague sx  Features gastric ca - Mucosal irregularity and ulceration, apple-core, filling defect , Pseudoachalasia, Linitis Plastica  Gastric ulcers - filling defect (bulls eye), radiating folds, ulcer collar (Hampton’s line) 3. CT: for staging in ca, look for perforation in ulcer 4. CXR : air under diaphgram (perf) 5. CT TAP, EUS : mets and staging

MANAGEMENT 1) 2) 3) 4) 5)

Clear airway to pvt aspiration - ETT Resuscitation (2 large bore, O2, fluid, CVP) Blood for ix, catheter for i/o, gastric lavage bfore OGDS, Sengstaken if suspect variceal Early meds – PPI (omeprazole), abx but not in ulcer, stop offending drugs OGDS- in 12H if high risk 24H low risk

Pharmacology  PUD  Gastroprotect (PPI, H2 antag,antimuscarinic)  Neutralization acid ( antacids )  Mucosal protect (Bismuth, sucralfate)  H.pylori eradication : MOA 

Variceal    

Vasopressin + GTN : to reduce portal pressure Octreotide : to preventt re-bleed Cefotaxime, ceftriaxone : prophlxs abx PPI and beta blocker

Surgical  PUD – partial gastrotectomy, vagotomy, highly selective vagotomy  

Variceal – TIPPS, splenorenal, portocaval Cancer  Sub/total gastrotomy  Chemo ( 5FU, cisplatin) and radiotx in bone mets

65

Together in Delivering Excellence (T.I.D.E) Common/Possible Question in Exam + Answer

1. When we decide to transfuse blood?  Sbp<110mmhg, postural hypotension  Pulse>110/min  Hb < 8g/dl  Angina or cvs disease with hb < 10g/dl 2. PUD 1. 2 aggrasive factor ( pepsin and gastric xtvt) 2. 5 protective (pg, high mucosal blood flow to remove proton, mucus, bicarb, epitheliat regenration) 3. Forrest classification to asses risk of rebleeding 4. 3 major complications of pud are haemorrhage, perforation and gastric outlet obstruction 5. Complication of surgery in pud : recurrence, small stomach syndrome, early/late dumping, bile vomit, malignant transformation, gallstone, nutrition def (b12, calcium and low) 6. Discharge patient with ppi, f/up to rescope in 6 weeks to look for heal or malignant transform, h.pylori eradication 3. GASTRIC CA 1. Most common adenocarcinoma 90%. Other 10% : scc, gist, leiomyosarcoma 2. Stomach layers : serosa, musc propria ( longitudinal, circular, oblique), submucosa, mucosa 3. Staging 4. Complication gastrotomy :  early  bleed, infection, anastomose leak, injury to surrounding esp pancreas  Late  early satiety, intestinal hurry, dumping syndr, biliary reflus to stomach, afferent limb syndrome, ntrient def 4. VARICEAL BLEED 1. Sites of portosystemic shunt : lower end esophagus, upper end anal canal, bare area of liver, paraumbilical region, retroperitoneal area. 2. Sengstaken Blakemore : 3 tubes (gastric ballon, esophageal ballon, gastric aspiration). Keep in fridge, deflate 6 hourly to prevent pressure necrosis, use max 48H 3. Complications: aspiration pneumonia, resp obstruction, esophageal ulcer and rupture, rebleed, uncontrolled varices 4. Contraindication : basal skull #, esophageal tear, severe facial injury 5. TIPPS : for Child B C. after fail medical and OGDS. Via IJV and SVC 6. Complication TIPPS : encephalopathy , liver capsule perforation, shunt stenosis 7. Surgery : for Child A, pt on long term beta blocker, chronic banding and sclerotherapy 8. CHILDS PUGH score –

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Together in Delivering Excellence (T.I.D.E) Lower Git Bleed [Miza] HISTORY 1.

Nature of bleeding - Mixed (higher colon) or coating the stool (haemorrhoid) - Torrential or drops or clot? - Malaena (come from upper GI) - Haematochezia, bright color (lower) vs darker color (higher) - Any mucus?

2.

Aetiology clues (to rule out)

UGIB

Diverticulosis

Colorectal CA

Colitis

Hemorrhoid

Coagulopathy

3.

Any malena, hematemesis, coffee ground vomitus Hx of PUD, gastritis, varices, cancer stomach, Mallory Weiss tear Usually torrential bleedingthat stop spontaneously, altered clot Hx of prev bleeding episodes Constitutional symptoms: LOW, LOA, fatigue Change in bowel habit tenesmus Symptom of anaemia Prev hx/ family hx of GIT or ovarian cancer Infective: any fever, night sweat, nausea vomiting, diarrhea, abd pain, recent travel/ contact hx, eating seafood, prev TB exposure, BCG vaccine Inflammatory: any hx of CD or UC, joint, liver, eye and skin manisfestation Iscahemic: artherosclerosis, risk factor, prev MI, stroke Bleeding to passing motion Any mass noticed at anus Hx of constipation, hard stool, low fibre diet, chronic straing, recent pregnant Any hx of bleeding disorder Easily bleeding, petechiae

PHYSICAL EXAMINATION

General Pallor, confusion Vital sign: HR. RR, BP, Temp Sign of dehydration Supraclavicular lymph node Skin manifestation of IBD Stigmata of CLD Abdomen: Scar Any palpable mass – to r/o Colorectal CA. if mass palpable describe the mass- location, size, shape, consistency, margin, mobility, tenderness, attached to underlying structure or skin, surrounding skin DRE -

Proctoscopy: To look for internal haemorrhoid

MANAGEMENT 1.

Resuscitation (RAINBOVV) a. Give O2, insert 2 large bore IV cannulae with fast infusion of srytalloid (NS 500ml over ½ hour) b. Infuse colloids if ongoing blood loss while waiting for the whole blood (GXM) c. Catheterize and monitor urine output, insert NGT on suction to detect UGIB d. Continuous vital sign monitoring & I/O chart, CVP, stool chart e. ECG + cardiac enzymes to detect MI f. Take blood for investigation (see next column )

2.

Identify source and stop bleeding. Arrange urgent colonoscopy. Diagnostic: identify cancer, diverticulosis, angiodysplasia, areas of inflammation or bleeding Therapeutic: clip, diathermize, or inject adrenaline/sclerosant into bleeding vessel.

3.

Treat according to cause:

Complications - Anaemia symptoms: SOB, postural giddiness, palpitation, chest pain, decrease effort tolerance, fatigue, syncope - Symptom of dehydration & shock: extreme thirst, confusion, pallor, decrease urine output

NVESTIGATION Laboratory 1. FBC: to look for sign of anemia 2. BUSE: look for hydration status, any ARF from shock, electrolyte imbalance- replace 3. Coagulation profile : PT/PTT – to rule out coagulopathy and correct it present 4. LFT – to r/o bleeding varices 5. ABG – may have metabolic acidosis in shock due to organ ischaemia – IV bicarb, dialysis if severe 6. GXM - 4 pint, to check for blood compatibility 7. ECG – for anesthesia assessment Imaging 1. 2.

Erect and supine AXR: to look for intestinal obstructionceacel distention, near perforation Erect CXR: in perforated tumor to detect air under diaphgram

Mass, blood, anal fissure, haemorrhoid

UGIB Diverticulosis Colorectal CA Colitis Haemorrhoid Coagulopathy

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Together in Delivering Excellence (T.I.D.E) Common/Possible Question in Exam + Answer 1.

Define Upper GI and lower GI Upper GI start from mouth until above ligament of Treits ( duodeno-jejunal junction) Lower GI start from below ligament of Treits until anus.

2.

Indication of colonoscopy Diagnostic Hematemesis Dyspepsia (<55 y.o) Gastric biopsy Duodenal biopsy Persistent vomiting Iron Deficiency Anaemia

Therapeutic Tx of bleeding lesion Variceals banding and sclerotherapy Stricture dilatation Palliation eg stent insertion, laser therapy Argon plasma coagulation for suspected vascular abnormality

Indication of upper GI endoscopy Diagnostic Rectal bleeding Iron deficiency anaemia Persistent diarrhea Biopsy of lesion seen on barium enema Assessment or suspicion of IBD Colon cancer survellance

Therapeutic Polypectomy Angiodysplasia Decompression Pseudo-obstruction Volvolus

3.

4.

Staging of Colon cancer (American Joint Committee on Cancer)

5.

Differences between Cohn Disease and Ulcerative colitis

6.

Stage of haemorrhoid

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Together in Delivering Excellence (T.I.D.E) Appendicular Mass [Rozana] HISTORY Appendicular mass = A mass of inflamed tissue located in the right lower quadrant, which surrounds an acutely inflammed and/or ruptured appendix with appendicitis. 

Common complication of acute appendicitis



Mass consists of greater omentum with oedematous caecal wall & loops of distal small intestine with inflamed appendix in centre  natural phenomenon to contain spread of infection



Sx : RIF , pain, anorexia, constipation

PHYSICAL EXAMINATION General : tachycardia, feverish Specific :  Tender irregular mass RIF beneath some rigidity of the overlying musculature  Other sign : rovsing (pain > in RIF than LIF when LIF is pressed), psoas ( pain on extending hip if retrocaecal appendix), cope (pain on flexion and internal rotation of right hip if appendix in close relation to obturator internus)

INVESTIGATION Laboratory  FBC : neutrophil leukocytosis  elevated CRP

MANAGEMENT Appendix mass + pt’s condition satisfactory  conservative = Ochsner – Sherren regime (nature has already localized the lesion + surgery at this time is difficult) 

Imaging  U/S – helpful in assessing the nature & size of mass  Laparotomy/colonoscopy : exclude colonic tumor

     

A: Analgesic, Antibiotic (metronidaole + cefuroxime), antipyretic B: Bed rest C: Charting (vital sign, size of the mass) D: Diet (Keep Nil by Mouth) E: Exploratory laparotomy KIV.(only in suspicion of abscess) F: Fluid maintenance (to correct dehydration) Interval appendicectomy should be performed 3 months later to prevent recurrence



If pt p/w lower abdominal mass and demonstrates feature of generalized peritonitis +/- bowel obstruction, operative intervention indicated



However early surgery is now regards as a preferred method. Laparoscopic appendicectomy is safe and should be a preferred method compared to open surgery even though in emergency setting.

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Together in Delivering Excellence (T.I.D.E) Obstructive Jaundice [Hidayah] HISTORY

PHYSICAL EXAMINATION

1.

Obstructive jaundice : yellow sclera, tea colored urine, pale stool

1. 2.

2.

Exclude pre&hepatic jaundice :  sx viral hepatitis (prodrome fever, malaise, arthralgia, myalgia, N&V)  risk factor viral hepatits (travel hx, ingestion of seafood, fmly hx of hepatitis (esp mother&siblings), blood transfusion, drug abuse, needlestick injuries, sexual contact)  Alcohol intake(pancreatitis,cirrhosis)  Drug hx (traditional med). OCP (intrahepatic cholestasis) statin (hepatotoxicity)  Hx of chronic liver dis.

3.

3.

4.

5. 6. 7. 8.

INVESTIGATION 1.

Benign/Malignant

Vitals: fever,hemodynamically stable General : Jaundice, pallor, any abdominal distention,leg swelling Peripheries : stigmata of CLD,scretch marks,conjunctival pallor Abdomen : Ascites, hepatosplenomegaly (cirrhosis&portal HPT), mass per abdomen, palpable gallbladder(courvoisier’s law) DRE : pale stool Lymph node: cervical & supraclavicular LN Bony tenderness Respi examination

To confirm obstructive jaundice LFT : bilirubin raised(+/- direct>indirect normal 3:7), raised ALP II. gamma-glutamyltransferase-if dx ambiguous. I.

Benign  Recurrent spikes of similar jaundice that resolves on their own times (suggest obstruction : stones,stricture)  Young pt with painful jaundice  Previous hx of gallstone/biliary colic sx  Previous biliary surgery/ibd (sclerosing cholangitis)

Malignancy  Old pt, new onset of jaundice & progressively worsening  No associated pain  Constitutional sx  Mets sx (bone pain, neck lump, dyspnea)  Late pain, constant & relentless (pancreatic ca)

4.Complication  Sx of cholangitis (fever,chills,rigor,RHC pain,jaundice)  Pruritus  Pancreatitis(gallstone as a cause)  Decompesation (heapatic encephalopathy,fetor hepaticus, worsening ascites)  Fat malabsorption (steatorrhea,fat soluble vit deficiency ADEK-coagulopathy.

2.

To confirm inflammation/infection I. FBC: Hb, WBC II. Renal profile : electrolyte(nutritional status), U:C ratio III. Coagulation profile prolong PT (vit k malabsorption, liver dysfx) IV. Tumor marker : CA 19-9, CEA (cholangioca&pancreatic ca) V. Blood C&S : TRO HBS sepsis (if fever&febrile) VI. GXM : in case op

3. I.

Imaging HBS US  choledolithiasis - duct dilate>8cm  Gallstone dis/cholecystitis - GB stone/sludge, thickned GB wall, pericholecystic fluid, fat stranding  cx gall stone  liver consistency (fatty/cirrhotic)

II. III.

CTAP : if suspect perforated,TRO ca CXR : ARDS in cholangitis,p.effusion



MANAGEMENT According to cause

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Together in Delivering Excellence (T.I.D.E) Common/Possible Question in Exam + Answer Notes [any classification,staging, mnemonic etc] 1.

Define jaundice:  Yellowish discoloration of kin, sclera and mucus membrane d/t bilirubin, a yellowish pigment  Usually clinically evident when serum bilirubin >3mg/dl (51.3umol/L)  Normal bilirubin: 3-17 umol/L

2.

Bilirubin transport

3.

Causes  Painless: CA,HOP,cholangioca,Periam ca  painful: Stricture,hepatic causes

Intraluminal Benign 1.Gallstone 2.Parasitic infection (schistosomiasis)

Mural Benign 1. Stricture (post instrumentation & post inflammation) 2. Primary sclerosing cholangitis 3. Choledochal cyst Malignant 1. Cholangiocarcinoma

Extramural Benign 1. Mirizzi syndrome 2. Pancreatitis Malignant 1. Head of pancreas ca 2. Periampullary ca 3. Mets to porta hepatis

4.

What is Corvoisier’s Law  If the gallbladder is enlarged& patient is jaundiced, the cause is unlikely to be gallstone

5.

Whait is Charcot’s triad  triad of fever, RHC pain &jaundice : suggest cholangitis.

6.

Urine & blood biochemistry in jaundice - Liver enzyme in ix of jaundice  ALP (alkaline phosphatase) & GGT : markers of cholestatis  ALT (alanine aminotransferase) & AST (aspartate aminotransferase) : markers of hepatocellular injury  AST: ALT ratio>1 → alcoholic hepatitis (remember ST out)

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Together in Delivering Excellence (T.I.D.E) Multi-nodular Goitre (MNG) [Alliah] HISTORY 

Definition  Enlarged and diffusely heterogenous thyroid gland



Epidemiology  6x more common in woman



Check list hx for MNG :  Establish details of the swellingonset,duration,progression,recent growth,pain  Other neck symptoms(local) - discomfort during swallowing, SOB,pain and hoarseness of voice  General sx - sx of endocrine dysfunction  Past medical hx - hx of radiation to the neck during childhood  Family hx of autoimmune disease



DDx  Anaplastic carcinoma of thyroid  Autoimmune thyroiditis

PHYSICAL EXAMINATION General  Moderate body built. Neither nervousness nor lethargic  Skin - normal (no sweating;not dry)  Hair - normal  Hands – no wasting or puffiness  Normal PR with no fine tremor  No eye signs  There may be general signs of thyrotoxicosis or in elderly pt with very long-standing nodular goitres, the signs of myxoedema. Specific  A nodular swelling in front of the neck which moves upwards on swallowing  Non – tender  Smooth surface but assymetrical nodular  Firm in consistency  Neither skin or nerby muscle attachment  No signs of airway obstruction  Cervical LN not palpable  No bruits over the gland

INVESTIGATION Laboratory 1)

2)

3)

TFT  To exclude mild hyperthyroidism  TSH : normal (0.5-5mu/L)  Free T4 : normal (9-24)  Free T3 : normal (2.2-5.4) Thyroid antibodies  To exclude autoimmune thyroiditis  Thyroid peroxidase (TPO) antibody – up to 25units/ml  Anti-thyroglobulin titres : significant when > 1:100 titres FNAC  Will only be required for dominant swelling in a generalised goitre

Imaging 1) 2)

Plain radiographs of chest and thoracic inlet  To exclude tracheal deviation or compression U/S and CT scan

MANAGEMENT Pharmaco  Thyroxine Surgical  Total thyroidectomy and lifelong replacement of thyroxine  Conventional subtotal thyroidectomy – leave up to 8g of relatively normal tissue in each remnant

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Together in Delivering Excellence (T.I.D.E) Common/Possible Question in Exam + Answer 1.

Classification of thyroid swelling Simple goitre (euthyroid)  Diffuse hyperplastic (physiological,puberty,pregnancy)  MNG

Toxic  Diffuse (Grave’s Dz)  Multinodular  Toxic adenoma

Neoplastic (Benign & Malignant)  Inflammatory  Autoimmune (Hashimoto’s dz)  Granulomatous (De Quarvain’s thyroiditis)  Fibrosing (Riedel’s thyroiditis)  Infective (acute and chronic)  Other - amyloid

2.

Complication 1) Tracheal obstruction  Due to gross lateral displacement or compression in lateral or AP plane by retrosternal extension of goitre 2) Secondary thyroitoxicosis (up to 30% pt)  Transient episodes of mild hyperthyroidism 3) Carcinoma (incidence 5-10%)

3.

Indication for surgery  Cannot be treated medically – failed or unsuitable for medical tx  Cancer  Compression on neighbouring structures  Cosmetic  Compliance/cost problems – with long term medical therapy

4.

Postoperative complication after thyroidectomy (mostly H’s, One I’s, One T’s)

   

IMMEDIATE (< 24hrs) Haemorrhage with hematoma formation Hoarness or airway compression Hyperthyroidism Tracheomalacia

 

EARLY (< 1m) Infection Hypoparathyroidism leading to hypocalcemia

   

LATE (> 1m) Hypothyroidism Hyperthyroidism Permanent hypoparathyroidism Hypertrophic scarring or keloid formation

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Together in Delivering Excellence (T.I.D.E) Hematuria [Ain] HISTORY

PHYSICAL EXAMINATION

Definition : >3 rbc/hpf  DDX     1.

2.

Haemoglobinuria Myoglobinuria pseudohematuria(menses) meds causing discolouration (rifampicin,phenytoin)

Which part of urine stream is blood stained?  Initial phase-bleeding from urethra distal to urogenital diaphragm  Throughout urination – upper urinary tract or upper bladder  End of urine stream- bladder neck or prostatic urethra

Painful hematuria

Painless hematuria

UTI Pyelonephritis Hydronephrosis Renal cysts Ureteric stone BPH,strictures tumour

Malignancy- RCC, bladder,prostate Drugs Glomerulonephritis ITP/HSP Bleeding diathesis Infection-malaria,schistosomiasis Exercise-joggers hematuria

Severity – any clots,s/s of anemia Ass. symptoms –frequency, dysuria, LUTS symptom, fever  DDX : nephrolithiasis, pyelonephritis, UTI, malignancy, bladder outflow obstruction. 5. Others – drug hx, malignancy symptom, recent travelling, sore throat, medical illness eg: coagulopathy, autoimmune ds INVESTIGATION

 



  

Is it painful or painless?

3. 4.



 

Urine – dipstick, UFEME ,urine cytology for malignant cells, urine phase contrast, urine C&S Blood – FBC,BUSE,PT/APTT,GXM Imaging : Upper tract - imaging, lower tract - cystoscopy Plain KUB : stone, size of kidney Ultrasounds of kidney :renal size, stones, hydronephrosis, hydroureters Intravenous urogram (IVU) – C/I in contrast allergy, renal impairment (cr>200),on metformin cause lactic acidosis, asthma given steroids 3 days b4 study, pregnancy CT Urogram/IVP Cystoscopy : detection of bladder tumour, biopsy can be taken at the same time Kidney biopsy –suspect glomerular disease

  

Vital sign: hypotension and tachycardia are seen in patients who are haemodynamically unstable from acute blood loss,high temperature in infection Sign of anemia – pallor of conjunctiva, skin Periorbital, scrotal, and peripheral oedema: may indicate hypoalbuminaemia from glomerular or renal disease. Cachexia: may indicate malignancy. Abdomen- renal/bladder mass, palpable bladder (AUR),flank tenderness, suprapubic tenderness Scrotum – varicocele on the left (RCC of left kidney with extension of tumour to renal vein, block testicular vein from drained to left renal vein) External genitalia - blood from urethra, trauma, laceration Digital rectal examination – prostate enlargement ( BPH vs cancer) The presence of a urethral catheter, suprapubic catheter, ureteral stent, or nephrostomy tube may signify an iatrogenic cause of bleeding that is generally benign

MANAGEMENT Depends on disease  Asymptomatic (isolated) hematuria generally does not require treatment. In conditions associated with abnormal clinical, laboratory, or imaging studies, treatment may be necessary, as appropriate, with the primary diagnosis.  Surgical intervention may be necessary in certain anatomical abnormalities, such as ureteropelvic junction obstruction, tumor, or significant urolithiasis.  Consultations are required in patients with urinary tract anomalies and in some patients with systemic diseases (eg, bleeding disorders, collagen vascular diseases, sickle cell nephropathy).  Referral to a urologist is required when clinical evaluation and workup indicates a tumor, a structural urogenital abnormality, or an obstructing calculus.

74

Together in Delivering Excellence (T.I.D.E) Common/Possible Question in Exam + Answer

Urine dipstick Positive for hematuria

No blood cell

urine microanalysis

blood cell present If no proteinuria (isolated hematuria) -need to ix for systemic ds Coagulation studies,complete blood count,hb electrophoresis

Myoglobinuria or hemoglobinuria

If proteinuria-suspect glomerular ds and require kidney biopsy

If pyuria and bacteriuria –obtained urine culture (if –ve,consider interstitial nephritis)

Causes of hematuria : Pre-renal

• • • •

Renal

• • •

Post-renal

• • •

Drugs: analgesics(NSAIDS), anticoagulants, CPM, OCP Systemic : sickle cell diasease, haemophilia, ITP Metabolic: hypercalciurea, DM Vascular: AV malformations, renal artery ds,renal vein thrombosis Glomerular: post-strep AGN, IgA nephropathy, lupus nephritis Interstitial: polycystic kidney disease, stone, malignancy Vascular: HSP, Wagener granulomatosis Infections of ureter, bladder, prostate, urethra Cancer of ureter, bladder, prostate, urethra Stone

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Together in Delivering Excellence (T.I.D.E) Prostate Cancer [Fatin] HISTORY o

o

o

o

Epidemiology : th  4 most common cancer among men  Peak age : 65-75 y.o Risk factor :  Age  Obesity  FHx  A/w ↑BP S&S :  Asymptomatic – incidental finding on DRE  Obst LUTS (hesitancy, staining on urinate, weak stream, prolonged micturition, terminal dribbling, incomplete voiding)  Cx LUTS – hematuria, infection, stone, obst uropathy @renal failure  IPSS (incomplete voiding, frequency, intermittency, urgency, weak stream, straining, nocturia) Complication :  Metastatic sx – lower back pain (from Batson venous plexus)  Other place: LN, rectum, bladder, lower ureter

PHYSICAL EXAMINATION

o

o

o

INVESTIGATION o

Diagnosis :  Transrectal ultrasound (TRUS) with core biopsy (2 specimen) -histology GLEASON score – degree of differentiation/microscopic appearance  PSA level <4 ng/ml –normal 4-10 ng/ml – local ca <30 ng/ml –metastatic

o

Metastatis  Chest x-ray – lung met  MRI prostate and CT scan TAP- staging  Bone scan – bone met

o

TNM staging : T1 – accidental finding T2 – PR finding 2a -1/2 of 1 lobe 2b – 1 lobe 2c – 2 lobes T3 – extra prostate spread 3a – prostate capsule 3b – seminal vesicle extension T4 – adjacent structure other than seminal vesicle 4a – 4b – pelvic wall, abdominal wall N0 – no regional LN N1 – regional LN MO – no distant met M1a – non regional LN met M1b – bone M1c – other sites (liver, brain, lung)

Specific :  DRE – hard, irregular, nodular, asymmetric area  BPH – smooth, enlarge, symmetrical Other :  Percuss spine for bone tenderness How to stage :  Clinical examination – palpable tumor T2  TRUS biopsy – staging purpose  CT scan abdomen and pelvic – tumor extension and node status  Bone scan –bone met

MANAGEMENT o

Stage 1 &2 (T1,T2) – locally invasive  Active surveillance – wait and see for pt not for surgery (old patient / early stage)  3-6 months  DRE & PSA level  Radical prostatectomy – remove prostate, seminal vesicle, prostatic urethra  Cx : incontinence, erectile dysfx  Radiotherapy – brachytherapy  Cx : cystitis, urethral stricture, proctitis

o

Stage 3 (T3 N1) – locally advance  Surgery  Radical radiotherapy  Hormonal manipulation  Orchidectomy (remove testes)  LHRH agonist/GnRH agonist e.g Zoladex, Goserelin (flare response -> castration level) s/e : HOT FLUSH, GYNAECOMASTIA, LIVER PROB, SWEATING, LOSS LIBIDO  + anti- androgen – prevent testosterone flare

o

Stage 4 (T4 Met) – advance (palliative treatment)  Hormone therapy  Adrenal suppression – ketoconazole  Glucocorticoid – dexamethasone, predinisolone  Chemotherapy – docetaxel + prednisolone

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Together in Delivering Excellence (T.I.D.E) 1.

Mc Neal classification (prostate zone)  Central  peripheral –carcinoma  transitional – BPH

2.

Pathology – adenocarcinoma/ glandular ca

3.

Causes of ↑ PSA level  prostate ca  BPH >50 g  post ejaculation  urethral injury  UTI  iatrogenic (flexible scope)

4.

Source of testosterone  testes  adrenal gland  fat

5.

Family history of – BRCA1, BRCA2, HPC1

6.

Pre-op assmnt of TRUS w biopsy  take consent  bowel prep –ducalex/ravin supp 3 days b4 procedure  analgesic – on table b4 procedure (lignocaine)  antibiotic – 3 days b4, 2 days after - quinolone –penetrate prostate -metronidazole  after TRUS – no ridding - no heavy lifting - no SI

7.

Function of prostate  secretes an alkaline fluid at the time of ejaculation.  alkaline fluid helps neutralize the acidic environment of the female vaginal tract, prolonging the lifespan of sperm and providing better motility

8.

What is PSA (prostate specific antigen)?  protein / tumor marker produced by epithelial cells of the prostate gland

77

Together in Delivering Excellence (T.I.D.E) Renal Calculi [Dalilah] HISTORY 1.

RENAL STONES Asymptomatic unless stone gets lodge in the pelviureteric junction May cause hydronephrosis and subsequent infection Vague flank pain

2.

URETERIC STONES (even small stones can cause severe symptoms as the ureter is narrow) Ureteric colic pain (severe intermittent loin to groin pain ) Hematuria (gross or microscopic ) Irritative symptoms ( frequency, urgency) Signs of pyonephrosis ( upper urinary tract infection symptoms ) ; fever + chills + rigors, very ill due to sepsis

3.

BLADDER STONES May be asymptomatic Irritative symptoms ( frequency, urgency) Hematuria If infection present ( dysuria, fever ) INVESTIGATION

For diagnosis 1. KUB radiograph Radioopaque stone ( 90% of renal stones) False negative; too small, false positive; phlebolith (round with lucent centre),stools. Kidney; kidney size , stone Ureter ; trace the path of ureter, ureteric stones Bladder; bladder stones 2. Intravenous radiogram To visualize stone Can show dilated urinary system secondary to stone obstruction (hydroureter/hydronephrosis) 3. Ultrasound of kidney/ bladder Features of stones ; echogenic rim, posterior acoustic shadowing For complications 4. Urine test ( dipstick, UFEME, Urine c n s) -hematuria, pyuria 5. 6.

Intravenous urogram Dilated urinary system ( hydronehprosis, hydroureter ) MAG-3- renogram To give differential function of each kidney Normal ; 50% on each side, out of 100% of both kidney combined

PHYSICAL EXAMINATION GENERAL  signs of anaemia ( pale hand, conjunctiva)  very ill, in pain, cachecic, febrile, tachycardia ( in case of sepsis) SPECIFIC  no guarding, no rebound ( symptoms are out of proportion to sign)  tender suprapubic area ( in case of acute urinary retention )  positive renal punch (in case of pylonephritis)  kidney ballootable ( in case of hydronephrosis)

MANAGEMENT Conservative 1. Stone smaller than 5 mm should be treated conservatively (60% will passed out ); only treat if they do not pass after 4 to 6 weeks, or got symptoms 2. Treat UTI 3. Treat underlying disease eg; hypercalcemia 4. Diet -high fluid intake -low salt diet -restriction of red meat, dairy product, refined sugar -increase citrus fruit intake Surgical Indications :  S/S ; constant pain  complication  Obstruct urine flow  UTI  Significant bleeding  Kidney size increase 

unlikely to resolve with conservative treatment :  Does not pass after one month  Too large to pass spontaneously Types : 1. PCNL (percutaneous nephrolithotomy) – more than 20 mm (large stone ) 2. ESWL (extracorporeal shock wave lithotripsy) – 5 to 10 mm ( small stone) 3. Ureterorenoscopy with lithotripsy (URS + LL) – Stones along ureter 4. Cystolitholapaxy –bladder stone (for stone crushing) *renal stone 5 to 10 mm : Either ESWL OR PCNL *can refer ANDRE SURGICAL NOTES for more info

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Together in Delivering Excellence (T.I.D.E) Common/Possible Question in Exam + Answer 1. 2. 3. 4.

