USA Pharm Exam 3 – Practice Questions & Answers
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Terms in this set (137)
first-pass metabolism of orgainic -ISDN undergoes first-pass metabolism to form
nitrates (ISDN, ISMN) ISMN
-ISMN does not undergo first-pass metabolism when
given PO
first-pass metabolism of NTG -bioavailability of NTG very low due to first-pass
-SL route avoids this but dose is limited
effects of cholestyramine on plasma -as add-on therapy for additional LDL lowering when
LDL and absorption of lipid-soluble combined w/ drug of other class (dec LDL by 15-
dietary components and drugs 30%)
-may adsorb other drugs and fat soluble vitamins
(take other drugs 1-2 hr before or 4-6 hr after)
explain MOA of cholestyramine -an anion exchange resin that releases chloride in
including effects on enterohepatic exchange for anions of bile acids in the small
recirculation of bile acids intestine
-resulting insoluble BAS-bile acid complex is not
absorbed (interrupts enterohepatic recirculation and
inc fecal elimination and inc conversion of
intracellular cholesterol to bile acids
Explain the mechanism of Mechanism: strongly inhibits lipolysis in adipose
antihyperlipidemic action of niacin, tissue: decreased fatty acid release; decreased
including effects on: lipolysis, hepatic synthesis of TG; decreased hepatic VLDL
lipoprotein lipase, HDL levels production
- LDL is a VLDL degradation product; decreased LDL
- decreased TG production
,niacin effect on lipoprotein lipase - increased activity of lipoprotein lipase: increased
clearance of VLDL lowers TG
niacin effect on HDL levels - inhibits hepatic uptake of HDL-C but does not
prevent cholesterol removal from HDL; increases
amount of circulating HDL that removes cholesterol
from peripheral tissues
Describe the effects of niacin on 5-25% reduction in LDL, 20-50% reduction in TG, 15-
plasma TG, LDL, and HDL 35% increase in HDL
state the two principal indications for Indicated as adjunct to diet, alone or in combination
niacin (Types IIa and IIb, Types IV and with a bile acid sequestrant, for reduction of elevated
V) TC and LDL levels in patients with heterozygous
primary hypercholesterolemia (types IIa and IIb)
when the response to diet and other
nonpharmacologic measures is inadequate; adjunct
therapy for treatment of very high serum TG (types IV
and V) who are at risk for pancreatitis.
State the major ADR associated with Major ADR is mild to severe cutaneous flushing,
use of niacin. Explain the mechanism sensation of warmth, redness, itching, and burning
and methods for prophylaxis about 1-2 hr post-dose. Prostaglandin D2-mediated
effect; prophylactic aspirin may be beneficial (325
mg about 30 min before each dose). Tolerance
develops over several weeks for many patients, but
some still may have to d/c niacin
Explain the mechanism by which stimulates lipoprotein lipase activity: reduction of
fibrates stimulate lipoprotein lipase VLDL, decreases serum TG
activity and reduce serum TG - activation of peroxisome proliferator-activated
receptor (PPARα) which regulates numerous aspects
of lipid metabolism
- stimulation of PPARα reduces expression of genes
that code for apoC-III; apoC-III inhibits lipoprotein
lipase
- removal of this inhibition stimulates lipoprotein
lipase and enhanced VLDL clearance
, Comment on the incidence of Incidence of myopathy is low, but may be increased
myopathy when the statin-fibrate when combined with a statin; muscle breakdown
combination is used. (rhabdomyolysis) has been reported with this
combination
State the major disease state Hepatic, gall bladder, and renal disease
contraindications for fibrates
State the indications for gemfibrozil Gemfibrozil is indicated as adjunctive therapy to diet
regarding Types IV and V for:
hyperlipidemias - hypertriglyceridemia (types IV and V) in patients at
risk for pancreatitis and who do not respond to diet;
consider therapy for TG 1000-2000 mg/dL with a
history of pancreatitis or of recurrent abdominal pain
typical of pancreatitis
State the indications for fenofibrate Fenofibrate is indicated as adjunctive therapy to diet
regarding Types IV and V for:
hyperlipidemias - adjunctive therapy to diet for reduction of LDL, TC,
TG and apoB in types IIa and IIb
- adjunct to diet in patients with very high TG
concentrations (types IV and V hyperlipidemias) who
are not appropriately controlled by diet alone and
are at risk of pancreatitis
statin effects on HMG-CoA reductase Mechanism: "blocks cholesterol synthesis in the liver"
- competitive inhibition of the enzyme HMG-CoA
reductase which catalyzes the early rate-limiting step
in cholesterol biosynthesis (conversion of HMG-CoA
to mevalonate)
statin effects on hepatic LDL reduces hepatocellular cholesterol; up-regulation of
receptors hepatic LDL receptors and subsequent increased
LDL clearance
- induce an increase in high-affinity LDL receptors;
