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Cardiology Exam > CV Pathology 2 > Flashcards

CV Pathology 2 Flashcards

1
Q

troponin - overview

A

*biomarker of myocardial damage
*normally regulate calcium-mediated contraction of cardiac muscle
*serum elevation = cardiac myocyte death (infarction, myocarditis, trauma)
-serum levels rise in 2-4 hours and peak 24-48 hours after an acute infarct
-levels may be higher and peak earlier with reperfusion = washout from necrotic tissue

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2
Q

ischemic heart disease - overview

A

*group of related entities resulting from myocardial ischemia
*imbalance between myocardial perfusion and cardiac O2 demand
*chief cause of mortality in US

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3
Q

ischemic heart disease - pathogenesis

A

*coronary artery disease: decreased blood flow caused by atherosclerosis

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4
Q

ischemic heart disease - clinical variants

A
  1. chronic coronary syndromes:
    a. stable angina = fixed stenosis
    b. prinzmetal = coronary spasm
  2. acute coronary syndromes:
    a. unstable angina = fixed stenosis with thrombosis
    b. myocardial infarction = obstruction with NECROSIS
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5
Q

myocardial infarction (MI) - overview

A

*necrosis of heart muscle resulting from ischemia
*increased incidence with age and atherosclerosis risk factors

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6
Q

myocardial infarction (MI) - pathogenesis

A

*acute thrombotic obstruction of coronary artery due to rupture of atherosclerotic plaque
*disruption typically sudden
*hemorrhage into plaque or additional thrombosis
* > 30 min = irreversible myocyte coagulative necrosis

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7
Q

myocardial infarction (MI) - transmural vs. endocardial

A
  1. transmural infarct:
    -FULL THICKNESS MYOCARDIAL NECROSIS
    -caused by COMPLETE OBSTRUCTION of coronary vessel
    -causes STEMI
  2. endocardial infarct:
    -only inner portion myocardial necrosis
    -obstruction of distal coronary vessels or severe/incomplete obstructions
    -causes NSTEMI
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8
Q

normal appearance of myocardium

A

*viable nuclei
*cross-striations
*intercalated discs

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9
Q

myocardial infarction (MI) - morphology 4-8 hours post-MI

A

*microscopic coagulative necrosis detectable:
-loss of nuclei (karyolysis)
-beginning loss of cross-striations
wavy CONTRACTION BANDS () extending across the fibers

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10
Q

myocardial infarction (MI) - morphology 12-24 hours post-MI

A

*gross and microscopically identified hemorrhage
*prominent contraction bands

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11
Q

myocardial infarction (MI) - morphology 1-3 days post-MI

A

*necrosis elicits NEUTROPHILIC INFILTRATE

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12
Q

myocardial infarction (MI) - morphology 3-7 days post-MI

A

*influx of MACROPHAGES
*removing necrotic myocytes and neutrophil fragments

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13
Q

myocardial infarction (MI) - morphology 10-14 days post-MI

A

*granulation tissue
*healing requires ingrowth of new vessels from the infarct margins
*large infarcts take longer to heal than smaller ones

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14
Q

myocardial infarction (MI) - morphology 2-8 weeks post-MI

A

*healing well underway
*EXTENSIVE COLLAGEN DEPOSITION (scar)
*MI size determines clinical sequelae

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15
Q

myocardial infarction - complication: arrhythmia

A

*90% develop some rhythm disturbance
*ex: ventricular fibrillation (causes the majority of deaths occurring prior to hospitalizations)

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16
Q

myocardial infarction - complication: contractile dysfunction

A

*impaired function proportional to size of damage
*ex. transmural infarct causes severe pump failure (cardiogenic shock)

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17
Q

myocardial infarction - complication: mural thrombus

A

*stasis due to diminished myocardial contractility
*endocardial damage fosters mural thrombosis with risk for left-sided thromboembolism

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18
Q

myocardial infarction - complication: papillary muscle dysfunction/rupture

A

*leads to post-infarct regurgitation
*mechanical complications most prevalent 3-14 days after MI

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19
Q

myocardial infarction - complication: ventricular dilation/aneurysm

A

*weakened necrotic muscle → stretching, thinning, and dilation of infarcted region
*large transmural infarctions → ventricular aneurysms
*prone to mural thrombosis
*mechanical complications most prevalent 3-14 days after MI

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20
Q

myocardial infarction - complication: myocardial rupture

A

*usually occurs < 5 days
*left ventricular rupture → rapidly fatal cardiac tamponade
*ventricular septal rupture → left-to-right shunt
*mechanical complications most prevalent 3-14 days after MI

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21
Q

myocardial infarction - complication: pericarditis

A

*transmural infarction → painful fibrinohemorrhagic pericarditis
*typically appears 2-3 days after infarction
*resolves after a few days

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22
Q

valvular heart disease - overview

A

*cardiac dysfunction caused by valvular disease
*usually acquired; more common on left side of heart
*abnormal flow = murmurs (auscultated), thrills (palpated)

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23
Q

valvular stenosis - overview

A

*failure to open completely
*forward flow obstruction
*due to chronic process (calcification or scarring)

24
Q

valvular insufficiency - overview

A

*failure to close completely
*regurgitation of blood (backflow)
*disease of valve cusps or tendinous cords or papillary muscles, e.g. endocarditis

25
Q

degenerative valve disease - overview

A

*degenerative changes in valvular extracellular matrix causing valve dysfunction
*related to repetitive mechanical stresses

26
Q

degenerative valve disease due to calcifications

A

*age-associated “wear and tear”
*clinical: usually asymptomatic
*pathogenesis: repeated valve injury → exacerbated blood flow → endothelial injury → Ca2+ deposition
*heaped-up calcified masses on cusp outflow side:
-protrude/impede valve opening (stenosis)
-cusps show thickened fibrosis

27
Q

degenerative valve disease due to alterations in the extracellular matrix

A

*idiopathic
*ballooning/hooding of leaflets:
-enlarged, redundant, thick, rubbery, floppy leaflets
*deposition of myxomatous (mucoid) material:
-increased proteoglycan and decreased fibrillar collagen/elastin
-fibrosis with scarring

28
Q

rheumatic heart disease - overview

A

*cardiac manifestation of rheumatic fever
*acute immunologically-mediated, multisystem inflammatory disease that occurs after group-A beta-hemolytic streptococcal infections

29
Q

rheumatic heart disease - clinical features

A

*evidence of preceding group A streptococcal infection (10 days to 6 weeks)
*acute rheumatic fever
*signs of carditis: pericardial friction rubs, cardiac dilation, mitral insufficiency, CHF

30
Q

rheumatic heart disease - pathogenesis

A

*tissue damage caused by combination of anti-M protein antibodies and T cell-mediated reactions
*CD4+ T cells recognize streptococcal peptides AND host antigens elicit cytokine-mediated inflammation

31
Q

rheumatic heart disease - pathology

A

*pancarditis = all layers of heart affected
1. pericarditis → fibrinous exudate
2. myocarditis: ASCHOFF BODIES
-collections of T-lymphocytes, scattered plasma cells, and plump, activated macrophages with necrosis (see image)
-scattered in interstitial tissue
3. valvulitis:
-FIBRINOID NECROSIS (fibrin deposition along closure lines)
-vegetations (small thrombotic verrucae)

32
Q

infective endocarditis - overview

A

*microbial infection of heart valves or mural endocardium with underlying tissue damage
*marked by presence of vegetations = infected thrombus with organisms

33
Q

infective endocarditis - pathogenesis

A

*microorganism seeds the bloodstream (bacteremia usually)
*acute = destructive infections by highly virulent organisms in NORMAL valves (STAPH AUREUS)
*chronic = infections by low virulence organisms in previously abnormal valves (Strep viridans)

34
Q

infective endocarditis - clinical presentation

A

*rapid onset of fever, chills, weakness
*murmurs in majority of patients

35
Q

infective endocarditis - gross pathology

A

*vegetations are friable, bulky, destructive:
-fibrin and inflammatory cells
-bacteria or other organisms
*vegetations are prone to embolization:
-often contain virulent organisms
-abscesses, septal infarcts, or mycotic aneurysms

36
Q

infective myocarditis - overview

A

*infectious agents or inflammatory processes targeting the myocardium
*usually VIRAL

37
Q

infective myocarditis - pathogenesis

A

*viral infection (classically, Coxsackie viruses)
*injury stems from direct cytopathic effects or by secondary immune response damage

38
Q

infective myocarditis - pathology

A

*myocardial inflammation and edema
*may resolve without significant sequelae
*heal by progressive fibrosis

39
Q

dilated cardiomyopathy - mechanism of failure

A

*impairment of contractility (systolic dysfunction)

40
Q

dilated cardiomyopathy - causes

A

*genetic (~50%)
*alcohol, peripartum, myocarditis, etc

41
Q

dilated cardiomyopathy - gross morphology

A

*four-chamber dilation & hypertrophy
*ischemic appearance

42
Q

dilated cardiomyopathy - microscopic morphology

A

*non-specific, with myocyte hypertrophy and interstitial fibrosis

43
Q

hypertrophic cardiomyopathy - mechanism of failure

A

*impairment of compliance (diastolic dysfunction)

44
Q

hypertrophic cardiomyopathy - causes

A

GENETIC

45
Q

hypertrophic cardiomyopathy - gross morphology

A

*thick-walled without ventricular dilation
*disproportionate septal thickening

46
Q

hypertrophic cardiomyopathy - microscopic morphology

A

*marked myocyte hypertrophy & disarray
*interstitial fibrosis

47
Q

restrictive cardiomyopathy - mechanism of failure

A

*impairment of compliance (diastolic dysfunction)

48
Q

restrictive cardiomyopathy - causes

A

*systemic disorders affecting myocardium
*amyloidosis
*radiation-induced fibrosis
*Loeffler syndrome
*endomyocarditis

49
Q

restrictive cardiomyopathy - gross morphology

A

*ventricles normal size
*atria dilated

50
Q

restrictive cardiomyopathy - microscopic morphology

A

*interstitial deposition/fibrosis (amyloid, eosinophilia, endomyocardial fibrosis)

51
Q

atrial myxoma - overview

A

*benign neoplasm arising from primitive multipotent mesenchyme
*most common primary tumor of the heart
*familial syndromes associated with myxomas

52
Q

atrial myxoma - clinical symptoms

A

*elaboration of IL6 causes fever & malaise
*valvular obstruction
*embolization of fragments

53
Q

atrial myxoma - pathology

A

*left atrium:
-pedunculated with stalk (usually 2-6 cm; ball valve obstruction of mitral or tricuspid valve)
-gelatinous amorphous extracellular matrix (scattered myxoma cells, abnormal vessel-like formations)

54
Q

papillary fibroelastoma

A

*benign tumor of valvular endocardium
*hair-like projections

55
Q

rhabdomyoma

A

*benign tumor of myocytes
*bizarre, markedly enlarged myocytes (Spider cells)
*usually associated with tuberous sclerosis

Cardiology Exam (52 decks)

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