Bob Flashcards
Outline the mechanism of action of aspirin in the prophylaxis of thromboembolism.
Aspirin is a NSAID irreversible inhibitor, non-specific inhibitor of cox enzymes inhibiting the synthesis of prostaglandin and thromboxane( causes platelet activation, activated platelets can trigger thrombus formation with risk of thromboembolism) reason bob is a risk is because of AF (ineffective flow, you get pooling of blood)
Asprin inhibits formation of thromboxane- works because platlets cannot make any enzymes because they have no neuclous
Bob states that when he runs out of enteric-coated aspirin, he just takes half a tablet of his normal aspirin. Explain how this might affect Bob’s risk for gastrointestinal upsets, ulceration or gastric bleeding
Risk for GI upsets is increased because the normal/uncoated aspirin starts to break down in the stomach and is a direct irritant to the stomach lining. However the risk for ulceration and GI bleeding remains the same because this is caused by the inhibition of prostaglandin synthesis. Inhibition of PG’s occurs whether or not the aspirin in broken down in the stomach (uncoated aspirin) or in the small intestine (enteric coated aspirin).
Explain the rationale for prescribing metoprolol following a myocardial infarction.
Metoprolol is Beta-1 selective blocker.
Antagonises effects of catecholamines on myocardium.
- decrease hr
- decrease force of contraction
- decrease conduction volocity.
Results in
• decrease workload and metabolic demand
• decrease risk dysrhythmias
• some peripheral vasodilation decreased afterload
Because of this, there is a decrase in cardica workload. Following an MI, there may be cell death, and due to the fact the MI happened in the first place.
Bob’s metoprolol is “controlled release”. Explain the purpose(s) of providing metoprolol in this form?
Formulated so active drug is realised slowly into gi tract for active absorption
Get slow sustain release of the drug- this is a advantage because gives a steady concentration therapeutic level over a longer time, no peak plasma concentration (less risk for ADR’s), you do not have to take the drug as often this is good for compliance
Maintains a steady plasma concentration
Bob knows he should be taking his simvastatin tablet at night. He asks you why. Explain the reason for this in relation to the mechanisms of action of simvastatin.
Endogenous cholesterol synthesis increases during night time.
lowers LDL stops Cholestrol transport and further formation of plaque
Simvastatin should not be taken in combination with drugs that inhibit the action of CYP3A4 as the risk of developing adverse effects of simvastatin are greatly increased”. Explain this statement.
CYP3a4 is enzyme pathway for metabolism of simvastation you get increased risk for toxicity if you take it with drugs like erythomic, interaction with grapefruit juice.
Prolongs action of drug.
- Bob rarely uses his GTN spray. He is reluctant to use it because it makes him dizzy and gives him a severe headache. State the advice you would give to Bob about using his GTN and these adverse effects. Provide rationales for your advice.
1) Use GTN Spray when you get chest pain you risk damaging heart
Sit down
Reduces oxygen demand for heart
2) Getting headache because it is causing vasodilation in brain, effect wears off in 5 mins, it goes away with regular use
3) Hypotension- vasodilation of venous blood vessels, decreases venous return, decrease cardiac output, blood pressure this is why you get dizzy advice is to sit down or lie flat and stand up slowly and try to sit down for 15 mins after taking drug ( this is when effect will wear off)
Outline the rationale for providing Bob with a loading dose of digoxin to commence therapy.
Digoxin has a large VD and long half life (steady states takes 4 half life) due to distribution into tissues of a high VD drug, fill up tissues faster by giving a loading does- therefore plasma concentration goes higher sooner therefore reach steady state sooner
Bob has a blood test two days after commencing digoxin to check the concentration of digoxin in his plasma. State why this is considered necessary for digoxin therapy?
Narrow therapeutic index – easy to go over the minimum toxic concentration, this is problem because (older person renal impairment, less lean body mass less VD increase risk for toxicity )
(toxic effects of drug mimics therapeutic effects of drug), Signs and symptoms of toxicity is close to signs of disease you are treating this is why you cannot just look at a person need to do a blood test
Outline three reasons digoxin should be used with caution in older adults.
1) Renal impairment – because of reduced clearance, excreted unchanged from kidneys
2) Polypharmacy– if a person has hypokalaemia (eg diuretics) it changes action of digoxin causes increased sensitivity – increased risk of dysrhythmias
3) Less lean body mass, leads to decreased VD leads to increased plasma concentration increased risk of toxicity
4) increased sensitivity to the drug
- State the mechanism of action of warfarin in the prophylaxis of thromboembolism
Warfarin supresses coagulation by decreasing production of clotting facotors.
4 clotting factors. VII, IX, X and prothrombin.
Vatimine K dependent factors.
Works by inhibiting vitamine K epoxide reductase complex. And enzyme that is required to convert vitamine k into an active form.
Antagomisn of vatmine k activation.
Decreased plalettle clotting.
Decreased risk of thromboembolism.
why is bob asprin discontinued.
Competition between drugs for protein binding site
E.g Warfarin and aspirin
Aspirin displaces warfarin off protein binding sites
More warfarin circulating free in plasma
Pronounced effects from warfarin
Increased risk of bleeding
Explain why Bob is prescribed 3 mg of warfarin for the first five days of therapy but after this dose is according to INR.
Half life’s of the clotting factors
It does not have a full effect on prothrombin times because it takes 5 days this is when the INR will start to increase
5-7 days for warfarin to have a full effect, does needs to be prescribed carefully in response to the INR
Admin drugs to target INR of between 2 and 3
- Bob’s dose of warfarin is targeted to his INR
a. What does this mean?
b. State the target value for Bob’s INR in treating his AF
a. What does this mean?
International normalised ratio – comparing Bobs pro thrombin time to a international standard of 1 (you and I who are not on warfarin our INR would be 1)
B. Aim for warfarin therapy is 2-3 or sometimes 2-4.
- Bleeding is the most serious adverse event associated with warfarin therapy. Advise Bob how he can minimise this risk and what signs might indicate active bleeding.
Advice
1) Do not alter his diet – vitamin K intake, increase the intake the INR will go down because warfarin will be less effect, if he decreases his vitamin K it will go down (increased risk of thromboembolism )
2) No over the counter prescribed or herbal remedies do not start or stop any medication with out consultation with doctor it can interfere with metabolism of warfarin
3) Always attend blood test – follow up to check if does is ok
4) NSAIDS (aspirin) interfere with clotting via a separate pathway and does not show up on his INR will increase the risk of bleeding
