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3P03 Review

The document discusses pharmacokinetic (PK) and pharmacodynamic (PD) modeling concepts. It covers PK parameters, compartmental models including one, two, and three compartment models, and modeling drug administration methods like intravenous bolus, infusion, and oral dosing. Mathematical models are used to estimate drug concentration over time based on these concepts.

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Sheila Kwok
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21 views4 pages

3P03 Review

The document discusses pharmacokinetic (PK) and pharmacodynamic (PD) modeling concepts. It covers PK parameters, compartmental models including one, two, and three compartment models, and modeling drug administration methods like intravenous bolus, infusion, and oral dosing. Mathematical models are used to estimate drug concentration over time based on these concepts.

Uploaded by

Sheila Kwok
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
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PK Concepts

PK: drug absorption, distribution, elimination kinetics, predict disposition

PD: interaction b/w [drug] and receptor response

PK-PD model: drug intensity over time

Drug binds protein, work better with plasma

Bigger therapeutic window, easier dosing control, less toxic side effects

Mathematical model and stats: estimate drug dose/efficacy over time

PK parameter: constant for a drug

PK function: relate ind to dep (i.e. time to [drug])

3 models categories:
Empirical: no mech explained; simple ([plasma] vs. body weight)

Physiological: need sample tissue, monitor drug flow; ideal but need data

Compartmental: if know tissue [drug], binding; used most

1st order: drug metabolized in liver

0 order: drug metabolism is saturable (or aspirin, phenytoin with xs)

If VD > Cp, drug leaving fast, no drug found in tissue

Double dosage doesn’t mean double duration time

Cl rate is not constant, but can be expressed as constant (=k)

IV bolus
- Not useful for treatment

- Can avoid large spike in conc

- Avoid drug rxns like pH, solubility issues

- Give massive dose at first to overcome distribution phase

- Drug instantly in circulation

Urinary extraction data lim


- Need to have some unmodified drug in urea

- No intf in quantification assay

- Frequent, empty bladder

- Wait 7 t1/2

- pH of urine

1 compartment model: only worry elimination, ignore distribution

2 compartment model
- Non-linear distribution: diff rates in diff tissues

- Plasma: central comp, rapid EL

- Tissues: peripheral comp, varied EL rates

- Drug slowly end up in tissues

- Elimination mostly from central, act like 1 comp (drop in same rate)

Residual method to find A, B, α, β, k, k12, k21

- Plot Cp vs time in log scale

- Extend linear part to find y-int (log B)

- Sub data from linear, find β

- For non-linear, find Cp’

- Find Cp - Cp’, plot over time (line a)

- Find A, α with same method

- Find k values

β: elimination from central


- Drug declines more slowly, β < k

- K is true elimination constant

- Use t 1/2 β to find dose

3 compartment model

IV infusion
- Precise control of Cp

- Infusion 0 order, constant rate

- Slow rate over long time

- Rate in = out

- Reach SS if elimination 1st order, approach SS if 0 order

- 4.23 half lives required for SS

> 1 compartment
- Double infusion rate, double Cp

- SS indep on: t, R

- Dep on: half life, VD, Cl

- If right DL selected, reach SS faster

> 2 compartment
- Can’t get to SS instantly

- VD not constant

- Assume Cp = C body at SS

- a: normal, no loading dose

- c: fast infusion

- b, d: with loading dose

Drug (oral)
- Fat soluble: passive diffusion

- Bind carrier protein: active transport


- Exposed to liver first

- Water soluble: pass aq channel - Might be metab b4 reach rest of body

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