Shared Flashcard Set


Functional Bowel Disorders

Additional Accounting Flashcards




How are the following gut sites affected by FBDs?
small intestine/colon
biliary tract
o Esophagus: function (non-cardiac) chest pain, functional heartburn
o Stomach/duodenum: functional (non-ulcer) dyspepsia, functional vomiting
o Small intestine/colon: IBS, functional bloating
o Biliary tract: sphincter of Oddi dysfunction
describe the Rome criteria for dx of IBS
o Recurrent abdominal pain or discomfort >=3 days per month in the last 3 months that has 2 of 3 following defecation features:
 Relieved by defecation
 Onset associated with change in stool frequency (>3/d diarrhea, <3/wk constipation)
 Onset associated with altered stool form (loose watery diarrhea, hard pellets constipation)
Neurogenic factors in FBD?
Motor, sensory, CNS dysfunction, altered fluid secretion, neurotransmitters => neurogenic defects in FBD

Functional aspects:  Motor: likely relevant to symptoms related to transit (diarrhea, constipation, N/V), unproved relation to pain
 Sensory/CNS: likely relevant to pain (60-70% have heightened perception), unproved relation to symptoms relating to transit
 Secretory: possibly relevant to stool consistency/frequency
Motor dysfunction - what can go wrong w/ contractions?
 Intense contractions that cause pain (spasms)
 Propulsive contractions that accelerate transit (e.g. diarrhea)
• Gastrocolonic response as a cause of diarrhea in IBS: increased motility is seen in IBS pts
• Mediated by parasympathetics
 Occlusive contractions that delay transit (e.g. constipation, bloating, N/V)
 Loss of contractions leading to delayed transit (e.g. constipation, bloating, N/V)
 Altered tone/compliance (e.g. fecal urgency, fullness, bloating)
Sensory: hyperalgesia, allodynia, altered referral patterns?
heightened sensation of gut stimulation due to abnormal activity of sensory nerves
 Hyperalgesia: heightened sensation of painful stimuli
 Allodynia: pain received with stimuli not normally painful
 Altered referral patterns: pain perceived more diffusely than normal
Areas of the CNS that are dysfunctional in FBD
heighted sensation of gut stimulation due to abnormal activity of pain pathways in brain
 Increased activation of anterior cingulated cortex (ACC)
 Activation of multiple new sites in prefrontal cortex (PFC)
 ACC and PFC deal with emotional aspects of pain
in altered fluid secretion, the balance of what gets altered?
altered balance in cholinergic secretory and adrenergic absorptive pathways in intestine
The main neurotransmitter that => neurogenic defects? where is it released from, what does it do, and when is it released in higher amounts?
 Serotonin (5-HT) as possible mediator
• Released by mucosal enterochromaffin cells with noxious stimulation
• Activates peristalsis – abnormalities cause increased/decreased transit
• Activates sensory pathways that mediate pain
• Increased release after meals in IBS

Other neurotransmitters:  Criteria to be considered a cause of FBD: presence of defect correlates with disease, normal controls do not possess defect, defect can cause symptoms
What is the relation of celiac disease to FBD?
 Definition: small intestinal inflammation due to gluten exposure
 Clinical: symptoms similar to IBS, anemia, bone disease, risk of malignancy
 Increased celiac disease prevalence in pts with IBS symptoms
 Therapy: some respond to gluten-free diet
How do cytokine abnormalities contribute to IBS?
o Cytokine abnormalities in IBS: study showed increaseTNF, IL1 and IL6 in IBS pts
What are clinical diseases that contribute to inflammatory processes in FBD?
o Clinical evidence: up to 25% of IBS pts report onset after infection, 6-25% of Campylobacter pts develop IBS, recent associations with C. diff and viral GE
What is the role of diet in IBS?
 Carbohydrates: malabsorption of simple sugars in IBS
• Lactase deficiency: prevalence depends on race
• Fructose: in fruits and soft drinks (60% absorbed), excess hydrogen production with >25gm, increased hydrogen production in intolerant pts
• Sorbitol: in fruits and artificial sweetener, excess hydrogen production with >5gm
 Gas formers: gas formation with complex carbohydrates
• Some IBS pts are more susceptible to forming gas from complex carbs
How does the gut flora in the colon vs. small intestine contribute to IBS?
 Colonic flora
• Colonic flora consists of thousands of bacterial species (1010-12 CFU/ml) – most uncharacterized
• Differences in microbial genomes of feces from IBS pts vs. controls identified in many bacteria
 Small intestinal bacterial overgrowth
• Normal luminal bacterial counts are much less than colon (7-8 magnitudes lower)
• 13-84% of IBS pts have abnormal upper gut bacteria (>105 CFU/ml)
• 40% respond to antibiotics
What Sx are present in Constipation IBS and what diet/medications contribute to this?
 Sx: pellet-like stools; straining and incomplete evaluation
 Review diet Hx: adequate fluids and fiber (recommended 20-30g/day, fruit/veggies only 1-2gm/serving)
 Review mediations: anti-HTN, narcotics, analgesics, anticholinergics, antidepressants can all slow down the bowel
What Sx are present in Diarrhea IBS and what diet/medications contribute to this?
 Sx: frequent, loose, urgent stools; incomplete evacuation; non-nocturnal symptoms
 Review diet Hx: fruits, soft drinks, juices containing fructose; sugar-free gum and candy/mints with sorbitol; dairy products (lactose)
 Review meds: Mg containing antacids, analgesics, PPIs
What Sx are present in Pain IBS and what diet/medications contribute to this?
 Sx: pain that is variable in location and severity; usually crampy, but may be sharp, dull or non-descript; associated gas and bloating; often exacerbated by meals or stress; non-nocturnal
 Review diet Hx: poorly digested sugars, air swallowing

No meds...
What would you expect TSH levels to be in a) constipation or b) diarrhea
a) High (hypothyroidism)
b) Low (hyperthyroidism)
What serology do you want to do for celiac disease?
tissue transglutaminase
What's the difference between lactose and glucose dependent hydrogen breath tests?
 Hydrogen breath test:
• if lactose deficient, administering lactose will cause colonic bacteria to produce hydrogen gas (human tissue does not do this) which can be measured
• if bacterial overgrowth, administering glucose will produce hydrogen
Goals in targeting neurogenic factors for FBD
o Modulate gut motor function: slow transit (for diarrhea), accelerate transit (for constipation), reduce spasm (for pain)
o Modulate secretion: increase secretion (for constipation)
o Modulate heightened sensation/CNS factors
 Antidepressants – TCAs, SSRIs
 Other visceral analgesics – pregabalin, gabapentin
3 classes of drugs for diarrhea IBS
Opiates, 5-HT3 antagonists, antispasmodics
What is the physiologic action of Diphenoxylate? and what 2 other drugs are in this same class?
Opiate antidiarrheals: loperamide, diphenoxylate, codeine
 Physiologic actions: increase non-propagative colonic contractions, enhance water and ion absorption, increase anal tone and decrease rectal sensation
 Clinical effects: slows colon transit, decreases stool frequency, improves consistency; may cause cramps
What is dicyclomine meant for? and what's its mechanism and the other drug in the class?
o Antispasmodics for pain- and diarrhea-predominant IBS
 E.g. dicyclomine, hyoscyamine
 Action: blunt cholinergically-mediated motor complexes (e.g. gastrocolonic response) – slow transit
 Clinical effects: reduce pain (esp. postprandial), may worsen symptoms in constipation-type IBS, may prevent postprandial diarrhea and fecal urgency
You think it's best to give a potent anti-diarrheal to decrease stool frequency and reduce pain in a patient who reports shitting his pants all the time and lots of pain, but know that you can only give this drug for really severe cases b/c it causes SE of ischemic colitis and severe constipation. Which drug is this?
o 5-HT3 antagonists for diarrhea-predominant IBS (not used as much)
 E.g. alosetron – most potent anti-diarrheal
 Physiologic actions: slow transit, reduce sensation, decrease intestinal secretion
 Clinical effects: decreases stool frequency, improves consistency, reduces pain
• Restricted to severe cases due to SE of ischemic colitis, severe constipation
Why would you give desipramine to a patient with IBS? what are other drugs in this class and how do they work?
o Tricyclic antidepressants for pain-predominant IBS
 E.g. amitriptyline, nortiptyline, desipramine
 Action: reduce sensory transmission, central antidepressant effect?, slows transit
 Clinical effects: reduces pain and diarrhea independent of mood effects
You decide to give a Cl-channel activator that works by activating guanylate cyclase. What are you doing here and which two drugs could you potentially give?
o Secretory stimulants for constipation-predominant IBS
 E.g. lubiprostone, linaclotide (investigational)
 Physiologic actions: chloride channel activator, guanylate cyclase activator – basically cause intestine to make more water
 Clinical effects: increase stool frequency, improve stool consistency, may produce nausea, cramps, possible cause of birth defects
What are drugs like paroxetine or citalopram good for?
improving Sx of depression (paroxetine), bloating, and pain, constipation.

These are SSRIs (also including fluoxetine)
Visceral analgesics are used to either reduce rectal hypersensitivity or increase rectal sensory threshold. What two drugs are used for this?
 Gabapentin reduces rectal hypersensitivity, increases compliance in diarrhea-predominant IBS
 Pregabalin increases rectal sensory thresholds for first sensation, desire to defecated and pain in IBS pts
 No clinical trials to date
is Psych treatment ever indicated for IBS?
yes for the worst cases
how long after a gluten free diet can you expect a symptom response in a celiac px? will there be a histologic response?
o Gluten-free diet for celiac disease only (avoid wheat, barley, rye, oats) – symptom response within 2 weeks, though histologic response is slower
Metamucil is a fiber supplement. what other treatmetns exist in the same class and what are their actions?
 Fiber supplements for constipation-predominant IBS
• E.g. psyllium, methylcellulose, calcium polycarbophil
• Action: water retention and bulking, stimulations fermentation, accelerates transit
• Clinical effects: increases stool frequency, improves consistency (has no effect on pain or diarrhea, may worse bloating)
T/F: Polyethylene glycol can sometimes be used as a neurogenic factor to help with constipation.
False: this is in the class of osmotic laxatives
 Osmotic laxatives for constipation-predominant IBS
• E.g. hypertonic salt (milk of magnesia), nonabsorbable sugar (lactulose), isotonic electrolyte (polyethylene glycol)
• Action: hydrate stool
• Clinical effects: increase stool frequency, improve stool consistency; may produce cramps and discomfort
What three things can you give to modify the gut flora?
 Antibiotics: for documented bacterial overgrowth, but concern about long-term use (resistant organisms) without bacterial overgrowth
 Probiotics: replace “pathogenic” bacteria, best for gaseous symptoms
• Modulate immune responses, enhance epithelial barrier, anti-microbial effects
 Prebiotics: oligosaccharides promote growth of specific “good” bacteria (e.g. bifidobacteria) and BEST FOR REDUCING DISCOMFORT/PAIN!
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