Nina Cooper
EMQ Lecture Notes
Respiratory SHORTNESS OF BREATH Case 1: 68, ex-smoker SOB on exertion, over years Wheezy for a few years Regular productive cough
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Investigations: postbronchodilator Spirometry o FEV1 % lower FEV1:FVC o Classic = gradual onset, smoker, productive cough Destruction of alveolar space ! decreased gas exchange ! chronic bronchitis
Mycobacteria, bacilli, acid-fast = appear red with ZN stain Treatment – RIPE o Rifampicin – Rifampicin – flu-like symptoms, hepatitis, stains contacts orange Isoniazid – Isoniazid – hepatitis, o neuropathy Pyrazinamide – Pyrazinamide – hepatitis, o arthralgia, gout Ethambutol – Ethambutol – ocular o toxicity + colour vision loss
Case 3: Steatorrhoea, diabetes Recurrent infections Dilated airways Clubbing • • • •
COPD Smoker/ex smoker Wheeze Chronic cough Regular sputum production Exertional breathlessness Frequent winter “bronchitis”
ASTHMA May/may not smoke Wheeze Chronic nonnonproductive cough Night time waking with breathlessness or wheeze Significant diurnal variation FHx asthma FHx atopy
Cystic Fibrosis Autosomal recessive rece ssive Carrier freq. 1 in 22 for Caucasians Defective Cl- excretion leads to viscous mucous Increased infections Also assoc. with di abetes and infertility Bronchiectasis = permanent dilation of bronchioles and elastic damage Signet rings seen on CT Past history of infections e.g. pertussis = bronchiectasis • •
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Case 2: Fever Cough Weight loss Red Ziehl-Nielson Stain • • • •
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Case 4: Shipyard worker End-inspiratory crackles Progressive Progressive dyspnoea Non-productive cough Clubbing • • •
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Long-standing cough (>2 weeks) Racial profiling in EMQs – normally Asian Systemic symptoms include weight loss, anorexia, fever and night sweats Investigations: o CXR: cavitatory nodules Sputum samples o Microscopy o Culture in Lowenstein Jensen medium for 4-6 weeks
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Mesothelioma Secondary to asbestosis (shipbuilding/power stations) or pneumocoliosis (coal worker) Leads to impaction ! fibrosis ! end inspiratory crackles Also seen in idiopathic id iopathic pulmonary pulm onary fibrosis (cryptogenic fibrosing •
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Nina Cooper
alveolitis) = progressive dyspnoea and non-productive cough
Case 5: Farmer Many flu-like illnesses over winter • •
Hypersensitivy Pneumonitis (EAA) • Farmer's lung lung - one of the most common forms. Due to exposure to mouldy hay. The major antigen is Saccharopolyspora rectivirgula • Bird-fancier's lung lung - one of the most common forms. Due to exposure to avian proteins, eg pigeons, parakeets • Cheese-worker's lung lung - exposure to cheese mould, Penicillium casei . • Malt worker's lung lung - exposure to Aspergillus clavatus cla vatus in in mouldy malt • Hot tub lung lung - exposure to Mycobacterium avium in in poorlymaintained hot tubs • Chemical worker's lung lung - trimellitic anhydride, diisocyanate and methylene diisocyanate diisocyanate act as the antigens during the manufacture of plastics, polyurethane foam and rubber. • Mushroom worker's lung lung exposure to thermophilic actinomycetes in mushroom compost
EMQ Lecture Notes
Pancoast’s Tumour Impinges on brachial plexus and sympathetic chain Leads to Horner’s syndrome PTOSIS o ANHYDROSIS o MYOSIS o •
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Case 3: Weight loss Cough Headaches Worse bending over • • • •
Metastases Liver: anorexia, nausea, weight loss, RUQ pain Bone: pain, fractures Adrenals: usually usual ly asymptomatic asymptoma tic Brain: SOL •
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Case 4: Lower back pain Tired Constipated Hypercalcaemia • • • •
Squamous Cell Carcinoma 35% of all lung cancers Arises from epithelial ep ithelial cells cell s Releases PTHrP Same actions as PTH: bone reabsorption, tubular calcium reabsorption Hypercalcaemia: stones, moans, groans, bones • • • •
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LUNG CANCER Case 1: SOB Weight loss Oedamatous Flushed • • • •
SVC Syndrome Blockage causes oedema of face and arms e.g. due to tumour Facial flushing Dilated veins over arms, neck and chest Morning headaches •
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Case 5: Recent haemoptysis Dyspnoea Truncal obesity Moon face • • •
Case 2: Ptosis R arm pain • •
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Nina Cooper
EMQ Lecture Notes
Small Cell Carcinoma 20% of all lung cancers 2 year survival: 20-40% limited disease, <5% extensive Neuroendocrine origin – often secrete polypeptide hormones Early metastases Paraneoplastic syndromes
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Cushing’s Ectopic ACTH production Moon face Truncal adiposity Muscle wasting Thin skin and striae
siADH
LambertEaton Cancer Antibodies produces against ADH tumour Hyponatraemia interfere Nausea with preMalaise synaptic Ca Confusion Channels Hyporeflexia Weakness Improves after exercise MG worsens with exercise
Adenocarcinoma Goblet cell origin 30% LC Most common type in nonsmokers Mets common • • •
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HAEMOPTYSIS Systematic Approach How much? Mixed in? Risk of asphyxiation? From where? Upper airway o Lower airway – o liquid/clots, pink/red? o Stomach – haematemesis – black/coffee grounds Age? o Children = pneumonia, foreign body Young adults adul ts = infection, o AI Old = cancer, chronic o disease, CCF Risk factors o Smoking o Travel o Anticoagulant drugs/ bleeding problems o HIV •
Case 1: SOB Coughing blood – mixed in with sputum Fever • •
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Pneumonia Radiological pulmonary shadowing LRTI = no radiological changes CAPs are spread by droplet inhalation Present with cough, fever and pleuritic chest pain Cough is initially dry but later becomes productive productive and may be blood-stained Examination reveals bronchial breath sounds and coarse creptitations in affected area Severity is assessed via CURB-65 o CRP o Urea o RR BP o Age >65 o Can be lobar or bronchopneumonia (patchy alveolar consolidation in both lobes) Investigations = CXR and sputum MCS Treatment = relevant abx: oral amoxicillin or IV clarithromycin + oral co-amoxiclav • • •
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Pathogens S. pneumonia Young and middle m iddle aged ag ed o o 30% all CAPs o Rapid-onset o High fevers, rigors and pleuritic chest pain o Rusty-coloured Rusty -coloured sputum CXR shows lobar o consolidation Chlamydophila Chlamydophila pneumonia Mild pneumonia in o younger people o Assoc. with sinusitis, pharyngitis and laryngitis o CXR shows small segmental infiltrates Mycoplasma pneumonia Adolescents and you ng o adults •
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Nina Cooper
EMQ Lecture Notes
Cause epidemics in 3 year cycles o Few chest signs Present erythema o nodosum, pericarditis and haemolytic anaemia CXR shows patchy/lobar o consolidation and hilar lymphadenopathy Staph. aureus o Complicates an underlying pneumonia o Can arise from other foci e.g. osteomyelitis Abscesses on XR - Cavities o with air-fluid levels Pneumocytisis jiroveci Pneumocystisi pneumonia o = PCP o Most common AIDSdefining illness o Dry cough, fever, SOB, weight loss and night sweats o Low O2 sats Widespread infiltrates on o CXR Legionella pneumophila o Legionnaire’s disease o Localised epidemics o Dry cough, myalgia, malaise and GI symptoms o Low sodium and low albumin Air conditioning units o Chlamydophila psittaci Contracted from birds o o Bacteria shed through faeces and nasal discharges o Fever, arthralgia, diarrhoea, conjunctivitis and headache o Hepatosplenomegaly recognised CXR = patchy lower lobe o consolidation Klebsiella pneumoniae o Purulent dark sputum o CXR = upper lobe consolidation o
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Case 2: 70M 40 pack year history Blood in sputum
Lung Cancer NSCC = 80% SCC = 20% See above notes. • • •
Case 3: 3 year old child Coughing up blood Happened when came back from nursery • • •
Inhaled Foreign Body Most common cause in young children •
Case 4: 2-3 cups of coffee-like appearance Been drinking •
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Oesophagial Varices Dilated veins at distal end of oesophagus Caused by portal HTN secondary to liver disease o Poor blood flow and high resistance ! backpressure ! tributary formation Also see caput meducae, o varices on rectum and spider naevi Weak and prone to o rupture Bleeding worsened by fact that can no longer metabolise vit K due to LF! •
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Case 5: 20 year old male from Bangladesh Coughing up blood for few weeks Bilateral hilar lymphadenopathy •
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Risk factors o Hx o HIV o Travel o Homeless Investigations: CXR, ZN staining, HIV serology BHL can be caused by TB or sarcoid
Nina Cooper
EMQ Lecture Notes
ASTHMA Case 1: 8M 6 month history of night cough and intermittent wheeze Small for age Mild eczema • •
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Stepwise Management of Asthma New diagnosis Started on step 1 = short acting B2 agonist e.g. salbutamol, terbutaline Step 2: step 1 + low dose inhaled steroid e.g. budesonide, fluticasone Step 3: step 2 + high dose inhaled steroid or long acting B2 agonist e.g. salmeterol Step 4: high dose inhaled steroids + long acting B2 agonist + other drugs e.g. theophyllines, anticholinergics (ipratropium), leukotriene antagonists (montelukast), mast cell stabilisers (sodium cromoglicate) Step 5: step 4 + oral steroids (prednisolone) •
Pt is too breathless to finish sentences o RR>25 Pulse >100bpm o Peak flow <50% predicted o Should treat immediately with 60% oxygen via facemask, back-to-back nebulisers and systemic steroids (either oral prednisolone or intravenous hydrocortisone) Patients should have their sats measured continuously and have regular PEFR readings + serial ABGs o
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Case 4: 21F, known asthma SOB Barely talk, silent chest, RR 36 per min Appears to be some improvement with O2, salbutamol nebs and steroids Peak flows still at 30% of best • • •
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Life-threating Exacerbation of Asthma Features Fatigue or exhaustion Central cyanosis Decreasing consciousness Bradycardia Silent chest or poor respiratory effort Peak flow <33% predicted/best •
Case 2: 16M Poorly controlled chronic asthma Managed with long acting B2 agonist and high-dose inhaled steroids Parents want to know if anything else can be given • •
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Stepwise Management of Asthma See above
Case 3: 23 year old man with known asthma A&E with SOB Widespread wheeze Breathless to talk HR 115BPM RR 36 •
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Severe Exacerbation of Asthma Features of severe asthma •
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Additional treatment required – IV MAGNESIUM SULPHATE If deteriorates may require intubation/ventilation •
Nina Cooper
EMQ Lecture Notes
Cardiology MURMURS
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Case 1: Anacrotic pulse (slow-rising) Breathlessness Syncope Pain • • • •
Aortic Stenosis Ejection systolic murmur Characteristic breathlessness, syncope and angina on exertion • •
Case 2: 26F Pink frothy sputum Atypical pain MI • • • •
Mitral Regurgitation Can present acutely or chronically Acute = backflow, leading to pink sputum Mitral valve prolapse causes atypical pain – seen in young Graham Steell murmur heard if the regurgitation backflows through the pulmonary valve too, due to LA problem Inferior MI can cause rupture of the posteromedial papillary muscle while anterolateral infarctions can cause rupture of the anterolateral papillary muscle This leads to acute mitral regurgitation (RV papillary rupture is rare but can cause regurgitation of the tricuspid valve) Complete rupture of the papillary muscle is fatal and causes wideopen MR Those with incomplete rupture need emergency cardiac surgery with inotropic support considered for transient stabilisation prior to this • •
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Case 3: IV drug user Low pitch murmer Loudest in apex • • •
Louder on inspiration Pulsating uvula
Aortic Regurgitation Multiple signs due to collapsing pulse De Musset’s (rhythmic o bobbing/nodding of head in synchrony with beating of the heart) Duroziez’s sign (systolic o and diastolic murmurs heard over the femoral artery when it is gradually compressed with the stethoscope) o Watson Hammer Pulse (Large volume collapsing pulse) Corrigan’s pulse (rapid o upstroke and collapse of the carotid pulse) Quinky’s sign (pulsation o of capillaries in nail bed) o Traube’s sign (a 'pistol shot' systolic sound heard over the femoral artery) Austin flint murmur = loudest in apex, mid-diastolic or pre-systolic, heard in severe aortic regurgitation Decrescendo diastolic murmur •
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Case 4: 30F SLE Muffled heart sounds • • •
Pericardial Effusion Lupus -> pericarditis Adversely affects heart function = cardiac tamponade Transudative (congestive heart failure, myxoedema, nephrotic syndrome), Exudative (tuberculosis, spread from empyema) Haemorrhagic (trauma, rupture of aneurysms, malignant effusion). Malignant (due to fluid accumulation caused by metastasis) • •
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Nina Cooper
Case 5: 22M Positive vasalva manoeuvre Harsh ejection systolic murmur
EMQ Lecture Notes
HEART FAILURE
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EMQ: • •
HOCUM Hypertrophic Obstructive Cardiomyopathy Disease of myocardium without known cause Cause of sudden cardiac death Valsalva maneuver increases the intensity of HOCUM murmurs, namely those of dynamic subvalvular left ventricular outflow obstruction (decreases AS, PS, TR) •
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80F IHD Dyspnoea Orthopnoea PND
Upon examination, you hear fine inspiratory creps + normal ECG Blood test = BRAIN NATRIURETIC PEPTIDE (check for LV HF) Fine insp creps = pulmonary oedema •
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Her BNP is positive. What should the next test be? GOLD STANDARD = TRANSOESOPHAGEAL ECHO FIRST LINE = TRANSTHORACIC DOPPLER ECHO •
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She is admitted. What should the first line treatment be? ACE INHIBITOR •
Patent Ductus Arteriosus Tachycardia Respiratory problems dyspnoea - shortness of breath Continuous machine-like heart murmur Cardiomegaly Left subclavicular thrill Bounding pulse Widened pulse pressure • •
She is discharged, but later presents with a chronic dry cough. Secondary treatment: ANG-II RECEPTOR ANTAGONIST •
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6 months later, she is put on enalapril (ACE inhibitor), atenolol (B-blocker) and furosemide (diuretic) Next = SPIRONOLACTONE Can cause gynaecomastia, menstrual disturbances etc. • •
Nina Cooper
INFECTIVE ENDOCARDITIS
EMQ Lecture Notes
Fast AF No discernable P waves Chaotic excitation Irregularly irregular Typical = old, palpitations, SOB, fatigue, syncope Paroxysmal = <24h, stops itself Persistent = >7 days, requires cardiaversion Permanent = doctor and patient have lost hope of sinus rhythm • •
EMQ: • • • • • • • •
22F IV Drug User Tricuspid murmur Petechiae Microvascular haematuria Janeway lesions Clubbing Splinter haemorrhages
Modified Duke criteria for Infective Endocarditis. MAJOR: Positive blood culture o Typical organism in 2 separate cultures or o Persistently positive +ve cultures) Endocardium involved Positive echo o Or new valvular o regurgitation Minor Predisposition (cardiac lesion, IVD user) Fever >38c Vascular/immunological signs Positive blood culture that does not meet criteria Positive echo that doesn’t meet major criteria Diagnosis: 2 major / 1 major + 3 minor / 5 minor •
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Causes can be cardiac or non-cardiac (infection, thyroxtoxicosis) Investigations ECG Ambulatory monitoring • •
Case 2: 36M Palpitations 150bpm • • •
Atrial Flutter Narrow complex tachycardia Atrial Rate = 250-350bpm Ventricular Beat = 150bpm with a 2:1 block Saw tooth appearance on ECG Acute = shock them • • •
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May show signs of septic shock. MANAGE: ABC, fluid resuscitate FBC ECG Echo Manage w MC&S • • • • •
Has MRSA = give IV VANCOMYCIN
ARRHYTHMIAS Case 1: 85F Acute SOB + pain Irregular rhythm HR 190 • • • •
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Case 3: 56M Previous MI Broad complex tachycardia • • •
Ventricular Tachycardia Broad complex = ventricular problem (i.e. not from SAN) •
Nina Cooper
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Risk = previous MI or inherited syndromes Emergency as can turn into VF -> ischaemia/infarction
EMQ Lecture Notes
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Back pain since prosthetic valve put in 4/52
Suspected Infective Endocarditis
Case 4: 24M Palpitations Pre- excitation • • •
Wolff-Parkinson White Often benign, 1-3/1000 people Non-conductive AV septum is bypassed by an accessory pathway (bundle of Kent) Pre-excitation, slurred upstroke = delta wave • •
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Case 5: 84M HR 32 Broad QRS • • •
Case 3: 72M Shoes too small Exertional dyspnoea No PMHx • •
Complete Heart Block Broad QRS = conduction outside of normal pathways SAN – spontaneous AVN – slower spontaneous (~30bpm) See P waves in unison + QRS randomly appearing •
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Suspected Heart Failure First line – BNP for HF if no previous MI If previous MI = stress echo •
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INVESTIGATIONS Case 1: 54 Diabetic SOB Central crushing chest pain • • • •
Suspected ACS Do ECG first •
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Suspected Mitral Regurgitation TTE •
Case 5: 55M Hyperlipidaemia Central chest pain on exertion Relieved by rest • • • •
Nina Cooper
EMQ Lecture Notes
syndrome, neoplasm from local tumour invasion, uraemia and autoimmune conditions such as RA and SLE.
Diagnosing Stable Angina Coronary angiography Then exercise ECG/CT calcium scoring • •
CHEST PAIN
Case 3: Central crushing chest pain Bradycardia • •
Case 1: 70M BMI 35 Collapse running Tearing pain to back BP 190/120 ! 160/90 • • • • •
Dissected Thoracic Aortic Aneurysm Higher risk in connective tissue disorders Can cause hemiplegia, acute limb ischaemia, MI if CA involvement •
MI CT Calcium Scoring RULE OUT Low risk factors Atypical pain
Functional Imaging
Angiography
INTERMEDIATE Low risk factors Atypical pain Women Includes stress echo, MPS with SPECT and cardiac MRI
RULE IN High risk Typical pain Can carry out procedure?
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Case 2: 32M Stabbing pain Worse lying down/coughing Improved by sitting upright Pericardial rub audible • •
Bradycardia -> inferior MI Management = MONA LISA MORPHINE OXYGEN NITRATES ASPIRIN
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LOOP DIURETIC I V ACCESS STREPTOKINASE ANTIPLATELETS
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Pericarditis Positional pain Can be caused by infection, SLE, rheumatic rever ! pericardial effusion The classical finding on examination is a friction rub which is said to sound like ‘walking on snow’ There may be diffuse ST elevations on ECG, an effusion on echocardiography and blood results suggesting inflammation Complications include tamponade and constrictive pericarditis Prior viral infection is a risk factor with the most common pericardial infection being viral Bacterial purulent pericarditis also occurs Inflammation is due either to direct viral attack or immune mediated damage Other risk factors include male gender, post-MI (both ‘early’ and Dressler’s), post-pericardiotomy • •
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Case 4: Sharp chest pain, worse on inspiration (pleuritic) Haemoptysis Sudden onset •
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Pulmonary Embolism Antiphospholipid syndrome can cause DVTs, leading to PE First-line = CTPA D-Dimers = non-specific •
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Wells Scoring
Nina Cooper
Case 5: 70F Similar pain to her angina, but no relief with GTN Woke up from sleep Previous episode 1/12 ago • •
EMQ Lecture Notes
Case 3: Myalgia Polyuria Polydipsia • • •
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Conn’s Syndrome Aldosterone-secreting tumour Raised Na, Low K, normal renal function Diagnosis: raised aldosterone, suppressed renin Surgical excision + spironolactone •
Unstable Angina Episodic Has PMHx Occurs at rest <20min Crescendo effect – gets worse, last longer, more frequent • • • •
Prinzmetal’s Angina ST Elevation Wake from sleep Female, age 50 Vasospasmic (functional, not stenosis) Ca channel blocker (NOT B blocker) See same ECG signs as pericarditis •
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Case 4: Middle aged Hep B +ve • •
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Polyarteritis Nodosa Necrotising vasculitis Associated with microaneurysms, MI Higher risk in hep B endemic areas ANCA +ve in <10% Gold standard diagnosis = histology • •
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HYPERTENSION
Case 5: Arteriopath 61M T2DM Kidneys fail 2/52 after ACE started •
Case 1: Tachycardia HTN Anxiety Weight loss • • •
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Phaeochromocytoma 10% rule: malignant, bilateral, extra adrenal, hereditary Diagnose with 24h catecholamines Require a/B blockade, then surgical removal •
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Case 2: 18 Radial-femoral delay Ejection systolic murmur • • •
Aortic Coarctation Interscapular murmur Decreased femoral pulses Seen in those with Turner’s Distal to L subclavian = no radialradial delay • • • •
Renal Artery Stenosis Normally due to atherosclerosis (rarer = Takayasu’s arteritis, thromboembolism) Suspect if htn resistant to optimal treatment Diagnosis: USS, gold standard = renal angiography ACE inhibitors drastically reduce GFR in those with RAD Causes acute renal failure – U&Es should be checked before and after starting ACEi •
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Nina Cooper
EMQ Lecture Notes
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Statin therapy, blood sugar control in diabetics and BP control with antihypertensives may also be necessary Those with LMS disease, 3 vessel disease or a reduced EF may benefit from CABG Single vessel disease may benefit from PCI
CASE 2/3 A 55 year old man is admitted to A&E with chest pain which is central in origin and came on while he was waiting for his bus. Troponin and CK-MB are not elevated. An overweight 63 year old male with a history of hypertension presents with cardiac
ANGINA CASE 1
sounding chest pain while watching TV. However, his cardiac biomarkers are not elevated. An ECG is ordered which shows ST depression and T wave inversion = Unstable Angina Characterised by chest pain at rest ECG will typically show ST depression and T wave inversion Acute management includes antiplatelets and antithrombotics to reduce damage and complications Long term management aims at reducing risk factors Key risk factors include obesity, hypertension, smoking, hyperlipidaemia, FH, DM and positive FH People with diabetes may again present with atypical symptoms Cardiac biomarkers will not be elevated although in a patient who has had an acute MI days earlier, troponin may remain elevated (remains elevated up to 10-14 days after release) All patients with presumed cardiac chest pain should in the first instance get oxygen, morphine •
A 73 year old banker complains of chest pressure which comes on predictably on exertion. It is relieved when he sits down and rests.
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= Stable Angina Resting ECG is often normal Patient is asymptomatic. During exercise stress ECG (most often the Bruce Protocol) there will be ST segment depression during exercise indicative of ischaemia and the patient will complain of chest pain Those unable to exercise to an adequate level may need stress myocardial perfusion imaging or stress echocardiography 1st line treatment involves lifestyle changes and antiplatelet therapy with aspirin. Anti-anginal therapy will also be given, first line being betablockade •
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Nina Cooper
and GTN with antiplatelet therapy in the absence of contraindications CASE 4 A 59 year old woman complains of chest pain. ECG shows ST segment depression. However, a subsequent coronary angiogram is normal = Syndrome X Chest pain with usual ST segment changes associated with coronary artery disease but with normal coronary arteries It is treated with calcium channel blockers such as nifedipine
EMQ Lecture Notes
CASE 6 A 44 year old female complains of a two week history of tight chest pain which occurs when she is lying down. = Decubitus Angina This patient has chest pain which occurs on lying down, which is decubitus angina by definition •
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CARDIOLOGY DRUGS Alpha 1 agonist Alpha 1 agonists such as phenylephrine are vasoconstrictors Also have a use as a mydriatic They are used as nasal decongestants as a result of their vasoconstrictor effect •
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Alpha 2 agonist Used for treatment of glaucoma Decrease production of aqueous fluid by the ciliary bodies of the eye and also by increasing uveoscleral outflow •
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Beta 1 agonist Used to treat hypotension and bradycardias E.g. dobutamine •
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Beta 2 agonist E.g. salbutamol Used for bronchial smooth muscle relaxation •
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Beta blocker Lower heart rate, CO and MABP during exercise Also act to reduce renin release as well as the release of NA Use ranges from migraine prophylaxis, anxiety and •
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Nina Cooper
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hypertension to thyrotoxicosis, post-MI and chronic heart failure Also useful in arrhythmias where they act to increase the refractory period of the AVN. Calcium channel blockers can increase A-V block, slowing down heart rate and worsening severe heart failure, bradycardia and sick sinus syndrome.
Calcium channel blocker Non rate slowing e.g amlodipine - leads to arterial vasodilation by action on vascular smooth muscle cells It can lead to unwanted ankle oedema, headache, hypotension and palpitations Used for hypertension and angina The palpitations a patient may experience are due to reflex tachycardia from arterial vasodilation Rate-slowing calcium channel blockers also exist such as verapamil and diltiazem and uses for these also include arrhythmias such as paroxysmal SVT and AF •
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EMQ Lecture Notes
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the renal and vascular actions of Ang II Uses: hypertension, heart failure
Organic Nitrates Uses o Angina Acute and chronic heart o failure BP control during o anaesthesia Mechanism of action: Release nitric oxide (NO) in smooth muscle cells (nitrates) or stimulate guanylate cyclase (nicorandil) to cause vasodilation Reduce preload (venous return) Venodilation Reduce afterload (peripheral resistance) Vasodilation Example: Glyceryl trinitrate, nicorandil Chronic use can lead to tolerance It is also weakly antiplatelet and has a weak direct action to vasodilate the coronary arteries •
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Spironolactone Aldosterone antagonist (potassium-sparing diuretic) Used to treat oedema Used to potentiate loop/thiazide diuretics •
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ACE inhibitor Prevent the conversion of angiotensin I to angiotensin II by ACE Uses o Hypertension o Heart failure Post-myocardial infarction o o Diabetic nephropathy Progressive renal o insufficiency Patients at high risk of o cardiovascular disease E.g. Enalapril •
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Angiotensin Receptor Blocker E.g. losartan Antagonists of type 1 (AT1) receptors for Ang II, preventing •
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Loop diuretic Used in pulmonary oedema due to LVF Reduces breathlessness and reduces preload Used for patients with chronic HF E.g. furosemide and bumetanide •
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Thiazides Inhibit sodium reabsorption at the beginning of the distal convoluted tubule Act within 1-2 hours Management of HTN – low dose produces maximal effects with little biochemical disturbances E.g. bendroflumethiazide, indapamide •
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Nina Cooper
MISC. CAUSES OF CHEST PAIN CASE 1 A 32 year old woman has a 2 day history of intermittent attacks of a sharp pain over the lower left side of her chest. The pain is exacerbated by movements of the rib cage and the patient tells you it becomes difficult to breathe. She has also felt feverish. = Borneholme Disease Bornholm disease is caused by Coxsackie B virus Symptoms include the fever seen as well as the characteristic attacks of severe pain in the lower chest Exacerbated by small movements of the rib cage, which make it difficult for the patient to breathe •
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CASE 2 A 22 year old woman complains of pain in her breast. Upon deep palpation, you notice tenderness over the right lower inner quadrant. = Costochondritis Inflammation of the costal cartilage
EMQ Lecture Notes
CASE 4 A 70 year old man presents 1 month post- MI with pain on inspiration, a low-grade fever and central sharp chest pain, made better by leaning forwards. = Dressler’s Syndrome Characterised by pleuritic chest pain, low-grade fever and pericarditis, which may be accompanied by pericardial effusion It usually presents two to five weeks after the initial episode, with pain and fever that may suggest further infarction The pain is the main symptom, often in the left shoulder, often pleuritic, and worse on lying down. There may be malaise, fever and dyspnoea Rarely, it may cause cardiac tamponade or acute pneumonitis A pericardial friction rub may be heard. The typical sound of pericarditis is described as like the sound of boots walking over fresh snow •
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CASE 3 A 40 year old man complains of pain and swelling over the ribs = Tietze’s Syndrome Inflammation of the costal cartilage Similar to constochondritis but has swelling •
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Nina Cooper
EMQ Lecture Notes
GI Medicine ANATOMY OF ALIMENTARY TRACT
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Lies deep to ribs 5-11 The common hepatic artery runs in association with the bile duct + portal vein in the free edge of the lesser omentum (the hepatoduodenal ligament part) The common hepatic is a branch of the aorta, and then divides into the R + L hepatic (with the cystic artery supplying the gall bladder branching off the R hepatic)
Gall Bladder/Biliary Tree Gall bladder stores + concentrates bile Sphincter of oddi controls passage of juices through the ampulla of vater Spleen Beneath ribs 9 through 11 on the left side. 10th rib is axis of spleen •
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Topographical Anatomy Costal margin: Formed by the medial borders of the 7th through 10th costal cartilages Rectus sheath: from xiphoid process and 5th through 7th costal cartilages pubic symphysis and pubic crest. Contains rectus abdominis muscle Linea alba: A slight indentation that can sometimes be seen extending from the xiphoid process to the pubic symphysis Inguinal Ligament: From ASIS to pubic tubercle of pelvis. Folded inferior edge of external abdominal aponeurosis. Separates abdominal region from thigh Umbilicus: At approximate level of intervertebral disc between the L3 and L4. Marks the T10 dermatome •
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Kidneys • •
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Oesophagus Pierces diaphragm at T10 •
Stomach Foregut structure Found in epigastric/left hypochondriac region • •
Located in loin region Left kidney is higher than right (pelvis at L1/2 on left and L2/3 on right)
Duodenum Brunner’s glands – found in second part of duodenum C-shape surround head, body and uncinate process of pancreas L2 level Blood supply = foregut (coeliac trunk) – ends at ampulla of vater •
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Nina Cooper
Ileum/Jejunum Blood supply = midgut (SMA) arterial arcades, with connecting vasa recta The jejunum makes up the proximal 2/5 of the SI, with the ileum forming the distal 3/5 The jejunum diameter > ileum It is difficult to distinguish the jejunum from the ileum by diameter alone, but there are other features, particularly the arterial arcades + vasa recta The jejunum has less o prominent arterial arcades with longer vasa recta o The ileum has prominent arterial arcades with a shorter vasa recta •
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EMQ Lecture Notes
VOMITING Case 1 • • • •
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Large Intestine The large intestine consists of the caecum (most proximal), vermiform appendix, ascending colon, hepatic flexure, transverse colon, splenic flexure, descending colon, sigmoid colon + rectum Distinguishing features: fatty tags (appendices epiploicae), ribbons of longitudinal muscle (taeniae coli) + segmented/pocketed haustra walls 2 openings: Ileocaecal orifice – acts as o valve preventing movement of substances back into small intestine o Appendix Blood supply = midgut until splenic flecture ! IMA/hindgut •
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Innervation of Gut Abdominal viscera is supplied by the autonomic nervous system Parasympathetic sensory innervation regulated the reflex gut function: o Vagus nerve o Pelvic splanchnic nerves S2-S4 Sympathetic sensory innervation mediate pain: Thoracic splanchnic T5o T12 (greater, lesser, least) o Lumbar splanchnic L1+L2 •
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80F 2 day hx of nausea and vomiting Slightly confused PMHx: AF, osteoarthritis, HTN (recently diagnosed) 3/52: started on low dose bendroflumethiazide Also takes digoxin and co- dydramol O/E: 36.8C, 56BPM, irregularly irregular HR, BP 145/85 Mild epigastric tenderness Na 138, K 3.1, urea 8.6, creatinine 142
Digoxin Toxicity Hypokalaemia secondary to use of diuretic (bendroflumethiazide) predisposes to digoxin toxicity Vomiting ! further hyperkalaemia Patients are nauseated and have a low HR •
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Case 2 • •
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25 student 8h hx of frequent vomiting, “unable to keep anything down” Cramp-like abdo pain Pale, clammy, shivering Hb 14.7, WCC 11.8, Platelet 368, Na 135, K 3.4, urea 7.7, creatinine 70
Gastroenteritis Secondary to staphylococcus aureus Short history due to preformed enterotoxin from food contaminated with staph. Vomiting starts shortly after consumption of food Other causative organisms of vomiting-predominant food poisoning include Bacillus cereus , however the hx is typically shorter (1-2h) and symptoms start later after ingestion Also occurs with Salmonella, Campylobacter and Shigella , but the predominant symptoms are lower abdominal pain, diarrhoea or dysentery •
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Nina Cooper
EMQ Lecture Notes
Case 3 • •
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4 week old baby 4/7 projectile vomiting of curdled milk shortly after every feed 2cm palpable mass in epigastric region
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Case 3 •
Gastric Outflow Obstruction Neonatal pyloric stenosis Occurs at 3-6 weeks old Characteristic = projectile vomiting after every meal Disorder is due to hypertrophy of circular muscle in pyloric region Dehydration and severe electrolyte disturbances eventually arise Treated surgically with a ramstedt pyloromyotomy
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persistently high serum gastrin levels Use of PPIs can suppress secretion e.g. lansoprazole
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45M Several episodes of vomiting fresh blood Drowsy MCV = 106 Platelets = 167 WCC = 11.7 INR 2.1
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HAEMATEMESIS
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Case 1 •
Oesophageal Varices Massive haematemesis + bloods = likely to point to varices Raised MCV due to alcoholinduced bone marrow toxicity Raised INR due to severe hepatic dysfunction Normally caused by portal htn secondary to cirrhosis Upper GI endoscopy = confirmation Need to correct coagulopathy ! FFP + vit K Sengstaken-Blakemore tube can be used for balloon tamponade of bleeding in emergency situations
70M 40% burns to body Several episodes of haematemesis
Gastric Erosion Stress ulceration ! erosion of stomach is a complication of serious burns = Curling’s ulcer Other traumatic causes e.g. sepss, organ failure and intracranial lesions (Cushing’s ulcer) Risk of bleeding is reduced with mucosa-protecting agent or prophylactic antacids •
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CONSTIPATION Case 1 • • •
Case 2 • •
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32F 1 year of recurrent peptic ulceration Taking 40mg of omeprazole Endoscopy reveals 2cm actively bleeding ulcer in duodenum CT shows 2cm mass in pancreas
Zollinger-Ellison Syndrome Rare disorder caused by gastrinsecreting tumour Either found in pancreatic islet cells or duodenal wall Large amounts of HCl produced due to gastrin secretion Diagnosis is suspected in pts with recurrent ulceration and •
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66M 3/12 hx of difficulty passing stool Previously opened daily Now straining, producing worm- like stools with mucus Tenesmus
Carcinoma of Colon/Rectum Short hx of change in bowel habit to constipation Mucus + tenesmus are common in low rectal tumours •
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Case 2 • • •
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28F Chronic schizophrenia Abdominal pain, bloating and constipation Opens 2x weekly with passage of hard stool Also complains of dry mouth
Nina Cooper
Iatrogenic Antipsychotic treatments (e.g. chlorpromazine) have anticholinergic side effects Leads to decreased motility of GIT and decreased glandular secretions ! dry mouth Also can cause difficulty passing urine, blurred vision + others Will see iatrogenic constipation with iron and opiate use •
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EMQ Lecture Notes
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Case 3 • •
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92F Falls and fractures right neck of femur Six days post-op, complains of colicky lower abdo pain Not opened bowels for 6-days post-op Faeces are palpable in left colon and on DRE Faecal loading seen on AXR
Simple Constipation Treatment = alleviate causative factors e.g. reduced food intake, low-fibre diet, lack of exercise and mobility Common in elderly too Use of laxatives should be shortterm •
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Groans, moans, stones, bones Abdo pain, vomiting, constipation Polyuria, polydipsia Depression, anorexia, weight loss Fatigue Hypertension Confusion Pyrexia Renal stones Ectopic calcification Causes Malignancy o Sarcoidosis o Primary o hyperparathyroidism
Case 5 • • • •
26F Constipation Struggled for a few years Topical GTN and dietary advice is not helping
Anal Fissure Constipation due to pain Tx o High fibre, high fluid diet o Topical lidocaine o Topical GTN ! headaches o Botox Surgical o • •
Case 6 Case 4 • •
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56M Short hx of abdo pain and difficulty opening bowels Not passed faeces for 6 days and now struggling to pass urine 6/12 hx of cough with occasional haemoptysis – puts down to being a smoker Wife thinks he has lost weight
Hypercalcaemia Likely to have carcinoma of bronchus (cough + haemoptysis) Can get hypercalcaemia with lung cancer due to malignant infiltration of bone (osteolysis + Ca release) or due to ectopic secretion of an PTH-like hormone Bowel can also be affected by auto-antibodies to myenteric neurones in association with SCC of the lung ! intestinal pseudoobstruction
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8 year old Constipation Distended abdomen Normally fit Healthy and balanced diet
Aganglionosis E.g. Hirchsprung’s disease Absence of ganglion cells in GIT Therefore impaired/absent nervous control Usually diagnosed as an infant • • •
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DIARRHOEA
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Case 1 • • •
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93F Severe chest infection 10 days broad-spec abx, nebs + O2 Develops profuse, offensive, greenish diarrhoea
Clostridium difficile
Nina Cooper
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Antibiotic induced diarrhoea Carried by 3-5% population Treatment with oral metronidazole or vancomycin Enterotoxin is responsible for the diarrhoea and cytotoxin is responsible for the pseudomembrane
EMQ Lecture Notes
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Case 5 •
Case 2 • •
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22M Severe abdominal cramps, vomiting and watery diarrhoea Several hours after eating poorly reheated chinese takeway Stool samples confirm gram positive, aerobi bacilli
Bacillus cereus Associated with poorly reheated rice Takes between 1-16h for symptoms to present •
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Middle aged couple 1 week hx of watery, severe diarrhoea and foul-smelling belches Several days after returning from Russia Cysts and trophozoites seen on stool microscopy
Giardia lamblia Commonly found in Eastern Europe and Russia Causes malabsorption and watery diarrhoea Characteristic = foul smelling flatus Causes villous atrophy in SI Can exist in cyst and trophozoite form Causes acute-phase IgM response Treat with rehydration and oral metronidazole •
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65F Diarrhoea Struggled with infrequent bowel motions most of her life
Overflow Diarrhoea History of chronic constipation/obstruction Liquid stool passes obstruction •
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Case 6 • • • •
Case 3 •
Self-limiting diarrhoea for up to 10 days Can cause toxic dilatation of colon in immunocomprimised patients Hydration + nutrition + electrolyte support
18F Diarrhoea Recently started OCP Similar episodes in the past which she manages with lifestyle modification
Lactose Intolerance Drug adjuvants can cause problems too OCP and POP both contain lactose Intolerance is due to hypersensitivity (reproducible, adverse reaction). Non-immune mediated •
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Case 7 • • • •
62M Bloody diarrhoea Intense abdominal pain Therapy for heart palpitations
Ischaemic Colitis
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WEIGHT LOSS
31M HIV +ve Profuse watery diarrhoea, weight loss and fever Dilated descending colon on AXR Oocysts present on stool sample
Cryptosporidium
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22F Hypopigmented patches on dorsum of hands Weight loss, loose stools and oligomenorrhoea Examination: onycholysis, fine tremor, resting tachycardia + warm peripheries
Nina Cooper
EMQ Lecture Notes
Thyrotoxicosis •
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Hypopigmentation = vitiligo – associated with many autoimmune disorders Signs of grave’s disease Acropachy (pseudoo clubbing of the nails) Orbitopathy (eye disease) o o Pre-tibial myxoedema Start pts on carbimazole or propylthiouricil
Bulbar Palsy •
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51F Weight loss, anorexia and swelling of abdomen Unwell, pale, signs of a left pleural effusion, hepatomegaly and shifting dullness in abdomen Multiple opacities in both lung fiels
Carcinomatosis •
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Signs of disseminated malignancy – ascites, hepatomegaly and multiple pulmonary mets Most likely cause = ovarian cancer – presents late with intra-abdo mets
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Case 1 • •
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72M 6/12hx of progressive difficulty swallowing Now only swallows small amounts of fluid Lost 10kg in weight Wasted appearance
Oesophageal Carcinoma • •
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Rapidly progressing dysphagia Weight loss + hypoproteinaemia = highly suggestive Histological diagnosis confirmed by oesophagoscopy Size of lesion seen on barium swallow ! apple core lesion
50F Chest pain associated with regurgitation of solids and liquids, occurring shortly after swallowing Dilated oesophagus + tapering lower oesophageal segment Oesophageal manometry demonstrates failure of relaxation of lower oesophageal sphincter
Achalasia •
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DYSPHAGIA
Palsy of tongue, muscles of mastication/deglutition and facial muscles due to loss of function of brainstem motor nuclei Signs of LMN disease Seen in motor neurone disease, but also Guillain-Barré, polio and brainstem tumours NEVER affects extraocular movements – how you distinguish from myasthenia gravis
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Failure of relaxation of lower oesophageal sphincter Presents between ages 30-60 Diagnosis = beak-like tapering on barium swallow
Case 4 • • •
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26M Undergone renal transplant 3 day hx of odynophagia and difficulty swallowing Barium swallow + endoscopy show generalised ulceration of oesophagus DHx: oral pred + ciclosporin
Oesophageal Candidiasis •
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Short hx of symptoms + immunosuppression Also seen in AIDS
DISEASES OF THE STOMACH
Case 2 • •
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45M 6/12hx of progressive difficulty with speech and swallowing Weakness of facial muscles bilaterally Absent jaw jerk
Case 1 • •
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63F 2/12 hx of anorexia, weight loss and epigastric pain Iron-deficiency anaemia
Nina Cooper
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Endoscopy shows thickened and rigid gastric wall without an obvious mass lesion Biopsies show numerous signet- ring cells diffusely infiltrating the mucosa
EMQ Lecture Notes
Kaposi’s Sarcoma Endoscopic + histological features = typical Also HIV +ve •
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Adenocarcinoma Weight loss + anorexia + irondeficiency anaemia (chronic bleeding) Leather bottle stomach = gastric carcinoma which diffusely infiltrates all layers of the gastric wall Signet-ring cells = poorly differentiated adenocarcinoma
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Active Chronic Gastritis Caused by h. pylori infection Presence of neutrophils shows active inflammation Nb. 90% of h. pylori infections cause duodenal ulcers •
51M 3 month hx of weight loss + dyspepsia Endoscopy shows heavy mucosal folds + 2cm antral ulcer Biopsy shows heavy infiltrate of atypical lymphocytes with clusters of intraepithelial lymphocytes
MALT Lymphoma Lymphoma of mucosa-associated lymphoid tissue Normal gastric mucosa is devoid of lymphocytes – any infiltrate signifies disease DD lies between gastritis and lymphoma Atypical + intraepithelial involvement + thickened folds + ulceration = infiltration is lymphomatous MALT lymphomas are the most common type of primary gastric lymphoma and are usually lowgrade B cell type •
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INFLAMMATORY BOWEL DISEASE Case 1 • • • •
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26M, HIV +ve 2 week hx of dyspepsia and epigastric pain Endoscopy shows purple, plaque like lesions Biopsies show slit-like vascular spaces surrounded by proliferating spindle cells
34F Known UC 2 week hx of worsening jaundice ERCP shows beading of intrahepatic ducts
Sclerosing Cholangitis Cholestatic jaundice with relatively raised alk phos Beading ! strictures and dilatations Principally associated with UC
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42M Long hx of epigastric discomfort related to meals Endoscopy shows diffuse erythema in antrum w/o obvious ulceration Antral biopsies show infiltrate of lymphocytes, plasma cells and neutrophils in the gastric mucosa Staining shows h. pylori infection
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27M CD Several small bowel resections Severe right sides loin pain, rigors and haematuria Urine microscopy shows pus cells and red cells but no organisms
Oxalate Renal Stones Oxalate is normally bound to calcium in terminal ileum, rendering it insoluble in the colon With multiple bowel resections, this does not occur and so leads •
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Nina Cooper
to hyperoxaluria and stone formation
Case 3 • •
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EMQ Lecture Notes
Hepatitis A RNA virus spread by faeco-oral route Causes acute illness – associated with jaundice, diarrhoea and fever Anti-HVA IgM response seen and later IgG seen •
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26M 6/52 hx of weight loss, passage of blood and mucus per rectum associated with diarrhoea Complains of red, watery eyes UC diagnosed
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Anterior Uveitis Related to disease activity and can be associated with presenting symptoms Equal presentation in UC and CD •
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19F 4 week hx of abdo pain and bloody diarrhoea Enlarging ulcer on left shin
61F Known polycythaemia rubra vera admitted with worsening pruritis and jaundice Icteric, tender hepatomegaly, ascites, peripheral oedema (marked sacral pad)
Budd-Chiari Syndrome Hepatic vein obstruction secondary to thrombosis as a result of polycythaemia rubra vera Disorder is known as Budd Chiari Syndrome Arises secondary to thrombogenic disorders Rarely can be due to congenital web within HPV Diagnosis confirmed by USS/venography of HV and IVC Treament: anticoagulation and treatment of underlying cause •
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Pyoderma Gangrenosum More common in UC Seen in IBD, vasculitic disorders and haematological malignancies • •
JAUNDICE Case 1 • • •
74M Acute chest infection Pyrexial, icteral sclerae, RLL pneumonia
Gilbert’s Syndrome Unconjugated hyperbilirubinea Associated with acute illness Autosomal dominant inheritance Acute illness + raised bilirubin No other signs of deranged LFTs •
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Primary Biliary Cirrhosis Signs of chronic liver disease associated with acute jaundice Autoantibodies are highly suggestive of PBC Heralded by onset of pruritis + antimitochondrial antibody Liver biopsy to determine stage + prognosis Prognostic markers include albumin, bilirubin, PT, evidence of cirrhosis and portal HTN Liver transplantation may be considered •
Case 2 41M Acute jaundice, nausea, vomiting, diarrhoea 3 weeks after returning for SE asia o Bilirubin 43 o AST 432 o ALT 522 o Albumin 35 o INR 1.2 Acute phase IgM response demonstrated
52F 6 week hx of worsening jaundice, pruritis and weight loss Spider naevi, hepatomegaly, jaundice Antimitochondrial antibodies – strongly positive Anti-smooth muscle antibodies and anti-LKM antibodies - negative
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Nina Cooper
Case 5 • •
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EMQ Lecture Notes
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Obese 71m 2 week hx of worsening jaundice, dark urine and pale stools Dilated CBD and gallbladder, no gallstones
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Deposited as haemosiderin ! fibrosis ! cirrhosis Can deposit in pancreas ! DM and heart ! HF Darkened skin is due to raised levels of melanotrophin
Case 3 Carcinoma of the Head of the Panreas Symptoms of obstructive jaundice Painless therefore ASSUME pancreatic cancer Other causes include cholangiocarcinoma, herpatic tumours and obstructing tumours at ampulla of Vater Diagnosis confirmed by ERCP/CT
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DISEASES OF THE LIVER
17M Symptoms and signs of chronic liver disease High transaminases Chronic inflammation in portal tracts + moderate fibrosis on biopsy Prominent accumulation of copper-associated protein in periportal hepatocytes Low serum caeruloplasmin + Cu
Wilson’s Disease Inherited autosomal recessive disorder Cooper accumulates in liver and basal ganglia of brain Chr 13 defect ! abnormal coppertransporting ATP-ase and failure of liver to excrete Cu in bile Accumulation leads to chronic hepatitis and cirrhosis In the brain ! neurological disability Children present with hepatic problems, adults present with neurological disease Pathognomonic sign = Kayser Fleischer ring = Cu deposition in cornea •
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42M African LFTs abnormal – high transaminases Moderate-severe inflammation seen on biopsy with mild fibrosis Special stains identify antigens from a dsDNA virus within the cytoplasm of many hepatocytes
Chronic Hepatitis B dsDNA = hepatitis B Not often preceeded by an acute hepatitic illness Leads to hepatocyte damageby causing expression of viral antigens on the cell surface ! destruction by immune system • •
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Causes of Ascites Abdominal trauma Acute pancreatitis (high serum amylase) Alcoholic cirrhosis (high yGT) Bacterial peritonitis CCF Hepatic vein occlusion Malignant mesothelioma Nephrotic syndrome (assoc. with hypercholesterolaemia) Ovarian carcinoma (see adenocarcinoma cells in ascitic fluid) Tuberculosis (granulomas in ascitic fluid) • •
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51M Pain in right hypochondrium Hepatomegaly 2cm below costal margin Darkened skin compared to before LFTs show markedly raised transaminases Biopsy shows cirrhosis and heavy deposition of haemosiderin within the cytoplasm of hepatocytes and bile duct epithelium
Genetic Haemochromatosis Defect in chr 6, near HLA-A locus Excessive absorption of iron in SI • •
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Nina Cooper
EMQ Lecture Notes
HEP B SEROLOGY
Resolved Infection Acute infection Vaccinated Low infectivity carrier Naive
sAg -
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sAg: surface antigen; eAg: e antigen; eAb: e antibody; cAb: core antibodu • •
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DNA virus Signs: fever, malaise, jaundice, hepatomegaly, arthralgia, urticarial, deranged LFTs Long term consequences: o Fibrosis o Cirrhosis o Hepatocellular carcinoma
DISORDERS OF THE PANCREAS
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Most common pancreatic neoplasm and occurs in the elderly Presents with painless jaundice Weight loss + anorexia also occur
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56M, chronic alcoholic Repeated attacks of abdo pain precipitated by bouts of heavy drinking Loose, pale, greasy stools Calcification in peritoneal cavity
Chronic Pancreatitis Upper abdo pain which develops gradually after meals/drinking Pain radiates to back and is relieved by sitting rowards Calcification = chronic calcifying pancreatitis ! intraductal calculi Can lead to pancreatic insufficiency •
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Case 4 Case 1 • • •
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36F Long hx of gallstones 12hr hx of severe abdominal pain radiating to back Tachycardic, tachypnoeic, hypotensive Mildly raised bilirubin 6x serum amylase level USS shows stone in CBD
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20M Fainted during rugby match Dizzy, palpitations then blacked out Previous episodes related to sport/exercise
Insulinoma Pancreatic islet-cell tumours than secrete insulin Hypoglycaemia associated with exercise/fasting Mostly cytologically benign •
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Acute Haemorrhagic Pancreatitis Sudden onset abdominal pain + signs of shock Common causes = alcohol and gallstones Diagnosis depends on serum amylase Raised amylase is also seen in other abdo emergencies (e.g. perf’ed DU) but if >5x normal = likely to be acute pancreatitis •
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DRUG SIDE EFFECTS
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75F Painless obstructive jaundice 5cm mass on head of pancreas Malignant glandular cells on aspirate
Adenocarcinoma Aspirate = diagnostic •
Drug Isoniazid Ethambutol Rifampicin
Pyrazinamide Streptomycin
Side Effect Peripheral neuropathy Colour blindness Hepatic enzyme inducer, liver toxicity, OCP failure Liver toxicity Ototoxicity
Nina Cooper
EMQ Lecture Notes
GI Surgery UPPER GI DISEASE Case 1 (Gallstones) 41F Fever, abdo pain, nausea RUQ pain Intense shaking Icteral sclera •
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Cholecystitis can occur in absence of gallstones Investigations include USS and ERCP Treat via interventional elective cholecystectomy
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Jaundice Increase in serum bilirubin Heme in RBCs broken down by macrophages in spleen/bone marrow ! unconjungated bilirubin Conjugated in liver Excreted into GI tract via biliary tree Converted into urobilinogen in terminal ileum Excretion: kidneys (via blood), sterabilogen (via faeces) and reexcreted by liver • •
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= Curling’s Ulcer
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Pre-hepatic: unconjugated hyperbilirubinaemia e.g. hereditary spherocytosis Hepatic: mix ! problem with liver excretion e.g. hepatitis, cirrhosis, drugs, humours Post-hepatic: conjugated hyperbilirubinaemia ! obstruction; gallstones/tumours/infection
Gallstones/Biliary Colic Contraction of gallbladder against an obstruction Triggered by eating fatty foods Severe pain radiating to back Associated with nausea Positive murphy’s sign Tachycardia, non guarding Female, fat, fertile, forty •
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73 Persistent unexplained dyspepsia Dysphasia Melaena
= Gastric Carcinoma Red flags = anorexia, melaena, progressive symptoms, age >55
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56 Hyperpigmented skin in left axilla (acanthosis nigrans) Progressive anaemia and dyspepsia
= Gastric Carcinoma Acanthosis nigricans Microcytic anaemia Dyspepsia, nausea, anorexia, weight loss, satiety Virchow’s node Persistent unexplained dyspepsia Vomiting of fresh blood Leather bottle stomach, rigid thick gastric wall CT/MRI staging Signet ring cells on biopsy Treatment: partial/complete gastrectomy • • •
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Stagnant bile ! ASCENDING CHOLANGITIS Charcot’s triad (fever, rigors, jaundice) Gram –ve (e.coli) Urgen investigations – watch BP
21 Severe burns Vomiting blood Pyrexial
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Nina Cooper
Case 4 • • •
32 CLO test positive Abdominal pain after meals
= Peptic Ulcer
Case 5 • • •
45 GI surgeon (?stressful) Raised INR Haematemesis after stag night
EMQ Lecture Notes
Malignant vs. Chronic Ulcers Malignant ! ulcerating, heaped up epithelium around crater, rolled, raised, everted Chronic ! boundaries, fibrous scar tissue, inflammation, necrosis Kaposi’s sarcoma ! AIDS, purple plaques/lesions in fundus, spindle cells •
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Pyloric Stenosis Projective vomiting Succession splash Hypokalaemia Metabolic alkalosis Seen in babies • •
= Oesophageal Varices
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Oesophageal Carcinoma Progressive, rapid dysphagia, weight loss, cachexia Low serum protein Diagnosis via oesophagoscopy Size assessed via barium swallow – apple core appearance • • •
Achalasia Lower oesophageal sphincter failure Food regurg Looks like beak line on swallow •
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Oesophageal Stricture Impact pain Regurgitation Barium swallow; benign ! PPI, dilatation; malignant ! resection • • •
Oesophageal Varices Haematemisis + macrocytic anaemia (direct effect on bone marrow) Raised INR (liver toxicity) Seen in alcoholics – portal HTN secondary to liver disease •
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Barrett’s Oesophagus Metaplasia of distal oesophageal mucosa, consequence of GORD Diagnosis with endoscopy, biopsy Treatment with regular surveillance, PPI or mucosal ablation Can progress to gastric carcinoma (30-40x more likely if untreated) •
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Mallory Weiss Tear Students, beer race Tear in mucosa at G-O junction Repeated retching and vomiting Bloods normal Self-limiting • • • • •
Acute Erosive Gastritis NSAIDs, alcohol, chemotherapy, stress Melaena and anaemia seen Burns ! curling’s ulcer Intracranial lesion ! cushing’s ulcer •
Peptic vs. Duodenal Ulcer Peptic Duodenal Pain immediately Pain 2-3h after after meals meals/at night
Chronic Gastritis vs. MALT Lymphocytes in stomach is bad Chronic gastritis = h. pylori, plasma cell and lymphoid follicles, differentiated, erythematous, typical lymphocytes MALT = B cell type lymphoma, intraepithelial involvement, thickened folds, atypical lymphocytes • •
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Zollinger-Ellison Syndrome Recurrent peptic ulceration Haematemsis Gastrin-secreting tumour from the G cells of the pancreas (also in the stomach and duodenum) Increased HCl in gastric antrum Multiple ulcers throughout upper GIT Distal ulceration ! diarrhoea • • •
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Nina Cooper
Investigation Raised gastrin levels in serum US, CT, angiography 60% malignant; mets to local LNs, liver • • •
Treatment Lansoprazole, surgical resection MEN1 = multiple endocrine neoplasia 1 (ZES presents as part of it) • •
Case 5 • • • •
EMQ Lecture Notes
PaO2 < 8kPa (60mmhg) Age > 55 years Neutrophils: (WBC >15 x109/l Calcium < 2mmol/l R enal function: (Urea > 16mmol/l) Enzymes: (AST/ALT > 200 iu/L or LDH > 600 iu/L) Albumin < 32g/l Sugar: (Glucose >10mmol/L) Pancreatic Pseudocyst Possible complication of pancreatitis Fever from infection and haemorrhage into lesser sac Symptoms of pancreatitis and fullness •
40 banker LUQ pain Radiating to back Hypotensive and tachycardic
= Acute pancreatitis
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Insulinoma Pancreatic islet cell tumour Hypoglycaemia upon fasting/exercise Mostly benign Palpitations, dizziness, fainting, diplopia, confusion Your typical young athlete •
Triad = HTN, low BP + resp failure Single best marker of prognosis? = Serum urea Amylase = raised 5x ! likely to be pancreatitis but can be duodenal ulcer
Case 6 • •
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Pancreatic Adenocarcinoma Painless, progressive jaundice Bad prognosis Risk factors: DM, smoking, alcohol 5th most common cause Courvoisier’s law: if the gall bladder is palpable and the patient is jaundiced, obstruction of the bile duct is unlikely to be a stone (i.e. a tumour!) Stone ! inflammation ! fibrosis ! non-distensable GB Older population, dark urine, pale stools, ALP>AST (obstructive) Inv: tumour marker CA19-9 (also increased in biliary tract malignancies), CT Palliative treatment Whipple’s – pancreatoduodenectomy: resection of head of pancreas + CBD + GB + distal stomach + duodenum •
52 chronic alcoholic Presents with fullness, epigastric pain and nausea Jaundice Palpable GB
= Pancreatic Carcinoma
Causes = IGETSMASHED Acute Pancreatitis Alcohol abuse Epigastric pain, radiates to back, relieved by sitting forwards Clinical dehydration ! hypokalaemia Haemorrhagic ! anaemia Retching Inv: bloods and USS of liver WCC: raised, neutrophilia Modified Glasgow criteria = prognostic (PANCREAS) • •
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A score >= 3 indicates Acute Severe Pancreatitis A score < 3 indicates Acute Mild Pancreatitis
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Abdominal Masses Case 1 •
60M
Nina Cooper
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Severe acute onset abdo pain BP 90/60, HR 150 Expansile umbilical mass
• •
•
•
•
•
AAA •
EMQ Lecture Notes
Screening for men >65 <4cm = reviewed annually 4-5.5cm = reviewed every 6 months Indications for elective repair o >5.5cm o Growth >1cm/year
•
Case 5 • • • •
Case 2 • • • • •
30M, Nigerian Abdominal mass and high fever Mass in LUQ Moves with respiration Cannot palpate above it
Presents with abdo pain, fever, mass If caused by spinal TB, also back pain Differential = femoral hernia Affected hip often held in flexed position
65yo alcoholic Epigastric tenderness Palpable mass CT shows fluid filled round mass in epigastrium
Pancreatic Pseudocyst Late complication in 20% pancreatitis, especially alcoholic Typically 6-8 weeks after episode Thick wall surrounding fluid Can occur in pancreas or lesser peritoneal sac Complications: abscess, vessel erosion, duodenal obstruction, rupture CT/US guided drainage if large •
• •
Splenomegaly Haematological e.g. CML Portal HTN e.g. cirrhosis Storage diseases e.g. Gaucher’s disease Systemic diseases Infections • • •
•
•
•
•
•
Case 6 Case 3 • • •
• •
•
72F RIF mass Firm, irregular and 5cm in diameter Lower edge is palpable Hb 9.5, WCC 5, MCV 70, Pk 150
• •
• • •
Caecal Carcinoma Caecal lesions = weight loss and anaemia Sigmoid colon/rectal lesion – change in bowel habit/PR bleed Be suspicious if >40yo presenting with acute appendicitis •
•
•
•
50M 2 year history of dyspepsia Sudden onset, severe epigastric pain Worse on movement One episode haemetemisis O/E = cold, sweaty, shallow breaths Abdo is rigid and bowel sounds absent CXR shows air under the diaphragm
•
Perforated Peptic Ulcer Free air under diaphragm = perforation Patient is shocked with abdo pain + worse with movement If diaphragmatic irritation, referred pain to shoulder tip Do erect CXR Immediate treatment = drip and suck, analgesia, antibiotics, PPI •
Case 4 • •
• •
45M, Indian Tender swelling below right inguinal ligament Right hip held in flexed position Complains of excrutiating pain despite taking paracetamol earlier
Psoas Abscess Secondary to lumbar TB •
•
•
• •
Case 7 • •
28M Hx of UC
Nina Cooper
•
•
•
Acute abdo pain, nausea, vomiting and bloody diarrhoea Febrile, tachycardic and distended abdomen AXR shows transverse colon with diameter of 6.5cm
Toxic Megacolon Can lead to perforation, sepsis and shock >6cm dilatation = diagnostic Toxic megacolon can be treated with intravenous fluids, antibiotics and steroids Colonoscopy contraindicated •
• •
•
Appendicitis Clinical Diagnosis Inflammation of vermiform appendix Causes = faecolith, lymphoid hyperplasia, infection (parasitic/viral) Tx: non operative vs. operative McBurney’s point Rovsing’s sign •
•
• • •
EMQ Lecture Notes
Investigation: colonoscopy (likely bowel cancer) Haemorrhoids Disrupted and dilated anal cushions 3, 7, 11 o’clock when in lithotomy position 1st degree - internal 2nd – prolapse on defecation, spontaneously reduce 3rd – prolapse but require digital reduction 4th – persistent prolapse Tx: conservative, sclerosing agents, banding, haemorrhoidectomy •
•
• •
•
• •
Case 10 75M Hx of AF Abdo pain, vomiting and rectal bleeding Blood is dark with altered constituency O/E: pale, tachycardic, cold peripheries Tender abdomen Bowel sounds difficult to here • • •
•
•
Case 8 • •
• •
•
65M Referred by GP with altered bowel habit and rectal bleeding over 8 weeks Blood is bright red and painless Reports tenesmus and weight loss
•
Mesenteric Ischaemia Hallmark: persisting abdo pain that is out of proportion for the clinical findings in high-risk patients Mesenteric angiography to differentiate between occlusive/non-occlusive causes Treatment: surgical, revascularisation or thrombolysis Embolus ! embolectomy Thrombus ! aorto-mesenteric bypass •
•
Investigation: Flexible sigmoidoscopy Colorectal Cancer Predisposing factors: IBD, FAP, polyps, smoking, low fibre diet Genetics: 1st degree relative 1:17, two 1st degree relatives = 1:10 Tx: must stage (TNM) ! chemoradiation/surgery Flexi sig – visualisation rectum and sigmoid, allows for biopsy •
•
•
• •
•
•
Case 11 45F RUQ and R shoulder pain Fever Murphy’s sign positive • • •
Case 9 • •
• •
•
83F Tiredness and weight loss over 6 weeks Mass in RIF Loss of 10kg
Investigation: USS
Case 12 23M •
Nina Cooper
• •
•
Abdominal pain Started over umbilicus and now in RLQ Tachycardic, tender RIF and Rovsing’s sign postive
Investigation: Predominantly clinical, USS in females
EMQ Lecture Notes
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EMQ Lecture Notes
Neurology Case 1: Left sided weakness Unable to move arm 2hrs since onset • • •
Management of Stroke Consider thrombolysis until 4.5h AFTER onset of symptoms: alteplase or streptokinase Contraindicated in Haemorrhagic stroke o Improving symptoms o o Severely impaired or altered mental state o At high risk of bleeding o Pregnancy o Recent trauma, surgery or lumbar puncture Alteplase = recombinant tissue plasminogen activator If contraindicated use aspirin •
•
Artery Regions and Symptoms
•
MCA
•
• •
Case 2 •
•
Able to speak, but sentences make little sense
• •
Very common Contralateral weakness Greater face/arms than legs Dysphasia Neglect
ACA Types of Stroke Middle cerebral artery affected Wernicke’s area = UNDERSTANDING Broca’s area = speech formation “broken speech”
•
•
•
•
•
Rare Contralateral weakness Greater in legs than arms/face
•
PCA •
Receptive vs. Expressive Dysphasia Receptive: o Wernicke’s aphasia o Left tempero-parietal damage o Can speak fluently but doesn’t make sense Grammatical mistakes o Jumbled sentences o Potential inability to o comprehend language Expressive: o Broca’s aphasia o Left frontal lobe o Cannot initiate language o Few disjointed words o Unable to construct sentences •
•
Varied visual defects
Vertebral Artery More common than PCA Causes lateral medullary syndrome AKA Wallenberg’s syndrome DANISH Acute vertigo (damage to VESTIBULAR NUCLEUS) Cerebellar signs – ataxia/pastpointing/dysdiadochokinesia = damage to cerebellar penduncle Ipsilateral horner’s syndrome PTOSIS o ANHIDROSIS o MIOSIS o • •
• • •
•
•
Posterior Inferior Cerebellar Artery Less common than VA •
Nina Cooper
• • • •
Lateral medullary syndrome Acute vertigo Cerebellar signs Ipsilateral horner’s syndrome
EMQ Lecture Notes
1 = moderate risk: warfarin (INR 2-3) or novel drug treatment (dabigatran) >2 = high risk: DABIGATRAN (or warf)
CHF or LVEF <40% = 1 HTN = 1 AGE >75 = 2 DIABETES = 1 STROKE/TIA/THROMBOEMBOLISM = 2 V ASCULAR DISEASE = 1 AGE 65-74 = 1 SEX CATEGORY: FEMALE = 1
HEADACHE Case 1: 18F 2/12 pain above eye since started revising Feels sick Lies in dark room to recover • •
•
Case 3: 57yo M T2DM Confusion, dizziness, anxious, loses consciousness Regains consciousness after 5 minutes • • •
•
Most likely to be HYPOGLYCAEMIA
•
Migraine >2: Unilateral/bilateral headache Pulsating Worsened by physical activity + >1 Nausea/vomiting Photophobia/phonia 1/3 occur with aura Visual Sensory Speech •
Autonomic Signs: Sweating Anxiety Tremor Palpitations Tremor Dizziness •
• •
• • •
Triggers: stress, depression, menstruation, menopause, food
• •
Tension Headache Band across forehead Associate with stress Classically EMQ of student doing exams •
Neuroglycopenic signs Confusion Drowsiness Visual problems Seizures Coma Hemiparesis (rare) • •
• •
• • • •
Case 4: Who should you anticoagulate? CHA2DS2-VASc SCORING 0 = no therapy
Case 2: 74M Recent onset, severe headache Fatigue Weight loss Sore throat Red face • • • • • •
Nina Cooper
Temporal Arteritis Granulomatous infiltration of small -> large size arteries Most common in ELDERLY Decreased pulsatility of temporal pulse ESR >50 New onset of headaches See abnormal MULTINUCLEATED GIANT CELLS Jaw claudication Scalp tenderness Associated with polymyalgia rheumatic • •
• • •
• • •
EMQ Lecture Notes
!
Pia Mater Extradural Haemorrhage Sharp Bang Loss consciousness > lucid period > compression of brain > coning of brainstem > vomiting > drowsiness > neurological symptoms > death • •
Subdural Haemorrhage Seen in ELDERLY and ALCOHOLICS – brain shrinks, veins stretch and can rupture Slow bleeding Symptoms progressively develop over weeks/months Classic = fall, progressively worsening headache > neurological deficits Also more likely in anticoagulated patients •
•
Rarer manifestations 10% show respiratory symptoms Weight loss Fever Fatigue Bruits of subclavian, axillary and brachial arteries Temporal redness • • • • •
•
•
•
•
Case 3: 58M Indian Electric shooting pain when brushing teeth Thinning beard • • •
Case 5: 34M 45 minute headaches every night Bangs head on floor to relieve severe pain • •
•
•
Trigeminal Neuralgia Paroxysmal attacks, varying in 220 minutes in length Sharp/intense/burning/stabbing sensation Trigger factors in trigger area e.g. brushing teeth in V3 Tic douloueux Caused by compression of the trigeminal nerve root (15% tumour) •
•
•
• •
Cluster Headaches Severe orbital, supraorbital or temporal pain Lasts 15min-3hr Occurs in clusters Often wakes people up at night Agitations • • • •
Cranial Autonomic Features Ipsilateral lacrimation Ipsilateral conjunctival infection Ipsilateral rhinorrhoea Ipsilateral ptosis Ipsilateral oedema of eyelid • • • •
Case 4: • •
• •
82F Progressively worsening headache Too much alcohol More forgetful than usual
Skull ! = middle meningeal artery (extradural) Dura Mater ! = venous (subdural) Arachnoid Mater
•
Case 6: 19M Pakistani parents 2 months of weight loss and headaches Worse since getting a cold Waking in the night with pain • • •
• •
Space-Occupying Lesion Progressively worsening over time •
Nina Cooper
•
•
•
Progressively worsening neurological signs Heaches which is present on waking Worse on coughing, sneezing, defaecating, bending over
EMQ Lecture Notes
•
= CJD •
• • •
DEMENTIA Case 1: 65M, HTN Severe memory loss and slowness of thought over weeks Wife reports memory problems for one year Marked deterioration 2/12
•
•
• •
•
•
= Vascular Dementia
Case 2: 85F Increasingly forgetful over past few years Deteriorated – fails to recognise immediate family on occasions Often doesn’t make sense when speaking • •
•
Passed away 3 months later Rapidly progressive -> death within months Myoclonus Memory loss, personality change, hallucination PRION proteins -> sponge-like degeneration of brain tissue Commonly sporadic (sCJD) but can be variant (vCJD) due to eating contaminated meat (mad cow disease)
Case 5: Wife of 75M reports frequent episodes of slowness and inattentiveness for hours Patient tells you he has been experiencing vivid visual hallucinations Patient has increased tone in both arms Slow to follow motor instructons •
•
•
•
= Lewy body Dementia (Parkinsonian features)
•
Alzheimer’s
Vascular Dementia
= Alzheimer’s
Case 3: 61M Recently become increasingly aggressive Shouting inappropriate remarks in public Increasingly cold and irritable towards own family • •
•
Memory loss Impaired speech/verbal ability Loss of executive function Visuo-spatial symptoms (gets lost)
•
= Pick’s disease (fronto-temporal dementia)
Case 4: 72F Rapid decline in cognitive function over days Memory/speech affected Jerky myoclonic movements of her limbs •
Gradual
Stepwise
Old age, FHX
CV risk factors + previous stroke
Most Common
•
• •
Pick’s Lewy Body Disease (Frontotemporal) Disinhibition Hallucinations Personality (visual) change Sleep Inappropriate disturbance behaviour Resembles Memory Alzheimer’s often Memory, preserved language and understanding all affected Earlier onset Fluctuating (<65) impairment Parkinsonism: tremor, rigidity, bradykinesia Histology shows lewy bodies
Case 6: Ex-American Football player Deterioration in memory • •
Nina Cooper
• •
•
Poor mood Struggles to find right words when speaking Continues to worsen over years
= Chronic Traumatic Encephalopathy Athletes e.g. boxers, football players who experience recurrent head trauma Develop features of alzheimer’s in their 40s •
•
COLLAPSE Case 1: 21M Large amounts of dilute urine Tremor and dizziness after sport, then collapses •
EMQ Lecture Notes
Carotid Sinus Syncope Shaving, head turning -> dizziness and syncope Epilepsy AURA Tonic-clonic sequence Tongue-biting, incontinence Post-ictal confusion •
• • • •
Generalised Seizures No localizing features Tonic-clonic = loss of consciousness, increased tone and jerking Absence = brief pause midsentence Myoclonic = single sudden jerk of limb/trunk • •
•
•
• •
= Hypoglycaemia DIABETICS Incorrect medication dose, missed meals or exercise Tremor, sweating, dizziness • •
•
Case 2: 36F Collapse after finding out about death of close family member Unconscious for a few minutes Limbs continue to move, making frequent, erratic movements • •
• •
= Vaso-vagal syncope Emotion/pain/fear/standing for too long Nausea, going pale Clonic jerking (no stiffness) •
• •
Simple Partial Seizure Restricted to one part of brain, no LOC Can vary from motor disturbance (Jacksonian) to a “funny turn” or strange sensation No post-ictal confusion or amnesia •
•
•
Case 3: 28F Smacking lips and strange chewing movements at work Stares blankly at colleagues during episodes Patient confused afterwards with no recollection Felt “déjà vu” earlier in the day • •
•
•
•
= Complex partial seizure Typically start with an aura, which is the simple partial component -> Automatisms such as lip smacking, wandering around Awareness is impaired •
•
•
Stokes-Adams Attacks ARRHYTHMIA -> reduced CO and LOC Pale, slow/absent pulse -> flushing upon recovery •
•
Drop Attacks Elderly woman Weakness of legs -> fall with no LOC or confusion • •
Case 4: 16M Stiff and shakes violently Right arm was shaking before collapse • • •
= Partial seizure with secondary generalisation Begins as a partial seizure (sensory/motor/automatism) Develops into LOC and convulsions •
•
Nina Cooper
Status Epilepticus Seizures lasting >30 minutes with no consciousness regained inbetween Tonic-clonic •
EMQ Lecture Notes
NMJ •
•
•
Treatment Open and maintain airway, 100% O2 IV Lorazepam bolus + 50% glucose o Rectal diazepam or oral midazolam if IV access impossible If seizures continue, IV Phenytoin If still no response -> general anaesthetic
