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This document covers the Genitourinary system, including the anatomy and physiology of the kidneys, substances secreted by the kidneys, urinary system components, and process overview. It also discusses kidney functions in drug metabolism, tubular reabsorption, tubular secretion, and implications in drug therapy. Finally, it includes disease spotlights and nursing responsibilities related to drug administration.
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WEEK 13: GENITOURINARY SYSTEM Anatomy and Physiology of the Genitourinary System The Kidney Primary Functions: Excretion, regulation of fluid balance, electrolyte composition, and acid-base balance. Health Impact: Overall health is dependent on proper kidney function. Substanc...
WEEK 13: GENITOURINARY SYSTEM Anatomy and Physiology of the Genitourinary System The Kidney Primary Functions: Excretion, regulation of fluid balance, electrolyte composition, and acid-base balance. Health Impact: Overall health is dependent on proper kidney function. Substances Secreted by the Kidneys: 1. Renin: Regulates blood pressure. 2. Erythropoietin: Stimulates red blood cell production. 3. Calcitriol: Active form of vitamin D for bone homeostasis. Urinary System Components: Two kidneys, two ureters, one urinary bladder. Each kidney has one million nephrons, the functional units. Process Overview: 1. Blood enters the nephron through renal arteries and passes through the glomerulus. 2. Water and small molecules filter into Bowman’s Capsule → proximal tubule → loop of Henle → distal tubule. 3. Filtrate becomes urine after leaving the nephron and entering collecting ducts. Key Structures: Ureter: Smooth muscle fiber (25–30 cm long, 3–4 mm diameter). Urinary Bladder: Muscular sac above/behind the pubic bone, pear-shaped. Kidney Functions in Drug Metabolism Tubular Reabsorption: Reabsorption of water (178.5 L/day), glucose, amino acids, and essential ions (sodium, chloride, calcium). Tubular Secretion: Substances like potassium, phosphate, and ammonium are secreted into urine. Implications in Drug Therapy: Damaged kidneys impair reabsorption and excretion, affecting serum drug levels. Examples: Penicillin G, NSAIDs, and furosemide. Renal Failure Definition: Decline in kidney function leading to inability to maintain fluid/electrolyte balance or excrete waste. Diagnostic Tools: 1. Urinalysis: Detects blood cells, protein, ketones, glucose, microorganisms, etc. 2. Imaging: CT, MRI, ultrasound. 3. GFR: Best marker for kidney function. Treatment Goals: Maintain blood flow and adequate urine output. Complications and Treatments: Compli Pathogene Treatment cation sis Anemia Insufficient Epoetin alfa erythropoieti (Procrit, n Epogen) Hyperk Inadequate Polystyrene alemia potassium sulfate, dietary excretion restriction Hyperp Impaired Calcium hospha phosphate acetate, dietary temia excretion restriction Hyperv Sodium/wat Loop/thiazide olemia er retention diuretics, sodium restriction Metabo Inability to Sodium lic excrete bicarbonate Acidosi metabolic s acids Drugs Acting on the Renal System Diuretic Classes: 1. Thiazide Diuretics: ○ First-line for hypertension, promotes calcium reabsorption. ○ Adverse effects: Hypokalemia, hypercalcemia, hyperglycemia. 2. Loop Diuretics (High-Ceiling): ○ Act on the loop of Henle, used for heart failure, edema, rapid diuresis. ○ Adverse effects: Electrolyte loss, hyperuricemia, glucose intolerance. 3. Carbonic Anhydrase Inhibitors: ○ Used for glaucoma, blocks bicarbonate reabsorption. 4. Potassium-Sparing Diuretics: ○ Retains potassium, indicated for hyperaldosteronism. ○ Example: Spironolactone (aldosterone antagonist). 5. Osmotic Diuretics: ○ Pulls water into renal tubules (e.g., mannitol for glaucoma, cranial pressure). Disease Spotlights 1. Edema: Caused by heart failure, liver disease, or renal disease. Treated with diuretics and addressing the underlying cause. 2. Hypertension: Persistent high BP managed with diuretics to reduce fluid volume. 3. Glaucoma: Increased intraocular pressure treated with diuretics to reduce fluid. Drugs for Urinary Tract Conditions 1. Anti-Infectives: ○ Antibiotics or urine acidifiers to inhibit bacterial growth. 2. Antispasmodics: ○ Relieve smooth muscle spasms in urinary tract infections. 3. Analgesics: ○ Phenazopyridine for pain relief in urinary tract irritation. 4. Bladder Protectants: ○ Pentosan polysulfate sodium for interstitial cystitis. 5. BPH Treatments: ○ Alpha-blockers (relax smooth muscle) and testosterone inhibitors (e.g., finasteride). Nursing Responsibilities Administer drugs properly (with food, early in the day). Monitor for adverse effects, fluid balance, and cardiac rhythm. Educate patients about their medication and dietary needs. WEEK 14: PAIN AND INFLAMMATION MANAGEMENT Anti-Inflammatory Drugs General Overview Anti-inflammatory agents: ○ Inhibit prostaglandin biosynthesis. ○ Provide analgesic, antipyretic, and anticoagulant effects. Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) Cyclooxygenase (COX) Function: Converts arachidonic acid into prostanoids (prostaglandins, thromboxanes). Role in Prostaglandin Synthesis: ○ Prostaglandins promote inflammation, pain, and fever but also protect the stomach lining and support platelet function. Types of NSAIDs Seven Groups: ○ Salicylates ○ Para-chlorobenzoic acids ○ Phenylacetic acids ○ Propionic acid derivatives ○ Fenamates ○ Oxicams ○ Selective COX-2 inhibitors Common Over-the-Counter NSAIDs: ○ Aspirin (Bayer, Bufferin) ○ Ibuprofen (Advil, Motrin IB) ○ Naproxen (Aleve) Key Therapeutic Effects 1. Relieve pain (analgesic). 2. Suppress inflammation. 3. Reduce fever (antipyretic). First-Generation NSAIDs 1. Salicylates Example: Aspirin (Acetylsalicylic Acid, ASA). ○ Mechanism: Inhibits prostaglandin synthesis and platelet aggregation. ○ Uses: Anti-inflammatory, antiplatelet therapy (e.g., for cardiac disorders). 2. Para-Chlorobenzoic Acids Example: Indomethacin (Indocin). ○ Uses: Rheumatoid arthritis, gouty arthritis, osteoarthritis. 3. Phenylacetic Acid Derivatives Examples: ○ Diclofenac Sodium (Voltaren-XR): Minimal antipyretic effects. ○ Ketorolac (Toradol): Injectable NSAID for short-term pain management. 4. Propionic Acid Derivatives Example: Ibuprofen (Motrin). ○ Uses: Mild pain, inflammation, and fever. ○ Advantages: Less severe GI irritation compared to aspirin. 5. Fenamates Examples: Meclofenamate, Mefenamic Acid (Ponstel). ○ Uses: Acute and chronic arthritic conditions. ○ Side Effects: GI irritation, edema, dizziness. 6. Oxicams Example: Piroxicam (Feldene). ○ Advantages: Long half-life, ideal for chronic arthritis. General Side Effects Gastric irritation. Sodium and water retention. Avoid alcohol to reduce GI complications. Second-Generation NSAIDs 7. Selective COX-2 Inhibitors Example: Celecoxib (Celebrex). ○ Benefits: Reduced GI side effects compared to non-selective NSAIDs. ○ Indication: Severe arthritis requiring long-term treatment. Corticosteroids Examples: Prednisone, Prednisolone, Dexamethasone. Uses: Control inflammation by suppressing inflammatory processes. Drawbacks: Numerous side effects; not first-line for arthritis. Disease-Modifying Antirheumatic Drugs (DMARDs) Types: 1. Immunosuppressive Agents (e.g., Methotrexate). 2. Immunomodulators (e.g., Anakinra, TNF blockers). 3. Antimalarials (mechanism unclear). Antigout Drugs Allopurinol Mechanism: Reduces uric acid production, preventing uric acid crystal formation in joints. Opioid Analgesics General Overview Derived from opium poppy (opiates) or synthesized (opioids). Effects: Analgesia, euphoria, sedation. Adverse Effects: Respiratory depression, nausea, constipation, tolerance, and addiction. Mechanism of Action Interact with opioid receptors: 1. Mu 2. Kappa 3. Delta Types of Opioids 1. Weak Agonists (e.g., Codeine): Moderate pain relief, cough suppression. 2. Strong Agonists (e.g., Meperidine): Risk of serotonin syndrome, hyperpyrexia. 3. Mixed Agonist-Antagonists (e.g., Nalbuphine): Lower addiction and respiratory depression risks. 4. Antagonists (e.g., Naloxone): Reverse opioid toxicity. Common Uses Severe pain, acute MI, end-of-life care (dyspnea), and preoperative anesthesia. Nursing Responsibilities 1. Monitor for bleeding (gums, stool). 2. Administer NSAIDs with food to prevent GI upset. 3. Educate patients to avoid alcohol and aspirin with NSAIDs. 4. Ensure patients inform healthcare providers of NSAID use before procedures. 5. Monitor renal function, especially in elderly patients. History of Chemotherapy Paul Ehrlich: Conceptualized chemotherapy targeting pathogens without harming hosts. Key milestones: ○ Sulfa drugs (1930s) ○ Penicillin discovery (1929, clinical trials in 1940) Key Definitions Chemotherapy: Use of drugs to treat diseases. Antimicrobial agents: Chemotherapeutic agents specifically for infections, including: ○ Antibacterials ○ Antifungals ○ Antiprotozoals ○ Antivirals Antimicrobials: How They Work Target pathogen-specific processes, sparing the host. Common mechanisms: 1. Inhibit cell wall synthesis. 2. Damage cell membranes. 3. Inhibit nucleic acid synthesis. 4. Inhibit protein synthesis. 5. Inhibit enzyme activity. Key Classes of Antibacterial Agents 1. Penicillins: ß-lactam antibiotics; inhibit cell wall synthesis. 2. Cephalosporins: ß-lactam class; categorized into five generations by spectrum. 3. Carbapenems: Broad-spectrum, strong efficacy against resistant strains. 4. Glycopeptides: Effective against Gram-positive bacteria (e.g., Vancomycin). 5. Tetracyclines: Broad-spectrum, bacteriostatic, inhibit protein synthesis. 6. Aminoglycosides: Broad-spectrum, bactericidal, inhibit protein synthesis but toxic. 7. Macrolides: Variable effect (bacteriostatic/cidal), inhibit protein synthesis. 8. Fluoroquinolones: Broad-spectrum, inhibit DNA synthesis. 9. Sulfonamides: Inhibit folic acid production, bacteriostatic. Special Antimicrobial Agents Antifungals: Interfere with sterols or nucleic acid synthesis. Antiprotozoals: Target DNA/RNA or metabolism. Antimalarials: Act at different Plasmodium life cycle stages. Antivirals: Challenge due to intracellular replication; HIV drug combinations are prominent. Drug Resistance Superbugs: Multidrug-resistant organisms complicate treatment. Resistance Mechanisms: ○ Mutation altering drug binding sites or permeability. ○ Enzyme production (e.g., ß-lactamase) to inactivate drugs. ○ Efflux pumps expelling drugs. Strategies to Combat Resistance Rational prescription: Narrow-spectrum drugs, proper dosage. Patient adherence: Complete prescribed courses, avoid self-medication. Education: Address overuse and misuse in healthcare and communities. Empiric Therapy Initiated before lab results to save lives, relying on clinical judgment.