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CPR 2 Exam 1 > Vascular Pathology > Flashcards

Vascular Pathology Flashcards

1
Q

What is an AVM?

A

Arteries and veins without intervening capillaries

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2
Q

“Tangle of worms” with pulsatile arteriovenous shunting with high blood flow is indicative of what?

A

AVM

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3
Q

AVM causes what type of cardiac failure?

A

High-output

Due to shunting of blood into venous circulation

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4
Q

In what population does AVM occur more frequently?

A

Males

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5
Q

When is AVM typically diagnosed?

A

Childhood

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6
Q

What is a surgically created AVM?

A

Arteriovenous fistula for hemodialysis or chemotherapy

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7
Q

What AVM can cause hematuria?

A

AVM of bladder

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8
Q

What are symptoms of an AVM of the brain?

A

Seizure

Intracerebral hemorrhage

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9
Q

What is a focal abnormality of an artery due to underlying defect in the media?

A

Berry (saccular) Aneurysm

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10
Q

Where is a berry (saccular) aneurysm typically found?

A

Anterior cerebral artery

Anterior communicating artery

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11
Q

What are risk factors for berry (saccular) aneurysm?

A

HTN

Smoking

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12
Q

Berry (saccular) aneurysms are associated with which diseases?

A

AD Polycystic kidney disease
Marfan syndrome
Ehlers Danlos syndrome

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13
Q

Subarachnoid hemorrhage is associated with what?

A

Berry (saccular) aneurysm

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14
Q

What are symptoms of a subarachnoid hemorrhage?

A 
Neck pain
Vomiting
Double vision
Seizures
LOC
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15
Q

Berry (saccular) aneurysm rupture often happens with what?

A

Straining with stool

Sexual orgasm

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16
Q

What is a dilation of artery due to infectious process that damages the vessel wall?

A

Mycotic aneurysm

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17
Q

What are the three causes of mycotic aneurysm?

A

1) Septic emboli (infective endocarditis)
2) Extension of an adjacent infectious process
3) Circulating organisms directly infecting the arterial wall

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18
Q

What is a focal, irregular thickening of medium and large muscular arteries?

A

Fibromuscular dysplasia

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19
Q

What arteries does fibromuscular dysplasia typically impact?

A

Renal
Carotid
Splanchnic
Vertebral

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20
Q

Fibromuscular dysplasia is upregulated in women due to what?

A

Estrogen

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21
Q

Fibromuscular dysplasia shows what on angiography?

A

String of beads

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22
Q

What artery does fibromuscular dysplasia most commonly impact?

A

Renal artery

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23
Q

Renal artery stenosis in fibromuscular dysplasia leads to activation of what?

A

RAAS

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24
Q

Activiation of RAAS in renal artery stenosis results in what?

A

Renovascular HTN (bruit sometimes heard)

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25
Q

What maintains blood volume and vascular tone?

A

Renin-angiotensin-aldosterone system

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26
Q

When is renin released?

A

Low volume
Low peripheral resistance
Decreased glomerular filtration rate

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27
Q

Where is renin released?

A

By juxtaglomerular cells in the afferent arterioles in the kidneys

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28
Q

Renin cleaves circulating angiotensinogen to form what?

A

Angiotensin I

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29
Q

Angiotensin I is cleaved to form angiotensin II by what?

A

ACE

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30
Q

Angiotensin II does what?

A

Vasoconstrict

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31
Q

Volume expansion caused the myocardial cells to release what?

A

Atrial natriuretic peptide

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32
Q

What does atrial natriuretic peptide cause?

A

Sodium excretion
Vasodilation
Decreased BP

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33
Q

HTN is a risk factor for what?

A

Atherosclerosis

End organ damage

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34
Q

What are the unmodifiable risk factors for primary HTN?

A

Age (older)

Genetics (blacks, higher risk)

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35
Q

What are the modifiable risk factors for primary HTN?

A

Stress
Obesity
Physical inactivity
Increased salt consumption

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36
Q

What are the renal causes of secondary hypertension?

A 
Renovascular disease
Renal artery stenosis
Fibromuscular dysplasia
Atherosclerosis
Polycystic kidney disease
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37
Q

What are the endocrine causes of secondary hypertension?

A

Primary aldosteronism
Cushing syndrome
Pheochromocytoma

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38
Q

What are the cardiovascular causes of secondary hypertension?

A

Coarctation of the aorta

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39
Q

Primary hyperaldosteronism causes HTN with what?

A

Hypokalemia

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40
Q

What symptoms are associated with the HTN due to primary alderosteronism?

A

Neuromuscular changes (weakness, muscle cramps, paraesthesias, visual disturbances)

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41
Q

What are the three causes of hyperaldosteronism?

A

Bilateral nodular hyperplasia of adrenal gland
Adenoma
Hybrid glomerulosa cells responsive to ACTH

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42
Q

What are the four causes of Cushing syndrome?

A

Tumor in anterior pituitary
Tumor in adrenal
Paraneoplastic Cushing
Iatrogenic Cushing syndrome (oral steroids)

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43
Q

What is a pheochromocytoma?

A

Tumor of the chromaffin cells of the adrenal medulla

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44
Q

What is secreted by a pheochromocytoma?

A

Epinephrine

Norepinephrine

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45
Q

Norepinephrine causes what?

A

Alpha-1 activation -> peripheral vasoconstriction

Beta-1 activation -> increased cardiac output

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46
Q

Epinephrine causes what?

A

Beta-1 activation -> increased cardiac output

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47
Q

What are the clinical symptoms of pheochromocytoma?

A 
Paroxysm of elevated blood pressure
Tachycardia
Palpitations
Headache
Diaphoresis
Tremor
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48
Q

How do you diagnose pheochromocytoma?

A

Elevation of urinary or plasma metanephrines

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49
Q

What syndrome is pheochromocytomas assocaited with?

A

MEN 2

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50
Q

What do pheochromocytomas look like on gross examination?

A

Golden brown color

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51
Q

What is MEN 1?

A

Pituitary adenoma
Parathyroid hyperplasia
Pancreatic tumors

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52
Q

What is MEN 2A?

A

Parathyroid hyperplasia
Medullary thyroid carcinoma
Pheochromocytoma

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53
Q

What is MEN 2B?

A

Mucosal neuromas
Marfanoid body habitus
Medullary thyroid carcinoma
Pheochromocytoma

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54
Q

What is the rule of 10s for pheochromocytomas?

A

10% are malignant
10% are extraadrenal
10% of sporatic are bilateral
10% are not associated with hypertension

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55
Q

What happens with renal artery stenosis?

A

HTN
Decreased GFR
Chronic kidney disease
Increased creatinine

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56
Q

What are the two causes of renal artery stenosis?

A

Atherosclerosis

Fibromuscular dysplasia

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57
Q

What is adult coarctation of the aorta?

