Pathopharmacology Exam Review PDF

Summary

This document appears to be a past paper or practice questions covering topics in pathopharmacology. The contents include various bacterial infections, antibiotics, immune system responses, and antiviral drugs. Key aspects include the discussion of hypersensitivity reactions, autoimmune disorders, and various types of pulmonary disorders, including treatments.

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1. exotoxin endotoxin Toxins secreted by bacteria that can cause Toxins secreted by bacteria that can cause damage to the host by destroying cells or damage to the host by destroying cells or disrupting normal cellula...

1. exotoxin endotoxin Toxins secreted by bacteria that can cause Toxins secreted by bacteria that can cause damage to the host by destroying cells or damage to the host by destroying cells or disrupting normal cellular metabolism. disrupting normal cellular metabolism. 2. infectivity communicability virulence The ability of a pathogen to The ability of a pathogen to The ability of a invade and multiply in the invade and multiply in the microorganism to cause host. host. severe disease or harm to the host. 3. Narrow spectrum Penicillin and narrow spectrum Aminoglycoside Cephalosporin treat gram-positive treat gram negative 4. Cephalosporin first generation higher generation treat gram positive and has more bacterial treat gram positive, negative, and less resistant bacterial resistant 5. Antibiotics that treat MRSA infection Vancomycin Inhibits cell wall synthesis used for severe infections including MRSA. Fifth generation cephalosporin Used for infections associated with MRSA. (Ceftaroline) 6. Antibiotics that treat Pseudomonas infection Fourth generation cephalosporin Used to treat health care- and hospital- (Cefepime): associated pneumonias, including those caused by Pseudomonas. 7. Inhibit cell wall of bacteria: Penicillin Cephalosporin Vancomycin Carbapenems 8. Protein inhibitors: Macrolides Aminoglycosides Tetracyclines 9. DNA and folic acid inhibitor: Sulfa and Trimethoprim 10. allergic reactions Penicillin and cephalosporins with Sulfa Antibiotics: Common mild reactions Penicillin allergies as more include rash, drug fever, and common, with anaphylaxis being photosensitivity. the most severe reaction characterized by bronchospasm, laryngeal edema, and hypotension. 11. Aminoglycosides SE: Ototoxicity nephrotoxicity 12. Grape fruit juices = P-450 inhibitor 13. Opioid SE constipation decrease RR sedation euphoria hypotension 14. Cyclosporine SE: nephrotoxicity, hepatotoxicity, and increase chance of infection 15. NSAID SE GI side effect nausea vomiting abdominal pain GI bleeding nephrotoxicity 16. Glucocorticoids SE: Hypertension, increase chance of infection, Hyperglycemia, breakdown of skin, muscle, and bones, and GI side effect (nausea, vomiting, abdominal pain), GI bleeding. 17. Hypersensitivity type IV: delayed response only T lymphocytes involved no antibody present Ex: PPD test and contact dermatitis 18. Autoimmune disorders: Lupus RA Graves Type 1 DM 19. Hypersensitivity type I: Mast cells, IgE, genetic link, prompt reaction 20 mins, mild hives and rash, life-threatening Anaphylaxis 20. Hypersensitivity type II and III: IgG, and IgM, causing autoimmune disorders, transfusion reaction and Rh disease of fetus 21. C-pain fibers unmyelinated slow poor localized 22. delta pain fibers located in skin fast highly localized 23. Threshold and tolerance pain 24. Why we have referred pain? Pain perceived at a location other than the site of the painful stimulus. Often occurs due to the sharing of sensory pathways between the site of injury and the referred area. 25. Benefits of low grade fever Kills invading microorganisms Promotes lysosomal breakdown and autodestruction of infected cells Increases lymphocytic transformation and phagocytic motility Augments antiviral interferon production Augments phagocytosis 26. Danger of hyperthermia Heat cramps, exhaustion, heatstroke Nerve damage at temperatures ≥ 41°C (105.8°F) leading to convulsions Death at temperatures ≥ 43°C (109.4°F) 27. Active Immunity: Passive Immunity: This occurs when an individual's immune This occurs when a person is given system responds to a foreign substance antibodies to a disease rather than (antigen) and produces antibodies. This producing them through their immune can happen through natural exposure to a system. This can happen naturally, such as pathogen or through vaccination. antibodies passed from mother to baby through breast milk, or artificially through antibody-containing blood products. Example: Getting vaccinated against Example: Receiving antibodies for rabies measles. after exposure to the virus. 