Brainscape's Knowledge GenomeTM

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


See full index

Gastrointestinal (farm) > Metabolic disease (Yr 4) > Flashcards

Metabolic disease (Yr 4) Flashcards

1
Q

what are some factors that are involved in the control of calcium homeostasis in the body?

A

parathyroid hormone
calcitonin
vitamin D

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

how does parathyroid affect calcium?

A

causing calcium to mobilise from bone (stores)
increases absorption from the gut (requires magnesium)

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

what is required for calcium absorption from the gut that is triggered by parathyroid hormone?

A

magnesium

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

how does calcitonin effect calcium?

A

reduces calcium absorption and availability

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

how does vitamin D affect calcium?

A

increased absorption from gut

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

what does the amount of ionised calcium in the blood depend on?

A

pH of blood (reduced binding with reduced pH hence reduced availability)

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

when does acute milk fever occur?

A

at/after calving

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

what are the clinical signs of acute milk fever?

A

initial tremors (hyperexcitation)
recumbent (muscles not working)
no faeces/urine (if there is faeces it will be dry)
postural bloat
slow HR/pulse

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

what are some differentials for recumbent cows after calving?

A

milk fever
acute coliform mastitis (endotoxaemia)
botulism
acute disease (salmonella…)
injury at calving

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

how is hypocalcaemia treated?

A

calcium borogluconate
phosphate supplementation
place in sternal recumbency

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

what is the role of phosphorous in the body?

A

essential compound of ATP (energy)

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

how can hypocalcaemia be prevented?

A

reduce calcium in diet (<0.7%) or massively increase it during dry period (>1.7%)
maximise DMI during dry period
DCAD dry ration
calcium binder during dry period to increase calcium mobilisation

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

why is low calcium fed during dry period?

A

tone the parathyroid during calving so more calcium is able to be mobilised more efficiently
high magnesium during dry period (essential for Ca absorption mediated by parathyroid hormone)

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

what is the aim of a DCAD diet?

A

reduces pH in blood (produces acidic urine)
this aims to trigger calcium mobilisation

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

how is a partial DCAD diet done?

A

control diet for minimum of 14 days pre-calving by giving low potassium forages and magnesium chloride flakes

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

when does hypocalcaemia occur in sheep?

A

pre-lambing (linked to stress - movement, weather, inadequate feeding…)

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

what is hypomagnesaemia also known as?

A

grass staggers

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

what is the cause of hypomagnesaemia?

A

magnesium output (in milk) is higher than input (in diet) as body is unable to store magnesium

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

what can affect the ability of the body to absorb magnesium from the diet?

A

high potassium (seen hen grazing lush/well fertilised pastures)

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

what are the clinical signs of hypomagnesaemia?

A

early - twitch/hypersensitive
recumbent and convulsing
(sheep usually found dead)

21
Q

what are some increased risk factors for hypomagnesaemia?

A

lush pasture
high yielding dairy cattle
stress - weather, movement, handling…

22
Q

how is hypomagnesaemia treated?

A

control convulsions (xylazine)
calcium IV
slow magnesium IV

23
Q

what is glucose produced from via gluconeogenesis?

A

propionate (also acetate and butyrate)

24
Q

how does adipose tissue produce energy?

A

lipolysis to give NEFA and glycerol

25
Q

what does the udder produce lactose from?

A

glucose (also propionate)

26
Q

where is glucose stored as glycogen?

A

liver

27
Q

what is the function of liver in relation to NEFA?

A

metabolise NEFAs to ketones
re synthesis NEFAs to fat

28
Q

what are ketone bodies?

A

energy source for muscle (not milk production or brain)

29
Q

what is the role of insulin?

A

facilitate glucose entry to cells and decrease gluconeogenesis
suppresses NEFA being converted to ketones

30
Q

what does glucagon stimulate?

A

gluconeogenesis and ketogenesis

31
Q

how does adrenaline effect ketosis?

A

stimulates lipolysis and NEFA release

32
Q

what are the clinical signs of ketosis?

A

reduced milk yield
selective appetite (refuse concentrates)
ketones in blood
firm shiny faeces
nervous ketosis (wall licking, kicking, blind…)

33
Q

what is the treatment for clinical ketosis?

A

oral propylene glycol
corticosteroids (dexamethasone)
IV glucose
vitamin B1 and 12
kexxtone bolus (monensin)

34
Q

why would you give a clinical ketosis cow corticosteroid?

A

stimulate gluconeogenesis

35
Q

how do kexxtone boluses aid ketosis treatment?

A

inhibit gram-positive bacterial growth in rumen which produce most of the acetate and lactate responsible for ketones
rumen produces more propionate and hence more glucose production can occur

36
Q

how can subclinical ketosis be tested for?

A

beta hydroxybutryrate in blood
NEFA in blood (indicates fat mobilisation)

37
Q

what does high beta-hydroxybutyrate indicate?

A

energy shortage and hence ketosis

38
Q

how can nutritional status of a cow be monitored?

A

BCS, DMI intake, cutting, rumen fill, faeces…
production targets/peaks
milk quality
biochemistry (metabolic profiles)

39
Q

what is the target BCS for cattle for most of the year?

A

2.5 (3 at start of drying off)

40
Q

what diagnostic markers can be used for monitoring metabolic and nutritional status?

A

beta hydroxybutryrate
NEFA
glucose
fat
protein
milk urea

41
Q

what is the cut-off for beta hydroxybutyrate for ketosis testing?

A

> 1.2 (this indicates ketosis)

42
Q

what does high beta hydroxybutyrate suggest?

A

ketosis

42
Q

what are high NEFAs suggestive of?

A

fat mobilisation

43
Q

when should you do metabolic profiling of cows?

A

take a random selection from…
early lactation (10-20 days)
mid lactation (80-150 days)
late dry cows (within 10 days of calving)
(allow 2 weeks after any major diet change)

44
Q

how can milk quality be a monitor for nutrition?

A

milk protein - low equates to energy deficiency
butterfat - low equates to lack of fibre
(fat/protein ratio to energy to fibre ratio)

45
Q

what are the two types of proteins measured in digestible crude protein?

A

effective rumen degradable protein (micro-organism feed)
undegradable dietary protein (passes through rumen into abomasum)

46
Q

what is needed for the effective rumen degradable protein to be taken up by the micro-organisms?

A

energy - if there isn’t enough energy milk urea will rise as the proteins won’t be able to be used by the microbes

47
Q

how can ketosis be minimised with dry period management?

A

low energy
maximise DMI
monitor BCS
avoid fat cows (they mobilise more fat)

Gastrointestinal (farm) (10 decks)

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