A

Congenital narrowing of the aorta opposite the ligamentum arteriosum

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58
Q

What does adult coarctation of the aorta cause?

A

HTN in upper extremities
Hypotension in the lower extremities
Limb claudication

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59
Q

What is coarctation of the aorta in adults associated with?

A

Bicuspid aortic valve

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60
Q

Coarctation of the aorta is most common in what population?

A

Males

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61
Q

When is a bruit heard?

A

Significant obstruction of a larger vessel

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62
Q

Where is a bruit heard with renal artery stenosis associated with fibromuscular dysplasia?

A

Epigastric abdominal bruit which radiates to the back or side

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63
Q

Where is a bruit heard with coarctation of the aorta?

A

Carotid bruit

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64
Q

Pyelonephritis and polycystic kidney disease can be a secondary cause of what?

A

HTN

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65
Q

How does parenchymal kidney disease cause hypertension?

A

Activation of the renin-angiotensin system due to renal ischemia

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66
Q

Why does concentric left ventricular cardiac hypertrophy occur?

A

Left ventricle is attempted to pump blood against increased vascular resistance

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67
Q

Concentric left ventricular cardiac hypertrophy leads to what?

A

Cardiomegaly (which then leads to heart failure, which then leads to fluid back up in the lungs, which then leads to dyspnea)

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68
Q

What are heart and aorta effects due to HTN?

A

Cardiac hypertrophy
Chronic heart failure
Ischemic heart disease
Aortic dissection

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69
Q

What are kidney effects due to HTN?

A

Proteinuria

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70
Q

What are brain and eye effects due to HTN?

A

Multi-infarct dementia
Cerebrovascular hemorrhage/strone
Increased intracranial pressure/papilledema (headache/vision changes)
Retinopathy (AV nicking)

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71
Q

What do patients with untreated HTN die from?

A

Ischemic heart disease/CHF

Stroke

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72
Q

Hyaline arteriosclerosis due to what?

A

Increased smooth muscle matrix synthesis and plasma protein leakages across damaged endothelium

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73
Q

Which drug class is hyaline arteriosclerosis seen in?

A

Calineurin inhibitors (T-cell immunosuppressive drug)

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74
Q

What is the hyaline material composed of in hyaline arteriosclerosis?

A

Precipitated plasma proteins

C3

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75
Q

Hyaline arteriosclerosis can lead to what downstream?

A

Ischemia

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76
Q

Homogenous pink (hyaline) thickening of the vessel wall leads directly to what?

A

Luminal narrowing

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77
Q

Hyaline arteriosclerosis manifests as what in the kidney?

A

Hyaline nephrosclerosis

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78
Q

Hyaline nephrosclerosis causes what?

A

Impairment of renal blood supply
Ischemic glomerulosclerosis
Leads to RAAS activation -> HTN

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79
Q

What is a hypertensive crisis?

A

Systolic greater than 180-200

Diastolic greater than 120

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80
Q

What is a hypertensive emergency?

A

Hypertensive crisis with end organ damage

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81
Q

What end organ damage is seen in hypertensive emergencies?

A 
Renal failure
Encephalopathy
Acute heart failure
Retinal hemorrhages and exudates
Papilledema
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82
Q

Papilledema is typically found with what?

A

Increased CSF pressure

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83
Q

What does the kidney show in hypertensive emergencies?

A

Necrotizing arteriolitis
Hematuria
Increased creatinine
Renal failure

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84
Q

What is malignant hypertension?

A

Markedly increased hypertension

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85
Q

Hyaline arteriolosclerosis occurs with what type of hypertension?

A

Chronic

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86
Q

Hyperplastic arteriolosclerosis occurs with what type of hypertension?

A

Severe

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87
Q

In hyperplastic arteriolosclerosis the smooth muscle forms what?

A

Concentric lamellations with a thickened reduplicated basement membrane

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88
Q

“Onion skinning” is found in what type of arteriolosclerosis?

A

Hyperplastic

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89
Q

What accompanies lamellations in malignant hypertension?

A

Fibrinoid deposits

Vessel wall necrosis (especially in the kidney)

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90
Q

Hyaline arteriolosclerosis causes what kidney appearance?

A

Cortical scarring
Shrunken kidney with granular surface
Thinned cortex

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91
Q

Hyperplastic arteriolosclerosis causes what kidney appearance?

A

Numerous petechial hemorrhages

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92
Q

What does arteriosclerosis mean?

A

Hardening of the arteries
Arterial wall thickening
Loss of elasticity

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93
Q

What are the three types of arteriosclerosis?

A

1) Arteriolosclerosis
2) Atherosclerosis
3) Monckeberg medial sclerosis

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94
Q

What are the two types of arteriolosclerosis?

A

Hyaline

Hyperplastic

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95
Q

In what vessels does arteriolosclerosis occur?

A

Small arteries and arterioles

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96
Q

What are complications of arteriolosclerosis?

A

Downstream ischemic injury

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97
Q

What happens in atherosclerosis?

A

Atheromatous plaque formation

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98
Q

What are complications with atherosclerosis?

A 
Stenosis/occlusion
Plaque rupture
Aneurysm
Thrombus
Atheroembolism
Microemboli
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99
Q

What is Monckeberg medial sclerosis?

A

Calcification of muscular arteries and internal elastic membrane

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100
Q

What type of arteriosclerosis is an age related degenerative process?

A

Monckeberg medial sclerosis

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101
Q

What is the number one cause of death in the US?

A

Myocardial infarction

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102
Q

What are the nonmodifiable risk factors for aterosclerosis?

A

Genetic abnormalities
Family history
Increasing age
Male gender

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103
Q

What is the genetic inheritance for atherosclerosis?

A

Multifactoral inheritance (AD= familial hypercholesteremia)

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104
Q

At what age is atherosclerosis most common?

A

40-60s

Increasing age= increasing risk

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105
Q

What is a protective effect for atherosclerosis?

A

Premenopausal estrogenized women (only younger women)

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106
Q

What is the most important factors for developing atherosclerosis?

A

Genetic predisposition

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107
Q

Are risk factors for atherosclerosis synergistic or additive?

A

Synergistic

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108
Q

What are modifiable risk factors for atherosclerosis?

A 
Hyperlipidemia
Hypertension
Cigarette smoking
Diabetes
Metabolic syndrome
Inflammation
Hyperhomocysteinemia
Lipoprotein a
Factors affecting homeostasis
Lack of exercise
Competitive, stressful lifestyle
Obesity
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109
Q

Which cholesterol delivers cholesterol to peripheral tissues?

A

LDL

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110
Q

Which cholesterol mobilizes cholesterol from the periphery?

A

HDL

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111
Q

How do statins work?

A

Inhibit HMG-CoA reductase (enzyme key in producing LDL cholesterol)

Decreases LDL, increases HDL

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112
Q

How can HDL be increased?

