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CPR 2 Cardiac Section > Vascular Pathology > Flashcards

Vascular Pathology Flashcards

1
Q

What characteristic of the vessels has the most influece on pressure within the vessel?

A

-the radius

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2
Q

What is an arteriovenous malformation?

A

-a connection between arteries and veins w/o intervening capillaries

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3
Q

What happens when there are large or multiple arteriovenous malformations (AVM’s) that are shunting blood from arterial to venous circulation?

A

–forces the heart to pump additional volume, which leads to high-output cardiac failure

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4
Q

What are some injurious causes of AVM’s?

A
  • rupture of an arterial aneurysm into an adjacent vein
  • penetrating injury that pierce arteries and veins
  • inflammatory necrosis or adjacent vessels
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5
Q

In what population are AVM’s most commonly diagnosed?

A
  • men

- late childhood or early adulthood

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6
Q

When would an AVM be medically indicated and surgically created?

A

-an arteriovenous fistula to provide access for chronic hemodialysis or chemotherapy

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7
Q

What is a Berry (Saccular) Aneurysm and where are they typically found?

A
  • focal, abnormal arterial dilation d/t underlying media defect
  • Circle of Willis near the branch of the Anterior Cerebral A. and the Anterior Communicating A. (40%)
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8
Q

What are major risk factors of a Berry Aneurysm?

A
  • HTN

- smoking

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9
Q

What conditions are associated with Berry Aneurysms?

A
  • AD PKD
  • Marfan Syndrome
  • Ehlers Danlos Syndrome
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10
Q

What is the most common cause of subarachnoid hemorrhages?

A

-Berry Aneurysm rupture

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11
Q

What causes Berry Aneurysm rupture?

A
  • acute increases in intracranial pressure

ex: straining w/ BM’s or orgasms

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12
Q

How would a patient present with a ruptured Berry Aneurysm?

A
  • “worst headache of my life”
  • neck pain
  • vomiting
  • double vision
  • seizures
  • loss of consciousness
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13
Q

What are possible causes of a Mycotic Aneurysm?

A
  • septic emboli (ex: from infective endocarditis)
  • could be an extension of adjacent infectious process or from circulating organisms that directly infect the arterial wall
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14
Q

What is Fibromuscular Dysplasia?

A

–focal, irregular thickening in medium and large muscular arteries (ex: RENAL, carotid, splanchnic, etc.)

–likely a developmental etiology (high incidence in first-degree relatives)

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15
Q

What is the most common population to be affected by Fibromuscular Dysplasia?

A

-young women

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16
Q

What does Fibromuscular Dysplasia look like on angiography and what would you find on physical exam?

A
  • “string of beads”

- epigastric abdominal bruit d/t renovascular HTN caused by Fibromuscular Dysplasia (present in 50%)

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17
Q

What level of blood vessels regulates peripheral vascular resistance?

A
  • arterioles

- influenced by neural and hormonal factors

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18
Q

What is the main cause of primary HTN?

A

–90-95% idiopathic (essential HTN)

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19
Q

What are risk factors of HTN?

A

Unmodifiable Risk Factors: age, genetics (ex: blacks have increased risk)

Modifiable Risk Factors: stress, obesity, physical inactivity, high salt consumption

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20
Q

What are some causes of secondary HTN?

A
  • kidney (renovascular disease, renal A. stenosis)
  • endocrine (pheochromocytoma)
  • cardiovascular (coarctation of the aorta)
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21
Q

How is the category of severity determined for HTN?

A

-whichever number is higher

ex: 144/86 would be Stage 2
S144 = Stage 2
D86 = Stage 1

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22
Q

What are the categories of severity of HTN?

A 
Normal S<120 and D<80 (ex: 116/76)
Elevated S120-129 and D<80 (ex: 124/76)
Stage 1 S130-139 or D80-89 (ex: 134/84)
Stage 2 S140+ or D90+ (ex: 146/96)
HTN Crisis S>180 and/or D>120 (ex: 184/124)
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23
Q

What is Primary Hyperaldosteronism?

A

-HTN w/ hypokalemia

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24
Q

What causes Cushing Syndrome (which is an endocrine-related cause of secondary HTN)?

A
  • tumor secretes ACTH, which increases cortisol secretion (pituitary or adrenal tumor, lung cancer, etc.)
  • iatrogenic (ex: steroids)
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25
Q

What are clinical characteristics of Cushing Syndrome?

A
  • “moon face” and increased facial hair growth
  • weight gain in neck, back, and belly
  • weak muscles in upper arms and legs
  • skin bruises easily and heals poorly
  • stretch marks
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26
Q

What is Pheochromocytoma (an endocrine-related cause of secondary HTN)?

A
  • tumor of chromaffin cells in the adrenal gland
  • releases epi/norepi to act on B1 and alpha1 receptor
  • increases cardiac output
  • constricts blood vessels
  • associated w/ MEN syndrome
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27
Q

What is the clinical presentation of Pheochromocytoma?

A
  • HTN
  • tachycardia, palpitations
  • headache
  • diaphoresis
  • tremor
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28
Q

How do you test for Pheochromocytoma?

A

-elevated urinary or plasma metanephrines (breakdown product of catecholamines)

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29
Q

What are the characteristics of Renal A. Stenosis (a renal cause of secondary HTN)?

A
  • could be d/t atherosclerosis
  • could be d/t Fibromuscular Dysplasia
  • HTN decreases GFR and causes chronic kidney Dz
  • increased creatinine
  • can hear an abdominal bruit
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30
Q

What are characteristics of Coarctation of the Aorta (a CV cause of secondary HTN)?

A
  • associated w/ bicuspid aortic valves
  • more common in men
  • HTN in the upper extremities
  • htn in the lower extremities
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31
Q

What are the end organ effects of HTN on the heart and aorta?

A
  • cardiac hypertrophy
  • chronic heart failure
  • ischemic heart disease
  • acute aortic dissection
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32
Q

What are the end organ effects of HTN on the kidney?

A

-renal dysfxn and failure

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33
Q

What are the end organ effects of HTN on the brain and eye?

A
  • -multi-infarct dementia
  • -cerebrovascular hemorrhage
  • -stroke
  • -increased intracranial pressure and papilledema
  • -retinopathy
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34
Q

What are the most common causes of death in untreated HTN patients?

A
  • 50% die of ischemic heart disease or heart failure

- 33% die of stroke

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35
Q

What is Hyaline Arteriolosclerosis (a HTN Vascular Dz)?

A

-homogenous pink hyaline thickening of the vessel wall, leading to a narrow lumen; CHRONIC HTN

  • increased smooth muscle matrix synthesis
  • increased leakage of plasma proteins
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36
Q

What other factor besides HTN might cause hyaline arteriosclerosis?

A

-side effect of calcineurin inhibitors

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37
Q

What is hyaline nephrosclerosis?

A

-arteriolar narrowing leads to impaired renal blood supply and ischemic glomerulosclerosis

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38
Q

Is a HTN crisis the result of a slow or rapid rise in BP?

A
  • rapid

- systolic >180; diastolic >120

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39
Q

What is a HTN Emergency?

A

–HTN crisis w/ end organ damage (often superimposed on pre-existing benign HTN)

-renal failure, encephalopathy, acute heart failure, retinal hemorrhages/exudates +/- papilledema

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40
Q

What is Hyperplastic Arteriolosclerosis (a HTN Vascular Dz)?

A
  • smooth muscle forms concentric lamellations (“onion skinning”) that cause a narrow lumen
  • occurs in SEVERE HTN
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41
Q

In malignant HTN, what else is seen besides lamellations that are seen in Hyperplastic Arteriolosclerosis?

A

-fibrinoid deposits and vessel wall necrosis (particularly in the kidney)

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42
Q

What is atherosclerosis?

A
  • “gruel” and “hardening”
  • atheromatous plaque formation
  • stenosis/occlusion
  • plaque rupture
  • aneurysm
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43
Q

What is Monckeberg Medial Sclerosis?

A
  • -age-related degenerative process
  • -calcification of muscular arteries (internal elastic membrane)

–no narrowing of lumen; not clinically significant

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44
Q

True or False: MI’s are responsible for almost 25% of all deaths in the US and is the number 1 cause of mortality

A

True

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45
Q

What are major non-modifiable risk factors for atherosclerosis?

