GI2- Equine Colic 1

  1. What is the relevant normal physiology of the small intestine? (3)
    digestion and absorption of carbohydrates and proteins, active fluid secretion to hydrate ingesta (isotonic, buffered--> normally reabsorbed in large intestine), movement of ingesta aborally
  2. What is the vicious cycle of SI obstruction?
    fluid sequestration- starts moving back towards stomach <--> bowel distention <--> ileus <--> gastric distention
  3. What are causes of simple/non-strangulating SI obstructions? (7)
    • Intraluminal: feed impaction, foreign body, Parascaris impaction, enterolith
    • Extraluminal: extramural mass, one organ causing an outflow disturbance of another, adhesions
  4. What are the classifications of strangulating obstructions? (2)
    • hemorrhagic strangulating obstruction (arterial supply not lost)
    • ischemic strangulating obstruction (arterial supply lost)
    • can progress from HSO to ISO
  5. Contrast complete and incomplete luminal obstructions.
    • Complete: accumulation of solids, liquids, and gases--> acute onset of clinical signs
    • Incomplete: accumulation of solids and some liquids--> slower onset of signs of obstruction
  6. What are the types of simple obstructions? (3)
    mechanical (stricture, intraluminal, extraluminal), malposition (visceral displacements), functional (ileus, enteritis)
  7. Describe the pathophysiology of simple obstructions.
    vascular supply is unaffected, distention and increased intraluminal pressure--> compresses mural wall vessels--> edema and increased mucosal permeability--> distention moves orally (toward the mouth)--> fluid accumulation--> gas accumulation--> motility increases then decreases as high stretch receptors get activated
  8. With simple SI obstruction, increased intraluminal pressure leads to... (4)
    distention of lumen, venous collapse in intestinal wall, edema and thickening, fluid/ingesta starts moving orally (if obstruction doesn't pass)
  9. What contributes to shock with simple SI obstruction? (4)
    third-spacing of fluids within the obstructed lumen, sweating and increased insensible losses, reduced/absent volume intake, endotoxemia can develop with intestinal stasis (bacterial overgrowth and bacterial translocation/ increased absorption of bacterial toxins
  10. With a proximal SI simple obstruction, ____(2)____ losses are high, leading to ___________ and __________; treatment is with ___________.
    Cl- and K+; metabolic alkalosis (Cl-); decreased absorption (K+); isotonic saline and K+
  11. A distal SI simple obstruction there are minimal ___________, but over time, ...
    electrolyte derangements; lactate increases and bicarb decreases, leading to metabolic acidosis.
  12. How does large intestine simple obstruction lead to shock? (2)
    hypovolemia (fluids not absorbed normally), obstructive shock (distention of all intestine--> obstructions vena cava)
  13. What are the types of strangulating obstructions? (2)
    • hemorrhagic: occlusion of intestinal lumen, lymphatic drainage, and venous drainage
    • ischemic: occlusion of lumen, lymphatics, veins, and arteries
  14. What are potential causes of strangulating obstructions? (4)
    • herniation (visceral displacement into a location causing vascular impairment)
    • torsion/volvulus
    • intussusception
    • bands (lipoma, congenital remnants, omentum)
  15. What are the pathologic consequences of strangulating obstruction and how do they develop? (3)
    • Necrosis: sequential loss of all layers--> oxygen dependent and tissues with high metabolic rate die first
    • Motility: initial increase then completely absent
    • Pain: inflammation, visceral distension, mesenteric stretching
  16. Why are strangulating lesions so severe?
    there is minimal collateral blood supply to most sections of bowel (end arterial system), mucosal enterocytes have an order of vulnerability to hypoxic/ischemic insult
  17. With strangulating lesions, the ___________ are most susceptible to necrosis, and the ___________ are least susceptible.
    tips of villi; crypts
  18. Strangulating lesions and/pr inflammatory GI lesions are very common causes of __________ in adult horses.
  19. With SI obstruction, pain is mostly a result of...
    distention, especially of the stomach.
  20. What are the most common tumors to cause intraluminal/intramural SI obstructions?
    leiomyoma, leiomyosarcoma
  21. What is Hemorrhagic bowel syndrome?
    jejunal hemorrhage, usually a single clot, causes low fecal output and dehydration; BROWN SWISS
  22. What is the most common cause of extraluminal SI obstruction?
  23. Where does intussusception most commonly occur?
    ileocecocolic junction
  24. What are the most common locations of volvulus in cattle? (2)
    • duodenal sigmoid flexure: acutely painful then quiet, severe alkalosis
    • jejunal volvulus: very painful, ischemia, distention, shock
  25. What are the clinical signs of mesenteric root torsion/ intestinal volvulus in cattle? (5)
    • acute onset of ischemia and distention--> abdominal distention
    • feces scant to absent
    • rectal palpation reveals distended bowel loops
    • tachycardia
    • dehydrated
  26. What is the only type of SI obstruction that is accompanied by a fever?
    physiologic obstruction: severe ileus--> stomach distention
  27. Describe the clinical presentation of colonic impaction?
    slower onset of signs as impaction worsens and moves orally
  28. Why is colonic displacement so common in horses?
    there is no mesentery holding the large colon in place
  29. Describe the clinical presentation of colonic displacement in horses.
    • rarely any vascular derangements and minimal gas distention
    • milder onset of abdominal pain
    • main systemic signs are due to dehydration (usually no endotoxemia or sepsis)
  30. Describe the clinical presentation of large intestinal volvulus in horses.
    rapid onset ischemia, severe gas distention, shock due to sepsis and hypovolemia, tachycardia, abdominal distention, severe pain
  31. Describe extraluminal large intestine obstruction in cattle.
    lymphoma or fat necrosis--> mild onset of disease, gradual occlusion of intestinal lumen--> lack of feces, abdominal distention
  32. How does enterocolitis/ anterior enteritis present in horses?
    severe pain acutely followed by depression
  33. How does peritonitis present in horses?
    low grade pain and depression
  34. How does grain overload present in horses?
    causes colitis and intestinal/stomach distention
Card Set
GI2- Equine Colic 1
vetmed GI2