Pathoma Ch 8 - Cardiology Flashcards
1
Q
What is the leading cause of death in the US?
A
IHD (ischemic heart disease)
2
Q
What causes IHD?
A
Usually due to atherosclerosis of coronary arteries which decreases blood blood to myocardum
3
Q
What are the RFs for IHD?
A
similar to those of atherosclerosis–incidence increases with age
4
Q
What is angina?
A
Chest pain that is reversible
5
Q
What is the hallmark of reversible cellular injury?
A
swelling
6
Q
After how many minutes of decreased blood flow/chest pain does myocardium undergo non-reversible damage?
A
20 minutes
7
Q
Which portion of the heart wall is most susceptible to ischemic damage?
A
endocardium
8
Q
What is stable angina?
A
(no chest pain at rest), chest pain that arises with exertion or emotional stress
9
Q
What causes stable angina?
A
Atherosclerosis of coronary arteries with >70% stenosis: decreased blood flow is not able to meet the metabolic demands of myocardium during exertion
10
Q
What does angina represent into terms of injury?
A
Reversible injury to myocytes (no necrosis)
11
Q
How does stable angina present?
A
chest pain lasting
12
Q
What is evident on EKG with stable angina?
A
ST-segment depression due to subendocardial ischemia
13
Q
How is stable angina relieved?
A
rest or nitroglycerin
14
Q
What causes unstable angina?
A
usually due to rupture of atherosclerotic plaque with thrombus and INCOMPLETE occlusion of coronary artery
15
Q
What kind of injury does unstable angina represent?
A
Reversible injury to myocytes (no necrosis)
16
Q
What is evident on EKG with unstable angina?
A
ST-segment depression due to subendocardial ischemia
17
Q
How is unstable angina relieved?
A
nitroglycerin
18
Q
What risk is posed by unstable angina?
A
Progression to MI
19
Q
What is prinzmetal angina?
A
Episodic chest pain unrelated to exertion
20
Q
What causes prinzmetal angina?
A
Coronary vasospasm (BV clamping down)
21
Q
What kind of injury does prinzmetal angina represent?
A
reversible injury to myocytes (no necrosis)
22
Q
What is evident on EKG with prinzmetal angina?
A
ST-segment elevation due to transmural ischemia (entire wall is cut from blood supply)
23
Q
How is prinzmetal angina relieved?
A
nitroglycerin or CCB
24
Q
What is the MoA of nitroglycerin?
A
dilates arteries and veins–major MoA is vasodilation of veins so less blood returns to heart > decreased preload > decreased stress on myocardium
25
What is myocardial infarction?
necrosis of cardiac myocytes
26
What is the most common cause of MI?
Usually due to rupture of atherosclerotic plaque with thrombus and COMPLETE occlusion of artery
27
What are some other causes of MI?
coronary artery vasospasm, emboli, vasculitis (ex: kawasaki disease)
28
How does vasculitis cause MI?
damage to vessel wall exposes SEC and TF > thrombosis
29
What causes coronary artery vasospasm?
prinzmetal angina and cocaine
30
What are the clinical features of MI?
severe, crushing chest pain lasting >20 minutes that radiates to the left arm or jaw, diaphoresis and dyspnea; nitroglycerin does not relieve symptoms
31
Why does an MI cause dyspnea?
Pulmonary congestion and edema are caused because heart isn't pumping well
32
Which areas of the heart are usually affected by infarction? Which are generally spared?
Affected: LV Spared: RV and both atria
33
What artery is most commonly involved in MI? What is second most common?
Most: LAD (45% of cases) Second: RCA
34
What does occlusion of left LAD lead to?
infarction of anterior wall and anterior septum of LV
35
What does occlusion of RCA lead to ?
infarction of posterior wall, posterior septum, and papillary muscles of LV
36
What does occlusion of left circumflex lead to?
infarction of lateral wall of LV
37
What does the initial phase of infarction lead to?
subendocardial necrosis involving
38
What is shown on EKG during initial phase of infarction?
ST depression
39
What does continued infarction lead to?
continued or severe ischemia leads to transmural necrosis which involves most of myocardial wall (transmural infarction)
40
What is shown on EKG with transmural infarction?
ST-segment elevation
41
Which lab tests are used to detect MI? What are they looking for?
Troponin I and CK-MB; looking to see if there has been irreversible damage to myocytes: hallmark is membrane damage > myocyte enzymes in the blood
42
Which lab test is most sensitive and specific marker for MI?
Troponin I (gold standard)
43
When do Troponin I levels begin to rise? When do they peak? When do they return to normal?
Levels rise 2-4 hours post infarction, peak at 24 hours and return to normal by 7-10 days
44
What is CK-MB useful for?
Detecting reinfarction that occurs days after initial MI (recall: Troponin I doesn't return to normal for 7-10 days so can't be used to assess reinfarction)
45
When do CK-MB levels begin to rise? When do they peak? When do they return to normal?
Rise 4-6 hours after infarction, peak at 24 hours and retun to normal by 72 hours
46
What is the treatment for MI?
aspirin and/or heparin, supplemental O2, nitrates, BB, ACEi, fibrinolysis or angioplasty
47
Why are aspirin and heparin used to tx MI?
limit thrombosis
48
Why is supplemental O2 a used to tx MI?
minimized ischemia
49
Why are nitrates used to tx MI?
vasodilate veins and coronary arteries (reduce preload/stress on heart)
50
Why are beta blockers used to tx MI?
slows heart rate, decreasing O2 demand and risk for arrhythmia
51
Why are ACEi used to tx MI?
decrease LV dilation; angiotensin II constricts peripheral BVs, blocking this decreases afterload on heart (ATII also increases BV volume via aldosterone)
52
What do fibrinolysis and angioplasty do?
open blocked vessel
53
What are potential complications of fibrinolysis and angioplasty?
Contraction band necrosis and reperfusion injury
54
What is contraction band necrosis?
Reperfusion of irreversibly-damaged cells results in Ca influx, leading to hypercontraction of myofibrils
55
What is reperfusion injury?
Return of oxygen and inflammatory cells may lead to free radical generation, further damaging myocytes
56
Why do cardiac enzymes continue to go up after angioplasy?
reperfusion injury results in more damage to myocytes which would cause cardiac enzyme levels to continue to rise
57
What are complications of MI related to?
Gross and microscopic changes
58
What is a feared complication very early after MI occurs? How is this handled?
Arrhythmia; tx with BB
59
What gross and microscopic changes appear
none
60
What complications can arise
Cardiogenic shock (massive infarction), CHF and arrhythmia
61
What gross and microscopic changes appear 4-12 hours after infarction?
G: dark discoloration M: coagulative necrosis (remove nucleus from cell)
62
What complications can arise 4-12 hours after infarction?
arrhythmia
63
What gross and microscopic changes appear 1-3 days after infarction?
G:yellow pallor (WBC in myocardium--acute inflammation always follows necrosis) M: neutrophils
64
What complications can arise 1-3 days after infarction?
fibrinous pericarditis; presents as chest pain with friction rub (only get this with transmural infarction)
65
What gross and microscopic changes appear 4-7 days after infarction?
G:yellow pallor M: macrophages--eat up dead and necrotic debris
66
At what point will the cardiac wall be the weakest?
4-7 days after infarction--when macrophages are present
67
What complications can arise 4-7 days after infarction?
Rupture of ventricular free wall leads to cardiac tamponade; rupture of interventricular septum leads to shunt; rupture of papillary muscle leads to mitral insufficiency
68
What BV supplies the papillary muscle?
RCA
69
What is mitral insufficiency?
Blood regurgitating back into atria during systole
70
What gross and microscopic changes appear 1-3 weeks after infarction?
G: red border emerges as granulation tissue enters from edge of infarct M: granulation tissue (base/scaffold for scar) with plump fibroblasts, collagen and BV
71
What complications can arise 1-3 weeks after infarction?
None listed
72
What gross and microscopic changes appear months after infarction?
G: white scar M: fibrosis
73
What is sudden cardiac death?
unexpected death due to cardiac disease; occurs without symptoms or
74
What complications can arise months after infarction?
anuerysm, mural thrombus (from stasis along wall of scar), Dressler syndrome
75
What is Dressler syndrome?
pericarditis that arises 6-8 weeks after infarction due to autoimmune phenomenon
76
What is the most common etiology of SCD?
acute ischemia
77
What % of patients with SCD have preexisting severe atherosclerosis?
90%
78
What is the most common cause of SCD?
fatal ventricular arrhythmia
79
What are some less common causes of SCD?
mitral valve prolapse, cardiomyopathy, cocaine abuse
80
What is CHF? How is it divided?
Pump failure; right and left-sided failure
81
What causes left-sided heart failure?
ischemia, HTN, dilated cardiomyopathy (4 chamber dilation of heart--stretches muscle so it won't work as well), MI and restrictive cardiomyopathy (can't fill heart appropriately)
82
What causes the clinical features of left-sided heart failure?
decreased forward perfusion and pulmonary congestion
83
What does decreased flow to kidneys lead to (decreased forward perfusion)?
activation of renin-angiotensin system; fluid retention exacerbates CHF (via aldosterone)
84
How does pulmonary congestion present clinically?
dyspnea, paroxysal nocturnal dyspnea (due to increased venous return while lying flat), orthopnea and crackles
85
What are some consequences of pulmonary congestion?
Small, congested capillaries may burst leading to intra-alveolar hemorrhage--marked by hemosiderin -laden macrophages
86
What are heart failure cells?
hemosiderin -laden macrophages; macrophages consume lots of iron
87
What is the mainstay of tx for left-sided heart failure?
ACEi
88
What is the most common cause of right-side heart failure?
Left-sided heart failure
89
What are some other important causes of right-side heart failure?
left to right shunt, chronic lung disease (cor pulmonale)--hypoxia > constriction of BV
90
What are the clinical features of right-side heart failure?
ALL DUE TO PULMONARY CONGESTION; jugular venous distention, painful hepatosplenomegaly with characteristic "nutmeg liver"--leads to cardiac cirrhosis, dependent pitting edema
91
What causes pitting edema in right-side heart failure?
Increased hydrostatic pressure
92
When do congenital heart defects arise?
During embyrogenesis (weeks 3-8)
93
What is the prevalence of congenital heart defects? What is their hereditary pattern?
1%, most defects are sparoadic
94
What are some examples of congenital heart defects?
Ventricular septal defects, atrial septal defect, patent ductus arteriosus, tetralogy of fallot, transposition of great vessels, truncus arteriosus, tricuspid atresia, coarcatation of the aorta
95
What does increased pulmonary resistance eventually lead to?
reversal of shunt leading to late cyanosis (Eisenmenger syndrome) with right ventricular hypertrophy, polycythemia and clubbing
96
What is VSD?
Defect in septum that divides right and left ventricles
97
Why does increased pulmonary resistance lead to polycythemia?
Deoxygenated blood in systemic circuit leads to hypoxemia > release of EPO > polycythemia
98
What does increased blood flow through pulmonary circulation result in?
hypertrophy of pulmonary vessels and pulmonary HTN
99
What is the most common congenital heart defect?
VSD
100
How do defects with right-to-left shunt is usually present?
cyanosis after birth (may be relative asymptomatic at birth)
101
With what is VSD associated?
fetal alcohol syndrome
102
What does VSD cause?
left to right shunt because wall between ventricles is not completely formed
103
What determines the extent of shunting?
size of defect and age at presentation
104
How does VSD present?
small defects are often asymptomatic; large defects can lead to Eisenmenger syndrome (increased volume in pulmonary circuit--pulmonary HTN but shunt can reverse because pressure in pulm system exceeds that of LV)
105
What is the tx for VSD?
surgical closure; small defects may close spontaneously
106
What is truncus arteriosus?
Characterized by single large vessel arising from both ventricles--truncus fails to divide
107
How does truncus arteriosus present?
Early cyanosis, deoxygenated blood from right ventricle and mixed with oxygenated blood from left ventricle, before pulmonary and aortic circulation separate
108
What is ASD?
Defect in septum that divides right and left ventricle
109
What is PDA?
Failure of ductus arteriosus to close
110
With what is PDA associated?
Congential rubella
111
What is most common type of ASD? With what condition is it associated?
Ostium secundum (90% of cases); Down syndrome
112
What does ASD result in?
left to right shunt and split S2 on auscultation
113
What causes split S2 on auscultation in ASD?
increased blood in right heart delays closure of pulmonary valve
114
What is an important complication of ASD?
Paradoxical emboli--embolus on right side that crosses over to left side
115
What is the result of PDA?
right to left shunt between aorta and pulmonary artery
116
What purpose does ductus arteriosus serve during development?
shunts blood to pulmonary atery to aorta, bypassing lungs
117
How does ductus arteriosus present? how does it progress?
Asymptomatic at birth with continuous 'machine-like' murmur; may lead to Eisenmernger syndrome
118
What is Eisenmernger syndrome?
reversal of shunt > lower extremity cyanosis
119
What is tricuspid atresia?
Tricuspid valve orifice fails to develop, right ventricle is hypoplastic
120
What maintains the patency of the ductus arteriosus?
PGE
121
What is the tx of PDA?
indomethacin
122
How does indomethacin work?
decreases PGE, resulting in PDA closure (PEF maintanes patency of ductus arteriosus)
123
What is tetralogy of fallot?
Characterized by 1. stenosis of right ventricular outflow tract; 2. right ventricular hypertoprhy; 3. VSD; 4. aorta that arrides the VSD
124
What does tetralogy of fallot lead to?
right to left shunt leads to early cyanosis; degree of stenosis determines degree of cyanosis
125
What causes right to left shunt in tetralogy of fallot?
because of stenosis, blood from RV goes into aorta
126
How do patients handle cyanotic spell with tetralogy of fallot?
They learn to squat: increased arterial resistance (increased pressure on right side of heart) decreases shunting and allow more blood to reach lungs
127
When do patients with tetralogy of fallot get cyanotic spell?
During exercise
128
How does tricuspid atresia present?
Cyanosis
129
What appears on X-ray with tetralogy of fallot?
Boot-shaped heart
130
What is transposition of the great vessels?
Characterized by pulmonary artery arising from left ventricle and aorta rising from right ventricle: results in two independent circuits that don't mix (need to create an opening between 2 circuits/maitain PDA)
131
With what is transposition of great vessels associated?
maternal diabetes
132
How does transposition of great vessels present?
early cyanosis: pulmonary and systemic circuits don't mix
133
What is required for survival in transposition of great vessels?
Creating of shunt after birth (allowing blood to mix)
134
What is the tx for transposition of great vessels?
PGE can be administered to maintain a PD until definitive surgical repair is performed
135
With what other condition is tricuspid atresia often associated?
ASD, resulting with left-to-right shunt (not sending blood to right ventricle)
136
What is coarctation of the aorta?
Narrowing of the aorta
137
How is coarctation of the aorta divided?
Infantile and adult forms
138
What is the result of transposition of great vessels associated?
hypertrophy of right ventricle and atrophy of left ventricle
139
With what is the infantile form of coarctation of the aorta associated with?
