Pathology Flashcards

Question

``` Angina Means Due to Myocytes damage? Types ```

Answer 1

Chest pain due to ischemic myocardium 2° to coronary artery narrowing or spasm no myocyte necrosis Stable angina Prinzemetal(variant) angina Unstable angina

Answer 2

Stable—usually 2° to atherosclerosis exertional chest pain in classic distribution ST depression on ECG resolving with rest or nitroglycerin.

Answer 3

Chest painoccurs 2° to coronary artery spasm Occurs at rest transient ST elevation on ECG Known triggers include tobacco, cocaine, and triptans, but trigger is often unknown. Treat with Ca2+ channel blockers, nitrates, and smoking cessation (if applicable).

Answer 4

Increase in frequency or intensity of chest pain or any chest pain at rest. thrombosis with incomplete coronary artery occlusion +/− ST depression and/or T-wave inversion on ECG no cardiac biomarker elevation (unlike NSTEMI)

Answer 5

Distal to coronary stenosis, vessels are maximally dilated at baseline. Administration of vasodilators (e.g., dipyridamole, regadenoson) dilates normal vessels and shunts blood toward well-perfused areas flow and ischemia in poststenotic region. Principle behind pharmacologic stress tests.

Answer 6

Most often acute thrombosis due to rupture of coronary artery atherosclerotic plaque. Acute onset typical chest pain Autonomic symptoms Lasting more than1/2hr Not responding to rest or GTN transmural, ECG may show ST elevations (STEMI) subendocardial, ECG may show ST depressions (NSTEMI) Cardiac biomarkers are diagnostic.

Answer 7

Death from cardiac causes within 1 hour of onset of symptoms most commonly due to a lethal arrhythmia (e.g., ventricular fibrillation). Associated with CAD (up to 70% of cases), cardiomyopathy (hypertrophic, dilated), hereditary ion channelopathies (e.g., long QT syndrome, Brugada syndrome).

Answer 8

Progressive onset of HF over many years due to chronic ischemic myocardial damage

Answer 9

LAD>RCA>LCX ``` 0-4hrs 4-24hrs 1-3days 3-14days 2wks -several months ```

Answer 10

None None Arrythmias HF Cardiogenic shock

Answer 11

Gross- Dark mottling Pale with Tetrazonium stain ``` LM- Early coagulative necrosis- release of necrotic cell contents into blood edema hemorrhage wavy fibers. Neutrophils appear. ``` Reperfusion injury may cause contraction bands (due to free radical damage and hyper contraction from high Ca influx) Complications Arrythmia HF Cardiogenic shock

Answer 12

Gross- Hyperaemia LM- Extensive coagulative necrosis. Tissue surrounding infarct shows acute inflammation with neutrophils. Complications -post MI fibrinous pericarditis

Answer 13

Gross- Hypereamic border Pale yellow soft middle Softest on day 10(high risk of rupture) LM- Macrophages cause phagocytosis Granulation tissue formation in the border Complications - Free wall rupture -tamponade papillary muscle rupture -mitral regurgitation interventricular septal rupture - VSD LV pseudoaneurysm (risk of rupture).

Answer 14

Gross- Re canalized vessel White gray area LM- Contracted scar complete ``` Complications - Dressler syndrome(AI pericarditis) HF arrhythmias true ventricular aneurysm (risk of mural thrombus). ```

Answer 15

ECG ``` ST elevation (STEMI, transmural infarct) ST depression (NSTEMI) hyperacute (peaked) T waves T-wave inversion new left bundle branch block pathologic Q waves or poor R wave progression (evolving or old transmural infarct). ``` Trop I- more specific CK-MB Cardiac troponin I rises after 4 hours High for 7–10 days CK-MB rises after 6–12 hours Normal in 48 hours predominantly found in myocardium but can also be released from skeletal muscle. Useful in diagnosing reinfarction following acute MI because levels return to normal to normal after 48 hours.

Answer 16

STEMI More necrosis Affects entire wall ST elevation on ECG, Q waves NSTEMI Subendocardial infarcts Due to ischemic necrosis of

Answer 17

Anteroseptal (LAD)-V1-V2 Anteroapical (distal LAD) -V3-V4 Anterolateral (LAD or LCX) -V5-V6 Lateral (LCX)-aVL,I InFerior (RCA)-II,III,aVF

Answer 18

Cardiac arrhythmia— important cause of death before reaching hospital common in first few days. LV failure and pulmonary edema. Cardiogenic shock (large infarct high risk of mortality). Ventricular free wall rupture -cardiac tamponade papillary muscle rupture -severe mitral regurgitation interventricular septum rupture -VSD Ventricular pseudoaneurysm formation (contained free wall rupture)— CO, risk of arrhythmia, embolus from mural thrombus; greatest risk approximately 3–14 days post-MI (as with rupture). True ventricular aneurysm—outward bulge during contraction (“dyskinesia”), associated with fibrosis arises 2 weeks to several months after MI. Postinfarction fibrinous pericarditis—friction rub (1–3 days post-MI). Dressler syndrome—autoimmune phenomenon resulting in fibrinous pericarditis (several weeks post-MI).

Answer 19

Unstable angina/NSTEMI— Anticoagulation (e.g., heparin) antiplatelet therapy (e.g., aspirin + clopidogrel), β-blockers, ACE inhibitors, statins. Symptom control with nitroglycerin and morphine. STEMI—In addition to above, reperfusion therapy most important (percutaneous coronary intervention preferred over fibrinolysis). PCI better Within

Answer 20

Dilated -most common Hypertrophic Restrictive

Answer 21

Most common cardiomyopathy (90% of cases) ``` Often idiopathic or familial. Other etiologies include A-Alcohol abuse B-Beriberi C-Coxsackie B virus myocarditis C-chronic Cocaine use C-Chagas disease, D-Doxorubicin toxicity hemochromatosis sarcoidosis peripartum cardiomyopathy. ``` Findings: S3, systolic regurgitant murmur HF-systolic dilated heart on echocardiogram balloon appearance of heart on CXR. Treatment: Na+ restriction, ACE inhibitors, β-blockers, diuretics, digoxin, ICD, heart transplant. Eccentric hypertrophy (sarcomeres added in series

Answer 22

60–70% of cases are familial autosomal dominant commonly a β-myosin heavy-chain mutation Can be associated with Friedreich ataxia. Causes syncope during exercise Diastolic HF sudden death in young athletes due to ventricular arrhythmia. Findings: S4, systolic murmur. May see mitral regurgitation due to impaired mitral valve closure. Treatment: cessation of high-intensity athletics use of β-blocker non-dihydropyridine Ca2+ channel blockers (e.g., verapamil) ICD if patient is high risk. Marked ventricular hypertrophy often septal predominance Obstructive hypertrophic cardiomyopathy (subset)—asymmetric septal hypertrophy and systolic anterior motion of mitral valve outflow obstruction dyspnea, possible syncope.

Answer 23

sarcoidosis amyloidosis postradiation fibrosis endocardial fibroelastosis (thick fibroelastic tissue in endocardium of young children) Löffler syndrome (endomyocardial fibrosis with a prominent eosinophilic infiltrate) hemochromatosis (dilated cardiomyopathy can also occur). Diastolic dysfunction ensues. Can have low- voltage ECG despite thick myocardium (especially amyloid).

Answer 24

Clinical syndrome of cardiac pump dysfunction congestion and low perfusion. ``` LHF/RHF LHF Systolic dysfunction— low contractility reduced EF, high EDV often 2° to ischemia/MI or dilated cardiomyopathy. ``` Diastolic dysfunction— low compliance 2° to myocardial hypertrophy preserved EF, normal EDV RHF most often results from left HF. Isolated right HF -due to cor pulmonale. ACE inhibitors or angiotensin II receptor blockers, β-blockers (except in acute decompensated HF), and spironolactone reduce mortality. Thiazide or loop diuretics are used mainly for symptomatic relief. Hydralazine with nitrate therapy improves both symptoms and mortality in select patients. LHF 1.Orthopnea- Shortness of breath when supine: venous return from redistribution of blood (immediate gravity effect) exacerbates pulmonary vascular congestion. 2.PND- Breathless awakening from sleep: venous return from redistribution of blood, reabsorption of edema, etc. 3.Pulmonary oedema- pulmonary venous pressure pulmonary venous distention and transudation of fluid. Presence of hemosiderin-laden macrophages (“HF” cells) in lungs. RHF 1.Hepatomegaly(Nutmeg liver)- central venous pressure resistance to portal flow. Rarely, leads to “cardiac cirrhosis.” 2.JVD- High venous pressure. 3.High central venous pressure -fluid transudation Refer book

Answer 25

Hypovolemic Cardiogenic Obstructive Distributive

Answer 26

