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243 Cards in this Set
- Front
- Back
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Presentation: Pancreatic Adenocarcinoma
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1. Abdominal pain radiating to back
2. Weight loss (due to malabsorption and anorexia) 3. Migratory thrombophlebitis—redness and tenderness on palpation of extremities (Trousseau’s syndrome) 4. Obstructive jaundice with palpable gallbladder (Courvoisier’s sign) |
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Causes: Acute Pancreatitis
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"GET SMASHED"
Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune disease, Scorpion sting, Hypercalcemia/Hyperlipidemia, ERCP, Drugs |
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Associated symptoms: Acute Pancreatitis
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Can lead to DIC, ARDS, diffuse fat necrosis,
hypocalcemia (Ca2+ collects in pancreatic calcium soap deposits), pseudocyst formation, hemorrhage, infection, and multiorgan failure |
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Associated symptoms: Chronic pancreatitis
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Chronic pancreatitis can lead to pancreatic insufficiency → steatorrhea, fat-soluble vitamin deficiency, and diabetes mellitus
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Define: Charcot's triad
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For cholangitis:
1. Jaundice 2. Fever 3. RUQ pain |
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Labs: Hemochromatosis
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↑ ferritin, ↑ iron, ↓TIBC → ↑transferrin saturation.
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Treatment: Hemochromatosis
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Phlebotomy, deferoxamine chelation
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Classic presentation: Hemochromatosis
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Micronodular cirrhosis, diabetes, and skin bronzing → "bronze diabetes"
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Associated symptoms: Wilson's Disease
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"ABCD"
Asterixis Basal ganglia degeneration (Parkinsonianisms) Ceruloplasmin ↓, Cirrhosis, Corneal deposits (Kayser-Fleischer rings) Dementia |
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Treatment: Wilson's disease
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Penicillamine chelation
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Basics: Dubin-Johnson syndrome
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Conjugated hyperbilirubinemia due to defective liver excretion. Grossly black liver. Benign.
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Basics Crigler-Najjar, Type I
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Absent UDP-glucuronyl transferase. Presents early in life; patients die within a few years.
Findings: jaundice, kernicterus, ↑ unconjugated bilirubin. |
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Basics Crigler-Najjar, Type II
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Deficient UDP-glucuronyl transferase, far less severe than type I. Responds to phenobarbital, which ↑ BUGT synthesis.
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Basics Gilbert syndrome
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Mildly ↓ UDP-glucuronyl transferase or ↓ bilirubin uptake. Asymptomatic. Elevated unconjugated bilirubin without overt hemolysis. No clinical consequences.
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Basics: Rotor's syndrome.
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Idiopathic conjugated hyperbilirubinemia. Mild. No black liver.
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Basics: Budd-Chiari syndrome
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Occlusion of IVC or hepatic veins with centrilobular congestion and necrosis, leading to congestive liver disease (hepatomegaly, ascites, abdominal pain, and eventual liver
failure). May develop varices and have visible abdominal and back veins. Absence of JVD. Associated with polycythemia vera, pregnancy, and hepatocellular carcinoma. |
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Basics: Physiologic jaundice of the newborn.
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At birth, immature UDP-glucuronyl transferase → unconjugated hyperbilirubinemia → jaundice/kernicterus. Treat with phototherapy to solubilize bilirubin.
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Layers of the Gut Tube.
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Layers of gut wall (inside to
outside): 1. Mucosa—epithelium (absorption), lamina propria (support), muscularis mucosae (motility) 2. Submucosa—includes Submucosal/Meissner’s plexus 3. Muscularis externa— includes Myenteric/Auerbach's plexus 4. Serosa/adventitia |
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Connects/Contains: Falciform Ligament.
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Connects liver to anterior abdominal wall.
Contains ligamentum teres. Remnant of fetal umbilical vein. |
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Connects/Contains: Hepatoduodenal Ligament.
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Connects liver to duodenum.
Contains portal triad (hepatic artery, portal vein, common bile duct) Connects lesser and greater sacs. |
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Connects/Contains: Gastrohepatic ligament.
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Connects liver to lesser curvature of stomach.
Contains gastric arteries. Separates right greater and lesser sacs. |
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Connects/Contains: Gastrocolic Ligament.
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Connects greater curvature to transverse colon.
Contains gastroepiploic arteries. A component of the greater omentum. |
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Connects/Contains: Gastrosplenic Ligament.
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Connects greater curvature to spleen.
Contains short gastric arteries. Separates left greater and lesser sacs. |
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Connects/Contains: Splenorenal Ligament.
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Connects spleen to posterior abdominal wall.
Contains splenic artery and vein. |
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Frequency of Basal Electric GI Rhythms.
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Stomach: 3 waves/min
Duodenum: 12 waves/min Ileum: 8–9 waves/min |
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Histology: Esophagus.
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Nonkeratinized stratified squamous epithelium.
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Histology: Stomach.
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Gastric glands.
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Histology: Duodenum.
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Villi and microvilli ↑ absorptive surface. Duodenum > jejunum > ileum.
