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Step 1 - Cardiovascular > Pathology > Flashcards

Pathology Flashcards

1
Q

Early cianosis

A

Right to left shunts. Blue babies

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2
Q

Right to left shunts

A

5 Ts:

  1. Truncus arteriosus: 1 vessel
  2. Transposition: 2 vessels
  3. Tricuspid atresia: 3= Tri
  4. Tetralogy of fallot: 4= Tetra
  5. TAPVR = 5 letters= total anomalous pulmonary venous return
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3
Q

Lack of aorticopulmonary septum formation

A

Persistent truncus arteriosus

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4
Q

Separation of systemic and pulmonary circulations

A

Transposition of great vessels

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5
Q

Not compatible with life unless a shunt is present

A

Transposition of great vessels

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6
Q

Transposition of great vessels prognosis

A

Without surgical intervention most infants die within first few months of life

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7
Q

Requires both ASD and VSD for viability

A

Tricuspid atresia

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8
Q

Most common cause of early childhood cyanosis

A

Tetralogy of fallot

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9
Q

Anteriosuperior displacement of the infundibular septum

A

Tetralogy of Fallot

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10
Q

Tetralogy of fallot

A

PROVe

  1. Pulmonar infundibular stenosis
  2. Right ventricular hypertrophy: boot-shaped heart
  3. Overriding aorta
  4. VSD
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11
Q

Determinant for prognosis in tetralogy of Fallot

A

Pulmonar infundibular stenosis

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12
Q

Treatment of tetralogy of Fallot

A

Early surgical correction

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13
Q

Squatting effect over tetralogy of Fallot

A

it increases systemic vascular resistance, decreasing right to left shunt (lower pressure difference), thus improving cyanosis.

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14
Q

Pulmonary veins drain into right heart circulation

A

TAPVR: total anomalous pulmonary venous return

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15
Q

TAPVR usually associates

A

ASD or PDA to allow for right to left shunting to mantain CO

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16
Q

Caused by lithium exposure in utero

A

Ebstein anomaly

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17
Q

Ebstein anomaly

A

Displacement of tricuspid valve leaflets downward into RV
Artificially atrializes the ventricle
Tricuspid regugitation + Right Heart Failure

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18
Q

Tet spells

A

Cyanotic episodes: crying, fever and exercise cause exacerbation of RV outflow obstruction, increasing right to left flow across VSD

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19
Q

Acyanotic presentation, it may occur later

A

Left to right shunts

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20
Q

Frequency of Left to right shunts

A

VSD>ASD>PDA

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21
Q

Most common congenital heart defect

A

Ventricular septal defect

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22
Q

Presentation of VSD

A
  • asymptomatic at birth
  • manifests later or remains asymptomatic
  • most selfe resolve
  • larger lesions lead to LV overload and HF
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23
Q

May lead to paradoxical emboly

A

ASD

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24
Q

Atrial septal defects are caused by defects in

A

Ostium secundum: more frequent, isolated

Ostium primum: rare, associate other cardiac anomalies

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25
Q

Continuous machine like murmur

A

Patent ductus arteriosus

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26
Q

Uncorrected _____ can result in late cyanosis in the lower extremities

A

Patent ductus arteriosus

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27
Q

Eisenmenger syndrome

A

Uncorrected left to right shunt: VSD, ASD, PDA
High pulmonary blood flow: pulmonary arterial hypertension: RVHypertrophy to overcompensate: shunt becomes right to left
Causes:
- Late cyanosis
- Clubbing
- Polycitemia

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28
Q

Aortic narrowing near insertion of ductus arteriosus

A

Coarctation of the aorta

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29
Q

Coarctation of aorta associates

A
  1. Bicuspid aortic valve
  2. Turner syndrome
  3. Other heart deffects
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30
Q

Notched ribs appearence on CXR

A

Coarctation of aorta: intercostal arteries enlarge due to collateral circulation: arteries erode ribs

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31
Q

Hypertension in upper extremities and weak, delayed pulse in lower extremities: brachial-femoral delay

A

Coarctation of aorta

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32
Q

Coarctation of aorta complications

A
  1. Heart failure
  2. Risk of cerebral hemorrhage= berry aneurisms
  3. Aortic rupture
  4. Endocarditis
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33
Q

Alcohol exposure in utero leads to

A 
VSD
PDA
ASD
Tetralogy of fallot
Left to right + TofF
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34
Q

Congenital rubela leads to

A

PDA
Pulmonary artery stenosis
Septal defects

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35
Q

Down syndrome heart deffects

A

AV septal defect: endocardial cushion defect
VSD
ASD

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36
Q

Infant of diabetic mother heart deffect

A

Transposition of great vessels

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37
Q

Marfan syndrome heart defects

A

Mitral valve prolapse: hiperlaxitud
Thoracic aortic aneurysm and dissection
Aortic regurgitation

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38
Q

Turner syndrome heart defects

A

Bicuspid aortic valve

Coarctation of aorta

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39
Q

Williams syndrome heart defects

A

Supravalvular aortic stenosis

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40
Q

22q11 syndromes heart deffects

A

Truncus arteriosus

Tetralogy of Fallot

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41
Q

Define hypertension

A

Persistent systolic BP>140, diastolic BP>90

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42
Q

90% of hypertension is…

A

Primary=essential

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43
Q

10% of hypertension is due to

A

Renovascular disease

1º hyperaldosteronism

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44
Q

String of beads in renal artery

A

Fibromuscular dysplasia

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45
Q

Hypertensive urgency

A

> 180/120 hypertension WITHOUT acute end organ damge

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46
Q

Hypertensive emergency

A

Severe hypertension with evidence of acute end organ damage:

  • Brain: encephalopathy, stroke
  • Eyes: retinal hemorrhages/exudates, papilledema
  • Heart: MI/HF, aortic disection
  • Kidney: injury, microangiopathic hemolytic anemia
  • Eclampsia
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47
Q

Hiperlipidemia signs

A
  1. Xanthomas: lipid-laden histiocytes. Eyelids: xanthelasma
  2. Tendinous xantoma: achilles
  3. Corneal arcus: common in elderly: arcus senilis
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48
Q

Calcification of internal elastic lamina and media of medium sized arteries

A

Mönckberg sclerosis: medial calcific sclerosis

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49
Q

Pipestem appearance on xray

A

Mönckberg sclerosis

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50
Q

Mönckberg sclerosis and blood flow

A

DOESNT obstruct

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51
Q

Types of arteriolosclerosis

A
  1. Hyaline: thickening in essential hypertension or Dm

2. Hyperplasic: onion skinning in severe hypertension

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52
Q

Arteriosclerosis

A

Hardening of arteries with arterial wall thickening and loss of elasticity

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53
Q

Atherosclerosis

A

Disease of elastic arteries and large and medium sized muscular arteries: form of arteriosclerosis caused by buildup of cholesterol plaques

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54
Q

Location of atherosclerosis

A

Abdominal aorta > coronary artery>popliteal artery>carotid artery

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55
Q

Symptoms of atherosclerosis

A

Angina

Claudication

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56
Q

Progression of atherosclerosis

A

endothelial cell dysfunction: macrophage and LDL accumulation: foam cell formation: fatty streaks: smooth muscle cell migration: proliferation and exrtacellular matrix deposition: fibrous plaque: complex atheromas

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57
Q

Localised pathological dilation of the aorta

A

Aortic aneurism

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58
Q

Palpable pulsatile abdominal mass

A

Abdominal aortic aneurysm

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59
Q

Abdominal aortic aneurysm is associated with

A

Atherosclerosis

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60
Q

Thoracic aortic aneurysm is associated with

A

Cystic medial degeneration

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61
Q

Risk factors for thoracic aneurysm

A
  • HTA
  • Bicuspid aortic valve
  • Connective tissue disease: Marfan
  • 3ary syphilis: endarteritis obliterans of vasa vasorum
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62
Q

Most frequent location of traumatic aortic rupture

A

Aortic isthmus: proximal descending aorta distal to origin of left subclavian artery

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63
Q

Aortic dissection

A

Longitudinal intimal tear forming a false lumen

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64
Q

Types of aortic dissection

A

Standford type A: Ascending aorta

Standford type B: Descending aorta

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65
Q

Treatment of Standford type A aortic dissection

A

Surgery

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66
Q

Treatment of Standford type B aortic dissection

A

Medically:

  • Beta blockers
  • Vasodilators
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67
Q

Necrosis in angina

A

No myocyte necrosis

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68
Q

Chest pain due to ischemic myocardium 2º to coronary artery narrowing or spasm

A

Angina

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69
Q

Types of Angina

A
  1. Stable
  2. Variant-Prinzmetal
  3. Unstable
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70
Q

Stable Angina

A
  • 2º to atherosclerosis
  • Exertional chest ain in classic distribution
  • ST depression on ECG usually
  • Resolves with rest or nitroglicerin
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71
Q

Variant Angina

A
  • AT REST
  • 2ª to coronary artery spasm
  • Transient ST elevation on ECG
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72
Q

Risk factors for Variant Angina

A

Smoking

HTA and hypercholesterolemia are not

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73
Q

Triggers Variant Angina

A

Cocaine
Alcohol
Triptans: 5HT1 agonist for migraine

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74
Q

Treatment of Variant Angina

A

Ca channel blockers
Nitrates
Smoking cessation

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75
Q

Stable angina is secondary to

A

Atherosclerosis

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76
Q

Unstable angina is secondary to

A

Thrombosis

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77
Q

Unstable angina

A
  • Secondary to thrombosis with incomplete coronary artery oclusion
  • +- ST depression and or T wave inversion
  • NO CARDIC biomarker elevation (unlike NSTEMI)
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78
Q

NSTEMI vs Unstable angina

A

Unstable angina has no cardiac biomarker elevation

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79
Q

Principle behind pharmacologic stress tests with coronary vasodilators

A

Coronary steal syndrome

  • Dipyridamole
  • Regadenoson
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80
Q

Coronary steal syndrome

A

Administration of vasodilators dilates normalvessels and shunts blood towards well perfused areas, diverting flow away from stenosed vessels, leading to ischemia in myocardium perfused by these

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81
Q

Sudden cardiac death

A

Death from cardiac causes within 1 hour of onset of symptoms, most commonly due to a lethal arrhythmia

82
Q

Prevent Sudden cardiac death

A

Implantable cardioverter defibrillator

83
Q

Sudden cardiac death is associated with _______ up to 70% of cases

A

Coronary artery disease
Other causes:
-Cardiomyopathy
-Hereditary ion channelopathies: long QT syndrome, Brugada syndrome

84
Q

Progressive onset of heart failure over many years due to chronic ischemic myocardial damage

A

Chronic ischemic heart disease

85
Q

Myocardial infarction most common cause

A

Acute thrombosis due to rupture of coronary artery atherosclerotic plaque

86
Q

Cardiac biomarkers in myocardial infarction

A

Elevated (diagnostic)

  • CK-MB
  • Troponins
87
Q

ST segment elevation MI

A

Transmural infarct
Full thickness of myocardial wall involves
ST elevation on ECG
Q waves

88
Q

Non ST segment elevation MI

A

Subendocardial infarct

ST depression on ECG

89
Q

Part of the heart wall specially vulnerable to ischemia

A

Subendocardium: inner 1/3 rd

90
Q

Occluded coronary arteries causing myocardial infarction frequency

A

Left anterior descending > Right Coronary Artery > Circumflex

91
Q

Myocardial infarction symptoms

A
  • Diaphoresis
  • Nausea and vomiting
  • Severe retrosternal pain
  • Pain in left arm and or jaw
  • Shortness of breath
  • Fatigue
92
Q

