Pharmacology Flashcards
three names used to identify a drug
- chemical name
- generic
- trade name
T/F groups of generic drugs usually have vastly different names
false, drugs in the same family tend to have similar names, especially the suffix
what is the FDAs legal mandate
- drugs must have a favorable benefit/risk ratio
- drugs must have phased trials that prove utility and safety
phases of a clinical trial (5)
- preclinical
- phase I
- phase II
- phase III
- phase IV
preclincial trials
focuses on animal testing to deteremine toxicity
phase I trials
testing a small group of healthy subject to determine a drug doesnt cause disease
phase II trials
testing on ill patients
Phase III trials
main trial to determine risk, usually many subjects in many locations
phase IV trials
post-marketing surveillance
what would be the different mandates needed to be met in developing a drug for tension headaches vs small cell lung cancer
tension headaches already have effective treatment, so the new treatment but be both safer and effective than the current treatment
small cell lung cancer doesn’t have an effective treatment so a lower risk/reward ratio is acceptable
what similarities are common in the same drug class
- biochemisty
- indications
- mechanism
- side effects
T/F drugs in the same family are basically identicl
false
what is the main method of drug action
interatction with cell receptors
what is the main determinant of a drugs level of effect
the amount of the drug in the blood
what is an example of a tissue that is impermeable to most drugs
the blood brain barrier, choroid plexus
what are two factors that influence the amount of a drug found in the blood
drug absorption and elimination
what are two main methods of drug elimination
hepatic and renal
four main receptor types
- ligand gated ion channels
- G protein linked receptors
- enzyme linked receptors
- intracellular receptors
why is a proton pump inhibitor more effective treatment of heartburn than inhibiting gastrin, histamine, or AcH
because gastrin, histamine, and AcH all feed into the proton pump, if you block the pump the action of the other three don’t matter
T/F one ligand fits a receptor best, and most other ligands don’t fit at all
true, but specificity isn;t perfect only relative to others
what is necessary for a ligand to activate a receptor
high ligand concentration
cross reactivity
the ability for a ligand to activate closely related receptors
receptor regulation
as ligand increases, receptor production decreases
decreasing ligand concentration increases receptor production
how does excessive or constant administrion of a drug limit its effectiveness
down regulation of receptors
what is an example of a drug that will get less effective with frequent use
beta II agonist inhaler
what are three ways the clinical intervention can manipulate ligand receptor interaction
- increase/decrease ligand concentration
- changing receptor function
- changing receptor affinity
two primary routes of drug adminstration
- enteral
- parenteral
two routes of enteral adminstration
oral and rectal
6 methods of parenteral adminstration
- intravenous
- intramuscular
- subcutaneous
- transdermal
- inhaled
- transmucosal
what are three pros of oral administration
2 cons
pros: cheap, easy, concentrated effect on the esophagus and stomach
cons: absorption issues, first pass effect
first pass effect
any drug adminstered orally must first pass through the liver and be metabolized before it can enter the blood
5 key questions to decide between enteral vs parenteral
- is the drug compatible with either method
- oral restrictions
- need for rapid onset
- better dosing with one method or the other
- is the patient compliant for enteral dosing
why are adverse drug reactions so common
- polypharmacy
- lack of compliance
four majo causes of ADRs
- allergic reactions
- inherent drug toxicity
- dosing errors
- drug interactions
what percent of ADRs are caused by allergies
5-10%
in the case of an allergic reacton to a drug, what are two possible causative factors
reaction to the drug itself or its metabolite or delivery method
theraputic index
the comparrison of the blood concentration needed for a drug to have a theraputic effect vs the level that produces toxicity
narrow theraputic index
there is little margin between a theraputic dose and a toxic dose
two key issues in understanding drug interactions
- we don’t know all the OTC, herbal, or illegal substances being used
- not everyone has the same reactions to a drug
a good philosophy when prescribing
use as much as necessary but as little as possible
pharmacogenomics
the study of genetic influences that produce variations in drug metabolism
two processes of drug metabolism
- absorption
- elimation
two phases of elimination
phase I (oxidation)
phase II (conjugation)
what happens in phase I elimation
the drug is usually rendered inactive through oxidation
what happens in phase II elimination
the drug is conjugated with bile or urea to be more soluable in feces or urine
what is CYP-450
where is it found
what does it do
cytochrome p450 enzymes
found in the liver or GI tract
phase I oxidation
how is a drug eliminated through the urine
it is oxidized into a soluable metabolite or conjugated into a polar species that will dissolve in urine
how is a drug eliminated through feces
a drug or an oxidative metabolite can be conjugated into a non-polar species which binds to bile and is excreted into feces
how many CYP enzymes are present in humans
50 enzymes in 17 families
T/F many different CYP enzymes function in drug metabolism
false, 8 isoforms of CYP 1, 2, and 3 families account for 92% of drug metabolism
two CYPs that you should know
CYP 2D6, CYP 3A4/5
how does genetic diversity influence a persons capacity for drug metabolism
several ethnic groups have varying levels of presence or activity in CYP enzymes
genetic diversity in CYP 2D6
absent in 7% of caucasians, hyperactive in 30% of east asians
what does CYP 2D6 do?
what is the effect of genetic variation on this enzyme
metabolizes codeine into morphine
if the enzyme isnt present codeine won’t work, if its hyperactive it will work too well
T/F CYP action is not effected by external forces
false it can be inhibited or induced
why do CYP inducers do
- increase enzyme activity
- lower circulating levels of the drug
- reduce drug effectiveness
what do CYP inhibitors do
- decrease enzyme activity
- increase circulating levels of the drug
- increase risk of side effects and toxicity
what enzyme inactivates calcium channel blockers
CYP 3A4-5
what do calcium channel blockers do
treat HTN, chest pain, arrythmias
three inducers of CYP 3A activity
carbamazepine
rifampin
st johns wort
if a patient taking a calcium channel blocker started taking St Johns wort, what might happen to his blood pressure
it could go up because St Johns wort will induce CYP 3A activity and decease the blood concentration
if a person taking calcium channel blockers for high blood pressure also begins taking erythromycin, what will happen to his blood pressure
the blood pressure will go up because erythromycin inhibits CYP 3A4-5 and decrease the circulating amount of the drug
