Metabolic causes of CNS disease

Question 1

electrolyte imbalances etiology

Answer 1

from profuse diarrhea, gastric reflux, extreme exertion, renal failure, transport stress and lactation

hyponatremia, hypernatremia, hypocalcemia and hypomagnesemia

Question 2

electrolyte imbalances diagnosis

Answer 2

measurement of serum and sometimes CSF electrolyte concentrations

thorough PE, chem panel

Question 3

electrolyte imbalances tx

Answer 3

correction of electrolyte disturbances via IV therapy with electrolyte supplementation

treatment of underlying disorder

Question 4

what is hypomagnesemic tetany

Answer 4

nervous irritation or tetany associated wtih decreased levesl of serum magnesium

common in ruminants

Question 5

grass tetany

Answer 5

grass stagger or lactation tetany

seen in dairy cattle overwintered indoors on poor quality, then turned out on lush grass pasture in spring

beef cows with calves in similar conditions

Question 6

milk tetany

Answer 6

seen in 2-4 month old vealer calves on poor quality milk replacer diet

Question 7

transport tetany

Answer 7

any age or species of ruminants

seen after extended truck or rail transport of 24 hour or greater duration

esp if feed and water withheld

Question 8

pathogenesis of hypomagnesemic tetany

Answer 8

serum magnesium levesl almost always less than 1 mg/dl

the onset of clinical signs closely associated with low CSF levels of Mg

Question 9

clinical findings in hypomagnesium tetany

Answer 9

signs limited to nervous dysfunction

hx of recent turnout onto pasture

early signs: alert, anxious expression, muscle twitching and fasciculations

progressive sxs: hyperesthesia, continuous bellowing, frenzied galloping, collapse with full blown convulsions (episodic)

death within 1-2 hours of first signs

Question 10

DDx of hypomagnesium tetany

Answer 10

rabies

lead poisoning

nervous ketosis

Question 11

diagnosis of hypomagnesium tetany

Answer 11

serum mg less than 1 mg/dl

clinical response to tx

Question 12

polioencephalomalacia epidemiology

Answer 12

occurs sporadically or as a herd problem

herd outbreaks following management changes

morbidity: 25%, mortality: 50%

mostly 6-18 months of age

Question 13

polioencephalomalacia pathogenesis

Answer 13

thiamine deficiency

inolved with glucose metabolism (esp in brain)

production may be reduced after a change in diet

high concentrate ration

thiamine analogues

decreased glucose production

thiaminase-1 producing bacteria in rumen

high dietary sulfur, amprolium, bracken fern, molasses-urea diet with no roughage

intracellular edema –>neuronal degeneration and laminar necrosis

Question 14

polioencephalomalacia clinical signs

Answer 14

blindness

PLR normal

opsithonotic

incoordinated

depression with excitement

dorsomedial strabismus

later signs: muscle tremors

terminal signs: recumbency with opisthotonos, convulsions, coma and death

24-48 hours

Question 15

clinical pathology of polioencephalomalacia

Answer 15

CBC normal

increased serum pyruvate levels, decreased blood lactate

CSF: normal to mild protein elevation

necropsy: diffuse cerebral edema, UV fluorescence observed in necrotic areas

Question 16

polioencephalomalacia diagnosis

Answer 16

response to early thiamine therapy

determination of sulfur content of diet (<0.4%)

cattle: r/o lead poisoning, hypovitaminosis A, TME
sheep: r/o enterotoxemia, focal symmetrical encephalomalacia
goats: r/o caprine leukoencephalomyelitis, enterotoxemia, listeriosis, pregnancy toxemia, lead poisoning and meningoencephalitis

Question 17

polioencephalomalacia treatment

Answer 17

thiamine q 6 hours until recovered

remove grain, put on forage ration

response in 6-8 hours

corticosteroids

severe cases response poorly

Question 18

Nervous ketosis epidemiology

Answer 18

wasting form: more ommon

nervous form: hypoglycemia

Question 19

nervous ketosis clinical signs

Answer 19

belligerence

delirium

awkward stance

head pressing

licking

intermittent nervous signs lasting 1-2 hours

Question 20

nervous ketosis diagnosis

Answer 20

urine or milk ketones

reponse to IV glucose therapy

intermittent signs

Question 21

nervous ketosis tx

Answer 21

IV glucose

oral propylene glycol

Question 22

DDx of nervous ketosis

Answer 22

listeriosis

rabies

pseudorabies

polioencephalomalacia

lead poisoning

Question 23

hypovitamosis A epidemiology

Answer 23

drought conditions

poor quality stored feed

young, growing animals

Question 24

hypovitamosis A clinical syndromes

Answer 24

blindness due to stenosis of optic foramen, increase in CSF pressure, pupils dilated and unresponsive to light

encephalopathy-increasing CSF pressure, clonic tonic convulsions

progressive paresis or paralysis-destruction of peripheral nerves

Question 25

hypovitamosis A diagnosis

Answer 25

serum vitamin A concentrations

analysis of ration

Question 26

hypovitamosis A tx

Answer 26

vitamin A

Question 27

hepatoencephalopathy etiology

Answer 27

acute hepatitis

chronic liver disease

neonatal foals

Question 28

hepatic encephalopathy risk factors

Answer 28

equine origin biologicals (tetanus antitoxin, vaccines, plasma)

portal-systemic shunt

Question 29

hepatic encephalopathy pathophysiology

Answer 29

increased ammonia

ammonia plus glutamate

GI derived toxins

decreased BCA:AAA ratio

increased GABA activity

Question 30

hepatoencephalopathy dx

Answer 30

confirmation of liver disease

increase SDH, AST, bile acids

Question 31

hepatoencephalopathy tx

Answer 31

px grave

maintain blood glucose

electrolyte disturbances

Question 32

hepatoencephalopathy clinical signs

Answer 32

depression, head pressing, yawning, ataxia, blindness, seizures, aimless wandering

anorexia, weight loss, icterus, photosensitization