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X Pharmacological Treatment Of Disease > Lipid Lowering Drugs > Flashcards

Lipid Lowering Drugs Flashcards

1
Q

what are the main lipid lowering drug group?

A

statins

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2
Q

what is cholesterol needed for?

A
  • As a component of cell membranes
  • For synthesis of steroid hormones
  • As a component of bile salts
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3
Q

are steroids fat soluble or water soluble?

A

fat soluble

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4
Q

what is the base structure of a steroid?

A

tetracyclic

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5
Q

what are the 3 sources of cholesterol?

A

Intestinal absorption
Peripheral synthesis
Hepatic synthesis

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6
Q

what does the liver do in terms of the source of cholesterol?

A

acts as the main regulatory organ that determines LDL-C levels in the blood

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7
Q

what is the structure of a lipoprotein?

A

a hydrophilic coat and a hydrophobic core

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8
Q

what is the hydrophilic coat of a lipoprotein made up of?

A

• Phospholipids
• Free cholesterol
• Associated proteins
(apoproteins /apolipoproteins)

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9
Q

what is the hydrophobic core of a lipoprotein made up of?

A

Trigylcerides and/or cholesterol esters

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10
Q

what are the 6 classes of lipoproteins?

A 
Chylomicrons
Chylomicron remnants
VLDL
IDL
LDL
HDL
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11
Q

what do chylomicrons do?

A

transport of ingested lipids to tissues

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12
Q

what do chylomicron remnants do?

A

ingested cholesterol => liver

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13
Q

what do VLDLs do?

A

transport of lipids from the liver to tissues

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14
Q

what do IDLs do?

A

intermediate density (VLDL remnant)

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15
Q

what do LDLs do?

A

supplies cholesterol to tissues that require it

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16
Q

what do HDLs do?

A

transports cholesterol from tissues to the liver

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17
Q

what are the two lipid pathways?

A

endogenous

exogenous

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18
Q

what does the endogenous pathway do?

A

liver -> tissues

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19
Q

what does the exogenous pathway do?

A

tissues -> liver

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20
Q

what is the sequence of events of the exogenous pathway?

A
  1. lipids in GI tract from diet → chylomicrons
    2a. chylomicrons pass through vascular endothelium via lipoprotein lipase, into the peripheral tissues and becomes a free fatty acid
    2b. turned into chylomicron remnant via lipoprotein lipase - returns to the liver as cholesterol

bile acids and cholesterol can enter GI tract via the bile duct, and return to the liver via the portal vein

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21
Q

what is the sequence of events of the endogenous pathway?

A
  1. cholesterol leaves the liver and is turned into VLDL
  2. VLDL is turned into LDL via lipoprotein lipase
  3. LDL can enter the peripheral tissues or act on LDL receptors on the liver
  4. LDL is returned to cholesterol in the liver

also

  1. cholesterol from cell leaves the peripheral tissues as HDL
  2. HDL is turned into VLDL which turns into LDL, or is turned into LDL directly
  3. LDL returns to the liver as cholesterol
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22
Q

what is the major lipid of a chylomicron?

A

triglyceride

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23
Q

what is the major lipid of VLDL?

A

triglyceride

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24
Q

what is the major lipid of IDL?

A

cholesteryl ester

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25
Q

what is the major lipid of LDL?

A

cholesteryl ester

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26
Q

what is the major lipid of HDL?

A

cholesteryl ester

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27
Q

what is cholesterol?

A

a sterol
fluidity/robustness of cell membranes
precursor for steroid hormones
important in vitamin D synthesis and bile acids

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28
Q

how is cholesterol synthesised in the liver?

A

HMG-CoA reductase → mevalonic acid → cholesterol

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29
Q

how is cholesterol delivered to cells?

A
  1. LDL particles bind to specific receptor sites on the surface of peripheral cells
  2. LDL-receptor is endocytosed
  3. LDL particle is delivered to lysosomes
  4. Cholesterol is released by enzyme activity.
  5. Receptor is recycled to the surface
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30
Q

what happens when free cholesterol accumulates in the cell?

A

new LDL receptor synthesis is inhibited and the entry of more LDL is prevented

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31
Q

what does the free cholesterol in cells do?

A
  1. Esterified with fatty acids => cholesterol esters, (storage form of cholesterol)
  2. Synthesis of membranes & other cell components
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32
Q

how does atherosclerosis occur?

A

LDL → oxidised → taken up by foam cells

changes in endothelium → monocytes/leukocytes → attracted to cells → differentiated to macrophage

macrophage releases cytokines
→ further damage to endothelium
→ smooth muscle migration to make fibrous cap

33
Q

what are the 6 classes of hyperlipidaemia?

A

type I, IIa, IIb, III, IV, V

34
Q

what is type I hyperlipidaemia and what does it consist of?

A

Familial Hyperchylomicronaemia

increase in chylomicron

35
Q

what is type IIa hyperlipidaemia and what does it consist of?

A

Familial Hypercholesterolaemia

increase in LDL

36
Q

what is type IIb hyperlipidaemia and what does it consist of?

A

Familial Mixed Hyperlipidaemia

increase in VLDL and LDL

37
Q

what is type III hyperlipidaemia and what does it consist of?

A

Familial Dysbetalipoproteinaemia

increase in IDL

38
Q

what is type IV hyperlipidaemia and what does it consist of?

A

Familial Hypertriglyceridaemia

increase in VLDL

39
Q

what is type V hyperlipidaemia and what does it consist of?

A

Familial Mixed Hypertriglyceridaemia

increase in chylomicron and VLDL

40
Q

which types of hyperlipidaemia are the most important? (increase cholesterol (LDL))

A

type IIa/IIb

41
Q

how do statins work?

A

inhibiting HMG-CoA reductase

42
Q

which pathway do statins inhibit?

A

endogenous cholesterol synthesis

43
Q

what happens when endogenous synthesis is inhibited?

A

Synthesis is prevented, causing an increase in the expression of hepatocye LDL receptors and removal of LDLs from the circulation.

44
Q

statins inhibit the synthesis of cholesterol - what else do they do?

A

increase the uptake of LDL

45
Q

which statin is derived from Aspergillus terreus?

A

lovastatin

46
Q

lovastatin, what other examples of statins are there?

A

Simvastatin, fluvastatin, lovastatin, rosuvastatin,

atorvastatin, pravastatin

47
Q

what are the side effects of statins?

A 
Myopathy
rhabdomyolysis (muscle wasting)
48
Q

what drug interactions are there with statins?

A

drugs associated with myopathy

49
Q

examples of Bile Acid Binding Resins

A

chlolestyramine, colestipol, cholesevelam

50
Q

what do bile acid binding resins do?

A

Sequester bile acids in the intestine

prevent their reabsorption via hepatic portal vein

51
Q

what happens as a result of sequestering bile acids in the intestine?

A

1.decreased absorption of exogenous cholesterol

  1. increased metabolism of endogenous cholesterol into bile acids in the liver
    - increased LDL receptors on liver
    - increased LDL blood removal
52
Q

what are the side effects of bile acid binding resins?

A

Bloating, flatulence, heartburn, constipation

53
Q

what are the drug interactions of bile acid binding resins?

A
  • interfere with absorption of other drugs

- decrease absorption of fat-soluble vitamins, e.g. vitamin A, E, D, K

54
Q

what is another name for nicotinic acid?

A

niacin

55
Q

what does nicotinic acid /niacin do?

A

inhibits production of VLDLs

inhibits lipolysis in adipocytes

56
Q

what does the inhibition of VLDL production by nicotinic acid lead to?

A

reduction in LDL and total cholesterol concentrations

57
Q

what does the inhibition of lipolysis in adipocytes by nicotinic acid lead to?

A

reduction in the delivery of FFAs to the liver and TG synthesis

58
Q

what is the mechanism of action of nicotinic acid?

A

IN THE HEPATOCYTE:

  1. decreased fatty acid mobilisation
  2. decreased TG synthesis
  3. decreased VLDL synthesis
  4. decreased VLDL secretion

VLDL enters the systemic circulation and its turned into LDL…….

IN THE SYSTEMIC CIRCULATION

  1. increase in HDL
  2. decrease in LDL
  3. decrease in lipolysis to LDL
  4. decreased VLDL
59
Q

what is the name for the nicotinic acid receptor?

A

HCA2

60
Q

how does the nicotinic acid receptor work?

A

usually.. adrenaline and noradrenaline stimulate Gs receptor on the cell which would stimulate adenylate cyclase.

NICOTINIC ACID stimulates the nicotinic acid receptor (Gi) which INHIBITS adenylate cyclase - this inhibits the rest of the process….

both the Gs and Gi act on adenylate cyclase.

adenylate cyclase catalyses the reaction of ATP to cAMP

cAMP -> PKA -> HSL.

triglycerides -> HSL -> FFA which leaves the cell to the liver.

the inhibition of adenylate cyclase lowers cAMP, PKA, HSL and FFA

61
Q

what is a side effect of niacin?

A

niacin flush

62
Q

what do fibrates mainly do?

A

Stimulate lipoprotein lipase

63
Q

what happens when lipoprotein lipase is stimulated?

A

promotes lipolysis of VLDLs

limits availability of free fatty acids for TG synthesis in the liver

64
Q

what other things do fibrates do?

A

Accelerate clearance of LDLs from the circulation by the liver
Increase HDL concentrations

65
Q

what is the mechanism of action of fibrates?

A
  • bind to PPAR-α
  • PPAR-α is a nuclear receptor expressed in hepatocytes, skeletal muscle, macrophages and the heart
  • leads to changes in the expression of genes involved in lipoprotein metabolism.
66
Q

examples of fibrates

A

gemfibrozil, fenofibrate, bezafibrate, ciprofibrate

67
Q

what is an example of a Cholesterol Uptake Inhibitor?

A

ezetimibe

68
Q

what do cholesterol uptake inhibitors do?

A

Inhibit cholesterol uptake (and plant stanols) from the duodenum into the enterocyte

69
Q

how do cholesterol uptake inhibitors work?

A

block transport protein NPC 1L1

70
Q

for type I hyperlipidaemia, how should you treat it?

A

no treatment effective

71
Q

for type IIa hyperlipidaemia, how should you treat it?

A

Statin and/or ezetimibe

72
Q

for type IIb hyperlipidaemia, how should you treat it?

A

Fibrates, statin, nicotinic acid

73
Q

for type III hyperlipidaemia, how should you treat it?

A

Fibrates

74
Q

for type IV hyperlipidaemia, how should you treat it?

A

Fibrates

75
Q

for type V hyperlipidaemia, how should you treat it?

A

Fibrates, niacin, VLDL and statin

76
Q

what are PC5K9 inhibitors?

A

reduce cholesterol more than statins

77
Q

how do PC5K9 inhibitors work?

A

bind to monoclonal antibodies

send LDL to lysozome - stop receptors from being recycled

78
Q

what is an example of a PC5K9 inhibitor?

A

evolocumab

X Pharmacological Treatment Of Disease (9 decks)

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