1
Q
Ch43 – What is the primary use of immunosuppressants?
A
Prevent organ rejection and treat autoimmune diseases by reducing immune activation.
2
Q
Ch43 – What are calcineurin inhibitors?
A
Drugs that inhibit calcineurin → prevent IL-2 production → suppress T-cell activation.
3
Q
Ch43 – Prototype calcineurin inhibitor?
A
Cyclosporine.
4
Q
Ch43 – Major adverse effects of cyclosporine?
A
Nephrotoxicity (most important), hypertension, tremor, hirsutism, gingival hyperplasia.
5
Q
Ch43 – What increases risk of cyclosporine toxicity?
A
CYP3A4 inhibitors (azoles, macrolides, grapefruit juice).
6
Q
Ch43 – Tacrolimus advantages vs cyclosporine?
A
More potent and less cosmetic side effects but higher risk of diabetes and neurotoxicity.
7
Q
Ch43 – Tacrolimus major adverse effects?
A
Nephrotoxicity, neurotoxicity, tremor, hyperglycemia.
8
Q
Ch43 – Why monitor drug levels for calcineurin inhibitors?
A
Narrow therapeutic window and drug interactions increase toxicity risk.
9
Q
Ch43 – Mechanism of glucocorticoids in immunosuppression?
A
Suppress cytokines, reduce leukocyte activity, inhibit inflammatory mediators.
10
Q
Ch43 – Major adverse effects of long-term glucocorticoids?
A
Hyperglycemia, osteoporosis, adrenal suppression, infection risk, weight gain, gastric ulcers, mood changes.
11
Q
Ch43 – Why taper glucocorticoids?
A
Prevent adrenal crisis and allow HPA axis recovery.
12
Q
Ch43 – Contraindications/cautions for glucocorticoids?
A
Active infections, peptic ulcer disease, uncontrolled diabetes, severe osteoporosis.
13
Q
Ch43 – Effects of glucocorticoids on wound healing?
A
Impaired collagen synthesis → delayed healing.
14
Q
Ch44 – What is the first-line disease-modifying drug for RA?
A
Methotrexate.
15
Q
Ch44 – Mechanism of methotrexate (low-dose)?
A
Inhibits folate metabolism and reduces immune cell proliferation (anti-inflammatory).
16
Q
Ch44 – Major adverse effects of methotrexate?
A
Hepatotoxicity, bone marrow suppression, stomatitis, GI upset, pulmonary fibrosis.
17
Q
Ch44 – What supplement must be given with methotrexate?
A
Folic acid to reduce toxicity.
18
Q
Ch44 – Methotrexate in pregnancy?
A
Contraindicated (Category X).
19
Q
Ch44 – Monitoring for methotrexate?
A
CBC, LFTs, renal function regularly.
20
Q
Ch44 – What are biologic DMARDs?
A
Targeted immune-modifying agents like TNF-alpha inhibitors (etanercept, adalimumab).
21
Q
Ch44 – Major risk of TNF-alpha inhibitors?
A
Serious infections: TB, fungal infections, reactivation of latent diseases.
22
Q
Ch44 – Screening required before biologics?
A
TB skin test/IGRA and hepatitis B screening.
23
Q
Ch44 – Hydroxychloroquine use?
A
Mild RA and lupus; also used for malaria prophylaxis.
24
Q
Ch44 – Major adverse effect of hydroxychloroquine?
A
Retinal toxicity (rare); requires baseline and annual eye exams.
25
Ch44 – Drug for acute gout attack?
NSAIDs first-line; colchicine or glucocorticoids if NSAIDs contraindicated.
26
Ch44 – Mechanism of colchicine?
Inhibits microtubules → reduces leukocyte migration and inflammation.
27
Ch44 – Colchicine adverse effects?
Severe diarrhea, GI upset, myelosuppression with chronic use.
28
Ch44 – Drug for chronic gout (urate lowering)?
Allopurinol or febuxostat.
29
Ch44 – Allopurinol mechanism?
Xanthine oxidase inhibitor → decreases uric acid production.
30
Ch44 – Allopurinol major adverse effect?
Severe hypersensitivity syndrome (rash → SJS/TEN).
31
Ch44 – Interaction warning: allopurinol and azathioprine?
Allopurinol increases azathioprine levels → severe toxicity; reduce azathioprine dose.
32
Ch45 – What are hematopoietic growth factors?
Drugs that stimulate bone marrow to produce blood cells (e.g., RBCs, WBCs).
33
Ch45 – Prototype erythropoiesis-stimulating agent (ESA)?
Epoetin alfa.
34
Ch45 – When are ESAs used?
Anemia of chronic kidney disease, chemotherapy-induced anemia.
35
Ch45 – Major risks of ESAs?
Hypertension, thrombotic events, stroke, rapid tumor progression at high Hgb levels.
36
Ch45 – Target hemoglobin when using ESAs?
Avoid >11 g/dL due to increased cardiovascular risk.
37
Ch45 – Monitoring for epoetin alfa?
Hgb levels weekly until stable; blood pressure closely.
38
Ch45 – Prototype colony-stimulating factor for neutropenia?
Filgrastim (G-CSF).
39
Ch45 – Filgrastim major adverse effect?
Bone pain; rare splenic rupture.
40
Ch45 – When is filgrastim used?
Neutropenia from chemotherapy, stem cell mobilization.
41
Ch45 – Iron deficiency anemia first-line treatment?
Oral ferrous sulfate.
42
Ch45 – How should oral iron be taken?
On empty stomach with vitamin C to enhance absorption; avoid calcium, antacids.
43
Ch45 – Adverse effects of oral iron?
Constipation, dark stools, nausea.
44
Ch45 – IV iron indications?
Intolerance to oral iron, malabsorption, severe deficiency requiring rapid replacement.
45
Ch45 – Risk of IV iron?
Anaphylaxis (especially iron dextran); newer agents safer.
46
Ch45 – Vitamin B12 deficiency treatment?
Cyanocobalamin (IM or high-dose oral).
47
Ch45 – Folate deficiency treatment?
Oral folic acid supplementation.
48
Ch45 – Why distinguish B12 vs folate deficiency?
Folate corrects anemia but not neurologic damage; untreated B12 deficiency causes irreversible neuropathy.
49
Ch40 – What is the first-line treatment for uncomplicated malaria caused by P. falciparum?
Artemisinin-based combination therapy (ACT), e.g., artemether–lumefantrine.
50
Ch40 – Mechanism of artemisinin derivatives?
Produce free radicals inside parasite → damage proteins → rapid parasite clearance.
51
Ch40 – Drug used for malaria prophylaxis in travelers?
Atovaquone–proguanil, doxycycline, or mefloquine (depending on location/resistance).
52
Ch40 – Mefloquine major adverse effects?
Neuropsychiatric symptoms: anxiety, depression, psychosis, nightmares; avoid in psychiatric history.
53
Ch40 – What drug treats hypnozoite liver stages of P. vivax and P. ovale?
Primaquine.
54
Ch40 – Required test before primaquine?
G6PD deficiency screening → risk of hemolysis.
55
Ch40 – What is the first-line treatment for toxoplasmosis in immunocompromised patients?
Pyrimethamine + sulfadiazine + leucovorin.
56
Ch40 – First-line treatment for Giardia?
Metronidazole or tinidazole.
57
Ch40 – First-line treatment for Entamoeba histolytica?
Metronidazole followed by paromomycin.
58
Ch40 – Drug of choice for pinworms (Enterobius)?
Albendazole or mebendazole; repeat in 2 weeks.
59
Ch40 – Mechanism of albendazole?
Inhibits microtubule synthesis → immobilizes and kills helminths.
60
Ch40 – Side effects of albendazole?
GI upset, elevated LFTs; avoid in pregnancy unless necessary.
61
Ch40 – Drug for Strongyloides or onchocerciasis?
Ivermectin.
62
Ch40 – Major ivermectin adverse effects?
Itching, rash, lymphadenopathy (from parasite die-off).
63
Ch40 – Special instruction for scabies treatment with ivermectin?
Often used when topical therapy fails or in crusted scabies.
64
65
Ch41 – First-line treatment for head lice (Pediculosis)?
Permethrin 1% lotion (OTC).
66
Ch41 – Mechanism of permethrin?
Neurotoxin that disrupts sodium channel function in parasites → paralysis.
67
Ch41 – When should permethrin be repeated?
Day 9 to kill newly hatched lice.
68
Ch41 – Alternative for permethrin-resistant lice?
Malathion lotion or spinosad topical.
69
Ch41 – Safety note for malathion?
Flammable; avoid heat sources and hair dryers.
70
Ch41 – First-line treatment for scabies?
Permethrin 5% cream from neck down, left on 8–14 hours.
71
Ch41 – When is oral ivermectin used for scabies?
Severe/crusted scabies or outbreaks where topical therapy impractical.
72
Ch41 – Symptoms after treatment (pruritus) indicates what?
Persistent itching is normal for weeks and does not mean treatment failure.
73
Ch42 – What is active immunity?
Immunity from the body’s own antibody production after infection or vaccination.
74
Ch42 – What is passive immunity?
Immediate temporary immunity using preformed antibodies (IVIG, maternal antibodies).
75
Ch42 – Example of live attenuated vaccines?
MMR, varicella, intranasal influenza, yellow fever.
76
Ch42 – Contraindications for live vaccines?
Pregnancy, severe immunosuppression (HIV with low CD4, chemotherapy).
77
Ch42 – Are live vaccines safe during breastfeeding?
Yes (except smallpox and yellow fever).
78
Ch42 – Examples of inactivated vaccines?
Influenza IM, Tdap, Hep A, Hep B, HPV, pneumococcal, meningococcal.
79
Ch42 – Who should receive Tdap?
Pregnant patients every pregnancy (27–36 weeks), adults requiring booster every 10 years.
80
Ch42 – What is herd immunity?
Indirect protection when a sufficient proportion of population is immune.
81
Ch42 – Vaccine contraindication vs precaution?
Contraindication: do NOT give. Precaution: weigh risk–benefit; may delay.
82
Ch42 – What vaccines must be delayed after IVIG?
Live vaccines (MMR, varicella) due to antibody interference.
83
Ch42 – Screening before HPV vaccine?
No Pap or pregnancy testing required.
84
Ch42 – Most common adverse effect of all vaccines?
Injection-site pain, low-grade fever, mild myalgias.
85
Ch42 – Vaccine counseling for parents/patients?
Mild fever and soreness are normal; serious reactions are rare; report adverse events to VAERS.
86
Ch42 – Who should always get influenza vaccine?
Everyone ≥6 months; especially pregnant, elderly, chronic diseases, healthcare workers.
87
Ch37 – What is the primary goal of HIV therapy?
Durable viral suppression (undetectable viral load), immune restoration, reduced morbidity/mortality, and prevention of transmission.
88
Ch37 – Recommended initial treatment for HIV?
Combination antiretroviral therapy (ART) with at least 3 active drugs, typically: 2 NRTIs + 1 INSTI.
89
Ch37 – What are NRTIs?
Nucleoside/nucleotide reverse transcriptase inhibitors that block viral DNA synthesis.
90
Ch37 – Prototype NRTI?
Tenofovir (TDF or TAF).
91
Ch37 – Major toxicities of NRTIs?
Lactic acidosis, hepatic steatosis, lipodystrophy (rare with newer NRTIs).
92
Ch37 – Tenofovir (TDF) major adverse effects?
Nephrotoxicity and decreased bone mineral density.
93
Ch37 – Tenofovir (TAF) advantage over TDF?
Less renal and bone toxicity.
94
Ch37 – Emtricitabine adverse effect?
Hyperpigmentation of palms/soles (rare).
95
Ch37 – What are NNRTIs?
Non-nucleoside reverse transcriptase inhibitors — bind directly to RT enzyme to inhibit replication.
96
Ch37 – Prototype NNRTI?
Efavirenz.
97
Ch37 – Efavirenz adverse effects?
CNS depression, vivid dreams, dizziness, suicidal ideation, teratogenic in 1st trimester.
98
Ch37 – NNRTI drug interactions?
Many CYP interactions; can lower hormonal contraceptive effectiveness.
99
Ch37 – What are protease inhibitors (PIs)?
Block viral protease enzyme → prevent viral maturation.
100
Ch37 – Prototype PI?
Atazanavir or ritonavir-boosted protease inhibitors.
101
Ch37 – Major adverse effects of PIs?
Dyslipidemia, insulin resistance, lipodystrophy, hepatotoxicity, GI upset.
102
Ch37 – Why is ritonavir used as a booster?
Potent CYP3A4 inhibitor → increases levels of other PIs.
103
Ch37 – PI drug interactions?
Many — strong CYP inhibition → avoid statins like simvastatin/lovastatin.
104
Ch37 – What are INSTIs?
Integrase strand transfer inhibitors — block integration of viral DNA into host genome.
105
Ch37 – Prototype INSTI?
Dolutegravir.
106
Ch37 – Dolutegravir advantages?
High barrier to resistance, well tolerated, once-daily dosing.
107
Ch37 – Dolutegravir adverse effects?
Insomnia, weight gain, neural tube defect risk in early pregnancy (small but noted).
108
Ch37 – What are entry inhibitors?
Block HIV entry into host cells — e.g., maraviroc (CCR5 antagonist).
109
Ch37 – What test must be done before starting maraviroc?
CCR5 tropism testing — only effective for CCR5-tropic virus.
110
Ch37 – Treatment goal viral load?
Undetectable (<20–50 copies/mL).
111
Ch37 – NP teaching point for HIV therapy?
Strict adherence required; missed doses lead to resistance.
112
Ch38 – What drugs are used for chronic HBV?
Tenofovir (TDF/TAF) or entecavir.
113
Ch38 – Mechanism of tenofovir in HBV?
Nucleotide analog that inhibits viral DNA polymerase.
114
Ch38 – Major risks of tenofovir in HBV patients?
Renal toxicity, decreased bone mineral density (TDF).
115
Ch38 – Can HBV medications be stopped abruptly?
No — stopping can trigger severe hepatitis flare.
116
Ch38 – What drugs are used for HCV?
Direct-acting antivirals (DAAs): NS5A inhibitors, NS5B polymerase inhibitors (e.g., sofosbuvir), and NS3/4A protease inhibitors.
117
Ch38 – Goal of HCV treatment?
Sustained virologic response (SVR) = cure.
118
Ch38 – Sofosbuvir mechanism?
Nucleotide analog NS5B polymerase inhibitor.
119
Ch38 – Major advantage of DAAs?
Very high cure rates (>95%), once-daily dosing, minimal side effects.
120
Ch38 – Major contraindication for ribavirin?
Pregnancy (Category X) — causes severe birth defects.
121
Ch38 – What must female patients and male partners do if ribavirin is used?
Use two forms of contraception during therapy and 6 months after.
122
Ch38 – Common side effects of DAAs?
Fatigue, headache; generally well tolerated.
123
Ch39 – What is the first-line regimen for active TB?
RIPE therapy: Rifampin, Isoniazid, Pyrazinamide, Ethambutol.
124
Ch39 – Mechanism of isoniazid (INH)?
Inhibits mycolic acid synthesis in mycobacterial cell walls.
125
Ch39 – Major adverse effects of INH?
Hepatotoxicity, peripheral neuropathy.
126
Ch39 – How to prevent INH neuropathy?
Give pyridoxine (vitamin B6).
127
Ch39 – Risk factors for INH hepatotoxicity?
Older age, alcohol use, pregnancy/postpartum, pre-existing liver disease.
128
Ch39 – Mechanism of rifampin?
Inhibits bacterial RNA polymerase → broad antimicrobial effect.
129
Ch39 – Major adverse effects of rifampin?
Hepatotoxicity, red-orange body fluids, GI upset.
130
Ch39 – Key rifampin drug interactions?
Strong CYP inducer → decreases levels of warfarin, OCPs, HIV drugs, many others.
131
Ch39 – Mechanism of pyrazinamide?
Disrupts mycobacterial membrane function; exact mechanism unclear.
132
Ch39 – Major adverse effects of pyrazinamide?
Hyperuricemia, hepatotoxicity.
133
Ch39 – Mechanism of ethambutol?
Blocks arabinosyl transferase → inhibits cell wall synthesis.
134
Ch39 – Major adverse effect of ethambutol?
Optic neuritis (red/green color blindness).
135
Ch39 – What monitoring is required for ethambutol?
Baseline and periodic vision testing.
136
Ch39 – Treatment duration for active TB?
Usually 6 months minimum (2 months RIPE + 4 months INH + rifampin).
137
Ch39 – Drug used for latent TB?
INH for 6–9 months or rifampin for 4 months (depending on tolerance and risk).
138
Ch39 – NP teaching for TB therapy?
Adherence essential; avoid alcohol; monitor for jaundice, neuropathy, vision changes; warn about orange urine (rifampin).
139
Ch34 – Mechanism of action of metronidazole?
Forms toxic free radicals that damage DNA → bactericidal against anaerobes and protozoa.
140
Ch34 – Spectrum of metronidazole?
Anaerobes (Bacteroides, C. difficile), protozoa (Giardia, Trichomonas, Entamoeba).
141
Ch34 – First-line treatment for mild-to-moderate C. difficile infection?
Oral vancomycin or fidaxomicin; metronidazole is now alternative only.
142
Ch34 – First-line treatment for bacterial vaginosis?
Metronidazole (oral or gel).
143
Ch34 – First-line for trichomoniasis?
Metronidazole 2 g PO single dose.
144
Ch34 – Major adverse effects of metronidazole?
Metallic taste, GI upset, disulfiram-like reaction with alcohol, peripheral neuropathy (prolonged use).
145
Ch34 – What must patients avoid when taking metronidazole?
Alcohol during therapy and 48–72 hours after completion.
146
Ch34 – Metronidazole in pregnancy?
Safe in 2nd and 3rd trimester; avoid high-dose single treatment in 1st trimester unless necessary.
147
Ch34 – Does metronidazole interact with warfarin?
Yes — increases INR and bleeding risk. Monitor closely.
148
Ch35 – Mechanism of amphotericin B?
Binds to ergosterol in fungal cell membranes → creates pores → cell death.
149
Ch35 – Is amphotericin B fungistatic or fungicidal?
Fungicidal.
150
Ch35 – Spectrum of amphotericin B?
Broad: systemic fungi (Candida, Aspergillus, Cryptococcus, Histoplasma).
151
Ch35 – Major adverse effects of amphotericin B?
Nephrotoxicity, electrolyte disturbances (hypokalemia, hypomagnesemia), infusion reactions (fever, chills, rigors).
152
Ch35 – How to reduce infusion reactions with amphotericin B?
Premedicate with acetaminophen, diphenhydramine, and possibly steroids; slow infusion.
153
Ch35 – Why monitor kidney function with amphotericin B?
Nephrotoxicity is dose-limiting; requires frequent BUN/Cr and electrolyte monitoring.
154
Ch35 – Mechanism of azole antifungals?
Inhibit ergosterol synthesis by blocking fungal CYP450 enzymes.
155
Ch35 – Prototype azole?
Fluconazole.
156
Ch35 – Spectrum of fluconazole?
Candida (except C. krusei), Cryptococcus; good CSF penetration.
157
Ch35 – Major adverse effects of azoles?
Hepatotoxicity, QT prolongation, CYP inhibition → drug interactions.
158
Ch35 – Important azole drug interactions?
Increase levels of warfarin, statins, some antidiabetics, and some antipsychotics.
159
Ch35 – When should NPs avoid azoles?
Severe liver disease, concurrent QT-prolonging medications without monitoring.
160
Ch35 – What are echinocandins and example?
β-glucan synthesis inhibitors (cell wall); example: caspofungin.
161
Ch35 – When are echinocandins used?
Invasive Candida infections; alternative for patients intolerant to azoles.
162
Ch36 – Mechanism of acyclovir?
Inhibits viral DNA polymerase after activation by viral thymidine kinase.
163
Ch36 – What viruses does acyclovir treat?
HSV-1, HSV-2, VZV.
164
Ch36 – Most effective use of acyclovir?
Early initiation in HSV outbreaks or for suppression therapy.
165
Ch36 – Main adverse effects of oral acyclovir?
GI upset, headache, rash.
166
Ch36 – Main adverse effects of IV acyclovir?
Nephrotoxicity (crystalluria) and neurotoxicity.
167
Ch36 – How to prevent acyclovir nephrotoxicity?
Adequate hydration; slow IV infusion.
168
Ch36 – Mechanism of valacyclovir?
Prodrug of acyclovir with better oral bioavailability.
169
Ch36 – What antiviral is used for CMV?
Ganciclovir or valganciclovir (not acyclovir).
170
Ch36 – Major adverse effects of ganciclovir?
Bone marrow suppression (neutropenia, thrombocytopenia).
171
Ch36 – Mechanism of oseltamivir (Tamiflu)?
Neuraminidase inhibitor → prevents viral release from host cells.
172
Ch36 – When must oseltamivir be started to be effective?
Within 48 hours of flu symptom onset.
173
Ch36 – Oseltamivir common adverse effects?
Nausea, vomiting, headache.
174
Ch36 – Who should always be treated with antivirals for influenza?
Pregnant patients, older adults, immunocompromised, hospitalized, and high-risk chronic disease groups.
175
Ch36 – Mechanism of zanamivir?
Inhaled neuraminidase inhibitor for influenza.
176
Ch36 – Contraindication for zanamivir?
Asthma or COPD due to risk of bronchospasm.
177
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178
Ch31 – Mechanism of action of sulfonamides?
Inhibit bacterial folic acid synthesis by blocking para-aminobenzoic acid (PABA) utilization.
179
Ch31 – Are sulfonamides bactericidal or bacteriostatic?
Bacteriostatic (unless combined with trimethoprim).
180
Ch31 – Prototype sulfonamide?
Sulfamethoxazole.
181
Ch31 – Major clinical uses of sulfonamides?
UTIs, Nocardia, some skin infections (MRSA), Pneumocystis prophylaxis when combined with TMP.
182
Ch31 – Major adverse effects of sulfonamides?
Hypersensitivity reactions, Stevens–Johnson syndrome (SJS/TEN), photosensitivity, hemolysis in G6PD deficiency, crystalluria.
183
Ch31 – Why avoid sulfonamides in pregnancy?
Risk of kernicterus in newborns due to bilirubin displacement.
184
Ch31 – Why avoid sulfonamides in infants <2 months?
Increased risk of bilirubin toxicity/kernicterus.
185
Ch31 – Drug interactions with sulfonamides?
Increase warfarin, phenytoin, sulfonylurea levels via CYP inhibition.
186
Ch31 – NP teaching for sulfonamides to reduce crystalluria?
Encourage adequate hydration.
187
188
Ch32 – Mechanism of trimethoprim?
Inhibits dihydrofolate reductase → blocks folate synthesis.
189
Ch32 – Why is trimethoprim bacteriostatic alone?
Incomplete folate blockade; becomes bactericidal when combined with sulfamethoxazole.
190
Ch32 – TMP-SMX mechanism?
Sequential blockade of folate synthesis → bactericidal synergy.
191
Ch32 – TMP-SMX clinical uses?
UTIs, MRSA skin infections, Pneumocystis jirovecii pneumonia (PJP), prostatitis, some GI infections.
192
Ch32 – TMP-SMX adverse effects?
Hyperkalemia, renal impairment, SJS/TEN, bone marrow suppression (anemia, leukopenia), photosensitivity.
193
Ch32 – Why does TMP-SMX cause hyperkalemia?
Trimethoprim acts like potassium-sparing diuretic (amiloride-like).
194
Ch32 – Which patients should avoid TMP-SMX?
Renal impairment, pregnancy, breastfeeding infants <2 months, folate deficiency.
195
Ch32 – Drug interactions of TMP-SMX?
Increases warfarin levels → INR monitoring needed; increases phenytoin levels.
196
Ch32 – Why is TMP-SMX commonly used for MRSA skin infections?
Good oral bioavailability and reliable MRSA coverage.
197
Ch32 – NP teaching for TMP-SMX?
Maintain hydration, avoid excessive sun, monitor for rash, check for sulfa allergy.
198
199
Ch33 – Mechanism of fluoroquinolones?
Inhibit bacterial DNA gyrase and topoisomerase IV → bactericidal.
200
Ch33 – Prototype fluoroquinolones?
Ciprofloxacin and levofloxacin.
201
Ch33 – Spectrum of ciprofloxacin?
Strong gram-negative coverage including Pseudomonas; weak gram-positive activity.
202
Ch33 – Spectrum of levofloxacin?
Respiratory fluoroquinolone: good gram-positive + atypicals + moderate gram-negative.
203
Ch33 – Major black box warning for fluoroquinolones?
Tendon inflammation/rupture (especially Achilles).
204
Ch33 – Who is at highest risk for tendon rupture?
Older adults, patients on steroids, transplant patients.
205
Ch33 – Other major adverse effects of fluoroquinolones?
QT prolongation, peripheral neuropathy, CNS effects (confusion, seizures), C. difficile risk, dysglycemia.
206
Ch33 – Why avoid fluoroquinolones in pregnancy and children?
Damage to developing cartilage and bone.
207
Ch33 – NP caution with fluoroquinolones and warfarin?
INR elevation; increased bleeding risk.
208
Ch33 – Drug interactions with fluoroquinolones?
Chelation with calcium, magnesium, iron, and antacids → reduced absorption.
209
Ch33 – How should fluoroquinolones be administered to avoid chelation?
Take 2 hours before or 4–6 hours after antacids, dairy, or supplements.
210
Ch33 – NP consideration: Which infections should avoid fluoroquinolone use unless necessary?
Uncomplicated sinusitis, bronchitis, and simple UTIs — due to risks outweighing benefits.
211
Ch33 – Fluoroquinolones and blood glucose?
Can cause hypo- or hyperglycemia, especially in diabetics.
212
Ch33 – Why avoid fluoroquinolones in myasthenia gravis?
They exacerbate muscle weakness (black box warning).
213
Ch33 – Which fluoroquinolone is best for Pseudomonas?
Ciprofloxacin.
214
Ch33 – Which fluoroquinolones are best for pneumonia?
Levofloxacin and moxifloxacin (respiratory fluoroquinolones).
215
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216
Ch28 – Mechanism of action of vancomycin?
Inhibits cell wall synthesis by binding to D-Ala-D-Ala chains; bactericidal against gram-positive organisms.
217
Ch28 – What organisms does vancomycin cover?
MRSA, MSSA, Streptococci, Enterococci (not VRE), C. difficile (oral).
218
Ch28 – Why is vancomycin not absorbed orally?
Large, hydrophilic molecule → must be given IV except for C. difficile infection.
219
Ch28 – Major adverse effects of vancomycin?
Nephrotoxicity, ototoxicity, Red Man Syndrome, neutropenia.
220
Ch28 – What causes Red Man Syndrome?
Histamine-mediated flushing from rapid infusion; not a true allergy.
221
Ch28 – How to prevent Red Man Syndrome?
Infuse slowly over ≥1 hour; premedicate with antihistamines if needed.
222
Ch28 – When are trough levels required for vancomycin?
Serious infections (MRSA bacteremia, endocarditis) or renal impairment; target ~15–20 mcg/mL for severe infections.
223
Ch28 – Why monitor kidney function with vancomycin?
Risk of nephrotoxicity increases with high troughs or concurrent nephrotoxins.
224
Ch28 – What drug is used for VRE?
Linezolid or daptomycin.
225
Ch28 – Mechanism of linezolid?
Protein synthesis inhibitor (50S); active against MRSA and VRE.
226
Ch28 – Major risk of linezolid?
Bone marrow suppression (thrombocytopenia), serotonin syndrome with SSRIs.
227
Ch28 – Why is daptomycin not used for pneumonia?
It is inactivated by lung surfactant.
228
229
Ch29 – Mechanism of action of tetracyclines?
Bind to 30S ribosomal subunit → inhibit protein synthesis (bacteriostatic).
230
Ch29 – Prototype tetracycline?
Doxycycline.
231
Ch29 – Spectrum of tetracyclines?
Broad: atypicals (Mycoplasma), Rickettsia, Lyme disease, acne, MRSA skin infections.
232
Ch29 – Major adverse effects of tetracyclines?
Photosensitivity, GI upset, esophagitis, tooth discoloration, inhibition of bone growth.
233
Ch29 – Why avoid tetracyclines in pregnancy and children <8?
Cause permanent tooth discoloration and bone growth suppression.
234
Ch29 – Key administration teaching for tetracyclines?
Avoid calcium, iron, antacids, and dairy → reduce absorption; take with water and sit upright to prevent esophagitis.
235
Ch29 – Drug interactions with tetracyclines?
Chelation with metals (Ca, Fe, Mg, Zn).
236
Ch29 – Mechanism of action of macrolides?
Bind to 50S ribosomal subunit → inhibit protein synthesis.
237
Ch29 – Prototype macrolide?
Azithromycin (others: erythromycin, clarithromycin).
238
Ch29 – Clinical uses of macrolides?
Atypical pneumonia, pertussis, strep infections, COPD exacerbations, chlamydia.
239
Ch29 – Major adverse effects of macrolides?
QT prolongation, GI upset, hepatotoxicity.
240
Ch29 – Which macrolides are strong CYP inhibitors?
Erythromycin and clarithromycin; azithromycin is NOT a CYP inhibitor.
241
Ch29 – NP caution with macrolides and cardiac risk?
Avoid in patients with QT prolongation, electrolyte abnormalities, or on other QT-prolonging medications.
242
243
Ch30 – Mechanism of aminoglycosides?
Bind to 30S ribosome → disrupt protein synthesis; bactericidal.
244
Ch30 – Prototype aminoglycoside?
Gentamicin.
245
Ch30 – Spectrum of aminoglycosides?
Aerobic gram-negative organisms (e.g., Pseudomonas, Enterobacteriaceae).
246
Ch30 – Why must aminoglycosides be given parenterally?
Not absorbed orally.
247
Ch30 – Major adverse effects of aminoglycosides?
Nephrotoxicity, ototoxicity, neuromuscular blockade.
248
Ch30 – Why monitor drug levels with aminoglycosides?
Narrow therapeutic index; high troughs correlate with toxicity.
249
Ch30 – What increases nephrotoxicity risk?
Concurrent nephrotoxins (vancomycin, NSAIDs), dehydration, older age.
250
Ch30 – Why avoid aminoglycosides in pregnancy?
Risk of fetal ototoxicity.
251
Ch30 – When are aminoglycosides used with β-lactams?
Synergy for severe gram-negative infections or enterococcal endocarditis.
252
Ch30 – Which aminoglycoside is used for tuberculosis?
Streptomycin.
253
Ch30 – Early sign of ototoxicity the NP must screen for?
Tinnitus or high-frequency hearing loss.
254
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255
Ch25 – Define bactericidal vs bacteriostatic drugs.
Bactericidal = kill bacteria directly. Bacteriostatic = inhibit growth, rely on host immunity to clear infection.
256
Ch25 – What is selective toxicity?
Ability of antimicrobials to target microbial cells without harming human cells.
257
Ch25 – Main mechanisms of drug resistance?
Enzyme production (β-lactamase), target site alteration, decreased permeability, efflux pumps.
258
Ch25 – What is spontaneous mutation?
Random DNA changes causing resistance to one drug; occurs gradually.
259
Ch25 – What is conjugation?
Bacterial DNA transfer via plasmids → rapid multi-drug resistance (e.g., gram-negative rods).
260
Ch25 – Major factors contributing to resistance?
Inappropriate prescribing, broad-spectrum use, stopping early, agriculture antibiotic use.
261
Ch25 – What is prophylactic antimicrobial use?
Antibiotics given to prevent infection (e.g., surgical prophylaxis, endocarditis prophylaxis).
262
Ch25 – Surgical prophylaxis recommended agent?
Cefazolin (unless MRSA risk → vancomycin).
263
Ch25 – What determines antibiotic selection?
Organism identity, sensitivity, infection site, patient factors (renal function, allergies, pregnancy).
264
Ch25 – When should cultures be obtained?
Before starting antibiotics whenever possible.
265
Ch25 – What is empiric therapy?
Initial treatment before organism identified; based on likely pathogens + local resistance patterns.
266
Ch25 – What is definitive therapy?
Targeted treatment based on culture and sensitivity results.
267
Ch25 – What is superinfection?
New infection during antibiotic treatment (e.g., C. difficile, Candida) due to disrupted normal flora.
268
Ch25 – Signs of C. difficile infection?
Watery diarrhea, abdominal pain, leukocytosis; risk increases with clindamycin, cephalosporins, fluoroquinolones.
269
270
Ch26 – Mechanism of penicillins?
Weakening bacterial cell wall by inhibiting transpeptidases (PBP enzymes) → cell lysis.
271
Ch26 – Are penicillins bactericidal or bacteriostatic?
Bactericidal.
272
Ch26 – Major adverse effect of penicillins?
Allergic reactions: rash, urticaria, anaphylaxis.
273
Ch26 – What percentage of penicillin-allergic patients have cross-reactivity with cephalosporins?
About 1–2% (lower than historically believed). Highest with 1st-generation cephalosporins.
274
Ch26 – What is penicillin G used for?
Syphilis, strep infections, some pneumococcal infections.
275
Ch26 – Why can’t penicillin G be given orally?
Unstable in stomach acid.
276
Ch26 – Aminopenicillins spectrum?
Broader gram-negative coverage: H. influenzae, E. coli, Enterococci.
277
Ch26 – Prototype aminopenicillins?
Amoxicillin, ampicillin.
278
Ch26 – Which aminopenicillin is most commonly used in outpatient NP practice?
Amoxicillin (better oral absorption).
279
Ch26 – Penicillinase-resistant penicillins (anti-staphylococcal) and example?
Resistant to staph penicillinase; used for MSSA. Example: nafcillin.
280
Ch26 – Why are penicillinase-resistant penicillins ineffective against MRSA?
MRSA alters its PBPs (PBP2a) → prevents binding.
281
Ch26 – What is an extended-spectrum penicillin?
Piperacillin — covers Pseudomonas when combined with tazobactam.
282
Ch26 – Most common reason for penicillin treatment failure?
Inactivation by β-lactamases.
283
Ch26 – Beta-lactam/beta-lactamase inhibitor combinations?
Amoxicillin-clavulanate; piperacillin-tazobactam.
284
Ch26 – Common adverse effect of amoxicillin–clavulanate?
Diarrhea (due to clavulanate).
285
Ch26 – Penicillin allergy management?
Avoid all penicillins; consider cephalosporins if low-risk reaction; use non–beta-lactams for severe allergy.
286
287
Ch27 – Mechanism of cephalosporins?
β-lactam antibiotics that inhibit cell wall synthesis; bactericidal.
288
Ch27 – Trend across cephalosporin generations?
↑ gram-negative activity and ↑ resistance to β-lactamase as generation increases.
289
Ch27 – 1st-generation cephalosporin prototype and uses?
Cefazolin — surgical prophylaxis, MSSA, streptococci.
290
Ch27 – 2nd-generation cephalosporin prototype?
Cefuroxime.
291
Ch27 – 3rd-generation cephalosporin prototype?
Ceftriaxone.
292
Ch27 – Why avoid ceftriaxone in neonates?
Risk of biliary sludging and kernicterus.
293
Ch27 – 4th-generation cephalosporin prototype?
Cefepime — broad spectrum including Pseudomonas.
294
Ch27 – 5th-generation cephalosporin prototype?
Ceftaroline — covers MRSA.
295
Ch27 – Main adverse effects of cephalosporins?
Allergic reactions, bleeding (especially cefotetan, ceftriaxone), C. difficile risk.
296
Ch27 – Drug interactions with cefotetan/cefoperazone?
Disulfiram-like reaction with alcohol; risk of bleeding due to vitamin K interference.
297
Ch27 – What are carbapenems used for?
Very broad-spectrum, severe infections, resistant organisms.
298
Ch27 – Prototype carbapenem?
Imipenem-cilastatin.
299
Ch27 – Why is cilastatin added to imipenem?
Prevents renal metabolism of imipenem → increases drug levels.
300
Ch27 – Big risk of carbapenems?
Seizures (especially imipenem) at high doses or renal impairment.
301
Ch27 – Why reserve carbapenems?
Overuse promotes multi-drug resistance; used only when other agents ineffective.
302
Ch27 – Cephalosporin dosing considerations?
Most require renal dose adjustment except ceftriaxone.
303
Ch27 – NP teaching: Cephalosporins and allergy?
Cross-reactivity low; safe for most non-anaphylactic penicillin allergies.
304
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305
Ch22 – What is the primary mechanism of first-generation antipsychotics (FGAs)?
Strong dopamine D2 receptor antagonism in the mesolimbic pathway.
306
Ch22 – What symptom cluster do FGAs primarily improve?
Positive symptoms: hallucinations, delusions, agitation.
307
Ch22 – Major adverse effect of FGAs?
Extrapyramidal symptoms (EPS): dystonia, akathisia, parkinsonism, tardive dyskinesia.
308
Ch22 – Prototype high-potency FGA?
Haloperidol.
309
Ch22 – Prototype low-potency FGA?
Chlorpromazine.
310
Ch22 – Difference between high- and low-potency FGAs?
High potency = more EPS, fewer anticholinergic/sedative effects. Low potency = more sedation, hypotension, anticholinergic effects, less EPS.
311
Ch22 – What is acute dystonia?
Sudden muscle spasms (neck, jaw, eyes) occurring hours–days after starting FGAs.
312
Ch22 – Treatment for acute dystonia?
IM or IV benztropine or diphenhydramine.
313
Ch22 – What is akathisia?
Inner restlessness and need to move; very distressing.
314
Ch22 – Treatment for akathisia?
Beta blockers (propranolol), benzodiazepines, or switch antipsychotic.
315
Ch22 – What is pseudoparkinsonism?
Bradykinesia, rigidity, tremor from dopamine blockade.
316
Ch22 – Treatment for pseudoparkinsonism?
Benztropine or amantadine; consider dose reduction.
317
Ch22 – What is tardive dyskinesia (TD)?
Late-appearing irreversible involuntary movements (tongue, lips, face).
318
Ch22 – Drugs used to treat TD?
VMAT-2 inhibitors: valbenazine, deutetrabenazine.
319
Ch22 – What is neuroleptic malignant syndrome (NMS)?
Life-threatening reaction: muscle rigidity, hyperthermia, autonomic instability, elevated CK.
320
Ch22 – Treatment of NMS?
Stop drug, supportive care, cooling, IV fluids, dantrolene or bromocriptine.
321
Ch22 – Major cardiovascular risk of FGAs?
QT prolongation and sudden cardiac death.
322
Ch22 – Why avoid FGAs in older adults with dementia?
Black box warning: increased mortality (mainly from CV events and infections).
323
Ch22 – Mechanism of second-generation antipsychotics (SGAs)?
Weak D2 blockade + potent 5-HT2A blockade.
324
Ch22 – What symptom clusters do SGAs help with?
Positive and negative symptoms; improved tolerability.
325
Ch22 – Major metabolic risks of SGAs?
Weight gain, hyperlipidemia, insulin resistance → metabolic syndrome.
326
Ch22 – Prototype SGA?
Clozapine.
327
Ch22 – Major adverse effects of clozapine?
Agranulocytosis, seizures, myocarditis, metabolic syndrome.
328
Ch22 – Required monitoring for clozapine?
Weekly → biweekly → monthly CBC with ANC monitoring.
329
Ch22 – SGAs with highest metabolic risk?
Clozapine and olanzapine.
330
Ch22 – SGAs with lowest metabolic risk?
Aripiprazole, ziprasidone, lurasidone.
331
Ch22 – Why is aripiprazole unique?
Partial D2 agonist → lower EPS and prolactin levels.
332
333
Ch23 – What is the primary mechanism of lithium?
Unclear; modulates glutamate, serotonin, dopamine; stabilizes neuronal excitability.
334
Ch23 – Therapeutic use of lithium?
Bipolar disorder: acute mania and long-term mood stabilization.
335
Ch23 – Therapeutic serum range of lithium?
0.6–1.2 mEq/L (narrow therapeutic index).
336
Ch23 – Why is serum monitoring essential for lithium?
Small increases in serum levels can cause toxicity.
337
Ch23 – Early signs of lithium toxicity?
Nausea, vomiting, diarrhea, fine tremor, polyuria, thirst.
338
Ch23 – Advanced signs of toxicity?
Coarse tremor, confusion, ataxia, seizures, ECG changes.
339
Ch23 – Severe toxicity signs?
Coma, convulsions, kidney failure, death.
340
Ch23 – What conditions increase lithium toxicity risk?
Dehydration, hyponatremia, diuretics, NSAIDs, ACEIs/ARBs.
341
Ch23 – Why do diuretics increase lithium levels?
Sodium loss increases lithium reabsorption in the kidneys.
342
Ch23 – Why avoid NSAIDs with lithium?
They decrease renal blood flow → increase lithium levels.
343
Ch23 – Safer analgesic alternative for patients on lithium?
Acetaminophen.
344
Ch23 – Lithium and pregnancy considerations?
Category D; risk of Ebstein anomaly (heart defect). Use only if benefits outweigh risks.
345
Ch23 – Major long-term risks of lithium?
Hypothyroidism, renal impairment, nephrogenic diabetes insipidus.
346
Ch23 – Required baseline labs before lithium?
TSH, renal function, electrolytes, pregnancy test.
347
Ch23 – How often should lithium levels be checked?
5–7 days after dose change; then every 3–6 months.
348
349
Ch24 – Other first-line pharmacologic options for bipolar disorder?
SGAs (quetiapine, lurasidone), valproate, lamotrigine, carbamazepine.
350
Ch24 – Why is valproate useful in bipolar disorder?
Effective for mania and rapid cycling; faster onset than lithium.
351
Ch24 – Major risks of valproate?
Hepatotoxicity, pancreatitis, teratogenicity (neural tube defects).
352
Ch24 – Lamotrigine use in bipolar?
Best for bipolar depression and maintenance; prevents depressive episodes.
353
Ch24 – Major adverse effect of lamotrigine?
Life-threatening rash (SJS/TEN) with rapid dose escalation.
354
Ch24 – Why must lamotrigine be titrated slowly?
To reduce rash risk; strict schedule required.
355
Ch24 – Carbamazepine use in bipolar?
Useful for mania; good for patients who do not tolerate lithium or valproate.
356
Ch24 – Adverse effects of carbamazepine?
Aplastic anemia, agranulocytosis, hyponatremia, rash (SJS/TEN).
357
Ch24 – Which antipsychotics are approved for bipolar depression?
Quetiapine, lurasidone, olanzapine + fluoxetine combo.
358
Ch24 – Which SGAs have lower metabolic effects?
Lurasidone, ziprasidone, aripiprazole.
359
Ch24 – Why avoid antidepressant monotherapy in bipolar disorder?
Can trigger mania or rapid cycling; usually require mood stabilizer co-treatment.
360
Ch24 – NP counseling for bipolar meds?
Strict adherence essential, avoid dehydration, monitor mood changes, watch for toxicity symptoms, maintain regular follow-ups.
361
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Ch19 – What is the primary goal of antiepileptic drug (AED) therapy?
Prevent seizures with minimal adverse effects and minimal disruption to quality of life.
363
Ch19 – Mechanisms of action of AEDs (general)?
Suppress sodium influx, suppress calcium influx, enhance GABA activity, or antagonize glutamate.
364
Ch19 – Why must AEDs be tapered rather than stopped abruptly?
Abrupt withdrawal can trigger status epilepticus or seizure recurrence.
365
Ch19 – Prototype sodium channel–blocking AED?
Phenytoin.
366
Ch19 – Major adverse effects of phenytoin?
Gingival hyperplasia, ataxia, diplopia, rash, hirsutism, cognitive impairment.
367
Ch19 – Phenytoin therapeutic range?
Narrow: 10–20 mcg/mL.
368
Ch19 – Why does phenytoin require careful monitoring?
Nonlinear pharmacokinetics → small dose changes cause large serum concentration changes.
369
Ch19 – Serious toxicity risks of phenytoin?
Stevens–Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), dysrhythmias, hypotension (IV).
370
Ch19 – Drug interactions with phenytoin?
Strong CYP inducer → decreases levels of warfarin, oral contraceptives, glucocorticoids.
371
Ch19 – NP teaching for phenytoin and oral contraceptives?
Phenytoin reduces OCP effectiveness → use backup contraception.
372
Ch19 – Prototype broad-spectrum AED for partial/tonic-clonic seizures?
Carbamazepine.
373
Ch19 – Key risks of carbamazepine?
Bone marrow suppression (aplastic anemia, agranulocytosis), SJS/TEN (especially HLA-B*1502 positive Asian ancestry), hyponatremia.
374
Ch19 – Lab monitoring for carbamazepine?
CBC, sodium, drug levels.
375
Ch19 – Prototype AED used for absence seizures?
Ethosuximide.
376
Ch19 – Prototype GABA-enhancing AED?
Valproic acid.
377
Ch19 – Major risks of valproic acid?
Hepatotoxicity, pancreatitis, teratogenicity (neural tube defects), thrombocytopenia.
378
Ch19 – Lab monitoring for valproic acid?
LFTs, platelets, drug levels.
379
Ch19 – Why avoid valproate in pregnancy?
High teratogenic risk → neural tube defects, cognitive impairment.
380
Ch19 – Safer AED options in pregnancy?
Lamotrigine, levetiracetam (though monitoring still required).
381
Ch19 – Lamotrigine major risk?
Life-threatening rash (SJS/TEN), especially with rapid dose escalation.
382
Ch19 – Levetiracetam benefits?
Minimal drug interactions, well tolerated, safe in pregnancy categories.
383
Ch19 – Status epilepticus first-line treatment?
IV benzodiazepines (lorazepam), followed by longer-acting AEDs (phenytoin/fosphenytoin).
384
Ch19 – NP counseling point: adherence with AEDs?
Strict adherence essential; missed doses can trigger seizures.
385
386
Ch20 – Parkinson’s disease pathophysiology?
Degeneration of dopaminergic neurons in the substantia nigra → dopamine deficiency and excess acetylcholine activity.
387
Ch20 – Cornerstone drug for Parkinson’s disease?
Levodopa combined with carbidopa.
388
Ch20 – Mechanism of levodopa?
Dopamine precursor converted to dopamine in the brain.
389
Ch20 – Mechanism of carbidopa?
Inhibits peripheral breakdown of levodopa → increases CNS availability and reduces peripheral side effects.
390
Ch20 – Why must levodopa always be given with carbidopa?
Prevents peripheral metabolism → reduces nausea, improves efficacy, lowers dose need.
391
Ch20 – Major adverse effects of levodopa?
Dyskinesias, nausea, orthostatic hypotension, psychosis, motor fluctuations (‘on-off’ phenomenon).
392
Ch20 – Dietary teaching for levodopa?
Avoid high-protein meals, which reduce drug absorption and transport across BBB.
393
Ch20 – Long-term complication of levodopa therapy?
Motor fluctuations and dyskinesias.
394
Ch20 – Prototype dopamine agonists?
Pramipexole, ropinirole.
395
Ch20 – Benefits of dopamine agonists?
Less motor fluctuation and dyskinesia than levodopa; can delay need for levodopa.
396
Ch20 – Adverse effects of dopamine agonists?
Hallucinations, sleep attacks, impulse-control disorders (gambling, shopping).
397
Ch20 – MAO-B inhibitors mechanism?
Inhibit breakdown of dopamine in the CNS (e.g., selegiline, rasagiline).
398
Ch20 – Risk of combining MAO-B inhibitors with SSRIs/SNRIs?
Serotonin syndrome.
399
Ch20 – COMT inhibitors mechanism?
Inhibit peripheral breakdown of levodopa (ex: entacapone).
400
Ch20 – Major side effect of entacapone?
Orange/brown urine discoloration.
401
Ch20 – Anticholinergics role in Parkinson’s?
Reduce tremor by balancing dopamine/acetylcholine, used mainly in younger patients.
402
Ch20 – Why avoid anticholinergics in older adults with Parkinson’s?
High risk for confusion, urinary retention, constipation, blurred vision.
403
404
Ch21 – Alzheimer’s disease pathophysiology?
Neuronal degeneration, reduced cholinergic transmission, amyloid plaques, neurofibrillary tangles.
405
Ch21 – Two main drug classes for Alzheimer’s?
Cholinesterase inhibitors and NMDA receptor antagonists.
406
Ch21 – Prototype cholinesterase inhibitor?
Donepezil.
407
Ch21 – Mechanism of donepezil?
Inhibits acetylcholinesterase → increases acetylcholine in the brain.
408
Ch21 – Benefits of cholinesterase inhibitors?
Modest improvement in cognition, memory, activities of daily living; slow symptomatic decline.
409
Ch21 – Common adverse effects of cholinesterase inhibitors?
Nausea, diarrhea, bradycardia, syncope, insomnia.
410
Ch21 – Why monitor heart rate with donepezil?
Bradycardia risk → syncope and falls, especially in older adults.
411
Ch21 – Contraindications for cholinesterase inhibitors?
Sick sinus syndrome, conduction abnormalities, significant bradycardia.
412
Ch21 – Prototype NMDA antagonist?
Memantine.
413
Ch21 – Mechanism of memantine?
Blocks pathologic glutamate overactivation of NMDA receptors → protects against excitotoxicity.
414
Ch21 – Benefits of memantine?
Improves symptoms in moderate–severe Alzheimer’s; well tolerated.
415
Ch21 – Common memantine side effects?
Dizziness, headache, constipation.
416
Ch21 – Can donepezil and memantine be used together?
Yes — combination therapy is common for moderate–severe disease.
417
Ch21 – Non-pharmacologic interventions for Alzheimer’s?
Structured routines, caregiver support, safety modifications, cognitive stimulation.
418
Ch21 – NP counseling for caregivers?
Disease progression is expected; medications slow decline but do not reverse it. Focus on safety and support.
419
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420
Ch16 – Mechanism of action of local anesthetics?
Block sodium channels in neurons, preventing depolarization and conduction of pain signals.
421
Ch16 – Why are local anesthetics less effective in infected (acidic) tissue?
Low pH reduces the amount of anesthetic in the lipid-soluble form needed to cross nerve membranes.
422
Ch16 – Two major classes of local anesthetics?
Amides (lidocaine, bupivacaine) and esters (procaine, chloroprocaine).
423
Ch16 – How to differentiate amides vs esters?
Amides have an 'i' in the prefix (lidocaine, bupivacaine). Esters generally do not.
424
Ch16 – Prototype amide anesthetic?
Lidocaine.
425
Ch16 – Prototype ester anesthetic?
Procaine.
426
Ch16 – Why is epinephrine sometimes added to local anesthetics?
Vasoconstricts → prolongs anesthesia duration, reduces systemic absorption, decreases bleeding.
427
Ch16 – When should epinephrine NOT be used with anesthetics?
Areas with end-artery blood flow: fingers, toes, nose, ears, penis → risk of ischemia or necrosis.
428
Ch16 – Early signs of systemic local anesthetic toxicity?
Tinnitus, metallic taste, circumoral numbness, dizziness, agitation.
429
Ch16 – Late signs of local anesthetic toxicity?
Seizures, CNS depression, cardiovascular collapse, arrhythmias.
430
Ch16 – Which local anesthetic has the highest cardiotoxicity risk?
Bupivacaine.
431
Ch16 – Treatment for severe local anesthetic systemic toxicity?
IV lipid emulsion therapy + airway/ventilatory support.
432
Ch16 – Are local anesthetics safe in pregnancy?
Lidocaine is generally safe; use lowest effective dose.
433
Ch16 – Why do children have higher risk of toxicity from local anesthetics?
Lower protein binding and higher systemic absorption.
434
435
Ch17 – Mechanism of general anesthetics?
Enhance inhibitory neurotransmission (GABA) and/or block excitatory neurotransmission (glutamate) to induce unconsciousness, amnesia, and analgesia.
436
Ch17 – Stages of anesthesia?
Induction → Maintenance → Emergence.
437
Ch17 – Prototype inhalation anesthetic?
Isoflurane (older) or sevoflurane (common).
438
Ch17 – Risks of inhalation anesthetics?
Hypotension, respiratory depression, malignant hyperthermia (with volatile agents + succinylcholine).
439
Ch17 – What is malignant hyperthermia?
A rare genetic reaction causing muscle rigidity, hyperthermia, tachycardia, acidosis, and hyperkalemia triggered by certain anesthetics.
440
Ch17 – Treatment for malignant hyperthermia?
Immediate discontinuation of trigger + IV dantrolene + cooling + supportive care.
441
Ch17 – Why is nitrous oxide used?
Strong analgesic effects; weak anesthetic → often combined with other agents.
442
Ch17 – Major risk of nitrous oxide?
Nausea/vomiting; long-term exposure → B12 deficiency.
443
Ch17 – Prototype IV anesthetic: propofol — mechanism?
Potentiates GABA; induces rapid unconsciousness.
444
Ch17 – Key advantages of propofol?
Rapid onset and recovery, antiemetic effects.
445
Ch17 – Major risks of propofol?
Profound respiratory depression, hypotension, risk for abuse, propofol infusion syndrome (rare).
446
Ch17 – Why avoid propofol in egg/soy allergy?
Emulsion contains egg lecithin/soybean oil (though true cross-reactivity is rare).
447
Ch17 – Ketamine mechanism and uses?
NMDA receptor antagonist → dissociative anesthesia; used for procedural sedation, bronchodilation.
448
Ch17 – Major adverse effects of ketamine?
Emergence reactions (hallucinations), increased HR/BP, increased intracranial pressure.
449
Ch17 – Why is ketamine preferred in asthmatics?
Provides bronchodilation.
450
Ch17 – Why avoid ketamine in heart disease?
Sympathomimetic effects increase cardiac workload and BP.
451
452
Ch18 – Mechanism of centrally acting muscle relaxants?
Depress polysynaptic neuronal transmission in the CNS → reduce muscle spasm and pain.
453
Ch18 – Prototype centrally acting muscle relaxant?
Cyclobenzaprine.
454
Ch18 – Common uses of muscle relaxants?
Acute musculoskeletal spasms, low back pain, tension-type injuries; NOT effective for spasticity disorders.
455
Ch18 – Major side effects of cyclobenzaprine?
Sedation, dry mouth, dizziness, anticholinergic effects.
456
Ch18 – Why avoid cyclobenzaprine in older adults?
High anticholinergic burden → fall risk, confusion; Beers Criteria says to avoid.
457
Ch18 – Cyclobenzaprine contraindications?
MAOI use (serotonin syndrome), hyperthyroidism, significant cardiac disease.
458
Ch18 – Difference between spasm and spasticity?
Spasm = acute, localized muscle contraction. Spasticity = chronic increased tone due to CNS damage (multiple sclerosis, cerebral palsy).
459
Ch18 – Drugs used for spasticity?
Baclofen, tizanidine, diazepam, dantrolene.
460
Ch18 – Mechanism of baclofen?
GABA-B receptor agonist → reduces excitatory neurotransmission in spinal cord.
461
Ch18 – Major risk of abrupt baclofen withdrawal?
Hallucinations, seizures, rebound spasticity — potentially life-threatening, must taper.
462
Ch18 – Tizanidine mechanism and key side effect?
Alpha-2 agonist → reduces spasticity; causes hypotension and sedation.
463
Ch18 – Dantrolene mechanism and use?
Acts directly on skeletal muscle by reducing calcium release; used for malignant hyperthermia and spasticity.
464
Ch18 – Diazepam role in spasticity?
Enhances GABA-A → useful for spasticity but limited by sedation and dependence risk.
465
Ch18 – Why avoid combining muscle relaxants with other CNS depressants?
Additive sedation → increased fall risk, respiratory depression, impaired cognition.
466
Ch18 – NP counseling for muscle relaxants?
Avoid alcohol/CNS depressants, do not drive until effects are known, use short-term only (usually ≤2–3 weeks).
467
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468
Ch13 – What is the mechanism of action of opioid agonists?
They bind to mu (μ) and kappa (κ) receptors in the CNS, inhibiting pain transmission and altering pain perception.
469
Ch13 – Prototype opioid agonist?
Morphine.
470
Ch13 – Major clinical uses of opioid agonists?
Moderate to severe pain, acute pain, postoperative pain, cancer pain, MI-related pain, and sometimes cough/diarrhea (specific agents).
471
Ch13 – Common adverse effects of opioids?
Respiratory depression, sedation, constipation, miosis, nausea, urinary retention, hypotension, pruritus.
472
Ch13 – Why does opioid-induced respiratory depression occur?
Activation of mu receptors decreases responsiveness of brainstem respiratory centers to CO₂.
473
Ch13 – Which patients are most at risk for opioid respiratory depression?
Opioid-naive patients, older adults, underlying lung disease, sleep apnea, concurrent CNS depressants.
474
Ch13 – Opioid tolerance develops to which effects?
Analgesia and euphoria (rapid tolerance), respiratory depression (slower). NOT to constipation or miosis.
475
Ch13 – Why is constipation persistent with chronic opioid use?
Mu receptors in the GI tract slow motility; tolerance does not develop. Requires prophylaxis.
476
Ch13 – What should NPs prescribe to prevent opioid-induced constipation?
Stimulant laxative (senna or bisacodyl) + stool softener; consider peripherally acting mu antagonists for refractory cases.
477
Ch13 – What is the mechanism of action of naloxone?
Pure opioid antagonist that displaces opioids from mu receptors, reversing respiratory and CNS depression.
478
Ch13 – When should naloxone be co-prescribed?
High-dose opioids, opioid + benzo use, history of overdose, high-risk respiratory conditions.
479
Ch13 – What is the difference between physical dependence and addiction?
Dependence = physiologic adaptation with withdrawal on stopping. Addiction = compulsive use despite harm. Patients on chronic opioids may be dependent but not addicted.
480
Ch13 – What are signs of opioid withdrawal?
Yawning, sweating, rhinorrhea, anxiety, cramps, diarrhea, piloerection; uncomfortable but rarely life-threatening.
481
Ch13 – Why must long-term opioids be tapered?
Prevent withdrawal, avoid rebound pain, reduce physiological stress.
482
Ch13 – What drug is used for opioid-use disorder?
Buprenorphine (partial agonist), methadone (full agonist), or naltrexone (antagonist).
483
Ch13 – Why is buprenorphine safer than full agonists?
Partial agonist → ceiling effect on respiratory depression; lower abuse and overdose risk.
484
485
Ch14 – What is the mechanism of NSAIDs?
Inhibit COX enzymes (COX-1 and/or COX-2), reducing prostaglandin synthesis → decreases inflammation, pain, and fever.
486
Ch14 – Difference between COX-1 and COX-2?
COX-1 = protective functions (GI mucosa, platelets, renal perfusion). COX-2 = inflammation and pain.
487
Ch14 – Prototype nonselective NSAID?
Ibuprofen.
488
Ch14 – Prototype COX-2 selective NSAID?
Celecoxib.
489
Ch14 – Benefits of COX-2 inhibitors?
Less gastric ulceration vs traditional NSAIDs.
490
Ch14 – Major risk of COX-2 inhibitors?
Increased cardiovascular risk (MI, stroke).
491
Ch14 – Major adverse effects of NSAIDs?
GI bleeding/ulcers, renal injury, hypertension, fluid retention, bleeding risk.
492
Ch14 – Why do NSAIDs worsen renal function?
They decrease prostaglandin-mediated afferent arteriole dilation → reduced renal blood flow.
493
Ch14 – Which patients are high-risk with NSAIDs?
Older adults, CKD, HF, dehydration, ACEI/ARB + diuretic combo (‘triple whammy’).
494
Ch14 – What is the black box warning for NSAIDs?
Increased risk of cardiovascular events and GI bleeding.
495
Ch14 – Counseling point: taking NSAIDs with food?
Reduces dyspepsia but does NOT prevent ulcers.
496
Ch14 – Preferred NSAID in breastfeeding?
Ibuprofen (low milk transfer, short half-life).
497
Ch14 – Why avoid NSAIDs in pregnancy (3rd trimester)?
Premature closure of ductus arteriosus; inhibits labor; increases bleeding risk.
498
Ch14 – What is ketorolac’s major limitation?
Should not be used >5 days due to high risk of GI bleeding and renal toxicity.
499
500
Ch15 – Mechanism of acetaminophen (APAP)?
Inhibits prostaglandin synthesis in the CNS; minimal anti-inflammatory effect.
501
Ch15 – Maximum daily dose of acetaminophen for adults?
Typically 3,000 mg/day OTC; up to 4,000 mg/day under provider supervision.
502
Ch15 – Why is acetaminophen overdose dangerous?
Causes hepatic necrosis due to toxic metabolite (NAPQI) accumulation when glutathione is depleted.
503
Ch15 – Early symptoms of acetaminophen toxicity?
Nausea, vomiting, diaphoresis → then improvement → then hepatic failure (RUQ pain, jaundice).
504
Ch15 – Antidote for APAP overdose?
N-acetylcysteine (NAC). Most effective within 8–10 hours.
505
Ch15 – Which patients require lower max APAP dosing?
Chronic alcohol use, malnutrition, fasting, underlying liver disease.
506
Ch15 – Why does alcohol increase APAP hepatotoxicity?
Induces CYP2E1, increasing production of the toxic NAPQI metabolite.
507
Ch15 – Is acetaminophen safe in pregnancy?
Generally considered first-line for pain/fever in pregnancy; use lowest effective dose.
508
Ch15 – Why choose APAP over NSAIDs in certain patients?
Safe for platelet function, fewer GI risks, safer in CKD and cardiovascular disease.
509
Ch15 – Drug combinations that contain acetaminophen (risk for accidental overdose)?
Many opioids (hydrocodone/APAP, oxycodone/APAP), cold/flu products, sleep aids.
510
Ch15 – Teaching point for patients using multiple OTC products?
Check all labels to avoid exceeding the daily maximum; APAP is hidden in many combination meds.
511
Ch15 – What lab test is essential in suspected APAP overdose?
Serum acetaminophen concentration + nomogram to determine need for NAC therapy.
512
Ch15 – Why is APAP preferred for children with fever?
Less GI irritation and no Reye’s syndrome risk (unlike aspirin).
513
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514
Ch7 – What are the two major divisions of the autonomic nervous system (ANS)?
Sympathetic (fight-or-flight) and parasympathetic (rest-and-digest) divisions.
515
Ch7 – What neurotransmitter is released by all preganglionic neurons?
Acetylcholine (ACh) is released by both sympathetic and parasympathetic preganglionic neurons.
516
Ch7 – What neurotransmitter is released by most sympathetic postganglionic neurons?
Norepinephrine.
517
Ch7 – What neurotransmitter is released by parasympathetic postganglionic neurons?
Acetylcholine.
518
Ch7 – Define cholinergic receptors and list their two major types.
Receptors that respond to acetylcholine. Types: Nicotinic (N and M) and muscarinic receptors.
519
Ch7 – Define adrenergic receptors and list their major subtypes.
Receptors that respond to epinephrine/norepinephrine. Subtypes: α1, α2, β1, β2, and β3.
520
Ch7 – What physiological effects occur with α1 receptor activation?
Vasoconstriction, increased BP, mydriasis, bladder sphincter contraction.
521
Ch7 – What physiological effects occur with β1 receptor activation?
Increased heart rate, increased contractility, increased renin release from kidneys.
522
Ch7 – What physiological effects occur with β2 receptor activation?
Bronchodilation, vasodilation in skeletal muscle, uterine relaxation, glycogenolysis.
523
Ch7 – What physiological effects occur with muscarinic receptor activation?
Increased secretions, bronchoconstriction, bradycardia, miosis, GI motility, bladder contraction.
524
Ch7 – What is the clinical relevance of understanding receptor selectivity?
It helps predict therapeutic effects, side effects, and drug interactions, guiding safer NP prescribing.
525
526
Ch8 – What is the mechanism of action of muscarinic agonists?
They bind and activate muscarinic receptors, mimicking parasympathetic (cholinergic) actions.
527
Ch8 – What is the prototype muscarinic agonist and what is it used for?
Bethanechol — used to treat urinary retention by stimulating bladder contraction.
528
Ch8 – What are common adverse effects of muscarinic agonists?
Bradycardia, hypotension, increased secretions, bronchoconstriction, diarrhea, abdominal cramps.
529
Ch8 – Contraindications for muscarinic agonists?
Asthma/COPD, bradycardia, hypotension, PUD, urinary or GI obstruction.
530
Ch8 – What patient teaching is important for bethanechol?
Take on an empty stomach to reduce nausea; report wheezing, dizziness, or severe abdominal cramping.
531
Ch8 – What is the mechanism of muscarinic antagonists?
They block acetylcholine at muscarinic receptors, inhibiting parasympathetic activity.
532
Ch8 – Prototype muscarinic antagonist and its uses?
Atropine — used for bradycardia, pre-anesthesia drying secretions, and cholinergic toxicity.
533
Ch8 – Common side effects of muscarinic antagonists?
Dry mouth, blurred vision, constipation, urinary retention, tachycardia.
534
Ch8 – Why is atropine dangerous for glaucoma patients?
It increases intraocular pressure due to mydriasis → can precipitate acute angle-closure glaucoma.
535
Ch8 – List common anticholinergic drugs used clinically.
Atropine, oxybutynin, tolterodine, scopolamine, benztropine, antihistamines with anticholinergic properties.
536
Ch8 – What teaching is important for patients on anticholinergic drugs?
Avoid overheating (reduced sweating), increase fiber/fluids for constipation, caution with driving due to blurred vision.
537
Ch8 – What is cholinesterase?
Enzyme that breaks down acetylcholine, terminating its action.
538
Ch8 – What is the mechanism of cholinesterase inhibitors?
They prevent ACh breakdown, increasing cholinergic receptor activation.
539
Ch8 – Give two common cholinesterase inhibitors and their uses.
Donepezil (Alzheimer’s disease), neostigmine (myasthenia gravis).
540
Ch8 – Signs of cholinergic crisis.
Excessive secretions, bronchoconstriction, bradycardia, muscle weakness, miosis, diarrhea — may lead to respiratory paralysis.
541
Ch8 – Antidote for cholinesterase inhibitor overdose?
Atropine.
542
Ch8 – Why must NPs use caution with cholinergic drugs in asthma/COPD?
They cause bronchoconstriction and increased secretions, worsening airway obstruction.
543
544
Ch9 – What is the mechanism of adrenergic agonists (sympathomimetics)?
They activate adrenergic receptors (α or β), mimicking sympathetic stimulation.
545
Ch9 – Prototype catecholamine and its features?
Epinephrine — short half-life, given parenterally, potent α1, α2, β1, β2 activation.
546
Ch9 – Clinical uses of epinephrine?
Anaphylaxis, cardiac arrest, severe hypotension, bronchospasm.
547
Ch9 – Major adverse effects of epinephrine?
Hypertensive crisis, dysrhythmias, angina, hyperglycemia, extravasation injury (with norepinephrine).
548
Ch9 – Why is epinephrine first-line for anaphylaxis?
It reverses bronchoconstriction (β2), increases BP (α1), and improves cardiac output (β1).
549
Ch9 – What is norepinephrine primarily used for?
Severe hypotension and shock due to strong α1 and β1 activity.
550
Ch9 – Why must norepinephrine be given through a central line?
High risk of extravasation causing severe vasoconstriction and tissue necrosis.
551
Ch9 – What drug treats extravasation from catecholamines?
Phentolamine (α-blocker) injected locally.
552
Ch9 – What are noncatecholamine adrenergic agonists and why are they useful?
Longer half-life, can be taken orally, cross BBB (e.g., albuterol, phenylephrine).
553
Ch9 – Mechanism and clinical use of albuterol?
Selective β2 agonist causing bronchodilation — used for acute asthma relief.
554
Ch9 – Side effects of albuterol?
Tremor, tachycardia (from β1 spillover), nervousness, hypokalemia at high doses.
555
Ch9 – What is phenylephrine used for clinically?
Selective α1 agonist used for nasal congestion, hypotension, and eye dilation.
556
Ch9 – What is the danger of overusing topical nasal decongestants like phenylephrine?
Rebound congestion (rhinitis medicamentosa).
557
Ch9 – What are adrenergic antagonists (blockers)?
Drugs that block α or β receptors, reducing sympathetic tone.
558
Ch9 – Prototype nonselective beta blocker?
Propranolol.
559
Ch9 – Prototype selective beta1 blocker?
Metoprolol.
560
Ch9 – Major contraindication to nonselective beta blockers?
Asthma/COPD — blocking β2 causes bronchoconstriction.
561
Ch9 – Why are beta blockers tapered rather than stopped abruptly?
Abrupt stopping can cause rebound tachycardia, ischemia, or angina due to upregulated receptors.
562
Ch9 – Key adverse effects of beta blockers?
Bradycardia, fatigue, depression, sexual dysfunction, heart block, worsened asthma (nonselective).
563
Ch9 – What are alpha blockers used for?
α1 blockers (e.g., prazosin) used for BPH and hypertension by relaxing smooth muscle.
564
Ch9 – Side effect of alpha blockers NPs must warn patients about?
First-dose orthostatic hypotension → dizziness/falls.
565
Ch9 – Clonidine mechanism of action.
Central α2 agonist → decreases sympathetic outflow → lowers BP.
566
Ch9 – Important warnings for clonidine.
Sedation, dry mouth, bradycardia; **rebound hypertension** if abruptly stopped.
567
Ch9 – Why does understanding adrenergic pharmacology matter for NPs?
It guides safe prescribing of asthma meds, antihypertensives, cardiac drugs, and emergency meds while preventing dangerous interactions or contraindications.
568
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569
Ch10 – Why do many CNS drugs take weeks to show full effect?
Adaptive changes in the brain (receptor regulation, increased synaptic remodeling) require time; clinical response often lags behind pharmacologic action.
570
Ch10 – What is the blood–brain barrier and why is it clinically significant?
A selective barrier that restricts drug entry to the CNS; lipid-soluble and transport-carried drugs cross more easily. Limits treatment options for CNS diseases.
571
Ch10 – Define physical dependence in relation to CNS drugs.
Physiologic adaptation to a drug; abrupt discontinuation leads to withdrawal symptoms. Not the same as addiction.
572
Ch10 – What is tolerance and which CNS drug classes commonly cause it?
Reduced response to the same dose requiring higher doses for effect. Common with opioids, benzodiazepines, barbiturates.
573
Ch10 – Why must NPs taper many CNS drugs?
Avoid withdrawal symptoms, prevent rebound effects, and reduce risk of seizures (especially with benzos, barbiturates, some antidepressants).
574
Ch10 – What is the major safety issue with combining CNS depressants?
Additive respiratory depression, sedation, and risk of fatal overdose (e.g., opioids + benzos + alcohol).
575
Ch10 – Why do children often react paradoxically to some CNS drugs?
Immature neural pathways can cause excitation instead of sedation with antihistamines or benzos.
576
577
Ch11 – What is the mechanism of SSRIs?
Block reuptake of serotonin (5-HT), increasing serotonin levels in synapses.
578
Ch11 – Prototype SSRI?
Fluoxetine.
579
Ch11 – Clinical uses of SSRIs?
Depression, anxiety disorders, PTSD, OCD, panic disorder, PMDD.
580
Ch11 – Major adverse effects of SSRIs?
Sexual dysfunction, GI upset, insomnia or somnolence, weight changes, serotonin syndrome, initial anxiety.
581
Ch11 – What is serotonin syndrome?
A potentially life-threatening toxicity with agitation, confusion, sweating, tremor, hyperreflexia, fever, and autonomic instability; often from interacting serotonergic drugs.
582
Ch11 – What drugs increase risk of serotonin syndrome?
MAOIs, TCAs, tramadol, linezolid, triptans, St. John’s wort, MDMA.
583
Ch11 – Why must SSRIs be tapered?
To prevent withdrawal symptoms: dizziness, anxiety, irritability, flu-like symptoms, sensory disturbances.
584
Ch11 – What is the mechanism of SNRIs?
Block reuptake of serotonin and norepinephrine.
585
Ch11 – Prototype SNRI?
Venlafaxine.
586
Ch11 – Major side effects of SNRIs?
Hypertension, insomnia, nausea, sweating, sexual dysfunction.
587
Ch11 – Mechanism of tricyclic antidepressants (TCAs)?
Block reuptake of norepinephrine and serotonin, also block histamine, alpha-1, and muscarinic receptors.
588
Ch11 – Why are TCAs dangerous in overdose?
They cause lethal cardiac dysrhythmias (QT prolongation, ventricular arrhythmias) and severe anticholinergic toxicity.
589
Ch11 – Prototype TCA?
Amitriptyline.
590
Ch11 – Common TCA side effects?
Sedation, orthostatic hypotension, dry mouth, constipation, urinary retention.
591
Ch11 – Why should TCAs be avoided in older adults?
High anticholinergic burden increases risk of falls, confusion, constipation, urinary retention.
592
Ch11 – Mechanism of MAOIs?
Inhibit monoamine oxidase → increases serotonin, norepinephrine, dopamine levels.
593
Ch11 – Major danger with MAOIs?
Hypertensive crisis from tyramine-containing foods (aged cheese, cured meats, draft beer).
594
Ch11 – Why are MAOIs rarely first-line?
Severe dietary restrictions, many drug interactions, and risk of serotonin syndrome.
595
Ch11 – What are atypical antidepressants and an example?
Antidepressants with unique mechanisms; example: Bupropion (dopamine–NE reuptake inhibitor).
596
Ch11 – Why is bupropion useful in patients with sexual dysfunction from SSRIs?
Minimal sexual side effects and can counter SSRI-related sexual dysfunction.
597
Ch11 – Contraindications for bupropion?
Seizure disorder, eating disorders, abrupt alcohol/benzo withdrawal.
598
Ch11 – Time frame for therapeutic effect of antidepressants?
1–3 weeks for improvement; 4–8 weeks for full effect.
599
Ch11 – NP counseling point for antidepressant initiation?
Symptoms may temporarily worsen (anxiety/agitation); continue therapy and follow up closely.
600
601
Ch12 – What is the mechanism of benzodiazepines?
Enhance GABA activity by increasing frequency of chloride channel opening → CNS depression.
602
Ch12 – Sample benzodiazepine and its use.
Lorazepam — used for anxiety, alcohol withdrawal, seizures, acute agitation.
603
Ch12 – Key safety concern with benzodiazepines?
Respiratory depression, especially with opioids/alcohol; dependence and withdrawal risk.
604
Ch12 – Benzodiazepine withdrawal symptoms?
Anxiety, tremors, insomnia, hypertension, seizures — potentially life-threatening.
605
Ch12 – Why are benzos preferred over barbiturates?
Higher safety margin, lower risk of fatal respiratory depression, less abuse potential.
606
Ch12 – Mechanism of barbiturates?
Potentiate GABA by increasing duration of chloride channel opening; strong CNS depressants.
607
Ch12 – Clinical risk of barbiturates?
Profound respiratory depression, coma, death; high abuse and dependence risk.
608
Ch12 – What is the mechanism of buspirone?
Non-benzodiazepine anxiolytic that acts on serotonin receptors (partial 5-HT1A agonist); no sedation or dependence.
609
Ch12 – Advantages of buspirone vs benzos?
No dependence, no abuse potential, no interaction with CNS depressants.
610
Ch12 – Disadvantage of buspirone?
Delayed onset (2–4 weeks) — not useful for acute anxiety.
611
Ch12 – Mechanism of Z-drugs (zolpidem
zaleplon
612
Ch12 – Side effects of Z-drugs?
Complex sleep behaviors (sleepwalking, sleep-driving), daytime drowsiness, dependency risk.
613
Ch12 – What teaching is needed for zolpidem?
Take immediately before bed with at least 7–8 hours available for sleep; avoid alcohol; risk for next-day impairment.
614
Ch12 – Why are sedative-hypnotics risky in older adults?
Increased fall risk, cognitive impairment, delirium — strongly discouraged in Beers Criteria.
615
Ch12 – What is the role of melatonin agonists (e.g.
ramelteon)?
616
Ch12 – First-line recommendation for chronic insomnia?
Non-pharmacologic therapy: sleep hygiene, CBT-I.
617
Ch12 – Why should NPs use caution prescribing multiple CNS depressants?
Synergistic respiratory depression significantly increases overdose risk.
618
Front
Back
619
Ch4 – What is the FDA’s role in drug approval?
The FDA evaluates new drugs for safety and efficacy before approval, regulates labeling, monitors post-marketing safety (Phase IV), and can issue warnings, require REMS programs, or withdraw drugs if necessary.
620
Ch4 – Describe the four phases of new drug development.
Phase I: safety and PK in healthy volunteers; Phase II: small patient group to evaluate effectiveness and optimal dosing; Phase III: large trials confirming safety/efficacy; Phase IV: post-marketing surveillance to detect rare or long-term adverse effects.
621
Ch4 – What is a REMS program and why might an NP encounter it?
A Risk Evaluation and Mitigation Strategy (REMS) is required by the FDA for drugs with serious safety concerns. Prescribers may need certification, patient counseling, labs, or enrollment in monitoring systems (e.g., isotretinoin, clozapine).
622
Ch4 – Why is post-marketing surveillance (Phase IV) critical?
Some adverse effects are too rare to appear in clinical trials. Real-world use reveals new risks, drug interactions, prescribing trends, and unexpected harms, prompting labeling changes or withdrawals.
623
Ch4 – Define medication reconciliation and explain its value.
A systematic review of all medications a patient is taking to prevent omissions, duplications, interactions, and dosing errors during transitions of care. Reduces adverse events and improves safety.
624
Ch4 – What is a black box warning and how should NPs address it during prescribing?
It is the FDA’s strongest safety warning for serious or life-threatening risks. NPs should discuss risks/benefits with the patient, document counseling, consider safer alternatives, and monitor closely.
625
Ch4 – What is the purpose of an IND (Investigational New Drug) application?
It allows manufacturers to begin clinical trials by demonstrating to the FDA that the drug appears safe for initial human testing.
626
Ch4 – Define orphan drug and explain its significance.
A drug developed for rare diseases affecting fewer than 200,000 people in the U.S. Qualifies for incentives like market exclusivity and tax credits, improving access for underserved conditions.
627
Ch4 – What is medication error reporting (e.g.
MedWatch) used for?
628
629
Ch5 – What defines a drug–drug interaction?
A pharmacokinetic or pharmacodynamic alteration in drug response caused by the presence of another drug, supplement, or substance. Can increase toxicity or reduce therapeutic effect.
630
Ch5 – What patient populations are at highest risk for clinically significant drug interactions?
Older adults, patients with polypharmacy, those with renal/hepatic impairment, and patients taking narrow therapeutic index drugs (warfarin, lithium, digoxin).
631
Ch5 – Describe pharmacokinetic interactions.
One drug alters the absorption, distribution, metabolism, or excretion of another (e.g., CYP inhibition increasing serum levels).
632
Ch5 – Describe pharmacodynamic drug interactions.
Two drugs act at the same site or on related systems, producing additive, synergistic, or antagonistic effects (e.g., benzodiazepines + opioids increasing sedation).
633
Ch5 – What are CYP450 inducers and what is the clinical effect?
Inducers increase the activity of metabolic enzymes, lowering levels of substrate drugs and reducing effectiveness (e.g., rifampin reduces levels of many drugs).
634
Ch5 – What are CYP450 inhibitors and why are they important?
Inhibitors reduce metabolism of substrate drugs, increasing concentrations and risk of toxicity (e.g., azole antifungals increase levels of statins or warfarin).
635
Ch5 – Name major CYP inducers.
Rifampin, carbamazepine, phenytoin, St. John’s wort, phenobarbital.
636
Ch5 – Name major CYP inhibitors.
Macrolides (except azithromycin), azole antifungals, amiodarone, protease inhibitors, cimetidine, grapefruit juice.
637
Ch5 – Why is grapefruit juice clinically significant?
It inhibits intestinal CYP3A4, increasing levels of many drugs (e.g., calcium channel blockers, statins, benzodiazepines).
638
Ch5 – Give an example of a pharmacodynamic synergistic interaction with clinical risk.
Opioids + benzodiazepines → severe respiratory depression, sedation, and overdose risk.
639
Ch5 – Give an example of a pharmacodynamic antagonistic interaction.
NSAIDs may blunt antihypertensive effects of ACE inhibitors or diuretics by altering renal prostaglandins.
640
Ch5 – What drug classes commonly interact with warfarin?
Antibiotics (especially TMP-SMX, fluoroquinolones, macrolides), antifungals, antiepileptics, SSRIs, antiplatelets, NSAIDs, and many herbal products. Most interactions ↑ bleeding risk.
641
Ch5 – What patient counseling is needed when starting/stopping drugs that interact with warfarin?
Notify prescriber, increase INR monitoring, report bleeding/bruising, maintain consistent vitamin K intake, and avoid new OTC/herbal products without consultation.
642
Ch5 – How does renal impairment influence drug–drug interactions?
Reduced clearance increases concentration of renally eliminated drugs, heightening risk of toxicity and interactions even at standard doses.
643
Ch5 – What are important drug–herbal supplement interactions NPs should watch for?
St. John’s wort (induces CYP), ginkgo (↑ bleeding), ginseng (↓ warfarin effect), garlic (↑ bleeding), kava/valerian (↑ sedation).
644
645
Ch6 – What is an adverse drug reaction (ADR)?
Any harmful or unintended response to a drug given at normal doses. Can be predictable (Type A) or unpredictable (Type B).
646
Ch6 – Describe Type A (augmented) adverse reactions.
Dose-dependent, predictable from drug’s pharmacology (e.g., hypoglycemia with insulin). Represent the majority of ADRs.
647
Ch6 – Describe Type B (bizarre) adverse reactions.
Idiosyncratic, unpredictable, often immune-mediated (e.g., anaphylaxis, Stevens–Johnson syndrome). Less common but serious.
648
Ch6 – Name risk factors for experiencing an adverse drug reaction.
Polypharmacy, older age, renal/hepatic impairment, female sex, genetic variations, high doses, narrow therapeutic index drugs.
649
Ch6 – What is an allergic drug reaction?
An immune-mediated response requiring prior sensitization. Types range from mild rash to life-threatening anaphylaxis. Not dose-dependent.
650
Ch6 – List signs of anaphylaxis NPs must recognize quickly.
Hypotension, wheezing, stridor, angioedema, urticaria, respiratory distress, rapid onset after exposure.
651
Ch6 – First-line treatment for anaphylaxis?
IM epinephrine in the mid-outer thigh, repeat every 5–15 min as needed, plus airway support, oxygen, IV fluids, H1/H2 blockers, corticosteroids.
652
Ch6 – What is Stevens–Johnson syndrome (SJS) and how is it managed?
A severe mucocutaneous reaction from drugs (e.g., sulfonamides, anticonvulsants). Stop the offending agent immediately, treat in burn/ICU settings, and provide supportive care.
653
Ch6 – What defines hepatotoxicity as an ADR?
Drug-induced liver injury evidenced by elevated liver enzymes, jaundice, abdominal pain, dark urine, or failure. Common with acetaminophen overdose, isoniazid, valproate, statins (rare).
654
Ch6 – How should NPs monitor liver toxicity risk with medications?
Check baseline and periodic LFTs for hepatotoxic drugs, avoid alcohol, review other hepatotoxic meds, and counsel patients to report jaundice or RUQ pain.
655
Ch6 – What is nephrotoxicity and what drugs commonly cause it?
Kidney injury caused by drugs such as NSAIDs, ACE inhibitors/ARBs (in at-risk patients), aminoglycosides, amphotericin B, contrast dye, calcineurin inhibitors.
656
Ch6 – Describe the concept of QT prolongation as an ADR.
Many drugs prolong the QT interval, increasing risk of torsades de pointes. Risk increases with multiple QT drugs, electrolyte abnormalities, or underlying cardiac disease.
657
Ch6 – Which drug classes commonly prolong the QT interval?
Fluoroquinolones, macrolides, azole antifungals, antipsychotics, some antidepressants (TCAs, citalopram at high doses), and certain antiarrhythmics.
658
Ch6 – What is a boxed warning for antidepressants in youth?
Increased risk of suicidal ideation in children, adolescents, and young adults, especially early in treatment or dose changes.
659
Ch6 – How do NPs differentiate an adverse drug reaction from disease progression?
Timeline of onset, dose relationship, improvement when drug is stopped (dechallenge), recurrence upon re-exposure (rechallenge—rarely done intentionally), and ruling out other causes.
660
Ch6 – Explain the purpose of reporting ADRs to MedWatch.
Improves national safety surveillance, identifies rare events, informs labeling changes, and contributes to safer prescribing.
661
Ch1 – Define pharmacotherapeutics and how it differs from general pharmacology.
Pharmacotherapeutics is the clinical use of drugs to prevent, diagnose, or treat disease and improve patient outcomes. Pharmacology is the broader science of drugs (how they work, how the body handles them, interactions) whether or not they are being used in a specific patient.
662
Ch1 – What are the three main goals of rational prescribing for NPs?
1) Maximize therapeutic benefit, 2) Minimize risk of harm (adverse effects, interactions, misuse), and 3) Use resources responsibly (cost, access, adherence) while respecting patient preferences.
663
Ch1 – List the core steps in the rational prescribing process.
1) Define the patient’s problem, 2) Specify the therapeutic objective, 3) Choose a drug based on efficacy, safety, suitability, and cost, 4) Write a clear prescription, 5) Educate the patient, and 6) Monitor effectiveness and safety and adjust as needed.
664
Ch1 – What information should always be included in a complete prescription written by an NP?
Patient identifiers (name, DOB), date, drug name (generic preferred), strength, dose, route, frequency, duration or quantity, indication when appropriate, refills, special instructions, and prescriber information (name, credentials, DEA if controlled, NPI, contact).
665
Ch1 – Differentiate between generic and brand-name drugs from a clinical standpoint.
Generic drugs must have the same active ingredient, strength, dosage form, and route as the brand, with bioequivalence within an accepted range. Clinically, they are usually interchangeable, but small PK differences may matter for narrow therapeutic index drugs or certain formulations (e.g., some anticonvulsants, levothyroxine).
666
Ch1 – What is off-label prescribing and what is the NP’s responsibility when doing it?
Off-label prescribing is using an approved drug for an indication, age group, route, or dose not specifically approved by the FDA. The NP must ensure there is sound evidence or guideline support, discuss risks/benefits with the patient, document the rationale, and monitor carefully.
667
Ch1 – Explain what a Black Box Warning indicates.
A Black Box Warning is the FDA’s strongest warning, placed in a drug’s labeling when there is a serious or life-threatening risk. It does not prohibit use but alerts prescribers to specific dangers and the need for careful risk–benefit evaluation and monitoring.
668
Ch1 – What factors should an NP consider when selecting a specific drug for a patient?
Disease factors (severity, comorbidities, organ function), patient factors (age, pregnancy, genetics, adherence, preferences), drug factors (efficacy, safety profile, interactions, route, dosing schedule), and system factors (cost, formulary, access).
669
Ch1 – How does health literacy impact pharmacotherapeutic outcomes?
Low health literacy is associated with poor understanding of indications and dosing, decreased adherence, and increased risk of adverse outcomes. NPs should use plain language, teach-back, and written instructions tailored to the patient’s literacy level.
670
Ch1 – Give three strategies to improve medication adherence in primary care.
1) Simplify regimens (once-daily dosing, combo pills), 2) Use shared decision-making to align treatment with patient values, and 3) Provide clear education and follow-up, including reminders, pill boxes, or digital supports if appropriate.
671
Ch1 – Why is it important for NPs to understand schedules of controlled substances?
Schedules (I–V) reflect abuse potential and accepted medical use. They determine prescribing authority, refill limits, documentation, and monitoring requirements. Misunderstanding can lead to unsafe prescribing or legal/regulatory violations.
672
Ch1 – Describe key components of safe opioid prescribing for NPs.
Use opioids only when benefits outweigh risks, set clear functional goals, start with the lowest effective dose, avoid dangerous combinations (e.g., opioids + benzodiazepines), check PDMP data, use written treatment agreements when appropriate, and reassess regularly.
673
Ch1 – How do clinical practice guidelines support pharmacotherapeutic decision making?
Guidelines synthesize evidence and expert opinion into recommendations for first-line, second-line, and alternative therapies, including dosing and monitoring. They help standardize care, improve outcomes, and reduce unwarranted practice variation.
674
Ch1 – What is polypharmacy and why is it clinically important?
Polypharmacy is commonly defined as taking multiple medications (often ≥5). It increases the risk of interactions, adverse drug events, nonadherence, and prescribing cascades, especially in older adults and those with multiple comorbidities.
675
Ch1 – Distinguish between a medication error and an adverse drug reaction (ADR).
A medication error is any preventable event that may cause or lead to inappropriate medication use or patient harm. An ADR is a harmful or unintended response to a drug given at normal doses; ADRs can occur even when no error is made.
676
Ch2 – Define pharmacokinetics and list its four main processes.
Pharmacokinetics is what the body does to the drug. The four processes are absorption, distribution, metabolism (biotransformation), and excretion.
677
Ch2 – Define pharmacodynamics in contrast to pharmacokinetics.
Pharmacodynamics is what the drug does to the body (mechanism of action, dose–response relationships, receptor binding, therapeutic and toxic effects), whereas pharmacokinetics is how the body handles the drug over time.
678
Ch2 – What is bioavailability and why does it matter for oral drugs?
Bioavailability is the fraction of an administered dose that reaches the systemic circulation unchanged. For oral drugs, factors like first-pass metabolism, formulation, and GI variables affect bioavailability, which influences dosing and interchangeability of products.
679
Ch2 – Explain first-pass metabolism and give an example of a drug affected by it.
First-pass metabolism is the metabolism of a drug in the gut wall and liver before it reaches systemic circulation after oral administration, reducing bioavailability. Drugs like propranolol and nitroglycerin are significantly affected, which is why some are given sublingually or via non-oral routes.
680
Ch2 – Define half-life (t½) and its clinical relevance.
Half-life is the time required for the plasma concentration of a drug to decrease by 50%. It determines dosing intervals, time to steady state, and how long it takes for a drug to be eliminated after discontinuation.
681
Ch2 – Approximately how many half-lives are needed to reach steady state with repeated dosing?
It typically takes about 4–5 half-lives of a drug to reach steady-state plasma concentrations with regular dosing.
682
Ch2 – What is a loading dose and when might it be used?
A loading dose is a higher initial dose designed to quickly achieve therapeutic plasma levels, useful for drugs with long half-lives when rapid effect is needed (e.g., some antiarrhythmics, certain antibiotics).
683
Ch2 – Define therapeutic index and explain its significance.
The therapeutic index is a ratio comparing a drug’s toxic dose to its effective dose. A narrow therapeutic index means there is a small margin between effective and toxic levels, requiring close monitoring (e.g., warfarin, digoxin, lithium).
684
Ch2 – Differentiate between agonist
partial agonist
685
Ch2 – What is potency versus efficacy in pharmacodynamics?
Potency refers to the amount of drug needed to produce a given effect (more potent = lower dose needed). Efficacy refers to the maximal effect a drug can produce. A drug can be more potent but not more efficacious than another.
686
Ch2 – Name three patient factors that can significantly alter drug absorption.
1) Gastric pH and motility, 2) Presence of food or other drugs in the GI tract, and 3) Integrity of GI mucosa or gut transit time (e.g., after bowel surgery, in severe diarrhea).
687
Ch2 – How does protein binding affect distribution and potential for drug interactions?
Highly protein-bound drugs are largely inactive while bound; only free drug is active. Competition for binding sites (e.g., between warfarin and another highly bound drug) can increase free drug levels and risk of toxicity.
688
Ch2 – Why do hepatic and renal function need to be considered before prescribing many medications?
Impaired hepatic function can reduce metabolism, and impaired renal function can reduce excretion, leading to drug accumulation and toxicity. Doses may need to be reduced or dosing intervals extended based on liver tests and estimated GFR/creatinine clearance.
689
Ch2 – Describe pharmacogenomics and its relevance to NP prescribing.
Pharmacogenomics studies how genetic variation influences drug response. Certain polymorphisms (e.g., CYP2D6, CYP2C19, HLA alleles) can affect efficacy and toxicity. NPs should recognize when genetic testing may guide drug choice or dosing (e.g., some antidepressants, clopidogrel, abacavir).
690
Ch2 – Define a type A (augmented) vs type B (bizarre) adverse drug reaction.
Type A reactions are dose-dependent, predictable from the drug’s known pharmacology (e.g., hypotension with antihypertensives). Type B reactions are idiosyncratic, not clearly dose-related, and often immune or genetic in origin (e.g., anaphylaxis, SJS).
691
Ch3 – Why are pregnant patients considered a special population for pharmacotherapy?
Pregnancy alters pharmacokinetics (↑ plasma volume, altered protein binding, ↑ renal blood flow, changes in hepatic enzymes), and drugs may affect the developing fetus, especially during organogenesis. Prescribing must weigh maternal benefit against fetal risk.
692
Ch3 – During which gestational period is the risk of teratogenic structural defects highest?
The risk of major structural malformations is highest during organogenesis, roughly weeks 3–8 of gestation, when organs are forming.
693
Ch3 – What general principles guide prescribing in pregnancy?
Use non-pharmacologic measures when reasonable; avoid unnecessary drugs; choose agents with the best safety data; use the lowest effective dose for the shortest time; avoid known teratogens; and collaborate with obstetric providers when risks are significant.
694
Ch3 – How have pregnancy drug risk categories changed in labeling?
Older letter categories (A, B, C, D, X) have been replaced by narrative labeling that describes data on pregnancy, lactation, and reproductive potential, including known risks and clinical considerations, to support individualized risk–benefit decisions.
695
Ch3 – What are key considerations when prescribing for a lactating patient?
Consider if the drug passes into breast milk in clinically significant amounts, the infant’s age and health, timing doses to minimize infant exposure (e.g., dose after breastfeeding), using drugs with better lactation safety data, and monitoring the infant for sedation, irritability, poor feeding, or GI issues.
696
Ch3 – Why are infants and young children at higher risk for drug toxicity?
Organ systems are immature: reduced hepatic metabolism, reduced renal clearance, different body water/fat distribution, and variable protein binding. These factors alter PK, so weight-based dosing and pediatric-specific references are essential.
697
Ch3 – Describe the basic principle of pediatric drug dosing.
Most pediatric doses are calculated based on weight (mg/kg) or body surface area and should never exceed recommended adult maximum doses. Use pediatric-specific drug references and double-check calculations.
698
Ch3 – List two major pharmacokinetic changes in older adults that affect drug therapy.
1) Decreased renal function (↓ GFR) leading to reduced drug clearance, and 2) Changes in body composition (↑ fat, ↓ total body water, ↓ lean mass) and sometimes reduced hepatic blood flow, altering distribution and metabolism.
699
Ch3 – What is the Beers Criteria and how is it used?
The Beers Criteria is a guideline listing potentially inappropriate medications and situations for older adults. NPs use it to identify drugs with higher risk of adverse effects in geriatrics and to consider safer alternatives or closer monitoring.
700
Ch3 – Give three strategies to reduce adverse drug events in older adults.
1) Regularly review the full medication list (including OTC and supplements), 2) De-prescribe unnecessary drugs, starting low and going slow with new meds, and 3) Monitor closely for side effects that may present atypically (falls, confusion, anorexia).
701
Ch3 – Why is renal function more important than age alone when adjusting doses?
Chronologic age does not reliably predict kidney function. Many older adults have reduced GFR despite normal serum creatinine due to low muscle mass. Dose adjustments should be based on estimated renal function (e.g., eGFR or CrCl), not age alone.
702
Ch3 – Name two high-risk drug classes commonly implicated in serious adverse events in older adults.
Common examples include anticoagulants (e.g., warfarin, DOACs), hypoglycemics (especially insulin and some sulfonylureas), opioids, and sedative-hypnotics/benzodiazepines.
703
Ch3 – What is a prescribing cascade
and why is it problematic in geriatrics?
704
Ch3 – List key elements of shared decision-making when prescribing for special populations.
Clearly present options, benefits, and risks; explore patient values and preferences; consider life stage, comorbidities, and social context; agree on a plan; and arrange follow-up to reassess effectiveness and safety.
705
Strep throat – first-line medication?
Penicillin V or amoxicillin. MOA: inhibits bacterial cell wall synthesis by binding PBPs.
706
Strep throat – second-line medication?
Cephalexin or azithromycin. MOA: inhibits bacterial protein synthesis at the 50S ribosome.
707
Acute otitis media – first-line therapy?
Amoxicillin. MOA: inhibits bacterial cell wall synthesis.
708
Acute otitis media – second-line therapy?
Amoxicillin-clavulanate. MOA: beta-lactam antibiotic plus beta-lactamase inhibitor.
709
Bacterial sinusitis – first-line medication?
Amoxicillin-clavulanate. MOA: inhibits cell wall synthesis and beta-lactamase enzymes.
710
Bacterial sinusitis – alternative therapy?
Doxycycline. MOA: inhibits bacterial protein synthesis at the 30S ribosome.
711
Community-acquired pneumonia (healthy adult) – first-line?
Amoxicillin or doxycycline. MOA: cell wall inhibition or 30S ribosomal inhibition.
