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
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)
3
Q
Fails to divide into pulmonary trunk and aorta due to lack of aorticopulmonary septum formation
A
Truncus arteriosus
4
Q
Defect that usually accompanies truncus arteriosus
A
VSD
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
6
Q
Required in transposition of the great vessels to maintain life
A
Shunt (VSD, PDA, or patent foramen ovale)
7
Q
Cause of transposition of great vessels
A
Failure of aorticopulmonary septum to spiral
8
Q
Complication of truncus arteriosus
A
Fluid overload leading to heart failure
9
Q
Chromosomal abnormality associated with truncus arteriosus
A
22q11 deletion (DiGeorge syndrome)
10
Q
Risk factors associated with transposition of great vessels
A
Diabetes, rubella, poor nutrition, alcohol, age > 40 years
11
Q
Anatomic anomaly that causes hypoplastic RV requiring ASD or VSD for viability
A
Tricuspid atresia
12
Q
What is tricuspid atresia
A
Absence of tricuspid valve
13
Q
Most common cause of early childhood cyanosis and caused by anterosuperior displacement of the infundibular system
A
Tetralogy of Fallot
14
Q
Most important determinant for prognosis in Tetralogy of Fallot
A
Pulmonary infundibular stenosis
15
Q
CXR finding in tetralogy of Fallot
A
Boot-shaped heart
16
Q
Conditions found in tetralogy of Fallot
A
Pulmonary infundibular stenosis
Right ventricular hypertrophy
Overriding aorta
VSD
17
Q
How does squatting improve cyanosis in tetralogy of Fallot
A
Increases SVR and decreases right-to-left shunt
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
19
Q
Required to maintain cardiac output in TAPVR
A
ASD or PDA to maintain right-to-left shunting
20
Q
Anatomic anomaly in which tricuspid valve leaflets are displaced downward into RV, artificially “atrializing” RV
A
Ebstein anomaly
21
Q
Most common cause of Ebstein anomaly
A
Lithium exposure in utero
22
Q
Associated conditions with Ebstein anomaly
A
Tricuspid regurgitation and HF
23
Q
Set of conditions that present as acyanotic early on with cyanosis occurring years later
A
Left-to-right shunts
24
Q
Types of left-to-right shunts
A
VSD > ASD > PDA
25
Most common congenital cardiac defect presenting as asymptomatic at birth, may manifests weeks later or remain asymptomatic
VSD
26
Structures with increased O2 saturation in VSD
RV and pulmonary artery
27
Structures with increased O2 saturation in ASD
RA, RV, and pulmonary artery
28
Most common ASD finding
Ostium secundum defects
29
Maintains patency of PDA
PGE synthesis and low O2 tension
30
Findings in PDA
Late cyanosis in lower extremities, continuous "machine-like" murmur
31
Consequence of uncorrected left-to-right shunt
Eisenmenger syndrome
32
Mechanism of Eisenmenger syndrome
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
33
Presentation in Eisenmenger syndrome
Late cyanosis, clubbing, and polycythemia
34
Turner syndrome patient presents with HTN in upper extremities and weak, delayed pulse in lower extremities, and notched ribs on CXR - diagnosis
Coarctation of the aorta
35
Cause of notched ribs on CXR in coarctation of the aorta
Intercostal arteries enlarge and erode ribs
36
Aortic narrowing near insertion of ductus arteriosus associated with bicuspid aortic valve, other heart defects and Turner syndrome
Coarctation of the aorta
37
Congenital heart defects associated with alcohol exposure
VSD, PDA, ASD, tetralogy of Fallot
38
Congenital heart defects associated with congenital rubella
PDA, pulmonary artery stenosis, septal defects
39
Congenital heart defects associated with Down syndrome
AV septal defects, VSD, ASD
40
Congenital heart defects associated with infant of diabetic mother
Transposition of great vessels
41
Congenital heart defects associated with Marfan syndrome
MVP, thoracic aortic aneurysm and dissection, aortic regurgitation
42
Congenital heart defects associated with prenatal lithium exposure
Ebstein anomaly
43
