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pharm exam 2 > hyperlipidemia > Flashcards

hyperlipidemia Flashcards

1
Q

hyperlipidemia

A

serum cholesterol > 200

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2
Q

hyperlipidemia: causes

A

genetic, dietary, lifestyle

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3
Q

hyperlipidemia: tx goals changed- ACC/AHA guidelines

A
  • risk based
  • updated in 2018
  • statins remain the mainstay of therapy
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4
Q

high intestiny (>/50)

A
  • atorvastatin
  • rosuvastatin
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5
Q

moderate intensity (30-40%)

A
  • atorvastatin
  • rosuvastatin
  • simvasatin
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6
Q

low intensity (<30%)

A
  • simvastatin
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7
Q

statins/ HMG-CoA reductase inhibitors: MOA

A

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

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8
Q

statins/ HMG-CoA reductase inhibitors: indications

A

o Hyperlipidemia
o ASCVD

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9
Q

statins/ HMG-CoA reductase inhibitors: common side effects

A

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

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10
Q

when are statins administered?

A

at night

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11
Q

Statins/HMG-CoA reductase inhibitor: common interactions

A

o Gemfibrozil or niacin + statin = increased risk of rhabdo

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12
Q

Ezetimibe (Zetia): MOA

A

works by inhibiting the intestinal absorption of cholesterol

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13
Q

Ezetimibe (Zetia): contraindicated

A

with statins in pts with liver disease

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14
Q

Ezetimibe (Zetia)

A
  • can be used as monotherapy
  • well tolerated
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15
Q

ENHANCE study (2008)

A

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

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16
Q

Bile Acid Sequestrants: drug examples

A

o Cholestyramine, colestipol, colesevelam

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17
Q

Bile Acid Sequestrants: MOA

A
  • Sequester bile acids
  • Liver increases production of bile acids using cholesterol
  • Bile acids are excreted in the gut
18
Q

Bile Acid Sequestrants: side effects

A

GI SE common–diarrhea, GI upset, gassiness

19
Q

Bile acid sequestrants

A

unsure effect of CV morbidity/mortality

20
Q

PCSK9 inhibitors: MOA

A
  • 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
21
Q

PCSK9 inhibitors: side effects

A

not too many SEs–> only nasal pharyngitis

22
Q

PCSK9 inhibitors:

A

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

23
Q

Fibrates: MOA

A

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

24
Q

Fibrates: common agents

A

Fenofibrate, gemfibrozil

25
Q

Fibrates: contraindications

A
  • Gemfibrozil should be avoided with statins
  • Increased serum statin levels = increased risk for rhabdo
26
Q

fibrates: primary role is

A

hypertriglyceridemia

27
Q

nitrates: indications

A
  • Management of acute and chronic angina
  • Anal fissure
  • CHF/MI
  • Peri/intraoperative BP management
28
Q

nitrates: MOA: vasodilation

A

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

29
Q

common side effects nitrates

A
  • Headaches -pts with migraine hx at higher risk
  • Flushing
  • Dizziness
  • Hypotension
  • Syncope
  • Reflex tachycardia
30
Q

nitrates: interactions

A
  • 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)
31
Q

nitrates: admin (all formulations)

A
  • Start low and go slow”
  • Avoid abrupt discontinuation (rebound angina)
  • Avoid EtOH use
  • Avoid abrupt position changes
32
Q

nitrates: sublingual/buccal (rapid acting)

A
  • Patient should be seated when using
  • Dry mouth may affect absorption – use spray
33
Q

nitrates: oral

A
  • Take at prescribed intervals
  • Store in tightly closed amber glass containers
  • Replace q6months if bottle open
34
Q

nitrates: transdermal

A
  • Rotate application sites
  • Still require nitrate free interval
  • Exercise may increase speed of absorption
  • Gloves!!!
35
Q

rapid acting nitrates

A
  • 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
36
Q

long acting nitrates

A
  • Use: chronic prophylaxis of angina
  • Oral – significant hepatic first pass metabolism
    -Isosorbide dinitrate
    -Isosorbide mononitrate
  • Transdermal
    -2% Ointment
    -Patch
37
Q

tolerance nitrates

A
  • 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
38
Q

cardiac glycoside: digoxin
MOA

A

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

39
Q

cardiac glycoside: digoxin
indications

A
  • Afib
  • Treatment resistant heart failure
  • SVT
40
Q

cardiac glycoside: digoxin

A

o Narrow Therapeutic Index
o Many drug/drug interactions

41
Q

cardiac glycoside: digoxin
digoxin toxicity

A
  • Can lead to lethal arrhythmias, hyperkalemia
  • S/S: N/V, diarrhea, blurry vision with yellow tint/halos, disorientation, weakness
42
Q

digoxin toxicity tx

A

digibind

pharm exam 2 (3 decks)

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