T3 - Hyperlipidaemias Flashcards

1
Q

when was the framingham heart study established and what was the purpose?

A

established in 1948 with the purpose to identify risk factors that contribute to CVD in those without CVD history

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2
Q

what are the six major risk factors for CVD established from the FHS?

A

hypertension, smoking, obesity, high blood cholesterol, diabetes and low physical activity

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3
Q

what risk factors does QRISK3 take into account?

A

age, sex, cholesterol:HDL ratio, BP, diabetes smoking

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4
Q

what QRISK score means a patient should go on primary prevention of lipid lowering therapy?

A

> 10

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5
Q

what is primary prevention of lipid lowering therapy?

A

statins

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6
Q

in what situation may the QRISK score not be suitable for assessing risk?

A

in those with familial hypercholesteroleaemia or other inherited lipid metabolism disorders

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7
Q

does a full lipid profile require a fasting blood sample?

A

no

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8
Q

what three factors may lead to consideration of familial HCE?

A

total cholesterol >7.5mmol/L, history of HCE or premature CHD

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9
Q

what is the dose and statin of choice for primary prevention?

A

20mg of atorvastatin

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10
Q

what is the drug of choice and dose for secondary prevention (ie with previous history of CVD)

A

80mg atorvastatin

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11
Q

what condition may be caused by lipid disorders and what is this associated with

A

pancreatitis associated with high serum triglycerides

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12
Q

what ligand does LDL R recognise and where is this found?

A

ApoB-100 in the plasma membrane of LDL

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13
Q

where are most LDL Rs present?

A

on hepatocytes in the liver

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14
Q

what drug is used in patients that do not tolerate statins well?

A

ezetimibe

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15
Q

what is the mechanism of action of ezetimibe and what does it cause?

A
  • potent selective inhibitor of cholesterol absorption in the SI
  • decreases cholesterol and Tis
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16
Q

what is the mechanism of action of bile acid sequestrates and what does this cause?

A

bind bile acids in the intestine and stop recycling by interrupting enterohepatic circulation

  • this causes increased conversion of cholesterol to bile acids in the liver
  • also increases LDL R expression to remove cholesterols from the blood
17
Q

what enzyme do fibrate drugs activate and what does this cause?

A

lipoprotein lipase

  • causes increased peripheral lipolysis, decreased hepatic TG production and increased reverse cholesterol transport
  • decreases TG and increases HDL
18
Q

what does omega 3 inhibit and what does it promote?

A

inhibits lipogenesis and promotes beta oxidation of fatty acids

19
Q

what is the result of PCSK9 inhibitors and in what circumstance is it given?

A

increased LDL R on hepatocyte surface therefore increased LDL absorption
- only given to very high risk patients

20
Q

what are the three main patterns of lipoprotein abnormalities?

A

1) HCE
2) mixed hyperlipidaemia (dyslipidaemia)
3) hypertriglycerideamiea

21
Q

how is HCE characterised?

A

raised total and LDL cholesterol

- familial

22
Q

which patients is mixed HLE commonly seen in and what influences it?

A

patients with glucose intolerance and diabetes

- often influenced by lifestyle

23
Q

what may hypertriglycerideaemia cause?

A

pancreatitis

24
Q

what is the inheritance pattern of familial HCE and what is the incidence?

A

autosomal dominant and 1 in 200-250

25
where are most mutations found in familial HCE and where are they found in 3% of all cases?
- most common mutations in LDL R | - 3% mutations in ApoB or GOF in PCSK9
26
why may females develop CVD later in life?
they are protected by oestrogen
27
what is the clinical presentation of familal HCE? (5 things)
tendon xanthoma (cholesterol accumulation in tendons), corneal arcus, skin bump, intimal thickening, diffuse arterial narrowing and low flow velocity
28
how is familial HCE treated?
- low sat fat diet and exercise - statins for all patients at any age - may add cholesterol inhibitor eg ezetimibe - anti PCSK9 - LDL aphesis - surgical removal of LDL - self help and DNA testing