Brainscape's Knowledge GenomeTM

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


See full index

CV Pharmacology > Lipid-Altering Drugs > Flashcards

Lipid-Altering Drugs Flashcards

1
Q

List the 4 HMG CoA-R Inhibitors

A

Atorvastatin
Lovastatin
Simvastatin
Statin

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

Bile-Acid binding resin

A

Cholestyramine

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

Niacin

A

.

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

List the 3 fibric acids (fibrates)

A

PPAR activators
Gemfibrozil
Fenofibrate

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

Cholesterol absorption inhibitor

A

Ezetimibe

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

Omega-3 Fatty acid

A

.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Proprotein convertase subtilisin/kesin 9 (PCSK9)

A

.

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

microsomal triglyceride transfer protein

A

.

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

Apolipoprotein B-100

A

.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Statin MOA

A
  • competitive inhibitor or active site on HMG CoA reductase (sterically prevent substrate from binding)
  • structural analog
  • rate-limiting step in cholesterol biosynthesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Statin pharmacokinetics

A
  • extensive first pass metabolism (good thing! prevents drug from getting into circulation)
    • LIMITS SYSTEMIC BIOAVAILABILITY
    • TARGETS LIVER (site of action)
  • HIGH PLASMA-PROTEIN BINDING
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Statin activation

A

All statins except simvastatin and lovastatin are in HYDROXY ACID form (active)
- PRO-DRUGS: sim. and lova. are administered as INACTIVE LACTONES, transformed in liver

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

Statin metabolism

A

ator, lova, and simva are metabolized by CYP 3A4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Statin half-lives

A

Variable

  • Lova 1-4 hrs
  • Simva 1-2 hrs
  • Atorva 20 hrs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Statin SE

A
  • MYOPATHY
    • associated with genetic mut (SLCO1B1 - reduced hepatic uptake)
  • RHABDOMYOLYSIS
    • marked CK and creatinine elevation (breakdown of muscle fibers) –> renal damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Which drugs will increase myopathy associated with increased plasma concentrations of statins?

A

drugs met by 3A4

  • macrolide abx (erythromycin)
  • azole antifungals (itraconazole)
  • cyclosporine
  • HIV protease inhibitors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Statin CIs

A

liver disease

PREGNANT/LACTATING or likely to become pregnant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Statin lipoprotein profile: TGs

A

o TG: the higher the baseline TG level, the greater the TG-lowering effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Statin lipoprotein profile: LDL

A

decrease by 20-55% - BEST

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Statin lipoprotein profile: HDL

A

increase by 5-10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Statin clinical use:

A

first-line therapy in hypercholesterolemia when at risk for MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Cholestyramine MOA

A

Highly positively charged → binds negatively charged bile acids –>excreted in stool –> hepatic bile-acid synthesis increases –> liver chol. content decreases –> stimulates production of LDL receptors

23
Q

what is the dominant mechanism for controlling LDL plasma concentration?

A

regulation of LDL receptor pathywas

24
Q

cholestyramine SE

A

o Constipation/bloating
o Interferes with absorption of other drugs
o Modest INCREASE in TG – with time, returns to baseline

25
Q

cholestyramine lipoprotein profile: TG

A
  • Normal levels – only transient increase

* >250 mg/dL – further significant increase

26
Q

cholestyramine lipoprotein profile: LDL

A

decreased by 12-15%

27
Q

cholestyramine lipoprotein profile: HDL

A

increase by 4-5%

28
Q

use of cholestyramine:

A

o Hypercholesterolemia (not recommended for pts with increased TG)
• 2nd tx: used if statins are insufficient
o 11-20y

29
Q

what is the main effect of niacin?

A

decrease TG (does not decrease cholesterol)

30
Q

Niacin MOA at adipose

A

inhibits FFA mobilization

31
Q

niacin MOA at liver

A

decreases syntheiss of VLDL-TG

32
Q

niacin method of admin

A

oral - 3 different formulations (intermediate, long acting, extended release)

33
Q

SE of niacin

A
  • pt compliance/SE
  • Both elevated TG and cholesterol
  • Low HDL
  • Care when combined with statins
34
Q

niacin CIs

A

o Peptic ulcer
o Gout
o Hepatic Disease
o Diabetes

35
Q

what is the risk when combining niacin with statins?

A

increases risk of myopathy (unk. mechanism)

36
Q

niacin lipoprotein profile: TG

A

decreased by 35-50%

37
Q

niacin lipoprotein profile: LDL

A

decreased by 25%

38
Q

niacin lipoprotein profile: HDL

A

increased by 15-30%

39
Q

niacin lipoprotein profile: Lp(a)

A

reduced by 40% → may be risk factor

40
Q

niacin uses

A

o Hypercholesterolemia & hyper-TG
• High LDL + low HDL
o Typically not 1st-line therapy for hypercholesterolemia
• Severe cases that do not respond to resins
• d/t SE
o Only lipid-lowering drug that reduces Lp(a)

41
Q

Ezetimibe MOA

A

o Protein transporter – Niemann Pick C10-like protein or NPC1L1
o Decreased rate of cholesteryl ester incorporation into chylomicrons → reduced cholesterol flux from intestine to liver

42
Q

Ezetimibe met

A

PRODRUG – met via glucuronidation

43
Q

Ezetimibe admin and T1/2

A

oral; 22hrs

44
Q

ezetimibe SE

A

well tolerated

- absorption decreased by cholestyramine

45
Q

Ezetimibe lipoprotein profile: TG

A

decreased by 5%

46
Q

Ezetimibe lipoprotein profile: LDL

A

decreased by 15-20%

47
Q

Ezetimibe lipoprotein profile: HDL

A

increased by 1-2%

48
Q

Ezetimibe uses

A

o Primary hypercholesterolemia
o Combined with statins
• Simvastatin + ezetimibe
• Further decreases in LDL-cholesterolemia
• Two differing pharmacological approaches

49
Q

Fibrates MOA

A

– primarily lower levels of TG-rich lipoproteins via regulation of TX

50
Q

which fibrate is the prodrug?

A

fenofibrate

51
Q

which fibrate has the longer T 1/2?

A

fenofibrate (20 hrs) (gemfibrozil 1 hr)

52
Q

fibrate SE

A

o Well tolerated
• GI
• Increased risk of gall stones
• Heme/hepatic function abnormalities
• Increased CK if combined with statin → renal failure
• CI – renal impairment
• Gemfibrozil can increase systemic statin concentrations by blocking transporter in liver

53
Q

fibrate uses

A

o Pts with high TGs + low HDL associated with metabolic syndrome/DM-II
o Not used as primary therapy in patients with elevated hypercholesterolemia w/o hyper-TG

54
Q

fibrate lipoprotein profile

A 
o	TG – decreases 30-50%
o	LDL – decreases 15-20%
•	Highly variable
•	2nd generation drugs (fenofibrate) more likely to decrease LDL 15-20% in patients with TG <400 mg/dL
o	HDL – increases 5-15%

CV Pharmacology (2 decks)

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