Osmosis High-Yield Notes Gastrointestinal Pathology PDF

Title Osmosis High-Yield Notes Gastrointestinal Pathology
Course Medicine
Institution Baylor College of Medicine
Pages 174
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NOTES

NOTES BILIARY TRACT DISEASES GENERALLY, WHAT ARE THEY? PATHOLOGY & CAUSES ƒ Diverse spectrum of diseases affecting biliary system (gallbladder, bile ducts, liver) ƒ Bile stored in gallbladder ĺ stasis/chemical constituents change ĺ precipitate to solid stone ĺ travel down biliary tract ĺ obstruction ĺ decreased bile drainage ĺ symptoms

SIGNS & SYMPTOMS ƒ Symptoms vary, based on location Ɠ ¡îĿŠɈŏîƭŠēĿČĚɈĿŠIJĚČƥĿūŠɈĿŠǷîƥūƑNj response, sepsis ƒ Right upper quadrant (RUQ) epigastric pain ƒ Jaundice ƒ Nausea, vomiting ƒ Fever, chills ĺ sepsis

Magnetic resonance cholangiopancreatography (MRCP) ƒ MRI for detailed images of hepatobiliary, pancreatic systems Endoscopic retrograde cholangiopancreatography (ERCP) ƒ Down esophagus, stomach, duodenum, ducts ĺ contrast medium injected into ducts ĺ X-ray shows narrow areas/ blockages Ɠ Complications: pancreatitis (most common); intraluminal/intraductal bleeding, hematomas; perforation; infection (cholangitis, cholecystitis); cardiopulmonary complications (cardiac arrhythmia, hypoxemia, aspiration)

LAB RESULTS ƒ See table

TREATMENT DIAGNOSIS DIAGNOSTIC IMAGING

MEDICATIONS ƒ Antibiotics

CT scan/ultrasound ƒ Locations of stones, gallbladder wall ƥĺĿČŒĚŠĿŠijɓĿŠǷîƥĿūŠ

SURGERY

X-ray ƒ Pigmented gallbladder stones (radiopaque)

OTHER INTERVENTIONS

194 OSMOSIS.ORG

ƒ Cholecystectomy

ƒ Sepsis management, biliary drainage, ERCP

Chapter 28 Biliary Tract Diseases

ASCENDING CHOLANGITIS osms.it/ascending-cholangitis PATHOLOGY & CAUSES ƒ Acute infection of bile duct caused by intestinal bacteria ascending from duodenum ƒ Bacterial infection of bile duct superimposed on obstruction of biliary tree; due to choledocholithiasis ƒ Gallstones form in gallbladder ĺ slip out ĺ travel through cystic bile duct, lodge in common bile duct ĺ obstruction of ŠūƑŞîŕċĿŕĚǷūDžĺ bacteria ascend from duodenum to bile duct ĺ infect stagnant bile, surrounding tissue

ƒ Common bacteria: E. coli, Klebsiella, Enterobacter, Enterococcus ƒ Medical emergency

RISK FACTORS ƒ Gallstones (most common) ƒ Stenosis of bile duct due to neoplasm/injury from laparoscopic procedure

OSMOSIS.ORG 195

COMPLICATIONS

LAB RESULTS

ƒ Sepsis, septic shock Ɠ High pressure on bile duct ĺ obstruction ĺ cells lining ducts widen ĺ bacteria, bile enter bloodstream ƒ Multiorgan failure

ƒ Assess infection, jaundice Ɠ Increased WBC Ɠ Increased serum C-reactive protein (CRP) Ɠ Elevated LFTs: ALP, GGT, ALT, AST

SIGNS & SYMPTOMS ƒ Charcot’s triad Ɠ RUQ pain, jaundice, fever/chills ƒ Reynold’s pentad Ɠ Charcot’s triad + hypotension/shock, altered consciousness Ɠ ƙƙūČĿîƥĚēDžĿƥĺƙĿijŠĿǶČîŠƥŞūƑċĿēĿƥNjɈ mortality

DIAGNOSIS DIAGNOSTIC IMAGING Ultrasound, ERCP ƒ Biliary dilation ƒ Bile duct wall thickening ƒ Evidence of etiology (stricture/stone/stent)

TREATMENT MEDICATIONS ƒ ŠƥĿċĿūƥĿČƙʋT×ǷƭĿēƙ

SURGERY ƒ Cholecystectomy Ɠ Avoid future complications

OTHER INTERVENTIONS ƒ ERCP Ɠ Removes gallstones ƒ Shockwave lithotripsy Ɠ High frequency sound waves break down stone ƒ Stent Ɠ Widen bile ducts in areas of stricture

Figure 28.1 The pathophysiology of ascending cholangitis.

196 OSMOSIS.ORG

Chapter 28 Biliary Tract Diseases

BILIARY COLIC osms.it/biliary-colic PATHOLOGY & CAUSES ƒ AKA “gallbladder attack” ƒ Gallstones lodged in bile ducts ĺ temporary severe abdominal pain ƒ After meal, gallbladder contracts ĺ gallstone ejected into cystic duct, lodged ĺ gallbladder contracts against lodged stone ĺ severe abdominal pain ƒ Pain subsides when gallstone dislodged

SIGNS & SYMPTOMS ƒ Pain Ɠ Severe right upper quandrant pain; radiates to right shoulder/shoulder blades Ɠ Intensity increases for 15 minutes, plateaus for few hours (< six), subsides Ɠ Starts hours after meal/at night/laying Ƿîƥ ƒ Nausea, vomiting, anorexia

CAUSES ƒ ƒ ƒ ƒ ƒ

Gallstones Narrow bile duct Pancreatitis Duodenitis Esophageal spasms

RISK FACTORS ƒ More common in individuals who are biologically female ƒ Obesity ƒ Pregnancy ƒ ijĚʓȅȁ

COMPLICATIONS ƒ Acute cholecystitis Ɠ TŠǷîƥĿūŠūIJijîŕŕċŕîēēĚƑDžîŕŕ Ɠ Gallstone doesn’t dislodge from cystic duct

DIAGNOSIS ƒ Recurrent symptoms

DIAGNOSTIC IMAGING Ultrasound ƒ ūŠǶƑŞîƥĿūŠūIJūċƙƥƑƭČƥĿūŠ X-ray, CT scan, MRI

TREATMENT SURGERY ƒ Cholecystectomy Ɠ Gallbladder removal Ɠ 'ĚǶŠĿƥĿDŽĚ

OTHER INTERVENTIONS ƒ Pain, symptom management

OSMOSIS.ORG 197

CHOLECYSTITIS (ACUTE) osms.it/acute-cholecystitis PATHOLOGY & CAUSES ƒ Stone lodged in cystic duct/common bile duct ĺ îČƭƥĚĿŠǷîƥĿūŠ ĺ pain Ɠ ȊȁʣūIJîČƭƥĚČĺūŕĚČNjƙƥĿƥĿƙƑĚƙūŕDŽĚƙ within month as stone dislodges ƒ Fatty meal ĺ small intestine cholecystokinin (CCK) signals gallbladder to secrete bile ĺ gallbladder contracts ĺ stone lodged in cystic duct ĺ blocks ċĿŕĚǷūDžĺ irritates mucosa ĺ mucosa ƙĚČƑĚƥĚƙŞƭČƭƙɈĿŠǷîƥūƑNjĚŠǕNjŞĚƙĺ ĿŠǷîƥĿūŠɈēĿƙƥĚŠƥĿūŠɈƎƑĚƙƙƭƑĚ ƒ Cholesterol stones Ɠ More potent ability to stimulate ĿŠǷîƥĿūŠČūŞƎîƑĚēƥūƎĿijŞĚŠƥ gallstones ƒ Possible progressions Ɠ Stone ejected out of cystic duct ĺ cholecystitis subsides, symptoms subside Ɠ Stone remains in place ĺ pressure builds ĺ pushes down on blood vessels supplying gallbladder ĺ ischemia ĺ gangrenous cell death ĺ gallbladder walls weaken ĺ perforation/rupture ĺ bacteria seeds to bloodstream ĺ sepsis ĺ medical emergency Ɠ Stone lodged in common bile duct ĺ ċŕūČŒƙǷūDžūIJċĿŕĚūƭƥūIJŕĿDŽĚƑ ƒ Bacterial growth (cholangitis) Ɠ Cholelithiasis ĺ stone descends to cystic duct ĺ cholecystitis ĺ stone descends from cystic duct, lodges in common bile duct ĺ choledolithiasis ĺ secondary infection due to obstruction ĺ cholangitis Ɠ Most commonly E. coli, Enterococci, Bacterioides fragilis, Clostridium

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Acalculous cholecystitis ƒ ČƭƥĚĿŠǷîƥĿūŠūIJijîŕŕċŕîēēĚƑDžĿƥĺūƭƥ gallstones/cystic duct obstruction; high morbidity, mortality rate ƒ ȆɝȂȁʣūIJîČƭƥĚČĺūŕĚČNjƙƥĿƥĿƙČîƙĚƙ ƒ ¤îƑĚɈēĿIJǶČƭŕƥƥūēĿîijŠūƙĚ ƒ Multifactorial etiology ƒ Often occurs in critically ill individuals/ following major surgery ƒ Pathogenesis Ɠ Gallbladder ischemia, reperfusion injury Ɠ Bacterial invasion of ischemic tissue

COMPLICATIONS ƒ Biliary peritonitis (from rupture) ƒ Gallbladder ischemia ĺ rupture ĺ sepsis ƒ Acalculous cholecystitis

Figure 28.2 A CT scan in the coronal plane demonstrating a thickened, oedematous gallbladder, indicative of acute cholecystitis.

Chapter 28 Biliary Tract Diseases

SIGNS & SYMPTOMS ƒ Midepigastric pain ĺ dull right upper quadrant pain radiates to right scapula/ shoulders (esp. after a meal in chronic cholecystitis) ƒ Hypoactive bowel sounds; nausea, vomiting, anorexia; jaundice; low grade fever ƒ Blumberg’s sign/rebound tenderness Ɠ RUQ pain when pressure rapidly released from abdomen; peritonitis (secondary to gallbladder perforation/ rupture) ƒ Positive Murphy’s sign Ɠ Sudden cessation of inhalation due to ƎîĿŠDžĺĚŠĿŠǷîŞĚēijîŕŕċŕîēēĚƑƑĚîČĺĚƙ ĚNJîŞĿŠĚƑɫƙǶŠijĚƑƙ Ɠ Examiner asks individual to exhale ĺ places hand below right costal margin in midclavicular line ĺ individual instructed to breathe in ĺ cessation due to pain Ɠ Differentiates cholecystitis from other causes of right upper quadrant pain

Diffusion-weighted MRI ƒ Differentiate between acute, chronic cholecystitis Ultrasound ƒ Gallstones/sludge Ɠ Gallbladder wall thickening, distention Ɠ Air in gallbladder wall (gangrenous cholecystitis) Ɠ ¡ĚƑĿČĺūŕĚČNjƙƥĿČǷƭĿēIJƑūŞƎĚƑIJūƑîƥĿūŠɓ exudate

LAB RESULTS ƒ Elevated ALP Ɠ Concentrated in liver, bile ducts Ɠ Bile backs up, pressure in ducts increase ĺ cells damaged, die ĺ ALP released ƒ Elevated leukocyte count

TREATMENT MEDICATIONS ƒ Antimicrobials

SURGERY ƒ Cholecystectomy

DIAGNOSIS DIAGNOSTIC IMAGING Cholescintigraphy/hepatic iminodiacetic acid (HIDA) scan ƒ Radioactive tracer injected into individual ĺ marked HIDA taken up by hepatocytes, excreted in bile ĺ drains down hepatic ducts ƒ Location of blockage

OSMOSIS.ORG 199

CHOLECYSTITIS (CHRONIC) osms.it/chronic-cholecystitis PATHOLOGY & CAUSES ƒ Obstruction of cystic duct (not infection) ĺ ĿŠǷîƥĿūŠūIJijîŕŕċŕîēēĚƑDžîŕŕ ƒ ūŠƙƥîŠƥƙƥîƥĚūIJĿŠǷîƥĿūŠēƭĚƥū gallstones repeatedly blocking ducts Ɠ Changes gallbladder mucosa ĺ deep grooves (Rokatansky–Aschoff sinus) Ɠ Pain esp. after meal; gallbladder attempts to secrete bile to small intestine for digestion ƒ Fatty meal ĺ small intestine cholecystokinin (CCK) signals gallbladder to secrete bile ĺ gallbladder contracts ĺ stone lodged in cystic duct ĺ blocks ċĿŕĚǷūDžĺ irritates mucosa ĺ mucosa ƙĚČƑĚƥĚƙŞƭČƭƙɈĿŠǷîƥūƑNjĚŠǕNjŞĚƙĺ ĿŠǷîƥĿūŠɈēĿƙƥĚŠƥĿūŠɈƎƑĚƙƙƭƑĚ ƒ Cholesterol stones Ɠ More potent ability to stimulate ĿŠǷîƥĿūŠČūŞƎîƑĚēƥūƎĿijŞĚŠƥ gallstones ƒ Possible progressions Ɠ Stone ejected out of cystic duct ĺ cholecystitis subsides, symptoms subside Ɠ Stone remains in place ĺ pressure builds ĺ pushes down on blood vessels supplying gallbladder ĺ ischemia ĺ gangrenous cell death ĺ gallbladder walls weaken ĺ perforation/rupture ĺ bacteria seeds to bloodstream ĺ sepsis ĺ medical emergency Ɠ Stone lodged in common bile duct ĺ ċŕūČŒƙǷūDžūIJċĿŕĚūƭƥūIJŕĿDŽĚƑ ƒ Bacterial growth (cholangitis) Ɠ Cholelithiasis ĺ stone descends to cystic duct ĺ cholecystitis ĺ stone descends from cystic duct, lodges in common bile duct ĺ choledolithiasis ĺ secondary infection due to obstruction ĺ cholangitis Ɠ Most commonly E. coli, Enterococci, Bacterioides fragilis, Clostridium

200 OSMOSIS.ORG

COMPLICATIONS ƒ Biliary peritonitis (from rupture) ƒ Gallbladder ischemia ĺ rupture ĺ sepsis ƒ Porcelain gallbladder (chronic cholecystitis) Ɠ ĺƑūŠĿČƙƥîƥĚūIJĿŠǷîƥĿūŠĺ ĚƎĿƥĺĚŕĿîŕǶċƑūƙĿƙɈČîŕČĿǶČîƥĿūŠ Ɠ Bluish discoloration of gallbladder; becomes hard, brittle Ɠ Bile stasis ĺ calcium carbonate bile salts to precipitate out ĺ deposit into walls Ɠ Increased risk of gallbladder cancer ƒ Acalculous cholecystitis

SIGNS & SYMPTOMS ƒ Midepigastric pain ĺ dull right upper quadrant pain radiates to right scapula/ shoulders (esp. after a meal in chronic cholecystitis) ƒ Hypoactive bowel sounds; nausea, vomiting, anorexia; jaundice; low grade fever ƒ Blumberg’s sign/rebound tenderness Ɠ Right upper quadrant pain when pressure rapidly released from abdomen; peritonitis (secondary to gallbladder perforation/rupture) ƒ Positive Murphy’s sign Ɠ Sudden cessation of inhalation due to ƎîĿŠDžĺĚŠĿŠǷîŞĚēijîŕŕċŕîēēĚƑƑĚîČĺĚƙ ĚNJîŞĿŠĚƑɫƙǶŠijĚƑƙ Ɠ Examiner asks individual to exhale ĺ places hand below right costal margin in midclavicular line ĺ individual instructed to breathe in ĺ cessation due to pain Ɠ Differentiates cholecystitis from other causes of right upper quadrant pain

Chapter 28 Biliary Tract Diseases

DIAGNOSIS DIAGNOSTIC IMAGING Cholescintigraphy/hepatic iminodiacetic acid (HIDA) scan ƒ Radioactive tracer injected into individual ĺ marked HIDA taken up by hepatocytes, excreted in bile ĺ drains down hepatic ducts ƒ Location of blockage Diffusion-weighted MRI ƒ Differentiate between acute, chronic cholecystitis Ultrasound ƒ Gallstones/sludge Ɠ Gallbladder wall thickening, distention Ɠ Air in gallbladder wall (gangrenous cholecystitis) Ɠ ¡ĚƑĿČĺūŕĚČNjƙƥĿČǷƭĿēIJƑūŞƎĚƑIJūƑîƥĿūŠɓ exudate

Figure 28.3 Endoscopic retrograde cholangiopancreatography demonstrating gallstones in the cystic duct.

LAB RESULTS ƒ Elevated ALP: concentrated in liver, bile ducts Ɠ Bile backs up, pressure in ducts increase ĺ cells damaged, die ĺ ALP released ƒ Elevated leukocyte count

TREATMENT MEDICATIONS

Figure 28.4 Histological appearance of cholestasis in the liver. There is build up of bile pigment in the hepatic parenchyma.

ƒ Antimicrobials

SURGERY ƒ Cholecystectomy

OSMOSIS.ORG 201

202 OSMOSIS.ORG

Chapter 28 Biliary Tract Diseases

GALLSTONE osms.it/gallstone PATHOLOGY & CAUSES ƒ Solid stones inside gallbladder composed of bile components ƒ Form based on imbalance of chemical constituents ĺ precipitate out to form solid stone

TYPES ƒ

îƥĚijūƑĿǕĚēċNjŕūČîƥĿūŠ (choledocholithiasis, cholelithiasis) or major composition (cholesterol, bilirubin stones)

Choledocholithiasis ƒ Gallstones in common bile duct ĺ ūċƙƥƑƭČƥĿūŠūIJūƭƥǷūDžƥƑîČƥ Ɠ Stasis, infection (primary cause) Ɠ Affects liver function; may cause liver damage Cholelithiasis ƒ Gallstones in gallbladder Ɠ Primary cause: imbalance of bile components Ɠ ĿŕĚǷūDžūƭƥūIJŕĿDŽĚƑŠūƥūċƙƥƑƭČƥĚēɒŕĿDŽĚƑ function not affected Cholesterol stones ƒ qūƙƥČūŞŞūŠɈȉȁʣ ƒ Composed primarily of cholesterol ƒ Cholesterol precipitation out of bile: supersaturation; inadequate salts/acids/ phospholipids; gallbladder stasis ƒ Radiolucent (not visible on X-ray) Bilirubin stones (pigmented stones) ƒ Composed primarily of unconjugated bilirubin Ɠ Formed from nonbacterial, ŠūŠĚŠǕNjŞîƥĿČĺNjēƑūŕNjƙĿƙūIJČūŠŏƭijîƥĚē bilirubin ƒ Occurs when too much bilirubin in bile ƒ Combines with calcium ĺ solid calcium bilirubinate

Figure 28.5 Cholesterol gallstones.

ƒ Radiopaque (visible on X-ray) ƒ Can be caused by excessive extravascular hemolysis Ɠ Extravascular hemolysis ĺ macrophages consume RBCs ĺ increased unconjugated bilirubin production ĺ too much unconjugated bilirubin for liver to conjugate ĺ unconjugated bilirubin binds to calcium instead of bile salts ĺ precipitate out to form black pigmented stones ƒ Brown pigmented gallstone: gallbladder/ biliary tract infection Ɠ Stones enter common bile duct Ɠ Brown pigment due to unconjugated/ hydrolyzed bilirubin, phospholipids: infectious organism brings hydrolytic ĚŠǕNjŞĚƙĺ hydrolysis of conjugated bilirubin, phospholipids ĺ combine with calcium ions ĺ precipitate out to form stones Ɠ Common infections: E. coli, Ascaris lumbricoides, Clonorchis sinensis (trematode endemic to China, Korea, Vietnam) Ɠ Commonly seen in Asian populations

OSMOSIS.ORG 203

RISK FACTORS ƒ More common in individuals who are biologically female, who use oral contraceptive Ɠ Ĺ estrogen ĺĹ cholesterol in bile + bile hypomotility ĺĹ risk of gallstones ƒ Obesity ƒ Rapid weight loss Ɠ Imbalance in bile composition ĺĹ risk of calcium-bilirubin precipitation ƒ Total parenteral nutrition (prolonged)

COMPLICATIONS ƒ ĺūŕĚČNjƙƥĿƥĿƙɚĿŠǷîƥĿūŠūIJijîŕŕċŕîēēĚƑɛ ƒ Ascending cholangitis ƒ Blockage of common, pancreatic bile ducts ƒ Gallbladder cancer: history of gallstones ĺ Ĺrisk of gallbladder cancer

DIAGNOSIS DIAGNOSTIC IMAGING Ultrasound, CT scan, X-ray, ERCP ƒ ×ĿƙƭîŕĿǕĚƙƥūŠĚƙ

LAB RESULTS ƒ Elevated bilirubin levels ƒ Liver function tests (LFTs) Ɠ Elevated gamma-glutamyl transferase (GGT), alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate transaminase (AST)

SIGNS & SYMPTOMS ƒ May be asymptomatic ƒ Sudden, intense abdominal epigastric/ substernal pain; radiates to right shoulder/ shoulder blades ƒ Nausea/vomiting; jaundice; abdominal tenderness, distension; fever, chills; ǷîƥƭŕĚŠČĚɈċĚŕČĺĿŠij ƒ See mnemonic for summary

MNEMONIC: 6 Fs Typical clinical presentation of an individual with gallstones Fat Female Fertile Forty Fatty food intolerance Flatulence

204 OSMOSIS.ORG

Figure 28.6 Abdominal ultrasound demonstrating cholelithiasis. The gallstones cast an acoustic shadow.

TREATMENT ƒ Necessary only if symptomatic

MEDICATIONS ƒ Bile salts Ɠ Dissolve cholesterol stones

Chapter 28 Biliary Tract Diseases

SURGERY ƒ Cholecystectomy

OTHER INTERVENTIONS ƒ Pain management ƒ Shock wave therapy (lithotripsy) Ɠ High-frequency sound waves fragment stones

Figure 28.7 Numerous gallstones, of mixedtype, in a cholecystectomy specimen. The wall of the gallbladder is thickened and ǶċƑūƥĿČɈČūŠƙĿƙƥĚŠƥDžĿƥĺŕūŠijɠƙƥîŠēĿŠij disease.

PRIMARY SCLEROSING CHOLANGITIS (PSC) osms.it/primary-sclerosing-cholangitis PATHOLOGY & CAUSES ƒ Autoimmune disorder in which T-cells attack, destroy bile duct epithelial cells in genetically predisposed individuals exposed to environmental stimuli Ɠ HLA-B8, HLA-DR3, HLA-DRw52a ƒ Associated with ulcerative colitis, Crohn’s disease ƒ ¬ČŕĚƑūƙĿƙɈĿŠǷîƥĿūŠūIJĿŠƥƑîɠɈ extrahepatic ducts ƒ ĚŕŕƙîƑūƭŠēċĿŕĚēƭČƥƙĿŠǷîŞĚēɈēĿĚĺ ǶċƑūƙĚ ƒ Death of epithelial cells lining bile ducts ĺ bile leaks into interstitial space, bloodstream ƒ “Beaded” appearance of bile ducts Ɠ Stenosis of affected ducts, dilation of unaffected ducts ƒ Severity depends on bilirubin levels, encephalopathy, presence/absence of ascites, serum albumin level, prothrombin time

COMPLICATIONS ƒ Portal hypertension Ɠ Fibrosis builds around bile ducts ĺ constricts portal veins ĺĹ pressure ƒ Hepatosplenomegaly Ɠ Portal hypertension ĺċîČŒƭƎūIJǷƭĿēɈ enlargement of spleen, liver ƒ Cirrhosis Ɠ ¤ĚČƭƑƑĚŠƥČNjČŕĚūIJĿŠǷîƥĿūŠɈĺĚîŕĿŠij ĺ tissue scarring ĺǶċƑūƙĿƙ ƒ Ĺ risk of cholangiocarcinoma, gallbladder cancer, hepatocellular carcinoma

SIGNS & SYMPTOMS ƒ May remit, recur spontaneously ƒ Jaundice, RUQ pain, weight loss, pruritus (deposition of bile salts, acids in skin), hepatosplenomegaly ƒ Liver failure Ɠ Ascites, muscle atrophy, spider angiomas, increased clotting time, dark urine, pale stool

OSMOSIS.ORG 205

DIAGNOSIS DIAGNOSTIC IMAGING MRCP ƒ Intrahepatic and/or extrahepatic bile duct dilation; multifocal or diffuse strictures ERCP ƒ Intrahepatic and/or extrahepatic bile duct dilation; multifocal or diffuse strictures

LAB RESULTS ƒ Liver function tests (LFTs) Ɠ Elevated conjugated bilirubin, ALP, GGT ƒ Elevated serum IgM antibody, p-ANCA (targets antigens in cytoplasm/nucleus of ŠĚƭƥƑūƎĺĿŕƙɒȉȁʣūIJĿŠēĿDŽĿēƭîŕƙDžĿƥĺ¡¬ ɛ ƒ Bilirubinuria ƒ Liver biopsy Ɠ Stage disease, predict prognosis

Figure 28.8 Cholangiogram demonstrating multiple biliary strictures in a case of primary sclerosing cholangitis.

OTHER DIAGNOSTICS ƒ Histology Ɠ ɨ~ŠĿūŠɠƙŒĿŠǶċƑūƙĿƙɩ: concentric rings ūIJǶċƑūƙĿƙîƑūƭŠēċĿŕĚēƭČƥɈƑĚƙĚŞċŕĚƙ onion skin

TREATMENT ƒ No effective treatment

MEDICATIONS ƒ Treat symptoms, manage complications, not curative (e.g. antibiotics) ƒ Immunosuppressants, chelators, steroids

SURGERY ƒ Liver transplant Ɠ Advanced liver disease

206 OSMOSIS.ORG

Figure 28.9 Histological appearance of primary sclerosing cholangitis. There is ūŠĿūŠɠƙŒĿŠǶċƑūƙĿƙūIJƥĺĚċĿŕĿîƑNjēƭČƥƙɍ

NOTES

NOTES COLORECTAL POLYP CONDITIONS

GENERALLY, WHAT ARE THEY? PATHOLOGY & CAUSES ƒ Colorectal polyps: overgrowths of epithelial cells lining colon/rectum ƒ Usually benign, can turn malignant

TYPES Adenomatous polyps/colonic adenomas ƒ Gland-like polyps caused by tumor suppressor gene mutation in adenomatous polyposis coli (APC) ƒ Characterized by accelerated division of epithelial cells ĺ epithelial dysplasia ĺ polyp formation ƒ No malignant potential by itself; requires mutations in other tumor suppressants (KRAS, p53) ƒ OĿƙƥūŕūijĿČČŕîƙƙĿǶČîƥĿūŠ Ɠ Tubular: pedunculated polyp, protrudes out in lumen Ɠ Villous:ƙĚƙƙĿŕĚɈČîƭŕĿǷūDžĚƑɠŕĿŒĚ appearance; more often malignant Ɠ Tubulovillous: characteristics of tubular, villous polyps Serrated polyps ƒ Saw-tooth appearance microscopically ƒ Contain methylated CpG islands ĺ silencing of DNA-repair genes, others ĺ more mutations ĺ malignancy Ɠ Small polyps (most common): AKA hyperplastic polyps; rarely malignant Ɠ Large polyps:ūIJƥĚŠǷîƥɈƙĚƙƙĿŕĚɈ malignant

TŠǷîƥūƑNjƎūŕNjƎƙ ƒ Caused by ĿŠǷîƥūƑNjċūDžĚŕēĿƙĚîƙĚƙ Ɠ Crohn’s disease, ulcerative colitis ƒ Not malignant

CAUSES ƒ Genetic mutations ƒ TŠǷîƥūƑNjČūŠēĿƥĿūŠƙɚĚɍijɍ ƑūĺŠɫƙ disease)

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