Hyperlipidaemia Flashcards

(64 cards)

1
Q

What is hyperlipidaemia?

A

Elevated levels of lipids (cholesterol and triglycerides) in the blood

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2
Q

Why are lipids necessary?

A

They are essential for cell membranes, hormone production, and energy storage.

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3
Q

What is the main risk of hyperlipidaemia?

A

Development of atherosclerosis → fatty plaque build-up → cardiovascular disease (MI, stroke, PAD)

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4
Q

What is the role of LDL?

A

“Bad cholesterol” – delivers cholesterol to tissues, contributes to plaque formation

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5
Q

What is the role of HDL?

A

“Good cholesterol” – removes cholesterol from tissues, transports it to the liver for excretion

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6
Q

What is the role of VLDL?

A

Transports triglycerides and some cholesterol from the liver to tissues

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7
Q

What is the role of chylomicrons?

A

Transport dietary triglycerides from intestines to tissues

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8
Q

What imbalance is common in hyperlipidaemia?

A

↑ LDL and triglycerides, ↓ HDL

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9
Q

What happens to dietary lipids in the intestine?

A

Fatty acids + glycerol → triglycerides → packaged into chylomicrons

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10
Q

What enzyme breaks down triglycerides in chylomicrons?

A

Lipoprotein Lipase (LPL) → releases free fatty acids for storage or energy

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11
Q

What are chylomicron remnants?

A

Cholesterol-rich particles left after triglyceride removal, processed by the liver

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12
Q

What does the liver secrete after processing remnants?

A

VLDLs (containing triglycerides and cholesterol)

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13
Q

What happens to VLDLs in circulation?

A

LPL removes triglycerides → VLDLs become IDLs

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14
Q

What is the fate of IDLs?

A

Taken up by the liver or converted into LDLs

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15
Q

What is the role of LDLs in metabolism?

A

Deliver cholesterol to cells for membranes and hormone synthesis

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16
Q

What are the two broad categories of hyperlipidaemia?

A

Primary (familial/genetic) and secondary (acquired)

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17
Q

What are examples of primary hyperlipidaemia?

A

Familial hypercholesterolaemia, familial combined hyperlipidaemia, familial hypertriglyceridaemia, familial dysbetalipoproteinaemia

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18
Q

What are common causes of secondary hyperlipidaemia?

A

Diet (high fat), obesity, diabetes, hypothyroidism, alcohol, certain drugs

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19
Q

Why is hyperlipidaemia clinically important?

A

It is a major modifiable risk factor for cardiovascular disease

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20
Q

What causes Type 1 Familial Hyperlipidaemia?

A

Lipoprotein Lipase or ApoC2 deficiency → impaired triglyceride breakdown → ↑ chylomicrons

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21
Q

What characterises Type 2A Familial Hypercholesterolemia?

A

↑ LDL due to LDL receptor mutations → high “bad cholesterol.”

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22
Q

What characterises Type 2B Familial Hypercholesterolemia?

A

↑ LDL + ↑ VLDL due to defective lipoprotein regulation

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23
Q

What causes Type 3 Dysbetalipoproteinemia?

A

Defective ApoE → impaired clearance of VLDL & chylomicron remnants → ↑ risk of atherosclerosis

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24
Q

What causes Type 4 Familial Hypertriglyceridaemia?

