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3: MED1 Y3 - Cardiovascular [2] > [17] Hyperlipidaemia > Flashcards

[17] Hyperlipidaemia Flashcards

1
Q

What is hyperlipidaemia?

A

Hyperlipidaemia is the term used to denoate raised serum levels of one or more of;

  • Total cholesterol (TChol)
  • Low density lipoprotein cholesterol (LDL-C)
  • Triglycerides (TGs)
  • Both TChol and TG (combined hyperlipidaemia)
    *
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2
Q

What is the clinical relevance of hyperlipidaemia?

A

Many types of hyperlipidaemia carry an increased risk of cardiovascular disease, being one of the three main modifiable risk factors

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3
Q

What is dyslipidaemia?

A

A wider term that includes low levels of high-density lipoprotein cholesterol (HDL-C)

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4
Q

What are lipids?

A

A structurally diverse group of compounds

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5
Q

What are the types of lipids?

A
  • Triacylglycerols
  • Fatty acids
  • Cholesterol
  • Phospholipids
  • Vitamins A, D, E, and K
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6
Q

Are lipids hydrophilic or hydrophobic?

A

Hydrophobic

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7
Q

What is the result of lipids being hydrophobic?

A

They are insoluble in water, and therefore need to be transported in the blood bound to carriers

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8
Q

How are lipids transported in the blood?

A
  • Bound to albumin
  • In lipoprotein particles
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9
Q

What % of lipids are bound to albumin?

A

2%, mainly fatty acids

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10
Q

What % of lipids are carried as lipoprotein particles?

A

98%

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11
Q

How is cholesterol obtained?

A

Some from the diet, most synthesised in liver

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12
Q

What is the physiological role of cholesterol?

A
  • Essential component of membranes that modulates fluidity
  • Precursor of steroid hormones
  • Precursor of bile acids
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13
Q

What steroid hormones have cholesterol as their precursor?

A
  • Cortisol
  • Aldosterone
  • Testosterone
  • Oesotrogen
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14
Q

In what form is cholesterol transported around the body?

A

Cholesterol esters

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15
Q

What are lipoproteins?

A

A biochemical assembly, whose purpose is to transport hydrophobic lipid molecules in water, as in blood or extracellular fluid

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16
Q

What is the importance of lipoproteins?

A

Many enzymes, transporters, structural proteins, antigens, adhesions, and toxins are lipoproteins

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17
Q

What is the outer shell of lipoproteins made of?

A

A phospholipid monolayer with small amounts of cholesterol

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18
Q

What does the outer shell of lipoproteins contain?

A

Integral apolipoproteins and peripheral apolipoproteins

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19
Q

Give two examples of integral apolipoproteins

A
  • apoA
  • apoB
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20
Q

Give two examples of peripheral lipoproteins

A
  • apoC
  • apoE
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21
Q

What is found inside the lipoprotein?

A
  • Triacylglycerols
  • Cholesterol esters
  • Fat soluble vitamins
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22
Q

What are cholesterol esters?

A

Cholesterol linked to fatty acids

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23
Q

What are the classes of lipoprotein named according to?

A

Density

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24
Q

What are the classes of lipoproteins?

A
  • Chylomicrons
  • VLDL (very low density lipoproteins)
  • IDL (intermediate density lipoproteins)
  • LDL (low density lipoproteins)
  • HDL (high density lipoproteins)
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25
Q

What does each class of lipoprotein contain?

A

A variable content of apolipoprotein, triglyceride, cholesterol, and cholesterol ester

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26
Q

What does each class of lipoprotein associated with it?

A

A particular complement of associated proteins, known as apolipoproteins

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27
Q

How many major classes of lipoproteins are there?

A

6

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28
Q

What are the important apolipoproteins?

A

apoB and apoAI

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29
Q

What is apoB associated with?

A
  • VLDL
  • IDL
  • LDL
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30
Q

What is apoAI associated with?

