(A) Match the pairs

Set I

Column ‘A’ Column ‘B’

1) Bone seeker a) Barium

2) Blue line b) Lead toxicity

3) Garlic odour c) Phosphorus

4) Shifting lameness d) Flurosis

5) Blind staggers e) Sub acute selenium poisoning

6) Peat scours f) Molybdenosis

7) Haemolytic crisis g) Copper toxicity

8) Dhurrin h) Cyanide

9) Chocolate colour blood I) Nitrite toxicity

10)BAL j) Mercury

Set II
1. Spectacled disease a) Molybdenosis
2. Minamata disease b) Mercury poisoning

3) Itai-itai disease c) Cadmium toxicity

4) Alkali disease d) Chronic Selenosis

5) Smell of bitter almonds e) Cyanide poisoning

6) Garlic odour f) Phosphorous poisoning

7) Ammonical odour g) Urea toxicity

8) Plumbism h) Chronic lead poisoning

9) Methaemoglobinaemia I) Nitrite poisoning

10)Crystals in brain j) Oxalate toxicity

Set III

1. Lead a) Delta amino levulinate dehydratase

2. Cyanide b) Cytochrome oxidase

3. Fluorine c) Aconitase

4. Arsenic d) Inhibition of Lipoic acid

5. Nitrite e) Methhaemoglobin formation

6. Selenium f) Glutathione peroxides

7. Molybdenum toxicity g) Copper deficiency

8. Oxalate h) Hypocalcaemia

9. Urea I) Systemic acidosis

10. Mercury j) Ptylism

Set IV

1) Arsenic toxicity a) BAL

2) Lead toxicity b) Calcium EDTA

3) Copper toxicity c) Ammonium

molybdate

4) Cyanide toxicity d)sodium nitrite+ sodium

thiosulphate

5) Molybdenum toxicity e) Copper sulphate

6) Nitrite toxicity f) Methylene blue

7) Selenium toxicity g) Sulphates

8) Fluorine toxicity h) Calcium salts

9) Urea I) Vinegar

10) Charcoal j) Universal antidote

Set V

1) Bright red mucus membrane a) Cyanide toxicity

2) Ascitis with severe thirst b) salt poisoning

3) Easy peeling of intestinal mucosa c) arsenic poisoning

4) Radio opacity of long bones d) Lead poisoning

5) Ammonical odour e) urea poisoning

6) Mottling of teeth f) Flurosis

7) Hoof elongating with skin lesions g) Selenosis

8) Change in colour of hair h) Molybdenosis

9) Enlarge spleen I) Copper poisoning

10) Crystals in brain and kidney j) oxalate poisoning

Set VI

1) Paints, diesel containers a) Lead toxicity

2) Young offshoots of Jawar b) Cyanide toxicity

3) Foot rot baths c) Copper toxicity

4) High Soya in feed d) Urea toxicity

5) Damage /contaminated silage e) Oxalate poisoning

6) Use of rock phosphate in mineral mixtures f) flurosis

7) Counter irritant ointments g) mercury toxicity

8) High soil pH, use of growth promoters h) Nitrite toxicity

9) Obligatory accumulate plants-Astregalus I) Selenosis

10) Less copper in soil j) Molybdenosis

A B
1. Hypericin/Fagopyrin (f) a). Teratogenic plants
2. Lantana camara (e) b). Sorghum
3. Oxalate poisoning (h) c). Thiamine deficiency
4. Linamarin (i) d). Bitter almonds
5. Amygdalin (d) e). Secondary photosensitization
6. Veratrum spp. (a) f). Primary photosensitization
7. Dhurrin (b) g). Haemorrhages
8. Sweet clover (g) h). Renal injury
9. Bracken fern (c) i). Linseed

A B
1. Sorghum (d) a). Photosensitization
2. Hypericum perforatum (a) b). Oxalate containing plant
3. Atriplex (b) c). Selenium containing plant
4. Astragalus spp. (c) d). HCN
5. Euphorbia spp. (g) e). Convulsive poison
6. Abrus precatorius. (h) f). Scopalamine
7. Lantana spp. (i) g). Nitrate rich plant
8. Datura spp. (f ) h). Sui poisoning
9. Nux vomica ( e) i. Mal de playa

I. Match the following:

1. Fang mark (3) 1) Botulinum
2. Nephrotoxic mycotoxin (1) 2) Snake bite
3. Neurotoxic bacterial toxin (2) 3) Ochrotoxin
4. Rodenticide (4) 4) ANTU
5. Phytotoxin in cotton (5) 5) Gossypol
6. Rubratoxin (7) 6) Anticoagulant rodenticide
7.Warfarin (6) 7) Penicillium species
8. Mimosine (9) 8) Salmonellosis
9. Food borne infection (10) 9) Nontoxic to poultry
10. Red squill (8) 10) Cigar tail

Match the following:

1. Toad (2) 1) Respiratory failure
2. Cobra bite (1) 2) Bufogenin
3. Haemotoxins (4) 3) krait
4. Neurotixins (3) 4) Pit vipers
5. Aldrin (6) 5) Ichthyo toxins
6. Fish (5) 6) Halogenated hydrocarbons
7. Sarin (8) 7) Herbicide
8. Dinitrophenol (7) 8) Organophosphorus insecticide
9. Direct additive (10) 9) Hydrocyanic acid
10. Indirect additive (9) 10) Molasses

Match the following:

1. Ionophores (2) 1) CS syndrome

2. Type I pyrethroids (1) 2) Atropine sulphate & diazepam
3. Type II pyrethroids (4) 3) Bufo vulgaris
4. Pyrethroids (6) 4) T syndrome
5. Poisonous toads (3) 5) Salinomycin
6. Organochlorine (7) 6) Monosodium glutamate
7. Chemical food additive (5) 7) Barbiturates
8. Thiocarbonates (9) 8) Herbicides
9. Derries (8) 9) Weedicides
10. Bipyrydiles (10) 10) Rotenone

Match the following:

1. Bipyridium herbicide 2 1) Chrysanthemum cinerariaefolium
2. Pyrethrum 1 2) Paraquat
3. OPI 4 3) Reversible inhibitor of AChE
4. Carbamates 3 4) Irreversible inhibitor of AChE
5. Copper Sulphate 6 5) OPI
6. TEPP 5 6) Molluscicides
7. Red squill 8 7) Coumarin derivatives
8. Warfarin 7 8) Urginea maritima
9. Heterocyclic compounds 10 9) Rodenticide
10. Reserpine 9 10) Triazenes

Match the following:

1. Herbicide 2 Melilotus alba
2. Warfarin 3 DNOC
3. Carbamates 1 Aminocarb
4. Cobra 5 Haemotoxic
5. Vipers 4 Neurotoxic
6. Metaldehyde 6 Molluscicides
7.Mimosine 8 Salmonellosis
8. Food borne infection 7 Cigar tail
9. Food intoxication 10 Naja naja
10. Common cobra 9 Botulism

. Match the following:

1. King cobra 3 Bangaurus calrulens
2. Indian krait 1 Naja henna
3. Black krait 2 Bangaurus niger
4. Direct acting OPI 6 Water insoluble
5. Indirect acting OPI 4 Dichlorovos
6. Organochlorine insecticide 5 Malathion
7. Endosulfan 9 Neuropoisons
8. Red squill 7 Oil soluble
9. Chlorinated hydrocarbons 10 Pit vipers
10.Crotalidae 8 Non-toxic to poultry

Match the following:

1. Organochlorine insecticides 2 Miosis
2. Organophosphorus insecticides 1 Mydriasis
3. Zinc phosphide 4 Pulmonary oedema
4. ANTU 3 Lethal synthesis
5. Red squill 6 Direct irritant to gut
6. Fluoroacetate 5 Scilliroside
7. Strychnine 8 Occupational poisoning
8. Insecticides 7 Malicious poisoning
9. DDT 10 Krait
10. Elapidae 9 Accidental poisoning

Match the following:

1. Lethal dose 2 Dose to cause 50 % lethality
2. LD 50 1 Dose to cause death
3. Toad 3 Bufomarines
4. American poisonous toad 6 Cardiotoxic steroids
5. Elapidae 4 Pit vipers
6. Crotolidae 5 Cobra
7. Black widow spider 10 Melittin
8. Food intoxication 7 Latrodactus mactans
9. Toxic dose 8 Salmonellosis
10. Honey bee 9 Dose to produce toxic effect

Match the following:

1.Safest rodenticides 2 Mammalicides
2.Tick toxins 3 Red squill
3. Strychnine 1 Wood ticks
4. Sodium fluoroacetate 4 Pulmonary odema
5. ANTU 7 Inhibition of citric acid cycle
6. Fish 5 Saxitoxin
7. Shellfish 6 Ichthyotoxins
8. Puffer fish 10 Ciguatoxin
9. Moray eel 8 Nonsystemic insecticide
10. EPN 9 Tetradotoxin
 Match the following:
1. Cuso4 2 Sea onion
2. Red squill 1 Growth promoters
3. Warfarin 4 Depilatory effect
4. Mimosine 3 Vitamin K
5. Rapid death 6 Viper bite
6. Prolonged death 5 Cobra bite
7. Organophosphates 8 Mydriasis
8. Organochlorines 7 Miosis
9. Carbamates 10 T syndrome
10. Pyrethroids 9 Reversible inhibitors of AChE

Match the following:

1. Pyrethroids 2 Reserpine
2. Alkaloidal rodenticide 1 CS syndrome
3.Growth promoters 4 Norbromide
4. Selective rodenticide 3 CuSo4
5. Molluscide 6 Toxophene
6. Chlorinated camphene 5 ETC
7. Dinitro compounds 7 Metaldehyde
8. Clotting disturbances 10 Chelating agents
9. ANTU 8 Warfarin
10. BAL 9 Rodenticide

Match the following:

1. Organophosphates 3 Aspergillus species
2. BAL 1 2-PAM
3. Aflatoxin 4 Rodenticide
4. ANTU 2 Chelating agent
5. Strychinine 6 Gastric lavage and atropine sulphate
6. Red squill 5 Anticonvulsants
7. Zinc Phosphide 9 Vitamin K
8. Thallitoxicosis 7 Gastric lavage and 5% NaHCO3
9. Warfarin 10 Glycerol monoacetate
10. Sodium fluoroacetate 8 Diphenyl thiocarbazone and PPB

Bold Number is the key of answer

(B) Multiple Choice questions

1. Hazard/ toxicity is the probability of getting the poison.

2. Cyanide cause histotoxic/ anoxic anoxia.
3. Mucous membranes are cyanotic/ bright red in cyanide poisoning.
4. Jawar contents dhurrin/ amygdalin as cyanogenic glycoside.
5. Cyanide poisoning is more common in cattle/ horses than sheep.
6. Sodium nitrate/ nitrite is used in treatment of cyanide poisoning.
7. Rumen microbes contents a enzyme α- glucosidase/ β-glucosidase
which is responsible for release of cyanide from its glycoside.
8. Lead lines are observed during chronic lead toxicity on gums/ long
bones.
9. Blue line is observed on gum/ long bone during plumbism.
10. Intranuclear eosinophilic/ basophilic inclusions are observed in liver/
kidney in chronic lead poisoning.
11. Basophilic striplings of RBC/ WBC are observed in lead poisoning.
12. δ- amino levulinate dehydrogenase is inhibited by mercury/ lead.
13. The specific antidote for lead toxicity is Disodium calcium EDTA/
Disodium potassium EDTA.
14. EDTA/ Succimer is orally acting chelator for lead poisoning.
15. Anaemia is commonly observed during chronic copper/ lead toxicity.
16. Behavioural symptoms are observed/ not observed in lead toxicity.
17. Intermittent/ continuous treatment with EDTA is advocated in lead
poisoning.
18. Sodium calcium EDTA is given I.M./ I.V. to treat lead toxicity.
19. Minamata episode is related with inorganic/ organic mercury toxicosis.
20. Minamata episode was due to mercury/ arsenic poisoning.
21. Stomatitis and other signs related to oral cavity are observed during
mercury/ copper toxicity.
22. The soluble form of BAL, DAM/ DMSA is used for treating mercury
poisoning, as it is less toxic.
23. BAL/ EDTA is the specific antidote for mercury poisoning.
24. BAL is administered at the dose of 10- 15 mg/ kg / 3-5 mg/ kg I.M.
25. BAL should always be given I.V. / I. M.
26. Calomel, corrosive sublimate are the source of inorganic/ organic
mercury poisoning.
27. BAL is the specific antidote for mercury/ lead poisoning.
28. Pentavalent/ trivalent arsenicals are more toxic.
29. Organic/ Inorganic arsenic compounds are more toxic.
30. Arsenicals are more/ less toxic than arsenates.
31. Trivalent arsenicals inhibit decarboxylation of ketoacids as it binds with –
SH group of lipoic acid/ cysteine.
32. In acute/ chronic arsenic toxicity the skin and keratinized tissue gets
affected.
33. Easy peeling of gastric mucosa which is due to submucosal oedema is
diagnostic for ANTU/ arsenic toxicity.
34. In chronic arsenic poisoning hooves/ ruminal contents are the preferred
material for diagnosis.
35. Mee’s lines are absent on nails during mercury/ arsenic poisoning.
36. Subacute selenosis is also known as blind staggers/ alkali disease.
37. Maximum selenium is present in obligatory/ facultative accumulator
plant.
38. Obligatory/ non-accumulator selenium plants are most important
sources for selenium poisoning in animals.
39. Inorganic/ organic selenium compounds are more toxic.
40. In selenosis/ fluorosis there is absence of skin lesions.
41. Symptoms are exhibited suddenly/ slowly during chronic copper
poisoning.
42. Copper poisoning is more common in cattle/ sheep.
43. Symptoms of chronic copper poisoning are observed in three/ two
phases.
44. Hemoglobinurea and jaundice are characteristic symptoms during
mercury/ copper poisoning.
45. D- penicillamine is specific antagonist for lead/ copper toxicity.
46. Low pH of soil will favour nitrate poisoning/ chronic selenosis.
47. Decaying organic matter and silo juices are source for cyanide/ nitrate
poisoning.
48. Chances of nitrate poisoning increase/ decrease when excessive
manure, fertilizers are used.
49. Excessive sulphur and phosphorus in soil increases/ decrease the
chances of nitrate poisoning.
50. Nitrates are more/ less toxic than nitrites.
51. Hemoglobin is reduced/ oxidized to methhaemoglobin by nitrates.
52. Death occurs when 20 % / 80% hemoglobin gets converted to
methhaemoglobin during nitrate poisoning.
53. Blood is dark brown/ bright red in nitrate toxicity.
54. The specific antidote for nitrate poisoning is of oxidizing agent /
reducing agent.
55. Methylene blue/ leucomethylene blue is actual reducing agent, which
converts methhaemoglobin to hemoglobin during nitrate poisoning.
56. Methylene blue is administered @ 8.8/ 4.4 mg/kg in cattle.
57. Methylene blue should be given by I.M./ I.V. route during nitrate toxicosis.
58. Vitamin C can be given in nitrate/ cyanide poisoning.
59. Red phosphorus/ white phosphorus is more toxic.
60. Red phosphorus/ yellow phosphorus is non-toxic.
61. Phosphorus poisoning causes ammonical/ garlic odour to breath.
62. Urea poisoning leads to smell of bitter almond/ ammonia.
63. Chance of selenosis/ fluorosis increase by the use of rock phosphate.
64. Fluorine causes formation of hydroxyapatite/ fluoroapatite leading to
faulty mineralisation.
65. Mottling of teeth is observed during osteofluorosis/ dental fluorosis.
66. In fluorosis shifting/ permanent lameness is observed.
67. Elongation of hooves along with spontaneous fracture is characteristic of
selenosis/ fluorosis.
68. Fluorine blocks aconitase/ decarboxylase.
69. Molybdenum levels are high if phosphorus is high/ low.
70. Molybdenosis occurs if copper/ ammonia levels are low.
71. Sulphates should be less/ more in soil to avoid molybdenosis.
72. Change in colour of hair is observed during selenium/ molybdenum
toxicity.
73. Spectacled appearance results from molybdenosis/ fluorosis.
74. Molybdenosis is treated with copper sulphate/ ammonium molybdate.
75. Salt toxicity is common in poultry/ sheep.
76. Salt toxicity is also referred as water/ sodium deprivation syndrome.
77. Salt toxicity is mainly potassium/ sodium toxicosis.
78. The common postmortem finding in salt toxicity is liver congestion/
ascites.
79. Blindness may be observed in salt/ chronic selenium toxicity.
80. Fever is present in salt toxicity/ organochlorine toxicity, which is
differentiating point between the two.
81. Perivascular eosinophilic infiltration in meninges is observed in poultry/
pigs during salt toxicity.
82. Toxicology/ toxinology is the study of toxins.
83. Venom is a type of bacterial toxin/ zootoxin.
84. Malacious poisoning is intentional/ accidental poisoning.
85. Ability to produce cancer is teratogenicity/ carcinogenicity.
86. Ability to produce abnormalities in foetus is teratogenicity/
carcinogenicity.
87. In chronic/ acute toxicity the dose of toxicant is large.
88. Selective toxicity is beneficial/ harmful phenomena.
89. Cyanogenic glycosides are toxic/ non-toxic.
90. Vitamin B 12a / Vitamin B 12b is advocated in cyanide poisoning.
91. Vinegar is given orally during nitrite/ cyanide poisoning.
92. Out of total absolute lead maximum lead bound to RBC/ bones.
93. In cattle the dose of Disodium calcium EDTA is 75 mg/ kg / 25 mg/kg I.V.
94. Obligatory selenium accumulators contain selenium between 100 –1000
ppm/ 1000-10000 ppm.

95. A diseased state resulting from entry of a specific toxin into the body of the
host is called as …..
1. Infection
 2. Infestation
3. Intoxication ,

96. Access of the toxin into the blood stream is called as

1. Toxaemia.
2. Infection
3. Infestation

97. The ability of a microorganism to produce the toxin is

1. Toxigenecity
2. Teratoenicity
3. Mutagenicity

98. The term toxin is derived from the Latin word

1. Toxicum
2. Toxinum
3. Toxirom

99. A specific substance elaborated by microorganisms (bacteria or fungi),

which causes a specific disease state is called as
1. Toxin
2. Poison
3. Venom

100. The major toxins are produced by

1. Bacteria and fungi
2. Plants
3. Metals

101. The bacterial toxins are of two types as

1. Endotoxins and Exotoxins.
2. Ocratoxins and Aflatoxins
3. Ergotoxin and rubratoxin

102. The lipopolysaccharide portion of the cell wall of Gram negative bacteria
are called as
1. Endotoxin.
2. Ocratoxins
3. Aflatoxins

103. The toxins released into the media or surroundings where the bacteria grow
are called as
1. Exotoxins.
2. Ergotoxin
3. Rubratoxin

