Concise and complete series

Toxicology
inaminute
Aashir Hussain

euIDE

EVIDENce
2

CHAN OF Gusroev
 Chapter 1

cONTENTS
GENERAL TOXICOLoGY
6
GENERAL TOXICOLOGY Terms tounderstand
16 Toxicolog8Y.
cORROSIVES Branch of sciencedeals with
22 poison concerningtheir source,
ORGANIC POISON properties, action, toxicity,
symptom produced, lethal dose,
33 fatal period, treatment and specific autopsy findings.
IRRITANTS (Inorganic) Poison.
41 Anything or substance when administeredthrough any
SEDATIVEAND HYPROTICS possible route and that causes damage to the body.
43
AGRICULTURE POISONS Poison intent to cause harm

46 Medicine intent to save a life.

CARDIAC POISON Fataldose
48 A minimum amount to cause the death of a
8 NALGESICS AND ANTI PYRETICS sufficient
living

organism.
50
9 STIMULANTS Fatal period
52 The time required by a fatal dose to kill.

10 ASPHYXIANTS Active principle

54 A substance in poison capable of causing
11 DHATURA significant damaging
effect e.g.
58
12 CEREBELLOTOXICAGENTS Tobacco Nicotine active principle

Note Itcontains selective poisons

toxins
of the important
only. Rest
should be done from G-friends
toxicology

Dr Azan
Compiled by
 8 GENERAL TOXICOLOGay
9

1.1 Classification

e.g.
Suicidal

organophosphat
e opium, KCN
of human poisoning
Homicidal

e.g. Thallium,
organophosphate,
strychnine,
arsenic
.
Accidental
Can occur due
Use of
chemicals
2. During
C.Nervous SYstem effects
1.Cerebellum effecting
Somniferous
tntOxicated
Deliriumsdhatura.
Opioids.

alcohol, anaesthesia,
sedative-hypnotics

drugs 2.PNS effecting.e.g. conium

Properties for pesticide
ideality:- Prop for ideality. 3.Spinalcord affecting, e.g. Nux-vomica
1. Cheap.
1. Cheep
2. Easy
3 Child p.Muscular
1.
system effecting
2. Easy to Digitalis 2. Nicotine
telling in
available
get acids Asphyxia causing.
3. No bad 3. Tasteless
4. Biting of 1.Co.
4. Can mix
smell 2.C02
with food poisoning
4. Short animals. 3.War gas
water
fetal 1.3Effects of poisons
5. Small lethal
period 1.Localaction e.g
5. Small dose i. By corrosion
fetal ii. Atropine cause dilating of the pupil.
period 2.Remote actions
6. Smal Effects at a site away from that local application site.

lethal a. Specific>1. Opium+ alcohol Brain.

dose 2.Digitalis>heart.
b. The shock produced by corrosives
non-specific
1.2 Distribution of poisons
3.General actions. Itto those absorbed poisons which
refers
A.Corrosives
affect more than one tissue
of the body. eg Ar
Acids Hg, Phrd!
HCL, H2SO4, HNO3 4.Both local + remote e.g (oxalic) Silv
Mineral acid
oxalic,, carbolic 5.Delayed complications e.g. (corrosions)
Organic acid
Vegetable acid > Hydrocyanic 14 Factors affectingpoisons
Alkalis Form
carbonates.
Sodium, Potassium and ammonium Physical.
B.Irritable Gases>liquids>solids(reactivityorder)
Inorganic Chemical
Become inert for example, acid and alkali combination OR
None Met4baic Br,

Metallic>
Organic
R Cl,

Zn, Ar, Radioactive s become more

Mechanical.
toxic in Some combinations.

Vegetable poison castoroil, ergot, capsicum etc. Depends upon the surface area

1. Dose to poison.
Animal Poison Scorpion,spiders All poisonous animals.+
hussain
TOXICOLoGY IN A MINUTE By Dr Aashirhussain TOXICOLOGY IN A MINUTE By DrAashir
10
GENERAL TOXICOLOGy 11

as therapeutic.
used
Small dose often effects.
toxic Temperature
cause
Large doses severity to the
more se Pulse
2. Mode of administration
of increasing Blood pressure
order
The route in Respiratory rate
follows
victim isas ous<Intraperi
Clothes
Topical<Oral<intradermal<IM<Subcutaneous<lnt The smell of body/ vomits-
toneal<inhalation</V
of the body. to lethal opium has a typical garlic smell
3. Conflation(Age) are more prone Skin, pallor, dry, hot, needle
older adults
Childs and to young marks, pigmentation
as compared
damage Eyesdilated/constricted
4. Environment. the poison
is high, Oral cavity, gum lines, staining
environment
If temp.of the Convulsions
also increases
response in the body: Polyneuritis
The fate of poison urine, faeces, milk, Coma
of poison: Vomiting,
Excretion
1) iii. Systemic examination
sweat is the guardian of
respiration, liver CNS reflexes
the liver (the
2) Metabolism: In CVS
of poisons)
thebody againstall types &
effects on thebody: All signs symptoms of Respiratory system
3) Adverse 3) Laboratory investigations:
are produced
poisoning lavage
retention in the body e.g. arsenic e.g. blood,vomitus, urine, gastric
4) Retention: Poison 4) Experiments on animals
1.6 Diagnosis of poisoning:
5) Miscellaneous:
In the living: X-rays e.g. lead poisoning
1) History: Ultrasound
From patient, relative, police or any other
ECGaconite poisoning
person MRI (CT scan)
with meals
Onset/ relationship

State of thebody
In the dead:
of police paper):
1) History(thestudy
Course of symptoms recorded by police
FIR, S/S observed before death,
Involvement of more than one individual & internal
2) Post mortem examination (external
or actual
Falsepoisoning >pretending PM)
Withdrawal syndrome 3) Chemical analysis
2) Clinical examination: Ekaninatim 4) Experiments on animals
i. ABC (Ai3Wag Bzeathirg Ciseuulatr on ) 5) Miscellaneous:
ii.
GPE (GEntiul vhgShCay ERawwination ) X-ray, biopsy,
MRI (CT scan)
General appearance/behavior poisonin
1.7General treatment
hussain
TOXICOLOGY IN A MINUTE ByDr
Aashir
TOXICOLOGY IN A MINUTE By Dr Aashir hussain
 12

functins GENERAL TOXICOLOGY 13

and circulatory
withan
AlM: Maintain respiratory
to remove
poison.
attempt 2 Cleaning the stomach before and upper endoscopy in
Seguence ofManagement unabsorbed
poison. someone. Who has been vomiting blood
1. Elimination of
The route is
essential. 3. Collecting stomach acid for thetest
like a co-first step
l from
is removal.
4 Relieving pressure in someone with a blockage in the
For inhaled,
artificial respirator intestine
source and giving
it possible. cONTRANDICATION
immediately Loss of airway protective reflex
should be avoided. 1.
Aspiration and snake bite a 2 Ingestion of a corrosive substance eg strong acid or
one's live hypnotic
Injected the alkali.
is applied
near injectedsite
tourniquet 3. Ingestion of a hydrocarbon with high aspiration
and poison removal is
The wound is excised potential
done. 4. The patient is at risk of hemorrhage or GIT perforation
washed out immediately
Contact poison is
should not be allowed tosta PROCEDURE
Ingested poison 1. Intubatepatient.
in the stomach
for a long time. 2. Place the patient in the left lateral decubitus pasition

.Itis removal from the stomach by 2 procesSec

es. with head 20 degrees downward.
1. Emesis 3 Externally measure the length of the lavage tube
needed to reach the stomach.
a. Mechanical emesis is indúced by strutting post
drawback is 4. Lubricatean appropriately sized lavage tube and genty
pharyngeal wall. The major
effectiveness. pass through the esophagus to the stomach.
b. Chemical induced by chemicals. S1es Adults and adolescents: 36-40french.
i. House available>e.g. warm water mustard hig Children22-28 french/
laveqeConfirm
Ekacf fa powder. placement oftube by.
Aspiration of gastric contents.
1pecdauÁ ii.
Ipecacinduces vomiting early < 30 mint
Auscultation of air over the epigastrium.
Plas due to Gll stimulate> 30 Brain
stimulation. 6. Using a funnel or lavage syringe, aspirate any stomach
Steng Eno)Eii. Soup solutions >e.g. liquid contents.
detergent.
iv. Salt solutions but now contraindicated as they Gently instil 200-250 ml warmed saline into the
can cause hyperosmolarity if absorbed. stomach for adults or 10-15 ml/kg for_children
(to

2. maxtmüm 250ml)
Gastriclavage
8. Allow instilled saline to flow out of the tube and into
Commonly called stomach pumping or
irrigation is the processof
gastric the bucket near the bed.
cleaning out the
Repeat instillation and drainage until the eftluent
is
the stomach. contents of 9.

INDICATION clear.
1. With 10. Once effluent is clear, may instill activated charcoal if
patient has ingested
poison. indicated.

TOXICOLOGY IN A MINUTE
By DrAashir hussain hussain
TOXICOLOGY IN A MINUTE By DrAashir
 GENERAL AICOL
TOXIcoLoa

15
14 ENERAL TOXICOLOGY
pojso
work against
damage to the
dotes orcompoundedwithout any damaPe
BAL (B%ondhe- Alveolas Lavage
1.8.Anti
ofpoison 3. Penicillamine(Cu, Pb,Hg)
The substances
effect
4. Desferrioxamine used for iron poisoning
neutralization
body. s0. Write medical + legal duties of Mo during poisonscase?
fal.
in high doses.
Indications duties
A Emetic gastric
Poisonis already
lavage
absorbed
route
is not
used.
Medical The doctor should
1, try their level best to save a life

of poison 2. Start treatment start.

TYPES
Ingestion by occupying 3. Maintain secrecyof patient.
Impairabsorption 4. Informing the condition of the patient to a relative.
1. antidotes
ysical
of 5. Immediate referral if needed.
space absorption. banana.
food e.g.
1. Bulk Legalduties
2. Fats, oils. 1. An official record of primary data.
charcoal. 2. Careful recording.
3. Activated
2. Chemical
antidotes. with poison and convers
rt Time of entry.
reaction
chemical Sign+symptom
Theyforma
them to less toxic. Clinical examination.
for alkali poison.
1. Acid (dilate) Vital sign.
for acid poison.
2. Alkali (dilate)
Record of ongoing treatment.
acid.
3. Lime for oxalic
3. Public health involvement like in food poisoning
3. Drugs antidotes. (Pharmacological)
to p0ison or compete
functions
opposite 4 The death certificate is never given before police
They produce forboth.
for receptors that are identical arrival.

e.g 5. Proper collection of samples and washing contents of

1. Atropine
for > Pilocarpine. stomach etc.

2.Diazepam Strychnine 6. Medicolegal report.

4. Uaiversal antidotes 7. Detail record maintaining.
for unknown poison or when mixtures of
Q. Collection, preservation and dispatch of the
It is used

poison are intake.

It contains the following. (MnemonicPTM) specimen?
1. adsorb alkalis. Ans. From practical Notebook.
Powdered charcoal 2/4
2.
Milk of magnesia % Acid neutralizes.
3.
Strong Tea (TannicAcid)% precipitates

Chelating agent
1.
EDTA.(Ar, Pb,Hg)

hussain
TOXICOLOGY IN A
MINUTÉ By DrAashir hussain t TOXICOLoGY IN A MINUTE By Dr Aashir

MAn
 16 17
CORROSIVES

Chapter
2
tube or lavage.
1. Gastric

CORROSIVES
Su feu CO)
2. Carbonates of Alkali (due to production of

PM (Post-Mortem features) canusMES )

2.1. Mineral Acid hsty White
1. Chalky teeth.
1.Sulphuric
Acid
is mostly coloress, without me 2. Black Tongue.
Sutphuricacid activity.
with hygroscopic 3. Dilated Pupils.
making liquid ofvitriol. 4. Face stained with corrosion.
Other namesOil
5. Stomach perforations.
Mechanism of action by dehydration. 6. Gastric contents in the Peritoneal Cavity.
tissue
Acid damage to conversion
of hemoglohi
due bin
Tissueblack/brown Legal Importance
1. most common.
Accidentals
to hematin.
Edema 2. Suicide Less common.
White necrotic membrane-swelling
shock> Death. 3. VitreolageIt isthrowing acidatEemeone.
Asphyxia
Signsand symptoms
2. Nitric Acid HNO3
wíth
Englaersa
fumeforming and these
1. Black / Brown vomit. Yellow colour liquid
fumes affect airwaymembranes.
2. Chalky White teeth.
3. Speaking+ Swallowingimpaired.
the mouth, contains a corrosive
Other Name Acd
Red Spiit}itL
Aqua fortis
4. Face Area, mainly around
1. 3-Engiaves's
2. Yellow acid.
burn area.
from other acids., of action.
Special features of sulphuric Mechanism
1. Fumes damage mucus membrane.
in the GIT tract.
1.
Seyere burning pain combines with organic matter to form
2. Nitric acid
2. Patient is
extremely Thirsty.
3. Productionof effervescence in contact
with the alkaline picric acid.
That is the reason for yellow tissues.
ground.
4. Clothes staining

Management
+ dark blackvomiting.
(Sane f amorphine.
cesosie)
Bhue Coloted uxine A reaction

Signsand symptoms
called xanthoproteic reaction.

of tissues.
eBls
1.
Relieving pain by analgesics
1. Yellow staining V'otiu)
2. Giving jce to suck for relieving thirst. 2. Respiratoryirritation more profound.
3.
Fluids to combat dehydration.
3. Intense suffocation. yelle
the
as sulphuric, except
4.
Steroids toavoid shock. All other features are the same
involved due to acid's
5. The milk of magnesia is a system is more
properantidote, or not available if respiratory
alternatives like
limewater or simple water are used. fumingnature.
6. Skin
7.
burnsarewashed immediately with plenty
of water. 3.Hydrochloricacid acid.
Eyes,if involved, are washed by sodium 1.Non-corrosive
solution. bicarbonate soluble.
2. Extremely
Things avoidduring
treatment 3. Stain clothes red. 4-Del Sarn skin
hussain
ByDrAashir
TOXICOLOGY IN A MINUTE TOXICOLoGY IN A MINUTE
ByDr Aashir hussain
 SIVE
18 19
UCT fethes CORROSIVES

Qther Names
1. Muriatic
acid.
Aetrer r 3dag 5. Urinary output is measured regularly as it is

of Salts. HCL nephrotoxic.

2.Spirit
HNO 6. symptomatic treatment
HSO 15-20ml
20-30ml
Post Mortem features
Fatal
10-15ml
1. Dark liquid in thestomach.
24h
dose 24h 2. Cloudy areas ofcalcium oxalate
24h
Fatal 3. Blood vessels of the sub-mucus layer show as dark
Period
Acids lines.
2.2. Organic
Medico-legal
( Oxalic acid.
1.Crystalline
in appearance.
actions
when taken into the
1. Suicidal most common.
2. To erase writing.
2.ACId with remote 3. Açcidental common.
body. 4.Homicidal.care
Other names.Sugar Acid Christison'ssaying substance of
Mechanism ofaction
The local damage mucus membrane
a
When person, aftertaking a crystalline with
strong acid taste,encountersseizuresand vomiting
It is no
Remote >form calcium oxalates abdomen pain and weak pulsedies before onehour.
1. Acid combine with serum calcium
activity
other substance butonly oxalicacid poisontmE D
>serum calcium decreases>muscle
increases>convulsions>collapse Carboticacid
2. It is also nephrotoxic. 1. Coaltarderivatiye.
3. Narcotic features. 2. Phenolic odour.
Signsand symptomns Other names Phenol
Depends on acid concentration. of action.
Mechanism
1. First sign is a burn on the GIT tract when swallowed. 1. Cause coagulativenecrosis.
2Vomitis specificblack ffe aiaUnkd 2. RemoteactienS-OnCNS.
3.Narcotics featuresathigh doses.
CNS 4. Nervous system Tingling.
= +
Halmai Signs and
1.
symptoms
White marks on chin+cheek.
Vyinay g%5.Nephrotic system Oliguria hematuria 2. Burns on GIT tract.
Management S.Skin is cold.
1.Immediatestomach wash.
4. PinPoint Pupils
2. Stomach wah is not done with warm water because it in héthie
5. Labored Breathing
dissolves more acid. (lungs)ffelty
6. Oligouria (kidney)
3.Chalk given at once. Ratio (30gram per
20gram of Carboluria
acid)
Features include
4.calcium gluconateisgivenPO--OU It a
is renal failuredue
to direct toxicity.
the yrine containing
hemolysis, hypotension, albuminuria,
TOXICOLOGY IN A MINUTE By DrAashir
hussain DrAashirhussain
 SNE 21
cORROSIVES
20
bolic prod
product.
metabolic da and after
andphenol'sairturninto
acid, with Management
free carbolic
free contact 1. Immediate treatment
into green.
urine
comes smoky 2. Stomach wash.
become
some time 3. Oxygen support.
wash.
Manarement
1.Stomach 4(Dicobalttetracemate specificantidote.
+Sodium Bicarbonate choice.
white ormilk. 6. Methylene blue (aqua.)is
2.IVsaline like egg
7. Also amylnitrite, sodium nitrite and sodium thiosulfate
3.Demulcents ifneeded. and
nd
4.Oxygen
is given +MgSOis given is a is used as antidotes

water
5T0% gtycerin+ Post Mortem appearance
antidote Asphyxia signs.
specifi
featurees with phenolic smell External
Postmortem the stomach 1. Bitter almond smell.
1.Mucoidin
2.Lungsconges
ted. 2. Pink patch at face (due to cynomethemoglobin)
Stomach.
Rugaein 3.Pink Post-mortem staining
3Prominent on chin
4. Whitemarks 4.Blue Nails.
5. Prominent bright eyes with dilated pupils.
Medicolega is Suicidal.
Themostcommon Oxalic Carbolic
internal
10-15gm 1. Pink mucosa
of GIT tract. spet/dss
15-20gm at pleura. lesdanglka
Fatal dose
2h 3h 2Petechial.haemorrhaggs
the that is bloody.
Fatal period 3. Froth in airway
Veghabe7 acidHCN/des Cgand almond smell body cavities.

A
Hydrocyanic
Acid gas
with a bitter almond smell. r,b 4. Bitter in

Other names> Prussicacid, cyanogen

Medicolegal
1. Mostly suicidal.
Cfage
Mechanism of action.
1. Cyanogen>inhibits cytochrome
oxidase >lead to
2. Accidental during disinfection.

cellular asphyxia.
2. Also damage
the mucus membrane by corrosive
action.

Signs andsymptoms
1. When taken through the mouth, produce the
following effects.

a.Brain confusionsand headache.

b. GIT
bitter almond smellthrough the mouth.
c.Muscularsystem power ofMuscles islost.
d. Unconsciousnessalso occurs at a
late stage.
2.
When inhaledproducesdeath atthe spot.

A Ru IN A MINUTE ByDr Aashir hussain

IRRITANTS (INORGANIC) 33

4
Chapter
IRRITANTS (Inorganic)
Non.Metallic.
4.1Phosphorous
White crystalline
1. Becomeyellow in the air.
2. Present initranslucent,

Luminous cylinders.
pextn
3. Insoluble in water.
4. Soluble in an organic solvent.

Redamorphous.
1. Inert.

2 Non-luminous.

Mechanism ofaction
1. Disrupt cellular oxidation (protoplasmic poison).
2. Disturb blood circulation in the bone.
3. Also, effect liver metabolic sequences.
Signsand symptoms
Primary phase Secondary phase
1. Effect GIT tract. 1. Distended abdomen.
2. Burning pain in 2. Pale faces

the GIT tract. 3. At first, the liver enlarged

3. Garlic taste and due to fatty
odour. degeneration(necrobiosis)
but later is shrunken due
to necrosis.
4. In between the primary
and secondary phase,
there is a remission phase
for 2 to 3 days.
Chronic (When encounteredforlong times in industries
like match industry)
 IRRITANS(Inorgan
IRRITANTs (INORGANIC) 35
34

Specific 2. Extreme toxic to affinity to form bonding

1. Multiple dischargint enzymeshas
General and weight within sinuses in the with their Sulphur containing group.
1. Weakness jaw which contains Signs andsymptoms
loss.
foulsmellypus Acute poison Chronic poison
2. Pain injoints.
(phossy jaw)
1. Small dose: It 4
contains stages
Jaundice
2 Foothache
3. Teeth loss.
GIT symptoms are
more during small
1.GIT disturbance stage
1. loss ofappetite
doses. 2. Diarrhea.
Mallore 4, Bones sequestrations,
Nausea burning 3. Nausea.
5. Bone formations in the
pains in GIT tract. 4 vomiting.
bonemarrow.
Intensethirst.
Rice watery
Management Chronic stools.

1.
Acute
Stomach wash.
1. Source removal
2. Surgery of
cl Coffee ground
vomiting
2. No demulcents. sequestered bone.
3. 0.2 % CuSo4
2. Large doses:- 2.Catarrhalstage
4.Symptomatic treatment Headaches 1. Inflamed mucus

Post mortem appearances Vertigo

membrane.
1. Garlic like
smellnatural.
2. Conjunctivitis
from orifices. Spasms
2.Blood discharge Coppes Collapse (Coma) 3. Flue like symptoms
3. Jaundice.
of the liver. Death (within 2 4. Head fullness
4.

5.
Fatty degeneration
Corrosive changes in the
mucus membrane of theGIT hours)
3.Skinrash stage
3d
tract.

6. Kidney + heart degenerations.

1 Skin irritation.
2. Thebrown pigment
Medico-legal
of skin (Rain drop
1. Accidental in industries involving phosphorous e.g.
Bomb appearance)
plus fireworks
3. Palms+soles
Metallic
4.2 Arsenic Hyperkeratosis.
4. Hairs falling.
Only its oxides and sulfides are poisonous as they
absorbedfrom GIT in relation to
are
pure arsenic which is
meests 5. Brittle nails.
6. White bands on
unabsorbed.
Other names
capillary poison.
Mechanism of action
gmedrdn nails(Mee's

Lines)
1. Highly
interfere with cellular
metabolisms mett 7.Normocytic anemia

TOXICOLOGY IN A MINUTE TOXICOLOGY IN A MINUTE By Dr Aashir hussain

By DrAashir hussain
 IRRITANTS
norgani
1RRIANTS (INORKANIC)
36 37

aC
thrombocytopenia
and
and
disturbance befocetd hais/rAik
4.Nervous
1. Hands foot 7. Lungs specifically
bdyhstk poib
S/ 2 Muscles tenderne ess Congested
fe
fadestds4 3. Drowsiness.
vision impair
ess.
Medico-legal 5aaNagO
1. Both suicidal and homicidal
use
7t PorSoy
4. is common as
a) easily available.
b)Tasteless.
c)Odourless. d)Small lethal dose.
e)Used as cattle poison. E)Abortifacient.

Management f)Aphrodisiac(sexualdesire stimulant)

Chronic
4.3 Mercury
1. Source removal of
Acute the Only those compounds of mercury are poisonous
patient. which are soluble.It includes their chlorides, nitrate,
1. Stomach wash
ferric
oxide 2. BAL injection. Oxide, sulphide,sulphate and cyanide.
2.(Hydrated
antidote
3. IV sodium Other names
(specific
antidote thiosulphate, which i 1.Para.2.Quick silver.
3. Universal choice.
sometimes also usSed
alternative Mechanism of action
Butler
or Ghee in acute
poisoning. Same as arsenic.
4.

(Demulcents) 4. B
Vitamin complex Iy Sign and symptoms
(e.g. 5. Symptomatic Acute poisoning
5. Purgatives Hydragyrism (chronic)
sodium sulphate) treatment. 1. When ingested, it 1. Teeth loss
6. BAL injection. causes a metallic 2. Painful groins.

alkali tab
NoSL7h kses
7. Maintain dehydration taste and burning 3. Blue-blackgum lines.
for thirst.
sensations on the
8 Ice sucking 4. Discolorationof the lens

9
10.
Morphine
Symptomatic
for pain. Arihis
He
Selubil
Caha
GIT tract. There is
the appearance of a
inthe eye
(Mercurialentis)
treatment. greyish-white 5. Tremors that affect

POST MORTEM APPEARANCE mucus membrane hands, arms, legs and

Acute Chronic with acorroded tongue which are coarse
1. Fatty degeneration is
1. Cyanosed appearance tongue. and intentional(Hatters
the internal organs. 2. Early death within 2
2. Jaundice shake)henere
3 Rigor mortis timne
2. GIT congestion. hours convulsions + 66. Shyness, irritabitity,Toss
increased. 3. Peripheral neuropathy coma.
= ofmemory insomnia
4 Stomach Red 4. Anemic 3. Late death
mercury erethism)
velvety Ulcerativecolitis.
5. Red mucosa Uremia
6. Petechial hemorrhage death
inthemyocardium 4. When inhaled

hub-Dna TOXICOLOGY IN A MINUTE By Dr Aashir hussain

TOXICOLOGY IN AMINUTE
By Dr Aashir hussain
 Janie
IRRITANTS (INORGANIC)
38 39

4. Arterioles and
salivation,
causes and 6. Mitochondrial
capillaries toxin
spasms. 7. Cause
pneumonitis 5. microcytic
Nephritis.
renalfailure. Treatment Chronic Sign and symptom
anemia

1. Source removal. 1. Acute

polsoning
Acute
wash 2. Symptomatic 1. Only
poisoningwhich causes
1. Stomach treatment 2. Colicky constipation.
albumin abdominal pain.
2. Egg is given 3 Oliguria Ateetm
3. Charcoal
sometimes.
4 Leg cramps.
5. Limbs paralysis.
4. BAL/Penicillamine 6. Lead
encephalopathy>in case of tetraethyl lead
5. Symptomatic
poisoning
treatment
Postmortem
appearance
Chronic 7 Black grey
stools
1. Necrosis of large
8 Basophilic stripling
Acute
intestine
2. Chronic poisons
(Plumbism) Ua
1Whittongue General
2. Grey white 2. Other features are 1. Pale face (vasospasm)
on GIT similarto acute
appearance 2. Hypochromic anemia.
tract poisoning. 3. Hypertension +Nephritis.
3. Toxic nephritis 3. Accidental only
4. Sterility in both genders.
4. Fatty degenerations 5. Menstrual disturbance.
of organs
GIT Specific signs(zombie signs)
5. Ulcer+ inflamed
Lead line Lead colic
tract
Blue-black line in gums due Intermittent abdominal pain
to deposition of relieved by pressure. There is

4.4 Lead when inhaled as subepitheliallead also constipation.

-
severe damage
Cause more are more
Its compounds
to ingestion. sulphidegranules
compared
to pure torm because of their Lead palsy Lead
encephalopathy
dangerous as compared 1. 1. Delusions
Wrist drop
solubility.
2. Foot drop 2. Loss of vision
Other names Due to degeneration 3. Insomnia
1. SEESA
of nerves 4. Headache
2. Plumbum
5.Hallucination
Mechanism ofaction
1. Same as arsenic 3 Impair reproductive Management Ladnét
ability by inducing Acute Chronic
2. Impair heme
1. Stomach wash 1. Source removal
synthesis infertility.

hussain
TOXICOLoGY IN A MINUTE By DrAashir
TOXICOLOGY IN A MINUTEBy Dr Aashir hussain
 9an AND HYPROTICS
sEDATIVE
40 e
L' for 41
2.
one
BAL week Chapter5
Penicillin for 35-7

SEDATIVE AND HYPROTICSs

by 3.
2 Pain relief
days.
morphine Vit.D
3 Calcium
salt+
4. Symptomatic
treatment.
51 The most common
Barbiturates
administration use
sedative-hypnotics in IV form
for anesthesia.
EDTA They are CVS
depressants
Penicillinamine Cas
5. Symptomatic Long-3cting
rance 1. Time of effect 1-12 h iate-scting
treatment
ortem2 1 Time of effect =half
2. Fetal dose =3-4g
Chroni hour to 8h
Acute Blue-black lines on 3 Example = 2. =2-3
Fetal dose g8

The intestine Gums phenobabitone 3 Example =

biack Erythrobliasts
contains Amylobarbitone
feces. yperpiasia Short-actig uiteasihort-actng
Sigrsof
1. Time of effect = 1. Used for
20mints to 4h anaesthesia
gastroeriteritis
=
2. Fetal dose 1-2g duration

3 Example = 2 Fetal dose=

Medicolegal Iimp.is due to drilling water fromn
1g8

Chronic poisoning
expected
(ahyount
cyclobarbitone 3 Example =
household old
lead pipes
gevnedY thiopentone sodium

45 Copper
Only some
hepetolaialle
salts are poisonous.
Another name is
Acute paisoninE
Sigmand sumptams

It produces green lines

on Gums. Wilson's CNS EVES
Tamba. in the eyes.
diseaseis specific forcopper deposition 1. Confusion 1. Diplopia

46 Thallium loss of hairs and

it also resists
2. Ataxia 2. Pupil constrict
Its poisoning causes 3. Slurred speech first them dilate

putrefaction. 4. Excitement
Arsenic Mercury Lead Flaccid limbs
5.
Fatal dose 120-200mgs 1-2gms When the CVS Reso
absorbed Slow periodic
1. Blood pressure
dose is > 0.5 decreased breathing (chyne

gm 2. Tachycardia
stroke breathing)

May occur
Fatal 12-48 h From a few 12-48 h

period hours to 5 respiratory

failure
days Face
SON
hussain
MINUTE ByDr Aashir
TOXICOLOGY TOXICOLOGYINA
 POISONS
GRICULTORE
42
Cyanosed face
6 43
blisters chapter
1. Barbiturate of
found
on site
friction
such as
AGRICULTUREPOISONSS
clefts
ofinter Linsecticides 2.Herbicides
etc (Paraquat)
axilla 3.Metallic
digitals,
Organo-phosphate compounds
use during psychothe rapy.
2 Chronic
Only
1.
poisonin
prolonged
casts urine.
during in (A).Alkyl (B).Aryl
and
sugar are pres
resent.
2. Albumin, of acute poisoning
3. CNS Symptoms 1. Malathion
Managementrespirator.
an artificial 2.HETP 1.PARATHION
1. Maintain airway by 3.TEPP
KMNO4. 2.DIAZINON
2. Gastric lavage by
body.
3. Warning the
6.1.Organophospihate
4. Dialysis.
The classification is
charcoal. givenabove. These
5. Activated poisons can
treatment. reach the body through inhalation, ingestion
6. Symptomatic and skin
absorption.
Postmortem appearanoe VMechanism ofattion
1. Signs of asphyxia.
2. Mouth and nose froth. Organophosphate poisoninhibits cholinesterase at

3. Face cyanosed. synapses and myoneural junction.

4. Tablets in the stomach. Acetylcholine accumulates that cause.
yper-excited both voluntaryand
5 Renal tubules regeneration. involuntary muscles.

Medicolega Sign and symptomms

1. Mostly accidental. 1 The SequenoDE siEmappearanmoeanects
2. Sometimes suicidal. 1. Involuntarymuscles 2. Secretoryglands. 3.

Voluntary muscles. 4 Brain centers.

5.2Chioralhydrate
It has a sweet taste and aromatic smell. Signs
bitter Early sigETS
and symptoms arethe same as barbiturates.
CNS EYE

Headaches
1. Pin point Pupils

2. Lacrimation
SKIN
1. Sweating

1. Nausea diarrhea

andVomiting
TODXICOLOGY IN A MINUTE husSsain
By Dr Aashir hussain TOXICOLOGY INANMINUTEByDr
Aashir
44 POISONS
OIsON AGRICUL

Salivation Musculoskeletal nortem appea 45

1. Chest constriction Post as asphyxia. ance
Tears
or red tears 2. Muscular twitching Same Face cyanosed.
Chromogenic in
1
due to porphyrin 2.Mouth+Nose froth
lacrimalglands 3 Kerosene like smel
a utes > coma death
4. A green ubstance in
1. Pulmonary edema the
5. Mucus is congested. stomach.
convulsions
FATALDO0SE 6. Lungs hyperemia.
HETP Parathion
TEPP 7. Pulmonary oedema
160mg 8. Dilated
IV 5mg
80mg capillary.

350mg 1. Accidental in Medicoleg

Oral 25mg 175mg agricultures
2. Suicidal also common as
paisoningE readily
Differentials
for argamophosphate availab
1. Atropineoverdose.
2. Heroin overdose.

3
4.
Narcotic
Mushroom
overdose.
poisoning.
Management
1. Removal of the patient from the source.
2. Removal of all clothes.

3. Skin wash.
4. Gastric lavage.

5 airway is maintained by an artificial respirator and

aspiration of secretions.

Specific ANTIDOTE Atropine sulphate is given 2mg

after every 20mints until the followingsigns
appear.
Flushface
Dry mouth
Pupils dilated
Warm skin
Fast pulse
7. Pralidoximeis
given which reactivates
8. Diuretics and cholinesterase.
saline purgatives
9. given.
Symptomatic treatment.

TOXICOLoGY IN A MINUTE
By Dr Aashir hussain DrAashir hussain
IN
 POISON
CARDIAC
46 47
7
Chapter other name is "mitha
POISON Its

includeaconitine,
zahar". Its active
principles

CARDIAC is plantpoison. Death withinsix hours

Jesaconinine
by
and hypo-aconitine.
ventricular fibrillation or
7.1. Digitalisit respiratory
7.1 paralysis.
Other names 7.3. Nicotine
Fox glove. Also called tobacco its active
principle include
nicotine and lobeline. It
Active princjple initially stimulates
1. Digitoxin. autonomic ganglia then depresses it. Clonidine is
2. Digitolin used for weaning away a person from chronic
3. Digitalein. tobacco addiction. Autopsy shows dark colour
4. Digitonin blood and pulmonary oedema.
in limited dose
has
ofaction lirect
Mechanism areglycosides and in tarting the f ct
They
muscle and help
restarting ailing
the heart it causes heart block
action on is exceeded, by
the dose
heart. When causes ventricular fibrillation
also
rate. It
slowingits
signs CNS
GIT
+ 1. Depression
diarrhoea
Nausea,vomiting, 2. Headache
pain Respiratory
CVS
1. Breathing rate down
1. Extra systoles
2. Coma convulsion
2. Fibrillation

3. Heart block
death
Management
Monitory ECG is essential.

1. Atropine for bradycardia.

2. Potassium salts for extra systoles.

3. Novocain, propranolol. (Specific antidote)

4. Fluid balance.
5. Symptomatic treatment.
Fetaldose = 3-4mg (digoxin)
Medicolegal
Mostly accidental intake.
No specific postmortem signs.
7.2.
Aconite

DrAashir hussain
TOXICOLOGY IN A MINUTE
By Dr Aashir hussain TOXICOLOGY IN A MINUTE By
 NALGEs AND ANTI
RETI NALGES PYRETICS
48 49
8
ANDANTI PYRI has three
It
Chapter
NALGESICS
PYRETI GIT STAGE
1.Severe vomiting.
stagesof sign's
appearance.

an acidictaste 2.However, the patient

81 Apirin
White powder
with is
fully conscious.
symptoms LATENT STAGE
Signsanmd GIT
Occur after 24 hr
ONS 1. Melena Malaise.
Mucosa erodes
1. Tinnitus Epigastric pain
3. Hematemesis
2. Headache HEPATIC STAGE (UQ)
4. Diarrhea
Occur after 3 days to five days
Respiration
Imp changes occur.
Sikin 1. Rate is increased,
1.Liver failure.
1. Rashes 2. Hyper ventilatioOn 2.GIT hemorrhages.
2. Cyanosis 3. Pulmonary edema 3.Brain edema.
3. Flushes 4. Cause ofdeath 4.Renaltubular necrosis.
Ear
5.Cardiomyopathy
Renal 1. Deafness The third stagesigns are also present in post mortem findings.
Renal failure (acute) 2. Buzzing ofear TREATMENT
1. Shifting to the hospital is an immediate step.
MIANAGEMENT
2. Gastric lavage.
1. Stomach wash.
3. Methionine or n-acetyl cysteine prevents liver

2. IV fluids.
achersis. damage by increasing glutathione.
3. Forced alkaline
4. Blood transfusion.
4 Dextrose.
5. Bicarbonate infusions.
5. Peritoneal dialysis.
6. Hypertonicglucosesol V.
6. Symptomatic 7. Symptomatic treatment.
Post mortem appearance Aspirin Paracetamol
1. Aspirin in the stomach. dose 20 tablets
fatal 4-10gm
2. Petechial hemorrhage. Unknown 2-5 days
Fatal
3. Lungs edema.
period
4. GIT mucosa eroded.
Medicolegalaccidental mostly.
8.2. Acetaminophen
paracetamol and is metabolic of
Also called

phenacetin,most cases are accidental.

Sien and sympioms

hussain
TOXICOLOGY IN AMINUTE ByDrAashir TOXICOLOGY INA MINUTE By DrAashir
hussain
50 STIMULANTS 51
STIMULANTS
Chapter 9
Hallucinations (feeling of sand
STIMULANTS particles under skin or
insect crawling over thebody) refer
as Coke Bug Or
formication.
9.1. Cocaine
1. powerful stimulant.
It is a 3. In women, increased erotic desire
leaves of the coca plant. is noted.
2. Obtained from 4. In men, sexual perversions are noted
3. Novocain is a syntheticanalogue. 5. black teeth (homosexuality)

Other names. 6. nasal septum perforations

1. Coke.
Management
2. White lady.
Acute
Chronic
Passages of intake. 1. Injected ones are 1. Gradualwithdrawal
Chewing limited by tourniquet 2. Bromocriptine or
2. Smoking.
application. lithium forcocaine
3. IV.
2. Locallyapplied should craving.
Sign and symptoms.
1. Acute poisoning&
be washed. 3 Psychotherapy
3. Swallowed should be
It has three stages.

1.Early stimulationstage.
removed by stomach
1. Excitement. wash.
2. Euphoria. 4. Diazepam for
3. Dry mouth. convulsions.

4 Vertigo 5. Propranolol for BP

5. Muscle 6. Ice bath for fever
twitching
6. Mydriasis. (cocainefever)
7. Hallucinations 7. Artificial respiration
(Lilliputianform)
2.Latestimulationstage 8. Symptomatic
1.
Hyperthermia (cocainefever) POSTMORTEM FINDINGS
2. Convulsions 1. Brain and lungs oedema.
3. Cyanosis 2. Congestionof viscera.

4. 3. Nasal ulcers.
Respiratory failure.
3 Stage ofdepression MEDICOLEGAL
1. Muscle importance.
paralysis.
Loss of reflexes. 1. Aphrodisiac.
3. Coma for ENT surgery
2. Topical anaesthesia
death.
2.Chronic poisoning 3. Mostly accidental.
1. Addict
loss of (cocainism)
interest in
family,friends.
TOXICOiOC
 ASPHYXIANTS STIMULANTS
53
52
4. If

Chapter 10
intracranial
pressure
5. Convulsions increased, give
mannitol.
are
controlled by
6. Resting of diazepam.
ASPHYXIANTS 7.
patient.

by incomplete
by incomplete Antibiotics+symptomatictreatment.
10.1. Carbon.monoxiroduces Post mortem finding
gas produces and
matter and
is colorless
Non-irritant 1. Bright cherry red
of organic post mortem
combustion co staining only specific for
poisoning. (pinkish)
odorless. for hemoglobin 2. Skin blisters.
times more affinity
1. The co has
250 oxygen and combine
than that of oxygen.
It displaces
that
3. Mouth +
nose > forth.
and form carboxyhemoglobin 4. The bright cherry red color
with hemoglobin is measured
by of blood,tissue and viscera.
5.
and whose level Brain edema.
cause anoxia 6.
Myocardialnecrosis.
spectrophotometry. (over 15% when
with myoglobin MedicoieKal imeertance
Co also combines
1. Acidental
absorbed) mostly.
2. Sometimes
3. Cardio-toxic. homicidal.

Sign and symptoms

Note
ofCO in blood. The collection of
depend upon saturation 10-20% specimens in living is taken from a peripheral
Signs veinabout 10ml blood. While in dead 20-30ml of blood is
(1-4%) 4-6% 1. Skin flushes.
this
urban Smokers have taken from both sides of the heart.
People of 2. Shortness of
areas saturator
breath 10.2. Carben dioxide
Heavy poisonous gas results from the complete combustion of
40-50% an
20-30% 30-40% organic compound. It is also colorless and Odourless. In

Confusion Drunkenness
1. Ear 1. high concentration, the vagal nerve that results in
it inhibits
2. Vision loss. respiratory failure. At 40% concentration,
it causes dyspnea
buzzing.
2. Muscles Nausea, and muscular weakness. At 50% cause coma cord death.
diarrhea
weaknesSs. 10.3. Hydrogen suiphide
3. Headache vomiting 1. Rotten egg smell specific for hydrogen sulphide.
70% Inhibit action of cytochrome oxidase, thus damage
5060% 60-70%
1. Respiratory
Chyne- stroke Coma cellular respiration.
failure 3. Damage multiple organs like produce as a headache,
breathing8
2. Death and
vertigo coma while affecting CNS. It produces
MANAGEMENT conjunctivitis in the eyes. Also damages the heart and
1. Removal from the source. causes myocardialdepression. Pneumonia and
2. Artificial respiration e.g. 100% oxygen. (do not wait for bronchitis in the respiratory system.
4. Rotten egg smell and bluish green post-mortem
labs)
3. Maintaining body warm. staining

TOXICOLoGY INAMINUTEBy DrAashirhussain

TOXICOLOoGY IN A MINUTE ByDrAashirhussain
 DHATURA DHATURAA
54
55
Chapter 11 1.Stomach wash
ine or
DHATURA The ALBA are
2.Physostigmine
neostigmineis
3.Symptomatic treatment specific antidote
flowercolor.
into two on the basis of bell like shape. Post mortem signs
DIvIded both having
and Nigerare black,with 1.Asphyxsia sign
wte of dhatura can kill 5 persons.
1 fruit 2.Seeds of dhatura don't
Other name putrified
Medicolegal
1.Atropa belladonna 1.Aphrodisiac
2.Thorn apple 2.Accidental
Active principal
3.Stupefyingpoison
1.Hyoscine 11.2 Cannabis indica
2.Scopolamine The active
principal is called
3.Atropine Other forms with cannabinol and is brain stimulant.
Mechanism of action. percentageof active
of acetylcholine followingtable principal is
givenin
(competitive)
They are basically antagonist
and symptoms Bhang 15 Majun 15%
Signs Ganja 25%
The 9Ds areimportant
% active active
Charas
active
2 principal
30-40
principal principal active
Delirium Drowsiness
dose principal
3 Fatal
Fatal dose Fatal dose
Dry mouth Dry skin is
10gm is
8gm per
6 is 2gm per
5 per kg of
kg of body kg of
Difficulty in
Dilated blood vessels body
body
swallowing weight
weight
Contents Contents Contents Contents
Dilated pupils 1.dry
Difficulty in talking 1.bhang 1.flowers 1.exudate
leaves 2.milk of female obtained
2.fruits 3.butter from
plants
3.shoots 4.sugar which are leaves

9.drunkun gait dried and stem

Signs Signs Signs Signs
1.extreme 1.same as 1.same as Lethal
happinesss bhang signs bhang and Signs are
in which plus there noted
majun plus
person is delusions there is

sings and drowsiness

Management
dance that
TOXICOLoGY IN A MINUTE ByDrAashirhussain
TOXICOLOGY IN A MINUTE By Dr Aashir hussain
 RA
DHATURA
56
57
1.Stomach wash
2.Isolation
is followed
by deep 3.Tracheostomy
4.Phenobarbital IV
sleep
3.Barbiturates
Management >specific antidote
1. Stomach wash 4.Muscle relaxants
e.g diazepam
2. Strychnineinjection 5.Urineacidification
3.Symptomatic treatment 6.Symptomatic treatment
Medicolegal importance Medicolegal importance
1.Stupefying poison 1.Aphrodisiac
use or
2.Run amok the continued 2.Arrow poison
caused by a
characterized by
t is a psychotic disturbance
is 3.Accidental
even use ofcannabisIt murders He first
first time to commit Difference
person betweenstrychnine
frenzied desire ofthe real or imaginary poisoning & tetanus:
whom he may have
a
Kiis person against his way until the strychnine
who comes in Tetanus
then anyone history of poisoning
enmity and
kills
killer) no Fever History ofinjury
homicidalhabit is made (serial Fever
set is rapid
11.3SPINAL POISON Delayed in
eralized convulsions and onset
STRYCHNOS CONVEX affect all the

FROM SEEDS PF NUX VOMICA,IS scles of Convulsions start with face, lock
body. Chest is fixed jaw OCcurs
ALKALOID OBTAINED SIDE AND GREY during Chest is not fixed
early.

ON ONE SIDE AND CONCAVE ON OTHER

vulsions during seizures

COLORED.ONLY SEEDSARE POISONOUS nplete relaxation between

the seizures
Relaxation between
spasm is never
ACTIVE PRINCIPAL complete

1.STRYCHNINE ality usually in few hours

Death is rare in few hours and
may be delayed for
2.logonin
days.
MECHANISM OF ACTION investigation: Poison positive
Lab
investigation: test is
Microbiological positive
It is brain stimulant

SIGNS
ONLY BROKEN SEEDS PRODUCE FOLLOWING SIGNS
1.INTENSE BITTER TASTE
2.BLOOD STAINED FROTH FROM MOUTH
3.FACE AND NECK MusCLES STIFFNESS
4.MUSCLE TWITCHING
5.0PISTHOTONOS =BODY IN ARC POSITION WITH ONLY HEAD
AND HEEL TOUCHING THE GROUND
6.convulsions

MANAGEMENT
 CEREE
CEREBELLOTOXIC AGENTS
58 59
12
Chapter AGENTS Mental
excitement
Laughing
CEREBELLOTOXIC Hallucinations

2.Stuporstage
Sensibility
Somniferous (ALKALOIDS)also called white Headache
12.1 Opium and morphinesomniferum obtain opium(unripe
of "papaver to Sleepiness
The capsules dried
which is Pupil constricted
contain liquid
pOppy thud have sensationon the
Itching
opium body
only) have small 3.Narcosisstage
capsules
ripe poppy Deep sleep
ne effects. and don't contain opium
Pin point
"khaskhaas"
therapeutic pupil
are known as lsoquinoline Cold skin
eeds
ACTIVE PRINCIPLE BP
Phenanthrenegroup Nicotine
group Papaverine Pulse
Morphine Respiratory rate
Codeine Management
Heroin Stomach wash
Tolerance dose Body warming
dose
Therapeutic Nalorphine
Drug 100mg (specific
antidote)
15-30mg Symptomatictreatment
Morphine Post Mortem
1. Black PM appearance
60mg
10-15mg 2 .Nails blue lividity
Heroin
60mg 3.Opium smell
10-15mg 4. Dilated neck veins
Opium 5. Heroin lungs
(edema of lungs and
airway froth).
Medico-legalaspects:
i. ldeal suicidal
poison
doses i.
Lethal Aphrodisiac
Morphine 500mg ii. Cattle poison
Heroin 200 mg 12.2 Ethyl alcohol

Sign and symptoms Liquid with a burning taste. it is a CNS depressant.

It causes CNS stimulation and then depression, so it passes Mechanism
through 3 stages. Ethanol acts directly on neuronal membranes at ion transport
1.Excitementstage. level
HRT 1. 1 region affected is reticulo activating system which
causes disruption of motor & thought process.

TOXICOLOGY IN A MINUTE By DrAashirhussain TOXICOLOGY IN A MINUTE By DrAashir hussain

 CEREBELLOTOXIC AGENTS
CEREBELLOTOXIC AGENTS
60
61
cortex causingbehavior
of cerebral 2.Early and
prolong Rigor mortise
2. Suppression 3.Fatty liver
order from
changes. CNS in descendin8 4.Dark blood
3. Ethanol depresses
medulla. edema
5.Cerebral
cortex to
in 12.3 Methanol:
Sign and symptoms on dose intake bloo d It is
alcohol used
3 stages depends in
anti-freeze and its 5% concentration is
It passes through denaturant for ethanol in used as
1.Excitement stage(<100mg/d) Other names: wood spirit

Mechanism: alcohol,Colombian spirit, wood

Person feel happy naphtha.
Rapid formation of formic
Sing and dance for acid and its
accumulation is
metabolic acidosis ocular responsible
Get angry easily Signs and symptoms; toxicity.

Sexual desiret 1) Central nervous

Excitement effects, euphoria, muscle weakness,
lost stage(100-200mg/dl) suppression of
inhibition, coma convulsions. &
2.Co-ordination 2) headache,delirium
dilated pupils
3) Intense Gl pain, cold
Alcohol smell in breath clammy extremities
4) decreased visual acuity, retinal edema
Slurred speech & dilated pupil with absenceof light
5) Fixed reflex
Memory loss
6)depressedrespiratory & heart rate
Staggering gate
7) metabolic acidosis
Can't able to stand straight
Fatal dose: 30-240OmL
3. Narcosis stage(300mg/dl)
Management
Deep sleep
DecreaseBP Stomach wash
Correction of acidosis by infusion of sodium bicarbonate.
Hypothermia Ethanol(specific antidote) is given PO or IV. Ethanol
Macewan's sign(on pinching face the contracted pupil dilate
shows increase affinity for alcohol dehydrogenase
and slowly return back)
Vision loss
enzyme and form acetaldehyde & then acetic acid is

formed which is less toxic.

Respiratory failure
Fatal dose: blood
Hemodialysis
2350mg% in
Leucorarin calcium (folate analog)
Fatal period: 12-24hr
Symptomatic treatment
Management
Alcoholism:
1.Stomach wash
Due to chronic use of alcohol it's dependence and addiction is
2.IV hyper-tonic glucosesolution
develop.
3.Electrolytes management three are included in alcoholism:
Following
4.Symptomatic treatment
1) Delirium tremens: excitement, delirium, fears
Post Mortem appearance
2) Korsakoff's psychosis:
1.Alcohol smell
It last for 4 month to 2 year due to thiamine deficiency.

TOXICOLoGY IN A MINUTE
TOXICOLoGY IN A MINUTE By DrAashir
hussain
By DrAashir hussain
 CEREBELLOTOXIC
62 AGENTS

COAT RACK)
Signs (mnemonic
ataxia, retrograde
Confusion, ophthalmoplagia,
amnesia and confabulation.
homicidal &
amnesia, anterograde suicidal tendencies
tendenciee
3)
3) Acute hallucinosis:

Treatment of alcoholism:
of alcohol
Slowly withdrawal
Hypnotic & psychotherapy
diet
Good nourishing
Alcohol withdrawal syndrome:
time, brain repeatedly exposed to
Alcohol intake for prolong

high doses of alcohol.

lead to symptoms of
If sudden stoppage
or reduction in usage
by intoxication.)
withdrawal (opposite to those produced
Features:
1. Tremors of hands
2. Agitation and anxiety
pulse rate, RR,
3. Autonomic NS over activity (increase
Temp).
to return to drinking.
4. Insomnia Gl upsets leads
5. Withdrawal seizures.
confusion & fluctuating
6. Delirium tremens (mental
consciousness)
7. Alcoholic hallucinosis; objects appears distorted,
shadowsseems to move,shouting or snatches of music
may be heard.
Treatment:
vitamin B daily.

Benzodiazepine;(short half life)

diazepam (Longer half life) are usually preferred.

Aversion therapy:
250 mg, it interferes with oxidative
Disulfiram
metabolism of ethanol. Due to this acetaldehyde level
increases which causes Side effects of halitosis, pruritus,

drowsiness,impotence, peripheral neuropathy,

depression,psychosis, hepatotoxicity.