Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Sys Path II > Stomach > Flashcards

Stomach Flashcards

1
Q

Which stomach of Ru is most closely related to the simple-stomached animals in terms of structure & function?

A

abomasum
(third compartment of new world camelids)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the structure of the fundic part of the stomach?

A
  • fundic mucosa is lined by numerous folds & produces HCl acid (parietal cells) & pepsinogen (chief cells)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the structure of the pyloric part of the stomach?

A
  • lined by epithelium w/ mucous-secreting glands.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the structure of the esophageal part of the stomach in some species?

A

in Eq, Sw, & Rat, the esophageal part (pars esophagea) is nonglandular & lined by stratified squamous epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the dividing line btwn the nonglandular and the glandular epithelium in the horse?

A

margo plicatus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the steps of a postmortem examination of the stomach/abomasum?

A
  • open along the greater curvature & gently scrape away ingesta to examine mucosa, do not wash w/ water
  • examine the quality & quantity of the gastric contents & remove them
  • examine the gastric mucosa, in particular the colour, thickness, & integrity of the mucosal surfaces
  • examine the content for presence of blood (if needed to perform occult blood test)
  • always take fundic mucosa for histo, plus obviously pathologic changes
  • If Haemonchosis is suspected, first tie off pylorus & cardia to collect content for worm count, & then open the abomasum in a bucket/tray
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Who does simple gastric dilation occur in?

A
  • a variety of animals including primates
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Explain gastric dilation & volvulus in Dogs?

A
  • in large, deep-chested breeds of dogs, distended stomach w/ food & gas can rotate on mesenteric axis counter clockwise (180, 270, or 360 degrees when the abdomen is viewed from the dorsal aspect), resulting in a gastric volvulus w/ an obstructed esophagus that prevents eructation & thus further contributes to gastric dilation
  • the spleen, attached to the stomach by the gastrosplenic ligament, rotates w/ the stomach & is thus folded back upon itself & located in the R cranial abdomen against the diaphragm
  • both gastric & splenic vein are compressed, resulting in a congested & edematous gastric wall (venous infarction in later stages) & congested spleen, b/c the arterial blood supply remains patent longer than venous drainage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are predisposing factors to gastric dilation & volvulus in dogs?

A
  • hereditary predisposition (large breeds)
  • obstruction of the cardia that prevents eructation & emesis
  • obstruction of the pylorus that prevents passage of gastric contents
  • repeated episodes of gastric dilation, overfeeding, &/or postprandial exercise, that contribute to stretching & relaxation of the gastrohepatic ligament
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the cause of death w/ gastric dilation & volvulus in dogs?

A
  • acid-base imbalance
  • increased intragastric pressure interferes w/ venous return from portal circulation
  • myocardial depressant factors released from pancreas
  • decreased cardiac output & shock
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What does gastric dilation & volvulus look like in Sw?

A
  • torsion of the stomach or the small intestine is one of the main causes of sudden death in adult breeding stock
  • the twist can involve the stomach, the spleen, part of the liver, &/or the intestine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What does gastric dilation & rupture look like in Eq?

A
  • acute gastric dilation & rupture in equids occurs most frequently as a terminal event in small intestinal obstruction, ileus, & displacement
  • it can also be the result of rapid ingestion of fermentable feeds or grains, a situation analogous to grain overload w/ lactic acidosis in cattle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does gastric dilation & rupture look like in non-human primates?

A
  • in research facilities occasionally develop acute gastric dilation associated w/ food restriction & accidental overfeeding
  • this cause is unknown, but two principal factors seem to be the intragastric fermentation associated w/ Clostridium perfringens, & abnormal gastric function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

In other animals what is gastric/abomasal dilation usually secondary to?

A
  • ulcers, pyloric stenosis, overeating, gastritis/abomesitis, vagal indigestion, etc.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the clinical consequences of gastric dilation?

A
  • severe distention compromises respiration & cardiovascular function & electrolyte balance
  • gastric rupture (usually along the major curvature) is often the ultimate cause of death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How do you distinguish btwn ante-mortem & post-mortem gastric rupture?

A
  • the only reliable indicator of ante-mortem rupture of the stomach is the presence of hemorrhage along the margins & evidence of acute inflammation (ex: fibrin strands)
  • if these changes are not present on gross exam, histo exam of the margins is recommended to rule out postmortem distention & rupture of the stomach/abomasum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Who does abomasal displacement and volvulus usually occur in in cows?

A
  • high-producing dairy cattle during the first 6 weeks after parturition
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the causes of abomasal displacement & volvulus in cattle?

A
  • abomasal atony due to heavy grain feeding (volatile fatty acids decrease motility)
  • impaired movement of ingesta & gas formation
  • hypocalcemia at the onset of lactation -> decreased strength of muscle contractions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the clinical features of a displaced abomasum (right or left sided)?

A
  • anorexia, dehydration, decreased amount of feces, ketouria, characteristic high-pitched ping subsequent to percussion over displaced abomasum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is important about a left-sided abomasal displacement?

A
  • most common
  • generally nonfatal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is important about a right-sided abomasal displacement?

A
  • occurs only in 10-15%
  • it is considered more significant b/c it may progress to abomasal volvulus resulting in an abomasal venous infarction & death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is important about Clostridium septicum in abomasitis?

A
  • it is a cause of hemorrhagic abomasitis w/ submucosal emphysema of lambs & occasionally calves (a disease known as BRAXY)
  • this disease is most common in Europe, but it occasionally also occurs in North America
  • generally, the disease follows ingestion of frozen feeds contaminated w/ the causative Clostridium spp.
  • the lesions are produced by the exotoxin of the bacteria, & death therefore is due to an exotoxemia (similar to Clostridial myositis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is fundic mucosal infarction in pigs?

A
  • in many cases of septicemia in pigs (ex: salmonellosis, swine dysentery, Glasser’s disease, & colibacillosis), venular thromboses occur in the fundic mucosa/submucosa resulting in congestion, hemorrhage, venous infarction, & ulceration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is gastritis often associated w/ clinically?

A

vomiting, dehydration, & metabolic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what are the different types of gastritis?

A
  • acute mild gastritis
  • canine hemorrhagic gastroenteritis (acute hemorrhagic diarrhea syndrome)
  • chronic gastritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Who is acute mild gastritis most common in and why?

A
  • dogs rather than cats due to less discriminating eating habits
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the clinical signs of acute mild gastritis?

A

vomiting & inappetence w/o systemic signs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the causes of acute mild gastritis?

A
  • ingestion of spoiled or contaminated food, foreign objects, toxic plants, chemicals, NSAIDs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the prognosis of acute mild gastritis?

A
  • not fatal & transient
  • it is successfully diagnosed & treated clinically (feed withdrawal & antiemetics)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Who does canine hemorrhagic gastroenteritis (acute hemorrhagic diarrhea syndrome) most often occur in?

A

most often occurs in smaller breeds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the cause of canine hemorrhagic gastroenteritis (acute hemorrhagic diarrhea syndrome)?

A

not clear but infection w/ Clostridium perfringens of unknown type is suspected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the clinical signs of canine hemorrhagic gastroenteritis (acute hemorrhagic diarrhea syndrome)?

A
  • hematemesis & hematochezia (often w/ hemoconcentration > PCV .60%)
  • on presentation, animal may be moribund & may die due to cardiovascular collapse, renal failure, &/or DIC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What would you see on endoscopy/necroscopy for canine hemorrhagic gastroenteritis (acute hemorrhagic diarrhea syndrome)?

A
  • diffuse hemorrhagic necrosis of gastrointestinal superficial mucosa (most severe in colon)(w/ Clostridial bacteria identified by histo)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Parvo vs canine hemorrhagic gastroenteritis (acute hemorrhagic diarrhea syndrome)?

A
  • parvoviral enteritis may have similar gross appearance, but histologically there is cryptal necrosis in the small intestines & it DOES NOT AFFECT THE STOMACH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the clinical signs of chronic gastritis?

A
  • emesis & if intestines are also affected than diarrhea & occasionally hematochezia
  • dehydration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are the different types of chronic gastritis?

A
  • eosinophilic gastritis as part of gastroenteritis or gastroenterocolitis
  • lymphoplasmacytic gastritis
  • hyperplastic (also called hypertrophic) gastritis in dogs
  • uremic gastritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Who is eosinophilic gastritis as part of gastroenteritis or gastroenterocolitis seen in?

