Pharm 1 USMLE Flashcards
28 y/o chemist presents w/ MPTP exposuree. what NT is depleted
dopamine
woman taking tetracycline exhibits photosensitivity. What are the clinical manifestations?
rash on sun exposed retions of body
African American man who goes to Africa develops a hemolytic anemia after taking malarial prophylaxis. what is the enzyme deficiency
glucose 6 phosphate dehydrogenase
farmer presents w/ dyspnea, salivation, miosis, diarrhea, cramping, and blurry vision. What caused this, and what is the MOA
insecticide poisoning; inhibition of acetylcholinesterase
27 y/o female w/ hx of psych illness now has urinary retention due to a neuroleptic. What do you tx it with?
bethancechol
pt w/ recent kidney transplant is on cyclosporine for immunosuppression. Requires antifungal agent for candidiasis. What antifungal drug would result in cyclosporine toxicity
ketoconazole
pt is on carbamazepine. What routine workup should always be done?
LFTs
23 y/o female who is on rifampin for TB prophylaxis and on birth control (estrogen) gets pregnant. why
rifampin augments estrogen metabolism in the liver, rendering it less effective
what is the volume of distribution
relates the amount of drug in the body to the plasma concentration
=amount of drug in body/plasma drug concentration
Vd of plasma protein bound drugs can be altered by dzs in these 2 organ systems
liver and kidney
what is clearance (CL)
relates the rate of elimination to the plasma concentration
Cl=rate of elimination of drug/plasma drug concentration
what is the half life (t1/2)
the time required to change the amount of drug in the body by 1/2 during elimination (or constant infusion). A drug infused at a constant rate reaches about 94% of steady state after 4 t(1/2_
t(1/2)=0.7xVd/Cl
what is concentration of drug in the body after 1 half life
50%
what is concentration of drug in the body after 2 half lives
75%
what is concentration of drug in the body after 3 half lives
87.5%
what is concentration of drug in the body after 4 half lives
~94%
Cp =
target plasma concentration
F=
bioavalability
Loading dose=
Cp x Vd/F
maintenance dose=
CpxCL/F
what happens to the loading dose and maitenance dose in pts will impared renal or hepatic fxn
loading dose remains the same
maitenence dose is decreased
this order elimination describes a constant rate of elimination regardless of C (i.e. constant AMOUNT of drug eliminated per unit time). Cp decreases linearly with time. E.g., etoh, phenytoin, and asprin (at high or toxic concentrations)
zero order elimination
image. p. 195
this order elimination describes a rate of elimination proportional to the drug concentration (i.e., constant FRACTION of drug eliminated per unit time). Cp decreases exponentially with time.
first order elimination
image. p. 195
In drugs with 1st order kinetics rate of elimination is ________ plasma concentration (Cp).
image. p. 195
proportional to
In drugs with 0 order kinetics rate of elimination is ________ plasma concentration (Cp).
image. p. 195
independant of
give some examples of phase I metabolism
reduction, oxidation, hydrolysis.
describe the metabolites of phase I metabolism(aka are they active)
slightly polar, water soluble, often still active
give some examples of phase II metabolism
acetylation, glucuronidation, sulfation
describe the metabolites of phase II metabolism(aka are they active)
yields very polar, inactive metabolites (renally excreted
what pump is key in phase I metabolism
cytocrome P-450
by what method are drugs metabolized in phase II metabolism
conjugation
what phase of metabolism do geriatric pts lose first
phase I
competitive antagonist shifts the curve _______
to the right
noncompetitive antagonist shifts the curve ______
downward
EC50:
dose causing 50% of maximal effect.
Kd:
concentration of drug required to bind 50% of receptor sites
image p. 196-percent of maximum efect as a fx of dose
in a system with spare receptors, the EC50 is lower than the Kd, indicating that to achieve 50% of maximum effect, <50% of the receptors must be activated.
image p. 197-percent of maximum efect as a fx of dose
comparison of dose-response curves for a full agonist and a partial agonist. The partial agonist acts on the same receptor system as the full agonist but cannot produce an equivalently large effect (it has lower maximal efficacy) no matter how much the dose is increased. A partial agonist may be more potent (as in the figure), less potent, or equally potent; potency is an indipendant factor
what is the therapeutic index
mean toxic dose/mean effective dose
TD50/ED50
high TI is good
on average how long does it take for a drug to be in In-vitro stidues
2 yts
on average how long does it take for a drug to be in animal stidues
2 years
this phase of clinical testing for a drugs looks at if it is safe, and the pharmakinetics
phase 1
this phase of clinical testing for a drugs looks at if it works in pts
phase 2
this phase of clinical testing for a drugs looks at does it work, in a double blind study
phase 3
this phase drug development involves postmarketing surveillance
phase 4
On average how many years of drug development does it take to file a NDA (new drug application)
9
how long after filing of application does patent expire on a drug and generics become available
20 years
given the receptor, give the G-protein class and the major fx: α1
increases vascular smooth mm contraction
G protien class: q
given the receptor, give the G-protein class and the major fx: α2
Decrease sympathetic outflow, decrease insulin release
G protien class: i
given the receptor, give the G-protein class and the major fx: ϐ1
increase heart rate, increase contractility, increase renin release, increase lipolysis, incease aqueous humor formation
G protien class: s
given the receptor, give the G-protein class and the major fx: ϐ2
vasodilation, bronchodilation, increase glucagon release
G protien class: s
given the receptor, give the G-protein class and the major fx: M1
CNS
G protien class: q
given the receptor, give the G-protein class and the major fx: M2
decrease heart rate
G protein class: i
given the receptor, give the G-protein class and the major fx: M3
increase exocrine gland secretions
G protein class: q
given the receptor, give the G-protein class and the major fx: D1
relaxes renal vascular sm mm
G protein class: s
given the receptor, give the G-protein class and the major fx: D2
modulates NT release, esp in the brain
G protein class:i
given the receptor, give the G-protein class and the major fx: H1
increase nasal and bronchial mucus production, contraction of bronchioles, pruritis, and pain
G protein class:q
given the receptor, give the G-protein class and the major fx: H2
increase gastric acid secretion
G-protein class:s
given the receptor, give the G-protein class and the major fx: V1
increase vascular sm mm contraction
G-protein class:q
given the receptor, give the G-protein class and the major fx: V2
increase H2O permeability and reabsorption in the collecting tubules of the kidney
G-protein class:s
release of NE from a sympathetic nn ending is modulated by ______, acting on these receptors.
NE, ACH, ATN II, othr substances
presynaptic α2 autoreceptors
Bethanechol is a cholinomimetic with direct agonist actions. Give its clinical applications
postop and neurogenic ileus and urinary retention
it acts by activating Bowel & Bladder smooth mm. It is resistant to AChE
Carbachol, pilocarpine is a cholinomimetic with direct agonist actions. Give its clinical applications
Used for glaucoma
it activates ciliary mm of eye (open angle), pupillary sphicter (narrow angle); It is resistant to AChe
Neostigmine is a cholinomimetic with indirect agonist actions, it acts on anticholinesterases. Give its clinical applications
postop & neurogenic ileus and urinary retention, myasthenia gravis, reversal of neuromuscular jxn blockade (postop)
It acts by inceasing endogenous ACh
Pyridostigmine is a cholinomimetic with indirect agonist actions, it acts on anticholinesterases. Give its clinical applications
used to tx myasthenia gravis
It acts by inceasing endogenous ACh, thereby increasing strength
Edrophonium is a Pyridostigmine is a cholinomimetic with indirect agonist actions, it acts on anticholinesterases. Give its clinical applications
myasthenia gravis (short acting)
It acts by inceasing endogenous ACh
physostigmine is a cholinomimetic with indirect agonist actions, it acts on anticholinesterases. Give its clinical applications
glaucoma (crosses blood brain barrier) and atropine OD
works by increasing endogenous ACh
Echothiophateis a cholinomimetic with indirect agonist actions, it acts on anticholinesterases. Give its clinical applications
Glaucoma
works by increasing endogenous ACh
give some signs of cholinesterase inhibitor poisoning
Diarrhea (abd cramping), Urination, Miosis, Bronchospasm, Bradycardia, Exitation of skeletal mm and CNS, Lacrimation, Sweating, and Salivation,
mneu: DUMBBELSS
or SLUD effects
what can cause cholinesterase inhibitor poisoning
Parathion and other organophosphates
how do you tx cholinesterase inhibitor poisoning
Antidote–atropine (muscarinic antagonist) plus pralidoxime (chemical antagonist used to regenerate active cholinesterase)
Atropine, homotropine, and tropicamide are cholinoreceptor blockers taht act on they eye to do what?
produce mydriasis and cycloplegia
Benzotropine is a cholinoreceptor blocker that acts on the CNS to tx?
Parkinson’s dz
Scopolamine is a cholinoreceptor blocker that acts on the CNS to tx?
Motion skickness
Ipratropium is a cholinoreceptor blocker that acts on the Respiratory system to tx?
Asthma, COPD
Methscopolamine, oxybutin, glycopyrrolateis a cholinoreceptor blocker that acts on the GU system to tx?
urgency in mild cystitis and reduce bladder spasms
atropine is a muscarinic _______
antagoinist
mneu: blocks SLUD:
salivation, Lacrimation, Urination, Defication
give the effect atropine would have on the eye
pupil dilation, cycloplegia
give the effect atropine would have on the airway
decrease secretions
give the effect atropine would have on the stomach
decrease acid secretion
give the effect atropine would have on the gut
decrease motility
give the effect atropine would have on the bladder
decrease urgency in cystitis
what would an atropine toxicity look like
increase body temp; rapid pulse; dry mouth; dry, flushed skin; cycloplegia; constipation; disorientation
SE: Hot as a hare Dry as a bone Red as a beet Blind as a bat Mad as a hatter
watch out cuz atropine can cause this in the elderly
acute angle-closure glaucoma
watch out cuz atropine can cause this in men with BPH
urinary retention