CH8 - Cardiac Pathology Flashcards
1
Q
What is ischemic heart disease (IHD)?
A
Group of syndromes related to myocardial ischemia
2
Q
What is the leading cause of death in the US?
A
ischemic heart disease (IHD)
3
Q
What is ischemic heart disease (IHD) usually due to?
A
atherosclerosis of coronary arteries, which decreases blood flow to the myocardium
4
Q
What are the risk factors for IHD?
A
They are similar to those of atherosclerosis; incidence increases with age.
5
Q
What is stable angina?
A
chest pain that arises with exertion or emotional stress.
6
Q
What is stable angina due to?
A
atherosclerosis of coronary arteries with > 70% stenosis;
7
Q
Why does stable angina arise with exertion?
A
decreased blood flow is not able to meet the metabolic demands of the myocardium during exertion
8
Q
What does stable angina represent?
A
reversible injury to myocytes (no necrosis)
9
Q
How does stable angina present?
A
As chest pain lasting < 20 minutes that radiates to the left arm or jaw, diaphoresis, and shortness of breath
10
Q
What does the EKG show in stable angina?
A
ST-segment depression due to subendocardial ischemia
11
Q
What is stable angina relieved by?
A
rest or nitroglycerin
12
Q
What is unstable angina?
A
chest pain that occurs at rest.
13
Q
What is unstable angina usually due to?
A
rupture of an atherosclerotic plaque with thrombosis and incomplete occlusion of a coronary artery
14
Q
What does unstable angina represent?
A
reversible injury to myocytes (no necrosis)
15
Q
What does the EKG show in unstable angina?
A
ST-segment depression due to subendocardial ischemia
16
Q
What is unstable angina relieved by?
A
Nitroglycerin
17
Q
In unstable angina there is a high risk of what?
A
progression to myocardial infarction
18
Q
What is prinzmetal angina?
A
episodic chest pain unrelated to exertion.
19
Q
What is prinzmetal angina due to?
A
coronary artery vasospasm
20
Q
What does prinzmetal angina represent?
A
reversible injury to myocytes (no necrosis)
21
Q
What does the EKG for prinzmetal angina show?
A
ST-segment elevation due to transmural ischemia.
22
Q
What is prinzmetal angina relieved by?
A
nitroglycerin or calcium channel blockers
23
Q
What is myocardial infarction?
A
Necrosis of cardiac myocytes
24
Q
What is myocardial infarction usually due to?
A
rupture of an atherosclerotic plaque with thrombosis and complete occlusion of a coronary artery
25
In addition to atherosclerotic plaque what are some other causes of myocardial infarction?
coronary artery vasospasm (due to Prinzmetal angina or cocaine use), emboli, and vasculitis (e.g., Kawasaki disease).
26
What are the clinical features for myocardial infarction?
include severe, crushing chest pain (lasting > 20 minutes) that radiates to the left arm or jaw, diaphoresis, and dyspnea; symptoms are not relieved by nitroglycerin.
27
In myocardial infarction what does the infarction usually involve?
the left ventricle (LV); right ventricle (RV) and both atria are generally spared.
28
What artery is most commonly involved artery in MI?
LAD; left anterior descending artery ? 45% of cases
29
What does occlusion of the left anterior descending artery (LAD) lead to?
infarction of the anterior wall and anterior septum of the LV
30
What does occlusion of right coronary artery (RCA) lead to?
infarction of the posterior wall, posterior septum, and papillary muscles of the LV;
31
What is the 2nd most commonly involved artery in MI?
RCA, right coronary artery
32
What does occlusion of the left circumflex artery lead to?
infarction of lateral wall of the LV.
33
What does the initial phase of infarction lead to?
subendocardial necrosis involving < 50% of the myocardial thickness (subendocardial infarction);
34
What does the EKG show for the initial phase of infarction?
(subendothelial infarction) ST-segment depression.
35
After the initial phase of infarction, what does continued or severe ischemia lead to?
transmural necrosis involving most of the myocardial wall (transmural infarction)
36
What does the EKG show in transmural infarction?
ST-segment elevation
37
What do the laboratory tests detect for myocardial infarction?
elevated cardiac enzymes.
38
What is the most sensitive and specific marker (gold standard) for Ml?
troponin I
39
What are the troponin I levels after 2-4 hours?
Levels rise 2-4 hours after infarction
40
When do troponin I levels peak?
at 24 hours
41
When do troponin I levels return to normal?
By 7-10 days.
42
What is CK-MB is useful for?
detecting reinfarction that occurs days after an initial MI
43
When do creatine kinase MB (CK-MB) levels rise?
4 - 6 hours after infarction
44
When does creatinine kinase MB levels peak?
They peak at 24 hours
45
When does creatinine kinase MB levels return to normal?
by 72 hours.
46
What does treatment for myocardial infarction include?
1) Asprin 2) Supplemental O2 3) Nitrates 4) beta-blockers 5) ACE inhibitor 6)Fibrinolysis or angioplasty
47
How does aspirin and/or heparin help treat MI?
limits thrombosis
48
How does supplemental 02 help treat MI?
minimizes ischemia
49
How do nitrates help treat MI?
vasodilate coronary arteries
50
How does beta-blockers help treat MI?
slows heart rate, decreasing O2 demand and risk tor arrhythmia
51
How does ACE inhibitors help treat MI?
decreases LV dilation
52
How does fibrinolysis or angioplasty help treat MI?
opens blocked vessel
53
What happens in fibrinolysis or angioplasty post-MI?
it opens bloced vessel; 1) contraction band necrosis 2) reperfusion injury
54
What is contraction band necrosis?
After fibrinolysis or angioplasty post-MI there is reperfusion of irreversibly damaged cells resulting in calcium influx, leading to hypercontraction of myofibrils
55
What is reperfusion injury?
After fibrinolysis or angioplasty post-MI, the return of oxygen and inflammatory cells may lead to free radical generation further damaging myocytes
56
< 4 hours from time of infarction what are the gross and microscopic changes?
No gross changes, and no microscopic changes
57
What are the complications < 4 hours from time of infarction?
Cardiogenic shock (massive infarction), congestive heart failure, and arrhythmia
58
4-24 hours from time of infarction what are the gross and microscopic changes?
[Gross] Dark discoloration and [microscopic] Coagulative necrosis
59
What are the complications from 4-34 hours from the time of infarction?
arrhythmia
60
1-3 days from time of infarction what are the gross and microscopic changes?
[gross] Yellow pallor, [microscopic] Neutrophils
61
What are the complications for 1-3 days from time of infarction?
Fibrinous pericarditis presents as chest pain with friction rub
62
What does fibrinous pericarditis present as?
chest pain with friction rub
63
4-7 days from time of infarction, what are the gross and microscopic changes?
[gross] Yellow pallor, [Microscopic] Macrophages
64
What are the complications 4-7 days from time of infarction?
Rupture of ventricular free wall, interventricular septum, or papillary muscle
65
What does rupture of ventricular free wall lead to?
cardiac tamponade
66
What does rupture of interventricular septum lead to?
shunt,
67
What does rupture of papillary muscle lead to?
mitral insufficiency
68
1-3 weeks from time of infarction, what are the gross and microscopic changes?
[gross] Red border emerges as granulation tissue enters from edge of infarct, [microscopic] Granulation tissue with plump fibroblasts, collagen, and blood vessels
69
Months from time of infarction, what are the gross and microscopic changes?
[gross] White scar, [microscopic] Fibrosis
70
What are the complications for 1 Month from the time of infarction?
Aneurysm, mural thrombus, or Dressier syndrome
71
What is sudden cardiac death?
Unexpected death due to cardiac disease, occurs without symptoms or <1 hour after symptoms arise
72
What is sudden cardiac death usually due to?
fatal ventricular arrhythmia
73
What is the most common etiology for sudden cardiac death?
acute ischemia; 90% of patients have preexisting severe atherosclerosis.