28. What is Superinfection? A superinfection is an infection that occurs on top of an existing infection, usually due to the disruption of normal microbial flora by antibiotics, allowing opportunistic pathogens to overgrow. 29. COPD Barrel Chest A physical characteristic often seen in advanced COPD where the chest becomes rounded and enlarged due to chronic overinflation of the lungs. 30. Glucorticoid inhalers = use daily regardless of having asthma or not 31. Main pathogenesis in emphysema = The destruction of the alveoli (air sacs) in the lungs, leading to decreased surface area for gas exchange and difficulty in breathing 32. Main pathogenesis in chronic bronchitis = increase in mucus production and inflammation in the airways, leading to coughing and difficulty in breathing. 33. Albuterol = beta 2 agonist treats asthma by opening the airways (bronchodilator) 34. Different types of pleural effusions Transudative Caused by fluid leaking into the pleural space due to increased pressure or low protein content, often seen in heart failure or cirrhosis. Exudative Caused by inflammation, infection, or malignancy, leading to fluid with high protein content and cellular debris. Hemorrhagic Contains blood, often due to trauma or malignancy. Chylous Contains lymph fluid, often due to injury or obstruction of the thoracic duct. 35. Signs and symptoms of acute asthma SOB Wheezing Chest tightness Coughing 36. Pathogenesis of asthma chronic inflammation of the airways leading to hyperresponsiveness bronchoconstriction airflow obstruction Allergens, infections…etc. 37. Temperature Benefit of fever Kills invading microorganisms Promotes lysosomal breakdown and autodestruction of infected cells Increases lymphocytic transformation and phagocytic motility Augments antiviral interferon production Augments phagocytosis 38. and their stages: what is the s/s or consequence of different stages of hyperthermia? Hyperthermia Heat Cramps: Painful muscle contractions due to loss of fluids and electrolytes. Heat Exhaustion Symptoms include heavy sweating, weakness, dizziness, nausea, and headache. Heatstroke A medical emergency where body temperature exceeds 41°C (105.8°F), causing confusion, seizures, and potential death. 39. Bacterial Infection a. Identify the factors of infection: including chain of transmission: Pathogenicity, microbial adherence, invasion, communicability, virulence, immunogenicity, infectivity, bacteremia or septicemia, portal of entry. pathogenicity communicability virulence Microorganism’s ability The ability to spread the The ability of a to infect and cause disease from one microorganism to cause disease in the host. individual to another. severe disease or harm to the host. b. What factors in an individual increase the risk of infection? Malnutrition, age, chronic illness, stress, immunosuppression, recent antibiotic use. c. For bacterial infection describe the following: Exotoxins Endotoxins Toxins secreted by bacteria. Components of the outer membrane of Gram-negative bacteria, released upon bacterial cell death. d. endospores role and mechanism: Endospores are a form of bacterial resistance; they can withstand extreme conditions and germinate when conditions are favorable, thus ensuring the survival of the bacterium. e. Limitations/complications of antibiotic use (i.e., antimicrobial resistance- understand thoroughly) Antimicrobial resistance: Bacteria become resistant to antibiotics, making infections harder to treat. This can result from overuse or misuse of antibiotics. 40. Antimicrobials Grape fruit juices = P-450 inhibitor i. b. Aminoglycosides: narrow-spectrum Treat gram negative protein inhibitor SE: Ototoxicity, and nephrotoxicity 41. Nosocomial infections known as hospital-acquired infections, are infections that patients acquire during their stay in a healthcare facility. These infections can be caused by bacteria, viruses, fungi, or parasites and are often associated with medical procedures or devices like catheters and ventilators. 42. Superinfection A superinfection is an infection that occurs on top of an existing infection, usually due to the disruption of normal microbial flora by antibiotics, allowing opportunistic pathogens to overgrow. 43. Bactericidal Bacteriostatic Bactericidal: Antibiotics that kill bacteria Antibiotics that inhibit the growth and directly. reproduction of bacteria, allowing the immune system to eliminate the infection. Example: Penicillin. Example: Tetracyclines. 44. Gram Positive Gram Negative Gram Positive Bacteria: Have a thick Gram Negative Bacteria: Have a thin peptidoglycan cell wall that retains the peptidoglycan cell wall and an outer crystal violet stain, appearing purple under membrane, which does not retain the a microscope. crystal violet stain, appearing pink under a microscope. Example: Staphylococcus aureus. Example: Escherichia coli. 45. MRSA Pseudomonas Treated with antibiotics like Vancomycin Treated with Fourth-generation and Fifth-generation cephalosporins cephalosporins (Cefepime) and other (Ceftaroline). antibiotics like Piperacillin-tazobactam. 46. antimicrobial class: Penicillin Inhibits cell wall synthesis. Side effects: Allergic reactions, gastrointestinal issues. Cephalosporins Inhibit cell wall synthesis. Side effects: Allergic reactions, gastrointestinal issues. Vancomycin Inhibits cell wall synthesis. Side effects: Nephrotoxicity, ototoxicity. Macrolides Inhibit protein synthesis. Side effects: Gastrointestinal issues, hepatotoxicity. Aminoglycosides Inhibit protein synthesis. Side effects: Ototoxicity, nephrotoxicity. Tetracyclines Inhibit protein synthesis and DNA/folic acid synthesis. Side effects: Photosensitivity, gastrointestinal issues. Sulfa antibiotics: Inhibit DNA/folic acid synthesis. Side effects: Allergic reactions, kidney issues. 47. Gentamicin Cephalosporin: Inhibit cell wall of bacteria: Cephalosporins inhibit cell wall synthesis. first generation treat gram positive and has more bacterial resistant, higher generation treat gram positive, negative, and less bacterial resistant: 48. including Vancomycin: inhibit cell wall of bacteria Penicillin group (B-lactam): Penicillin (B-lactam): Inhibits cell wall synthesis. Vancomycin Inhibits cell wall synthesis. 49. Tetracycline protein inhibitor broad-spectrum action 50. Sulfa: DNA/ folic acid inhibitor 51. Macrolides protein inhibitor 52. Immune Dysfunction 53. Active Immunity: Passive Immunity: This occurs when an individual's immune This occurs when a person is given system responds to a foreign substance antibodies to a disease rather than (antigen) and produces antibodies. This producing them through their immune can happen through natural exposure to a system. This can happen naturally, such as pathogen or through vaccination. antibodies passed from mother to baby through breast milk, or artificially through antibody-containing blood products. Example: Getting vaccinated against Example: Receiving antibodies for rabies measles. after exposure to the virus. 54. Describe autoimmune disorders Autoimmune disorders occur when the immune system mistakenly attacks the body's own tissues, recognizing them as foreign. This leads to inflammation and damage to various organs and tissues. 55. Autoimmune disorders: Lupus systemic lupus erythematosus (SLE), is a chronic autoimmune disease where the body's immune system mistakenly attacks its own healthy tissues and organs RA a chronic autoimmune disease that primarily affects the joints. It causes inflammation, pain, and stiffness in the joints, which can lead to damage and disability over time Graves an autoimmune disorder that causes the thyroid gland to produce too much thyroid hormone. Type 1 DM an autoimmune disease that occurs when the body's immune system destroys the pancreas' insulin- producing cells. 56. Differentiate among the four hypersensitivity reactions and what immunoglobulins are involved in the hypersensitivities i. Hypersensitivity 1 Mast cells & basophils, IgE, genetic link, prompt reaction 20 mins, mild hives and rash, life-threatening Anaphylaxis (Allergens) 2 Immediate, specific antibodies attacking specific antigens Ex: Graves disease and myasthenia gravis -Transfusion Reaction - Rh disease of fetus 3 Non-tissue specific, system unable to remove antigen-antibody immune complexes Ex: Lupus 4 delayed response, and only T lymphocytes involved, no antibody present. PPD test and contact dermatitis (Mediated by T cells only and no antibodies) 57. Allergies (include anaphylaxis) i. Describe the role of histamine in the allergic Histamine is released by mast cells response. during an allergic reaction, causing symptoms like vasodilation, increased vascular permeability, and bronchoconstriction. ii. can cause allergic reactions Penicillin, Cephalosporin, and sulfa These can cause allergic reactions antibiotics ranging from mild rashes to severe anaphylaxis. 