Complication 1-3 days after myocardial infarction

A

Fibrinous pericarditis

93
Q

Complication 3-14 days after myocardial infarction

A

RUPTURES

  1. Free wall rupture: tamponade
  2. Papillary muscle rupture: mitral regurgitation
  3. Interventricular septal rupture: macrophage-mediated structural degradation
  4. Left ventricle pseudoaneurism: risk of rupture
94
Q

Complication 0-24 hours after myocardial infarctions

A
  1. Heart failure
  2. Ventricular arrythmia
  3. Cardiogenic shock
95
Q

Complication 2 weeks-months after myocardial infarction

A

Dressler syndrome
Heart failure
Arrythmias
True ventricular aneurysm: risk of mural thrombus

96
Q

Dressler syndrome

A

Autoimmune inflammatory reaction (pericarditis) to myocardial neo-antigens formed as a result of the MI

97
Q

Myocardial infarction diagnoses

A
  1. First 6 hours: ECG (GS)
  2. Cardiac troponin I: rises after 4 hours, peaks at 24 hours, lasts 7-10 days. more specific
  3. CK-MB: rises after 6-12 hours, peaks at 16-24 hours. Useful dx reinfarction following acute MI as it stabilises after 48 hours
98
Q

STEMi V1-V2

A

Anteroseptal: LAD

99
Q

STEMI v3-V4

A

Anteroapical: distal LAD

100
Q

STEMI V4-V5

A

Anterolateral: LAD or LCX

101
Q

STEMI I, aVL

A

Lateral: LCX

102
Q

STEMI II, III, aVF

A

Inferior: RCA

103
Q

STEMI v7-V9

ST depression in V1-V3 with tall R waves

A

Posterior: PDA

104
Q

Myocardial infarct complications

A
  1. Cardiac arrythmia
  2. Post infarction fibrinous pericarditis
  3. Papillary muscle rupture
  4. Interventricular septal rupture
  5. Ventricular pseudoaneurysm formation
  6. Ventricle free wall rupture
  7. True ventricular aneurysm
  8. Dressler syndrome
  9. LV failure and pulmonary edema
105
Q

Protect against free wall rupture

A

LV hypertrophy

Previous MI

106
Q

Autoimmune phenomenon resulting in fibrinous pericarditis

A

Dressler syndrome

107
Q

Unstable angina/NSTEMI treatment

A 
Anticoagulation: heparin
Antiplatelet therapy: aspirin
ADP receptor inhibitor: clopidogrel
Beta blockers
ACE inhibitors
Statin
Syptom control: nitroglycerin and morphine
108
Q

STEMI treatment

A 
Reperfusion therapy: Percutaneous coronary intervention >fibrinolysis
Anticoagulation: heparin
Antiplatelet therapy: aspirin
ADP receptor inhibitor: clopidogrel
Beta blockers
ACE inhibitors
Statin
Symptom control: nitroglycerin and morphine
109
Q

Types of cardiomyopathies

A
  1. Dilated cardiomyopathy
  2. Hypertrophic cardiomyopathy
  3. Restrictive cardiomyopathty
110
Q

Most common cardiomyopathy

A

Dilated: 90% of cases

111
Q

Balloon appearance of heart on CXR

A

Dilated cardiomyopathy

112
Q

Cardiomyopathy with systolic disfunction

A

Dilated cardiomyopathy

113
Q

Eccentric hypertrophy of heart

A

Dilated cardiomyopatht: sarcomers added in series

114
Q

Causes of dilated cardiomyopathy

A
  1. Idiopathic
  2. Familial
  3. Alcohol abuse
  4. Wet Beri Beri
  5. Coxsackie B viral myocarditis
  6. Chronic Cocaine use
  7. Chagas disease
  8. Doxorubicin toxicity
  9. Hemochromatosis
  10. Sarcoidosis
  11. Peripartum cardiomyopathy
115
Q