104. The example of neurotoxin is

1. Botulinum toxin and tetanospasmin.
2. Cholaragen.
3. Diphtheria toxin and haemolysins.

105. The example of Enterotoxins is

1. Botulinum toxin and tetanospasmin.
2. Cholaragen.
3. Diphtheria toxin and haemolysins.

106. The example of Histotoxin is

1. Botulinum toxin and tetanospasmin.
 2. Cholaragen.
3. Diphtheria toxin and haemolysins.

107 . BotulinumToxin is produced by

1. Clostridium botulinum.
2. Ciostridium tetani,
3. Vibrio cholerae.

108. Tetanospasmin is produced by

1. Ciostridium tetani,
2. Clostridium botulinum.
3. Vibrio cholerae.

109. Cholaragen (enterotoxin) is produced by

1. Vibrio cholerae.
2. Clostridium botulinum.
3. Ciostridium tetani,

110. Diphtheria Toxin (cytotoxin) is produced by

1. Corynebacterium diphtheriae.
2. Clostridium botulinum.
3. Ciostridium tetani,

111. Haemolysins causes

1. Lysis of red blood cells.
2. Lysis of platelets
3. Lysis of WBC

112. The Streptolysin 0 and streptolysin S. are produced by

1. Streptococcus species
2. Staphylococus spp.
3. Clostridium spp.

113. Leucocidin, the cytotoxins elaborated by

1. Staph, aureus
2. Streptococcus species
3. Clostridium spp.

114. Lecithinase ,the cytotoxins elaborated by

1. Clostridium perfringens,
2. Staphylococus spp.
3. Clostridium spp.

115. Leucocidin selectively causes lysis of

1. Leucocytes.
2. Erythrocytes

116. Lecithinase causes lysis of

1. Red blood cells
2. Platelets
3. WBC

117. The toxicity resulting from the ingestion of mold (fungi) infested feeds (grain
or fodder) is called
1. mycotoxicosis
 2. Plant toxicity
3. mineral toxicity

118. Toxins causing liver and kidney damage are

1. Aflatoxins, rubratoxins and T-2 toxin
2. Slaframine and ergotoxins
3. Tremortin-A and satratoxins

119. Toxins causing nervous derangement are

1. Tremortin-A and satratoxins
2. Aflatoxins, rubratoxins and T-2 toxin
3. Ergotoxins

120. Toxins causing lameness are

1. Ergotoxins
2. Slaframine and ergotoxins
3. Tremortin-A and satratoxins

121. Toxins causing oestrogenlc effect are

1. Zearalenone
2. Slaframine and ergotoxins
3. Tremortin-A and satratoxins

122. Toxins causing histaminergic effect are

1. Slaframine and ergotoxins
2. Ergotoxins
3. Tremortin-A and satratoxins

123. Aflatoxins are produced by

1. Aspergillus spp.
2. Venoms
3. Plants

124. The toxicosis produced by aflatoxins is called as

1. aflatoxicosis.
2. Ocratoxicosis
3. Rubratoxicosis

125. Rubratoxins are produced by

1. Penidllium rubrum
2. Aspergillus spp.
3. Venoms

126. T-2 Toxin is produced mainly by the molds belonging to

1. Fusarium spp.
2 Aspergillus spp.
3. Atriplex spp.

127. T-2 toxin causes

1. Hepatic as well as renal toxicity.
2. Toxicity of brain
3. Toxicity to reproductive organs

128. Ergotoxins are produced by the fungi of genus

1. Claviceps
2. Fusarium spp.
3 Aspergillus spp.
129. The plants which contain (HCN) are called as
1. Cyanogenic plants.
2. Oxalate rich plants
3. Selenium accumulators

130. An example of commonly occuring cyanogenetic plant is

1 Sorghum halepense (Johnson grass)
2. Tribulus terestris
3. Vinca rosea

131. Among domestic livestock the most susceptible animals for HCN poisoning
are
1. Cattle and buffaloes
2. Sheep and Goat
3. Dog and cat

132. Among domestic livestock the more resistant animals for HCN poisoning
are
1. Sheep
2. Cattle
3. Dog and cat

133. For the diagnosis of HCN in plant material the test used is
1. sodium picrate paper test.
2. Benedicts test
3. Barium chloride test

134. The treatment of cyanogenetic plant poisoning consists of

1. sodium nitrite and sodium thiosulfate
2. Atropine sulphate
3. 2-PAM

135 The dose of sodium nitrite and sodium thiosulfate in Cattle and buffaloes is
1) 3 G of sodium nitrite, 15 G of sodium thiosulfate injected
intravenously.
2) 30 G of sodium nitrite, 150 G of sodium thiosulfate injected
intravenously.
3) 35 G of sodium nitrite, 5 G of sodium thiosulfate injected intravenously.

136. The dose of sodium nitrite and sodium thiosulfate in Sheep and goats is
1. sodium nitrite1 G and sodium thiosulfate 2.5 G injected
intravenously.
2. sodium nitrite10 G and sodium thiosulfate 25 G injected intravenously.
3. sodium nitrite 50 G and sodium thiosulfate 10 G injected intravenously.

137. The abnormal dermal reaction that appears in lightly pigmented skin areas
of the animals due to ultra-violet activation of certain metabolites or toxic
substances (photodynamic) present In the peripheral circulation is due to …
1. Photosensitization.
2. Fungal infection
3. Bacterial infection

138. The example of plants containing photodynamic substance is

1. Hypericum perforatum
2. Sorghum spp.
3. Vinca spp.
139. Secondary Photosensitization is also called as
1. Hepatogenous photosensitization.
2. Enterogenic photosensitization
3. Endocrine photosensitization

140. The plants causing secondary photosensitization is

1. Lantana camara,
2. Sorghum
3. Wheat

141. The example of oxalate-rich plants is

1. Atriplex spp.
2. Sudan grass
3. Lantana camara

142. Treatment of oxalate poisoning in animals is done with

1. lime water or dicalcium phosphate
2. EDTA
3. Atropin sulphate

143. The example of obligate selenium accumulator plant is

1. Astragalus species
2. Sorghum
3. Wheat

144. The example of Facultative selenium accumulator plant is

1. Aster spp.
2. Sorghum
3. Wheat

145. The example of Passive selenium accumulator plant is

1. Corn,
2. Sorghum
3. Wheat

146. The example of Nitrate rich plant is

1. Amaranthus spp.,
2. Sorghum
3. Wheat

147. The abrus poisoning is due to the seeds of

1. Abrus precatorius
2. Sudan grass
3. Lantana

148. The abrus poisoning is also called as..

1. sui poisoning
2. Spectacle disease
3. Hydrocynic acid poisoning

149. The lantana poisoning is due to grazing of livestock on

1. Lantana camara
2. Sorghum
3. Wheat

150. The Ipomoea plant contains toxic principle

1. ipomeanols
2. Withanin
 3. Nerin

151. The Nerium plant contains toxic principle

1. Nerin
2. ipomeanols
3. Withanin

152. The Datura Poisoning resulting from ingestion of fruit, seeds and leaves of
1. Datura alba
2. Parthenum
3. Nerium

153. The Castor Poisoning resulting from ingestion of fruit, seeds and leaves of
1, Ricinus communis
2. Veratrum plants
3. Datura alba

154. Plants causing Teratogenecity is

1. Veratrum plants
2. Datura alba
3. Parthenum

155. Plants Causing Delay In Blood Coagulation is

1. sweet clover
2. Veratrum plants
3. Datura alba

156. Plants Causing Thiamlne Deficiency is

1. Pteridium plants
2. sweet clover
3. Veratrum plants

157. Red squill is obtained from

i) Plant ii) Animals
iii) Reptiles iv) Amphibians

158. Warfarin is an antagonist of

i) Vit.A ii) Vit. K ii) Vit.E iv) Vit.C

159. Endrin is an
i) OCI ii) OPI iii) Carbamate iv) none

160. Aldicarb is an
i) OCI ii) OPI iii) Carbamate iv) none

161. Mydriasis is seen in poisoning of

i) OCI ii) OPI iii) Carbamate iv) all

162. Behavioural changes are seen in poisoning of

i) OCI ii) OPI iii) both iv) none

163. The toxins produced by lower animals are called

i) Venoms ii) Bacterial toxins iii) Poison iv) Viral toxins

164. Snakes toxins are comprise of potent

i) Neurotoxic ii) Haemotoxic iii) Both iv) none
165. The deadly poisonous snake family
i) Elapine ii) Viperine iii) Both iv) None

166. The venom of cobra & krait is mainly

i) Neurotoxic ii) Haemotoxic iii) Both iv) None

167. The most susceptible species to venomous snake bite

i) Goat ii) Sheep iii) Cattle iv) Horse

168. Viper snakes are mainly

i) Haemotoxic ii) Neurotoxic iii) Cardiotoxic iv) Carcinogenic

169. Rattle snakes are mainly

i) Neurotoxic ii) Cardiotoxic iii) Haemotoxic iv) None

170. The neurotoxic venoms cause paralysis of

i) Sensory nerve ii) motor nerve iii) both iv) none
171. The cause of death in snakebite is
i) Respiratory paralysis ii) shock iii) oedema iv) all

172. Curare like effect is seen in bite of

i) Cobra ii) Krait iii) Pit viper iv) both i&ii

173. Polyvalent antisnake venom should be given

i) P/O ii) I/V iii) I/M iv) S/C

174. 2-PAM is given by

i) P/O ii)I/V iii)I/M iv) S/C

175. Toxins of toad are secreted by the glands of

i) Adrenal ii) Thyroid iii) Skin iv) Both

176. Scorpion venoms contain

i) Neurotoxic protein ii) Haemotoxic protein
iii) Haemorrhage iv) none

177. Excessive amount of ACh is released in

i) Spider venom ii) Snake venom iii) Bee sting iv) toad toxin

178. Bufogenins are cardiogenic

i) Alkaloid ii) Glycosides iii) Resins iv) both ii&iii

179. Snake bite causes

i) Flaccid paralysis ii) spastic paralysis
iii) Motor paralysis iv )Both ii&iii

180. Symptoms of tick paralysis are

i) Ascending flaccid paralysis ii) Descending flaccid paralysis
iii) Ascending spastic paralysis iv) Descending spastic paralysis

