Lecture 23 - Alimentary 4 Flashcards

1
Q

Briefly explain the mechanism of dehydration and shock in the ruminants:

A
  1. Fermentation of readily digestible carbohydrate causes increased osmotically active particles within the rumen
  2. Osmotic pull of water from ECF into the rumen
  3. Some material from rumen reaches large intestine
  4. Further fermentation results in osmotic diarrhoea
  5. The net result is hypovolaemic shock
  6. Bacteria and bacterial products (endotoxins) are then able to cross compromised ruminal wall
  7. This leads to endotoxic shock
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2
Q

What are the two different products of lactic acidosis in ruminants?

A

D-lactate (accumulation in rumen and blood)

L-lactate (used to host)

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3
Q

How does metabolic acidosis result in ruminal stasis?

A

Initially, it is by the direct effect of SCFAs (especially butyrate) - later on is due to damaged ruminal wall, hypovolaemia, metabolic acidosis and systemic toxaemia

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4
Q

How should rumen fluid collected appear normally and how will it appear in cases of ruminal acidosis?

A

Normally, protozoa keep particulate matter suspended in fluid - settling quickly occurs when the protozoa die .

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5
Q

What is the name of the bacteria that are shown below?

A

Gram positive Lactobacilli

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6
Q

What is the name of the condition that is shown below ‘star gazing cow’ relate this to ruminal acidosis ?

A

Ruminal acidos may lead to destruction of thiamine producing bacteria . This leads to a thiamine deficiency and polioencephalomalacia. The cow has opisthotonus and is showing a star gazing attitude

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7
Q

What are the two different types of bloat that are seen within cattle?

A

Free-gas bloat (fermentation is normal) - acute or chronic

Frothy (legume) bloat - feremntation is abnormal

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8
Q

What is the cause of failure of eructation (free gas bloat) and describe the appearance of the animal?

A

Free-gas bloat is associated with intermittant obstruction of the cardia - note the distended left paralumbar fossa

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9
Q

What is the pathophysiology of failure of eructation - frothy bloat?

A

Feeding of lush pasture that are high in chloroplast and in soluble protein results in the production of a stable foam that traps gas (stable foam resembles whipped egg white) and blocks the cardia and prevents eructation.

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10
Q

How do the clinical signs for frothy bloat differ to those seen in free gas bloat?

A

Signs similar to free gas bloat except absence of large asculatable ‘ping’ despite marked left flank distention

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11
Q

What are some sequale to frothy bloat?

A

Ruminal distention can rapidly lead to compression of the thorax, cardiopulmonary failure, recumbancy and death

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12
Q

What are primary cycle and secondary contraction cycles of the reticulum and the rumen?

A

Primary cycle - emptying and mixing contractions

Secondary cycle - contractions related to eruction of gas

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13
Q

What nerve controls forestomach motility?

A

The vagus nerve

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14
Q

Briefly describe how forestomach contractions are mediated:

A

The regulation is mainly via long vagovoagal reflexes. Sensory information from forestomach receptors is transmitted via vagus to integrating. The vagus nerve also conveys efferent signals from dorsal vagal nucleus back to the forestomach muscle

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15
Q

What are the four main abnormalities of motility (provide an example of each)?

A
  1. Depression of the gastric centrers in the centrla nervous system - anaesthesthics, drugs, pain, pyrexia
  2. Lack of excitatory reflex inputs via tension receptors in the forestomach (anorexia, vagus indigestion)
  3. Block of motor pathways (usually secondary to drugs such as atropine or to hypocalcaemia)
  4. Increased inhibitory reflexes inputs via epithelial receptors in forestomachs (ruminal distention, acids, abomasal or small intestine distention)
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16
Q

What is meant by “hardware disease” in cattle?

A

Traumatic reticuloperitonitis - caused by ingesting baling metallic objects e.g. bailing wire

17
Q

What are some of the potential outcomes of traumatic reticoluperitonitis?

A

Objects collect in reticulum where they may:

  1. Sit harmlessly and slowly dissolve
  2. Penetrate wall and cause local peritonitis
  3. Penentrate wall and cause generalised peritonitis
  4. Penetrate wall, causing peritonitis and migrate cranially through diaphragm
18
Q

What are the clinical signs seen with traumatic reticuloperitonitis?

A
  1. Sudden drop in milk production
  2. Anorexia
  3. Depression
  4. Fever
  5. Increased heart rate and respiratory rate
  6. Cranial abdominal pain (positive grunt test or withers pinch test)
19
Q

What clinical signs may be seen with chronic localised traumatic reticuloperitoniits (TRP)?

A

Weight loss, poor lactation, rough hair coat and vagal indigestion

20
Q

What is the name of the conditon shown below? Privde a potential cause:

A

Fibrinous pericarditis in a cow with TRP.

21
Q

What are the two different types of vagal indigestion that have been described?

A

2 main types has been described:

  • Failure of digesta transport into and through omasum is the most common form of the disease
  • Failure of pyloric outflow - impairing abomasal emptying is less common
22
Q

What are the theories surrounding vagal indigestion?

A
  1. Disruption of mechanoreceptors in chronically inflammed wall of reticulum and rumen limits generation of secondary signals travelling to brain via vagus nerve - disrupts vagal motor signals neccesary for normal activity
  2. Chronic inflammation of the reticulum - with peritoneal adhesions - disrupts primary and secondary reticulomrumenal motility patterns
  3. Primarty vagus nerve damage anywhere along length - may also cause disease - occurs in very small number of cases
23
Q

What are the clinical signs that are normally seen as a result of vagal indigestion?

A
  1. Reduced feed intake with normal water consumption
  2. Decreased milk production
  3. Bradycardia (>60 bpm) - less than 30% of cases
  4. Variable rumen sounds (absent or hypermotile) - usually increases (3-6/min) but ineffective contractions
  5. Viewed from behind “papple” or L-shape - rumen gas cap and digesta filling of ventral sacs