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Vascular Flashcards

1
Q

atherosclerosis

A

disease of arterial intimal thickening due to lipid accumulation, chronic inflammation, and repair
muscular and elastic arteries
contains: calcification, cholesterol clefts, necrotic core, fibrous cap

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2
Q

modifiable risk factors for athersclerosis

A

multiplicative

  1. smoking
  2. HTN
  3. obesity
  4. DM
  5. dyslipidemia
    also: inflammation (high CRP) and physical inactivity
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3
Q

atherosclerosis pathogenesis

A

injured endothelial cells and dysfunction-> increase permeability and leukocyte and platetlet adhesion-> accumulation of lipid in tunica intima-> monocyte recruitment-> foam cell-> recruit sm. muscle cells and T cells-> Sm. muscle cell proliferation and ECM deposition

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4
Q

How does hyperlipidemia contribute to atherogenesis?

A

high levels of cholesterol increases local reactive oxygen species causing membrane and mitochondrial damage and accelerate NO decay

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5
Q

foam cells formation

A

macrophages (sm. muscles too) take up modified LDL through scavenger receptors that lack feedback inhibition and are unable to degrade them
release GF, cytokines, chemokines

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6
Q

What is the role of inflammation in atherosclerosis?

A

cholesterol crystal and FFA activate inflammasome leading to activation of IL-1: recruits leukocytes
inflammatory cells breakdown ECM and result in unstable plaques
IL-1 and TNF-a: decrease superoxide dismutase, NO, PG

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7
Q

factors implicated in sm. muscle proliferation in atherosclerosis

A

PDGF, FGF, TGF-alpha

stabilizes plaques

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8
Q

neovascularization of later atherosclerosis

A

O2 can’t get through thickened artery

hemorrhage into plaque making it prone to rupture

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9
Q

internal elastic lamina

A

separates tunica intima and tunica media

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10
Q

arteriovenous fistula

A

direct connection between arteries and veins bypassing capillaries

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11
Q

fibromuscular dysplasia

A

focal irregular arterial wall thickening with intimal and medial hyperplasia and fibrosis leading to luminal stenosis
renal, carotid, splanchnic or vertebral arteries in young women

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12
Q

hyperplastic arterioloscerosis

A

concentric wall thickening due to smooth muscle hyperplasia and hypertrophy
onion skinning
cause: malignant HTN, scleroderma can cause similar look of large interlobar renal arteries, lupus

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13
Q

fibrinoid change/necrosis

A

leakage of plasma protein into wall with or without necrosis

cause: malignant HTN or vasculitis (esp. polyarteritis nodosa)

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14
Q

hyaline arteriolosclerosis

A

wall thickening due to leakage of plasma protein into wall and increased secretion of matrix by smooth muscle cells
cause: HTN, DM
differential should include amyloidosis (larger vessels) and fibrinoid change

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15
Q

medial calcific sclerosis

A

Monckeberg

degenerative calcification of internal elastic lamina spreading into tunica media

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16
Q

canakinumab

A

trial drug
anti-interleukin-1B Ab
Tx:unstable plaque in acute coronary syndrome

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17
Q

What makes a plaque unstable?

A

thin fibrous plaque: prone to rupture and release thrombogenic material form necrotic

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18
Q

colchicine

A

gout drug that can be used at low doses in athersclreosis

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19
Q

angiogram

A

shows lumen of vessels only

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20
Q

intravascular ultrasound

A

shows wall and lumen of vessels

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21
Q

mechanism of acute coronary syndrome

A

rupture of atherosclerotic plaque due to erosion of fibrous cap (usually thin) and release of thrombogenic material
ruptured plaques: large lipid core, thin cap, abundant inflammatory cells, calcification

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22
Q

erosion of atherosclerotic plaque

A
  1. oxidative stress and hypochlorous acid cause endothelial cell apoptosis producing TF
  2. modified LDL can induce MMP-14 -> MMP-2-> degradation of type IV collagen
  3. Lp-PLA2-> MCP-1, ICAM-1, VCAM-1 -> endothelial cells vasodilator less in response to NO and undergo apoptosis
  4. Lp-PLA2-> MCP-1 on macrophages-> IL-1beta
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23
Q

What causes atthersclerotic events?

