Pharm 35 Flashcards

Statin MOA

A) Blocks NPC1L1 transport

B) Inhibits HMG-CoA reductase

C) Activates PPAR-alpha

D) Targets apoB-100 mRNA

Which adverse effect is most classically associated with statin therapy?

A) Myopathy

B) Cholesterol gallstones

C) Severe constipation

D) Hyperuricemia

A patient is started on a statin for high LDL. Which routine laboratory monitoring is most appropriate because of potential hepatic toxicity?

A) Serum amylase

B) Troponin

C) LFTs

D) Urinalysis

A patient taking simvastatin is prescribed a strong macrolide antibiotic and develops increased statin toxicity risk. Which cytochrome P450 enzyme is most relevant?

A) CYP2D6

B) CYP1A2

C) CYP2C9

D) CYP3A4

A patient with severe hypertriglyceridemia is treated with a fibrate. Which lipoprotein is predominantly reduced by this drug class?

A) Chylomicron remnants

B) HDL

C) VLDL

D) Lp(a)

A fibrate improves hypertriglyceridemia by activating a nuclear receptor that increases lipoprotein lipase activity. Which mechanism is correct?

A) PPAR-alpha agonism

B) NPC1L1 blockade

C) HSL inhibition

D) PCSK9 blockade

A patient is prescribed gemfibrozil with a statin and develops muscle tenderness. Which lab is most appropriate to monitor for the major overlapping toxicity?

A) Bilirubin

B) CK

C) Amylase

D) TSH

Which adverse effect best matches fibrate therapy?

A) Hyperuricemia

B) Facial flushing

C) Cholelithiasis

D) Gingival hyperplasia

A patient with dyslipidemia receives niacin, which lowers free fatty acid delivery to the liver by blocking what?

A) HSL inhibition

B) PPAR-alpha activation

C) MTP inhibition

D) Bile acid binding

Niacin decreases hepatic production of which lipoproteins by reducing adipose free fatty acid release?

A) HDL and chylomicrons

B) LDL and VLDL

C) IDL and HDL

D) Lp(a) and HDL

Which adverse-effect cluster is most characteristic of niacin?

A) Myopathy, CK rise, rhabdomyolysis

B) Gallstones, nausea, constipation

C) Flushing, hyperuricemia, hepatotoxicity

D) Tendon rupture, cough, edema

A dyslipidemic patient needs the medication class with the greatest HDL-raising effect. Which drug is most appropriate?

A) Ezetimibe

B) Cholestyramine

C) Fenofibrate

D) Niacin

A patient with high LDL is started on cholestyramine. Which lipoprotein effect is expected from bile acid resin therapy?

A) LDL decreases; VLDL increases

B) HDL decreases; LDL increases

C) VLDL decreases; LDL increases

D) Chylomicrons decrease; HDL decreases

A patient taking cholestyramine reports what adverse effects

A) Flushing and hyperuricemia

B) Constipation and nausea

C) Myopathy and CK elevation

D) Cough and angioedema

A patient taking both a fibrate and a bile acid resin develops biliary colic. Which GI complication is especially increased by this combination?

A) Pancreatitis

B) Peptic ulcer disease

C) Cholelithiasis

D) Ischemic colitis

Which mechanism best describes ezetimibe?

A) Binds bile acids

B) Activates PPAR-alpha

C) Blocks HMG-CoA reductase

D) Inhibits intestinal cholesterol absorption

A drug prevents intestinal cholesterol uptake by blocking the brush-border cholesterol transporter. Which specific target is inhibited?

A) MTP

B) NPC1L1

C) PCSK9

D) ApoB-100

A patient who consumes minimal dietary cholesterol is still prescribed ezetimibe to increase biliary cholesterol loss. Can ezetimibe still inhibit cholesterol reabsorption? A) Yes B) No

A patient taking ezetimibe is monitored for hepatic adverse effects. Which labs are most appropriate?

A) CK only

B) Troponins

C) LFTs

D) Urine ketones

A patient with familial hypercholesterolemia is treated with a drug that blocks assembly of apoB-containing lipoproteins by inhibiting microsomal triglyceride transfer protein. Which drug mechanism is this?

A) PCSK9 inhibition

B) NPC1L1 inhibition

C) ApoB-100 antisense

D) MTP inhibition

A patient receives mipomersen for severe hypercholesterolemia. Which mechanism best describes this medication?

