Nursing Oral Revalida Reviewer

EAVALMONTE

DISEASE

SIGNS AND SYMPTOMS

LAB LA B FI FIND NDIN INGS GS

PATH PA THOP OPHY HYSI SIOL OLOG OGY Y

Diagnosis 1.History taking & PE 2. ECG – ST segment depression & T wave inversion 3. Stress test – treadmill = abnormal ECG 4. Serum cholesterol & uric acid increase 5. Cardiac catheterizationProvides the MOST DEFINITIVE source of diagnosis by showing the presence of the atherosclerotic lesions

atherosclerosis ↓ reduced coronary tissue perfusion ↓ diminished myocardial oxygenation ↓ anaerobic metabolism ↓ increased lactic acid production ↓ chest pain

ANGINA PECTORIS-

A clinical syndrome characterized by paroxysmal chest pain usually relieved by REST or NGT nitroglycerin, nitroglycerin, resulting from temp myocardial ischemia. Predisposing Predisposing Factor: 1. sex – male 2. black raise 3. hyperlipidemia hyperlipidemia 4. smoking 5. HPN 6. DM 7. oral contraceptive contraceptive prolonged 8. sedentary lifestyle 9. obesity 10.hypothyroidism Precipitating factors 4 E’s 1. Excessive physical exertion 2. Exposure to cold environment Vasoconstriction 3. Extreme emotional

1. Initial symptoms – Levine’s sign – hand clutching of chest 2. Chest pain – sharp, stabbing excruciating pain. Location – substernal -radiates back, shoulders, axilla, arms & jaw muscles -relieve by rest or NGT 3. Dyspnea 4. Tachycardia 5. Palpitation 6.diaphoresis 7. Dizziness and syncope

DRUG STUDY/ NRSG RESPONSIBILIT IES 1. Nitroglycerine1.) Enforce CBR 2.) Administer meds 1st dose NTG – NTG – small doses – give 3 – 5 min venodilator 2nd dose NTG – 3 Large dose – – 5 min vasodilator 3rd & last dose – 3.) Administer O2 3 – 5 min inhalation Still painful after 4.) Semi-fowler 3rd dose – notify 5.) Diet- Decrease doc. MI! Keep in Na and saturated a dry place. fats Avoid moisture & 6.) Monitor VS, I&O, heat, may ECG inactivate the 7.) HT: Discharge drug. planning: 2. Monitor S/E: a. Avoid orthostatic precipitating factors hypotension – – 4 E’s dec bp b. Prevent transient complications – MI headache c. Take meds before dizziness physical exertion-to 3. Rise slowly achieve maximum from sitting therapeutic effect of position 4. ASPIRIN drug B. Beta d. Importance of blockers – follow-up care. propanolol Administer with foods NURSING INTERVENTIONS

EAVALMONTE response 4. Excessive intake of food –

DISEASE MYOCARDIAL INFARCTION – heart attack – terminal stage of CAD - Characterized by necrosis & scarring due to permanent malocclusion Predisposing factors 1. sex – male 2. black raise 3. hyperlipidemia hyperlipidemia 4. smoking 5. HPN 6. DM 7. oral contraceptive contraceptive prolonged 8. sedentary lifestyle 9. obesity 10. hypothyroidism hypothyroidism 11. obesity 12. stress

SIGNS AND SYMPTOMS



1. chest pain – excruciating, vice like, visceral pain located substernal or precodial area (rare) - radiates back, arm, shoulders, axilla, jaw & abd muscles. - not usually relived by rest r NTG 2. dyspnea 3. erthermia 4. initial increase/decre ase in BP/tachybrady 5. mild restlessness &

1. ECG- the ST segment is ELEVATED. T wave inversion, ECG tracing – ST segment increase, widening or QRS complexes – means arrhythmia in MI indicating PVC 2. Myocardial enzymeselevated Creatinine Phospokinase, Lactic acid dehydrogenase and Troponin levels 3. CBC- may

Interrupted coronary blood flow ↓ myocardial ischemia ↓ anaerobic myocardial metabolism for several hours ↓ myocardial death ↓ depressed cardiac function ↓ triggers autonomic nervous system response ↓ further imbalance of myocardial O2 demand and supply

NURSING INTERVENTIONS

1. Narcotic analgesics – Morphine SO4 – to induce vasodilation vasodilation & decrease levels of anxiety. 2. Administer O2 inhalation – low inflow (CHF-increase (CHF-increase inflow) 3. Enforce CBR without BP a.) Bedside commode 4. Avoid valsalva maneuver 5. Semi fowler 6. General liquid to soft diet – decrease Na, saturated fat, caffeine 7. Monitor VS, I&O & ECG tracings 8. Take 20 – 30 ml/week – wine,

C. ACE inhibitors – captopril D. Ca antagonist nefedipine DRUG STUDY/ NRSG RESPONSIBILIT IES

1. ANALGESIC The choice is MORPHINE SULFATE It reduces pain and anxiety Relaxes bronchioles to enhance oxygenation 2. Vasodilators Vasodilators 1. NTG 2. Isordil - Antiarrythmic Antiarrythmic 1. LYDOCAINE blocks release of norepenephrine 2. Brithylium - Beta-blockers – lol 1. Propanolol (inderal) - ACE inhibitors pril Prevents

EAVALMONTE

DISEASE

CONGESTIVE HEART FAILURE(LEFT) Inability of the heart to pump sufficiently - Backflow Predisposing factors: 1.) 90% mitral valve stenosis – due RHD, aging RHD affects mitral valve – streptococcal streptococcal infection Dx: - Aso titer – anti streptolysine O > 300 total units - Steroids - Penicillin - Aspirin

apprehensions 6. occasional findings a.) split S1 & S2 b.) pericardial friction rub c.) rales /crackles d.) S4 (atrial gallop)

show elevated WBC count 4. Test after the acute stage- Exercise tolerance test, thallium scans, cardiac catheterization 5. serum cholesterol & uric acid increase

SIGNS AND SYMPTOMS

LAB FINDINGS

1. Dyspnea 2. Orthopnea (Diff of breathing sitting pos – platypnea) 3. Paroxysmal nocturnal dysnea – PNOnalulunod 4. Productive cough with blood tinged sputum 5. Frothy salivation 6. Cyanosis

CXR may reveal cardiomegaly 2. ECG may identify Cardiac hypertrophy 3. Echocardiogra m may show hypokinetic heart 4. ABG and Pulse oximetry may show decreased O2 saturation 5. PCWPPulmonary

brandy/whisky to induce vasodilation. vasodilation. 9. Assist in surgical; CABAG

formation of angiotensin II Limits the area of infarction 1. Captopril – - Ca – antagonist 1. Nifedipine - Thrombolitics or fibrinolytics– fibrinolytics– to dissolve clots/ thrombus

PATHOPHYSIOLOGY


DRUG STUDY/ NRSG RESPONSIBILIT IES

LEFT Ventricular pump failure ↓ back up of blood into the pulmonary veins ↓ increased pulmonary capillary pressure ↓ pulmonary congestion

1. Administer meds 2. Administer O2 inhalation – high! @ 3 -4L/min via nasal cannula 3. High fowlers 4. Restrict Na! 5. Provide meticulous skin care 6. Weigh pt daily. Assess for pitting edema. Measure abdominal girth daily & notify MD 7. Monitor V/S, I&O, breath sounds

M – morphine SO4 to induce vasodilatation A– aminophylline & decrease anxiety D – digitalis (digoxin) D - diuretics O - oxygen G - gases

LEFT ventricular failure ↓ decreased cardiac output ↓ decreased perfusion to

EAVALMONTE Complication: Complication: RS-CHF Aging – degeneration / calcification of mitral valve Ischemic heart disease 1. CAD 2. Valvular heart diseases 3. Hypertension Hypertension 4. MI 5. Cardiomyopathy Cardiomyopathy 6. Lung diseases 7. Post-partum 8. Pericarditis and cardiac tamponade

DISEASE

CONGESTIVE HEART FAILURE(RIGHT) Inability of the heart to pump sufficiently sufficiently - Backflow Predisposing factor 1. 90% - tricuspid stenosis 2. COPD 3. Pulmonary embolism

7. Rales/ crackles – due to fluid 8. Bronchial wheezing 55 9. PMI – displaced lateral – due cardiomegaly 10. Pulsus alternons – weak-strong pulse 11. shock 12. S3 – ventricular gallop 13.cerebralan oxia 14. Oliguria SIGNS AND SYMPTOMS

