Inorganic irritant poisons

Arsenious oxide-sankhya, somlakhar or arenic trioxide ——most toxic

Arsenic disulphide / red arsenic

Arsenic trisulphide-Yellow arsenic

Copper arsenite-sceele’s green

Copper acetoarsenite-paris green

Arsenic salts

Inhibits ATP formation by combining with the mitochondiral enzymes of sulfydryl group especially pyruvate dehydrogenase and certain phosphates leading to uncoupling of mitochondrial oxidative phosphorylation.

inhibits transformation of thiamine inot acetyl coa and succinyl coa

inhibits cellular glucose uptake, gluconeogenesis and fatty caicd oxidation further preventing the formation of ateyly coa

MOA of arsenic

120-200mg

1-2days

Fatal dose of arsdenic

Clinical features of acute arsenic poisoning

Subacute arsenic poisoning

Rain drop pigmentation, Mee’s lines,Flexor eczema, painless perforation of nasal septum, bone marrow depression, peipheral neutopathy resembling sensorymototr type as in gullian bares syndrome, weakness of the extensor muscles leading to foot drop and wrist drop.

Features of chronic poisoning

BAL or dimercaprol-3-5mg/kg im 4hrly 2 days, 6 hrly 1 day and 12 hrly for 10 days

Antidote for arsenic poisoning

RIgor mortis early and lasts for longer suration

body is emacitated

putrefaction is delayed

blood tinged vomitus and fecal matter may be present on the clothes.

eyeballs are sunken and skin cyanosed

stomach-edematous, swollen, flea bittenn appearance, red velvety mucosa.

Stomach has mucin covering that may have arsenic particlescongetsion more marked at crest of fugal

Inflammation more at greater curvature posterior part and cardiac endbrain edema necrosis, hemorrhagic encephalitis.

PM findings of arsenic

Lead acetate, carbonate, chromate, monoxide, tetroxide most toxic, sulphide least toixc

Toxic compounds of lead

gasoline

petrol, automobile exhaust, house paints, battery making, steel welding and cutting

Sources of lead poisoning

inghiibts mitochondrial oxidative phosphorylation by combining with sulfhydrl group,

inhibits enzymes responsible for heme synthesis—-causing anemia leading to hemolysis

Mechanism of action of lead poisoning

vomitting, constipation, diarrohea, headcahe, lethargy, myalgia,abdominal pain, metallic taste, ataxia, convulsion,coma

features of acute lead poisoning

anemia

basophilic stippling

burtonian line due to the deposition of granules in the gingiva, formed due to the formation of lead sulphide from the h2s released from decomposed protein in the mouth

Bone line’lead line -deposition of lead in the epiphyses of growing long bones.

Constipation, Colic of intestine,ureters and BVs , Cabot;s ring -figure 8 in RBCS

Drop-foot and wrist due to the weaknedd of the muscles and degeneration of nerves due to the interference with phosphocreatine metabolism.

Encephalopathy-associated with tetraethyl lead

Face pallor-earliest and most consistent sign

Gout

Features of chronic lead poisoning

Severe poisoning with encephalopathy -BAL-4mg'/kg immediately repeat same dose at 4hourly interval until blood level falls below 8ug/100ml.

then reduce to 12mg/kg/day in 3 divided doses

calcium sodium edta-75mg’kg’day—— reduce to 50 mg

oral chealtion with d penicillamine 10mg /kg/day

if no encephalopathy-reduced doses

moderate ko lagi only edta

mild ko lagi d penicllamine -3omg/kg/day

treatment of lead poisoning

PM finings of lead poisoning

inorganic- mercuric form and mercurous form

mercuric chloride and mercurous chloride mercuric cuphide, cyanide, oxide, iodide.

organic- methyl mercury

dimethyl mercury ethyl mercury phenyl mercury

toxic compounds of mercury

clinical features of merury

Blue MEAT

Blue line, Mercuria lentis, Erethism, acrodynia, tremors

Chronic mercury poisoning is characterised by

Danbury tremors

intially fine ——later coarse and involuntary. termor begins first in the hands, procedes towards the lips and tongue and finally involves the arms and legs.

in advancedd case-hatters shake and glasssblowers shakes. concussion mercularis-severe form of tremors in which no activity is possible.

Tremors associated with mercury poisoning

mercury depositions in the anterior capsule of the lens

on slit lamp examination malt brown reflex is seen.

mercuria lentis

neuropsychiatric disorders present in mercury posioning

characterised by- anxiety amnesia depression, mood instalbility, loss of confiedence, constant blushin, suciede melanchonia, insomina, delusions and hallucination

mad hatters syndrome

Erethism

hypersensitivity reaction isiosyncriatic

characterised by-

paresthesia, pink, puffy, peeling of skin, painful

Acrodynia

minamata disease

hunter rusell syndrome

other disease caused due to hg poisoning

removal of further exposure

demulcents

saline purgatives

oral hygiene

chealting agents

d penicillamine-25-40mg'/kg/day in 4 divided doses in case of children

adult-250mg/kg/day in 4 times a day

DMSA
DMPS

BAL

treatment of mercury posioning

Copper sulphate-blue vitrol

copper carbonate0mountain green

copper subacetate-verdigris

copper asenite-scheels green

copper acetoarsenite-paris green

Copper toxic compounds

copper sulphate-20-30gm

copper subacetate- 15gm

fata period -1-3days

fatal dose of copper

clincial feeatures of copper poisoning

PM findings of copper poisoning

chalcosis bulbi- kayser fleischer ring, sunflower cataract, golden plaques depsoited at posterior pole of retina that reflects with metalic sheen.

Vineyard sprayerslungs-due to chronic exposure to bordeaux solution(1-2percent copper sulfate solution neutralised with lime)

Copper realted terminologies

potassium ferrocyanide

Antidote for copper poisoning

cadmium

ouch ouch disease or itai disease is casued by

replaces calcium present in the bone-leads to bone softening-osteomalacia

cadmium moa

Thallium poisoning

Poisoner’s poison

forms-thallium acetate, thallium sulphate

BAN

butterfly rash, behavioural change

alopecia with madarosis, aldrich mee’s lines

neuropathy-similar to arsenic

CF

Iron posioning

white- garlicky odour, luminiscent, ocidative, fuming,inflammable, highly toxic

red- sab opposite of white and non toxic

forms of phosphorous

WHite- rodenticide, insecticide, ffertilizers, bombs, smoke screens fireworks

red- matchsticks

Uses of phosphorous

protoplasmic poison and affetts celular oxidation

cardio and heapatotoxic

moa of phosphorous

clinical features of phosphorous

similar to acute

phossy jaw or glass jaw- osteomyelitis of the lower jaw. initial toothache, swelling, loosening of teeth.

features of chronic poisoning pf phosphorous

milk, oily or fatty food should not be given as it increases absorption

what should not be done in the treatment of phosphorous poisoning

Pm finding of phos poisoning