A
  • genetic abnormalities (multifactorial inheritance)
  • family history
  • increasing age (40-60’s)
  • male sex
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46
Q

True or False: premenopausal estrogenized women have an increased risk of atherosclerosis

A

False; there is a Protective Effect against atherosclerosis

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47
Q

What are major modifiable risk factors for atherosclerosis?

A
  • hyperlipidemia
  • HTN
  • cigarette smoking
  • diabetes
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48
Q

What increases LDL?

A
  • animal products

- trans fat (fried foods, snack foods)

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49
Q

What decreases LDL?

A
  • soluble fiber

- statins (inhibit HMG CoA reductase which makes LDL)

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50
Q

What increases HDL?

A
  • exercise

- moderate alcohol consumption

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51
Q

What decreases HDL?

A
  • obesity

- smoking

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52
Q

What is the physiological process behind how cigarette smoking increases risk of atherosclerosis?

A
  • cigarette smoking increases free radicals and ROS
  • ->causes endothelial dysfxn
  • ->causes platelet activation
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53
Q

What is the physiological process behind how diabetes increases risk of atherosclerosis?

A

-increased glucose causes oxidative stress, which causes inflammation

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54
Q

How does the endothelium respond to turbulent flow, HTN, cigarette smoking, etc.?

A
  • becomes activated (pro-thrombotic, pro-inflammatory)
  • expresses procoagulants
  • expresses adhesion molecules
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55
Q

What is the structure of plaque?

A
  • rests against the internal elastic membrane
  • necrotic ctr (cell debris, cholesterol crystals, calcium)
  • fibrous cap (macrophages, lymphocytes, collagen)
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56
Q

Where do most atherosclerotic lesions forms?

A
  • areas of flow disturbance or branch points

- near endothelial injury/dysfxn

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57
Q

What growth factors cause smooth muscle cell proliferation and collagen deposition (ECM)?

A
  • -PDGF (by platelets, macrophages, endothelial cells)
  • -fibroblast GF
  • -TGF-alpha
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58
Q

Which vessel in the body is the most heavily involved with atherosclerosis?

A

-abdominal aorta

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59
Q

What is the definition of an aneurysm?

A

-an excessive localized abnormal dilation of a blood vessel or ventricular wall

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60
Q

What is the difference between a true aneurysm and a false aneurysm?

A

A true aneurysm has an intact vessel wall

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61
Q

What causes Marfan Syndrome?

A
  • mutation in the FBN1 fibrillin gene

- increased TGF-B causes elastic tissue weakening

62
Q

What are clinical features of Marfan Syndrome?

A
  • aortic aneurysm and dissection
  • flexible joints
  • tall, thin, w/ disproportionately long legs, arms, digits
  • intraocular dislocation
  • pectus carinatum or excavatum
63
Q

What are clinical features of Ehlers Danlos Syndrome?

A
  • hyperelastic fragile skin
  • joint hypermobility
  • abnormal wound healing
  • mitral valve prolapse
64
Q

What causes Ehlers Danlos Syndrome?

A

-mutation in collagen

65
Q

What are the clinical manifestations of tertiary syphillis caused by T. pallidum?

A
  • can affect brain, skin, organs, and CV system
  • obliterative endarteritis of vasa vasorum
  • thoracic aneurysm
  • aortic valve regurge (diastolic decrescendo murmur)
  • aorta w/ rough, pitted, tree bark appearance
66
Q

What is the primary risk factor of a AAA?

A

-atherosclerosis

67
Q

What is the at-risk population for a AAA?

A

-male smokers >50yrs old

68
Q

Where is the most typical location of a AAA?

A
  • below the renal arteries

- above the aortic bifurcation

69
Q

What is the clinical presentation of a (symptomatic) AAA?

A
  • pulsatile abdominal mass
  • abdominal pain, back pain

-if ruptured … severe acute pain and htn

70
Q

At what size is a AAA considered for surgical repair?

A

–5 cm (3-15% risk of rupture)

71
Q

What are significant features of the Inflammatory Type of AAA?

A
  • IgG4
  • T lymphocytes
  • fibroinflammatory infiltrate weakens wall
  • responds to steroids
  • prominent fibrosis
72
Q

What is the primary risk factor of a Thoracic Aortic Aneurysm?

73
Q

What is the clinical presentation of a Thoracic Aortic Aneurysm?