Congenital heart defects associated with Turner syndrome
Bicuspid valve, coarctation of the aorta
44
Congenital heart defects associated with Williams syndrome
Supravalvular aortic stenosis
45
Congenital heart defects associated with 22q11 syndromes
Truncus arteriosus, tetralogy of Fallot
46
Plaques or nodules composed of lipid-laden histiocytes in skin, especially the eyelids seen in type II familial hypercholesterolemia
Xanthomas
47
Lipid deposit in tendon, especially Achilles seen in type II familial hypercholesterolemia
Tendinous xanthoma
48
Lipid deposit in cornea, common in elderly, early in life in type II familial hypercholesterolemia
Corneal arcus
49
Hardening of arteries, with arterial wall thickening and loss of elasticity in small arteries and arterioles
Arteriosclerosis
50
Types of arteriosclerosis
Hyaline and Hyperplastic
51
Type of arteriosclerosis with thickening of vessel walls in essential HTN or DM
Hyaline arteriosclerosis
52
Type of arteriosclerosis with "onion skinning" in severe HTN with proliferation of smooth muscle cells
Hyperplastic arteriosclerosis
53
Type of sclerosis causing calcification of internal elastic lamina and media of medium sized vessels
Monckeberg sclerosis
54
X-ray finding in Monckeberg sclerosis
"Pipestem" appearance of medium sized vessels
55
Layer of artery not affected in Monckeberg sclerosis
Intima
56
A form of arteriosclerosis caused by buildup of cholesterol plaques affecting elastic arteries and large to medium-sized muscular arteries
Atherosclerosis
57
Arteries more commonly affected in atherosclerosis in order of incidence
Abdominal aorta > coronary artery > popliteal artery > carotid artery
58
Modifiable risk factors in atherosclerosis
Smoking, HTN, hyperlipidemia, DM
59
Nonmodifiable risk factors in atherosclerosis
Age, sex, family history
60
Gender and age group most commonly affected by atherosclerosis
Older men and postmenopausal women
61
Symptoms of atherosclerosis
Angina, claudication or asymptomatic
62
Complications of atherosclerosis
Aneurysms, ischemia, infarcts, peripheral vascular disease, thrombus, emboli
63
Common findings in atherosclerosis
Foam cells, fatty streaks
64
Growth factors involved in smooth muscle cell migration
PDGF and FGF
65
Foam cells
Lipid-laden macrophages
66
Important in pathogenesis of atherosclerotic plaque formation
Inflammation
67
First step in formation of atherosclerotic plaque
Endothelial cell dysfunction
68
Presents with abdominal and/or back pain, which is a sign of leaking, dissection or imminent rupture
Aortic aneurysm
69
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
Abdominal aortic aneurysm
70
Risk factors associated with abdominal aortic aneurysm
Tobacco use, increased age, male sex, family history
71
Most common location of abdominal aortic aneurysms
Between level of renal arteries and aortic bifurcation
72
Mechanism of thoracic aortic aneurysm associated with HTN
HTN causes hyaline sclerosis of vasa vasorum causing ischemia and thinning of aortic wall
73
Mechanism of thoracic aortic aneurysm associated with 3rdtiary syphilis
Tertiary syphilis destroys vasa vasorum causing endarteritis obliterans
74
Mechanism of thoracic aortic aneurysm associated with Marfan syndrome
Elastic properties of fibrillin are compromised
75
Mechanism of thoracic aortic aneurysm associated with Ehler-Danlos syndrome
Collagen proteins disrupted
76
Complication of thoracic aortic aneurysm
Rupture or aortic root dilatation causing aortic valve regurgitation
77
Classic signs of abdominal aortic aneurysms
Severe left flank pain, pulsating mass with heartbeat, hypotension
78
Signs and symptoms of thoracic aortic aneurysms
Usually asymptomatic but can present with severe back and abdominal pain
79
Most common cause of traumatic aortic rupture
Blunt trauma like rapid deceleration injury or crush injury and penetrating trauma
80
Most common location of traumatic aortic rupture
Aortic isthmus (just distal to left subclavian artery at site of ductus arteriosus)
81
Aortic dissection involving ascending aorta, may extend to aortic arch or ascending aorta and result in aortic regurgitation or cardiac tamponade
Stanford type A
82
Aortic dissection involving only descending aorta below ligamentum arteriosum
Stanford type B
83
Treatment for Stanford type B aortic dissection
B-blockers then vasodilators
84
Treatment for Stanford type A aortic dissection
Surgery
85
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
Aortic dissection
86
CXR finding in aortic dissection
Mediastinal widening
87
Complications in aortic dissection
Organ ischemia, aortic rupture or death
88
Exertional chest pain that resolves with rest or nitroglycerin usually 2ndary to atherosclerosis
Stable angina
89
Findings in stable angina
ST depression on ECG with no cardiac markers
90
CP occurring at rest triggered by cocaine, alcohol, or triptans 2ndary to coronary artery vasospasms
Prinzmetal angina
91
Treatment for Prinzmetal angina
Ca channel blockers, nitrates and smoking cessation
92
Thrombosis with complete coronary artery occlusion with increased frequency or intensity of CP at rest
Unstable angina
93
Risk factors associated with Prinzmetal angina
Smoking
94
Findings in Prinzmetal angina
Transient ST segment elevations on ECG and no cardiac markers
95
Findings in unstable angina
ST segment depression with T-wave inversions on ECG and no cardiac markers
96
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.
Coronary steal syndrome
97
Caused by progressive onset of HF over many years due to chronic ischemic myocardial damage
Chronic ischemic heart disease
98
Most common cause of MI
Acute thrombosis due to rupture of coronary artery atherosclerotic plaque causing elevation of cardiac enzymes
99
Presents with ST elevation on ECG with Q-waves, transmural damage involving full thickness of myocardial wall
STEMI
100
Presents with ST depression on ECG with subendocardial infarcts and subendocardium ischemic damage
NSTEMI
101
Commonly occluded coronary arteries in order of incidence
LAD > RCA > circumflex artery
102
Common symptoms in MI
Diaphoresis, nausea, vomiting, severe retrosternal pain, pain in left arm and/or jaw, SOB and fatigue
103
When is early coagulative necrosis with release of necrotic cell contents into blood first seen in an MI
0-24 hours after MI
104
What are the characteristic cells 0-24 hours after acute MI
Neutrophils
105
In what stage of MI is reperfusion injury seen
0-24 hours after MI
106
Injury associated with generation of free radicals, leading to hypercontraction of myofibrils through influx of free calcium seen within 0-24 hours after MI
Reperfusion injury
107
Dark mottling, pale with tetrazolium stain is seen how long after an MI
0-24 hours
108
Complications associated within 0-24 hours after MI
Ventricular arrhythmia, HF, cardiogenic shock
109
Complication associated within 1-3 days after MI
Postinfarction fibrinous pericarditis
110
Hyperemia with extensive coagulative necrosis is seen how long after MI
1-3 days
111
Acute inflammation with neutrophils surrounding infarcted tissue is seen how long after MI
1-3 days
112
Complication of free wall rupture from MI
Cardiac tamponade
113
Causes mitral regurgitation after MI
Papillary muscle rupture
114
Macrophage-mediated structural degradation seen after MI usually affects with heart structure
Interventricular septum
115
Maximally yellow, hyperemic border with central yellow-brown softening is usually seen how long after MI
3-14 days
116
Interventricular septal rupture is seen how long after MI
3-14 days
117
Free wall rupture causing tamponade is seen how long after MI
3-14 days
118
Mitral regurgitation from papillary muscle rupture is seen how long after MI
3-14 days
119
Complication seen 2 weeks to several months after MI presenting with fever, pleuritic pain, pericarditis and/or pericardial effusion
Dressler syndrome
120
Gray-white contracted scar with recanalized artery is seen how long after MI