Dilated cardiomyopathy treatment

A
  1. Na restriction
  2. ACE inhibitors
  3. Beta blockers
  4. Diuretics
  5. Digoxin
  6. ICD
  7. Heart transplant
116
Q

Ventricular apical ballooning due to increased sympathetic stimulation (stressful situations)

A

Takotsubo cardiomyopathy

117
Q

Most common cause of hypertrophic cardiomyopathy

A

60-70% of cases are familial, autosomal dominant due to mutations encoding sarcomeric proteins such as myosin binding protein C and beta myosin heavy chain

118
Q

Associated with Friedreich ataxia

A

Hypertrophic cardiomyopathy

119
Q

Causes syncope during exercise

May lead to sudden death in young athletes due to ventricular arrythmia

A

Hypertrophic cardiomyopathy

120
Q

Cardiomyopathy with diastolic dysfunction

A

Hypertrophic

Restrictive

121
Q

Ventricular concentric hypertrophy: sarcomers added in parallel

A

Hypertrophic cardiomyopathy

122
Q

Hypertrophic obstructive cardiomyopathy

A

Subset of hypertrophic cardiomyopathy
- Asymetrical septal hypertrophy + systolic anterior motion of mitral valve: outflow obstruction: dyspnea, possible syncope

123
Q

Treatment of hypertrophic cardiomyopathy

A
  • Cessation of high intensity atheltics
  • use of beta blocker or non dihydropyridine Ca channel blockers
  • ICD if patient is at high risk
124
Q

Infiltrative cardiomyopathy

A 
Restrictive cardiomyopathy:
-postradiation fibrosis
-Loffler syndrome
-Endocardial fibroelastosis
-Amyloidosis
-Sarcoidosis
-Jemocromatosis
Puppy LEASH
125
Q

Sarcoidosis and hemochromatosis produce

A

Dilated > restrictive cardiomyopathy

126
Q

Loeffler syndrome

A

Endomyocardial fibrosis with a prominent eosinophilic infiltrate

127
Q

Cor pulmonale

A

Isolated right HF due to pulmonary cause

128
Q

Dercrease heart failure mortality

A

ACE inhibitors
ARB
Beta blockers: except acute descompensated
Spironolactone

129
Q

Presence of hemosiderin laden macrophages in lungs

A

Heart failure cells: pulmonary edema

130
Q

Left heart failure produces

A

Orthopnea
Paroxysmal nocturnal dyspnea
Pulmonary edema

131
Q

Right heart failure produces

A

Hepatomegaly: nutmeg liver
Jugular venous distension
Peripheral edema

132
Q

Shock

A

Inadequate organ perfusion and delivery of nutrients for normal tissue and cellular function

133
Q

Types of shock

A
  1. Hypovolemic
  2. Cardiogenic
  3. Obstructive
  4. Distributive
134
Q

Skin in shock

A

Always cold and clammy except in distributive shock:

