Metals - Shokry

Question 1

Sources of copper toxicosis

Answer 1

Excess copper
Molybdenum deficiency (6:1)
Unavailable sulfate

Question 2

Accumulation of copper in the liver is due to

Answer 2

Imbalances between copper, molybdenum and sulfate

Question 3

What is secondary copper toxicosis

Answer 3

Liver damage causes copper accumulation by hepatocytes

Question 4

How long does copper accumulation take

Answer 4

2-10 wks

Question 5

Release of copper from the liver and excess in the blood causes

Answer 5

Oxidation of erythrocyte membranes increasing fragility and causing hemolytic crisis

Question 6

Copper oxidizes hemoglobin to

Answer 6

methemoglobin

Question 7

Clinical signs of copper

Answer 7

Sudden weakness, anorexia, pale MM, icterus, hemoglobinuria, dyspnea

Question 8

Lesions seen with copper

Answer 8

Icterus, Hemolysis, Methemoglobin
Liver enlarged, yellow, friable
Kidney enlarged, hemorrhagic, bluish, friable (gunmetal)
Blackberry Spleen

Question 9

Treatment for copper toxicosis

Answer 9

Ammonium tetrathiomolybate

D-penicillamine - 6 days

Question 10

Which species is most susceptible to molybdenum

Answer 10

Cattle

Question 11

Which species are resistant to molybdenum

Answer 11

Horses and pigs

Question 12

molybdenum is absorbed ____ and excreted in _____

Answer 12

Absorbed from GI and excreted in milk at toxic levels

Question 13

Clinical signs of molybdenum

Answer 13

Severe diarrhea (green w/ gas bubbles) 8-10 d post
Rough hair coat and depigmentation (eyes)
Weight loss, osteoporosis, lameness, pica

Question 14

Treatment for molybdenum

Answer 14

Copper glycinate/sulfate

Question 15

What are organic arsenics used for

Answer 15

Improve weight gain and feed efficiency

Control enteric infection - swine, poultry

Question 16

organic arsenics toxicity is enhanced by

Answer 16

dehydration, renal insufficiency

Question 17

What is the mode of action for organic arsenics

Answer 17

Peripheral nerve demyelination and axonal damage

Question 18

Clinical signs for arsanilic acid in swine

Answer 18

3-5 days
Incoordination
Partial parlysis
Blindness
Still have good appetite

Question 19

Clinical signs for arsanilic acid in poultry

Answer 19

Anorexia, depression, coma, death

Question 20

Clinical signs for Roxarsone in swine

Answer 20

Sudden onset
Marked hyperexcitability
Tremors
Collapse, coma
No blindness

Question 21

Clinical signs of roxarsone in poultry

Answer 21

Incoordination/ataxia

Question 22

organic arsenics lesions in swine

Answer 22

Erythema
Muscle atrophy
Peripheral nerve and optic nerve degeneration

Question 23

Which form of inorganic arsenic is most toxic

Answer 23

Trivalent

Question 24

inorganic arsenic is absorbed by

Answer 24

GI, skin, inhalation

Question 25

Where are the highest concentrations of inorganic arsenic

Answer 25

Liver, Kidney, Hair/Hoof

Question 26

Milk from poisoned cows contains ______ of inorganic arsenic

Answer 26

Toxic levels

Question 27

MOA of inorganic arsenic

Answer 27

Inhibits/slows citric acid cycle

Question 28

inorganic arsenic peracute signs

Answer 28

Sudden death, colic, collapse, death

Question 29

inorganic arsenic acute signs

Answer 29

Rapid onset, staggering, salivation, thirst, diarrhea

Question 30

inorganic arsenic subacute signs

Answer 30

Same + bloody diarrhea, partial paralysis of hind limbs, death

Question 31

Lesions associated with inorganic arsenic

Answer 31

GI edema/hemorrhage, sloughing Liver/kidney damage Capillary degeneration

Question 32

What sample should be taken for inorganic arsenic

Answer 32

Urine antemortem | Liver/kidney postmortem

Question 33

What is increased with inorganic arsenic

Answer 33

PCV, BUN

Question 34

What chelator is used with inorganic arsenic

Answer 34

Dimercaprol

Question 35

Selenium acts as an antioxidant by

Answer 35

Prevention of peroxide accumulation through reduction of glutathoine

Question 36

Selenium and Vit E prevents what

Answer 36

Cellular degeneration and cell membrane damage

Question 37

What type of soil promotes selenate formation

Answer 37

alkaline

Question 38

Selenium toxicity is reduced by

Answer 38

High protein diet and binding elements such as copper

Question 39

Selenium targets which organs

Answer 39

Liver, Kidney, Spleen

Question 40

Selenium acute signs - Oral

Answer 40

Colic, bloat, dark diarrhea | Respiratory distress, frothy

Question 41

Selenium acute signs - Parenteral

Answer 41

Neuroligical

Question 42

Selenium subacute Cattle

Answer 42

Blind staggers Stage 1 - poor appetite, wandering/circling Stage 2 - Incoordination, foreleg weakness (on knees) Stage 3 - Hypothermia, emaciation, clouded cornea, paresis, coma, death

Question 43

Selenium subacute swine

Answer 43

Porcine Focal Symmetrical Poliomyelomalacia Incoordination, lameness, parlysis Alopecia, hoof abnormalities/separation

Question 44

Selenium chronic toxicosis - Alkali Disease

Answer 44

Rough hair, hair loss (mane/tail) Hoof deformities Lameness, stiffness Partial blindness, anemia, emaciation, birth defects

Question 45

Selenium acute lesions

Answer 45

Hemorrhagic enteritis Organ congestion Pulmonary edema Rotten/garlic gut smell

Question 46

Selenium chronic lesions

Answer 46

Abnormal hooves, cardiac damage, hepatic necrosis

Question 47

Selenium treatment

Answer 47

Saline cathartics | Acetylcysteine