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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
Q

90-95% of HTN- cause?

A

-idiopathic (essential HTN)

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26
Q

5% of HTN- cause?

A

secondary HTN

  • renal or adrenal disease
  • renal a stenosis
  • endocrine
  • CV
  • neurologic
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27
Q

risk factors for essential HTN

A
  • high Na intake
  • obesity
  • stress
  • smoking
  • physical inactivity
28
Q

malignant HTN- characterized by?

A
  • 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
Q

BP =

A

CO x PVR

CO= SV x HR

30
Q

most important determinant of SV?

A

filling pressure- reg thru sodium homeostasis

31
Q

PVR- constrictors

A
  • ang II
  • catecholamines
  • thromboxane
  • leukotrienes
  • endothelin
32
Q

PVR- dilators

A
  • prostaglandins
  • Kinins
  • NO
33
Q

blood volume and vascular tone- maintained by?

A

renin-angiotensin-aldosterone system!

-low volume- renin released by JG cells- cleaves angiotensinogen to form angI–ACE–> angII

34
Q

angII- fxns

A
  • vascular constriction
  • aldosterone secretion by adrenal gland
  • increase tubular Na reabs
35
Q

volume expansion- induces?

A
  • myocardial release of ANP (atrial natriuretic peptide)

- leads to Na excretion/diuresis and vasodilation

36
Q

secondary HTN- renovascular HTN

A

-renal a stenosis- causes dec glomerular flow- induces renin secretion

37
Q

single-gene disorders that cause HTN

A
  • 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
Q

mech’s of essential HTN

A
  • genetic factors
  • reduced renal Na excretion
  • vasoconstrictive influences
  • environmental factors
39
Q

hyaline arteriosclerosis- morphology

A
  • increased smooth m matrix syn
  • plasma protein leakage (across damaged endo)
  • homogenous pink (hyaline) thickening of vessel wall- lumen narrows
40
Q

hyperplastic arteriosclerosis

A
  • seen in severe HTN

- smooth m cells form concentric lamellations (onion skinning)- lumen narrows

41
Q

arteriolosclerosis- 3 general patterns

A
  • 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
Q

atherosclerosis- morphology

A
  • fibrous cap- smooth m cells, macrophages, foam cells
  • necrotic center- cell debris, chol crystals, foam cells
  • media
43
Q

atherosclerosis- constitutional risk factors

A
  • family history- most important!!
  • age
  • gender- premenopausal women protected
44
Q

atherosclerosis- MAJOR modifiable risk factors

A
  • hyperlipidemia (LDL)- hypercholesterolemia is sufficient to initiate lesion development!!
  • HTN
  • smoking
  • diabetes mellitus- induces hypercholesterolemia
45
Q

atherosclerosis- MINOR modifiable risk factors

A
  • 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
Q

CRP

A

acute phase reactant

  • expression increased by IL-6
  • binds to bacteria, act the classical complement cascade
47
Q

response to injury model for atherosclerosis

A

-chronic injury and/or dysfxn of endo- leads to chronic infl and attempts to repair the tissue

48
Q

atherosclerosis progression- sequence

A
  • 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
Q

atheroscloersis- arterial wall changes

A
  • 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
Q

2 most important causes of endo dysfxn are?

A
  • hemodynamic disturbances

- hypercholesterolemia

51
Q

endo injury- hemodynamic disturbances

A

-lesions occur at openings of exiting vessels, branch points, posterior abomdinal aorta- due to disturbed flow patterns

52
Q

enjo injury- circulating lipids/hypercholesterolemia

A
  • 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
Q

dyslipoproteinemias- include?

A

lipoprotein abnormalities

  • increased LDL chol levels
  • dec HDL chol levels
  • inc levels of abnormal lipoprotein
54
Q

contributes to the initiation and progression of atherosclerotic lesions??

A

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
Q

atherosclerosis- smooth m prolif and matrix deposition

A
  • 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
Q

atherosclerosis- morphology

A
  • fatty streaks

- atherosclerotic plaques

57
Q

atherosclerosis- most common sites of involvement

A
  • abdominal aorta (most common!)
  • coronary a’s
  • popliteal a’s
  • internal carotid a’s
  • circle of wilis
58
Q

atherosclerotic plaques- 3 principal componets

A
  • smooth m cells, macrophages, T-cells
  • extracellular matrix- collagen, elastic fibers, proteoglycans
  • intracellular and extracellular lipid
59
Q

atherosclerotic plaques- complications

A
  • rupture and ulceration- may lead to thrombosis
  • hemorrhage
  • embolism
  • aneurysm formation
60
Q

major consequences of atherosclerosis

A
  • MI
  • stroke
  • aortic aneurysms
  • PVD (gangrene of legs)
61
Q

atherosclerotic stenosis

A
  • 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
Q

acute plaque change- 3 categories

A
  • rupture/fissuring- exposes thrombogenic plaque constituents- thrombus may form!!!
  • erosion/ulceration- also exposes thrombogenic
  • hemorrhage into plaque- expands its volume
63
Q

plaques responsible for MI and other acute coronary symptoms are ?

A

asymptomatic before the acute change!!

64
Q

what stabilizes the plaque?

A

fibrous cap!- undergoes continuous remodeling- can also make it more susceptible to rupture!
-collagen- major structural component!

65
Q

vulnerable plaque

A
  • 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
Q

extrinsic influences can contribute to acute plaque changes

A
  • BP

- vasoconstriction- increases physical stress

Cardiovascular II (13 decks)

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