What is the type of renal stones? How renal stones are classified ? Which stones are radioopaque, which stones are radiolucent ? Treatment modalities based on size,types, location of stones.. ( when to use PCNL, ESWL)

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Together in Delivering Excellence (T.I.D.E)

O&G Notes

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Together in Delivering Excellence (T.I.D.E) Pregnancy Induced Hypertension [Hamizah] HISTORY Risk factors: Primigravida, age>40, pregnancy interval>10 years, prior PE in a pregnancy by same partner,multiple pregnancy, Fly history of PE , obese, renal dz, DM, essential HPT, autoimmune dz (SLE,antiphospholipid syndrome) Clinical features -maternal manifestations: Presenting complaints: Weight gain & edema, headache, blurred vision, epigastric/ RUQ pain, SOB, oliguric, hemorrhagic manifestation, per vaginal bleeding (abruption) fetal mv (assess fetal well being) Complications: A. Maternal  Heart: high output, pulmonary edema  Placental abruption (d/t necrosis of distal end spiral arteries)  Hematology: thrombocytopenia  Renal: renal failure, nephrotic syndrome  Liver: subcapsular hemorrhage, infarction, rupture, congestion  Lung: aspiration pneumonia (during fits)  CNS: eclampsia, cerebral hemorrhage, retinal detachment B. Fetal  IUGR  Oligohydramnios

PHYSICAL EXAMINATION General examination  Vitals(BP, HR, RR, spo2)  Weight  Pallor, petechiae, edema Chest examination  (crepitations in pulmonary edema) Abdominal examination Epigastric or right upper quadrant tenderness Neurological examination Hyperreflexia, clonus Visual field testing Obs examination Symphysial fundal height (small for dates?) Palpate for fetal lie & presentation Palpate for uterine tenderness (woody hard indicate abruption) Estimated liquor volume DopTone for fetal heart sound

INVESTIGATION Maternal 1. FBC - Anemia(d/t hemolysis in HELLP) 2. Thrombocytopenia 3. Renal profile + serum uric acid 4. Raised serum creatinine & urea 5. Raised serum uric acid level in PE 6. 24 hr urinary total protein 7. Liver function test 8. Raised AST, ALT 9. Indirect hyperbilirubinemia 10. Coagulation profile 11. PT & APTT +/- d-dimers, fibrinogen (for DIVC) Fetal U/S  Estimated fetal weight, fetal lie & presentation, liquor volume, umbilical artery Doppler flow HELLP SYNDROME -Hemolysis (anemia) -Elevated liver enzyme (AST/ALT>70iu/L) -Low platelet (<100)

MANAGEMENT Antenatal  Identify risk factors & observe BP  PE, urinalysis, BP  Confirm diagnosis:  Mild PIH-outpatient  Severe PIH, PE- admission Outpatient management Antenatal clinic visit: - Every 4 weeks if not on treatment, normal biophysical profile, good fetal growth - Every 2 weeks if on treatment Tests:  Urinalysis (protein)  BP  SFH & liquor volume  BUSE,FBC,serum uric acid Fetal surveillance: US monthly, FKC Inpatient/ admission 1. BP 4 hourly 2. SFH & liquor volume 3. Daily OE chart, urine protein 4. FBC, BUSE, serum uric acid 5. LFT, coagulation profile (HELLP) 6. IO chart 7. Fetal surveillance:-FKC, CTG, US 8. AntiHPT agent only use of DBP>100mmHg (aim:90-100mmHg) 9. Dexamethasone if early delivery expected (<34 weeks) Intrapartum management i. BP/ pulse half hourly ii. To cont oral antihypertensive treatment iii. Strict IO chart iv. Adequate analgesia (preferable epidural analgesia) v. CTG monitoring vi. Shortened 2nd stage-assisted delivery, episiotomy vii. NO syntometrine/ ergometrine viii. Use syntocinon 10 units Portpartum management 1. Beware sx of IE & pulmonary edema 2. BP monitoring 3. ½ hourly for at least 2-4 hours before sending to postnatal ward 4. 4 hourly in ward for 24-48 hours before d/c 5. Antihypertensive should be cont & stopped later on postnatal review 6. IO chart 7. Daily urine albumin, PE chart Anti HPT med Aim: to keep DBP btw 90-100mmHg Drugs

MOA

Start dose (mg/day)

Max dose (mg/day)

Adverse effect

Methydopa

Centrally acting

250 TDS

3000

Depression, drowlsy

Labetolol

a&B blockers

100 TDS

2000

Nifedipine

CCB

15 TDS

60

Hydralazine

vasodilator

25

300

Heart block, IUGR, hypoglycaemia, bronchoconstriction Headache, flushing Tachycardia, hypotension

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Together in Delivering Excellence (T.I.D.E) Questions: Definition:   

BP of 140/90 mmHg or more taken on 2 occasion at least 4 hour apart; OR An increase in systolic BP of 30 mmHg or/and diastolic BP of 15 mmHg compared to pre-pregnancy level Single reader of Diastolic BP more than 110mmHG.

1) GESTATIONAL HYPERTENSION   

Is hypertension after 20th week of gestation in a previously normotensive woman x proteinuria Condition return to norm within 6 weeks after labour

2) PRE- ECLAMPSIA  

Develop after 20 weeks gestation New onset proteinuria (>0.3g/24 hr urine collection)

3) CHRONIC HYPERTENSION  

Presence of hypertension of at least 140/90 mmHg before 20th week of pregnancy or beyond 6 weeks postpartum. Includes essential & secondary hypertension.

4) CHRONIC HYPERTENSION WITH SUPERIMPOSED PRE-ECLAMPSIA    

Development of pre-eclampsia in patient with pre-existing hypertension Criteria used should include: worsening of hypertension proteinuria

5) ECLAMPSIA  

criteria for PE met presence of generalised tonic-clonic seizures which cnt be attributed to other causes



signs & symptoms of IE:

Headache, nausea & vomiting, visual disturbance, RUQ/ epigastric pain, frothy urine, pregressive edema at independent site

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Together in Delivering Excellence (T.I.D.E) MANAGEMENT OF ECLAMPSIA 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11.

Call for help Left lateral position Secure airway, prevent pt injury Wait for convulsion to abate, if not iv diazepam 10mg bolus Max oxygenation-mask or intubation Catheterization for io chart Neurological examination Bishop score Prophylactic anticonvulsant therapy BP control Cervix favourable-vaginal delivery ; cervix unfavourable- c-sec

Anticonvulsive therapy MgSO4 à Maintainance dose: *IV infusion of 1g/hour * 5ml MgSO4 + 45ml 5%Dextrose sol. Infuse at 20ml/hour( syringe pump) OR * 10ml MgSO4 in 500ml D5% at 33 dpm (drips) Duration: – continue for 24hours after last fit or after delivery Monitoring for MgSO4 therapy: 1.Investigations  BUSE,FBC  Serum Ca2+,Mg  Renal function test (urea,uric acid,creatinine)  Coagulation profile  UFEME  ECG  GXM 2. STOP !!! If present signs of Mg toxicity: (a) RR < 16/min (b) Urine output < 25ml/hr (c) patellar reflex absent (d) Serum Mg > 3.5mmol/L (therapeutic range: 1.7-3.5) (e) BP < 90/60 mmHg 3. Antidote: Ca gluconate 10%-10ml Antihypertensive therapy initiatiate parenterally if BP> 160/110mmHg

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Together in Delivering Excellence (T.I.D.E) Placenta Praevia [Alliah] HISTORY Definition  Placenta that has implanted into lower segment of uterus after 28wks of gestation Risk factor  Multiple pregnancy  Multiparity  Previous C-sec/ERPOC/uterine surgery  Uterine structural abn. S&S

   

   

Assisted conception Advanced maternal age (>40) Previous episode Smoking

PHYSICAL EXAMINATION General   

Stable and less distress pt condition May appear pale BP,PR and pulse volume may fluctuate

Specific    

Soft and non-tender abdomen Fetal readily palpable Fetal not engaged,abnormal presentation and lie Usually normal fetal heart

Unprovoked painless PV bleeding Nature : fresh blood and intermittent Usually normal fetal movement Less distressed pt condition

Complications Maternal  Life-threatening haemorrhage-shock  Placenta accreta  PPH  Need of c-sec  Infection DDx

Fetal  Malpresentation  Fetal abn.  IUGR  Premature labor  Fetal hypoxia  Fetal death

 Placenta Abruptio  Vasa previa  Local causes

INVESTIGATION Laboratory FBC

Hb- to check for anemia TWBC & Platelet –to establish baseline * both Hb and platelet can be affected severely with massive blood loss (anemia and DIC)

GXM Coagulation profile (when indicated) Renal profile Imaging 1) Transabdominal & Transvaginal U/S  To locate placenta  To confirm diagnosis  TVS : esp. when locating posterior PP that obscured by overlying fetus & more accurate 2) Color Doppler U/S  To diagnose in pt high risk of placenta accreta (previous c-sec)

MANAGEMENT Conservative  Pt with minor and major (no previous bleeding) PP Consider : - Distant house-hospital - Transportation - Educational level & know how to take care herself Educate : - Rest and no heavy work - Avoid SI - Avoid abdominal massage - Immediate come to hosp. If presence of contraction pain * Pt with major PP (had previous bleeding) : should admit from 34weeks Acute Resuscitation (RAINBOVV) +  V/S monitoring hourly  Pad chart monitoring  Assess baby : CTG and US  Give IM Dexamethasone if < 34wks  Check maternal rhesus status Caesarean Section Emergency  Gestational age > 36 wks of gestation  Irrespective of gestational age if : profuse bleeding &/or fetal distress Elective  At 38 or 39 wks  If : a) placenta edge <2cm from internal os b) posterior or thick (> 1cm) * Minor PP – SVD if placenta minimum 2cm away from cervical os

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Together in Delivering Excellence (T.I.D.E) 1.

Classification UK Type I. Lateral : < 5cm from os II. Marginal : edge at int.os  Anterior  Posterior III. Assymetrical cover os IV. Symmetrical cover os @ anterior & posterior

Minor

Major

US Complete : covering os Partial : partially cover os Marginal : edge within 2 cm from int.os Low-lying : edge within 25cm from int.os

2.

How can you diagnosed placenta accreta?  Color Doppler U/S (whether there is blood flow to the bladder)  MRI  Grey scale U/S

3.

When we opt for McAfee Regime?  Bleeding is not life-threatening & baby is still premature [expectant mx]  Components : a) Admit pt to the ward b) Close observation for any further bleeding c) Availability of atleast 2 units of gxm d) Availability of the ot

4.

If now pt is 38 weeks & pt admitted for elective LSCS. How do u prepare this patient?  Consent (operation, blood transfusion & explain future risk of Csec and the need for Csec the next pregnancy, risk for hysterectomy)  FBC - check for Hb (aim at least 11g/dl)  GXM 4 pints  CBD should be done in OT

5.

Mode of anaesthesia in this patient? GA  Not spinal because spinal can cause hypotension  In PP surgery, there will be lots of blood loss & patient can go further hypotensive  GA - is easy to control the circulation in case the surgery went complicated

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Together in Delivering Excellence (T.I.D.E) PPROM (Preterm Pre-Labour Rupture Of Membrane) [Baisyatul] HISTORY 1.

2.

3.

Presenting complain Sudden gush of warm fluid vaginally, usually followed by continuous dribble, colourless fluid Volume ( soaked sarong/ pad) Must distinguish from leaking urine ( ask about frequency, urgency, dysuria) as incontinence or ITI may present in similar way Smell ( urine smell, foul smelly, odourless) Vaginal discharge- UTI Per-vaginal bleed-( a/w abruption) Uterine irritability or contractions Fetal movement may reduce, frequency or strength also reduced Risk factor assessment Prev history of preterm labour/PPROM Twin pregnancy Polyhydramnions Uterine/cervical abnormalities (fibroids) Recurrent antepartum haemorrhage Infection ( fever, vaginal discharge) Smoking Cocaine abuse Low BMI mother Asses complication Chorioamnionitis ( maternal pyrexia, vaginal discharge, uterine tenderness )

1.

PHYSICAL EXAMINATION General examination: Signs of infection: tachycardia, high temperature, flushed appearance

2.

Abdominal examination: Uterus smaller than date due to oligohydramnions Malpresentation (beware cord prolapse) Uterine tenderness if chorioamnionitis present

3.

Sterile speculum examination (definitive diagnostic tool) Preferably after patient has been resting supine for 20-30 minutes A pool of amniotic fluid in posterior fornix Visualize the cervix; fluid may be seen trickling through the external os and dilatation of cervix can be assessed

Digital vaginal examination should be avoided: Can stimulate prostaglandin production Introduce organism into cervical canal

INVESTIGATION Maternal Check pool of liquor by: a) Litmus paper (red to blue) b) Nitrazine test (turn to black) c) Ferning test (microscopic examination to look for fetal epithelial cells) Full blood count: check WBC, CRP for early marker for infection High vaginal swab: culture for gonorrhoea, Chlamydia, trachomatis Low vaginal swab: GBS Urine FEME: to rule out UTI

1. 2.

Fetal Serial CTG (beware of increasing baseline heart rate or fetal tachycardia early sign for intrauterine infection Ultrasound: look for AFI, fetal biophysical profile Fetal fibronectin is a useful confirmatory test if doubt about diagnosis

5.

3. 4.

6. 7.

8.

MANAGEMENT Admit patient (inpatient management) Monitor patient (Vigilance for chorioamnionitis) Clinical (Maternal fever, tachycardia, uterine pain/tenderness, purulent vaginal discharge, fetal tachycardia) Laboratory investigations e.g. total white count and differential count, C-reactive protein, HVS C&S Biophysical profile of fetus IM dexamethasone nd 12mg stat, repeat 2 dose after 12 hour Prophylaxis antibiotic Erythromycin 250mg orally 6hourly for 10 days To reduce risk of chorioamnionitis If chorioamnionitis: cephalosporin + metronidazole (augmentin) immediately Discharged after observe 48-72 hous if no more leaking liquor, no infection, no labor symptoms Delivery indicated if: Chorioamnionitis is diagnosed Fetal distress occurs Post-natal: Maintain vigilance and screening for infection. Neonatal screen for sepsis

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Together in Delivering Excellence (T.I.D.E) COMMON QUESTIONS 1. Complications Maternal complication: 1) Infection - Associated with 30% subclinical chorioamnionitis with PPROM. 2) Abruptio placenta is evident in 4-7% of women with PPROM. 3) Psychosocial sequelae, particularly related to PPROM, with the disruption created by maternal hospitalisation and continued observation associated with uncertain fetal/neonatal prognosis. 4) Increased likehood of operative delivery associated with induction of labour will increased the chance of maternal complications. 5) Increased incidence of marginal cord insertion and Battledore placenta which may account for increased incidence of retained placenta. This in turn may be associated with the known increase in the incidence of primary and secondary post-partum hemorrhage. 6) Associated with 10% incidence of endomyometritis Fetal complication: 1) Prematurity and risks of prematurity like RDS, NEC, intraventricular hemorrhage, etc. 2) Neonatal sepsis - 2-4% 3) Oligohydroamnios tetrad characterised by facial anomalies, limb position defects, pulmonary hypoplasia and impaired growth, all of which will lead to neonatal morbidity. 4) Fetal hypoxia due to greater risks of cord prolapse, cord compression and abruptio placenta 5) Neonatal morbidity will be increased due to mechanical difficulties encountered with delivery either by vaginal or abdominal route as a result of increased incidence of malpresentations and reduced volume of amniotic fluid 2. Advise upon discharge - No sexual intercourse - Come back if leak again, contraction pain, infection - Frequently follow up antenatally 3. Role of tocolytic in PPROM - No significant benefit in prolongation of pregnancy to term - Allow course of steroid for fetal lung maturation to be completed - To facilitate transfer of undelivered mother to a unit that able to provide appropriate neonatal care Reference: 1. Obstetric 10 Teachers 19th edition (MOST) 2. Specialist notes 3. Student notes o&g

87

Together in Delivering Excellence (T.I.D.E) Heart Disease (HD) in pregnancy [Hidayah]

HISTORY  Epidemiology : 1 % of pregnancy  Risk factors : 1. CHD 2.hypercholesterolemia 3. Family hx of HD , hypercholesterolemia 4.hx of RHD during childhood  History 1. Diagnosis -type of lesion, when/where/how?, causes (CRHD,CHD,HPT), procedure( exercise test,echo), surgical/corrective done?, any improvement/residual? Medication& diet, compliance/f.up, cx, admitted before? 2. Symptom – fatigue at rest, exertional chest pain, orthopnea, PND, palpitation, exertional syncope, NYHA classification* 3. Any pre conceptional advice – surgical advice?, explain about mother& fetal risk, willing for frequent f.up&long stay in ward, should have early booking. 4. Booking- when, ix,echo&result, early u/s for dating (risk of prematurity), u/s for CHD~20W 5. Symptom that may aggravated heart failureAnemia (pallor, lethargic), UTI (dysuria, frequency), URTI (running nose, sorethroat) 6. Pregnancy- in labour ? fetal movement

PHYSICAL EXAMINATION General o Anemia o Clubbing, infective endocarditis signs, o xanthoma o Pulses (arrhythmias) o Blood pressure o Jugular venous pressure o Cyanosis o Dental carries o ankle edema Abdomen examination (as usual)  Uterus smaller than date or any abnormalities Chest examination  Shifted apex beat  Murmur  Basal crepitation

INVESTIGATION Maternal 1. 2. 3. 4. Fetal

FBC – Hb , WBC ( can aggrevate HF) Urine FEME (TRO UTI) ECG Echocardiogram

1. CTG : to look evidence of fetal hypoxia 2. U/S : detailed detection of fetal anomalies, AFI, fetal growth&placentation.

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Together in Delivering Excellence (T.I.D.E) MANAGEMENT Preconception 1. Fully accessed 2. Treat aggresively any medical illness (try to stabilize before pregnancy) 3. If surgery needed, do b4 pregnancy (mitral valve replacement in MS) 4. Counselling about: Effect of haemodynamic changes&maternal risk Effect of fetal growth & preterm Genetic transmission Effect of maternal drug & compliance Need for frequent admission & long stay 5. Encourage complete family earlier&discourage from multiple pregnancy.

 Time and mode of delivery 1. Mild & moderate heart dis Aim for spontaneous vaginal delivery Avoid induction of labour if possible 2. Admit patient early, wait for birth if : Severe heart disease Develop acute heart failure 3. Prepare for preterm labour for severe heart dis pt (high chance to deliver at 32-34W in severe MS) 

Intrapartum 1. Aim delivery within 6 H 2. Stop heparin b4 pregnancy (clexane stop 6H b4 delivery) 3. Prop up to left lateral tilt 4. Continue ECG, CTG & pulse oximeter 5. Give oxygen (3L/min) 6. Give epidural anaestesia 7. AB prophylaxis (in severe cases) IV ampicillin 2g stat & 8 H later 2x doses IV gentamicin 800mg & 8H later 2x dose 8. Avoid fluid overload by close monitoring during fluid therapy nd 9. Shortened 2 stage by using instrumental delivery rd 10. For 3 stage, give syntocinon(don’t give ergometrine)



Postpartum 1. Keep pt in labour room for 6-24H after delivery 2. Give Lasix 40mg stat (to prevent fluid overload during ntrapartum) 3. Admit ward at least 1 w 4. Close monitoring (i/o chart, BP, PR, RR, ECG) 5. Look for any complication 6. Continue prophylaxis AB for 5 days 7. Advise for contraception (POP,barriermethods, sterilizationBTL)



Management of Heart Failure 1. Inform cardiologist,obstetrics,anes-send to CCU/ICU 2. Semi-recumbent (propup) 3. Oxygen 4. Morphine (pain relief&dilate vein) 5. Frusemide 6. Digoxin-dysrhytmia 7. Endotracheal intubation 8. Assisted aspiration 9. Cardiac surgery 10. Leg exercise/stocking (prevent DVT)

Antenatal  Booking 1. All mother examined carefully for CVS abn. 2. If suspected, refer to cardiologist & do echo 3. Known case should book early 4. Cases should be managed in combined clinic 

Antenatal 1. Regular antenatal checkup  Assess maternal : ( sx HF and NYHA), ECG, vital sign  Assess fetal : detailed scan for congenital anomalies, serial growth scan to detect IUGR, Fetal kick chart, CTG. 2. Avoid factor aggravate HF and treat Anemia Infection- UTI, URTI Hyperthyroidism Arrhytmia Multiple gestation 3. Advise about : rest, no smoking, compliance to hematinic, care about infection, dental checkup (prevent I.E) 4. Anticoagulant indicated in pt congenital heart disease who have pulmonary HPT or artificial valve replacement. 3 types of regime :  Continue warfarin throughout pregnancy, replace heparin for delivery (1-2w prior to delivery st  Replace warfarin with heparin in 1 trimester,other same st as 1 regime  Use heparin throughout pregnancy

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Together in Delivering Excellence (T.I.D.E) Common/Possible Question in Exam + Answer 1.

CVS Normal physiology in pregnancy a.

b. c. d. e. f. g.

2.

Risk stratification - maternal risk Low risk (mortality <10%)

1. 2. 3.

CO= SV x HR

st

CO ↑ in 1 trimester 30-50%, max at 20-24W d/t :  ↑ Stroke volume in early pregnancy  ↑HR in late pregnancy *bcoz of this pt prone to develop acute pulmonary edema at 20-24W nd Blood volume ↑40% , accelerated in 2 trimester, peak at 24W  Primi-1200ml, Multi-1500ml,Twins 2000ml Falli in systemic vascular resistance & BP d/t AV shunt in placenta & vasodilator effex=ct of progesterone ↑ in pulmonary blood flow but ↓ in pulmonary vascular resistance. Term , uterus compression on IVC, ↓30% CO During labour, anxiety, pain & uterine contraction ↑CO bout 50% Immediately after delivery  ↑ venous return d/t relief of caval compression & auto transfusion from contracting uterus.  HR & CO ↓within hours post delivery

Acyanotic heart disease Uncomplicated AR/MR Uncomplicated septal defect (ASD/VSD)

Moderate risk (mortality 5-15%) 1. 2.

High risk (mortality 25-50%)

Coarctation of aorta Prosthetic valve on coagulation

1. 2. 3. 4. 5.

3.

Risk factor to develop heart failure     

4.

5.

Systemic ventricular dysfunction (ejection fraction<30%,NYHA class III-IV) Pulmonary HPT Cyanotic heart dis Aortic pathology (dilated aortic root >4cm,Marfan syndrome) MS&AS (severe)

Respi / urinary infection Anaemia Obesity Corticosteroid Tocolytics

    

Multiple gestation HPT Arrhythmias Pain related stress Fluid overload

Stages of heart failure

Side effect of anticoagulant Warfarin : maternal bleeding (at vitamin K & FFP during labour, fetal intracranial hemorrhage and teratogenicity. Heparin : usage more than 6 month causing osteoporosis

6.

Complication of heart dis in pregnancy : Maternal 1. Heart failure 2. Arrythmia 3. Acute pulmonary edema

Fetal 1. Preterm labour 2. IUGR 3. Congenital heart disease 4. Maternal cyanosis (fetal hypoxia) 5. Effect of maternal drug (teratogenesis, growth restriction, fetal loss)

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Together in Delivering Excellence (T.I.D.E) Abnormal Lie/ Breech Presentation [Amy] HISTORY o

o o o o o

o

Age, Parity – high parity increase risk, Gravida, LMP, POA-prematurity, EDD **unstable lie : lie of fetus change time to time beyond 37 weeks U/L GDM or PIH – macrosomia, fetal abn eg hydrocephalus, anencephalus Gynaecology problem/surgery done eg menorrhagia, mass – uterine fibroid , scar History of antepartum bleeding – placenta praevia Congenital abn – uterine malformation Scan done  No of gestation – multiple gestation  Liquor volume – poly/oligohydramnios  Fetal growth - macrosomia  Fetal abnormalities Fetal movement - IUD

PHYSICAL EXAMINATION Inspection Broad fundus – transverse Palpation SFH smaller than date – transverse/oblique No presenting part felt over brim Try to feel for uterine fibroid

Type of abnormal lie : 1. Transverse 2. Oblique 3. Unstable lie

Breech presentation Palpation : longitudinal lie, firm lower pole, limbs to one side, hard head at fundus Auscultation : fetal heart heard above umbilicus VE : no head in pelvis. Soft buttock felt and hard irregular sacrum. Type of breech presentation : 1. Extended breech ** 2. Flexed breech

3.

INVESTIGATION 1. 2.

3.

GSH– before ECV Ultrasound o Confirm gestation no and age – prematurity o Normality – congenital abn o Biometry – IUGR, macrosomia o Viability – IUD o AFI – oligo/polyhydramnios o To confirm lie/presentation of fetus o Uterus – fibroid, placenta praeviae CTG

Footling breech

MANAGEMENT External Cephalic Version (ECV) – breech o Nulliparous : 36w, multi : 37w o NBM 6h and request GSH o Prepare for c-sec if ECV failed. o Administer tocolytics eg. Nefidipine, Salbutamol o Fetal heart rate monitoring before and after o No more than 2 attempts at version o Before depart, check FH, PV discharge/bleeding o If failed, elective c-sec at 38-39 w or vaginal breech delivery – spontaneous breech delivery, assisted breech delivery, total breech extraction OR Stabilizing Induction – unstable lie 1. Vaginal delivery if cervix favourable 2. Ensure longitudinal lie & cephalic presentation 3. IV Syntocinon to start uterine contraction 4. Keep close watch to have continuing cephalic presentation 5. ARM when uterine contraction regular with : o Stabilizing head into pelvis by assistant o ARM when uterine contraction to prevent amniotic fluid embolism o Slow release of liquor 6. VE to exclude cord prolapsed. If failed, elective c-sec at 38weeks.

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Together in Delivering Excellence (T.I.D.E) 1.

Definitions o Lie : relationship between longitudinal axis of fetus to longitudinal axis of maternal uterus o Presentation : part of fetus that present in pelvic brim

2.

Complications o Antenatal : risk PPROM and cord prolapsed o Intrapartum Fetal o rapid compression and decompression cause intracranial injury o Cord compression – delay will cause birth asphyxia o Abdominal viscera damage Mother o Uterine rupture/cervical lacerations/perineal laceration o Uterine atony/haemorrhage

3.

ECV **women should be counselled successful rate is 50% Easier to perform if : o Multiparous o Adequate liquor volume o Breech free above pelvic brim o Flexed breech Contraindications: Absolute : o Where c-sec is required o Footling breech o APH within 7days o Abnormal CTG o Major uterine anomaly o Ruptured membrane o Multiple pregnancy

Relative : o SGA with abnormal Doppler parameter o Proteinuric PE o Oligohydramnios o Major fetal abnormalities o Scarred uterus o Unstable lie

Risk of ECV : o Placenta abruption o Uterine rupture o Rupture of membrane o Cord accident o Transplacental haemorrhage o Fetal bradycardia 4.

Vaginal breech delivery- unfavourable : o Other CI for vaginal delivery eg. Praeviae, compromised fetal condition o CPD o Footling or kneeling breech o Large baby (>3.8kg) o IUGR (<2.0kg) o Previous c-sec

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Together in Delivering Excellence (T.I.D.E) Anemia in Pregnancy [Aiman]

HISTORY Active symptom:  Weakness/lethargy  Headache  Palpitation  Shortness of breath  Dizziness Further history: 1. Hx of bleeding (APH) 2. Current pregnancy – APH, Multiple pregnancy, infection - if diagnose with anemia - how?when?who?hb level at booking, when diagnose, during subsequent follow up and latest? On what treatment? compliance? 3. Hx of previous pregnancy – PPC, spacing, infection, anemia 4. Family hx of anemia require blood transfusion (her thallasemia status and family) 5. Diet hx – vege

Complication: INVESTIGATION Bedside: Urine dipstic : proteinuria suggest UTI Lab:  FBC (at booking and repeat back at 28weeks-RCOG)  Hb : anemia  MCV(80-95fl) and MCHC(20-35g/dL) i. normal(normocytic normochromic) – haemolysis, blood loss ii. lower(microcytic hypochromic) – IDA, thallasemia, anemia of chronic disease iii. higher(macrocytic) – folic acid or vit b12 deficiency, aplastic anemia Specific:  Serum ferritin: lower than normal (less than 10mg/dl)= IDA  Electrophoresis : normal or not – for thallasemia

PHYSICAL EXAMINATION General Examination  Pallor palm and conjunctiva  Increase respiratory rate  Angular stomatitis, glossitis, koilonychias – suggest anemia due to IDA Others CVS : can presented with CCF (ankle oedema, basal crepitation) and murmur due to hyperdynamic blood flow

Differential Diagnosis : IDA (most common in Malaysia, due to poor spacing) Thallasemia Sickle cell Folic acid deficiency MANAGEMENT In Malaysia: all pregnant lady was prescribe with iron supplement as prevention And screening done during booking # Management depends on cause and severity of anemia For IDA Antenatal:  Trial of iron therapy or iron supplement – if IDA, patient HB will increase in 2-3 weeks time (diagnostic and therapeutic)  Patient with severe anemia require referrel to specialist centre for further management  Target is >10g/dL hb prior to delivery Intra:  GSH rd  PPH prevention – active management during 3 stage  Start transfusion if severe anemia or excessive blood loss Post:  Iron supplement  Counselling regarding contraception and spacing Admission:  When need for transfusion (moderate, >37weeks with sign of labour or severe or with complication)  When have active blood loss

93

Together in Delivering Excellence (T.I.D.E) 1. Hb level (expected to be lower than normal in pregnant lady): Anemia @booking <11g/dL 2nd and 3rd trimester <10.5g/dL Or (<10.5g/dL – RCOG, <11g/dL – WHO) Mild (8-10g/dL), moderate (6-8g/dL), severe (<6g/dL) 2. Risk factor a. b. c. d.