•
E.g. myasthenia gravis, Lamberteaton syndrome, organophosphate poisoning, botulism Affects multiple muscle groups LMN signs
•
•
•
Muscle •
•
•
•
E.g. muscular dystrophy, hypothyroidism Tend to result in muscle wasting and specific functional difficulties relating to proximal weakness Signs of proximal myopathy include difficulty in getting out of chairs and difficulty climbing stairs
Case 1: 65F Sudden-onset right sided weakness of face and arm History of HTN – takes amlodipine Right arm is rigid and hyper- reflexic •
WEAKNESS Approaching Weakness: categorise into UMN and LMN, or Brain/SC/PNs/NMJ/muscle • •
UMN • • •
Spasticity Hyper-reflexia Babinksi
• •
•
•
= CVA
Case 2: 50M Smoker 6 month hx of SOB and 2 day hx of haemoptysis Weight loss of 1 stone in 1 month Peripheral nerve examination shows weakness in arms/legs, but improved when repeated later •
LMN •
•
Muscle wasting Floppy paralysis Fasciculations
• •
•
Brain • •
•
UMN signs Focal signs according to lesion e.g. hemiparesis, haemianopias General signs e.g. headache, vomiting
Spinal Cord E.g. MS, transverse myeltitis, trauma, malignancy UMN signs Focal lesions e.g. vision (optic neuritis, nystagmus), bladder/bowel incontinence, bulbar signs (swallowing, speech) •
• •
Peripheral Signs Spinal root compression, plexus injuries Look for LMN signs •
•
•
= Lambert Eaton Syndrome Paraneoplastic (assoc. with small cell lung cancer) or autoimmune Antibodies against presynaptic calcium channel Proximal muscle weakness and gait abnormalities •
•
•
Case 3: 40F Droopy eyelids Hard to swallow, cannot complete meal • • •
Nina Cooper
• •
EMQ Lecture Notes
Hyperthyroidism Voice trails off at end of sentences
= Myaesthenia Gravis Antibody against ACh receptor Oculomotor/bulbar signs predominate • •
•
•
Happened 6 months ago but resolved spontaneously Reduced fine touch sensation in both feet + weakness
= Multiple Sclerosis Optic neuritis is most common presentation Weakness Fatigue Paraesthesia Paralysis Relapsing-remitting, secondary progressive, primary progressive •
• • • • •
RR: get better, then relapse, then get better Eventually can progress to secondary progressive PP: death at 5-10 years
ALCOHOL Impacts on Brain Liver Nutrition Trauma Social Other substance abuse Immunosuppression • • • •
LE Improves with exercise
MG Worsens with exercise
Less Ca in cleft, therefore requires multiple APs before muscle moves
More weakness over time as need Ache to break down the ACh to free up receptors
Case 4: 4M Not able to run like peers Waddle when walks Falls over frequently Difficulty climbing stairs Positive Gower’s sign
• • •
Case 1: 45F Post-op (gall bladder) Agitated, shouting incoherently and convinced she is covered in spiders • • •
• • • • • •
= Muscular Dystrophy
Case 5: 30F 2 day hx of pain and loss of vision in left eye • •
= Delirium Tremens Alcohol withdrawal state Agitation, confusion, fluctuating consciousness, seizures, arrhythmias, visual/tactile hallucinations Treat with benzodiazepines (CHLORDIAZEPOXIDE) • •
•
Case 2: Known alcoholic Slurred speech, cannot walk straight, floppy sat in chair Blood alcohol level = 0 • •
•
Nina Cooper
EMQ Lecture Notes
•
= Cerebellar Syndrome DANISH Dysdiadochokinesia Ataxia Nystagmus Intention tremor Slurred speech Hypotonia
Alcoholics also get other types of dementia (10% causes)
• • • • • • •
Case 3: 39M 40 units a week for 5 years Numbness/tingling in toes for 4 months Impotence
Wernicke’s Encephalopathy Confusion Ataxia Opthalmoplegia TX: IV Pabrinex (thiamine [B1], riboflavin [B2], nicotinamide [B3], pyridoxine [B6], ascorbic acid [vit C] • • • •
• • •
•
Case 6: 60M Reducing GCS Swollen abdomen Yellow sclera Sickly sweet smell of breath = FETOR HEPATICUS • • • •
= Peripheral Neuropathy Commonest cause are DIABETES and B12 DEFICIENCY Glove & stocking distribution Usually symmetrical Can also cause impotence and autonomic dysfunction (B12 def) •
• • •
•
= Decompensated Liver Failure Leads to hepatic encephalopathy Inverted sleep-wake cycle = first sign Due to ammonia and other waste substances crossing BBB Lethargy, personality change Worsening confusion and LOC Signs of liver failure e.g. fetor hepaticus, jaundice Cure = transplant • •
•
Case 4: 60 year old publican Increasingly confused over weeks Vomiting for few days Intermittent consciousness • •
• •
= Subdural haemorrhage Cerebral atrophy (alcohol!) Frequent falls (drunk!) Clotting disorder (liver failure!) DD: CVS, other intracerebral bleed, SOL, meningitis, encephalitis) • • • •
Case 5: 50M, Irish Mumbling incoherently Not sure where he is Complains of double vision Recalls the prime minister as “Bertrand Ebstein” Claims “came on moped which he borrowed from Robbie” • • • • •
•
= Wernicke-Korsakoff’s Syndrome Due to untreated Wernicke’s Anterograde amnesia Confabulation • • •
• • •
•
NERVE INJURY Nerve Median Nerve (C6-T1)
Feature Wasting of thenar eminence Loss of sensation in lateral palmar surface of 3 and a half digits Test for weakness in abductor pollicis brevis Frequently affected in carpal tunnel syndrome
Ulnar Nerve (C8-T1)
Wasting of hypothenar eminence Sensory loss over medial one and a half digits Test for weakness of abductor digiti minimi “Claw hand”
Radial Nerve (C5-T1)
Weakness of wrist extension ! wrist drop Anaesthesia over fist dorsal interosseous muscle
Klumpke’s Palsy
Erb’s Palsy
Paralysis of intrinsic muscles of hand Loss of sensation in ulnar distribution Horner’s syndrome sometimes present
Loss of shoulder abduction and elbow flexion Arm held internally rotated “Waiter’s tip”
Common Peroneal Nerve (L4-S1)
Weakness in dorsiflexion and eversion of the foot Sensory loss over dorsum of foot Hit in side of knee
Tibial Nerve (L4-S3)
Inability to invert food or stand on tip-toe Sensory loss on sole of foot
Stroke: Symptoms and Signs Site of Stroke Anterior Circulation
Posterior Circulation
Symptoms/Signs Unilateral weakness/sensory deficit Homonymous hemianopia Higher cerebral dysfunction e.g. dysphasia/neglect
Cranial nerve palsy/cerebellar signs Vertigo, dysarthria, ataxia, choking Isolated homonymous hemianopia
Dominant Frontal Lobe (Broca’s Area)
Patient can understand you Replies in broken speech = Broca’s (expressive) dysphasia
Dominant Temperoparietal Lobe (Wernicke’s Area)
Patient has impaired comprehension Speech is fluent with jargon = Wernicke’s (receptive) dysphasia
PICA Thrombosis (Lateral Medullary Syndrome)
Vertigo, vomiting, dysphagia Ipsilaterally: ataxia, Horner’s, nerve V/VI palsy Contralaterally: loss of pain/temperature/sensation in face
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HEADACHES: SUMMARY Name
Site
Character
Severity
Time
Migraine
Unilateral or bilateral
Can be pulsation
Moderate – severe
4-72 hours
Tension Headache Temporal arteritis
Temporal Band
Band-like
Mild
N/a
Temporal
General pain
Moderate severe
New onset
Sharp, stabbing, burning
Intense
2s-20min
Trigeminal Neuralgia
V2/3
Cluster Headaches
Unilateral, orbital or supraorbital
Hot metal poking into eye
Extremely severe
15min – 3hrs
Subdural
General
General
Progressively worsens
Worsens over weeks/months
Extradural
General
General
Severe
Worsens over hours
SOC
General
General
Increases in severity – can be very painful
Progresses over months
Associated Symptoms Nausea, vomiting, photophobia, photophonia None at all
Predisposing Factors Caffeine, chocolate
High Risk Groups Women
Stress
Students
Polymyalgia rheumatica, respiratory symptoms, jaw claudication Caused by shaving, brushing teeth, wind on face etc. Running, red and swollen eye Runny nose Worsening neuro signs
Parvovirus B19
>50 years old
None
15% have tumour
None
All ages
Fall or head injury
Elderly, anticoagulated, EtOH
Worsening neuro signs after lucid interval Worsening neuro signs
Large head injury
Worse in morning, coughing, sneezing, bending over
Nina Cooper
EMQ Lecture Notes
Renal Medicine PHYSIOLOGICAL KIDNEY FUNCTION
Case 2 • •
Main role is waste removal Occurs in glomerulus Mainly creatinine, urea and drugs Also involved in reabsorption of Na and H2O Rapid exchange of Na and K in the DCT
•
•
•
•
•
54M Stage 3 CRF Bone pain Ca low Alk phos high
•
•
Renin-Angiotensin-Aldosterone Axis Involved in regulating BP Renin coverts ang – ang I Then converted to ang-II by ACE Results in water retention via aldosterone • • • •
Test to confirm pathology DEXA scan Diagnosis = renal osteodystrophy • •
Renal Osteodystrophy High phosphate due to inadequate excretion Low Ca due to low calcitriol and poor renal reabsorption Increased PTH Increased bone reabsorption Osteoporosis on DEXA = bone density scan Give Ca and Vit D supplements to reduce PTH levels •
•
• •
Vitamin D Regulation Kidney controls how much Ca is reabsorbed •
Phosphate High phosphate ! PTH secretion Therefore must regulate phosphate excretion to stop bone reabsorption and high blood Ca • •
Acid-Base Balance H+ and HCO3- regulated by kidney •
•
•
Case 3 • •
• • • •
RBCs • •
EPO produced by kidney Influenced RBC formation (and some platelets)
CHRONIC RENAL FAILURE
Case 1 • • • •
17 child Chronic renal failure Severe anaemia Iron studies within normal limits
Most appropriate treatment Recombinant erythropoietin injection •
35F Kidney transplant 6 months ago Swelling in neck Constipation, low mood Calcifications in kidney GFR normal
Diagnosis Tertiary hyperparathyroidism •
Hyperparathyroidism Primary = problem with parathyroid (adenoma) – autonomous secretion of PTH Secondary = physiological reaction to low Ca or high Phos ! high PTH Tertiary = prolonged secondary hyperparathyroidism, so parathyroidism becomes autonomous ! inappropriate PTH secretion Used to being in CRF o therefore gland doesn’t know what to do after transplant as Ca is normal! •
•
•
Nina Cooper
•
•
She has stones + groans + moans = hypercalcaemia Swelling in neck suggests a thyroid/parathyroid problem – it is hyperplasia
CRF Overview
Drugs contraindicated in renal failure Potassium sparing diuretics NSAIDs Gentamicin • • •
EMQ Lecture Notes
•
•
•
•
ACE-I to control BP and save renal function Statins and aspirin to reduce CVS risk Erythropoietin or iron supplementation for anaemia Avoid nephrotoxic drugs e.g. NSAIDs
Eventually Haemodialysis Peritoneal dialysis Transplant • • •
CRF • • •
GFR <60ml/min for >3 months 5 stages End stage is <15ml/min
• • • •
Case 1 •
Causes •
HAEMATURIA
HTN DIABETES GLOMERULONEPHRITIS Renal vascular disease Recurrent pyelonephritis
Symptoms and Signs Fatigue, anorexia, weakness Vomiting, metallic, pruritis (hyperuricaemia) Bone pain Dyspnoea, ankle swelling Pallor, easy bruising HTN (secondary to fluid retention + decreased renin) • •
•
Likely diagnosis Transitional cell carcinoma •
Case 2 • • •
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Investigations Urine dip: protein + blood Low Hb (normocytic normochromic anaemia – also seen in acute blood loss) Raised urea and creatinine Hypocalcaemia and Hyperphosphataemia o Secondary hyperparathyroidism Hyperkalaemia Usually small kidneys on USS – can be polycystic Renal osteodystrophy on DEXA scan • •
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Commonest pathogens E-coli Klebsiella Proteus • • •
Gut bacteria are mainly gram negative therefore abx that can be used are Nitrofurantoin Ciprofloxacin Augmentin = penicillin + clavulanic acid (B-lactamase inhibitor) Trimethoprim • • •
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Case 3 •
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23F Burning on passing urine Dipstick +ve for blood, leukocytes and nitrites
Best Treatment Nitrofurantoin
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Management Careful fluid balance Sodium restriction (K restriction if hyperkalaemia) Phosphate restriction Vitamin D and Ca supplementation
60M with a 40 pack year history Frank haematuria
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18 gap year student 4 week history of terminal haematuria Intermittent fevers and malaise Eosinophil markedly raised Returned from Malawi a month ago
Nina Cooper
EMQ Lecture Notes
Likely diagnosis Schistosomiasis Key is terminal = terminal = lower down in urinary tract (malaria causes haemolysis therefore blood would be present throughout)
Best way to confirm diagnosis Abdo ultrasound ultrasoun d (she has gallstones)
Schistosomiasis Lots of different species S. Haematobium causes urinary schisto (commonly in Africa and the Middle East) Transmission: drinking/swimming in water with schisto eggs Increased risk of squamous cell squamous cell carcinoma carcinoma of the bladder
Differential Diagnosis Bilirubinuria (in obstructive jaundice) Myoglobinuria Food e.g. beetroot Drugs e.g. rifampicin, nitrofurantoin Porphyria (urine darkens on standing)
Case 4
MIXED RENAL SBAs/EMQs
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RUQ pain Thinks passing blood in urine
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35 year old man comes to A&E with severe left flank pain Comes in waves
Most appropriate next step CT KUB •
Renal Colic Ask about Loin to groin pain o (writhing in agony!) Haematuria o o Frequency o Dysuria o Rigors o Fever o Hx of stones or recurrent UTIs Abx: nitrofurantoin, nitrofuranto in, ciprofloxacin, augmentin (if infection present) •
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Differentials for Renal Colic Biliary colic Pyelonephritis Acute pancreatitis pancrea titis Acute appendicitis appe ndicitis Dissecting aortic aneurysm Epidiymo-orchitis • • • • • •
Management Analgesia and an d anti-emetic anti-eme tic CT KUB If septic, consider surgical drainage • • •
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Case 1 • • • •
50M ITU admission Severe sepsis Develops acute RF
Indications for Dialysis in ARF Persistent Persistent hyperkalaemia Volume overload overlo ad refractory due to diuretics e.g. pulmonary oedema Severe metabolic acidosis Uraemic complications e.g. encephalopathy, pericarditis • •
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Urine Dipstick Testing False-negatives False-negatives for haematuria are rare, hence a dipstick that is negative for haem theoretically theoretically excludes haematuria Haematuria +ve test = haemoglobinuria, myoglobinuria, haematuria UTI +ve but –ve nitrate ! not all organisms have nitrate reductases OR the urine dwell time in the bladder is too short for conversion Dipstick insensitive to non-albumin protiens e.g. Bence-Jones proteins (seen in myelomas ! light chains) Glycosuria due to “renal glycosuria” can be due to genetic conditions, DM or pregnancy •
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Case 2
Case 5 •
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45F BMI 35
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Patient in ITU Granular muddy brown casts in urine
Nina Cooper
Acute Tubular Necrosis Most common cause of ARF in hospital 3 stages Initiation: Hypovolaemia, o myoglobinuria, toxins Maintenance: oliguria, o hyperkalaemia, fluid overload, increasing creatinine/BUN o Recovery: gradual increase in urine output leading to high-volume high-volume diuresis. Can get hypokalaemia and other electrolyte imbalances •
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EMQ Lecture Notes
Renal Arteriography Arteriography MRI/CT taken over EXCEPT in polyarteritis nodosa Multiple aneurysms and irregular constrictions in the alrger vessels with occlusion of the smaller penetrating arteries • • •
DMSA • •
MCUG • •
Urinary Casts Means it is a tubular problem Cylindrical structures formed in the tubular lumen therefore pathology is intrarenal Red blood cell casts Glomerulonephritis o White blood cell casts o Acute pyelonephritis pye lonephritis o Tubulointerstitial nephritis Granular casts o Acute tubular tubula r necrosis
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Radionuclear Looks for scars – therefore have to look 4-6months after atypical/recurrent UTIs
Micturating cystourethrogram Catheter administered contrast Can be used in paeds for vesicoureteral reflux and gynae for urodynamic studies
Case 4 • • •
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24 Severe gm-ve sepsis Becomes oliguric with rising urea and creatinine Difficulty hearing everyone
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Caused by gentamicin Kidney damage + hearing loss 8th CN damage ! irreversible hearing loss and vertigo Think of 2 boxers – punches kidneys first then your head off •
Case 3 •
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Paediatric FY1 writing discharge summary Young boy has just recovered from acute pyelonephritis
Scan he will need for follow up in 4-6 weeks = DMSA Scan Basic Genitourinary Imaging Plain abdo x-ray o Uric acid stones are radiolu radiolucent USS: UT obstruction, hydronephrosis, renal mass and PKD CT KUB: Gold standard for kidney stones MRI: Renal vein thrombosis, RCC, replacing renal angiography
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Chloramphenicol Not used in western world Causes anaemia, aplastic anaemia, aplastic anaemia and gray baby syndrome • •
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IV Urogram Kidney anatomy Detects renal stones US taking over • • •
Doxycycline Photosensitivity reactions Photosensitivity reactions GI upset Tooth discolouration • • •
Erythromycin GI discomfort Skin rashes • •
Imipenem GI upset Skin rash Seizures • • •
Nina Cooper
EMQ Lecture Notes
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Nephrotic vs. Nephritis Nephrotic Pro Proteinuria (>3.5g/24h) – (>3.5g/24h) – causes frothy urine Hypoalbuminaemia (<25g/L) Generalised oedema (perio (periorbital) Also risk of o Thromboembolism – renal vein thrombosis (loss of antithrombin and proteins C/S ! procoagulant) High infection risk (loss of o Ig) Hyperlipidaemia – liver o tries to produce more albumin and at same time pumps out lipids
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Alport’s Syndrome Syndr ome X-linked, type 4 collagen mutation – major structural structur al component in in kidneys, eyes, ears Haematuria, sensoorineural hearing loss, severe ocular abnormalities •
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Case 6 • • •
Nephritic Inflammatory process Haematuria (RBC casts) HTN Azotemia (high (hig h urea, high creatinine but no clinical symptoms)/oliguria Proteinuria <3.5g/day
Auditory nerve deafness, corneal dystrophy and ocular lens dislocation Urinalysis shows microscopic haematuria
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54M Haematuria Abdominal Abdomina l discomfort CT scan of the abdomen shows PKD and liver cysts
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Nephrotic Acute poststreptococcal glomerulonephritis
Both Diffuse prolipherative glomerulonephritis
Rapidly progressive glomerulonephritis Berger’s IgA glomerulonephropathy
Mebranoproliferative glomerulonephritis
Nephritic Focal segmental glomerulonephritis Membranous glomerulonephritis Minimal change disease
Autosomal Dominant Domina nt PKD Adult Adult (a (autosomal dominant) Multiple, large, bilateral cysts gradually destroying kidneys Presents with progressive UTIs, haematuria, HTN, flank pain Muts in PKD1/2 Associated with polycystic kidney kid ney disease, berry aneurysms and mitral valve prolapse • •
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Autosomal Recessive Recessiv e PKD Can cause RF in utero Potter’s syndrome Neonatal period ! HTN, portal HTN and progressive renal failure Associated with congenital hepatic he patic fibrosis • •
Amyloidosis Alport syndrome Diabetic glomerulonephropathy
Membranous GN - most common cause of nephrotic syndrome nephrotic syndrome in adults
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Case 7 •
Minimal change disease – most common in children Berger’s – most common cause of acute GN worldwide
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Case 5 • •
12M FHx renal disease – males more than females
13F, Caucasian Discoloured urine 3 weeks earlier had facial impetigo that was treated Urinalysis shows haematuria, mild proteinuria and occasional RBC casts
Post-streptococcal GN Discoloured urine 3 weeks ago – typical presents 1-4 weeks later • •
Nina Cooper
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Facial impetigo/URTI infection ! both caused by staph RBC cast = nephritic syndrome Immune complexes deposit in glomeruli Frequently seen in children Resolves spontaneously
EMQ Lecture Notes
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Renal biopsy was taken ! podocyte infusion on EM
Minimal Change Glomerulonephritis Usually post URTI but can be caused by immunisation and allergy Light micros = normal EM = podocyte fusion Responds to corticosteroids Most common cause of GN in children •
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Berger’s (IgA Nephropathy) Acute gastroenteritis or URTI Usually 1-3 days after start of infection IgA deposits in mesangium causing micro/macroscopic haematuria Resolves within 2-3days and usually benign 30% can progress to ESRF over 20 years • •
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Case 10 20F Butterfly rash Puffiness around eyes, mouth and ankles HTN Blood/protein in urine • • •
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Case 8 • • •
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26M Haemoptysis Condition worsens ! few weeks later has renal failure Significant haematuria and HTN Renal biopsy shows linear immunofluorescence
Goodpasteure’s Syndrome Middle aged, haemoptysis, linear immunofluorescence Antibodies formed against alveolar and glomerular basement membrane (type 4) Whole of glomerular membrane is destroyed ! linear pattern •
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Lupus Nephritis Primary = involves only glomeruli Secondary = involves glomeruli and other organs Immune complexes circulate in blood and deposit in glomeruli – causes an inflammatory process Spectrum from nephrotic ! nephritic ! RF • •
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Case 11 58M Obese Blood in urine Abdo CT shows right sided renal mass Biopsy ! rounded and polyglonal cells with abundant clear cytoplasm • • • •
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Wegener’s Granulomatosis (Granulomatosis with polyangitis) Small vessel vasculitis (c-ANCA +ve) URTI – nasal septum perf, chronic sinusitis, mastoiditis Renal: haematuria, red cell casts LRTI – haemoptysis •
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Grawitz Tumour Man + old + obese = risk for renal cell carcinoma RCC also known as clear cell carcinoma and grawitz tumour Clear cell = loads of fat ! look like yellow/gold upon excision 70-90% renal tumours, mean age 55 Arises from renal tubule epithelium Other RF = von-Hippel Lindau and smoking Metastasise to lung and bone •
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Case 9 •
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7M, Caucasian Stung by bee 2 weeks ago Generalised urticarial Required hospitalisation Later developed a puffy face and now reports foamy urine
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Nina Cooper
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Haematuria + abdo (flank) pain + renal mass
EMQ Lecture Notes
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Case 12 76M Progressive lower back pain for 2 months Nagging and constant pain – not relieved by rest/position change Urinary urgency, notcutria, frequency and hesistancy
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Painless haematuria (NO casts) Recurrent UTIs Voiding irritability Pee SAC Phenacetin o Smoking o o Aniline dies o Cyclophosphamide
Squamous Cell Carcinoma 10% cancers Associated with chronic inflammation/irritation Developed = long term catheters Developing = schistosomiasis • •
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Prostatic Carcinoma Mets to bone ! pain Adenocarcinoma 80% peripheral zone presents as above with weight loss, bone pain, raised ALP = mets DRE = craggy, nodular, loss midline sulcus BPH: hyperplasia of transitional zoneincreases over time naturally Irritative symptoms = nocturia, frequency Obstructive symptoms = poor stream, hesitancy, dribbling, terminal haematuria, overflow incontinence, UTIs
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Case 13 3 year old Large abdo mass and haematuria
ACUTE RENAL FAILURE Pre Renal Renal Hypoperfusion
Renal Glomerular disease
Post-Renal Obstruction
Calculus Volume depletion Oedematous states
Tubular injury e.g. ATN
Enlarged prostate
Vasculitis Bladder tumour
Hypotension Cardiovascular
Acute interstitial diseases e.g. NSAIDs
Blood clot Urethral stricture – normally due to cystoscope
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Wilm’s Tumour Commonest intra-abdo tumour <10yrs Peak 2-4 years Presentation = large flank mass +/- haematuria Nephroblastoma (mesoderm: kidney, fat, bone) Rapidly growing •
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Case 14 62M Used to work in rubber industry Recurrent UTIs and painly haematuria • •
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Transitional Cell Carcinoma M:F 4:1 Peak 60-70 • •
Case 1 • • • • • •
90F Complains of back pain GP prescribes diclofenac 5 days later ! A&E Generally unwell and confused In ARF
Intersitial Renal Failure NSAIDs Diclofenac – strong NSAID usually prescribed for renal colic and muscular pain Inhibits prostaglandins – required to maintain renal perfusion pressure Analgesic nephropathy ! more long term, aspirin/paracetamol, renal scarring • •
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Case 2 • •
12M D&V
Nina Cooper
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Urea 23.1, creatine 220, K 5.7, Na 134 Stool sample shows E. Coli O157
EMQ Lecture Notes
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CT shows no visible damage to kidneys
Hypovolaemia Causes pre-renal failure •
Haemolytic uraemic syndrome ARF Microangiopathic haemolytic anaemia Thrombocytopenia Nephrotoxins ! RBC and platelet destruction Supportive treatment: ? temporary dialysis •
RENAL INVESTIGATIONS
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Case 1
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Case 3 • • •
