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toxicology
it is a study of a drug, toxin, chemical or natrually occuring substance
most reporte poising invovle ..
everday house hold items such as medicnies, cleaning supplies, comsmetics, and personal care items.
all resusitations begin with the simple atidone....DONT
Dextose
Oxygen
Naloxone
Thiamine
Dextrose
part of DONT..
Hypoglyceima is a common cause of coma and stupor... and shoud be asses or treated empiricallly in all patietns with deceased level of consciouness..
One ampule of D50 only raise the blood sugar by about
60mg..in average 70kg
Oxygen
part of the DONT...

airway protention and asisted ventilation lead to successful recovery for most paitents with acute drug induced coma...
In regards to the O of DONT

you must continusly monitor airway patency and protective reflexes....b/c
as one continues to absorb a drug it cna lead to abrupt changes in the level of unconsicouness and increaeed risk of acute pulmonary aspiration of gastric contens... or res. arrest.
Does a pulse oximeter guage ventilation...
no, it esitmates oxygen content... it also does not accurately estimate oxygen saturation in patients with CO poisning.. you need a Cooximetry..
Naloxone
part of DONT.. it is based on the premise that patients with depressed airway reflexes or hypoventilation may respond ot reversla agents such as naloxone.. or flumazenil
Naloxone conintues to be used widely as an empiric antidoet for any patient with even a vague supsicin of
opiate intoxication.
how come you dont want to use Flumanezil for the N of DONT
becasue it might induce seizures in patients who have also ingested TCA or other congestoins. and it might interfere with benzos..
all patietns with clasic signs RR <12 pupis mitoic, and needle marks should be given...
naloxone
beware of withdraw from what of the DONT..
naloxone
Thiamine..
part of the DONT. it is given for the following
Alltered mental status (wernkies encepthopahty)

Malnoushed pts

Hx of Alchol

Vomiting prolonged Hx

Pts who are chronically ill
what are the decontamination methonds
Gastric Lavage
Activated Charcol
Multple Dose activated Charol
Whole Bowel Irrigation
Gastric Lavage
A dectonamination method.

in certain stduyes gastirc lavae was associated with a higher incidence of medical intensive care unit adminssons and aspiratoin pneumonia.

you should consider gastirc lavage if the patient has massive ingestion, presents early, or is severly ill, without antecedent vomiting.

also consider gastirc lavage for substances not bound to charcoal.. or substacnes that delay gastirc emptying or for Bezoars
what are the toxins that are poorly bound by actived charcoal
Caustics
Heavy metals.. Li
Alcholos
Rapid onset/Absor. (CN, lq)
Cl an Iodine
Othres (insouble tablet form)
Aliphatics (petrol distillate)
Laxitives (Na Mg Salts)
What are the toxins that form Bezoars
Baribituates
Iron
Glutethamide
Meprobamate
Entirc Coated tablets
Salicylates
Sust. release tablets
Activated Charcoal
typen of Decon. method

it is as effective of gastric empthing.

Acitvated Charcoal is recommended in all cases of orally adminstreed dru intoxicatoins excetp if the durg is not bound by charcoal
Activated Charcoal is safe although vomiting and diarrhea are seen when..
cathartics such as sorbital are added.
one can get constipatoins with actvated charcoal when...
cathartics are withheld.
what is a serous adverse effect of Activated Charcoal...
pulomnay aspiratoin of actived charcoal along with gastric contents..
Multpile Dose Activated charcoal...
it is type of Decon. rxn

aslo refered as gastro int. dialysis
MDAC is thought to produce its benifincal effect by ...
interrupting the enteroenteric and in some cases the enterohepatic recirclation of drugs.... also it that any remaing unabosrbed drug may be adsorbed to the repeated doses of activated charcoal..
Whole Bowel irrigation..
a type of Decon. Methoud..
Basically you give polyethylene glycol to flugh out the GI tract and Decrease the time avaibble for the drug to be absorbed...
What is the reccomendation forn WBI
it is reccmended in cases involinbg body packers and in situations in whcih LARGE amounts of drug or toxin may still be present in the gi Tract due to concretoins or Bezoars formation (think FE) or when sustained release is invovled (Ca Channle Blocker)
What is a toxidrome
they are collectoins of symptoms characterstic for specfic agent groups..
Anticholinergic Mneu.
Hot as a hare mad as a hatter dry as a bone and Red as a beet

HR Inc
Blood Pressue Inc
Pupil sixe Inc
Mental Status Agitated
Skin Dry
Bladder Normal
Bowel Sound Decreassed
Sympthomemit
HR inc
BP inc
Pupil size Inc
Mental Status Agitated
Skin Wet
Bladder Size Norm
Bowel Sound Normal
what is Opoid synd
Depressed mental status
Miosis
Decreased Respiratoins... this is why they die
Cholinergic Toxidrome
Musc. Symptoms
Diarrhea
Urination
Miosis
Bronchorrhea
Emeiss
Lacrimation
Salvation
Cholinergic toxidrome
Nicotinic Symptoms
M mydriasis
T Tremor
W Weak
tH HTN
F fasculations.
what are the agetns that cause cholinergic toxidreom
Anticholinesterases(organophosphates)

Carbmates (physo and neo stimgmine)
Sedative Hypnotic toxidrome
Depressoin #1!!!!!
bradypnea
Hypotension
Ataxia
Hyprefle
What are causes of Sedateve hypnic toxidroem
Benzo
Barbs
ethanol
Skel Muscl Relax
Salicaityes toxidroem
SOB
increased Breathing
N/V
Tinnitus.....
Diaphories
ToxicoKinetics..Absoptoin
First order
the physical sate of malecule affects it. its faster if
...lq
...non inon
...molec size is small
Bioavil.
the fractoin of dose that is abosrbed and reaches the blood stream..
First Pass t
this refers to met. that occurs befor eth agent recahces the systemic circ.
Liver
Stomach
Stomach and the first pass effect for some compounds...
Cocaine.. it hydroxed by watere

Ethanol... Alcohol dehydro.
Distributoin
this refers to the movement of the agent form the blood to the tissues getting to the target organ..
redistr.
an has concentrated in and endorgan such as the brain.. and overtime.. the agent redistributes from the brain back into the bloodstream; re-elevating blood levels in a delayed fashion.
protein binding
only unbound drug is active.. and hemodialysis can not remove bound drug.
Volume of disr. (Vd)
a measure of the apparent space that a dose of drug would distribue into if the congentratoin of the durg was equal thoughout that volume
the Vd is increased for..
fat soulbe agetns.. since it is able to cross many membranes and enter many compartments
a very large Vd reflects that
most of the drug is not in the plamsa... Vd>1L/kg that is large... thus not good for hemodyalsis.
first order kinetics
a stey fractoin amount is revoved per unit time.

THE ENZYMES ARE NOT SATURATED...

ITS DONE IN 5 HALFLIVES
ZERO ORDER KINITECS
A STEADU ABSOULTE AMOUNT IS REMOVED PER UNIT TIME

THE ENZME IS SATURATED. THUS HIGHER CONCENTRATOINS OF THE DRUG WILL NOT BE MET. FASTER

ETHANOL IS THE CLASSIC EXAMPLE
ACETMANIPHEN IN REGARDS TO DRUG MET.
THE ORGINAL COMPUND IS NON TOXIC.. AND 5% OF THE DRUG IS MET TO NAPQ1... WHICH IS HEPATOTOXIC... AND GLUTHATONE IS A KEY SULFOR DONOR TO GET RID OF NAPQ1.. THUS IF THE IS REPLEATED YOU CAN GIVE.. N-ACTEYL CYSTEINE..
NAPQI IS PRUDUCED BY
CYP 2EI
WHY DO CHRONIC ALCHOLICS HAVE INCREASED TOXCIITY REALTED TO ACETMANIOPHEN...
BY THEY HAVE REVVED UP CYP2EI METBOLISM.
ALKALINE DIRUESIS WILL INCREASE THEE EXCREAOTIN OF
WEAK ACIDS
SUCH AS PHEONBARBITAL AND ASPIRIN.
ACID DIURESIS MAY BE EFFECTVIE AGAING
WEAK BASES SUCH AS AMPHE AND PHENCYCLIDINE... BUT THIS IS RARELY DONE B/C IT IS VERY DANDEROUS
How is enhancing elmination done
Alakine dirues
Acid Diuress
Hemodialiss
Pulse does of activaed charcoal
Pulse dose of activated charcaol.. it
enhances elmmination of drugs such as theophylline and phenobarb
what are some of the indicatoins for enghaced eliminaton of posions
drug has small volume of dist
metobiltes. if toxic must be removied

supportive measu are not suff
toxciity must be reverisble and plasma [] dependent
ACPM toxcity 5-8 days
fulminant hepatic failure
what is key assemst for acetaminophen
Acet. Level at 4 hours from the timee of ingestion.
when is nomogram not helpful in a ACPM toxicity
if the time of overdose not known.
beware of Tylenoal Er and Coningest with anticholin such as tyleonal PM which have diphendydramine..
in these cases you may need to do more than one APAP levle to determine if the patient is at rsik
in ACPM toxciity what test should you follow
LFT and coagulation Profile INR, PT/PTT
if thee PT is greater than the number of hours from the time of ingestion in regards to ACPM toxciity you need to..
prepare for liver transplant
in regards to aboptoin in tx of ACPN toxcity
charcoal decreas absortpin and is more effective if given early and does not decrase the efficacy of NAC
in readards to distrubion in ACPM tox
small vd but dont do hemodial
in reards to met and Acpm tox
THIS IS THE KEY FACTOR IN DETERMING SUCCESS OF ANTIDOE

NAPQI.. WHEN HEPATIC GLUTATHONE STORE DECREASE BY 70% NAPQI STARTS BINDING AND DESTROING CELLUAR PROTEINS AND MEMRANE

NAC ACTS TO REPLENISH GLUTHIONNE STORES..

GIVES CENTROLOBAR NECROSIS
WHAT INDUCES CYP2EI
ALCOHOL
CARBAMAZAPINE
DILATIN
ISONIZID
PHENOBARBITAL
ACUTE SALICYLATE TOXCITY
TACHYPNEA HYPERNIEA
N/V
DIZZY
DIAPHOR
TINNITS
RES. ALAKLIS
MET. ACIDOSIS
WHAT ARE SOME OF THE LAB FINDINGS OF SALCYL TOXCIITY
ANION GAP ACIDO
DOES NOT HAVE A NORMOGRAM (WHERE A SINGLE LEVEL CAN ACCURTLY REFECT TOXCIITY IF WAS ACUTE EXPOSURE)
THE PROBMLEM WITH PLASMA SAILICATY [] IS THAT THE LEVEL CAN BEGIN TO DECREASE WHILE THE PATIENT IS GETTING WORSE
WHATS 2 THINGS YOU MUST ASSCESS IN SALICALY TOXCIITY
1. SALICIALTYE LEVEL
2. CLINICAL SYMPTOMS AT THE SAME TIME

THE PREMISE IS THAT LEVELS MAY DECREAE B/C IT IS EITHER BEING ELMINATED OR B/C IT IS ENTERING THE CENTRLA COMPARTMENT IE BRAIN OR OTHER TISSUES THUS THE PTS SYMPOTSM ARE WORSEING.
IN REGARDS TO SALYCL TOX ABSORTPION
CHARCOAL DECREASE
IN REGARDS SALCY TOX.. MET. AND ELMIN
MDAC-- GIVES YOU INCREASED ELEMINATOIN.

ION TRAPPING URINE ALKALINIZATION
....THIS IS IMPAIRED BY HYPOVOL OR HYPOKAL

HEMODIAL...B/C SAL HAVE SMALL VD....ASLO CORRECTS FLUID AND ACID BASE ABONRMALITIES... USED IN SICKER PTS WHO HAVE ACID BASE ABNOR. OR CERBAL EDEMA
IN REGARDS TO SACLY POISING.. WHY USE MDAC
B/C SALICYLATES CLASICALY ARE ASSOIATED WITH DELAYED GASTRIC EMPTYING

AND ASPRIN TABLETS HAVE BEEN ASSOCATED WITH FOMRATION OF CONCREATOINS.. AND THESE CONCRETIONS MAY EVENTALLY BREAK UP AND INCREASE RELEASE OF MORE SALICYLATE.
IN CHRONIC SALICYALTE POISING YOU SEE
ALTEREND METNAL STATUS
Methylsalicylate (oil of winter green
one teaspoon ahd 4000mg salciylates
one teaspoon can be toxic to children
What are the various prepartions of Fe
Fumarate
Sulfate
glutmate
what are the phases of Fe poisning
1. local toxic effects N/V GI ulcers, GI bleeding

2. 6-24 hrus following the intial overdose.. Gi symptoms diminsh

stage 3 12-24 hrsHYPOVOLEMA, VD, Cardiac Depressoin, no oxidative phospholatoin, METABLIC ACIDOSS

Stage 4 Hepatic failure 2-4 days

Stage 5 rare .. stricturues and caring of GI
in regards of Fe tox Absorptoin
DONT NOT GIVE CHARCOAL
BEWARE OF BEZOARS
DO WBI....
IN Regards to Fe tox Dist.
total iron binding capcity may be altered after acute overdose but it should not be used as indicator of toxicity...

free iron rapidly diffused into cells and tissues ESPCIALLY THE LIVER.

TX IS MOT EFFECTIVE IF A CHELATION IS PROVIDED PRIOR TO DISTRIB INTO TISSUES
IN REARGDS TO FE TOX ELMINATION.
Deferoxamine.. a specific chelator for acute iron overdose...
IN THE PRESCENCE OF FERIC IRON DEFEROXAMINE FORMS A COMPLEX CALLED..
FERRIOXAMINE WHICH IS EXCRETTEDN BY THE KIDNEYS..
DEFEROXAMINE CHELATES..
FREE IRON AND IRON TRANSPORTED B/W TRNAFERRITIN AND FERRTIN, BUT NOT THE FE PRESENT IN HgB, Hemosiderin or ferrtin.
what are the indications for the treament of Deferoxamine...
Met. acidosis
repetive Vomiting, toxic app.
lethary
Gi bleeding or signs of shock.
hypotension

give IV
CO poisoning
it is the most common casue of toxic death excpet for alchool
it reulst for combustion and smoke inhlaltion.
what is the most common misdais of CO
viral illness
consdier Co poising when
a group comes in wiht the same sympotms
why do you get met. acidois in CO poisning
b/c of hypoxica, thus get lactate formation.
whats the pathophys of CO posining..
it binds to hb 200-250 times more avidly than that of oxygen.

it shigs oxyhemoblgin curve to the left. thus decreaseing oxygen unloading.

binds to cytochorme oxidase.. cells can not use oxygen.
you get serous toxicity when carbosyhembogling is >
25%w
whats key in looking at CO levels
that levels do not corrlate with toxciity.. patients comatose du to Co can have very low levels after the exposure
CarboxyHb levels are determeined by a
co-oximeter.
How do you treat CO poisning.
Oxygen.. and remove patietn from the exposin envirmonemtn.
in regards to CN toxciity
it is rapidly distrubed to RBC and tissues.. and detoxifactoin occurs via the combination of CN with Sulfur to form Thiocynate.. and thiocynate is harmless and renally eliminated.
What is the pathy phys of CN
CN has a high affinty for metals.. and its most siginifacnt effect is casued by binding to ferric iron of Mito cyto. oxidase .. this is thee same blook seen above with CO...

the body ability to use oxygen is very rapidly stopped and the body shifts to anaeroic met. and a very rapid lactic acidosis
how do diagnosise CN
reconzide the situatoin.. jeweler or labrotry worker..

Artereial blood gass.. see severe met. acidosis b/c of lactate
how to treat Cn
if given orally Charcoal
high flow oxygen
Cyanide kit....
what the cynadie kit
two nitrates
... amyl nitrate for inalif or sodium nitrate for Iv admin

IV sodum thiosulfate
when do you use nitrates for CN posinng ...
only use on symptomatic patients b.c it has its own toxicity..

the theoritcal mech is... nitrates oxidize Fe Hb to Fe 3 and methhb avidly binds Cn thus rmoving CN form the Cirulatoin.
How does Sodium thiosulfate work... in regards to CN poisning.
it increases the detoxifcation rate of Cn b donating a sulfur molecule to the enzyme Rhodanase which catalyzes the formatoin of less toxic thiocynate
What are the big three alcholis
Ethylen Glycol
Isopropanol
Methanol...
What is the acute toxciity of the alcohols..
intially CNS toxciity.. Intoxicated...
whats more intoxicating IPA, EG, ME
IPA
EG is rapidly metabloized to...
calcium oxlate which precipitates in the kidneys and other vital organs to produce direct toxciity
ME produes the classic
Snow storm visual changes in the context of N/V and met. acidosi
which alcohol does not give you Metablic acidosis
IPA, but it does give osmolar gap...
if a pt comes in with sigle digit HCO3 leves and has sever met. acidoss and is not DKA must be considered to have
EG or ME.. but CN can casue this as well
IN regards to Alchol tox
Abosption
CHARCOAL IS NOT HELPFUL
.1ML/KG OF EG RAISED BLOOD TO
20MG/DL
IN REGARDS TO ALCHOL TOX
DISTR.
HAS SMALL VD... HEMODIA. GOOD
MET.IN REGARDS TO ALCHO TOX
THE metbolsim of alchols occurs in a serous of steps that involoe alchol dehydrogenase and aldehyde dehydrogensase.
EG and its met
glycolic acid
glyoxylic acid
oxalic acid
all contr. to its anion gap
ME and its mets
formate.. causes anion gap and ocular toxciity
Isopropanol and its met
converted to acetone and has not anion gap......
Fomepizole
this inhibits alcoohl dehydrogenase therefore stopping the conversoin of toxic alocholol to tis toxic met.
Folinic acid
it enchances the met. of folate in ME toxciity
Thiamine, pyridoxine, Mg
all enhance the met. of blyoxlic acid to less toxic metl in EG
IN regars to n Alcohol tox.. elimn
Dialysis.. this is important if met. can not be blocked.. helpfl given dose dep. kinietics..
methamph.
it is the crystalline form and is smoked,, it has 15-20 timees thee effect of amphet... called ICE>...
what are the mood modfing amphet..
MDMA
MDA
MDEA
amphetamines and its derivatives are all structally based on what structure..
phenylethylamine..

they are weak bases
what is the patho phys of aphe
Direct Apha agonist
Decrease the reuptake of NE and DA
whats different in regards to the mood enhancin amphet
they can release sertonin and block its reuptake,,, thus may cause sertonin syndrome (Rigiid hyperreflex, and hyperprexia)
What is the rebound phase..
this is regards the amphetimine.. it is a phase of prolonged sleep and voracoious eating
whats the treament of amphye toxicity
Charcoal
Alkalin urine ?
why not use Acid urine, in tx of amphem since it is a weak base..
b/c it also inreases myoglobin precipatoin, thus if rhabodyolyis is present it can increase renal failure..
the tertiary amines in TCA are more potent inhibiros of ..
5HT reuptake
the seconday amines of TCA are more potent inhiotrs of
NE reuptake
What is the effect of TCA
amine reuptake inhibition
AntiCholin effet
Alph Blocking effect.. hyopten
Quinidine like effect.. cardiac dist. and hypotension

GABA INHIB.. RES. FOR SEIZURES
Quinidine like effect of TCA is due to
membrane depressant effects on Na channels of the distal conduction system that cuases cardiac conduction dist. and hypotne.
TCA acute toxciity you see
a wide complex tachy that looks like a VT
a young dry agitated seizing pt, with a wide complex tachy is almost alwyas a
TCA overdose
every overdose pt requiera a
EKG
In regards to TCA tox abso
Charcoal
inregards to TCA tox DIS
LARGE VOL OF DIS.. NOT DIAL...BUT SODIUM BICARB MAY LIMIT BINDING OF TRYCYL TO SODIUM CHANNELS
IN REGARDS TO TCA TOX MET
AMITRIPTYLINE AND IMIPRAMINE ARE MET TO SECONDARY AMINES NORTRIPTYLINE AND DESIPRAMINE
WHAT ARE THE KEYS TO TX FOR TCA TOXCIITY
MAINTAIN PERFUSOIN...
TREAT THE CARDIO EFFECTS(QUIINIDIE LIKE EFFECTS)

SEZIURES LOWER PH>>ENCHANCE QUINDINE LIKE EFFECT THUS TREAT SEIZRUES. WITH BENZOS

GIVE NA BICARB..

HYPTOTEN. GIVE A DIRECT AGENT NE

ANTICHOLN TOX.. DONT GIVE PHYSOSTIGMINE...OR FLUMAZANIL, OR TYPE iA ANTIARRHYTHIMCS..
MAO
IT IS AN INTRACELLUALR ENZYME, IN MOST CELLS EXCETP RBC... IT DEGRADES ENDOGNES AND EXONG. BIOGENIC AMINE BEFORE THEY GO BACK INTO VESICLES
MAO-I
INCREASE NERUOAMINES ACTIVITY IN CNS, THUS INCREASE EXCITMENT
MAOI IN THE PRESENCE OF AGENTS THAT INCREASE THE RELAEE OF NERUOAMINES...
HUGE HYPERADRENERGIC RESPONSE..
MEPERIDDINE..
IT IS AN OPIOD THAT BINDS TO MU KAPPA AND DELTA RR

NORMEPERIDINE IS RENALLY ELIMINATED..
NORMEPERDINE AS SOME NON OPIOD ACTOINS..
IT IS HALF THE ANALGEISC BUT TWICE THE NERUTOXICITY OF MEPERIDINE..

CAUES AGITATOIN, TREMOR, AND MYOCLONUS AND SIZURES..
MEPERIDINE.. CAN CUASE
DECREASE NERUONAL REUPTAKE OF 5HT AND THUS CAN CAUSE SERTONIN SYNDROME.
Coccain.. alkaloid..its periphrial effects
decrease the reuptake of epi and ne and increase relae of NE
Coocain the central effects..
in relase of NE and other excitrory amino acides and decrease reuptake of 5ht, da and other excitory amino acids.
what is serotonin sydnrome...
it is a potentially fatal interaction, that occurs when multpile serotonergic agetns are in a person at one time..
5ht met is primarly done by
MAO b/c it is a poor substrate of COMT

in the setting of MAOI and when IC stores of serotonin are expandid any precipitant that icnrease serotonin in the synape (either by increase relase or by decrease reuptake) is potentially catastrophic...