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atherosclerosis Flashcards

1
Q

does the risk for atherosclerosis increase or decrease with age?

A

risk increases with age

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2
Q

is atherosclerosis more prevalent in males or females?

why?

A

more prevalent in males bc estrogen protects against atherosclerosis (usually catch up after menopause)

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3
Q

what are genetic risk factors for atherosclerosis?

A
  • inherited mutations can lead to increased predisposition

- e.g. mutation in LDL receptors leads to accumulation in cholesterol

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4
Q

what are risk factors for atherosclerosis associated with family history?

A

can be multifactorial - based on inherited genes or other factors

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5
Q

how does smoking effect the risk of atherosclerosis?

A
  • can initate or accelerate the disease
  • effects endothelial cells resulting in poor vascualr tone, increased vasoconstriction, oxidation and prothrombotic products
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6
Q

what is the effect of diabetes mellitus on atherosclerosis?

A

associated with increased endothelial dysfunction and lipid levels

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7
Q

what is the effect of hypertension on atherosclerosis?

A

accelerates development of atheromas

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8
Q

what is the effect of hyperlipidemia on atherosclerosis?

A

increases lipid level in blood increasing likelihood of plaque buildup

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9
Q

what is coronary artery disease and what is it caused by?

what can it lead to?

A
  • most common cardiovascular disease
  • casued by atherosclerosis
  • can lead to chest pain, heart attack or death
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10
Q

what are the 3 characteristics of atherosclerosis?

A
  • endothelial dysfunction
  • vascular inflammation
  • build-up of lipids, cholesterol, Ca and other cellular debris
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11
Q

define atherosclerosis

A

when build up of plaque clogs the arteries

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12
Q

what is the contemporary theory for the pathology of atherosclerosis?
give a general explanation for this theory.

A
  • response-to-injury hypothesis
  • states: atherosclerosis develops as healing response to endothelial injury
  • thus, endo dysfuntion is the critical triggering event
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13
Q

what can cause endothelial dysfunction?

A

hemodynamic forces, hyperlipidemia,

hypertension, smoking, toxins, viruses, etc.

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14
Q

what happens once vascular endothelial cells are damaged? (explain altherosclerosis in detail)

A
  • blood contents enter intima of bv
  • LDLs and VDLs are oxidized, monocytes are transformed into macrophages
  • sm cells in tunica media migrate to intima and (w macrophages) engulf LDLs of foam cells
  • engulfing progresses forming an atherosclerotic cap
  • fatty streaks form and progress
  • eventually the complete plaque is formed (now called atheromatus plaque)
  • there’s progressive accumulation of lipids within the tunica intima and plaque grows
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15
Q

what is the first visual manifestation of atheroscleoris?

A

formation of fatty acid streaks

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16
Q

is an atheromatus plaque stable? can it progress?

A
  • clinically stable (not thrombus prone)

- can progress to structurally unstable (thrombus prone)

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17
Q

progression of atherosclerosis (when do symptoms start)?

A
  • earliest event = plaque grows and begins closing off vessel (still symptomless)
  • if builds slowly - once occlusion = 75% now critical and symptoms show (usually chest pain)
  • if acute change in plaque (usually thrombus superimposed on plaque) - symptoms show
  • once the plaque is severe the patient is subject to major complications (heart attack, aneurism)
18
Q

fully formed plaque will be composed of:

A

necrotic tissue at the center and a fibrous cap

19
Q

compare healthy vs atherosclerotic cardiac muscle cells

A
  • healthy = striated with nuceli and intercalated discs
  • atherosclerotic = dying (coloured spots through the muscle shown as result of imflammatory cells recruited to contain the necrotic tissue)
20
Q

what is the clinical presentation of atherosclerotic plaque development leading to blood clot formation?

A

(1) early lesion (endo damage) - no symptoms
(2) plaque growth (damages inner wall of bv, fatty deposits accumulate narrowing arteries) - mild symptoms
(3) plaque ruptutes - spills cholesterol, etc. into bloodstream
(4) causes clot to form and block blood flow to specific part of body

21
Q

hyperlidemia increases the risk of what stage of atherosclerotic development?

A

plaque growth

22
Q

define cardiac tamponade.

is it considered a medical emergency?

