Hyperlipidemia Flashcards
Hyperlipidemia classes of medication?
- Cardiac glycosides
- Hyperlipidemia treatment
- Bile acid sequesterants
- Cholestrol absorption inhibtor
- PC5K-9 Inhibitor
Cardiac glycosides drug and two effects?
Digoxin
Positive ionotrope
Negative chronotrope
Positive ionotrope of digoxin?
- The heart has two channels, Na+/K+ pump and the Na+/Ca2+ pump
- Digoxin will block the Na+/K+ pump and not the Na+/Ca2+ pump
- With accumulated Na+ in the cell, the Na+/Ca2+ pump will be overactive and increase Ca2+ and influx and Na+ efflux
- Increased Calcium increases cardiac contractility and cardiac output. This increases the oxygen demand by the heart.
Digoxin negative chronotrope effect?
- Digoxin will increase vagal nerve activity on the SA and AV node
- This will block the conduction through the AV node and decrease SA node firing
- Thisrecp will increase the sensitivity of SA and AV node to ACh
- This will utimately activate the M2 muscuranic recepetor in the heart and this will decrease heart rate
Digoxin two ultimate effects on the heart
The ultimate positive ionotropic effect is increased contractility and and cardiac output
The ultimate negative chronotrope effect is bradycardia
Hypokalemia effects on Digoxin efficacy?
Digoxin binds on the same site as potassium on the Na+/K+pump.
Thus, decreased Potassium means no competition for binding and this potentiates the effects of digoxin and can cause toxicity and thus can cause hyperkalemia
Types of hyperlipidemia treatment?
- HMG-CoA Reductase inhibitor
- Fibrates
Statins MOA?
In the liver,
-HMG-CoA is converted to mevalonic acid by HMG-CoA reductase
-Mevalonic acid is then converted into cholesterol
-Statins inhibit HMG-CoA reductase and thus a decrease in the production of mevalonic acid and cholesterol
Most effective drug in the lowering of LDL?
HMG-CoA reductase inhibitors/Statins
HMG-CoA Reductase inhibitors drugs?
SAR Statin(Sars Satan)
Simvastatin
Atorvastatin
Rouvastatin
HMG-CoA Reductase inhibitors effect on LDL receptors?
When body detects decrease cholesterol in the blood, the liver increases synthesis of liver LDL receptors.
As a result, LDL in the blood will bind to LDL receptors on the liver and be internalised
HMG-CoA Reductase inhibitors effects on:
LDL
Cholesterol
HDL
Triglycerides
Decreased LDL
Decreased Cholesterol
HDL remains the same
Decreased Triglycerides
Good and bad cholesterol?
Good cholesterol-HDL
Bad cholesterol-LDL
Fibrates drugs?
Bezafibrates
Gemfibrozil
Fibrates MOA?
Increased PPAR-gamma, agonist, thus increased HDL
Increased LPL
Fibrates effect :
LDL
Cholesterol
HDL
Triglycerides
Apo-AI & Apo-AII
FFA & Lipids
Increased LDL
Decreased Cholesterol
Increased HDL
Decreased Triglycerides
Increased Apo-AI & Apo-AII
Deposition FFA & Lipids
Which drug is effective in increasing HDL?
Fibrates
Fibrates & Statins S/E?
Rhabdomyolysis
Myalgia
Increased Liver enzymes(can damage liver)
Why are statins and fibrates CI from each other?
They exacerbate S/E
Bile acid sequestrants drugs?
Cholestyramine
Bile acid synthesis?
Digestion and absorption of lipids in the GIT
Cholestyramine MOA?
Cholestyramine binds negatively charged bile acids and salts in the small intestines
-Thus preventing their absorption of lipids
-Cholestyramine-bile acids complex eliminated from the body
Systematic effects of cholestyramine and why?
Little few systematic effects because the cholestyramine-bile acid complex is eliminated from tehir body
Cholestyramine effect on LDL receptors?
-The liver upregulates the expression of the LDL-receptors in its surface in response to decreased lipid content
-This will increase LDL binding of the liver
