toxicology Flashcards
narcoric drug and psychotropic act was passed in
1985
drugs used for narcoanalysis
sodium pentathal( thiopentone sodium) P sodium amytal A sodium seconal S scopolamine S PASS
most common form of arsenic used is ?
arsenic trioxids
fatal dose of arsenic
0.1-0.2 gm .
which poison delays putrefaction and can be found in bones hairs and nails for several yrs
arsenic
which metal can be found from from completely decomposed bodies ,charred bones , ashes
arsenic
stages of chronic arsenic poisoning
1st 》 stage of gasttoenteritis
2nd 》catarrhal stage
3rd》skin rash resembles fading measels rash
4th 》nervous disturbance mixed sensory and motor neuropathy mimicking gullian barre
symmetrical sensory neuropathy with glove and stocking is diagnostic of arsenic poisoning
moa of arsenic poisoning
interferes with cellular respiration by combing with sulphhydryl grps of mitochondrial enzymes
it particularly adhers with vascular endothelium
leading to increased permeabilty and vascular damge
patchy brown raindrop type hyperpigmentation of palms and soles
and blistering is seen in
arsenic
poisoning
mees lines are seen n ??
arsenic poisoning
&thallium poisoning
they r white transverse opaque bands crossing nails indicating areas of arrested growth
red velvety stomach mucosa is seen in
arsenic poisoning
features of arsenic poisoning
M 》 marsh test M》mees lines N》neuritis N》numbness O》 odour garlic on breath P》putrefaction is retarded P》paraesthesia and numbness mixed sensory and motor neuropathy R》rain drop hyperpigmentation R》red velvety stomach mucosa R》rigor mortis lasts longer
treatment of arsenic poisoning
hydrate ferric salt is given
as it forms harmless salt
BAL as a antidotes
alkali are contraindicated
gutziet test is for ?
arsenic poisoning
difference bw arsenic and cholera
ARSENIC CHLOERA
throat pain before vomiting after vomiting
purging after vomiting before vomiting
stools initially bloody thn rice rice watery
watery
tenesmus + -
voice normal rough
conjunctiva inflamed not inflamed
father of toxicology
paracelsus
father of modern toxicology
mathieu orfila
poisoning with irritant poisons can be mistaken for
gastroenteritis
which metal poison can be detected by analysing bone / burnt bone
arsenic
black foot ds ie severe gangrene of lower limbs is seen in
arsenic poisoning
a pinch of which poison can kill as many as 5 persons
arsenic
in chronic arsenic poisoning greatest amt is found in
liver 》kidney 》spleen,hair,nails ,bone marrow
a poisoning where cadaveric rigidity is lasting longer is
arsenic
rigor mortis is not seen in ?
fetus < 7 mnths
septicemia conditions
in which conditions rigor mortis appears early and passes off early
these r conditions where muscle is exhausted and glycogen stores r depleted
like
1 chronic ds like TB ;cancer ,typhoid ,cholera
2 convulsive disorders as strychnine poisoning
3 violent deaths as cut throat ,fire arms ,electocution ,lightening
conditions in which rigor mortis appears early and lasts longer
drowning
rigor mortis lasts longer in following conditions
drowning
CO
arsenic
early dissappearnce of rigor mortis is seen in
bacterial infection widspread as gas gangrene
delayed onset rigor mortis is seen in
▪asphyxia
▪apoplexy
▪severe hrge
▪pneumonia ▪paralysis of muscle due to nervous ds
A young woman employed as a dental laboratory technician complains of conjunctivitis, skin irritation, and hair loss. On examination, she has perforation of the nasal septum and a “milk and roses” complexion. These signs and symptoms are most likely due to
(A) Acute mercury poisoning
(B) Chronic inorganic arsenic poisoning
(C) Chronic mercury poisoning
(D) Excessive use of supplementary iron tablets
The “milk and roses” complexion, which results from vasodilation and anemia, is a characteristic of chronic inorganic arsenic poisoning, whereas patients with lead poisoning often have a gray pallor. Other signs and symptoms of arsenic poisoning include gastrointestinal distress, hyperpigmentation, and white lines on the nails. We hope you were not led astray by her employment. The answer is B.
green blue skin hair and perspiration is seen in
copper poisoning
claptons lines is seen in
copper poisoning greenish lines on margins of gums due to copper sulphide poisoning
in chronic arsenic poisoning following samples can be sent for lab analysis except nail hair bone blood
in chronic poisoning arsenic is rapidly cleared from blood and
is deposited various tissue therefore arsenic can be detected in blood in acute cases only
plumbism or saturism is another name of ?
chronic lead poisoning
facial pallor is earliest
and most consistent
sign of
chronic lead poisoning
clinical features of lead poisoning r
A anaemia
ALA levels inc
anorexia
arthralgia
abortion
atrophy of optic nerve
B
basophilia punctuate, brutonian line(blue line present in upper jaw)
C
colic and constipation
increased coproporphyrin
cerebral edema
D pure motor palsy
drop
wrist ,foot
E
encephalopathy eosinophilia
emaciation
F
facial pallor
foul breath
fanconi syn
G
gonadal dysfunction
gout like pictures
H
headache
hallucination
high bp
I
impotence
irritability
insomniaclinical features of lead poisoning r
A anaemia B basophilia punctuate, brutonian line C colic and constipation increased coproporphyrin D drop wrist ,foot E encephalopathy eosinophilia F facial pallor
osteomyelitis of jaw with multiple discharging sinuses and necrosis
and foul smelling pus is seen in ?
chronic phosphorous poisoning or phos jaw
characteristic loosening of teeth ,necrosis of gums and sequesteration of mandible
earliest sign of lead poisoning is
- facial pallor
* puntate basophilia
earliest sign of lead poisoning is
facial pallor
most common features of lead poisoning are
colic and constipation
lead poisoning can be detected from urine by finding
coproporphyrin aminolevulinic
lead
lead poisoning can be detected from blood by finding
- zn protophorphyrin •free erythrocyte protoporphyrin
- basophilic stippling
- lead
least toxic salt of lead is
lead suphide
least common complications of lead poisoning is
peripheral neuropathy
acute yellow fatty liver is caused by which poisoning
phosphorous arsenic
poison which is illuminous
waxy
translucent
has garlicky smell and taste
yellow or white phosphorous
which substance is brownish blue ,soft,scaly,with metallic lustre and unpleasant taste gives violet colored vapour
iodine
phossy jaw is caused by red / yellow phosphorous
yellow phosphorous
match stick on its surface has
potassium chlorate
and antimony sulphide
it is stricked agnst match box hving
red phosphorous
only free P in the body is significant T/F
T
pressence of phosphorous in viscera is of no use
viscera for chemical examination if phosphorous poisoning is suspected is preserved in ?
saturated saline
as luminousity is lost in rectified spirit
hg or quick silver is poisonous if swallowed
T/F
F
not poisonous because not absorbed but its vapors are poisonous
clinical finding of
hydragyrism
M membranous colitis E erethism A acrodynia T tremors S salivation gigivitis
wht is mercuria lentis
brownish deposition of mercury on ant lens capsule
it is an early feature seen on slit lamp examinations as malt brown reflex
wht is danbury tremors
hatters or glass blowers shake
seen in mercury poisoning moderately coarse intentional tremors affecting hands 》lips 》tongue 》arms 》legs
wht is erethism
seen in hg poisoning in people working in mirror glass blowing industry
personality disturbance characterised by shyness,irritability, loss of memory and insomnia
wht is acrodynia
also k/a pink ds idiosyncratic hypersensitivity seen in children 5P Pinkish Puffy Painful Paraesthesa Peeling of skin and sheddingof teeth
clinical feature of mercury poisoning
Peter SMELL BLACK TEA
P pink ds
peeling of skin
painful puffy hands
proximal convulted tubule necrosis
Salivation
Minimata ds
membranous colitis
membranous glomerulonephritis
E erythrism
L lens deposition
black line on gums
T tremors
E erethism
A acrodyniamost poisonous hg salt
mercury chloride
name poisonous salts of copper
•copper subactetate (verdigris)
•copper sulphate
(blue vtriol,nilatutia)
fatal dose of cu sulphate
30 gm
fatal dose of cu subacetate
15gm
skin jaundiced urine ,hair,froth,mucosa,perspiration becomes blue green in
copper poisoning
name the salt which acts as both poison and antidote
copper sulphate it act as antidote for phosphorous poisoning
fatal period for copper is
1-3 days
clinical feature of aluminium phosphide poisoning
garlic odour and blood stained froth gryish black residues sticking to mucosa of stomach cardotoxotic liver necrosis bleeding diathesis
mc cause of death in alphos poisoning
cardiogenic
moa of celphos poisoning
aluminium phosphide on coming in contact with moisture ad liberates
phosphine gas which is mitochondrial toxin inhibits
etc cyt oxidase
preservative for all poisons is ?
saturated nacl also for carbolic acid but excluding other acids
preservative for acids
rectified spirit
blood for alcohol examination
potassium oxalate(anticoagulants) naflouride ( enzyme inhibitors)and so
features of carbolic acid poisoning
5C’s
•corrosive poison causes corrosion of lips, mouth, tongue,stomach
•CNS depressant •constricted pupils
•carbol uria
ie smoky green brown urine
• cartilage and corneal discoloration
• stomach mucosa is thickened and leathery
names of nephrotoxic poisons causing proximal convulted tubular necrosis and proteinuria
mnemonic C Last Menstrual
Period
cadmium carbolic acid (phenol) L lysol M mercury P phenol
proximal tubule proteinuria
and painful bone lesions are seen in overdose of
cadmium
osteomalcia bone pains multiple pathological #s waddling gait golden yellow staining of teeth emphysema anemia itai-itai ds is feature of
cadmium poisoning
substances which delay putrefaction are
arsenic phenol(carbolic acid )
metal fume fever is common in chronic poisoning of
zn
first colourless or slightly green at first but turns dark smoky green or even black n air due to oxidation is feature of
this is k/a carboluria seen in carbolic acid poisoning
urine in phenol poisoning contains hydroquinone and pyrocatechol further oxidation of hydroquinone and pyrocatechol caeses green discoloration
carbolic acid in urine can be confirmed by ??
add •ferric chloride 》urine turns blue
•bromine water》white precipitate of tribrom phenol
•Benedict and fehling solution is reduced
bluish green frothy discharge from mouth is seen in ??
copper poisoning
a presin come in emergency with rigor and chills and clinical feature resembles malaria which poisoning it is likely
zinc poisoning
presents as self limiting influenza like syndrome expoure to zinc oxide fumes
temperatures return to normal with sweating and chills like malaria symptoms
which is least common complications of celphos poisoning
oesophageal strictures and fistula occur in few survivors in late stages survivors are already very few
which barium salt is used in gi xray
barium sulphate
barium sulphide is used as
hair remover / depilatory
barium carbonate is
rat poison when ingested causes gi irritation on absorption it causes cramps,stiffness, weakness and paralysis of all muscles including heart
boiled lobster poisoning is seen in
boric acid poisoning boric acid is used as antiseptic or antifungal agent in baby talcum powder or as pesticide agnst ants and cockroaches causes ERYTHRODERMIC RASH followed by desquamation and exfoliation
borax is ??
k/a sodium borate , sodium tetraborate
over exposure causes repsiratory irritation
including n/v/d
in severe poisoning erythematosus and exfoliative rash , unconsciousness, respiratory depression and renal failure
prussic acid is another name of
hydrocynaic acid
scheeles acid is another name of
HCN
NAture of pupils in cynaide poisoning
fixed and dilated pupils are seen
moa of cyanide poisoning
inhibits cytochrome oxidase enzymes for oxygen utilisation in cells
death due to ,histotoxic anoxia
treatment for cyanide poisoning
*amyl nitrite
sodium nitrite they both promote
methhaemoglobin formation
* dicobalt EDTA chelate cyanide into harmless product
* hydroxocobalmine
* ventilation with 100%o2
*exchange transfusion or blood administration
characteristic smell on postmortem of cyanide poisoning
bitter almonds
color of postmortem staining of hcn
cherry red
fine froth may be present at mouth
eyes may be bright ,glistening with dilated pupils
internal appearence of hcn poisoning
characteristic bitter almond
smell from viscera of the body
mucous membranes appear congested and red
all vessels including veins appear red as they contain oxygenated blood
blood stained froth may be presnt in the trachea
principal behind giving nitrite in cyanide poisoning
cyanide s hve a better affinity for methhaemoglobin and nitrite convert haemoglobin into methhaemoglobin which combines with cyanide to form non toxic cyanmethhaemoglobin which in presence of sulphate donor like thiosulphate converts cyanide to thiocyante which is excreted in urine
principal behind giving vitb12 in cyanide poisoning
detoxify cyanide by forming cyanocobalamine by giving hydoxyl grp and then binding cyanyl grp which is excreted in urine or converted to thiocyanate by na thiosulphate
cobalt edta principal behind giving it in
cyanide poisoning
edta chelates cyanide to form a nontoxic product tht is excreted in urine it has more rapid action ,efficacious and less toxic thn nitrites
caustic poison erodes mucosa because
commonest cause of chemical burns
hydoxyl ions produces saponification of fat
cellular dehydration
coagulation of cellular protein and conversion of haemoglobin to haematin
which type of cattle poison occurs due to ingestion of linseed plants
hydrocyanic acid
non poisoning salt of cyanide is
potassium ferrocyanide
fatal dose of
carbolic acid
20 drops of pure phenol
40 drops of carbolic disinfectant
substances used to erase wrting inattempt to forgery is
oxalic acid
symptoms of oxalic acid poisoning
shock
hypocalcemia presenting as tingling ,numbness, twitching, trousseous and chvostek and convulsions
nephrotoxic lead to oxaluria
treatment of oxalic acid poisoning
never use warm water as causes more solublisation of acid
any preparation calcium lactate which converts poison into insoluble calcium oxalate is antidote for oxalate poisoning
effect of carbolic acid on mucosa is
initially green white or brown white which turns to brown or grey which is leathery and thickned
effect of h2so4 on mucosa is
brown discoloration of stomach with erosion and perforation
bloating paper appearence
effect on mucosa of HNO3
yellow discoloration of mucosa and skin
HCL and carbolic acid
greyish yellow stains
black colored mucosa is due to
KOH,NaOH
yellow or white grey mucosa
phosphorous
yellow discoloration of mucosa is with hno3 》phosphorous
brick red to brown color mucosa is due to
KCN
putrefaction
is retarded in deaths due to
poisoning •strychnine •carbolic acid •chronic heavy metals eg arsenic •zn chloride ANAEMIA DEBILITY WASTING DS
in HNO3 color of urine is
brown
in barbiturates poisoning color of urine is of
liquid gold
poisons causing miosis
PCM MO is Barred
Phenol
Choral hydrate
Morphine Muscarine and nicotine
Barbiturates
postmortem findings of carbolic acid are?
leathery stomach
pct necrosis
delays putrefaction
magenstrasse is ??
area which has greatest damage it is route which is followed by acidic agents in stomach in filled stomach along the lesser curvature and in empty stomach lower 1/2 sparing fundus
oochronosisis is seen in ?
carbolic acid poisoning pigmentation of cornea and various cartilage due to hydroquinone and pyrocatechol
which of the substances is given to erase ink to foreigners
oxalic acid
which poison causes tetany and torsseuseu sign +ve
oxalic acid
antidote for oxalic acid poisoning is
calcium gluconate
TOC for h2so4,HNo3,HCl is ??
weak solution of noncarbonated alkalies like CaO,MgO,non flatulent antacids
egg albumin
milk
wht is vitriloage
throwing of any corrosive on another person
sec 326 A
Sec 326B
perforation of stomach is more common due to ingestion of
h2so4
also causes brown discoloration of mucosa
most common site of damge in case of acid
stomach as already acidic
most common site of damage in case of alkali
oesophagus because it neutralizes acidity in stomach
type of necrosis by acids
coagulative necrosis
type of necrosis by alkali
liquefactive necrosis
fatal period of h2so4 is ??
12-24hrs
damge site of dry flame or heat burns is
at or above the site of contact no tricke marks
features of damge by chemical and steam/liquid burns
at and below the contact site so trickle marks are present
singing of hair is present in dry / moist burns
dry
red line is present in dry or wet burns or chemical
dry and moist burns not in chemical burns
postmortem appearence in carbon monoxide poisoning is
- bright cherry red discoloration of skin ,mucosa,mucus membrane nailbeds
- blisters on areas tht contact ground or appositional skin
- blood is thin and red coloured
- congestion of all organs
- Parkinson
at wht saturation hb with CO profound coma with shallow respiration occurs
50-60%
wht saturation of CO in blood is rapidly fatal
> 80%
cherry red discoloration is seen at which saturation of CO
30-40%
upper limit of CO In air is
0.01%
symptoms of carbon monoxide poisoning start when conc is
> 10%
at following blood concentration the clinical picture will simulate an alcoholic
50%
%of COHb causing death is
80%
in low CO con 4% symptoms produced will be
none
diffusion of oxygen at tissue level is affected in all following poisoning ?
phosgene CO
cyanide
simple asphyxiants heavier thn air is
methane
Carbon dioxide
Nitrogen when inhaled they exclude the o2
wht is Japanese detergent
suicide technique
it involves mixing of house hold chemicals like bath sulphur with toilet bowl cleaner to produce deadly poisonous hydrogen sulphide gas cloud it is used in closed spaces like car to achieve instant death
American substitute a common insecticide for bath sulphur as it is not there in us
love drug or adam or hug drug is another name of?
ecstasy it produces general symptoms stimulants ,tismus and bruxism within 1/2-1 hr
name rave drugs
▪ecstasy
▪gamma hydroxy butyrate(k/a georgia home boy,scoop water or liquid ecstasy )
▪ROHYPNOL
(k/a roofie,ropes,ropies,roches)
chemical name for ecstasy is
MDMA
wht is k/ a knock out drops or
mickey finn
or
dry wine
sedative chloral hydrate
it is given food or drink to make person suddenly helpless for rape and robbery
it is combined with alcohol which is k/a mickey finn used to increase potency of alcohol
chloral hydrate physical nature
peculiar pungent odour
crystalline used as a hypnotic
IT RAPIDLY DETERIORATES AFTER DEATH CHEMICAL ANALYSIS OF THE VISCERA SHOULD BE DONE AS AN URGENCY
how does ethylene oxide affects kidney
it is a bitter sweet non volatile liquid used as antifreeze it is cns depressant and affects kidney by forming calcium oxalate crystals
methods of determining blood and urine alcohol method
A KBC CASE A alcohol dehydrogenase method K ozelka and hine test Breath analysis Chromatography Cavett test
formulas for alcohal level in blood
widmarks formula
wht is wernicke encephalopathy
acute rxn to severe thiamine deficiency it is reversible characterized by GOA G global confusion O opthalmoplegia A ataxia
wht is korsakoff syndrome
chronic complications of severe thiamine deficiency 》wernicke encephalopathy characterized by A amnesia
C confabulation
it is irreversible
most common symptoms alcohol withdrawal
mild hangover( most common) sever •delirium tremens most severe clouding of consciousness, disorientation, visual hallucinations •alcoholic seizures • alcoholic Hallucination
fomepizole is a inhibitor of
alcohol dehydrogenase
primary agent responsible for toxic effects of methanol
formic acid which more toxic thn formaldehyde which inturn is more toxic thn methanol
clinical feature of methanol poisoning
Hi RADIO CiTy •Hypothermia •respiratory depression •anionic metabolic acidosis •dyspnea •increased osmolar gap •odour of spirit in breath •opaque vision •cyanosis •tubular necrosis
which of the following does not cause hyperpyrexia Maoi alcohol atropine amphetamine
alcohol it causes peripheral vasodilatation thus gives a feeling of warmth but inturn causes loss of heat thus hypothermia
morbid jealousy and mcewans signs
micturation syncope
munich beer heart
is diagnostic of ?v
case of alcohol intoxication, pupils are contracted, but on external painful stimulation of the person, e.g. by pinching or slapping, causes pupil to dilate followed by slow constriction again. This is called as McEwan’s sign and if this is positive, it is suggestive of alcoholic coma.
stages of alcoholic poisoning is
Acute alcohol poisoning is considered when blood alcohol concentration exceeds 150 mg/100 ml beyond his/
her capacity consumed by any preparation containing alcohol either in small doses at short intervals, or in one big dose.
SIGNS & SYMPTOMS
1. Stage of Excitement
Blood level: 50–80mg/100 ml of blood
Blood alcohol concentration (BAC): 0.05-0.1%
2. Stage of In-coordination
Blood level: 80–150 mg/100 ml of blood
Blood alcohol concentration (BAC): 0.15-0.25%
3.Intoxicated 150to 300 mg%
4 Stage of Coma
Blood level: >400mg/100 ml of blood
Blood alcohol concentration (BAC): > 0.25%
mcewan sign is +ve
wht is micturation syncope and Munich beer heart
▪when person gets up from bed for micturation in night probaly due to sudden upright posture there is syncope in alcoholic
▪munich heart is dilated cardiomyopathy in alcoholic
also there is •nystagmus in direction of gaze independant of head position
best method of treatment of methyl alcohal is
ethyl alcohol
fatal dose is absolute alcohal in adults is
150ml
fatal dose of methanol
60-250ml
treatment of methanol poisoning
1 gastric lavage using using sodium biborate infusion
2.oral or iv nahco3to combat acidosi
3.folinic acid speeds up elimination of folinic acid
4.ethanol iv is competitive inhibitor
do check glucose level as it causes hypoglycaemia 5.fomepizole
6.hemodialysis is treatment of choice in severe poisoning
6.eyes should be protected from light
an pt presents with pyrexia,constricted pupil,hypotension, cyanosis,stupor progresses to coma poisoning is due to phenobarbitone cannabis dhatura diphenhydramine
phenobarbitone
as it only causes
constriction of pupil
cannabis intoxication features r
- conjunctival injection
- increased appetite
- inc HR
- dry mouth
- flash backs
- amotivational syndrome
- colours appear brighter and richer
urine is alkalinized in ____ poisoning
barbiturates salicylates poisoning
urine is acidified in ??
