Pathology Flashcards

Question

2-4 Hours Post-MI

Answer 1

Can only see areas of infarction with TTC staining

Answer 2

* Micro * Wavy fibers * Pyknosis * Hyperesosinophilia * Hemorrhage * Gross * Mottling

Answer 3

* Left * Pyknosis * Hypereosinophilia * Few PMNs * Right * Dark contraction bands * Nuclei absent * Acute inflammation starting

Answer 4

* PMNs infiltrate * Loss of striations * Loss of nuclei

Answer 5

Inflammatory cells including MΦ Necrotic myocytes

Answer 6

* Hyperemic border * Depressed sunken yellow area * Highest risk for rupture of the infarcted area

Answer 7

Very early granulation tissue

Answer 8

MΦ Numerous capillaries Immature collagen

Answer 9

More developed vessels ↑ Collagen Maturing granulation tissue

Answer 10

Continued in-growth of capillaries Fibroblasts w/ collagen deposition

Answer 11

* Generally reperfusion beneficial * **"New" cellular injury may occur** 1. Infiltrating WBCs generate oxygen free radicals 2. Apoptosis 3. Microvascular injury ⇒ hemorrhage and endothelial cell swelling 4. Occlusion of capillaries ⇒ prevent reperfusion 5. **Contraction band necrosis**

Answer 12

* ½ of all deaths due to acute MI **occur within 1 hour of onset** * 30% overall mortality in the 1^st year * _Risk factors:_ * Advanced age * Female gender * DM * Previous MI * 75% have post-MI complications

Answer 13

**Full thickness hole through part of the heart** * Ventricular free wall * Hemopericardium ⇒ cardiac tamponade * Highest risk 3-7 days post MI * Ventricular septum * L to R shunt ⇒ murmur and CHF * Papillary muscle * Acute, severe MR

Answer 14

* _Fibrinous_ or _fibrino-hemorrhagic_ ⇒ **bread and butter appearance** * Usu. occurs 2-3 days post transmural MI * Usually resolves

Answer 15

Usually seen with MI of the adjacent posterior LV and ventricular septum

Answer 16

New necrosis adjacent to an existing infarct

Answer 17

Stretching, thinning, and dilation of the infarcted region. Seen most often in anteroseptal infarcts.

Answer 18

Focal abnormal in contraction ⇒ stasis Endocardial damage ⇒ thrombogenic surface

Answer 19

* **Late complication** * Bounded by scarred myocardium * **Usually from large anteroseptal MI that has undergone expansion** * Bulges during systole * **Rupture does not occur** * Complications * Mural thrombus * Arrhythmias * Heart failure

Answer 20

"Progressive late heart failure" * Exhaust compensatory hypertrophy of viable myocardium ⇒ **cardiac decompensation** * Slow progressive onset of CHF s/p MI * Accounts for ~ 50% of cardiac transplants * **Enlarged, heavy heart with LV hypertrophy and dilation**

Answer 21

* 80-90% due to IHD * Typically due to a lethal arrhythmia * Increased cardiac mass is an independent risk factor * Prognosis improved w/ automatic defibrillators

Answer 22

* Produced by **atrial cells** * Causes: * Vasodilation * Natriuresis * Diuresis

Answer 23

* Ensure synchronous contraction through **electrical coupling** * Ischemia and myocardial disease ⇒ abnl spatial distribution of gap junctions * Contributes to electromechanical dysfunction and heart failure

Answer 24

* _Chambers_ * ↑ LA cavity size * ↓ LV cavity size * Sigmoid septum * _Valves_ * AV calcification * MV annular calcification * Fibrosis of leaflets * Buckling of mitral leaflets towards LA * Lambl excrescences ⇒ small filiform processs on the closure lines of aortic and mitral valves * _Epicardial coronary arteries_ * Tortuosity * ↑ Cross-sectional luminal area * Calcification * Atherosclerosis * _Myocardium_ * ↑ Mass * ↑ Subepicardial fat) * Brown atropy * Lipofuscin deposition * Basophilic degeneration (by-product of glycogen metabolism * Amyloid deposits * _Aorta_ * Dilated ascending aorta with rightward shift * Elongated thoracic aorta * Sinotubular junction calcification * Elastic fragmentation and collagen accumulation * Atherosclerosis