2 weeks to several months
121
Type of collagen seen in scar 2 weeks to several months after MI
Type I collagen
122
Cardiac biomarker useful in diagnosing reinfarction following acute MI
CK-MB
123
Cardiac biomarker that is more specific for MI
Troponin I
124
Gold standard for diagnosing MI
ECG within first 6 hours
125
Significance of Q-waves
Transmural MI (STEMI)
126
Significance of T-wave inversions
Transmural MI (STEMI)
127
Coronary vessel infarcted with ST elevations or Q waves in leads V1-V2
LAD (anteroseptal)
128
Coronary vessel infarcted with ST elevations or Q waves in leads V3-V4
distal LAD (anteroapical)
129
Coronary vessel infarcted with ST elevations or Q waves in leads V5-V6
LAD or LCX (anterolateral)
130
Coronary vessel infarcted with ST elevations or Q waves in leads I, aVL
LCX (Lateral)
131
Coronary vessel infarcted with ST elevations or Q waves in leads II, III, aVF
RCA (Inferior)
132
Coronary vessel infarcted with ST elevations or Q waves in leads V7-V9, ST depression sin V1-V3 with tall R waves
Posterior (PDA)
133
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
Cardiac arrhythmia
134
Occurs 1-3 days after MI with friction rub and pain relieved by leaning forward
Postinfarction fibrinous pericarditis
135
Occurs 2-7 days after MI resulting in mitral regurgitation and risk increased due to single blood supply from PDA
Papillary muscle rupture
136
Occurs 3-5 days after MI from macrophage-mediated degradation
Interventricular septal rupture
137
Occurs 3-14 days after MI with decreased CO, risk of arrhythmia, embolus from mural thrombus and contained within free wall rupture
Ventricular pseudoaneurysm formation
138
Occurs 5-14 days after MI causing cardiac tamponade; LVH and previous MI are protective
Ventricular free wall rupture
139
Occurs 2 weeks to several months after MI causing dyskinesia and outward bulge with contraction associated with fibrosis
True ventricular wall rupture
140
An autoimmune phenomenon occurring several weeks after MI resulting in fibrinous pericarditis
Dressler syndrome
141
Can occur 2ndary to LV infarction, VSD, free wall rupture, papillary muscle rupture with mitral regurgitation
LV failure and pulmonary edema
142
Symptom control for unstable angina or NSTEMI
Nitroglycerin and morphine
143
Preventive treatments for angina or NSTEMI
Anticoagulation- heparin
Antiplatelet therapy (Aspirin) + ADP inhibitors (clopidogrel)
B-blockers, ACE inhibitors, statins
144
STEMI treatment
Anticoagulation- heparin
Antiplatelet therapy (Aspirin) + ADP inhibitors (clopidogrel)
B-blockers, ACE inhibitors, statins
Reperfusion therapy - percutaneous coronary intervention
145
When are B-blockers contraindicated in angina, NSTEMI, or STEMI
HoTN, bradycardia or pulmonary edema
146
Most common cardiomyopathy
Dilated cardiomyopathy
147
Findings in dilated cardiomyopathy
HF, S3, systolic regurgitant murmur, dilated heart on echo, balloon heart on CXR
148
Treatment for dilated cardiomyopathy
Na restriction, ACE inhibitors, B-blockers, diuretics, digoxin, ICD, heart transplant
149
Causes of dilated cardiomyopathy
```
ABCCCD:
Alcohol abuse
Beriberi (wet)
Coxsackie B
Cocaine use
Chagas disease
Doxorubicin
```
150
Type of hypertrophy seen in dilated cardiomyopathy
Eccentric hypertrophy - sarcomeres added in series
151
Inheritance pattern of hypertrophic cardiomyopathy
Autosomal dominant
152
Type of dysfunction that ensues dilated cardiomyopathy
Systolic dysfunction
153
Mutation in hypertrophic cardiomyopathy
Mutations in genes encoding sarcomeric proteins like myosin binding protein C and B-myosin heavy chain
154
Complication of hypertrophic cardiomyopathy
Sudden death in young athletes due to ventricular arrhythmia
155
Findings in hypertrophic cardiomyopathy
S4, systolic murmur, mitral regurgitation due to impaired mitral closure
156
Treatment for hypertrophic cardiomyopathy
Cessation of high intensity athletics, B-blockers or non-dihydropyridine CCBs (verapamil)
ICD in high risk patients
157
Endomyocardial fibrosis with a prominent eosinophilic infiltrate
Loffler syndrome
158
Type of dysfunction that ensues hypertrophic cardiomyopathy
Diastolic dysfunction
159
Caused by asymmetric septal hypertrophy and systolic anterior motion of mitral valve causing outflow obstruction
Hypertrophic Obstructive Cardiomyopathy (HOCM)
160
Causes of restrictive/infiltrative cardiomyopathy
```
Puppy LEASH:
Postradiation fibrosis
Loffler syndrome
Endocardial fibroelastosis
Amyloidosis
Sarcoidosis
Hemochromatosis
```
161
Cardiomyopathy with low voltage ECG despite thick myocardium
Restrictive cardiomyopathy
162
Thick fibroelastic tissue in endocardium of young children
Endocardial fibroelastosis
163
Type of dysfunction that ensues restrictive cardiomyopathy
Diastolic dysfunction
164
Type of dysfunction characterized by reduced EF, increased EDV and decreased contractility 2ndary to ischemia, MI or dilated cardiomyopathy
Systolic dysfunction
165
Type of dysfunction characterized by preserved EF, normal EDV and decreased compliance 2ndary to myocardial hypertrophy
Diastolic dysfunction
166
Most common cause of RHF
Left Heart Failure (LHF)
167
Isolated right heart failure due to pulmonary causes
Cor pulmonale
168
When are B-blockers contraindicated in HF
Acute decompensated HF
169
Drugs that decrease mortality in HF
ACE inhibitors or ARBs, B-blockers, spironolactone
170
Drug used mainly for symptomatic relief of HF
Thiazide diuretics
171
Combo drugs that improve both symptoms and mortality in select patients
Hydralazine with nitrate therapy
172
Shortness of breath when lying down
Orthopnea
173
Mechanism of orthopnea
Immediate increased venous return from redistribution of blood worsens pulmonary vascular congestion
174
Breathless awakening from sleep
Paroxysmal nocturnal dyspnea
175
Mechanism of paroxysmal nocturnal dyspnea
Increased venous return from redistribution of blood and reabsorption of peripheral edema
176
Increased pulmonary venous pressure causing pulmonary venous distention and transudation of fluid
Pulmonary edema
177
Classic microscopy finding in pulmonary edema
Hemosiderin-laden macrophages in lungs (HF-cells)
178
Signs of left heart failure
Orthopnea, paroxysmal nocturnal dyspnea, pulmonary edema
179
Caused by increased central venous pressure causing increased resistance to portal flow and seen in RHF
Hepatomegaly (nutmeg liver)
180
Sign caused by increased venous pressure seen in neck
Jugular venous distention
181
Sign caused by increased venous pressure and causing fluid transudation
Peripheral edema
182
Signs of right heart failure
Hepatomegaly, jugular venous distention, peripheral edema
183
Inadequate organ perfusion and delivery of nutrients necessary for normal tissue and cellular function; may be reversible but life threatening if not treated promptly
Shock
184
Type of shock caused by hemorrhage, dehydration or burns and presents with cold, clammy skin
Hypovolemic shock
185
Effects of hypovolemic shock on hemodynamics
Preload - severely decreased
CO - decreased
Afterload - increased
186
Effects of obstructive shock on hemodynamics
Preload - increased or decreased
CO - severely decreased
Afterload - increased
187
Effects of distributive shock caused by sepsis or anaphylaxis on hemodynamics
Preload - decreased
CO - increased
Afterload - severely decreased
188
Effects of distributive shock caused by CNS injury on hemodynamics
Preload - decreased
CO - decreased
Afterload - severely decreased
189
Type of shock caused by acute MI, HF, valvular dysfunction, arrhythmia, tamponade, PE or tension pneumothorax
Cardiogenic or obstructive shock
190
Effects of cardiogenic shock on hemodynamics
Preload - increased or decreased
CO - severely decreased
Afterload - increased
191
Treatment for hypovolemic shock
IV fluids
192
Treatment for cardiogenic shock
Inotropes, diuresis
193
Treatment for obstructive shock
Relieve obstruction
194
Treatment for distributive shock
IV fluids, pressors
195
Round white spots on retina surrounded by hemorrhage
Roth spots
196
Tender raised lesions on finger or toe pads
Osler nodes
197
Small, painless erythematous lesions on palm or sole
Janeway lesions
198
Acute cause of bacterial endocarditis
S aureus
199
Valves commonly affected by S aureus in bacterial endocarditis
Mitral valve
200
Gross findings found on pathology of heart valve in acute bacterial endocarditis
Large vegetations on previously normal valve
201
Subacute cause of bacterial endocarditis
Streptococcus viridans from prior dental procedures
202
Gross findings found on pathology of heart valve in subacute bacterial endocarditis
Small vegetations on damaged heart valve
203
Symptoms of bacterial endocarditis
```
FROM JANE:
Fever
Roth spots
Osler nodes
Murmur
Janeway lesions
Anemia
Nail-bed hemorrhage
Emboli
```
204
Valve commonly affected by S aureus in IV drug users
Tricuspid valve
205
Significance of negative cultures in bacterial endocarditis
```
Infection from Coxiella, Bartonella or HACEK organisms:
Haemophilus
Aggregatibacter
Cardiobacterium
Eikenella
Kingella
```
206
Early heart valve lesion in rheumatic heart disease
Mitral regurgitation
207
Late heart valve lesion in rheumatic heart disease
Mitral stenosis
208
Late sequelae of rheumatic fever
Rheumatic heart disease
209
Most commonly affected heart valves in rheumatic heart disease in order of incidence
Mitral valve > aortic valve > > tricuspid valve
210
Mechanism of rheumatic heard disease
Immune mediated type II hypersensitivity reaction; antibodies to M protein cross-react with self antigens
211
Lab findings in rheumatic heart disease
Positive ASO titers and throat cultures
Increased ESR and CRP
Increased PR interval
Leukocytosis
212
Microscopic findings in rheumatic heart disease
Anitschkow cells within Aschoff bodies
213
Granulomas with Anitschkow cells found inside
Aschoff bodies
214
Enlarged macrophages with ovoid, wavy, rod-like nucleus that look like caterpillars
Anitschkow cells
215
Common signs of Rheumatic fever
```
JONES criteria: O = heart
Joint - migratory polyarthritis
O- carditis
Nodules in skin - subcutaneous
Erythema marginatum
Sydenham chorea
```
216
Inflammation of the pericardium presenting with sharp pain, aggravated by inspiration and relieved by sitting up or leaning forward
Acute pericarditis
217
ECG findings in acute pericarditis
Widespread ST segment elevation and/or PR depression
218
Complication in acute pericarditis that presents with friction rub
Pericardial effusion
219
Most common cause or acute pericarditis
Idiopathic; presumed viral
220
Less common causes of acute pericarditis
Bacterial, neoplasia, autoimmune, uremia, cardiovascular, radiation therapy
221
Compression of the heart by fluid decreasing cardiac output and equilibration of diastolic pressure in all heart chambers
Cardiac tamponade
222
Syndrome in cardiac tamponade characterized by hypotension, distended neck veins, and distant heart sounds
Beck triad
223
ECG findings in cardiac tamponade
Low-voltage QRS and electrical alternans
224
Causes electrical alternans
Swinging movement of heart in large effusion
225
Decrease amplitude of systolic BP by > 10 mmHg during inspiration
Pulsus paradoxus
226
Findings in cardiac tamponade
Beck triad, pulsus paradoxus, and increased HR
227
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
Syphilitic heart disease
228
Cause of atrophy of vessel wall in syphilitic heart disease
Destruction of vasa vasorum by 3rdtiary syphilis
229
Most common primary cardiac tumor in adults
Myxoma
230
Most common site for myxomas
Left atrium
231
Presents with multiple syncopal episodes and early diastolic "tumor plop" sound with gelatinous material on histology
Myxoma
232
Most frequent primary cardiac tumor in children with hamartomatous growth on histology and associated with tuberous sclerosis
Rhabdomyoma
233
Increase in JVP on inspiration instead of normal decrease
Kussmaul sign
234
Common causes of Kussmaul sign
Constrictive pericarditis, restrictive cardiomyopathies, right atrial or ventricular tumors
235
Usually affects elderly females with unilateral headache, jaw claudication and impaired vision
Giant cell arteritis
236
Complication of giant cell arteritis
Irreversible blindness due to ophthalmic artery occlusion
237
Biopsy findings in giant cell arteritis
Focal granulomatous inflammation with segmental lesions
238
Treatment for giant cell arteritis
High dose corticosteroids prior to biopsy to prevent blindness
239
Lab findings suggestive of giant cell arteritis
Increased ESR
240
Usually affects Asian females < 40 years, presents with weak upper extremity pulses, fever, night sweats, arthritis, myalgias, skin nodules, ocular disturbances
Takayasu disease
241
Common findings in Takayasu disease
Granulomatous thickening and narrowing of aortic arch at branch points and proximal vessels with increased ESR
242
Treatment for Takayasu disease
Corticosteroids
243
Usually affects middle-aged men, presents with HBV seropositivity, fever, weight loss, malaise, headache, cutaneous eruptions, renal damage, and GI symptoms
Polyarteritis nodosa
244
Classic image finding in Polyarteritis nodosa
String of pearls on blood vessels
245
Blood vessels commonly affected in Polyarteritis nodosa
Renal and visceral vessels - NO pulmonary vessels
246
Typical biopsy findings in Polyarteritis nodosa
Transmural inflammation of the arterial wall with Fibrinoid necrosis
247
Treatment for Polyarteritis nodosa
Corticosteroids and cyclophosphamide
248
Commonly affects Asian children < 4 years old and presents with conjunctival injection, rash, adenopathy, strawberry tongue, hand-foot changes and fever
Kawasaki disease
249
Complication of Kawasaki disease
Coronary artery aneurysm; thrombosis or rupture can cause death
250
Treatment of Kawasaki disease
IV immunoglobulins and aspirin
251
Commonly presents in heavy smokers < 40 years old with intermittent claudication causing gangrene, autoamputation of digits and superficial nodular phlebitis
Buerger disease
252
Treatment for Buerger disease
Smoking cessation
253
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
Granulomatosis with polyangiitis (Wegener)
254
Commonly presents with triad of:
1. Focal necrotizing vasculitis
2. Necrotizing granulomas in the lung and upper airway
3. Necrotizing glomerulonephritis
Granulomatosis with polyangiitis (Wegener)
255
Lab findings in Granulomatosis with polyangiitis (Wegener)
PR3-ANCA/c-ANCA positive
256
CXR findings in Granulomatosis with polyangiitis (Wegener)
Large nodular densities
257
Treatment for Granulomatosis with polyangiitis (Wegener)
Cyclophosphamide, rituximab, corticosteroids
258
Necrotizing vasculitis commonly involving lung, kidney and skin with pauci-immune glomerulonephritis and palpable purpura with no nasopharyngeal symptoms
Microscopic polyangiitis
259
Lab findings in microscopic polyangiitis
MPO-ANCA/p-ANCA positive
260
Treatment for microscopic polyangiitis
Cyclophosphamide and corticosteroids
261
Vasculitis that presents with asthma, sinusitis, skin nodules or purpura, peripheral neuropathy and can involve heart, GI, kidneys with eosinophilia
Eosinophilic granulomatosis with polyangiitis (Churg-Strauss)
262
Lab findings in eosinophilic granulomatosis with polyangiitis (Churg-Strauss)
MPO-ANCA/p-ANCA, increased IgE levels
263
Most common childhood systemic vasculitis often following URI
Henoch-Schonlein purpura
264
Henoch-Schonlein purpura classic triad
Skin: palpable purpura on buttocks/legs
Arthralgias
GI: abdominal pain (intestinal hemorrhage, melena)
265
Vasculitis can be 2ndary to IgA immune complex deposition and associated with IgA nephropathy (Berger disease)
Henoch-Schonlein purpura
266
Inherited disorder of blood vessels presents with blanching skin lesions, recurrent epistaxis, skin discolorations, AVMs, GI bleeding and hematuria
Hereditary hemorrhagic telangiectasia
267
Inheritance pattern for hereditary hemorrhagic telangiectasia
Autosomal dominant
