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Year 4 > Bovine GIT > Flashcards

Bovine GIT Flashcards

1
Q

The bacteria in the rumen are mostly gram what?

A

Gram positive

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2
Q

How long does it take rumen microbes to adapt to a new diet?

A

3 weeks

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3
Q

Out of fibre and FME (fermentable metabolisable energy), which has the highest rate of fermentation?

A

FME (fast)

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4
Q

Give some examples of FMEs

A

Starches

Sugars

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5
Q

What is glucose metabolise into in the rumen?

What is this then metabolised into?

A

Pyruvate

  • > Acetic acid (absorbed)
  • > Propionic acid (absorbed)
  • > Butyric acid (absorbed)
  • > CO2 (vented)
  • > Methane (vented)
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6
Q

What should rumen pH be?

A

6-7

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7
Q

How does a low rumen pH lead to ruminal acidosis?

A

Low pH -> kills microbes, encourages growth of lactobacilli (produce D-lactic acid which can’t be metabolised)
Efficiency of digestion falls if pH falls (destroys papillae)
Undigested particles pass through to hindgut -> osmotic diarrhoea (loose faeces), colonic acidosis (damage to colon wall -> fibrin casts in faeces)
Low pH also destroys rumen papillae -> rumenitis

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8
Q

Give some factors that affect rumen pH

A

Amount of VFAs being produced
Type of acid produced (lactic acid= strong)
Rate of fermentation (fibre-slow, concentrates (FME)-fast)
Rate of acid removal (absorption across rumen wall-papillae)
Buffering by saliva (chewing the cud)

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9
Q

What % of cows should be chewing the cud at any one time?

A

70%

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10
Q

What does saliva contain that is so important for a healthy rumen?

A

Sodium bicarbonate (buffers the acid in the rumen)

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11
Q

Why should dairy cows have plenty of long fibre?

A 
Encourages cudding (bicarbonate in saliva buffers acid in rumen)
Forms a rumen mat (home to microbes; keeps food particles in rumen to be digested)
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12
Q

A rumen pH of what value is indicative of SARA (sub-acute ruminal acidosis)?

A

<5.5

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13
Q

What does swishing tails indicate?

A

Sore bums (due to acidic faeces)

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14
Q

How might the faeces of a SARA infected cow appear?

A

Loose and soft
Long fibre present
Undigested grains present
May see fibrin casts (from inflamed colon)

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15
Q

Give some effects of SARA

A

Reduced DMI
Reduced digestibility (reduced energy intake, negative energy balance)
Immunosuppression (susceptible to disease)
Poor milk yields
Milk butterfat may be low (not always)

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16
Q

Give some health effects of SARA

A 
Displaced abomasum (VFAs enter abomasum -> atony)
Digestive upsets
Ketosis (negative energy balance)
Lameness (ulcers, white line lesions)
Mastitis
Immunosuppression
Infections eg endocarditis
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17
Q

Give some fertility effects of SARA

A

Cows not seen bulling

Poor conception rates

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18
Q

How can you diagnose SARA?

A

Measure rumen pH 2-4 hours after feeding (gold standard) (<5.5)
Sieve faeces (undigested grain, long fibres over 1/2 inch, mucus casts)
History (nutritional management)
Condition score (>0.5 loss in CS from dry-peak lactation)
Observe the group (eg tail swishing, cudding)
Clues (eg fertility, lameness, LDA, ketosis)

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19
Q

When should you measure rumen pH?

A

2-4 hours after feeding

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20
Q

How would you sample rumen pH in a herd?

A

Sample 2 groups: cows calved 14-21 days ago, and cows calved 60-80 days ago.
First group are still adapting to ration, second group have adapted so have maximal DMI
Sample 6 cows from each group
Diagnosis confirmed when 2 cows from either group are below threshold pH (ie <5.7)

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21
Q

How do you sample rumen pH?

A 
Restrain cow
Obtain sample at level of stifle, 6-8" behind last rib
Clip and scrub
LA
3-5" needle, 16-18G
Read sample on pH meter immediately
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22
Q

What is included in a ‘far off diet’?

A

Grass silage and straw

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23
Q

Give the following values for grass silage:
Energy
Protein
Dry matter

A

Energy: 10.5-12MJ ME/kg DM
Protein: 14-16%
Dry matter: 20-35%

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24
Q

Give the following values for maize silage:
Energy
Protein

A

Energy: 11-11.5 ME
Protein: 8-9%

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25
Q

Why is it better to add hay rather than straw to a diet when adding fibre?

A

Hay is more palatable

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26
Q

When does acute ruminal acidosis occur?

A

When overeating grain

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27
Q

What clinical signs would you see with acute ruminal acidosis?

A 
Distended rumen 
Ataxia
Diarrhoea (profuse and smelly)
Depression
Recumbency and shock 
Anorexia
Dilated pupils
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28
Q

What would you see with peracute ruminal acidosis?

A

Severe ataxia or recumbency, apparently blind, severe dehydration

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29
Q

How would you treat mild acute, subacute and peracute ruminal acidosis?

A

Mild: give hay and observe
Subacute: oral antacids (magnesium hydroxide/carbonate), hay
Peracute: rumenotomy (empty rumen contents), sodium bicarbonate iv, balanced fluids, calcium borogluconate (source of calcium)

NSAIDs
Antibiotics eg oral penicillin
Animal may be severely dehydrated so give water

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30
Q

How can you prevent ruminal acidosis?

A

Take care when introducing grain to fattening animals
Good fibre source
Correct mixing of diets

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31
Q

Which part of the rumen acts as a home for microbes?

A

Fibre mat

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32
Q

Give some conditions that may occur in the dairy cow after calving

A 
Milk fever (hypocalcaemia)
RFM/metritis/endometritis
Mastitis
Displaced abomasum
Ketosis
Fertility issues
Lameness
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33
Q

Why does milk fever occur?

A

Hypocalcaemia +/- hypophosphataemia

Drain on Ca2+ due to colostrum/milk demands from calf

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34
Q

What is the role of parathyroid hormone?

A

Mobilisation of calcium from bone stores

Increased absorption from gut (requires Mg2+)

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35
Q

What is the role of calcitonin?

A

Reduces calcium absorption and availability

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36
Q

What is the role of vitamin D?

A

Increased calcium absorption from gut

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37
Q

Ca2+ is present in the blood in which 2 ways?

A

Bound (chiefly to albumin)

Ionised (active Ca2+)

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38
Q

How does pH affect binding of Ca2+ in blood?

A

Reduced binding with reduced pH

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39
Q

What are the roles of Ca2+ in the body?

A

Muscle function (every muscle and gland requires Ca2+ to function)
Nerve impulses
Immune response

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40
Q

What are the clinical signs of acute milk fever?

A

At/after calving:
Initial hyper-excitement, tremor
Recumbent (muscles stop working)
Guts/gland stop working: no faeces/ urination, dry nose, bloat, slow pulse/HR

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41
Q

Give a common clinical sign of hypophosphataemia

A

Peri-parturient haemoglobinuria (red urine)

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42
Q

How can you treat hypocalcaemia?

A

IV calium borogluconate 40% (don’t administer too fast -> arrhythmias)
Hypocalcaemia is often complicated by hypophosphataemia so give foston (organic phosphorus) IV

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43
Q

Sub-clinical hypocalcaemia is a risk factor for which other diseases?

A

Immune function depression
Coliform mastitis
Metritis/endometritis
‘Post-partum depression’

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44
Q

How can you prevent hypocalcaemia?

A 
Aim to tone up the parathyroids
Feed low calcium diet pre-calving
Feed high magnesium diet pre-calving 
Boluses at calving?
Maximise DMI pre-calving
DCAD diets: aim for a negative DCAD before calving -> induces a compensated metabolic acidosis (causes mobilisation of calcium)
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45
Q

When does hypocalcaemia occur in sheep?

A

Pre-lambing; stress

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46
Q

How do you treat hypocalcaemia in sheep?

A

20ml Ca2+ borogluconate IV

or get farmer to give 80ml SC at many sites

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47
Q

What is ‘grass staggers’?

A

Hypomagnaesmia

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48
Q

Give some clinical signs of hypomagnaesaemia

A

Peracute/acute-often found dead
Early-twitching, hypersensitive, occasionally aggressive
Recumbent and convulsive- EMERGENCY

Sheep usually found dead

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49
Q

Give some trigger factors for hypomagnaesaemia

A

Lush pastures (Spring)
High milk output
Stress-weather, movement, handling (noradrenaline binds Mg)

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50
Q

How do you treat hypomagnaesemia?

A

Be quiet- risk of setting off convulsions
Control convulsions with xylazine iv
Give Ca2+ 40% IV, then slowly give up to 200ml MgSO4 IV

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51
Q

How can you prevent hypomagnaesaemia?

A

Move off affected pasture
Give additional Mg (dairy cows-high Mg cake; beef cows-mineral supplements, boluses, give straw to slow gut transit time and give Mg more chance to be absorbed)

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52
Q

Where does the reticulum lie?

A 
Opposite 6-8th rib on LHS
Lies ventrally (is in contact with the ventral body wall)
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53
Q

Give the clinical signs of traumatic reticulitis

A 
SUDDEN milk drop (eg 20l to 5l)
Hunched up appearance
Stiff gait
Inappetence, dull, depressed
Often fed a TMR
May grunt spontaneously (pain)
Increased temp 39.5
Reduced rumen contractions
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54
Q

How often do rumen contractions occur?

A

3 rumen/reticular contractions in 2 mins

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55
Q

What are the 2 types of rumen contractions?

A

Primary (starts in reticulum, works backwards to rumen. Biphasic. Mixing)
Secondary (moves gas to the cardia. Starts in caudal rumen and moves forwards. Belches afterwards)
(2 primary for every 1 secondary)

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56
Q

How can you diagnose traumatic reticulitis?

A

Eric Williams Test- gold standard. Listen over trachea, feel rumen contractions in left flank (hands on L sub-lumbar fossa) (will slow with reticulitis, pain on reticular contraction)
Withers pinch-abdominal pain
Pole test-abdominal pain
Faeces-stiffer with long fibre

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57
Q

What 3 scenarios may you encounter when doing the Eric Williams test on a cow with traumatic reticulitis?

A

Reduction in primary cycles
Grunt (pain) immediately prior to primary cycle
Breath holding prior to primary cycle

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58
Q

What are the problems with swallowing a wire and it penetrating the medial reticulum?

A

Damage to vagus
Abscess in medial wall
No pain receptors

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59
Q

What clinical signs would you have with traumatic pericarditis?

A 
Increased pulse 
Increased temp
Very ill
Heart sounds:
-Initially: pericardial rub ('grating')
-Later: very quiet/absent
-Later: 'washing machine sounds'
Can be fatal
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60
Q

How would you identify whether traumatic pericarditis had developed into heart failure?
What is the prognosis?

A

Distended jugular veins
Visible jugular pulse
Sub-mandibular oedema
Euthanasia

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61
Q

Give some consequences of traumatic reticuloperitonitis

A

Vagus nerve injury (penetration in medial wall of reticulum)

Reticular adhesions

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62
Q

Give some consequences of vagus nerve injury resulting from traumatic reticulopericarditis

A

Dorsal vagus nerve injury: achalasia of reticulo-omasal orifice -> food can’t pass into omasum -> enlarged rumen +/- bloat
Pyloric branch of ventral vagus nerve: achalasia of pylorus -> food can’t leave abomasum -> abomasal impaction
Hypermotility or hypomotility of rumen (depends on fibre types damaged)

63
Q

Give some clinical findings of a cow with traumatic reticulopericarditis and subsequent vagus indigestion

A 
Inappetence
'10 to 4' appearance (distension of abdomen in lower right quarter-enlarged rumen)
Hypo/hypermotile rumen motility
Dehydration
Scant faeces
Sometimes ping on lower right flank
64
Q

How can you treat traumatic reticuloperitonitis?

