Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Food animal production > Bovine Neurological disease > Flashcards

Bovine Neurological disease Flashcards

You may prefer our related Brainscape-certified flashcards:
Gourmet Food flashcards
1
Q

What is the typical presentations of bovine neurological disease?

A 
recumbency (downers)
gait abnormalities
abnormal head posture
sick
aint doing right
difficulty eating
blindness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What should you try to assess with a distance exam?

A
  1. behavior
  2. vision
  3. gait
  4. ability to eat
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How do you examine the 12 cranial nerves? (restrained)

A
  1. vision
  2. sensation and response
  3. hearing
  4. vestibular system
  5. mastication and swallowing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How do you do a spinal evaluation?

A
  1. examine the animal as moves freely and driven
  2. attempt to assess limb placement and motion
    (requires experience)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is a key comonent of neurological disease (time)

A

the timeline–what is onset, progression?

acute, subacute, chronic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the timeline of progression, treatment of polio?

A

Fairly rapid progression, rapid improvement with thiamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the timeline of progression of rabies?

A

rapid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is an issue with doing a neuro exam in calvess?

A

they are very stoical and hard to get a response to most stimuli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is an issue with downer cows?

A

It is difficult to assess limb function. May need to use panniculus, shock prod.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are additional diagnostic tests that can be used for neuro cows?

A
  1. chemistry–Mg, Ca, urea, glucose (hypocalcemia, hypomagnesiuma, urea poisoning, glucose–neuro ketosis) CK/AST—down cows
  2. CBC–meningitis, cerebral abscess
  3. CSF–menigitis, neoplasia, trauma
  4. lead
  5. vit A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Are CBCs very useful?

A

no, the inflammation in the brain is rarely reflected in the CBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Are CSF taps useful?

A

could do in a calf but in a cow very very difficult

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the best diagnostic test for neurologic dz in cattle?

A

you

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How do you assess blindness in cattle?

A
  1. distant exam
  2. pupillary light reflex
  3. menace response
    (check palpebral reflex first)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are three conditions typified by blindness?

A
  1. lead poisoning
  2. polioencephalomalacia. a) vit B1 deficiency, b) sulfate induced
  3. vitamin A deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the signalment for lead poisoning in cattle?

A
  1. any age, any animal, calves may be slightly more common

2. any bizarre behavior patterns (e.g. uncontrollable walking)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are characteristics on distance exam of lead poisoning?

A
  1. ataxia (drunkeness)
  2. weakness (recumbency)
  3. convulsions
  4. aimless wandering
  5. headpressing
    6 opsithotonus
  6. teeth grinding
  7. bellowing
    9 . hyperasthesia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the source of lead in lead poisoning?

A

car batteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What will you see when looking for a “car battery”

A

The individual lead sheets and old paper that separated them because the casing has been frozen and broken apart
Grey, white because the acid has dried–residue crystals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What does lead taste like?

A

sweet, covered in salt crystals. cows like to pick it up and chew it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is a source of lead besides car batteries

A

1) paint
(white and green
usually an issue for bottle fed calves in an old barn)
2) crank case oil–not really major

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are features on the physical exam of lead poisoning?

A
  1. Disruption of normal GI function (decreased rumination, mild bloat, tenesmus, constipation or diarrhea)
  2. blindness!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is more common, acute or chronic lead poisoning?

A

acute (1/2lb in cows, 2oz calve)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How is lead poisoning diagnosed?

A

1) blood lead levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What blood tubes must be used to analyze lead poisoning?

A

HEPARINIZED BLOOD SAMPLE (can’t use EDTA because it binds lead)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are ways can check for lead poisoning besides blood sample?

A
  1. Ca-EDTA adminsitration and measure urinary excretion
  2. measure urinary delta ALA excretion
  3. fecal lead
  4. radiograph
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What can you do post mortem to diagnose lead?

A
  1. lead in reticulum and rumen

2. check levels in KIDNEY (or liver)–kidney better

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Do you teat lead poisoning in cows?

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the theoretical treatments for lead?

A
  1. remove access to lead
  2. chelation therapy–Ca-EDTA to promote excretion
  3. thiamine
  4. rumenotomy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the problems with teatment of lead poisoned cows?

A

Not safe to eat even with treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the two types of polioecephalomalacia?

A
  1. thiamine deficiency

2. sullfate toxicity

32
Q

What are the signs on a distance exam of polio?

A
  1. blindness
  2. ataxia
  3. tremors
  4. recumbency
  5. convulsions
  6. opisthotonus
33
Q

What is the pathophysiology of thiamine deficiency/polio?

A
  1. thiamine normally made in rumen
  2. thiamine needed for pentose phoshate pathway of glycolysis
  3. main energy producing pathway in brain
  4. without thiamine brain cells die
34
Q

What are the causes for thiamine deficiency in cattle (that normally have thiamine made in rumen)

A
  1. thiamine antagonists-amprolium–used for cocidiosis
  2. rumen thaminases–produced by bacterial fermentation–IN RUMENAL acidosis–predisposition to colonization by thiaminase producing bacteria–
  3. ingested preformed thaminases (braken fern), fish meal
35
Q

Which animals usually get thiamine deficiency due to the colonization of bacteria that produce thiaminases?

A
  1. feedlot–number

2. dairy

36
Q

How is polio diagnosed and differentiated from lead?

A

They are blind BUT the eye responds to light (pupillary light reflex maintained)
GI motility is normally ok
otherwise signs very similar to lead poisoning

37
Q

How do you finalize polio diagnosis?

A 
1. PM examination of the brian
cerebral edema
mild yellow discoloration
FLouresces under UV light
2. no simple lab tests--eryhtrocyte transketolase
38
Q

What is the treatment for polio?

A
  1. Thiamine!

10mg/kg IV then 10mg/kg IM every 3 hours for 5 teatments

39
Q

What is the prognosis for polio?

A

good if caught early!

40
Q

What should you remember if one animal has gotten polio (thiamine deficiency)?

A

Leave a bottle because it is likely a feed issue and may have to treat others

41
Q

Can sulfate toxicity be distinguished from thiamine deficiency?

A

NO not clinically or PM

42
Q

What is the typical source of sulfate?

A

water (slough wter may be particularly bad in drought years)

43
Q

What is the level of sulfate that is toxic?

A

2000-7000ppm range

44
Q

What are sources of sulfate besides water?

A
  1. hay and grain grown in highh sulfate areas

2. plans that accumulate sulfate–kochia, canadian thistle

45
Q

What minerals can be protective against sulfate toxicity?

A
  1. copper and molybdenum (high levels can protect from sulfate toxicity)
46
Q

How is sulfate toxic

A

Not clear
May be that sulfate is converted to H2S in rumen, erucated, injaled and absorbed in lung and transported to the brain in blood where it exerts toxic effect

47
Q

What happens if you treat an animal with thiamine that has sulfate toxicity?

A

they still die. thiamine treatment does not work

48
Q

What do you do if cows are dying of sulfate poisoning?

A

fix the water problem–hard to get producer during august during harvest

49
Q

What are the three syndromes of vitamin A deficiency?

A
  1. adult cattle on scurb patsures
  2. feedlot steers
  3. neonatal calves
50
Q

Why do adult cows with vit A deficiency have infertility?

A

vit A is required for corpus luteum (yellow)

51
Q

What are the presenting signs for vit A?

A 
night blindness-rare
blindness-esp feedlot steers
weak animals dying shortly after birth
repro problems
poor hair coat
paralysis
convulsions
52
Q

What colour plants is vit A in?

A

green things–easily produced from beta carotene–carotenes freely available in green coloured feed

53
Q

Where do neonates get their vitA?

A

in colostrum. VitA crosses the placent poorly (why colostrum is yellow)

54
Q

Why does it take pastured animals a long time of poor feed to get vit A deficiency?

A

It takes months because they have good liver stores

55
Q

How do feed lot animals get vit A deficiency?

A

toxicity of chlorinated napthalenes

56
Q

What is vit A required for?

A

maintenance of epithelial surfaces

57
Q

Why do animals get blindness with vit A

A

the low vit A means that epithelial surfaces are not maintained, replaced with keratinized epithelium, thickened arachnoid results in decreased CSF absorption and there is increased pressure on optic nerve and they go blind

(also failure to remodel bone as animal regrows)

58
Q

How is vit A deficiency typically diagnosed?

A
  1. response to therapy,
  2. signs,
  3. liver biopsy (other methods not practical)
  4. plasma vit A
  5. diet calculations
  6. CSF pressure
  7. optho exam
59
Q

What is the treatment for vit A deficiency?

A

injectible vit A

60
Q

What is the prognosis for calves with vit A deficiency if treated?

A

good, with improvement within 48hrs

61
Q

What are the two ways mentation can be altered?

A
  1. depression

2. excitability

62
Q

What are the two causes of disease that affect forebrain?

A
  1. infectious

2. metabolic

63
Q

What are the signs of acetonemia/ketosis?

A
  1. hyperexcitability

2. deranged licking

64
Q

How is acetonemia/ketosis diagnosed?

A

urine dip stick

65
Q

How is ketosis treated?

A

glucose IV, good quality feed

66
Q

What animals get hypocalcemia?

A
  1. post-partum dairy cows

2. late pregnancy beef cows

67
Q

What is calcium needed for?

A
  1. heart function
  2. muscle function
  3. brain function–hypocalcemic animals become hyperexcitable then depressed
68
Q

What animals get hypomagnesemia?

A
  1. often cattle on lush pasture
69
Q

What is the progression of hypomagnesemia?

A

rapid
found dead with signs of struggling
(dead convulsing)

70
Q

What is the treatment of hypomagnesemia

A

magnesium but must be careful not to give them too much

71
Q

What are the signs of urea toxicity?

A
  1. bizarre behavioral signs in animal fed a urea supplement
  2. severe abdominal pain
  3. frothing at the nose and mouth
  4. hypersensitivity
  5. aggression
  6. muscle tremor weakenss
  7. dypnea
  8. bellowing
72
Q

What is the pathogenesis of urea poisoning?

A

urea turned into ammonia in the rumen and causes the neuro effects

73
Q

What is the history of urea poisoning>

A
  1. animals fed urea suplements as cheap non-protein nitrogen source
  2. urea as fertilizer
  3. conversion of urea to ammonia is facilitated by soybean meal (urease)
74
Q

How does death occur with urea poisoning?

A

resp depression

75
Q

How is urea poisoning diagnosed?

A

blood ammonia–difficult to do, must be on ice, here they have to do at human hospital

76
Q

What is the treatment for urea poisoning?

A

4L vinegar orally to acidify rumen

rumen lavage

77
Q

Is treatment for urea poisoning likel to be successful?

A

no

Food animal production (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions