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. - Review prescription. - Prepare medication. - Administer to patient. - Document administration. -...

**[PHARMACY EXAM REVISION 2024]** **WEEK ONE MEDICATION SAFETY** **Medication Management Pathway** - The green and orange sections are the most relevant to nurses. - Review prescription. - Prepare medication. - Administer to patient. - Document administration. - 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. - 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 - 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 ]** - Evidence-based medicine requires healthcare professionals to appraise medical literature and understand treatment effects. - Key outcome measures in clinical trials include **absolute risk (AR)**, **absolute risk reduction (ARR)**, **relative risk (RR)**, and **relative risk reduction (RRR)**. - **Absolute risk** is the chance of an outcome occurring in a group. - **Absolute risk reduction (ARR)** reflects the difference in risk between treated and untreated groups. It's more clinically relevant as it reflects baseline risks. - **Number needed to treat (NNT)** is the reciprocal of ARR and indicates how many people need to be treated to prevent one adverse outcome. - **Relative risk (RR)** compares the probability of an outcome between treated and untreated groups. - **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. - **ARR** and **NNT** are more useful for assessing real-world clinical effects than **RRR**. - 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. - Low-dose thiazide (or thiazide-like diuretics). - Angiotensin Converting Enzyme (ACE) inhibitors (generic names end in -pril). - Angiotensin II Receptor Blockers (ARBs; also known as sartans) (generic names end in-sartan). - 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: - Benzothiazepines: Diltiazem (available in Australia). - 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 ventricular nodal cells Effect on 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 | **B Blockers in | **B Blockers | **B Blocker and | | pregnancy** | Breastfeeding** | and adverse | drug | | | | effects.** | interaction** | +=================+=================+=================+=================+ | Beta-blockers | Metoprolol, | **Common**\ | Beta-blockers | | may cause | labetalol and | Bradycardia, | reduce blood | | pharmacological | propranolol are | hypotension, | pressure, | | effects, such | preferred to | transient | cardiac | | as bradycardia, | atenolol as | worsening of | contractility | | in the fetus | they are more | heart failure | and conduction, | | and neonate. | extensively | (when treatment | therefore | | However, | protein bound | starts), | administration | | occasionally | and therefore | bronchospasm, | with other | | certain b | less likely to | dyspnoea, cold | medications | | blockers are | pass into | extremities, | that also have | | used in | breast milk. | fatigue, | these effects | | pregnancy. | | dizziness.  | increases risk | | | | | of hypotension, | | Labetalol is | | **Infrequent or | heart failure | | the b blocker | | rare**\ | and | | of choice used | | Hallucinations, | bradyarrhythmia | | to treat | | insomnia, | 's. | | hypertension in | | nightmares, | | | pregnancy.  | | heart block, | Monitoring | | | | rash, alopecia, | blood pressure | | Atenolol should | | impotence. | and heart rate | | be avoided in | | | are | | the early | | | recommended.  | | stages of | | | | | pregnancy, and | | | It is | | given with | | | recommended | | caution later, | | | that combing | | due to its | | | b-blockers and | | association | | | verapamil be | | with | | | avoided (unless | | intrauterine | | | under | | fetal growth | | | specialist | | retardation. | | | supervision). | +-----------------+-----------------+-----------------+-----------------+ **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): - Reduced ejection fraction (LVEF \ - **Nurses and midwives** routinely administer vaccines and must stay informed using resources like the **Australian Immunisation Handbook**. - **Routine vaccines** for those aged 15-49 include annual influenza and meningococcal vaccines. DTP is recommended for all, especially during pregnancy. - **Pregnancy immunization**: Pertussis, influenza, and COVID-19 vaccines are recommended to protect the mother and newborn. - **Pre-term infants** can receive vaccines based on their chronological age, with close monitoring. - Adverse effects should be reported to the **Therapeutic Goods Administration (TGA)**. - **Vaccine administration tips**: use separate injection sites, do not mix vaccines in syringes, observe patients for 15 minutes post-vaccination. **WEEK 10 COMPLEMENTARY MEDICINES AND VTE PROPHYLAXIS** **What is in complementary medicines?** Are non-prescription alternative medicine that aims to achieve the healing effects of medicine despite the lacking biological plausibility, testability, repeatability or evidence of effectiveness. **The risks, info and problems of complementary medicines:** - **Lack of awareness**: Many Australian consumers and health professionals are unfamiliar with the drug regulatory system, particularly for complementary medicines. Labels may be unreliable, especially for products sourced from overseas. - **Limited education**: Health professionals often lack structured education about complementary medicines and their potential effects, making it hard to assess the therapeutic or toxicological risks. - **Importance of documentation**: When recording complementary medicines, it is essential to note the brand name, dose, and duration, not just the active ingredients, to fully assess the potential for drug interactions. - **AUST L and