A

Poor prognosis-slaughter

Can do rumen lavage, fluid therapy and laxatives, rumenotomy

65
Q

When might you perform a rumenotomy?

A

Unable to relieve bloat via stomach tube

Recurring chronic bloat

66
Q

What is the definition of bloat?

A

Accumulation of rumen gas sufficient to change the contour of the rumen
Visible distension

67
Q

What are the 2 types of bloat?

A

Frothy bloat

Free gas bloat

68
Q

Give the pathogenesis of frothy bloat

A

Froth forms in rumen (dietary- clovers)
Covers gas receptors in cardia
Failure to eructate

69
Q

How can you treat frothy bloat?

A

Dose with surfactant to get rid of froth

Emergency: 4”-6” incision through rumen

70
Q

What causes free gas bloat?

A

Excess carbohydrates
Secondary to other conditions eg wire, vagus indigestion
Secondary to chronic pneumonia

71
Q

How can you relieve free gas bloat?

A

Pass stomach tube
Trochar in emergency
‘Red devil’ trochar with chronic bloat

Can stitch a trochar in and leave it there/do a rumenostomy (hole) if cow keeps bloating

72
Q

How does fatty liver occur in cows?

A

Non-essential fatty acids are metabolised to ketones in the liver, then re-synthesised to fat

73
Q

Why don’t we want to overcrowd dry cows and cause stress?

A

Adrenaline stimulates lipolysis and non-essential fatty acid release

74
Q

Ketone bodies are an energy source for what?

A

Muscle

75
Q

Where is glycogen stored?

A

Liver

76
Q

What are the functions of insulin?

A

Enables glucose entry into cells (and glucose use by muscle cells)
Decreases liver gluconeogenesis
Suppresses NEFA entry to mitochondria and ketogenesis
Stimulates lipogenesis in adipose tissue and in liver

77
Q

Why don’t we want to overcrowd dry cows and cause them stress?

A

Adrenaline release -> stimulates lipolysis and NEFA release -> lose weight -> fat mobilisation syndrome and ketosis

78
Q

How is the liver affected by fat mobilisation syndrome?

A

Yellow fatty liver

79
Q

How does fat mobilisation syndrome result in ketosis?

A

Insufficient propionate from rumen -> insufficient oxalo-acetate
Acetyl CoA formed from fat mobilisation (negative energy balance) and acetate/butyrate (from rumen) cannot enter Kreb’s cycle
Acetyl CoA is instead mobilised to ketones

80
Q

Give some clinical signs of clinical ketosis

A

Reduced milk yield
Selective appetite (refuses concentrates)
Ketone bodies in blood
Firm ‘shiny’ faeces

81
Q

Give some clinical signs of nervous ketosis

A

Obsessive licking
Hyper-excited
Twitchy

82
Q

Give the treatment for clinical ketosis

A

Oral propylene glycol
Corticosteroid
Glucose 40% iv
Combination of above

83
Q

What could you measure in blood to diagnose sub-clinical ketosis?

A

beta-hydroxy butyrate (cut-off value= 0.9mmol/L)

NEFAs in blood (cut-off value= > 0.4mmol/L) (Indicates fat metabolism)

84
Q

What is sub-clinical ketosis?

A

An excess of circulating ketone bodies without clinical signs of ketosis

85
Q 
What are the ideal body condition scores for: 
Drying off
Dry period
Early lactation
Mid lactation
A

Drying off: 2.5 (-3.0)
Dry period: 2.5 (-3.0)
Early lactation: 2.0 -2.5
Mid lactation: 2.5 (-3.0)

86
Q

Who loses more condition: a fat cow or a thin cow?

A

Fat cow as they have a smaller appetite

87
Q

When do we want a dairy cow to have maximal DMI (appetite)?

A

Dry period

4-10 weeks post-calving

88
Q

How do we prevent fat mobilisation syndrome and ketosis occurring?

A 
Feed in dry period:
-Low energy
-Maximise DMI (comfort, palatable diet, ad-lib food)
Monitor condition score
Avoid fat cows!
89
Q

Who will get fat and why:
Mabel: conceives to 1st service at 85 days
Buttercup: conceives to 6th service at 210 days
Give a negative consequence of this

A

Buttercup
Longer lactation, long period of high energy food and low yield
Will get fat in late lactation so will be fat in dry period
Will get fat mobilisation syndrome in next lactation (fat cows become thin -> infertile)

90
Q

What causes Johne’s disease?

A

Mycobacterium avium subspecies paratuberculosis

91
Q

Regarding Johne’s disease, where is MAP found?

A

Macrophages

92
Q

With Johne’s disease, what are the stages of MAP infection?

A

Susceptible
Infected but not infectious (cell-mediated response is fine)
Infectious (cell-mediated response starts to fail)
Resistant

93
Q

What are the clinical signs of Johne’s disease?

A 
Weight loss
Profuse diarrhoea (often with bubbles)
Animal remains bright and eating
Older animals (>3 yrs old)
Often after calving (stress)
94
Q

What are the clinical signs of sub-clinical Johne’s disease?

A

Reduced milk yield
Mastitis and high SCC
Infertility, lameness, LDA

95
Q

Cows with Johne’s disease are how many times more likely to be lame?

A

5 x more likely

96
Q

Cows with Johne’s disease are how many times more likely to develop mastitis/SCC problems?

A

2 x more likely

97
Q

What is the major route of transmission of Johne’s disease?

How else is it transmitted?

A

Oro-faecal route
Also:
Via colostrum and milk (dam colostrum or pooled colostrum)
In utero
Dirty environment
Dam faeces: teat, contamination of environment

98
Q

Who is most at risk from Johne’s disease?

A

Calves less than 12 months old

99
Q

At what age do dairy cows most commonly show clinical signs of Johne’s disease?

A

5 yrs old (middle age)

100
Q

What does it mean if a cow is ELISA +ve for Johne’s?

A

Losing immune control -> likely to be infectious

101
Q

For a cow to be classed as a ‘super shedder’ of Johne’s, how much bacteria would be present in their faeces?

A

> 1 million cfu/g faeces

102
Q

How can you diagnose Johne’s disease?

A 
Faecal culture (gold standard) and/or PCR (detects shedders)
ELISA (detects antibody, high probability of being a shedder if +ve)
103
Q

What is sensitivity (of a test)?

A

Ability to detect true positives

104
Q

What is specificity (of a test)?

A

Ability to detect true negatives

105
Q

What is the gold standard test for diagnosing Johne’s disease?

A

Faecal culture

106
Q

How can you reduce transmission of Johne’s disease to young stock?

A

Reduce risk factors (eg clean calving pens, only feed dams colostrum, keep young stock away from adults)
Cull animals likely to be shedding the infection

107
Q

Describe a test and cull scheme for Johne’s disease

A

Annual ELISA test: all adults > 2 yrs old
Cull all positives
Cull daughters

We are culling those that are likely to be infectious, not those that are infected

108
Q

How can you control Johne’s disease in beef suckler herds?

A

Outdoor calving (or move outside immediately when calved)
Cull daughters
Clip and clean teats before calving
Ensure bull is clean before purchasing

109
Q

When would you vaccinate against Johne’s? Does the vaccine prevent infection?

A

2nd week of life

No-reduces shedding and reduces incidence of clinical disease

110
Q

Why must you leave a 60 day gap between doing TB testing and a MAP ELISA?

A

Cross-reaction between MAP and TB test (avian part) -> false negatives

111
Q

Give some diseases of the abomasum

A 
Dilation and displacement (most common)
-LDA
-Right-sided dilation and displacement
Abomasal ulcers
Geo-sedimentum abomasi (sand impaction)
112
Q

What are the risk factors for abomasal disease?

