Pharmacy Exam Revision 2024 PDF

PHARMACY EXAM REVISION 2024 WEEK ONE MEDICATION SAFETY Medication Management Pathway - The green and orange sections are the most relevant to nurses. o Review prescription. o Prepare medication. o Administer to patient. o Document...

PHARMACY EXAM REVISION 2024 WEEK ONE MEDICATION SAFETY Medication Management Pathway - The green and orange sections are the most relevant to nurses. o Review prescription. o Prepare medication. o Administer to patient. o Document administration. o Monitor patient response. Medication incident - Any problems that arise in prescribing, dispensing, or administrating a medicine. (Does not need to cause harm to be an incident). Medication error - Any preventable event that may cause or lead to inappropriate medication use or patient harm. o Can result: § Adverse event (ADE) causes patient harm. Includes harm caused by medication errors and harm caused by an expected side effect of medication. § Near miss where a patient is nearly harmed. § Neither harm nor potential for harm. Common Causes of Medication Errors: Errors can occur during prescribing, dispensing, and administering medications. Common causes include staff fatigue, distractions, interruptions, heavy workload, and night shifts. Poor communication, especially during transitions of care (e.g., hospital admission, discharge, transfers between wards or facilities), increases the risk of errors. Insufficient patient information (e.g., age, weight, allergies) can lead to inappropriate medication choices. Use of error-prone abbreviations, unclear dose expressions, and inconsistent documentation practices. Medication history errors during hospital admissions, leading to unintended changes in treatment. Incorrect formulation immediate release instead of slow release Diltiazem immediate release vs-controlled release tablets o Solution – separate storage places for immediate release and controlled release Prevention Strategies: Near misses occur when a potential error is identified and corrected before reaching the patient. Ensuring accurate patient identification and medication matching can prevent errors. Clear communication of medication changes and accurate documentation, especially at care transition points, is crucial.  Using reliable resources to verify medication dosages and avoiding error-prone terminologies. Regular review and verification of patient-specific clinical information to develop safe treatment plans. Encouraging healthcare professionals to ask for clarification if medication orders are unclear or ambiguous. Medication Safety Principles – Swiss cheese models - Inherent weakness = human error – tiredness, hungry, angry, late and (look alike, sound alike medications) - Safeguards = health practitioner training, safety software and policies. 6/7 rights of medication administration 1. Right patient 2. Right drug 3. Right dose 4. Right route 5. Right time 6. Right documentation 7. Right to refuse WEEK 2 PHARMACOKINETICS AND PHARMACODYNAMICS What is pharmacokinetics and pharmacodynamics? Pharmacodynamics = the study of the effects of the drugs on the body. For example, what receptors does the drug activate and what other affects does it have. It also describes the relationship between drug concentration in the body and drug response. Pharmacokinetics = is the study of the effect the body has on the drug. It describes the relationship between drug dose and the resultant concentration of drug in the body over time. Pharmacodynamics and pharmacokinetics data can be combined to provide a description of the time course of drug response. Clinical pharmacokinetics studies the movement of drugs into, within, and out of the body, focusing on systemic circulation. The goal is to achieve the desired drug concentration at its site of action for a specific time. Drug effects are often linked to drug concentration at the site of action, usually within tissues. Direct measurement of drug concentrations at receptor sites is impractical (e.g., digoxin's receptor sites in the myocardium). Plasma, blood, or serum concentrations are used as surrogate markers for drug concentration at the site of action = this means using the blood as an estimate of the drug dose and levels at the site. Changes in plasma drug concentration are assumed to reflect changes in tissue drug concentration. As plasma drug concentration increases, tissue drug concentration typically increases proportionally. Concentration-time curves show how drug concentration changes over time after administration (oral or intravenous).  The shape of the concentration-time curve is influenced by the route of administration and pharmacokinetic properties. A drug reaches steady state after about 4-5 half-lives; at steady state, plasma concentrations remain constant with regular dosing. Therapeutic drug monitoring (TDM) is the measurement of plasma drug concentration to optimize therapy and minimize toxicity. TDM should only occur when a drug has reached steady state. Drugs suitable for TDM often have a high toxicity risk, a narrow therapeutic range, an unpredictable dose-response relationship, and available assays. Example: Vancomycin, an antibiotic with a half-life of 4-6 hours, reaches steady state in 30 hours; trough levels are measured to prevent toxicity. TDM ensures safe and effective drug therapy by monitoring plasma drug concentrations at appropriate times. WEEK 3 CLINICAL EVIDENCE AND THERAPEUTIC DECISIONS Therapeutic Clinical Evidence - Evidence-based medicine (EBM) uses the best available scientific evidence from clinical research to guide patient care decisions. - Clinical experience, knowledge, and patient values are integral in decision-making along with scientific evidence. - EBM aims to improve treatment planning, quality of care, and patient outcomes. - Identifying well-conducted research is essential for finding the best evidence. - Main types of studies include randomized controlled trials (RCTs), cohort studies, case-control studies, and qualitative studies. - RCTs are the most reliable for determining treatment effectiveness, comparing interventions with controls (either no treatment or another treatment). - Case-control studies compare groups with and without a specific medical condition to identify risk factors and are usually retrospective. - Cohort and case-control studies are "observational studies." - Clinical trials are crucial for determining the safety and effectiveness of treatments, often conducted in phases: Phase I: Small groups (20-80 participants) to assess safety and dosage. Phase II: Larger groups (several hundred) to evaluate efficacy and safety. Phase III: Large groups (hundreds to thousands) to compare treatment to standard or experimental interventions. Phase IV: Post-marketing studies to monitor long-term effectiveness and side effects in the general population. - Certain populations (e.g., medically complex patients, pregnant women, children) are often excluded from clinical trials, leading to gaps in safety evidence for these groups. - Randomized trials provide estimates of treatment effects, and understanding both relative and absolute measures is key in assessing risks and benefits. - Systematic reviews summarize multiple RCTs and are useful for synthesizing evidence. - Different study types have pros and cons; it’s important to ask why a specific study type was chosen and if it is appropriate for the research question. Absolute Risk Measures o Evidence-based medicine requires healthcare professionals to appraise medical literature and understand treatment effects. o Key outcome measures in clinical trials include absolute risk (AR), absolute risk reduction (ARR), relative risk (RR), and relative risk reduction (RRR). o Absolute risk is the chance of an outcome occurring in a group. o Absolute risk reduction (ARR) reflects the difference in risk between treated and untreated groups. It’s more clinically relevant as it reflects baseline risks. o Number needed to treat (NNT) is the reciprocal of ARR and indicates how many people need to be treated to prevent one adverse outcome. o Relative risk (RR) compares the probability of an outcome between treated and untreated groups. o Relative risk reduction (RRR) measures the percentage reduction in risk, often used in media and by pharmaceutical companies to present impressive results, but it may overestimate treatment benefits. o ARR and NNT are more useful for assessing real-world clinical effects than RRR. o Caution is needed when generalizing ARR and NNT to different populations with varying baseline risks. Local baseline risks can be used to calculate population specific ARR and NNT. Resources for therapeutic decisions Product information (TGA, MiMs, CMI): Strengths: Current regulatory status, pharmacokinetics/dynamics, side effects, contraindications. Limitations: May be outdated, hard to interpret in clinical context due to legal language. Australian Medicines Handbook (AMH): Strengths: Current regulatory status, clinical summaries, drug interactions, adverse effects in context. Limitations: Not freely available, not referenced. Answering questions with evidence: Paracetamol vs NSAIDs for osteoarthritis: NSAIDs more effective but riskier; conflicting information from AMH and Cochrane reviews. SSRIs and bleeding risk: Limited evidence; observational studies suggest possible risk; AMH and therapeutic guidelines mention bleeding but lack references. Pregabalin in pregnancy: Little evidence from trials or observational studies; product info suggests caution, AMH advises limited data, and therapeutic guidelines offer management tips. WEEK 4 CARDIOVASCULAR SYSTEM Pharmacological Management of Hypertension Principles to determine quality use of medicines Clinical Efficacy and safety: Is the treatment clinically effective and safe to use? Patient factors: Are there any patient specific factors such as age and ethnicity that need to be taken into consideration? Other concomitant medications: Are there any drug interactions that could occur? Pregnancy and breastfeeding: Some medications cause harm to the foetus or are excreted in breast milk. Other medical conditions: Some medications may have favourable or undesirable properties in specific medical conditions. Let’s look at the Clinical Efficacy and Safety of Antihypertensive medications The Therapeutic Guidelines recommend the following medications as suitable first line agents in the management of uncomplicated elevated blood pressure ( that is elevated blood pressure without other comorbidities ) in non-pregnant adults. o Low-dose thiazide (or thiazide-like diuretics). o Angiotensin Converting Enzyme (ACE) inhibitors (generic names end in -pril). o Angiotensin II Receptor Blockers (ARBs; also known as sartans) (generic names end in- sartan). o Dihydropyridine calcium channel blockers (CCBs) (generic names end in -pine). Angiotensin-converting enzyme (ACE) inhibitors and Angiotensin receptor antagonists (ARA). ACE inhibitors (ACEi) are used to manage hypertension, chronic heart failure, and post- myocardial infarction. Site of action: Angiotensin I and II receptors in the renin–angiotensin–aldosterone system (RAAS). RAAS role: Controls blood pressure and fluid volume. Angiotensin II: Vasoconstrictor, stimulates aldosterone secretion, increases sodium reabsorption, blood pressure, and blood volume. Renin released by kidneys in response to low sodium or hypotension. ACEi mechanism: Blocks conversion of angiotensin I to II, reduces aldosterone, enhances sodium excretion, prevents bradykinin breakdown (vasodilator), lowers blood pressure. Common ACEi examples: Enalapril, captopril. Side effects: Common: Hypotension (especially after first dose), persistent non-productive cough. Serious: Hyperkalemia (with potassium-sparing diuretics), angioedema (requires immediate discontinuation). Contraindications: History of hypersensitivity or angioedema with ACEi. Bilateral/unilateral renal artery stenosis. Pregnancy (can cause fetal complications). Monitoring: Potassium and renal function before starting and 2 weeks after. Alternative class: Angiotensin receptor antagonists (ARAs or sartans) block angiotensin II receptors, have similar uses, but don’t cause cough. Calcium Channel Blockers Calcium channel blockers (CCBs) are first-line medications for hypertension. Two main types: Dihydropyridines: Predominantly cause vasodilation of peripheral blood vessels; preferred for treating hypertension. Non-dihydropyridines: Reduce heart rate and contractility with less vasodilation. Divided into: o Benzothiazepines: Diltiazem (available in Australia).  o Phenylalkylamines: Verapamil (affects heart rate and contractility more than peripheral vasodilation). Dihydropyridines in Australia: Six available, including nifedipine (short-acting, also available as controlled-release). Adverse effects: Dihydropyridines: Vasodilatory side effects like headache, dizziness, flushing, peripheral oedema (common, dose-dependent). Can cause reflex tachycardia (short-acting forms) leading to palpitations and chest pain. Non-dihydropyridines: Verapamil commonly causes constipation; can slow heart rate and worsen cardiac output. Contraindications: Non-dihydropyridines (diltiazem, verapamil) are contraindicated in heart failure with reduced ejection fraction. Indications: Hypertension, angina, and some arrhythmias (verapamil). Site of Action Effect Amlodipine Diltiazem Verapamil Peripheral smooth muscle Hypotensive +++ ++ ++ effects Coronary smooth muscle Anti-anginal effects ++ ++ ++ Myocardium cardiac muscle Reduces + ++ ++ contractility Sino atrial node and atrial Effect on + ++ +++ ventricular nodal cells conduction Heart rate Minimal Minimal Reduces Reduction in after load Decreased +++ ++ ++ peripheral resistance What is coronary heart disease? Coronary heart disease (CHD) occurs when a coronary artery clogs and narrows because of a build-up of plaque known as atherosclerosis. B – Blockers In the body the nervous system consists of two branches § The parasympathetic nervous system and the sympathetic nervous system (SNS). Activation of the SNS increases heart rate and force of contraction through the activation of β1 adrenoceptors located in the myocardium and the cells of the sinoatrial node and conducting tissue. The SNS is stimulated when the neurotransmitter noradrenaline is released and this in turn releases catecholamines, adrenaline with small amounts of noradrenaline. This results in an increase in heart rate and force of contraction of the heart. This in turn leads to an increase in cardiac output and myocardial oxygen requirements. There are two main classes of adrenergic receptors: alpha- and beta-adrenoceptors which are subdivided into the following: § β1 receptors are predominantly located in the heart, kidneys and smooth muscle in the gastrointestinal tract. § β2 receptors are predominantly located in the lungs. Video Explanation of B Blockers Beta-blockers are used to manage various conditions, including hypertension, angina, tachyarrhythmias, heart failure with reduced ejection fraction, and post-myocardial infarction. They act as competitive antagonists on beta receptors in the heart, lungs, kidneys, and other organs. Cardio selective beta-blockers (e.g., atenolol, bisoprolol) target beta1 receptors in the heart and are preferred for patients with controlled asthma or COPD due to less risk of bronchospasm. Nonselective beta-blockers (e.g., propranolol) affect both beta1 and beta2 receptors and can cause bronchospasm, making them unsuitable for asthma patients. Beta- blockers are contraindicated in bradycardia and poorly controlled asthma and should be used cautiously in diabetics due to masking hypoglycaemia. They are started at low doses and tapered off gradually to avoid rebound effects like angina or hypertension.  B Blockers in pregnancy B Blockers in B Blockers and B Blocker and drug interaction Breastfeeding adverse effects. Beta-blockers may cause Metoprolol, Common Beta-blockers reduce blood pharmacological effects, such as labetalol and Bradycardia, pressure, cardiac contractility bradycardia, in the fetus and propranolol are hypotension, transient and conduction, therefore neonate. However, occasionally preferred to worsening of heart administration with other certain b blockers are used in atenolol as they failure (when treatment medications that also have these pregnancy. are more starts), bronchospasm, effects increases risk of extensively dyspnoea, cold hypotension, heart failure and Labetalol is the b blocker of protein bound extremities, fatigue, bradyarrhythmia’s. choice used to treat and therefore dizziness. hypertension in pregnancy. less likely to pass Infrequent or rare Monitoring blood pressure and into breast milk. Hallucinations, heart rate are recommended. Atenolol should be avoided in insomnia, nightmares, It is recommended that combing the early stages of pregnancy, heart block, rash, b-blockers and verapamil be and given with caution later, due alopecia, impotence. avoided (unless under specialist to its association with supervision). intrauterine fetal growth retardation. WEEK 5: HEART FAILURE, ASTHMA, CHRONIC OBSTRUCTIVE PULOMONARY DISEASE The heart failure syndrome occurs when there is inadequate oxygen delivery to peripheral tissues (at rest or during exercise), due to dysfunction of the heart or when adequate oxygen delivery can be maintained only with an elevated left ventricular filling pressure. Heart failure is a condition or a collection of symptoms that weaken or stiffen the heart. It is characterised with signs and symptoms that include: Some causes of heart failure include: Coronary artery disease Hypertension Valvular heart disease Congenital: atrial septal defect, ventricular septal defect, aortic coarctation Arrhythmias Medication management of Heart Failure Heart failure is often caused by coronary heart disease, high blood pressure, and cardiomyopathy. It results in the heart's inability to pump enough oxygenated blood to meet the body's needs. The heart compensates by enlarging, pumping faster, and developing more muscle. Over time, these compensations worsen, leading to symptoms like fatigue, breathlessness, and edema. Heart failure is classified by left ventricular ejection fraction (LVEF): o Reduced ejection fraction (LVEF