A

HDL

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31
Q

How are apolipoproteins related to the phospholipid bilayer?

A

They can be integral or peripheral

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32
Q

What is the structural role of apolipoproteins?

A

Packing water insoluble lipid

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33
Q

What is the functional role of apolipoproteins?

A
  • Acting as a co-factor for enzymes
  • Acting as ligands for cell-surface receptors
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34
Q

Where are chylomicrons loaded?

A

In the small intestine

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35
Q

Where do chylomicrons enter from the small intestine?

A

The lymphatic system

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36
Q

What is added to chylomicrons before they enter the lymphatic system?

A

apoB-48

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37
Q

Where to chylomicrons travel once they have entered the lymphatic system?

A

To the thoracic duct

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38
Q

Where does the thoracic duct empty into?

A

The left subclavian vein

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39
Q

What is added to chylomicrons once it enters the blood?

A

apoC and apoE

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40
Q

What does apoC on chylomicrons bind to?

A

Lipoprotein lipase (LPL) on adipocytes and muscle

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41
Q

What happens when apoC on chylomicrons binds to LPL on adipocytes and muscles?

A

The chylomicron releases fatty acids, which enters cells and depletes chylomicrons of their fat content

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42
Q

What happens when the triglyceride content of chylomicrons is depleted to about 20%

A

apoC dissociates and the chylomicron becomes a chylomicron remnant

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43
Q

What happens to chylomicron remnants?

A

They return to the liver, and the LDL receptor on hepatocytes binds apoE

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44
Q

What happens when the LDL receptor on hepatocytes binds the apoE on chylomicrons?

A

It causes the chylomicron remnant to be taken up by receptor mediated endocytosis

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45
Q

What happens once chylomicron remnants have been taken into the hepatocytes?

A

Lysosomes release the remaining contents for their use in metabolism

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46
Q

Where is VLDL made?

A

In the liver

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47
Q

What is the purpose of VLDL?

A

Transporting TAG to other tissues

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48
Q

What is added to VLDL during its formation?

A

apoB100

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49
Q

What is added to VLDL in the blood?

A

apoC and apoE

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50
Q

Where does the apoC and apoE added to VLDL in the blood come from?

A

HDL particles

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51
Q

What does VLDL bind to?

A

Lipoprotein lipase on endothelial cells in muscle and adipose

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52
Q

What happens when VLDL binds to LPL on muscle and adipose tissue?

A

It starts to become depleted of TAG

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53
Q

What happens to fatty acids release from VLDL in muscle?

A

They are taken up and used for energy production

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54
Q

What happens to the fatty acids released from VLDL in adipose?

A

The fatty acids are used for the re-synthesis of TAG and stored as fat

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55
Q

What happens as the TAG content of VLDL drops?

A

VLDL particles dissociate from the LPL enzyme complex and return to the liver

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56
Q

What happens if the VLDL TAG content depletes to about 30%?

A

The particle becomes an IDL particle

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57
Q

Why is the IDL particle short lived?

A

As they can be taken up by the liver, or rebind to the LPL enzyme to further deplete TAG content

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58
Q

What happens to IDL on depletion to about 10%?

A

It loses apoC and apoE, and becomes a LDL particle

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59
Q

What is the primary function of LDL?

A

Provide cholesterol from the liver to the peripheral tissues

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60
Q

How does LDL get into the peripheral tissue?

A

Peripheral cells express LDL receptors, and take up LDL via the process of receptor mediated endocytosis

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61
Q

Why is LDL not cleared effectively by the liver?

A

Because it does not have apoC or apoE, and the liver has high affinity for apoE

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62
Q

How does the half life of LDL in the blood compare to VLDL or IDL?

A

It is much longer

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63
Q

What is the result of LDL having a much longer half life in the blood?

A

It is more susceptible to oxidative damage

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64
Q

What happens to oxidised LDL?

