Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
56 Cards in this Set
- Front
- Back
What is the most common toxicosis in sheep?
|
copper - excess copper in concentrate portion of the feed
|
|
At what Cu: Mo ratio does copper toxicosis occur in the sheep?
|
> 10:1
|
|
What dog breed has an inherited copper accumulation problem?
|
Bedlington terriers
|
|
Where does copper build up over weeks and months?
|
the liver - during this period, the animal is asymptomatic
|
|
What is the trigger that releases Cu from the liver?
|
stress --> causes hepatic necrosis
|
|
What are the clinical signs of Cu toxicosis in sheep?
|
hepatic --> RBC --> renal
|
|
What type of epidemic surve would you see with Cu toxicosis?
|
sporadic epidemic curve --> high mortality with low morbidity
|
|
What color are the kidneys in copper toxicosis?
spleen |
gun metal
blackberry jam colored |
|
What can be done to check the status of a sheep heard for copper toxicosis?
dogs? |
test samples of the liver on dead sheep
-buccal mucosa or blood on Bedlingtons |
|
What is the treatment for copper toxicosis in sheep?
prevention? |
ammonium tetrathiomolybdate - helps Cu excretion
- Na molybdate can be used for prevention |
|
What is the treatment for dogs with copper toxicosis?
|
trientine - more expensive
|
|
What year of penny will have zinc in it?
|
1983 and after
|
|
What are the acute clinical signs of zinc toxicosis?
|
GI, RBC, hepatic, renal
(pancreatic lesions) |
|
What are the choronic clinical signs of zinc toxicosis?
|
GI, RBC, hepatic, renal and bone
(pancreatic acinar lesions) |
|
What is unique about CHRONIC zinc toxicosis?
|
decreased bone formation
|
|
Name some situations where lead is absorbed more?
|
-young animals
-acidic environment -animals deficient in Ca, Zn, or Fe absorb more |
|
Is Pb a cumulative toxicant?
|
yes
|
|
Where is early lead deposited?
|
on RBCs and in kidney and liver
|
|
7-10 days after absorption, where is most Pb?
|
in bone - it acts as a sink
|
|
Does Pb cross the BBB and placenta?
|
yes
|
|
What is the primary excretion route for Pb?
|
feces; bile adds to this
-urinary route is important only in Chelation therapy |
|
What does Pb bind in the body?
|
A number of SH groups of a number of key metabolic enzymes
-may compete with or replace Zn in enzymes |
|
What are the most important systems affected clinically by Pb and what are the minor?
|
MAJOR: GI and CNS
MINOR: PNS, hemopoietic is most sensitive, renal |
|
What is the MoA that lead acts on the brain?
the blood? |
damage to BBB and demyelination
-enzymes of heme synthesis are inhibited (ALA-dehydratase and synthetase) |
|
What is the acute syndrome seen with Pb poisoning?
|
GI Syndrome
-anorexia, vomit -initially, see constipation, followed by diarrhea - may have some blood in the feces -cattle have rumen stasis or sluggishness |
|
After the acute GI syndrome with lead poisioning, what comes next?
-this occurs with small quantities of lead over weeks to months |
Chronic - CNS syndrome
-depression to hysteria -barking/muscle tremors -behavioral changes -seizures (clonic-tonic) -CNS signs in dogs may be intermittent and hard to diagnsoise -Cows - blindness, bellowing, head bobbing, ataxia, ear twitching -Horses - roaring -water fowl - droopy wings |
|
What should you use to collect blood for lead sampling?
tissues? |
EDTA or heparin
- unclotted blood - plasma - liver and kidney > 10ppm |
|
What are differentials of lead poisoning in dogs?
|
GI - gastritis, arsenic
CNS - distemper, encepalitis, organochlorines, strychnine, metaldehyde, OPs, Carbamate |
|
What are differentials of lead poisoning in cattle?
|
GI - simple indigestion, polio, arsenic
CNS - hemophilus, polio, grass tetany, nervous acetonemia, brain abcess, neoplasia, organochlorines, urea, salt |
|
What is the treatment of lead poisoning?
|
-chelation therapy - no FDA approved product for veterinary use
-use CaNa2 EDTA to prevent hypocalcemia and treat for 2-5 days -SA use only |
|
EDTA is highly polar and chelates extracellular Pb? Where does it primarily chelate from?
-what is a down to using EDTA? |
bone, not soft tissue
-can be nephrotoxic |
|
What product that is approved for use in humans removed Pb from soft tissues and bone?
-what animals is it good to use in? |
DMSA - succimer
-esp good in birds (Pb or Zn) -also in dogs and cats |
|
What treatment for Pb poisoning is orally active, SH containing chelator? What is is MOST useful for?
|
penicillamine
-most useful for copper, but can be used for Pb, As, and Zn -good for chronic toxicities |
|
What therapy is very useful in cattle for the treatment of lead poisioning?
|
thiamin - B1
-maintains nerve cell membranes |
|
Which saline cathartic is best to use for lead poisoning?
|
MgSO4 - insoluble Pb ppt formed
|
|
What are sources for inorganic arsenic in cattle?
-dogs and cats? |
-old pesticides, ashes from salt treated lumber
- sweet syrupy ant baits |
|
Which form of aresenic is most toxic?
|
trivalent form (3+)
|
|
How is the trivalent form of arsenic best absorbed?
|
GI and skin
-high in liver and kidney |
|
How is inorganic arsenic excreted?
|
rapidly in urine and feces, and bile to intestine
|
|
Does inorganic arsenic cross the BBB?
the placenta? |
NO - BBB
Yes - placenta |
|
What does inorganic arsenic combine with and and what does it shut down?
|
combines with SH groups of key metabolic enzymes (Lipoic Acid) and shuts down cellular respiration
|
|
What does inorganic arsenic have direct corrosive action on?
|
cappillaries and is a potent toxicant to the vascular system
|
|
What are the main systems affected by inorganic arsenic in the acute form?
|
GI and vascular
-intense abdominal pain -rapid, severe, watery diarrhea (blood) -severely hyperemic gut (BRICK RED) |
|
What are the main systems affected by inorganic arsenic in the subacute form? -lesser
|
GI and vascular
- profuse, water diarrhea -severely hyperemic gut (brick red) -PU/PD initially--> oliguria and proteinuria --> anuria -cool extremetis due to poor circulation -may see death in 4-7 days |
|
Is chronic arsenic poisioning common in animals?
|
no
|
|
What are the major lesions seen with inorganic arsenic poisoning?
|
-hyperemic gut - brick red
-massive mucosal edema and fluids - atonic gut |
|
Is inorganic arsenic poisoning fast or slow?
|
rapid onset time
|
|
What are sample you can take to test for inorganic arsenic?
-antemortem -post mortem |
antemortem - vomit, feces, urine, hair
post mortem - liver and kidney >10 ppm |
|
Are cathartics recommended for use with inorganic arsenic poisoning?
|
no
|
|
What are the 3 antidotal therapies for the treatment of inorganic arsenic poisioning and which one is the best?
|
1 - BAL - expensive
2 - DMSA - much safer and better than BAL (BEST) 3 - sodium thiosulfate |
|
What is the prognosis for inorganic arsenic poisoning?
|
guarded to poor - most die
|
|
How should the diet be with inorganic arsenic poisoning for recovery?
|
bland
|
|
What are ORGANIC arsenicals used for>
|
feed additives
-lack of water, dehydration, and renal disease with high concentration increases toxicity |
|
What do organic arsenicals cause - MoA?
|
demyelination and axonal damage - peripheral neuropathy
|
|
What is the main system affected by organic arsenicals?
|
PNS
-become weak, may be bland, ataxic -dog sitting -LATER - bright and alerts, will eat if feed is brought to them |
|
What are the main animals affected by organic arsenical poisoning?
|
swine and poultry
|