A patient with high LDL is started on atorvastatin. Which enzyme is directly inhibited?
A) PCSK9
B) HMG-CoA reductase
C) PPAR-alpha
D) Intestinal cholesterol transporter
B. HMG-CoA reductase
Which drug class includes atorvastatin, simvastatin, rosuvastatin, and pravastatin?
A) Fibrates
B) PCSK9 inhibitors
C) Bile acid sequestrants
D) Statins
D. Statins
Statins lower cholesterol by acting primarily in which organ?
A) Intestine
B) Kidney
C) Liver
D) Pancreas
C. Liver
HMG-CoA reductase normally helps the liver perform which process?
A) Break down triglycerides
B) Make cholesterol
C) Bind bile acids
D) Degrade LDL receptors
B. Make cholesterol
Blocking HMG-CoA reductase causes which direct effect?
A) More bile acid absorption
B) More VLDL secretion
C) More PCSK9 activity
D) Less liver cholesterol synthesis
D. Less liver cholesterol synthesis
After statins reduce liver cholesterol, the liver increases which surface proteins?
A) LDL receptors
B) ApoA-I proteins
C) PCSK9 proteins
D) Bile acid receptors
A. LDL receptors
Increased hepatic LDL receptors cause which blood effect?
A) Less LDL clearance
B) More HDL breakdown
C) More LDL removal
D) More VLDL secretion
C. More LDL removal
Statins are mainly used for which lipid abnormality?
A) High triglycerides
B) Low HDL only
C) High bile acids
D) High LDL
D. High LDL
A patient is prescribed rosuvastatin to reduce plaque risk. Which clinical goal fits best?
A) Prevent atherosclerosis
B) Treat constipation
C) Increase VLDL secretion
D) Block vitamin absorption
A. Prevent atherosclerosis
Statins help prevent heart disease mainly by lowering which lipoprotein?
A) HDL
B) Albumin
C) Chylomicrons
D) LDL
D. LDL
Which adverse effect is associated with statins?
A) Constipation
B) Bloating
C) Myopathy
D) Tendon rupture
C. Myopathy
Which organ toxicity is associated with statins?
A) Liver dysfunction
B) Lung fibrosis
C) Kidney stones
D) Bone marrow failure
A. Liver dysfunction
Fenofibrate and gemfibrozil belong to which class?
A) Statins
B) PCSK9 inhibitors
C) Bile acid sequestrants
D) Fibrates
D. Fibrates
Which name clue helps identify fenofibrate and gemfibrozil?
A) “fib” in name
B) “statin” suffix
C) “cumab” suffix
D) “three Cs” clue
A. “fib” in name
Fibrates directly activate which receptor?
A) HMG-CoA reductase
B) PCSK9
C) PPAR-alpha
D) ApoA-I
C. PPAR-alpha
Activating PPAR-alpha mainly increases breakdown of which lipid?
A) Triglycerides
B) LDL receptors
C) Bile acids
D) Intestinal cholesterol
A. Triglycerides
Fibrates are mainly used to lower which lipid?
A) LDL
B) HDL
C) Bile acids
D) Triglycerides
D. Triglycerides
Compared with LDL lowering, fibrates are mainly better for lowering what?
A) Cholesterol absorption
B) Triglycerides
C) PCSK9 activity
D) Bile acid binding
B. Triglycerides
Fibrates can also cause a small increase in which lipoprotein?
A) LDL
B) VLDL
C) HDL
D) Chylomicrons
C. HDL
A patient with very high triglycerides is started on gemfibrozil. Which mechanism explains the benefit?
A) Blocks PCSK9
B) Activates PPAR-alpha
C) Binds bile acids
D) Blocks cholesterol absorption
B. Activates PPAR-alpha
Which adverse effect is associated with fibrates?
A) Cough
B) Tendon rupture
C) Bradycardia
D) Myopathy
D. Myopathy
Fibrates share which side effect with statins?
A) Constipation
B) Liver dysfunction
C) Decreased absorption
D) Visual changes
B. Liver dysfunction
Colestipol, cholestyramine, and colesevelam belong to which class?
A) Statins
B) Bile acid sequestrants
C) Fibrates
D) Sterol absorption inhibitors
B. Bile acid sequestrants
Which memory clue was given for bile acid sequestrants?
A) “floxacin” ending
B) “statin” suffix
C) “cumab” ending
D) The three Cs
D. The three Cs
Bile acid sequestrants work in which location?
A) Gut
B) Liver cytosol
C) Blood plasma
D) Kidney tubule
A. Gut
Bile acid sequestrants directly bind what?
A) LDL receptors
B) HMG-CoA reductase
C) Bile acids
D) ApoA-I
C. Bile acids
Bile acids are made from which molecule?
A) Triglycerides
B) Cholesterol
C) Glucose
D) Amino acids
B. Cholesterol
If bile acids are trapped and excreted, what must the liver use more of?
A) Potassium
B) Glucose
C) Albumin
D) Cholesterol
D. Cholesterol
Bile acid sequestrants lower LDL because the liver uses cholesterol to make what?
A) New bile acids
B) VLDL
C) ApoA-I
D) PCSK9
A. New bile acids
Which clinical effect results from bile acid sequestrants?
A) HDL drops severely
B) LDL decreases
C) VLDL secretion increases
D) Triglycerides vanish
B. LDL decreases
Which listed drug is a bile acid sequestrant?
A) Atorvastatin
B) Ezetimibe
C) Fenofibrate
D) Colestipol
D. Colestipol
Which listed drug is a bile acid sequestrant?
A) Cholestyramine
B) Rosuvastatin
C) Gemfibrozil
D) Evolocumab
A. Cholestyramine
Which listed drug is a bile acid sequestrant?
A) Alirocumab
B) Niacin
C) Colesevelam
D) Bempedoic acid
C. Colesevelam
Which side effect is associated with bile acid sequestrants?
A) Myopathy
B) Hyperkalemia
C) Bronchoconstriction
D) Constipation
D. Constipation
A patient on cholestyramine develops abdominal gas and fullness. Which adverse effect fits?
A) Liver dysfunction
B) Bloating
C) Tendon rupture
D) Neurotoxicity
B. Bloating
Bile acid sequestrants can decrease absorption of what?
A) LDL receptors only
B) Liver cholesterol only
C) Other drugs and vitamins
D) Bone marrow cells only
C. Other drugs and vitamins
Which side effect set best matches bile acid sequestrants?
A) Constipation, bloating, decreased absorption
B) Rash, fever, hyperkalemia
C) Myopathy, liver dysfunction
D) GI upset, neurotoxicity, tendon rupture
A. Constipation, bloating, decreased absorption
A patient taking colesevelam has reduced absorption of another medication. Which mechanism explains this?
A) PPAR-alpha activation
B) Gut binding effect
C) PCSK9 blockade
D) HMG-CoA reductase inhibition
B. Gut binding effect
Which lipid-lowering class works by making the body excrete bile acids in stool?
A) Fibrates
B) Statins
C) PCSK9 inhibitors
D) Bile acid sequestrants
D. Bile acid sequestrants
Ezetimibe belongs to which drug category?
A) PCSK9 inhibitor
B) Sterol absorption inhibitor
C) Fibrate
D) Bile acid sequestrant
B. Sterol absorption inhibitor
Ezetimibe acts primarily in which body site?
A) Liver
B) Kidney
C) Pancreas
D) Intestine
D. Intestine
Ezetimibe directly blocks absorption of what?
A) Cholesterol
B) Triglycerides
C) Bile acids
D) ApoA-I
A. Cholesterol
Ezetimibe lowers LDL by decreasing cholesterol entry from where?
A) Kidney
B) Muscle
C) Gut
D) Pancreas
C. Gut
A patient with high LDL is started on ezetimibe. Which mechanism best explains its effect?
A) Activates PPAR-alpha
B) Blocks cholesterol absorption
C) Blocks PCSK9
D) Binds bile acids
B. Blocks cholesterol absorption
Less intestinal cholesterol absorption causes which blood effect?
A) HDL disappears
B) VLDL secretion increases
C) PCSK9 increases
D) LDL goes down
D. LDL goes down
Which listed drug is a sterol absorption inhibitor?
A) Ezetimibe
B) Niacin
C) Fenofibrate
D) Evolocumab
A. Ezetimibe
Which pairing is correct?
A) Ezetimibe—PPAR-alpha activator
B) Ezetimibe—bile acid binder
C) Ezetimibe—intestinal cholesterol absorption blocker
D) Ezetimibe—PCSK9 blocker
C. Ezetimibe—intestinal cholesterol absorption blocker
Niacin decreases secretion of which lipoprotein from the liver?
A) HDL
B) LDL
C) Chylomicrons
D) VLDL
D. VLDL
Less VLDL secretion eventually leads to less of which lipoprotein?
A) LDL
B) HDL
C) Albumin
D) ApoA-I
A. LDL
Niacin decreases breakdown of which apolipoprotein?
A) ApoB-100
B) ApoA-I
C) ApoC-II
D) ApoE
B. ApoA-I
ApoA-I helps increase which lipoprotein?
A) LDL
B) VLDL
C) HDL
D) Chylomicrons
C. HDL
Niacin is best known in these notes for increasing which lipid?
A) LDL
B) VLDL
C) Bile acids
D) HDL
D. HDL
Which drug is described as the best for raising HDL?
A) Ezetimibe
B) Niacin
C) Fenofibrate
D) Cholestyramine
B. Niacin
Niacin lowers LDL indirectly by decreasing which precursor lipoprotein?
A) HDL
B) Albumin
C) VLDL
D) LDL receptors
C. VLDL
Evolocumab and alirocumab belong to which class?
A) Statins
B) PCSK9 inhibitors
C) Fibrates
D) Bile acid sequestrants
B. PCSK9 inhibitors
Which name clue helps identify evolocumab and alirocumab?
A) “statin” suffix
B) “fib” in name
C) “cumab” suffix
D) “three Cs” clue
C. “cumab” suffix
PCSK9 inhibitors directly block which protein?
A) ApoA-I
B) PPAR-alpha
C) HMG-CoA reductase
D) PCSK9
D. PCSK9
PCSK9 normally breaks down which liver surface proteins?
A) LDL receptors
B) HDL proteins
C) Bile acid receptors
D) Sodium channels
A. LDL receptors
Blocking PCSK9 allows LDL receptors to do what?
A) Break down faster
B) Stay alive longer
C) Leave the liver
D) Stop binding LDL
B. Stay alive longer
When LDL receptors stay alive longer, the liver does what?
A) Releases more LDL into blood
B) Stops clearing LDL
C) Pulls more LDL from blood
D) Makes more VLDL
C. Pulls more LDL from blood
PCSK9 inhibitors cause which lipid effect?
A) HDL disappears
B) Triglycerides always rise
C) VLDL secretion increases
D) LDL drops a lot
D. LDL drops a lot
Which listed drug is a PCSK9 inhibitor?
A) Evolocumab
B) Fenofibrate
C) Ezetimibe
D) Colestipol
A. Evolocumab
Which listed drug is a PCSK9 inhibitor?
A) Simvastatin
B) Alirocumab
C) Gemfibrozil
D) Niacin
B. Alirocumab
Bempedoic acid acts primarily by inhibiting what?
A) Cholesterol biosynthesis
B) Bile acid absorption
C) ApoA-I breakdown
D) PCSK9 degradation
A. Cholesterol biosynthesis
Bempedoic acid inhibits cholesterol biosynthesis in which organ?
A) Intestine
B) Liver
C) Kidney
D) Muscle
B. Liver
Bempedoic acid causes the liver to make less what?
A) HDL
B) ApoA-I
C) Cholesterol
D) Bile acid binders
C. Cholesterol
After bempedoic acid decreases liver cholesterol, the liver increases what?
A) VLDL secretion
B) PCSK9 breakdown
C) Triglyceride storage
D) LDL receptors
D. LDL receptors
Bempedoic acid lowers blood LDL by causing which effect?
A) More LDL pulled from blood
B) Less bile acid excretion
C) More VLDL secretion
D) More cholesterol absorption
A. More LDL pulled from blood
Which drug inhibits cholesterol biosynthesis in the liver?
A) Cholestyramine
B) Bempedoic acid
C) Gemfibrozil
D) Niacin
B. Bempedoic acid
Which class mainly lowers LDL by increasing hepatic LDL receptors after blocking liver cholesterol synthesis?
A) Fibrates
B) Bile acid sequestrants
C) Niacin
D) Statins
D. Statins
Which class mainly lowers LDL by preventing the degrading of LDL receptors?
A) PCSK9 inhibitors
B) Bile acid sequestrants
C) Fibrates
D) Sterol absorption inhibitors
A. PCSK9 inhibitors
Which class lowers LDL by blocking intestinal cholesterol absorption?
A) Fibrate
B) Sterol absorption inhibitor
C) Beta blocker
D) Sulfonamide
B. Sterol absorption inhibitor
Which class lowers LDL by binding bile acids in the gut?
A) Statins
B) Fibrates
C) Bile acid sequestrants
D) PCSK9 inhibitors
C. Bile acid sequestrants
Which class mainly lowers triglycerides through PPAR-alpha activation?
A) PCSK9 inhibitors
B) Statins
C) Sterol inhibitors
D) Fibrates
D. Fibrates
Which drug is most associated with raising HDL in these notes?
A) Niacin
B) Ezetimibe
C) Atorvastatin
D) Colestipol
A. Niacin
Which lipid-lowering agents share myopathy and liver dysfunction as listed side effects?
A) Niacin and ezetimibe
B) Statins and fibrates
C) PCSK9 inhibitors and sequestrants
D) Bempedoic acid and niacin
B. Statins and fibrates
Which drug lowers LDL by blocking intestinal absorption rather than liver synthesis?
A) Rosuvastatin
B) Ezetimibe
C) Pravastatin
D) Bempedoic acid
B. Ezetimibe
Which drug lowers LDL by blocking receptor degradation rather than cholesterol synthesis?
A) Simvastatin
B) Cholestyramine
C) Alirocumab
D) Niacin
C. Alirocumab
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) Atorvastatin
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
(B) Cholestyramine
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
(E) Pravastatin
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
(D) Increased triglyceride hydrolysis by lipoprotein lipase
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
(B) Cholelithiasis
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
(E) Increased triglyceride
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
Niacin can exacerbate both hyperuricemia and glucose intolerance.
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
(B) Alanine and aspartate aminotransferase
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
(C) Decreased gastrointestinal absorption of cholesterol