morphine
amphetamine poisoning
TOC of barbiturates poisoning
hemodialysis 》forced alkaline diuresis
barbiturates poisoning presents with??
features of shock ie hemoconcentration and oliguria therefore urine is highly concentrated and deep yellow ie liquid gold is slang used for amphetamine addicts
urine appears liquid gold in which poisoning
amphetamine
antidote for benzodiazepines toxicity is ???
flumazenil
opium is derived from
unripe capsule of papaver somniferum
boy died in emergency room with white froth in mouth the poisoning is due to
opium or drowning
white leathery froth is present in
opium poisoning and drowning
drugs used
in herion \opioid intoxication
naloxone nalmefene naltrexone physostigmine thiamine glucose
drugs used opioid withdrawal
methadone clonidine
buprenorphine naloxone, naltrexone,nalmefene
constricted pupil is feature of opium withdrawal and overdose
opium overdose
type of respiration in morphine poisoning
slow
symptoms of opoid withdrawal
yawning dysphoric mood and insomnia with water loss from
various orifices ie lacrimation , salivation ,diarrhoea, vomiting rhinorohea
opium poisoning is featured by
- constricted pupil
- respiratory depression 3.hallucination
- tachycardia
- tachypnea
1,2,3
all are adultrants of heroin except charcoal quinine chalk powder fructose mannitol talc
charcoal
give various forms of cannabis
bhang
majun
ganja
charas or hashish
bhang is derived from
dried leaves and fruit shoots
ganja is derieved from
dried flowering tops of female plant
charas or hashish is derived from
resinou exudates from leaves and stem of plant
runamok amotivational syndrome are symptoms of
cannabis poisoning
clinical features of cocaine poisoning
B》 black tongue and teeth
U》ulceration and very rarely perforation of nasal septum
M》magnan syndrome or cocaine bugs or formification or tactile hallucinations P
persecuting delusions and perversions mainly homosexuality and libidinous
tactile hallucinations is the most characteristic of
cocaine poisoning
black tongue is seen i n abuse of
cocaine
a sensation of grains of sands under the skin is feature of
cocaine poisoning
angel dust is ?
phencyclidine
speed bal is cocaine +___
heroin
name cardiac poison
D 》digitalis O》oleander N 》nicotine Has 》hyocyanic acid A 》aconite Queen 》quinine
name the deliriant poisons
hi 》hyoscyanamus niger A B 》atropa belladona C 》cannabis indica D 》dhatura opium nd lead poisoning
color of root of aconite plant
outer dark brown
white internally which becomes pink on exposure to air
fatal period for aconite is
2-6 hrs
monks hood is another f
aconite ,monks hood ,blue rocket ,mitha bish ,wolf bane
wht is wolfbane or mitha bish
aconite
clinical features of aconite
gi 》on ingestion there is tingling ,numbness burning sensation from mouth to stomach
nervous system 》 mind remains clear till last paralysis of respiratory centre
muscular 》muscle weaknes
pupil dilate and contract ie hippus and later remain dilated
cardiovascular》 chest pain,hypotension first tachycardia then bradycardia
HYPERSALIVATION
symptons OPC poisoning
muscarinic B3 Bronchoconstriction Bradycardia Blurring of vision
S》sweating salivation L 》lacrimation red tears chromolacryorrhea U》 urination D》diarrhoea G》gastrointestinal distress E》emesis
smell of pt of opc poisoning
kerosene like
name poison causing miosis
Phenol M morphine P pontine hrge . chloral hydrate barbiturates Iridocyclitis
poisons causing mydriasid
Viper》viper venom D》dhatura A》atropine N》nux vomica C》cyanide cocaine calotropis CO cholroform Party 》 Parasympatholytic drugs palsy of 3rd nerve Atrophy optic nerve R》 retinal detachment int opthalmoplegia
color of postmortem lividity in cyanide poisoning
brick red
pm staining is also ka
suggilation vibices
darkening of death
wht is the time when pm staining starts to appear
commenses within 1 hr
fixed in 4-6 hrs
maximum bw 6-12 hrs
and persists till putrefaction sets in
colour of bright red pm lividity is
CO
HCN
Burn
cold
colour of pm staining is dark brown/ yellow possible poison is
phosphorous
opium produces ____ colour of pm lividity
black
clostridium produces ____ colour of lividity
bronze colour
h2s produces ____colour of lividity
blue green
odour during pm is burnt rope possible diagnosis is
cannabis
nux vomica is
seeds containing strychnine and used as cattle poison
moa of strychinine poisoning
it stimulants all parts of cns especially the ant horn cells of spinalcord greatly increasing reflux activity
inhibits the inhibition of
the ant horn cells of spinal cord resulting in excitation to any slight stimulus
cerebral cortex and respiratory centre is stimulated
signs symptoms of strychinine poisoning is
•convulsions affect all muscle at a time
•risus sardonicus contraction of jaw
•ophisthotonus
hyperextension of body effecting antigravity muscles
•bending forward of the body (emprosthotonus)
• bending sidewards of the body (pleurosthotonus)
•MIND REMAINS CLEAR TILL END
difference bw tetanus and strychinine
poisoning
tetanus is gradual in onset and strychinine is sudden in onset
•all muscles r involved in strychinine poisoning at same tine but not tetanus
•muscles r never completely relaxed in b/w fits in case of tetanus where as they r relaxed in case of strychnine
in nnuxvomica poisoning following are also to be preserved •long bone •brain •muscles •skin
brain
nux vomica contains 2 alkaloids strychinine and ____
brucine
respiratory depression is caused by all except
opium
barbiturates strychinine
gelsemine
strychinine
symptoms of dhatura poisoning is
atropine poisoning presents with symptoms of bronchodilation
,tachycardia ,mydriasis(blind as a bat)
hyperthermia ( hot as a hare)
dilation of skin leading to flushing (red as a beet), dryness of skin and mucous
(dry as bone )
difficulty in talking,swallowing, constipation ,urinary retention
