Patient Drugs

Question 0

HMG-Coa reductase

Answer 0

HMG-CoA reductase (or 3-hydroxy-3-methyl-glutaryl-CoA reductase or HMGCR) is the rate-controlling enzyme (EC 1.1.1.88& EC 1.1.1.34) of the mevalonate pathway, the metabolic pathway that produces cholesterol and other isoprenoids. Normally in mammalian cells this enzyme is suppressed by cholesterol derived from the internalization and degradation of low density lipoprotein (LDL) via the LDL receptor as well as oxidized species of cholesterol. Competitive inhibitors of the reductase induce the expression of LDL receptors in the liver, which in turn increases the catabolism of plasma LDL and lowers the plasma concentration of cholesterol, an important determinant of atherosclerosis.[1] This enzyme is thus the target of the widely available cholesterol-lowering drugs known collectively as the statins. HMG-CoA reductase is anchored in the membrane of the endoplasmic reticulum, and was long regarded as having seven transmembrane domains, with the active site located in a long carboxyl terminal domain in the cytosol. More recent evidence shows it to contain eight transmembrane domains.[2]

Question 1

Simvastatin

Answer 1

Trade name: zocor
Hypolipidemic drug
MOA: an HMG_coa reductase inhibitor
Interferes with cholesterol biosynthesis
It prevents conversion of the enzyme HMG-CoA to mevalonate
Therapeutic effect: decreases LDL, cholesterol, VLDL and plasma triglyceride. Slightly increase serum HDL concentration
Pharmacokinetics:
Protein binding: 95%
We’ll absorbed from GI tract, undergoes extensive first pass metabolism, hydrolized to active metabolites. Half life less than 3 hours. Eliminated in feces

Question 2

Cholesterol synthesis

Answer 2

All animal cells manufacture cholesterol for their use, with relative production rates varying by cell type and organ function. About 20–25% of total daily cholesterol production occurs in the liver; other sites of higher synthesis rates include the intestines, adrenal glands, and reproductive organs. Synthesis within the body starts with one molecule of acetyl CoA and one molecule of acetoacetyl-CoA, which are hydrated to form 3-hydroxy-3-methylglutaryl CoA (HMG-CoA).[34] This molecule is then reduced to mevalonate by the enzyme HMG-CoA reductase. This is the regulated, rate-limiting and irreversible step in cholesterol synthesis and is the site of action for the statin drugs (HMG-CoA reductase competitive inhibitors).

Question 3

Mavik( trandoropril)
1. Ace inhibitor ( angiotensin converting enzyme)
2 use for tx of hypertension and CHF
3. Causes vasodilation
4. It blocks angiotensin converting enzyme which is part of renin-angiotensin system which regulates bp

Answer 3

Mavik( trandoropril)
1. Ace inhibitor ( angiotensin converting enzyme)
2 use for tx of hypertension and CHF
3. Causes vasodilation
4. It blocks angiotensin converting enzyme which is part of renin-angiotensin, aldosterone system which regulates bp

Question 4

Ace inhibitors

Answer 4

Angiotensin-converting enzyme inhibitors reduce the activity of the renin-angiotensin-aldosterone system (RAAS) as the primary etiologic (causal) event in the development of

1. hypertension in people with diabetes mellitus, as part of the insulin-resistance syndrome
2. or as a manifestation (outward indication) of renal disease.[2]