3.2.2 Dyslipidemia

Question 1

Define Dyslipidemia

Answer 1

Elevation of:
- Cholesterol
- LDL
- Triglycerides

Lowering of HDL

Question 2

What are the 2 major lipids in plasma?

Answer 2

1. Cholestrol
- “building blocks”
- major component of cell membranes
- precursor to steroids & bile acid
- Plasma = esterified form
- Cell membrane = free / unestrified

**2. Triglicerides”
- “energy source / fuel provider”
- glycerol + 3 free fatty acids bound by estrification (triacylglycerols)
- stored: adipose tissue
- release op fatty acids during fasting stage as lipase enzyme action

Question 3

How doe cholestrol & triglyceride transport in plasma?

Answer 3

By transporters (lipoproteins)

Question 4

What does a lipoprotein consists of?

Answer 4

Core:
- insoluble lipid
- hydrophobic

Outer layer:
- partly lipid soluble
- partly water

3 components:
- free cholestrol
- phospholipids
- apoproteins

Question 5

What are the functions of apoproteins?

Answer 5

• stabilisation of lipoproteins
• regulator of lipoprotein metabolism
• secretion of lipoproteins
  Carry protective effect to prevent atherosclerosis

Question 6

How is “species of lipoprotein” classified?

Answer 6

• big size = LDL = dominant cor lipid content
• small size = HDL = dominant apoprotein content

Question 7

Describe the exogenous lipoprotein pathway

Answer 7

• dietary TG & Cholesterol packaged with ApoB48 to form Chylomicrons
• Cm = largest of lipoprotein subspecies
• Cm enable transport of fatty acids to muscle or adipose tissue for storage
• Cm remnants = left overs after TG & apo removal
• Cm remnants taken up by liver for metabolism

Question 8

Describe the endogenous lipoprotein pathway

Answer 8

• TG & cholesterol from liver are secreted to CLDL -> transport lipids to periphery
• LPL most important enzyme in pathway -> removes components of VLDL
• liver synthesises cholesterol
• hepatic TG synthesis depends on fatty acids from adipose tissue, lipogenesis from carbohydrate intake & chylomicron remnant intake
• LDL = carrier for cholestrol in plasma
• low LDL receptor activity = high LDL levels
• HDL cleans up excess cholestrol

Question 9

How does atherosclerosis form?

Answer 9

LDL + inflam process (monocytes, macrophages, O2 free radicals)

Endotelial damage + Foam cell formation + platlet adhesion + growth factor release
=
Smooth muscle proliferation = accumulation of connective tissue
=
ATHEROSCLEROSIS

Question 10

What is the HDL two fold protective effect?

Answer 10

1. Reverse cholestrol transport
2. Anti oxidative activity

Question 11

What is the feature of an atherosclerotic plaque?

Answer 11

NOT TRIGLYCERIDE ACCUMULATION
- TG rich lipoproteins contain cholesterol esters that are atherogenic

Question 12

What 2 dysfunctions does increased triglyceride cause?

Answer 12

• acute pancreatitis (inflam)
• retinal vein thrombosis

Question 13

Examples of secondary dyslipidemia

Answer 13

• DM
• Hypothyroidism
• Nephronic syn
• Alcohol excess
• Steroid hormones
• Retinois acids
• HAART

Question 14

Familial hypercholesterolemia

Answer 14

• LDL receptor abnormality
• very common
• LDL >5mmol/l
• very high risk for death if untreated (M 50%; W 15%)

Signs & Symptoms
- Bilateral thick achilles tendon (Tendinous xanthomata)
- xanthelasma (yellow on eye)
- Corneal arcus (ring around eye)

Question 15

Primary isolated hypertriglyceridemia

Answer 15

• Autosomal dominant
• Very high VLDL output by liver
• High ratio of TG to ApoB
• Low HDL & LDL
• Recurrent abdom pain and pancreatitis

Question 16

Secondary dyslipidemia: Metabolic syndrome

Answer 16

• Cental abdom obesity
• Hypertension
• Insulin resistance
• acanthosis nigricans & skin tags
• High TG, low HDL, high ApoB

Question 17

What is the difference between primary and secondary prevention?

Answer 17

*Primary** - ID patient before event happen
Secondary - after event happened, prevent another event from happening