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RACP Written 2018 > Cardiology - Lipids > Flashcards

Cardiology - Lipids Flashcards

(60 cards)

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1
Q

What is the role of apolipoproteins?

A

Activate enzymes needed for lipoprotein metabolism

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2
Q

What is the function of apoprotein component of lipoproteins?

A

Structural support
Receptor recognition
Enzymatic activity

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3
Q

Where is ApoB-100 made?

A

In the liver

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4
Q

Where is ApoB-48 made?

A

In the intestine

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5
Q

What is Apo-AI?

A

The major protein in HDL that has been inversely correlated with arteriographic evidence of coronary disease

it activates the enzyme lecithin-cholesterol acyltransferase (LCAT)

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6
Q

What does LCAT (lecithin-cholesterol acyltransferase) do?

A

allows the HDL particle to convert cholesterol obtained from peripheral tissues to cholesterol ester

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7
Q

What is Apo-B 100

A

The primary apoprotein of LDL which allows recognition of the particle by the LDL receptors on cell surfaces

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8
Q

What are the genes that synthesise Apo-B48 and Apo-B 100

A

Trick question. They are made by the same gene.

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9
Q

Where is Apo-E found?

A

In VLDL particles AND in chylomicrons, IDLs and HDLs.

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10
Q

What does ApoE do?

A

ApoE helps remove chylomicrons from the serum to the liver

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11
Q

What is the characteristic pathology of Type III hyperlipoproteinaemia?

A

Most Type III hyperlipoproteinaemia patients are homozygous to apoprotein E2/2 genotype

Characterised by premature atherosclerosis
(BOTH hyperchol and hypertriglyceridaemia)

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12
Q

SECONDARY causes of VLDL overproduction

A

Excessive VLDL secretion by liver is seen in:

  • high carb diets
  • alcohol
  • obesity
  • nephrotic syndrome
  • cushing’s syndrome
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13
Q

What are the two PRIMARY causes of excessive VLDL production by the liver?

A

Familial combined hyperlipidaemia (FCHL)

Lipodystrophy

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14
Q

What are the features of Familial Combined Hyperlipidaemia (FCHL)?

A
  • elevated TG and LDL-C
  • low HDL
  • Cause of hyperlipidaemia in 20% of those with IHD <60yrs old
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15
Q

What are the features of lipodystrophy?

A
  • Truncal adiposity with decreased fat in buttocks and extremities
  • insulin resistance and T2DM
  • hepatosteatosis
  • elevated TG and LDL-C
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16
Q

What are the PRIMARY causes of impaired lipolysis of TG-rich lipoprotein (with VERY HIGH triglycerides)?

A 
Familial chylomicronaemia syndrome
Familial hypertriglyceridaemia (FHTG)
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17
Q

Features of Familial chylomicronaemia syndrome

A

PROFOUNDLY elevated chylomicrons
Fasting TG VERY high

Recurrent pancreatitis
Lipaemia retinalis
Xanthomas
Hepatosplenomegaly

** NOT associated with coronary artery disease **

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18
Q

What is the inheritance of the two types of familial chylomicronaemia syndrome?

A

LPL deficiency: Autosomal Recessive

Apo-C II Deficiency: Autosomal Recessive

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19
Q

What are the features of familial hypertriglyceridaemia (FHTG)?

A

ELEVATED fasting TG
Average/low LDL-C
Low HDL-C

NOT ELEVATED APO-B
NOT ASSOC. WITH CAD

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20
Q

What are the dyslipidaemias caused by impaired hepatic uptake of ApoB-containging lipoproteins?

A

Type 3 Hypercholesterolaemia
Sitosterolemia
Cholesterol Ester Storage Disease

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21
Q

What is Type 3 Hypercholesterolaemia?

A

aka Autosomal Dominant Hypercholesterolaemia due to Mutations in PCSK9

dyslipidaemia caused by impaired hepatic uptake of ApoB-containging lipoproteins

  • autosomal dominant
  • rare
  • responds well to PCSK9 inhibition
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22
Q

What mutation causes Type 3 Hypercholesterolaemia?

A

Mutation in PCSK9

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23
Q

What is Sitosterolaemia?

A

rare, autosomal recessive

dyslipidaemia caused by impaired hepatic uptake of ApoB-containging lipoproteins

Mutations in ATP-Binding Cassette (ABCG5 and ABCG8)
ALSO get anisocytosis, poikilocytosis and splenomegaly
–> respond VERY WELL to dietary modification and ezetimibe

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24
Q

What mutation causes Sitosterolaemia?

A

Mutations in ATP-Binding Cassette (ABCG5 and ABCG8)

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25
What is Cholesterol Ester Storage Disease?
aka Lysosomal Acid Lipase Deficiency dyslipidaemia caused by impaired hepatic uptake of ApoB-containging lipoproteins ``` Autosomal recessive Elevated LDL-C Low HDL-C FATTY liver Non-obese NOT insulin resistant ```
26
What are the dyslipidaemias due to impaired hepatic Apo-B uptake?
Type 3 hyperlipoproteinaemia | = Familial Dysbetalipoproteinaemia (FDBL)
27
What is Type 3 Hyperlipoproteinaemia?
aka Familial Dysbetalipoproteinaemia (FDBL) dyslipidaemia due to impaired hepatic Apo-B uptake Autosomal recessive Mixed hyperlipidaemia Usually due to mutation in ApoE gene (only ApoE2 and ApoE3
28
What are the dyslipidaemias due to inherited low levels of Apo-B lipoproteins?
Abetalipoproteinaemia Familial hyperbetalipoproteinaemia PSCK9 Deficiency
29
What is Abetalipoproteinaemia?
A dyslipidaemia due to inherited low levels of Apo-B lipoproteins Rare autosomal recessive Associated neuro: - loss of tendon reflexes - reduced lower limb vibration and proprioception - ataxia and spastic gait - pigmented retinopathy
30
What are the dyslipidaemias due to impaired hepatic uptake of ApoB containing lipoproteins?
Secondary causes: - hypothyroidism - CKD Primary causes: - Type 1 hypercholesterolaemia (= Familial Hypercholesterolaemia "FH") - Type 2 hypercholesterolaemia (= Familial Defective APOB-100)
31
What is Type 1 hypercholesterolaemia?
aka Familial Hypercholesterolaemia "FH" A dyslipidaemia due to impaired hepatic uptake of ApoB containing lipoproteins Features: - AUTOSOMAL DOMINANT - due to loss of function mutation in LDL receptor - NORMAL TG - elevated lipoprotein (a) - VERY HIGH risk coronary artery disease (needs statin and PCSK9 inhibitor) - liver transplant is also an option
32
What is Type 2 Hypercholesterolaemia?
aka Familial Defective APOB-100 A dyslipidaemia due to impaired hepatic uptake of ApoB containing lipoproteins Features: - AUTOSOMAL DOMINANT - NORMAL TG - ELEVATED LDL-C - increased risk CAD
33
What are the treatment targets for 2013 ACC/AHA Guidelines?
No treatment targets
34
When do you initiate primary prevention for hyperlipidaemia as per 2013 ACC/AHA Guidelines?
Age >21yrs with LDL-C >=4.9mmol/L - initiate high intensity statin - aim for AT LEAST 50% reduction in LDL-C - if the LDL-C remains >=4.9 despite maximum statin then add in a non-statin drug If LDL-C level is 1.9 - 4.9mmol/L WITH DIABETES: - initiate statin age 40 - 75yrs IF their 10yr ASCVD risk >=7.5% give high intensity - IF they are <45yrs or >75yrs only CONSIDER a statin IF LDL-C level is 1.9 - 4.9mmol/L WITHOUT DIABETES: - if aged 45-75yrs AND 10yr risk >=7.5% then start moderate or high intensity statin - CONSIDER if age <45yrs or >75yrs
35
According to the 2013 ACC/AHA Guidelines for primary prevention for hyperlipidaemia in age >21yrs with LDL-C >=4.9mmol/L
- initiate high intensity statin - aim for AT LEAST 50% reduction in LDL-C - if the LDL-C remains >=4.9 despite maximum statin then add in a non-statin drug
36
According to the 2013 ACC/AHA Guidelines for primary prevention for hyperlipidaemia If LDL-C level is 1.9 - 4.9mmol/L WITH DIABETES:
- initiate statin age 40 - 75yrs IF their 10yr ASCVD risk >=7.5% give high intensity - IF they are <45yrs or >75yrs only CONSIDER a statin
37
According to the 2013 ACC/AHA Guidelines for primary prevention for hyperlipidaemia IF LDL-C level is 1.9 - 4.9mmol/L WITHOUT DIABETES:
- if aged 45-75yrs AND 10yr risk >=7.5% then start moderate or high intensity statin - CONSIDER if age <45yrs or >75yrs
38
What are the HIGH intensity statins? When using them what do you aim for?
Aim to lower LDL-C by 50% Atorvastatin 40 - 80mg Rosuvastatin 20 - 40mg
39
What are the MODERATE intensity statins? When using them what do you aim for?
Aim to lower LDL-C by 30 - 50% ``` Atorvastatin 10-20mg Rosuvastatin 5-10mg Simvastatin 20-40mg Pravastatin 40-80mg Lovastatin 40mg Fluvastatin ```
40
What is the MoA of statins?
Competitively inhibit 3-hydroxy-3-methylglutaryl Coenzyme A (HMG-CoA) reductase (rate limiting step in cholesterol production)
41
Common side effects of statins
Myopathy and rhabdo Autoimmune necrotising myopathy Sleep disturbance (insomnia and nightmares) Elevated transaminases
42
Rare side effects of statins
``` Pancreatitis Paraesthesias Peripheral neuropathy and sexual dysfunction Interstitial lung disease Thrombocytopenia ```
43
Benefits of statins?
Reduce risk MI Reduce risk stroke Reduce revascularity procedures Mortality benefit
44
Mechanism of action of cholestyramine?
Bile acid sequestrant/resin Binds bile acids in intestinal lumen to prevent bile acid resorption - -> increased demand for cholesterol to be converted to bile acid synthesis - -> increases LDL uptake and removal from plasma
45
Side effects of cholestyramine?
Exacerbates hyperTRIGLICERIDAEMIA (so avoid if TG >3mmol/L) Avoid if complete biliary obstruction Constipation Aggravation of haemorrhoids and diverticulosis Fat soluble vitamin deficiencies
46
Benefits of cholestyramine?
Reduce LDL by 15-20% | Reduces risk of nonfatal MI/death secondary to CVS in men without heart disease and total cholesterol >6.8mmol/L
47
Mechanism of action of Nicotinic Acid?
Suppresses fatty acid release from peripheral tissue especially adipose tissue If dosed >1g daily: - Reduced LDL - Reduced Triglycerides - Elevated HDL - Reduced Lipoprotein (a)
48
Side effects of Nicotinic Acid?
Peptic ulcer disease GORD In coronary artery disease it is associated with AF Vasodilation (results in hypotension) Macula oedema and reversible vision loss
49
Benefits of Nicotinic Acid?
``` Reduces total chol Reduces LDL-C Reduces triglycerides Increases HDL-C Reduces coronary artery disease Reduces CVS events ``` NO MORTALITY BENEFIT
50
What is the mechanism of action of Ezetimibe?
Reduces absorption of dietary and biliary cholesterol by inhibiting its transport across the intestine wall --> increases demand for cholesterol and increases LDL uptake
51
Side effects of Ezetimibe?
Headache Diarrhoea Raised transamnases
52
Benefits of Ezetimibe?
Reduces LDL by 18% | ONLY evidence is in combo with a statin
53
Mechanism of action of Fibrates
Activate peroxisome activated nuclear receptors and modulate lipoprotein synthesis and catabolism
54
Side effects of Fibrates
``` GIT disturbance Gallstones Pancreatitis Leukopenia Myopathy ```
55
Benefits of Fibrates
Reduce LDL by 5-15% Greatest benefits if HDL <1 and TG>2.3 Reduces non-fatal MI Reduces risk retinopathy Reduces risk progression of albuminuria NO EFFECT on MORTALITY
56
What is PCSK9?
PCSK9 = Proprotein Convertase Subtilisin-Kexin Type 9 PCSK9 binds to LDL Receptor on hepatocytes to stimulate ingestion of the LDL-R with degradation of the LDL-R-PCSK9 complex. Because of reduced numbers of LDL-R on surface there is higher blood levels of LDLs
57
What do PSCK9 inhibitors do?
Bind to PCSK9 to stop it binding to LDL-R
58
What are the names of the PCSK9 inhibitors?
Alirocumab Evolocumab Bococizumab
59
What are the benefits of PCSK9 inhibitors?
Reduce major CVS events Reduce lDL Bococizumab reduces CVS events in high risk patients
60
Neurocognitive adverse events are seen in which PCSK9 inhibitor?
Bococizumab

RACP Written 2018 (167 decks)

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