Pharm Flashcards
Receptors that work on Gi
M2, a2, D2 (MAD2s inhibit)
Receptors that work on Gs
B1,b2, D1, H2, V2
Receptors that work on Gq
H1, a1,v1, m1, m3 (cutesies HAV 1 M&M)
Alpha 1 effects
Increases vascular smooth muscle contraction (increase TPR,increase BP)
pupillary dilation
intestinal and sphincter muscle contraction
Alpha 2 effects
Inhibits sympathetic outflow, negative feedback on presynaptic nerves
decreases insulin release (found on pancreatic cells)
Beta 1 effects
Found mainly on heart and kidney: increases heart rate, contractility, increase renin release
Beta 2 effects
Smooth muscle relaxation (peripheral vasodilation, broncodilation, GI, utuers, bladder), causes decreasedTPR, reflex tachycardia, decrease uterine tone
Increases insulin release, increased glycogenolysis
Dopamine 1 effect
Relaxes renal vascular smooth muscle
Dopamine 2 effect
Modualtes transmitter release in the brain
Histamine 1 effect
Increases nasal and bronchial mucus production, contract bronchioles, pruritis
Histamine 2 effect
Increases gastric acid secetion
Vasopressin 1
increases vascular smooth muscle contraction
Vasopressin 2
Increases H2O permeability and RAB in collecting tubules
Definition of Km
[S] at which V = 1/2Vmax
This value is related to affinity of enzyme for substrate
Km
Vm is directly proportional to…
Enzyme concentration
Line-weaver burke plot:
X axis, Y axis, slope
X axis: -1/Km
Y axis: 1/Vm
Slope: Km/Vm
Origins of Parasympathetic NS
CN III, VII, IX, X, S2/S3
Which is more selective, PNS or SNS, and why?
PNS because longer preganglionic fibers, which allow one nerve-one organ effect. SNS has shorter preganglionic fibers and postganglionic fibers branch and affect multiple targets
Equation for Volume of distribution
Vd = amount of drug in body/plasma drug concentration
Half life equation
T1/2 = 0.7xVd/CL
Clearance (CL) equation
CL = rate of eliminiation of drug/plasma drug concentration = (Vd) * (Ke) = 0.7*Vd/t1/2
Loading Dosage equation
Dose = Volume of distribution * target plasma concentration / bioavailability
Vd depdendent, not affected by renail/iver disease
Maintainance Dose equation
Dose = target plasma concentration * clearance / bioavailability
which drugs have zero order elimination?
PEA
Phenytoin,Ethanol, Aspirin
Phase I of metabolism does what? and done by what system?
Done by CytP450 in liver, yields slightly polar molecules, still somewhat active
ROH - Reduction, oxidation, hydrolysis
What phase of metabolism is lost first in elderly patients?
Phase I
Phase II of metabolism includes what?
Conjugation reactions - methylation, glucordination, aceylation, sulfation
yields polar, inacative metabolites
Therapeutic index =
LD50/ED50
Hemicholinum
Blocks choline entry into nerves
Vasamicol
blocks packaging of Ach into vesicles
Botulinum fxn
Decreases ACh release into synapse
Black Widow Spider Toxin
Causes release of Ach into synapse, causing paralysis
Metyrsoine fxn
blocks conversion of Tyrosine to Dopa by blocking tyrosine hydroxylase
Reserpine
Inhibits NE packaging into vesicles
Amphetamine
Stimulates release of NE into synapse
Guanethidine, bretylium
Blocks NE release into synapse
Ephedrine, Tyramine
Stimulates release of NE into synapse
Cocaine, TCA
blocks NE reuptake by pre-synaptic neuron
Feedback on pre-synaptic neuron via 3 signals
M2: inhibits NE release
A2: inhibits NE release
AII: promotes NE release
MOA, Clinical indications for Bethanechol
Direct Cholinergic Agonist
Activates bowel and bladder smooth muscle
Used for post op ileus, neurogenic ileus and urinary retention
MOA, Clinical indications for carbhachol
Direct cholinergic agonist, used for glaucoma and relief of IOP
MOA, Clinical indications for Pilocarpine
Contracts ciliary muscle of eye, pupillary sphincter, resistant to AChE
Used for stimulatoin of sweat, tears, and saliva
Used for open/closed angle Glaucoma
MOA, Clinical indications for Methacholine
Challenge test for asthma dx, direct cholinergic agonist, stimulates muscarinic receptors in airway when inhaled
MOA, Clinical indications for Neostigmine
Acetylcholinesterase Inhibitors
Post op and neurogenic ileus, urinary retention, myasthenia gravis, reversal of NMJ blockade
MOA, Clinical indications for pyridostigmine
Increases endogeneous ACh bc acetylcholineesterase inhibtor
myasthenia gravis
MOA, Clinical indications for edrophonium
Cholinergic that blocks acetylcholinesterase
used for dx of MG
MOA, Clinical indications for physostigmine
Blocks acetylcholineesterase fxn, increases ACh
Used for Atropine overdose and anticholingeric toxicity
MOA, Clinical indications for Donepeil,
Block acetylcholine function, causing increased ACh, used for Alzhemiers
MOA, Clinical indications for Rivastigmine, Gamantine
Block acetylcholine function, causing increased Ach, used for Alzhemiers
Cholinesterase Inhibitor Poisoning Sx
DUMBBELSS
Diarrhea, urination, miosis, bradycardia, bronchospasm, exciation of skeletal muscle, lacrimation, sweating, salivation
Cause and tx for cholinesterase inhibitor poisoning
Insectasides (Organophosphates)
Tx: atropine, pralidoxime
MOA, Clinical indications for Atropine
muscarinic antagonist
MOA, Clinical indications for benztropine
muscarininc antagonisns, used for parkinsons
MOA, Clinical indications for scopolamine
muscarininc antagonist, used formotion sickness and to decreased oral secretions (eg ICU pt)
MOA, Clinical indications for ipratropium, tiatropium
Muscarninc antagonist at level of lungs for COPD and asthma pts, by decreasing bronchoconstriction
MOA, Clinical indications for oxybutynin, tolteridine, trospium
Muscarininc antagonist at GU system to reduce urgency and decrease ladder spasms
Sx of atrophine toxicity
Caused by excessive anticholnergic sx bc its an antimuscarinic
Hot as a hare, dry as a bone, red as a bat, blind as a bat, mad as a hatter
increased body temp,dry flushed skin, cyclooplegia, constipated, disoriented
MOA, Clinical indications for epinephrine
sympathomimetic, beta and alpha agonist
Anaphylaxis, asthma, hypotension
MOA, Clinical indications for norepinephrine
sympathomimetic, primarily alpha effects, some B1 effect
hypotension (but decreases renal perfusion), septic shock
MOA, Clinical indications for isoproternol
sympathomimetic, Beta effects only
Used for torsade de pointes,bradyarrythmias
MOA, Clinical indications for Dopamine
sympathomimetic, low dose: dopamine
Med dose: beta receptors
high dose: alpha receptors
Used for shock, heart failure
MOA, Clinical indications for dobutamine
sympathomimetic, primarily B1 effects
increases Hr and contractility, heart failure, cardiac stess test
MOA, Clinical indications for phenylephrine
sympathomimetic, Increases alpha effects
causes vasoconstiction and ocular mydriasis,decongestant for rhinitis
MOA, Clinical indications for albuterol, salmeterol, terbutaline
sympathomimetic, Primarily B2,some B1 effect. Acute asthma (metaproternol, albuterol), salmetrol for long term asthma or COPD control
terbutaline helps with uterine relaxation
MOA, Clinical indications for amphetamine
indirect sympathetomemimetc, releases stored catecholamines, used for narcolepsy, ADD
MOA, Clinical indications for ephedrine
releases stored catecholamines, used for nasal decongestion
MOA, Clinical indications for cocaine
blocks reputake of NE at cleft
Used for vasoconstriction and local anesthesia
MOA, Clinical indications for clonidine
alpha 2 agonist, used to decrease BP, acts centrally
MOA, Clinical indications for methyldopa
central alpha 2 agonist, decreases BP, especially pregnancy induced BP
MOA, Clinical indications for phenoxybenzamine
irreversible nonselective alpha blocker, used for phenochromacytoma
MOA, Clinical indications for phentolamine
reversible nonselective alpha blocker, used for pts on MAO inhibitors who have eaten tyramine containing foods
MOA, Clinical indications, and toxicity for prazosin, terazosin, doxazosin
alpha1 blocker, used for HTN and urinary retension in BPH, can cause 1st dose orthostaiss, reflex tachy, and rebound HTN