Exam 1 Review: Pharmacology and Pain Management PDF

Module 1: Pharmacokinetics (PK), Pharmacodynamics (PD), and Pharmacogenomics (PG) 1. Define Pharmacokinetics (PK), Pharmacodynamics (PD), and Pharmacogenomics (PG). Pharmacokinetics (PK): The study of what the body does to a drug, including Absorption, Distribution, Metabolism, and Ex...

Module 1: Pharmacokinetics (PK), Pharmacodynamics (PD), and Pharmacogenomics (PG) 1. Define Pharmacokinetics (PK), Pharmacodynamics (PD), and Pharmacogenomics (PG). Pharmacokinetics (PK): The study of what the body does to a drug, including Absorption, Distribution, Metabolism, and Excretion (ADME). Pharmacodynamics (PD): The study of what a drug does to the body, including mechanisms of action and dose-response relationships. Pharmacogenomics (PG): The study of how genetic variations affect drug response and metabolism. 2. Identify factors responsible for interpatient variability in drug response. Genetic differences in enzyme activity (e.g., CYP450 variations). Age-related changes in metabolism and elimination. Presence of diseases (e.g., liver or kidney disease). Drug-drug interactions affecting metabolism or excretion. Food intake affecting drug absorption. 3. Interpret key PK and PD parameters. Bioavailability: The proportion of the drug reaching systemic circulation. Half-life (t½): The time it takes for plasma drug concentration to reduce by half. Volume of Distribution (Vd): The extent of drug distribution in the body. Clearance (CL): The rate at which a drug is eliminated from circulation. Therapeutic Index (TI): The margin between effective and toxic doses. 4. Select appropriate candidates for therapeutic drug monitoring (TDM). Patients on drugs with a narrow therapeutic index (e.g., digoxin, lithium). Patients with altered metabolism (e.g., liver/kidney impairment). Patients experiencing toxicity or poor response to therapy. 5. Describe current and possible future roles of PG in clinical practice. Current: Identifying genetic polymorphisms affecting drug metabolism (e.g., CYP2D6 variations for antidepressants and opioids). Future: Personalized drug regimens to optimize treatment and minimize adverse effects. 6. Apply knowledge of PK, PD, and PG principles to individual patient scenarios, including the use of TDM. Adjust drug doses based on a patient’s metabolism (e.g., slow CYP2D6 metabolizers need lower opioid doses). Monitor plasma drug levels in high-risk drugs like phenytoin. Use genetic testing to determine optimal anticoagulant therapy. Key Medications Affecting PK and PD CYP450 System and Drug Metabolism 1. Warfarin o PD: Inhibits vitamin K-dependent clotting factors (II, VII, IX, X). o PK: Metabolized by CYP2C9, CYP1A2, and CYP3A4. o Adverse Effects: Bleeding, bruising, warfarin skin necrosis. o Considerations: CYP2C9 polymorphisms affect dosing. 2. Phenytoin (Dilantin®) o PD: Prolongs inactivation of sodium (Na+) channels, stabilizing neurons. o PK: Highly protein-bound, nonlinear kinetics. Metabolized by CYP2C9, CYP2C19. o Adverse Effects: Gingival hyperplasia, hepatotoxicity, ataxia, nystagmus, teratogenicity. o Monitoring: Therapeutic range 10-20 mcg/mL (total), 1-2 mcg/mL (free). 3. Carbamazepine (Tegretol®) o PD: Blocks Na+ channels, reducing neuron excitability. o PK: Auto-induces CYP3A4, decreasing its own levels over time. o Adverse Effects: Aplastic anemia, hepatotoxicity, rash (esp. Steve Johnson Syndrome in HLA-B*1502 allele). o Monitoring: Therapeutic range 4-12 mcg/mL. 4. Omeprazole (Prilosec®) o PD: Proton pump inhibitor (PPI), reduces gastric acid secretion. o PK: Metabolized by CYP2C19, affects clopidogrel activation. o Adverse Effects: Osteoporosis, hypomagnesemia, increased risk of C. difficile infection. Avoid with clopidogrel due to interaction. Module 2: Pain Management 1. Explain the Differences Between Nociceptive and Neuropathic Pain Nociceptive Pain: o Caused by tissue damage, detected by nociceptors.  o Subtypes: § Somatic: Localized pain from muscles, bones, or joints (e.g., arthritis, laceration). § Visceral: Internal organ pain, often cramping or squeezing (e.g., appendicitis, kidney stones). o Treatment: NSAIDs, acetaminophen, opioids. Neuropathic Pain: o Caused by nerve damage or dysfunction (e.g., diabetic neuropathy, postherpetic neuralgia). o Characterized by: § Hyperalgesia: Increased pain response. § Allodynia: Pain from normally non-painful stimuli. o Treatment: Anticonvulsants (gabapentin, pregabalin), antidepressants (amitriptyline, duloxetine), topical agents (lidocaine, capsaicin). 2. Compare and Contrast Classes of Analgesic Medications Non-Opioid Analgesics: o Acetaminophen: Reduces pain and fever but lacks anti-inflammatory effects; risk of hepatotoxicity. o NSAIDs: Inhibit COX enzymes to reduce inflammation (e.g., ibuprofen, naproxen); risk of GI bleeding and renal impairment. Opioids: o Used for severe pain, bind to opioid receptors to inhibit pain perception. o Examples: Morphine, oxycodone, fentanyl, hydromorphone. o Risks: Respiratory depression, addiction, tolerance. Adjuvant Analgesics: o Primarily for neuropathic pain or multimodal pain management. o Examples: Gabapentin (anticonvulsant), duloxetine (SNRI), lidocaine patches (local anesthetic). 3. Select an Appropriate Candidate for Migraine Prophylaxis and Create an Analgesic Regimen Migraine Prophylaxis Indications: o Frequent migraines (>5 per month). o Contraindications to acute therapies or risk of medication overuse. Regimen: o Prophylaxis: § First-line: Beta-blockers (propranolol), CGRP antagonists (erenumab), anticonvulsants (topiramate). o Acute Migraine Relief: § Triptans (sumatriptan, rizatriptan): 5-HT1 agonists that cause vasoconstriction.  § NSAIDs + triptans for severe pain. § Avoid opioids (ineffective, risk of dependence). 4. Identify the Role of Non-Opioid Analgesics in the Management of Pain First-line for mild to moderate pain (preferred over opioids). Used alone or as adjuncts to reduce opioid use. Lower risk of dependence, overdose, and respiratory depression. Examples: o Acetaminophen for osteoarthritis. o NSAIDs for inflammatory pain (e.g., arthritis, musculoskeletal pain). 5. Review the Various Opioid Classes and Specific Opioid Medications Opioid Structural Classes: o Phenanthrenes: Morphine, codeine, oxycodone, hydromorphone. o Phenylpiperidines: Fentanyl, meperidine. o Phenylheptanes: Methadone. Functional Classes: o Full agonists: Morphine, oxycodone, fentanyl. o Partial agonists: Buprenorphine. o Antagonists: Naloxone, naltrexone (opioid reversal agents). 6. Calculate an Equianalgesic Dose of an Opioid Regimen When Converting to Another Regimen Conversion Example: Morphine 90 mg/day to oxycodone o Morphine to oxycodone ratio: 30 mg morphine = 20 mg oxycodone. o Total oxycodone dose: (90 mg morphine ÷ 30 mg) × 20 mg = 60 mg oxycodone/day. o Adjust for cross-tolerance (~25% reduction): 60 mg × 0.75 = 45 mg/day oxycodone. o Dosing recommendation: Oxycodone ER 20 mg BID + Oxycodone IR 5 mg Q6H PRN. Key Takeaways for Exam Nociceptive pain is treated with NSAIDs/opioids, while neuropathic pain requires adjuvants (gabapentin, antidepressants). Acetaminophen is safer but lacks anti-inflammatory effects; NSAIDs reduce inflammation but risk GI/renal toxicity.  Opioids are reserved for severe pain, with high risks of addiction and respiratory depression. Triptans and CGRP antagonists are first-line for migraines, while opioids are avoided. Equianalgesic opioid conversion accounts for cross-tolerance to prevent overdose. Non-Opioid Analgesics 1. Acetaminophen (Tylenol®) PD: Inhibits prostaglandin synthesis in CNS, analgesic and antipyretic; weak COX-1 & COX-2 inhibitor. NO ANTI-INFLAMMATORY. PK: Hepatic metabolism via glucuronidation/sulfation; toxic dose leads to NAPQI accumulation. Adverse Effects: Hepatotoxicity (especially with alcohol use), rash, anaphylaxis. Max Dose: 4g/day (adults), 2g/day (cirrhosis). 2. NSAIDs (Non-Steroidal Anti-Inflammatory Drugs) Ibuprofen (Advil®, Motrin®), Naproxen (Aleve®), Celecoxib (Celebrex®) PD: Inhibit COX-1 and COX-2, reducing prostaglandin synthesis (anti-inflammatory, analgesic, antipyretic). PK: Renal elimination, half-life varies (ibuprofen: 2-4h, naproxen: 12-17h). Adverse Effects: GI ulcers/bleeding, renal impairment, cardiovascular risk (esp. with COX-2 inhibitors). Opioid Analgesics 1. Morphine PD: μ-opioid receptor agonist, inhibits pain transmission. PK: Hepatic metabolism (via glucuronidation); renally cleared active metabolites (morphine-6-glucuronide). Adverse Effects: Respiratory depression, constipation, hypotension, pruritus. Conversion: 10 mg IV = 30 mg PO. 2. Oxycodone (OxyContin®, Percocet®) PD: μ-opioid receptor agonist. PK: Metabolized by CYP3A4 and CYP2D6. Adverse Effects: Similar to morphine; higher risk of CYP interactions. High addiction risk. Note: Often combined with acetaminophen. 