A
  • accumulation of fluid in the pericardial sac
  • compresses heart muscle and blood flow
  • medical emergency
23
Q

state the 2 hemodynamic forces and explain how they can influence atherosclerosis

A

(mechanical forces exerted by blood flow)

(1) pressure: acts perpendicular to vessel wall & affects vascular sm cells
(2) shear stress: acts parallel to vessel walls (exherted longitudinally in direction of bf) & affects endo cells
- influenced by type of blood flow
- both forces can damage artery walls leading to atherosclerosis

24
Q

explain laminar blood flow and how it is related to atherosclerosis

A
  • normal condition of blood flow

- research has shown laminar slow induces endo cells to express genes that protect against atherosclerosis

25
Q

explain turbulent blood flow and how it is related to atherosclerosis

A
  • laminar blood flow can become turbulent in aterial curves or at branches
  • now have incresed shear stress
  • blood can swirl around and cause dysfunction in the endo cells or contribute to the accumulation of fats - leading to atherosclerosis
26
Q

explain observable changes in endothelial cell morphology when exposed to physiological shear stress (>15 dynes/cm^2)

A
  • cells are elongated and aligned to the direction of blood flow
  • do this to increase the aerodynamics of their shape
  • minimizes interference with vessel components
27
Q

explain observable changes in endothelial cell morphology when exposed to low arterial l shear stress (0-1 dynes/cm^2)

A

-cells have a cobblestone appearance

28
Q

explain the regulatory features of laminar sheer stress

A
  • endothelial cells express genes like KFL2 or Nrf2
  • act in a protective manner & help inhibit the expression of NFkB (pro-inflammatory transcription factor)
  • blocks oxidative stress/inflammatory pathways
  • limits thrombosis
29
Q

explain the regulatory features of turbulent sheer stress

A
  • expression of protective genes is lost
  • NFkB is upregulated to create a pro-inflammatory environment in bvs
  • allows recruitment of monocytes & macrophages to initate plaque formation
  • also enables sm cells to proliferate
30
Q

compare quiescent phenotypes (laminar) to activated phenotypes (turbulent) of coagulation factors

A
  • quiescent: increased PGL2, NO, tPA and decreased platelet aggregation
  • activated: decreased PGL2, NO, tPA and increased platelet aggregation
31
Q

compare quiescent phenotypes (laminar) to activated phenotypes (turbulent) of endothelium

A
  • quiescent: decreased proliferation, apoptosis and increased alignment
  • activated: increase proliferation, apoptosis and decreased alignment
32
Q

compare quiescent phenotypes (laminar) to activated phenotypes (turbulent) of the inflammatory state

A
  • quiescent: decreased sm proliferation and leukocyte adhesion (anti-inflamm)
  • activated: increased sm proliferation and leukocyte adhesion (pro-inflamm)
33
Q

what are xanthomas? where are they found?

A
  • cholesterol deposits under the skin

- found in joints, eyelids & ankle tendons

34
Q

what are lipoproteins used for?

A

the trandport of lipids in the blood plasma

35
Q

what are 4 lipoproteins and what do they do?

A

(1) CMs (least dense) carry triglycerides from intestine to tissues
(2) VLDLs deliver triglycerides to cells
- converted into intermediary IDL
(3) LDLs main transporter of cholesterol to tissues
- synthesized from VLDL/IDLs
(4) HDLs (most dense) mediator of reverse cholesterol transport

36
Q

explain the process of reverse cholesterol transport

A
  • diet absorbed and transformed into triglycerides & cholesterol
  • CM/VLDLs transport to fat cells
  • synthesized into LDLs - used for bodily functions
  • HDL associates with cholesterol released by LDL and transports it back to the liver
37
Q

how does HDL mediate reverse cholesterol transport (2)

A

(1) direclty binds and deposits cholesterol into liver

(2) interacts with VLDL/LDL causing them to deposit their cholesterol in the liver

38
Q

how do lipids influence atherosclerosis?

A
  • dysfunctional endo cells mediate adhesion/migration of leukocytes with VCAM-1 receptor
  • increased lipids promotes increased expression of VCAM-1
  • suggests hyperlipidemia promotes atherosclerosis through leukocyte adhesion
  • also excess lipids in blood reduces blood flow (more viscous)
39
Q

define primary hyperlipidemia

A
  • result of a genetic disorder

- e.g. gene mutation or receptor protein defects

40
Q

define secondary hyperlipidemia

A
  • acquired - usually as a result of environmental influences or existing health condition
  • e.g. diabetes, hyperthyroidism, pancreatitis
  • diet rich in sugar/fat increases risk
41
Q

explain treatment approaches for hyperlipidemia

A
  • life-style changes (exercise)
  • modified diet
  • statins (drug)
42
Q

explain how statins work (2 fronts)

A
  • lower cholesterol levels by inhibiting cholesterol biosyntesis at the liver by increasing expression of LDL receptors
  • also increase KLF2 expression

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