A

-symptoms are d/t compression of adjacent structures

  • breathing difficulties (respiratory tree)
  • dysphagia (esophagus)
  • cough (recurrent laryngeal nerve)
74
Q

What is an aortic dissection?

A

–intimal tear w/ blood-filled channel separating media

–can progress to rupture (excruciating anterior CP)

75
Q

What is the clinical triad of an aortic dissection?

A
  • thoracic pain
  • pulse abnormalities
  • mediastinal widening on CXR
76
Q

What are the causes of an aortic dissection?

A
  • HTN (especially in men ages 40-60)

- connective tissue disorders (Marfan, Ehlers Danlos)

77
Q

Where is the aortic dissection most common?

A
  • proximal to the L common carotid A.
  • -Debakey Type 1
  • -Type A
78
Q

What are the characteristics of Giant Cell (Temporal) Arteritis?

A
  • -most common vasculitis in older adults (>50yrs) in US
  • -affects temporal, vertebral, and opthalmic aa.
  • -important to Dx b/c vision loss can occur
  • -T-cell mediated autoimmune response
  • -Dx by temporal A. biopsy (anti-endothelial, ASMA Ab’s)
79
Q

What is Takayasu Arteritis?

A
  • granulomatous autoimmune vasculitis of large-to-medium arteries in certain HLA types
  • more common in younger adults (<50yrs)
80
Q

What is the clinical presentation of Takayasu Arteritis?

A

-thickened aorta and major branch vessels
(pulmonary, coronary, renal)

  • weak upper extremity pulses
  • ocular disturbances
81
Q

What are the characteristics of Polyarteritis Nodosa?

A
  • -systemic vasculitis of small-to-medium vessels
  • -young adults (33% have Hep B)
  • -immune-complex mediated
  • -commonly involves renal vessels and the GI tract
  • -classic presentation = rapidly accelerating HTN
82
Q

What is Kawasaki Disease (Mucocutaneous Lymph Node Syndrome)?

A
  • -infancy or early childhood
  • -large-to-medium vessels (prefers coronary A.)
  • -infectious (viral) trigger w/activated T-cells
83
Q

What is the clinical presentation of Kawasaki Disease (Mucocutaneous Lymph Node Syndrome)?

A
  • fever
  • “strawberry tongue”
  • conjunctivitis
  • erythema of palms and soles
  • cervical lymphadenopathy
84
Q

What are the fatal complications of Kawasaki Disease (Mucocutaneous Lymph Node Syndrome)?

A
  • MI
  • coronary A. rupture

-must treat with IVIG within the first 10 days of symptoms

85
Q

What is Churg-Strauss Syndrome (Allergic Granulomatosis and Angiitis)?

A

-small vessel necrotizing vasculitis associated w/ asthma, hypereosinophilia, and lung infiltrates

86
Q

What does the inflammation of Churg-Strauss Syndrome resemble?

A
  • Polyarteritis Nodosa or Microscopic Polyangiitis

- -w/ the addition of eosinophils and granulomas

87
Q

What disease marker is present in Churg-Strauss Syndrome (Allergic Granulomatosis and Angiitis)?

A
  • -MPO-ANCA mostly

- -less than half have ANCA

88
Q

What is the clinical presentation of Churg-Strauss Syndrome (Allergic Granulomatosis and Angiitis)?

A
  • palpable purpura
  • GI tract bleeding
  • renal disease (glomerulosclerosis)

-myocardial involvement (cardiomyopathy/myocarditis and infarction) in 60% of patients

89
Q

What accounts for almost half of the deaths in Churg-Strauss Syndrome?

A

-cardiomyopathy/myocarditis and infarction

90
Q

What is Granulomatosis w/ Polyangiitis (Wegner’s Granulomatosis?

A

–small-to-medium vessel necrotizing granulomatous vasculitis of respiratory tract (pneumonitis, sinusitis)

91
Q

What are the characteristics of Granulomatosis w/ Polyangiitis (Wegner’s Granulomatosis)?

A

+/- necrotizing renal pathology
(necrotizing crescentic glomerulonephritis)

  • -males, 40’s, T-cell mediated hypersensitivity rxn
  • -PR3-ANCA (c-ANCA)
92
Q

What are the clinical symptoms of Granulomatosis w/ Polyangiitis (Wegner’s Granulomatosis)?