``` Systemic inflammatory response syndrome ≥ 2: fever/hypothermia tachycardia tachypnea leukocytosis/leukopenia ``` First sign of shock is tachycardia. Multiple organ dysfunction syndrome (MODS) is the end result of shock.

Answer 27

bacteria FROM JANE Fever (most common symptom) new murmur Roth spots (round white spots on retina surrounded by hemorrhage) Osler nodes (tender raised lesions on finger or toe pads) Janeway lesions (small,painless,erythematous lesions on palm or sole) glomerulonephritis septic arterial or pulmonary emboli splinter hemorrhages on nail bed Multiple blood cultures necessary for diagnosis. Acute—S. aureus (high virulence). Large vegetations on previously normal valves Rapid onset. Subacute—viridans streptococci (low virulence). Smaller vegetations on congenitally abnormal or diseased valves. Sequela of dental procedures. Gradual onset. S. bovis (gallolyticus) is present in colon cancer, S. epidermidis on prosthetic valves. Mitral valve is most frequently involved. Tricuspid valve - associated with IV drug abuse (don’t “tri” drugs). Associated with S. aureus, Pseudomonas, and Candida. Culture ⊝—most likely Coxiella burnetii, Bartonella spp., HACEK (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella) Endocarditis may also be nonbacterial (marantic/thrombotic) 2° to malignancy, hypercoagulable state, or lupus(Libermann sacks) Transeosophageal Echo to see valves

Answer 28

A consequence of pharyngeal infection with group A β-hemolytic streptococci. After2-3 weeks Late sequelae include rheumatic heart disease, which affects heart valves—mitral > aortic >> tricuspid (high-pressure valves affected most). Early lesion is mitral valve regurgitation; late lesion is mitral stenosis. Rheumatic granuloma- Aschoff bodies -giant cells Anitschkow cells -enlarged macrophages with ovoid, wavy, rod-like nucleus anti- streptolysin O (ASO) titers. Anti DNAse B titres ``` Immune mediated (type II hypersensitivity) not a direct effect of bacteria. ``` Antibodies to M protein cross-react with self antigens (molecular mimicry). Treatment/prophylaxis: penicillin. J♥NES (major criteria): Joint (migratory polyarthritis) -large joints ♥ (carditis)-pan carditis Nodules in skin (subcutaneous) Erythema marginatum Sydenham chorea Minor- None specific-fever /ESR high Prior group a infection-ASOT/anti DNAse b titres Pan carditis Endocarditis involve valves-small vegetations Aschoff bodies in myocardium Death due to myocarditis High risk of chronic disease CHRONIC RHEUMATIC HEART DISEASE A. Valve scarring that arises as a consequence of rheumatic fever B.Results in stenosis with a classic 'fish mouth' appearance 1. Almost always involves the mitral valve;thickening of chordae tendineae and cusps 2. Occasionally involves the aortic valve; fusion of the commissures 3. Other valves are less commonly involved. C. Complications include infectious endocarditis.

Answer 29

Commonly presents with sharp pain, aggravated by inspiration, relieved -sitting up and leaning forward. Presents with friction rub. ECG changes include widespread ST-segment elevation and/or PR depression. Causes include idiopathic (most common-presumed viral), confirmed infection (e.g., Coxsackievirus), neoplasia, autoimmune (e.g., SLE, rheumatoid arthritis), uremia cardiovascular (acute STEMI or Dressler syndrome), radiation therapy.

Answer 30

Compression of heart by fluid (e.g., blood, effusions) in pericardial space Low CO. Equilibration of diastolic pressures in all 4 chambers. Findings: Beck triad (hypotension, distended neck veins, distant heart sounds), High HR pulsus paradoxus. ``` ECG shows low-voltage QRS electrical alternans (due to “swinging” movement of heart in large effusion). ``` Pulsus paradoxus— in amplitude of systolic BP by > 10 mmHg during inspiration. Seen in cardiac tamponade, asthma, obstructive sleep apnea, pericarditis, croup.

Answer 31

3° syphilis disrupts the vasa vasorum of the aorta(end arteritis obliterans) -atrophy of vessel wall -dilatation of aorta and valve ring. calcification of aortic root and ascending aortic arch. Leads to “tree bark” appearance of aorta. Can result in aneurysm of ascending aorta or aortic arch, aortic insufficiency.

Answer 32

Most common heart tumor is a metastasis. Lung/breast/lymphomas/melanomas Mostly affect the pericardium-effusions Myxomas Rhabdomyomas Myxomas- Most common 1° cardiac tumor in adults 90% occur in the atria (mostly left atrium) “ball valve” obstruction in the left atrium associated with multiple syncopal episodes early diastolic “tumor plop” sound. Rhabdomyomas- Most frequent 1° cardiac tumor in children associated with tuberous sclerosis Benign Ventricles

Answer 33

Increased JVP on inspiration instead of a normal reduction Inspiration -negative intrathoracic pressure not transmitted to heart -impaired filling of right ventricle -blood backs up into venae cavae -JVD. constrictive pericarditis restrictive cardiomyopathies right atrial or ventricular tumors.

Answer 34

Rare blood vessel malignancy in the head, neck, and breast areas. Usually in elderly on sun-exposed areas. Associated with radiation therapy chronic postmastectomy lymphedema. Hepatic angiosarcoma associated with vinyl chloride and arsenic exposures. Very aggressive and difficult to resect due to delay in diagnosis.

Answer 35

Benign capillary skin papules found in AIDS patients Caused by Bartonella henselae infections. Frequently mistaken for Kaposi sarcoma, but has neutrophilic infiltrate.

Answer 36

``` Benign capillary hemangioma elderly Does not regress Frequency increase with age. ```

Answer 37

Cavernous lymphangioma neck Associated with Turner syndrome.

Answer 38

``` Benign painful red-blue tumor under fingernails Arises from modified smooth muscle cells of the thermoregulatory glomus body. ```

Answer 39

Endothelial malignancy most commonly of the skin but also mouth, GI tract, and respiratory tract. Associated with HHV-8 and HIV. Frequently mistaken for bacillary angiomatosis, but has lymphocytic infiltrate.

Answer 40

Polypoid capillary hemangioma ulcerate and bleed. Associated with trauma and pregnancy

Answer 41

Benign capillary hemangioma of infancy Appears in first few weeks of life (1/200 births) grows rapidly regresses spontaneously by 5–8 years old.

Answer 42

Reduction in blood flow to the skin due to arteriolar (small vessel) vasospasm response to cold or stress color change from white (ischemia) to blue (hypoxia) to red (reperfusion). Most often in the fingers A and toes. Raynaud disease when 1° (idiopathic) Raynaud syndrome when 2° to a disease process such as mixed connective tissue disease, SLE, or CREST (limited form of systemic sclerosis) syndrome. Treat with Ca2+ channel blockers.

Answer 43

Large- Temporal Takayasu Medium- Polyarteritis nodosa Kawasaki dis Buergers dis(pollyangitis obliterance) ``` Small- Granulomatosis with polyangitis(wegners) Microscopic polyangitis Eosinophilic Granulomatosis with polyangitis HSP ```

Answer 44

Usually elderly females. Unilateral headache (temporal artery) jaw claudication. May lead to irreversible blindness due to ophthalmic artery occlusion. Associated with polymyalgia rheumatica. commonly affects branches of carotid artery. Focal granulomatous inflammation ESR-high Temporal artery bx Treat with high-dose corticosteroids prior to temporal artery biopsy to prevent blindness.

Answer 45

Young adults. Hepatitis B seropositivity in 30% of patients. Fever, weight loss, malaise, headache. GI: abdominal pain, melena. Hypertension, neurologic dysfunction, cutaneous eruptions, renal damage. Typically involves renal and visceral vessels not pulmonary arteries. Immune complex mediated. Transmural inflammation of the arterial wall with fibrinoid necrosis. Innumerable renal microaneurysms and spasms on arteriogram. Treat with corticosteroids, cyclophosphamide.

Answer 46

Wegners Granulomatosis ``` Upper respiratory tract: perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis. ``` Lower respiratory tract: hemoptysis, cough, dyspnea. Renal: hematuria, red cell casts. Triad: Focal necrotizing vasculitis Necrotizing granulomas in the lung and upper airway Necrotizing glomerulonephritis PR3-ANCA c-ANCA (anti-proteinase 3). CXR: large nodular densities. Treat with cyclophosphamide, corticosteroids.

Answer 47

Necrotizing vasculitis lung, kidneys, and skin pauci-immune glomerulonephritis palpable purpura. Presentation similar to granulomatosis with polyangiitis but without nasopharyngeal involvement. No granulomas. MPO-ANCA/p-ANCA H (anti- myeloperoxidase). Treat with cyclophosphamide, corticosteroids.

Answer 48

Asthma, sinusitis, skin nodules or purpura, peripheral neuropathy (e.g., wrist/foot drop). Can also involve heart, GI, kidneys (pauci- immune glomerulonephritis). Granulomatous, necrotizing vasculitis with eosinophilia MPO-ANCA/p-ANCA, IgE level high

Answer 49

Most common childhood systemic vasculitis. Often follows URI. Classic triad: Skin: palpable purpura on buttocks/legs J Arthralgias GI: abdominal pain Vasculitis 2° to IgA immune complex deposition. Associated with IgA nephropathy (Berger disease).

Answer 50

Refer book

Answer 51

Refer book

Answer 52

Usually Asian females