DRUGS: Lipid D/O Flashcards
What Classes of Drugs under Lipid D/O (5)
- HMG-COA Reductase Inh. (Statins)
- Nicotinic Acid
- Fibric Acid Derv./Fibrates
- Bile Acid Binding Resins (BAS)
- Sterol Absorption Inh.
What class of Drugs:Lipid D/O stated below:
▪️Aka: Statins
▪️MOA: Concept: De Novo Cholesterol Biosynthesis - process of self-production of cholesterol by the liver; usually happens at night (Liver= peaks @ night)
▪️Uses
- 1st line: hypercholesterolemia
- For stabilization of atheromatous plaque formation (4-6 months)
▪️-statins except: Cilostatin, Nystatin, Somatostatin
▪️Teratogenic or C/I: Pregnancy
HMG-COA Reductase Inh.
What are the effects of Statins?
▪️↓ Cholesterol
▪️↓ LDL
▪️↑ HDL
2 Classification of DOA of HMG-CoA Reductase Inh. (Statins)
- Short-acting (t1/2: 1-3 hrs.)
- Long-acting (can be taken anytime of the day)
What type of DOA of HMG-CoA Reductase Inh. (Statins) stated below
▪️t1/2: 1-3 hrs
▪️taken @ night
▪️majority of statins except Ator & Rosu
Short-acting Statins
What type of DOA of HMG-CoA Reductase Inh. (Statins) stated below
▪️can be taken anytime of the day
▪️Atorvastatin (Lipitor): t1/2: 14 hrs
▪️Rosuvastatin: t1/2: 19 hrs
Long-acting Statins
What drug is stated below:
Most effective in the management of hypercholesterolemia
Rosuvastatin (Crestor)
What class of Drugs:Lipid D/O stated below:
▪️Form of Niacin (B3) [Nicotinic Acid- has a hypolipidemic effect, Niacinamide x)
▪️MOA:
1. Activates lipoprotein lipase (LPL)
2. (-) synthesis & release of VLDL
3. (-) HDL catabolism- most effective (breakdown)
4. (-) lp(a) lipoprotein
▪️Uses:
- Mgt. hypertriglyceridemia
- Mgt. lp(a) hyperlipoproteinemia
Nicotinic Acid
What are the effects of the ff:
- Activates lipoprotein lipase (LPL)
- (-) synthesis & release of VLDL
- (-) HDL catabolism- most effective (breakdown)
- (-) lp(a) lipoprotein- bad lipoprotein
- ↓ TGs
- ↓ VLDL
- ↑ HDL
- ↓ risk: Angina Pectoris
T/E of Nicotinic Acid
What treatment is used when the patient becomes red (erythema) due to nicotinic acid
NSAIDs such as ASA/Ibuprofen to block COX
- the redness or flushing occurs due to PGs
What class of Drugs:Lipid D/O stated below:
▪️MOA:
- Peroxisome Proliferator Activated Receptor
- PPAR-a-agonists
- activates LPL:↓TGs
- activates ApoAl, ApoAll proteins: ↑ HDL
- (-) ApoCIII proteins: ↓VLDL
▪️Uses:
- 1st line: hypertriglyceridemia
- Mgt. Metabolic Syndrome
Fibric Acid Derivatives/Fibrates
What class or category of Drugs:Lipids belongs the ff. drugs:
▪️Fenofibrate
▪️Clofibrate-T/E: hepatobiliary CA
▪️Gemfibrozil
Fibric Acid Derivatives/Fibrates
What class of Drugs:Lipid D/O stated below:
▪️Aka: BA (Bile Acid) Sequestrants
▪️MOA: (-) biliary recycling
= ↓ cholesterol, ↓ LDL, ↑ HDL
▪️Uses:
- add ons on statins for hypercholesterolemia
- Antidote for oral poisonings such as for Warfarin and Digoxin
Bile Acid Binding Resins
What class or category of Drugs:Lipids belongs the ff. drugs:
▪️ Cholestyramine
▪️ Colestipol
▪️ Colesevelam
Bile Acid Binding Resins
What class of Drugs:Lipid D/O stated below:
▪️Drug Ezetimibe belongs here
▪️MOA: (-) Niemann-Pick C1-Like 1 Transporter (NPC1L1)
▪️Use: co-admin w/ statins for hypercholesterolemia [Simvastatin + Ezetimibe (Vytorin) ]
Sterol Absorption Inh.
