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159 Cards in this Set
- Front
- Back
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Congenital diaphragmatic hernia
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Left lung hypoplasia, herniation of stomach and spleen into thorax.||Failure of pleuroperitoneal fold fusion.|
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Gastrochisis
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Failure of lateral body folds to fuse; extrusion of abdominal contents through abdominal folds. Not covered by peritoneum.|||
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Omphalocele
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Persistence of herniation of abdominal contents into umbilical cord, covered by PERTIONEUM.|||
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Tracheoesophageal fistula
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Most common subtype is blind upper esophagus with lower esophagus connected to trachea. Results in cyanosis, choking and vomiting with feeding, and polyhydramnios.|Air in the stomach coming from the trachea.||
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Congenital pyloric stenosis
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Hypertrophy of the pylorus causes obstruction. Palpable "olive" mass in epigsatric region and nonbilious projectile vomiting at ~2 weeks of age. Empties liquids not solids.|Hypocholemic metabolic alkalosis.|1/600 live births; first born males.|Surgical incision.
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Damage to falciform ligament
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Damages ligamentum teres (fetal umbilical veins)||Connects liver to anterior abdominal wall.|
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Damage to hepatoduodenal ligmaent
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Damages the portal triad (hepatic artery, portal vein, common bile duct).||Connects liver to duodenum; greater and lesser sacs.|
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Damage to gastrohepatic ligament
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Damages gastric arteries.||Connects liver to lesser curvature of stomach; seperates right greater and lesser sacs.|
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Damage to gastrocolic ligament
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Damages gastroepiploic arteries.||Connects greater curvature and transverse colon.|
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Damage to gastrosplenic ligament
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Damages short gastric arteries.||Connects greater curvature nad spleen.|
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Damage to spenorenal ligament
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Damages splenic artery and vein.||Connects spleen to posterior abdominal wall.|
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Periportal hepatitis
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Viral hepatitis|||
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Centrilobular hepatitis
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Affected first by ischemia, has P-450 system, more sensitive to toxic injury and alcoholic hepatitis.|||
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Sliding hiatal hernia
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|"Hourglass stomach." |Most common diaphragmatic hernia. GE junction is dipslaced. Abdominal structures enter thorax. Due to defect in pleuroperitoneal membrane.|
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Paraesophageal diaphragmatic hernia
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Hypoplastic left lung.|Bowl sounds in thorax.|GE junction is normal; stomach cardia (near esophagus) moves into thorax.|
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Indirect inguinal hernia
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Occurs in infants due to patent processus vaginalis. May result in hydrocele. More common in males.|Herniated gut is covered in all 3 layers of spermatic fascia.|Herniation throug hinternal (deep) inguinal ring, external (superficial) inguinal ring, and into the scrotum. Later to inferior epigastric artery.|
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Direct inguinal hernia
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Usually in older men.|Herniated gut is only covered by external spermatic fascia.|Herniation through the inguinal triangle. Medial to the inferior epigastric artery. Goes through only the external (superficial) inguinal ring.|
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Femoral hernia
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More common in women. Leading cause of bowel incarceration.||Hernaition below the inguinal ligament through the femoral canal; lateral to pubic tubercle.|
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Warthin's tumor
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Benign parotid tumor; hetertropic salivary tissue trapped in a lymph node, or surrounded by lymphatic tissue.|||
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Pleomorphic salivary adenoma
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Most common parotid tumor, MOBILE, painless (no nerve invasion, and benign with high rate of recurrence due to irregular margins (hard to completely remove surgically).|||
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Mucoepidermoid carcinoma
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Most common malignant tumor of parotid gland. Will present with pain due to facial nerve invasion.|||
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Globus sensation
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Globus hystericus or globus pharyngis; feeling of having a "lump" in one's throat without clinical or radiographic evidence, often triggered by strong emotion (benign).|||
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Achalasia
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Failure of relaxation of the LES due to loss of myenteric (Auerbach's) plexus. Uncoordinated peristalsis leading to progressive dysphagia (firist solids, later liquids).|High LES opening pressure. Barium swallow shows dilated esophagus with an area of distal stenosis. "Bird's beak" sign.|Associated with increase risk of esophageal squamosu cell carcinoma. Secondary achalasia may arise from Chagas' disease. Scleroderma has esophageal dysmotility with pressure proximal to LES.|
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Gastroesophageal reflux disease
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Heart burn and regurgitation upon lying down. May also present with noctural cough and dyspnea. ADULT ONSET ASTHMA|Esosinophilia.|Leads to Barrett's esophagus (columnar metaplasia).|
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Esophageal varices
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Massive hematemesis of submucosal veins of lower 1/3rd of esophagus. Worse prognosis and more bleeding than Mallory-Weiss syndrome.||History of alcoholism; portal hypertension. Due to flow via left gastric vein.|Balloon tamponade.
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Mallory-Weiss syndrome
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Mucosal lacerations at the gastroesophageal junction due to severe vomiting. Leads to PAINFUL hematemesis (vs painless = esophageal varices). Found in alcoholics and bulimics.|||
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Boerhaave syndroem
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Transmural esophageal rupture due to violent retching.|||
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Esophageal strictures
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Associated with lye (sodium hydroxide) and acid reflux.|||
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Esophagitis
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Associated with GERD, infection (HSV-1: punched-out ulcers; CMV: linear ulcers; Candida: white speudomembrane), or chemical ingestion (radiation).|Must see eosinophils on biopsy for reflux esophagitis.|Leads to Barrett's esophagus (columnar metaplasia).|
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Plummer-Vinson syndrome
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Female with triad of dysphagia (due to esophageal webs), glossitis, iron deficiency anemia.||Increased incidence of squamous cell carcinoma of esophagus.|
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Barrett's esophagus
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||Glandular metaplasia; replacement of stratified squamous epithelium with columnar epithelium in distal esophagus. Due to GERD. Associated with esophagitis, ulcers, and increased risk of esophageal adenocarcinoma.|
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Esophageal adenocarcinoma
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Lower 1/3rd of the esophagus.||Requires Barrett's esophagus metaplasia. Due to esophageal web/esophagitis, Zenker's diverticula. Usually white male.|
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Esophageal squamous cell carcinoma
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Upper 2/3rds of the esophagus. (usually mid)||Due to alcohol, achalasia, cigarettes/tobacco, prior lye (sodium hydroxide) ingestion. Usually African-American.|
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Celiac sprue
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Diarrhea, steatorrhea, weight loss, weakness, dermatitis herpetiformis (vesicular lesions on elbows). Commonly seen in patients on a high fiber diet for first time.|HLA-B8, DR, and DQ. IgA antibodies to gliadin and tissue tansglutaminase. Blunting of villi, lymphocytes in lamina propria, crypt hyperplasia. Screen by serum transglutaminase Ab.|Affects proximal small bowel. Autoimmune mediated hypersensitivity to gliadin leading to steatorrhea. Decreased absorption in jejunum. Moderate increase of T-cell lymphoma risk. |
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Tropical sprue
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Diarrhea, steatorrhea, weigth loss, weakness. |Blunting of villi, crypt hyperplasia.|Due to bacterial overgrowth. Can affect entire small bowel.|Antibiotics.
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Whipple's disease
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Diarrhea, arthralgias, cardiac and neurological (altered mental status, peripheral neuropathy)symptoms. Occurs in older men.|PAS-positive macrophages in intestinal lamina propia, mesenteric nodes.|Infection with Tropheryma whippeli (gram positive).|Antibiotics.
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Lactase deficiency
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Osmotic diarrhea. Self-limited lactase deficiency following injury (e.g. viral gastroentritis).|Normal-appearing villi. Absence of blood glucose elevation with administration indicates deficiency. ||
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Pancreatic insufficiency
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Malabsorption of fat and fat-soluble vitamins (ADEK).|Increase neutral fat in stool.|Due to CF, obstructing cancer, and chronic pancreatitis.|
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Abeta-lipoproteinemia
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Presents in early childhood with malabsorption and neurological manifestations.|Fat accumulation in enterocytes.|Decreased synthesis of apo B; inability to generate chylomycrions. Low blood cholesterol, VLDL.|
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Acute gastritis
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Erosive gastritis.|PMNs.|Disruption of mucosal barrier leads to inflammation. Can be caused by physiological stress, ***NSAIDS (decreased PGE2), alcohol, uremia, burns (Curling's ulcer), and brain injury (Cushing's ulcer).|
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Curling's ulcer
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Burn resulting in acute erosive gasttritis.||Low plasma volume leads to sloughing of gastric mucosa.|
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Cushing's ulcer
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Brain injury resulting in acute erosive gastritis.|Elevated ICP.|Increased vagal stimulation leads to elevated ACh and higher H+ production.|
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Chronic gastritis type A
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Nonerosive gastritis of the fundus/body.|Lymphocytes, plasma cells, macrophages. Hypochlorhydria.|Due to autoimmune disorders characterized by autoantibodies to parietal cells, pernicious anemia, and achlorhydria. Increased risk of gastric adenocarcinoma.|
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Chronic gastritis type B
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Nonerosive gastritis of the antrum.|Chronic "active" gastritis; PMNs present.|Most common type; due to H. hyplori infection. Increased risk of MALToma and gastric adenocarcinoma.|
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Ménétrier's disease
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Protein losing enteropathy (peripheral edema) and diarrhea.|Cerebriform appearance of rugae.|Gastric hypertrophy with protein loss, parietal cell atrophy, and increased mucous cells. Precancerous. Rugae of stomach are so hypertrophied that they look like brain gyri.|
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Gastric adenocarcinoma intestinal type
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Often presents with acanthosis nigricans. Early satiety (due to mass in the stomach). Weight loss and anorexia.|Resembles colonic adenocarcimona with malignant ulcers on lesser curvature of the stomach (heaped, irregular borders with necrotic base). |Liver and nodal metastasis. Due to nitrosamines (smoked food), pickled vegetables, achlorhydria, chronic gastritis, type A blood. |
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Gastric adenocarcinoma diffuse type
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Often presents with acanthosis nigricans. Weight loss and anorexia. Krukenberg's tumor on metastasis.|Signet ring cells; grossly thickened and leathery stomach (linitis plastica).||
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Sign of Leser-Trelat
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Sudden appearance of multipe seborrheic keratosis indicating an underlying malignancy (GI especially gastric adenocarcinoma or lymphoid).|||
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Virchow's node
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Nontender enlarged left supraclavicular lymph node.||Sign of gastric adenocarcinoma metastasis.|
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Sister Mary Joseph's nodule
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Subcutaneous periumbilical metastasis.||Sign of gastric adenocarcinoma metastasis.|
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Krukenberg's tumor
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Bilateral metastasis to ovaries. Abundant mucus, signet ring cells.||Diffuse type gastric adenocarcinoma metastasis.|
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Gastric ulcer
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Pain GREATER with meals. Weight loss. Older patients. Risk of hemorrage (posterior>anterior). Most common cause of upper GI bleeds.|Positive urease breath test. Goes down to the muscular layer (irreversible unlike stress ulcers). Well defined ulcer borders and radiating folds (vs carcinoma).|70% caused by H. pylori infection. Chronic NSAID use also implicated. Due to decreased mucosal protection against gastric acid. Increased risk of gastric carcinoma.|PPI, clarithromycin, and amoxicillin (or metronidazole).
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Duodenal ulcer
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Pain DECREASES with meals. Weight gain. Risk of hemorrhage (posterior > anterior) and perforation ( anterior > posterior).|Hypertrophy of Brunner's glands. Clean, "punched-out" margins unlike raised/irregular margins of carcinoma. No increased risk of carcinoma.|100% caused by H.pylori infection. Due to elevated gastric acid secretion (Zollinger-Ellison sndrome) or decreased mucosal protection. Associated with blood group O. More common than gastric ulcers.|PPI, clarithromycin, and amoxicillin (or metronidazole).
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Crohn's disease
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Mucoid diarrhea. Migratory polyarthritis, erythema nodosum, immunologic disorders, kidney stones. May also have strictures, perianal fistulas and fissures, malabsorption and nutritional depletion (B12).|Transmural inflammation. COBBELSTONE MUCOSA (linear ulcers), creeping fat, bowel wall thickening. String sign. Noncaseating granulomas and lymphoid aggregates (TH1).|Disorder response to intestinal bacteria. Affects terminal ileum and colon but can occur anywhere in the GI tract. Skip lesion, rectal sparing. Increased risk of colorectal cancer.|Corticosteroids, infliximab.
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Ulcerative colitis
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Blood diarrhea. Malnutrition, toxic megacolon, colorectal carcinoma (worse with right-sided or pancolitis). Assocaited with pyoderma gangrenosum, ankylosing spondylitis, uveitis, primary sclerosing cholangitis.|Mucosal and submucosal inflammation only. Friable mucosal pseudopolyps with freely hanging mesentary. Loss of haustra; "lead pipe" appearance on imaging. NO GRANULOMAS!|Autoimmune (HLA-B27). Continuous colonic lesions, always with rectal involvement. |Sulfasalazine, 6-mercaptopurine, infliximab, colectomy.
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Irritable bowel syndrome
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Recurrent abdominal pain asosciated with paint hat improves with defection, change in stool frequency, change in apperance of stool. May present with diarrhea, constipation, or alternating.|No structural abnormalites. Chronic symptoms.|Generally caused by stress (or infection).|Treat symptoms.
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Appendicitis
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All age groups. Initial difuse periumbilical pain (T10) that localized at McBurney's point (1/3rd distance from ASIS to ubilicus). Nausea, fever; may perforate and cause pertionitis.|Must see PMNs in the muscularis mucosa.|In kids: lymphoid hyperpalsia after viral infection, enterobius vermicularis. Adults: obstruction, fecalith. |
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Diverticulum
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Blind pouch protruding from alimentary tract that communicates with the lumen of the gut. Most often in signmoid colon.|True has all 3 gut wall layers (Meckel's); false have only mucosa and submucosa. |Most diverticula (esophagus, stomach, duodenum colon) are acquired and termed "false" in that they lack or have an attenuated muscularis externa. Occurs especially where vasa recta perforate muscularis externa.|
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Colonic diverticulosis
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Many false diverticula. Common (>50%) in 60+ years of age. Often asymptomatic or assoocitaed with vague discomfort and/or painless rectal bleeding.||Caused by increased intraluminal pressure and focal wekaness in colonic wall. Assocaited with low-fiber diet. Most common in sigmoid colon.|
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Diverticulitis
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Elderly. Inflammation of diverticula cuasing LLQ pain, fever, leukocytosis. May perforate and cause peritonitis, abscess formation, or bowel stenosis. May cause bright red rectal bleeding. May also cause colovesical fistula => pneumaturia.||"Left-sided appendicitis."|Antibiotics.