increased LDL extraction; reduced plasma levels of
LDL
| Verified Solutions
Save
Terms in this set (137)
first-pass metabolism of orgainic -ISDN undergoes first-pass metabolism to form
nitrates (ISDN, ISMN) ISMN
-ISMN does not undergo first-pass metabolism when
given PO
first-pass metabolism of NTG -bioavailability of NTG very low due to first-pass
-SL route avoids this but dose is limited
effects of cholestyramine on plasma -as add-on therapy for additional LDL lowering when
LDL and absorption of lipid-soluble combined w/ drug of other class (dec LDL by 15-
dietary components and drugs 30%)
-may adsorb other drugs and fat soluble vitamins
(take other drugs 1-2 hr before or 4-6 hr after)
explain MOA of cholestyramine -an anion exchange resin that releases chloride in
including effects on enterohepatic exchange for anions of bile acids in the small
recirculation of bile acids intestine
-resulting insoluble BAS-bile acid complex is not
absorbed (interrupts enterohepatic recirculation and
inc fecal elimination and inc conversion of
intracellular cholesterol to bile acids
Explain the mechanism of Mechanism: strongly inhibits lipolysis in adipose
antihyperlipidemic action of niacin, tissue: decreased fatty acid release; decreased
including effects on: lipolysis, hepatic synthesis of TG; decreased hepatic VLDL
lipoprotein lipase, HDL levels production
- LDL is a VLDL degradation product; decreased LDL
- decreased TG production
,niacin effect on lipoprotein lipase - increased activity of lipoprotein lipase: increased
clearance of VLDL lowers TG
niacin effect on HDL levels - inhibits hepatic uptake of HDL-C but does not
prevent cholesterol removal from HDL; increases
amount of circulating HDL that removes cholesterol
from peripheral tissues
Describe the effects of niacin on 5-25% reduction in LDL, 20-50% reduction in TG, 15-
plasma TG, LDL, and HDL 35% increase in HDL
state the two principal indications for Indicated as adjunct to diet, alone or in combination
niacin (Types IIa and IIb, Types IV and with a bile acid sequestrant, for reduction of elevated
V) TC and LDL levels in patients with heterozygous
primary hypercholesterolemia (types IIa and IIb)
when the response to diet and other
nonpharmacologic measures is inadequate; adjunct
therapy for treatment of very high serum TG (types IV
and V) who are at risk for pancreatitis.
State the major ADR associated with Major ADR is mild to severe cutaneous flushing,
use of niacin. Explain the mechanism sensation of warmth, redness, itching, and burning
and methods for prophylaxis about 1-2 hr post-dose. Prostaglandin D2-mediated
effect; prophylactic aspirin may be beneficial (325
mg about 30 min before each dose). Tolerance
develops over several weeks for many patients, but
some still may have to d/c niacin
Explain the mechanism by which stimulates lipoprotein lipase activity: reduction of
fibrates stimulate lipoprotein lipase VLDL, decreases serum TG
activity and reduce serum TG - activation of peroxisome proliferator-activated
receptor (PPARα) which regulates numerous aspects
of lipid metabolism
- stimulation of PPARα reduces expression of genes
that code for apoC-III; apoC-III inhibits lipoprotein
lipase
- removal of this inhibition stimulates lipoprotein
lipase and enhanced VLDL clearance
, Comment on the incidence of Incidence of myopathy is low, but may be increased
myopathy when the statin-fibrate when combined with a statin; muscle breakdown
combination is used. (rhabdomyolysis) has been reported with this
combination
State the major disease state Hepatic, gall bladder, and renal disease
contraindications for fibrates
State the indications for gemfibrozil Gemfibrozil is indicated as adjunctive therapy to diet
regarding Types IV and V for:
hyperlipidemias - hypertriglyceridemia (types IV and V) in patients at
risk for pancreatitis and who do not respond to diet;
consider therapy for TG 1000-2000 mg/dL with a
history of pancreatitis or of recurrent abdominal pain
typical of pancreatitis
State the indications for fenofibrate Fenofibrate is indicated as adjunctive therapy to diet
regarding Types IV and V for:
hyperlipidemias - adjunctive therapy to diet for reduction of LDL, TC,
TG and apoB in types IIa and IIb
- adjunct to diet in patients with very high TG
concentrations (types IV and V hyperlipidemias) who
are not appropriately controlled by diet alone and
are at risk of pancreatitis
statin effects on HMG-CoA reductase Mechanism: "blocks cholesterol synthesis in the liver"
- competitive inhibition of the enzyme HMG-CoA
reductase which catalyzes the early rate-limiting step
in cholesterol biosynthesis (conversion of HMG-CoA
to mevalonate)
statin effects on hepatic LDL reduces hepatocellular cholesterol; up-regulation of
receptors hepatic LDL receptors and subsequent increased
LDL clearance
- induce an increase in high-affinity LDL receptors;
increased LDL extraction; reduced plasma levels of
LDL
