Pathophysiology of the Acute Abdomen Flashcards

1
Q

contrast somatic pain to visceral pain

A

somatic pain:
1. skin, muscles, bone
2. easy to pinpoint location
3. sources: cuts, burns, broken bones, etc.
4. role in abdominal pain:
-parietal pain: peritonitis, surgical incisions

visceral pain:
1. internal organs
2. diffuse in character, poorly localized
3. mechanisms:
-distension
-traction of mesentery
-ischemia
-chemicals (inflammatory processes)

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2
Q

describe the 5 steps of the pain pathway

A
  1. transduction: via sensory nerve endings and nociceptors
  2. transmission: via sensory nerves
  3. modulation: in the spinal cord
  4. projection to the brain
  5. perception in the cerebral cortex
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3
Q

describe first order neurons

A

A-delta and C fibers

  1. free nerve endings, sensitive to specific stimuli
  2. visceral afferents travel with sympathetic autonomic nervous system
  3. parietal (somatic) afferents travel with associated spinal nerve roots

responsible for transmission and transduction

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4
Q

describe second order neurons

A
  1. visceral afferents travel with sympathetic autonomic nervous system ascending tracts
  2. parietal (somatic) afferents travel with associated ascending spinal tracts
  3. action potentials may be modulated (augmented or inhibited)

responsible for modulation and projection

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5
Q

describe perception of pain

A
  1. perception of visceral input is similar to somatic input
  2. visceral input contributes to interoceptive system, which conveys important info about homeostasis to the body
  3. can illicit various responses:
    -endocrine
    -autonomic
    -behavioral
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6
Q

describe visceral distension and traction initiate pain

A
  1. distension of hollow viscous or traction of mesentery result in
  2. circumferential stretch of organ or stretch of mesentery, which leads to
  3. activation of the first order free nerve endings with MECHANORECEPTORS
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7
Q

describe how visceral ischemia initiates pain

A
  1. inadequate blood supply
    -leads to to inadequate oxygen delivery and inadequate removal of waste
  2. results in
    -decreased pH
    -lactate production
    -ATP
  3. which activate first order free nerve endings with CHEMORECEPTORS
    =why a heart attack hurts
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8
Q

describe how chemicals initiate pain

A
  1. local tissue injury causes inflammation and release of inflammatory mediators
    -bradykinin, prostaglandin, serotonin, glutamate, substance P, etc.
  2. results in direct activation and sensitization of free nerve endings (hyperalgesia) of CHEMORECEPTORS
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9
Q

describe nonstrangulating lesions

A
  1. origin of pain:
    -distension: of gastric/intestinal wall and visceral peritoneum
    -traction/stretch of viscera/mesentery
  2. may be medically or surgically managed
    -prognosis often good/guarded
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10
Q

what are the types of nonstrangulating lesions?

A
  1. functional: no physical blockage
    -spasmodic colic
    -tympany
  2. mechanical: physical blockage preventing movement
    -intraluminal: impaction, FB

-extraluminal: displacement, non GI mass (neoplasia, abscess, etc.)

-intramural: neoplasia, focal eosinophilic enteritis

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11
Q

describe strangulating lesions

A
  1. origin of pain:
    -distension of intestinal wall

-traction/stretch of visceral and/or parietal peritoneum

-ischemia: in any unperfused area

  1. requires IMMEDIATE SURGICAL management
    -prognosis often guarded/poor
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12
Q

what are the types of strangulating lesions?

A
  1. gastrointestinal:
    -GDV
    -intussusception
    -strangulating lipoma
    -colon volvulus
    -mesenteric torsion
  2. non-GI
    -liver lobe torsion
    -splenic torsion
    -uterine torsion
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13
Q

describe nonstrangulating ischemic lesions

A

uncommon!

  1. origin of pain:
    -ischemia of intestinal wall and visceral peritoneum

-distension of intestinal wall

-stretch of visceral/parietal peritoneum

  1. includes:
    -strongylus vulgaris causing verminous arteritis

-shock causing hypoperfusion

-mesenteric thromboembolism

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14
Q

describe inflammatory lesions

A
  1. origin of pain:
    -chemicals: release inflammatory mediators that act on the intestinal wall, visceral and parietal peritoneum

-distension: of intestinal wall and visceral and parietal peritoneum

  1. often medically managed
    -prognosis depends on cause
  2. include: any -itis!
    GI: esophagitis, gastritis, enteritis, typhlitis, colitis
    -non GI: pancreatitis, peritonitis, cholecystitis (mucocele or cholelith)
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15
Q

describe species differences with abdominal pain

A
  1. pathophysiology same across species
  2. but consider differences in anatomy and physiology
    -ruminants vs. monogastric, hindgut vs foregut, ideal diet for species versus actual diet
  3. some lesions occur commonly in many (neoplasia)
  4. some lesions are species specific
    -strangulating lipoma: horse thing
  5. foreign bodies much more common in young dogs
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