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Cardiovascular II > Vascular Path Robbins Part 1 > Flashcards

Vascular Path Robbins Part 1 Flashcards

1
Q

blood vessels- 3 concentric layers

A 
-intima 
(internal elastic lamina)
-media
(external elastic lamina)
-adventitia
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2
Q

intima- consists of

A
  • endo cells (single layer) on basement membrane

- demarcated from the media by internal elastic lamina

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3
Q

media- consists of

A

smooth m cells

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4
Q

media- in elastic a’s (aorta)

A

-have high elastin content

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5
Q

media- in muscular a’s

A
  • composed predominantly of circumferentially oriented smooth m cells
  • smooth m contraction and relaxation- reg by inputs from autonomic NS and local metabolic factors
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6
Q

principal points of physiologic resistance to blood flow

A

arterioles

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7
Q

adventitia- consists of

A
  • separated from the media by external elastic lamina

- loose CT containing n fibers, vasa vasorum (small arterioles that supply the outer portion of the media)

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8
Q

a’s divided into 3 types

A
  • large/elastic arteries (aorta, major branches of aorta)
  • medium-sized/muscular a’s- smaller branches of aorta)
  • small a’s (<2 mm diameter) and arterioles (20-100 um diameter)
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9
Q

capillaries- size? consists of

A
  • 7-8 um diameter (size of red cell)
  • have endo cell lining, but no media
  • pericytes (resemble smooth m cells) lie deep to endo
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10
Q

veins- diff from a’s

A
  • larger diameters, larger lumens, thinner/less organized walls
  • contains 2/3 of total blood volume
  • less rigid walls-subject to dilation and compression, as well as infiltration by tumors and infl process
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11
Q

lymphatics

A
  • thin-walled channels- lined by specialized endo
  • provide conduits to return interstitial tissue fluid and infl cells to bloodstream
  • can also transport microbes and tumor cells- important potential pathway for disease dissemination
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12
Q

vascular anomalies

A
  • berry aneurysms
  • arteriovenous fistula
  • fibromuscular dysplasia
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13
Q

berry aneurysms- found where? asssoc with? can cause?

A
  • circle of willis
  • autosomal dominant polycystic kidney disease
  • fatal subarachnoid hemorrhage
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14
Q

arteriovenous fistulas- arise from? can cause?

A
  • direction connections b/w a’s and v’s that bypass the capillary bed
  • most often developmental defects
  • may arise secondary to infl, trauma, rupture
  • can rupture- leads to hemorrhage
  • can cause high-output cardiac failure- by shunting blood from arterial to venous circulation, forcing heart to pump additional volume
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15
Q

fibromuscular dysplasia

A
  • focal thickening of intima and media of medium/large muscular a’s- results in stenois
  • “string of beads”
  • young women- most often
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16
Q

endo cells- normal state

A

-nonthrombogenic surface

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17
Q

endo cells- activated state- what stimuli?

A
  • turbulent blood flow
  • HTN
  • complement, bacterial products, lipid products, glycation end products
  • viruses
  • hypoxia, acidosis
  • tobacco smoke components
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18
Q

activated endo cells- characterized by expression of?

A
  • adhesion molecules
  • procoagulants, anticoagulants
  • vasoactive factors, GFs
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19
Q

endothelial dysfxn- characterized by?

A
  • procoagulation
  • proinfl
  • smooth m stimulation
  • partly responsible for initiation of thrombus formation, atherosclerosis, and vascular lesions of HTN
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20
Q

predominant cellular element of vascular media- fxns

A

vascular smooth m cells

  • roles in vascular repair and pathologic processes
  • can proliferate when stimulated
  • can syn collagen, elastic, proteoglycans, GFs, cytokines
  • responsible for vasoconstriction.dilation
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21
Q

vascular injury- assoc with?

A

endo cell dysfxn or loss

  • stim smooth m recruitment/proliferation (from media to intima)
  • assoc matrix syn
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22
Q

vascular injury- stereotypical response?

A

-intimal thickening!!

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23
Q

HTN- risk factor for?

A
  • atherosclerosis, aortic dissection
  • Hypertensive heart disease (cardiac hypertrophy and HF)
  • stroke
  • hypertensive renal disease
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24
Q

hypertensive vascular disease- increased prevalence in?

A
  • advancing age

- african americans

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25
90-95% of HTN- cause?
-idiopathic (essential HTN)
26
5% of HTN- cause?
secondary HTN - renal or adrenal disease - renal a stenosis - endocrine - CV - neurologic
27
risk factors for essential HTN
- high Na intake - obesity - stress - smoking - physical inactivity
28
malignant HTN- characterized by?
- small % of HTN pts show a rapidly rising BP that if untreated leads to death within 1-2 yrs - severe HTN (>200/120), renal failure, retinal hemorrhages/exudates
29
BP =
CO x PVR | CO= SV x HR
30
most important determinant of SV?
filling pressure- reg thru sodium homeostasis
31
PVR- constrictors
- ang II - catecholamines - thromboxane - leukotrienes - endothelin
32
PVR- dilators
- prostaglandins - Kinins - NO
33
blood volume and vascular tone- maintained by?
renin-angiotensin-aldosterone system! | -low volume- renin released by JG cells- cleaves angiotensinogen to form angI--ACE--> angII
34
angII- fxns
- vascular constriction - aldosterone secretion by adrenal gland - increase tubular Na reabs
35
volume expansion- induces?
- myocardial release of ANP (atrial natriuretic peptide) | - leads to Na excretion/diuresis and vasodilation
36
secondary HTN- renovascular HTN
-renal a stenosis- causes dec glomerular flow- induces renin secretion
37
single-gene disorders that cause HTN
- gene defects affecting enzymes in aldosterone metabolism (aldosterone synthase, 11-B hydroxylase 17alpha-hydroxylase)- increase secretion in aldosterone- inc Na/water reabs - mutations affecting proteins that influence Na reabs- Liddle syndrome- gain-of-fxn mutation in epit Na channel protein that increases distal tubular reabs of Na in response to aldosterone
38
mech's of essential HTN
- genetic factors - reduced renal Na excretion - vasoconstrictive influences - environmental factors
39
hyaline arteriosclerosis- morphology
- increased smooth m matrix syn - plasma protein leakage (across damaged endo) - homogenous pink (hyaline) thickening of vessel wall- lumen narrows
40
hyperplastic arteriosclerosis
- seen in severe HTN | - smooth m cells form concentric lamellations (onion skinning)- lumen narrows
41
arteriolosclerosis- 3 general patterns
- arteriosclerosis- small a's/arterioles (variants- hyaline and hyperplastic) - Monckeberg medial sclerosis- calcification of walls of muscular a's, typically involving internal elastic membrane - atherosclerosis- most freq and clinically important
42
atherosclerosis- morphology
- fibrous cap- smooth m cells, macrophages, foam cells - necrotic center- cell debris, chol crystals, foam cells - media
43
atherosclerosis- constitutional risk factors
- family history- most important!! - age - gender- premenopausal women protected
44
atherosclerosis- MAJOR modifiable risk factors
- hyperlipidemia (LDL)- hypercholesterolemia is sufficient to initiate lesion development!! - HTN - smoking - diabetes mellitus- induces hypercholesterolemia
45
atherosclerosis- MINOR modifiable risk factors
- inflammation- CRP is a marker! - hyperhomocystinemia - metabolic syndrome - lipoprotein a- altered form of LDL that contains apo B-100 portion of LDL linked to Apo A - factors affecting hemostasis
46
CRP
acute phase reactant - expression increased by IL-6 - binds to bacteria, act the classical complement cascade
47
response to injury model for atherosclerosis
-chronic injury and/or dysfxn of endo- leads to chronic infl and attempts to repair the tissue
48
atherosclerosis progression- sequence
- endo injury and dysfxn- causes vascular perm, leukocyte adhesion, thrombosis - accum of lipoproteins and its oxidized forms in vessel wall - monocyte adhesion to endo- foam cells! - platelet adhesion - factor release- induces smooth m cell recruitment - smooth m cell prolif, extracellular matrix prod, recruitment of T cells - lipid accumulation
49
atheroscloersis- arterial wall changes
- chronic endo injury - endo dysfxn - macrophage act, smooth m recruitment - macrophages and smooth m cells engulf lipid (foam cells) - smooth m proliferation, extracellular matrix deposition
50
2 most important causes of endo dysfxn are?
- hemodynamic disturbances | - hypercholesterolemia
51
endo injury- hemodynamic disturbances
-lesions occur at openings of exiting vessels, branch points, posterior abomdinal aorta- due to disturbed flow patterns
52
enjo injury- circulating lipids/hypercholesterolemia
- lipids in plaques are predominantly chol and chol esters - accum in intima, taken up by macrophages, partially oxidized - modified LDL accum in macrophages- foam cells and fatty streak form - stim infl response!
53
dyslipoproteinemias- include?
lipoprotein abnormalities - increased LDL chol levels - dec HDL chol levels - inc levels of abnormal lipoprotein
54
contributes to the initiation and progression of atherosclerotic lesions??
chronic infl!! - infl triggered by accum of chol crystals and free fa's in macrophages - recognized by inflammasome- leads to IL-1 secretion - macrophages and T-lymphocytes recruited - infl cytokines- act endo cells and GFs stim smooth m cells to migrate to intima and proliferate
55
atherosclerosis- smooth m prolif and matrix deposition
- intimal expansion from foam cells and extracellular lipid, infl and smooth m cells and increased ECM- atheromatous plaque formed - soft fibrofatty plaque becomes covered with a fibrous cap (dense collagen fibers)- center is necrotic (lipid, debris, foam cells, thrombus)
56
atherosclerosis- morphology
- fatty streaks | - atherosclerotic plaques
57
atherosclerosis- most common sites of involvement
- abdominal aorta (most common!) - coronary a's - popliteal a's - internal carotid a's - circle of wilis
58
atherosclerotic plaques- 3 principal componets
- smooth m cells, macrophages, T-cells - extracellular matrix- collagen, elastic fibers, proteoglycans - intracellular and extracellular lipid
59
atherosclerotic plaques- complications
- rupture and ulceration- may lead to thrombosis - hemorrhage - embolism - aneurysm formation
60
major consequences of atherosclerosis
- MI - stroke - aortic aneurysms - PVD (gangrene of legs)
61
atherosclerotic stenosis
- plaques continually grow (cycling thru injury-healing process) - lumen shrinks- leads to ischemia downstream- critical stenosis- 70% occluded! - chronic ischemia of myocardium, bowel, brain, extremities (intermittent claudication)
62
acute plaque change- 3 categories
- rupture/fissuring- exposes thrombogenic plaque constituents- thrombus may form!!! - erosion/ulceration- also exposes thrombogenic - hemorrhage into plaque- expands its volume
63
plaques responsible for MI and other acute coronary symptoms are ?
asymptomatic before the acute change!!
64
what stabilizes the plaque?
fibrous cap!- undergoes continuous remodeling- can also make it more susceptible to rupture! -collagen- major structural component!
65
vulnerable plaque
- thin fibrous cap (not much collagen) | - infl in plaque- can accelerate fibrous cap degradation and inhibit its resn- reduces the amt of collagen! weakens it
66
extrinsic influences can contribute to acute plaque changes
- BP | - vasoconstriction- increases physical stress

Cardiovascular II (13 decks)

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