A

Exercise

Moderate alcohol intake

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113
Q

What decreased HDL?

A

Smoking

Obesity

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114
Q

What increases LDL?

A 
Animal products 
Trans fat (fried, snack food)
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115
Q

What decreases LDL?

A

Soluble fiber

Statins

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116
Q

How do cigarettes promote atherosclerosis?

A

ROS and free radicals cause endothelial dysfunction and platelet activation through oxidization of LDL

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117
Q

How does diabetes promote atherosclerosis?

A

Sugar causes oxidative stress which damages blood vessels and increases inflammation

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118
Q

How does hyperhomocysteine increase aterosclerosis?

A

Oxidative stress leading to damage of the endothelium

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119
Q

C-reactive protein correlates with what?

A

Inflammatory activity

Cardiac risk

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120
Q

Pack per day for years doubles risk of what?

A

Ischemic heart disease

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121
Q

Diabetes doubles your chances of what?

A

Myocardial infarction

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122
Q

Hyperhomocysteinemia is associated with what?

A

Increased coronary atherosclerosis
Increased peripheral vascular disease
Increased stroke

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123
Q

What cytokine is associated with c-reactive protein?

A

IL-6

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124
Q

What makes up metabolic syndrome?

A 
Abdominal obesity
Increased triglycerides
Low HDL
Hypertension
Insulin resistance
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125
Q

What is function of endothelium?

A

Non-reactive barrier that keeps blood and plasma going throughout the body smoothly in laminar flow

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126
Q

What causes endothelial activation?

A 
Turbulent flow
Hypertension
Cytokines
Complement
Bacterial products
Lipid products
Advanced glycation end-products
Hypoxia
Acidosis
Viruses
Cigarette smoke
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127
Q

What happens in activated endothelium?

A

Increased expression of procoagulants
Adhesion molecules and proinflammatory factors
Altered expression of chemokines, cytokines, and growth factors

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128
Q

Activated endothelium is the key to driving the pathogenesis of what?

A

Atherosclerosis

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129
Q

What are the steps in vascular injury?

A

1) Recruitment of smooth muscle cells or smooth muscle precursor cells to intima
2) Smooth muscle cell mitosis
3) Elaboration of extracellular matrix

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130
Q

What are the two parts of an atherosclerotic plaque?

A

Fibrous cap

Necrotic center

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131
Q

What makes up the fibrous cap of an atherosclerotic plaque?

A 
Smooth muscle cells
Macrophages
Foam cells
Lymphocytes
Collagen elastin
Proteoglycans
Neovascularization
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132
Q

What makes up the necrotic center of an atherosclerotic plaque?

A

Cell debris
Cholesterol crystals
Foam cells
Calcium

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133
Q

Where is fibrous cap located in the atherosclerotic plaque?

A

Adjacent to the lumen

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134
Q

What is the atherosclerotic plaque surrounded by?

A

Internal elastic lamina

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135
Q

What happens when vessels become completely occluded?

A

Neovascularization

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136
Q

What lipid is atheromatous plaques primary consisted of?

A

LDL (which accumulates in the intima)

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137
Q

When monocytes take up oxidized LDL what cytokine is released to recruit additional monocytes?

A

IL-1

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138
Q

Where does atherosclerosis typically occur?

A

Branch points

Posterior abdominal aorta

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139
Q

What are the steps for atherosclerosis?

A

1) Chronic endothelial injury
2) Endothelial dysfunction
3) Macrophage activation with smooth muscle recruitment
4) Engulfment of lipid with fatty streak deposition
5) Proliferation of smooth muscle with extracellular matrix deposition

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140
Q

Which growth factors are important for smooth muscle cell proliferation and extracellular matrix deposition?

A

PDGF
Fibroblast growth factor
TGF-alpha

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141
Q

What releases PDGF?

A

Platelets
Macrophages
Endothelial cells
Smooth muscle cells

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142
Q

What are the most extensively involved vessels with atherosclerosis?

A

Abdominal aorta
Coronary arteries
Internal carotid arteries
Circle of Willis

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143
Q

What is the earliest gross indication of atherosclerosis?

A

Superficial flat yellow fatty streaks

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144
Q

What are fatty streaks made of?

A

Lipid filled macrophages on the intimal surface

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145
Q

What does severe atherosclerosis look like grossly?

A

Ulcerated plaques with calcification and associated blood clots

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146
Q

What does a fatty streak turn into?

A

Fibrofatty plaque

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147
Q

What causes a fibrofatty plaque to turn into an advanced/vulnerable plaque?

A 
Cell death/degeneration
Inflammation
Plaque growth
Remodeling of plaque and wall extracellular matrix
Organization of thrombus
Calcification
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148
Q

What are the three clinical outcomes of atherosclerotic changes?

A

1) Aneurysm and rupture
2) Occlusion by thrombus
3) Progressive plaque growth

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149
Q

What causes aneurysm and rupture with atherosclerosis?

A

Mural thrombosis
Embolization
Wall weakening

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150
Q

What causes occlusion by thrombus with atherosclerosis?

A 
Plaque rupture
Plaque erosion
Plaque hemorrhage
Mural thrombosis
Embolization
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151
Q

What causes critical stenosis with atherosclerosis?

A

Progressive plaque growth

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152
Q

What are clinical effects of atherosclerosis on the brain?

A

Thrombus causes infarction or stroke

Vascular rupture leas to intracerebral hemorrhage

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153
Q

What are clinical effects of atherosclerosis on the kidney?

A

Renal artery stenosis -> HTN
Ischemic injury with uremia
Renal failure

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154
Q

What is the principle cause of abdominal aortic aneurysms?

A

Atherosclerosis

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155
Q

Obstruction of visceral organs due to atherosclerosis causes what?

A

Chronic mesenteric ischemia nd infarction

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156
Q

Peripheral vascular disease causes what?

A

Claudication

Gangrene

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157
Q

Atherosclerosis can cause what in the heart?

A

Ischemic heart disease -> stenosis -> myocardial infarction

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158
Q

What is an excessive locational abnormal dilation of a blood vessel or ventricular wall?

A

Aneurysm

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159
Q

What is a “true” aneurysm?

A

Intact but thinned muscular wall at the site of dilation

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160
Q

What is a “false” aneurysm?

A

Defect though the wall of the vessel communicating with an extravascular hematoma that freely communicates with the intravascular space (pulsating hematoma)

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161
Q

What arises when blood enters a defect in the arterial wall and tunnels between layers?

A

Arterial dissection

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162
Q

Which aneurysm bulges out on one side?

A

Saccular

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163
Q

Which aneurysm bulges out on all sides of the vessel?

A

Fusiform

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164
Q

Where does a ventricular aneurysm occur?

