Pathoma Cardiac Pathology Flashcards

1
Q

Three subtype of angina and what each is all about

A

1. Stable Angina: CP that arises with exertion or emotional stress. >70% stenosis. REVERSIBLE injury to myocytes w/o necrosis. Lasts <20 min. ST depression. Tx: rest, nitro

2. Unstable Angina: CP that occurs at rest. Due to rupture of atherosclerotic plaque with thrombosis and INCOMPLETE occlusion of coronary artery. REVERSIBLE injury. ST depression. High risk to progress to MI. Tx: nitro

3. Prinzmetal Angina: episodic CP unrelated to exertion. REVERSIBLE injury. Due to coronary artery vasospasm. ST elevation due to transmural ischemia. Tx: nitro, CCB

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2
Q

Myocardial Infarction and what are 3 most common arteries involved

A
  • Necrosis of cardiac myocyte.
  • Due to rupture of atherosclerotic plaque with thrombosis and COMPLETE occlusion of a coronary artery.
    1. Left anterior descending artery (LAD) –>anterior wall and anterior septum (45% of cases)
    2. Right Coronary Artery (RCA) –> posterior wall, posterior septum, papillary muscles LV (2nd most common)
    3. Left Circumflex Artery (LCA) –> infarction lateral wall of LV
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3
Q

Treatment of MI

A
  1. ASA w/ w/o heparin, limits thrombosis
  2. O2 to minimize ischemia
  3. Nitrates: vasodilate veins* and coronary arteries
  4. B-blocker: slow HR, decrease demand of heart
  5. ACE-I: decrease blood volume, decrease TPR
  6. fibrinolytics (tPA) or angioplasty (stent)
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4
Q

Two complications after angioplasty of coronary vessels after an acute MI

A

1. Contraction band necrosis: reperfusion leads to an influx of calcium, leading to hypercontraction of myofibrils (despite cell being dead with no nucleus)

2. Reperfusion injury: return of O2 and inflammatory cells may lead to free radical generation. (often see an additional increase in troponin after angioplasty due to formation of free radicals)

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5
Q

<4 hours after MI

A
  • NO gross changes, NO microscopic changes
  • Can see cardiogenic shock (massive infarction), CHF, arrhythmia
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6
Q

4-24 hours post MI

A

-Dark Discoloration

-Coagulative necrosis

-Complication of arrhythmia

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7
Q

1-3 days post MI

A

-Yellow pallor

-Neutrophils due to Acute Inflammation

-Complication of fibrinous pericarditis that presents as CP with friction rub

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8
Q

4-7 days post MI

A
  • Yellow pallor
  • macrophages present that are eatingup necrotic debris.

Risk of rupture of ventricular free wall HIGHEST now can lead to cardiac tamponade. Risk of rupture of interventricular septum leading to shunt, rupture of papillary muscle leading to mitral insufficiency (esp if RCA infarct)

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9
Q

1-3 months post MI

and Months after MI

A

1-3 months

  • Red border emerges as grnaulation tissue enters from edge of infarct
  • Granulation tissue with plump fibroblasts, collagen (type 1 Collagen), and blood vessels

Months

White scar, with fibrosis, risk of aneuysm, mural thrombus or Dressler syndrome (Ab against pericardium)

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10
Q

Causes of left sided HF

A
  • Ischemia
  • hypertension
  • dilated cardiomyopathy
  • MI
  • Restrictive cardiomyopathy
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11
Q

Clinical features of left sided HF

A

-pulm congestion leading to pulmonary edema

-dyspnea, paroxysmal nocturnal dyspnea (due to increased venous return when lying flat), orthopnea, crackles

  • Small congested capillaries burst, leading to intraalveolar hemorrhage marked by hemosiderin-laden macrophages
  • decreased blood flow to kidneys resulting in activation of RAAS

-tx: ACE-I

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12
Q

Right sided heart failure causes and presentation

A

Causes: left sided heart failure, left to right shunt, cor pulmonale

Clinical: JVD, hepatosplenomegaly (with nutmeg liver) leading to cardiac cirrhosis, pitting edema (due to increased hydrostatic pressure)

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13
Q

Right sided HF vs Left sided HF

A
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14
Q

Ventricular Septal Defect (VSD)

A

-Defect in septum that divides right and left ventricles.

-most common congenital heart defect

L–> R shunt

Can result in Eisenmenger syndrome (reversal of shunt)

Tx: surgical closure

Associated with fetal alcohol syndrome****, Cri-du-chat syndrome

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15
Q

Atrial Septal Defect

A

-Most common type is ostium secundum (90% of cases)

-Ostium primum type is associated with Down Syndrome

-Results in L –> R shunt, split S2 on auscultation due to increased blood in right heart delays closure of pulmonary valve

-Paradoxical emboli can occur (instead of going to lung to cause PE, go to left side of circulation, end up going to brain or other circulation places)

-Distinct from patent foramen ovale in that septa are missing tissue rather than unfused.

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16
Q

Patent Ductus Arteriosus (PDA)

A
  • Failure of ductus arteriosus to close
  • Associated with congenital rubella
  • Left –> Right shunt between aorta and pulm artery resulting in pulm HTN

-Machine-like murmur

-May lead to Eisenmenger syndrome, resulting in lower extremity cyanosis (because past branch point of aorta)

Tx: Indomethacin (decreases PGE). PGE KEEEEPS PDA open

17
Q

Tetralogy of Fallot

A

1. Stenosis of right ventricular outflow tract

2. right ventricular hypertrophy

3. VSD

4. Aorta that overrides the VSD

-Right –> Left shunt

-pts learn to squat, increases arterial resistance by decreasing shunting and allowing more blood to reach lungs

-Boot shaped heart on X-ray

18
Q

Transposition of great vessels associated with what and treated with what?

A

-Maternal diabetes

  • presents with early cyanosis
  • Need to create a shunt after birth, give PGE to keeeep PDA patent until surgery can be performed
19
Q

Coarctation of Aorta

A

-Narrowing of the aorta. Two types

1. Infantile: associated with PDA, coarctation distal to aortic arch but proximal to PDA. Lower extremity cyanosis. Associated with Turner Syndome

2. Adult: not associated with PDA. Hypertension in upper extremities and weak pulses in lower extremities. Collateral ciruclation develops across intercostal arteries, engorged arteries cause “notching of ribs”Associated with Bicuspid Aortic Valve

20
Q

Cause of acute rheumatic fever

A

2-3 weeks post Group A beta hemolytic streptococi

Caused by molecular mimicry, bacterial M protein resembles proteins in human tissue

21
Q

3 types of pancarditis in Acute Rheumatic Fever

A

1. Endocarditis: Mitral valve > Aortic valve. Small vegetations along lines of closure that lead to regurgitation

2. Myocarditis: Aschoff bodies that are characterized by foci of chronic inflammation, reactive histiocytes with slender wavy nuclei (Anitschkow cells) MOST common cause of death

3. Pericarditis: leads to friction rub and CP

22
Q

Aortic Stenosis

A

Systolic Murmur

Usually due to fibrosis and calcification. Increased risk with bicuspid aortic valve

-May also arise as a consequence of Chronic Rheumatic Valve Disease, coexisting mitral stenosis and fusion of the aortic valve commissures.

-Systolic ejection click followed by crescendo-decrescendo

-Concentric LVH, angina and syncope with exercise, microangiopathic hemolytic anemia (RBC damaged produces schistocytes)

23
Q

Aortic Regurgitation

A

Diastolic Murmur

-Due to aortic root dilation (syphilitic aneurysm and aortic dissection), or valve damage (infectious endocarditis)

-Early blowing diastolic murmur

-Wide pulse pressure (increased systolic, decreased diastolic)

-Bounding pulse (water-hammer pulse), pulsating nail bed, head bob

-Eccentric hypertrophy (due to volume overload)

24
Q

Concentric vs eccentric LV hypertrophy

A

Concentric: Aortic Stenosis, Hypertrophic Cardiomyopathy. Sarcomeres added in PARALLEL

Eccentric: Aortic Regurgitation, Dilated Cardiomyopathy. Sarcomeres added in SERIES

25
Q

Mitral Valve Prolapse

A

Ballooning of mitral valve back into LA during systole

  • Seen in 2-3% of US adults
  • Due to myxoid degeneration (accumulation of ground substances) of the valve, making it floppy

-Mid-systolic click, followed by regurgitation murmur

-Seen in Marfan and Ehlers-Danlos

26
Q

Mitral Regurgitation

A
  • Reflux of blood LV–>LA during systole
  • Arises as a complication of mitral valve prolapse
  • Also arise from LV dilation, infective endocarditis, acute rheumatic heart disease, papillary muscle rupture after MI (day 4-7 most likely)
  • Holosystolic blowing murmur, louder with squatting (increased afterload) and expiration (increased venous return)

Can lead to volume overload and left sided heart failure

27
Q

Mitral Stenosis

A
  • Narrowing of mitral valve orifice
  • Usually due to chronic rheumatic valve disease
  • Opening SNAP followed by diastolic rumble
  • Can lead to pulm congestion, pulm HTN with R sided HF, AFIB and mural thrombi
28
Q

Most common overall cause of endocarditis

A

-Steptococcus viridans: a low virulence organism that infects PREVIOUSLY damaged valves. Results in small vegetations that do not destroy valves

=Also called subacute endocarditis

29
Q

Endocarditis in IV drug users affects which valve and what bug?

A

S. Aureus and affects tricuspid valve

Results in large vegetations that destroy the valve

30
Q

HACEK organisms are what and what do they cause?

A

-Associated with endocarditis with negative blood cultures

Haemophilus

Actinobacillus

Cardiobacterium

Eikenella

Kingella

31
Q

Clinical features of bacterial endocarditis include

A
  • Fever
  • Murmur
  • Janeway lesions (erythematous lesions on palms and soles)
  • Osler nodes (painful lesions on fingers and toes)
  • Roth spots (due to embolization of septic vegetations)
32
Q

Libman-Sacks endocarditis

A

-due to sterile vegetations that arise in association with SLE. Vegetations ar epresent on surgce and undersurface of mitral valve

BOTH SIDES OF VALVE

33
Q

Dilated Cardiomyopathy

A

-Dilation of all four chambers of heart.

-MOST common form of cardiomyopathy

  • Systolic dysfunction leading to R+L HF, mitral and tricuspid regurgitation and arrhythmia (think stretching)
  • Causes: idiopathic (mostly), myocarditis (coxsackie A or B), ETOH, Drugs (doxorubicin, cocaine), Pregnancy, hemochromatosis
34
Q

Hypertrophic Cardiomyopathy

A
  • Hypertrophy of LV
  • Genetic mutations in SARCOMERE proteins, AD
  • Decreased CO

LVH–> diastolic dysfunction

S4 present

Syndope with exercise, sudden death

-Myofiber concentric hypertrophy with disarray

35
Q

Restrictive Cardiomyopathy

A
  • Decreased compliance of ventricular endomyocardium that restricts filling during diastole
  • Caused by: amyloidosis, sarcoidosis, endocardial fibroelastosis (children), Loeffler syndrome(endomyocardial fibrosis with an eosinophilic infiltrate and eosinophilia)
  • Presenents as congestive heart failure, low voltage EKG with diminished QRS
36
Q

Myxoma

A
  • Benign mesenchymal tumor with a gelatinous appearance and abundant ground substance.
  • MOST COMMON primary cardiac tumor in adults
  • Forms a pedunculated mass in the LA that can cause syndope due to obstruction of mitral valve

90% in LA

37
Q

Rhabdomyomas

A

-benign hamatoma of cardiac muscle

-Most common primary cardiac tumor in CHILDREN

-Associated with tuberous sclerosis