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what part of the stomach contains stratified squamous epithelium?
non glandular portion (continuous with esophagus epithelium)
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what 3 receptors are required for the secretion of gastric acid? what pump then allows for secretion of HCl? 4
- histamine 2
- gastrin
- acetylcholine
- H-K-ATPase pump
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since the stratified squamous portion of the stomach has no protective layer from HCl, how is it protected from acid injury?
- highly impermeable until pH <2.5 (then damage would occur)
- feed bolus in lower portion protects from exposure to HCl/bile acid
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what are glandular mucosa defenses against HCl? 4
- mucus barrier
- HCO3 secretion
- rapid regeneration and repair
- reflux of basic duodenal secretions
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how does grain affect pH environment in stomach?
- less chewing required so less saliva
- more VFAs produced in gastric fluid
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what is legume forage (alfalfa) effect on pH in stomach?
great buffering effect - protects squamous epithelium from exposure to HCl
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How does exercise affect gastric physiology?
- withholding feed and feeding high concentration diets incr. risk of mucosal injury
- strenuous exercise decr. pH in upper portion
- "sloshing effect"
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what is role of prostaglandins in gastric physiology?
- PGI2 - vasodilation so adequate blood flow
- PGE2 - encourages mucus secretion to protect mucosa
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where are erosions/ulcers usually found in the stomach? how does this compare to where foals get ulcers?
- squamous epithelium along margo plicatus
- (foals get primary gastric/duodenal ulcer disease)
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what are some risk factors associated with adult horses acquiring EGUS? 6
- housing in stalls, meal feeding
- stress, show horses
- high CHO diets
- incr. exercise intensity; race horses
- NSAIDs
- H. pylori
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what are some clinical signs associated w/EGUS in adults? 6
- mild intermittent colic (coincides with meals)
- decr. appetite; failure to finish grain
- loss of body condition
- poor hair coat
- alterations in attitude
- (so CS may not be severe or obvious)
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how do you definitively diagnose EGUS?
gastroscopy on fasted patient
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what is expected PCV/TS on patient with EGUS? Will there be blood in the feces?
- normal PCV/TS (no anemia)
- not even occult blood in feces - microbes break it down
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what is the difference between grade 0 and 1 ulcer?
- 0: WNL
- 1: mucosa intact, squamous hyperkeratosis
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how is grade 2, 3, and 4 ulcer described?
- 2: small single/multifocal lesions
- 3: large, superficial
- 4: extensive lesions/deep ulcerations
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what do you do for a suspected EGUS patient if scoping not available?
- treat anyway - response to tx is considered diagnostic
- (improved attitude/appetite/coat/resolution of colic)
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what is the goal of EGUS treatment?
- incr. gastric pH and decr. HCl secretion
- (incr. roughage, decr. grain, meds to alter HCl secretion)
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what are some examples of H2 receptor antagonists? 4
- ranitidine (extended period of therapy required)
- cimetidine (high doses req)
- famotidine
- nizatidine
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what are advantages of using Omeprazole (H+pump inhibitor) instead of histamine blockers? 4
- in addition to decr. HCl, can also promote healing of ulcer
- low doses can PREVENT ulcer formation
- only licenced product for tx/prevention
- single daily dose
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what is MOA for sucralfate? what are some disadvantages of this med? 4
- adheres to ulcerated mucosa
- stimulates mucus secretion
- enhances mucosal blood flow and PGE2 synthesis
- (does NOT promote healing of ulcers and can interfere w/absorption of other meds)
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antacids like maalox can coat/soothe stomach but what is problem with using these meds?
- requires high doses every 2 hours
- (can be helpful in tx of foals)
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how is treatment different with pyloric ulcers?
may need prolonged therapy; more difficult to resolve
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how is gastric impaction treated?
- gastric lavage via NGT w/warm water
- DSS detergent to break up impaction
- bethanecol to encourage emptying
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what is a differential cause of gastric impaction if horse lives in UK or South America?
equine dysautonomia (grass sickness)
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In addition to gastric rupture secondary to dilation, what is a reason the stomach would rupture without distention? how is this treated?
- ischemic infarct of portion of stomach
- result of gastric ulceration
- -gastric rupture is a terminal event - no tx -euthanize
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what is most common stomach neoplasia in horses?
- squamous cell carcinoma in teen/geriatrics
- -can met; no effective therapy
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what is the hallmark of malabsorption?
weight loss
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what diagnostic tool is most reliable in evaluating the small intestine?
ultrasound
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is small intestine palpable on rectal palpation?
not in normal/healthy patient but can feel if distended (always an abnormal finding)
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Colic signs and copious gastric reflux is a symptom of acute or chronic SI disease? what are expected peritoneal fluid findings? what would US show?
- acute
- elevated TP
- US: dilated loops of SI
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what is classic indication of chronic SI disease? how is chronic SI disease demonstrated on US?
- weight loss (+/- signs of colic)
- thickened walls (+/- dilation)
- -chronic patients can have acute episodes
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In horses, IBD is typically defined by which cells? how is definitive diagnosis made?
- granulocytic = eosinophils, lymphocytes, macrophages
- need histopathology
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Which form of IBD is NOT associated with weight loss?
idiopathic focal eosinophilic enteritis (IFEE - focal and acute)
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What is appetite like with IBD? Is there signs of pain? Diarrhea?
- weight loss despite good appetite
- intermittent colic
- diarrhea NOT typical sign of SI disease
-
Is total protein affected by IBD?
- yes, PLE
- hypoalbuminemia w/o liver disease or proteinuria
- peripheral edema
-
what would glucose absorption curve look like with IBD? what would abdominocentesis show?
- flat line, no peak
- elevated protein but this is not specific
-
what is treatment for IBD?
immunosuppressive doses of steroids - largely unsuccessful and can trigger laminitis
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what type of surgery can be done for IBD?
if intramural lesions are present, resection is indicated
-
what signalment is associated with granulomatous enteritis?
young standardbred; genetic predisposition
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what would histopath show to indicate granulomatous enteritis? what is the cause?
- macrophages ("granulomatous")
- unknown cause (may include Mycobacterium avium)
-
which form of IBD has a dermatitis component? old or young horses?
- multisystemic eosinophilic epitheliotropic enterocolitis (MEED)
- young
- *diarrhea* also component of MEED
-
what cell is seen on histopath? cause?
- tissue eosinophilia (also lymphs and macrophages)
- hypersentitivity? eosinophils in GI but also other tissues/organs
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Which form of IBD is rare and histopath shows lymphs and plasma cells in lamina propria w/ villous atrophy?
lymphocytic-plasmacytic enterocolitis
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Which form of IBD will have NO evidence of PLE?
idiopathic focal eosinophilic enteritis (newly discovered syndrome)
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how is IFEE treated that differs from the other form of IBD?
IFEE usually responds to surgical decompression without required resection (other forms usually require resection of lesions)
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does IFEE present with acute signs or persist quietly/chronic?
acute signs of colic
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what obligate intracellular bacterium infects young foals (4-6mo) and is transmitted via fecal-oral route?
lawsonia intracellularis
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what are some risk factors associated with lawsonia problems?
- overcrowding, diet change, transport, weaning
- (usu. seen in Fall, Winter)
-
what is the hallmark sign of lawsonia?
chronic wasting
-
is there a PLE associated w/Lawsonia infections? what is appearance of intestines?
- yes, severe hypoproteinemia (and peripheral edema)
- corrugated, thickened SI w/mucosal ulceration
-
What part of the intestine does Lawsonia have an affinity for? what does this cause?
*crypt cells* - decreased brush border enzyme capacity - can't absorb nutrients - wt. loss +/- malabsorptive diarrhea
-
what do CBC results show with lawsonia infection? 5
- mod-severe hypoproteinemia
- mild anemia
- hyperfibrinogenemia
- neutrophilic leukocytosis
- prerenal azotemia/electrolyte imbalances if diarrhea
-
what is the gold standard for diagnosing lawsonia? what is prognosis for positive results?
- isolation/culture from tissue (difficult; Warthin Starry silver stain)
- good 93% survival (but smaller stature; slower growth)
-
What sample is needed for PCR of lawsonia?
- PCR on tissue is sensitive and specific
- (false pos. if use feces)
-
what antibiotics are appropriate for tx of lawsonia?
- Abs that target intracellular organisms
- -tetracyclines (oxy then doxy up to 17days)
- -macrolides (erythromycin) + rifampin
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what is a characteristic sign of duodenal-proximal jejunal enteritis (DPJ)?
high volumes of enterogastric reflux (due to excessive fluid/electrolyte secretion into SI)
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is DPJ functional or mechanical ileus? is it painful?
- functional ileus
- abdominal pain and distention
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How would you describe gross lesions of duodenum with DPJ?
- serositis - bright red to dark ecchymotic hemorrhages
- fibrinopurulent serosal exudate
- hyperemia/edema
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Is surgery needed for patients with DPJ?
no, but need to distinguish DPJ from mechanical obstructions that do require sx
-
Since DPJ is an inflammatory syndrome, what are expected PE findings? 5
- *fever* (Ddx from mechanical obst.which will not have fever)
- tachycardia, tachypnea
- decr. borborygmi; mild/mod/severe colic pain
- dehydration/volume depletion
- endotoxemia
-
how do you distinguish DPJ from mechanically obstructed patient?
- decompression of reflux in DPJ will lead to relief/depression
- decompression in obstruction/strangulation will not help pain symptoms
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how will US differ in DPJ vs. obstructed/surgery patient?
- DPJ- thickened walls, fluid filled loop distention, poor motility
- sx case: dilation, no motility, sediment line
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what are peritoneal fluid findings for DPJ?
- dark yellow/orange (but NOT serosanguinous as will obstruction/deteriorated bowel)
- high protein (>2.5)
- normal to slightly elevated WBC (higher WBC with deterioration)
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what is treatment for DPJ? 7
- gastric decompression (indwelling stomach tube)
- IV fluids to replace losses
- NSAIDs/lidacain CRI (caution ulcers)
- prokinetics (metaclopramide, bethanecol, erythromycin)
- +/- Abs (if WBC very low may need)
- NPO at least 3 days; TPN
- laminits prophylaxis (inflammation -endotoxemia)
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what are some complications associated with DPJ and treatment? 7
- laminitis
- thrombophlebitis
- adhesions within peritoneum (fibrinous exudates on serosa)
- peritonitis
- esophagitis/pharyngitis - rupture
- cardiac arrythmias (balance electrolytes, acid/base)
- $$$ - several days in hospital
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