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Questions and Answers
Who developed a synthetic chemical that would target infection-causing cells without affecting human cells?
What significant discovery was made by Alexander Fleming?
Which of the following is NOT a classification of anti-infectives?
What is one mechanism of action for anti-infective agents?
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What term describes the ability of microorganisms to adapt to anti-infective drugs over time?
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How can bacteria acquire resistance to anti-infective drugs?
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What can cause natural resistance to anti-infectives?
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What happens to some strains of bacteria previously controlled by penicillin?
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What is the primary action of aminoglycosides?
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Which of the following is NOT a common medication classified as an aminoglycoside?
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What side effect is most associated with aminoglycoside therapy?
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What is a common contraindication for the use of aminoglycosides?
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How are aminoglycosides primarily excreted from the body?
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What is the recommended maximum duration for amikacin treatment due to its toxicity?
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Which pharmacokinetic property is true for aminoglycosides?
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Which adverse effect requires monitoring urinalysis in patients receiving aminoglycosides?
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Which antibiotic is indicated for prostatitis?
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What is a common adverse effect of macrolides?
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Which statement is true regarding the pharmacokinetics of macrolides?
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What is a contraindication for using lincosamides?
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Which of the following antibiotics is classified as a monobactam?
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Which of the following antibiotics is indicated for chronic bronchitis?
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What are the adverse effects associated with the use of monobactams?
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How should macrolides be administered for optimal absorption?
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What is a common type of fungal infection in humans?
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What is the primary component of fungal cell walls that provides resistance to antibiotics?
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Which of the following antifungal treatments is used for systemic mycoses?
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What form of antifungal medication can be used topically?
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Which antifungal medication is commonly used in the treatment of vaginal thrush?
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What is a potential side effect of systemic antifungal medications?
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What is the mechanism of action of antifungal medications?
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What is a common indication for using topical antifungal treatments?
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What is the primary use of lamivudine?
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Which adverse effect is associated with abacavir?
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What is a contraindication for protease inhibitors?
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Which condition is NOT an indication for zidovudine?
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What adverse effect can occur due to tenofovir?
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Which class of drugs blocks protease activity essential for HIV maturity?
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What condition is reserved for treatment with integrase inhibitors?
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Which of the following is a characteristic of hepatitis C?
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Study Notes
Development of Anti-infective Therapy
- Paul Ehrlich (1920s): Pioneered the search for synthetic chemicals that targeted infection-causing cells without harming human cells.
- Penicillin (late 1920s): Discovered in a mold sample.
- Sulfonamides (1935): Introduced as an effective anti-infective agent.
- Alexander Fleming: Recognized for discovering penicillin while observing a mold (Penicillium notatum) contaminating a petri dish containing Staphylococcus aureus bacteria.
Anti-Infective Agents
- General term for medicines inhibiting or killing infectious organisms.
- Exert effects on foreign organisms that cause infection.
Mechanism of Action
- Interfering with Bacterial Cell Wall Biosynthesis: Prevents bacteria from building their protective outer layer.
- Preventing Use of Essential Substances: Blocks the invading organism's access to nutrients crucial for growth.
- Interfering with Protein Synthesis: Disrupts the production of vital proteins within the infectious organism.
- Interfering with DNA Synthesis: Impedes the replication of the invading organism's genetic material.
- Altering Cell Membrane Permeability: Causes leakage of essential cellular components, ultimately leading to cell death.
Classifications of Anti-Infectives
- Antibiotics: Target bacterial infections.
- Antivirals: Fight viral infections.
- Antifungals: Treat fungal infections.
- Antitubercular: Specifically used against tuberculosis.
- Antiprotozoal: Used against single-celled parasitic organisms.
- Antimalarial: Target malaria parasites.
- Anthelmintics: Treat worm infections.
Resistance
- Natural Resistance: Microorganisms naturally unaffected by certain drugs due to lacking the specific target or process targeted by the anti-infective.
- Acquired Resistance: Microorganisms develop the ability to resist an anti-infective over time.
Acquiring Resistance
- Producing Deactivating Enzymes: Some bacteria produce enzymes (like penicillinase) to break down the antibiotic before it can work.
- Altering Binding Sites: Bacteria modify the target sites on their membranes or ribosomes, making them inaccessible to the anti-infective drug.
Aminoglycosides
- Powerful antibiotics used for serious infections caused by gram-negative aerobic bacilli.
- Usually given by injection but can be used for ear or eye infections as drops.
- Bactericidal: Kills bacteria.
- Target organisms: E. coli, Proteus, Pseudomonas.
- Mechanism: Inhibit protein synthesis in susceptible gram-negative bacteria, leading to cell death.
Aminoglycosides Pharmacokinetics
- Poorly absorbed from the GI tract: But rapidly absorbed following IM injection, reaching peak levels within an hour.
- Widely distributed: Crosses the placenta and enters breast milk.
- Excreted unchanged in urine: Half-life typically 2-3 hours.
Aminoglycosides Contraindications
- Known allergies: To the drug.
- Renal or hepatic disease: Can worsen organ function.
- Hearing loss: May exacerbate pre-existing hearing impairment.
Aminoglycosides Adverse Effects
- Ototoxicity: Damage to the eighth cranial nerve (hearing and balance), leading to dizziness, tinnitus, and hearing loss.
- Nephrotoxicity: Damage to the kidneys, monitored by urinalysis and kidney function tests.
Aminoglycosides Drug-to-Drug Interactions
- Diuretics: Can increase the risk of nephrotoxicity.
- Neuromuscular blockers: May enhance their effects.
Common Aminoglycosides
- Gentamicin (Garamycin)
- Streptomycin
- Amikacin (Amikin)
- Kanamycin (Kantrex)
- Neomycin (Mycifradin)
- Tobramycin (Nebcin, Tobrex)
Amikacin
- Not used for extended periods (7-10 days) due to toxicity to bone marrow, kidneys, and GI tract.
Nursing Responsibilities for Aminoglycosides
- Assessment: Vital signs, electrolyte levels, hearing ability, renal function.
- Baseline renal function studies: Review before and during therapy.
- Weight: Assess patient weight.
- Administer IM dose: Deep into large muscle mass (ventral gluteal).
Aminoglycosides Side Effects to Report
- Ototoxicity: Dizziness, tinnitus, progressive hearing loss
- Nephrotoxicity: Increasing BUN, creatinine; decreasing urine output; decreasing specific gravity.
Cephalosporins
- Similar in structure and activity to penicillin:
- Effective against: 3rd generation (P. aeruginosa), Salmonella, Shigella.
- Mechanism: Interfere with bacteria's cell-wall-building ability during division.
- Indications: Treat infections caused by susceptible bacteria.
Cephalosporins Pharmacokinetics
- Well absorbed from the GI tract:
- Metabolized in the liver:
- Excreted in the urine:
Cephalosporins Contraindications
- Allergies: To cephalosporins or penicillin (cross-reactivity).
Cephalosporins Adverse Effects
- GI tract: Nausea, vomiting, diarrhea.
Cephalosporins Drug-to-Drug Interactions
- Aminoglycosides: May enhance their effects.
- Oral anticoagulants: May increase the risk of bleeding.
Fluoroquinolones
- Powerful broad-spectrum antibiotics:
- Mechanism: Inhibit DNA gyrase, a bacteria-specific enzyme, disrupting DNA replication and cell division.
-
Indications: Treat various bacterial infections including:
- Lower respiratory tract infections
- Infectious diarrhea
- Skin, bone, and joint infections
- UTIs
- Prostatitis
- Chronic bronchitis
- Mild to moderate community-acquired pneumonia
- Selected sexually transmitted diseases.
Macrolindes
- Antibiotics that interfere with protein synthesis in susceptible bacteria.
- Indications: Treat infections of respiratory, dermatologic, urinary tract, and GI systems caused by susceptible bacteria.
- Mechanism: Bind to bacterial cell membranes, altering protein function and causing cell death.
- Bacteriostatic: Slows bacterial growth, or bactericidal: Kills bacteria, depending on the concentration.
Macrolindes Pharmacokinetics
- Absorbed in the GI tract:
- Metabolized in the liver:
- Excreted in bile and feces:
Macrolindes Contraindications
- Allergy: To the drug.
- Hepatic dysfunction: Can worsen liver problems.
Macrolindes Adverse Effects
- GI symptoms: Nausea, vomiting, diarrhea.
Macrolindes Drug-to-Drug Interactions
- Digoxin: May increase digoxin levels.
- Oral anticoagulants: May enhance their effects.
- Theophylline: May increase theophylline levels.
- Corticosteroids: May increase the risk of stomach ulcers.
Common Macrolindes
- Azithromycin
- Clarithromycin
- Dirithromycin
- Erythromycin
Nursing Responsibilities for Macrolindes
- Oral Administration: Give with a full glass of water, 1 hour before or 2 hours after meals for best absorption.
- Hepatic Function: Monitor hepatic enzymes (alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, and bilirubin) for abnormalities.
- Hydration: Monitor hydration status if GI reactions occur.
Lincosamides
- Similar to macrolides but more toxic:
- Indications: Severe infections.
- Mechanism: Similar to macrolides.
Lincosamides Pharmacokinetics
- Well absorbed from the GI tract (oral) or IM injection.
- Metabolized in the liver:
- Excreted in urine and feces:
Lincosamides Contraindications
- Hepatic impairment: Can worsen liver function.
- Renal impairment: Can worsen kidney function.
Lincosamides Adverse Effects
- GI reactions: Nausea, vomiting, diarrhea.
Common Lincosamides
- Clindamycin
- Lincomycin
Monobactams
- Unique structure with little cross-resistance:
-
Indications: Treat infections caused by susceptible bacteria:
- UTIs
- Skin infections
- Intra-abdominal infections
- Gynecologic infections.
- Mechanism: Disrupt bacterial wall synthesis, leading to leakage of cellular content and cell death.
Monobactams Pharmacokinetics
- Well absorbed from IM injections:
- Excreted unchanged in urine:
Monobactams Contraindications
- Allergy: To the drug.
Monobactams Adverse Effects
- GI: Nausea, vomiting, diarrhea.
- Hepatic: Enzyme elevation.
Common Monobactams
- Aztreonam
- Azactam
Antivirals
- Target viral infections:
-
Mechanism: Act on specific stages of the viral life cycle, like:
- Nucleosides Reverse Transcriptase Inhibitors (NRTIs): Compete with natural nucleosides within a human cell, preventing the virus's replication.
- Protease Inhibitors: Block protease activity essential for viral maturity.
- Integrase Inhibitors: Interfere with the integration of viral DNA into the host's DNA.
Nucleoside Reverse Transcriptase Inhibitors (NRTIs)
- Indications: Combination therapy for HIV infection in adults and children, chronic hepatitis B, and prevention of maternal HIV transmission.
- Contraindications: Pregnancy (except for zidovudine), hepatic dysfunction, severe renal impairment, bone marrow suppression.
NRTIs Adverse Effects
- Abacavir: Serious, potentially fatal hypersensitivity reactions (fever, chills, rash, fatigue, GI upset, flu-like symptoms).
- Didanosine: Serious pancreatitis, hepatomegaly, neurological problems.
- Emtricitabine, tenofovir: Severe, fatal hepatomegaly with steatosis.
- Zidovudine: Severe bone marrow suppression.
- Tenofovir: Changes in body fat distribution.
Protease Inhibitors
- Mechanism: Block protease activity within the HIV virus, preventing its maturation.
- Indications: Combination therapy for treatment of HIV infections.
- Contraindications: Pregnancy, lactation, hepatic dysfunction, patients taking antidiabetic drugs.
- Darunavir: Not for children under 3 years old due to potential toxicity.
Protease Inhibitors Adverse Effects
- GI: Nausea, vomiting, diarrhea, anorexia.
- Liver: Elevated cholesterol and triglyceride levels.
- Skin: Rashes, pruritus, Steven Johnson syndrome.
Integrase Inhibitors
- Mechanism: Block the integration of viral DNA into the host's DNA.
- Indications: Reserved for patients with previous antiviral treatment and evidence of viral replication.
-
Contraindications:
- Hypersensitivity to any component of the drug. Not for use as initial HIV treatment, children, or nursing mothers.
- Adverse Effects: Headache, dizziness, rhabdomyolysis, myopathy.
Anti-Hepatitis B and C Agents
- Hepatitis B: Serious viral liver infection spread through blood, blood products, sexual contact, or contaminated needles.
- Hepatitis C: Leading cause of liver transplants due to progressive liver disease.
Antifungals
- Target fungal infections: Used to treat mycoses (fungal infections).
- Fungi: Different from bacteria, with cell walls made of chitin and polysaccharides, making them resistant to antibiotics.
-
Types:
- Systemic: Treat systemic fungal infections, potentially toxic to the host.
- Topical: Used for skin and mucous membrane infections.
Antifungals Mechanism
- Fungicidal: Kills the fungus.
- Fungistatic: Prevents the fungus from growing.
Antifungal Indications
- Common Infections: Ringworm, athlete's foot, fungal nail infections, vaginal thrush, severe dandruff.
- Serious Infections: Aspergillosis (lungs), fungal meningitis (brain).
Antifungal Forms
- Cream, gel, ointment, spray: Topical
- Capsule, tablet, liquid: Oral
- Injection: Systemic
- Pessary (small tablet): Vaginal
Common Antifungal Medicines
- Topical: Clotrimazole (Canesten), econazole, miconazole, terbinafine (Lamisil).
- Oral/Systemic: Fluconazole (Diflucan), ketoconazole (Daktarin), nystatin (Nystan), amphotericin.
Drugs for Systemic Antifungal Treatment
- Azole derivatives: Fluconazole, isavuconazole, itraconazole, posaconazole, voriconazole.
- Echinocandins: Anidulafungin, caspofungin, micafungin.
- Flucytosine:
Antifungal Pharmacokinetics
- Route: Oral or IV.
- Onset: Oral (slow) takes 1-2 hours, IV (rapid) takes 1 hour.
- Peak: 1-2 hours (oral), 1 hour (IV).
- Duration: 2-4 days (oral and IV).
- Metabolism: Liver.
- Excretion: Kidney (urine).
Antifungal Side Effects
- Generally mild and short-lived.
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