Cardiac Pathology (Pathoma)

Question 1

Stable angina

Answer 1

Chest pain that arises w/ exertion or emotional stress.

Due to atherosclerosis of coronary arteries w/ > 70%

Represents reversible injury (cellular swelling) to myocytes.

Presents w/ chest pain ( amt of time myocardium can withstand lack of blood flow) that radiates to the left arm or jaw. Diaphoresis. Shortness of breath.

Subendocardial ischemia. Shows ST segment depression.

Relieved by rest or nitroglycerin (decrease preload)

Question 2

Unsatble angina

Answer 2

Chest pain occurs at rest (or w/ less exertion)

Due to the formation of a thrombosis which partially** blocks coronary artery.

Reversible injury to myocytes.

ST depression

Relieved by Nitro

High risk of progression to MI (part of acute coronary syndrome)

Question 3

Prinzmetal angina

Answer 3

Due to coronary artery vasospasm that leads to episodic chest pain unrelated to exertion.

Represents reversible injury

ST elevation due to transmural ischemia.

Nitro or Ca blockers relieve sx.

Question 4

Myocardial Infarction

Answer 4

Necrosis of cardiac myocytes.

Classically due to thrombosis and *complete occlusion of the coronary artery.

Other causes include coronary artery vasospasm (prizmetal’s >20 min), emboli, and vasculitis (Kawasaki)

Presents w/ severe crushing chest pain (>20 minutes) that radiates to the left arm or jaw. Diaphoresis. Dyspnea. Symptoms not relieved by Nitro.

Usually involves the Left Vent. LAD>RCA>Left circumflex

Initial phase - subendocardial necrosis (ST depression).

Will progress to transmural (STEMI)

Test for elevated cardiac enzymes (leaking of enzymes due to membrane damage = irreversible injury)

Troponin I is most sensitive and specific marker. Rises 2-4hrs post infarction. Peaks at 24 hrs. Returns to normal by 7-10 days.

CK-MB is useful for detecting reinfarction. Rises in 4-6 hrs and peaks at 24. Returns to n ormal by 72 hours.

Rx is ASA/heparin. Supplemental 02. Nitrates. B-blocker. ACEI.

Fibrinolysis or angioplasty(preferred). Can cause contraction band necrosis due to repurfusion post MI.

Question 5

MI in LAD

Answer 5

Affects anterior wall of LV and anterior IV septum

Question 6

MI in RCA

Answer 6

Affects posterior LV wall and posterior IV septum. Feeds papillary muscle –> highest risk for papillary muscle rupture in RCA MI.

Question 7

MI in Left Circumflex

Answer 7

Affects lateral wall of LV.

Question 8

Troponin I

Answer 8

Most sensitive and specific marker. Rises 2-4hrs post infarction. Peaks at 24 hrs. Returns to normal by 7-10 days.

Question 9

CK-MB

Answer 9

Useful for detecting reinfarction. Rises in 4-6 hrs and peaks at 24. Returns to n ormal by 72 hours.

Question 10

Contraction band necrosis

Answer 10

Repurfusion post MI. Returning blood flow –> large return of calcium –> large contraction of dead cells

Question 11

Repurfusion injury

Answer 11

ROS futher injury the myocardium.

Classically seen if cardiac markers continue to rise post angioplasty.

Question 12

MI complications

Answer 12

Gross changes = none

Microscopic changes = none

Complications - cardiogenic shock (massive infarction), CHF, and arrhythmia (MCC of death)

Question 13

MI complications 4-24 hrs.

Answer 13

Gross = dark discoloration

Micro = coagulative necrosis (loss of nucleus –> pyknosis, karryolexis, karryolisis)

Complications - arrhythmia

Question 14

MI complications 1-3 days

Answer 14

Gross = yellow pallor

Micro = neutrophils

Complications - fibrinous pericarditis (chest pain w/ friction rub –> can only occur in transmural infarction!)

Question 15

MI complications 4-7 days

Answer 15

Gross = yellow pallor

Micro = macrophages

Complications - rupture of ventricular free wall (tamponade), IV septum rupture (shunt), or papillary muscle (mitral insufficiency. Esp in RCA MI.)

Question 16

MI complicatiopns 1-3 weeks

Answer 16

Gross = red border emerges as granulation tissue enters from edge of infarct

Micro = granulation tissue w/ plump fibroblasts, collagen, and blood vessels

Question 17

Months

Answer 17

Gross = white scar made of type I collagen

Micro = fibrosis

Complications = aneurysm (not as strong), mural thrombus (not as contractile –> stasis –> thrombus), or dressler syndrome (AI pericarditis)

Question 18

Progression of Microscopic MI

Answer 18

1 Day - 1 Week - 1 Month

1 day of coagulative necrosis —> 1 week of inflammation (nphils –> macrophages) –> granulation tissue from one week to one month –> scar

Question 19

Sudden cardiac death

Answer 19

Unexpected death due to cardiac disease

Occurs w/o sx or

Question 20

Chronic Ischemic Heart Disease

Answer 20

Poor myocardial function due to chronic ischemic damage (with or without infarction)

Progresses to CHF

Question 21

Left sided heart failure

Answer 21

Failure of the pump

Causes: Ischemia, HTN (hypertrophy –> ischemic damage) , dilated CM (stretched muscle = less contractile) , MI, restrictive CM (can’t fill)

Pulmonary conjestion is key clinical problem. Pulmonary edema w/ dyspnea, PND, orthopnea, and crackles.

Heart-failure cells (hemosiderin laden macrophages) in lungs.

Decreased forward perfusion –> activation of RAAS –> fluid overload and increased TPR –> positive feedback.

Mainstay of treatment is ACEI to lower TPR and fluid.

Question 22

Right-sided heart failure

Answer 22

MCC is Left sided heart failure.

Other causes: L-R shunt and chronic lung disease (cor pulmonale)

Clinical features: JVD, painfuls H/Smegaly (may lead to cardiac cirrhosis), dependent pitting edema.

Question 23

Cardiac Congenital Defects

Answer 23

Usually arise in embryogenesis from weeks 3-8.

Seen in 1% of live births.

Most are sporadic.

Question 24

VSD

Answer 24

Defect in septum

MC congenital heart defect

*Associated w/ FAS.

Can be asx if small.

If large –> eventual pulmonary HTN –> reversal (Eisenmenger’s syndrome) –> cyanosis.

Rx: Surgery if symptomatic/larger

Question 25

ASD

Answer 25

Defect usually from ostium secundum. Ostium primum type is associated w/ Downs*. Presents w/ L-->R shunt w/ fixed split of S2. Can cause paradoxical emboli.

Question 26

PDA

Answer 26

Failure of DA to close. *Associated w/ congenital rubella Asx at birth w/ holocystolic "machine-like" murmur. **Cyanosis in lower extremity later in life in Eisenmenger syndrom --> PDA attaches to aorta after the great vessels Rx: Indomethacin

Question 27

Tetrology of Fallot

Answer 27

4 problems: 1. Pulmonary Stenosis, 2. VSD. 3. Overriding aorta on VSD 4. RVH R-->L shunt. Stenosis is key for degree of shunting. Kids become very cyanotic when exercising (relieved by squatting --> increase arterial pressure --> decrease shunting) *Boot shaped heart on CXR

Question 28

Transposition of Great Vessels

Answer 28

Separate circuits that don't mix. Early cyanosis. Only survival if can create L-->R shunt (i.e. give prostaglandins and/or create ASD) **Associated w/ maternal diabetes

Question 29

Trunctus Arteriosis

Answer 29

One large vessel arising from both vessels. Due to truncus failing to divide. Early cyanosis

Question 30

Tricuspid Atresia

Answer 30

Tricuspid valve fails to develop RV is hypolastic Associated w/ ASD resulting in R-->L shunt Presents w/ early cyanosis

Question 31

Coarctation of aorta

Answer 31

Infantile Form: Associated w/ PDA. Coarctation lies distal to aortic arch, but proximal to PDA (low pressure after block --> allows blood from PDA to enter descending aorta Presents w/ lower extremity cyanosis *Associated w/ Turner Syndrome Adult form: Coarctation lies distal to arch (not associated w/ PDA). HTN in upper extremities and hypotension in lower extremities. Associated w/ bicuspid aortic valve. *Collateral circulation develops across intercostal arteries (enlarged and notching of ribs)

Question 32

Acute Rheumatic Fever

Answer 32

Systemic complication of pharyngitis due to group A B-hemolytic strep Affects children 2-3 weeks post strep throat *Caused by molecular mimicry; bacterial M protein resembles human tissue. (Type II HS) Diagnosis based on Jones criteria: 1.)Evidence of prior strep infection (ASO or anti-DNase B titer) 2.) Minor criteria (fever and elevated ESR) 3.) Major criteria: J- Joint problems (migratory polyarthritis) O- Heart problems (draw O as heart). Inflammation of all 3 layers of heart N - Nodules E - Erythema marginatum (rash that is more red at margins) S - Sydenham's Chorea * Key long term sequelae are due to heart (pancarditis). 1.)Endocarditis --> vegetation on mitral valve (can involve aortic as well). --> regurge early, stenosis late. 2. ) *Myocarditis --> presence of Aschoff bodies (focus of chronic inflammation w/ Nischow cells (histiocytes w/ catepllar nucleus). MCC of death in acute phase. 3. ) Pericarditis --> frictrion rub Acute attack resolves, but many cases become chronic disease. Repeat exposure to strep --> relapse of acute phase. Increases the risk of valvular disease. Can result in scarring of mitral valve --> mitral stenosis (thickening of chordae tendinae and cusps w/ **fusion of commisures) AKA fishmouth appearance of valve. Ocasionally involves aortic valve --> fusion of commisures. Key complication is endocarditis (Strep. mutans)

Question 33

Aortic stenosis

Answer 33

Usually due to calcification and fibrosis (wear and tear) Presents in late adulthood (

Question 34

Aortic Regurgitation

Answer 34

MC arises due to isolated root dilatation. Can occur secondary to syphillitic aortic aneurysm. Or valve damage (I.e. infectious endocarditis --> valve damage) Clinical features: Early, blowing, diastolic murmur. Bounding pulses, pulsating nail bed, headbobbing, Wide pulse pressure. (Increased SV and regurge) LV dilitation and eccentric hypertrophy Rx: is valve replacement when LV HF begins.

