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Toxicology Final Ingrid > Poisonings > Flashcards

Poisonings Flashcards

1
Q

Ethiology of DNOC poisoning

A

insecticide, herbicide, acaricide and fungicide

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2
Q

Mechanism DNOC

A

Inhibit oxidative phosphorylation in tissues
Decreased synthesis of energy rich compounds
Stimulation of metabolism in organism
Methemoglobinaemic agent

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3
Q

Symptoms DNOC

A

Yellow mucus membranes, skin and feathers.
Hyperpnoea, dyspnoea, sweating (increased body temp.), spasms, muscle weakness, oliguria, rapid rigor mortis after death

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4
Q

Therapy DNOC

A

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.

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5
Q

CHTA of DNOC

A

Yellow colour
Alkaline environment: forms salt in yellow solution
Acidic environment: insoluble
pH change

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6
Q

Ethiology of warfarin poisoning

A

effective agent in rodenticides

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7
Q

Mechanism of warfarin poisoning

A

Anticoagulant
Inhibit production of prothrombin in liver
Prolongs clotting time of blood
Damages capillaries

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8
Q

Symptoms of warfarin poisoning

A

Dehydration - rats leave to find water
Cats & dogs - internal bleeding - blood in vomit, urine, diarrhea
Bleeding from natural body openings
Haematoma
Haemorrhages in brain

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9
Q

Treatment of warfarin poisoning

A

Blood transfusion
Vitamin K or K1

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10
Q

CHTA warfarin

A

Chromatographic - blue on yellow background

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11
Q

Ethiology of aflatoxins

A

Produced by Aspergillus flavus and Aspergillus parasiticus, naturally in environment

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12
Q

Mechanism of aflatoxins

A

Effect liver
Severe hepatocellular necrosis - high doses

Low doses cause reduced growth rate and enlarged liver

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13
Q

Symptoms aflatoxins

A

Loss of apetite, vomiting, jaundice, bruising, bleeding, diarrhea

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14
Q

Therapy aflatoxin

A

Symptomatic and supportive

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15
Q

CHTA aflatoxins

A

chromatography:
B1 & B2 stain blue
G1 & G2 stain green
UV screening of raw material

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16
Q

Ethiology Organophosphates

A

insecticide

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17
Q

Mechanism organophosphates

A

Inhibit acetylcholinesterase by binding to enzymes –> overabundance of acetylcholin at neuroreceptor –> stimulate ANS, CNS and smooth muscles.
Contain sulphur - more toxic

18
Q

Symptoms organophosphate poisoning

A

Salivation, diarrhea, vomiting, cramps, seizures

19
Q

Therapy organophosphate

A

Atropin

20
Q

CHTA organophosphates

A

TLC and GC

21
Q

Ethiology of MCPA

A

herbicides and algicides

22
Q

Mechanism of MCPA

A

Inhibit ribonuclease synthesis
Uncoupling of oxidative phosphorylation
Demyelinisation of peripheral nerves

23
Q

Symptoms MCPA

A

Fatigue, vomiting, nausea, diarrhea, anorexia, tremor, ataxia, increased body temperature, hyperventilation, hypoxemia, stiffness in hindlimb muscles - paralysis, coma

24
Q

CHTA of MCPA

A

Yellow stain on blue background with BTB
Dark stain under UV light with AgNO3

25
Q

Therapy of MCPA

A

Symptomatic and supportive

26
Q

Describe screening method for detection of Aspergillus flavis in cereals

A

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.

27
Q

Ethiology of atropine

A

Natural alkaloid in solanaceous plants. Parasympathetic compound that penetrate the blood-brain barrier.

28
Q

Mechanism of atropine

A

Prevents binding of acetylcholine to its receptors:
* spasmolytic effect on smooth muscles
* depressant effect on secretion from glands

29
Q

Symptoms of atropine intoxication

A

Facial flushing
Dry mucus membranes
pupils unreactive to light
tachycardia
hypertension
disorientation
delirium
In high doses: hyperthermia, hallucination, fatigue, coma

30
Q

CHTA of atropine

A

TLC - orange/brown colour

31
Q

Therapy of atropine poisoning

A

Symptomatic:
* Beta blockers and diazepam
In life-threatning situation: physostigmine
In per-oral ingestion: activated charcoal

32
Q

Therapy of lead poisoning

A
  1. BAL (dimercaprol) acts to chelate lead both intracellularly and extracellularly. 2 BAL + lead –> complex secreted in urine
  2. 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.
33
Q

Mechanism of cyanide

A

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.

34
Q

Ethiology of ethylene glycol intoxication

A

automobil and radiator antifreeze

35
Q

Mechanism of Zn3P2 poisoning

A

In acid environment of stomach or in contact with water, hydrogen phosphide (PH3) is released.

36
Q

Clinical symptoms of Zn3P2 poisoning

A

Apathy
Agitation
Rigidity
Black vomit and faeces
Vomitting
Staggered moving
Spasms
Death
Large stomach

37
Q

Therapy of urea poisoning

A

acetic acid, vinegar or hydrochloric acid

38
Q

Treatment of mercury poisoning

A

Use of chelating agents (BAL, CaEDTA)
Gastric lavage
Activated charcoal

39
Q

Treatment of cyanide poisoning

A
  1. Formation of methemoglobin by administration of nitrites - MtHb-CN
  2. Application of sodium thiosulfate - SCN- which is excreted in urine
40
Q

Mechanism of NaCl poisoning

A

Change in osmotic proportion and irritant effect on digestive system

Toxicology Final Ingrid (8 decks)

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