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Special Pathology - GIT > Stomach > Flashcards

Stomach Flashcards

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1
Q

Rumen tympany

A

aka bloat; accumulation of gas in the rumen

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2
Q

frothy bloat

A

formation of stable foam - balance between pro and anti-foaming factors is upset

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3
Q

Three causes of frothy bloat

A
  1. Primarily dependent on leguminous diets high in soluble protein (bloat inducing legumes, such as alfalfa and clover, are up to 4.5% soluble protein).
  2. Decreased saliva production; saliva has anti-acid and anti-foaming properties.
  3. Decreased rumen pH promotes formation of a stable foam from soluble proteins
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4
Q

Free gas bloat

A

physical or functional defects affecting the esophagus, esophageal groove or vagus nerve can prevent eructation;

  1. Esophagus: obstruction by foreign bodies (apple) or by extra-esophageal compression (lymphosarcoma).
  2. Failure to eructate - lesion involving vagus nerve (abscess, chronic pneumonia) or localized reticuloperitonitis involving the left ventral wall of the reticulum (adhesions and pain interfere with the cardia clearing reflex)
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5
Q

Traumatic reitculoperitonitis

A

aka hardware disease; penetration of the reticulum by a sharp foreign body

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6
Q

Sequelae of Traumatic reitculoperitonitis

A
  • Localized peritonitis with or without abscesses may involve the diaphragm, spleen, and liver.
  • Foreign body penetration through the diaphragm causing traumatic reticulopericarditis.
  • Adhesions or abscesses between reticulum and diaphragm causing omasal transport failure (indigestion), or chronic bloat.
  • Adhesions or abscesses that cause decreased abomasal motility and impaction (indigestion)
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7
Q

Acute carbohydrate engorgement leads to _____.

A

Rumen lactic acidosis

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8
Q

How does acute carbohydrate engorgement lead to rumen lactic acidosis?

A
  • Quantities of readily digestible carbohydrates are rapidly consumed
  • Rumen flora produce excessive volatile fatty acids
  • Rumen pH lowered
  • Lowere rumen pH favors overgrowth of streptococci and lactobacilli that produce excessive amounts of lactic acid
  • As volative fatty aicds and lactic acid levels increase rumen pH drops from normal pH of 5.5 - 7.5 to 5.0 - 4.0, causing acidosis
  • The osmotic effect of fatty acids draws fluid from the circulation into the rumen
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9
Q

The result of acute carbohydrate engorgement/rumen lactic acidosis:

A
  • Dehydration, hypovolemia, acidosis, rumen atony, splashy rumen, and toxemia; bloat (frothy or free gas) may also occur
  • Rumenitis appears as “matting” and loss of rumen papilli
  • Areas of infarction may develop due to mycotic infection of rumen wall blood vessels
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10
Q

Sequellae of acute carbohydrate engorgement/rumen lactic acidosis

A
  • Opportunistic pathogens like Fusobacterium and fungi invade the rumen wall
  • Mycotic infection of rumen wall and blood vessels
  • This condition may occur subclinically.
  • Bacterial transportation to liver causes abscesses in liver
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11
Q

Vagal indigestion

A
  • Damage of vagus nerve causes outflow dysfunction
  • Abscesses, lymphosarcoma, traumatic reticuloperitonitis
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12
Q

What kind of dogs are most at risk to gastric dilatation/volvulus?

A

large, deep-chested young dogs

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13
Q

What has been hypothesized to predispose dogs to gastric dilatation/volvulus?

A

Delayed gastric emptying

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14
Q

Describe gastric dilatation/volvulus in dogs

A
  • Gas distended stomach contains fluid and ingesta mixed with frothy mucoid substrate.
  • Gastric dilatation may be accompanied by volvulus with gastric ischemia/infarction
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15
Q

Sequellae to gastric dilatation/volvulus in dogs

A
  • Decreased VENOUS return via compression of caudal vena cava and portal vein leads to decreased cardiac output and hypotensive shock.
  • Reduced function of the hepatic mononuclear phagocytic system allows endotoxins to accumulate.
  • Disseminated intravascular coagulation (DIC) develops in the presence of endotoxins, venous stasis, hypoxia and metabolic acidosis
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16
Q

Abomasal displacement in cattle

A
  • Post parturient condition in high producing dairy cows on high grain rations
  • Hypocalcemia causes low muscle tone ⇒ Abomasal atony is believed to play a role in this condition⇒Abomasum becomes distended with gas and rises to right or left side.
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17
Q

Abomasal displacement in cattle: LDA vs RDA

A
  • LDA is not usually a cause of death
  • RDA is life threatening
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18
Q

Gastric distention is mainly seen in ______, and may be seen in _____.

A

mainly horses; may see in nonhuman primates

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19
Q

Gastric distension results from…….

And can result in ……

A
  • Gaseous distention of the stomach results from engorgement of grain or other palatable food
  • Ileus develops
  • May have reflux of intestinal content in horses with small bowel obstruction
  • Can result in gastric rupture
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20
Q

Acute gastritis is characterized as?

A
  • Multifocal or diffuse.
  • Characterized by hemorrhage, congestion and edema with damage or loss of surface epithelium
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21
Q

Common causes of acute gastritis:

Common causes of acute abomasitis:

A
  • Nonsteroidal anti-inflammatory drugs
  • Toxic metabolites such as found in uremic dogs
  • Acute abomasitis may be caused by clostridia, mycotic agents, parasites, and systemic viral infections
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22
Q

Uremic gastritis is ______, and is most common in _____.

A
  • Mineralization of basement membranes, glands, vessels, and interstitium of mucosa
  • Most common in carnivores with chronic renal failure and uremia
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23
Q

What disease does the common name “braxy” stand for?

A
  • acute emphysematous abomasitis caused by infection with Clostridium septicum
24
Q

Chronic gastritis

A
  • prolonged exposure to agents that cause gastritis or to other factors can result in chronic inflammation of the stomach
25
Q

Hypertrophic gastritis: lesions - grossly and microscopically, cause

A
  • Gastric mucosa is thrown into thick folds resembling convolutions of the brain.
  • Diffuse or focal
  • Microscopically–severe epithelial hyperplasia, and infiltrates of mononuclear inflammatory cells
  • Cause is unknown, associated with protein losing gastropathy, diarrhea
26
Q

Parietal cell hyperplasia leads to thickening of mucosa with ______ syndrome.

A

Zollinger Ellison Syndrome

27
Q

Dog breeds susceptible to hypertrophic gastritis

A
  • Basenji
  • Beagle
  • Boxer
  • Bull terrier
28
Q
  • What is Chronic hypertrophic pyloric gastropathy?
  • What kinds of dogs does it most commonly involve (small/large, young/old, male/female)
  • Symptoms
  • Cause
  • Associations
  • Gross lesions
  • Is it neoplastic?
A
  • Hypertrophy of mucosa or smooth muscle
  • Small breeds of dogs, middle aged or older
  • Males >>>>> females
  • Chronic vomiting, weight loss, gastric distention
  • Non-neoplastic
  • Unkown cause
  • Commonly associated with inflammation in mucosa
  • Enlarged mucosal folds
29
Q

Eosinophilic gastritis:

  • Description
  • Lesions
  • May be accompanied by?
  • Cause?
    • May predispose rottweiler’s with this syndrome:
A
  • Extensive fibrosis with eosinophil infiltration may cause flattening of gastric rugae and marked thickening of the stomach wall
  • Focal or diffuse
  • May be accompanied by arteritis
  • Likley a hypersensitivity response to agents unkown
  • May occur in a hypereosinophilic syndrome in rottweilers
30
Q

Lymphocytic-Plasmacytic Gastritis

A
  • Chronic gastritis and gastric ulcers have been associated with gastric infection by spiral-shaped microorganisms in the genus Helicobacter.
  • Multiple species are affected including dogs, cats, ferrets and non-human primates
31
Q

Gastric mucosal barrier consists of certain gastrointestinal defense mechanisms which cannot be defined on a strictly anatomic basis. They are characterized by a number of physiochemical processes which seek to ……

Anatomic components include:

A
  • ….maintain normal mucosal function by limiting the back diffusion of H+ ions.
  • Mucous layer, epithelial cells, and vasculature
32
Q

Five components of gastric mucosal barrier

A
  1. Gastric mucus
  2. Regulation of intramural pH
  3. Mucosal regeneration
  4. Cytoprotective functions of prostaglandins
33
Q

Components of the Gastric Mucosal Barrier:

Gastric mucus

A
  • Thin layer adherent to the lipid membranes of surface epithelial cells.
  • Protects against luminal pepsin and provides a mixing barrier for surface neutralization of H+ ions by HCO3- ions secreted from the underlying epithelium
34
Q

Components of the gastric Mucosal Barrier:

Regulation of Intramural pH

A
  • Normal mucosal blood flow ensures adequate oxygenation and energy substrates
  • provides a pool of HCO3- ions and a means of disposal of back diffused H+ ions
35
Q

Components of the gastric mucosal barrier:

Mucosal Regeneration

A
  • Gastric epithelium has a high proliferation rate which enables continual replacement of shed cells and restitituion of epithelial integrity following acute damage (providing the basement membrane remains intact)
36
Q

Components of Gastric Mucosal Barrier:

Cytoprotective functions of prostaglandins

A
  • Prostaglandins are saturated, oxygenated fatty acids found in almost every mammalian cell.
  • Prostaglandins of the E type occur in copious amounts in the gastrointestinal system in general.
  • Current evidence indicates that prostaglandins play an important role in maintaining integrity of the gastroduodenal mucosa by virtue of their antisecretory and cytoprotective properties
  • Protective effects of prostaglandins:
    • Decrease gastric acid secretion
    • Increase mucus and bicarbonate secretion
    • Increase mucosal blood flow
    • Enhance cell regeneration
37
Q

Breakdown of the gastric mucosal barrier

A
  • The gastric mucosal barrier can be disrupted in any number of situations that permit back diffusion of H+ ions, especially when the ability to neutralize or remove H+ ions from the mucosa also is impaired.
  • Back diffusion of H+ ions triggers a series of events that ultimately increases the amount of acid entering the surface epithelial cells and subepithelial tissues
38
Q

Acute hemorrhagic gastritis ⇒ ______ ⇒ _______

A

Acute hemorrhagic gastritis ⇒ gastric erosions ⇒ multiple small acute peptic ulcers

39
Q

Acute gastric erosions and ulcers:

  • Factors that may be involved in pathogenesis:
  • These factors lead to:
A
  • Irritation by drugs - NSAID’s cause direct epithelial toxicity and inhibit prostaglandin synthesis
  • Excess acid secretion via hypergastrinemia
  • Reflux of bile and duodenal contents into the stomach
  • Mucosal ischemia - caused by shock or hypotension (trauma, sepsis, burns, hypothermia) is likely an extremely important factor. Hypoxemia compromises integrity of the protective surface barrier and allows back-diffusion of acid through the damaged mucosal surface

Reduced effectiveness of the normal intact gastric mucosal barrier via direct injury to epithelial cells, back-diffusion of acid and pepsin and reduced mucosal perfusion or ischemia causes gastric mucosal damage that can progress to acute gastric ulcers.

40
Q

Chronic Gastric Ulcers

  • Description
  • Location
  • How do they differ from acute ulcers?
A
  • Usually solitary and may occur at any level of gastrointestinal tract (esophagus, stomach, duodenum) exposed to the action of acid-peptic juices
  • Most occur in the pyloric antrum and proximal duodenum
  • Chronic ulcers differ from acute ulcers because they are usually solitary and have a predilection for specific locations in the stomach and duodenum
  • There appears to be overlap in the pathogenesis of chronnic and acute ulcers as far as casues and role of decreased mucosal resistance to injury
41
Q

Gastric/Duodenal Ulcer Disease in Small Animals

Describe pathogenesis of each clinical conidtion:

  1. Cirrhosis
  2. Chronic Renal failure
  3. Mast Cell Tumor
  4. Gastrinoma
  5. Chronic Pancreatitis
  6. Gastric neoplasms
A
  1. Uncertain (multifactorial)
  2. Vascular/toxic metabolic products?
  3. Hiastmaine stimulates H+ secretion, vascular dilation
  4. Gastrin stimulates H+ secretion
  5. Decreased bicarbonate in pancreatic juices
  6. Neoplastic cell infiltrates
42
Q

Gastric/Duodenal Ulcer Disease in Large Animals

Describe the anatomic area selected and the pathogensis for each animal listed:

  1. Foals <4 months
  2. Adult horses
  3. Young Cows
  4. Swine
A
  1. Foals - stomach and duodenum - unkown/stress, NSAID’s
  2. Adult horses - squamous area, often asymptoamtic - unclear/NSAIDs
  3. Young cows - abomasum - uknown (seen during postpartum period)
  4. Swine - esophageal area of stomach - multifactorial (finley ground pelleted ration; hot weather)
43
Q

Pyloric Stenosis

  • Associated with ….
  • Interferes with ….
  • Causes…..
A
  • Narrowing of pylorus/thickening of pyloric area
  • Interference with gastric emptying
  • Projectile vomiting
44
Q

Gastric Parasites - Equine

  • Gastrophilus intestinalis* vs Gastrophilus nasalis
  • Both produce these lesions:
A
  • Gastrophilus intestinalis
    • Bots - fly larvae attach to the stratified squamous portion of the gastric mucosa
  • Gastrophilus nasalis
    • Bots - fly larvae attach to the glandular portion of the gastric mucosa
  • Both produce 1-2 mm ulcers at attachment site
45
Q

Gastric Parasites - Equine

Draschia megastoma

A
  • Filarid worm found in 2.5 - 3.0 cm diameter noduels (brood pouch) on the margo plicatus
  • Focal or multifocal granulomatous gastritis in horses
  • Eggs released through pore, pass out in feces, consumed by fly larvae that are the intermediate hosts
  • Not usually associated with clinical signs
46
Q

Gastric Parasites - Ruminants

  • Ostertagia* sp.
  • Acute vs Chronic
A
  • Infest cattle and buffalo
  • Reside in the mucosa
  • Ingest blood products
  • Acute - hemorrhagic inflammation
  • Chronic - loss of glands, fibrosis of the mucosa; achlorhydria (low production of gastric acid) and unthriftiness
47
Q

Gastric Parasites - Ruminants

Haemonchus contortus

A
  • Blood sucking nematode that infests small ruminants
  • Reside on the surface of the gastric mucosa
  • Releases anti-coagulant causing hemorrhagic in abomasum - usually in sheep
48
Q

Gastric Parasites - Cat

  • Ollulanus tricuspis*
  • What types of lesions does it cause?
A
  • Mild gastritis that can lead to fibrosis of the mucosa
49
Q

Gastric Parasites - Cat

  • Gnathostoma* sp.
  • What types of lesions does it cause?
A
  • Granulomatous masses in submucosa (5 cm or more in diameter)
50
Q

Gastric Parasites - Pigs

Hyostrongylus rubidus

A
  • Thin sow syndrome
  • Gastric mucosa is thickened, catarrhal, cobblestoned
  • Mucus metaplasia of parasitized and adjacent glands
  • Formation of submucosal lymphoid follicles
51
Q

Gastric Tumor:

Leiomyoma

A
  • Benign
  • Smooth muscle tumor
  • Clinically significant when they obstruct gastric inflow or outflow
52
Q

Gastric Tumor:

Adenomatous polyps

A
  • Benign
  • Epithelial tumors of the gastric mucosa in dogs
  • May cause vomiting
53
Q

Gastric Tumor:

Adenocarcinoma

A
  • Malignant
  • Occur most often in the dog and cat; chow dogs appear to have an increased risk
  • Causes vomiting and weight loss
  • Pyloric antrum often involved
  • Ulceration and thickening of the stomach wall is common - this may result in a flask-shaped stomach
  • Metastases occur in the regional lymph nodes, lungs, and other organs
54
Q

Gastric Tumor:

Lymphosarcoma

A
  • Malignant
  • Stomach of the dog and cat
  • Abomasum of bovine
  • Nodular or diffuse infiltrates of neopasltic lymphoid cells can infiltrate all layers of the stomach and may produce gastric ulcers
55
Q

Gastric Tumors:

Squamous Cell Carcinoma

A
  • Malignant
  • Large cauliflower-like or ulcerated mass in the squamous part of the stomach in the horse
  • Transmural infiltration with implatnation of the peritoneal surface is common
  • Often metastasize widely before detection
56
Q

Gastric Tumors:

Leiomyosarcoma

A
  • Malignant counterpart of leiomyoma (smooth muscle tumor)
  • Tumor cells are more undifferentiated and mitotic activity is greater
  • Invasion of adjacent structures and metastasis may occur

Special Pathology - GIT (5 decks)

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