Chronic Diarrhea and Malabsorption: Chronic Diarrhea and Malabsorption: Bile and Fat

0:00Welcome to Board Pearls. This is episode two of two of the Chronic Diarrhea and Malabsorption chapter, in the Stomach and Small Bowel Disorders module. This episode covers bile acids, microscopic colitis, fat and blood in the stool, and the workup that comes back empty. A man with diarrhea after cholecystectomy shows why bile acids in the colon cause diarrhea, where it happens, and how it's diagnosed without the reference scan, and a woman with a long ileal resection shows why the same drug would hurt her. An older man on several culprit drugs shows who gets microscopic colitis, which drugs cause it, and why biopsies must come from both sides of the colon, and a woman with celiac disease shows how the two diseases travel together. A man with greasy stools shows how steatorrhea is proven, how a failing pancreas is separated from a damaged small bowel, and how enzymes are dosed, and a woman with a normal pancreas shows the mucosal causes. A man with bloody diarrhea shows how the colonoscopy pattern names an inflammatory cause. And a woman whose full workup comes back empty shows how to retake the history and run empiric trials in the right order, and a man at the end of that road shows when the label of irritable bowel finally applies.

1:14Here's the first patient. A forty-six-year-old man had a laparoscopic cholecystectomy eight months ago. Since then he's had urgent, watery diarrhea three to six times a day, often within half an hour of eating, sometimes waking him at night, with two episodes of incontinence. There's no blood and no weight loss. His celiac serology, calprotectin, thyroid-stimulating hormone, TSH, and stool infection tests are normal. His primary care doctor has called it irritable bowel.

1:46Urgent watery diarrhea, often after meals and at night, that began after a cholecystectomy points to bile acid diarrhea, and the irritable bowel label is premature. Seeing why starts with how bile acids normally cycle. The liver secretes conjugated bile acids into the duodenum, where they solubilize dietary fat. In the terminal ileum, the apical sodium-dependent bile acid transporter reabsorbs about ninety-five percent of them, and they return to the liver through the portal vein. Only about five percent are lost in the stool each cycle, and the liver replaces them.

2:21The ileum has a second job, and failure of either one floods the colon. It releases a hormone, fibroblast growth factor nineteen, FGF19, that suppresses the liver enzyme cholesterol seven-alpha-hydroxylase, CYP7A1, and slows bile acid production. So the ileum both recovers bile acids and sets how many new ones are made.

2:45Once in the colon, bile acids cause diarrhea directly. Above roughly three to five millimoles per liter, they act on a receptor on colon cells called TGR5, which stops the colon absorbing water and electrolytes and makes it secrete. The result is urgent, watery, often nocturnal diarrhea, sometimes with incontinence. Eating releases bile, so his diarrhea comes soon after meals.

3:09Bile acid diarrhea happens in four settings, and his history places him in one. The first is disease or resection of the terminal ileum: Crohn ileitis, an ileocecal resection, radiation injury, ischemia, or lymphoma. The second is idiopathic bile acid diarrhea, in which the ileum doesn't make enough FGF19, so the liver overproduces bile acids. About thirty percent of patients labeled irritable bowel with diarrhea have measurable bile acid malabsorption, much of it this type.

3:43The other two settings are anatomy and drugs. The third is altered anatomy or motility after cholecystectomy, vagotomy, or gastrectomy, which disrupts the normal cycling of bile acids. Chronic watery diarrhea beginning within months of a cholecystectomy, with urgency and incontinence, is the classic picture, and it's his. The fourth is drugs, with metformin and lenalidomide as the prototypes, so his medication list still matters, because a drug like metformin can add to the same diarrhea.

4:13Confirming it is harder than suspecting it. The reference test, the selenium-75 homocholic acid taurine, SeHCAT, scan, measures retention of a swallowed radiolabeled synthetic bile acid at seven days. Retention under fifteen percent is abnormal: ten to fifteen is mild, five to ten moderate, and under five severe. But it isn't available in the United States.

4:37The tests that are available measure the liver's response. C4, seven-alpha-hydroxy-four-cholesten-three-one, is an intermediate in bile acid synthesis, and it's high when the liver ramps up production to replace losses. Fasting FGF19 is low in the idiopathic form. A forty-eight-hour stool bile acid measurement is rarely available outside research. In practice, the most useful test is a trial of a bile acid sequestrant, which binds bile acids in the gut so they can't act on the colon. A response within one to two weeks supports the diagnosis and treats it.

