Ch 12-Cardiac Path-Galbraith PDF's Flashcards

(94 cards)

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
When will you see microscopic granulation tissue after an MI?
7-10 days it begins to form, can last up to 14 days
26
About how long does it take to form a dense collagenous scar following an MI?
~2 months
27
Contraction band necrosis is associated with ___
Reperfusion injury; dead myocytes contract d/t Ca influx
28
What is the most cardiac myocyte-specific lab test to determine an MI?
Troponin I and T
29
When does Troponin I typically peak after onset of chest pain in an MI?
About 24-30 hours
30
When does CK-MB usually peak after onset of chest pains with an MI?
About 18 hours
31
Half of all MI deaths occur within 1 hour of onset, and are usually secondary to a ___
Fatal arrhythmia
32
What are some more common complications of an MI?
``` Contractile dysfunction Fibrinous pericarditis Myocardial rupture Infarct expansion Ventricular aneurysm ```
33
___ precipitates sudden cardiac death in 80-90% of cases
Coronary artery disease
34
Sudden cardiac death is due to a __ most often arising from ischemia-induced myocardial irritability
Fatal arrhythmia
35
Left-sided hypertensive heart disease is usually due to ___ HTN Right-sided hypertensive heart disease is usually due to ___ HTN
Systemic Pulmonary
36
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?
Diastolic dysfunction can result in LA enlargement Can lead to A fib
37
Acute cor pulmonale may arise from a large __
Pulmonary embolus
38
Chronic stenosis may cause ___ overload hypertrophy --> CHF Chronic insufficiency (regurgitation) may cause ___ overload hypertrophy --> CHF
Pressure Volume
39
___ 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.
Calcification aortic stenosis
40
What type of "cells" can be found on affected valves in calcific aortic stenosis?
Osteoblast-like cell
41
Where do calcific deposits occur in mitral annular calcification?
Fibrous annulus (fibrous ring) Normally does not affect valve function
42
What gender and age group is more likely to have mitral annular calcification?
F > M | > 60 years
43
When do valve leaflets prolapse back into the LA with a mitral valve prolapse?
Systole --> Mid-systolic click
44
Who is more likely to have a mitral valve prolapse?
F : M --> 7:1 ratio
45
What is the buzzword associated with leaflets becoming thickened and rubbery d/t proteoglycans deposits in mitral valve prolapse?
Myxomatous degeneration
46
Rheumatic fever is a multisystem inflamm disorder following pharyngeal infx with ___
Group A streptococcus
47
The pathogenesis of rheumatic heart disease is an immune response to streptococcal ___ proteins that cross react with cardiac self-ags.
M
48
What are other common features of rheumatic fever?
``` 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
What is the morphologic feature associated with pancarditis in acute RF?
Aschoff bodies
50
In chronic RHD, mitral leaflet thickening, fusion and shortening of commisures, fusion and thickening of tendinitis cords will result in __
Mitral stenosis
51
what type of valvular disorder is mostly associated with RF?
Mitral stenosis
52
__ is a rapidly progressive, destructive infx of a previously normal valve. It requires surgery in addition to ABx
Acute infective endocarditis
53
__ is a slower-progressing infx of a previously deformed valve (such as in RHD). It can often be cured with ABx alone
Subacute infective endocarditis
54
What are some predisposing conditions for infective endocarditis?
Valvular abnormalities: RHD, prosthetic valves, MV prolapse, calcific stenosis, bicuspid AV Bacteremia: ANother site of infx, dental work/surgery, contaminated needles, compromised epithelium
55
Which valves are more commonly affected in infective endocarditis?
Left-sided valves more commonly affected Right-sided valves often involved in IV drug abusers
56
What is the classic feature of infective endocarditis?
Friable, bulky, destructive valvular vegetations Friability leads to septic emboli Vegetations are mixtures of fibrin, inflamm cells, and orgs
57
What type of symptoms do infective endocarditis pts usually present with?
Nonspecific symptoms --> fever, weight loss, fatigue Murmurs usually present with left-sided lesions
58
This org is often involved in infective endocarditis d/t dental work and valve abnormalities
Strep viridans
59
This org causes infective endocarditis of normal valves, abnormal valves, and IV drug abusers.
Staph aureus
60
This org is associated with infective endocarditis of prosthetic valves
Staph epidermidis
61
Aside from strep viridans, staph aureus, and staph epidermidis, what other orgs are associated with infective endocarditis?
``` H-Hemophilus A-Actinobacillus C-Cardiobacterium E-Eikenella K-Kingella ```
62
Describe what happens to the the following features of the myocardium and chambers as you age: LV chamber size: ___ Epicardial fat: ___ Myocardial changes: ___
Decreased LV size Increased epicardial fat Lipofuscin and basophilic degeneration, fewer monocytes, increased collagen fibers
63
Nonbacterial thombotic endocarditis is associated with ___
MALIGNANCIES (Esp. mucinous adenocarcinomas) Sepsis Catheter-induced endocardial trauma
64
What is the most common type of cardiomyopathy?
Dilated (90%)
65
What type of dysfunction is associated with dilated cardiomyopathy?
Systolic dysfunction Progressive cardiac dilation and systolic dysfunction, usually with dilated hypertrophy
66
Dilated cardiomyopathy is thought to be familial in 30-50% of cases and due to ___ mutations and is autosomal dominant (usually)
TITIN Alcohol strongly linked to DCM, so is myocarditis, cardiotoxic drugs/substances (Doxorubicin, cobalt Fe overload)
67
Describe the morphology of Dilated cardiomyopathy
Dilation of all chambers Mural thrombi common Functional regurgitation of valves
68
What is a classical presentation of Dilated cardiomyopathy?
Usually manifests between 20-50 yrs old Progressive CHF --> dyspnea, exertional fatigue, decreased ejection fraction Arrhythmias Embolism
69
___ 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.
Takotsubo cardiomyopathy BROKEN HEART SYNDROME
70
In Arrhythmogenic RV cardiomyopathy, RV failure and arrhythmias cause __ which can lead to sudden death
V tac and V fib It is familial (usually autosomal dominant)
71
Desmosome and intercalated dysfunctions are associated with this cardiomyopathy:
Arrhythmogenic RV cardiomyopathy
72
__ is a genetic disorder leading to myocardial hypertrophy and diastolic dysfunction, leading to decreased stroke volume and often ventricular outflow obstruction
Hypertrophic cardiomyopathy
73
In Hypertrophic cardiomyopathy, numerous mutations are known involving sarcomeric proteins, most commonly ___
B-myosin heavy chain
74
Describe the morphology of hypertrophic cardiomyopathy:
Massive myocardial hypertrophy, often with marked septal hypertrophy Microscopically, myocytes disarray
75
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
Hypertrophic cardiomyopathy
76
___ 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
Restrictive cardiomyopathy
77
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 __
Transthyretin
78
When amyloid deposits in the interstitium of the myocardium of a ___ cardiomyopathy results
Restrictive
79
What is the most common causative agent/org responsible for myocarditis?
Coxsackie A and B viruses most common
80
What are some non-infectious causes of myocarditis?
Immune-mediated rxns, including RF, SLE, drug hypersensitivity
81
The single most common genetic cause of congenital heart disease is ___
Trisomy 21
82
What are the 3 left-to-right shunt congenital heart disorders (Galbraith slides)
ASD VSD PDA
83
___ 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
ASD
84
___ 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
VSD
85
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
PDA
86
What type of murmur do you hear with a PDA?
Harsh, machinery-like murmur
87
What are the 3 R-->L shunts (Galbraith slides)?
Classic TOF Transposition of great arteries W/ VSD Transposition of great arteries W/O VSD
88
What are the 4 cardinal features of TOF?
VSD Obstruction of RV outflow tract Aorta overrides the VSD RV hypertrophy
89
What does the heart look like in TOF?
"BOOT-SHAPED"--> heart is enlarged d/t RV hypertrophy
90
The clinical severity of TOF depends on the degree of ___
Subpulmonary stenosis
91
Which form of coarctation of the aorta generally has a PDA?
Infantile
92
What are the characteristics of a coarctation of the aorta with a PDA that manifests at birth?
May produced cyanosis in lower half of body
93
What are the characteristics of a coarctation without PDA?
Usually asymptomatic HTN in UE's, Hypotension in LE's Claudication and cold LE's May eventually see concentric LV hypertrophy
94
What is the greatest determinant of cyanosis in TOF?
Degree of pulmonary stenosis