delirium( mad as wet hen )
muttering delirium
pill rolling tremors
carphologia picking up of imaginary threads from clothes, bed sheets
9 ds 1 dry hot skin ( hot as hare) 2 dilation of cutaneous blood vessels ie ( red as beet ) 3.dilation of pupils ( blind as abat) 4.dry as a bone dryness if mouth and mucosa 5 dysphagia 6 difficulty talking 7.delirium ( mad as wet hen )
dhatura or atropine poisoning
treatment of atropine poisoning is
physostigmine doc sc/iv
gastric lavage with tannic acid
cold sponging
diazepam for convulsions
treatment
for amanita muscaria and amanita phylloides
atropine is antidote they produce parasympathetic symptoms
dhatura seeds resemble
capsicum seeds
thorn apple is
dhatura alba
dhatura niger
a child is brought with dilated pupil ,dry mouth ,delirium the substance is atropine /sympathetic
atropine
women consumes several amitryplline following can be done except •nahco3 infusion •gastric lavage •diazepam to control seizures •atropine as a antidotes
atropine as a antidotes as tca itself has anticholinergicssideeffects
ci for atrophine poisoning is
narrow angle glaucoma •belladonna poisoning
•prostatic hypertrophy
atropine is doc for
- opc poisoning
* mushroom poisoning
most common way of commiting suicide is by
use of insecticide
see which are alkyl phosphates and aryl phosphate
?
most specific test for opc poisoning is
plasma
cholinestrase
aashtma like symptoms r seen in ___
poisoning
opc
atropine reverses which effect of opc poisoning
only muscarinic effect not nicotinic like respiratory muscle paralysis
a person is hving bp of 90/50 should we give vasopressor
no give if bp is less thn 60
carbamate
poisoning should we give oximes
no
plant penicillin is
endrin
20yr old pt comes with pinpoint pupil ,fasiculations,no fever dx is head injury opc atropine pontine hrge
pinpoint pupil is only seen in opc and pontine hrge but difference is tht pontine hrge there is fever,but no fever in opc poisoning so ans is opc
oximes r ineffective in
carbamate poisoning edrophorium, neostigmine propxur donepizil
cause of pinpoint pupil
BPH SOOCH B》Barbiturates slightly constricted but dilate in later stage of asphyxia P》phenol H》hrge pontine S》syphilis O》opc O》opium C》choral hydrate H》horner syndrome
in which poisoning pupil alternately constrict and dilate remains dilated in later stage
aconite poisoning
acridor pear smell is in which poisoning
paraldehyde
shoe polish odour is produced in poisoning of
nitrobenzene
rotten eggs odour is due to which poisoning
hydrogen sulphide
disulphiram
garlic odour is produced in which poisoning
- arsenic
- zinc phosphide
- aluminium phosphide
blue green pm staining is seen in
h2s
blue hypostasis
h2s bluish green
aniline (deep blue)
cuso4 blue
red brown lividity is seen in
aniline
bromide nitrite
whereas phosphorous
produces dark brown
fecl3 is used in diagnosis of
phenol
best site for collection of samples for toxicology
femoral vein》subclavian , jugular , ililac vessels 》root of aorta 》svc》heart
which poison turns to black on exposure to silver nitrate
celphos on coming in contact with moisture liberates phosphine which on reacting with agno3 gives black colour
urine is stored in
?
toluene for chemical analysis
thymol
for general purpose
sample to look for uric acid is send in ?
alcohal
specimen for virological purposes is sent in
50% glycerine
sodium flouride is
used for preservation of
samples for alcohal and 3C’s
cocaine
cyanide and
CO analysis
specimens for toxicological analysis is preserved in ?
saturated sodium chloride
lee jones test is used for
ie adding ferrous sulfate, sodium hydroxide ,heat,HCL to gastric
content s used to differentiate cyanide from salicylates
name few elapids
cobra
krait
coral snake
name few vipers
russel viper
green pit viper
type of venom by vipers
neurotoxic
type of venom by vipers
vasculotoxic (hemolysis ,cytolysis )
moa elapid bite
act on motor nerve cells like curare and cause paralysis of muscle in following order mouth 》throat 》respiratory muscle
moa of viper bite
endothelial cells damage and rbc hemolysis
local symptoms at the site of bite is severe in which snake bite
viper
rest both hve minimal symptoms
priapism occurs with bite of e
Spanish fly
russel viper belongs to
viperidae
pit viper belongs to
crotalidae
cobra ,krait belongs to
elapidae
venom is produced by
salivary glands
the characteristic features poisonous snake are
POISONOUS NON POISONOUS
long fangs hollow several small teeth2 rows
compressed tails not so
nocturnal habit not so
belly scales are large,complete small cover entire breath donot cover entire breath
head scales r small large
ophitoxemia means
poisoning by snake venom
venom of sea snake is mostly
myotoxic
which is a non poisonous
snake
viper,krait,sea snake ,rat snake
rat snake
stability of snake venom is dependant on
disulphide bond
treatment of 6 hrs old with only mild local edema is
wait and watch ?
first treatment for snake bite is
immobisation or splinting of limb
scorpion bite resembles
resembles neuro toxic cobra and ,krait
polyvalent venom is against
4 common species in india common cobra krait, russel viper, saw scale viper
abrus precatorius is used as
it contains abrin whose mechanism is similiar to viper snake and is used to kill cattle as sui
other name of abrus precatorius
indian or Buddhist rosary /prayerbead
,crab eye
rati
most potent toxins in plant kingdom is
ricin from ricinus communis more poisonous tn cobra and 6000 time thn cyanide
which substance is used as
agent to inflict artificial bruise
semicarpus anacardium
socrates was killed by?
hemlock or conium maculatum
clinical features of hemlock or conium maculatum poisoning are
gastric irritation, pain , vomiting, 》followed by increasing ascending paralysis to affect respiratory muscles
breath ha mousy odour
how much of croton seed oil is fatal ?
20 drops
vegetable viper snake poison is
abrus
activated charcoal is not useful in
alcohal
corrosive heavy metal
hydrocarbon cyanide
contraindications of gastric lavage are
- corrosive poisoning alkaleis ,acid organic acids except carbolic acid
- convulsant poisoning eg strychinine •kerosene poisoning
in salicylate poisoning treatment recommended is
forced diuresis
urine is alkanised
in ?
salicylates barbiturates
hemoperfusion with charcoal is used in poisoning with
amphetamine antidepressant atropine barbiturates benzodiazepines chloroquine opium strychinine
hemodialysis is not useful in ?
copper sulphate kerosene oil,
benzodiazepines OPC ,
digitalis
c-oil-BORD
hemodialysis is useful in
aspirin barbiturates chloral hydrate
methyl alcohal,ethyl alcohol ,ethylene glycol and theophylline
gastric lavage is
indicated in all cases of acute poisoning
ideally because of
fear of aspiration
complications of kerosene poisoning is
pneumonia
do we give corticosteroids in the treatment of kerosene poisoning
no corticosteroids, prophylactic antibiotics, emesis induction ,gastric lavage and use of activate charcoal are not recommended • fever and leukocytosis are early features of kerosene poisoning induced pneumonitis occurring within hours
xray finding occur in few hrs
treatment of paracetamol poisoning
gastric lavage useful in <4hrs
•< 2.5 l fluid daily as pcm leads to fluid retention •nacetylcysteine to prevent hepatic damage
•hemodialysis and hemoperfusion
antidote for strychinine poisoning
short acting barbiturates like phenobarbitone
antidote for cyanide
poisoning
amyl/sodium nitrite and sodium thiosulphate
antidote for ethylene glycol
fomepizole /ethanol
contraindications of BAL
cadmium and iron poisoning
bal is agent of choice for
mercury also used for gold cu bismuth nickel arsenic antimony
treatment of iron poisoning is
- gastric lavage with nahco3 and desferrioxamine •mgoh2
- injectable desferrioxamine (agent of choice in acute poisoning)
- hemodialysis
most prominent means of committing suicide in india are ?
hanging >consuming poison>self immolation >drowning
wht is parasuicide
non fatal act of suicide in which aim is not death most common cause is sublethal drug overdose 》wrist slash
most imp indication
for edta is
lead poisoning
has no role in hg poisoning
doc for transfusion siderosis
deferiprone
gunch/indian liquorice is another name of
abrus precatorius
egg shaped seeds with black spot at 1 end is
abrus precatorius
abrin is active principal in
abrus precatorius
fatal dose of croton
20 drops
4 seeds
castor plant is
ricinus communis
fatal dose of ricinus communis is
10 seeds ricin 6 mg
jamalghota is
croton
best preservative for viscera is
rectified spirit
rectified spirit is not used in
alcohal
phenol
phosphorous
paraaldehyde
histopathology specimen is preserved in
formalin
arsenic poison resembles
cholera
fading measeles
addison ds
thallium poisoning resembles which disease
natural death
Gullian barre
porphyria
opc resembles which ds
bronchial ashtma
opc resembles which ds
bronchial ashtma
ideal homicidal poison is??
thallium
triad of thallium poisoning
gastroenteritis
polyneuritis
hair loss
tabby cat striations are seen in
heart show fatty degeneration in thallium poisoning
wht is signe de sourcil
the eyebrow sign seen in thallium poisoning
outer 1/3 rd of eye brow falls characteristic of thallium poisoning
acne is seen in which poisoning
bromides
which is ideal suicidal poison
cyanide
most commonly used suicidal poisons r
opc
name stupefying agents
dhatura
cannabis
chloral hydrate
dry wine is
chloral hydrate
abortifacient drugs r
calotropis oleander aconite ergot lead
cattle poison are
abrus oleander calotropis aconite opc strychinine curare snake venom
arrow poison is
abrus croton calotropis aconite strychinine curare snake venom
drugs not included in NDPS act are
alcohal
paracetamol
nicotine
schedule C includes
biological and special products
schedule E includes
poisons
schedule F includes
vaccine and sera
schedule G includes
hormonal preprations
schedule H include
drugs /poisons sold on prescription of RMP
schedule L includes
antibodies
antihistamines
chemotherapeutic drugs
schedule X includes
potential drug of abuse
best method to induce emesis is
gag reflex or hypertonic saline
only pharmaceutical agent recommended to induce vomiting is
ipecacuanha
gastricl lavage is useful withinn
3hrs of ingestion of poison
acute yellow fatty liver is caused by ??
arsenic
most common presentation of gastroenteritis is
gastroenteritis
beus lines are seen in
chronic stsyemic disease
diffrential of mees lines
beus line 》chronic systemic ds
muehrcke’s line 》hypoprotenemia
golden hair are seen in
arsenic and cadmium poisoning
copper also
arsenic trioxide is used in treatment of
AML
arsenic crosses BBB??
no
test of arsenic are
reinsch test marsh test gutziet test neutron activation analysis absorption spectroscopy
ptysalism is seen in
copper poisoning
vineyard sprayers disease is due to
copper sulphate solution
chronic opthalmic exposure of copper results in
chalcosis oculi 》copper deposition in cornea,lens,vitreous
kayser Fleischer rings》deposition in desmets membrane
chalcosis lentis is ant subcapsular catract sunflower cataract
smelters fever is
metal fume fever due to Zn
Monday morning fever is seen in
Zn poisoning metal fume fever
most effective treatment of plumbism is
calcium disodium versenate
xray finding of lead poisoning
increased radioopaque bands of lines at metaphysis of long bones is seen in children
symptoms of iodine poisoning
intense thirst
blue colored vomiting with iodine odour
urine is scanty and red brown in colour
symptoms of iodism
it is chronic iodine poisoning painful parotits resembling mumps pain over frontal sinus running nose wasting and emaciation
which phosphorous is toxic
white phosphorous is highly toxic
wht is smoking stool syndrome
faint fumes coming from stools in phosphorous poisoning
lumiecent vomiting and feaces r diagnostic of
phosphorous poisoning
treatment of phosphorous poisoning is
- gastric lavage with kmno4 as it oxidises phosphorous into phosphoric acid and phosphates
- CUSO4
- vitK
- avoid oil and fat
- hemodialysis
fulminant poisoning is seen when amt of phosphorous ingested is
more thn 1 gm
antidote for phosphorous poisoning is
copper sulphate as it coats the phosphorous particles with insoluble copper phosphide
postmortem findings of phosphorous poisoning
in acute poisoning jaundice is seen
the gastric and intestinal contents smell of garlic
mucosa becomes yellowish or greyish white
multiple small hrge r seen
liver becomes swollen, yellow, easily ruptured
after a week yellow atrophy appears
diwali poison are
phosphorous mercuric cyanide (small tablets when put to flame produce snake like appearence) antimony arsenic strontium
brown malt reflex is seen in
mercuria lentis chronic mercury poisoning
bilateral deposit of mercury on ant capsule of lens it has no effect on visual acuity
liver changes in celphos poisoning
centrizonal hrgic necrosis
TOC for celphos poisoning is
MgSO4
activated charcoal and paraffin for adsorption and excretion of PH3
gastric lavage +_____= black colour
silver nitrate due to phosphine gas in gastric lavage
treatment of choice for flouride poisoning
calcium
liquid gold is
urine of amphetamine addicts as urine of amphetamine addicts is itself addicting people used to sell their urine so it is k/a liquid gold
marasmus is seen in which poisoning
phenol poisoning
effect of phenol on respiratory centre
depressant
lee jones test is used for
cyanide poisoning based on prussian blue reagent
coffee ground appearence of vomica is seen in
oxalic acid poisoning
changes in contents of stomach in oxalic acid poisoning
stomach contents are gelatinous and brownish due to acid hematin formation
stomach is reddened,eroded,almost black in colour
test done for CO poisoning is
kunkels test tannic acid test
wetzel test
hoppe seyler test
bilateral symmetrical necrosis of lenricular nuclei and punctate hrge in white matter is seen in
CO poisoning
universal antidote contains
mag oxide 2 acid neutralise charcoal 1 c/i corrosive alcohal heavy metals CN tannic acid 1 percipitates alkaloid
most desirable method of alcohol estimation for medicolegal purposes
gas chromatography
____ metabolism is disrupted in chronic alcohalism
tryptophan
legal limit of alcohol prescribed by motor vehicle act is
30 mg% of blood alcohol level
critical limit leading to incoordination of muscles in alcoholic is
150mg % bal
rate of fall of BAC Is
15mg%/hour
urine contains more alcohol than blood t/f
true
blood for alcohal estimation in postmortem is taken from
femoral vein
BAC =_____×Breath alcohol concentration
2.3
BAC =__ × Urine alcohal conc
0.75
BAC _____vitrous humor conc
0.8
earliest clinical presentation in methanol poisoning is
abdominal cramps
wht is mellanby effect
the behavioural impairment at given blood alcohol level is more when blood alcohol levels are rising than when it is falling
TOC for methanol poisoning
hemodialysis
smack is
heroin
other names of heroin
brown sugar
junk
dope
smack
cutting in is
adulteration of heroin
love drug is
MDA
eve is
MDEA
ecstasy is
MDMA also k/a rave drugs
date rape drug is
alcohal
barbiturates
rohyphol(fluntrazepam)
chloral hydrate (knockout drops/mickey finn)
hot shot is
heroin +strychnine
crack is
cocaine + baking soda
it is sniffed
mickey finn is
chloral hydrate +alcohal
tests done to detect opium.is
marquis test
deniges test
husemanns test
most potent prepration of cannabis is
charas
route of cocaine addiction
snorting
skin popping
most common substance abuse in india
tobacco
most common illicit substances abuse in India
cannabis
most common illicit substances abuse in world
cannabis
most common date rape drug is
alcohol
3rd supralabial
touches both eye and nostril in
common cobra
4th infralabial is largest in
common krait
central rows of hexagonal scales
common krait
PASV starts with
10 vials
fixation of toxin of common cobra
post synaptic region
neostigmine is useful
fixation of toxin of
common krait
presynaptic region
no role of neostigmine
wht is mercurialism
caused by iv inj of mercury
causes thrombophlebitis
granuloma
pul embolism
who is ophiophagus
hannah
king cobra
naja
naja is
common cobra
echis carinatus
saw scaled viper
bangarus ceruleus is
banded krait
best emetic
ipeac
best emetic
ipeac
best purgative best cathartic
sorbitol
