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PATHO I > Vascular Disorders and Tumors > Flashcards

Vascular Disorders and Tumors Flashcards

1
Q
A
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1
Q

What is the endothelial cell marker for angiosarcoma?

A

CD31

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2
Q

What are the risk factors for hepatic angiosarcomas?

A

VAT
* Vinyl chloride
* Arsenic
* Thorotrast

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3
Q

What is the cause of Kaposi Sarcoma?

A

HHV-8 (Herpesvirus-8)

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4
Q

What is the most common HIV-related malignancy?

1000x higher increased risk

A

AIDS-associated (epidemic) KS

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5
Q

Endemic African KS is more common in what patient population?

A

Younger people

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6
Q

What type of bacteria is associated with Bacillary angiomatosis?

A

GNB

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7
Q

What specific bacteria is commonly found to cause Bacillary angiomatosis?

A

Bartonella henselae

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8
Q

How do GNB induce bacillary angiomatosis?

A
  • Bacteria cause host to produce HIF-1α
  • Drives VEGF production
  • Leads to vascular proliferation
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9
Q

Cavernous hemangiomas are associated with what other disease?

A

Hippel-Lindau disease (CNS)

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10
Q

What is the difference between a Cherry hemangioma and a Strawberry hemangioma?

A

Cherry hemangioma
* Adults, benign, do not regress

Strawberry hemangioma
* Newborns, extremely common, grow for months then regress; gone by 1-7 yo

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11
Q

Osler-Weber-Rendu Disease is also called?

A

Hereditary hemorrhagic telangiectasia

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12
Q

HHT shows what type of inheritance pattern?

A

Autosomal dominant

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13
Q

What signaling pathway is disrupted to lead to telangiectasias in HHT?

A

TGF-β signaling

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14
Q

A port wine stain is characteristic of which disease?

A

Sturge-Weber Syndrome

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15
Q

Sturge-Weber Syndrome occurs along the distribution of which nerve?

A

Trigeminal Nerve

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16
Q

S/Sx of Sturge-Weber Syndrome.

A
  • Facial port wine nevi (stain) along trigeminal nerve
  • Benign vascular tumor of arachnoid and pia mater (leptomeninges)
  • Mental retardation
  • Seizures
  • Glaucoma
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17
Q

What does -ectasia mean?

A

local dilation of a structure

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18
Q

Telangiectasia describes what? Is commonly seen in?

A
  • Permanent dilation of small vessels that form discrete red lesions
  • Spider telangiectasias are common to the face, neck, or upper chest
  • Most associated with hyperestrogenic states (e.g., pregnancy, cirrhosis)
19
Q

What is nevus flammeus?

A
  • Birthmark in a port-wine/flame coloration
  • Due to capillary malformations
  • Composed of dilated vessels
  • May deepen in color and usually will not fade
20
Q

What is the most common form of vascular ectasias?

A

Nevus flammeus

21
Q

Benign vascular tumors display what type of cell feature?

A

monolayer of normal-appearing endothelial cells

22
Q

What is the cause of lymphangitis?

A

Bacterial seeding of lymphatic vessels
* Inflamed lymphatics are red, painful SQ streaks
* Typically associated with tender enlargement of draining lymph nodes (acute lymphadenitis)

Can appear as ascending streaks as they go to center of body

23
Q

What is the difference between DVT and VTE?

A

DVT
* Formation of blood clots in deep vein, typically in LE

VTE
* Formation of blood clot in vein (e.g., DVT or PE)

24
Q

Why do DVTs go unrecognized?

A
  • In 50% of pts, they lead to pain and edema
  • However, in 50% they are asymptomatic due to venous collateral channels
25
Q

What is a rare post-partum DVT?

A

Pelvic venous plexus DVT

26
Q

Portal vein thrombosis can occur do to?

A
  • Peritoneal infections (peritonitis)
  • Appendicitis
  • Pelvic abscesses
27
Q

Trousseau Syndrome is associated with what type of vascular manifestation?

A

Thrombophlebitis migrans

28
Q

Thrombophlebitis is usually associated with what visceral cancers?

A
  • Pancreatic adenocarcinoma
  • Gastric adenocarcinoma
29
Q

How do visceral cancers (e.g., pancreatic or gastric adenocarcinomas) cause thrombophlebitis migrans?

A
  • Tumor releases mucin which reacts with platelets leading to microthrombi
  • Recurrent & migratory as it disappears and reoccurs elsewhere
30
Q

What does phlebitis mean?

A

Venous inflammation

31
Q

Venous thrombosis is accompanied by what?

A

Inflammation

32
Q

What are the 3 H’s of Virchow’s Triad?

A
  • Hypercoagulability
  • Venous stasis
  • Endothelial wall dysfunction/damage (vessel wall injury)
33
Q

What are characteristics of chronic venous insufficiency?

A
  • Leg swelling (edema)
  • Skin color and texture changes
  • Venous ulcers
34
Q

How does chronic venous insufficiency lead to ulceration?

A
  • Varicose veins –> Chronic venous congestion & poor vessel drainage
  • Leakage of Plasma proteins & edema –> decreased O2 supply –> hypoperfusion and hypoxia that leads to atrophy and ulceration (stasis dermatitis)
35
Q

How does skin dispigmentation occur in chronic venous insufficiency?

A

Extravasated RBCs –> degradation –> release of hemosiderin –> brown skin pigmentation: yellow-brown or red-brown

36
Q

What is the pathogenesis of varicose veins?

A

Prolonged venous pressure –> dysfunction of venous valves –> varicose veins

37
Q

What is the mechanism behind varicose veins seen in pregnancy?

A

Prolonged elevation of venous pressure caused by compression of inferior vena cava by the gravid uterus during pregnancy

38
Q

How does cocaine cause vasospastic angina?

A
  • Leads to increased SANS output
  • Increased HR, BP, contractility will lead to an increase of O2 demand
  • SANS leads to coronary spasm and vasoconstriction, thrombi formation leading to a decrease of O2 demand
  • Overall, SANS stimulation leads to ischemia, infarction, and possibly death
  • Cocaine also decreases Na+ transport leading to arrhythmia (QT & QRS prolongation) and decreased LV function
  • This leads to possible death
39
Q

What is stress cardiomyopathy?

E.g., Broken heart syndrome

A
  • Stress induced LV ballooning
  • Stress –> increased catecholamines –> increased HR & contractility –> vasospasm
  • Becomes “octopus trap”-like (e.g., Japanese Octopus Trap – Tako-Tsubo)
40
Q

What is prinzmetal angina?

A

Vasospasm of cardiac arterial or arteriolar beds that may lead to MI (if 20-30 mins duration)

41
Q

Vasospastic angina is a toxic effect of which drug?

A

Cocaine

42
Q

What is the basic histopathological difference between primary and secondary Reynaud’s (RP)?

A
  • Primary: normal capillaroscopic pattern
  • Secondary: abnormal capillaroscopic pattern with a **decrease in capillary density **
43
Q

Describe secondary RP.

A
  • ≥30 yo
  • secondary to other diseases (e.g., scleroderma, hyperviscocity, PAD, trauma, β-blockers, EPI, smoking)
  • Nail fold capillary exam is abnormal
  • digital ulceration, scarring, tissue death (gangrene)
  • asymmetric
44
Q

Describe primary RP.

A
  • < 30 yo
  • Idiopathic
  • Nail fold exam is normal
  • Digital arteries are commonly involved
  • Usually benign (w/o ulceration or necrosis)
  • Symmetric
45
Q

In primary RP what do the arteries and arterioles respond to?

A

Clear lines of demarcation to cold or emotional stress

PATHO I (8 decks)

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