Exam 1 Flashcards
DEA regulating how NPs prescribe vs state
DEA tells us about controlled substances
- what schedule the drug belongs to
STATE- regulates medications and who can prescribe within the state
Clinical trial process
- process of making a new drug
- has to be approved by FDA
Preclinical: testing on animals (monitor toxic effects, efficacy, reactions)
-after data collected in animals, then application sent tonFDA for approval to continue to clinical trials
Clinical trials:
-phase 1: 20-100 healthy people- testing absorption, distribution, metabolism and elimination. Most effect dose and routes are determined- focuses on safety
-phase 2: hundreds of patients with disease get drug and test same as phase 1
-phase 3: DFA approval needed then double blinded study with thousands of people
-phase 4: post market DFA approves drug (monitor long term effects. Compare to similar drugs on market)
Imp qualities for a conscientious prescriber?
Trust, open communication, polypharmacy, vitamins, holistic assessment, allergies, pregnant
Pros vs cons prescribing medications vis EMR vs paper
EMR:
Pros- ready at pharmacy, easy to read, catches drug interactions, present normal dosages to pick from
Cons- call if mess up, need script for schedule 2
Paper:
Cons- handwriting, lose it, wait at pharmacy, can’t track
Side effect vs adverse effect
Side effect: expected, secondary unwanted effect occurs d/t drug therapy. Ex/N/V
Adverse effect: unintended pharmacological effect when medication administered correctly
Ex: anaphylactic, rash
Pharmacodynamics
What the drug does to the body
A set of processes by which drugs produce specific biochemical or physiologic changes in the body
Can a drug create an effect?
No. It can speed up and slow down something that is already occurring in the body
What can effect pharmacodynamics?
Age Gender Ethnicity Weight Potency of drug Liver/kidney fnc Genetics Nutrition Diet Route Pharmacogenomics Disease Drug-drug competition
Ligand
Any chemical, endogenous or exogenous, that interacts/ binds to a receptor
Exogenous (purely drugs- body doesn’t make them)
Ex: medications, hormones
Endogenous (exist in the body)
Ex: hormones, neurotransmitters
Agonist vs antagonist
Agonist: binds to receptor, memetic effect, affinity and efficacy
Antagonist : binds to receptor with affinity but no efficacy
Full agonist
Partial agonist
Inverse agonist
Full: maximum effect with a few receptors activated ex albuterol
Partial: produce submaximal effect- all receptors are activated but not getting full effect
Ex: subaxone decrease pain but not getting high
Inverse: binds to the same receptor sites but gives opposite effect
Antagonist types
Antagonist: has affinity but no efficacy ( binding but no affect)
Ex: beta blockers
Chemical antagonist; drug forms with a bond with a second drug making it unavailable for interaction
Competitive: both ligands go to the active site- one will have more affinity and therefore bind to the receptor leaving more free drug of the other less affinity
Non competitive (allosteric): binds to a different site other than the active site, changing the active site and not allowing the effect
Physiologic: drug produces opposite affect through different pathways
Synergism
Taking two drugs to make a greater effect. Important because we can prescribe two drugs together that can lead to positive or negative effect
Ex: oxycodone and Tylenol
Ex: aspirin and Coumadin
Four types of receptors
1) G-protein coupled
2) Gated ion channel
3) enzyme linked receptors
4) intracellular receptors
G-protein coupled receptors
-most common
-requires second messenger
-transmembranous
-interact with a Ligand and receptor to produce conformational change in the function of the cell
Ex: beta blockers
Gated ion channel receptors
- Bind to generate an action potential,
- open and close to allow certain ions to pass through (effect pos/ meg charges)
- only first messenger
Ex: lidocaine
Enzyme linked receptors
- cytokines, tyrosine kinase activated
- transmembranous
- substrate binds to receptor which binds to enzyme causing action
- limited by down regulation
Ex: insulin
Intracellular receptors
-second messenger
- goes through membrane to attach
-lipid soluble
Ex sex hormones, glucocorticoids
Affinity
Binding strength to receptor
Efficacy
Max affect the drug will have on the body
Potency
Amount of drug needed for an effect, more morphine than diluadid to reach same effect
-concentration of drug you need minimal 60% of dose reach effect
Which ligand has affinity but no efficacy?
Antagonist
Selectivity vs specificity
Selectivity : ligand will have more affinity toward a receptor (ex alpha and beta receptors)
Specificity : lock and key, receptor can only accept certain ligands
How would you order the steps for signal transduction?
1) a ligand binds to the cell surface receptor
2) the receptor activates a protein at the cell membrane
3) the second messenger molecule is released
4) final target causes response
First messenger
Starts the signal process from the Cell surface- passes a message to the second messenger
Second messenger
-don’t always use one
- message is sent to the cell and causes the movement and signal to do the work on the inside of the cell- amplify the signal
Ex: cyclic AMP, calcium ions
Are second messengers usually required for hydrophilic it lipophilic ligands ?
Hydrophilic
Therapeutic index
Related the dose of a drug require to produce a desired effect to that which produces an undesired effect
Drug has a low therapeutic index
You need to watch closely, Increased risk for toxicity and adverse effects
Ex Coumadin INR between 2-3
Drug has high therapeutic index
Safer drug. More room for error, less monitoring
Upregulation
Cell receives a weak signal from repeated administration of drug
“Famine” not enough insulin for the amount of receptors, receptors working hard, call in help (add more receptors)
Down regulation
Body will absorb receptors because they aren’t doing anything. Causes harder time finding receptors, more breakthrough pain meds causing drug tolerance, reduces sensitivity to a message
Plenty of ligand available to receptor, so receptors get lazy and decrease
What happens if you stop a beta blocker?
Upregulation and rebound hypertension
Pharmacokinetics
- what the body is doing to the drug
- absorbed> distributed and metabolized > excreted
- factors affecting pharmacokinetics: age, pregnancy, hepatic/renal diseases, drug interaction, nutritional status