Capillary Wedge Pressure is increased in LEFT sided CHF and CVP is increased in RIGHT sided CHF 6. ABG – PCO2 increase, PO2 decrease = = hypoxemia = resp acidosis

the brain, kidney and other tissues ↓ oliguria, dizziness

8. Institute bloodless phlebotomy. Rotating tourniquet or BP cuff rotated clockwise q 15 mins = to promote decrease venous return 9. Diet – decrease salt, fats & caffeine

LAB FINDINGS

PATHOPHYSIOLOGY



1. Peripheral dependent, pitting edema 2. Weight gain 3. Distended neck vein 4. hepatomegaly 5. Ascites

Diagnosis: 1. CXR – cardiomegaly 2. CVP – measures the pressure at R atrium Normal: 4 to 10 cm of water Increase CVP >

RIGHT ventricular failure ↓ blood pooling in the venous circulation ↓ increased hydrostatic hydrostatic pressure ↓ peripheral edema

1. Administer meds 2. Administer O2 inhalation – high! @ 3 -4L/min via nasal cannula 3. High fowlers 4. Restrict Na! 5. Provide meticulous skin care 6. Weigh pt daily.

a.) Cardiac glycosides Increase myocardial = increase CO Digoxin (Lanoxin). Antidote: digivine Digitoxin: metabolizes in

EAVALMONTE 4. Pulmonic stenosis 5. Left sided heart failure

DISEASE

HYPERTENSIONA systolic BP greater than 140 mmHg and a diastolic pressure greater than 90 mmHg

SIGNS AND SYMPTOMS

1. Headache 2. Visual changes 3. chest pain

10 – hypervolemia Decrease CVP <4– hypovolemia Flat on bed – post of pt when giving CVP Position during CVP insertion – Trendelenburg to prevent pulmonary embolism & promote ventricular filling. 3.Echocardiogr aphy – enlarged heart chamber / cardiomyopath y 4.Liver enzyme SGPT ( ALT)

RIGHT ventricular failure ↓ blood pooling ↓ venous congestion in the kidney, liver and GIT

Assess for pitting edema. Measure abdominal girth daily & notify MD 7. Monitor V/S, I&O, breath sounds 8. Institute bloodless phlebotomy. Rotating tourniquet or BP cuff rotated clockwise q 15 mins = to promote decrease venous return 9. Diet – decrease salt, fats & caffeine

liver not in kidneys not given if with kidney failure. b.) Loop diuretics: Lasix – effect with in 1015 min. Max = 6 hrs c.) Bronchodilators: Aminophillin (Theophyllin). Avoid giving caffeine d.) Narcotic analgesic: Morphine SO4 induce vasodilaton & decrease anxiety e.) Vasodilators – NTG f.) Antiarrythmics arrythmics – Lidocaine

LAB FINDINGS

PATHOPHYSIOLOGY



1. Health history and PE 2. Routine laboratory-

1. Health history and PE 2. Routine laboratory-

Diuretics Beta blockers Calcium channel blockers

EAVALMONTE over a sustained period, based on two or more BP measurements. Primary HPN- Idiopathic Secondary HPN- Due to other conditions like Pheochromocytoma, renovascular hypertension, Cushing’s, Conn’s , SIADH Major Risk factors 1. Smoking 2. Hyperlipidemia Hyperlipidemia 3. DM 4. Age older than 60 5. Gender- Male and post menopausal W 6. Family History 7. Smoking 8. Obesity 9. High salt intake 10. Low potassium intake

4. dizziness 5. N/V 6. Blurring of vision 7. Epistaxis

urinalysis, urinalysis, ECG, lipid profile, BUN, serum creatinine , FBS 3. Other labCXR, creatinine clearance, 24huour urine protein

urinalysis, ECG, lipid profile, BUN, serum creatinine , FBS 3. Other lab- CXR, creatinine clearance, 24-huour urine protein 4. Avoid stress. 5. Provide information information about anti-hypertensive drugs Instruct proper compliance and not abrupt cessation of drugs even if pt becomes asymptomatic/ improved condition 6. Promote Home care management Instruct regular monitoring of BP Involve family members in care Instruct regular follow-up

ACE inhibitors A2 Receptor blockers Vasodilators -nadolol(corgard) -metoprolol (lopressor) clonidine(catapre ss) -hydralazine (apresoline) captopril(capoten ) diltiazem(cardize m) nifedipine(calcibl oc) -verapamil

EAVALMONTE DISEASE

BUERGER DISEASEAcute inflammatory disorder affecting small to medium sized arteries & veins of lower extremities. extremities. Male/ feet

Predisposing factors: - Male - Smokers

SIGNS AND SYMPTOMS

LAB FINDINGS

1. Intermittent claudication claudication – leg pain upon walking Relieved by rest 2. Cold sensitivity & skin color changes White bluish Pallor cyanosis red rubor 3. Decrease or diminished peripheral pulses - Post tibial, Dorsalis pedis 4. Tropic changes 5. Ulcerations 6. Gangrene formation

1. Oscillometry – decrease peripheral pulse volume. 2. Doppler UTZ – decrease blood flow to affected extremities. 3. Angiography – reveals site & extent of malocculsion.

PATHOPHYSIOLOGY


1. Encourage a slow progression of physical activity a.) Walk 3 -4 x / day b.) Out of bed 2 – 3 x a / day Inflammation Inflammation of the 2. Meds arteries a.) Analgesic ↓ b.) Vasodilator thrombus formation c.) Anticoagulant Anticoagulant ↓ 3. Foot care mgt like occlusion of the vessels DM – a.) Avoid walking barefoot b.) Cut toe nails straight c.) Apply lanolin lotion – prevent skin breakdown d.) Avoid wearing constrictive garments 4. Avoid smoking & exposure to cold environment 5. Surgery: BKA (Below the knee amputation) 6. Stop smoking.

Cause is UNKNOWN Probably an Autoimmune disease


-Pentoxyfylline (Trental) reduces blood viscosity and improves supply of O2 blood to muscles -Cilostazol (Pletaal) inhibits platelet aggregation and increases vasodilatation

EAVALMONTE

DISEASE

BRONCHIAL ASTHMAreversible inflammation lung condition due to hyerpsensitivity hyerpsensitivity leading to narrowing of smaller airway.

1. Extrinsic Asthma – called Atropic/ allergic asthma a.) Pallor b.) Dust c.) Gases d.) Smoke 64 e.) Dander f.) Lints 2. Intrinsic AsthmaCause: HeredItary Drugs – aspirin, penicillin, b blockers Food additives – nitrites Foods – seafood, chicken, eggs, chocolates, milk Physical/ emotional

SIGNS AND SYMPTOMS

1. C – cough – non productive to productive 2. D – dyspnea 3. W – wheezing on expiration 4. Cyanosis 5. Mild apprehension & restlessness 6. Tachycardia & palpitation 7. Diaphoresis

LAB FINDINGS

1. Pulmo function test – decrease lung capacity 2. ABG – PO2 decrease

PATHOPHYSIOLOGY


1. CBR – all COPD 2. Medsa.) Bronchodilator through inhalation or metered dose inhaled / pump. Give 1 s t before corticosteroids b.) Corticosteroids – due inflammatory. Given 10 min after adm bronchodilator bronchodilator c.) Mucolytic/ expectorant d.) Mucomist – at bedside put suction machine. e.) Antihistamine Antihistamine 2. Force fluid 3. O2 – all COPD low inflow to prevent resp distress 4. Nebulize & suction 5. Semifowler – all COPD except emphysema due


EAVALMONTE stress Sudden change of temp, humidity &air pressure

late stage 6. HT a.) Avoid pred factors b.) Complications: Complications: c.) Adherence to medications

3. Mixed type

DISEASE

PANCREATITISacute or chronic inflammation of pancreas leading to pancreatic edema, hemorrhage & necrosis due to auto digestion. Bleeding of pancreas Cullen’s sign at umbilicus Predisposing factors: 1. Chronic alcoholism 2. Hepatobilary disease 3. Obesity 4. Hyperlipidemia Hyperlipidemia 5. Hyperparathyroidism Hyperparathyroidism 6. Drugs – Thiazide diuretics, pills Pentamidine HCL (Pentam) 7. Diet – increase saturated fats

