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GI

  1. __________ is an effective emetic in cats
    Xylazine (Rompun)
  2. _________ is a broad spectrum antiemetic by virtue of an action in the emetic center
    Maropitant (cerenia)
  3. ___________ SHOULD NOT be used as an appetite suppressant/weight control drug in cats
    Dirlotapride (silentrol)
  4. ________ is the most effective drug for hypomotilit/megacolon-related constipation in cats
    Cisapride
  5. anti-ileus effect of lidocaine related to ___________
    Blockage of pain impulses
  6. the __________ effect of ________ and __________ contribute to their effectiveness in diarrhea related to inflammatory bowel disease
    • Anti-inflammatory
    • metronidazole
    • tylosin
  7. ________ can potentially bind concurrently administered oral drugs, preventing their absorption
    Sucralfate
  8. Small vs large bowel diarrhea: 
    Tenesmus
    frequency
    urgency
    stool volume
    mucus
    fresh blood
    vomiting
    weight loss
    • Image Upload 2
    • small bowel also more associated with failure to thrive, changes in appetite, borborygmi, flatus, abdominal discomfort, ascites and edema
  9. Dilation
    Expansion within normal parameters
  10. dilitation
    Stretching beyond normal limits
  11. distension
    Expansion (normal or abnormal) due to increased intraluminal pressure
  12. GDV view and what you see on the other view
    • R lat
    • change in OPACITY NOT a change in SHAPE
    • Double bubble!! vs gastric compartmentalization
  13. functional ileus, rad signs
    • lack of peristaltic contractions
    • Normal vs mild to moderate diffuse SI enlargement (filled with gas, fluid or combination)
    • imaging in rarely helpful in forward flow (diarrhea)
  14. mechanical ileus and radiographic patterns
    • Physical obstruction of intestine
    • severe segmental small-intestinal enlargment
    • small intestinal foreign body
    • linear foreign body. 
    • SI full of gas, liquid or combination
    • imaging is rarely helpful in forward flow cases (diarrhea)
  15. focal SI enlargement ddx
    intestinal mass (neoplasm, granuloma, abscess
  16. segemntal SI enlargement
    • Larger portion than focal enlarged.  
    • Usu SI obstruction, pancreatitis, regional peritonitis
  17. diffuse SI enlargement ddx
    • Entire SI
    • infectious/inflammatory, metabolic, downstream obstruction
  18. Radiographic signs of mesenteric torsion
    • Severe diffuse small intestinal enlargement
    • vascular compression of root of mesentery
  19. difference between constipation, obstipation and megacolon on radiographs
    None
  20. mural filling defect
    eccentrically located place with no contrast on at least one radiographic view (central on some).  Central on all is luminal.
  21. lumen filling defect
    Centrally located place with no contrast on ALL radiographic views.  Mural is eccentric
  22. List the 5 Fs of abdominal distension
    • Fat
    • feed
    • fetus
    • flatus
    • fluid
  23. Understand the pathophysiology behind the top 5 etiologies of bloat
    • hypocalcemia: failure of rumen muscle contraction
    • frothy bloat: too much grain or legume traps air into froth, doesn't stimulate cardia to eructate 
    • ruminal acidosis: too many carbs, decreased pH, increased VFA production, osmotic draw of water, gas not touching cardia, stretch receptors stop contractions 
    • choke: esophageal obstruction prevents eructation
    • positional: gas cap not touching cardia due to position (laying down), no eructation
  24. treatments for acute ruminal distension
    • Orogastric tube long enough to reach gas cap
    • knife/trochar
    • bloat whistle
    • surgical fistula
  25. explain the difference between acute and chronic ruminal distension
    • acute: bloat
    • chronic: vagal syndrome, vagal indigestion - "papple". Soft and doughy.  Vagus damaged.  Could be hardware disease or pyloric outflow obstruction
  26. list the causes of ruminal distension in calves
    • "idiopathic": bronchopneumonia causing enlarged mediastial lymph nodes that don't allow eructation
    • ruminal drinkers: failure of esophageal groove in calves that drink milk from a bucket
  27. recommendations to pet owners for worms (5)
    • fecal exams (floatation with centrifugation) 4x in the first year, then 2x/year.  
    • Deworm puppies and kittens starting at 2 weeks, then every 2 weeks until they start HWP that kills hooks and roundworms
    • treat nursing dams at same time as litters
    • prompt/frequent fecal removal
    • prevent hunting
  28. why are parasitic worms prevalent? (5)
    • really well adapted to infect hosts
    • MANY eggs/day to contaminate environment
    • eggs long-lived in environment (esp roundworms)
    • can infect prey, and infect predators through prey
    • capable of vertical transmission
    • treatment is not curative (reinfection common, and young or arrested worms not killed)
  29. species of roundworms (4)
    • toxocara canis
    • toxocara cati
    • toxascaris leonina
    • baylisascaris procyonis
  30. how dogs (4) and cats (3) get infected with roundworms
    • dogs: transplacental (ALL puppies infected), transmammary, ingestion from soil, ingestion of paratenic host (mammal, earthworm, cockroach, bird).
    • cats: transmammary (rare), ingestion from soil, ingestion from paratenic host (mammal, earthworm, cockroach, bird)
  31. pathology and clinical signs of ascarids (5, 11)
    • light to moderate: asymptomatic, vomiting, diarrhea, mucus in feces, growth retardation
    • heavy: disseminated granulomas in tissues (liver, lungs, kidneys, heart, eyes in dogs), eosiniphilia (cats), cough (cats), hypertrophy or atrophy of intestinal layers, vomiting, mucoid gastroenteritis, diarrhea, growth impairment, emaciation (dogs), death (dogs).
  32. products that treat ascarids and hookworms
    • nemex
    • panacur
    • drontal plus
    • heartgard plus
    • iverhart max
    • sentinel
    • advantage multi
    • trifexis
  33. Hookworm species (4) and best/worst
    • ancylostoma caninum - the most pathogenic
    • ancylostoma braziliese - cutaneous
    • ancylostoma tubaeforme
    • uncinaria stenocephala - the mildest, asymptomatic
  34. how dogs (4) and cats (3) get infected with hookworms
    • dogs: cutaneous, from soil, from paratenic host (mammals, cockroaches, birds), transmammary
    • cats: cutaneous, from soil, from paratenic hosts
  35. clinical signs of hookworm infection
    • anemia (blood loss)
    • inappetance
    • ill-thrift
    • emaciation (protein loss)
    • diarrhea
    • slimy or bloody diarrhea
    • death
  36. zoonosis of hookworms
    • cutaneous larva migrans (skin, A. braziliense)
    • visceral larva migrans
    • ocular larva migrans
  37. causes of ptyalism in horses and cattle (2 and examples, 3 most common)
    • inability to swallow: choke, neuro like botulism, EPM and Guttural Pouch Mycosis
    • excessive production: red clover toxicity (slaframine, PNS), mouth injury/irritation, gastric/esophageal ulceration in foals
    • stomatitis (mercury, plant awns, NSAIDSs, Baytril, dental stuff)
    • losing saliva shouldn't upset equine acid/base, but cows can get a profound metabolic acidosis from lost bicarb
  38. causes of and dx of Lumpy Jaw
    • actinomyces bovis - NOT a commensal (in soil)
    • eats away at bones (osteomyelitis, mandible or maxilla become soft).  Will continue to eat, not painful.  
    • Eventually ruptures and seeds environment
  39. causes of and dx of Wooden tongue
    • actinobacillus lignieresii - a commensal!  Must be an INJURY.  Painful
    • fibrosing disease of any soft tissue.  Eathing sticks, foxtails, sharp feed, etc. 
    • dx: soft tissue becoming hard. 
    • Corynebacterium or Actinomyces can cause wooden tongue in horses (infrequent)
  40. causes (4) of pharyngeal trauma in cattle.  MO (3)
    • balling guns, stomach tubes, choke (apple or potato!), esophageal feeders in calves
    • MO: trueperella pyogenes, fusobacterium necrophorum, bacterioides spp
  41. esophageal groove dysfunction in calves
    • when bucket-fed calves put milk in the rumen, not the abomasum, because the esophageal groove malfunctions. 
    • causes bloat, intermittent anorexia, poor growth and grey feces.  Predisposes to abomasitis
    • wean or switch to bottle (or smaller nipple), feed consistent temp milk.
  42. equine "grass mumps"
    pathophysiology unknown, related to green pasture.  Swelling of parotid salivary glands.  No medical concern.  Take off pasture to tx.  Sometimes returns when they're returned to pasture.
  43. signs/diagnose (5), treat (4) and prevent esophageal choke in horses (including complications)
    What about in Friesian horses?
    • signs/dx: excessive salivation, retching, coughing, saliva and food dripping from nostrils.  Try to pass tube and can't - definitive diagnosis.
    • tx: tranquilize (stress and lower head), REMOVE food and water.  This may be enough (4-6h), or could gently lavage and push with tube.  Give buscopam (PNS), GA if needed.  Then IV fluids, no food, maybe abx for aspiration
    • prevention: dental health, good food with no beet pulp, wet food for geriatric, don't feed excited or sedated horses. Don't let them eat too fast.
    • Friesian: megaesophagus, chronic choke, may also have trouble with gastric emptying
  44. Classical presentation and signs of a patient with acute abdomen
    • Praying position
    • pain can be regional, focal or diffuse
  45. stabilize and manage a patient with acute abdomen (and why you do each thing).
    • Restore abnormalities in major body systems
    • maximize delivery of O2 (put on O2 or give fluid therapy)
    • analgesia
    • dx underlying pathology
    • +/- empirical abx (septic!)
    • +/- sx
    • 1. Rapid stabilization. 2. Early ID. 3. Attention to co-morbid conditions.  4. Timely definitive therapy
    • Assess resp, CV, perfusion and mentation (these things kill quickly)
    • Oxygen is never wrong unless you're on fire
    • fluids in hypovolemic shock cases (hemoab? GDV?), manage dehydration?
    • abdominocentesis to check for intracellular bacteria, creatinine/potassium (uroabdomen), glc/lactate (septic or neoplasia), amylase/lipase (pancreatitis), bilirubin (biliary peritonitis). Or diagnostic peritoneal lavage if can't get fluid
    • abdominal rads (+/- further imaging) - dx
    • analgesia - opioids like fentanyl or methadone
    • Surgical exploration if no ddx is forthcoming
    • feeding tube as needed
  46. rational dx approach to acute abdomen patient.  What is your ER database and why?
    • Hx, PE (resp, CV, perfusion, mentation - these things kill fast)
    • QATs (anemia/hemorrhage?Ok for sx? Organ screening)
    • blood gas (shock = acidosis)
    • electrolytes (dx, tx abnormalities)
    • +/- lactate (shock = acidosis, check status of tx)
    • peripheral blood smear (septic?)
    • effusion evaluation (septic? Dx)
    • CBC
    • chemistry
    • coag (DIC? OK for sx?)
    • blood type (transfusion later?)
    • urine
  47. when is abdominocentesis indicated in an acute abdomen, and describe
    • whenever present in companion animals, or suspect
    • Can do single quadrant, four quadrant, ultrasoundguided (this is best).  Find a pocket on U/S, avoid midline.  
    • Diagnostic peritoneal lavage: fuse 20-22mL/kg, massage or walk and aspirate (can't run chem on this, microscope only)
    • Put in EDTA and red top, save some for culture, put some on a slide.  Compare results to peripheral
  48. analysis of abdominal fluid: understand indications and interpretation of cytology, aerobic/anaerobic c/s, cell count and TP concentration, as well as biochem tests (glc, lactase, amylase, lipase, creatinine, potassium, total bilirubin)
    • cytology: direct stain vs centrifuges, look for intracellular bacteria, neutrophils with lipid vacuoles, bile pigments etc
    • aerobic/anaerobic c/s: bacteria sensitivity 
    • cell count, TP concentration: transudate, modified transudate, exudate
    • glc/lactase:  septic peritonitis or neoplasia
    • amylase/lipase: pancreatitis
    • creatinine/potassium: uroabdomen
    • total bilirubin: biliary peritonitis
  49. describe approach to traumatic wounds involving the abdomen (including bite wounds and penetrating wounds)
    • SURGICAL EXPLORATION of WOUND
    • medical, surgery or medical stabilization before therapy.
    • Open (remove crushed tissue)
    • debride
    • lavage
    • close using appropriate drainage or leave open.  
    • FULL exploratory if abdomen is penetrated.
  50. what does the presence of free air in abdominal cavity mean on abdominal X-ray of a patient with acute abdomen
    • Seen between liver and diaphragm
    • gastric necrosis and/or stomach rupture
  51. most likely signalment and risk factors of dogs GDV
    • Adults
    • lg to giant breeds (even with short legs!)
    • deep chests
    • first-degree relative with GDV
    • eating too fast
    • being nervous
    • raised food bowl
    • feeding large volume or once daily
    • high fat or oil in dry food
  52. list reported risk factors for increased mortality associated with GDV (7)
    • Increased lactate (with minimal decreases in serial collection)
    • gastric necrosis
    • splenectomy
    • partial gastrectoy or splenectomy 
    • pre-and post-operative arrhythmias
    • increased duration of clinical signs
    • increased high mobility group box I (HMGB1)
  53. Pathophysof GDV including gastric distension (3), gastric volvulus, splenic involvement (4)
    • Gastric distension: swallowing Air, food, fluid. Pressure decreases venous return (shock), congestion of splanchnic vessels (breakdown of gut mucosal barrier, bacterial translocation, SIRS, DIC), increased gastric wall pressure (ischemia, infection, ulceration, necrosis, perforation, peritonitis)
    • gastric volvulus: twists to occlude pylorus (clockwise), pylorus ends on left side
    • splenic involvement: usually rotates with the stomach and short gastric ligaments and vessels cause congestion and splenomegaly,infarct and thrombosis, torsion, avulsed branches of arteries tear and cause hemoabdomen
  54. classic presentation and clinical signs of GDV
    • presentation: large, deep chested dog with acute history of agitation and non-productive retching
    • PE reveals distended, tympanic abdomen (probably), ptylism with thick, ropey saliva +/- shock.
  55. how is dx of GDV made (or confirmed)-detailed and specific!!
    • Suspicion from clinical signs (stabilize! And take QATs for trends)
    • R lat radiograph
  56. Stabilize and treat a GDV, understand the principles a behind your interventions
    • IV fluids including hypertonic saline for hypotension
    • lidocaine IV to decrease arrhythmias, RLat rads, decompression via trocarization or orogastic if necessary, SURGERY
  57. what is in emergency database of a GDV and why?
    • QATs: baseline values, monitoring trends
    • venous blood gas: acid/base, electrolytes likely to be wrong, need correction
    • lactate: gauge shock, perfusion, monitor serially
    • coag: DIC! Ok for sx
  58. What lab tests have prognostic values for GDV (usefulness and limitation)
    serial lactate: decreasing is a good prognosis, but not great data
  59. What does the presence of free air in the abdominal cavity or gastric pneumnotosis mean on an abdominal X-ray of a patient with a GDV?  How does this affect prognosis?
    • free air: between liver and diaphragm.From gastric necrosis an/or stomach rupture
    • gastric pneumotosis: gas dissection of gastric mucosa, may be gastric necrosis, increases likelihood of gastric resection
  60. Describe in detail the step-by-step procedure recommended to achieve gastric decompression in GDV?  Include oro-gastric tube and trocarization.
    • after fluid therapy!
    • Orogastric tube: measure from tip to last rib, lubricate, tube into esophagus(PALPATE), gently rotate in, you'll get a rush of stomach gas and efflux.  Lavage.
    • trocharization: clip and prep, "ping" 16g or 18g poke.  Can usu pass tube afterwards.
  61. Why is correction of shock/dehydration prior to intestinal surgery important?
    • optimizing bowel perfusion prior to surgical trauma reduces the risk of dehiscence.  
    • Also for higher likelihood of surgery survival
  62. Steps required to enter abdominal cavity for an exploratory laparotomy
    • optimize exposure: good light, table height, wide clip preparing for extended incision.  Clip prepuce to the side
    • incision from xiphoid to midway between umbilicus and pubis.  
    • resect falciform ligament: gets in the way and becomes useless and traumatized, can be necrotic and cause dehiscence
    • Balfour retractors
    • use stay sutures and pack lap pads around organs.
  63. How to use stay sutures and lap sponges to improve exposure
    • use 3-0 PDS sutures on either side of intended incision, tag with hemostats and clip to drapes.  This elevates and maintains exposure.  
    • Saline-soaked lap pads pack encroaching structures out of field and maintain exposure (also can catch spillover)
  64. List 2 ways to reduce tissue trauma when handling bowel
    • handle as little as possible!  
    • Atraumatic forceps (debakey, NOT rat tooth!)
    • use stay sutures instead of forceps wherever possible to avoid repetitive handling
    • avoid dessication
  65. List two ways to reduce patient exposure to bacterial contaminants in an open bowel surgery
    • use additional lap sponges and a secondary waterproof barrier to drape around bowel loop before opening (secondary barrier principle)
    • change gloves and instruments after the dirty part! After R&A and before closing
    • use assistant's fingers (or doyen bowel clamps) to section off bowel
    • have a "receiving zone" for the gross stuff that's coming out. "Landing zone for the schmoo"
    • DO NOT CUT THE COLON
  66. Suture type, suture size, needle type and suture patterns appropriate for SA intestinal surgery
    • 3-0 or 4-0 PDS (NO braided, catgut or monocryl)
    • curved, round-bodied taper point needle (separates rather than cuts for smallest hole and leakproof seal)
    • simple interrupted 2-3mm from incision and 3mm apart, using SUBMUCOSAL layer. 
    • simple continuous maybe okay in SI but not LI
  67. Role of prophylactic abx in SA intestinal sx
    • it is a clean-contaminated procedure so need them during sx only.  
    • 30 mins prior then every 60-90 mins.  
    • discontinue after sx is over unless septic or major spillage.
  68. benefits of early feeding following intestinal surgery
    • feeding within 12h of surgery promotes intestinal healing and prevents ileus
    • this decreases mortality, length of stay and risk of dehiscence
    • NG/NE tube (or E tube for longer) if necessary
  69. risks that should be discussed with O prior to SA intestinal sx
    • possibility of negative explore
    • GI dehiscence in 5-20%
    • incisional infection 5%
    • Prolonged hospital stays (24-48h normal, some need 4-5d)
  70. why are linear FB cases considered higher sx risk?
    bowel is under tension, risk of ischemic injury and large areas of traumatized bowel, prone to further trauma from surgical manipulation
  71. when performing a surgical explore for FB, why prox duodenum should be looked at first
    • if plicated, this is a linear FB and needs to be handled differently.
    • Normally run the bowel.  In linear, minimal handling!!  Check the tongue and pylorus and cut the string first.  String could cut the bowel--iatrogenic perforation
  72. steps for removal of linear FB
    • Normal clip, prep, incision, balfour retractors.
    • Look at proximal bowel (plicated)
    • check under the tongue, cut string if present
    • gastrotomy (stay sutures, pack off, suction, reach in and cut as close to pylorus as you safely can to "release" the duodenum)
    • milk FB downstream into one section of bowel that HASN't been involved
  73. catheter technique for removing an embedded linear FB
    • If intestine stays bunched after gastrotomy, make single enterotomy, thread red rubber over the string for atraumatic removal, then cut at the other end and remove from that side.  
    • Manages any FB with only a gastrotomy and two enterotomies.
  74. how to plan and steps involved for intestinal R&A
    • If a piece of bowel is really really angry, take it out! Both sides must be very viable, so take the WHOLE angry area. 
    • Both sides should have good feeder vessels.  Ligate and cut everything between, don't forget the one that runs along the intestine.  
    • If two sides aren't the same size, cut the smaller side on an angle (blood vessel side longer) so they match up and everyone has good blood supply. Nice to pile lap pads under to start, gives you a more visible field
    • close mesenteric side first, always do the hardest sutures first.
    • close mesentery but be SO CAREFUL not to accidently loop in feeder vessels
    • Omentalize
    • DO NOT CUT THE COLON
  75. Why you shouldn't perform a colostomy if an FB is in the colon
    If it made it to the colon, it will pass.  Colon has LOTS of bacteria and doesn't heal as well as SI.
  76. Why are healing of colon and rectum delayed compared to rest of GI tract
    • poor collateral circulation
    • large numbers of bacteria
    • high intraluminal pressure
    • collagen lysis > synthesis in first 3-4d, so ONLY suture holding together and preventing dehiscence and septic peritonitis
  77. Common complications of rectal surgery, explain possible reasons for occurrence (4/8)
    • dehiscence
    • infection
    • stricture formation (rare in SI but common in LI)
    • incontinence
    • Due to:
    • tension
    • poor suture placement
    • disruption of blood supply
    • incontinence: 1. removal of >4cm, 2. removal of distal 1.5cm, 3. removal of >50% of EAS, 4. 360 degree resection
  78. common rectal (3), perianal (2) and anal sac (1) tumors, including dx, tx, prognosis
    • benign rectal: adenomatous polyps
    • malignant rectal: adenocarcinoma in dogs, lymphoma in cats
    • perianal: adenomas in MI dogs, hepatoid tumors (not in cats)
    • anal sac: CHANG
  79. techniques for anal gland removal and how to avoid complications
    • open: incision from duct out through skin.  Cuts across anal sphincter and if you don't get whole sac you'll have a fistula
    • closed: put something in duct to map hole, then incise from outside.  Avoids EAS, sac is closed so easier to get whole thing (esp with wax)
    • Ecollar, analgesia, ice and abx ointment as a leakage barrier. 
    • complications: incisional, scooting, inflammation, fecal incontinence from excessive removal of EAS, draining tract from piece of sac remaining.  Use closed!
  80. common causes of perineal hernia, common tx techniques and when sx is an emergency
    • weakening of pelvic diaphragm.  
    • Common in male intact, straining (prostate etc), docked tails or barkers
    • treatment: medical (prevent constipation and causative factors.  Not ideal) or surgery to put it back.  
    • Sx is an emergency when bladder or viscera are entrapped!
  81. rotavirus in foals
    • most common proven cause of diarrhea in foals
    • 3d-5mo, younger is more severe
    • risk for gastric ulceration
    • very contagious
    • ELISA, EM or PCR (best)
    • hydration, ulcer prophylaxis, lactaid etc
    • vaccinate mom
  82. clostridium perfringens type A in foals
    • often blamed but rarely proven as causes of diarrhea.
    • NetF toxin, translocation
    • 1-7d
    • hyponatremia, hypochloremia, azotemia, hypokalemia, metabolic acidosis
    • antiserum and vaccination
    • abx (metro, kpen)
  83. clostridium perfringens type C in foals
    • <5d
    • LIFE-THREATENING
    • beta toxin (necrotic) causes bloody diarrhea
    • cytology of blood culture, peritoneal fluid.
    • abx (metro)
  84. clostridium difficile in foals
    • <7d
    • toxins found in stool of normal foals.
    • caused by abx in adults, not foals.
    • abx (metro)
  85. salmonella in foals and weanlings
    • translocation of bacteria from gut common, so high mortality
    • neonates, then a few months old, not between
    • bacteremia common
    • mare culture positive but asymptomatic
    • give abx based on c/s
  86. coronavirus in foals
    Only cause diarrhea with co-infection (crypto)
  87. cryptosporidium parvum in foals
    Only cause diarrhea with co-infection (coronavirus)
  88. diarrhea in foals (causes)
    • clostridium difficile (1-7d)
    • clostridium perfringens type A (1-4d)
    • clostridium perfringens type C (1-7d)
    • rotavirus (3d-5mo)
    • salmonella (first 2 wks)
    • beta coronavirus + cryptosporidianeonatal septicemia
    • foal heat (7-12d) (change in microbiome)
  89. non-specific tx for foal enteritis
    • fluids
    • anti-ulcer
    • parenteral nutrition
    • probiotics
    • analgesia for colic
  90. diarrhea in weanlings, yearlings
    • proliferative enteropathy/lawsonia intracellularis (3-11mo)
    • rhodococcus equi enterocolitis (3wk-9mo)
    • abx-induced diarrhea
    • salmonella (after 6wk)
    • (also neorickettsia risticii, listeria, brachyspira, coronavirus, parasites)
  91. lawsonia intracellularis/proliferative enteropathy in weanlings/yearlings
    • 3-11mo
    • found in feces of unaffected
    • LOW TOTAL PROTEIN (leukocytosis and anemia), increased CK, electolytes, "wagon wheel" in SI
    • dx via clinical signs, fecal PCR and serology
    • abx (oxytet to doxy)
    • good px with tx but MONTHS to gain weight
    • can cause coagulopathy, DIC.  May be associated with parasites and renal failure
  92. Rhodococcus equi enterocolitis in weanlings/yearlings
    • 3wks-9months
    • infect peyer's patches.  FEVER (not seen with r. equi pneumonia)
    • Other organ systems can be affected (lung abscesses, uveitis, synovitis)
    • a r/o dx? fecal swab, VapA-plasmids, leukoCYTOSIS unlike most diarrheas
    • clarithro/azithro + rifampin
    • px good unless bone infection or abdominal abscesses (weight loss before diarrhea)
  93. antibiotic induced diarrhea in weanlings/yearlings
    • macrolides (careful after 3-4mo!), trimethroprim-sulfamethoxazole, rifampin
    • within 2-6d of treatment
    • hyponatremia, hypchloremia, dehydration, decreased protein, azotemia, neutropenia with left shift
    • metro, fluids, low-dose NSAIDs, transfaunation
  94. most common gastric tumors in c/d
    LSA in cat stomach, carcinoma in a dog
  95. where to cut stomach for a gastrotomy
    • over lesion or in mid-body, away from blood supply in greater curvature.
    • Use have to incise both layers separately, seromuscularis and mucosa fall away from each other.
  96. bile is present in vomit when
    pylorus is unobstructed.  Alkalosis may develop is pylorus IS obstructed
  97. how to close the stomach after gastrotomy
    • 2-layer closure with 2-0 or 3-0 absorbable
    • mucosa: simple continuous
    • seromuscularis: simple continuous or inverting (Cushings - make straight lines over incision).  Don't enter gastric lumen with these sutures!  Just seromuscularis.  
    • lavage abdomen if leakage occurred (around your packed off towels.
  98. peri- and post-op care for gastrotomy
    • peri-op abx q90min-2h
    • fluids until drinking (12-24h)
    • famotidine and sucralfate
    • offer water and blended bland food at 12-24h -- healing is faster if they eat!!
  99. pathophysiology of GDV (7)
    • older dog = lax ligaments of stomach
    • deep chested have acute angle between esophagus and stomach
    • rapid ingestion = aerophagia = gastric distension (most gas in stomach is swallowed air)
    • acute angle prevents eructation (one-way valve)
    • Pylorus rotates VENTRALLY AND TO THE LEFT
    • hypovolemic shock (compressed VC and portal vein = sequestration of blood, no blood to central body of stomach, gastric wall compression compromises further, splenic rotation exacerbates)
    • venous stasis, necrosis, infarcts cause DIC
  100. IN GDV, the pylorus always rotates
    ventrally and to the left
  101. GDV sx and px
    • ventral midline
    • decompress stomach with tube or trochar
    • grab what is on the dog's left and pull it to the right until you have a normal stomach
    • Look for necrotic tissue in stomach (body, cardia), spleen (rare).  Resect necrotic (20% of dogs, decreases prognosis to 70% mortality)
    • incisional gastropexy
    • lavage and suction drains if ruptured
    • fluids, abx q2h
    • px: 15-30% if no resection, 50-70% with resection
  102. incisional gastropexy
    • adhesion between pyloric antrum and right ventrolateral body wall
    • incisions in seromuscular (ONLY) of pylorus and peritoneum and transversus abdominus caudal to 13th rib
    • suture. Routine abdominal closure.
  103. post-op GDV sx care
    • fluids, abx
    • monitor for DIC
    • H2 blockers and sucralfate
    • analgesia (NOT NSAID)
    • feed after 24-72h
    • ECG - arrhythmias in 50% due to myocardial hypoxia from decreased venous return 12-48h later, no tx usu needed)
  104. TGE in piglets (transmissible gastroenteritis)
    • all ages
    • necropsy: acidic diarrhea, lacteals clear (no resorption, villi wiped out), thin intestinal wall
    • highly contagious coronavirus
    • <2wks piglets: vomiting, watery diarrhea, death
    • finishing pigs and adults: inappetence and diarrhea, occasional vomiting
    • Dx: FAT, direct EM, viral isolation, PCR
    • tx: NONE
    • prevention: vaccines or grind intestines of piglet and feed to sow (IgA in milk)
    • enters via starlings, visitors, swine
  105. PED in piglets
    • all ages, fecal spread
    • very contagious coronavirus
    • necropsy: acidic diarrhea, lacteals clear. Blunted villi, crypts preserved.
    • <2wks: v, d, death, horrid smell
    • finishing and adults: mild d, inappetance, occasional v
    • reportable
    • PCR, histology, immunohistochem
    • aggressive feedback of feces or piglet intestines to sows. Commercial vax only partially effective
    • BIOSECURITY.  Not zoo
  106. mucohemorrhagic diarrhea differentials in older piglets
    • swine dysentery (>7d, esp grow/finish)
    • salmonellosis (post-weaning)
    • trichuriasis/whipworms (post-weaning)
    • ileitis/lawsonia intracellulitis (post-weaning)
  107. coccidiosis in piglets
    • 5-14d (sometimes older)
    • Isospora suis
    • oocysts 2-3d AFTER scours, shedding sporadic.  Merozoites (blue bananas) in impression smears. Diarrhea doesn't respond to abx (amprolium)
    • Hygiene, all-in, all-out
  108. clostridium perfringens in piglets
    • piglets 1-7-14d
    • bloody diarrhea
    • necrohemorrhagic SI, sometimes LI with gas bubbles
    • gram + rods
    • Vax sows 2-5wks before farrowing
    • give 2-5cc antitoxin orally before 12h (gut still open) to stop outbreak.
  109. medication for enteric diseases in swine
    • expect a response in 24h (wrong dx or rx!)
    • treat parenterally or via water if off feed
    • oral pump to medicate piglets
    • therapeutic level of abx NOT GROWTH PROMOTANT LEVEL (illegal)
  110. mgmt to control enteric diseases in swine
    • BIOSECURITY!!!
    • All-in, all-out
    • sanitation
    • facility design (cleanable, no wildlife, separate ages)
    • keep warm (drafts, bedding/flooring)
    • proper nutrition (lamb milk replacer)
    • vax for mom and antibodies in milk for neonates (TGE, PED, rotavirus, e coli, clostridium perfringens, lawsonia)
  111. colibacilosis in swine
    • enterotoxigenic strains adhere to mucosa which causes fluid loss into intestines
    • inherited and acquired resistance (sows better than gilts)
    • neonatal to post-weaning
    • necropsy: alkaline diarrhea, white lacteals (bicarb lost, fat resorbed)
    • tx: oral abx, electrolytes, keep warm
    • prevention: keep clean, warm, dry and draft-free. remove sow feces. Vax sow
  112. Edema disease in swine
    • shigatoxin from e coli
    • thriving piglet dies suddenly 1-2wks after weaning.
    • Ataxia, convulsions, constipation or diarrhea, palpebral edema, edema of stomach wall or spiral colon
  113. rotavirus in swine
    • suckling or weaned pig
    • grey diarrhea
    • villous atrophy, but less severe than TGE
    • dx by FAT, EM, immunohistochem
    • vax sows prefarrowing, hygiene
  114. swine dysentery
    • Brachyspira hyodysenteriae
    • starting to reappear in midwest
    • carrier pigs, mice, manure
    • diarrhea with blood, mucus, bad smell.  Dehydration, wasting, death
    • necropsy: diffuse lesions in LI, foul smell.  Culture shows spirochetes
    • remove manure and disinfect (in summer when herd size down, medicate EVERYONE).  Control rodents.
  115. salmonellosis in swine
    • salmonella enterica choleraesuis and typhimurium (zoonotic)
    • postweaning piglets
    • marked fever, septicemia, enterocolitis. Mortality low but POOR FEED CONVERSION
    • prophylactic abx (used approved route, dose, etc because feed animal)
    • button ulcers and intestinal casts
  116. ileitis in swine
    • Lawsonia intracellularis
    • acute: sudden death, bloody diarrhea, anemia, melena
    • chronic: yellow-brown diarrhea, depressed feed intake, wasting without fever
    • abx (tylosin), and blue vax in NON-CHLORINATED water or by IM
  117. whipworm in swine
    • trichuris suis
    • survive 6 years in soil!  Pigs on dirt!
    • anorexia and bloody mucoid diarrhea, visible parasites on fibronecrotic membrane in LI in 3-4wks
    • bipolar egg
    • fenbendazole (safeguard
  118. gastric ulcers in swine
    • dead pig looks very white (bleeds to death), feces are small and dark. 
    • Ulcerated pars esophagus (patch of stomach, clean margins)
    • from stress!  Miss meals, hot, mixing, transport, simultaneous feed drops
    • food ground too small
  119. lamb/kid health is based on (7)
    • health and nutrition of dam
    • colostrum consumption
    • further nutrition of kid/lamb
    • sanitation
    • dipping navels (2-7% tincture of iodine)
    • separation of groups
    • comfort and ventilation
  120. lamb/kid colostrum
    • feed within 2h
    • 50 mL/kg QID first day (1oz/lb TID)
    • heat-treat to 56 for 60min
    • Johne's!!
    • Tube feed if needed (18 french) only if it can hold head up!!
  121. causes of diarrhea in neonate lamb/kids
    • e coli
    • cryptosporidiosis
    • rotavirus
    • caprine herpesvirus
    • lamb dysentery
    • salmonellosis
    • indigestion
  122. colibacillosis in lamb/kids
    • <10d
    • secretory diarrhea from enterotoxigenic strains
    • fluids
    • SANITATION and colostrum
    • in feces of normal goat kids
    • colostrum means shouldn't need to vax
    • oral electrolytes
    • NO BAYTRIL (FELONY)
  123. Floppy kid disease
    • metabolic acidosis without diarrhea or dehydration
    • 3-10d old (also lambs, occasional calf, cria)
    • cause unknown (e coli? Overfeeding?)
    • depressed, weak, no suckle, abdominal distension, cold extremities, low temp or fever.  Ill 24-36h
    • tx with bicarb/baking soda, pepto. Take off milk (TOO MUCH). Abx to prevent septicemia
  124. cryptosporidosis in lamb/kid
    • cryptosporidium parvum
    • intracellular protzoa, extracytoplasmic under brush border
    • >3wk (esp 5-10d)
    • ZOONOTIC, alcohol gel doesn't kill
    • white or yellow watery diarrhea, depression, poor haircoat, poor appetite, dehydration, acidosis, death if severe, mixed infections common
    • dx: fecal float, acid fast stain
    • tx: more and better colostrum, better sanitation, oral electrolytes. Lactaid.  Raise them in a box!
  125. lamb dystentery
    • clostridium perfringens (C)
    • <3wks old (beta toxin destroyed by trypsin in older animals)
    • hemorrhagic enterotoxemia, abdominal pain, rapid death
    • everyone should get the vax (for mom)
  126. Salmonellosis in lamb/kid
    • contamination at parturition, stress, food/water deprivation, concurrent abortions, death of adults.  
    • dx: culture of feces and lymph nodes (always large in young)
  127. Indigestion in lambs, kids
    cow milk to young lambs (kids can tolerate), excessive intake, indigestible (cheap) milk replacers (need low lactose, high fat and protein)
  128. causes of diarrhea in older kids and lambs (5)
    • coccidiosis
    • intestinal strongyles
    • enterotoxemia
    • salmonellosis
    • indigestion/rumen acidosis
  129. coccidiosis in lambs/kids
    • >3wks old (have it until proven otherwise)
    • "mucky butt"
    • species-specific eimeria
    • diarrhea and ill thrift
    • milk is protective so post-weaning.  poor nutrition, vit E/selenium deficiencies, crowding, wet environment, feet and feces in feeders!
    • small white foci on intestinal wall, absorption impaired
    • merozoites early, can have LOTS without disease.  Rebound after tx because coccidioSTATS while developing immunity. Limit shedding. 
    • Tx entire group prophylactically (decoquinate)
    • keep clean and dry, group by age (2 wks), keep dairy kids away from adults
  130. intestinal strongyles in sheep/goats
    • pasture problem (small and damp), L3 in dewdrops on grass. 
    • pasture rotation, cold winters help.  
    • Deworm ONLY those in need--resistance!!  Cull those that need lots of deworming.  Make sure to use correct dose PO, rotate drug group annually and super-double-dose new purchase
    • Fenbendazole (goat label dose is wrong)
  131. Enterotoxemia type D in lambs and kids
    • clostridium perfringens type D
    • >3wks (trypsin ACTIVATES this one)
    • abdominal pain, sudden death, neuro signs, fluid and fibrin in pericardial sac, pulpy kidney.
    • Antitoxin gives 3 week protection to those not already symptomatic, time for vax to work
  132. causes of diarrhea in adult small ruminants (6)
    • salmonellosis
    • indigestion/rumen acidosis
    • enterotoxemia (can kill adults)
    • intestinal strongyles (can kill adults)
    • paratuberculosis (can kill adults, usu no diarrhea)
    • toxemia from mastitis or metritis
  133. indigestion/rumen acidosis in adult small ruminants
    • roughage (fiber) digestion in the rumen produces acetate and pH >6, and bicarb in saliva from cud chewing buffers rumen. 
    • No cud to chew after grain, and soluble carbs produce propionate and butyrate and drop pH lower.  Bacteria produce lactic acid and lower it even more
    • acid absorbed from rumen = systemic acidosis
    • fluid pulled into rumen = dehydration, splashy rumen.  Rumen protozoa die, but some bacteria thrive, gram + dysbiosis
    • dx: aspirate rumen fluid and check with pH paper
    • tx: HAY, water, B vitamins, oral bicarb, abx, calcium, flunixin, transfaunation. 
    • FEED ROUGHAGE, free-choice bicarb, no sudden diet changes
  134. causes of chronic weight loss in small ruminants (6)
    • malnutrition: poor feed, social, dental, minerals, blind, lame
    • parasites: coccidia, haemonchus, strongyles, liver flukes, lungworms, tapeworms, keds, sarcoptic mange
    • chronic infections: paratuberculosis, caseous lymphadenitis, chronic pneumonia or mastitis, OPP, CAE, scrapie
    • neoplasia: 
    • renal amyloidosis
    • abomasal emptying defect
  135. paratuberculosis in small ruminants
    • mycobacterium avium subspecies paratuberculosis = Johne's Disease
    • incubates > 1 year, slowly progressive (2-7y before clinical signs), hastened by stress/poor condition things.
    • Nonspecific signs, like poor production, ill thrift, 10-20% diarrhea, weight loss, alopecia, hypoproteinemia, increased parasites.
    • fecal-oral, transplacental, transmammary, intra-species
    • suspect when you have good management and a few emaciated, lots of parasites
  136. dx of lg bowel diarrhea (5)
    • signs: tenesmus, frequency, increased urgency, mucus, fresh blood
    • systemically healthy: fecal float and culture, symptomatic
    • unwell: chem/CBC/UA, colonoscopy (L LAT!), U/S (rads rarely useful). R/O metabolic, systemic dz.
    • ALWAYS take a biopsy with coloscopy (good for histo)
  137. tx of lg bowel diarrhea
    • withhold food for 24h then introduce easily assimilable diet (rice with single protein like cottage cheese).  Add fiber like psyllium (bind bacteria, absorb water, promote motility). 
    • fenbendazole to kill whips
    • specific tx for specific dz (campylobacter, salmonella, giardia)
  138. acute non-specific colitis
    • commonly from dietary indiscretion, FB, etc
    • clinical: sudden-onset severe, often blood/mucoid diarrhea +/- vomiting. Rectal may reveal evidence of indiscretion
    • tx: symptomatic. NPO, then bland diet, protectants. If dehydration or systemic, fluids and pursue. +/- loperamide
  139. chronic colitis
    • ALWAYS should be confirmed by biopsy of mucosa (need histopath).  
    • fecal exam and culture, basic chem/CBC/UA
    • imaging, coloscopy with biopsy. 
    • falls under IBD umbrella (increased cellularity of lamina propria)
    • Lymphoplasmacytic enteritis: increased lymphocytes and plasma cells, most common
    • Granulomatous colitis: macrophages
  140. lymphocytic plasmacytic colitis
    • most common type of chronic colitis, characterized by mucosal infiltration of lymphocytes and plasma cells.
    • cause undetermined, but inflammation from lots of factors (environment, immune, MO etc)
    • tx: diet (digestible, novel protein, hydrolyzed?), abx or immunosuppressives, not sure which works for which.  tx response within 2 wks
  141. granulomatous colitis/histiocytic colitis
    • less common than lymphocytic plasmacytic
    • mucosal infiltration of macrophages +/- neutrophils and lymphocytes, plasma cells. 
    • underlying infection?
    • Cultures from abdomen everywhere and special stains, imaging of chest and abdomen.
    • Don't immunosuppress until infectious agents excluded. 
    • px guarded to poor without underlying cause
  142. Granulomatous Colitis in Boxer Dogs
    • aka histiocytic Ulcerative Colitis
    • severe lg bowel diarrhea with profound weight loss, anemia, hypoalbuminemia.  Mucosal infiltration with macrophages, mucosal ulceration and loss of goblet cells
    • E coli
    • enrofloxacin (except now some are resistant, so don't tx until you KNOW)
  143. colonic neoplasia
    • most are malignant.
    • adenocarcinoma (infiltrative and ulcerative), LSA (diffuse), polyps (benign, pre-malignant?)
    • more in rectum than colon
  144. Constipation dx
    • infrequent and difficult evacuation of feces
    • R/O peri-anal and postural causes of painful or refusal. 
    • Rectal (FB, mass, stricture)
    • neuro (megacolon could be dysautonomia)
    • severe or recurrent gets a CBC/Chem/UA
    • rads to check for megacolon
    • proctoscope/coloscopy
    • nothing?  Idiopathic megacolon
    • tx: alleviate constipation (lactulose, enemas, manual deobstipation), fluids if dehydrated (constipation + vomiting), remove underlying cause, prevent recurrence (laxatives, bulking agents)
    • cisapride (pro-kinetic) may help.
  145. diarrhea definition and patho-mechanisms (4)
    • feces containing excess water, resulting in an increase in fluidity, volume or frequency of bowel movements. 
    • osmotic, secretory, permeability and motility.  Often more than one involved.
  146. cobalamin and folate
    • cobalamin decrease: diet, ileal disease, intestinal bacteria, EPI, receptor abnormality. Pancreatic or enteric dz in cats.
    • folate increase: diet, supplementation, intestinal bacteria, low intestinal pH, EPI
    • folate decrease: diet, proximal SI disease, drugs like sulfasalazine
  147. fecal alpha-1 antiprotease
    test to confirm GIT as a site of protein loss
  148. Exocrine Pancreatic insufficiency (causes, % gone, dx, cbc/chem results, cobalamin/folate, vit E)
    • lack of effective pancreatic exocrine secretions in SI, usu due to atrophy (dogs) or chronic pancreatitis (cats), or excessive pancreatic acid, protein malnutrition or hypoplasia.
    • 90% gone before signs are noted
    • dx via LOW TLI (<2.5 for dogs, normal is >5)
    • weight loss, chronic SI diarrhea, ravenous. CBC/chem unremarkable, low cholesteral increased ALT. Low cobalamin, high folate. Vitamin E low. Cats may get Vit K deficiency
    • Tx: powdered enzymes or whole pancreas. normal diet or digestable fat. Could need oxytet to get flora under control.
  149. major diagnostic tool for chronic diarrhea
    intestinal biopsy
  150. most common histopathological diagnoses in dogs with chronic diarrhea (3)
    • inflammatory bowel disease (lymphoplasmacytic enteritis)
    • lymphangiectasia
    • lymphoma
  151. minimal change enteropathy tx (low disease activity, normal histopath, normal cobalamin and albumin
    • empirical parasite tx
    • dietary trial: + = diet responsive enteropathy
    • abx trial: + = antibiotic responsive enteropathy
  152. IBD (3)
    • etiopathogenesis unclear
    • lymphoplasmacytic enteritis: most common form. responds to hydrolyzed diet, abx/tylosin or immunosuppressive (one or all, try in that order if mild or all at once if severe)
    • granulomatous or neutrophilic enteritis: not common, bacterial or fungal/algal. Culture, special stains. DON'T immunosuppress
    • lymphangiectasia and crypt cysts/abscesses: abnormal distension of lymphatics. local or portal hypertension. Drops protein-rich lymph into intestines and makes granules on mesentery. v, d, hypoproteinemia, chylothorax. PLE! cause not determined, tx is symptomatic/supportive.
  153. Feline GI lymphoma (low grade T cell alimentary lymphoma)
    • lymphoma = diverse group of lesions, often fatal (T cell responds to chemo.)
    • mucosal and submucosal neoplastic lymphocytes.
    • ulceration, perforation, obstruction, malabsorption. 
    • middle and older cats, weight loss, v, SI d, inappetance. 
    • hypoalbuminemia, chronic dz or iron def anemia, low cobalamin, folate low, high TLI (pancreatitis or pancreatic lymphoma)
  154. How to tell IBD from GI lymphoma in cats
    • hypoalbuminemia in GI lymphoma not IBD usu
    • intestinal perforation in Gi lymphoma
    • concurrent renomegaly or splenomegaly in GI lymphoma
    • reactive hyperplasia in LN in GI lymphoma
    • Hard to tell!
  155. Canine pancreatitis basic info
    • Chronic: fibrosis, DM, EPI
    • etiology and pathogenesis poorly understood, but when digestive enzymes activated in pancreas (should be in zymogen until activated by trypsin), may fuse with lysosomes
    • pancreas may down-regulate trypsin?
    • systemic inflammatory syndrome, electrolytes, acid-base, fluids.
  156. canine pancreatitis  clinical signs, signalment, lab results, tests
    • middle to older, overweight.Hyperlipidemia, hx of dietary or toxin or drug.  
    • Signs: Lethargy, anorexia, hunched stance, vomiting, airhead, increased rr and enlarged abdomen. Dehydration to shock.
    • Lab: pre-renal and renal azotemia, increased liver enzymes, hyperbilirubinemia, lipemia, hyperglycemia, hypoproteinemia, hypocalcemia, metabolic acidosis, electrolyte derangement (usu low), increased serum amylase and lipase sometimes (not a slam dunk). 
    • Tests: trypsinogen activation peptide (TAP), pancreatic lipase immunoreactivity (TLI, cPL) seem best, but TLI (trypsin-like immunoreactivity) is common.
  157. Canine pancreatitis prognosis and treatment
    • severe is guarded while mild is good.  TAP increased in poor prognosis, also shock or major chem abnormalities.
    • Tx goals: restore biliary outflow, remove necrotic if present. 
    • Tx: supportive to restore abnormalities, analgesia with opioids, NPO vs enteric feeding. Free choice once app returns as long as not high-fat. Decrease obesity.
  158. Feline pancreatitis: clinical signs, cause, tests, lab results, tx goals, prognosis, sequelae
    • clinical signs: lethargy, anorexia, weight loss
    • cause: don't know
    • tests: no single test!  Usu co-morbidity. fPL vs exploratory/biopsy
    • lab results: increased ALT, bilirubin, cholesterol, glc, low K and Ca. Ca most useful.
    • tx goals: maintain/restore tissue perfusion, limit bacterial translocation, inhibit inflammation and pancreatic enzymes, enteral nutritional support, analgesia.  Sx if needed for biliary system, remove necrosis, place feeding tube.
    • prognosis: always guarded (esp suppurative). Low iCa is worse.
    • sequelae: EPI due to end stage chronic (low cobalamin and TLI)
  159. Ways vomiting is caused (4)
    • 1. Drugs, toxins, uremia, infection to CRTZ to vomiting center
    • 2. Vestibular to CRTZ and/then vomiting center
    • 3. Disease of GIT, liver, pancreas, genitourinary, peritoneum to vomiting center
    • 4. Cerebral to vomiting center
  160. tx for the happy healthy vomitor
    • Systemically unwell, longer than a week, hematemesis, bloody diarrhea or abdominal pain.
    • PCV/TP for hydration, feces for endoparasites. Allow to self-limit.
  161. What to ask of a vomiting animal
    • Distinguish vomiting from regurg
    • nature of vomitus
    • frequency, progression, duration, time related to feeding
    • access to FB, toxins, diet
    • vax
    • past medical history
    • check the tongue in cats!!
  162. 4 main causes and clinical signs of gastric disease (9)
    • inflammation, ulceration, neoplasia, obstruction
    • vomiting, hematemesis, melena, retching, burping, hypersalivation, abdominal distension, abdominal pain, weight loss
    • PE frequently normal
  163. tx options for gastric disease
    • Fluids (vomiting common)
    • decrease acid: Block H2 (famotidine), gastrin, ACh,  adenylyl Cyclades (omeprazole)
    • mucosal protection: misoprostol/PGE2 analog (good for NSAID), sucralfate
    • antiemetics: metoclopramide (dopamine and serotonin), chlorpromazine (alpha1, alpha2, H1, H2, D2), ondansetron (serotonin), maropitant (NK-1)
    • abx: only in barrier dysfunction
    • analgesia: opioids
  164. Parasitic Gastritis in dogs, cats, both
    • ollulanus tricuspis in cat stomach. Fenbendazole
    • Physalloptera: stomachs of dog and cat. Pyrantel pamoate
    • gnathostoma (cats), spirocera (dogs), aonchotheca (cats)
  165. helicobacter gastritis
    • lymphoplasmacytic infiltration of the stomach
    • treat biopsy-confirmed helicobacter AND gastritis
    • tx not agreed upon.  Combo of abx?
  166. lymphocytic plasmacytic gastritis of unknown cause treatment
    Tx with diet (Ag-resistant for 2 wks) +/- steroids. THen immunosuppression.
  167. delayed gastric emptying/motility disorders
    • Outflow obstruction or defective propulsion
    • suspect if vomiting 8-10-16hrs after a meal.  Projectile with pyloric stenosis. 
    • Can sometimes see abdominal distension, weight loss, melena, abdominal discomfort, distension, bloating and anorexia
    • tx: underlying cause. Check for ulcers, FB, inflammation, stenosis etc. Dietary modification probably good (semi-liquid protein and fat restricted diets fed small amts frequently with rice), prokinetic (cisapride and erythromycin most effective)
  168. Salmonella in adult horses
    • Many are carriers--foals get sick and mares don't. So stress, abx, lack of food etc. 
    • lab: hyponatremia, hypochloremia, neutropenia with left shift, azotemia, hemoconcentration.
    • tx as with any colitis: fluids/colloids, low-dose flunixin, "icing" the feet, bio-sponge. Abx not proven to work.
  169. Neorickettsia risticii/Potomac Horse Fever in adult horses
    • More laminitis than salmonella but looks similar.
    • Fresh water snails and caddisflies.
    • Fever 2-3D after infection then at 7d with diarrhea, toxemia.
    • IV tetracycline
  170. Clostridium difficile colitis in adult horses
    • Usu during abx administration (3-4d after)
    • colic, abdominal bloat and ileus
    • metro, bio-sponge and trans-faunation
  171. difference between foal and adult horse diarrhea
    foals usually have SI diarrhea.  Adults have colitis.  If they have SI disease, the colon can compensate so diarrhea rarely seen
  172. clostridium perfringens type A colitis in adult horses
    • thought to be a frequent cause but rarely proven. 
    • enterotoxins, beta 2 toxin, alpha toxins
    • metro, penicillin, bio-sponge, transfaunation
    • Type C rarely a prob in adult horses
  173. NSAID-induced colitis in adult horses
    • colic, renal dysfunction, hypoproteinemia with low-volume diarrhea
    • U/S shows thickened colon wall (lots of fluid in colon common for ALL colitis)
    • misoprostol, omeprazole, analgesia (torb or lidocaine CRI)
    • feed low-bulk, high fiber diet
  174. Cyathostomiasis colitis in adult horses
    • mostly yearlings and adults
    • progressive diarrhea, severe weight loss, hypoproteinemia in late fall through early spring
    • moxidectin +/- dexamethasone
  175. coronavirus colitis in adult horses
    • usu enteritis, so diarrhea is rare.  Possibly necrotizing enteritis at tips of villi, crypt necrosis. 
    • fever, anorexia, leukopenia, not diarrhea
    • fall-spring
    • dx: hx, clinical, fecal PCR
    • Tx: supportive
  176. things you can feel on an equine rectal
    • bladder
    • spleen
    • nephrosplenic space
    • inguinal ring
    • small colon
    • L kidney
    • SI mesentery
    • repro structures
    • things you can almost feel: SI, duodenum, LI, cecum
  177. things you shouldn't feel on an equine rectal
    • SI, duodenum, LI, cecum
    • tight bands (colonic or mesentery)
    • abdominal mass
    • pain on palpation
    • crepitation
  178. abdominocentesis sample in equines
    • look at color, consistency, turbidity, particles, smell.  Should be clear and light yellow
    • nucleated cell count <5,000
    • total protein <2.0
    • RBC count
    • lactate <0.7
    • cytology and culture
  179. abdominocentesis changes/values with ischemia in equines
    • normal to increase RBC (>10,000), orange to red
    • erythrophagia
    • increased TP, turbid, >3.0
    • WBC 5,000 - 80,000 with strangulation
    • suppurative inflammation (leaks bacteria after a few hours)
    • GI rupture or leakage (end-stage)
  180. serosanguinous abdominal fluid in equines
    go to surgery!
  181. peritonitis abdominocentesis in equines
    • WBC > 100,000
    • actinobacillus, strep, e coli, bacterioides, clostridium
    • MEDICINE, not surgery, though abdominal lavage may be helpful
  182. L-Lactate in equine abdominocentesis and what it indicates
    • abnormal tissue perfusion, anaerobic metabolism.  
    • if globally hypovolemic, similar increase in systemic and peritoneal lactate
    • if abdominal problem, 2x increase in peritoneal vs systemic lactate.  much higher in strangulating.
  183. ultrasound signs of gastric reflux in equine
    • enlarged gastric echo (>4 ICS)
    • swirling luminal fluid
  184. ultrasound signs of gastric impaction in equine
    • enlarged gastric echo (>4 ICS)
    • sharp acoustic shadow
  185. ultrasound signs of gastric rupture in equine
    • flocculant free fluid
    • fibrinous "lacy" appearance of serosal surfaces
    • free peritoneal gas
  186. Ultrasound signs of small intestinal strangulation in equine
    • thickened, edematous walls (>5mm)
    • minimal peristalsis
  187. signs of equine enteritis
    • increased or decreased (abnormal) peristalsis
    • bowel wall diffusely thickened.
  188. signs of intussusception in equines
    target lesion
  189. ultrasound signs of nephrosplenic entrapment in equines
    • difficulty visualizing left kidney
    • spleen displaced off body wall
  190. ultrasound signs of right dorsal displacement and volvulus in equines
    colonic vasculature along RIGHT BODY WALL, should not show on U/S.  Thickened left colon
  191. post-op peritonitis on ultrasound in equine
    variable echogenetic free fluid with possible fibrin tags on serosal surfaces
  192. hemoabdomen on ultrasound in equine
    echogenic swirling or "smoke-like" appearance
  193. Equine Colics with _______ _______ and __________ are more likely to need surgery than those with _______ ________ and ___________
    • acute onset and rapid course
    • slow onset and progression
  194. 4 causes of abdominal pain in equines
    • intestinal distension
    • intestinal spasm or hypermotility
    • intestinal ischemia
    • inflammation of peritoneum or bowel
  195. Interpretation (equine): 
    sudden decrease in pain in an animal with severe colic
    slow decline in signs of pain
    pain uncontrollable with analgesics
    pain increasing in severity or chronic unrelenting pain
    low grade or intermittent pain
    • sudden decrease in pain in an animal with severe colic: rupture of stomach or other viscus
    • slow decline in signs of pain: necrosis of strangled segment. Nerves damaged
    • pain uncontrollable with analgesics: go to surgery
    • pain increasing in severity or chronic unrelenting pain: surgical intervention likely needed
    • low grade or intermittent pain: conservative management
  196. Pulse rate as an indicator for equine surgery
    not good
  197. how do equines get dehydrated in colic
    sequestration of fluid proximal to obstructed SI +/- endotoxemia
  198. interpretation (equine): 
    increased intestinal sounds
    decreased or absent sounds
    • increased: "spasmodic" colic, early intestinal obstruction
    • decreased: ischemia, overdistension of bowel, chronic obstruction, peritonitis, drugs
    • normal or increased indicate not strangulation or other major pathological change.  cases that need sx usu have decreased or absent bowel sounds.
  199. Indications for surgery (10, equine)
    • severe pain
    • abnormal rectal (SI tight like a tube is strangulation, just feel it is enteritis)
    • abnormal U/S (enteritis looks like strangulation, but VERY dilated...)
    • abnormal belly tap (serosanguinous. Enteritis just turbid)
    • progressive abdominal distension (maybe trochar)
    • progressive deterioration of CV
    • progressive deterioration despite medical therapy
    • absent borborygmi (med or sx, but sx more likely)
    • large amounts of gastric reflux (but look for other factors)
    • high heart rate (pain, endotoxemia, hypovolemia. Not necessarily sx)
  200. 3 top differentials for a high equine heart rate
    • pain
    • endotoxemia
    • hypovolemia
  201. LDA: 
    Path
    Ping/succination
    appearance
    acid/base: 
    tx 
    px
    • most common left-sided ping (and most common surgical disorder), usu in first 6wk of lactation. High concentrate diet = gas, floats. 
    • Ping/succination: dorsal 1/3 of left abdomen from 8th intercostal to paralumbar fossa, somewhat circular.  Lg fluid filled viscous under rib cage
    • appearance: sprung rib cage
    • acid/base: hypochloremic metabolic alkalosis
    • tx: surgical.  Toggle pin fixation vs open surgical technique. 
    • px: good
  202. free gas rumen bloat: 
    Ping
    appearance
    tx
    • Ping/succination: dorsally on left, 8th intercostal to paralumbar fossa, higher than LDA. Can be heard dorsally over midline. Horizontal line at ventral edge, not like LDA. 
    • appearance: papple!  L paralumbar fossa balloons outward
    • tx: Ororumen tube will relieve gas/ping. Can blow in and hear bubbles.
  203. rumen void/collapse ping: 
    Ping/succination
    appearance
    tx
    • Ping/succination: dorsal half to third of left abdomen, 10th space to paralumbar fossa. No fluid detected. 
    • appearance: sunken paralumbar fossa.
    • tx: look for underlying disease.  Feed.
  204. pneumoperitoneum: 
    Path
    Ping/succination
    appearance
    other signs in PE
    • Path: free gas or air, usu post-laparotomy or after rupture.
    • Ping/succination: bilaterally in top third of abdomen to midline.  No fluid wave
    • appearance: apple!  Dorsal abdominal distension. 