Brunner’s glands (submucosa) and crypts of Lieberkühn. |
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Histology: Jejunum.
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Jejunum has largest number of goblet cells in the small intestine.
Plicae circulares and crypts of Lieberkühn. |
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Histology: Ileum.
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Peyer’s patches (lamina propria, submucosa), plicae circulares (proximal ileum), and crypts of Lieberkühn.
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Histology: Colon.
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Colon has crypts but no villi.
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Overview: Myenteric Plexus.
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AKA Auerbach's plexus.
Coordinates motility along entire gut wall. Contains cell bodies of some parasympathetic terminal effector neurons. Located between inner (circular) and outer (longitudinal) layers of smooth muscle in GI tract wall |
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Overview: Submucosal Plexus.
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Regulates local secretions, blood flow, and absorption.
Contains cell bodies of some parasympathetic terminal effector neurons. Located between mucosa and inner layer of smooth muscle in GI tract wall. |
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1/3s: Esophageal Anatomy.
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Upper 1⁄3: Striated muscle.
Middle 1⁄3: Striated and smooth muscle. Lower 1⁄3: Smooth muscle. |
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Blood/Innervation/Vertebral Level: Foregut.
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Celiac artery, vagus nerve, T12/L1.
Stomach to proximal duodenum; liver, gallbladder, pancreas, spleen (mesoderm) |
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Blood/Innervation/Vertebral Level: Midgut.
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SMA/vagus/L1.
Distal duodenum to proximal 2/3 of transverse colon. |
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Blood/Innervation/Vertebral Level: Hindgut.
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IMA/Pelvic nerves/L3.
Distal 1/3 of transverse colon to upper portion of rectum; splenic flexure is a watershed region |
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Branches: Celiac Trunk.
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Common hepatic, splenic, and left gastric arteries.
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Portosystemic Anastomoses.
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Left gastric v. ↔ esophageal v.
Paraumbilical v. ↔ superficial and inferior epigastric vv. Superior rectal v. ↔ middle and inferior rectal vv. Splenic v. ↔ left renal v. |
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Define: Pectinate Line.
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Formed where hindgut meets ectoderm within the rectum.
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Layers: Anterior Abdominal Wall.
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Skin → superficial fascia → external oblique m. → internal oblique m. → transversus abdominis m. → transversalis fascia → extraperitoneal fat → peritoneum
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Retroperitoneal Structures.
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1. Duodenum (2nd, 3rd, 4th
parts) 2. Descending colon 3. Ascending colon 4. Kidney and ureters 5. Pancreas (except tail) 6. Aorta 7. IVC 8. Adrenal glands 9. Rectum |
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Celiac Trunk Anastomoses.
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Gastroepiploic aa. and gastric aa.
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Overview: Diaphragmatic Hernia.
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Abdominal structures enter the thorax; may occur in infants as a result of defective development ofpleuroperitoneal membrane. Most commonly a hiatal hernia, in which stomach herniates upward through the esophageal hiatus of the diaphragm.
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Overview: Indirect Inguinal Hernia.
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Goes through the INternal (deep) inguinal ring, external (superficial) inguinal ring, and INto the scrotum. Enters internal inguinal ring lateral to inferior epigastric artery. Occurs in INfants owing to failure of processus vaginalis to close. Much more common in males.
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Overview: Direct Inguinal Hernia.
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Protrudes through the inguinal (Hesselbach’s) triangle. Bulges directly through abdominal wall medial to inferior epigastric artery. Goes through the external (superficial) inguinal ring only. Covered by external spermatic fascia. Usually in older men.
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Overview: Femoral Hernia.
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Protrudes below inguinal ligament through femoral canal below and lateral to pubic tubercle. More common in women.
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Hernias and the Inferior Epigastric Artery.
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Direct: Lateral to inferior epigastric a.
Indirect: Medial to inferior epigastric a. |
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Source: Gastrin
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G cells of gastric antrum.
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Source: CCK
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I cells of duodenum and jejunum.
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Source: Secretin.
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S cells of duodenum.
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Source: Somatostatin.
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D cells of GI mucosa and pancreatic islets.
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Source: GIP
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K cells of duodenum and jejunum.
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Source: VIP
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Parasympathetic ganglia in sphincters, gallbladder, and small intestine
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Source: Motilin
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Mo cells of small intestine.
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Source: Ghrelin.
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P/D1 cells of stomach.
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Action: Gastrin.
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↑ gastric H+ secretion
↑ gastric motility ↑ growth of gastric mucosa |
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Action: CCK
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↑ pancreatic secretion
↑ gallbladder contraction ↓ gastric emptying |
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Action: Secretin.
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↑ pancreatic HCO3- secretion
↓ gastric acid secretion ↑ bile secretion |
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Action: Somatostatin.