A
  • lungs: cavities, bleeds, lung infiltrates
  • nose: congestion, nosebleeds, saddle nose
  • kidneys: glomerulonephritis
93
Q

What is Microscopic Polyangiitis?

A

-necrotizing vasculitis of small vessels (arterioles, capillaries, venules) of any organ system, especially the kidneys and lungs

94
Q

What are the characteristics of Microscopic Polyangiitis?

A
  • -uniform disease stage activity in all vessels
  • -MPO-ANCA
  • -no significant immunoglobulin deposition in lesions
95
Q

What are the clinical symptoms of Microscopic Polyangiitis?

A
  • hematuria, proteinuria
  • hemoptysis
  • cutaneous purpura
  • muscle weakness
  • bowel pain and bleeding
96
Q

What are the characteristics of Behcet’s Disease

A
  • -small-to-medium vessel NEUTROPHILIC vasculitis
  • -associated w/ HLA-B51

Tx: steroids

97
Q

What is the classic clinical triad of Behcet’s Disease?

A
  • oral aphthous ulcers
  • genital ulcers
  • uveitis

-often presents w/ arthritis

98
Q

What is Thromboangiitis Obliterans (Buerger Disease)?

A
  • segmental, thrombosing, acute and chronic vasculitis of small and medium vessels (particularly tibial and radial arteries)
  • luminal necrosis and granulomatous inflammation
99
Q

What population is at risk for Thromboangiitis Obliterans (Buerger Disease)?

A

-heavy smokers, <35yrs

100
Q

What are the characteristics of Thromboangiitis Obliterans (Buerger Disease)?

A
  • -hypersensitivity or toxic rxn to cigarettes
  • -anti-endothelial Ab’s

–affects HLA haplotypes of certain ethnic groups (Israeli, Indian, Japanese)

101
Q

What is the disease process of Thromboangiitis Obliterans (Buerger Disease) and the progression of symptoms?

A
  • thrombosis —> vascular insufficiency —> tissue death

- Raynaud’s Phenomenon —> intermittent claudication —> severe pain at rest —> ulceration —> gangrene

102
Q

What are the characteristics of Raynaud’s Phenomenon?

A
  • vasospasm of small arteries and arterioles (especially fingers and toes) induced by cold or emotion
  • “red, white, and blue” (proximal vasodilation, central vasoconstriction, and distal cyanosis)
103
Q

What are the characteristics of Primary Raynaud’s Phenomenon?

A
  • symmetric involvement of the digits
  • young women
  • episodic
  • spontaneous remission
104
Q

What are the characteristics of Secondary Raynaud’s Phenomenon?

A
  • asymmetric involvement of digits that worsens w/ time

- a component of other arterial diseases (SLE, scleroderma, thromboangiitis obliterans)

105
Q

What are some causes of myocardial vascular contraction?

A
  • high levels of vasoactive mediators
  • -exogenous (cocaine, caffeine)
  • -endogenous (epinephrine)
  • elevated thyroid hormones
  • -increased sensitivity to catecholamines
  • autoantibodies and T cells in scleroderma
106
Q

What is Takotsubo Cardiomyopathy (“Broken Heart Syndrome”)?

A

-sudden surge of catecholamines w/ emotional distress

—> stimulates cardiac muscle cells, triggers constriction and causes ischemic cardiomyopathy or cardiac death

107
Q

What are the characteristics of varicose veins?

A
  • sustained intraluminal pressure leads to valvular incompetence
  • stasis, thrombus, edema, pain, ischemia of overlying skin (stasis dermatitis), poor wound healing, superimposed infection
108
Q

What is the risk of thrombi from superficial veins vs. risk of thrombi from deep veins?

A

-risk of thrombi from superficial veins is rare

109
Q

What are the characteristics of portal HTN?

A
  • venous HTN, most commonly d/t cirrhosis
  • esophageal varices, hemorrhoids, caput medusae
  • splenomegaly
110
Q

What are the clinical symptoms of Superior Vena Cava Syndrome?

A

-venous dilation in head, neck, chest wall, and arms (with cyanosis)

  • facial swelling, neurologic manifestations
  • respiratory distress if pulmonary vessels compressed
111
Q

What could be causes of Superior Vena Cava Syndrome?

