M13 - Lipid Pharm Flashcards
Statins (MOA/AE/Tests)
*FIRST line therapy
MOA: inhibit HMG CoA reductase = increase LDL R exp. = decrease LDLC (and decrease TGs)
AE:
-Hepatotoxicity
-SKM toxicity (mmmr)
*should get baseline LFTs (ALT/AST) and CK
Increased SKM tox with:
1. Increased statin dose
2. Drug-drug interactions
3. Low thyroid hormone levels
4. Low vitamin D levels
Ezetimibe (MOA/AE)
MOA: inhibits NPC1L, increase LDL R exp. = decrease LDLC
AE: minimal
Cholestyramine, Colestipol, Colesevelam (MOA/AE)
BA Sequestrants
MOA: increase LDL R exp. = decrease LDLC
AE: very safe bc not absorbed systemically
-GI (bloat/constipation/nausea/flatulence)
-Can affect GI abs. of other drugs/fat sol vits
Alirocumab, Evolocumab (MOA/AE)
PCSK-9 Inhibitors (monoclonal antibody, SC inj)
MOA: increase LDL R exp. = decrease LDLC
AE:
-Inject site rxn
-Allergic rxn
Niacin (MOA/AE)
MOA: activate gpcr on adipose, decrease TG synthesis = decrease VLDL and LDLC
AE: FIDHHHH
-Flushing, itching, dyspepsia, headache
-Hepatotoxicity
-Hyperglycemia
-Hyperuricemia
*Increased risk of SKM toxicity with statins
Fenofibrate, Gemfibrozil (MOA/AE)
FIBrates
MOA: activate PPARα, decrease VLDL, may increase LDLC (increase fatty acid ox. also)
AE:
-GI (dyspepsia, abd. pain, diarrhea, constipation)
-Increase gallstone formation
-Increase risk of SKM tox with statins (esp. gem)
Highest LDL-C Lowering
Statins, PCSK9 inhibitors
Highest TG Lowering
Fibrates, Niacin, Statins
Highest HDL-C Raising
Niacin
Used for: Central DI
Desmopressin (ADH congener)
MOA: increase water permeability of CNT and
CD = increase water reabsorption
AE: Hyponatremia
Used for: Hyperthyroidism
Anti-thyroid drugs (Meth and PTU)
MOA: inhibit thyroid peroxidase, decrease levels of TH
AE:
-Rash
-Hepatotoxicity
-Agranulocytosis
Meth preferred; PTU = black box warning for
hepatotoxicity (reserved for intolerance to methimazole or 1st trimester pregnancy)
