Pharmacology for Nurses: Essential Exam Prep & Practice Questions. 2025/26 Exam Updates.
Pharmacology Nursing is the study of how medications affect the human body and how nurses can
safely administer and monitor these medications. It includes understanding drug classifications, dosage
calculations, side effects, interactions, and the nursing responsibilities involved in medication
administration. Nurses must be knowledgeable about pharmacokinetics, pharmacodynamics, and
patient education to ensure safe and effective medication use.
1st generation cephalosporins - ✔✔-Cefazolin, cephalexin
Use: Gram- positive cocci, Proteus mirabilis, E. coli, Klebsiella pneumoniae. Cefazolin used prior to
surgery to prevent S. aureus wound infections
1st generation H1 blockers - ✔✔-Diphenhydramine, dimenhydrinate, chlorpheniramine
1st generation H1 blockers mechanism, use, and toxicity - ✔✔--Mechanism: reversible inhibitors of H1
histamine receptors.
-Use: allergy, motion sickness, sleep aid.
-Toxicity: sedation, antimuscarinic, anti-α-adrenergic.
2nd generation cephalosporins - ✔✔--Cefoxitin, cefaclor, cefuroxime
-Use: gram-positive cocci, Haemophilus influenzae, Enterobacter aerogenes, Neisseria spp., Proteus
mirabilis, E. coli, Klebsiella pneumoniae, Serratia marcescens.
2nd generation H1 blockers - ✔✔-Loratadine, fexofenadine, desloratadine, cetirizine
2nd generation H1 blockers mechanism, use, and toxicity - ✔✔--Mechanism: reversible inhibitors of H1
histamine receptors.
-Use: Allergy.
-Toxicity: far less sedating than 1st generation because of decreased entry into CNS.
3rd generation cephalosporins - ✔✔--Ceftriaxone, cefotaxime, ceftazidime)
-Use: serious gram-negative infections resistant to other β-lactams. Ceftriaxone—meningitis, gonorrhea,
disseminated lyme disease; ceftazidime—Pseudomonas
,4th generation cephalosporins - ✔✔--Cefepime
-Use: gram-negative organisms, with activity against Pseudomonas and gram-positive organisms.
5-fluorouracil (5-FU) mechanism - ✔✔--Pyrimidine analog bioactivated to 5F-dUMP, which covalently
complexes folic acid.
-This complex inhibits thymidylate synthase decreasing dTMP and decreasing DNA synthesis.
5-fluorouracil (5-FU) toxicity - ✔✔-Myelosuppression, which is not reversible with leucovorin (folinic
acid)
5-fluorouracil (5-FU) use - ✔✔-Colon cancer, pancreatic cancer, basal cell carcinoma (topical)
5th generation cephalosporins - ✔✔--Ceftaroline
-Use: broad gram-positive and gram-negative organism coverage, including MRSA; does not cover
Pseudomonas.
6-mercaptopurine (6-MP), Azathioprine, 6-thioguanine (6-TG) clinical use - ✔✔-Preventing organ
rejection, rheumatoid arthritis, IBD, SLE; used to wean patients off steroids in chronic disease and to treat
steroid-refractory chronic disease.
6-mercaptopurine (6-MP), Azathioprine, 6-thioguanine (6-TG) mechanism - ✔✔--Purine (thiol) analogs
leading to decreasedde novo purine synthesis.
-Activated by HGPRT. Azathioprine is metabolized into 6-MP.
6-mercaptopurine (6-MP), Azathioprine, 6-thioguanine (6-TG) toxicity - ✔✔--Myelosuppression, GI,
liver.
-Azathioprine and 6-MP are metabolized by xanthine oxidase; thus both have increase toxicity with
allopurinol or febuxostat.
Abciximab clinical use - ✔✔-Antiplatelet agent for prevention of ischemic complications in patients
undergoing percutaneous coronary intervention
,Abciximab target - ✔✔-Platelet glycoproteins IIb/IIIa
IIb times IIIa equals "absiximab"
ACE inhibitors (drugs, mechanism, use, toxicity) - ✔✔-Captopril, enalapril, lisinopril, ramipril
-Mechanism: inhibit ACE -> decrease AT II -> decrease GFR by preventing constriction of efferent
arterioles. Levels of renin increase as a result of loss of feedback inhibition. Inhibition of ACE also
prevents inactivation of bradykinin, a potent vasodilator.
-Use: hypertension, HF, proteinuria, diabetic nephropathy. Prevent unfavorable heart remodeling as a
result of chronic hypertension. In diabetic nephropathy, intraglomerular pressure, slowing GBM
thickening
-Toxicity: cough, Angioedema (contraindicated in C1 esterase inhibitor deficiency), Teratogen (fetal renal
malformations), increased Creatinine (decreased GFR), Hyperkalemia, and Hypotension. Avoid in
bilateral renal artery stenosis, because ACE inhibitors will further decrease GFR causing renal failure.
Acetaminophen (mechanism, use, toxicity) - ✔✔--Mechanism: reversibly inhibits cyclooxygenase,
mostly in CNS. Inactivated peripherally.
-Use: antipyretic, analgesic, but not anti-inflammatory. Used instead of aspirin to avoid Reye syndrome in
children with viral infection.
-Toxicity: overdose produces hepatic necrosis; acetaminophen metabolite (NAPQI) depletes glutathione
and forms toxic tissue byproducts in liver. N-acetylcysteine is antidote—regenerates glutathione.
Acetaminophen toxicity antidote - ✔✔-N-acetylcysteine (replenishes glutathione)
Acetazolamide (mechanism, use, toxicity) - ✔✔--Mechanism: carbonic anhydrase inhibitor. Causes self-
limited NaHCO3 diuresis and decreased total body HCO3− stores.
-Use: glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness, pseudotumor cerebri.
-Toxicity: hyperchloremic metabolic acidosis, paresthesias, NH3 toxicity, sulfa allergy.
Acetazolamide as a glaucoma drug - ✔✔--Mechanism: diuretic; decrease aqueous humor synthesis via
inhibition of carbonic anhydrase
, -No pupillary or vision changes
AChE inhibitor/organophosphate toxicity antidote - ✔✔-Atropine > pralidoxime
Acid suppression therapy general overview image - ✔✔-
Acute gout drugs - ✔✔-NSAIDs (naproxen, indomethacin), glucocorticoids, colchicine
Acyclovir, famciclovir, valacyclovir clinical use - ✔✔--HSV and VZV. Weak activity against EBV. No
activity against CMV. Used for HSV- induced mucocutaneous and genital lesions as well as for
encephalitis. Prophylaxis in immunocompromised patients. No effect on latent forms of HSV and VZV.
Valacyclovir, a prodrug of acyclovir, has better oral bioavailability.
-For herpes zoster, use famciclovir.
Acyclovir, famciclovir, valacyclovir mechanism of resistance - ✔✔-Mutated viral thymidine kinase.
Acyclovir, famciclovir, valacyclovir MoA - ✔✔-Guanosine analogs. Monophosphorylated by HSV/VZV
thymidine kinase and not phosphorylated in uninfected cells few adverse effects. Triphosphate formed by
cellular enzymes. Preferentially inhibit viral DNA polymerase by chain termination.
Acyclovir, famciclovir, valacyclovir toxicity - ✔✔-Obstructive crystalline nephropathy and acute renal
failure if not adequately hydrated. Mutated viral thymidine kinase.
Adalimumab, infliximab clinical use - ✔✔-IBD, rheumatoid arthritis, ankylosing spondylitis, psoriasis
Adalimumab, infliximab target - ✔✔-Soluble TNF-α
Etanercept is a decoy TNF-α receptor and not a monoclonal antibody
Adenosine - ✔✔--Antiarrhythmic
-Increase K+ out of cells hyperpolarizing the cell and increasing intracellular Ca2+.
