EGUS Flashcards
1
Q
What is EGUS?
A
EGUS is an umbrella term used to describe erosive and ulcerative diseases of the equine stomach.
2
Q
What are the two primary conditions encompassed by EGUS?
A
Equine Squamous Gastric Disease (ESGD)
Equine Glandular Gastric Disease (EGGD)
3
Q
What is ESGD?
A
Ulceration affecting the squamous mucosa of the stomach.
4
Q
What are the subclasses of ESGD?
A
Primary ESGD
Secondary ESGD
5
Q
What characterizes Primary ESGD?
A
Occurs without any underlying gastrointestinal abnormalities.
Often associated with factors such as diet, management, and exercise.
6
Q
What characterizes Secondary ESGD?
A
Occurs due to delayed gastric outflow caused by anatomical or functional abnormalities.
Examples include pyloric stenosis or other forms of gastric retention.
7
Q
What is EGGD?
A
Ulceration affecting the glandular mucosa of the stomach.
8
Q
What factors are suggested to contribute to the pathogenesis of EGGD?
A
Breakdown of mucosal defences.
Possible contributions from NSAID use.
Bacterial infections.
Stress and other physiological stressors.
9
Q
Why is EGGD not currently subclassified further?
A
The pathogenesis of EGGD is unclear, preventing further subclassification.
10
Q
What does EGUS represent?
A
A spectrum of erosive and ulcerative diseases affecting different regions of the equine stomach.
11
Q
Why is differentiating between ESGD and EGGD essential?
A
It is crucial for understanding the underlying causes and appropriate treatment strategies.
12
Q
What is typically seen in Primary ESGD?
A
Horses with no other gastrointestinal abnormalities.
13
Q
What is strongly associated with Primary ESGD?
A
Management practices, such as feeding regimes and exercise intensity.
14
Q
What is the pathophysiology of Primary ESGD?
A
Involves increased exposure of the squamous mucosa to gastric acid.
15
Q
What are the risk factors for Primary ESGD?
A
Periods of fasting or intermittent feeding.
High-grain diets leading to increased gastric acid production.
Intense exercise that may cause acid splash onto the squamous mucosa.
16
Q
What causes Secondary ESGD?
A
Conditions that cause delayed gastric outflow.
17
Q
What are common causes of Secondary ESGD?
A
Anatomical abnormalities like pyloric stenosis.
18
Q
What results from Secondary ESGD?
A
Prolonged exposure of the squamous mucosa to gastric acid.
19
Q
How is the pathogenesis of EGGD compared to ESGD?
A
It is less understood compared to ESGD.
20
Q
What mechanisms are proposed for EGGD?
A
What mechanisms are proposed for EGGD?
21
Q
What factors may contribute to EGGD?
A
NSAID usage disrupting the protective mechanisms of the glandular mucosa.
Bacterial infections, particularly Helicobacter species, although conclusive evidence in horses is lacking.
Stress, which may alter gastric blood flow and mucus production, contributing to ulcer formation.
22
Q
What research gaps exist for EGGD?
A
Further studies are needed to elucidate the exact mechanisms.
Investigation into the role of specific bacteria, the impact of stress, and the effectiveness of various treatments.
23
Q
What percentage of untrained Thoroughbred racehorses are affected by ESGD?
A
Approximately 37% of untrained Thoroughbred racehorses.
24
Q
What does the prevalence of ESGD in untrained Thoroughbreds indicate?
A
It indicates that some level of ulceration can occur even before training begins, likely due to management and feeding practices.
25
What is the prevalence of ESGD in Thoroughbred racehorses within 2-3 months of the start of race training?
The prevalence rises dramatically to between 80-100%.
26
What does the high prevalence of ESGD during training underscore?
The significant impact of intense physical activity and associated management practices on the development of squamous gastric ulcers.
27
What is the initial prevalence of ESGD in Standardbred racehorses before training?
Around 44%.
28
How does the prevalence of ESGD change during the training period for Standardbreds?
It increases to 87%.
29
What does the increase in ESGD prevalence during training for Standardbreds highlight?
The role of exercise and training-related stress in ulcer development.
30
What is the prevalence of ESGD in endurance horses during the off-season?
Approximately 48%.
31
What does the off-season prevalence of ESGD in endurance horses suggest?
Endurance horses are at risk of ulceration even when not actively competing, possibly due to ongoing management factors.
