300 Nursing Pharmacology Flashcards by Drug Class Deck

If you can name the class, the nursing priorities should come with it.

300 cardsLast updated 2026-08-30

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Nursing pharmacology gets messy when names pile up faster than patterns stick. You may recognize a drug on sight, then stall on what the class does, what changes absorption or excretion, or which adverse effects need your attention right away. The hard part is not recognizing the term. It is pulling the right nursing focus and watch-outs back out when you need them. This deck cuts the subject into 300 cards that stay at class and concept level, so knowledge transfers across brand names. The sections are principles (40), cardiovascular (55), neuro-and-psych (50), infection-and-immunity (50), endocrine-and-gi (55), and respiratory-and-renal (50). Each card covers a class, suffix, or concept, asks what it is, and answers with the meaning and the thing to watch for. A card on Absorption, Fluoroquinolones, or -zolamide trains the same pattern of recall every time. When these cards are on a spaced-repetition schedule, the items you can answer cleanly stop crowding your reviews, and the ones you miss keep coming back until they settle. The deck leaves out doses and treatment instructions on purpose, so your time stays on mechanism, nursing priorities, and adverse-effect patterns that carry from one drug name to the next.

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What's inside

Showing 100 representative cards from the full 300-card deck.

Front	Back
Absorption — what is it?	Movement of a drug from the administration site into the bloodstream. Vomiting, diarrhea, poor perfusion, or food and antacid interactions that reduce uptake.
Excretion — what is it?	Removal of drugs or metabolites from the body, mainly by the kidneys. Accumulation and toxicity when kidney function declines or dehydration occurs.
Half-life — what is it?	Time needed for the amount of drug in the body to fall by about half. Accumulation with repeated dosing or prolonged toxicity after an overdose.
Hepatic impairment — what is it?	Reduced liver function that can lower metabolism, change protein binding, and alter first-pass handling. Excess sedation, bleeding, jaundice, or rising toxicity with usual doses.
Pharmacodynamics — what is it?	Study of what a drug does to the body, including receptor effects and clinical response. Additive effects with drugs that act on the same system.
Potency — what is it?	Amount of drug needed to produce a given effect compared with another drug. Unexpected toxicity or poor control after a formulation or agent change.
Therapeutic index — what is it?	Margin between effective exposure and toxic exposure. A narrow index means less room for error. Small changes in therapy, missed doses, or interactions causing toxicity or loss of control.
Oral route — what is it?	Drug is swallowed and absorbed through the gastrointestinal tract. Aspiration, vomiting, tube feed or antacid interactions, and first-pass loss of effect.
Intravenous route — what is it?	Drug is delivered directly into the bloodstream for immediate systemic availability. Infiltration, phlebitis, infection, and immediate severe reactions.
Rights of administration — what is it?	Safety framework to verify the correct patient, drug, dose, route, time, and related documentation or reason. Look alike or sound alike drugs, interruptions, allergy conflicts, and transcription errors.
Maintenance dose — what is it?	The repeated dose schedule that replaces drug eliminated from the body and keeps levels in the desired range. Accumulation and toxicity if clearance falls. Loss of effect if missed doses or interactions lower levels.
Cytochrome P450 induction — what is it?	Increased CYP enzyme activity that speeds metabolism of affected drugs and lowers their concentration. Treatment failure or withdrawal can occur while the inducer is present. Toxicity can appear after it is stopped. Some inducers also reduce hormonal contraceptive effectiveness.
Synergism — what is it?	Combined drug effect is greater than expected from simply adding the individual effects. Profound CNS depression, respiratory depression, or severe hypotension.
Idiosyncratic reaction — what is it?	An unusual unpredictable response not explained by the drug's usual action. Rash, confusion, severe agitation, or organ injury out of proportion to expected effects.
Rectal route — what is it?	Medication is inserted into the rectum for local treatment or systemic absorption when oral use is limited. Erratic absorption. Avoid or question use with rectal bleeding or recent rectal surgery.