3. Fentanyl (Duragesic®, Actiq®)  PD: Highly potent μ-opioid receptor agonist. PK: Hepatic metabolism (CYP3A4), rapid onset (~1 min IV), lipophilic. Adverse Effects: Chest wall rigidity (high-dose IV), profound respiratory depression. Notes: 100 mcg IV = 10 mg morphine IV. Module 3: Controlled Substances & Prescribing Regulations 1. Review State and Federal Regulations Pertaining to the Prescribing of Controlled Substances Controlled substances are classified into Schedules I–V based on abuse potential and medical use. o Schedule I: No accepted medical use, high abuse potential (e.g., heroin, LSD, ecstasy, marijuana at the federal level). o Schedule II: High abuse potential but accepted medical use (e.g., oxycodone, fentanyl, methadone, hydrocodone, morphine, cocaine). o Schedule III–V: Lower abuse potential (e.g., ketamine, benzodiazepines, cough syrups with codeine). Prescribing laws: o Schedule II: No refills, requires a new prescription each time. o Schedule III–V: Can have up to five refills within six months. DEA Requirements: o Prescribers must have a DEA registration number. o Schedule II prescriptions must be hand-signed and dated the day they are written. o State laws may impose stricter regulations than federal laws. 2. Identify the Necessary Components of a Controlled Substance Prescription A valid prescription must include: Patient information: Full name and address. Prescriber information: Name, address, DEA number. Medication details: Drug name, strength, dosage form, quantity, directions for use. Refills: Allowed only for Schedule III–V (maximum five refills in six months). Signature: Must be manually signed by the prescriber. Additional requirements for Schedule II: No refills allowed, written prescriptions only (except in emergencies). 3. Describe Your State’s Prescription Monitoring Program (PMP) PMPS are state-run electronic databases tracking controlled substance prescriptions. Purpose: Detect misuse, doctor shopping, and potential diversion of controlled substances. Mandatory Checking: Some states require prescribers to check the PMP before issuing prescriptions for opioids or other high-risk drugs. 4. Discuss Ethical and Legal Standards of Prescribing Controlled Substances Prescriptions must be for a legitimate medical purpose and within the prescriber’s scope of practice. o Example: Dentists should not prescribe ADHD medications. Prescribers and pharmacists share responsibility in ensuring prescriptions are valid. Pre-signing prescription blanks is prohibited. Best practices include: o Using tamper-resistant prescription pads. o Writing out the quantity in both numerical and word form (e.g., “30 (thirty)”). o Reporting suspicious prescription activity to the DEA. 5. Discuss Substances of Abuse and the Appropriate Treatment Opioids: High risk of dependence and overdose. Treatment includes: o Medication-Assisted Treatment (MAT): § Methadone (Schedule II): Requires DEA registration for addiction treatment. § Buprenorphine (Schedule III): Requires DEA waiver to prescribe for opioid use disorder. § Naltrexone: Opioid antagonist, blocks opioid effects. o Naloxone (Narcan®): Opioid reversal agent, available IV, IM, or intranasally. Alcohol: o Treatment options: § Naltrexone: Reduces cravings. § Acamprosate: Helps maintain abstinence. § Disulfiram: Causes aversive reaction to alcohol. o Withdrawal requires benzodiazepines (e.g., diazepam, lorazepam). Benzodiazepines: Used for anxiety and insomnia but can be addictive. o Tapering required to avoid withdrawal symptoms (e.g., seizures, agitation, insomnia). Nicotine: o Treatment options: § Nicotine replacement therapy (patches, gum, lozenges). § Varenicline (Chantix®): Blocks nicotine receptors.  § Bupropion (Zyban®): Aids smoking cessation by increasing dopamine and norepinephrine. Key Takeaways for Exam Schedule II drugs require written prescriptions, no refills, and strict monitoring. A valid controlled substance prescription must include patient info, drug details, DEA number, and manual signature. State PMPs are essential tools to track opioid prescribing and prevent abuse. Ethical prescribing ensures medications are used for legitimate medical purposes within a provider’s scope of practice. Substance use disorders require individualized treatment, including MAT for opioids and behavioral therapy for all addictions. Benzodiazepines (Schedule IV Controlled Substances) 1. Alprazolam (Xanax®) PD: Enhances GABA-A receptor activity, leading to CNS depression. PK: Metabolized by CYP3A4, short half-life (~6-12h). Adverse Effects: Sedation, dependence, respiratory depression (esp. with opioids). Notes: Avoid in elderly (fall risk). 2. Diazepam (Valium®) PK: Long half-life (~30-60h), active metabolites prolong effects. PD: GABAergic inhibition. Indications: Anxiety, muscle spasms, alcohol withdrawal. Adverse Effects: Sedation, confusion, Notes: Used for alcohol withdrawal. Module 4: CNS Agents & Psychotropics 1. Review Commonly Used CNS Agents Antidepressants: o SSRIs: Fluoxetine, Sertraline (increase serotonin levels, first-line for depression and anxiety). o SNRIs: Venlafaxine, Duloxetine (increase serotonin & norepinephrine, used for depression and neuropathic pain).  o Atypical Antidepressants: Bupropion (dopamine & norepinephrine effects, used for depression and smoking cessation; avoid in seizure risk), Mirtazapine (enhances serotonin & norepinephrine, causes sedation and weight gain). o TCAs: Amitriptyline, Nortriptyline (older, significant anticholinergic effects, sedating). o MAOIs: Phenelzine, Tranylcypromine (reserved for treatment-resistant cases, requires dietary restrictions to avoid hypertensive crisis). Antipsychotics: o Typical (First-Generation, FGAs): Haloperidol (dopamine receptor blockade, high risk of extrapyramidal symptoms (EPS)). o Atypical (Second-Generation, SGAs): Quetiapine, Aripiprazole (dopamine & serotonin receptor blockade, lower EPS risk but higher metabolic side effects). Mood Stabilizers: o Lithium: Gold standard for bipolar disorder, requires serum monitoring due to narrow therapeutic index. o Anticonvulsants for mood stabilization: Valproate, Lamotrigine (used in bipolar disorder). Anxiolytics: o Benzodiazepines: Lorazepam, Diazepam (enhance GABA, used for acute anxiety, risk of dependence). o Buspirone: Non-sedating, takes weeks to show effects, used for long-term anxiety management. Stimulants: o Methylphenidate, Amphetamines: Increase dopamine and norepinephrine, used for ADHD. 2. Important Counseling Points for CNS Agents Antidepressants: o May take 4–6 weeks for full effect. o Risk of increased suicidal ideation in young adults (18–24 years). o Avoid abrupt discontinuation to prevent withdrawal symptoms. Antipsychotics: o Adherence is critical to avoid relapse. o Monitor for metabolic syndrome (SGAs: weight gain, dyslipidemia, diabetes risk). o EPS risk is higher with FGAs (dystonia, tardive dyskinesia). Mood Stabilizers: o Lithium: Maintain consistent hydration and sodium intake. Watch for toxicity signs (tremors, confusion, nausea). o Monitor weight, thyroid, and renal function regularly. Anxiolytics: o Benzodiazepines: Risk of dependence, limit use to short-term. o Buspirone: Takes weeks for effect, not sedating.  Stimulants: o Take in the morning to avoid insomnia. o Monitor appetite and growth in children. 3. Developing an Optimal Psychotropic Regimen Patient-Specific Factors: o Age: Lower doses in older adults due to metabolic changes. o Comorbidities: Avoid bupropion in seizure history, use caution with lithium in kidney disease. o Medication History: Prior response to specific agents is critical. Medication-Specific Factors: o Pharmacokinetics: Half-life, metabolism (e.g., CYP450 interactions). o Adverse Effects: Tailor treatment to minimize side effects (e.g., avoiding weight gain in obese patients). o Cost & Accessibility: Consider insurance coverage and affordability. 