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Pharmacology > Lipid Lowering Therapies > Flashcards

Lipid Lowering Therapies Flashcards

1
Q

What level of LDL is considered indication for lipid-lowering therapies?

A

160mg/dL

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2
Q

What non-pharmacological treatments can be used in hypercholesterolaemia?
How effective are these?

A

Diet
Exercise
Weight Reduction
Modest reduction in LDL and increase in HDL

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3
Q

What is the first line treatment for hyperlipidaemia?

A

HMG CoA reductase inhibitors

aka statins

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4
Q

What is the mechanism of action of statins?

A

Statins are analogues of HMG. They have a strong affinity for the enzyme and bind effectively to inhibit HMG CoA reductase. This reduces intracellular supplies and upregulates expression of LDL receptors. This reduces serum cholesterol.

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5
Q

Give some examples of statins:

A

Lovastatin, simvastatin, pravastatin, atorvastatin, fluvastatin, pitavastatin, rosuvastin.

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6
Q

Rank the statins in order of potency. 1 being most potent.

A
  1. Pitavastatin
  2. Rosuvastatin
  3. Atorvastatin
  4. Simvastatin
  5. Pravastatin
  6. Lovastatin
  7. Fluvastatin.
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7
Q

What are the indications for statin therapy?

A

All types of hyperlipidaemia except familial hypercholesteraemia as lack of LDL receptor means that mechanism is not effective at reducing serum cholesterol.

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8
Q

Describe the PK’s of statins:

A

Prava- and Fluvastatin are almost completely absorbed after oral administration and are active as such. Lovastatin and atorvastatin are 30-50% absorbed and are hydrolysed to active form. Excretion is primarily by bile and faeces however some renal excretion can occur. Simvastatin half life 5 hours, others much longer.

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9
Q

What are the ADR’s of statins?

A

Liver problems - monitoring required.

Myopathy/Rhabdomyolysis - RARE - more common in HRH

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10
Q

DDI’s/Contraindications of statins?

A

May increase warfarin levels - monitor INR frequently

Not to be used in pregnant and nursing mothers, children or teenagers.

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11
Q

What is second line treatment for hypercholesteraemia?

A

Ezetimibe

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12
Q

What is the mechanism of action of Ezetimibe?

A

Selectively inhibits absorption of dietary and biliary cholesterol in the small intestine. This reduction in intracellular hepatic stores prompts clearance of cholesterol from the serum.

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13
Q

What are the PKs of Ezetimibe?

A

Metabolised in the liver and small intestine and excreted by bile and renal excretion. Half life 22 hours.

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14
Q

How effective are statins?

A

Very effective at reducing LDL
Modestly effective at increasing HDL
Slightly effective at decreasing triglyceride

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15
Q

How effective is niacin?

A

Slightly effective at reducing LDL
Very effective at increasing HDL
Effective at reducing triglycerides

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16
Q

How effective are fibrates?

A

Slightly effective at reducing LDL.

Effective at increasing HSL. Very effective at decreasing triglycerides.

17
Q

Describe the mechanism of action of Niacin:

A

Inhibits lipolysis in adipose tissues. Reduction in VLDL and LDL levels and triglycerides.

18
Q

Indications for niacin?

A

Familial hyperlipidaemias
Severe hypercholesteraemia
Best agent at increasing HDL.

19
Q

What are the PK’s of niacin?

A

Administered orally, converted to nicotinamide in the body. Niacin and its metabolites are excreted in the urine.

20
Q

ADR’s of Niacin?

A 
Intense Cutaneous flush and pruritus (can be avoided when administered with aspirin or given as sustained release)
Nausea and abdo. pain
Hyperuricaemia and gout.
Impaired glucose tolerance
Hepatotoxicity.
21
Q

Gives some examples of Fibrates:

A

Fenofibrate - more effective

Gemfibrozil

22
Q

What is the mechanism of action of fibrates?

A

PPARS (Perioxisome Proliferator activated receptors) are activated by fibrates. This leads to a decreased production of apoproteins and increased expression of lipoprotein lipase. Reduced triacylglyceride concentration.
increases expression of apoplipoproteins for HDL

23
Q

What are the PKs of fibrates?

A

Completely absorbed after oral dose. Distributed widely bound to albumin. Extensive biotransformation. Excreted in urine.

24
Q

ADR’s of fibrates?

A

GI effects - mild which lessen as therapy continues.
Lithiasis - increase biliary cholesterol excretion so increased predisposition to gallstone formation.
Myositis - Patients with renal insufficiency may be at risk.

25
Q

DDIs and contraindications of fibrates?

A

Competition for binding sites on binding proteins with coumarin anticoagulants - monitor INR - May elevate levels of sulfonylureas.
- Not known in pregnancy and lactating women.
Not to be used in those with severe hepatic and renal dysfunction or those with pre-existing gallbladder disease.

26
Q

Give some examples of Bile-acid binding resins:

A

Cholestryamine
Colestipol
Colesevalam

27
Q

Describe the mechanism of action of bile-acid binding resins.

A

They are anion exchange resins that bind negatively to bile acids and bile salts in the small intestines. This resin/bile acid complex is excreted in the faeces thus preventing them from returning via the enterohepatic circulation to the liver. This causes the liver to increase synthesis of bile acids from cholesterol reducing intracellular cholesterol. This causes up regulation of LDL receptors and reduction in serum cholesterol.

28
Q

What are the therapeutic uses of bile-acid binding resins?

A

Type IIA
Type IIB hyperlipaemias
Cholestryamine can also relieve pruritus caused by bile acid accumulation in patients with biliary obstruction.

29
Q

What are the PK’s of Bile acid-binding resins?

A

Taken orally - insoluble so they are neither absorbed or metabolically altered by the intestine. Totally excreted in faeces.

30
Q

What are the ADR’s of Bile acid-binding resins

A

GI effects - constipation, nausea and flatulence
Impaired absorption - at high doses impairs with absorption of fat soluble vitamins
Drug interactions - interfere with the intestinal absorption of many drugs - therefore they should be taken 1-2hrs before or 4-6hrs after.

Pharmacology (8 decks)

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