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Cardio > vascular Pathology > Flashcards

vascular Pathology Flashcards

0
Q

Response of vascular smooth muscle to injury (minor and major)

A
  • in minor injuries: adjacent endothelial cells migrate to restor luminal surface
  • in major injuries: smooth muscle is stimulated to migrate to intima (bad) and create collagen (worse)
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1
Q

Review:

  • inter-endothelial attachment protein
  • expressed in HEVs for niece Tcell attachment
  • binds integrins for stable adhesion
A
  • CD31
  • CD34
  • CD54
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2
Q

Stenosis outcomes

A
  • chronic ischemia
  • rupture -> thrombus
  • complete progressive occlusion
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3
Q

5 leading Causes of death in 2010

A 
1 heart disease 
2 malignant neoplasms 
3 chronic lower resp diseases
4 Cerebrovascular disease 
5 accidents
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4
Q

Clinically significant stages of atherosclerosis

A
  • fiberoatheroma (lipid core with fibrotic layer): stage IV

- complicated lesion with surface defect and adherent hematoma or thrombosis: stage V

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5
Q

Plaque structure

A
  • cells (smooth muscle cells, foam cells, lymphocytes)
  • matrix
  • lipid (in necrotic core)
  • neovascularization
  • important: media is thinned at base of plaque: rupture/ulceration significant risk
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6
Q

Preclinical stage

A
  • Generally 40-50 yearsish. Silent until age related comorbidities show up
  • exception: familial hypercholesterolemia and TIIDM
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7
Q

Diagnosis of atherosclerosis

A
  • angiography is gold standard

- one clear artery doesn’t guarantee another (patchy)

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8
Q

Tissue ischemia in atherosclerosis

A
  • may be direct occlusion
  • may also be decreased Plat in collateral vessels
  • lower ext gangrenous ulcers and bowel ischemia are common presentations of mesenteries and LEx atherosclerosis
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9
Q

Risk factors for MandM in atherosclerosis

A
  • synergistic

- HTN, cholesterol LDL/HDL ratio, smoking male, genetics

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10
Q

Heterozygous familial hypercholesterolemia

A
  • LDL receptor mutation: LDL>220 Mg/dL

- 1:500

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11
Q

Familial defective apoprotein B

A
  • Apo B 100

- 1:700

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12
Q

Familial combined hyperlipidemia

A
  • unknown etiology
  • LDL and trigs elevated
  • HD! Suppressed
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13
Q

Inflammatory conditions effecting development if atherosclerosis

A
  • high CRP
  • homocysteine (B12 deficiency)
  • lipoprotein LPa
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14
Q

Berry aneurysm

- incidence, location, rupture risk, clinical sequela

A
  • 2 %
  • 90% are in MCA/ACA near branch points
  • Marfan and Ehlers danlos at increased risk for rupture
  • results in subarachnoid hemorrhage
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15
Q

Fibromuscular dysplasia

A
  • Segmental lesions affecting renal, carotid, splanchnic, vertebral
  • renovascular HTN: decreased afferent pressure -> JG cells -> renin release
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16
Q

Etiology of HTN

A
  • 90% essential: unknown
  • secondary: renal lesions most common (glomerulonephritis, renal artery stenosis et al)
    > CV: coarctation of aorta, poly arteritis nodosa
    > endocrine
    > Neuro: increased ICP
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17
Q

Hyaline arteriolesclerosis

A
  • thickening of media and intima by hyaline material in HTN

- sequelae: diffuse renal ischemia, worsening HTN

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18
Q

True vs. false aneurysm

A
  • true aneurysm has all three walls dilated

- false aneurysm has had the media and the intima separated

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19
Q

Cystic media degeneration

A
  • ischemic degeneration of medial layer of aorta due to stenosis of vaso vasorum
  • risk factor for AAA
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20
Q

Thoracic aortic aneurysm etiology and sequelae

A
  • rare
  • most are HTN in origin
  • infectious etiology: syphillis
  • sequelae: encroachment on esophagus, lungs, mediastinum, bones; aortic valvular insufficiency with LVH, coronary artery obstruction, rupture (uncommon)
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21
Q

Aortic aneurysms

A

Class A: surgical emergency
- proximal to descending aorta
Class B: distal to arch

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22
Q

Raynaud’s phenom vs disease

A
  • disease is primary, less severe, presents younger and essentially an exaggerated vasomotor response
  • phenomena is typically secondary to disease process (arterial stenosis) presents in more variable age group,
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23
Q

Vasculitis

A
  • rarely infectious, typically immune mediated
  • large: GTA (giant cell, takayasu’s, the other one)
  • medium: PK (polyarteritis nodosa, kawasakis)
  • small: Good Small White CHurch (goodpastures, SLE vasc, Wegeners, Churg-Strauss)
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24
Q

Polyarteritis nodosa

A
  • NO LUNG involvement (pan no pulm)
  • obliterated arterial lumen, trans mural neutrophils
  • transmural necrotizing inflammation of muscular arteries (sans lung)
  • on continuous inflammation (esp bifurcations)
  • microaneurysms, ischemia with ulceration, hemorrhage with necrosis and infarct
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25
Q

Kawasakis disease

A
  • aka mucocutanious lymphnode syndrome
  • PAN-like arteritis of medium vessels in young kids
    > mucocutaneous erythema, palmar and pedal erythema, desquamation
  • autoantibodies against smooth muscle
  • cardiac sequelae most significant pathology (rare)
26
Q

Cardiac sequelae of Kawasakis etiology and treatment

A
  • coronary vasculitis
  • coronary aneurysms (large)
  • fatal in ~ 1%
  • epidemic in Japan and Hawaii, but #1 acquired heart diseas in kids in us
  • Aspirin and IVIG
27
Q

Wegeners granulomatosis (it’s a klr)

A
  • classic triad: upper resp lesions, lung lesions (necrotizing capsulitis) kidney lesions
  • all three together are uncommon presentation clinically
28
Q

Infectious arteritis

A
  • bacteria or fungi esp. Aspergillus and mu or (angioinvasive)
  • infarction and aneurysm rupture
29
Q

Varicose veins

A
  • pathenogenesis: venous stasis
  • can be painful, unsightly
  • pulmonary emboli rare (only 1 of three in virchows)
  • varices in esophagus and anorectal junction due to portal HTN
30
Q

Phlebothrmbitis (thrombophlebitis)

A
  • not an inflammatory state, thrombosis within vein
  • immobilization with inactivity
  • Vircows triad: venous stasis, endothelial injury, hypercoagulable state
  • most originate in deep leg veins
31
Q

Clinical manifestations of thrombophlebitis

A
  • few signs of early disease
  • first symptom often embolus
  • leg edema, redness, pain
  • Homan sign: pain in popliteus upon abrupt dorsiflexion
32
Q

Pulmonary thromboembolus

A
  • # 1 cause of sudden death in post op PTs
  • lines of Zahn in antemortem clots
  • can be visualized in ventilation/perfusion scan
33
Q

SVC/ IVC syndrome

A
  • 90% neoplasm, 10% thrombosis
  • facial edema, dilated head/neck veins (SVC)
  • leg edema, distention of superficial abdomen, if renal veins effected massive proteinuria
    > hepatocellular and renal cell CA
34
Q

Lymphangiitis

A
  • typically GAStrep
  • inflammation along lymphatic drainage pathway
  • bacteremia -> sepsis; monitor closely
35
Q

Lymphadema

A
  • primary is rare, defects in lymph drainage, or agenesis

- secondary much more common: inflammation or cancer

36
Q

Weird complication of large hemangioma

A
  • high output cardiac failure

- don’t remove heagioma unless necessary

37
Q

Vascular ectasias

A
  • talengectasia

- osler-weber-rendu disease: talengectasias of mouth and tongue; risk of lethal intestinal bleed

38
Q

Bacillary angiomatosis

A
  • opportunistic infection presenting as vascular proliferations of blood vessels
  • Infection typically GNBac (often Bartonella)
39
Q

Vascular tumors: intermediate grade and malignant

A 
- intermediate:
   > kaposis sarcoma (assoc with HIV and HHV8) coalescing patches and plaques 
   > hemagioendothelioma 
- malignant:
   > angiosarcoma 
   > hemangiopericericytoma
40
Q

Arterioloslerosis

A
  • similar to atherosclerosis but generally localized t heart and kidneys
41
Q

Boot shaped heart with

- overriding aorta, VSD, pulmonary stenosis r vent hypertrophy

A
  • tetralogy of fallot
  • untreated 30 year survival is ~ 10%
  • right to left shunting
42
Q

Neonat with lower body cyanosis

A
  • coarctation of the aorta
43
Q

Pulmonary atresia/stenosis

A
  • results in post-stenotic pulmonary dilation
44
Q

Circumferential infarct

A
  • subendocardial infarction

> can be due to global hypoperfusion in presence of reduced atherosclerotic vessels

45
Q

Kerley B lines on roentgenogram

A
  • represent pulmonary edema (vascular and interstitial)

- especially in interlobar speta

46
Q

Panners don’t mine for gold so polyart nod doesn’t involve lung. Wegener is the coal miner

A

,

47
Q

Osler-Weber-Rendu disease

A

Oropharyngeal Talengectasias

- potentially lethal GI bleeds

48
Q

C-ANCA/P-ANCA

A
  • C-ANCA: Wegeners

- P-ANCA: microscopic polyangiitis, Churg-Strauss

49
Q

Anti-endothelial cell Abs

A

Associated with kawasakis

50
Q

Pulseless (weakened pulse in UEX), similar to giant cell arteritis except pathology in aorta

A

Takayasu’s

- more common in japanese

51
Q

Hypersensitivity type as units of small/medium blood vessels, hemoptysis, hematuria, muscle pain/weakness, palpable cutaneous purpura

A

Microscopic polyangiitis

- fragmenting neutrophils: leukocytoklastic vasculitis

52
Q

Allergic symptoms with eosinophilic rhinitis

A
  • Churg- Strauss

- ANCAs probably responsible for vascular manifestation

53
Q

Beurgers disease (thromboangiitis obliterans)

A
  • smokers
  • cold sensitivity, raynauds, chronic ulcers in fingers toes, feet
  • stop smoking
54
Q

Most common infectious vasculitis

A
  • mucor/aspergillus
55
Q

Most common vascular tumor

A
  • hemangioma (capillary variant)
56
Q

Pedunclulated rapidly growing hemangioma

A
  • pyogenic granulomas

- can occur in pregnant women

57
Q

Exquisitly painful benign tumor typically under finger nail bed

A

Glomus tumor

- excision is curative

58
Q

Large facial vasicular lesion in presence of mental deficiency

A
  • Sturge-Weber syndrome
59
Q

kaposis sarcoma variants (4)

A
  • KS preceded by HHV8 (requires a cofactor to progress as a tumor)
  • chronic: Eastern European men, NOT assoc with HIV
  • Lymph: African variant NOT assoc with HIV
  • transplant assoc is aggressive: not assoc with HIV (immunosuppressive)
  • AIDS assoc IS assoc with AIDS
60
Q

Malignant tumor arising due to exposure to arsenic, radiation or PVC

A
  • angiosarcoma
61
Q

Fragmented neutrophils

A
  • microscopic angiitis
62
Q

Munkeyburg phenomena

A
  • benign calcification of media of arteries not constricting flow.
    Show up on x ray

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