GI Flashcards
Anterior 2/3 of tongue
a. Origin
b. Taste
c. Sensation
d. Motor
a. 1st arch
b. Facial nerve (7)
c. CN V3
d. CN XII (12)
Posterior 1/3
a. origin
b. taste
c. sensation
d. motor
a. 3rd and 4th arch
b. Glossopharyngeal (9)
c. CN 9
d. CN X11 (12)
Causes of Glossitis
B12, Niacin, Riboflavin deficiency
Oral hairy leukoplakia
white patch on tongue caused by EBV (in immunocompromised patients)
Oral thrush
White spot on buccal mucosa/tongue
Caused by candida albicans
Apthous ulcers causes
Canker sore
Citrus fruits, B12 deficiency
Parotid secretions
Serous secretions
Submandibular gland
Serous AND mucinous secretions
Sublingual gland
Mucinous secretions
Secretions in sympathetic vs. parasympathetic
Sympathetic - very thick secretion by superior cervical ganglion
Parasympathetic - serous secretion by CN 5 and 7
Xerostomia
Sjogrens
Antihistamines
Anticholinergic
Sialolithiasis
Stone in salivary gland duct that prevents release of saliva
Most common place of salivary gland
parotid
Most common tumor of salivary gland
Pleomorphic adenoma
2nd most common benign tumor of salivary gland
Warthin tumor
Most common malignant salivary tumor
Mucoepidermoid tumor
Sublingual gland - benign vs. malignant tumor
> 70% change it is malignant
a. foregut
b. midgut
c. hindgut
a. pharynx to duodenum (Celiac artery)
b. duodenum to proximal 2/3 of transverse colon (SMA)
c. distal 1/3 transverse colon to anal canal above pectinate line (IMA)
Developmental defects of anterior abdominal wall due to failure of:
a. rostral fold closure
b. lateral fold closure
c. caudal fold closure
a. sternal defecs
b. omphalocele, gastroschisis
c. bladder exstrophy
Extrusion of abdominal contents through abdominal folds, NOT covered by peritoneum
Gastroschisis
Persistence of herniation of abdominal contents into umbilical cord, SEALED by peritoneum
Omphalocele
Cause of duodenal atresia
Failure to recanalize (trisomy 21)
Cause of jejunal, ileal, colonic atresia
Due to vascular accident
Drooling, choking, vomiting with first feeding
Esophageal atresia with distal tracheoesophageal fistula
Gasless abdomen on CXR
Pure esophageal atresia
Palpable olive mass in epigastric region and NONbilious projectile vomiting in 2-6 week old infant. Cause? Result?
Pyloric stenosis from hypertrophy of pylorus
Results in hypokalemic, hypochloremic metabolic alkalosis
What tissues are they derived from?
a. Pancreas
b. Spleen
a. Endoderm (from hepatic diverticulum)
b. Mesoderm (still supplied by foregut)
a. Cause of annular pancreas
b. Cause of pancreas divusm
a. Abnormal migration; ventral pancreatic bud encircles 2nd part of duodenum –> bilious vomiting
b. Ventral and dorsal pancreatic parts fail to fuse; mostly asymptomatic –> may cause pancreatitis, abdominal pain
Retroperitoneal structures
Suprarenal glands (adrenals) Aorta and IVC Duodenum (2nd through 4th parts) Pancreas (except tail) Ureters Colon (ascending, descending) Kidneys Esophagus (thoracic portion) Rectum
Contents of Hepatoduodenal ligament
Portal vein
Proper Hepatic artery
Common bile duct
Falciform ligament connects:
liver to anterior abdominal wall
Gastrohepatic ligament connects and contains what?
Connects liver to lesser curvature of stomach; contains gastric arteries
Layers of gut wall (inside to outside)
Mucosa - epithelium, lamina propria, muscularis mucosa
Submucosa - Submucosal nerve plexus (Meissner); secrets fluid
Muscularis externa - includes Myenteric nerve plexus (Auerbach), motility
Serosa - (when intraperitoneal), Adventitia (when retroperitoneal)
Erosions affect which layers of gut wall?
Ulcers affect which layers of gut wall?
Erosions are MUCOSA ONLY
Ulcers extend into submucosa, inner or outer muscular layer
Digestive tract histology
a. Esophagus
b. Stomach
c. Duodenum
d. Jejunum
e. Ileum
f. Colon
a. Nonkeratinized stratified squamous epithelium
b. Gastric glands
c. Villi and microvilli increase absorptive surface; brunner glands (secrete bicarbonate) and crypts of Lieberkuhn
d. Plicae circulares and crypts of Lieberkuhn
e. Peyer patches, plicae circulares, crypsts of Lieberkuhn
f. Colon has crypts of Liberkuhn but no villi; abundant goblet cells
Branches of celiac trunk
Common hepatic artery
Splenic artery
Left gastric artery
Branches of common hepatic artery
Proper hepatic artery
Right gastric artery
Gastroduodenal artery
Branches of gastroduodenal artery
Anterior superior pancreaticoduodenal artery
Right gastro-omental (epiploic) artery
Anastomoses of celiac trunk
Right gastro-omental and left gastro-omental (epiploic)
Left and right gastrics
Portosystemic anastomoses (sign and vessels involved)
a. Esophagus
b. Umbilicus
c. Rectum
a. Esophageal varices; left gastric –> esophageal
b. Caput medusae; paraumbilical –> small epigastric veins of anterior abdominal wall
c. Anorectal varices; superior rectal –> middle and inferior rectal
What is Pectinate line?
Pathology above pectinate line?
Pathology below pectinate line?
- Where endoderm (hindgut) meets ectoderm
- Above the pectinate line –> internal hemorrhoids (NOT PAINFUL, visceral innervation), adenocarcinoma
- Below pectinate line –> external hemorrhoids (PAINDUL, pudendal nerve innervation), squamous cell carcinoma
Arterial supply and venous drainage above pectinate line
Lymphatic drainage
- arterial supply - Superior rectal artery from IMA
- venous drainage - superior rectal vein –> inferior mesenteric vein –> portal system
- lymphatic drainage - internal iliac lymph nodes
Arterial supply, venous drainage and lymphatic drainage below pectinate line
- arterial supply: inferior rectal artery (branch of internal pudendal artery)
- venous drainage: inferior rectal vein –> internal iliac vein –> common iliac vein –> IVC
- lymphatic drainage: superficial inguinal nodes
Zones of liver and what they are susceptible to
- Zone 1: periportal zone; affected first by viral hepatitis; ingested toxins
- Zone 2: intermediate; yellow fever
- Zone 3: pericentral vein zone; affected 1st by ischemia, contains p450 system, most sensitive to metabolic toxins, site of alcoholic hepatitis
a. Sliding hiatal hernia
b. Paraesophageal hernia
a. most common, gastroesophageal junction is displaced upward (hourglass stomach)
b. gastroesophageal junction is normal, funds protrudes into the thorax
Common location of diaphragmatic hernia
Left side due to relative protection of right hemidiaphragm by liver
Indirect vs. Direct inguinal hernia
a. site of protrusion
b. lower border
c. medial border
d. lateral border
a. indirect = deep inguinal ring, direct = Hesselbach triangle
b. BOTH = inguinal ligament
c. indirect = inferior epigastric vessels, direct = rectus abdominis muscle
d. indirect = XXX, direct = inferior epigastric vessels
Femoral hernia
Protrudes below inguinal ligament through femoral canal below and lateral to pubic tubercle; more common in females
Which kind of hernia most commonly becomes incarcerated and descends into scrotum?
Indirect inguinal hernia
What do these cells secrete?
a. G cells
b. D cells
c. I cells
d. S cells
e. K cells
a. Gastrin
b. Somatostatin
c. CCK
d. Secretin
e. Glucose dependent insulinotropic peptide
a. Regulation of Gastrin
b. Actions of Gastrin
a. Increased by stomach distension/alkalinization/amino acids/vagal stimulation/peptides and decreased by pH
When would gastrin levels be increased?
In ZE, in chronic atrophic gastritis (H. pylori) and in chronic PPI use
a. Regulation of Somatostatin
b. Actions of Somatostatin
a. Increased by acid, decreased by vagal stimulation
b. It decreases gastric acid and pepsinogen secretion, decreases pancreatic and small intestine fluid secretion, decreases gallbladder contraction, decreases insulin and glucagon release and decreases splanchnic blood flow
Uses of Somatostatin analog (Octreotide)
Variceal bleeding
Acromegaly
Insulinoma
Carcinoid syndrome
a. Regulation of CCK
b. Actions of CCK
a. Increased by fatty acids and amino acids
b. Increases pancreatic secretion and gallbladder contraction, decreases gastric emptying and causes relaxation of Sphincter of Oddi
a. Regulation of Secretin
b. Actions of Secretin
a. Increased by acid and fatty acids in duodenum
b. Causes increased pancreatic bicarbonate secretion and increased bile secretion, causes decreased gastric acid secretion
a. Regulation of GIP
b. Actions of GIP
a. Increased by fatty acids, amino acids and ORAL glucose
b. Exocrine: decreased gastric H+ secretion, Endocrine: Increased insulin release
a. Regulation of Motilin
b. Actions of Motilin
a. Increased in fasting state
b. Produces migratory motor complexes (motilin receptor agonists are used to stimulate intestinal peristalsis - Erythromycin)
a. Regulation of VIP (vasoactive intestinal peptide)
b. Actions of VIP
a. Increased by distension and vagal stimulation, Decreased by adrenergic input
b. Increases intestinal water and electrolyte secretion, increases relaxation of intestinal smooth muscle and sphincters
VIPoma
Pancreatic tumor that secretes VIP
Causes copious watery diarrhea, hypokalemia and achlorhydria
Source and action of:
a. Intrinsic factor
b. Gastric acid
c. Pepsin
d. HCO3
a. Parietal cells –> binds Vitamin B12 for uptake in ileum
b. Parietal cells –> decrease stomach pH
c. Chief cells –> protein digestion
d. Mucosal cells and Brunner glands –> neutralizes acid
Regulation of:
a. Intrinsic factor
b. Gastric acid
c. Pepsin
d. HCO3
a. —-
b. Increased by histamine, Ach and gastrin; decreased by Somatostatin, GIP, prostaglandin and secretin
c. Increased by vagal stimulation and local acid
d. Increased by pancreatic and biliary secretion with secretin
How does Gastrin increase acid production?
It causes increased acid secretion primarily through its effects on ECL cells leading to histamine release (rather than direct effect on parietal cells)
Intracellular signaling of: (all on parietal cells)
a. Ach acting on M3 receptor (vagus)
b. Gastrin acting on CCK receptor
c. Histamine acting on H2 receptor
d. Prostaglandins on parietal cell
e. Somatostatin on parietal cell
a. Gq –> IP3/Calcium –> activates H+/K+ ATPase (proton pump)
b. Gq –> IP3/Calcium –> activates proton pump (more importantly it activates ECL cells)
c. Gs –> increases cAMP –> activates proton pump
d. Gi –> decreases cAMP –> inhibits proton pump
e. Gi –> decreases cAMP –> inhibits proton pump
Carbohydrate absorption
ONLY monosaccharides are absorbed by enterocytes
Glucose and galactose taken up by SGLT1 (Na dependent)
Fructose taken up by facilitated diffusion by GLUT-5
All transported to blood but GLUT2 transporter
What is the D-xylose absorption test?
It distinguishes GI mucosal damage from other causes of malabsorption
Where are they absorbed?
