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CVM II > Vascular Part II > Flashcards

Vascular Part II Flashcards

1
Q

What is vasculitis and the clinical presentation?

A

Inflammation of vessels
Clinical presentation may depend on the location of the affected vessel, but pt frequently show nonspecific signs and symptoms
Fever, malaise,arthralgias, myalgias

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2
Q

How is vasculitis classified?

A

Infectious vs noninfectious

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3
Q

What is noninfectious vasculitis mediated by?

A

immunologic injury
Immune complex deposition or autoAbs

Immunosuppressive therapy needed

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4
Q

What is immune complex vasculitis and what may it be seen in?

A

Deposition of antigen-ab complexes in vascular walls

may be seen in SLE, drug hypersensitivity, secondary to exposure to infectious agent

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5
Q

What are antineutrophil cytoplasmic antibodies?

A

ANCA
heterogenous group of abs reactant with cytoplasmic enzymes found in neutrophil granules, monocytes, and endothelial cells
Activate neutrophils which release ROS

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6
Q

Anti-proteinase 3 or C-ANCA is directed against what?

A

Neutrophil azurophilic granule constituent

Associated with GPA or Wegener granulomatosis

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7
Q

What is anti-myeloperoxidase or p-ANCA directed against

A

Lysosomal constituent involved in generating oxygen free radicals
Seen in microscopic polyangiitis or Chur-Strauss syndrome

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8
Q

How are ANCAs useful?

A

Diagnostic markers for ANCA-associated vasculitides

Titers often mirror inflammation lvls so generally follow disease severity

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9
Q

What is giant cell arteritis?

A

also called temporal arteritis
Most common vasculitis in older pts
Focal granulomatous inflammation of medium and small aa
Chiefly cranial vessels, can involve aorta

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10
Q

What is the morphology of Giant cell arteritis?

A

chronic (T-cell) inflammation of aa in head, especially temporal arteries
Medial granulomatous inflammation
Multinucleated giant cells
Fragmentation of elastic lamia
Healed sites - scarring of media and intimal thickening

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11
Q

What arteries are involved in Giant cell arteritis?

A

Temporal
Cranial vessels
Opthalmic a (50%) –> vision loss
Aorta

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12
Q

What is the clinical presentation of temporal arteritis?

A

Presents with headache and facial pain

Systemic symptoms - flulike

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13
Q

How is giant cell arteritis diagnosed?

A

Surgical biopsy of temporal a of 1 cm

Sites of involvement may be patchy and focal

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14
Q

Treatment for giant cell arteritis ?

A

Steroids or antitumor necrosis factor therapy

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15
Q

What is Takayasu arteritis?

A

narrowing of lumen; vasculitis of aortic arch and major branch vessels
Pulseless disease
Pulmonary, coronary and renal aa may be involved
upper extremities pulseless

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16
Q

Giant cell arteritis typically seen in what pts?

A

50 and older

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17
Q

Describe a typical pt with Takayasu arteritis?

A

Weak pulse and low BP in upper extremities
Less than 50 y/o
ocular and neurologic disturbances
HTN occuring secondary to renal a disease

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18
Q

What are the histological features of Takayasu arteritis?

A

same as Giant cell arteritis but in a pt less than 50

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19
Q

What is Polyarteritis nodosa? PAN?

A

Systemic vasculitis
Immune complex mediated
Necrotizing vasculitis involving small-medium aa
No ANCAs

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20
Q

What vessels are involved in Polyarteritis nodosa (PAN)?

A 
renal vessels
Heart
Liver
GI tract
NOT pulmonary vessels
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21
Q

Describe a typically pt with PAN?

A

any age group, but classically young
1/3 have chronic hep B
(HBsAg-HBsAb)

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22
Q

What is usually effective in treating Polyarteritis nodosa?

A

Immunosuppressive therapy

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23
Q

Describe the lesions seen in Polyarteritis nodosa?

A

Transmural necrotizing inflammation - contains neutrophils, eosinophils, lymphocytes and Mo
Fibroid necrosis of vessel wall
Inflammation not circumferential
Thickened intima

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24
Q

In PAN, the inflamed vessel wall may become susceptible to what?

A

thrombus formation/occlusion -> ischemic
Aneurysm
Rupture

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25
Q

What is Kawasaki disease?

A

Acute arteritis of infants and small children (80% less than 4 yo)

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26
Q

What vessels does Kawasaki disease typically involve

A

Coronary arteries

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27
Q

What can Kawasaki disease lead to?

A

Affected sites may form aneurysms -> thrombosis or rupture -> acute MI

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28
Q

What is the presenting picture of Kawasaki disease?

A

Erythema of conjunctiva, oral mucosa, palms and soles
Rash
Cervical LN enlargement (mucocutaneous LN syndrome)

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29
Q

What is the treatment for kawasaki disease?

A

Usually self-limited.

IVigs and aspirin are indicated to lower risk of cornonary event

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30
Q

What is Microscopic polyangiitis?

A

Necrotizing vasculitis involving arterioles, capillaries and venules

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31
Q

What vessels are affected in microscopic polyangiitis?

A

Vessels of many organ systems

Renal glomeruli and lung capillaries most common

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32
Q

What are commonly associated with Microscopic polyangiitis?

A 
Necrotizing glomerulonephritis (90%) and pulmonary capillaritis
MPO-ANCA
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33
Q

Describe the histologic findings of Microscopic polyangiitis

A

Segmental necrotizing inflammation with fibrinoid necrosis

Many apoptotic neurtrophils w/i and around vessel walls (leukocytoclastic vasculitis)

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34
Q

What can improve long-term survival w Microscopic polyangiitis?

A

Cyclosporine and steroids

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35
Q

What is Churg-Strauss syndrome?

A

Small vessel necrotizing vasculitis

Associated with Athma, allergic rhinitis, hyereosinophilia, lung infiltrates, extravascular granulomas

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36
Q

What is Churg-Strauss syndrome associated with that sets it apart from PAN or m. polyangiitis?

A

Eosinophils, granulomas, asthma, allergic rhinitis

Less than half show ANCA positivity

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37
Q

What is the cause of mortality in pts with Churg-Strauss syndrome? What possibly causes this?

A

Many organ systems may be involved but eosinophilic infiltrates are implicated in cardiomyopathy that develops in 60% of pts
Cardiac involvement -> death in approx half of pts

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38
Q

What is Behcet disease

A

Vasculitis of small-medium vessels w the additional findings:
Aphthous ulcers of oral cavity
Genital ulcers
Uveitis

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39
Q

What is the typical triad that presents with Bechet disease?

A

Apthous ulcers of the oral cavity
Genital ulcers
Uveitis

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40
Q

Describe vessel inflammation in Bechet disease

A

neutrophilic and morhpologically nonspecific

May involve visceral organ systems with subsequent aneurysm formation

41
Q

What is the marker for Microscopic polyangiitis

A

MPO-ANCA

42
Q

What is the marker for Bechet disease?

A

HLA-B51

43
Q

What is mortality related to in a pt with Bechet disease?

A

Sever neurologic involvement or rupture of vascular aneurysms

44
Q

What is effective i the treatment of Bechet disease?

A

Steroids or TNF-antagonist therapies

45
Q

What is Granulomatosis with polyangiitis?

A

GPA or Wegener granulomatosis

Necrotizing vasculitis

46
Q

What triad comes with Granulomatosis with polyangiitis?

A

Necrotizing granulomas of the upper and lower respiratory tracts
Necrotizing or granulomatous vasculitis, most prominently in respiratory tract
Focal necrotizing, often crescentic, glomerulonephritis

47
Q

What is the marker for Granulomatosis with polyangiitis?

A

PR3-ANCA - 95%

48
Q

What is the Tx for granulomatosis with polyangiitis?

A

Immunosuppressive therapy
Cyclophosphamide, steroids, and TNF antagnonists
*untreated, 80% mortality in one year

49
Q

What are the clinical features of granulomatosis with polyangiitis?

A

Male, 40 yo

Persistent pneumonitis and sinusitis, renal disease, and nasopharyngeal ulceration

50
Q

What is the morphology of granulomatosis with polyangiitis?

A

Upper respiratory tract: Sinonasal and pharyngeal inflammation with granulomas and vasculitis
LRT: multple necrotizing granulomas, may coalesce and cavitate

51
Q

What is thromboangiitis obliterans?

A

Acute and chronic thrombosing vasculitis of small and medium vessels
Tibial arteries
Radial arteries

52
Q

Describe a pt with thromboangiitis obliterans

A 
Young adult 
Smokers 
Vasculitis in distal extremities
Spasms 
Vascular insufficiency of extremities
53
Q

What is the morphology of thromboangiitis obliterans?

A

Acute lesions: neutrophilic infiltrates with mural thrombi and containing microabscesses, ofthen with giant cell formation
Secondary involvement of adjacent vein and nerve

54
Q

What are the symptoms of a pt with thromboangiitis obliterans?

A

Nodular phelbitis
Raynaudlike cold sensitivity
Leg claudiction
Vascular insufficiency –> pain even at rest, skin ulcers, and ultimately gangrene

55
Q

What is Raynaud?

A

Excessive vasospasm of small arteries and arterioles

Fingers and toes

56
Q

What are the symptoms of Raynaud?

A

pain
pallor
Cyanosis
Prlonged vasospasm -> tissue necrosis

57
Q

What is primary Raynaud?

A 
induced by cold or emotion
Symmetric involvement of digits
3-5% general population
Young women
Benign course
58
Q

What is secondary raynaud phenomenon?

A 
Component of another arterial disease such as 
SLE
Scleroderma
Thromboangiitis obliterans
Asymmetric involvement of digits 
Worsens with time
59
Q

What is myocaardial vessel vasospasm?

A

Excessive vasoconstriction of myocardial aa or arterioles
Cardiac raynaud
Histo: contraction band necrosis

60
Q

Myocardial vessel vasospasm may cause what?

A

ischemia or infarct
sudden cardiac death
Fatal arrhythmia
Ischemic dilated cardiomyopathy

61
Q

What is myocardial vessel vasospasm caused by?

A

circulating vasoactive agents, which may be endogenous
Epinephrine - release by pheochromocytomas Increased sensitivity of vessels to catecholamines - Thyroid hormone
Increased caatecholamine - extreme psycological stress

62
Q

What are varicose veins?

A

Abnormal dilation of veins with valvular incompetence, secondary to sustained intraluminal pressure
Stasis, congestion, throbus, edema and ischemia of overlying skin (stasis dermatitis)

63
Q

Varicose veins are common with what type of pts?

A

10-30% of adults
Obesity and pregnancy increase risk
Hereditary venous defects
Prolonged standing

64
Q

What are esophageal varices caused by?

A

Portal HTN (often due to cirrhosis) opens portosystemic shunts. Blood directed to veins at gastroesphageal junction, rectum (hemorrhoids), and periumbilicus (caput medusa)

65
Q

Why are esophageal varices clinically important?

A

they may fatally rupture

Called exsanguination

66
Q

what are hemorrhoids?

A

dilation of venous plexus at anorectal junction
Extremely common
Pain, bleeding and may ulcerate
Secondary to pregnancy and chronic constipation

67
Q

What is thrombophlebitis?

A

Venous thrombosis and inflammation

68
Q

What does thrombophelbitis almost always involve?

A

> 90% deep veins in the legs

Can be asymptomatic

69
Q

What leads to increased risk of DVT in LE ?

A

prolonged inactivity

Systemic hypercoagulability - Factor V leiden

70
Q

What is Trousseau sign?

A

migratory thrombophlebitis
Malignancy-associated hypercoagulability
Pts w cancer may experience hypercoagulability as a paraneoplastic syndrome

71
Q

What is Trousseau sign often seen with?

A

mucin-producing adenocarcinomas
Mucin - thrombogenic
Adenocarcinomas of lung, ovary, pancreas

72
Q

What is the classic case of Trousseau sign?

A

Venouts thromboses appear at one site, disappear, and reappear at a different site

73
Q

What are hemangiomas?

A

Common benign tumor showing localized increase in neoplastic blood vessels
Sites: skin, mucous membranes of head/neck and liver

74
Q

Describe capillary hemangioma

A

Most common
Skin, mucous membranes
Unencapsulated
Thin-walled capillaries, tightly packed together

75
Q

Congenital (juvi/strawberry) hemangiomas

A

Variant of capillary hemangioma
Present at birth
Grows rapidly then begins to regress at 1-3 years

76
Q

Describe cavernous hemangioma

A

Irregular, dilated vascular channels making a lesion with an indistinct borer
Unencapsulated
Skin, liver, CNS
DO NOT REGRESS
thrombosis, and dystrophic calcification common
More likely to bleed

77
Q

Describe Pyogenic granuloma

A 
Lobular capillary hemangioma 
Not pyogenic or granuloma 
Ulcerated polypoid variant 
Proliferating capillaries 
Rapidly growing, often oral mucosa - ulcerate
78
Q

What is a simple lymphangioma?

A

Benign lymphatic analog of hemangiomas
No RBCs
Subcutis of head/neck and axillae
Exudate-filled, blisterlike blebs composed of small lymphatic channels

79
Q

What is a cavernous lympangioma?

A 
Cystic hygroma
Neck or axilla of children 
Can be large 
Seen in Turner syndrome 
Simple surgical resection difficult 
Dilated lymph vessels
80
Q

What is a glomus tumor?

A 
Benign tumors arising from glomus bodies (thermoregulation),
Distal fingers 
Smooth muscle origin 
PAINFUL 
Excision curative
81
Q

What is a Bacillary angiomatosis?

A

Vascular proliferation in response to gran negative Bartonela bacilli
Lesions localized, forming red papules
Proliferation of capillaries with plump endothelial cells
Occurs in immunocompromised

82
Q

How can bartonella bacilli be identified?

A

PCR or visualized with Warthin-Starry stain

83
Q

What is an effective treatment for Bacillary angiomatosis?

A

Macrolide antibiotics

84
Q

What is epithelioid hemangioendothelioma

A 
Neoplastic endothelial cells 
Plump and cuboidal - resemble epithelium
Vascular channels difficult to recongize
Metastasisin 20-30% 
Variable clinical behavior
85
Q

What is Kaposi sarcoma?

A

Vascular tumor caused by HHV8

86
Q

What is AIDS-associated KS

A

Most common form seen in US
Most common AIDS related malignant tumor
May spread to LN and viscera
Occur anywhere in skin and mucous membranes, LN, GI tract or viscera

87
Q

What is Chronic/Classic KS?

A

Older men from middle eastern
Mediterranean or eastern european descent
NOT associated with HIV
Tumor localized to skin
Ashkenasi jew
Red purple cutaneous plaques and nodules on LE

88
Q

What is African/edemic KS?

A

Not associated with HIV
Pts younger than 40
Can involve LN
Cutaneous lesions are sparse, can be aggressive

89
Q

What is Transplant-associated KS?

A

Not associated with HIV
T cell immunosuppression
Can spread to LN and viscera can be aggressive and fatal

90
Q

Describe patches

A

Pink-purple, usally confined to distal LE

Dilated, irregular EC-lined spaces, interspersed lymphocytes, plasma cells, an Mo

91
Q

Describe raised plaques

A

Dilated, jagged vascular channels lined by plump spindle cellsaccompanied by perivascular aggregates

92
Q

Describe nodular lesions

A

neoplasic
LN and visceral involvement
African and AIDS associated diseases
Plump spindle-shaped cells, slitlike vascular spaces filled with erythrocytes

93
Q

Describe angiosarcoma

A 
Malignant endothelial tumor 
Older; m=f
May occur anywhere
Common: skin, soft tissue, breast, liver
Locally invasive and may metastasize
5 year survival around 30%
Chronic lymphedema can develop, ipsilateral arm years after radical mastectomy for breast cancer 
Dilated lymphatic vessels
94
Q

What would best confirm angiosarcoma?

A

CD31

95
Q

What is vascular ectasis?

A

Common lesions characterized by local dilations of preexisting vessels; they are not true neoplasms
Nexus flammeus
Spider telangiectassis
Hereditary hemorrhagic telangiexcasia

96
Q

What is Nevis flammeus?

A

Birthmark
Macular cutaneous lesion that show only dermal vessel dilations; most regress
Port wine stain: variant that persist and grow along w child
Sturge-weber syndrome: port-wine stain + leptomeningeal angiomatous masses, mental retardation, seizures, hemiplegia, and skull radiopacities

97
Q

What are spider telangiectasis?

A

Minute subcutaneous arterioles, often pulsatile, arranged in radial fashion around a central core
Typically occur above the waist
Associated with hyperestrogenic states - pregnancy or cirrhosis

98
Q

What is hereditary hemorrhagic telangiexcasia?

A

Also older-weber-tendu disease
Rare, AD disorder caused by mutations in genes encoding components of the TGF-B signaling pathway
Multiple small aneurysmal telangiexcasia on skin and mucous membranes
Pts present with epistaxis, hemoptysis, or GI or GU bleeding

CVM II (4 decks)

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