Answer 25

_6 principal mechanisms underlie heart failure:_ 1. Pump failure 2. Obstruction to flow 3. Regurgitant flow 4. Shunted flow 5. Conduction abnormalities 6. Rupture of heart or major vessel

Answer 26

A primary abnormality of the myocardium. * Primary vs secondary * Classified based on morphology * Dilated * Hypertrophic * Restrictive

Answer 27

"Congestive cardiomyopathy" * Progressive dilation and contractile dysfunciton * Most common form ⇒ 90% * Onset 20-50 y/o

Answer 28

* **Familial** ⇒ 25-35% * Most AD w/ variable penetrance * Typically affect cytoskeleton * Also proteins of sarcomere, mitocondria, nuclear envelope * **X-linked form** * **Mutation in dystrophin gene** * Presents in teens to early 20's * Rapidly progressive * **Acquired** * **Toxin-induced** * ETOH and acetaldehyde directly toxic to myocardium * Thiamine deficiency may contribute * Chemotherapeutic agents like doxorubicin * **Inflammatory** ⇒ myocarditis * Coxsackie B virus and other enteroviruses * **Pregnancy associated** * Occurs in late pregnancy or weeks-months postpartum * HTN, volume overload, nutritional deficiencies, immune rxn may be involved

Answer 29

* Gross * Enlarged globular heart * Usu. all chambers dilated * Micro * Myocyte hypertrophy and stretching * Nulcear enlargement * Interstitial fibrosis * Inflammatory infiltrates

Answer 30

"Idiopathic hypertrophic subaortic stenosis (IHSS)" * Symmetic and asymmetrical patterns * 30% w/ outflow obstruction * Loss of compliance ⇒ **diastolic dysfunction** * **Systolic function usually hyperdynamic** * _Etiology:_ * Familial ⇒ 50% * Friedreich ataxia * Storage diseases * Infants of diabetic mothers * Pathophysiology: mutations in structural proteins of scarcomere ⇒ **diastolic dysfunction, myocyte hypertrophy, and disarray**

Answer 31

* Mutations in structural proteins of sarcomere * β myosin heavy chain most common * Autosomal dominant

Answer 32

* HTN heart disease w/ age related subaortic septal hypertrophy * Aortic stenosis * Amyloidosis

Answer 33

* LVH affects septum most * Endocardial fibrosis * Myocyte hypertrophy and disarry with interstitial fibrosis

Answer 34

* Loss of compliance ⇒ **diastolic dysfunction** * Least common type * Often associated with **systemic disease** * Causes: * _Direct_ * Toxic * Methylsergide * Anorectic agents * Radiation * Infectious * Infiltration * Genetic * Idiopathic * _Indirect_: infiltration by something other than cardaic muscle * Glycogen storage diseases * Amyloidosis * Hemachromatosis * Sarcoidosis

Answer 35

* Often d/t compensatory changes in the heart * CO doesn't meet demand * ↑ Peripheral resistance * Volume overload * Cardiac dysfunction

Answer 36

Pattern dependent on etiology. * **Concentric hypertrophy** ⇒ seen with conditions that ↑ afterload * HTN * Aortic stenosis * **Non-concentric / Eccentric hypertrophy** ⇒ seen with volume overload * ↓ Capillary to myocyte ratio * ↑ Fibrous tissue * Abnormal protein synthesis

Answer 37

CO insufficient to meet requirements of peripheral tissues. * HTN, valvular disease, MI, etc ⇒ **↑ cardiac work** * ↑ Wall stretch ⇒ hypertrophy and/or dilation * **↓ Renal perfusion** ⇒ RAAS activation ⇒ sodium and salt retention * **Down regulation of neurohumoral receptors** * _May be due to:_ * Loss of blood, arrhythmia, obstructed flow, regurg, or primary pump failure

