Nursing Field Notes / Pharmacology · Foundations Course

Pharmacokinetics ⏳

What the Body Does to the Drug

NG-262 Pharmacology ADHD-friendly visual edition

Pharmacokinetics = the journey a drug takes through the body: in, around, changed, and out. Four steps — Absorption, Distribution, Metabolism, Excretion (ADME) — explain why a pill takes longer to work than a shot, why liver failure changes your dosing, and why some drugs need blood levels drawn. Every other pharmacology page on this site leans on these concepts.

📄 Simple Nursing original — opens in Drive →

🚶 ADMEAbsorption → Distribution → Metabolism → Excretion.

🔄 First-pass effectOral drugs get metabolized by the liver before reaching the body.

⏳ Half-lifeTime for the body to eliminate 50% of the drug.

🎯 Therapeutic indexNarrow window drugs need blood levels — peak & trough.

🚶

THE ADME JOURNEY

STEP 1 · IN, AROUND, OUT

Every drug you'll ever give follows the same 4-stop route through the body.

🚶 ADME — the drug's route through the body

🧠 "A Dizzy Man Excretes" — Absorption, Distribution, Metabolism, Excretion. Say it in order every time you think about a drug's journey.

① Absorption — getting into the blood

Moves the drug from the site of administration into body fluids via active transport, passive transport, or pinocytosis.

IV/IM = fastest absorption; IV = 100% bioavailability, no absorption step at all
Oral = slowest — depends on GI motility, pH, food, and solubility
Affected by: route, solubility, condition of body tissues

🧠 "Straight to vein, straight to work." IV skips absorption entirely — that's why it's the fastest route in an emergency.

② Distribution — only free drug works

The systemic circulation carries the drug to body tissues. Depends on protein binding, blood flow, and solubility.

Drug binds albumin or stays free — only free circulating drug is active
Low albumin (liver disease, malnutrition, elderly) → more free drug → higher effect/toxicity risk
Fat-soluble drugs cross the blood-brain barrier more easily

🧠 "Bound and gagged does nothing." A drug stuck to albumin is inactive until it's released.

③ Metabolism — the liver changes it

Also called biotransformation — the body changes the drug to be more or less active, and more excretable.

Mostly the liver (cytochrome P450 enzymes); also kidneys, lungs, plasma, intestinal mucosa
Liver disease → drugs metabolize slower → higher risk of toxic accumulation

🧠 "Liver = the drug's chemistry lab." It rebuilds the molecule before the kidneys can flush it.

④ Excretion — eliminating the drug

After the liver renders it inactive, it's excreted mainly by the kidneys via urine.

Other routes: bile/feces, lungs (volatile drugs), sweat, breast milk
Renal failure = drug accumulation risk — dose adjustments needed

🧠 "Bad kidneys, bad exit — the drug gets stuck inside." Always check renal function before dosing in older or renally-impaired clients.

🔄

FIRST-PASS & THE 3 PHASES

STEP 2 · WHY ROUTE CHANGES THE DOSE

Same drug, same dose, different route — the amount that actually reaches circulation can be wildly different.

🔄 First-pass effect — oral drugs get "taxed" by the liver first

First-pass effect: the concentration of an oral drug is greatly reduced before it ever reaches systemic circulation, because it's absorbed through the intestine, travels via the portal vein, and passes through the liver first. Sublingual, rectal, and IV routes bypass some or all of this.

🧠 "Oral pays a liver toll before it can spend itself in the body." That's why oral doses of some drugs are much higher than IV doses of the exact same drug.

💧 Pharmaceutic phase — getting dissolved

The drug must dissolve before it can be absorbed. Liquids and IV meds are already dissolved → absorb fastest.

CAUTION A tablet/capsule must pass through the GI tract to dissolve. Enteric-coated / time-released capsules are built to dissolve only in the alkaline environment of the small intestine.

🧠 Never crush an enteric-coated or extended-release tablet — it destroys the coating meant to protect the stomach or delay release.

🩸 Pharmacokinetic phase — this whole page

This phase is ADME itself — how the drug is transported and distributed through absorption, distribution, metabolism, and excretion.

🧠 Pharmaceutic → Pharmacokinetic → Pharmacodynamic. Dissolve it, move it, then let it act.

🎯 Pharmacodynamic phase — what the drug does

Deals with the drug's action and effect on the body — two mechanisms: alteration in cellular function or alteration in cellular environment.

Primary effect = the desired therapeutic effect
Secondary effect = any other effect — e.g. sildenafil was developed for hypertension, its secondary effect treats erectile dysfunction

🧠 A secondary effect isn't a mistake — sometimes it becomes the drug's most famous use.

⏳

HALF-LIFE & THERAPEUTIC WINDOW

STEP 3 · TIMING THE DOSE

This is the math behind why dosing schedules exist — and why some drugs need blood levels drawn.

⏳ Half-life decay curve — 50% gone every interval

Half-life (t½) = the time it takes for the body to eliminate 50% of the drug. A short half-life needs frequent dosing; a long half-life needs infrequent dosing — but takes longer to reach a stable ("steady state") level.

🧠 "Half, half, half again." Each half-life cuts what's left in half — it never technically hits zero, but after ~4–5 half-lives it's clinically gone.

📍 Onset, peak, and duration

Onset of action = time to reach a therapeutic effect after administration
Peak concentration = when the absorption rate equals the elimination rate (the highest point)
Duration = how long the drug keeps producing a therapeutic effect

🧠 "Onset starts it, peak is the top, duration is how long it lasts."

🎯 Therapeutic index — narrow vs. wide window

🧠 Narrow window = tight rope, no net. Too little = no effect; too much = toxicity — with barely any room in between.

🧪 Why this matters clinically

The therapeutic index is the range between the minimum effective concentration and the minimum toxic concentration. Narrow-index drugs (digoxin, warfarin, lithium, phenytoin, theophylline, aminoglycosides) require routine blood levels and careful dose titration — this connects directly to peak/trough monitoring and toxic ranges & antidotes.

🧠 "Wide window, wing it a little; narrow window, watch it like a hawk."

⚠️

REACTIONS & INTERACTIONS

STEP 4 · WHEN THE MATH GOES WRONG

Different words for different kinds of "this didn't go as planned" — the vocabulary examiners love to mix up.

🚨 Adverse, allergic, anaphylactic, angiedema — severity ladder

Term	What it means
Adverse drug reaction	Undesirable effect — mild, severe, or life-threatening; can occur at first dose or after repeated doses
Allergic reaction	Immune-mediated hypersensitivity — the body treats the drug as a foreign invader; can be immediate or delayed
Anaphylactic shock	🚨 Extremely serious, usually immediate — requires emergency treatment to support BP & breathing; can be fatal
Angiedema	Fluid collects in subcutaneous tissue — most commonly eyes, lips, mouth, throat → airway risk

🧠 "Adverse is the category, allergic is the cause, anaphylaxis is the emergency, angiedema is the swelling."

🧪 Toxic, cumulative, idiosyncratic, tolerance

Toxic reaction — levels build up because the body can't excrete the drug
Cumulative effect — seen in liver/kidney disease; one dose isn't cleared before the next is given
Idiosyncrasy — an unusual, unpredictable reaction, often genetic
Drug tolerance — decreased response over time, requiring a higher dose (e.g., opioids)

🧠 "Toxic builds up, tolerance wears off." Opposite problems, both from repeated dosing.

🔗 Drug interactions — additive vs. synergistic vs. antagonistic

Type	Effect
Additive	Combined effect equals the sum of each drug given alone
Synergistic	Combined effect is greater than expected — e.g. hypnotics + alcohol → increased CNS depression
Antagonistic	One drug blocks another — e.g. naloxone reverses opioids

🧠 Synergy stacks the danger, antagonism cancels it out.

🍽️ Food-drug interactions & other key terms

Food interaction — some foods increase or decrease drug metabolism (e.g. grapefruit juice + many CYP3A4 drugs)
Teratogen — any substance causing abnormal fetal development
Pharmacogenomics — genetic makeup alters how a person responds to a drug

🧠 EXAM TIP influence on metabolism also includes age, weight, disease state, and route — not just genetics or food.

🧭 Sympathomimetic vs. sympatholytic vs. parasympathomimetic vs. parasympatholytic

Term	Effect
Sympathomimetic	Mimics the sympathetic nervous system ("fight or flight")
Sympatholytic	Blocks/inhibits sympathetic nervous system transmission
Parasympathomimetic (cholinergic)	Stimulates the parasympathetic nervous system via acetylcholine (ACh)
Parasympatholytic (anticholinergic)	Reduces parasympathetic nervous system activity

🧠 "Mimetic mimics, lytic blocks." Pair that with sympathetic (fight/flight) vs. parasympathetic (rest/digest) and you can predict the effect of almost any autonomic drug.

⚡

QUICK RECALL

SAY IT OUT LOUD

🚶 ADMEAbsorption → Distribution → Metabolism → Excretion

🔄 First-passOral drugs lose potency through the liver first

⏳ Half-lifeTime to eliminate 50% — sets dosing frequency

🎯 Narrow indexDigoxin/warfarin/lithium need blood levels

🎯 Cover & check — 4 rapid-fire questions

Q1: What do the letters ADME stand for?

Absorption, Distribution, Metabolism, Excretion — the four pharmacokinetic phases a drug moves through.

Q2: What is the first-pass effect, and which routes avoid it?

Oral drugs travel via the portal vein through the liver before reaching systemic circulation, reducing the amount that's active. IV bypasses it completely; sublingual and rectal routes bypass some of it.

Q3: Define half-life.

The time it takes for the body to eliminate 50% of the drug from the blood.

Q4: Why do narrow therapeutic index drugs like digoxin need routine blood levels?

Because the gap between an effective dose and a toxic dose is very small — peak and trough levels catch dangerous accumulation before it causes toxicity.