Associated with PDA and Turner syndrome
140
Where does coarctation of aorta lie in infantile form?
distal or aortic arch but proximal to PDA
141
How does infantile coarctation of aorta present
lower extremity cyanosis in infants, often at birth
142
Where does coarctation of aorta lie in adult form?
distal to aortic arch (pressure before narrowing is increased, pressure after narrowing is decreased)
143
Which is more common,metastatic tumors in the heart or primary tumors in the heart?
Metastatic tumors
144
Is adult for of coarctation of aorta associated with PDA?
no
145
Why does collateral circulation develop across intercostal arteries?
blood is trying to get around narrowing
146
How do intercostal arteries run?
right along lower surface of ribs
147
How does coarctation of aorta in adulthood present on x-ray?
'notching' of ribs due to engorged arteries
148
How does adult form of coarctation of aorta present?
hypertension of upper extremities and hypotension with weak pulses in lower extremities; classically discovered in adulthood
149
What do valvular lesions usually cause?
stenosis (decreased caliber of valve orifice, makes it hard for blood to get through) or regurg
150
What is acute rheumatic fever?
systemic complication of phyarngitis due to group A beta-hemolytic stres
151
Who is affected by rheumatic fever?
children 2-3 weeks after an episode of "strep throat"
152
What causes rheumatic fever?
molecular mimicry; bacterial M protein resumeles protein in human tissue (get damage to human tissues)
153
On what is dx of rheumatic fever based?
Jones criteria--evidence of prior group A beta-hemolytic strep infection with presence of major and minor factors
154
How is evidence of prior group A beta-hemolytic strep infection demonstrated?
elevated ASO (anti-strepsolyn O) or anti-DNase B titers
155
What are the major Jones criteria?
migratory polyarthritis, pancarditis, subcutaneous nodules, erythemia marginatum, sydeham chorea (Joints, O-heart, Nodules, Erythema marginatum, Sydeham chorea)
156
What is migratory arthritis?
swelling and pain in a large joint (ex wrist, knee, ankle) that resolves and then "migrates" to involve another large joints
157
What is pancarditis?
Inflammation of all layers of heart
158
What is endocarditis?
mitral valve is involved more than aortic valve; characterized by small vegetations along lines of closure that lead to regurg
159
How is myocarditis characterized?
Aschoff bodies: characterized by foci of chronic inflammation, reactive histiocytes with slender, wavy nuclei (Anitschkow cells), giant cells and fibrionoid material
160
What is the most common cause of death during acute phase of rheumatic fever?
Myocarditis
161
What does pericarditis lead to?
friction rub and chest pain
162
What is chronic rheumatic heart disease?
valve scarring that arises as a consequence of rheumatic fever
163
How does rheumatic fever resolve?
acute attack usually resolves but may progress to chronic rheumatic heart disease; repeat exposure to group A (beta-hemolytic) strep results in relapse of acute phase and increases risk for chronic disease
164
What is the result of chronic rheumatic heart disease?
stenosis with classic 'fish-mouth' appearance
165
What is sydeham chorea?
rapid, involuntary muscle movements
166
Which valves are involved in chronic rheumatic heart disease?
Almost always involves mitral valve--leads to thickening of chordae tendinae and cusps (stenosis); occasionally involves aortic valve--leads to fusion of commissures which reduces size of orifice
167
What is aortic stenosis?
narrowing of the aortic valve orifice; normally opening is 4cm2 but with stenosis it's less than 1
168
What causes aortic stenosis?
fibrosis and calcification from "wear and tear"
169
What is a potential complication of chronic rheumatic heart disease?
infectious endocarditis
170
When does aortic stenosis present?
late adulthood (>60)
171
What increases risk for aortic stenosis?
Bicuspid aortic valve: normal valve has 3 cusps, fewer cusps results in increased "wear and tear" (stenosis will present earlier)
172
What is the relationship between aortic stenosis and chronic rheumatic valve disease?
aortic stenosis can arise as a consequence of chronic rheumatic valve disease
173
What valves do rhuematic disease affect?
always involves mitral valve, may or may not involve aortic valve
174
How can chronic rheumatic valve disease be distinguished from "wear and tear"?