Answer 38

* Causes: * Ischemic heart disease * HTN * AV or MV disease * Non-ischemic myocardial diseases * Effects: * Congestion of pulmonary vasculature * ↓ Peripheral blood pressure and flow * Sequelae of left HF: * Secondary atrial enlargement * Pulmonary congestion and edema * ↓ Renal perfusion * Cerebral hypoxia

Answer 39

* Leakage of congested capillaries into alveolar spaces * Results in hemosiderin deposition in MΦ ⇒ **siderophages** (**"Heart failure cells")**

Answer 40

* Causes: * Left-sided HF ⇒ most common * Cor pulmonale * Chronic pulmonary HTN * Effects: * Passive congestion of liver * Renal congestion * Pleural effusions * Anasarca * RVH

Answer 41

* Many pts have right and left HF * Treatment * Diuretics ⇒ ↓ fluid overload * ACEi ⇒ ⊗ RAAS * β-blockers ⇒ ↓ systemic vascular resistance

Answer 42

Important for management, diagnosis is clinical. * Kidney function * Electrolytes * CXR * BNP * ECHO

Answer 43

* **Diastolic HF** * LVEF \> 50% * Thickened and stiff chambers * Heart can't fill * **Systolic HF** * LVEF \< 40% * Dilated and thin chambers * Heart can't pump

Answer 44

"CHF w/ preserved systolic function" * More common * **Seen in older pts with hx of HTN** * **Stiff ventricles with impaired filling leading to inadequate pumping** * Sensitive to HR and volume overload * Acute presents with similar sx to systolic HF * SOB, orthopnea, PND, edema * Management * Acutely treat with diuresis * Long-term goal to control BP

Answer 45

"CHF with reduced LVEF" * Generally due to **cardiomyopathies** * Different types * **Ischemic heart disease** * CAD * MI * CABG * **Non-ischemic cardiomyopathies** * Familial * Viral * Drug and ETOH * Hypo or hyper thyroid disease * Chemotherapy (Doxorubicin and Herceptin) * Toxins (cobalt) * Infections like HIV * Valvular heart disease

Answer 46

* Manage modifiable factors * Medications * Beta-blockers * ACEi * Mineralocorticoid inhibitors * Patient education * Avoid NSAIDS

Answer 47

* **Non-compliance ⇒ leading cause** * Ischemia * Inadequate treatment * Arrhythmias * Miscellaneous * HTN * No definite factor

Answer 48

* Maternal rubella infection ⇒ PDA * Environmental acquired congenital heart defect * ETOH * Thalidomide * Maternal DM

Answer 49

* Atrioventricular septal defects (endocardial cushion defect) * VSD * ASD * PDA

Answer 50

* VSD * Double outlet right ventricle * PDA

Answer 51

VSD, ASD, PDA

Answer 52

aortic coarctation

Answer 53

Mitral valve prolapse Aortic root dilatation

Answer 54

Truncus arteriosus

Answer 55

Tetralogy of Fallot

Answer 56

Supravalvar aortic and pumonary stenosis

Answer 57

Congenital heart defects with initial L→R shunt and later development of a R→L shunt

Answer 58

VSD with reversal of flow due to pulmonary HTN Occures when pulmonary pressure = systemic pressure

Answer 59

* Abnormal opening in atrial septum allowing communication between left and right atria * 3 types classified by location on septum * **Secundum ASD** ⇒ 90% * @ Fossa ovale * **Primum ASD** ⇒ 5% * Near AV valves * Usually ass. w/ cleft anterior mitral leaflet * **Sinus venous ASD** ⇒ 5% * Near entrance of SVC * Usu. w/ anomalous connections of right pulmonary veins * Pulmonary blood flow 2-4x nl * **Most isolated well tolerated ⇒ asymptomatic till 30 y/o** * **Mumur often present**

Answer 60

* **Most common congenital cardiac anomaly** * Described by location and size * **Membranous vs muscular** * 50% of small muscular VSD close spontaneously * Large defects usu. membranous or infundibular * Stay open with sign. shunt * L to R shunt ⇒ RV dilation and hypertrophy * Eisenmenger's syndrome

Answer 61

* 90% are isolated * **Most w/o functional difficulties @ birth** * **Harsh "machine-line" murmur** * **Initial L to R shunt ⇒ Eisenmenger** * Close ASAP * Sometimes need to keep open ⇒ Prostaglandin E

Answer 62

* **From abnl development of embryologic AV canal** * Superior and inferior cushions fail to fuse * **Incomplete closure of AV septum** * **Inadequate formation of tricuspid and mitral valves** * **In complete form ⇒ all 4 chambers freely communicate** * \> ⅓ with complete AVSD have Downs

Answer 63

* Most common cyanotic congenital heart disease * 10% of all CHD * Features: * **VSD** ⇒ membranous, malaligned * **RV** outflow tract obstruction * Most severe form is pumonary valve atresia * **Aorta overriding septal defect** ⇒ dextroposition * **RVH** ⇒ compensatory * Clinical manifestations * **R to L shunt ⇒ cyanosis** * Pulmonary arteries hypoplastic * Aorta enlarged * Subpulmonary stenosis protects pulmonary vasculature from pressure overload ⇒ **RV failure rare**

Answer 64

* **Persistent presence of one arterial trunk arising from the ventricles** * Due to failure of separation into pulmonary artery and aorta * **Single great artery receives blood from both ventricles** * Accompanied by **underlying VSD** * Blood from RV and LV mix ⇒ **early systemic cyanosis** * ↑ Pulmonary blood flow ⇒ **risk of irreversible pulmonary HTN**

Answer 65

* Discordant ventriculo-arterial connections * **LV ⇒ pulmonary artery / RV ⇒ aorta** * _Need mixing of systemic venous and arterial blood to live_ * **VSD** (35%) * **PFO and PDA** (65%) * RVH, LV atrophy * Fix with arterial switch operation * Need to consider abnl of coronary arteries

Answer 66

**A narrowing, or constriction, in a portion of the aorta.** * **Infantile form** * **Tubular hypoplasia of aortic arch** _proximal to PDA_ * Sx early in life * **Adult form** * **Ridge of proliferative intimal tissue** usually in a _post-ductal position_ * Ass. with **male sex** except for **Turner's syndrome** * Bounding pulses in BUE * Can develop _collaterals_ via **enlarged intercostal and internal mammary arteries** * Visible erosions "**notching**" on underside of ribs on CXR

Answer 67

* **Obstruction @ pulmonary valve** * Varied severity * Isolated or part of complex * _Clinical manifestations:_ * **RVH** * **± Post-stenotic dilation of pulmonary artery** * **± Pulmonary trunk hypoplasia** * **Complete atresia of PA** ⇒ no communication b/t RV and lungs * See hypoplastic RV and ASD

Answer 68

* **Valvular AS** * **Cusps hypoplastic, dysplastic, or abnl #** * Less severe forms compatible with life * 80% isolated * May see dense, porcelain-like endocardial fibroelastosis of LV * **Subaortic stenosis** * **Thickened band (discrete type) or collar (tunnel type) of dense endocardial fibrous tissue** * Below level of the cusps * **Supravalvular AS** * **Ascending aortic wall thickened ⇒ luminal constriction** * May be related to developmental d/o affecting multiple organ systems * Includes hypercalcemia of infancy (Williams syndrome) * Can be caused by elastin mutations

Answer 69

Constellation of findings: * **Severe congenital valvular aortic stenosis/atresia** * LVOT obstruction ⇒ **LV and ascending aorta hypoplasia** * **PDA ⇒** allows flow into aorta and coronary arteries * Nearly always fatal in first week of life when ductus closes

Answer 70

Most cases are viral.