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Zenker's diverticulum
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False diverticulum. Herniation of mucosal tissue at junction of pharynx and esophagus. Presneting symptoms are halitosis, dysphagia, obstruction.|Only mucosa and submucosa.||
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Meckel's diverticulum
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True diverticulum. Causes melena, RLQ pain, intussusception, volvulus, or obstruction near the terminal ileum.|Ectopic acid-secreitng gastric mucosa and/or pancreatic tissue. 2 inchs long, 2 feet from ileocecal valve, 2% of the population, first 2 years of life, 2 types of epithelia. Dx by pertechnetate study ectopic uptake.|Persistence of the vitelline duct or yolk stalk. Most common congenital anomaly of the GI tract.|
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Omphalomesenteric cyst
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Cystic dilation of vitelline duct.|||
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Intussusception
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Compromises blood supply. Repeated episodes of a child doubling over in pain with every migrating motor complex.|Currant jelly stools.|Unusual in adults (associated with intraluminal mass or tumor). Majority of causes occur in children (usually idoipathic; may be adenovirus). "Telescoping" of 1 bowel segment into distal segment, commonly at ileocecal junction. |
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Iatrogenic volvulus
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Presents with ostipation (not moving any food contents and can't pass gas). Occurs in small bowel.|Step ladder or staircase appearance.|Generally during surgery.|
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Sigmoid volvulus
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Twisting of portion of bowel around its mesentary. Can lead to obstruction and infarction. May ooccur at cecum and sigmoid colon where there is redundant mesentery. Usually in elderly.|Step ladder or staircase appearance.||
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Duodenal atresia
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Early bilious vomiting in an infant with proxmial stomach distention.|Double-bubble sign on x-ray.| |
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Meconium ileus
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Meconium plug obstructs intestine, preventing stool passage at birth.||Associated with cystic fibrosis.|
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Necrotizing enterocolitis
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Necrosis of GI mucosa and possible perforation. Colon usually involved but can involve entire GI tract.||Associated with prematurity (weak immune system).|
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Ischemic colitis
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Pain 30-40 minutes after eating (doesn't respond to antacids) and weight loss; bloody stools. Typically affects elderly.|Transmural infarction.| Commonly at splenic flexure and distal colon. History of MI, atrial fibrillation, and atherosclerosis.|Bowel ressection.
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Post operative adhesion
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Acute bowel obstruction, commonly from a recent surgery. Can have well-demarcated necrotic zones and fibrous bands.||Most common cause of small bowel obstruction.|
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Angiodysplasia
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Tortuous dilation of vessels leading to right sided colon bleeding in elderly patient. |Confirmed by angiography.|More often found in cecum, terminal ileum, and ascending colon.|
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Hyperplastic colonic polyps
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Most common non-neoplastic polyp in colon (>50% in rectosigmoid colon);.|||
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Juvenile colonic polyps
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A child with a solitary rectal polyp that prolapses and bleeds.|||
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Juvenile polyposis syndrome
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Multiple juvenile polyps in stomach and colon, increase risk of adenocarcionma.|||
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Peutz-Jeghers syndrome
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Nonmalignant hamartomatous polyps throughout GI tract, hyperpigmented mouth, lips, hands, and genitalia.||Autosomal dominant. Assocaited with visceral malignancies (lung, pancreas, breast, uterus, colon). POLYPS ARE NOT CANCEROUS.|
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Familial adenomatous polyposis
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Thousands of polyps; pancolonic; always involve rectum.|Must have at least 100 to make a diagnosis.|Autosomal dominant mutation of APC gene on c5q. Two hit hypothesis. 100% progress to CRC in the 30s or earlier.|Total colectomy.
