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

What is the definition of constipation?

- Variable, but:

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


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


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 


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


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 


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


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 


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


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 



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 


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



What is the pediatric etiology of constipation?


- ORGANIC: 5% 

1. Anatomic 

2. Metabolic

3. Neuropathic 

4. Drugs 

5. Endocrine CT disorder 

6. Lead intoxication or botulism 


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


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


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 


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 


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

- 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 


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 


What are Sitzmarks? Potential results?

- 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)


What is anorectal manometry? When is it useful?

- 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 


Who gets severe idiopathic chronic constipation? Complaints?

- Mostly women

- Complaints include:

1. Infrequent defecation

2. Excessive straining when defecating

3. Or both


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


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 


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%


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


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) 


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


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


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 


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 


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 


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)


What is going on here?

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

- Hirschsprung's 


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 


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


What is this?

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


What are these?

- 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 


What are these?

- Chagas disease 


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


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

- 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 


What are these?

- 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