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CPR Exam 1 > Blood Vessels Pt. 2 > Flashcards

Blood Vessels Pt. 2 Flashcards

1
Q

What are the most common vessels to be affected by vasculitis?

A

arterioles, capillaries and venuoles

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2
Q

What is the difference between non-infectious and infectious vasculitis?

A

infectious: immune mediated inflammation

- can indirectly induce a noninfectious vasculitis

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3
Q

What is the major cause of noninfectious vasculitis?

A 
immune response (local or systemic)
KNOW these:
- giant cell (teporal) arteritis
- polyarteritis nodosa (PAN)
- granulomatosis with polyangitis (Wegener granulomatosis)
- thromboangitis obliterans (Buerger dz)
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4
Q

What is immune complex vasculitis?

A

autoantibody production and formation of immune complexes

  • deposition of Ag-Ab complexes in vascular walls
  • seen in systemic immunologic diseases (SLE), and drug hypersensitivity (PCN acts as hapten binding to serum proteins, streptokinase acts as a foreign protein)
  • secondary exposure to infectious agent
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5
Q

What is Antineutrophil cytoplasmic antibodies (ANCA)?

A

a heterogeneous group of antibodies reactant with cytoplasmic enzymes found in neutrophil granules, monocytes and endothelial cells

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6
Q

What is PR3-ANCA?

A

anti-proteinase-3: associated with polyangiitis

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7
Q

What is MPO-ANCA?

A

anti-myeloperoxidase: induced by Rx, propylthiouracil

- associated with microscopic polyangiitis and Churg-Strauss syndrome

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8
Q

What do ANCAs do?

A

they activate neutrophils, which then release ROS

- “pauci-immune” due to ANCE Ab directed against cellular constituents and do NOT form circulating immune complexes

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9
Q

What is Giant cell (temporal) arteritis and aortitis?

A

most common vasculitis among older patients

  • may present with constitutional symptoms (fever, fatigue, wt loss), facial pain, headache
  • chronic T cell-mediated (CD4>CD8) inflammation of arteries in the head, especially temporal arteries
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10
Q

What happens in chronic inflammation of the arteries?

A
  • granulomatous inflammation, often with multinucleated giant cells
  • fragmentation of the elastic lamina and intimal thickening
  • sites of involvement within artery may be patchy and focal
  • double vision* or involvement of opthalmic artery may lead to vision loss -> hallmark
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11
Q

What is Takayasu arteritis?

A

characterized by ocular disturbances and marked weakening of pulses of upper extremities (pulseless disease is hallmark)

  • sx: weak pulse and low BP in upper extremities
  • granulomatous vasculitis of medium and larger arteries
  • similar histologically to giant cell arteritis EXCEPT”
    • > INVOLVES THE AORTIC ARCH (AORTITIS) AND MAJOR BRANCH VESSELS
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12
Q

What are the symptoms of Takayasu arteritis?

A

initially nonspecific
- later, vascular sx dominate: decrease in BP, weak carotid and UE pulses, visual deficits, renal hemorrhages, total blindness and neuro deficits
distal aorta sx: claudication (pain) in legs, pulm art -> pulm HTN, coronary art -> MI, renal art -> systemic HTN

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13
Q

What is Polyarteritis nodosa (PAN)?

A

systemic vasculitis, likely immune complex mediated

involves: renal vessels, heart, liver, GI tract
- > pulmonary vessels are spared

classically seen in young adults, 1/3 of pt have chronic hepatitis B*** (hallmark)
- HBsAg-HBsAb complexes are found in involved vessels

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14
Q

When do you see segmental transmural necrotizing inflammation?

A

In PAN. it has a predilection for branch points

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15
Q

What are the first signs of PAN?

A

ulcerations, infarcts, ischemic atrophy or hemorrhage

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16
Q

What are the inflamed vessel walls susceptible to in PAN?

A
  • thrombus
  • aneurysm
  • rupture
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17
Q

What is the classic presentation of PAN?

A

typically involves some combination of

  • rapidly accelerating HTN due to renal artery involvement
  • abdominal pain and blood stools caused by vascular gastrointestinal lesions
  • diffuse myalgias and peripheral neuritis mostly affecting motor nerves
  • renal involvement is often prominent and a major cause of mortality
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18
Q

What happens in PAN goes untreated?

A

Often fatal! Immunosuppression can yield remission or cure in 90% of cases

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19
Q

What is Kawasaki disease?

A

acute arteritis of infants and small children** (80% <4 y/o)

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20
Q

What is usually involved in Kawasaki disease?

A

coronary arteries

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

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21
Q

What are clinical findings in Kawasaki’s?

A
  • erythema of the conjunctiva, oral mucosa, palms and soles, desquamative rash
  • cervical lymph node enlargement “mucocutaneous lymph node syndrome”

NOTE: usually self-limiting, but IV-immunoglobulins and aspirin are indicated to lower risk of coronary event

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22
Q

What is microscopic polyangiitis?

A

necrotizing vasculitis involving arterioles, capillaries and venules

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23
Q

What is the difference between PAN and microscopic polyangiitis?

A

unlike PAN, all lesions of microscopic polyangiitis tend to be of the same age in any given patient and are distributed more widely

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24
Q

What vessels does microscopic polyangiitis affect?

A

vessels of many organ systems, but renal glomeruli and lung capillaries are most common (90% of necrotising glomerulonephritis)

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25
Q

What are most cases of microscopic polyangiitis associated with?

A

MPO-ANCA

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26
Q

What is seen histologically in microscopic polyangiitis?

A

segmental necrotizing inflammation with fibrinoid necrosis

  • usually see many apoptotic neutrophils
  • leukocytoclastic vastilitis, or hypersensitivity vasculitis
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27
Q

What are the major symptoms of microscopic polyangiitis?

A

hemoptysis, hematuria, proteinuria, bowel pain or bleeding, muscle pain or weakness, palpable cutaneous purpura

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28
Q

What is Churg-Strauss syndrome?

A

aka allergic granulomatosis and angiitis
- is small vessel necrotizing vasculitis associated with asthma, allergic rhinitis, hypereosinophilia, lung infiltrates, extravascular granulomas

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29
Q

What can the inflammation of Churg-Strauss resemble?

A

PAN or microscopic polyangiitis, with the addition of eosinophils and granulomas

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30
Q

What organ systems are involved in Churg-Strauss?

A

multisystem disease with cutaneous involvement (palpable purpura), GI tract bleeding, and renal disease
- myocardial involvement may give rise to cardiomyopathy, heart is involved in 60% of patients and accounts for half of deaths in the syndrome

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31
Q

What is Behcet disease?

A

vasculitis of small-medium vessels with classic triad of sx:

  1. aphthous ulcers (canker sores)
  2. genital ulcers
  3. uveitis (eye inflammation, reddening)
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32
Q

What HLA gene is Behcet associated with?

A

HLA-B51

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33
Q

What is disease mortality related to in Behcet disease?

A

severe neurologic involvement or rupture of aneurysms

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34
Q

What is granulomatosis with polyangiitis?

A

Aka Wegener granulomatosis, is a necrotizing vasculitis featuring:

  • necrotizing granulomas of upper/lower respiratory tracts
  • necrotizing or granulomatous vasculitis most prominently in the respiratory tract
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35
Q

How would you characterize necrosis of granulomatosis with polyangiitis?

A

focal necrotizing, often crescentic glomerulonephritis

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36
Q

What is granulomatosis with polyangiitis associated with?

A

PR3-ANCA (up to 96% of cases)

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37
Q

What is a form of T cell-mediated hypersensitivity response to normally “innocuous” inhaled microbial or environmental agents

A

granulomatosis with polyangiitis

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38
Q

What are the clinical features of granulomatosis with polyangiitis?

A

M>F, average age 40

sx: persistent pneumonitis and sinusitis, renal disease, nasopharyngeal ulceration
- rashes, myalgias, articular involvement, neural inflammation, fever

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39
Q

What happens is granulomatosis with polyangiitis is left untreated?

A

rapidly fatal, 80% mortality at one year

tx: steriods, cyclophosphamide, TNF agonists

40
Q

What is the morphology of granulomatosis with polyangiitis?

A
  • upper respiratory tract: sinonasal and pharyngeal inflammation with granulomas and vasculitis (granulomas with geographic patterns of central necrosis, accompanying vasculitis)
  • lower resp tract: multiple necrotizing granulomas, which may coalesce and cavitate**
41
Q

What is Thromboangiitis obliterans (Buerger disease)?

A
  • segmental, thombosing vasculitis of small and medium vessels
  • especially affects tibial and radial arteries
  • may lead to vascular insufficiency of the extremities (chronic ulcerations can lead to gangrene)
  • pt almost always heavy smokers, <35 y/o, most have hypersensitivity to intradermally injected tobacco products
42
Q

What ethnic groups are associated with Buerger disease?

A

Israeli, Indian subcontinent, Japanese

43
Q

What are the symptoms of Thromboangiitis obliterans?

A

** severe pain, even at rest**, chronic extremity ulcerations leading to gangrene

early manifestations: cold-induced Raynaud phenomenon, leg pain induced by exercise that is relieved on rest (intermittent claudication), instep foot pain, superficial nodular phlebitis (venous inflammation)

44
Q

What are the agents of direct invasion of infectious vasculitis?

A

pseudomonas, aspergillus, mucor

45
Q

Why are mycotic aneurysms a concern in infectious vasculitis?

A

because vascular infections weaken the arterial walls, or induce thrombosis/infarction

46
Q

What is the Raynaud phenomenon?

A

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

47
Q

What is Primary Raynaud phenomenon?

A

Aka Raynaud disease, induced by cold or emotion, symmetric involvement of the digits
- estimated 3-5% of population, young women, benign course

48
Q

What is secondary Raynaud phenomenon?

A

component of another arterial disease such as SLA, scleroderma, thromboangiitis obliterans, asymmetric involvement of digits
- worsens with time

49
Q

What is myocardial vessel vasospasm?

A

Aka cardiac Raynaud, is excessive vasoconstriction of myocardial arteries or arterioles that may cause ischemia or infarct

50
Q

What usually causes myocardial vessel vasospasm?

A

circulating vasoactive agents, which may be endogenous (Epi, pheochromocytoma), or exogenous (cocaine)

51
Q

What is the outcome of myocardial vessel vasospasm?

A

sudden cardia death or Takotsubo cardiomyopathy (broken heart syndrome, assoc with emotional distress)

52
Q

What causes varicose veins?

A

abnormal dilation of veins with valvular incompetence, secondary to sustained intraluminal pressure
- stasis, congestion, thrombus, edema, pain and ischemia of overlying skin (stasis dermatitis)

53
Q

What is rare to be seen in varicose veins?

A

embolism from thrombi of superficial lower extremity veins (unlike DVT, which is not rare to see)

54
Q

What is esophageal varices?

A

portal HTN (d/t cirrhosis) opens portosystemic shunts which direct blood to veins at the gastroesophageal junction

55
Q

Why are esophageal varices clinically important?

A

because they may fatally rupture

56
Q

What are hemorrhoids?

A

dilation of the venous plexus at the anorectal junction

- cause pain, bleeding, may ulcerate

57
Q

What is thrombophlebitis?

A

venous thrombosis and inflammation

- almost always (>90%) involves deep veins in the legs, can be complete asymptomatic

58
Q

What is the single most important risk factor for developing a deep venous thrombosis in the lower extremities?

A

prolonged inactivity/immobilization

NOTE: systemic hypercoagulability may also increase the risk of DVT

59
Q

What is the most serious potential consequence of thrombophlebitis?

A

pulmonary embolism

60
Q

What is migratory thrombophlebitis? (Trousseau sign)

A

patients with cancer may experience hypercoagulability as a paraneoplastic syndrome

61
Q

Where is Trousseau sign particularly seen?

A

mucin-producing adenocarcinomas (music thought to be thrombogenic)

62
Q

What is seen in a classic case of migratory thrombophlebitis?

A

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

63
Q

What is thrombophlebitis associated with?

A

adenocarcinomas of the lung, ovary and pancreas

64
Q

What is Superior Vena Cave syndrome?

A

neoplasms that compress of invade the SVC

- bronchogenic carcinoma, mediastinal lymphoma, or aortic aneurysm

65
Q

What is the characteristic clinical complex that SVC obstruction causes?

A
  • marked dilation of the veins of the head, neck and arms with cyanosis
  • pulmonary vessels can also be compressed -> respiratory distress***
66
Q

What is Inferior Vena Cava syndrome?

A

neoplasms that compress or invade the IVC, or thrombosis of the hepatic, renal or lower extremity veins that propagate cephalad

67
Q

What two types of carcinoma tend to grow in veins, occlude the IVC and extend into the right atrium?

A

Hepatocellular carcinoma and renal cell carcinoma

68
Q

What does IVC syndrome cause?

A

induces marked lower extremity edema, distention of the superficial collateral veins of the lower abdomen
- renal involvement -> massive proteinuria***

69
Q

What is lymphangitis?

A

accute inflammation and spread of bacterial infection into lymphatics

70
Q

What is the most common infectious agent of lymphangitis?

A

group A b-hemolytic streptococci

71
Q

What are the symptoms of lymphangitis?

A

red, painful subcutaneous streaks (inflamed lymphatics), and painful enlargement of draining LN (lymphadenitis)

72
Q

What specific markers are used to detect malignant tumors?

A

CD31 and von Willebrand factor

73
Q

What are hemangiomas?

A

common tumors, localized increase in neoplastic blood vessels

  • common sites include skin and mucous membranes of the head and neck, and in the liver
  • congenital (juvenile “strawberry”) hemangiomas often regress
74
Q

What is a capillary hengioma?

A

MOST COMMON, thin-walled capillaries, tightly packed together

75
Q

What is a cavernous hemangioma?

A

irregular, dilated vascular channels that make a lesion with an indistinct border
- more likely to involve deep tissue, more likely to bleed d/t larger vessel involvement

76
Q

What is a pyogenic granuloma?

A

Aka lobular capillary hemangioma

  • type of capillary hemangioma
  • rapidly growing, often in oral mucosa*** (may ulcerate), can develop following trauma
77
Q

What is a granuloma gravidarum?

A

tumor that develops in the gingiva of pregnant women

78
Q

What is a simple lymphangioma?

A

appear very similar to capillary hemangiomas, but WITHOUT RBCs
- subcutis of head/neck and axillae

79
Q

What is a cavernous lymphangioma?

A

Aka cystic hygroma, in the neck or axilla of children

- can be large, often seen in Turner syndrome***

80
Q

What is a Glomus tumor?

A

Aka glomangioma, paraganglioma

  • benign, painful tumor arising from glomus bodies (dermis layer of skin, but smooth muscle origin, not endothelial)
  • most often appear in distal fingers
81
Q

What is Bacillary angiomatosis?

A

a vascular proliferation in response to gram negative Bartonella bacilli

  • occurs on the skin of the immunocoprimised
  • lesions are localized, forming red papules
  • Tx: macrolide antiobiotics
82
Q

What does Bacillary angiomatosus look like histologically?

A

proliferation of capillaries with plump endothelial cells

83
Q

What histo stain is used to identify Bacillary angiomatosis?

A

Warthin-Starry stain

84
Q

What is epithelioid hemangioendothelioma?

A

neoplastic endothelial cells are plump and cuboidal, resembling epithelium. vascular channels may be difficult to recognize
- variable clinical behavior, with metastasis in 20-30%

85
Q

What causes Kaposi Sarcoma?

A

human herpesvirus 8

86
Q

What are the 4 distinct clinical forms of Kaposi Sarcoma?

A
  1. AIDS-associated KS
  2. Classic KS
  3. Endemic African KS
  4. Transplant-associated KS
87
Q

What is AIDS-associated KS?

A
  • Most common form in US
  • most common AIDS-related malignant tumor
  • may spread to lymph nodes and viscera
88
Q

What is classic KS?

A
  • older men from middle eastern, mediterranean or eastern european descent
  • NOT associated with HIV
  • tumors localized to skin
89
Q

What is Endemic African KS?

A
  • NOT associated with HIV
  • patients ,40
  • can involve lymph nodes
90
Q

What is Transplant-associated KS?

A
  • NOT associated with HIV, but with T-cell immunosuppression

- can spread to lymph nodes and viscera

91
Q

What is an angiosarcoma?

A

malignant endothelial tumor

  • can be induced by radiation exposure, can arise in setting of lymphedema (upper extremity after radical mastectomy)
  • may occur everywhere, but most common on skin, soft tissue, breast and liver
  • hard to treat, 5 year survival 30%
92
Q

What is associated with arsenic, pesticides, Thorotrast (contract agent) and polyvinyl chloride?

A

Hepatic angiosarcoma

93
Q

What is a balloon angioplasty?

A

rupture of occluding plaque, and limited dissection produced

- abrupt reclosure can result from extensive dissection, thus 90% of angioplasties followed by stent placement

94
Q

What are drug-eluting stents?

A

leach antiproliferative drugs to block smooth muscle activation
- just a temporary fix

95
Q

What vasculature is utilized in small bore grafts?

A

saphenous vein or left internal mammary arteries

CPR Exam 1 (18 decks)

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