Gastric diseases

Question 1

EGUS

Answer 1

Equine Gastric Ulcer Syndrome

On any surface that might be affected by gastric acid

Hyperkeratosis— perforation (more sever)

Along margo plicatus usually

Question 2

What are the 2 main components of EGUS

Answer 2

Equine squamous gastric disease (ESGD) can be primary or secondary

Equine glandular gastric disease (EGGD)- can be analysed anatomically or descriptively

Question 3

Primary ESGD

Answer 3

In intensive management

Otherwise normal GIT

Question 4

Secondary ESGD

Answer 4

Secondary to delayed gastric emptying from other diseases

Question 5

Locations of EGGD

Answer 5

Cardia

Fundus

Antrum

Pylorus

Question 6

Description of different types of EGGD

Answer 6

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

Question 7

Prevelance

Affected breeds and age groups

Answer 7

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

Question 8

Causes and pathophys

Answer 8

Imbalance of inciting and protective factors

Question 9

What are the inciting factors

Answer 9

HCl

Pepsin

Bile acids

Question 10

What are the protective factors

Answer 10

Mucus bicarbonate

Adequate circ

PGE2

Gastroduodenal motility

Question 11

Acid exposure: HCl

Answer 11

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)

Question 12

Bile salts and acids

Answer 12

Duodenogastric reflux may happen normally

Causes irritation after 14 hrs fast

Question 13

Pepsin

Answer 13

Chief cells

Proteolytic on gastric mucosa

Question 14

Extrinsic factors

Answer 14

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

Question 15

Gastric ulcers in newborn foals Causes

Answer 15

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

Question 16

Gastric Ulcers in Newborn foals Clinical signs and treatment

Answer 16

Clinical signs: anorexia, Dx, colic, sudden death

Therapy: H2 antags! ranitidine and sucralfate

PPI’s???

NO NSAIDS!!!

Question 17

Sucklings and Weanings

Answer 17

Sq mucosa along greater curv

Clinical signs: Dx, no appetite, poor growth and BC

Question 18

Gastroduodenal ulcer disease in foals

Answer 18

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

Question 19

Yearlings and Adult horses

Answer 19

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

Question 20

Squamous ulcer grading system

Answer 20

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

Question 21

Treatment of ulcers

Answer 21

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

Question 22

Acute gastric dilation and impaction

Answer 22

Draught

Innapropriate feeding- feed swells after feeding

• Corn
• Fresh green hay or alfalfa
  
  • bread

Question 23

Acute gastric dilation and impaction pathogenesis

Answer 23

Fermentation produces gas, VFA’s and lactate

FLuid influx

Gastic dilation– colic

P on diaphragm- resp compromised

Decr venous return

Hypovol shock

Gastric rupture

Question 24

Acute gastric dilation and impaction: clinical signs

Answer 24

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

Question 25

Acute gastric dilation and impaction: diagnosis

Answer 25

Nasogastric tubing

US

Question 26

Acute gastric dilation and impaction: Differentials

Answer 26

Primary vs secondary gastric content- ileus, enteritis, impaction

Gastric diseases: inflamm, ulcer, obstruction, neoplasm

Spasmodic colic

Question 27

Acute gastric dilation and impaction: treatment

Answer 27

Spasmolytics, analgesics

Stomach tubing and lavage

IV fluids

Prognosis is good if caught early, more prolonged there is a risk of gastric rupture

Complications:

• acute laminitis
• haem gastritis
  
  • colitis

Question 28

Gastric parasites

Answer 28

Gasterophilosis

Draschia megastoma

Question 29

Gastric squamous cell carcinoma

Answer 29

Older!! >20

Weight loss and poor appetite

Anaemia

Slow progression

Diagnose via gastroscopy sometimes may be visible on US