ACE inhibitors — what is it?	Block formation of angiotensin II. This lowers vasoconstriction and aldosterone, reducing blood pressure and cardiac workload. Dry cough, angioedema, hyperkalemia, and rising creatinine. Report facial swelling at once.
Beta blockers — what is it?	Block beta receptors to slow heart rate and reduce contractility and renin release. Lowers blood pressure and oxygen demand. Bradycardia, heart block, fatigue, and bronchospasm with nonselective agents. They can mask hypoglycemia.
Loop diuretics — what is it?	Block sodium and chloride reabsorption in the loop of Henle. Produce strong diuresis and reduce edema. Dehydration, hypotension, hypokalemia, and ototoxicity. Low potassium can increase digoxin toxicity risk.
Potassium-sparing diuretics — what is it?	Promote mild diuresis while conserving potassium. Some agents also block aldosterone effects. Hyperkalemia, endocrine effects with some agents, and worsening kidney function.
Class I antiarrhythmics — what is it?	Block fast sodium channels to slow impulse conduction in cardiac tissue. QRS widening, reduced contractility, and proarrhythmia.
QT prolongation — what is it?	Delayed ventricular repolarization on ECG that can be drug induced and can lead to torsades de pointes. Syncope, palpitations, torsades de pointes, and sudden rhythm deterioration.
Heparins — what is it?	Enhance antithrombin activity to inhibit clotting factors. Used for rapid anticoagulation. Bleeding and heparin-induced thrombocytopenia. Avoid unnecessary IM injections and other bleeding risks.
Direct oral anticoagulants — what is it?	Directly inhibit thrombin or factor Xa to reduce clot formation without routine INR monitoring. Bleeding and accumulation with renal impairment. Strong P-gp or CYP3A4 interactions can alter effect.
Statins — what is it?	Inhibit hepatic cholesterol synthesis and increase LDL receptor activity. Lower LDL and cardiovascular risk. Myopathy, rhabdomyolysis, and liver injury. Some interacting drugs raise toxicity risk.
Bile acid sequestrants — what is it?	Bind bile acids in the gut so cholesterol is used to make more bile acids. Lower LDL. Constipation, bloating, and reduced absorption of many medicines and fat-soluble vitamins.
Cardiac glycosides — what is it?	Increase contractility and slow AV conduction. Can improve symptoms in heart failure and control some atrial rhythms. Digoxin toxicity, bradycardia, AV block, and arrhythmias. Low potassium increases risk.
SGLT2 inhibitors — what is it?	Promote urinary glucose and sodium loss and reduce heart failure events, even in some patients without diabetes. Genital infections, dehydration, ketoacidosis, and worsening hypotension.
Alpha-1 blockers — what is it?	Block peripheral alpha-1 receptors to relax arterioles and veins. They can also improve urinary outflow in BPH. First-dose syncope, dizziness, and additive hypotension with PDE-5 inhibitors or alcohol.
First-dose phenomenon — what is it?	Marked hypotension after the initial dose of some vasodilating antihypertensives, especially alpha-1 blockers. Syncope, dizziness, and injury from falls.
Osmotic diuretics — what is it?	Filtered osmoles that pull water into the renal tubule, increasing urine output and lowering intracranial or intraocular pressure. Pulmonary edema, dehydration, and worsening heart failure.
Sequential nephron blockade — what is it?	Using diuretics at different nephron sites to overcome persistent fluid retention. Severe volume depletion, hypokalemia, hyponatremia, and renal injury.
Rate control — what is it?	Slowing the ventricular response in tachyarrhythmias without necessarily restoring sinus rhythm. Bradycardia, hypotension, AV block, and worsening heart failure.
AV nodal blockade — what is it?	Slowing conduction through the AV node to terminate or control supraventricular tachyarrhythmias. Bradycardia, hypotension, and higher-degree heart block.
Glycoprotein IIb/IIIa inhibitors — what is it?	IV antiplatelet drugs that block the final common pathway of platelet aggregation. Major bleeding and thrombocytopenia.
Anticoagulation reversal — what is it?	Using antidotes or factor replacement to rapidly reduce anticoagulant effect during serious bleeding or urgent procedures. Recurrent thrombosis after reversal and infusion reactions with reversal products.
PCSK9 inhibitors — what is it?	Monoclonal antibodies that prevent LDL receptor breakdown, greatly increasing LDL clearance. Injection-site reactions, hypersensitivity, and cost-related nonadherence.
Omega-3 fatty acids — what is it?	Lower triglycerides, especially at prescription strength, by reducing hepatic VLDL production. GI upset, bleeding tendency, and more atrial fibrillation episodes in susceptible patients.
