Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

pharmacology GMU > Antihyperlipidemic agents > Flashcards

Antihyperlipidemic agents Flashcards

1
Q

Dyslipidemia

A

overproduction of deficiency in lipoprotein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

types of dyslipidaemia?

A

primary: disorder of lipoproteins metabolism due to genetics
secondary: disorder of lipoproteins metabolism due to some diseases like diabetes mellitus, hypothyroidism ,hypopituitarism etc

risk factors includes diet, obesity, hypertension, smoking, alcohol and sedentary lifestyle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

lipoprotein?

A

theses are spherical particles of water soluble proteins transporting neutral lipids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

types of lipoproteins? CTC

A

cholesterol: essential component of cell mea, myelin sheet, brain and bile salt that digest dietary fats.
serves as building blocks for steroid hormone synthesis.

triglyceride: major form of dietary fats that provides energy
chylomicrons: large LP that delivers triglycerides to skeletal muscle and fat tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

types of hyper-lipoproteinemia?

A

type 1- familial LP lipase deficiency
type 2A- familial hyper-cholesterolemia
type 2B- familial combined hyperlipidemia, most common, causes is generally multifactorial

type 3- familial dysbeta-lipoproteinemia
type 4- hypertriglyceridemia- common, genetic or multifactorial
type 5- familial combined hyperlipidemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

classification of anti-hyperlipidemic agents?

A
  1. MHG-CoA reductase inhibitor- statins (rosuva,simva,ator)
  2. bile acid binding resin (sequestrates)- cholestyramine, colistipol- (choli)
  3. fibrates- gemfibrozil, bezafibrate, fenofibrate
  4. inhibitor of VLDL secretion and lipolysis- nicotinic acid
  5. cholesterol uptake inhibitor- Ezetimibe
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

HMG-CoA reductase inhibitors (statin)

A

These are the most efficacious and best tolerated hypo-lipidemic agents.
Mechanism- they inhibit HMG-CoA reductase enzyme which leads to inhibitoion of the conversion of HMG-CoA to mevalonic acid. thus, describing the synthesis of cholesterol by 20-50% which leads to increase in LDL receptor on the liver cells; there is increased uptake and breakdown of LDL & IDL decreasing the LDL & TG level up to 30%, the HDL is increased by 20%.

they are pleiotropic
improve endothelial dysfunction
increase NO bioavailability
inhibit inflammatory response etc

maximum effect- combined with bile sequestrants/ nicotinic acid

HMG-CoA reductase activity is maximum at midnight, hence statin are given at bedtime to obtain maximum effect
atorvastatin & rosuvastatin haave a long plasma T1/2 (18-24h) they can be taken at any time of the day

all statin are metabolized by CYP3A4(except rosuva & fluva which are metabolized by CYP2C9), thus inhibitors of these isoenzymes alters the blood level of statin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

teurapetic use of statin

A

drugs of 1st choice in primary hyperlipidemia
secondary HL
Arherosclerotic vascular disease
coronary artery disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

adverse effect

A
  • headache, nausea, GI disturbance
  • sleep disturbance (love, simva crosses BBB)
  • muscle pain may lead to rhabdomyolysis
  • myopathy are common when combined with –b gemfibrozil/nicotinic acid/CYP3A4 inhibitor.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

drug interaction

A

drugs that inhibits CYP3A4 (cyclosporin, erythromycin, itraconazole) increases plasma conc of statin

drugs which induces CYP3A4 (phenytoin) decreases their blood level and efficacy.
note: rosuva $ fluva are metabolized by CYP2C9
drugs that inhibit CYP2C9- ketoconazole, amiodarone, metronidazole)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

bile acid (BA) binding resin (sequestrants)-Chole

A

cholestyramine, colestipol, cholesevelam

bile acid is synthesized in liver by cholesterol, secreted into duodenum for absorption of dietary fat, then reabsorbed to the liver by portal circulation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

mechanism of BA binding resin?

A

resin bounded to bile acid is non-absorbable; so it get excreted preventing resorption to liver
to compensate for the loss the synthesis of cholesterol increases leading to decrease in cholesterol pool, leading to up regulation of LDL receptors; as a result LDL-cholesterol conc is reduced
there is a small rise in HDL and TG- TG because bile acid suppresses hepatic TG production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

uses of BA binding resin

A 
type 2A
type 2B (raised VLDL)-used with niacin
relieving pruritus in cholestasis and bile salt accumulation patients
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

adverse effect of BA binding resin

A

constipation, gi distress, interfere with absorption of many drugs
increased triglyceride level on prolonged use
induce HMG-CoA reductase, hence not suitable as mono therapy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

fibrates

A

gemfibrozil, bezafibrates, clofibrates, fenofibrate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

mechanism of action of fibrates

A 
they activate PPAR-ALPHA (peroxisomal proliferation activated receptor-alpha) which leads to:
increased peripheral lipolysis
decreased hepatic TG production
enhanced LP lipase activity
conversion of cholesterol to HDL
17
Q

uses of fibrates

A

drug of choice for treating hypertriglyceridemia (type 3&4)
treats type 2B along with niacin

note: fenofibrites is uricosuric hence it is used in patients with hyperlipidemia & hyperuricemia coexist

18
Q

adverse effect of fibrtaes

A

epigastric distress, diarrhea, dyspepsia
myopathy
+ liver enzymes & risk of gall stones
impotence

19
Q

drug interaction of fibrates

A

+ action of oral anticoagulants (coumarin)

+ the risks of myopathy, rhabdomyolysis when given with statin

20
Q

CI of fibrates

A

hepatic disease with elevated serum transaminase

pergnancy & lactation

21
Q

EZETIMIBE -CHOLESTEROL UPTAKE INHIBITORS

A

inhibits NPC1-LI (niemann-pick C1-like 1) protein involved in intestinal absorption of cholesterol
there is uptake of LDL from plasma

22
Q

uses of EZETIMIBE

A

type 2B & type 2A as mono therapy or with statin

23
Q

adverse effect of EZETIMIBE

A

GIT discomfort, avoid in patients with liver dysfunction

24
Q

nicotinic acid/ niacin

A

inhibits VLDL secretion and lipolysis in adipose tissue thereby reducing the level of free fatty acid
as a result TG synthesis is reduced in liver
leads to reduction in plasma VLDL,LDL & LP and + HDLch

it is inexpensive and can be used alone

decreases TG -40%,VLDL-35%, LDL-25% & +HDL- 25-30%

25
Q

uses of niacin

A

type2B and 4 both LDL & VLDL are +

high risk for CHD (high TG & low HDL)

26
Q

adverse effect of naicin

A

cuteness rash & pruritus, dry skin
gi distress, hepatic dysfunction
hyperuricemia, hyperglycemia

27
Q

CI of niacin

A

hepatic impairment
diabetes
hyperuricemia
gastric ulcers

pharmacology GMU (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions