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39 Cards in this Set
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In general from what age should adults have their lipid levels checked and how frequently should they be checked if the result is normal? |
Adults should have their blood lipids assessed every five years starting at 45 years of age ATSI adults should have lipid tests performed every five years from 35 years of age |
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Lipid levels should be interpreted in the context of what? |
Absolute CVD risk assessment after 45 years of age (35 years of age for ATSI peoples) |
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For patients with low CVD risk <10% what intervention should be done and how often should their lipids be tested? |
Provide lifestyle advices Repeat lipids every 5 years |
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For patients with moderate CVD risk 10-15% what intervention should be done and how often should their lipids be tested? |
Provide intensive lifestyle advice Consider pharmacotherapy = if not reaching target after 6/12 OR if family history of premature CVD or patient is ATSI, South Asian, Middle Eastern, Maori or Pacific Islander descent. Repeat lipids every two years. |
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For patients with high CVD risk >15% OR clinically determined high risk factors what intervention should be done and how often should their lipids be tested? |
Provide intensive lifestyle advice Commence cholesterol-lowering therapy (simultaneously with antihypertensive unless CI) Repeat lipids every 12/12 |
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What are the clinically determined high risk factors, putting someone in the high risk group for cholesterol and lipids? |
Diabetes + >60 years of age Diabetes + microalbuminuria CKD; persistent microalbuminuria or stage 3a/4 Previous dx of familial hypercholesterolaemia SBP ≥180 mmHg or DBP ≥110 mmHg Serum total cholesterol >7.5 mmol/L ATSI peoples aged >74 years Existing CVD - event or symptomatic |
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How is a definitive diagnosis of high lipids made? |
If lipid levels are abnormal, a second confirmatory sample should be taken on a separate occasion (as levels may vary between tests) before a definitive diagnosis is made. A fasting sample should be used when assessing elevated TGs. |
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What dietary advice should be given to the patient with dyslipidaemia? |
Effective dietary changes for improving lipid levels include: Reducing saturated and trans fats Replacing saturated fats with monounsaturated and polyunsaturated fats Increasing soluble fibre Introducing plant sterol–enriched milk, margarine or cheese products. |
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What lifestyle advice should be given to assist in lowering lipid levels? |
Advise to aim for healthy targets: Encourage any physical activity and aim for at least 30 minutes of moderate-intensity physical activity on most, if not all, days Recommend smoking cessation Suggest a target waist measurement <94 cm for men and <80 cm for women, and a BMI <25 kg/m2 Recommend salt restriction ≤4 g/day (65 mmol/day sodium) Encourage limiting ETOH to ≤2 SD/day for males and ≤1 SD/day for females |
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When using pharmacotherapy for primary prevention what lipid levels should we aim for? |
Lipid-lowering therapy for primary prevention should (while balancing risks and benefits) aim towards: total cholesterol <4.0 mmol/L HDL-C ≥1.0 mmol/L LDL-C <2.0 mmol/L non-HDL-C <2.5 mmol/L TG <2.0 mmol/L |
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When lipid lowering is started how long does it take to have an effect on lipid levels? And how long is it normally prescribed for? |
Most lipid levels respond to therapy within 2 to 3 weeks and usually stabilise within 1 to 3 months. Treatment of dyslipidaemia is generally life long. Before starting drug therapy, confirm that the dyslipidaemia is not secondary to a treatable problem. |
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What are some of the secondary causes of dyslipidaemia that need to be excluded? |
ETOH use Oestrogen use Type 2 diabetes Obesity Renal impairment Smoking Drug therapy Hypothyroidism Nephrotic syndrome Cholestasis Anorexia nervosa |
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In order to decrease CVD events which lipid level are we most trying to change? And which medication is used to do this? |
Decreasing the number of CVD events is related mainly to the extent of lowering of atherogenic lipoproteins, reflected by reduction in LDL-C and non–HDL-C. Although this benefit is not drug specific, the weight of evidence favours the use of statins. |
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What are some of the common statins used in the treatment of dyslipidaemia and at what dose? |
Atorvastatin = 10 - 80 mg daily Pravastatin = 20 - 80 mg daily Rosuvastatin = 5 - 40 mg daily Simvastatin = 10 - 80 mg daily Fluvastatin = 20 - 80 mg daily |
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When starting statins one should prescribe the lowest dose possible and titrate the medication over what time period? |
