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Flashcards in Bilal - Constipation/Megacolon Deck (39):
1

What is the definition of constipation?

- Variable, but:

1. Infrequent BM: <2/wk for 12 months

OR 

2. Infrequent BM: <3/wk for 12 mos w/straining, feeling of incomplete evacuation, hard stool at least 25% of time

2

What are the 3 patterns of colonic contractions?

- Motor func depends on contraction of CIRCULAR layer of smooth muscle:

1. Short duration stationary motor contractions: short areas of colon (focal); mix fecal material and extract water/electrolytes (15 sec)

2. Long duration: stationary or propagate short distances (orad or aboral direction); mixing and local propulsion (last up to a few mins)

3. Giant migrating complexes (MMC): propagate aborally over extended distances, causing mass mvmt of feces (1-2x/d) after water/electrolyte absorption-> may be precipitated by colonic distention 

3

How does food intake affect colonic motility?

- Causes INC segmental activity via gastrocolic reflex, which may be mediated by CCK, which is responding to food in the stomach

- Response is proportional to the caloric content of a meal -> very heavy meal may induce exaggerated reflex

- Not the same food coming out; just that the entire body is connected

4

What hormones (4) influence colonic motility?

- CCK: INC frequency & amplitude of segmental contractions

- Prostaglandins

1. PGF: stimulates longitudinal muscle contraction -> propagative

2. PGE: INH circular muscle contraction, so constipating

- Serotonin: mediates intestinal peristalsis & secretion in GI tract as well as modulation of pain perception

1. INC peristalsis

2. INC secretion

3. Modulates pain 

5

What is the role of serotonin in the colon? Rxs?

- Serotonin (5-HT) is an important neurotransmitter in the brain-gut interaction

- Released by enterochromaffin cells: 80% of total body 5-HT in the GI tract

1. 5-HT3 receptor antagonists have offered some help in alleviating pain in IBS and functional dyspepsia

2. 5-HT4 receptor agonists have a pro-kinetic effect in humans

6

What are the differences b/t functional constipation and IBS-D?

- Both have symptoms >=3 mos, and onset >=6 mos prior to diagnosis 

1. IBS-C predominant: starts with abdominal PAIN (have to have pain here; gets better with bowel movements)

2. Functional: NO pain, no alternating diarrhea 

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7

What is the epi of constipation?

- Prevalence: 12-19% 

- More common in ppl with: 

1. Little daily physical activity 

2. Low income 

3. Poor education 

- In pts >65-y/o, esp. females

8

What is the non-drug-induced etiology of chronic constipation (table)?

- 1o colorectal disorder: less prevalent, and falls under idiopathic constipation (he would put IBS in here)

- 2o: something else going on that is causing the constipation

1. Rule out 2o causes and drugs first, then think about primary/IBS 

- Neurogenic: peripheral or central

- Non-neurogenic: metabolic and myopathic 

 

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9

What are some drugs associated with constipation?

- Rule out 2o causes and drugs first, then think about primary/IBS

- Zofran (5-HT3 INH) given for nausea 

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10

What things might you think about when elderly person presents with constipation?

- ENDOCRINE/METABOLIC disease: DM, hypothyroid

- NEURO disease: autonomic neuropathy, cerebro-vascular disease, MS, Parkinson's, spinal cord injury

- PSYCH conditions: anxiety, depression 

- STRUCTURAL ABNORMALITIES: anorectal conditions (fissures, hemorrhoids, rectal prolapse, rectocele), obstructive colonic lesions 

- LIFESTYLE: dehydration, low cal diet, low fiber diet, immobility

- IATROGENIC: meds 

11

What is the pediatric etiology of constipation?

- FUNCTIONAL: 95% 

- ORGANIC: 5% 

1. Anatomic 

2. Metabolic

3. Neuropathic 

4. Drugs 

5. Endocrine CT disorder 

6. Lead intoxication or botulism 

12

What is the difference b/t pediatric func constipation and func fecal retention?

- Functional constipation: infants and pre-school

1. 2-wk duration of pebble-like, hard stools

- Functional fecal retention: common cause of chronic constipation

1. Fear and toilet refusal from infancy to 16-y/o

13

What are the important components in constipation diagnosis?

- Hx and PE; other medical conditions

- Evaluate current medication

- Rule out thyroid disorders or electrolytes problem

- Colonoscopy or barium enema (rarely done now)

- Colon transit of markers

- Anorectum manometry

14

What should you do with pts who present w/chronic constipation unresponsive to conservative tx?

- Rule out 2o causes 

- Do colonoscopy, if indicated 

- Other test to rule out 1o causes: transit, manometry 

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15

Who should get lab data (colon complaints)?

- Labs should be performed in pts w/rectal bleeding, weight loss of ≥10 pounds, a family hx of colon cancer or inflam bowel disease, anemia, or (+) fecal occult blood tests, as well as a person with short-term history of constipation

1. Complete blood cell count (CBC)

2. Serum glucose, creatinine, Ca2+

3. Thyroid-stimulating hormone (TSH)

- Looking for red flags for cancer or IBD (UC, Chron’s)

- REMEMBER: 60-y/o w/severe constipation for past 3 months -> more worried than person who comes in with chronic history of the same problem 

16

What technique was used to get these images? Difference b/t the 2?

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- LEFT: normal colon 

- RIGHT: colonic malignancy 

- Do NOT underestimate importance of colonoscopy in pts >50, esp. those with new-onset constipation

- 1/20 Americans have colon cancer after age 50 

17

What imaging (and other) techniques can be emplyed in the evaluation of constipation?

- Plain films of the abdomen for diagnosis of: 

1. Megacolon

2. Impaction

- Barium Enema

- Colon Transit Study *(sitzmark study)

- Defecography

- Manometry 

18

What are Sitzmarks? Potential results?

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- Used after colonoscopy; different techniques 

- Pt takes 1 capsule on day 0; check x-ray on day 5

1. If >80% of marker passed by day 5 (5 or fewer markers left), then colon transit normal

- Capsules contain 24 radiopaque ring markers

- ATTACHED IMAGES of potential results: 

1. Normal colonic transit

2. Colonic inertia: delayed passage of marker through prox colon and no INC in motor activity after meals or with admin of laxatives (SLOW)

3. Outlet delay: markers move normally through colon, but stagnate in rectum (more common in pelvic floor dyssenergia; problem in defection process)

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19

What is anorectal manometry? When is it useful?

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- Pressure in rectum goes up, pressure in sphincter goes down in normal person

1. If pressure in sphincter area is high when pt is trying to defecate, this is abnormal

- Helpful, but in severe cases 

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20

Who gets severe idiopathic chronic constipation? Complaints?

- Mostly women

- Complaints include:

1. Infrequent defecation

2. Excessive straining when defecating

3. Or both

21

What pelvic floor muscle is important in defecation?

- Puborectalis: unique, “sling-like” muscle that wraps around the rectum 

- In resting phase, in a contracted state, and keeps rectum angled where it meets the anus, working as a sphincter to prevent accidental leakage of stool

- When it relaxes, sphincter relaxes

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22

What is the difference b/t normal defection and pelvic floor dyssynergia?

- NORMAL: relaxation of puborectalis and external anal sphincter muscles, together with INC intra-abdominal pressure and INH of colonic segmenting activity

- DYSSYNERGIC: ineffective defecation associated with a failure to relax, or inappropriate contraction of, the puborectalis and external anal sphincter muscles 

1. Will see outlet delay on sitzmark study 

23

What is the etiology of severe idiopathic constipation?

- One study: 

1. Slow transit constipation: 11%

2. Dyssynergic defecation: 13%

3. Combo of the two: 5%

4. IBS: 71%

24

What are some of the txs for constipation?

- PT. EDUCATION: INC fluid and fiber intake -> do NOT underestimate importance of dietary changes 

- LAXATIVES: over-the-counter

- OTHER PHARMA: 

1. Lubiprostone: Cl- channel activator that INC secretion of electrolytes in the colon

2. 5HT4 agonists, Prucalopride

- DISIMPACTION: pts with a fecal impaction

- BIO-FEEDBACK for pelvic dysfunction

- SURGERY: sub-total colectomy with ileorectal anastomosis (can get ischemic colitis; will have a little diarrhea forever after this) 

25

How are fiber and laxatives used to tx constipation?

- Fiber supplementation can improve symptoms

1. Usually combine fiber supplement w/ laxative or osmotic agent

- BULK-FORMING laxatives: methylcellulose (pill), calcium polycarbophil 

- SURFACTANTS (stool softeners): docusate sodium 

- OSMOTIC agents: polyethylene glycol (Golytely, Miralax), lactulose

1. Less side effects, and easier to tolerate 

- STIMULANT laxatives: bisacodyl (diphenylmethane), senna (anthraquinones)

1. Can cause more pain, side effects

- SUPPOSITORIES: more rapid -> glycerin, bisacodyl

26

Name 3 pharma therapies for constipation (not laxatives).

- LUBIPROSTONE: locally-acting Cl- channel activator that enhances chloride-rich intestinal fluid secretion

- MISOPROSTOL: PG analog that can stimulate colonic activity

- PRUCALOPRIDE: 5HT4 pro-kinetic agent 

1. Available in Europe and Canada, but not in US

27

What is Hirschsprung disease? Epi?

- Congenital aganglionic megacolon: disorder characterized by obstipation from birth and colonic dilatation proximal to a spastic, non-relaxing and non-propulsive segment of distal bowel

- Obstipation: severe or complete constipation

- EPI: 1:5000-8000 live births and 4:1 M > F 

1. 10% of cases in Down's

2. Most cases sporadic, but a few familial 

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28

What is the pathogenesis of Hirshsprung? Late consequences?

- Absence of ganglion cells in lg bowel (so bowel remains spastic) submucosa (Meissner) and muscle wall (Auerbach) 

1. Func obstruction, so progressive dilatation and hypertrophy proximal to aganglionosis

- LATER: massive distention outruns hypertrophy, wall becomes thinned and ruptures

1. Mortality: superimposed enterocolitis w/fluid and electrolyte disturbances; perforation with peritonitis

- Heterogeneous defects in genes regulating:

1. Migration and survival of neuroblasts

2. Neurogenesis

3. Receptor tyrosine kinase activity

- Rectum ALWAYS involved, and sigmoid in most cases; rarely the entire colon 

29

What is the clinical presentation of Hirschsprung's?

- Initial presentation: failure to pass meconium 

1. Obstructive constipation, occasional passage of stool

2. Bouts of diarrhea, abdominal distention

- Spastic, and a lot of stool above it, so pressure above can sometimes cause leakage of stool via diarrhea; stops when pressure goes down, so they have constipation again 

30

How is Hirschsprung's diagnosed?

- RECTAL BIOPSY: have to do this b/c gold standard for diagnosis -> dx if ganglion cells are absent 

- Abdominal radiographs: massively dilated colonic segment

- Contrast enema

- Anorectal manometry: heightened pressure (see attached image)

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31

What is going on here?

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- Abdominal radiograph (left) and contrast enema (right) showing dilated colon 

- Hirschsprung's 

32

What is the tx for Hirschsprung's?

- Surgical resection of aganglionic segment of bowel

- Normal ganglionic bowel brought down and anastomosed to the anus

- Sphincter function is generally preserved 

33

What are 5 causes of acquired (toxic) megacolon?

- C. diff pseudomembranous colitis: diarrhea initially, but colon may get overwhelmed, leading to constipation and loss of albumin (can even perforate)

1. If colitis is severe, the colon will resign

- Inflammatory bowel disease (IBD: UC or Crohn's)

- Obstruction: tumor or inflammatory stricture

1. Always rule this out when you see a massively dilated colon; may or may not see big mass -> may have to go in with a scope next

2. Pseudo-obstruction (adynamic colon): rare, elderly, after an infection 

- Functional disorder associated with PSYCH disease and medication

- Chagas disease: trypanosomes invade bowel wall and destroy enteric plexus (inflam of the ganglia)

1. People coming in from South America

- NOTE: acquired megacolon is a rare, but fatal condition

34

What is this?

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- Toxic megacolon: can be fatal, and can be caused by the 2 attached images 

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35

What are these?

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- Chagas disease: infection of T. cruzi in myenteric plexus causing loss of ganglion cells in dilated portion of colon (attached) 

- Live in thatched roofs 

- Invade Meissner's plexus: submucosa 

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36

What are these?

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- Chagas disease 

37

What is the general organization of the GI wall histo (image)?

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38

What is the difference b/t these 2 images? Disease? Biopsy method? Staining?

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- Normal colon wall (left) vs. Hirschsprung's disease (congenital aganglionic megacolon; right) 

- Has to be a rectal suction biopsy because you have to get deep enough

1. May have sibling diagnosed with this

- May do sequential biopsies up the colon, starting at the rectum to see where the ganglion cells start

- Can re-stain with CALRETININ to ensure there are no ganglion cells (ignore 4th image; just shows non-specific staining)

1. Box 3 is up-close image of 2

2. Usually, ganglion cells come in little clusters 

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39

What are these?

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- Normal ganglion cells in the GI tract 

- Ganglion cells: lots of cytoplasm and prominent nucleoli off to the side

- Usually, ganglion cells come in little clusters