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GI- Week 1 > Colon and Constipation > Flashcards

Colon and Constipation Flashcards

1
Q

What is the definition of constipation?

A

Infrequent (less than 2/week) BM for 12 months or

Infrequent (less than 3/week) BM for 12 months with straining/feeling of incomplete evacuation/hard stool at least 25% of the time

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2
Q

Motor function/motility of the colon depends on contraction of what?

A

the circular layer of smooth muscle

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3
Q

What are the 3 patterns of circular smooth muscle contraction?

A
  • Stationary-motor contractions (short duration)
  • Long duration colonic contractions
  • giant migrating complexes of the colon
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4
Q

What is the primary function of stationary-motor contraction

A

these are present over short areas of colon, persist for less than 15 seconds, and cause mixing of fecal-material and extraction of water

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5
Q

What is the purpose of long duration colonic contractions?

A

these may be stationary or propagate for short distances, may travel in orad or aboral directions, and assist in mixing and local propulsion of feces

Migrates towards rectum in distal colon

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6
Q

What is the purpose of giant migrating complexes of the colon?

A

these propagate over extended distances and cause mass movement of feces. They normally occur 1-2x/day and may be precipitated by colonic distension

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7
Q

What is a gastrocolic reflux?

A

this is a phenomenon mediated by CCK in which ingesting food can cause an almost simultaneous increase in distal colon motility resulting in defecation of stored food almost right after eating. This response is proportional to the caloric content of the meal

It involves an increase in motility of the colon in response to stretch in the stomach and byproducts of digestion in the small intestine. Thus, this reflex is responsible for the urge to defecate following a meal. The small intestine also shows a similar motility response. The gastrocolic reflex helps make room for more food

Clinically, the gastrocolic reflex has been implicated in pathogenesis of irritable bowel syndrome: the very act of eating or drinking can provoke an overreaction of the gastrocolic response in some patients with irritable bowel syndrome due to their heightened visceral sensitivity, and this can lead to abdominal pain, diarrhea, or constipation

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8
Q

____ causes increased frequency and amplitude of segmental contractions

A

CCK

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9
Q

What other neurotransmitters are involved in colonic motility and function?

A

Prostaglandin F stimulates longitudinal muscle contraction

Prostaglandin E inhibits circulat muscle contraction

Serotonin mediates intestinal peristalsis and secretion in the Gi tract as well as modulation of pain perception

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10
Q

Notes on serotonin in the GI

A

80% of the total body 5-HT (serotonin) is located in the GI tract and is released by enterchromaffin cells.

5-HT3 receptor antagonists have offered some help in alleviating pain in IBS and functional dyspepsia and 5-HT4 receptor agonists have a prokinetic effect in humans

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11
Q

How is IBS defined by the Rome III Criteria?

A

Recurrent abdominal pain/discomfort 3+days/month for the past 3 mos, associated with 2+ of the following:

  • imporvement with defecation
  • onset associated with change in stool frequency
  • onset associated with change in stool form

IBS is subtyped by predominant stool pattern

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12
Q

A pt. that suffers from straining, sensation of incomplete evacuations, and constipation but no pain would be diagnosed with what?

A

functional constipation

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13
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A
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14
Q

What are the main categories of chronic constipation causes?

A
  • neurogenic disorders
  • IBS
  • drugs
  • non-neurogenic disorders
  • idiopathic
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15
Q

What are some neurogenic causes of constipation?

A

peripheral- Hirschsprungs disease, DM, Chaga’s disease

central- MS, spinal cord injury, Parkinson’s

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16
Q

What are some non-neurogenic disorders that cause constipation?

A

hypothyroidism

hyper OR hypocalcemia

pregnancy

myotonic dystrophy

systemic sclerosis

porphyria

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17
Q

What are some drugs that cause constipation?

A

Anticholinergics, antidepressants, antipsychotics

cation-containing agents (iron supplements, aluminum (antacids))

opiates

antiHTNs

5-HT antagonists

CCBs

vinca alkaloids

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18
Q
A
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19
Q

What is functional constipation? Who is it common in?

A

Functional constipation, known as chronic idiopathic constipation (CIC), is constipation that does not have a physical (anatomical) or physiological (hormonal or other body chemistry) cause. It may have a neurological, psychological or psychosomatic cause. A person with functional constipation may be healthy, yet has difficulty defecating.

Common in infants and pre-school aged children

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20
Q

What is functional fecal retention?

A

It is defined by passage of big, hard stools at infrequent intervals, days or weeks apart; and by the child trying to avoid having a bowel movement by stiffening and straightening his or her legs and buttocks.

Functional fecal retention is most often due to frightening or painful defecation experiences, which result in voluntary avoidance of passing stools. Repeated retention of feces causes an increase in size of stools leading to more painful defecation experiences and further attempts at avoidance.

21
Q

How should chronic constipation be approached?

A

try to elucidate secondary causes with an H&P, and if none can be found, move on to a colonoscopy (if over 50)

22
Q

What should be done if nothing is found on colonoscopy?

A

do a colon transit marker to help see how the colon is moving plus anorectal manometry/ballon expulsion test

23
Q

When should labs be included in a workup of constipation?

A

in pts. with:

  • rectal bleeding
  • weight loss of 10+ lbs
  • fam Hx of colon cancer or Inflammatory bowel disease, anemia, or positive fecal occult blood tests
  • short term Hx of new constipation in an older pt.
24
Q

What labs should be included in these pts.?

A
  • CBC
  • serum glucose,
  • creatinine,
  • calcium
  • TSH
25
Q
A
26
Q
A
27
Q

Severe idiopathic chronic constipation is more common in _____

A

women

28
Q
A
29
Q

What muscles might be involved in pelvic outlet delay?

A

the anal sphincters and the puborectalis muscle.

In normal defecation these muscles relax (together with increased intraabdominal pressure and inhibition of colonic segmenting activity), but in dyssynergic defecation one of these or both does not relax

30
Q
A
31
Q

What are some fiber supplementation options?

A

these include bulk forming laxatives such as Metamucil, methylcellulose, and calcium polycarbophil (FiberCon)

32
Q

What are some other laxative agents?

A

Stool softeners such as docusate sodium (e.g. Colace)

Osmotic agents such as polyethylene glycol (miralax) and lactulose

Stimulant laxatives such as bisacodyl and senna (which might cause pain and discomfort)

Suppositories with glycerin or bisacodyl

Disimpaction

33
Q

What is Lubiprostone?

A

A secretagogue that promotes defecation by locally acting on a chloride channel to enhance chloride-rich intestinal fluid secretion

34
Q

What are some other laxative drugs?

A

Misoprostol

Prucalopride, a 5-HT4 prokinetic agent

Linaclitde

35
Q

What is Hirschsprung disease?

A

A congenital disorder chracterized by obstruction/constipation from birth and colonic dilation proximal to a spastic, non-relaxing and nonpropulsive segment of distal bowel

36
Q

What causes Hirschsprung?

A

absence of ganglion cells in large bowel (usually the rectum and sigmoid area), causing functional obstruction and proximal distention

Mainly due to failure of neural crest cells to migrate to the colon appropriately during prenatal development

37
Q

How common is Hirschsprung disease?

A

1:5000 births, 4:1 males, and 10% associated with Down syndrome

Most cases: sporadic, a few familial

38
Q

What are the gene defects related to Hirschsprung?

A
  • migration and survival of neuroblasts
  • neurogenesis
  • receptot tyrosine kinase activity
39
Q

How does Hirschsprung disease progress?

A

the absence of ganglia in the submucosa (meissner) and muscle (Auerbach) causes distal spasitity that causes progresses proximal dilation and hypertrophy. Later in the disease, distension predominates and the gut wall becomes thinned and ruptures

40
Q

What parts of the colon are commonly involved in Hirschsprung?

A

rectum is always involved, rectum and sigmoid in most cases, and rarely the entire colon

41
Q

What is the source of most mortality associated with Hirschsprung?

A

superimposed entercolitis with fluid and electrolyte disturbances, and perforation with peritonitis

42
Q

Hirschsprung

A
43
Q

How is Hirschsprung diagnosed?

A

rectal biopsy (gold standard) with absence of ganglion cells (which are inhibitory to contraction)

Adjuvant: abdominal radiographs, contrast enema, anorectal manometry

44
Q
A
45
Q

What are the main causes of acquired megacolon?

A
  • obstruction (rule out first)
  • C. diff pseudomembranous colitis
  • Inflammatory bowel disease (UC or CD)
  • Functional disorders
  • Chagas disease (trypanosomes invade bowel wall and destroy enteric plexus (inflammation of the ganglia))
46
Q

What is active inflammation?

A

the presence of neutrophils in the glands of the GI tract

47
Q
A
48
Q
A

GI- Week 1 (20 decks)

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