The dose should be titrated every 4 - 8 weeks to achieve target lipid levels. Maximum response to a dose can be expected within 4 weeks of initiation or dose increase. High doses of statins should only be used in patients who have not achieved target lipid levels on lower doses. |
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When should other drugs be added to statin therapy? |
Other drugs should be added to statin therapy when target lipid levels have not been achieved with the maximum tolerated dose of statin OR in patients who are unable to tolerate statins. |
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What are the additional medications that can be added to statin therapy, or used in patients who cannot tolerate statin therapy? |
Ezetimibe, bile acid binding resins, nicotinic acid and fibrates. Depending on requirements, combinations of statin, ezetimibe, nicotinic acid and fenofibrate are feasible. |
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What is the role of fish oil in treating dyslipidaemia? |
Fish oil lowers triglycerides but does not reduce LDL-C. The sugar cane derivative policosanol has been shown to be ineffective. |
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If using ezetimibe what dose is used? |
Ezetimibe 10 mg orally, daily. Has a synergistic effect when used in combination with a statin, but also well tolerated and lowers lipids when used instead of statins. |
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When are bile acid binding resins used in dyslipidaemia? And when should they not be used? |
If LDL-C is still not well controlled, or there are adverse effects from ezetimibe, consider adding a bile acid binding resin to statin therapy. Bile acid binding resins are mainly used in combination with statins, but they can be used alone or in combination with other drugs, including ezetimibe. Resins increase triglyceride levels and are inappropriate in mod-severe hypertriglyceridaemia. |
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Which bile acid binding resin medications can be used and at what dose? |
Cholestyramine 4 - 8 g orally, daily in the morning, increasing up to 24 g daily in divided doses if required OR Colestipol 5 - 10 g orally, daily in the morning, increasing up to 30 g daily in divided doses if required. Assess the patient's tolerance of the dosage after 4 - 6 weeks. |
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What are some of the common adverse effects of bile acid binding resins? |
GIT adverse effects. The drug must be thoroughly mixed with an adequate volume of fluid (eg fruit juice) to minimise upper GIT disturbance. To minimise constipation, increase soluble fibre and fluid intake, with or without laxative use. Bile acid binding resins may influence LFTs via bile acid metabolism, but they are not systemically absorbed so no monitoring is required. They can interfere with absorption of other drugs taken concurrently, particularly oral anticoagulants, thyroxine, cyclosporin and digoxin. |
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When is nicotinic acid used in the treatment of dyslipidaemia? |
Nicotinic acid is rarely used because it is poorly tolerated, mainly due to flushing. Gastric irritation, gout and impaired glucose tolerance can also occur. Flushing may be minimised by giving nicotinic acid with food, increasing the dose gradually, and using prophylactic aspirin. Patients taking nicotinic acid should have their blood glucose, plasma urate, CK and LFTs monitored at initiation and dose adjustment. |
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When are fenofibrates used in treating dyslipidaemia? |
The addition of fenofibrate may lead to a 5% to 10% reduction of LDL-C. Although product information warns against combination use, studies suggest that combining fenofibrate with a statin does not increase the risk of myopathy beyond the level seen with statin monotherapy. |
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When a patient has predominant elevation of their triglycerides what medication is indicated? And at what triglyceride levels should this medication be used? |
Drug therapy with a fibrate and/or fish oil is indicated if: Triglyceride elevation is severe (>10 mmol/L) Triglyceride >4 mmol/L and is associated with low HDL-C (<1 mmol/L) Triglyceride elevation is associated with increased absolute CVD risk. |
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What dose of fenofibrate or fish oil should be used in hypertriglyceridaemia? |
Fenofibrate 145 mg orally, daily (reduce dose in patients with renal impairment) OR Gemfibrozil 600 mg orally, twice daily AND/OR Fish oil (1.2 - 3.6 g of omega-3) orally, daily. |
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What other factors are central to the management of hypertriglyceridaemia? |
Dietary modification, behavioural risk factor modification (eg weight loss, increased physical activity, alcohol avoidance) and diabetic control. It is not appropriate to manage severe triglyceride elevation (>10 mmol/L) with statin monotherapy; max doses of fish oil and fibrate are usually needed, and special dietary measures and careful surveillance required. Some cases are extremely resistant to treatment and may warrant referral for specialist management. |
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In a patient with absolute CVD risk high, LDL-C elevated and triglycerides mildly to moderately elevated (up to 4 mmol/L) what is the recommended first line treatment? |
Statin therapy |
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In a patient with absolute CVD risk high, LDL-C elevated and triglycerides >4 mmol/L, what is the recommended first line treatment? |
Statins alone are unlikely to achieve ideal levels of both triglycerides and total cholesterol. Fibrates are appropriate first-line therapy in this situation, but their effect on total cholesterol is limited. Treat for predominant elevation of triglycerides. |
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What is the best treatment for cases of mixed hyperlipidaemia in which a lipid abnormality is persistent or more severe? |
A combination of a cholesterol-lowering drug and a triglyceride-lowering drug is necessary. Safe and effective combinations include: Statin + fish oil Fibrate + ezetimibe Where necessary, statin + fenofibrate or statin + nicotinic acid, may also be used with caution. |
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What are the 2 serious side effects of lipid modifying drugs? |
Liver dysfunction Muscle problems |
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What monitoring should be done to check for these side effects and how frequently should this be done? |
Liver and muscle biochemistry - ALT and CK Tested at baseline and when the response of lipids is assessed (1 - 2 months after initiation or dosage adjustment). It is no longer considered necessary to routinely monitor LFTs and CK unless the patient develops symptoms or signs of liver dysfunction or muscle problems. |
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At what level of CK elevation should statins be stopped? Can patients with mild muscle symptoms still be treated with statins? |
If asymptomatic CK elevation is detected, measurement should be repeated after avoidance of exercise for several days. Treatment may continue provided CK does not exceed 5 times the upper limit of normal. Consider whether a drug interaction or other acute event (eg trauma, surgery) precipitated CK elevation.Patients who experience mild muscle symptoms still benefit from the maximum tolerated dose of statin. Low-dose intermittent therapy (second daily or twice weekly) is often effective and well tolerated. |
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At what level of ALT or CK, and with what symptoms should statins be stopped? |
Previously normal ALT is persistently > 3x ULN CK is >10 x ULN CK is >5 x ULN and muscle symptoms Persistent unexplained muscle pain Persistent unexplained muscle weakness. |
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In treating dyslipidaemia when is it important to check blood glucose levels? |
High-dose statins may slightly impair glucose metabolism, while nicotinic acid can cause impaired glucose tolerance as well as hyperuricaemia and gout. Check blood glucose before starting therapy, and repeat 1- 2 months after starting therapy or adjusting the dose. |
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How common is familial hypercholestrolaemia? What is its inheritance? In which patients should be consider familial hypercholestrolaemia may be present? |
Familial hypercholesterolaemia is a dominantly inherited condition that affects > 1 in 500 people and accelerates CVD by 20 - 40 yrs. Consider in patients with severely elevated LDL, or those with tendon xanthomata or a strong family history of premature CVD events. Approximately 50% of family members are affected, so identification by family cascade screening is important. |
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How is familial hypercholestrolaemia diagnosed? |
Diagnosis requires exclusion of secondary causes of hypercholesterolaemia AND Clinical evaluation = using the Dutch Lipid Clinic Network Score. Cases of definite or probable familial hypercholesterolaemia should be confirmed by genetic diagnosis to assist family cascade screening via specialised clinics. Cases of possible familial hypercholesterolaemia should be reviewed regularly (every 2 years) to identify additional features, especially evidence of the development of CVD. |
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How is familial hypercholestrolaemia managed? |
The usual principles of lipid-modifying therapy apply to the management of familial hypercholesterolaemia, but combination therapy and additional monitoring may be required. Detailed information on management is available in the Familial Hypercholesterolaemia Australasia Network consensus model of care. |
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What are some of the other side effects of statins? |
Common - myalgia, mild transient GI symptoms, headache, sleep disturbance (eg insomnia, nightmares), dizziness, elevated ALT. Rare - myopathy, rhabdomyolysis, renal failure, hepatitis, liver failure, pancreatitis, alopecia, paraesthesia, peripheral neuropathy, sexual dysfunction, memory loss, gynaecomastia, hypersensitivity, anaphylaxis, angioedema, toxic epidermal necrolysis, interstitial lung disease, thrombocytopenia, visual disturbances (blurred vision, diplopia). |
