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TOX > Pesticides DONE > Flashcards

Pesticides DONE Flashcards

1
Q

members of organophosphorus

A

Parathion , Malathion

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2
Q

moa of organophosphorus

A

irreversible binding of their phosphate radicals to the
cholinesterase enzyme forming phosphorylated enzymes.

within 48, the enzymy complex loses an alkyl group called aging

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3
Q

Clinical picture of organophosphorus

A

Cholinergic syndrome
* Muscarinic receptors effects: (DUMBBLES)
Diarrhea, Urine incontinence, Miosis, Bronchospasm, Bradycardia, Lacrimation, Emesis and Salivation.
2. Nicotinic receptors effects:
Musculoskeletal: Fasciculation — paralysis.
3. Cardiovascular (Sympathetic ganglia):
Tachycardia & hypertension followed by bradycardia &
hypotension.
4. CNS effects
- Stage of stimulation: anxiety, irritability, and convulsions.
- Stage of depression: coma, and depression of both respiratory & cardio-vascular centers.

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4
Q

causes fasciculation then paralysis

A

OPP

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5
Q

causes tachycardia and hypertension followed by bradycardia and hypotension

A

OPP
Parathion malathion

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6
Q

other effects of OPP

A

metabolic acidosis
hyperglycemia
non-cardiogenic P edema

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7
Q

intermediate syndrome of OPP

A

paralysis of proximal muscles of the limbs, neck flexor muscles, and respiratory muscles.
not responsive to atropine or oximes

3 days to 30 days

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8
Q

Delayed peripheral neuropathy of OPP

A

begins by paresthesia (glove & stocking), and pain
in the calves followed by weakness
“toe drop” that rapidly progresses to flaccid paresis.
treatment is difficult & no role of antidotes

3 weeks

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9
Q

Differential diagnosis of OPP

A

Carbamate
Other causes of miosis such as opioids and sedative-hypnotics.
gastro-enteritis & Guillain-Barre syndrome.

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10
Q

Guillain Barre syndrome like

A

OPP poisoning

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11
Q

cause of death of OPP poisoning

A
  • Respiratory failure due to peripheral and central actions:
  • Peripheral: bronchospasm; increased bronchial secretion; and paralysis of respiratory muscles.
  • Central: depression of R.C.
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12
Q

investigations of OPP

A

1.Routine lab investigation.
- ABG: Metabolic Acidosis.
- Blood glucose: Hyperglycemia.
2.Cholinesterase levels: decrease of its levels
3.Detection of para-nitrophenol (metabolite of organophosphate)
in urine.
4.Chest X-ray: pneumonia, non-cardiogenic pulmonary edema.
5.ECG: arrhythmia.

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13
Q

25% depression in its level is an indicator of
OPP poisoning).

A

Cholinesterase levels:

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14
Q

metabolite of organophosphate

A

para-nitrophenol

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15
Q

what is para-nitrophenol

A

metabolite of organophosphate in urine.

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16
Q

Treatment of OPP

A
  • Prophylactic for workers:
    monitoring of the cholinesterase level.
    Protective clothing, masks, gloves & boots.
    Frequent washing of hands and body
  • Curative:
    ABC.
    2- Decontamination:
    GIT:
    Gastric lavage:
    Cuffed endotracheal tube to prevent aspiration (petroleum distillate
    vehicle).
    Cathartics.
    Skin: Skin wash with copious water.
    Eyes: Irrigation of the eyes with copious amount of tape water for at least 15 minutes.**
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17
Q

needs prophylactic treatment

A

inoraganic corrosives
OPP

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18
Q

Antidotes of OPP

A

Atropine
Oximes
Obidoxime
Pralidoxime

19
Q

obidoxime r2

A

antidote of OPP

20
Q

Toxogonin r2

A

antidote of OPP

21
Q

white eschars turn brown in

A

phenol poisoning

22
Q

are reversible cholinesterase inhibitors — accumulation
of acetylcholine -—

A

CARBAMATES

23
Q

Difference between carbamates & organophosphates:

A
  • reversible cholinesterase inhibitors so they are less toxic
    & of shorter duration than organophosphates.
  • Rapid onset 15 — 120 minutes)
  • Carbamate poorly cross the blood brain barrier, so no CNS effects.
  • Carbamates have no long-term sequelae.
  • cholinesterase values are not reliable because return to normal within few hours
  • oximes are no indicated
24
Q

clinical picture of naphtalene poisoning

A

1) Blood:
“Hemolysis&raquo_space; hemoglobinuria (especially Persons with G6PD
deficiency) leads to dark urine and renal failure.
Met-Hemoglobinemia.
2) Other manifestations:
=Nausea, vomiting, and diarrhea.
=Coma and convulsions.

24
Q

worsen condition of patient G6PD deficiency

A

naphtalene

25
Q

mechanism of action of naphtalene

A

Naphthalene toxic metabolites combine with:
Hemoglobin > met-hemoglobin.
Cell wall structures > hemolysis.

26
Q

make dark urine

A

naphthalene

26
Q

investigations of naphtalene

A
  1. Routine lab investigations:
    “CBC: Hemolysis.
    «Kidney function test: Renal failure.
  2. Toxicological screening for naphthalene.
  3. Urine analysis: hemoglobinuria
  4. Met-hemoglobin level.
26
Q

treatment of severe hemlysis

A

blood transfusion

27
Q

treatment of naphtalene

A

ABC
GIT: as OPP: GL & catharitics
symptomatic:
blood transfusion in sever hemolysis
methylene blue for Met-Hemoglobinemia.
Care of the kidneys.
Monitoring the urine output.
Hemoglobinurea: alkalinization of urine and diuresis.

28
Q

mechanism of action of aluminum phosphide

A

AIP releases phosphine gas in the presence of HCI in the stomach, which is rapidly absorbed throughout the gastrointestinal tract, leading to systemic toxic effects involving the heart, lung, kidney, liver

Phosphine gas causes failure of cellular respiration due to the effect on mitochondria, inhibition of cytochrome C oxidase and formation of highly reactive hydroxyl radicals.

28
Q

treatment of met hemoglobinemia

A

Methylene blue

29
Q

Clinical picture of AIP

A

1.Gastrointestinal: Nausea, vomiting & abdominal pain.

2.Cardiac: intractable shock, sever hypotension, cardiac arrhythmia

3.Respiratory: Pulmonary edema, cough & dyspnea.

4.Hepatic: Centrilobular necrosis.

  1. Metabolic: sever metabolic acidosis which may be not responding to treatment.
30
Q

causes intractable shock

A

AIP

31
Q

main managment of AIP

A

supportive

32
Q

treatment of AIP

A

1-Supportive treatment: early and good supportive care can
decrease fatality (see general)
2- GIT decontamination:
«Avoid water ingestion as it increase phosphine gas release
«Gastric lavage with coconut oil or paraffin oil
“Activated charcoal may be helpful
3-Symptomatic treatment: for hypotension, cardiogenic shock and liver and renal failure

33
Q

Gastric lavage with coconut oil or paraffin oil in

A

AIP

34
Q

Avoid water ingestion after poisoning of

A

AIP

35
Q

moa of Warfarin

A

It acts as vitamin K antagonist&raquo_space; inhibits the
biosynthesis of vitamin K- dependent coagulant factors
ll, Vil, LX and X. These effects are gradually developed
over several days.

36
Q

Clinical picture of warfarin

A

Bleeding:
- Hematuria, blood in stool, epistaxis, bruising and
menorrhagia.
- Hemorrhage into the airway with resultant airway obstruction.
- Intracranial hemorrhage.

36
Q

investigation of warfarin

A

Prothrombin time (PT),
(International Normalized ratio) (INR),
partial thromboplastin time (PTT),
thrombin time & and fibrinogen concentration.

37
Q

treatment of warfarin toxicity

A

1-Supportive treatment: ABC (see general toxicology).
2-GIT decontamination:
- Gastric lavage.
- Activated charcoal.
3-Antidote: Vitamin K1
Given orally or IV
4-Symptomatic: Bleeding:
- Blood transfusion,
- Vitamin k-dependent factors,
- Packed red blood cells or Fresh-frozen plasma (FFP).

38
Q

antidote of warfarin

A

vit K 1

TOX (10 decks)

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