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LHW GIT Flashcards

1
Q

Describe the fate of ERDP once it enters the rumen

A
  1. Broken down by microbes to NH4 and then used as microbial protein, excess in digested in the abomasum/ small intestine
  2. If energy is insufficient the NH4 is absorbed across the rumen wall and converted to urea
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2
Q

Give an example of molecules that are used as FME by the cow

A

Starch/ sugar

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3
Q

Give an example of a rumen undegradable protein and describe its fate once it enters the rumen.

A
  1. Soya. Passes through the rumen and is digested in the abomasum/ small intestine.
  2. Higher biological value/ quality
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4
Q

Give examples of molecules used for energy by the cow.

A
  1. Long chain carbohydrates – cellulose – fibre – butterfat
  2. Short chain carbohydrates – sugars and starches - FME
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5
Q

Outline the cause of rumenal acidosis. And the possible sequelae

A
  1. Imbalance of microbial population
  2. Build-up of fermentation products – volatile fatty acids (acetate, butyrate, propionate)
  3. With excess VFAs acetyl CoA builds up (rather than entering the Krebs cycle) and ketones are produced
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6
Q

What is the maintenance DMI for a cow?

A

2% of BW, increases to 3-4% when lactating

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7
Q

Describe the equation for calculating energy requirements of a lactating cow.

A

Maintenance (65-70MJ) + 5MJ/ litre of milk

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8
Q

Describe how the energy requirements of the cow change from the dry period into transition.

A

Energy requirements increase from 90 to 110 MJ/day but DMI decreases with increasing foetal load

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9
Q

What is fat mobilisation syndrome?

A

Decreased DMI during the dry period leads to NEB which continues into lactation and reduces milk yield.

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10
Q

Which bacteria of the rumen produce ketonic acids for FME production?

A

Cellulolytic, hemicellulolytic, pectinolytic and amylolytic

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11
Q

Which bacteria are responsible for lactic acid production in the rumen? What is the fate of this substance within the rumen?

A
  1. Strep bovis an amylolytic bacteria
  2. Lactic acid is usually an intermediate of ketonic acids which is converted by acid utilising bacteria to acetate, butyrate and propionate.
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12
Q

How does a change in environment within the rumen lead to SARA?

A
  1. Overload of concentrates leads to an increased VFA production
  2. Ph within the rumen decreases and cellulolytic bacteria are unable to perform their function
  3. Lactic acid producing bacteria continue to work and produce lactic acid (which cannot be absorbed by the rumenal wall) leading to further Ph decrease
  4. Reduced digestive efficiency
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13
Q

What is the pathophysiology of SARA?

A

Fluctuating Ph of the rumen due to overfeeding of concentrates – combatted by giving TMR ration ad lib!

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14
Q

What clinical signs are associated with SARA?

A
  1. Decreased rumen ph
  2. Weight loss
  3. Loose faeces
  4. Tail swishing
  5. Undigested grains in faeces
  6. Dirty cows
  7. Mucus casts in faeces
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15
Q

What are the clinical effects of SARA?

A
  1. Reduced DMI
  2. Reduced digestibility
  3. Immunosuppression
  4. Poor milk yield/ quality
  5. DA, Ketosis, lameness, mastitis, poor fertility
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16
Q

How can SARA be managed in the dairy herd?

A
  1. Increase long fibre content of the diet in fresh calved cows
  2. Reduced parlour fed concentrates
17
Q

What clinical signs are associated with a case of acute ruminal acidosis? Describe the pathophysiology of each.

A
  1. Distended rumen – atony due to acid build up
  2. Ataxia
  3. Diarrhoea – osmotic due to increased acid
  4. Depression
  5. Recumbency and shock – diarrhoea and hypovolaemia and pressure on the aorta leading to poor venous return
18
Q

What treatment options may be employed in a case of acute rumenal acidosis?

A
  1. Antacids
  2. Stomach tube
  3. Rumenotomy
  4. Fluids
  5. NSAIDS
19
Q

You are presented with a cow that has been chronically losing weight, though bright and has profuse diarrhoea. What disease process may you suspect? How is the pathogen transmitted?

A
  1. MAP – Johne’s
  2. Faecal-oral, colostrum, milk, in utero
20
Q

What is the pathophysiology of hypocalcaemia in the cow?

A
  1. Reduced muscular/ glandular function – bloat, tremors, dry nose reduced urination/ defacation
  2. Reduced immune function
21
Q

What differentials may be suspected for the recumbent, bloated post-calving cow?

A
  1. Acute coliform mastitis
  2. Botulism
  3. Hypocalcaemia
  4. Septicaemia
  5. Calving injury
  6. Trauma
22
Q

When giving calcium IV why must the infusion be given slowly?

A

Avoiding heart arrhythmias

23
Q

Describe the pathophysiology of fat mobilisation syndrome.

A
  1. Negative energy balance
  2. Insufficient propionate and hence oxalo acetate
  3. Acetyl CoA is formed in excess
  4. Ketones produced
  5. OR fat resynthesis
  6. Acetone and BHB produced
24
Q

How can hypocalcaemia be avoided?

A
  1. Ca bolus at calving
  2. Induce mild hypo prior to calving
25
Q

What biochemical calues are measured in diagnosis of FMS?

A
  1. Beta-hydroxybutyrate (>1.4mmol/L)
  2. NEFA – pre-calving
26
Q

What is the Eric Williams test for traumatic reticulitis?

A
  1. Concurrent listening to tracheal grunting with pre-rumenal contractions over the sub-lumbar fossa
  2. Grunting occurs prior to contraction
27
Q

What diagnostic tests can be used for a suspected case of traumatic reticulitis?

A
  1. Eric Williams
  2. Wither pinch
  3. Pole test
  4. WBC count
  5. Exploratory rumenotomy
28
Q

Name an explain a sequela to traumatic reticulitis.

A
  1. Vagus indigestion – wire penetration of the vagus nerve
  2. Rumen/ pyloric outflow disturbance, rumenal distension
  3. Alteration
29
Q

How are cases of frothy and free gas bloat treated differently?

A
  1. Frothy – give surfactant (cannot be treated with trocar)
  2. Free gas – trocar/ red devil
30
Q

Describe the possible sequelae to LDA, why does each occur?

A
  1. Metabolic acidosis and hypochloraemia – reduced ingesta outflow and continued hydrochloric acid secretion
  2. Hypokalaemia due to alkalosis (K+ into cells)
31
Q

Describe the pathogenesis of LDA.

A

High conc diet, increased VFAs, NEFAs, hypokalaemia, hyperinsulinaemia. Abomasal atony and increased gas production, dilation and hence movement of the unattached middle section of the abomasum.

32
Q

With which type of torsion during an RDA will there be most complications and why?

A

Left torsion – more likely to end in ischemia and necrosis.

33
Q

How would a cow with ARA present? Outline for a subacute to peracute case.

A
  1. Sub-acute - Still bright and eating, +/- distended abdomen and scour
  2. Acute - Ataxic, anorexic, dilated pupils
  3. Per-acute - Severe ataxia/ recumbency, blindness, severe dehydration, foul smelling diarrhoea
34
Q

What therapeutics are used in the treatment of ARA?

A
  1. Oral antacids - MgCO3
  2. NaC2O4 - beware hypernautraemia and gas production
  3. Relieve bloat with a stomach tube
  4. Rumenotomy
  5. Sodium bicarbonate IV
  6. Balanced fluids
35
Q

Why may you use NSAIDs in a case of ARA?

A

Cows are usually endotoxic (NSAIDs antiendotoxaemic)

36
Q

Why may it be unlikely for an ARA cow to be hypocalcaemic?

A

Their low blood pH prevents calcium-albumin binding

37
Q

What is the role of calcium in the body?

What clinical signs are seen with deficiency?

A
  1. Muscle/ glandular function - dry nose, ileus, tremors
  2. Nerve impulse propagation
  3. Immune response
38
Q

What differentials may be associated with a recumbent cow?

A
  • Acute coliform mastitis - check TPR
  • Botulism
  • Acute septicaemia
  • Calving injury - post calving, dystocia
  • Hypocalcaemia - post calving
  • Trauma
39
Q

What treatment protocol would be used with a case of hypocalcaemia

A

IV 40% calcium borogluconate - SLOWLY

IV foston (Ph)

Get into sternal recumbency

Gastrointestinal (15 decks)

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