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Farm Animal Final Year > Metabolic Disease With Neuro Signs > Flashcards

Metabolic Disease With Neuro Signs Flashcards

1
Q

What is the aetiology of hypomagnesaemia?

A
  • Multifactorial, related to Mg in diet and presence of competing cations (K, Na)
  • No feed back mechanism to control Mg concentration, Mg excess excreted in urine
  • Main absorption in forestomachs, increases with Na:K ration >5:1
  • Alteration in CNS and peripheral nerve function
  • There are reserves in bone but there is poor short term mobilisation
  • Chronic hypomagnesaemia increases chances of hypocalcaemia
  • Sheep; similar, but not as common
  • Calves; similar not as common
  • Morbidity 2-12%
  • Mortality approx. 30%, higher in beef (due to short course of disease, 5-10 hours)
  • Important disease for beef and dairy farmers
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2
Q

Name risk factors of hyppomagnesaemia

A
  • lush pastures which have received large applications of fertilizers containing high levels of nitrogen and potassium, ammonia in rumen impairs Mg absorption
  • Bucket fed calves (milk is low in Mg)
  • (Silage from) Pastures low in Mg, generally poor quality pasture
  • Pasture species, season, soil type, climate, DMI etc
  • Risk period: peak lactation/late pregnancy
  • Most common is a combination of factors: inadequate energy intake, low Mg content, cold, wet ,windy weather
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3
Q

Name clinical signs of hypomagnesaemia

A
  • Tetanic muscle spasms
  • Whole body tremor
  • Bellowing
  • Aggressive
  • Blindness
  • Elevated pounding heart rate
  • Hypertonicity and seizures (vs flaccid muscles and recumbency in hypo Ca)
  • Hyper alertness, hyper responsiveness, hyperesthesia
  • Eventually animals fall on their side in convulsions
  • Sudden death after excitement / therapy
  • Frothing at the mouth
  • Retraction of eyelids
  • Pricking of the ears
  • Nystagmus
  • Opisthotonus
  • Elevated heart rate and strong
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4
Q

Name 3 differentials for hypomagnesaemia (4)

A
  • Acute lead poisoning
  • Rabies
  • Nervous ketosis
  • BSE
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5
Q

How can we diagnose hypomagnesaemia?

A
  • Clinical signs and history
  • Serum Mg reference range 1.7-3 mg/dL (tetany average 0.5 mg/dL)
  • Response to Tx
  • Sometimes concurrent hypocalcaemia
  • Aqueous humour or cerebrospinal fluid magnesium concentration, even up to 12h post mortem
  • Non-specific necropsy findings
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6
Q

How can we treat hypomagnesaemia?

A
  • Safest general recommendation: 400ml Ca-Mg bottle, 50 ml for sheep
  • Combined with SC concentrated solution of Mg salt
  • IV magnesium salts can be dangerous: cardiac dysrhytmias, medullary depression, respiratory failure
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7
Q

How can we prevent hypomagnesaemia?

A
  • Prophylactic oral therapy (biological availability for Mg carbonate, Mg oxide, Mg sulfate is 44%, 51% and 58% respectively)
  • Top dressing pasture, daily drenching, dusting, spraying, provision in drink water, magnesium buckets
  • Intraruminal Mg bolus
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8
Q

What is staggers?

A

Hypomagnesaemia

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9
Q

What does chronic hypomagnesaemia increase the chance of?

A

Hypocalcaemia

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10
Q

What causes the signs of hypocalcaemia?

A

•Decreased calcium ions at the axonal membrane initially result in tetany, ultimately there is enough of a loss of calcium at the neuromuscular synaptic membranes so as to reduce acetylcholine release causing degrees of paralysis. Cattle appear to be more susceptible the neuromuscular blockade, that masks the tetany seen only very early in the course of disease.

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11
Q

A) What is the effect of hypocalcaemia on the heart?

B) What causes the effect on heart rate?

A

A) Tachycardia and weak heart rate

B) Low calcium and the heart muscle doesn’t function as well and the contraction isn’t as good. So the heart rate increases to keep the pressure up.

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12
Q

What is nervous ketosis?

A

Hypogylcaemia

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13
Q

What is the aetiology of hypoglycaemia?

A
  • Multifactorial
  • Disease in cattle and sheep occur in different parts of pregnancy-lactation cycle
  • Energy balance; inadequate nutrition
  • Cattle respond readily to treatment, sheep highly fatal
  • Excess ketone bodies (see lecture Yr 2 GI)
  • Prolonged course (several days) results in evident brain lesions: cerebro-cortical neuronal necrosis
  • Possible effects (hypo-glycaemic encephalopathy) on fetuses of affected ewes
  • Neonatal large animals (starvation, cold exposure, other diseases)
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14
Q

Name clinical signs of hypoglycaemia

A
  • Muscle weakness
  • Tremor
  • Head pressing
  • Compulsive licking (self/objects)
  • Ataxia
  • Blindness
  • Hyperesthesia
  • Anorexia
  • Drop in milk
  • Opisthotonus / stargazing
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15
Q

Name 3 differentials of hypoglycaema in cattle (4)

A
  • Rabies
  • Hypomagnesaemia
  • BSE
  • Lead poisoning
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16
Q

Name 2 differentials of hypoglycaema in sheep (3)

A
  • Listeriosis
  • Cerebral abscess
  • Rabies
17
Q

How can we diagnose hypoglycaemia?

A
  • Clinical signs and history
  • Ketones (breath, urine, milk)
  • BOH/BHB (serum β-hydroxy butyrate)
  • Non specific necropsy findings (twin lambs and fatty liver)
18
Q

How can we treat hypogylcaemia?

A
  • Dextrose IV (400 ml 50%, not SC!)
  • Oral propylene glycol (225 g 2x/day for 2 days)
  • Glucocorticosteroids (reduce milk yield)(40 mg dexamethasone sodium phosphate or 5 mg flumethasone)?
  • Insulin (off label; where economics allow)?
  • Induced parturition or caesarean in ewes
19
Q

What is swayback?

A

Hypocupremia

20
Q

What is the aetiology of hypocupremia?

A
  • Dietary deficiency of Cu in the dam during gestation
  • Copper is necessary for myelin formation
  • Bilateral symmetric loss of myelin in the dorsolateral spinal cord tracts
  • Low copper in perinatal period causes abnormal mitochondria function and cytochrome-c oxidase activity in the CNS.
  • Lambs and kids may be affected clinically at birth with tetraparesis or develop pelvic limb ataxia at 2-4 months of age.
  • Unweaned lambs from birth till 1-2 months of age
  • Congenital form only when Cu deficiency is extreme (born dead, weak, unable to stand)
  • Also called enzootic ataxia
21
Q

Name clinical signs of hypocupraemia

A
  • Excessive joint flexion, knuckling over fetlocks, wobbling, falling
  • Appetite unaffected
  • Depression
  • Tremors
  • Wool abnormalities (loss of crimp, depigmentation)
  • Anaemia, scouring, unthriftiness, infertility (adults)
  • Incoordination starts with hindlimbs, erratic movement
  • Spastic paralysis
  • Blindness
22
Q

Name 5 differentials of hypocupraemia (7)

A
  • Congenital anomalies of spinal cord
  • Trauma
  • Spinal abscess
  • Ischemic myelopathy
  • Border disease
  • Cerebellar hypoplasia (daft lamb disease)
  • Hypothermia
23
Q

How can we diagnose hypocupraemia?

A
  • clinical signs & history
  • microscopic examination nervous tissue: histopathologic lesions characteristic of myelin degeneration
  • low concentrations of liver copper (tissue levels more reliable than serum)
24
Q

How can we treat hypocupraemia?

A
  • Supplementing copper (oral, injectable, bolus) usually unsuccessful due to advanced lesions in nervous system
  • Determine copper, molybdenum, sulphur, iron to prevent further cases
25
Q

What is the aetiology of hepatic encephalopathy?

A
  • Detoxification of especially nitrogenous waste is reduced; hyperammonemia, hypoglycemia
  • Hepatotoxic encephalopathy : alkaloid ingestion (congenital liver failure in newborn)
  • Severe acute or chronic liver disease (i.e. cirrhosis)
  • Congenital acquired porto-systemic shunt>rare in LA
  • Hyperammonemia: inadvertent exposure to ammonia containing feedstuff or fertilizer causes elevated blood ammonia concentration, not necessarily concurrent with evident liver disease
26
Q

Name 5 plants which can poison and cause neuro signs (8)

A

–Ragwort (Hepatic encephalopathy)

•Important Poisoning; see GI module

–Bracken

•Important Poisoning (See CCN. See Urinary module)

–Horsetail (See CCN)

–Hemlock

–Hemlock Water dropwort (Tuberous roots known as “Dead mans fingers)

–Black nightshade

–Rhododendron

–Laburnum

27
Q

Name clinical signs of Hepatic encephalopathy

A
  • Blindness
  • Aimless wandering
  • Compulsive activity
  • Aggression
  • Ataxia
  • Facial and ear tremors
  • Seizures
  • Coma (death)
  • Tenesmus / urine spillage / rectal prolaps
28
Q

Name 2 differentials of hepatic encephalopathy (3)

A
  • Staggers
  • Nervous ketosis
  • BSE
29
Q

How can we diagnose Hepatic encephalopathy?

A
  • Blood ammonia
  • Liver biopsy
  • Histology: astrocyte proliferation, hypertrophy with swollen pale nuclei (Alzheimer type 2 astrocytes
30
Q

How can you treat Hepatic encephalopathy?

A
  • Difficult
  • Remove hepatotoxins from environment
31
Q

How can low magnesium lead to hypocalcemia?

A

i. Low magnesium intake inhibits calcium absorption in the intestine
ii. Hypomagnesemia (low blood magnesium level) inhibits PTH release
iii. Hypomagnesemia makes neuromuscular irritability worse:

Neuromuscular irritability proportional to:

32
Q

When do sheep get hypoglycaemia and why?

A

Before parturition - energy demand of growing lots of lambs

33
Q

When do cows get hypoglycaemia and why?

A

Post parturition - energy demand is huge

Farm Animal Final Year (131 decks)

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