AUST R numbers**: These numbers on packaging indicate whether a product is listed or registered in the Australian Register of Therapeutic Goods (ARTG). Absence of these numbers may signal the product is not approved for marketing in Australia. - **Country of origin**: Products from overseas may follow different manufacturing standards, which could affect their quality. - **Risks**: Adverse reactions to complementary medicines, such as hepatotoxicity from black cohosh or interactions with prescription drugs (e.g., St John's wort with certain medications), are well documented. These interactions can alter drug efficacy or increase toxicity, particularly in cancer chemotherapy. - **Regulatory differences**: Unlike registered medicines, complementary medicines undergo minimal scrutiny by the Therapeutic Goods Administration (TGA). Listed medicines do not require proof of contents or efficacy, and the ingredients are accepted on trust without pre-approval of labelling. - **Challenges in predicting interactions**: Assessing drug interactions requires knowledge of both pharmacodynamics and pharmacokinetics, as well as understanding the limitations of drug-interaction checkers. **Drug interactions with complementary medicines.** - Many individuals see these as safe alternatives to prescription medicines and often do not declare that they are taking them when asked by a health professional, during part of a routine medication history. - Several complementary medicines interact with other drugs. - **Familiarity with Interactions**: Health professionals are expected to understand the interactions of common complementary medicines or know where to find this information. Although manufacturers may not provide interaction details, evidence from case reports, research, and online resources helps predict and prevent interactions. - **Complementary Medicines in Australia**: These include herbs, vitamins, minerals, and other supplements, largely regulated as unscheduled medicines and often self-selected by consumers. Up to 60% of Australians use complementary medicines regularly, and about 50% use them alongside conventional medications. - **Risk of Drug Interactions**: With many Australians using complementary medicines, especially vulnerable groups (e.g., elderly, chronic disease patients), prescribers must ask about these products to predict potential drug interactions based on known pharmacodynamic and pharmacokinetic data. - **Polypharmacy**: The use of complementary medicines alongside multiple prescription drugs (polypharmacy) increases the risk of interactions. Studies show that many elderly people and veterans using both have significant risks for drug interactions, some of which can be serious. - **Mechanisms of Interaction**: Complementary medicines interact via pharmacodynamic (overlapping actions) or pharmacokinetic mechanisms (changes in absorption, distribution, metabolism, or excretion). Herbal medicines, due to their complex chemistry, often interact with the cytochrome P450 system and P-glycoprotein, leading to potential drug interactions. **Venous Thromboembolism (VTE)** Venous thromboembolism is a disease which encompasses deep vein thrombosis (DVT) and pulmonary embolism (PE) is a major health care problem resulting in significant mortality, morbidity and expenditure in healthcare resources. The prevention of VTE is an important patient safety strategy in hospital settings where patients are at a risk of VTE therefore, the role of nurses is to have a comprehensive understanding of the classification and clinical application of the medicine and to administer the medication according to the rights of safe drug administration. **VTE Risk Assessment tools:** [Risk assessment scoring:] which stratifies a patient's level of VTE risk (high, medium or low risk). [Risk factor recognition:] identifies whether a patient has risk factors for VTE without assigning a score or level of risk. Safe and effective use of prevention methods: **[Medicines:]** Medicines are the preferred method for preventing venous thromboembolism (VTE) in most at-risk patients due to their superior efficacy compared to mechanical compression. Commonly used medications for VTE prevention include: - **Low molecular weight heparins (LMWH)** and heparins - **Direct oral anticoagulants (DOACs)**, including direct thrombin inhibitors and Factor Xa inhibitors - **Vitamin K antagonists** Less commonly used medicines include: - **Danaparoid** (for patients with heparin-induced thrombocytopenia) - **Aspirin** **VTE PREVENTION METHODS** When developing local policies and supporting individual clinical judgment for venous thromboembolism (VTE) prevention, particularly with anticoagulants (high-risk medicines that increase bleeding risk), the following factors should be considered: - **Thrombosis and bleeding risk**: Assess the patient\'s clinical condition, reason for admission, and individual risk factors for thrombosis and bleeding. - **Extremities of body weight**: VTE prevention doses for patients under 50kg or over 120kg, or with a BMI over 30kg/m², are uncertain. Specialist advice may be needed, and close monitoring for signs of thrombosis or bleeding is required. - **Medication interactions**: Consider potential interactions with other medications the patient is taking. - **Kidney and liver function**: Monitor kidney function (Creatinine Clearance) and liver function, and assess the need for an antidote based on the patient\'s condition. - **Patient beliefs**: Account for personal beliefs (e.g., needle phobia or religious views) that might affect their treatment. - **Adherence**: Consider dosing frequency, the patient\'s ability to self-administer, and the need for a dose administration aid (DAA) if necessary.