Pharmacy & Pharmacology Subscriber guide

Pharmacokinetics and Pharmacodynamics for Veterinary Technicians

Pharmacy and Pharmacology (D1 A, F; K12) 10 min read, 2,303 words Last verified

What the body does to a drug and what the drug does to the body, explained for technicians: bioavailability, half-life, volume of distribution, receptor types and the species and breed differences the VTNE tests.

Introduction

Pharmacokinetics (PK) is what the body does to a drug: absorption, distribution, metabolism and excretion, often shortened to ADME. Pharmacodynamics (PD) is what the drug does to the body: which receptor it binds and how strong the effect is.1 You do not need to fit curves on the job. You do need to know why an oral dose is bigger than an IV dose, why a loading dose is ordered, why a Collie gets a lower acepromazine dose and why a cat must never get acetaminophen. These ideas explain the "why" behind many orders you carry out and many VTNE questions.

Key facts

  • An IV dose is the reference for 100% bioavailability.1
  • Bioavailability (F) is the rate and extent to which a drug is absorbed into the circulation.1
  • Elimination half-life is the time for plasma concentration to fall by 50%.1
  • Steady state, and near-complete elimination after stopping, both take 3 to 5 half-lives.1
  • A loading dose reaches the target concentration fast; it does not make the drug reach true steady state faster.1
  • A narrow therapeutic index means a small gap between an effective and a toxic concentration (gentamicin is the classic example).13
  • A partial agonist (buprenorphine, butorphanol at mu) has a lower maximum effect than a full agonist.2
  • Dogs homozygous for the ABCB1-1Δ (MDR1) mutation are susceptible to toxicity from ivermectin, loperamide and vincristine.5

How the VTNE tests this

  • Define the terms: match bioavailability, first-pass effect, half-life or volume of distribution to a description (Domain 1 Task A; Knowledge 12).7
  • Predict timing: how long until steady state, or until a drug is mostly gone, from a given half-life.
  • Classify drug action: full agonist, partial agonist, agonist-antagonist or antagonist, and what a reversal agent does (Domain 1 Task F).7
  • Spot the species or breed risk: cats and glucuronidation, herding dogs and MDR1, patients with kidney or liver disease.
  • Calculate: a loading dose from volume of distribution, or an oral dose adjusted for bioavailability.

Core concepts

Absorption and bioavailability

A drug given IV goes straight into the blood, so IV dosing defines 100% bioavailability.1 Any other route (PO, IM, SC) is extravascular: the drug must be absorbed first, so plasma concentration rises to a peak (Cmax) and then falls.1 Oral bioavailability varies widely. Metronidazole is 60% to 100% bioavailable by mouth, and many fluoroquinolones exceed 80% in small animals, but oral ciprofloxacin in ruminating cattle is only 0% to 20%.89

First-pass effect

Blood from the gut passes through the liver before it reaches the rest of the body. Drugs that the liver extracts very efficiently show high first-pass metabolism and low oral bioavailability.1 That is why some drugs need a much larger oral dose than IV dose. In a dog with a portosystemic shunt, blood bypasses the liver, so oral bioavailability of these drugs can rise sharply and oral doses must be lowered.1

Distribution and volume of distribution

Apparent volume of distribution (Vd) is the volume the drug would need to fill if its plasma concentration were the same everywhere. It is calculated as dose divided by plasma concentration, in L/kg.1 "Apparent" means it does not say where the drug went, only that it left the plasma.1 Water-soluble drugs stay mostly in extracellular fluid (20% to 30% of body weight). Lipid-soluble drugs enter cells and usually have a Vd above 0.6 L/kg. Digoxin in dogs has a mean Vd of 13 L/kg because it binds heavily in tissues.1

Many drugs bind plasma proteins, mainly albumin. Most NSAIDs are up to 99% protein bound, and only the small unbound fraction is active in tissues.10

Metabolism and excretion

The liver and kidneys are the two main clearance organs. Metabolism changes the drug, and the metabolites are then excreted, usually by the kidneys.1 Renal clearance depends mostly on renal blood flow. When kidney function falls, the veterinarian may lower the dose or lengthen the interval, guided by serum creatinine.1

Half-life and steady state

Half-life depends on both clearance and Vd: it gets longer when Vd is larger and shorter when clearance is higher.1 After a drug is stopped, 50% is gone after one half-life, 75% after two and 87.5% after three; for practical purposes most of it is gone after 3 to 5 half-lives.1 With repeated dosing the same numbers apply in reverse: 50% of the steady-state level after one half-life, 87.5% after three and 93.6% after four. The full response to a drug, good or toxic, cannot be judged until steady state is reached.1 Half-life also drives withdrawal and milk discard times in food animals.1

Pharmacodynamics: receptors and dose response

The size of a drug's effect reflects how many receptors it occupies.1 Receptors are finite, so they can be saturated.2 Drugs are grouped by intrinsic efficacy, meaning how strongly they switch the receptor on:2

  • Full agonist: gives the largest possible effect at its best concentration (morphine at the mu receptor).
  • Partial agonist: its maximum effect (Emax) is lower than a full agonist's. Butorphanol and buprenorphine level off before respiratory depression is usually seen.2
  • Agonist-antagonist: an agonist at one receptor and an antagonist at another. Butorphanol is a kappa agonist, a partial mu agonist and a delta antagonist.2
  • Competitive antagonist: binds the receptor with no intrinsic efficacy and blocks the agonist. It shifts the agonist dose-response curve to the right.2 Reversal agents work this way.

Potency is how much drug it takes to reach an effect; efficacy is the maximum effect possible. A drug can be more potent yet have lower maximal efficacy.3 The therapeutic index compares the toxic concentration with the effective concentration. A small index means a dose increase is more likely to cause toxicity.3 Repeated dosing can also cause tolerance, a reduced response, for example from receptor downregulation.2

Receptor occupancy by full agonist, partial agonist and competitive antagonist Full agonist Partial agonist Competitive antagonist Receptor Receptor Receptor Large effect Smaller ceiling effect No effect; blocks agonist e.g. morphine (mu) e.g. buprenorphine (mu) e.g. naloxone (mu)
Figure 1. Receptor occupancy. A full agonist fits and fully activates the receptor. A partial agonist binds but activates it less, so its maximum effect is lower. A competitive antagonist sits in the site without activating it and keeps agonists out, which is how reversal agents work. Original diagram, VTNE Exam Prep.

Procedure or technique

How the technician applies PK and PD at the treatment table:

  1. Check the route on the order. An oral dose and an IV dose of the same drug are often different numbers. Never swap routes without a new order from the veterinarian.
  2. Flag patient factors before you draw up. Note age, hydration, kidney or liver disease, low albumin, species and breed. Age, breed, drug interactions and kidney or liver disease all change dosing needs.1
  3. Ask about MDR1 status in herding breeds before giving ivermectin, loperamide, vincristine, acepromazine or butorphanol, and tell the veterinarian if it is unknown (Figure 3).56
  4. Time samples for therapeutic drug monitoring exactly as ordered. Monitoring matters most for narrow therapeutic index drugs such as gentamicin.1 Record the dose time and sample time.
  5. Give doses on time. If a drug with a short half-life is given at a long interval, concentrations swing, and an anticonvulsant may leave the patient at risk of seizures just before the next dose.1
  6. Keep the reversal agent ready when an agonist sedative or opioid is used, and record the time of reversal and the patient's response.
  7. Watch and record the response. Note when the effect starts, how deep it is and how long it lasts, especially after a dose change.
Table 1. Routes of administration: absorption and bioavailability
RouteAbsorption step?BioavailabilityTechnician notes
IVNo; drug enters plasma directly100% by definitionFastest onset; a wrong dose cannot be retrieved
IM, SCYesUsually high; varies by drugFluoroquinolone absorption after IM or SC dosing is rapid
POYes, then first pass through the liverVariable: 60% to 100% for metronidazole; often over 80% for small animal fluoroquinolones; 0% to 20% for ciprofloxacin in ruminating cattleFluoroquinolone peaks come 1 to 3 hours after an oral dose; food and other drugs can change absorption

Sources: Merck Veterinary Manual, Pharmacokinetics; Quinolones; Nitroimidazoles.189

Flowchart: reading the curve and screening for MDR1

Plasma concentration-time curves after IV and oral doses, with MEC and MTC lines MTC: minimum toxic concentration MEC: minimum effective concentration IV: starts at peak Oral: Cmax after absorption Therapeutic window Time after dose Plasma concentration
Figure 2. Plasma concentration over time after one IV dose (solid line) and one oral dose of the same drug (dotted line). The IV curve starts at its highest point and only falls. The oral curve rises while the drug is absorbed, peaks lower because of incomplete bioavailability and first-pass loss, then falls. The drug works while it sits between the minimum effective concentration (MEC) and the minimum toxic concentration (MTC). Schematic, not drawn to scale. Original diagram, VTNE Exam Prep.
Decision tree: screening a dog for MDR1 risk before giving a P-glycoprotein substrate drug Order: ivermectin, loperamide, vincristine, acepromazine or butorphanol. Herding breed? Is the dog's MDR1 (ABCB1) result on file as normal/normal? No or unknown Yes No Tell the veterinarian before giving; dose may be reduced or drug changed Give as ordered; monitor and record the depth and length of effect If given: watch closely for deep, long sedation or neuro signs
Figure 3. MDR1 screening before giving a P-glycoprotein substrate. Collies, Australian shepherds, Shetland sheepdogs, Old English sheepdogs and several other breeds commonly carry the mutation. The technician's job is to flag the risk, not to change the dose. Original diagram, VTNE Exam Prep.

Species differences

Cats. Cats have low glucuronyl transferase activity, so their capacity for glucuronidation, a major phase II conjugation pathway, is limited.4 They clear acetaminophen mainly by sulfation; when that pathway saturates, toxic metabolites form. The result is methemoglobinemia (brown or muddy mucous membranes) and liver injury, usually after 40 to 50 mg/kg but sometimes at 10 mg/kg.4 Meloxicam is handled by oxidation in cats, not glucuronidation.10

Dogs with the MDR1 mutation. P-glycoprotein is an efflux pump in the blood-brain barrier. The ABCB1-1Δ mutation leaves it truncated and nonfunctional, so substrate drugs reach the brain in higher amounts.5 In a study of rough-coated Collies, homozygous mutant dogs given acepromazine 0.04 mg/kg IV were sedated more deeply and for longer, and the authors advise reduced doses with careful monitoring.5 Butorphanol is also thought to be a P-glycoprotein substrate, and there are anecdotal reports of increased sedation in these dogs.5

Ruminants. The rumen changes oral absorption. Oral ciprofloxacin is barely absorbed in ruminating cattle.8

Table 2. Species, age and disease factors that change drug handling
PatientPK or PD changeExampleTechnician action
CatLimited glucuronidationAcetaminophen causes methemoglobinemiaNever give; tell owners never to give human pain pills
Herding-breed dog (MDR1 mutant)Nonfunctional P-glycoprotein in the blood-brain barrierIvermectin, loperamide, vincristine toxicity; deeper acepromazine sedationCheck genotype; flag to veterinarian
Ruminating cattlePoor oral absorption of some drugsOral ciprofloxacin 0% to 20% bioavailableFollow route on order and label
NeonateLarger VdDistribution differs from adultsNever scale adult doses without an order
GeriatricSmaller VdDistribution differs from young adultsMonitor response closely
DehydrationVd decreasedKidney clearance may also fallReport hydration status
Kidney diseaseLower renal clearanceDose cut or interval lengthenedTrack creatinine; time doses exactly
Portosystemic shuntReduced first-pass metabolismOral bioavailability risesExpect lower oral doses

Sources: Merck Veterinary Manual; Deshpande et al. 2016.1458

Calculation

Loading dose from volume of distribution. Rearranging Vd = dose ÷ concentration gives dose = Vd × target concentration.1

Example: phenobarbital Vd is 0.6 L/kg and the target plasma concentration is 10 mg/L.1

Dose = 0.6 L/kg × 10 mg/L = 6 mg/kg (the L cancels). For a 20 kg dog: 6 mg/kg × 20 kg = 120 mg IV.

Adjusting for oral bioavailability. An oral dose must be divided by F.1 If F were 0.8, the oral loading dose would be 6 mg/kg ÷ 0.8 = 7.5 mg/kg.

Half-life timing. A drug with a 12-hour half-life reaches steady state in about 3 to 5 half-lives: 36 to 60 hours.

  • Tell cat owners that human pain relievers such as acetaminophen can kill a cat even at small doses.4
  • Tell owners of herding breeds that MDR1 testing exists and that the result should be on the record before certain drugs are used.5
  • Explain to owners of pets on long-term drugs such as phenobarbital that the full effect takes days and that doses should not be skipped or doubled.
  • In food animals, half-life underpins withdrawal and milk discard times; follow the label or the veterinarian's written withdrawal time.1
  • Only the veterinarian changes a dose, route or interval. The technician observes, records and reports.

Common mistakes and exam traps

  • Bioavailability is the fraction that reaches the circulation, not the fraction absorbed from the gut. A drug can be fully absorbed yet have low F because of first-pass metabolism.
  • A loading dose gets the concentration up quickly. It does not change the drug's half-life or the 3 to 5 half-lives needed for true steady state.1
  • A large Vd means the drug leaves the plasma for the tissues. It does not tell you where it went.1
  • Potency and efficacy are different: the lower dose is the more potent drug, but the bigger maximum effect is the more efficacious one.3
  • Partial agonists have a ceiling; giving more buprenorphine does not give morphine-level effect.2
  • The cat question is about glucuronidation (phase II conjugation), not about kidney clearance.4

Quick review

  1. PK is what the body does to the drug (ADME); PD is what the drug does to the body.
  2. IV is the 100% bioavailability reference.
  3. First-pass liver metabolism lowers oral bioavailability.
  4. Vd = dose ÷ plasma concentration; loading dose = Vd × target concentration.
  5. Half-life is the time for plasma concentration to fall by half.
  6. Steady state and washout each take 3 to 5 half-lives.
  7. Liver and kidneys are the main clearance organs.
  8. Narrow therapeutic index drugs need careful dosing and often drug monitoring.
  9. Full agonist: maximum effect. Partial agonist: ceiling. Competitive antagonist: blocks, no effect of its own.
  10. Cats glucuronidate poorly; never give acetaminophen.
  11. MDR1 mutant herding dogs: ivermectin, loperamide, vincristine toxicity; reduced acepromazine dose.

Test yourself

5 questions written for this guide. Pick an answer, then check it.

Question 1A 25 kg dog needs an IV loading dose of a drug with a volume of distribution of 0.7 L/kg. The target plasma concentration is 20 mg/L. What total IV dose does this give?

Show answer

Answer: B. 350 mg

Dose = Vd x target concentration = 0.7 L/kg x 20 mg/L = 14 mg/kg; 14 mg/kg x 25 kg = 350 mg. A (140 mg) multiplies Vd by 20 and by 10 kg, not 25 kg. C (500 mg) ignores Vd and multiplies 20 mg/L by 25 kg. D (714 mg) divides by Vd instead of multiplying.

Source Pharmacokinetics, Merck Veterinary Manual

Question 2A drug has an elimination half-life of 8 hours and is started at a fixed dose every 8 hours. When can the veterinarian first fairly judge whether the dose is working?

Show answer

Answer: B. After 24 to 40 hours of dosing

Steady state takes 3 to 5 half-lives (3 x 8 to 5 x 8 = 24 to 40 hours), and response cannot be assessed until then. A is one half-life, only 50% of steady state. C uses days instead of half-lives. D: a loading dose reaches steady-state concentration sooner but is not required to judge response.

Source Pharmacokinetics, Merck Veterinary Manual

Question 3A 3-year-old Australian shepherd is scheduled for sedation with acepromazine. No MDR1 (ABCB1) test result is in the record. What should the technician do first?

Show answer

Answer: C. Tell the veterinarian before giving the drug

Australian shepherds commonly carry the ABCB1-1 mutation, and mutant dogs have deeper, longer acepromazine sedation; the veterinarian decides whether to reduce the dose. A ignores a known breed risk. B changes a dose without an order. D is wrong twice: technicians do not substitute drugs, and butorphanol is also thought to be a P-glycoprotein substrate, with anecdotal reports of increased sedation in these dogs.

Source Effect of the canine ABCB1-1 mutation on acepromazine sedation, J Vet Intern Med 2016

Question 4Buprenorphine is added to a dog's plan, and later the dose is increased with little extra pain relief. Which property best explains this?

Show answer

Answer: A. It is a partial mu agonist with a ceiling effect

A partial agonist has a lower maximum effect (Emax) than a full agonist, so raising the dose eventually adds little. B: a pure antagonist has no effect of its own. C and D are about absorption, which would not explain a plateau after a dose increase in a drug that is already working.

Source Drug Action in Animals: Pharmacodynamics, Merck Veterinary Manual

Question 5An owner gives her cat an acetaminophen tablet. Why is the cat at much greater risk than a dog would be?

Show answer

Answer: D. Cats have limited glucuronidation in the liver

Cats have low glucuronyl transferase activity, so they rely on sulfation, which saturates and produces toxic metabolites that cause methemoglobinemia. A, B and C are not the reason given for feline acetaminophen toxicity.

Source Toxicoses From Human Analgesics in Animals, Merck Veterinary Manual

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Figure credits

  • Figure 1 Original diagram, VTNE Exam Prep
  • Figure 2 Original diagram, VTNE Exam Prep
  • Figure 3 Original diagram, VTNE Exam Prep

References

  1. Merck Veterinary Manual. Pharmacokinetics. merckvetmanual.com (accessed 2026-10-31) merckvetmanual.com/pharmacology/pharmacology-introduction/pharmacokinetics
  2. Merck Veterinary Manual. Drug Action in Animals: Pharmacodynamics. merckvetmanual.com (accessed 2026-10-31) merckvetmanual.com/pharmacology/pharmacology-introduction/drug-action-in-animals-pharmacodynamics
  3. Merck Manual Professional Edition. Dose-Response Relationships. merckmanuals.com (accessed 2026-10-31) merckmanuals.com/professional/clinical-pharmacology/pharmacodynamics/dose-response-relationships
  4. Merck Veterinary Manual. Toxicoses From Human Analgesics in Animals. merckvetmanual.com (accessed 2026-10-31) merckvetmanual.com/toxicology/toxicities-from-human-drugs/analgesics-toxicity
  5. Deshpande D, Hill KE, Mealey KL, Chambers JP, Gieseg MA. The effect of the canine ABCB1-1Δ mutation on sedation after intravenous administration of acepromazine. J Vet Intern Med. 2016;30(2):636-641. PMC4913601 pmc.ncbi.nlm.nih.gov/articles/PMC4913601/
  6. Merck Veterinary Manual. Analgesics Used in Animals. merckvetmanual.com (accessed 2026-10-31) merckvetmanual.com/therapeutics/pain-assessment-and-management/analgesics-used-in-animals
  7. AAVSB. 2023 Veterinary Technician National Examination Content Outline. aavsb.org (accessed 2026-10-31) aavsb.org/wp-content/uploads/2025/04/AAVSB-2023-Veterinary-Technician-National-Examination-Content-Outline-2.pdf
  8. Merck Veterinary Manual. Quinolones, Including Fluoroquinolones, for Use in Animals. merckvetmanual.com (accessed 2026-10-31) merckvetmanual.com/pharmacology/antibacterial-agents/quinolones-including-fluoroquinolones
  9. Merck Veterinary Manual. Nitroimidazoles Use in Animals. merckvetmanual.com (accessed 2026-10-31) merckvetmanual.com/pharmacology/antibacterial-agents/nitroimidazoles
  10. Merck Veterinary Manual. Nonsteroidal Anti-inflammatory Drugs in Animals. merckvetmanual.com (accessed 2026-10-31) merckvetmanual.com/pharmacology/anti-inflammatory-agents/nonsteroidal-anti-inflammatory-drugs

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