712
Community-acquired pneumonia with comorbidities – first-line?
Amoxicillin-clavulanate plus macrolide OR respiratory fluoroquinolone. MOA: PBPs plus 50S inhibition or DNA gyrase inhibition.
713
Community-acquired pneumonia – second-line?
Levofloxacin. MOA: inhibits bacterial DNA gyrase and topoisomerase IV.
714
Pertussis – first-line treatment?
Azithromycin. MOA: inhibits bacterial protein synthesis at the 50S ribosome.
715
Uncomplicated UTI – first-line medication?
Nitrofurantoin. MOA: damages bacterial DNA.
716
Uncomplicated UTI – alternative medication?
Trimethoprim-sulfamethoxazole. MOA: sequential inhibition of folate synthesis.
717
Complicated UTI – first-line therapy?
Fluoroquinolone. MOA: inhibits bacterial DNA gyrase.
718
Outpatient pyelonephritis – first-line therapy?
Ciprofloxacin. MOA: inhibits DNA gyrase.
719
Pyelonephritis in pregnancy – first-line therapy?
Ceftriaxone. MOA: inhibits bacterial cell wall synthesis.
720
Bacterial vaginosis – first-line medication?
Metronidazole. MOA: free radical formation causing DNA strand breakage.
721
Trichomoniasis – first-line treatment?
Metronidazole single dose. MOA: DNA disruption via free radicals.
722
Chlamydia – first-line medication?
Doxycycline. MOA: inhibits bacterial protein synthesis at 30S ribosome.
723
Chlamydia in pregnancy – first-line medication?
Azithromycin. MOA: inhibits bacterial protein synthesis at 50S ribosome.
724
Gonorrhea – recommended treatment?
Ceftriaxone plus doxycycline. MOA: cell wall inhibition plus 30S ribosomal inhibition.
725
Syphilis – first-line treatment?
Penicillin G. MOA: inhibits bacterial cell wall synthesis.
726
Syphilis with penicillin allergy (non-pregnant)?
Doxycycline. MOA: inhibits bacterial protein synthesis.
727
Non-purulent cellulitis – first-line therapy?
Cephalexin. MOA: inhibits bacterial cell wall synthesis.
728
Purulent cellulitis (MRSA) – first-line?
Trimethoprim-sulfamethoxazole or doxycycline. MOA: folate inhibition or 30S ribosome inhibition.
729
Severe MRSA infection – first-line therapy?
Vancomycin. MOA: binds D-Ala-D-Ala preventing cell wall synthesis.
730
C. difficile infection – first-line medication?
Oral vancomycin. MOA: inhibits bacterial cell wall synthesis.
731
C. difficile infection – alternative medication?
Fidaxomicin. MOA: inhibits bacterial RNA polymerase.
732
Influenza – first-line antiviral therapy?
Oseltamivir. MOA: neuraminidase inhibition preventing viral release.
733
HSV infection – first-line therapy?
Acyclovir or valacyclovir. MOA: inhibits viral DNA polymerase.
734
Herpes zoster – first-line therapy?
Valacyclovir. MOA: inhibits viral DNA synthesis.
735
HIV initial therapy – preferred regimen?
Two NRTIs plus one INSTI. MOA: inhibits reverse transcription and viral integration.
736
Hepatitis B – first-line medication?
Tenofovir or entecavir. MOA: inhibits viral DNA polymerase.
737
Hepatitis C – first-line therapy?
Direct-acting antivirals. MOA: inhibit viral polymerase and replication proteins.
738
Malaria prophylaxis – first-line?
Atovaquone-proguanil. MOA: mitochondrial electron transport inhibition and folate inhibition.
739
Malaria uncomplicated infection – first-line therapy?
Artemether-lumefantrine. MOA: free radical formation damaging parasite proteins.
740
Lyme disease – first-line medication?
Doxycycline. MOA: inhibits bacterial protein synthesis.
741
Disseminated Lyme disease – first-line therapy?
Ceftriaxone. MOA: inhibits bacterial cell wall synthesis.
742
Rocky Mountain spotted fever – treatment of choice?
Doxycycline. MOA: inhibits bacterial protein synthesis.
743
Pinworm infection – first-line therapy?
Albendazole. MOA: inhibits parasite microtubule formation.
744
Giardiasis – first-line therapy?
Metronidazole. MOA: damages protozoal DNA.
745
Bacterial meningitis – empiric therapy?
Ceftriaxone plus vancomycin. MOA: cell wall inhibition.
746
Bacterial meningitis age >50 – additional drug?
Ampicillin. MOA: inhibits bacterial cell wall synthesis.
747
Otitis externa – first-line therapy?
Topical fluoroquinolone. MOA: DNA gyrase inhibition.
748
Necrotizing fasciitis – key antibiotic therapy?
Broad-spectrum beta-lactam plus clindamycin. MOA: cell wall inhibition and toxin suppression.
749
Infective endocarditis – empiric therapy?
Vancomycin. MOA: inhibits bacterial cell wall synthesis.
750
Active tuberculosis – first-line therapy?
RIPE regimen. MOA: inhibits mycolic acid synthesis, RNA polymerase, and cell wall synthesis.
751
Strep throat – first-line medication?
Penicillin V or amoxicillin. MOA: inhibits bacterial cell wall synthesis by binding PBPs.
752
Strep throat – second-line medication?
Cephalexin or azithromycin. MOA: inhibits bacterial protein synthesis at the 50S ribosome.
753
Acute otitis media – first-line therapy?
Amoxicillin. MOA: inhibits bacterial cell wall synthesis.
754
Acute otitis media – second-line therapy?
Amoxicillin-clavulanate. MOA: beta-lactam antibiotic plus beta-lactamase inhibitor.
755
Bacterial sinusitis – first-line medication?
Amoxicillin-clavulanate. MOA: inhibits cell wall synthesis and beta-lactamase enzymes.
756
Bacterial sinusitis – alternative therapy?
Doxycycline. MOA: inhibits bacterial protein synthesis at the 30S ribosome.
757
Community-acquired pneumonia (healthy adult) – first-line?
Amoxicillin or doxycycline. MOA: cell wall inhibition or 30S ribosomal inhibition.
758
Community-acquired pneumonia with comorbidities – first-line?
Amoxicillin-clavulanate plus macrolide OR respiratory fluoroquinolone. MOA: PBPs plus 50S inhibition or DNA gyrase inhibition.
759
Community-acquired pneumonia – second-line?
Levofloxacin. MOA: inhibits bacterial DNA gyrase and topoisomerase IV.
760
Pertussis – first-line treatment?
Azithromycin. MOA: inhibits bacterial protein synthesis at the 50S ribosome.
761
Uncomplicated UTI – first-line medication?
Nitrofurantoin. MOA: damages bacterial DNA.
762
Uncomplicated UTI – alternative medication?
Trimethoprim-sulfamethoxazole. MOA: sequential inhibition of folate synthesis.
763
Complicated UTI – first-line therapy?
Fluoroquinolone. MOA: inhibits bacterial DNA gyrase.
764
Outpatient pyelonephritis – first-line therapy?
Ciprofloxacin. MOA: inhibits DNA gyrase.
765
Pyelonephritis in pregnancy – first-line therapy?
Ceftriaxone. MOA: inhibits bacterial cell wall synthesis.
766
Bacterial vaginosis – first-line medication?
Metronidazole. MOA: free radical formation causing DNA strand breakage.
767
Trichomoniasis – first-line treatment?
Metronidazole single dose. MOA: DNA disruption via free radicals.
768
Chlamydia – first-line medication?
Doxycycline. MOA: inhibits bacterial protein synthesis at 30S ribosome.
769
Chlamydia in pregnancy – first-line medication?
Azithromycin. MOA: inhibits bacterial protein synthesis at 50S ribosome.
770
Gonorrhea – recommended treatment?
Ceftriaxone plus doxycycline. MOA: cell wall inhibition plus 30S ribosomal inhibition.
771
Syphilis – first-line treatment?
Penicillin G. MOA: inhibits bacterial cell wall synthesis.
772
Syphilis with penicillin allergy (non-pregnant)?
Doxycycline. MOA: inhibits bacterial protein synthesis.
773
Non-purulent cellulitis – first-line therapy?
Cephalexin. MOA: inhibits bacterial cell wall synthesis.
774
Purulent cellulitis (MRSA) – first-line?
Trimethoprim-sulfamethoxazole or doxycycline. MOA: folate inhibition or 30S ribosome inhibition.
775
Severe MRSA infection – first-line therapy?
Vancomycin. MOA: binds D-Ala-D-Ala preventing cell wall synthesis.
776
C. difficile infection – first-line medication?
Oral vancomycin. MOA: inhibits bacterial cell wall synthesis.
777
C. difficile infection – alternative medication?
Fidaxomicin. MOA: inhibits bacterial RNA polymerase.
778
Influenza – first-line antiviral therapy?
Oseltamivir. MOA: neuraminidase inhibition preventing viral release.
779
HSV infection – first-line therapy?
Acyclovir or valacyclovir. MOA: inhibits viral DNA polymerase.
780
Herpes zoster – first-line therapy?
Valacyclovir. MOA: inhibits viral DNA synthesis.
781
HIV initial therapy – preferred regimen?
Two NRTIs plus one INSTI. MOA: inhibits reverse transcription and viral integration.
782
Hepatitis B – first-line medication?
Tenofovir or entecavir. MOA: inhibits viral DNA polymerase.
783
Hepatitis C – first-line therapy?
Direct-acting antivirals. MOA: inhibit viral polymerase and replication proteins.
784
Hypertension – first-line medications?
Thiazide diuretic, ACE inhibitor, ARB, or calcium channel blocker. MOA: natriuresis, RAAS inhibition, or calcium channel blockade.
785
Hypertension in diabetes – preferred first-line?
ACE inhibitor or ARB. MOA: blocks RAAS and reduces intraglomerular pressure.
786
Hypertension in pregnancy – first-line?
Labetalol or nifedipine. MOA: alpha/beta blockade or calcium channel inhibition.
787
Heart failure with reduced EF – foundational therapy?
ACE inhibitor/ARB/ARNI, beta blocker, SGLT2 inhibitor. MOA: neurohormonal blockade and natriuresis.
788
Heart failure fluid overload – first-line?
Loop diuretic. MOA: inhibits Na-K-2Cl transporter in loop of Henle.
789
Atrial fibrillation rate control – first-line?
Beta blocker or diltiazem. MOA: slows AV nodal conduction.
790
Atrial fibrillation anticoagulation – first-line?
Direct oral anticoagulant (apixaban). MOA: factor Xa inhibition.
791
Hyperlipidemia – first-line therapy?
Statins. MOA: inhibit HMG-CoA reductase reducing cholesterol synthesis.
792
Asthma rescue therapy – first-line?
Short-acting beta agonist. MOA: beta-2 stimulation causing bronchodilation.
793
Asthma controller therapy – first-line?
Inhaled corticosteroid. MOA: suppresses airway inflammation.
794
COPD maintenance therapy – first-line?
LABA or LAMA. MOA: bronchodilation via beta-2 or muscarinic blockade.
795
Type 2 diabetes – first-line medication?
Metformin. MOA: decreases hepatic gluconeogenesis and improves insulin sensitivity.
796
Type 2 diabetes with ASCVD – preferred add-on?
GLP-1 receptor agonist. MOA: enhances glucose-dependent insulin secretion.
797
Hypothyroidism – first-line therapy?
Levothyroxine. MOA: synthetic T4 replacement.
798
Hyperthyroidism – first-line medication?
Methimazole. MOA: inhibits thyroid hormone synthesis.
799
GERD – first-line therapy?
Proton pump inhibitor. MOA: irreversible inhibition of gastric H+/K+ ATPase.
800
Depression – first-line medication?
SSRI. MOA: inhibits serotonin reuptake.
801
Generalized anxiety disorder – first-line?
SSRI or SNRI. MOA: serotonin and norepinephrine reuptake inhibition.
802
Bipolar disorder – first-line mood stabilizer?
Lithium. MOA: modulates ion transport and neurotransmitter signaling.
803
Schizophrenia – first-line therapy?
Second-generation antipsychotic. MOA: dopamine D2 and serotonin 5-HT2A blockade.
804
ADHD – first-line medication?
Stimulant (methylphenidate). MOA: increases dopamine and norepinephrine.
805
Osteoporosis – first-line therapy?
Bisphosphonates. MOA: inhibit osteoclast-mediated bone resorption.
806
Gout acute flare – first-line?
NSAIDs. MOA: cyclooxygenase inhibition reducing inflammation.
807
Gout chronic management – first-line?
Allopurinol. MOA: inhibits xanthine oxidase reducing uric acid production.
808
Migraine acute treatment – first-line?
Triptans. MOA: serotonin 5-HT1B/1D agonists causing vasoconstriction.
809
Migraine prevention – first-line?
Beta blockers or topiramate. MOA: reduces neuronal excitability.
810
Seizure disorder – first-line?
Levetiracetam. MOA: modulates synaptic vesicle protein SV2A.
811
Alzheimer disease – first-line therapy?
Donepezil. MOA: acetylcholinesterase inhibition increasing acetylcholine.
812
Parkinson disease – first-line therapy?
Levodopa-carbidopa. MOA: dopamine precursor plus peripheral decarboxylase inhibition.
813
Iron deficiency anemia – first-line therapy?
Oral ferrous sulfate. MOA: replaces iron for hemoglobin synthesis.
814
B12 deficiency – first-line therapy?
Cyanocobalamin. MOA: vitamin B12 replacement for DNA synthesis.
815
Anaphylaxis – first-line medication?
IM epinephrine. MOA: alpha-1 vasoconstriction and beta-2 bronchodilation.
816
Allergic rhinitis – first-line therapy?
Intranasal corticosteroid. MOA: suppresses local nasal inflammation.
817
Motion sickness – first-line therapy?
Scopolamine. MOA: muscarinic receptor blockade.
818
Nausea and vomiting – first-line antiemetic?
Ondansetron. MOA: serotonin 5-HT3 receptor antagonism.
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