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Cardiovascular Exam I > Drugs for Lipid Disorders > Flashcards

Drugs for Lipid Disorders Flashcards

1
Q

5 drug categories used to tx lipid disorders

A

HMG-CoA reductase inhibitors (statins)

Niacin (nicotinic acid, vit B3)

Fibric acid derivatives (fibrates)

Bile acid sequestrants (resins)

Cholesterol absorption inhibitors

[note: new treatments not categorized — lomitapide, mipomersen, evolocumab, alirocumab]

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2
Q

Drugs included in HMG-CoA reductase inhibitor class used to tx lipid disorders

A 
Atorvastatin
Fluvastatin
Lovastatin
Pitavastatin
Pravastatin
Rosuvastatin 
Simvastatin
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3
Q

Drugs included in fibric acid derivatives class used to tx lipid disorders

A

Fenofibrate

Gemfibrozil

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4
Q

Drugs included in bile acid sequestrants class used to tx lipid disorders

A

Cholestyramine
Colesevelam
Colestipol

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5
Q

Cholesterol absorption inhibitor used to tx lipid disorders

A

Ezetimibe (Zetia)

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6
Q

Management of hyperlipoproteinemia involves dietary measures first, UNLESS the patient has what risk factor(s)?

A

Evident coronary or peripheral vascular disease

Pts with familial hypercholesterolemia — always require drug therapy in addition to diet

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7
Q

What dietary components tend to contribute to development of hyperlipoproteinemia?

A

Total fat, sucrose, and fructose increase VLDL

Alcohol can cause significant hypertriglyceridemia by increasing hepatic secretion of VLDL

Excess calories in general increase synthesis and secretion of VLDL

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8
Q

During weight loss, LDL and VLDL levels may be much lower than can be maintained during neutral caloric balance. Thus, dietary changes sufficient for lipid management can only be made after weight loss has stabilized for how long?

A

1 month

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9
Q

General dietary recommendations for control of hyperlipoproteinemia

A

Limit total calories from fat to 20-25% of daily intake

Limit saturated fats to less than 8% of daily intake

Limit cholesterol to less than 200 mg/day

[goal is to reduce serum cholesterol range from 10-20% by adhering to these]

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10
Q

What are the most effective agents in reducing LDL levels and the best tolerated class of lipid lowering agents?

A

HMG-CoA reductase inhibitors (Statins)

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11
Q

Oral absorption of the statins varies from 40-75%, with the exception of _____ which is almost completely absorbed.

Statin absorption is enhanced by ____; it has extensive first-pass metabolism and half lives range from 1-3 hours with the exception of ______ (14 hrs), ______ (12 hrs), and ______ (19 hrs)

A

Fluvastatin

Food; atorvastatin, pitavastatin, rosuvastatin

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12
Q

Most of the absorbed dose of statin is excreted in the ____ (5-20% urine)

A

Bile

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13
Q

What 3 statins are primarily metabolized by CYP3A4?

A

Lovastatin
Simvastatin
Atorvastatin

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14
Q

What 2 statins are metabolized primarily by CYP2C9?

A

Fluvastatin

Rosuvastatin

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15
Q

Of the statins, _____ undergoes limited CYP450 biotransformation and _____ is not metabolized by CYP450s

A

Pitavastatin; pravastatin

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16
Q

MOA of statins

A

Statins are structural analogs of HMG-CoA (initial precursor of cholesterol) and inhibit HMG-CoA reductase, the RL step in cholesterol synthesis

Inhibiting de novo cholesterol synthesis depletes the intracellular supply of cholesterol, which causes the cell to increase the number of specific cell-surface LDL receptors that can bind and internalize circulating LDLs

Increased expression of surface LDL receptors reduces circulating LDL levels by 20-55%

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17
Q

List statins from most potent to least potent

A

[most potent]

Atorvastatin, Rosuvastatin

Simvastatin

Pitavastatin, lovastatin, pravastatin

Fluvastatin

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18
Q

Therapeutic benefits of statins

A

Plaque stabilization

Improvement of coronary endothelial function

Inhibition of platelet thrombus formation

Anti-inflammatory effects

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19
Q

Statins are effective in lowering plasma cholesterol levels in ALL types of hyperlipidemias. They can be used alone or with ____, ____, or _____

A

Resins; niacin; ezetimibe

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20
Q

Why are statins primarily taken at night? Which ones are not taken at night?

A

Cholesterol synthesis occurs predominantly at night — get maximal effect at this time

Longer-acting statins not taken at night = atorvastatin, pitavastatin, rosuvastatin

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21
Q

Adverse effects of statins on liver and muscle

A

Liver — elevations of serum aminotransferases up to 3x nml (improves when drug is stopped)

Muscle — creatine kinase activity may increase, particularly in active patients; Rhabdomyolysis (leading to myoglobinuria) can occur rarely and lead to renal injury; Myopathy can occur with monotherapy, but with increased incidence in pts concomitantly taking statins and fibrates

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22
Q

Drug interactions of concern with statins

A

Statins increase warfarin levels —> increased likelihood of bleeding

Use with caution with other agents that inhibit, compete with, or induce CYP450 enzymes (except pravastatin and pitavastatin to a lesser extent)

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23
Q

Contraindications to statin use

A

Contraindicated in pregnancy, lactating p ts, or likely to become pregnant

Not recommended in pts with liver disease or skeletal m. myopathy

Use in children is restricted to those with homozygous (sometimes heterozygous) familial hypercholesterolemia

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24
Q

How does Niacin alter the lipid profile?

A

Decreases TGs, LDL, Lp(a)

Increases HDL

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25
Q

Niacin is converted to nicotinamide and is incorporated into NAD. It is well-absorbed and distributed to mainly ____, _____, and ____ tissue

It has extensive first pass metab with a half-life of about 60 minutes (meaning dosing is 2-3x daily)

A

Hepatic; renal; adipose

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26
Q

MOA of niacin for lipid disorders

A

Inhibits lipolysis of triglycerides in adipose tissue (the primary producer of circulating FFAs)

By reducing circulating FFAs, the liver produces less VLDL and LDL levels decrease

Catabolic rate for HDL is also decreased

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27
Q

What happens to fibrinogen and tissue plasminogen activator levels on niacin therapy?

A

Fibrinogen levels reduced

tPa levels increased

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28
Q

AEs of niacin used to tx lipid disorder

A

Most common complaint is intense cutaneous flush accompanied by uncomfortable warmth that occurs after each dose when drug is started, or with dose increase (can take ASA or daily ibuprofen to mitigate prostaglandin-mediated flushing)

Others: pruritis, rashes, dry skin or mucous membranes, and acanthosis nigricans

May cause hepatotoxicity (monitor liver enzymes from baseline)

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29
Q

In what pt populations should niacin tx be avoided?

A

Avoid in pts with hepatic disease or acive peptic ulcer

Use with caution in pts with DM d/t niacin-induced insulin resistance, which can cause hyperglycemia (pts with insulin resistance often show signs of acanthosis nigricans d/t elevated insulin levels)

30
Q

What must be done to ensure proper absorption of fibric acid derivatives like gemfibrozil and fenofibrate

A

Take with a meal! —> >90% absorption

Not absorbed well on empty stomach

[note half life of gemfibrozil is 1.5 h, fenofibrate half life is 20 h]

31
Q

MOA of fibrates gemfibrozil and fenofibrate

A

Agonists for peroxisome proliferator-activated receptor alpha; when activated, PPARalpha binds to DNA, regulating the expression of genes encoding proteins involved in lipoprotein structure and function (LPL, apo A-I, apo A-II expression increased and apo C-III is decreased)

Major effect is increased oxidation of FAs in liver and striated muscle; increased lipolysis of TG via lipoprotein lipase while intracellular lipolysis in adipose tissue is decreased

32
Q

Effect of fibrates gemfibrozil and fenofibrate on lipid profile

A

VLDL levels decrease, LDL levels modestly decrease in most pts (can increase as TGs are reduced)

HDL levels increase moderately

33
Q

Fibrates are useful in the tx of what types of hypertriglyceridemias?

