Gastrointestinal

Chronic condition in which retrograde flow of stomach contents causes irritation of the esophageal lining. Main mechanism is due to transient relaxations of the LES. Risk factors: - Increased intra-abdominal pressure (obesity, pregnancy)- Sliding hiatal hernia- CNS depressants- Smoking, alcohol, caffeine- Associated with asthma Presentsation:- Heartburn (exacerbation when lying down)- Belching, regurgitation- Dysphagia.- Chronic nonproductive cough, hoarseness (laryngopharyngeal reflux) - Macroscopic: mucosal erythema/edema, erosions/ulcerations in severe cases- Histology: basal zone hyperplasia, elongation of the lamina propria papillae, scattered eosinophils and neutrophils Treatment: PPIs Complications:- Gastrointestinal bleeding (esophageal ulceration, hematesis, melena)- Esophageal adenocardinoma (Barrett's esophagus)- Difficulty with swallowing (esophageal stricture)

Autoimmune distruction of the parietal cells found predominantly in the upper glandular layer of the gastric body and fundus.→ Achlorhydria → hypergastrinemia→ Lack of intrinsic factor → vitamin B12 deficiency → pernicious anaemiaAutoantibodies against intrinsic factor → " Histology: CD4-predominate inflammatory infiltrate, oxyntic gland atrophy, intestinal metaplasia.

- a small amount of unconjugated bilirubin is present as an albumin-free anion in plasma. This fraction may in increase in severe hemolytic disease of the newborn (erythroblastosis fetalis) and may diffuse into the brain of infants - the accumulation of unconjucated bilirubin in the brain can cause severe neurologic damage

Hepatic conjugating enzyme UGT1A1 catalyzes the glucuronidation of bilirubin. Hereditary unconjugated hyperbilirubinemias:- Crigler-Najjar syndrome: complete UGT1A1 deficiency, fatal- Gilbert syndrome: some activity Hereditary conjugated hyperbilirubinemia- Dubin-Johnson syndrome- Rotor syndrome - All are autosomal recessive

Characterized by intestinal metaplasia – replacement of nonkeratinized stratified squamous epithelium with intestinal epithelium (nonciliated columnar with goblet cells) in distal esophagus. - Due to gastroesophageal reflux disease (GERD). - Most common in white males between 40-60 years of age. - The physiological transformation zone ("Z-line") between squamous and columnar epithelium is shifted upwards. - ↑ risk of esophageal adenocarcinoma.

Squamous cell carcinoma- Risk factors: Alcohol, smoking, diet low in fruits/vegetables, hot liquids, caustic strictures, achalasia- Upper 2/3 Adenocarcinoma- Risk factors: GERD, Barrett esophagus, obesity, smoking, achalasia- Lower 1/3 and may invade the gastric cardia Symptoms:- Dysphagia with possible odynophagia (pain swallowing)- Weight loss

Autosomal dominant disorder in which patients develop thousands of polyps as teenagers.- Pancolonic, always involves rectum - Mutation of the adenomatous polyposis coli (APC) tumor suppressor gene on chromosome 5q21. 2-hit hypothesis. - Prophylactic colectomy or else 100% progress to CRC. Variants:- Gardner syndrome- Turcot syndrome

= Lynch syndromeAutosomal dominant mutation in mismatch repair genes (MHL1, MSH2, MSH6, PMS2) with subsequent microsatellite instability. ~80% progress to CRC - Proximal colon always involved (right side).- Associated with endometrial, ovarian, and skin cancers. Diagnostics:- Identification via Amsterdam II criteria.- Genetic testing: Immunohistochemistry testing (detects microsatellite instabilities); confirm with DNA sequencing

Esophageal atresia with distal tracheoesophageal fistula is the most common (85%).- Often presents as polyhydramnios in utero (due to inability of fetus to swallow amniotic fluid). - Drooling, choking, foaming, and vomiting with first feeding. - Cyanosis is 2° to laryngospasm (to avoid reflux-related aspiration). Clinical test: failure to pass nasogastric tube into stomach. CXR: Air-filled stomach situated at the level of the 3rd thoracic vertebra

Protrusion of peritoneum through an opening, usually at a site of weakness. Contents may be at risk for incarceration (not reducible back into abdomen/pelvis) and strangulation (ischemia and necrosis). Complicated hernias can present with tenderness, erythema, fever. Diaphragmatic hernia- May occur due to congenital defect of pleuroperitoneal membrane or from trauma.- Hiatal hernia – stomach herniates upward through the esophageal hiatus of the diaphragm- Sliding hiatal hernia – gastroesophageal junction is displaced upward as gastric cardia slides into hiatus; "hourglass stomach". Most common type.- Paraesophageal hiatal hernia – gastroesophageal junction is usually normal but gastric fundus protrudes into the throax. Indirect inguinal hernia- Goes through the internal (deep) inguinal ring lateral to inferior epigastric arteries, external (superficial) inguinal ring, and into the scrotum. - Follows the path of descent of the testes; covered by all 3 layers of spermatic fascia.- Caused by failure of processus vaginalis to close (can form hydrocele).- May be notices in infants or discovered in adulthood. Much more common in males. Direct inguinal hernia- Protrudes through the inguinal (Hesselbach) triangle.- Bulges directly through parietal peritoneum medial to inferior epigastric artery but lateral to the rectus abdominis.- Goes through the external (superficial) inguinal ring only.- Covered by external spermatic fascia.- Usually in older men due to an acquired weakness in the transversalis fascia. Femoral hernia- Protrudes below inguinal ligament through femoral canal below and lateral to pubic tubercle.- Most common in females, but overall inguinal hernias are the most common.- More likely to present with incarceration or strangulation than inguinal hernias.

Failure of LES to relax due to loss of myenteric (Auerbach) plexus due to loss of postganglionic inhibitory neurons (which contain NO and VIP). - 2° achalasia (pseudoachalasia) may arise from Chagas disease (T cruzi infection) or extraesophageal malignancies (mass effect or paraneoplastic). Diagnosis: All patients should initially undergo upper endoscopy and/or barium esophagram to rule out pseudoachalasia.- Barium swallow shows dilated esophagus with area of distal stenosis ("bird's beak").- Manometry is the confirmatory test. Findings include uncoordinated or absent peristalsis with high LES resting pressure → progressive dysphagia to solids and liquids (vs obstruction – solids only). - ↑ risk of esophageal squamous cell carcinoma

Gastritis featuring massive hyperplasia of gastric mucosa → hypertrophied rugae (look like brain gyri). - Causes excess mucus production with resultant protein loss and parietal cell atrophy with ↓ acid production. Presentation:- Epigastric pain- Anorexia- Weight loss- Vomiting- Edema (due to protein loss) - Precancerous.

Recurrent abdominal pain associated with >2 of the following- Related to defecation- Change in stool frequency- Change in form (consistency) of stool - No structural abnormalities.- Most common in middle-aged women. - Chronic symptoms may be diarrhea-predominant, constipation-predominant, or mixed. Pathophysiology is multifaceted. First-line treatment is lifestyle modification and dietary changes. 

Acute inflammation of the appendix due to obstruction by fecalith (adults) or lymphoid hyperplasia (children). - Initial diffuse periumbilical pain migrates to McBurney point (1/3 the distance from right anterior superior iliac spine to umbilicus) - Nausea, fever, vomiting, anorexia, may perforate → peritonitis- May elicit psoas, obturator and Rovsing signs (referred pain from LLQ to RLQ), guarding and rebound tenderness. - Visceral abdominal (dull, non-localized) pain is most often due to luminal distension and stretching of smooth muscles and is carried by general visceral afferent fibers of the autonomic nervous system. - Somatic (severe, well-localized) pain is usually due to irritation of the parietal peritoneum and is worsened with deep inspiration or pushing on the abdominal wall. Differential: diverticulitis (elderly), ectopic pregnancy (use β-hCG to rule out), pseudoappendicitis.

Diverticulum: Blind pouch protruding from the alimentary tract that communicates with the lumen of the gut. Most diverticula (esophagus, stomach, duodenum, colon) are acquired and termed "false diverticula".- "True" diverticulum – all 3 gut wall layers outpouch (eg, Meckel)- "False" diverticulum – only mucosa and submucosa outpouch. Occur especially where vasa recta perforate muscularis externa. Diverticulosis: Many false diverticula of the colon, commonly sigmoid. Common (in ~50% of people >60 years). Caused by ↑ intraluminal pressure and focal weakness in colonic wall. Associated with obesity and low-fiber/high-fat/red meat diets.- Often asympatomatic or associated with vague discomfort.- Complications include diverticular bleeding (painless hematochezia), diverticulitis. Diverticulitis: Inflammation of diverticula with wall thickening, classically causing LLQ pain, fever, leukocytosis. Treat with antibiotics.- Complications: abscess, fistula (colovesical fistula → pneumaturia), obstruction (inflammatory stenosis), perforation (→ peritonitis).

