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Equine Clinical Studies > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

Define Colic

A

A collection of clinical signs observed
interpreted as evidence of pain originating
from within the abdominal cavity.

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2
Q

What may help you distinguish a normal, rolling horse to one rolling out of pain?

A

A normal, happy horse will get up and shake afterwards

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3
Q

In what age of horses would you see parascaris equorum?

A

Less than 1 year

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4
Q

What age of horses would you see Lawsonia intracellularis?

A

6 months - yearling

Or because Jamie has different shit on different slides - 3-7 months

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5
Q

What is the normal temperature of a horse?

A

37-38.5 degrees C

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6
Q

What is the normal HR of a horse?

A

36 +/- 10

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7
Q

What is the purpose of nasogastric intubation?

A
  • Asses for presence of fluid accumulation in the stomach
  • Relieve stomach distention to avoid rupture and relieve pain
  • Administer enteral fluid therapy if no reflux returned
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8
Q

What action would you take if a horse presents with signs of colic and a HR or >60?

A

Immediately pass a stomach tube

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9
Q

What structures may be palpated in the left dorsal quadrant when palpating per rectum?

A

Caudal edge of spleen
Nephrosplenic space
Nephrosplenic ligament
Left kidney

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10
Q

What structures may be palpated in the right dorsal quadrant when palpating per rectum?

A

Caecal base

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11
Q

What structures may be palpated in the left ventral quadrant when palpating per rectum?

A

Pelvic flexure of large colon

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12
Q

What structures may be palpated in the right ventral quadrant when palpating per rectum?

A

Caecum

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13
Q

What structures may be palpated at the dorsal midline when palpating per rectum?

A

Aorta

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14
Q

What structures may be palpated at the ventral midline when palpating per rectum?

A

Female reproductive organs
Bladder
Small colon

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15
Q

At what point do you take abdominal fluid from?

A

The most ventral part of the midline, possibly slightly to the right

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16
Q

What aspects of abdominal fluid can be assessed?

A
  • Colour
  • Transparency
  • Protein
  • Cytology
  • Microbiology
  • Lactate analysis
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17
Q

What is a normal abdominal fluid protein level and what does it mean when its elevated?

A

Less than 20 g/L, increase = intestinal injury

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18
Q

What is lactate an indicator of and how is it interpreted?

A

Lactate is an indicator of tissue ischaemia and when peritoneal lactate is higher than plasma lactate it indicates the ischaemia is within the abdominal cavity.

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19
Q

Which two sites may damaged intestine hide from leaking lactate into peritoneal fluid?

A

Epiploic foramen and inguinal ring (into scrotal sack)

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20
Q

What are the four treatment goals of the colic patient?

A

Relieve pain
Restore tissue perfusion
Restore metabolic status
Manage secondary complications

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21
Q

What is the onset and duration of action of flunixin?

A

15 minutes to onset, 12 hours duration

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22
Q

Why is meloxicam in some cases considered superior to flunixin for treating colic?

A

It causes less retardation of the small intestinal mucosal repair after ischaemia.

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23
Q

What side effects are seen with a2 agonists?

A

Decrease in GIT motility, CV and respiratory depression and ataxia.
Increased sweating and urine production, rarely xylazine rage

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24
Q

When is N-Butylscopolammonium bromide indicated?

A

Spasmodic colic or with hypermotility.

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25
Q

How do you calculate the size of a horses stomach?

A

1.5% of its body weight

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26
Q

What is the use of dioctyl sodium succinate (DSS) and what can it not be administered with?

A

It reduces surface tesion and allows water and fate to penetrate the ingesta. It can not be administered with paraffin oil.

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27
Q

What is the triadan number for the left wolf tooth?

A

205

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28
Q

What is the triadan number for the last molar on the bottom right?

A

411

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29
Q

When do the deciduous incisors erupt in foals?

A

‘01 ~6 days
‘02 ~6 weeks
‘03 ~6 months

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30
Q

When do a horse’s permanent incisors erupt?

A

‘01 - 2.5 years (in wear @ 3)
‘02 - 3.5 years (in wear @ 4)
‘03 - 4.5 years (in wear @ 5)

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31
Q

Which is the last permanent cheek tooth to errupt?

