Gastric Disease in Horses Flashcards

1
Q

Name some disorders of the equine stomach

A
  • EGSD – squamous disease in adults
  • EGGD – glandular gastric disease in adults
  • Gastric disease in foals – important but not that common
  • Gastric rupture – primarily adults but not always
  • Gastric impaction - primarily adults but not always
  • Habronemiasis – main parasitic disease in the stomach
  • Gasterophilus – just educate owners it’s a pointless disease to treat for
  • Gastric neoplasia
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2
Q

What is the pathology of ESGD (equine squamous gastric disease)?

A
  • EQUINE SQUAMOUS DISEASE
  • Acid dependent disease
  • Equine stomach split into 2. One part (above margo line??) doesn’t have same protective things to protect against acid – when acid splashes off onto the surface of the squamous region. Anything that REDUCES GASTRIC PH will have an impact on this disease – especially if its low for a longer period of time.
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3
Q

With equine squamous gastric disease (ESGD), what is there an imbalance between?

A

Imbalance between:

–Mucosal aggressive factors

  • HCl
  • Pepsin
  • Bile acids
  • Other organic acids

–Mucosal protective factors absent in squamous region

  • Bicarbonate
  • Mucus
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4
Q

Name some mucosal aggressive factors

A
  • HCl
  • Pepsin
  • Bile acids
  • Other organic acids
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5
Q

Name some mucosal protective factors absent in squamous region

A
  • Bicarbonate
  • Mucus
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6
Q

What plays a very important role in enhancing blood flow and promoting the secretion of the mucus-bicarbonate layer?

A

PGE2

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7
Q

What happens if mucosal blood is affected?

A
  • PGE2 plays a very important role in enhancing blood flow and promoting the secretion of the mucus-bicarbonate layer
  • THUS ANYTHING that affects mucosal blood flow WILL predispose animals to the development of gastric disease
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8
Q

What stimulates the production of surface PL’s, enhance mucosal repair and control [Na] within cells preventing cell swelling and death?

A

PG’s also stimulate production of surface PL’s, enhance mucosal repair and control [Na] within cells preventing cell swelling and death

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9
Q

In foals and adults, what are some things that can cause a reduction in gastric blood flow?

A

•Need at least disruption of mucosal protective factors which often relates to a reduction in gastric blood flow – lots of things that can disrupt blood flow but no evidence to suggest the likely causation

–Stress

–NSAIDs

–Furosemide

–Hypovolaemia – colic, D+, sepsis

–Anorexia, no feeding or intermittent feeding – boidy not going to send blood to gastric mucosa as not stimulated – no gastrin being produced from those methods of masticating and development of salivary production

–Ileus

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10
Q

What are some things that are likely to cause ESGD in adult horses?

A
  • Squamous region less protected than the glandular region
  • Likely prolonged exposure to HCl, pepsin and VFA’s
  • Gastric pH likely important in this form of disease
  • Lower pH if not buffered with food

–Ileus (inc also in bile acids in stomach)

  • More carbohydrates in diet – more likely to have more VFA’s in stomach – dissociated at low pH – more likely to cause disease
  • Stress – impact on gastrin production and will ultimately the amount of acid that is in the stomach

-Buffering with food, primarily fibre

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11
Q

Which horses is ESGD (squamous ulceration) more common in?

A
  • Complex and multifactorial
  • 60-95% prevalence – depends on population!
  • Often thought of as a disease of the performance horse, but common in brood mares also

–Race horses have more carbs and less fibre in their diets

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12
Q

What are the clinical signs of ESGD in adult horses?

A
  • In 95% cases (not always this high) this causes NO DISEASE
  • Most of the disease proposed to be caused by this condition is drug company driven – drugs to treat this are very expensive!! Need to work out which horses needs treating and which ones have clinical signs
  • Many horses with grade 2 (3) ulcers or less, are unlikely to have clinical signs
  • Rarely MAY cause (if grade 3 or above)

–….. May have mild acute or recurrent colic

–decreased appetite and then weight loss/ reduction in body condition BUT NOT IN THE FACE OF A NORMAL APPETITE

–poor performance – unwilling to move forward**

–attitude changes – behaviour changes e.g. girthing pain, colt backed**

–** - most likely clinical signs, can be really tricky to differentiate from other causes of poor performance or having a bad attitude!

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13
Q

What are some clinical signs of grade 3+ ulcers with ESGD in adult horses?

A

–May have mild acute or recurrent colic

–decreased appetite and then weight loss/ reduction in body condition BUT NOT IN THE FACE OF A NORMAL APPETITE

–poor performance – unwilling to move forward**

–attitude changes – behaviour changes e.g. girthing pain, colt backed**

–** - most likely clinical signs, can be really tricky to differentiate from other causes of poor performance or having a bad attitude!