A

-neoplasms (lung carcinoma, lymphoma)

112
Q

What could be causes of Inferior Vena Cava Syndrome?

A

-neoplasms (hepatocellular carcinoma, renal cell carcinoma, or thomosis such as a DVT)

113
Q

What are the clinical symptoms of Inferior Vena Cava Syndrome?

A
  • lower extremity edema

- distention of superficial lower abdominal veins

114
Q

What are the clinical characteristics of Thrombophlebitis?

A
  • venous thrombosis and inflammation
  • typically in deep veins of the leg
  • edema, cyanosis, erythema, pain
  • serious consequence: PE
115
Q

What are the risk factors of Thrombophlebitis?

A
  • prolonged inactivity/immobilization
  • hypercoagulable states (factor mutations, estrogen)

-tumor (thrombotic paraneoplastic syndrome, migratory thrombophlebitis); pancreatic or lung carcinoma

116
Q

What are the characteristics of Lymphangitis?

A
  • -inflammation of lymphatic channels
  • -common cause: Group A B-hemolytic strep
  • -inflamed lymphatics (painful red streaks)
117
Q

What is Lymphadenitis?

A

-painful enlargement of draining lymph nodes

118
Q

What are the characteristics of Primary Lymphedema?

A

-congenital defect

-familial Milroy Disease
lymphatic agenesis or hypoplasia

119
Q

What are the characteristics of Secondary Lymphedema?

A
  • -blockage of previously normal lymphatics
  • -causes: tumor, surgery, post-irradiation fibrosis

–peau d’orange (draining lymphatics of skin overlying breast cancer are filled w/ tumor cells)

120
Q

What are examples of vascular ectasias?

A
  • -nevus simplex
  • -port-wine stain
  • -Sturge-Weber Syndrome
121
Q

What are characteristics of a nevus simplex (a type of vascular ectasia)?

A
  • the most common type of vascular ectasia
  • simple birthmark (~50% of infants)
  • common sites: forehead, eyelid, nose, upper lip
  • ectatic vessels in upper dermis
  • most regress
122
Q

What are characteristics of a Port-Wine Stain (nevus flammeus)?

A
  • progressive ectasia of vascular plexus
  • rare (0.3% of newborns)
  • persist into adulthood
123
Q

What are characteristics of Sturge-Weber Syndrome?

A
  • -trigeminal n. port-wine stain
  • -mental retardation, seizures, hemiplegia
  • -leptomeningeal capillary-venous malformation
  • -skull radio-opacities
  • -eye abnormalities (esp. glaucoma)
124
Q

What is a telangectasia?

A

-a permanent dilation in small vessels and capillaries forming a discrete lesion

125
Q

What are the characteristics of a spider telangectasia?

A
  • central red papule w/ radial red lines
  • face, neck, and upper chest
  • can be induced by increased circulating estrogen
  • -(pregnancy, liver disease)
126
Q

What are the characteristics of Hereditary Hemorrhagic Telangectasia (Osler-Weber-Rendu Disease)?

A
  • autosomal dominant
  • mutation in TGF-B signaling pathway
  • abnormal vessels in skin, mucus membranes, organs
  • telangectasias and AVM’s occur
  • Sx depend on location (nosebleeds, hematuria, etc.)
127
Q

What is a hemangioma?

A
  • common benign vascular tumor of children and adults
  • most common benign tumor in infants and children
  • frequently found on the head and neck
  • usually superficial, but may be internal (esp. liver)
128
Q

What is a Capillary Hemangioma?

A
  • -most common type
  • -skin, mucus membranes, viscera
  • -red spot
  • -thin-walled capillaries, tightly packed together
129
Q

What is a Congenital /Infantile/Juvenile Hemangioma (“Strawberry”)?

A
  • present at birth, usually regress

- subtype of capillary hemangioma

130
Q

What is a Cavernous Hemangioma?

A
  • irregular, dilated vascular channel w/ indistinct border
  • more likely to involve deep tissue
  • more likely to bleed
  • seen in VHL
131
Q

What is a Pyogenic Granuloma (Lobular Capillary Hemangioma)?

A
  • type of capillary hemangioma
  • rapidly growing, often in oral mucosa or on finger
  • may ulcerate
  • 25% develop after a trauma
  • gingiva of pregnant women
132
Q

What is a Glomus Tumor?