A

↑ VLDL production in the liver → ↑ triglycerides

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25
How does diabetes cause hyperlipidaemia?
Insulin resistance → ↑ VLDL production + ↓ HDL
26
How does hypothyroidism cause hyperlipidaemia?
↓ thyroid hormones → reduced lipid metabolism → ↑ LDL
27
Which medications can cause hyperlipidaemia?
Thiazide diuretics and others that alter fat metabolism
28
What are the treatment goals in hyperlipidaemia?
↓ LDL-C, ↑ HDL-C, ↓ triglycerides → prevent atherosclerosis & CV events
29
What is the mechanism of statins?
Inhibit HMG-CoA reductase → ↓ cholesterol synthesis → ↑ LDL receptor expression → ↑ LDL clearance
30
What are pleiotropic effects of statins?
Improve endothelial function, reduce oxidative stress, stabilise plaques
31
When are statins used?
First-line therapy for primary & secondary prevention of CVD
32
Examples of statins?
Atorvastatin, Simvastatin, Rosuvastatin
33
How are statins dosed?
Once daily; simvastatin at night, atorvastatin/rosuvastatin any time
34
What monitoring is needed with statins?
LFTs before and after 3 months; lipid profile every 3 months
35
Common side effects of statins?
Myopathy, rare rhabdomyolysis, ↑ liver enzymes, GI disturbances
36
Key counselling for statins?
Take consistently; report muscle pain; avoid grapefruit juice (esp. simvastatin)
37
What is the mechanism of ezetimibe?
Inhibits NPC1L1 transporter in intestine → ↓ cholesterol absorption → ↑ LDL receptor expression → ↓ LDL
38
When is ezetimibe used?
Add-on to statins if LDL remains high or in statin intolerance
39
Example of ezetimibe?
Ezetimibe (Ezetrol)
40
How is ezetimibe dosed?
Once daily, with or without food; often combined with statins.
41
What monitoring is needed with ezetimibe?
Lipid profile; LFTs if combined with statins
42
Common side effects of ezetimibe?
Diarrhoea, abdominal pain, fatigue, arthralgia (usually mild)
43
Key counselling for ezetimibe?
Maintain healthy diet; remind patients of monitoring if combined with statins
44
Why is pharmacological management of hyperlipidaemia important?
Reduces risk of atherosclerosis, heart attacks, strokes, and cardiovascular mortality
45
What is the mechanism of fibrates?
PPAR-α agonists → ↑ lipoprotein lipase expression → ↓ triglycerides, ↑ HDL, ↓ VLDL production
46
What is the rationale for using fibrates?
Effective in hypertriglyceridaemia; moderately increase HDL; sometimes combined with statins in mixed dyslipidaemia
47
Examples of fibrates?
Fenofibrate, Gemfibrozi
48
How are fibrates dosed?
Once or twice daily, usually with meals
49
What monitoring is required with fibrates?
Lipid profiles, liver function tests, renal function tests
50
Common side effects of fibrates?
GI disturbances, gallstones, myopathy (especially with statins)
51
Key counselling for fibrates?
Report muscle pain/weakness; combine with diet/exercise for best effect.
52
What is the mechanism of PCSK9 inhibitors?
Monoclonal antibodies block PCSK9 → ↑ LDL receptors on hepatocytes → ↑ LDL clearance
53
What is the rationale for using PCSK9 inhibitors?
For familial hypercholesterolaemia or high CV risk patients not controlled with statins/ezetimibe
54
Examples of PCSK9 inhibitors?
Alirocumab, Evolocumab
55
How are PCSK9 inhibitors dosed?
Subcutaneous injection every 2–4 weeks.
56
What monitoring is required with PCSK9 inhibitors?
Regular lipid profiles
57
Common side effects of PCSK9 inhibitors?
Injection site reactions, flu-like symptoms, fatigue
58
Key counselling for PCSK9 inhibitors?
Teach injection technique; stress adherence; report persistent flu-like symptoms or injection site issues
59
What dietary changes help manage hyperlipidaemia?
↓ saturated/trans fats; ↑ soluble fibre (oats, beans, lentils); plant sterols/stanols
60
How does exercise help?
Regular aerobic activity (≥150 min/week) → ↑ HDL, ↓ triglycerides
61
How does weight loss help?
Losing 5–10% body weight → ↓ LDL/triglycerides, ↑ HDL
62
Why is smoking cessation important?
Smoking ↓ HDL and damages vessels → quitting improves lipid profile and CV risk
63
How does alcohol intake affect lipids?
Excess alcohol ↑ triglycerides; moderation reduces risk
64
Why combine lifestyle changes with drug therapy in hyperlipidaemia?
Lifestyle modifications enhance drug efficacy, reduce LDL/triglycerides, raise HDL, and improve CV outcomes