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First Pass Metabolism
(decr bioavailability)

destroyed before gets to target system by enzymes in GI tract. If survives --> liver where gets metabolized. Ex=AMINOGLYCOSIDES (insulin)=why no oral admin yet

first pass metabolism (aka presystemic metab)
Q

the fraction of drug lost in liver or gut wall
Ex=propranolol, lidocaine (arythmia), nitrates (angina)

enterohepatic circulation

oral-->metab by bacteira w/glucuronidase-->absorbed in SI-->into liver via portal vein-->GLUCORONIDATION here-->through bile duct-->back into SI-->metab again etc...

Example of enterohepatic circulation?

BC pills: bact in that intest metab & help w/enterohepatic circulation. If on abx, bact can't break down bc pills= lowers processing of them, gets excreted instead of metabolized =BABY.

SUBLINGUAL

-no first pass metabolism
-directly into submand vein, then sup vena cava, then heart w/i minutes

RECTAL

-Lower rectum=direct link to syst circulation
-Upper rectum=direct to liver
-About 50% bipasses liverthrough lower rectum, still better

TRANSDERMAL DELIVERY

-Smooth plasma [], no spikes like when take in am, pm etc...
-no first pass metabolism
-convenient
-Probs? poss tolerance so must remove 8-10hrs

What if drug water soluble?

probably won't work well, needs to be fat sol

RESPIRATORY DELIVERY

-alveolar epothelium huge SA for lipid sol drugs
-rapid action b/c huge blood supply

INTRAVENOUS

-immediate action
-no gastric acid/first pass metab
-ok w/unconcious patients

INTRAMUSCULAR

-mild irritant drugs ok
-quick absorption
IMPT: of on anti-coag drugs like hep, don't give IM b/c=hamartoma!!!!

SUB-Q

-insulin & heparin, self-admi is poss
-prob inj insulin IM is that if work out, get lots blood to that m, then get huge insulin rel=low bp=bad

INTRATHECAL

-into subarachnoid space, piercing meninges
-prob=headache, meningitis

EPIDURAL

-not piercing meninges=less complications

What is pharmokinetics?

-effects of pH on absorption of drug
-only non-ionized are lipid sol and can cross cell membrane
-ionized are water sol no cross memb, gets peed out

Weak acids & weak bases?

-drugs either weak acids or weak bases, strong acids & bases not used b/c always protonated thus dont' cross memb
-form changes based on surrounding pH

HA <--> H+ + A- = weak acid, a proton donor
BH+ <--> H+ + B = base, accepts proton

What happens to acidic drug in acidic env?

Stays unionized b/c can't donate proton to anyone

What happens to basic drug in basic env?

Stays unionized b/c no protons to accept

What do you want to do if get acidic drug poisioning (acetominaphin)?

make urine alkaline, drug gets ionized, then excreted

What effect does pH have on ionization of a drug?

-weak acids become ionized as pH goes up, or as the pH-pKa gest more positive (in a more basic medium)

-weak bases become ionized as pH decr or as pH-pKa gets more negative (in an acidic env)

What's the equation for Bioavailability?
Q

Fraction of drug reaching systemic circulation

F=fg X (1-ER)
F=bioavailability
fg=amt absorbed
1-ER=amnt escap 1st pass metab

IV=100% bioavailability

How to figure out oral dose?

Oral dose=IV dose/F (oral bioavailability)

What must 2 drugs have in common to be BIOEQUIVALENT?
Q

1) Same Cmax (max plasma [] attained by drug)
2) Same Tmax (time at which max [] is reached)
...they must reach same plasma [] at same time w/i 20% margin

What is volume of distribution equation?
Q

Vd = D/Co

D=total amt of drug in body
Co=drug [] in plasma

Note: loading dose dep on vol, maint dose dep on clearance

What are the general Vd's of our body spaces?

3L=vascular areas
11L=ecf (like mannitol can't penetrate cell walls)
42L=total body water (ecf & icf...alcohol)
>42L=w/i cells or tissues

Note: babies have high high total body water, old people have least, women have less then men, which affects dosing

What do acidic drugs bind?

Basic ones?

Acidic = albumin (b/c slightly basic)
Basic = glycoproteins (b/c acidic)
-Plasma protein bound drugs can not leave vascular compartments & aren't free to be used if bound

What's the danger w/giving sulfonamides to babies?

It displaces bilirubin from binding sites can cause jaundice and kernicterus problems. ALSO it displaces some of the WARFARIN bound to proteins=more avail and free=BLEEDING PROBS!

What is metabolism again?

makes drug more water sol, happens in liver mostly, phase 1 & 2 reactions

What does phase 1 & 2 metabolism phases do?

Phase 1-uses cytochrome p450
Phase 2-conjugate rxn, adds water sol molecule so can be excreted

What factors do you need to know to predict whether drug is in ionized or un-ionized form? Q

1) acid/basic nature of the drug
2) pKa of the drug
3) pH of the surrounding

Biotransformation:
1)Inactivation
2)Active metabolite from inactive drug example?
3)Active metabolite from active drug ex?

1)what happens w/metabolism usually
2)L-Dopa-->dopa & Enalapril-->enalaprilat
3)Codeine-->morphine & imipramine-->desipramine

What drugs inhibit CPY450 enzyme?
Q

cimetidine
Clarithromycin
erythromycin
grapefruit juice
SSRI

What drugs induce/help CPY450 enzyme?
Q

alcohol
carbamazepine
phenobarbital
phenytoin
rifampin
st john's wort

What's the deal w/ abscence of cytochrome P450 2D6 in some caucasians?
Q

can't convert codeine to morphine, get little if any pain relief from codeine
...rem: some east african's have hyperactive cyto P450 so they can OD on codeine be careful!!

If you want to excrete an acidic drug, what do you do? "ASAP"

Make urine basic (alkaline)
Use: sodium bicarb, potassium citrate & acetazolamide

If you want to excrete a basic drug, what do you do?

Make urine acidic
Use:ammonium chloride, vit-C, cranberry juice

What is FIRST ORDER KINETICS?

-rate of elim proportional to plasma [] of drug
-follows same order of breakdown over time:
80mg->40->20->10->5
-most drugs are 1st order kinetics
-all amounts [] taper off at same place b/c dep on 1/2 life NOT how much you give them. Remember:steady state dep solely on 1/2 life

Eq for half life?

t1/2=0.7 X Vd/CL
...what is Vd again? dose/drug left in body

What is steady state?

rate in=rate out
only used in 1st order kinetic drugs

What is the time to reach a steady state dependent on?
Q

only on drug's 1/2 life NOT on dose size or freq of administration
we want drugs to be at steady state in body

Time & Steady State?

-50% steady state reached at 1 1/2 life, at 1st dose
-75% at 2 1/2 lifes, at 2nd dose
-90% at 3.3 1/2 lifes
-96.85% of steady state reached at 5 1/2 lifes. THIS WHERE WE CONSIDER THEM AT A STEADY STATE, WHAT WE GIVE THEM IS WHAT COMES OUT

If it takes 5 1/2 lives to reach steady state, how many take to get rid of all drugs?

5

Does rate of infusion of drug affect time to reach steady state?

NO! b/c ss only dep on drug's 1/2 life HOWEVER, if rate of infusion is doubled, then plasma level of drug at SS is doubled

...time to reach SS always same b/c 1/2 life det it, it's the [] that changes!!

Lower 1/2 life drug gets to SS sooner than longer 1/2 life one

...

What is the definition for clearance?

vol of plasma that is completely cleared of drug in a given time

Clearance=rate of elim/plasma drug []

How do you calculate for a corrected dose based on P w/say kidney disease or decreased clearance?

Corrected dose=avg dose per day X patients CL/normal CL

Loading dose equation?

maint dose X 2
...loading dose brings us right up to theraputic rance w/out waiting

Drug [] at steady state equation?

Css=dose X F/ CL X t

What is the problem with a narrow theraputic range & what are the drugs w/this?

Warfarin, digoxin,
harder to manage, to keep w/i small range

What is a receptor?

drug binds here, produces an effect
-propagates signal to inside of cell
-amplify signal
-adapt , if body wants to reduce effect of drug, can down regulate R's (see w/long term use of drug...TOLERANCE)

Definition of affinity?

drug bind to R, how STRONG drug binds R has nothing to do with activating anything

What is intrinsic activity?

ability of drug to activate it's R & prod response...once bound, how can you or can you activate the R

What is an AGONIST?

Binds to R & activates it...produces a response
an agonist has both affinity & intrinsic activity

Examples of AGONISTS?

morphine
epinephrine

What is an ANTAGONIST?

binds R but doesn't activate it
has affinity but no intrinsic activity

Examples of antagonists?

atenolol
metoprolol
prazosin...all a/b blockers

What is a PARTIAL AGONIST?
Q

binds & activates R, but produces sub-maximal response when compared to agonist., it competitively antagonizes the pure agonist

Example of partial agonist?

Aripiprazole for schizophrenia & bipolar

What are examples of intra-nuclear R's?

-steroids, thyroxine, Vit-D
-must be lipid sol to cross membrane
-involves synth of proteins, takes days

What is potency?

-amount of drug needed to produce the desired response
-on graph, closer to Y axis=most potent

What is efficacy?

-max response of the drug
-on graph, highest line=most efficacy

What is theraputic index?

-ratio of median lethal dose (LD50) to median effective dose (ED50)
-low therapeutic index=bad drugs, not a lot of room to play to find good dose

Drugs w/ low therapeutic index?
"Tiger WouLD's"

-Theophylline
-Warfarin
-Lithium
-Digoxin

What is a physiologic antagonist?
Q

-binds to different receptor & produces opposite effect of the drug it's antagonizing...different R's & opposite effects
-Ex: histamine binds to R & vasodilates & bronchoconstricts. Epinephrine=it's physiologic antagonist, it binds DIFFERENT Beta R and causes bronchodilation and alpha R & causes vasoconstriction
-Proprinolol poisioning: bind beta R=bradycardia, treat by stimul glucagon R=incr heart contraction

What is a competitive/reversible antagonist?

-decr potency NOT EFFICACY
-see parallel shift of DRC to R

What is a non-competative/irreversible antagonist?

-binds R irreversibly or it binds to a different site than the agonist
-see non-parallel shift in DRC to R
-decreases efficacy

Examples of non-competative drugs?
"Papa Dan's"

-proton pump inh
-allapurinol
-phenoxybenzamine for pheochromocytoma
-aspirin
-digoxin

To know:
Focus more on drugs inducing/inhibiting cyt p450
How to make urine more acidic or alkaline?
1st and 0 order kinetics
Know the 0 order drugs
Maintenance dose is dependent on CL
Vd formula? Used to calculate loading dose
Know maintenance dose formula
Loading dose formula
Half life 2 formulas
Have to know when drug reaches steady state and time to reach it
Therapeutic index of drug
Drug antagonism

...

What are spare receptors?

-R's that exist if max drug response can be obtained w/ out using all R's. See non-linear rel between R occupancy & response on graph (linear rel when no spare R's)

What decreases w/ an irreversible noncompetative antagonist?

only efficacy!, but w/super high dose, both efficacy & potency decrease on DRC

In old people, is Phase 1 or Phase 2 reactions lost most?

-Phase 1 lost when liver starts to loose function.
-Lorazipam only metabolized by phase 2 conjugation reactions, so best to use these types drugs w/old folks.

What is tachyphylaxis?

-give successive doses too quickly, get decreased response

What is R sensitization or Up-regulation?

-prolonged use of R blocker=body senses & up regulates more R;s
-Ex=beta blockers, so if all sudden stop taking beta blocker's, now have tons extra R's NE acts on all of them=tachycardia!!!!

What are the 3 phases of drug development clinical trials?

Phase 1-give to healthy P, test for side-effects tests for safety

Phase 2-give to small amt of people does it work?

Phase 3-give to bigger # of people simulates regular use in larger population

What are the 5 categories for teratogenicity?

A=folic acid safe
B=no evidence of risk
C=not sure
D=Bad, evidence of risk
E=Super bad, deff risk thalidomide

What is atropine & who is it contraindicated in?

PNS blocker, old men b/c poss retention of urine

What is the major neurotransmitter in PNS?

Ach

Where do the SNS & PNS start?

-SNS=thoracolumbar
-also know SNS has diffuse action, affects many organs
-short pre-gangli, long post-ganglia
-Ex: Ach rel onto adrenal medulla-->causes rel Epi (major one) NE (minor one, becomes major in pheochromocytoma)!!
-PMS=craniosacral
-long pre-ganglionic, short post ganglionic on organ it's affecting

How is PNS Ach synth, what R's does it act on, what causes it's release & how is it inactivated?

-Synth by acetyltransferase (ChAT)
-Acts on both nicotinic & muscarinic R's
-Ca is influxed-->vesicle w/Ach released
-Inactivated by acetyl cholinesterase in synaptic cleft. most impt way it's destroyed super fast in miliseconds. This enzyme inhibitor is a major class of drugs
...remember Ach made from choline & acetyl CoA & is recycled after broken down & transported back into axon to be used again

What are the 2 types of acetyl cholinesterase & where are they located?

-Acetyl cholinesterase (true)-at all neuromuscular jncts, hydrolizes Ach only

-Butyryl cholinesterase (pseudo)-in plasma & liver, hydrolizes procaine (local anisthetic) & succinylcholine AKA suxamethonium

What are the 2 major types of Ach muscarinic R's and where are they?

-M2:heart, causes decr adenyl cyclase, decr cAMP, K channel opens, K in, hyperpolarize, decr HR
-mimics vagal activity
-causes decr in heart contraction (even though will incr HR w/ low dose)

-M3:Everywhere, causes incr PLC, incr IP3 & DAG, ca enters cell, rel of vessicles w/NT
-on BV's, causes vasodilation via NO
-respiratory tract, causes bronchoconstriction & increase in secretions

How does Ach cause vasodilation?

binds M3 R, causes rel NO, acts on cGMP=vasodilation via smooth m relaxation

What R does Ach bind to & what does it do in the GI tract?

-binds M3 R
-increases tone, peristalsis,secretions & relaxes sphincter

What R does Ach bind in urinary bladder & what does it do?

-binds M3 R
-contracts detrusor & relaxes trigone & spincter

What R does Ach bind in eye & what does it do?

-binds M3 R
-on sphincter M, pupil constriction
-causes accommodation: ciliary m's contract, susp lig relax, lense conves = near vision
-to see something far away, cilliary m's relax, lense flattens

What is parasympathetic control of accomodation?
Q

-relaxed cilliary m=flat lense=see distant object
-contract cilliary m=convex, thick, round lense=near vision

What are the major cholinergic agonists & what kind of affects do they have?

-Ach, methacholine, carbachol, bethanechol, cevimeline, pilocarpine
-diffuse effects so many actions all over act on both nicotinic & muscarinic R's

What are the nicotinic partial agonists & why are these good?

-varenicline "chantix" smoking cessation
-good b/c in the presence of a full agonist nicotine, they act as antagonists. Keeps R turned on at low level so body thinks nicotine coming in

What is anti-AchE & what does it do?

-inhibits AchE in synaptic regions
-prolonge existence of Ach

What are irreversible anti-AchE agents?

-Insecticides
-organophosphorous compunds
-parathion
-malathion
-nerve gass
-soman
-sarin
-tabun
-dytios tight binding to AchE for lifetime, but early on can still hydrolize the bond before covalent bonding happens=can reverse if super early in rxn.

What are reversible (carbamate) anti-AchE agents?

-Medically used:
-Edrophonium
-Neostigmine
-physostigmine
-pyridostigmine
-tacrine
-Insecticides:
-Carbaryl (Sevin) BAD
-Propoxur (Baygon)

What kind of drug is edrophonium & what's it used for?

-reversible anti-AchE
-myasthenia gravis, works for 5-15 min

What's neostigmine & what's it used for?

-reversible anti-AchE, doesn't enter CNS b/c quaternary amine
-myasthenia gravis, works for 1-2 hrs
-bad oral absorption

What's physostigmine & what's it used for?

-reversible anti-AchE lipid sol, enters CNS
-glaucoma, or atropine poisioning,works for 1-2 hours
-good oral absorption

How do irreversible Anti-AchE agents work?

-organophosphorous compounds react w/esteric site of enzyme, which is then hyrolized very slow or not at all
-over time AchE ages by losing one alkyl group and eventually becomes totally resistant to hydrolysis=permanent

What is the cholinesterase reactivator & what's it used for?

-PAM!!! (pralidoxime), attaches to anionic site of AchE if there's also organophosphorous agent there & releases the enzyme
-nerve gas & organophosphorus poisioning
-don't use for OD of neostigmine OR other carbamate poisioning

What do you use for tx of organophosphate instecticide poisioning?

ATROPINE BABY!!!, it blocks muscarinic R's!!! AKA it's ANTI-MUSCARINIC or PARASYMPATHOLYTIC

What do you use to treat glaucoma besides physostigmine?

-carbachol - cholinomimetic (Ach like)
-pilocarpine -" "

What do you use for paralysis/atony of bladder or GI like after Sx?

-bethanechol -cholinomimetic
-neostigmine = best -" "

What can you use to Dx bronchial hyper reactivity?
Q

-Methacholine -cholinomimetic

What's good to use for OD of tricyclic anti-depressants (TCA's) or anti-muscarinic agents?

-sodium bicarb

What would you give a p after general anesh to recover from blockage of nicotinic R's of skeletal m while being on ventilator?
Q

-neostigmine (cholinomimetic) ...BUT it will increase Ach levels EVERYWHERE so must give small dose of atropine w/it don't get bradycardia.

What can you use to treat alzheimers?

-donepezil -cholinomimetic
-galantamine -" "
-rivastigmine - " "
-tacrine - " '

What can you use to treat xerostomia (sjogren's)

-pilocarpine -cholinomimetic
-cevimeline - " "

In the PNS, how is Ach degraded usually?

AchE

In the SNS, how are Ne & Epi degraded usually?

Re-uptake . Ne & Epi take lots of energy to make, so don't want to degrade it like Ach in the PNS.

Where is AchE located?
What about Butyryl Cholinesterase?

-in all neuromuscular junctions
-like AchE, in plasma & liver. Hydrolyzes procaine (local anisth) & succinylcholine (suxamethonium)

How does Botulinum toxin block rel of Ach?

-degrades SNAP-25 that's req for vessicle fusion & rel of Ach

How do we metabolize catecholameines (NE)?

-MAO: acts on NE after it's taken back into axoplasm via NET
-COMT: acts on NE after goes into circulation, mostly in LIVER

What are the 2 types of MAO reuptakes & where are they located?

-MAO A: anywhere in body
-MAO B: Brain

What does MAO A metabolize?

NE, 5-HT, Dopamine, tyramine

What are the MAO A inhibitors (keeps catacholamines in cleft longer)?

-phenelzine
-tranylcypromine
...anti-depressants

What's the "cheese reaction"?

If on a MAO inhibitor, you're inhibiting MAO in the GI tract too. Tyramine (a catecholamine) is in wine & cheese, it you inhibit MAO, you can't metabolize tyramine, it builds up & enters CNS & nerves & promotes the release of NE=super high amounts of NE--> hypertension & possible stroke

Where are MAO B inhibitors located, & what do they metabolize?

-selegiline & rasagiline
-Brain
-metabolize dopamine, norepi & 5-HT

good parkinsons tx

Where are nicotinic nerve R's & what do they do?

adrenal medula & autonomic ganglia
open Na/K ch

Where are nicotinic muscle R's & what do they do?

neruomuscular jnctn
open Na/K ch

Where are M1 (Gq) PNS r's and what do they do?

-ganglia, CNS
-incr PLC, IP3 & DAG=let Ca in

Where are M2 (Gi) PNS r's & what do they do?

-Heart
-decr AC, cAMP, opens K+ ch=hyperpolarize & decr HR

Where are M3 (Gq) PNS r's & what do they do?

-everywhere!!!!!
-incr PLC, IP3 & DAG=let Ca in
-have all expected PNS effects on organs
eye:constr pupil via sphincter m

What happens if you relax the ciliary M?

flatten lense= can see distant objects

What happens if you contract ciliary M?

make lense rounder/thicker=can see near objects

Where are A1 (Gq) SNS r's & what do they do?

-Eye: contr radial fibers=mydriasis
-Arterioles/veins: contr=incr BP
-Bladder: contract trigone=urinary retention don't give w/BPH already hard to Pee

Where are A2 (Gi) SNS R's & what do they do?

-decr AC & cAMP
-platelet aggregation & pancreas decr insuin rel
-decr NE rel

Where are B1 (Gs) SNS R's & what do they do?

-incr cAMP, PKA = let ca in
-heart, contr cardiac m
-kid, incr renin rel

Where are B2 (Gs) SNS R's & what do they do?

-incr cAMP, PKA=let Ca in
-dilate BVs to skel m, see tremor
-inhibit MLK in smooth m=decr contraction, thus causing vasodilation
-relax uterus
-dilate bronchioles

Where are Dopa 1 SNS R's & what do they do?

-stimulate AC & cAMP
-vasodilate renal veain= inr blood flowgood in shock saves kidney

Where are Dopa-2 (Gi) SNS R's & what do they do?

-inhibit AC, decr cAMP, open K+ channels=hyper polarize
-in brain

What is prazosin (minipress) & what is it used for?

-reversible selective a-1 blocker
-tx for HT & BPH urinary retention
...give first low dose at bed so don't get postural hypotension b/c of FIRST DOSE PHENOMENON

What is phenoxybenzamie & what's it used for? What must you also use w/it and why?

-irrevers nonselective a-blocker
-tx for PHEOCHROMOCYTOMA...(rem that cause incr. rel NE & Epi, need to block both those to treat it, so must also give b-blocker.
...GIVE A-BLOCKER 1ST THEN B if use B 1st get severe hypertensive crisis & stroke

What are B-blockers used for?
What is the 1 situation where you wouldn't use them?

-In every cardiovascular problem & hypertension
EXCEPT Prinzmetal's Angina (a vasospastic angina at rest)

What are the ABCS's of beta blockers (adverse effects*?
Q

AV block, bradycardia
Bronchial asthma and COPD
Cold extremities
Depression/DM contraindicatins

What are the uses of B-blockers?

-hypertension b/c decreases CO & thus resistance
-CAD
-CCF, low dose in mild & moderate cases
-Glaucoma (one of the best types of drugs for this)
-Hyperthyroidism (treats palpatations & tremors from this)
-Migraine
-Anxiety
-Prev esoph varacies in portal HT/chirrhosis

What's the "Black Box Warning" for B-blockers?

must taper dosage down and gradually pull P off it over 1-2 weeks don't stop suddenly!!!

If not can get angina pectoris and MI if don't

What are ganglionic blockers and what effects do they produce?

-competative antagonists against nicotinic r's in autonomic ganglia
-decrease PNS effects EXCEPT in ARTERIOLES, VEINS & SWEAT GLANDS will decr SNS effects!

What affect does Ganglionic blockers have in atrerioles/veins & sweat glands?

-wellll here they will block SNS effects (block PNS effects everywhere else)
-arterioles/veins if block SNS effect see vasodilation
-sweat glands=if block SNS effects see anhydrosis

What are the 2 ganglionic blockers?

-mecamylamine
-trimethaphan

What's a role of ganglionic blockers?

-block reflex changes (sudden changes in BP)

What's chronic simple glaucoma & what's it due to?

-b/c of increased production of aqueous humor
-therapy aims to decrease this production

What are the 4 types of drugs to treat glaucoma?

1) beta blockers, decr form of aq humor by decreasing cAMP watch out for bronchospasm in asthmatics
2) alpha-2 agonists, " "
3) carbonic anhydrase inh, " "
4) cholinomimetics, incr outflow by effecting ciliary & sphincter m's (but low choice b/c this usually isn't the prob w/glaucoma

What are the effects of PROPRANOLOL beta blocker on the heart?

-neg ionotropic effects, so decr contration
-neg chronotropic action, so decr HR-->longer diastole=better blood flow
-decr AV conduction, good for A-fib

What are the effects of PROPRANOLOL beta blocker on the eye?

-glaucoma TX best choice!! b/c decr aqueous humor production

What are the effects of PROPRANOLOL beta blocker on the respiratory tract?

-causes bronchoconstriction so don't use in asthma or COPD p's!!!!! If must use, use B1 selective one (b/c remember B2's are in the bronchioles)

What are the metabolic side-effects of PROPRANOLOL beta blocker?

-blocks hypogycemia warning signals, so in DM P, use B1 selective one BUT if DM p has MI, benefits outweigh the risks here

What are the 4 selective B1 only blockers?

-Atenolol
-Metoprolol
-Esmolol

-Acebutolol

What receptor binds Ach to constrict pupil (meiosis)?

-M3

What receptor binds NE? to dilate pupil (mydriasis)?

-A1, by contracting radial fibers

Accommodation is purely under PNS CONTROL, so involves only M3 R's thus only muscarinic drugs can affect accommodations.

-If use muscarinic agonist get contr ciliary M and get blurry vision b/c focusing for near objects.

-If block muscarinic Ach R's then can't accomodate, can't see near, can only see far.

BLURRY VISION=MUSCARINIC DRUG!

Does an alpha blocker affect accommodation?

NO NO NO NO NO!!! how you can tell it's alpha blocker & not M3 agonist!

P comes in complaining of blurry vision...what kind of drug is it (binds to what R)?

-muscarinic agonist, b/c only PNS & muscarinic drugs will affect accommodation

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