58. Immune System Medications Glucocorticoid drugs: Reduce inflammation and suppress the immune system. Side effects: Hypertension, increased risk of infection, hyperglycemia, breakdown of skin, muscle, and bones, GI side effects, GI bleeding. Cyclooxygenase inhibitors: Reduce inflammation and pain. Side effects: GI issues, increased risk of bleeding. Cyclosporine An immunosuppressant used to prevent organ rejection. Side effects: Nephrotoxicity, hepatotoxicity, increased risk of infection. 59. glucocorticoid drugs cyclooxygenase inhibitors, Knows the: i. Cyclosporine: Side effects: nephrotoxicity, hepatotoxicity, and increase chance 1. of infection Mechanism of actions and side effects of : Glucocorticoid drugs: Reduce inflammation and suppress the immune system. Side effects: Hypertension, increased risk of infection, hyperglycemia, breakdown of skin, muscle, and bones, GI side effects, GI bleeding. Cyclooxygenase inhibitors: Inhibit the COX enzyme, immunosuppressant, Reduce inflammation and pain. Side effects: GI issues, increased risk of bleeding. Cyclosporine An immunosuppressant used to prevent organ rejection. Side effects: Nephrotoxicity, hepatotoxicity, increased risk of infection. 60. Inflammation Inflammation is the body's response to injury or infection, characterized by redness, swelling, heat, pain, and loss of function. 61. Types of Exudate Serous Clear, watery fluid. Fibrinous Thick, sticky, and contains high levels of fibrin. Purulent Contains pus, indicating infection. Hemorrhagic Contains blood, indicating bleeding. 62. Complement Cascade function: Opsonization Opsonization is a process where pathogens are marked for destruction by the immune system. The complement cascade enhances the ability of antibodies and phagocytic cells to clear microbes and damaged cells. 63. inflammation Localized Inflammation that occurs at the site of injury or infection. General Systemic inflammation affecting the entire body. 64. Role in inflammation: Macrophages Phagocytose pathogens and release cytokines to mediate the inflammatory response. Neutrophils Phagocytose pathogens and release free radicals to kill microbes. 65. Pain and Pain medication Pain Process Involves the transmission of pain signals from the site of injury to the brain. Pain Pathway: Nerve fibers transmit pain signals to the central nervous system. Types of Pain: Acute, chronic, referred pain. Referred Pain: Pain perceived at a location other than the site of the painful stimulus Threshold Pain threshold is the minimum intensity at which a person perceives pain. Tolerance Pain tolerance is the maximum level of pain a person can endure. i. characteristics of pain fibers? Delta Pain Fibers Fast-paced, highly localized, found in the skin. C Pain Fibers Unmyelinated, slow, poorly localized. ii. Mechanism of Like morphine, Side effects constipation, action and side work by binding decreased effects of opioid to opioid respiratory rate, medications like receptors in the sedation, Morphine brain to reduce euphoria, pain. hypotension. iii. Narcan Reverses the effects of opioids. iv. Buprenorphine A partial opioid agonist used for pain and opioid dependence. v. Clonidine Mechanism Centrally acting alpha-2 adrenergic agonist that reduces sympathetic outflow, resulting in decreased blood pressure. Uses Hypertension, ADHD, pain management in certain cases. Side Effects Drowsiness, dry mouth, constipation, and bradycardia. vi. Ultram Mechanism Centrally acting analgesic that binds to opioid receptors and inhibits reuptake of norepinephrine and serotonin. Uses Moderate to moderately severe pain. Side Effects: Dizziness, nausea, constipation, headache, somnolence. vii. NSAID what are they? Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) are medications used to reduce inflammation, pain, and fever. How do they work?: NSAIDs inhibit the enzyme cyclooxygenase (COX), which is involved in the production of prostaglandins. Prostaglandins are responsible for inflammation, pain, and fever. side effects: GI bleeding -Ulcers Abdominal pain Nausea Vomiting 66. Antiviral and antifungal: Understanding mechanism of action and side effects a. Acyclovir Mechanism of Action: Inhibits viral DNA polymerase, preventing viral DNA synthesis. Side Effects: Nausea, diarrhea, headache, nephrotoxicity (at high doses), and stinging sensations (topical). b. Flu Vaccines Mechanism of Action: Stimulate the immune system to produce antibodies against the influenza virus. Side Effects: Soreness at the injection site, mild fever, muscle aches. c. Protease Inhibitors (as a group) Mechanism of Action: Inhibit the protease enzyme in HIV, preventing the maturation of infectious viral particles. Side Effects: Hyperglycemia, lipodystrophy, elevated liver enzymes, gastrointestinal disturbances. List: nelfinavir (Viracept). d. Tamiflu Mechanism of Action: Inhibits neuraminidase, an enzyme that helps the flu virus spread. Side Effects: Nausea, vomiting, headache. e. Efavirenz Mechanism of Action: Non-nucleoside reverse transcriptase inhibitor (NNRTI) for HIV treatment. Side Effects: CNS effects (dizziness, insomnia), rash, liver enzyme elevations. f. Nelfinavir Mechanism of Action: HIV protease inhibitor. Side Effects: Diarrhea, nausea, rash. g. Zidovudine Mechanism of Action: Nucleoside reverse transcriptase inhibitor (NRTI) for HIV treatment. Side Effects: Anemia, neutropenia, gastrointestinal disturbances. h. Voriconazole Mechanism of Action: Inhibits fungal cell membrane synthesis. Side Effects: Visual disturbances, liver enzyme elevations, skin reactions. i. Amphotericin B Mechanism of Action: Binds to ergosterol in fungal cell membranes, causing cell death. Side Effects: Nephrotoxicity, infusion reactions (fever, chills), electrolyte imbalances. j. Azoles as a group Mechanism of Action: Inhibit fungal cell membrane synthesis. Side Effects: Liver enzyme elevations, gastrointestinal disturbances, skin reactions. k. HIV: Modes of transmission, expected lab findings, dx of AIDS. HIV Modes of Transmission: Sexual contact, blood transfusions, needle sharing, mother-to-child during childbirth or breastfeeding. Expected Lab Findings Decreased CD4+ T-cell count, increased viral load. Diagnosis of AIDS: Diagnosed when CD4+ T-cell count falls below 200 cells/mm³ or when opportunistic infections/cancers occur. l. superficial, mucocutaneous, and Primary or deep. Fungal Infections: Superficial: Affecting skin, hair, and nails (e.g., ringworm, athlete's foot). Mucocutaneous: Affecting mucous membranes (e.g., oral thrush). Primary or Deep: Affecting internal organs (e.g., histoplasmosis). 67. Additonal Information 68. Efavirenz: Can it be taken with meals? Taken on an empty stomach to reduce side effects such as dizziness and drowsiness. 69. Nelfinavir: Common side effects Diarrhea, nausea, rash. 70. 9. Pulmonary diseases and treatments i. T.B. medications Rifampin, Isoniazid, Pyrazinamide, Ethambutol = RIPE to treat active TB Mechanism: Target various aspects of Mycobacterium tuberculosis. Side Effects: Hepatotoxicity, peripheral neuropathy (Isoniazid), gastrointestinal disturbances, optic neuritis (Ethambutol). 71. Pathophysiology: 72. TB: TB Testing Results: Positive tuberculin skin test (TST) or interferon-gamma release assays (IGRA). Adherence Crucial for effective treatment and prevention of drug resistance. Drug Resistance Can occur with improper use or incomplete treatment. Latent TB: Inactive, non-contagious, but Active TB: Contagious, symptomatic, can become active requires treatment. Transmission: Airborne, spread through respiratory droplets. 73. Pulmonary: a. Pulmonary Pulmonary embolism (PE) composed of an embolus, usually a blood clot, that lodges in the pulmonary arteries and obstructs blood flow to the lungs. Clinical manifestations can include sudden shortness of breath, chest pain, cough (sometimes with bloody sputum), rapid breathing, rapid heart rate, lightheadedness, and low blood pressure. Prevention involves anticoagulant therapy compression stockings. Pulmonary Edema: Clinical Manifestations: Shortness of breath, pink frothy sputum, crackles in lungs. Primary Cause: Left-sided heart failure. Pneumonia Clinical Manifestations: Fever, cough, chest pain, difficulty breathing. Pathogenesis: Inflammation and infection of the lung parenchyma. Virchow's Triad: Components: Endothelial injury, hypercoagulability, stasis of blood flow. 74. Pulmonary disorders hypoxemia: Low blood oxygen levels. Hypoxia: Low oxygen in tissues. Ventilation/Perfusion (V/Q) Mismatch: Imbalance between air reaching the alveoli and blood reaching the alveoli. Asthma Extrinsic: ** Status Asthmatics: Severe, prolonged asthma attack not responsive to usual treatment. Pathogenesis Immune response to allergens, leading to airway inflammation and bronchoconstriction. Clinical Manifestations: Wheezing, shortness of breath, chest tightness. 75. COPD and barrel chest: COPD: A = Emphysema Alveoli destruction B= Chronic Bronchitis Excess Mucus production Barrel Chest: Increased anterior- posterior diameter of the chest. 76. Pneumothorax pleural effusion Air in the pleural space causing lung abnormal accumulation of fluid in collapse. Air in the pleural space causing the pleural space between the lung collapse. lungs and chest wall. 1. Transudative effusions - Caused by imbalances in hydrostatic or oncotic pressure, such as heart failure, cirrhosis, or nephrotic syndrome. The fluid is typically clear and protein-poor. 2. Exudative effusions - Caused by inflammation or injury, such as pneumonia, cancer, or pulmonary embolism. The fluid is protein-rich. 3. Empyema - A collection of pus in the pleural space due to bacterial infection. 4. Hemothorax - An accumulation of blood in the pleural space, often from trauma or surgery. 5. Chylothorax - An accumulation of lymphatic fluid high in triglycerides in the pleural space. Pulmonary medications Albuterol (SABA): Mechanism Beta-2 agonist that opens airways by relaxing bronchial muscles. Use Treats asthma by providing quick relief. When to use: Rescue Inhaler Glucocorticoids Mechanism Reduce inflammation in the airways. Side Effects: Hypertension, increased infection risk, hyperglycemia, breakdown of skin, muscles, bones, GI side effects, GI bleeding. Usage Need to be used daily, even when not experiencing asthma symptoms. ********* Long-acting Beta Agonists (LABA): Indication: Used for long-term control of asthma symptoms. 77. Singulair Mechanism: Leukotriene receptor antagonist that helps reduce airway inflammation and bronchoconstriction. 78. how it work in treating Asthma, their side effects, and patient teaching Corticosteroids Mechanism: Reduce inflammation in the airways. Side Effects: Hypertension, increased infection risk, hyperglycemia, breakdown of skin, muscle, and bones, GI side effects (nausea, vomiting, abdominal pain), GI bleeding. Patient Teaching: Importance of daily use, potential side effects, and proper inhaler technique. Inhibit Cell Wall Synthesis Inhibit Protein Inhibit DNA/Folic Acid Beta-lactams 1. Aminoglycosides Sulfonamides & trimethoprim 1.penicillins 2. Tetracyclines 2. cephalosporins 3. macrolides 3. Carbapenems 4.vancomycin Antimicrobial Treat MOA: SE: MOR: Treats MRSA : or Pneumonia Penicillin -Narrow Inhibits Allergic reaction 1. Prevents N/A Spectrum = cell wall target Gram + synthesi reach s 2. -Broad Inactivatio Spectrum = n by Gram - & bacterial Gram + enzymes 3. -Extended- Penicillin- Spectrum binding Penicillin = proteins Piperacillin production (Anti- – these Pseudomonal change the ) shape Cephalosporins **4th gen Inhibits -Anaphylactic Both (Cefepime) cell wall shock 4th gen = treats synthesi -Superinfection pseudomona pseudomona s – PBPs s s Penicillin 5th gen= **5th gen Binding MRSA (ceftaroline) Proteins treats MRSA to disrupt Carbapenems Broad Inhibit Abdominal pain N/A spectrum = cell wall Nausea Gram - & + synthesi Vomiting s Vancomycin Treats MRSA Inhibits -Ototoxicity MRSA & C.diff cell wall -Redman synthesi syndrome s Thrombophlebiti s Tetracyclines Broad Inhibits -GI issues Pneumonia **Doxy treats spectrum protein -Discoloration of acne** -Lyme synthesi teeth *Minocycline disease s -Teratogenic -Peptic ulcer disease Macrolides Broad Inhibits 1.GI issues N/A spectrum protein 2. arrhythmia - synthesi prolonged QTs s 3. super infection Aminoglycosides Narrow Inhibits Ototoxicity and * Narrow Spectrum = protein Nephrotoxicity Therapeutic Gram - synthesi index) s Tri Broad Inhibits photosensitivity Spectrum folic Bactrim acid/DN (combo of A both) = treats UTI Sulfa Broad Inhibits photosensitivity Spectrum folic Bactrim acid/DN (combo of A both) = treats UTI

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