Hyperlipidemia Flashcards

1
Q

What are the different types of lipoproteins?

A

HDL - mainly phosphoplipids
LDL - mainly cholesterol
vLDL - mainly triglycerdies
Chylomicrons

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2
Q

What are the different categories of hyperlipidemia?

A

Primary Hyperlipidemia - increased LDLs only
Familial Primary Hyperlipidemia
Secondary Hyperlipidemia
Mixed Hyperlipidemia - increased LDLs + triglycerides

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3
Q

What are the different risk factors of hyperlipidemia?

A
  • Family history of hyperlipidemia
  • Xanthalasma
  • Corneal Arcus at < 50 years old
  • Those at risk of CVD
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4
Q

What are the risk factors of CVD?

A
  • Family History
  • Diabetes or impaired glucose tolerance
  • Hypertension
  • Smoking
  • Low socio-economic background
  • High BMI
  • Hyperlipidemia
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5
Q

What are the clinical features of hyperlipidemia?

A
  • Xanthomata - yellow lipid deposits

- Xanthelasma - congregation of yellow plaques around eye lids or just below eyes

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6
Q

What are the causes of hyperlipidemia?

A
  • High fat diet
  • Sedentary lifestyle
  • Obesity
  • Diabetes
  • Genetics
  • Family History
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7
Q

What is the pathophysiology of hyperlipidemia?

A
  • Hyperlipidemia sees high levels of LDLs

Lipoproteins in the form of micells are taken up into small intestinal cells from the lumen of the small intestine. Here, they are broken down into their basic units, monoglycerides and fatty acids. Fatty acids, monoglycerides, cholesterol and apoproteins are packaged into chylomicrons and released into the blood. In the blood, the chylomicrons travel to the liver, where they bind to the LDL receptors on hepatocytes.

Glucose also enters hepatocytes via the glucose transporter. Glucose undergoes a series of reactions to form glycerol and ACoA. ACoA can be converted into malonyl CoA, which in turn can be converted into fatty acids. Alternatively, ACoA can also form cholesterol through the action of HMG-CoA reductase.

Glycerol and fatty acids combine together to form triglycerides. the triglycerdies, apoproteins and cholesterol are then packaged together at Golgi into lipoproteins.

Empty HDLs pick up excess cholesterol in circulation and return to hepatocytes. vLDLs are broken down by lipases to LDLs and then to IDLs

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8
Q

What are the investigations done for suspected hy[erlipidemia?

A

Blood tests - cholesterol levels

Urinanalysis - proteinuria

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9
Q

What is the management of hyperlipidemia?

A

Conservative or medical

CONVERVATIVE MANAGEMENT:

  • Cardio protective diet
  • Physical activity
  • Weight management
  • Reduce alcohol intake
  • Smoking cessation

MEDICAL MANAGEMENT - depends on whether prevention is primary or secondary

=> Primary prevention:

Atrovastatin 20mg OD in the following cases:
- 10 year CVD risk ≥ 10%
OR
- Type 1 Diabetes
OR
- CKD if eGFR < 60

=> Secondary prevention

Atorvastatin 80mg BD in the following cases:
- Ischaemic Heart Disease
OR
- Cerebrovascular Disease
OR 
- Peripheral Artery Disease
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10
Q

What is the follow up protocol for those started on statins?

A

Patients followed up at 3 months:

  • Full lipid profile repeated
  • If non HDL has not fallen by 40% lifestyle changes are discussed
  • Atorvastatin dose may be increased to 80mg
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