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14
Q

What is the diagnosis for ESGD?

A

Gastroscopy

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15
Q

What is the treatment for ESGD?

A

•Omeprazole – a proton- pump inhibitor

–Licensed for the horse (SID)

–Expensive although getting cheaper – many insurance companies won’t pay for this unless definitively diagnosed. £350 – 500 per month for treatment but a months treatment will fix 90% of these horses.a

–Prophylactic and therapeutic doses licensed – may not be appropriate to use prophylactically

•Ranitidine – H2-blocker – some work done on it, but almost no one uses it

–More effective in rested than competing horses – doesn’t work in working horses really

–Not licensed, slightly cheaper but needs giving TID (3xdaily)

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16
Q

How does omeprazole work for the treatment of ESGD?

Cost?

A

•Omeprazole – a proton- pump inhibitor

–Licensed for the horse (SID)

–Expensive although getting cheaper – many insurance companies won’t pay for this unless definitively diagnosed. £350 – 500 per month for treatment but a months treatment will fix 90% of these horses.a

–Prophylactic and therapeutic doses licensed – may not be appropriate to use prophylactically

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17
Q

How does ranitidine work for the treatment of ESGD?

License?

A

•Ranitidine – H2-blocker – some work done on it, but almost no one uses it

–More effective in rested than competing horses – doesn’t work in working horses really

–Not licensed, slightly cheaper but needs giving TID (3xdaily)

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18
Q

How can you prevent ESGD?

A
  • About manipulation and management of the diet. 75% of horses probably don’t need what they got given in a bucket – hay or haylage would reduce the prevalence of this disease. Little and often feeds is better (closer to wild)
  • Dietary management if possible

–Small feeds little and often

–Frequently not possible

–More fibre in diet

–Small feeds prior to exercise as the work can increase risk of acid splash into squamous mucosa

  • Low dose omeprazole – licensed for this purpose – anecdotally this is become less common
  • Pectin-lethicin compounds – dietetics – shown to have some efficacy

–Also found in sugar beet – high in pectin, has some evidence to show its effective as a preventative

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19
Q

How can you use dietary management to prevent ESGD?

A

•Dietary management if possible

–Small feeds little and often

–Frequently not possible

–More fibre in diet

–Small feeds prior to exercise as the work can increase risk of acid splash into squamous mucosa

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20
Q

What drugs/medications can you use to prevent ESGD?

A
  • Low dose omeprazole – licensed for this purpose – anecdotally this is become less common
  • Pectin-lethicin compounds – dietetics – shown to have some efficacy

–Also found in sugar beet – high in pectin, has some evidence to show its effective as a preventative

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21
Q

Describe this

A

Shows image of squamous and glandular mucosa – line is the middle is margo plicatus . If we see lesions, will see them just running in squamous mucosa just above the margo line

22
Q

What is the margo plicatus?

A

A region called the margo plicatus is present which separates the glandular and non-glandular parts of the equine stomach. The non-glandular area is lined with squamous epithelium (not columnar)

23
Q

Describe grades 1-4 on squamous ulceration (from the EGUS council)

A

1- mildest, mucosa still intact but hyperkeratinisation on the surface – variation of normal sometimes, unlikely to have clinical signs

2- multiple small multifocal lesions that are ulcers. Can be extensive, sometimes don’t cause CS’s – if a lot, more likely to treat

3 – more larger and extensive that might be deeper, some might bleed – much more likely to have CS’s

4 – deep craters, often very large and end up having to heal in a way a skin wounds would – contract and granulate – much longer to do this!

24
Q

What is EGGD?

A
  • “New”/ emerging disease – increasing in prevalence,
  • Compared to EGUS is less common, but increasing in prevalence based on recent literature
  • More likely associated with clinical signs
  • Likely multi-factorial and is a syndrome
  • Is a gastritis
  • Appears to wax and wane so may run a prolonged course – might be 3-6 months to fix!
25
Q

What is EGGD thought to be caused by?

A

•We need to determine what underlying cause is – we literally have no idea!

–Thought maybe to be immune-mediated (may relate to diet) or infectious (become less likely now though)

26
Q

What is the problem with using biopsies to diagnose for EGGD?

A

•Biopsies are problematic and difficult!

–Transendoscopic not representative of full thickness

–Disease only manifests at pyloric antrum, but often whole glandular region affected

27
Q

What are the presenting signs of EGGD?

A
  • Changes in temperament including nervousness and aggression
  • Cutaneous sensitivity manifested as biting of the flanks and resentment of girthing, grooming, leg aids or rugging
  • Changes in rideability including reduced willingness to work and reluctance to go forward
  • Unexplained weight loss
  • Reduced appetite or altered eating patterns
  • Colic (mild and possibly recurrent)
28
Q

What are the different risk factors for EGGD?

A

Different risk factors to squamous disease

–Undertaking more exercise per days of the week

–Less common in those performing at a higher level – less stressed and different management

–Less likely to be lame, calmer, more likely to have weigh loss secondary to reduce appetite

–Increased number of carers…different management?/stress?

–If they work more than 5 days a week, the risk starts to increase

–Horses that have multiple keepers – increased risk

29
Q

What is the diagnosis for EGGD?

A

Gastroscopy

30
Q

What is the treatment for EGGD?

A

•Treatment

–Omeprazole monotherapy is NOT appropriate – only 20% get better!

–Three options:

  • Oral omeprazole and sucralfate – increases mucosal blood flow (not for its ‘ulcer-lining’ effects – only 20% get better with oral therapy!
  • Misoprostol – 60-75% get better – increases PGE2
  • Injectable omeprazole – NEW KID ON THE BLOCK, ONCE A WEEK IM, data for this at the moment – injectable does seem to be more effective than oral, might suggest it does have a role to play and this might be about acid suppression, might be about something else
  • NO evidence for antimicrobials
  • Steroids for refractory cases – in those horses where nothing else works! INHIBIT COX AND LOX, REDUCE GASTRIC BLOOD FLOW AND INCREASE CORTISOL – WHICH IS WHAT STRESS DOES- SO WHY DOES IT WORK?! NO IDEA – BUT DOES SEEM TO WORK IN SOME CASES
  • Omeprazole reduces acid secretion, but by itself orally doesn’t work very well. Sucralfate – crap bandage, but increases PGE and mucosal blood flow – certainly seems to increase usefulness with omeprazole
31
Q

What are some recommendations for the preventions for EGGD?

A
  • Provide a minimum of 2 rest days from work per week
  • Turn-out where possible provided the horse does not become stressed by turn-out. Some horses that are not accustomed to turn-out may be less stressed in a stable environment
  • Minimise changes in equine companions and human carers
  • Minimise management changes and other potential stressors
  • Feed 2 litres of chaff or an equivalent volume of forage 30 mins prior to exercise
  • Feed 250g sugar beet twice daily or pectin-lethicin supplements
  • Add corn oil to diet
32
Q

What is gastric disease in foals?

How do thye preesnt?

A

Gastric disease in foals - glandular disease

  • Very serious issue – life threatening disease!
  • Often of concern in sick, septic, Perinatal Asphyxia Syndrome, stressed and hospitalised foals
  • Present with moderate to severe colic signs in young foals
  • Bruxism and ptyalism older foals (preweaning)
  • Gastric disease leads to oesophageal (reflux) and pyloric/ duodenal strictures and gastric rupture (older foals)

–Increased risk of strictures

•Ischaemic damage and reduction in mucosal blood flow and not of acid damage - may ultimately contribute

–Therefore omeprazole is NOT an appropriate treatment for these guys!

33
Q

What does reduction in gastric acid in goalds lead to?

What does this mean we should avoid and what should we promote?

A

•Acid in the stomach is there for a reason

–Acid helps to reduce live bacterial load entering the intestines from food and environment

–If we use acid suppressants - increases risk of D+ - so we want to increase blood flow rather than suppressing acid!

  • Reduction in gastric acid predisposes foals particularly to developing severely secondary bacterial infections caused by Clostridial disease esp C. difficile
  • As the acid is a secondary problem, the focus should be on returning gastric blood flow to normal rather than suppressing acid
34
Q

How can you diagnose gastric disease in foals?

A

Gastroscopy, Faecal occult blood, contrast radiography, abdominal ultrasound, peritoneocentesis

35
Q

What is the treatment and prognosis for gastric disease in foals?

A

•Treatment: VERY controversial – two camps – become less controversial, still older vets that want to give omeprazole to every foal but more have move to treatment with sucralfate

–Omeprazole (or ranitidine) OR

–**Sucralfate**

–If concurrent oesophageal ulceration – sucralfate always

•Prognosis: Much less favourable than either ESGD or EGGD in adults

36
Q

What is gastric disease in pigs?

What do clinical signs include

A
  • Common condition growing pigs (up to 60% at slaughter) and then in sows (5% prevalence) – often around cardia
  • Clinical signs incl

–Anorexia

–Vomiting

–Signs associated with anaemia

–Teeth grinding

–Black faeces

–Dead (due to haemorrhage)

–Weight loss in growers with a chronic form

37
Q

What are common causes for gastric disease in pigs?

A
  • As in horses multifactorial
  • Various nutritional factors have been identified

–low protein, low fibre, high energy, high wheat, vitamin E, selenium or Zn def, high levels of iron, copper or calcium, high unsaturated fats, whey and skimmed milk based diets

•Physical aspects of the feed

–More ground worse; pelleted diets better

•Management issues

–Irregular feeding patterns and shortage of feeder space, increased stocking densities, stress, transportation, excessive aggression between animals, poor stockmanship, fluctuating environmental temperatures

•Other disease

–Link between pneumonia and sepsis; Helicobacter

•Breed

38
Q

What is the diagnoses and main differential diagnoses for gastric disease in pigs?

A
  • Diagnosis – clinical signs and post mortem examination; faecal occult blood test
  • Main DDx

–Eperythrozoonosis

–Hyostrongylus rubidus (gastric worm)

–Porcine enteropathy

39
Q

What is gastric rupture in adults horses often secondary to?

What happens afterwards?

Diagnosis?

A

–Secondary to small intestinal strangulating lesions – very specific way of presenting:

•Often have been painful and then become pain free

–Because of decreased pressure

–Then they:

–Horses quickly progress to septic shock because of peritonitis

  • Reluctant to move
  • HR>100BPM
  • Purple MM
  • No GI borborygmi

–Diagnosis – peritoneal tap

40
Q

What is gastric rupture in foals often secondary to?

A

–As in adults, but rarer

–Secondary to perforating gastric ulcers

•Most likely secondary to necrotising enterocolitis (bacterial infection)

41
Q

What can gastric impaction be caused by?

A
  • Acute or chronic
  • Usually associated with anorexia, weight loss if chronic to colic signs if acute
  • Primary or secondary motility disorder
  • Rarely associated with poor quality forage, foreign objects or improper mastication
  • Can see secondary to dental disease, gorging(primarily sugar beet they get hold of) or inadequate water consumption and DEHYDRATION (e.g. endurance horses, but usually rare in other horses)
42
Q

What is the diagnosis for gastric impaction?

A

Diagnosis – Idea when pass a nasogastric tube – hitches and gets stuck and often don’t get fluid back; gastroscopy (convincing diagnosis is still being full after 24 hrs of food being witheld); abdominal ultrasound, (abdominal radiographs in ponies and sm horses), surgery

43
Q

What is the treatment for gastric impaction?

A

•Treatment

–The longer the stomach is distended, the less likely its functions will return

–Aggressive gastric lavage – Coke (I recommend caffeine free – send them wild!!) – coke has stable bubbles and carbonic acid stabilised in these bubbles has a big positive impact on breaking down the fibre mat

–Pro-motility agents –erythromycin and metaclopormide

–(Surgery to empty)

44
Q

What is habronemiasis?

A

Cause summer sores around the mucosa, sometimes around the eyes, usually mucosa of mouth – fly related disease – eggs get laid, larvae hatch and larve go burrowing and get themselves into oesophagus and into stomach and GIT – develop and end up with worms

45
Q

How important is Habronemiasis?

What is the diagnosis and differential diagnoses?

A
  • Usually of little consequence
  • Q common in terms of causing summer sores
  • Penetrates and migrates to the stomach
  • Usually of little consequence
  • Susceptible to avermectins administered q 4 weeks for 3 doses
  • Can cause pyloric outflow obstruction rarely
  • Present with mild, recurrent colic
  • Intermittent tachycardia and NG reflux
  • DX: Gastroscopy and biopsy
  • DDX: SCC, EGGD
46
Q

What is the difference between these 2 pictures?

A

Left – normal

Right – horse that was confirmed to have habronemiasis

47
Q

What is the life cycle of gasterophilus?

A
  • Adult flies are active in middle of day in warm months
  • Lay their white/yellow sticky eggs on the legs of horses. Flies 1-1.5cm in length-look like small bumblebees
  • Eggs hatch spontaneously or when stimulated by the horse’s saliva whilst grooming
  • L3 attaches to squamous gastric mucosa along the margo pliacatus (Gastrophilus intestinalis) or to the dorsoproximal part of the duodenum (Gasterophilus nasalis)
  • Larvae then survive here for 10-12 months before passed out to pupate in faeces
48
Q

What is the importance of gasterophilus?

What is it responsive to?

A

•Totally unimportant in terms of clinical disease

–IF in vvvv high numbers could block duodenum – this form v rare in UK

•IS a condition that needs client management

–Get very upset when pupae are passed in faeces

  • Often see a few in horses
  • Very responsive to avermectins
  • NOT a cause of poor performance

49
Q

How common is gastric squamous cell carcinoma?

What do they present with?

Diagnosis?

Treatment?

A
  • Most common tumour of the stomach, but RARE – 3 cases in referral practice in 14 years
  • Present with weight loss, recurrent, chronic, mild colic, anorexia and depression
  • Can metastasise to local LN and lungs
  • No treatment – resection not possible, not really responsive to any treatment we have available to us
  • Dx: Gastroscopy (cant always see) and abdominal ultrasound
50
Q

What is this?

A

Gastric squamous cell carcinoma

Looks like very deep ulcer, but doesn’t have other changes to mucosa you would expect to disease