32
What is the prevalence of ESGD in endurance horses during competition?
Ranges from 66-93%.
33
What does the increased prevalence of ESGD during competition periods indicate?
The additional stress and physiological demands placed on horses during long-distance events.
34
What is the prevalence of EGGD in leisure and sport horses?
Ranges from 54-64%.
35
What does the prevalence of EGGD in leisure and sport horses indicate?
Glandular gastric disease is a significant concern in horses not engaged in high-intensity racing or endurance activities, suggesting the influence of diet, management, and possibly stress.
36
What is the prevalence of EGGD in Australian Thoroughbreds?
Ranges from 47-65%.
37
What does the prevalence of EGGD in Australian Thoroughbreds emphasize?
EGGD is a common condition in Thoroughbreds globally, not just in high-performance athletes.
38
What do differences in ulcer prevalence between disciplines highlight?
The impact of the type and intensity of activity on the development of gastric ulcers.
39
Which horses show the highest prevalence of ESGD?
Racehorses (both Thoroughbreds and Standardbreds).
40
What does the high prevalence of ESGD in racehorses suggest?
The high-intensity, high-stress environment of race training and competition.
41
What do endurance horses demonstrate about the impact of physical exertion?
High prevalence during competition indicates the impact of prolonged physical exertion over long distances.
42
What do significant rates of EGGD in leisure and sport horses implicate?
Factors such as diet and general management practices.
43
What does the consistency in prevalence rates across different regions suggest?
Fundamental aspects of equine management, diet, and training are universally influential in the development of gastric ulcers.
44
What adjustments could be critical in reducing the incidence of EGUS?
Adjustments in training intensity, feeding practices, and stress management.
45
Why is regular monitoring for signs of EGUS crucial?
Particularly in high-risk populations such as racehorses and endurance horses.
46
What preventive measures could help mitigate high prevalence rates of EGUS?
Dietary adjustments, acid suppressive therapy, and stress reduction strategies.
47
What did the postmortem study of 3,715 horses over 72 years find regarding breed and ulceration?
Thoroughbred and Standardbred breeds are more likely to have ulcers than cold-blooded horses.
48
What did the postmortem study find regarding sex and ulceration?
Stallions had a higher prevalence of ulcers compared to mares and geldings.
49
What did two large cross-sectional studies find about the likelihood of ESGD in Thoroughbred racehorses?
No significant effect of age or sex on the likelihood of having ESGD.
50
What association was found between ESGD and age in Standardbred racehorses?
No association with the presence of ESGD, but increasing age was associated with worsening ulcer severity, especially in geldings.
51
What were the findings of the retrospective study of 684 sport and leisure horses in the UK?
No effect of age, sex, or month of presentation on the prevalence of ESGD or EGGD. A significant association between the Thoroughbred breed and the presence of ESGD in horses of any age was found.
52
What are the implications of the findings regarding breed and sex?
Factors like intensity or duration of exercise may outweigh potential age or sex effects. Thoroughbreds may be predisposed to ESGD, indicating a breed-specific risk.
53
How can trainers and the location of training yards influence ESGD risk?
Horses trained in urban areas are 3.9 times more likely to have gastric ulcers compared to those in rural areas.
54
What social and environmental factors increase the risk of ESGD?
Lack of direct contact with other horses, solid barriers instead of rails, and preference for talk radio over music radio in barns.
55
Feeding which forage is associated with an increased risk of EGUS?
Straw feeding.
56
How does lack of water access in the paddock affect the risk of EGUS?
Increases the risk of EGUS.
57
What is the general consensus on pasture turnout for reducing EGUS risk?
Generally considered to reduce the risk, but evidence is conflicting.
58
What are the positive findings regarding pasture turnout?
Horses with some access to turnout are less likely to have ESGD, and lower risk is observed in Thoroughbred racehorses turned out with other horses.
59
What conflicting evidence exists regarding pasture turnout?
No effect of pasture quality or time spent at pasture on ESGD prevalence in Thoroughbred racehorses, and no differences in intragastric pH in horses fed ad libitum grass hay and grain twice a day, regardless of housing conditions.
60
What is the belief regarding free access to fibrous feed and gastric ulceration?
Widely considered to reduce the risk, but strong evidence is lacking.
61
What are the study findings on alfalfa hay and grain diets?
They result in higher gastric pH and less gastric squamous mucosa injury compared to brome grass hay or coastal Bermuda hay with no grain.
62
What is the effect of a high fiber diet compared to an iso-energetic low fiber diet?
A high fiber diet can result in more severe ESGD lesions.
63
How does the time between forage meals affect the likelihood of ESGD?
Increased time between forage meals (>6 hours) increases the likelihood of ESGD compared to more frequent feeding (<6 hours).
64
What is consistently associated with an increased risk of ESGD?
Increased starch/grain intake.
65
What are the study findings on grain intake and ulceration?
Nonexercising animals fed grain at 1% of body weight an hour before hay showed a marked increase in ulceration. Exceeding 2 g/kg bodyweight of starch intake per day is linked to a two-fold increase in the likelihood of ESGD grade ≥2/5.
66
What is the effect of intermittent water access on EGUS risk?
Increases the risk of EGUS. Horses without constant access to water in their paddock are more than 2.5 times more likely to have EGUS grade ≥2/5.
67
How does fasting affect ESGD?
Recognized as a significant risk factor, with intermittent starvation causing and increasing the severity of ESGD. Used as an experimental model to produce ESGD.
68
Can horses with EGUS be asymptomatic?
yes, horses can be asymptomatic or exhibit various degrees of clinical signs depending on the severity and location of the ulcers.
69
What behavioral changes are commonly perceived to be linked to ulcers?
Nervousness, aggression, and self-mutilation.
70
Which type of horses are more likely to have ESGD based on nervous dispositions?
Show horses with nervous dispositions.
71
How does aggression affect ESGD in racehorses?
Aggression might limit ESGD.
72
What is the association between crib-biting and ESGD?
Crib-biting is associated with ESGD, but the mechanism is unclear.
73
What performance issues are linked to EGUS?
Poor performance, resistance to training, and decreased work ethic.
74
How does recurrent colic relate to EGUS?
Frequent bouts of colic or abdominal discomfort are strongly associated with gastric ulcers, particularly ESGD.
75
What percentage of horses with recurrent colic had gastric ulcers in one study?
83% of horses with recurrent colic had gastric ulcers; 28% had colic attributable to ulceration.
76
What appetite and weight changes can indicate EGUS?
Inappetence, weight loss, and slow eating.
77
What coat condition can be an indicator of chronic health issues like EGUS?
A dull, rough, or unkempt coat.
78
What faecal changes might accompany EGUS?
Intermittent or chronic diarrhoea and changes in manure consistency.
79
What are the specific clinical signs for ESGD?
Pain and discomfort, increased salivation, teeth grinding, and stretching.
80
What are the clinical characteristics of EGGD?
Fewer specific signs, subtle discomfort, weight loss, poor body condition, and chronic low-grade colic.
81
What is the association between ESGD and performance in Thoroughbred and Standardbred racehorses?
ESGD is significantly associated with decreased performance.
82
How is poor performance linked to the presence of ulcers in horses?
Poor performance is linked to the presence of ulcers, independent of severity or number.
83
What performance improvements have been observed post-treatment with omeprazole?
Some case studies report improved performance post-treatment with omeprazole.
84
What effects does ESGD induced by intermittent feed deprivation have on horses?
Results in reduced time to fatigue, lower increases in maximal oxygen uptake, and shorter stride length in untreated horses.
85
Why does the committee not support diagnosing EGUS based solely on clinical signs?
The clinical signs are nonspecific and poorly associated with the presence of EGUS.
86
What are the most prevalent clinical signs of EGUS at a population level?
Reduced appetite and poor body condition.
87
What does the committee recommend for confirming EGUS?
EGUS should be confirmed by performing gastroscopy.
88
What is the primary diagnostic tool for identifying gastric ulceration in horses?
Gastroscopy
89
What are the preparation steps for a gastroscopy procedure in horses?
Horses should be fasted for at least 12-16 hours and water withheld for 4-6 hours before the procedure. Sedation is typically required, and the stomach is insufflated with air for better visualization.
90
What areas of the stomach must be examined during gastroscopy to avoid missing lesions?
The entire stomach, including the pylorus and proximal duodenum, squamous and glandular mucosa, margo plicatus, antrum, pylorus, and proximal duodenum.
91
Is there a relationship between the presence of ESGD and EGGD?
No, the presence of one type of lesion cannot predict the presence or absence of the other.
92
Are there any reliable haematological or biomechanical markers for diagnosing gastric ulceration?
Currently, no reliable markers exist.
