Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pathology > Heart > Flashcards

Heart Flashcards

1
Q

Three mechanisms that initially maintain cardiac output in HF

A

1) Frank-Starling, 2) hypertrophy and/or dilation, 3) neurohormonal (adrenergic, RAAS, and ANP)

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

Effect of pressure overload

A

Parallel formation of new sarcomeres = hypertrophy (lalaki to cope)

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

Effect of volume overload

A

Series formation of new sarcomeres = dilation (dadami to cover greater volume)

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

Common causes of left-sided HF

A

Ischemic heart disease, HTN, aortic and mitral valve diseases, primary myocardial diseases

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

Common causes of right-sided HF

A

Left-sided HF (most common) and cor pulmonale

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Organ more affected by left-sided HF than right-sided HF

A

Lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Organs hypoperfused by left-sided HF

A

Kidneys (prerenal azotemia) and brain (hypoxic enceph)

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

More prominent finding in right-sided HF due to third spacing

A

Effusions and ascites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Most common genetic cause of congenital heart disease

A

Trisomy 21

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

Marks the irreversibility of CHD lesions

A

Pulmonary HTN

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

Most common type of ASD

A

Ostium secundum (90%)

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

ASD adjacent to AV valves

A

Ostium primum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Associated with ostium primum

A

AV valve defects and VSD

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

ASD near the entrance of the SVC

A

Sinus venosus

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

Clinical findings pointing to ASD

A

Widely fixed split S2 (due to prolonged ejection of RV and increased blood flow across PV), and murmur (pulmonic stenosis-like due to increase blood flow across PV)

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

Most common congenital heart defect

A

VSD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Most common type of VSD

A

Perimembranous (90%), other types include infundibular and muscular

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

Cut-off size for VSD that would determine if clinically symptomatic or well-tolerated

A

> 10 mm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

T or F: Small muscular VSDs are more likely to close than membranous

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Vast majority of VSDs that close do so before age __

A

Four years of age

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

Adult remnant of PDA

A

Ligamentum arteriosum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Embryonic structure represented by median umbilical ligament

A

Urachus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Embryonic structure represented by medial umbilical ligament

A

WALA (mediaNNNN ang urachus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

CHD associated with continuous, machinery-like murmur

A

PDA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Administered to infants relying on PDA to survive other CHDs

A

PGE2 (alprostadil), a prostaglandin analogue (vs indomethacin, which can be used to close the PDA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Most common cyanotic heart disease overall

A

TOF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Most common cyanotic heart disease in newborns

A

TGA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Defect causing TOF

A

Anterosuperior displacement of infundibular septum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Components of TOF

A

RVH, VSD, overriding aorta, pulmonary outflow obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Couer en sabot

A

Boot-shaped heart on CXR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

The degree of ___ determines clinical consequences

A

PS (if mild, “pink TOF” that acts like VSD; if considerable, then classic TOF with tet spells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Epidemiologic profile of patients with TGA

A

Infant of diabetic mothers and male (3:1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Frequently associated abnormalities in TGA necessary for survival

A

PFO, ASD, PDA (50% also have VSD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Radiographic appearance of TGA

A

Egg on a string or apple on a stem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Location of infantile coarctation of the aorta

A

Tubular hypoplasia proximal to the PDA (preductal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Location of adult coarctation of the aorta

A

Coarctation opposite the ligamentum arteriosum distal to arch vessels (postductal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Associated genetic syndrome with infantile coarctation of the aorta

A

Turner syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Clinical findings of infantile coarctation

A

Lower extremity cyanosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Clinical findings of adult coarctation

A

Upper extremity hypertesion with rib notching on CXR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Most common cause of ischemic heart disease

A

Atherosclerosis of epicardial coronary arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Earliest detectable feature of myocyte necrosis

A

Sarcolemmal membrane disruption, leading to myocardial proteins in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Length of time to loss of contractility in IHD

A

<2 mins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Length of time to loss of irreversible cell injury in IHD

A

20-40 mins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Three patterns of infarction

A

Transmural, subendocardial, multifocal microinfarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Pattern of infarction leading to regional permanent occlusion that occurs in STEMI

A

Transmural

46
Q

Pattern of infarction leading to transient or partial occlusion or global hypotension (circumferential) occuring in NSTEMI

A

Subendocardial

47
Q

Most commonly involved coronary arteries in MI

A

LAD > RCA > L circumflex

48
Q

Gross morphology of infarcts after 2-3 hours

A

Triphenyltetrazolium chloride pale zone

49
Q

Gross morphology of infarcts after 12-24 hours

A

Reddish-blue (stagnated, trapped blood) or dark mottling, with conversion to pale tan, soft infarct

50
Q

Gross morphology of infarcts after 10-14 days

A

Bounded by hyperemic zone of granulation (conversion to fibrous scar)

51
Q

Microscopic morphology of infarcts after 6-12 hours

A

Ischemic coagulative necrosis

52
Q

Microscopic morphology of infarcts after 1-3 days

A

Acute inflammation with PMNs

53
Q

Microscopic morphology of infarcts after 3-7 days

A

Macrophages

54
Q

Microscopic morphology of infarcts after 1-2 weeks

A

Granulation tissue

55
Q

Most sensitive and specific cardiac troponins

A

Trop T and trop I

56
Q

Cardiac biomarker used to assess reinfarction

57
Q

Cardiac biomarkers that peak within 24 hours

A

Trop I and CK-MB

58
Q

Cardiac biomarkers that return to normal in 5-10 days

59
Q

Cardiac biomarkers that return to normal in 48-72 hours

60
Q

Fibrinous pericarditis post MI

A

Dressler syndrome

61
Q

Unexpected death from cardiac causes either without symptoms or within 1 to 24 hours of symptom onset

