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sam dr green > disorders of the stomach > Flashcards

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
Q

tx for physaloptera rara

A
  • Pyrantel pamoate
    • Nemex, strongid
  • •Ivermectin
  • •Fenbendazole
  • •Removal during gastroscopy
26
Q

px for physalotera rara

A

Excellent
•Vomiting usually resolves after worm removal
•UNCOMMON disease

27
Q

congenital lesions of chro. hypetrophic pyloric gastropathy

A

hypertrophy of smooth mm.

28
Q

l acquired lesions of chr. hypertrophic pyloric gastropathy

A
  • Circular muscle hypertrophy (Type 1)
  • Muscular hypertrophy and mucosal hyperplasia (Type 2)
  • Primarily mucosal hyperplasia (Type 3)
29
Q

causes of chr. hypertrophic pyloric gastropathy

A

nknown

30
Q

clinical features and signalment of chr. hypertrophic pyloric gastropathy

A
  • 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
Q

dx for chr. hypertrophic pyloric gastropathy

A
  • 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
Q

tx for chro. hypertrophic pyloric gastropathy

A
  • Surgery
  • •Pyloroplasty
  • •Complicated surgery
  • •Must be performed by skilled surgeon
33
Q

px for chr. hypertrophic pyloric gastropathy

A

Dependent on surgery
•Good to excellent

34
Q

sequela to gdv

A
  • 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
Q

cause for gdv

A

unknown

36
Q

risk factors for gdv

A
  • 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
Q

clinical features of gdv

A
  • Nonproductive retching
  • •Salivation
  • •Abdominal pain
  • •Marked abdominal distension (later stages)
    • Tympany
    • NOTalways obvious!! (large, heavily muscled dogs)
  • •Depression, weakness, collapse, moribund
38
Q

dx for gdv

A
  • 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
Q

sign of poor px for gdv

A

increased lactate levels

40
Q

tx for gdv

A
  • Aggressive fluid therapy / shock therapy
  • •Gastric decompression
  • •Surgery
41
Q

post operative concerns for gdv

A
  • Cardiac arrhythmias
  • •Viability of spleen and stomach
  • •Gastric motility
  • •Gastric ulceration
  • •Reperfusion injury
  • •Bacterial translocation
  • •Sepsis/SIRS
  • •Coagulopathy -DIC
  • •MODS
    • Pancreatitis
    • ARF
42
Q

px for gdv

A
  • 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
Q

prevention for gdv

A
  • Minimize risk factors
  • •Discuss prophylactic gastropexy for @risk dogs
  • •Minimize excitement before and after feeding
44
Q

etiology for bilious diarrhoal syndrome

A
  • Gastroduodenal reflux
  • •Empty stomach for prolonged period (overnight)
45
Q

clinical features of bilious diarrhoal syndrome

A

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
Q

dx for bilious diarrheal syndrome

A
  • Appropriate history
  • •Resolution with appropriate treatment
    • •Diagnosis of exclusion, must rule out
    • Obstruction, foreign body
    • Inflammation, neoplasia
    • Non GI disorders
    • Etc.
47
Q

tx for bilious vomitus syndrome

A
  • Feed dog extra meal late at night
  • •Prevents prolonged periods of empty stomach
  • •+/-gastric prokinetics
48
Q

px for bilious vomiting syndrome

A

Excellent
•Vomiting usually resolves with feeding
•Dogs remain healthy even if vomiting persists

49
Q

Superficial lesions involving the gastric mucosa

A

gastric erosions

50
Q

cause of gastrointerstinal ulceration erosions

A
  • 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
Q

clinical features of gastrointestinal ulceration erosions

A
  • 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
Q

dx for GUE

A
  • 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
Q

tx for GUE

A
  • 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
Q

px for GUE

A
  • Favorable
    • If underlying cause controlled
    • If therapy prevents perforation of ulcer
55
Q

common stomach neoplasias in dog

A
  • Carcinoma (Chows!!!)
  • Lymphoma –typically diffuse
  • Leiomyomas
  • Leiomyosarcomas
56
Q

common stomach neoplasia of cat

A

Lymphoma –typically diffuse

57
Q

clinical features of stomach neoplasias

A
  • Asymptomatic until disease is advanced
  • •Anorexia most common sign
  • •Vomiting (advanced disease, obstruction)
  • •Weight loss
  • •GI bleeding
  • •Polyps –rarely cause signs
58
Q

dx for stomach neoplasia

A
  • 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
Q

tx for stomach neoplasia

A
  • Surgery
    • Carcinoma -complete excision difficult
    • Leiomyoma / leiomyosarcoma more resectable
  • •Chemotherapy (lymphoma)
    • most chemoresponsive
60
Q

px for stomach neoplasia

A
  • Carcinoma –poor (unless detected early)
  • •Lymphoma –usually poor (dog worse than cat)
  • •Leiomyoma / leiomyosarcoma –surgery may be curative if caught early
61
Q
A

sam dr green (10 decks)

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