Gastric diseases Flashcards
(29 cards)
EGUS
Equine Gastric Ulcer Syndrome
On any surface that might be affected by gastric acid
Hyperkeratosis— perforation (more sever)
Along margo plicatus usually
What are the 2 main components of EGUS
Equine squamous gastric disease (ESGD) can be primary or secondary
Equine glandular gastric disease (EGGD)- can be analysed anatomically or descriptively
Primary ESGD
In intensive management
Otherwise normal GIT
Secondary ESGD
Secondary to delayed gastric emptying from other diseases
Locations of EGGD
Cardia
Fundus
Antrum
Pylorus
Description of different types of EGGD
Focal/multi-focal or diffuse
Mild/moderate or severe
Flat and haemorrhagic or flat and fibrinosuppurative
Depressed with or withour blood clots or depressed and fibrinosuppurative
Prevelance
Affected breeds and age groups
Thorough and Standardbreds: 70-94%
Sport: 58%
Avg population: 10.3%
- rare in draught!
- on margo plicatus sq mucosa along lesser curv
Foals: 25-57%
- Glandular and gastroduodenal ulcers
Causes and pathophys
Imbalance of inciting and protective factors
What are the inciting factors
HCl
Pepsin
Bile acids
What are the protective factors
Mucus bicarbonate
Adequate circ
PGE2
Gastroduodenal motility
Acid exposure: HCl
Parietal cells continuosly
pH 2-6- depends on diet (saliva is alkaline)
Stim: gastrin which responds to increased gastric dilation and rising pH, hist and Ach (vagus nerve)
Inhibitors: somatostatin and epidermal growth factor (in saliva)
Bile salts and acids
Duodenogastric reflux may happen normally
Causes irritation after 14 hrs fast
Pepsin
Chief cells
Proteolytic on gastric mucosa
Extrinsic factors
NSAID’s: COX-1 inhib: decr blood flow and mucus prod
Stress
Diet
- Conc feeds
- low fibre
- decr saliva
- intermittent feeding
- starvation
Delayed gastric emptying
During exercise: Intraabd and gastric P incr and gastric fluid line rises
Gastric ulcers in newborn foals Causes
Gastric pH <2 within 48hrs
Mothers mik buffers the gastric acid
Hyperplasia and hyperkeratosis of sq mucosa
Glandular mucosa along GREATER curv
Concurrent diseases:
- Decr GI motility
- Splanchnic hypoperfusion
- Speticaemia
Gastric Ulcers in Newborn foals Clinical signs and treatment
Clinical signs: anorexia, Dx, colic, sudden death
Therapy: H2 antags! ranitidine and sucralfate
PPI’s???
NO NSAIDS!!!
Sucklings and Weanings
Sq mucosa along greater curv
Clinical signs: Dx, no appetite, poor growth and BC
Gastroduodenal ulcer disease in foals
Ranges from diffuse inflamm to sever ulceration and thickening of duodenal wall
Delayd gastric emptying
Bruxism
Gastroesophageal reflux
Asp pneumonia
May lead to:
- Gastric or duodenal rupture
- Stricture
- Ascending cholangiohepatitis
Outbreaks associated with rotavirus
Yearlings and Adult horses
Usually SQ mucosa along greater curv
(if on fundus or pylorus will be on glandular mucosa)
Bleeding without anaemia or hypoproteinaemia
Clinical signs: anorexia, colic after feeding, poor performance, poor BC
Squamous ulcer grading system
0: intact epithelium
1: hyperaemia and hyperkeratosis
2: small single or small multifocal lesions
3: large single or multifocal lesions or extensive supf lesions
4: multiple deep, bleeding ulcers
Treatment of ulcers
Continuous feeding of good quality food
PPI’s: omeprazole
H2 antags- ranitidine IV: limited in adults, used in neonates
PGE2-Misoprostol PO
Sucralfate PO- stim mucus and PGE2 production
Acute gastric dilation and impaction
Draught
Innapropriate feeding- feed swells after feeding
- Corn
- Fresh green hay or alfalfa
- bread
Acute gastric dilation and impaction pathogenesis
Fermentation produces gas, VFA’s and lactate
FLuid influx
Gastic dilation– colic
P on diaphragm- resp compromised
Decr venous return
Hypovol shock
Gastric rupture
Acute gastric dilation and impaction: clinical signs
Sudden onset with fast progression
Severe continuous colic
Profuse sweating
Tahcycard
Decr GI motility
No rectal findings
Haemoconc
incr lactate in the blood
US shows enlarged stomach