Answer 71

Classifies myocarditis based on endomyocardial biopsy findings.

Answer 72

* Lymphocytic myocarditis * Hypersensitivity myocarditis * Giant cell myocarditis * Sarcoid myocarditis * Infectious myocarditis

Answer 73

* **Most common form** * **Associated with myocyte injury** * **Most cases are viral** * Focal, patchy, or diffuse pattern * Gross appearance * Normal ⇒ Enlarged and dlidated with mottling * Dx with clinical findings, serology, histopathology, ISH, molecular probes, and PCR

Answer 74

* _Etiologies_ * **Typically caused by drugs** * Sulfonamides, methyldopa, PCN * Parasitic infections * Taenia, Echinococcus, Schistosoma, Tricinella, Toxoplasma, Trypanosomiasis * Hypereosinophilic syndromes * Asthmatic bronchitis * **Eosinopril-rich inflammatory infiltrate in myocardium**

Answer 75

* Chagas disease due to Trypanosoma cruzii * Toxoplasma * Diphtheria * Trichinosis

Answer 76

**Characterized by infiltrates of histiocytes and lymphocytes with granuloma formation.** * Idiopathic * Sarcoidosis * Granulomatous infections * Mycobacteria and fungi * See necrotizing granulomas * Hypersensitivity * Rheumatoid disases * Rheumatic fever

Answer 77

* **Unknown etiology** * Rapidly progressive * Frequently fatal * **Mixed inflammatory infiltrate including multinucleated giant cells** * **Multifocal myocyte necrosis** * No granulomas

Answer 78

* Causes * Bacteria and some fungi * Due to generalized sepsis or direct spread from infective endocarditis * Early viral and idiopathic myocarditis * Ischemia/Infarct

Answer 79

* May be **asymptomatic with no sequelae** * May result in **acute heart failure, arrhythmia, or sudden death** * Most have **fatigue, dyspnea, palpitations, precordial discomfort, fever** * Dilated cardiomyopathy may result over time

Answer 80

* Pericardial disorders can cause * **Fluid accumulation** * **Inflammation** * **Fibrous constriction** * **Usually associated with disease elsewhere in the heart or systemic disease** * Isolated pericardial disease rare

Answer 81

* **Most often develop d/t pericarditis** * Exceptions include **cardiac rupture** and **myxedema** (hypothryoidism) * Pericardium may be distended by: * **Serous fluid** * **Blood** ⇒ hemopericardium * **Pus** ⇒ purulent pericarditis * **Gas/air** ⇒ pneumopericardium

Answer 82

**Slowly accumulating effusions dilate the pericardium.** * Can reach \> 500 ml and remain asymptomatic * CXR ⇒ globular enlargement of the heart shadow * EKG ⇒ low-voltage QRS complexes in all 6 limb leads

Answer 83

**Rapidly developing fluid collections.** * **200-300 ml may cause cardiac tamponade** * Compress atria and venae cavae * Can compress ventricles * Cardiac filling restricted * Seen with * Hemopericardium d/t ruptured MI site * Proximal aortic dissection

Answer 84

* **Hemopericardium d/t ventricular wall rupture s/p MI** * **Proximal aortic dissection** * **Bacterial or fungal infections** * **HIV-associated infections** * **Neoplastic involvement** * ~ 20% of large effusions with no obvious cause constitute the initial presentation of unrecognized cancer

Answer 85

Unless intrapericardial pressure immediately decreased, pulmonary blood flow stops and cardiac arrest follows.

Answer 86

* Dyspnea and tachypnea * Pericardial pain * Diaphoresis * Peripheral cyanosis * **Beck's triad** ⇒ hypotension, muffled heart sounds, JVD * **Paradoxical pulse** ⇒ abnormally large drop in systemic arterial pressure during inspiration * **Varying degrees of reduced CO and shock** * Diaphoresis, cool extremities, depressed sensorium

Answer 87

* Occurs with pericardial effusion and tamponade * **Beat-to-beat shift in QRS axis** * **Associated with mechanical swinging of the heart** * Electrical alternans + sinus tach virtually dx of cardiac tamponade

Answer 88

* **Air within the pleural cavity** * **Can lead to cardiac tamponade** * Causes * Complication of respiratory therapy in infants * Seen with pneumothorax and pneumomediastinum * Spontaneously in asthma * Blunt chest trauma * S/p pericardiectomy

Answer 89

* **Severe pleuritic pain in anterior chest** * May radiate to arms and back * **Pericardial friction rub** * Best heart at the left sternal border at end expiration * EKG ⇒ diffuse ST elevations in all leads

Answer 90

* Most common types: * **Fibrinous** ⇒ "dry', little or no serious effusion * **Serofibrinous** ⇒ "wet", ass. w/ serous effusion * Causes: * **Noninfectious inflammatory diseases** * **Rheumatic fever** * **Dressler syndrome** * **Uremia** * SLE, Scleroderma * Tumors * **Infection of contiguous tissues** * Preceding viral infection * Other causes: * **1-3 days post MI** * Radiation * Post-surgical

Answer 91

* **Due to infection of pericardial space** * Direct extension from adjacent tissues * Hematogenous or lymphatic spread * Inoculation during procedure * Up to 500 ml of exudate * Serosa reddened and granular * Extension ⇒ **mediastinopericarditis** * Usu. results in organization and scarring ⇒ **constrictive pericarditis**

Answer 92

* Most often caused by malignancy * Bacterial infections esp. Tb * Pts w/ bleeding diathesis * S/p cardiac surgery

Answer 93

* **Presumed to be Tb until proven otherwise** * Rarely fungal infections * Occurs by direct spread from Tb foci * Frequently progresses to disabling, fibrocalcific, chronic constrictice pericarditis

Answer 94

* **Can develop from any type of acute pericarditis** * Fibrous thickenings ⇒ **soldier's plaque** * Delicate, stringy adhesions may damage pericardial sac ⇒ adhesive pericarditis * **Rarely interferes with cardiac function**

Answer 95

* **Obliteration of pericardial sac with adherence of outer pericardium to surrounding structures** * Pulls during systole ⇒ cardiac strain * Inc. workload ⇒ hypertrophy and dilation

Answer 96

* **Fusion of visceral and parietal layers ⇒ thick fibrous scar** * **Compresses the heart** * Prevents hypertrophy & dilation * **Heart cannot respond to inc. peripheral demand** * **See DOE, weight loss, fatigue, ankle edema** * May require pericardiectomy * Most common w/ pericardial disease d/t: * **Tb** * **Radiation therapy** * **Prior cardiac surgery** * Chest trauma * Uremia * Metastatic tumor * Develops months to years after acute insult

Answer 97

* **Primary tumors** * Much lower incidence * Myxoma most common * **Metastatic tumors** * Far more common * Can originate from anywhere * Sarcomas and germ cell tumors common

Answer 98

* Most common primary tumor in adults * 90% in atria * L:R = 4:1 * Derived from multipotent mesenchymal cells * Gelatinous "myxoid" consistency with soft, irregular surface

Answer 99

* Abundant myxoid matrix * Stellate, endothelia, SM, and undiff. cells * Inflammation and hemorrhage may be present

Answer 100

* Occur in subepicardium or subendocardium \> myocardium * Most in LV, RA, or atrial septum * Lipomatous hamartoma of cardiac valves ⇒ rare * Gross and micro appearance of adipose tissue

Answer 101

* **Most common primary cardiac tumor in kids** * Protrude into ventricle * **Often seen with tuberous sclerosis** * May cause outflow obstruction * Composed of skeletal muscle dervied cells * **Spider cells**

Answer 102

* **Malignant vascular tumor** * Anastomosing vascular channels lined by atypical cells * Hemorrhage and necrosis common