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OD2 (S1&2) > PHARM - Lipid Lowering Drugs - Week 4 > Flashcards

PHARM - Lipid Lowering Drugs - Week 4 Flashcards

1
Q

Define dyslipidaemia.

A

Abnormal lipid profile

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2
Q

What can dyslipidaemia lead to (3)?

A

Atherosclerosis and stroke.
Increases the risk of myocardial infarction.

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3
Q

Name three forms forms of dyslipidaemia.

A

Hypercholesterolaemia
Hypertriglyceridaemia
Mixed Hyperlipidaemia

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4
Q

What level of cholesterol confers a high risk of hypercholesterolaemia, and what is the target range (mmol/L)?

A

> 7.5mmol/L is high risk
Treatment target is <4mmol/L

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5
Q

Are normal total cholesterol levels healthy?

A

Not necessarily

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6
Q

What are the target levels for total cholesterol, triglycerides, HDLs, and LDLs (fasting obviously)?

A

Total - <4.0mmol/L
Triglycerides - <2.0mmol/L
HDL - >1.0mmol/L
LDL - <2.5mmol/L

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7
Q

What are 5 modifiable risk factors for dyslipidaemia?

A

Stop smoking
Avoid alcohol
Weight reduction
Increase exercise
Modify diet

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8
Q

Name three secondary causes of dyslipidaemia.

A

Obesity
Diabetes
Hypothyroidism

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9
Q

What two dietary compound intakes are reduced in a diet modified for treating hypercholesterolaemia?

A

Saturated and trans fatty acids

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10
Q

Does the mediterranean diet reduce risk of hypercholesterolaemia by reducing LDLs?

A

No, it doesnt reduce LDLs, but still lowers risk.

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11
Q

What dietary compounds can be used to reduce LDL cholesterol?

A

Plant sterol esters

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12
Q

What is the effect of fish oils in terms cholesterol levels (2)?

A

Reduces triglycerides
Increases HDLs

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13
Q

Which is the good cholesterol, LDL or HDL?

A

HDL

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14
Q

Consider patients with a low risk vs >moderate risk of hypercholesterolaemia. What kind of intervention is ideal for these two populations?

A

Low risk - lifestyle/diet intervention
>Moderate risk - pharmacological intervention

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15
Q

Name two sources of cholesterol, and where in the body it is absorbed.

A

Animal fat and eggs, absorbed in the intestines

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16
Q

What is the RDA for cholesterols? Why is this so?

A

None set, de novo synthesis, primarily in the liver, is adequate.

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17
Q

Which organ is cholesterols stored for export, and in what form?

A

Stored in the liver for export in VLDLs

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18
Q

What is cholesterol converted to?

A

Bile salts

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19
Q

Where are bile salts stored?

A

Gall bladder

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20
Q

What three synthesis processes are cholesterols used for?

A

Steroid hormone production
Vitamin D synthesis
Membrane synthesis

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21
Q

Name 5 forms of lipoproteins that transport cholesterol in the blood.

A

Chylomicrons
VLDLs
LDLs
IDLs
HDLs

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22
Q

Name three kinds of bad cholesterols, and why they are so (and what they contain that makes this so).

A

VLDLs
LDLs
IDLs
They contain alipoprotein B-100, which can transport lipids into the artery walls

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23
Q

What is the good cholesterol, and why is this so?

A

HDLs
They can retreive cholesterol from artery walls

24
Q

What is the rate-limiting step for cholesterol synthesis?

A

Conversion of HMG-CoA to mevalonic acid by HMG-CoA reductase enzyme

25
Q

What are statins, and what form of dyslipidaemia do they treat, and how (5)?

A

They are structural analogues of HMG-CoA
They decrease mevalonic acid, therefore cholesterol
-There is a compensatory increase in LDL receptors
-Increased clearance of LDL (with bound cholesterol) from the blood
-Decreased plasma total cholesterol and LDL
-Increased plasma HDL

26
Q

What are level of cholesterol and triglycerides are indications for hypercholesterolaemia and mixed hyperlipidaemia?

A

Hypercholesterolaemia - high LDL
Mixed hyperlipidaemia - high LDL and triglycerides

27
Q

How long after beginning statin treatment is there greater benefit?

A

After 1-2 years of se, there is greater benefit.

28
Q

Why do statins have poor compliance?

A

Related to perceived lack of efficacy rather than side effects

29
Q

What kind of fruit juice increases the toxicity of statins, and what must be done?

A

Grapefruit juice, which must be avoided

30
Q

Which pathway is responsible for drug-drug interactions involving statins?

