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Pharmacology CP > Lipid-Lowering Drugs > Flashcards

Lipid-Lowering Drugs Flashcards

1
Q

What is primary hyperlipidaemias?

A
  • Monogenic (severe and rare)
  • -> E.g. familial hypercholesterolaemia
  • Polygenic (moderate and common)
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2
Q

What does secondary hyperlipidaemia involve?

A
  • Very common

- Alcohol, hypothyroidism, diabetes, diet

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3
Q

What are the classes of lipid-lowering drugs?

A
  • Statins e.g. simvastatin, atorvastatin
  • Fibrates, e.g. clofibrate
  • Nicotinic acid
  • Drugs that reduce cholesterol absorption from gut
  • Others
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4
Q

Give examples of drugs that reduce cholesterol absorption from gut

A
  • Anion-exchange resins (e.g. cholestyramine)
  • Lipase inhibitor (orlistat)
  • Nutraceuticals (phytosterols)
  • Cholesterol transporter NPC1L1 inhibitor (ezetimibe)
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5
Q

Give examples of other classes of lipid-lowering drugs

A
  • PCSK9 inhibitors

- Maybe fish oils

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6
Q

What are the lipoproteins?

A
  • Triglyceride (Structural)
  • Phospholipid (structural)
  • Cholesterol (structural)
  • Apolipoprotein- LP without lipid
  • Chylomicron
  • VLDL
  • LDL
  • HDL
  • Get smaller and denser
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7
Q

Describe triglyceride as a structural component of a lipoprotein

A
  • Glycerol backbone, 3 fatty acids
  • Important for energy and are stored in adipose tissue
  • Carried in lipoproteins in interior lipoprotein
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8
Q

Describe phospholipid as a structural component of lipoprotein

A
  • One fatty acid replaced with phosphate
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9
Q

Describe cholesterol as a structural component of a lipoprotein

A
  • Impermeabilise cell membranes

- Without these, water flows through

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10
Q

Describe a chylomicron as a lipoprotein

A
  • Takes large amounts of triglycerides form the gut to liver
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11
Q

Describe VLDL as a lipoprotein

A
  • Very low-density lipoprotein

- Transports from liver to tissue

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12
Q

Describe LDL as a lipoprotein

A
  • Low-density lipoprotein
  • Carry from tissue
  • Excessive LDL cholesterol with or without triglycerides is known as type 2 hyperlipidaemia- associated with CVD
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13
Q

Describe HDL as a lipoprotein

A
  • High-density lipoprotein
  • Tissues to liver
  • Repeat the cycle
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14
Q

What are the risk factors for atheroma/ CAD?

A
  • Raised total cholesterol (>5mmol/l)
  • Raised LDL cholesterol (>3mmol/l)
  • Reduced HDL (<1mmol/l)
  • Raised triglycerdies- acute pancreatitis
  • If lipids not effectively handled, deposited in areas of endothelial damage- might be caused by smoking of high BP
    • atheroma–> angina–> MI/ ischaemic stroke
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15
Q

How are lipids packaged in the gut following digestion?

A
  • Dietary fat (cholesterol and triglycerides)
  • Packaged into chylomicron
  • Transports to a liver cell
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16
Q

What happens after cholesterol and triglyceride packaged into a chylomicron reach the liver cell?

A
  • They are packages up to VLDLs and sent to the periphery
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17
Q

What happens if inadequate amounts of cholesterol are found in the diet?

A
  • Acetyl CoA pathway

- HMG CoA reductase (hydroxymethylglutaryl coenzyme A reductase)

18
Q

What does LDL do with cholesterol and triglycerides after VLDLs?

A
  • Removes fatty acids for burning for energy or muscles or storing in adipose tissue for future use
  • Activated by lipoprotein lipase- controlled by insulin
19
Q

What happens to LDL after is deposits fatty acids?

A
  • LDL and HDL return to liver cells where there are LDL receptors
  • Vital role in regulating cholesterol in circulation
20
Q

What happens to excess LDL?

A
  • LDL remains too long becomes oxidised and is a risk for atheroma
21
Q

What is the purpose of liver cells?

A
  • Aim to maintain their internal cholesterol
22
Q

How can HMG CoA reductase be inhibited?

A
  • Statins
23
Q

How might the liver prevent excess circulating LDL?

A
  • By inducing expression of LDL receptors
24
Q

Give some examples of statins

A
  • Simvastatin
  • Pravastatin
  • Fluvastatin
  • Atorvastatin
25
Q

What do Statins do?

A
  • Inhibit HMG CoA reductase
  • Compensatory increase in hepatic LDL receptors clears plasma LDL cholesterol (20-50%)
  • Decrease triglycerides (25%)
  • Increase HDL (15%)
26
Q

What do statins treat?

A
  • First line for hypercholesterolaemia to reduce progression of atherosclerosis
  • Primary prevention of MI and stroke
  • Secondary prevention of MI and stroke
27
Q

What are some other effects of statins?

A
  • Reduced vascular inflammation and thrombosis
  • Improved endothelial function and plaque stability\
  • Reduced cancer deaths (prostate and colorectal cancers)
28
Q

What are some unwanted effects of statins?

A
  • Myalgia (<5%)
  • Rhabdomyolysis (muscle breakdown –> acute renal failure)
  • More common, and 10x higher with a fibrate)
29
Q

What do fibrates do?

A
  • Activate and enhance activity of lipoprotein lipase
  • May also reduce release of VLDL
  • Reduce amount of cholesterol going through cycle
  • Reduce risk of excess LDL
30
Q

Give examples of fibrates

A
  • Clofibrate

- Fenofibrate

31
Q

What is the mechanism of fibrates?

A
  • Activate PPAR alpha (peroxisome proliferator-activated receptor α)
  • Decreases synthesis of VLDL
  • Activates lipoprotein lipase
  • Redues plasma triglycerides by 20-50%
  • LDL decreased and HDL increased
32
Q

What are fibrates?

A
  • First line drugs for hyper-TG (Reduces pancreatitis
  • Effects on CAD are variable (gemfibrozil best)
  • Can be combined with statins
33
Q

What are the side effects of fibrates?

A
  • NVD
  • Myositis/flu
  • Gall stones
34
Q

What does nicotinic acid do?

A
  • Inhibits diacylglycerol acyltransferase-2 (DGAT2)
  • -> Prevents cholesterol and TG combination to produce VLDLs
  • Reduces TG synthesis and release from liver
  • Lowers plasma TF by 20-50% and LDL by 10-20%
  • Combines with fibrates for hypertriglyceridemia
35
Q

What are the side effects of nicotinic acid?

A
  • Flushing (prostaglandins)
  • Itching
  • Dizziness
  • Palpitations
  • Hyperglycaemia
  • Gout
  • Poorly tolerated
  • Acipimox better tolerated by less effective
36
Q

How do ion exchange resins affect bile acids?

A
  • Bile acids normally emulsify fats in gut for better absorption
  • Ion exchange resin forms complex with bile acids, so dietary lipids are not emulsified but excreted
  • Not absorbed in the gut
  • Also clear plasma LDL cholesterol
37
Q

Give examples of anion exchange resins

A
  • Cholestyramine

- Colestipol

38
Q

How are ion exchange resins administered?

A
  • Combination therapy for severe hyperlipidaemia

- Side effects- gut only (bloating, NVD, decreased fat-soluble vitamin absorption)

39
Q

What are lipase inhibitors?

A
  • E.g. orlistat

- Blocks breakdown of TG to fatty acids within the gut

40
Q

What are nutraceuticals?

A
  • E.g. plant sterols
  • Reduce gut absorption of cholesterol
  • But no by much and rather expensive
41
Q

What is ezetimibe and what does it do?

A
  • Inhibits intestinal cholesterol transport (NPC1L1)
  • Halves cholesterol absorption and reduced plasma LDL-C by 15%
  • Used as adjunct to diet and statins in hypercholesterolaemia
42
Q

What are PCSK9 inhibitors and give examples?

A
  • E.g. alirocumab and evolocumab
  • Monoclonal Abs block pro protein converts subtilisin/kexin type 9
  • Reduces degradation of LDL receptors on hepatocytes by PCSK9
  • Reduces plasma LDL-C by 45-70%
  • Given subcutaneously every 2 wks for resistant primary hypercholesterolaemia (combined with statins and other drugs)

Pharmacology CP (11 decks)

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