4. Drug Interactions, Monitoring, and Contraindications Clinically Significant Drug Interactions: o SSRIs + MAOIs: Risk of serotonin syndrome (agitation, tachycardia, fever, clonus). o Lithium + NSAIDs/Diuretics: Increased lithium levels → toxicity risk. o Benzodiazepines + CNS Depressants (alcohol, opioids): Additive sedation, respiratory depression. Key Monitoring Parameters: o Antidepressants: Mood changes, weight, QTc interval (citalopram). o Antipsychotics: Lipids, glucose, weight (SGAs), EPS monitoring (FGAs). o Lithium: Serum levels (therapeutic range: 0.6–1.2 mEq/L), thyroid, renal function. o Stimulants: Blood pressure, heart rate, growth in children. Contraindications: o Bupropion: Seizure or eating disorder history. o Clozapine: Risk of agranulocytosis, requires frequent CBC monitoring. o Lithium: Avoid in significant renal impairment. Key Takeaways for Exam SSRIs are first-line for depression/anxiety but take 4–6 weeks for full effect. FGAs have higher EPS risk, while SGAs have higher metabolic risk. Lithium requires serum monitoring and hydration balance to prevent toxicity.  Avoid benzodiazepines long-term due to dependence risk; consider buspirone for anxiety instead. Monitor weight, glucose, and lipids with SGAs to prevent metabolic syndrome. Check lithium, thyroid, and renal function periodically in bipolar treatment. Antidepressants 1. Selective Serotonin Reuptake Inhibitors (SSRIs) Fluoxetine (Prozac®), Sertraline (Zoloft®), Escitalopram (Lexapro®) PD: Block presynaptic serotonin reuptake (↑ 5-HT). PK: Hepatic metabolism (CYP2D6, CYP3A4), long half-life (fluoxetine: ~7-9 days). Adverse Effects: Sexual dysfunction, GI upset, serotonin syndrome. Notes: 4 to 6 weeks for full effect. 2. Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs) Duloxetine (Cymbalta®), Venlafaxine (Effexor®) PD: Increases serotonin & norepinephrine. PK: Venlafaxine increases BP; Duloxetine is hepatotoxic. Adverse Effects: Hypertension (venlafaxine), hepatotoxicity (duloxetine). Notes: Venlafaxine used for neuropathic pain. Module 5: Anticonvulsants & Seizures 1. Review Common Anticonvulsant Medications Anticonvulsants are divided into classic and modern agents. Classic Anticonvulsants: o Phenytoin, Carbamazepine, Phenobarbital o Require therapeutic drug monitoring. o Strong CYP3A4 inducers, leading to multiple drug interactions. o Highly protein-bound, meaning small dose changes can result in large serum fluctuations. Modern Anticonvulsants: o Levetiracetam, Lamotrigine, Topiramate o Minimal need for drug level monitoring. o Fewer drug-drug interactions. o Broad-spectrum efficacy across multiple seizure types. 2. Propose an Appropriate Anticonvulsant Regimen in a Given Patient Case Partial Seizures: o First-line: Levetiracetam (500–3000 mg daily, divided). o Alternative: Lamotrigine (requires slow titration to prevent rash). Generalized Tonic-Clonic Seizures: o First-line: Valproic Acid (monitor LFTs due to hepatotoxicity risk). o Alternative: Lamotrigine or Topiramate. Absence Seizures: o Ethosuximide or Valproic Acid are most effective. o Avoid Phenytoin and Phenobarbital as they can worsen absence seizures. 3. Emergency Management of Seizures A seizure lasting >5 minutes or multiple seizures without recovery is considered status epilepticus, requiring urgent intervention. Step 1: Benzodiazepines (first-line for acute seizures) o Lorazepam 4 mg IV push o Midazolam 10 mg IM o Diazepam 10–20 mg PR Step 2: Longer-acting anticonvulsants to prevent seizure recurrence o Phenytoin, Fosphenytoin, or Valproic Acid Step 3: If seizures persist, escalate to o Phenobarbital, Levetiracetam, Lacosamide, or Propofol/Ketamine infusion. Non-Pharmacologic Emergency Measures: Position patient on their side to prevent aspiration. Remove dangerous objects from the surroundings. DO NOT place objects in the mouth. Call 911 if seizure lasts >5 minutes. 4. Treatment Considerations for Epilepsy in Pregnancy Key Risks: o 25–30% of pregnant patients experience increased seizure frequency due to changing drug metabolism. o Seizures can cause miscarriage, trauma, fetal hypoxia, and acidosis. Preferred Medications: o Levetiracetam and Lamotrigine (lower teratogenic risk). o Avoid Valproic Acid, Phenytoin, and Phenobarbital due to high teratogenic risk. Drug Clearance Changes in Pregnancy:  o Increased clearance: Phenytoin, Carbamazepine, Lamotrigine. o Decreased clearance: Levetiracetam, Oxcarbazepine. o Monitor drug levels frequently and adjust doses accordingly. Supplementation: o Folic Acid (≥4 mg daily) 3 months before conception to prevent neural tube defects. o Vitamin K (before birth) if taking Phenytoin, Carbamazepine, Phenobarbital (reduces neonatal bleeding risk). 5. Strategies for Withdrawing Anticonvulsant Medications Consider Withdrawal If: o Seizure-free for 2–5 years. o No abnormal EEG and low relapse risk. Tapering Recommendations: o Gradual dose reduction over several months to prevent withdrawal seizures. o Monitor for recurrence, as 60% of patients relapse after stopping treatment. Risk of Relapse Higher If: o Generalized tonic-clonic or partial seizures were present. o Longer disease duration and abnormal EEG findings exist. Key Takeaways for Exam Anticonvulsants are classified as "classic" (e.g., Phenytoin, Carbamazepine) or "modern" (e.g., Levetiracetam, Lamotrigine). Status Epilepticus requires urgent treatment with Benzodiazepines, followed by long- acting anticonvulsants. Pregnancy considerations: Avoid Valproic Acid, use Levetiracetam/Lamotrigine instead. Withdrawal of therapy should be gradual, with high relapse risk in certain seizure types. Common Anticonvulsants 1. Valproic Acid (Depakote®) PD: Inhibits GABA degradation, Na+ channel modulation. PK: Highly protein-bound, metabolized in liver. Adverse Effects: Hepatotoxicity, pancreatitis, teratogenicity. Notes: Contraindicated in pregnancy. 2. Lamotrigine (Lamictal®) PD: Inhibits Na+ channels, stabilizing neuronal membranes. PK: Hepatic metabolism, slow titration required,  Adverse Effects: Steven-Johnson syndrome (SJS) risk—requires slow titration. Notes: Must titrate slowly to avoid rash. Module 6: Asthma, COPD, Allergic Rhinitis 1. Identify Risk Factors for Asthma, COPD, and Allergic Rhinitis Asthma: o Environmental: Allergens (dust mites, pollen, mold, pet dander), air pollution, occupational exposures. o Genetic: Family history of asthma or atopy. o Lifestyle: Smoking, obesity, sedentary behavior. o Other: Respiratory infections, exposure to cold air or exercise. COPD: o Smoking: Leading cause; includes secondhand smoke exposure. o Environmental: Air pollution, occupational exposure to dust and chemicals. o Genetic: Alpha-1 antitrypsin deficiency. o Other: History of childhood respiratory infections. Allergic Rhinitis: o Environmental: Exposure to allergens like pollen, mold, dust mites, and pet dander. o Genetic: Family history of atopy (allergic rhinitis, asthma, eczema). o Seasonal Factors: Spring and fall when pollen counts are high. o Other: Urban living, pollution exposure. 2. Medications Used for Asthma, COPD, and Allergic Rhinitis Asthma: o Rescue Medications: Short-acting beta-2 agonists (SABA) like Albuterol. o Maintenance Therapy: § Inhaled corticosteroids (ICS): Fluticasone, Budesonide. § Long-acting beta-2 agonists (LABA): Salmeterol, Formoterol (always combined with ICS). § Leukotriene receptor antagonists: Montelukast. § Biologics: Omalizumab (for severe asthma with allergic or eosinophilic phenotypes). COPD: o Bronchodilators: § Short-acting muscarinic antagonists (SAMA): Ipratropium. § Long-acting muscarinic antagonists (LAMA): Tiotropium, Umeclidinium. § LABA: Indacaterol, Salmeterol.  o Anti-inflammatory: § ICS: Fluticasone, Budesonide (used selectively for frequent exacerbations and high eosinophil counts). o Combination Inhalers: § LABA + LAMA: Formoterol/Glycopyrronium. § LABA + ICS: Salmeterol/Fluticasone. § Triple therapy: LABA + LAMA + ICS (Trelegy®). o Adjuncts: Roflumilast (PDE-4 inhibitor), Azithromycin (for former smokers). Allergic Rhinitis: o First-Line Therapy: Intranasal corticosteroids (Fluticasone, Budesonide). o Antihistamines: § Oral: Loratadine, Cetirizine (second-generation, less sedating). § Intranasal: Azelastine (more effective than oral antihistamines). o Decongestants: Oxymetazoline (limit to 3 days to avoid rebound congestion). o Adjuncts: Montelukast (useful for patients with both allergic rhinitis and asthma). 3. Pharmacologic Regimens for Asthma, COPD, and Allergic Rhinitis Asthma Regimens: o Mild Intermittent: SABA PRN. o Mild Persistent: Low-dose ICS + SABA PRN. o Moderate Persistent: Low-dose ICS + LABA, or medium-dose ICS. o Severe Persistent: High-dose ICS + LABA ± biologic (e.g., Omalizumab for allergic asthma). o Considerations: Monitor adherence, inhaler technique, and adjust therapy based on symptom control. COPD Regimens (GOLD Guidelines): o Mild Symptoms (GOLD A): SABA or SAMA PRN. o Moderate Symptoms (GOLD B): LABA or LAMA. o Frequent Exacerbations (GOLD C): LAMA. o Severe Symptoms/Exacerbations (GOLD D): LABA + LAMA ± ICS or triple therapy. o Considerations: Include Roflumilast for FEV1 < 50% with chronic bronchitis and Azithromycin for former smokers. Allergic Rhinitis Regimens: o Mild Symptoms: Oral antihistamine (e.g., Loratadine). o Moderate-Severe Symptoms: Intranasal corticosteroids (e.g., Fluticasone). o Persistent Congestion: Add intranasal antihistamine or Montelukast for concurrent asthma. o Considerations: Address patient adherence and educate on proper nasal spray technique. 4. Patient Education for Medications Asthma and COPD: o Inhaler Use: § Demonstrate proper technique for MDIs, DPIs, or nebulizers. § Use spacers with MDIs for patients with coordination issues. o Adherence: § Reinforce daily ICS use for asthma control. § Avoid overuse of rescue inhalers (SABAs). o Side Effects: § Rinse mouth after ICS use to prevent thrush. § Monitor for beta-agonist effects (tachycardia, tremors). COPD-Specific Education: o Smoking Cessation: Essential for slowing disease progression. o Vaccinations: Annual influenza and pneumococcal vaccines to reduce exacerbations. o Pulmonary Rehabilitation: Improves quality of life in moderate to severe COPD. Allergic Rhinitis: o Intranasal Corticosteroids: Correct spray technique to avoid epistaxis. o Antihistamines: Second-generation preferred to reduce sedation. o Decongestants: Limit oxymetazoline use to avoid rebound congestion. Key Takeaways for Exam Asthma: o ICS is the foundation of therapy; LABAs must be combined with ICS. o Montelukast has an FDA Boxed Warning for neuropsychiatric effects. o Biologics (Omalizumab, Mepolizumab) are reserved for severe eosinophilic or allergic asthma. COPD: o GOLD guidelines classify COPD severity and guide therapy selection. o LABAs and LAMAs are preferred for maintenance; ICS is used selectively in frequent exacerbators. o Roflumilast and Azithromycin are adjuncts for specific COPD subtypes. Allergic Rhinitis: o Intranasal corticosteroids (Fluticasone, Budesonide) are first-line. o Second-generation antihistamines (Cetirizine, Loratadine) are preferred for systemic relief. o Montelukast is an option for patients with concurrent asthma. Module 6: Asthma & COPD Medications 1. Short-Acting Beta Agonists (SABAs) SABAs are rescue medications for acute bronchospasm. a) Albuterol (Ventolin®, ProAir®) PD: β2 agonist—Relaxes bronchial smooth muscle. PK: Inhaled, rapid onset. Onset: 5 min; Duration: 4-6 hours. Adverse Effects: Tachycardia, tremors, hypokalemia. Notes: First-line rescue inhaler for asthma attacks. b) Levalbuterol (Xopenex®) PD: Selective β2 agonist, smooth muscle relaxation PK: Inhaled, rapid onset. Onset: 5-10 min; Duration: 5-8 hrs. Adverse Effects: Less tachycardia than albuterol, tremors. Notes: Preferred in patients with cardiac disease. c) Terbutaline (Brethine®) PD: β2 agonist, bronchodilation. PK: Oral and subcutaneous forms available Adverse Effects: Hypotension, tachycardia, hyperglycemia. Notes: Rarely used due to systemic effects. 2. Long-Acting Beta-Agonists (LABAs) LABAs are bronchodilators used for long-term asthma control, but must be used with ICS in asthma to prevent increased mortality risk. a) Salmeterol (Serevent®) PD: β2 agonist—Relaxes bronchial smooth muscle. PK: Onset: 15-30 min; Duration: ~12 hours. Adverse Effects: Tachycardia, tremors, headache. Notes: BBW: NEVER use as monotherapy in asthma (↑ mortality risk). b) Formoterol (Foradil®) PD: β2 agonist, bronchodilation via cAMP activation PK: Onset: ~5 min, Duration: ~12 hours. Adverse Effects: QT prolongation, palpitations, hypokalemia. Notes: Often combined with ICS (e.g., Symbicort® = budesonide + formoterol). c) Vilanterol (Breo Ellipta®) PD: Ultra-LABA, smooth muscle relaxation. PK: Onset: ~5 min, Duration: ~24 hours.  Adverse Effects: Increased HR, headache, tremor. Notes: Once-daily dosing; combined with fluticasone. 3. Inhaled Corticosteroids (ICS) ICS are first-line therapy for long-term asthma control due to their anti-inflammatory effects. a) Fluticasone (Flovent®) PD: Inhibits inflammatory mediators, reduces airway hyperreactivity. PK: Liver metabolism (CYP3A4); minimal systemic absorption. Adverse Effects: Oral candidiasis (thrush), hoarseness, cough. Notes: Rinse mouth after use to prevent thrush. b) Budesonide (Pulmicort®) PD: Decreases airway inflammation, suppresses cytokines. PK: Rapid lung absorption, hepatic metabolism (CYP3A4) Adverse Effects: Dysphonia, Oral candidiasis (thrush), cough. Notes: Preferred in pregnancy for asthma control. Rinse mouth after use to prevent thrush. c) Beclomethasone (QVAR®) PD: Suppresses inflammatory cells in airways. PK: Hepatic metabolism, minimal systemic absorption Adverse Effects: Sore throat, hoarseness, oral candidiasis. Notes: Used for maintenance therapy. d) Mometasone (Asmanex®) PD: Reduces airway inflammation and bronchial hyperresponsiveness. PK: Liver metabolism, low systemic bioavailability. Adverse Effects: Oral candidiasis (thrush), dysphonia, cough. Notes: High potency; used once daily. COPD Medications LABAs and anticholinergics (LAMA) are first-line for COPD maintenance therapy. 1. Long-Acting Beta-Agonists (LABAs) in COPD a) Indacaterol (Arcapta Neohaler®) PD: β2 agonist, long-acting bronchodilator PK: Onset: 5 min, Duration: ~24 hours.  Adverse Effects: Tachycardia, palpitations, tremors. Notes: Once-daily dosing, COPD only (not for asthma). b) Olodaterol (Striverdi Respimat®) PD: β2 agonist, smooth muscle relaxation. PK: Onset: 5 min, Duration: ~24 hours. Adverse Effects: Tachycardia, QT prolongation. Notes: Used in COPD, often combined with LAMAs. 2. Long-Acting Muscarinic Antagonists (LAMA) / Anticholinergics LAMAs are first-line therapy for COPD, reducing bronchoconstriction by blocking acetylcholine. a) Tiotropium (Spiriva®) PD: Blocks M3 receptors, reducing bronchoconstriction. PK: Long-acting, once-daily dosing. Adverse Effects: Dry mouth, urinary retention, glaucoma risk. Notes: Preferred for COPD maintenance. b) Aclidinium (Tudorza Pressair®) PD: M3 receptor antagonist, long-acting bronchodilation. PK: Onset: 5 min, Duration: ~12 hours. Adverse Effects: Blurred vision, dry mouth, cough Notes: Twice-daily dosing. c) Umeclidinium (Incruse Ellipta®) PD: M3 receptor antagonist, inhibits bronchoconstriction. PK: Onset: 10 min, Duration: ~24 hours. Adverse Effects: Dry mouth, constipation. Notes: Once-daily inhaler. d) Glycopyrrolate (Seebri Neohaler®) PD: Blocks M3 receptors, smooth muscle relaxation. PK: Onset: 5 min, Duration: ~12 hours. Adverse Effects: Urinary retention, blurred vision. Notes: Used in combination with LABAs. 3. Short-Acting Muscarinic Antagonists (SAMA) / Anticholinergics SAMAs are used for acute COPD exacerbations. a) Ipratropium (Atrovent®) PD: M3 receptor antagonist, inhibits bronchoconstriction. PK: Onset: 15 min, Duration: 4 to 6 hours. Adverse Effects: Dry mouth, headache, blurred vision. Notes: Used as PRN for COPD; less effective in asthma. 4. Combination Therapies (ICS + LABA or LAMA + LABA) The following are combination therapies that include inhaled corticosteroids (ICS) + long- acting beta-agonists (LABA) or long-acting muscarinic antagonists (LAMA) + LABA: 1. Advair Diskus® contains fluticasone + salmeterol and is used for asthma and COPD. 2. Symbicort® contains budesonide + formoterol and is used for asthma and COPD. 3. Breo Ellipta® contains fluticasone + vilanterol and is used for asthma and COPD, with the advantage of once-daily dosing. 4. Anoro Ellipta® contains umeclidinium + vilanterol and is indicated for COPD only as a LAMA + LABA combination. 5. Stiolto Respimat® contains tiotropium + olodaterol and is used for COPD only as a LAMA + LABA combination. Key Takeaways ICS (e.g., Fluticasone, Budesonide) = First-line for asthma but not COPD monotherapy. LABAs (e.g., Salmeterol, Formoterol) = Must be combined with ICS in asthma but used alone in COPD. LAMAs (e.g., Tiotropium, Umeclidinium) = First-line for COPD maintenance. SABAs (e.g., Albuterol, Levalbuterol) = Rescue therapy for asthma and COPD. Module 7: Hypertension & Dyslipidemia 1. Define Hypertension and Goal Blood Pressure Hypertension is defined as systolic blood pressure (SBP) ≥140 mmHg and/or diastolic blood pressure (DBP) ≥90 mmHg based on repeated measurements. Goal Blood Pressure (BP): o General population & low-risk patients: