Part 5.2-BLOOD-DYSLIPIDEMIA

Dyslipidemia refers to:
a. Abnormal glucose profile
b. Abnormal lipid profile
c. Abnormal electrolyte profile
d. Abnormal blood pressure

b. Abnormal lipid profile

Hypercholesterolemia is characterized by:
a. Increased LDL with decreased HDL
b. Increased serum triglycerides only
c. Decreased cholesterol only
d. Increased platelet count

a. Increased LDL with decreased HDL

Hypertriglyceridemia is defined as:
a. Increased LDL only
b. Increased HDL only
c. Increased serum triglycerides
d. Decreased triglycerides

c. Increased serum triglycerides

HMG-COA reductase Inhibitor MOA

a. Increasing triglyceride synthesis
b. Inhibiting the first committed step in cholesterol biosynthesis
c. Blocking intestinal triglyceride absorption
d. Activating vitamin K synthesis

b. Inhibiting the first committed step in cholesterol biosynthesis

Cholesterol synthesis peaks during:
a. Morning exercise
b. Fasting
c. Afternoon meals
d. Height of sleep

d. Height of sleep

HMG-CoA reductase inhibitors are commonly known as:
a. Fibrates
b. Statins
c. Bile acid sequestrants
d. PCSK9 inhibitors

b. Statins

Which statins are long-acting and may be taken anytime?
a. Simvastatin and Pravastatin
b. Atorvastatin and Rosuvastatin
c. Gemfibrozil and Fenofibrate
d. Ezetimibe and Cholestyramine

b. Atorvastatin and Rosuvastatin

Which statins are short-acting and should be taken at bedtime?
a. Simvastatin and Pravastatin
b. Atorvastatin and Rosuvastatin
c. Gemfibrozil and Fenofibrate
d. Ezetimibe and Cholestyramine

a. Simvastatin and Pravastatin

HMG-COA reductase Inhibitor Adverse effects:

Fibromyalgia or Myalgia?

Muscle pain (Myositis) or Dermatomyositis?

Rhabdomyolysis or Acute kidney injury (AKI)?

Myalgia

Muscle pain (Myositis)

Rhabdomyolysis

Fibric acid MOA
a. Increasing activity of lipoprotein lipase (LPL)
b. Inhibiting cholesterol synthesis
c. Blocking bile acid recycling
d. Inhibiting intestinal cholesterol uptake

a. Increasing activity of lipoprotein lipase (LPL)

Lipoprotein lipase (LPL) functions to:
a. Increase LDL production
b. Break down triglycerides into fatty acids and glycerol
c. Increase bile acid synthesis
d. Block cholesterol transport

b. Break down triglycerides into fatty acids and glycerol

LPL: takes up and breaks down triglyceride into fatty acid and glycerides or glycerol = lowers serum triglyceride

Examples of fibric acid derivatives include:

a. Simvastatin and Pravastatin
b. Atorvastatin and Rosuvastatin
c. Gemfibrozil and Fenofibrate
d. Ezetimibe and Cholestyramine

c. Gemfibrozil and Fenofibrate

Drug of choice for hypertriglyceridemia is:
a. Statins
b. Fibric acid derivatives (fibrates)
c. Ezetimibe
d. Vitamin K

b. Fibric acid derivatives (fibrates)

Major adverse effects of fibrates include:
a. Hepatotoxicity and flushing only
b. Myalgia, myositis, and rhabdomyolysis
c. Hypertension and edema
d. Bleeding and thrombocytopenia

b. Myalgia, myositis, and rhabdomyolysis

-same with statins

Nicotinic acid is a form of:
a. Vitamin A
b. Vitamin C
c. Niacin
d. Riboflavin

c. Niacin

Nicotinic acid lowers lipids primarily by:
a. Inhibiting synthesis and release of VLDL from the liver
b. Increase activity of the enzyme lipoprotein lipase (LPL)
c. Blocking intestinal bile acids
d. Increasing LDL receptor destruction

a. Inhibiting synthesis and release of VLDL from the liver

Nicotinic acid is mainly used as:
a. Drug of choice for hypercholesterolemia
b. Alternative for hypertriglyceridemia
c. DOC for hypertriglyceridemia
d. Alternative for hypercholesterolemia

b. Alternative to fibrates for hypertriglyceridemia

Adverse effects of nicotinic acid include:
a. Hepatotoxicity at high doses and flushing
b. Myalgia at high doses and flushing
c. Intracerebral hemorrhage at high doses and myalgia
d. Osteoporosis at high doses and myalgia

a. Hepatotoxicity at high doses and flushing

Which drugs are bile acid binding resins (bile acid sequestrants)?
a. Fenofibrate and Gemfibrozil
b. Cholestyramine and Colestipol
c. Evolocumab and Alirocumab
d. Simvastatin and Pravastatin

b. Cholestyramine and Colestipol

Bile acid sequestrants work by:
a. Increasing bile acid recycling
b. Inhibiting recycling of bile acids
c. Inhibits synthesis and release of VLDL
d. Increase activity of the enzyme lipoprotein lipase (LPL)

b. Inhibiting recycling of bile acids

Bile acid sequestrants are commonly used as:
a. Add-ons to statins
b. Replacement for statins
c. First-line drugs for hypercholesterolemia
d. First-line drugs for hypertriglyceridemia

a. Add-ons to statins

Ezetimibe is classified as a:
a. Statin
b. Fibric acid derivative
c. Cholesterol transport inhibitor
d. Vitamin K antagonist

c. Cholesterol transport inhibitor

Ezetimibe lowers cholesterol by:
a. Inhibiting intestinal cholesterol uptake via NPC1L1 transporter
b. Increasing triglyceride synthesis
c. Blocking thrombin formation
d. Activating bile acid recycling

a. Inhibiting intestinal cholesterol uptake via NPC1L1 transporter

Ezetimibe is commonly used as:
a. Monotherapy for stroke
b. Add-on therapy with statins
c. Drug of choice for HIT
d. Antiplatelet agent

b. Add-on therapy with statins

PCSK9 inhibitors means

a. Platelet coagulation synthesis kinase 9
b. Plasma cholesterol suppressor kinase 9
c. Proprotein convertase subtilisin/kexin 9
d. Peripheral cholesterol signaling kinase 9

c. Proprotein convertase subtilisin/kexin 9 (PCSK9)

PCSK9 inhibitors include:
a. Simvastatin and Pravastatin
b. Evolocumab and Alirocumab
c. Fenofibrate and Gemfibrozil
d. Cholestyramine and Colestipol

b. Evolocumab and Alirocumab

PCSK9 inhibitors work by:
a. Destroying LDL receptors
b. Inhibiting PCSK9, increasing LDL receptors and cholesterol uptake
c. Increasing VLDL synthesis
d. Blocking intestinal triglyceride absorption

b. Inhibiting PCSK9, increasing LDL receptors and cholesterol uptake

Evolocumab is mainly used for:
a. Drug of choice in the management of hypertriglyceridemia
b. Hypercholesterolemia refractory to other drugs
c. Used as an add-on for statins
d. Anticoagulation in pregnancy

b. Hypercholesterolemia refractory to other drugs