Gastrointestinal Flashcards

1
Q

GI embryo - foregut, midgut, hindgut

A

Foregut - pharynx to duodenum

Midgut - duodenum to proximal 2/3 of transverse colon

Hindgut - distal 1/3 of transverse colon to anal canal above pectinate line

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2
Q

Developmental defects of anterior abdominal wall due to failure of:

A

Rostral fold closure - sternal defects

Lateral fold closure - omphalocele, gastroschisis

Caudal fold closure - bladder exstrophy

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3
Q

Duodenal atresia

A

Failure to recanalize (trisomy 21)

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4
Q

Jejunal, ileal, colonic atresia

A

Due to vascular accident (apple peel atresia)

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5
Q

Midgut development

A

6th week - midgut herniates through umbilical ring

10th week - returns to abdominal cavity + rotates around superior mesenteric artery (SMA)

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6
Q

Gastroschisis

A

extrusion of abdominal contents through abdominal folds; not covered by peritoneum

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7
Q

Omphalocele

A

Persistence of herniation of abdominal contents into umbilical cord, sealed by peritoneum

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8
Q

Tracheoesophageal anomalies

A

Esophageal atresia (EA) with distal tracheoesophageal fistula (TEF) is the most common (85%)

Results in drooling, choking, and vomiting with first feeding. TEF allows air to enter stomach (visible on CXR). Cyanosis is secondary to laryngospasm (to avoid reflux-related aspiration). Clinical test: failure to pass nasogastric tube into stomach

In H-type, the fistula resembles the letter H. In pure EA the CXR shows gasless abdomen

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9
Q

Congenital pyloric stenosis

A

Hypertrophy of the pylorus causes obstruction. Palpable “olive” mass in epigastric region and nonbilious projectile vomiting at about 2-6 weeks old. Occurs in 1/600 live births, more often in firstborn males.

Results in hypokalemic hypochloremic metabolic alkalosis (secondary to vomiting of gastric acid and subsequent volume contraction). Treatment is surgical incision (pyloromyotomy)

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10
Q

Pancreas and spleen embryo

A

Pancreas - derived from foregut. Ventral pancreatic buds contribute to uncinate process and main pancreatic duct. The dorsal pancreatic bud alone becomes the body, tail, isthmus, and accessory pancreatic duct. Both the ventral and dorsal buds contribute to the pancreatic head.

Annular pancreas - ventral pancreatic bud abnormally encircles 2nd part of duodenum; forms a ring of pancreatic tissue that may cause duodenal narrowing

Pancreatic divisum - ventral and dorsal parts fail to fuse at 8 weeks. Common anomly; mostly asymptomatic, but may cause chronic abdominal pain and/or pancreatitis

Spleen - arises in mesentery of stomach (hence is mesodermal) but is supplied by foregut (celiac artery)

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11
Q

Retroperitoneal structures

A

Retroperitoneal structures include GI structures that lack a mesentery and non-GI structures. Injuries to retroperitoneal structures can cause blood or gas accumulation in retroperitoneal space

SAD PUCKER

Suprarenal (adrenal) glands
Aorta and IVC
Duodenum (2nd through 4th parts)
Pancreas (except tail)
Ureters 
Colon (descending and ascending)
Kidneys
Esophagus (thoracic portion)
Rectum (partially)
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12
Q

Falciform ligament

A

Connects liver to anterior abdominal wall

Contains:
Ligamentum teres hepatis (derivate of fetal umbilical vein)

Derivative of ventral mesentery

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13
Q

Hepatoduodenal ligament

A

Connects liver to duodenum

Contains:
Portal triad - proper hepatic artery, portal vein, common bile duct

Pringle maneuver - ligament may be compressed between thumb and index finger placed in omental foramen to control bleeding

Borders the omental foramen, which connects the greater and lesser sacs

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14
Q

Gastrohepatic ligament

A

Connects liver to lesser curvature of stomach

Contains:
Gastric arteries

Separates greater and lesser sacs on the right.

May be cut during surgery to access liver sac

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15
Q

Gastrocolic ligament

A

Connects greater curvature and transverse colon

Contains:
Gastroepiploic arteries

Part of grater omentum

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16
Q

Gastrosplenic ligament

A

Connects greater curvature to spleen

Contains:
Short gastrics
Left gastrorpiploic vessels

Separates greater and lesser sacs on the left

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17
Q

Splenorenal

A

Connects spleen to posterior abdominal wall

Contains:
Splenic artery and vein
Tail of pancreas

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18
Q

Layers of gut wall

A

MSMS

Mucosa - epithelium, lamina, propria, muscularis mucosa

Submucosa - includes Submucosal nerve plexus (Meissner), Secretes fluid

Muscularis externa - include Myenteric plexus (Auerbach), Motility

Serosa (when intraperitoneal), adventitia (when retroperitoneal)

Frequencies of basal electric rhythm (slow waves)
Stomach - 3 waves/min
Duodenum - 12 waves/min
Ileum - 8-9 waves/min

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19
Q

Digestive tract histology

A

Esophagus - Nonkeratinized stratified squamous epithelium

Stomach - gastric glands

Duodenum - Villi and microvilli increase absorptive surface 
Brunner glands (HCO3 secreting cells of submucosa) and crypts of Lieberkuhn

Jejunum - Plicae circulares and crypts of Lieberkuhn

Ileum - Peyer patches (lymphoid aggregates in lamina propria, submucosa), plicae circulares (proximal ileum), and crypts of Liberkuhn. Largest number of goblet cells in the SI

Colon - Colon has crypts of Lieberkuhn but no villi; abundant goblet cells

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20
Q

Superior mesenteric artery syndrome

A

When the transverse portion (third part) of duodenum is entrapped between SMA and aorta, causing intestinal obstruction

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21
Q

GI blood supply and innervation

A

1) Foregut embryologic origin

Celiac Artery
Vagus Nerve (parasymp)
Vertebral level = T12/L1

Pharynx (Vagus only) and lower esophagus (celiac artery only) to proximal duodenum; liver, gallbladder, pancreas, spleen (mesoderm)

2) Midgut

SMA
Vagus (parasymp)
L1

Distal duodenum to proximal 2/3 of transverse colon

3) Hindgut

IMA
Pelvic (parasymp)
L3

Distal 1/3 of transverse colon to upper portion of rectum; splenic flexure is a watershed region between SMA and IMA

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22
Q

Celiac trunk

A

Branches of celiac trunk = Common hepatic, splenic, and Left Gastric. These constitute the main blood supply of the stomach

Short gastrics have poor anastomoses if splenic artery is blocked.

Strong anastomoses exist between:
L and R gastroepiploics
L and R gastrics

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23
Q

Portosystemic anastomoses

A

1) Esophagus - Esophageal varices

L gastric vein and esophageal vein

2) Umbilicus - Caput medusae

Paraumbilical veins - small epigastric veins of the anterior abdominal wall

3) Rectum - Anorectal varices (NOT internal hemorrhoids)

Superior rectal vein - middle and inferior rectal veins

Varices of gut, butt, and caput are commonly seen with portal HTN

Treatment with a transjugular intrahepatic portosystemic shunt (TIPS) between the portal vein and hepatic vein relieves portal HTN by shunting blood to the systemic circulation bypassing the liver

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24
Q

Pectinate (Dentate) line

A

Formed where endoderm (hindgut) meets ectoderm

1) Above pectinate line - internal hemorrhoids, adenocarcinoma

Arterial supply from superior rectal artery (branch of IMA)

Venous drainage: superior rectal vein - inferior mesenteric vein - portal system

Internal hemorrhoids receive visceral innervation and are therefore NOT PAINFUL

Lymphatic drainage to internal iliac lymph nodes

2) Below pectinate line - external hemorrhoids, anal fissures, squamous cell carcinoma

Arterial supply from inferior rectal artery (branch of internal pudendal artery)

Venous drainage: inferior rectal vein - internal pudendal vein - internal iliac vein - common iliac vein - IVC

External hemorrhoids receives somatic innervation (inferior rectal branch of pudendal nerve) and are therefore PAINFUL if thrombosed

Lymphatic drainage to superficial inguinal nodes

Anal fissure - tear in the anal mucosa below the Pectinate line: Pain while Pooping; blood on “toilet” Paper. Located Posteriorly since this area is Poorly Perfused

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25
Liver anatomy
Apical surface of hepatocytes faces bile canaliculi. Basolateral surface faces sinusoids Zone 1 - periportal zone - affected 1st by viral hepatitis - ingested toxins (cocaine) Zone 2 - intermediate zone - Yellow Fever Zone 3 - pericentral vein (centrilobar) zone - Affected 1st by ischemia - Contains cytochrome P-450 system - Most sensitive to metabolic toxins - Site of alcoholic hepatitis
26
Femoral region
Organization - Lateral to Medial: Nerve-Artery-Vein-Empty space-Lymphatics You go from lateral to medial to find your NAVEL Femoral triangle - Contains femoral vein, artery, nerve Venous near the penis Femoral sheath - fascial tube 3-4 cm below inguinal ligament. Contains femoral vein, artery, and canal (deep inguinal lymph nodes) but not femoral nerve
27
Biliary structures - stones
Gallstones that reach the confluence of the common bile duct and pancreatic ducts at the ampulla of Vater can block both the common bile and pancreatic ducts (double duct sign), causing both cholangitis and pancreatitis, respectively Tumors that arise in head of pancreas can cause obstruction of common bile duct alone leads to painless jaundice
28
Diaphragmatic hernia
Abdominal structures enter the thorax; may occur due to congenital defect of pleuroperitoneal membrane, or as a result of trauma. Commonly occurs on left side due to relative protection of right hemidiaphragm by liver Most commonly a hiatal hernia, in which stomach herniates upward through the esophageal hiatus of the diaphragm Sliding hiatal hernia - most common. Gastroesophageal junction is displaced upward; "hourglass stomach" Paraesophageal hernia - gastroesophageal junction is usually normal. Fundus protrudes into the thorax
29
Indirect inguinal hernia
Goes through internal (deep) inguinal ring, external (superficial) inguinal ring, and into the scrotum. Enters internal inguinal rung lateral to inferior epigastric artery. Occurs in infants owing to failure of precessus vaginalis to close (can form hydrocele). Much more common in males An indirect inguinal hernia follows the path of descent of the testes. Covered by all 3 layers of spermatic fascia
30
Direct inguinal hernia
Protrudes through the inguinal (Hasselbach) 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 MDs dont LIe Medial to inferior epigastric artery = Direct Lateral to inferior epigastric artery = Indirect
31
Femoral hernia
Protrudes below inguinal ligament through femoral canal below and lateral to pubic tubercle. More common in females Leading cause of bowel incarceration
32
Hasselbach triangle
Inferior epigastric vessels Lateral border of rectus abdominis Inguinal ligament
33
Gastrin
``` 1) Source: G cells (antrum of stomach, duodenum) ``` 2) Action: Increases gastric H secretion (lower pH) Increases growth of gastric mucosa Increases gastric mucosa 3) Regulation: Increased by stomach distention/alkalinization, amino acids, peptides, vagal stimulation Decreased by pH
34
Somatostatin
``` 1) Source: D cells (pancreatic islets, GI mucosa) ``` 2) Action: Decreased gastric acid and pepsinogen secretion Decreased pancreatic and SI fluid secretion Decreased gallbladder contraction Decreased insulin and glucagon release 3) Regulation: Increased by acid Decreased by vagal stimulation 4) Notes: Inhibits secretion of GH, insulin, and other hormones (encourages somato-stasis). Octreotide is an analog used to treat acromegaly, insulinoma, carcinoid syndrome, and variceal bleeding
35
Cholecystokinin
``` 1) Source: I cells (duodenum, jejunum) ``` ``` 2) Action: Increases pancreatic secretion Increases gallbladder contraction Decreases gastric emptying Increases sphincter of Oddi relaxation ``` 3) Regulation: Increased by fatty acids, amino acids 4) Notes: CCK acts on neural muscarinic pathways to cause pancreatic secretion
36
Secretin
``` 1) Source: S cells (duodenum) ``` 2) Action: Increases pancreatic HCO3 secretion Decreases gastric acid secretion Increases bile secretion 3) Regulation: Increased by acid, fatty acids in lumen of duodenum 4) Notes: Increased HCO3 neutralizes gastric acid in duodenum, allowing pancreatic enzymes to function
37
Glucose-dependent insulinotropic peptide (GIP)
``` 1) Source: K cells (duodenum, jejunum) ``` 2) Action: Exocrine - Lowers gastric H secretion Endocrine - Increases insulin release 3) Regulation: Increased by fatty acids, amino acids, oral glucose 4) Notes: Also known as gastric inhibitory peptide Oral glucose load leads to increased insulin compared to IV equivalent due to GIP secretion
38
Motilin
1) Source: Small intestine 2) Action: Produces migrating motor complexes (MMCs) 3) Regulation: Increased in fasting state 4) Notes: Motilin receptor agonists (erythromycin) are used to stimulate intestinal peristalsis
39
Vasoactive intestinal polypeptide (VIP)
1) Source: Parasympathetic ganglia in sphincters, gallbladder, small intestine 2) Action: Increases intestinal water and electrolyte secretion Increases relaxation of intestinal smooth muscle and sphincters 3) Regulation: Increased by distention and vagal stimulation Decreased by adrenergic input 4) Notes: VIPoma - non alpha, non B islet cell pancreatic tumor that secretes VIP Copious Watery Diarrhea, Hypokalemia, and Achlorhydria (WDHA syndrome)
40
Nitric Oxide
1) Source: 2) Action: Increases smooth muscle relaxation, including lower esophageal sphincter (LES) 3) Regulation: 4) Notes: Loss of NO secretion is implicated in increased LES tone of achalasia
41
Intrinsic factor
``` 1) Source: Parietal cells (stomach) ``` 2) Action: Vitamin B12-binding protein (required for B12 uptake in terminal ileum) 3) Regulation: 4) Notes: Autoimmune destruction of parietal cells leads to chronic gastritis and pernicious anemia
42
Gastric acid
``` 1) Source: Parietal cells (stomach) ``` 2) Action: Lowers stomach pH 3) Regulation: Increased by histamine, ACh, gastrin Decreased by somatostatin, GIP, prostaglandin, secretin 4) Notes: Gastrinoma: gastrin-secreting tumor that causes high levels of acid and ulcers refractory to medical therapy (like PPIs)
43
Pepsin
``` 1) Source: Chief cells (stomach) ``` 2) Action: Protein digestion 3) Regulation: Increased by vagal stimulation, local acid 4) Notes: Pepsinogen (inactive) is converted to pepsin (active) in the presence of H
44
HCO3
``` 1) Source: Mucosal cells (stomach, duodenum, salivary glands, pancreas) and Brunner glands (duodenum) ``` 2) Action: Neutralizes acid 3) Regulation: Increased by pancreatic and biliary secretion with secretin 4) Notes: HCO3 is trapped in mucus that covers the gastric epithelium
45
Pancreatic secretions - general
Isotonic fluid; low flow - high Cl, high flow - high HCO3
46
a-amylase
Pancreatic secretion Role: Starch digestion Secreted in active form
47
Lipases
Pancreatic secretion Role: Fat digestion
48
Proteases
Pancreatic secretion Role: Protein digestion Includes trypsin, chymotrypsin, elastase, carboxypeptidases Secreted as proenzymes also known as zymogens
49
Trypsinogen
Pancreatic secretion Role: Converted to active enzyme trypsin - activation of other proenzymes and cleaving of additional trypsinogen molecules into active trypsin (positive feedback loop) Converted to trypsin by enterokinase/enteropeptidase, a brush-border enzyme duodenal and jejunal mucosa
50
Carbohydrate absorption
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 D-xylose absorption test: distinguishes GI mucosal damage from other causes of malabsorption
51
Vitamin/Mineral absorption
Iron - absorbed as Fe in duodenum Folate - absorbed in small bowel B12 - absorbed in terminal ileum, along with bile salts, requires intrinsic factor IFB = Iron First Bro Clinically relevant in patients with small bowel disease or after resection
52
Peyer patches
Unencapsulated lymphoid tissue found in lamina propria and submucosa of ileum. Contain specialized M cells that sample and present antigens to immune cells B cells stimulated in germinal centers of Peyer patches differentiate into IgA-secreting plasma cells, which ultimately reside in lamina propria. IgA receives protective secretory component and is then transported across the epithelium to the gut to deal with intraluminal antigen Think of IgA, the Intra-Gut-Antibody. And always say "secretory IgA"
53
Bile
Composed of bile salts (bile acids conjugated to glycine or taurine, making them water soluble), phospholipids, cholesterol, bilirubin, water, and ions. Cholesterol 7a-hydroxylase catalyzes rate-limiting step of bile synthesis Functions: Digestion and absorption of lipids and fat-soluble vitamins Cholesterol excretion (body's only means of eliminating cholesterol) Antimicrobial activity (via membrane disruption)
54
Bilirubin
Heme is metabolized by heme oxygenase to biliverdin, which is subsequently reduced to bilirubin. Unconjugated bilirubin is removed from blood by liver, conjugated with glucuronate, and excreted in bile Direct bilirubin - conjugated with glucuronic acid; water soluble Indirect bilirubin - unconjugated; water insoluble
55
Salivary gland tumors
Generally benign – in parotid gland 1) Pleomorphic adenoma: (benign mixed tumor) – most common. Presents as painless, mobile mass. Made of chondromyxoid stroma and epithelium and recurs if incompletely excised or ruptured during surgery. 2) Mucoepidermoid carcinoma: most common malignant tumor. Has mucous and Squamous parts. Painless, slow growing mass. 3) Warthin tumor (papillary cystadenoma lymphomatosum): benign cystic tumor with germinal centers
56
Achalasia
(absence of relaxation): Failure of relaxation of LES due to loss of myenteric plexus. High LES resting pressure and uncoordinated peristalsis – progressive dysphagia to solids and liquids (vs obstruction – solid only). Ba swallow shows dilated esophagus with an area of distal stenosis. Associated with higher risk of esophageal squamous cell carcinoma. “Birds beak” on Ba swallow. Secondary achalasia = can come from chagas disease (T. Cruzi infection) or Malignancies (mass effect or paraneoplastic)
57
Boerhaave Symdrome
Esophageal Transmural, usually distal esophageal with pneumomediastinum due to violent retching; surgical emergency
58
Eosinophilic esophagitis
Infiltration of eosinophils in the esophagus in atopic patients. Food allergens - dysphagia, heartburn, strictures. Unresponsive to GERD therapy
59
Esophageal strictures
Associated with lye ingestion and acid reflux
60
Esophageal varices
Dilated submucosal veins in lower 1/3 of esophagus secondary to portal HTN. Common in alcoholics, may be source of upper GI bleeding
61
Esophagitis
Associated with reflux, infection in immunocompromised (Candida: white pseudomembrane, HSV-1: punched-out ulcers, CMV: linear ulcers) or chemical ingestion
62
Gastroesophageal reflux disease
GERD Commonly presents as heartburn and regurgitation upon lying down. May also present with nocturnal cough and dyspnea, adult-onset asthma. Decrease in LES tone
63
Mallory-Weiss syndrome
Mucosal lacerations at the gastroesophageal junction due to severe vomiting. Leads to hematemesis. Usually found in alcoholics and bulimics.
64
Plummer-Vinson Syndrome
Triad of: Dysphagia, Iron deficiency anemia, Esophageal Webs "DIE" May be associated with glossitis. Increased risk of esophageal squamous cell carcinoma (Plumbers DIE)
65
Sclerodermal esophageal dysmotility
Esophageal smooth muscle atrophy leads to lower LES pressure and dysmotility. This causes acid reflux and dysphagia leading to stricture, Barrett esophagus, and aspiration. Part of CREST syndrome
66
Barrett esophagus
Glandular metaplasia - replacement of nonkeratinized stratified squamous epithelium with intestinal epithelium (nonciliated columnar with goblet cells) in distal esophagus. Due to chronic acid reflux (GERD). Associated with esophagitis, esophageal ulcers, and increased risk of esophageal adenocarcinoma
67
Esophageal cancer
Can be squamous cell carcinoma or adenocarcinoma. Typically presents with progressive dysphagia (first solid, then liquids) and weight loss; poor prognosis. Risk factors are AABCDEFFGH ``` Achalasia Alcohol - Squamous Barrett esophagus - adeno Cigarettes - both Diverticula (Zenker) - squamous Esophageal web - squamous Familial Fat (obesity) - adeno GERD - adeno Hot liquids - squamous ``` Worldwide, squamous cell is more common. Adenocarcinoma is most common type in America Squamous cell - upper 2/3 Adenocarcinoma - lower 1/3
68
Acute gastritis (erosive)
Disruption of mucosal barrier leading to inflammation Can be caused by: 1) NSAIDs - lower PGE2 leading to lower gastric mucosa protection 2) Burns (Curling ulcer) - lower plasma volume - sloughing of gastric mucosa 3) Brain injury (Cushing ulcer) - increased vagal stimulation leads to increased ACh which raises H production Especially common among alcoholics and patients taking daily NSAIDs (patients with RA) "Burned by a curling iron" "Always cushion the brain"
69
Chronic gastritis (nonerosive)
1) Type A (fundus/body) - Autoimmune disorder characterized by Autoantibodies to parietal cells, pernicious Anemia, and Achlorhydria. Associated with other autoimmune disorders 2) Type B (antrum) - Most common type. Caused by H Pylori infection. Increased risk of MALT lymphoma A comes before B A = autoimmune = first part of stomach B = bacteria = second part of stomach (antrum)
70
Menetrier Disease
Gastric hyperplasia of mucosa leading to hypertrophied rugae, excess mucus production with resultant protein loss and parietal cell atrophy with decreased acid production. Precancerous. Rugae of stomach are so hypertrophied that they look like brain gyri
71
Stomach cancer
Commonly gastric adenocarcinoma; lymphoma; carcinoid (rare). Early aggressive local spread with node/liver metastases. Often presents with weight loss, early satiety, and in some cases acanthosis nigricans 1) Intestinal - associated with H pylori, dietary nitrosamines (smoked foods), tobacco smoking, achlorhydria, chronic gastritis. Commonly on lesser curvature; looks like ulcer with raised margins 2) Diffuse - not associated with H pylori; signet ring cells (mucin-filled cells with peripheral nuclei); stomach wall grossly thickened and leathery (linitis plastica) Virschow node = involvement of left supraclavicular node by metastasis from stomach Krukenberg tumor = bilateral metastases to ovaries. Abundant mucin-secreting, signet-ring cells Sister Mary Joseph nodule = subcutaneous periumbilical metastasis
72
Gastric vs Duodenal Ulcers in Peptic ulcer disease
1) Gastric Pain - can be greater with meals - weight loss H pylori - 70% Mechanism - decreased mucosal protection against gastric acid Other causes - NSAIDs Risk of carcinoma - increased Other - Biopsy margins to rule out malignancy 2) Duodenal Pain - decreases with meals - weight gain H Pylori - 100% almost Mechanism - Decreased mucosal protection or increased gastric acid secretion Other causes - Zollinger-Ellison Syndrome Risk of carcinoma - generally benign Other - Hypertrophy of Brunner glands
73
Ulcer complications
