Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathoma > Pathoma Ch 8 - Cardiology > Flashcards

Pathoma Ch 8 - Cardiology Flashcards

1
Q

What is the leading cause of death in the US?

A

IHD (ischemic heart disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What causes IHD?

A

Usually due to atherosclerosis of coronary arteries which decreases blood blood to myocardum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the RFs for IHD?

A

similar to those of atherosclerosis–incidence increases with age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is angina?

A

Chest pain that is reversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the hallmark of reversible cellular injury?

A

swelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

After how many minutes of decreased blood flow/chest pain does myocardium undergo non-reversible damage?

A

20 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which portion of the heart wall is most susceptible to ischemic damage?

A

endocardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is stable angina?

A

(no chest pain at rest), chest pain that arises with exertion or emotional stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What does angina represent into terms of injury?

A

Reversible injury to myocytes (no necrosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does stable angina present?

A

chest pain lasting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is evident on EKG with stable angina?

A

ST-segment depression due to subendocardial ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How is stable angina relieved?

A

rest or nitroglycerin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What causes unstable angina?

A

usually due to rupture of atherosclerotic plaque with thrombus and INCOMPLETE occlusion of coronary artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What kind of injury does unstable angina represent?

A

Reversible injury to myocytes (no necrosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is evident on EKG with unstable angina?

A

ST-segment depression due to subendocardial ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How is unstable angina relieved?

A

nitroglycerin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What risk is posed by unstable angina?

A

Progression to MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is prinzmetal angina?

A

Episodic chest pain unrelated to exertion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What causes prinzmetal angina?

A

Coronary vasospasm (BV clamping down)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What kind of injury does prinzmetal angina represent?

A

reversible injury to myocytes (no necrosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How is prinzmetal angina relieved?

A

nitroglycerin or CCB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is myocardial infarction?

A

necrosis of cardiac myocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the most common cause of MI?

A

Usually due to rupture of atherosclerotic plaque with thrombus and COMPLETE occlusion of artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are some other causes of MI?

A

coronary artery vasospasm, emboli, vasculitis (ex: kawasaki disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How does vasculitis cause MI?

A

damage to vessel wall exposes SEC and TF > thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What causes coronary artery vasospasm?

A

prinzmetal angina and cocaine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the clinical features of MI?

A

severe, crushing chest pain lasting >20 minutes that radiates to the left arm or jaw, diaphoresis and dyspnea; nitroglycerin does not relieve symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Why does an MI cause dyspnea?

A

Pulmonary congestion and edema are caused because heart isn’t pumping well

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Which areas of the heart are usually affected by infarction? Which are generally spared?

A

Affected: LV Spared: RV and both atria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What artery is most commonly involved in MI? What is second most common?

A

Most: LAD (45% of cases) Second: RCA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What does occlusion of left LAD lead to?

A

infarction of anterior wall and anterior septum of LV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What does occlusion of RCA lead to ?

A

infarction of posterior wall, posterior septum, and papillary muscles of LV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What does occlusion of left circumflex lead to?

A

infarction of lateral wall of LV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What does the initial phase of infarction lead to?

A

subendocardial necrosis involving

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is shown on EKG during initial phase of infarction?

A

ST depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What does continued infarction lead to?

A

continued or severe ischemia leads to transmural necrosis which involves most of myocardial wall (transmural infarction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is shown on EKG with transmural infarction?

A

ST-segment elevation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Which lab tests are used to detect MI? What are they looking for?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Which lab test is most sensitive and specific marker for MI?

A

Troponin I (gold standard)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

When do Troponin I levels begin to rise? When do they peak? When do they return to normal?

A

Levels rise 2-4 hours post infarction, peak at 24 hours and return to normal by 7-10 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is CK-MB useful for?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

When do CK-MB levels begin to rise? When do they peak? When do they return to normal?

A

Rise 4-6 hours after infarction, peak at 24 hours and retun to normal by 72 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is the treatment for MI?

A

aspirin and/or heparin, supplemental O2, nitrates, BB, ACEi, fibrinolysis or angioplasty

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Why are aspirin and heparin used to tx MI?

A

limit thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Why is supplemental O2 a used to tx MI?

A

minimized ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Why are nitrates used to tx MI?

A

vasodilate veins and coronary arteries (reduce preload/stress on heart)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Why are beta blockers used to tx MI?

A

slows heart rate, decreasing O2 demand and risk for arrhythmia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Why are ACEi used to tx MI?

A

decrease LV dilation; angiotensin II constricts peripheral BVs, blocking this decreases afterload on heart (ATII also increases BV volume via aldosterone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What do fibrinolysis and angioplasty do?

A

open blocked vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are potential complications of fibrinolysis and angioplasty?

A

Contraction band necrosis and reperfusion injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is contraction band necrosis?

A

Reperfusion of irreversibly-damaged cells results in Ca influx, leading to hypercontraction of myofibrils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is reperfusion injury?

A

Return of oxygen and inflammatory cells may lead to free radical generation, further damaging myocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Why do cardiac enzymes continue to go up after angioplasy?

A

reperfusion injury results in more damage to myocytes which would cause cardiac enzyme levels to continue to rise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What are complications of MI related to?

A

Gross and microscopic changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is a feared complication very early after MI occurs? How is this handled?

A

Arrhythmia; tx with BB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What gross and microscopic changes appear

A

none

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What complications can arise

A

Cardiogenic shock (massive infarction), CHF and arrhythmia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What gross and microscopic changes appear 4-12 hours after infarction?

A

G: dark discoloration M: coagulative necrosis (remove nucleus from cell)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What complications can arise 4-12 hours after infarction?

A

arrhythmia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What gross and microscopic changes appear 1-3 days after infarction?

A

G:yellow pallor (WBC in myocardium–acute inflammation always follows necrosis) M: neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What complications can arise 1-3 days after infarction?

A

fibrinous pericarditis; presents as chest pain with friction rub (only get this with transmural infarction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What gross and microscopic changes appear 4-7 days after infarction?

A

G:yellow pallor M: macrophages–eat up dead and necrotic debris

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

At what point will the cardiac wall be the weakest?

A

4-7 days after infarction–when macrophages are present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What complications can arise 4-7 days after infarction?

A

Rupture of ventricular free wall leads to cardiac tamponade; rupture of interventricular septum leads to shunt; rupture of papillary muscle leads to mitral insufficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What BV supplies the papillary muscle?

A

RCA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What is mitral insufficiency?

A

Blood regurgitating back into atria during systole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What gross and microscopic changes appear 1-3 weeks after infarction?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What complications can arise 1-3 weeks after infarction?

A

None listed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What gross and microscopic changes appear months after infarction?

A

G: white scar M: fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What is sudden cardiac death?

A

unexpected death due to cardiac disease; occurs without symptoms or

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What complications can arise months after infarction?

A

anuerysm, mural thrombus (from stasis along wall of scar), Dressler syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What is Dressler syndrome?

A

pericarditis that arises 6-8 weeks after infarction due to autoimmune phenomenon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What is the most common etiology of SCD?

A

acute ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What % of patients with SCD have preexisting severe atherosclerosis?

A

90%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What is the most common cause of SCD?

A

fatal ventricular arrhythmia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What are some less common causes of SCD?

A

mitral valve prolapse, cardiomyopathy, cocaine abuse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What is CHF? How is it divided?

A

Pump failure; right and left-sided failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What causes left-sided heart failure?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What causes the clinical features of left-sided heart failure?

A

decreased forward perfusion and pulmonary congestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What does decreased flow to kidneys lead to (decreased forward perfusion)?

A

activation of renin-angiotensin system; fluid retention exacerbates CHF (via aldosterone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

How does pulmonary congestion present clinically?

A

dyspnea, paroxysal nocturnal dyspnea (due to increased venous return while lying flat), orthopnea and crackles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What are some consequences of pulmonary congestion?

A

Small, congested capillaries may burst leading to intra-alveolar hemorrhage–marked by hemosiderin -laden macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What are heart failure cells?

A

hemosiderin -laden macrophages; macrophages consume lots of iron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What is the mainstay of tx for left-sided heart failure?

A

ACEi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

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

A

Left-sided heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What are some other important causes of right-side heart failure?

A

left to right shunt, chronic lung disease (cor pulmonale)–hypoxia > constriction of BV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What are the clinical features of right-side heart failure?

A

ALL DUE TO PULMONARY CONGESTION; jugular venous distention, painful hepatosplenomegaly with characteristic “nutmeg liver”–leads to cardiac cirrhosis, dependent pitting edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What causes pitting edema in right-side heart failure?

A

Increased hydrostatic pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

When do congenital heart defects arise?

A

During embyrogenesis (weeks 3-8)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What is the prevalence of congenital heart defects? What is their hereditary pattern?

A

1%, most defects are sparoadic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What are some examples of congenital heart defects?

A

Ventricular septal defects, atrial septal defect, patent ductus arteriosus, tetralogy of fallot, transposition of great vessels, truncus arteriosus, tricuspid atresia, coarcatation of the aorta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What does increased pulmonary resistance eventually lead to?

A

reversal of shunt leading to late cyanosis (Eisenmenger syndrome) with right ventricular hypertrophy, polycythemia and clubbing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What is VSD?

A

Defect in septum that divides right and left ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Why does increased pulmonary resistance lead to polycythemia?

A

Deoxygenated blood in systemic circuit leads to hypoxemia > release of EPO > polycythemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

What does increased blood flow through pulmonary circulation result in?

A

hypertrophy of pulmonary vessels and pulmonary HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

What is the most common congenital heart defect?

A

VSD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

How do defects with right-to-left shunt is usually present?

A

cyanosis after birth (may be relative asymptomatic at birth)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

With what is VSD associated?

A

fetal alcohol syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What does VSD cause?

A

left to right shunt because wall between ventricles is not completely formed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What determines the extent of shunting?

A

size of defect and age at presentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

How does VSD present?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

What is the tx for VSD?

A

surgical closure; small defects may close spontaneously

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

What is truncus arteriosus?

A

Characterized by single large vessel arising from both ventricles–truncus fails to divide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

How does truncus arteriosus present?

A

Early cyanosis, deoxygenated blood from right ventricle and mixed with oxygenated blood from left ventricle, before pulmonary and aortic circulation separate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What is ASD?

A

Defect in septum that divides right and left ventricle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

What is PDA?

A

Failure of ductus arteriosus to close

110
Q

With what is PDA associated?

A

Congential rubella

111
Q

What is most common type of ASD? With what condition is it associated?

A

Ostium secundum (90% of cases); Down syndrome

112
Q

What does ASD result in?

A

left to right shunt and split S2 on auscultation

113
Q

What causes split S2 on auscultation in ASD?

A

increased blood in right heart delays closure of pulmonary valve

114
Q

What is an important complication of ASD?

A

Paradoxical emboli–embolus on right side that crosses over to left side

115
Q

What is the result of PDA?

A

right to left shunt between aorta and pulmonary artery

116
Q

What purpose does ductus arteriosus serve during development?

A

shunts blood to pulmonary atery to aorta, bypassing lungs

117
Q

How does ductus arteriosus present? how does it progress?

A

Asymptomatic at birth with continuous ‘machine-like’ murmur; may lead to Eisenmernger syndrome

118
Q

What is Eisenmernger syndrome?

A

reversal of shunt > lower extremity cyanosis

119
Q

What is tricuspid atresia?

A

Tricuspid valve orifice fails to develop, right ventricle is hypoplastic

120
Q

What maintains the patency of the ductus arteriosus?

A

PGE

121
Q

What is the tx of PDA?

A

indomethacin

122
Q

How does indomethacin work?

A

decreases PGE, resulting in PDA closure (PEF maintanes patency of ductus arteriosus)

123
Q

What is tetralogy of fallot?

A

Characterized by 1. stenosis of right ventricular outflow tract; 2. right ventricular hypertoprhy; 3. VSD; 4. aorta that arrides the VSD

124
Q

What does tetralogy of fallot lead to?

A

right to left shunt leads to early cyanosis; degree of stenosis determines degree of cyanosis

125
Q

What causes right to left shunt in tetralogy of fallot?

A

because of stenosis, blood from RV goes into aorta

126
Q

How do patients handle cyanotic spell with tetralogy of fallot?

A

They learn to squat: increased arterial resistance (increased pressure on right side of heart) decreases shunting and allow more blood to reach lungs

127
Q

When do patients with tetralogy of fallot get cyanotic spell?

A

During exercise

128
Q

How does tricuspid atresia present?

A

Cyanosis

129
Q

What appears on X-ray with tetralogy of fallot?

A

Boot-shaped heart

130
Q

What is transposition of the great vessels?

A

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
Q

With what is transposition of great vessels associated?

A

maternal diabetes

132
Q

How does transposition of great vessels present?

A

early cyanosis: pulmonary and systemic circuits don’t mix

133
Q

What is required for survival in transposition of great vessels?

A

Creating of shunt after birth (allowing blood to mix)

134
Q

What is the tx for transposition of great vessels?

A

PGE can be administered to maintain a PD until definitive surgical repair is performed

135
Q

With what other condition is tricuspid atresia often associated?

A

ASD, resulting with left-to-right shunt (not sending blood to right ventricle)

136
Q

What is coarctation of the aorta?

A

Narrowing of the aorta

137
Q

How is coarctation of the aorta divided?

A

Infantile and adult forms

138
Q

What is the result of transposition of great vessels associated?

A

hypertrophy of right ventricle and atrophy of left ventricle

139
Q

With what is the infantile form of coarctation of the aorta associated with?

A

Associated with PDA and Turner syndrome

140
Q

Where does coarctation of aorta lie in infantile form?

A

distal or aortic arch but proximal to PDA

141
Q

How does infantile coarctation of aorta present

A

lower extremity cyanosis in infants, often at birth

142
Q

Where does coarctation of aorta lie in adult form?

A

distal to aortic arch (pressure before narrowing is increased, pressure after narrowing is decreased)

143
Q

Which is more common,metastatic tumors in the heart or primary tumors in the heart?

A

Metastatic tumors

144
Q

Is adult for of coarctation of aorta associated with PDA?

A

no

145
Q

Why does collateral circulation develop across intercostal arteries?

A

blood is trying to get around narrowing

146
Q

How do intercostal arteries run?

A

right along lower surface of ribs

147
Q

How does coarctation of aorta in adulthood present on x-ray?

A

‘notching’ of ribs due to engorged arteries

148
Q

How does adult form of coarctation of aorta present?

A

hypertension of upper extremities and hypotension with weak pulses in lower extremities; classically discovered in adulthood

149
Q

What do valvular lesions usually cause?

A

stenosis (decreased caliber of valve orifice, makes it hard for blood to get through) or regurg

150
Q

What is acute rheumatic fever?

A

systemic complication of phyarngitis due to group A beta-hemolytic stres

151
Q

Who is affected by rheumatic fever?

A

children 2-3 weeks after an episode of “strep throat”

152
Q

What causes rheumatic fever?

A

molecular mimicry; bacterial M protein resumeles protein in human tissue (get damage to human tissues)

153
Q

On what is dx of rheumatic fever based?

A

Jones criteria–evidence of prior group A beta-hemolytic strep infection with presence of major and minor factors

154
Q

How is evidence of prior group A beta-hemolytic strep infection demonstrated?

A

elevated ASO (anti-strepsolyn O) or anti-DNase B titers

155
Q

What are the major Jones criteria?

A

migratory polyarthritis, pancarditis, subcutaneous nodules, erythemia marginatum, sydeham chorea (Joints, O-heart, Nodules, Erythema marginatum, Sydeham chorea)

156
Q

What is migratory arthritis?

A

swelling and pain in a large joint (ex wrist, knee, ankle) that resolves and then “migrates” to involve another large joints

157
Q

What is pancarditis?

A

Inflammation of all layers of heart

158
Q

What is endocarditis?

A

mitral valve is involved more than aortic valve; characterized by small vegetations along lines of closure that lead to regurg

159
Q

How is myocarditis characterized?

A

Aschoff bodies: characterized by foci of chronic inflammation, reactive histiocytes with slender, wavy nuclei (Anitschkow cells), giant cells and fibrionoid material

160
Q

What is the most common cause of death during acute phase of rheumatic fever?

A

Myocarditis

161
Q

What does pericarditis lead to?

A

friction rub and chest pain

162
Q

What is chronic rheumatic heart disease?

A

valve scarring that arises as a consequence of rheumatic fever

163
Q

How does rheumatic fever resolve?

A

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
Q

What is the result of chronic rheumatic heart disease?

A

stenosis with classic ‘fish-mouth’ appearance

165
Q

What is sydeham chorea?

A

rapid, involuntary muscle movements

166
Q

Which valves are involved in chronic rheumatic heart disease?

A

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
Q

What is aortic stenosis?

A

narrowing of the aortic valve orifice; normally opening is 4cm2 but with stenosis it’s less than 1

168
Q

What causes aortic stenosis?