SIGNS AND SYMPTOMS

LAB FINDINGS

1. Severe Lt epigastric pain – radiates from back &flank area - Aggravated by eating, with DOB 2. N/V 3. Tachycardia 4. Palpitation due to pain 5. Dyspepsia – indigestion 6. Decrease bowel sounds 72 7. (+) Cullen’s sign ecchymosis of umbilicus hemorrhage 8. (+) Grey

1. Serum amylase & lipase – increase 2. Urine lipase – increase 3. Serum Ca – decrease 4. WBC 5. UTZ

PATHOPHYSIOLOGY



Autodigestion Autodigestion of 1. Administer meds. pancreatic tissue 2. Withold food & ↓ fluid – aggravates Hemorrhage, Necrosis pain and Inflammation Inflammation 3. Assist in Total ↓ Parenteral Nutrition KININ ACTIVATION will (TPN) or result to increased hyperalimentation permeability Complications Complications of ↓ TPN Loss of Protein-rich fluid 1. Infection into the peritoneum 2. Embolism HYPOVOLEMIA 3. Hyperglycemia Hyperglycemia 4. Institute stress mgt tech a.) DBE b.) Biofeedback 5. Comfy position Knee chest or fetal like position 6. If pt can tolerate food, give increase CHO, decrease fats,

a.) Narcotic analgesic Meperidine Hcl (Demerol) Don’t give Morphine SO4 – will cause spasm of sphincter. b.) Smooth muscle relaxant/ anti cholinergic - Ex. Papavarine Hcl Prophantheline Bromide (Profanthene) c.) Vasodilator – NTG d.) Antacid – Maalox e.) H2 receptor antagonist Ranitidin

EAVALMONTE Turner’s spots – ecchymosis of flank area 9. Hypocalcemia

DISEASE

APPENDICITISInflammation Inflammation of the vermiform appendix

ETIOLOGY: usually fecalith, lymphoid hyperplasia, foreign body and helminthic obstruction

and increase CHON 7. Complications: Complications: Chronic hemorrhagic pancreatitis

(Zantac) to decrease pancreatic stimulation f.) Ca – gluconate


SIGNS AND SYMPTOMS

LAB FINDINGS

PATHOPHYSIOLOGY


1. Abdominal pain: begins in the umbilicus then localizes in the RLQ (Mc Burney’s point) 2. Anorexia 3. Nausea and Vomiting 4. Fever 5. Rebound tenderness and abdominal rigidity (if perforated) 6. Constipation

1. CBC- reveals increased WBC count 2. Ultrasound 3. Abdominal Xray

Obstruction of lumen ↓ increased pressure ↓ decreased blood supply ↓ bacterial proliferation and mucosal inflammation ↓ Ischemia ↓ Necrosis ↓ rupture

1. Preoperative care NPO Consent Monitor for perforation and signs of shock Monitor bowel sounds, fever and hydration status POSITION of Comfort: RIGHT SIDELYING in a low FOWLER’S Avoid   

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EAVALMONTE or diarrhea

Laxatives, enemas & HEAT APPLICATION 2. Post-operative Post-operative care Monitor VS and signs of surgical complications Maintain NPO until bowel function returns If rupture occurred, expect drains and IV antibiotics 

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DISEASE IRON DEFICIENCY ANEMIAResults when the (dietary intake of) iron is inadequate to produce hemoglobin Causes: 1. Increase demand for Iron- rapid growth in

SIGNS AND SYMPTOMS



1. Pallor of the skin and mucous membrane 2. Weakness and fatigue 3. General malaise 4. Pica

1. CBC- Low levels of Hct, Hgb and RBC count 2. low serum iron, low ferritin 3. Bone marrow aspirationMOST definitive

Decreased stores of iron ↓ depletion of hemoglobin synthesis ↓ reduced oxygen carrying capacity ↓ tissue hypoxia



1. Provide iron richfoods -Organ meats (liver) -Beans -Leafy green vegetables -Raisins and molasses 2. Administer iron

1. Oral Iron -FeSO4- 325mg (65mg) -Fe Fumarate 325mg (107mg) -Treatment for 612 mos. Iron should not 

EAVALMONTE infancy and adolescence, pregnancy, EPO tx. 2. Increase Iron Lossmenstruation, menstruation, blood donation, bleeding 3. Decrease iron intake or absorption- Crohn’s disease, postgastrectomy, gastrectomy, acute or chronic inflammation 

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5. Brittle nails 6. Smooth and sore tongue 7. Angular cheilosis

4. Fecalysis w/ occult blood

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1mg iron lost daily due to exfoliation of skin and mucous cells Ave loss in menstruation is 50ml or 0.7mg/day Pregnancy req. 25mg/day

DISEASE APLASTIC ANEMIAA condition characterized by decreased number of RBC as well as WBC and

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Oral preparations tablets- Fe fumarate, sulfate and gluconate Advise to take iron ONE hour before meals (to optimize absorption) Practice good oral hygiene

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be taken with antacid because it decreases absorption Take it with vitamin C It stains teeth Drink it with a straw

2. Treat the cause 3. Blood Transfusion

SIGNS AND SYMPTOMS

1. Fatigue 2. pallor 3. dyspnea 4.bruising or



1. CBCdecreased blood cell numbers

Toxins cause a direct bone marrow depression ↓


1. Assess for signs of bleeding and infection 2. Instruct to avoid


1. Bone marrow transplantation 2. Immunosupressa

EAVALMONTE platelets Causes:

bleeding 5. retinal hemorrhages 6. Infection

1. Environmental toxinspesticides, benzene 2. Certain drugsChemotherapeutic agents, chloramphenicol, phenothiazines, Sulfonamides 3. Heavy metals 4. Radiation 5. Idiopathic

DISEASE

SIGNS AND SYMPTOMS

2. Bone marrow aspiration confirms the anemiahypoplastic or acellular marrow replaced by fats


Acellular bone marrow exposure to ↓ offending agents decreased production of blood elements ↓ PANCYTOPENIA



nt drugs 3. Rarely, steroids 4. Blood transfusion


SICKLE CELL ANEMIA-

-Results from

1. Anemia – Hgb 7-10g/dL

1. Anemia – Hgb 7-10g/dL

Low O2 ↓

1. Manage the pain -Support and

1. No safe and effective tx

EAVALMONTE inheritance of sickle hgb 2. Jaundice gene (HbS) from both 3. Enlarged parents bones in the -The RBC change shape, skull and face upon deoxygenation deoxygenation 4. because of Tachycardia, polymerization polymerization of the cardiac abnormal sickle murmurs and hemoglobin. cardiomegally -This process damages 5. Thrombosis the red blood cell which may membrane causing affect any sickling or cresent organs shape 6. -abN hgb leads to Splenomegaly chronic hemolytic 7. schemic anemia manifesting at 1 symptoms yr. causing back -SC crisis occurs at high and chest altitude, unpressurized pains planes, strenuous 8. Non-healing exercise and resp. ulcers infections 3 Nsg priority 1. a/w – avoid deoxygenating deoxygenating activities - High altitude is bad 2. Fluid deficit – promote hydration 3. Pain & comfort

cause defective hemoglobin to acquire a rigid, crystal-like Cshaped configuration configuration ↓ Sickled RBCs will adhere to endothelium ↓ pile up and plug the vessels ischemia results ↓ pain, swelling and fever

elevate acutely inflamed joint -Relaxation techniques Analgesics 2. Prevent and manage infection -Monitor status of patient -Initiate prompt antibiotic therapy 3. Promote coping skills -Provide accurate information -Allow patient to verbalize her concerns about medication, prognosis and future pregnancy 4. Monitor and prevent potential complications -Provide always adequate hydration -Avoid cold, temperature that may cause vasoconstriction

2. BM transplant BT in ACS, strokes, Pregnancy 3. Hydroxyureainduces production of HgbF

EAVALMONTE

DISEASE FOLIC ACID DEFICIENCY (MEGALOBLASTIC ANEMIA)-anemias characterized by abnormally large RBC secondary to impaired DNA synthesis due to deficiency of Folic acid and/or vitamin B12 Causes:

1. Alcoholism 2. Malabsorption Malabsorption 3. Diet deficient in vegetables, or excessively heated or cooked with large amount of water 4. Long term anticonvulsant medication 5. Use of antimetabolites 6. Increased folate demand states as pregnancy and growth spurts like infancy and adolescence

SIGNS AND SYMPTOMS

1. Easy fatigability 2. Pallor 3. Dyspnea 4. Chest pain 5. Light headedness 6.Tachycardia or palpitations



1. Blood smear 2. Bone marrow examination 3. Serum folate <150ng/ml 4. Schillings test normal 5. (-) neurologic manifestations

Decreased folic acid ↓ impaired DNA synthesis in the bone marrow ↓ impaired RBC development, impaired nuclear maturation but CYTOplasmic maturation continues ↓ large size


1. Folic acid supplementation 1 mg/day oral supplementation 2. Dietary enhancement: Foods rich in Folate: asparagus,broccoli, spinach, lettuce,banana,liver, organ meats, peas,beans and nuts


EAVALMONTE

DISEASE VITAMIN B12 DEFICIENCY (PERNICOUS ANEMIA) -Vitamin B12 deficiency+ intrinsic factor deficiency= Pernicious Anemia

- megaloblastic, megaloblastic, chronic anemia due to deficiency of intrinsic factor leading to Hypochlorhydria – decrease Hcl acid secretion. Lifetime B12 injections. With CNS involvement.

