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57 Cards in this Set
- Front
- Back
What is:
a. systemic inflammation b. systemic inflammatory response syndrome (SIRS) |
a. inflammatory response to blood borne microbial mols, tissue derived enzymes, pro-inflammatory mediators, etc.
b. 2 or more of the following: tachypnea, tachycardia, fever or hypothermia, neutrophilia or neutropenia |
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What is
a. sepsis b. endotoxemia c. septic shock |
a. systemic inflammatory response triggered by a microbial mol (infection, damaged gut barrier, etc.)
b. systemic inflammation triggered by Gram (-) bacterial endotoxin c. sepsis w/ signs of shock |
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What is the pathophysiology of sepsis?
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infection or mucosal damage allows microbes (usually bacteria) to access systemic circulation
systemic inflammation triggered: most commonly by Gram (-) bacterial lipopolysaccharide (LPS) poor perfusion: neutrophil & platelet aggregates, thrombi, hemodynamic shock (peripheral vasodilation, poor cardiac output) tissue injury: ischemia, edema (d/t ↑ vascular permeability), leukocyte products (reactive O2 intermediates, degradative enzymes) multiorgan dysfunction/failure: laminitis, CV, liver, kidneys |
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What are the clinical signs of sepsis?
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tachycardia, tachypnea, pyrexia or hypothermia, leukocytosis or leucopenia
other: hyperemic mm, depression, edema signs of shock: prolong CRT, poor peripheral pulses, hypotension, weakness, trembling, cool extremities |
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What are common lab findings w/ sepsis?
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CBC: hemoconcentration (↑ PCV, TP), systemic inflammation (↑ fibrinogen, leukocytosis, neutropenia w/ L shift: classic, thrombocytopenia)
Chem: azotemia, ↑ liver enzymes, high gap lactic acidosis U/A: concentrated, hematuria, proteinuria |
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How is sepsis diagnosed?
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hx
typical clinical signs typical lab findings blood culture (lacks sensitivity in adults) look for source |
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What is the tx for sepsis?
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summary tx plan
SIRS - 2-4 L J5 plasma - flunixin IV TID-QUID if hypotensive - LRS bolus (20 L), then at 2x maintenance - if still hypotensive: 10 ml/kg hetastarch, consider pressors (neonates) monitor PE, BP, colic, feet, veins, PCV/TP, creatinine, LFTs, urine ABs: if neutrophil count < 1000 OR septicemia suspected or documented nutrition - high quality diet if tolerated: high fat - +/- parenteral nutrition preventing laminitis - circulatory support: incl. colloids - anti-inflammatories: aspirin (↓ platelet clumping), pentoxifylline? (↑ deformability of RBCs & WBCs), hand walk, ice feet |
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What are the principles of treating sepsis?
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stop absorption/tx source: hasten GI mucosal healing, drain abscesses, tx infections
antagonize LPS effects ↑ perfusion: ↑ BP, improve blood distribution, ↓ endothelial permeability (vascular leak syndrome) control coagulation/platelet activation |
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What are some causes of acute diarrhea in adult horses?
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infectious: Salmonella, Neorickettsia risticii, Clostridium difficile, Clostridium perfringens
toxic: NSAIDs, cantharidin, arsenic, ABs misc.: grain overload, sand enteropathy |
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What is the pathophysiology of diarrhea in adult horses?
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mucosal injury -->
- absorption of bacterial products: local inflammation, or endotoxemia/SIRS/sepsis - enterocyte hypersecretion --> massive fluid loss (isotonic) --> dehydration, electrolyte & acid-base imbalances - protein loss: albumin +/- globulin - motility dysfunction: hypomotility early (colic), then hypermotility (diarrhea) |
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What are the clinical signs of acute diarrhea?
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fever: usually 1st sign seen
scant to profuse diarrhea, +/- colic sepsis & dehydration: depression, anorexia, tachycardia, tachypnea, tacky hyperemic mm, prolonged CRT, limb edema, weak peripheral pulses, cool extremities |
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What are the lab findings assoc. w/ acute diarrhea?
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CBC: mature neutropenia w/ ↑ bands, ↑ fibrinogen, thrombocytopenia
Chem: hypoproteinemia, hypoglycemia, hyponatremia, hypokalemia, hypocalcemia (esp. cantharidin), metabolic acidosis, azotemia, +/- ↑ liver enzymes, bile acids, hyperbilirubinemia |
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How is acute diarrhea diagnosed?