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↓ gastric acid and pepsinogen secretion
↓ pancreatic and small intestine fluid secretion ↓ gallbladder contraction ↓ insulin and glucagon release |
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Action: GIP
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↓ gastric H+ secretion (exocrine)
↑ insulin release (endocrine) |
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Action: VIP
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↑ intestinal water and electrolyte secretion
↑ relaxation of intestinal smooth muscle and sphincters |
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Action: GI Nitric Oxide
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↑ smooth muscle relaxation (including lower esophageal sphincter)
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Action: Motilin.
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Produces migrating motor complexes.
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Action: Ghrelin.
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↑ growth hormone, cortisol, and prolactin secretion.
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Regulation: Gastrin.
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↑ by stomach distention, amino acids, peptides, vagal stimulation
↓ by stomach pH < 1.5 |
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Regulation: CCK.
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↑ by fatty acids, amino acids
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Regulation: Secretin.
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↑ by acid, fatty acids in lumen of duodenum
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Regulation: Somatostatin.
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↑ by acid
↓ by vagal stimulation |
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Regulation: GIP
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↑ by fatty acids, amino acids, oral glucose
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Regulation: VIP
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↑ by distention and vagal stimulation
↓ by adrenergic input |
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Regulation: Motilin
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↑ in fasting state
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Regulation: Ghrelin
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↑ before meals
↓ after meals |
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Overview: VIPoma.
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Islet cell tumor; classically causes WDHA syndrome: watery diarrhea, hypokalemia, and achlorhydria.
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Source: Intrinsic Factor.
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Gastric parietal cells.
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Source: Gastric Acid.
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Gastric parietal cells.
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Source: Pepsin.
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Gastric chief cells.
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Regulation of Gastric Acid.
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↑ by histamine, ACh, gastrin
↓ by somatostatin, GIP, prostaglandin, secretin |
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Sources: Saliva.
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Parotid glands: serous fluid
Submandibular and sublingual glands: mucinous fluid |
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Functions: Saliva.
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1. α-amylase (ptyalin) begins starch digestion; inactivated by low pH on reaching stomach
2. Bicarbonate neutralizes oral bacterial acids, maintains dental health 3. Mucins (glycoproteins) lubricate food 4. Antibacterial secretory products 5. Growth factors that promote epithelial renewal |
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Nervous Input: Salivation
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Controlled by both sympathetics from superior cervical ganglia (T1-T3) and parasympathetics from facial and glossopharyngeal nerves.
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Overview: Carbohydrate Absorption.
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Only monosaccharides (glucose, galactose, fructose) are absorbed by enterocytes. Glucose and galactose are taken up by SGLT1 (Na+ dependent). Fructose is taken up by facilitated diffusion by GLUT-5. All are transported to blood by GLUT-2.
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Overview: Salivary Amylase
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Starts digestion, hydrolyzes α-1,4 linkages to yield disaccharides (maltose and α-limit dextrans).
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Overview: Pancreatic Amylase
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Highest concentration in duodenal lumen, hydrolyzes starch to oligosaccharides and
disaccharides. |
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Overview: Oligosaccharide Hydrolases
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At brush border of intestine, the rate-limiting step in carbohydrate digestion, produce monosaccharides from oligo- and disaccharides.
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Overview: Pancreatic Enzymes.
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α-amylase—starch digestion, secreted in active form.
Lipase, phospholipase A, colipase—fat digestion. Proteases (trypsin, chymotrypsin, elastase, carboxypeptidases)—protein digestion, secreted as proenzymes also known as “zymogens.” Trypsinogen—converted to active enzyme trypsin by enterokinase/enteropeptidase, an enzyme secreted from duodenal mucosa. Trypsin activates other proenzymes and more trypsinogen (positive feedback loop). |
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Absorption: Iron.
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Absorbed as Fe2+ in duodenum.
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Absorption: Folate.
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Absorbed in jejunum.
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Absorption: B12
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Absorbed in ileum along with bile acids.
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Overview: Peyer's Patches.
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Unencapsulated lymphoid tissue found in lamina propria and submucosa of small intestine. Contain specialized M cells that take up antigen.
B cells in Peyer's patches differentiate into IgA-secreting plasma cells. |
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Composition: Bile
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Composed of bile salts (bile acids conjugated to glycine or taurine, making them water
soluble), phospholipids, cholesterol, bilirubin, water, and ions. |
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The Only Method for Meaningful Cholesterol Excretion.
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As bile salts!
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Heme Excretion.
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Heme → biliverdin → unconjugated bilirubin → conjugated bilirubin (UDP glucuronyl transferase) → bile → urobilinogen
80% of urobilinogen is excreted in feces as stercobilin; 20% is reabsorbed. The vast majority of this (>90%) is recirculated to the liver and reexcreted as bile. A small amount (<10%) is excreted by the kidneys as urobilin. |
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Overview: Salivary Gland Tumors.
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Generally benign and occur in parotid gland. Types include pleomorphic adenoma, Warthin’s tumor, and mucoepidermoid carcinoma.
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Overview: Pleomorphic Salivary Gland Adenoma.
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Most common salivary gland tumor; painless, movable mass; benign with high rate of recurrence.
