Pharmacokinetics Flashcards
pharmacokinetics
how meds travel through the body
absorption
transmission of meds from location of admin to bloodstream
pattern of absorption
- rate of absorption determines how soon it will take effect
- amount absorbed determines intensity of effect
- route of admin affects rate and amount
oral absorption
- barriers: meds must pass through epithelial cells of GI tract
- absorption pattern: varies greatly because of
- stability and solubility of med
- GI pH and emptying time
- presence of food in stomach or intestines
- other concurrent meds
- forms of meds (enteric-coated, liq)
sublingual, buccal absorption
- barriers: swallowing before dissolution allows gastric pH to inactivate meds
- absorption pattern: quick absorption systemically via highly vascular mucous membranes
rectal, vaginal absorption
- barriers: presence of stool in rectum or infectious material in vagina limits tissue contact
- absorption pattern: easy with both local and systemic effects
inhalation absorption
- barriers: inspiratory effort
- absorption pattern: rapid absorption via alveolar capillary networks
intradermal, topical (ID, top)
- barriers: close proximity of epidermal cells
- absorption pattern:
- slow, gradual
- effects mostly local, but somewhat systemic, especially with lipid-soluble meds passing through SC fatty tissue
sublingual (SL)
under the tongue
buccal
between the cheek and gum
subcutaneous (SC, subQ, SQ), intramuscular (IM)
- barriers: large spaces between cells of capillary walls mean no significant barrier
- absorption pattern:
- solubility of med in water: highly soluble meds absorb rapidly (10-30 min); poorly soluble meds absorb slowly
- blood perfusion at site of injection: high perfusion means rapid absorption; low perfusion means slow
intravenous (IV)
- barriers: none
- absorption pattern:
- immediate: enters bloodstream directly
- complete: reaches blood in its entirety
distribution
transport of meds to sites of action by bodily fluids
factors affecting distribution
- circulation: inhibited blood flow or perfusion can delay distribution
- permeability of cell membrane: med must be able to pass through tissues to target area; lipid-solubles and those with transport system can cross BBB and placenta
- plasma protein binding: meds compete for protein-binding sites in bloodstream, primarily albumin. binding affects how much of med will travel to target; meds competing can lead to toxicity
metabolism (biotransformation)
- changes meds into less active or inactive forms via enzyme action
- primarily in liver
- also in kidneys, lungs, intestines, and blood
factors affecting rate of metabolism
- age:
- infants: limited med-metabolizing capacity
- in general, hepatic med metabolism declines with age; varies with pt
- increase in some med-metabolizing enzymes:
- can metabolize particular med sooner, requiring higher dosage to maintain therapeutic level
- can cause increase in metabolism of other concurrent-use meds
- first-pass: liver inactivates some meds; requires nonenteral route (SL, IV) to bypass effect
- similar metabolic pathways: same metabolic pathway metabolizes two meds
- can alter rate of metabolism of one or both
- can lead to med accumulation
- nutritional status: lack of factors necessary for specific enzyme production impairs med metabolism
outcomes of metabolism
- increased renal excretion
- inactivation of meds
- increased therapeutic effect
- activation of pro-meds (pro-drugs) into active forms
- decreased toxicity when actives are inactivated
- increased toxicity when inactives are activated
excretion
- elimination of meds from the body, primarily via kidneys
- also via liver, lungs, intestines, exocrine glands (i.e. breast milk, sweat, tears, etc.)
How does kidney function affect medication excretion?
meds remain in the body longer, increasing duration and intensity of response
What levels should be monitored in a pt with kidney dysfunction?
BUN and creatinine
therapeutic level
plasma med level that is effective and not toxic
therapeutic index (TI)
- indicates safety margin of drug concentration
- high TI = wide margin
- low TI = narrow margin, close monitoring of med levels in blood
When is plasma level at its highest?
- when elimination = absorption
- consider route of admin when measuring
- refer to drug ref. or pharmacist for peak times
When do you check trough levels for meds with low TI?
immediately before next dose
plateau
med’s concentration in plasma during a series of doses
half-life (t½)
- time for med in the body to drop by 50%
- affected by liver and kidney function
- usually takes four half-lives to achieve steady blood concentration (intake = metabolism and excretion)
short half-life
- meds leave body in 4-8 hrs
- short dosing interval to keep MEC from dropping between doses
long half-life
- meds leave more slowly
- over 24 hrs
- greater risk for med accumulation and toxicity
- can be given at longer intervals
- take longer to reach steady state