68M History of IHD Generally unwell after “new tablet” from GP for HTN
Pre-renal Failure Renal artery stenosis Block ACE ! reduced Ang-II ! effert arterioles cannot constrict ! decrease GFR ! ARF ACEi and ARBs are contraindicated in patients with RAS Doppler US – check for RAS Gold-standard = angiography • •
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Renal Colic CT KUB = first investigation Loin ! groin pain Vomiting, pallor, sweating, fever, haematuria 90% radiopaque Key sites: renal pelvis, PUJ, VUJ Cannot see urate/xanthine stones Give diclofenac analgesia Associated with zidovudine and other HIV meds Treatment o Hydration o NSAIDs o If large ! shockwaves, surgery • • •
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Case 4 •
70M A&E ! confusion and abdo pain Large suprapubic mass Urea 16 Creatinine 130
Case 2 •
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Post-renal failure Prostatic hypertrophy Leads to urinary retention High pressure in renal pelvis ! decline in renal function Treat: urinary catheter •
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30M Ambulance after motorcycle accident Large blood loss Urea 20 Creatinine 220 K 5.7 Na 138
34F 2 day hx pain passing urine, frequency and offensive smell +ve nitrates and leukocytes + Blood, + protein
UTI •
Case 5 •
25M Severe flank pain and vomiting 4 episodes today Pale, sweaty and tender in right loin Urine dipstick o +++ Blood o + Protein o No nitrites/leukocytes
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MSU – MC&S First line ! dipstick Before starting abx, send of MSU then start broad-spectrums Once sensitivities are known, adjust abx therapy
Case 3 • •
16M Renal transplant
Nina Cooper
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Decline in renal function over 2 weeks Pain around transplant site US shows no significant abnormalities
Transplant Rejection US guided renal biopsy Used for diagnosis and severity Acute = steroids, chronic = re-list for transplantation • • •
Case 4 • • • •
2M Recurrent UTIs Failing to thrive Strong FHx for vesico-ureteric reflux
Vesicoureteric Reflux UTI in kids Urine enters ureters and renal pelvis during micturition Leads to renal scarring and failure First to USS Also DMSA scan and micturating cysturethrogram • •
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Case 5 •
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27M, Indian 8 week history of weight loss, night sweats, loin pain and dysuria Urine dip shows blood and leucocytes Urine sample shows “no growth”
TB •
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Three early morning urine samples for MC&S and Ziehl Neelson staining Sterile pyuria – always renal TB See leucocytes with negative culture Non-specific symptoms may resemble UTI Positive mantoux
EMQ Lecture Notes
Nina Cooper
EMQ Lecture Notes
Haematology & Rheumatology RHEUMATOLOGY Sjogren’s Syndrome Schirmer’s test – filter paper left for 5 minutes, dry if got sjogren’s Xerophthalmia (dry eyes, conjunctivitis – sand in my eyes) Arthritis Xerostomia (dry mouth, dysphagia) •
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Temporal Arteritis Jaw claudication Unilateral headache Irreversible blindness due to retinal artery occlusion Treat with steroids • • •
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Scleroderma CREST syndrome Calcinosis – calcium deposits in skin Raynaud’s Esophageal dysfunction Sclerodactylyl – thickening and tightening of the skin on fingers and hands Telangiectasia – red marks on skin surface • •
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Osteoarthritis Heberden’s and bouchard’s B – Below – Bouchard’s • •
Dermatomyositis Heliotrope rash Gottren’s papules Autoimmune – combining inflammatory myopathy and cutaneous involvement Myopathy ! prox muscle weakness >50 years old = cancer CK elevated • • •
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Rheumatoid Arthritis Swan neck and boutonniere deformities Z-thumb Dorsal interossei wasting Joint subluxation Rheumatoid nodules Ulnar deviation •
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Nina Cooper
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Scars Prominent ulnar styloid
EMQ Lecture Notes
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Nails of hand are pitted and lifted of skin at distal edges Scaly rash
Psoriatic Arthritis Asymmetric and patchy involvement DIP involvement Dactylitis (sausage fingers) 5% of those with psoriasis •
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Tophaceous Gout Multiple large tophi affecting the wrists and several finger joints •
Case 3: 31M Red/itchy eyes for 8 hours Pain on urination and diffuse joint pain for one month Negative test for gonorrhoea/chlamydia Negative for rheumatoid factor but HLA-B27 positive Diarrhoea 2/12 ago • • •
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Reiter’s Syndrome
Case 4: 27M 6/12 hx of lower back pain Stiffness wakes him up in the night Worse in morning Severe lumbar spine limitation Negative for ANA/RF but HLA B27 positive •
MISC. RHEUM
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Case 1: 75 woman Sudden onset pain in right knee Red, swollen and painful Temp = 38.6 • • • •
Gout • • •
Needle shaped Negatively birefringent X-ray finding shows chrondrocalcinosis
Acute Hot Swollen Joint Trauma, septic arthritis and crystal arthropathy (gout/pseudogout) Septic: may see pus, culture s.aureus/streptococcus/gonorrhea Pseudogout = positive biregringent, rhomboid shaped weakly •
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Ankylosing Spondylitis Disease of spine and sacroiliac joints Fusion of joints = bamboo spine Extra articular features = 5 A’s o Anterior uveitis o Achilles tendonitis o Apical lung fibrosis Aortic incompetence o Amyloidosis in kidneys o •
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Seronegative Spondyoarthropathies Arthritis without RF Strongly associated with HLA-B27 More common in men Enteropathic Arthritis Crohn’s and UC o Reactive Arthritis After acute GI/chlamydia o CAN’T SEE: Conjunctivitis o and anterior uveitis • • •
Case 2: 56f Pain in hands and swelling of fingers Mainly in DIPs • •
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Nina Cooper
EMQ Lecture Notes
o o
CAN’T PEE: urethritis CAN’T CLIMB A TREE: arthritis
HAEMOLYTIC ANAEMIA •
= Premature RBC haemolysis Normal RBC lifespan = 120 days Classification = intrinsic or extrinsic Intrinsic = RBC problem o ! Hereditary spherocytosis ! PK/G6PD deficiency ! HbC ! SCA ! Paroxysmal nocturnal haemoglobinuria Extrinsic o ! Autoimmune ! MIHA (microangiopathic) ! MAHA (macroangiopathic haemolytic anaemia) ! Infection (malaria) Confirming haemolysis LOW Hb o Unconjugated bilirubin is o HIGH Urine urobilinogen is HIGH o o LDH – HIGH (found in RBCs) o Blood film – typical signs for each o Haptolobin LOW if intravascular– mops up free Hb •
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Case 2: Child admitted with septicaemia Platelets 30, APTT 60s, PT 20s and low fibrinogen • •
DIC •
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Case 1: 7F Nigeria Screaming that bones in hand/leg are excruitatingly painful Hb = 90
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Sickle Cell Anaemia • • •
Abnormality in B-globin chain Glu" Val at position 6 Causes of sickling o Hypoxic conditions – Hb stick together in RBC = high altitude, anaesthesia
and excessive exercise o Dehydration – increased MCHC, increased chance of sickling Infection and inflammation o Trait: symptoms only in extreme hypoxia Diagnosis: electrophoresis and neonatal screening
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Microangiopathic Haemolytic Anaemia o Thrombocytic thrombocytopenia purpura (TTP) Haemolytic uraemic o syndrome DIC o DIC Widespread activation of o coagulation system Common in obstetric o complication o Septicaemias o Cancers (pancreatic carcinomas or AML) TTP o Widespread activation of platelets o Genetic o Autoimmune process o Pentagon: CNS abnormalities ! Fever ! ! Renal pathology Thrombocytopenia ! ! MIHA HUS Widespread activation of o platelets o E-coli infection TTP vs. HUS : both thrombocytopenia but HUS more renal and not CNS DIC vs. TTP/HUS: doesn’t have thrombocytopenia but raised DDimers
Nina Cooper
Case 3: 24 teacher Atypical pneumonia Yellow sclera Patient has a positive coomb’s test
EMQ Lecture Notes
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FBC shows mild anaemia Osmotic fragility test positive Negative Coombs test
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Hereditary Spherocytosis 1/5000 North Europeans Autosomal dominant Weak scaffolding in RBC membrane structure – membrane gets damaged causing a spherical RBC Gets stuck in spleen Osmotic fragility: hypertonic solution, water should move into RBC ! no extra membrane, cannot expand • •
Autoimmune Haemolytic Anaemia Coombs test: binds to autoantibodies for RBCs Myocoplasma pneumonia ! cold agglutinin haemolytic anaemia >50% of patients with mycoplasmic pneumonia develop cold agglutinin HA •
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LEUKAEMIA AND LYMPHOMA Case 1: 5 year old boy Seizures and lymphadenopathy Investigations reveal pancytopenia (everything down in bloods) • • •
Case 4: 28 Mediterranean couple Honeymoon to Namibia Husband becomes unwell Blood film shows bite cells and Heinz bodies • • • •
G6PD Deficiency 5-7% worlds population Mediterranean and African populations X linked recessive Pathology: hexomonophosphate shunt pathways, no production of NADPH, no free radicals mopped up but GSH, therefore damage to RBCs from free radicals (oxidative attack and haemolysis) Oxidative crisis: infection, drugs (primaquine, quinine), fava beans Symptoms usually 2-3 days following oxidative stress and self limiting Heinz bodies: identified with a supra vital stain Bite cells: due to macrophage removal of membrane • •
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ALL
Case 2: 40M Severe haemorrhage Blood films shows schistocytes (broken down RBCs) • • •
APML
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Case 3: 72M Weight loss, fever and night sweats Symptoms get better with Imatinib • •
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CML
Case 4: 16F Afro-Caribbean Mass on jaw Starry sky appearance on jaw • • • •
Case 5: Northern European boy Enlarged spleen • •
Burkitt’s Lymphoma
Nina Cooper
Case 5: 51m Pain on drinking alcohol Reed Sternberg Cells Haematology starts him on radiotherapy in combination with ABVD
EMQ Lecture Notes
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Nodular Sclerosing Hodgkin’s Lymphoma
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BLOOD CELL LINEAGE
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GOLD STANDARD – BM aspirate, 20% blasts Investigations FBC: pancytopenia, o increase in WCC Definitive diagnosis if o >20% blasts in BM aspirate (Jamshidi needle, PSIS) Management o Supportive: blood products, broad spec abx, co-trimoxazole, hydration, allopurinol, rasburicase WBC >200 ! o hyperviscosity, leukophoresis o Renal failure ! dialysis Treatment o Systemic chemotherapy o In AML, give for 3 years as have to target BBB/testes Stem cell transplant o
AML • • •
Should have no blasts on films – live in BM LEUKAEMIAS Progeny of single transformed cells Acute lymphoblastic leukaemia Acute myeloid leukaemia Chronic myeloid leukaemia Men > Women L comes before M in alphabet, AML can be a form of CML Therefore age of presentation o Kids for ALL AML and CML in older o patients
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ALL • • • •
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Increased risk in Down’s More common in age 1-3 80% 5 year survival if young Presentation: B SYMPTOMS, anaemia, lymphadenopathy, bone pain, easy bruising, multiple infections CNS involvement: headache, vomiting, meningism, cranial nerve palsy Testes in Boys
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Mean age 60-70 (OLD PEOPLE) Tranlocation of t(8,21) Acute promyelocytic leukaemia = subtype of AML, medical emergency as high risk of bleeding and DIC, septic shock and hyperviscosity syndrome Presentation: older men, short presentation of B symptoms, anaemia, easy bruising, multiple infections Investigations o Pancytopenia (aleukaemic leukaemia) o Auer rods and lysine acetylation (APML = GIANT CELLS, schistocytes) Definitive diagnosis = o >20% BM cells in aspirate Immunophenotyping/cytog o enic analysis for risk stratification o Myeloperoxidase, sudan black B, non specific esterase APML ! give ATRA (or arsenic trioxide), only 30% cure AML ! supportive therapy, systemic chemotherapy via central venous catheter
Nina Cooper
CML •
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Philadelphia chromosome t(9,22) ! BCR-ABL fusion protein leading to increased tyrosine kinase activation In old people Precursor to AML Presentation: old man with incidental finding or long presentation of B symptoms Splenomegaly, bruising and bleeding, gout, hyperviscosity, retinal haemorrhage Bi/triphasic disease o Chronic (5% blast cells) o Acceleration (10-19%) o Blast crisis (20% - Auer rods) Investigations o FBC ! anaemia of chronic disease, increased WCC Blood film shows o increasing blast cells FISH analysis – checks for o fusion genes Management o Imatinib if Philadelphia chromosome positive and in chronic phase – inhibits tyrosine kinase Blast crisis ! allogenic o SCT Still refractory: donor o lymphocyte fusion
EMQ Lecture Notes
80% non-Hodgkins, 20% Hodgkins More lazy the lymphoma, the worse the prognosis •
Hodgkins One site of swollen lymph nodes Spreads adjacently Male > female Bimodal distribution ! classical 20s, nodular lymphocyte predominant in 50s Classical: nodular o sclerosing (related to EBV) Lymphocyte depleted – o bad prognosis Present with B symptoms, rubbery neck node, pain on drinking alcohol and tobacco intolerance Nodular Sclerosing: Reed Sternberg/Hodgkin cells, Owl’s eyes inclusions Lymphocyte Predominant: L and H cells, can return as B cell lymphoma Staging: 1-4, A/B with PET o 1 = lone LN o 2 = spread to neighbour LN o 3 = spread below diaphragm o 4 = extends beyond LNs Manage with ABVD and extensive radiotherapy • • • •
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Non-Hodgkin’s Lymphoma Can be a B cell or T Cell Divided into low grade and high grade High grade = good prognosis due to fast dividing rate, can be targeted B cells are CD3 negative, T cells are CD3 positive •
LYMPHOMA Cancer of the lymph nodes – controlled degree of genomic instavility accentuated by Inherited Viral; EBC, HTLV Enviromntal; mutagens and chronic immune stimulation Iatrogenic; radiotherapy, chemotherapy Immunosuppression • • •
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B Cell Lymphoma: LOW GRADE CLL: chronic lymphocytic leukaemia (actually a lymphoma!) o Occurs in elderly “Fragile” o o Smudge/smear cells under microscopy Treatment: GO-GO o (rituximab), SLOW-GO, NO-GO (supportive treatment, chlorambucil) •
Nina Cooper
EMQ Lecture Notes
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Has CD5+ve marker as so premature
MALT Chronic antigen stimulation e.g. chronic h. pylori infection Associated with Sjogren’s o and thyroiditis o Only lymphoma that can be treated without chemo o Give triple therapy: PPI and 2 x abx Mantle Zone Lymphoma o Males Affects GI tract o Cyclin D1 + CD5+ve o o
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B Cell Lymphoma: HIGH GRADE Diffuse large B Cell lymphoma Burkitt’s Lymphoma o Mass in jaw o Associated with EBV o Give R-CHOP • •
T Cell Lymphoma CD3 +ve Large numbers of aggressive T Cells Enteropathy associated: Crohn’s • •
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Nina Cooper
Haematology
Year 3 Notes
Overview
ANAEMIA = LOW concentration of haemoglobin Normal for ! = 110-140, " = 130-150 Indication for transfusion if symptomatic and <80 •
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Symptoms Tiredness SOB •
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Examination Conjunctival pallow Tachycardia – hyperdynamic state causing flow murmur • •
Classification: via MCV Normal = 80-100 Microcytic = <80 Macrocytic = >80
Major: require lifelong blood transusions o Intermedia: nontransfusion dependent Only cure = BM transplant and cord blood transplantations Chronic blood transfusions ! iron overload Manage with iron chelation (desferioxamine) Signs o Hepatosplenomegaly o Extramedullary erythropoiesis ! jaw protrusion abd big forehead Hair-on-end XR o appearance o
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Microcytic Anaemia IRON DEFICIENCY Dietary ! vegetarian/vegan Increased loss Crohn’s/Coeliac/Short o bowel syndrome ! Malabsorption Loss in bowel e.g. o bleeding o Menstruation Treat with ferrous sulphate/fumarate – will see darkened stool and causes constipation
Macrocytic Anaemia B12/FOLATE DEFICIENCY Lack in diet Lack absorption • •
• •
•
HERIDITARY: Thalassaemia Seen in mediterraneans ! /" types o 4! alleles and 2" alleles Alpha – severity depends on number of genes mutated One gene = no effect o Two genes = symptoms o of mild anaemia = alpha thalassaemia trait o Three genes = HbH disease – require lifelong chronic blood tranfusions o Four genes = death in utero Beta • •
•
•
B12/Folate Required for purine synthesis, which is key for RBC production Therefore abnormal RBCs are produced Need to check for coeliac in young – check for anti-endomysial antibodies •
•
•
Pernicious Anaemia Lack of intrinsic factor – binds to B12/folate Can be due to antibody against parietal cells (which produce IF) or antibody directly against IF itself Nb. Absorption occurs in the ileum Use schilling test to diagnose pernicious anaemia Give vitamin B12 to o saturate stores Radiolabelled vitamin B12 o given alone, if this is low in the urine then there is a malabsorptive problem o Radiolabelled IF/Vit B12 are given ! if the urine level increases then there •
•
• •
Nina Cooper
Year 3 Notes
is a lack of IF and so it must be replaced
Other Causes Alcohol •
Simple = macrocytic Can develop into megaloblastic Hypothyroidism Liver disease Drugs o Methoxtrxate Phenytoin o Leads to functional folate o deficiency o o
• • •
Megaloblastic Anaemia Large erythroblasts with immature nuclei in BM Hypersegmented neutrophils
X-linked recessive – seen in men more o Cannot protect cell from reactive oxidative species Triggered by o Moth balls " " Fava beans " Nitrofurantoin " Anti-malarials " Infection G6PD Deficiency o RBC haemolysis o G6PD = protective against oxidative stress Occurs after exposure to o dapsone/antimalarials Denatured Hb ! HEINZ o BODIES o
•
•
•
ACQUIRED Autoimmune Haemolytic Anaemia Use Coomb’s Test/DAT Check for RBC antibodies Cold-activated = mycoplasma infection Warm-activated = lymphoproliferativedisease e.g. CML/lymphoma + SLE Paroxysmal cold haemoglobinuria = Donalth-Landsteiner Test Paroxysmal Noctural haemoglobinuria = Ham’s Test •
Haemolytic Anaemia Same symptoms + signs as usual anaemia PLUS Jaundice (prehepatic) due to increased unconjugated bilirubin Can be intravascular or extravascular •
•
•
Causes of Haemolytic Anaemia SICKLE CELL HbS o Typically African/Afroo Caribbean child Trait ! few symptoms, o only at altitude or extreme hypoxia o Risk with parvovirus: RBCs have a shorter lifespan in SSA, and you cannot synthesize enough RBCs quickly enough to recover ! manage with abx, transfusion, oxygen and analgesia o Deep seated bony pain = BM infarction o Give SC morphine HEREDITARY SPHEROCYTOSIS o Mutation in spectrin ! spherical RBCs Buzzword = osmotic o fragility test ENZYMATIC DEFICIENCY o E.g. G6PD •
•
•
• •
•
•
•
Non-autoimmune = Microangiopathic Haemolytic Anaemia Diseases of small BVs ! haemolysis HUS: Haemolytic Uraemic Syndrome o E-coli ! blood cell haemolysis TTP: thrombotic thrombocytopenic purpura Clots and low platelets o Rash o Affects brain o DIC: disseminated intravascular coagulation o Septic/post-natal/vascular insult o Low platelets Pro and anti thrombotic o state Low fibrinogen and clots o Manage with fluids, O2, o abx and stop the bleeding •
•
•
•
Nina Cooper
Year 3 Notes
Metal Heart Valve RBCs hit metal and get fragmented Causes haemolytic anaemia
Essential thrombocythaemia Platelets >600 Usually old/middle-aged patients Increased clot risk
Normocytic Anaemia Chronic disease Liver disease Blood loss (acute)
LEUKAEMIA
•
•
•
• • •
• •
ALL: Acute Lymphocytic Leukaemia Commonest cancer of childhood Assoc. with Down’s Syndrome AML <3 + downs ALL >3 + downs •
Anaemia of Chronic Disease Rheumatoid arthritis ! can get folate/B12 deficiency secondary to methotrexate use Cancer Chronic inflammation Vague symptoms •
• • •
• • •
Presentation Enlarged LNs Hepatosplenomegaly Prone to infections Low platelets = bleed Low RBCs = anaemic • • •
Aplastic Anaemia Pancytopenia Hypocellular BM Absent reticulocytes •
• •
• •
MYELOPROLIFERATIVE DISORDERS Polycythaemia Rubra Vera Myeloproliferative disorder V167F mutation in JAK2 kinase causes uncontrolled stem cell proliferation, usually of the RBC line Present with headaches, dizziness and stroke Hyper mast cell degranulation can cause severe pruritis, characteristically after hot baths/showers (aquagenic) and peptic ulcers Patients may also present with gout due to elevated cell turnover, splenomegaly and plethora • •
•
•
•
Blood Film: Blast cells Treat with chemotherapy and BM transplant AML: Acute Myeloid Leukaemia More common in adults Although also seen in those under 3 with down’s Auer rods seen on film Subtype: acute promyelocytic anaemic (APML) RARA-PML is a fusion o protein o Treat with transretenoic acid (vitamin A) • •
• •
CLL: chronic lymphocytic leukaemia More likely to die with than from Normally incidental finding Chronically raised WBC count Smear cells seen on film • • • •
Secondary Polycythaemia Condition causing excessive RBC production COPD ! chronic low levels of oxygen EPO-secreting tumour
CML: chronic myeloid leukaemia Seen in those aged 25-40 years Due to Philadelphia chromosome = BCR-ABL mutation (9,22) Treat with imatinib
Idiopathic Erythrocytosis Isolated erythrocytosis with no change in WVC or platelets High risk of AML progression
LYMPHOMA
•
•
•
•
•
• •
•
Either Hodgkin’s or Non-Hodgkin’s Hodgkin’s Lymphoma Reed-Sternberg /owl-shaped cells seen •
Nina Cooper
• • • • • • • •
Continuous spread Painful LNs after ethanol Lymphadenopathy Hepatosplenomegaly Infection Bleeding Anaemia Treat with ABVD chemotherapy
Non-Hodgkin’s Non-continuous spread Burkitt’s lymphoma Black people o Mass on jaw o Fast growing and o disfiguring Treat with R-CHOP chemotherapy
Year 3 Notes
•
•
• •
•
<1 = greater chance of clot o >1 = greater chance of bleeding Aim for 2-3 in most patients, but for 3-4 in metallic heart valve If INR is too high, give vitamin K INR>6: ?bleeding o ! Yes: IV vitamin K + FFP ! No: Oral vitamin K Monitors EXTRINSIC pathway (a pEt) o
•
For PE/DVT X1, known cause " 3 months warfarin X1, unknown cause " 6 months Recurrent " 1 year then review •
•
Different Subtypes and Management Use B staging A = no sweats, weight loss of fevers B = B symptoms o FLAWS o Fever, Lethargy, Appetite Loss, Weight Loss, Sweating
•
• •
Heparin •
•
MYELOMA • • • • •
Cancer of plasma cells in BM Lack of antibody production Unexplained backache Pathological fractures Recurrent bacterial infections
• •
Protamine sulfate = reverser of unfractionated heparin Nothing easily reverse LMWH Monitor w APTT = INTRINSIC (apInt)
Haemophilia X-linked, only seen in males A: factor 8 (stabilizes vWF, therefore loss " decreased vWF) B: factor 9 (AKA Christmas Disease) Causes hypocoagulable state • •
•
•
COAGULATION
Warfarin Inhibits vitamin K Blocks clotting factors II, VII, IX, X and C&S C/S are anticoagulant and get blocked quicker than the clotting factors, so you initially get a hypercoagulable state Give LMWH with warfarin to prevent clots, until INR is in target range Given for PE/DVT, AF, metallic heart valve • •
Von Willebrand Disease Males and females VWF starts the coagulation cascade Causes excessive bleeding • •
•
•
•
•
Vitamin K Deficiency Seen in liver disease Vitamins ADEK are fat soluble Therefore seen in pancreatitis and biliary tree problems too • • •
Low platelets and clotting factors leads to an increased of bleeding Low platelets Fine bleeding o Gums/mucosa o Petechiae o Low CFs o Haemarthroses o Delayed bleeding •
INR Targets PT is affected by warfarin INR shows how the clotting of a patient compares to someone else in their age group (i.e. is a ratio) o 1 = normal • •
•
Nina Cooper
•
Protein C/S deficiency
Essential Thrombocythaemia Clonal proliferation of megakaryocytes Epistaxis (nosebleeds) Bleeding from gums and GIT Picture of thrombosis and bleeding •
• • •
Idiopathic Thrombocytopenic Purpura (ITP) Platelet dysfunction Menorrhagia + epistaxis + purpura Antibody of platelet leads to removal by reticuloendothelial system, reducing platelet lifespan to just a few hours • •
•
Year 3 Notes
Disorder
INR
APTT
Thrombin Time
Platelet Count
Bleeding Time
!
!!
!!
N
N
!!
!!
!!
"
!
Liver Disease
!
!
N/!
N/ "
N/!
Platelet Defect
N
N
N
N
!(!)
!!
!
N
N
N
N
!!
N
N
N
N
!!
N
N
!(!)
Heparin DIC
Vitamin K Deficiency
Haemophilia Von Willebrand’s
Notes
! AST
HYPOCOAGULABLE Name
Description
HYPERCOAGULABLE Features
PLATELET DISORDERS: low platelets fine bleeding from gums/mucosa, petechiae Aplastic anaemia, megaloblastic anaemia, marrow Decreased BM infiltration (leukaemia/myeloma), marrow production of suppression e.g. cytotoxic drugs, radiotherapy platelets Clonal proliferation of Epistaxis (nosebleeds) Essential megakaryocytes Bleeding from gums Thrombocytaemia and GIT Picture of thrombosis and bleeding ITP Idiopathic Thrombocytopenic Purpura
HUS Haemolytic Uraemic Syndrome
Platelet dysfunction: Antibody to platelet leads to removal by reticuloendothelial system, reducing platelet lifespan to just a few hours Initially endothelial damage triggers thrombosis, platelet consumption and fibrin strand deposition, mainly in the renal vasculature. This leads to decreased platelets and increased bleeding risk.