1) Hemorrhage Gastric, duodenal (posterior > anterior). Ruptured gastric ulcer on the lesser curvature of stomach leads to bleeding from L gastric artery. An ulcer on the posterior wall of duodenum leads to bleeding from gastroduodenal artery 2) Perforation Duodenal (anterior > posterior) May see free air under diaphragm with referred pain to the shoulder via phrenic nerve
74
Malabsorption syndromes - general
Can cause diarrhea, steatorrhea, weight loss, weakness, vitamin and mineral deficiencies ``` Celiac Disease Disaccharidase deficiency Pancreatic insufficiency Tropical sprue Whipple Disease ```
75
Celiac Disease
A malabsorption syndrome Autoimmune-mediated intolerance of gliadin (gluten protein found in wheat) leads to malabsorption and steatorrhea Associated with HLA-DQ2, HLA-DQ8 Also associated with Northern European decent, dermatitis, herpetiformis, lower bone density Findings = anti-endomysial, anti-tissue transglutaminase, and anti-gliadin antibodies; blunting of villi; and lymphocytes in lamina propria. Moderately increased risk of malignancy (T cell Lymphoma) Lower mucosal absorption primarily affects distal duodenum and/or proximal jejunum Tx = gluten-free diet
76
Disaccharidase Deficiency
A malabsorption syndrome 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 (viral enteritis) Lactose intolerance test: (+) for lactase deficiency if administration of lactose produces symptoms and serum glucose rises
77
Pancreatic insufficiency
A malabsorption syndrome Due to cystic fibrosis, obstructing cancer, chronic pancreatitis. Causes malabsorption of fat and fat-soluble vitamins (ADEK) as well as B12 Increased neutral fat in stool D-xylose absorption test - normal urinary excretion in pancreatic insufficiency; lower excretion with intestinal mucosal defects or bacterial overgrowth
78
Tropical sprue
A malabsorption syndrome Similar findings as celiac sprue (affects small bowel), but responds to antibiotics. Cause is unknown, but seen in residents of or recent visitors to tropics
79
Whipple Disease
A malabsorption syndrome Infection with Tropheryma whipplei (gram positive) PAS (+) foamy macrophages in intestinal lamina propria, mesenteric nodes. Cardiac symptoms, Arthralgias, and Neurologic symptoms are common. Most often occurs in older men
80
Crohn Disease
1) location - Any portion of GI tract, usually the terminal ileum and colon. Skip lesions, rectal sparing. 2) Gross morphology - Transmural inflammation - fistulas. Cobblestone mucosa, creeping fat, bowel wall thickening ("string sign" on Ba swallow XR), linear ulcers, fissures 3) Microscopic morphology - Noncaseating granulomas and lymphoid aggregates (Th1 mediated) 4) Complications - Strictures (leading to obstruction), fistulas (including enterovesical fistulae, which can cause recurrent polymicrobial UTIs), perianal disease, malabsorption, nutritional depletion, colorectal cancer, gallstone 5) Intestinal manifestation - Diarrhea that may or may not be bloody 6) Extraintestinal manifestations - Migratory polyarthritis, erythema nodosum, ankylosing spondylitis, pyoderma gangrenosum, aphthous ulcers, uveitis, kidney stones 7) Tx - Corticosteroids, azathioprine, antibiotics (ciprofloxacin, metronidazole), infliximab, adalimumab
81
Ulcerative Colitis
1) location - Colitis = colon inflammation. Continuous colonic lesions, always with rectal involvement 2) Gross morphology - Mucosal and submucosal inflammation only. Friable mucosal pseudopolyps with freely hanging mesentery. Loss of haustra - "lead pipe" on imaging 3) Microscopic morphology - Crypt abscesses and ulcers, bleeding, no granulomas (Th2 mediated) 4) Complications - Malnutrition, sclerosing cholangitis, toxic megacolon, colorectal carcinoma (worse with right sided colitis or pancolitis) 5) Intestinal manifestation - Bloody diarrhea 6) Extraintestinal manifestations - Pyoderma gangrenosum, erythema nodosum, primary sclerosing cholangitis, ankylosing spondylitis, aphthous ulcers, uveitis 7) Tx - 5-aminosalicylic preparations (mesalamine), 6-MP, infliximab, colectomy UC causes ULCCCERS ``` Ulcers Large Intestine Continuous, Colorectal carcinoma, Crypt abscesses Extends proximally Red diarrhea Sclerosing cholangitis ```
82
Irritable Bowel Syndrome
Recurrent abdominal pain associated with at least 2 of the following: Pain improves with defecation Change in stool frequency Change in appearance of stool No structural abnormalities. Most common in middle-aged women. Chronic symptoms. May present with diarrhea, constipation, or alternation symptoms. Pathophysiology is multifaceted. Treat the symptoms
83
Appendicitis
Acute inflammation of the appendix due to obstruction by fecalith (in adults) or lymphoid hyperplasia (in children) Initial diffuse perumbilical pain migrates to McBurnery point (1/3 the distance from right anterior superior iliac spine to umbilicus). Nausea, fever; may perforate - peritonitis; may elicit psoas, obturator, Rovsing sign, guarding and rebound tenderness on exam Ddx = diverticulitis (elderly), ectopic pregnancy (use B-hCG to rule out) Tx = appendectomy
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Diverticulum
Blind pouch protruding from the alimentary tract that communicates with the lumen of the gut. Most diverticula (esophagus, stomach, duodenum, colon) are acquired and are termed "false" in that they lack or have an attenuated muscularis externa. Most often in sigmoid colon "True" diverticulum - all 3 gut wall layers outpouch (Meckel) "False" diverticulum or pseudodiverticulum - only mucosa and submucosa outpouch. Occur especially where vasa recta perforate muscularis externa
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Diverticulosis
Many false diverticula of the colon, commonly sigmoid. Common (in 50% of people > 60) Caused by increased intraluminal pressure and focal weakness in colonic wall. Associated with low-fiber diets. Often asymptomatic or associated with vague discomfort. A common cause of hematochezia. Complications include diverticulitis, fistulas
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Diverticulitis
Inflammation of diverticula classically causing LLQ pain, fever, leukocytosis. May perforate - peritonitis, abscess formation, or bowel stenosis. Give antibiotics May also cause colovesical fistula (fistula with bladder) - pneumaturia Sometimes called "left-sided appendicitis" due to overlapping clinical presentation
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Zenker diverticulum
Pharyngoesophageal FALSE diverticulum herniation of mucosal tissue at Killian triangle between the thyropharyngeal and cricopharyngeal parts of the inferior pharyngeal constrictor Presenting symptoms = dysphagia, obstruction, foul breath from trapped food particles (halitosis) Most common in elderly males
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Meckel diverticulum
TRUE diverticulum. Persistence of the vitelline duct. May contain ectopic acid-secreting gastric mucosa and/or pancreatic tissue. *Most common congenital anomaly of GI tract. Can cause melena, RLQ pain, intussusception, volvulus, or obstruction near terminal ileum. Contrast with omphalomesenteric cyst = cystic dilation of vitelline duct Dx = pertechnetate study for uptake by ectopic gastric mucosa The five 2's 2 inches long 2 feet from ileocecal valve 2% of population Commonly presents in first 2 years of life May have 2 types of epithelia (gastric/pancreatic)
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Malrotation
Anomaly of midgut rotation during fetal development leading to improper positioning of bowel, formation of fibrous bands (Ladd bands) Can lead to volvulus, duodenal obstruction
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Volvulus
