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Cardiovascular-First Aid 2017 > Pathology > Flashcards

Pathology Flashcards

1
Q

Presents with early cyanosis, often diagnosed prenatally or immediately after birth requiring urgent surgical treatment or maintenance of PDA

A

Right-to-left shunts

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2
Q

Types of right-to-left shunts

A 
Truncus arteriosus (1 vessel)
Transposition  (2 vessel)
Tricuspid atresia (3 vessel)
Tetralogy of Fallot (4 vessel)
TAPVR (5 letters in name)
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3
Q

Fails to divide into pulmonary trunk and aorta due to lack of aorticopulmonary septum formation

A

Truncus arteriosus

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4
Q

Defect that usually accompanies truncus arteriosus

A

VSD

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5
Q

Anatomic anomaly where the aorta arises from the right ventricle and the pulmonary artery from the left ventricle leading to separation of systemic and pulmonary circulations

A

Transposition of the Great vessels

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6
Q

Required in transposition of the great vessels to maintain life

A

Shunt (VSD, PDA, or patent foramen ovale)

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7
Q

Cause of transposition of great vessels

A

Failure of aorticopulmonary septum to spiral

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8
Q

Complication of truncus arteriosus

A

Fluid overload leading to heart failure

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9
Q

Chromosomal abnormality associated with truncus arteriosus

A

22q11 deletion (DiGeorge syndrome)

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10
Q

Risk factors associated with transposition of great vessels

A

Diabetes, rubella, poor nutrition, alcohol, age > 40 years

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11
Q

Anatomic anomaly that causes hypoplastic RV requiring ASD or VSD for viability

A

Tricuspid atresia

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12
Q

What is tricuspid atresia

A

Absence of tricuspid valve

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13
Q

Most common cause of early childhood cyanosis and caused by anterosuperior displacement of the infundibular system

A

Tetralogy of Fallot

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14
Q

Most important determinant for prognosis in Tetralogy of Fallot

A

Pulmonary infundibular stenosis

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15
Q

CXR finding in tetralogy of Fallot

A

Boot-shaped heart

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16
Q

Conditions found in tetralogy of Fallot

A

Pulmonary infundibular stenosis
Right ventricular hypertrophy
Overriding aorta
VSD

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17
Q

How does squatting improve cyanosis in tetralogy of Fallot

A

Increases SVR and decreases right-to-left shunt

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18
Q

Pulmonary veins fail to enter left atrium and drain into right heart circulation and usually associated with ASD or PDA

A

Total anomalous pulmonary venous return

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19
Q

Required to maintain cardiac output in TAPVR

A

ASD or PDA to maintain right-to-left shunting

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20
Q

Anatomic anomaly in which tricuspid valve leaflets are displaced downward into RV, artificially “atrializing” RV

A

Ebstein anomaly

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21
Q

Most common cause of Ebstein anomaly

A

Lithium exposure in utero

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22
Q

Associated conditions with Ebstein anomaly

A

Tricuspid regurgitation and HF

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23
Q

Set of conditions that present as acyanotic early on with cyanosis occurring years later

A

Left-to-right shunts

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24
Q

Types of left-to-right shunts

A

VSD > ASD > PDA

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25
Q

Most common congenital cardiac defect presenting as asymptomatic at birth, may manifests weeks later or remain asymptomatic

A

VSD

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26
Q

Prognosis for VSD

A

Most self-resolve, larger lesions may lead to LV overload and HF

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27
Q

Structures with increased O2 saturation in VSD

A

RV and pulmonary artery

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28
Q

Presents with loud S1 and wide, fixed-split S2 and may lead to paradoxical emboli

A

ASD

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29
Q

Structures with increased O2 saturation in ASD

A

RA, RV, and pulmonary artery

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30
Q

Cause of ASD

A

Missing septal tissue between atria

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31
Q

Most common ASD finding

A

Ostium secundum defects

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32
Q

Maintains patency of PDA

A

PGE synthesis and low O2 tension

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33
Q

Consequence of uncorrected PDA

A

Progressive RVH and/or LVH and HF

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34
Q

Findings in PDA

A

Late cyanosis in lower extremities, continuous “machine-like” murmur

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35
Q

Drug used to maintain patency of PDA

A

Indomethacin

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36
Q

Consequence of uncorrected left-to-right shunt

A

Eisenmenger syndrome

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37
Q

Mechanism of Eisenmenger syndrome

A

Early left-to-right shunt since LVP > RVP then pulmonary vasculature remodels causing pulmonary arterial hypertension leading to RVH; becomes right-to-left shunt since RVP > LVP