IDA – poor spacing, poor diet(vege), blood loss(worm,infection) Thallasemia Folic acid deficiency Others – myeloproliferaive disorder

3. Complication a. Inability to withstand haemorrhage b. Increase risk of : i. Infection ii. Cardiac failure iii. PPH c. Fetal : low birth weight, IUGR d. Spontaneous abortion in Thallasemia 4. Diet consultation on how to take iron supplement Take on empty stomach, 1 hour before meals, take with Vit. C (juice or supplement) to maximize absorption, and avoid taking antacid, tea or coffee Type

Name

Advantage

Oral iron

Ferrous fumarate(TD) Ferrous sulphate(TD)

Cheap Easy to take

Parenteral iron

Dextrin Imferon

For severe anemia

Disadvantage Dark stool Nausea and vomiting Not compliance Anaphylactic reaction Pain and discolouration at injected area Skin necrosis

*Parenteral iron can be considered from the second trimester onwards and during the third trimester for women with confirmed iron deficiency who fail to respond to or are intolerant of oral iron

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Together in Delivering Excellence (T.I.D.E) UTI In Pregnancy [Aiman] HISTORY Lower UTI  Dysuria, frequency, urgency  Occasional suprapubic pain and hematuria  Cloudy urine

PHYSICAL EXAMINATION General Examination - Depends on severity Tenderness (urethra, suprapubic, loin area)

Acute pyelonephritis(rapid progress hr to day)  Fever + chilss and rigors, flank pain  Varying degree of dysuria, frequency, urgency Mild: appear well Severe: very ill, vomiting, dehydration, abdominal and loin pain Current pregnancy – infection (vaginal discharge) - if diagnose with UTI - how?when?who? when diagnose? On what treatment? compliance? Further history: Previous history of UTI U/L: DM, HIV, STD, obstruction(stone, tumour, stricture), neurogenic bladder

Tachycardia + Tachypnea + Febrile + + in acute pyelonephritis

Differential Diagnosis : Acute pyelonephritis Cystitis Urethritis Acute appendicitis Acute pelvic inflammatory disease VE examination

Complication:    

Miscarriage Premature birth PPROM Low birth weight

INVESTIGATION Bedside: Urine dipstick (midstream urine – must send within 4hr sample taken) proteinuria, pH, *leukocyte esterase, *nitrites *if positive with symptom 90% is UTI, if negative less likely to be UTI Imaging: USS – screen for hydronephrosis, kidney stone, abscess

MANAGEMENT 1. Increase fluid intake 2. Increase bladder empty (adequate urine output to flush out microorganism) 3. Antibiotic Ampicillin/amoxicillin – T. amoxicillin + clavulanate (augmentin) 625mg BD for x7-14/7 -

Lab:  Urinalysis – urine microscopy (white cell count >10WBC/microL, bacteria, pyuria, rbc cast)  Urine C + S – on cysteine-lactose-electrolyte-deficient(CLED) medium using urostrip method (in complicated case or when to change regime) + in pyelonephritis  ABG - Respiratory alkalosis PaCo2 <32mmHg  FBC - Leukocytosis <4000 or >12000 cells/mL  BUSE,Creatinine – Renal function  LFT  Blood culture and sensitivity Specific: Urinalysis

Cephalosporin (not effective, not active against proteus, and affecting normal flora)  Cephalexin – 0.5-1g BD x3-7/7  Cefuroxime – 250-500mg BD x3-7/7 [usually in pregnancy (complicated UTI) longer course is needed for 1-2 weeks] Follow up after 1-2 weeks complete antibiotic + urinalysis and culture 4.

Antipyretic

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Together in Delivering Excellence (T.I.D.E) 1. Why more in female: a. Close to anus (short proximity to anus) b. Its opening to labia c. Short urethra length d. Used of spermicide (diaphragm, cervical cap, condom), insertive rectal intercourse 2. Why in pregnancy is higher(detected in 2-85 of pregnancy): a. Predispose factor for UTI: i. Reduce urethral tone ii. Reduce ureteral peristalsis iii. Temporary incompetence of vesicoureteral valves. iv. Bladder catheterization before or during delivery increase risk b. Obstruction (pelvis or abdominal tumour, stricture, renal stone) 3. Etiology: a. Uncomplicated (most common): E.coli b. Complicated: wide range from gram +ve to –ve c. Community acquired: (Escherichia coli, Klebsiela pneumonia, Proteus mirabilis, Staphylococcus saprophyticus, Enterococcus faecalis) d. Hospital acquired: (E.coli, Pseudomonas aeruginosa, Proteus sp., Enterobacter) 4. Pathogenesis : a. Ascending route (mostly) Normal flora vs gram –ve bacilli(abnormal flora) b. Hematogenous c. Lymphatic (rare) 5. Bacterial virulence factor (not all E.coli strain capable – belongs to serogroup O, K, and H)  Bacterial adherence to uroepithelial celss (hairlike proteinaceous surface and p. fimbrae)  Produce cytotoxins, hemolysin and aerobactin (a siderophore to scavenging iron) – make it resisaant to bacteriacidal action of human serum

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Together in Delivering Excellence (T.I.D.E) Uterus smaller than date [Nur Diana] HISTORY

PHYSICAL EXAMINATION

*Condition:

*Symphysial-fundal height (SFH) < 3cm of gestational age

*Causes: 1. Wrong date 2. Oligohydramnios 3. Missed miscarriage 4. Intrauterine death 5. Fetal growth restriction (FGR) 6. GDM 7. Anemia 8. PIH / pre eclampsia

*Examine fetal heart rate by using pinard

*Complication: Fetal hypoxia, stillbirth INVESTIGATION

*Serial ultrasound – to detect any FGR, liquor amount

MANAGEMENT

* is tailored accordingly to treat the cause.

(oligohydramnious). *A detail fetal anomaly scan *Doppler study of umbilical artery flow *investigations to find out the causes

*What are the causes of FGR? *What do you understand by the term symmetrical & asymmetrical FGR? A. Symmetrical FGR  is more common  usually begins late in pregnancy  manifested as restriction of weight followed by length  but the head continues to grow at normal or near-normal rates B.

Asymmetrical FGR  is less common  begins early in pregnancy  manifested as generalized growth restriction

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Together in Delivering Excellence (T.I.D.E) Uterus Larger Than Date [Sofia] HISTORY st

PHYSICAL EXAMINATION

1. Ask LMP in detail, 1 scan n subsequent scan for REDD

PHYSICAL EXAMINATION (like usual flow of PE)(+ve findg)

2. Ask rgrdg causes of polyhydramnios (AFI >25 / deepest pool >8)  Maternal GDM- ask indication of MOGTT in the pt and result  Fetal: multiple pregnancy(d/t TTTS): when, where & how, risk factor(assisted conception, family hx of multiple preg, high parity, adv maternal age) , increase symptoms of pregnancy (hyperemesis, abd discmfrt, GERD, SOB, frequency, leg swellg), ask complication (TTTS, single fetal demise) :fetal abN: esophageal atresia, tracheoesophageal fistula, duodenal atresia, anecephaly,  placenta: chorioangioma, AV fistula  ask d AFI value  ask complication of polyhydramnios (malpresentation, abN lie, preterm labour)

A.

Polyhydramnios:  Abd distention w tense shiny skin (not really)  Tense on palpation  SFH & fundal height larger than date  Difficult to palpate fetal part or poles  abN lie or presentation  +ve fluid thrill

B.

Multiple pregnancy:  SFH larger than date  2 fetal poles  2 fetal heart sound MANAGEMENT

#Management for polyH, GDM refer dodi’s short notes 3. Ask regarding s/s of uterine fibroid / pelvic mass: menseswhether had heavy bleeding, pelvic pain, recurrent miscarriage, pressure symptoms (frequency, urinary retention, constipation, varisoce vein, leg edema) ask regrdg complication of fibroid to pregnancy: fetal malpresentation, IUGR, preterm labour, placenta previa, PPH, obstructed labour)

1.

4. Ask for macrosomic baby: whether pt DMT2 or GDM, MOGTT indication & result, risk factor(famly hx, past hx of GDM), if GDM or DM as regardg compliance to mdctn n diet in detail, HbA1c, s/s of DM (polyuria, polydipsia, recurrent UTI, vaginal candidiasis), previous baby weight

Establish the cause- if DM, need to optimize the glycemic control, if due to TTTS, can do amniodrainage & laser ablation of anastomose placental vessel, if d/t fetal aBN, monitor fetal wellbeing  Amniocentesis: for severe poly, symptomatic poly, failed indomethacine, cx: preterm labour, chorioamnionitis, PPROM & abruption  Indomethacine (PG-E)- reduce liquor amount by antagonist anti diuretic effect of ADH on collecting duct, shud discontinued at 32-35w d/t risk of premature closure of ductus arteriosus, cerebral vasoC, impaired renal fx

2.

Ultrasound- like describe earlier

5. Baby well being (fetal kick chart)

3.

Admit if- maternal discomfort, risk of preterm labour (give dexamethasone), risk of membrane rupture (risk of cord prolapsed & placenta abruption)

4.

Time of delivery: 38-39w

5.

Mode of delivery: a) Spontaneous vaginal delivery- if cervix favourable & longitudinal lie b) Elective c-sec- if poly + transverse lie

6. Details of ultrasound (any fetal abN, AFI, any pelvic mass, fibroid, position of placenta) 7. S/S of labour INVESTIGATION

1. 2. 3. 4. 5. 6.

FBC to look at Hb level BUSE- for baseline GSH Ultrasound- like I describe earlier CTG- for fetal wellbeing GDM ix- refer dody’s notes

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Together in Delivering Excellence (T.I.D.E) Common/Possible Question in Exam + Answer 1.

UTERUS LARGER THAN DATE?       

Wrong date (LMP) Polyhydramnious (excess amount of Amniotic Fluid in Uterus) Larger baby (macrosmia) ( d/t GDM: dodi akn cover) Multiple pregnancy Molar pregnancy Uterine fibroids Pelvic mass

2.

Uterus smaller than the dates?  Wrong date (LMP)  Oligo hydramnious  Smaller baby (microsmia)  Head engaged too deeply  Genetic (maternal paternal small size)  Intrauterine Growth Restriciton (IUGR)  Intrauterine death (IUD)  Transverse lie

3.

Amniotic fluid index  Summation of all max vertical pool (4 quadrants) rd  3 trimester value: (N: 10-25)  <5cm : oligo  <10cm : reduce  25cm : polyhydramnios

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Together in Delivering Excellence (T.I.D.E) Dysmenorrhoea [Farhan] HISTORY  Definition: painful menstruation  Primary (absent of pelvic pathology) vs secondary (presence of pelvic pathology)  Risk factor for severe dysmenorrhea: i. Early menarche ii. Nulliparity iii. Long menstruation period iv. Heavy menstruation v. Smoking vi. Positive family history  Primary dysmenorrhoea: i. occurs 6 to 12 months following menarche ii. pain: lower abdominal and cramping in nature; may radiate to the back and to the inner thigh, lasts from 8 to 72 hours and accompanies menstrual flow or precedes it by only a few hours

iii. a/w other systemic symptoms such as vomiting, nausea, diarrhoea, fatigue, and headache  Secondary dysmenorrhea: i. occurs years after menarche (30s – 40s) ii. pain: not consistently related to menstruation alone, may worsens as menstruation progress iii. a/w irregular bleeding pattern, heavy periods, dyspareunia, vaginal discharge iv. common causes: endometriosis, chronic pelvic inflammatory disease, adenomyosis, intrauterine polyps, submucosal fibroids INVESTIGATION  Urine pregnancy test  FBC: to exclude anaemia  WBC, ESR, and CRP: raised WBC with a high ESR and CRP  acute/chronic inflammatory disease, but not specific  Swabs: for chlamydia and gonorrhoea from the endocervix and posterior fornix of the vagina  Tumour markers such as Ca-125: should be checked in the presence of an ovarian mass, but non-specific and levels can be elevated in endometriosis  Ultrasonography: fibroids, adnexal pathology, endometriomas, and intrauterine contraceptive devices are best assessed with ultrasonography  Laparoscopy: aids in the diagnosis of endometriosis, adhesions, and pelvic inflammatory disease and at the same time can offer treatment  MRI and CT pelvis and/or abdomen

 Hysteroscopy

PHYSICAL EXAMINATION    i.

ii.

iii. iv.

Do a complete pelvic examination, external gentalia, speculum and bimanual examination Primary dysmenorrhea: usually unremarkable Secondary dysmenorrhea Endometriosis: positive in ~40% of the time with adnexal, rectovaginal, and uterine tenderness, together with cervical excitation. Acute or chronic inflammatory disease: tender pelvic examination and abnormalities such as the presence of adnexal masses (usually bilateral) may occur, particularly in chronic disease. Speculum examination, in acute cases, may reveal a purulent vaginal discharge and an erythematous vagina and cervix. Fibroid uterus: suggested by an enlarged uterus with an irregular contour. Adenomyosis: a tender and globular shaped enlarged uterus is frequently palpable during bimanual examination

MANAGEMENT  Primary dysmenorrhea: to provide relief from cramping pain and associated symptoms  Secondary dysmenorrhea: pain control and treat the underlying cause  NSAIDs: decrease menstrual pain by decreasing intrauterine pressure and lowering prostaglandin F2α (PGF2α) levels in menstrual fluid. e.g. Ibuporfen, Diclofenac, Mefenamic acid, Naproxen  Oral contraceptives: COCPs, the levonorgestrel intrauterine device, and depot medroxyprogesterone acetate provide effective pain relief and are associated with reduced menstrual flow. It may be necessary to add an NSAID to the OC.  Others: direct application of heat, diet e.g. low fat vegetarian, fish oil, vitamin E

 Prevention: exercise, smoking cessation

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Together in Delivering Excellence (T.I.D.E) 1. How does Prostaglandin cause pain?     

↑ prostaglandin production cause : ↑ uterine cramping  uterine ischaemia and pain cause hypersensitization of pain terminal to physical and chemical stimuli studies shown ↑ PG production during 1st 48-72 hours of menses ↓ PG can decrease the pain

2. How do birth control pills reduce cramping?   

↓ thickness of the endometrium and change the hormone status to the same levels as those found in the early proliferative stage lowest level of PG production ↓ cramping, uterine ischaemia and pain

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Together in Delivering Excellence (T.I.D.E) Ovarian CA [Rafidah] HISTORY Epidemiology

PHYSICAL EXAMINATION GENERAL    

Lifetime risk in general population 1:70 (1.4%) Mean age 64 yrs old Women with hereditary cancer present early with mean age of 54 years Epithelial ovarian ca >50 yrs Malignant Germ cell tumour younger than 20 yrs old

SPECIFIC

Aetiology and Risk factor Decreased risk of ovarian Ca  Multiparity  OCP  Tubal ligation  Hysterectomy

Increased risk of ovarian ca  Nulliparity  Intrauterine device  Endometriosis  Cigarette smoking  Obesity  Early menarche  Late menopause  Clomiphene citrate > 1 year  Hereditary ovarian ca – BRCA1,BRCA 2, HPNCC

S&S         

Pallor Loss of weight Cachexia(late) Palpable left supraclavicular LN

Asymptomatic Abnormal uterine bleeding d/t hormone producing ovarian cancer such as granulosa cell tumour Gastrointestinal sx: bloating, abdominal distension, abdominal discomfort Abdominal mass Respi sx due to abdominal distension, plueral effusion, or metastases Constituitional sx: LOW, LOA, lethargy Persistent pelvic and abdominal pain Acute sx are rare, this result from pain due to torsion, rupture, infection, or intracystic hemorrhage Bowel and urinary sx if being compressed

Abdominal examination  

Bimanual examination 

1) 2) 3)

CA 125 >35iu/ml (epithelial ovarian ca more in serous type) CEA in mucinous AFP (in germ cell tumour such as endodermal sinus tumour, immature teratoma, dysgerminoma 4) Hcg in choriocarcinoma 5) Inhibin and estrogen in granulosa cell tumour 6) Androgen in sertoli leydig cell tumour 7) FBC – anemia 8) BUSE – electrolyte imbalance 9) LFT - metastasise 10) Chest xray - metastasise

Imaging a. Ultrasound : Features of malignancy – bilaterality, presence of solid areas, papillary projection, ascites, hydronephrosis, or liver secondaries b. CT scan: To identify lymphadenopathy and detect peritoneal tumour deposit, assessment of operability

Endoscopy 

Done in those with occult blood or significant intestinal sx



To exclude primary colonic cancer with ovarian metastases

Adenexal mass – fixed/ immobile if spread to surrounding structure

Chest examination   

Palpation: Reduced chest expansion Reduced vocal fremitus Percussion: stony dull Auscultation: reduced breath sound and vocal resonance

Breast examination 

INVESTIGATION Laboratory

Abdominal distension Fluid thrill +ve in gross ascites, shifting dullness in mild ascites

Breast lump (breast ca may metastasise to ovarian

MANAGEMENT (EOC) STAGE 1a, 1b, 1c TAHBSO – the best therapeutic management Omentectomy is also done - as it harbour microscopic disease All clinically stage 1c will be given post operative adjuvant chemotherapy •

In stage 1a or 1b additional features such as grade of tumour , histological type need to be considered => 1a or 1b with grade 2 or grade 3 tumour, risk of relapse is high – it is recommended to give adjuvant chemo • If patient wish to keep fertility, consider conservative fertility sparing surgery (justified after careful exploration to exclude metastatic disease) • Unilateral salpingo-oophorectomy • Omentectomy • Peritoneal biopsy • Pelvic/paraortic disecction STAGE 2a, 2b 2c

•

TAHBSO with omentectomy is the treatment of choice in many centres

• Adjuvant therapy include systemic chemotherapy ADVANCED STAGE : STAGE 3 & 4  Patients who have had cytoreduction (debulking) should receive adjuvant chemotherapy  Patients who could not undergo primary cytoreduction prior to chemotherapy due to physical unfitness: interval debulking may be considered after three cycles of systemic chemotherapy (neoadjuvant chemo)

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Together in Delivering Excellence (T.I.D.E) Chemotherapy Can be given as:   

Primary treatment Adjunct following surgery relapsedisease

First line treatment:  -

-

Combination of platinum compound with paclitaxel (given as outpatient basis, 3 weeks apart for 6 cycles) Platinum Most effective chemotherapeutic agent in ovarian cancer MOA: heavy metal cause cross linkage of DNA strand, thus arresting cell replication Eg: carboplatin (less renal toxic, less nausea), cisplatin (more S/E compared to carboplatin) Paclitaxol MOA: work by causing microtubular damage to cell, thus prevent replication and cell division Given together with steroid to prevent high sensitive reaction, side effect of peripheral neuropathy, neutropenia, myalgia and loss of total body hair.

FIGO staging Stage I IA IB IC II IIA IIB IIC III IIIA IIIB IIIC IV

FIGO definition Growth limited to one ovaries Limited to one ovaries: no external tumour. Capsule intact, no ascites Limited to both ovaries: no external tumour, capsule intyact, no ascites Either IA or IB, but tumour on surface of ovary or with capsule rupture or with ascites positive for tumour cells Growth limited to pelvis Extension and/or metastasise to uterus or tubes Extension to other pelvic organ As IIA, or IIB, but tumour on surface of ovary or with capsule ruptured or with ascites positive for tumour cells Growth limited to abdominal peritoneum or positive retroperitoneal or inguinal lymph nodes Tumour grossly limited to pelvis with negative nodes but histologically confirmed microscopic peritoneal implant Abdominal implants <2cm in diameter Abdominal implants >2cm diameter or positive retroperitoneal or inguinal lymph nodes Growth involving one or both ovaries with distant metastases Must have positive cytology on pleural effusion, liver parenchyma

Prognostic factor in ovarian cancer -

Stage of disease Volume of residual disease post surgery Histological type and grade of tumour Age at presentation

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Together in Delivering Excellence (T.I.D.E) Endometrial Mass (Zuraidah) PHYSICAL EXAMINATION

HISTORY Endometriosis : presence of endometrial tissue outside both the uterine cavity & myometrium Adenomyosis : endometrial tissue found within the myometrium Fibroid : benign tumors of uterine smooth muscle (leiomyoma)

Endometriosis

Adenomyosis

Uterine fibroid

History  Peak in 30-45years of age  20 dysmenorrhea- pain begin prior to onset of the menses, increase intensity during flow, gradually improves as bleeding settles  Acute/chronic  Pain in lower abdomen, back or perineum  Abnormal bleeding, irregular, menorrhagia  Deep dyspareunia  Infertility  Occur in older multiparous women 0  2 dysmenorrhea  Cyclic, cramping uterine pain  Severe menorrhagia  Distended abdomen (symmetrical)  Occurs in reproductive age  Risk factor: nulliparity, obesity, +ve family hx  Usually asymptomatic  Symptoms  Menorrhagia (submucous)  Dysmenorrhea (slight discomfort to colicky pain at suprapubic, low backache  Acute abdomen/pelvic pain: degenerated/ torsion of fibroid  Urinary sx (pressure)  Sbfertility :mechanical distortion/occlusion

INVESTIGATION Laboratory 1. FBC -  hb, mild leukocytosis in endometriosis 2. ESR – elevated in endometriosis 3. CA 125 – elevated in endometriosis & adenomyosis Imaging Endometriosis

Adenomyosis

Fibroid

Ultrasound  May found  Thickened endometrioma ( myometrium chocolate cyst) - cyst  Ill-defined containing echogenic heterogenous material (inside of echotexture cyst looks full of within white shadows with myometrium layering rather than uniformly dark:presence of blood) MRI Definitive ix as it  detect lesion > 5mm provides excellent in size, particularly in images of deep tissue, eg: myometrium, rectovaginal septum endometrium & areas of adenomyosis Laparoscopy Dx only confirmed - gold standard by histology after - typical endometrial hysterectomy appearance “powder burn” – small brown/ black puckered lesion look like remaining cigarette burn

 hypoechoic, but can be sooechoic or even hyper compared to N myometrium  calcification is seen as echogenic foci with shadowing  cystic areas of necrosis or degeneration

Hysterosalpingograp hy/ hysteroscopy - detect submucous fibroid

General  Anemic – pallor, conjunctiva pale  Lethargy Specific Endometriosis  Palpable mass  Tender – if rebound tenderness + rigid abdomen indicate of large endometrioma ruptures, spilling blood into peritoneal cavity (acute abdominal pain)  Pelvic exam – areas of tenderness / palpabe mass d/t adhesions or endometrioma.  Rectovaginal exam – tender nodular indurations along the uterosacral ligaments Adenomyosis  Pelvic exam: - Symmetrical enlarged uterus & tender all over - Soft and boggy uterus Fibroid    

Uterus palpable if > 14w Usually non tender, if present only occur over one localized fibroid (d/t degeneration) Firm in consistency & well defined margin Pelvic exam : - Enlarged uterus - regular/ irregular - uterus not felt separate from the swelling - cervix move with movement of swelling - move side to side

MANAGEMENT Adenomyosis:  definitive tx is hysterectomy with or without ovarian conservation Endometriosis Medical 1. Analgesic : NSAIDs 2. Combined oral contraceptive (COC) – taken continuously for 6m – induce amenorrhea 3. Progestogens – if COC is at risk 4. Gonadotropin releasing hormone (GnRH) agonist – relieve severity of sx by induce state of hypogonadotropic hypogonadism/ pseudomenopause with low circulating estrogen Surgical 1. Laparoscopic with diathermy, laser vaporization or excision – drained & inner cyst lining should be excised 2. Hysterectomy & bil salpingooophorectomy (definitive)  for severe/ progressive dz  women whose completed families followed by HRT

Fibroid Conservative Asymptomatic & detected incidentally  repeat clinical exam/ us after 612month interval Medical 1. Gonadotropin releasing hormone (GnRH) agonist – shrinking fibroids by downregulate the pituitary thus reduce estrogen level. Limited to use in preparation for surgery (myomectomy or hysterectomy) Surgical 1. Hysteroscopic removal – menorrhagia a/w submucous fibroid or fibroid polyp 2. Myomectomy  bulky fibroid that causes pressure sx  preservation of fertility 3. Hysterectomy (definitive) 4. Uterine artery embolization (UAE) – embolization of both uterine arteries under radiological guidance. Lead to shrinkage of fibroid & reduction in menstrual blood loss

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Together in Delivering Excellence (T.I.D.E)

Types of fibroid Submucous fibroid – whorled tumour located adjacent to & bulging into the endometrial cavity Intramural fibroid – centrally within myometrium Subserosal fibroid – at the outer border of the myometrium Pedunculated fibroid – attached to the uterus by a narrow pedicle containing blood vessels

Different types of degeneration in fibroid?     

Red Hyaline Cystic Calcification Malignant/sarcomatous

105

Together in Delivering Excellence (T.I.D.E) Miscarriage [IQbaL] HISTORY Definition : Spontaneous loss of pregnancy at or before 24 weeks gestation 10-20% incidence in confirmed pregnancy Majority at 1st trimester Risk factors (RF) a) Embryonic  Chromosomal abnormalities b) Maternal  Advanced maternal age (>35yo, dec good no. of good Oocytes)  Genital tract infection (bacterial vaginosis)  Medical/endocrine disorder  Uterine abnormalities  Drugs/chemicals

INVESTIGATION 1. 2. 3. 4. 5.

UPT FBC – infection (anemia, TRO septic miscarriage) Rhesus blood group Serum B-hCG titre – to confirmed pregnancy Tran-vaginal US  Key Dx of miscarriage provided serum B-hCG >1500UI/L i. empty gestational sac ii. no visible yolk sac iii. crown-rump length > 7mm but no fetal heart activity  Help to differentiate btw complete/incomplete

Key diagnostic factors

i. ii.

Presence of RF

Vaginal bleeding with or without clots Other diagnostic factors  Suprapubic pain, low back pain  Recent post-coital bleed



Uterine structural abnormality

Chronological History Confirmed pregnant? UPT done? Hx post-coital? Any atypical blood clot expelled? Severity of vaginal bleeding? – flooding, clots, inc in duration & no. of pads used per day, anemic sx Important TRO ectopic pregnancy (pelvic/suprapubic pain a/w fainting attack or unexplained anaemia) Recent genital infection? Fever? Hx of recent trauma

PHYSICAL EXAMINATION GENERAL  Clinically well  If ill-looking – significant blood loss SPECIFIC A. CVS  Any pale, tachycardia, hypotension (anemic)  Dyspnea (ectopic pregnancy) B.

Abdominal-pelvic  Size of uterus

C.

Perineum  Any local lesion that lead to bleeding

Speculum examination  Early pregnancy tissue?  Cervical Os : open/closed?  Laceration, cervical ectropion?

MANAGEMENT Initial Management  Monitoring : BP, pulse rate, temperature  Lab Ix : Hb level, GXM ( if pt is severely compromised)  Pt with miscarriage can have expectant, medical or surgical management Expectant No intervention May have unplanned surgery if bleed heavily Surgical ERCP (evacuation of product of conception) Successful rate : 95-100% Risk of cervical trauma, subsequent cervical incompetence, uterine perforation, intrauterine adhesion & post-operative pelvic infection Medication Prostaglandin : Orally (misoprostol) or vaginally (Gemeprost) Increase rate of successful : prostaglandin + Mifepristone (progesterone agonist) Counselling To ensure pt understand most miscarriage are nonrecurrent

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Together in Delivering Excellence (T.I.D.E) WHO classification Type

THREATENED [cervical os CLOSE]

Clinical Presentation

U/S finding

Management i. ii. iii. iv.

 Unprovoked vaginal bleed  With/out lower abd pain  Occur <22 weeks gestation

v. Intra-uterine pregnancy

INEVITABLE [cervical os OPEN]

 Painful vaginal bleed  POC at cervical  If excessive bleeding  hypovolemic shock Ferguson reflex (oxytoxin release) # Pregnancy will not continue  proceed to incomplete/ complete miscarriage

vi. i. ii. iii. iv. v.

i. INCOMPLETE [cervical os OPEN]

COMPLETE [cervical os CLOSED]

Missed miscarriage [cervical os CLOSED]

 Painful vaginal bleed  POC partially expelled

 Minimal pain or bleeding

 With/out pain and bleeding

Retained POC

No retained POC

 Fetal pole present but no fetal heartbeat  Gestational sac present (diameter >20mm) but no fetal pole identified

REASSURE pt Admit if excessive bleeding TCA scan in 1-2 weeks Advice : proper rest at home, no strenuous or heavy work, no SI until 12th week gestation & no further bleed Give Duphaston : to restore luteal f(x) & relax smooth ms of uterus Anti-D immunoglobulin if indicated Stabilized pt Manual evacuation : digitally or with sterile ovum or sponge-holding forceps Analgesic Counselling Anti-D immunoglobulin if indicated

ii. iii. iv. v.

Controlled bleeding (IV/IM Ergometrine or IM syntometrine) Surgical evacuation (D&C) Analgesic Counselling Anti-D immunoglobulin if indicated

i. ii. iii.

Analgesic Counseling Anti-D immunoglobulin if indicated

i.

ii.

Cervical softening (vaginal gemeprost 1mg, oral/vaginal misoprostol) 2-3 hour before evacuation Surgical evacuation under GA/reginal anaesthesia

Complication Septic miscarriage : ascending bacterialinfection secondary to incomplete miscarriage or termination of pregnancy  Common organism : E.coli, bacteroids, streptococci  Symptoms : unwell, fever, lower abd pain. Foul smelling vaginal discharge  Signs : spiking temperature, lower/pelvic pain, guarding  U/S : presence of POC  Management o Admit pt o Ix : FBC, Blood C&S, swab from endocervix fot C&S, BUSE and creat & LFT o Fluid resuscitation o Anti-biotic (cover gram positive, negative & anaerobes DIFFERENTIAL DIAGNOSIS CONDITION Differentiating signs/symptoms Differentiating test  TAS is diagnostic : no intrauterine gestational sac, complex or cystic adnexal mass with/out free fluid in pouch of Douglas  Atypical symptoms that can be missed ( iliac fossa/suprapubic pain, unexplained pallor, tachycardia or syncope  Serial serum B-hCG + single measure of Ectopic pregnancy progesterone : to distinguish between early viable,  O/E : adnexal tenderness or suggestion of haemoperitoneum poor prognosis or ectopic gestation  If in doubt, laparoscopy to confirm Dx : distended, ruptured or haemorrhagic fallopian tube or other extra-uterine preg site.  Uterine size more larger than expected gestational age  TAS : classic Snow-storm appearance Hydatidiform mole ( Molar )  Pregnancy Sx are marked  Partial hydatidiform : reveal fetus but unusuallooking placenta  Very rare : passed some molar, grape-like tissue  Suprapubicpain + DYSURIA & FEVER  Urine microscopy and culture Cystitis  May have haematuria Pregnancy co-excisting with a  May be suspected from appearances of the ecto-cervix on  Confirm after U/S or by spontaneous avulsion of bleeding cervical polyp/ large speculum examination polyp ectropion

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Together in Delivering Excellence (T.I.D.E)

ORTHOPAEDIC

Notes

108

Together in Delivering Excellence (T.I.D.E) Osteomyelitis [Fatin] HISTORY *Inflammation of bone caused by infection o Epidemiology :  cause by Staph A. (H.influenza in children)  site : children (metaphysis and epiphysis of long bone) & adult (spine, pelvic & foot if has DFU) o Causes :  Hemato spread – UTI, pneumonia  Local infection – infected puncture wound  Direct contamination – open #, iatrogenic (surgry) o Risk factor :  DM, Sickle cell dz, peripheral vascular dz, chronic dz, alcohol, steroid Rx recent injury, ortho surgery o S&S :  Pain, malaise, fever  Swelling, redness, tender, warmth, ↓ROM o Complication :  Spread-septic arthritis (joint), metastatic OM (other bone)  Shortening / deformity (physis is damage)  Chronic OM –pain, fever, redness, swelling, discharge sinus  No- union fracture

PHYSICAL EXAMINATION General  Ill looking, in pain  Vital sign : fever, tachycardia  Sign of septicemia Specific  Swelling, redness, tender, warmth, ↓ ROM  Chronic – discharge, sinus, non-heal ulcer ∆∆ 1. 2. 3. 4.

INVESTIGATION o

Laboratory  FBC- leukocytosis  ESR - ↑  Blood culture  Needle aspiration

MANAGEMENT o

o o

Imaging  X-ray - Acute : First 10 days –normal finding Later – periosteal rxn, lytic area, soft tissue swelling - Subacute (Brodie’s abcess) : lytic area surrounded by sclerotic bone - chronic : sequestrum, involucrum, cloaca, sinus tract  Bone scan – positive b4 x-ray changes appear

Abscess Malignant bone tumour (Osteosarcoma, Ewing sarcoma Lymphoma 4) Metastatic bone tumour

Non-surgical  Antibiotic (3-6/52)  Adult : cloxacillin & fusidic acid rd  Children : 3 gen cephalosporin (gram –ve)  Analgesic Surgical  Drainage of abcess  Debridement of infected, dead bone  Bone graft/ packing material  Removal of implant

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Together in Delivering Excellence (T.I.D.E) Common/Possible Question in Exam + Answer 1.

List the factors that predispose to post-traumatic infection. a) Inadequate debridement. b) Early closure of the wound. c) Unfixed / unstable fracture. d) Wound tension. e) Tight dressing. f) Haematoma formation. g) Use of foreign material implant eg. Internal fixation.

2. What are the complication of osteomyelitis? I. General :  Septicaemia  Metastatic abcsess ii. Local :  Septic arthritis  Spontaneous fracture  Shortening/ Deformity  Chronic osteomyelitis. 3.

Why metaphysis is affected in children  Highly vascular  Thin cortex  Hairpin like arrangement of capillary – blood stasis  Lack of pmn

4.

Pathogenesis

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Together in Delivering Excellence (T.I.D.E) Fracture – Malunion & Non Union [Rozana] HISTORY 

Non union = bone/fracture fails to unite within expected time, with the evidence of cessation of fracture healing.



Malunion = The partial and incorrectly angled joining of two or more large fracture fragments



Risk factor/causes :  Malunion : Failure to reduce a fracture adequately, Failure to hold reduction while healing proceeds, Gradual collapse of comminuted or osteoporotic bone.  Non union : Inadequate blood supply, Infection, Inadequate fracture immobilisation , Intact fellow bone, interposition, Smoking, NSAID



Specific :  Malunion : tenderness, deformity & shortening of the limb, surgical scars , swelling , Limitation of movements, 

Non union : painless, deformity

Sx :  Malunion : pain, loss of function, deformity, swelling, crepitus, abnormal movement, or positioning of a limb, soft tissues  Non union : painless, deformity INVESTIGATION

I.

PHYSICAL EXAMINATION

Imaging :  Non union : a) Atrophic non-union : - Bone looks inactive / cessation of fracture healing (Bone ends are often tapered / rounded), Relatively avascular b) Hypertrophic non-union : - bone gap, Excessive bone formation on the side of the gap, (callus) 

Malunion : Present of fracture line , altered anatomical position

MANAGEMENT i. Non union mx  Depends on the factors : Infection, Inadequate blood supply, Inadequate immobilisation  Mx aimed at optimizing 1)biology (infection, blood supply, bone graft), 2) mechanics (skeletal stabilization)  Atrophy – Fixation & bone grafting  Hypertrophy – Rigid fixation ii. Malunion  Angulation in a long bone (> 15 degrees) & Marked rotational deformity → Osteotomy & internal fixation +/- bone graft  Shortening (> 3cm) in 1 of the lower limbs → A raised boot OR Bone operation

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Together in Delivering Excellence (T.I.D.E) Common/Possible Question in Exam + Answer Notes [any classification,staging, mnemonic etc] 



Indication for ORIF a. Failed conservative rx b. 2# in 1 limb c. Bilateral identical # d. Intraarticular # e. Open # Emergency mx for open #  7 ‘As’ o ATLS  Correct shock , give blood >1.5 L lost or continued bleeding, control of bleeding may require surgery o Assesment  Neurovascular status, soft tissues and photograph wound (reduces number of wound inspection) o Antisepsis  Take swab form wound  Use copious irrigarion with sterile 0.9% saline  Cover with a large antiseptic soaked dressing o Alignment  Align # and splint (+ pain relief) o Anti tetanus

o o 

Cx

    









 Check status and immunize appropriately Antibiotics rd  3 gen cephalosporin eg. Ceftriaxone 1g/24h +/- IV mtronidazole if grossly contaminated Analgesia  Intravenous opiate analgesia titrated to effect

Immediate Internal bleeding External bleeding Organ injury Nerve/ skin injury Vessel injury (limb ischaemia)

   

Later – local Skin necrosis/ gangrene Pressure sores Infection Non/ delayed union

   

Later – general Venous/ fat embolism PE Pneumonia Renal stones

Gustillo classification of open # o Type I - low energy wounds <1cm long eg coz by bone piercing skin o Type II – low energy wound >1cm, causing moderate tissue damage o Type III – all high energy injuries irrespective of wound size  IIIA – adequate local soft tissue coverage  IIIB - inadequate local soft tissue coverage  IIIC – implies arterial injury needing repair Methods of traction (hold the reduction) o Skin traction – uses adehesive strapping to attach the load, cons : load cannot be great & sensitivity to adhesive o Fixed - Thomas splint, weight can be added over a pulley to relieve pressure on ischial tuberosity o Skeletal traction – pin thru bone, bigger forces can be employed o Balanced – weight of limb against the load, enable pt to easily lift leg off bed o Gallow’s – suitable for children up to 2 years, buttock rise above the head FES o Clinical condition in which circulating fat emboli/macroglobules lead to multisystem dysfunction o Common in long bone fracture and pelvic fracture, more frequent in closed fracture than open fracture. o Usually asymptomatic, few patient develop S&S of multiorgan dysfunction ( triad of brain, skin, lungs) o Source of fat emboli – bone marrow o Management is supportive, with an estimated mortality rate of 5 -15 % site of bone graft taken? o

ilium and the fibula are the most common sites for bone-graft harvesting

Radiographic Determinants of Healing: - restoration of cortical continuity (look for healing on 4 cortices - AP and lateral views); - loss of distinct fracture line; - presence of callus (w/ IM nail or external fixator)

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Together in Delivering Excellence (T.I.D.E) Gouty Arthritis [Farhan ] HISTORY  Monoarticular pain with edema and inflammation  >50% occurs at MTP of big toe (podagra)  Other joints are ankle, foot, small joints of hands, wrist, elbow and knee  Can be polyarticular (10%)  Male predominance (4:1)  Caused by deposition of monosodiumurate crystals in/near joints  Precipitated by e.g. trauma, surgery, starvation, infection or diuretics (thiazide)  Acute vs chronic attack  Causes (primary vs secondary): i. Hereditary ii. High purine diet iii. Alcohol excess iv. Diuretics v. Leukaemia vi. Cytotoxics (tumour lysis)  Comorbidities: i. Cardiovascular disease ii. Hypertension iii. Diabetes mellitus iv. Chronic renal failure  Complications: i. Severe degenerative arthritis ii. Secondary infections iii. Urate nephropathy iv. Renal stones v. Fractures (in joints with tophi) INVESTIGATION

PHYSICAL EXAMINATION Acute:  Pyrexia often present  Red, warm, tender and painful joint(s)  Usually monoarticular  Most common MTP joints Chronic:  Tophi (chalky coloured nodules on pinna, tendons, joints) Chronic arthritis (secondary OA, restriction of joint movements) MANAGEMENT Asymptomatic hyperuricaemia should not be treated 1. Treat acute attacks  Use high-dose NSAIDs or coxib  If contraindicated; use colchicine  Steroids can be used  Rest and elevate joints  Ice packs may help

2. Prophylaxis for acute flares  Allopurinol 100mg/24hr, increasing every 2 weeks (max 900mg/24hr) o SE: rash, fever, WCC low o Can trigger acute attack, so wait until 3 weeks after acute attack and cover with NSAIDs or colchicine 1. Serum urate – high level not diagnostic, low level does not o Excreted through kidney (beware in renal exclude diagnosis impairment) 2. 3. 4. 5.

WBC – often raised ESR – often raised Synovial fluid analysis – Negative birefringent (under polarized light), needle shaped crystals X-rays – soft tissue swelling, punched-out erosions (difference from RA: maintenance of joint space, does not involve joint capsule, absence of periarticular osteopenia)

 Febuxostat (80mg/24hr) o Alternative if allopurinol is contraindicated or not tolerated o SE: increase LFT o Metabolised and excreted by liver 3. Diet (low purine, hydration) and exercise

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Together in Delivering Excellence (T.I.D.E) Differential diagnosis

Differentiating signs

Pseudogout  Presentation may be identical to that of gout  Is less common in young age (<50)  Is more likely to affect wrist and knee joints (proximal)







Differentiating tests







X-ray: Chondrocalcinosis  (radiographic calcification of cartilage in certain  joints) is usually present. Ultrasound: Calcium pyrophosphate deposits are found deeper in the cartilage and are less  homogenous (lumpybumpy) than the superficial double contour sign seen in gout. Synovial fluid: Calcium pyrophosphate crystals; are rhomboid-shaped, weakly positively birefringent crystals.

Rheumatoid Arthritis A chronic systemic inflammatory disease. Check extraarticular involvement; lympadenopathy, vasculitis, pleural & pericardial effusion Chronic tophaceous and polyarticular gout may present like RA, and tophi can be misdiagnosed as rheumatoid nodules. Symmetrical swollen, painful, and stiff small joints of hands and feet. Worse in morning.

X-ray: Juxta-articular osteopenia Synovial fluid is inflammatory (WCC 1 – 50000/mm^3), but no monosodium urate crystals are found. Anticyclic citrullinated peptide (anti-CCP) has a high specificity (98%), but a low sensitivity and it may be useful in the early detection of patients who will have severe RA.

  



  

Septic Arthritis Presentation may be identical to that of gout. Occurs in both sexes and at any age. Risk factors for infection, such as intravenous drug use and immunocompromise, may be present.

Synovial fluid microscopy and culture may be Gram positive and show growth. Blood cultures may grow the causal bacteria. X-ray & CRP may be normal. Co-existence of crystals and infection in the joint is not uncommon.

Purine content food High (avoid) – liver, anchovies, sardines, mackerel (kembung), crab, shrimps, scallops and other shellfish Moderate (eat in moderation) – red meat, chicken, soya beans, peas, spinach, cauliflower, asparagus, mushrooms Low – dairy products, eggs, pasta/noodles, bread, fruits, nuts, cereal products

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Together in Delivering Excellence (T.I.D.E) Bone Tumor [Rafidah] HISTORY

PHYSICAL EXAMINATION

Epidemiology 

Malignant common in adult (except osteosarcoma and ewing sarcoma in young) In pt over 50 years bone mets seen more frequently than all primary malignant bone tumour



  

Ill or in pain Cachexia Pale

Specific

Risk factor   

General

Smoking Previous irradiation Bone mets – previous history of malignancy(breast, prostate, kidney, lung, thyroid, bladder and GIT)

 Lump Inspection (location, size, number, shape, skin changes, surrounding skin, scar, dilated vein, discharge) Palpation (tenderness, temperature, surface, margin ,arise from the bone (non mobile side horizontally and vertically) or muscle (mobile horizontally but not vertically) or above the muscle (mass disappear when the muscle contracted), consistency, pulsatile, expansile, slipping sign, fluctuation test, transillumination test) Auscultation(bruit) If the mass near to the joint, assess for effusion and ROM Assess the peripheral nerve and peripheral pulses

 

S&S     

Mass palpable, rapidly progressive increase in size Pain at rest/ night pain LOA,LOW Loss of function Asymptomatic but later presented with pathological # - any break in midshaft should be regarded a pathological until proven otherwise Neurological symptom – paraesthesia or numbness cause by pressure or stretching of peripheral nerve Back pain – mets Systemic review – ask about symptom in respective system that suggestive of malignancy (To look for primary tumour causing metastasise to the bone)

  

Complication 

Metastasize – lung



Pathological fracture

  

Other examination: Metastasise:  Spine – deformity or tenderness  Lungs  liver – ascites, hepatosplenomegaly  lymph node      

Primary cancer (based on history) Thyroid Breast Lungs Prostate (DRE) Kidney

INVESTIGATION

MANAGEMENT I.

Laboratory     

FBC Serum ALP ESR Serum protein electrophoresis – abnormal globulin fraction in myeloma Bence jones protein in urine - myeloma

  -

Imaging  Plain radiograph 1) Description  Type of xray  Age (skeletally immature vs mature)  Solitary or multiple  Lucency(lytic) vs density(blastic)  Site(bone and area – metaphysis,diaphysis, epiphysis)  Feature: a) zone of transition(wide or narrow) b) periosteal reaction c) cortical destruction or cortical thickening - stipled calcification inside vacant area is characteristic of cartilage tumour  CT&MRI

-to assess true extent opf tumour and its relationship to surrounding structures - deciding how much tissue to remove in local extent of the tumour  Bone scan

-to reveal site of small tumour or presence of skip lesion/silent secondary deposits

Biopsy – for diagnosis and planning treatment Others: chest xray, ct chest

 -

ii.

Surgical Tumour excision : Intracapsular excision Marginal excision Wide local resection Radical resection Limb salvage Done if certain that there are no skip lesions and functional limb can be preserved Amputation High grade lesion Doubt whether lesion intracompartmental Local control for tumour resistant to chemo and radio rx

Non surgical

  -

Multi agent chemotherapy methotrexate, doxorubicin, cyclophosphamide, vincristine and cisplatinum rx 8-12 weeks preop, maintenance another 6-12month postop Radiotherapy adjunctive rx for high grade tumour inaccessible sites inoperable because of their size, proximity to major blood vessel for marrow cell tumour such as multiple myeloma for metastatic deposits for palliative local tumour control where no surgery is planned

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Together in Delivering Excellence (T.I.D.E) 1.

Enneking classification

GRADE (SURGICAL)

G0 – BENIGN G1 – LOW GRADE MALIGNANT G2 – HIGH GRADE MALIGNANT

SITE

T0 – BENIGN INTRACAPSULAR & INTRACOMPARTMENTAL T1(A) – INTRACOMPARTMENTAL T2(B) – EXTRACOMPARTMENTAL

METASTASIS

M0 – NO REGIONAL/DISTANT METS M1 – REGIONAL / DISTANT METS

2.

What is intracompartmental and extracompartmental?  Intracompartmental: lesion confined to an enclosed tissue space (e.g. a bone, a joint cavity, muscle group within its fascial envelope)  Extracompartmental: extend into interfascial or extrafascial plane with no natural barrier to proximal or distal spread

3.

Malignancy vs benign in radiograph

Malignant ill defined Irregular Break of cortex Periosteal reaction – codman’s triangle, lamellated, sun burst appearance Wide zone of transition

Benign Well defined Regular cortical destruction Thick, wavy, uniform callus formation due to chronic irritation Narrow zone of transition

4. How is it benign periosteal reaction can be differ from the malignant type? In the case of benign, slowly growing lesion, the periosteum has time to lay down thick new bone and remodel it into a more normal-appearing bone while aggressive periostitis dows not have time to consolidate 5. Complication of biopsy Hemorrhage, wound breakdown, infection, pathological fracture 6. Commonest site for bone mets? Vertebrae,pelvis, proximal half of the femur and humerus

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Together in Delivering Excellence (T.I.D.E) Diabetic Foot Ulcer [Zuraidah] HISTORY Definition:  A diabetic foot is a spectrum of condition as a cx of DM to the foot, ranging from nerve, skin, fascia, muscle, tendon, bone and blood vessels General and Medical History  History of presenting foot complaints and duration  painful/not, rest pain/ claudication  Duration of diabetes, management and control  Cardiovascular, renal, ophthalmic evaluation & other co morbidities  Social history – alcohol / tobacco / occupation / dietary habits  Current medication and antibiotic use  Allergies  Past Medical & Surgical history  Cultural habits – walks barefoot / wets feet at work / wear socks / walks alot  Patients’ perception of Diabetes Mellitus, necessity of weight and diet control  Able to afford diabetic drugs History of Foot Problems  Daily activity and current diabetic foot status  Footwear – shoes / slippers / sandals / use different footwear / Fit  Foot-care – aware of foot problem / inspect foot / wash feet / proper nailclipping / attend podiatry  Callus formation  Deformities and previous foot surgery  Neuropathy and ischemic symptoms  Skin & nail problems – sweaty feet / fungal infections / skin disease / blisters/ Ingrown toenails History of Foot Ulcer  Site, size, duration, odour and type of drainage  Precipitating event or trauma  Recurrences – number of times  Associated infections  Frequency of hospitalizations and treatment given  Wound care / measures to reduce plantar pressure  Patient compliance  Previous foot trauma or surgery  Features of Charcot’s joint INVESTIGATION Laboratory 1. Full Blood Count 2. Erythrocyte Sedimentation Rate (Esr) 3. Blood Glucose 4. Renal Function Test 5. Urinalysis 6. Glycosylated Haemoglobin Level (Hba1c) 7. Ulcer Swab Culture 8. Tissue Biopsy 9. X-ray- AP and lateral view to exclude osteomyelitis and gas gangrene 10. Ankle-brachial systolic index( by Doppler u/s)  Normal->0.9  >0.5-Ulcer healing  <0.5-Impendent gangrene  <0.4-Amputation needed

PHYSICAL EXAMINATION General  alert conscious, any septic looking  Vital signs Specific  System – CVS, RESPI, CNS– look for cx Local examination 1) Features of neuropathic vs ischemic ulcer (see table in notes) 2) Ulcer assmnt Site Size Wound bed

Infection signs

Exudate Wound edge

Depend on types Length, width, depth and location, preferably with clinical photograph Appearance: • Black (necrosis) • Yellow, red, pink • Undermined • Odour Be aware that some signs (fever, pain, increased white blood count/ ESR) may be absent. Evaluate the ulcer for signs of infection, inflammation and oedema. Copious, moderate, mild, none Callus and scale, maceration, erythema, oedema

Evaluation of vascular status  pulses (dorsalis pedis, posterial tibial, popliteal, femoral) / capillary refill  edema/ temperature gradient/ color changes  changes of ischemia (trophic changes) Evaluation of neurological status  vibration perception : tuning fork 128hz  pressure & touch :cotton wool(light), monofilament 10g (Semmes Weinstein)  -pinprick (pain) /2 point discrimination / temperature  deep tendon reflex (ankle,knee)/ clonus /Babinski /Romberg’s test

MANAGEMENT The aim is to obtain wound closure as soon as possible and to prevent recurrence. Principles of Treatment  Debridement of necrotic tissue  Wound care  Reduction of plantar pressure (off-loading)  Treatment of infection  Vascular management of ischaemia  Medical management of co morbidities  Surgical management to reduce or remove bony prominences and / orimprove soft tissue cover   Reduce risk of recurrence

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Together in Delivering Excellence (T.I.D.E) Common/Possible Question in Exam + Answer 1) Pathophysiology of the ischemic foot? Occlusive vascular dz involving both microangiopathy & atherosclerosis of large & medium sized artery. 2) pathophysiology of diabetic neuropathy and types of neuropathy? accumulation sorbitol + fructose in Schwann cells -- Increase IC osmolality --influx of water caused osmotic cell injury -- damage schwann cell (segmental demyelination ) -- axon degeneration irreversibly -- disrupt neural function -- Diabetic neuropathy

Characteristics

Clinical presentations

Sensory neuropathy • Loss of protective sensation • No perception of shoes rubbing or temp changes

Autonomic neuropathy • Reduced sweating - dry cracked skin • Increased blood flow - warm foot

Motor neuropathy • Dysfx of the motor nerves that control the movement of the foot. Limited joint mobility may increase plantar pressure • Foot deformities develop

• Unaware of a foot ulcer/ lack of discomfort when a wound is being probed

• Dry skin with cracks and fissures • Bounding pulses • Dilated dorsal veins • Warm feet

• Hammer toes • High medial Longitudinal arch, leading to prominent Metatarsal heads and pressure points over the plantar forefoot • Clawed toes • Altered gait

3) Wagner’s classification?

4) How to monitor diabetic at annual review?  Eyes : visual acuity, fundoscopy  Sensory system : touch, pinprick & vibration  Deep tendon reflex  CVS: BP, peripheral pulses  Biochemistry : urine & blood sugar, albumin, Hba1c, creatinine

Notes Neuropathic vs ischemic ulcer Clinical signs Foot deformities Foot temperature/ footpulse

Neuropathic ulcer

Clawed toes, possible high arch, possible Charcot deformities

Warm, palpable pulse

Ischaemic ulcer No specific deformities. Possible absent toes/forefoot from previous amputations Cold or decreased temperature, pulse may be absent or reduced Pale/bluish. Pronounced redness when lowered (dependent

Skin colour

Normal or red

Skin condition

Dry skin due to decreased sweating

Thin, fragile and dry.

Ulcer location

On the plantar aspects (forefoot 80%) of the foot/toes,

Distal/tips of the toes, heel, or margins of the foot

Callus present

Commonly seen on the weight bearing areas and is generally thick

Not usually. If present, distal eschar or necrosis

Ulcer characteristics

Usually painless, with a “punched out” appearance (granulation or deeper base) surrounded by callus

rubor), blanching on elevation

Painful, especially with necrosis or slough Sensation may be present but decreased if there is associated

Sensation

Reduced or absent sensation to touch, vibration, pain, and pressure

Ankle reflexes

Usually not present

Usually present

Foot pulses

Present and often bounding. Dilated, prominent veins

Absent or markedly reduced

neuropathy

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Together in Delivering Excellence (T.I.D.E) Osteoarthritis/Rheumatoid Arthritis [Ain] HISTORY Osteoarthritis : Chronic joint disorder in which there is progressive softening and disintregation of articular cartilage accompanied by new growth of cartilage and bone at the joint margins (osteophytes) and capsular fibrosis. Rheumatoid arthritis : Chronic systemic inflammatory disorder involving mainly the joints with a peripheral symmetrical nonsuppurative disorder.

PHYSICAL EXAMINATION OA    

The information needed to help diagnose includes: 

 

  

 





Description of the symptoms : Pain,swelling,stiffness,deformity,reduced range of motion Details about when and how the pain or other symptoms began : acute vs chronic Do you have any general symptoms that seem to affect your whole body, such as fatigue, weight loss, or fever? : RA involved systemic, OA doesn’t cause whole body symptom Does exercises help your pain or make it worse. Details about other medical problems that exist : in RA most common involves lung, heart n eyes Location of the pain, stiffness or other symptoms : which joint, unilateral/bilateral, duration of stiffness How the symptoms affect daily activities – driving, working, List of current medications and complication of drugs : prolong NSAID used, methotrexate, cytotoxic drug in RA - Assess detailed about risk factor in hx - Assess complication RA involves systemic response- osteoporosis, carpal tunner syndrome, heart problems, lung disease ( pleuritic/effusion/interstitial pulmonary fibrosis),anemia, cervical myelopathy, mononeuritis multiplex OA more localized – foot pain, reduce mobility, septic arthritis after arthroplasty, gout

Antalgic gait



Joint swelling, warmth, and tender.(the small joints of the hands and feet are affected in a relatively symmetric distribution)

  

Presence of fluid on the joint-(effusion)



The presence of bumps (rheumatoid nodules) over pressure points in the body.



Extra-articular involvement of organs such as the skin, heart, lungs, and eyes.

Varus deformity Quadriceps wasting Bony bumps on the finger joint closest to the fingernail (Heberden's nodes),bony bumps on the middle joint of the finger (Bouchard's nodes), or bony bumps at the base of the thumb.

 Tenderness and/or swelling in weight-bearing joints such as the hips and knees.

 Pain, limited movement, and/or a creaking noise or feeling (crepitus) that occurs when the joints are moved. Eg; knee examination

      

RA

Swelling and tender joint Crepitus Limited rom Contracture Varus stress test positive Joint line tendernes Osteophytes

Decreased range of motion Joint and tendon destruction: deformities such as ulnar deviation, boutonniere and swan-neck deformities, hammer toes, genu varus/valgus

Important findings in the physical exam include the:

 Pattern of symptoms in the affected joints.  Presence of swelling or tenderness in the joints.

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Together in Delivering Excellence (T.I.D.E) INVESTIGATION Laboratory : FBC Inflammatory marker : ESR,CRP Rheumatoid factor : RA Synovial fluid analysis : high WBC indicate inflammatory or infection response/other cause of arthritis eg. Gout, RA, septic arthritis Anti-citrullinated protein antibody (anti-CCP ) : in RA Anti-nuclear antibody (ANA)- TRO other form of arthritis eg. SLE

MANAGEMENT Main principle in OA treatment : 1) Relieve pain – analgesic, NSAID 2) Increase movement – physiotheraphy ( increase in range n power) 3) Reduce load – walking stick,soft-soled shoes, weight reduction, avoid prolong activity Principle in RA : To control joint inflammation To prevent joint damage and disability

Pharmacological (medical)

# there is no specific lab ix for OA compared to RA,mainly its by clinical dx as well as x-ray.

OA -analgesic eg.PCM,tramal -steroid oral/injection - NSAID eg. Ibuprofen, naproxen, celecoxib

Imaging : X-ray OA

RA

-Loss/narrowing of joint space. -Osteophytes. -Subchondral cyst. -Subchondral sclerosis. -deformity

-Juxta-articular osteopenia. -Soft tissue swelling. -Loss of joint space. Advanced :– -Bony erosion -subluxation

-

MRI



To detect arthritis. MRI can be helpful in evaluating joint damage, particularly damage to the spine, knee, or shoulder.



Non medical/ conservative

-Rest, reduce weight, use of public transport -physiotheraphy -occupational theraphy

Surgery

-osteotomy -arthroplasty (eg.total knee replacement) -arthrodesis

RA -oral steroid eg. Prednisone - NSAID - DMARD (disease modifying anti-rhuematic drugs) Within 3 months after onset of symptom eg. Methotrexate, penicillamine, tumor necrosis factor antagonist -occupational theraphy -physiotheraphy

-arthroscopy/synovectomy (to remove debris or inflamed tissue from a joint)

-arthroplasty (joint replacement) -carpal tunnel release -cervical spinal fusion -finger & hand surgery

To track the progress of disease. In repeat scans, MRI can determine how fast the arthritis is progressing

Common/Possible Question in Exam + Answer 1.

Classification of osteoarthritis

Common OA question. 1. What is radiological features changes? - as mentioned above 2. Whats common joint affected ? knee joint 3. Treatments? as mentioned above 4. Indication for surgery ? severe intolerable pain,pain at rest,affect normal function

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Together in Delivering Excellence (T.I.D.E) 2.

Difference of OA/RA

3.

American rheumatic association criteria for RA

‘ RF RISES ‘ - R : rheumatoid factor F : finger/hand joint involved for > 6 weeks R : rheumatoid nodules I : involvement of 3 or more joint area S : stiffness (morning) >1 hour for > 6 weeks E : erosion on xray S : symmetrical arthritis > 6 weeks 4.

Detailed history about risk factor OA (mainly affect cartilage) Age Older age >45 y.o Family hx

-

Sex

Equal Men < 55 y.o Women >later in life Non-immune -age,genetic,previous injury to joint,obesity,hormone

Trigger

RA (mainly affect synovium) At any age even in children Average : 30- 50 y.o More in RA Women > men 3:1

Autoimmune -genetic,infection,hormone,smoking

bilaterally,symmetrical,destructive and performing polyarthropathy.

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Together in Delivering Excellence (T.I.D.E) PERSONAL NOTES

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