A

Site of previous MI

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165
Q

What is cystic medial degeneration?

A

Normal elastin of the media is disrupted and replaced with areas of amorphous ground substance

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166
Q

What causes cystic medial degeneration?

A

Marfan
Ehlers Danlos
Systemic HTN

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167
Q

How does systemic HTN cause cystic medial degeneration?

A

Narrowing of small arterioles which feed the aorta leading to aortic ischemia, scarring, and inadequate ECM synthesis

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168
Q

What do vessels with cystic medial degeneration look like in Marfan syndrome?

A

Elastin fragmentation with areas without elastin fibers that are filled with proteoglycans

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169
Q

Marfan syndrome is caused by a mutation in what gene?

A

FBN1 (fibrillin gene)

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170
Q

What does the FBN1 or fibrillin gene do?

A

Needed for structural integrity of connective tissue

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171
Q

Is there increased or decreased TGF-beta in Marfan syndrome?

A

Increased

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172
Q

In Marfan syndrome fibirllin in unable to bind what?

A

TGF-beta

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173
Q

Increased TGF-beta activity weakens what?

A

Elastic tissue

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174
Q

What are symptoms of Marfan syndrome?

A 
Tall stature
Long fingers
Subluxation/dislocation of lenses
Pectus excavatum
Mitral valve prolapse
Aortic aneurysm
Aortic dissection
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175
Q

Ehlers danlos is due to a mutation in what?

A

Collagen

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176
Q

What are symptoms of ehlers danlos?

A 
Hyperelastic, fragile skin
Joint hypermobility
Lens subluxation
Abnormal wound healing
Widened scars
Bruising
Mitral valve prolapse
Kyphscoliosis
Rupture of colon, cornea, large arteries
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177
Q

What is syphillis caused by?

A

Spirochete Treponema pallidum

178
Q

What skin lesion is seen on initial infection with syphillis?

A

Red chancre lesion in the genital or anal area

179
Q

Tertiary syphillis presents after a latency period of how long?

A

5 years

180
Q

What organ systems does tertiary syphillis impact?

A 
Brain (neurosyphillis)
Skin
Bones
Organs (gumma formation)
Heart (obliterative endarteritis)
181
Q

What is a gumma formation?

A

Plasma rich inflammatory lesions

182
Q

What is obliterative endarteritis?

A

Concentric endothelial and fibroblastic proliferation of small vessels

183
Q

Where does obliterative endarteritis occur with tertiary syphillis?

A

Vaso vasorum (which feeds thoracic aorta causing ischemia and aneurysm formation)

184
Q

What two cardiovascular conditions occur with tertiary syphillis?

A

Obliterative endarteritis

Aortitis

185
Q

What appearance does an aortic aneurysm due to tertiary syphillis have?

A

Tree bark appearance (aorta becomes rough and pitted with concomitant calcification)

186
Q

What is the most important risk factor for abdominal aortic aneurysms?

A

Atherosclerosis

187
Q

What are risk factors for abdominal aortic aneurysms?

A

Smoking
Male
Age

188
Q

What is the typical location for abdominal aortic aneurysms?

A

Below renal arteries, above aortic bifurcation

189
Q

What do abdominal aortic aneurysms typically contain?

A

Bland laminated mural thrombus

190
Q

What vasculature does abdominal aortic aneurysms impact?

A

Renal
Superior mesenteric arteries
Iliac arteries

191
Q

How do the major of AAA patients present?

A

Aymptomatically

192
Q

In 1/3 of asymptomatic AAA patients there is what?

A

Pulsatile abdominal mass

193
Q

In 2/3 of asymptomatic AAA patients it is found during what?

A

Radiology finding or work up for peripheral vascular disease

194
Q

What are the non-ruptured symptoms of AAA?

A

Pain in abdomen, back

195
Q

What are the ruptured symptoms of AAA?

A

Severe acute pain
Pulsatile abdominal mass
Hypotension

196
Q

What is the size of AAA where surgical bypass is considered?

A

5 cm

197
Q

5-10% of AAA are what type?

A

Inflammatory with abundant lymphoplasmacytic inflammation

198
Q

What is a chronic inflammatory disease thought to represent an autoimmune disease in which numerous lymphocytes and IgG4 secreting plasma cells are associated with prominent fibrosis?

A

IgG4 related disease

199
Q

What organs is IgG4 related disease most common?

A 
Pancreas (autoimmune pancreatitis)
Biliary tree (sclerosing cholangitis)
Major salivary glands
Orbit of eye
Retroperitoneum
200
Q

What happens in IgG4 related disease and AAA?

A

Weakening of the wall with a fibroinflammatory infiltrate

201
Q

What treats IgG4 disease?

A

Steroids

202
Q

What is seen on histology of IgG4 disease with AAA?

A

Spindle fibroblastic-type cell proliferation admixed with clusters of plasma cells and lymphocytes

203
Q

What is primary risk factor for thoracic aortic aneurysm?

A

HTN

204
Q

What are conditions associated with thoracic aortic aneurysms?

A

Tertirary syphillis
Connective tissue disease (Marfan syndrome)
Vasculitis (giant cell aortitis, Takayasu)

205
Q

What are clinical symptoms of thoracic aortic aneurysms?

A

Breathing difficulties
Dysphagia
Cough (recurrent laryngeal nerve)

206
Q

When is surgical repair or endovascular placement of graft material considered for thoracic aortic aneurysm?

A

5.5 cm

207
Q

What is the clinical triad for aortic dissection?

A

1) Abrupt onset of thoracic pain with a sharp, tearing or ripping character
2) Variation of pulse (absence of proximal extremity or carotid pulse) and a greater than 20 mim of mercury BP difference between arms
3) Mediastinal widening on CXR as blood expands the vessel

208
Q

Where is the pain in aortic dissection?

A

Radiates to the back and move downward as dissection progresses

209
Q

How does death occur with aortic dissection?

A

Rupture of dissection through the adventitia into the pericardial, pleural, or peritoneal cavities

210
Q

Is cystic medial degeneration associated with aortic dissection?

A

Yes

211
Q

What are the two caused os aortic dissection?

A

1) HTN (men, 40-60)

2) Connective tissue disorders (Marfan syndrome, Ehlers Danlos)

212
Q

A tear in the intima of the aorta causes development of what?

A

Hematoma

213
Q

How does a hematoma become a dissecting aneurysm?

A

Hematoma in the media dissects longitudinally

214
Q

What is a double barreled aorta?

A

Intimal tear further down the aorta that reconnects the false lumen back to the aorta

215
Q

How does a false aneurysm become a chronic dissection?

A

False channel is endothelized overtime

216
Q

Do chronic dissections have the potential for future rupture?

A

Yes

217
Q

What is type A dissection?

A

Proximal intimal tear in the ascending aorta

218
Q

What is the most common type of aortic dissection?

A

Type A

219
Q

What is a type B dissection?

A

Proximal intimal tear in the aortic arch or the descending arota

220
Q

Which type of aortic dissection is more prone to external rupture into the mediastinum or pericardial cavity requiring surgical intervention?

A

Type A

221
Q

How are uncomplicated type B dissections handled?

A

Medical management

222
Q

What are the large vessel vasculitis?

A

Giant cell arteritis

Takayasu arteritis

223
Q

What are the medium vessel vasculitis?

A

Polyarteritis nodosa

Kawasaki disease

224
Q

What are the small vessel vasculitis?

A 
Microscopic polyangiitis
Wegener granulomatosis
Churg-Strauss syndrome
SLE vasculitis
Henoch-Schonelin purpura
Cryoglobulin vasculitis
Goodpasture disease
225
Q

What is the most common vasculitis in older adults in the US?

A

Giant cell arteritis

226
Q

What is a T-cell mediated vasculitis that affects the arteries of the scalp and head?

A

Giant cell arteritis

227
Q

What is the most common feature of giant cell arteritis?

A

Headache

also facial pain, fever, ocular diagnoses, fatigue/flu like symptoms

228
Q

Ocular symptomatology occurs in half the patients with what?

A

Giant cell arteritis

229
Q

Why is it important to catch giant cell arteritis quickly?

A

Can spread to ophthalmic artery and cause permanent blindness

230
Q

What is used to diagnose giant cell arteritis?

A

Temporal artery biopsy

231
Q

How is giant cell arteritis treated?

A

High dose corticosteroids

232
Q

What is seen on the temporal biopsy for someone with giant cell arteritis?

A

Intimal thickening with granulomatous inflammation and fragmentation of the internal elastic lamina

233
Q

Which vasculitis is a granulomatous autoimmune vasculitis associated with certain HLA subtypes?

A

Takayasu arteritis

234
Q

What populations are primarily affected by Takayasu arteritis?

A

East Asia
India
Latin America

235
Q

What age and gender is most commonly associated with Takayasu arteritis?

A

Female aged 15-40

236
Q

What are the symptoms of Takayasu arteritis?

A 
Ocular disturbances
Weakened pulses in upper extremities 
Fatigue
HTN
Fever
Decreased weight
237
Q

What is seen on histology for Takayasu arteritis?

A

Perivascular mononuclear infiltrate which can evolve to marked destruction with fibrosis and giant cells

238
Q

What is a systemic vasculitis of small to medium vessels associated with hepatitis B?

A

Polyarteritis nodosa

239
Q

What age group is typically affected by polyarteritis nodosa?

A

Young adults

240
Q

What is the pathophysiology associated with polyarteritis nodosa?

A

Immune complex mediated disease with Hep B surface antigen/Hep B surface antibody complexes in vessels

241
Q

What vessels does polyarteritis nodosa impact the most?

A 
Renal vessels
Heart
Liver
GI tract
Peripheral nerves
Skin
242
Q

What is seen histologically with polyarteritis nodosa?

A

Fibrinoid necrosis with embedded inflammatory cells within the wall

243
Q

How does polyarteritis nodosa typically present?

A 
Rapidly accelerating HTN (renovascular HTN)
Abdominal pain
Hematochezia
Myalgias
Peripheral neuritis of the motor neurons
244
Q

Polyarteritis nodosa is fatal with renal involvment unless given what therapy?

A

Immunosuppression

245
Q

What is an acute multisystem vasculitis of large to medium vessels which presents in early childhood and infancy?

A

Kawasaki disease

246
Q

What are the symptoms of Kawasaki disease?

A 
Conjunctivitis
Rash (genital)
Adenopathy (cervical)
Strawberry tongue
Hands (palmar erythema and swelling)
Burn (fever)
247
Q

Kawasaki disease has a preference for which artery?

A

Coronary artery

248
Q

What causes Kawasaki disease?

A

Activated T cells (+ monocytes/macrophages) which are provoked by a viral illness

249
Q

What causes death in Kawasaki disease?

A

Aneurysmal rupture of coronary arteries

250
Q

Depress ventricular function can result in which vasculitis?

A

Kawasaki disease

251
Q

What is given to treat Kawasaki disease?

A

Aspirin and IVIG

252
Q

What is another name for Kawasaki disease?

A

Mucocutaneous lymph node syndrome

253
Q

What is a small vessel vasculitis with upper respiratory involvement, asthma, peripheral blood esosinophilia, and pulmonary infiltrates?

A

Churg-Strauss syndrome

254
Q

What are found in a biopsy for Churg-Strauss syndrome?

A

Eosinophils with granulomas

255
Q

What lab finding is positive for Churg-Strauss syndrome?

A

MPO-ANCAs

256
Q

What organs systems are involved in Churg-Strauss syndrome?

A

Skin (palpable purpura)
GI tract bleeding
Renal disease (focal and segmental glomerulosclerosis)

257
Q

What causes death in patients with Churg-Strauss?

A

Cardiomyopathy/myocarditis with infarction

258
Q

How is Churg-Strauss treated?

A

Steroids

Cyclophosphamide

259
Q

What is a necrotizing granulomatous vasculitis which affects small to medium sized vessels of the upper and lower respiratory tract including the sinonasal tract and lung?

A

Granulomatosis with polyangiitis/Wegner’s granulomatosis

260
Q

What respiratory tract conditions are seen in granulomatosis with polyangiits?

A

Pneumonia with infiltrates
Chronic sinusitis
Nasopharyngeal ulceration

261
Q

What renal conditions is seen with granulmatosis with polyangiitis?

A

Necrotizing crescentic glomerulnephritis

262
Q

What population is most commonly affected with granulomatosis with polyangiitis?

A

Middle aged

263
Q

What is the pathogenesis of granulomatosis with polyangiitis?

A

T-cell hypersensitivity reaction mediated by inhaled environmental or microbial material

264
Q

What serologic test can identify granulomatos with polyangiits?

A

PR3-ANCA (C-ANCA)

265
Q

What lung findings are seen with granulomatosis with polyangiitis?

A

Cavities
Bleeds
Infiltrates

266
Q

What nasal findings are seen with granulomatosis with polyangiitis?

A

Stuffiness
Nose bleeds
Saddle nose

267
Q

What is the treatment for granulomatosis with polyangiitis?

A

Steroids
Cyclophosphamide
TNF-antagonists

268
Q

What lesions are seen on histology with granulomatosis with polyangiitis in the lung?

A

Tan, nodular centrally cavitating lesions

269
Q

What lesions are seen on histology with granulomatosis with polyangiitis in the kidney?

A

Necrotizing crescentic glomerulonephritis

270
Q

Which vasculitis has uniform stage of disease activity in all vessels?

A

Microscopic polyangiitis

271
Q

What are the symptoms associated with microscopic polyangiitis?

