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Cardiovascular 3 > Peripheral Venous Diseases > Flashcards

Peripheral Venous Diseases Flashcards

1
Q

The stasis of blood, hypercoagulability, and vascular damage are the 3 components to which triad?

A

Virchow’s triad

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2
Q

This is the condition when a DVT in a proximal vein in the lower extremity dislodges and travels to the lungs, obstructing the pulomary artery.

A

Pulomary embolism

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3
Q

True or False: there is a decrease in alveolar-arterial oxygen gradient in a PE.

A

False- it’s increased. you can inhale the O2 fine but can’t get it in the blood cuz of the blockage.

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4
Q

The increase in these mediators make things worse in a PE by causing vasoconstriction in the vasculature.

A

Vasoactive + bronchoconstrictive mediators

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5
Q

The increased resistance in the pulomary system leads to the increased stress in which heart chamber?

A

RV

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6
Q

This is the syndrome from a venous valvular damage and/or persistent occlusion from a DVT, which may lead to chronic leg swelling, stasis pigmenetation and skin ulcerations.

A

Postphelbitic syndrome

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7
Q

This is teh condition where there is unilateral leg swelling, edema, localized warmth + erythemia, and tenderness.

A

DVT

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8
Q

What are the radiological tests u can perform to screen for a DVT?

A

ultrasound + D-dimer

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9
Q

What is the % sensitivity in screening for a DVT in a proximal leg vein?

A

95%

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10
Q

What is the % sensitivity in screening for a DVT in a calf vein?

A

75%

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11
Q

Which scan can u do to Dx a pelvic vein thrombus?

A

MRI

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12
Q

Which leads show an inverted T waves on EKG with a PE?

A

V1-4 (from RV strain) or S1-Q3-T3 (waves in each leads)

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13
Q

Which lab marker is elevated in PE, which is released dur to RV stain?

A

BNP

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14
Q

This is the test to confirm the Dx of a PE, given that the pt can tolerate the contrast.

A

CT angiography

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15
Q

What do u do if the pt cannot tolerate the contrast to Dx a PE?

A

do a VQ scan

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16
Q

Which 2 drugs can u give for the anticoagulation Tx of a DVT?

A

heparin IV bridged to coumadin

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17
Q

How long is the pt on coumadin for the Tx of a PE after Dx?

A

3-6 months.

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18
Q

What is the thing u can surgically put into the vein to “catch” the DVT if the pt cannot take anticoagualnts?

A

intravascular filter

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19
Q

Which 2 drugs can u give for the prophylaxis of a PE?

A

LMWH (or UFH) and low dose oral warfarin

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20
Q

These are abnormally dilated, tortuous veins from prolonged increase in tinraluminal pressure and loss of vessel wall support.

A

Varicose veins

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21
Q

WHy can liver cirrhosis cause esophageal varices and hemorrhoids?

A

from portal vein HTN –> opening of the porto-systemic shunts that increase blood flow to the veins

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22
Q

Where does 90% of thrombophlebitis (phlebothrombosis) occur in the body?

A

Deep leg veins

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23
Q

What is the biggest risk factor for thrombophlebitis?

A

prolonged immovilization

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24
Q

What is the biggest and most serious complicaiton to thrombophlebitis?

A

PE

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25
Q

This is the syndrome from neoplasma that compres or invade the SVC, leading to dilation of the veins of the head, neck and arms with cyanosis.

A

SVC syndrome

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26
Q

If the IVC is compressed (in IVC syndrome), by neoplasms, what happens in the lower legs and urine?

A

edema, distention of the veins in the lower abdomen, and massive proteinuria.

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27
Q

This is acute inflammation of the lymphatics, tpyically from bacterial spread.

A

Lymphangitis

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28
Q

What is the most common bacteria to cause lymphangitis?

A

Beta hemolytic strep.

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29
Q

What are the specific Sx to lymphangitis?

A

red, painful subQ streaks, painful enlargement of the lymph nodes.

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30
Q

This is the condition where there’s an increase in the hydrostatic pressure in the lymphatics from a distal obstruction, leading to increased interstitial fluid accumulation.

A

Lymphadema

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31
Q

What is the specific skin coloration to lymphadema?

A

Orange peel appearance.

32
Q

If we call a condition a “primary lymphadema,” waht must be the causitive agent?

A

GENETICS. Like you have an isolated defect like in the familial Milroy disease, which causes lymphatic agenesis or hypoplasia.

33
Q

And if we call a condition a “secondary lymphadema,” what must be the causitive agent?

A

BLOCKAGE. Like a tumor, surgery, fibrosis, filariasis, or thrombosis.

34
Q

These are very common tumors, characterized by increased numbers of normal or abnormal vessels filled with blood.

A

Hemangiomas

35
Q

Where in the body are hemangiomas typically found?

A

Head or neck

36
Q

This type of hemangioma is the most common subtype, typically occur in the mouth and lips, and include juvenile hemangiomas.

A

Capillary hemangiomas

37
Q

This type of hemangioma involves large dilated vascular channels, typically in deep structures, and can be destructive, which is why if it’s int he brain its no bueno.

A

Carvernous hemangioma

38
Q

This type of capillary hemangioma is a rapidly growing pedunculated rednodule on the skin or gingival mucosa, and typically occur after trauma.

A

Pyogenic granuloma

39
Q

Where can pregnant women get pyogenic granulomas, which typically regress after pregnancy?

A

Gingiva

40
Q

These are benign lymphatic analogues of blood vessel hemangiomas.

A

lymphangiomas

41
Q

This type of lymphangioma is made of small lymphatic channels, occur mainly in the head region, and have NO RBC’s.

A

Simple (capillary) lymphangioma

42
Q

This type of lymphangioma is typically in the neck or axilla of children, common in Turners, can be pretty effin big, and are composed of massivly dilated lymphatic spaces lined by endothelial cells and separated by interveining connective tissue stroma containing lymphoid aggregates.

A

Cavernous lymphangioma (cystic hygroma)

43
Q

These are the tumors that make big men cry because they are exquisitely painful tumors under the fingernails arising from modified SM cells of the glomus body.

A

Glomus tumor (glomangioma)

44
Q

These are common lesions characterized by local dilation of preexisting vessels. They are NOT true neoplasms.

A

Vascular ectasias

45
Q

This is a term used for a congenital anomaly or acquired exaggeration of preformed bessels in the skin, composed of capillaries, venules, and arterioles, that creates a discrete red lesion.

A

Telangiectasias

46
Q

This is a flat lesion on the head, ranging from light pink-purple, typically called a “birthmark”

A

Nevus flammeus

47
Q

This is a form of nevus flemmus which occurs on the head, thickens the skin, doesnt fade, and is deeply purple.

A

Port wine stain

48
Q

Lesions in a trigeminal nerve distribution can cause these angiomatous masses in the cortical leptomeninges in the cortical leptomeninges and ipsilateral facial port wine nevi.

A

Sturge-Weber Syndrome

49
Q

These are non-neplastic vascular lesion on the face, neck, or upper chest, and commonly assocaited with hyper-estrogenic states like in pregnancy.

A

Spider telangiectasia

50
Q

This AD disorder is when telangiectasias are malformations of dilated capillaries and veins, spread all over the body, and can rupture, causing nosbleeds, GI bleeds, or hematuria.

A

Hereditatary Hemorrhagic Telangiectasia (Osler-Weber-Rendu disease)

51
Q

This is a vascular proliferation resulting from an opportunistic infection in immunocompromised pts, typically involving the skin, bone, brain, and other organs.

A

bacillary Angiomatosis

52
Q

What are the 2 bugs that can cause Bacillary Angiomatosis?

A

Batronella Henselae (from cats) or B. Quintana (trench fever, from lice)

53
Q

What types of pt’s usually get kaposi sarcoma (KS)?

A

AIDS

54
Q

Chronic KS is typically found in what patient demographic?

A

Ashkenazi Jews

seriously these people get everything

55
Q

Is chronic KS associated with AIDS?

A

Nope.

56
Q

What is the morphology of the nodules in chronic KS?

A

multiple red to purple skin plauqes or nodules, usually in the distal or lower extremities.

57
Q

Lymphadenopathic KS has the same general geographic distribution as what type of cancer?

A

Burkitt lymphoma

58
Q

Lymphadenopathic KS is prevalent among what patient demographic?

A

South African Bantu children

59
Q

Is lymphadenopathic KS assocaited with HIV?

A

No

60
Q

What are the clinical manifestations of lymphadenopathic KS?

A

sparse skin lesions, lymphadenopathy, tumors in the viscera and are very aggressive.

61
Q

THis type of KS is from solid organ trasnplantation.

A

Transplant-associated KS (lolefn 9egnwrgiwnrg)

62
Q

What are the very bad clinical manifestations of transplant-associated KS?

A

very aggressive, nodule, mocosal, and visceral involvement, can be fatal.

63
Q

How can u reduce the incidence of AIDS-assocaited KS in AIDS pts?

A

Antiretroviral therapy

64
Q

What is the main causitive agent in KS?

A

KS Herpesviridae

65
Q

True or false: KSHV is a lytic and latent infection in endothelial cells.

A

True!

66
Q

Which substances are derived from HIV-infected T cells or inflammatory cells to cause local proliferation in the infection?

A

Cytokines

67
Q

In latent infected cells, KSHV proteins disrupt normal cellular proliferation and prevent apoptosis by disrupting which intracellular regulator?

A

p53 and producing a viral homologue of cyclin D

68
Q

Are most cases of KSHV asymptomatic?

A

yes

69
Q

What type of therapy can u use to get rid of the lesions?

A

surgery, radiation, or chemo.

70
Q

This is a wide SPECTRUM of vascular neoplasms, and an intermediate between benign, well-differentiated hemangiomas, and highly manlignant angiosarcomas.

A

Hemangioendothelioma

71
Q

This type of hemangioendothelioma is a vascular tumor of adults around medium-sized arteries and large veins.

A

Epithelioid Hemangioendothelioma

72
Q

These are malignant endothelial neoplasms that resemble hemangiomas, occur in older adults, and often involve the skin, soft tissue, breast, and liver.

A

Angiosarcomas

73
Q

These are rare tumors from the pericytes and commonly involves the lower extremities and retroperitoneum.

A

Hemangiopericytoma

74
Q

What is the morphology of hemangiopericytomas?

A

numerous branching capillary channels and gaping sinusoidal spaces enclosed within spindle shaped cells.

75
Q

What % of hemangiopericytomas metastisize?

A

50% toi lungs, bone, or liver.

Cardiovascular 3 (8 decks)

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