Chapter 8 cardiac pathology Flashcards
1
Q
Define stable angina
A
chest pain that arises with exertion or emotional stress
2
Q
How does stable angina present?
A
chest pain last less than 20 minutes that radiates tot he left arm or jaw, diaphoresis and SOB
3
Q
EKG shows ST segment depression due to subendocardial ischemia in what two types of angina?
A
Stable angina and unstable angina
4
Q
EKG shows ST segment elevation due to transmural ischemia in what type of angina?
A
Prinzmetal angina
5
Q
Stable angina is relieved by what?
A
rest and nitroglycerin
6
Q
Define unstable angina
A
chest pain that occurs at rest
7
Q
unstable angina has a high risk of progressing to?
A
MI
8
Q
unstable angina is usually due to?
A
rupture of an atherosclerotic plaque with thrombosis and incomplete occlusion of a coronary artery
9
Q
Define prinzmetal angina
A
episodic chest pain unrelated to exertion
10
Q
prinzmetal angina is due to?
A
coronary artery vasospasm
11
Q
myocardial infarction is usually due to?
A
rupture of an atherosclerotic plaque with thrombosis and complete occlusion of a coronary artery
12
Q
clinical features of MI include
A
severe, crushing chest pain (> 20 min) that radiates to the left arm or jaw, diaphoresis and dyspnea; symptoms are not relieved by nitroglycerin
13
Q
MI usually involves what part of the heart?
A
left ventricle
14
Q
occlusion of which coronary artery leads to infarction of the anterior wall and anterior septum of the LV
A
left anterior descending artery (LAD)
15
Q
What is the most commonly involved artery in MI (45% of cases)?
A
left anterior descending artery (LAD)
16
Q
What is the 2nd most commonly involved artery in MI?
A
right coronary artery
17
Q
occlusion of which coronary artery leads to infarction of the posterior wall, posterior septum and papillary muscles of the LV?
A
right coronary artery
18
Q
initial phase of the MI is characterized by?
A
subendocardial necrosis involving <50% of the myocardial thickness; EKG shows ST-segment depression
19
Q
Continued or severe ischemia seen in MI is characterized by?
A
transmural necrosis involving most of the myocardial wall; EKG shows ST segment elevation
20
Q
What is the most sensitive and specific marker for MI?
A
Troponin I; it is the gold standard!
21
Q
How does troponin I levels change post MI?
A
levels rise 2-4 hours after infarction
peak at 24 hours
return to normal by 7-10 days
22
Q
What is CK-MB useful for in regards to MI?
A
useful for detecting reinfarction that occurs days or after an initial MI
23
Q
How do CK-MB levels change post MI?
A
levels rise 4-6 hours after infarction
peak at 24 hours
return to normal by 72 hours
24
Q
explain contraction band necrosis
A
reperfusion of irreversibly-damaged cells results in calcium influx, leading to hypercontraction of myofibrils
25
explain reperfusion injury
return of oxygen and inflammatory cells may lead to free radical generation, further damaging myocytes
26
What changes and complications occur <4 hours post MI?
No gross changes; No microscopic changes; complications include cardiogenic shock, CHF, arrhythmia
27
What changes and complications occur 4-24 hours post MI?
Gross changes - dark discoloration
Microscopic changes - coagulative necrosis
Complications - arrhythmia
28
What changes and complications occur 1-3 days post MI?
Gross changes - Yellow pallor due to WBCs
Microscopic changes - Neutrophils
Complications - Fibrinous pericarditis, presents as chest pain with friction rub
29
What changes and complications occur 4-7 days post MI?
Gross changes - Yellow pallor due to WBCs
Microscopic changes - Macrophages
Complications - rupture of ventricular free wall (leads to cardiac tamponade), IV septum (leads to shunt) or papillary muscle (leads to mitral insufficiency)
30
What changes and complications occur 1-3 weeks post MI?
Gross changes - red border emerges as granulation tissue enters from edge of infarct
Microscopic changes - granulation tissue with plump fibroblasts, collagen and blood vessels
Complications - none
31
What changes and complications occur months post MI?
Gross changes - white scar
Microscopic changes - fibrosis
Complications - Aneurysm, mural thrombus or Dressler syndrome
32
What is Dressler's syndrome?
pericarditis that occurs 6-8 weeks post MI; Ab is produced against the myocardium
33
Causes of left sided heart failure
ischemia, HTN, dilated cardiomyopathy, myocardial infarction, restrictive cardiomyopathy
34
Mainstay treatment of left sided heart failure
ACE inhibitor
35
Dyspnea, paroxysmal norturnal dyspnea, orthopnea and crackles seen in left sided heart failure is due to?
pulmonary congestion that leads to pulmonary edema
36
Heart failure cells seen in left sided heart failure are ?
hemosiderin laden macrophages
37
Decreased flow in the kidneys, which can happen in left sided heart failure leads to?
activation of the renin-angiotensin system => resultant fluid retention exacerbates CHF
38
What is the most common cause of right sided heart failure?
left sided heart failure
39
Clinical features of right sided heart failure are mainly due to ?
congestion
40
What are the clinical features of right sided heart failure?
jugular venous distension; painful hepatosplenomegaly with characteristic "nutmeg liver"; dependent pitting edema
41
Eisenmenger syndrome
increase pulmonary resistance from a left to right shunt leads to a reversal of the shunt causing late cyanosis with right ventricular hypertrophy, polycythemia and clubbing
42
When does cyanosis present in defects with right to left shunting?
shortly after birth
43
Down syndrome is associated with what type of atrial septal defect?
Ostium primum type
44
Atrial septal defect results in what type of shunt and what is heart on auscultation?
results in left to right shunt; split S2 heard on auscultation (increased blood in right heart delays closure of pulmonary valve)
45
What is an important complication of atrial septal defect?
paradoxical emboli
46
Patent ductus arteriosus is associated with which congenital infection?
congential rubella
47
What type of shunting results from a patent ductus arteriosus?
left to right shunting between the aorta and the pulmonary artery
48
How does PDA present at birth?
asymptomatic with a holosytolic machine like murmur
49
What is used to treat a PDA
Indomethacin - decreases PGE (PGE keeps the DA patent so decreasing it would cause closure)
50
How does tetrology of fallot present on chest xray?
boot shaped heart
51
What are the 4 characteristics of the tetrology of fallot?
stenosis of the right ventricular outflow tract; right ventricular hypertrophy; VSD; aorta that overrides the VSD
52
patients with a tetrology of fallot engage in what action during a cyanotic spell
they learn to squat - this increases arterial resistance which decreases shunting from the right to the left and allows more blood to reach the lungs
53
What is transposition of the great vessels characterized by?
pulmonary artery arises from the left ventricle and the aorta arises from the right ventricle
54
What condition is transposition of the great vessels associated with?
maternal diabetes
55
What is required for survival in patients with transposition of the great vessels?
A PDA in order for the circuits to mix
56
Name the four congenital defects that can cause early cyanosis?
tetrology of fallot; transposition of the great vessels; truncus arteriosus; tricuspid atresia
57
What type of shunting generally presents as cyanosis shortly after birth?
right to left shunting
58
What characterizes truncus arteriosus?
a single large vessel arising from both ventricles
59
What characterizes tricuspid atresia?
tricuspid valve orifice fails to develop; RV is hypoplastic; often associated with ASD
60
What characterizes the infantile form of coarctation of the aorta?
associated with PDA; coarctation lies after the aortic arch but before the PDA
61
How does the infantile forms of coarctation of the aorta present?
lower extremity cyanosis, often at birth
62
Infantile form of coartation of the aorta is associated with what condition?
Turner syndrome
63
What characterizes the adults form of coarctation of the aorta?
is not associated with PDA; coarctation lies after the aortic arch
64
How does the adult form of coarctation of the aorta present?
HTN in the upper extremities; hypotension with weak pulses in the lower extremities; collateral circulation develops across intercostal arteries causing notching on ribs
65
Coarctation of the aorta in adults is associated with what type of valve abnormality?
bicuspid aortic valve
66
What evidence indicates prior group A beta hemolytic streptococcal infection
elevated ASO or anti-DNase B titers
67
Major criteria of acute rheumatic fever
migratory polyarthritis; pancarditis; subcutaneous nodules; erythema marginatum; sydenham chorea
68
Myocarditis caused by acute Rheumatic fever is characterized by what components?
Aschoff bodies (foci of chronic inflammation); Anitschkow cells (reactive histiocytes with slender, wavy nuclei); giant cells and fibrinoid material
69
Chronic rheumatic heart disease is characterized by?
valve scarring; stenosis with a classic "fish mouth" appearance; almost always involves MITRAL VALVE
70
Aortic stenosis is usually due to?
fibrosis and calcification from "wear and tear"; presents late in adulthood (>60)
71
What can increase risk of aortic stenosis?
bicuspid aortic valve; normally there are 3 cusps, fewer cusps result in increased wear and tear
72
Aortic stenosis can cause what to be heard during auscultation?
systolic ejection click followed by crescendo - decrescendo murmur
73
What is aortic regurgitation?
back flow of blood from the aorta into the LV during diastole
74
Aortic regurgitation causes hyperdynamic circulation due to increased pulse pressure b/c?
diastolic pressure decreases due to regurgitation while systolic pressure increases due to increased stroke volume
75
How does hyperdynamic circulation seen in aortic regurgitation present?
bound pulse; pulsating nail bed (Quincke pulse); head bobbing
76
What is mitral valve prolapse?
ballooning of the mitral valve into the LA during systole
77
What causes MV prolapse?
myxoid degeneration (accumulation of ground substance) of the valve making it floppy
78
MV prolapse is seen in what two conditions?