Warm and dry

135
Q

Hypovolemic shock treatment

A

IV fluids

136
Q

Cardiogenic shock treatment

A

Inotropes

Diuretics

137
Q

Obstructive shock treatment

A

Relieve obstruction

138
Q

Distributive shock treatment

A

IV fluids

Pressors

139
Q

Most common symtoms of bacterial endocarditis

A

Fever

140
Q

Acute endocarditis is due to

A

S aureus: high virulence

Large vegetations on previously normal valves

141
Q

Subacute endocarditis is due to

A

Viridans streptococci: low virulence

smaller vegetations on congenitally abdnormal or diseased valves

142
Q

Endocarditis in patients with colon cancer

A

S bovis: gallocyticus

143
Q

Endocarditis in patients with prostetic valves

A

S epidermidis

144
Q

Marantic/thrmobotic/non bacterial endocarditis

A

Malignancy
Hypercoagulable state
SLE

145
Q

Valve most frequently envolved in endocarditis

A

Mitral

146
Q

Endocarditis associated with IV drug abuse

A

Tricuspid: dont tri drugs

147
Q

IV drug abuse endocarditis microorganisms

A

S aureus
Psedomonas
Candida

148
Q

Negative culture in suspected endocarditis

A

Coxiella burnetti: Q fever
Bartonella spp
HACEK: haemophilus, aggregatibacter, cardiobacterium., eikenella, kingella

149
Q

Endocarditis findings

A

FROM JANE:

  • Fever
  • Roth spots: white in retina surrounded by hemorrage
  • Osler nodes: immune complex deposition
  • Murmur
  • Janeway lesions: erythematous lesions in palm/soles
  • Anemia
  • Nail-bed hemorrage
  • Emboli
  • Glomerulonephritis
150
Q

Consequence of pharyngeal infection with group A beta hemolytic streptococci

A

Rheumatic fever

151
Q

Pathology findings in rheumatic fever

A
  1. Aschoff bodies: granuloma with giant cells
  2. Anitschkow cells: enlarged macrophages with rod like nucleus
  3. High antistreoptolysin O titers: ASO
152
Q

Prophylaxis of rheumatic fever

A

Penicillin

153
Q

Rheumatic fever is due to

A

Immune mediated type II hypersensitivity. antibodies to M protein cross react with self antigens: molecular mimicry

154
Q

JONES major criteria for Rheumatic fever

A 
J♥NES
Joint migratory polyarthritis
♥Carditis
Nodules in skin subcutaneous
Erythema marginatum
Sydenham chorea
155
Q

Commonly presents with:

  • sharp pain
  • aggravated by inspiration
  • relieved by sitting up and leaning forward
A

Acute pericarditis

156
Q

Complication of acute pericarditis

A

Pericardial effusion: friction rub

157
Q

ECG changes in pericarditis

A

WIDESPREAD:
ST segment elevation
PR depression

158
Q

Compression of the heart by fluid in pericardial space

A

Cardiac tamponade: low Cardiac output

159
Q

Equilibration of diastolic pressures in all 4 chambers

A

Cardiac tamponade

160
Q

Findings of cardiac tamponade

A 
Beck triad!
- Hypotension
- Distended neck veins
- Distant heart sounds
High heart rate
Pulsus paradoxus
161
Q

Cardiac tamponade ECG

A

Low voltage QRS

Electrical alternans: swinging movement of heart in large effusion

162
Q

Pulsus paradoxus

A

Decreasing in amplitude of systolic blood presure by >10 mmHg during inspiration

  • Cardiac tamponade
  • Asthma
  • Obstructive sleep apnea
  • Pericarditis
  • Croup
163
Q

Calcification of aortic root, ascending aortic arch and thoracic aorta

A

Syphilitic heart disease

164
Q

Tree bark appearance of aorte

A

Syphilitic heart disease: result in aortic aneurysm or insufficiency

165
Q

Most common heart tumor

A

Metastasis

166
Q

Most common primary cardiac tumor

A

Mixoma

167
Q

90% of mixomas occour in

A

Atria: left atrium

168
Q

Ball valve obstruction in left atrium + multiple syncopes

A

Myxoma

169
Q

Most frequent primary cardiac tumor in children

A

Rhabdomyomas

170
Q

Associated with tuberous sclerosis

A

Rhabdomyomas

171
Q

Kussmaul sign

A

Rise in Jugular venous pressure on inspiration instead of a normal dicrease:
- constrictive pericarditis
-restrictive cardiomyopathies
-right atrial or ventricular tumors
Impaired filling of ventricle: blood backs up into venae cavae