A

PM4 at 4 years

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32
Q

When to bottom incisor cups disappear?

A

‘01 - 6
‘02 - 8
‘03 - 9

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33
Q

When do bottom incisor dental stars appear?

A

‘01 - 8
‘02 - 9
‘03 - 10

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34
Q

What is the difference between and overjet and an overbite.

A

An overjet is rostral projection of the maxillary incisors while an overbite is rostral and ventral projection.

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35
Q

Is there any treatment for parrot mouth?

A

orthodontic braces +/- bite plate but only if done young. If not, will require life long dental care.

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36
Q

What are the 3 phases of eating

A

Prehension
Mastication
Deglutition (swallowing)

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37
Q

What drug predisposes to choke?

A

a2 agonist sedatives

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38
Q

What are the 4 main sites of oesophageal obstruction in horses?

A

Post pharynx
Thoracic inlet
Base of heart
Cardia of stomach

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39
Q

Discuss the diagnosis of choke

A
  • Clinical signs
  • Palpation
  • Inability to pass a NGT to stomach
  • Endoscopy
  • Radiography +/- contrast
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40
Q

Discuss the treatment of choke

A
  • Heavy sedation
  • Stomach tube, lavage with water +/- obstetrical lubricant
  • Oxytocin to stimulate smooth muscle contraction of distal oesophagus (efficacy?)
  • Guaifenesin for skeletal muscle relaxation
  • Withhold food and water
  • IV fluids
  • Correct electrolyte and acid-base abnormalities
  • Anti-inflammatory medicine
  • Antibiotics
  • Surgery (rately required)
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41
Q

What do mucus cells secrete what is its function?

A

Bicarbonate rich mucus, protects the epithelium from acid

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42
Q

What do parietal cells secret and what is its function?

A

Hydrochloric, acid which activates pepsinogen

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43
Q

What do chief cells secret and what is its function?

A

Pepsinogen, which is activated by HCl to pepsin which aids in digestion of proteins

44
Q

What do G cells secret and what is its function?

A

Gastrin, which acts to relax proximal stomach and enhance contractions in the distal stomach

45
Q

In what portion of the stomach gets the majority of ulcers?

A

Squamous

46
Q

Give examples of anti-ulcer drugs and their mechanism of action

A

Ranitidine - H2 antagonist
Omeprazole - proton pump inhibitor
Antacids - neutralisation
Sucralfate - reacts with HCl in stomach to form a protective barrier

47
Q

What is the normal wall thickness of the equine small intestine?

A

Less than 2mm

48
Q

What is the normal diameter of the equine small intestine?

A

Less than 4cm

49
Q

Name a prokinetic drug for the treatment of ileus

A

lignocaine

metaclopramide

50
Q

Explain the clinical signs of Lawsonia intracellularis infection

A

Chronic weight loss due to malabsorption
Intermittent mild colic
Hypoproteinaemia - Oedema
US - thick SI

51
Q

How do you diagnose Lawsonia intracellularis?

A

Serology

PCR - Ileum (surgical collection) or fecal (not as good)

52
Q

How do you treat Lawsonia intracellularis?

A

Antibiotics (Macrolides, tetracyclines) and supportive care such as colloid therapy for hypoproteinaemia

53
Q

Outline the treatment of proximal enteritis

A
  • REFLUX, indwelling NGT
  • May require surgical decompression
  • Prokinetics
  • IV fluids (large volumes)
  • Parenteral nutrition
  • Anti-inflammatories
  • Polymyxin B for endotoxin
  • +/- Antibiotics
54
Q

What age group of horses would you see inflammatory bowel disease?

A

Adult horses

55
Q

What is inflammatory bowel disease characterized by?

A

Pronounced cellular infiltration of the small and large intestines.

56
Q

What are the clinical signs of IBD?

A 
Chronic wasting
\+/- diarrhoea
\+/- colic
Hypoproteinaemia
Anaemia
57
Q

Which part of endotoxins is highly variable between bacteria serotypes?

A

O-specific chain

58
Q

Which part of endotoxins is the toxic principle?

A

Lipid A

59
Q

What are the main two organs which fail in the face of endotoxaemia?

A

Kidneys and laminae

60
Q

What are the 6 main treatment strategies for endotoxaemia?

A
  1. Inhibition of LPS release into circulation
  2. Scavenging of LPS to prevent direct effect and interaction with inflammatory cells
  3. Inhibition of cellular activity by LPS
  4. Inhibition of mediator synthesis
  5. Interference with effects of inflammatory mediators
  6. Supportive care
61
Q

How can you attempt to inhibit endotoxin release into circulation?

A

Antimicrobial therapy, however note that these kill bacteria and may increase endotoxin initially

62
Q

How can you attempt to scavenge LPS in a horse with endotoxaemia?

A
  • Immunotherapy (vaccination, anti-serum against LPS)

- Polymixin B (binds to lipid A of LPS)

63
Q

What portion of LPS does polymixin B bind to?

A

Lipid A

64
Q

What side effect must be considered before using polymixin B

A

Nephrotoxicity

65
Q

How may you attempt to inhibit cellular activation by LPS in a horse with endotoxaemia?

A

Ethyl Pyruvate blocks the production of proinflammatory mediators via blocking the activation of NF-kB

66
Q

How may you attempt to inhibit inflammatory mediator synthesis in a horse with endotoxaemia?

A
  • NSAIDs
  • Pentoxifylline
  • DON’T USE CORTICOSTERIODS
  • Antioxidants (DMSO, Allopurinol)
  • Lignocaine
67
Q

What sort of supportive care would you be giving an endotoxaemic horse?

A
  • Fluids
  • CV support
  • Manage coagulopathies
  • Treatment/prevention of laminitis
  • Nutritional support
68
Q

What is the most important risk factor associated with adhesion in horses?

A

Recent abdominal surgery

69
Q

What type of surgery predisposes horses to caecal impaction?

A

Musculoskeletal and opthalmology cases - high levels of pain

70
Q

What are the clinical signs of caecal impaction

A

May be very mild and intermittent signs of colic, however rupture may occur with no significant signs of abdominal pain. Main signs are decrease fecal production and decreased borborygmi.

71
Q

How is caecal impaction diagnosed?

A

Abdominal palpation per rectum will reveal a tight, ventral caecal band palpable on the right of the abdomen

72
Q

What is the difference between primary and secondary caecal tympany?

A

Primary - rapid gas production or reduced caecal motility

Secondary - outflow obstruction aboral to caecum (colon displacements)

73
Q

What is the difference between primary and secondary caecal perforation?

A

Primary - broodmares after parturition w/o evidence of caecal outflow obstruction
Secondary - caecal outflow obstruction

74
Q

What are the functions of the caecum?

A

Water reabsorption, electrolyte reabsorption and initiation of microbial digestion of complex carbohydrates

75
Q

Explain the two parts of reperfusion injury.

A

Part 1 - Ischaemia
No oxygen -> no ATP -> Membrane ion pump function altered and mitochondrial dysfunction -> cell membrane failure and influx of Ca, Na and H2O -> Cell necrosis -> Reactive oxygen species and proinflammatory cytokines
Part 2 - Reperfusion
Leucocyte chemotaxis & activation -> ROS -> damage to cell membranes -> further necrosis -> proinflammatory mediators -> Vicious cycle

76
Q

What are the first two organs that circulating toxins and inflammatory products reach after traversing the portal system?

A

Heart and lungs

77
Q

What are the major implications of reperfusion injury?

A

Ileus, loss of absorption and increased secretion of the intestines. Endotoxaemia,

78
Q

DMSO is available at 99% concentration. Is this fine to administer to a horse with endotoxaemia or reperfusion injury?

A

No, must be

79
Q

How many taenia does each segment of the colon have and which have haustra?

A 
Right and left ventral - 4 w/ H
Left dorsal - 1 no H
Right dorsal - 3 no H
Transverse - 2 no H
Descending - 2 w/ H
80
Q

What are the functions of the colon?

A

Microbial digestion and fluid absorption

81
Q

What may be heard on abdominal auscultation in a horse with sand impaction?

A

“surf sounds” in the ventral abdomen

82
Q

How may sand impaction be diagnosed?

A

Fecal sand sedimentation
Ultrasound
Abdominal radiographs - need very high power
History and clinical exam findings

83
Q

How may sand impaction be treated?

A

Treat primary large colon impaction first

Then administer psyllium mucilloid and paraffin oil. May scald hind limbs, so protect with vaseline

84
Q

How may sand impaction be prevented?

A

Remove access to sand

Psyllium 1 cup in feed BID for 1 week per month

85
Q

What may be seen on ultrasound with a left dorsal displacement / nephrosplenic entrapment of the colon?

A

Inability to identify the left kidney

86
Q

What treatment can be considered for dorsal displacement of the colon?

A 
IV fluids and withhold feed
Phenylephrine - alpha agonist
jog
GA and roll
Surgery - standing flank or ventral midline
87
Q

What may be found on abdominal palpation per rectum in a horse with right dorsal displacement of the colon?

A

Gas distention, inability to locate pelvic flexure

88
Q

Define peritonitis and list the ways it may be classified.

A

Inflammation of the mesothelial lining of the peritoneum, categorised as:

  • Diffuse/localised
  • Acute/chronic
  • Septic/sterile
  • Primary/Secondary
89
Q

What is a normal amount of gastric reflux in a horse?

A
90
Q

Why can there be an in an increase in serum GGT in horses with right dorsal displacement?

A

Direct pressure on common bile duct

91
Q

Why must opioids be administed only with/after an a2 agonist?

A

Otherwise agitation and hyperexcitability is common

92
Q

How many taenial bands does the descending colon have?

A

2

93
Q

Small colon obstructions are strongly associated with what infectious agent?

A

Salmonella

94
Q

When is an enema useful in a horse?

A

Only in foals :)

95
Q

What are the factors that adversely affect surgical outcome of horses with discending colon obstructive disease?

A
  • Poor blood supply
  • High concentration of collagenase
  • High intraluminal concentration of bacteria
  • High musculat activity
  • Presence of particulare faeces
96
Q

Where do most rectal tears occur and why?

A

25-30cm from anus at 10-12 o’clock position because the thickness of circular muscle decrease and it is a weak area due to penetration of terminal arteries

97
Q

Explain the grading of rectal tears

A

Grade 1 - mucosa and submucosa only
Grade 2 - muscularis only
Grade 3 - mucosa, submucosa and muscularis (serosa intact)
Grade 4 - mucosa, submucosa, muscularis and serosa (total tear)

98
Q

Explain the types of rectal prolapse

A

Type 1 - prolapse of mucosa, submusosa
Type 2 - Prolapse of full thickness rectum
Type 3 - Prolapse of full thickness rectum and intusseption of rectum/colon
Type 4 - Intusseption through anus

99
Q

How may you diagnose Clostridium perfringens?

A

PCR test for toxigenic strains, ELISA for extoxin. Large number of G+ive rods suggestive, faecal culture does not confirm disease - present in normal horses.

100
Q

What age of horses are you most likely to see Clostridium perfringens in?

A

Often enterocolitis in neonatal foals with haemorrhagic diarrhoea and death, less commonly adult horses

101
Q

How do you treat Clostridium difficile infection?

A

Metronidazole, vancomycin if resistant.

102
Q

What part of the equine GIT is most sensitive to NSAID toxicity?

A

Right dorsal colon - wall will be thickened

103
Q

What are the 5 mechanisms of weight loss in horses?

A
  • Decreased intake
  • Maldigestion/Malabsorption
  • Inappropriate utilisation of absorbed nutrients
  • Increased requirements
  • Increased losses
104
Q

Most significant diarrhoeal disease involves what part of the GIT?

A

Colon, may be SI in foals

105
Q

What are the principles of treatment of horses with diarrhoea?

A
  • Replace, maintain circulation volume
  • Replace electrolytes
  • Control endotoxinaemia & sepsis
  • Binding of enterotoxins
  • Control secondary consequences
  • Nutritional support
  • Re-establish normal GIT flora
106
Q

Discuss fluid therapy for horses with diarrhoea

A

Replace deficit - kg x %dehydration
Maintenance - Adults 60mL/kg/day, Neonates 100mL/kg/day (I think)
Account for losses

107
Q

How may you bind toxins in a horse with diarrhoea?

A

Activated charcoal, Bio-sponge

Equine Clinical Studies (2 decks)

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