IHD hyperlipideamia overview Flashcards

(50 cards)

1
Q

What is hyperlipidaemia?

A
  • Abnormally high fats in the blood
  • Cholesterol and/or triglycerides
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Which lipid is most associated with cardiovascular disease?

A
  • LDL cholesterol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Why is cholesterol treated clinically?

A
  • Reduce cardiovascular disease risk
  • Prevent MI, stroke, angina, and PAD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What proportion of heart attacks are related to high cholesterol?

A
  • About one third
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is atherosclerosis?

A
  • Fatty plaque formation in arteries
  • Causes narrowing and stiffening
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Outline the development of atherosclerotic plaque.

A
  • LDL enters artery wall
  • LDL oxidised
  • Macrophages ingest LDL
  • Foam cells form
  • Atheroma develops
  • Plaque rupture
  • Thrombus → MI or stroke
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What usually causes a myocardial infarction?

A
  • Plaque rupture followed by clot formation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Is hyperlipidaemia symptomatic?

A
  • Usually asymptomatic for decades
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Physical signs of severe hyperlipidaemia?

A
  • Xanthomas
  • Xanthelasma
  • Corneal arcus (<45 suggests FH)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What complication is caused by very high triglycerides?

A
  • Acute pancreatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Lifestyle causes of hyperlipidaemia?

A
  • Saturated fat diet
  • Smoking
  • Alcohol excess
  • Inactivity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How does saturated fat raise cholesterol?

A
  • Increases hepatic LDL production
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is familial hypercholesterolaemia?

A
  • Genetic LDL receptor disorder causing very high LDL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Pathophysiology of FH?

A
  • Defective LDL receptors
  • LDL remains in blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Consequences of FH?

A
  • Premature coronary disease
  • Early MI (men ~50, women ~60)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Prevalence and treatment of FH?

A
  • ~1 in 250 people
  • Requires medication from childhood (~5 yrs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Non-modifiable cardiovascular risk factors?

A
  • Age
  • Male sex
  • South Asian ethnicity
  • Family history
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Why does menopause increase risk?

A
  • Loss of oestrogen
  • Reduced HDL protection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Secondary causes of hyperlipidaemia?

A
  • Type 2 diabetes
  • Hypothyroidism
  • Kidney disease
  • Liver disease
  • Obesity/central adiposity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Why does hypothyroidism raise LDL?

A
  • Decreases LDL receptor activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Normal lipid targets?

A
  • Total cholesterol <5 mmol/L
  • LDL <3 mmol/L
  • HDL >1 male, >1.2 female
  • TG <1.7 mmol/L
22
Q

Is fasting required for lipid tests?

23
Q

What is non-HDL cholesterol?

A
  • All atherogenic lipoproteins (LDL + VLDL + IDL)
24
Q

Why is non-HDL cholesterol used?

A
  • Represents all “bad” lipids
25
Relationship between LDL and non-HDL cholesterol?
- LDL ≈ non-HDL − 0.8 mmol/L
26
What is QRISK3?
- Calculator estimating 10-year CVD risk
27
When should QRISK3 not be used?
- Established CVD - FH - Type 1 diabetes - CKD - Pregnancy
28
Why not use QRISK3 in these groups?
- Already high risk
29
Effect of lowering LDL by 1 mmol/L?
- ~25% reduction in cardiovascular events
30
Primary prevention treatment threshold?
- QRISK ≥10%
31
Primary prevention target?
- ≥40% LDL/non-HDL reduction
32
Secondary prevention treatment?
- High-intensity statin immediately
33
First-line statin after MI?
- Atorvastatin 80 mg (do not delay)
34
Secondary prevention lipid targets?
- LDL ≤2.0 mmol/L - Non-HDL ≤2.6 mmol/L
35
Mechanism of statins?
- Inhibit HMG-CoA reductase - Increase LDL receptors - Increase LDL clearance
36
Main LDL-lowering effect of statins?
- Increased hepatic LDL removal
37
Mechanism of ezetimibe?
- Blocks NPC1L1 transporter - Reduces intestinal cholesterol absorption
38
Mechanism of bempedoic acid?
- Inhibits ATP-citrate lyase - Increases LDL receptors
39
Mechanism of PCSK9 inhibitors?
- Prevent LDL receptor destruction - Given by injection
40
Mechanism of inclisiran and dosing?
- siRNA blocking PCSK9 production - Day 0 → 3 months → every 6 months
41
When is icosapent ethyl used?
- Persistent high triglycerides despite statins
42
When are fibrates used?
- Hypertriglyceridaemia
43
Tests before starting statins?
- Lipids - LFTs - Thyroid function - Renal function
44
Statin follow-up monitoring?
- 2–3 months - 1 year
45
What test for statin muscle pain?
- Creatine kinase
46
Common statin side effects?
- Headache - GI upset - Raised liver enzymes
47
Serious statin complication?
- Rhabdomyolysis → kidney failure
48
Statin diabetes risk?
- ~3 extra cases per 100 people over 5 years - Benefit outweighs risk
49
Risk factors for statin intolerance?
- Older age - Female - Hypothyroidism - Alcohol - Renal/liver disease - Drug interactions
50
What happens if statins are stopped?
- Increased heart attack risk