A

Cytochrome pathways

31
Q

What three things can increase statin levels?

A

Some antibiotics, antifungals, and fibrates

32
Q

What three things can decrease statin levels?

A

Phenytoin, barbiturates, and verapamil

33
Q

Taking statins causes a mild serum elevation to which enzyme and in what percentage of patients?
What should be done as a precaution?

A

Serum aminotransferase in >2% of patients.
Patients should be monitored at 2-4 month intervals, and dose reduced if necessary

34
Q

Taking statins causes a minor elevation to which enzyme (non-serum), and what two symptoms can it lead to?

A

Minor increase in creatine kinase, and can lead to muscle pain and tenderness

35
Q

Name 4 common adverse effects of statins.

A

Mild GI symptoms, headaches, insomnia, and dizziness

36
Q

Name 4 rare but serious adverse effects of statins.

A

Myopathy
Rhabdomyolysis
Renal failure
Liver failure

37
Q

Is pregnancy a contraindication to statins? Why/why not?

A

Yes, it causes impaired foetal myelination

38
Q

In what three cases should statins be withholded?

A

During infection, pre-surgery, and post-trauma

39
Q

What are bile acid sequestrants, and how (in 5 statements) do they work?

A

They are polymeric cationic exchange resins
-They bind bile acid, preventing gut absorption
-Increased demand for cholesterol for bile acid synthesis
-Causes upregulation of hepatic LDL receptors
-Removal of LDL from plasma
-More cholesterol metabolism

40
Q

What two forms of dyslipidaemia are an indication for bile acid sequestrants?

A

Hypercholesterolaemia
Mixed hyperlipidaemia

41
Q

Name 4 common adverse effects of bile acid sequestrants.

A

Abdominal discomfort
Bloating
Constipation
Flatulence

42
Q

Name 5 rare adverse effects of bile acid sequestrants.

A

Increased triglycerides
Faecal impaction
Decreased absorption of fat soluble vitamins
Steatorrhoea (excess fat in faeces)

43
Q

Will taking bile acid sequestrants reduce other drug absorption?

A

Yes, not just anions, but also neutral or cationic charges.

44
Q

What form of dyslipidaemia is the drug ezetimibe used to treat, and how? Does it affect bile salt/fat soluble vitamin absorption? What cholesterol does it lower?

A

For hypercholesterolaemia.
Specifically inhibits cholesterol absorption in the intestine by binding to a sterol transporter (Neimann-Pick C1-like 1 protein).
It lowers LDL.

45
Q

Name 2 possible side effects of ezetimibe.

A

Diarrhoea
Headache

46
Q

Is ezetimibe well tolerated? Is it used in isolation or in combination with other drugs?

A

Well tolerated
Used in combination

47
Q

Describe the treatment - humanised PCSK9 monoclonal antibody - the dyslipidaemia it is used to treat, how it does so, what PCSK9 is, how it is administered, and how often.

A

PCSK9 is an enzyme that attaches to LDL receptors. Blocking this enzyme can increase LDL recycling and lower LDL levels.
Humanised PCSK9 monoclonal antibodies are used to treat familial hypercholesterolaemia.
It is injected once every 2-4 weeks.

48
Q

Name 3 common adverse effects of humanised PCSK9 monoclonal antibodies.

A

Injection site reactions
Nasopharyngitis
Upper respiratory tract infections

49
Q

What is used to treat hypertriglyceridaemia?

A

Fibrates

50
Q

What are fibrates an agonist for? What does this result in?

A

An agonist for the nuclear receptor peroxisome proliferator activated receptor α (PPARα)

51
Q

What effect do fibrates have on triglycerides levels, triglyceride lipolysis, HDLs, and LDLs?

A

Increases lipolysis of triglycerides
Moderate reduction of triglyceride levels
Moderate increase in HDLs
Variable effects on LDLs

52
Q

Are fibrates used in isolation?

A

No, generally used as an adjunct to dietary changes as well.

53
Q

What two compounds increase when taking fibrates?

A

Serum aminotransferase and/or creatinine

54
Q

What is a common adverse effect of fibrates?

A

GI disturbances

55
Q

What are two rare adverse effects of fibrates?

A

Gallstones
Arrythmia

56
Q

Where do the following work:
Ezetimibe
Bile acid resins
Fibrates
Statins
PCSK9 inhibitors

A

Ezetimibe - intestine
Bile acid resin - intestine
Fibrates - capillaries
Statins - liver
PCSK9 inhibitor - liver

OD2 (S1&2) (174 decks)

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