74
What are the less common causes for sudden cardiac death?
mitral valve prolapse, cardiomyopathy, and cocaine abuse
75
What is chronic ischemic heart disease?
Poor myocardial function due to chronic ischemic damage (with or without infarction);
76
What does chronic ischemic heart disease progress to?
congestive heart failure (CHF)
77
What is congestive heart failure?
Pump failure; divided into right- and left-sided failure
78
What are the causes of left-sided heart failure?
ischemia, hypertension, dilated cardiomyopathy, myocardial infarction, and restrictive cardiomyopathy
79
What are the clinical features for left-sided heart failure due to?
decreased forward perfusion and pulmonary congestion.
80
What are the clinical features for left-sided heart failure?
1) decreased perfusion and pulmonary congestion 2) activation of rennin angiotensin system
81
In left-sided heart failure what does pulmonary congestion lead to?
pulmonary edema.
82
In left-sided heart failure why is there paroxysomal nocturnal dyspnea?
Its due to increased venous return when lying flat
83
In left-sided heart failure, pulmonary edema results in what?
dyspnea, paroxysmal nocturnal dyspnea, orthopnea, and crackles
84
How can left-sided heart failure lead to intra-alveolar hemorrhage?
Small, congested capillaries may burst, leading to intraalveolar hemorrhage
85
In left-sided heart failure what is intra-alveolar hemorrhage marked by?
hemosiderin-laden macrophages (heart-failure cells)
86
In left sided heart failure how are the kidneys involved?
Decreased flow to kidneys leads to activation of renin-angiotensin system
87
In left sided heart failure does the kidney affect the rennin angiotensin system?
Fluid retention exacerbates CHF
88
What is the main treatment for left sided heart failure?
treatment is ACE inhibitor.
89
What is right-sided heart failure most commonly due to?
left-sided heart failure;
90
Aside from left sided heart failure what are some other important causes for right sided heart failure?
Left to-right shunt and chronic lung disease (cor pulmonale)
91
What are the clinical features for right sided heart failure due to?
congestion
92
What are the clinical features for right sided heart failure?
1. Jugular venous distension 2. Painful hepatosplenomegaly with characteristic nutmeg liver; may lead to cardiac cirrhosis 3. Dependent pitting edema
93
In right sided heart failure what is the dependent pitting edema due to?
increased hydrostatic pressure
94
What are the congenital heart defects?
Arise during embryogenesis
95
When do congenital heart defects usually arise?
usually weeks 3 through 8
96
In what percentage of live births do you see congenital heart defects?
seen in 1% of live births
97
Most congenital heart defects are?
sporadic.
98
Congenital heart defects often result in?
shunting between left (systemic) and right (pulmonary) circulations.
99
Defects with left-to-right shunting
may be relatively asymptomatic at birth, but the shunt can eventually reverse
100
What does increased flow through the pulmonary circulation result in?
hypertrophy of pulmonary vessels and pulmonary hypertension.
101
What does increased pulmonary resistance eventually result in?
reversal of shunt
102
What does the reversal of shunt in congenital defects with left to right shunt lead to?
late cyanosis (Eisenmenger syndrome) with right ventricular hypertrophy, polycythemia, and clubbing.
103
What do defects with right-to-left shunting usually present as?
cyanosis shortly after birth.
104
What is ventricular septal defect (VSD)?
Defect in the septum that divides the right and left ventricles
105
What is the most common congenital heart defect?
ventricular septal defect (VSD)
106
What is ventricular septal defect (VSD) associated with?
fetal alcohol syndrome
107
What does ventricular septal defect (VSD) result in?
left-to-right shunt,
108
What determines extent of shunting in ventricular septal defect (VSD)?
size of defect and age at presentation
109
What happens with small defects in ventricular septal defect (VSD)?
they are often asymptomatic
110
What happens with large defects in ventricular septal defect (VSD)?
can lead to Eisenmenger syndrome
111
What is the treatment for ventricular septal defect (VSD)?
involves surgical closure; small defects may close spontaneously
112
What is atrial septal defect?
Defect in the septum that divides right and left atria;
113
What is the most common type of atrial septal defect?
It is ostium secundum (90% of cases)
114
What type of atrial septal defect is type is associated with Down syndrome?
Ostium primum
115
What does atrial septal defect result in?
left-to-right shunt and split S2 on auscultation
116
Why is there split S2 on auscultation in atrial septal defect?
increased blood in right heart delays closure of pulmonary valve
117
What is an important complication of atrial septal defect?
Paradoxical emboli
118
What is patent ductus arteriosus?
Failure of ductus arteriosus to close
119
What is patent ductus arteriosus associated with?
congenital rubella
120
What does patent ductus arteriosus result in?
left-to-right shunt between the aorta and the pulmonary artery
121
During development what does the ductus arteriosus normally do?
shunts blood from the pulmonary artery to the aorta, bypassing the lungs
122
What are the symptoms for patent ductus arteriosus?
Asymptomatic at birth with holosystolic machine-like murmur; may lead to Eisenmenger syndrome, resulting in lower extremity cyanosis
123
What does the treatment for patent ductus arteriosus involve?
indomethacin, which decreases PGE2 resulting in PDA closure
124
What is the effect of PGE on patent ductus arteriosus?
PGE maintains patency of the ductus arteriosus
125
What is tetralogy of fallot?
It is characterized by (1) stenosis of the right ventricular outflow tract, (2) right ventricular hypertrophy, (3) VSD, and (4) an aorta that overrides the VSD
126
In tetralogy of fallot what does the right-to-left shunt lead to?
early cyanosis;
127
In tetralogy of fallot what determines the extent of shunting and cyanosis?
the degree of stenosis
128
In tetralogy of fallot what patient behavior is observed?
they learn to squat in response to a cyanotic spell
129
In tetralogy of fallot why does squatting help with the cyanotic spell?
increased arterial resistance decreases shunting and allows more blood to reach the lungs.
130
What is seen on x-ray in tetralogy of fallot?
Boot-shaped heart on x-ray
131
What is transposition of the great vessels characterized by?
pulmonary artery arising from the left ventricle and aorta arising from the right ventricle
132
What is the transposition of the great vessels associated with?
maternal diabetes
133
What does transposition of the great vessels presents with?
early cyanosis; pulmonary and systemic circuits do not mix.
134
In transposition of the great vessels what is required for survival?
creation of shunt (allowing blood to mix) after birth is required for survival.
135
What is the effect of PGE in transposition of the great vessels?
can be administered to maintain a PDA until definitive surgical repair is performed.
136
What does transposition of the great vessels result in?
hypertrophy of the right ventricle and atrophy of the left ventricle
137
What is truncus arteriosus?
Characterized by a single large vessel arising from both ventricles 1. Truncus fails to divide.
138
What does truncus arteriosus present with?
early cyanosis
139
Why is there early cyanosis in truncus arteriosus?
deoxygenated blood from right ventricle mixes with oxygenated blood from left ventricle before pulmonary and aortic circulations separate
140
What is tricuspid atresia?
Tricuspid valve orifice fails to develop; right ventricle is hypoplastic.
141
What is tricuspid atresia often associated with?
ASD, resulting in a right-to-left shunt; presents with early cyanosis,
142
What is coarctation of the aorta?
Narrowing of the aorta,
143
What is coarctation of the aorta classically divided into?
infantile and adult forms
144
What is the infantile form of coarctation of the aorta associated with?
a PDA
145
In the infantile form of coarctation of the aorta where is the coarctation located?
after (distal to) the aortic arch, but before (proximal to) the PDA
146
What does the infantile form of the coarctation of the aorta present as?
lower extremity cyanosis in infants, often at birth
147
What is the infantile form of coarctation of the aorta associated with?
Turner syndrome
148
What is the adult form of coarctation of the aorta associated with?