Marfan syndrome and Ehlers-Danlos syndrome
79
How does MV prolapse present on auscultation?
mid-systolic click followed by crescendo murmur
80
What action increases the click and murmur heard on auscultation with MV prolapse?
squatting - increases systemic resistance decreases left ventricular emptying
81
What is mitral regurgitation?
reflux of blood from the LV into the left atrium during systole
82
What can be heard on auscultation for mitral regurgitation?
holosystolic blowing murmur - louder with squatting due to increased systemic vascular resistance decreases ventricular emptying and expiration due to increase return to LA
83
How does mitral stenosis present on auscultation?
opening snap followed by diastolic rumble
84
What is the most common cause of endocarditis overall?
Strep viridans - low virulence organism that infects previously damaged valves
85
What is the laboratory profile of strep viridans?
alpha hemolytic; bile esculin negative; optochin resistant
86
What is the most common cause of endocarditis in IV drug users?
Staph aureus
87
What valve is most commonly affected by staph aureus?
tricuspid valve
88
Endocarditis as a result of staph aureus infection causes what kind of vegetation?
results in large vegetations that destroy the valve
89
Endocarditis as a result of strep viridans infections causes what kind of vegetation?
results in small vegetations that do not destroy the valve
90
Endocarditis from prosthetic valves is associated with what bacteria?
Staph epidermidis
91
Strep bovis is associated with endocarditis in patients with what underlying condition?
colorectal carcinoma
92
Clinical features of bacterial endocarditis?
Janeway lesions (nontender lesions on palms, soles); Osler nodes (tender lesions on fingers, toes); splinter hemorrhages on nail bed
93
What is Libman Sacks endocarditis?
sterile vegetations that arise in association with SLE; vegetations are present on the surface AND undersurface of the mitral valve and cause mitral regurgitation
94
What is the most common form of cardiomyopathy?
dilated cardiomyopathy
95
dilated cardiomyopathy is characterized by?
dilation of all four chambers of the heart
96
the most common cause of dilated cardiomyopathy is?
idiopathic (also associated with alcohol use, pregnancy and doxorubicin)
97
What is hypertrophic cardiomyopathy?
massive hypertrophy of the LV
98
what is the most common cause of hypertrophic cardiomyopathy?
genetic mutations in sarcomere proteins; most commonly AD
99
biopsy of hypertrophic cardiomyopathy will show what?
myofiber hypertrophy with disarray
100
What are the clinical features of hypertrophic cardiomyopathy?
decreased CO b/c LV hypertrophy leads to diastolic dysfunction where ventricle cannot fill; sudden death; syncope with exercise
101
What is a common cause of sudden death in young athletes?
hypertrophic cardiomyopathy
102
What is restrictive cardiomyopathy?
decreased compliance of the ventricular endomyocardium that restricts filling during diastole
103
What are some causes of restrictive cardiomyopathy?
amyloidosis, sarcoidosis, hemochromatosis, endocardial fibroelastosis, Loeffler syndrome (associated with eosinophilia)
104
How does restrictive cardiomyopathy present?
as congestive heart failure
105
What is a classic finding on low voltage EKG that indicates restrictive cardiomyopathy?
diminished QRS amplitude
106
Name the cardiac tumor --- benign mesenchymal tumor with a gelatinous appearance and abundant ground substance, most common primary cardiac tumor in adults; forms a pedunculated mass in the LA
Myxoma
107
Name the cardiac tumor --- benign hemartoma of cardiac muscle; most common primary cardiac tumor in CHILDREN; associated with TUBEROUS SCLEROSIS; usually in ventricle
Rhabdomyoma
108
T/F metastatic tumors are more common in the heart than primary tumors
T
109
Metastasis to the heart most commonly affect which part?
pericardium - results in pericardial effusion
110
What are some common metastases to the heart?
breast and lung carcinoma, melanoma, lymphoma
111
Risk for free wall rupture is greatest after how many days post MI and why?
After 5-10 days; macrophages have degraded important structural components as they replace neutrophils, the heart is maximally soft and prone to rupture
112
When is the heart at greatest risk for undergoing a ventricular aneurysm post MI and why?
around 7-8 weeks; dense type I collagen replaces the primitive type III collagen, this puts the heart at risk for undergoing a ventricular aneurysm as the scar tissue has diminished contractile properties it can become weak