If-channel inhibitors — what is it?	Slow the sinus node by blocking the funny current, reducing heart rate without lowering contractility. Bradycardia, atrial fibrillation, and luminous visual phenomena.
Preload reduction — what is it?	Lowering venous return and cardiac filling pressure to ease congestion and dyspnea. Hypotension, dizziness, and renal hypoperfusion.
Sulfonamide diuretics — what is it?	Many loop and thiazide diuretics contain a sulfonamide group. Cross-reactivity with sulfa allergy is possible but not common. Hypersensitivity reactions such as rash, fever, or rare severe skin injury. Stop and escalate if they appear.
Protease-activated receptor-1 antagonists — what is it?	Antiplatelets that block thrombin-mediated platelet activation. They reduce arterial thrombosis risk but do not dissolve clots. Major bleeding. Concurrent use with other drugs that raise bleeding risk may change the plan of care.
Opioids — what is it?	Strong analgesics that bind opioid receptors to reduce pain perception and response. Respiratory depression, hypotension, constipation, urinary retention, and additive CNS depression with sedatives.
Local anesthetics — what is it?	Drugs that block sodium channels in nerves to stop sensation in a limited area. CNS toxicity, seizures, dysrhythmias, and hypotension. Vasoconstrictor mixtures can worsen ischemia in end artery areas.
Hydantoins — what is it?	Sodium channel blocking anticonvulsants used for focal and tonic-clonic seizures. Nystagmus, ataxia, gingival overgrowth, rash, liver injury, and severe tissue damage with extravasation.
Iminostilbenes — what is it?	Sodium channel blocking anticonvulsants used mainly for focal seizures and trigeminal neuralgia. Hyponatremia, severe rash, dizziness, blood dyscrasias, and reduced effect of hormonal contraceptives.
SSRIs — what is it?	Antidepressants that selectively block serotonin reuptake to improve mood and anxiety symptoms. Sexual dysfunction, GI upset, insomnia or somnolence, serotonin syndrome, and increased bleeding with NSAIDs or anticoagulants.
Tricyclic antidepressants — what is it?	Older antidepressants that block norepinephrine and serotonin reuptake and also have anticholinergic effects. Anticholinergic effects, QT changes, orthostatic hypotension, and dangerous overdose toxicity.
First-generation antipsychotics — what is it?	Antipsychotics with strong dopamine blockade that reduce positive psychotic symptoms. Acute dystonia, parkinsonism, akathisia, tardive dyskinesia, hyperprolactinemia, and neuroleptic malignant syndrome.
Benzodiazepines — what is it?	Anxiolytics and sedatives that enhance GABA to reduce anxiety and promote sleep or muscle relaxation. Respiratory depression with opioids or alcohol, confusion, dependence, withdrawal seizures, and paradoxical agitation.
Dopamine precursor therapy — what is it?	Treatment that supplies levodopa to restore brain dopamine, often paired with peripheral decarboxylase inhibition. Nausea, orthostasis, dyskinesias, hallucinations, and wearing-off or on-off motor fluctuations.
COMT inhibitors — what is it?	Adjunct Parkinson drugs that prolong levodopa effect by blocking catechol-O-methyltransferase. Worsening dyskinesia, diarrhea, hypotension, hallucinations, and possible liver toxicity with some agents.
Adjuvant analgesics — what is it?	Drugs not classed as primary analgesics that enhance pain relief or target specific pain types, especially neuropathic pain. Additive CNS depression, falls, anticholinergic effects, or mood changes depending on the adjuvant used.
Opioid tolerance — what is it?	Reduced response to an opioid over time so more drug may be needed for the same effect. Respiratory depression after opioid switching because cross-tolerance is incomplete.
Barbiturates — what is it?	Strong CNS depressants that enhance GABA activity. Some are used for seizures and sedation. Respiratory depression and major enzyme induction that lowers levels of many other drugs.
Carbonic anhydrase inhibiting anticonvulsants — what is it?	Antiseizure agents that partly work through carbonic anhydrase inhibition, including topiramate and zonisamide. Kidney stones, metabolic acidosis, decreased sweating, and overheating.
Norepinephrine-dopamine reuptake inhibitors — what is it?	Antidepressants that raise norepinephrine and dopamine, often improving energy and concentration. Seizures, agitation, insomnia, hypertension, and stronger stimulant effects.
Antihistamine anxiolytics — what is it?	Sedating H1 blockers used short term to relieve anxiety or acute agitation. Anticholinergic effects, oversedation, and QT prolongation with some agents.