Menorrhagia Epistaxis Purpura ! megakaryocytes in bM
Abdominal pain Bloody diarrhoea ARF
Name
Description
Features
CONGENITAL
Factor Von Leiden
Mutation of factor V ! resistance to protein C
Increased risk of DVT 5% Caucasians – suspect if <45 Increased risk of VTE
Protein C Deficiency
Congenital absence of Protein C
Protein S Deficiency
Vitamin K-dependent anticoagulant, causing activation of factor V and VIII
DVT DIC PE
Blood Group O
Lower levels of factor VII and VWF naturally
4x increased risk
Bernard Soulier Syndrome
Glycoprotein Ib deficiency = receptor for VWF
Glanzmann’s Thrombaesthenia
Glyocoprotein IIb/IIIa deficiency = receptor for fibrinogen
CLOTTING FACTOR DISORDERS: Low CFs haemarthroses and delayed bleeding Haemophilia A: factor 8 (Stabilises VWF) B: factor 9 (Christmas disease) Liver Disease Decreased clotting factor production Decreased absorption of vitamin K Abnormalities of platelet function Malabsorption Vitamin K deficiency ! reduced synthesis of factors II, VII, IX, X
Von Willebrand Disease
VWF starts clotting cascade ! absence leads to hypocoagulable state
Bleeding gums Menorrhagia Epistaxis ! Bleeding time Bleeding gums/GIT Menorrhagia Epistaxis ! Bleeding time ACQUIRED
X-linked Males only Crippling arthropathy Haemathroses Alcoholic/chronic liver disease patient Bleed a lot
Have a malabsorptive picture + hypocoagulable state Treat with FFP/vit K Vitamins ADEK are fat soluble, therefore also see if have pancreatitis or a biliary tree problem Males and females Normal PT + platelets Abnormal PTT Abnormal bleeding time
Disease
Antiphospholipi d Syndrome
Malignancy, sickle cell anaemia, nephortic syndrome, polycythaemia vera, essential thrombocytosis Autoimmune hypercoagulable state caused by antiphospholipid antibodies
Iatrogenic
OCP use
Other
Obesity
Arterial and venous thrombosis Multiple miscarriage
Year 3 EMQ Notes
Haematology
Nina Cooper
LEUKAEMIA, LYMPHOMA & MYELOMA Name Myeloma
B Cell Lymphoma
Description Myeloma = Cancer of the bone marrow Affects the plasma cells – (antibody producing cells) Non-Hodgkin’s
Seen in older people
Hodgkin’s Lymphoma
T Cell Lymphoma
Reed-Sternberg Cell (special type of B cell) Continuous LN spread
Non-Hodgkin’s
Symp toms Unexplained backache Pathological fractures Recurrent bacterial infections
Malaise Widespread, intractable itch Appetite loss Weight loss Lethargic, low mood Fevers Night sweats Enlarged, rubbery LN Pain in LN after drinking Hepatomegaly/splenomegaly Infection Bleeding Anaemia Fatigue Weight loss Night sweat
Di agnostics Bone Marrow Aspirate showing increased plasma cells Ig profile Biopsy LN
Owl-shaped cells (ReedSternberg Cells)
Lymphoblastic change Invades CNS
Treatment Chemotherapy with autologous stem cell transplantation
R-CHOP
ABVD chemotherapy
Remission induction with chemotherapy Consolidation: Maintenance by clearing CNS of residual cells Stem cell transplant
Can causes rashes/lumps if cutaneous TCL Can also be caused by NK cells Chronic Myeloid Leukaemia
Philadelphia chromosome (9,22) translocation = BCR ABL
Insidious onset Aged 25-40 years
Hypercellular BM Cytogenetic testing
Imatinib
Year 3 EMQ Notes
Chronic lymphocytic leukaemia
Haematology
Seen in elderly More likely to die with than from
Acute Myeloid Le ukaemia Adults Seen in <3s with Down’s APML = subtype, treat with vitamin A (transretinoic acid) RARA-PML fusion protein Acute Lymphocytic Leukaemia
Cancer of childhood Associated with Down’s
Often asymptomatic
Nina Cooper
Chronically raised WCC Smear cells seen
Depends on stage If asymptomatic, don’t treat
General weakness Fatigue Weight loss Blood in urine/stools Bruising easily Hepato/splenomegaly Enlarged LNs Hepatosplenomegaly Prone to infections Low platelets = bleed Low RBCs = anaemic
Auer Rods
Blast Cells
Can treat with chemo Chemotherapy Radiotherapy Radiotherapy BM transplant
Chemo BM transplant
Year 3 EMQ Notes
Nina Cooper
CLINICAL HAEMATOLOGY Blood Film Sign
Cause
Sickle Cells
Sickle Cell Anaemia
Spherocytes
Hereditary Spherocytosis
Dacrocytes
Myelofibrosis
Target Cells
Obstructive jaundice Liver disease Haemoglobinopathies Hyposplenism
Rounded Macrocytes
Alcoholic liver disease
Oval Macrocytes
Vitamin B12/folate deficiency
Polychromatic Macrocytes
Young RBCs
Irregularly Contracted Cells
Oxidant damage
Elliptocytes
Hereditary
Pencil Cells
Iron Deficiency (elliptocytes)
Fragments
Mechanical stress
Rouleaux
Plasma protein abnormalities
Agglutinates
Antibody causing agglutination
Howell-Jolly Body
Nuclear remnant from cell, due to poor splenic function
Left Shift
Severe bacterial infection
Toxic granulation
Infection, inflammation, necrosis Pregnancy
Hypersegmented neutrophil
Lack of vitamin B12/folate
Heinz Body
Haemolytic anaemia
Bence Jones Protein (urine)
Light chain, related to lytic lesions
Fibrin Split Products
DIC
Tests •
•
•
•
•
Ham’s test: paroxysmal noctural haemoglobinuria Coomb’s test: autoimmune haemolytic anaemia Metabisulfite test: mimics accelerated deoxygenation, for sickle cell Osmotic fragility test: hereditary spherocytosis Reticulocyte test: aplastic anaemia, hypersplenism
Year 3 EMQ Notes
Nina Cooper
Stains Stain Sudan Black Myeloperoxidase Tartrate-resistant acid phosphatase Leukocyte alk phos
Mechanism Preferentially stains myeloblasts against lymphoblasts n/a n/a
Clinical Use Differentiates AML and ALL Extramedullary leukaemia Hairy cell leukaemia
Elevated in polycythaemia vera, essential thrombocytosis and myelofibrosis Depressed inparoxysmal nocturnal haemoglobinuria and CML
Blood Transfusion Reactions •
•
•
•
•
Tissue related lung injury 2-6hr after transfusion, inflammatory process causes sequestration of neutrophils o within the lungs Antibodies form against donor WCs and attack the patient’s lungs (which share the o HLA antigens) Symptoms include fever, hypotension, cyanosis and pulmonary oedema o Immediate haemolytic transfusion reaction Immune destruction of transfused cells o o Hypotension, tachycardia, nausea, abdo pain, loin pain Occurs within 24hrs o Delayed haemolytic transfusion reaction Same symptoms, >24hrs o IgA deficiency ! anaphylactic-type reaction if patient is re-transfused at later date Antibodies to IgA are produced during first exposure o o Retransfusion leads to bronchospasm, laryngeal oedema and hypotension Febrile non-haemolytic transfusion reaction o WC antibodies react with leukocytes in blood transfusion o Usually have hx of previous transfusions Fevers, rigors and discomfort o
Coagulation Disease
Abnormality
Factor V deficiency
Warfarin/ Vit K Deficiency Glanzmann’s Thrombaesthesia
Bernard Soulier Syndrome
PT
PTT
PLATELETS
Lack of factor V ! no input from extrinsic pathway
!
!
normal
BLEEDING TIME normal
Inhibition of factors II, VII, IX, X
!
!
normal
normal
normal
normal
normal
!
normal
normal
normal
!
Platelets lack GLP IIb/IIIa, so fibrinogen binding is disrupted GLP Ib (receptor for VWF) is deficient
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Nina Cooper
Rheumatology
Year 3 Notes
Overview
ARTHRITIS •
RHEUMATOID ARTHRITIS >30 minutes of stiffness in the morning Deforming polyarthropathy Proximal IPJs affected Nodules on elbows/tendon sheaths •
•
•
•
•
•
•
Rheumatoid Hands Ulnar deviation of fingers Subluxation of MCPs Z shaped thumbs Boutonniere’s deformity Swan necking • • • • •
Bloods: RhF (IgM against IgG), anti-CCP
Urethritis o Arthritis Most commonly post-GU/GI infection See penile ulcers + plaques on soles/palms Seronegative Also get enteropathic arthritis secondary to IBD o
ANKYLOSING SPONDYLITIS Young men Bamboo spine – fusion of the vertebrae 95% HLA-B27 +ve “?” posture • •
• •
SEPTIC ARTHRITIS Inflammation of joint Will be just ONE swollen hot joint S.aureus or GU infection on aspirate •
Treat with DMARDs Biologics include infliximab Methotrexate Etanocept • •
• •
•
CONNECTIVE TISSUE DISEASE
Affects other parts of body too Fibrotic lung disease Seen as part of Felty’s syndrome Rheumatoid Arthritis o Splenomegaly o o Neutropenia Caplan’s Syndrome o Rheumatoid Arthritis o Pneumoconiosis o Lung Nodules on XR • •
•
SLE • • • • •
Autoimmune Drug induced: penicillamine/gold Malar rash Fatigue Joint pain
Bloods: anti-dsDNA, anti-histone, antismith
PSORIATIC ARTHRITIS Looks like rheumatoid but has skin/nail changes Affects people who have psoriasis
Management: immunosuppression Hydroxychloroquine Biologics Acute: steroids
OSTEOARTHRITIS Worst at night Degenerative Seen in weight-bearing joints Affects distal IPJs Heberden’s (distally) and Bouchard’s (proximally) nodes
SJOGREN’S Autoimmune attack on exocrine glands Schirmer’s test: for dry eyes See lacrimation o Positive if not producing o enough tears Also get dry mouth/vagina Bloods: anti-Ro, antil-La Can be primary or secondary to SLE, RA Symptom constellation = sicca Xerostermia o
•
•
• • • • •
• • •
•
•
•
REACTIVE ARTHRITIS Reiter’s Syndrome Can’t see, Can’t Pee, Can’t Climb a Tree Uveitis o • •
• •
•
Nina Cooper
Year 3 Notes
o o o o
Keratoconjunctivitis Chronic bronchitis Vaginal dryness Signs of arthritis
SYSTEMIC SCLEROSIS Cutaneous Anti-centromere CREST syndrome o Calcinosis o Raynaulds o Esophagitis o Scleradectomy (thickening of skin, beak nose, small mouth) Telangiectesis o Diffuse: anti-SCL70 = anti-DNA topoisomerase Get CREST syndrome + organ fibrosis • • •
•
•
VASCULITIS
LARGE VESSEL Giant cell (temporal) Arteritis o Ix: biopsy showing skip lesions Mx: high dose steroids o Associated with o polymyalgia rheumatic Takayasu arteritis o Japanese women o Fibrosis of aortic branches o Pulseless limb •
•
MEDIUM VESSEL Kawasakis Children o Coronary artery o aneurysms Skin manifestations o Polyarteritis nodosa o Associated with HBV •
•
POLY/DERMATOMYOSITIS Muscle inflammation + skin involvement Proximal muscles affected Anti-JO1, raised CK Associated with malignancy Gottron’s papules Heliotrope rash (purple around eye) Shawl sign •
• • • • •
•
CRYSTALS
Gout • • • • •
•
•
Middle aged men 1st MTP of big toe Swollen, hot, painful Uric acid crystals Normal gout Negatively birefringent o Needle shaped o Triggers: meat, alcohol, thiazide diuretics Management o Acute: NSAIDs, colchicine o Chronic: allopurinol Interacts with azathioprine !
Pseudogout Occurs in knee (and elsewhere) Calcium pyrophosphate crystals Pseudogout Positively birefringent o Brick shaped o • • •
SMALL VESSEL Wegener’s Churg-Strauss P-ANCA positive o Asthma o Eosinophilia o o SE of monteleukast Microscopic polyangitis o P=ANCA o Pulmonary and renal symptoms Henoch-Schonlein Purpura Children o Triad o Purpura on buttocks/legs Abdo pain Renal failure • •
•
•
!
! !
Nina Cooper
EMQ Lecture Notes
Oncology Carcinoma Tumour from epithelial surface Ulcerated mass Rolled edge Tissue invasion Necrosis Bleeding Obstruction/perforation of a lumen
Case 4
Local Excision For benign/minimally invasive malignant tumours Basal cell carcinoma Small SCC Pleomorphic adenoma Lipoma
Burkitt’s lymphoma
• • • • • • •
• • • • • •
6M, Ethiopian 4 week hx of swelling jaw Progressively enlarging Hx of EBV infection Minor disruption of teeth No laryngeal obstruction
•
Case 5
•
•
•
•
•
•
•
•
EPONYMOUS NEOPLASMS
•
35F Bulky mass in left breast Overlying skin is red and tender Contour of breast is distorted Mixed connective tissue and epithelial elements on biopsy
Case 1 • •
•
2M Abdominal distension, haematuria Large nodular mass on left kidney
Wilm’s Tumour
Case 2 • •
•
32M architect, homosexual 2 week hx of indigestion and dysphagia Multiple purple bruise-like lesions on R arm
Kaposi’s Sarcoma
•
•
•
• •
OTHERS Ewing’s sarcoma: rare bone cancer in children (“blue cell”) Grawitz tumour: RCC •
•
TUMOUR MARKERS
Case 1 • • • •
45F Irregular 4cm lump in breast Fixed to overlying skin Bloody discharge from nipple
Ca15-3
Case 3 •
Brodie’s Tumour AKA Phyllodes tumour Mostly benign, good prognosis
55M Progressive weakness of L hand Wasting of intrinsic muscles of hand (T1 nerve root) Mild ptosis and meiosis on L face
Pancoast Tumour
•
High levels suggest metastatic breast disease
Case 2 • • •
•
56M Anorexia and jaundice Bilirubin 350 umol/L, AST 55 IU/L and ALP of 750 IU/L Gallbladder is palpable
Ca19-9 • •
Pancreatic cancer Monitors response to therapy
Nina Cooper
EMQ Lecture Notes
Case 3 • • • • •
70M Difficulty passing urine Haematuria Back pain DRE shows irregular, hard mass
PSA • •
Measure of prostate cancer Treatment success and progression
Case 4
•
82F Constipation, tenesmus and lower abdominal pain Lost 5kg in 1 month
•
Carcinoembryonic antigen
• •
CEA
Case 5 • • •
50M, hep C Jaundice, RUQ pain Weight loss and appetite loss
Alpha-Fetoprotein Hepatocellular carcinoma •
Malignancy Hepatocellular Ca
Carcinogen Aflatoxin B1
Mesothelioma
Abestos
Prostate Ca Bladder Ca
Cadmium Aniline dyes/rubber industry
Endometrial Ca
Oestrogen
GI Lymphoma
Coeliac
Gastric Ca
Pernicious anaemia
Cervical Ca
Unprotected sex with multiple partners
Lymphoma
EBV
Nina Cooper
EMQ Lecture Notes
Breast, Lumps, Vascular GENERAL LUMPS Case 1 • • • •
35F Lump on scalp Painless, attached to skin Has a punctum
Sebaceous Cyst Occurs anywhere with sebaceous glands (not palms/soles) Intradermal Easily infected Tx: incision •
•
•
Recently diagnosed with EBV
Lymph Node Inflamed due to infection or infiltration Infection o EBV TB o HIV o Syphilis o Infiltration o Malignancy o Sarcoidosis •
•
•
• •
Case 5 •
Case 2 • • •
68F Firm, painless lump on elbow PMHx: Arthritis and pulmonary fibrosis
Rheumatoid Nodule Subcutaneous, collagenous granulomes Found on extensor surfaces (elbows/hands) In established rheumatoid arthritis Up to 25% RA patients Treat RA with methotrexate ! pulmonary fibrosis OR she gets pulmonary fibrosis due to inflammation from RA •
•
•
• • •
21M Painless lump on top of foot Appeared a few weeks ago Transilluminates
Ganglion (cyst) Dorsum of hand or foot Herniation of synovial joint or tendon sheath Thin-walled cysts Contain mucinous fluid “Bible cyst” Tx: leave it, aspiration or excision • •
• • • •
• •
Examining a Lump 6 S’s Site Size Shape Surface Smoothness Surroundings • • •
Case 3 • • • • •
•
45M Lump on a scar on abdomen Recently had a stoma reversal Present all the time Solid + itches sometimes
• •
3 T’s
•
Tender Temperature Transilluminate
•
Pulsatile
• •
Keloid •
• •
Hypertrophy of vascularised collagen Extend outside the scar Tx: excision or steroids (topical/injections)
Case 4 • • •
P
NECK LUMP INVESTIGATIONS Case 1
22M Lump on jaw Firm, not fixed to skin
• • •
27M Pain in jaw Hurts when eats
Nina Cooper
• •
EMQ Lecture Notes
Swollen, tender and red No fever
•
Sialolithiasis Stone in Salivary Gland Sialogram = best investigation Recurrent, unilateral Pain, worse on eating
•
Case 2
•
• •
•
• •
• • •
•
66F Pain in jaw Small, hard lump adjacent to earlobe Getting bigger over past few months
Parotid Tumour Unilateral lump near ear “Displaces the earlobe” = classic EMQ Facial pain = ? parotid tumour compressing facial nerve Best investigation = excision biopsy Salivary gland tumours o 80% parotid o Of these, 80% are pleomorphic adenomas 80% are in superficial o lobes Tx: surgery +/- radiotherapy – beware of facial nerve (VII) • •
•
•
•
•
•
Case 4 • •
•
Acute Chronic
Mumps/HIV Stone Tumour (fixed) ALL, sarcoid etc.
23M Painless and mobile from side- to-side but not up and down Sits anterior to sternocleidomastoid
Carotid Body Pathology Either aneurysm or rupture Best investigation = angiography Duplex USS cannot differentiation RARE Usually firm, but can be soft and pulsatile Classically move sideways but not up/down • • • • •
•
Case 5 • •
•
Unilateral
Congenital malformation of branchial arches = therefore <20yo Don’t tend to be problematic unless fistulate or become infected Cholesterol crystals can be found on FNA Tx: leave/excise (close to carotids/jugulars therefore risky) Best investigation = final needle aspirate
Bilateral
35F Uneven borers, smooth, slightly fluctuant Not fixed to skin or deeper structures
Mumps/HIV Lipoma Autoimmune disease
• • •
• •
Reassure patient Benign, fatty lump Occurs wherever fat can expand (not scalp, palms) Symptomatic only with pressure Malignant change is rare
Case 3 • • •
•
18M Lump in neck Anterior border of right sternocleidomastoid, half way up neck Growing slowly, causing no trouble
Branchial Cyst
ULCERS
Case 1 • • • •
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65M Painless wound in R leg Present for 2 months 3cmx4cm ulcer covering medial malleolus Shallow bed is covered in granulation tissue Surrounded by sloping edges
Nina Cooper
Venous Ulcer Caused by superficial/deep venous incompetence Gaiter region, covering the medial malleolus Lipodermatosclerosis Brown discoloration (haemosiderin deposition due to pooling of blood and iron breakdown) Extensive, can be painless •
EMQ Lecture Notes
Case 3 • •
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27F Altered bowel habit and rectal bleeding Large ulcerating lesion on left leg with dark red edges
Pyoderma Gangrenosum Recurring nodulo-pustular ulcers, with tender red/blue necrotic edge Purulent Associated with IBD, but also alcoholic hep, Wegener’s, myeloma •
• •
Case 2 • • •
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60M T2DM Large ulcerating lesion over left toes Lesion has well demarcated adges Leg is cool to touch Hairless Dorsalis pedias and posterior tibial pulses are absent
Case 4 • • • • •
Arterial Ulcer AKA ischaemic Caused by large vessel disease (atherosclerosis) or small vessel disease (vasculitis) Located distally Punched out appearance Absent pulses Low ABPI Shiny, hairless skin Arteriopath, smoking, diabetes, CVD VERY painful
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60M, obese Ulceration on sole of right foot Deep and penetrating skin Appears well perfused No pain Ankle reflexes are absent bilaterally
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Neuropathic Repetitive trauma with absent/reduced sensation Diabetes Lack of ankle reflexes Seen on weight-bearing areas •
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Nina Cooper
Case 5 • • •
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66M Retired marines officer Large scar from burn sustained in a war Painless 3cm area of irregular ulceration within scar Surrounded by raised edge Blood-stained discharge from base No regional lymphadenopathy
Marjolin’s Ulcer Eponymous name for a SCC arising in an area of previous inflammation e.g. long-standing venous ulcer or third degree burn (clue: WAR VETERENS) Features include o Painless o Blood-stained discharge o Raised edge LN spread rare o •
•
EMQ Lecture Notes
Carotid Body Tumour Babies Tumour of paraganglion cells Moves side/side but not up/down Pressure ! dizziness Pulsatile and has a bruit Diagnosed: carotid angiography • • • • • •
Case 1 • • • • •
Lymphoma Lethargy Weight loss LN painful after alcohol Night sweats Itchy • • • • •
Case 2 • •
•
• •
NECK LUMPS
30M Lump in posterior triangle Enlarging slowly for 2 months Feverish, itchy, sweaty Lost 8kg unintentionally
25M Painful swelling bulging from under anterior border of sternocleidomastoid Soft, fluctulant but tender on examination Present since was a child Started causing trouble after recent pneumonia
Branchial Cyst 2/3 up sternocleidomastoid Remnant of second branchial cleft Smooth, non-tender fluctuant lump Enlarged + painful after respiratory infection Present from childhood Diagnosed: FNA showing yellow fluid with cholesterol crystals • •
3 Main Locations for Neck Lumps Anterior Triangle o Branchial cyst Carotid body tumours o (ABC) o Midline Thyroiglossal cust o Thyroid goitre o o Dermoid cyst Posterior Triangle o Cervical ribs o Cystic hygromas o Pharyngeal pouches (2C, 2P) o •
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Anywhere Lymph nodes Lipoma Sebaceous cysts
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Case 3 • • • •
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70F Mass in right jaw Slowly growing for 6 months Past week – unable to move right side of face Hard, irregular lump extending behind angle of mandible
Salivary Duct Carcinoma Hard, irregular pass •
Nina Cooper
•
Facial nerve involvement
EMQ Lecture Notes
•
Case 4 • •
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28M Lump in posterior triangle of neck Difficulty finishing meals Regurgitates food at night
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Cold, pulses absent (popliteal, posterior tibila and dorsalis pedis) Fixed flexion deformity – cannot flex knee or toes Apyrexial, HR 85
Acute Limb Ischaemia Surgical emergency requiring revascularisation within 4-6h to save limb Mainly due to in situ thrombosis or emboli •
Pharyngeal Pouch Weakening and protrusion of pharyngeal wall through Killian’s dehiscense Elderly man Dysphagia, regurgitation of food Gurgling sensation Aspiration at night Bad breath •
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• • • • •
Signs – 6 Ps Pale Pulseless Painful Perishing cold Paraesthesia* Paralysis* • • • •
Case 5 • •
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3 month old baby Lump on base of neck, posterior to stenocleidomastoid Transilluminates
Cystic Hygromas Congenital collection of lymphatic sacks Clear fluid Soft, fluctuant •
• •
VASCULAR SURGERY
Case 1 •
•
*indicates amputation necessary Management Options Percutaneous transluminal angioplasty: short stenosis in large arteries Surgical bypass: extensive atheromatous disease with good distal run off e.g. femoral popliteal bypass, femoral distal bypass Acutely: surgical embolectomy or thrombolysis Amputation: useless limb e.g. flixed flexion deformity OR dead limb e.g. extensive necrosis In addition to other signs, LOSS OF SENSATION or PARALYSIS point to gangrene •
•
•
•
Conditions met to qualify for elective AAA repair
•
AAA Repair Greater than 5.5cm + otherwise fit for surgery, OR Smaller aneurysm that is now causing symptoms e.g. back pain, OR Smaller aneurysm growing at >1cm/yr <5.5cm = monthly ultrasound surveillance Repair can be open/endovascular •
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Case 2 • • • •
56M Homeless Severe pain in right leg Pale compared to left leg, from below knee to toes
Ankle Brachial Pressure Index (ABPI) Measured by divided ankle systolic BP by brachial systolic BP Should be >1 >1.3 = walls are so calcified that they cannot be compressed by a BP cuff 0.6-0.9 = peripheral vascular occlusive disease e.g. intermittent claudication 0.3-0.6 = critical limb ischaemia <0.3 = impending gangrene •
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Buerger’s Test Used to assess arterial supply to lower limbs •
Nina Cooper
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Raise patients legs to 45 degrees and held there for 2 minutes The time taken for the legs to show signs of pallor is noted Rapid = poor arterial o supply Legs are then allowed to hang independently off the side of the bed o Rate at which colour returns = rate of venous filling If there is arterial insufficiency, after 2-3 mins the foot on the affected side will develop a reactive hyperaemia ! crimson coloured foot (due to vasoldilation from anaerobic metabolics built up during elevation) Can be positive in one or both of the lower limbs
Amaurosis Fugax Transient monocular loss of vision Result of atherogenic emboli arising from the carotid artery territory, which unilaterally obstruct the lumen of the retinal artery circulation Other causes include cardiac emboli and temporary vasospasm of retinal artery (in young people during exercise) Giant cell arteritis can cause chronic granulomatous inflammation of the central retinal artery which produces similar symptoms to amaurosis fugax • •
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•
EMQ Lecture Notes
o
o o
Varicose Veins Asymptomatic ! treat conservatively o Avoid long periods of standing o Compression stockings o Lose weight Walk more o Or injection sclerotherapy ! for below knee varicosities o Increase the amount of intravascular granulation tissue If QOL is severely aggected e.g. due to pain, ulceration, thrombophlebitis, then surgery is an option You can ligate the o saphenofemoral/saphenop opliteal junctions o Or multiple avulsions of the varicosities and endoluminal radiofrequency ablation of long saphenous Low molecular weight heparin has been shown to be effective for the use of DVT prophylaxis in those undergoing surgery •
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Necrotising Fasciitis Infection of deep layers of the skin and subcutaneous tissues which spreads within the fascial plain of the tissue Group A strep = most common Usually starts at the site of local trauma Features include swelling, erythema, vesicle and bullae formation on the skin Very ill with fever +- diarrhoea and vomiting Confirm diagnosis with blood culture and aspiration of pus Requires debridement – emergency •
Trendelenburg’s Tourniquet Test SFJ is occluded using a tourniquet Assesses where the level of venous insufficiency occurs If the varoscosities do not fill, then the defect lies above the tourniquet • •
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Carotid Endarterectomy Patients with symptomatic carotid artery stenosis >70-80% are candidates for carotid endarterectomy Simply the procedure to unblock the carotids Post operative complications o 66% get post-op HTN •
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5-8% stroke risk (carotid artery stenosis or haemorrhagic) 5% CN injury 1% get patch rupture or infection
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Nina Cooper
EMQ Lecture Notes
Aortic Dissection Defined as a surgical emergency Split in the intimal lining of the tunica media of the aorta ! double lining or rupture into the pericardium ! cardiac tamponade CT scan used for rapid diagnosis MRI = higher sensitivity and goldstandard, but takes longer • •
• •
Raynaud’s Syndrome Digital ischaemia due to reflex vasospasm of normal arterioles Digital pallow ! cyanosis ! reactive hyperaemia Secondary Reynauds can occur as a result of scleroderma, SLE, polyarteritis nodosa, RA, cervical rib, cryoglobulinaemia, polycythaemia and drugs such as B blockers and ergot alkaloids •
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Popliteal Aneurysms 80% of all peripheral aneurysms More likely to have an aortic aneurysm as well • •
Case 1 • • •
24F Breast lump 1.5cm discrete, smooth mobile lump
Fibroadenoma Benign neoplasm Arises from stroma Most common breast lump in under 30s Hard, smooth and mobile “Breast mouse” • • •
• •
Fibroadenosis AKA fibrocystic changes Lumpy/bumpy chest Multiple cysts and nodules Menstrual cycle Sometimes pain Oestrogen-induced hyperplasia Small cysts – dilation/unfolding lobules Fibrosis – rupture of cysts ! fibrosis Adenosis – increase in acini • • • • • • •
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Branches of the external carotid Superior thyroid Ascending Pharyngeal Lingual Facial Occipital Posterior auricular Maxillary Superficial temporal • •
Case 2 •
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34F Large lump, hot and painful Gave birth 6 weeks ago
• • • •
“ S ome Aggressive L overs F ind P ositions M ore S timulating”
O dd
Acute mastitis Infection of the breast Often in the first month of breastfeeding Bacteria from skin ! spread to ducts Caused by staph aureus, strep pyogenes, empidermidis Causes inflammation, pus and sometimes fever Abscess – more inflammation and fever, not helped by abx • •
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BREAST
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Case 3 • • •
56F White nipple discharge Poorly defined periareolar mass
Duct Ectasia Dilatation Blockage Chronic inflammation and fibrosis Poorly defined palpable periareolar mass • • • •
Nina Cooper
• • • •
Mostly painless White cheesy discharge 5th-6th decade Often multiparous
