disorders of the stomach Flashcards

1
Q

vomiting of sudden onset presumed to be caused by gastric mucosal insult or inflammation

A

acute gastritis

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2
Q

causes of acute gastritis

A
  • Dietary indiscretion or intolerance
  • Foreign body
  • Drugs or toxins (NSAIDs)
  • Parasites
  • Infectious, viral, bacterial (poorly characterized)
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3
Q

primary acute gastritis

A

Injury mediated directly by injurious substance

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4
Q

secondary acute gastritis

A
  • Injury occurs in directly due to systemic disease Medated by
    • Increased secretion of gastric acid
    • Reduced mucosal blood flow
    • Alteration of gastric mucosal barrier
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5
Q

clinical features of acute gastritis

A
  • Dogs > cats
  • •Acute onset vomiting
  • •Anorexia
  • •+/-ADR
  • •Fever, abdominal pain uncommon
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6
Q

tx for acute gastritis

A
  • Work-up unnecessary in mostcases
  • •Common problem, cause seldom identified
  • •Presumptive diagnosis
    • History (exposure to garbage, drugs, etc.)
    • Physical exam (NSF except for nausea, mild abdominal discomfort)
    • Rapid response to symptomatic treatment
  • Full diagnostic evaluation required if
    • Systemic illness or fever
    • Abdominal pain or suspicion of foreign body
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7
Q

tx for acute gastritis

A
  • Symptomatic
  • •NPO x 24 hours
  • •Fluids (SQ, IV)
  • •+/-H2receptor antagonists, proton pump inhibitors
  • •+/-Antiemetics
  • •Dietary modification
    • Small amounts of water
    • Slow introduction of bland diets
  • •If signs do not resolve within 1 -2 days, full diagnostic workup should be performed
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8
Q

px for acute gastritis

A
  • Excellent
  • •Must maintain
    • Fluid balance
    • Electrolyte balance
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9
Q

etiology for hemorrhagic gastroenteritis

A

unknown

multiple theories

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10
Q

clinical features of hemorrhagic gastroenteritis

A
  • Dogs (small breed more common)
  • •No history of dietary indiscretion
  • •Hematemesis
  • •Hemorrhagic diarrhea (hematochezia)
    • “raspberry jam” appearance
  • •Peracute / acute onset
  • •Rapid progression, rapid debilitation
    • Can present in hypovolemic shock
  • •Depression, abdominal discomfort common
  • •Pyrexia uncommon
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11
Q

dx for hemorrhagicgastroenteristis

A

presumptive dx

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12
Q

tx for hemorrhagic enteritis

A
  • Hospitalize!!
  • •IV fluid therapy (aggressive!!)
  • •IV antibiotics (ampicillin)
  • •Other symptomatic therapy
    • NPO
    • Antiemetics
    • H2receptor antagonists
    • (Fenbendazole)
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13
Q

px for hemorrhagic gastroenterisits

A
  • Good for most animals
    • If treated early and effectively
  • •Recurrences are possible
  • •Poor prognostic indicators
    • Hypoproteinemia
    • Sepsis
  • •Potential to be a fatal disease
    • Circulatory collapse
    • DIC
    • ARF
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14
Q

cause of chronic gastritis

A
  • cause rarelly identified
  • When other causes of chronic vomiting ruled out **AND **inflammation present on histopathology
  • Chronic gastritis usually due to
    • Food allergy
    • Occult parasitism
    • Immune reaction to bacterial pathogens
    • Immune reaction to unknown pathogens
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15
Q

clinical features of chr. gastritis

A
  • May be asymptomatic (26% -48%)
  • •Decreased appetite / anorexia
    • May be ONLYclinical sign
  • •Chronic vomiting
    • Intermittent (once weekly)
    • Frequent (multiple times daily)
  • •Weight loss, melena, hematemesis (variable)
  • •May have concurrent dermatologic signs
    • Dietary sensitivity (food allergy)
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16
Q

dx for chr. gastritis

A
  • Rule out other causes of chronic vomiting/anorexia
    • MDB
    • T4, HW, FeLV, FIV (cats)
    • Abdominal imaging (radiographs, ultrasound)
    • (ACTH, bile acids)
  • •Histopathology requiredfor definitive diagnosis
    • Gastroscopy
    • Laparotomy (full thickness biopsy)
  • •Interpret histopathology cautiously
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17
Q

tx for chr. gastritis

A
  • Variable (dependent on histopathology)
  • •No universal approach
  • •(Antiparasitics -fenbendazole)
  • •Dietary therapy
    • Low fat, low fiber (low residue diets)
    • Novel protein, hydrolyzed protein diets
  • •H2receptor antagonists
  • •Corticosteroids / Budesonide
  • •Other immunosuppressants
    • Cyclosporin (Atopica)
    • Azathioprine (Imuran)
    • Chlorambucil (Leukeran)
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18
Q

px for chr. gastritis

A
  • Extremely variable
  • •Often good for lymphocytic/plasmacytic gastritis
  • •Often good for eosinophilic gastritis (dogs)
  • •Progression of lymphocytic gastritis to lymphoma?
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19
Q

cs of helicobacter associated dz

A
  • Most are asymptomatic
  • •Nausea, anorexia, vomiting
  • •Lymphocytic infiltrates (gastritis)
  • •+/-neutrophilic infiltrates (gastritis)
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20
Q

dx for helicobacter associated dz

A
  • Gastric biopsy, special stains (Giemsa, Warthin-Starry)
  • •Location of organism (crypts ?)
  • •Presence of inflammation (gastritis)
  • •PCR
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21
Q

tx for helicobacter associated dz

A

Multiple drug combinations suggested

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22
Q

px for helicobactwr associated dz

A
  • Many respond well
    • Resolution of clinical signs
    • Clearance of organism
  • •Cause and effect still uncertain
  • •Some animals may not respond
    • Other diseases present?
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23
Q

One worm can cause intractable vomiting

name the worm

A
  • physaloptera rara
  • dogs
  • animal otherwise bar
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24
Q

dx for physaloptera rara

A
  • Ova rarely found in fecal (few eggs passed)
  • •Most diagnosed via gastroduodenoscopy
    • May be single worm infections
    • Can be difficult to find
  • •Some diagnosed with empirical treatment
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25
tx for physaloptera rara
* Pyrantel pamoate * Nemex, strongid * •Ivermectin * •Fenbendazole * •Removal during gastroscopy
26
px for physalotera rara
Excellent •Vomiting usually resolves after worm removal •UNCOMMON disease
27
congenital lesions of chro. hypetrophic pyloric gastropathy
hypertrophy of smooth mm.
28
l acquired lesions of chr. hypertrophic pyloric gastropathy
* Circular muscle hypertrophy (Type 1) * Muscular hypertrophy and mucosal hyperplasia (Type 2) * Primarily mucosal hyperplasia (Type 3)
29
causes of chr. hypertrophic pyloric gastropathy
nknown
30
clinical features and signalment of chr. hypertrophic pyloric gastropathy
* dogs\>cats * males\> females * congenital lesions * shortly after weaning up to 1 yr old * acquired lesions * old dogs * Any animal can be affected * Chronic vomiting * Shortly after eating * May be projectile * Animals otherwise BAR (may have weight loss)
31
dx for chr. hypertrophic pyloric gastropathy
* MDB * +/-Hypochloremic, hypokalemic metabolic alkalosis * coz its upper gi dz * •Presence of gastric outflow obstruction * Ultrasound (thickened pyloric musculature) * Contrast radiography * Gastroduodenoscopy * Increased folds of normal appearing mucosa at pylorus * Redundant antral mucosa, may be inflamed * Fluoroscopy * Exploratory surgery * Serosa appears normal * Pylorus thickened when palpated * Difficulty passing finger through pylorus * **_•Histopathology to rule out infiltrative disease_**
32
tx for chro. hypertrophic pyloric gastropathy
* Surgery * •Pyloroplasty * •Complicated surgery * •Must be performed by skilled surgeon
33
px for chr. hypertrophic pyloric gastropathy
Dependent on surgery •Good to excellent
34
sequela to gdv
* Gastric outflow is obstructed * •Progressive distension with air * •Splenic torsion may occur concurrently * •Obstruction: hepatic portal vein, posterior vena cava * •Mesenteric congestion, decreased CO * •Hypovolemic shock * •Compromise to gastric blood supply * •Gastric wall necrosis
35
cause for gdv
unknown
36
risk factors for gdv
* large breed dogs * Offspring of parents who had GDV * Increasing age * Faster speed of eating * Once daily feeding * Raised feeding bowl and aerophagia * Personality (happy dogs \< GDV)
37
clinical features of gdv
* Nonproductive retching * •Salivation * •Abdominal pain * •Marked abdominal distension (later stages) * Tympany * NOTalways obvious!! (large, heavily muscled dogs) * •Depression, weakness, collapse, moribund
38
dx for gdv
* Physical exam findings (presumptive) * Tympanic anterior abdomen * Tachycardia * Pale MM * Hypothermia * Depression * Arrhythmias (VPCs, ventricular tachycardia) * •Radiographs (perform AFTERstabilization) * **•Inability to pass stomach tube is NOTdiagnostic**
39
sign of poor px for gdv
increased lactate levels
40
