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Cardiovascular Medicine-Unit 1 > Ch 12-Cardiac Path-Galbraith PDF's > Flashcards

Ch 12-Cardiac Path-Galbraith PDF's Flashcards

1
Q

Describe morphologic changes of heart valves as you age:

A

Aortic and mitral valve annular calcification
Fibrous thickening
MV leaflets buckling toward LA —> increased LA size
Lambl excrescences

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2
Q

Describe the vascular changes in the heart as you age:

A

Coronary atherosclerosis

Stiffening of the aorta

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3
Q

Loss of myocardial contractile function is a __ dysfunction

Loss of ability to fill the ventricles during ventricular filling is a ___ dysfunction

A

Systolic

Diastolic

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4
Q

In the setting of pressure overload, myocytes become ___ and the LV wall thickness increases concentrically

In the setting of volume overload, myocytes ___, and ventricular dilation is seen

A

Thicker

Elongate

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5
Q

What is left-sided heart failure commonly a result of?

A

Myocardial ischemia
HTN
Left-sided valve disease
Primarily myocardial disease

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6
Q

In left ventricular dysfunction, you can get left atrial dilation which can lead to:

A

A fib, stasis, thrombus

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7
Q

What are some symptoms of pulmonary congestion and edema from left-sided heart failure?

A

Cough
Dyspnea
Orthopnea
Paroxysmal nocturnal dyspnea (pillow orthopnea)

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8
Q

Describe what happens to glomerular perfusion in left-sided failure and its consequences:

A

Decreased ejection fraction may result in decreased glomerular perfusion –> stimulates release of renin –> increased volume

Prerenal azotemia

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9
Q

What is the most common cause of right-sided heart failure?

A

Left-sided heart failure

Isolated right-sided heart failures results from any cause of pulmonary HTN (parenchymal lung disease, primary pulm HTN, pulm vasoconstriction)

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10
Q

In primary right-sided heart failure, describe what happens to the following as the venous system becomes markedly congested:
Liver: __
Spleen: __
Peritoneal, pleural, and pericardial spaces: ___
Edema?
Renal: __

A 
Liver congestion (NUTMEG liver)
Splenic congestion (SPLENOMEGALY)
Effusions
Edema in dependent areas (ankle)
Renal congestion
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11
Q

___ is described as a stenosis occlusion of a coronary artery with a “squeezing” or burning sensation (when walking up stairs/exercising), relieved by rest or vasodilators

A

Stable angina

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12
Q

__ is characterized as an episodic coronary spasm, relieved with vasodilators

A

Prinzmetal angina

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13
Q

__ is characterized by pain, increasing in frequency, duration, and severity, eventually at rest. There is usually a rupture of a plaque, with a partial thrombus. Up to 50% may have evidence of myocardial necrosis

A

Unstable or “crescendo” angina

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14
Q

Nearly 90% of infarcts are caused by ___

A

Atheromatous plaque

Other causes: embolus, vasospasm, ischemia secondary to vasculitis, shock ,hematologic abnormalities

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15
Q

Describe the classic presentation of an MI:

A 
PROLONGED CHEST PAIN (>30 min) --> crushing, stabbing, squeezing, tightness; radiating down left arm or to left jaw
DIAPHORESIS
Dyspnea
Nausea-vomiting
Up to 25% are asymptomatic
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16
Q

Describe the levels of lactate and ATP during an MI

A

Lactate increases, ATP decreases

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17
Q

What are the areas of infarct with permanent occlusion of the LAD?

A

Apex, LV anterior wall, anterior 2/3 of septum

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18
Q

What are the areas of infarct with permanent occlusion of the RCA?

A

RV free wall, LV posterior wall, posterior 1/3 of septum

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19
Q

What are the areas of infarct with permanent occlusion of the LCX?

A

LV lateral wall

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20
Q

Describe the damage in a transient/partial obstruction non-transmural infarct:

A

Regional subendocardial infarct

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21
Q

Describe the damage in a global hypotension non-transmural infarct:

A

Circumferential subdendocardial infarct

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22
Q

Describe the damage in a small intramural vessel occlusion non-transmural infarct:

A

Microinfarcts

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23
Q

___ stains tissue containing lactate dehydrogenase red (after an MI)

A

Triphenyltetrazolium chloride

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24
Q

What are some gross and microscopic morphologic changes seen immediately after an MI?

A

Nothing

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25
Q

When will you see microscopic granulation tissue after an MI?

A

7-10 days it begins to form, can last up to 14 days

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26
Q

About how long does it take to form a dense collagenous scar following an MI?

A

~2 months

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27
Q

Contraction band necrosis is associated with ___

A

Reperfusion injury; dead myocytes contract d/t Ca influx

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28
Q

What is the most cardiac myocyte-specific lab test to determine an MI?

A

Troponin I and T

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29
Q

When does Troponin I typically peak after onset of chest pain in an MI?

A

About 24-30 hours

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30
Q

When does CK-MB usually peak after onset of chest pains with an MI?

A

About 18 hours

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31
Q

Half of all MI deaths occur within 1 hour of onset, and are usually secondary to a ___

A

Fatal arrhythmia

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32
Q

What are some more common complications of an MI?

A 
Contractile dysfunction
Fibrinous pericarditis
Myocardial rupture
Infarct expansion 
Ventricular aneurysm
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33
Q

___ precipitates sudden cardiac death in 80-90% of cases

A

Coronary artery disease

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34
Q

Sudden cardiac death is due to a __ most often arising from ischemia-induced myocardial irritability

A

Fatal arrhythmia

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35
Q

Left-sided hypertensive heart disease is usually due to ___ HTN

Right-sided hypertensive heart disease is usually due to ___ HTN

A

Systemic

Pulmonary

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36
Q

In left-sided heart disease, pressure overload results in LV hypertrophy (LV wall is concentrically thickened). What happens to the LA and what type of dysfunction and arrhythmia can result?

A

Diastolic dysfunction can result in LA enlargement

Can lead to A fib

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37
Q

Acute cor pulmonale may arise from a large __

A

Pulmonary embolus

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38
Q

Chronic stenosis may cause ___ overload hypertrophy –> CHF

Chronic insufficiency (regurgitation) may cause ___ overload hypertrophy –> CHF

A

Pressure

Volume

39
Q

___ is the most common valve abnormality. The prevalence increases with age (60-80 yrs), “wear and tear” is associated with chronic HTN, hyperlipidemia, inflammation. The bicuspid valves show an accelerated course and can get ossification of valves.

A

Calcification aortic stenosis

40
Q

What type of “cells” can be found on affected valves in calcific aortic stenosis?

A

Osteoblast-like cell

41
Q

Where do calcific deposits occur in mitral annular calcification?

A

Fibrous annulus (fibrous ring)

Normally does not affect valve function

42
Q

What gender and age group is more likely to have mitral annular calcification?

A

F > M

> 60 years

43
Q

When do valve leaflets prolapse back into the LA with a mitral valve prolapse?

A

Systole –> Mid-systolic click

44
Q

Who is more likely to have a mitral valve prolapse?

A

F : M –> 7:1 ratio

45
Q

What is the buzzword associated with leaflets becoming thickened and rubbery d/t proteoglycans deposits in mitral valve prolapse?

A

Myxomatous degeneration

46
Q

Rheumatic fever is a multisystem inflamm disorder following pharyngeal infx with ___

A

Group A streptococcus

47
Q

The pathogenesis of rheumatic heart disease is an immune response to streptococcal ___ proteins that cross react with cardiac self-ags.

A

M

48
Q

What are other common features of rheumatic fever?

A 
J-Joints (migratory polyarthritis)
O-O supposed to look like a heart for heart problems 
(pancarditis)
N-Nodules (subQ nodules)
E-Erythema marginatum (rash)
S-Syndenham chorea
49
Q

What is the morphologic feature associated with pancarditis in acute RF?

A

Aschoff bodies

50
Q

In chronic RHD, mitral leaflet thickening, fusion and shortening of commisures, fusion and thickening of tendinitis cords will result in __

A

Mitral stenosis

51
Q

what type of valvular disorder is mostly associated with RF?

A

Mitral stenosis

52
Q

__ is a rapidly progressive, destructive infx of a previously normal valve. It requires surgery in addition to ABx

A

Acute infective endocarditis

53
Q

__ is a slower-progressing infx of a previously deformed valve (such as in RHD). It can often be cured with ABx alone

A

Subacute infective endocarditis

54
Q

What are some predisposing conditions for infective endocarditis?

A

Valvular abnormalities: RHD, prosthetic valves, MV prolapse, calcific stenosis, bicuspid AV

Bacteremia: ANother site of infx, dental work/surgery, contaminated needles, compromised epithelium

55
Q

Which valves are more commonly affected in infective endocarditis?

A

Left-sided valves more commonly affected

Right-sided valves often involved in IV drug abusers

56
Q

What is the classic feature of infective endocarditis?

A

Friable, bulky, destructive valvular vegetations

Friability leads to septic emboli

Vegetations are mixtures of fibrin, inflamm cells, and orgs

57
Q

What type of symptoms do infective endocarditis pts usually present with?

A

Nonspecific symptoms –> fever, weight loss, fatigue

Murmurs usually present with left-sided lesions

58
Q

This org is often involved in infective endocarditis d/t dental work and valve abnormalities

A

Strep viridans

59
Q

This org causes infective endocarditis of normal valves, abnormal valves, and IV drug abusers.

A

Staph aureus

60
Q

This org is associated with infective endocarditis of prosthetic valves

A

Staph epidermidis

61
Q

Aside from strep viridans, staph aureus, and staph epidermidis, what other orgs are associated with infective endocarditis?

A 
H-Hemophilus
A-Actinobacillus
C-Cardiobacterium
E-Eikenella
K-Kingella
62
Q

Describe what happens to the the following features of the myocardium and chambers as you age:

LV chamber size: ___
Epicardial fat: ___
Myocardial changes: ___

A

Decreased LV size
Increased epicardial fat
Lipofuscin and basophilic degeneration, fewer monocytes, increased collagen fibers

63
Q

Nonbacterial thombotic endocarditis is associated with ___

A

MALIGNANCIES (Esp. mucinous adenocarcinomas)
Sepsis
Catheter-induced endocardial trauma

64
Q

What is the most common type of cardiomyopathy?

A

Dilated (90%)

65
Q

What type of dysfunction is associated with dilated cardiomyopathy?

A

Systolic dysfunction

Progressive cardiac dilation and systolic dysfunction, usually with dilated hypertrophy

66
Q

Dilated cardiomyopathy is thought to be familial in 30-50% of cases and due to ___ mutations and is autosomal dominant (usually)

A

TITIN

Alcohol strongly linked to DCM, so is myocarditis, cardiotoxic drugs/substances (Doxorubicin, cobalt Fe overload)

67
Q

Describe the morphology of Dilated cardiomyopathy

A

Dilation of all chambers
Mural thrombi common
Functional regurgitation of valves

68
Q

What is a classical presentation of Dilated cardiomyopathy?

A

Usually manifests between 20-50 yrs old
Progressive CHF –> dyspnea, exertional fatigue, decreased ejection fraction
Arrhythmias
Embolism

69
Q

___ is due to excess catecholamines following extreme emotional of psychological stress. It appears > 90% women ages 58-75, the symptoms and signs resemble an acute MI and there is apical ballooning of the LV with abnormal wall motion and contractile dysfunction.

A

Takotsubo cardiomyopathy

BROKEN HEART SYNDROME

70
Q

In Arrhythmogenic RV cardiomyopathy, RV failure and arrhythmias cause __ which can lead to sudden death

A

V tac and V fib

It is familial (usually autosomal dominant)

71
Q

Desmosome and intercalated dysfunctions are associated with this cardiomyopathy:

A

Arrhythmogenic RV cardiomyopathy

72
Q

__ is a genetic disorder leading to myocardial hypertrophy and diastolic dysfunction, leading to decreased stroke volume and often ventricular outflow obstruction

A

Hypertrophic cardiomyopathy

73
Q

In Hypertrophic cardiomyopathy, numerous mutations are known involving sarcomeric proteins, most commonly ___

A

B-myosin heavy chain

74
Q

Describe the morphology of hypertrophic cardiomyopathy:

A

Massive myocardial hypertrophy, often with marked septal hypertrophy

Microscopically, myocytes disarray

75
Q

Consequences of extensive ___ can lead to foci of myocardial ischemia, LA dilation and mural thrombus, diminished CO and increased pulm congestion leading to exertional dyspnea, arrhythmias, and Sudden death

A

Hypertrophic cardiomyopathy

76
Q

___ is due to decreased ventricular compliance (increased stiffness), leading to diastolic dysfunction. It may be secondary to depositio of material within the wall (amyloid) or increased fibrosis (radiation). The ventricles are usually normal size, but both atria can be enlarged

A

Restrictive cardiomyopathy

77
Q

Amyloid is an EC deposition of proteins which form an insoluble B-pleated sheet. It may be systemic (due to myeloma) or restricted to the heart which is usually __

A

Transthyretin

78
Q

When amyloid deposits in the interstitium of the myocardium of a ___ cardiomyopathy results

A

Restrictive

79
Q

What is the most common causative agent/org responsible for myocarditis?

A

Coxsackie A and B viruses most common

80
Q

What are some non-infectious causes of myocarditis?

A

Immune-mediated rxns, including RF, SLE, drug hypersensitivity

81
Q

The single most common genetic cause of congenital heart disease is ___

A

Trisomy 21

82
Q

What are the 3 left-to-right shunt congenital heart disorders (Galbraith slides)

A

ASD
VSD
PDA

83
Q

___ is usually asymptomatic until adulthood. The L–>R shunting causes volume overload on the right side which may lead to pulmonary HTN, Right heart failure, paradoxical embolization, and may be closed surgically with normal survival

A

ASD

84
Q

___ is the most common form of congenital heart disease. Many smaller defects close spontaneously but Large ones may cause significant shunting leading to RV hypertrophy, pulmonary HTN which can ultimately reverse flow through the shunt, leading to cyanosis

A

VSD

85
Q

A ___ may fail to close when infants are hypoxic, and/or have defects associated with increased pulmonary vascular pressure (VSD). It produces a harsh, machinery-like murmur. Large shunt can increase pulm pressure and eventually shunt reversal and cyanosis

A

PDA

86
Q

What type of murmur do you hear with a PDA?

A

Harsh, machinery-like murmur

87
Q

What are the 3 R–>L shunts (Galbraith slides)?

A

Classic TOF
Transposition of great arteries W/ VSD
Transposition of great arteries W/O VSD

88
Q

What are the 4 cardinal features of TOF?

A

VSD
Obstruction of RV outflow tract
Aorta overrides the VSD
RV hypertrophy

89
Q

What does the heart look like in TOF?

A

“BOOT-SHAPED”–> heart is enlarged d/t RV hypertrophy

90
Q

The clinical severity of TOF depends on the degree of ___

A

Subpulmonary stenosis

91
Q

Which form of coarctation of the aorta generally has a PDA?

A

Infantile

92
Q

What are the characteristics of a coarctation of the aorta with a PDA that manifests at birth?

A

May produced cyanosis in lower half of body

93
Q

What are the characteristics of a coarctation without PDA?

A

Usually asymptomatic

HTN in UE’s, Hypotension in LE’s
Claudication and cold LE’s
May eventually see concentric LV hypertrophy

94
Q

What is the greatest determinant of cyanosis in TOF?

A

Degree of pulmonary stenosis

Cardiovascular Medicine-Unit 1 (6 decks)

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