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HLB Cardiac > Dyslipidaemias: diagnosis, pharmacotherapy and prevention > Flashcards

Dyslipidaemias: diagnosis, pharmacotherapy and prevention Flashcards

1
Q

What does cholesterol mean?

A
  • cholos = bile - steros = solid - ol = alcohol
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2
Q

What does atherosclerosis mean?

A
  • atheros = greek work for glue - sclerosis = german for hardening
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3
Q

What is the basic structure of a triglyceride?

A
  • glycerol backbone - three fatty acids
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4
Q

What is a lipoprotein?

A
  • proteins that are soluble in water - able to carry lipids around the body
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5
Q

What are the 3 main components of lipproteins?

A

1 - cholesterol 2 - triglycerides 3 - apoproteins

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6
Q

What is the primary aspect of lipoproteins that determines the structure and function?

A
  • apoproteins
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7
Q

What is the main element of the core of lipoproteins?

A
  • cholesterol esters - triglycerides
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8
Q

What is the main element of the outer surface of lipoproteins?

A
  • apoproteins - phospholipids - cholesterol free
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9
Q

What is the major difference between free and esterified cholesterol?

A
  • free = biologically active but cytotoxic - ester = safe/protected form for storage
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10
Q

What are the 2 different lipoproteins that we need to be aware of that are commonly measured in the blood?

A
  • low density lipoproteins (LDL) - high density lipoproteins (HDL)
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11
Q

Why are low density lipoproteins (LDL) classed as the bad lipoproteins?

A
  • they contain the majority of the bodies cholesterol - stored in body as fat
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12
Q

Where is the majority of the cholesterol in the body prodcued?

A
  • liver
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13
Q

What is 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA)?

A
  • intermediate precursor of cholesterol
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14
Q

What is the rate limiting step and the target of statins in an attempt to reduce cholesterol synthesis?

A
  • 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase - HMG-CoA converted to Mevalonate
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15
Q

How are bile acids formed?

A
  • synthesised in liver from cholesterol
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16
Q

What is the function of bile acids?

A
  • secreted into GIT by gall-bladder - act as emulsifiers for fat digestion
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17
Q

What is the basic principle of exogenous lipid transport?

A
  • lipids digested in GIT - processed into chylomicrons - absorbed into lymphatic system
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18
Q

Once chylomicrons have been absorbed during exogenous lipid transport, how are triglycerides and fatty acids absorbed by capillaries?

A
  • lipoprotein lipase released from capillaries - triglycerides released from chylomicrons
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19
Q

Once chylomicrons have moved throughout the body, what happens to the remnants of them during exogenous lipid transport?

A
  • remnants rich in cholesterol return to liver - cholesterol and bile are secreted into GIT
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20
Q

What is the basic principle of endogenous lipid transport?

A
  • liver processing of lipoproteins - lipoproteins delivered around the body
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21
Q

In endogenous lipid transport what are the 2 main lipoproteins released from the liver?

A
  • very low density lipoproteins (VLDL) - low density lipoproteins (LDL)
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22
Q

In endogenous lipid transport very low density lipoproteins (VLDL) are created and released from the liver into the circulation. What is the first thing that happens to them in the capillaries?

A
  • lipoprotein lipase is released from capillaries - TAG and fatty acids are released from VLDL and absorbed by capillaries
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23
Q

In endogenous lipid transport once very low density lipoproteins (VLDL) have had most of their TAGs absorbed by capillaries, what do VLDL become?

A
  • intermediate lipoproteins
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24
Q

In endogenous lipid transport what happens to the intermediate lipoproteins that are formed from VLDL?

A
  • enter the liver - processed into low density lipoproteins
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25
Q

In endogenous lipid transport what happens to low density lipoproteins (LDL)?

A
  • LDLs are transported to peripheries - LDL receptors bind to LDL - cholesterol is stored in tissues
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26
Q

What is the reverse pathway involved in lipid transport?

A
  • free cholesterol in tissues is absorbed by high density lipoproteins (HDL) - HDL transport cholesterol to liver for processing
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27
Q

What are the 3 pathways for lipid transport in the body?

A

1 - exogenous 2 - endogenous 3 - reverse

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28
Q

What is included in total cholesterol, and what is the healthy target?

A
  • LDL and HDL - <5mmol/L - LDL/HDL ratio >3.5
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29
Q

What is the healthy target for LDL?

A
  • <3mmol/L
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30
Q

What is the healthy target for HDL?

A
  • >1.5mmol/L
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31
Q

What is the healthy target for triglycerides?

A
  • 0.5 - 2mmol/L
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32
Q

What is primary dyslipidaemia?

A
  • error in metabolism - generally caused by genetics
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33
Q

What are the 2 most common things affected by primary dyslipidaemia?

A
  • abnormal lipoprotein structure - abnormal lipoprotein receptors
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34
Q

What is the Frederick classification?

A
  • classification of dyslipidaemia
35
Q

What is familial hypercholesterolaemia type IIa?

A
  • very high LDL cholesterol
  • >5mmol/L even from birth
  • >7/5mmol/L for total cholesterol
36
Q

What causes familial hypercholesterolaemia type IIa?

A
  • autosomal (non sex chromosome specific) dominant genes
  • 1 inherited = bad
  • 2 inherited = really bad
37
Q

What do the specific mutations in familial hypercholesterolaemia type IIa cause?

A
  • mutations causing absence or very low LDL receptors
  • cholesterol remains in blood
  • increased risk of atherosclerosis
38
Q

Is familial hypercholesterolaemia type IIa common?

A
  • no - 0.5% of the population
39
Q

What is familial combined hyperlipidaemia type IIb?

A
  • moderatley high levels of LDL, VLDL and triglycerides
40
Q

What causes familial combined hyperlipidaemia type IIb?

A
  • autosomal (non sex chromosome specific) dominant genes
  • 1 inherited = bad
  • 2 inherited = really bad
  • can be a number of genetic causes
41
Q

How common is familial combined hyperlipidaemia type IIb?

A
  • relatively common
  • 10% of population
42
Q

What are 2 very common clinical presentations, what may be useful in identifing a patient with familial combined hyperlipidaemia type IIb?

A
  • insulin resistance
  • obesity
43
Q

In familial combined hyperlipidaemia type IIb what is the most common apolipoprotein affected?

A
  • mutated apolipoprotein B-100 (ApoB-100)
  • overproduction of ApoB-100
  • common in LDL and VLDL
44
Q

Familial combined hyperlipidaemia type IIb accounts for 20% of what premature what?

A
  • premature ischemic heart disease
  • premature = anyone <70%
45
Q

What is familial hypertriglyceridaemia type IV?

A
  • elevated triglycerides
  • >5mmol/L
  • cholesterol can be normal
46
Q

What are 3 very common clinical presentations of patients with familial hypertriglyceridaemia type IV?

A
  • insulin resistance
  • obesity
  • eruptive xanthomas
47
Q

What is one of the most common finding in patients with familial hypertriglyceridaemia type IV that is difficult to understand why it happens?

A
  • acute pancreatitis
  • seen in patients with triglyceride levels >10mmol/L
48
Q

What causes familial hypertriglyceridaemia type IV and is it common?

A
  • multiple genetic defects
  • 1% of population
49
Q

What is familial hyperchylomicronamia type I?

A
  • increased chylomicrons
  • deficiency in lipoprotein lipase of capillaries
  • blood is creamy
  • genetic defects
50
Q

What is familial dysbetalipoproteinemia type III?

A
  • decreased apoprotein E
  • poor clearance of cholesterol by liver
  • causes palmar xanthomas
  • genetic defects
51
Q

What is xanthelasmata?

A
  • xanthos is greek for yellow
  • elesma greek for plate/near eye
  • fatty deposits around the eyes
  • normally macrophages containing lipids
52
Q

What is tendon xanthoma?

A
  • fatty build up in tendons
53
Q

What is palmar xanthoma?

A
  • fatty build up on palms of hands
  • common in familial dysbeta-lipoproteinemia
54
Q

What is eruptive xanthoma?

A
  • red/pink lumps - itchy and raised
  • common in hypertriglyceridaemia
55
Q

Are there any operations for hyperlipidaemia?

56
Q

What is the most common advice given to someone with hyperlipidaemia?

A
  • lifestyle interventions
57
Q

What is the first line of defence for a patient with hyperlipidaemia?

58
Q

What is the mechanism of action for statins?

A
  • inhibit HMG-Coa reductase in liver - HMG-CoA does not become mevalonate
59
Q

What are the main effects on lipoproteins and triglycerides following statins?

A
  • ⬇️ LDL, total cholesterol and TAG - ⬆️ HDL
60
Q

What are the 2 most common statins prescribed?

A
  • atorvastatin (MOST COMMON) - simvastatin
61
Q

Statins have been shown to reduce all cause mortality, but what does that mean?

A
  • reduced death from any cause
62
Q

In addition to reducing cholesterol what can statins do to atherosclerosis plaque formation?

A
  • reducing inflammation from cytokines - reduce cholesterols in necrotic core - both stabilise the atherosclerosis
63
Q

What is the most common side effect from statins?

A
  • myalgia (muscle pain)
64
Q

In addition to myalgia, what other side effects can be seen with statin use?

A
  • rhabdomyolysis (muscle breakdown) - arthralgia (joint pain) - liver dysfunction
65
Q

What is the Framlington study?

A
  • study of CVD risk in the town of Framlington, USA
66
Q

What was the first risk score for cardiovascular disease?

A
  • Framlington risk score
67
Q

What are the 2 most common risk scores used in the UK?

A
  • Q-Risk - JBS3
68
Q

Which cardiovascular risk score do NICE recommend using?

69
Q

When do NICE recommend someone should be prescribed a statin?

A
  • patient has a >10% risk of developing CVD in next 10 years
70
Q

When patients are prescribed statins, how often do NICE recommend patients blood biochemistry should be tested?

A
  • every 3 months
71
Q

What is the target for LDL reduction recommend by NICE for someone taking a statin?

A
  • >40% reduction in LDL
72
Q

Are statins the only drug recommended by NICE based on estimated risk?

73
Q

What are fibrates?

A
  • drugs that aim to increased catabolism (b oxidation) - increased uptake of fats
74
Q

Bezafibrate is the first line drug of choice for patients with hypertriglycaemia. What is the mechanism of action for this drug?

A
  • increased activation of lipoprotein lipase - reduces TAG and LDL - increased HDL
75
Q

What are the common side effects of Bezafibrate?

A
  • myalgia - GIT disturbances (diarrhoea)
76
Q

Cholestyramine acts in the GIT and is a bile salt sequestrants, what is the mechanism of action of this drug?

A
  • reduces bile absorption - reduces cholesterol and LDL
77
Q

What are the side effects of Cholestyramine, a bile salt sequestrants?

A
  • reduces all fat absorption - reduces fat soluble vitamines (ADEK) - GIT disturbances (diarrhoea)
78
Q

Ezetimbe is an alternative to Cholestyramine, what is the mechanism of action of Ezetimbe?

A
  • inhibits cholesterol absorption only - commonly used alongside statins
79
Q

What are the side effects of Ezetimbe?

A
  • mild GIT disturbances (diarrhoea)
80
Q

What are PCSK9 receptors?

A
  • enzyme that binds to LDL receptors - maintains cholesterol homeostasis
81
Q

Evolocumab is a PCSK9 inhibitor, what does this drug do?

A
  • monoclonal antibody (mab at end of name) - inhibits PCSK9 enzyme - increased LDL receptors and decreased cholesterol in blood
82
Q

Evolocumab is a PCSK9 inhibitor that has been shown to be effective at reducing LDL, TAG and and increased HDL, but it is expensive. Which patients would generally be prescribed this drug?

A
  • hypercholesterolemia patients - patients non-response to statin
83
Q

What are the common side effects of Evolocumab a PCSK9 inhibitor?

A
  • cough - flu like symptoms

HLB Cardiac (24 decks)

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