A

It is taken up by macrophages that then transform to foam cells

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65
Q

What is the clinical relevance of foam cells?

A

They contribute to the formation of atherosclerotic plaques

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66
Q

What do cells requiring cholesterol express?

A

LDL reecptors on their plasma membranes

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67
Q

What acts as a ligand for LDL receptors expressed by cells requiring cholesterol?

A

The apoB-100 on LDL

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68
Q

What happens when LDL binds to receptors expressed by cells requiring cholesterol?

A

The receptor/LDL complex is taken into the cell by endocytosis into an endosome, which then fuses with lysosomes for digestion to release cholesterol and fatty acids

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69
Q

What is LDL receptor expression controlled by?

A

Cholesterol concentration in the cell §

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70
Q

How is HDL producted?

A
  • Nascent HDL is synthesised by the liver and intestine
  • HDL particles can bud off from chylomicrons and VLDL as they are digested by LPL
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71
Q

How does nascent HDL develop?

A

It accumulates phospholipids and cholesterol from cells lining blood vessels, and the hollow core progressively fills to produce a more globular shape

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72
Q

Why is HDL clinically important?

A

Because it has the ability to remove cholesterol from cholesterol-laden cells and return it to the liver. This is an important process for blood vessels, as it reduces the likelihood of foam cells and atherosclerotic plaque formation

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73
Q

What happens to mature HDL?

A

It is taken up by the liver via specific receptors

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74
Q

What is type I hyperlipoproteinaemia?

A

Increased chylomicrons found in fasting plasma

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75
Q

What causes type I hyperlipoproteinaemia?

A

Defective lipoprotein lipase

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76
Q

Is there a link between type I hyperlipoproteinaemia and coronary heart disease?

A

No

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77
Q

What is type IIa hyperlipoproteinaemia caused by?

A

A defective LDL receptor

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78
Q

Is type IIa hyperlipoproteinaemia associated with coronary heart disease?

A

Yes, which may be severe

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79
Q

What causes type IIb hyperlipoproteinaemia?

A

Defect unknown

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80
Q

Is type IIb hyperlipoproteinaemia associated with CHD?

A

Yes

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81
Q

What is type III hyperlipoproteinaemia?

A

Raised IDL and chylomicron remnants

82
Q

What causes type III hyperlipoproteinaemias?

A

Defective apoE

83
Q

Is type III hyperlipoproteinaemia associated with CHD?

A

Yes, but the condition is rare

84
Q

What causes type IV hyperlipoproteinaemia?

A

Defect unknown

85
Q

Is type IV hyperlipoproteinaemia associated with coronary heart disease?

A

Yes

86
Q

What is type V hyperlipoproteinaemia?

A

Raised chylomicrons and VLDL in fasting plasma

87
Q

What causes type V hyperlipoproteinaemia?

A

Cause unknown

88
Q

Is type V hyperlipoproteinaemia associated with CHD?

A

Yes

89
Q

How does raised serum LDL lead to atheroma?

A

Raised serum LDL increases the oxidized LDL, which is recognised and engulfed by macrophages. Lipid laden macrophages called foam cells accumulate in the intima of blood vessel walls to form a fatty streak, which can evolve into an atherosclerotic plaque

90
Q

How can atherosclerotic plaques cause pathology?

A

They grow and enrough on the lumen of the artery causing angina.

If the plaque ruptures, it triggers acute thrombosis (clot) by activating platelets and the clotting cascade, which can lead to stroke or MI

91
Q

What are the causes of hyperlipiaemia?

A
  • Medical conditions
  • Drugs
  • Pregnancy
  • Obesity
  • Alcohol abuse
  • Inherited disorders
92
Q

What medical conditions can cause hyperlipidaemia?

A
  • Hypothyroidism
  • Obstructive jaundice
  • Cushing’s syndrome
  • Anorexia nervosa
  • Nephrotic syndrome
  • Diabetes mellitus
  • CKD
93
Q

What drugs can cause hyperlipidaemia?

A
  • Thiazide diuretics
  • Glucocorticoids
  • Ciclosporin
  • Anti-retroviral therapy
  • Beta-blockers
  • COCP
  • Atypical antipsychotics
94
Q

What inherited disorders can cause hyperlipidaemia?

A
  • Familal dyslipidaemias
  • Familial hypercholesterolaemia
  • Familial combined hyperlipidaemia
  • Apoprotein disorders
95
Q

When should familial hypercholesterolaemia be suspected?

A
  • When adults have a raised TChol concentration (typically >7.5mmol/L) and there is a personal or family history of premature CHD
  • When secondary causes of hypercholesterolaemia have been ruled out
96
Q

When can a definite diagnosis of familial hypercholesterolaemia be made, according to the Simon Broom diagnostic criteria?

A
  • A TChol level of >7.5mmol/L and a LDL-C of >4.9mmol/L, and
  • Tendon xanthomata, or evidence of signs of these in a first or second degree relative, or
  • DNA evidence of an LDL receptor mutation, familial defective apo-B-100, or PCSK9 mutation
97
Q

When can a possible diagnosis of familal hypercholesterolaemia be made, according to the Simon Broom diagnostic criteria?

A
  • A TChol level of >7.5mmol/L and a LDL-C of >4.9mmol/L, and
  • A family history of MI in a second-degree relative of 50 years or younger, or first degree relative 60 years or younger, or
  • Family history of raised TChol greater than 7.5mmol/L
98
Q

How might hyperlipidaemia present?

A
  • Discovered during routine screening, or as part of risk-assessmentfor co-morbidities
  • Premature arcus senilis
  • Tendon xanthomata
99
Q

What is arcus senilis?

A

A white or grey opaque ring in the corneal margin

100
Q

What is a tendon xanthomata?

A

Hard, non-tender nodular enlargement of tendons, most commonly found on knuckles and Achilles tendon

101
Q

What investigations are done in hyperlipidaemia?

A
  • Lipid profile
  • Fasting blood glucose
  • Renal function
  • LFTs
  • TSH
  • DNA testing
102
Q

What should be included in a lipid profile?

A
  • TChol
  • LDL-C
  • HDL-C
  • TGs
103
Q

Why is a fasting sample required for a lipid profile?

A

TGs rise dramatically after a meal

104
Q

Why is a fasting blood glucose required in the management of hyperlipideaemia?

A

To exclude hyperlipidaemia secondary to diabetes mellitus

105
Q

Why is renal function testing required in hyperlipidaemia?

A

To exclude CKD

106
Q

What are LFTs required in the investigation of hyperlipidaemia?

A

To rule out liver disease, if statins have to be initiated

107
Q

When is a TSH done in the investigation of hyperlipidaemia?

A

If dyslipidaemia is present

108
Q

Why is TSH done in investigation of dyslipidaemia?

A

To exclude myxoedema

109
Q

What is the aim of treatment of hyperlipidaemia?

A

Prevent or reduce the risk of complications of CVD

110
Q

What does risk-reduction involve in the management of hyperlipidaemia?

A
  • Non-drug measures, such as addressing lifestyle factors
  • Drug treatment using lipid-lowering therapy
111
Q

What drug is offered in primary prevention of hyperlipidaemia?

A

Atorvastatin

112
Q

What does of atorvastatin should be offered in the primary prevention of hyperlipidaemia?

A

20mg

113
Q

Who should be offered atorvastatin in the primary prevention of hyperlipidaemia?

A
  • People who have a 10% or greater 10 year risk of developing cardiovascular disease
  • 85 years or older
  • Have type 1 diabetes, and;
    • Are older than 40 years
    • Have had diabetes for more than 10 years
    • Have established neuropathy
    • Have other cardiovascular risk factors
  • Have chronic kidney disease
114
Q

What are statins?

A

HMG-CoA reductase inhibitors

115
Q

What do statins do?

A

Lower elevated LDL-C, resulting in a substantial reduction in coronary events and death from CHD

116
Q

Who are statins considered first-line in?

A

Patients with elevated risk of atherosclerotic cardiovascular disease

117
Q

What are the therapeutic benefits of statins?

A
  • Plaque stabilisation
  • Improvement of coronary endothelial function
  • Inhibition of platelet thrombus formation
  • Anti-inflammatory activity
118
Q

What is the mechanism of action of statins?

A

Statins are competitive inhibitors of HMG-CoA, which is the rate limiting step in cholesterol synthesis.

119
Q

What is the result of the inhibition of de novo cholesterol synthesis by statins?

A

It means the intracellular supply of cholesterol is depleted

120
Q

What is the result of the depletion of intracellular cholesterol supplies by statins?

A

It causes the cell to increase the number of cell surface LDL receptors, which bind and internalise circulating LDLs. This reduces plasma cholesterol.

121
Q

By what mechanisms do statins decrease plasma cholesterol?

A
  • Decreasing cholesterol synthesis
  • Increasing LDL catabolism
122
Q

Other than decreasing plasma cholesterol, what can statins do?

A
  • Decrease triglyceride levels
  • Increase HDL cholesterol in some patients
123
Q

What are the therapeutic uses of statins?

A

Statins are effective in lowering plasma cholesterol levels in all types of hyperlipidaemias

124
Q

What cause of hyperlipidaemia are statins much less effective in treating?

A

Familal hypercholesterolaemia

125
Q

Why are statins much less effective in treating patients with familial hypercholesterolaemia?

A

Patients who are homozygous for familial hypercholesterolaemia lack LDL receptors, and therefore benefit from statins is much less

126
Q

What are the adverse effects of statins?

A
  • Elevated liver enzymes
  • Myopathy and rhabdomyolysis
  • Drug interactions
127
Q

What should be done due to the potential for statins to elevate liver enzymes?

A

LFTs should be evaluated prior to starting therapy, or if the patient develops symptoms of liver dysfunction

128
Q

Why is it important to check liver function with statin therapy?

A

As hepatic insufficiency can cause drug accumulation

129
Q

How common are myopathy and rhabdomyolysis as side effects of statins?

A

Rare, but have been reported

130
Q

What was true of the patients in most reported cases of myopathy and rhabdomyolysis with statin treatment?

A

They had renal insufficiency, or were taking drugs such as erythromycin, gemfibrozil, or niacin

131
Q

What is simvastatin metabolised by>

A

Cytochrome P450 enzymes

132
Q

What effect might inhibitors of cytochrome P450 enzymes have when a patient is taking simvastatin?

A

May increase the risk of rhabdomyolysis

133
Q

What should be measured in patients on statins who have muscle complaints?

A

​Plasma creatinine kinase

134
Q

What are the common side effects of statins?

A
  • Nosebleeds
  • Sore throat
  • Non-allegic rhinitis
  • Headache
  • Nausea
  • GI disturbance
135
Q

What drug might statins interact with?

A

Warfarin - statins increase the effect of warfzrin

136
Q

What is the result of statins interacting with warfarin?

A

The INR must be measured regularly

137
Q

Where are statins contraindicated?

A

Pregnancy and lactation

138
Q

Are the statins administered in their active form?

A

Simvastatin and lovastatin are lactones are are hydrolysed to their active form.

Other statins are administered in thier active form

139
Q

Are the statins well absorbed after oral administration?

A

Variable

140
Q

Where are the statins metabolised?

A

Liver

141
Q

Do statins undergo first-pass metabolism?

A

Yes, significantly

142
Q

What is the result of the significant first-pass metabolism of the statins?

A

Their predominant effects are in the liver

143
Q

Do statins have active metabolites?

A

Some do

144
Q

How are statins excreted?

A

Primarily through bile and faeces, but some urinary elimination occurs

145
Q

What is the half life of statins?

A

Variable

146
Q

How do the potencies vary between statins?

A

Different statins have different potencies, with atorvastatin having a higher potency than simvastatin

147
Q

What is involved in secondary prevention in hyperlipidaemia?

A

Start statin treatment with atorvastatin in people with cardiovascular disease

148
Q

What does of atorvastatin is used in secondary prevention?

A

80mg

149
Q

When might a lower dose of atorvastatin be used in secondary prevention?

A
  • Potential for drug interactions
  • High risk of adverse effects
  • Patient prefers it
150
Q

What should be done if a person is not able to tolerate a high-intensity statin regime?

A

Aim to treat at the maximum tolerated dose

151
Q

When is ezetimibe therapy recommended?

A
  • Monotherapy for treatment of primary hypercholesterolaemia in adults who cannot tolerate statin therapy
  • Co-administration with initial statin therapy to treat primary hypercholesterolaemia if serum or total LDL cholesterol concentration is not appropriately controlled
  • If change from initial staitn therapy is being considered
    *
152
Q

What is the clinical use of benxzafibrate?

A

It is an adjunct to diet and other appropriate measures in mixed hyperlipidaemia if statins are contraindicated or not tolerated

NICE advises against its use

153
Q

What is the clinical use of nicotinic acid?

A

It is an adjunct to statins in dyslipidaemia, or alone if statins aren’t tolerated

NICE advises against its use

154
Q

By how much can ezetimibe lower LDL cholesterol?

A

Approx. 17%

155
Q

What is the result of the modest statin-lowering effects of ezetimibe?

A

If is often used as an adjunct to statin therapy, or in statin-intolerant patients

156
Q

What is the mechanism of action of ezetimibe?

A

It selectively inhibits reabsorption of dietary and biliary cholesterol in the small intestine, leading to a decrease in the delivery of intestinal cholesterol to the liver. This causes a reduction of hepatic cholesterol stores, and an increase in clearance of cholesterol from the blood

157
Q

Are adverse effects common with the use of ezetimibe?

A

No, they are uncommon

158
Q

What are the contraindications for ezetimibe?

A

Patients with moderate or severe hepatic insufficiency

159
Q

How is ezetimibe metabolised?

A

By the small intestine and liver via glucuronide conjugation

160
Q

How is ezetimibe excreted?

A

Biliary and renal excretion

161
Q

Give two examples of fibrates

A
  • Benzofibrate
  • Fenofibrate
162
Q

What are fibrates?

A

Derivates of fibric acid

163
Q

What do fibrates do?

A

Lower serum triglycerides and increase HDL levels

164
Q

What are PPARs?

A

Peroxisome proliferator activated receptors - they are members of the nuclear receptor family that regulates lipid metabolism

165
Q

What do PPARs function as?

A

Ligand-activated transcription factors

166
Q

What activates PPARs?

A

Binding to their natural ligands or anti-hyperlipidaemic drugs

167
Q

What are the natural ligands for PPARs?

A

Fatty acids or eicosanoids

168
Q

What happens when PPARs are activated?

A

They bind to peroxisome proliferator response elements, which ultimately leads to decrased TAG concentration through increased expression of lipoprotein lipase, and decreasing apolipoportein CII concentration

169
Q

How do fibrates increase cholesterol?

A

By increasing the expression of apo AI and apoAII

170
Q

What are the therapeutic uses of fibrates?

A

They are used in the treatment of hypertriglyceridaemias

171
Q

What kind of hypertriglyceridaemias are fibrates particularly useful in?

A

Type III hyperlipidaemia

172
Q

What happens in type III hyperlipidaemias?

A

Intermediate-density lipoprotein particles accumulate

173
Q

What are the adverse effects of fibrates?

A
  • Mild GI disturbance
  • Gallstones
  • Myositis
  • Drug interactions
174
Q

What happens to the adverse effect of GI disturbance with fibrate as therapy progresses?

A

It lessens

175
Q

Why do fibrates cause a predisposition to gallstone formation?

A

Because they increase biliary cholesterol excretion

176
Q

What should be done as a result of myositis being a potential adverse effect of fibrates?

A

Muscle weakness or tenderness should be evaulated

177
Q

Who might be at increased risk of myositis caused by fibrates?

A

Patients with renal insufficiency

178
Q

What drug might interact with fibrates?

A

It increases the effects of warfarin

179
Q

What should be done due to fibrates potentially increasing the effects of warfarin?

A

Monitor INR regularly AGAIN OBVIOUSLY I HATE THIS JUST GIVE THEM BLOODY RIVAROXIBAN

180
Q

What are the contraindications to fibrates?

A

They should not be used in patients with severe hepatic or renal dysfunction, or pre-existing gallbladder disease

181
Q

Are fibrates well absorbed after oral administration?

A

Yes, completely

182
Q

Describe the distribution of fibrates

A

They distribute widely, bound to albumin

183
Q

What happens to fenofibrate in the body?

A

Fenofibrate is a prodrug which is convereted to the active moiety fenofibric acid

184
Q

Do fibrates undergo biotransformation?

A

Yes, extensively

sorry this is a bit of a leading question lol why would it ask if the answer was no

185
Q

whos my best boy

A

eddie

186
Q

i wonder if you’ll ever actually get 186 cards deep in hyperlipidaemia

A

if you do let me know hheheh

187
Q

How are fibrates excreted?

A

In the urine as glucuronide conjugates

188
Q

What is nicotinic acid also known as?

A

Niacin

189
Q

How effective is nicotinic acid?

A

It can reduce LDL-C by 10-20%, is the most effective agent for increasing HDL-C, and lowers triglycerides by 20-35% at typical doses of 1.5-3g/day

190
Q

What can nicotinic acid be used in combination with?

A

Statins

191
Q

What combination of nicotinic acid and statins is available?

A

A fixed-dose combination of lovostatin and long-acting nicotinic acid

192
Q

What is the mechanism of action of nicotinic acid?

A

At therapeutic doses, it strongly inhibits lipolysis in adipose tissue, thereby reducing production of free fatty acids. The liver normally uses circulating free fatty acids as a major precursor for tryglyceride synthesis, and so reduced liver triglyercide levels decrease hepatic VLDL production, which in turn reduces LDL-C plasma concentrations

193
Q

What are the therapeutic uses of nicotinic acid?

A

It is useful in the treatment of familial hyperlipidaemias

It is also used to treat other severe hypercholesterolaemiaes, often in combination with other agents

194
Q

What are the adverse effects of nicotinic acid?

A
  • Intense cutaneous flush accompanied by uncomfortable feeling of warmth
  • Pruritis
  • Nausea and abdominal pain
  • Hyperuricaemia and gout
  • Impaired glucose tolerance
  • Hepatotoxicity
195
Q

What mediates the flush caused by nicotic acid?

A

Prostaglandins

196
Q

How can the adverse effect of flush with nicotinic acid be decreased?

A

Administration of aspirin prior to nicotinic acid

197
Q

How can some of the bothersome initial adverse effects of nicotinic be reduced?

A

Slow titration of the dosage, or usage of sustained release formulations

198
Q

Why does niacin predispose to hyperuricaemia and gout?

A

Because it inhibits tubular secretion of uric acid

199
Q

When should the use of nicotinic acid be avoided?

A

In hepatic disease

200
Q

How is nicotinic acid administered?

A

Orally

201
Q

What happens to nicotinic acid in the body>

A

It is convereted to nicotinamide, which is incorporated into the cofactor NAD+

202
Q

How are nicotinic acid and its derivates excreted?

A

Into the urine

3: MED1 Y3 - Cardiovascular [2] (19 decks)

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