Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

ischemic heart disease - pathogenesis

A

*coronary artery disease: decreased blood flow caused by atherosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

myocardial infarction (MI) - overview

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

normal appearance of myocardium

A

*viable nuclei
*cross-striations
*intercalated discs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

*gross and microscopically identified hemorrhage
*prominent contraction bands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A

*necrosis elicits NEUTROPHILIC INFILTRATE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

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

A

*influx of MACROPHAGES
*removing necrotic myocytes and neutrophil fragments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

myocardial infarction - complication: arrhythmia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

myocardial infarction - complication: contractile dysfunction

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

myocardial infarction - complication: papillary muscle dysfunction/rupture

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

myocardial infarction - complication: pericarditis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
degenerative valve disease - overview
*degenerative changes in valvular extracellular matrix causing valve dysfunction *related to repetitive mechanical stresses
26
degenerative valve disease due to calcifications
*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
degenerative valve disease due to alterations in the extracellular matrix
*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
rheumatic heart disease - overview
*cardiac manifestation of rheumatic fever *acute immunologically-mediated, multisystem inflammatory disease that occurs after group-A beta-hemolytic streptococcal infections
29
rheumatic heart disease - clinical features
*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
rheumatic heart disease - pathogenesis
*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
rheumatic heart disease - pathology
*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
infective endocarditis - overview
*microbial infection of heart valves or mural endocardium with underlying tissue damage *marked by presence of vegetations = infected thrombus with organisms
33
infective endocarditis - pathogenesis
*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
infective endocarditis - clinical presentation
*rapid onset of fever, chills, weakness *murmurs in majority of patients
35
infective endocarditis - gross pathology
*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
infective myocarditis - overview
*infectious agents or inflammatory processes targeting the myocardium *usually VIRAL
37
infective myocarditis - pathogenesis
*viral infection (classically, Coxsackie viruses) *injury stems from direct cytopathic effects or by secondary immune response damage
38
infective myocarditis - pathology
*myocardial inflammation and edema *may resolve without significant sequelae *heal by progressive fibrosis
39
dilated cardiomyopathy - mechanism of failure
*impairment of contractility (systolic dysfunction)
40
dilated cardiomyopathy - causes
*genetic (~50%) *alcohol, peripartum, myocarditis, etc
41
dilated cardiomyopathy - gross morphology
*four-chamber dilation & hypertrophy *ischemic appearance
42
dilated cardiomyopathy - microscopic morphology
*non-specific, with myocyte hypertrophy and interstitial fibrosis
43
hypertrophic cardiomyopathy - mechanism of failure
*impairment of compliance (diastolic dysfunction)
44
hypertrophic cardiomyopathy - causes
GENETIC
45
hypertrophic cardiomyopathy - gross morphology
*thick-walled without ventricular dilation *disproportionate septal thickening
46
hypertrophic cardiomyopathy - microscopic morphology
*marked myocyte hypertrophy & disarray *interstitial fibrosis
47
restrictive cardiomyopathy - mechanism of failure
*impairment of compliance (diastolic dysfunction)
48
restrictive cardiomyopathy - causes
*systemic disorders affecting myocardium *amyloidosis *radiation-induced fibrosis *Loeffler syndrome *endomyocarditis
49
restrictive cardiomyopathy - gross morphology
*ventricles normal size *atria dilated
50
restrictive cardiomyopathy - microscopic morphology
*interstitial deposition/fibrosis (amyloid, eosinophilia, endomyocardial fibrosis)
51
atrial myxoma - overview
*benign neoplasm arising from primitive multipotent mesenchyme *most common primary tumor of the heart *familial syndromes associated with myxomas
52
atrial myxoma - clinical symptoms
*elaboration of IL6 causes fever & malaise *valvular obstruction *embolization of fragments
53
atrial myxoma - pathology
*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
papillary fibroelastoma
*benign tumor of valvular endocardium *hair-like projections
55
rhabdomyoma
*benign tumor of myocytes *bizarre, markedly enlarged myocytes (Spider cells) *usually associated with tuberous sclerosis

Cardiology Exam (52 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions