Diseases of the Small & Large Intestines Flashcards

1
Q

How is the small intestine usually palpated on rectals? How does it feel when diseased?

A

not felt or seen

felt and seen due to distension

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2
Q

How is reflux location dependent?

A

comes up in much larger amounts and faster higher up in the GIT (small intestine)

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3
Q

What aspects of fluid are analyzed following abdominocentesis?

A
  • color
  • protein
  • WBCs
  • lactate
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4
Q

What 3 bacteria are thought to be involved in the development of duodenitis proximal jejunitis (DPJ)?

A
  1. Clostridium difficile - toxin A = inflammatory, toxin B = smooth muscle paralysis
  2. Clostridium perfringens
  3. Salmonella
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5
Q

What feeding practices are thought to cause DPJ?

A

high amounts of concentrate and grass

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6
Q

What is DPJ? What 3 things does it cause?

A

inflammation, edema, and hemorrhage in the duodenum and proximal jejunum

  1. serositis with petechia and ecchymosis
  2. increased secretion
  3. decreased motility
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7
Q

What other organs are typically involved with DPJ?

A

pancreas and liver

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8
Q

What are the most common clinical signs associated with DPJ? How does it compare to (strangulating) obstructions?

A
  • acute colic
  • depression, fever
  • dehydration
  • tachycardia, tachypnea
  • ileus

pain wanes after NG decompression, but depression remains

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9
Q

What laboratory findings are used to diagnose DPJ? NG tube?

A
  • leukopenia
  • dehydration (increased PCV/TP)
  • electrolyte and acid-base abnormalities
  • increased liver enzymes

large volume of orange-brown, fetid reflux

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10
Q

What is found on rectal palpation, U/S, and abdominocentesis in patients with DPJ?

A

multiple loops of distended SI

distended SI and decreased motility

yellow, turbid to serosanguinous fluid with increased TP and normal WBC

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11
Q

What are the main 2 ways to treat DPJ? How are sequelae treated?

A
  1. NG decompression every 2 hrs
  2. correct fluid and electrolyte losses

combat endotoxemia and inflammation with Banamine, Polymyxin (good for G-), DMSO, and laminitis prevention

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12
Q

What are the main 2 antimicrobials used to treat DPJ? What is added?

A
  1. Penicillin IV
  2. Metronidazole per rectum

Gentamycin when there is low WBCs

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13
Q

What treatment is usually added for prolonged recover of DPJ?

A

prokinetic agents/motility modifiers

  • Lidocaine
  • Metoclopramide
  • Erythromycin
  • Cisapride
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14
Q

What response is expected in patients with improving DPJ? What nutrition should be provided while they are improving?

A
  • improved hydration
  • decreased HR and reflux
  • increased attitude

avoid oral food for several days and provide parenteral nutrition

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15
Q

What 5 complications are associated with DPJ?

A
  1. peritonitis
  2. infarction
  3. aspiration pneumonia
  4. adhesions
  5. laminitis
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16
Q

What causes equine proliferative enteropathy (EPE)? In what horses is it most common? When/where?

A

Lawsonia intracellularis

weanlings and foals (<1 y/o)

August-February in North America

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17
Q

How is equine proliferative enteropathy (EPE) transmitted? What history is commonly associated? What risk factor increases infection rate?

A

oro-fecal disease of pigs (subclinical)

housed with pigs or where a pig pen used to be, exposure to rodent reservoirs

stress

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18
Q

Where in the GIT does EPE affect? What causes disease? What does this result in?

A

distal jejunum and ileum (farther down the SI)

invasion of bacterial into proliferating crypts in the ileum = excessive mitosis and hyperplasia

  • thick and corrugated mucosa
  • decreased absorption
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19
Q

What are the most common clinical signs associated with EPE?

A
  • anorexia caused by malabsorption and protein loss
  • lethargy, fever, weight loss
  • colic, diarrhea
  • peripheral edema (protein loss!)
  • concurrent disease
20
Q

What laboratory and U/S findings are seen with EPE?

A

non-specific hypoproteinemia and hypoalbuminemia

thickened SI with excessive abdominal fluid

21
Q

What molecular and serological testing is commonly done to diagnose EPE?

A
  • PCR on fecal samples or rectal swabs
  • serology for IPMA (immune peroxidase monolayer assay)
  • silver stain of biopsy

(Lawsonia intracellularis)

22
Q

What antimicrobials are recommended for younger and older horses with EPE? What other 3 medications can be used?

A

YOUNG (foals <500 lbs) - macrolides, like Azithromycin and Clarithromycin

OLDER (weanling, yearling, adults) - oxytetracycline IV, then oral doxycycline

Rifampin, Chloramphenicol, Minocycline

23
Q

What supportive treatment is recommended for EPE?

A

colloids to replace lost proteins, parenteral nutrition, and antiulcers until diarrhea, hypoproteinemia, and thickened intestine resolve

24
Q

How is EPE prevented?

A
  • separate affected foals
  • regular PEs, TP, and serological status checks
  • pest control
  • extra-label pig vaccine given rectally
25
Q

What is the pathophysiology of inflammatory bowel disease (IBD)? What clinical signs are most commonly seen?

A

intestinal thickening with protein-losing enteropathy

  • progressive weight loss despite appetite
  • intermittent abdominal discomfort
  • edema
26
Q

What laboratory abnormalities are seen with IBD? How is it diagnosed and treated?

A

anemia, hypoproteinemia

U/S, absorption test, biopsy

steroids, surgery for idiopathic focal eosinophilic enteritis

27
Q

How is an absorption test performed? How do patients with IBD test?

A
  • 18-24 hr fast
  • obtain a baseline blood sample
  • administer a 10% solution of D-glucose or D-xylose per NG tube
  • collect blood sample every 30 mins for 4 hr and graph —> should have a peak at 60-120 mins

the peak will be much lower in patients with IBD

28
Q

What causes Ascarid impaction in horses? When is this most common?

A

heavy infestation of Parascaris equorum

  • weanling foals
  • poor deworming history
29
Q

What are the most common clinical signs associated with Ascarid impaction? How is it diagnosed?

A
  • unthriftiness, poor haircoat
  • colic 1-5 days after deworming

NG reflux containing dead ascarids or distended SI seen on U/S or rectal

30
Q

What medical treatments are recommended for ascarid impaction?

A
  • intestinal lubricants
  • IV fluids
  • pain control
  • slow onset antihelmintic Fenbendazole (Panacur)
31
Q

What is the most common site of small intestinal intra-luminal impaction?

A

ileus

32
Q

Where do horses most commonly experience ileal impaction? What are some risk factors?

A

South Eastern US, where coastal Bermuda hay is more commonly used

  • adults
  • ileal hypertrophy
  • infiltrative bowel disease
  • tapeworms - Anoplocephala perfoliata
33
Q

What clinical signs are associated with ileal impaction? How is it diagnosed?

A
  • colic
  • progressive abdominal distension
  • decreased gut sounds

rectal exam and U/S show distended SI, NG reflux
(normal abdominocentesis)

34
Q

What medical treatment is recommended for ileal impaction? When is surgery necessary?

A
  • NG reflux
  • pain control
  • IV fluids

intense pain, changed abdominal fluid

35
Q

Where can the cecum be auscultated? What does it sound like?

A

upper right abdominal quadrant

opening or flushing drain

36
Q

What are 5 major predisposing factors that contribute to pelvic flexure impaction?

A
  1. poor ability to chew
  2. coarse roughage
  3. decreased water intake
  4. motility decrease
  5. excessive fluid loss
37
Q

What clinical signs are associated with pelvic flexure impaction?

A
  • slow onset, mild/severe, intermittent pain
  • anorexia
  • abdominal distension
  • decreased fecal output
  • heart rate increasing with pain
38
Q

What are the 2 major histories associated with pelvic flexure impaction?

A
  1. horse moves from pasture to stall and begins to eat excessive amounts of straw or hay due to boredom
  2. water supply broken/frozen over in the winter
39
Q

In what 3 ways is pelvic flexure impaction diagnosed?

A
  1. no reflux from NG tube
  2. impaction on rectal exam - feeling of distension in the lower left abdomen without saccules
  3. normal abdominocentesis
40
Q

How is pelvic flexure impaction treated?

A
  • no feeding, allow water if no reflux
  • pain management
  • fluids + laxatives - mineral oil (more of a marker, where feces will be coated when impaction is resolved), magnesium sulfate, DSS
41
Q

What are the 3 major predisposing factors that contribute to sand impaction? Where is it most commonly found?

A
  1. access to sandy soil
  2. feeding hay or grain on sandy ground
  3. pica caused by lack of roughage and mineral content

lowest part of large intestine at the ventral diaphragmatic/sternal flexure

42
Q

What clinical signs are associated with sand impaction?

A
  • acute, intermittent. severe, or chronic pain
  • anorexia
  • abdominal distension
  • decreased fecal output
  • heart rate varies with levels of pain
  • diarrhea
43
Q

How is sand impaction diagnosed? What is not recommended?

A

MAY NOT FIND SAND

  • auscultation at ventral midline behind xiphoid = ocean sounds
  • rectal palpation, sand in feces - add water to fecal balls in palpation sleeve and see if sedimentation is present in the fingers

ABDOMINOCENTESIS - weight of sand in large intestine pulls it down and makes it fragile = easily perforated by needle

44
Q

What are 3 ways to treat sand impaction?

A
  1. pain management
  2. limit feed
  3. fluids + laxatives: psyllium hydrophilic mucilloid (Metamucil) every 6 hr until impaction resolves, then SID for a week and probiotics

surgery recommended for larger loads

45
Q

Why must laxative usage be done carefully when treating sand impaction?

A

Metamucil can form a gel in the intestines

46
Q

How can sand impaction be prevented?

A
  • prevent overgrazing in sandy pasture
  • do not feed off the ground - use a trough
  • prophylactic psyllium (SandRID, SandClear)