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Salmonellosis: fecal culture (5 consecutive samples) or fecal PCR
Potomac Horse fever: buffy coat PCR C. perfringens: culture or PCR for toxins C. difficile: fecal cytotoxin immunoassay cantharidin toxicity: ID of blister beetles, cantharidin assay (urine, feces, GI contents) |
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What is the tx for acute diarrhea?
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fluids
- crystalloids: maintenance + fluid deficit + on-going lossses - colloids: if hypoproteinemic or evidence of septic/endotoxemic shock - plasma: 6-8 L initially - hetastarch: often used after initial plasma administration - electrolyte/acid-base balance mucosal protectant: bismuth subsalicylate BIP or psyllium TID-QID tx sepsis nutrition - good quality grass hay/grass - pelleted feed: - AVOID enteral nutrition - +/- parenteral nutrition absorbent powders: only administer to horses w/ normal intestinal motility - biosponge (di-tri-octahedral smectite) 0.5-1 lb BID: absorbs Clostridial toxins - activated charcoal: 1 lb BID specific therapy - AVOID ABs if possible - Clostridiosis: Metronidazole PO - Poto. Horse fever: Oxytetracycline IV - Salmonellosis: Enrofloxacin or Chloramphenicol |
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What are some causes of chronic diarrhea in adult horses?
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parasitism (top ddx: always R/O), malnutrition, ulcerative colitis, IBD, sand enteropathy, Salmonellosis, neoplasia, chronic peritonitis, chronic liver dz/fibrosis (rare), chronic R heart failure (rare)
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What are the clinical signs of chronic diarrhea?
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wt. loss, +/- colic, +/- peripheral edema (if hypoproteinemic)
rarely dehydrated & rarely have systemic inflammation |
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What lab findings are assoc. w/ chronic diarrhea?
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CBC/Chem: usually normal
+/- hypoproteinemia,+/- anemia of chronic inflammation, +/- electrolyte imbalances |
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How is chronic diarrhea diagnosed?
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hard to dx
fecal float, sand test, peritoneal fluid analysis, fecal culture, abd. U/S, rectal bx |
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What is the tx for chronic diarrhea?
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- parasites: fenbendazole for 5 d. followed by ivermectin for encysted cyathosomes
- sand: psyllium powder - switch to all hay diet or pelleted feed - chronic Salmonellosis: probiotics? - metronidazole for 2 wks - misoprostol, iodochlorhydroxyquin - steroids: last resort |
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What is the pathophysiology of right dorsal ulcerative colitis?
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- NSAID toxicity
- dehydration may play a role - usually performance horses or sick horses in hospital being treated for something else - mucosal injury d/t inhibition of PG production - usually localized, but may be diffuse |
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What are the clinical signs of acute & chronic R dorsal ulcerative colitis?
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acute: colic, mild to moderate diarrhea, anorexia, edema (d/t PLE)
chronic: intermittent colic, wt. loss, intermittent diarrhea, anorexia, edema |
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What lab findings are assoc. w/ R dorsal ulcerative colitis?
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CBC: anemia of chronic inflammation or chronic blood loss, leukocytosis or leucopenia
chem.: panhypoproteinemia peritoneal fluid: normal to ↑ WBCs |
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How is R dorsal ulcerative colitis diagnosed?
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R/O other causes
U/S: not very sensitive (can only see ~1/3 or R dorsal colon): thickness > 5 mm: abnormal |
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What is the tx for R dorsal ulcerative colitis?
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30-60 d. of tx
rest low fiber roughage: pelleted feed; avoid hay, grain, & grass psyllium mucilloid: promotes epi healing misoprostol: promotes mucosal healing colloids if hypoproteinemic tx systemic problems: sepsis/endotoxemia analgesia: butorphanol, fentanyl |
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What is the pathogenesis of gastric ulcer dz (protective & harmful factors)?
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chemical damage d/t acid & bile salts
predominantly occurs at margo plicatus, but may also occur at antrum, duodenum protective factors: saliva, roughage mat (buffer), mucus, epithelial integrity (PGs), gastric emptying harmful factors: disruption of roughage mat, NSAIDs, mucosal ischemia, pooling of acid or bile salts |
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What are some risk factors for
a. squamous gastric ulcers b. glandular gastric ulcers |
a. occupation/training: 90% of racehorses, 50% of show horses; intermittent feeding, anorexia, or withholding food; stress
b. illness, post-op colics; gastric outflow obstruction; NSAID toxicity; Helicobacter infection? |
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What are the clinical signs of gastric ulcer dz in
a. adults b. foals |
a. colic (chronic, intermittent, or after a meal), occasional hypersalivation, occasional bruxism (grinding teeth), reluctance to eat
b. colic (more common & more severe than in adults), hypersalivation, bruxism, mild non-hemorrhagic diarrhea |
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How is gastric ulcer dz diagnosed?
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gastric endoscopy: only means of definitive dx
response to therapy |
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What is the tx for gastric ulcer dz?
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drugs: 2-4 wks of therapy needed
- proton pump inhibitor (omeprazole): tx of choice - H2 blocker (ranitidine) - sucralfate: give if signs of colic (promotes healing of glandular mucosa) - magnesium or aluminum hydroxide (antacid) to relieve acute signs: give if signs of colic management/diet - ↓ stall confinement - frequent feeding: GRAZING - less grain, more roughage: alfalfa hay - corn oil (↑ PGE-2), high fat diet? - modify training prevention: low dose omeprazole PO daily during training/racing |
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What is the pathophysiology of esophageal obstruction (choke)?
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functional or mechanical obstruction --> reflux of saliva & food material --> mucosal injury, possible ulceration, stretching of wall, rupture
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What are some clinical signs of esophageal obstruction?
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esophageal dysphagia: anorexia, hypersalivation (loss of bicarb, Na), nasal d/c (food material, saliva, water), cough, gagging, extension of neck when eating, swelling in cervical region, dehydration
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What lab findings are assoc. w/ esophageal obstruction?
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hemoconcentration: ↑ PCV, TP
electrolyte & acid/base abnormalities: hyponatremia, hypokalemia, metabolic acidosis mild azotemia |
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How is esophageal obstruction diagnosed?
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establish obstruction: clinical signs, ability to pass NG tube (careful: risk of perforation), endoscopy, U/S, rads +/- contrast
look for underlying cause |
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What is the tx for esophageal obstruction?
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obstruction relief
- lavage: -single NG tube: standing, sedate w/ detomidine -double NG tubes (ingress & egress tube), general anesthesia w/ ET tube sx: rare (FBs, strictures, ruptures, masses) diet: bran mashes, slurry from pelleted food, avoid hay or grass until function is normal hydration: IV or rectal administration - soften the impaction - replace fluid deficits - correct electrolyte/acid-base imbalances esophageal motility: ace, X/T, & detomidine or oxytocin |
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What is the pathogenesis & signalment of proliferative enteropathy?
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- Lawsonia intracellularis infection
- transmission: fecal-oral - organism promotes epithelial proliferation (hypertrophy) in SI --> malabsorption, PLE - signalment: 1-6 mo. old |
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What are the clinical signs of proliferative enteropathy?
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thin, +/- colic, diarrhea +/- melena, peripheral edema
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How is proliferative enteropathy diagnosed?
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- U/S
- definitive dx: serology or fecal PCR (specific but very insensitive) - can do tissue PCR post-mortem |
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What is the tx for proliferative enteropathy?
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Doxycycline: tx of choice
erythromycin, azithromycin, chloramphenicol also used supportive care: fluids, colloids |
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What is the pathophysiology & signalment for IBD?
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- inappropriate immune response to a pathogen or other Ag OR appropriate immune response to a persistent pathogen or other Ag
- depending on segment(s) involved, may have malabsorption syndrome, diarrhea, or both - many horses w/ R dorsal ulcerative colitis have underlying IBD signalment: 1-6 yrs old |
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What are the clinical signs of each of these types of IBD?
a. MEED b. EC c. GE d. LPE |
a. MEED: wt. loss, diarrhea (50%), dermatitis
b. EC: chronic intermittent colic c. GE: wt. loss, diarrhea (33%), dermatitis d. LPE: wt. loss, diarrhea (33%) also peripheral edema, poor appetite |
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What lab findings are assoc. w/ IBD?
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anemia of chronic inflammation or blood loss
possible leukocytosis: eosinophilia, lymphocytosis depending on dz +/- ↑ fibrinogen panhypoproteinemia |
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How is IBD diagnosed?
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- abd. U/S: look for thick intestines
- carbohydrate absorption test: tests for malabsorption peritoneal fluid analysis - intestinal bx: definitive dx (transendoscopic or surgical) - rectal bx: do if animal has diarrhea |
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What is the tx for IBD?
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- colloids
- remove Ag source: ex. anthelmintics if eosinophilic dz - resection of intestines if segmental (EC) immunosuppression: Dex (tx of choice to begin therapy), prednisolone (long term therapy) |
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What is the pathophysiology of peritonitis?
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- infection: acute or chronic
- intestinal rupture: acute & usually fatal - intestinal abscess: Gram (-) enterics or others - massive inflammatory response - absorption of bacterial products --> endotoxemia - fibrin deposition, pocket formation, intestinal adhesions |
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What clinical signs are assoc. w/ peritonitis?
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wt. loss, pyrexia, anorexia, colic, diarrhea, +/- sepsis
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How is peritonitis diagnosed?
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- peritoneal fluid analysis: WBC, protein, glucose, pH
- U/S - rectal exam |
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What is the tx for peritonitis?
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broad spectrum ABs
- aminoglycoside + penicillin: 1st choice - other possibilities: enrofloxacin, doxycycline, chloramphenicol - add metronidazole if anaerobes suspected (ex. perforation) tx systemic effects (sepsis), analgesia abdominal lavage - done if bacteria seen on cytology, if systemically ill or WBC in peritoneal fluid > 100,00 cells/uL |
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What is the pathophysiology of proximal enteritis?
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- severe inflammatory dz of duodenum & proximal jejunum
- etiology unknown: Clostridium difficile?, mycotoxins? - mucosal barrier damage --> inflammation --> hypersecretion, functional ileus, gastric fluid accumulation |
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What are some clinical signs of proximal enteritis?
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acute colic, fever, signs of sepsis (depression, tachycardia, tachypnea, hyperemic mm, prolonged CRT), dehydration, nasogastric reflux (reddish orange), NO diarrhea
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What lab findings are assoc. w/ proximal enteritis?
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CBC: leucopenia followed by leukocytosis, hemoconcentration, ↑ fibrinogen, thrombocytopenia
Chem: hyponatremia, hypochloridemia, hypokalemia, hypocalcemia, metabolic acidosis, +/- abnormal organ function tests (ex. liver) |
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How is proximal enteritis diagnosed?
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pyrexia, non-turgid distended bowel loops on rectal exam, peritoneal fluid analysis (normal WBC, RBC, ↑ TP), gastric decompression --> ↓ pain, ↓ HR, depression, gastric fluid (fetid, orange-red), large volume), U/S (diameter < 6 cm, wall > 6 mm, little motility)
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What is the tx for proximal enteritis?
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gastric decompression
fluid therapy - IV isotonic fluids: deficit + maintenance + replacement of gastric reflux losses - electrolytes: K, Ca gluconate, bicarb - colloids ABs - metronidazole: Clostridiosis is possible etiology - broad spectrum AB if severe neutropenia analgesia/anti-inflammatory - lidocaine: tx of choice - flunixin: risk of potentiating mucosal damage - butorphanol: CRI tx sepsis/endotoxemia mucosal protectants: ranitidine, omeprazole prokinetics - lidocaine: tx of choice - metoclopramide: 2nd choice - erythromycin: 3rd choice nutrition - NPO while refluxing > 2-4 L/4 hrs - gradually put back on food - parenteral nutrition if NPO > 72 hrs |
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ddx for intermittent colic w/ or w/o weight loss
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R dorsal ulcerative colitis, obstructive GI dz, gastric ulcers, IBD, neoplasia, sand enteropathy, parasites (cyathosomes), peritonitis, dental dz, EIA
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ddx for intermittent colic w/ bruxism or salivation
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gastric ulcers, gastric neoplasia, gastric impaction, esophagitis, gastric outflow obstruction, R dorsal ulcerative colitis
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ddx for esophageal dysphagia
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obstructive
-intraluminal: simple impaction or FB -extraluminal: intramural mass (ex. SCC), extramural mass (ex. abscess or tumor), vascular ring anomaly, congenital anomaly, stricture, diverticulum -functional: esophagitis neuromuscular: CN 9 or 10 dysfunction, botulism, selenium/vitamin E deficiency, megaesophagus pain: esophagitis |
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ddx for proximal enteritis signs
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proximal enteritis, peritonitis, small intestinal obstruction (strangulating or non-strangulating), gastric outflow obstruction, Salmonellosis
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ddx for weight loss w/ or w/o colic
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IBD, parasites, malnutrition, liver dz, renal failure, EIA, neoplasia, intra-abdominal abscess, dental dz, sand enteropathy, gastric ulcers, chronic dz of other systems
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