Credit test 1 "essay q's"

Question 1

Write etiology of poisoning, mechanism of action, clinical symptomatology, therapy and chemical toxicological
analysis in NaCl poisoning

Answer 1

• Sodium Chloride is used as feed additive. Chloride and sodium ions are the natural part of the animal and plant tissues. Most frequent cause of intoxication is the ingestion of forage with a high content of NaCl, overdosage or inadequate mixing of NaCl in the diet and shortage of water. Sodium Chloride poisoning occurs after the acception of lethal doses of NaCl – depends on species. Second cause is food intake with high content of NaCl and also the animals are short of water
  Clinical symptoms
• Pigs: thirst, salivation, pruritus, diarrhoea, excitation incoordinated moving, spasms, paralysis of hind legs, death within 24 h
• Cattle: in acute poisoning – thirst, regurgitation, abdominal pains, diarrhoea, ataxia, rotation, blindness and in chronic –gastroenteritis, mass loss and dehydration
• Poultry: thirst, dyspnoe, fluid discharge from beak, weakness, diarrhoea and leg paralysis
  Therapy
  Oral administration of fresh water or i.v. / i.m. administration of calcium preparations

Question 2

Write etiology of poisoning, mechanisms of action, clinical symptomatology, therapy and chemical-toxicological
analysis in zinc phosphide poisoning

Answer 2

• Zinc phosphide has been used widely as a rodenticide. Upon ingestion, it gets converted to phosphine gas in the body,
  which is subsequently absorbed into the bloodstream through the stomach and the intestines – gets captured by the liver
  and the lungs. Phosphine gas produces various metabolic and nonmetabolic toxic effects
  Clinical signs
• Acute: Fever, nausea, shock, weak heart beat, low blood pressure, loss of consciousness
• Other: vomiting, diarrhoea, cyanosis, rales, restlessness - Clinical symptoms often seen in 30 min after exposure
• It irritates the mucous membrane of stomach and causes the dilation of the gastrointestinal tract → causes stomach pain,
  hyper reflectivity when touched, twitching, hypersensitivity and hypersalvation
  Zinc phosphide
• Is a dark grey powder, not soluble in water, commonly sold in bait pellets, paste or tracking powder

Question 3

Clinical symptoms of NaCl poisoning

Answer 3

in pigs are thirst, salivation, pruritus, diarhoea, then excitation, incoordinated moving, spasms, paralysis of hind legs, death within 24 h. Affected pigs may be blind, deaf, apathic, anorhectic and non-reactive to external stimuli.

Question 4

Sources of intoxication of NaCl

Answer 4

ingestion of forage with a high content of NaCl, overdosage or inadequate mixing of NaCl in the diet and shortage of water. 
Sodium chloride (NaCl) poisoning occurs after the acception of lethal doses of NaCl.

Question 5

Clinical signs of urea intoxication (20-60min)

Answer 5

o Increase in rumen content pH
o Tremor
o Fibrillation (mainly on face and ears)
o Exophthalmos, increased resp rate
o Expressive jugular pulse
o Pulmonary edema
o Groaning (abdom pain)
o Staggering
o Foamy salivation
o Grinding teeth
o Bloating
o Cyanosis
o Hyperthermia
o Tonic-clonic convulsions
o Death within 2h

Question 6

Therapy of urea poisoning in cattle

Answer 6

0.5-3% acetic acid (HCl 0.1-0.3%) – 3-5L for cattle, 1L for sheep

Question 7

Diagnosis of intoxication

Answer 7

VALUES:
NH3 in blood – over 0.4 mmol/l 

NH3 in rumen – over 100 mmol/l 

pH in rumen – 7.0 – 7.9 

pH in blood – 7.0 

urea in blood ( >12 mol/l)

Question 8

Clinical symptoms of MtHb intoxication

Answer 8

depression, weakness, rapid breathing, discoloration of skin and mucos membranes, jaundice, vomiting, hypothermia, swelling of face or jaw.

Question 9

Clinical symptoms of zinc phosphate intoxication

Answer 9

Lack of appetite
Garlic/rotten fish smelling breath
Rapid and or difficulty breathing
Lethargy
Weakness
Abdominal bloat or pain
Diarrhea and gas
Vomiting
Drooling
Seizures or convulsions
Coma
Death

Question 10

Clinical symptoms of MtHb intoxication: (Long answer)

Answer 10

Condition which a part of the normal blood pigment, hemoglobin, is present as methemoglobin. This can be caused by nitrites which penetrates the erythrocytes and oxidize Fe2+ to Fe3+. Fe3+ is not able to bind O2 and transport it to tissues. MtHb is under normal circumstances present in RBCs in low concentrations and excess MtHb is reconverted to hemoglobin in the RBCs by intraerythrocytary methemoglobin reductase. The altered hemoglobin result in hypoxia and later anoxia. Clinically manifested by cyanosis, which induce blue mucous
membrane. Other signs are dyspnoe, open mouth breathing, ataxia, weakness and death
- Colour of blood will be brownish