A 
Hematuria
Proteinuria
Hemoptysis
Cutaneous purpura
Muscle weakness
Bowel pain
Bleeding
272
Q

Is there deposition of immunoglobin in microscopic polyangiitis?

A

No

273
Q

What is found on histology for microscopic polyangiitis?

A

Leukocytoclastic picture with neutrophils infiltrating small blood vessels

274
Q

What vessels does microscopic polyangiitis impact?

A

Arterioles
Capillaries
Venules

275
Q

Various stages of disease activity are seen within different vessels in what vasculitis?

A

Polyarteritis nodosa

276
Q

What is the classic triad for Behcet’s disease?

A

1) Oral aphthous ulcers
2) Genital ulcers
3) Uveitis

277
Q

What HLA is Behcet’s disease associated with?

A

HLA-B51

278
Q

What is seen in the GI system with Behcet’s disease?

A

Ulcerations

279
Q

What inflammatory cell is required for diagnosis of Behcet’s disease?

A

Neutrophils

280
Q

How is Behcet’s disease treated?

A

Steroids

TNF-antagonists

281
Q

What is another name for thromboangiitis obliterans?

A

Berger disease

282
Q

What arteries does thrombangiitis obliterans typically impact?

A

Tibial artery

Radial artery

283
Q

What occludes the vessel in thromboangiitis obliterans?

A

Microabscess (granulomatous)

284
Q

What population is thromboangiitis obliterans found?

A

Smokers > 35 years old

285
Q

What is the pathophysiology of thromboangiitis obliterans?

A

Hypersensitivty/toxic reaction to cigarette smoke

Anti-endothelial antibodies

286
Q

What ethnic groups are commonly affected with thromboangiitis obliterans?

A

Israeli
Indian
Japanese

287
Q

What is the symptom progression for thromoangiitis obliterans?

A

Raynaud’s -> intermittent claudication -> sever pain at rest -> ulceration -> gangrene

288
Q

What is the pain in claudication due to?

A

Lack of oxygen in tissues

289
Q

Raynaud is secondary to what diseases?

A

Systemic lupus
Scleroderma
Thromboangiitis obliterans

290
Q

What provokes an attack of Raynaud’s?

A

Cold temperature
Emotion
Stress

291
Q

Is primary Raynaud’s symmetric or asymmetic?

A

Symmetric

292
Q

Does primary or secondary Raynaud’s spontaneously remit?

A

Primary

293
Q

The aorta is involved in which vasculitis?

A

Giant cell arteritis

Takayasu arteritis

294
Q

Eosinophils are rare in which vasculitis?

A

Giant cell arteritis

295
Q

Eosinophils are required in which vasculitis?

A

Churg-Strauss

296
Q

Neutrophils are required in which vasculitis?

A

Behcet disease

297
Q

Granulomas are required in which vasculitis?

A

Granulomatosis with polyangiitis

298
Q

Thrombosis is required in which vasculitis?

A

Berger disease

299
Q

PR3-ANCA is positive in which vasculitis?

A

Granulomatosis with polyangiitis

300
Q

MPO-ANCA is positive in which vasculitis?

A

Churg-Strauss

Leukocytoclastic vasculitis

301
Q

Which vasculitis is associated with polymyalgia rheumatica?

A

Giant cell arteritis

302
Q

Which vasculitis is associated with asthma, atopy, and sinusitis?

A

Churg-Strauss syndrome

303
Q

Which vasculitisis is associated with Hep B?

A

Polyangiitis nodosa

304
Q

Which vasculitis is associated with young smokers?

A

Berger disease

305
Q

Which vasculitis is associated with orogenital ulcers?

A

Behcet’s disease

306
Q

What is thought of as a cardiac Raynaud’s phenomenon?

A

Myocardial vessel vasospasm

307
Q

What are the three main causes of myocardial vessel vasospasm?

A

1) High levels of vasoactive mediators
2) Elevated thyroid hormones
3) Autoantibodies and T-cells in scleroderma

308
Q

What is excessive vasoconstriction of myocardial arteries or arterioles causing ischemia or infarct?

A

Myocardial vessel vasospasm

309
Q

What are the sources of high levels of vasoactive meditors?

A

Exogenous (cocaine, caffeine)

Endogenous (epinephrine/norepinephrine in pheochromocytoma)

310
Q

What is Takotsubo cardiomyopathy?

A

“broken heart syndrome”

311
Q

What is the pathophysiology of Takotsubo cardiomyopathy?

A

Emotional distress causes sudden surge of catecholamines which stimulates cardiac muscle cells and triggers constriction of coronary arteries (leads to ischemic cardiomyopathy or death)

312
Q

Hyperthyroidism with elevated thyroid hormone increases the sensitivity to what?

A

Catecholamines (leading to vasospasm)

313
Q

What population is broken heart syndrome seen in?

A

Elderly women

314
Q

What are varicose veins?

A

Abnormally dilated twisted veins which occur from prolonged, increased intraluminal pressure leading to incompetence of the venous valves and dilation

315
Q

Which veins do varicose veins typically occur with?

A

Superficial veins (with stasis, edema, and thrombosis)

316
Q

What is stasis dermatitis?

A

Ischemia of overlying skin with hemolysis of extravasated RBCs and ulcerations

317
Q

What does the skin look like with varicose veins?

A

Yellow and shiny (due to extravasated RBCs)

318
Q

Is embolism common with varicose veins?

A

No

319
Q

Is pruritis associated with varicose veins?

A

Yes

320
Q

What does portal hypertension lead to?

A 
Esophageal varices
Splenomegaly
Hemorrhoids
Distended superficial epigastric veins
Caput medusae
321
Q

What causes superior vena cava syndrome?

A

Compression or invasion of the superior vena cava which causes obstruction of blood flow

322
Q

What is the most common cause of superior vena cava syndrome?

A

Intrathoracic malignancy

323
Q

What are the two most common malignancies that cause superior vena cava syndrome?

A

Bronchogenic lung carcinoma

Lymphoma

324
Q

What are other causes of superior vena cava syndrome?

A

Aneurysm
AV fistula
Mediastinal fibrosis

325
Q

What are the symptoms of superior vena cava syndrome?

A

Dilation of veins of head, neck, chest, and arms
Cyanosis
Facial swelling
Neurologic manifestations
Respiratory distress (pulmonary vessels compressed)
Confusion
Headaches
Exacerbated as the patient bends forward/lies down

326
Q

What causes inferior vena cava syndrome?

A

Hepatocellular carcinoma
Renal cell carcinoma
Thrombosis (DVT)
Tumoral vein invasion

327
Q

What are the symptoms of inferior vena cava syndrome?

A

Lower extremity edema

Distension of superficial lower abdominal veins

328
Q

What is a venous thrombosis with an associated inflammatory response due to clot formation?

