S21 Cardio biochemistry Atherosclerosis Flashcards

1
Q

formation fo ahterosclerotic plaque

A

modified LDLs readily penetrate arterial endothelia; increases adhesion expression

less LDL receptor mediated uptake and more scavenger (SR-B1) uptake promoting monocyte differentiation to macrophage and foam cells

monocytes and platelets recruited to sub-endothelial space: elicit inflammatory response.

LDL degraded to produce foam cell macrophage with accumulated cholesterol. foam cells secrete factors to activate SMC proliferation and ECM deposition.

dying macrophage leave behind other atherosclerotic plaque on innermost layer of artery

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2
Q

II-A (hypercholesterolemia)

A

common

familial hypercholesterolemia, combined hyperlipidemia
polygenic hypercholesterolemia

LDL elevated

CHOL elevated

severe atherogenicity

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3
Q

II-b (combined hyperlipemia)

A

most common

familial combined hyperlipidemia

unclassified

LDL, VLDL elevated

CHOL, TG elevated

Severe atherogenicity

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4
Q

IV (endogenous hyperlipemia)

A

common

Familial hypertriglyceridemia (mild)
Familial combined hyperlipidemia
Sporadic combined hypertriglyceridemia
Tangier’s Disease

VLDL elevated

TG elevated

mild to moderate atherogenicity

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5
Q

Monogenic hyperlipoproteinemias

A

gene defects causing hyperlipoproteinemias are often monogenic and fall into 4 categories
- Aloliprotein disorders: Apo A, B, CII, E

  • Enzyme disorders: lipoprotein lipase, hepatic lipase, lecithin: cholesterol Acyl transferase
  • Receptor Disorder: LDL Receptor, Cholesterol Ester Transfer Protein, Microsomal Transfer Protein, ABC1 transfer protein
  • other: chylomicron retention disease

LDL receptor mutations (5 types_

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6
Q

apoB100 deficiencies often present with

A

xanthomas of eyes, skin and feet

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7
Q

Metabolic syndrome is defined by

A

hypertriglyceridemia >150
low HDL cholesterol <5o in women, <40 in men

hypertension >130/85 mmHg

increased waist circumference >35 in women, >40 in men

elevated fasting blood glucose >100 mg/dl

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8
Q

insulin in lipid metabolism

A

suppresses adipocyte lipolysis by hormone sensitive lipase

surpasses hepatic VLDL production
stimulates uptake of FFA from TRL into adipocytes and non-hepatic peripheral tissues by LPL

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