A) ApoB-100 antisense oligonucleotide

B) PPAR-alpha receptor activation

C) Bile acid sequestration

D) HMG-CoA reductase inhibition

A patient receives evolocumab for refractory high LDL. Which mechanism best explains its LDL-lowering effect?

A) Inhibits bile acid absorption

B) Inhibits PCSK9 activity

C) Blocks hepatic triglyceride transfer

D) Inhibits hormone-sensitive lipase

How do alirocumab and evolocumab increase hepatic LDL receptor availability?

A) Increase bile acid excretion

B) Activate lipoprotein lipase

C) Prevent LDL receptor digestion

D) Inhibit hepatic VLDL secretion

A patient taking evolocumab has a dramatic improvement in one lipid fraction. Which lipoprotein is most strongly reduced

A) HDL

B) Chylomicrons

C) VLDL

D) LDL

A patient with elevated LDL and atherosclerotic vascular disease needs first-line lipid therapy that reduces hepatic cholesterol synthesis and increases hepatocyte LDL receptors. Which drug class best matches?

A) Statins

B) Fibrates

C) Niacin

D) Bile acid sequestrants

Which set contains only statins listed as commonly used HMG-CoA reductase inhibitors?

A) Fenofibrate, gemfibrozil, ezetimibe

B) Atorvastatin, simvastatin, rosuvastatin

C) Colestipol, colesevelam, cholestyramine

D) Evolocumab, alirocumab, bempedoic acid

Compared with atorvastatin, simvastatin, rosuvastatin, and pitavastatin, which listed statins are noted as similar but somewhat less efficacious?

A) Ezetimibe, niacin, colestipol

B) Fenofibrate, gemfibrozil, alirocumab

C) Fluvastatin, pravastatin, lovastatin

D) Evolocumab, colesevelam, bempedoic acid

A patient with high LDL and recent acute coronary syndrome is started on a drug that modestly lowers triglycerides while upregulating LDL receptors. Which therapy is most appropriate?

A) Ezetimibe

B) Gemfibrozil

C) Colestipol

D) Atorvastatin

Which clinical application best matches statin therapy?

A) Elevated LDL and ASCVD prevention

B) Digitalis toxicity and pruritus

C) Hypertriglyceridemia and pruritus

D) Phytosterolemia and ASCVD prevention

A patient with severe hypertriglyceridemia is treated with fenofibrate. Which mechanism best explains the benefit?

A) Blocks NPC1L1 transporter

B) Activates PPAR-alpha

C) Complexes PCSK9

D) Binds intestinal bile acids

Which drug pair belongs to the fibrate subclass?

A) Colestipol and colesevelam

B) Ezetimibe and bempedoic acid

C) Evolocumab and alirocumab

D) Fenofibrate and gemfibrozil

A fibrate improves hypertriglyceridemia by changing VLDL secretion and lipoprotein lipase activity. Which effect pattern is correct?

A) Decreases VLDL; increases LPL

B) Increases VLDL; decreases LPL

C) Decreases LDL receptors; lowers HDL

D) Blocks bile acids; raises LDL

Which lipid effect is expected from fibrates in addition to decreased VLDL secretion?

A) Decreased apo A-I production

B) Increased HDL

C) Increased phytosterol absorption

D) Increased LDL catabolism blockade

A patient with hypertriglyceridemia is prescribed a PPAR-alpha agonist. Which medication is most likely?

A) Ezetimibe

B) Cholestyramine

C) Gemfibrozil

D) Evolocumab

A patient with elevated LDL, pruritus, and possible digitalis toxicity receives a medication that binds bile acids in the gut. Which drug is specifically listed in this subclass?

A) Niacin

B) Colestipol

C) Fenofibrate

D) Bempedoic acid

Which mechanism best describes bile acid sequestrants?

A) Prevent bile acid reabsorption

B) Inhibit hepatic MTP

C) Complex circulating PCSK9

D) Reduce apo A-I catabolism

Bile acid sequestrants lower LDL through which compensatory hepatic response?

A) Downregulate LDL receptors

B) Upregulate LDL receptors

C) Block LDL receptor recycling

D) Complex LDL receptors directly

Which set contains bile acid sequestrants listed as similar to colestipol?