SIGNS AND SYMPTOMS

LAB FINDINGS

PATHOPHYSIOLOGY

1. weakness, fatigue, listlessness 2. Neurologic manifestations due to affected neuromyelination . E.g. Paresthesias in the extremities, extremities, loss of balance and position sense 3. Gastric manifestation: weight loss, anorexia, N/V, diarrhea/constipa tion, steatorrhea 4. Smooth, sore

1. Peripheral blood smearshows giant RBCs, WBCs with giant hypersegmented nuclei 2. Very high MCV 3. Schilling’s test (shows absorption of tagged B12) 4. Intrinsic factor antibody test

↓Intrinsic factor production by the parietal cells of the stomach ↓ ↓Vitamin b12 absorption ↓ ↓RBC production ↓ ↓DNA Synthesis in maturing RBC ↓ Impairment of integrity of cells (mouth, stomach, anus, vagina,)



1. Enforce CBR 2. Diet – high high calorie or CHO. Increase CHON, iron & Vit C 3. Avoid irritating mouthwashes. mouthwashes. Use of soft bristled toothbrush is encouraged. 4. Avoid applying electric heating pads – can lead to burns 5. Provide assistance in ambulation 6. Avoid too much heat and cold

1. Administer B12 injections at monthly intervals for lifetime as ordered. IMdorsogluteal or ventrogluteal. Not given oral – due pt might have tolerance to drug

EAVALMONTE -Intrinsic factor binds with Vit. B12 to promote absorption in the terminal ileum

beefy tongue

Causes:

1. Strict vegetarian diet 2. Gastrointestinal malabsorption such as Crohn's disease, Gastrectomy and ileal resection 3. Absence of intrinsic factor DISEASE

SIGNS AND SYMPTOMS

LAB FINDINGS

1. Skin is ruddy 2. Splenomegaly 3. headache 4. dizziness, blurred vision 5. Angina, dyspnea and thrombophlebitis

1. CBC- shows elevated RBC mass 2. Normal oxygen saturation 3 Elevated WBC and Platelets

PATHOPHYSIOLOGY



1. Primary role of the nurse is EDUCATOR 2. Regularly asses for the development of complications 3. Assist in weekly phlebotomy 4. Advise to have cool or tepid bath for itchiness and use cocoa butter based lotion 5. Advice to avoid alcohol intake to

1. To reduce the high blood cell massPHLEBOTOMY 2. Hydroxyureadecrease marrow function 3. Allopurinoldecrease uric acid caused by increase in cell turn over 4. Dipyridamole/AS A- decrease viscousity of

POLYCTHEMIA-

-Refers to an INCREASE volume of RBCs -The hematocrit is ELEVATED to more than 55% -The overproduction of red blood cells may be due to a primary process in the BM or it may be a reaction to chronically low O2 level or, rarely, a malignancy -Classified as Primary or Secondary

Myeloproliferative d/o, hypoxia ↓ The stem cells grow uncontrollably ↓ The bone marrow becomes HYPERcellular and all the blood cells are increased in number ↓ -Blood becomes thick and viscous causing sluggish circulation Increased blood

EAVALMONTE viscosity causes thromboembolism

decrease risk of bleeding

Causes:

-Organ infiltration causes hepato,splenomegaly

-Secondary polycythemia - caused by either natural or artificial increases in the production of erythrocytes -Physiologic polycythemia occurs in individuals living at high altitudes -Other causes include smoking, renal or liver tumors, or heart or lung diseases that result in hypoxia

DISEASE IDIOPATHIC THROMBOCYTOPENI A PURPURA-Autoimmune disorder in which IgG is formed that binds the platelet -Platelet with Ab is destroyed as it passes the spleen and by

blood 5. Chemotherapy to suppress bone marrow

-Capillary overdistention overdistention causes rupture, then hemorrjage, hemorrjage, then hypovolemia.

SIGNS AND SYMPTOMS

LAB FINDINGS

1. Platelet count less than 20T 2. Easy bruising 3. Heavy menses Petechiae and Ecchymoses of skin 4. Bleeding from mucous

1. Platelet count decreases, mild anemia 2. BMA: increase megakaryocyt es

PATHOPHYSIOLOGY

Viral illness, Pregnancy, SLE, Sulfa drugs ↓ Antibody (Ab) Formation ↓ Ab attaches to platelet ↓ Platelet destruction by WBC and Spleen ↓



1. Prevent bruising Treatment 2. Protect from started when infection there is bleeding 3. Administer meds or Platelet count orally, rectally or IV of <10T even rather than IM; hold w/o bleeding pressure on site for 1. Stop the 5 mins medication that 4. Avoid aspirin caused ITP 5. Provide client 2.

EAVALMONTE Macrophages -Destruction of platelets result in count less than 100,000/mm3

membranesmouth, GIT and lungs spleen not enlarge

Decrease Platelet ↓ Hematoma/ecchymosis/bl eeding

Causes:

-Exact cause is unknown but sometimes associated with: Viral illness, SLE and pregnancy, sulfa drugs

DISEASE

SIGNS AND SYMPTOMS

LAB FINDINGS

PATHOPHYSIOLOGY

teaching and discharge planning 6. Pad crib and playpen 7. Provide soft toys 8. Provide protective headgear during toddlerhood 9. Use soft toothbrush 10. Avoid contact sports

Immunosuppress ion- block the binding receptor on macrophages so that platelets are not destroyed Prednisone, Cyclophosphami de, Azathioprine 3. Splenectomyeffective only in 50% of patients IV immunoglobulinalso binds receptors 4. Chemotheraphy(Vincristine) binds receptors



HEMOPHILIA-

-Two clinically indistinguishable disease characterized characterized by bleeding disorder due to genetic defect

1. Bleeding in soft tissues, muscles and weight bearing joints 2. Bleeding in any body parts

1. prolonged PTT, decrease Factor VIII or IX level

1. Educate about their condition 2. Teach about activity restrictions to decrease episodes of trauma and bleeding

BT- FFP, cryoprecipitate, FVIII&IX conc.

EAVALMONTE -Gene is carried by females and manifest only in males -Frequently dx at birth due to cepalhematoma and bleeding after circumcision

3. Avoid medications medications such as ASA, NSaids, alcohol 4. Avoid injections 5. Precaution on Dental procedures 6. Patients should be encouraged to wear identifications identifications bands 7. Warm compress are avoided

-Hemophilia A -Hemophilia B

DISEASE PEPTIC ULCER DISEASE

-Excoriation / erosion of submucosa & mucosal lining due to: a.) Hypercecretion of acid – pepsin

SIGNS AND SYMPTOMS

According to location 1. Stress ulcer 2. Gastric ulcer 3. Duodenal ulcer – most common

LAB FINDINGS

1. Endoscopic exam 2. Stool from occult blood 3. Gastric analysis – N – gastric

PATHOPHYSIOLOGY

Disturbance in acid secretion and mucosal protection ↓ Increased acidity or decreased mucosal resistance


Nursing Mgt: 1. Diet – bland, non irritating, non spicy 2. Avoid caffeine & milk/ milk products Increase gastric acid secretion