5:11Before settling on the diagnosis, the mimics are excluded. Celiac disease is excluded with serology, and chronic pancreatitis with fecal elastase. Bacterial overgrowth deconjugates bile acids and causes similar symptoms, so a breath test or a rifaximin trial is used when it's suspected. His elastase is normal, and he has no risk factors for overgrowth.

5:36The sequestrant trial is also his treatment, and its practical rules decide whether he sticks with it. Cholestyramine starts at four grams once daily and increases to four grams two to four times a day, up to sixteen grams a day, taken before meals and at bedtime. It binds other drugs, so other medications are taken one hour before or four hours after it. It also binds fat-soluble vitamins, and it causes bloating and constipation.

6:02The alternatives are easier to take. Colesevelam, three point seven five grams a day as six six-hundred-twenty-five-milligram tablets or one point eight seven five grams twice daily, is better tolerated, because tablets avoid the gritty powder and cause less bloating. Colestipol, five to thirty grams a day in divided doses, is a third option. Loperamide can be added, and a moderate-fat diet helps, since dietary fat triggers bile release. Because so many patients labeled irritable bowel with diarrhea have bile acid malabsorption, sequestrants are part of irritable bowel treatment too.

6:36He starts cholestyramine four grams before breakfast, then twice daily. Within ten days his stools are formed and the urgency is gone. He finds the powder hard to take and switches to colesevelam, which keeps him well.

6:50The second patient shows that the length of ileum lost changes everything. A thirty-eight-year-old woman with Crohn disease had one hundred fifty centimeters of ileum removed and has large-volume, greasy, foul-smelling diarrhea and weight loss. The rule is about one hundred centimeters. With less than one hundred removed, bile acids spill into the colon and cause watery bile acid diarrhea, but the liver keeps up, the pool is preserved, and fat is still absorbed, so that patient responds to a sequestrant.

7:18Her resection is past that line. With more than one hundred removed, losses exceed what the liver can replace, the pool shrinks below the level needed to form micelles, and the result is steatorrhea. Her colon actually sees lower bile acid concentrations, because her high stool volume dilutes them. A sequestrant would bind the few bile acids she has left and worsen her fat malabsorption without helping the diarrhea. Her treatment is a low-fat diet with medium-chain triglycerides, which are absorbed without bile acids, plus fat-soluble vitamins.

7:51The third patient has watery diarrhea from the colon's own lining. A sixty-nine-year-old man has had watery, non-bloody diarrhea for five months, six to eight times a day, with urgency and two stools most nights. He has mild cramps that ease after a bowel movement, and he's lost four pounds. He smokes half a pack a day. He takes lansoprazole for heartburn, sertraline, started a year ago, and naproxen for knee pain. His blood count, TSH, C-reactive protein, CRP, celiac serology with total immunoglobulin A, IgA, and stool infection panel are normal.

8:32An older man with chronic watery, non-bloody diarrhea, a normal workup so far, and several culprit drugs is the typical picture of microscopic colitis. It's the leading cause of chronic watery diarrhea in people over sixty, peaking in the seventh decade. Women are affected more often, especially with the collagenous type, but men get it too. Symptoms are chronic watery, non-bloody diarrhea, sometimes more than ten stools a day; nocturnal stools in about a quarter; urgency; incontinence; mild cramps; and mild weight loss. Severe weight loss, blood, or rapid decline should prompt a search for another diagnosis.

9:12The mechanism is an immune injury to the colon's surface lining, set off by genetic risk, autoimmune tendency, smoking, and drugs. The injured lining absorbs less sodium and chloride and secretes chloride. So the diarrhea is secretory, with an osmotic gap under fifty, persisting during a fast, and often at night.

9:33His drugs and habits matter now, because removing them will be the first treatment. The clearest links are nonsteroidal anti-inflammatory drugs, NSAIDs; proton pump inhibitors, PPIs, with lansoprazole the strongest and omeprazole also recognized; selective serotonin reuptake inhibitors, SSRIs, such as sertraline and fluoxetine; H2 blockers, with ranitidine historically implicated before its withdrawal in the United States; simvastatin; carbamazepine; ticlopidine; and acarbose. Smoking, current or former, roughly doubles the risk, independent of drugs. He has naproxen, lansoprazole, sertraline, and smoking: four modifiable risk factors.

10:18The diagnosis is made only on biopsy, and where the biopsies come from decides whether it's made. The colon almost always looks normal, at most mildly red, swollen, or fragile, so random biopsies of normal-looking mucosa are mandatory. They must come from both the right and left colon, ideally the cecum, ascending, transverse, and rectosigmoid, because the lymphocytic infiltrate and collagen band are denser on the right. Left-only sampling misses about ten percent of cases, so a flexible sigmoidoscopy isn't enough. His colonoscopy looks normal, and the right colon biopsies show a thickened collagen band under the surface lining, with less impressive left-sided changes.

11:00The pathologist separates the two types, and both from inflammatory bowel disease, IBD. Lymphocytic colitis has more than twenty intraepithelial lymphocytes per one hundred surface cells, twenty-five by some thresholds, with more inflammatory cells in the lamina propria. Collagenous colitis has a subepithelial collagen band thicker than ten microns, against a normal of about three, confirmed with a trichrome stain, patchy and densest on the right.

11:27Both types share features that separate them from IBD. Both show damaged surface cells that flatten, vacuolate, and detach, and in both the crypt architecture is preserved, unlike IBD, where crypts are distorted. He has collagenous colitis. The two types are treated the same way.

11:45His treatment is staged by severity, following the American Gastroenterological Association, AGA, guideline. First, the causative drugs and smoking are stopped, which sometimes cures it and is always the starting point. Loperamide helps mild symptoms. Bismuth subsalicylate, two hundred sixty-two milligrams, two to three tablets three times a day for six to eight weeks, is a low-cost option for mild to moderate disease.

12:11For moderate to severe disease, or symptoms that persist after the drugs are stopped, budesonide nine milligrams a day for six to eight weeks is first line, with a response in about four in five. It acts locally because the liver clears most of it on first pass. After the course, it's tapered.

12:29Relapse is common, so the plan after budesonide is set in advance. Relapse after stopping occurs in sixty to eighty percent, and relapsing patients go on maintenance budesonide three to six milligrams a day. Cholestyramine helps when bile acid diarrhea overlaps, which it often does. Five-aminosalicylic acid, five-ASA, drugs have weak evidence. Refractory disease goes to azathioprine, six-mercaptopurine, or methotrexate, or to an anti-tumor necrosis factor, anti-TNF, drug or vedolizumab, based on small case series.

13:07He stops naproxen and lansoprazole and enters smoking cessation, and his psychiatrist moves him to another antidepressant. After a month he still has four loose stools a day, so he starts budesonide nine milligrams, and within three weeks his stools are formed. He tapers after eight weeks, relapses two months later, and goes on budesonide three milligrams a day.

13:29The fourth patient shows that the link with celiac disease runs both ways. A forty-one-year-old woman with celiac disease confirmed two years ago follows a strict gluten-free diet, checked by a dietitian, and her tissue transglutaminase has normalized, but she still has watery diarrhea. Microscopic colitis is fifty to seventy-two times more common in celiac disease, so her next step is colonoscopy with random right and left colon biopsies, not a repeat duodenal biopsy.

13:58The link works in reverse too. A patient with refractory microscopic colitis, malabsorption, iron deficiency, or major weight loss should be tested for celiac disease, sometimes with a duodenal biopsy even when serology is negative. Thyroid disease, rheumatoid arthritis, psoriasis, and type one diabetes are also more common in microscopic colitis.

14:22The fifth patient's stools are fatty, not watery, and that changes the workup. A fifty-seven-year-old man drank heavily for twenty years and has had three admissions for pancreatitis. For six months he's had three to four bulky, pale, foul-smelling stools a day that float, leave an oily film, and are hard to flush. He's lost twenty-two pounds despite eating well. He has trouble driving at night. His calcium and vitamin D are low, and his international normalized ratio, INR, is one point six, though he takes no anticoagulant.

15:01His history already points to steatorrhea, and probably to its cause. Greasy, foul, floating stools with weight loss despite good intake are its signature, and so is loss of the fat-soluble vitamins A, D, E, and K. His low calcium and vitamin D come from vitamin D malabsorption. His prolonged INR without an anticoagulant comes from vitamin K deficiency. His trouble driving at night is night blindness from vitamin A deficiency. And three bouts of pancreatitis point at a cause.

15:32The workup follows how fat absorption works, because it fails in two distinct ways. In the lumen, pancreatic lipase breaks fat down, and bile acids carry the products to the lining in micelles, and failure here is maldigestion. Then the mucosa takes up and packages the fat, and failure here is malabsorption. So the workup is one split, pancreas or mucosa, with too few luminal bile acids as a second, smaller cause of maldigestion.

16:01Steatorrhea is proven first. The reference test is quantitative fecal fat: one hundred grams of fat a day for at least three days, with a seventy-two-hour stool collection. Normal is under seven grams a day, up to fourteen can occur with diarrhea alone, and over fourteen is the usual cutoff for steatorrhea in a patient with diarrhea. Over thirty grams a day is typical of pancreatic insufficiency, while fourteen to thirty is more common in mucosal disease.

16:28The collection is unpleasant and rarely done routinely, so screens exist. A Sudan stain of a single stool is the bedside screen, showing fat globules under the microscope, but it misses mild cases. An acid steatocrit, which measures fat in a centrifuged sample, is a third option.

16:46Pancreas is then separated from mucosa with fecal elastase, a pancreatic enzyme that survives transit, measured on one random stool. Under two hundred micrograms per gram supports pancreatic insufficiency, and under one hundred is severe. Watery stool dilutes it and makes it falsely low, so a formed or semi-formed sample is collected when possible. The cholecystokinin-secretin test is the historical reference but is rarely used outside referral centers.

17:14His fecal fat is forty-two grams a day, his elastase is forty on a semi-formed sample, and computed tomography, CT, shows pancreatic calcifications. He has pancreatic insufficiency from chronic pancreatitis. The other pancreatic causes are chronic pancreatitis from other causes, hereditary, autoimmune, or idiopathic; pancreatic cancer; cystic fibrosis; a Whipple resection; and severe acute pancreatitis that destroyed much of the gland.

17:43His treatment is pancreatic enzyme replacement, dosed by lipase. It's twenty-five thousand to fifty thousand units with each meal and ten thousand to twenty-five thousand with each snack, taken with the first bite of food. Fat-soluble vitamins are replaced, including vitamin K for his INR, and the diet is moderate in fat, not very low in fat. He starts fifty thousand units with meals and twenty-five thousand with snacks, plus vitamins A, D, and K. His stools become formed, his INR normalizes, and he regains weight over three months, with support to stay off alcohol.

18:19His pancreatitis carries one more risk to watch for. Chronic pancreatitis is a cause of bacterial overgrowth, which deconjugates bile acids and adds its own fat malabsorption, so incomplete response to enzymes should raise it.

18:33The sixth patient shows where the answer lies when the pancreas is fine. A thirty-four-year-old woman has six months of greasy stools, bloating, and fifteen pounds of weight loss, with iron deficiency and low vitamin D. Her fecal elastase is three hundred twenty, normal. So the problem is mucosal, and the workup is upper endoscopy with at least four biopsies from the distal duodenum and one or two from the bulb, plus tissue transglutaminase IgA with total IgA.

19:00Celiac disease is the most common finding, and the rest of the mucosal list each has a clue. Tropical sprue affects a returning traveler with combined folate and B12 deficiency. Whipple disease shows periodic acid-Schiff-positive macrophages. Autoimmune enteropathy shows loss of goblet and Paneth cells with deep crypt cell death. Common variable immunodeficiency shows low immunoglobulins. Eosinophilic gastroenteritis, bacterial overgrowth, and drug-induced enteropathy, such as from olmesartan, complete the common causes.

19:34A few mucosal causes have findings outside the duodenum. Intestinal lymphangiectasia shows dilated lacteals and causes protein loss, with low albumin and low lymphocytes, confirmed by an alpha-one antitrypsin clearance test. Short bowel syndrome follows the one-hundred-centimeter rule. Chronic mesenteric ischemia causes pain after meals, weight loss, and an abdominal bruit, seen on CT angiography.

20:01Her iron deficiency fits celiac disease, which damages the duodenum, where iron is absorbed. Her tissue transglutaminase is high and her duodenal biopsies show villous atrophy. She starts a gluten-free diet with a dietitian.

20:16The last cause of fatty stool is too few bile acids in the lumen. Fat isn't absorbed when luminal bile acids fall below the level needed to form micelles. That happens in severe cholestasis, such as primary biliary cholangitis or primary sclerosing cholangitis; in bacterial overgrowth, where deconjugated bile acids precipitate; and after more than one hundred centimeters of ileal resection. Treatment is the cause plus medium-chain triglycerides for calories, because they're absorbed without micelles. The older D-xylose test, once used to separate mucosal from pancreatic disease, has been replaced by direct testing.

20:54The seventh patient's stools carry blood, and that sends the workup to the colon. A sixty-one-year-old man has bloody diarrhea with crampy pain, and his fecal calprotectin is over one thousand. Inflammatory diarrhea is bloody, leukocyte-positive, and often febrile, with a calprotectin usually over two hundred fifty, and values over one thousand to two thousand are seen in active IBD and severe infectious colitis. The workup is colonoscopy with ileoscopy and segmental biopsies, plus a multiplex PCR stool infection panel.

21:28The colonoscopy and biopsy pattern usually names the cause. Pseudomembranes with a positive C. difficile toxin test mean C. difficile colitis. Discontinuous deep ulcers with skip lesions and granulomas point to Crohn disease. Continuous distal-predominant inflammation with crypt distortion and basal plasmacytosis points to ulcerative colitis. Watershed necrosis at the splenic flexure or rectosigmoid, with viable deeper crypts, points to ischemic colitis. Telangiectasias in a prior radiation field point to radiation colitis. Owl-eye inclusions in large ulcers of an immunocompromised host point to cytomegalovirus. Invasive infections, herpes simplex colitis, cancer, and lymphoma are also on the list. His shows watershed necrosis at the splenic flexure, ischemic colitis.

22:19The eighth patient has had every test, and nothing has been found. A thirty-nine-year-old woman has had watery diarrhea for a year, four to six times a day, with some urgency and no blood. A blood count, metabolic panel, TSH, and celiac serology with total IgA are normal. Her calprotectin and elastase are normal, an infection panel is negative, stool electrolytes give an indeterminate osmotic gap, and her fecal fat is normal. Upper endoscopy with duodenal biopsies, colonoscopy with right and left colon biopsies, and CT enterography are all normal. She asks what's left.

23:00She has obscure chronic diarrhea, and before another test, the history is taken again, because a careful repeat history catches a substantial share of unexplained diarrhea before any new test. The medication list is reread, including over-the-counter products, the surgical history is rechecked, and she's asked for a week-long diet diary. She mentions a cholecystectomy three years ago that no one had recorded, and her diary shows sugar-free gum through the day and several glasses of milk. That raises bile acid diarrhea, a sorbitol osmotic load, and possible lactose intolerance.

23:34The small bowel needs a closer look only when features point there. Capsule endoscopy is for suspected small bowel disease earlier tests haven't shown: subtle Crohn disease, NSAID injury such as diaphragm-like strictures, small bowel lymphoma, or sprue patterns too far down for a duodenal biopsy. Patency is confirmed first, with a patency capsule or cross-sectional imaging, in anyone with obstructive symptoms or known strictures, because a capsule can lodge.

24:05Enteroscopy follows when tissue or treatment is needed. Push enteroscopy reaches the proximal jejunum, and single- or double-balloon enteroscopy reaches further, for biopsy, dilation, or tattooing a lesion for surgery. She has no bleeding, iron deficiency, weight loss, or obstructive symptoms, so a capsule isn't needed now.

24:25Empiric trials come next, ordered by how common the condition is, so the likeliest answer is tested first. A bile acid sequestrant for one to two weeks comes first, because bile acid diarrhea is common, especially with irritable bowel overlap or after cholecystectomy. Rifaximin, five hundred fifty milligrams three times a day for fourteen days, comes second, for overgrowth and dysbiosis, which overlap with irritable bowel with diarrhea in a substantial minority.

24:54The diet trials follow. A lactose-free diet runs for two to four weeks. A diet low in fermentable oligosaccharides, disaccharides, monosaccharides, and polyols, a low-FODMAP diet, runs for four to six weeks, with structured reintroduction. And an enzyme trial is reasonable when elastase is borderline or steatorrhea is suspected.

25:17A gluten-free trial is a special case. If it helps, later celiac testing becomes unreliable, so human leukocyte antigen, HLA, DQ2 and DQ8 typing comes first, and a negative result essentially excludes celiac disease.

25:33Her cholecystectomy makes a sequestrant her first trial. On colesevelam, her stools fall from five a day to two, with less urgency. She stops the gum and switches to lactose-free milk, and the rest of her symptoms settle. She had bile acid diarrhea with two osmotic contributors.

25:50Targeted tests are added only when the picture fits, because each has a specific trigger. A neuroendocrine panel is for prominent secretory features or red flags such as flushing, low potassium, ulcers, a thyroid nodule, or a rash. It includes chromogranin A, vasoactive intestinal peptide, gastrin off PPIs, calcitonin, somatostatin, glucagon, and urine five-hydroxyindoleacetic acid, with DOTATATE imaging when a tumor is suspected.

26:21The other targeted tests answer narrower questions. Anorectal manometry is for fecal incontinence, which is mistaken for diarrhea more often than expected. Quantitative immunoglobulins look for common variable immunodeficiency in a patient with chronic diarrhea plus sinus and lung infections or past giardiasis. A urine and stool laxative screen is added when factitious disease is plausible. She has none of those features.

26:46When all of that is exhausted, the patient is referred. Specialized chronic diarrhea centers regularly find what the first workup missed. They find bile acid diarrhea; carbohydrate malabsorption, including sucrase-isomaltase deficiency by genetic testing; idiopathic secretory diarrhea, sporadic or in outbreaks, which eventually resolves on its own; microscopic colitis missed because random biopsies weren't taken; laxative use; hormone-secreting tumors; fecal incontinence; an unasked-about drug; and pancreatic insufficiency.

27:21The last patient shows when the irritable bowel label finally applies. A forty-four-year-old man with a normal workup has run every empiric trial without benefit. He has diarrhea with abdominal pain related to bowel movements, meets the Rome criteria, and has no alarm features. Only now does irritable bowel with diarrhea apply.

27:42His treatment follows that diagnosis. It's loperamide; rifaximin; eluxadoline, which is contraindicated without a gallbladder; a bile acid sequestrant for overlap; and a tricyclic or serotonin-norepinephrine reuptake inhibitor, SNRI, neuromodulator. Alosetron is reserved for severe disease in women. Given how often the label turns out to hide bile acid diarrhea, food intolerance, overgrowth, microscopic colitis, or celiac disease, applying it early means missing something treatable.

28:13Here are the traps the boards set in these patients. Diarrhea after a cholecystectomy isn't irritable bowel until bile acids are considered. SeHCAT isn't available in the United States. Cholestyramine isn't taken with other medications, and long-term sequestrants need fat-soluble vitamins watched. And a sequestrant isn't given after more than one hundred centimeters of ileal resection.

28:37The microscopic colitis traps follow. A normal-looking colon doesn't end the workup without biopsies, and the left colon alone isn't enough. Preserved crypts mean it isn't IBD. Budesonide doesn't come before stopping the PPI, NSAID, or SSRI and addressing smoking, and it isn't stopped without a plan for relapse. And a celiac patient with persistent watery diarrhea needs colon biopsies, not a repeat duodenal biopsy.

29:04The fatty diarrhea traps come next. Elastase isn't sent on watery stool. Enzymes are taken with the first bite, not after the meal, and a pancreatic patient doesn't need a very low-fat diet. A high INR in malabsorption means vitamin K. And low albumin with low lymphocytes points to lymphangiectasia.

29:24The obscure diarrhea traps close the list. A new test doesn't come before retaking the history. A capsule isn't given without confirming patency. A gluten-free trial doesn't come before HLA typing. Empiric trials are run in order of likelihood. Fecal incontinence can present as diarrhea. Eluxadoline isn't given without a gallbladder. And the irritable bowel label doesn't come before organic disease is excluded and the trials are done.

29:51So, start to finish. Too many bile acids in the colon cause urgent, often nocturnal watery diarrhea through TGR5, after ileal disease, from low FGF19, after cholecystectomy, or from drugs. A sequestrant trial usually makes the diagnosis. After more than one hundred centimeters of ileal resection, the problem becomes fat malabsorption, treated with a low-fat diet and medium-chain triglycerides.

30:18Microscopic colitis is watery secretory diarrhea in older adults with a normal-looking colon. Biopsy both sides, stop NSAIDs, PPIs, SSRIs, and smoking, and give budesonide, with low-dose maintenance for relapse.

30:33Fatty diarrhea is proven by fecal fat over seven grams a day, with over thirty favoring the pancreas. Elastase under two hundred points to pancreatic insufficiency, treated with lipase-dosed enzymes taken with the first bite, vitamins, and a moderate-fat diet. A normal elastase means duodenal biopsies and celiac serology. Bloody diarrhea with a high calprotectin goes to colonoscopy, where the pattern names the cause.

30:59When the workup is empty, retake the history, run empiric trials in order of likelihood, add targeted tests only when the picture fits, refer when those are exhausted, and only then apply the irritable bowel label.

31:13That completes the Chronic Diarrhea and Malabsorption chapter. The next chapter is irritable bowel syndrome, starting with a patient with constipation-predominant disease.

31:23For the full chapter, the practice vignettes, and the topic-tagged question bank, head to board pearls dot com. You'll find the rest of the series on Apple Podcasts, Spotify, or wherever you listen to podcasts. That brings us to the end of episode two of two of chapter twelve, and I'll see you in the next one.