With chronic rheumatic valve disease there will be mitral stenosis and fusion of aortic valve commissures
175
What does a systolic ejection click represent?
blood forcing valve open
176
Why is there often a prolonged asymptomatic stage with aortic stenosis? What can be found on PE during this stage?
cardiac compensation; systolic ejection click followed by crescendo-decrescendo murmur
177
What are some complications of aortic stenosis?
concentric LV hypertrophywhich may progress to heart failure, angina and syncope with exercise, microangiopathic hemolytic anemia
178
What is mitral valve prolapse?
ballooning of mitral valve into left atrium during systole--becomes floppy (valve gets stretched backwards during prolapse so that can lead to regurg)
179
How does aortic stenosis cause angina and syncope with exercise?
limited ability to increase blood flow across stenotic valve leads to decreased perfusion of brain and myocardium
180
How does aortic stenosis cause microangiopathic hemolytic anemia?
RBCS are damaged (producing schistocyes) while crossing calcified valve
181
What is aortic regurgitation?
backflow of blood from aorta into the left ventricle during diastole
182
What is the most common cause of aortic regurgitation?
Isolated root dilation (aortic root is part where aorta comes off valve-Ben thinks)
183
What are other causes of aortic regurgitation?
aortic root dilation (ex: syphilitic aneurysm and aortic dissection) or valve damage (infectious endocarditis)
184
How does aortic root dissection cause aortic regurgitation?
pulls on valve outward so orifice becomes bigger
185
What is the treatment for aortic stenosis?
Replacement after onset of complications
186
What are the clinical features of aortic regurgitation?
early, blowing diastolic murmur, hyperdynamic circulation due to increased pulse pressure
187
What is pulse pressure?
difference between systolic and diastolic pressures
188
What is the treatment for aortic regurgitation?
valve replacement once LV dysfunction develops
189
Why does pulse pressure increase in aortic regurgitation?
diastolic pressure decreases due to regurg while systolic pressure increases due to increased SV
190
How does hyperdynamic circulation due to increased pulse pressure present?
bounding pulse (water-hammer pulse), pulsating nail bed (Quincke pulse) and head bobbing
191
What is eccentric hypertrophy?
involves one part of ventricle
192
In what % of the US population is mitral valve prolapse seen?
2-3% of adults
193
What causes MVP?
Myxoid degeneration (accumulation of ground substance on the valve which makes it floppy--etiology is unknown (may be seen in Marfan or Ehler-Danlos syndromes)
194
What does mitral valve prolapse present?
Incidental mid-systolic click followed by a regurgitation murmur; usually asymptomatic
195
What effect do changes in position have on click and murmur in MVP?
Click and murmur become softer with squatting: increased systemic resistance decreases left ventricular emptying
196
What is mitral regurgitation?
Reflux of blood from left ventricle into left atrium during systole
197
What causes mitral regurg?
Usually arises as complication of mitral valve prolapse; other causes: LV dilatation, infective endocarditis, acute rheumatic heart disease, papillary muscle rupture after MI
198
What causes LV dilatation? How does it cause mitral regurg?
left sided cardiac failure; LV dilation stretches valve outward increasing size of orifice
199
What are the clinical features of mitral regurg?
Holosystolic "blowing" murmur; louder with squatting and expiration
200
Why is the mitral valve regurg murmur louder with squatting?
increased systemic resistance decreases left ventricular emptying
201
Why is the mitral valve regurg murmur louder with expiration?
increased return to LA (VERY IMPORTANT)
202
What does mitral regurg result in?
Volume overload and left sided heart failure
203
What is mitral stenosis?
Narrowing of mitral valve orifice
204
What causes mitral stenosis?
usually due to rheumatic heart disease
205
What are the clinical features of mitral stenosis?
opening snap followed by diastolic rumble
206
What does mitral stenosis lead to?
Volume overload > dilatation of left atrium
207
What does dilatation of left atrium lead to?
pulmonary congestion with edema and alveolar hemorrhage (heart failure cells); pulmonary HTN with eventual right-sided heart failure; A-fib with associated risk of mural thrombi
208
What are heart failure cells?
hemosiderin laden macrophages
209
How does dilatation of left atrium lead to A-fib and thrombosis?
Stretching of atrial wall disrupts conduction system, also causes stasis of blood
210
With what is adult form of coarctation of aorta associated?
bicuspid aortic valve
211
What is the most common primary cardiac tumor in children?
rhabdomyoma
212
What are some common metastases to the heart?
Breast and lung carcinoma, melanoma and lymphoma
213
What part of the heart do metastases commonly affect?
Pericardium, resulting in a pericardial effusion
214
What is endocarditis?
inflammation of endocardium that lines surface of cardiac valves, usually due to bacterial infection
215
What is the most common overall cause of endocarditis?
strep viridans
216
How does strep viridans cause endocarditis? What results?
low-virulence organism that infects previously damaged vessels (ex: chronic rheumatic heart disease, mitral valve prolapse); results in subacute endocarditis (small vegetations that do not destroy valve)
217
Once small vegetation from strep viridans form on valves what happens?
TF and subendothelial collagen from damaged endocardial surface are exposed > thrombotic vegetations (platelets and fibrin) > transient bacteremia leads to trapping of bacteria in vegetations
218
With what procedures is subacute endocarditis from strep viridans a risk? What can be done?
Dental procedures; prophylactic abx decrease risk
219
What is the most common cause of endocarditis among drug users? Why?
Staph aureus; iv drug user has infection skin (strep gets right into veins > heart > tricuspid valve)
220
How does staph aureus cause endocarditis? What results?
high-virulence organism that infects normal valves, most commonly the tricuspid; acute endocarditis results (large vegetations destroy valve)
221
What pathogen is associated with endocarditis of prosthetic valves?
Staph epidermidis
222
What pathogen is associated with endocarditis in patients with underlying colorectal carcinoma?
Strep bovis
223
What pathogen is associated with endocarditis of with negative blood cultures?
HACEK organisms: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella
224
Why are HACEK organisms associated with endocarditis with negative blood cultures?
They are difficult to grow
225
What are the clinical features of endocarditis?
fever, murmur, Janeway lesions, Roth spots, Osler nodes, splinter hemorrhages in nail bed, ACD
226
Why does endocarditis cause fever?
bacteremia
227
Why does endocarditis cause murmur?
vegetations on heart valve
228
What are Janeway lesions? What causes them?
erythematous non-tender lesions on palms and soles--from embolization of septic vegetations
229
Where do splinter hemorrhages appear with endocarditis? Why?
in nail bed--from embolization of septic vegetations
230
What are Osler nodes? What causes them?
tender lesions on fingers or toes--from embolization of septic vegetations ("ouch, ouch, osler")
231
What are Roth spots? What causes them?
retinal hemorrhages with white or pale centers--from embolization of septic vegetations
232
How does endocarditis cause Janeway lesions, Roth spots and Osler nodes?
embolization of septic vegetations
233
Why does endocarditis cause ACD?
chronic inflammation
234
What are the lab findings in endocarditis?
Positive blood cultures (except with HACEK) ACD (increased ferritin, decreased TIBC, decreased serum iron, decreased %sat, decreased Hb, decreased MCV)
235
What tool is useful for detecting lesions on valves?
transesophageal echocardiogram
236
What is the result of endocarditis from strep viridans?
small vegetations that don't destroy valve--subacute endocarditis
237
What is nonbacterial thrombotic endocarditis?
caused by sterile vegetations that arise in associateion with a hypercoagulable state or underlying adenocarcinoma
238
What valve do nonbacterial thrombotic vegetations tend to affect? What results?
mitral valve along lines of closure; mitral regurg
239
What is rhabdomyoma?
benign hamartoma of cardiac/striated muscle (benign mass)
240
What is Libman-Sacks endocarditis?
endocarditis due to sterile vegetations that arise in association with SLE
241
Where do Libman-Sacks vegetations present? What results?
characteristically on surface and undersurface of mitral valve; mitral regurg
242
What is cardiomyopathy?
Group of myocardial disease that result in cardiac dysfunction
243
What is most common form of cardiomyopathy?
dilated cardiomyopathy
244
What is dilated cardiomyopathy?
dilation of all four chambers of the heart
245
What is hypertrophic cardiomyopathy?
massive hypertrophy of left ventricle
246
What are some other causes of dilated cardiomyopathy?
genetic mutations (usually autosomal dominant) myocarditis Alcohol abuse drugs pregnancy pregnancy hemochromatosis
247
How does myocarditis cause dilated cardiomyopathy?
lymphocytic infiltrate in the myocadium
248
What is the result of myocarditis?
Chest pain, arrhythmia with sudden death or heart failure; dilated cardiomyopathy is a late complication
249
What generally causes myocarditis that leads to dilated cardiomyopathy?
Coxsackie A and B
250
When in pregnancy does dilated cardiomyopathy present?
seen during late pregnancy or soon (weeks to months) after childbirth
251
Which drugs cause dilated cardiomyopathy?
doxorubicin, cocaine
252
What causes hypertrophic cardiomyopathy?
usually due to genetic mutations in sarcomere proteins
253
What is the most common form of hypertrophic cardiomyopathy?
autosomal dominant
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What is the most common cause of dilated cardiomyopathy?
idiopathic
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What is the treatment for dilated cardiomyopathy?
heart transplant
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What are the clinical features of hypertrophic cardiomyopathy?
Decreased CO, sudden death due to ventricular arrhythmias, syncope with exercise
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How does hypertrophic cardiomyopathy cause decreased CO?
left ventricular hypertrophy leads to diastolic dysfunction--ventricle cannot fill because of lack of compliance
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How does hypertrophic cardiomyopathy cause decreased sudden death?
hypertrophic cardiomyopathy is a common cause of sudden death in young athletes
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How does hypertrophic cardiomyopathy cause decreased syncope with exercise?
sub-aortic hypertrophy of the ventricular septum results in functional aortic stenosis--preferential involvement of IVS right beneath aortic valve
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What is restrictive cardiomyopathy?
Decreased compliant of ventricular endomyocardium that restricts filling during diastole
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What causes restrictive cardiomyopathy?
Amyloidosis, sarcoidosis, endocardial fibroelastosis (in children), Leoffler syndrome
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How does sarcoidosis cause restrictive cardiomyopathy?
granulomas in wall of heart makes it difficult for heart to stretch
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What is endocardial fibroelastosis? In whom is it seen?
dense layer of fibrosis and elastic tissue endocardium, cannot be stretched
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What is Loeffer syndrome?
endomyocardial fibrosis with an eosinophilic infiltrate and eosinophilia--also hemachromatosis
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How does restrictive cardiomyopathy present?
CHF
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What EKG findings present with restrictive cardiomyopathy?
low-voltage EKG with diminished QRS amplitude (because you have all this material in the wall)
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Where does rhabdomyoma usually arise?
in the ventricle
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What is the most common primary cardiac tumor in adults?
myxoma
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What are the different kinds of cardiac tumors?
myxoma, rhabdomyoma, metastases
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Why can't cardiac cells form tumors?
cardiac cells are permanent
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What is myxoma?
benign mesenchymal tumor with a gelatinous appearance and abundant ground substance (this is what makes it look gelatinous) on histology
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How and where does myxoma usually arise? How does it present?
Usually forms pedunculated mass (grows off stalk) in left atrium that causes syncope due to obstruction of mitral valve