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Overview: Warthin’s Tumor.
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Benign; heterotopic salivary gland tissue trapped in a lymph node,
surrounded by lymphatic tissue. |
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Overview: Mucoepidermoid Carcinoma.
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Most common malignant salivary gland tumor.
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Overview: Achalasia.
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Failure of relaxation of lower esophageal sphincter due to loss of myenteric (Auerbach’s) plexus. High LES opening pressure and uncoordinated peristalsis → progressive dysphagia. Associated with an ↑ risk of esophageal carcinoma.
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Labs: Achalasia
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Barium swallow reveals characteristic "bird's beak" on plain film.
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Common Causes: Esophagitis.
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Associated with reflux, infection (HSV-1, CMV, Candida), or chemical ingestion.
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Overview: Plummer-Vinson Syndrome.
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Triad of:
1. Dysphagia (due to esophageal webs) 2. Glossitis 3. Iron deficiency anemia |
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Presentation: GERD.
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Commonly presents as heartburn and regurgitation upon lying down. May also present with nocturnal cough and dyspnea.
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Overview: Barrett's Esophagus.
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Glandular metaplasia—replacement of nonkeratinized (stratified) squamous epithelium with intestinal (columnar) epithelium in the distal esophagus. Due to chronic acid reflux (GERD).
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Presentation: Esophageal Carcinoma.
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Progressive dysphagia (solids → liquids) → weight loss.
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Risk Factors: Esophageal Carcinoma.
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"ABCDEF"
Alcohol/Achalasia Barrett's esophagus Cigarettes Diverticuli Esophagitis Familial |
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Location: Esophageal Adenocarcinoma.
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Lower 1/3.
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Location: Esophageal Squamous Cell Carcinoma.
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Upper and middle 1/3.
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Incidence: Squamous vs. Adenocarcinoma of the Esophagus.
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Worldwide, squamous is #1; in the US, adenocarcinoma is #1
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Overview: Celiac Sprue.
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Autoantibodies to gluten (gliadin) in wheat and other grains. Proximal small bowel primarily.
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Overview: Tropical Sprue.
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Probably infectious; responds to antibiotics. Similar to celiac sprue, but can affect entire small bowel.
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Overview: Whipple’s Disease.
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Infection with Tropheryma whippelii (gram positive); PAS positive macrophages in intestinal lamina propria, mesenteric nodes. Arthralgias, cardiac and neurologic symptoms are common. Most often occurs in older men.
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Overview: Disaccharidase Deficiency.
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Most common is lactase deficiency → milk intolerance. Normal-appearing villi. Osmotic diarrhea. Since lactase is located at tips of intestinal villi, self-limited lactase deficiency can occur following injury (e.g., viral diarrhea).
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Common Causes: Pancreatic Insufficiency.
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Due to cystic fibrosis, obstructing cancer, and chronic pancreatitis.
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Presentation: Pancreatic Insufficiency.
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Malabsorption of fat and fat-soluble vitamins. Steatorrhea.
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Overview: Abetalipoproteinemia.
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↓ synthesis of apo B → inability to generate chylomicrons → ↓ secretion of cholesterol, VLDL into bloodstream → fat accumulation in enterocytes. Presents in early childhood with malabsorption and neurologic manifestations.
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Findings: Celiac Sprue.
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Findings include antibodies to gliadin and tissue transglutaminase, blunting of villi, and lymphocytes in the lamina propria.
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Classic Finding: Celiac Sprue.
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Associated with dermatitis herpetiformis.
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Overview: Ménétrier’s Disease.
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Gastric hypertrophy with protein loss, parietal cell atrophy, and ↑ mucous cells. Precancerous. Rugae of stomach are so hypertrophied that they look like brain gyri.
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Basic Pathogenesis: Acute Gastritis.
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Disruption of mucosal barrier → inflammation. Erosive.
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Common Causes: Acute Gastritis.
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Can be caused by stress, NSAIDs (↓ PGE2 → ↓ gastric mucosa production), alcohol, uremia, burns (Curling ulcers), and brain injury (Cushing ulcers)
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Overview: Cushing Ulcers.
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Cushing ulcer: ↑ ICP → ↑ vagal stimulation → ↑ ACh→ ↑H+ production → acute gastritis
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Overview: Curling Ulcers.
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Curling ulcer: burn injury → ↓ plasma volume → sloughing of gastric mucosa → acute gastritis
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Overview: Type A Chronic Gastritis.
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Autoimmune gastritis affecting the fundus and body. Antibodies ton parietal cells and intrinsic factor.
AKA "atrophic gastritis" Manifests with pernicious anemia and achlorhydria. |
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Overview: Type B Chronic Gastritis.
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Caused by H. pylori. Most common gastritis. Affects antrum. Increased risk of gastric MALToma.
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Overview: Krukenberg's Tumor.
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Bilateral metastases from stomach to ovaries.
Abundant mucus and signet ring cells. |
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"Sister Mary Joseph’s Nodule"
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Subcutaneous periumbilical
metastasis from the stomach. |
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Overview: Gastric Neoplasms.
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Almost always adenocarcinoma. Early aggressive local spread and node/liver mets.
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Common Causes: Stomach Cancer.
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Associated with dietary nitrosamines (smoked foods), achlorhydria, chronic gastritis, type A blood.
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"Linitus Plastica"
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Widespread, diffusely infiltrative gastric adenocarcinoma with extensive gastric thickening.
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Common Features: Stomach Cancer.
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Signet ring cells, acanthosis nigricans are common features.
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PUD: Gastric Ulcers.
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Pain can be Greater with meals—weight loss. Often occurs in older patients. H. pylori infection in 70%; chronic NSAID use also implicated.
Due to ↓ mucosal protection against gastric acid. |
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PUD: Duodenal Ulcers.
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Pain Decreases with meals—weight gain. Almost 100% have H. pylori infection.
Due to ↑ gastric acid secretion (e.g., Zollinger-Ellison syndrome) or ↓ mucosal protection. |
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Common Complications: Duodenal PUD.
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Common complications include bleeding, penetration into pancreas, perforation, and obstruction.
No inherent malignant potential. |
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Pathology: Duodenal PUD.
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Hypertrophy of Brunner’s glands. Ulcer beds tend to have clean, “punched-out” margins unlike the raised/irregular margins of carcinoma.
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Etiology: Crohn's.
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Disordered response to intestinal bacteria.
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Etiology: Ulcerative Colitis.
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Autoimmune.
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Locations: Crohn's.
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Any portion of the GI tract, from mouth to anus. Particularly prevalent within the terminal ileum and colon.
RECTAL SPARING! |
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Location: Ulcerative Colitis.
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Continuous colonic lesions, always with rectal involvement.
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Gross Morphology: Crohn's.
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Transmural inflammation, "cobblestone" mucosa (skip lesions), creeping fat, linear ulcers, fistulas, fissures.
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Gross Morphology: Ulcerative Colitis.
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Mucosal and submucosal inflammation only. Friable mucosal pseudopolyps with freely hanging mesentery. Loss of haustra → “lead pipe” appearance on imaging.
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Microscopic Morphology: Crohn's.
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Noncaseating granulomas and lymphoid aggregates.
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Microscopic Morphology: Ulcerative Colitis.
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Crypt abscesses and ulcers, bleeding, no granulomas.
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Complications: Crohn's.
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Strictures, fistulas, perianal disease, malabsorption, nutritional depletion.
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Complications: Ulcerative Colitis.
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Malnutrition, toxic megacolon, colorectal carcinoma.
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Intestinal Manifestations: Crohn's.
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Diarrhea that may or may not be bloody.
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Intestinal Manifestations: Ulcerative Colitis.
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Bloody diarrhea.
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Extraintestinal Manifestations: Crohn's.
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Migratory polyarthritis, erythema nodosum, ankylosing spondylitis, uveitis, immunologic disorders.
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Extraintestinal Manifestations: Ulcerative Colitis.
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1° sclerosing cholangitis, pyoderma gangrenosum.
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Tx: Crohn's.
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Corticosteroids, infliximab.
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Tx: Ulcerative Colitis.
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ASA preparations (sulfasalazine), infliximab, colectomy.
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Overview: IBS.
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Recurrent abdominal pain associated with ≥ 2 of the following:
1. Pain improves with defecation 2. Change in stool frequency 3. Change in appearance of stool No structural abnormalities. May present with diarrhea, constipation, or alternating. Pathophysiology is multifaceted. Treat symptoms. |
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Differential: Appendicitis.
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Diverticulitis (elderly), ectopic pregnancy (use β-hCG to rule out).
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Presentation: Appendicitis.
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Initial diffuse periumbilical pain → localized pain at McBurney’s point. Nausea, fever; may perforate → peritonitis.
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True vs. False Diverticula.
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“True” diverticulum—all 3 gut wall layers outpouch.
“False” diverticulum or pseudodiverticulum—only mucosa and submucosa outpouch. Occur especially where vasa recta perforate muscularis externa. |
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Overview: "Divertuclum"
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Blind pouch protruding from the alimentary tract that communicates with the lumen of the gut.
Most diverticula (esophagus, stomach, duodenum, colon) are acquired and are termed “false” in that they lack or have an attenuated muscularis externa. Most often in sigmoid colon. |
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Overview: "Diverticulosis"
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Many diverticula. Common, particularly > 60. Caused by ↑ intraluminal pressure and focal weakness in colonic wall. Associated with low-fiber diets. Most often in sigmoid colon.
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Presentation: Diverticulosis.
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Often asymptomatic or associated with vague discomfort and/or painless rectal bleeding.
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Extraintestinal Manifestations: Ulcerative Colitis.
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1° sclerosing cholangitis, pyoderma gangrenosum.
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Tx: Crohn's.
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Corticosteroids, infliximab.
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Tx: Ulcerative Colitis.
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ASA preparations (sulfasalazine), infliximab, colectomy.
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Overview: IBS.
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Recurrent abdominal pain associated with ≥ 2 of the following:
1. Pain improves with defecation 2. Change in stool frequency 3. Change in appearance of stool No structural abnormalities. May present with diarrhea, constipation, or alternating. Pathophysiology is multifaceted. Treat symptoms. |
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Differential: Appendicitis.
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Diverticulitis (elderly), ectopic pregnancy (use β-hCG to rule out).
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Presentation: Appendicitis.
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Initial diffuse periumbilical pain → localized pain at McBurney’s point. Nausea, fever; may perforate → peritonitis.
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True vs. False Diverticula.
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“True” diverticulum—all 3 gut wall layers outpouch.
“False” diverticulum or pseudodiverticulum—only mucosa and submucosa outpouch. Occur especially where vasa recta perforate muscularis externa. |
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Overview: "Diverticulum"
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Blind pouch protruding from the alimentary tract that communicates with the lumen of the gut.
Most diverticula (esophagus, stomach, duodenum, colon) are acquired and are termed “false” in that they lack or have an attenuated muscularis externa. Most often in sigmoid colon. |
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Overview: "Diverticulosis"
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Many diverticula. Common, particularly > 60. Caused by ↑ intraluminal pressure and focal weakness in colonic wall. Associated with low-fiber diets. Most often in sigmoid colon.
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Presentation: Diverticulosis.
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Often asymptomatic or associated with vague discomfort and/or painless rectal bleeding.
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Overview: "Diverticulitis"
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Inflammation of diverticula classically causing LLQ pain, fever, leukocytosis. May perforate → peritonitis, abscess formation, or bowel stenosis. Tx with antibiotics.
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Possible Complications: Diverticulitis.
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May cause bright red rectal bleeding. May also cause colovesical fistula (fistula with bladder) → pneumaturia.
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Overview: Zenker's Diverticulum.
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False diverticulum. Herniation of mucosal tissue at junction of pharynx and esophagus.
Presenting symptoms: halitosis (due to trapped food particles), dysphagia, obstruction. |
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Overview: Meckel's Diverticulum.
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Persistence of the vitelline duct or yolk stalk. May contain ectopic acid–secreting gastric mucosa and/or pancreatic tissue.
Most common congenital anomaly of the GI tract. |
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Complications: Meckel's Diverticulum.
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Can cause bleeding, intussusception, volvulus, or obstruction near the terminal ileum.
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"The Five 2s": Meckel's Diverticulum.
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The five 2’s:
2 inches long. 2 feet from the ileocecal valve. 2% of population Commonly presents in first 2 of life. May have 2 types of epithelia (gastric/pancreatic). |
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Overview: Intussusception.
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“Telescoping” of 1 bowel segment into distal segment; can compromise blood supply.
Unusual in adults (associated with intraluminal mass or tumor). Majority of cases occur in children (usually idiopathic; may be viral [adenovirus]). Abdominal emergency in early childhood. |
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Overview: Volvulus.
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Twisting of portion of bowel around its mesentery; can lead to obstruction and infarction. May occur at cecum and sigmoid colon, where there is redundant mesentery.
Most common among elderly. |
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Overview/Pathogenesis: Hirschsprung’s Disease.
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Congenital megacolon characterized by lack of ganglion cells/enteric nervous plexuses (Auerbach’s, Meissner's) in segment on intestinal biopsy.
Due to failure of neural crest cell migration. |
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Presentation: Hirschspring's Disease.
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Presents as chronic constipation early in life. Dilated portion of the colon proximal to the aganglionic segment, resulting in a “transition zone.” Involves rectum. Usually failure to pass meconium.
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Overview: Duodenal Atresia.
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Causes early bilious vomiting with proximal stomach distention (“double bubble”) due
to failure of recanalization of small bowel. Associated with Down syndrome. |
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Overview: GI Angiodysplasia.
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Tortuous dilation of vessels → bleeding. Most often found in cecum, terminal ileum, and ascending colon. More common in older patients.
Accounts for 20% of major episodes of lower intestinal bleeding; intestinal hemorrhage may be chronic and intermittent or acute and massive. |
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Overview: Ischemic Colitis.
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Reduction in intestinal blood causes ischemia. Pain after eating → weight loss. Commonly occurs at splenic flexure and distal colon. Typically affects elderly.
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Overview: Colonic Polyps.
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Masses protruding into gut lumen → sawtooth appearance. 90% are non-neoplastic. Often rectosigmoid.
Adenomatous polyps are precancerous. Malignant risk is associated with ↑ size, villous histology, ↑ epithelial dysplasia. Precursor to colorectal cancer. The more villous the polyp, the more likely it is to be malignant |
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Overview: Hyperplastic GI Polyps.
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Most common non-neoplastic polyp in colon (> 50% found in rectosigmoid colon).
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Overview: Juvenile GI Polyps.
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Mostly sporadic lesions in children < 5 years of age. 80% in rectum. If single, no malignant potential.
Juvenile polyposis syndrome—multiple juvenile polyps in GI tract, ↑ risk of adenocarcinoma. |
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Overview: Peutz-Jeghers Syndrome.
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Autosomal-dominant syndrome featuring multiple benign GI hamartomas and mucocutaneous hyperpigmentation. Associated with ↑ risk of CRC and other malignancies.
Single polyps are not malignant. |
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Epidemiology: CRC.
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3rd most common cancer; 3rd most deadly in United States. Most patients are > 50 years of age. ~ 25% have a family history.
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Overview: FAP.
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Familial adenomatous polyposis
Autosomal-dominant mutation of APC gene on chromosome 5q. Two-hit hypothesis. 100% progress to CRC. Thousands of polyps;pancolonic; always involves rectum. |
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Overview: Gardner’s Syndrome
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FAP + osseous and soft tissue tumors, retinal hyperplasia.
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Overview: Turcot’s Syndrome.
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FAP + malignant CNS tumor. TURcot = TURban.
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Overview: HNPCC.
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AKA "Lynch Syndrome"
Autosomal dominant mutation of DNA mismatch repair genes. ~ 80% progress to CRC. Proximal colon is always involved. |
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Risk Factors: CRC.
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IBD, Streptococcus bovis bacteremia, tobacco use, large villous adenomas, juvenile polyposis syndrome, Peutz-Jeghers syndrome.
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Presentation: CRC.
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Distal colon—obstruction, colicky pain, hematochezia.
Proximal colon—dull pain, iron deficiency anemia, fatigue. |
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Dx: CRC.
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Iron deficiency anemia in older males.
Screen patients > 50 years of age with stool occult blood test and colonoscopy. “Apple core” lesion seen on barium enema x-ray. CEA tumor marker. |
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Molecular Pathogenesis of CRC.
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There are 2 molecular pathways that lead to CRC:
1. Microsatellite instability pathway (15%): DNA mismatch repair gene mutations → sporadic and HNPCC syndrome. Mutations accumulate, but no defined morphologic correlates. 2. APC/β-catenin (chromosomal instability) pathway (85%): Loss of APC, K-RAS mutation, and loss of p53 |
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Epidemiology: Carcinoid Tumors.
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Comprise 50% of all small bowel tumors.
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Classic Symptoms: Carcinoid Syndrome.
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Classic symptoms: wheezing, right-sided heart murmurs, diarrhea, flushing.
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Causes: Micronodular Cirrhosis.
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Metabolic insults: Wilson's, hemochromatosis, alcoholism, etc.
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Causes: Macronodular cirrhosis.
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Usually due to significant liver injury leading to hepatic necrosis (e.g., post-infectious or drug-induced hepatitis). ↑ risk of hepatocellular carcinoma.
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DDx: Elevated LFTs.
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Viral hepatitis (ALT > AST)
Alcoholic hepatitis (AST > ALT) Myocardial infarction (AST) |
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DDx: Elevated GGT.
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Various liver diseases; ↑ with heavy alcohol consumption.
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DDx: Elevated Alk Phos
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Obstructive liver disease, hepatocellular carcinoma, bile duct disease, bone disease
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DDx: Elevated Lipase.
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Acute pancreatitis.
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DDx: Elevated Amylase
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Acute pancreatitis, mumps
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Overview: Reye's Syndrome
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Rare, often fatal childhood hepatoencephalopathy.
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Findings: Reye's Syndrome.
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Findings: mitochondrial
abnormalities, fatty liver (microvesicular fatty change), hypoglycemia, coma. |
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Mechanism: Reye's Syndrome
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Mechanism: aspirin metabolites ↓ β-oxidation by reversible inhibition
of mitochondrial enzyme. |
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Most Common Cause: Reye's Syndrome
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Associated with viral infection (especially VZV and influenza B) that has been treated with salicylates.
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Overview: Hepatic Steatosis.
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Short-term change with moderate alcohol intake. Macrovesicular fatty change that may be reversible with alcohol cessation.
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Overview: Alcoholic Hepatitis.
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Requires sustained, long-term consumption. Swollen and necrotic hepatocytes with neutrophilic infiltration. Mallory bodies are present.
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Overview: Alcoholic Cirrhosis.
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Final and irreversible form of alcoholic liver disease. Micronodular, irregularly shrunken liver with “hobnail” appearance.
Sclerosis around central vein. |
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Manifestations: Alcoholic Cirrhosis.
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Has manifestations of chronic liver disease (e.g., jaundice, hypoalbuminemia)
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Overview: Hepatocellular Carcinoma.
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Most common 1° malignant tumor of the liver in adults.
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Risk Factors: Hepatocellular Carcinoma.
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incidence is associated with hepatitis B and C, Wilson’s disease, hemochromatosis, α1-antitrypsin deficiency, alcoholic cirrhosis, and carcinogens (e.g., aflatoxin in peanuts).
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Findings: Hepatocellular Carcinoma.
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Jaundice, tender hepatomegaly, ascites, polycythemia, and hypoglycemia.
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Marker: Hepatocellular Carcinoma.
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↑ α-fetoprotein.
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Route of Metastasis: Hepatocellular Carcinoma.
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Commonly spread by hematogenous dissemination.
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Overview: "Nutmeg Liver"
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Due to backup of blood into liver. Commonly caused by right-sided heart failure and Budd-Chiari syndrome. The liver appears mottled like a nutmeg. If the condition persists, centrilobular congestion and necrosis can result in cardiac cirrhosis.
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Overview: α1-Antitrypsin Deficiency
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Misfolded gene product protein accumulates in hepatocellular ER. ↓ elastic tissue in lungs → panacinar emphysema. PAS-positive globules in liver. Codominant trait.
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Overview: Wilson's Disease.
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Inadequate hepatic copper excretion and failure of copper to enter circulation as ceruloplasmin. Leads to copper accumulation, especially in liver, brain, cornea, kidneys, and joints.
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Pathophysiology: Primary Biliary Cirrhosis
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Autoimmune reaction → lymphocytic infiltrate + granulomas. ↑ serum mitochondrial antibody.
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Presentation: Primary Biliary Cirrhosis
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Pruritus, jaundice, dark urine, light stools, hepatosplenomegaly.
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Presentation: Secondary Biliary Cirrhosis
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Pruritus, jaundice, dark urine, light stools, hepatosplenomegaly.
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Presentation: Primary Sclerosing Cholangitis
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Pruritus, jaundice, dark urine, light stools, hepatosplenomegaly.
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Labs: Primary Biliary Cirrhosis
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↑ conjugated bilirubin, ↑ cholesterol, ↑ alkaline phosphatase.
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Labs: Secondary Biliary Cirrhosis
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↑ conjugated bilirubin, ↑ cholesterol, ↑ alkaline phosphatase.
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Labs: Primary Sclerosing Cholangitis
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↑ conjugated bilirubin, ↑ cholesterol, ↑ alkaline phosphatase.
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Overview: Primary Biliary Cirrhosis
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Inflammatory autoimmune disease mainly affecting the intrahepatic bile ducts. Characterized by nonsuppurative, inflammatory destruction of medium-sized intrahepatic bile ducts. Accompanied by portal inflammation, scarring, and eventual development of cirrhosis and liver failure.
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Overview: Primary Sclerosing Cholangitis
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Chronic cholestatic disorder characterized by non-specific inflammation, fibrosis, and strictures of both intra- and extrahepatic bile ducts.
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Antibodies: Primary Sclerosing Cholangitis
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Anti-smooth muscle and anti-nuclear antibodies.
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Antibodies: Primary Biliary Cirrhosis
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Anti-mitochondrial antibodies targeting the E2 component of the pyruvate dehydrogenase complex.,
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Most Common Causes: Secondary Biliary Cirrhosis (Adult)
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Extrahepatic cholelithiasis, malignancies of the biliary tree or pancreatic head, and strictures from surgical procedures.
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Most Common Causes: Secondary Biliary Cirrhosis (Children)
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Biliary atresia, cystic fibrosis, choledochal cysts.
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Pathophysiology: Secondary Biliary Cirrhosis
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Extrahepatic biliary obstruction → ↑pressure in intrahepatic ducts → injury/fibrosis and bile stasis.
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Pathophysiology: Primary Sclerosing Cholangitis.
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Unknown cause of concentric bile duct fibrosis → alternating strictures and dilation with “beading” of intra- and extrahepatic bile ducts.
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Pathogenesis: Gallstones.
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Form when solubilizing bile acids and lecithin are overwhelmed by ↑ cholesterol and/or bilirubin or gallbladder stasis.
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Two Types of Gallstones.
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Cholesterol stones and pigment stones.
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Common Causes: Cholesterol Stones.
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Associated with obesity, Crohn’s disease, cystic fibrosis, advanced age, clofibrate, estrogens, multiparity, rapid weight loss, and Native American origin.
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Common Causes: Pigment Stones
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Seen in patients with chronic hemolysis, alcoholic cirrhosis, advanced age, and biliary infection.
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Complications: Cholelithiasis.
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Can cause ascending cholangitis, acute pancreatitis, bile stasis, cholecystitis.
Can fistulize with duodenum. |
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"Gallstone Ileus"
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Gallbladder fistulizes with small bowel → gallstone/s occludes ileocecal valve → ileal obstruction.
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Overview: Cholecystitis.
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Inflammation of gallbladder. Usually from gallstones; rarely ischemia or infectious CMV). ↑ alkaline phosphatase if bile duct becomes involved (e.g., ascending cholangitis).
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Markers: Pancreatic Adenocarcinoma.
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CEA and CA-19-9 tumor markers.
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Overview: Pancreatic Adenocarcinoma.
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Prognosis averages 6 months or less; very aggressive; usually already metastasized at presentation; tumors more common in pancreatic head (→ obstructive jaundice).
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Epi: Pancreatic Adenocarcinoma.
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↑ risk in Jewish and African-American males.
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