a. Iron
b. Folate
c. Vitamin B12
a. As Fe 2+ in duodenum
b. In small bowel
c. In terminal ileum (requires intrinsic factor)
What are 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
Rate limiting step of bile synthesis
Cholesterol 7 alpha hydroxylase
Excretion of bilirubin
- Conjugated bilirubin made into Urobilinogen by gut bacteria
- Urobilinogen excreted in feces as Stercobilin or enters Enterohepatic circulation and goes to liver OR kidney
- Urobilinogen that goes to Kidney is excreted in urine as Urobilin (yellow) 10%
- Urobilinogen that goes to Liver (90%) is used again
a. Cause of Achalasia
b. Presentation
c. Imaging findings
d. Complications/Associations
a. LES fails to relax due to loss of myenteric Auerbach plexus –> high LES resting pressure and uncoordinated peristalsis (Secondary achalasia could be due to Chagas disease or malignancy)
b. Progressive dysphagia to solids AND liquids
c. Barium swallow shows bird’s beak (dilated esophagus with area of distal stenosis)
d. Increased risk of esophageal squamous cell carcinoma
Boerhaave syndrome
Rupture of esophagus –> Transmural, usually distal esophageal with pneumomediastinum due to violent retching
Surgical EMERGENCY
Infiltration of eosinophils in the esophagus in atopic patients
Eosinophilic esophagitis; causes dysphagia, heartburn, strictures
Lye ingestion and acid reflux association
Esophageal stricture
Associated with reflux, infection in immunocompromised or chemical ingestion
a. white pseudomembrane, hyphae
b. punched-out ulcers
c. Linear ulcers with clear perinuclear halo in cells
Esophagitis
a. Candida
b. HSV-1
c. CMV
Dysphagia, Iron deficiency anemia, Esophageal webs, Glossitis –> increases risk of what?
Plummer Vinson syndrome
a. Increases risk of esophageal squamous cell carcinoma
Esophagus association with CREST syndrome
Esophageal dysmotility from smooth muscle atrophy –> decreased LES pressure –> acid reflux and dysphagia
Metaplasia seen in Barrett esophagus
Risk of what kind of cancer?
Replacement of nonkeratinized stratified squamous epithelium with intestinal epithelium (non-ciliated columnar with goblet cells)
Risk of esophageal adenocarcinoma
Risk factors for
a. Esophageal Adenocarcinoma
b. Esophageal Squamous cell carcinoma
c. Both
a. Barrett esophagus, Obesity, GERD, Caucasian
b. Alcohol, Diverticula, Esophageal web, Hot liquids, African americans
c. Cigarettes
Causes of acute gastritis
- NSAIDs –> decreased PGE2 –> decreased gastric mucosa protection
- Burns (Curling ulcer) –> decreased plasma volume –> sloughing of gastric mucosa
- Brain injury (Cushing ulcer) –> increased vagal stimulation –> increased Ach –> increased H+ production
Chronic gastritis causes
- Type A (fundus/body) –> Autoimmune destruction with auto Abs to parietal cells –> pernicious anemia, Achlorhydria
- Type B (antrum) –> Most common type; caused by H. pylori infection
Type B chronic gastritis increases risk of what?
MALT lymphoma
Gastric hyperplasia of mucosa?
What does it cause?
Menetrier disease (protein losing gastroenteropathy) Hypertrophied rugae, excess mucus production with resultant loss of protein and parietal cell atrophy with decreased acid production
Acanthosis nigricans, weight loss, early satiety
Gastric adenocarcinoma
Types of gastric adenocarcinoma
- Intestinal - associated with H. pylori, dietary nitrosamines, tobacco, achlorhydria, chronic gastritis
2 Diffuse - NOT associated with H. pylori; Signet ring cells seen; stomach all is grossly thickened and leathery (linitis plastica)
Linitis plastica
Seen in diffuse gastric adenocarcinoma
Stomach wall looks leathery and thickened
Signet ring cells
Munin-Filled cells with peripheral nuclei - seen in diffuse gastric adenocarcinoma
Involvement of left supraclavicular node by metastasis from stomach
Virchow node
Bilateral gastric adenocarcinoma metastases to ovaries
Krukenberg tumor
Subcutaneous periumbilical metastasis of gastric adenocarcinoma
Sister Mary Joseph nodule
Compare:
a. Gastric ulcer
b. Peptic ulcer
a. Pain greater with meals (weight loss), H. pylori in 70%, from decreased mucosal protection against gastric acid, also caused by NSAIDs, increased risk of carcinoma
b. Pain decreases with meals (weight gain), H. pylori in 100%, from decreased mucosal production or increased gastric acid secretion, associated with ZE, generally benign
H. pylori treatment
PPI + Clarithromycin + Amoxicillin
PPI + Bismuth + Metronidazole + Tetracycline
Complications of ulcers
- Hemorrhage - generally posterior;
2. Perforation - generally anterior; may see free air under diaphragm with referred pain to shoulder via phrenic nerve
Blunting of villi, Lymphocytes in lamina propria
Celiac disease
Risk of malignancy in Celiac disease?