Most common cause of gastric outlet obstruction in infants (1:600).  - Palpable "olive" mass in epigastric region, visible peristaltic waves, and nonbilious projectile vomiting at ~2-6 weeks old.- "Hungry vomiter": Demands food after vomiting, strong rooting and sucking reflex. - More common in firstborn males- Associated with exposure to macrolides, exposure to nicotine, bottle feeding- Results in hypokalemic hypochloremic metabolic alkalosis (2° to vomiting of gastric acid and subsequent volume contraction) - Ultrasound shows thickened and lengthened pylorus. Treatment: surgical incision (pyloromyotomy)

Persistence of the vitelline (omphalomesenteric) duct (connects lumen to yolk sac). True diverticulum. "Rule of 2s":- Approximately 2% of the population- Within 2 feet (60 cm) of the ileocecal valve- Approximately 2 inches (5 cm) long- 2x in males- Symptomatic by the age of 2 - May contain ectopic acid-secreting gastric mucosa and/or pancreatic tissue. - Most common congenital anomaly of GI tract.- Can cause hematochezia/melena, RLQ pain, intussusception, volvulus, or obstruction near terminal ileum. Diagnosis: pertechnetate study for uptake by heterotopic gastric mucosa

Pharyngoesophageal false diverticulum. - Esophageal dysmotility causes herniation of mucosal tissue at Killian triangle between the thyropharyngeal and cricopharyngeal parts of the inferior pharyngeal constrictor. Symptoms:- Halitosis (bad breath)- Dysphagia- Obstruction- Gurgling- Aspiration- Neck mass

Congenital megacolon characterized by lack of ganglion cells/enteric nervous plexus (Auerbach's and Meissner's plexuses) in distal segment of colon. Due to failure of neural crest cell migration. Associated with mutations in RET. Presentation:- Bilious emesis, abdominal distension- Failure to pass the first stool (meconium) within 48 hours of delivery → chronic constipation- Dilated portion of the colon proximal to the aganglionic segment = "transition zone" - Risk ↑ with Down syndrome- Explosive expulsion of feces (squirt sign) → emtpy rectum on digital exam- Diagnosed by absence of ganglionic cells of rectal suction biopsy. Treatment: Resection

Etiology: Alcohol consumption (♂ >210 g per week; ♀ >140 g per week) Hepatic steatosis: Macrovesicular fatty change that may be reversible with alcohol cessation. Alcoholic hepatitis: Requires sustained, long-term consumption.- Swollen and necrotic hepatocytes with neutrophilic infiltration.- Mallory bodies (intracytoplasmic eosinophilic inclusions of damaged keratin filaments)- AST > ALT ratio usually >2:1  Alcoholic cirrhosis: Final and usually irreversible form.- Regenerative nodules surrounded by fibrous bands in response to chronic liver injury → portal hypertension and end-stage liver disease.- Sclerosis around central vein (area III) may be seen in early disease.

Thrombosis or compression of hepatic veins with centrilobular congestion and necrosis → congestive liver disease (hepatomegaly, ascites, abdominal pain, varices, abdominal pain, liver failure). Etiology:- Secondary to conditions with hypercoagulable states→ Polycythemia vera, postpartum state, clotting disorders- Secondary to invasion or compression of hepatic veins→ Hepatocellular carcinoma, renal carcinoma Presentation:- Absence of JVD.- Abdominal pain, tender hepatomegaly- Ascites, abdominal distension- Portocaval anastomoses- May cause nutmeg liver (mottled appearance) Diagnostics: Imaging with Doppler, CT/MRI with contrast

Autosomal recessive mutations in hepatocyte copper-transporting ATPase (ATP7B gene; chromosome 13) → ↓ copper incorporation into apoceruloplasmin and excretion into bile → ↓ serum ceruloplasmin. - Age of onset 5-35 years Presentation:- Liver disease (eg, HCC, hepatitis, cirrhosis)- Neurologic disease (eg, parkinsonism, tremor, dementia, dysarthria, dystonia, psychiatric disease)- Kayser-Fleischer rings (deposits in Descemet membrane of cornea)- Renal disease (eg, Fanconi syndrome) Diagnosis:- ↓ serum ceruloplasmin (degradation if not bound to copper)- ↑ free serum copper but ↓ total serum copper- ↑ urinary copper excretion- Coombs-negative hemolytic anemia Treatment: Chelation with penicillamine or trientine, oral zinc

- Autosomal recessive with incomplete penetrance.- C282Y > H63D mutation on HFE gene, located on chromosome 6; associated with HLA-A3. - Defective binding of transferrin to its receptor → liver stops producing hepcidin → unregulated ferroportin on basolateral surface of enterocytes causes ↑ intestinal absorption through DMT1 on lumen side (↑ ferritin, ↑ iron, ↓ TIBC → ↑ transferrin saturation).- Iron overload can be 2° to chronic transfusion therapy (eg, β-thalassemia major).  - Iron accumulates in liver, pancreas, skin, heart, pituitary, joints. - Hemosiderin (iron) can be identified on liver MRI or biopsy with Prussain blue stain. Presentation:- After age 40 (vs Wilson diseasse) when total body iron >20 g.- Iron loss through menstruation slows progression in women.- Fatigue, lethargy- Classic triad of cirrhosis, diabetes mellitus, skin pigmentation ("bronze diabetes").- Restrictive cardiomyopathy (classic) or dilated cardiomyopathy (reversible).- Hypogondism, erectile dysfunction, loss of libido, amenorrhea (due to pituitary/gonadal accumulation).- Arthropathy (calcium pyrophosphate deposition; typically MCP joints II and III)- HCC is common cause of death. Treatment: repeated phlebotomy, chelation with deferasirox, deferoxamine, oral deferiprone

Anomaly of the midgut rotation during fetal development → improper positioning of bowel (small bowel clumped on the right side), formation of fibrous bands (Ladd bands). - Can lead to volvulus, duodenal obstruction

At birth, immature UDP-glucuronosyltransferase → unconjugated hyperbilirubinemia → jaundice/kernicterus (deposition of unconjugated, lipid-soluble bilirubin in brain, particularly basal ganglia). - Occurs after first 24 hours of life and usually resolves without treatment in 1-2 weeks. - Peak total serum bilirubin <15 mg/dL- Daily rise in bilirubin levels <5 mg/dL/day Treatment: Phototherapy (non-UV) isomerizes unconjugated bilirubin to water-soluble form.

Mildly ↓ UDP-glucuronosyltransferase conjugation and impaired bilirubin uptake.- Most commonly inherited hyperbilirubinemia.- Prevalence 3-7% in the US. - Asymptomatic or mild jaundice usually with stress, illness, or fasting. - ↑ unconjugated bilirubin without overt hemolysis. No treatment required.

Absent UDP-glucuronosyltransferase.- Presents early in life, patients die within a few years. Findings: - Excessive, persistent neonatal jaundice- Neurological symptoms caused by kernicterus (bilirubin deposition in brain) - ↑ unconjugated bilirubin (20-50 mg/dL) Treatment: - Plasmapheresis (unconjugated bilirubin is bound to albumin, which is removed)- Phototherapy (renders unconjugated bilirubin water-soluble)- Liver transplant is curative. Type II is less severe and responds to phenobarbital, which ↑ liver enzyme synthesis.

Defective MRP2 receptor → Impaired excretion of conjugated bilirubin into the bile canaliculi.- Benign. - Onset occurs during adolescence.- Mild-to-moderate jaundice.- May worsen because of medications (particularly contraceptives) or pregnancy.- Grossly black liver due to impaired excretion of epinephrin metabolites that accumulate within lysosomes. (Rotor syndrom is similar, but milder in presentation without black liver. Due to impaired hepatic uptake and excretion.)

- Hirschsprung's disease - Chagas disease - obstruction (neoplasm, inflammatory stricture) - toxic - visceral myopathy

- brain trauma --> elevated intracranial pressure  --> increased vagal stimulation --> ulcers in esophagus, stomach, duodenum

- complication of severe burns/trauma - reduced plasma volume leads to ischemia of the gastric mucosa/duodenal ulcer

Acute upper gastrointestinal bleeding caused by partial-thickness mucosal lacerations at gastroesophageal junction due to severe vomiting. Etiology:- Severe vomiting- Usually found in alcoholics and bulimics Presentation:- Hematemesis- Epigastric or back pain

Autosomal dominant syndrome featuring numerous hamartomas throughout GI tract, along with mucocutaneous hyperpigmentions (eg, mouth, lips, hands, genitalia). - Associated with ↑ risk of breast and GI cancers (eg, colorectal, stomach, small bowel, pancreatic).   - Enteroscopy: <20 polyps, primarily jejunum

- FAP + osseous and soft tissue tumors (eg, osteomas, desmoid tumors, sebaceous cysts, lipomas, fibromas) - Congenital hypertrophy of retinal pigment epithelium - Impacted/supernumerary teeth

FAP/Lynch syndrome + malignant CNS tumor (eg, medulloblastoma, glioma)

Autosomal dominant syndrome in children (typically < 5 years) with incomplete penetrance. - Numerous hamartomatous polyps in the colon, stomach, small bowel. - Associated with ↑ risk of CRC

Progressive chronic inflammation of the intra- and extrahepatic bile ducts.- Classically in middle-aged men with IBD. Features:- Signs of cholestasis: jaundice, pruritus, fatigue, acute cholangitis- Later signs of cirrhosis: portal hypertension, splenomegaly, liver failure Imaging: MRCP, ERCP- Concentric "onion skin" bile duct fibrosis → alternating strictures and dilation with "beading" of intra- and extrahepatic bile ducts  - Associated with ulcerative colitis - p-ANCA ⊕- ↑ IgM- ↑ risk of cholangiocarcinoma and gallbladder cancer

Chronic progressive liver disease of autoimmune origin → lymphocytic infiltrate + granulomas → destruction of intralobular bile ducts. - Classically in middle-aged women.- Most common cause of vanishing bile duct syndrome. Presentation:- Fatigue (usually the first symptom)- Pruritus- Hepatomegaly- Jaundice- Maldigestion- Xanthelomas - Anti-mitochondrial antibody (AMA) ⊕, ANA ⊕- ↑ IgM- Associated with other autoimmune conditions (eg, Sjögren syndrome, Hashimoto thyroiditis, CREST, rheumatoid arthritis, celiac disease)

Intestinal hypomobility without obstruction → constipation and ↓ flatus. - Distended/tympanic abdomen with ↓ bowel sounds. Associated with:- abdominal surgeries- opiates- hypokalemia- sepsis Treatment: bowel rest, electrolyte correction, cholinergic drugs (stimulate intestinal motility)

- Mainly occurs in adults >60 years- Young people with atrial fibrillation, vasculitis, or hypercoagulable states Etiology:- Embolic occlusion of SMA (~50%): generally resulting from atrial fibrillation, MI, endocarditis- Arterial thrombosis (~25%): due to preexisting visceral atherosclerosis, arteritis, aortic aneurysm, dissection- Venous thrombosis Sudden interruption of blood flow → hemorrhagic infarction and small bowel necrosis- SMA most commonly affected (distal duodenum until splenic flexure) Presentation:- Periumbilical pain that is out of proportion to clinical findings- Nausea and vomiting- May see red "current jelly" stools (DD intussusception) Diagnosis: CT angiography

"Intestinal angina": atherosclerosis of celiac artery, SMA, or IMA → intestinal hypoperfusion → postprandial epigastric pain → food aversion and weight loss. - Abdominal bruit caused by stenosis of mesenteric arteries - Thumbprintin is the pathognomonic radiographic finding.

Gastric ulcer- Pain increases with meals → weight loss- 70% H pylori infection- Mechanism: ↓ mucosal protection, NSAIDs- ↑ risk of carcinoma- Biopsy margins to rule out malignancy (especially intestinal gastric carcinoma) Duodenal ulcer:- Pain decreases with meals → weight gain- 90% H pylori infection- Mechanism: ↓ mucosal protection, ↑ gastric acid secretion, Zollinger-Ellison syndrom- Generally benign- Hypertrophy of Brunner glands

Most commonly benign and in parotid gland. Tumors in smaller glands more likely malignant. - Typically present as painless mass/swelling. Facial pain or paralysis suggests malignant involvement of CN VII. Pleomorphic adenoma (benign mixed tumor) – most common salivary gland tumor. Composed of chondromyxoid stroma and epithelium and recurs if incompletely excised or ruptured intraoperatively. May undergo malignant transformation. Warthin tumor (papillary cystadenoma lymphomatosum) – benign cystic tumor with germinal centers. Typically found in smokers. Bilateral in 10%; multifocal in 10%. Mucoepidermoid carcinoma – most common malignant tumor, has mucinous and squamous components.

Infiltration of eosinophils in the esophagus often in atopic patients (eg, asthma, allergic rhinitis).  - Food allergens → dysphagia, food impaction. - Esophageal rings and linear furrows often seen on endoscopy. - Unresponsive to GERD therapy.

Triad of dysphagia, iron deficiency anemia, and esophageal webs. - May be associated with glossitis. - Increased risk of esophageal squamous cell carcinoma.

Transmural esophageal rupture with pneumomediastinum.- In >90% of cases, the rupture occurs in the distal third of the esophagus on the left dorsolateral wall surface. Etiology: Excessive intake of alcohol in the past, repeated episodes of vomiting, childbirth, seizures, prolonged coughing, endoscopy. Presentation:- Vomiting and/or retching- Severe retrosternal pain- Subcutaneous emphysema may be due to dissecting air (creptitus may be felt in the neck region or chest wall). Diagnostics:- CXR: Widened mediastinum, pneumomediastinum- Contrast esophogram with gastrografin (barium not indicated because inflammatory) - Surgical emergency

Acute gastritisErosions can be caused by:- NSAIDs – ↓ PGE2 → ↓ gastric mucosa protection- Burns (Curling ulcer) – hypovolemia → mucosal ischemia- Brain injury (Cushing ulcer) – ↑ vagal stimulation → ↑ ACh → ↑ H+ production- Especially common among alcoholics and patients taking daily NSAIDs (eg, patients with rheumatoid arthritis). Chronic gastritis- Mucosal inflammation, often leading to atrophy (hypochlorhydria → hypergastrinemia) and intestinal G-cell metaplasia (↑ risk of gastric cancers).- H pylori: Most common. ↑ risk of peptic ulcer disease, MALT lymphoma. Affects antrum first and spreads to body of stomach.- Autoimmune: Autoantibodies to parietal cells and intrinsic factor. ↑ risk of pernicious anemia. Affects body/fundus of stomach.

Most commonly gastric adenocarcinoma; lymphoma, GI stromal tumor, carcinoid. - Early aggressive local spread with node/liver metastases. - Often presents late, with weight loss, abdominal pain, early satiety, and in some cases acanthosis nigricans or Leser-Trélat sign.- Associated with blood type A. Intestinal-type adenocarcinomas:- Associated with H pylori, dietary nitrosamines (smoked foods), smoking, achlorhydria, chronic gastritis. - Grow as nodular, polypod, and well-demarcated masses that rapidly expand within the gastric lumen.- Commonly on lesser curvature- Often ulcerate/bleed, look like ulcer with raised margins Diffuse:- Not associated with H pylori- Signet ring cells (mucin-filled cells with peripheral nuclei)- Plaquelike appearance, ill-defined, infiltrate large areas of the stomach wall- Stomach wall grossly thickened and leathery (linitis plastica) Virchow node – involvement of left supraventricular node by metastasis from stomach.Kruckenberg tumor – bilateral metastases to ovaries. Abundant mucin-secreting, signet ring cells.Sister Mary Joseph nodule – subcutaneous periumbilical metastasis.

Hemorrhage: - Gastric, duodenal (posterior > anterior).- Most common complication.- Ruptured gastric ulcer on the lesser curvature of stomach → bleeding from left gastric artery.- An ulcer on the posterior wall of duodenum → bleeding from gastroduodenal artery. Perforation: - Sudden onset of intense, stabbing pain, followed by diffuse abdominal pain (beginning peritonitis)- Duodenal (anterior > posterior)- May see free air under diaphragm with referred pain to the shoulder via irritation of phrenic nerve. Obstruction: Pyloric channel, duodenal- Postprandial, nonbilious vomiting, succession splash

Lactase deficiency resulting in incomplete hydrolysis of lactose into glucose and galactose. The fermentation of undigested lactose by gut bacterial leads to increased production of short-chain fatty acids (eg, acetate, butyrate, propionate) that acidify the stool. - Normal appearing villi, except when 2° to injury at tips of villi (eg, viral enteritis). - Osmotic diarrhea with ↓ stool pH (colonic bacteria ferment lactose). - Lactose hydrogen breath test: ⊕ for lactose malabsorption if post-lactose breath hydrogen rises >20 ppm compared with baseline.