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

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
Side effects statins
Muscular side effects and GI disturbances
26
Ezetimibe target organ
GI tract
27
MOA ezetimibe
Selective cholesterol absorption inhibitor - inhibits cholesterol at brush border at small intestine Increases LDL cholesterol uptake into cells = decreased blood levels
28
Ezetimibe side effects
Fatigue, diarrhoea, abdo pain
29
Colestyramine target organ
GI tract
30
Colestyramine MOA
Binding bile acids, reducing reabsorption which reduces conversion of cholesterol into bile acids
31
Colestyramine side effects
Intestinal obstruction and acidosis
32
Fibrates MOA
Activate PPAR to break down triglycerides
33
Fibrates side effects
Myositis-like syndrome if renal function impaired
34
Nicotinic acid MOA
Reduces production of TGs and VLDL which are converted to LDL in blood
35
Side effects nicotinic acid
vasodilatation - skin flushing
36
methylcellulose MOA
Attracts water into colon = softer and bulkier stool | Swelling ins Atomach = reducing hunger