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Systemic Pharmaco > Lipid-Lowering Drugs > Flashcards

Lipid-Lowering Drugs Flashcards

1
Q

What is the function of lipoproteins?

A

Transport hydrophobic lipids

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2
Q

Lipoproteins are separated by ultracentrifugation (density).

The greater the content of ______ in the lipoprotein, the lower the ______ of the lipoprotein.

The greater the content of ______, the higher the ______ of the lipoprotein.

A

TG, density

Protein, density

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3
Q

Rank the lipoproteins from highest to lowest density

A

CM > VLDL > IDL > LDL > HDL > free fatty acids/albumin

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4
Q

What are chylomicrons?

Where are they formed? What type of lipids do they carry?

A
  • Formed in mucosal epithelial cells of the small intestine
  • Contain mainly dietary lipids
  • Transported to adipose tissue for storage
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5
Q

What are VLDLs?

Where are they formed? What type of lipids do they carry?

A
  • Synthesized in hepatocytes

- Contain mainly endogenous lipids

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6
Q

How are the TGs in CMs and VLDLs lost?

A

Apo C2 activates endothelial lipoprotein lipase, releasing FFAs for takeup by:

  1. Adipocytes (for storage)
  2. Muscle cells (ATP production)
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7
Q

What are IDLs?

What are they also called? What are they derived from? What can they become?

A

Also called ßVLDL or VLDL remnants

  • Derived from TG depletion of VLDL
  • Taken up by liver for reprocessing or upon further TG depletion, becomes LDL
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8
Q

What are LDLs?

Why are they also known as “bad” cholesterol?

A

When present in excessive numbers, LDLs deposit cholesterol in and around smooth muscle fibers in arteries, forming fatty plaques, increasing risk of coronary artery disease

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9
Q

What are HDLs?

Where are they formed? What is their function? Why are they known as “good” cholesterol?

A
  • Made in the liver
  • Remove excess cholesterol from body cells and the blood and transport it to the liver for elimination
  • High HDL levels are associated with decreased risk of coronary artery disease
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10
Q

What is the exogenous pathway of cholesterol transport?

A
  1. TGs in CMs hydrolysed in LPL in tissues
  2. CM remnants bind to receptors on hepatocytes and undergo endocytosis
  3. Chol is stored, oxidised to bile acids, or secreted in bile
  4. Or it may enter endogenous pathway in VLDL
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11
Q

What is the endogenous pathway of cholesterol transport?

A
  1. Chol and newly synthesized TGs transported from liver as VLDLs to muscle & adipose tissues
  2. TGs hydrolysed
  3. VLDLs become LDLs
  4. Hepatocytes take up LDL by endocytosis via LDL receptors
  5. Chol can return to plasma from tissues in HDL
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12
Q

What is the cause of type I familial hyperchylomicronemia? What is the lipid profile?

A

LPL deficiency

  • High TG
  • Atherosclerosis risk NE
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13
Q

What is the cause of type IIa familial hypercholesterolemia? What is the lipid profile?

A

Decreased no. of LDL receptors, decreased LDL uptake

  • High chol
  • High atherosclerosis risk
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14
Q

What is the cause of type IIb familial combined (mixed) hyperlipidemia? What is the lipid profile?

A

Overproduction of VLDL by liver

  • High chol & TG
  • High atherosclerosis risk
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15
Q

What are the classes of drugs used in hyperlipidemias?

A
  1. Niacin
  2. Fibrates
  3. Resins
  4. HMG-CoA reductase inhibitors
  5. Inhibitors of intestinal sterol absorption
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16
Q

What is the MOA of niacin?

A
  1. Strongly inhibits lipolysis of TGs into FFAs
    - Lower TG and chol in VLDL & LDL
  2. Increase HDL-chol levels (most potent)
  3. Decrease circulating fibrinogen, increase tissue plasminogen activator
    - Reverse thrombosis associated w hypercholesterolemia & atherosclerosis
17
Q

How is niacin administered?

A

Oral

- Converted to nicotinamide in body

18
Q

What are the clinical uses of niacin?

A

Widely used, esp for treatment of:

  1. Type IIb – familial combined hyperlipidemia (VLDL overproduction)
  2. Type IV – familial hypertriglyceridemia (VLDL overproduction &/or decreased removal)
19
Q

What are the adverse effects of niacin?

