hyperlipidemia

Question 1

hyperlipidemia

Answer 1

serum cholesterol > 200

Question 2

hyperlipidemia: causes

Answer 2

genetic, dietary, lifestyle

Question 3

hyperlipidemia: tx goals changed- ACC/AHA guidelines

Answer 3

• risk based
• updated in 2018
• statins remain the mainstay of therapy

Question 4

high intestiny (>/50)

Answer 4

• atorvastatin
• rosuvastatin

Question 5

moderate intensity (30-40%)

Answer 5

• atorvastatin
• rosuvastatin
• simvasatin

Question 6

low intensity (<30%)

Answer 6

• simvastatin

Question 7

statins/ HMG-CoA reductase inhibitors: MOA

Answer 7

prevent the production of mevalonate – the building block of cholesterol
o Reduced intrahepatic cholesterol synthesis
o Upregulates expression of LDL receptor gene = more LDL receptors on the liver = lower LDL/triglycerides and higher HDL

Question 8

statins/ HMG-CoA reductase inhibitors: indications

Answer 8

o Hyperlipidemia
o ASCVD

Question 9

statins/ HMG-CoA reductase inhibitors: common side effects

Answer 9

o Myalgia
o Myopathy (can lead to rhabdo)
o Headache
o GI symptoms
o Elevated LFTs (<1% of patients)
o Increased risk for DM/hyperglycemia
o ? Cognitive decline

Question 10

when are statins administered?

Answer 10

at night

Question 11

Statins/HMG-CoA reductase inhibitor: common interactions

Answer 11

o Gemfibrozil or niacin + statin = increased risk of rhabdo

Question 12

Ezetimibe (Zetia): MOA

Answer 12

works by inhibiting the intestinal absorption of cholesterol

Question 13

Ezetimibe (Zetia): contraindicated

Answer 13

with statins in pts with liver disease

Question 14

Ezetimibe (Zetia)

Answer 14

• can be used as monotherapy
• well tolerated

Question 15

ENHANCE study (2008)

Answer 15

reduced cholesterol by 15-20% but no reduction in atherosclerotic plaque

Question 16

Bile Acid Sequestrants: drug examples

Answer 16

o Cholestyramine, colestipol, colesevelam

Question 17

Bile Acid Sequestrants: MOA

Answer 17

• Sequester bile acids
• Liver increases production of bile acids using cholesterol
• Bile acids are excreted in the gut

Question 18

Bile Acid Sequestrants: side effects

Answer 18

GI SE common–diarrhea, GI upset, gassiness

Question 19

Bile acid sequestrants

Answer 19

unsure effect of CV morbidity/mortality

Question 20

PCSK9 inhibitors: MOA

Answer 20

• PCSK9 is an enzyme that degrades LDL receptors on the liver
• Inhibitors bind to PCSK9 resulting in inhibition of receptor degradation  more LDL receptors  lower serum LDL

Question 21

PCSK9 inhibitors: side effects

Answer 21

not too many SEs–> only nasal pharyngitis

Question 22

PCSK9 inhibitors:

Answer 22

o Shown to decrease ASCVD morbidity and mortality
o Cost is going down but still expensive
o Reserved for lipid specialists

Question 23

Fibrates: MOA

Answer 23

Increase lipoprotein lipase activity–> more rapid degredation of triglycerides and LDL

Question 24

Fibrates: common agents

Answer 24

Fenofibrate, gemfibrozil

Question 25

Fibrates: contraindications

Answer 25

* Gemfibrozil should be avoided with statins * Increased serum statin levels = increased risk for rhabdo

Question 26

fibrates: primary role is

Answer 26

hypertriglyceridemia

Question 27

nitrates: indications

Answer 27

* Management of acute and chronic angina * Anal fissure * CHF/MI * Peri/intraoperative BP management

Question 28

nitrates: MOA: vasodilation

Answer 28

Peripheral arteries & veins * Causes less blood return to the heart decreasing filling volume (preload) * Decreases the workload of the heart Coronary arteries * Causes increased blood flow and oxygen supply to the myocardium * Increases oxygenation of the heart muscle

Question 29

common side effects nitrates

Answer 29

* Headaches -pts with migraine hx at higher risk * Flushing * Dizziness * Hypotension * Syncope * Reflex tachycardia

Question 30

nitrates: interactions

Answer 30

* Caution with anti-hypertensives or any med that may cause hypotension * Contraindicated with PDE-5 Inhibitors * Anticholinergic agents may decrease absorption of SL and buccal formulations (dry mouth)

Question 31

nitrates: admin (all formulations)

Answer 31

* Start low and go slow” * Avoid abrupt discontinuation (rebound angina) * Avoid EtOH use * Avoid abrupt position changes

Question 32

nitrates: sublingual/buccal (rapid acting)

Answer 32

* Patient should be seated when using * Dry mouth may affect absorption – use spray

Question 33

nitrates: oral

Answer 33

* Take at prescribed intervals * Store in tightly closed amber glass containers * Replace q6months if bottle open

Question 34

nitrates: transdermal

Answer 34

* Rotate application sites * Still require nitrate free interval * Exercise may increase speed of absorption * Gloves!!!

Question 35

rapid acting nitrates

Answer 35

* Use: acute angina, acute angina prophylaxis * Sublingual/Buccal (avoids the first pass effect) -Tablet (0.3mg, 0.4mg, 0.6mg) -Spray (0.4mg) * Repeat q 5 minutes for up to 3 administrations – then call 911 * Refill yearly to ensure potency

Question 36

long acting nitrates

Answer 36

* Use: chronic prophylaxis of angina * Oral – significant hepatic first pass metabolism -Isosorbide dinitrate -Isosorbide mononitrate * Transdermal -2% Ointment -Patch

Question 37

tolerance nitrates

Answer 37

* Loss of ability of the smooth muscle to vasodilate in response to nitrates * Occurs with continuous exposure * Must have a 10–12-hour nitrate free interval per day

Question 38

cardiac glycoside: digoxin MOA

Answer 38

Inhibits Na/K ATPase resulting in increased cardiac contractility and decreased AVE conduction/heart rate

Question 39

cardiac glycoside: digoxin indications

Answer 39

* Afib * Treatment resistant heart failure * SVT

Question 40

cardiac glycoside: digoxin

Answer 40

o Narrow Therapeutic Index o Many drug/drug interactions

Question 41

cardiac glycoside: digoxin digoxin toxicity

Answer 41

* Can lead to lethal arrhythmias, hyperkalemia * S/S: N/V, diarrhea, blurry vision with yellow tint/halos, disorientation, weakness

Question 42

digoxin toxicity tx

Answer 42

digibind