A 
Usually seen in early lactation
Usually housed animals
Imbalance of fibre and concentrate
Associated with ketosis and fat mobilisation syndrome
Hypocalcaemia 
Concurrent inflammatory disease
Poor comfort
Lameness
ie anything that reduces DMI
113
Q

What is the primary event to occur in LDA? (left displaced abomasum)

A

Abomasal atony (inflammatory cytokines inhibit motility -> stops moving -> fills with gas from excess VFAs-> lifts to the left)

114
Q

Give the clinical signs of LDA

A

Reduced milk yield (not as marked or sudden as ‘wire’)
Ketosis
Selective appetite-prefers fibre
Usually 0-4 weeks post-calving
Characteristic ‘ping’
Absence of rumen sounds over displaced abomasum

115
Q

When casting a cow to fix an LDA, what recumbency should the cow be in?

A

Right lateral recumbency
Then roll to dorsal
Then roll over to left lateral

116
Q

What are the advantages and disadvantages of casting a cow to fix an LDA?

A

Advantages:

  • Cheap
  • Non-invasive

Disadvantages:

  • Least successful
  • Risk of ulcer rupture
117
Q

What is toggling?

A

Method of fixing an LDA
Cheap but nasty method
Can get complications: abomasal fistula, can misplace toggles, cow can pull toggles out

118
Q

What are the surgical methods of fixing an LDA?

A

Left & right-sided approach - 2 surgeons
Left side (Utrecht)
Right side
Right paramedian approach - cow is cast

119
Q

When doing a left and right-sided approach to the surgical method of fixing an LDA, where is the abomasum sutured to?

A

Pulled up to right incision and ‘sows ear’ part is sutured into wound closure

120
Q

How should you care for a cow after LDA surgery?

A

Antibiotics
Treat underlying condition eg ketosis
High fibre diet

121
Q

Give the progression of a right displaced abomasum

A

Aetiology not fully understood
Similar to LDA
Atony of abomasum -> dilation and distension -> displacement -> torsion

122
Q

What are the metabolic consequences of dilation with RDA?

A 
Pooling of H+ and Cl- in abomasum 
Upper intestinal obstruction
Metabolic alkalosis
Hypochloraemia
Dehydration
123
Q

What is the outcome of a cow with a right displaced abomasum that has full torsion?

A

Euthanasia (very hard to fix)

124
Q

What are the metabolic consequences of displacement and torsion with RDA?

A 
Mucosal damage (due to increased luminal pressure)
Cytokine release and endotoxaemia
Metabolic acidosis
Severe dehydration
125
Q

Give the 9 clinical signs of the dilation and displacement phase of a RDA

A 
Inappetent/depressed
Reduced faeces
Dehydrated
Tachycardia
Pale, dry mm
Doughy rumen
Reduced rumen turnover
Ping (middle to upper 1/3 of abomasum)
Tense viscus rectally
126
Q

What are the treatment options for RDA if only dilation/displacement is present?

A

Medical- Ca 40%, metaclopromide, fluids

Surgical- drain and replace

127
Q

What are the treatment options for a torsion in a cow with RDA?

A

Surgery

Slaughter

128
Q

What post-operative care should you give after surgery to fix a RDA?

A 
Fluid therapy: 50-100 litres (Hartmanns like)
NSAIDS
Antibiotics 
Oral KCl (50g daily)
Ca 40%
Propylene glycol
129
Q

Give the clinical signs of a cow with caecal dilation

What about with volvulus?

A

1st few months of lactation
Anorexia
Decreased milk yield
Reduced faeces
Mild abdominal discomfort
Ping in upper right flank (right lumbar fossa)
Rectally: distended, recognisable viscus

With volvulus: as above but with dehydration, tachycardia, abdominal pain

130
Q

Describe the aetiology behind caecal dilation and volvulus

A 
Excess carbohydrates are fermented in caecum
Increased VFAs
Reduced pH
Caecal atony
Accumulation of ingesta and gas
131
Q

What are the risk factors for caecal dilation and volvulus?

A

Nutritional

SARA

132
Q

What would you find on a rectal exam on a cow with caecal distension and volvulus?

A

Distension: long cylindrical, movable organ. Blind end points to pelvic cavity
Volvulus: points cranial and lateral/medial

133
Q

How can you treat a cow with caecal distension and volvulus?

A

Good quality hay
TLC
Surgery to correct torsion

134
Q

What age group of cattle get abomasal ulcers?

A

Mature cattle

135
Q

How may you identify a cow with an abomasal ulcer?

A 
Abdominal pain
Melena (black faeces) due to acute abomasal haemorrhage
Pale mm
Sudden onset anorexia
Tachycardia
Perforation:
- Hypovolaemia
- Unable to stand
136
Q

What can happen as a result of a perforation of an abomasal ulcer?

A

Acute local/diffuse peritonitis

137
Q

Give some possible causes of abomasal ulcers

A

Stress (lactation, transport)
High levels of grain (SARA)
Secondary to LDA/RDA

138
Q

Give the pathogenesis of abomasal ulcers

A

Injury to gastric mucosa -> diffusion of H+ ions into tissue -> damage

139
Q

Give the 4 types of abomasal ulcers

A

Type 1:

  • Non-perforating
  • Minimal amounts of intra-luminal haemorrhage

Type 2:

  • Major blood vessel perforates
  • Severe blood loss
  • Melena

Type 3:

  • Perforating ulcer
  • Acute, local peritonitis (localised by greater omentum)

Type 4:

  • Perforating ulcer
  • Diffuse peritonitis
140
Q

In which part of the abomasum do ulcers occur in cows and calves?

A

Cows: fundus
Calves: pylorus

141
Q

How do you treat an abomasal ulcer?

A

Antacids: Magnesium oxide po 800g/450kg daily
Blood transfusion/fluids (if haematocrit <12%)
Surgical excision
NO NSAIDS OR STEROIDS

142
Q

What are the clinical signs of a cow with oesophageal obstruction (choke)?

A 
Inability to swallow
Regurgitation of food and water
Drooling
Bloat
Anxiety/restless
Stop eating
143
Q

What is the usual cause of oesophageal obstruction?

A

Potatoes

144
Q

Give some extra-luminal causes of oesophageal obstruction

A

Pressure by surrounding organs (only occasionally)

  • Mediastinal abscesses
  • Tuberculous lymph nodes
145
Q

Where are the 2 locations that choke (oesophageal obstruction) usually occurs?

A

Cervical oesophagus above larynx

Base of heart/cardia

146
Q

How do you treat oesophageal obstruction (choke)?

A

Many self-resolve
Starve and observe
Sedate (Buscopan)
Flunixin (NSAID)
Can sedate and pull object out with your hand/push into rumen
If unsuccessful, trocharise rumen and feed via rumen until obstruction passes

147
Q

What are the 4 grades of abomasal ulcers?

A

1) Erosion/ulcer without haemorrhage
2) Haemorrhagic
3) Perforated with acute localised peritonitis
4) Perforated with peritonitis within the omental bursa

148
Q

Which volatile fatty acids are produced by:
Cellulose (fibre)
FME

A

Cellulose: acetate
FME: proprionate

149
Q

What is the ‘Dolly Parton effect’?

A

Large concentrate feeds cause spikes in rumen pH

150
Q

What fibre length causes cows to start sorting?

A

> 4”

151
Q

What is the ideal concentrate:fodder ratio?

A

60:40

152
Q

How can you distinguish first cut from second cut grass silage?

A

First cut: more leafy

Second cut: contains seeds

153
Q

When does SARA tend to occur?

A

After calving when dry cows are changed abruptly from a high-fibre diet to a higher-concentrate milking cow diet. Not enough time for ruminal papillae and bacteria to adjust -> rapid production and accumulation of VFAs. Therefore transition diet is very important!

Year 4 (51 decks)

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