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► Med Notes > Cardiology_2 > Flashcards

Cardiology_2 Flashcards

1
Q

Truncus arteriosus gives rise to what?

A

ascending aorta and pulmonary trunk

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2
Q

which congenital cardiac defect is associated with 22q11 syndromes?

A

truncus arteriosus • ToF

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3
Q

which congenital cardiac defects are associated with Down syndrome?

A

ASD • VSD • AV septal defect (endocardial cushion defect)

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4
Q

which congenital cardiac defects are associated with congential rubella?

A

septal defects • PDA • PA stenosis

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5
Q

which congenital cardiac defects are associated with turner syndrome?

A

coarctation of the aorta (preductal)

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6
Q

which congenital cardiac defects are assciated with Mafan’s syndrome?

A

aortic insufficiency and dissection (late complication)

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7
Q

which congenital cardiac defects are associated with infants of diabetic mothers?

A

transposition of great vessels

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8
Q

hypertension is defined as what?

A

BP >= 140/90

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9
Q

what are the risk factors for hypertension?

A

↑ age • obesity • smoking • genetics • black>white>asian

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10
Q

90% of hypertension is what?

A

1° (essential) and related to ↑ CO and ↑ TPR

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11
Q

10 % of hypertension is what?

A

mostly 2° to renal disease

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12
Q

features of malignant hypertension?

A

severe • >180/120 • rapidly progressing

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13
Q

hypertension predisposes to what?

A

athersclerosis • LVH • stroke • CHF • renal failure • retinopathy • aortic dissection

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14
Q

what are the signs of hyperlipidemia?

A

atheromas • xanthomas • tendinous xanthoma • corneal arcus

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15
Q

what are atheromas?

A

plaques in blood vessel wall

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16
Q

what are xanthomas?

A

plaques or nodules composed of lipid-laden histiocytes in the skin, especially the eyelids

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17
Q

what do you call a xanthoma of the eyelid?

A

xanthelasma

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18
Q

what is a tendinous xanthoma?

A

lipid depost in the tendon, especially the achilles

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19
Q

what is corneal arcus?

A

lipid deposit in cornea, nonspecific (arcus senilis)

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20
Q

what are the 3 classes of arteriosclerosis?

A

Monckberg • arteriosclerosis • atherosclerosis

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21
Q

what is Monckberg arteriosclerosis?

A

calcification in the media of the arteries, especially radial or ulnar

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22
Q

severity of monckberg arteriosclerosis?

A

usually benign • does not obstruct blood flow • intima not involved

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23
Q

typical presentation of monckberg arteriosclerosis?

A

pipestem arteries

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24
Q

what are the two subtypes of arteriosclerosis?

A

hyaline • hyperplastic

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25
Q

what is hyaline arteriosclerosis?

A

thickening of small arteries in essential hypertension or DM

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26
Q

what is hyperplastic arteriosclerosis?

A

onion skinning in malignant hypertension

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27
Q

what is atherosclerosis?

A

fibrous plaques and atheromas form in intima of arteries

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28
Q

what type of disease is atherosclerosis?

A

disease of elastic arteries and large and medium sized muscular arteries

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29
Q

what are the modifiable risk factors for atherosclerosis?

A

smoking • hypertension • hyperlipidemia • diabetes

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30
Q

what are the non-modifiable risk factors for atherosclerosis?

A

age, gender (↑ in men and postmenopausal women), and positive family history

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31
Q

what is important in the pathogenesis of atherosclerosis?

A

inflammation

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32
Q

what is the progression of atherosclerosis?

A

endothelial cell dysfunction → macrophage and LDL accumulation → foam cell formation → fatty streaks → smooth muscle cell migration (involves PDGF and FGF), proliferation and ECM deposition → fibrous plaque → complex atheromas

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33
Q

important histological finding in atherosclerosis?

A

cholesterol crystals

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34
Q

what are the complications of atherosclerosis?

A

aneurysms • ischemia • infarcts • peripheral vascular disease • thrombus • emboli

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35
Q

what is the relative frequency of location of atherosclerosis?

A

abdominal aorta > coronary artery > popliteal artery > carotid artery

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36
Q

what are the symptoms of atherosclerosis?

A

angina • claudication • but can be asymptomatic

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37
Q

what is an aortic aneurysm?

A

localized pathologic dilation of the aorta

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38
Q

what are the 2 types of aortic aneurysm?

A

AAA • TAA

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39
Q

AAA is associated with what?

A

atherosclerosis

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40
Q

AAA occurs more frequently in who?

A

hypertensive male smokers> 50yo

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41
Q

TAA is associated with what?

A

hypertension, cystic medial necrosis (Marfan’s) and historically 3° syphilis

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42
Q

what happens in aortic dissection?

A

longitudinal intraluminal tear forming a false lumen

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43
Q

aortic dissection associated with what?

A

hypertension • bicuspid aortic valve • cystic medial necrosis • inherited connective tissue disorders (Marfans)

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44
Q

aortic dissection presents how?

A

tearing chest pain radiating to the back

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45
Q

in aortic dissection, CXR shows what?

A

mediastinal widening

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46
Q

possibilities for the false lumen in aortic dissection?

A

can be limited to the ascending aorta, propagate from the ascending aorta, or propagate from the descending aorta

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47
Q

aortic dissection can result in what?

A

pericardial tamponade • aortic rupture • death

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48
Q

what are the ischemic heart disease manifestations?

A

angina • coronary steal syndrome • myocardial infarction • sudden cardiac death • chronic ischemic heart disease

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49
Q

pathology involved in angina?

A

CAD narrowing >75% • no myocyte necrosis

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50
Q

stable angina is mostly 2° to what?

A

atherosclerosis

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51
Q

presentation of stable angina?

A

ST depression on ECG • retrosternal chest pain with exertion

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52
Q

Prinzmental angina occurs when?

A

at rest 2° to coronary artery spasm

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53
Q

ECG finding in prinzmental angina?

A

ST elevation

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54
Q

pathology involved in unstable angina?

A

thrombosis with incomplete coronary artery occlusion

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55
Q

presentation of unstable/crescendo angina?

A

ST depression on ECG • worsening chest pain at rest or with minimal exertion

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56
Q

what happens in coronary steal syndrome?

A

vasodilator may aggravate ischemia by shunting blood from area of critical stenosis to an area of higher perfusion

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57
Q

myocardial is most often due to what?

A

acute thrombosis due to coronary artery atherosclerosis with complete occlusion of coronary artery with myocyte necrosis

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58
Q

ECG findings in MI?

A

ECG initially shows ST depression progressing to ST elevation with continued ischemia and transmural necrosis

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59
Q

what is sudden cardiac death?

A

death from cardiac causes within 1 hour of onset of symptoms, most commonly due to a lethal arrhythmia (V-fib)

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60
Q

sudden cardiac death is associated with what?

A

CAD up to 70% of cases

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61
Q

what is chronic ischemic heart disease?

A

progressive onset of CHF over many years due to chronic ischemic myocardial damage

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62
Q

relative frequency of coronary artery occlusion in MI?

A

LAD >RCA > circumflex

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63
Q

what are the symptoms of MI?

A

diaphoresis • nausea • vomiting • severe retrosternal pain • pain in left arm and or jaw • shortness of breath • fatigue

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64
Q

what are the gross findings within 0-4h of MI?

A

none

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65
Q

what are the LM findings within 0-4h of MI?

A

none

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66
Q

what are the risks within 0-4h of MI?

A

arrhythmia • CHF • exacerbation • cardiogenic shock

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67
Q

what are the gross findings within 4-24h of MI?

A

infarct and dark mottling; pale with tetrazolium stain distal to occluded artery

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68
Q

what are the LM findings within 4-12h of MI?

A

early coagulative necrosis • edema • hemorrhage • wavy fibers

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69
Q

what is the risk within 4-12h of MI?

A

arrhythmia

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70
Q

what are the LM findings within 12-24h of MI?

A

contraction bands from reperfusion injury • release of necrotic cell content into blood • beginning of neutrophil migration

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71
Q

what is the risk within 12-24h of MI?

A

arrhythmia

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72
Q

what are the gross findings within 1-3 days of MI?

A

hyperemia

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73
Q

what are the LM findings within 1-3days of MI?

A

extensive coagulative necrosis • tissue surrounding infarct shows acute inflammation • neutrophil migration

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74
Q

what is the risk within 1-3 days of MI?

A

fibrinous pericarditis

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75
Q

what are the gross findings within 3-14days of MI?

A

hyperemic border; • central yellow-brown softening • maximally yellow and soft by 10 days

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76
Q

LM findings within 3-14days of MI?

A

macrophage infiltration followed by granulation tissue at the margins

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77
Q

what is the risk within 3-14 days of MI?

A

free wall rupture leading to tamponade, papillary muscle rupture, ventricular aneurysm, interventricular septal rupture due to macrophages that have degraded important structural components

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78
Q

what are the gross findings 2weeks-months post MI?

A

recanalized artery • gray white

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79
Q

LM findings 2 weeks-months post MI?

A

contracted scar complete

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80
Q

risk 2weeks-months post MI?

A

dressler’s syndrome

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81
Q

what is the gold standard for dx of MI in first 6h?

A

ECG

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82
Q

use of cardiac troponin I in diagnosis of MI?

A

rises after 4 hours and is elevated for 7-10 days; more specific than other protein markers

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83
Q

use of CK-MB in diagnosis of MI?

A

useful in diagnosing reinfarction following acute MI because levels return to normal after 48 hours

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84
Q

CK-MB predominantly found where?

A

in myocardium but can also be released from skeletal muscle

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85
Q

ECG changes in MI?

A

ST elevation (transmural infarct) • ST depression (subendocardial infarct) • Q waves (transmural infarct)

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86
Q

necrosis in transmural infarct?

A

↑ necrosis

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87
Q

subendocardial infarcts due to what?

A

ischemic necrosis of < 50% of ventricle wall

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88
Q

transmural infarct affects how much of cardiac structure?

A

affects entire wall

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89
Q

subendocardial infarct affect what structure?

A

subendocardium especially vulnerable to ischemia

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90
Q

ECG in transmural infarcts?

A

ST elevation • Q waves

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91
Q

ECG in subendocardial infarct?

A

ST depression

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92
Q

Q waves in V1-V4, where is the infarct?

A

Anterior wall (LAD)

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93
Q

Q waves in V1-V2, where is the infarct?

A

Ateroseptal (LAD)

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94
Q

Q waves in V4-V6, where is the infarct?

A

anterolateral (LCX)

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95
Q

Q waves in I, aVL, where is the infarct?

A

lateral wall (LCX)

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96
Q

Q waves in II, III, aVF, where is the infarct?

A

inferior wall (RCA)

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97
Q

in MI, what is an important cause of death before reaching hospital?

A

cardiac arrhythmia

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98
Q

cardiac arrhythmia in MI is common when?

A

in first few days

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99
Q

what are the complications of MI?

A

cardiac arrhythmia • LV failure and pulmonary edema • Cardiogenic shock • Ventricular free wall rupture • papillary muscle rupture • IVS rupture • ventricular aneurysm formation • postinfarction fibrinous pericarditis

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100
Q

what is Dressler’s syndrome?

A

autoimmune phenomenon resulting in fibrinous pericarditis (several weeks post MI)

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101
Q

factors associated with cardiogenic shock in MI?

A

large infarct- high risk of mortality

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102
Q

in MI ventricular free wall rupture →?

A

cardiac tamponade

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103
Q

in MI, papillary muscle rupture→?

A

severe mitral regurgitation

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104
Q

in MI, IVS rupture→?

A

VSD

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105
Q

factors associated with ventricular aneurysm formation in MI?

A

↓ CO • risk of arrhythmia • embolus from mural thrombus

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106
Q

when is the greatest risk for ventricular aneurysm formation in MI?

A

1 week post MI

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107
Q

what is the most common cardiomyopathy?

A

dilated (congestive) cardiomyopathy 90%

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108
Q

dilated cardiomyopathy is usually what origin?

A

often idiopathic, up to 50% familial

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109
Q

specific etologies of dilated cardiomyopathy include what?

A

ABCCCD • Alcohol abuse • wet Beriberi • Coxsackie b virus myocarditis • chronic Cocaine use • Chaga’s disease • Doxorubicin toxicity • hemochromatosis • peripartum cardiomyopathy

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110
Q

what are the findings in dilated cardiomyopathy?

A

S3 • dilated heart on U/S • balloon appearance on chest X ray

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111
Q

what is the treatment for dilated cardiomyopathy?

A

Na+ restriction • ACE inhibitors • diuretics • digoxin • heart transplant

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112
Q

what happens in hypertrophic cardiomyopathy?

A

hypertrophied interventricular septum is too close to mitral valve leaflet, leading to outflow tract obstruction

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113
Q

60-70% of hypertrophic cardiomyopathy are of what origin?

A

familial • AD • βmyosin heavy chain mutation

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114
Q

hypertrophic cardiomyopathy is associated with what?

A

Friedreich’s ataxia

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115
Q

morphologic findings in hypertrophic cardiomyopathy?

A

disoriented, tangled, hypertrophied myocardial fibers

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116
Q

what is a cause of sudden death in young athletes?

A

hypertrophic cardiomyopathy

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117
Q

what are the findings in hypertrophic cardiomyopathy?

A

normal sized heart • S4 • apical impulses • systolic murmur

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118
Q

what is the treatment for hypertrophic cardiomyopathy?

A

β blocker or non-dihydropyridine calcium channel blocker (verapamil)

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119
Q

what ensues in hypertrophic cardiomyopathy?

A

diastolic dysfunction

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120
Q

gross appearance in hypertrophic cardiomyopathy?

A

asymmetric concentric hypertrophy (sarcomeres added in parallel)

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121
Q

pathogenesis of hypertrophic cardiomyopathy?

A

proximity of hypertrophied interventricular septum to mitral leaflet obstructs outflow tract, resulting in systolic murmur and syncopal episodes

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122
Q

major causes of restrictive/obliterative cardiomyopathy include what?

A

sarcoidosis • amyloidosis • postradiation fibrosis • endocardial fibroelastosis • Lofflers syndrome • hemochromatosis

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123
Q

what is endocardial fibroelastosis?

A

thick fibroelastic tissue in endocardium of young children

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124
Q

what is Loffler’s syndrome?

A

endomyocardial fibrosis with a prominent eosinophilic infiltrate

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125
Q

what ensues in restrictive/obliterative cardiomyopathy?

A

diastolic dysfunction

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126
Q

what is CHF?

A

a clinical syndrome that occurs in patients with an inherited or acquired abnormality of cardiac structure or function, which is characterized by a constellation of clinical symptoms (dyspnea, fatigue) and signs (edema, rales)

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127
Q

in CHF RHF most often results from what?

A

LHF

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128
Q

isolated RHF is usually due to what?

A

cor pulmonale

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129
Q

which drugs reduce mortality in CHF?

A

ACE inhibitors • β blockers • ARBs • spironolactone

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130
Q

when do you not give β blockers in CHF?

A

acute decompensated HF

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131
Q

which drugs are used for symptomatic relief in CHF?

A

thiazides • loop diuretics

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132
Q

which drugs improve symptoms and mortality in select patients with CHF?

A

hydralazine with nitrate therapy

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133
Q

what are the abnormalities seen in CHF?

A

cardiac dilation • dyspnea on exertion • LHF • RHF

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134
Q

what is the cause of cardiac dilation in CHF?

A

greater ventricular EDV

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135
Q

what is the cause of DOE in CHF?

A

failure of cardiac output to ↑ during exercise

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136
Q

what are the manifestations of LHF in CHF?

A

pulmonary edema/PND • orthopnea

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137
Q

what is the cause of pulmonary edema/PND in CHF?

A

↑ pulmonary venous pressure→ pulmonary venous distentions and transudation of fluid

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138
Q

histological finding in LHF in CHF?

A

presence of hemosiderin laden macrophages (heart failure cells) in the lungs

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139
Q

what is the cause of orthopnea in CHF?

A

↑ venous return in supine position exacerbates pulmonary vascular congestion

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140
Q

what are the manifestations of RHF in CHF?

A

hepatomegaly (nutmeg liver) • peripheral edema • jugular venous distention

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141
Q

what is the cause of hepatomegaly (nutmeg liver) in CHF?

A

↑ central venous pressure → ↑ resistance to portal flow

142
Q

rarely, hepatomegaly in RHF leads to what?

A

cardiac cirrhosis

143
Q

what is the cause of peripheral edema in CHF?

A

↑ venous pressure → fluid transudation

144
Q

what is the cause of jugular venous distention in CHF?

A

↑ venous pressure

145
Q

what are the symptoms of bacterial endocarditis?

A

Bacteria FROM JANE: • Fever • Roth spots • Osler nodes • Murmur • Janeway lesions • Anemia • Nail-bed hemorrhage • Emboli

146
Q

what is the most common symptom of bacterial endocarditis?

A

fever

147
Q

what are roth spots?

A

round white spots on retina surrounded by hemorrhage

148
Q

what are osler’s nodes?

A

tender raised lesions on finger or toe pads

149
Q

what are janeway lesions?

A

small, painless, erythematous lesions on palm or sole

150
Q

what is necessary for diagnosis of bacterial endocarditis?

A

multiple blood cultures

151
Q

organism that causes acute bacterial endocarditis?

A

S aureus

152
Q

virulence of organism that causes acute bacterial endocarditis?

A

S aureus (high virulence)

153
Q

presentation in acute bacterial endocarditis caused by S aureus?

A

large vegetations on previously normal valves

154
Q

what is the onset of acute bacterial endocarditis caused by S aureus?

A

rapid onset

155
Q

organism that causes subacute bacterial endocarditis?

A

viridans streptococcus

156
Q

virulence of the organism that causes subacute bacterial endocarditis?

A

low virulence

157
Q

presentation in subacute bacterial endocarditis?

A

smaller vegetations on congenitally abnormal or diseased valves

158
Q

subacute bacterial endocarditis can be sequelae of what?

A

dental procedures

159
Q

what is the onset of subacute bacterial endocarditis?

A

more insidious onset

160
Q

endocarditis may be nonbacterial secondary to what?

A

malignancy • hypercoagulable state • lupus (marantic/ thrombotic endocarditis)

161
Q

S bovis is present in which cause of endocarditis?

A

colon cancer

162
Q

S epidermidis is present in which cause of endocarditis?

A

prosthetic valves

163
Q

which valve is most frequently involved in bacterial endocarditis?

A

mitral

164
Q

tricuspid valve endocarditis is associated with what?

A

IV drug use (dont TRI DRUGS)

165
Q

tricuspid endocarditis is associated with which organisms?

A

S aureus • Pseudomonas • Candida

166
Q

what are the complications of bacterial endocarditis?

A

chordae rupture • glomerulonephritis • suppurative pericarditis • emboli

167
Q

rheumatic fever is a consequence of what?

A

pharyngeal infection with group A β hemolytic streptococci

168
Q

early deaths in rheumatic fever due to what?

A

myocarditis

169
Q

late sequelae of rheumatic fever include what?

A

rheumatic heart disease

170
Q

relative frequency of valves affected by rheumatic heart disease?

A

mitral > aortic&raquo_space; tricuspid (high pressure vavles affected most)

171
Q

early lesion in rheumatic fever is what?

A

MR

172
Q

what is the late lesion in rheumatic fever?

