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CPR Exam 1 > Infectious Vasculitis > Flashcards

Infectious Vasculitis Flashcards

1
Q

Direct invasion of what agents may cause infectious vasculitis?

A

Pseudomonas
Aspergillus
Mucor

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2
Q

What is the general pathogenesis of infectious vasculitis?

A

Vascular invasion as part of localized tissue infection, or less commonly hematogenous spread

Septicemia or embolization from infective endocarditis

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3
Q

What conditions may result from infectious vasculitis?

A

Mycotic aneurysms = vascular infections weaken arterial walls
Thrombosis
Infarction

Inflammation induced thrombosis of meningeal vessels in bacterial meningitis can eventually cause infarction of underlying brain tissue

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4
Q

What are the DOs of blood vessel hyperreactivity?

A

Raynaud phenomenon

Myocardial vessel vasospasm

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5
Q

Describe what Raynaud Phenomenon is generally.

A

Excessive vasospasm of small arteries and arterioles, especially fingers and toes
“red, white, and blue” = proximal vasodilation, central vasoconstriction, and distal cyanosis

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6
Q

Describe Primary Raynaud Phenomenon.

A

Induced by cold or emotion; symmetric involvement of digits
Estimated 3-5% general population; YOUNG WOMEN
BENIGN course

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7
Q

Describe Secondary Raynaud Phenomenon.

A

Component of another arterial disease (SLE, scleroderma, thromboangiitis obliterans)
Asymmetric involvement of digits
Worsens with time

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8
Q

Describe Myocardial vessel vasospasm.

A

Excessive vasoconstriction of myocardial arteries or arterioles (“cardiac Raynaud”) - may cause ischemia or infarct

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9
Q

What is the pathogenesis behind Myocardial vessel vasospasm?

A

High levels of vasoactive mediators can precipitate prolonged myocardial vessel contraction

Usually caused by circulating vasoactive agents, which may be endogenous (epinephrine, pheochromocytoma), or exogenous (cocaine)

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10
Q

What is the outcome of Myocardial vessel vasospasm?

A

Sudden cardiac death

Takotsubo cardiomyopathy = “broken heart syndrome”, associated with emotional distress

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11
Q

What are varicose veins?

A

Abnormal dilation of veins with valvular incompetence, secondary to sustained intraluminal pressure

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12
Q

What Sx may you see with varicose veins?

A

Stasis, congestion, thrombus, edema, pain and ischemia of overlying skin (stasis dermatitis)

Poor wound healing and superimposed infections are common complications

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13
Q

Where do embolisms generally form in regards to varicose veins?

A

Embolism from thrombi of superficial lower extremity veins are RARE

They are more likely to form as DVTs (deep vein thrombosis)

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14
Q

What are esophageal varices? Why are they clinically important?

A

Portal HTN (often due to cirrhosis) opens portosystemic shunts which direct blood to veins at the gastroesophageal junction

Clinically important cause they may rupture

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15
Q

Portal HTN causes esophageal varies. What other conditions may it lead to?

A

Hemorrhoids = rectum

Caput medusa = periumbilical veins

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16
Q

What happens in caput medusae in relation to the abdominal wall?

A

In portal HTN, the umbilical vein (normally obliterated at birth) can dilate

Blood shunted from periumbilical veins –> umbilical vein –> abd wall

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17
Q

What are hemorrhoids?

A

Dilation of the venous plexus at the anorectal junction

Extremely common, and cause pain, bleeding, ulcers

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18
Q

What is thrombophlebitis?

A

Venous thrombosis and inflammation

Almost always (>90%) involves deep veins in the legs - can be completely asymptomatic

Pulmonary embolism is a serious consequence

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19
Q

What are the risks for DVT?

A

Single most important = prolong inactivity/immobilization

Systemic hypercoagulability

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20
Q

What is migratory thrombophlebitis?

A

Trousseau sign

Pts with cancer may experience hypercoagulability as a paraneoplastic syndrome

Particularly seen with mucin-producing adenocarcinomas (mucin through to be thrombogenic) = Associated with adenocarcinomas of lung, ovary, pancreas

Classic case - appear to one site, disappear, reappear elsewhere

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21
Q

What is Superior vena cava syndrome?

A

Neoplasms compress or invade SVC (bronchogenic carcinoma, mediastinal lymphoma, or aortic aneurysm)

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22
Q

What Sx does SVC syndrome produce?