A

– well-circumscribed mesenchymal tumor (typically benign) of modified smooth muscle arising from glomus body responsible for thermoregulation

-bluish, painful, esp. w/ temperature changes

133
Q

Where is a Glomus Tumor commonly seen?

A
  • most commonly in upper extremity (esp. fingers)

- subungual location is common

134
Q

What is a Lymphangioma?

A
  • benign lymphatic neoplasm

- Two Types: Simple or Cavernous (Cystic Hygroma)

135
Q

What are the characteristics of a Simple Lymphangioma?

A
  • common in head and neck

- predilection for axillary region

136
Q

What are the characteristics of a Cavernous Lymphangioma (Cystic Hygroma)?

A
  • neck or axilla of children
  • large (up to 15 cm)
  • massively dilated lymphatic spaces
  • common in Turner Syndrome (also seen in Trisomy 21)
  • can be difficult to resect
137
Q

What is a Bacillary Angiomatosis

A
  • reactive vascular proliferation to Bartonella bacilli
  • -ex: B. henselae … Cat Scratch Fever
  • -ex: B. quintana … Trench Fever

-bacteria seen on Warthin Starry stain (silver stain)

138
Q

What are the characteristics of Bacillary Angiomatosis?

A
  • benign lesion
  • red papules
  • occurs in immunocompromised (HIV, transplant pts)
  • Tx: abx
139
Q

What is Kaposi Sarcoma?

A
  • -angioproliferative disorder caused by HHV-8
  • -intermediate grade (borderline) vascular tumor
  • -can affect lymph nodes, GI tract, and other organs
140
Q

What is the clinical presentation of Kaposi Sarcoma?

A

–red-purple nodules or plaques on lower limbs, genitals, face, and back

141
Q

What are the characteristics of Classic (Sporadic) Kaposi Sarcoma?

A
  • Mediterranean, Eastern European, or Middle Easterns
  • older men (3:1 M:F)
  • distal lower extremities
  • indolent
142
Q

What are the characteristics of Endemic (African) Kaposi Sarcoma?

A
  • -African children < 10 yrs
  • -lymph nodes +/- cutaneous involvement
  • -also cutaneous manifestations in adults
143
Q

What are the characteristics of Iatrogenic Kaposi Sarcoma (related to immunosuppression)?

A
  • -related to T-cell immunosuppression in transplant pts

- -may be widespread

144
Q

What are the characteristics of AIDS-associated Kaposi Sarcoma?

A
  • -most common type in the US
  • -most common type of AIDS-related malignancy
  • -disseminates
  • -widely aggressive course
145
Q

What are the stages of Kaposi Sarcoma?

A

1) Patch Stage - dilated channels w/blood and small hyperchromatic nuclei
2) Plaque Stage - infiltrative proliferation of spindle cells and irregular vascular channels
3) Tumor Stage - nodular mass of spindle cells

146
Q

What is angiosarcoma?

A
  • malignant vascular tumor
  • locally invasive
  • frequently metastasizes
147
Q

What are specific risk factors for angiosarcoma?

A
  • Liver: arsenic, thorotrast, PVC production
  • lymphedema s/p axillary LN dissection
  • radiation for carcinoma
148
Q

What are the characteristics of Balloon Angioplasty?

A
  • compresses and can rupture the occluding plaque

- abrupt reclosure can result from thrombosis or spasm

149
Q

What devices are used concomitantly with balloon angioplasty?

A

–metallic stents or drug-eluting stents

150
Q

What are the characteristics of metallic stents, which are an expandable metallic mesh?

A

–can cause endothelial injury and immediate thrombosis —> thus, antithrombolytic drugs are given

–long-term: proliferative in-stent restenosis in 33% of pts within 9 mos.

151
Q

What are the characteristics of drug-eluting stents?

A

–releases an anti-proliferative to block smooth muscle activation

–restenosis at 1yr is decreased by 65%

152
Q

What are the characteristics of vascular grafts?

A

-synthetic or autologous replacement or bypass of vessel (synthetic is only used in large vessels)

–long-term patency of saphenous v. = 50% at 10yrs

–long-term patency of internal mammary a. = 90% at 10yrs

CPR 2 Cardiac Section (6 decks)

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