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AM2 > Ruminal Metabolism > Flashcards

Ruminal Metabolism Flashcards

1
Q

Acidosis two types

A

SARA pH

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2
Q

What causes rumen pH to fall

A

Excess starch hence shift towards amylolytic flora

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3
Q

Process of acidosis

A

Increase of starch causes incr in VFA and decr in pH
Increase in lactate producing bacteria S.Bovis so incr in lactate
pH

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4
Q

Which VFA supports gluconeogenesis

A

Proprionate

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5
Q

How can you control pH

A

Yeast supplements - scavenge O2 giving anaerobic environment for bacterial growth

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6
Q

Which is main VFA produced

A

Acetate

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7
Q

Solutions to lack of glucose eg at lactation

A

Utilise oxaloacetate from KA
Burn fat releasing acetyl CoA
BUT
Reduced efficiency of KCA if less oxaloacetate Nx too much acetyl CoA
Acetyl CoA metabolised to ketone bodies in liver and supplies tissues instead of glucose and builds up toxic level

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8
Q

Signs of ketosis

A

Pear drops
Lethargic
Loss in body weight

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9
Q

Treatment of ketosis

A

Dextrose (500ml 50%) IV
propylene glycol and glycerol drench
Glucocorticoids

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10
Q

Prevention of ketosis

A

Balanced ration

Maintain BCS

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11
Q

Cause of hepatic lipidosis

A

Excess energy intake during dry period
Negative energy balance at calving
Body fat mobilised faster than it is used up
NEFA in blood and stored by liver

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12
Q

What does fatty liver occur with

A

Metritis
Mastitis
DA
Hypocalcaemia

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13
Q

Prevention of fatty liver

A

Monitor BCS in dry period, don’t let >3.5
minimise NEB so less fat mobilisation
Minimise stress

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14
Q

DA causes

A

Hypo motility of abomasum

Incr concentrates and decr roughage

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15
Q

Signs of LDA

A 
Decr milk
Gas production
Decr appetite/anorexia
Alkalosis and hypokalaemia
Secondary ketosis common
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16
Q

Signs of RDA

A

LDA PLUS
ischaemia
Blood supply to GIT compromised
Necrosis

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17
Q

DA treatment

A

Surgical
Manipulation
Roll

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18
Q

Prevention of DA

A 
promote DMI and rumen fill immediately after calving
Feed TMR
avoid rapid dietary changes
Feed enough roughage
Treat ketosis
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19
Q

Causes of retained placenta

A 
Dystocia
Twins
Stillbirth
Abortion
Low Se
Hypocalcaemia
Old age
Previous history
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20
Q

Treatment of retained placenta

A

Trimming of excess tissue don’t manually remove

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21
Q

Prevention of retained placenta

A

Se supplementation

Cull repeat offenders

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22
Q

Hypocalcemia/ mikl fever causes

A

Too much calcium in dry period
Not enough vit D or Mg in dry period
Ca:P ratio too low (excess P)
Jersey cow is prone

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23
Q

Milk fever signs

Three stages

A

1

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24
Q

How do vit D and Mg prevent milk fever

A

Regulate calcium reabsorptiom

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25
Q

Milk fever prevention

A

Low calcium diet in dry period
DCAD diet- low pH improves calcium absorption
- promotes parathyroid gland to use bone calcium
-use low K diet S it blocks Mg
Vit D in feed

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26
Q

Cause of twin lamb disease

A

Poor rationing in pregnancy
Sheep outdoors in poor weather
Ketosis

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27
Q

Signs of twin lamb disease

A

Don’t want to move
Ketone bodies
Disturbed vision

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28
Q

Treatment of twin lamb disease

A

Dextrose IV bonus (500mg 50%)
Propylene glycol and glycerol drench
Glucocorticoids

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29
Q

Prevention of twin lamb disease

A

Good nutrition in last 8w pregnancy

Concentrate supplementation

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30
Q

Cause of hypo magnesaemia

A

Pasture low in Mg

Fertiliser use reduces pasture uptake of Mg

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31
Q

Signs of hypo magnesaemia

A

Frothing at mouth
Muscle twitching and teeth grinding
Dead stock at pasture

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32
Q

Treatment of hypo magnesaemia

A 
Mg sulphate (200ml 50%) SC
Hay treated 60g Mg oxide daily
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33
Q

Prevention of hypo magnesaemia

A

Her age dusted with Mg oxide (500g a cow)
Herbage sprayed with 2% Mg sulphate
Mineral licks
Boluses

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34
Q

Causes of cerebrocortical necrosis

A

Vit b1 deficiency /thiamine deficiency
Carb rich and roughage poor ration causes SUBCLINICAL lactic acidosis
Destruction of thiamine in GI tract

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35
Q

Signs of CCN

A

circle collapse leg-kicking

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36
Q

Treatment of CCN

A

early thiamine may cure but not if lesion advanced

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37
Q

Prevention of CCN

A

Diet ensuring no SARA

Prophylactic vitamins

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38
Q

Causes of swayback

A

Low Cu causes underdevelopment of myelin sheaths in lambs

Poor absorption of Cu due to copper thhiomolybdate formation

39
Q

Prevention of swayback

A

CoSeCure boluses

Supplement copper but with CARE as sheep accumulate copper in liver and toxicity occurs at 25mg/kg

40
Q

Cause of pine

A

Lack of Co

Inability to make vit B12 in rumen

41
Q

Signs of pine

A

Unthrifty
Dull fleece
No appetite

42
Q

Treatment of pine

A

IM injection of vit B12

Drenching up to 1ml/kg cobalt sulphide

43
Q

Prevention of pine

A

CoSeCure boluses

44
Q

Cause of white muscle disease

A

Se and vit E deficiency
Low bioavailability of inorganic Se
Se incorporated into organic form on pasture

45
Q

What does Se do

A

Cofactor for reduction of antioxidant enzymes
Cofactor for thyroid hormone deiodinases
Removes reactive oxygen species
Controls metabolic rate

46
Q

Signs of white muscle disease

A

Acute and rapid wasting of skeletal muscle

Unable to stand

47
Q

Treatment of white muscle disease

A

IM or SC injection of young lambs with 0.75-1.5mg Se as potassium selenate
Injection of 34-68mg vit E

48
Q

Prevention of white muscle disease

A

Supplement dams ration in late gestation
Injection of newborn lambs with Se and vit E prep
CoSeCure bolus
SelPlex

49
Q

Aphosphorosis cause

A

Phosphorus deficiency due to poor diet or grazing soil low in P

50
Q

Signs of aphosphorosis

A 
Rickets
Stiff joints
Poor fertility
Decr milk
Chew strange things
51
Q

Treatment of a phosphorosis

A

Oral P supplementation (won’t work on vomiting or diarrhoea)

Sodium phosphate salts

52
Q

Prevention of aphosphorosis

A

P fertiliser on depleted soil

0.42% DM P conc for high yielders

53
Q

Signs of vit a deficiency

A 
Night blindness
Infertility
Rough coat
Impaired immunity
Weak/dead lambs 
Xerophthalmia (dry conjunctiva)
54
Q

Treatment of vit a deficiency

A

Retinol injection and vit a supplement in feed

55
Q

Goitre causes

A

Iodine deficiency causing decr thyroxine

Goitrogens reduce T3 and or T4 production and release

56
Q

Signs of goitre

A

Enlarged thyroid gland

Weak or hailess young

57
Q

Treatment of goitre

A

Potassium iodide oral dosing

Intra ruminal boluses provide slow release of iodine

58
Q

Prevention of goitre

A

Add iodine to conc rations

Rapeseed treated to eliminate goitrogens

59
Q

Clover disease causes

A

Phytoestrogens produced in clover gives infertility as cysts form in uterus and cervix and uterus doesn’t contract normally

60
Q

What conditions In Rumen support microbial growth

A

Temp/moisture /pH
Supply of nutrients
Removal of products of digestion and fermentation

61
Q

How are VFA produced

A

From pyruvate by fermentation

62
Q

What are the three VFAs

A

Acetate butyrate propionate

63
Q

Why drive towards propionate production

A

So less methane produced as acts as hydrogen sink

64
Q

What diet produces acetate

A

High fibre

65
Q

What is the fate of acetate

A

Converted to acetyl CoA in liver, used in kerbs

Milk fat precursor

66
Q

What diet favours propionate

A

High concentrate

67
Q

What is fate of propionate

A

20% to lactate during absorption across rumen wall, enters gluconeogenic pathway via PEP
80% to glucose VIA OXALOACETATE

68
Q

What favours butyrate

A

High fibre

69
Q

What is destiny of butyrate

A

B hydroxybutyrate in absorption, passed to liver and converted to acetyl CoA , or used as energy source

70
Q

How is methane formed

A

Reduction of co2, h2 from acetate and butyrate production

71
Q

What should be pH of rumen

A

6.7+/- 0.5

72
Q

What provides buffer

A

Saliva- 180L a day produced

73
Q

What is dietary protein made up of

A

Microbial protein DMTP (from non-protein N)

dietary Undegraded protein RUP

74
Q

What uses amino acids as energy

A

Low energy FME diets, form branched VFAs

75
Q

What is the fate of urea

A

Converted to ammonia by bacterial urease in the rumen, excreted in urine

76
Q

What causes low ammonia levels

A

Low dietary protein

77
Q

What causes high ammonia levels

A

More protein degraded than microbial protein formed

78
Q

What is optimal rumen ammonia conc

A

8mM

79
Q

Efficiency of dietary N utilisation and reason

A

20% retention in rumen
Different rates of degradation of carbs and protein gives low efficiency of microbial protein syn
BALANCE OF RDP AND FME IMPROVES EFFICIENCY

80
Q

Glycerol base lipids

A

Neutral triacylglycerol

Structural glycolipids and phospholipids

81
Q

Non glycerol base lipids

A

Steroids
Vitamins
PGs
Waxes

82
Q

How much energy per mole lipid

A

409 mole ATP

83
Q

PUFA:SUFA

A

> 0.45 for healthy cell function and membrane fluidity

84
Q

Lipid recommendations

A

Omega 6: omega 3

85
Q

Where does most of lipid in diet come from

A

Chloroplast of plants- thylakoids has membrane lipid (omega 3 mainly)

86
Q

Fatty acids in beef

A

MUFA»SUFA>PUFA

87
Q

Process of bio hydrogenation

A

Protozoa act on cells causing lipolysis to FFAs (incr by red clover)
FFAs undergo bio hydrogenation, PUFA (92% omega 3 and 86% omega 6) lost
Fish oil decr sat fat 18:0 and incr trans Fat 18:1

88
Q

Role of PPO in red clover

A

Oxidises phenols to quinones in presence of oxygen which bind to proteins

89
Q

What causes milk fat depression (fat lowered up to 50%)

A

Highly polyunsaturated fats- plant oils, oil seeds
Low roughage and high conc
High 18:1 trans fat

90
Q

What does SREBP1 do

A

Up regulates de novo synthesis, esterification and desaturation

91
Q

What drives metabolic disorders

A

Losing control of rumen pH

92
Q

Unsustainability of the Holstein

A

Yield requires energy and protein beyond levels available from pasture
Consumes more than body weight of cereals per lactation- using human resources
Producing cereals uses polluting fertiliser
Ill equipped to digest a grain rich diet- SARA, DA

93
Q

Proposed solutions to global food security

A

International network of ‘model farms
Global network of ‘farm platforms’
Critical zone observations

94
Q

How do PUFAS affect butterfat

A

Toxic to rumen bacteria, have to be converted from 18:2 and 18:3 to 18:0 by biohydrogenation
A low rumen pH will cause 18:2 or 18:3 to create intermediate c10-t12 TFA which causes milk fat depression as down regulates SREBP1 reducing de novo synthesis of c4-c14 FAs

AM2 (5 decks)

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