181. The common toxin of fish poisoning is

i) Saxitoxin ii) Tetradotoxin iii) Ciguatoxin iv) both i &ii

182. Organic phosphate insecticide mainly act as

i) Neuropoison ii) Anticholine esterase
iii) Antimuscarnic iv) Choline esterase

183. The following is a neuropoison

 i) OPI ii) OCI iii) Pyrethroids iv) Carbamate

184. DNOC is a
i) Herbicide ii) Insecticide iii) Rodenticide iv) all

185. 2-PAM is
i) Oxime reactivator ii) choline esterase reactivator
iii) none iv) both i & ii

186. An example of oxime reactivator

i) 2-PAM ii) MINA iii) DNOC iv) all v) both i & ii

187. Irreversible blockade of AChE is caused by

i) OPI ii) OCI iii) Pyrethroids iv) Carbamate

188. ANTU causes

i) Pulmonary oedema ii) Kidney failure
iii) Hepatotoxicity iv) CNS effects

189. Reversible blockade of of AChE is caused by

i) OPI ii) OCI iii) Pyrethroids iv) Carbamate

190. TEPP is a
i) Direct acting OPI ii) Indirect acting OPI
iii) Direct acting OCI iv) Direct acting OCI

191. Fentrothion is an
i) Direct acting OPI ii) Indirect acting OPI
iii) Direct acting OCI iv) Direct acting OCI

192. Fentrothion is converted into

i) Fenoxon ii) Fentoxon iii) Paraxon iv) None

193. OPI inhibits

i) True cholinesterase ii) False choline esterase
iii) Both iv) None

194. OCI poisoning should be differentiated from

i) Strychnine poisoning ii) lead poisoning
iii) OPI poisoning iv) all of the above

195. Miosis is seen in the poisoning of

i) OPI ii) OCI iii) Pyrethroids iv) Carbamate

196. Major sources of pesticide poisoning are

i) Accidental exposure ii) intentional exposure
iii) Occupational exposure iv) all

197. Organochlorines are the ________generation insecticides

i) First ii) second iii) Third iv) Fourth

198. Organophosphates are the ________generation insecticides

i) First ii) second iii) Third iv) Fourth

199. __________possess potential insecticidal properties without

Mammalian toxicity
i) Pyrethroides ii) carbamates iii) OPI iv) OCI
200. Permethrin is an
i) Type I pyrethroids ii) Type II pyrethroids
iii) Type I carbamates iv) Type II carbamates

201. Allethrin is an
i) Type I pyrethroids ii) Non alpha pyrethroid
iii) Type II pyrethroids iv) Both i)&ii)

202. Deltamethrin is an
i) Type I pyrethroids ii) Type II pyrethroids
iii) Type I carbamates iv) Type II carbamates

203. Cypermethrin is an
i) Type I pyrethroids ii) Alpha pyrethroid
iii) Type II pyrethroids iv) Both i)&ii)

204. Chlorinated Hydrocarbon poisoning is characterized by

i) Behavioural changes ii) Neurologic symptoms
iii) Cholinergic symptoms iv) All

205. OPI poisoning is characterized by

i) Muscaranic symptoms ii) Nicotinic symptoms
iii) CNS symptoms iv) All

206. 2-PAM is contraindicated in poisoning of

i) OPI ii) Pyrethroid iii) Carbamate iv) OCI

207. In T- syndrome ‘T’ refers to

i) Tachycardia ii) Tremors iii) Tachyphylaxis iv) Both i)&ii)

208. CS-Syndrome is seen in poisoning of

i) Type I pythroids ii) Type II pyrethroids
iii) Carbamates iv) Both i)&ii)

209. Na Flouroacetate inhibits

i) Krebs cycle ii) Citric acid cycle iii) Glycolysis iv) Both i)&ii)

210. _________is the safest rodenticide

i) Red squill ii) Zinc Phosphide iii) Warfarin iv) Both i)&ii)

211. Toxic principle of Red squill is

i) Scilliroside ii) Phosphine iii) Alkaloid iv) All

212. Red squill is more toxic to

i) Male ii) Female iii) Both iv) None

213. Zinc phosphide toxicity is due to

i) Zinc ii) Phosphine gas iii) Phosphoric acid iv) Phosphorous

214. Impairment of blood clotting is associated with

i) Red squill ii) ANTU iii) Warfarin iv) Zinc Phosphide

215. Dinitrocompounds interfere with

i)Electron transport chain ii) Krebs cycle
iii) Glycolysis iv) HMP pathway

216. Paraquat is
i) Insecticide ii) Weedicide iii) Rodenticide iv) All
217. Thallium toxicosis is due to inhibition of
i) Sulfhydryl enzymes ii) AChE
iii) Superoxide formation iv) H202

218. Commonly used insecticides are

i) Organochlorines ii) Organophosphates
iii) Both i & ii iv) Chlorates

219. Commonly used Herbicides are

i) Bipyridal compounds ii) Pyrethroids
iii) Chlorates iv) Both i &iii

220. Commonly used redenticides are

i) Strychnine ii) Zinc phosphate
iii) Red squill iv) Both ii &iii

221. Commonly used mammalicides

i) OPC ii) Strychnine
iii) Red squill iv) Both ii &

222. Most common source of Rodenticides poisoning

i)Ingestion of rodent baits by dogs, cats or grazing livestock
ii)Malicious poisoning
iii)Accidental contamination of animal feeds
iv)all

223. Organochlorine insecticides causes membrane

i) Depolarization ii) Repolarization
iii) Hyperpolarization iv) All

224. Pesticides are classified on their mode of action

i) Stomach poisons ii) Contact poisons
iii) Fumigants iv) All

225. --------------- is known as chlorinated camphene

i) Dieldrin ii) Toxophene
iii) DDT iv) Endosulfan

226. An example of stomach and contact poison is

i) Dieldrin ii) Toxaphene
iii) Both i & ii iv) None

227. _____________insecticide group is having excellent insecticidal

activity and low mammalian toxicity.
i) OPI ii) OCI
iii) Pyrethroids iv) Carbamates

228. ------------ is proved to be safe in use under a variety of field

conditions.
i) Carbamates ii) Pyrethroids iii) Amitraz iv) DDT

229. Treatment of OCI consists of

i) Atropine So4 ii) Barbiturates
iii) IV calcium borogluconate iv) All

230. Commonly used Molluscides

i) Metaldehyde ii) Methiocarb
 iii) DNOC iv) Both i &ii

231. --------------- is a selective rodenticide

i) Red squill ii) Warfarin
iii) Zinc Phosphate iv) Norbromode

232. Food supplementation of ionophores is contradicted

i) Bovines ii) Canines
iii) Equines iv) Caprines

233. ------------------ is an alkaloidal rodenticide

i) Red squill ii) Warfarin
iii) Reserpine iv) Norbromide

234. The substance which is having growth activity several times

greater than that of dried thyroid gland.
i) OPI ii) OCI
iii) Pyrethroid iv) Carbamates

235. Anabolic steroids affects of age or puberty

i) Delayed ii) Reduced
iii) No effect iv) None

236. Atropine So4 is not used commonly in toxicity

i) OPI II) OCI
iii) Pyrethroid iv) Carbamates

237. Arsenicides are used as a feed additive in the form of

i) Arsanilic acid ii) Arsenic acid
iii) Potassium arsenalate iv) Sodium arsenalate

238. CUSO4 is used as growth promoter mainly

i) Pig ration ii) Calf ration
iii) Canine food iv) All of the above

239. Organophosphates cause

i) Miosis ii) Mydriasis
iii) Cycloplegia iv) None of the above
Bold letter is the key of answer
(C) Correct wherever necessary:

1) Trivalent arsenicals inhibit decarboxylation of ketoacids.

2) Arsenicals bind with biotin.

3) Chronic arsenic toxicity leads to involvement of keratinized tissue.

4) Submucosal edema of intestine is observed during ANTU poisoning.

5) Lipoic acid may be given in arsenic poisoning.

6) The transverse lines observed on nails during mercury poisoning are called

as Mee’s lines.

7) Sub acute selenium poisoning is called as alkali disease.

8) Chronic selenium poisoning is referred as blind staggers

9) Facultative selenium accumulators content 1000 –10000 ppm selenium

10) Obligatory accumulators are selenium contenting plants accumulating

maximum selenium

11) Non-accumulators are most important plants source for selenium toxicity.

12) Organic selenium compounds are less toxic than inorganic selenium

compounds

13) Selenosis in dog is also referred as dog murrain

14) Sodium arsenic is indicated during arsenic poisoning

15) Copper has inverse relationship between molybdenum and sulphur

16) In chronic copper toxicity the symptoms are exhibited acutely.

17) Copper toxicity is treated with molybdenum and vice verse

18) Third phase of chronic copper poisoning is of haemolytica crisis

19) During chronic copper toxicity jaundice, hemoglobinurea is commonly

observed.

20) D-peniocllimine is given to reduce lead levels in liver

21) High pH of soil favour nitrate poisoning

22) Low molybdenum and sulphur favors nitrate poisoning

23) High sulphur and phosphorous in soil increases chances of nitrate;

poisoning

24) Excess use of fertilizer manures and herbicides such as 2-4D causes

increase indicate of nitrate toxicity in animals.

25) Nitrites are converted to nitrate, which are more toxic.

26) Nitrites converted hemoglobin to methaemoglobin to caused toxicity

27) Death during nitrate toxicity occurs when 20% hemoglobin in converted to

methaemoglobin

28) Blood is chocolate brown in color during nitrate poisoning

29) Methylene blue is converted to leucomethylene blue with the help of NADP

30) Leucometh7yle blue converted hemoglobin to methaemoglobin during

nitrate toxicosis

31) Methylene blue is administered by I/v route

32) Methylene blue is given at the dose of 8.8 mg/kg b.w.in cattle

33) Vitamin C can be administered in place of methylene blue during nitrate

poisoning

34) Red phosphorus is non toxic

35) Yellow phosphorus is non toxic

36) Use of rock phosphate in DCP leads to occurrence of flurosis

37) Fluorine causes formation of hydroxyuappetite in bones leading to faulty

mineralization

38) Molting of teeth are exhibited during osteo flurosis

39) Shifting lameness is observed during flurosis

40) Bones are white and chalky during Selenosis

41) Low phosphorus and high sulphate predisposes for molybdenosis

42) Copper and molybdenum levels are inversely related

43) In pigs copper and molybdenum levels are inversely related

44) Copper sulphate is used for treatment of molybdenum poisoning

45) Salt toxicity is called as water deprivation induced sodium toxicosis.

46) Deprivation of water increase salt toxicity

47) Pigs exhibit dog sitting posture in salt toxicity

48) Blindness is always observed in blind staggers

49) Salt toxicity and toxicity is organochlorine is differentiated on the basis of

fever

50) In cattle perivascular eosinophilic infiltration in meninges in seen during salt

toxicity

51) Toxicology deals with study of all poisons

52) All venous are Zoo toxins and all zoo toxins are venom

53) Teratogenecity is ability to produce cancers.

54) Carcinogenecity is ability to produce cancers.

55) Ingestion of large dose at a time causes chronic toxicity.

56) Selective toxicity is harmful phenomenon.

57) Cyanide inhibits cytochrome oxidase enzyme.

58) Cyanide leads to anoxic anoxia.

59) Jawar has amygdalin as cyanogenic glycoside

60) Linamarin is present as cyanogenic glycoside in linseed.

61) Sodium thiosulphate and sodium nitrate is given as antidote for cyanide

toxicity.

62) The enzyme β-glycosidase is necessary for release of cyanide in rumen.

63) Mucus membranes are cyanotic and there is a respiratory distress in

cyanide toxicity.

64) Smell of bitter almonds is experienced during postmortem of animal died of

cyanide toxicity.

65) Orally vinegar is given during cyanide and nitrite toxicity

66) Lead lines are observed during chronic lead poisoning whereas blue line is

seen during chronic mercury poisoning.

67) Out of total absorbed lead, maximum is bound to bones.

68) Anaemia is commonly observed during Plumbism.

69) Mercury inhibits δ-amino-lavulinate dehydratase enzyme

70) Succimer is orally active lead chelator.

71) Disodium EDTA is administered i/v to treat Lead poisoning

72) In dogs Disodium calcium EDTA is given @ 25 mg/kg b.w. (i/v)

73) Minamata incidence was due to inorganic mercury toxicosis

74) Basophilic stipplings of RBCs are observed during lead toxicity

75) Organic mercurials are more toxic than inorganic mercu5rials.

76) Inoganic mercury poisoning lead to inflammation to gums loosing of teeth

and ptylism.

77) BAL is less toxic than DAMSA

78) Dimercaprol must be given i/v

79) The dose of BAL is 3-5 mg/kg i/m.

80) Behavioral symptoms are common in mercury poisoning

81) D-penicllimine is given in copper as well as mercury poising

82) Nigeta disease is related with arsenic poising

83. A pesticide is a chemical, which kills insects. Insecticide

84 . Pest may be defined as economical species. uneconomical
85. Organochlorine pesticides are generally termed as muscle poisons. nerve
86. Organochlorine insecticides act as irreversible AntiCholine Esterase. OPI
87. OPI act as reversible AChE. Irreversible
88. Carbamates act as irreversible AChE. reversible
89. Pyrethroids act as irreversible AChE. carbamates
90. 2-PAM is a choline esterase inhibitors. reactivators
91. 2-PAM is a Anticholinesterase reactivator. Cholinestrase
92. Organochlorine causes miosis. Mydriasis
93. Organophosphate causes moisis. organochlorine
94. BHC is an OPI. OCI
95. Malathion is a nerve poison. DDT
96. All weedicides are pesticides but all pesticides are not weedicidal, Pesticide
97. Exact mechanism of toxicity of OPI is not known. OCI
98. Red squill is obtained from ground onion. Sea
99. Rat can vomit and hence succumb to toxicity. cannot
100. Warfarin toxicity is due to antagonism of vitamin C Vit. E
101. Strychnine is a rodenticide. Mammalicide
102. ANTU is a violent convulsive poison. Strychnine
103. Thiamine causes thalli toxicosis.] Thalium
104. Sodium fluoroacetate inhibits electron transport chain. Citric acid cycle
105. Red squill causes massive pulmonary oedema. ANTU
106. Phosphine gas is formed in the GIT from zinc phosphate. Phosphide
107. Toxins produced by the bacteria are called zootoxins. Lower animals
108. The toxins produced by mammals are called venoms. Lower animals
109. Pit viper venom is a neurotoxin. Haemotoxic
110. The venom produced by krait is haemotixic. Neurotoxic
111.The venom of pit viper causes irreversible blockade of neuromuscular
transmitter. Cobra or Krait
112. Krait belongs to family Elapine snakes. Viperine
113. Cobra venom is a neurotoxic and belongs to viperine family. Elapine
114. Clinical signs of krait bite are characterized by hemolytic syndrome.
neorotoxic
115. Scorpion may cause sudden death in the animals. May not
116. Scorpion venom containing a toxin similar to bolulinus toxin. Neorotoxic
protein
117. Bufogenin and bufotalin are the neurotoxic bufotoxin. Cardiotoxic
glycoside
118. Bufogenin and bufatalin are the two alkaloids liberated by toad venom.
Glycoside
119. Neurotoxic bufatalin causes paralysis of nerves by persistent
repolarisation through Na + IONS. Depolarisation
120. Tick paralyis is very commonly seen in Rhinocerus. Calf, kids and lambs
121. Neostigmine has antagonistic effects of antisnake venom. Synergestic
122. Application of torniquet reduces the life of snake bitten animals. Prolongs
123. Zinc phosphide is converted into laughing gas. Phosphine
124. Bifotoxon causes paralysis of skeletal muscles. Motar nerves
125. Tick toxins cause paralysis of motor nerves. Skeletal muscels
126. Staphylococcal food poisoning is an example of food infection. Intoxication
127. Salmonellosis is an example of food intoxication. Food infection
128. Oxalate is having depilatory effect. Mimosine
129. Urea poisoning is common in horses. Ruminants
130. Paraquat is commonly used rodenticide. Weedicides
131. Zinc phosphide is commonly used insecticide. rodenticides
132. DDT keeps the Na+ channels in the close state for a prolonged period of
the time causing hyperactivity at nervous system. open
133. Behavioural changes are seen in anticholinesterase insecticides. OCI
134. Organophosphate toxicity symptoms resemble rabies. OCI
135. Universal antidote is contraindicated in organochlorine insecticides. OPI
136. Organophosphate poisoning should be differentiated from lead
poisoning. Phosphide
137. Zinc phosphate is an example of rodenticide. OCI
138. Nicotinic cholinergic signs are seen in organochlorine insecticide toxicity.
OPI
139. Oxime reactivators combine with the esteratic site of AChE. Anionic
140. Carbamate irreversibly carbamylate anionic site Esteratic
141. Pyrethroids are natural insecticides obtained from Chrysanthemum
spps. flowers. Pyrethrins
142. Type I pyrethroids cause C-S syndrome. T
143. Type II pyrethroids cause T syndrome. CS
144. Deltamethrin is a type I pyrethroid. Type II
145. Permethrin is a type II pyrethroid.] Type I
146. DNOC is a commonly used insecticide. Weedsides
147. Zinc phosphide is directly stimulant to CNS. Gut
148. Fluoroacetate as such is toxic but becomes highly toxic after its
conversion in the body to fluorocitrate. Non toxic
149. Red squill contains an cardiac alkaloid . scillirosids. Glycoside
150. Red squill is very toxic rodenticide in poultry. Non toxic
151. Horse appears to be most resistant to venomous than any other species.
Susceptible
152. Cobra bite causes local swelling. Dose not
153. Death is rapid in viper bites. Prolong
154. Death is prolonged in cobra bites. Rapid
155. KMNO4 should be used locally at snakebite. Never
156. Dinitro compounds act by interfering with Krebs cycle of energy
metabolism. ETC
157. Red squill is more toxic to male rats than females. Female
158. Red squill is obtained from Urginea maritima fungi. Plant
159. Toxins of lower animals are called as Phytotoxins. Zoo toxin

(D) Definitions:

1) Toxinology 2) Poison / Toxicant 3) Toxin

4) Venom 5) Toxicity 6) Hazard

7) Toxicokinetic 8) Toxicodynamics 9) Toxicology

10) LD50 11) Carcinogenecity 12) Mutegencicity

13) Teratogenecity 14) Lethal synthesis 15) Antidote

16) Chelate 17) Mycotoxin 18) Phytotoxin

19) Zootoxin 20) Malicious poisoning 21) Acute toxicity

22) Sub acute toxicity 23) Chronic toxicity 24) Cumulative toxicity

25) Delayed toxicity 26) Plumbism 27) Blue line

28) Lead lines 29) Arsenolysis 30) Selenium accumulators

31) Selenium obligatory accumulators 32) Blind staggers

33) Alkali disease 34) Plumbism 35) Teart disease

36) Dog murrain 37) Spectacled disease 38) Minamata disease

39) Nigeta disease 40) Allergy

41. Chemical which kills the pests. Pesticides

42. Chemicals used to eradicate or destroy the noxious weeds Weedicides
43. Chemicals which destroy the rodent pests. Rodenticides
44. Clinical signs of OCI poisoning Delayed neurotoxicity
45. Conversion of metabolite causing toxicity to body Antimetabolite
46. Alpha Naphthyl thio urea ANTU
47. Toxicosis due to a rodenticide thallium Thallitoxicosis
48. It is used as a mammalicide and clovulsive poison Strychnine
49. The venom of Vipers and rattle snakes Haemotoxic venom
50. The venom of cobra and krait Neurotoxic venom
51. A neurotoxic produced by poisonous toads Bufotoxin
52. The toxins of salivary galnds of ticks Tick paralysis
53. It is an organochlorine insecticide DDT
54. Oxime reactivators 2-PAM
55. Used in OPC poisoning to reactivate esteratic site. Oxime reactivators
56. Mono sodium glutamate Chinese restaurant syndrome
57. Antidote of snake bite Polyvalent antisnake venom serum
58. Neurotoxins bind specifically to cholinergic receptors and NM junction
produce curare like effect and respiratory paralysis. Flaccid paralysis
59. Salivation.lacrimation,urination and defecation SLUD
60. Chemical used to kill the insects Insecticide
61. Any substance depresses the body health or entirely destroys life. Poison
62. Poison or toxin secreted by specialised glands of an animal. Venom
63. Toxins produced by lower animals. Zootoxin
64. Drugs or chemicals intentionally added to foods. Direct additive
65. That occurs as a environmental contaminant. Indirect additive
66. Toxins produced by fish. Ichthyotoxin
67. Toxicosis due to secretion of tick’s salivary glands Tick toxicosis
68. Chemicals used to destroy noxious weeds. Herbicides
69. Venoms produced by bees causing intense pain, local odema at the site of
sting. Bee stings
70. These marks used to locate the site of snake bite Fang marks
71. Paralysis due to tick’s toxicosis Tick paralysis
72. Used in the treatment of OPI poisoning AntiChE’s
73. A gas produced by zinc phosphide in rat stomach Phosphine
74. Diseases caused by ingestion of microbial toxins along with food Food
intoxication
75. Toxic substances present in animal feeds and fodder Food toxicants
76. Conversion of inactive substance into active toxic substance inside the
animal body. Lethal synthesis
77. Syndrome due to acute organo phosphate toxicity Jake leg or Ginger jake
paralysis
78. Part per billion ppb
79. Parts per million ppm
80. Likelihood of poisoning of a living organism due to particular toxicant
Hazard/Risk
81. Daily dose of a chemical residue taken during the entire life time
Acceptable daily intake
82. Concentration of chemical that produces no harmful effect No
effect/Maximum no adverse effect
83. Non carcinogenic chemical residue permitted in food Finite tolerance
84. No chemical residue in food due to its extreme toxic properties Negligible
tolerance Zero tolerance
85. Type I pyrethroids induced tremors T syndrome
86. Type II pyrethroids induced choreoathetosis-salivation CS syndrome
87. Any foreign substance to body Xenobiotic
88. Active part of toxic substances Toxicant
89. Dose to produce toxic symptoms Toxic dose
90. Dose to produce lethality Lethal dose
91. No observed effect level/ no observed adverse effect level NOEL/NOAEL
E) Give reasons :

1) Organic arsenicals are non toxic

2) Hooves, hairs and nails are collected in chronic arsenic poisoning

3) Mussel lining of intestine gets easily peeled off n arsenic toxicity

4) Organic selenium compounds are more toxic than inorganic selenium

compounds

5) Use of fertilizer / manure increases the chances of nitrate poisoning

6) Fluorine causes blockage of TCA cycle

7) In molybdenum poisoning osteoporosis is commonly observed

8) Molybdenosis leads to spectacle disease

9) Salt toxicity is called as water deprivation induced sodium toxicosis

10) Salt toxicity is sodium deprivation syndrome

11) Hazardous nature depends on conditions

12) Selective toxicity is a beneficial phenomenon

13) Consumption of physically damage plants milled planted etc increases the

extent of cyanide toxicity

14) Cabbage soybean although contains cyanide are not toxic

15) Orgnomercurials are more toxic than inorganic mercury poisoning

16) In acute selenium poisoning the breath has garlic odou8r

17) Arsenic are used in treatment of selenium toxicity

18) Copper toxicity is treated with molybdate salts

19)Cyanide toxicity is due to cytotoxic anoxia

20)Horses/pigs are less susceptible to cyanogenic plant poisoning as compared

to ruminants

21)Sheep are less susceptible to cyanogenic plant poisoning as compared to

cattle

22)Methaemoglobinaemia has toxicological as well as therapeutic significance

23)In cyanogenic plant poisoning the mucosae are bright red in colour at initial

stages and cyanotic at the terminal stages

24)Very young shoots of jowar are highly toxic

25)Blindness may occur in photosensitized animals

26)Hepatogenous photosensitization is called secondary photosensitization

27)Parthernium-lnduced photosensitization is called primary photosensitization

28)Lantana-induced photosensitization is called secondary photosensitization

29)Mold-infested hay can also cause oxalate poisoning

30)Haemorrhages occur due to feeding on oxalate-rich plants

31)Renal damage occurs in oxalate poisoning

32)Following mold infestation the sweet clover hay becomes toxic

33)Acute Nuxvomica poisoning in dogs is characterized by nervous signs,

34)Abrus precatorius poisoning is called Sui (needle) poisoning

35)Kaner poisoning is characterized by cardiac failure

36)Methaemoglobinaemia also has therapeutic purpose.

37)Why oxime reactivators are not used in carbamate toxicity? Due to

inhibition of AchE by carbamylation.

38)Strychnine is a violent convulsive poison? Antagonims of glycine mediated

postsynaptic inhibition in spinal motor nerves.

39)ANTU causes pulmonary oedema? Interferes with effective uptake of

oxygen from pulmonary alveoli.

40)Warfarin causes coagulant defect? Interferes with normal function of Vit.

K.

41)Red squill is a safest rodenticide? It has no major adverse effects.

42)Paraquat causes pulmonary injury? Due to damage to cellular membrane

and interferes with gas transport.

43)Neostigmine has synergistic effect with polyvalent antisnake venom serum?

Due to its anti AChE action.

44)Application of torniquet prolongs the life of the snake bitten animal? Due to

inhibition of transport of poison from the site of snake bite.

45)Scorpion or bee stings cause intense pain. Due to release of histamine and

proteolytic enzymes.

46)Generalized muscle paralysis occurs following a bite from a cobra or krait.

Due to irreversible blockade of neuromuscular transmission.

47)Bufotoxin causes paralysis of motor nerves Due to increased sodium ion

permeability.

48)Tick toxins cause paralysis of skeletal muscles. By preventing synthesis or

release of ACh from motor nerve terminals.

49)Organochlorine insecticide cause neuronal hyper excitability. Decreased

firing threshold.

50)Symptoms of organophosphate insecticide toxicity persist for longer periods

than the toxicity with carbamates. Irreversible inhibition of AChE.

51)Cholinergic signs characterize organic phosphate/ carbamate toxicity

symptoms. Due to inhibition of AChE.

52)Death in acute organic phosphate insecticide toxicity occurs due to

respiratory failure. Neuromuscular blockade of respiratory muscle.

53)Oily purgatives should not used in animals, which are acutely intoxicated with

insecticides. Because it retains the insecticides inside the GIT.

54)Fluoroacetate impairs cellular respiration. Inhibits of kreb cycle.

55)Warfarin causes hemorrhages. Inhibits Vit. K.

56)Strychnine is a convulsive poison. Antagonims of glycine mediated

postsynaptic inhibition in spinal motor nerves.

57)ANTU toxicity in dogs is characterized by respiratory distress. Causes

massive pulmonary oedema.

58)The action of fluoroacetate involves formation of antimetabolite. Due to

formation of fluorocitrate.

59)Atropine is the antidote of carbamate or organic phosphate insecticide

toxicity. To control the parasympathetic signs.

60)2-PAM is specific antidote of organic phosphate insecticide toxicity. Due to

reactivation of AChE.

61)Overfeeding of molasses is toxic to animals. Due to its high content of

potassium carbonate

62)Overfeeding of urea is toxic to animals. Due to liberation of excess

ammonia.

63)Acidosis develops in urea intoxication. Due to enhanced glycolysis and

lactate production.

64)Cotton seed cake feeding may pose health hazard to pigs. It contains

gossypol.

65)Long term feeding of Leucaene leaves as green fodder to livestock is not

advisable. Due to its adverse effects like hepatic necrosis, ascites and

renal damage.

66)Prolonged feeding of leucaena leaves in heifers may result in infertility. Due

to content of HCN.

67)Selenium toxicity causes depletion of reduced glutathione.

68)Copper poisoning is more common in sheep.

69)Methylene blue is repeated cautiously during treatment of nitrate poisoning.

70)Molybdenosis causes scouring.

71)Water deprivation aggravates salt toxicity.

72)Treatment of salt toxicity is not easy.

73)Highly toxic compounds may be less hazardous.

74)Many times the circumstantial evidence is more important than clinical

evidence in diagnosing poisoning cases.

75)In the initial stage of treatment of poisoning case vomition and diarrhoea

should not be stopped.

76)Extent of poisoning changes from species to species

77)Incidence of cyanide poisoning is more in ruminants as compared to

monogastric animals.
78)Sodium nitrite should be given before sodium thiosulphate during the

treatment of cyanide toxicosis.

79)Disodium Calcium- EDTA is administered in a schedule during the treatment

of lead poisoning.

80)Lipoic acid is indicated for arsenic toxicity.

81)Although selenium non-accumulators have less selenium as compared to

obligatory accumulators but they are important source for selenium toxicity

to animals.

82)Nitrate poisoning is common in agriculturally developed states Adrenergic

drugs are avoided during treatment of nitrate poisoning.

(F) Answer in one sentence

1. What is Toxicology?

2. What is a poison?

3. What is hazard and how it differs form toxicity?

4. What is venom?

5. Explain the term Intoxication?

6. Explain carcinogenecity?

7. What is Mutagenecity?

8. What is median lethal dose?

9. Explain malacious poisoning?

10. What is acute poisoning?

11. What is chronic toxicity?

12. Explain delayed toxicity?

13. What do you mean by selective toxicity?

14. Explain what is teratogenecity?

15. Name the five evidences for diagnosis of toxicity case?

16. Name the contents of universal antidote?

17. Explain the term toxicokinetics?

18. What do you mean by toxicodynamics?

19. Explain lethal synthesis?

20. What is allergy?

21. Name three cyanogenic glycosides?

22. What is the enzyme inhibited by cyanide?

23. Where are lead line observed?

24. Where is the blue line present during the plumbism?

25. What is specific antidote for lead toxicity?

26. What was the cause of minamata incidence?

27. What is a Nigeta disease?

28. What is mercurial ptylism?

29. What is the specific antidote for mercury toxicity?

30. What is alkali disease?

31. What is subacute selenium toxicity refereed as?

32. Which is specific antidote for copper poisoning?

33. What type of odour is observed during phosphorus toxicity?

34. What type o phosphorus is toxic?

35. In which form flurosis is exhibited?

36. What type of lameness is observed in flurosis?

37. Molybdenosis depends on which other minerals?

38. Which reducing agent can be used in treating nitrate poisoning?

39. What materials you will collect for diagnosis of nitrate poisoning?

40. What material is collected for diagnosis of copper toxicity of sheep?

41. Copper toxicity is seen in which species?

42. What material is collected for diagnosis of chronic arsenic poisoning?

43. What specific material is to be collected to diagnose flurosis?

44. What are the material; collected for diagnosis of chronic selenosis?

45. Neurotoxic Produced by cobra and krait.

46. Haemotoxic venom Produced rattle snake and vipenrs.

47. Scorpion venom. Produced by scorpion sting.

48. Bufotoxin Produced by poisonous toads.

49. Spider venom Produced by Spiders Black widow spider

50. Tick toxins Toxins produced from salivary glands of ticks.
51. Venom Poison or toxin secreted by specialized galnd of
animals.
52. Toxin Depresses the health or entirely destroy the life.
53. Zootoxin Produced by lower animals.
54. Oxime reactivators used in OPI poisoning Eg. 2-PAM.
55. ANTU Amino naphthyl thio urea, a rodenticide.
56. Anticholine esterase Eg. Neostogmine used in carbamate
poisoning.
57. Bee stings multiple in nature and cause severe local swelling.
58. Phosphine gas produced in stomach of rat.
59. 2-PAM oxime reactivator antidote of OPI poisoning.
60. Pesticides chemicals to control pests.
61. Insecticides chemicals to control insects.
62. Rodenticides chemical to kill rodents.
63. Poison any substance interfere with physiological functions.
64. Herbicides killing or damaging unwanted plants.
65. Weedicide killing or damaging unwanted weeds.
66. Ichthyotoxins toxins produced by fish.
67. Tick toxins toxins liberated by salivary galnd of ticks.
68. Tick paralysis paralysis due to tick toxins.
69. Antimetabolite conversion of fluroacetate into fluorocitrate in
fluoroacetate poisoning.
70. Direct feed additive Drugs or chemical sintentionally added to
foods.
71. Indirect feed additive That occurs as a environmental
contaminant.
72. Violent convulsion conversions caused by strychnine.
73. Parasympathetic signs in OPC toxicity salivation, lacrimation,
urination, defecation.
74. PPb parts per billion.
75. Haemotoxicity toxicity to haemopoitic system.
76. Toad toxins toxins liberated by toads skin glands.
77. Cardiotoxic glycosides of toad bufogenic toad toxins.
78. Mechanism of action of toad toxins cardiotoxic glycosides.
79. Tick causing tick paralysis Dermacentor, lxodes.
80. Intentional additives Urea, Molasses.
81. Incidental additives Gogssypol, mimosine.
82. Food intoxication due to ingestion of microbial toxins with foods.
83. Name two ionophores used as feed additives monesin,
salinomycin.
84. Antidote of OPC poisoning 2-PAM
85. Mechanism of carbamate toxicity irreversible inhibition of AChE.
86. Food toxicants toxic substances present in animal feeds and
fooders.
87. Name two toxicants naturally present in feed and fodder. Gossypol,
HCN, nitrates.
88. Name two direct additives Iodinated casein, antibiotics.
89. Name two indirect additives Oxalates and selenium.
90. Food infection Ingestion of food with contaminated pathogenic
microorganism.
91. Name two venomous snakes Cobra Krait.
92. Reversible inhibitors of AChE Aldicarb, Carbaryl.
93. MINA Mono iso nitrosamine.
94. Anticoagulant rodenticide Warfarin.
95. T-Syndrome Tremor syndrome
96. CS Syndrome Choreoathetosis / salivation.
97. NOEL/NOAEL no observed effect level.
98. Ppt parts per trillion.
99. ppm parts per million.
100. Bound form of HCN
101. Linamarin
102. Dhurrin
103. Amygdalin
104. Cytochrome oxidase
105. Hypericin
106. Fagopyrin
107. Parthenin
108. Phylloerythrin
109. Photodynamic substance
110. Congenital porphyries
111. Predilection sites
112. Cyanogenic glycosidase.
113. Acute ergotism is characterized by nervous signs.
114. Chronic ergotism is characterized by gangrene/necrosis of
extremities.
115. ' Botulinum toxin causes respiratory paralysis
116. Tetanus toxin causes violent convulsions
117. Diphtheria toxin is called a cytotoxin or Histotoxins
118. Leucocidin is called a haemolysis
119. Cholaragen is called an enterotoxin
120. Aflatoxicosis results in immunosuppression
121. Aflatoxicosis results in hepatotoxicity
122. Zearalenone is called an estrogenic toxin
123. Slaframine is called an histaminergic toxin.

(G) Differentiate between

1. Zootoxin and Phytotoxin

2. Toxin and Venom

3. Toxicology and Toxinology

4. Blue lines and lead lines

5. Salt toxicity and Organochlorine poisoning

6. Blind stagger and Alkali disease

7. Selenium facultative and obligatory accumulators

8. Nitrite and cyanide poisoning

9. Toxicity and Hazard

10. Acute toxicity and Chronic toxicity

11. Teratogenecity and Mutagenecity

12. Teratogenecity and Carcinogenecity

13. Mycotoxin and zootoxin

14. Selective toxicity and Delayed toxicity

15. Delayed toxicity and Chronic toxicity

16. Lewisite and antilewisite

17. Antidote and Chelate

18. Dhurrin and Amygdalins

19. Free HCN and bound form of HCN

20. Methaemoglobin and hemoglobin

21. Primary photosensitization and secondary photosensitization

22. Chlorophyll and phylloerythrin

23. Phytotoxin and mycotoxins

24. HCN and Dhurrin

25. Acute ergotism and chronic ergotism

26. Nervous ergotism and gangrenous ergotism

27. Bacterial toxins and mycotoxins

28. Tetanospasmin and aflatoxin

29. Neurotoxin and enterotoxin

30. Aflatoxins and ergotoxins

31. Phytotoxin and mycotoxins

32. Botulinum toxin and tetanus

33. Zearalenone and Slaframine

34. Endotoxin and exotoxin

35. Zootoxin and venom

36. Insecticides & Pesticide

37. Poison& Venom

38. Symptoms of OPI & CHC’s

39. Direct and indirect feed additive

40. Mechanism of toxicosis of OPI & Carbamates poisoning

41. Mechanism of toxicosis of OPI & CHC

42. Treatment of OPI &CHC Poisoning

43. Treatment of OPI & Carbamate poisoning

44. Snake bite and Bees string

45. ANTU & Zinc Phosphide

46. Herbicide & Rodenticide

47. Haemotoxic & Neurotoxic snakes

48. Carbaryl& Malathion

49. Parathion & DDT

50. Parathion &2-PAM

51. Food intoxication & Food infection

52. Mimosine & Gossypol

53. Food toxicants & Food intoxication

54. Toxic dose & Lethal dose

55. Accidental poisoning & Malicious poisoning

56. Direct and indirect acting OPI

(H) Write Short notes

1. Haemolytic crisis in chronic copper toxicity
2. Factors aggravating nitrate poisoning
3. Treatment of nitrate poisoning
4. Circumstantial and clinical evidences of poisoning
5. Supportive and specific treatment of poisoning case
6. Sources of poisons
7. Mechanism of action of different toxicants
8. Metabolism of toxicants
9. General and specific antidotes
10. Line of treatment of cyanide toxicity
11. Sources of lead poisoning
12. Mechanism of toxicity of arsenic
13. Symptoms of arsenic poisoning
14. Seleniferous plants
15. Mechanism of selenium toxicity
16. Symptoms of chronic copper toxicity in sheep
17. Symptoms of molybdenum poisoning
18. Symptoms of salt poisoning and its treatment
19. Factors modifying toxicity of a compound
20. Classification of toxicants
21. Antidotal therapy
22. Pathological and analytical evidences for diagnosis of poisoning
23. Differential diagnosis of heavy metal toxicities
24. Bacterial toxins
25. Botulinum toxin
26. Tetanus toxins
27. Aflatoxins
28. Nervous ergotism
29. Rubratoxins
30. Gangrenous ergotism
31. T-2 toxin
32. Zearalenone
33. Cyanogenic glycosides
34. Oxalate poisoning
35. Aflatoxicosis
36. Ergotism
37. Teratogenic plants
38. Plants causing delay in blood coagulation
39. Plants causing thiamine deficiency
40. Biochemical basis of cyanide toxicity
41. Photosensitization
42. Lantana poisoning
43. Datura poisoning
44. Nuxvomica poisoning
45. Castor poisoning
46. Kaner poisoning
47. Biochemical basis of treatment of cyanogenic plant poisoning.
48. Sui poisoning
49. Venoms and stings
50. Bacterial toxins
51. Rodenticides
52. Rubratoxicity
53. Poison
54. Venom
55. Teratogen
56. Zootoxin
57. Snake venoms
58. Insecticides
59. Herbicides
60. Weedicides
61. Sources of Poisoning
62. Symptoms of OPI
63. Symptoms of CHC
64. Symptoms of Carbamate toxicity
65. ANTU toxicity
66. Warfarin toxicity
67. Zinc Phosphide toxicity
68. Herbicide poisoning
69. Treatment of snakebite
70. Bee Stings
71. Ichthyotoxins
72. Tick toxins
73. Hazards of feed additives
74. Feed additives and Preservatives
75. Toxic effects of hormones and Anabolic steroids
76. Toxic effects of Ionophores
77. Toxic effects of antibacterial feed additives.

(I) Answer in Brief

1. What are the general principles of diagnosis of poisoning case?

2. Explain the general line of treatment of poisoning case

3. What are general mechanisms by which toxicants acts?

4. How are poisons absorbed?

5. Explain metabolism of toxicants

6. Write the symptoms and post mortem lesions observed during cyanide

toxicity

7. What is the mechanism of cyanide toxicosis?

8. Write the different mechanisms through which lead causes toxicity

9. Enlist the symptoms observed during inorganic mercury poisoning

10. Which are the different forms of the arsenic and grade their toxicities

11. Which are the different source of arsenic poisoning in animals

12. Write about the treatment of arsenic toxicity

13. What are the symptoms observed in blind staggers?

14. Enlist the symptoms of chronic selenosis

15. Give differentiating diagnostic features for selenium and fluorine toxicity

16. Give the source of copper poisoning in sheep

17. What are the post mortem lesions observed in chronic copper poisoning?
18. Enumerate the different mechanisms through which fluorine causes toxicity

19. Give symptoms of osteofluorosis

20. What are the mechanisms of actions of nitrate toxicity?

21. How methylene blue acts in treatment of nitrate poisoning

22. Give the differentiating diagnostic points between cyanide and nitrate

poisoning

23. Explain the sequence of events during salt toxicity

24. What are the symptoms observed during salt toxicity in poultry

25. Differential diagnosis of snakebite.

26. General management of snake bite

27. Three A’s of snake bite treatment.

28. Four families most poisonous snake.

29. Clinical signs of snake bite patient.

30. Line of treatment of Bee’s and Scorpion bitten dog.

31. Tick toxins and Ichthyotoxins

32. Common fish poisonings

33. ANTU Poisoning

34. Warfarin poisoning

35. Zinc phosphide poisoning

36. Red squill poisoning

37. Secondary poisoning and lethal synthesis

38. Mechanism of toxicity of Dinitro compounds.

39. Mechanism of toxicity of OPC poisoning.

40. Mechanism of toxicity of Carbamate toxicity

41. Muscarnic and Nicotinic symptoms of OPI toxicity.

42. Behavioural changes in DDT poisoning

43. Neurological symptoms of Lindane poisoning

44. Cholinergic manifestation in animals poisoned with endosulfan.

45. Clinical signs of synthetic pyrethroid toxicity.

46. Short notes on i) Haemotoxin ii) Neurotoxin

47. Line of treatment of Organochlorine insecticide poisoning .

48. Line of treatment of OPI poisoning .

49. Expand DAM,MINA 2-PAM, ANTU&NOEL

50. Clinical signs of 2,4-D toxicity.

51. Mechanism of action of snake venom

52. Toads

53. NOAEL

54. Tolerance level.

(J) SUBJECTIVE QUESTIONS:

1. Describe the source, mechanism, clinical symptoms, differential diagnosis

and treatment of cyanide poisoning in animals.
2. Describe the source, mechanism, clinical symptoms, differential diagnosis
and treatment of nitrate poisoning in animals.
3. Describe the source, mechanism, clinical symptoms, differential diagnosis
and treatment of lead poisoning in animals.
4. Describe the source, mechanism, clinical symptoms, differential diagnosis
and treatment of mercury poisoning in animals.
5. Describe the source, mechanism, clinical symptoms, differential diagnosis
and treatment of arsenic poisoning in animals.
6. Describe the source, mechanism, clinical symptoms, differential diagnosis
and treatment of copper poisoning in animals.
7. Describe the source, mechanism, clinical symptoms, differential diagnosis
and treatment of fluorosis in animals.
8. Describe the source, mechanism, clinical symptoms, differential diagnosis
and treatment of selenium poisoning in animals.
9. Describe the source, mechanism, clinical symptoms, differential diagnosis
and treatment of molybdenum poisoning in animals.
10. Describe the source, mechanism, clinical symptoms, differential diagnosis
and treatment of salt poisoning in animals.
11. Give differential diagnosis of:
a. Selenium and fluorine toxicity

b. Nitrate and cyanide poisoning

c. Selenium and ergot poisoning

 d. Lead and arsenic toxicity

e. Arsenic and mercury toxicity

f. Lead and mercury toxicity

g. Molybdenum and selenium toxicity

h. Copper and lead toxicity

i. Salt and organochlorine toxicity

j. Salt and lead toxicity

12. Describe the sources, mechanism of toxicosis, symptoms, diagnosis and

treatment of Cyanogenic plant poisoning.
13. What is photosensitization? Discuss various types and write in brief the
symptoms and Line of treatment of photosensitized animals.
14. List any four important toxic plants of your locality and mention their active
principles, Mechanism of toxicosis; symptoms and treatment of their toxicity
in animals.
15. Give the classification of mycotoxins. Describe in brief the various types
with important Clinical signs.
16. What is toxinology ? Give the classification of toxins along with their source.
Describe ergotism.
17. What are bacterial toxins? Give their classification along with source.
Describe Poisoning with tetanus toxin.
18. What are mycotoxins"? Give their classification with examples. Describe
aflatoxicosis In poultry.19
19. What is ergot? What are its toxins? Describe chronic ergot poisoning in
animals.
20. Write the name of the toxic principle, important symptoms and line of
treatment of Toxicity of the following plants:
a. Abrus precatorlus b. Parthenium hysterophorus
c. Thevetia peruviana d. Sorghum vulgare
e. Ipomoea carnea f. Nerium oleander
g. Lantana camara h. Datura stromonium
21. Name the important food toxicants. Describe urea toxicosis in
ruminants.
22. What are zootoxins? Give their classification.
23. Describe the snake venoms giving a brief account of their toxic nature,
clinical signs and treatment of snake victims.
24. Give the line of treatment of the following.
 a) Snake bitten animals
b) Bee sting in a dog
c) Tick paralysis in a lamb
25. Write short notes on
a) Toad toxins b) Scorpion venom
c) Tick paralysis d) Bee sting f) spider venom
26. Describe the source, symptoms, diagnosis and treatment of
Organochlorine insecticides toxicity in livestock.
27. Describe the source, symptoms, diagnosis and treatment of
Organophosphate insecticide toxicity in livestock.
28. Carbamate toxicity.
29. Pyrethroid toxicity.
30. What are rodenticides? Name the commonly used rodenticide. Describe
the source, mechanism of toxicosis, symptoms and treatment of ANTU
and Warfarin.
31. What are rodenticides? Name the commonly used rodenticide.Describe
the source, mechanism of toxicosis, symptoms and treatment of Zinc
hosphide and red squill.
32. Define herbicide? Classify on the basis of chemicals nature with example.
Write sources, clinical signs, diagnosis and treatment of 2,4-D.
33. Define herbicides? Classify on the basis of chemicals nature with
example. Write sources, clinical signs, diagnosis and treatment of
Dinitrophenol.
34. Write in detail the mechanism of toxicosis , symptoms and treatment of
Organophosphate toxicity in a cow.
35. Write in detail the mechanism of toxicosis, symptoms and treatment of
Organochlorine insecticide toxicity in a bullock.
36. Write in detail of synthetic pyrethroid toxicity in a dog.
37. Write in detail of carbamate insecticide toxicity in livestock.
38. Name four commonly used OPI. Describe mechanism of toxicosis,
symptoms and treatment of OPI poisoning.
39. Define food toxicants., Classify them. Describe in detail toxicity caused by
Hydrocyanic acid.
40. Name four commonly used Organochlrine insecticide. write source,
symptoms, And line of treatment of Organochlorine poisoning.
41. Name two each commonly used pyrethroids and carbamates. Write
source, symptoms and line of treatment of carbamate toxicity in goat.

(K) Describe in brief the mechanism of toxicosis of the following:

1. Hydrocyanic acid
2. Photodynamic substance
3. Oxalates (in blood and on kidney)
4. Sweet clover hay
5. Oxalates
6. Strychnine
7. Lantana
8. Datura
9. Ergotoxins
10. Aspergillosis
11. Tetanospasmin
12. Enterotoxin
13. Rubratoxins
14. Histotoxins
15. Endotoxin
16. Teratogenic toxin
17. Estrogenic toxin
18. Histaminergic toxin
19. Exotoxin
20. Ergotoxins
21. Tetanus toxin.
22. Zearalenone
23. Botulinum toxin
24. Aflatoxins
25. Slaframine
26. Peritrem-A