A

Useful in management of hypertriglyceridemias where VLDL predominates, dysbetalipoproteinemia, and hypertriglyceridemia that ressults from tx with viral protease inhibitors (e.g., saquinavir, indinavir, or nelfinavir for HIV therapy)

34
Q

GI, liver, and muscle AEs associated with fibrates

A

GI: mild GI disturbances are most common AE but usually subside; increased risk of cholelithiasis (d/t increase in cholesterol content of bile)

Liver: increased serum transaminases (up to 3x normal)

Muscle: myositis can occur (evaluate for muscle weakness and tenderness); myopathy and rhabdomyolysis have been reported (increased risk when fibrates and statins combined)

35
Q

Fibrates may potentiate the actions of what drug?

In what pt populations should they be avoided?

A

Potentiate actions of anticoagulants

Use with caution in pts with biliary tract disease or in those at high risk for cholelithiasis (e.g., women, obese pts, Native Americans)

Avoid in pts with hepatic or renal dysfunction; safety has not been established in pregnant or lactating women

36
Q

Large polymeric cationic exchange resins that are insoluble in water; neither absorbed nor metabolically altered by the intestine; totally excreted in the feces

A

Bile acid sequestrants (colestipol, cholestyramine, colesevelam)

37
Q

MOA of colestipol, cholestyramine, and colesevelam

A

Positively charged compounds bind negatively charged bile acids (metabolites of cholesterol) and increase bile acid excretion up to 10-fold

Increased excretion of bile acids enhances the conversion of cholesterol to bile acids in the liver via 7alpha-hydroxylation; the decline in hepatic cholesterol stimulates an increase in hepatic LDL receptor, which enhances LDL clearance and lowers levels; however, this effect is partially offset by enhanced cholesterol synthesis caused by upregulation of HMG-CoA reductase

38
Q

Combined use of a ____ substantially increases the effectiveness of resins/bile acid sequestrants

A

Statin

39
Q

Therapeutic uses for bile acid sequestrants

A

Used to tx primary hypercholesterolemia (reduces LDL by ~20%) - prescribed as monotherapy or in combo with niacin for tx of type IIa and type IIb hyperlipidemias

Used to relieve pruritis in pts who have bile salt accumulation (e.g., from biliary obstruction)

40
Q

AEs of bile acid sequestrants

A

Most common are GI effects - constipation, nausea, flatulence

41
Q

Drug interactions and pts in which bile acid sequestrants should be avoided

A

Resins impair the absorption of numerous drugs: tetracycline, phenobarbital, digoxin, warfarin, pravastatin, fluvastatin, aspirin, and thiazide diuretics (as a result, any medication except niacin should be given at least 1 hr before or at least 2 hrs after)

Avoid or use with caution in pts with diverticulitis, preexisting bowel disease, or cholestasis

42
Q

T/F: ezetimibe is highly water insoluble and the majority is excreted in the feces with a 22 hr half life

A

True

43
Q

MOA of ezetimibe

A

Selectively inhibits intestinal absorption of cholesterol and phytosterols (plant sterols); thought to inhibit the transport protein NPC1L1; effective even in the absence of dietary cholesterol d/t inhibition of reabsorption of cholesterol excreted in the bile

44
Q

Effect of ezetimibe on lipid profile

A

On average, lowers LDL by 18%, TGs by 6%, and raises HDL slightly by 1.3%

45
Q

Therapeutic uses for ezetimibe

A

Used to tx various causes of elevated cholesterol levels

For primary hypercholesterolemia: as monotherapy or in combo with statin

For homozygous familial hypercholesterolemia: in combo with atorvastatin or simvastatin

For mixed hyperlipidemia: in combo with fenofibrate

46
Q

AEs and contraindications to ezetimibe

A

No significant drug interactions are reported; avoid administration of ezetimibe and bile acid sequestrants d/t impaired ezetimibe absorption

47
Q

Statins rely on functional LDL receptors to achieve an LDL lowering effect and thus will not work in pts with what condition? What are some drug options?

A

Homozygous familial hypercholesterolemia (mutations lead to dysfunctional LDL receptors)

New txs include lomitapide and mipomersen

48
Q

MOA of lomitapide

A

Directly binds and inhibits microsomal triglyceride transfer protein (MTP) which is located in the lumen of the ER

MTP inhibition prevents the assembly of apo-B containing lipoproteins in enterocytes and hepatocytes resulting in reduced production of chylomicrons and VLDL and subsequently reduces plasma LDL-C concentrations

49
Q

AEs and drug interactions with lomitapide

A

Substrate and inhibitor of CYP3A4, causing interactions with many drugs

Most common AEs are GI symptoms, increased aminotransferase levels, and hepatic fat accumulation

50
Q

MOA of mipomersen

A

Antisense oligonucleotide that targets apolipoprotein B-100 mRNA and disrupts its function

[apoB-100 is the ligand that binds LDL to its receptor and is important for transport and removal of atherogenic lipids]

51
Q

AEs associated with mipomersen

A

Injection site reactions

Flu-like symptoms, HA, elevation in liver enzymes >3x normal (discontinue if elevation persists or if accompanied by clinical symptoms like hepatic stenosis)

52
Q

PJ is a 4.5-year-old boy. At his checkup, the pediatrician notices cutaneous xanthomas and orders a lipid panel. Repeated measures confirm that the patient’s serum cholesterol levels are high (936 mg/dL). Further testing confirms a diagnosis of homozygous familial hypercholesterolemia. Which of the following interventions will be least effective in this patient?

a. atorvastatin
b. ezetimibe
c. lomitapide
d. mipomersen
e. niacin

A

a. atorvastatin

Homozygous familial hypercholesterolemia is caused by mutations leading to dysfunctional LDL receptors incapable of taking up LDL from the bloodstream. Options B–E would have a cholesterol- lowering effect. Lomitapide and mipomersen are specifically indicated for patients with familial hypercholesterolemia. Reductase inhibitors such as atorvastatin rely on functional LDL receptors to achieve a LDL-lowering effect and thus will not work in patients with homozygous familial hypercholesterolemia. The answer is A.

53
Q

A 46-year-old woman with a history of hyperlipidemia was treated with a drug. Below are her lipid panel results as well as normal values. Which of the following drugs is most likely to be the one that this patient received?

Before tx: TGs 1000, Total chol 640, LDL 120, VLDL 500, HDL 20

6 months after tx: TGs 300, total chol 275, LDL 90, VLDL 150, HDL 40

normal values: TGs <150, total chol <200, LDL <130, VLDL <30, HDL >35

a. Colestipol
b. ezetimibe
c. gemfibrozil
d. lovastatin
e. niacin

A

c. gemfibrozil

This patient presents with striking hypertriglyceridemia, elevated VLDL cholesterol, and depressed HDL cholesterol. Six months after drug treatment was initiated, her triglyceride and VLDL cholesterol have dropped dramatically and her HDL cholesterol level has doubled. There are 2 drugs that are most likely to have achieved all of these desirable changes: niacin and gemfibrozil. Both of these agents can cause the effects seen above (decrease TGs and increase HDL). Due to the high TG level before treatment, however, a fibrate is more likely to be chosen as a single agent based on the basic pharmacology compared to niacin.

54
Q

A 35-year-old woman appears to have familial combined hyperlipidemia. Her serum concentrations of total cholesterol, LDL cholesterol, and triglyceride are elevated. Her serum concentration of HDL cholesterol is somewhat reduced.

If this patient is pregnant, which of the following drugs should be avoided because of a risk of harming the fetus?

a. cholestyramine
b. ezetimibe
c. fenofibrate
d. niacin
e. pravastatin

A

e. pravastatin

The HMG-CoA reductase inhibitors are contraindicated in pregnancy because of the risk of teratogenic effects

55
Q

A 35-year-old woman appears to have familial combined hyperlipidemia. Her serum concentrations of total cholesterol, LDL cholesterol, and triglyceride are elevated. Her serum concentration of HDL cholesterol is somewhat reduced.

The patient is started on gemfibrozil. Which of the following is a major mechanism of gemfibrozil’s action?

a. Increased excretion of bile acid salts
b. increased expression of high-affinity LDL receptors
c. increased secretion of VLDL by the liver
d. increased triglyceride hydrolysis by lipoprotein lipase
e. reduced uptake of dietary cholesterol

A

d. increased triglyceride hydrolysis by lipoprotein lipase

A major mechanism recognized for gemfibrozil is increased activity of the lipoprotein lipase associated with capillary endothelial cells. Gemfibrozil and other fibrates decrease VLDL secretion, presumably by stimulating hepatic fatty acid oxidation

56
Q

A 35-year-old woman appears to have familial combined hyperlipidemia. Her serum concentrations of total cholesterol, LDL cholesterol, and triglyceride are elevated. Her serum concentration of HDL cholesterol is somewhat reduced.

The patient is started on gemfibrozil.. Which of the following is a major toxicity associated with gemfibrozil therapy?

a. bloating and constipation
b. cholelithiasis
c. hyperuricemia
d. liver damage
e. severe cardiac arrhythmia

A

b. cholelithiasis

A major toxicity of the fibrates is increased risk of gallstone formation, which may be due to enhanced biliary excretion of cholesterol

57
Q

A 43-year-old man has heterozygous familial hypercholesterolemia. His serum concentrations of total cholesterol and LDL are markedly elevated. His serum concentration of HDL cholesterol, VLDL cholesterol, and triglycerides are normal or slightly elevated. The patient’s mother and older brother died of myocardial infarctions before the age of 50. This patient recently experienced mild chest pain when walking upstairs and has been diagnosed as having angina of effort. The patient is somewhat overweight. He drinks alcohol most evenings and smokes about 1 pack of cigarettes per week.

Consumption of alcohol is associated with which of the following changes in serum lipid concentrations?

a. decreased chylomicrons
b. decreased HDL cholesterol
c. decreased VLDL cholesterol
d. increased LDL cholesterol
e. increased triglyceride

A

e. increased triglyceride

Chronic ethanol ingestion can increase serum concentrations of VLDL and triglycerides. This is one of the factors that places patients with alcoholism at risk of pancreatitis. Chronic ethanol ingestion also has the possibly beneficial effect of raising, not decreasing, serum HDL concentrations.

58
Q

A 43-year-old man has heterozygous familial hypercholesterolemia. His serum concentrations of total cholesterol and LDL are markedly elevated. His serum concentration of HDL cholesterol, VLDL cholesterol, and triglycerides are normal or slightly elevated. The patient’s mother and older brother died of myocardial infarctions before the age of 50. This patient recently experienced mild chest pain when walking upstairs and has been diagnosed as having angina of effort. The patient is somewhat overweight. He drinks alcohol most evenings and smokes about 1 pack of cigarettes per week.

If the patient has a history of gout, which of the following drugs is most likely to exacerbate this condition?

a. colestipol
b. ezetimibe
c. gemfibrozil
d. niacin
e. simvastatin

A

d. niacin

Niacin can exacerbate both hyperuricemia and glucose intolerance.

59
Q

A 43-year-old man has heterozygous familial hypercholesterolemia. His serum concentrations of total cholesterol and LDL are markedly elevated. His serum concentration of HDL cholesterol, VLDL cholesterol, and triglycerides are normal or slightly elevated. The patient’s mother and older brother died of myocardial infarctions before the age of 50. This patient recently experienced mild chest pain when walking upstairs and has been diagnosed as having angina of effort. The patient is somewhat overweight. He drinks alcohol most evenings and smokes about 1 pack of cigarettes per week.

After being counseled about lifestyle and dietary changes, the patient was started on atorvastatin. During his treatment with atorvastatin, it is important to routinely monitor serum concentrations of which of the following?

a. blood urea nitrogen
b. alanine and aspartate aminotransferase
c. platelets
d. red blood cells
e. uric acid

A

b. alanine and aspartate aminotransferase

The 2 primary adverse effects of the HMG-CoA reductase inhibitors are hepatotoxicity and myopathy. Patients taking these drugs should have liver function tests performed before starting therapy, and at regular intervals as needed during therapy. Serum concentrations of alanine and aspartate aminotransferase are used as markers of hepatocellular toxicity.

60
Q

A 43-year-old man has heterozygous familial hypercholesterolemia. His serum concentrations of total cholesterol and LDL are markedly elevated. His serum concentration of HDL cholesterol, VLDL cholesterol, and triglycerides are normal or slightly elevated. The patient’s mother and older brother died of myocardial infarctions before the age of 50. This patient recently experienced mild chest pain when walking upstairs and has been diagnosed as having angina of effort. The patient is somewhat overweight. He drinks alcohol most evenings and smokes about 1 pack of cigarettes per week.

Six months after beginning atorvastatin, the patient’s total and LDL cholesterol concentrations remained above normal, and he continued to have anginal attacks despite good adherence to his antianginal medications. His physician decided to add ezetimibe. Which of the following is the most accurate description of ezetimibe’s mechanism of an action?

a. decreased lipid synthesis in adipose tissue
b. decreased secretion of VLDL by the liver
c. decreased GI absorption of cholesterol
d. increased endocytosis of HDL by the liver
e. increased lipid hydrolysis by lipoprotein lipase

A

c. decreased GI absorption of cholesterol

The major recognized effect of ezetimibe is inhibition of absorption of cholesterol in the intestine.

61
Q

52 year-old male presents to his general practitioner’s office for his annual physical exam. He follows a low saturated fat diet and jogs 2 miles 3x/week. He does not smoke and has no family history of premature coronary heart disease (CHD). Current medications include enalapril. Physical examination is normal. BP was 144/88, total chol 261, HDL 45, LDL 200, TG 80

What are the risk factors for CAD in this pt?

A

52 y/o male

Hypertensive and on medication (enelapril. = ACE inhib) for his HTN

LDL is 200 mg/dL

62
Q

52 year-old male presents to his general practitioner’s office for his annual physical exam. He follows a low saturated fat diet and jogs 2 miles 3x/week. He does not smoke and has no family history of premature coronary heart disease (CHD). Current medications include enalapril. Physical examination is normal. BP was 144/88, total chol 261, HDL 45, LDL 200, TG 80

what is the MOA of the drug that is most appropriate?

A. agonist for peroxisome proliferator-activated receptor alpha

b. bind to bile acids in the GI tract and increase excretion
c. incorporate into NAD
d. inhibit absorption of cholesterol
e. inhibit RL enzyme in cholesterol synthesis

A

e. inhibit RL enzyme in cholesterol synthesis

63
Q

52 year-old male presents to his general practitioner’s office for his annual physical exam. He follows a low saturated fat diet and jogs 2 miles 3x/week. He does not smoke and has no family history of premature coronary heart disease (CHD). Current medications include enalapril. Physical examination is normal. BP was 144/88, total chol 261, HDL 45, LDL 200, TG 80

what is the most potent drug of choice? least potent?

A

Most potent = atorvastatin

Least potent = fluvastatin

64
Q

52 year-old male presents to his general practitioner’s office for his annual physical exam. He follows a low saturated fat diet and jogs 2 miles 3x/week. He does not smoke and has no family history of premature coronary heart disease (CHD). Current medications include enalapril. Physical examination is normal. BP was 144/88, total chol 261, HDL 45, LDL 200, TG 80

what genetic changes would you expect if simvastatin is prescribed?

a. decreased expression of HDL receptors
b. decreased formation of chylomicrons
c. increased expression of VLDL
d. increased expression of LDL receptors
e. increased expression of peroxisome proliferator-activated receptor alpha

A

d. increased expression of LDL receptors

65
Q

An asymptomatic female is screened with a lipid profile during her annual physical by her primary care provider. She has type 2 diabetes (controlled with medication) and is approximately 20% overweight. Her fasting lipoprotein profile is as follows: total chol 644, HDL 24, LDL 160, TG 2300.

what are the risk factors for CAD in this pt?

A

T2D, obesity, high total cholesterol and TG, low HDL

66
Q

An asymptomatic female is screened with a lipid profile during her annual physical by her primary care provider. She has type 2 diabetes (controlled with medication) and is approximately 20% overweight. Her fasting lipoprotein profile is as follows: total chol 644, HDL 24, LDL 160, TG 2300.

Where is the most likely genetic mutation/deficiency causing the elevations in this patients TG levels?

a. chylomicrons
b. HDL receptor
c. Insulin receptor
d. LDL receptor
e. lipoprotein lipase

A

e. lipoprotein lipase

67
Q

An asymptomatic female is screened with a lipid profile during her annual physical by her primary care provider. She has type 2 diabetes (controlled with medication) and is approximately 20% overweight. Her fasting lipoprotein profile is as follows: total chol 644, HDL 24, LDL 160, TG 2300.

Assuming the pt is heterozygous for a mutation in lipoprotein lipase, which class of agents used to tx hyperlipidemias would be most effective in treating this pts elevated TG levels?

a. bile acid sequestrants
b. ezetimibe
c. fibrates
d. niacin
e. statins

A

c. fibrates

[fibrates are the best at reducing TGs!]

68
Q

52 year-old male presents to his general practitioner’s office for his annual physical exam. He follows a low saturated fat diet and jogs 2 miles 3x/week. He does not smoke and has no family history of premature coronary heart disease (CHD). Current medications include enalapril. Physical examination is normal. BP was 144/88, total chol 261, HDL 45, LDL 200, TG 80

After taking simvastatin for one week, he returns to the office complaining of leg and arm pain. Which lab value would you expect to find at this time?

a. ALT = 80 U/L (13-40 U/L)
b. creatine kinase = 150 U/L (15-105 U/L)
c. fasting serum glucose = 180 mg/dL (74-106)
d. HDL = 65 mg/dL (>40)
e. LDL = 185 mg/dL (<130 mg/dL)

A

b. creatine kinase = 150 U/L (15-105 U/L)

69
Q

52 year-old male presents to his general practitioner’s office for his annual physical exam. He follows a low saturated fat diet and jogs 2 miles 3x/week. He does not smoke and has no family history of premature coronary heart disease (CHD). Current medications include enalapril. Physical examination is normal. BP was 144/88, total chol 261, HDL 45, LDL 200, TG 80

The pt responds to simvastatin with a 40% reduction of LDL over the next 3 mos and then is lost to follow up for 5 years. he presents at age 57 for another PE and is 25 lbs heavier and smoking 1/2 ppd. BP is now 148/95, LDL is 200, TGs are 310, HDL is 28, and total chol is 290. An agent is prescribed as an addition to simvastatin that will increase his risk of myopathy. which agent is prescribed?

a. colestipol
b. ezetimibe
c. gemfibrozil
d. niacin
e. rosuvastatin

A

c. gemfibrozil

70
Q

52 year-old male presents to his general practitioner’s office for his annual physical exam. He follows a low saturated fat diet and jogs 2 miles 3x/week. He does not smoke and has no family history of premature coronary heart disease (CHD). Current medications include enalapril. Physical examination is normal. BP was 144/88, total chol 261, HDL 45, LDL 200, TG 80

Which cholesterol absorption inhibitor can be prescribed in combo with simvastatin to further decrease his LDL levels?

a. colestipol
b. ezetimibe
c. gemfibrozil
d. niacin
e. rosuvastatin

A

b. ezetimibe

Cardiovascular Exam I (8 decks)

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