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Gastro > Constipation, Hirschprung, Megacolon > Flashcards

Constipation, Hirschprung, Megacolon Flashcards

1
Q

Definition of constipation:

A 
Infrequent BM <3/wk for 12 mo 
AND at least 25% of time:
  straining
  feeling of incomplete evacuation
  hard stool
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2
Q

In normal colon, motor function depends on contraction of

A

circular layer of smooth muscle

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3
Q

3 patterns of contractions:

A

short duration
long duration
giant migrating complexes

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4
Q

How are short duration colonic contractions characterized?

A

stationary motor contr, present over short areas of colon + persisting for <15s

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5
Q

What is the physiologic function of short duration colonic contractions?

A

mixing of fecal material and extraction of water

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6
Q

How are long duration colonic contractions characterized?

A

stationary or propagating (short distances) contractions, which may travel in orad or aboral direction

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7
Q

What is the physiologic function of long duration colonic contractions?

A

Assists in mixing and local propulsion of feces

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8
Q

long duration colonic contractions cause migration towards:

A

rectum in distal colon

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9
Q

How are giant migrating complexes of the colon characterized?

A

aboral propagating over extended distances

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10
Q

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

A

causes mass movement of feces

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11
Q

Giant migrating complexes of the colon normally occur ____ (how freq?), and may be precipitated by:

A

1-2 times per day

colonic distention

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12
Q

How does food affect colonic motility?

A

causes increased segmental activity

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13
Q

Gastro-colic reflux may be mediated by:

A

CCK

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14
Q

Motility in response to food intake is proportional to:

A

caloric content of meal

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15
Q

CCK causes:

A

increased frequency & amplitude of segmental contractions

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16
Q

PgF stimulates:

A

longitudinal muscle contraction

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17
Q

PgE inh:

A

circular muscle contraction

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18
Q

Serotonin mediates:

A

intestinal peristalsis
secretion in GI tract
modulation of pain perception

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19
Q

Serotonin is released by:

__% of serotonin is located in GIT

A

enterochromaffin cells

80

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20
Q

What do 5HT3-R antagonists treat?

A

IBS pain

functional dyspepsia

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21
Q

2 types of constipation?

A

functional

IBS-C

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22
Q

Constipation is more common in pts with:

A

little daily physical activity
low income
poor education

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23
Q

Constipation: Epidemiology

A

F>M

~65 y/o

24
Q

Major causes of chronic constipation?

A 
neuropathic disorders
IBS-C
drugs
pregnancy
hyper/hypo-Ca
hypothyroidism
idiopathic
25
Q

Drugs associated with constipation?

A 
analgesics
anticholinergics
Fe-supplements
Cation-containing (Al)
CCB
neurally-active
26
Q

What lifestyle characteristics cause constipation in elderly?

A

dehydration
low calorie diet
low fiber diet
immobility

27
Q

Constipation: Pediatric Etiology

A

95% functional

5% organic (which includes lead intoxication)

28
Q

Functional constipation:
Epidemiology?
Symptoms?

A

infants + pre-school age

2wks pebble-like, hard stools

29
Q

Functional fecal retention:
Epidemiology?
Etiology?

A

common cause of chronic constipation infancy to 16 years old

fear and toilet refusal

30
Q

What should you rule out when diagnosing constipation?

A

thyroid disorders or electrolytes problem

31
Q

What tests would you perform to dx constipation?

A

Colonoscopy or Barium Enema

Colon transit of markers

Anorectum Manometry

32
Q

Which patients with constipation should you get lab data for?

A 
rectal bleeding
wt loss of ≥10 pounds
family hx of colon CA or IBD
anemia
(+) fecal occult blood
33
Q

What labs should you perform for constipation?

A 
CBC
glu
creatinine
Ca
TSH
34
Q

Plain films of the abdomen help in the diagnosis of:

A

Megacolon

Impaction

35
Q

Colon Transit Study:
Methods?
Normal results?

A

methods: take Sitzmarks capsule, check Xray on day 5
normal: >80% ring markers passed by day 5

36
Q

Severe Idiopathic Chronic Constipation more commonly affects (M, F)

A

F

37
Q

Severe Idiopathic Chronic Constipation:

Symptoms?

A

infrequent defecation, excessive straining when defecating, or both

38
Q

Sitz marker study:

Colonic inertia results?

A

delayed passage of marker through proximal colon

no increase in motor activity after meals or with laxatives

39
Q

Sitz marker study:

Outlet delay?

A

markers move normally through the colon but stagnate in rectum
(more common in pelvic floor dyssenergia)

40
Q

How is the pelvic floor involved in normal defecation?

A

puborectalis, ext/int sphincter relax

increased intraabdominal pressure

inhibition of colonic segmenting activity

41
Q

What causes dyssynergic defecation?

A

failure to relax or inappropriate contraction of the puborectalis and external anal sphincter muscles

42
Q

abnormalities that can produce severe idiopathic chronic constipation:

A

Slow transit constipation
Dyssynergic defecation
Irritable bowel syndrome

43
Q

What is Hirschsprung Disease?

A

Congenital disorder characterized by:

  • -obstipation from birth
  • -colonic dilatation proximal to a spastic, non-relaxing and nonpropulsive segment of distal bowel
44
Q

Hirschsprung Disease/Congenital Aganglionic Megacolon

Epidemiology?

A

Males > female : 4:1

10% of cases in Down’s Syndrome

Most cases: sporadic, a few familial

45
Q

Hirschsprung Disease/Congenital Aganglionic Megacolon

Pathogenesis?

A

Absence of ganglion cells in submucosa and musc wall of large bowel

46
Q

Hirschsprung Disease/Congenital Aganglionic Megacolon is caused by what genetic defects?

A

Heterogeneous defects in genes regulating:

  • migration + survival of neuroblasts
  • neurogenesis
  • receptor TK activity
47
Q

What causes mortality in Hirschsprung Disease?

A

Superimposed enterocolitis with fluid and electrolyte disturbances

perforation with peritonitis

48
Q

What parts of the bowel are involved in Hirschsprung Disease/Congenital Aganglionic Megacolon?

A

rectum
sigmoid (usually)

entire colon = rarely

49
Q

What is the consequence of the abnormalities present in Hirschsprung Disease/Congenital Aganglionic Megacolon?

A

functional obstruction

progressive dilation and hypertrophy proximal to aganglionosis

later: massive distension outruns hypertrophy, wall becomes thinned + ruptures

50
Q

Hirschsprung Disease/Congenital Aganglionic Megacolon:

Clinical presentation?

A
  • -failure to pass meconium
  • -obstructive constipation with occasional passage of stool
  • -bouts of diarrhea + abdominal distention
51
Q

Gold standard for Hirschsprung Disease/Congenital Aganglionic Megacolon diagnosis?

A

rectal biopsy showing absence of ganglionic cells

52
Q

Treatment of Hirschsprung Disease/Congenital Aganglionic Megacolon?

A

Surgical resection of the aganglionic segment of bowel

Sphincter function is generally preserved

53
Q 
Acquired Megacolon (“Toxic Megacolon”):
Infectious causes?
A

Clostridium difficile pseudomembranous colitis

Chagas Disease: trypanosomes invade bowel wall and destroy enteric plexus

54
Q 
Acquired Megacolon (“Toxic Megacolon”):
Non-Infectious causes?
A

Inflammatory bowel disease

Obstruction (tumor or inflammatory stricture)

Functional disorder associated with pyschiatric disease and medication

55
Q

Can Acquired Megacolon be fatal?

A

YES!

56
Q

Anorectal Malformations:
Epidemiology?
Treatment?

A

1:3000 live births

surgery

57
Q

Anorectal Malformations:

Pathogenesis (3 possible)?

A

Failure of urorectal septum formation in cloaca (week 7)

failure of anal membrane opening (week 8)

malformations in urinary tract and/or trisomy 21

Gastro (25 decks)

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