Pharmacology Flashcards
Endogenous
Substance created w/in body
Exogenous
Substance created outside of body
Titration
Slowly increasing dosage to build tolerance to adverse drug reactions (ADRs)
Tachyphylaxis
Tolerance that develops over hours or days
Types of intramolecular bonds
Covalent (usually irreversible in body) > ionic > hydrogen > hydrophobic
Signaling mechanisms
- Intracellular - drug crosses membrane to intracellular receptor
- Binds w/ transmembrane protein - Ed Scissorhands or scissors in drawer
- Binds w/ and opens/closes transmembrane channel
- G-protein systems
Catecholamines
Epi, Norepi, Dopamine
Made by adrenal glands and derived from tyrosine
Agonists (full, partial and inverse)
Cause an action
Full - has maximum effect
Partial - less than max effect
Inverse - causes action opposite of an agonist
Antagonists (reversible, irreversible, competitive and noncompetitive)
Blocks an agonist’s action at the receptor
Reversible vs irreversible - whether agonist can also bond or not; covalent bond vs others
Comp. vs noncomp. - binds at same or different site as agonist
Tapering
Slowly weaning off drug to avoid adverse withdrawal symptoms
Mixed agonist/antagonist
Drug w/ agonist effect at one receptor and antagonist effect at another
Not common
Common ADRs
GI upset
Hypersensitivity (allergic rx)
Note: ADRs are a type of unpleasant/unwanted side effect
Pregnancy categories
A - controlled studies show no fetal risk
B - no fetal risk evidence in human studies; fetal harm remote
C - fetal risk not excluded, adequate studies lacking; risk outweighed by benefit
D - evidence of fetal risk from human studies; benefit may outweigh risk
X - contraindicated
Drug schedule classifications
CI - high abuse potential, no accepted medical use
CII - high abuse potential, accepted medical use (w/ restrictions)
CIII - less abuse potential
CIV - low abuse potential (includes OTC)
CV - lowest abuse potential (includes OTC)
Type IV Hypersensitivity
T cell-mediated, slow rx, only requires one exposure, often fatal, Steven-Johnson syndrome or toxic epidermal necrolysis (like burns)
Acetaminophine
Analgesic, antipyretic
Tylenol
Analgesic, , antiinflammatory, NSAID, non-selective COX inhibitor
Type I Hypersensitivity
B cell mediated, involves IgE antibodies, rapid rx, requires two exposures, anaphylaxis
Pharmokinetics
How body affects a drug - absorption, metabolism, excretion
Pharmodynamics
How a drug affects the body
Types of DDIs
Pharmakokinetic - changes how drug is absorbed, distributed, metabolized or excreted; usually less drug-specific b/c it affects everything that uses that pathway
Pharmacodynamic - changes how a drug affects the body; a drug’s pharmacodynamic DDIs may be more varied from interacting drug to interacting drug
Polypharmacy
Individual taking many drugs
ADR
Adverse Drug Reaction
Therapeutic threshold
Window between minimum effective dosage and maximum effective dosage (dosage between ED50 to TD50)
Inert drugs
Bind to a receptor w/ no direct physiological effect (may have indirect effects)
T/F - Most drug effects show a linear change in relation to concentration
False - usually show a greater change at low concentrations - slope becomes flatter at higher doses
MEC
Minimum effective concentration
Peak effect/max efficacy
Dose where drug has maximum effect
Onset of effect
Time between administration and desired effect
Therapeutic index
LD50/TD50 - wider TI implies a safer drug
Can vary between effects of the same drug (Ibu. for pain vs inflammation
What must be assumed w/ an enhanced response to a given drug dose?
Increase in drug sensitivity
What is one way to help avoid tolerance?
Giving drugs in bursts or taking periodic breaks (four days on, one day off)
Hyperreactivity is not hypersensitivity
True
Metric conversions
kilo (1000) — hecto (100) — deka (10) — base — deci (.1) — centi (.01) — (.001)
Half-life
Time required to eliminate 50% of absorbed dose of a drug
How do you avoid first pass metabolism?
Enter bloodstream somewhere where you will go to the heart before the liver.
Avoid delivery through intestines or hepatic portal
Parenteral administration
w/ a needle - IV, IM, sub cu, intradermal, IO, intrarticular, intralesional, intrathecal (through dura and into spinal canal and CSF), epidural
What type of administration route are sublingual and buccal?
Topical
Neither are suitable for high-dose drugs
Avoids first pass metabolism
Characteristics of classic topical admin.
Pros - Cheap, treats affected site, low risk of systemic effects, easy to self-administer
Cons - variability in effects, systemic absorption possible, local toxicity
Characteristics of respiratory admin.
Pros - good for systemic and local administration, easy to self-administer, cheap, can bypass first-pass metabolism, fast onset
Cons - high potential for abuse, systemic effect for respiratory ailments
Nasal - good perfusion and surface area, may go directly into CSF
Characteristics on enteral admin.
Pros - cheap, easy, safe
Cons - variable absorption, upset stomach, first-pass metabolism
Infiltration
Fluid from parenteral admin ends up outside vessel
Extravasation
Infiltration that causes a blister
Lbs/kg
2.2 lbs/kg
mL/tsp
5 mL/tsp
Enterohepatic circulation
Drug goes through liver, is concentrated and excreted in stomach bile and reabsorbed in GI tract.
Extends duration of drug in body.
Clearance
Clearance = (elimination rate)/(drug concentration) = liters/hour
Volume of fluid that would be cleared of the drug
Types of drug metabolism
Phase I - uses CYP450 system (mostly isoenzymes CYP3A4 and CYP2D6) to oxidize/reduce/hydrolize drugs; alters pharmacodynamics
Phase II - uses other enzymes to conjugate (add glucuronic acid, sulfate, glycine); affects polarity and H20 solubility and increases clearance
T/F - Molecular charge affects glomerular filtration
False
Factors that affect tubular reabsorption
pH - weak acids more readily reabsorbed
Nonionized drugs more easily reabsorbed
More alkaline urine increases excretion of weak acids
Biliary excretion
Concentration and excretion of drug through liver bile.
Usually involves Phase II metabolism
Pulmonary excretion
Works for volatile (usually unchanged) drugs that passively diffuse into lungs.
Breast milk excretion
Mostly lipid soluble drugs.
Relatively acidic milk can concentrate weak bases - opt for drugs w/ lower pKa
Plasma half-life (elimination half-life)
Time it takes to clear half the drug concentration
Often used to help set dosing intervals.
Estimation - total elimination equals 5 x half-life
Dosing to effect
Used when half-life is altered
Uses other, physiological marker (effectiveness or toxicity) to determine dosing
Efficacy half-life
Time it takes for a drug to lose half its effect
Cmax
Peak serum concentration
Loading dose
A stronger initial dose that helps decrease the time until onset of effect
Steady-state
Point where drug intake equals drug excretion and plasma concentration is steady
Css = steady state concentration
Tmax
Time it takes to reach Cmax
COX
Cyclooxygenase
COX-1 - GI activity, kidney perfusion, platelet clotting
COX-2 - inflammation, pain and swelling