Increased risk of T cell lymphoma
Histology in Lactase deficiency
Normal appearing villi
Cause of self limiting lactase deficiency
Viral enteritis (lactase is at tips of intestinal villi)
Causes of pancreatic insufficiency
Results of pancreatic insufficiency
CF, Obstructing cancer, Chronic pancreatitis
Malabsorption of fat (steatorrhea) and fat soluble vitamins (A, D, E, K)
CF effects on pancreas
Decreases secretion of fluid into pancreatic ducts in CF –> enzymes accumulate in ducts and can digest pancreas –> cause pancreatic insufficiency
Difference between tropical sprue and Celiac disease?
Tropical sprue has similar findings to Celiac but it RESPONDS to antibiotics; seen in residents or visitors of Tropics
PAS + foamy macrophages in lamina propria
Symptoms?
Whipple disease (Tropheryma whipplei, gram positive) Cardiac symptoms, Arthralgias, Neurologic symptoms, Hyperpigmentation, Weight loss, Lymphadenopathy
Crohn’s
a. Location
b. Gross morphology
c. Histology
d. Complications
e. Intestinal manifestation
f. Extraintestinal manifestatin
g. Treatment
a. Any portion of GI tract, usually the terminal ileum and colon; skip lesions and rectal sparing
b. Transmural inflammation –> fistulas; cobblestone mucosa, creeping fat, bowel wall thickening, linear ulcers, fissures (String sign on barium swallow)
c. Non-caseating granulomas and lymphoid aggregates (TH1)
d. Strictures (obstruction), fistulas, perianal disease, malabsorption, nutritional depletion, colorectal cancer, gallstones
e. Diarrhea (may or may not be bloody)
f. Migratory polyarthritis, erythema nodosum, ankylosing spondylitis, pyoderma gangrenosum, apthous ulcers, uveitis, kidney stones
g. Corticosteroids, Azathioprine, ABx, Infliximab, Adalimumab
Ulcerative colitis
a. Location
b. Gross morphology
c. Histology
d. Complications
e. Intestinal manifestation
f. Extra-intestinal manifestation
g. Treatment
a. Colon inflammation, continuous, always with rectal involvement
b. Mucosal and submucosal inflammation ONLY, friable musocal pseudopolyps; loss of haustra (lead pipe appearance)
c. Crypt abscesses and ulcers; bleeding, no granulomas (TH2)
d. Malnutrition, sclerosing cholangitis, toxic megacolon, colorectal carcinoma
e. Bloody diarrhea
f. Pyoderma gangrenosum, erythema nodosum, sclerosing cholangitis, ankylosing spondylitis, aphthous ulcers, uveitis
g. 5-aminosalicylic preparations, 6 mercaptopurine, Infliximab, Colectomy
Ulcerative colitis (ULCCCERS)
Ulcers Large intestine Continous, Colorectal carcinoma, Crypt abscesses Extends proximally Red diarrhea Sclerosing cholangitis
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
True vs. False Diverticula
True = all 3 gut layers out pouch False = only mucosa and submucosa out pouch (occur especially where vasa recta perforate muscular externa)
Most common location of diverticula
Sigmoid colon
Diverticulosis
- Cause
- Symptoms
- Associations
Many false diverticula of colon (sigmoid usually)
- Increased intraluminal pressure and focal weakness in colonic wall
- Vague discomfort, Hematochezia
- Low fiber diets, Diverticulitis, fistulas
Diverticulitis
-Complications
Inflammation of diverticular causing LLQ pain, fever, leukocytosis
-May perforate –> peritonitis, abscess formation, bowel stenosis or cause colovesical fistula
Caused by CF and Hirschsprung
Meconium ileus
Common in post op
Intestinal ileus
Currant jelly stools
Intussuception
Virus associated with intussuception
Adenovirus
Cause of Hirschsprung disease
Failure of neural crest cell migration; associated with mutations in RET gene
Pain out of proportion to physical findings
Acute mesenteric ischemia, ischemic colitis
Tortuous dilation of vessels causing hematochezia
Angiodysplasia; seen more in elderly; most often in cecum, terminal ileum and ascending colon
Double bubble on X ray
Duodenal atresia (proximal stomach distension)
Intestinal hypomotility WITHOUT obstruction
Associations
Ileus
Associated with abdominal surgeries, opiates, hypokalemia, sepsis
Necrotizing enterocolitis
Seen in premature, formula-fed infants with immature immune system –> causes necrosis of intestinal mucosa with possible perforation
Characteristics of polyps:
a. Hyperplastic
b. Hamartomatous
c. Adenomatous
d. Serrated
a. NON neoplastic; smaller and majority in rectosigmoid
b. NON neoplastic; solitary lesions do not have significant risk of malignant transformation; NORMAL colonic tissue with distorted architecture (Peutz Jeghers and juvenile polyposis)
c. Neoplastic; mutations in APC or KRAS via chromosomal instability pathway - Tubular histology has LESS malignant potential than villous
d. Premalignant; via CpG hypermethylation phenotype pathway with micro satellite instability and mutations in BRAF (Saw tooth pattern)
a. AD mutation of APC tumor suppressor gene on chromosome 5q
b. FAP + malignant CNS tumor
c. FAP + osseous and soft tissue tumor, congenital hypertrophy of retinal pigment epithelium, impacted teeth, lipomas
d. AD syndrome featuring hamartomas throughout GI tract, hyper pigmented mouth/lips/hands/genitalia; associated with increased risk of small bowel, colorectal, stomach, breast and pancreatic cancers
e. AD syndrome in children featuring numerous hamartomatous polyps in the colon, stomach, small bowel; associated with increased risk of CRC
a. Familial adenomatous polyposis
b. Turcot syndrome
c. Gardner syndrome
d. Peutz Jeghers syndrome
e. Juvenile polyposis syndrome
AD mutation in DNA mismatch repair genes with subsequent micro satellite instability –> 80% progress to CRC. Proximal colon always involved. Associated with enodmetrial, ovarian and skin cancers
Lynch syndrome
Risk factors for colorectal cancer
Adenomatous and serrated polyps, familial cancer syndromes, IBD, tobacco use, diet of processes meat with low fiber
Presentation of colorectal cancer (depending on location)
Ascending: exophytic mass, iron deficiency anemia, weight loss
Descending: infiltrating mass, partial obstruction, colicky pain, hematochezia
Bacteria associated with colorectal cancer
Streptococcus bovis (Group D Strep - growth in bile, NOT in NaCl)
Apple core lesion on barium enema x-ray
Colorectal cancer
CEA tumor marker
Good for monitoring recurrence of colorectal cancer
NOT good for screening
2 molecular pathways that lead to colorectal cancer
- Microsatellite instability pathway (15%): DNA mismatch repair gene mutations –> Lynch syndrome
- APC/B-catenin (chromosomal instability) (85%) –> sporadic cancer
Relationship of aspirin and colon adenocarcinoma
Increased COX2 is linked to colon adenocarcinoma
Aspirin may decreased adematous polyp formation
Histology of liver cirrhosis
Diffuse bridging fibrosis and nodular regeneration via stellate cells
AST > ALT
Alcoholic hepatitis
ALT > AST
Viral hepatitis
gamma glutamyl transpeptidase
Increased in various liver and biliary diseases (NOT elevated in bone disease like ALP)
Most specific marker for acute pancreatitis
Lipase
Findings in Reye syndrome
Mitochondrial abnormalities Fatty liver (microvesciular fatty change) Hypoglycemia Vomiting Hepatomegaly Coma
Associations with Reye syndrome
Viral infection that was treated with Aspirin- especially VZV and influenza B
Mechanism of Reye syndrome
Aspirin metabolites decrease Beta oxidation by reversible inhibition of mitochondrial enzymes
Macrovesicular fatty liver change
Hepatic steatosis (Microvesicular = Reye syndrome)
Swollen and necrotic hepatocytes with neutrophilic infiltration
Alcoholic hepatitis
Intracytoplasmic eosinophilic inclusions of damaged keratin filaments
Mallory bodies - seen in alcoholic hepatitis
Micro nodular irregularly shrunken liver with hobnail appearance; sclerosis around central vein (zone III)
Alcoholic cirrhosis
Fatty infiltration of hepatocytes –> cellular ballooning and eventual necrosis
Non-alcoholic fatty liver disease
Cause of hepatic encephalopathy
Cirrhosis –> portosystemic shunts –> decreased NH3 metabolism –> neuropsych dysfunction
Triggers of hepatic encephalopathy
- Increased NH3 production and absorption (dietary protein, GI bleed, constipation, infection)
- Decreased NH3 removal (renal failure, diuretics)
Balloon degeneration (hepatocyte swelling), mononuclear cell infiltration, councilman bodies
Viral hepatitis
Aflatoxin from Aspergillus
Hepatocellular carcinoma
Tumor marker of Hepatocellular carcinoma
Increased alpha fetoprotein
Benign liver tumor (collection of dilated blood vessels) that occurs at age 30-50; biopsy is C/I because of risk of hemorrhage
Cavernous hemangioma
Rare, benign liver tumor related to oral contraceptive or anabolic steroid use
Hepatic adenoma (resect if > 5 cm)
Malignant liver tumor of endothelial origin
Associations
Angiosarcoma
Associated with arsenic, vinyl chloride
Nutmeg liver with absence of JVD
Budd Chiari syndrome (thrombosis or compression of hepatic veins)
Budd Chiari associations
Hyper coagulable states
Polycythemia vera
Postpartum state
HCC
PAS+ globules in liver, Autosomal Recessive inheritance
Alpha 1 antitrypsin deficiency
Grossly black liver
Conjugated hyperbilirubinemia
Dubin Johnson syndrome - caused by defective liver excretion
Wilson disease characteristics
Decreased Ceruloplasmin Cirrhosis Corneal deposits (Kayser Fleischer rings) Copper accumulation Carcinoma Hemolytic anemia Basal ganglia degeneration (Parkinson symptoms) Asterixis Dementia, Dyskinesia, Dysarthria
Wilson disease defect
Autosomal recessive (chr 13); defect in hepatocyte copper transporting ATPase (ATP7B gene)
Defect causing primary Hematochromatosis
C282Y or H63D mutation on HFE gene
Associated with HLA-A3
Biliary tract disease –> lymphocytic infiltrate + granulomas –> destruction of intralobular bile ducts
Primary Biliary Cirrhosis
Features of Primary Biliary Cirrhosis
Anti-mitochondrial antibody
Other autoimmune conditions (CREST, Sjogren, RA, Celiac)
Onion skin bile duct fibrosis –> beading of intra and extra hepatic bile ducts on ERCP
Primary sclerosing cholangitis
Features of Primary Sclerosing Cholangitis
Hypergammaglobulinemia (IgM)
p-ANCA
Ulcerative colitis
Associations of cholesterol stones
Obesity, Crohn disease, advanced age, clofibrate, estrogen therapy, multiparty, rapid weight loss, Native American origin
Imaging of:
a. Cholesterol stones
b. Pigment stones
a. Radiolucent with 10-20% opaque because of calcifications
b. Black = adiopaque, Calcium bilirubinate, hemolysis; Brown = radiolucent, infection
Associations of pigment stones
Patients with chronic hemolysis, alcoholic cirrhosis, advanced age, biliary infections, total parenteral nutrition
Triad of Cholangitis
Fever
RUQ pain
Jaundice
(Pentad = plus hypotension and altered mental status)
Porcelain gallbladder
Calcified gallbladder due to chronic cholecystitis; usually found incidentally on imaging
CA 19-9 Tumor marker
Pancreatic adenocarcinoma
Risk factors for pancreatic adenocarcinoma
Tobacco use Chronic pancreatitis Diabetes Age > 50 Jewish and African-Americal males
Trousseau syndrome
Migratory thrombophlebitis (redness and tenderness on palpation of extremities) Seen with pancreatic adenocarcinoma
