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Human Pharmacy > Dyslipidaemia > Flashcards

Dyslipidaemia Flashcards

1
Q

What drugs can cause lipidaemia?

A

Beta blockers –> dec HDL-C, inc TG
Diuretic = inc TC

Oral contraceptives = atherogenic effect at high dose

Lipid neutral cardiac drugs = ACEi, ARBs, CCB, nitrates, hydralazine, methyldopa, clonidine

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2
Q

List drugs that manage hypercholesterolaemia

A

Bild acid binding resins

Ezetimibe

Fibric acid derivatives

Nicotinic acid

Statins

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3
Q

List the relevant bile acid binding resins

A

cholestyramine, colestipol

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4
Q

Discuss the efficacy of bile acid binding resins

A

Moderately effective, very safe, commonly used in younger populations

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5
Q

What is the MOA for bile acid binding resins?

A

Large MW polymers containing chloride ions (exchanged for bile acids in gut) bind to bile acid –> binds to bile-acid resin complex –> complex is excreted –> prevent enterohepatic cycling of bile

Forces liver to synthesise more bile from cholesterol –> LDL taken from blood + inc LDL-R on liver

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6
Q

What drug interactions are associated with bile acid binding resins?

A

digoxin, thiazides, frusemide, thyroxin

take other meds 1 hr before or 4-6 hrs after

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7
Q

What is ezetemibe?

A

cholesterol absorption inhibitor –> block absorption from gut

It is an adjunct therapy to diet and statins, can be used alone

Combined = more effective that simvastatin or ezetimibe alone

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8
Q

What is the MOA of ezetemibe?

A

absorbed from intestines and localised in brush border of small intestines –> inhibit absorption of biliary and dietary cholesterol —> dec delivery of chol –> inc LDL-R

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9
Q

List the ADRs of ezetemibe

A

Well tolerated

headache, myalgia

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10
Q

What is the MOA of fibric acid derivates?

A

Inc PPARalpha-mediated lipoprotein lipase expression

Also dec expression of apolipoprotein C-III (inhibits LPL)

Inc LDL-R expression

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11
Q

What are some ADRs of fibric acid derivates?

A

GI disturbances, pancreatitis, photosensitivity, blood cell deficiencies, rhabdomyolysis, other myopathies

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12
Q

Which drugs interact with fibric acid derivates?

A

HMG-CoA reductase inhibitors

Cholestryamine

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13
Q

Discuss niacin (Vit B3) role in hyperlipidaemia treatment and MOA

A

MOA = inhibits TG production (secondary) and VLDL secretion (primary = due to inhibition of lipolysis in adipose tissue –> reduces supple of free fatty acids)

It dec the LDL occupying HDL —> inc blood HDL

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14
Q

What are the ADRs of Niacin?

A

Vasodilation + flushing + pruritis of skin

Elevated liver enzymes, hepatitis

Nacine induced insulin resistance –> sever hyperglycaemia

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15
Q

What drug interact with Naicin?

A

statins –> myopathy

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16
Q

List the relevant HMG-COA reductase inibitors

A

atorvastatin, fluvastatin, lovastatin, pravastatin, rosuvastatin, simvastatin

17
Q

Briefly discuss some facts about statins

A

highly effective, good safety record with once daily dosing = good patient compliance

Most taken at bedtime –> inhibit nocturnal cholesterol biosynthesis

Low oral bioavailability due to first pass metabolism

18
Q

Which statins can be taken at any time of the day?

A

Atorvastatin, rosuvastatin = longer half lives

19
Q

Which statins are pro drugs?

A

lovastatin, simvastatin

activated in the liver

20
Q

What is the MOA of statins?

A

Competitive inhibitors of HMG-CoA reductase –> inhibits the conversion of HMG-CoA to mevalonic acid –> inhibiting cholesterol biosynthesis

21
Q

What affect do statins have on cholesterol?

A

Inc LDL-R –> dec serum LDL –> less LDL available to form vLDL

10% inc HDL, 20-40% dec in LDL

Serum TG = decreased

22
Q

List some ADRs of statins

A

myalgia, GIT disturbances, elevated hepatic enzymes, mild GI distress

hepatotoxicity, pancreatitis, diabetes, alopecia, CNS

Most serious = rhabdomyolysis

23
Q

Discuss statin-induced rhabdomyolysis

A

Inihbit chol synthesis –> statins alter muscle cell mem comp

Early stage statin myopathy = myalgia w/ elevated CK (reversible 2-3 wks w/ no statins)

Later stage = myositis (muscle inflam) –> muscle pain, leakage of muscle CK into plasma, elevated CK

Late stage = myositis becomes rhabdomyolysis –> muscle cells destroyed –> myoglobin accumulate in kidney –> acute renal failure (dark urine)

24
Q

Which drugs interact with HMG-CoA reductase inhibitors?

A

Fibric acid derivates = cause myopathies

Other drugs metabolised by CYP3A4 and CYP2C9

Erythromycin and itraconazole

Warfarin

25
Q

What statins are metabolised by CYP3A4?

A

Atorvastatin, simvastatin

26
Q

What statins are metabolised by CYP2C9?

A

Rosuvastatin, fluvastatin

Human Pharmacy (11 decks)

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