Lead Flashcards

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?

A

Vit D

25
Q

What is the excretion?

A

kidney

milk - minor

26
Q

Why are young animal more susceptable?

A

low iron milk diet

iron competes with lead

27
Q

What can be submitted antemortem to confirm Dx?

A

heparinized blood (WHOLEBLOOD) in RBC
rumen contents
fecal contents

28
Q

What can be submitted postmortem?

A

liver and kidney (best)
rumen, fecal (variable)
brain (poor)

29
Q

What is detected on clin path?

A
anemia
basophilic stippling
increased ESR
anisocytosis
hypochromia
leptocytes
altered enzymatic activity

kidney damage
- proteinuria, glucouria

30
Q

What else can be seen diagnostically?

A

increased radiographic density
growth plates in bone
stomach or rumen contents

31
Q

What is the treatment for food animals?

A

discouraged

  • food safety
  • prognosis
  • potential repro problems
32
Q

What are some treatment chelation therapys?

A
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
Q

What other treatment options are there for lead?

A
thiamin (IV)
- chelates and cheap
MgSO4 (oral)
- acts as laxative and binds lead
sedation
rumen lavage
rumenotomy
zinc supplementation
rumen transplant
34
Q

What is the best treatment?

A

calcium EDTA + thiamin (IV)

35
Q

What is used for supportive therapy?

A

force feeding
oral fluids
mannitol (helps reduce swelling in the brain)
edema

36
Q

What is the epidemiology of lead?

A

young animals in season when batteries are changed (harvesting)
- may and august

37
Q

what is the economic implications of lead?

A
expensive in cattle 
meat and milk residues
lack of approved medications 
reportable disease in alberta
- must cull