tx for gdv
* Aggressive fluid therapy / shock therapy * •Gastric decompression * •Surgery
41
post operative concerns for gdv
* Cardiac arrhythmias * •Viability of spleen and stomach * •Gastric motility * •Gastric ulceration * •Reperfusion injury * •Bacterial translocation * •Sepsis/SIRS * •Coagulopathy -DIC * •MODS * Pancreatitis * ARF
42
px for gdv
* Variable –dependent on speed of dx and tx * •18% -28% mortality rates reported * •Lactate as prognostic indicator * 99% dogs with blood lactate levels \< 6 mmol/L survived GDV * 58% survival in dogs with lactate \> 6 mmol/L * High lactate also predictive of gastric necrosis at sx * •Chance of recurrence with surgery? * \< 7% chance of volvulus with surgery * Can have gastric dilatation
43
prevention for gdv
* Minimize risk factors * •Discuss prophylactic gastropexy for @risk dogs * •Minimize excitement before and after feeding
44
etiology for bilious diarrhoal syndrome
* Gastroduodenal reflux * •Empty stomach for prolonged period (overnight)
45
clinical features of bilious diarrhoal syndrome
Clinical features * •Vomiting in otherwise normal dog * •Vomiting usually occurs once daily * •Typically vomitus is bile-stained fluid * •Often late at night, or just before morning meal
46
dx for bilious diarrheal syndrome
* Appropriate history * •Resolution with appropriate treatment * •Diagnosis of exclusion, must rule out * Obstruction, foreign body * Inflammation, neoplasia * Non GI disorders * Etc.
47
tx for bilious vomitus syndrome
* Feed dog extra meal late at night * •Prevents prolonged periods of empty stomach * •+/-gastric prokinetics
48
px for bilious vomiting syndrome
Excellent •Vomiting usually resolves with feeding •Dogs remain healthy even if vomiting persists
49
Superficial lesions involving the gastric mucosa
gastric erosions
50
cause of gastrointerstinal ulceration erosions
* Stress (hypovolemia, sepsis) * •NSAIDs –MAJOR cause of GUE * Multiple NSAIDs * Switching NSAIDs without washout period * NSAIDs + steroids * Switching from NSAIDs to steroids (or steroids to NSAIDs) without washout period * Steroids •MCT, gastrinoma •Renal disease, liver disease / PSS •Hypoadrenocorticism (Addison’s disease) •Chronic gastritis / IBD, (foreign body) •Neoplasia
51
clinical features of gastrointestinal ulceration erosions
* Dogs \> cats * •Anorexia –**principal sign** * •+/-vomiting (fresh/digested blood) * •Anemia * •Hypoproteinemia * •Most animals not painful in abdomen * •Ulcers may perforate/heal over before peritonitis occurs * May cause local abscess / fever / pain * •Perforation -peritonitis
52
dx for GUE
* Presumptive * Evidence of GI blood loss without coagulopathy * Elimination of other causes of GI blood loss * •Imaging * Contrast radiographs * Ultrasound * Endoscopy –**MOSTsensitive & specific diagnostic tool** * •Biopsy * to r/o infiltrative dz
53
tx for GUE
* Dependent on cause * •Gastrinomas -H2receptor antagonists (palliative) * •Symptomatic therapy * Acid reduction (H2receptor antagonists, PP inhibitors) * Fluids * Gastric protectants –sucralfate * •If life threatening bleeding OR no response to therapy (3-6 days) * Surgery to resect ulcer * Must perform endoscopy first
54
px for GUE
* Favorable * If underlying cause controlled * If therapy prevents perforation of ulcer
55
common stomach neoplasias in dog
* Carcinoma (Chows!!!) * Lymphoma –typically diffuse * Leiomyomas * Leiomyosarcomas
56
common stomach neoplasia of cat
Lymphoma –typically diffuse
57
clinical features of stomach neoplasias
* Asymptomatic until disease is advanced * •**Anorexia most common sign** * •Vomiting (advanced disease, obstruction) * •Weight loss * •GI bleeding * •Polyps –rarely cause signs
58
dx for stomach neoplasia
* Iron deficiency anemia without obvious blood loss (suggests GI bleeding) * •Hypoglycemia (leiomyoma, leiomyosarcoma) * •Radiographs * •Contrast radiographs * might be helpful * •Ultrasound * FNA / cytology * see thickning and can aspirate * •Endoscopy (limitations) * hard to get a good representation * •Histopathology * •Exploratory surgery
59
tx for stomach neoplasia
* Surgery * Carcinoma -complete excision difficult * Leiomyoma / leiomyosarcoma more resectable * •Chemotherapy (lymphoma) * most chemoresponsive
60
px for stomach neoplasia
* Carcinoma –poor (unless detected early) * •Lymphoma –usually poor (dog worse than cat) * •Leiomyoma / leiomyosarcoma –surgery may be curative if caught early
61