biochemistry 7 Flashcards

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1
Q

what is atherogenesis

A

process that leads to narrowing or sudden complete occlusion of the arterial lumen
- lipid deposition in the subendothrlial layer

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2
Q

what are the arteriosclerotic cardiovascular diseases

A
  • coronary heart disease
  • stroke
  • peripheral vascular disease
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3
Q

what are the complications of atherosclerosis

A
  • renal artery disease
  • aneurysms
  • coronary heart disease
  • stroke
  • peripheral artery disease
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4
Q

what are the major stages of atherosclerosis

A

1) endothelial dysfunction
2) formation of lipid layer within the intima
3) monocytes and smooth muscle cells migrate into vessels wall forming macrophages
4) foam cell formation - cholesterol as detergent
5) degradation of extracellular matrix —-> plaque formation and displacement

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5
Q

what is calcification and what does it cause

A
  • calcium build up in plaques
  • > 5 years after plaque formation
  • problem in over 40s
  • arteries stiff, reduced expansion/contraction
  • more difficult to treat
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6
Q

what does a normal endothelial cell do

A
  • high kruppel-like factors (KLF2,KLF4) - anti-inflammatory control
  • low NFxB - proinflammatory factors
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7
Q

what does dysfunctional endothelium cells do

A
  • KLF factors suppressed
  • NFxB predominates - increases expression of cell-adhesive moclules and promotes adhesion of monocytes and T lymphocytes to the endothelium
  • decreases NO production - promotes vasoconstriction
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8
Q

what are the inflammatory autoimmune conditions and what do they do

A
  • rheumatologic disorders
  • systemic lupus erythematosus
  • they elevate systemic inflammation
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9
Q

what are the risk factors for elicit pro-inflammatory cytokines

A
  • Interleukin-1 (IL-1)
  • Tumour necrosis factor-alpha (TNF-α)
  • Interferon (IFN)
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10
Q

what are the accentuated traditional factors for atherosclerosis

A
  • dyslipidemia
  • smoking
  • hypertension
  • physical inactivity
  • insulin resistance
  • obesity
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11
Q

how does HDL protect against atherosclerosis

A
  • HDL removes cholesterol from macrophages
  • cholesterol returned o liver - generates bile salts or excretion
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12
Q

what occurs when there is a blockage of cholesterol transferred to HDL

A
  • premature atherosclerosis
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13
Q

what is the function of cholesterol

A
  • modulates membrane fluidity
  • some nerve cells have 25% plasma membrane
  • precursor for steroid hormones
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14
Q

how much cholesterol is found in the brain

A
  • 25% of bodies cholesterol
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15
Q

what changes in pathways can cause Parkinson’s disease

A
  • decreased cholesterol
  • increases eicosanoids
  • increases DAG, TAG and glycerophosphoinositol
  • decreased sphingomyelin
  • increased ceramide and gangliosides
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16
Q

what are the treatments to decrease fat

A
  • decreased fat intake
  • exercise
  • medical intervention
17
Q

what does increasing LDL receptors via treatment do

A
  • increased DL uptake from the blood —> increase cholesterol clearance
18
Q

what happens when using treatment to decrease cholesterol precursors

A
  • inhibit bile salt - ingesting a charged resin that binds to bile salts decreasing reabsorption
  • inhibits HMG CoA reductase - by statins which decreases cholesterol synthesis
19
Q

what do PCSK9 inhibitors to

A
  • targets LDL receptors via degradation
  • inhibitors are monoclonal antibodies
20
Q

what do fibrates do

A
  • agonists of PPAR alpha transcription factor
  • stimulates lipoprotein lipase - decreases plasma triglyceride concentration and increases HDL
21
Q

what does niacin do

A
  • binds niacin receptors
  • reduce free fatty acid release from adipose
  • inhibits HDL uptake by the liver
    overall:
  • raise HDL
  • lower LDL
  • lower triglycerides
22
Q
A