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57 Cards in this Set
- Front
- Back
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Autocrine
Paracrine Endocrine cell cell communication examples |
- Signaling chemicals coming from a cell act on their own
receptors (e.g., norepinephrine acting on the presynaptic receptors and cytokines acting on lymphocytes). -Signaling chemicals influence the function of neighboring cells and cells present in the close vicinity (e.g., histamine, serotonin). -Signaling chemicals are carried to the distant sites and act on discrete organs (insulin, estrogen, testosterone, etc.). -Direct communication occurs through interaction of signaling molecules anchored on the cell membranes CTcell-B cell interaction, HIV [gp120J-T cell [CD4J interaction). |
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receptors?
throxine, hydrothyronine? estrogen? loose receptor example |
- extracellular, plasma bound, intracellular
- binds all receptors - only bind intracellular - TBG, ANP-C, IgG |
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affinity
intrinsic activity agonist antagonist partial agonist |
- persistent ability with which the
drug binds to the specific receptors on the cell membrane - The intrinsic activity of a drug is the inherent property of the drug to impart biological signals -drugs that can produce the maximal response in any given tissue are termed full agonists -antagonists can have full (1.0) affinity, but their intrinsic activity is Always zero (0). -can bind with full affinity, the same as a full agonist, but can produce only a partial effect |
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differential effects of epinephrine
receptor and function lungs ateries heart eye hair viens |
blocker B2 - methoxanine ?
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agonist and antagonist
adrenergic alpha |
alpha 1
phenylephrine antag Phentolamine Tolazoline Prazosin alpha 2 clonidine antag Phentolamine• Tolazoline Yohimbine |
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agonist and antagonist
adrenergic beta |
beta1
isoproterenol dobutamine antag Propranolol Timolol Metoprolol Atenolol beta 2 isoproterenol terbutaline antag Propranolol Timolol Butoxamine |
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bradycardia
tachycardia |
- constricted
- dialated, isoproterenol, B1 |
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heteroreceptors!
potentiate adrenergic stim ? blocker? control diaherria? |
angiotensin II
neuro peptide y diphenoxylate binds adropine? |
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flow chart
acetylcholine lung gentitals heart GI tract bladder lacrimal eye ateries sweating |
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dry mouth, dry skin, tachycardia- meds
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adropine
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know different receptors, second messengers w/ Alpha, beta, M1, M2, M3
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a
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direct acting cholinomimetics
indirect acting block |
bind to receptors,
- acetylcholine esterase |
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cholinergic Muscarinic ag antag
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M1
carbachol antag atropine pirenzepine M2 carbachol antag atropine M3 antag atropine |
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cholinergic nicotinic ag antag
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Nn
antag HexaMethonium Nm antag Tubercurarine succinylcholine |
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atropine effects
diphenoxylate binds atropine diphenoxynate |
dilate pupil-> not completely artopine and phenylephrine
M1 opiate receptor , block acetylcholine release thro M1 |
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phenoxylbenzamine
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permanent bind alpha 1
dilate pupil |
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Atropine effects
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• (Mydriasis): temporary pupil dilation
• GI tract: decreased muscle actions and secretions • Bronchiolar smooth muscle: decreased muscle actions and secretions (asthma) • Brain: Blockage of CNS receptors (Parkinson’s, motion sickness) • Urinary bladder: Relaxation of detrusor muscle and constriction of spincter (urinary incontinence) • Heart: Tachycardia (M2 blocker SA node) • Salivary glands: decreased saliva secretion • Sweat glands: decreased sweating |
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inhibitors?
cooperatively req? |
competitive, un, non inhibition(allosteric)
multiple subunits |
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acetylcholineesterase inhibitors
myestinia gravis treating glacoma |
- edrophonium for diagnosis, neostigmine, physostigmine
-important acute or chronic (C- timinol, A- vilocarpine, physostigmine) indirect cholinomamatics |
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condition pupil dialated
aqueous humor release -treat with |
timinol and another one (pupil hint)
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Prevent organophospahte bond
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-PAM, pralidoxime
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nerve gas
first thing then |
-atropine
- physostigmine, neostigmine |
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Penicillins
which enzyme inhibited |
- transpeptidase
-cuz 2 B alanines |
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which kill gram -ve
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-amox, ampi
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penicilinase resistant
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-methi
-nafi -oxa -cloxa -dicloxa |
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know combos
Augmentin Unasyn |
-amox + clavulanic acid
-ampi + sulbactum timentin? |
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which enzyme produce 6-aminopenicillinic acid (6-APA)
beta-lactamase produce |
- bacterial penicillin amidase
-penicilloic acid |
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5-florouracil inhibiting thymidine synthase
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for rectal cancer
-fDUMP |
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xanthine oxidase inhibitor
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treat gout
-allopurinol, suicide |
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receptor theories
clarks assumptions are |
-stimulus is elicited when receptor molecule occupied by agonist
-drug-receptor complex formed readily and is rapidly reversible -maximal stim occurs when all sites occupied -occupation of one does not affect the tendency of others to be occupied |
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PD2 value-
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-affinity of ligand for receptor
- log Kd conc |
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calc intrinsic activity aka alpha
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Gaddum eq.
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rate theory
antagonist agonist partial?? |
by Paton
rate 0 rate max acybutanol, betalol?? |
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dose response curve if shift right?
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-antagonist present, need more conc for same effect, Kd value increase w/ comped. antag
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pA2 vs pA10 which smaller
comp. antag |
-PA10
-change .95 |
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kind of inhibtor
difference of low conc vs high |
w/ non comp. antag
shifting right at low, Kd increaing Emax decreasing high doses, |
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what the hell is this what does it tell us
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partial + full agonist/ partial effect at full conc.
dose relation Kd (sumthin bout this) |
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select preferred drug from graphs
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max efficicacy, max potency
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therapeutic index
first dose producing max effect |
- calc ratio Ld50/Ed50
- ceiling dose |
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conc drug 1/3 of Kd effect is total # receptors?
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D / Kd +D
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tolerance
tachyphylaxis |
-gradual decrease in effectiveness of drug over long time period
-loss of response on repeated administration -ex angiotensin II |
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how fast is each type response
ion channels steriods DNA second messenger kinases |
-ion channels- milliseconds
-second messengers- seconds -kinases -minutes -steriods and DNA- hours |
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know secondary messengers
2nd messengers good for |
-cAMP, cGMP, Ca++,
arachidonic acid, 4,5-phosphoinositol, 4,5-biphosphate (PIP2), Inositol 1, 4, 5-triphosphate, 1, 2-diacylglycerol -amplifying |
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heat shock protein 90
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inactivates steroid receptor until ligand binds- then transcription
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phosphorlation and consequences
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- activate, inhibit
-ex. glycogen synthesis controlled by both, (lots Ca degradation) |
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EGF receptor
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-dimerization triggered by EGF
-autophos happens -phosphorlates other crap |
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phos or nonphos--> Beta arrestin binds which
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-phos
-phos kick off Gs -Gs protein inhibited until unphos |
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activating guanylate cyclase activity
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-GC activated by ANP binding ANP receptor
-on inside GC, make cGMP from GTP then dilate -this how NO works |
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3 units of G protein, where bind
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-alpha, beta, gamma
-bind alpha -if alpha s, make cAMP, if alpha i inhibit AC |
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Na, K gating, potential range for gates
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Na- inactive -90mV inside open
-activated (-90- +35mV) both open -inactivated (-90 - +35mV) inside closed, out open K- same as Na but... -open just as Na is closing |
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nicotine bind ______open Na channel, where bind
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-nicotinic receptor
-subunits 5 -2 alpha, beta, gamma, delta -binds alpha |
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channel typpes, potential ranges, tests to determine channel
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GABA complex
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-open Cl- channel, hyperpolarize
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GABA complex
benzodiaziphone Barbituate |
-potentiate effect
-open channel more freq, - long last current -both +ve allosteric, coop |
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GABA antagonist
inverse agonist |
-bicululline (comp),
-picrotoxin (noncomp), directly inhibit channel bind benzodiaphine decreasing opening |
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Barbituates
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-potentiate GABA effect
-allosterically relieve picrotoxin inhibited channel |
