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CV > Quiz 1 Drugs > Flashcards

Quiz 1 Drugs Flashcards

1
Q

Mechanism of Atorvastatin

A

Competitive inhibitor for active site on HMG CoA reductase (rate limiting step of cholest. synth); [structural analogs of HMG CoA intermediate] -> decr plasma cholesterol by INCREASING gene expression of LDL RECEPTOR

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2
Q

Indications of Atorvastatin

A

First line use for hypercholesterolemia when at risk for MI

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3
Q

Side Effects of Atorvastatin

A

Elevated serum levels of hepatic enzymes; hepatitis; and myalgia, rhabdomyolysis, and other myopathies (muscle pain, weakness). Teratogen

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4
Q

Pharmakokinetics of Atorvastatin

A

Extensive 1st pass eff (liver) -> limits syst bioavail, targets liver (site of action); high plasma prot binding; half-life: 20 hrs

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5
Q

Contraindications of Atorvastatin

A

Metabolized by CYP3A4; incr risk myopathy w/ erythromycin, gemfibrozil, or naicin; those hypersensit, active liver dis, & pregnant

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6
Q

First line use for hypercholesterolemia when at risk for MI

A

Atorvastatin, Lorvastatin, Simvastatin

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7
Q

Statins have greater effect on LDL or HDL?

Lorvastatin, Atorvastatin, Simvistatin

A

Greater effect on LDL; higher the baseline TG level = greater lowering effect

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8
Q

Mech of Lorvastatin

A

Competitive inhibitor for active site on HMG CoA reductase (rate limiting step of cholest. synth);> decr plasma cholesterol by INCREASING gene expression of LDL RECEPTOR
**prodrugs, administered as lactones (transformed in liver to active form)

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9
Q

Difference in mechanism of Lorvastatin and Atorvastatin

A

Lorvastatin is a PROdrug and activated in liver

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10
Q

Toxicity of Lorvastatin:

A

All Statins same: Elevated serum levels of hepatic enzymes; hepatitis; and myalgia, rhabdomyolysis, and other myopathies (muscle pain, weakness). Teratogen

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11
Q

PharmK of Lorvastatin

A

Extensive 1st pass eff (liver) -> limits syst bioavail, targets liver (site of action); high plasma prot binding; half-life: 1-4 hours

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12
Q

Contraindications of All Statins

A

Metabolized by CYP3A4; incr risk myopathy w/ erythromycin, gemfibrozil, or naicin; those hypersensit, active liver dis, & pregnant

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13
Q

Simvastatin and Lorvastatin are the same except:

A

Simvustatin half life = 1-2 hours

Lorvastatin = 1-4 hours

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14
Q

What are the HMG CoA Reductase Inhibitors

Statins?

A

Atorvastatin
Lovastatin
Simvastatin

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15
Q

Rate limiting step in cholesterol biosynthesis

A

HMG CoA reductase

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16
Q

How do statins prevent substrate binding?

A

• statins inhibit HMGR by binding to the active site of
the enzyme, thus stericallypreventing substrate from
binding

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17
Q

How are statins similar and different from HMGR

A

• statins inhibit HMGR by binding to the active site of
the enzyme, thus sterically preventing substrate from
binding
All differ from HMG-CoA by being more bulky and more hydrophobic

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18
Q

DOMINANT MECHANISM FOR

CONTROLLING LDL PLASMA CONCENTRATIONS

A

REGULATION OF HEPATIC LDL RECEPTOR PATHWAY IS

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19
Q

characteristic Side effect of statins

A

characterized by intense myalgia, first in arms/thighs then in entire body
along with fatigue
serum creatine kinase levels increased 10-fold (rare)

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20
Q

MYOPATHY RISK FACTORS are greater when taking statins with

A

gemfibrozil

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21
Q

associated with increased risk of myopathy in

Chinese population

A

Simvastatin plus niacin

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22
Q

are statins safe to take when pregnant?

A

no

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23
Q

first line therapy in patients who are at high risk for MI

due to hypercholesterolemia

A

Statins

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24
Q

What pts should not use statins even though they have elevated cholesterol

A

The exception is patients with homozygous familial hypercholesterolemia, who have very attenuated responses to the usual doses of statins because both alleles of the LDL receptor gene code for dysfunctional LDL receptors; the partial response in these patients is due to a reduction in hepatic VLDL synthesis associated with the inhibition of HMG-CoA reductase–mediated cholesterol synthesis

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25
Q

Cholestyramine is what type of medication?

A

Bile Acid-Binding Resins

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26
Q

What is the only way cholesterol is excreated from body?

A

amount of bile salts (not reabsorbed) excreted (0.8 g/day) accounts for only mechanism for cholesterol excretion

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27
Q

How does cholestryramine increase bile acid excretion in feces

A

anion-exchange resins that readily exchange chloride ions
for bile salts in the small intestine and increase bile acid
excretion in the feces

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28
Q

What is the rate limiting step of bile acid conversion? What effect does cholesteryamine have on it

A

7 alpha hydroxylase; the increased excretion of bile acids lowers feedback inhibition thus increase breakdown of hepatic cholesterol

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29
Q

Increased catabolism of cholesterol from cholesteryamine will increase activity of?

A

hepatic HMG CoA reductase

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30
Q

How does cholestyramine lower plasma LDL-cholesterol?

Two mechanisms

A

increasing rate of removal of cholesterol through receptor-mediated catabolism
- liver responds to lowering of its cholesterol content by
forming more LDL receptors (similar to statins)

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31
Q

PharmK of cholestyramine:

A
  • quaternary amine; hygroscopic powder administered as
    chloride salt and insoluble in water
  • not absorbed but can interfere with absorption of other agents
  • time delay before effects seen (1-2 weeks)
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32
Q

Key Adverse effects of Cholestyramine

A

mostly GI, gritty consistancy, modest elevation of plasma TGs

33
Q 
Lipoprotein Profile after pt has been on cholesteryamine
patient with normal TG:
patient with TG > 250 mg/dl:
LDL-C: 
HDL-C:
A

TG increase transiently
significant further increase in TGs
reduced by 12-25%; dose-dependent; larger doses associated with more adverse GI effects
increase by 4-5%

34
Q

Uses of Cholesteryamine

A

management of primary hypercholesterolemia; but NOT if pt has elevated TGs!!!!

35
Q

Mech of Niacin/Nicotinic Acid in adipose

A

inhibits breakdown of TG by hormone-sensitive lipase–> reduces transport of FFAs to the liver and decreases TG synthesis in liver.
(niacin couples to Gi in the GCPR, stimulates Gi path–> inhibition cAMP–>decreases hormone-sensitive lipase
activity, TG breakdown and release of free fatty acids)

36
Q

Mech of Niacin in the liver

A

decreases synthesis of VLDL-TG
-inhibits DGAT2 (key in catalyzing final reduction in TG synthesis) thus decreased TG to make VLDL and increases apoB degredation

37
Q

PharmK of Niacin

A
  • Different formulations
  • immediate release (IR) (quick absorbed-more sides)
  • long acting release, sustained release (SR)
    (absorbed slowly, increased risk of hepatotoxicity)
  • extended release (ER)
    once per day, less side effects
38
Q

Major side effect of taking Niacin

A

production of intense cutaneous flush and pruritus
Devos 1 to 2 hours after taking drug = poor compliance, disappears with continued use
flush dt PGDs (take with aspirin)

39
Q

What pts should not take Niacin?

A

Pts with diabetes, peptic ulcer, gout or hepatic dysfnx

40
Q

Use of niacin with _____ may cause myopathy

A

statins

41
Q

Lipoprotein Profile after pt has been on Niacin
TGs:
LDL-C:
HDL-C:

A

TGs reduced by 35-50% (w/in 4-7 days)
LDL-C reduced by 25% (takes 3-5 wks)
HLD-C increased by 15-30%
***also can reduce Lp(a) which is independent risk factor for 2-3 fold increase in CAD

42
Q

Clinical Uses of Niacin

A

hypertriglyceridemias and elevated LDL-cholesterol

**particularly useful in patients who present with both low HDL and high LDL

43
Q

only lipid-lowering drug that reduced Lp(a) levels (40% reduction)

A

Niacin

44
Q

Is Niacin a recommended tx for hypercholesterolemia?

A

second or third choice for hypercholesterolemia because of troublesome side effects

45
Q

inhibits cholesterol transfer from intestinal lumen into

intestinal cell.

A

Eztimibe

46
Q

Mech of Ezitimibe

A

binds to NPCL1 and decreases rate of CE incorporation into chylomicrons–decreases flux of cholesterol from intestine–> liver thus reduces cholesterol–> VLDL

47
Q

How does Ezitimibe lower plasma LDL-C

A

increaess expression of LDL receptors

48
Q

PharmK of Ezitimibe

A
  • oral administration

- rapid glucuronidation to active metabolite

49
Q

Adverse sides of Eztimibe

Contraindications

A

generally well tolerated

- Bile-acid sequestrants inhibit absorption of ezetimibe, Don’t administered together

50
Q

Lipoprotein profile for Ezitimibe
LDL:
TG:
HDL:

A

reduced by 15-20%
reduced by 5%
increased 1-2%

51
Q

Clinical uses of Eztitimbe?

A

monotherapy for treatment of primary hypercholesterolemia in patients resistant to statins

52
Q

Do we prescribe Ezitimibe with Statins?

Pros, Cons?

A

Statins stop cholesterol biosynthesis
Ezetimibe inhibit cholesterol intestinal absorption
–see possible benefit with reduction of LDL by 60% BUT increased risk of myopathy

53
Q

Gemfibrozil and Fenofibrate are examples of

A

Fibric Acids/PPARactivators or agnonists

54
Q

Primary fnx of fibric acids?

A

Lower TG’s

55
Q

Mech of fibric acids

A

bind to PPARalpha (expressed 1˚ in liver and brown
adipose)
PPAR bind as heterodimers with retinoid X receptor to specific response elements and alter the transcription rate of target genes

56
Q

What happens as a result of fibric acids binding to PPAR alpha?

A

more lipolysis and plasma clearance of TG-lipoP
–activates LPL and reduces procution of apoCIII, a LPL inhibitor
reduces FFA for TG synthesis
inhibits denova FA synthesis
increases HDL (makes more apoAI and apoAII)

57
Q

How are Gemfibrozil and Fenofibrate simular and different in regards to PharmK

A

Both oral admin and highly bound to plasma proteins
Gemfibrozil 1/2 = 1.1 hrs
Fenofibrate = 20 hours and is metabolized to active metabolite

58
Q

Side effects of fibric acids

A

usually well tolerated with GI disturbances

increased gall stones, possible blood/liver fnx abnormalities

59
Q

What pts shouldn’t use fibric acids

A

ones with renal failure

60
Q

When using gemfibrozil + statin we increase….

A

creatine kinase— leads to renal failure

61
Q

Typical Lipoprotein Profile after use of fibric acids
TG:
LDL:
HDL:

A

TG: decrease by 30-50%
LDL: decrease by 15-20% highly variable
HDL: increase by 5-15%

62
Q

What does the lipoprotein profile for patient using fibric acids depend on?

A

highly dependent on starting lipoprotein profile, presence or absence of a genetic hyperlipoproteinemia

63
Q

approved for treatment in individuals with very high serum

triglycerides greater than 750 mg/dl

A

Use Fibric Acids

64
Q

When is it appropriate to use Fibric Acids to tx hypercholesterima

A

Only when patient has hypertriglyceridemia as well

65
Q

treatment of hypertriglyceridemia (Fredrickson types IV and V)

A

Fibric Acids

66
Q

recommended for patients 11 to 20 years of age

- most often used as second agents if statins do not lower LDL

A

cholestyramine

67
Q

approved for use as monotherapy or in combination statins or fibrates for the treatment of hypercholesterolemia.

A

Ezetimibe

68
Q

hypertriglyceridemia AND elevated LDL

  • side effects limit its use
  • useful in patients with both hypertriglyceridemia and low HDL
A

Niacin

69
Q

Drugs of choice for hypertriglyceridemia

A
  1. Fibric Acids
  2. Niacin
  3. Omega 3s
70
Q

When do we recommend omega 3 fish oil?

A

Adjunct to diet therapy in the treatment of hypertriglyceridemia

71
Q

Adverse effect of omega 3s?

A

fish allergies, may increase LDL, may increase liver enZ, prolonged bleeding.

72
Q

a mediator of hepatic LDL receptor degradation

A

(PCSK9) Inhibitors

73
Q

Role of PCSK9 in LDLR regulation

A

hepatic LDLR controlled via STEB-2 and PCSK9:
PCSK9 binds LDLRs–> get internalized and directs Rs for destruction–> so DECREASE LDLRs at cell surface
***PCSK9 antibody stops PCKS9 bindng to LDLR-LDL complex = increased LDLRs on cell surface

74
Q

Individuals with GOF mutations in PCSK9 seen in families with FH… what do the mutations cause?

A

increase the affinity of PCSK9 for LDLR, result in high cholesterol levels and a significantly
increased incidence of coronary heart disease

75
Q

How is LOF mutation of PCSK9 a good thing?

A

prevent interaction with LDLR…LDL-C levels reduced by up to 40% and the risk of coronary heart disease is reduced by up to 88%

76
Q

Adverse effects of PCKS9 inhibitors

A

IG well tolerated… injection site rxns

77
Q

Uses of PCKS9 inhibitors

A

for men and women with hypercholesterolemia

78
Q

Mech of MTP (Microsomal triglyceride transfer protein) inhibitors?

A

MTP plays an important role in the hepatic assembly

of plasma lipoproteins by mediating the transfer of triglycerides to VLDL

CV (11 decks)

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