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USMLE Step I Pathology > Cardiac Pathology (Pathoma) > Flashcards

Cardiac Pathology (Pathoma) Flashcards

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USMLE® Step 1 flashcards
1
Q

Stable angina

A

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)

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2
Q

Unsatble angina

A

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)

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3
Q

Prinzmetal angina

A

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.

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4
Q

Myocardial Infarction

A

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.

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5
Q

MI in LAD

A

Affects anterior wall of LV and anterior IV septum

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6
Q

MI in RCA

A

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

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7
Q

MI in Left Circumflex

A

Affects lateral wall of LV.

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8
Q

Troponin I

A

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

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9
Q

CK-MB

A

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

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10
Q

Contraction band necrosis

A

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

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11
Q

Repurfusion injury

A

ROS futher injury the myocardium.

Classically seen if cardiac markers continue to rise post angioplasty.

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12
Q

MI complications

A

Gross changes = none

Microscopic changes = none

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

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13
Q

MI complications 4-24 hrs.

A

Gross = dark discoloration

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

Complications - arrhythmia

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14
Q

MI complications 1-3 days

A

Gross = yellow pallor

Micro = neutrophils

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

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15
Q

MI complications 4-7 days

A

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.)

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16
Q

MI complicatiopns 1-3 weeks

A

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

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

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17
Q

Months

A

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)

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18
Q

Progression of Microscopic MI

A

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

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19
Q

Sudden cardiac death

A

Unexpected death due to cardiac disease

Occurs w/o sx or

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20
Q

Chronic Ischemic Heart Disease

A

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

Progresses to CHF

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21
Q

Left sided heart failure

A

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.

22
Q

Right-sided heart failure

A

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.

23
Q

Cardiac Congenital Defects

A

Usually arise in embryogenesis from weeks 3-8.

Seen in 1% of live births.

Most are sporadic.

24
Q

VSD

A

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

25
Q

ASD

A

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.

26
Q

PDA

A

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

27
Q

Tetrology of Fallot

A

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

28
Q

Transposition of Great Vessels

A

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

29
Q

Trunctus Arteriosis

A

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

Early cyanosis

30
Q

Tricuspid Atresia

A

Tricuspid valve fails to develop

RV is hypolastic

Associated w/ ASD resulting in R–>L shunt

Presents w/ early cyanosis

31
Q

Coarctation of aorta

A

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)

32
Q

Acute Rheumatic Fever

A

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)

33
Q

Aortic stenosis

A

Usually due to calcification and fibrosis (wear and tear)

Presents in late adulthood (

34
Q

Aortic Regurgitation

A

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.

35
Q

Mitral Valve Prolapse

A

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.

36
Q

Mitral Regurgitation

A

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.

37
Q

Mitral stenosis

A

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.

38
Q

Strep viridans

A

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.

39
Q

S. aurues

A

MCC in IV drug-use

High-virulence –> infects normal valves (tricuspid)

Large vegetations that destroy valve (acute endocarditis)

40
Q

S. epidermidids

A

Endocarditis in prostetic valves

41
Q

Strep bovis

A

Endocarditis in patients w/ underlying CRC.

42
Q

HACEK Organisms

A

Endocarditis w/ negative blood cultures.

Hemophilus
Actinobacillus
Cardiobacterium
Eikinella
Kingella
43
Q

Infectious Endocarditis

A

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.

44
Q

Nonbacterial throbotic endocarditis

A

Sterile vegetations that arise w/ hypercoaguable state or underlying adenocarcinoma.

Vegetations arise on mitral valve and result in regurge

45
Q

Libmann Sachs Endocarditis

A

LSE w/ SLE

Sterile

*Vegetations on both sides of mitral valve (results in mitral regurge)

46
Q

Dilated Cardiomyopathy

A

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

47
Q

Hypertrophic Cardiomyopahty

A

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

48
Q

Restrictive CM

A

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

49
Q

Myxoma

A

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.

50
Q

Rhabdomyoma

A

Benign hamartoma of cardiac muscle.

MC primary cardiac tumor in children; **Associated w/ tuberous sclerosis.

Usually arises in ventricle

51
Q

Metastasis

A

More common than primary tumor

Common metastasis include: breast, lung, melanoma, and lymphoma

MC involves pericardium resulting in exudative pericardial effusion

USMLE Step I Pathology (14 decks)

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