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Gardner's syndrome
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Familial adenomatous polyposis, osteomas and soft tissue tumors, retinal hyperplasia, epidermal inclusion cysts, fibromatosis, and impacted/supernumerary teeth.|Must have at least 100 to make a diagnosis.||
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Turcot's syndrome
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Familial adenomatous polyposis plus malingant CNS tumor (gliomas).|Must have at least 100 to make a diagnosis.||
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Colorectal cancer
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Rectosigmoidal > ascending > descending in frequency. Iron deficiency anemai in males (>50 years of age) and postmenopausal women raises suspicion. Screen patietns > 50 years of age with stool occult blood test and colonsocopy.|CEA tumor marker. "Apple core" lesion on barium enema x-ray. Ascending presents with exophytic mass, irony deficiency, and weight loss. Descending presents with infiltration mass, partial obstruction, colicky pain, hematochezia.|3rd most commona nd 3rd most deadly in US. Most patients are >50 years of age and 25% have family history. Increased risk by IBD, Streptococcus bovis bactremia, tobacco use, large villous adenomas, juvenile polyposis syndrome, Peutz-Jeghers syndrome.|
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Hereditary nonpolyposis colorectal cancer
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80% progression to CRC. Proximal colon always involved. Increased risk of endometrial and ovarian carcinoma.|Multiple areas of dysplastic mucosa.|Autosomal dominant mutation of DNA mismatch repair genes (microsatellite instability).|
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Carcinoid syndrome
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Recurrent diarrhea, salivation, cutaneous flushing of face, asthmatic wheezing/bronchospasms, telangiectasia. Right sided heart failure (sacral/pedal edema, nutmeg liver, elevated JVP).|5-hydroxyindoleatic acid (5-HIAA) in urine. "Defnese core bodies " on EM. Stain with synaptophysin, chromogranin.|Rare syndrome caused by carcinoid tumors (neuroendocrine/neural crest cells), especially metastatic small bowel tumors, which secrete high levels of serotonin (5-HT) . Not seen if tumor is limited to GI tract (5-HT undergoes first-pass metabolism in liver). Most common tumor of appendix and small bowel.|
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Moecular pathogensis of colorectal cancer
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||Two pathways. 1st is the microsatellite instability (15%); DNA mismatch repair gene mutations lead to sporadic and HNPCC syndrome Mutations oaccumulate, but no defined morphological correlaties. 2nd is the APC/beta-catenin (chromosomal instability) pathway (85%). Loss of APC gene (decreased intracellulr adhesion and increased proliferation) => K-RAS mutation (unregulated intracellular signal transduction, adenoma) => loss of p53 (carcinoma).|
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Portal hypertension
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Esophageal varices (hematemesis, melena), splenomegaly, caput medusae, ascites, portal hypertensive gastropathy, hemorrhoids.||Portosystemic shunts alleviate portal hypertension; esophageal varices, caput medusae, hemorrhoids.|
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Liver failure
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Coma, scleral icterus, fetor hepaticus (musty breath), spider nevi, gynectomastia, jaundice, testicular atrophy, asterixis, bleeding tendency (low clotting factors), anemia, pedal edema.|||
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Elevated AST and ALT
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Viral hepatitis (ALT>AST), alcoholic hepatitis (AST> ALT)|||
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Elevated GGT (gamma-glutamyl transpeptidase)
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Various liver diseases; increase with heavy alcohol consumption.|||
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Elevated alkaline phosphatase
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Obstructive liver disease (hepatocellular carcinoma), bone disease, bile duct disease.|||
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Elevated amylase
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Acute pancreatitis, mumps.|||
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Elevated lipase
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Acute pancreatitis.|||
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Micronodular cirrhosis
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Nodules < 3 mm, uniform size. Due to metabolic insult (e.g., alcohol, hemochromatosis, Wilson's disease).|||
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Macronodular cirrhosis
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Nodules > 3 mm, varied size. Usually due to significant liver injury leading to hepatic necrosis (e.g., postinfectious or druginduced hepatitis).||Leads to portal hypertension, liver failure, hepatocellular carcionma.|
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Reye's syndrome
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Childhood hepatoencephalopathy; mitochondrial abnormalities, microvesicular steatosis, hypoglycemia, vomiting, hepatomegaly, coma. ||Associated with viral infection (VZV and influenza B) that is treated with salicylates. Aspirin metabolites decrease beta oxidation by reversible inhibiton of mitochondrial enzyme. Contraindicate aspirin in children, use acetaminophen.|
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Nonalcoholic hepatic steatosis
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||Associated with obesity, hyperinsulinemia, insulin resistance, and DM2. |
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Alcoholic hepatic steatosis
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|Macrovesicular fatty change that may be reversible with alcohol cessation.|Short-term change with moderate alcohol intake.|
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Alcoholic hepatitis
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Can be asymptomatic or have RUQ pain, hepatomegaly, jaundice.|Mallory bodies (cytoskeletal intermediate fillaments). AST>ALT; ratio >1.5. Swollen and necrotic hepatocytes with neutrophilic infilitrates. Fatty change.|Requires sustained, long-term consumption. Leads to cirrhosis.|
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Alcoholic cirrhosis
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Has manifestations of chronic liver disease (jaundice, hypoalbuminemia).|Micronodular, irregularly shrunken liver with "hobnail" appearance. Sclerosis aroudn central vein (zone III). |Final and irrversible form. |
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Hepatocellular carcinoma/hepatoma
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Jaundice, tender hepatomegaly, ascites, polycythemia, and hypoglycemia. May lead to Budd-Chiari syndrome.|Elevated alpha-fetoprotein, elevated EPO (polycythemia!).|Most common primary malingant tumor of liver in adults. Increased risk with HepB/C, Wilson's disease, hemochromatosis, alpha1-antitrypsin deficiency, alcoholic cirrhosis, and carcinogens (alfatoxin from Aspergillus). Hematogenous dissemination. |
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Cavernous hemangioma
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Common benign liver tumor; age 30-50.|Contraindicate biopsy due to risk of hemorrhage.||
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Nutmeg liver
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Backup of blood into liver due to right-sided heart failure or Budd-Chiari syndrome. Centrilobular congestion and necrosis can result in cardiac cirrhosis.|Mottled nutmeg appearance.||
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Budd-Chiari syndrome
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Hepatosplenomegaly, ascites, adominal pain, and eventual liver failure. May develop varices and have visible abdominal and back veins. Absence of JVD.|Centrilobular congestion and necrosis leading to congestive liver disease. "Nutmeg" appearance.|Occlusion of IVC or hepatic veins. Associated with hypercoagulable state (YOUNG FEMALE ON ORAL CONTRACEPTIVES), polycythemia vera, pregnancy, and hepatocellular carcionma.|
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alpha1-antitrypsin deficiency
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Hepatic cirrhosis, panacinar emphysema.|PAS-positive hepatocytes.|PiZZ genotype. Codominant trait on chromosome 14; misfolded gene product protein aggregates in hepatocellular endoplasmic reticulum. |
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Physiologic neonatal jaundice
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Immature UDP-glucuronyl transferase leads to unconjugated hyperbilirubinemia and jaundce. Extreme cases may have kernicterus. Resolves within 1 week.|||Phototherapy (converts UCB to water-soluble form).
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Hepatocellular jaundice
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|Direct and indirect hyperbilirubinemia; elevated urine bilirubin; normal or decreased urine urobilinogen.||
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Obstructive jaundice
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|Direct hyperbilirubinemia; elevated urine bilirubin; decreased urine urobilinogen.||
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Hemolytic jaundice
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|Indirect hyperbilirubinemia; acholuria (absent urien bilirubin); increased urine urobilinogen.||
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Gilbert's syndrome
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Asymptomatic; no clinical consequences. Jaundice related to physiological stress (fasting, infection).|Elevated unconjugated bilirubin without overt hemolysis.|Decreased UDP-glucuronyl transferase or decreased bilirubin uptake.|
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Crigler-Najjar syndrome type I
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Presents early in life; patients die within a few years. Jaundice, kernicterus (bilirubin deposition in brain).|Elevated unconjugated bilirubin.|Absent UDP-glucuronyl transferase. |Plasmapheresis and phototherapy.
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Crigler-Najjar syndrome type II
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Less severe and responds to phenobarbital which induces liver enzyme synthesis.|||
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Dubin-Johnson syndrome
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Benign condition but have jaundice.|Conjugated hyperbilirubinenmia. Grossly black liver.|Due to defective liver excretion of conjugated bilirbuin.|
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Rotor's syndrome
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Similar to Dubin-Johnson syndrome but even milder (jaundice).|Normal appearing liver. Mild conjugated hyperbilirubinemia.|Due to defective liver excretion of conjugated bilirbuin.|
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Wilson's disease
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Copper accumulation especially in cortex (dementia), putamen (parkinsonian sx; dyskinesia and dysarthria, asterixis), hepatic cirrhosis, cornea (Kayser-Fleischer ring), kidney, and joints. Elevated risk of hepatocellular carcinoma. Hemolytic anemia.|Low ceruloplasmin levels. Can also dx by slit lamp.|Autosomal recessive (ATP7B). Inadequate hepatic copper excretion and failure of copper to enter circulation as ceruloplasmin.|Penicillamine.
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Hemochromatosis
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Micronodular cirrhosis, diabetes mellitus and skin pigmentation ("bronze diabetes"). Results in dilated cardiomyopathy, testicular atrophy, and elevated risk of hepatocellular carcinoma.|HLA-A3. Elevated ferritin, elevated serum iron, low TIBC, increased transferrin saturation. Prussian blue stain of hepatocytes.|Deposition of hemosiderin. If primary due to autosomal recessive defect. Secondary due to chronic transfusion therapy (beta-thalassemia).|Repeated phlebotomy, deferoxamine.
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Secondary biliary cirrhosis
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Pruritus, jaundice, dark urine, light (clay-colored) stools, hepatosplenomegaly. Complicated by ascending cholangitis.|Elevated conjugated bilirubin, elevated cholesterol, elevated ALP.|Due to extrahepatic biliary obstruction (gallstone, biliary stricture, chronic pancreatitis, panceatic head carcinoma). Elevated pressure in intrahepatic ducts leads to fibrosis and bile stasis.|
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Primary biliary cirrhosis
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Bone pain, pruritus, xanthelasma, jaundice, dark urine, light (clay-colored, acholic) stools, hepatosplenomegaly. More common in women.|Elevated conjugated bilirubin, elevated cholesterol, elevated ALP. Elevated serum mitochondrial autoantibodies (IgM).|Autoimmune reaction leading to lymphocytic infiltrate and granulomas. Associated with CREST, rheumatoid arthritis, celiac disease.|
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Primary sclerosing cholangitis
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Pruritus, jaundice, dark urine, light (clay-colored) stools, hepatosplenomegaly. More common in men.|p-ANCA. Elevated conjugated bilirubin, elevated cholesterol, elevated ALP. Hypergammaglobulinemia (IgM). Beaded appearance of bile ducts on ERCP.|Unknown cause of concentric "onion skin" bile duct fibrosis. Associated with ulcerative colitis. Can lead to secondary biliary cirrhosis.|
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Biliary colic
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Obstruction of common bile duct by gallstones causes bile duct contraction (RUQ pain). May present without pain in diabetes.|||
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Cholesterol cholelithiasis
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Jaundice, fever, RUQ pain, tea colored urine, clay-colored stools. Murphy's sign positive - inspiratory arrest on deep palpation due to pain. Most often causes cholecystitis, aslo ascending cholangitis, acute pancreatitis, and bile stasis.|80% radiolucent (some may be opaque due to calcium). Elevated cholesterol, decreased bile salts. Dx with radionuclide scan, ultrasound.|Risk factors are female, fat, fertile (pregnant) and forty. Associated with obesity, Crohn's disaease, CF, advanced age, clofibrate/gemfibrozil/cholestyramine, estrogens, multiparity, rapid weight loss, and Native Americans.|Cholecystectomy.
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Pigment cholelithiasis
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Jaundice, fever, RUQ pain, tea colored urine, clay-colored stools. Murphy's sign positive - inspiratory arrest on deep palpation due to pain. Most often causes cholecystitis, aslo ascending cholangitis, acute pancreatitis, and bile stasis.|Radiopaque. Elevated unconjugated bilirubin, decreased bile salts. Black stones = hemolysis; brown stones = infection. Dx with radionuclide scan, ultrasound.|Seen in patients with chronic hemolysis, alcoholic cirrhosis, advanced age, and biliary infection. Also Ascaris or Clonorchis.|Cholecystectomy.
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Acute cholecystitis
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Right shoulder or tip of the right scapula pain.|Elevated ALP if bile duct becomes involved (ascending cholangitis). Lymphocytosis.|Due to gallstones; rarely from ischemia or infectious (CMV). |Cholecystectomy.
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Chronic cholecystitis
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|Dystrophic calcification; "porcelain gallbladder". Rokitansky-Aschoff sinuses.|Wall of gallbladder has become thickened and fibrotic. Predisposed to carcinoma of the gallbladder.|
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Ileocecal valve obstruction
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Due to gallstone; fistula between gallbladder and small instestine.|Air in biliary tree.||
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Acute pancreatitis
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Epigastric abdominal pain radiating to the back, anorexia, nausea. Can lead to DIC, ARDS, hyperglycemia, hypocalcemia (Ca2+ collects in pancreatic calcium soap deposits), pseudocyst formation, hemorrhage, infection, and multiorgan failure.|Elevated amylase (rises first) and elevated lipase (higher specificity, 24-48 hrs post injury). Enzymatic fat necrosis.|Autodigestion of pancreas by trypsin. Caused by gallstones, ethanol, trauma, steroids, mumps, autoimmune disease, scorpion stings***, hypercalcemia/hypertriglyceridemia (>1000), ERCP, sulfa drugs.|Conservative management; NPO.
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Chronic pancreatitis
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Can lead to pancreatic insufficiency (steatorrhea, ADEK deficiency, diabetes mellitus, and elevated risk of pancreatic adenocarcionma). Pseudocysts.||Strongly associated with alcoholism and smoking.|
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Pancreatic adenocarcinoma
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Presents with abdominal pain raiding to back, weight loss (fat malabsorption/anorexia), migratory thrombophlebitis (Trousseau's), obstructive jaundice with palpable gallbladder (Courvoisier's sign).|CA 19-9 tumor marker; CEA less specific. Elevated ALP and conjugated bilirubin if it arises from head of pancreas.|Arises from DUCTS of the pancreas (not acini). Very aggressive (6 month prognosis); metastasized by presentation. Risk factors are smoking (NOT alcohol), chronic pancreatitis (>20 years), >50 years of age, and Jewish/African American males. Body and tail adenocarcionmas have poorer prognosis due to late detection.|Whipple procedure
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External hemorrhoid
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Pain is so severe the patient can't sit down.||Seen in pregnant women (tell them to lay on left side so IVC isn't constricted). Associated with thrombosis.|
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Internal hemorrhoid
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Present with bleeding; painless.||Portal hypertension.|
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Systemic mastocytosis
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Gastric acid hypersecretion (histamine), pruritis, utricaria, diarrhea, nausea, vomiting, cramps, hypotension, tachycardia, bronchospasm.||Abnormal proliferation of mast cells and increased histamine secretion.|
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Cowden syndrome
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"Characterized by macrocephaly, intestinal hamartomatous polyps, and benign skin tumors, typically trichilemmomas, papillomatous papules, and acral keratoses.
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Melanosis coli
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Mimics colitis or malignancy.|Black pigmentation of colon due to ingestion of laxative pigment by macrophages.|History of laxative abuse.|
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Pseudomembranous colitis
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Diarrhea, fever, abdominal cramps.|Yellow exudative membrane on colon. DIAGNOSED BY C. DIFFICLE TOXIN IN STOOL.|Most commonly due to clindamycin or ampicillin. Overgrowth of C. difficile|Metronidazole, vancomycin.
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Mesenteric lymphadenitis
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Mimics appendicitis||Caused by Yersinia enterolitica or viral infection.|
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Tubular adenoma
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|Tall cells with hyperchromatic nuclei. Pedunctulated tubule.|Less likely to cause cancer (5-10%).|
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Villous adenoma
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|Broad based, finger like projections. Sessile villous.|Has more dysplasia so higher incidence of cancer (50%+). Typically seen in the rectum|
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Right sided colonic adenocarcinoma
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Pain, palpable mass, iron deficiency anemia. Occult bleeding (difficult to detect).|Presents as fungating polypoid mass in lumen. CEA tumor marker for RECURRANCE (can't make initial dx).||
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Left sided colonic adenocarcinoma
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Pencil thin stools, cycling diarrhea and constipation, bright red rectal bleeding.|"Apple core" lesion (stenosis of lumen). CEA tumor marker for RECURRANCE (can't make initial dx).|More infiltrative so there is worse prognosis vs right sided tumors.|
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Carcinoid tumor of the appendix
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Generally asymptomatic until it metastasizes to the liver.|||
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Amebic liver abscess
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|Necrotic abscess filled with brown pastellike material "anchovy paste".|Cuased by Entamoeba histolytica. Spread via fecal-oral route.|
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Liver cell adenoma
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Right sided abdominal pain. |Well circumscribed benign liver tumor.|Associated with oral contraceptive use.|
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Metastasis to the liver
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|Multiple lesions of the liver.|Most common cancer of the liver (GI, melanoma, breast, lung, etc.)|
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Hepatic hemangiosarcoma
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||Associated with vinyl chloride use.|
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Viral hepatitis
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|Elevated conjugated and unconjugated bilirubin. Elevated AST and ALT (ALT>AST). Lobular disarray. Councilman bodies (apoptosis).||
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Hepatitis B
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Hepatocellular carcinoma.|Hepadnavirus (enveloped dsDNA). Ground-glass hepatocyte appearance in carrier state. HBsAg (initial infection, chronic state, NOT window period). HBcAg (window period). HBeAg (indicates transmissibility, window period).|Spread via sex, IV drug abuse.|
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Hepatitis A
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Anicteric in children; icteric and more severe in adults.|Picornavirus (naked ssRNA+). Anti-HAV IgM. Ballooning degeneration (hepatocyte swelling), mononuclear infiltrate, Councilman bodies.|Spread via fecal-oral route.|
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Hepatiis C
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Hepatic cirrhosis, hepatocellular carcinoma.|Flavivirus (naked +ssRNA).|Spread by IV drug abuse.|
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Hepatitis D
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Fulminant hepatitis with hepatits B coinfection.|Deltavirus (-ssRNA, circular).|Spread via fecal-oral route.|
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Hepatitis E
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20-25% mortality rate in pregnant females..|Hepevirus (naked +ssRNA).|Spread via fecal-oral route.|
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Cholesterolosis
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May predispose to gallstones.|Yellow speckling of red-tan mucosa "strawberry gallbladder".|Accumulation of cholesterol-laden macrophages in mucosa of gallbladder. |
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Gallbladder adenocarcinoma
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Older female with history of gallstones.|Enlarged palpable gallbladder. "Porcelain" appearance due to dystrophic calcifications.|Poor prognosis. Metastasis to liver.|
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Cholangiocarcinoma
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|Adenocarcinoma.|Carcinoma of intrahepatic bile ducts. Caused by Clonorchis sinensis (Chinese liver fluke) or primary sclerosing cholangitis.|
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Bile duct carcinoma
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|Adenocarcinoma.|Carcinoma of the extrahepatic bile ducts.|
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Klatskin tumor
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|Adenocarcinoma.|Carcinoma of the bifurcation of the left and right hepatic bile ducts.|
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Acute acalculous cholecystitis
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RUQ pain secondary to ischemia and stasis.||Acute inflammation of the gallbladder in absence of gallstones. Seen in the hopsitalized (trauma, etc.) and severely ill.|Antibiotics.
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Brown pigment acute cholecystitis
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|Elevated beta-glucuronidase.|Due to infection (Escherichia coli, Ascaris lumbricoides, Opisthorchis sinensis). Beta-glucuronidase hydrolyzes conjugated bilirubin, increasing the insoluble unconjugated form.|
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Black pigment acute cholecystitis
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||Due to chronic hemolysis.|
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Biliary atresia
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Jaundice, dark urine, light-colored stools, hepatomegaly in an infant.|Intrahepatic cholestasis, proliferation of bile ducts. Elevated direct bilirubin, ALP, GGT.|Congenital obstruction of extrahepatic bile ducts. Leads to biliary cirrhosis if untreated.|
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Hepatorenal syndrome
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Rapid decrease in renal function due to hepatic cirrhosis.|||
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Intestinal malrotation
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Presents with acute volvulus.|Small bowel on right side, cecum in epigastrum.||
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Spontaneous bacterial peritonitis
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Associated with cirrhosis and ascites. Fever, chills, abdominal tenderness, general malaise.||Caused by S. pneumonia in children, E. coli in adults.|
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