Drug Classes for Dyslipidemias (+ example, MOA, AEs)

Question 1

Statins (Example, MOA, AEs)

Answer 1

Example: Atorvastatin

MOA: Inhibits HMG-CoA reductase
(dec. intracellular cholesterol –> inc. LDL-R expression –> inc. hepatic uptake of LDL-C –> dec. LDL-C in blood)

AEs: Hepatotoxicity
Skeletal muscle toxicity (can be affected by dose + DDI)

*best results for dec. LDL-C

Question 2

Cholesterol Absorption Inhibitors (Example, MOA, AEs)

Answer 2

Example: Ezetimibe

MOA: Inhibits NPC1L1 transporter [that moves cholesterol –> blood]
(dec. absorption of cholesterol from GI –> dec. incorporation of cholesterol into chylomicrons –> dec. cholesterol delivery to liver –> dec. intracellular cholesterol –> inc. LDL-R expression –> inc. hepatic update of LDL-C –> dec. LDL-C

AEs: minimal

Question 3

Bile Acid Sequestrants (Example, MOA, AEs)

Answer 3

Example: Cholestyramine

MOA: binds BA in the intestines [to prevent recycling] (inc. fecal excretion of BAs –> dec. intracellular BAs –> inc. BA synthesis –> dec. intracellular cholesterol –> inc LDL-R expression –> inc. hepatic uptake of LDL –> dec. LDL-C

AEs: GI - bloating, constipation, nausea, gas (due to acid build up on GI tract)

Question 4

PCSK9 Inhibitors (Example, MOA, AEs)

Answer 4

Example: Alirocumab

MOA: monoclonal antibody binds to PCSK-9 [a protein that results in bind/degrade of LDL-R]
(inc. LDL-R expression –> inc. hepatic update of LDL –> dec. LDL)

AEs: Injection site reactions
Allergic reactions

*better efficacy than statins

Question 5

Nicotinic Acid (Example, MOA, AEs)

Answer 5

Example: Niacin

MOA: Activates niacin receptors (Gi- coupled) on fat cells [to dec amount of cAMP]
(dec. HSL –> dec. lipolysis –> dec. release if fatty acids –> dec. hepatic TG synthesis –> dec. VLDL –> dec. LDL C)

AEs: Flushing
Itching
Dyspepsia
Headache
Hepatotoxicity
Hyperglycemia
Hypperuricemia