A

MS

173
Q

Rheumatic fever is associated with what?

A

Aschoff bodies • Anitschkow’s cells • elevated ASO titers

174
Q

what are Aschoff bodies?

A

granuloma with giant cells

175
Q

what are anitschkow’s cells?

A

activated histiocytes

176
Q

immunology of rheumatic fever?

A

Type II HSR; not a direct effect of bacteria • Ab to M protein

177
Q

symptoms of Rheumatic fever?

A

FEVERSS: • Fever • Erythema marginatum • Valvular damage • ESR ↑ • Red hot joints (migratory polyarthritis) • Subcutaneous nodules • St. Vitus’ dance (Sydenham’s chorea)

178
Q

acute pericarditis commonly presents with what?

A

sharp pain, aggravated by inspiration, and relieved by sitting up and leaning forward • friction rub

179
Q

ECG findings in acute pericarditis?

A

widespread ST-segment elevation and/or PR depression

180
Q

acute fibrinous pericarditis is caused by what?

A

Dressler’s syndrome, • uremia • radiation

181
Q

fibrinous pericarditis presents with what?

A

loud friction rub

182
Q

what are the causes of serous pericarditis?

A

viral • noninfectious inflammatory diseases

183
Q

course of viral serous pericarditis?

A

often resolves spontaneously

184
Q

non infectious inflammatory diseases that cause acute serous pericarditis?

A

RA • SLE

185
Q

what causes suppurative/purulent pericarditis?

A

bacterial infections with pneumococcus or streptococcus

186
Q

frequency of purulent pericarditis?

A

rare with antibiotics

187
Q

what happens in cardiac tamponade?

A

compression of heart by fluid (blood effusions) in pericardium leading to ↓ CO

188
Q

what happens to pressures in cardiac tamponade?

A

equilibration of pressures in all 4 chambers

189
Q

what are the findings in cardiac tamponade?

A

hypotension • ↑ venous pressure (JVD) • distant heart sounds • ↑ HR • pulsus paradoxus

190
Q

what is pulsus paradoxus?

A

↓ in amplitude of systolic blood pressure by >=10mHg during inspiration

191
Q

pulsus paradoxus seen in what?

A

severe cardiac tamponade • asthma • OSA • pericarditis • croup

192
Q

what happens in syphilitic heart disease?

A

3° syphilis disrupts the vasa vasorum of the aorta with consequent atrophy of the vessel wall and valve ring

193
Q

in syphilitic heart disease you may see what?

A

calcification of the aortic root and ascending aortic arch

194
Q

syphilitic heart disease leads to what appearance?

A

tree bark appearance of the aorta

195
Q

syphilitic heart disease can result in what?

A

aneurysm of the ascending aorta or aortic arch and aortic insufficiency

196
Q

what are the most common primary cardiac tumors in adults?

A

myxomas

197
Q

90% of cardiac myxomas occur where?

A

in the atria (mostly left atrium)

198
Q

myxomas are usually described as what?

A

ball valve obstruction in LA associated with multiple syncopal episodes

199
Q

what is the most frequent primary cardiac tumor in children?

A

rhabdomyomas

200
Q

cardiac rhabdomyomas are associated with what?

A

tuberous sclerosis

201
Q

most common heart tumor is what?

A

mets from melanoma or lymphoma

202
Q

what is Kussmaul’s sign?

A

↑ in JVP on inspiration instead of normal ↓

203
Q

what happens in Kussmaul’s sign?

A

inspiration → negative intrathoracic pressure not transmitted to the heart→ impaired filling of RV → blood backs up into the venae cavae→ JVD

204
Q

Kussmaul’s sign may be seen in what?

A

constrictive pericarditis • restrictive cardiomyopathies • RA or RV tumors • cardiac tamponade

205
Q

Raynaud’s phenomenon affects what type of vessels?

A

small vessels

206
Q

what happens in Raynaud’s phenomenon?

A

↓ blood flow to the skin due to arteriolar vasospasm in response to cold temperature or emotional stress

207
Q

Raynauds phenomenon is most often seen where?

A

fingers • toes

208
Q

when is it called Raynaud’s disease?

A

when primary (idiopathic)

209
Q

when is it called Raynaud’s syndrome?

A

when secondary to a disease process such as mixed connective tissue disease, SLE, or CREST

210
Q

temporal arteritis generally affects who?

A

elderly females

211
Q

symptoms in temporal arteritis?

A

unilateral headache (temporal artery) • jaw claudication

212
Q

temporal arteritis may lead to what?

A

irreversible blindness die to ophthalmic artery occlusion

213
Q

temporal arteritis is associated with what?

A

polymyalgia rheumatica

214
Q

temporal arteritis most commonly affects which vessels?

A

branches of carotid artery

215
Q

pathology/labs seen in temporal arteritis?

A

focal granulomatous inflammation • ↑ ESR

216
Q

what is the treatment for temporal arteritis?

A

high dose corticosteroids

217
Q

Takayasu arteritis typically affects who?

A

asian females <40yo

218
Q

symptoms of takayasu arteritis?

A

pulselessness disease: • fever • night sweats • arthritis • myalgias • skin nodules • ocular disturbances

219
Q

pathology/labs seen in takayasu arteritis?

A

granulomatous thickening of aortic arch, proximal great vessels • ↑ ESR

220
Q

what is the treatment for takayasu arteritis?

A

corticosteroids

221
Q

what are the large artery vasculitis disorders?

A

temporal arteritis and takayasu arteritis

222
Q

what are the medium vessel vasculitis disorders?

A

polyarteritis nodosa • kawasaki disease • Buerger’s disease (thromboangitis obliterans)

223
Q

polyarteritis nodosa affects who?

A

young adults

224
Q

viral association with polyarteritis nodosa?

A

HBV seropositivity in 30% of patients

225
Q

symptoms of polyarteritis nodosa?

A

fever • weight loss • malaise • headache • abdominal pain • melena • HTN • neuro dysfunction • cutaneous eruptions • renal damage

226
Q

polyarteritis nodosa typically involves which vessels?

A

renal and visceral vessels, not pulmonary arteries

227
Q

immunology of polyarteritis nodosa?

A

IC mediated

228
Q

pathology/labs seen in polyarteritis nodosa?

A

transmural inflammation of the arterial wall with fibrinoid necrosis • lesions are of different stages • many aneurysms and constrictions on arteriogram

229
Q

treatment for polyarteritis nodosa?

A

corticosteroids • cyclophosphamide

230
Q

kawasaki disease affects who?

A

asian children < 4yo

231
Q

symptoms associated with kawasaki disease?

A

fever cervical lymphadenitis • conjunctival injection • changes in lips/oral mucosa (strawberry tongue) • hand-foot erythema • desquamating rash

232
Q

children with kawasaki disease may develop which complications?

A

coronary aneurysms → MI, rupture

233
Q

treatment for kawasaki disease?

A

IV immunoglobulin and aspirin

234
Q

Buerger’s disease affects who?

A

heavy smokers, males <40yo

235
Q

symptoms in Buerger’s disease?

A

intermittent claudication may lead to gangrene, autoamputation of digits, superficial nodular phlebitis • raynauds phenomenon

236
Q

what is the pathology seen in buerger’s disease?

A

segmental thrombosing vasculitis

237
Q

what is the treatment for buergers disease?

A

smoking cessation

238
Q

what are the small vessel vasculitis disorders?

A

microscopic polyangitis • Wegener’s granulomatosis (granulomatosis with polyangitis) • Churg strauss syndrome • Henoch Schonlein purpura

239
Q

what is microscopic polyangitis?

A

necrotizing vasculitis commonly involving lung, kidneys, and skin with pauci immune glomerulonephritis and palpable purpura

240
Q

pathology/labs seen in microscopic polyangitis?

A

no granulomas • p-ANCA

241
Q

what is the treatment for microscopic polyangitis?

A

cyclophosphamide and corticosteroids

242
Q

what are the upper respiratory tract symptoms of wegener’s granulomatosis?

A

perforation of nasal septum, • chronic sinusitis • otitis media • mastoiditis

243
Q

what are the lower respiratory symptoms of Wegener’s granulomatosis?

A

hemoptysis • cough • dyspnea

244
Q

what are the renal manifestations of wegener’s granulomatosis?

A

hematuria • red cell casts

245
Q

what is the triad that characterizes wegener’s granulomatosis?

A

focal necrotizing vasculitis • necrotizing granulomas in the lung and upper airway • necrotizing glomerulonephritis

246
Q

what are the labs seen in wegeners granulomatosis?

A

c-ANCA • CXR: large nodular densities

247
Q

what is the treatment for wegeners granulomatosis?

A

cyclophosphamide • corticosteroids

248
Q

what are the symptoms of Churg-strauss syndrome?

A

asthma • sinusitis • palpable purpura • peripheral neuropathy (wrist/foot drop) • can also involve heart, GI, pauci-immune glomerulonephritis

249
Q

pathology/labs seen in Churg strauss syndrome?

A

granulomatous, necrotizing vasculitis with eosinophilia • p-ANCA, elevated IgE level

250
Q

what is the most common childhood systemic vasculitis?

A

henoch-schonlein purpura

251
Q

henoch-schonlein purpura often follows what?

A

URI

252
Q

what is the classic triad of henoch schonlein purpura?

A

skin: palpable purpura on buttocks/legs • arthralgia • GI: abdominal pain, melena, multiple lesions of same age

253
Q

pathology seen in henoch schonlein purpura?

A

vasculitis secondary to IgA complex deposition • associated with IgA nephropathy

254
Q

what is a strawberry hemangioma?

A

benign hemangioma of infancy

255
Q

strawberry hemangioma appears when?

A

first few weeks of life (1/200 births)

256
Q

course of strawberry hemangioma?

A

grows rapidly and regresses spontaneously at 5-8 years of age

257
Q

what is a cherry hemangioma?

A

benign capillary hemangioma of the elderly

258
Q

course of cherry hemangioma?

A

does not regress

259
Q

incidence of cherry hemangioma?

A

frequency ↑ with age

260
Q

what is a pyogenic granuloma?

A

polypoid capillary hemangioma that can ulcerate and bleed

261
Q

pyogenic granuloma is associated with what?

A

trauma and pregnancy

262
Q

what is a cystic hygroma?

A

cavernous lymphangioma of the neck

263
Q

cystic hygroma is associated with what?

A

Turner syndrome

264
Q

what is a glomus tumor?

A

benign painful red-blue tumor under fingernails

265
Q

glomus tumor arises from what?

A

modified smooth muscle cells of the glomus body

266
Q

what is bacillary angiomatosis?

A

benign capillary skin papules found in AIDS patients

267
Q

bacillary angiomatosis is caused by what?

A

Bartonella henselae infections

268
Q

bacillary angiomatosis is frequently mistaken for what?

A

kaposi sarcoma

269
Q

what is angiosarcoma?

A

rare blood vessel malignancy typically occuring in the head, neck, and breast areas

270
Q

angiosarcoma is associated with what?

A

patients receiving radiation therapy, especially for BRCA and hodgkins lymphoma

271
Q

course of angiosarcoma?

A

very aggressive and difficult to resect due to delay in diagnosis

272
Q

what lymphangiosarcoma?

A

lymphatic malignancy associated with persistent lymphedema (post radical mastectomy)

273
Q

what is kaposi sarcoma?

A

endothelial malignancy most commonly of the skin but also mouth, GIT, and respiratory tract

274
Q

kaposi sarcoma is associated with what?

A

HHV-8 and HIV

275
Q

kasposi sarcoma is frequently mistaken for what?

A

bacillary angiomatosis

276
Q

what is sturge-weber disease?

A

congenital vascular disorder that affects capillary sized blood vessels.

277
Q

Sturge-weber disease manifests how?

A

with port wine stain (nevus flammeus) on face • ispilateral leptomeningeal angiomatosis (intracerebral AVM) • seizures • early onset glaucoma

278
Q

what are the antihypertensive therapies for essential hypertension?

A

diuretics • ACEI • ARBs • Ca channel blockers

279
Q

what are the antihypertensive therapies used in CHF?

A

diuretics • ACEI/ARBs (compensated CHF) • K+ sparing diuretics

280
Q

β blockers must be used cautiously in what?

A

decompensated CHF

281
Q

β blockers are contraindicated in what?

A

cardiogenic shock

282
Q

what are the antihypertensive therapies used in DM?

A

ACEI/ARBs • Ca channel blockers • diuretics • β blockers • α blockers

283
Q

ACEIs are protctive against what in DM?

A

diabetic nephropathy

284
Q

which drugs are Ca channel blockers?

A

nifedipine • verapamil • diltiazem • amlodipine

285
Q

MOA of Ca channel blockers?

A

block voltage dependent L type calcium channels of cardiac and smooth muscle and thereby reduce muscle contractility

286
Q

relative effect on smooth muscle of Ca channel blockers?

A

Vascular smooth muscle- amlodipine=nifedipine>diltiazem>verapamil

287
Q

relative effect on heart of Ca channel blockers?

A

heart- verapamil>diltiazem>amlodipine=nifedipine • Verapamil-ventricle

288
Q

clinical use of Ca channel blockers?

A

hypertension • angina • arrhythmias (not nifedipine) • prinzmental’s angina • Raynauds

289
Q

toxicity of Ca channel blockers?

A

cardiac depression • AV block • peripheral edema • flushing • dizziness • constipation

290
Q

MOA of hydralazine?

A

↑cGMP→smooth muscle relaxation • vasodilates arterioles > veins • ↓ afterload

291
Q

clinical use of hydralazine?

A

severe hypertension • CHF • first line tx for htn in pregnancy, with methyldopa • frequently coadministered with β blocker to prevent reflex tachycardia

292
Q

toxicity of hydralazine?

A

compensatory tachycardia (CI in angina/CAD), fluid retention, nausea, HA, angina • Lupus like syndrome

293
Q

commonly used drugs for malignant hypertension treatment?

A

nitroprusside • nicardipine • clevidipine • labetalol • fenoldopam

294
Q

features of nitroprusside for malignant hypertension?

A

short acting • ↑ cGMP via direct release of NO

295
Q

toxicity of nitroprusside?

A

can cause cyanide toxicity

296
Q

MOA of fenoldopam?

A

dopamine D1 receptor agonist→ coronary, peripheral, renal, splanchnic vasodilation→ ↓BP and ↑ natriuresis

297
Q

MOA of nitroglycerine, isosorbide dinitrate?

A

vasodilate by releasing NO in smooth muscle, causing ↑ cGMP in and smooth muscle relaxation • dilates veins»arteries • ↓preload

298
Q

clinical use of GTN, ISDN?

A

angina • pulmonary edema

299
Q

toxicity of GTN, ISDN?

A

reflex tachycardia, hypotension, flushing, HA, “monday disease” in industrial exposure

300
Q

what is monday disease in industrial GTN, ISDN exposure?

A

development of tolerance for the vasodilating action during the work week and loss of tolerance over the weekend results in tachycardia, dizziness, and HA upon reexposure

301
Q

what is the goal of antianginal therapy?

A

reduction of myocardial O2 consumption (MVO2) by decreasing >=1 of the determinants of MVO2: EDV, BP, HR, contractility, ejection time

302
Q

effect of nitrates on EDV?

A

↓

303
Q

effect of β blockers on EDV?

A

↑

304
Q

effect of nitrates+ β blockers on EDV?

A

no effect or ↓

305
Q

effect of nitrates on BP?

A

↓

306
Q

effect of βblockers on BP?

A

↓

307
Q

effects of nitrates + βblockers on BP?

A

↓

308
Q

effect of nitrates on contractility?

A

↑ (reflex response)

309
Q

effects of β blockers on contractility?

A

↓

310
Q

effect of nitrates + βblockers on contractility?

A

little/no effect

311
Q

effect of nitrates on HR?

A

↑ (reflex)

312
Q

effect of βblockers on HR?

A

↓

313
Q

effect of nitrates + β blockers on HR?

A

↓

314
Q

effect of nitrates on ejection time?

A

↓

315
Q

effect of β blockers on ejection time?

A

↑

316
Q

effect of nitrates + βblockers on ejection time?

A

little/no effect

317
Q

effect of nitrates on MVO2?

A

↓

318
Q

effect of β blockers on MVO2?

A

↓

319
Q

effect of nitrates + βblockers on MVO2?

A

↓↓

320
Q

how do Ca channel blockers compare to the effects of nitrates and beta blockers on MVO2?

A

nifedipine is similar to nitrates • verapamil is similar to beta blockers

321
Q

which are the partial β agonists contraindicated in angina?

A

pindolol and acebutalol

322
Q

effect of HMG-CoARI’s on LDL?

A

↓↓↓

323
Q

effect of HMG-CoARIs on HDL?

A

↑

324
Q

effect of HMGCoARI’s on TG?

A

↓

325
Q

MOA of HMGCoARIs?

A

inhibit conversion of HMG-CoA to mevalonate, a cholesterol precursor

326
Q

AE of HMGCoARIs?

A

hepatotoxicity (↑LFT) • rhabdomyolysis

327
Q

effect of niacin on LDL?

A

↓↓

328
Q

effect of niacin on HDL?

A

↑↑

329
Q

effect of niacin on TG ?

A

↓

330
Q

MOA of niacin?

A

inhibits lipolysis in adipose tissue; • reduces hepatic VLDL secretion into circulation

331
Q

AE of niacin?

A

red, flushed, face which is ↓ by aspirin or long term use • hyperglycemia (acanthosis nigricans) • hyperuricemia (exacerbates gout)

332
Q

effect of bile acid resins on LDL?

A

↓↓

333
Q

effect of bile acid resins on HDL?

A

slightly ↑

334
Q

effect of bile acid resins on TG?

A

slightly ↑

335
Q

MOA of bile acid resins?

A

prevent intestinal reabsorption of bile acids; liver must use cholesterol to make more

336
Q

AE of bile acid resins?

A

patients hate it- • tastes bad and causes GI discomfort • ↓ absorption of fat soluble vitamins • cholesterol gallstones

337
Q

effect of ezetimibe on LDL?

A

↓↓

338
Q

effect of ezetimibe on HDL ?

A

no effect

339
Q

effect of ezetimibe on TG?

A

no effect

340
Q

MOA of ezetimibe?

A

prevent cholesterol reabsorption at small intestinal brush border

341
Q

AE of ezetimibe?

A

rare ↑ in LFTs • diarrhea

342
Q

effects of fibrates on LDL?

A

↓

343
Q

effects of fibrates on HDL?

A

↑

344
Q

effects of fibrates on TG?

A

↓↓↓

345
Q

MOA of fibrates?

A

upregulate LPL→↑TG clearance

346
Q

AE of fibrates?

A

myositis • hepatotoxicity • cholesterol gallstones

347
Q

PK of digoxin?

A

75% bioavailability • 20-40% protein bound • t1/2=40h • urinary excretion

348
Q

MOA of digoxin?

A

direct inhibition of Na+/K+ ATPase leads to indirect inhibition of Na+/Ca++ exchanger/antiport • ↑[Ca++]i → positive inotropy • stimulates vagus → ↓ HR

349
Q

clinical use of digoxin?

A

CHF • atrial fibrillation

350
Q

why use digoxin in CHF?

A

↑ contractility

351
Q

why use digoxin in atrial fibrillation?

A

↓conduction at AV node and depression of SA node

► Med Notes (62 decks)

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