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57 Cards in this Set

  • Front
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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
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
What is the pathophysiology of sepsis?
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
What are the clinical signs of sepsis?
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
What are common lab findings w/ sepsis?
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
How is sepsis diagnosed?
hx
typical clinical signs
typical lab findings
blood culture (lacks sensitivity in adults)
look for source
What is the tx for sepsis?
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
What are the principles of treating sepsis?
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
What are some causes of acute diarrhea in adult horses?
infectious: Salmonella, Neorickettsia risticii, Clostridium difficile, Clostridium perfringens

toxic: NSAIDs, cantharidin, arsenic, ABs

misc.: grain overload, sand enteropathy
What is the pathophysiology of diarrhea in adult horses?
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)
What are the clinical signs of acute diarrhea?
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
What are the lab findings assoc. w/ acute diarrhea?
CBC: mature neutropenia w/ ↑ bands, ↑ fibrinogen, thrombocytopenia

Chem: hypoproteinemia, hypoglycemia, hyponatremia, hypokalemia, hypocalcemia (esp. cantharidin), metabolic acidosis, azotemia, +/- ↑ liver enzymes, bile acids, hyperbilirubinemia
How is acute diarrhea diagnosed?
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)
What is the tx for acute diarrhea?
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
What are some causes of chronic diarrhea in adult horses?
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)
What are the clinical signs of chronic diarrhea?
wt. loss, +/- colic, +/- peripheral edema (if hypoproteinemic)

rarely dehydrated & rarely have systemic inflammation
What lab findings are assoc. w/ chronic diarrhea?
CBC/Chem: usually normal

+/- hypoproteinemia,+/- anemia of chronic inflammation, +/- electrolyte imbalances
How is chronic diarrhea diagnosed?
hard to dx

fecal float, sand test, peritoneal fluid analysis, fecal culture, abd. U/S, rectal bx
What is the tx for chronic diarrhea?
- 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
What is the pathophysiology of right dorsal ulcerative colitis?
- 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
What are the clinical signs of acute & chronic R dorsal ulcerative colitis?
acute: colic, mild to moderate diarrhea, anorexia, edema (d/t PLE)

chronic: intermittent colic, wt. loss, intermittent diarrhea, anorexia, edema
What lab findings are assoc. w/ R dorsal ulcerative colitis?
CBC: anemia of chronic inflammation or chronic blood loss, leukocytosis or leucopenia

chem.: panhypoproteinemia
peritoneal fluid: normal to ↑ WBCs
How is R dorsal ulcerative colitis diagnosed?
R/O other causes

U/S: not very sensitive (can only see ~1/3 or R dorsal colon): thickness > 5 mm: abnormal
What is the tx for R dorsal ulcerative colitis?
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
What is the pathogenesis of gastric ulcer dz (protective & harmful factors)?
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
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?
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
How is gastric ulcer dz diagnosed?
gastric endoscopy: only means of definitive dx

response to therapy
What is the tx for gastric ulcer dz?
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
What is the pathophysiology of esophageal obstruction (choke)?
functional or mechanical obstruction --> reflux of saliva & food material --> mucosal injury, possible ulceration, stretching of wall, rupture
What are some clinical signs of esophageal obstruction?
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
What lab findings are assoc. w/ esophageal obstruction?
hemoconcentration: ↑ PCV, TP
electrolyte &

acid/base abnormalities: hyponatremia, hypokalemia, metabolic acidosis

mild azotemia
How is esophageal obstruction diagnosed?
establish obstruction: clinical signs, ability to pass NG tube (careful: risk of perforation), endoscopy, U/S, rads +/- contrast

look for underlying cause
What is the tx for esophageal obstruction?
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
What is the pathogenesis & signalment of proliferative enteropathy?
- Lawsonia intracellularis infection
- transmission: fecal-oral
- organism promotes epithelial proliferation (hypertrophy) in SI --> malabsorption, PLE

- signalment: 1-6 mo. old
What are the clinical signs of proliferative enteropathy?
thin, +/- colic, diarrhea +/- melena, peripheral edema
How is proliferative enteropathy diagnosed?
- U/S
- definitive dx: serology or fecal PCR (specific but very insensitive)
- can do tissue PCR post-mortem
What is the tx for proliferative enteropathy?
Doxycycline: tx of choice

erythromycin, azithromycin, chloramphenicol also used

supportive care: fluids, colloids
What is the pathophysiology & signalment for IBD?
- 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
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
What lab findings are assoc. w/ IBD?
anemia of chronic inflammation or blood loss
possible leukocytosis: eosinophilia, lymphocytosis depending on dz
+/- ↑ fibrinogen
panhypoproteinemia
How is IBD diagnosed?
- 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
What is the tx for IBD?
- 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)
What is the pathophysiology of peritonitis?
- 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
What clinical signs are assoc. w/ peritonitis?
wt. loss, pyrexia, anorexia, colic, diarrhea, +/- sepsis
How is peritonitis diagnosed?
- peritoneal fluid analysis: WBC, protein, glucose, pH
- U/S
- rectal exam
What is the tx for peritonitis?
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
What is the pathophysiology of proximal enteritis?
- severe inflammatory dz of duodenum & proximal jejunum
- etiology unknown: Clostridium difficile?, mycotoxins?
- mucosal barrier damage --> inflammation --> hypersecretion, functional ileus, gastric fluid accumulation
What are some clinical signs of proximal enteritis?
acute colic, fever, signs of sepsis (depression, tachycardia, tachypnea, hyperemic mm, prolonged CRT), dehydration, nasogastric reflux (reddish orange), NO diarrhea
What lab findings are assoc. w/ proximal enteritis?
CBC: leucopenia followed by leukocytosis, hemoconcentration, ↑ fibrinogen, thrombocytopenia

Chem: hyponatremia, hypochloridemia, hypokalemia, hypocalcemia, metabolic acidosis, +/- abnormal organ function tests (ex. liver)
How is proximal enteritis diagnosed?
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)
What is the tx for proximal enteritis?
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
ddx for intermittent colic w/ or w/o weight loss
R dorsal ulcerative colitis, obstructive GI dz, gastric ulcers, IBD, neoplasia, sand enteropathy, parasites (cyathosomes), peritonitis, dental dz, EIA
ddx for intermittent colic w/ bruxism or salivation
gastric ulcers, gastric neoplasia, gastric impaction, esophagitis, gastric outflow obstruction, R dorsal ulcerative colitis
ddx for esophageal dysphagia
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
ddx for proximal enteritis signs
proximal enteritis, peritonitis, small intestinal obstruction (strangulating or non-strangulating), gastric outflow obstruction, Salmonellosis
ddx for weight loss w/ or w/o colic
IBD, parasites, malnutrition, liver dz, renal failure, EIA, neoplasia, intra-abdominal abscess, dental dz, sand enteropathy, gastric ulcers, chronic dz of other systems