Lead Flashcards

(37 cards)

1
Q

What is the most common poisoning of livestock?

A

lead

- but it affects all species

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2
Q

what is the cause of the biochemical or subcellular effects of lead?

A

affinity of lead for SH (sulfhydryl) or imidazole groups

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3
Q

The binding of lead to various macromolecules impair which functions?

A

enzymes - substrate
mitochondria - decrease ATP
reproduction - chromosomal damage
immune system - immunosuppression

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4
Q

In which organ systems are the cellular and clinical affects most aparent?

A

GI
nervous
hemopoetic

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5
Q

What are the GI effects of lead?

A

irritation, gastroenteritis, rumestasis in cattle

diarrhea/constipation

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6
Q

What are the nervous effects?

A

encephalopathy
- capillary damage causes hemorrhage and congestion in the brain followed by edema and malacia
blindness and peripheral nerve degeneration
no direct harm to brain
affects vascular supply –> edema and swelling

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7
Q

What are the hemopoetic effects?

A
anemia
reduced iron uptake
RBC fragility
heme synthesis altered
by enzymes containing SH
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8
Q

What are the effects on the kidey?

A

degenerative changes

  • tubular necrosis, nephritis, fibrosis and yaline degen
  • acid fast inclusions bodies are present
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9
Q

What are the effects on the liver?

A

mild degen

little clin significance

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10
Q

What are the MSK effects?

A

osteoporosis

- common in sheep

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11
Q

What are the affects on the resp system?

A

impaired neuro = impaired swallowing mech and cause aspiration pneumonia

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12
Q

What are the acute and subacute syndromes characterized by? two general systems?

A

GI and neuro

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13
Q

How long does the acute syndrome last? which age?

A

lasts 24h
usually younger animals
one or two in herd

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14
Q

What are the clinical signs of acute poisoning?

A

behaviour
- mania, frenzy, charging fences, bellowing, head pressing

locomotor
- staggering an muscle tremors

nervous phenomena

  • champing jaws, blindess, snapping eyelids
  • hyperesthesia
  • intermittent tonic-clonic convulsions
  • opisthotonus

GIT

  • frothing, salivation (impaired swallowing
  • rumen stasis
  • abdominal pain
  • abnormal eructation
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15
Q

How long does the subacute poisoning last? which age?

A

adults typically 3-4d

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16
Q

What are the clinical signs of subacute poisoning?

A

behavioural

  • dullness
  • head pressing

locomotor

  • abnormal gait
  • incoordination, muscle tremors, staggering, often stand immobile, occasionally circle

nervous
- blind, depression, hyperesthesia, head bobbing, convulsions absent

GIT
– grinding teeth, rumen stasis, salivation, anorexia, diarrhea/constipation, abdominal pain

17
Q

What is the main difference between subacute and acute?

A

lasts longer and no convulsions with subacute

18
Q

What are signs/type is specific to sheep?

A

osteoporosis

usually subacute

19
Q

What type and signs are specific to horses?

A

chronic

  • colic, pharyngeal paralysis (roaring)
  • aspiration pneumonia
  • no convulsions
20
Q

What type and signs are specific to pigs?

A

primarily GIT - vomiting

few CNS signs

21
Q

what type and signs are specific to dogs/cats?

A

similar to pigs

  • vomiting
  • hyperexcitability
  • convulsions
  • altered hysterical bark
22
Q

What are some sources of lead?

A

paint, oil, lubricants, lead toys, lead shot, batteries, used crankcase, old shingles, industrial contam

23
Q

What is the absorption and distribution?

A

higher absorption in young animal

cumulative
half life is many month
enters blood distributes rapidly to liver and kidney (1d)
displace Ca
does not accumulate in brain

gut>blood>kidney>liver>bones

24
Q

What Vitamin from sun can increase absorption?

25
What is the excretion?
kidney | milk - minor
26
Why are young animal more susceptable?
low iron milk diet | iron competes with lead
27
What can be submitted antemortem to confirm Dx?
heparinized blood (WHOLEBLOOD) in RBC rumen contents fecal contents
28
What can be submitted postmortem?
liver and kidney (best) rumen, fecal (variable) brain (poor)
29
What is detected on clin path?
``` anemia basophilic stippling increased ESR anisocytosis hypochromia leptocytes altered enzymatic activity ``` kidney damage - proteinuria, glucouria
30
What else can be seen diagnostically?
increased radiographic density growth plates in bone stomach or rumen contents
31
What is the treatment for food animals?
discouraged - food safety - prognosis - potential repro problems
32
What are some treatment chelation therapys?
``` penicillamine (oral) british antiLewistie IV - short acting, lipid soluble - penetrate CNS Calcium EDTA (IV) - no longer approved for livestock succimer (oral) - best for dogs but hard to get ```
33
What other treatment options are there for lead?
``` thiamin (IV) - chelates and cheap MgSO4 (oral) - acts as laxative and binds lead sedation rumen lavage rumenotomy zinc supplementation rumen transplant ```
34
What is the best treatment?
calcium EDTA + thiamin (IV)
35
What is used for supportive therapy?
force feeding oral fluids mannitol (helps reduce swelling in the brain) edema
36
What is the epidemiology of lead?
young animals in season when batteries are changed (harvesting) - may and august
37
what is the economic implications of lead?
``` expensive in cattle meat and milk residues lack of approved medications reportable disease in alberta - must cull ```