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38
Q

Presentation in Eisenmenger syndrome

A

Late cyanosis, clubbing, and polycythemia

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39
Q

Turner syndrome patient presents with HTN in upper extremities and weak, delayed pulse in lower extremities, and notched ribs on CXR - diagnosis

A

Coarctation of the aorta

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40
Q

Cause of notched ribs on CXR in coarctation of the aorta

A

Intercostal arteries enlarge and erode ribs

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41
Q

Preductal coarctation

A

Coarctation is before ductus arteriosus

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42
Q

Postductal coarctation

A

Coarctation is after ductus arteriosus

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43
Q

Aortic narrowing near insertion of ductus arteriosus associated with bicuspid aortic valve, other heart defects and Turner syndrome

A

Coarctation of the aorta

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44
Q

Congenital heart defects associated with alcohol exposure

A

VSD, PDA, ASD, tetralogy of Fallot

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45
Q

Congenital heart defects associated with congenital rubella

A

PDA, pulmonary artery stenosis, septal defects

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46
Q

Congenital heart defects associated with Down syndrome

A

AV septal defects, VSD, ASD

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47
Q

Congenital heart defects associated with infant of diabetic mother

A

Transposition of great vessels

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48
Q

Congenital heart defects associated with Marfan syndrome

A

MVP, thoracic aortic aneurysm and dissection, aortic regurgitation

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49
Q

Congenital heart defects associated with prenatal lithium exposure

A

Ebstein anomaly

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50
Q

Congenital heart defects associated with Turner syndrome

A

Bicuspid valve, coarctation of the aorta

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51
Q

Congenital heart defects associated with Williams syndrome

A

Supravalvular aortic stenosis

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52
Q

Congenital heart defects associated with 22q11 syndromes

A

Truncus arteriosus, tetralogy of Fallot

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53
Q

Plaques or nodules composed of lipid-laden histiocytes in skin, especially the eyelids seen in type II familial hypercholesterolemia

A

Xanthomas

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54
Q

Lipid deposit in tendon, especially Achilles seen in type II familial hypercholesterolemia

A

Tendinous xanthoma

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55
Q

Lipid deposit in cornea, common in elderly, early in life in type II familial hypercholesterolemia

A

Corneal arcus

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56
Q

Hardening of arteries, with arterial wall thickening and loss of elasticity in small arteries and arterioles

A

Arteriosclerosis

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57
Q

Types of arteriosclerosis

A

Hyaline and Hyperplastic

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58
Q

Type of arteriosclerosis with thickening of vessel walls in essential HTN or DM

A

Hyaline arteriosclerosis

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59
Q

Type of arteriosclerosis with “onion skinning” in severe HTN with proliferation of smooth muscle cells

A

Hyperplastic arteriosclerosis

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60
Q

Type of sclerosis causing calcification of internal elastic lamina and media of medium sized vessels

A

Monckeberg sclerosis

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61
Q

X-ray finding in Monckeberg sclerosis

A

“Pipestem” appearance of medium sized vessels

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62
Q

Layer of artery not affected in Monckeberg sclerosis

A

Intima

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63
Q

A form of arteriosclerosis caused by buildup of cholesterol plaques affecting elastic arteries and large to medium-sized muscular arteries

A

Atherosclerosis

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64
Q

Arteries more commonly affected in atherosclerosis in order of incidence

A

Abdominal aorta > coronary artery > popliteal artery > carotid artery

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65
Q

Modifiable risk factors in atherosclerosis

A

Smoking, HTN, hyperlipidemia, DM

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66
Q

Nonmodifiable risk factors in atherosclerosis

A

Age, sex, family history

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67
Q

Gender and age group most commonly affected by atherosclerosis

A

Older men and postmenopausal women

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68
Q

Symptoms of atherosclerosis

A

Angina, claudication or asymptomatic

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69
Q

Complications of atherosclerosis

A

Aneurysms, ischemia, infarcts, peripheral vascular disease, thrombus, emboli

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70
Q

Common findings in atherosclerosis

A

Foam cells, fatty streaks

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71
Q

Growth factors involved in smooth muscle cell migration

A

PDGF and FGF

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72
Q

Foam cells

A

Lipid-laden macrophages

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73
Q

Important in pathogenesis of atherosclerotic plaque formation

A

Inflammation

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74
Q

First step in formation of atherosclerotic plaque

A

Endothelial cell dysfunction

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75
Q

Presents with abdominal and/or back pain, which is a sign of leaking, dissection or imminent rupture

A

Aortic aneurysm

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76
Q

Associated with atherosclerosis and presenting with palpable, pulsatile abdominal mass commonly below renal arteries caused by oxidative stress, vascular smooth muscle apoptosis or chronic transmural inflammation

A

Abdominal aortic aneurysm

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77
Q

Risk factors associated with abdominal aortic aneurysm

A

Tobacco use, increased age, male sex, family history

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78
Q

Most common location of abdominal aortic aneurysms

A

Between level of renal arteries and aortic bifurcation

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79
Q

Mechanism of thoracic aortic aneurysm associated with HTN

A

HTN causes hyaline sclerosis of vasa vasorum causing ischemia and thinning of aortic wall

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80
Q

Mechanism of thoracic aortic aneurysm associated with 3rdtiary syphilis

A

Tertiary syphilis destroys vasa vasorum causing endarteritis obliterans

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81
Q

Mechanism of thoracic aortic aneurysm associated with Marfan syndrome

A

Elastic properties of fibrillin are compromised

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82
Q

Mechanism of thoracic aortic aneurysm associated with Ehler-Danlos syndrome

A

Collagen proteins disrupted

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83
Q

Complication of thoracic aortic aneurysm

A

Rupture or aortic root dilatation causing aortic valve regurgitation

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84
Q

Classic signs of abdominal aortic aneurysms

A

Severe left flank pain, pulsating mass with heartbeat, hypotension

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85
Q

Signs and symptoms of thoracic aortic aneurysms

A

Usually asymptomatic but can present with severe back and abdominal pain

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86
Q

Most common cause of traumatic aortic rupture

A

Blunt trauma like rapid deceleration injury or crush injury and penetrating trauma

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87
Q

Most common location of traumatic aortic rupture

A

Aortic isthmus (just distal to left subclavian artery at site of ductus arteriosus)

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88
Q

Aortic dissection involving ascending aorta, may extend to aortic arch or ascending aorta and result in aortic regurgitation or cardiac tamponade

A

Stanford type A

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89
Q

Aortic dissection involving only descending aorta below ligamentum arteriosum

A

Stanford type B

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90
Q

Treatment for Stanford type B aortic dissection

A

B-blockers then vasodilators

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91
Q

Treatment for Stanford type A aortic dissection

A

Surgery

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92
Q

Longitudinal intimal tear forming a false lumen that can present with tearing, sudden-onset chest pain, radiating to the back with unequal BP in arms

A

Aortic dissection

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93
Q

CXR finding in aortic dissection

A

Mediastinal widening

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94
Q

Complications in aortic dissection

A

Organ ischemia, aortic rupture or death

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95
Q

Exertional chest pain that resolves with rest or nitroglycerin usually 2ndary to atherosclerosis

A

Stable angina

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96
Q

Findings in stable angina

A

ST depression on ECG with no cardiac markers

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97
Q

CP occurring at rest triggered by cocaine, alcohol, or triptans 2ndary to coronary artery vasospasms

A

Prinzmetal angina

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98
Q

Treatment for Prinzmetal angina

A

Ca channel blockers, nitrates and smoking cessation

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99
Q

Thrombosis with complete coronary artery occlusion with increased frequency or intensity of CP at rest

A

Unstable angina

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100
Q

Risk factors associated with Prinzmetal angina

A

Smoking

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101
Q

Findings in Prinzmetal angina

A

Transient ST segment elevations on ECG and no cardiac markers

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102
Q

Findings in unstable angina

A

ST segment depression with T-wave inversions on ECG and no cardiac markers

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103
Q

Condition in which blood is shunted away from areas of heart perfused by stenosed arteries to areas that are well-perfused after administration of vasodilators causing ischemia in areas supplied by stenosed arteries.

A

Coronary steal syndrome

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104
Q

Caused by progressive onset of HF over many years due to chronic ischemic myocardial damage

A

Chronic ischemic heart disease

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105
Q

Most common cause of MI

A

Acute thrombosis due to rupture of coronary artery atherosclerotic plaque causing elevation of cardiac enzymes

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106
Q

Presents with ST elevation on ECG with Q-waves, transmural damage involving full thickness of myocardial wall

A

STEMI

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107
Q

Presents with ST depression on ECG with subendocardial infarcts and subendocardium ischemic damage

A

NSTEMI

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108
Q

Commonly occluded coronary arteries in order of incidence

A

LAD > RCA > circumflex artery

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109
Q

Common symptoms in MI

A

Diaphoresis, nausea, vomiting, severe retrosternal pain, pain in left arm and/or jaw, SOB and fatigue

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110
Q

When is early coagulative necrosis with release of necrotic cell contents into blood first seen in an MI

A

0-24 hours after MI

111
Q

What are the characteristic cells 0-24 hours after acute MI

A

Neutrophils

112
Q

In what stage of MI is reperfusion injury seen

A

0-24 hours after MI

113
Q

Injury associated with generation of free radicals, leading to hypercontraction of myofibrils through influx of free calcium seen within 0-24 hours after MI

A

Reperfusion injury

114
Q

Dark mottling, pale with tetrazolium stain is seen how long after an MI

A

0-24 hours

115
Q

Complications associated within 0-24 hours after MI

A

Ventricular arrhythmia, HF, cardiogenic shock

116
Q

Complication associated within 1-3 days after MI

A

Postinfarction fibrinous pericarditis

117
Q

Hyperemia with extensive coagulative necrosis is seen how long after MI

A

1-3 days

118
Q

Acute inflammation with neutrophils surrounding infarcted tissue is seen how long after MI

A

1-3 days

119
Q

Complication of free wall rupture from MI

A

Cardiac tamponade

120
Q

Causes mitral regurgitation after MI

A

Papillary muscle rupture

121
Q

Macrophage-mediated structural degradation seen after MI usually affects with heart structure

A

Interventricular septum

122
Q

Maximally yellow, hyperemic border with central yellow-brown softening is usually seen how long after MI

A

3-14 days

123
Q

Interventricular septal rupture is seen how long after MI

A

3-14 days

124
Q

Free wall rupture causing tamponade is seen how long after MI

A

3-14 days

125
Q

Mitral regurgitation from papillary muscle rupture is seen how long after MI

A

3-14 days

126
Q

Complication seen 2 weeks to several months after MI presenting with fever, pleuritic pain, pericarditis and/or pericardial effusion

A

Dressler syndrome

127
Q

Gray-white contracted scar with recanalized artery is seen how long after MI

A

2 weeks to several months

128
Q

Type of collagen seen in scar 2 weeks to several months after MI

A

Type I collagen

129
Q

Cardiac biomarker useful in diagnosing reinfarction following acute MI

A

CK-MB

130
Q

Cardiac biomarker that is more specific for MI

A

Troponin I

131
Q

Gold standard for diagnosing MI

A

ECG within first 6 hours

132
Q

Significance of Q-waves

A

Transmural MI (STEMI)

133
Q

Significance of T-wave inversions

A

Transmural MI (STEMI)

134
Q

Coronary vessel infarcted with ST elevations or Q waves in leads V1-V2

A

LAD (anteroseptal)

135
Q

Coronary vessel infarcted with ST elevations or Q waves in leads V3-V4

A

distal LAD (anteroapical)

136
Q

Coronary vessel infarcted with ST elevations or Q waves in leads V5-V6

A

LAD or LCX (anterolateral)

137
Q

Coronary vessel infarcted with ST elevations or Q waves in leads I, aVL

A

LCX (Lateral)

138
Q

Coronary vessel infarcted with ST elevations or Q waves in leads II, III, aVF

A

RCA (Inferior)

139
Q

Coronary vessel infarcted with ST elevations or Q waves in leads V7-V9, ST depression sin V1-V3 with tall R waves

A

Posterior (PDA)

140
Q

Occurs within the first few days after an MI and is an important cause of death before reaching the hospital and within the first 24 hours post MI

A

Cardiac arrhythmia

141
Q

Occurs 1-3 days after MI with friction rub and pain relieved by leaning forward

A

Postinfarction fibrinous pericarditis

142
Q

Occurs 2-7 days after MI resulting in mitral regurgitation and risk increased due to single blood supply from PDA

A

Papillary muscle rupture

143
Q

Occurs 3-5 days after MI from macrophage-mediated degradation

A

Interventricular septal rupture

144
Q

Occurs 3-14 days after MI with decreased CO, risk of arrhythmia, embolus from mural thrombus and contained within free wall rupture

A

Ventricular pseudoaneurysm formation

145
Q

Occurs 5-14 days after MI causing cardiac tamponade; LVH and previous MI are protective

A

Ventricular free wall rupture

146
Q

Occurs 2 weeks to several months after MI causing dyskinesia and outward bulge with contraction associated with fibrosis

A

True ventricular wall rupture

147
Q

An autoimmune phenomenon occurring several weeks after MI resulting in fibrinous pericarditis

A

Dressler syndrome

148
Q

Can occur 2ndary to LV infarction, VSD, free wall rupture, papillary muscle rupture with mitral regurgitation

A

LV failure and pulmonary edema

149
Q

Symptom control for unstable angina or NSTEMI

A

Nitroglycerin and morphine

150
Q

Preventive treatments for angina or NSTEMI

A

Anticoagulation- heparin
Antiplatelet therapy (Aspirin) + ADP inhibitors (clopidogrel)
B-blockers, ACE inhibitors, statins

151
Q

STEMI treatment

A

Anticoagulation- heparin
Antiplatelet therapy (Aspirin) + ADP inhibitors (clopidogrel)
B-blockers, ACE inhibitors, statins
Reperfusion therapy - percutaneous coronary intervention

152
Q

When are B-blockers contraindicated in angina, NSTEMI, or STEMI

A

HoTN, bradycardia or pulmonary edema

153
Q

Most common cardiomyopathy

A

Dilated cardiomyopathy

154
Q

Findings in dilated cardiomyopathy

A

HF, S3, systolic regurgitant murmur, dilated heart on echo, balloon heart on CXR

155
Q

Treatment for dilated cardiomyopathy

A

Na restriction, ACE inhibitors, B-blockers, diuretics, digoxin, ICD, heart transplant

156
Q

Causes of dilated cardiomyopathy

A 
ABCCCD:
Alcohol abuse
Beriberi (wet)
Coxsackie B 
Cocaine use
Chagas disease
Doxorubicin
157
Q

Type of hypertrophy seen in dilated cardiomyopathy

A

Eccentric hypertrophy - sarcomeres added in series

158
Q

Inheritance pattern of hypertrophic cardiomyopathy

A

Autosomal dominant

159
Q

Type of dysfunction that ensues dilated cardiomyopathy

A

Systolic dysfunction

160
Q

Mutation in hypertrophic cardiomyopathy

A

Mutations in genes encoding sarcomeric proteins like myosin binding protein C and B-myosin heavy chain

161
Q

Complication of hypertrophic cardiomyopathy

A

Sudden death in young athletes due to ventricular arrhythmia

162
Q

Findings in hypertrophic cardiomyopathy

A

S4, systolic murmur, mitral regurgitation due to impaired mitral closure

163
Q

Treatment for hypertrophic cardiomyopathy

A

Cessation of high intensity athletics, B-blockers or non-dihydropyridine CCBs (verapamil)
ICD in high risk patients

164
Q

Endomyocardial fibrosis with a prominent eosinophilic infiltrate

A

Loffler syndrome

165
Q

Type of dysfunction that ensues hypertrophic cardiomyopathy

A

Diastolic dysfunction

166
Q

Caused by asymmetric septal hypertrophy and systolic anterior motion of mitral valve causing outflow obstruction

A

Hypertrophic Obstructive Cardiomyopathy (HOCM)

167
Q

Causes of restrictive/infiltrative cardiomyopathy

A 
Puppy LEASH:
Postradiation fibrosis
Loffler syndrome
Endocardial fibroelastosis
Amyloidosis
Sarcoidosis
Hemochromatosis
168
Q

Cardiomyopathy with low voltage ECG despite thick myocardium

A

Restrictive cardiomyopathy

169
Q

Thick fibroelastic tissue in endocardium of young children

A

Endocardial fibroelastosis

170
Q

Type of dysfunction that ensues restrictive cardiomyopathy

A

Diastolic dysfunction

171
Q

Type of dysfunction characterized by reduced EF, increased EDV and decreased contractility 2ndary to ischemia, MI or dilated cardiomyopathy

A

Systolic dysfunction

172
Q

Type of dysfunction characterized by preserved EF, normal EDV and decreased compliance 2ndary to myocardial hypertrophy

A

Diastolic dysfunction

173
Q

Most common cause of RHF

A

Left Heart Failure (LHF)

174
Q

Isolated right heart failure due to pulmonary causes

A

Cor pulmonale

175
Q

When are B-blockers contraindicated in HF

A

Acute decompensated HF

176
Q

Drugs that decrease mortality in HF

A

ACE inhibitors or ARBs, B-blockers, spironolactone

177
Q

Drug used mainly for symptomatic relief of HF

A

Thiazide diuretics

178
Q

Combo drugs that improve both symptoms and mortality in select patients

A

Hydralazine with nitrate therapy

179
Q

Shortness of breath when lying down

A

Orthopnea

180
Q

Mechanism of orthopnea

A

Immediate increased venous return from redistribution of blood worsens pulmonary vascular congestion

181
Q

Breathless awakening from sleep

A

Paroxysmal nocturnal dyspnea

182
Q

Mechanism of paroxysmal nocturnal dyspnea

A

Increased venous return from redistribution of blood and reabsorption of peripheral edema

183
Q

Increased pulmonary venous pressure causing pulmonary venous distention and transudation of fluid

A

Pulmonary edema

184
Q

Classic microscopy finding in pulmonary edema

A

Hemosiderin-laden macrophages in lungs (HF-cells)

185
Q

Signs of left heart failure

A

Orthopnea, paroxysmal nocturnal dyspnea, pulmonary edema

186
Q

Caused by increased central venous pressure causing increased resistance to portal flow and seen in RHF

A

Hepatomegaly (nutmeg liver)

187
Q

Sign caused by increased venous pressure seen in neck

A

Jugular venous distention

188
Q

Sign caused by increased venous pressure and causing fluid transudation

A

Peripheral edema

189
Q

Signs of right heart failure

A

Hepatomegaly, jugular venous distention, peripheral edema

190
Q

Inadequate organ perfusion and delivery of nutrients necessary for normal tissue and cellular function; may be reversible but life threatening if not treated promptly

A

Shock

191
Q

Type of shock caused by hemorrhage, dehydration or burns and presents with cold, clammy skin

A

Hypovolemic shock

192
Q

Effects of hypovolemic shock on hemodynamics

A

Preload - severely decreased
CO - decreased
Afterload - increased

193
Q

Effects of obstructive shock on hemodynamics

A

Preload - increased or decreased
CO - severely decreased
Afterload - increased

194
Q

Effects of distributive shock caused by sepsis or anaphylaxis on hemodynamics

A

Preload - decreased
CO - increased
Afterload - severely decreased

195
Q

Effects of distributive shock caused by CNS injury on hemodynamics

A

Preload - decreased
CO - decreased
Afterload - severely decreased

196
Q

Type of shock caused by acute MI, HF, valvular dysfunction, arrhythmia, tamponade, PE or tension pneumothorax

A

Cardiogenic or obstructive shock

197
Q

Effects of cardiogenic shock on hemodynamics

A

Preload - increased or decreased
CO - severely decreased
Afterload - increased

198
Q

Treatment for hypovolemic shock

A

IV fluids

199
Q

Treatment for cardiogenic shock

A

Inotropes, diuresis

200
Q

Treatment for obstructive shock

A

Relieve obstruction

201
Q

Treatment for distributive shock

A

IV fluids, pressors

202
Q

Round white spots on retina surrounded by hemorrhage

A

Roth spots

203
Q

Tender raised lesions on finger or toe pads

A

Osler nodes

204
Q

Small, painless erythematous lesions on palm or sole

A

Janeway lesions

205
Q

Acute cause of bacterial endocarditis

A

S aureus

206
Q

Valves commonly affected by S aureus in bacterial endocarditis

A

Mitral valve

207
Q

Gross findings found on pathology of heart valve in acute bacterial endocarditis

A

Large vegetations on previously normal valve

208
Q

Subacute cause of bacterial endocarditis

A

Streptococcus viridans from prior dental procedures

209
Q

Gross findings found on pathology of heart valve in subacute bacterial endocarditis

A

Small vegetations on damaged heart valve

210
Q

Symptoms of bacterial endocarditis

A 
FROM JANE:
Fever
Roth spots
Osler nodes
Murmur
Janeway lesions
Anemia
Nail-bed hemorrhage
Emboli
211
Q

Valve commonly affected by S aureus in IV drug users

A

Tricuspid valve

212
Q

Significance of negative cultures in bacterial endocarditis

A 
Infection from Coxiella, Bartonella or HACEK organisms:
Haemophilus
Aggregatibacter
Cardiobacterium
Eikenella
Kingella
213
Q

Early heart valve lesion in rheumatic heart disease

A

Mitral regurgitation

214
Q

Late heart valve lesion in rheumatic heart disease

A

Mitral stenosis

215
Q

Late sequelae of rheumatic fever

A

Rheumatic heart disease

216
Q

Most commonly affected heart valves in rheumatic heart disease in order of incidence

A

Mitral valve > aortic valve > > tricuspid valve

217
Q

Mechanism of rheumatic heard disease

A

Immune mediated type II hypersensitivity reaction; antibodies to M protein cross-react with self antigens

218
Q

Lab findings in rheumatic heart disease

A

Positive ASO titers and throat cultures
Increased ESR and CRP
Increased PR interval
Leukocytosis

219
Q

Microscopic findings in rheumatic heart disease

A

Anitschkow cells within Aschoff bodies

220
Q

Granulomas with Anitschkow cells found inside

A

Aschoff bodies

221
Q

Enlarged macrophages with ovoid, wavy, rod-like nucleus that look like caterpillars

A

Anitschkow cells

222
Q

Common signs of Rheumatic fever

A 
JONES criteria: O = heart
Joint - migratory polyarthritis
O- carditis
Nodules in skin - subcutaneous
Erythema marginatum
Sydenham chorea
223
Q

Inflammation of the pericardium presenting with sharp pain, aggravated by inspiration and relieved by sitting up or leaning forward

A

Acute pericarditis

224
Q

ECG findings in acute pericarditis

A

Widespread ST segment elevation and/or PR depression

225
Q

Complication in acute pericarditis that presents with friction rub

A

Pericardial effusion

226
Q

Most common cause or acute pericarditis

A

Idiopathic; presumed viral

227
Q

Less common causes of acute pericarditis

A

Bacterial, neoplasia, autoimmune, uremia, cardiovascular, radiation therapy

228
Q

Compression of the heart by fluid decreasing cardiac output and equilibration of diastolic pressure in all heart chambers

A

Cardiac tamponade

229
Q

Syndrome in cardiac tamponade characterized by hypotension, distended neck veins, and distant heart sounds

A

Beck triad

230
Q

ECG findings in cardiac tamponade

A

Low-voltage QRS and electrical alternans

231
Q

Causes electrical alternans

A

Swinging movement of heart in large effusion

232
Q

Decrease amplitude of systolic BP by > 10 mmHg during inspiration

A

Pulsus paradoxus

233
Q

Findings in cardiac tamponade

A

Beck triad, pulsus paradoxus, and increased HR

234
Q

Findings include atrophy of vessel wall and dilatation of aorta and valve ring with calcification of aortic root, ascending arch, and thoracic duct causing a “tree bark” appearance of aorta

A

Syphilitic heart disease

235
Q

Cause of atrophy of vessel wall in syphilitic heart disease

A

Destruction of vasa vasorum by 3rdtiary syphilis

236
Q

Most common primary cardiac tumor in adults

A

Myxoma

237
Q

Most common site for myxomas

A

Left atrium

238
Q

Presents with multiple syncopal episodes and early diastolic “tumor plop” sound with gelatinous material on histology

A

Myxoma

239
Q

Most frequent primary cardiac tumor in children with hamartomatous growth on histology and associated with tuberous sclerosis

A

Rhabdomyoma

240
Q

Increase in JVP on inspiration instead of normal decrease

A

Kussmaul sign

241
Q

Common causes of Kussmaul sign

A

Constrictive pericarditis, restrictive cardiomyopathies, right atrial or ventricular tumors

242
Q

Usually affects elderly females with unilateral headache, jaw claudication and impaired vision

A

Giant cell arteritis

243
Q

Complication of giant cell arteritis

A

Irreversible blindness due to ophthalmic artery occlusion

244
Q

Biopsy findings in giant cell arteritis

A

Focal granulomatous inflammation with segmental lesions

245
Q

Treatment for giant cell arteritis

A

High dose corticosteroids prior to biopsy to prevent blindness

246
Q

Lab findings suggestive of giant cell arteritis

A

Increased ESR

247
Q

Usually affects Asian females < 40 years, presents with weak upper extremity pulses, fever, night sweats, arthritis, myalgias, skin nodules, ocular disturbances

A

Takayasu disease

248
Q

Common findings in Takayasu disease

A

Granulomatous thickening and narrowing of aortic arch at branch points and proximal vessels with increased ESR

249
Q

Treatment for Takayasu disease

A

Corticosteroids

250
Q

Usually affects middle-aged men, presents with HBV seropositivity, fever, weight loss, malaise, headache, cutaneous eruptions, renal damage, and GI symptoms

A

Polyarteritis nodosa

251
Q

Classic image finding in Polyarteritis nodosa

A

String of pearls on blood vessels

252
Q

Blood vessels commonly affected in Polyarteritis nodosa

A

Renal and visceral vessels - NO pulmonary vessels

253
Q

Typical biopsy findings in Polyarteritis nodosa

A

Transmural inflammation of the arterial wall with Fibrinoid necrosis

254
Q

Treatment for Polyarteritis nodosa

A

Corticosteroids and cyclophosphamide

255
Q

Commonly affects Asian children < 4 years old and presents with conjunctival injection, rash, adenopathy, strawberry tongue, hand-foot changes and fever

A

Kawasaki disease

256
Q

Complication of Kawasaki disease

A

Coronary artery aneurysm; thrombosis or rupture can cause death

257
Q

Treatment of Kawasaki disease

A

IV immunoglobulins and aspirin

258
Q

Commonly presents in heavy smokers < 40 years old with intermittent claudication causing gangrene, autoamputation of digits and superficial nodular phlebitis

A

Buerger disease

259
Q

Treatment for Buerger disease

A

Smoking cessation

260
Q

Presents with upper respiratory tract symptoms: nasal septum perforation, chronic sinusitis, otitis media, and mastoiditis; lower respiratory tract symptoms: hemoptysis, cough, and dyspnea; renal symptoms: hematuria, red cell casts

A

Granulomatosis with polyangiitis (Wegener)

261
Q

Commonly presents with triad of:

  1. Focal necrotizing vasculitis
  2. Necrotizing granulomas in the lung and upper airway
  3. Necrotizing glomerulonephritis
A

Granulomatosis with polyangiitis (Wegener)

262
Q

Lab findings in Granulomatosis with polyangiitis (Wegener)

A

PR3-ANCA/c-ANCA positive

263
Q

CXR findings in Granulomatosis with polyangiitis (Wegener)

A

Large nodular densities

264
Q

Treatment for Granulomatosis with polyangiitis (Wegener)

A

Cyclophosphamide, rituximab, corticosteroids

265
Q

Necrotizing vasculitis commonly involving lung, kidney and skin with pauci-immune glomerulonephritis and palpable purpura with no nasopharyngeal symptoms

A

Microscopic polyangiitis

266
Q

Lab findings in microscopic polyangiitis

A

MPO-ANCA/p-ANCA positive

267
Q

Treatment for microscopic polyangiitis

A

Cyclophosphamide and corticosteroids

268
Q

Vasculitis that presents with asthma, sinusitis, skin nodules or purpura, peripheral neuropathy and can involve heart, GI, kidneys with eosinophilia

A

Eosinophilic granulomatosis with polyangiitis (Churg-Strauss)

269
Q

Lab findings in eosinophilic granulomatosis with polyangiitis (Churg-Strauss)

A

MPO-ANCA/p-ANCA, increased IgE levels

270
Q

Most common childhood systemic vasculitis often following URI

A

Henoch-Schonlein purpura

271
Q

Henoch-Schonlein purpura classic triad

A

Skin: palpable purpura on buttocks/legs
Arthralgias
GI: abdominal pain (intestinal hemorrhage, melena)

272
Q

Vasculitis can be 2ndary to IgA immune complex deposition and associated with IgA nephropathy (Berger disease)

A

Henoch-Schonlein purpura

273
Q

Inherited disorder of blood vessels presents with blanching skin lesions, recurrent epistaxis, skin discolorations, AVMs, GI bleeding and hematuria

A

Hereditary hemorrhagic telangiectasia

274
Q

Inheritance pattern for hereditary hemorrhagic telangiectasia

A

Autosomal dominant

Cardiovascular-First Aid 2017 (5 decks)

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