A

fibrosis and calcification from “wear and tear”

169
Q

What is a potential complication of chronic rheumatic heart disease?

A

infectious endocarditis

170
Q

When does aortic stenosis present?

A

late adulthood (>60)

171
Q

What increases risk for aortic stenosis?

A

Bicuspid aortic valve: normal valve has 3 cusps, fewer cusps results in increased “wear and tear” (stenosis will present earlier)

172
Q

What is the relationship between aortic stenosis and chronic rheumatic valve disease?

A

aortic stenosis can arise as a consequence of chronic rheumatic valve disease

173
Q

What valves do rhuematic disease affect?

A

always involves mitral valve, may or may not involve aortic valve

174
Q

How can chronic rheumatic valve disease be distinguished from “wear and tear”?

A

With chronic rheumatic valve disease there will be mitral stenosis and fusion of aortic valve commissures

175
Q

What does a systolic ejection click represent?

A

blood forcing valve open

176
Q

Why is there often a prolonged asymptomatic stage with aortic stenosis? What can be found on PE during this stage?

A

cardiac compensation; systolic ejection click followed by crescendo-decrescendo murmur

177
Q

What are some complications of aortic stenosis?

A

concentric LV hypertrophywhich may progress to heart failure, angina and syncope with exercise, microangiopathic hemolytic anemia

178
Q

What is mitral valve prolapse?

A

ballooning of mitral valve into left atrium during systole–becomes floppy (valve gets stretched backwards during prolapse so that can lead to regurg)

179
Q

How does aortic stenosis cause angina and syncope with exercise?

A

limited ability to increase blood flow across stenotic valve leads to decreased perfusion of brain and myocardium

180
Q

How does aortic stenosis cause microangiopathic hemolytic anemia?

A

RBCS are damaged (producing schistocyes) while crossing calcified valve

181
Q

What is aortic regurgitation?

A

backflow of blood from aorta into the left ventricle during diastole

182
Q

What is the most common cause of aortic regurgitation?

A

Isolated root dilation (aortic root is part where aorta comes off valve-Ben thinks)

183
Q

What are other causes of aortic regurgitation?

A

aortic root dilation (ex: syphilitic aneurysm and aortic dissection) or valve damage (infectious endocarditis)

184
Q

How does aortic root dissection cause aortic regurgitation?

A

pulls on valve outward so orifice becomes bigger

185
Q

What is the treatment for aortic stenosis?

A

Replacement after onset of complications

186
Q

What are the clinical features of aortic regurgitation?

A

early, blowing diastolic murmur, hyperdynamic circulation due to increased pulse pressure

187
Q

What is pulse pressure?

A

difference between systolic and diastolic pressures

188
Q

What is the treatment for aortic regurgitation?

A

valve replacement once LV dysfunction develops

189
Q

Why does pulse pressure increase in aortic regurgitation?

A

diastolic pressure decreases due to regurg while systolic pressure increases due to increased SV

190
Q

How does hyperdynamic circulation due to increased pulse pressure present?

A

bounding pulse (water-hammer pulse), pulsating nail bed (Quincke pulse) and head bobbing

191
Q

What is eccentric hypertrophy?

A

involves one part of ventricle

192
Q

In what % of the US population is mitral valve prolapse seen?

A

2-3% of adults

193
Q

What causes MVP?

A

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
Q

What does mitral valve prolapse present?

A

Incidental mid-systolic click followed by a regurgitation murmur; usually asymptomatic

195
Q

What effect do changes in position have on click and murmur in MVP?

A

Click and murmur become softer with squatting: increased systemic resistance decreases left ventricular emptying

196
Q

What is mitral regurgitation?

A

Reflux of blood from left ventricle into left atrium during systole

197
Q

What causes mitral regurg?

A

Usually arises as complication of mitral valve prolapse; other causes: LV dilatation, infective endocarditis, acute rheumatic heart disease, papillary muscle rupture after MI

198
Q

What causes LV dilatation? How does it cause mitral regurg?

A

left sided cardiac failure; LV dilation stretches valve outward increasing size of orifice

199
Q

What are the clinical features of mitral regurg?

A

Holosystolic “blowing” murmur; louder with squatting and expiration

200
Q

Why is the mitral valve regurg murmur louder with squatting?

A

increased systemic resistance decreases left ventricular emptying

201
Q

Why is the mitral valve regurg murmur louder with expiration?

A

increased return to LA (VERY IMPORTANT)

202
Q

What does mitral regurg result in?

A

Volume overload and left sided heart failure

203
Q

What is mitral stenosis?

A

Narrowing of mitral valve orifice

204
Q

What causes mitral stenosis?

A

usually due to rheumatic heart disease

205
Q

What are the clinical features of mitral stenosis?

A

opening snap followed by diastolic rumble

206
Q

What does mitral stenosis lead to?

A

Volume overload > dilatation of left atrium

207
Q

What does dilatation of left atrium lead to?

A

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
Q

What are heart failure cells?

A

hemosiderin laden macrophages

209
Q

How does dilatation of left atrium lead to A-fib and thrombosis?

A

Stretching of atrial wall disrupts conduction system, also causes stasis of blood

210
Q

With what is adult form of coarctation of aorta associated?

A

bicuspid aortic valve

211
Q

What is the most common primary cardiac tumor in children?

A

rhabdomyoma

212
Q

What are some common metastases to the heart?

A

Breast and lung carcinoma, melanoma and lymphoma

213
Q

What part of the heart do metastases commonly affect?

A

Pericardium, resulting in a pericardial effusion

214
Q

What is endocarditis?

A

inflammation of endocardium that lines surface of cardiac valves, usually due to bacterial infection

215
Q

What is the most common overall cause of endocarditis?

A

strep viridans

216
Q

How does strep viridans cause endocarditis? What results?

A

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
Q

Once small vegetation from strep viridans form on valves what happens?

A

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
Q

With what procedures is subacute endocarditis from strep viridans a risk? What can be done?

A

Dental procedures; prophylactic abx decrease risk

219
Q

What is the most common cause of endocarditis among drug users? Why?

A

Staph aureus; iv drug user has infection skin (strep gets right into veins > heart > tricuspid valve)

220
Q

How does staph aureus cause endocarditis? What results?

A

high-virulence organism that infects normal valves, most commonly the tricuspid; acute endocarditis results (large vegetations destroy valve)

221
Q

What pathogen is associated with endocarditis of prosthetic valves?

A

Staph epidermidis

222
Q

What pathogen is associated with endocarditis in patients with underlying colorectal carcinoma?

A

Strep bovis

223
Q

What pathogen is associated with endocarditis of with negative blood cultures?

A

HACEK organisms: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella

224
Q

Why are HACEK organisms associated with endocarditis with negative blood cultures?

A

They are difficult to grow

225
Q

What are the clinical features of endocarditis?

A

fever, murmur, Janeway lesions, Roth spots, Osler nodes, splinter hemorrhages in nail bed, ACD

226
Q

Why does endocarditis cause fever?

A

bacteremia

227
Q

Why does endocarditis cause murmur?

A

vegetations on heart valve

228
Q

What are Janeway lesions? What causes them?

A

erythematous non-tender lesions on palms and soles–from embolization of septic vegetations

229
Q

Where do splinter hemorrhages appear with endocarditis? Why?

A

in nail bed–from embolization of septic vegetations

230
Q

What are Osler nodes? What causes them?

A

tender lesions on fingers or toes–from embolization of septic vegetations (“ouch, ouch, osler”)

231
Q

What are Roth spots? What causes them?

A

retinal hemorrhages with white or pale centers–from embolization of septic vegetations

232
Q

How does endocarditis cause Janeway lesions, Roth spots and Osler nodes?

A

embolization of septic vegetations

233
Q

Why does endocarditis cause ACD?

A

chronic inflammation

234
Q

What are the lab findings in endocarditis?

A

Positive blood cultures (except with HACEK) ACD (increased ferritin, decreased TIBC, decreased serum iron, decreased %sat, decreased Hb, decreased MCV)

235
Q

What tool is useful for detecting lesions on valves?

A

transesophageal echocardiogram

236
Q

What is the result of endocarditis from strep viridans?

A

small vegetations that don’t destroy valve–subacute endocarditis

237
Q

What is nonbacterial thrombotic endocarditis?

A

caused by sterile vegetations that arise in associateion with a hypercoagulable state or underlying adenocarcinoma

238
Q

What valve do nonbacterial thrombotic vegetations tend to affect? What results?

A

mitral valve along lines of closure; mitral regurg

239
Q

What is rhabdomyoma?

A

benign hamartoma of cardiac/striated muscle (benign mass)

240
Q

What is Libman-Sacks endocarditis?

A

endocarditis due to sterile vegetations that arise in association with SLE

241
Q

Where do Libman-Sacks vegetations present? What results?

A

characteristically on surface and undersurface of mitral valve; mitral regurg

242
Q

What is cardiomyopathy?

A

Group of myocardial disease that result in cardiac dysfunction

243
Q

What is most common form of cardiomyopathy?

A

dilated cardiomyopathy

244
Q

What is dilated cardiomyopathy?

A

dilation of all four chambers of the heart

245
Q

What is hypertrophic cardiomyopathy?

A

massive hypertrophy of left ventricle

246
Q

What are some other causes of dilated cardiomyopathy?

A

genetic mutations (usually autosomal dominant) myocarditis Alcohol abuse drugs pregnancy pregnancy hemochromatosis

247
Q

How does myocarditis cause dilated cardiomyopathy?

A

lymphocytic infiltrate in the myocadium

248
Q

What is the result of myocarditis?

A

Chest pain, arrhythmia with sudden death or heart failure; dilated cardiomyopathy is a late complication

249
Q

What generally causes myocarditis that leads to dilated cardiomyopathy?

A

Coxsackie A and B

250
Q

When in pregnancy does dilated cardiomyopathy present?

A

seen during late pregnancy or soon (weeks to months) after childbirth

251
Q

Which drugs cause dilated cardiomyopathy?

A

doxorubicin, cocaine

252
Q

What causes hypertrophic cardiomyopathy?

A

usually due to genetic mutations in sarcomere proteins

253
Q

What is the most common form of hypertrophic cardiomyopathy?

A

autosomal dominant

254
Q

What is the most common cause of dilated cardiomyopathy?

A

idiopathic

255
Q

What is the treatment for dilated cardiomyopathy?

A

heart transplant

256
Q

What are the clinical features of hypertrophic cardiomyopathy?

A

Decreased CO, sudden death due to ventricular arrhythmias, syncope with exercise

257
Q

How does hypertrophic cardiomyopathy cause decreased CO?

A

left ventricular hypertrophy leads to diastolic dysfunction–ventricle cannot fill because of lack of compliance

258
Q

How does hypertrophic cardiomyopathy cause decreased sudden death?

A

hypertrophic cardiomyopathy is a common cause of sudden death in young athletes

259
Q

How does hypertrophic cardiomyopathy cause decreased syncope with exercise?

A

sub-aortic hypertrophy of the ventricular septum results in functional aortic stenosis–preferential involvement of IVS right beneath aortic valve

260
Q

What is restrictive cardiomyopathy?

A

Decreased compliant of ventricular endomyocardium that restricts filling during diastole

261
Q

What causes restrictive cardiomyopathy?

A

Amyloidosis, sarcoidosis, endocardial fibroelastosis (in children), Leoffler syndrome

262
Q

How does sarcoidosis cause restrictive cardiomyopathy?

A

granulomas in wall of heart makes it difficult for heart to stretch

263
Q

What is endocardial fibroelastosis? In whom is it seen?

A

dense layer of fibrosis and elastic tissue endocardium, cannot be stretched

264
Q

What is Loeffer syndrome?

A

endomyocardial fibrosis with an eosinophilic infiltrate and eosinophilia–also hemachromatosis

265
Q

How does restrictive cardiomyopathy present?

A

CHF

266
Q

What EKG findings present with restrictive cardiomyopathy?

A

low-voltage EKG with diminished QRS amplitude (because you have all this material in the wall)

267
Q

Where does rhabdomyoma usually arise?

A

in the ventricle

268
Q

What is the most common primary cardiac tumor in adults?

A

myxoma

269
Q

What are the different kinds of cardiac tumors?

A

myxoma, rhabdomyoma, metastases

270
Q

Why can’t cardiac cells form tumors?

A

cardiac cells are permanent

271
Q

What is myxoma?

A

benign mesenchymal tumor with a gelatinous appearance and abundant ground substance (this is what makes it look gelatinous) on histology

272
Q

How and where does myxoma usually arise? How does it present?

A

Usually forms pedunculated mass (grows off stalk) in left atrium that causes syncope due to obstruction of mitral valve

Pathoma (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions