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CPR Exam 1 > Infectious Vasculitis > Flashcards

Infectious Vasculitis Flashcards

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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
What is lymphangitis?
Acute inflammation and spread of bacterial infection into lymphatics
26
What is the most common agent of lymphangitis?
Group A B-hemolytic streptococci
27
What Sx do you see with lymphangitis?
Red, painful subcutaneous streaks (inflamed lymphatics) Painful enlargement of draining LN (lymphadenitis) Can progress to cellulitis and focal abscesses; or bacteremia and sepsis
28
What is primary lymphedema?
Isolated congenital defect, of familial Milroy Dz (lymphatic agenesis or hypoplasia)
29
What is secondary or obstructive lymphedema?
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
What is peau d' orange (orange peel)?
Seen with secondary or obstructive lymphedema Skin overlying breast cancer, draining lymphatics clogged with tumor cells
31
Describe vascular tumors, benign and malignant.
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
What is ectasia?
Any local dilation of a structure
33
What is telangiectasia?
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
What is Nevus Flammeus?
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
Describe a Port wine stain.
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
What is Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu disease)?
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
What are the benign vascular tumors?
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
What is a hemangioma? Where are the common sites? What happens with congenital hemangiomas?
Common tumors; localized increase in neoplastic blood vessels Common sites = skin & mucous membranes of head & neck, and in liver Congenital hemangiomas often regress
39
What is a capillary hemangioma?
Most common | Thin-walled capillaries, tightly packed together
40
What is a cavernous hemangioma?
Irregular, dilated vascular channels making a lesion with an indistinct border More likely to involve deep tissue, more likely to bleed
41
What is a pyogenic granuloma (lobular capillary hemangioma)?
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
What is a simple lymphangioma?
Appear very similar to capillary hemangiomas, but w/o RBCs Subcutis of head/neck and axillae
43
What is a cavernous lymphangioma cystic hydroma)?
Neck or axilla of children Can be large (up to 15 cm) Large cavernous lymphangiomas of the neck seen in turner syndrome
44
What is a Glomus tumor?
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
What is bacillary angiomatosis?
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
What are the Intermediate-Grade (Borderline) vascular tumors?
Epithelioid hemangioendothelioma Kaposi Sarcoma
47
What is Epithelioid Hemangioendothelioma?
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
What is Kaposi Sarcoma caused by?
HHV8
49
What are the 4 distinct clinical forms of KS?
Aids-associated KS Classic KS Endemic African KS Transplant-assoc KS
50
What is AIDS-associated KS?
Most common form seen in US Most common AIDS-related malignant tumor May spread to lymph nodes and viscera
51
What is classic KS?
Older men from middle eastern, Mediterranean, or eastern European descent Not associated with HIV Tumors localized to skin
52
What is endemic African KS?
Not associated with HIV. Pts <40 Can involve lymph nodes
53
What is transplant-associated KS?
Not associated with HIV, but with T-cell immunosuppression Can spread to LN and viscera
54
What are the malignant vascular tumors?
Angiosarcoma | Hemangiopericytoma
55
What is a Angiosarcoma? Who does it affect more? How can it be induced?
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
What is hepatic angiosarcoma associated with?
Arsenic, pesticides, thorotrast (contrast agent), polyvinyl chloride
57
Where do angiosarcomas occur? What is the survival rate?
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
What is the pathology behind vascular intervention?
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
What are types of endovascular stenting?
Balloon angioplasty Coronary stents Drug-eluting stents
60
What is a balloon angioplasty?
Rupture of occluding plaque Limited dissection produced Abrupt reclosure can result form extensive dissection; thus 90% of angioplasties are followed by stent placement
61
What is a coronary stent?
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
What are Drug-eluting stents? What are the drugs?
Leach antiproliferative drugs to block smooth muscle activation Decrease restenosis at 1 yr by 50-80% Paclitaxel and Sirolimus
63
What are vascular replacements?
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
What can you use for small bore grafts (coronary arteries)?
Saphenous vein = 50% patency at 10 yrs Left internal mammary arteries = 90% patency at 10 yrs

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