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Pharma > Agents Used In Dyslipidaemias > Flashcards

Agents Used In Dyslipidaemias Flashcards

1
Q

What are some risk factors of CHD?

A

Smoking
HTN
Obesity
DM

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2
Q

What are primary dyslipidemias?

A

Hereditary diseases affecting the lipoprotein metabolism

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3
Q

What are the secondary dyslipidemias?

A 
DM
Nephrotic syndrome
Kidney failure
Hypothyroidism
Anorexia nervous a
Alcoholism
Liver disease
Medication
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4
Q

What are the drug tarts of lipoprotein metabolism in the order of atherogenicity?

A

LDL
VLDL
Chylomicrons
HDL

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5
Q

What is another word for HMG-CoA reductase inhibitors?

A

Statins

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6
Q

Name the HMG-CoA reductase inhibitors

A 
Lovastatin
Simvastatin 
Pravastatin
Atorvastatin 
Fluvastatin 
Rosuvastatin
Mevastatin
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7
Q

What is the mechanism of action of statins?

A

They competitively inhibit HMG-CoA reductase

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8
Q

What is the result of using HMG-CoA reductase inhibitors?

A 
Depletion of intracellular cholesterol supply from the liver
Increased LDL receptor expression
Decreased plasma LDL
Slight decreased VLDL
Slight increased HDL
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9
Q

What are some other benefits of using statins?

A 
Stabilisation of atherosclerotic plaques
Decreased vascular inflammation 
Improvement of endothelial function
Increased fibrinolysis 
Anti thrombotic effect
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10
Q

What are the clinical indications of statins?

A

Secondary prevention of MI or stroke
Primary prevention of arterial disorders (HTN, PVD)
Familial hypercholesterolemia (Type IIa)
Severe dyslipidemias

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11
Q

Which statin is used to treat familial hypercholesterolemia (Type IIa)?

A

Atorvastatin

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12
Q

How are statins administered?

A

Orally

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13
Q

Which enzyme metabolises statins?

A

CYP3A4

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14
Q

Which enzyme metabolises fluvastatin?

A

CYP2C9

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15
Q

Which enzyme metabolises rosuvastatin?

A

CYP2C9

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16
Q

Which statins are metabolised by CYP2C9?

A

Fluvastatin

Rosuvastatin

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17
Q

Which statin is independent of CYP?

A

Pravastatin

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18
Q

When is Pravastatin recommended?

Why?

A

In the case of drug interactions

Because it is independent of CYP

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19
Q

What is the half life of statins?

A

Short half life except for atorvastatin and rosuvastatin

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20
Q

Which statins have a half life of 14-18h?

A

Atorvastatin

Rosuvastatin

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21
Q

What are the drug interactions of statins?

A

Drugs which are CYP inhibitors also inhibit the metabolism of statins

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22
Q

What is a side effect of Gemfibroxil?

A

It increases rhabdomyolysis

It will decrease the clearance of statins

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23
Q

What are the adverse effects of statins?

A 
Increased plasma liver enzymes 
Increased creatine kinase 
GI symptoms
Skin rashes
Neurological effects (dizziness and insomnia)
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24
Q

When are statins contraindicated?

A

Pregnancy

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25
Q

What is the result/cause of increased CK?

A

Myalgia
Myosotis
Myopathy
Rhabdomyolysis

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26
Q

When using statins, when is there a high risk for rhabdomyolysis?

A 
In elderly 
In kidney and or hepatic problems
In hypothyroidism 
In trauma or severe physical activity 
In drug interactions (fibrates, macrolides)
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27
Q

What sort of drugs are bile acid binding resins?

A

Polymers

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28
Q

Name the bile acid binding resins

A

Cholestyramine
Coolest iPod
Colesevelam

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29
Q

What are the adverse effects of Bile acid binding resins?

A

GI symptoms
Steatorrhea
Decreased appetite
Decreased absorption of lipophilic vitamins (ADEK)

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30
Q

How are bile acid binding resins administered?

A

Orally

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31
Q

How are bile acid binding resins absorbed?

A

They are not absorbed or altered in the intestines

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32
Q

What are bile acid binding resins combined with?

Why?

A

Statins

To avoid the liver producing more cholesterol

33
Q

What is the clinical indication of bile acid binding resins?

A

Type IIA and IIB dyslipidemias

34
Q

What is the clinical indication for Cholestyramine?

A

Decreases pruritus from patients with accumulation of bile salts

35
Q

what is the clinical indication of Colesevelam?

A

DM2 due to its glucose lowering effects

36
Q

What is the mechanism of action of bile acid binding resins?

A

They bind bile acids and bile salts in the small intestine - this complex is then excreted in the feces, decreasing the bile acid concentration

Hepatocytes produce more bile acids from cholesterol decreasing IC cholesterol concentration and increasing the hepatic uptake of cholesterol-containing LDL

LDL decreases
VLDL and TG moderate increase

37
Q

What is the mechanism of action of Colesevelam?

A

Inhibits the absorption of the bile acids

38
Q

Name the cholesterol absorption inhibitor?

A

Ezetimibe

39
Q

What is the mechanism of action of Ezetimibe?

A

Inhibits the absorption of cholesterol and phystosterols

40
Q

What is the clinical indication of Ezetimibe?

A

Adjunct to statins (synergy)
Decreases LDL
Hypercholesterolemia and phytosterolemia

41
Q

How is Ezetimibe admistered?

A

Orally

42
Q

Is Ezetimibe absorbed or not absorbed?

A

Absorbed

43
Q

How is Ezetimibe metabolised?

A

It is metabolised in the liver and small intestines via glucuronidation (not by CYP enzymes)

44
Q

What are the side effects of Ezetimibe?

A

GI distress

Hepatotoxicity if given with Statins

45
Q

Name the fibrates

A

Gemfibrozil
Fenofibrate
Bezafibrate
Ciprofibrate

46
Q

What is the clinical indication of fibrates?

A

Hypertriglyceridemia

47
Q

How are fibrates administered?

A

Orally

48
Q

Are fibrates absorbed or not?

A

Completely absorbed

49
Q

When do you take fibrates?

Why?

A

Only taken during a meal for its absorption

50
Q

What are fibrates drug interactions?

A

Statins

Anticoagulants (competition with coumarin for plasma proteins)

51
Q

When are fibrates counterindicated?

A

Pregnancy

Alcoholism

52
Q

What are the adverse effects of fibrates?

A 
GI symptoms 
Cutaneous symptoms 
Increased liver enzymes 
Myositis
Rhabdomyolysis
CNS symptoms such as insomnia and dizziness
53
Q

What does PPAR-alpha stand for?

A

Peroxisome proliferator activated receptors alpha

54
Q

What are PPAR alphas?

A

They control gene expression and regulate the lipid metabolism

55
Q

What are the ligand for PPAR alpha ?

A

FA
Eicosanoids
(Fibrates)

56
Q

What is the mechanism of action of fibrates?

A

They bind to and activate PPAR alpha receptors

57
Q

What is the result of Fibrate binding to PPAR alpha?

A
  • Increased LPL activity - VLDL secretion is inhibited - decreased VLDL
  • Increased LDL receptor leading to slight decrease in LDL
  • Slight increase in HDL
  • Decreased lipolysis in fat tissue leading to decreased TG
58
Q

What are some other effects of fibrates?

A

Decreased fibrinogen
Decreased insulin resistance
Decreased inflammation in the endothelium

59
Q

How is Niacin administered?

A

Orally

60
Q

What are the contraindications of Niacin?

A 
Ulcer
Diabetes
Metabolic syndrome 
Gout 
Pregnancy 
Childhood
61
Q

What are the adverse effects of Niacin?

A 
Flushing, itching, rash
GI disturbances
Hepatotoxicity 
Increased insulin resistance
Decreased Uric acid elimination
62
Q

How do we prevent the Niacin induced cutaneous flushing, rash etc..?

A

NSAIDs

63
Q

The use of NSAIDs for prophylactic treatment for the Niacin induced rash suggests what?

A

That the rash and flushing are PGD2 mediated

64
Q

What is the clinical indication of Niacin?

A

Hypercholesterolemia
Hypertriglyceridemia
Low HDL

65
Q

What are the effects of combining Niacin with Laropiprant?

A

This combination inhibits the PGD2 receptors and thus decreases unwanted side effects

66
Q

What is the mechanism of action of Niacin on adipocytes?

A

Niacin inhibits TG synthesis through inhibition of FA formation, decreasing TG

Decreased fat release
Decreased VLDL release from the liver
Decreased LDL

67
Q

What is the effect of Niacin on macrophages?

A

Stimulation of COX-2 leading to an increase in PGE2 and PGD2. This increase leads to unwanted effects such as cutaneous vasodilation, burning sensation of face and upper body.

68
Q

What is the effect of Niacin on LPL?

A
  • Niacin activates LPL resulting in increased liver degradation of intracellular Apo-B. Decreased VLDL and LDL
  • Inhibits Apo-AI degradation leading to increased HDL half life
69
Q

Name the CETP inhibitors

A

Darcetrapib

Torcetrapib

70
Q

What is the mechanism of action of Darcetrapib and Torcetrapib?

A

CETP inhibitors

71
Q

What is the effect of CETP inhibitors?

A

They inhibit the cholesterol ester transfer protein leading to decreased cholesterol transport from HDL to LDL

72
Q

Name the MTP inhibitors

A

Lomitapide

73
Q

What is the mechanism of action of Lomitapide?

A

Lomitapide inhibits MTP leading to decreased Apo-B level. As a result, VLDL, IDL and LDL decrease

74
Q

What does MTP stand for?

A

Microsomal triglyceride transfer protein

75
Q

What is the action of Mipomersen?

A

Inhibitor of Apo-B translation

76
Q

Name the PCSK9 inhibitors

A

Alirocumab

Evolocumab

77
Q

What is the mechanism of action of Alirocumab and Evolocumab?

A

They are PCSK9 inhibitors

78
Q

What is the mechanism of action of Omega-3 fatty acids?

A

They work partly via the PPAR system
Increase LPL activity in the endothelium and decrease lipogenesis in the liver
Inhibition of fat synthesis
Promote beta oxidation of fatty acids

Pharma (23 decks)

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