Pharmacology Nursing is the study of how medications affect the human body and how nurses can
safely administer and monitor these medications. It includes understanding drug classifications, dosage
calculations, side effects, interactions, and the nursing responsibilities involved in medication
administration. Nurses must be knowledgeable about pharmacokinetics, pharmacodynamics, and
patient education to ensure safe and effective medication use.
1st generation cephalosporins - ✔✔-Cefazolin, cephalexin
Use: Gram- positive cocci, Proteus mirabilis, E. coli, Klebsiella pneumoniae. Cefazolin used prior to
surgery to prevent S. aureus wound infections
1st generation H1 blockers - ✔✔-Diphenhydramine, dimenhydrinate, chlorpheniramine
1st generation H1 blockers mechanism, use, and toxicity - ✔✔--Mechanism: reversible inhibitors of H1
histamine receptors.
-Use: allergy, motion sickness, sleep aid.
-Toxicity: sedation, antimuscarinic, anti-α-adrenergic.
2nd generation cephalosporins - ✔✔--Cefoxitin, cefaclor, cefuroxime
-Use: gram-positive cocci, Haemophilus influenzae, Enterobacter aerogenes, Neisseria spp., Proteus
mirabilis, E. coli, Klebsiella pneumoniae, Serratia marcescens.
2nd generation H1 blockers - ✔✔-Loratadine, fexofenadine, desloratadine, cetirizine
2nd generation H1 blockers mechanism, use, and toxicity - ✔✔--Mechanism: reversible inhibitors of H1
histamine receptors.
-Use: Allergy.
-Toxicity: far less sedating than 1st generation because of decreased entry into CNS.
3rd generation cephalosporins - ✔✔--Ceftriaxone, cefotaxime, ceftazidime)
-Use: serious gram-negative infections resistant to other β-lactams. Ceftriaxone—meningitis, gonorrhea,
disseminated lyme disease; ceftazidime—Pseudomonas
,4th generation cephalosporins - ✔✔--Cefepime
-Use: gram-negative organisms, with activity against Pseudomonas and gram-positive organisms.
5-fluorouracil (5-FU) mechanism - ✔✔--Pyrimidine analog bioactivated to 5F-dUMP, which covalently
complexes folic acid.
-This complex inhibits thymidylate synthase decreasing dTMP and decreasing DNA synthesis.
5-fluorouracil (5-FU) toxicity - ✔✔-Myelosuppression, which is not reversible with leucovorin (folinic
acid)
5-fluorouracil (5-FU) use - ✔✔-Colon cancer, pancreatic cancer, basal cell carcinoma (topical)
5th generation cephalosporins - ✔✔--Ceftaroline
-Use: broad gram-positive and gram-negative organism coverage, including MRSA; does not cover
Pseudomonas.
6-mercaptopurine (6-MP), Azathioprine, 6-thioguanine (6-TG) clinical use - ✔✔-Preventing organ
rejection, rheumatoid arthritis, IBD, SLE; used to wean patients off steroids in chronic disease and to treat
steroid-refractory chronic disease.
6-mercaptopurine (6-MP), Azathioprine, 6-thioguanine (6-TG) mechanism - ✔✔--Purine (thiol) analogs
leading to decreasedde novo purine synthesis.
-Activated by HGPRT. Azathioprine is metabolized into 6-MP.
6-mercaptopurine (6-MP), Azathioprine, 6-thioguanine (6-TG) toxicity - ✔✔--Myelosuppression, GI,
liver.
-Azathioprine and 6-MP are metabolized by xanthine oxidase; thus both have increase toxicity with
allopurinol or febuxostat.
Abciximab clinical use - ✔✔-Antiplatelet agent for prevention of ischemic complications in patients
undergoing percutaneous coronary intervention
,Abciximab target - ✔✔-Platelet glycoproteins IIb/IIIa
IIb times IIIa equals "absiximab"
ACE inhibitors (drugs, mechanism, use, toxicity) - ✔✔-Captopril, enalapril, lisinopril, ramipril
-Mechanism: inhibit ACE -> decrease AT II -> decrease GFR by preventing constriction of efferent
arterioles. Levels of renin increase as a result of loss of feedback inhibition. Inhibition of ACE also
prevents inactivation of bradykinin, a potent vasodilator.
-Use: hypertension, HF, proteinuria, diabetic nephropathy. Prevent unfavorable heart remodeling as a
result of chronic hypertension. In diabetic nephropathy, intraglomerular pressure, slowing GBM
thickening
-Toxicity: cough, Angioedema (contraindicated in C1 esterase inhibitor deficiency), Teratogen (fetal renal
malformations), increased Creatinine (decreased GFR), Hyperkalemia, and Hypotension. Avoid in
bilateral renal artery stenosis, because ACE inhibitors will further decrease GFR causing renal failure.
Acetaminophen (mechanism, use, toxicity) - ✔✔--Mechanism: reversibly inhibits cyclooxygenase,
mostly in CNS. Inactivated peripherally.
-Use: antipyretic, analgesic, but not anti-inflammatory. Used instead of aspirin to avoid Reye syndrome in
children with viral infection.
-Toxicity: overdose produces hepatic necrosis; acetaminophen metabolite (NAPQI) depletes glutathione
and forms toxic tissue byproducts in liver. N-acetylcysteine is antidote—regenerates glutathione.
Acetaminophen toxicity antidote - ✔✔-N-acetylcysteine (replenishes glutathione)
Acetazolamide (mechanism, use, toxicity) - ✔✔--Mechanism: carbonic anhydrase inhibitor. Causes self-
limited NaHCO3 diuresis and decreased total body HCO3− stores.
-Use: glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness, pseudotumor cerebri.
-Toxicity: hyperchloremic metabolic acidosis, paresthesias, NH3 toxicity, sulfa allergy.
Acetazolamide as a glaucoma drug - ✔✔--Mechanism: diuretic; decrease aqueous humor synthesis via
inhibition of carbonic anhydrase
, -No pupillary or vision changes
AChE inhibitor/organophosphate toxicity antidote - ✔✔-Atropine > pralidoxime
Acid suppression therapy general overview image - ✔✔-
Acute gout drugs - ✔✔-NSAIDs (naproxen, indomethacin), glucocorticoids, colchicine
Acyclovir, famciclovir, valacyclovir clinical use - ✔✔--HSV and VZV. Weak activity against EBV. No
activity against CMV. Used for HSV- induced mucocutaneous and genital lesions as well as for
encephalitis. Prophylaxis in immunocompromised patients. No effect on latent forms of HSV and VZV.
Valacyclovir, a prodrug of acyclovir, has better oral bioavailability.
-For herpes zoster, use famciclovir.
Acyclovir, famciclovir, valacyclovir mechanism of resistance - ✔✔-Mutated viral thymidine kinase.
Acyclovir, famciclovir, valacyclovir MoA - ✔✔-Guanosine analogs. Monophosphorylated by HSV/VZV
thymidine kinase and not phosphorylated in uninfected cells few adverse effects. Triphosphate formed by
cellular enzymes. Preferentially inhibit viral DNA polymerase by chain termination.
Acyclovir, famciclovir, valacyclovir toxicity - ✔✔-Obstructive crystalline nephropathy and acute renal
failure if not adequately hydrated. Mutated viral thymidine kinase.
Adalimumab, infliximab clinical use - ✔✔-IBD, rheumatoid arthritis, ankylosing spondylitis, psoriasis
Adalimumab, infliximab target - ✔✔-Soluble TNF-α
Etanercept is a decoy TNF-α receptor and not a monoclonal antibody
Adenosine - ✔✔--Antiarrhythmic
-Increase K+ out of cells hyperpolarizing the cell and increasing intracellular Ca2+.
