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NEU2 > Metabolic diseases in farm animals > Flashcards

Metabolic diseases in farm animals Flashcards

1
Q

Describe the aetiology of hypomagnesaemia

A
  • Related to Mg in diet and presence of competing cations (K, Na)
  • No feedback mechanism to control Mg concentration
  • Main absorption in forestomachs, increases with increasing Na:K ratio (>5:1)
  • Only short term mobilisation of reserve in bone
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2
Q

What is a potential complication of chronic hypomagnesaemia?

A

Increases chances of hypocalcaemia

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3
Q

Compare hypomagnesaemia in adult cattle to that in sheep and calves

A
  • Sheep: similar but less common

- Calves: similar, but less common other than milk fed white veal calves (not UK)

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4
Q

Explain the mortality of hypomagnesaemia in beef cattle

A
  • ~30%
  • Due to short course of disease (5-10 hours from start to death)
  • Beef animals looked at less than dairy
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5
Q

What is the effect of hypomagnesaemia on the nervous system?

A

Alteration in CNS and peripheral nerve function

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6
Q

Identify risk factors for hypomagnesaemia

A
  • Lush pastures with large applications of fertilisers
  • Bucket fed calves
  • Silage from/pastures low in Mg, generally poor quality pasture
  • Pasture species, season, soil type, climate, DMI
  • Increased risk in lactation/late pregnancy
  • Cold, wet, windy
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7
Q

Explain why hypomagnesaemia occurs in lactation/late pregnancy

A
  • Hypocalcaemia 48 hours after calving, hypomagnesaemia seen later
  • Combination of calcium and magnesium deficit that predisposes to hypomagnesaemia
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8
Q

Explain why lush pastures with high levels of fertiliser increase the risk of hypomagnesaemia

A
  • High levels of nitrogen and potassium and ammonia

- Compete for mg absorption in rumen

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9
Q

Describe the clinical signs of hypomagnesaemia

A
  • Tetanic muscle spasms
  • Whole body tremor
  • Bellowing, aggressive
  • Blindness
  • Elevated, pounding heart rate
  • Hypertonicity and seizures
  • Hyper alertness, hyper responsiveness, hyperaesthesia
  • Convulsions
  • Sudden death after excitement/therapy
  • Frothing at mouth
  • Retraction of eyelids
  • Pricking of ears
  • Nystagmus
  • Opisthotonus
  • Bloating
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10
Q

List the differential diagnoses for hypomagnesaemia

A
  • Acute lead poisoning
  • Rabies
  • Nervous ketosis
  • BSE
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11
Q

Outline the method for the diagnosis of hypomagnesaemia

A
  • Clinical signs and history
  • Serum Mg low
  • Response to treatment
  • May have concurrent hypocalcaemia
  • Aqueous humour or CSF Mg concentration
  • Non-specific necropsy findings (rule out other conditions)
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12
Q

Explain the value of testing the aqueous humour or CSF Mg concentrations

A
  • Can be done up to 12 h post mortem
  • Useful where several dead cows in field
  • Sample from the eye for aqueous humour
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13
Q

Describe the treatment of hypomagnesaemia

A
  • Safest general recommendation: 400ml Ca-Mg bottle, 50ml for sheep
  • Combined with SC concentrated solution of Mg salt
  • Ideally give Mg SC, calcium IV
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14
Q

What are the risks of administering Mg IV?

A
  • Cardiac dysrhythmias
  • Medullary depression
  • Respiratory failure
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15
Q

Outline the preventative methods for hypomagnesaemia

A
  • Prophylactic oral therapy (low bioavailability, give slightly more than “right” amount)
  • Top dressing of pastures, daily drenching
  • Dusting, spraying
  • Provision in drinking water (better absorption of MgCl), magnesium buckets
  • Intraruminal Mg bolus
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16
Q

Compare the bioavailability of Mg carbonate, Mg oxide, Mg sulfate in cows

A
  • Mg carbonate: 44%
  • Mg oxide: 51%
  • Mg sulfate: 58%
17
Q

Explain how chronic hypomagnesaemia increases the chances of hypocalcaemia

A
  • Low Mg intake inhibits ca absorption in intestine

- HypoMg inhibits PTH release

18
Q

Explain how the neuromuscular blockade that masks tetany in hypomagnesaemia occurs

A
  • Only very early in disease
  • HypoMg worsens neuromuscular irritability
  • Decreased Ca ions at axonal membrane initially result in tetany, looks like hypoMg
  • Enough loss of Ca at neuromuscular synaptic memrbanes to reduce Ach release causing degrees of paralysis
19
Q

Describe the aetiology of hypoglycaemia/nervous ketosis in cattle

A
  • After calving due to increase in milk production
  • Negative energy balance is main factor
  • Excess ketone body production
  • prolonged course leads to evident brain lesions
  • May occur in neonatal large animals due to starvation, cold exposure or other diseases
20
Q

When does nervous ketosis typically occur in sheep?

A

Before lambing due to energy requirements of fast growing lambs

21
Q

Describe the development of brain lesions with nervous ketosis

A
  • Mainly sheep
  • Cerebro-cortical neuronal necrosis
  • Hypoglycaemic for a few days
22
Q

Compare the prognosis of nervous ketosis in sheep and cows

A
  • Sheep: highly fatal, possible effects (hypo-glycaemic encephalopathy) on fetuses
  • Cattle respond readily to treatment
23
Q

Describe the clinical signs of nervous ketosis in cattle and sheep

A
  • Muscle weakness, tremor
  • Head pressing
  • Compulsive licking
  • Ataxia
  • Blindness
  • Hyperaesthesia
  • Anorexia
  • Drop in milk production
  • Opisthotonus
24
Q

List the differentials for nervous ketosis in cattle

A
  • Rabies
  • Hypomagnesaemia
  • BSE
  • LEad poisoning
  • Listeriosis
25
Q

List the differentials for nervous ketosis in sheep

A
  • Listeriosis
  • Cerebral abscess
  • Rabies
26
Q

Describe the diagnosis of nervous ketosis

A
  • Clincal signs, history
  • Ketones (breath, urine, milk)
  • BOH/BHB serum levels
  • Non-specific necropsy findings (twin lambs in sheep, fatty liver in cows)
27
Q

Describe the treatment for nervous ketosis in cattle and sheep

A
  • Dextrose IV (400ml 50%)
  • Oral propylene glycol (225g BID for 2 days)
  • Glucocorticoids (reduce milk yield, 40mg dex sodium phosphate or 5mg flumethasone)
  • Insulin (off label use, where economics allow, must give glucose first)
  • induced parturition or caesar in ewes
28
Q

Describe the aetiology of hypocupraemia in sheep

A
  • Dietary deficiency of Cu in dam during gestation
  • Copper required for myelin formation
  • Bilateral symmetric loss of myelin in dorsolateral spinal cord tracts
  • Low copper perinatal period causes abnormal mitochondria function and cytochrome-C oxidase activity in CNS
  • Lambs and kids) may be affected clinical at birth or shows delayed onset
  • Congenital only when Cu deficiency extreme
29
Q

What is hypocupraemia also known as?

A

Swayback, enzootic ataxia

30
Q

Describe the clinical signs of hypocupraemia

A
  • Excessive joint flexion, knuckling over fetlocks, wobbling, falling
  • Appetite unaffected
  • Depression
  • Tremors
  • Wool abnormalities (loss of crip, depigmentation)
  • Anaemia, scouring, unthriftiness, infertility in adults
  • Incoordination starting with hindlimbs, erratic movement
  • Spastic paralysis
  • Blindness
31
Q

List the differential diagnoses for hypocupraemia

A
  • Congenital abnormalities of spinal cord
  • Trauma
  • Spinal abscess
  • Ischaemic myelopathy
  • Border disease
  • Cerebellar hypoplasia
  • Hypothermia
32
Q

Outline the diagnosis of hypocupraemia

A
  • Clinical signs, history
  • Microscopic examination of nervous tissue (characteristic lesions of myelin degeneration)
  • Low concentrations of liver copper
33
Q

Outline the treatment of hypocupraemia

A
  • Supplement copper (oral, injectable, bolus) but usually unsuccessful due to advanced nature of lesions
  • Correct copper, molybdenum, sulphur, iron to prevent further cases
34
Q

Describe the aetiology of hepatic encephalopathy in cattle

A
  • Reduced detoxification of compounds esp, nitrogenous waste due to liver damage
  • Hyperammonaemia, hypoglycaemia
  • Severe acute or chronic liver disease
  • Congenital acquired porto0systemic shunt
  • Hepatotoxic encephalopathy due to plants
  • Hyperammonaemia
35
Q

Explain how hyperammonaemia may occur in cattle and lead to hepatic encephalopathy

A
  • Exposure to ammonia containing feedstuffs or fertiliser
  • Urea in total mixed ration drives protein building in rumen, but also raises ammonia in blood, liver unable to cope
  • Leads to hepatic encephalopathy without liver disease
36
Q

Describe the clinical signs of hepatic encephalopathy

A
  • Blindness
  • Aimless wandering (dazed)
  • Compusive activity
  • Aggression
  • Ataxia
  • Facial and ear tremors
  • Seizures
  • Coma (death)
  • Tenesmus/urine spillage/rectal prolapse
  • +/- photosensitisation
37
Q

List the differentials for hepatic encephalopathy in cattle

A
  • HypoMg
  • Nervous ketosis
  • BSE
38
Q

Outline the diagnosis of hepatic encephalopathy in cattle

A
  • Blood ammonia
  • Liver biopsy (easy)
  • Histology: astrocyte proliferation, hypertrophy with swollen pale nuclei
39
Q

Outline treatment of hepatic encephalopathy in cattle

A
  • Difficult
  • Put in quiet environment and hope they recover
  • Remove hepatotoxins from environment if cause

NEU2 (23 decks)

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