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Cardiovascular II > Vascular Path Robbins Part 3 > Flashcards

Vascular Path Robbins Part 3 Flashcards

1
Q

vasculitis- clinical presentation

A

vasculitis- clinical presentation -infl of vessels

-nonspecific- fever, malaise, arthralgias, myalgias

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2
Q

vasculitis- classified as

A
  • noninfectious- mediated by immunologic injury (immune complex depositions, autoab’s)- indicates immunosuppressive therapy!!
  • infectious- pathogenic organisms invading the vessel wall
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3
Q

major cause of noninfectious vasculitis

A

local or systemic response

  • immune complex deposition
  • ANCAs
  • antiendothelial cell ab’s
  • autoreactive T cells
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4
Q

immune complex vasculitis- what is it? may be seen in?

A
  • deposition of ag-ab complexes in vascular walls- infl rxn occurs
  • systemic immunologic diseases (SLE)
  • drug hypersensitivity
  • secondary to exposure to infectious agent
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5
Q

antineutrophil cytoplasmic ab’s (ANCAs)- 2 types, act what?

A
  • anti-proteinase-3 (PR3-ANCA; c-ANCA)
  • anti-myeloperoxidase (MPO-ANCA; p-ANCA)
  • ANCA titers
  • act neutrophils- release ROS
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6
Q

PR3-ANCA- assoc with?

A

granulomatosis with polyangiitis

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7
Q

MPO-ANCA- assoc with?

A
  • microscopic polyangiitis

- Churg-Strauss syndrome

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8
Q

possible mech for ANCA vasculitis

A
  • drugs or cross-reactive microbial ag’s induce ANCA formation
  • infection, endotoxin exposure, or infl stimulus- elicits cytokines that upreg the surface expression of PR3 and MPO on neutrophils
  • ANCAs react with cytokine-act cells
  • ANCA-act neutrophils- cause tissue injury
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9
Q

granulomatous arteritis- 3 types

A
  • Giant cell (temporal) arteritis
  • Takayasu arteritis
  • Granulomatosis with polyangiitis
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10
Q

Giant Cell (Temporal) Arteritis- affects who? morphology?

A
  • most common vasculitis in older pts
  • chronic (T-cell mediated) infl of a’s, esp temporal a’s
  • medial granulomatous infl, w/ multinucleated giant cells
  • fragmentation of elastic lamina
  • patchy and focal
  • healed sites- scarring of medial, intimal thickening
  • ophthalmic a- vision loss
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11
Q

Takayasu arteritis- affects who? presentation?

A
  • similar morphology to giant cell arteritis
  • aortic arch and major branch vessels (“pulseless disease”)
  • pulm, coronary, renal a’s may be involved
  • younger age group! (<50)
  • weak pulse, low BP in UE’s
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12
Q

PAN (polyarteritis nodosa)- involves? age group? assoc with? therapy?

A
  • systemic vasculitis, immune complex mediated
  • renal vessels, heart, liver, GI tract
  • pulm vessels spared!!
  • classically young adult!
  • chronic hepatitis B- HBsAg-HBsAb complexes- 1/3 of pts
  • immunosuppressive therapy
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13
Q

PAN (polyarteritis nodosa)- morphology

A
  • transmural necrotizing infl- small/medium a’s
  • fibrinoid necrosis of vessel wall
  • typically not circumferential!!
  • susceptible to thrombus formation/occlusion, aneurysm, rupture
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14
Q

PAN- classic presentation

A
  • young adult
  • rapidly accelerating HTN due to renal involvement
  • abdominal pain and bloody stools- vascular GI lesions
  • diffuse myalgias
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15
Q

Kawasaki disease- age? involves? presenting picture? treatment?

A
  • infants/small children (<4 yrs)
  • coronary a’s- can form aneurysms- thrombosis/rupture- acute MI!!
  • erythema of conjunctiva, oral mucosa, palms, and soles; cervical LN enlargement (“mucocutaneous LN syndrome”)
  • usually self-limited
  • IVIg and aspirin- lowers risk of coronary event
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16
Q

microscopic polyangiitis- affects? assoc with? morphology?

A
  • necrotizing vasculitis of arterioles, capillaries, venules
  • many organ systems- renal glomeruli and lung capillaries most common!
  • MPO-ANCA (most cases)
  • segmental necrotizing infl with fibrinoid necrosis
  • apoptotic neutrophils (“leukocytoclastic vasculitis!”)
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17
Q

Churg-Strauss Syndrome- assoc with?

A
  • Eosinophils!!
  • small vessel necrotizing vasculitis- assoc with asthma, allergic rhinitis, hypereosinophilia
  • eosinophils and granulomas!
  • <1/2 show ANCA positivity
  • many organ systems
18
Q

Behcet disease- triad? assoc with?

A
  • vasculitis of small/medium vessels
  • aphthous ulcers of oral cavity, genital ulcers, uveitis!!
  • neutrophilic
  • HLA-B51
19
Q

Granulomatosis with polyangiitis- involves? assoc with? therapy?

A

(Wegener granulomatosis)

  • necrotizing vasculitis; granulomas
  • upper/lower resp tracts, focal necrotizing often crescentic glomerulonephritis!!
  • PR3-ANCA (95%)
  • immunosuppressive therapy
20
Q

Granulomatosis with polyangiitis- clinical presentation

A
  • males, age 40
  • persistent pneumonitis and sinusitis, renal disease, nasopharyngeal ulceration
  • if untreated- 80% mortality in 1 yr
21
Q

Thromboangiitis obliterans- involves? affects who? leads to?

A

(Buerger Disease)

  • thrombosing vasculitis!- tibial, radial a’s!!
  • almost always smokers, young adults
  • leads to vascular insuff of extremities
  • may involve adj v’s and n’s- pain!
  • chronic ulcerations- gangrene
22
Q

infectious vasculitis- most common agent

A

Pseudomonas

-Aspergillus, Mucor

23
Q

Raynaud Phenomenon

A
  • vasospasm of small a’s and arterioles, esp in fingers and toes (sometimes nose, earlobes, lips)
  • digits- “red, white, and blue” from proximal to distal
24
Q

primary raynaud phenomenon- induced by?

A
  • induced by cold or emotion
  • symmetric involvement of digits
  • young women; 3-5% of population
  • benign course
25
Q

secondary raynaud phenomenon

A
  • component of another arterial disease, such as SLE, scleroderma, thromboangiitis obliterans
  • asymmetric involvement of digits
  • worsens with time!!
26
Q

myocardial vessel vasospasm- caused by?

A
  • vasoconstriction of myocardial a’s or arterioles (“cardiac Raynaud”- may cause ischemia or infarct
  • circulating vasoactive agents- epinephrine or cocaine
  • MI can occur after 20-30 min
27
Q

myocardial vessel vasospasm- can result in?

A
  • sudden cardiac death

- Takotsubo cardiomyopathy (“Broken heart syndrome”)- ischemic dilated cardiomyopathy

28
Q

varicose veins- what are they? risks?

A
  • abnormal dilations of v’s with valvular incompetence, secondary to sustained intraluminal P
  • incompetenence of venous valves- results in stasis, congestion, thrombus, edema, ischemia of overlying skin (stasis dermatitis), ulcerations
  • obesity, pregnancy
  • embolism from thrombi of superficial LE v’s- rare!!
29
Q

esophageal varices- caused by?

A
  • portal HTN (cirrhosis) opens portosystemic shunts which direct blood to v’s at the gastroesophageal jxn
  • may fatally rupture!!
30
Q

other varices

A
  • rectum- hemorrhoids

- periumbilicus- caput medusa

31
Q

hemorrhoids

A

dilation of venous plexus at anorectal jxn

  • common!!
  • pain, bleeding, may ulcerate
32
Q

thrombophlebitis- most where?

A

(also called phlebothrombosis)

  • venous thrombosis and infl
  • 90% in deep v’s in legs- can be completely asymptomatic!!
33
Q

risk factor for DVT in LE?

A
  • prolonged activity/immobilization- single most important!
  • systemic hypercoagulability (may also increase risk)
  • mechanical factors that slow venous return- CHF, pregnancy, obesity
34
Q

most common serious clinical complication of DVT?

A

-pulmonary embolism- often 1st manifestation of thrombophlebitis

35
Q

migratory thrombophlebitis - assoc with?

A

(Trousseau sign)

  • assoc with cancer- hypercoagulability!
  • mucin-producing adenocarcinomas
  • venous thromboses appear at 1 site, disappear, and reappear at another site
  • adenocarcinomas of lung, ovary, pancreas
36
Q

superior vena cava syndrome- caused by? effects

A
  • neoplasms or aortic aneurysms that compress or invade the SVC
  • dilation of v’s of head, neck, arms with cyanosis
  • pulm vessels may be compressed- resp distress
37
Q

inferior vena cava syndrome-caused by? effects?

A
  • neoplasms that compress or invade IVC
  • thrombosis of hepatic, renal, or LE v’s that moves cephalad
  • hepatocellular carcinoma and RCC- grow within v’s!
  • obstruction- LE edema, distention of superficial collateral v’s of lower abdomen, proteinuria (with renal v involvement)
38
Q

lymphangitis- what is it? caused by? manifested by?

A

acute infl elicited by the spread of bacterial infections into lymphatics

  • group A B-hemolytic streptococci- most common
  • dilated and filled with exudate of neutrophils/monocytes
  • red, painful subcutaneous streaks and painful enlargement of draining LNs (lymphadenitis)
39
Q

primary lymphedema- due to?

A

isolated congenital defect or familial Milroy disease (heredofamilial congenital lymphedema)
-lymphatic agenesis or hypoplasia

40
Q

secondary or obstructive lymphedema- due to?

A

blockage of a previously normal lymphatic

  • malignant tumors
  • surgical procedures that remove regional groups of LNs
  • postirradiation fibrosis
  • filariasis
  • postinfl thrombosis and scarring
41
Q

persistent edema from cancer- leads to?

A
  • peau d’orange appearance of overlying skin- seen in breast cancers (lymphatics clogged with tumor cells)
  • chylous ascites (abdomen), chylothorax, chylopericardium- caused by rupture of dilated lymphatics (secondary to obstruction from a tumor)

Cardiovascular II (13 decks)

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