lipid modification Flashcards

1
Q

What are the high intensity statins, and their doses?

A
  • Atorvastatin 20mg, 40mg, 80mg
  • Rosuvastatin 10mg, 20mg, 40mg
  • Simvastatin 80mg
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2
Q

MHRA advice - simvastatin

A
  • increased risk myopathy with high dose simvastatin (80mg)
  • consider only in pt with severe hypercholesterolaemia and high risk of CV complications who have not achieved their treatment goal s on lower doses
  • benefit vs risk only!
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3
Q

What to do if pt still has high triglyceride levels even after LDL-C has reduced adequately with statins

A
  • Add e.g. fenofibrate
  • Fibrates more effective in reducing triglyceride concentration
  • Max. dose 200 mg daily with concurrent use of a statin!
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4
Q

What to offer pt with familial hypercholesteorlaemia and why

A
  • High risk of premature CHD
  • Offer lifelong lipid modifying therapy to all pt
  • And advice on lifestyle changes to all pt
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5
Q

what is the primary target for reducing CV risk with lipid modifying treatment

A

Non-HDL cholesterol (replaced LDL cholesterol)

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6
Q

what are the healthy levels of all cholesterol

A
  • Total cholesterol <5mmol/L
    ○ TOO HIGH = 5-6.4 mmol/L
    ○ VERY HIGH = 6.5-7.8 mmol/L
    ○ EXTREMELY HIGH = >7.8mmol/L
  • Non-HDL <4mmol/L
  • HDL >1mmol/L
    ○ HDL is the good cholesterol which absorbs cholesterol in the blood and carries it back to liver
    ○ High levels of HDL can lower risk for heart disease and stroke
  • LDL <3mmol/L
    ○ Bad cholesterol
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7
Q

healthy levels of triglyceride, fasting and non-fasting

A
  • Fasting triglyceride <1.7mmol/L
  • Non-fasting triglyceride
    <2.3mmol/L
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8
Q

primary prevention of CVD with high intensity statin treatment should be offered to people

A
  • 25-84yrs (incl T2D) if estimated 10 year risk of developing CVD using QRISK3 is 10% or more, and lifestyle modification is ineffective/inappropriate
  • T1D (w/o need for formal risk assessment) who are >40, diabetes >10years, established nephropathy, other CVD RF
  • CKD (w/o need for formal risk assessment)
  • familial hypercholesterolaemia
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9
Q

consider offing lipid modification therapy for primary prevention of CVD to

A
  • all people with T1D (w/o need for formal risk assessment)
  • 85 or over, esp smokers/hypertension, taking into account risk vs benefit. pt pref, lifestyle modification, comorbid, polypharmacy, frailty, life expectancy (w/o need formal risk assessment)
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10
Q

before offering lipid modification treatment for primary prevention, what interventions and tests hold be implemented? (LIPID PROFILE)

A
  • clinical findings, lipid profile and FHx to judge likelihood of familial lipid disorder
  • exclude possible secondary causes (e.g. excess alcohol, uncontrolled DM, hypothyroid, liver disease, nephrotic syndrome)
  • discuss benefit of lifestyle modifications and optimise management of other modifiable CVD RF
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11
Q

Before giving lipid modification therapy, perform baseline blood tests (if not already done as part of the CV risk assessment) and a clinical assessment. Include all of the following:

A
  • take at least one lipid sample to measure full lipid profile
  • lipid measurement: total cholesterol, HDL-C, non-HDL-C, triglycerides
  • fasting sample not needed
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12
Q

What to do if a pt has total cholesterol >7.5 mmol/L and FHx premature CHD

A
  • consider possibility of familial hypercholesterolaemia
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13
Q

What do to if a pt has total cholesterol >9.0 mmol/L or non-HDL cholesterol >7.5 mmol/L

A
  • arrange for specialist assessment, even in absence of 1st degree FHx premature CHD
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14
Q

What to do if a pt has triglyceride >20 mmol/L that is not the result of excess alcohol or poor glycaemia control

A

Refer for urgent specialist review

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15
Q

What to do if a pt has triglyceride levels between 10-20mmol/L

A
  • repeat measurement with fasting test, after 5 days but within 2 weeks
  • review for potential secondary causes of hyperlipidaemia
  • seek specialist advice if conc remains above 10mmol/L
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16
Q

what to do if a pt has triglyceride conc between 4.5-9.9mmol/L

A
  • be aware that CVD risk may be underestimated by risk assessment tools
  • optimise management other CVD RF present
  • seek specialist advice if non-HDL cholesterol is >7.5 in this group of pt
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17
Q

What interventions and tests should I implement before starting lipid modification treatment for the primary prevention of cardiovascular disease? (CK)

A
  • Creatinine kinase: ask if persistent generalised unexplained muscle pain
  • if present, measure CK level
  • if raised by less than 5x UL of normal, start statin treatment at lower dose
  • if 5x UL normal, remeasure after 7 days
  • if still 5x UL normal, do not start statin treatment - seek specialist advice
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18
Q

What interventions and tests should I implement before starting lipid modification treatment for the primary prevention of cardiovascular disease? (LFTs)

A
  • alanine aminotransferase or aspartate aminotransferase
  • if abnormal, further investigations to determine cause e.g. NAFLD
  • do not routinely exclude treatment for people who have liver enzymes elevated by less than 3x UL normal
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19
Q

What interventions and tests should I implement before starting lipid modification treatment for the primary prevention of cardiovascular disease? (renal function)

A
  • including eGFR
  • CKD does not preclude the use of lipid lowering drugs as these pt are at increased risk of CVD
  • however specific doses are recommended depending on stage of CKD
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20
Q

What interventions and tests should I implement before starting lipid modification treatment for the primary prevention of cardiovascular disease? (HbA1c)

A
  • to diagnose DM
  • do not stop lipid lowering treatment due to acute elevations in blood glucose
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21
Q

What interventions and tests should I implement before starting lipid modification treatment for the primary prevention of cardiovascular disease? (TFTs)

A
  • TSH in pt with symptoms of under or overactive thyroid
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22
Q

5 factors that also need to be included in a clinical assessment before starting statin therapy

A
  • Alcohol consumption.
  • Blood pressure.
  • Body mass index.
  • Smoking status.
  • Diabetes status
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23
Q

When should I advise lipid modification therapy for secondary prevention of cardiovascular disease?

A
  • Advise adults to start lipid modification therapy if they have established CVD disease
  • e.g. past or current history of myocardial infarction, angina, stroke, transient ischaemic attack, or peripheral arterial disease
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24
Q

Which first-line lipid modification therapy is recommended for secondary prevention of CVD?

A
  • Offer high intensity statin treatment unless this is contraindicated (for example in pregnancy).
  • If the person is already taking a different statin for secondary prevention of cardiovascular disease, switch to a high intensity one
  • if they are taking simvastatin 80mg, speak to them about switching to e.g. atorvastatin 80mg, as there is increased myopathy risk
  • ideal: atorv 80mg daily, lower dose if interactions/increased risk adverse events/ pt requests to start with lower dose
  • need to do it alongside lifestyle measures e.g. increased exercise, reduced alcohol, good diet
25
Q

Should you offer statin in combination with bile acid sequestrates, nicotinic acid, omega-3 fatty compounds or a fibre in combination with a statin?

A

No

26
Q

What drug can you consider to treat people with primary hypercholesterolaemia

A

ezetimibe

27
Q

secondary care treatment options for people with primary non familial hypercholesterolaemia or mixed dyslipidaemia

A

aliorocumab
evolocumab

28
Q

How should I manage someone who is already taking a different statin for secondary prevention of cardiovascular disease?

A
  • discuss benefits of changing to high intensity treatment with atorv 80mg (or lower if necessary) or a medium intensity statin (e.g. simv 20 or 40mg)
  • if pt unwilling to change to atorv 80mg, reassure them they will still get benefit from current treatment
  • if pt is stable on high intensity statin simv 80, speak to them about switching to high intensity atorv instead
29
Q

How should I follow up a person after initiating lipid modification therapy for secondary prevention of CVD?

A
  • after 3 months of high intensity strain treatment, measure total cholesterol, HDL-C and non-HDL-C
  • aim of treatment: >40% reduction in baseline non-HDL-C levels
30
Q

What to do if >40% reduction in non-HCL-C is not achieved after 3 months high intensity statin

A
  • discuss adherence and timing of dose
  • optimise adherence to diet and lifestyle measures
  • consider increasing dose if <80mg atorv, if pt is judged to be at higher risk of cVD because of comorbids, risk score, or clinical judgement
31
Q

what to do if > 40% reduction in non-HDL-C is still not achieved after appropriate dose titrations of atorvastatin, or because dose titration is limited by adverse effects

A

Consider ezetimibe co-administered with atorvastatin for people with primary hypercholesterolaemia (consider seeking specialist advice).

32
Q

monitoring - statins

A
  • recheck LFTs within 3 months of starting treatment, and again at 12 months.
  • further monitoring is not necessary unless clinically indicated (for example symptoms or signs of hepatotoxicity develop).
33
Q

how often should you review statin treatment, and what should you discuss

A
  • annually
  • consider performing a non-fasting blood test for non-HDL-C to inform the discussion
  • discuss adherence and lifestyle factors
  • discuss with people who are stable on a low- or medium-intensity statin the likely benefits and potential risks of changing to a high-intensity statin
34
Q

what to do if unexplained muscle symptoms e.g. pain, tenderness, weakness occur

A
  • check CK (do not measure in asymptomatic people)
  • if CK <5x UL normal, reassure that symptoms unlikely to be due to statin and explore other causes
  • stop statin if CK 5x or more UL normal
  • consider stopping treatment if muscular symptoms severe and cause daily discomfort, even if CK levels are not >5x UL normal
35
Q

If other adverse effects are reported when taking high-intensity statin treatment, discuss the following possible strategies with the person:

A
  • stopping statin and trying again when symptoms resolves to check if they are related to statin use
  • reduce dose within same intensity group
  • changing to a statin in a lower intensity group
36
Q

For people taking ezetimibe monotherapy (if statins are contraindicated or not tolerated), consider the following combination if ezetimibe alone does not control low-density lipoprotein cholesterol well enough.

A
  • NUSTENDI: ezetimibe with bempedoic acid
37
Q

When would you offer icosapent ethyl in people already taking a statin

A
  • for people at high risk of CV events and have raised fasting triglycerides (1.7mol/L or above), if they have established CVD< and LDL-C between 1.04-2.60mmol/L
38
Q

When would you offer inclistiran as an option for treating primary hypehoeolsolaemia or mixed dyslpiademia ask an adjunct to diet

A
  • Hx of CV events e.g. ACS (unstable angina, MI), coronary or other arterial revascularisation procedures, CHD, ischaemic stroke, PAD

and

  • LDL-C conc persistently >2.6mmol/L or more desire max tolerated lipid lowering therapy
39
Q

Pt with primary heterozygous familial hypercholesterolaemia who have contraindications to, or are intolerant of statins, can be considered for treatment with

A

ezetimibe as monotherapy

40
Q

Treatment with fibrate or bile acid sequestrant (e.g. cholestyramine or colestipol HCl) can be considered under specialist advice in pt who…

A

statin or ezetimibe are inappropriate/not tolerated

41
Q

Combination of a statin + fibrate

A

carries an increased risk of muscle-related SE (including rhabdomyolysis) and should be used under specialist supervision

42
Q

concomitant use of gemfibrozil + statin

A

increases risk of rhabdomyolysis considerably - DO NOT USE THIS COMBINATION

43
Q

Name some filtrates

A
  • gemfibrozil
  • fenofibrate
  • bezofibrate
  • ciprofibrate
44
Q

name the medium intensity statins and doses

A
45
Q

name the low intensity statins and their doses

A
46
Q

which statins need to be taken at bed time and why

A

Simvastatin, pravastatin & fluvastatin
Because these have shorter half lives
Cholesterol is synthesised at night

47
Q

MOA statins

A

Statins competitively inhibit 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase, an enzyme involved in cholesterol synthesis, especially in the liver.

48
Q

MHRA advice - all statins, myasthenia graves

A
  • small no. of new onset, or exacerbations of myasthenia graves or ocular myasthenia
  • most cases, pt recover after stopping statin treatment
  • symptom onset ranged from a few days to 3 months after starting statin treatment
  • refer pt who present with suspected new onset mg symptoms after starting statin to neurologist
  • pt should inform HCP of Hx MG or OM as it may exacerbate symptoms
  • pt to continue taking statin unless advised to stop
  • pt to inform Dr of symptoms e.g. weakness arms legs that worsens after activity, double vision, drooping eyelids, difficulty swallowing, SOB
  • seek immediate medical attention if severe breathing or swallowing problems
49
Q

cautions for all statins

A
  • RF for muscle toxicity incl myopathy or rhabdomyolysis e.g. elderly, P/FHx muscle disorders, Hx liver disease, high alcohol intake
  • hypothyroidism should be managed adequately before starting treatment with statin
50
Q

Common SE all statins

A
  • arthralgia
  • asthenia
  • constipation
  • diarrhoea
  • dizzy
  • flatulence
  • GI discomfort
  • headache
  • muscle complaints
  • nausea
  • sleep disorders
  • thrombocytopenia
51
Q

statins & diabetes

A

Statins should not be discontinued if there is an increase in the blood-glucose concentration as the benefits continue to outweigh the risks.

52
Q

statins & interstitial lung disease

A

If patients develop symptoms such as dyspnoea, cough, and weight loss, they should seek medical attention.

53
Q

conception and contraception with statins

A

adequate contraception is required during treatment and for 1 month afterwards.

54
Q

use in pregnancy - statins

A

Statins should be avoided in pregnancy (discontinue 3 months before attempting to conceive) as congenital anomalies have been reported and the decreased synthesis of cholesterol possibly affects fetal development.

55
Q

use in BF - statins

A

avoid

56
Q

use in HI, all statins

A

In general, manufacturers advise caution (risk of increased exposure); avoid in active disease or unexplained persistent elevations in serum transaminases.

57
Q

monitoring requirements for all statins BEFORE treatment

A
  • one full lipid profile (non-fasting): TC, HDL, non-HL, triclyceride
  • TSH
  • renal function
  • LFTs
  • CK in pt with persistent, generalised unexplained muscle pain
  • FBGC or HbA1c in pt at high risk DM
58
Q

ongoing monitoring requirements for all statins

A
  • FBGC or HbA1c in pt at high risk DM after 3 months of starting
  • Liver function within 3 months, and at 12 months of treatment