Exam - pharma Flashcards
Aspirin MOA
- specific for MI
- general effects
- side effects
- relevant pharmacokinetic parameters (half life, bioavailability)
- Anticoagulant: affects platelet aggregation by binding irreversibly to the COX1 and COX 2 enzymes to
- This results in the COX 1 pathway activation where the effects include antiplatelet aggregation.
- It also contributes to some unwanted effects on this pathway such as removal of GI protection which can result in the gastric side effects including ulcer and GI bleeding. Main side effects are GI (nausea, vomiting, heartburn) and bruising/bleeding.
- Half life of aspirin CR is ~3-4 hours.
Statins
- specific MOA
- general effects
- side effects
- relevant pharmacokinetic parameters (half life, bioavailability)
- inhibit HMG-CoA reductase, which blocks it from completing the synthesis of cholesterol. Results in lower serum cholesterol levels
- undergo first-pass metabolism
- half life 14hrs, peak 1-2hrs, duration 20-30hrs
- Most effective at night when the liver is processing the most lipids.
- Side fx: headache, flatulence, abdominal pain, cramps, nausea/vom/const.
- avoid grapefruit juice, alters the drug’s metabolism.
Beta blockers
- specific MOA
- general effects
- side effects
- relevant pharmacokinetic parameters (half life, bioavailability)
- competitively block beta(1) adrenergic receptors on the heart, decr. SNS influence and the excitability of the heart.
- Decr. CO, which lowers BP and cardiac workload.
- also block beta2 receptors on bronchiole smooth mm causing bronchoconstriction
- side effects associated w blockade of the SNS. Incl. dizziness, heart failure, arrythmias, gastric pain, flatulence, diarrhoea/vom
- half life 3-4hrs
SNS responsible for incr. HR, BP and contraction, thus blocking these actions reduces demand for O2
GTN
- Relaxes vascular smooth mm which decr. venous return and BP, reducing left ventricular workload and decr. myocardial O2 consumption
- vasodilation decreases preload and relaxation of vessels decreases afterload.
- half life 1-4mins
- adverse effects incl. headache/dizziness/tachycardia, nausea/vomiting, hypotension.
Clopidogrel
- specific MOA
- general effects
- side effects
- relevant pharmacokinetic parameters (half life, bioavailability)
- inhibits platelet activation and aggregation
- Inhibits receptor P2Y12, a chemoreceptor on platelet cell membranes.
- Used in combination with acetylsalicylic acid (aspirin) to prevent thrombosis after angioplasty.
- Adverse effects: bleeding and bruising, headache, dizziness, neusea and GI distress
Insulin
- Activate insulin receptors to phosphorylate tyrosine residues of intracellular proteins and enzymes; alters their shape –> changes metabolic activities
- Short acting (Ben: Humalog): onset of action approx. 30-60mins (subcut), peak action 2-4hrs, duration of action up to 8hrs. (NB: can be given IV in emergencies but half life 5 mins when given via this route so effect disappears in approx. 30mins)
- Longer acting (Ben: Humulin NPH): insulin is precipitated into crystals and suspended in solution to slow absorption. Size of crystals determines rate of absorption, onset and duration. Subcut only. Onset approx 1-2hrs, max. effect approx. 4-12hrs, duration approx. 24hrs
Sulphonylurea drugs: Oral hypoglycaemics
e.g. metformin
- decr. liver gluconeogenesis, incr. glucose utilization by peripheral cells, decr. LDL and VLDL and incr. HDL
- slow onset, peak 2-2.5hrs, duration 10-16hrs.
- half life 6.2 and then 17hrs
- unwanted effects: hypoglycaemia, and commonly GI upset, ie. anorexia, diarrhoea, nausea
Sympathomimetics
E.g. salbutamol, salmeterol
- Act to open the airways
- Agonists at beta 2 adrenergic receptors on bronchiole smooth muscle
- Side effects due to stimulation of beta1 receptors and include: tachycardia, palpitations, tremor and anxiety
Anticholinergic drugs
e.g. ipratropium
- block muscarinic acetylcholine (mACh) receptors on bronchiole smooth muscle
- Prevents the activation by ACh which causes bronchoconstriction
- so, blocking mACh receptors on bronchiole smooth muscle –> bronchodilation
Corticosteroids
e.g. hydrocortisone, prednisone
- Switch on/off specific genes that code for proteins involved in the inflammatory process or its regulation.
- Can take hours to exert the full therapeutic effect.
Common anticoagulants for stroke
Clopidogrel – Inhibits receptor P2Y12, a chemoreceptor on platelet cell membranes.
Warfarin – Inhibits vitamin K-epoxide reductase.
Heparin – Inhibits antithrombin III, which ultimately inactivates blood clotting factor Xa and inhibits blood clotting.
Aspirin – Blocks prostaglandin synthetase action.
Dabigatran – Competitive direct inhibitor of thrombin (factor IIa).
Dipyridamole – Inhibits the phosphodiesterase enzyme.
Common antihypertensives for stroke
Candesartan – Angiotensin II blocker.
Cilazapril – ACE inhibitor. Blocks the production of angiotensine II, which narrows blood vessels.
Clonodine – Alpha 2 adrenergic agonist.
Felodipine – Calcium channel blocker. Causes the blood vessel walls to relax and open up.
Frusemide – Diuretic. Rid the body of excess fluid.
Metoprolol – Beta blocker. Reduce blood pressure by affecting the nerve impulses to the heart and blood vessels.
Common protective drugs for stroke
- Paracetamol – Anti-inflammatory analgesia and hypothalmic regulation to avoid unwanted fevers.
- Omeprazole – Proton pump inhibitor. Protects against gastroesophageal reflux.
- Nimodipine – Calcium channel blocker. Used to protect against vasospasm.
- Gliclazide – A sulfonylurea which acts by stimulating β cells of the pancreas to release insulin.
- Diazepam – Acts on the gamma-aminobutyric acid (GABA) receptor, in the limbic system and thalamus, producing a calming effect.
rtPA § What it is § What it does/how it works § When it is used § Risks § Contraindications
- Fibrinolytic, tissue plasminogen activator, enzyme.
- Is a protease that turns plasminogen into plasmin, which is a molecule that cuts apart the fibrin strands holding blood clots together. Reverses any coagulation
- ischemic strokes; as soon as possible (<4.5hrs after stroke, preferably <3hrs, otherwise loses effectiveness)
- Uncontrollable bleeding and fatality in about 1 of every 15 patients.
- recently had surgery, already have a coagulation/bleeding disorder, any other bleeding risks, significant hypertension
Corticosteroids
hydrocortisone, methylprednisone, predisone
- switch on/off specific genes that code for proteins involved in the inflammatory process or its regulation.