A

Sudden cardiac death

62
Q

Most common cause of sudden cardiac death

63
Q

Most common mechanism of sudden cardiac death

A

Arrhythmia (asystole or v fib)

64
Q

Most common cause of arrhythmia

A

Ischemic injury

65
Q

Earliest change seen in left-sided HHD

A

Increase in transverse diameter of myocytes, leading to variable cell or nuclear enlargement with interstitial fibrosis

66
Q

Seen in acute cor pulmonale from left-sided HHD

A

RV dilation

67
Q

Seen in chronic cor pulmonale from left-sided HHD

A

RV hypertrophy, dilation, and possible R-sided HF

68
Q

Most common cause of MVP

69
Q

Most common known cause of MVP

A

Fibrillin-1 gene defect (Marfan’s)

70
Q

In MVP, marked thickening of spongiosa with deposition of mucoid material

A

Myxomatous degeneration

71
Q

Antibodies and CD4 T cells directed vs streptococcal M proteins also recognize cardiac self-antigens

A

Molecular mimicry

72
Q

Composed of T-cells, plasma cells, and macrophages

A

Aschoff body (seen in RF)

73
Q

Plump, activated macrophages with condensed chromatin pattern (“slender wavy ribbon”), also known as caterpillar cells

A

Anitschkow cells

74
Q

Most commonly involved valve in RHD

A

Mitral > aortic > tricuspid >pulmonic

75
Q

Calcification and fibrous bridging of valvular commisures seen in RHD

A

Fish mouth or button hole deformity

76
Q

Small vegetations along lines of closure overlying foci of fibrinoid necrosis seen in RHD

77
Q

Subendocardial irregular thickenings due to regurgitant jets seen in RHD

A

MacCallum plaques

78
Q

Hallmark of infective endocarditis

A

Vegetations

79
Q

Common organisms in acute IE

A

Staph aureus (also in IV drug users), damage more pronounced

80
Q

Common organisms in subacute IE

A

Viridans strep and HACEK organisms

81
Q

Most commonly affected valves in IE

A

Aortic and mitral

82
Q

Two kinds of non-infective vegetations

A

Nonbacterial thrombotic endocarditis (NBTE) or marantic endocarditis, and Libman-Sacks endocarditis (in SLE)

83
Q

Consequence of IE vegetations

A

Septic embolus

84
Q

Associated with marantic endocarditis

A

Systemic hypercoagulable states, mucinous adenoCA, endocardial trauma

85
Q

Three broad categories of cardiamyopathies

A

Dilated CM, hypetrophic CM, restrictive CM

86
Q

Dysfunction in dilated CM

A

Systolic (impaired contractility)

87
Q

Dysfunction in hypertrophic CM and restrictive CM

A

Diastolic (impaired compliance)

88
Q

Genetic neurological disease associated with hypertrophic CM

A

Friedreich ataxia

89
Q

Other associated causes of hypetrophic CM

A

Friedreich ataxia, storage diseases, infant of diabetic mothers

90
Q

Causes of restrictive CM

A

Amyloidosis, radiation-induced fibrosis, endomyocardial fibrosis

91
Q

Most common viral causes of myocarditis

A

Coxsackie A and B, enteroviruses

92
Q

Parasitic causes of myocarditis

A

T. cruzi (Chagas disease) and Trichinella spiralis

93
Q

Most common helminthic cause of myocarditis

A

Trichinella spiralis

94
Q

Most common primary cardiac tumor in adults

95
Q

Most common primary cardiac tumor in children

A

Rhabdomyoma

96
Q

Location of myxoma

97
Q

Location of rhabdomyoma

A

Ventricles

98
Q

Conditions associated with myxoma

A

McCune-Albright and Carney complex

99
Q

Condition associated with rhabdomyoma

A

Tuberous sclersosis

100
Q

Number of mxyoma

A

Usually solitary

101
Q

Number of rhabdomyoma

A

Usually multiple

102
Q

Thin strands of cytoplasm from nucleus to nuclear membrane, found in rhabdomyoma

A

Spider cells

103
Q

Beck’s triad of cardiac tamponade

A

Hypotension, engorged neck veins, muffled heart sounds

104
Q

Radiographic appearance of pericardial effusion

A

Water-bottle appearance

105
Q

Most common type of acute pericarditis

A

Fibrinous/serofibrinous

106
Q

Most common cause of hemorrhagic pericarditis

107
Q

Most common cause of caseous pericarditis

108
Q

Two types of chronic pericarditis

A

Adhesive mediastinopericarditis, constrictive pericarditis

109
Q

Clinical findings of adhesive mediastinopericarditis

A

Systolic retraction of the rib cage and diaphragm, pulsus paradoxus

110
Q

Clinical findings of constrictive pericarditis

A

Diastolic dysfunction

111
Q

Clinical findings of acute pericarditis

A

Pericardial friction rub, chest pain relieved when leaning forward

Pathology (13 decks)

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