A) Fenofibrate and gemfibrozil

B) Evolocumab and alirocumab

C) Cholestyramine and colesevelam

D) Niacin and ezetimibe

Which clinical applications best match bile acid sequestrants?

A) Hypertriglyceridemia and Lp(a)

B) Familial hypercholesterolemia only

C) Acute coronary syndrome only

D) Elevated LDL, digitalis toxicity, pruritus

A patient with elevated LDL and phytosterolemia is started on ezetimibe. Which target does ezetimibe block?

A) HMG-CoA reductase

B) PPAR-alpha

C) PCSK9

D) NPC1L1

Ezetimibe decreases LDL and phytosterols primarily by inhibiting cholesterol absorption at which site?

A) Intestinal brush border

B) Hepatic sinusoid

C) Renal collecting duct

D) Adrenal zona glomerulosa

Which effect best matches ezetimibe therapy?

A) Increases apo A-I catabolism

B) Inhibits biliary cholesterol reabsorption

C) Increases VLDL secretion

D) Decreases LDL receptor expression

A patient with elevated VLDL and Lp(a) receives niacin. Which mechanism best explains its HDL effect?

A) Blocks bile acid absorption

B) Complexes PCSK9

C) Decreases apo A-I catabolism

D) Inhibits sterol transport

Which lipid effect pattern best matches niacin?

A) Increases HDL; decreases Lp(a), LDL

B) Decreases HDL; increases VLDL, LDL

C) Decreases HDL; decreases phytosterols only

D) Increases LDL; decreases triglycerides only

Niacin lowers VLDL primarily by reducing secretion from which organ?

A) Intestine

B) Kidney

C) Adrenal gland

D) Liver

A patient asks why sustained-release niacin is not interchangeable with extended-release niacin. Which concern is emphasized?

A) More renal toxicity

B) More pulmonary toxicity

C) More hepatic toxicity

D) More thyroid toxicity

A patient with familial hypercholesterolemia has incomplete response to other lipid-lowering therapy. Which medication class complexes PCSK9?

A) Bile acid sequestrants

B) Sterol absorption inhibitors

C) PCSK9 monoclonal antibodies

D) Fibrates

Evolocumab lowers LDL by complexing PCSK9. What is the downstream receptor effect?

A) Inhibits LDL receptor catabolism

B) Increases LDL receptor destruction

C) Blocks NPC1L1 transporters

D) Decreases lipoprotein lipase activity

Which drug is listed as similar to evolocumab?

A) Colesevelam

B) Alirocumab

C) Pitavastatin

D) Gemfibrozil

Which clinical situation best matches PCSK9 monoclonal antibody use?

A) Digitalis toxicity with pruritus

B) Hypertriglyceridemia as first-line therapy

C) Familial hypercholesterolemia with incomplete response

D) Phytosterolemia from intestinal absorption

A patient with elevated LDL receives bempedoic acid. Which mechanism best matches this medication?

A) Activates PPAR-alpha

B) Binds intestinal bile acids

C) Complexes PCSK9

D) Inhibits hepatic cholesterol biosynthesis

Bempedoic acid reduces cholesterol synthesis and produces which compensatory hepatic effect?

A) Upregulates LDL receptors

B) Downregulates LDL receptors

C) Increases VLDL secretion

D) Blocks apo A-I synthesis

Which pairing correctly matches lipid drug class with its primary clinical application?

A) Fibrates; hypertriglyceridemia

B) Ezetimibe; digitalis toxicity

C) Bile resins; familial hypercholesterolemia

D) Niacin; acute coronary syndrome

A patient with elevated LDL but no prior cardiovascular event is started on a statin to reduce future atherosclerotic events. Which clinical application is being used?

A) Digitalis toxicity treatment

B) Primary prevention

C) Phytosterolemia treatment

D) Hypertriglyceridemia rescue

A patient with prior myocardial infarction and elevated LDL is prescribed high-intensity statin therapy to prevent recurrent events. Which clinical application is being used?

A) Secondary prevention

B) Pruritus treatment

C) Biliary cholesterol excretion

D) Familial triglyceride clearance

Bile acid sequestrants reduce LDL partly because binding bile acids forces the liver to convert more cholesterol into bile acids. Which mechanism is this?

A) Reduced apo A-I catabolism

B) Increased cholesterol catabolism

C) Increased VLDL secretion

D) Blocked PCSK9 binding