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1

Local Anesthetics (LA)

1-structures

2-pH levels for LA

3-neuron sensitivity ot LA block

1- 
-lipophilic domain---entry of LA into axon
-intermediate chain---amides=metabolize in liver (long acting) &&& esters=metabolize in blood (short acting)
-hydrophilic N terminal= inhibitory Na Channels

2-more acidic= more charged LAs are
but the LA must be uncharged for it to enter into neurons
once in the neruon it becomes charged again, causing Na channel block 
***channels more active= greater inhibition of LAs

3-sensitivity isn't equal
small= first to be blocked (sensory---convey pain)
large= last to be blcoked (motor)
high frequency (sensory)= preferential to low frequency (motor)
*fast first, slow last &&& small first, big last 
*size matters
*if both axons are same size the myelinated ones are blocked first (bc there is less resistance) 

2

1-surface anesthesia

2-infiltration/field block anesthesia

3-nerve block anesthesia

4-intravenous regional anesthesia 

5-epidural block 

6-spinal block

1-topical---very little anesthesia

2-subcutaneous injection---numbs distal to injection
 

3-peripheral nerves or plexus---less LA needed (group)

4-injection of LA into vein w/ tight flow

5-space w/in vertebral canal but superficial to dural sac
-not limited to injection site of L2
-less risk for puncture headache 
-catheter for long term pain reduction 

6-CSF in subarachnoid space 
-limited to injection site below term of spinal cord L2
-less time/discomfort
-less LA needed---bc no metablosim in CSF
-intense nerve blocks 

3

1-absorption

2-distribution

3-metablosim

4-excretion

1-dependent upon: site of injectioncoadmin w/ vasoconstrictors (epi & levonordefrin)
---
vasoconstrictors are given so drugs stay where its supposed too---if given w/in BV bundle it will leave the body quickly

2-given to all tissues---passes BB barrier= CNS side effects
-esters metabloized in plama= too fast to be redis at low doses
-amides taken up by everything but muscle & gut
-amides highly bound to plasma proteins---affected by cancer & etc

3-amides metabolized in liver (CYP 3A4) & esters by plasma esterases
-CSF doesnt have esterase---so less LA needed for spinal block ---so give esters

4-water soluble metabolizes taken away in urine
acidification of urine promote excretion

4

1-epinephrine

2-side effects

3-CNS

1-helps LA stay longer so less LA needed
-dec rate of absorption & prolonged anesthesia via vasocontriction at site 
-reduces amt of LA needed to reach effect 
-can vasodilate skeletal muscle=inc toxicity
-shouldnt be given at peripheral sites= hemostasis= bleeding 

2-adverse effects bc of accidental intravascular injection of LA

3-seizures then depression
low conc- sleepiness, dizziness, restlessnes, euphoria
high conc- shivering---CNS depression= resp failure->death
-restlessness & tremor---tonic convulsions
-barbiturates treat convulsions

5

1-cardio system

2-peripheral nervous system

3-blood

4-allergic reactions

5-pregnancy

1-minimal changes in electrical excitability, conduction rate & force of contraction
-@ high levels= depression of cardiac excitability to collapse
-all LA are vasodilators except cocaine
-Bupivacaine= cardiotoxic= hypotension & arrhythmias

2-prolonged sensory & motor deficits (prilocaine)
 

3-high doses of prilocaine or benzocaine=
conversion of hemoglobin to methemoglobin= O2 not carried causing anemia

4-allergic reactions---mainly ester LA
allergic dermatitis & asthma attacks

5-LA can cross placental barrier...so CNS, peripheral & cardiac can be affected

6

Amides

1-lidocaine

2-bupivacaine

3-mepivacaine

4-prilocaine

5-articaine

1-most widely used LA
-for all types of local anesthesia
-good diffusion & penetration

2-longest duration of action of all LA (good for long term procedures)
-more sensory than motor block so its useful in analgesia during labor 
-not needed for intravenous anesthesia bc of cardiotoxic potential (blocks Cardiac Ca channels)

3-similar to lidocaine in potency & toxicity
-not topical 
-if sulfite allergies---3% mepivacaine solution w/o epi in it
 

4-less toxic & effective than lidocaine
-if sulfite allergies---4% prilocaine solution w/o epi in it
-infiltration anesthesia---not topical
-if intravascular= anemia by methemoglobin

5-metabolized in 2 places
-rapid metabolized in plasma & the rest in the liver

7

Esters

1-benzocaine

2-cocaine hydrochloride

1-topical for surface anesthesia---skin & mucous
-toxicity bc of methemoglobin, but toxicity low 
-poor H20 solubility, not well absorbed 

2-topical only
-drug well absorbed via mucous membranes 
-high abuse potential
-only LA that is vasoconstrictive
-low toxicity= nervousness/convulsions/cardiac failure
-if w/ epi= inc cardiac toxicity

8

Anesthetic state

1-amnesia

2-immobility in response to noxious stimulation

3-attenuation of autonomic response to noxious 

3a-balance anesthesia

4-preop surgery

5-induction & maintenance of anesthesia

6-post op recovery

1-depressing neuronal activity in hippocampus

2-inhibiting conscious brain acitivity or reflexes
---absolute relaxation

3-sensing of pain the autonomic system will inc HR & BP
-combo drug therapy to reduce neuronal activity
-sensory neurons sense pain, causing reflex of BP inc

3a-multiple classes of drugs to get certain anesthesia
-relaxers, opoids, N2O, inhaled IV etc

4-serotonin receptor antagonist & histamine antagonist to prevent vomiting & acid reflux---reduce regurgitation (bc of lower esophageal sphincter)

5-intravenous GAs are faster acting than inhaled
-some inhaled = unpleasant orders but inhaled are used for maintenance
"balanced anesthesia"

6-hypertensive
-emergence excitement---restless, crying, moaning
-hypothermia---give NSAIDS
 

9

1-inhaled GAs
 

2-pharmacokinetics
a-high water solubility
b-low water solubility
c-blood/gas partition coefficient 

3-N2O speed of induction vs Halothane

4-potency

1-N2O is a gas---others are voltaile

2-effect of gas is proportional to conc of CNS
-rate of GA diffusion= rate of aesthetic induction/recovery
-inhaled GA rate of recovery= imp---faster effects of inhaled GA wear off post-surgery, faster the patient can recover & spend less time in recovery

2a-slow induction---long time for GA to fully dissolve in blood before entering CNS

2b-rapid induction---GA not soluble in blood and goes from blood to CNS

2c-measure of water solubility---GA in blood/ GA in lung

3-N2O= poorly sobule in blood---rapid inudction(low#)
Halothane= very soluble in blood= slow induction(high#)

4-Minimum alveolar concentration---conc of inhaled GA in 50% of patients to not respond to pain (pin prick)
-proportional to lipid solubility
-inc speed of induction= dec H20 solubility
-N20= doesnt take long to saturate blood to brain
-Halothane= takes long to saturate bc more soluble

10

1-Nitrous Oxide (N2O)

1a-acture exposure

1b-chronic exposure

2-isoflurane

3-sevoflurane

1-weak anesthetic---rapid inudction & recovery 
20% inhaled air= analgesia 
30-80% inhaled air= sedation
-analgesic can be abolished with opoid antagonist---so uses opoid receptors 
-colorless & odorless
-used to relieve anxiety 

1a-depresses ventilary response to hypoxia
-air pockets expand 
-change BP
-doesnt trigger malig hyperthermia
 

1b- infertility & abortion
-blood dyscrasias 
-neuro deficits
-dec vit B12---reduced myelin & nucleic acids

2-inhaled GA
-eliminated unchanged via the lungs (not really metabolized)
-dec in BP, vasodilation only
-tachycardia
-dec ventilary= hypoxia

3-reacts w/ dried out soda lime to produce CO---airway burns possible fire
-non-irritating to airways & induce anesthesia
-eliminated unchanged via lungs (not really metabolized)
-dec in BP, vasodilation
-short term renal damage

11

1-pharmacodynamics

2-pharmacokinetics

3-pharmacotherapeutics

4-pharmaceutics

5-toxicology

1-branch of pharm that deals w/ biochemical & physiological effects of drugs & mechansms underlying effects

2-deals w/ quantitative description of the time course for absorption, distribution, metabolism & excretion of drugs

3-deals w/ use of drugs in tx of specific disease 

4-chemistry, compounding, formulation & dosage

5-adverse effects of drugs & other agents

12

1- actions of body

2-actions of the drug on the body

3-ADME overview

4-narrow therapeutic

5-wide therapeutic

1-ADME---absorption, distribution, metabolism, & excretion

2-therapeutic effects, side effects, & toxic effects

3-oral tablet taken, drug is dissolved, absorbed into GI, goes into plasma, bound to drug or free drug (only unbound)
drug can be metabolized & have some sort of effect

4-chemo agents & general anesthetics IV 

5-polyethylene glycol (miralax)

13

1-bioavailability 

2-factors that determine blood levels of a drug

3-enteral 

4-parenteral (injection)

5-topical

6-inhalation

1-fraction or percentage of drug dose that reaches systemic circulation---determined from area under the time vs plasma conc curve

2-amt given, route of admin, rate & extent of absorption (epi & levon reduce these in anesthetic), distribution to tissues, & rate/extent of excretion

3-drug intro at some part of the GI tract (SI)
oral ingestion

4-intravenous---no absorption, very rapid of high BP
intraarterial---not very common, invasive
intramuscular---drugs w/ slow/erratic absorption from GI
subcutaneous---<2 mL vol given
intrathecal---direct injection into subaracnoid

5-skin, more keratinized than mucous membranes---less systemic---keratinized skin= less likely it'll absorb
-mucous membranes= systemic 

6-general anesthetics---asthma medications

14

1-absorption of drugs

2-passive, paracellular transport

3-passive diffusion
 

4-active, facilitated diffusion

5-active, drug transport

1-for drug to be absorbed must pass through intracellular gaps or cell membrane

2-limited to small sized molecules 

3-most common drug transport & greatly affected by pH
----materials move down conc 
---small quicker than large
---lipid solubility
---pH effects- only non-ionized forms can cross membranes

4-no input of energy, requires conc gradient---glucose w/ GLUT4 transporters in muscles cells

5-5-fluorouracil chemo agent

15

1-acidic drugs

2-basic drugs

3-pKa

4- influencing drug absorption

1-aspirin---non-ionized (absorbed) at low pH & ionized (not absorbed) at high pH

2-codeine---non-ionized (absorbed) at high pH & ionized (not absorbed) at low pH

3-pKa is the pH at which half the drug is in ionized form.  
pKa= pH + log (protonated drug)/(non-protonated drug)

4-H20 solubility, area of absorbing 
Blood flow to area---epi & levono = vasoconstrictors & dec BF
rate of gastric emptying & transity 
presence of food, lipids or drugs

16

1-oral/nasal mucosa absorption

2-stomach abosrption

3-small intestines absorptions

4-formulations

5-BB barrier

6-placental barrier

7-binding to plasma proteins

8-sites of loss 

1-neutral drugs/weak bases are absorbed
-first pass metabolism by the liver

2-acidic environment---favors ionization of most drugs
-bc of small surface area & low pH, few drugs absorbed from stomach

3-large pH gradient---acidic & basic---portal hepatic circulation delivers drugs to liver (main metabolism) 
-some drugs can be metabolized on first pass (first pass effect)

4-eneteric coating & sustained release 

5-prevents passage of large or ionized molecules---less of a barrier in kids as in adults
 

6-similar to BB barrier but less selective

7-albumin is the most imp. one---bound drug cant distribute to tissues 

8-fat & GI & others 

17

1-liver

2-kidney


3-fat

4-brain

5-fetus

6-teeth, gingiva & saliva

7-volume distribution

1-large BF, drug metabolism, portal-hepatic first pass

2-high BG, site of excretion

3-low BF, slow accum of lipid soluble drugs, site of loss

4-BB barrier, small lipid soluble can cross

5-placental barrier isnt stong

6-applied topically or injected, pH can affect

7-not true volume---volume which drug would have to be dissolved to acct for all drug at conc in plasma
= amt of drug in body/concentration in plasma

18

1-drug metabolism

2-microsomal oxidation of drugs (phase 1)

3-non-microsomal

4-reductions

5-hydrolyses

6-conjugation reactions (phase 2)

1-active drug (non-polar) then metabolized into inactive drug (polar)

2-"pinched off"---pieces of smooth ER 
highest conc in liver 
contain mixed function oxidases & cyto P450
induction & inhibition of microsomal drug metabolizing

3-some oxidative enzymes arent associated 
in hepatic & extrahepatic 

4-microsomal & non-microsomal

5-mostly non-microsomal

6-coupling of drugs or metabolites to small polar molecules
-microsomal & non-microsomal

19

1-kinetics

2-factors affecting metabolism

renal excretion
3-filtration

4-tubular secretion 

5-reabsoprtion 

6-biliary & fecal excretion

1-determined by conc of drug in relation to the saturation of the metabolic enzymes

2-age, disease, nutrition, genetic factors & duration of tx

3-low MW drugs are readily filtered
-drug bound to plasma protein isnt excreted
-alterations in GFR can affect drug excretion 

4-active process
-system for organic acids & base
-competition of drugs for transport systems

5-passive
-lipophilic are reabsorbed---hydrophilic remain in tubules
-pH effects on acids/bases---acidic urine favors excretion of basic drugs, basic urine favors excretion of acidic drugs

6-secretion of conjugates in bile
enterohepatic cycling
 

20

1-clearance

2-kinetics of drug elimination

3-plateau principle

1-rate of elimination/ concentration
-elimination of the drug from the blood by all routes

2-elimination of most drugs= 1st order kinetics some are 0 order kinetics
1st order elimination= depends on conc of drug that is present, exponentialfixed half life
0 order elimination= rate of metabolism doesnt depend on conc of drug, linear, no fixed half life

3-time course of drug action w/ multiple dosing regimens
-double the dose---inc conc but will take a while to reach the plateau
loading dose- give a relatively high dose of drug to achieve blood level 
maintenance dose- once high level, cut back to lower dose to maintain blood level

21

1-agonist

2-competitive antagonism

3-affinity

4-intrinsic activity

5-potency

6-efficacy

1-drug interacts w/ receptors to activate mechanisms/transduction 
---affinity & intrinsic activity

2-binds to the same site but has different reation
prevents agonist from binding to the receptor
---affinity & no intrinsic activity

3-propensity of drug to bind to a given receptor

4-describes ability of a drug to initiate response---activates receptor or initiates specific signaling

5-refers to amt of drug needed to produce a given effect 

6-refers to ability of a drug to produce an effect w/o regard to conc

22

Q image thumb

1-Drug A= more potent than Drug B (Drug A bc takes less nM to do the same amt Drug B---less needed to have a given response)
Drug A & B= similar efficacies
Drug A= more potent & more efficacious than Drug C (drug A taller)

23

1-graded dose response relationship

2-threshold dose

3-potency

4-maximal effect (efficacy)

5-slope

6-bio variation

7-quantal dose response relationship

1-shows intensity of a drug effect in a subject 

2-dose below which no effect is seen

3-position of curve on X axis---pharmacokinetics of drug & ability of drug to bind to receptor & produce an effect

4-determined by both pharmacokinetics of drug & ability to produce an effect 

5-varying the dose will affect response
very steep slope= slight inc in drug dose= large inc in response 
shallow slope= small inc in dose= less effect on intensity

6-give same dose to diff subjects= may have diff intensities 
-diff doses of a drug may be needed to produce same intensity in diff people

7-% of subjects in a pop that exhibit a response of a given intensity as a function of drug dose
-compare effects of diff drugs in a population
-comparing doses of a single drug that will produce different effects in a pop

24

1-intravenous GAs

2-propofol

3-etomidate

4-ketamine

1-fast acting drugs---surgical anesthesia
-highly lipophilic
-goes to CNS & spinal cord

2-MJ death
-heavy sedation---only used if heart is healthy & isnt high TAG level 
-not H20 soluble 
-very fatty
-enhanced GABA 
-dec in BP, vasodilation & contractility
-dec ventilation 
-anti-emetic---*widely used bc of this
 

3-intravenous GA
-same action of propofol except it is emetic

4-water soluble---comes concentrated 
analgesia ---doesn't need an opoid
battlefield use
-competitive antagonist & inhibition of Na channels
-no pain on injection
-hallucinations= drug of abuse "special k"
-modest dec in ventilation rate= bronchodilator
-inc BP, inc CO, inc HR...good for pts w/ hypotension
-frequent peeing

25

1-GA Adjuncts

2-benzodiazepines

3-opiods

4-hypothermia

5-malig hyperthermia

1-drugs used in addition to GA---dec the dose of GA to get anesthesia (balanced anesthesia)

2-Midazolam
-used for pre-op sedation (amnesia)
-dec brain metabolic rate, dec BP & dec ventilation
-H20 soluble
-no pain on injection w/ rapid onset 

3-fentanyl
-potent analgesics (only ketamine isnt opoid)
-minimize reflex to noxious stimuli 
-dec ventilation---why you can die from overdose= stop brathing 
-incapacitate individuals (hostage) 

4-core body temp is below 36 celsius 
-common in long operations...many GAs cause vasodilation= heat loss 
-cardiac arrest, unstable angina & MI
tx= heat

5-adverse to inhaled GA
-core body temp increases to over 42 bc of uncontrolled muscle rigidity
-most inhaled GAs, except N20 cause malig hyper
-genetically susceptible
-bc of aberrant skeletal muscle myocyte---ryanodine Ca channels dont close= loss of heat---fatigued myocte lyse= release of K

---tx= dantrolene---ryanodine receptor inhibitor-treats spasms

26

1-NMJ blockers

2-nondepolarizing (competitive) NMJ blockers

3-depolarizing NMJ blockers

1-causes relaxation of skeletal muscles
-dont pass BB barrier w/ no CNS effect
-intravenous
-small fast muscles, limb trunk, intercostal & diaphragm
-dantrolene treats malig hyperthermia & controls muscle spasms

2-rocuronium---competitive antagonist
-block of gang muscarinic receptors= tachycardia
steroidal
liver metabolism
very rapid---relax larynx & jaw for tracheal intubation

3-succinylcholine---very short/fast
-initial fasciculations in chest & abs
-degraded by plasma choline esterase 
-post ions enter neg charged cell---excessive opening of receptors by SCh results in dec electrochemical force= less positive entry in presence of AcH= less muscle response 

27

1-autonomic nervous

Anatomical Organizaton

2-origin
 

3-length of pregang fibers

 

1-independent---not under direct conscious control
-concerned w/ CO, BF & digestion
-Symp= fight or flight---stress response
-Parasymp=rest & digest= more active
---both are always on

2-symp=thoracocolumbar
parasymp=craniosacral

3-symp=ganglia are near spinal cord= short fibers
parasymp=gagnlia are closer to effect=far from spinal cord= long fiber

28

1-parasymp

2-symp

3-symp cholinergic

4-adrenal medulla

5-myasthenia gravis

1-pregang fibers enter ganglia at synpase---AcH released to bind to nicotinic---releasing AcH---going to postgang muscarinic
*always muscarinic for parasymp

2-pregang fibers enter ganglia at synpase---AcH released to bind to nicotinic---releasing NE---going to postgang adrenergic (alpha or beta)
alpha= BV---to shunt blood away from GI to skeletal
beta= inc BF in skeletal muscle

3-pregang fibers enter ganglia at synpase---AcH released to bind to nicotinic---releasing AcH---going to postgang muscarinic in SWEAT glands via SYMP system

4-pregang fiber innervates medulla---releases AcH &binds to nicotinic & releases Epi into bloodstream for a generalized effect by activating adrenergic receptors throughout

5-nicotinic receptors are destroyed= muscle weakness
-tx= AcH esterase inhibitors to inc levels of AcH by nicotinic receptors

29

1-nicotonic receptors

2-muscarinic receptors

3-Alpha receptors

4-Beta Receptors

1-Nn= neural= autonomic & adrenal medulla
Nm= neurmoscular junction

2-parasymp organs, brain & sweat glands
-usually w/ secretion modulation or increase in secretion
-SM contractions
-most drugs= nonselective 
 

3-a1= BV, urinary sphincer & eye for SM contraction
a2=pancreas (inhibition of insulin secretion), GI sphincters & CNS

4-B1= heart (inc rate/contraction) kidney (inc renin)
B2= SM relaxation---skeletal BV 
B3=bladder (SM relaxation)

30

1-eye

2-secretory 

3-heart 

3-BV of mucosa etc

5- BV of skeletal muscle

6-airways

1-symp= dilation (mydriasis) a1
inc aqueous humor b2 
parasymp=constriction (miosis) & contraction (muscarinic)

2-symp= dry mouth, viscous---a & b
inc resp secretions= b2
parasymp= inc secretions (watery)

3-symp= SA, ventricles, AV= inc = B1 & B2
parasymp= SA, ventricles, & AV= dec

4-symp= constriction- a1 a2
parasymp= dilation

5-symp= constriction a1 & dilation B2
parasymp= dilation 

6-symp= relaxation b2
parasymp= constriction

31

1-GI tract
 

2-urinary bladder wall & sphincter

3-kidney JG cells

4-Uterus

5-male sex organs

6-liver/fat cells

7-goose bumps

1-symp= relaxation a1,a2,b1,b2
dec motility
parasymp= inc motility & spasms

2-symp= relaxation B2 & b3
contraction A1
parasymp= constriction & relaxation

3-symp=inc renin secretiom---B1

4-symp= contraction---a1
relaxation---B2

5= symp= ejaculation
parasymp= erection

6-symp= inc glucose B2 & fatty acid output B1

7-contraction a1 & secretion (muscarinic)

32

1-bladder

2-botox

1-symp= when bladder is filling you have B2 & B3 on the bladder so you have relaxation so you can fill the bladder
A= SM contraction of sphincter (keeping it closed)
parasymp= involuntary muscarinic 
---contraction of muscle lining bladder & relaxation of sphincter (so it can be released

2-blocks AcH release by inhibiting fusion of vesicle w/ plasma membrane to stop release of AcH---stops wrinkles by paralyzing the tissue

33

1-muscarinic agonists

2-actions of muscarinic agonists

3-adverse muscarinic agonists

4-contraindications of muscarinic agonists

1-acetylcholine
bethanechol
pilocarpine
cevimeline

2-***think parasymp
inc GI motility
Dec HR
Dec BP---Dec CO & vasodilation
Contraction of bladder & relaxation of sphincter
Miosis
& Dec intraocular pressure
Stimulation of secretions 

3-bc of excessive muscarinic
---hypotension, bradycardia, bronchoconstriction, diarrhea, cramping, incontinence, sweating

4-if they have asthma, cardio, peptic ulcer, hyperthyroidism, weakened bladder or obstruction
---if they have tehse then dont give agonists

34

1-bethanechol

2-pilocarpine

3-cevimeline

4-acetylcholine

5-cholinesterase inhibitor

6-irreversible inhibitor 

1-promote GI motility ---fixing digestive type stuff 
---so GI & peeing

2-tx of glaucoma
-tx of salivary gland dysfunction---Sjorgens syndrome so it will inc salivary amts

3-salivary gland dysfunction---xerostomia

4-tx of glaucoma
easily degraded

5-edrophonium
physotigmine
neostigmine
pyridostigmine
rivastigmine
donepezil
carbmate insecticides

6-organophosphate insecticides---parathion malathion
sarin
DFP

35

1-cholinesterase inhibitor effects

2-cholinesterase inhibitors adverse

3-tx of cholinesterase inhibitor poisoning

4-neostigmine

5-pyridostigmine

6-edrophonium

1-*similar to para
preventing breakdown of AcH in synpase
-inc GI motility 
-contraction of bladder & relaxation of spincter
-bradycardia & hypotension 
-inc sec
-dec intraocular pressure
-stimulation of skeletal muscle (therapeutic) & paralysis of skeletal muscle (toxic doses)

2-toxic= crisis...overdose=poisoning 
SLUDGESalivation, Lacrimation, Urination, Defecation, GI distress, Emesis
-skeletal muscle fasciulation= paralysis & bradycardia
miosis

3-atropine then pralidoxime

4-tx of myasthenia gravis
-reversal of neuromuscular blockade
-Quaternary---dont enter CNS 
-long acting

5-tx of myasthenia gravis 
-reversal of neuromuscular blockade
-used in military as nerve agent
-Quaternary---dont enter CNS 
-long acting

6-dx of myasthenia gravis (transient improvement means they have myasthenia gravis)
-Quaternary---dont enter CNS 
-short

36

1-rivastigmine

2-donepezil

3-physostigmine

4-cholinesterase inhibitors contraindications

1-improvement in ability w/ Alzheimers---show a loss of cholinergic neurons 
-so raising levels of acetylcholine can reverse cholinergic deficit 

2-improvement in ability w/ Alzheimers---show a loss of cholinergic neurons 
-so raising levels of acetylcholine can reverse cholinergic deficit 

3-tx of poisoning w/ atropine
-nonquaternary---can get into CNS

4-asthma, cardio, peptic ulcer, GI obstruction

37

1-organophosphates insecticides

2-parathion

3-malathion

4-DFP/isoflurophate

1-parathion & malathion 

2-oxidized to active metabolites
-rapid in insects---insects cant easily detoxify these metabolites but can be toxic in humans
-absorbed in skin

3-oxidized to active metabolites
-rapid in insects---insects cant easily detoxify these metabolites but can be toxic in humans

4-potent & toxic & irreversible
tx of glaucome

38

1-pralidoxime

2-botulinum toxin

3-muscarinic antagonists

4-muscarinic antagonists physio

5-muscarinic antagonists therapeutic

1-cholinesterase reactivator
-used w/in 2 hrs following exposure

2-clostridium botulinum---canned foods
-toxin prevents release of acetylcholine from nerve ending
-affects autonomic nerve endings & neuromuscular junction (paralysis)

3-atropine
scopolamine
dicyclomine
glycopyrrolate
ipratropium
tiatropium
tolterodine
oxybutynin
tropicamide

4-***think symp effects
drying 
dec GI motility
relaxation of bladder & urine retention 
bronchodilation
mydriasis 
inc HR 

5-tx of GI disorders
urology
mydriatic (if have glaucoma dont use)
-prep anesthesia---reduce vagal tone & dry secretions
-antidote for poisoning

39

1-atropine 

2-scopolamine

3-muscarinic antagonists adverse

4-muscarinic antagonists contraindications

5-muscarinic antagonists tx for poisoning

1-cardiac stimulation in emergencies
-nightshade
-tx for poisoning 

2-prevention of motion sickness
-like atropine except it has CNS depressant (sedation & amnesia)
-orally & patch

3-dry mouth , dry skin, constipation, & urine retentionvisual disturbance, blurred, photophobia

4-glaucoma, prostatic hypertrophy 
cardio instability
severe ulcerative colitis (weakenes lining soooo you can get toxic megacolon, dont give to pt if has this)

5-admin of cholinesterase inhibitors
-ice baths to reduce hyperthermia
-pt in dark, prevent photophobia & excitement

40

1-dicyclomine

2-glycopyrrolate

3-ipratropium

4-tiatropium

1-nonquaternary---can cross BB barrier
-intestinal antispasmodic & tx of IBS

2-quaternary---no CNS effects 
-preop med to dry secretions & inhibit vagal

3-quaternary---via inhalation for tx of asthma & COPD
-few systemic effects

4-quaternary---via inhalation for tx of asthma & COPD
-few systemic effects

41

1-tolterodine

2-oxybutynin

3-solifenacin

4-tropicamide

1-tx of urinary incontinence bc of over active bladder

2-tx of urinary incontinence bc of over active bladder

3-tx of urinary incontinence bc of over active bladder

4-dilate the pupil for eye exams