Brainscape's Knowledge GenomeTM

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


See full index

LA DX & TX I > Exam 1 - FA Diffuse Brain Disease > Flashcards

Exam 1 - FA Diffuse Brain Disease Flashcards

1
Q

what 8 diseases/conditions are on your differential list for diffuse intracranial signs?

A
  1. polioencephalomalacia
  2. lead toxicity
  3. rabies
  4. water deprivation/salt water toxicity
  5. nervous coccidiosis
  6. urea toxicosis
  7. bacterial meningitis
  8. thrombotic meningoencephalitis (TEME)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the 2 most common causes of polioencephalomalacia?

A

thiamine deficiency & excess sulfates in feed/water

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

what animals are primarily affected by the thiamine deficiency form of polioencephalomalacia?

A

young cattle, sheep, goats, antelope, & deer

typically on a high concentrate low roughage diet

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

what is the mechanism of the thiamine deficient polioencephalomalacia?

A

decreased activity of transketolase enzyme in RBCs which decreases utilization of glucose in the tissue

decreases ATP

decreases utilization of glucose by the brain

end result - intracellular edema of the brain

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

what are the 5 main factors causing thiamine deficiency?

A

disturbances in metabolism

decreased synthesis rate

increased excretion

thiamine antimetabolites

feeds - DDG, corn gluten, kocia, & turnips

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

how does molasses cause a decreased rate of thiamine synthesis?

A

decreases propionate (glucose precursor) production

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

what are some examples of processes that cause disturbances in thiamine metabolism?

A

low intake & increased demand

clostridium - thiaminase I

bacillus - thiaminase II (excessive grain intake)

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

what is the mechanism of high sulfates causing polioencephalomalacia?

A

too much sulfur in the diet that preferentially selects for one particular population of bacteria - sulfates are used for respiration & then the bacteria release H2S gas

the H2S gas inhibits cytochrome oxidase activity

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

what animals are predisposed to developing polioencephalomalacia as a result of high sulfates?

A

animals with high sulfates in their diet

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

what is the first stage of disease seen in polioencephalomalacia?

A

spastic, uncoordinated movement/convulsions when excited/may or may not be blind, & hyperesthesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is the second phase seen of polioencephalomalacia?

A

blind/opisthotonus/star gazing (4th CN)/circles/head press/diarrhea

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

what is the 3rd phase of polioencephalomalacia?

A

lateral recumbency/paddling/death/head tilt/nystagmus

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

what is the hallmark sign of polioencephalomalacia?

A

acute onset of CNS signs with cortical blindness (PLR intact) & small ruminants that ‘act funny’

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

what can you look at in the blood diagnostically for polioencephalomalacia?

A

transketolase activity - giving thiamine may help you diagnostically

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is the treatment for polioencephalomalacia caused by thiamine deficiency?

A

thiamine 10-15mg/kg QID IM/SQ on day 1

TID for 2 more days

BID fpr 2 days

SID for 2 days

IV needs to be given in 5% dextrose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is the post-mortem diagnosis of polioencephalomalacia?

A

moist, swollen, yellow, cortical gyri, & cerebral coning

may fluoresce under UV light due to lipofuscin

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

what are some ways to prevent polioencephalomalacia caused by thiamine deficiency or high sulfates?

A

brewer’s yeast - extra thiamine source

increase roughage in diet - selects for favorable rumen bacteria

check sulfate levels in diet/water!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

when trying to diagnose polioencephalomalacia from excess sulfates, what should you do?

A

check water as a potential source!!!

on a herd basis - levels of sulfates can be measured chute side using a rumen gas cap test

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

what is the pathophysiology of lead toxicity?

A

lead binds to RBC & increase fragility of cells

this inhibits enzymes in heme synthesis

leads to poryphrin build up

inhibits the utilization of iron

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

what are common sources of lead toxicity?

A

BATTERIES!!

lead arsenate

grease/used motor oil/lead based paints

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

what is the most common presentation of lead toxicity?

A

encephalopathy

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

T/F: signs of acute lead toxicity should put rabies on your differential list

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what are the acute clinical signs of lead toxicity?

A

12-24 hours to develop

CNS/GI
cortical blindness with intact PLR
rumen atony/dead protozoa
cerebral signs
seizures

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

what are the clinical signs of chronic lead toxicity?

A

normocytic normochromic anemia
basophilic stippling
weight loss
lead stored in bone

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

how is lead toxicity diagnosed in most acute cases?

A

in a purple top - whole blood lead is > or = to 0.35ppm

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

how is lead toxicity diagnosed in most chronic cases?

A

blood levels may be normal - assess blood ALA levels/poryphrins

most will have a normal hemogram, but you may see an inappropriately responsive anemia with basophilic stippling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what lesion would you expect to see on necropsy for an animal with suspected lead toxicity?

A

polioencephalomalacia

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

what is the treatment for lead toxicity?

A

oral magnesium sulfate!!

Ca disodium EDTA 6.6% solution - 73mg/kg IV SID for 5 days, rest for 2 days, then repeat

thiamine 5-10mg/kg SID - decreases lead deposition & counters lead inhibition of thiamine synthesis

rumenotomy

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

what is the cause of rabies?

A

rhabdovirus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what is the pathophysiology of rabies?

A

saliva contamination or CNS fluids enter through a break in skin

migrates up neurons to the CNS where it replicates & goes to the salivary glands & nasal secretion

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

what is the incubation period of rabies?

A

3 weeks to 3 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what animals serve as reservoirs for rabies virus?

A

foxes, skunks, raccoons, & bats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what are the 3 forms of rabies?

A

furious

dumb

paralytic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what clinical signs are associated with the furious form of rabies?

A

tenesmus, hypersexuality, aggressive behavior, bellowing, paraphimosis, excitability, fear, & rage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what clinical signs are associated with the dumb form of rabies?

A

depression, anorexia, febrile, can’t drink, excessive salivation, flaccid tongue/anus/tail/bladder, circling, head pressing, strabismus, nystagmus, base wide stance, ptosis, dropped head & neck

36
Q

what clinical signs are associated with the paralytic form of rabies?

A

1st sign often unexplained astaxia & shifting leg lameness, decreased spinal reflexes, recumbency/flaccidity, & down 3-5 days & die at day 10

37
Q

what is the most common way that rabies is transmitted?

A

bites from an infected animal

38
Q

other than bites, how is rabies transmitted?

A

nervous tissue/CNS fluid, aerosol (bat caves), & milk

39
Q

how is rabies diagnosed?

A

post mortem only

FA stained hippocampus & cerebellum, negri bodies with a non-supperative encephalitis, & mouse inoculation

40
Q

how is rabies prevented?

A

vaccinate animals!! pest control!

41
Q

what is the common name for pseudorabies?

A

mad itch

42
Q

in what environments is pseudorabies seen?

A

where livestock come into contact with pigs

43
Q

what clinical signs of pseudorabies are seen in cattle, sheep, & goats?

A

ataxia, circling, GP deficits, nystagmus, excoriation, depression/aggression, & looks like rabies!!!

44
Q

how is pseudorabies diagnosed?

A

VI from nasal swabs, saliva, or nervous tissue & serology

45
Q

what is the pathophysiology of pseudorabies?

A

virus enters the skin or respiratory epithelium & travels to the CNS via axonal migration

46
Q

what clinical signs are seen in neonatal pigs with pseudorabies?

A

convulsions, tremors, ataxia, & possible acute death

47
Q

what is the pathophysiology of water deprivation causing salt toxicity?

A

Na ion concentration becomes higher in the brain than the CSF & blood due to the hyperosmolar CSF & brain tissue created during the time of water deprivation - this inhibits the pump to get Na out

idiogenic osmoles are created

when water is offered, the sodium content of the water is lower than the ion content of the CSF/tissues

water moves from area of greater concentration to lesser concentration (from blood to CSF & brain)

causes cerebral swelling!!!

48
Q

what clinical signs are seen with water deprivation/salt toxicity?

A

cerebral - from brain swelling

can get GI signs from high salt intake - severe diarrhea

49
Q

how is water deprivation/salt toxicity diagnosed post mortem?

A

inflammation of omasum, abomasal, & omasal surfaces (may be hemorrhagic & dark)

cerebral edema (coning)

in swine only - eosinophilic meningoencephalitis

50
Q

how is water deprivation/salt toxicity diagnosed antemortem?

A

clinical signs - pigs, sit & spin

history

CSF Na > than serum Na or serum & CSF Na > than 160 mEq/L

cerebral Na 1800 ppm or greater

histopathology

51
Q

how is water deprivation/salt toxicity prevented?

A

access to fresh water at all times

check salt levels in water & feed

52
Q

what is the treatment for water deprivation/salt toxicity?

A

frequent small amounts of water

IV mannitol to decrease edema

diazepam for seizures

hypertonic saline - helps lessen the gradient

if giving a scouring calf fluids & CNS signs develop - give IV fluids high in sodium to slow the movement of water into the brain

53
Q

what animals are at risk for developing water deprivation/salt toxicity?

A

show pigs held off water, scouring calves, calves fed exclusively milk without access to fresh water that are weaned & offered water, animals on automatic feeders that freeze

54
Q

what is the maximum tolerable salt level in feed for cows?

A

4% for lactating cows & 6% for non-lactating cows

55
Q

what is the maximum tolerable salt level in water for all livestock species?

A

5,000 PPM

56
Q

what lesion would you expect to see on necropsy of an animal with water deprivation/salt toxicity?

A

polioencephalomalacia

57
Q

what is the suggested pathophysiology of nervous coccidiosis?

A

seen most commonly following or during outbreaks of bloody diarrhea in weaning age calves (eimeria)

toxin liberated from the GI tract during coccidia infection

58
Q

what is the progression of disease of nervous coccidiosis?

A

intermittent in the beginning then frequency between normalcy decreases

59
Q

what are the clinical signs seen with nervous coccidiosis?

A

convulsions, paddling, opisthotonus, muscle tremors, tetanic spasms, & strabismus

60
Q

how is nervous coccidiosis diagnosed?

A

clinical signs & fecal float

61
Q

how is nervous coccidiosis prevented?

A

coccidiostats

62
Q

what is the treatment for nervous coccidiosis?

A

albon & vitamin A 1 time & then put in a quiet place, use diazepam for seizures

amprolium 50mg/kg SID 5 days

2-4mg/kg of calcium gluconate with magnesium SQ

63
Q

what animals are most commonly affected by urea toxicosis?

A

animals that aren’t accustomed to consuming urea

64
Q

what are the common sources/causes of urea toxicosis?

A

improper mixed

soybeans fed with urea

screw up - wrong bag in the feeder

65
Q

what is the pathophysiology of urea toxicity?

A

excessive amounts of NH3 are produced which causes the pH in the rumen to go up

this causes NH4 to be converted back to NH3

the high load of NH3 going to the liver overwhelms the ability of the liver to convert NH3 to urea to be excreted

NH3 is rapidly absorbed in the blood

66
Q

what are the clinical signs seen with urea toxicity?

A

salivation, bruxism, abdominal pain, dull/weak, hyperirritability, tetany, muscle tremors, & prostration/death (1-4 hours)

67
Q

how is urea toxicity diagnosed?

A

check sources/feeding history

rumen content pH > 8 rumenocentesis

freeze blood & rumen contents
NH3 content > 2mg/dl blood
>80mg/dl rumen content

68
Q

how is urea toxicity treated?

A

1/2 gallon vinegar in cold water - sheep gets 1 quart

rumenotomy

69
Q

what animals are typically at risk for bacterial meningitis?

A

young calves, lambs, kids, & piglets

70
Q

what is the suggested pathophysiology of bacterial meningitis?

A

failure of passive transfer, omphalitis, & likely e. coli is involved in the etiology

71
Q

what are the clinical signs of bacterial meningitis?

A

omphalitis, hypopyon, swollen joints, stiff/extended neck, hyperesthesia, opisthotonus, exaggerated spinal reflexes, & abnormal vocalization

72
Q

if I have a calf with suspected bacterial meningitis, what are my differentials for a calf that is dull without a suckle reflex?

A

hypoglycemia, hypothermia, septic, dehydrated, or acidotic

73
Q

how do you treat bacterial meningitis?

A

antibiotics/supportive fluids/nsaids

whole blood? - consider failure of passive transfer

74
Q

what is the suggested pathophysiology of thrombotic meningoencephalitis?

A

histophilus somni - vasculitis with thrombus formation & septic infarcts in various organs

causes endothelial cells to slough

75
Q

what are the clinical signs of thrombotic meningoencephalitis?

A

high fever, blind, GP deficits, very depressed/obtunded, nervous signs, ataxia, paralysis, & coma

76
Q

how is thrombotic meningoencephalitis?

A

hemorrhages in the retina

CSF - xanthochromia, neutrophils, total protein > 100mg/dl

CBC - neutropenia initially

77
Q

what is the toxic dose for urea in cattle?

A

1-1.5g/kg

78
Q

what is the toxic dose for urea in sheep?

A

2g/kg bw

79
Q

how is urea toxicity prevented?

A

adding urea slowly to diets so animals get accustomed to change

avoid screw ups with mixing & feeding

80
Q

how is bacterial meningitis prevented?

A

ensure passive transfer

81
Q

how is thrombotic meningoencephalitis treated?

A

oxytetracycline 5mg/lb IV BID

florfenicol 20mg/kg IV SID

ceftiofur

NSAIDS

82
Q

how is thrombotic meningoencephalitis prevented?

A

vaccine may reduce severity & incidence of CNS disease

need new vaccine

mass medicate LA 200 or aureomycin in feed (5-10mg/lb/cow/day)

lower stress

83
Q

what is the typical history of a cow presenting with nervous ketosis?

A

post partum dairy cow - negative energy balance

84
Q

what are the clinical signs of nervous ketosis?

A

excessive licking of themselves/inanimate objects, ataxia, blind, circling, & aggressive

85
Q

what is the treatment for nervous ketosis?

A

nervous signs will decrease as ketosis is addressed

treat the primary problem

IV dextrose 50%

transfaunate

86
Q

T/F: nervous ketosis is usually secondary to other diseases or conditions such as mastitis, metritis, etc

A

true

LA DX & TX I (45 decks)

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