NURS 5334 Pharm Study Guide Quiz 1-with 100% verified solutions-2024-2025.docx, Exams of Nursing

Download NURS 5334 Pharm Study Guide Quiz 1-with 100% verified solutions-2024-2025.docx and more Exams Nursing in PDF only on Docsity! NURS 5334 Pharm Study Guide Quiz 1-with 100% verified solutions- 2024-2025 MODULE 1 1. What are the BON rules and regulations for prescriptive authority for the advance practice nurse? 1. Texas is very restricted 2. Describe the pharmacokinetic processes of absorption, distribution, metabolism and elimination and how differences in these areas affect drug action. 1. Absorption 1. Drug’s movement from the site of administration into the blood. 2. Distribution 1. Drug’s movement from the blood into the interstitial space oftissues and from there into cells. 3. Metabolism 1. Biotransformation is the enzymatically mediated alteration of drug structure. 4. Elimination 1. Combination of metabolism and excretion 3. Compare and contrast pharmacokinetics and pharmacodynamics of special populations—pediatrics, older adults and those that are pregnant. 1. Pediatrics—they have organ immaturity, elderly—they have organ degeneration, loss of nephrons, excretion of drug is decreased and you have to give this population a lower dose of medication. Medication can pass through milk of lactating females. 4. Analyze a drug interaction to determine an appropriate course of action. 1. Basic mechanism of drug-drug interactions through pharmacokinetic interactions are altered absorption, altered distribution, altered metabolism, and altered renal excretion. 5. Identify medications with a narrow therapeutic index requiring drug level monitoring. 1. 6. Discuss the effect of ionization and pH on absorption. 1. Drugs that are weak acids are best absorbed in acidic environments. Acidic drugs accumulate on the alkaline side, basic drugs accumulate on the acidic side known as ion trapping. Ionization of the drugs is pH dependent, when the pH and the fluid on one side of the membrane differs from the pH on the other side, drug molecules tend to accumulate on the side where the pH most favors ionization. 7. Discuss factors affecting drug distribution. 1. Competition for protein binding and alteration of extracellular pH 8. Discuss barriers affecting drug distribution—such as placental membrane, blood brain barrier and volume of distribution. 1. Placental membrane: drugs are easily passed through the placental membrance 2. Blood brain barrier: the PGP pumps drugs back into the blood and thereby limits their access to the brain. 3. Volume of distribution: 9. Discuss the “first-pass effect”—what effect can this have on distribution of a drug? 1. Rapid hepatic inactivation of certain oral drugs. When drugs are absorbed by the 1. Neonates: drug remain in the stomach longer which increases the levels, low acidity can affect the absorption of acid labile drugs b) Parenteral? 1. Reponses are slow and erratic. 2. Infancy: absorption is more rapid than in neonates & adults 3. Best avoided in infants c) Transdermal? 1. Greater skin permeability which increases topical drug absorption and increases the risk for toxicity 2. Distribution a) Protein binding 1. Neonates: less protein-binding—increased availability of highly protein bound drugs such as phenytoin, diazepam, and phenobarbital. Reduced dosages needed in these highly bound drugs. b) Blood Brain Barrier 1. Not fully developed at birth, drugs have easy access to the CNS, doses should be reduced. 3. Metabolism a) Hepatic function? 1. Liver hasn’t reached full maturation—sensitive to drugs eliminated by the CYP450. Liver’s ability to metabolize drugs increases about one month after birth. b) T half life 1. Decreased by as much as 48-72 hours 4. Excretion a) Renal? 1. GFR is significantly reduced at birth, drugs eliminated by the kidneys must be given in a reduced dosage and longer dosing intervals. 7. What education needs to be given to parents? 1. What to do if child spits out medication or throws it up 2. Effective education: dosage size and timing, route, technique of administration, duration of treatment, how to store the drug, nature and time course of the desired response, nature and time course of adverse reactions. 8. How do you convert pounds to KG? 1. Divide weight by 2.2 9. What is definition of polypharmacy? Is polypharmacy always inappropriate? What is Beer’s List? 1. Polypharmacy: 3 or more prescription drugs in conjunction-+ with3 or more dietary supplements. 2. No 3. List that identifies drugs with a high likelihood of causing adverseeffects in the elderly 10. What are pharmacodynamic and pharmacokinetic differences in geri patients? 1. Absorption? a) GI 1. Produce less acid and fewer parietal cells 2. Bioavailability decreased 3. Rate of absorption decreased 2. Distribution? a) Lean Body Mass 1. Drugs accumulate in adipose tissues because lean muscle mass decreases by 20% b) Body Water 1. Decrease by 10-15%-drugs reach higher serum concentrations c) Albumin 1. Lowered—leads to higher levels of free or unbound drugs 3. Metabolism? a) Hepatic 1. Decreased with age—decreases drug clearance b) T half life 1. Increases—alters drug-drug interactions 4. Excretion? a) Renal 1. Decreases—which decreases renal clearance of drugs ANTIMICROBIALS 1. Differentiate Bacteriostatic and Bactericidal. 1. Bacteriostatic: can slow bacteria growth and do NOT cause cell death 2. Baterialcidal: directly lethal to the bacteria 2. What is the difference between broad spectrum and narrow spectrum? 1. Broad spectrum: active against a wide variety of microbes. 2. Narrow spectrum: only active against a few species of bacteria or micro-organisms 3. Which is preferred? 1. Narrow spectrum 4. What are antibiotic classifications? 1. Classifications by susceptible organisms 2. Classified by mechanism of action 5. What is empiric antibiotic use? Therapeutic use? 1. Initiate treatment before you know what the results of the test-- Treat with broad-spectrum antibiotic for initial treatment and once you get culture and drug sensitivity then you can use narrow spectrum antibiotic. 6. Which antibiotics work by weakening the cell wall? 1. Penicillins ■ Bacteriostatic: ECSTaTiC ■ E rythromycin ■ C lindamycin ■ Sulfamethoxazole ■ T rimethoprim ■ a ■ T etracycline ■ i ■ C hloramphenicol ■ Bacterialcidal: Very F inely Proficient At Cell Murder ■ V ancomycin ■ F luoroquinolones ■ P enicillin ■ A minoglycosides ■ C ephalosporins ■ M etronidazole 7. Beta Lactam? 1. Penicillins (penicillin G, Ampicillin, amoxicillin, pipercillin) 2. Carbapenems (ztreonam, Imipenem, Meropenem, Ertapenem) 3. Cephalosporins (Cefazolin, ceftriaxone, cefotetan) 4. Vancomycin 5. Lypoglycoproteins (telavancin) 6. Monobactrams (aztreonam) 7. Fosfomycin 8. What are the medications that react with PCN? 1. Aminoglycosides, bacteriostatic agents, and probenecid 9. What organisms are susceptible to PCN? 1. Gram-positive bacteria and gram-negative 10. Beta lactams 1. Penicillins, cephalosporins and carbapenems (drugs that end in -nem and -nam) b) Mechanism of action: weaken cell wall and promote bacterial lysis and death. Active only against bacteria that is undergoing growth and cell division. c) allergy potential between penicillin and cephalosporins* d) Allergic Reaction 1. Immediate: 2-30 minutes after dose 2. Accelerated: 1-72 hours after dose 3. Delayed: days to weeks 4. Treatment: epinephrine (IM or SubQ or IV), respiratory support. e) Drug-drug interactions: aminoglycosides, bacteriostatic agents, probenecid f) Penicillin G AKA Penicillin 1. Bactericidal to gram-positive and gram-negative bacteria. 2. Drug of choice g) Ampicillin and Amoxicillin 1. Broad spectrum 2. Gram-negative bacilli i. Haemophilus influenza ii. E. Coli iii. Salmonella iv. Shigella 3. Adverse reaction i. Rash ii. Diarrhea h) Piperacillin 1. Extended-spectrum penicillin 2. Fights against: pseudomonas, enterbacter, proteus, bacteroides fragilis, klebsiella 3. Administered: parenterally via IV Mediated by IgE antibodies i. Gram + bacteria ii. Only given IV iii. ONLY used in vancomycin-resistant infections 2. Adverse Effects i. Taste disturbance ii. Nausea iii. Vomiting iv. Foamy urine v. Red man syndrome vi. Prolong QT interval vii. BLACK BOX WARNING: mortality increases in pts. With hospital-acquired or ventilator- associated pneumonia and creatinine clearance <50. 3. Drug-drug interactions: NSAIDS or ACE Inhibitors (damage kidneys), Clarithromycin, ketoconazole (cause prolonged QT interval) 6. Monobactrams l) Aztreonam 1. Binds to PBP3 2. Narrow spectrum 3. Active against gram – bacteria i. Neisseria species ii. H. Influenza iii. Pseudomonas iv. Klebsiella v. Proteus vi. Serratia vii. Salmonella viii. Shigella 4. Highly resistant to beta lactamases 7. Fosfomycin a) Single dose therapy b) UTI caused by E. Coli or enterococcus faecalis c) Mechanism of action 1. Kills bacteria by partially preventing cross-linking of peptidoglycan strands d) Adverse effects 1. Diarrhea 2. Headache 3. Vaginitis 4. Nausea 5. Abdominal pain 6. Rhinitis 7. Drowsiness 8. Dizziness e) Take with or without food f) Symptoms improve within 2-3 days after taking BACTERIOSTATIC INHIBITORS (suppress growth, do not kill) 1. Tetracyclines (tetracycline, demeclocycline, doxycycline, minocycline) a) Broad spectrum b) Work against gram + and – c) Mostly used outpatient d) Extensive use = increased in bacterial resistance e) Uses 1. Chylamydial infections and other STDs 2. Helicobacter pylori (causes ulcers in the duodenal and gastric) 3. Acne 4. Skin infections 5. Anthrax (doxycycline) 6. Infectious disease 7. PUD 8. Periodontal disease 9. RA 10. RMSF 11. Pneumonia 12. Lyme disease f) Why can’t we give to children under 8 and pregnant women?* 1. Can irreversibly stain teeth (4 months-8 years old)* 2. Impact skeletal development in babies* g) Photosensitivity* 3. Wear sunscreen h) Adverse effects 1. Nausea, cramps, epigastric burning 2. Create superinfections—c. diff 3. Hepatotoxicity—IV form i) tetracycline with iron, vitamins, or calcium – bioavailability* 1. Impaired absorption of antibiotic 2. If you want to take iron, vitamins, or calcium leave 2 hours in between tetracyclines 2. Macrolides a) Broad spectrum b) Erythromycin 1. High dose IV is cidal 2. Low dose PO is static 3. Food increases absorption 4. Metabolized by CYP3A4 system 5. Drug-drug interactions: theophylline, carbamazepine, warfarin, verapamil, diltiazem, HIV protease inhibitors, simvastatin cipro 6. Uses i. Alternative to PCN in allergic patients ii. Atypical infections 1. Group A strep 2. Corynebacterium diphtheriae 3. Whooping cough 4. Chlamydia and Mycoplasma (walking pneumonia) 7. Side effects i. GI difficulties most common with oral erythromycin 1. N/V/D, abdominal cramping, hepatotoxicity ii. Less side effects with newer macrolides c) Azithromycin 1. Cause QT prolongations** d) Clindamycin (Cleocin) 1. Bacteriostatic 2. BLACK BOX WARNING: Promote severe c. diff in elderly patients 3. Uses i. Anaerobic bacteria, gram – and + 4. Used as alternate to penicillin 5. Adverse effects i. Hepatic toxicity ii. Blood dyscrasias iii. Diarrhea iv. Hypersensitivity reactions 3. Oxazolidiones (Zyvox or Linezolid) a) Used to treat VRE and MRSA b) Very expensive c) Limited use due to resistance d) Gram + bacteria, NO gram - bacteria 1. Enterococcus 2. MRSA 3. Staphylococcus epidermidis 4. Strep pneumonia e) Adverse effects 1. Diarrhea 2. Nausea 3. Vomiting 4. Headache 5. Myelosuppression f) Drug-drug interactions 1. MAOIs and Tedizolid 4. Ketolides 1. UTIs (main use) 2. Gram negative 3. Others i. Nocardiosis ii. Malaria iii. Ulcerative colitis iv. Toxoplasmosis v. Chlamydia d) Adverse effects 1. Skin, skin, skin i. Skin rashes & itching ii. Stevens-Johnson syndrome iii. Photosensitivity 2. Hematologic effects i. Hemolytic anemia ii. Kernicterus 3. Renal damage e) Drug-drug interactions** 1. Phenytoin, glipizide, glyburide (inhibit hepatic metabolism) 2. Thiazide (Celebrex) diuretics and sulfides (cross- hypersensitivity) f) Resistance to sulfonamides 1. Gonococci, meningococci, streptococci, shigellae g) Topical sulfonamides (silver sulfadiazine and mafenide) 1. Used to suppress colonization in pt. with 2nd and 3rd degree burns 2. Mafenide application painful i. Can cause acidosis 3. Sulfadiazine application pain free i. Systemic absorption, be careful in pt. with sulfa allergies 11. Trimethoprim a) Uses 1. Acute and uncomplicated UTIs 2. E. coli, proteus, klebsiella, Enterobacter, and staph b) Adverse effects 1. Hematologic 2. Hyperkalemia c) Do not use in pregnancy or lactation 12. Trimethoprim PLUS sulfamethoxazole (AKA Bactrim DS) a) Need to watch the plasma levels b) Therapeutic uses 1. UTI, otitis media, bronchitis, shigellosis, pneumocystis pneumonia, GI infection c) Dosage in CHILDREN is based on trimethoprim and not sulfamethoxazole (not the case in adults) d) Adverse effects 1. GI—nausea and vomiting 2. Rash 3. Hyperkalemia 4. Steven-Johnson syndrome 5. Blood dyscrasias 6. Kernicterus 7. Renal damage or crystal urea 8. Birth defects in 1st trimester DRUGS TO TREAT UTIs** 1. Uncomplicated UTIs a) Single dose therapy 1. For uncomplicated, non pregnant females b) Conventional therapy 1. For pregnant females c) Nitrofurantoin and Bactrim DS** d) If there’s resistance: fluoroquinolones are used** e) Fosomycin= single dose therapy f) Nitrofurantoin rapidly metabolized and concentrates in the bladder** 1. Used for acute cystitis, NOT pyleo 2. Acute and uncomplicate Pyleo a) Mild and moderate infection treat at home 1. First line: TMP, SMZ, Cipro and levofloxacin for 10- 14 days 2. Second line: augmentin (amoxicillin clavulanate AKA cephalexin) b) Severe infection requires hospitalization and IV antibiotics then once controlled you start oral antibiotics 3. Cipro, ceftrizxone, ceftazidime, ampicillin plus gentamicin, ampicillin/culbactam 3. Complicated UTIs a) Need to do a C&S and treat with broad spectrum until it comes back** 4. UTI relapse a) Long-term therapy: prophylactically low dose of TMP/SMZ 3x weekly for 6 months or TMP at bedtime for 6 months or nitrofurantoin for 6 months** 5. Postcoital cystitis a) Take nitrofurantoin and void after intercourse 6. Prostatitis** a) Signs & Symptoms 1. High fever, chills, malaise, myalgia, localized pain, dysuria, nocturia, urinary urgency, urinary frequency b) Causes 1. E. coli, indwelling urethral catheters, urethral instrumentation, or transurethral prosthetic resection c) Treatment 1. 2-4 weeks of fluroquinolone or doxycycline 7. UTI antiseptics a) Nitrofurantoin and methenamine** 1. Bacteriostatic 2. High concentrations=bactericidal 3. Uses i. Lower UTI ii. Prophylaxis iii. Recurrent infections 4. Not absorbed systemically (doesn’t work for kidney infections) 5. Adverse effects i. GI ii. Pulmonary iii. Hematologic (agranulocytosis, leukopenia, thrombocytopenia, megaloblastic anemia) iv. Peripheral neuropathy (irreversible) v. Hepatotoxicity vi. Birth defects (DO NOT GIVE TO PREGNANT FEMALES) 6. Methenamine i. Uses 1. Chronic lower UTIs ii. Adverse effects 1. Contraindicated in pt with renal and liver failure iii. Drug-drug interactions 1. Urinary alkalinizers 2. Sulfonamides 8. Floroquinolones (cipro) a) Broad spectrum b) PO and IV c) Resistance in N. Gonorrhoeae** 1. Excellent oral absorption (PO) d) Cipro 1. Uses (gram -) i. Anthrax* ii. Respiratory infections iii. UTIs iv. GI infections v. Bones, joints, soft tissue infecitons 2. Adverse Effects** i. Cartilage damage** 1. Ophthalmia can cause blindness iii. Single dose of ceftriaxone IM or IV 2. Prevention iv. 0.5% erythromycin ophthalmic ointment @ birth required by law c) Preadolescent 1. Weight >45kg: treatment same as adults 2. Weight <45kg: single dose of ceftiaxon for vaginitis, cervicitis, urethritis, pharyngitis, proctitis 3. Systemic is IM or IV ceftriaxone daily for 7 days 4. Nongonococcal urethritis a) Diagnosis: presence of polymorphonuclear leukocytes and negative culture for gonorrhea b) Azithromycin or doxycycline 1. Alternatives: erythromycin, levofloxacin or ofloxacin, metronidazole, tinidazole for trichomonas. c) Pelvic inflammatory disease 1. Cause: gonorrhea or chlamydia 2. Causes infertility 3. Broad coverage and combo therapy is required i. Inpatient: IV cefoxitin or cefotetan and doxycycline followed by oral doxycycline ii. Outpatient: ceftriaxone or cefoxitin and doxycycline, used with/without metronidazole d) Acute epididymitis (pain in back and testes) 1. Treat according to the organism 2. Ceftriaxone plus doxycycline or ofloxacin 3. Levofloxacin is added if pt. has anal intercourse e) Non-sexually transmitted disease (urinary tract instrumentation) 1. Ofloxacin f) Syphilis** 1. Primary: chancre, red, hard, protruding, and painless sore 2. Secondary: 2 weeks after chancre heals 3. Tertiary: 5-40 years after initial infection 4. Highly responsive to Penicillin G g) Bacterial vaginosis (fishy odor, pH <4.5)** 1. Non-pregnant women i. Metronidazole or clindamycin cream 2. Pregnant women i. Only oral clindamycin and metronidazole h) Trichimoniasis** 1. Metronidazole 2g PO once or Tinidazole 4g PO once i) Chancroid 1. Painful ragged ulcer at site of inoculation 2. Swollen lymph nodes 3. Azithromycin, ceftriaxone, cipro, erythromycin base j) Herpes simplex virus** 1. Acyclovir, famciclovir, valacyclovir i. Can be taken every day for suppressive therapy or can preserve it and take them when there’s an active outbreak ii. Vancyclovir 500mg taken daily can decrease transmission by 50% iii. Infants exposed at birth should be treated with acyclovir ANTIFUNGALS 5. Amphotericin B (broad spectrum, given IV) a) Uses 1. Some protozoa 2. Systemic mycoses b) Mechanism of action 1. Binds to ergosterol in the fungal cell membrane and increases permeability and the cell leaks intracellular cations reduces viability. Bacteria not affected. 2. Fungicidal or fungistatic c) Adverse effects 1. Infusion reactions i. Phlebitis 2. Renal damage causes hypokalemia (may need potassium and monitor creatinine) 3. Fever, chills, rigors, nausea, headache. 4. Hematologic effects: bone marrow suppression and normochromic normocytic anemia (monitor h&h) d) Drug-drug reactions 1. Hydrocortisone-high incidence of phlebitis 2. Aminogylcosides-nephrotoxic 3. Cyclosporins-nephrotoxic 4. NSAIDS-nephrotoxic e) BLACK BOX WARNING 1. Highly toxic, only used in the setting of life threatening infections. 6. Azoles (Itraconazole, fluconazole, voriconazole, ketoconazole, Posaconazole, isavuconazonium) a) Uses (orally) 1. Systemic mycoses b) Mechanism of Action 1. Inhibits the synthesis of the ergosterol and disrupts the fungal cell membrane . Inhibits fungal cytochrome p450 c) Adverse effects 1. Liver damage (monitor liver enzymes) 2. GI effects (N/V/D) d) Drug-Drug interactions (inhibit p450 drug metabolism) 1. Dofetilide (antiarrhythmic) 2. Warfarin 3. Cyclosporin 4. Lovastatin 5. Simvastatin 6. PPIs (inhibit absorption) 7. Cola (enhances absorption) e) BLACK BOX WARNING 1. Decrease in ventricular ejection fraction—should not be used in patients with heart failure or ventricular dysfunction 7. Echinocandins a) Caspofungin, Micafungin, Anidulafungin 1. Uses i. IV therapy of invasive aspergillus not responsive to amphotericin B, itraconazole, and candida infections 2. Adverse effects i. Fever ii. Phlebitis 3. Drug-drug interactions i. Drugs that induce cytochrome P450 may decrease levels ii. Decreases levels of tacrolimus iii. Combining with cyclosporine can increase risk for liver injury 8. Pyrimidine Analog b) Flucytosine 1. Uses i. Serious infections from candida and cryptococcus neoformans 2. Adverse effects i. Half life prolonged in patients in renal impairment (BLACK BOX WARNING) ii. Bone marrow suppression iii. Neutropenia or thrombocytopenia iv. Rarely fatal agranulocytosis v. Hepatotoxicity 3. Drug-drug interactions i. ?? 9. Which drugs treat? a) Tinea pedis 1. Terbinafine (topical) 2. Butenafine (topical) 3. Ciclopirox (topical) 5. Disturbed balance 13. Amikacin (injectable) a) Adverse effects 1. Nephrotoxic 2. Eighth cranial nerve damage (BLACK BOX WARNING) 14. Para-aminosalicylic acid a) Adverse effects 1. GI disturbances: N/V/D 2. Salt loading 3. Allergic reactions 4. Hepatotoxicity 5. Goiter 15. Ethionamide a) Adverse effects 1. GI disturbances: N/V/D 2. Hepatotoxicity 3. Peripheral neuropathy 4. CNS effects: convulsions, mental disturbance 5. Allergic reactions 6. Hypoglycemia 16. Cycloserine a) Adverse effects 1. Anxiety 2. Depression 3. Confusion 4. Hallucinations 5. Paranoia 6. Hyperreflexia 7. Seizures 8. Peripheral neuropathy 9. Hepatotoxicity 10. Folate deficiency 17. Bedaquiline [Sirturo] a) Adverse effects 1. BLACK BOX WARNING: prolonged QT 18. Treatment a) What is treatment for drug sensitive TB 1. Two phases i. Initial phase (8 weeks) 1. Eliminate actively dividing extracellular tubercle bacilli. 