A

up to 75% rupture
up to 25% erosion
most events are due to superimposed thrombosis

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24
Q

How do statins and aspirin prevent atherosclerotic event?

A

statins: reduce lipid content, making more fibrous, decrease macrophages
may be anti-thromboic, pro-fibrinolytic, vasodilatory
aspirin: anti-platelet

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25
What is the role of T cells in atherosclerotic plaques?
1. secrete IFN-gamma that inhibits sm. muscle cells from making collagen required for fibrous cap 2. boosts macrophage collagenases through its CD40 ligand
26
What is the role of macrophages in atherosclerotic plaques?
overproduces MMP-1, MMp-8, MMP-13 that degrade collagen
27
distribution of atherosclerosis
1. lower abdominal aorta 2. coronary arteries 3. popliteal arteries 4. internal carotid arteries
28
Which coronary arteries are most likely to have acute coronary disease?
1. LAD (1/2) 2. RCA (1/3) 3. LCX (1/6)
29
atherosclerotic stenosis
early stages: remodeling of artery expands it outward and preserves lumen, eventually impinges on lumen
30
critical stenosis
occlusion that produces tissue ischemia, 70% reduction of lumen cross section Sx develop: angina on exertion effects of occlusion depend on metabolic demand and arterial supply of tissue
31
general categories of acute plaque changes
1. rupture: releases thrombogenic plaque constituents into blood 2. erosion: exposes subendothelial basement membrane to blood 3. hemorrhage into atheroma: expanding its volume
32
When are MI most likely?
6am-12pm due to adrenergic stimulation associated with waking and rising also intense emotional distress
33
methotrexate use in atherosclerosis
inhibition of proliferation fibroblasts, sm. muscle cells, endothelial cells, lymphocytes that play a role in atherosclerosis
34
thrombosis of coronary arteries in the young
1. vasospasm (cocaine, amphetamines) 2. lupus anticoagulant in young woman hypercoaguable states lead to VENOUS thrombosis
35
atheroembolism
most likely in leg, renal, intestinal arteries from aorta | RARE in coronary arteries
36
dissection
tear of tunica intimal letting luminal blood under high pressure into the tunica media making a second lumen
37
ectasia
non-discrete, non-localized dilatation of blood vessel or duct
38
fibrillin
extracellular glycoproteins essential for structuring elastin fibers
39
Marfan syndrome
autosomal dominant inherited disease of defective fibrillin (FBNI gene) and excess TGF-beta leading to tall thin body habits and cystic medionecrosis of ascending aortic (dissections) Tx: beta-blockers
40
Ehlers-Danlos
usually autosomal dominant heterogeneous group of inherited disorders due to defects in synthesis or structure of fibrillar collagen COL3A1 gene for type III collagen spontaneous rupture of blood vessels and intestines
41
aortic aneurysm
elderly, fam. Hx, white males combination of atherosclerosis and predetermined degeneration of tunica media (increased MMP) other causes: Marfan, infection, vasculitis abdominal more common Sx: usually none; back pain if leaking Dx: imaging Tx: stent, surgery (not until 5 cm) complications: RUPTURE, thrombus, embolism, obstruction, aortoenteric fistula
42
aortic dissection
late, middle age, men blacks rarely obvious what causes it, medial dissection associated with cystic medial degeneration Sx: tearing chest pain or between scapulae that moves as dissection progresses, with or without altered mental status (carotid), arm pain/weakness (subclavian), collapse (rupture into pericardium or left pleural cavity) DX: CT, MRI, transesophageal echo Tx: reduce BP, surgery
43
giant cell arteritis
temporal arteritis elderly, white, female, N. European Hx Sx: headache, visual distrubance, jaw claudication, scalp tenderness complication: blindness inflammation: segmental, transmural, granulomatous, giant cells on internal elastic membrane innate and adaptive PAMP-> dendritic cells (TLR-4) produce IL-12 and IL-18 (also IL-2, IL-6) -> up regulate Th1 cell production of IFN-gamma, Th17 (IL-1, IL-23) and release homing CCL19 and CCL21-> bind CCR7 receptor-> arrest of dendritic cells -> trapped in arterial wall IFN-gamma-> VEGF and PDGF -> fibrosis and stenosis MMP-2 and MMP-9: destroy elastin Tx: anti-TNF and corticosteroids: suppress IL-1, IL-6, IL-17 (Th17)
44
Takayasu arteritis
young East Asian females cpture, hemopericardium (cardiac tamponade) Sx: pulseless arm, arm claudication, subclavian or aortic bruit, aortic or major branches stenosis, angina inflammation: segmental, transmural, necrotizing, loose granulomas (multinucleate giant cells) complications: aortic dissection, rupture, hemopericardium (cardiac tamponade) Tx: corticosteroids poor prognosis
45
polyarteritis nodosa
white, male, 40s Sx: neuropathy (wrist or foot drop), renal failure, ACUTE ABDOMEN, cholecystitis, pancreatitis, angina pectoris, livedo reticularis inflammation: segmental, transmural, nodular, FIBRINOID necrosis SPARES LUNGS, lesions at DIFFERENT PHASES complications: thrombosis, occlusion, rupture, aneurysm NO Ab prognosis: good with treatment
46
Kawasaki disease
East Asian children Sx: conjunctival injection, desquamtion rash, cervical lymphadenopathy, strawberry tongue, hand and foot erythema/ edema, fever complications: coronary aneurysm, thrombosis, MI, sudden death Tx: aspirin and IV immunoglobulin
47
microscopic polyangiitis
hypersensitivity or leukocytoclastic vasculitis all lesions SAME PHASE necrotizing glomerulonephritis and pulmonary capillarities common Ab: P-ANCA (MPO) segmental, fibrinoid necrosis Sx: hemoptysis, hematuria, proteinuria, bowel pain, bleeding, muscle pain/weakness, palpable purpura Tx: corticosteroids, immunosuppression
48
granulomatosis with polyangiitis
Wegner's, white, 40's necrotizing granulomatous: arteries and veins in upper and lower respiratory tract and kidneys GEOGRAPHIC with histiocytes Ab: C-ANCA (proteinase-3) Tx: corticosteroids, immunosuppression, rituximab
49
Churg-Strauss syndrome
allergic granulomatosis with polyangitis | asthma, eosinophilia, vasculitis
50
Buerger disease
young, male, smoker, Middle Eastern or South Asian thrombosing faso-occlusive disease of arteries and veins of limbs ischemic ulcers. gangrene moving distal to proximal granulomas and giant cells Tx: stop smoking and amputation
51
peripheral arterial disease
common, elderly, men chronic atherosclerotic occlusive disease of large and medium arteries, primarily legs Sx: intermittent claudication (during exercise), pain at rest is severe signs: lost pulses, bruits, pallor, skin/muscle atrophy, ulceration, necrosis Dx: Hx and physical Tx: exercise
52
acute arterial occlusion
uncommon thromboemboli mostly from heart Sx: pain, pallor, paralysis, paresthesia, pulselessness in legs (arms and brain too) Dx: Hx and physical Tx: anticoagulation, thrombolytics, surgery, thromboectomy SURGICAL EMERGNCY
53
large vessel vasculitis
1. Temporal (giant cell) arteritis 2. Takayasu arteritis PULSELESS
54
medium vessel vasculitis
1. polyarteritis nodosa 2. Kawasaki 3. Buerger INFARCTION
55
small vessel vasculitis
1. granulomatosis with polyangitis (Wegner's) 2. microscopic polyangitis 3. eosinophilic granulomatosis with polyangitis (Churg-Strauss) 4. Henoch-Sconlein purpura PALPABLE PURPURA
56
aneurysm
discrete localized dilatation of blood vessel (or heart)
57
cysitc medial degeneration
loss of sm. muscle cells and plastic fibers in tunica media of large arteries leads to: aneurysm
58
Type A aortic dissection
ascending aorta with/without other parts of aorta must have rapid Dx Tx: anti hypertensives, surgery
59
Type B aortic dissection
descending aorta alone | Tx: anti-hypertensives
60
vasculitis
inflammation of blood vessels most autoimmune most common Sx: fever, myalgia, arthralgia, malaise Dx: biopsy
61
palpable purpura
erythematous tender skin nodules
62
infectious vasculitis
``` caused by : 1. fungal (Aspergillus) 2. bacterial (pseudomonas) 3. viral (CMV) may cause mycotic aneurysm (even if not fungal) ```

SS- Cardio (16 decks)

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