Lipid-Modifying And Antiplatelet agents Flashcards
Statin: Mechanism of action and effect
Inhibits HMG-CoA reductase that is implicated in the conversion of HMG-CoA to mevalonate, a rate-determining step in the synthesis of cholesterol. Effect: reduction in cholesterol formation—> reduction in VLDL and LDL. It has some effects on increasing HDL and TG marginally.
Statin: Adverse effects
Muscle pain (myopathy) to more severe rhabdomyolysis.
Statin: If patient is in a lot muscle pain, weakness and cramp during treatment what do you check. Why is it of serious concern.
Rise in liver enzymes (ALT) and creatinine kinase concentration (x5) discontinue therapy.
Want to rule out rhabdomyolysis.
Statin: Caution/Contraindication
Caution: hepatic impairment, renal impairment (dose adjust initial 20 mg OD —> <30 mL/min).
Contraindicated: Pregnancy ( discontinue 3 months before attempting to conceive).
Statin: Why is myopathy implicated with Statins.
Statins lower CoQ10 in serum which is necessary in the mitochondrial oxidative chain reaction and reduction in tissue results in reduced ATP production. Leading to pain in muscle.
What hour of the day would you advise patient to take Atorvastatin 20mg OD.
Cholesterol synthesis is the greatest in early morning hours. So advise patient to take it at night (also to mitigate muscle pain during day too).
Statin: What drugs are you concerned with severe toxicity for rhabdomyolysis.
a. Atorvastatin + Clarithromycin
b. Carbamazepine + Atorvastatin
c. Ciclosporin + Atorvastatin
d. Alcohol + Atorvastatin
(a) and (c) increases risk of rhabdomyolysis due to its inhibitory effect on CYP3A4 increasing concentration of Atorvastatin.
What drug are you concerned with for hepatotoxicity
a. Atorvastatin + Clarithromycin
b. Carbamazepine + Atorvastatin
c. Ciclosporin + Atorvastatin
d. Alcohol (25 units/week) + Atorvastatin
e. Alcohol (10 units/week) + Atorvastatin
(d) it is more likely for hepatotoxicity.
How are Statin eliminated.
primarily bile filling hepatic/ and or extra hepatic metabolism.
Statin: Monitoring
a. Before treatment
b. During treatment
a) Before treatment:
1. Patient parameter: before starting—> full lipid profile (non-fasting) should be measured, including total cholesterol, HDL-cholesterol, non-HDL-cholesterol (calculated as total cholesterol minus HDL-cholesterol), and triglyceride concentrations, thyroid-stimulating hormone, and renal function.
2. Creatine kinase.
3. Diabetes: at high risk fasting blood-glucose concentration or HbA1c checked before starting statin treatment.
b) During treatment:
- Liver function test: liver enzymes should be measured before treatment and repeated within 3 months and at 12 months of starting treatment.
Monitoring efficacy treatment: lipid profile 3 months and 12 months. - Creatine kinase: In patient with unexplained muscle pain.
CASE STUDY 1: Patient X is 65 year old man who has H. Pylori infection and has been prescribed Clarithromycin. He currently takes the following medicine:
Gliclazide 80 mg OD, Atorvastatin 40 mg, Aspirin 75 mg and Clopidogrel 75 mg, Ramipril 40 mg.
a. What is the first line for H.pylori infection. What questions will you ask the patient.
b. What medicines would you stop and why. What would you add.
Why are anti platelets used.
To limit growth or, or decrease risk of arterial thrombosis. Act by inhibiting platelet aggregation.
Indication for Antiplatelet therapy.
Not to be used in primary prevention.
Secondary prevention of atherothrombotic events in people with acute coronary syndrome (ACS), angina, peripheral arterial disease (PAD).
Secondary prevention after myocardial infarction (MI), stent implantation, stroke or transient ischaemic attack (TIA).
What is recommendation of Antiplatelet therapy in angina
Prescribe aspirin 75 mg daily with stable angina/ unstable angina and continue indefinitely. In patient >65 prescribe PPIs.
What is the recommendation of Antiplatelet therapy in Acute Coronary Syndrome
DAPT therapy aspirin 75 mg dailyplus ticagrelor 90mg twice a day for 12 months.
