LHW GIT

Question 1

Describe the fate of ERDP once it enters the rumen

Answer 1

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

Question 2

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

Answer 2

Starch/ sugar

Question 3

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

Answer 3

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

Question 4

Give examples of molecules used for energy by the cow.

Answer 4

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

Question 5

Outline the cause of rumenal acidosis. And the possible sequelae

Answer 5

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

Question 6

What is the maintenance DMI for a cow?

Answer 6

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

Question 7

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

Answer 7

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

Question 8

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

Answer 8

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

Question 9

What is fat mobilisation syndrome?

Answer 9

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

Question 10

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

Answer 10

Cellulolytic, hemicellulolytic, pectinolytic and amylolytic

Question 11

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

Answer 11

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.

Question 12

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

Answer 12

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

Question 13

What is the pathophysiology of SARA?

Answer 13

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

Question 14

What clinical signs are associated with SARA?

Answer 14

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

Question 15

What are the clinical effects of SARA?

Answer 15

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

Question 16

How can SARA be managed in the dairy herd?

Answer 16

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

Question 17

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

Answer 17

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

Question 18

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

Answer 18

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

Question 19

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?

Answer 19

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

Question 20

What is the pathophysiology of hypocalcaemia in the cow?

Answer 20

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

Question 21

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

Answer 21

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

Question 22

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

Answer 22

Avoiding heart arrhythmias

Question 23

Describe the pathophysiology of fat mobilisation syndrome.

Answer 23

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

Question 24

How can hypocalcaemia be avoided?

Answer 24

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

Question 25

What biochemical calues are measured in diagnosis of FMS?

Answer 25

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

Question 26

What is the Eric Williams test for traumatic reticulitis?

Answer 26

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

Question 27

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

Answer 27

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

Question 28

Name an explain a sequela to traumatic reticulitis.

Answer 28

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

Question 29

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

Answer 29

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

Question 30

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

Answer 30

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

Question 31

Describe the pathogenesis of LDA.

Answer 31

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.

Question 32

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

Answer 32

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

Question 33

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

Answer 33

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

Question 34

What therapeutics are used in the treatment of ARA?

Answer 34

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

Question 35

Why may you use NSAIDs in a case of ARA?

Answer 35

Cows are usually endotoxic (NSAIDs antiendotoxaemic)

Question 36

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

Answer 36

Their low blood pH prevents calcium-albumin binding

Question 37

What is the role of calcium in the body? What clinical signs are seen with deficiency?

Answer 37

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

Question 38

What differentials may be associated with a recumbent cow?

Answer 38

* Acute coliform mastitis - check TPR * Botulism * Acute septicaemia * Calving injury - post calving, dystocia * Hypocalcaemia - post calving * Trauma

Question 39

What treatment protocol would be used with a case of hypocalcaemia

Answer 39

IV 40% calcium borogluconate - SLOWLY IV foston (Ph) Get into sternal recumbency