A
  1. Intense cutaneous flush & pruritus (hypersensitivity)

2. Hyperuricemia, gout

20
Q

What are the fibrates?

A

Gemfibrozil
Fenofibrate
Clofibrate

21
Q

What is the MOA of fibrates?

A

Activates the peroxisome proliferators-activated receptor-alpha (PPAR-a) pathway

  • Increased activity of LPL
  • More efficient breakdown of TGs
  • Decrease plasma TG levels
  • Decrease VLDL in part bc of decreased secretion by liver
  • HDL levels rise moderately
22
Q

What are the clinical uses of fibrates?

A

Treatment of:

  1. Type IV – familial hypertriglyceridemia (VLDL overproduction &/or decreased removal)
  2. Type III – familial dysbetalipoproteinemia (IDL overproduction or underutilization)
23
Q

What are the adverse effects of fibrates?

A
  1. GI effects: nausea
  2. Skin rashes (hypersensitivity)
  3. Gallstones
  4. Myositis (myocytes inflammation)
24
Q

What are the bile acid binding resins?

A

Cholestipol

Cholestyramine

25
Q

What is the MOA of bile acid binding resins?

A

Anion exchange resins bind negatively charged bile acids and bile salts in small intestine

  • Lower bile acid conc. w increased loss in feces
  • Hepatocytes increase conversion of chol to bile acids
  • Decrease in intracellular chol conc.
  • Increase hepatic uptake of LDL
  • Decrease in LDL
  • May increase VLDL but have little effect on HDL
26
Q

How is bile acid binding resins administered?

A

Oral only

27
Q

What are the clinical uses of bile acid binding resins?

A

Treatment of:

  1. Type IIa – familial hypercholesterolemia (decreased no. of LDL receptors)
    • niacin: LDL elevations in Type IIb– familial combined hyperlipidemia (VLDL overproduction)
28
Q

What are the adverse effects of bile acid binding resins?

A
  1. GI effects: constipation, nausea, flatulence (food for bacteria in gut)
  2. Impaired absorption of fat-soluble vitamins ADEK – will require supplements
29
Q

What are the HMG-CoA reductase inhibitors?

A

Atorvastatin
Simvastatin
Pravastatin
Fluvastatin

30
Q

What is the MOA of HMG-CoA reductase inhibitors?

A

Competitively inhibit HMG-CoA reductase (rate-limiting step in chol synthesis)

  • Lower chol levels
  • Upregulate LDL receptors on hepatocytes
  • Decrease LDL levels
31
Q

How and when are HMG-CoA reductase inhibitors administered?

A

Oral, first pass extraction

Given in the evening bc of nocturnal secretion

32
Q

What are the clinical uses of HMG-CoA reductase inhibitors?

A
  1. Effective in lowering plasma chol levels in all types of hyperlipidemias (1st line)
  2. Reduce risk of coronary events and mortality in patients with IHD
33
Q

What are the adverse effects of HMG-CoA reductase inhibitors?

A
  1. Liver: biomedical abnormalities in liver fn (increased liver enzymes)
  2. Muscle: myopathy (muscle weakness), rhabdomyolysis (breakdown of skeletal muscles causing tea-coloured urine)
34
Q

What are the inhibitors of intestinal sterol absorption?

A

Ezetimibe

35
Q

What is the MOA of the inhibitors of intestinal sterol absorption??

A

Selective inhibitor of chol transport protein NPC1L1 in intestine
- Chol not absorbed into body

36
Q

Will the absorption of intestinal sterol absorption be effective in the absence of dietary cholesterol?

A

Yes. It also inhibits absorption of bile salts for recycling

37
Q

What is the clinical use of inhibitors of intestinal sterol absorption?

A

Reduction of LDL (better effects w statin)

38
Q

The other drug is ezetimibe often combined with statins. Which statin? What is the combined drug called?

A

+ Simvastatin = Vytorin

39
Q

What is the adverse effects of inhibitors of intestinal sterol absorption?

A

Reversible impaired liver fn (low incidence – need to undergo routine liver fn test)

Systemic Pharmaco (6 decks)

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