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Pharmacology > Hyperlipidemia > Flashcards

Hyperlipidemia Flashcards

1
Q

Hyperlipidemia classes of medication?

A
  1. Cardiac glycosides
  2. Hyperlipidemia treatment
  3. Bile acid sequesterants
  4. Cholestrol absorption inhibtor
  5. PC5K-9 Inhibitor
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2
Q

Cardiac glycosides drug and two effects?

A

Digoxin

Positive ionotrope
Negative chronotrope

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3
Q

Positive ionotrope of digoxin?

A
  1. The heart has two channels, Na+/K+ pump and the Na+/Ca2+ pump
  2. Digoxin will block the Na+/K+ pump and not the Na+/Ca2+ pump
  3. With accumulated Na+ in the cell, the Na+/Ca2+ pump will be overactive and increase Ca2+ and influx and Na+ efflux
  4. Increased Calcium increases cardiac contractility and cardiac output. This increases the oxygen demand by the heart.
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4
Q

Digoxin negative chronotrope effect?

A
  1. Digoxin will increase vagal nerve activity on the SA and AV node
  2. This will block the conduction through the AV node and decrease SA node firing
  3. Thisrecp will increase the sensitivity of SA and AV node to ACh
  4. This will utimately activate the M2 muscuranic recepetor in the heart and this will decrease heart rate
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5
Q

Digoxin two ultimate effects on the heart

A

The ultimate positive ionotropic effect is increased contractility and and cardiac output

The ultimate negative chronotrope effect is bradycardia

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6
Q

Hypokalemia effects on Digoxin efficacy?

A

Digoxin binds on the same site as potassium on the Na+/K+pump.

Thus, decreased Potassium means no competition for binding and this potentiates the effects of digoxin and can cause toxicity and thus can cause hyperkalemia

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7
Q

Types of hyperlipidemia treatment?

A
  1. HMG-CoA Reductase inhibitor
  2. Fibrates
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8
Q

Statins MOA?

A

In the liver,

-HMG-CoA is converted to mevalonic acid by HMG-CoA reductase
-Mevalonic acid is then converted into cholesterol
-Statins inhibit HMG-CoA reductase and thus a decrease in the production of mevalonic acid and cholesterol

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9
Q

Most effective drug in the lowering of LDL?

A

HMG-CoA reductase inhibitors/Statins

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10
Q

HMG-CoA Reductase inhibitors drugs?

A

SAR Statin(Sars Satan)

Simvastatin
Atorvastatin
Rouvastatin

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11
Q

HMG-CoA Reductase inhibitors effect on LDL receptors?

A

When body detects decrease cholesterol in the blood, the liver increases synthesis of liver LDL receptors.

As a result, LDL in the blood will bind to LDL receptors on the liver and be internalised

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12
Q

HMG-CoA Reductase inhibitors effects on:

LDL
Cholesterol
HDL
Triglycerides

A

Decreased LDL
Decreased Cholesterol
HDL remains the same
Decreased Triglycerides

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13
Q

Good and bad cholesterol?

A

Good cholesterol-HDL
Bad cholesterol-LDL

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14
Q

Fibrates drugs?

A

Bezafibrates
Gemfibrozil

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15
Q

Fibrates MOA?

A

Increased PPAR-gamma, agonist, thus increased HDL

Increased LPL

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16
Q

Fibrates effect :

LDL
Cholesterol
HDL
Triglycerides
Apo-AI & Apo-AII
FFA & Lipids

A

Increased LDL
Decreased Cholesterol
Increased HDL
Decreased Triglycerides
Increased Apo-AI & Apo-AII
Deposition FFA & Lipids

17
Q

Which drug is effective in increasing HDL?

A

Fibrates

18
Q

Fibrates & Statins S/E?

A

Rhabdomyolysis
Myalgia
Increased Liver enzymes(can damage liver)

19
Q

Why are statins and fibrates CI from each other?

A

They exacerbate S/E

20
Q

Bile acid sequestrants drugs?

A

Cholestyramine

21
Q

Bile acid synthesis?

A

Digestion and absorption of lipids in the GIT

22
Q

Cholestyramine MOA?

A

Cholestyramine binds negatively charged bile acids and salts in the small intestines
-Thus preventing their absorption of lipids
-Cholestyramine-bile acids complex eliminated from the body

23
Q

Systematic effects of cholestyramine and why?

A

Little few systematic effects because the cholestyramine-bile acid complex is eliminated from tehir body

24
Q

Cholestyramine effect on LDL receptors?

A

-The liver upregulates the expression of the LDL-receptors in its surface in response to decreased lipid content
-This will increase LDL binding of the liver

25
Q

Cholestyramine effect :

LDL
Cholesterol
HDL
Triglycerides

A

Decreased LDL
Decreased Cholesterol
No effects on HDL
No effects Triglycerides

26
Q

Cholestyramine tolerance?

A

-Poorly tolerated because it takes like sea weed

27
Q

Cholestyramine S/E?

A

-Decreased Vitamin ADEK absorption(fat-soluble vitamins)
-GIT: Constipation, ingestion, bloating

28
Q

Cholestyramine DI?

A

Form indoluble complexes with other drugs

29
Q

Which drug causes flushing?

A

Nicotinic acid

30
Q

Cholesterol absorption inhibitor drug?

A

Ezetemide

31
Q

Cholesterol absorption inhibitor MOA?

A

-Blocks cholesterol absorption in the small intestines
-Therefore, less cholesterol in the liver

32
Q

Cholesterol absorption inhibitor effects on LDL receptor?

A

-Increases expression of LDL receptor on the liver(to increase cholesterol synthesis in the liver)
-LDL binds to LDL-receptors in the liver

33
Q

Cholesterol absorption inhibitor

LDL
Cholesterol
HDL
Triglycerides

A

Decreased blood LDL
Decreased Cholesterol
Remains unchanged HDL
Decreased Triglycerides

34
Q

Cholesterol absorption inhibitor tolerance?

A

Well tolerated

35
Q

PC5K–9 inhibitor drug?

A

Evolocummab

36
Q

PC5K–9 inhibitor effects:
-LDL
-Cholesterol
-HDL
-Potency

A

-LDL-Decreased
-Cholesterol-Decreased
-HDL-Remain unchanged
-Potency-Increased

37
Q

PC5K–9 inhibitor MOA?

A

Monoclonal antibody

PC5K–9 binds to LDL-receptor on the liver syrface

LDL-receptor degradation and increased LDL in the blood

Therefore PC5K-9 Inhibition

Inhibition of liver LDL-receptor degradation

Circulating LDL binds to the LDL-receptor

Decreased LDL in the blood

38
Q

PC5K–9 S/E?

A

-Influenza
-Nasopharyngitis
-Upper resp tract infections
-Back pain
-Injection-site reactions

Pharmacology (44 decks)

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