93
What is the promise and limitation of the sucrose permeability test for detecting gastric ulcers?
It shows promise for non-invasive detection by measuring sucrose concentration in the blood or urine, but its diagnostic accuracy has not been reported in clinical cases.
94
Why is empirical treatment without gastroscopy not recommended?
Due to the importance of distinguishing ESGD from EGGD and the potential treatment costs.
95
What is the Equine Gastric Ulcer Council 0–4 Grading System (1999) for ESGD?
Grade 0: Intact epithelium with no hyperkeratosis.
Grade 1: Intact mucosa with areas of hyperkeratosis.
Grade 2: Small, single or multifocal lesions.
Grade 3: Large single or extensive superficial lesions.
Grade 4: Extensive lesions with areas of apparent deep ulceration.
96
What is the current status of grading glandular lesions for EGGD?
Minimal data exist on the validity of grading glandular lesions.
97
What grading recommendation is given for EGGD?
A hierarchical grading system is not recommended until better defined. Descriptive terminology should be used to describe lesions.
98
What is a challenge for endoscopists regarding lesion importance?
Assigning clinical importance to individual lesions beyond just their endoscopic appearance.
99
What is suggested about the correlation between lesion severity and clinical signs?
More severe lesions are believed to result in more clinically significant disease, but the relationship may not be linear or consistent.
100
What is 'silent' or non-clinical gastric ulceration?
Many horses with EGUS do not exhibit clinical signs, which may mean subclinical ulcers.
101
What human comparison is made regarding mucosal integrity loss?
In humans, hyperemia of the glandular mucosa reflects acidification that activates sensory nerves and causes pain. A similar effect may exist in horses.
102
What variability is noted in treatment response?
Some horses with severe endoscopic disease do not show clinical signs and do not respond to treatment.
103
What does the committee recommend regarding the assessment of clinical relevance based on endoscopic appearance?
The assessment should not be based on endoscopic appearance alone. Clinicians should assess the relevance of lesions in light of the horse's recent usage, history, and presenting clinical signs.
104
What is the primary cause of ESGD?
Prolonged exposure of the squamous mucosa to gastric acid, leading to mucosal damage.
105
How does Hydrochloric Acid (HCl) contribute to ESGD?
Squamous mucosal cells are susceptible to damage from HCl, with severity depending on pH, concentration, and duration of exposure.
106
What role do Volatile Fatty Acids (VFAs) play in ESGD?
VFAs, byproducts of bacterial fermentation of dietary sugars, can penetrate the mucosal barrier and, in combination with HCl, exacerbate mucosal damage.
107
What is the mechanism of injury for ESGD?
HCl disrupts the outer cell barrier, causing cellular damage in deeper layers of the squamous epithelium, and VFAs enhance the extent of mucosal injury.
108
How does training and exercise contribute to ESGD?
Increased intra-abdominal pressure during exercise forces acidic gastric contents against the squamous mucosa, causing irritation and ulceration.
109
What is the correlation between training intensity and ESGD severity?
Intensive long-duration training increases the prevalence and severity of squamous lesions. The severity of ESGD is related to the intensity and duration of training.
110
How is the glandular mucosa protected against the acidic environment of the stomach?
By several defense mechanisms including mucus production, bicarbonate secretion, and adequate blood flow.
111
What leads to EGGD?
Disruption of the protective mechanisms, leading to mucosal damage despite the stomach’s naturally acidic conditions.
112
What is the role of Helicobacter pylori and other bacteria in EGGD?
Similar bacteria have been detected in horses, but their role in EGGD remains uncertain. Some studies have found Helicobacter-like organisms in horses with EGGD, while others have not.
113
How do NSAIDs contribute to EGGD?
NSAIDs can inhibit prostaglandin synthesis, crucial for maintaining mucosal blood flow and integrity. High doses of NSAIDs can cause ulceration, but standard clinical doses do not typically induce gastric ulcers when administered for short periods.
114
What does the high prevalence of EGGD in horse populations suggest?
Factors other than NSAID use are significant contributors to the prevalence of EGGD.
115
What is the committee's comment on the development of EGGD?
Multiple different mechanisms likely contribute to the development of EGGD in horses, similar to how different diseases with separate pathophysiologies result in peptic ulcer disease (PUD) in humans.
116
What are the central acid suppressors used in managing gastric ulcers?
Proton Pump Inhibitors (PPIs) and H2-Receptor Antagonists.
117
Which types of EGUS benefit from acid suppression treatment?
Both Equine Squamous Gastric Disease (ESGD) and Equine Glandular Gastric Disease (EGGD).
118
Which drug is the most studied PPI in horses and remains the drug of choice?
Omeprazole.
119
What is the role of H2-Receptor Antagonists in treating EGUS?
They competitively block the H2 receptor on parietal cells, with efficacy depending on maintaining plasma drug concentrations.
120
Why is omeprazole considered superior to ranitidine?
It is more effective for treating naturally occurring EGUS.
121
When is ranitidine used as an alternative?
When omeprazole is unavailable or ineffective.
122
Why has formulation variability increased for omeprazole?
Due to the expiration of the GastroGard® patent, leading to various formulations entering the market.
122
How is omeprazole protected from stomach acid degradation?
Through buffered paste or enteric-coated granules.
123
What do studies show about the bioavailability differences between GastroGard® and other formulations?
No significant bioavailability differences between GastroGard® and other formulations. Enteric-coated formulations have higher bioavailability compared to unprotected omeprazole.
124
What is the standard dose of GastroGard® for treating ESGD?
4 mg/kg PO once daily for 28 days.
125
What are the dosing recommendations for lower doses of omeprazole?
Buffered formulations: 2 mg/kg PO once daily.
Enteric-coated granules: 1 mg/kg PO once daily.
126
What is the recommended duration of treatment for ESGD?
Standard treatment period: 28 days, possibly reduced to 3 weeks if healing occurs by 21 days. Approximately 70-80% of ESGD lesions heal within 28 days.
127
Is the use of adjunctive therapies typically justified for ESGD?
No, adjunctive therapies are not typically justified for ESGD.
128
What are the challenges in treating EGGD with standard omeprazole treatment?
EGGD responds poorly to standard omeprazole treatment, often requiring longer treatment durations.
129
What role might bacteria play in EGGD?
Bacterial involvement is unclear, and antimicrobial treatment lacks strong evidence.
130
What is the role of failed mucosal defenses in EGGD?
Failed mucosal defenses significantly contribute to the pathogenesis of EGGD, making mucosal protectants a logical complement to treatment.
131
What is the best-studied mucosal protectant for EGGD and its mechanism of action?
Sucralfate: It adheres to ulcerated mucosa, stimulates mucus secretion, promotes prostaglandin E synthesis, and enhances blood flow.
132
What are the treatment recommendations for EGGD using combination therapy?
Omeprazole: 4 mg/kg PO once daily.
Sucralfate: 12 mg/kg PO twice daily.
Duration: Minimum of 8 weeks, with initial control examination at 4 weeks.
133
What is the committee's stance on the routine use of antimicrobials in treating EGGD?
Not justified until efficacy is appropriately documented due to the lack of evidence establishing bacteria as a contributory factor to EGGD.
134
What is the typical dose of omeprazole for ESGD prevention?
1.0 mg/kg PO once daily.
135
Is there a specific guideline for the prevention of EGGD?
No specific guidelines exist, and the efficacy of omeprazole as a prophylactic for EGGD is unclear.
136
What nutraceuticals show promise as prophylactics for both ESGD and EGGD?
Magnesium Hydroxide, Pectin-lecithin Complex, Saccharomyces Cerevisiae.
137
What are the potential benefits of using sea buckthorn berries?
Protective against EGGD in fasting models.
138
Are antacids justified as sole therapeutic agents?
No, they provide short-lived symptomatic relief but are not justified as sole therapeutic agents.
139
What is the ideal feeding recommendation to reduce EGUS risk?
Continuous access to good quality grass pasture or frequent feedings of hay (4-6 meals/day).
140
What is the recommended minimum hay intake for horses?
1.5 kg (DM)/100 kg bodyweight per day.
141
What is the recommendation for grain and concentrate feeding?
Feed sparingly, avoid sweet feed, and limit starch intake to ≤2 g/kg bodyweight per day or ≤1 g/kg bodyweight per meal.
142
How might corn oil reduce EGGD risk?
Corn oil (45 mL PO once daily) reduced gastric acid output and increased prostaglandin concentration in ponies.
143
What is the recommendation regarding water and electrolytes?
Provide continuous access to water and avoid electrolyte pastes or hypertonic solutions given PO; mixing electrolytes in feed or giving in lower doses in water is safe.