172
Q

Large vessel vasculitis

A
  1. Giant cell (temporal) arteritis

2. Takayasu arteritis

173
Q

Medium vessel vasculitis

A
  1. Polyarteritis nodosa: PAN
  2. Kawasaki disease: mucocutaneous lymph node syndrome
  3. Buerger disease: thromboangiitis obliterans
174
Q

Small vessel vasculitis

A
  1. Wegener Granulomatosis
  2. Microscopic polyangiitis
  3. Churg-Strauss granulomatosis
  4. Henoch-Schönlein purpura
175
Q

Jaw claudication and unilateral headache in an elderly female

A

Giant cell arteritis

176
Q

Vasculitis with high ESR (VSG)

A

Giant cell arteritis

Takayasu arteritis

177
Q

Treatment of giant cell arteritis

A

High dose corticosteroids prior to temporal artery biopsy to prevent blindness

178
Q

Complication of giant cell arteritis

A
  1. Irreversible blindness due to ophtalmic artery occlusion

2. Polymialgia rheumatica

179
Q

Weak upper extremity pulses, fever, night sweats, arthitis, myalgias, skin nodules, ocular disturbances in <40 years old asian woman

A

Takayasu arteritis

180
Q

Granulomatous thickening and narrowing of aortic arch and proximal great vessels

A

Takayasu arteritis

181
Q

Renal microaneurysms

A

Polyarteritis nodosa

182
Q

Pulmonary affection in polyarteritis nodosa

A

None

183
Q

Vasculitis with 30% hepatitis B seropositivity

A

Polyarteritis nodosa

184
Q

kawasaki disease presentation

A 
-Asian children <4 years old
CRASH
-Conjunctival injection
-RASH: polymorphous, desquamating
-Adenopathy cervical
-Strawberry tong: oral mucositis
-Hand foot changes: edema, erythema
-Fever
185
Q

Kawasaki disease treatment

A

IV immunoglobulin

Aspirin

186
Q

Vasculitis that may develop coronary artery aneurysms

A

Kawasaki disease

187
Q

Vascultisi in heavy smoker males younger than 40 years old

A

Buerger disease

188
Q

Treatment of Buerger disease

A

Smoking cessation

189
Q

High PR3-cANCA

A

Wegner granulomatosis

190
Q

Wegener granulomatosis findings

A
  1. Upper respiratory: Perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis
  2. Lower respiratory: hemoptysis, cough, dyspnea
  3. Renal: hematuria, red cell casts
191
Q

Wegner granulomatosis triad

A
  1. Focal necrotizing vasculitis
  2. Necrotizing granulomas in the lung and upper airway
  3. Necrotizing glomerulonephritis
192
Q

Wegener granulomatosis treatment

A

Cyclophosphamide

Corticosteroids

193
Q

Eosinophilic granulomatosis

A

Churg-Strauss

194
Q

pANCA and high IgE

A

Churg-Strauss granulomatosis

195
Q

Most common childhood ssytemic vasculitis

A

Henoch-Schönlein vasculitis

196
Q

Follows upper respiratory infection

A

Henoch-Schönlein vasculitis

197
Q

Associated with IgA nephropathy (Berger disease)

A

Henoch-Schönlein vasculitis

198
Q

Vasculitis secondary to Ig A immune complex deposition

A

Henoch-Schönlein vasculitis

199
Q

Henoch-Schönlein vasculitis triad

A
  1. Skin: palpable purpura on buttocks/legs
  2. Artharlgias
  3. Abdominal pain
200
Q

Osler-Weber-Rendu syndrome

A

hereditary hemorrhagic telangiectasia

201
Q

Osler-Weber-Rendu syndrome findings

A
  1. Telangiectasia
  2. Recurrent epistaxis
  3. Skin discolorations
  4. Arteriovenous malformation
  5. GI bleeding
  6. Hematuria

Step 1 - Cardiovascular (5 decks)

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