Question 35

Mitral Valve Prolapse

Answer 35

Ballooning of MV into LA during sytole Due to myxoid degeneration in valve making it floppy Etiology is unknown; More common in Marfan's and EDS. Presents w/ mid-systolic click followed by regurge murmur; usually asymptomatic Rare complications include: IE, Arrhythmia, severe mitral regurge. Rx: is valve replacement when complications occur.

Question 36

Mitral Regurgitation

Answer 36

Usually arises as a complication of MVP Other causes include LV dilation, IE, acute rheumatic heart disease, and papillary muscle post RCA MI. Clincally: Holosytsolic blowing murmur that gets louder w/ squatting or expiration.

Question 37

Mitral stenosis

Answer 37

Usually doe to chronic rheumatic valve disease Clinically: Opening snap w/ diastolic rumble. Volume overload leads to dilitation of LA --> pulmonary congestion; pulmonary HTN; A fib. Also dysphagia (esophagus) and hoarseness (left recurrent laryngeal nerve) due to LA being most posterior chamber.

Question 38

Strep viridans

Answer 38

MC overall cause of IE Low-virulence organism; infects previously damaged valves. Results in small vegetations that do not destoy valve. Pathogenesis - damaged endocardial surface --> thrombotic vegetations (platelets and fibrin) --> transient bactermia (dental procedure) --> trapping of bacteria in vegetations.

Question 39

S. aurues

Answer 39

MCC in IV drug-use High-virulence --> infects normal valves (tricuspid) Large vegetations that destroy valve (acute endocarditis)

Question 40

S. epidermidids

Answer 40

Endocarditis in prostetic valves

Question 41

Strep bovis

Answer 41

Endocarditis in patients w/ underlying CRC.

Question 42

HACEK Organisms

Answer 42

Endocarditis w/ negative blood cultures. ``` Hemophilus Actinobacillus Cardiobacterium Eikinella Kingella ```

Question 43

Infectious Endocarditis

Answer 43

Clinically presents w/ fever, murmur , septic emboli can cause Janeway lesions (painless on palms and soles) Osler nodes (painful on fingers and toes --> ouch ouch osler), splinter hemorrhages , anemia of chronic disease. Laboratory features: Positive blood cultures (spaced), AOCD (microcitic secondary to hepcidin) , TEE is useful for detecting lesions on valves.

Question 44

Nonbacterial throbotic endocarditis

Answer 44

Sterile vegetations that arise w/ hypercoaguable state or underlying adenocarcinoma. Vegetations arise on mitral valve and result in regurge

Question 45

Libmann Sachs Endocarditis

Answer 45

LSE w/ SLE Sterile *Vegetations on both sides of mitral valve (results in mitral regurge)

Question 46

Dilated Cardiomyopathy

Answer 46

Dilation of all 4 chambers resulting in sytolic dysfunction leading to biventricular CHF Complications include mitral and tricuspid regurge and arrhytmia. MCC of cardiomyopathy MC is idiopathic Can be due to genetic mutation, myocarditis (coxsackie virus), alcohol abuse (and thiamine deficiency), drugs, *pregnancy Rx = transplant

Question 47

Hypertrophic Cardiomyopahty

Answer 47

Massive hypertrophy of the LV. Preferrentially in septum. Due to genetic mutations in **sarcomere proteins (most commonly AD) Decreased CO. Diastolic dysfunction. Sudden death due to ventricular arrhythmias; common cause of sudden death in young athletes Syncope w/ exercise *Biopsy shows myofiber hypertrophy w/ dissarray

Question 48

Restrictive CM

Answer 48

Decreased compliance of ventricular endomyocardium Restricts filling during diastole Causes: amyloidosis, sarcoidosis, Hemochromatosis, Endocardial fibroelastosis (children), Loeffler syndrome (eosinophilc infiltrate) Presents w/ CHF w/ low voltage EKG and Diminished QRS amplitudes

Question 49

Myxoma

Answer 49

Mesenchymal proliferation w/ a gelatinous appearance. Abundant ground substance on histo MC primary cardiac tumor in adults MC is pedunculated (off a stalk) mass in LA causing syncope due to blocking of mitral valve.

Question 50

Rhabdomyoma

Answer 50

Benign hamartoma of cardiac muscle. MC primary cardiac tumor in children; **Associated w/ tuberous sclerosis. Usually arises in ventricle

Question 51

Metastasis

Answer 51

More common than primary tumor Common metastasis include: breast, lung, melanoma, and lymphoma MC involves pericardium resulting in exudative pericardial effusion