Pharmacology Flashcards
Vmax is proportional to
the enzyme concentration
Km is inversley proportional to
the affinity of the enzyme to its substate
Enzyme reaction showing a sigmoid curve
cooperative kinetics
Km =
saturation at 1/2 Vmax
Michaelis-Mentin kinetics
hyperbolic curve shape
Lineweaver-Burk plot gradient
Km/Vmax
How do reversible competitive inhibitors change Vmax and Km?
No change
Increase Km
How to irreversible competitive inhibitors change Vmax?
Decrease Vmax
No change
How do noncompetitive inhibitors change Vmx?
Decrease Vmax
No change
What do reversible compeititve inhibitors do?
decrese the potency
What do irreversible competitive inhibitors do?
decrease efficacy
What do noncompetitive inhibitors do?
decrease efficacy
Volume of distribution
volume occupied by drug in body relative to plasma concentration
Vd =
amount of drug in body/ plasma drug concentration
Clearance =
rate of elimination/ plasma drug concentration
= Vd x elimination constant
Half life =
0.693 x Vd / Clearance
when is steady state reached?
after 4-5 half lives
Loading dose =
(Cp x Vd) / F
Cp = target plasma concentration
F = bioavailability
Vd = volume of distribution
Maintenance dose =
(Cp x CL x dosage interval) / F
how should loading and maintenance doses change in renal and liver disease?
same loading dose, decrease maintenance dose
permissive interaction
A is required for the full effect of B
synergistic interaction
the effect of A+B is greater than the sum of the individual effects
tachyphylactic interactions
acute decrease in drug response after initial/ repeated administration
zero order kinetics
rate of elimination is always constant
first order kinetics
rate of elimination is proportional to drug concentration
drugs using zero order kinetics
PEA
Phenytoin
Ethanol
Aspirin
Rx for aspirin, methotrexate, phenobarbital OD and why
Bicarbonate
They are weak acids
Rx for amphetamine, TCA OD and why
ammonium chloride
they are weak bases
phase I drug metabolism
reduction, oxidation, hydrolysis
P-450
what phase of drug metabolism is lost first?
phase I
elderly
phase II drug metabolism
conjugation
–> polar and inactive
what will increase the side effects of a drug?
being a slow acetylator
what happens in conjucation phase II?
methylation, glucuronidation, acetylation, sulfation
efficacy
maximal effect a drug can produce
potency
amount of drug needed for a given effect
EC50 is
the dose of drug needed to give 50% of the maximum effect
theraputic index =
median toxic dose / median effective dose
very safe drug theraputic index will be
high
sympathetic NS
short pre-synaptic
P-ANS
long pre-synaptic
P-ANS receptors
Nicotinic ACh
Muscarinic ACh
S-ANS receptors
Nicotinic ACh
Muscarinic ACh, NE, D, Epinephrine
somatic receptors
voluntary motor nerve
ACh at NMJ
how muscarinic ACh receptors work
GPCR
sympathetic receptors and g protein classes
a1 - Q
a2 - I
B1, 2, 3 - S
action of a1
smooth muscle contraction, mydriasis, intestine and bladder contraction
action of a2
decrease sympathetic flow, decrese insulin, decrease lypolysis, increase plt aggregation, decrease aq humour production
action of B1
increase HR and contractility, lipilysis, renin release
action of B2
vasodilation, bronchodilation, lipolysis, insulin, decrease uterine tone, ciliary muscle relaxation, increase aq humour production
B3 action
lipolysis, thermogenesis in skeletal muscle
be free to take off your clothes and shiver!
M1 action
CNS, enteric nervous system
M2 action
decrease Hr and contractility of aorta
M3 action
exocrine secretion, gut peristalsis, bladder contraction, btonchoconstriction, miosis, accomodation
D1 action
relax renal vascular smooth muscle
D2 action
modulates transmitter release (brain)
H1 action
mucus production, vascular permeability, contraction of bronchioles, pruitus, pain
H2 action
gastric acid secretion
V1 action
vascular smooth muscle contraction
V2 action
H2O reabsorbtion in collecting duct
mneumonic for Q g protein class
A Very Quick MuMMy Must Hop
mneumonic for I g protein class
2 MAD I’s
mneumonic for S g protein class
you See, 3 Bees, 2 Honeypots and a Very Victorious Dog
action of Gq
phospholipase C –> PIP2 –> DAG –> PKC
–> IP3 –> Ca2+ rise
action of Gs
Adenylyl cyclase –> cAMP –> PKA –> Ca2+ rise, inhibits myosin light chain kinase
action of Gi
Inhibits Gs (Adenylyl cyclase –> cAMP –> PKA –> Ca2+ rise, inhibits myosin light chain kinase)
hemicholinium
stops formation of ACh
vesamicol
stops ACh entering vesicles
Botulinum
stops vesicle release
stops NA reuptake
cocaine, TCA, amphetamine
Increases NA release
amphetamine, ephedrine
Stops NA release
Bretylium, guanethidine
Reserpine
stops DA moving into vesicles
Metryrosine
analog of tyrosine, stops NA being synthesised
tyramine excess results in
why
htn crisis
excess tyramine displaces NA in vesicles, more NA diffuses into the cleft increasing sympathetic activation
cholinomimetics
bethanechol, carbachol, methacholine, pilocarpine
methacholine
stimualtes muscarinic receptors in airway
carbachol use
miosis for open angle glaucoma
bethanechol use
post op ileus, neurogenic ileus, urinary retention
anticholinesterases
neostigmine, edrophonium, donepezil, galantamine
edrophonium use
dgx myasthenia gravis
donepezil, galantamine, rivastigmine use
alzheimer disease
neostigmine use
ileus, urinary retention, myasthenia gravis, reverses NMJ block