Long-acting injectable antipsychotics — what is it?	Depot formulations that release antipsychotic medication slowly to improve adherence. Delayed adverse effects, missed-dose relapse, and post-injection sedation with some products.
Neuroleptic malignant syndrome — what is it?	A rare life-threatening reaction to dopamine blockade with rigidity, fever, autonomic instability, and confusion. Rhabdomyolysis, kidney injury, arrhythmias, and rapid deterioration.
Penicillins — what is it?	Beta-lactam antibiotics that block bacterial cell wall synthesis and work best against actively dividing bacteria. Anaphylaxis, rash, diarrhea, and C. difficile colitis.
Tetracyclines — what is it?	Broad-spectrum antibiotics that bind the 30S ribosomal subunit and stop bacterial protein synthesis. Photosensitivity, esophagitis, tooth discoloration, and reduced absorption with cations.
Neuraminidase inhibitors — what is it?	Influenza antivirals that block release of new virus from infected cells and work best when started early. Nausea, bronchospasm with inhaled therapy, and rare neuropsychiatric effects.
Azole antifungals — what is it?	Antifungals that inhibit ergosterol synthesis and are used for many yeast and mold infections. Hepatotoxicity, QT changes, and strong CYP interactions.
Rifamycins — what is it?	Antimycobacterial drugs that inhibit bacterial RNA polymerase and are core agents in tuberculosis treatment. Hepatotoxicity and many drug interactions, including reduced effect of hormonal contraceptives.
Live attenuated vaccines — what is it?	Vaccines made from weakened replicating organisms that mimic natural infection and create strong immunity. Vaccine-related infection in severely immunocompromised patients.
Calcineurin inhibitors — what is it?	Immunosuppressants that block T-cell activation by reducing interleukin-2 signaling. Nephrotoxicity, hypertension, tremor, and grapefruit interactions.
Carbapenems — what is it?	Broad-spectrum beta-lactam antibiotics that block bacterial cell wall synthesis and resist many beta-lactamases. Seizures can occur with high exposure or renal dysfunction. Also watch for C. difficile diarrhea.
Glycopeptides — what is it?	Cell wall inhibitors used mainly for serious gram-positive infections, including many MRSA infections. Nephrotoxicity and infusion-related flushing can require a slower infusion or a different agent.
Antiretroviral protease inhibitors — what is it?	Antiretrovirals that block HIV protease so new virions remain immature and noninfectious. Boosted regimens can cause major drug interactions. Hyperglycemia and fat redistribution are also concerns.
Antifungal antimetabolites — what is it?	Antifungals converted inside fungal cells to metabolites that disrupt DNA and RNA synthesis. Bone marrow suppression and liver injury can require dose adjustment or discontinuation.
Recombinant protein vaccines — what is it?	Vaccines made from purified antigens produced by recombinant technology. They contain no live organism. Severe allergy to a component changes the plan. Local soreness is common.
mTOR inhibitors — what is it?	Immunosuppressants that inhibit mTOR and reduce lymphocyte response to IL-2 signaling. Mouth ulcers, hyperlipidemia, proteinuria, and delayed wound healing can change therapy.
Rapid-acting insulin — what is it?	Insulin used at meals for very fast onset control of postprandial glucose. Hypoglycaemia if the meal is delayed or missed. Lipodystrophy from poor site rotation.
Sulfonylureas — what is it?	Stimulate pancreatic beta cells to release insulin and lower blood glucose. Hypoglycaemia is the main risk, especially with missed meals, alcohol or older age.
Thyroid hormone replacement — what is it?	Synthetic thyroid hormone used to replace deficiency in hypothyroidism. Overreplacement can cause palpitations, tremor and bone loss. Iron and calcium reduce absorption.
Glucocorticoids — what is it?	Cortisol-like steroids that suppress inflammation and immune activity. Hyperglycaemia, mood change, infection masking, GI irritation and bone loss with longer use.
Proton pump inhibitors — what is it?	Block the gastric proton pump, producing strong acid suppression. C difficile diarrhoea, low magnesium and reduced absorption of some medicines.
5-HT3 antagonists — what is it?	Prevent nausea and vomiting by blocking serotonin receptors in the gut and chemoreceptor trigger zone. Constipation, headache and QT prolongation risk.
Teratogens — what is it?	Drug or chemical exposures that can harm fetal development. Highest structural risk is during organ formation. Some exposures also cause later growth or neurodevelopment problems.