A

Obstruction produces a characteristic clinical complex:

  • Marked dilation of veins of head, neck, and arms w/ cyanosis
  • Pulmonary vessels can also be compressed –> respiratory distress
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23
Q

What is inferior vena cava syndrome?

A

Neoplasms that compress or invade IVC or thrombosis of the hepatic, renal, or lower extremity veins that propagates cephalad

Hepatocellular carcinoma and renal cell carcinoma = tend to grow within veins, can ultimately occlude the IVC, and extend into the right atrium

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24
Q

What Sx does IVC syndrome produce?

A

IVC obstruction induces: Marked lower extremity edema
Distension of the superficial collateral veins of lower abd
Renal involvement –> massive proteinuria

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25
Q

What is lymphangitis?

A

Acute inflammation and spread of bacterial infection into lymphatics

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26
Q

What is the most common agent of lymphangitis?

A

Group A B-hemolytic streptococci

27
Q

What Sx do you see with lymphangitis?

A

Red, painful subcutaneous streaks (inflamed lymphatics)

Painful enlargement of draining LN (lymphadenitis)

Can progress to cellulitis and focal abscesses; or bacteremia and sepsis

28
Q

What is primary lymphedema?

A

Isolated congenital defect, of familial Milroy Dz (lymphatic agenesis or hypoplasia)

29
Q

What is secondary or obstructive lymphedema?

A

Blockage of previously normal lymphatics

Ex: from Malignant tumor, surgical procedures (radical mastectomy with axillary node dissection), post irradiation fibrosis, filariasis, post inflamm thrombosis or scarring

Chylothorax, chylous ascites, chylopericardium

30
Q

What is peau d’ orange (orange peel)?

A

Seen with secondary or obstructive lymphedema

Skin overlying breast cancer, draining lymphatics clogged with tumor cells

31
Q

Describe vascular tumors, benign and malignant.

A

Benign tumors:
-Produce obvious vascular channels filled with blood cells lined by a monolayer of normal-appearing endothelial cells

Malignant tumors:

  • More cellular, more proliferative
  • Exhibit cytologic atypia
  • Do not form well-organized vessels
  • Endothelial derivation of neoplastic proliferations that don’t form distinct vascular lumina can usually be confirmed by immunohistochemical demonstration of endothelial cell-specific markers such as CD31 or vWF
32
Q

What is ectasia?

A

Any local dilation of a structure

33
Q

What is telangiectasia?

A

Permanent dilation of preexisting small vessels that form a discrete RED lesion - usually in the skin or mucous membranes

Congenital or acquired, not true neoplasms

Malformations or hamartomas

34
Q

What is Nevus Flammeus?

A

Birthmark
Most common form of vascular ectasia
Light pink to deep purple flat lesion of head or neck composed of dilated vessels
Most regress spontaneously

35
Q

Describe a Port wine stain.

A

Form of nevus flammeus

Grow during childhood, thicken, and don’t fade

Such lesions in distribution of trigeminal nerve = Sturge-Weber syndrome

Ipsilateral venous angiomas in the cortical leptomeninges, mental retardation, seizures, hemiplegia, skull radio-opacities

36
Q

What is Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu disease)?

A

Autosomal dominant DO cause by mutation in genes that encode components of TGF-B signaling pathway

Malformations composed of dilated capillaries and veins that are present at birth

Lesions spontaneously rupture, causing epistaxis, GI bleeding, hematuria

Widely dist. over skin and oral mucous membrane + resp, GI, and GU tract

37
Q

What are the benign vascular tumors?

A

Capillary hemangioma
Cavernous hemangioma
Pyogenic granuloma

Cavernous lymphangioma (Cystic hygroma) 
Simple (capillary) lymphangioma

Glomus tumor

Nevus flammeus
Spider telangiectasia
Hereditary hemorrhagic telangiectasis

Bacillary angiomatosis

38
Q

What is a hemangioma? Where are the common sites? What happens with congenital hemangiomas?

A

Common tumors; localized increase in neoplastic blood vessels

Common sites = skin & mucous membranes of head & neck, and in liver

Congenital hemangiomas often regress

39
Q

What is a capillary hemangioma?

A

Most common

Thin-walled capillaries, tightly packed together

40
Q

What is a cavernous hemangioma?

A

Irregular, dilated vascular channels making a lesion with an indistinct border

More likely to involve deep tissue, more likely to bleed

41
Q

What is a pyogenic granuloma (lobular capillary hemangioma)?

A

Type of capillary hemangioma (not pyogenic, not a granuloma)

Rapidly growing, often in oral mucosa (may ulcerate); 1/4 dev following trauma

Granuloma gravidarum (pregnancy tumor): gingiva of pregnant women

42
Q

What is a simple lymphangioma?

A

Appear very similar to capillary hemangiomas, but w/o RBCs

Subcutis of head/neck and axillae

43
Q

What is a cavernous lymphangioma cystic hydroma)?

A

Neck or axilla of children

Can be large (up to 15 cm)

Large cavernous lymphangiomas of the neck seen in turner syndrome

44
Q

What is a Glomus tumor?

A

Aka Glomangioma, paraganglioma

Benign tumors arising from glomus bodies, and most often appear in distal fingers

Of smooth muscle origin rather than endothelial

PAINFUL

45
Q

What is bacillary angiomatosis?

A

Vascular proliferation in response to gram (-) Bartonella bacilli

Occurs on the skin of immunocompromised patients

  • lesions are localized, forming red papules
  • micro = proliferation of capillaries with plump endothelial cells
  • bacteria can be identified with PCR, or visualized with a Warthin-Starry stain
  • macrolide abx are effective
46
Q

What are the Intermediate-Grade (Borderline) vascular tumors?

A

Epithelioid hemangioendothelioma

Kaposi Sarcoma

47
Q

What is Epithelioid Hemangioendothelioma?

A

Neoplastic endothelial cells are plump and cuboidal, resemble epithelium

Vascular channels may be difficult to recognize

Variable clinical behavior, with metastasis in 20-30%

48
Q

What is Kaposi Sarcoma caused by?

A

HHV8

49
Q

What are the 4 distinct clinical forms of KS?

A

Aids-associated KS
Classic KS
Endemic African KS
Transplant-assoc KS

50
Q

What is AIDS-associated KS?

A

Most common form seen in US

Most common AIDS-related malignant tumor

May spread to lymph nodes and viscera

51
Q

What is classic KS?

A

Older men from middle eastern, Mediterranean, or eastern European descent

Not associated with HIV

Tumors localized to skin

52
Q

What is endemic African KS?

A

Not associated with HIV.

Pts <40

Can involve lymph nodes

53
Q

What is transplant-associated KS?

A

Not associated with HIV, but with T-cell immunosuppression

Can spread to LN and viscera

54
Q

What are the malignant vascular tumors?

A

Angiosarcoma

Hemangiopericytoma

55
Q

What is a Angiosarcoma? Who does it affect more? How can it be induced?

A

Malignant endothelial tumor

Age = older, M=F

Can be induced by radiation exposure; can arise in setting of lymphedema (upper extremity after radial mastectomy)

56
Q

What is hepatic angiosarcoma associated with?

A

Arsenic, pesticides, thorotrast (contrast agent), polyvinyl chloride

57
Q

Where do angiosarcomas occur? What is the survival rate?

A

May occur anywhere, but most common sites = skin, soft tissue, breast, and liver (CD31 marker)

Locally invasive and may metastasize

5 yr survival around 30%

58
Q

What is the pathology behind vascular intervention?

A

Therapeutic intervention that injures the endothelium also tends to induce intimal thickening by recruiting smooth muscle cells promoting extracellular matrix deposition, analogous to atherosclerosis

59
Q

What are types of endovascular stenting?

A

Balloon angioplasty
Coronary stents
Drug-eluting stents

60
Q

What is a balloon angioplasty?

A

Rupture of occluding plaque
Limited dissection produced

Abrupt reclosure can result form extensive dissection; thus 90% of angioplasties are followed by stent placement

61
Q

What is a coronary stent?

A

Expandable tubes of metallic mesh

Due to endothelial injury may induce thrombosis

Long term = proliferative in-stent restenosis (1/3 pts within 6-12 mo)

62
Q

What are Drug-eluting stents? What are the drugs?

A

Leach antiproliferative drugs to block smooth muscle activation

Decrease restenosis at 1 yr by 50-80%

Paclitaxel and Sirolimus

63
Q

What are vascular replacements?

A

Synthetic or autologous vascular grafts

Synthetic large bore works for aorta, but small bore fail due to thrombosis or intimal hyperplasia at junction of the graft with the native vasc.

64
Q

What can you use for small bore grafts (coronary arteries)?

A

Saphenous vein = 50% patency at 10 yrs

Left internal mammary arteries = 90% patency at 10 yrs

CPR Exam 1 (11 decks)

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