A

Thrombophlebitis

329
Q

What is thrombophlebitis usually caused by?

A

DVT of the leg

330
Q

What are the symptoms of thrombophlebitis?

A

Edema
Cyanosis
Erythema
Pain

331
Q

What is the most serious potential consequence with thrombophlebitis?

A

Pulmonary embolism

332
Q

What is the most important risk factor for thrombophlebitis?

A

Prolonged inactivity/immobilization

333
Q

What are risk factors for thrombophlebitis?

A 
Prolonged inactivity/immobilization
Hypercoagulability states (clotting factor mutations, tumor, estrogenic states, factor V leiden)
Tumor: thrombotic paraneoplastic syndrome; migratory thrombophlebitis (trousseau sign)
334
Q

Mucin produdcing adenocarcinomas are thought to be more what?

A

Thrombogenic

335
Q

What is a paradoxical embolus?

A

Embolus crosses from venous to arterial circulation (patent ductus arteriosus, AV malformation, ASD)

336
Q

What is the most common cause of lymphangitis?

A

Group A beta-hemolytic streptococcus

337
Q

How does lymphangitis due to beta-hemolytic streptococcus present?

A

Erythematous, warm streaking
Cellulitis
Abscess formation with fever

338
Q

Inflamed lymphatics present as?

A

Red, painful subcutaneous streaks

339
Q

Lymphadenitis presents as?

A

Painful enlargement of draining lymph nodes

340
Q

What is lymphedema?

A

Swelling caused by fluid buildup due to blockage of lymphatics

341
Q

When does lymphedema occur in the axilla?

A

After axillary dissection

342
Q

What are the primary causes of lymphedema?

A

Congenital defect

Familial Milroy disease (lymphatic agenesis/hypoplasia)

343
Q

What are secondary/obstructive causes of lymphedema?

A

Malignant tumor
Surgical procedures (radical mastectomy with axillary node dissection)
Post-irradiation fibrosis

344
Q

What is peau d’orange?

A

Draining lymphatics of skin overlying breast cancer filled with tumor cells

345
Q

What is vascular ectasia?

A

Local dilation of a blood vessel

346
Q

What is nevus simplex?

A

Simple birth mark caused by a vascular ectasia in the upper dermis which is extremely common

347
Q

Does nevus simplex regress with time?

A

Yes

348
Q

What is another name for port-wine stains?

A

Nevus flammeus

349
Q

What are port wine stains?

A

Progressive actasisias that persist into adulthood

350
Q

What is Sturge-Weber syndrome?

A 
Trigeminal nerve facila port wine stain
Mental retardation, seizures, hemiplegia
Leptomeningial capillary-venous malformation
Skull radio-opacitis
Eye abnormalities: glaucoma
351
Q

A large facial telangiectasia in a child with mental deficiency would be a prototypical clinical presentation of what?

A

Sturge-Weber syndrome

352
Q

What causes Sturge-Weber syndrome?

A

Somatic mutations in fetal ectodermal tissue causes inappropriate maturation of blood vessel formation (not heritable)

353
Q

Where does a nevus simplex typically occur?

A

Forehead
Eyelid
Nose
Upper lip

354
Q

What is a non-neoplastic permanent dilation of small vessels and capillaries?

A

Telangectasia

355
Q

When is a spider telangiectasia seen?

A

Increased circulating estrogen levels (mostly seen on face, neck, and upper chest)

356
Q

Which hormone has dilating effects on small vessels causes telangiectasias?

A

Estrogen

357
Q

What are two conditions with hyperestrogenism?

A

Pregnancy

Liver Cirrhosis

358
Q

What causes impaired metabolism and inactivation of estrogen leading to increased estrogen?

A

Liver cirrhosis

359
Q

What is another name for hereditary hemorrhagic telangiectasia?

A

Osler-Weber-Rendu disease

360
Q

What is the inheritance pattern for hereditary hemorrhagic telangiectasia?

A

Autosomal dominant

361
Q

What is mutated in hereditary hemorrhagic telangiectasia?

A

TGF-beta signaling

362
Q

What happens in hereditary hemorrhagic telangiectasia?

A

Numerous telangectasias

AV malformations

363
Q

What are the symptoms associated with hereditary hemorrhagic telangiectasia?

A

Nosebleeds
GI
Hematuria

364
Q

What is a benign vascular tumor characterized by an increased proliferation of blood vessels filled with blood?

A

Hemangiomas

365
Q

In which populations are hemangiomas common in?

A

Infancy

Childhood

366
Q

Where are hemangiomas typically found?

A

Head

Neck

367
Q

Is malignant transformation of hemangiomas common?

A

No

368
Q

Von Hippel-Lindau has what type of hemangiomas?

A

Cavernous hemangiomas (vascular lesions in cerebellum, brain stem, retina, pancreas, liver)

369
Q

Where is pyogenic granulomas most common?

A

Lips

Mouth Fingers

370
Q

What is another name for pyogenic granulomas?

A

Lobular capillary hemangioma

371
Q

What are some associations with Von Hippel-Lindau?

A

Angiomatosis
Hemangioblastomas
Pheochromocytoma
Renal cell carcinoma
Pancreatic cysts (pancreatic serous cystadenoma)
Endolymphatic sac tumor
Bilateral papillary cystadenomas of the epididymis or broad ligament of the uterus

372
Q

What is the most common hemangioma?

A

Capillary hemangioma

373
Q

What is seen with capillary hemangiomas?

A

Red spot

Thin-walled capillaries, tightly packed together

374
Q

What is a strawberry/congenital/infantile/juvenile hemangioma?

A

Capillary hemangioma that is present at birth and regresses

375
Q

What is characteristic of cavernous hemangiomas?

A

Irregular, dilated vascular channels making a lesions with an indistinct border
Involves deep tissue, more likely to bleed

376
Q

Pyogenic granuloma is what type of hemangiomas?

A

Capillary hemangioma

377
Q

Where are pyogenic granulomas most common?

A

Oral mucosa

Finger

378
Q

What is granuloma gravidarum?

A

Pyogenic granuloma seen in the gingiva of pregnant women

379
Q

How does congenital juvenile hemangioma/strawberry hemangioma present grossly?

A

Red bumpy raised plaque

380
Q

How does congenital juvenile hemangioma/strawberry hemangioma present histologically?

A

Demarcated lobular collections fo blood vessels

381
Q

What is seen histologically with cavernous hemaniomas?

A

Enlarged vessel spaces filled with blood

382
Q

What is seen histologically with pyogenic granulomas?

A

Lobulated capillary proliferation of small vessels

383
Q

What are glomus bodies?

A

Dermal structures which act as natural arteriovenous shunts

384
Q

What is the function of glomus bodies?

A

Take blood away from the skin surface when the skin is exposed to a cold temperature preventing heat loss

385
Q

What type of cells are glomus cells?

A

Modified round smooth muscle cells

386
Q

Glomus tumor is what type of tumor?

A

Mesenchymal

387
Q

What does the glomus tumor look like grossly?

A

Bluish with predilection for the subungal location under the fingernail

388
Q

What are the symptoms with glomus tumors?

A

Pain elicited by changes in temperature or tactile stimulation

389
Q

Are glomus tumors benign?

A

Yes

390
Q

What is a lymphangioma?

A

Benign dermal neoplasm measuring up to 2cm comprised of endothelial lined spaces

391
Q

What is the key feature of lymphaniomas?

A

Dilated spaces without RBCs

392
Q

What is the second main types of lymphangioma?

A

Cystic hygroma (cavernous lymphangioma)

393
Q

What conditions are cystic hygromas associated with?

A

Turner syndrome
Down’s
Klinefelter syndrome

394
Q

What is the tratment for cystic hygroma?

A

Surgical excision

395
Q

Where are lymphangiomas found?

A

Head
Neck
Axilla

396
Q

Where are carvernous lymphangiomas found?

A

Neck

Axilla

397
Q

Are cavernous lymphangiomas large or small?

A

Large (>15 cm)

398
Q

What is a reactive vascular proliferation that is generated in response to Bartonella bacilli?

A

Bacillary angiomatosis

399
Q

Bartonella hensale causes what?

A

Cat scratch disease (necrotizing granulomatous lymphadentitis

400
Q

Bartonella quintana causes what?

A

Human body louse which served as a vector for transmitting trench fever in WWI

401
Q

Bacillary angiomatosis is seen in what populations?

A

Immunosuppressed (those with HIV, transplant patients)

402
Q

What is seen clinically with bacillary angiomatosis?

A

Red, smooth papules and nodules

403
Q

What is seen histologically with bacillary angiomatosis?

A

Lobular proliferation of capillaries and ectatic vessels lined by endothelial cells typically with background inflammatory cells such as neutrophils, lymphcytes, and histocytes

404
Q

What stain is used for bartonella microorganisms?

A

Warthin-Starry stain

405
Q

How is bartonella angiomatosis treated?

A

Antibiotics

406
Q

What is a vascular neoplasm that requires infection with HHV-8, a double stranded herpes virus?

A

Kaposi sarcoma

407
Q

How is Kaposi sarcoma classified?

A

Intermediate grade

Borderline tumor

408
Q

What are the symptoms of Kaposi sarcoma?

A 
Red-purple nodules/plaques
Lower limbs
Genitals
Face
Back
Lymph nodes
GI
409
Q

What are the four types of Kaposi sarcoma?

A

1) Classic (sporadic)
2) Endemic (African)
3) Iatrogenic (immunosuppresssion related)
4) AIDS associated

410
Q

What population does classic/sporadic Kaposi sarcoma affect?

A

Older men of Mediterranean, Eastern European, and Middle Eastern decent

411
Q

The African endemic variant of Kaposi sarcoma impacts who?

A

Lymph nodes and viscera of children (HIGH MORTALITY)

412
Q

Iatrogenic Kaposi sarcoma is assocaited with which drugs?

A

Calcineurin

413
Q

What is the most common types of Kaposi sarcoma in the US?

A

AIDS associated

414
Q

What are the three stages of Kaposi sarcoma on the skin?

A

1) Patch stage: red/purple macules
2) Plaques: red, thickened
3) Tumor: nodule formation

415
Q

What is seen on the histology of the patch stage of Kaposi sarcoma?

A

Dilated channels containing blood with small hyperchromatic nuclei

416
Q

What is seen on the histology of the plaque stage of Kaposi sarcoma?

A

Infiltrative proliferation of spindled endothelial cells and irregular vascular channels

417
Q

What is seen on the histology of the tumor stage of Kaposi sarcoma?

A

Nodule mass of spindled cells

418
Q

What is a malignant tumor of vascular origin?

A

Angiosarcoma

419
Q

What are the risk factors for liver angiosarcoma?

A

Arsenic
Thorotrast
Polyvinyl chorlide (PVC)

420
Q

What is arsenic used for?

A

Agricultureal pesticides
Treatment of wood as a preservative pesticide
Well water

421
Q

What is thorotrast used for?

A

Radioactive compound that was utilized as a radiocontrast agent for imaging

422
Q

PVC is what?

A

Synthetic plastic polymer

423
Q

When can lymphadema predispose someone to lymphangiosarcoma?

A

Lymphedema after axillary dissection such as in a radical mastectomy procedure for breast cancer

424
Q

Radiation therapy can induce mutations which cause what years after initial therapy?

A

Angiosarcoma

425
Q

What does angiosarcoma look like histologically?

A

Well to poorly defined vascular spaces often containing RBCs lined by endothelial cells with cytologic atypia

426
Q

What stains do angiosarcomas show?

A

CD31

CD34

427
Q

When is percutaneous coronary intervention used?

A

Significant coronary artery disease including patients who have had acute coronary syndrome including ST elevation MI, non-ST elevation MI, and unstable angina

428
Q

What are the two types of coronary intervention for significant stenosis by atherosclerotic plaque?

A

Balloon angioplasty

Endovascular stenting

429
Q

What is given immediately after coronary metallic stents?

A

Antithromboti drugs

430
Q

1/3 of patients with traditional metal stents what occurs?

A

Restenosis

431
Q

What drives the in-stent restenosis?

A

Endothelial injury of the stent on the vessel which drives smooth muscle proliferation and matrix synthesis (drug eluting stent in utilized to reduce local neointimal hyperplasia and proliferative in-stent restenosis

432
Q

What is the anti-restenotic drug used?

A

Siroliumus

433
Q

What does a balloon angioplasty do?

A

Compresses and rupture occluding plaque

Aburpt reclosure can result from thrombosis and spasm

434
Q

When are vascular grafts utlized?

A

Replace or bypass a vascular segment involved by significant atherosclerotic disease

435
Q

When are large synthetic grafts used?

A

When replacing large vessels like abdominal aortic aneurysm repair

436
Q

What are two examples of vascular grafts?

A

Coronary artery bypass grafts

Abdominal aortic aneurysm stent grafting

437
Q

What occurs in coronary artery bypass grafting?

A

Native arteries and/or veins are harvested and used to bypass the diseased atherosclerotic vessel

438
Q

Saphenous veins are easier to harvest and less technically demanding than internal mammary arteries by their failure is?

A

Higher

439
Q

What occurs in endovascular abdominal aortic aneurysm repaire?

A

Endovascular graft device is inserted usually using a femoral artery approach

440
Q

What is a CABG?

A

Coronary artery graft

441
Q

Which artery is used in a CABG?

A

Internal mammary artery

CPR 2 Exam 1 (20 decks)

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