Intermediate-acting insulin — what is it?	Basal insulin with a slower onset than mealtime insulin and a clear peak that can cover about half a day. Midday or nocturnal hypoglycaemia, especially if meals are missed or activity increases.
Inhaled corticosteroids — what is it?	Anti-inflammatory steroids delivered to the airways for controller therapy, not quick symptom relief. Oral candidiasis and dysphonia. Higher exposure can add systemic steroid effects.
Helicobacter pylori eradication — what is it?	Combination therapy using acid suppression plus antibiotics to clear H. pylori and reduce ulcer recurrence. Diarrhoea, candidiasis, and treatment failure if therapy is not completed.
Neurokinin-1 antagonists — what is it?	They block substance P at NK1 receptors and are used mainly to prevent delayed chemotherapy nausea and vomiting. Drug interactions, constipation, fatigue, and hiccups.
Insulin in pregnancy — what is it?	Insulin is usually the preferred glucose-lowering medicine when drug treatment is needed in pregnancy because it does not meaningfully cross the placenta. Hypoglycaemia and rapidly changing insulin requirements.
GLP-1 receptor agonists — what is it?	Incretin mimics that increase glucose-dependent insulin release, suppress glucagon and slow gastric emptying, lowering glucose and often promoting weight loss. Vomiting, dehydration and pancreatitis symptoms. Hypoglycaemia risk rises when used with insulin or a sulfonylurea.
-terol — what is it?	Often marks beta2 agonist bronchodilators that relax bronchial smooth muscle. Tremor, palpitations, tachycardia, or paradoxical bronchospasm. Low potassium can raise dysrhythmia risk.
First-generation antihistamines — what is it?	Older H1 blockers that reduce allergy symptoms and readily enter the brain. Confusion, dry mouth, urinary retention, or blurred vision. Use caution in glaucoma and BPH.
ARBs — what is it?	Block angiotensin II receptors. They lower pressure and can protect the kidney with less cough than ACE inhibitors. Hyperkalemia, dizziness, or angioedema. Dual RAAS blockade raises kidney injury risk.
Isotonic fluids — what is it?	Fluids with a similar tonicity to plasma that mainly expand the extracellular space. Fluid overload, especially in heart failure or kidney disease. Crackles and edema need reassessment.
Potassium replacement — what is it?	Replaces potassium needed for cardiac conduction and neuromuscular function. Hyperkalemia, nausea, or IV site pain. Digoxin effects change as potassium balance shifts.
Spacer use — what is it?	A chamber attached to a metered-dose inhaler that improves lung delivery and reduces drug left in the mouth. Poor technique can reduce effect and increase local steroid problems such as thrush.
H1 receptor blockade — what is it?	Prevents histamine from causing itching, sneezing, runny nose, and hives. Dry mouth, sedation, or blurred vision depending on the agent.
Urinary retention risk — what is it?	Antihistamine and decongestant effects can worsen bladder emptying, especially with outlet obstruction. Lower abdominal fullness, pain, or inability to void.
Colloid fluids — what is it?	Solutions with large molecules that tend to remain intravascular and expand plasma volume. Fluid overload, allergic reactions, or coagulation effects depending on the product.
Fluid overload — what is it?	Excess fluid in the intravascular or interstitial space that strains the heart and lungs. Crackles, dyspnea, hypertension, or jugular venous distention.
LABA monotherapy in asthma — what is it?	Using a long-acting beta2 agonist alone in asthma can relieve symptoms while airway inflammation remains untreated. Worsening asthma control masked by temporary relief. Tremor and palpitations can occur.
Intranasal antihistamines — what is it?	Local H1 blockers used for allergic rhinitis. They reduce sneezing, itching, and runny nose through nasal action. Bitter taste, nose irritation, epistaxis, and possible sedation.
Balanced crystalloids — what is it?	Crystalloid fluids whose electrolyte mix is closer to plasma than normal saline. Fluid overload. Some solutions contain potassium or calcium, which can affect selection.
Rescue inhaler overuse — what is it?	Frequent use of a quick-relief bronchodilator signals poor airway control rather than good prevention. Repeated beta agonist use can cause tachycardia, tremor, and low potassium. Shorter relief means the plan needs review.
-zolamide — what is it?	Suffix for carbonic anhydrase inhibitors. Systemic forms increase bicarbonate excretion, causing mild diuresis and alkaline urine. Metabolic acidosis, hypokalemia, kidney stones, paresthesias, or sulfonamide hypersensitivity.

Frequently asked

How is this deck split across topics?

The 300 cards are divided into principles (40), cardiovascular (55), neuro-and-psych (50), infection-and-immunity (50), endocrine-and-gi (55), and respiratory-and-renal (50). Inside those sections, the cards focus on drug classes, suffixes, and core concepts rather than isolated brand names.

What am I expected to recall on each card?

Each back uses the same fields: Meaning and Watch for. That keeps the review pattern steady whether the front says Absorption, Fluoroquinolones, or -zolamide.

Does this deck cover doses, titration, or full treatment plans?

No. It stays at class and concept level on purpose, so you can lock in mechanism, nursing priorities, and key risks before layering on protocol details.

Can I import the whole deck on the free plan?

Yes. Importing a saved deck runs no new AI generation and does not use your AI allowance, so the free plan imports all 300 cards. You can study, edit and delete them afterwards.

Will importing it twice create duplicates?

No. Cards you already have are skipped and only cards added in a revision come through. Including re-imports after deleting it, one official deck can be imported three times per account.

Can I use it on the web and in the mobile app?

Yes. The deck is added to your account rather than to a device, so the same cards and the same progress are there on the web, on iOS and on Android.

Can I edit the cards after importing?

Yes. Imported cards are yours: you can edit both sides, delete cards you do not need, change tags, and move cards to another deck.