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302 Scientific basis of medicine > Metabol 4) Lipid disorders > Flashcards

Metabol 4) Lipid disorders Flashcards

1
Q

Where do lipids come from?

A

Exogenous - from gut to tissues (ingested lipids)
Endogenous - from liver to tissues (synthesised lipids)
Lipids in blood
- fatty acids - bound to albumin
- cholesterol and triglyceride form lipoprotein complex

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2
Q

Why are lipoprotein particles water soluble?

A

Apoplipoproteins and other amphipathic molecules have detergent-like properties so they surround lipids to create lipoproteins

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3
Q

What affects a lipoproteins size and flotation density?

A

Triglyceride content
Cholesterol conent
Apo-lipoprotein content
Stage in circulation through body

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4
Q

What are the 5 major classes of lipoproteins?

A 
Chylomicrons
Very low-density lipoproteins
Intermediate density lipoproteins
Low density lipoprotein
High density lipoprotein
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5
Q

What is the function of the Al apoliprotein?

A

Lecithin: cholesterol acyl transferase activation

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6
Q

What is the function of apolipoprotein B-100?

A

LDLR ligand

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7
Q

What is the function of apoliproprotein B-48?

A

Principal apoprotein in chylomicron

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8
Q

What is the function of the apolipoprotein Cll?

A

Lipoprotein lipase inhibitor

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9
Q

What is the function of the apolipoprotein Clll?

A

LPL activator

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10
Q

What is the function of the apolipoprotein E?

A

Chylomicron remnant R ligand

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11
Q

What is the role of the liver in chylomicron metabolism?

A

Endogenous:

  • synthesis of triglyceride
  • export as VLDL
  • take up particles when triglyceride is removed
  • LDL delivers cholesterol to peripheral cells

Exogenous:
- liver produces bile acids and cholesterol which are involved in creation of micelles for lipid absorption from gut

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12
Q

Describe the stages of the exogenous lipid pathway

A

1) cholesterol and fatty acids from digestion are absorbed into intestinal mucosa cells
2) Re-esterified to cholesterol esters and triglycerides and packaged with phospholipids and lipoproteins
3) Secreted into lymphatic systems as chylomicrons
4) Enter systemic circulation via thoracic duct
5) Lipoprotein lipase from capillary walls hydrolyse triglycerides to fatty acids and glycerol
6) Fatty acids taken up by adipose or muscle cells and glycerol is processed by the liver –> reutilised to make triglyceride or converted to glucose
7) Chylomicron remnant is taken up by LDL receptors on the liver

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13
Q

What are normal serum lipid concentrations?

A

5.0mmol/L in individuals without cardiovascular disease

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14
Q

What are the healthy limits for fasting serum triglycerides?

A

1.7mmol/L

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15
Q

What are the healthy limits for HDL-C?

A

Lower limit is 0.9mmol/L for men and 1.2mmol/L in women

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16
Q

Give an example of a primary dyslipidaemia?

A

Familial hypercholesterolaemia

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17
Q

What is familial hypercholesterolaemia?

A

Autosomal dominant disorder of lipid metabolism

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18
Q

What are the features of familial hypercholesterolaemia?

A

Raised blood cholesterol (especially LDL-C)

Tendon and skin xanthomata (deposits of cholesterol)

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19
Q

Why is it difficult to diagnose familial hypercholesterolaemia?

A

Due to overlapping levels of cholesterol

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20
Q

What genetic mutations are implicated in familial hypercholesterolaemia?

A

APOB
PCSK9
LDLR

21
Q

What is APOB?

A

Protein that binds to LDL receptor

22
Q

What is PCSK9?

A

Protein involved in receptor degradation

23
Q

What are some examples of secondary dyslipidaemia?

A

Hypertriglyceridaemia

Hypercholesterolaemia

24
Q

What can cause hypertriglyceridaemia?

A 
Obesity
Diabetes mellitus
Excess alcohol
Renal failure
Gout
Drug treatments - thiazides, beta blockers, retinoid acid derivatives, oestrogen therapy
25
What can cause hypercholesterolaemia?
``` Hypothyroidism Nephrotic syndrome High saturated fat diet Cholestatic liver disease Anorexia nervosa ```
26
What is the BMI of obese class I?
30.0-34.9
27
What is the BMI of overweight?
25-29.9
28
What is the BMI of obese class II?
35-39.9
29
What is the BMI of obese class III?
≥40
30
How is BMI calculated?
Weight (kg) / height^2 (m2)
31
What molecules does adipose tissue release?
``` Leptin TNF-alpha PAI-1, haptoglobin, serum amyloid A IL-1 beta, IL-6, IL-10, TGF-beta NGF MCP-1, MIF, IL-8 Adiponectin VEGF ```
32
Why does high visceral fat increase cardiovascular risk?
Increased triglycerides Decreased HDL-cholesterol Increased glucose Increased insulin
33
What are the factors in metabolic syndrome?
``` Reduced glucose tolerance Hyperinsulinaemia Visceral oebsity Haemostatic disorders Hypertension Lipid disorders - elevated triglycerides - LDL-C normal or moderately elevated - HDL-C diminished ```
34
What is the waist circumference for identifying metabolic syndrome?
Men >94cm | Women >80cm
35
How is metabolic syndrome identified according to IDF criteria?
Waist circumference + 2 of: - fasting serum triglycerides ≥1.7mmol/L - serum HDL-C cholesterol lowered - BP ≥130/85mmHg - fasting glucose ≥5.6mmol/L or diagnosis of diabetes mellitus
36
What are some further consequences of visceral obesity?
``` Brain health - stroke, necrosis - brain size - cognitive function - dementia Respiratory diseases Heart diseases - heart failure - CHD - valve diseases - arrhythmias Diabetes Cancers Bone density PCOS HIV ```
37
What are some risk factors for coronary heart disease?
``` Lipid profile Obesity Inflammation / infection Blood pressure Socio-economic status Genetic factors Metabolic Smoking habit ```
38
What factors does the Framingham risk score include?
``` Age Total serum cholesterol / HDL cholesterol Systolic BP Smoking status Sex Left ventricular hypertrophy T2DM ```
39
What factors does the Q risk 2 score include?
``` Age Total serum cholesterol / HDL cholesterol Systolic BP Smoking status Sex Left ventricular hypertrophy T2DM BMI Family history Deprivation score Ethnicity AF Renal disease Rheumatoid arthritis ```
40
What drug classes can be used for lipid management in dyslipidaemia?
``` Statins Bile acid sequestrant Cholesterol absorption inhibitor PCSK inhibitors Fibric acid derivatives Fish oil ```
41
What is the mode of action of statins?
HMG-CoA reductase inhibitor
42
What is the mode of action of bile acid sequestrants?
Bind bile salts
43
What is the mode of action of PCSK inhibitors?
Block LDLR catabolism | Inhibit PCSK9 --> blocks PCSK9-LDL-R interaction --> increases LDL-R expression --> increases LDL-C clearance
44
What is the mode of action of fibric acid derivatives?
LPL stimulation
45
What statin should be used if there is low risk of CHD?
Lovastatin
46
What statin should be used with high risk of CHD (high cholesterol)
Pravastatin
47
What statin should be used for secondary prevention?
Simvastatin
48
What anti-atherogenic effects does a high HDL-C have?
Anti-inflammatory Antithrombotic Pro-endothelial

302 Scientific basis of medicine (28 decks)

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