Comprehensive Nursing Pharmacology: Fundamentals, Pharmacokinetics, Pharmacodynamics, GI, and Reproductive System Medications

Comprehensive practice flashcard set covering foundational pharmacology principles, pharmacokinetics, pharmacodynamics, GI medications, parenteral fluids, and reproductive pharmacology.

How does the lecture define pharmacology?

Pharmacology is the broadest term for the study or science of drugs.

What is the difference between pharmacokinetics and pharmacodynamics?

Pharmacokinetics is the study of drug absorption, distribution, metabolism, and excretion (ADME), whereas pharmacodynamics is the study of how drugs interact with body receptors to produce physiological effects.

How are pharmaceutics, pharmacotherapeutics, and pharmacognosy defined?

Pharmaceutics is the science of preparing and dispensing drugs, including dosage form design; pharmacotherapeutics is the treatment of pathological conditions through the use of drugs; and pharmacognosy is the study of drugs obtained from natural plant and animal sources.

What is the primary purpose and scope of Canada's Food and Drugs Act (1953)?

It is the main piece of drug legislation in Canada that protects consumers from contaminated, adulterated, and unsafe drugs and labelling practices; regulates advertising and selling of drugs, foods, cosmetics, and therapeutic devices; and categorizes drugs into schedules A through G.

Under the Controlled Drugs and Substances Act (1997), how are controlled drugs labeled and scheduled?

Controlled drugs require a prescription from a licensed medical practitioner and display the letter N and a designated symbol on their label. They are organized into eight schedules based on misuse, harm, and illegal production potential, with Schedule I containing the most dangerous drugs (opiates including opium, heroin, morphine, cocaine, fentanyls, and methamphetamine).

Under the Canadian Patent Act, how long do drug patents last, and what occurred regarding Ozempic in April 2026?

Drug patents generally last $20\text{ years}$ from the application filing date. In April 2026, after patent and regulatory protections ended, Health Canada approved the first generic alternative to Ozempic containing semaglutide.

How does the National Drug Scheduling Advisory Committee (NDSAC) classify non-prescription and prescription drugs into provincial schedules?

Schedule 1 requires a prescription; Schedule 2 includes non-prescription drugs kept behind the counter requiring pharmacist involvement; Schedule 3 includes non-prescription drugs sold in the self-selection area of a pharmacy; and Schedule 4 drugs may be sold in any retail outlet.

What is the distinction between a drug's chemical name, generic name, and trade/brand name?

The chemical name describes molecular and atomic structure (e.g., N-acetyl-p-aminophenol); the generic name is assigned by a federal body when first produced (e.g., acetaminophen); and the trade/brand name is given by manufacturers with the first letter capitalized followed by a trademark symbol (e.g., Tylenol™).

What distinguishes the four categories of medication errors: Near Miss, No Harm Event, Medication Error, and Critical Incident?

A Near Miss does not reach the patient and results in no harm; a No Harm Event reaches the patient but results in no harm; a Medication Error causes harm; and a Critical Incident results in serious harm.

What are the Ten Rights of Medication Administration?

1. The right patient
2. The right dose
3. The right medication
4. The right route
5. The right time
6. The right education
7. The right to refuse
8. The right assessment
9. The right evaluation
10. The right documentation

At what stages must medication reconciliation occur, and what are its three key steps?

Medication reconciliation must occur at facility entry, facility transfer, status change, and discharge. Its three sequential steps at each stage are: (1) Verification, (2) Clarification, and (3) Reconciliation.

What is bioavailability, and how does the first-pass effect impact it?

Bioavailability is the extent of drug absorption into the vascular bed. The first-pass effect occurs when enteral drugs pass from the GI tract via the mesenteric vein and portal vein directly to the liver for rapid metabolism before reaching general circulation, reducing bioavailability to less than $100\%$.

How do drug solubility and environmental pH determine the rate and extent of drug absorption?

Un-ionized drugs cross lipid cell membranes more easily, whereas ionized drugs cross less easily. Acidic environments favour the absorption of weak acids, and alkaline environments favour the absorption of weak bases. Furthermore, medications must be water-soluble to dissolve in GI fluids and fat-soluble to penetrate cellular membranes.

What is enterohepatic recycling, and what is a prime clinical example?

Enterohepatic recycling occurs when a drug excreted by the liver into bile enters the small intestine, is converted back to an absorbable form by gut bacteria, and is reabsorbed into the bloodstream via portal circulation, prolonging drug action (e.g., ethinyl estradiol in oral contraceptives).

What pharmacokinetic process and relationship between free and bound drug molecules is illustrated in this diagram?

Plasma protein binding: drugs bind reversibly to albumin. Bound drug molecules are too large to exit capillary pores and remain pharmacologically inactive reservoirs, whereas unbound (free) drug molecules diffuse across capillaries to produce therapeutic effects.

What clinical risk arises when a patient with low serum albumin receives a highly protein-bound drug?

Low albumin levels result in fewer binding sites, leading to an increased concentration of free (unbound) active drug in the bloodstream, which significantly increases the risk of drug toxicity.

What is the difference between Cytochrome P450 enzyme inducers and enzyme inhibitors?

Enzyme inhibitors decrease enzyme activity, slowing drug metabolism, increasing serum drug levels, and elevating toxicity risks; enzyme inducers increase enzyme activity, accelerating metabolism, lowering circulating drug levels, and potentially reducing clinical efficacy.

What are the three distinct steps of renal drug excretion?

1. Glomerular Filtration: Unbound low-molecular-weight drugs are forced through capillary walls into the tubular urine (protein-bound drugs are not filtered).
2. Passive Tubular Reabsorption: Lipid-soluble drugs move back into the blood along a concentration gradient (water-soluble/ionized drugs remain in urine).
3. Active Tubular Secretion: Active transport pumps move organic acids, bases, and protein-bound drugs from blood into tubular urine.

Why is sodium bicarbonate administered to alkalinize urine in acute aspirin (ASA) poisoning?

Aspirin is an acidic drug. Making the urine more basic causes aspirin molecules to become ionized in the renal tubules, preventing their passive tubular reabsorption and trapping them in the tubular lumen to accelerate urinary excretion.

What is a drug's half-life ($t_{1/2}$), and how many half-lives are typically required to reach complete elimination or steady state?

Half-life is the time required to remove half ($50\%$) of the original plasma drug concentration. It does not change with dose and typically takes approximately $5\text{ half-lives}$ to achieve complete elimination or to attain steady state.

What is the clinical rationale for administering a loading dose prior to maintenance dosing?

A loading dose is a larger initial dose given to rapidly achieve a therapeutic blood level without waiting the $4\text{ to }5\text{ half-lives}$ required at standard dosing intervals, particularly for medications with a long half-life (e.g., vancomycin).

When is a drug's trough level drawn, and what is its purpose in Therapeutic Drug Monitoring?

A trough level represents the lowest concentration of the drug in the bloodstream and is measured immediately before administering the next scheduled dose to ensure levels are therapeutic, avoid subtherapeutic dosing, and prevent toxic accumulation.

How does Modified Occupancy Theory explain drug action compared to Single Occupancy Theory?

Single Occupancy Theory states that response intensity is solely proportional to the number of receptors occupied, reaching maximum effect when all receptors are filled. Modified Occupancy Theory accounts for differing drug responses at identical receptors by incorporating affinity (binding strength), efficacy/intrinsic activity (ability to activate the receptor), and potency (dose needed).

In pharmacodynamics, what type of drug-receptor interaction is represented by this diagram?

Competitive antagonism: a drug competes directly with an endogenous agonist (such as norepinephrine [NE]) for the same receptor binding site ($\text{R}$), preventing agonist binding and blocking the physiologic effect.

How do non-competitive antagonists differ from competitive antagonists in their receptor binding mechanism?

Competitive antagonists compete directly with agonists for the same receptor site (e.g., atropine competing with acetylcholine); non-competitive antagonists bind to a completely different part of the receptor or ion channel to inactivate it, preventing agonist-induced activation regardless of agonist concentration (e.g., ketamine at the NMDA receptor).

How is the Therapeutic Index (TI) calculated, and what does a low TI value indicate?

The Therapeutic Index is calculated as $TI = \frac{LD_{50}}{ED_{50}}$ (the ratio of the lethal dose in $50\%$ of animals to the effective dose in $50\%$). A low TI (approaching $1$) indicates a narrow safety margin where therapeutic and toxic doses are very close, necessitating close clinical monitoring (e.g., warfarin).

What is the distinction between metabolic tolerance and tachyphylaxis?

Metabolic tolerance is an accelerated drug clearance occurring because the liver produces increased metabolizing enzymes over repeated dosing; tachyphylaxis is a rapidly developing tolerance that occurs quickly following rapid administration of a drug.

What characterizes an adverse drug reaction as iatrogenic, teratogenic, or mutagenic?

An iatrogenic reaction is an inadvertent, disease-like state produced by medical treatment; a teratogenic reaction causes structural or functional defects in an exposed developing fetus; and a mutagenic reaction induces permanent alterations in genetic material (DNA).

How do additive, synergistic, and potentiation drug interactions differ numerically and mechanistically?

An additive effect occurs when two drugs with similar actions equal the sum of individual effects ($1 + 1 = 2$, e.g., acetaminophen + ibuprofen); a synergistic effect produces a combined effect greater than the sum ($1 + 1 = 5$, e.g., opioid + benzodiazepine causing fatal respiratory depression); and potentiation occurs when a drug lacking its own direct effect enhances another drug ($0 + 1 = 2$, e.g., clavulanate protecting amoxicillin from beta-lactamase).

What chemical incompatibility occurs when intravenous phenytoin is co-administered with 5% Dextrose in Water (D5W)?

Phenytoin precipitates and crystallizes upon contact with D5W, occluding the IV tubing and preventing medication delivery; therefore, IV phenytoin must be diluted and flushed only with $0.9\%\text{ sodium chloride}$.

Why is the consumption of grapefruit juice contraindicated with certain orally administered drugs?

Grapefruit juice inhibits hepatic and intestinal Cytochrome P450 metabolizing enzymes, preventing drug breakdown, dramatically increasing systemic drug concentrations, and leading to severe toxicity or fatality.

What is Call to Action 22 of the Truth and Reconciliation Commission of Canada Report regarding healthcare delivery?

It calls upon those who can effect change within the Canadian healthcare system to recognize the value of Aboriginal healing practices and use them in the treatment of Aboriginal patients in collaboration with Aboriginal healers and Elders when requested.

What is the primary mechanism of action and major clinical limitation of antacids?

Antacids buffer and neutralize hydrochloric acid ($\text{HCl}$) in the stomach to raise gastric pH and relieve acute symptoms; they do not prevent or decrease the actual gastric acid overproduction.

What nursing implications and electrolyte considerations govern the administration of antacids?

Antacids should be taken $1\text{ hour}$ before or $3\text{ hours}$ after meals and at bedtime, administered with $240\,\text{mL}$ of water, and spaced $1\text{ to }2\text{ hours}$ away from other medications. Magnesium compounds cause diarrhea and must be avoided in renal impairment; aluminum and calcium compounds cause constipation.

How do Histamine-2 Receptor Antagonists (H2RAs) decrease gastric acidity, and what adverse reactions are associated with cimetidine and rapid IV push?

H2RAs block histamine at H2 receptors on parietal cells, decreasing acid output. Cimetidine can cause gynecomastia, impotence, loss of libido, and central confusion in elderly clients; rapid IV infusion of H2RAs can cause acute hypotension and bradycardia.

What is the mechanism of action of Proton Pump Inhibitors (PPIs), and what long-term adverse risks are associated with their chronic use?

PPIs bind irreversibly to the $H^+-K^+-\text{ATPase}$ enzyme pump in parietal cells, blocking all gastric acid secretion. Long-term use is associated with osteoporosis, Clostridium difficile (C. diff) enteric infections, chronic kidney disease (CKD), pneumonia, and an increased risk of myocardial infarction (MI).

How does sucralfate (Sulcrate) promote ulcer healing, and how must it be scheduled?

Sucralfate reacts locally with gastric acid to form a viscous, non-absorbable paste that selectively adheres to ulcerated mucosa. It does not alter gastric acidity and must be taken on an empty stomach $2\text{ hours}$ apart from other medications.

What is the mechanism and therapeutic indication of misoprostol (Cytotec), and what is a prominent adverse effect?

Misoprostol is a synthetic prostaglandin E analogue that suppresses gastric acid secretion and enhances mucosal defensive mucus production to prevent NSAID-induced gastric ulcers. It commonly causes abdominal cramping, diarrhea, and vaginal bleeding.

According to this diagram, which primary central nervous system sites and pathways coordinate the emetic reflex and serve as targets for antiemetic drugs?

The chemoreceptor trigger zone (CTZ) and the vomiting centre (medulla), which receive emetic signals from the labyrinth (inner ear), cerebral cortex, and gastrointestinal tract, targeted respectively by anticholinergics, antihistamines, neuroleptics, prokinetics, serotonin blockers, and cannabinoids.

What are the indications, mechanism, and serious adverse neurological effects of metoclopramide (Maxeran)?

Metoclopramide is a prokinetic agent that enhances gastrointestinal motility to treat GERD and gastroparesis. It can cause severe extrapyramidal symptoms (EPS) including dystonia, akathisia, parkinsonism, and irreversible tardive dyskinesia, and is contraindicated in seizure disorders and bowel obstruction.

What is the optimal timing for administering ondansetron (Zofran) to prevent postoperative nausea and vomiting?

Ondansetron is a 5-HT3 serotonin receptor antagonist that should be administered approximately $30\text{ minutes}$ prior to the end of the surgical procedure.

What visual side effect is expected with bismuth subsalicylate (Pepto-Bismol) administration?

Bismuth subsalicylate temporarily darkens the tongue and stool a blackish color, which is a benign effect that must be differentiated from melena/GI bleeding.

Why is diphenoxylate formulated with atropine sulfate in the antidiarrheal Lomotil?

Diphenoxylate is a synthetic opioid; sub-therapeutic anticholinergic atropine sulfate is combined with it to discourage abuse and overdose by causing unpleasant anticholinergic effects (dry mouth, tachycardia, blurred vision) if taken in excess.

What critical nursing instruction must accompany the administration of bulk-forming laxatives such as psyllium (Metamucil)?

They must be mixed and consumed with a full glass of water followed by adequate fluid intake to prevent esophageal obstruction or fecal impaction above intestinal strictures.

Why must 5% Dextrose in Water (D5W) be avoided in pediatric patients and clients with acute head injuries?

Although isotonic in the infusion bag ($170\text{ calories/litre}$), once dextrose is rapidly metabolized in the body, D5W leaves free hypotonic water that readily crosses the blood-brain barrier, precipitating or aggravating cerebral edema.

Based on the provided illustration, how do hypotonic, isotonic, and hypertonic intravenous fluids affect fluid movement and cellular volume?

Hypotonic fluids ($< 250\,\text{mEq/L}$) cause water to shift from the vascular space into dehydrated cells, causing them to swell; isotonic fluids ($310\,\text{mEq/L}$) produce zero net fluid movement across the cell membrane; and hypertonic fluids ($> 375\,\text{mEq/L}$) draw water out of edematous cells into the vascular compartment, causing cells to shrink.

What safety mandates apply to the administration of concentrated intravenous potassium chloride?

Potassium is a High Alert Medication available in premixed solutions of $10\text{ to }40\,\text{mEq/L}$. Concentrated potassium must NEVER be given IV push or bolus (which causes fatal cardiac arrhythmias) and MUST always be administered using an electronic infusion control pump.

How do colloid solutions such as 5% and 25% albumin work to expand vascular volume?

Colloids contain high-molecular-weight proteins that cannot cross semipermeable capillary membranes, significantly elevating plasma oncotic pressure to pull fluid from interstitial spaces into the vascular system to treat third-spacing, burns, and severe hypovolemia.

According to this biochemical pathway, how do PDE-5 inhibitors such as sildenafil, vardenafil, and tadalafil produce smooth muscle relaxation?

They block the phosphodiesterase type 5 (PDE-5) enzyme responsible for breaking down cyclic guanosine monophosphate (cGMP) into 5'-GMP, leading to sustained elevated cGMP levels, activation of protein kinase G (PKG), vascular smooth muscle relaxation, and enhanced corpus cavernosum blood inflow.

What absolute contraindication exists regarding PDE-5 inhibitors and cardiovascular vasodilators?

PDE-5 inhibitors must never be co-administered with organic nitrates (e.g., nitroglycerine) or alpha-blockers because concurrent enzyme inhibition and nitric oxide donor activity produce profound, life-threatening refractory hypotension.

What are the three primary mechanisms of action of combination hormonal contraceptives?

1. Inhibit hypothalamic secretion of gonadotropin-releasing hormone (GnRH), suppressing pituitary secretion of FSH and LH to completely prevent ovulation.
2. Thicken cervical mucus to create a physical barrier impenetrable by sperm.
3. Alter endometrial maturation to impair blastocyst implantation.

What is the regimen and cycle structure of the extended-cycle contraceptive Seasonale?

Seasonale follows a $91\text{-day}$ extended cycle consisting of $84\text{ consecutive days}$ of active hormonal tablets followed by $7\text{ days}$ of placebo tablets, resulting in withdrawal bleeding only four times per year.

What clinical warnings and time constraints apply to medroxyprogesterone acetate (Depo-Provera)?

Depo-Provera is a progestin-only injection administered deep IM every $3\text{ months}$; it should be restricted to a maximum duration of $\le 2\text{ years}$ because it causes progressive loss of bone mineral density.

What patient instruction is critical if the Evra transdermal contraceptive patch detaches for more than 24 hours?

If the patch is detached for longer than $24\text{ hours}$, contraceptive protection is compromised, a new patch must be applied immediately to start a new cycle, and a backup non-hormonal barrier method must be used for the next $7\text{ days}$.

What is the active ingredient, therapeutic window, and effectiveness limitation of Plan B emergency contraception?

Plan B contains levonorgestrel ($0.75\,\text{mg}$ or $1.5\,\text{mg}$ single dose) and must be taken as soon as possible within $72\text{ hours}$ ($3\text{ days}$) of unprotected intercourse (most effective within $24\text{ hours}$); its clinical effectiveness is diminished in women weighing over $165\text{ to }176\,\text{lbs}$.

What are the dual pharmaceutical components and mechanisms in Mifegymiso (RU-486)?

Mifegymiso consists of mifepristone (which blocks the progesterone receptors required to maintain the endometrium and gestational sac) followed by misoprostol (a synthetic prostaglandin that induces myometrial uterine contractions to expel the conceptus), approved for pregnancy termination up to $9\text{ weeks}$ gestation.

What laboratory and clinical risks must be monitored during gender-affirming testosterone therapy in transgender men?

Adverse risks include venous thromboembolism (VTE), elevated low-density lipoproteins (LDL) and serum triglycerides, decreased high-density lipoproteins (HDL), elevated serum creatinine levels, and hot flashes/fatigue if therapy is rapidly discontinued.