Twisting of portion of bowel around its mesentery; can lead to obstruction and infarction. Can occur throughout the GI tract. Midgut volvulus more common in infants and children. Sigmoid volvulus more common in elderly
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Intussusception
Telescoping of proximal bowel segment into distal segment, commonly at ileocecal junction. Compromised blood supply leads to intermittent abdominal pain often with "currant jelly" stools. Unusual in adults (associated with intraluminal mass or tumor that acts as lead point that is pulled into the lumen) Majority of cases occur in children (usually idiopathic; may be associated with recent enteric or respiratory viral infection) Abdominal emergency in early childhood, with bull's eye appearance on ultrasound
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Hirschsprung Disease
Congenital megacolon characterized by lack of ganglion cells/enteric nervous plexuses (Auerbach and Meissner) in segment of colon. Due to failure of neural crest cell migration. Associated with mutations in RET gene presents with bilious emesis, abdominal distention, and failure to pass meconium leading to chronic constipation Normal portion of the colon proximal to the aganglionic segment is dilated, resulting in a "transition zone." Involves rectum. Think of Hirschsprung as a giant spring that has sprung in the colon. Risk higher with Down Syndrome Diagnosed by rectal suction biopsy Tx = resection
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Acute mesenteric ischemic
Critical blockage of intestinal blood flow (often embolic occlusion of SMA) leading to small bowel necrosis causing abdominal pain out of proportion to physical findings May see red "currant jelly" stools
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Adhesion
Fibrous band of scar tissue; commonly forms after surgery; most common cause of small bowel obstruction. Can have well-demarcated necrotic zones
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Angiodysplasia
Tortuous dilation of vessels leads to hematochezia Most often found in cecum, terminal ileum, ascending colon. More common in older patients. Confirmed by angiography
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Duodenal atresia
Causes early bilious vomiting with proximal stomach distention ("double bubble" on XR) bc of failure of small bowel recanalization. Associated with Down Syndrome
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Ileus
Intestinal hypomotility without obstruction leading to constipation and decreased flatus; distended/tympanic abdomen with reduced bowel sounds. Associated with abdominal surgeries, opiates, hypokalemia, sepsis Tx = bowel rest, electrolyte correction, cholinergic drugs (stimulate intestinal motility)
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Ischemic colitis
Reduction in intestinal blood flow causes ischemia. Pain after eating leading weight loss. Commonly occurs at watershed areas (splenic flexure, distal colon) Typically affects elderly
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Meconium ileus
In cystic fibrosis, meconium plug obstructs intestine, preventing stool passage at birth
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Necrotizing enterocolitis
Seen in premature, formula-fed infants with immature immune system Necrosis of intestinal mucosa (primarily colonic) with possible perforation, which can lead to pneumatosis intestinalis, free air in abdomen, portal venous gas
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Colonic polyps
Small growths of tissue within the colon. May be neoplastic or non-neoplastic. Grossly characterized as flat, sessile, or pedunculated (on a stalk) on the basis of protrusion into colonic lumen. Generally classified by histologic type
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Hyperplastic polyps
Non-neoplastic Generally smaller and majority located in rectosigmoid area
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Hamartomatous polyps
Non-neoplastic Solitary lesions do not have a significant risk of malignant transformation. Growths of normal colonic tissue with distorted architecture Associated with Peutz-Jeghers syndrome and juvenile polyposis
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Adenomatous polyps
Neoplastic Via chromosomal instability pathway with mutations in APC and KRAS. Tubular histology has less malignant potential than villous; tubulovillous has intermediate malignant potential
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Serrated polyps
Premalignant Via CpG hypermethylation phenotype pathway with microsatellite instability and mutations in BRAF "saw-tooth" pattern of crypts on biopsy Up to 20% of cases of sporadic CRC
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Familial adenomatous polyposis (FAP)
Autosomal Dom mutation in APC tumor suppressor gene on chromosome 5q. 2 hit hypothesis 100% progresses to CRC unless colon is resected. Thousands of polyps arise starting after puberty; pancolonic; always involves rectum
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Gardner Syndrome
FAP+ osseous and soft tissue tumors, congenital hypertrophy of retinal pigment epithelium, impacted/supernumerary teeth
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Turcot Syndrome
FAP + malignant CNS tumor. "Turcot = Turban"
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Peutz-Jeghers Syndrome
Autosomal Dom syndrome featuring numerous hamartomas throughout GI tract, along with hyperpigmented mouth, lips, hands. genitalia Associated with higher risk of CRC
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Juvenile Polyposis Syndrome
Autosomal Dom syndrome in children (typically younger than 5) featuring numerous hamartomatous polyps in the colon, stomach, small bowel. Associated with higher risk of CRC
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Lynch Syndrome
Previously known as "hereditary nonpolyposis colorectal cancer (HNPCC)" Autosomal Dom mutation of DNA mismatch repair genes with subsequent microsatellite instability 80% progresses to CRC Proximal colon is always involved Associated with endometrial, ovarian, and skin cancers Can be identified clinically in families using 3-2-1 rule 3 relatives with Lynch Syndrome-associated cancers across 2 generations, 1 of whom must be diagnosed before age 50 years old.
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Colorectal cancer
Most patients are over 50. 25% have a family history Adenomatous and serrated polyps, familial cancer syndromes, IBD, tobacco use, diet of processed meat with low fiber Rectosignmoid > ascending > descending Ascending - exophytic mass, iron deficiency anemia, weight loss Descending - infiltrating mass, partial obstruction, colicky pain, hematochezia Rarely, presents with Strep Bovis bacteremia Dx = iron deficiency anemia in males (especially over 50 years old) and postmenopausal female raises suspicion Screen patients > 50 years old with colonoscopy, flexible sigmoidoscopy, or stool occult blood test Apple core lesion seen on Ba enema XR CEA tumor marker good for monitoring recurrence, not useful for screening
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Molecular pathogenesis of colorectal cancer
There are 2 molecular pathways that lead to CRC 1) Microsatellite instability pathway (15%): DNA mismatch repair gene mutation leads to sporadic and Lynch Syndrome. Mutations accumulate, but no defined morphologic correlates 2) APC/B-catenin (chromosomal instability) pathway (85%) leads to sporadic cancer Loss of APC gene puts normal colon at risk. (decreased intercellular adhesion and increased proliferation) KRAS mutation puts the at risk colon into and adenoma (unregulated intracellular signal transduction). Loss of tumor suppressor gene (p53, DCC) turns the adenoma into carcinoma (increased tumorigenesis) "order of events = AK 53"
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Cirrhosis and portal HTN
Cirrhosis - diffuse bridging fibrosis and nodular regeneration via satellite cells disrupts normal architecture of liver; increased risk of hepatocellular carcinoma (HCC) Etiologies: alcohol (60-70% of cases in the US), chronic viral hepatitis, biliary disease, genetic/metabolic disorders Portosystemic shunts partially alleviate portal HTN - esophageal varices, caput medusae, anorectal varices
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Serum markers of liver and pancreas pathology
1) Alkaline phosphatase (ALP) - cholestatic and obstructive hepatobiliary disease, HCC, infiltrative disorders, bone disease 2) Aminotransferases (AST and ALT) (often called "Liver enzymes") - Viral hepatitis (ALT > AST), Alcoholic hepatitis (AST > ALT) 3) Amylase - Acute pancreatitis, mumps 4) Ceruloplasmin - Reduced in Wilson Disease 5) y-glutamyl transpeptidase (GGT) - increased in various liver and biliary diseases (just as ALP can), but NOT in bone disease; associated with alcohol use 6) Lipase - Acute pancreatitis (most specific)
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Reye Syndrome
Rare, often fatal childhood hepatic encephalopathy. Findings: mitochondrial abnormalities, fatty liver (microvascular fatty change), hypoglycemia, vomiting, hepatomegaly, coma. Associated with viral infection (esp VZV and influenza B) that has been treated with aspirin. Mech: Aspirin metabolites lower B-oxidation by reversible inhibition of mitochondrial enzymes. Avoid aspirin in children, except in those with Kawasaki Disease*
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Alcoholic liver disease
1) Hepatic steatosis - Macrovascular fatty change that may be reversible with alcohol cessation 2) Alcoholic hepatitis - Requires sustained, long-term consumption. Swollen and necrotic hepatocytes with neutrophilic infiltration. Mallory bodies (intracytoplasmic eosinophilic inclusions of damaged keratin filaments) Make a toAST with alcohol - AST > ALT (ratio usually > 1.5) 3) Alcoholic cirrhosis - Final and irreversible form. Micronodular, irregularly shrunken liver with "hobnail" appearance. Sclerosis around central vein (zone 3) Manifestations of chronic liver disease (jaundice, hypoalbuminemia)
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Non-alcoholic fatty liver disease
Metabolic syndrome (insulin resistance) leads to fatty infiltration of hepatocytes causing cellular "ballooning" and eventual necrosis. May cause cirrhosis and HCC. Independent of alcohol use ALT > AST
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Hepatic encephalopathy
Cirrhosis leads to portosystemic shunts leading to reduced NH3 metabolism causing neuropsychiatric dysfunction Spectrum from disorientation/asterixis (mild) to difficult arousal or coma (severe). Triggers: Increased NH3 production and absorption (due to dietary protein, GI bleed, constipation, infection) Decreased NH3 removal (due to renal failure, diuretics, bypassed hepatic blood flow post-TIPS) Tx = lactulose (increases NH4 generation) and rifaximin
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Hepatocellular Carcinoma/Hepatoma
Most common primary malignant tumor of liver in adults. Associated with HBV (+/- cirrhosis) and all other causes of cirrhosis (including HCV, alcoholic and non-alcoholic fatty liver disease, autoimmune disease, hemochromatosis, alpha1 antitrypsin deficiency, Wilson Diseaes) and specific carcinogens (aflatoxin from Aspergillus) May lead to Budd-Chiari Syndrome Findings: jaundice, tender hepatomegaly, ascites, polycythemia, anorexia. Spreads hematogenously Dx = increased alpha-fetoprotein; ultrasound or contrast CT/MRI, biopsy
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Cavernous hemangioma
Liver tumor Common, benign liver tumor; typically occurs at age 30-50 years. Biopsy contraindicated bc of risk of hemorrhage
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hepatic adenoma
Liver tumor Rare, benign liver tumor, often related to oral contraceptive or anabolic steroid use; may regress spontaneously or rupture (abdominal pain and shock)
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Angiosarcoma
Liver tumor Malignant tumor of endothelial origin; associated with exposure to arsenic, vinyl chloride
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Metastases
Liver tumor GI malignancies, breast, and lung cancer. Most common overall**
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Budd-Chiari Syndrome
Thrombosis or compression of hepatic veins with centrilobular congestion and necrosis leads to congestive liver disease (hepatomegaly, varices, abdominal pain, eventual liver failure) Absence of JVD Associated with hypercoagulable states, polycythemia vera, postpartum state, HCC May cause nutmeg liver (mottled appearance)
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Alpha1-antitrypsin deficiency
Misfolded gene product protein aggregates in hepatocellular ER leading to cirrhosis with PAS (+) globules in liver. Codominant trait In lungs, lower alpha1 antitrypsin leads to uninhibited elastase in alveoli leading to less elastic tissue causing panacinar emphysema
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Jaundice
Abnormal yellowing of the skin and/or sclera due to bilirubin deposition. Occurs at high bilirubin levels ( > 2.5 mg/dL) in blood secondary to increased production or defective metabolism
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Unconjugated (indirect) hyperbilirubinemia
Hemolytic, physiologic (newborn), Crigler-Najjar, Gilbert Syndrome
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Conjugated (direct) hyperbilirubinemia
Biliary tract obstruction: gallstones, cholangiocarcinoma, pancreatic or liver cancer, liver fluke. Biliary tract disease: Primary sclerosing cholangitis Primary biliary cirrhosis Excretion defect: Dubin-Johnson syndrome, Rotor syndrome
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Mixed (direct and indirect) hyperbilirubinemia
Hepatitis, Cirrhosis
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Physiologic neonatal jaundice
At birth, immature UDP-glucuronosyltransferase leads to unconjugated hyperbilirubinemia causing jaundice/kernicterus (bilirubin deposition in brain, particularly basal ganglia) Tx = phototherapy (converts unconjugated bilirubin to water-soluble form)
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Gilbert Syndrome
Hereditary hyperbilirubinemia Mildly reduced UDP-glucuronosyltransferase conjugation and impaired bilirubin uptake. Asymptomatic or mild jaundice. Increased unconjugated bilirubin without overt hemolysis. Bilirubin increases with fasting and stress Very common. No clinical consequences
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Crigler-Najjar Syndrome, type 1
Hereditary hyperbilirubinemia Absent UDP-glucuronosyltransferase. Presents early in life; patients die within a few years Findings: jaundice, kernicterus (bilirubin deposition in brain), increased unconjugated bilirubin Tx = plasmapheresis and phototherapy Type 2 is less severe and responds to phenobarbital, which increases liver enzyme synthesis
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Dubin-Johnson Syndrome
Hereditary hyperbilirubinemia Conjugated hyperbilirubinemia due to defective liver excretion. Grossly black liver. Benign Rotor Syndrome** is similar but even milder and does not cause black liver
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Wilson Disease (hepatolenticular degeneration)
Inadequate hepatic copper excretion and failure of copper to enter circulation as ceruloplasmin. Leads to copper accumulatio, especially in liver, brain, cornea, kidneys (Fanconi syndrome), and joints Autosomal recessive inheritance (chromosome 13). Copper is normally excreted into bile by hepatocyte copper transporting ATPase (ATP7B gene) Treatment includes chelation with penicillamine or trientine, oral zinc Characterized by: Low Ceruloplasmin, Cirrhosis, Corneal deposits (Kayser-Fleischer rings). Copper accumulation, Carcinoma (HCC) Hemolytic anemia Basal ganglia degeneration (parkinsonian symptoms) Asterixis Dementia, Dyskinesia, Dysarthria Copper is Hella BAD
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Hemochromatosis
Hemosiderosis is the deposition of hemosiderin (iron), which stains blue; hemochromatosis is the disease caused by this iron deposition Classic triad of micronodular Cirrhosis, Diabetes Mellitus and Skin pigmentation - "Bronze Diabetes" results in HF, testicular atrophy, increased risk of HCC Disease may be primary (auto recess) or secondary to chronic transfusion therapy (B-thalassemia major) Increased ferritin Increased Fe Low TIBC All this = high transferrin saturation Can be identified on biopsy with Prussian blue stain total body iron may reach 50g, enough to set off metal detectors at airports Primary hemochromatosis due to C282Y or H63D mutation on HFE gene. Associated with HLA-A3 Iron loss through menstruation slows progression in women Treatment of hereditary hemochromatosis: repeated phlebotomy, chelation with defarasirox, deferoxamine, deferiprone (oral)
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Biliary tract disease - general
May present with pruritus, jaundice, dark urine, light-colored stool, hepatosplenomegaly. Typically with cholestatic pattern of LFTs (increased conjugated bilirubin, increased cholesterol, increased ALP)
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Secondary biliary cirrhosis
Extrahepatic biliary obstruction leads to increased pressure in intrahepatic ducts leading to injury/fibrosis and bile stasis Patients with known obstructive lesions (gallstones, biliary strictures, pancreatic carcinoma) May be complicated by ascending cholangitis
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Primary biliary cirrhosis
Autoimmune reaction leading to lymphocytic infiltrate + granulomas causing destruction of intralobular bile ducts Classically in middle-aged women Anti-mitochondrial antibody (+), including IgM Associated with other autoimmune conditions (CREST, Sjogren syndrome, RA, Celiac)
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Primary sclerosing cholangitis
Unknown cause of concentric "onion skin" bile duct fibrosis causing alternating strictures and dilation with "beading" of intra-and extrahepatic bile ducts on ERCP, magnetic resonance cholangiopancreatography (MRCP). Classically in young men with IBD Hypergammaglobulinemia (IgM). MPO-ANCA/p-ANCA (+) Associated with UC. Can lead to secondary biliary cirrhosis, cholangiocarcinoma
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Gallstones (cholelithiasis)
Increased cholesterol and/or bilirubin, lower bile salts, and gallbladder stasis all cause stones 2 types of stones 1) Cholesterol stones (radiolucent with 10-20% opaque due to calcifications) - 80% of stones. Associated with obesity, Crohn, advanced age, clofibrate, estrogen therapy, multiparity, rapid weight loss, Native American origin 2) Pigment stones (black = radiopaque, Ca bilirubinate, hemolysis; brown = radiolucent, infection) - seen in patients with chronic hemolysis, alcoholic cirrhosis, advanced age, biliary infections, total parenteral nutrition (TPN) Stones most often cause cholecystitis; also ascending cholangitis, acute pancreatitis, bile stasis Can also lead to biliary colic - neurohormonal activation (by CCK after a fatty meal) triggers contraction of gallbladder, forcing a stone into the cystic duct. May present without pain (in diabetes) Can cause fistula between gallbladder and small intestine, leading to air in biliary tree and allowing the passage of gallstones into the intestinal tract. Gallstone may obstruct ileocecal valve leading to gallstone ileus Diagnose with ultrasound. Treat with cholecystectomy if symptomatic ``` Risk factors = 4 F's Female Fat Fertile (pregnant) Forty ``` Charcot triad of cholangitis: Jaundice Fever RUQ pain
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Cholecystitis
Acute or chronic inflammation of gallbladder. Usually from cholelithiasis (gallstones); most commonly blocking the cystic duct leading to secondary infection; rarely ischemia or primary infection (CMV) Murphy sign (+) - inspiratory arrest on RUQ palpation due to pain. Increased ALP if bile duct becomes involved (ascending cholangitis) Diagnose with ultrasound or cholescintigraphy (HIDA, or hepatobiliary iminodiacetic acid scan)
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Porcelain gallbladder
Calcified gallbladder due to chronic cholecystitis; usually found incidentally on imaging Tx = prophylactic cholecystectomy due to high rates of gallbladder carcinoma
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Acute pancreatitis
Autodigestion of pancreas by pancreatic enzymes Causes: idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune disease, Scorpion sting, Hypercalcemia/Hypertriglyceridemia ( > 1000), ERCP, Drugs (sulfa drugs, NRTIs, protease inhibitors) - GET SMASHED Clinical presentation - epigastric abdominal pain radiating to back, anorexia, nausea Labs - high amylase and lipase (higher specificity) Can lead to DIC, ARDS, diffuse fat necrosis, hypocalcemia (ca collects in pancreatic Ca soap deposits), pseudocyst formation, hemorrhage, infection, multiorgan failure Complications - pancreatic pseudocyst (lined by granulation tissue, not epithelium; can rupture and hemorrhage)
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Chronic pancreatitis
Chronic inflammation, atrophy, calcification of the pancreas. Major causes are alcohol abuse and idiopathic Mutations in CFTR (cystic fibrosis) can cause chronic pancreatic insufficiency Can lead to pancreatic insufficiency leading to steatorrhea, fat soluble vitamin deficiency, diabetes mellitus Amylase and lipase may or may not be elevated (almost always elevated in acute pancreatitis)
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Pancreatic adenocarcinoma
Average survival - 1 year after diagnosis. Very aggressive tumor arising from pancreatic ducts (disorganized glandular structure with cellular infiltration); already metastasized at presentation; tumors more common in pancreatic head (leading to obstructive jaundice). Associated with CA 19-9 tumor marker (also CEA, less specific) ``` Risk factors: Tobacco use Chronic pancreatitis (especially more than 20 years) Diabetes Age > 50 Jewish and black males ``` Often presents with: Abdominal pain radiating to back Weight loss (due to malabsorption and anorexia) Migratory thrombophlebitis - redness and tenderness on palpation of extremities (Trousseau Syndrome) Obstructive jaundice with palpable, nontender gallbladder (Courvoisier sign) Tx = Whipple procedure, chemotherapy, radiation therapy