02-28 Diarrhea Flashcards

• Describe the normal fluid and electrolyte transport of the gut • Define diarrhea • Discuss the epidemiology and risk factors of diarrheal illnesses • Describe a framework to characterize the different pathophysiologic mechanisms leading to diarrhea • Discuss the differential diagnosis, appropriate workup and management of a patient presenting with acute diarrhea • Discuss the differential diagnosis, appropriate workup and management of a patient presenting with chronic diarrhe

1
Q

<p>In how many ways are the small intestines folded to increase surface area?</p>

A

<ul>
<li>folded into pliae circularis</li>
<li>villi</li>
<li>microvilli</li>
</ul>

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2
Q

<p>OBJECTIVE: Describe the normal fluid transport of the gut by segment.</p>

<ul>
<li>Which segments absorb: bile salts, Ca++, Fe++ and B12?</li>
</ul>

A

<p></p>

<p>Most water reabsorbed para-cellularly, amount varies by segment:</p>

<ul>
<li>Duodenum: gets 1500cc's from diet + 8000cc's of fluid from saliva, bile, pancreatic secretions, gastric secretions
<ul>
<li>absorbs Fe++ & Calcium</li>
</ul>
</li>
<li>Jejenum: reabsorbs 7000cc's</li>
<li>Ileum: reabsorbs 1500cc's
<ul>
<li>absorbs bile salts and B12</li>
</ul>
</li>
</ul>

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3
Q

<p>OBJECTIVE: Describe the normal electrolyte transport in the small bowel</p>

<ul>
<li>What is depicted here?</li>
</ul>

A

<p>Electrolyte transport is different in the villi than down in the crypts.</p>

<p><strong>VILLI</strong>(see image on reverse)</p>

<p>There are Na+/H+ exhangers and Na+/Nutritent (e.g. SGLT-1, salt-glucose)co-transporters throughout on the <u>villi</u></p>

<ul>
<li>Uses the gradient made by basolateral Na+/K+-ATPase</li>
</ul>

<p><strong>CRYPTS</strong>(see image here)</p>

<p><u>Apical Membrane</u>: chloride eggress</p>

<ul>
<li>No nutrient/Na+ co-trans or Na+/H+ exchangers</li>
<li>CFTR causes Cl- eggress
<ul>
<li>mutated in C.F.→ constipation</li>
</ul>
</li>
<li>This is controlled by cAMP: ↑[cAMP]→↑ secretion &↓ absorption
<ul>
<li>one mech: CFTR gets phosphor'd→ prolonged opening</li>
</ul>
</li>
</ul>

<p><u>Basolateral membrane</u>: Cl- eggress made possible by:</p>

<ul>
<li>basolateral Na/K/2Cl- carrier</li>
</ul>

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4
Q

<p>OBJECTIVE: How do you actually define diarrhea?</p>

A

<p>the quantitative determination of an increase in stool weight greater than 200 grams per 24 hours</p>

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5
Q

<p>OBJECTIVE: Discuss the epidemiology and risk factors of diarrheal illnesses</p>

A

<ul>
<li>2nd most common GI complaint</li>
<li>
<p>20% of all deaths in children less than 5 years of age worldwide are due to diarrhea</p>
</li>
<li>
<p>billions of cases/year</p>
</li>
</ul>

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6
Q

<p>OBJECTIVE: Describe a framework to characterize the different pathophysiologic mechanisms leading to diarrhea</p>

A

<p>With <strong>acute</strong> diarrhea, framework is basically infectious and either infiltrative (bloody) or not, viral or bacterial, etc.</p>

<p>With <strong>chronic</strong> better to think in four categories:</p>

<ol>
<li>osmotic
<ul>
<li>stops w/ fasting</li>
<li>
<p>&uarr; stool anion gap ( > 100)</p>
</li>
</ul>
</li>
<li>secretory
<ul>
<li>not better w/ fasting</li>
<li>no&nbsp;&uarr; in stool anion gap&nbsp;</li>
<li>&quot;NORMAL mechanism of secretion gets commandeered by an endogenous hormone or exogenous toxin&quot;&nbsp;(e.g. vibrio)</li>
</ul>
</li>
<li>inflammatory
<ul>
<li>not better w/ fasting</li>
<li>bloody mucoid stools</li>
<li>stool studies: fecal leukocytes</li>
<li>cause:&nbsp;epithelial&nbsp;destruction (e.g. IBD)</li>
</ul>
</li>
<li>dysmotility</li>
</ol>

<ul>
<li>abnl transit time&nbsp;&rarr; diarrhea</li>
<li>key is the history: surgery?&nbsp;</li>
<li>post-op is archetype: removal of anatomy causing dumping syndrome</li>
</ul>

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7
Q

<p>Stool anion gap?</p>

A

<p>multiply 2 x (Na+ stool + K+ stool) and subtracting from an estimated stool osmolality of 290 mosm/kg H2O</p>

<ul>
<li>Gap > 100 suggests osmotic diarrhea
<ul>
<li>stool [electrolyte] are ↓↓b/c of malabsorbed molecules still in lumen</li>
</ul>
</li>
</ul>

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8
Q

<p><em>Vibrio cholerae</em> diarrhea mechanism</p>

A

<p>vibrio enterotoxin ramps of adenylate cyclase→↑ cAMP→ more Cl- eggress & less reabsorption of Na+</p>

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9
Q

<p>OBJECTIVE: DDx, appropriate work-up &amp; mgmt of pt w/ ACUTE diarrhea?</p>

A

<p>.</p>

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10
Q

<p>OBJECTIVE: DDx, appropriate work-up &amp; mgmt of pt w/ CHRONIC diarrhea?</p>

A

<p><strong>DDx</strong></p>

<p><u>osomotic</u></p>

<p><u>secretory</u></p>

<ul>
<li>toxin-related (e.g. vibrio)</li>
<li>endocrine tumors (VIPoma, gastrinoma, carcinoid tumors secreting 5HIAA)</li>
<li>many laxatives (senna, phenolphthalein, bisacodyl)</li>
<li>lubiprostone</li>
</ul>

<p><u>inflammatory</u></p>

<ul>
<li>most commonly IBD</li>
<li>bacterial agents secreting cytotoxins
<ul>
<li>E.H.E.C.&nbsp;(O157:H7)</li>
<li>C difficile</li>
</ul>
</li>
<li>Invasive organisms
<ul>
<li>Shigella, Campylo., Salmonella, Yersinia</li>
</ul>
</li>
</ul>

<p><u>dysmotile</u></p>

<ul>
<li>post-op&nbsp;&rarr; dumping syndrome is archetype</li>
<li>dz assoc&#39;d w/ disordered motility (e.g. scleroderma or diabetes)</li>
<li><u>slow</u> intestinal transit with bacterial overgrowth
<ul>
<li>deconjugates bile acids &amp; prevents proper bile acid function&nbsp;&nbsp;steatorrhea</li>
</ul>
</li>
</ul>

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