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Pharmacology > Treatment of Dyslipidemia > Flashcards

Treatment of Dyslipidemia Flashcards

1
Q

Pathogenesis of Hyperlipoproteinemia

A

PREMATURE ATHEROSCLEROSIS - associated w/ elevated concentrations lipoproteins

📌elevated LDL
📌depressed HDL
📌 hypertriglyceridemia

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2
Q

Drugs most effective at LOWERING LDL CHOLESTEROL

A

STATINS
RESINS
EZETIMIBE
NIACIN

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3
Q

Drugs most effective in LOWERING TRIGLYCERIDE and VLDL and RAISING HDL

A

NIACIN

FIBRATES

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4
Q

Statins use in CAD

A

for STABILIZATION of atherosclerotic plaques

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5
Q

Drugs that causes FLUSHING

A

VANC

Vancomycin
Adenosine
Niacin
CCB

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6
Q

FIBRATES

A

Fibrates Upregulate Lipoprotein Lipase (FULL)

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7
Q

Familial hypercholesterolemia

A

NIACIN + STATIN

STATIN + EZETIMIBE

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8
Q

Familial Combined Hypercholesterolemia

A

NIACIN + RESIN

STATIN + FIBRATE

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9
Q

Disadvantageous Antihyperlipidemic Combinations

A

FIBRATE + RESIN - CHOLELITHIASIS (increased risk)
STATIN + RESIN - impaired statin absorption
STATIN + FIBRATE - increased risk of myopathy and rhabdomyolysis

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10
Q

Caused by mutations leading to dysfunctional LDL receptors incapable of taking up LDL from the bloodstream

A

Homozygous Familial Hypercholesterolemia

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11
Q

Most effective in increasing HDL levels

A

NIACIN

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12
Q

STATINS/HMG-CoA Reductase Inhibitors

A 
Simvastatin
Atorvastatin
Rosuvastatin
Fluvastatin
Pravastatin
Lovastatin
Pitavastatin
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13
Q

Side effects of STATINS/HMG-CoA Reductase Inhibitors

A 
HEPATOXICITY
myopathy
rhabdomyolysis
GI distress
teratogen
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14
Q

Most potent among the Statins

A

Atorvastatin

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15
Q

(-) hormone sensitive lipase

A

NIACIN/Nicotinic Acid/Vitamin B3

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16
Q

MOST EFFECTIVE for INCREASING HDL

A

NIACIN

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17
Q

Side effects of Niacin

A 
FLUSHING
myositis
itchy skin
hyperglycemia
hyperuricemia
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18
Q

Fibric Acid Derivatives

A

Gemfibrozil
Fenofibrate
Bezafibrate

19
Q

MOA of Fibric Acid Derivatives

A

PPAR-a agonists (Peroxisome Proliferation Receptor Alpha) – (+) lipoprotein lipase

(-) apo CIII
(+) apo C1 and CII

20
Q

Side effects of Fibric Acid Derivatives

A

rhabdomyolysis
stone formation
myositis
erectile dysfunction

21
Q

Bile Acid Binding Resins

A

Cholestyramine
Colesevelam
Colestipol

22
Q

Side effects of Bile Acid Binding Resins

A

stone formation

constipation

23
Q

Cholesterol Absorption Inhibitor

(-) binding sites - NPC1L1 and clathrin AP2

A

Ezetimibe

decrease LDL, TG
increase HDL

24
Q

Cholesterol Absorption Inhibitor

PCSK9 (-)

A

Evalocumab

Aliracumab

25
Q

Omega 3-FA

A

DHA

EPA

26
Q

HIGH LDL

A

diet and exercise

STATIN

EZETIMIBE

27
Q

HIGH VLDL

A

diet and exercise

STATIN

FIBRATE

28
Q

HIGH TRIGLYCERIDES

A

diet and exercise

FIBRATE

NIACIN

29
Q

LOW HDL

A

diet and exercise

NIACIN

30
Q

HIGH LDL

HIGH VLDL

A

diet and exercise

STATIN

EZETIMIBE or NIACIN

31
Q

HIGH LDL
HIGH TRIGLYCERIDES
LOW LDL

A

diet and exercise

STATIN + NIACIN + FIBRATES

32
Q

PJ is a 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

33
Q

A 46-year-old woman with a history of hyperlipidemia was treated with a drug. The chart below shows the results of the patient’s fasting lipid panel before treatment and 6 mo after initiating drug therapy. Normal values are also shown. Which of the following drugs is most likely to be the one that this
patient received?

(A) Colestipol
(B) Ezetimibe
(C) Gemfibrozil
(D) Lovastatin
(E) Niacin
A

(E) Niacin

34
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

Which of the following drugs is most likely to increase this patient’s triglyceride and VLDL cholesterol concentrations when used as monotherapy?

(A) Atorvastatin
(B) Cholestyramine
(C) Ezetimibe
(D) Gemfibrozil
(E) Niacin
A

(B) Cholestyramine

35
Q

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

36
Q

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

37
Q

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

38
Q

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

39
Q

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

40
Q

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

41
Q

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 gastrointestinal absorption of cholesterol
(D) Increased endocytosis of HDL by the liver
(E) Increased lipid hydrolysis by lipoprotein lipase

A

(C) Decreased gastrointestinal absorption of cholesterol

42
Q

Fibrate + Resin

A

Increased risk of cholelithiasis

43
Q

Statin + Resin

A

Impaired statin absorption

44
Q

Statin + Fibrate

A

Increased risk of myopathy, rhabdomyolysis

Pharmacology (72 decks)

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