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Cardiology > Lipid Disorders > Flashcards

Lipid Disorders Flashcards

1
Q

List the 3 types of lipid disorders (3)

A
  • Familial hypertriglycerideaemia
  • Type 3 hyperlipidaemia
  • Hypertriglyceridaemia (primary/secondary)
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2
Q

What is familial hypercholesterolaemia? (3)

A
  • Autosomal dominant
  • Raised cholesterol
  • Normal TG
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3
Q

What mutations lead to familial hypercholesterolaemia? And what genes are affected? (3)

A

LDL receptor pathway mutations

  • LDLR
  • APB
  • PCSK9
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4
Q

What are the signs of FH? And which is the most specific to FH?

A
  • Tendon xanthomata (most specific)
  • Xanthelasmata
  • Corneal arcus
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5
Q

What is tendon xanthomata?

A

Swellings on knuckles, knees, Achiles tendon

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6
Q

What is diagnostic for FH in adults? (3)

A
  • Cholesterol conc= above 7.5mmol
  • LDL = above 4.9mmol
  • Tendon xanthomas/in first/second degree relative

OR
- Positive genetic testing

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7
Q

What is diagnostic for FH in children? (3)

A
  • Cholesterol conc= above 6.7mmol
  • LDL = above 4mmol
  • Tendon xanthomas/in first/second degree relative

OR
- Positive genetic testing

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8
Q

What suggests possible FH? (3)

A
  • Cholestrol concs same as diagnostic FH
  • Family history of MI in younger than 50 yr 2nd degree relative/younger than 60 first degreee
  • Family history of raised cholesterol
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9
Q

What level is the cut off for raised cholesterol in adults?

A

7.5mmol

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10
Q

What level is the cut off for raised LDLs in adults?

A

4.9mmol

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11
Q

What level is the cut off for raised cholesterol in children?

A

6.7mmol

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12
Q

What level is the cut off for raised LDLs in children?

A

4mmol

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13
Q

How is familial hypercholesterolaemia managed? (4)

A
  • Repeat LDL measurement to confirm
  • Cascade testing = family history
  • Start high intensity statin treatment
  • Diet and lifestyle advice
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14
Q

What is the effects of statins on cholesterol synthesis? (2)

A
  • HMG CoA reductase is inhibited

- Increased LDL liver uptake

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15
Q

What is HMG CoA reductase being inhibited by statins mean?

A

HmG CoA is not converted to mevalonate, one of the precursors of cholesterol

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16
Q

What is type III hyperlipoproteinaemia? (4)

A
  • Autosomal recessive
  • Polymorphism of APOE2
  • Cholesterol increased
  • Triglycerides increased
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17
Q

What are the symptoms of type III hyperlipoproteinaemia? (2)

A
  • Palmar xanthomata

- Eruptive xanthoama on elbow/knee points

18
Q

What gene is linked to type III hyperlipoproteinaemia?

A

APOE2

19
Q

Is hyperlipoproteinaemia responsive to diet/statins?

A

Yes

20
Q

What are the 2 types of hypertriglyceridaemia?

A
  • Primary

- Secondary

21
Q

List 2 examples of primary hypertriglyceridaemia

A
  • Familial combined hyperlipidaemia

- Polygenic hypertriglyceridaemia

22
Q

List 3 examples of conditions causing secondary hypertriglyceridaemia

A
  • Uncontrolled diabetes
  • Hypothyroidism
  • Alcohol related liver disease
23
Q

What is the upper reference range for triglycerides?

A

2.3 mmol/L

24
Q

When taking a TG sample what condition does a patient need to be in compared to taking a cholesterol sample?

A

Patient = fasting in TG sample, not cholesterol

25
Q

What are the symptoms of severe hypertriglyceridaemia?

A
  • Eruptive xanthomata

- Lipaemia retinalis (white lines across retina)

26
Q

What non cardiac problem is associated with hypertriglyceridaemia?

A

Acute pancreatitis

27
Q

What puesdo condition is hypertriglyceridaemia associated with?

A

Psuedohyponatraemia

28
Q

What is the management of hypertriglyceridaemia? (4)

A
  • Drugs
  • Lose weight
  • Restrict saturated fats not carbs
  • Manage secondary causes e.g diabetes/thyroid functiion
29
Q

What drugs are used in all types of hyperlipdaemia? (3)

A
  • Statins
  • Ezetimibe
  • Bile acid sequestrant
30
Q

What drug is used in familial hypercholesterolaemia to reduce LDLs?

A

Fibrates

31
Q

What drug is used in homozygous familial hypercholesterolaemia only?

A

Apheresis

32
Q

List the common statins used in the UK. What is the most common? (5)

A
  • Atorvastatin (most common)
  • Simvastatin
  • Pravastatin
  • Fluvastatin
  • Rosuvastatin
33
Q

What is the strongest type of statin used in the UK? Can it be given in primary care?

A

Rosuvastatin - can’t be given in primary care

34
Q

What are the most common side effects of statins? (3)

A
  • Muscle pain
  • Myopathy
  • Rhabdomyolysis
35
Q

What should be checked when giving statins and why?

A
  • CK levels

- Could indicate rhabdomyolysis

36
Q

At what upper limit of the reference range should statins be stopped? And what is the next step? (2)

A

If 10x

- If pain persists, investigate further

37
Q

What is the effect of ezetimbe?

A

Decreases cholesterol absorption from gut by reducing exogenous pathway

38
Q

How is ezetimbe used in treatment? (2)

A
  • Not first line use

- In combo with statins for familial hypercholestrolaemia

39
Q

How much of the population does familial hypercholesterolaemia affect?

A

1:500

40
Q

What is puesdohyponatraemia?

A

measured sodium concentration is low, but the true physiological plasma sodium concentration is normal

41
Q

How can hyperlipidaemia lead to puesdohyponatraemia? (4)

A
  • More triglycerides in sample means less aqueous portion of sample
  • Sodium is in aqueous portion
  • Conc in aqueous portion is the same
  • Conc of sodium in total sample decreased
42
Q

What are the next steps when a hyponatraemic result is found in a patient with hyperlipidaemia? (2)

A
  • Check plasma osmolality of sodium is normal

- Contact biochem lab for blood gas sodium measurement

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