2. Isoniazid, rifampin, pyrazinamide, ethambutol ii. Continuation phase (18 weeks) 1. Eliminate persistent intracellular organisms 2. Isoniazid and rifampin b) Multi drug resistant? 1. Isoniazid resistant i. Treated for 6 months with 3 drugs 1. Rifampin, ethambutol, pyrazinamide 2. Rifampin resistant i. Treated for 18-24 months with 3 drugs 1. Isoniazid, ethambutol, pyrazinamide c) Extensively drug resistant? 1. Treatment is prolonged to at least 24 months 2. Use 2nd and 3rd line drug—less effective 3. Initial therapy can consist of 5,6,7 drugs i. Isoniazid, rifampin, pyrazinamide, ethambutol, amikacin or capreomycin, levofloxacin, cycloserine, ethionamide or PAS. 4. Last resort i. Infected tissue removed by surgery d) Patients with TB and HIV? 1. Rifabutin can be used but it can accelerate the metabolism of protease inhibitors and NNRTIs but not as much as rifampin. e) Latent TB? 1. Treated with one or two drugs 2. TB must be ruled out 3. Isoniazid alone daily or twice weekly for nine months or isoniazid daily or twice weekly for 6 months 4. Rifampin alone daily for 4 months, isoniazid plus rifapentines taken weekly for three months f) How do you promote treatment adherence? 1. Directly observed therapy i. Administration of each dose is done in front of representative of the health department 2. Intermittent dosing (2-3 times a week) g) How do you evaluate? 1. Three primary modes i. Bacteriologic evaluation of sputum 1. Evaluated monthly until 2 consecutives are negative ii. Chest radiographs 1. Done in pt with negative pretreatment sputum test 2. Repeat every 2 months after initial tx iii. Clinical evaluation 1. Fever, malaise, anorexia, cough must be evaluated at every clinic visit 2. Should be markedly decreased within 2 weeks ANTHELMINTICS 1. What are the antihemintics drugs? a) Drugs of choice 1. Mebendazole, albendazole, pyrantel pamoate, praziquantel, diethylcarbamazine, ivermectin. 2. Anthelmintic drugs are generally devoid of serious adverse effects 3. Important to match drug with infesting worm 4. Many worm infestations are both asymptomatic and self-limited, hence drug therapy can be optional ANTIVIRALS FOR NON HIV 1. Acyclovir a) Uses 1. 1st choice for herpes simplex virus or varicella zoster virus b) Adverse effects 1. IV i. Phlebitis ii. Nephrotoxicity iii. Neurotoxicity 2. Oral i. GI effects ii. Vertigo 2. Valacyclovir a) Uses 1. Herpes zoster, genital herpes, herpes labialis, cold sores, varicella, chicken pox b) Adverse effects 1. Hematologic affects: thrombocytopenia, aplastic anemia 2. Neurologic: psychosis, encephalopathy, seizures 3. GI affects 3. Famciclovir a) Uses 1. Genital HSV, herpes zoster, orolabial HSV b) Adverse effects 1. Blood dyscrasias i. Neutropenia ii. Thrombocytopenia 2. Stevens Johnson Syndrome 3. CNS—hallucinations, delirium c) Drug-drug interactions 1. Live varicella & zoster vaccine 4. Ganciclovir a) Uses a. Hyperglycemia, fat redistribution, hyperlipidemia, increased bleeding in pt with hemophilia, reduce bone density, elevation of serum transaminase 2. Drug-drug interactions iv. Integrase strand transfer inhibitors (raltegravir) 1. Adverse effects a. Insomnia, headache, rare hypersensitivity v. Fusion inhibitors (enfuvirtide AKA fuzeon) 1. Adverse effects a. Injection site reactions, ammonia, hypersensitivity reactions vi. CCR5 antagonists (maraviroc) 1. Adverse effects a. Hepatic toxicity, myocardial ischemia, orthostatic hypotension, immune reconstitution syndrome, increased risk for infection, potential risk for malignancy, upper respiratory infections, cough. c. What are laboratory tests used to guide treatment of HIV? i. Plasma HIV RNA or viral load assays d. What causes resistance in treatment of HIV? i. Nonadherence to treatment e. Which medications can be used in pregnancy? i. Same medications can be used in pregnancy that is used in non- pregnancy, just transmission occurs and lowers the maternal viral load. f. When is tenofovir/emtricitabine (Truvada) indicated? i. It is an HIV prophylaxis ii. Those considered high risk for HIV acquisition, those pt that have sexual partners with known HIV infection, sexually active with people who belong to the social networks with a high HIV population, or one or more of the following: don’t use condoms, have STI, engage in sex for money, men in prisons. LOCAL ANESTHESIA 1. What is MOA of local anesthetics? a. Suppress pain by blocking sodium channels and impulses, conduction along the axons and the selectivity of the anesthetic effects, only neurons located near the side of administration are affected and they suppress pain without generalized depression of the CNS 2. What 3 properties determines the ability of anesthetic to penetrate axon membrane? a. Molecular size, lipid solubility, degree of ionization at the tissue pH 3. Why are vasoconstrictors used in conjunction with local anesthetics? a. Delays the systemic absorption and prolongs anesthesia and reduces the risk of toxicity 4. What blood dyscrasia can occur from benzocaine? a. Methemoglobinemia-hgb is modified so it cant release O2 into the tissues and if enough hgb is converted to methemoglobin, death can result. 5. What are application guidelines for topical anesthetics to prevent systemic reactions? a. Apply the smallest amount needed, avoid application to large areas, avoid broken or irritated skin, avoid strenuous exercise, wrapping the site and heating the site. DRUGS FOR HEADACHES 1. What is pathophysiology of migraine? a. Neurovascular disorder that involves the dilation and inflammation of intracranial blood vessels. Vasodilation causes the pain. 2. What foods can trigger migraines? a. Aged cheeses, wine, cured meats, hot dogs, lunch meat, chocolate, Chinese food, canned soups, diet sodas, artificial sweeteners, yellow food coloring. 3. What drug classes are abortive medications? a. NSAIDs/aspirin b. Opioid analgesics: butorphanol and meperidine c. Serotonin 1B/1D receptor agonists: triptan d. Ergot alkaloids 4. What drug classes are preventive? What can happen with all preventive medications have if taken too frequently? a. Beta blockers, antiepileptic drug, tricyclic antidepressants, calcium channel blockers, botulism toxin, ACE inhibitors, Angiotensin 2 receptor blockers. b. Chronic headache 5. What are some herbal meds effective with migraines? What are their side effects? a. riboflavin B2 and coenzyme Q-10 b. Side effects: GI, liver damage and cancer 6. What is treatment for menstrual migraine? a. Tricyclic antidepressants, estrogen gel and patches HEADACHES 1. NSAIDs: First line 2. Seratonin 1B1D Receptor Agonists/Triptans a. What is MOA? i. Binds to receptors on the intracranial blood vessels and causes vasoconstriction, diminishes perivascular inflammation b. Side effects? i. Chest symptoms: heavy arms or chest pressure ii. Teratogenic iii. Vertigo, malaise, fatigue, tingling sensation, bad taste with intranasal form c. Drug/drug interactions? i. Ergot alkaloids, sumatriptan and all other triptans d. What is Treximet? i. Combination of Sumatriptan & Naproxen 3. Ergot Alkaloids a. What is MOA? i. Works by agonist activity at subtypes of serotonin receptors and specifically the 5HT1B and 5HT1D receptors. Suppresses the release of CGRP, to block inflammation associated with the trigeminal vascular system. b. Side effects? i. N/V ii. Overdose: causes ischemia secondary to constriction of the peripheral arteries. Extremities become cold, pale and numb. Muscle pain and then gangrene sets in. iii. Teratogenic c. Drug/drug interactions? i. Drugs that are CYP3A4 inhibitors ii. Triptans iii. SSRIs 4. What are primary treatments for cluster HA? a. Prophylaxis b. Glucocorticoids, verapamil, lithium 5. What are primary treatments for tension HA? a. Acetaminophen, NSAIDs (aspirin, ibuprofen, naproxen), butalbital OPIOIDS 1. What are 3 main classes of opioid receptors? a. Mu receptors b. Kappa receptors c. Delta receptors 2. What are 3 classifications of drugs that act as opioid receptors? a. Agonist b. Partial agonist c. Antagonist b. Cox 2: mediates inflammation and sensitizes receptors to painful stimuli, mediates fever, contributes to perception of pain, promotes vasodilation, contributes to colon cancer. i. Risk for MI and stroke 3. ASA a. Drug interactions? i. Anticoagulants (warfarin and heparin) ii. Glucocorticoids iii. Alcohol iv. Ibuprofen v. ACE inhibitors and ARBs b. Side effects? i. Ulceration and bleeding of GI ii. Reversible impairment of kidneys iii. Edema iv. Toxic levels—tinnitus, sweating, headache, dizziness v. Children <18 years old—Reye syndrome 4. Non ASA first generation NSAIDs –indications RA, OA a. Ibuprofen, Naproxen b. SAFETY ALERT: All first-generation NSAIDs are associated with an increased risk of GI bleeding that can lead to hospitalization or death 5. 2nd Generation NSAIDs-indications RA, OA a. Celecoxib, Meloxican i. What are drug/drug interactions 1. Warfarin (increases anticoagulant effect) 2. ACE inhibitors (decrease antihypertensive effects) 3. Lithium (increase levels) 4. Fluconazole (increases celecoxib levels) Both first and second generation pose the risk for heart disease, renal function, and GI bleed though Cox 2 pose less risk for GI 6. Acetaminophen a. No anti-inflammatory action b. What are side effects? i. Steven Johnson syndrome ii. Acute generalized pustulosis iii. Toxic epidermal necrolysis iv. Hepatic toxicity v. Hepatic necrosis vi. N/V/D, sweating c. Drug/drug? i. Alcohol (increase risk to liver) ii. Warfarin (increase risk of bleeding) d. Vaccines? i. Tylenol can blunt the immune response e. What is treatment for overdose? i. Acetylcysteine or Mucomyst GLUCOCORTICOIDS 1. What are therapeutic uses? a. Help mature lungs in a fetus b. Suppress immune response in inflammation c. Rheumatoid arthritis, systemic lupus, erythematosus, synovitis, osteoarthritis, gouty arthritis, allergic conditions, asthma, skin diseases (stigmas, psoriasis, mycosis, fungoides, seborrheic dermatitis, contact dermatitis, exfoliative dermatitis), neoplasms, suppression of allograft rejections. 2. What are metabolic effects? a. Protein synthesis is suppressed and fat deposits are mobilized and sodium retention and potassium excretion, inhibits the intestinal absorption of calcium and anti-inflammatory and immunosuppressant effects. 3. What are adverse effects? a. Adrenal insufficiency, osteoporosis, pneumocystis pneumonia, hyperglycemia, glycosuria, proximal myopathies in the proximal muscles of the arms and legs. 4. Drug/drug interactions? a. Diuretics (loss of potassium) b. NSAIDs (risk of GI bleed) c. Insulin and oral hypoglycemics d. Vaccines 5. How should these drugs be tapered? a. Taper the dosage to 50% of the physiologic value, monitor for signs of insufficiency RA 1. Chronic systemic inflammation including the synovial membranes of multiple joints 2. Shortens lifespan and increases risk of CV and stroke 3. Goal of treatment a. Reduce inflammation and pain while preserving function and preventing deformity 4. First line treatment: a. NSAIDs with DMARD 5. DMARDs a. Traditional i. Methotrexate, leflunomide, sulfasalazine, hydroxychloroquine, minocycline, Penicillamine, Azathioprine, Cyclosporine 6. Biological response modifiers a. Non-TNF i. Abatacept, rituximab, anakinra, tocilizumab b. Anti-TNF i. Infliximab, adalimumab, etanercept, certolizumab, golimumab 7. Oral JAK inhibitors a. Tofacitinib, Ruxolitinib All of these drugs suppress immune system COMMONLY USED NSAIDs DMARDS/TRADITIONAL 1. Methotrexate a. Adverse reactions? i. Hepatic fibrosis, bone marrow suppression, GI ulceration, pneumonitis (BLACK BOX) b. Bone Marrow? i. Suppression 2. Sulfasalazine a. GI side effects 3. GOUT 1. Cause a. Excessive production of uric acid b. Impaired renal excretion of uric acid 2. Flare up < 3 times per year