1. Antacids 2. H2 receptor antagonist Ex 1. Ranitidine (Zantac) 2. Cimetidine

EAVALMONTE b.) Decrease resistance to mucosal barrier Causes: 1. Hereditary 2. Emotional 3. Smoking – vasoconstriction – GIT ischemia 4. Alcoholism – stimulates release of histamine = Parietal cell release Hcl acid = ulceration 5. Caffeine – tea, soda, chocolate 6. Irregular diet/rapid eating 7. Ulcerogenic drugs – NSAIDS, aspirin, steroids, indomethacin, ibuprofen Indomethacin Indomethacin - S/E corneal cloudiness. Needs annual eye check up. 9. Gastrinoma 10. Microbial invasion – helicobacter pylori. DISEASE

Increase – duodenal 4. GI series – confirms presence of ulceration

↓ erosion and ulceration

3. Administer meds 4. Maintain patent IV line 4. VS, I&O & bowel sounds 5. Complications: a.) Hemorrhage – hypovolemic shock Late signs – anuria b.) Peritonitis c.) Paralytic ileus – most feared d.) Hypokalemia e.) Thromobphlebitis f.) Pernicious anemia

(Tagamet) 3. Tamotidine (Pepcid) - Avoid smoking – decrease effectiveness of drug - Administer antacid & H2 receptor antagonist – 1hr apart -Cemetidine decrease antacid absorption & vise versa Cytoprotective agents Ex 1. Sucralfate (Carafate) Provides a paste like subs that coats mucosal lining of stomach 2. Cytotec

SIGNS AND SYMPTOMS

LAB FINDINGS

PATHOPHYSIOLOGY


LIVER CIRRHOSIS-

Early sign –

1. Liver

Inflammation Inflammation causes liver

1. 1. CBR


EAVALMONTE -lost of architectural architectural design of liver leading to fat necrosis & scarring Causes:

1. Chronic alcoholism 2. Malnutrition – decreaseVit B, thiamin - main cause 3. Virus – 4. Toxicity- eg. Carbon tetrachloride 5. Use of hepatotoxic agents

hepatic encephalopathy 1. Asterixis – flapping hand tremors Late signs – headache, restlessness, disorientation, decrease LOC – hepatic coma. Early signs: a.) Weakness, fatigue b.) Anorexia, n/v c.) Stomatitis d.) Urine – tea color Stool – clay color e.) Amenorrhea f.) Decrease sexual urge g.) Loss of pubic, axilla hair h.) Hepatomegaly i.) Jaundice j.) Pruritus or urticaria

enzymesincrease SGPT (ALT) SGOT (AST) 2. Serum cholesterol & ammonia increase 3. Indirect bilirubin increase 4. CBC pancytopenia 5. PTT – prolonged 6. Hepatic ultrasonogram – fat necrosis of liver lobules

parenchymal cell destruction ↓ Fibrotic changes causes obstruction of hepatic blood flow and normal liver function ↓ Obstruction causes of hepatic blood flow and normal liver function ↓ Decreased liver function results changes in the body ↓ Decreased absorption and utilization of vit. Adek -ineffective detoxification of protein wates

2. Restrict Na! 3. Monitor VS, I&O 4. With pt daily & assess pitting edema 5. Measure abdominal girth daily – notify MD 6. Meticulous skin care 71 7. Diet – increase CHO, vit & minerals. Moderate fats. Decrease CHON Well balanced diet 8. Complications: a.) Ascites – fluid in peritoneal cavity Nursing Mgt: 1. Meds: Loop diuretics – 10 – 15 min effect 2. Assist in abdominal paracentesis paracentesis aspiration of fluid - Void before paracentesis paracentesis to prevent accidental puncture of bladder as trochar is inserted

EAVALMONTE

DISEASE CHOLECYSTITIS/ CHOLELITHIASIS-

- Inflammation of gallbladder with gallstone formation. Predisposing factor:

1. High risk – women 40 years old 2. Post menopausal women – undergoing estrogen therapy 3. Obesity 4. Sedentary lifestyle 5. Hyperlipidemia Hyperlipidemia 6. Neoplasm

SIGNS AND SYMPTOMS

LAB FINDINGS

1. Severe Right abdominal pain (after eating fatty food). Occurring especially at night 2. Fatty intolerance 3. Anorexia, n/v 4. Jaundice 5. Pruritus 6. Easy bruising 7. Tea colored urine 8. Steatorrhea

1. Oral cholecystogra m (or gallbladder series)confirms presence of stones

PATHOPHYSIOLOGY

Supersaturated bile, Biliary stasis ↓ Stone formation ↓ Blockage of Gallbladder ↓ Inflammation, Mucosal Damage and WBC infiltration ↓ Less bile in the duodenum ↓ Impaired fat digestion and absorption ↓ Vitamin ADEK malabsorption, STEATORHEA with increased gas formation Jaundice ACHOLIC stools



1. Meds – a.) Narcotic analgesic Meperdipine Hcl – Demerol b.) Anti cholinergic Atropine SO4 c.) Anti emetic Phenergan – Phenothiazide with anti emetic properties 2. Diet – increase CHO, moderate CHON, decrease fats 3. Meticulous skin care 4. Surgery: Cholecystectomy Nursing Mgt post cholecystectomy -Maintain patency of T-tube intact & prevent infection

a.) Narcotic analgesic Meperdipine Hcl – Demerol b.) Anti cholinergic Atropine SO4 c.) Anti emetic Phenergan – Phenothiazide with anti emetic properties

EAVALMONTE

DISEASE ULCERATIVE COLITIS-

-Ulcerative and inflammatory condition of the GIT usually affecting the large intestine -The colon becomes edematous and develops bleeding ulcerations -Scarring develops overtime with impaired water absorption and loss of elasticity Causes:

unknown

SIGNS AND SYMPTOMS

1. Anorexia 2. Weight loss 3. Fever 4. SEVERE diarrhea with Rectal bleeding 5. Anemia 6. Dehydration Dehydration 7. Abdominal pain and cramping

LAB FINDINGS

1. Sigmoidoscop y- increased mucosal friability, decreased mucosal detail, thick inflammatory exudates, edema, erosion 2. Stool specimenpositive for blood and mucus

PATHOPHYSIOLOGY

Inflammation edema of the mucous membrane of the colon and rectum leads to bleeding and shallow ulcerations ↓ Abscess formation causes bowel-wall shortening, thinning, fragility, hypermotility, hypermotility, and decreased absorption ↓ Mucosal ulcerations begin in the distal end of the colon and ascend the large intestine


1. Maintain NPO during the active phase 2. Monitor for complications complications like severe bleeding, dehydration, electrolyte imbalance 3. Monitor bowel sounds, stool and blood studies 4. Restrict activities 5. Administer IVF, electrolytes electrolytes and TPN if prescribed 6. Instruct the patient to AVOID gas-forming foods, MILK products and foods such as whole grains, nuts, RAW fruits and vegetables especially SPINACH, pepper, alcohol and caffeine 7. Diet progressionclear liquid LOW


Aminosalicylic agents

EAVALMONTE

DISEASE

DISSEMINATED INTRAVASCULAR COAGULATION- Acute hemorrhagic syndrome char by wide spread bleeding & thrombosis due to a def of clotting factors (Prothrombin & Fibrinogen

Predisposing factor: 1. Rapid BT 2. Massive trauma 3. Massive burns 4. Septicemia 5. Hemolytic reaction 6. Anaphylaxis Anaphylaxis 7. Neoplasia – growth of new tissue 8. Pregnancy

SIGNS AND SYMPTOMS

LAB FINDINGS

1. Petechiae – widespread & systemic (lungs, lower & upper trunk) 2. Ecchymosis – widespread 3. Oozing of blood from venipunctured site 4. Hemoptysis – cough blood 5. Hemorrhage 6. Oliguria – late sx

1. CBC – reveals decrease platelets 2. Stool for occult blood (+) Specimen – stool 3. Opthalmoscopi c exam – sub retinal hemorrhage 4. ABG analysis – metabolic acidosis

PATHOPHYSIOLOGY

residue, high protein diet 8. Administer drugsanti-inflammatory, antibiotics, antibiotics, steroids, bulk-forming agents and vitamin/iron supplements NURSING INTERVENTIONS

1. Monitor signs of bleeding – hema test + urine, stool, GIT 2. Administer isotonic fluid solution to prevent shock. 3. Administer O2 inhalation 4. Administer meds 47 a. Vit K aquamephyton b. Pitressin or vasopressin – to conserve water. 5. NGT – lavage - Use iced saline lavage 6. Monitor NGT output 7. Provide heplock


Vit K aquamephyton Pitressin or vasopressin – to conserve water.

EAVALMONTE 8. Prevent complication: hypovolemic shock Late signs of hypovolemic shock : anuria

DISEASE SIGNS AND SYMPTOMS ADDISON’S DISEASE-

-Steroids-lifetime Decreased adrenocortical hormones leading to: -a.) Metabolic disturbances (sugar) b.) F&E imbalancesimbalancesNa, H2O, K c.) Deficiency of neuromuscular function (salt & sex) Predisposing Factors:

1. Atrophy of adrenal gland 2. Fungal infections 3. Tubercular

1. T – tremors, tachycardia I - irritability R - restlessness E – extreme fatigue D – diaphoresis, depression 2. Decrease sexual urge or libidoDecreased Androgen 3.Loss of pubic and axillary hair 4. Pathognomonic sign– bronze like skin pigmentation due to decrease cortisol will

LAB FINDINGS

1. FBS – decrease FBS (N 80 – 120 mg/dL) 2. Plasma cortisol – decreased Serum Na – decreased (N 135 – 145 meg/L) 3. Serum K – increased (N 3.5 – 5.5 meg/L)

PATHOPHYSIOLOGY

Autoimmune Autoimmune theory: body produces antibodies, resulting in adrenal hypofunction Decreased aldosterone causes disturbances in sodium, water, and potassium metabolism Decreased cortisol causes abnormal metabolism of fat, protein, and carbohydrate



1. Monitor VS 2. Adm meds 3. Diet – increase calorie or CHO Increase Na, Increase CHON, Decrease K 4. Force fluid 5. Administer isotonic fluid as ordered 6. Meticulous skin care – due to bronze like 7. HT & discharge planning a) Avoid precipitating precipitating factors leading to Addisonian crisis 1. Sudden withdrawal crisis

Administer meds a.) Corticosteroids Corticosteroids (Decadron) or Dexamethazone - Hydrocortisone (cortisone)Prednisone 1. Adm 2/3 dose in AM & 1/3 dose in PM in order to mimic the normal diurnal rhythm. 2. Taper the dose (w/draw, gradually from drug) – sudden withdrawal can lead to addisonian crisis 3. Monitor S/E

EAVALMONTE infections Complication of Addison’s dse : Addisonian crisis 16. Results the acute exacerbation of Addison’s dse characterized by : Hypotension, hypovolemia, hyponatremia, hyponatremia, wt loss, arrhythmia DISEASE

CUSHING’S SYNDROME-

-increase secretion of adrenocortical hormone Predisposing Factors: 1. Hyperplasia of adrenal gland 2. Tubercular infection – milliary TB

stimulate pituitary gland to release melanocyte stimulating hormone.

SIGNS AND SYMPTOMS

LAB FINDINGS

1. Increase sugar – Hyperglycemia 3 P’s 1. Polyuria 2. Polydipsia – increase thirst 3. Polyphagia – increase appetite Classic Sx of DM – 3 P’s & glycosuria + wt loss 2. Increase susceptibility to infection – due to increased

1. FBS – increase↑ (N: 80-120mg/dL) 2. Plasma cortisol increase 3. Na – increase (135145 meq/L) 4. K- decrease (3.5-5.5 meq/L)

PATHOPHYSIOLOGY

2. Stress 3. Infection b) Prevent complications Addisonian crisis & Hypovolemic shock 8. Hormonal replacement therapy – lifetime 9. Important: follow up care

(Cushing’s syndrome S/Sx) a.) HPN b.) Hirsutism c.) Edema d.) Moon face & buffalo hump e.) Increase susceptibility susceptibility to infection sue to steroids- reverse isolation



1. Monitor VS, I&O 2. Administer meds 3. Restrict Na 4. Provide Dietary intake – low in CHO, low in Na & fats High in CHON & K 5. Weigh pt daily & assess presence of edema- measure abdominal girthnotify doc. 6. Reverse isolation 7. Skin care – due acne & striae 8. Prevent complication - Most feared –

a. K- sparing diuretics (Aldactone) Spironolactone - promotes excretion of NA while conserving potassium Not lasix due to S/E hypoK & Hyperglycemia!

EAVALMONTE corticosteroid 3. Hypernatrermia a. HPN b. Edema c. Wt gain d. Moon face Buffalo hump Hypokalemia Hirsutism – increase sex 6. Acne & striae 7. Increase muscularity of female

arrhythmia & DM (Endocrine disorder lead to MI – Hypothyroidism & DM) 9. Surgical bilateral Adrenolectomy 10. Hormonal replacement therapy – lifetime due to adrenal gland removal- no more corticosteroid!

DISEASE SIGNS AND SYMPTOMS

LAB FINDINGS

1. Increase in appetite – hyperphagia – wt loss due to increase metabolism 2. Skin is moist - perspiration 3. Heat intolerance 4. Diarrhea – increase motility 5. All VS

1. Serum T3 & T4 increased 2. Radio iodine uptake – increase 3. Thyroid scan – reveals enlarged TG

PATHOPHYSIOLOGY



HYPERTHYROIDISM

-Graves dse or thyrotoxicosis ( everything up except wt and mens) -Increased T3 & T4 Predisposing factors:

1. Autoimmune disease – release of long acting thyroid stimulator (LATS)

Increased thyroid 1. Monitor VS & I & O – hormones determine presence of ↓ thyroid storm or most Increased metabolic feared complication: rate, oxygen Thyrotoxicosis consumption, 2. Administer meds sympathetic activity and 3. Diet – increase cns function, altered calorie – to correct wt protein, fat, loss carbohydrate 4. Skin care – metabolism 5. Comfy & cool ↓ environment Changes in the body 6. Maintain siderailsdue

1. Prophylthiuracil (PTU) 2. Methymazole (Tapazole) Most toxic s/e agranulocytosisfever, sore throat, leukocytosis=inc wbc: check cbc and throat swab culture Most feared

EAVALMONTE Exopthalmos Enopthalmos – severe dehydration depressed eye 2. Excessive iodine intake 3. Hyperplasia of TG

increase = HPN, tachycardia, tachypnea, hyperthermia 6. CNS changes 8. Irritability & agitation, restlessness, tremors, insomnia, hallucinations 7. Goiter 8. Exopthalmos – pathognomonic sx 9. Amenorrhea

agitation/restlessness 7. Provide bilateral eye patch – to prevent drying of eyesexopthalmos 8. Assist in surgery – subtotal thyroidectomy Complication- thyroid storm


complication : Thrombosis – stroke CVS

LAB FINDINGS

PATHOPHYSIOLOGY



HYPOTHYROIDISM-decrease secretion of T3, T4 – can lead to MI / Atherosclerosis Atherosclerosis Adult – myxedema Child- cretinism – only endocrine dis lead to mental retardation Predisposing factor:

Early signs – 1. weakness and fatigue 2. Loss of appetite – increased lypolysis – breakdown of fats causing 3. atherosclerosis

1. Serum T3 T4 decrease 2. Serum cholesterol increase – can lead to MI 3. RA IU – radio iodine uptake – decrease

1. Monitor VS. Levothyroxine Check for s/sx of Thyroglobulin cardiovascular disorder. 2. Monitor daily weigh. 3. Diet, decrease calorie, increase fiber 4. Provide warm environment environment during

EAVALMONTE

1. `Iatrogenic causes – caused by surgery 2. Atrophy of TG due to: a. Irradiation b. Trauma c. Tumor, inflammation 3. Iodine def 4. Autoimmune – Hashimoto disease

= MI Wt gain 5. Cold intolerance – myxedema coma Constipation Late Sx – brittle hair/ nails Non pitting edema due increase accumulation of mucopolysachar ide in SQ tissue -Myxedema Horseness voice Decrease libido Decrease VS – hypotension bradycardia, bradypnea, and hypothermia Lethargy Memory impairment

cold climate. 5.


LAB FINDINGS

PATHOPHYSIOLOGY



DM TYPE 1-

-“Juvenile “ onset, common in children, non-obese “brittle dse”

1.) Polyuria 2.) Poydipsia 3.) Polyphagia 4.) Glycosuria 5.) Weight loss

1. FBS- > 126 2. RBS- >200 3. OGTT- > 200

Destruction of BETA cells ↓ decreased insulin production ↓

1. Insulin Therapy 2. Diet 3. Exercise 4. Regular Glucose Monitoring

Insulin Route: Subq -Do not massage site of injection.

EAVALMONTE -Insulin dependent diabetes mellitus Causes:

1. 90% hereditary – total destruction of pancreatic dells 2. Virus 3. Toxicity to carbon tetrachloride 4. Drugs – Steroids both cause hyperglycemia Lasix - loop diuretics

6.) Anorexia 7.) N/V 8.) Blurring of vision 9.) Increase susceptibility to infection 10.) Delayed/ poor wound healing

uncontrolled glucose production by the liver ↓ Hyperglycemia ↓ signs and symptoms Complication: DKA


-Store at room temp or ref. -Shake before using.

LAB FINDINGS

PATHOPHYSIOLOGY

1. FBS- > 126 2. RBS- >200 3. OGTT- >

Decreased insulin production ↓


DM TYPE 2-

-A type of DM characterized by

1. Asymptomatic 2. 3 P’s and 1G

1. Diet 2. Exercise 3. Regular Glucose


EAVALMONTE insulin resistance and impaired insulin production

200

Causes:

1. Unknown 2. Probably genetic and obesity

diminished insulin action ↓ Hyperglycemia ↓ signs and symptoms

Monitoring 4. Oral Hypoglycemic Agents (OHA)

Complication: HONKC H – hyper O – osmolar N – non K – ketotic C – coma


LAB FINDINGS

PATHOPHYSIOLOGY


PLACENTA PREVIA-

-it occurs when the

1. Abrupt, painless , bright

Ultrasound

Fertilized ovum ↓

1. Monitor vital signs & bleeding


EAVALMONTE placenta is improperly red vaginal implanted in the lower bleeding. uterine segment, sometimes covering TYPES: the cervical os. Abnormal 1. Low-lying – lower implantation of implantation of placenta. the placenta in - candidate for CS the lower rather than in the Causes: upper portion of the uterus 1. Increased parity 2. Marginal – 2. Advanced maternal placenta edge age approaches that 3. Past cesarian births of the cervical 4. Past uterine os curettage 3.partial – 5. Multiple gestations implantation 6. Decreased that occludes a vascularity vascularity of upper portion of the uterine segment cervical os 7. Use of cocaine 4. Complete ( totalis) – placenta that totally obstructs the cervical os

DISEASE

SIGNS AND SYMPTOMS

LAB FINDINGS

implantation implantation in uterus ↓ embryonic stage ↓ placenta arise in thropoblast tissues ↓ insufficient blood ↓ Placenta migrates to where there is sufficient blood supply ↓ placenta resides in lower part ↓ (low lying, total, partial, marginal) ↓ painless dark red bleeding ↓ Profuse bleeding ↓ Hypotension ↓ Hypovolemic shock ↓ Coma ↓ death

( weigh unused perineal pad, then weigh perineal pad soaked in blood, then subtract. The difference is the weight of the blood loss.) 2. Monitor fetal heart rate 3. Provide strict bed rest to minimize the risk to fetus. 4.observe for further bleeding episodes 5. Avoid vaginal examinations ( no ie). If ie is indicated, it should be done in a double set-up environment. ( meaning: or/dr) wherein the patient has already signed a consent form, preop

PATHOPHYSIOLOGY


DRUG STUDY/ NRSG

EAVALMONTE RESPONSIBILIT IES ABRUPTIO PLACENTA-it is the premature separation of the placenta form the implantation implantation site. It usually occurs after the twentieth week of pregnancy. Causes:

1.maternal hypertension ( chronic or pregnacy induced) 2. Advanced maternal age 3. Grand multiparity – more than 5 pregnancies 4. Trauma to the uterus 5. Sudden release of amniotic fluid that cause sudden decompression decompression of te uterus.

1. Painful dark red vaginal bleeding in covert type 2.painful bright red vaginal bleeding in overt type 3.hard, rigid, firm,board-like abdomen caused by accumulation of blood behind the placenta with fetal parts hard to palpate. 4. Abnormal tenderness due to distentionof the uterus with blood. 5. Sharp pain over the fundus as the placenta separates. 6. Signs of shock & fetal distress as the placenta separates.

Ultrasound

1. Infuse IV, prepare to administer blood 2. Type and crossmatch 3. Monitor FHR 4. Insert Foley 5. Measure blood loss; count pads 6. Report s/sx of DIC 7. Monitor v/s for shock 8. Strict I&O

EAVALMONTE


LAB FINDINGS

PATHOPHYSIOLOGY



1. Home management is allowed only if: A. Bp is 140/90 o below B. There is no proteinuria C. There is no fetal growth retardation D. The patient is not a young primipara. 2. Cbr 3. Diet should be high in protein & carbohydrates carbohydrates with moderate sodium restriction. 4. Provide detailed instructions about warning signs: A. Epigastric pain – aura to convulsion B. Visual disturbances C. Severe continuous

1. Hydralazine – ( apresoline ) antihypertensive 2. Magnesium sulfate ( mgso4) - drug of choice to treat & prevent convulsions. 3. Diuretics are not given & ivf is limited

ECLAMPSIA-

-with seizure! Increase BUN – glomerular damage. Provide safety. Causes:

1.maternal hypertension ( chronic or pregnacy induced) 2. Advanced maternal age 3. Grand multiparity – more than 5 pregnancies 4. Trauma to the uterus 5. Sudden release of amniotic fluid that cause sudden decompression decompression of te uterus.

1. All the signs & symptoms of preeclampsia 2. Convulsion followed by coma is the main difference of eclampsia & preeclampsia 3. Oliguria 4. Pulmonary edema

Actions of mgso4: Prevent convulsion B. Reduce blood pressure Check the following first before administering mgso4:

EAVALMONTE headache 5. A. Rest in left lateral position to promote blood supply to the placenta & the fetus. 6. Absence of pattelar reflex is sign of MGSO4 toxicity DISEASE SIGNS AND SYMPTOMS

LAB FINDINGS

1. BP decrease - Urine output - HR increase - Hct increase - Serum Na decrease - Serum K increase - Met acidosis Class: I. Partial Burn 1. 1 s t degree – superficial burns - Affects epidermis - Cause: thermal burn - Painful - Redness

(cont) II Full thickness Burns 1. Third & 4 th degrees burn - Affects all layers of skin, muscles, bones - Cause – electrical - Less painful - Dry, thick, leathery wound surface – known as ESCHAR – devitalized or

PATHOPHYSIOLOGY


Deep tendon reflex present +2 ( normal) 2. Rr should be at least 12 bpm 3. Urine output should be at least 30 ml/hr AntidoteCalcium Gluconate DRUG STUDY/ NRSG RESPONSIBILIT IES

BURNS-

- direct tissue injury caused by thermal, electric, chemical & smoke inhaled (TECS) Nursing Priority – infection (all kinds of burns) Head burn-priorityburn-prioritya/w 2nd priority for 1st & 2nd ° - pain 2nd priority for 3rd ° F&E Causes:

1. Therma Thermall- direct direct contact –

1. Home management is allowed only if: A. Bp is 140/90 o below B. There is no proteinuria C. There is no fetal growth retardation D. The patient is not a young primipara. 2. Cbr 3. Diet should be high in protein & carbohydrates carbohydrates with moderate sodium restriction. 4. Provide detailed instructions about

Mafenide acetate Morphine sulfate Lactated Ringers D5W

EAVALMONTE flames, hot grease, sunburn. 2. Electr Electric, ic, – wire wires s 3. Chem Chem.. – dir direc ectt contact – corrosive materials acids 4. Smok Smoke e – gas gas / fume inhalation

(erythema) & blanching upon pressure with no fluid filled vesicles 2. 2 nd degree – deep burns - Affects epidermis & dermis - Cause –chem. burns - very painful - Erythema & fluid filled vesicles (blisters)

necrotic tissue.


LAB FINDINGS

PATHOPHYSIOLOGY

1. Productive cough 2. Dyspnea at rest – due terminal 3. Anorexia & gen body malaise 4. Rales/ rhonchi 5. Bronchial wheezing 6. Decrease tactile fremitus

1. Pulmonary function test – decrease vital lung capacity 2. ABG – a.) Panlobular / centrolobular emphysema pCO2 increase pO2 decrease – hypoxema resp acidosis

Smoking ↓ Particle deposition in airways ↓ low level inflammatory response due to aging ↓ Disequilibrium between elastase and antielastase ↓ Destruction of elastic

warning signs: A. Epigastric pain – aura to convulsion B. Visual disturbances C. Severe continuous headache 5. A. Rest in left lateral position to promote blood supply to the placenta & the fetus. 6. Absence of pattelar reflex is sign of MGSO4 toxicity NURSING INTERVENTIONS


EMPHYSEMA-

-irreversible terminal stage of COPD - Characterized by inelasticity of alveolar wall leading to air trapping, leading to maldistribution maldistribution of gases. - Body will compensate over distension of thoracic cavity

1. CBR Aminophylline 2. Meds Theophylline 3. O2 – Low inflow 4. Force fluids Ventolin 5. High fowlers Salbutamol 6. Neb & suction 7. Institute Bricanyl P – posture Terbutaline E – end E – expiratory to Alupent prevent collapse of alveoli P – pressure

EAVALMONTE - Barrel chest

(should have vibration)– - There is progressive palpation – and irreversible “99”. Decreased alveolocapillary - with air or fluid destruction with 7. Resonance to abnormal alveolar hyperresonance enlargement causing – percussion alveolar wall 8. Decreased or destruction. The result diminished is INCREASED lung breath sounds compliance, 9. DECREASED oxygen Pathognomonic: diffusion and barrel chest – INCREASED airway increase post/ resistance! anterior diameter of Predisposing factor: chest 1. Smoking 10. Purse lip 2. Allergy breathing – to 3. Air pollution eliminated PCO2 4. High risk – elderly 11. Flaring of 5. Hereditary alai nares DISEASE SIGNS AND SYMPTOMS PLEURAL EFFUSION-

-referred to as ‘water on the lungs’ is the build up of excess fluid between the layers of the pleura of the lungs. The pleura

1. Dyspnea, dullness over affected area upon percussion, absent or decreased breath sounds

Blue bloaters b.) Panacinar/ Centracinar pCO2 decrease pO2 increase – hyperaxemia resp alkalosis Pink puffers

recoil ↓ Overdistention of alveoli ↓ Retention of CO2 ↓ Hypoxia and resp acidosis

8. HT a.) Avoid smoking

Complication: Pneumothorax – air in pleural space

LAB FINDINGS

PATHOPHYSIOLOGY

a. Chest x-ray positive if greater than 250 cc pleural fluid b. Pleural biopsy may reveal

Inflammation of airways ↓ Bronchial edema, increased mucus production, bronchoconstriction, bronchial spasm ↓


1. Assist with repeated thoracentesis. 2. Administer narcotics/sedatives as ordered to decrease pain. 3. Assist with


a. Antibiotics: either systemic or inserted directly into pleural space b. Fibrinolytic enzymes: trypsin,

EAVALMONTE are thin membranes that line the lungs and the inside chest cavity and act to lubricate and facilitate breathing. It is normally filled with 510 milliliters of serous fluid. Types: 1. TransudativeTransudativecaused by leaking into pleural space. This is caused by elevated pressure in or low protein content in the bld vessels/ CHF is a common cause.

over affected bronchogenic area, pleural carcinoma pain, dry cough, c. pleural friction Thoracentesis rub may contain 2. Pallor, blood if cause fatigue, fever, is cancer, and night pulmonary sweats (with infarction, or empyema) tuberculosis; positive for specific organism in empyema.

worsening of obstruction ↓ accumulation accumulation of fluids caused by oversecretion oversecretion ↓ multiplication of growth of microorganism ↓ Inflammation Inflammation in the epithelial wall ↓ fluid filled alveoli ↓ rupture of inflamed endothelial cells excess fluid accumulate in the pericardial space ↓ Pleural effusion

2. Exudative- results from leaky blood vessels caused by inflammation. inflammation. Often caused by lung disease, tb, pneumonia, drug reaction. DISEASE SIGNS AND SYMPTOMS

LAB FINDINGS

PATHOPHYSIOLOGY

1. Chest xraydifference between croup

Viral infection ↓ affects larynx and trachea

instillation of medication into pleural space (reposition client every 15 minutes to distribute the drug within the pleurae). 4. Place client in high-Fowler’s position to promote ventilation. 5. O2 6. ABG

streptokinase-. streptodornase to decrease thickness of pus and dissolve fibrin clots



CROUP-group of respiratory disease that often

1. Colds 2. low grade fever

1. Airway 2. Assess resp status

1. Antipyretic: Antipyretic: Acetaminophen to reduce fever

EAVALMONTE affects infants, and children under age 6, characterized by barking cough, whistling, stridor as the child breathes in, and hoarseness in the larynx. Types: 1. Larnygotracheobronch itis- acute viral infection of the larynx, bronchi, which causes obstruction below vocal cords. 2. Spasmodic laryngitis- sudden onset, occurring mainly at night and characterized by laryngeal obstruction at the level of vocal cord Causes: flu virus, adenovirus, rhinovirus, enterovirus, coxsacklevirus, measles virus, reovirus

3. stridor 4. seal bark cough 5. cyanosis 6. use of accessory muscles to breath 7. agitation 8. muffled voice 9. spontaneous cough

and epiglottis 2. Throat culturereveals identifies infectious agent and sensitivity to specific antimicrobial therapy 3. ABGreveals hypoxemia state that require oxygen therapy, decreased PH and changes and co2 levels indicating respiratory acidosis or failure in severe cases.

↓ subglottic edema ↓ airflow obstruction ↓ croup

3. NPO status 4. Immunization (haemophilus type B) 5. Facilitate hygiene 6. Proper hygiene 7. Administer meds

2. Bronchodilator to relax respiratory smooth muscle and relieve stridor 3. Corticosteroidsto reduce inflammation and edema around vocal cords 4. Antibiotics

EAVALMONTE

DISEASE TETRALOGY OF FALLOT-group of congenital heart conditions including pulmonic stenosis, ventricular hypertrophy, overriding aorta and ventricular septic defect.

Causes: 1. Unknown 2. Fetal alcohol syndrome

SIGNS AND SYMPTOMS

1. Rt ventricular hypertrophy 2. high degree of cyanosis 3. polycythemia 4. severe dyspnea – squatting position – relief , inhibit venous return facilitate lung expansion. 5. growth retardation – due no O2 6. tet spell or blue spellsshort episodes of hypoxia 7. syncope 8. clubbing of fingernails – due to chronic tissue hypoxia 9. mental retardation – due decreased O2 in brain




1. Chest X-raydecreased pulmonary vascular, enlarged right ventricle, a boot shape cardiac silhouette 3. Electrocardio Electrocardio graphy 4. diminished o2 saturation

atherosclerosis ↓ reduced coronary tissue perfusion ↓ diminished myocardial oxygenation ↓ anaerobic metabolism ↓ increased lactic acid production ↓ chest pain

1. O2 2. no valsalva maneuver , fiber diet laxative 3. morphine – hypoxia 4. propranolol – decrease heart spasms 5. palliative repair – BLT blalock taussig procedure Brock procedure – complete procedure


Morphine Propranolol

EAVALMONTE 10. boot shaped heart – x-ray

DISEASE RHEUMATIC HEART DISEASE-

SIGNS AND SYMPTOMS

Major Minor 1. polyarthritis -inflammation inflammation disease ff – multi joint an infection acquired by pain 1. group A Beta hemolytic arthralgia – strepto coccus joint pain -Affected body – cardiac 2. chorea – muscles and valves , sydenhamms musculoskeletal , CNS, chores or Integumentary st. vetaus Sorethroat before RHD dance-Aschoff – rounded purposeless nodules with nucleated involuntary cells and fibroblasts – hand and stays and occludes shoulder with mitral valve grimace 2. low grade fever 3. carditis – tachycardia erythema marginatum macular rashes SQ nodules 3. all lab




1. CBR 2. throat swab – culture and sensitivity 3. antibiotic mgt – to prevent recurrence 4. aspirin – antiinflammatory. Low grade fever – don’t give aspirin. S/E of aspirin: - Reyes syndrome – encephalopathyfatty infiltration of organs such as liver and brain


aspirin – antiinflammatory. Low grade fever – don’t give aspirin. S/E of aspirin: - Reyes syndrome – encephalopathyfatty infiltration infiltration of organs such as liver and brain

EAVALMONTE results increase antibody “ C reactive protein “ erythrocyte sedimentation rate “ anti streptolysin

Nursing Oral Revalida Reviewer

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