NR566 Midterm Study Guide (Week 1-4) PDF

**Week 1:** 1\. [Amphotericin B:] -Pharmacokinetics: a\. Absorption & Distribution: poorly absorbed by the GI tract, hence oral therapy cannot be used for systemic infection. Amphotericin must be administered IV. b\. Metabolism & Excretion: little is known about the elimination of amphotericin B...

**Week 1:** 1\. [Amphotericin B:] -Pharmacokinetics: a\. Absorption & Distribution: poorly absorbed by the GI tract, hence oral therapy cannot be used for systemic infection. Amphotericin must be administered IV. b\. Metabolism & Excretion: little is known about the elimination of amphotericin B, it is unknown if the drug is metabolized or ultimately removed from the body. Renal excretion is minimal. Complete elimination takes a long time, up to one year to fully leave the body. Dose or frequency reduction can be discussed in patients with renal impairment. -Minimizing Nephrotoxicity: infuse one liter of normal saline on days the drug is administered 2\. [Itraconazole:] \- Drug interactions: itraconazole inhibits CYP3A4, ultimately increasing levels of many other drugs (ciaspride, pimozide, dofetilide, and quinidine) 3\. [Caspofungin:] -Therapeutic use: Aspergillus & Candida infections -Adverse effects: (fever, phlebitis at the injection site), headache, rash, nausea, and vomiting 4\. [Griseofulvin:] -Indications: dermatophytic infections of the skin, hair, and nails 5\. [Oral Terbinafine:] -Indications: ringworm and onychomycosis (fungal infection of the nails) 6\. [Azole use in Older Adults:] older adults are at higher risk for achlorhydria than younger individuals and may not predictably absorb some antifungal agents. In addition, warfarin, phenytoin, and oral hypoglycemic agents are increased by azoles 7\. [Tinea Pedis Treatment:] topical fungal therapy, patients should wear cotton socks, change shoes often, and dry their feet after bathing 8\. [Systemic Mycoses Treatment of Choice:] Amphotericin B & azoles 9\. [Acyclovir:] -MOA: inhibits viral replication by suppressing the synthesis of viral DNA -Indication: Herpes simplex infections, Varicella Zoster infections, Herpes simplex genitalis -Route of Administration Considerations 10\. [Osteltamivir (Tamiflu):] -MOA: antiviral effects from inhibition of neuramininidase Administration: PO Indications: used for prevention and treatment of influenza in patients one year of age and older. Reduction of symptom duration, severity, and incidence of complications. Recommended for both prophylaxis and treatment of influenza in pregnant people. Prophylactic therapy for family members of someone with the flu and residents of nursing homes. \*\*Purpose of annual flu vaccine: protection against influenza \*\*Contraindications to the flu vaccine: pregnancy (pregnant people must receive the inactivated vaccine), allergy to the flu vaccine or a vaccine component (eggs), GBS within six weeks following a vaccine administration, moderate to severe acute illness at the time of vaccination 11\. [Palivizumab:] -Indications: prevention of RSV infection in premature infants and in young children with chronic lung disease 13\. [NRTI's:] \- MOA: inhibition HIV replication by suppressing synthesis of viral DNA -Adverse Effects: lactic acidosis, hepatic steatosis, pancreatitis, and myopathies 14\. [Protease Inhibitors (PI's):] -MOA: prevent HIV maturation by blocking the HIV enzyme protease -Adverse Effects: hyperglycemia and the development of diabetes, lipodystrophy (Cushing's appearance), hyperlipidemia, increased bleeding in people with hemophilia, elevation of serum transaminases (liver injury), and decreased cardiac conduction velocity (Prolonged PR interval or BBB) 15\. [Integrase Strand Transfer Inhibitors (INSTIs):] -MOA: target HIV by terminating the integration of HIV into DNA -Adverse effects: dizziness and insomnia, depression, suicidal ideation, and rhabdo 16\. [Chemokine Receptor 5 Antagonists (CCR5 Antagonists):] -MOA: block entry of HIV into CD4 T-cells 17\. [Albendazole:] -MOA: treatment of parenchymal neurocysticercosis by inhibition of polymerization of tubulin and hence prevents the formation of cytoplasmic microtubules, as a result, microtubule-dependent uptake of glucose is prevented 18\. [Mebendazole:] -MOA: drug of choice for most intestinal worms, prevents uptake of glucose by susceptible intestinal worms, which results in slow death 19\. [Enterobiasis Treatment Choices (Pinworm infection):] albendazole, mebendazole, and pyrantel pamoate (all family members of an infected individual should be treated simultaneously) **Week 2:** 20\. [Antibiotics:] -Determining drug susceptibility: first identify the microbe, then test for sensitivity -Infants: highly vulnerable to drug toxicity due to poorly developed kidney and liver function 21\. [Antibiotic Stewardship:] \- Prophylactic use of antibiotics: surgery, bacterial endocarditis, neutropenia, young women with recurrent UTI, oseltamivir for influenza, STD exposure \- Misue of antibiotic Drugs: attempted treatment of viral infections, treatment of fever of unknown origin, improper dosage, treatment in the absence of adequate bacteriologic information, omission of surgical drainage 22[. Penicillin:] \- Bacterial resistance: bacterial resistance of penicillin is determined by inability of penicillin to reach their targets, inactivation of penicillin by bacterial enzymes, and production of PBPs that have a low affinity for penicillin \- Penicillin V vs. Penicillin G: \*Penicillin V: Principle different to Penicillin G is stability. Penicillin V is stable in stomach acid, whereas penicillin G is not. Because of its acid stability, penicillin V is ok for oral therapy. Ok to take with meals. \* Penicillin G: first penicillin available. Bactericidal to most gram-positive bacteria and some gram-negative bacteria. Drug of choice for many infections \- MOA: penicillin weakens the cell wall, causing bacteria to take up excessive amounts of water and rupture (penicillins are bactericidal) -Gram-negative Penicillin Activity: Some penicillins are ineffective against gram-negative bacteria due to the gram-negative bacteria having a cell envelope that has three layers instead of two in gram-positive bacteria 23\. [Cephalosporins:] \- MOA: bactericidal drugs that bind to penicillin-binding proteins (PBPs) and disrupt cell wall synthesis and activate autolysins \*damage to the cell wall that causes cell death -Drug interactions: alcohol, drugs that promote bleeding (NSAIDs, anticoagulants, and antiplatelets) -Structure: B-lactams 24\. [Carbapenems:] -MOA: binds to two PBPs, causing weakening of the bacterial cell wall and subsequent cell lysis and death -Dose adjustments: elderly patients and those with renal impairment -Elimination: Renal 25\. [Vancomycin:] -MOA: inhibits cell wall synthesis and promotes bacterial lysis and death. Disrupts the cell wall by binding to molecules that serve as precursors for cell wall biosynthesis -C-diff Infection: gram-positive, spore-forming, anaerobic bacillus that infects the bowel. Treat with vancomycin, flagyl, or fidoxomicin -Adverse effects: renal impairment. Avoid concomitant use of additional nephrotoxic agents -Provider response to adverse effects: Monitor vancomycin trough levels 26\. [Aminoglycosides:] -Beneficial Drug Interactions: a\. Penicillins and aminoglycosides are frequently given together to enhance bacterial kill b\. Cephalosporins and vancomycin weaken the bacterial cell wall, and thereby act in concert with aminoglycosides to enhance the bacterial kill. -Drug interactions: ototoxic drugs (loop diuretics) & nephrotoxic drugs (amphotericin B, cephalosporins, polymyxins, vancomycin, aspirin, and NSAIDs) -MOA: disruption of bacterial protein synthesis -Cause of resistance: productive of enzymes that can inactive aminoglycosides -Adverse effects: ototoxicity, nephrotoxicity, neurotoxicity **Week 3:** +-----------------------------------+-----------------------------------+ | Chapter 50 | Chapter 51 | | ---------- | ---------- | | | | | - Estrogen | - Contraceptives | | | | | - Metabolic Actions | - Selection w/history of | | | thrombus | | - MOA | | | | - Drug Interactions with | | - Female Hypogonadism | Oral Contraceptives | | | | | - Interactions | - Oral contraceptives vs. | | | Other Contraceptives: | | - Cancer Palliation | Selection | | | | | - Routes of Administration | - Contraception During | | | Lactation | | - Progestins | | | | - Risk of Thrombotic Stroke | | - Contraindications | in Migraine Patients | | | | | - Menopausal Hormone | - | | Therapy (HT) | | | | - Oral Contraceptives | | - Hormone Therapy | | | | - Contraindications | | - Treatment of | | | Genitourinary Syndrome of | - Mechanism of Thrombosis | | Menopause | | | | | | - Patient Education | | | | | | - Treatment of Vasomotor | | | Symptoms | | | | | | - Management of Menopausal | | | Symptoms | | | | | | - Prevention of | | | Osteoporosis | | +===================================+===================================+ | Chapter 52 | Chapter 53 | | ---------- | ---------- | | | | | - Testosterone | - Phosphodiesterase-5 | | | Inhibitors | | - Anabolic Effects | | | | - ED Treatment | | - Clinical Pharmacology of | | | Androgens | - Sildenafil | | | Contraindications | | - Premature Epiphyseal | | | Closure | - | | | | | - Therapeutic Uses | - 5-α-Reductase Inhibitors | | | | | - Erythropoietic Effects | - Indications | | | | | - Replacement Therapy | - MOA | | | | | - Adverse Effects in Women | - Adverse Effects | | | | | | - Key prescribing | | | consideration | | | | | | - Finasteride Indications | | | | | | - α1-Adrenergic Antagonists | | | | | | - MOA | | | | | | - Adverse Effects | | | | | | - Drug Interactions | | | | | | - | | | | | | - Prostaglandin Analogs | | | | | | - Alprostadil Adverse | | | Effects | +-----------------------------------+-----------------------------------+ +-----------------------------------+-----------------------------------+ | National STD Curriculum | National STD Curriculum | | ----------------------- | ----------------------- | | | | | - Gonorrhea | - Acute PID | | | | | - Evaluation and Treatment | - Parenteral Treatment | | of Sex Partners | Regimen | | | | | - Treatment Guidelines for | - Parenteral Treatment | | Uncomplicated Gonococcal | Regimen Alternatives | | Infections | | | | - PID | | - | | | | - Treatment in the presence | | - Syphilis | of Gonorrhea | | | | | - Preferred Drug for All | - Treatment Indications: | | Stages | Oral vs Parenteral | | | | | - Treatment of Primary or | - BV | | Secondary Syphilis with | | | Penicillin Allergy | - Follow-up | | | | | - Preferred Drug for All | - Role of Probiotics | | Stages | | | | - Management of Male Sex | | - Evaluation and Treatment | Partners | | of Sex Partners | | | | - Chlamydia | | - HSV | | | | - Treatment during | | - Acyclovir MOA | pregnancy | | | | | - Episodic Treatment | - Management of Sex | | | Partners in Chlamydial | | - Types of therapies | Infections | | | | | - Treatment Duration: 1st | | | clinical episode | | +-----------------------------------+-----------------------------------+ Week 4 +-----------------------------------+-----------------------------------+ | Chapter 14 | Chapter 13 | | ---------- | ---------- | | | | | - Anticholinergic Drugs | - Bethanechol | | | | | - MOA | - MOA | | | | | - Overactive Bladder | - Adverse Effects | | | | | - mirabegron (Myrbetriq) | - General Action | | vs. anticholinergics | | | | - Therapeutic Use | | - Prescribing | | | Considerations | - GI Uses | | | | | - M3 Selectivity of | - Adverse Effects | | Darifenacin | | | | - Pharmacokinetics | | - Oxybutynin Side Effects | | | | Chapter 16 | | - Strategies to Reduce | ---------- | | Anticholinergic Side | | | Effects | - alpha-1 adrenergic antagonist | | | | | - Non-pharmacologic | - Baseline Assessment | | treatment options | | | | - High-Risk Patient | | - Assessment of Treatment | Identification | | Response | | | | - Adverse Effect | | - QT Prolongation Risk with | Minimization | | Solifenacin | | | | - Patient Education | | - Solifenacin Side Effects | | | | - Therapeutic Goal | | - Darifenacin Dose | | | Adjustments | - Monitoring Parameters | | | | | | - Therapeutic Effect | | | Evaluation | | | | | | Eastham, J.H. & Patel P. (2024) | | | | | | - phenazopyridine | | | | | | - MOA | | | | | | - Diagnostic Use | | | | | | - Contraindications | | | | | | - Interactions | +-----------------------------------+-----------------------------------+