Poisonings Flashcards
Ethiology of DNOC poisoning
insecticide, herbicide, acaricide and fungicide
Mechanism DNOC
Inhibit oxidative phosphorylation in tissues
Decreased synthesis of energy rich compounds
Stimulation of metabolism in organism
Methemoglobinaemic agent
Symptoms DNOC
Yellow mucus membranes, skin and feathers.
Hyperpnoea, dyspnoea, sweating (increased body temp.), spasms, muscle weakness, oliguria, rapid rigor mortis after death
Therapy DNOC
Application of barbiturates, sufficient amount of water, rehydration,
stabling in cold room, decontamination of skin with mild soap and water,
methemoglobin methylene blue if high conc.
CHTA of DNOC
Yellow colour
Alkaline environment: forms salt in yellow solution
Acidic environment: insoluble
pH change
Ethiology of warfarin poisoning
effective agent in rodenticides
Mechanism of warfarin poisoning
Anticoagulant
Inhibit production of prothrombin in liver
Prolongs clotting time of blood
Damages capillaries
Symptoms of warfarin poisoning
Dehydration - rats leave to find water
Cats & dogs - internal bleeding - blood in vomit, urine, diarrhea
Bleeding from natural body openings
Haematoma
Haemorrhages in brain
Treatment of warfarin poisoning
Blood transfusion
Vitamin K or K1
CHTA warfarin
Chromatographic - blue on yellow background
Ethiology of aflatoxins
Produced by Aspergillus flavus and Aspergillus parasiticus, naturally in environment
Mechanism of aflatoxins
Effect liver
Severe hepatocellular necrosis - high doses
Low doses cause reduced growth rate and enlarged liver
Symptoms aflatoxins
Loss of apetite, vomiting, jaundice, bruising, bleeding, diarrhea
Therapy aflatoxin
Symptomatic and supportive
CHTA aflatoxins
chromatography:
B1 & B2 stain blue
G1 & G2 stain green
UV screening of raw material
Ethiology Organophosphates
insecticide
Mechanism organophosphates
Inhibit acetylcholinesterase by binding to enzymes –> overabundance of acetylcholin at neuroreceptor –> stimulate ANS, CNS and smooth muscles.
Contain sulphur - more toxic
Symptoms organophosphate poisoning
Salivation, diarrhea, vomiting, cramps, seizures
Therapy organophosphate
Atropin
CHTA organophosphates
TLC and GC
Ethiology of MCPA
herbicides and algicides
Mechanism of MCPA
Inhibit ribonuclease synthesis
Uncoupling of oxidative phosphorylation
Demyelinisation of peripheral nerves
Symptoms MCPA
Fatigue, vomiting, nausea, diarrhea, anorexia, tremor, ataxia, increased body temperature, hyperventilation, hypoxemia, stiffness in hindlimb muscles - paralysis, coma
CHTA of MCPA
Yellow stain on blue background with BTB
Dark stain under UV light with AgNO3
Therapy of MCPA
Symptomatic and supportive
Describe screening method for detection of Aspergillus flavis in cereals
One layer of grains onto 15x15 cm frame
Observe in dark room under UV light
Green fluorescens - count the green grains
0-1 = negative
2-3 = feed can still be used
4+ = need further analysis for quantitative determination of aflatoxins –>
extract by chloroform, methanol or acetone. Pipette standard and sample onto chromatographic plate and observe under UV light after dissolvent has reached the top.
Ethiology of atropine
Natural alkaloid in solanaceous plants. Parasympathetic compound that penetrate the blood-brain barrier.
Mechanism of atropine
Prevents binding of acetylcholine to its receptors:
* spasmolytic effect on smooth muscles
* depressant effect on secretion from glands
Symptoms of atropine intoxication
Facial flushing
Dry mucus membranes
pupils unreactive to light
tachycardia
hypertension
disorientation
delirium
In high doses: hyperthermia, hallucination, fatigue, coma
CHTA of atropine
TLC - orange/brown colour
Therapy of atropine poisoning
Symptomatic:
* Beta blockers and diazepam
In life-threatning situation: physostigmine
In per-oral ingestion: activated charcoal
Therapy of lead poisoning
- BAL (dimercaprol) acts to chelate lead both intracellularly and extracellularly. 2 BAL + lead –> complex secreted in urine
- CaEDTA - forms stable, non-soluble, non-toxic, non-ionic complex with lead ions. Removed lead from the extracellular compartment of soft tissues, CNS and RBC, excreted in urine.
Mechanism of cyanide
Cyanide bind to iron Fe3+. Inhibit reoxidation of cytochrome oxidase - cellular hypoxia. Cyanide binds reversibly with cytochrome oxidase inhibiting the final step of oxidative phosphorylation - the transfer of electrons to oxygen.
Inhibit cellular respiration and formation of ATP.
Ethiology of ethylene glycol intoxication
automobil and radiator antifreeze
Mechanism of Zn3P2 poisoning
In acid environment of stomach or in contact with water, hydrogen phosphide (PH3) is released.
Clinical symptoms of Zn3P2 poisoning
Apathy
Agitation
Rigidity
Black vomit and faeces
Vomitting
Staggered moving
Spasms
Death
Large stomach
Therapy of urea poisoning
acetic acid, vinegar or hydrochloric acid
Treatment of mercury poisoning
Use of chelating agents (BAL, CaEDTA)
Gastric lavage
Activated charcoal
Treatment of cyanide poisoning
- Formation of methemoglobin by administration of nitrites - MtHb-CN
- Application of sodium thiosulfate - SCN- which is excreted in urine
Mechanism of NaCl poisoning
Change in osmotic proportion and irritant effect on digestive system
