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PHARMACOLOGY > Lipid lowering drugs + Atherosclerosis > Flashcards

Lipid lowering drugs + Atherosclerosis Flashcards

1
Q

what is atherosclerosis

A 
thickening of the inner arterial wall:
fatty materials (plaque)
chronic inflammation
reduced blood flow 
increased blood pressure
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2
Q

medical conditions associated with atherosclerosis

A
  1. coronary artery disease
  2. stroke
  3. peripheral vascular disease (narrowing of b.v > reduced blood flow to limbs)
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3
Q

relationship between blood cholesterol level and heart attack risk

A

increase in blood cholesterol level increases heart attack risk

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4
Q

how are lipids transported through the bloodstream

A

in lipoprotein complexes

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5
Q

where is most blood cholesterol found

A

LDL fraction

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6
Q

what ratio of cholesterol is beneficial

A

high HDL: LDL

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7
Q

plaque formation

A
  1. absorption of oxidized LDL-C - endothelial surface injury
  2. inflammatory response
  3. macrophage infiltration
  4. foam cell formation
  5. plaque enlarges - capped by sm cells
  6. cap ruptures:
    - RBC platelets are attracted
    - clots form
    - potential thrombosis
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8
Q

hyperlipidemia

A

high levels of lipids in blood

primary (genetic):
elevated LDL, VLDL, or chylomicrons
type II: highest risk for atherosclerosis

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9
Q

risk factors for secondary hyperlipidemia

A 
alcohol
smoking
obesity
diabetes mellitus
kidney disease
hypothyroidism
hypertension
liver disease
retinoic acid 
age
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10
Q

drugs used to treat atherosclerosis

A

STATINS

FIBRATES

Cholesterol absorption inhibitors:

  • BILE ACID-BINDING RESINS
  • EZETIMIBE

NIACIN

OMEGA-3 FATTY ACIDS

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11
Q

what is STATIN

A

HMG CoA reductase inhibitor (block enzyme needed to make cholesterol)
Prodrug: administered in inactive form - metabolized to active form
mimics the HMG CoA substrate intermediate

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12
Q

how does STATIN work

A

plasma LDL reduction

HMG CoA reductase inhibitor
direct cholesterol synthesis reduction
increased expression of LDL receptors

reduce vascular inflammation
reduce platelet aggregation
stabilisation of atherosclerotic plaques
immunosuppression

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13
Q

side effects of STATIN

A

GI disturbance

myositis (muscle inflammation)
myopathy (muscle weakness)

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14
Q

how does FIBRIN work

A

clofibrate

  1. activates PPARa - regulator of lipid metabolism in blood
    activation promotes fatty acid degradation
  2. promotes increased lipoprotein lipase activity
    - triglyceride degradation
    - reduces serum VLDL
  3. promotes decreased diacetyl acetyltransferase activity
    - DAT = triglyceride formation
  4. increased LDL uptake
  5. increased plasma HDL
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15
Q

side effects of FIBRATES

A

GI distress

rhabdomyolysis when given with a statin

interferes with metabolism of oral anticoagulants by competing for Cytochrome P450 drug-metabolizing enzymes

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16
Q

Cholesterol absorption inhibitors I:

A

BILE ACID BINDING RESINS

treat: hypercholesterolemia

-anion exchange resins, exchange Cl- for bile acids
= decrease bile acid + cholesterol reabsorption
increase LDL receptors

reduce plasma cholesterol + coronary heart disease

17
Q

side effects of BILE ACID RESIN

A

constipation

inhibits absorption of fat-soluble vitamins

should not be administered with medications that are primarily absorbed in the intestines

18
Q

Cholesterol absorption inhibitors II:

A

EZETIMIBE
competitive inhibitor of cholesterol absorption from intestine
- blocks binding of cholesterol to transporter
- moderate effect on LDL levels when used alone
-used in combination with low dose statin - benefit reduced tolerance to statins

Side effects: GI distress

19
Q

NIACIN

A

treats hypercholesterolemia
most effective - when used with bile binding resins

stimulates GPR109A = inhibit fat breakdown in adipose tissue
=decreases VLDL formation => increasing HDL fraction

20
Q

side effects of nicotinic acid

A

worsen cardiac arrhythmias
worsen gout/gall bladder/liver disease
GI distress
flushing/rash

reduced with extended-release niacin

21
Q

OMEGA-3 FATTY ACIDS

A

found in oily fish
reduce plasma triglycerides by increasing lipoprotein lipase + reducing synthesis of VLDL

eicosapentaenoic acid can replace arachnoid acid in cell membranes - decreased synthesis of prostaglandins (involved in platelet aggregation/inflammation)

not useful for treating high cholesterol // may elevateHDL fraction

22
Q

ACETYLSALICYLIC ACID

A

inhibits platelet aggregation by blocking Cox-1

23
Q

CLOPIDOGREL

A

anti-platelet

PHARMACOLOGY (24 decks)

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