Macrominerals Flashcards

1
Q

Are macrominerals large in size?

A

NO

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2
Q

What is hypomagnesia also known as?

A

Grass staggers

Grass tetany

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3
Q

Why does hypomagnesia arise?

A
  • No homeostatic mechanism for controlling Mg levels (cf. Ca)
  • deficiency arises when ^ demand v intake
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4
Q

What are the clinical signs associated with grass staggers?

A
  • range peracute to subclin
  • hyperaesthesia
  • twitchy ears
  • sensitive to sound/hand clap
  • staggers, collapses - signs of thrashing and struggle
  • jaw champing
  • sudden death
  • ^ HR
    > subclin
  • slow onset 3-4d
  • spasmodic urination/defeacation
  • mm tremor
  • staggering gait
  • ^ HR
  • usually post-partum so difficult to distinguish normal urogenital pain
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5
Q

What sample may be analysed by the lab post-mortem to ID hypomag?

A

Vitrium of the eye

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6
Q

What are hypomag cows reffered to as?? (By van winden )

A

Red cows

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7
Q

How is hypomag treated?

A

Urgently!

  • Bottle Ca borogluconate with Mg hypophosphate I/V slowly
  • Magnesium sulphate 25% s/c only (IC -> Cardiac arrest)
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8
Q

Where should you stand by a downer cow?

A

Behind the back

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9
Q

How may hypomagnesium be prevented?

A

Mg alone not v palatable

  • MgO mix with molasses
  • Mg bolus orally precalving
  • Mg in drinking water
  • Avoid K fertiliser (pig manure)
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10
Q

What are hypocalcaemic cows reffered to as?? (By van winden)

A

Blue cows

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11
Q

What is hypocalcaemia also known as?

A
  • Bovine parturient paresis
  • Hypocalcaemia
  • Acute flaccid paralysis
  • Milk fever
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12
Q

What are the normal levels of calcium in the blood?

A

2.3 - 3.2 mmol/l

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13
Q

Outline Ca homeostasis

A
  • Absorbed in GIT, kidney and bone
  • PTH regulates
  • Vit D3 converted in kidney and activated in liver works on GIT ONLY to ^ absorbtion
  • Calcitonin binds free Ca (low clinical impact)
  • Mg co-factor required to activate D3, produce/release PTH and other stages
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14
Q

What are the clinical signs associated with subclinical hypocalcamiea?

A
  • able to stand
  • hypersenstivie
  • excitable
  • tremors
  • ears twitching
  • ataxia
  • bloat or gas in gut [sm mm affected first]
  • slowed gut transit
  • v VFI
    > Blood Ca: 1.8-2.3
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15
Q

What are the clinical signs associated with moderate clinical milk fever?

A
  • recumbent (sternal)
  • depressed
  • dry muzzle
  • cold extremities
  • bloat
  • no defeacation (on rectal = full)
  • delayed/absent pupil responses
    > Blood Ca: 1.2 - 1.8
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16
Q

What are the clinical signs associated with severe clinical hypocalcaemia?

A
  • reduced consciousness
  • lateral recumbency
  • unresponsive
  • mm flaccidity
  • v CO
  • bloat
  • death
    > Blood Ca <1.2
17
Q

What is the treatment for milk fever hypocalcaemia@?

A
  • 20% Ca Borogluconate 400ml
    > Higher conc available but unneccesary, may -> hyperCa -> depressed PTH etc. -> yoyo between hypo hyper
  • low volume tx maxacal 100ml
  • some may have mg, p , glucose mixed in
    > Inject SLOW i/v and monitor HR - may -> cardiac arrest
  • sc deposit to prevent reoccurrence (usually to tide over until fresh food available)
18
Q

How can you tell an animal is recovering from milk fever?

A
  • sits up (may need assistance)
  • defeacates
  • eructates
19
Q

What is the cause of hypocalcaemia?

A
  • demand not met by supply
  • absorption from KIDNEY
  • GIT: dry cow ration too ^ in Ca -> v % absorption
  • feed intake in fat cows may be inadequate
  • BONE reserves low in old cows
    > amount of Ca available in each reserve inversely proportional to speed it can be released (ie. kidney small amount quickly, bone large amount slowly)
20
Q

Which cows are at risk of milk fever?

A
  • older
  • fatter
  • channel breeds
21
Q

How may hypocalcaemia be prevented?

A
  • LOW Ca in dry cow ration
  • High Ca milking cow ration
  • Supplement Mg
  • DCAB diet
  • drench or bolus around calving
22
Q

How are hypo-phosphoraemic cows described? How may this be identified?

A
  • “Happy downer”
  • Mg/Ca Tx doesn’t work
    NB: Make sure to check for other casues of being down - Fx, toxic, neuro problems etc.)
23
Q

What may cause v phosphorus?

A

^ Ca soil

24
Q

How is hypophosphatemia treated?

A

Foston I/v

25
Q

What is DCAB?

A

Dietary cation anion balance
- Cations subtract anions should = v pH blood
- allows PTH to be more effective and optimised Mg absorption
> achieved by v K in diet and ^ anions

26
Q

What are the cations?

A

Na and K

27
Q

What are the anions?

A

Cl and S

28
Q

What units are anions and cations analysed in?

A

mmol/kg DM

29
Q

Give examples of anions that can be fed in the diet. What are potential down sides to using these?

A
Magnesium chloride
Magnesium sulphate
Calcium chloride
Ammonium chloride 
-> unpalatable and may v DMI -> NEB, fatty liver, metabolic issues
30
Q

What should be monitored when using the DCAB diet?

A

Urine pH of several cows each week

  • aim for 5.5-6.5
  • NO LOWER THAN 5.0-5.5 (too many anions being absorbed)
  • aim for small range between cows so you know the diet is being well spread throughout the herd