Hyperlipidaemia and therapeutic approaches Flashcards

1
Q

Hyperlipidaemia

A

high LDL cholesterols

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2
Q

Dyslipidaemia

A

High levels of HDL-cholesterol

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3
Q

Chylomicrons

A

Transport TGs/cholesterol from intestine via lymph to blood

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4
Q

VLDL

A

High TG content, lipoprotein lipase converts VLDL Tis to FFA

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5
Q

LDL

A

high cholesterol content

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6
Q

Hypercholesterolemia

A

Elevated LDL-c

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7
Q

Lipid functions

A
Energy storage
Intracellular signalling
Base for steroid hormone synthesis 
vit D synthesis 
Insulation
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8
Q

Triglycerides

A

Glycerol backbone with 3x FFAs

Excess calories converted to Tis and transpired to fat cells for storage

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9
Q

Cholesterol

A

Steroid alcohol found in animal tissues
Mainly synthesised in liver
precursor of steroids, bile acids and vit D
Maintains cell membranes

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10
Q

Lipoproteins

A

Bind lipids and facilitate transport in water

Cell surface receptors are different for different apolipoproteins

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11
Q

Function of low cholesterol lipoproteins

A

Deliver endogenous TAG to peripheral tissues

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12
Q

Optimal levels of LDL-c

A

<1.8mmol/L

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13
Q

Optimal levels of cholesterol

A

<4.4mmol/L

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14
Q

Optimal levels of triglycerides

A

<1.1mol/L

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15
Q

Causes of primary dyslipidaemias

A
  • Genetic mutations
  • Familial hypercholesterolemia most common
  • Typically presents in children
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16
Q

Causes of secondary dyslipidaemias

A
  • Diet
  • Obesity
  • Diabetes
  • Hypothyroidism
  • Alcohol
  • CKD
  • Drugs
17
Q

Management of dyslipidaemias

A
  • Lifestyle - reduce total and saturated fat intake, weight loss, exercise
  • Statins: HMG-COA reductase inhibitors
  • Secondary pt first-line treatment is lifestyle changes
  • Plant sterols (stop body absorbing cholesterol) lower LDL-C and increase HDL-C
18
Q

Statins MOA

A

HMG-coA reductase inhibitors (important in cholesterol synthesis)

19
Q

Side effects of statins

A

Kidney problems
Muscle degeneration and ache
Paraesthesia

20
Q

PCSK9

A

Proprotein convertase subtilise/kexin type 9
Binds LDL for degeneration in lysosomes
Determines LDL-c concentration
This needs to be inhibited to allow LDL to be taken up from blood

21
Q

Ezetimibe

A

Impairs intestinal uptake of dietary and bile conjugated cholesterol
Used as add on to statins

22
Q

Side effects ezetimibe

A

Fatty stools

23
Q

Statin target organ

A

Liver

24
Q

Statin MOA

A

Inhibit HMG COA - involved in cholesterol synthesis

This causes liver cells to make more LDL receptors = increased clearance of LDL from blood stream

25
Q

Side effects statins

A

Muscular side effects and GI disturbances

26
Q

Ezetimibe target organ

A

GI tract

27
Q

MOA ezetimibe

A

Selective cholesterol absorption inhibitor - inhibits cholesterol at brush border at small intestine
Increases LDL cholesterol uptake into cells = decreased blood levels

28
Q

Ezetimibe side effects

A

Fatigue, diarrhoea, abdo pain

29
Q

Colestyramine target organ

A

GI tract

30
Q

Colestyramine MOA

A

Binding bile acids, reducing reabsorption which reduces conversion of cholesterol into bile acids

31
Q

Colestyramine side effects

A

Intestinal obstruction and acidosis

32
Q

Fibrates MOA

A

Activate PPAR to break down triglycerides

33
Q

Fibrates side effects

A

Myositis-like syndrome if renal function impaired

34
Q

Nicotinic acid MOA

A

Reduces production of TGs and VLDL which are converted to LDL in blood

35
Q

Side effects nicotinic acid

A

vasodilatation - skin flushing

36
Q

methylcellulose MOA

A

Attracts water into colon = softer and bulkier stool

Swelling ins Atomach = reducing hunger