EMQ Lecture Notes
Paget’s Disease Itchy Erythema Scale formation Erosion Nipple discharge Occurs in 1-4% breast cancers 60% with Paget’s have invasive carcinoma, 40% have DCIS (cannot palpate lump) • • • •
Periductal Mastitis Painful erythematous palpable subareolar mass Poorly defined periareolar mass No discharge Metplasia of squamous cells ! abscess formation ! abscess formation and inflammation Not associated with age/parity >90% smokers •
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BREAST INVESTIGATIONS
Case 1 • •
Case 4 • • •
31F Pain in breast Same time each month
Cyclical Breast Pain Associated with menstrual cycle Occurs in luteal phase (after rising of progesterone) •
32F 5cm unilateral irregular breast lump
USS •
Anyone under age of 40
Mammography Anyone over 40 •
•
USS + Mammography Lump and are 40 or over •
Case 5 • • • • •
52F Irregular lump on left breast Inverted nipple Unilateral bloody discharge Skin puckering
Invasive breast carcinoma Most common cancer in UK 1 in 8 women Ulceration Skin retraction Peau d’orange Swelling Discharge Eczema Nipple retraction or distortion Lump will be hard, fixated and can cause skin tethering •
Case 2 • •
56f 5cm unilateral irregular breast lump
USS + Mammography Less dense tissue than younger woman •
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Case 3 • •
36F Hot, red, painful breast lump
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65F Itchiness and discharge from nipple No lump
DCIS •
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Case 4
Case 6 •
Antibiotics Likely to be acute mastitis Might be abscess – will require draining if abx don’t work
No palpable lump
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26F Painful breasts at same time each month Multiple hard lesions less than 2cm in diameter
Reassure Can give ibuprofen •
Nina Cooper
Case 5 • •
47F White, low viscosity liquid discharge from her nipples
Prolactin White, low viscosity = breast milk Prolactinoma ! galactorrhoea • •
EMQ Lecture Notes
Nina Cooper
EMQ Lecture Notes
Endocrinology and Poisoning ENDOCRINE INVESTIGATIONS
Case 1 • • • • •
20M athlete Weight loss and fatigue Unable to gain weight Drinking water non-stop Polyuria
Random Blood Glucose T1DM Lack of insulin leads to release of glucagon, corticosteroids, adrenaline and GH This results in gluconeogenesis and glycogenolysis in the liver, releasing more glucose into the bloodstream This process is fed by breakdown of fat/muscle to fuel the liver The glucose gets so high that it is lost in the urine, causing an osmotic diuresis This makes you drink more, causing the polydipsia When the liver cannot keep up with the gluconeogenesis and glycogenolysis, it begins to produce ketones (acetone smells like pear) Ketones = acids, and so trigger vomiting via the CTZ This causes Kussmal breathing to blow off excess CO2 as well
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Failure to suppress on high-dose dexamethasone and exaggerated cortisol response to CRH Cushing’s syndrome = ectopic ACTH secretion Failure to suppress on o low-dose dexamethasone Loss of diurnal variation in o cortisol secretion Loss of cortisol response o to an insulin tolerance test Psuedo-Cushing’s Syndrome o Failure of suppression of serum cortisol on lowdose dexamethasone + characteristic body habitus of Cushing’s Elevated MCV and serum o GGT show cause = alcoholism o Normalises on cessation of drinking o
Case 3 • • •
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25M 3/12 hx polyuria and polydipsia PMHx ITU stay at HH following RTA Glucose 5.8
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Case 2 • • • •
65M Difficulty climbing stairs Exertional dyspnoea Has centripetal obesity, bruises, darkening palmar reases and recent onset DM
Diabetes Insipidus vs. Psychogenic Polydipsia Use water deprivation test DI: get up at night to drink water CENTRAL = pituitary tumour, trauma [car crash!] or tumour – treated by desmopressin NEPHROGENIC = hereditary or secondary – hypercalcaemia, lithium and demeclocycline Treatment: • •
Cushing’s Syndrome Due to a SCC – links to problems breathing Therefore order high dose dexamethasone test Acts like cortisol to depress ACTH – in Cushing’s this doesn’t happen Disease – pituitary adenoma •
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Nina Cooper
•
Central = intranasal desmopressin, nephrogen = thiazide diuretic
EMQ Lecture Notes
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Case 4 • • • • •
65M Hyponatraemia No medications Adrenal insufficiency High urine osmolality
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Case 5 • • •
Diagnosis: SIADH Opposite to DI Order CXR and head MRI Symptoms: generalised weakness, hyporeflexia, ataxia, lethargy, confusion Suspect if patient has hyponatraemia, hypo-osmolality and a high urine osmolality Indvestigations o Decreased osmolality o Inappropriate urine conc o Excess Na excretion in urine Treat: saline, demeclocycline Treating Na by >10mmol causes quadriplegia, pseudobulbar palsy, seizure, coma, death – don’t rush treatment Use demeclocycline and tolvapatan if water restriction is sufficient •
Neurones derived from olfactory epithelium – patients typically present with anosmia or hyposmia Frequently demonstrate colour blindness, cleft palate/lip Treatment = pulsed GnRH
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65m Coarse facial features Widely spaced teeth Headaches Ring keeps getting stuck on fingers
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Acromegaly Visual disturbance Slanting forehead Protruding jaw Oral glucose tolerance test = diagnosis o GH drops in increased glucose o Won’t decrease in acromegaly Due to a pituitary tumour Serium IGF=1: screening test for acromegaly, levels directly relate to amount of GH secretion of previous 24hrs Treatment = surgery • • • •
• •
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Case 6 • • • •
Young female Low mood, weakness, tearful Mild GI irritation Darkened skin creases
Addison’s Disease Short synACTHen test Inject ACTH ! increased cortisol Damage to adrenals means cortisol will NOT increase GI disturbance, weight loss, postural htn High potassium + low sodium due to lack of aldosterone • • •
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Case 7 •
Kallmann’s Syndrome Isolated hypogonadotrophic hypogonadism Caused by failure of development of hypothalamic neurones
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30F Generalised weakness and paraesthesia Severe HTN Raised sodium, low potassium, raised bicarbonate
Nina Cooper
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Darkened skin creases
Conn’s Syndomre Diagnose with plasma renin:aldosterone level Hypokalaemia, metabolic low alkalosis Can be unilateral or bilateral Renin low due to excess aldosterone •
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EMQ Lecture Notes
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Case 2 • •
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53F Weight gain, lethargy, constipation Started 5 months ago Mild, diffusely enlarged thyroid
35F Visual disturbance Cross street, cannot see cars on either side PMHx hypercalcaemia treated 3 years ago with neck surgery Pituitary studies are ordered What else?
Hashimoto’s Most common cause of hypothyroidism in western world Examination: moderately enlarged non-tender thyroid Anti-thyroglobulin Anti-microsomal Anti-thyroid Peroxidase Anti TSH-R
3 Ps: parathyroid tumour, pancreatic tumour, pituitary adenoma Pancreatic US (Zollinger-Ellison Syndrome – stomach tumour causing duodenal ulcers) MEN2b = signs of Marfan’s (Lincoln = men2b) Men2a = phaeochromocytoma, amyloid producing medullary thyroid tumour
Case 3
MEN1 •
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Case 8
Exophthalmos and pretibial myxoedema – GRAVE’S Autoimmune Overstimulation of TSH-R
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40F Mood swings, problems with attention, hand tremor Discomfort in neck Radiates to ears when swallowing Flu-like illness recently
De Quervain’s Thyroiditis Clue = flu-like illness Viral infection e.g. flu, coxsacchie, mumps Causing inflammation and release thyroid hormone Pain worse with swallowing Fever Hyperthyroid -> hypothyroid -> euthyroid Dx: clinical and high ESR Treatment: none, NSAIDs • •
THYROID DISEASE
Functions of Thyroid Increase BMR Physical and mental growth Maintain responsiveness of body to adrenergic drive • • •
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Case 1 • • •
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35F Insominia, palpitations Lost 5kg over 2 months despite eating whole KFC bucket every night Irritable Wear shorts Unsightly rash on shins
Case 4 • •
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Hyperthyroidism
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61F Difficulty breathing and swallowing Midline neck mass increasing in size over few months Thyroid is hard, immobile and enlarged No tenderness USS-guided biopsy shows increased fibrotic tissue
Nina Cooper
Riedel’s Thyroiditis Idiopathic fibrosis of thyroid Slow growing (rock like) Biopsy to distinguish from cancer TFTs normal, some develop hypo/hyperthyroidism None, palliative surgery if affecting oesophagus etc. • • •
EMQ Lecture Notes
Medullary Carcinoma Calcitonin = tumour marker Rare 5% Sporadic or part of MEN2 syndome • • •
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CALCIUM METABOLISM
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Case 5 • •
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Case 1
84F Lump in neck, growing rapidly for past month Problems swallowing Hard irregular mass on right side, fixed to overlying skin
Anaplastic Carcinoma Rare Elderly Die within 1 year Hard, rapidly enlarging Spread Causing tracheal compression of RPN injury • • • • •
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49M Increased tiredness, irritability and abdo pains Admitted to hospital with bones Raised serum PTH
Primary Hyperparathyroidism Bones, stones, moans, groans = hypercalcaemia Polyuria and polydipsia Hyperplasia or adenoma or parathyroid gland Increased PTH leading to increased Ca •
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Causes of Hypercalcaemia MALIGNANCY: Myeloma and bony mets also increase serum calcium VIT D INTOXICATION SARCOIDOSIS •
Case 6 • • •
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25F Left sided neck lump 2cm smooth, regular, firm lump that moves upwards when swallowing but not with tongue protrusion Cervical LNs present on left side of neck also
Papilary Carcinoma 90% Adolescents and young adults May spread to LNs Orphan Annie eyes (cleared-out appearance) Psammoma bodies (sady) Treatment = thyroidectomy +radio-iodine TSH-dependent so thyroxine for rest of life • • • •
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Causes of Hypocalcaemia CKD Gland failure = autoummune DiGeorge syndrome Post-thyroidectomy Hypomagnesaemia • • • • •
Pseudohypoparathyroidism Target cell resistance to PTH Low Ca and PTH is appropriately high • •
Case 2 • • •
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21F Thyroidectomy Numbness in extremities and muscle spasm Wrist flexes when taking BP
OTHER CANCERS
Follicular Carcinoma 20% Middle aged Spreads to lung and bone • • •
Hypoparathyroidism Trousseau’s sign = cuff leading to spasm = carpopaedal spasm Weakness, crampings, normal Also Chvostek’s sign •
• •
Nina Cooper
EMQ Lecture Notes
Case 3 • • • • •
63M CKD Tiredness and muscle cramps Chvostek’s sign elicited Raised PTH
MIXED EMQs Case 1 •
Secondary Hyperparathyroidism PTH increased due to low serum Ca Usually in CKD •
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Case 4 • •
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Same 63M Admitted to hospital a year later with severe loin to groin pain Increasingly depressed and irritable
Tertiary Hyperparathyroidism Prolonged period of secondary disease Parathyroids undergo hyperplasia due to loss of feedback control ! hypercalcaemia •
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40M Weight gain Stretch marks Cut won’t heal Cortisol suppressed by high dose dexamethasone only
Cushing’s Disease Disease = ACTH secreting pituitary adenoma Syndomre = ectopic sources e.g. adrenal adenoma, SCC •
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Case 2 • • • •
Female Received several units of blood Amenorrhoea Inability to lactate
Sheehan’s Syndrome Ischaemic necrosis of pituitary Hypopituitarism •
Case 5 • • •
•
56 smoker SOB, weight loss, haemoptysis Polyuria and bone pain in left leg
Case 3 • • •
26F HTN Muscle cramps Weakness Serum K = 2.9
PTHRP Secretion Causes ectopic secretion of PTH Signs of hypercalcaemia Pain due to bone breakdown
Conn’s Syndrome
Case 6
Case 4
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35F Symptoms of hyperkalaemia Lump in right neck Frequent headaches and palpitations Normal stature
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MEN2a • •
See primary hyperparathyroidism Palpitations due to phaeochromocytoma
60f oVERWEIGHT Loss peripheral vision Straie and alrge scars on lower abdomen Had recent surgery – not sure what for
Nelson’s Syndrome Bilateral adrenalism for Cushing’s ! existing pituitary adenoma grows rapidly (no negative feedback) ! visual problems, hyperpigmentation due to increased ACTH production •
Nina Cooper
Case 5 • • • • • •
30F Weight loss, tachycardia Feels hot all the time Clubbing Painful swelling of digits Eyes are bulging out of orbits
EMQ Lecture Notes
Papillary Tumour Younger patients •
MANAGEMENT OF DIABETES
Case 1 • •
Grave’s Disease Thyroid acropachy Exophthalmos
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Case 6 • • •
49F Lump in neck Hoarse voice
Riedels’ Thyroiditis See above •
Case 7 • • • • •
•
26F A&E via LAS Clutching stomach, doesn’t know where she is Eyes are sunken
IV Saline Dehydration •
DKA ! characterised by hyperglycaemia, ketoacidosis, ketonuria Mortality of 3-5% Complete lack of insulin ! increase in glucagon, cortisol, growth hormone, epinephrine Stimulates hepatic gluconeogenesis, glycogenolysis, lipolysis Lack of insulin leads to fatty acid metabolism and causes increased ketone production • •
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22M Sore throat recently Feels heart racing Weight loss Painful lump in neck
De Quervain’s See above •
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Presentation Nausea and vomiting due to hydroxybutyrate Sweet smelling breath due to acetone Severe dehydration - glycosuria, osmotic diuresis Ketoacidosis due to ketones Confusion: hyperosmolarity, dehydration and acidosis Diffuse abdominal pain •
•
Toxic Multinodular Goitre Lumpy irregular swelling of thyroid No eye sides Can cause Plummer’s Syndrome: autonomous hyperfunctioning nodules • • •
Simple Colloid Goitre Increased gland production of colloid due to increased thyroxine demand Low T4 and high TSH Simply due to iodine deficiency or pregnancy/puberty •
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Case 8 • • • • • •
64M 2 month hx of weight loss Hoarse voice Difficulty swallowing Lymphadenopathy Orphan Annie Eyes on histology
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Management IV normal saline – DEHYDRATION kills One drip is set up, then start insulin infusion Correct hypokalaemia •
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Case 2 • • •
54M Diabetic HbA1C of 8.5% six weeks after being started on metformin
Sulphonylurea HbA1C >6.5 •
! metformin
Nina Cooper
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Sulfonylurea given if not overweight e.g. glibenclamide (urea pisses off B cells and causes them to produce more insulin) If HHbA1C>6.5 still ! sulphonylurea + metformin Still not good and >7.5 ! thiazolidinediones or insulin Then if >7.5 = insulin + metformin + sulphonylurea
HbA1c •
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Chromatography of Hb gives HbA and HbA1 (4-6%) HbA1c = glycosylated form of HbA1 Reflects blood glucose over 120 day life span of erythrocyte 50% comes from last month, 25% from month before 6.5 – MAGIC NUMBER
Case 3 • •
EMQ Lecture Notes
•
Calms down after few minutes and appears to be falling asleep
Hypoglycaemic – give IV glucagon ABCDEFG Neuroglycopenia Irritable, tired, drowsy etc. 3 states o Conscious, orientated, able to swallow ! 15-20g carbohydrate – LUCOZADE o Conscious but confused, disorientated, unable to cooperate, aggressive but are able to swallow ! dextrogel squeezed into mouth, IM glucagon o Unconscious and or/having seizuires and/or very aggressive ! IV Glucose or IM glucagon • • • •
65M, white BP 155/85 on 2 consecutive visits to GP POISONING
Calcium Channel Blocker Over 55/black = Ca Channel blocker, Under 55 = ACE inhibitor Step 2: A+C Step 3: A+C+D (thiazide-like diuretic) •
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Case 1 • •
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78F Attempted suice by OD on prescription medicine Fatigued, bradycardic and can see yellow-green halos
Digoxin OD Affects cardiac ion channels – increases IC calcium Increased contractility and increases vagal tone to heart Dig ! AVN block Enhanced automaticity ! arrhythmias and supraventricular tachycardia OR bradycardia due to HB Yellow-green visual halos = xanthopsia Digibind = antidote •
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Case 4 • • •
67F DM Suddenly becomes aggressive, shouts at nurses for imprisoning her
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Case 2 • • •
14F Paracetamol OD 10 x 250mg tablets
Nina Cooper
•
EMQ Lecture Notes
Weighs 50kg
•
Reassure and Discharge For paracetamol toxicity must be <75mg per kilo, 75-150mg per kg = borderline, 150mg per kg = hepatocellular damage This pt has taken 2500mg overall, which is 50mg per kilo – therefore she is not at risk Otherwise you would give Nacetylcysteine •
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Paracetamol Primary cause of liver failure First few hours = nausea and vomiting, over 24-48hrs you get hepatotoxicity Signs = tenderness, jaundice, asterixis, foetor hepaticus, haemorrhage (II, VII, IX, X) 95% paracetamol detoxified by phase II enzymes and excreted by urine 5% converted to NAPQI via P450 enzymes! conjugated with GSH Too much paracetamol – enzymes are all occupied and so excess NAPQI is produced ! destructive in liver as not enough glutathione to bind Therefore need to give NAC to allow for more glutathione production and to conjugate the NAPQI NAC is most effective in first 8 hours • •
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Benzodiazepine Flumezanil -Ams bind to inhibitory GABA-A receptors Solitary OD causes sleepiness With alcohol it causes severe resp depression • •
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Case 4 • •
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UNKNOWN
DOSE
DOSE
<1 hr – CHARCOAL
<8 hours, measure levels, treat if above line
<8hrs: measure levels, NAC if above line
8-36hrs TREAT >36hrs, treat if above line
Case 3 • •
16F Drunk
UNKNOWN
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Case 5 • • •
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75M OD on prescription medication ABG shows mixed respiratory alkalosis and metabolic acidosis Seizure
Aspirin (salicylate) Stimulates resp centres to hyperventilate ! resp alkalosis Aspirin = acid therefore metabolic acidosis Vomiting Dehydration Hyperventilation Give ACTIVATED CHARCOAL straight away Measure urine pH Give IV sodium bicarbonate until becomes alkaline Haemodialysis if renal failure, heart failure, seizures •
Treat
4 yr old child 15 year old brother notes brother drank bottle of mother’s bright green medication Has respiratory depression and pinpoint pupils
Naloxone Prescription meds such as tramadol can be used for OD Bright green liquid = methadone Resp depression Pinpoint pupils
•
KNOWN
Took mothers “anxiety medication” Ends in “pam” RR is 6
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Nina Cooper
Poison
EMQ Lecture Notes
Digoxin
Key Features Tachycardia, bradycardia, yellow halo
Antidotes Digibind
Paracetamol
Tell you/ hepatic failure
N-acetyl-cysteine
Benzodiazepines
Drowsiness, respiratory depression
Flumezanil
Opiates
Resp. depression, pinpoint pupils
Naloxone
Salicylates
Tinnitus, vertigo, hyperventilation Metabolic acidosis, mixed respiratory alkalosis and metabolic acidosis
First 2 hours: Charcoal Urinary alkalisation: sodium bicarbonate
Organophosphorous insecticides
Farmer, inactivate cholinesterase: SLUD = salivation, lacrimation, urination, diarrhoea
Heparin
Bleeds
Protamine
Warfarin
Bleeds
Vitamin K
Beta blocker
Severe bradycardia or hypotension
Atropine and Glucagon
Carbon monoxide
Low sats but normal blood gas
Paraquat
Weed killers, alveolar failure
Atropine
100% oxygen Hyperbaric chamber
Activated charcoal
Nina Cooper
EMQ Lecture Notes
Infectious Diseases & Eponymous Syndromes INFECTIOUS DISEASES
Case 1: Elective in India Profuse rice watery stools
Malaise
•
Influenza
Cape Town in August = their winter Therefore, no mosquitos & increased risk of flu
•
• •
•
Cholera Rice water stools Gram -ve
• •
Dengue • •
DIARRHOEA
•
Shigella • • •
• •
Salmonella typhi Gram –ve motile bacilli Gradual onset Rose spots • • •
Gram +ve Pseuodomembranous colitis
• •
Campylobacter Self-limiting Hx of poultry or unpasteurized milk Gram –ve flagella, corkscrew • • •
Yersinia Plague Gm –ve facultative Anaerobe
Enteroamoeba Parasite Giardia Long-term diarrhea Water contamination • • • •
Case 2: Elective in Cape town Mild fever, headache • •
•
•
Falciparum = worst Non-specific symptoms: headache, fever, vomiting, diarrhoea Plasmodium Ovale/vivax stay in system “V&O do not go”
Influenza Non-specific symptoms: headache, fever, vomiting, diarrhoea A: birds B: seals C: pigs •
•
C. Diff
•
•
Common diarrhea Enterotoxigenic Most common in traveller
•
•
•
Malaria
E-Coli
•
•
Bloody diarrhea Acute presentation Gram –ve
Retrobulbar headache Rash Viral (RNA) Can cause facial flushing Dengue shock syndrome ! haemorrhagic fever
• •
TB •
Latent infection
Herpes virus HSVI/II: cold sores/genital III: varicella zoster – chicken pox and shingles IV: EBV, infectious mononucleosis V: CMV, immunocompromisied: systemic symptoms: fever, pneumonitis, colitis, hepatitis, retinitis, CVS VI/VII: rosida infection (children) VIII: Kaposi’s sarcoma (popular blotches): AIDS defining illness • •
• •
• •
Case 3: Travelling businessman Returns from Africa Headache and malaise • • •
Nina Cooper
•
No response to chloroquine, responds to quinine
Malaria •
•
Quinine/chloroquine are antimalarials 2-3 treatments Old: chloroquine (falc. now o resistant) o Quinine = new, best treatment o Artesanate since 2011/12
EMQ Lecture Notes
Case 7: Elective in Cape town •
HOSPITAL ACQUIRED INFECTIONS Klebsiella Gram –ve rod Pneumonia: currant jelly sputum Renal calculi (staghorn) Others: proteus (gm –ve bacilli), pseudomonas (gm –ve) • • • •
C. Difficile Gm +ve Abx use Toxic megacolon Pseudomembranous colitis •
Case 4: 23F Gap year Returns to UK Presents with bloody diarrhoea • • • •
• • •
PCP • •
Shigella
Case 5: Professor of ID Returns from South America 3x3 erythematous ulcer on left forearm, raised edge
• •
Pneumoncystis jivoreci Pneumonia in CD4<200; ITU intubated CXR unrevealing Histoplasmosis: ddx
• • •
Leishmaniasis Cutaneous: itchy papules, becomes erythematous ulcers with raised edges Visceral (Kala Azar): spreads via lymphatic and reticuloendothelial system; lymphadenopathy and constitutional system Mucocutanoues: lip, nose, pharynx etc. Protozoa Spread by sandlifes •
•
Case 8: 6 year old Itchy popular rash skin burrows in hand palms and finger webs • • •
Scabies
•
Case 9: Gardener presents to A&E with inability to eat Greets you with sardonic smile
•
Tetanus
•
•
•
Schistosomiasis
Case 10: 42yo South African man Blotches over legs Enjoys sexual intercourse • •
Lyme Disease
•
Case 6: 21yo Rockstar Acute pain in right knee Hot and swollen to touch Gram –ve diplococci
HIV
Neisseria gonorrhoea Rockstar: promiscuous? Chlamydia/gonorrhea = most common STDs
Case 11: HIV +ve man Headache and fevers Ring enhancing features on CT
! Kaposi’s
sarcoma
• • •
JC Virus: causes PML, AIDS-defining, hand moves around without him realising
•
•
• • •
Nina Cooper
EMQ Lecture Notes
Toxoplasmosis ANTIBIOTICS
Case 3: 29 businessman 3 day business trip Unwell for a week with muscle cramps and SOB Wife is upset as he forgot her birthday and never normally does Na = 128, K = 4.6 •
Lung Pathogens Typical
•
•
o o o o •
Strep. Pneumoniae Pneumococcus Rusty brown sputum Penicillin: amoxicillin
Atypical o
o o
o
Legionella ! LFTS: rise ! Low Na Mycoplasma E.g. dry cough, walking pneumonia Macrolide: clariothromycin, erythromycin
Exceptions C. diff: metronidazole Pneumonocystis carinii: cotrimoxazole HIV+ or immunosup. Boat shaped organisms on BAL with silver stain • •
• •
UTIs • •
Trimethroprim Nitrofurantoin
Case 1: 25m Previously well 1 week history of SOB, fever and productive cough Dullness to percussion Increased tactile vocal fremitus in right base • •
•
•
•
Clarithromycin Legionella In Edinburgh: probably in a hotel Can get CNS abnormalities: forgetful Low Na • • •
•
Case 4: 49F 1 week hx of lower abdominal pain Pain on urination Finding job increasingly difficult as she has to urinate so often • •
• •
Nitrofurantoin HEPATITIS B SEROLOGY Used to measure immunity following HVB immunization: Hepatitis B surface antibody (HBsAb)
•
•
Used to indicate acute HVB infection: Hepatitis B surface antigen (HBsAg)
•
Amoxicillin Streptococcal infection Nb. Flucloxacillin is for staph. aureus infections of the skin
Used to indicate chronic HVB infection if detected 6 months after original infection: Hepatitis B surface antibody (HBsAb)
• •
Case 2: 38 prostitute 1 week hx of dry cough and SOB on exertion Normal CXR • •
•
Co-trimoxazole Pneumocystis carinii Prostitute " HIV Normal CXR • • •
Used to indicate high infectivity in a chronic HVB carrier: Hepatitis B e antigen (HBeAb) High levels indicates low infectivity in a chronic HVB carrier Hepatitis B core antibody (HBcAb)
Nina Cooper
Surface antigen: outside, first to be shed If antigen is found in someone’s blood, they’ve got Hep B First way to detect a positive infection result If under 6 months, acute If over 6 months, chronic If VACCINATED, you will find the surface antibody only Core antigen: inside The core antigen should never be found in the blood The core antibody will be present in the blood and shows infection – present after 4 weeks o IgM: acute o IgG: chronic o If HBcAB is high, you are mounting a good response and you’re not highly infective E antigen: extra, not always there Indicates a high level of infectivity Requires aggressive treatment Absence = low infectivity •
•
• • •
•
•
• • •
EMQ Lecture Notes
Case 2: 22 student Abdo cramps, D&V Eaten a chinese take away from the night before Gm +ve bacilli • • •
•
Bacillus cereus 1-6h intubation period Reheated rice Sudden vomiting, minimal nonbloody diarrhea Self-limiting • • •
•
S. aureus Similar Gram +ve clusters 1-6h incubation Prominent vomiting • • • •
Case 3: 82F Hospitalised for CAP Fever and profound diarrhoea after 3 days in hostpital White/yellow membrane-like plaques on colonic mucosa Biopsy shows plaques made of fibrin and inflammatory cells • • •
•
TB DRUGS: RIPE RIPE: for 2 months RI: for following 4 months Isoniazid: peripheral neuropathy (give with pyridoxine – vit B6) Rifampicin: orange tears/urine, hepatitis, drug interactions Pyrazindamide: hepatotoxicity Ethambutol: optic neuritis (redgreen colour blindness) • • •
•
• •
DIARRHOEA CTD.
Case 1: 32M Profuse, watery diarrhoea Abdo cramps during trip to mexico Resolves without antibiotics • •
•
C. Difficile #1 HAI Anaerobic, spore-forming, gm +ve Follows cephalosporins/ fluoroquinolones 2 exotoxins o A: diarrhea o B: cytotoxic to colonic cells Diagnostic in stools Treat with oral/IV metronidazole Oral vancomycin if doesn’t work • • •
•
• • •
•
•
Case 4: Couple 1 week hx of watery diarrhoea, foul smelling stools and gas/abdo cramps Cysts and trophozoites • •
E. coli (traveller’s diarrhea) Can infect adults/kids Virulence factors affects severity ETEC: enterotoxigenic – traveller’s diarrhea, no invasion/inflammation EIEC: invasive ! necrosis and inflammation, blood and pus in stool EHEC: causes HUS • • •
•
•
•
Giardia • • • •
Eastern Europe/Russia Hikers MSM Bloating, abdo pain, malabsorption of protein
Nina Cooper
•
•
•
Fat and fould smelling non-bloody diarrhea Pear shaped trophozite cysts found in stool Treat with metronidazole
Entamoeba Histolytica Flask-shaped ulcers Bloody diarrhea RUQ pain (liver absecesses) • • •
EPONYMOUS SYNDROMES
Case 1: 20yo man Hemisection spinal cord Cannot move right leg but responds to pain Cannot feel pain in left leg • • •
•
Brown Séquard Syndrome Spinothalamic tract: crosses at level of SC Contralateral loss of fine touch/pain/temperature •
•
Case 2: 49M Increased urination and thirst Weakness and muscle cramps
EMQ Lecture Notes
• • • • •
Stiff hands, wrists and feet Pain worse in morning Palpable spleen Low neutrophils Raised CRP
Felty’s Syndrome Rheymatoid arthritis Splenomegaly Neutropenia • • •
Case 4: 55M A&E Confused Gaze palsy Thiamine started immediately Condition improves significantly days later • • • • • •
Wernicke’s encephalopathy Chronic alcoholism/severe nutritional deficiency Opthalmoplegia (horizontal nystagmus) Confusion Ataxia •
•
• •
• • •
Conn’s Syndrome Cushing’s Syndrome Syndrome: outside pit Disease: within pituitary
Because thiamine is a cofactor for the enzymes responsible for glucose metabolism, infusion of glucose will exacerbate the pre-existing thiamine deficiency precipitates Wernicke’s encephalopathy.
• •
Korsakoff’s Syndrome Irreversible Anterograde and retrograde amnesia Confabulation •
Nelson’s Cushing’s within pituitary Post bilateral adrenalectomy for pituitary adenoma High cortisol levels pre-surgery ! suppressed CRH Lowered cortisol ! increased CRH Unchecked growth of pituitary adenoma Hyperpigmentation (POMC) ! alpha… • •
•
• •
•
Wermer’s: MEN1 Sipple’s: MEN2
Case 3: 30F A&E • •
•
•
Case 5: 34 M asthmatic Wrist drop Eosinophilia and auto- antibodies to neutrophil myeloperoxidase • • •
Churg-Strauss Syndrome Small vessel vasculitis Palpable purpura Peripheral neuropathy (wrist, foot drop) Eosinophilia Late onset asthma • • •
• •
Nina Cooper
•
•
Histology: granulomatosis vasculitis P-ANCA (myeloperoxidase)
EMQ Lecture Notes
•
•
Case 6: 42F Spinning sensation Nausea and ringing in left ear Always uses right ear when using phone Feels fine between episodes • • • •
•
Ménière’s Disease Inner ear disorder Increased volume of endolymph Spontaneous episodic vertigo Unilateral tinnitus Unilateral sensorineural hearing loss Treat by relieving pressure • • • • •
•
Case 7: 32M Weakness and tingling Started in feet, now at knees Getting worse 2/5 strength in both legs, absent reflexes in knees PMHx: resp infection • • • • •
•
Guillain Barre Syndrome 1-28 days post resp/GI infection: CMV/EBV/campylobacter Molecular mimicry to myelin = autoimmune response to peripheral nerves Motor > sensory Ascending symmetrical paralysis Can affect autonomic NS ! cardiac irregularitis, HTN/HypoTN LP find albumino-cytological dissociation Mechanical ventilation, treatment with IVIG/plasma exchange •
•
• • •
•
•
Case 8: 2 weeks post MI Central chest pain, worse lying down and on inspiration Friction rub on auscultation • •
•
Dressler’s Syndrome Autoimmune 1 week ! few months post MI • •
Pericarditis: sharp, pleuritic chest pain, pericardial friction rub and pleural effusions on XR Give aspirin
Nina Cooper
EMQ Lecture Notes
Emergencies & Harder EMQs ULCERS
• • •
Case 1 • • •
• •
65M Painful wound on leg Knocked on coffee table 4 weeks ago ABPI = 1.1 Appears to have eczema
ABPI • • • • •
Venous • • • • • • •
•
Painful Shallow Flat Pink base Granulation tissue Normal ABPI Due to venous insufficiency (deep or superficial) Lipodermatosclerosis + haemosiderin deposition
• • • •
>1.0 normal <0.3 = impending gangrene 0.3-0.6: pain at rest 0.9-0.6: claudication Falsely high ABPI if incompressible vessels
Case 4 • • • • •
45m Sore on finger Painless Well defined borders Small flat spot that grew and became an open wound
Infective Typical of syphilis 3-90 day incubation period Chancre of primary syphilis Painless Well-defined Singular Firm Lesion appears at point of contact •
Case 2 •
Same sites as neuropathic Distal sites Paucity of hair, shiny skin, pale, nail dystrophy
65F Wound on heel Punched appearance 0.5cm deep Doesn’t hurt
• • • • • • •
Neuropathic Alcoholic, diabetes Microvascular angiogpathy and peripheral neuropathy Punched out Painless Deep Pink base Tips of toes/heels/malleoli • •
• •
Case 5 • • •
• • •
17M Melaena Admitted to hospital with severe burns
Curling’s Ulcer Acute duodenal ulcer Mucosal sloughing after plasma volume depletion • •
Case 3 • • • • •
70M Painful wound on dorsum Smoked for 40 years Punched out appearance Intermittent claudication
• • •
Case 1 • •
Arterial •
EMERGENCIES
Painful Cold Pulseless Fibrotic base
•
•
65M Headaches and tender scalp Stiff and painful shoulders in the morning for 2 weeks Jaw hurts when chewing
Nina Cooper
EMQ Lecture Notes
Prednisolone 40-60mg/d PO Temporal arteritis Pain due to assoc. with polymyalgia rheumatic Risk of sudden blindness Raised ESR, CRP, platelets Temporal artery biopsy Tx: decrease prednisolone after 57 days; continue for 2 days • •
• •
Case 4 • • • •
• •
Case 2 • • • • •
22M Known epilepsy Having seizure Started convulsing 30 mins ago >1 seizure, did not regain consciousness
55M Massive haematemesis Low BP, tachycardic 5 th finger of hand is bent close to palm
Terlipressin 2mg SC qds Oesophageal Varcies Shocked? (HR>100, BP <100, postural drop, urine output <30ml/hr) Yes: haemodynamically stabilise then endoscopy No: 2 big cannulae, resuscitate, endoscopy Terlipressin: vasopressin analogue splanchnic vasoconstrictor Then balloon tamponade •
•
•
•
100% oxygen Always do ABC Status epilepticus: seizures >30 mins without intervening consciousness Mortality and brain damage increase with attack length Aim to stop in <20mins Remember, not only tonic-clonic •
•
•
•
•
ACUTE ASHTMA MANAGEMENT
Case 1 • •
•
Same 22 year old man is still convulsing ! Lorazepam
2-4mg IV bolus
• •
13M 6/12 hx of coughing at night and wheeze Otherwise well Small for his age
Inhaled short-acting beta 2 agonist
Case 2 Wait 2 minutes and repeat previous treatment - still convulsing ! Phenytoin
IV
• • • • • •
Anaesthetist arrives ! General
Anaesthetic
• • •
•
Oxygen + short-acting B2 agonist (nebulised) + steroids Severe asthma 60% oxygen via facemask Back to back nebs Systemic steroids Monitor PEFR every 15 mins Serial ABGs • •
Case 3 •
25F Known asthma A&E ! SOB Widespread wheeze Too breathless to talk HR 115, RR 36
33F A&E after RTA Chest pain Right side is hyperresonant and reduced breath sounds Trachea is deviated to the left
Large-bore cannula to 2nd ICS, midclavicular line
• • • •
Case 3 • •
12F Poorly controlled asthma
Nina Cooper
•
•
EMQ Lecture Notes
Managed with LABA, monteleukast monteleukast and high dose steroids Mother asks if there is any other medication she can take?
Oral Steroids Moving from step 4 •
! step
5
• •
25F, pregnant Mild asthma Refuses to put any chemicals into her body as she has read it might harm the baby
Breathing techniques
Case 5 • • • •
•
35M A&E with SOB Barely talk, silent chest, RR:36 Improvement with oxygen, salbutamol nebs and steroids Peak flow still only 30% of best
IV magnesium sulphate Acute severe and not responding re sponding to treatment Or if life-threatening attack •
•
CALCIUM/PARATHYROID Case 1 • • • •
Significantly raised PTH
Secondary Hyperparathyroidism Hyperparathyroidism Poor kidney function ! calcium loss Loads of PTH produced but kidneys still cannot function well enough to retain Ca Therefore high PTH and low Ca Assoc. with renal osteodystrophy •
•
• •
Case 4 •
•
Case 3 • • • • •
40F Thyroidectomy Thyroidectomy yesterday Tingling lips General weakness Ca 1.8
Hypoparathyroidism Trousseau’s and Chvostek’s sign High phosphate, low Ca • •
Case 4 • • • • •
75M Weight loss, haemoptysis Smoking hx Corrected calcium of 2.8mmol/l Low PTH
PTHrp secretion Assoc. with squamous cell tumours Common cause of raised calcium in malignancy Treat with fluids and bisphosphonates If refractory: use calcitonin •
•
•
50M Polyuria, constipation, lethargy Corrected calcium 2.8 (2.2-2.6) PTH is significantly raised
•
Case 5 •
Primary Hyperparathyroidism Hyperparathyroidism High PTH, high Ca PTH can be normal, but this is inappropriate if the Ca is high Usually benign parathyroid adenoma Classical bone disease: osteitis fibrosa cystica
•
• •
• •
25F CRF has a corrected corrected Calcium of 2.6mmol Phosphate of 2.1 Significantly raised PTH
•
•
Tertiary Hyperparathyroidism History of CRF PTH significantly raised, raised Ca Autonomous function of of parathyroid glands after secondary stage • • •
Case 2 • •
• •
10F Chronic renal failure secondary to PKD Corrected Ca of 1.9 Phosphate of 2.5 (0.7-2.4)
Nina Cooper
EMQ Lecture Notes
Case 4
SBAS
•
Case 1 •
•
Benzodiazepine Benzodiazepine OD
Flumazenil Do not give if mixed BZD+TCA, as TCAs reduce seizure threshold •
Irregular rhythm Sawtooth pattern
Atrial Flutter Flutte r Re-entry circuits in atria Shows a heart block (1:2/3/4) • •
Case 5 Case 2 • • •
•
Afebrile pt ! blood blood results Markedly raised ALP Ca is 2.5
Tall prominent P in leads II, III and aVF
Right atrial hypertrophy P pulmonale Due to cor pulmonale Tall peaked p wave Lead II •
Paget’s disease of the bone Headache Back pain Hat doesn’t fit Isolated raised ALP • • • •
• • •
LA hypertrophy P mitrale Bifid P wave split into 2 and prolonged Best in V1 •
Other sources of ALP ALP: osteoblast action, liver, placenta, kidneys Signs of biliary obstruction (ALP > AST/ALT) •
•
•
•
LVH •
ECG SIGNS
• •
Case 1 • •
Sinus tachycardia S I, T III, Q III
Pulmonary Embolus Pain, SOB, tachycardia •
• • •
Flattened T waves Wide PR and U waves Also ST depression depre ssion
Hypokalaemia Hyperkalaemia: tall, tented T waves, flat P waves, wide QRS Hypocalcaemia: prolonged QT, symptoms of low Ca (tetany, carpopedal spasm)
•
Anterior MI
Case 7 Pathologic J waves
Hypothermia
Case 8 • • •
Tall R waves ST depression Inverted T waves in leads V1-3
Posterior MI ANTIHYPERTENSIVES
ST elevation in all leads
• •
Pericarditis Saddle shaped in all leads •
ST elevation in V1-6
Case 1
Case 3 •
Case 6
•
Case 2
Deep S in V1/2 Tall R in V5/6 LAD
• •
58M GP ! BP BP 220/100 Smoker Smoothly enlarged prostate, PSA normal
Nina Cooper
Doxazosin Enlarged prostate Give alpha 1 blocker ! for BPH • •
Case 2 Obese 47F 170/90 Blood glucose 11.3 Cholesterol 6.9
• • • •
Ramipril
Case 3 32F 24 weeks gestation Lethargy and malaise BP 160/80 Protein in urine
• • • • •
Methyldopa Alpha 2 agonist ag onist Only antihypertensive antihypertensive safe in pregnancy • •
Case 4 62 smoker Episodic chest pain Relieved by rest Normal glucose BP 160/90
• • • • •
Atenolol • •
Got angina Therefore give beta blocker to treat HTN and angina
Case 5 • • • •
•
86 male 6 weeks post MI Dry cough Aspirin, metoprolol, metop rolol, lisinopril and GTN spray GP stops lisinopril and exchanges it for another
Losartan
EMQ Lecture Notes
Nina Cooper
EMQ Lecture Notes
Treatment of Status Epilepticus ABC: Basic Resus
100% O2
IV Phenytoin – General Anaesthesisa ! Paralysis ! Ventilation
18mg/kg at rate of <50mg/min
Or IV Diazepam - 100MG IN 500ML OF 5% DEXTROSE
IV Cannula
Correction of hypotension, glucose etc. Give thiamine if alcoholism suspected
BENZODIAZEPINE: IV lorazepam, PO midazolam, IV/PR diazepam
Chromosomal Syndromes Name Down’s Syndrome
Abnormality Trisomy 21
• • • •
Edward’s Syndrome
Trisomy 18
• • • • • • • •
Patau Syndrome
Trisomy 13
• • • • •
Turner’s Syndrome
45X
• • • • • •
Klinefelter’s Syndrome
47XXY
• • • •
Key Features Epicanthal folds Round face Small eyes Single palmar crease
Small head Mostly female Cleft lip/palate Multiple heart defects Widely spaced eyes Ptosis Rocker bottom feet nd rd Webbed 2 /3 toe
Polydactyly Cyclopia Low set ears Abnormal genitalia Dextrocardia
Webbed neck Amenorrhoea Short stature Wideley spaced nipples Visual problems Hearing loss
Hypogonadism Small testicles Low testosterone Gynaecomastia
Image
DiGeorge Syndrome
Microdeletion at 22q11
•
• • • • •
William’s Syndrome
Microdeletion at 7q11
• • • • •
Cri-du-Chat
5p deletion
• • • • •
Triple X Syndrome
47 XXX
Congenital heart disease Palate defect Learning disability Recurrent infections Hypertelorism Characteristic facial features Elfin facial appearance Low nasal bridge Mental disability Heart defect Visuo-spacial disability
Cat-like cry Unusual facial features Behavioural problems Hypotonia Microcephaly
Not distinguishable from other females
Hyponatraemia Anorexia, nausea, malaise, headache, irritability, confusion, weakness, seizures, cardiac failure, oedema Dehydrated Not Dehydrated Urine osmolality Oedematous >20mmol/L: Nephrotic syndrome Addison’s Cardiac failure Renal failure Cirrhosis Diuretic excess Renal failure Osmolar diuresis Urine Osm >500 SIADH Urine osmolality <20mmol/L Osm <500mmol/kg, no Diarrhoea oedema Vomiting Water overload Fistulae Severe Burns hypothyroidism Trauma Glucocorticoid CF insufficiency Heat •
•
•
•
•
•
•
•
Hypernatraemia Lethargy, thirst, weakness, irritability, confusion, coma, fits + signs of dehydration Water loss in excess of Na loss Diarrhoea, vomiting, burns Excess Saline Diabetes insipidus Osmotic diuresis Primary aldosteronism • • • • •
•
Give water po or 5% dextrose IV
• •
•
•
•
• •
•
• •
Hypokalaemia K < 2.5mmol/L
K+ >6.5mmol
Muscle weakness, hypotonia, hyporeflexia, cramps, tetany, palpitations, arrhythmia
Fast irregular pulse, chest pain, weakness, palpitations, light-headedness
Small/inverted T waves, prominent U waves, prolonged PR, depressed ST
Tall tented T waves, small P waves, broad QRS, ventricular fibrillation
Causes
Causes
• • • • • • •
Diuretics D&V Cushing’s/steroids/ACTH Conn’s syndrome Alkalosis Bulimia Renal tubular failure
Treatment: oral K Hypocalcaemia SPASMODIC: S: spasms P: periorbital paraesthesiae A: anxious, irritable S: seizures M: muscle tone increased in smooth muscle (colic, wheeze, dysphagia) O: orientation impaired, confusion D: dermatitis I: impetigo herpetiformis C: chvostek’s sign • • • • •
• • • •
Hyperkalaemia
• • • • • • •
Treatment: underlying cause Hypercalcaemia “Bones, Stones, Groans, Moans” Abdominal pain Vomiting Constipation Polyuria/polydipsia Depression Anorexia, Weight loss Tiredness, Weakness HTN Confusion Renal stones/failure Ectopic calcification • • • • • • • • • • •
Raised Phosphate
Oliguric renal failure K-sparing diuretics Rhabdomyolysis Metabolic acdisosis Addison’s Burns ACE-I
• • • • • •
CKD Hypoparathyroidism Pseudohypoparathyroidism Acute rhabdomyolysis Vitamin D deficiency Hypomagnesaemia
Causes • • • • • •
Normal/low Phosphate Osteomalacia Acute pancreatitis Over-hydration Resp alkalosis
•
•
•
•
•
Malignancy Primary hyperparathyroidism Renal failure Addison’s TB Vitamin D overdose Raynaud’s Muscle tumour Endocrine tumours
• •
Urea Urea: waste product
Creatinine Indicative of renal function
Causes of hyperuricaemia: Drugs: cytotoxics, thiazides, loop diuretics, pyrazinamide Increased Cell Turnover: lymphoma, leukaemia, psoriasis, haemolsis, rhabdomyolysis, tumour lysis syndrome Reduced Excretion: primary gout, CKD, hyperparathyroidism, pre-eclampsia Other: htn, hyperlipidaemia
Rise = damage to nephrons – therefore use to monitor levels of kidney disease GFR: more sensitive indication of degree of renal impairment
Urate precipitation in renal tubules renal failure
ACIDOSIS
ALKALOSIS Metabolic Respiratory High pH, high HCO3 High pH, low CO2
Metabolic Low pH, low HCO3
Respiratory Low pH, High CO2
Raised Anion Gap Increased production/decrease d excretion of fixed/organic acids Lactic acid (shock. Infection, tissue ischaemia) Urate (renal failure) Ketones (DM, alcohol) Drugs/toxins (salicylates, biguanides, methanol)
T2 Respiratory failure Vomiting Most commonly Hypokalaemia COPD Burns Ingestion of base
•
•
• •
•
Normal Anion Gap Loss of HCO3/ingestion of H+ Renal tubular •
•
Hyperventilation
