what is a drug
a chemical substance used for preventing treating or diagnosing
pharmacodynamics
what drugs do to the body
pharmacokinetics
what the body does to the drugs
how does schuedule number related to the potential of abuse?
the higher schedule the lower the potential
what are the 4 phases for manufacturing a new drug?
en vitro, animal testing, clinical testing, marketing
what determines drug absorption and distribution
molecular size and solubility
why do you want drugs to be fat sol?
so they can pass through membranes and get anywhere in the body including the CNS
what are the 3 ways that drug actions are ended?
redistribution, excretion, metabolism
which organ is most important for excretion?
kidney
which organ is most important for metabolism
liver
what are the 2 phases of metabolism
redox reactions to increase polarity; or conjugation to increase molecule size
what is efficacy?
how large a response is
what is potency?
how much a drug is required to produce a response
what is the margin of safety?
difference b/t effective dose and toxic dose
therapeutic index
Ratio of toxic does over effective dose
parasympathetic pre-ganglionic
cholinergic
sympathetic pre-ganglionic
cholinergic
parasympathetic post-ganglionic
cholinergic
sympathetic post-ganglionic
adrenirgic
which r/c are stimulated by acetylcholine
muscarinic and nictonic
which type of r/c are stim by norepi and epi
alpha and beta
what enzyme breaks down ach
cholinesterase
what enzyme breaks down epi
monamine oxidase
what is significant about a quaterinary ammonium ion?
POLAR= lipid insoluble= not albe to pass Blood Brain Barrier
where are beta one r/c
heart
where are beta two r/c
bronchus
were are alpha one r/c
arterioles and iris
what happens when you stimulate b 1 r/c?
ionotropic (increased contraction force) and chronotropic (increased HR)
what happens when you stimulate b2 r/c?
broncodilation
what happens when you stimulate a1 r/c
vasoconstriction and mydriasis (dilation of pupil)
what happens when you stimulate muscarinic r/c in the sphincter muscle of eye
myosis (constriction of pupil)
what happens if you stimulate muscarinic r/c in arterioles?
vasodilation
what happens if you stimulate muscarinic r/c in the bronchioles
bronchoconstriction
stimulating of muscarinic r/c in GI and urinary tracts?
salivation, lacrimation, urination, diarrhea
what are two ways to mimic the parasympa nervous system?
stim muscarinic r/c or prevent breakdown of ACH
acetylcholine; category and MOI
parasympathomimetic; muscarinic and nicotinic agonist
bethanechol
parasympathomimetic; muscarinic agonist
pilocarpine
parasympathomimetic; marcarinic agonist
neostigmine
parasympathomimetic; reversible cholinesterase inhibitor
malathione
parasympathomimetic; irrevsible cholinesterase inhibitor (used in nerve gas)
how do you inhibit the parasympa nervous system
antagonise muscarinic r/c
atropine
parasympatholytic; muscarinic antagonist
scopolamine
parasympatholytic; muscarinic antagonist
iparatropium
parasympatholytic; muscarinic antagonist
how do you mimic the sympathetic nervous system?
stimulate adernergic r/c, promote release of norepi, prevent elimination of norepi
epinepherine
sympathomimetic; stimulates alpha and beta r/c
phenylephrine
sympathomimetic; alpha one r/c agonist
clonidine
sympathomimetic; alpha 2 agonist
isoproterenol
sympathomimetic; beta one and 2 agonist
albuterol
sympathomimetic; beta 2 agonist
amphetamine
sympathomimetic; stims release of norepi and dopamine
phenylzine
sympathomimetic; MAO inhibitor
how do you inhibit the sympathetic NS?
block the adrenergic r/c and deplete the stores of norepi
parazrocin
sympatholytic; alpha one antagonist
propranolol
sympatholytic; beta one and two antagonist
metoprolol
sympatholytic; beta one antagonist
reserpine
sympatholytic; promotes release of norepi, reduces reuptake resulting in depletion or norepi stores
how do antidepressants work?
increase neurotransmitters
how do antidepressants increase NT?
increase release, decrease metabolism and decrease reuptake
sertaline
antidepressant; selective serotonin reuptake inhibition
what do some ssris stimulate?
CRT2 center
what does the CRT2 center control?
located in center of brainstem that is very sensitive to chemical substances- responds by sending message to vomitting center
what does the CRT2 center make you do?
after it finds a chemical substance is makes the body vomit to get rid of the substance
trazadone
antidepressant; nonselective NT reuptake inhibition
side effects of all antidepressants
HT or Hypotension, tachycardia and insomnia
what do tricyclic antidepressants do
inhibit reuptake and promote release of NT including ACH
what do monoamine inhibitors do
increase amount of norepi, dopamine, and serotonin by decerasing metabolism
alprazolam
anxiolytic; gaba r/c agonist (decreases action potential)
what are the two types of analgesics
narcotic and non narcotic
what do narcotics stimulate
opiate r/c in thalamus
how do non narcotics work
block enzymes responsible for producing prostaglandins
what is the most commonly perscribed drug in north america
vicodin
hydrocodone
analgesic; opiate r/c agonist
what does hydrocodone do to the eye
causes miosis
tramadol
analgesic; weak opiate r/c agonist; serotonin reuptake inhibitor and norepi releaser
what are the two types of skeletal muscle relaxants
neuromuscular blockers and spasmatolytic
how do neuromuscular blockers work
produce paralysis by blocking nicotinic r/c by using competitive antagonist or depolarizing agents
when are neuromuscular blockers used?
inpatient when with anesthesiologist
how do spasmolytics work
inhibit the polysynaptic stretch reflex by stimulating gaba r/cs
alendronate
bone resorption inhibitor, inhibits osteoclasts
why does alendronate have a long half life?
because it attaches to osteoclasts which is a permanent structure
what is the difference b/t primary and secondary hypothyroidism
primary= pathology is in thyroid and secondary is in pituitary
what is a diffuse goiter?
goiter that has spread through all of the thyroid
wha is a toxic goiter
goiter with hyperthyroid dz- usually from graves dz
what is a nontoxic goiter
assoc with low or normal thyroid levels
levothyroxine
thyroid drug; bind to nuclear r/c that cause gene transcription and protein synthesis
what is levothyroxine used for
replacement therapy
what is the most commonly used trade name of levothyroxine?
synthroid
liothyronine
thyroid drug; bind to nuclear r/c that cause gene transcription and protein synthesis
which is more potent levothyroxine or liothyronine?
liothyronine is more potent
iodide salts
anti thyroid; inhibit the release of thyroid hormones
what are iodide salts used for
treatment of thyroid storm
propylthiouracil
antithyroid; inhibits several steps in thyroid synthesis
radioactive iodide
antithyroid; diagnostic and chemical ablation
insulin
antidiabetic; binds to insulin r/c which activates tyrokinase which phosphylates proteins, which alters metabolic enzymes to move glucose into cell from plasma
metformin
oral hypoglycemic; suppression of hepatic gluconeogenesis
what is the most serious side effect of metformin?
lactic acidosis
what is metfomin used for?
treatment of type 2 diabetes
piaglitasone
oral anti diabetic; decreases insulin resistance by regulating genes involved in glucose and lipid metabolism
glucagon
pancreatic hormone; binds to r/c in liver causing increased CAMP, glycogenolysis and gluconeogensis
wha is glucogon used for
emergency treatment of severe hypoglycemia