    • other: Hard to hear rumen sounds, and rectum collapses around your hand.
  205. Left sided pings (4)
    • Rumen tympany
    • rumen collapse/void
    • LDA
    • pneumoperitoneum
  206. right sided pings (6)
    + colic (2)
    • gas distension of proximal colon
    • RDA, +/- volvulus
    • pneumoperitoneum
    • pneumorectum
    • ventral sac of rumen
    • physometra
    • + colic
    • cecal dilatation +/- volvulus
    • small intestinal distension
  207. RDA +/- volvulus (RDA, RAV): 
    Path
    Ping/succination
    appearance
    acid/base
    colic
    tx 
    px
    • Path: progression faster than LDA, less common. Displacement can be considered volvulus? Controversial. COUNTERCLOCKWISE.  RAV is shock, RDA is stable. 
    • Ping/succination: 9th rib to 13th or slight paralumbar fossa on R side. More caudal if torn omentum. Fluid under ribs. Could be rumen tympany. 
    • appearance: sprung rib cage and half-moon distension on R. 
    • acid/base: hypochloremic metabolic alkalosis.  Severe RAV will switch to metabolic acidosis. 
    • colic: no
    • tx: surgery. Don't let the sun set on an RDA, it will turn into an RAV! (ER) Stabilize first if you can. Flunixin for reperfusion injury. 
    • px: >90% for RDA, 60-70% survival in RAV.
  208. distension of proximal colon: 
    Ping/succination
    appearance
    tx
    colic
    • Ping/succination: dorsal paralumbar fossa, width of a hand, 2-3 rib spaces. 
    • appearance: normal
    • tx: clinically insignificant
    • colic: no
  209. pneumorectum: 
    Ping/succination
    appearance
    colic
    • Ping/succination: rectum and distal colon, right dorsal third of caudal abdomen, from tuber coxae along dorsal paralumbar fossa
    • appearance: normal
    • colic: no
  210. physometra: 
    Path
    Ping/succination
    appearance
    colic
    • Path: endometritis resulting in fluid and gas accumulation in uterus, esp right horn. uncommon.
    • Ping/succination: lower right paralumbar fossa
    • appearance: normal
    • colic: no
  211. gas in distended ventral sac of rumen: 
    Path
    Ping/succination
    appearance
    colic
    • Path: 
    • Ping/succination: rare/inconsistent.  Mid abdomen in R paralumbar fossa. No fluid wave
    • appearance: papple
    • colic: no
  212. cecal dilatation and/or displacement:
    definitions (2)
    Path
    Ping/succination
    appearance
    rectal
    colic
    tx
    • Path: similar to LDA.  High concentrate diet = increased gas
    • definitions: cecal dilitation = no twist.  Dilitation and displacements = cecal torsion (rotation around long axis) or cecal volvulus/twist (dorsal or ventral retroflexion, more common).
    • Ping/succination: right mid abdomen to 10th or 11th, involving paralumbar fossa. Variable. "washing machine" sounds
    • appearance: distension of right paralumbar fossa
    • rectal: easily palpated (watermelon), hard to ID volvulus (unless no manure or folded tube felt)
    • colic: yes
    • tx: dilatation = supportive, withold feed, monitor 24h (sx if not improved).  volvulus = surgery and typhlectomy (cecal amputation to relieve gas)
  213. distension of SI:
    Path
    Ping/succination
    appearance
    colic
    rectal
    • Path: indigestion, obstruction, secondary to cecal disorders, hemorrhagic bowel syndrome (torsion, intussusception)
    • Ping/succination: variable on the right. "tinkling and splashing" from pooling fluid in SI
    • appearance: abdominal distension esp right mid and ventral abdomen. No/few feces
    • colic: yes
    • rectal: bicycle inner tube tires
  214. hemorrhagic bowel syndrome (HBS) (part of SI distension)
    Path
    Ping/succination
    appearance
    colic
    rectal
    tx 
    px
    • Path: many names. unknown why. Nutrition? Clostridium vs asper?
    • Ping/succination: mild r sided ventral
    • appearance: shocky, dead, abdominal distension
    • colic: yes
    • rectal: SI distension, melena or hemorrhage, clots and casts of blood.
    • tx: cull vs sx/medical. Milk clots through, DON'T resect. 
    • px: poor, 85-100% mortality
  215. intussusception, part of SI distension
    Path
    Ping/succination
    appearance
    acid/base
    colic
    tx 
    px
    • Path: invagination, unknown why. Parasites, enteritis, abrupt diet changes, drug causing motility, linear FB etc. Jejunojejunal most common but also later. Usu <2mo calves in spring.
    • Ping/succination
    • appearance: abdominal distension, raspberry jam feces
    • acid/base: hypokalemic, hypochloremic metabolic alkalosis
    • colic: yes
    • tx: surgical correction 
    • px: poor, 35-45% chance of survival
  216. right sided bloat and pings in calves (4)
    • right displacement of abomasum
    • ruptured abomasal ulcer (peritonitis and pneumoperitoneum)
    • abomasitis
    • cecal dilation/torsion
  217. abomasitis/clostridial abomasitis in calves: 
    signalment
    etiology
    presenting complaint
    ping/succinate
    tx:
    • signalment: either <1 wk or transition (4-6wks)
    • etiology: unknown. Changes in flora from diet? Clostridium overgrowth, sarcina.
    • presenting complaint: acute depression, anorexia, abdominal distension, R-sided bloat, colic, acute death
    • Ping/succinate: +/- on the right. Fluid wave
    • tx: CULL. Or penicillin, anti-toxin, supportive
    • px: 30-50% chance of survival
  218. bilateral abomasal distension in calves (4)
    • ruptured abomasal ulcer
    • uroperitoneum
    • intestinal atresia
    • intussusception
  219. Left sided abdominal distension and pings in calves (1(7), 1)
    • Rumen bloat: 
    •    Fibrous distension
    •    rumen putrefaction
    •    rumen acidosis
    •    rumenitis
    •    trichobezors
    •    secondary to lung disease
    •    secondary to abomasal disease
    • LDA
  220. Medications to help EXAM in equine colic
    • Anti-inflammatories/analgesics/sedatives
    • flunixin meglumine/Banamine (NSAID)
    • Buscopan (anti-spasmodic and anticholinergic)
    • alpha-2 (xylazine and detomidine)
    • opioids
  221. tx of impaction colic (equine in the field)
    LI/pelvic flexure
    ileal
    cecal
    small colon
    Sand
    • off feed
    • LI: cathartic (mineral oil, epsom salts and water via NG tube).  Respond in 12-48h.  flunixin PRN for pain
    • ileal: surgical unless minimal.
    • cecal: fluids, oral cathartics, but risk of cecal rupture.  Surgical otherwise
    • small colon: medical like other impactions, enemas with epsom salts or electrolytes and water.  Sx if deteriorates
    • sand: psyllium, pain meds, sx if non-responsive
  222. Tx of nephrosplenic entrapment colic (equine in the field)
    • attempt medical, >50% success
    • phenylephrine: alpha-1 agonist causes splenic contraction for 30 mins.  Then trot the horse so the colon falls off. A FEW >15yo horses got a coag and died. 
    • rolling: anesthesia, R lat recumbency, lift hind and ballotte, then flip and wake up, palpate.
  223. tx of peritonitis colic (equine in the field) (8)
    • usu from intestinal leakage, degeneration. Can be actinobacillus equuli, parasite migration, or in <2y, rhodococcus or strep equi.
    • ID and tx cause if possible
    • broad spectrum abx (culture and sensitivity), oral and lipophilic if abscesses.
    • flunixin/banamine
    • analgesia PRN
    • fluid, electrolyte, maybe colloid
    • heparin to prevent adhesions
    • anthelmintics
    • peritoneal lavage if necessary
  224. tx of spasmodic colic (equine in the field) (6)
    • mild colic
    • one gallon mineral oil
    • flunixin meglumine/banamine
    • discuss changes, teeth, deworming for cause
    • off grain for the day, hay and grass for a while
    • observation for water, fecal
    • call if re-colics
  225. tx of parasite colic (equine in the field)
    • decompression: relieve gastric reflux and SI fluid accumulation
    • analgesics, anti-inflammatories
    • IV fluid therapy
    • Sx if medical not working
    • large strongyles: surgery and removal in infarcted colon as needed
  226. endotoxemia in horses
    caused by
    sensitivity
    pathophys, sequelae
    supportive therapy
    • endotoxin in blood stream, colloquially clinical manifestation of inflammation 
    • cause: GI DISEASE (translocation)
    • sensitivity: horses are the most sensitive species to endotoxin
    • path: LPS stims macrophages, cytokines, triggers clotting system (DIC), endothelium (permeability and edema), leads to SIRS, sepsis, MODS.  Hyperdynamic phase becomes hypodynamic, poor prognosis
    • tx: correct inciting, fluids to dilute, immunotherapy (plasma to scavenge LPS), polymixin B (bind LPS), inhibit inflammation (banamine, anti-oxidants, liodcaine CRI, maybe pentoxifylline for laminitis)
  227. signs of equine colic
    • rolling
    • pawing
    • getting up and down
    • flank watching
    • frequently posturing to urinate and urinating only small volumes or not at all (but not blocked)
    • lifting upper lip
    • pacing stall
  228. field fluids plan for equine colic
    • IV very expensive, PO better and gets to source of problem (but not with obstruction or reflux! Not enough for severe dehydration)
    • 8-10L stomach capacity, empties every 20-30mins
    • repeat high volumes should isotonic (water with free choice salt OK for lower)
    • IV use hypertonic FOLLOWED by oral or isotonic
  229. indications for liver biopsy
    • investigation of chronic liver enzyme elevations
    • liver nodules/mass ID
    • allows characterization of liver disease (benign vs malignant neoplasia, inflammatory, infectious, infiltrative)
  230. techniques for liver biopsy
    • wedge: focal lesion on periphery
    • guillotine: focal lesion on periphery, pedunculated. Crush artifact from suture
    • center of lobe: skin punch technique on focal lesions, avoid hemorrhage and necrotic
    • no focal lesions: 1cm3 from at least 3 lobes, avoid caudate
    • not in necrotic or hemorrhagic areas, <50% of lobe thickness to avoid hepatic veins, 6mm minimum. 
    • control bleeding with tampanade, vertical mattress or gelfoam
  231. anatomic limitations to partial hepatectomy
    • can only remove solitary liver masses where resection doesn't compromise caudal VC (midline), portal vein (R side), or common bile duct (R side)
    • left lateral and medial lobes are easiest, anything on the right is dangerous. 
    • highly friable, risk of hemorrhage
    • overlapping mattress or staples
  232. common tumors of the liver
    • hepatoma: older dogs, well-demarcated, hepatocyte proliferation, often incidental. Very common.
    • hepatocellular carcinoma: most common malignant liver cancer in dog. Slow metastasis, get huge, liver enzyme elevation
  233. indications for splenectomy
    • splenic hematoma/trauma
    • splenic neoplasia/rupture
    • splenic torsion
    • partial (rarely) for focal splenic abscess, splenic trauma
  234. 3 techniques for splenectomy
    • hilar ligation: start at tail, double clamp 2-4cm sections of splenic vessels along hilus. Ligate before or after transecting between clamps. 2-0 or 0 absorbable. Then double ligate splenic artery, remove spleen and submit. 
    • three point ligation: ER splenectomy.  Triple ligate splenic (above pancreas branch), L gastroepiploic and short gastric arteries, 2 left on arteries and 1 removed with spleen. Much faster!  0 pds, crushing sutures. 
    • ligasure: computer cautery device can seal a 7mm vessel to withstand 3x normal systolic. double seal and then cut.
  235. three complications after splenectomy
    • hemorrhage (rare)
    • vascular compromise to left limb of pancreas
    • portal vein thrombosis
    • arrhythmia (anemia, hemoab)
  236. Difference between foal and adult equine gastric ulcers
    • Adult: in 90% of performance horses, but almost never perf, bleed, stricture (just affect performance)
    • foals: 50% of sick foals, often perf, duodenal stricture.  But rarely bleed.
  237. Risk factors in adults and foals for gastric ulcers
    • Adults: fasting, inadequate roughage/too much grain, exercise, transportation,stall confinement, "nervous", sick or hospitalized (NSAIDs, steroids)
    • foals: physiologic stress, hypoxia, delayed gastric emptying, prologed time between feedings, small meal size, prolonged recumbency, NSAIDs (HOSPITALIZATION)
  238. horse stomach anatomy and where they get ulcers
    • Squamous, non-glandular portion around esophagus, 80% of ulcers here
    • glandular on other side of Margo plicatus
    • many ulcers near pylorus, too
    • treatment completely different between squamous and glandular!
  239. pathogenesis of nonglandular ulcers
    • Excess acid: lack of forage, sloshing during exercise
    • decreased protective factors: exercise decreases blood flow and increases gastrin, less mucus/bicarb.(SNS)
    • Helicobacter NOT a proven factor
  240. clinical signs of gastric ulcers in adult horses
    • picky eaters, changes in appetite
    • poor BCS
    • rough hair coat
    • mild colic
    • behavior changes (grumpy, irritable, don't want to move)
    • poor performance (decreased stride length, mild anemia for few that bleed)
  241. diagnosis in adult horses with gastric ulcers
    • gastroscopy!  
    • Clinical signs vague, empirical treatment expensive and squamous vs pyloric treated differently (though meds are safe)
  242. treatment in adult horses with gastric ulcers
    squamous
    glandular
    • squamous: proton pump inhibitors (gastrogard best = omeprazole), sucralfate (increases blood flow, stops acid from getting into ulcer)
    • glandular: misoprostol (not in pregnant! PG analogue causing decreased acid, increased blood, bicarb, mucosa healing)
  243. prevention of gastric ulcers in adults
    • nutritional management: pasture, free-choice roughage, limited concentrate, vegetable oil
    • drugs: omeprazole (can be prophylactic)
    • supplements: antacids - but be careful of active ingredient!
  244. pathophys of foal ulcers
    • gastric pH >4 at birth, <2 by 1 week old.
    • nursing increases pH: stimulates saliva (alkaline), absorbs gastric acid secretions.  No nursing = acid!
  245. 3 stages of clinical signs of foals with ulcers
    • stage 1: colic, frequently lie on back
    • stage 2: bruxism, ptyalism
    • stage 3: poor appetite, poor BCS.  
    • Also resp distress, bloat, acute death!
  246. prevention and tx of foals with gastric ulcers
    • prevention
    • frequent feedings, prophylactic acid reduction, selective NSAIDs, prevent stress
    • treatment
    • H2 antagonist or proton pump blockers: ranitidine, omeprazole, pantoprazole
    • sucralfate
    • antacid cocktail: soothing and short-acting, via NG tube (pepto, maalox, sucralfate, AC, warm water, lidocaine)
    • gastric emptying drugs: metoclopramide, bethanechol
  247. pathophys and signalment of adult cattle with abomasal ulcers
    • late pregnancy to early lactation
    • highly volatile fatty acid production (acidic, high energy, finely ground food)
    • decreased abomasal blood flow
    • dereased abomasal motility
    • stress
    • current post-partum diseases (hypocalcemia, metritis, DAs)
  248. How does stress cause ulcer?
    • cortisol impairs epithelial replication (turnover is crucial to barrier function)
    • cortisol increases vagal stimulation to increase gastrin release (makes more HCl)
    • all this leads to barrier disturbance and allows more diffusion of H+ ions and pepsin into deeper layers of mucosa
  249. 3 syndromes of abomasal ulcers in cattle
    • perforation (localized vs diffuse peritonitis)
    • bleeding
    • in between (stretching can cause microhemorrhages, and DA causes retained Cl = acidic)
  250. localized peritonitis in cattle with perforating ulcers
    • acute leakage of abomasal contents is walled off by omentum and fibrinous adhesions - cows are AMAZING at this
    • adheres to parietal peritoneum and/or omentum
    • anorexic, febrile, rumen stasis, painful abdomen
    • reluctant to move, painful on deep palpation of ventral abdomen
    • Looks like hardware!
    • tx with dietary changes (no silage, high-moisture corn, concentrates, more fibrous diet) and medical (stall rest, broad abx, MAYBE IV proton pump blocker)
  251. diffuse peritonitis in cattle with perforating ulcers
    • acute, septic shock, recumbency, complete GI stasis and anorexia
    • grave prognosis, sudden death.  
    • Not much we can do
  252. bleeding ulcers in adult cattle
    • just like any ulcer, but in vascular area
    • melena, pale membranes, tachycardia, cool extremities
    • PE, PCV/TS, fecal occult blood test
    • improved abomasal physiology, blood transfusion
    • LSA!: bleeding, pyloric outflow obstruction, don't respond to blood transfusion or supportive. Abdominocentesis may show neoplastic cells.
  253. types of abomasal ulcers in calves
    • perforation: most common, 7d, 2-3wks. recombent, abdominal distension, resp distress, death.
    • bleeding: uncommonish
    • incidental: a little of each
    • abomasitis: usu bacterial, not really the same
  254. treatment and prevention of abomasal ulcers in calves
    • surgery for perforating
    • omeprazile, ranitidine
    • prevent: nurse frequently at right temp, avoid NSAIDs, no prophylactic acid inhibitors
  255. abomasitis/abdominal tympany in calves
    • etiology unknown.  Maybe greedy nursers?  Too much = bacterial overgrowth (clostridium perfringens A, sarcinia, salmonella typhimurium
    • acute bloat, rapidly progressive depression, recumbency, shock, death
    • Tx: emergent and intensive!  Pass ororumen tube, IV fluids, systemic abx, antitoxin?  Sx?
  256. Ulcers in camelids
    • Common
    • C3, acute perforation
    • tx with IV/SQ pantoprazole and sucralfate
  257. Left paralumbar fossa abomasopexy, left flank abomasopexy
    • for LDA
    • celiotomy in left paralumbar fossa, ID abomasum
    • ford interlocking suture along greater curvature (slip the mucosa)
    • leave the ends long, use needle to pass through cranial right paramedian area
    • tie suture ends together (ventral midline) when abomasum is in appropriate place
  258. Right paramedian abomasopexy
    • for LDA or RDA
    • cast cow on R, into dorsal recumbency (trough)
    • decompress PRN
    • pexy (slip mucosa), include into midline closure
    • advantages: good visualization, direct fixation
    • disadvantages: dorsal COMPROMISES P (no late gestation or resp dz). Vascular, poor exposure to cd abdomen
  259. R paralumbar fossa omentopexy
    • Standing.  EFAH SOC
    • R paralumbar fossa celiotomy.  Decompress and replace, incorporate a fold of omentum adjacent to pylorus into first layer of closure
    • advantage: minimal stress, access to intestinal, prophylactic OK, not too vascular
    • direct: indirect (omentum stretches/tears), long arms and limited visualization
  260. closed techniques for replacing a DA (3, advantages, disadvantages)
    • rolling: quick, non-invasive, recurs
    • blind tack: quick, cheap, measure pH to ID viscus. Could suture wrong organ, ascending infection/peritonitis, abomasal fistula
    • toggle pin: same as blind tack
  261. RDA, RAV
    • RDA often twist, LDA can't. Never let the sun set on an RDA because it will BECOME an RAV
    • Right paralumbar fossa celiotomy, left arm along greater curvature.  Twist clockwise, omentum may be twisted.
  262. hypochloremic hypokalemic metabolic alkalosis
    • anorexia
    • obstruction of abomasal outflow
    • sequestration of gastric contents
    • accumulation of HCO3 in ECF
    • if it goes on long enough, lactic acid will build up and cause a metabolic acidosis. Bad news.
  263. abomasal volvulus tx
    • decompress PRN
    • reduction. Three ways to be sure it's in the right place
    • follow pylorus to greater curvature of abomasum to the reticulum
    • follow cranial duodenum to liver
    • palpate omasum against R lat body wall
  264. complications of Abomasal volvulus (7)
    • peritonitis
    • abomasitis/omasitis
    • metabolic derangements
    • adhesions
    • vagal indigestion (papple!)
    • incisional complications
    • severe and prolonged can cause shock and acidosis, hyperkalemia can cause cell necrosis and rhabdomyolysis
  265. 2 cardinal rules of an RDA
    • don't let the sun set on an RDA
    • don't roll a cow if there's a possibility of volvulus
  266. Three most common causes of weight loss in the horse
    • inadequate feed
    • dentition
    • parasitism
  267. Classification of IBD is based upon __________
    infiltration (lyphocytic plasmacytic, granulomatous or eosinophilic)
  268. Horses with _____ or _______ IBD can also present with dermatitis resembling pemphigus foliaceous
    • Granulomatous
    • eosinophilic
  269. Horses with IBD often present with intermittent colic which may be due to ________, _______, ________, or _______
    • Inflammation
    • colonic spasm/displacement/gas from fermentation
    • masses
    • mural bands
  270. Definitive diagnosis of IBD is achieved by
    histopathology - biopsy!
  271. Three prongs of a tx plan for IBD include ______, ________, and __________
    • diet
    • anthelmintics
    • dexamethasone
  272. Strep equi infections are associated with weight loss by two mechanisms:
    • Internal abscess formation
    • immune-mediated myopathy
  273. The histopathological findings/infiltrates in immune-mediated myopathy
    infarctive purpura hemorrhagic
    acute rhabdomyolysis
    • lymphocytic muscular infilatration
    • neutrophilic vascular infiltration
    • macrophage muscular infiltration
  274. _________and ________ are administered to horses with S. equi associated immune mediated myopathy
    • penicillin
    • dexamethasone
  275. equine motor neuron disease is a disease in horses characterized by oxidative stress/loss of ventral horn motor neurons which has been attributed to genetic factors as well as a deficiency of _______
    Vitamin E
  276. Horses at risk for developing equine motor neuron disease are those with _______, _______, _________, and ________
    • minimal access to green pastures
    • fed grass hay (low vitamin E)
    • fed grain (low vitamin E)
    • maintainedon same premises for >18 months
  277. Horses with EMND differ from horses with vitamin E responsive myopathy in that the latter lack evidence of neurogenic atrophy in ______ muscle
    SCDM = sacrocaudalis dorsalis medialis
  278. The prognosis for horses with vitamin E responsive myopathy is ______ compared to horses with EMND
    better
  279. EMND differs from white muscle disease which is caused by __________ and is characterized by myofiber degeneration and necrosis
    Selenium deficiency
  280. mild elevations in CK and AST are expected to occur in EMND whereas ________ are found in horses with nutritional myopathy as well as infarctive purpura hemorrhagica
    Marked elevations
  281. Ostertagia ostertagi
    • abomasal worm of cattle, moroccan leather appearance
    • most important nematode parasite of cattle in NY
    • type 1 disease: bright green diarrhea, mid-july onward, normal infection. Less mortality more morbidity
    • type II disease: intermittent diarrhea with anorexia and thirst, late winter or early spring, arrested larvae wake up, less morbidity more mortality. more hypoalbuminemia
  282. Treatment of lactating dairy cows for parasites
    • TREAT HEIFERS
    • prevents disease, decreases time to first breeding
  283. importance of cryptosporidium parvum
    zoonotic.  vet students.  In CALVES
  284. Disease caused by haemonchus
    • anemia.  UNTIL PROVEN OTHERWISE
    • Famacha is just a chart
  285. Thing to remember about tapeworms
    not killed by avermectins
  286. Parascaris equorum and ivermectin
    Have resistance!!
  287. Strongylus vulgaris and colic
    clots break off causing blockage of blood to gut wall, which leads to necrosis and colic
  288. small strongyles and avermectins
    • There are now reports of resistance here, too!!!  
    • Egg reappearance periods have decreased
  289. cytoisospora suis
    no good drug approved to treat this (there is toltrazuril in Europe but the FDA says it's carcinogenic)
  290. Ascaris suum and how you tell adult pigs are infected
    milk spots and thumps, liver/lung migration
  291. The most common cause of diarrhea in calves <1wk of age is ___________
    Enterotoxigenic E Coli (ETEC)
  292. The most common protozoal cause of diarrhea in calves <3wks is _____________.  It's success as an enteric pathogen is attributed to ____________; _____________; and ____________
    • cryptosporidium Parvum
    • large # oocytes excreted
    • survives for months in moist environment
    • 10 oocysts enough for a infection
  293. The common mechanism of diarrhea induced by rotavirus and coronavirus infections is _____________ and _____________.  However, __________ is an added mechanism of diarrhea in coronavirus infections.
    • maldigestion/malabsorption
    • inflammation
  294. The major concern with Salmonella infections in young animals is the potential for ____________ to develop.  Hence, calves diagnosed with salmonellosis are typically treated with antimicrobials.
    Bacteremia
  295. The host-adapted Salmonella serovar in cattle is ___________. It primarily manifests clinically as _________ in contrast to diarrhea
    • Dublin
    • Pneumonia, septicemia
  296. In calves with diarrhea, neurological signs may occur as a consequence of _______________; _____________; ______________ or _________________
    • Metabolic acidemia (D-lactic acidosis, electrolyte losses, dehydration)
    • Hypoglycemia
    • septic/meningitis (e Coli, salmonella Dublin, or other salmonella)
    • neurotoxin (clostridia)
  297. Bradycardia occurs in diarrheic calves due to _______________ and/or ______________
    • Hypoglycemia
    • hyperkalemia (acidosis)
  298. Passage of frank blood and mucus is associated with infections due to ______________, ______________, ___________, __________ and ____________ in calves less than one month of age
    • coronavirus
    • crytposporidium
    • salmonella
    • clostridium perfringens
    • potentially BVD
  299. In treating calves with diarrhea, oral fluid replacement is opted if ___________________; IVFs are necessary if the calf is > ________% dehydrated
    • standing and suckle reflex
    • >8-10%
  300. If diarrheic calves are treated with antimicrobials, two choices include ___________ or ___________.  In contrast, calves should not be treated with ______________, _______________, __________, ____________. In addition, because of prolonged tissue residues, ___________ should not be administered to calves
    • Amoxicillin trihydrate
    • procaine penicillin
    • chloramphenicol, enrofloxacin, metronidazole
    • aminoglycocides
  301. Colostrum is an important management component to raising healthy calves.  It is recommended that the average newborn Holstein calf receive ______________ liters within the first 4 hours of life.
    4
  302. The three chemicals that are efficacious against Cryptosporidium, ___________, __________ and __________, are impractical to sue on farm settings because of the necessary contact times and their toxicities
    • Formaldehyde
    • hydrogen peroxide
    • ammonia
  303. In young stock (6-24 months of age), coccidiosis is a common cause of diarrhea.  The two most important species are ___________ and _____________.
    • eimeria bovis
    • eimeria zuernii
  304. Coccidial infections are treated with ____________ or ______________; prevention of infections is by inclusion of _____________ in the rations
    • amprolium
    • oral sulfa drugs
    • coccidiostats (monensin)
  305. BVD, an RNA virus, is a cause of multi-systemic disease affecting the ____________, __________ or ____________ systems
    reproductive, respiratory, GI
  306. Most of the viral biotypes that survive in nature are _____________.  When a PI is exposed to a _________, it may develop mucosal disease and either linger or die.
    • noncytopathic
    • cytopathic
  307. Typical BVD infections cause mild or subclinical disease characterized by __________, ____________, and _________
    • Fever
    • decreased milk production
    • diarrhea
  308. The three methods used to diagnose BVD infections include ____________; ______________ and _____________
    • viral isolation (takes weeks)
    • antigen detection (immunohistochemnistry on necropsy, Ag-capture ELISA on skin or milk)
    • PCR on pooled milk or blood
    • serology (not helpful in PI! They have no Abs!)
  309. Two strategies to prevent BVD losses from occurring in a herd are: ____________ and ___________
    • Test herd and new editions: eliminate PIs
    • vaccination: prevents FETAL infection, no PI = no shedding.  Killed in cow/pregnant, MLV in heifer, calf
  310. In cattle greater than 24 months of age, medications such as __________ or feed-related disorders such as ________ and __________ may cause acute diarrhea
    • Magnesium
    • Indigestion
    • ruminal acidosis (too much grain)
  311. On dairies, cattle are at risk for shedding salmonella if there is _________________, ______________, _______________, ________________
    • failure to store concentratesin an enclosed building (rodents, birds, etc)
    • access of cows to surface water or contaminated irrigation water (salmonella in manure, etc)
    • consumption of roughage from fields with contaminated manure
    • season (worst in summer, spring, fall)
  312. Supportive treatment of adult cattle with salmonella includes _____________, ___________, ______________, and _________________
    • IV fluids
    • Or oral (hypertonic saline followed by free access to water)
    • anti-inflammatories (flunixin)
    • antimicrobials to decrease translocation (oxytet, penicillin)
  313. ______________ is an acute onset diarrhea that typically occurs in a herd during the cold months.  It is thought to be due to ______________. Most cattle will recover spontaneously but others may require calcium and oral fluid supplementation
    • Winter dysentery
    • bovine corona virus
  314. MAP is a cause of chronic granulomatous bowel disease with secondary diarrhea in adult cattle.  The ___________ is the most susceptible to infection emphasizing the need to clean/disinfect maternity pens; separate them from calves and feed milk replacer or milk from healthy, low-risk cows.
    Young! Keep calves away from potential shedders' feces!
  315. (MAP) It is not until the infected bovid reaches stage _______ that clinical signs of gradual weight loss, ill thrift and intermittent diarrhea (without fever) occur.  Most of the cases will be antibody positive and fecal PCR+
    three
  316. Diagnosis of MAP is challenging: culture of feces or tissue (________, ___________) can be undertaken.  For fecal cultures, pass-through of environmental bacterial contaminants leads to false positives.
    Ileum, LN
  317. Antibody-based tests (KELA-ELISA), while specific, suffer from __________.  If positive, the animal has infection; if negative, may still have MAP infection.  Confirm with fecal culture.
    poor sensitivity
  318. Other less common causes of chronic diarrhea in adult cattle include _____________, _________ (due to chronic infectious or inflammatory concerns), _______________ and _____________.
    • BVD
    • amyloidosis (rare, due to chronic Ag)
    • Chronic salmonellosis
    • liver abscesses, portal cava syndrome
    • intestinal neoplasia
  319. 4 main organisms in calf diarrhea
    • ETEC (e Coli)
    • cryptosporidium
    • rotavirus
    • coronavirus
  320. 5 hemorrhagic diarrhea causes in calves
    • coronavirus
    • crytposporidium
    • salmonella
    • clostridium perfringens
    • potentially BVD
  321. how much colostrum should a calf get?  In IgG?
    4L in first 4h, IgG > 1000mg/dL or TP >5.5
  322. 2 main diarrhea causes in young stock (<2y, cattle)
    Eimeria, BVD
  323. How to ID effusion (8)
    • fluid wave doesn't work
    • visceral structures feel wet or slippery
    • abdominal distension
    • tachypnea due to cranial displacement of diaphragm
    • +/- abdominal pain
    • distended superficial abdominal veins
    • rads: ground glass appearance, could be local or general
    • U/S: enhanced by effusion (appears black +/- sparkles), can show hepatic vein distention and help with fluid sampling.
  324. abdominal fluid collection (SA - preparation, mechanisms)
    • be aware of bleeding tendencies
    • palpate immediately before to avoid viscera
    • empty urinary bladder first
    • avoid ventral midline - poke higher on flank to avoid seromas
    • DO NOT REMOVE LARGE VOLUMES before sampling small amounts. 
    • hypodermic needle and syringe vs butterfly vs catheter vs 14g catheter with tomcat. 
    • DON'T do abdominal lavage.
  325. What to do with abdominal effusion sample (tubes etc) (6)
    • EDTA for cytology
    • heparin for certain thing but NOT cytology
    • red top for chem - creat for uro, bilirubin for GB, high triglycerides and low cholesterol for chylous, 
    • red top for aerobic and anaerobic culture
    • microhematocrit for PCV, TP, xanthochrome (if bloody)
    • diff-quik neutrophils to see bacteria, gram stain to ID. Air dry slides rapidly.
  326. How to interpret a bloody effusion (5)
    • PCV compared to peripheral
    • look for platelets = fresh bleed (iatrogenic vs HSA vs coag or vasculitis)
    • check ACT - effusion shouldn't clot
    • color of plasma - xanthochromic/yellow without jaundice in P = RBC breakdown = chronic presence of RBC, not a new bleed
    • look for erythrophagocytosis = chronic RBC diapedesis or chronic hemorrhage
  327. post-hepatic effusion/ascites
    associated with vena cava or hepatic VEIN hypertension (CV failure, pericardial tampanade, VC constriction): protein-rich fluid from hepatic lymph drips from hepatic surface. Hepatomegaly usu.
  328. hepatic origin ascites
    • sinusoidal or portal hypertension due to hepatic fibrosis, causes sinusoidal hypertension. 
    • sinusoidal: fibrosis in space of Disse
    • pre-sinusoidal: impaired blood flow at portal triads obstruct flow into sinusoids
    • post-sinusoidal: impaired blood flow (fibrosis, inflammation, thromboembolism) at hepatic venules 
    • often pure transudate (but hepatic lymph?)
  329. pre-hepatic origin ascites
    • portal vein hypertension due to impaired blood flow in extrahepatic portion of portal veins (thrombosis, stenosis)
    • mesenteric lymph lower protein than hepatic lymph
    • abdominal neoplasia
    • abdominal carcinomatosis
  330. therapeutic abdominocentesis
    • large volume fluid removal of ascites.
    • to facilitate palpation or imaging (don't take too much!! And not before you know the composition!) or to alleviate discomfort from tense ascites
    • **refractory to diuretics and sodium restriction (to jump start)
    • can strip essential proteins
    • complication: post-paracentesis circulatory disfunction (PCD). several days after, can cause hepatic encephalopathy, hyponatremia, acute renal failure.
    • coupled with albumin administration in humans, DON'T USE HUMAN ALBUMIN in d/c
  331. mechanisms for managing ascites
    • sodium restriction. Avoid drugs that increase (mineralcortioid activity, NSAIDs)
    • cage rest (facilitate renal perfusion and sodium excretion)
    • sodium wasting diuretics (spironolactone, +/- furosemide, no more than 1.5% body weight/day)
    • if that doesn't work, colloid administration and/or therapeutic abdominocentesis
  332. when to use diuretics in ascites
    • ALWAYS WITH SODIUM RESTRICTIONS
    • discomfort
    • impairing vital organ function (reduced ventilation, reduced abdominal organ perfusion
    • unresponsive to cage rest and sodium restriction
    • spironolactone best but may not be fast enough, furosemide
    • no more than 1.5% body weight loss/day
    • not much info on colloids (don't use human albumin or hetastarch)
  333. Administered colloids/albumin in the IV compartment
    don't stay in vessels so transient influence--not a great treatment
  334. Fluids dosing should be based on
    LEAN BODY MASS
  335. drug dosing in hypoalbuminemia
    if protein or albumin bound, consider the impact of increased free drug!!
  336. How much albumin will 1 bag of fresh frozen plasma or whole blood provide?
    • 1 bag = 1 L = 1000mL
    • 100mL = 2.5 - 3.5gm albumin
    • 1000mL = 25-35gm albumin. 
    • 250 mL = 6-9gm albumin.
  337. Telmisartan (for fibrosis in chronic hepatitis or ductal plate malformations) with spironolactone can cause ____________
    hypotensive collapse.  Careful when combining drugs that affect RAAS!!!
Author
XQWCat
ID
333955
Card Set
GI
Description
Vb GI
Updated

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