Its not associated with a PDA
149
Where is the coarctation for the adult form of coarctation of the aorta?
coarctation lies after (distal to) the aortic arch
150
How does the adult form of coarctation of the aorta present?
as hypertension in the upper extremities and hypotension with weak pulses in the lower extremities; classically discovered in adulthood
151
In the adult form of coarctation of the aorta what is seen on x-ray?
Notching of ribs
152
Why is there notching of the ribs seen on x-ray for the adult form of coarctation of the aorta?
Collateral circulation develops across the intercostal arteries; engorged arteries cause notching of ribs on x-ray
153
What is the adult form of coarctation of the aorta associated with?
bicuspid aortic valve
154
What is the purpose of heart valves?
To prevent back flow
155
What are the has four valves of the heart?
tricuspid, pulmonary, mitral, and aortic
156
What does valvular lesions generally result in?
stenosis (decreased caliber of the valve orifice) or regurgitation (backflow)
157
What is acute rheumatic fever?
Systemic complication of pharyngitis due to group A beta-hemolytic streptococci
158
Who does acute rheumatic fever affect?
children 2-3 weeks after an episode of streptococcal pharyngitis strep throat
159
What is acute rheumatic fever caused by?
molecular mimicry, bacterial M protein resembles proteins in human tissue
160
What is diagnosis of acute rheumatic fever based on?
Jones criteria.
161
What evidence is needed for the Jones Criteria?
Evidence of prior group A beta-hemolytic streptococcal infection with the presence of major and minor criteria
162
What would indicate prior group A beta-hemolytic streptococcal infection?
Elevated ASO or anti-DNase B titers
163
What is the minor Jones criteria?
Minor criteria are nonspecific and include fever and elevated ESR.
164
What is the major Jones criteria?
1) migratory polyarthritis 2) pancarditis 3) subcutaneous nodules 4) erythema marginatum 5) Sydenham chorea
165
What is Migratory polyarthritis?
In Jones criteria, swelling and pain in a large joint (e.g., wrist, knees, ankles) that resolves within days and migrates to involve another large joint
166
What is Pancarditis?
a) endocarditis b) myocarditis c) pericarditis
167
In endocarditis which valve is involved more commonly?
Mitral valve is involved more commonly than the aortic valve.
168
How is endocarditis characterized?
by small vegetations along lines of closure that lead to regurgitation
169
What is myocarditis in pancarditis?
its with Aschotf bodies that are characterized by foci of chronic inflammation, reactive histiocytes with slender, wavy nuclei (Anitschkow cells), giant cells, and fibrinoid material
170
What is the most common cause of death during the acute phase?
myocarditis
171
What is pericarditis in pancarditis lead to?
friction rub and chest pain
172
What is involved with erythema marginatum in the major criteria of Jones criteria
annular, nonpruritic rash with erythematous borders, commonly involving trunk and limbs
173
What is Sydenham chorea in the major criteria of Jones criteria?
It is rapid, involuntary muscle movements
174
What usually happens to an acute attack of rheumatic fever?
usually resolves, but may progress to chronic rheumatic heart disease;
175
What does repeat exposure to group A beta-hemolytic streptococci result in?
relapse of the acute phase of rheumatic fever and increases risk for chronic disease.
176
What is chronic rheumatic heart disease?
Valve scarring that arises as a consequence of rheumatic fever
177
What does chronic rheumatic heart disease result in?
stenosis with a classic fish mouth appearance
178
What does chronic rheumatic heart disease almost always involve?
the mitral valve
179
What does the involvement of the mitral valve in chronic rheumatic heart disease lead to?
thickening of chordae tendineae and cusps
180
What does chronic rheumatic heart disease occasionally involve?
the aortic valve
181
What does the involvement of the aortic valve in chronic rheumatic heart disease lead to?
fusion of the commissures
182
What do complications in chronic rheumatic heart disease include?
infectious endocarditis
183
What is aortic stenosis?
Narrowing of the aortic valve orifice
184
What is aortic stenosis usually due to?
fibrosis and calcification from wear and tear
185
When does aortic stenosis present?
in late adulthood (> 60 years)
186
What does a bicuspid aortic valve increase the risk for?
aortic stenosis and hastens disease onset.
187
How many cusps does a normal aortic valve have?
three cusps,
188
What is the effect of fewer cusps on the aortic valve?
it results in increased wear and tear on each cusp
189
What is the relationship between aortic stenosis and chronic rheumatic fever?
aortic stenosis may arise as a consequence of chronic rheumatic valve disease;
190
What distinguishes rheumatic disease from wear and tear in aortic stenosis?
coexisting mitral stenosis and fusion of the aortic valve commissures
191
In aortic stenosis what happens during cardiac compensation?
it leads to a prolonged asymptomatic stage during which a systolic ejection click followed by a crescendo-decrescendo murmur is heard
192
What does the complications of aortic stenosis include?
1) Concentric left ventricular hypertrophy 2) angina and syncope with exercise 3) microangiopathic hemolytic anemia
193
In aortic stenosis what does concentric left ventricular hypertrophy lead to?
It may progress to cardiac failure
194
In aortic stenosis what does angina and syncope with exercise lead to?
Limited ability to increase blood flow across the stenotic valve leads to decreased perfusion of the myocardium and brain
195
In aortic stenosis what does microangiopathic hemolytic anemia lead to?
RBCs are damaged (producing schistocytes) while crossing the calcified valve
196
In aortic stenosis what does treatment involve?
valve replacement after onset of complications.
197
What is aortic regurgitation?
Backflow of blood from the aorta into the left ventricle during diastole
198
Aortic regurgitation arises due to what?
aortic root dilation (syphilitic aneurysm and aortic dissection) or valve damage (infectious endocarditis)
199
What is the most common cause of aortic regurgitation?
isolated root dilation
200
What are the clinical features for aortic regurgitation?
1. Early, blowing diastolic murmur 2. Hyperdynamic circulation due to increased pulse pressure
201
What is pulse pressure?
it is the difference between systolic and diastolic pressures
202
What is the relationship between pressure and aortic regurgitation?
Diastolic pressure decreases due to regurgitation, while systolic pressure increases due to increased stroke volume
203
How does aortic regurgitation present?
with bounding pulse (water-hammer pulse), pulsating nail bed (Quincke pulse), and head bobbing
204
What does aortic regurgitation result in?
LV dilation and eccentric hypertrophy (due to volume overload)
205
What is the treatment for aortic regurgitation?
valve replacement once LV dysfunction develops
206
What happens in mitral valve prolapse?
Ballooning of mitral valve into left atrium during systole
207
What is the incidence of mitral valve prolapse in US adults
Seen in 2-3% of US adults
208
What is mitral valve prolapse due to?
myeloid degeneration (accumulation of ground substance) of the valve, making it (loopy)
209
What is the etiology for mitral valve prolapse?
Unknown
210
What might mitral valve prolapse be seen in?
Marfan syndrome or Ehlers-Danlos syndrome
211
What does mitral valve prolapse present with?
an incidental mid-systolic click followed by a regurgitation murmur that is usually asymptomatic
212
With mitral valve prolapse, when does the mid-systolic click get louder?
Click and murmur become louder with squatting
213
Why does squatting make the mid-systolic click get louder in mitral valve prolapse?
increased systemic resistance decreases left ventricular emptying
214
What are the complications for mitral valve prolapse?
they are rare, but include infectious endocarditis, arrhythmia, and severe mitral regurgitation.
215
What is the treatment for mitral valve prolapse?
valve replacement.
216
What is mitral regurgitation?
Reflux of blood from the left ventricle into the left atrium during systole
217
Mitral regurgitation usually arises as a complication of what?
mitral valve prolapse
218
Aside from mitral valve prolapse, what are some other causes of mitral regurgitation?
Left ventricular dilatation (left-sided cardiac failure), infective endocarditis, acute rheumatic heart disease, and papillary muscle rupture after a myocardial infarction.
219
What are the clinical features for Mitral regurgitation?
1. Holosystolic [blowing] murmur;
220
In mitral regurgitation why is the holosystolic murmur louder with squatting?
increased systemic resistance decreases left ventricular emptying and expiration, increased return to left atrium
221
What does mitral regurgitation result in?
Volume overload and left-sided heart failure
222
What is mitral stenosis?
Narrowing of the mitral valve orifice
223
What is mitral stenosis usually due to?
chronic rheumatic valve disease
224
What are the clinical features for mitral stenosis?
1. Opening snap followed by diastolic rumble 2. Volume overload leads to dilatation of the left atrium
225
In mitral stenosis what does the dilation of the left atrium leading to volume overload result in?
i. Pulmonary congestion with edema and alveolar hemorrhage ii. Pulmonary hypertension and eventual right-sided heart failure iii. Atrial fibrillation with associated risk for mural thrombi
226
What is endocarditis?
Inflammation of endocardium that lines the surface of cardiac valves
227
What is endocarditis usually due to?
bacterial infection
228
What is the most common overall cause of endocarditis?
Streptococcus viridans
229
What is streptococcus viridans?
it is a low virulence organism that infects previously damaged valves (chronic rheumatic heart disease and mitral valve prolapse).
230
What does streptococcus viridans result in?
small vegetations that do not destroy the valve (subacute endocarditis)
231
How does streptococcus viridans affect the endocardial surface?
develops thrombotic vegetations (platelets and fibrin) on damaged endocardial surface, transient bacteremia leads to trapping of bacteria in the vegetations, prophylactic antibiotics decrease risk of endocarditis.
232
What is the most common cause of endocarditis in IV drug users?
Staphylococcus aureus
233
What is Staphylococcus aureus?
High-virulence organism that infects normal valves, most commonly the tricuspid.
234
What does Staphylococcus aureus result in?
large vegetations that destroy the valve (acute endocarditis)
235
What is Staphylococcus epidermidis associated with?
endocarditis of prosthetic valves
236
What is Streptococcus bovis associated with?
endocarditis in patients with underlying colorectal carcinoma
237
What are HACEK organisms associated with?
are associated with endocarditis with negative blood cultures.
238
HACEK
Haemophilus, Actinobacius, Cardiobacterium, Eikenella, Kingella
239
What are the clinical features of bacterial endocarditis?
1) Fever 2) Lesions 3) Janeway lesions 4) anemia of chronic disease
240
What is the fever in bacterial endocarditis due to?
bacteremia
241
What is the murmur in bacterial endocarditis due to?
vegetations on heart valve
242
What are the Janeway lesions, splinter hemorrhages in nail bed and osier nodes in bacterial endocarditis due to?
embolization of septic vegetations
243
What are Janeway lesions?
erythematous nontender lesions on palms and soles.
244
What are Osier nodes?
tender lesions on fingers or toes
245
What is anemia of chronic disease due to?
chronic inflammation
246
What are the laboratory findings for endocarditis?
1. Positive blood cultures 2. Anemia of chronic disease 3. Transesophageal echocardiogram is useful for detecting lesions on valves
247
What are the general lab findings of anemia of chronic diseae?
low Hb, low MCV; high ferritin, low TIBC, decreased serum iron, and decreased l% saturation
248
What is the transesophageal echocardiogram useful for?
detecting lesions on valves
249
What is non-bacterial thrombotic endocarditis due to?
sterile vegetations that arise in association with a hypercoagulable state or underlying adenocarcinoma.
250
What does non-bacterial thrombotic endocarditis result in?
Vegetations arise on the mitral valve along lines of closure and result in mitral regurgitation.
251
What is Libman-Sacks endocarditis due to?
sterile vegetations that arise in association with SLE.
252
What does Libman-Sacks endocarditis result in?
Vegetations are present on the surface and undersurface of the mitral valve and result in mitral regurgitation
253
What is cardiomyopathy?
Group of myocardial diseases that result in cardiac dysfunction
254
What are the types of cardiomyopathy?
Dilated cardiomypathy, hypertrophic cardiomyopathy, restrictive cardiomyopathy
255
What is dilated cardiomyopathy?
Dilation of all four chambers of the heart
256
What is the most common form of cardiomyopathy?
Dilated cardiomyopathy
257
What does dilated cardiomyopathy result in?
Results in systolic dysfunction (ventricles cannot pump),
258
What does the systolic dysfunction resulting from dilated cardiomyopathy lead to?
biventricular CHF
259
What are the complications of dilated cardiomyopathy?
mitral and tricuspid valve regurgitation and arrhythmia.
260
What is the most common cause of dilated cardiomyopathy?
Its idiopathic
261
What are some other causes of dilated cardiomyopathy?
1. Genetic mutation (usually autosomal dominant) 2. Myocarditis (usually due to coxsackie A or B) 3. Alcohol abuse 4. Drugs (doxorubicin) 5. Pregnancy
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In pregnancy, when is dilated cardiomyopathy?
Its seen during late pregnancy or soon (weeks to months) after childbirth
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What characterizes myocarditis leading to dilated cardiomyopathy?
characterized by a lymphocytic infiltrate in the myocardium
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What does dilated cardiomyopathy from myocarditis result in?
chest pain, arrhythmia with sudden death, or heart failure. Dilated cardiomyopathy is a late complication.
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What is the treatment for dilated cardiomyopathy?
heart transplant.
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What is hypertrophic cardiomyopathy?
Massive hypertrophy of the left ventricle
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What is hypertrophic cardiomyopathy usually due to?
genetic mutations in sarcomere proteins; most common form is autosomal dominant
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What are the clinical features for hypertrophic cardiomyopathy?
1. Decreased cardiac output 2. Sudden death due to ventricular arrhythmias 3. Syncope with exercise
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How does hypertrophic cardiomyopathy lead to syncope with exercise?
Subaortic hypertrophy of the ventricular septum results in functional aortic stenosis
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What is a common cause of sudden death in young athletes?
hypertrophic cardiomyopathy
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In hypertrophic cardiomyopathy what does the decreased cardiac output lead to?
Left ventricular hypertrophy leads to diastolic dysfunction (ventricle cannot fill).
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In hypertrophic cardiomyopathy, what does biopsy show?
myofiber hypertrophy with disarray
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What is restrictive cardiomyopathy?
Decreased compliance of the ventricular endomyocardium that restricts filling during diastole
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What are the causes of restrictive cardiomyopathy?
amyloidosis, sarcoidosis, hemochromatosis, endocardial fibroelastosis (in children), and Loeffler syndrome (endomyocardial fibrosis with an eosinophilic infiltrate and eosinophilia).
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What does restrictive cardiomyopathy present as?
congestive heart failure;
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What is the classic finding in restrictive cardiomyopathy?
low-voltage EKG with diminished QRS amplitude.
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What are the cardiac tumors?
Myxoma, rhabdomyoma
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What is myoxma?
Benign mesenchymal tumor with a gelatinous appearance and abundant ground substance on histology
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What is the most common primary cardiac tumor in adults?
myxoma
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What does myxoma usually form?
a pedunculated mass in the left atrium
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What does the pedunculated mass in the left atrium due to myxoma cause?
syncope due to obstruction of the mitral valve
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What is rhabdomyoma?
Benign hamartoma of cardiac muscle
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What is the most common primary cardiac tumor in children?
rhabdomyoma
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What is rhabdomyoma associated with?
Tuberous sclerosis
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Where does rhabdomyoma usually arise?
in the ventricle
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Which type of tumors are more common in the heart?
Metastatic tumors more than primary tumors
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What does common metastases to the heart include?
breast and lung carcinoma, melanoma, and lymphoma
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What does metastatic tumors in the heart most commonly involve? What does this result in?
the pericardium, resulting in a pericardial effusion