A

in dogs & less commonly in cats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is the etiology of eosinophilic gastritis as part of gastroenteritis or gastroenterocolitis?

A

etiology is poorly understood: 2 conditions should be considered when the diagnosis of eosinophilic gastroenteritis is made on an endoscopic biopsy of the stomach, duodenum , & colon (REMEMBER TO ALWAYS SAMPLE ALL 3 SITES WHEN DOING ENDOSCOPIC GIT BIOPSY TO INCREASE THE CHANCE OF YOUR DIAGNOSIS!!!):
1. Parasites
2. hypersensitivity reaction to unknown allergen or food intolerance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

why should you consider parasites w/ eosinophilic gastritis as part of gastroenteritis or gastroenterocolitis?

A
  • gastrointestinal parasites (ex: Toxocara canis, Physaloptera canis, Ollulanus tricuspis, Trichuris vulpis, Ancylostoma spp - last two can cause blood & protein loss) & their products induce variable degrees of eosinophilic inflammation occasionally w/ mild to moderate hyperplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

why should you consider a hypersensitivity reaction to an unknown allergen or food intolerance w/ eosinophilic gastritis as part of gastroenteritis or gastroenterocolitis?

A
  • most likely due to feed ingredients or preservatives or medications (allergens)
  • sometimes this is accompanied by a peripheral eosinophilia & skin disease
  • more severe aspect of this condition can present as hemorrhagic enteritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What will you see with endoscopy w/ eosinophilic gastritis as part of gastroenteritis or gastroenterocolitis?

A
  • the gross lesions of eosinophilic gastroenteritis are rather nonspecific (mild hyperemia & thickening of the mucosa, increased amounts of mucus)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

How do we diagnose eosinophilic gastritis as part of gastroenteritis or gastroenterocolitis?

A

Histo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is the cause of lymphoplasmacytic gastritis?

A

not determined - chronic irritative/antigenic stimulus by gastric bacteria (including Helicobacter spp.) suspected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is characteristic of hyperplastic (hypertrophic) gastritis in dogs?

A

thickened rugae secondary to hyperplasia of gastric glands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are the causes of hyperplastic (hypertrophic) gastritis in dogs?

A
  • chronic retention of gastric fluid & reflux of intestinal bile
  • immune-mediated process resulting in hyperplastic lymphoplasmacyctic gastritis
  • idiopathic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is FOCAL hyperplastic (hypertrophic) gastritis in dogs?

A

Antral (pyloric) hyperplastic (hypertrophic) gastritis:
- in older small breed dogs
- clinical signs of upper GI obstruction (post-prandial vomiting)
- diagnosis by endoscopy & radiography (endoscopic biopsy may not be useful diagnostic test b/c samples are taken only from the superficial mucosa)
- must be differentiated from pyloric obstruction due to pyloric muscular hypertrophy which presents w/ similar clinical signs (may need imaging or laparoscopy to differentiate from pyloric hyperplastic gastritis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is DIFFUSE hyperplastic (hypertrophic) gastritis in dogs?

A
  • chronic giant hypertrophic gastropathy is a rare disease in Ca which are affected by weight loss, D+, V+, & hypoproteinemia
  • cause is unknown
  • ante-mortem diagnosis is made by endoscopy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Who, besides Ca, can also get hyperplastic (hypertrophic) gastritis?

A
  • described also in primates & Eq due to parasitism
49
Q

What is the cause of uremic gastritis?

A

chronic renal disease/failure

50
Q

What would you see on endoscopy/necropsy in uremic gastritis? What about microscopic exam?

A
  • major gross lesions are nonspecific congestion & edema of the gastric mucosa w/ occasional ulceration
  • caused by injury to capillaries w/in the lamina propria associated w/ elevated concentrations of nitrogen-derived metabolic waste products in the systemic circulation from kidney failure
  • microscopic exam reveals mineralization of the glands, vessels, & lamina propria of the gastric mucosa
51
Q

gross lesions of uremia in dogs?

A
  • severe bilateral renal fibrosis (etc.) -> chronic renal failure
  • secondary bilateral parathyroid hyperplasia
  • bilateral erosive glossitis (+/- stomatitis)
  • mineralization of intercostal muscles
  • uremic gastritis w/ mid-mucosal mineralization
  • uremic pneumonitis
  • osteodystrophy fibrosa (osteopenia)
52
Q

What is an ulcer?

A
  • a mucosal defect in which the entire epithelial thickness w/ the basement membrane is lost
53
Q

What is a perforating ulcer?

A
  • penetration through the remaining tissue layers to the peritoneal cavity
54
Q

What is an erosion?

A
  • partial- thickness epithelial loss
55
Q

How are chronic ulcers different from acute ulcers?

A

chronic ulcers have an indurated rim caused by fibrosis & epithelial hyperplasia (attempts of epithelial regeneration)

56
Q

What would you see on endoscopy/ necropsy w/ gastric ulcers?

A
  • sharply demarcated areas of mucosal loss often covered w/ exudate
57
Q

What are the clinical signs of gastric ulcers?

A
  • vomiting & hematemesis
  • anorexia
  • abdominal pain
  • anemia secondary to gastric bleeding resulting in melena (digested blood in feces)
  • decreased production (ex: milk) & performance
  • exsanguination -> death
  • peritonitis & septicemia due to perforating ulcer -> death
58
Q

What is the pathogenesis of gastric ulcers?

A

conditions necessary for ulcer development could be boiled down to an imbalance btwn acid secretion & mucosal protection:
- high gastric acidity
- infection
- local disturbances in blood flow
- NSAIDs
- local disturbances or trauma to the mucosal epithelial barrier

59
Q

Relationship btwn high gastric acidity and the pathogenesis of gastric ulcers?

A
  • mast cell tumours in dogs & occasionally cats stimulate gastric HCl secretion through histamine release
  • gastrinoma: functional tumour of G-cells in duodenum or pancreatic islets that produce gastrin which increases the secretion of HCl & causes gastric ulceration (occurs rarely in Ca; in humans it is called Zollinger-Ellison syndrome)
60
Q

Relationship btwn infection and the pathogenesis of gastric ulcers?

A
  • in certain primates (including humans), a substantial portion of gastric & duodenal ulcers are the result of infection w/ Helicobacter pylori (this same bacterium has been epidemiologically linked to gastric adenocarcinoma)
  • in ferrets, Helicobacter mustelae acts similarly
  • in dogs & cats, similar gastric Helicobacter-like organisms (GHLOs) are present in the stomach, but their relationship w/ ulcer formation or neoplasia is not established at this stage (it appears that the stomachs of as many animals w/o ulcers are as heavily colonized by these bacteria as are those animals w/ ulcers)
61
Q

Relationship btwn local disturbances in blood flow and the pathogenesis of gastric ulcers?

A
  • stress-induced disturbance in blood flow by neurogenic, hypovolemic, or septic shock results in gastric ischemia
62
Q

Relationship btwn NSAIDs and the pathogenesis of gastric ulcers?

A
  • NSAIDs depress prostaglandin formation resulting in decreased blood perfusion, decreased secretion of bicarbonate (buffering system disrupted), & some of them have direct toxic effects on vascular endothelium (ex: phenylbutazone)
63
Q

Relationship btwn local disturbances or trauma to the mucosal epithelial barrier and the pathogenesis of gastric ulcers?

A
  • this injury can be due to back flush of bile salts from the duodenum or ingestion of lipid SOLVENTS ex: alcohol
64
Q

What are gastric ulcers like in horses?

A
  • ulceration is affecting almost always only pars esophagea
  • many foals are affected asymptomatically
  • some w/ severe gastric ulceration may have abdominal pain, bruxism (grinding of the teeth), ptyalism, & gastric reflux
  • in 40-90% of competitive & performance horses, ulceration of pars esophagea is present & is most severe in those that are worked the hardest
65
Q

What are gastric ulcers like in pigs?

A
  • ulceration is also affecting only pars esophagea
  • it occurs commonly in penned pigs & is associated w/ multiple factors: finely ground grain, ingredients in diets (large quantities of skimmed milk or whey), & stress of confinement rearing, etc.
  • occasionally, it is fatal due to exsanguination
66
Q

What are gastric ulcers like in cattle?

A
  • significance of abomasal ulceration ranges from subclinical to fatal
  • in calves, ulcers are associated w/ dietary changes or mechanical irritation of the abomasum by roughage
  • in dairy cattle, ulcers are associated w/ heavy grain feeding (lactic acidosis) at the time of parturition, displacement of the abomasum, BVD, impaction, torsion, & gastric lymphoma
67
Q

Relevancy of parasitism?

A
  • parasitic diseases are relatively easy to prevent & control by modern anthelmintics
  • accordingly, they are not v commonly encountered in clinical practice
  • however, resistance to drugs & climate change (more rain in the prairies) appear to be related to higher incidence of parasitic diseases in small Ru
68
Q

What are the gastric parasites of horses?

A
  • Gasterophilus intestinalis & Gasterophilus nasalis (equine bots) are commonly seen in Eq on inadequate deworming regimens (this may be a hint to check for more important pathogenic parasites ex: Strongylus vulgaris)
  • Bot fly (Gasterophilus intestinalis) lays eggs on the hairs of the distal limbs of the horse, & bot fly (Gasterophilus nasalis) lays its eggs around the nose of the horse.
  • the larvae hatch after being moistened & warmed by licking , invade oral mucosa, & travel to the pars esophagea (Gasterophilus intestinalis) & glandular stomach & duodenum (Gasterophilus nasalis)
  • both spp attach to the mucosa via their hooked mouthparts (maxillae)
  • the larvae pass in the feces (next year), pupate, & develop into flies
  • bot flies may annoy horses which may injure themselves by trying to get rid of the flies
  • larvae cause minimal damage which is usually clinically insignificant, but suggest inadequate deworming protocol
69
Q

What are important abomasal parasites of Ru?

A
  • haemonchus contortus
  • ostertagia ostertagi & Ostertagia circumcincta
70
Q

Who is Haemonchus contortus?

A
  • known as the barber pole worm
  • most common in sheep & goats
71
Q

What is the lifecycle of Haemonchus contortus?

A
  • hyperinfested pastures containing numerous 3rd-stage larvae are the source of infection which can be acute (sudden death), subacute (hypoproteinemia & anemia), or chronic (weight loss & eventual hypoproteinemia & anemia)
  • larvae on grasses are ingested by the host & enter the abomasum, where they may lie dormant w/in the gastric glands (hypobiosis) during periods of climatic adversity (cold or dryness)
  • hypobiosis may be terminated in females by stress of parturition during spring, which will follow w/ subsequent contamination of pastures & lamb infection
  • after development to adults, they exit from the abomasal glands to the surface, attach via a buccal tooth & suck blood
  • eggs pass in the feces, completing the life cycle
72
Q

what are the clinical signs of Haemonchus contortus?

A

they are blood feeders (loss of both erythrocytes & protein), therefore they cause:
- severe anemia -> pale mucous mbs
- hypoproteinemia -> generalized edema (bottle jaw)
- weight loss (non-specific sign)
- usually w/o D+ if not complicated by other GIT disorders

73
Q

How do we diagnose Haemonchus contortus?

A
  • presumptive diagnosis may be made based on observation of a large number of adult worms in abomasum together w/ severe hypoproteinemia (edema) & anemia observed clinically or at post mortem exam
  • the definitive diagnosis at necropsy is based on semiquantification of abomasal parasite load together w/ anemia & generalized edema due to hypoproteinemia
74
Q

Who affects calves w/ similar signs to Haemonchus contortus in sheep?

A

Haemonchus placei

75
Q

Who are Ostertagia ostertagi & Ostertagia circumcincta

A
  • cause ostertagiosis in cattle & sheep, respectively
76
Q

What are the lifecycles of ostertagia ostertagi & Ostertagia circumcincta?

A
  • animals ingest L3 larvae which burrow into the abomasum glands & molt into early stage of L4 larvae
  • if development into adult stage proceeds immediately ‘Type I’ disease occurs
  • if the larvae become dormant (hypobiosis), the disease will be delayed & it happens during synchronous maturation & emergence of hypobiotic larvae from the mucosa usually during winter (this is called Type II disease)
77
Q

How are abomasal glands significantly damaged by larval development & emergence w/ ostertagia ostertagi & Ostertagia circumcincta?

A
  • parietal & chief cells are replaced by mucus cells (mucous cells from metaplasia & hyperplasia) accompanied by inflammation
  • loss of parietal cell results in loss of acidic pH (abomasal achlorhydria)
  • intercellular junction btwn poorly differentiated mucus cells are not tight (leaky) resulting in: protein-losing gastropathy -> systemic hypoproteinemia; back-diffusion of pepsinogen into lamina propria & circulation)
78
Q

What are the clinical signs of ostertagia ostertagi & Ostertagia circumcincta?

A

inappetence, D+, wasting, generalized edema (due to hypoproteinemia)

79
Q

What would you see on necropsy w/ ostertagia ostertagi & Ostertagia circumcincta?

A
  • ‘Morocco leather’ or ‘cobblestone’ appearance of the abomasum of heavily infested animals
  • generalized edema due to hypoproteinemia (NO anemia)
  • diagnosis: above 2 findings are often sufficient for diagnosis (proper worm count w/ digestion of abomasal mucosa may be performed to confirm diagnosis
80
Q

Who causes mucosal thickening & mucus metaplasia/hyperplasia in the stomach of pigs?

A

Hyostrongylus rubidis

81
Q

What does neoplasia of the stomach look like in Eq?

A

SCC of the pars esophagea is v invasive & metastatic

82
Q

What does neoplasia of the stomach look like in Bo?

A

lymphoma is caused by the Bo leukemia virus & has an apparent predilection for the abomasum, R atrium, & uterus

83
Q

What does neoplasia of the stomach look like in Ca & Fe?

A

gastric adenocarcinoma is locally invasive & metastatic; lymphomasarcoma can also occur

84
Q
A

Fundic gland

85
Q

Postmortem exam of stomach or abomasum

A
86
Q

Postmortem exam of stomach or abomasum

A
87
Q

where should you take a sample of the stomach for histo?

A
88
Q
A

gastric dilation in rabbit

89
Q

Ca

A

gastric dilation & volvulus

90
Q

Eq

A

Gastric dilation & rupture

91
Q

Eq

A

gastric dilation & rupture

92
Q

Eq

A

gastric dilation & rupture (fibrinous)

93
Q

What 4 things happen when you obstruct a blood vessel?

A
  1. congestion
  2. edema
  3. hemorrhage
  4. necrosis/ischemia
94
Q

Calf

A

abomasal volvulus

95
Q

calf

A

abomasal volvulus (opened)

96
Q

calf

A

mycotic abomasitis

97
Q

calf

A

mycotic abomasitis & omasitis

98
Q
A

Hemorrhagic & emphysematous abomasitis (do not confuse w/ torsion)

99
Q
A

Hemorrhagic & emphysematous abomasitis (do not confuse w/ torsion - can see emphysema inside & not diffuse discolouration)

100
Q
A

hemorrhagic & emphysematous abomasitis

101
Q

ca & fe

A

gastritis

102
Q

Ca

A

hemorrhagic gastritis

103
Q
A

Physaloptera rara

104
Q
A

antral (pyloric) hyperplastic gastritis

105
Q
A

antral (pyloric) hyperplastic gastritis

106
Q
A

hyperplastic gastritis

107
Q

biopsy will reveal mineralization, Fe

A

uremic gastritis

108
Q

Eq

A

pars esophagea ulceration

109
Q

Ca

A

gastric ulcer w/ exsanguination

110
Q
A

perforating abomasal ulcer

111
Q

Eq

A

gasterophiliasis

112
Q
A

anemia

113
Q
A

Haemonchus contortus

114
Q
A

Haemonchus contortus

115
Q

What is this condition called?

A

bottle jaw

116
Q
A

Ostertagia ostertagi

117
Q
A

Ostertagia ostertagi

118
Q

Who?

A

Ostertagia ostertagi arrested larva (early L4) in fundic gland

119
Q

How do you need to change your sampling method for the stomach when you suspect Ostertagia ostertagi?

A

need to sample further down b/c mucus cells will be extended

Sys Path II (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions