NOTES

NOTES
BILIARY TRACT DISEASES

GENERALLY, WHAT ARE THEY?

Magnetic resonance
PATHOLOGY & CAUSES cholangiopancreatography (MRCP)
ƒ MRI for detailed images of hepatobiliary,
ƒ Diverse spectrum of diseases affecting pancreatic systems
biliary system (gallbladder, bile ducts, liver)
ƒ Bile stored in gallbladder ĺ stasis/chemical Endoscopic retrograde cholangiopancrea-
constituents change ĺ precipitate to tography (ERCP)
solid stone ĺ travel down biliary tract ĺ ƒ Down esophagus, stomach, duodenum,
obstruction ĺ decreased bile drainage ĺ ducts ĺ contrast medium injected into
symptoms ducts ĺ X-ray shows narrow areas/
blockages
Ɠ Complications: pancreatitis (most
SIGNS & SYMPTOMS common); intraluminal/intraductal
bleeding, hematomas; perforation;
ƒ Symptoms vary, based on location infection (cholangitis, cholecystitis);
Ɠ ¡îĿŠɈŏîƭŠēĿČĚɈĿŠIJĚČƥĿūŠɈĿŠǷîƥūƑNj cardiopulmonary complications (cardiac
response, sepsis arrhythmia, hypoxemia, aspiration)
ƒ Right upper quadrant (RUQ) epigastric pain
ƒ Jaundice LAB RESULTS
ƒ Nausea, vomiting ƒ See table
ƒ Fever, chills ĺ sepsis

TREATMENT
DIAGNOSIS
MEDICATIONS
DIAGNOSTIC IMAGING ƒ Antibiotics
CT scan/ultrasound
ƒ Locations of stones, gallbladder wall SURGERY
ƥĺĿČŒĚŠĿŠijɓĿŠǷîƥĿūŠ ƒ Cholecystectomy

X-ray
OTHER INTERVENTIONS
ƒ Pigmented gallbladder stones (radiopaque)
ƒ Sepsis management, biliary drainage,
ERCP

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ASCENDING CHOLANGITIS
osms.it/ascending-cholangitis
ƒ Common bacteria: E. coli, Klebsiella,
PATHOLOGY & CAUSES Enterobacter, Enterococcus
ƒ Medical emergency
ƒ Acute infection of bile duct caused
by intestinal bacteria ascending from
duodenum RISK FACTORS
ƒ Bacterial infection of bile duct ƒ Gallstones (most common)
superimposed on obstruction of biliary tree; ƒ Stenosis of bile duct due to neoplasm/injury
due to choledocholithiasis from laparoscopic procedure
ƒ Gallstones form in gallbladder ĺ slip out
ĺ travel through cystic bile duct, lodge
in common bile duct ĺ obstruction of
ŠūƑŞîŕċĿŕĚǷūDžĺ bacteria ascend from
duodenum to bile duct ĺ infect stagnant
bile, surrounding tissue

OSMOSIS.ORG 195
 COMPLICATIONS LAB RESULTS
ƒ Sepsis, septic shock ƒ Assess infection, jaundice
Ɠ High pressure on bile duct ĺ Ɠ Increased WBC
obstruction ĺ cells lining ducts widen Ɠ Increased serum C-reactive protein
ĺ bacteria, bile enter bloodstream (CRP)
ƒ Multiorgan failure Ɠ Elevated LFTs: ALP, GGT, ALT, AST

SIGNS & SYMPTOMS TREATMENT

ƒ Charcot’s triad MEDICATIONS
Ɠ RUQ pain, jaundice, fever/chills ƒ ŠƥĿċĿūƥĿČƙʋT×ǷƭĿēƙ
ƒ Reynold’s pentad
Ɠ Charcot’s triad + hypotension/shock, SURGERY
altered consciousness
ƒ Cholecystectomy
Ɠ ƙƙūČĿîƥĚēDžĿƥĺƙĿijŠĿǶČîŠƥŞūƑċĿēĿƥNjɈ
Ɠ Avoid future complications
mortality

OTHER INTERVENTIONS
DIAGNOSIS ƒ ERCP
Ɠ Removes gallstones
DIAGNOSTIC IMAGING ƒ Shockwave lithotripsy
Ultrasound, ERCP Ɠ High frequency sound waves break
ƒ Biliary dilation down stone
ƒ Bile duct wall thickening ƒ Stent
ƒ Evidence of etiology (stricture/stone/stent) Ɠ Widen bile ducts in areas of stricture

Figure 28.1 The pathophysiology of ascending cholangitis.

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BILIARY COLIC
osms.it/biliary-colic

PATHOLOGY & CAUSES SIGNS & SYMPTOMS

ƒ AKA “gallbladder attack” ƒ Pain
ƒ Gallstones lodged in bile ducts ĺ Ɠ Severe right upper quandrant pain;
temporary severe abdominal pain radiates to right shoulder/shoulder
ƒ After meal, gallbladder contracts ĺ blades
gallstone ejected into cystic duct, lodged Ɠ Intensity increases for 15 minutes,
ĺ gallbladder contracts against lodged plateaus for few hours (< six), subsides
stone ĺ severe abdominal pain Ɠ Starts hours after meal/at night/laying
ƒ Pain subsides when gallstone dislodged Ƿîƥ
ƒ Nausea, vomiting, anorexia
CAUSES
ƒ Gallstones
DIAGNOSIS
ƒ Narrow bile duct
ƒ Pancreatitis ƒ Recurrent symptoms
ƒ Duodenitis
ƒ Esophageal spasms DIAGNOSTIC IMAGING

RISK FACTORS Ultrasound

ƒ More common in individuals who are ƒ ūŠǶƑŞîƥĿūŠūIJūċƙƥƑƭČƥĿūŠ
biologically female X-ray, CT scan, MRI
ƒ Obesity
ƒ Pregnancy
ƒ ijĚʓȅȁ TREATMENT
SURGERY
COMPLICATIONS
ƒ Cholecystectomy
ƒ Acute cholecystitis
Ɠ Gallbladder removal
Ɠ TŠǷîƥĿūŠūIJijîŕŕċŕîēēĚƑDžîŕŕ
Ɠ 'ĚǶŠĿƥĿDŽĚ
Ɠ Gallstone doesn’t dislodge from cystic
duct
OTHER INTERVENTIONS
ƒ Pain, symptom management

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 CHOLECYSTITIS (ACUTE)
osms.it/acute-cholecystitis
Acalculous cholecystitis
PATHOLOGY & CAUSES ƒ ČƭƥĚĿŠǷîƥĿūŠūIJijîŕŕċŕîēēĚƑDžĿƥĺūƭƥ
gallstones/cystic duct obstruction; high
ƒ Stone lodged in cystic duct/common bile morbidity, mortality rate
duct ĺ îČƭƥĚĿŠǷîƥĿūŠ ĺ pain
ƒ ȆɝȂȁʣūIJîČƭƥĚČĺūŕĚČNjƙƥĿƥĿƙČîƙĚƙ
Ɠ ȊȁʣūIJîČƭƥĚČĺūŕĚČNjƙƥĿƥĿƙƑĚƙūŕDŽĚƙ
ƒ ¤îƑĚɈēĿIJǶČƭŕƥƥūēĿîijŠūƙĚ
within month as stone dislodges
ƒ Multifactorial etiology
ƒ Fatty meal ĺ small intestine
cholecystokinin (CCK) signals gallbladder ƒ Often occurs in critically ill individuals/
to secrete bile ĺ gallbladder contracts following major surgery
ĺ stone lodged in cystic duct ĺ blocks ƒ Pathogenesis
ċĿŕĚǷūDžĺ irritates mucosa ĺ mucosa Ɠ Gallbladder ischemia, reperfusion injury
ƙĚČƑĚƥĚƙŞƭČƭƙɈĿŠǷîƥūƑNjĚŠǕNjŞĚƙĺ Ɠ Bacterial invasion of ischemic tissue
ĿŠǷîƥĿūŠɈēĿƙƥĚŠƥĿūŠɈƎƑĚƙƙƭƑĚ
ƒ Cholesterol stones
COMPLICATIONS
Ɠ More potent ability to stimulate
ƒ Biliary peritonitis (from rupture)
ĿŠǷîƥĿūŠČūŞƎîƑĚēƥūƎĿijŞĚŠƥ
gallstones ƒ Gallbladder ischemia ĺ rupture ĺ sepsis
ƒ Possible progressions ƒ Acalculous cholecystitis
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
ċŕūČŒƙǷūDžūIJċĿŕĚūƭƥūIJŕĿDŽĚƑ
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 Figure 28.2 A CT scan in the coronal plane
Ɠ Most commonly E. coli, Enterococci, demonstrating a thickened, oedematous
Bacterioides fragilis, Clostridium gallbladder, indicative of acute cholecystitis.

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Diffusion-weighted MRI
SIGNS & SYMPTOMS ƒ Differentiate between acute, chronic
cholecystitis
ƒ Midepigastric pain ĺ dull right upper
quadrant pain radiates to right scapula/ Ultrasound
shoulders (esp. after a meal in chronic ƒ Gallstones/sludge
cholecystitis)
Ɠ Gallbladder wall thickening, distention
ƒ Hypoactive bowel sounds; nausea,
Ɠ Air in gallbladder wall (gangrenous
vomiting, anorexia; jaundice; low grade
cholecystitis)
fever
Ɠ ¡ĚƑĿČĺūŕĚČNjƙƥĿČǷƭĿēIJƑūŞƎĚƑIJūƑîƥĿūŠɓ
ƒ Blumberg’s sign/rebound tenderness
exudate
Ɠ RUQ pain when pressure rapidly
released from abdomen; peritonitis
(secondary to gallbladder perforation/ LAB RESULTS
rupture) ƒ Elevated ALP
ƒ Positive Murphy’s sign Ɠ Concentrated in liver, bile ducts
Ɠ Sudden cessation of inhalation due to Ɠ Bile backs up, pressure in ducts increase
ƎîĿŠDžĺĚŠĿŠǷîŞĚēijîŕŕċŕîēēĚƑƑĚîČĺĚƙ ĺ cells damaged, die ĺ ALP released
ĚNJîŞĿŠĚƑɫƙǶŠijĚƑƙ ƒ Elevated leukocyte count
Ɠ Examiner asks individual to exhale ĺ
places hand below right costal margin
in midclavicular line ĺ individual TREATMENT
instructed to breathe in ĺ cessation due
to pain MEDICATIONS
Ɠ Differentiates cholecystitis from other ƒ Antimicrobials
causes of right upper quadrant pain
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

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 CHOLECYSTITIS (CHRONIC)
osms.it/chronic-cholecystitis
COMPLICATIONS
PATHOLOGY & CAUSES ƒ Biliary peritonitis (from rupture)
ƒ Gallbladder ischemia ĺ rupture ĺ sepsis
ƒ Obstruction of cystic duct (not infection) ĺ
ĿŠǷîƥĿūŠūIJijîŕŕċŕîēēĚƑDžîŕŕ ƒ Porcelain gallbladder (chronic cholecystitis)
ƒ ūŠƙƥîŠƥƙƥîƥĚūIJĿŠǷîƥĿūŠēƭĚƥū Ɠ ĺƑūŠĿČƙƥîƥĚūIJĿŠǷîƥĿūŠĺ
gallstones repeatedly blocking ducts ĚƎĿƥĺĚŕĿîŕǶċƑūƙĿƙɈČîŕČĿǶČîƥĿūŠ
Ɠ Changes gallbladder mucosa ĺ deep Ɠ Bluish discoloration of gallbladder;
grooves (Rokatansky–Aschoff sinus) becomes hard, brittle
Ɠ Pain esp. after meal; gallbladder Ɠ Bile stasis ĺ calcium carbonate bile
attempts to secrete bile to small salts to precipitate out ĺ deposit into
intestine for digestion walls
ƒ Fatty meal ĺ small intestine Ɠ Increased risk of gallbladder cancer
cholecystokinin (CCK) signals gallbladder ƒ Acalculous cholecystitis
to secrete bile ĺ gallbladder contracts
ĺ stone lodged in cystic duct ĺ blocks
ċĿŕĚǷūDžĺ irritates mucosa ĺ mucosa SIGNS & SYMPTOMS
ƙĚČƑĚƥĚƙŞƭČƭƙɈĿŠǷîƥūƑNjĚŠǕNjŞĚƙĺ
ĿŠǷîƥĿūŠɈēĿƙƥĚŠƥĿūŠɈƎƑĚƙƙƭƑĚ ƒ Midepigastric pain ĺ dull right upper
ƒ Cholesterol stones quadrant pain radiates to right scapula/
Ɠ More potent ability to stimulate shoulders (esp. after a meal in chronic
ĿŠǷîƥĿūŠČūŞƎîƑĚēƥūƎĿijŞĚŠƥ cholecystitis)
gallstones ƒ Hypoactive bowel sounds; nausea,
ƒ Possible progressions vomiting, anorexia; jaundice; low grade
fever
Ɠ Stone ejected out of cystic duct ĺ
cholecystitis subsides, symptoms ƒ Blumberg’s sign/rebound tenderness
subside Ɠ Right upper quadrant pain when
Ɠ Stone remains in place ĺ pressure pressure rapidly released from
builds ĺ pushes down on blood vessels abdomen; peritonitis (secondary to
supplying gallbladder ĺ ischemia ĺ gallbladder perforation/rupture)
gangrenous cell death ĺ gallbladder ƒ Positive Murphy’s sign
walls weaken ĺ perforation/rupture ĺ Ɠ Sudden cessation of inhalation due to
bacteria seeds to bloodstream ĺ sepsis ƎîĿŠDžĺĚŠĿŠǷîŞĚēijîŕŕċŕîēēĚƑƑĚîČĺĚƙ
ĺ medical emergency ĚNJîŞĿŠĚƑɫƙǶŠijĚƑƙ
Ɠ Stone lodged in common bile duct ĺ Ɠ Examiner asks individual to exhale ĺ
ċŕūČŒƙǷūDžūIJċĿŕĚūƭƥūIJŕĿDŽĚƑ places hand below right costal margin
ƒ Bacterial growth (cholangitis) in midclavicular line ĺ individual
Ɠ Cholelithiasis ĺ stone descends to instructed to breathe in ĺ cessation due
cystic duct ĺ cholecystitis ĺ stone to pain
descends from cystic duct, lodges in Ɠ Differentiates cholecystitis from other
common bile duct ĺ choledolithiasis ĺ causes of right upper quadrant pain
secondary infection due to obstruction
ĺ cholangitis
Ɠ Most commonly E. coli, Enterococci,
Bacterioides fragilis, Clostridium

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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 Figure 28.3 Endoscopic retrograde
cholangiopancreatography demonstrating
Ɠ Gallbladder wall thickening, distention
gallstones in the cystic duct.
Ɠ Air in gallbladder wall (gangrenous
cholecystitis)
Ɠ ¡ĚƑĿČĺūŕĚČNjƙƥĿČǷƭĿēIJƑūŞƎĚƑIJūƑîƥĿūŠɓ
exudate

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 Figure 28.4 Histological appearance of

cholestasis in the liver. There is build up of
MEDICATIONS bile pigment in the hepatic parenchyma.
ƒ Antimicrobials

SURGERY
ƒ Cholecystectomy

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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 îƥĚijūƑĿǕĚēċNjŕūČîƥĿūŠ
(choledocholithiasis, cholelithiasis) or major
composition (cholesterol, bilirubin stones)

Choledocholithiasis
ƒ Gallstones in common bile duct ĺ
ūċƙƥƑƭČƥĿūŠūIJūƭƥǷūDžƥƑîČƥ Figure 28.5 Cholesterol gallstones.
Ɠ Stasis, infection (primary cause)
Ɠ Affects liver function; may cause liver
damage ƒ Radiopaque (visible on X-ray)
ƒ Can be caused by excessive extravascular
Cholelithiasis
hemolysis
ƒ Gallstones in gallbladder
Ɠ Extravascular hemolysis ĺ
Ɠ Primary cause: imbalance of bile macrophages consume RBCs ĺ
components increased unconjugated bilirubin
Ɠ ĿŕĚǷūDžūƭƥūIJŕĿDŽĚƑŠūƥūċƙƥƑƭČƥĚēɒŕĿDŽĚƑ production ĺ too much unconjugated
function not affected bilirubin for liver to conjugate ĺ
unconjugated bilirubin binds to calcium
Cholesterol stones
instead of bile salts ĺ precipitate out to
ƒ qūƙƥČūŞŞūŠɈȉȁʣ form black pigmented stones
ƒ Composed primarily of cholesterol ƒ Brown pigmented gallstone: gallbladder/
ƒ Cholesterol precipitation out of bile: biliary tract infection
supersaturation; inadequate salts/acids/ Ɠ Stones enter common bile duct
phospholipids; gallbladder stasis
Ɠ Brown pigment due to unconjugated/
ƒ Radiolucent (not visible on X-ray) hydrolyzed bilirubin, phospholipids:
infectious organism brings hydrolytic
Bilirubin stones (pigmented stones)
ĚŠǕNjŞĚƙĺ hydrolysis of conjugated
ƒ Composed primarily of unconjugated bilirubin, phospholipids ĺ combine with
bilirubin calcium ions ĺ precipitate out to form
Ɠ Formed from nonbacterial, stones
ŠūŠĚŠǕNjŞîƥĿČĺNjēƑūŕNjƙĿƙūIJČūŠŏƭijîƥĚē Ɠ Common infections: E. coli, Ascaris
bilirubin lumbricoides, Clonorchis sinensis
ƒ Occurs when too much bilirubin in bile (trematode endemic to China, Korea,
ƒ Combines with calcium ĺ solid calcium Vietnam)
bilirubinate Ɠ Commonly seen in Asian populations

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 RISK FACTORS
ƒ More common in individuals who
DIAGNOSIS
are biologically female, who use oral
contraceptive
DIAGNOSTIC IMAGING
Ɠ Ĺ estrogen ĺĹ cholesterol in bile + bile Ultrasound, CT scan, X-ray, ERCP
hypomotility ĺĹ risk of gallstones ƒ ×ĿƙƭîŕĿǕĚƙƥūŠĚƙ
ƒ Obesity
ƒ Rapid weight loss
LAB RESULTS
Ɠ Imbalance in bile composition ĺĹ risk
ƒ Elevated bilirubin levels
of calcium-bilirubin precipitation
ƒ Liver function tests (LFTs)
ƒ Total parenteral nutrition (prolonged)
Ɠ Elevated gamma-glutamyl transferase
(GGT), alkaline phosphatase (ALP),
COMPLICATIONS alanine aminotransferase (ALT),
ƒ ĺūŕĚČNjƙƥĿƥĿƙɚĿŠǷîƥĿūŠūIJijîŕŕċŕîēēĚƑɛ aspartate transaminase (AST)
ƒ Ascending cholangitis
ƒ Blockage of common, pancreatic bile ducts
ƒ Gallbladder cancer: history of gallstones ĺ
Ĺrisk of gallbladder cancer

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;
ǷîƥƭŕĚŠČĚɈċĚŕČĺĿŠij
ƒ See mnemonic for summary

Figure 28.6 Abdominal ultrasound

MNEMONIC: 6 Fs demonstrating cholelithiasis. The gallstones
Typical clinical presentation cast an acoustic shadow.
of an individual with
gallstones
Fat TREATMENT
Female
Fertile ƒ Necessary only if symptomatic
Forty
Fatty food intolerance MEDICATIONS
Flatulence ƒ Bile salts
Ɠ Dissolve cholesterol stones

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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 mixed-

type, in a cholecystectomy specimen. The
wall of the gallbladder is thickened and
ǶċƑūƥĿČɈČūŠƙĿƙƥĚŠƥDžĿƥĺŕūŠijɠƙƥîŠēĿŠij
disease.

PRIMARY SCLEROSING
CHOLANGITIS (PSC)
osms.it/primary-sclerosing-cholangitis
COMPLICATIONS
PATHOLOGY & CAUSES ƒ Portal hypertension
Ɠ Fibrosis builds around bile ducts ĺ
ƒ Autoimmune disorder in which T-cells
constricts portal veins ĺĹ pressure
attack, destroy bile duct epithelial cells
in genetically predisposed individuals ƒ Hepatosplenomegaly
exposed to environmental stimuli Ɠ Portal hypertension ĺċîČŒƭƎūIJǷƭĿēɈ
Ɠ HLA-B8, HLA-DR3, HLA-DRw52a enlargement of spleen, liver
ƒ Associated with ulcerative colitis, Crohn’s ƒ Cirrhosis
disease Ɠ ¤ĚČƭƑƑĚŠƥČNjČŕĚūIJĿŠǷîƥĿūŠɈĺĚîŕĿŠij
ƒ ¬ČŕĚƑūƙĿƙɈĿŠǷîƥĿūŠūIJĿŠƥƑîɠɈ ĺ tissue scarring ĺǶċƑūƙĿƙ
extrahepatic ducts ƒ Ĺ risk of cholangiocarcinoma, gallbladder
ƒ ĚŕŕƙîƑūƭŠēċĿŕĚēƭČƥƙĿŠǷîŞĚēɈēĿĚĺ cancer, hepatocellular carcinoma
ǶċƑūƙĚ
ƒ Death of epithelial cells lining bile ducts
ĺ bile leaks into interstitial space,
SIGNS & SYMPTOMS
bloodstream
ƒ May remit, recur spontaneously
ƒ “Beaded” appearance of bile ducts
ƒ Jaundice, RUQ pain, weight loss, pruritus
Ɠ Stenosis of affected ducts, dilation of
(deposition of bile salts, acids in skin),
unaffected ducts
hepatosplenomegaly
ƒ Severity depends on bilirubin levels,
ƒ Liver failure
encephalopathy, presence/absence of
ascites, serum albumin level, prothrombin Ɠ Ascites, muscle atrophy, spider
time 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
ŠĚƭƥƑūƎĺĿŕƙɒȉȁʣūIJĿŠēĿDŽĿēƭîŕƙDžĿƥĺ¡¬ ɛ
Figure 28.8 Cholangiogram demonstrating
ƒ Bilirubinuria multiple biliary strictures in a case of primary
ƒ Liver biopsy sclerosing cholangitis.
Ɠ Stage disease, predict prognosis

OTHER DIAGNOSTICS
ƒ Histology
Ɠ ɨ~ŠĿūŠɠƙŒĿŠǶċƑūƙĿƙɩ: concentric rings
ūIJǶċƑūƙĿƙîƑūƭŠēċĿŕĚēƭČƥɈƑĚƙĚŞċŕĚƙ
onion skin

TREATMENT
ƒ No effective treatment

MEDICATIONS
ƒ Treat symptoms, manage complications,
not curative (e.g. antibiotics) Figure 28.9 Histological appearance of
ƒ Immunosuppressants, chelators, steroids primary sclerosing cholangitis. There is
ūŠĿūŠɠƙŒĿŠǶċƑūƙĿƙūIJƥĺĚċĿŕĿîƑNjēƭČƥƙɍ
SURGERY
ƒ Liver transplant
Ɠ Advanced liver disease

206 OSMOSIS.ORG
 NOTES

NOTES
COLORECTAL POLYP CONDITIONS

GENERALLY, WHAT ARE THEY?

TŠǷîƥūƑNjƎūŕNjƎƙ
PATHOLOGY & CAUSES ƒ Caused by ĿŠǷîƥūƑNjċūDžĚŕēĿƙĚîƙĚƙ
Ɠ Crohn’s disease, ulcerative colitis
ƒ Colorectal polyps: overgrowths of epithelial
cells lining colon/rectum ƒ Not malignant
ƒ Usually benign, can turn malignant
CAUSES
TYPES ƒ Genetic mutations
ƒ TŠǷîƥūƑNjČūŠēĿƥĿūŠƙɚĚɍijɍ ƑūĺŠɫƙ
Adenomatous polyps/colonic adenomas disease)
ƒ Gland-like polyps caused by tumor
suppressor gene mutation in adenomatous
RISK FACTORS
polyposis coli (APC)
ƒ Family history
ƒ Characterized by accelerated division of
epithelial cells ĺ epithelial dysplasia ĺ ƒ Bowel wall injury (e.g. radiation exposure,
polyp formation ƙŞūŒĿŠijɈĿŠǷîƥūƑNjċūDžĚŕēĿƙĚîƙĚɛ
ƒ No malignant potential by itself; requires ƒ Risk increases with age
mutations in other tumor suppressants (K-
RAS, p53) COMPLICATIONS
ƒ OĿƙƥūŕūijĿČČŕîƙƙĿǶČîƥĿūŠ ƒ Malignancy
Ɠ Tubular: pedunculated polyp, protrudes Ɠ Depends on degree of dysplasia, size of
out in lumen polyp
Ɠ Villous:ƙĚƙƙĿŕĚɈČîƭŕĿǷūDžĚƑɠŕĿŒĚ
appearance; more often malignant
Ɠ Tubulovillous: characteristics of tubular, SIGNS & SYMPTOMS
villous polyps
ƒ Often asymptomatic
Serrated polyps ƒ If ulcerating
ƒ Saw-tooth appearance microscopically Ɠ Rectal bleeding, anemia symptoms (e.g.
ƒ Contain methylated CpG islands ĺ fatigue)
silencing of DNA-repair genes, others ĺ ƒ If large
more mutations ĺ malignancy
Ɠ Obstruction ĺ abdominal pain,
Ɠ Small polyps (most common): AKA constipation
hyperplastic polyps; rarely malignant
ƒ Malabsorption ĺ diarrhea
Ɠ Large polyps:ūIJƥĚŠǷîƥɈƙĚƙƙĿŕĚɈ
ƒ Some polyposis syndromes
malignant
Ɠ Extracolonic symptoms
Hamartomatous polyps
ƒ Mixture of tissues; disorganized mass
containing tissue found at site of polyp
ƒ Occur sporadically/in genetically inherited
conditions (Juvenile polyposis, Peutz–
Jeghers syndrome)

OSMOSIS.ORG 207
 DIAGNOSIS TREATMENT
DIAGNOSTIC IMAGING SURGERY
CT scan, MRI Polyp removal (polypectomy)
ƒ Hyperdense outpouchings of colonic wall
Colonic resection (colectomy)
into lumen; detection of metastases
ƒ If multiple polyps associated with polyposis
Endoscopy (colonoscopy) with biopsy syndromes/polyps with high-grade
ƒ Type of polyp, malignant potential (degree dysplasia
of dysplasia)

LAB RESULTS
ƒ TƑūŠɠēĚǶČĿĚŠČNjîŠĚŞĿîĺ decreased
red blood cell (RBC) count, low mean
corpuscular volume (MCV) levels
ƒ TƑūŠɠēĚǶČĿĚŠČNjîŠĚŞĿîĺ low ferritin,
serum iron, transferrin saturation
ƒ APC, RAS, etc. mutations
ƒ Assess asymptomatic family members for
risk

OTHER DIAGNOSTICS Figure 29.1 The gross pathological

appearance of a sessile colorectal polyp.
Digital rectal examination
ƒ Detection of distal rectal polyps; malignant
polyp, hard, irregular; benign polyps, softer,
pliable

Figure 29.2 Histological appearance of a

villous adenoma, characterised by a surface
composed of long villous projections. Figure 29.3 The histological appearance of
a tubular adenoma composed of compact
glands with variable levels of dysplasia.

208 OSMOSIS.ORG
 Chapter 29 Colorectal Polyp Conditions

FAMILIAL ADENOMATOUS
POLYPOSIS (FAP)
osms.it/familial-adenomatous-polyposis
Ɠ Abdominal mesenchymal desmoid
PATHOLOGY & CAUSES tumors: compress adjacent structures ĺ
obstruction/vascular impairment
ƒ Inherited condition; hundreds/thousands
Ɠ Other potential malignancies:
adenomatous polyps in colon
thyroid, pancreas, brain (glioma), liver
ƒ Autosomal dominant ĿŠĺĚƑĿƥîŠČĚɒȂȁȁʣ (hepatoblastoma)
penetrance; de novo mutations may occur

TYPES SIGNS & SYMPTOMS

Classic FAP ƒ Usually asymptomatic until malignancy
ƒ Most aggressive, frequent; ʑȂȁȁƎūŕNjƎƙîƥ ƒ Colonic manifestations
diagnosis; early onset Ɠ Palpable abdominal mass;
hematochezia (rectal bleeding); pain
Attenuated FAP (AFAP)
(esp. abdomen); diarrhea
ƒ ʒȂȁȁƎūŕNjƎƙîƥēĿîijŠūƙĿƙɚūŕĿijūƎūŕNjƎūƙĿƙɛɒ
later onset

Autosomal recessive FAP DIAGNOSIS

DIAGNOSTIC IMAGING
CAUSES
ƒ Germline mutation in APC gene (tumor Endoscopy with biopsy
suppressor) ĺ prevention of apoptosis ĺ
ūŕūŠūƙČūƎNjɈǷĚNJĿċŕĚƙĿijŞūĿēūƙČūƎNjɇ
cell overgrowth ĺ polyps
ƒ 'ĚƥĚČƥĿūŠūIJʓȂȁȁƎūŕNjƎƙɒʗȄȁƎūŕNjƙɈ
ƒ APC gene nonfunctional in FAP; slightly
AFAP
impaired in AFAP
ƒ Autosomal recessive FAP Esophagogastroduodenoscopy (EGD)
Ɠ Mutations of MUTYH gene on ƒ Gastric, duodenal adenomas
ČĺƑūŞūƙūŞĚȂ
Barium enema (with double contrast)
ƒ Filling defects
RISK FACTORS
ƒ Family history Abdominal CT scan
ƒ Hyperdense outpouchings of colonic wall
COMPLICATIONS into lumen
ƒ Malignancy if untreated
ƒ Extracolonic manifestations LAB RESULTS
Ɠ Congenital hypertrophy of retinal ƒ TƑūŠɠēĚǶČĿĚŠČNjîŠĚŞĿî
pigment epithelium (CHRPE) ƒ Ļ RBC, Ļ MCV
Ɠ Fundic gland polyps: sessile polyps in ƒ Ļ ferritin, Ļ serum iron, Ļ transferrin
stomach, usually not malignant saturation
Ɠ Duodenal adenomas: malignant ƒ APC mutations
potential

OSMOSIS.ORG 209
 OTHER DIAGNOSTICS
TREATMENT
Family history
ƒ Cancers, gastrointestinal (GI) tract diseases MEDICATIONS
ƒ Cyclooxygenase 2 inhibitors, other
Digital rectal examination ŠūŠƙƥĚƑūĿēîŕîŠƥĿɠĿŠǷîƥūƑNjēƑƭijƙ
ƒ Palpable mass (NSAIDs)
ƒ Epidermal growth factor receptor inhibitor:
Ophthalmic examination
erlotinib
ƒ CHRPE
ƒ Chemotherapy, if colon cancer

SURGERY
ƒ Frequent endoscopic check-ups to detect
ūŠƙĚƥūIJƎūŕNjƎūƙĿƙĚDŽĚƑNjȂɝȃNjĚîƑƙ
Ɠ If polyps detected ĺ surgical removal
(colectomy; proctocolectomy)

Figure 29.4 Endoscopic appearannce of

the colon in a case of familial adenomatous
polyposis.

Figure 29.5 A retinal photograph

demonstrating hypertrophy of the retinal
pigment epithelium in a case of familial
adenomatous polyposis.

GARDNER'S SYNDROME (GS)

osms.it/gardners-syndrome
ƒ Tumors outside colon
PATHOLOGY & CAUSES Ɠ Fibromas, lipomas, epidermoid cysts,
thyroid neoplasms, osteomas, desmoid
ƒ Variant of FAP with prominent extracolonic
ƒ Extracolonic polyps can arise in stomach,
manifestations
duodenum, spleen, kidneys, liver,
ƒ Inherited condition; numerous mesentery, small bowel; CHRPE lesions
adenomatous polyps in colon; extracolonic
polyps, tumors

210 OSMOSIS.ORG
 Chapter 29 Colorectal Polyp Conditions

CAUSES ƒ Supernumerary impacted teeth

ƒ APC, RAS, TP53 mutation; DCC deletion ĺ ƒ Multiple jaw osteomas, odontomas
furthers carcinogenesis
Digital rectal examination
ƒ Autosomal dominant inheritance
ƒ Palpable mass

COMPLICATIONS Ophthalmic examination

ƒ Malignancy in colon, thyroid, liver, kidneys ƒ CHRPE

ECG
SIGNS & SYMPTOMS ƒ Stomach, duodenum for polyps

ƒ Colonic manifestations
Ɠ Rectal bleeding, diarrhea TREATMENT
ƒ Extracolonic manifestations
ƒ No cure; palliative treatment
Ɠ Desmoid tumors (parietal bumps,
bleeding)
Ɠ Dental problems SURGERY
Ɠ Epidermoid cysts ƒ Excision of tumors/polyps with wide (8mm)
Ɠ Epigastric pain, bleeding, jaundice margin
Ɠ Malnutrition ĺmalaise, lethargy, fatigue ƒ Colectomy

OTHER INTERVENTIONS
DIAGNOSIS ƒ Radiotherapy, if recurrent

DIAGNOSTIC IMAGING
Endoscopy with biopsy

ūŕūŠūƙČūƎNjɈǷĚNJĿċŕĚƙĿijŞūĿēūƙČūƎNj
ƒ Direct visualization of adenomatous polyps
in colon

Abdominal CT scan
ƒ Hyperdense outpouchings of colonic wall
into lumen

Head/dental X-ray
ƒ Dental abnormalities

LAB RESULTS
ƒ TƑūŠɠēĚǶČĿĚŠČNjîŠĚŞĿî
Ɠ Ļ RBC, Ļ MCV
Ɠ Ļ ferritin, Ļ serum iron, Ļ transferrin
saturation
ƒ Tumoral markers (e.g. carcinoembryonic
antigen)
ƒ APC, RAS, TP53 mutations; DCC deletion

OTHER DIAGNOSTICS
Physical examination

OSMOSIS.ORG 211
 JUVENILE POLYPOSIS SYNDROME
osms.it/juvenile-polyposis

PATHOLOGY & CAUSES DIAGNOSIS

ƒ Numerous benign (AKA juvenile) polyps DIAGNOSTIC IMAGING
along GI tract
Endoscopic studies
ƒ Majority non-neoplastic hamartomas
polyps, in colorectum ƒ E.g. endoscopy, colonoscopy,
sigmoidoscopy
ƒ Criteria for diagnosis
CAUSES
Ɠ ʑǶDŽĚŏƭDŽĚŠĿŕĚƎūŕNjƎƙĿŠČūŕūŠɓƑĚČƥƭŞ
ƒ BMPR1A, SMAD4 mutations
Ɠ Multiple juvenile polyps in other areas of
ƒ Autosomal dominant inheritance; GI tract
incomplete penetrance
Ɠ Family history with any number of
ƒ 'ĚŠūDŽūŞƭƥîƥĿūŠƙɚȃȆʣɛ polyps
ƒ Biopsy, cytology
COMPLICATIONS
ƒ Increased risk of colorectal/extracolonic LAB RESULTS
adenocarcinoma; intestinal obstruction
ƒ TƑūŠɠēĚǶČĿĚŠČNjîŠĚŞĿî
Ɠ Ļ RBC, Ļ MCV
SIGNS & SYMPTOMS Ɠ Ļ ferritin, Ļ serum iron, Ļ transferrin
saturation
ƒ Hematochezia, anemia symptoms; ƒ BMPR1A, SMAD4 mutations
abdominal pain; diarrhea/constipation;
rectal prolapse
TREATMENT
SURGERY
ƒ Polypectomy
ƒ Surgical colectomy, proctocolectomy
Ɠ Malignant, ulcerating polyps

Figure 29.6 A juvenile retention polyp with

abundant edematous stroma and dilated
ČNjƙƥĿČƙƎîČĚƙǶŕŕĚēDžĿƥĺŞƭČĿŠɍ¹ĺĚƙƎîČĚƙ
are lined by cuboidal epithelium.

212 OSMOSIS.ORG
 Chapter 29 Colorectal Polyp Conditions

PEUTZ–JEGHERS SYNDROME
(PJS)
osms.it/peutz-jeghers

PATHOLOGY & CAUSES DIAGNOSIS

ƒ Inherited condition; benign hamartomatous DIAGNOSTIC IMAGING
polyps, in small bowel; also in colon,
stomach Endoscopy, colonoscopy, with biopsy
ƒ Associated with hyperpigmented (melanin- Capsule endoscopy
containing) macules on skin, mucosa
Abdominal CT scan
CAUSES ƒ Hyperdense outpouchings of colonic wall
into lumen
ƒ IV drug use
Ɠ Increases likelihood of infective
endocarditis LAB RESULTS
ƒ Congenital bicuspid aortic valve ƒ Fecal occult blood test
ƒ Diabetes, high blood pressure, smoking ƒ TƑūŠɠēĚǶČĿĚŠČNjîŠĚŞĿî
Ɠ Ļ RBC, Ļ MCV
COMPLICATIONS Ɠ Ļ ferritin, Ļ serum iron, Ļ transferrin
saturation
ƒ Very high risk of extracolonic malignant
transformation ƒ Tumor markers
Ɠ Breast, ovarian, cervical, testicular, Ɠ /Ɉ ɠȂȊɠȊɈ ɠȂȃȆ
pancreatic, thyroid cancer ƒ STK11 (LKB1) mutations
ƒ Mild malignant potential of polyps
OTHER DIAGNOSTICS
SIGNS & SYMPTOMS Diagnostic criteria
ƒ One of following
ƒ GI Ɠ ʓƥDžū¡cƎūŕNjƎƙČūŠǶƑŞĚēĺĿƙƥūŕūijĿČîŕŕNj
Ɠ Ulceration ĺ GI bleeding Ɠ ʓūŠĚ¡cƎūŕNjƎDžĿƥĺIJîŞĿŕNjĺĿƙƥūƑNj
(hematochezia/melena) ĺ symptoms of Ɠ PJS-associated mucocutaneous
anemia pigmentations
Ɠ Colicky abdominal pain
Ɠ Intussusception ĺ bowel obstruction, Digital rectal examination
bowel infarction ƒ Palpable mass
Ɠ Diarrhea, constipation
ƒ Pigmented lesions around oral mucosa,
nostrils, perianal area of extremities; fade
TREATMENT
after puberty
SURGERY
ƒ Polypectomy

MEDICATIONS
ƒ Cyclooxygenase 2 inhibitors (celecoxib)

OSMOSIS.ORG 213
 Figure 29.7 Histological appearance of a
Peutz-Jegher’s polyp. Figure 29.8 Multiple melanotic macules on
the skin and oral mucosa of a young boy with
Peutz-Jegher’s syndrome.

214 OSMOSIS.ORG
 NOTES

NOTES
ESOPHAGEAL DISEASE

GENERALLY, WHAT IS IT?

PATHOLOGY & CAUSES DIAGNOSIS
ƒ Pathologies of the esophagus ƒ TŠēĿDŽĿēƭîŕĺĿƙƥūƑNjɓČŕĿŠĿČîŕIJĚîƥƭƑĚƙɈ
ƒ Esophageal motility disorders esophagogastroduodenoscopy (EGD),
Ɠ Diseases interfering with correct barium swallow X-ray, esophageal
function of esophagus’ various muscular manometry, endoscopic biopsy
components
TREATMENT
CAUSES
ƒ Infections, autoimmune disease, anatomical ƒ See individual diseases
defects, irritative processes

SIGNS & SYMPTOMS

ƒ 'ĿIJǶČƭŕƥNjɓƎîĿŠDžĺĿŕĚƙDžîŕŕūDžĿŠijɈĚƙƎĚČĿîŕŕNj
spasm-type pain
ƒ 'ĿIJǶČƭŕƥNjDžĿƥĺIJūūēƑĚijƭƑijĿƥîƥĿūŠ

ACHALASIA
osms.it/achalasia
ƒ Affected individual lacks nonadrenergic,
PATHOLOGY & CAUSES noncholinergic, inhibitory ganglion cells
ĺ imbalanced excitation and relaxation
ƒ /ƙūƎĺîijĚîŕƙŞūūƥĺŞƭƙČŕĚǶċƑĚƙ fail ĺ incomplete lower esophageal sphincter
to relax ĺ lower esophageal sphincter relaxation, increased lower esophageal
ƑĚŞîĿŠƙČŕūƙĚēɓIJîĿŕƙƥūūƎĚŠ tone, lack of esophageal peristalsis
ƒ AKA esophageal achalasia, achalasia
cardiae, cardiospasm, esophageal
aperistalsis
CAUSES
ƒ Likely caused by underlying autoimmune
ƒ Progressive degeneration of ganglion cells
process triggered by previous viral
in myenteric plexus within esophageal wall
ĿŠIJĚČƥĿūŠɓijĚŠĚƥĿČƎƑĚēĿƙƎūƙĿƥĿūŠɓ
ĺ lower esophageal sphincter fails to relax
ŠĚƭƑūēĚijĚŠĚƑîƥĿDŽĚēĿƙĚîƙĚɓūƥĺĚƑĿŠIJĚČƥĿDŽĚ
ĺ loss of peristalsis in distal esophagus
process
ƒ Involves smooth muscle layer of
esophageal, lower esophageal sphincters

OSMOSIS.ORG 215
 ¡ƑĿŞîƑNjîČĺîŕîƙĿîɚŞūƙƥČūŞŞūŠɛ /ŠēūƙČūƎĿČċĿūƎƙNj
ƒ No known underlying cause ĺ failure of ƒ Hypertrophic musculature
distal esophageal inhibitory neurons ƒ ċƙĚŠČĚūIJƙƎĚČĿǶČŠĚƑDŽĚČĚŕŕƙDžĿƥĺĿŠ
myenteric plexus
¬ĚČūŠēîƑNjîČĺîŕîƙĿî
ƒ Esophageal cancer
ƒ Chagas disease OTHER DIAGNOSTICS
Ɠ Protozoan infection due to Trypanosoma /ƙūƎĺîijĚîŕŞîŠūŞĚƥƑNj
cruzi ĺloss of intramural ganglion ƒ Lower esophageal sphincter fails to relax
cells ĺ aperistalsis, incomplete lower upon wet swallow (< 75% relaxation)
esophageal sphincter relaxation
ƒ Lower esophageal pressure
Ɠ Normal < 26mmHg
SIGNS & SYMPTOMS Ɠ ČĺîŕîƙĿîʑȂȁȁŞŞOij
Ɠ sƭƥČƑîČŒĚƑîČĺîŕîƙĿîʑȃȁȁŞŞOij
ƒ DysphagiaƥūƙūŕĿēƙɓŕĿƐƭĿēƙɈūēNjŠūƎĺîijĿî ƒ Aperistalsis in esophageal body
(rarely), heartburn unresponsive to proton ƒ Relative increase in intraesophageal
pump inhibitor therapy, symptoms worsen pressure vs. intragastric pressure
progressivelys, regurgitation of undigested
food, substernal chest pain, hiccups
ƒ Weight loss TREATMENT
ƒ Coughing while lying horizontally,
aspiration of food ĺ recurrent pulmonary MEDICATIONS
complications ƒ Calcium channel blockers for mild to
moderate disease
ƒ Nitrates effective before dilatation occurs
DIAGNOSIS ƒ Antimuscarinic agents (rarely effective)
DIAGNOSTIC IMAGING ƒ ¡ƑūƥūŠƎƭŞƎĿŠĺĿċĿƥūƑƙɚîIJƥĚƑƙƭƑijĚƑNjɓ
ƎŠĚƭŞîƥĿČēĿŕîƥîƥĿūŠɛƥūƎƑĚDŽĚŠƥƑĚǷƭNJ
Barium swallow X-ray and continuous damage
ǷƭūƑūƙČūƎNj
ƒ Normal peristalsis not seen SURGERY
ƒ Acute tapering at lower esophageal
sphincter gîƎîƑūƙČūƎĿČOĚŕŕĚƑŞNjūƥūŞNj
ƒ Narrowing of gastroesophageal junction ƒ Esophageal dilatation via surgical cleaving
ɚċĿƑēɫƙċĚîŒɓƑîƥɫƙƥîĿŕîƎƎĚîƑîŠČĚɛ of muscle
ƒ Dilated esophagus above narrowing ƒ Only cut through outer muscle layers (those
ƒ ĿƑɠǷƭĿēŞîƑijĿŠūDŽĚƑċîƑĿƭŞČūŕƭŞŠēƭĚƥū failing to relax), leaving inner mucosal layer
lack of peristalsis intact

/ƙūƎĺîijĚîŕĚŠēūƙČūƎNjDžĿƥĺūƑDžĿƥĺūƭƥ /ŠēūƙČūƎĿČŞNjūƥūŞNj
ĚŠēūƙČūƎĿČƭŕƥƑîƙūƭŠē ƒ Peroral endoscopic myotomy, minimally
ƒ May appear normal invasive ĺ incision made through
esophageal mucosa, innermost circular
ƒ Unusually increased resistance to passage
muscle layer divided and extended through
of endoscope through esophagogastric
ŕūDžĚƑĚƙūƎĺîijĚîŕƙƎĺĿŠČƥĚƑɈȃČŞɓȁɍȉĿŠĿŠƥū
junction
gastric muscle
ƒ Retained food in esophagus on upper
endoscopy

216 OSMOSIS.ORG
    ĺîƎƥĚƑȄȁEsophageal Disease

OTHER INTERVENTIONS
ƒ Eat slowly, chew well, drink plenty of water
with meals, avoid eating near bedtime,
raise head off bed when sleeping with
pillows (promotes emptying of esophagus
with gravity)
ƒ DŽūĿēIJūūēƙƥĺîƥîijijƑîDŽîƥĚƑĚǷƭNJĺ
ketchup, citrus, chocolate, caffeine

ūƥūNJĿŠŏĚČƥĿūŠ
ƒ Paralyze muscle keeping lower esophageal
sphincter shut (causes scarring of sphincter
ĺ may complicate later myotomy)

¡ŠĚƭŞîƥĿČēĿŕîƥîƥĿūŠ
ƒ qƭƙČŕĚǶċƑĚƙƙƥƑĚƥČĺĚēɓƥūƑŠċNjIJūƑČĚIJƭŕ
ĿŠǷîƥĿūŠūIJċîŕŕūūŠƎŕîČĚēĿŠŕūDžĚƑ
esophageal sphincter Figure 30.1 A barium swallow demonstrating
the bird’s beak sign in achalasia. The proximal
ƒ Lowers basal lower esophageal tone by
esophagus is dilated.
disruption of muscular ring

BARRETT'S ESOPHAGUS
osms.it/barretts-esophagus
Ɠ ÀƎƑĿijĺƥɓƙƭƎĿŠĚƑĚǷƭNJ
PATHOLOGY & CAUSES Ɠ ¬ĿijŠĿǶČîŠƥŕNjŞūƑĚŕĿŒĚŕNjƥūēĚDŽĚŕūƎ
adenocarcinoma
ƒ Premalignant condition; metaplasia of cells
lining lower esophagus ¬ĺūƑƥɠƙĚijŞĚŠƥîƑƑĚƥƥɫƙ
ƒ sūƑŞîŕƙƥƑîƥĿǶĚēƙƐƭîŞūƭƙĚƎĿƥĺĚŕĿƭŞĺ ƒ Distance between z-line and
simple columnar epithelium, goblet cells ijîƙƥƑūĚƙūƎĺîijĚîŕŏƭŠČƥĿūŠʒȄČŞɓȂɍȃĿŠ
(usually native to lower gastrointestinal Ɠ Greater prevalence
tract)
Ɠ Shorter history of heartburn
ƒ Chronic acid exposure ĺƑĚǷƭNJĚƙūƎĺîijĿƥĿƙ
Ɠ Usually asymptomatic
(chronic irritation) ĺ metaplasia
Ɠ ¡ƑĚēūŞĿŠîŠƥŕNjƭƎƑĿijĺƥƑĚǷƭNJ
ƒ Bile acids ĺ intestinal differentiation ĺ
promotes cancer growth Ɠ Less mucosa involved ĺ lower
incidence of dysplasia

TYPES
RISK FACTORS
ƒ If z-line and gastroesophageal junction
coincide ĺ intestinal metaplasia at ƒ Bulimia
gastroesophageal junction ƒ Central obesity
Ɠ Associated with Helicobacter pylori ƒ Previous chemical damage to esophageal
epithelium (e.g. swallowing lye)
gūŠijɠƙĚijŞĚŠƥîƑƑĚƥƥɫƙ ƒ Smoking
ƒ Distance between z-line and ƒ Hiatal hernia
ijîƙƥƑūĚƙūƎĺîijĚîŕŏƭŠČƥĿūŠʑȄČŞɓȂɍȃĿŠ
Ɠ ƙƙūČĿîƥĚēDžĿƥĺŞūƑĚƙĚDŽĚƑĚƑĚǷƭNJ

OSMOSIS.ORG 217
 COMPLICATIONS
ƒ Esophageal adenocarcinoma
TREATMENT
MEDICATIONS
SIGNS & SYMPTOMS ¡ƑūƥūŠƎƭŞƎĿŠĺĿċĿƥūƑƙ
ƒ /ɍijɍūŞĚƎƑîǕūŕĚɒŞîŠîijĚîČĿēƑĚǷƭNJ
ƒ Often asymptomatic
ƒ ¬îŞĚîƙƑĚǷƭNJɈŠūƥɚĿŠĿƥĿîŕɛČîŠČĚƑūƭƙ ĺĚŞūƎƑĚDŽĚŠƥĿūŠ
changes ƒ sūŠēNjƙƎŕîƙƥĿČɓŕūDžɠijƑîēĚŕĚƙĿūŠ
ƒ GƑĚƐƭĚŠƥɈƎƑūŕūŠijĚēĺĚîƑƥċƭƑŠɈēNjƙƎĺîijĿîɈ Ɠ Aspirin, NSAIDS ĺinhibition of
hematemesis, epigastric pain, weight loss cyclooxygenase (COX-1 & 2) may
(due to painful eating) protect against progression of disease

DIAGNOSIS SURGERY
¹ƑĚîƥŞĚŠƥūIJēNjƙƎŕîƙƥĿČŕĚƙĿūŠƙ
DIAGNOSTIC IMAGING
ƒ Endoscopic mucosal resection, surgical
/ƙūƎĺîijūijîƙƥƑūēƭūēĚŠūƙČūƎNj removal of esophagus, radiation therapy,
ƒ Fiber optic camera inserted via mouth ĺ systemic chemotherapy
examine and biopsy esophagus, stomach,
duodenum OTHER INTERVENTIONS
ŠŠƭîŕĚŠēūƙČūƎĿČūċƙĚƑDŽîƥĿūŠ
LAB RESULTS
ƒ GūƑŠūŠēNjƙƎŕîƙƥĿČɓŕūDžɠijƑîēĚŕĚƙĿūŠƙ
ĿūƎƙNj
qîŠîijĚŞĚŠƥūIJîČĿēƑĚǷƭNJ
ƒ Specimen from
ƒ DŽūĿēɓƑĚēƭČĚĿŠƥîŒĚūIJIJūūēƙŒŠūDžŠƥū
esophagogastroduodenoscopy must
DžūƑƙĚŠƑĚǷƭNJɇČĺūČūŕîƥĚɈČūIJIJĚĚɈƥĚîɈ
contain goblet cells ĺ“intestinal
ƎĚƎƎĚƑŞĿŠƥɈîŕČūĺūŕɈIJîƥƥNjɓƙƎĿČNjɓîČĿēĿČIJūūēƙ
metaplasia” ĺmarker for progression of
metaplasia to dysplasia ĺadenocarcinoma ¹ƑĚîƥŞĚŠƥūIJēNjƙƎŕîƙƥĿČŕĚƙĿūŠƙ
ƒ Immunohistochemical staining assists in ƒ ¤îēĿūIJƑĚƐƭĚŠČNjîċŕîƥĿūŠ
diagnosis
Ɠ Electrical current used to destroy small
ƒ ĿūƎƙNjČŕîƙƙĿǶČîƥĿūŠ regions of tissue
Ɠ Nondysplastic ƒ Spray cryotherapy
Ɠ Low-grade dysplasia Ɠ gĿƐƭĿēŠĿƥƑūijĚŠƙƎƑîNjîƎƎŕĿĚēƥūƙŞîŕŕ
Ɠ High-grade dysplasia region of tissue ĺ freezing ĺ tissue
Ɠ Frank carcinoma death
ƒ Photodynamic therapy
OTHER DIAGNOSTICS Ɠ Chemical photosensitizer ĺcytotoxicity
DžĺĚŠƙƥĿŞƭŕîƥĚēċNjČĚƑƥîĿŠIJƑĚƐƭĚŠČNj
¬ČƑĚĚŠĿŠij of light
ƒ Biological malesɈʑȇȁNjĚîƑƙūŕēɈŕūŠij
ƙƥîŠēĿŠijƑĚǷƭNJɈŕĿIJĚĚNJƎĚČƥîŠČNjʑǶDŽĚNjĚîƑƙ
ƒ Anyone with diagnosis of Barrett’s
esophagus

/ƙūƎĺîijĚîŕƎOƙƥƭēĿĚƙ
ƒ /ƙƥîċŕĿƙĺĚIJǶČîČNjūIJƎƑūƥūŠƎƭŞƎĿŠĺĿċĿƥūƑ
treatment

218 OSMOSIS.ORG
    ĺîƎƥĚƑȄȁEsophageal Disease

Figure 30.2OĿƙƥūŕūijĿČîŕîƎƎĚîƑîŠČĚūIJƥĺĚƙƐƭîŞūČūŕƭŞŠîƑŏƭŠČƥĿūŠĿŠîČîƙĚūIJîƑƑĚƥƥɫƙ
esophagus. The underlying glandular epithelium contains goblet cells, indicating intestinal
metaplasia.

BOERHAAVE SYNDROME
osms.it/boerhaave-syndrome
Ɠ Chemical mediastinitis ĺ mediastinal
PATHOLOGY & CAUSES necrosis ĺ rupture of overlying pleura
ĺ contamination of pleural cavity ĺ
ƒ Rupture through esophagus caused by pleural effusion
increased intraesophageal pressure and Ɠ Effort rupture of cervical esophagus ĺ
negative intrathoracic pressure localized cervical perforation
ƒ ×ūŞĿƥĿŠijɓƑĚƥČĺĿŠijĺ unrelaxed Ɠ Spread of contamination slow due
esophagus, closed glottis ĺ increase to attachments of esophagus to
in esophageal pressure, slight drop in prevertebral fascia
intrathoracic pressure ĺ spontaneous
ƒ Usually occurs in anatomically normal
rupture of esophageal wall ĺ
esophagi
contamination of mediastinum with gastric
contents ĺ chemical mediastinitis
Ɠ Tears commonly occur at left RISK FACTORS
posterolateral aspect (distal esophagus), ƒ îƭƙƥĿČĿŠijĚƙƥĿūŠɈƎĿŕŕɓŞĚēĿČîƥĿūŠ
just above esophageal hiatus of esophagitis, eosinophilic esophagitis,
diaphragm Barrett’s esophagus, infectious ulcers,
Ɠ Can be fatal without treatment ĺ sepsis stricture dilatation

OSMOSIS.ORG 219
 ƒ Barium sulfate common contrast material,
SIGNS & SYMPTOMS but spillage into mediastinal and pleural
spaces ĺĿŠǷîƥūƑNjƑĚƙƎūŠƙĚĺ
ƒ Severe vomiting ĺprofound retrosternal ǶċƑūƙĿƙ
chest pain (may radiate to left shoulder) or
abdominal pain /ŠēūƙČūƎNjîDŽūĿēĚē
Ɠ Followed by painful swallowing ƒ May extend tear, introduce air into
(odynophagia), tachypnea, dyspnea, mediastinum
cyanosis, fever, shock
ƒ Mackler’s triad: chest pain, vomiting, LAB RESULTS
subcutaneous emphysema
ƒ Hemoglobin and hematocrit
ƒ Hamman’s sign:ČƑƭŠČĺĿŠijɓƑîƙƎĿŠijƙūƭŠēɈ
ƒ Assess severity of initial bleeding
ƙNjŠČĺƑūŠūƭƙDžĿƥĺĺĚîƑƥċĚîƥɇ
ƒ ¡ŕĚƭƑîŕĚIJIJƭƙĿūŠǷƭĿēŞîNjċĚĺĿijĺĿŠ
Ɠ Heard over precordium, left lateral
amylase (saliva), low pH
position
ƒ Leukocytosis
Ɠ Caused by mediastinal emphysema
ƒ Cervical perforation:ŠĚČŒƎîĿŠɈēĿIJǶČƭŕƥNj
ƙDžîŕŕūDžĿŠijɚēNjƙƎĺîijĿîɛɈēĿIJǶČƭŕƥNj
speaking (dysphonia), tenderness of
sternocleidomastoid
ƒ Intra-abdominal perforation: epigastric
pain (may radiate to left shoulder), back
pain, inability to lie supine, acute abdomen
pain

DIAGNOSIS
ƒ sūŠɠƙƎĚČĿǶČƙNjŞƎƥūŞƙĺ diagnostic delay,
poor outcome
ƒ Physical examination often unhelpful;
history important

DIAGNOSTIC IMAGING
ĺĚƙƥÝɠƑîNj
ƒ Early: free mediastinal air
ƒ Hours to days later: pleural effusion,
pneumothorax, widened mediastinum, Figure 30.3 A contrast swallow in an
subcutaneous emphysema individual with Boerhaave’s syndrome. The
ĺĚƙƥ ¹ƙČîŠ contrast has leaked into and accumulated in
the thoracic cavity.
ƒ /ƙūƎĺîijĚîŕDžîŕŕĚēĚŞîɓƥĺĿČŒĚŠĿŠijɈ
ĚNJƥƑîĚƙūƎĺîijĚîŕîĿƑɈƎĚƑĿĚƙūƎĺîijĚîŕǷƭĿēɈ
mediastinal widening, pneumothorax

GŕƭūƑūƙČūƎNj
ƒ Water soluble contrastɚijîƙƥƑūijƑîǶŠɛ
esophagram ĺ location and extent of
extravasation of contrast

ȃȃȁ OSMOSIS.ORG
    ĺîƎƥĚƑȄȁEsophageal Disease

SURGERY
TREATMENT ƒ 'ĚċƑĿēĚĿŠIJĚČƥĚēɓŠĚČƑūƥĿČƥĿƙƙƭĚ, repair
ēĚIJĚČƥɓƑĚƙĚČƥĿūŠūIJēĚIJĚČƥɓēĿDŽĚƑƙĿūŠ
MEDICATIONS
ƒ IV proton pump inhibitor ĺ reduce acidity,
irritation OTHER INTERVENTIONS
ƒ Prophylactic antibiotic therapy ƒ ¡îƑĚŠƥĚƑîŕɓĚŠƥĚƑîŕɚ ŏĚŏƭŠūƙƥūŞNjɓ¡/HƥƭċĚɛ
nutritional support

DIFFUSE ESOPHAGEAL SPASM

osms.it/esophageal-spasm

PATHOLOGY & CAUSES DIAGNOSIS

ƒ Esophageal motility disorder characterized DIAGNOSTIC IMAGING
by repetitive, non-peristaltic, spontaneous
contractions of the distal esophageal îƑĿƭŞƙDžîŕŕūDžNJɠƑîNjɚƭƎƎĚƑHTɛ
smooth muscle ƒ “Corkscrew” appearance is characteristic
ƒ Sphincter function = normal
/ŠēūƙČūƎNj
ƒ Exclude heart disease, mechanical
CAUSES intraluminal obstruction
ƒ Cause relatively unknown
ƒ Uncontrolled brain signals and extremely OTHER DIAGNOSTICS
ĺūƥɓČūŕēċĚDŽĚƑîijĚƙČîŠƥƑĿijijĚƑēĿƙĚîƙĚ
ȃȅɠĺūƭƑĚƙūƎĺîijĚîŕŞîŠūŞĚƥƑNj
COMPLICATIONS ƒ Shows uncoordinated esophageal
contractions of normal amplitude
ƒ gĚîēƙƥūēĿIJǶČƭŕƥNjƙDžîŕŕūDžĿŠijɈĿŞƎîĿƑĚē
îēDŽîŠČĚŞĚŠƥūIJIJūūēîŠēɓūƑƑĚijƭƑijĿƥîƥĿūŠ
TREATMENT
SIGNS & SYMPTOMS
ƒ No cure
ƒ Intermittent dysphagia
ƒ Atypical chest pain that mimics cardiac MEDICATIONS
chest pain; may radiate to jaw, arms, back ƒ sĿƥƑîƥĚƙɈČîŕČĿƭŞČĺĚŕċŕūČŒĚƑƙɈîŠēɓ
ƒ Food regurgitation relatively uncommon or botulinum toxin injections to lower
esophageal muscle; used to decrease
spasms
ƒ Antidepressants, anti-anxiety medications

SURGERY
ƒ Surgical esophagomyotomy rarely
considered

OSMOSIS.ORG 221
 GASTROESOPHAGEAL REFLUX
DISEASE (GERD)
osms.it/gastroesophageal-reflux
Ɠ Often felt shortly after eating meals
PATHOLOGY & CAUSES ɚDžūƑƙĚîIJƥĚƑŕîƑijĚŞĚîŕƙɓDžĺĚŠŕNjĿŠij
down)
ƒ eîČĿēƑĚǷƭNJ ƒ Halitosis, tooth decay
ƒ Failure of lower esophageal sphincter ĺ
ƎūūƑČŕūƙƭƑĚɓĿŠîƎƎƑūƎƑĿîƥĚƑĚŕîNJîƥĿūŠɚƎūūƑ
tone) of lower esophageal sphincter ĺ DIAGNOSIS
stomach contents re-enter esophagus
ƒ Commonly associated with decreased ƒ Can be diagnosed based on clinical
esophageal motility, gastric outlet symptoms, history alone
obstruction, hiatal hernia
DIAGNOSTIC IMAGING
RISK FACTORS
ƒ Obesity, pregnancy, smoking, hiatal hernia /ŠēūƙČūƎNj
ƒ Medications ƒ ÀƙĚēDžĺĚŠƥĺĚƑîƎĚƭƥĿČƑĚƙƎūŠƙĚƎūūƑɓ
concerning symptoms present (dysphagia,
Ɠ Antihistamines, calcium channel
anemia, blood in stool, wheezing, weight
blockers, antidepressants, hypnotics,
loss, voice changes)
glucocorticoids
ƒ Zollinger–Ellison syndrome, high blood ÀƎƎĚƑHTƙĚƑĿĚƙÝɠƑîNjƙDžĿƥĺċîƑĿƭŞČūŠɠ
calcium (increased gastrin production), trast
ƙČŕĚƑūēĚƑŞîɓƙNjƙƥĚŞĿČƙČŕĚƑūƙĿƙɚĚƙūƎĺîijĚîŕ ƒ Useful to identify complications
dysmotility)
ƒ /îƑŕNjƙƥîijĚƙūIJƑĚǷƭNJĚƙūƎĺîijĿƥĿƙɇijƑîŠƭŕîƑ
ƒ Visceroptosis nodular appearance of mucosa in distal
third of esophagus with numerous ill-
COMPLICATIONS ēĚǶŠĚēȂɝȄŞŞŕƭČĚŠČĿĚƙ
ƒ Esophagitis, esophageal strictures, Barrett’s ƒ Shallow ulcers and erosions
esophagus (premalignant condition), Ɠ Collections of barium in distal
esophageal adenocarcinoma, laryngitis, esophagus near gastroesophageal
ČĺƑūŠĿČČūƭijĺɈƎƭŕŞūŠîƑNjǶċƑūƙĿƙɈĚîƑîČĺĚɈ junction
asthma, recurrent pneumonia Ɠ Identify stricture (tapered area
of concentric narrowing in distal
esophagus)
SIGNS & SYMPTOMS
ƒ Acid taste in mouth, heartburn, retrosternal
LAB RESULTS
chest pain, early satiety, regurgitation, ƒ 24-hour esophageal pH monitoring in
odynophagia, increased salivation, lower esophagus
postprandial nausea and vomiting,
sore throat, sensation of lump in throat,
coughing, wheezing

222 OSMOSIS.ORG
    ĺîƎƥĚƑȄȁEsophageal Disease

ĿūƎƙNj
ƒ /ēĚŞîɈċîƙîŕĺNjƎĚƑƎŕîƙĿîɚŠūŠɠƙƎĚČĿǶČ
ĿŠǷîƥĿūŠɛ
ƒ gNjŞƎĺūČNjƥĿČĿŠǷîƥĿūŠɚŠūŠɠƙƎĚČĿǶČɛ
ƒ sĚƭƥƑūƎĺĿŕĿČĿŠǷîƥĿūŠɚƑĚǷƭNJɓ
Helicobacter gastritis)
ƒ /ūƙĿŠūƎĺĿŕĿČĿŠǷîƥĿūŠɚƭƙƭîŕŕNjƑĚǷƭNJɈ
ĿIJʑȃȁĚūƙĿŠūƎĺĿŕƙƎĚƑĺĿijĺɠƎūDžĚƑǶĚŕē
extending beyond distal esophagus, more
like eosinophilic esophagitis)
ƒ Elongation of papillae
ƒ Goblet cell intestinal metaplasia
ƒ ¹ĺĿŠŠĿŠijūIJƙƐƭîŞūƭƙČĚŕŕŕîNjĚƑ
ƒ Dysplasia
ƒ Carcinoma Figure 30.4 The histological appearance of
ƥĺĚƙƐƭîŞūƭƙɠŕĿŠĚēĚƙūƎĺîijƭƙĿŠîČîƙĚūIJ
OTHER DIAGNOSTICS ƑĚǷƭNJɍ¹ĺĚƎîƎĿŕŕîĚċĚČūŞĚĚŕūŠijîƥĚēîŠē
ƒ Esophageal manometry (excludes motility there is overgrowth of the basal cells (darker
disorder) blue) known as basal cell hyperplasia.
ƒ Short term trial of proton-pump inhibitors

TREATMENT
MEDICATIONS
ƒ Antacids neutralise acidity of gastric
secretions
ƒ OȃƑĚČĚƎƥūƑċŕūČŒĚƑƙēĚČƑĚîƙĚîČĿēĿǶČîƥĿūŠ
of gastric secretions
ƒ Proton pump inhibitors decrease
îČĿēĿǶČîƥĿūŠūIJijîƙƥƑĿČƙĚČƑĚƥĿūŠƙ
ƒ Prokinetics strengthen lower esophageal
sphincter (LES), causing stomach contents
to empty faster
ƒ Baclofen (GABAB agonist)
Ɠ Inhibits transient LES relaxations,
particularly in postprandial period
Ɠ Modestly effective, but rarely used due
ƥūIJƑĚƐƭĚŠƥēūƙĿŠijƑĚƐƭĿƑĚŞĚŠƥƙ

¬ƭƑIJîČĚîijĚŠƥƙîŠēîŕijĿŠîƥĚƙ
Figure 30.5 A contrast X-ray demonstrating ƒ Sucralfate (aluminium sucrose sulfate)
ijîƙƥƑūĚƙūƎĺîijĚîŕƑĚǷƭNJɍ¹ĺĚČūŠƥƑîƙƥ Ɠ Adheres to mucosal surface ĺ
medium was injected percutaneously into promotes healing, protects from peptic
the stomach and has migrated into the injury
esophagus.
ƒ Sodium alginate
Ɠ Polysaccharide derived from seaweed
ĺIJūƑŞƙîDŽĿƙČūƭƙijƭŞƥĺîƥǷūîƥƙ
within stomach ĺ reduced postprandial
acid pocket in proximal stomach

OSMOSIS.ORG ȃȃȄ
 SURGERY
sĿƙƙĚŠIJƭŠēūƎŕĿČîƥĿūŠ
ƒ Upper part of stomach wrapped around
lower esophageal sphincter ĺ strengthens
ƙƎĺĿŠČƥĚƑɈƎƑĚDŽĚŠƥƙîČĿēƑĚǷƭNJ

¹ƑîŠƙūƑîŕĿŠČĿƙĿūŠŕĚƙƙIJƭŠēūƎŕĿČîƥĿūŠ
ƒ Similar procedure to Nissen fundoplication,
performed transorally with endoscope

gTsÝƑĚǷƭNJŞîŠîijĚŞĚŠƥƙNjƙƥĚŞ
ƒ Titanium beads with magnetic cores
wrapped around weak native lower
esophageal sphincter ĺ attractive force
between beads closing sphincter ĺ force
of peristaltic wave of caused by swallowing Figure 30.6 An endoscopic view of
can transiently open beads an esophageal stricture, a potential
ČūŠƙĚƐƭĚŠČĚūIJƙĚDŽĚƑĚɈŕūŠijɠƙƥîŠēĿŠijƑĚǷƭNJɍ
OTHER INTERVENTIONS
gĿIJĚƙƥNjŕĚŞūēĿǶČîƥĿūŠƙ
ƒ Avoid lying down within three hours after
eating, wedge pillow when sleeping to
elevate head, weight loss, avoid certain
IJūūēƙɚČūIJIJĚĚɈîŕČūĺūŕɈČĺūČūŕîƥĚɈIJîƥƥNjɓ
îČĿēĿČɓƙƎĿČNjIJūūēƙɛɈƙŞūŒĿŠijČĚƙƙîƥĿūŠɈ
moderate exercise

MALLORY–WEISS SYNDROME
osms.it/mallory-weiss
CAUSES
PATHOLOGY & CAUSES ƒ Vomiting, straining, coughing, seizures,
blunt abdominal injury, nasogastric tube
ƒ Severe vomiting ĺ sudden increase placement, gastroscopy
in intra-abdominal pressure ĺ partial
thickness laceration at gastroesophageal
junction ĺ bleeding from mucosa RISK FACTORS
ƒ Also called gastroesophageal laceration ƒ Alcoholism, bulimia, food poisoning, hiatal
syndrome hernia, NSAID abuse, biological male sex
ƒ Laceration known as “Mallory–Weiss tear”, ɚȉȁʣɛɈĺNjƎĚƑĚŞĚƙĿƙijƑîDŽĿēîƑƭŞɚƙĚDŽĚƑĚ
involves mucosa and submucosa, not morning sickness in pregnancy)
muscular layer

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    ĺîƎƥĚƑȄȁEsophageal Disease

SIGNS & SYMPTOMS TREATMENT

ƒ Hematemesis after episode of violent ƒ In absence of comorbidities (esp. portal vein
ƑĚƥČĺĿŠijɓDŽūŞĿƥĿŠij ĺNjƎĚƑƥĚŠƙĿūŠɛɈƙĿijŠĿǶČîŠƥĺĚîŕĿŠijūČČƭƑƙĿŠ
ƒ Melena ǶƑƙƥȃȅɝȅȉĺūƭƑƙ
ƒ Bleeding associated symptoms may cease
îIJƥĚƑȃȅɝȅȉĺūƭƑƙ MEDICATIONS
ƒ Epigastric, back pain
¬ƭƎƎūƑƥĿDŽĚɚƎĚƑƙĿƙƥĚŠƥċŕĚĚēĿŠijƭŠČūŞɠ
ƒ Signs of hemodynamic instability
ŞūŠɛ
Ɠ Resting tachycardia, hypotension
ƒ Acid suppression
Ɠ IV proton pump inhibitor
DIAGNOSIS ƒ If nausea and vomiting persistent
Ɠ Antiemetics
DIAGNOSTIC IMAGING
/ŠēūƙČūƎNj SURGERY
ƒ Tears appear as red longitudinal breaks in /ŠēūƙČūƎNjɚIJūƑƙƎƭƑƥĿŠijɓūūǕĿŠijƥĚîƑƙɛ
mucosa, may be covered by clot
ƒ Cauterization, hemoclips (hemostasis of
small defects), endoscopic band ligation
LAB RESULTS (with or without epinephrine injection),
ƒ Hemoglobin, hematocrit (assess severity of arterial embolization
initial bleeding)

Figure 30.7 Endoscopic appearance of a

Mallory-Weiss tear.

OSMOSIS.ORG 225
 PLUMMER–VINSON SYNDROME
osms.it/plummer-vinson
DIAGNOSTIC IMAGING
PATHOLOGY & CAUSES
îƑĿƭŞĚƙūƎĺîijūijƑîƎĺNjɈDŽĿēĚūǷƭūƑūƙČūƎNjɈ
ƒ Triad of ĿƑūŠēĚǶČĿĚŠČNjîŠĚŞĿî, dysphagia, ĚƙūƎĺîijūijîƙƥƑūēƭūēĚŠūƙČūƎNj
cervical esophageal web ƒ Esophageal web
ƒ AKA Paterson–Brown–Kelly syndrome,
sideropenic dysphagia
LAB RESULTS
ƒ Premalignant disease
ƒ Anemia
Ɠ Complete blood cell count, peripheral
CAUSES blood smear, iron study
ƒ Exact cause unknown, likely connected to
ijĚŠĚƥĿČIJîČƥūƑƙɈŠƭƥƑĿƥĿūŠîŕēĚǶČĿĚŠČĿĚƙ
TREATMENT
RISK FACTORS
MEDICATIONS
ƒ Postmenopause
ƒ Iron supplementation, folate, vitamin B12
ĺČūƑƑĚČƥĿƑūŠēĚǶČĿĚŠČNjîŠĚŞĿî
COMPLICATIONS
ƒ /ƙūƎĺîijĚîŕɓƎĺîƑNjŠijĚîŕƙƐƭîŞūƭƙČĚŕŕ SURGERY
carcinoma
ƒ Mechanical widening of esophagus

SIGNS & SYMPTOMS

ƒ Esophageal signs and symptoms
Ɠ /ƙūƎĺîijĚîŕDžĚċƙɈēĿIJǶČƭŕƥɓƎîĿŠIJƭŕ
swallowing, Plummer–Vinson syndrome
at upper end of esophagus, Schatzki
ring lower end of esophagus
ƒ TƑūŠēĚǶČĿĚŠČNjƙĿijŠƙîŠēƙNjŞƎƥūŞƙ
Ɠ Glossitis, cheilosis, angular stomatitis,
koilonychia, splenomegaly, dizziness,
pallor, dyspnea

DIAGNOSIS
ƒ Presence of esophageal web in individual
DžĿƥĺĿƑūŠēĚǶČĿĚŠČNjîŠĚŞĿî Figure 30.8 An endoscopic view of an
esophageal web which is usually associated
with Plummer-Vinson syndrome.

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    ĺîƎƥĚƑȄȁEsophageal Disease

ZENKER'S DIVERTICULUM
osms.it/zenkers
¹ƙČîŠDžĿƥĺūƑîŕČūŠƥƑîƙƥ
PATHOLOGY & CAUSES
ƒ Distinct outpouching visible
ƒ Diverticulum (outpouching) of pharyngeal
mucosa through Killian’s triangle (area of
muscular weakness), between transverse
TREATMENT
ǶċƑĚƙūIJČƑĿČūƎĺîƑNjŠijĚƭƙŞƭƙČŕĚîŠē
ūċŕĿƐƭĚǶċƑĚƙūIJŕūDžĚƑĿŠIJĚƑĿūƑČūŠƙƥƑĿČƥūƑ ƒ ¬ŞîŕŕɓîƙNjŞƎƥūŞîƥĿČēĿDŽĚƑƥĿČƭŕîēūŠūƥ
muscle ƑĚƐƭĿƑĚƥƑĚîƥŞĚŠƥ
ƒ AKA pharyngoesophageal diverticulum,
pharyngeal pouch, hypopharyngeal SURGERY
diverticulum ƒ Neck surgery ĺ cricopharyngeal myotomy,
ƒ Pseudodiverticulum diverticulopexy
Ɠ Does not involve all layers of esophageal
wall ĺcontains mucosa, submucosa OTHER INTERVENTIONS
ƒ sūŠɠƙƭƑijĿČîŕĚŠēūƙČūƎĿČƥĚČĺŠĿƐƭĚ
CAUSES ƒ Endoscopic stapling
ƒ Uncoordinated swallowing, impaired ƒ Endoscopic laser
relaxation and swallowing, impaired
relaxation and spasm of cricopharyngeus
muscle ĺincreased pressures in distal
pharynx ĺ excessive lower pharyngeal
pressures ĺdiverticulum formation

RISK FACTORS
ƒ Biological maleʑȇȁNjĚîƑƙūŕē

SIGNS & SYMPTOMS

ƒ May be asymptomatic
ƒ 'ĿIJǶČƭŕƥNjƙDžîŕŕūDžĿŠij, sense of lump in
throat, cervical webs
ƒ Food trapping
Ɠ Regurgitation, cough, halitosis, infection

DIAGNOSIS
DIAGNOSTIC IMAGING
Barium swallow
ƒ Distinct outpouching visible
Figure 30.9 A barium swallow
ÀƎƎĚƑijîƙƥƑūĿŠƥĚƙƥĿŠîŕĚŠēūƙČūƎNj demonstrating a Zenker’s diverticulum,
ƒ Pouch visualized outlined on the right of the image.

OSMOSIS.ORG 227
 NOTES

NOTES
GASTRIC DISEASE

GENERALLY, WHAT IS IT?

PATHOLOGY & CAUSES TREATMENT
ƒ Diseases affecting gastric mucosa, gastric MEDICATIONS
outlet, etc. ƒ Proton pump inhibitor (PPI)
ƒ TŠǷîƥĿūŠēƭĚƥūĿŠIJĚČƥĿūŠɒƭŕČĚƑîƥĿūŠ ƒ ūƑƑĚČƥǷƭĿēɈĚŕĚČƥƑūŕNjƥĚēĚǶČĿƥƙ
ƒ 'ĿƙČūŠƥĿŠƭĚŠūŠƙƥĚƑūĿēîŕîŠƥĿɠĿŠǷîƥūƑNj
ēƑƭijƙɚs¬T'ƙɛ
SIGNS & SYMPTOMS
ƒ May be asymptomatic SURGERY
ƒ Epigastric pain, nausea, vomiting ƒ /ŠēūƙČūƎĿČŕĿijîƥĿūŠɓČūîijƭŕîƥĿūŠ
ƒ ŠĚŞĿîɒIJĚČîŕɈƭƑĿŠîƑNjĿŠČūŠƥĿŠĚŠČĚɒƭŕČĚƑƙɒ ƒ Surgical repair
ċŕĚĚēĿŠij
OTHER INTERVENTIONS
ƒ 'ĿĚƥîƑNjŞūēĿǶČîƥĿūŠɒĚNJĚƑČĿƙĚ
DIAGNOSIS ƒ DŽūĿēƙŞūŒĿŠij
DIAGNOSTIC IMAGING
ƒ /ŠēūƙČūƎNj

LAB RESULTS
ƒ Biopsy

228 OSMOSIS.ORG
 Chapter 31 Gastric Disease

CYCLIC VOMITING SYNDROME

osms.it/cyclic-vomiting
ƒ Autonomic:ŕĚƥĺîƑijNjɈƎîŕŕūƑɈĚNJČĚƙƙĿDŽĚ
PATHOLOGY & CAUSES ƙîŕĿDŽîƥĿūŠɈŕūDžijƑîēĚIJĚDŽĚƑ
ƒ Neurologic:ĺĚîēîČĺĚɈƎĺūƥūƎĺūċĿîɈ
ƒ ŠƭŠČūŞŞūŠēĿƙūƑēĚƑČĺîƑîČƥĚƑĿǕĚēċNj
phonophobia, vertigo
ƑĚČƭƑƑĚŠƥĚƎĿƙūēĚƙūIJDŽūŞĿƥĿŠijƙĚƎîƑîƥĚē
ċNjîƙNjŞƎƥūŞîƥĿČƎĚƑĿūēƙ ƒ ¬ūČĿîŕDžĿƥĺēƑîDžîŕ
ƒ Median onset age:ȆɝȇNjĚîƑƙūŕē
DIAGNOSIS
CAUSES
ƒ îƭƙĚƭŠŒŠūDžŠɒƥƑĿijijĚƑƙŞîNjĿŠČŕƭēĚ OTHER DIAGNOSTICS
psychological stress (e.g. interpersonal ƒ OĿƙƥūƑNjîŠēƎĺNjƙĿČîŕĚNJîŞĿŠîƥĿūŠ
ČūŠǷĿČƥɈĺūŕĿēîNjƙɛūƑƎĺNjƙĿČîŕƙƥƑĚƙƙɚĚɍijɍ Ɠ sūĿēĚŠƥĿǶîċŕĚūƑijîŠĿČČîƭƙĚ
ĿŠIJĚČƥĿūŠƙɈĚNJĺîƭƙƥĿūŠɛɈČĚƑƥîĿŠIJūūēƙɚĚɍijɍ ƒ Diagnostic criteria (Rome IV criteria)
ČūDžɫƙŞĿŕŒɈČĺūČūŕîƥĚɈČĺĚĚƙĚɈŞūŠūƙūēĿƭŞ
Ɠ ʓƥĺƑĚĚƑĚČƭƑƑĚŠƥɈēĿƙČƑĚƥĚĚƎĿƙūēĚƙ
glutamate) menses
of vomiting in the prior year, with
ƥDžūĚƎĿƙūēĚƙĿŠƥĺĚƎîƙƥƙĿNJŞūŠƥĺƙ
RISK FACTORS ūČČƭƑƑĿŠijîƥŕĚîƙƥūŠĚDžĚĚŒîƎîƑƥ
ƒ ĺĿŕēƑĚŠʑîēƭŕƥƙ Ɠ Variable intervals between vomiting
Ɠ In children:ŞĿƥūČĺūŠēƑĿîŕ'sēĚŕĚƥĿūŠƙ ĚƎĿƙūēĚƙîŠēîƙNjŞƎƥūŞîƥĿČċîƙĚŕĿŠĚ
îŠēƎūŕNjŞūƑƎĺĿƙŞƙ Ɠ ¬ƥĚƑĚūƥNjƎĿČîŕČĺîƑîČƥĚƑĿƙƥĿČƙƑĚijîƑēĿŠij
ƒ Females > males ƥĿŞĿŠijūIJūŠƙĚƥɈƙNjŞƎƥūŞƙɈîŠēēƭƑîƥĿūŠ
ƒ Family history of migraines
ƒ ƭƥūŠūŞĿČîċŠūƑŞîŕĿƥĿĚƙɚĚŕĚDŽîƥĚē
sympathetic tone)
TREATMENT
ƒ ONjƎūƥĺîŕîŞĿČɠƎĿƥƭĿƥîƑNjɠîēƑĚŠîŕîČƥĿDŽîƥĿūŠ
OTHER INTERVENTIONS
(Sato variant)
ƒ 'ƭƑĿŠijČNjČŕĿČDŽūŞĿƥĿŠijĚƎĿƙūēĚƙ
ƒ Chronic cannabis use
Ɠ T×ǷƭĿēƙɈîŠƥĿĚŞĚƥĿČƙɈƙĚēîƥĿDŽĚƙɒČūŞIJūƑƥ
ČîƑĚĿŠēîƑŒɈƐƭĿĚƥƑūūŞ
COMPLICATIONS
ƒ Erosive esophagitis Prevention
ƒ qîŕŕūƑNjɠØĚĿƙƙƥĚîƑ ƒ Prophylactic therapy
ƒ 'ĚĺNjēƑîƥĿūŠ Ɠ OȂɠîŠƥîijūŠĿƙƥƙɚĚɍijɍČNjƎƑūĺĚƎƥîēĿŠĚɛ
IJūƑČĺĿŕēƑĚŠʔǶDŽĚNjĚîƑƙūŕē
ƒ Electrolyte imbalance
Ɠ ¹ƑĿČNjČŕĿČîŠƥĿēĚƎƑĚƙƙîŠƥƙɚĚɍijɍ
ƒ ÀŠĿŠƥĚŠēĚēDžĚĿijĺƥŕūƙƙ
amitriptyline) > years of age
ƒ Abortive therapy
SIGNS & SYMPTOMS Ɠ ¹ƑĿƎƥîŠƙɒŠĚƭƑūŒĿŠĿŠɠȂƑĚČĚƎƥūƑ
antagonists
ƒ ¬NjŞƎƥūŞƙƥĚŠēƥūēĚDŽĚŕūƎîƥŠĿijĺƥɈĿŠƥĺĚ ƒ DŽūĿēîŠČĚūIJƥƑĿijijĚƑƙ
ĚîƑŕNjŞūƑŠĿŠijĺūƭƑƙɈūƑƭƎūŠîDžîŒĚŠĿŠij
ƒ ¡ƑūēƑūŞîŕƎĚƑĿūēĿƙČūŞŞūŠ
ƒ Gastrointestinal: vomiting which may
ĿŠČŕƭēĚċĿŕĚūƑċŕūūēɒƑĚƥČĺĿŠijɈîċēūŞĿŠîŕ
ƎîĿŠɈēĿîƑƑĺĚî

OSMOSIS.ORG 229
 GASTRIC DUMPING SYNDROME
osms.it/gastric-dumping

PATHOLOGY & CAUSES DIAGNOSIS

ƒ TîƥƑūijĚŠĿČƎūƙƥɠijîƙƥƑĿČƙƭƑijĚƑNjƙNjŠēƑūŞĚɒ DIAGNOSTIC IMAGING
ĿŞƎîĿƑĚēijîƙƥƑĿČŞūƥĿŕĿƥNjĺƑîƎĿēƙƥūŞîČĺ ƒ /ŠēūƙČūƎNj
emptying
ƒ Surgical intervention ĺēĿƙƑƭƎƥĿūŠĿŠ
LAB RESULTS
ijîƙƥƑĿČîŠîƥūŞNjɈŞƭČūƙîŕIJƭŠČƥĿūŠɈIJƭŠēƭƙ
tone, antropyloric regulatory mechanisms, ƒ Oral glucose challenge test elicits
ēƭūēĚŠîŕIJĚĚēċîČŒūŠŞūƥĿŕĿƥNjĺƑîƎĿē symptoms
emptying of stomach contents into ƒ ONjēƑūijĚŠċƑĚîƥĺƥĚƙƥîIJƥĚƑijŕƭČūƙĚ
ēƭūēĚŠƭŞ ingestion
ƒ ȆȁʣūIJĿŠēĿDŽĿēƭîŕƙƭŠēĚƑijūĿŠijijîƙƥƑĿČ
ƙƭƑijĿČîŕƎƑūČĚēƭƑĚƙ OTHER DIAGNOSTICS
ƒ qūƑĚČūŞŞūŠĿŠĿŠēĿDŽĿēƭîŕƙDžĺūîƑĚ ƒ HîƙƥƑĿČĚŞƎƥNjĿŠijƙƥƭēNj
biologically female ƒ ŕĿŠĿČîŕĿŠēĿČĚƙ
Ɠ Sigstad’s diagnostic index: > 7
Ɠ ×ĿƙĿČŒČŕîƙƙĿǶČîƥĿūŠɇheart rate
SIGNS & SYMPTOMS variations after oral glucose challenge
ƒ GI: ĚîƑŕNjƙîƥĿĚƥNjɒîċēūŞĿŠîŕČūŕĿČɒŠîƭƙĚîɈ
DŽūŞĿƥĿŠijɒĚNJƎŕūƙĿDŽĚēĿîƑƑĺĚîɒċŕūîƥĿŠijɒ TREATMENT
malabsorption
ƒ Vasomotor: ēĿîƎĺūƑĚƙĿƙɒƎîŕƎĿƥîƥĿūŠƙɒ MEDICATIONS
vertigo
ƒ /îƑŕNjēƭŞƎĿŠijƙNjŠēƑūŞĚ Acarbose
Ɠ ȄȁɝȇȁŞĿŠƭƥĚƙƎūƙƥɠŞĚîŕ ƒ TŠƥĚƑIJĚƑĚƙDžĿƥĺČîƑċūĺNjēƑîƥĚƑĚîċƙūƑƎƥĿūŠ
Ɠ ČČĚŕĚƑîƥĚēƙƥūŞîČĺĚŞƎƥNjĿŠijĺ
Octreotide
ĺNjƎĚƑūƙŞūŕîƑČūŠƥĚŠƥƙƎūƭƑĚēĿŠƥū
small bowel ĺ osmotic activity ĺ bowel ƒ Inhibits insulin release
ēĿƙƥĚŠƥĿūŠɈŞūƥĿŕĿƥNjƙƥĿŞƭŕîƥĚēĺ GI
symptoms OTHER INTERVENTIONS
ƒ gîƥĚēƭŞƎĿŠijƙNjŠēƑūŞĚ
'ĿĚƥîƑNjŞūēĿǶČîƥĿūŠ
Ɠ ȇȁɝȂȉȁŞĿŠƭƥĚƙƎūƙƥɠŞĚîŕ
ƒ DŽūĿēƙĿŞƎŕĚƙƭijîƑƙɈǷƭĿēĿŠƥîŒĚēƭƑĿŠij
Ɠ ČČĚŕĚƑîƥĚēƙƥūŞîČĺĚŞƎƥNjĿŠijĺĹ
ŞĚîŕƙɒŕūDžČîƑċūĺNjēƑîƥĚɈĺĿijĺƎƑūƥĚĿŠēĿĚƥ
ČîƑċūĺNjēƑîƥĚČūŠČĚŠƥƑîƥĿūŠĿŠƎƑūNJĿŞîŕ
intestine ĺƑîƎĿēijŕƭČūƙĚîċƙūƑƎƥĿūŠ
ĺƑîƎĿēɈƙƭƙƥîĿŠĚēĿŠƙƭŕĿŠƑĚƙƎūŠƙĚĺ
hypoglycemia ĺ vasomotor symptoms

230 OSMOSIS.ORG
 Chapter 31 Gastric Disease

GASTRITIS
osms.it/gastritis

ƒ Infectious
PATHOLOGY & CAUSES
Ɠ Most common cause (80%)
ƒ TŠǷîƥĿūŠūIJƥĺĚŕĿŠĿŠijūIJƥĺĚƙƥūŞîČĺ Ɠ H. pylori ĺ chronic gastritis ĺ gastric
ƒ qîNjūČČƭƑîƙîƙĺūƑƥĚƎĿƙūēĚūƑŞîNjċĚūIJ atrophy ĺ metaplasia ĺēNjƙƎŕîƙĿîĺ
îŕūŠijēƭƑîƥĿūŠ cancerɚîƙƙūČĿîƥĚēDžĿƥĺĿŠƥĚƙƥĿŠîŕɠƥNjƎĚ
gastric carcinoma)
Ɠ NjƥūƥūNJĿŠɠîƙƙūČĿîƥĚēijĚŠĚɚ îijɛɒ
TYPES carcinogenic virulence factor of H. pylori
Acute gastritis Ɠ sūƑŞîŕijîƙƥƑĿŠŕĚDŽĚŕƙɈŠūĺNjƎūČĺŕūƑĿēĿîɈ
ŠūîŠƥĿɠƎîƑĿĚƥîŕČĚŕŕɓîŠƥĿɠĿŠƥƑĿŠƙĿČIJîČƥūƑ
ƒ TŠǷîƥĿūŠūIJijîƙƥƑĿČŞƭČūƙîɒČūŞƎîƑĚƥū
îŠƥĿċūēĿĚƙɚČūŞƎîƑĚƥūîƭƥūĿŞŞƭŠĚ
ijîƙƥƑūƎîƥĺNjɚDžĿƥĺūƭƥîČƥĿDŽĚĿŠǷîƥĿūŠɛ
îƥƑūƎĺĿČijîƙƥƑĿƥĿƙɒĺNjƎūČĺŕūƑĿēĿîɈîŠƥĿɠ
ƒ Gastritis, gastropathy ƎîƑĿĚƥîŕɓîŠƥĿɠĿŠƥƑĿŠƙĿČIJîČƥūƑîŠƥĿċūēĿĚƙɛ
Ɠ ŕĿŠĿČîŕŕNjĿēĚŠƥĿČîŕɈĺĿƙƥūŕūijĿČîŕŕNjēĿƙƥĿŠČƥ Ɠ Gastric ulcers
Atrophic gastritis
ƒ AKA chronic gastritis, metaplastic gastritis,
gastric atrophy
ƒ ĺƑūŠĿČĿŠǷîƥĿūŠūIJijîƙƥƑĿČŞƭČūƙî
ĺ epithelial metaplasia, mucosal atrophy,
ijŕîŠēŕūƙƙ
Ɠ Metaplasia: reversible change of one
epithelium into another, response to
stress
Ɠ Intestinal metaplasia: goblet cells

CAUSES
Acute gastritis
ƒ ĚƑƥîĿŠŞĚēĿČîƥĿūŠƙɈîŕČūĺūŕɈ
ČūƑƥĿČūƙƥĚƑūĿēƙɈƭƑĚŞĿî
ƒ s¬T'ƙċŕūČŒČNjČŕūūNJNjijĚŠîƙĚĺĻ
ƎƑūƙƥîijŕîŠēĿŠ/ȃɈTȃƎƑūēƭČƥĿūŠĺĻ
ijîƙƥƑĿČēĚIJĚŠƙĚmechanisms (mucus, HCO3 Figure 31.1ĺĿijĺŞîijŠĿǶČîƥĿūŠĿŞîijĚūIJ
secretion) ĺ mucosal injury Helicobacter organisms within a gastric crypt.
ƒ H. pylori infection ĺ gastric mucosa Helicobacter are a common cause of gastritis.
ĿŠǶŕƥƑîƥĚƙîŠƥƑƭŞ, corpus ĺĿŠǷîƥĿūŠ
involving neutrophil, mononuclear cells
ƒ AlcoholɈČĿijîƑĚƥƥĚƙŞūŒĚɈČîIJIJĚĿŠĚĺ ƒ Autoimmune
ĿƑƑĿƥîƥĚƙɈĚƑūēĚƙƙƥūŞîČĺŞƭČūƙîŕĿŠĿŠij Ɠ qūƙƥČūŞŞūŠČîƭƙĚĿŠĿŠēĿDŽĿēƭîŕƙ
ƒ /NJƥƑĚŞĚƎĺNjƙĿūŕūijĿČîŕƙƥƑĚƙƙɚĚɍijɍƙĺūČŒɈ without H. pylori
sepsis, burns) Ɠ TŠĺĚƑĿƥĚēautoimmunity against intrinsic
factor, H+ɓe+ ATPase in parietal cells
Atrophic gastritis ĺĿŠĺĿċĿƥĿūŠūIJijîƙƥƑĿČîČĿēƙĚČƑĚƥĿūŠ
ƒ Two main causes:ĿŠIJĚČƥĿūƭƙîŠē ɚĺNjƎūČĺŕūƑĿēĿîɛɍĻ intrinsic factor ĺ
autoimmune

OSMOSIS.ORG 231
 cobalamin (BȂȃ) malabsorption ĺ
pernicious anemia DIAGNOSIS
Ɠ ONjƎūČĺŕūƑĿēĿîɚĿŞƎîĿƑĚēĿƑūŠîċƙūƑƎƥĿūŠ
ɓHɠČĚŕŕĺNjƎĚƑƎŕîƙĿîɈĺNjƎĚƑijîƙƥƑĿŠĚŞĿîĺ
LAB RESULTS
ĹŠĚƭƑūĚŠēūČƑĿŠĚƥƭŞūƑIJūƑŞîƥĿūŠɛ Endoscopic biopsy
ƓĹijîƙƥƑĿČîēĚŠūČîƑČĿŠūŞîɈ ƒ Distinguish gastropathy from gastritis,
ŠĚƭƑūĚŠēūČƑĿŠĚƥƭŞūƑƙ ŠūŠƙƎĚČĿǶČɒŞƭČūƙîŕĚƑūƙĿūŠƙɈĚƑNjƥĺĚŞîɈ
Ɠ 'îŞîijĚŕĿŞĿƥĚēƥūijîƙƥƑĿČIJƭŠēƭƙɈċūēNj absence of rugae
ƒ Infectious atrophic gastritis
RISK FACTORS Ɠ qƭŕƥĿIJūČîŕîƥƑūƎĺNjɒijîƙƥƑĿČɓēƭūēĚŠîŕ
ƭŕČĚƑƙɒĚƑNjƥĺĚŞîƥūƭƙɈŠūēƭŕîƑŞƭČūƙîɒ
Atrophic gastritis ƥĺĿČŒĚŠĚēƑƭijîŕIJūŕēƙĿŠĚîƑŕNjēĿƙĚîƙĚɈ
ƒ Infectious ŕūƙƙūIJƑƭijîŕIJūŕēƙĿŠŕîƥĚēĿƙĚîƙĚɒ
Ɠ OūƭƙĚĺūŕēČƑūDžēĿŠijɒƑƭƑîŕîƑĚîƙɒƎūūƑ ēîŞîijĚŕĿŞĿƥĚēƥūijîƙƥƑĿČîŠƥƑƭŞ
sanitation ƒ Autoimmune atrophic gastritis
ƒ Autoimmune Ɠ Diffuse atrophy, absent rugae, mucosal
Ɠ ƙƙūČĿîƥĚēDžĿƥĺOgɠ'¤ȄɈȉɈūƥĺĚƑ ƥĺĿŠŠĿŠijɈDŽĿƙĿċŕĚƙƭċŞƭČūƙîŕċŕūūē
îƭƥūĿŞŞƭŠĚēĿƙĚîƙĚƙɒŞūƑĚČūŞŞūŠĿŠ vessels
ċĿūŕūijĿČîŕŕNjɠIJĚŞîŕĚĿŠēĿDŽĿēƭîŕƙ
H. pylori detection
ƒ Serology, stool antigen test, urease breath
SIGNS & SYMPTOMS test, biopsy
ƒ Atrophic gastritis
ƒ May be asymptomatic Ɠ H. pylori ČƭƑDŽĚēċîČĿŕŕĿɚĺĚŞîƥūNJNjŕĿŠɈ
ƒ Epigastric pain, nausea, vomiting ĚūƙĿŠɒHĿĚŞƙîɒØîƑƥĺĿŠɠ¬ƥîƑƑNjƙƥîĿŠɛɒ
ƒ Mucosal ulcers intraepithelial neutrophil, plasma cell
invasion
ƒ Hemorrhage, hematemesis, melena
Other lab results
Autoimmune atrophic gastritis
ƒ Autoimmune atrophic gastritis
ƒ TƑūŠēĚǶČĿĚŠČNjîŠĚŞĿî
Ɠ ŠƥĿɠTGîŠƥĿċūēĿĚƙɈîŠƥĿɠƎîƑĿĚƥîŕČĚŕŕ
Ɠ ONjƎūČĺŕūƑĺNjēƑĿîĺēĿĚƥîƑNjĿƑūŠĿŠ
îŠƥĿċūēĿĚƙ
ferric form ĺĻ iron absorption ĺ iron
ēĚǶČĿĚŠČNj Ɠ Ĺ serum gastrin: parietal cell loss ĺ
îČĺŕūƑĺNjēƑĿîĺƭŠƑĚƙƥƑĿČƥĚēijîƙƥƑĿŠ
ƒ Pernicious anemia (symmetrical neuropathy
secretion
ƎƑĚēūŞĿŠîŠƥŕNjîIJIJĚČƥĿŠijŕūDžĚƑŕĿŞċƙɛ
ƓĻ serum pepsinogen: ijîƙƥƑĿČūNJNjŠƥĿČ
Ɠ ŠƥĿɠĿŠƥƑĿŠƙĿČIJîČƥūƑɚTGɛîŠƥĿċūēĿĚƙɈ
ŞƭČūƙîēîŞîijĚēĺĻ chief cells ĺĻ
Ļ cobalamin (BȂȃ) absorption ĺ
serum pepsinogen
ēĚƎŕĚƥĿūŠūIJȆɠŞĚƥĺNjŕɠƥĚƥƑîĺNjēƑūIJūŕîƥĚ
ĺ homocysteine cannot convert Ɠ Lymphocytosis, eosinophilia, plasma
into methionine ĺĿŞƎîĿƑĚēŞNjĚŕĿŠ ČĚŕŕĿŠDŽîƙĿūŠɒūNJNjŠƥĿČijŕîŠēēĚƙƥƑƭČƥĿūŠɒ
regeneration ĺƙƭċîČƭƥĚČūŞċĿŠĚē metaplasia (intestinal, pyloric,
ēĚijĚŠĚƑîƥĿūŠūIJƙƎĿŠîŕČūƑēƎūƙƥĚƑĿūƑ pancreatic)
columns
Ɠ ØĚĚƙƙɈƎîƑîƎŕĚijĿîɈƎîƑĚƙƥĺĚƙĿîƙɈ
îƥîNJĿîɈŕūƙƙūIJƎūƙĿƥĿūŠɓDŽĿċƑîƥĿūŠƙĚŠƙĚ
Ɠ ¬ƎîƙƥĿČĿƥNjɈČŕūŠƭƙɒîƥƑūƎĺĿČijŕūƙƙĿƥĿƙɒ
IJĚČîŕɓƭƑĿŠîƑNjĿŠČūŠƥĿŠĚŠČĚɒēĿîƑƑĺĚîɒ
ēĚŞĚŠƥĿî

232 OSMOSIS.ORG
 Chapter 31 Gastric Disease

TREATMENT
MEDICATIONS
Remove offending agents
ƒ s¬T'ƙɈîČĿēƙɓîŕŒîŕĿƙ

Eradicate H. pylori
ƒ Triple therapy
Ɠ ¡¡TʋČŕîƑĿƥĺƑūŞNjČĿŠʋîŞūNJĿČĿŕŕĿŠɚȃ
DžĚĚŒƙɛ
ƒ £ƭîēƑƭƎŕĚƥĺĚƑîƎNj
Ɠ ¡¡TʋċĿƙŞƭƥĺʋŞĚƥƑūŠĿēîǕūŕĚʋ
ƥĚƥƑîČNjČŕĿŠĚɚȂDžĚĚŒɛ

ūƑƑĚČƥDŽĿƥîŞĿŠēĚǶČĿĚŠČĿĚƙ
ƒ For Autoimmune atrophic gastritis
Figure 31.2 Histological appearance of
chronic gastritis. The lamina propria contains
numerous plasma cells.

Figure 31.3 The histological appearance

ūIJĿŠƥĚƙƥĿŠîŕŞĚƥîƎŕîƙĿîɈČĺîƑîČƥĚƑĿǕĚēċNj
the presence of goblet cells in the gastric
mucosa.

OSMOSIS.ORG 233
 GASTROPARESIS
osms.it/gastroparesis

PATHOLOGY & CAUSES SIGNS & SYMPTOMS

ƒ 'ĚŕîNjĚēijîƙƥƑĿČĚŞƎƥNjĿŠijɈŠūŞĚČĺîŠĿČîŕ ƒ Chronic nausea, vomiting
obstruction ƒ Early satiety, bloating
ƒ ċēūŞĿŠîŕƎîĿŠ
CAUSES
ƒ Most common cause
Ɠ TēĿūƎîƥĺĿČɓēĿîċĚƥĚƙ
DIAGNOSIS
ƒ TîƥƑūijĚŠĿČɚƎūƙƥɠƙƭƑijĿČîŕɓŞĚēĿČîƥĿūŠƙĿēĚ DIAGNOSTIC IMAGING
ĚIJIJĚČƥɛɈƎūƙƥɠDŽĿƑîŕ
ƒ qūƑĚČūŞŞūŠîŞūŠijĿŠēĿDŽĿēƭîŕƙDžĿƥĺ Endoscopy, CT scan, MRI
¹Ȃ'qƥĺȃ'qƙĚČūŠēîƑNjƥūŠĚƭƑūƎîƥĺNj ƒ /NJČŕƭēĚŞĚČĺîŠĿČîŕūċƙƥƑƭČƥĿūŠ

Gastric emptying scintigraphy

234 OSMOSIS.ORG
 Chapter 31 Gastric Disease

TREATMENT OTHER INTERVENTIONS

ƒ /NJĚƑČĿƙĚɒŕūDžIJîƥēĿĚƥ
MEDICATIONS
ƒ qĚƥūČŕūƎƑîŞĿēĚɚijîƙƥƑūĿŠƥĚƙƥĿŠîŕƎƑūŒĿŠĚƥĿČɛ
ƒ ¤ĚŞūDŽĚŞĚēĿČîƥĿūŠƙƥĺîƥŞîNjēĚŕîNjijîƙƥƑĿČ
emptying

PEPTIC ULCER
osms.it/peptic-ulcer

PATHOLOGY & CAUSES

ƒ ĺƑūŠĿČŞƭČūƙîŕƭŕČĚƑîƥĿūŠūIJƙƥūŞîČĺɓ
ēƭūēĚŠƭŞĚNJƥĚŠēƙĿŠƥūŞƭƙČƭŕîƑĿƙŞƭČūƙîɍ
ƒ Most common cause of upper
ijîƙƥƑūĿŠƥĚƙƥĿŠîŕċŕĚĚēĿŠijɒƎƑūNJĿŞîŕ
ēƭūēĚŠƭŞɓijîƙƥƑĿČîŠƥƑƭŞ
ƒ ƙƙūČĿîƥĚēDžĿƥĺČĺƑūŠĿČijîƙƥƑĿƥĿƙ
ƒ ĹîČĿēƙĚČƑĚƥĿūŠɈĻ protective mechanisms
ĺŞƭČūƙîŕēîŞîijĚĺ ulceration

RISK FACTORS
ƒ H. pylori infection (most common)
ƓĹijîƙƥƑĿČîČĿēƙĚČƑĚƥĿūŠɈĻēƭūēĚŠîŕ
HCO3 secretion
ƒ s¬T' Figure 31.4ŠĚŠēūƙČūƎĿČDŽĿĚDžūIJƥĺĚ
Ɠ ¡îƑƥĿČƭŕîƑŕNjŕūDžēūƙĚîƙƎĿƑĿŠ ijîƙƥƑĿČîŠƥƑƭŞDžĺĿČĺēĿƙƎŕîNjƙƥDžūēĿƙČƑĚƥĚ
ČūƑƥĿČūƙƥĚƑūĿēƙ ulcers.
ƒ Physiologic stress
Ɠ Cushing’s ulcer (intracranial
hypertension), Curling ulcer (severe SIGNS & SYMPTOMS
burns)
ƒ Psychological stress ƒ Up to 70% asymptomatic
ƒ ONjƎĚƑČĺŕūƑNjēĿî ƒ /ƎĿijîƙƥƑĿČċƭƑŠĿŠijƎîĿŠɒŞîNjŞĿŞĿČ
ƒ ¬ŞūŒĿŠij ŞNjūČîƑēĿîŕĿŠIJîƑČƥĿūŠ
ƒ ĺƑūŠĿČūċƙƥƑƭČƥĿDŽĚƎƭŕŞūŠîƑNjēĿƙĚîƙĚ Ɠ Usually occurs few hours after meal,
(COPD) worsens at night
ƒ ONjƎĚƑijîƙƥƑĿŠĚŞĿîɚèūŕŕĿŠijĚƑɠ/ŕŕĿƙūŠ Ɠ ¡îĿŠČĺîƑîČƥĚƑĿƙƥĿČîŕŕNjƑĚŕĿĚDŽĚēċNjIJūūēɓ
ƙNjŠēƑūŞĚɛ îŠƥîČĿēƙ
ƒ ¡îĿŠŞîNjƑîēĿîƥĚƥūċîČŒɈČĺĚƙƥɈŕĚIJƥɓƑĿijĺƥ
ƭƎƎĚƑîċēūŞĿŠîŕƐƭîēƑîŠƥƙ
ƒ sîƭƙĚîɈDŽūŞĿƥĿŠijɈČūIJIJĚĚɠijƑūƭŠēĚŞĚƙĿƙɈ
bloating, weight loss

OSMOSIS.ORG 235
 ƒ Surgical emergency
Ɠ Hematemesis, melena, positive guaiac
ƥĚƙƥĿIJƙŕūDžċŕĚĚē
Ɠ ČƭƥĚîċēūŞĚŠɒîċēūŞĿŠîŕijƭîƑēĿŠijɈ
peritonitis
Ɠ GI obstruction
ƒ HîƙƥƑĿČūƭƥŕĚƥūċƙƥƑƭČƥĿūŠɈǶƙƥƭŕîIJūƑŞîƥĿūŠ

DIAGNOSIS
DIAGNOSTIC IMAGING
Abdominal CT scan

Barium abdominal radiography

Endoscopy
ƒ Diagnostic, therapeutic Figure 31.5ċîƑĿƭŞƙƥƭēNjēĚŞūŠƙƥƑîƥĿŠij
the bullseye sign in a case of a gastric ulcer.

TREATMENT
MEDICATIONS
ƒ 'ĿƙČūŠƥĿŠƭĚs¬T'ƙɈîDŽūĿēƙŞūŒĿŠij
ƒ PPI

SURGERY
ƒ /ŠēūƙČūƎĿČŕĿijîƥĿūŠɓČūîijƭŕîƥĿūŠūIJċŕĚĚēĿŠij
ulcers

236 OSMOSIS.ORG
 NOTES

NOTES
GASTROINTESTINAL CANCERS

GENERALLY, WHAT ARE THEY?

ƒ Grading, TNM staging for treatment
PATHOLOGY & CAUSES Ɠ T: characteristic of primary Tumor (e.g.
invasion of nearby tissue)
ƒ Tumors arising from cells in gastrointestinal
Ɠ N: involvement of regional lymph Nodes
(GI) tract
Ɠ M: Metastasis; spread from primary
ƒ Multifactorial etiology; generally result from
tumor to other body parts
aberrant cellular signaling, unregulated
cellular growth
Ɠ Genetic alterations (e.g. point mutations, LAB RESULTS
îŞƎŕĿǶČîƥĿūŠƙɈƑĚîƑƑîŠijĚŞĚŠƥƙɈ
deletions) Biopsy
Ɠ /ƎĿijĚŠĚƥĿČĿŠǷƭĚŠČĚ (e.g. DNA ƒ Histopathological diagnosis
methylation, chromatin remodeling)
Ɠ Environmental factors (e.g. exposure to
ČîƑČĿŠūijĚŠƙɈČĺƑūŠĿČĿŠǷîƥĿūŠɛ
TREATMENT
ƒ Risk increases with age MEDICATIONS
ƒ Chemotherapy
SIGNS & SYMPTOMS
SURGERY
ƒ Highly variable clinical presentation; see ƒ See individual disorders
individual disorders
ƒ Fatigue, anorexia, weight loss
OTHER INTERVENTIONS
ƒ Radiation therapy
DIAGNOSIS
DIAGNOSTIC IMAGING
Imaging studies
ƒ Localization, staging

OSMOSIS.ORG 237
 CARCINOID TUMOR
osms.it/carcinoid-tumor
cells
PATHOLOGY & CAUSES
Ɠ Commonly located in ileum; may arise
from Meckel’s diverticulum
ƒ Uncommon, well-differentiated, slow-
growing neuroendocrine tumor; originates Ɠ Potential for lymph node/hepatic
in tubular digestive tract; also found in metastasis
bronchopulmonary system, genitourinary ƒ Appendix
tract Ɠ Originates from subepithelial endocrine
ƒ Benign/malignant; tendency for liver cells
metastasis Ɠ Relatively low potential for metastasis
ƒ Carcinoid: tumors of different
Hindgut tumors
morphology, less aggressive than GI tract
adenocarcinomas; low grade (proliferative ƒ Rectum, colon, cecum (most common)
activity); low mitotic rate
COMPLICATIONS
TYPES ƒ Depend on tumor’s location, size, local
ƒ Embryonic origin of GI tract (e.g. foregut, biochemical attributes
midgut, hindgut) Ɠ Local/distant metastasis
Ɠ Pain: obstruction, intussusception,
Foregut tumors (e.g. stomach) bowel ischemia, mechanical pressure
ƒ Type I from tumor
Ɠ Most common Ɠ Desmoplasia: intense, local reaction
Ɠ ~ƑĿijĿŠîƥĚƙIJƑūŞĚŠƥĚƑūČĺƑūŞîIJǶŠɠŕĿŒĚ characterized by overproduction
(ECL) cells of extracellular matrix proteins +
Ɠ In association with high gastrin levels ŞNjūǶċƑūċŕîƙƥČĚŕŕƎƑūŕĿIJĚƑîƥĿūŠĺ
secondary to chronic atrophic gastritis ǶċƑūƙĿƙɈūċƙƥƑƭČƥĿūŠ
Ɠ Small, usually benign Ɠ Carcinoid syndrome: tumor-related
ƒ Type II humoral factors (e.g. serotonin,
histamine, etc.) ĺČƭƥîŠĚūƭƙǷƭƙĺĿŠijɈ
Ɠ Originates from ECL cells
pruritic rash; excessive lacrimation;
Ɠ In association with high gastrin levels wheezing; diaphoresis
induced by gastrinomas (e.g. Zollinger–
Ellison syndrome) in conjunction with
multiple endocrine neoplasia type 1 SIGNS & SYMPTOMS
(MEN1)
Ɠ Often large, indolent; low-grade ƒ Often asymptomatic, discovered
malignancy incidentally (e.g. imaging, surgery,
ƒ Type III endoscopy)
Ɠ Not associated with high gastrin levels ƒ Vary according origin site
Ɠ Large, aggressive; local lymphatic/ Ɠ sūŠƙƎĚČĿǶČɈDŽîijƭĚîċēūŞĿŠîŕƎîĿŠ
hepatic metastases; produce serotonin Ɠ Loss of appetite, vomiting, diarrhea,
(5-HT) constipation
Midgut tumors ƒ Desmoplasia (with CT scan)
ƒ Small bowel (most common)
Ɠ Originates from intraepithelial endocrine

238 OSMOSIS.ORG
 Chapter 32 Gastrointestinal Cancers

DIAGNOSIS TREATMENT
DIAGNOSITC IMAGING MEDICATIONS
ƒ Somatostatin analogues suppress tumor
CT scan, MRI, labeled somatostatin recep-
proliferation, decrease symptoms
tor-based diagnostic imaging
ƒ Localization, TNM staging
ƒ Presence of hepatic lesions SURGERY
ƒ Surgical removal of tumor
Endoscopy with biopsy
ƒ Tumor visualization
ƒ Histopathological analysis, grading

LAB RESULTS
ƒ 5-hydroxyindoleacetic acid, chromogranin

Figure 32.2 Gross pathology of carcinoid

tumor of the terminal ileum.

Figure 32.1 Histological appearance of a

carcinoid tumor of the lung.

MNEMONIC: CARCinoid
Carcinoid syndrome
components
CƭƥîŠĚūƭƙǷƭƙĺĿŠij
Asthmatic wheezing
Right-sided valvular heart
lesions
Cramping and diarrhea

OSMOSIS.ORG 239
 CHOLANGIOCARCINOMA
osms.it/cholangiocarcinoma
(IDH1)
PATHOLOGY & CAUSES ƒ Risk increases with age
ƒ Slightly more common in individuals who
ƒ Rare bile duct cancers; arise from epithelial
are biologically male
cells of intrahepatic, extrahepatic bile ducts
(not including gallbladder, ampulla of Vater)
ƒ High fatality due to late diagnosis; highly COMPLICATIONS
proliferative ƒ Metastasis
ƒ Mostly adenocarcinomas; minority Ɠ Liver, lymph nodes, peritoneum, bone,
squamous cell carcinomas etc.
ƒ Bowel perforation, bleeding
TYPES
ƒ Determined by location (Bismuth–Corlette)
SIGNS & SYMPTOMS
Type I
ƒ gūČîƥĚēċĚŕūDžČūŠǷƭĚŠČĚūIJŕĚIJƥɈƑĿijĺƥ ƒ Often asymptomatic initially; malaise,
hepatic ducts weight loss, abdominal pain
ƒ Extrahepatic disease (when bile drainage
Type II obstructed)
ƒ gūČîƥĚēîƥČūŠǷƭĚŠČĚ Ɠ Right upper quadrant pain, jaundice,
pruritus, dark urine, clay-colored stools,
Type IIIa weight loss
ƒ Occludes common hepatic duct ƒ Intrahepatic disease
Type IIIb Ɠ Dull right upper quadrant pain, malaise,
ƒ Occludes right/left hepatic duct weight loss
ƒ ~ƥĺĚƑǶŠēĿŠijƙ
Type IV Ɠ Hepatomegaly, palpated mass
ƒ Multicentric

RISK FACTORS
ƒ Primary
Ɠ Existing liver, gallbladder disease:
primary sclerosing cholangitis (PSC);
chronic liver disease (e.g. viral hepatitis,
cirrhosis)
ƒ Congenital abnormalities of biliary tree
ƒ Genetic disorders
Ɠ Lynch syndrome; multiple biliary
papillomatosis
ƒ Obesity
Figure 32.3 Histological appearance of
ƒ gĿDŽĚƑǷƭŒĚĿŠIJĚČƥĿūŠɚƭŠēĚƑČūūŒĚēǶƙĺɛ a cholangiocarcinoma. There are normal
ƒ Intrahepatic cholangiocarcinomas hepatocytes in the top left of the image, with
Ɠ Associated with mutations in gene the tumour occupying the bottom right of the
encoding isocitrate dehydrogenase 1 image.

240 OSMOSIS.ORG
 Chapter 32 Gastrointestinal Cancers

DIAGNOSIS
ƒ History, physical examination
Ɠ Consistent with hepatobiliary disease

DIAGNOSTIC IMAGING
MRI, CT scan, PET, etc.
ƒ Detailed evaluation of lesion TNM staging

Transabdominal/endoscopic ultrasound
(EUS) with biopsy
ƒ Biliary obstruction, dilation of intrahepatic
ducts
ƒ Histolopathological analysis, grading

Figure 32.4 Histological appearance of a

LAB RESULTS
cholangiocarcinoma. This image shows the
ƒ Tumor markers tumor edge, with normal hepatocytes on the
Ɠ Carbohydrate antigen (CA) 19-9; right and tumor on the left. The tumor cells
carcinoembryonic antigen (CEA) form tubular structures and are surrounded
ƒ Liver function tests ċNjǶċƑūƙĿƙɍ
Ɠ Consistent with biliary obstruction,
cholestasis
Ɠ Elevated transaminases, gamma- TREATMENT
glutamyl transpeptidase, alkaline
phosphatase
MEDICATIONS
Ɠ Prolonged prothrombin time/elevated
ƒ Fluoropyrimidine-based chemoradiotherapy
INR
ƒ Chemotherapy
Ɠ Elevated bilirubin

SURGERY
ƒ Resection

OTHER INTERVENTIONS
ƒ Radiation

OSMOSIS.ORG 241
 COLORECTAL CANCER
osms.it/colorectal-cancer
ƒ Black people of African descent
PATHOLOGY & CAUSES
Ɠ Highest rates in United States
ƒ Common malignancy of large bowel/rectum ƒ More common in individuals who are
biologically male
ƒ Third most common cancer worldwide
ƒ Risk increases with age
ƒ Often arises from colonic epithelial tissue
ĺadenomatous polyp formation ĺ ƒ Protective factors
adenocarcinoma Ɠ Physical activity; regular use of aspirin,
ƒ High metastatic potential after penetrating ūƥĺĚƑŠūŠƙƥĚƑūĿēîŕîŠƥĿɠĿŠǷîƥūƑNj
muscularis mucosa drugs (NSAIDs)

RISK FACTORS COMPLICATIONS

ƒ Hereditary ƒ TƑūŠɠēĚǶČĿĚŠČNjîŠĚŞĿî (due to bleeding)
Ɠ Familial adenomatous polyposis; ƒ Local, distant metastasis
Lynch syndrome, MUTYH-associated ƒ Bowel obstruction
polyposis ƒ Cachexia
ƒ TŠǷîƥūƑNjċūDžĚŕēĿƙĚîƙĚ ƒ Bowel perforation ĺ peritonitis
ƒ Lifestyle
Ɠ Smoking, physical inactivity
ƒ Dietary
SIGNS & SYMPTOMS
Ɠ High alcohol consumption; processed ƒ May be asymptomatic initially
red meat; low consumption of fruits,
ƒ Vague constitutional symptoms
vegetables
Ɠ Fatigue, anorexia, weight loss
ƒ Obesity
ƒ Change in bowel habits
ƒ Diabetes mellitus, insulin resistance
Ɠ Narrowing of stool, constipation,
ƒ Low socioeconomic status
diarrhea
ƒ History of abdominal radiation
ƒ Rectal bleeding
ƒ Lack of screening colonoscopy
Ɠ Frank/occult
ƒ Rectal pain, tenesmus (feeling of
incomplete defecation)
ƒ Nausea, vomiting
Ɠ Bowel obstruction from advanced
malignancy

DIAGNOSIS
DIAGNOSTIC IMAGING
ūŕūŠūƙČūƎNjɓǷĚNJĿċŕĚƙĿijŞūĿēūƙČūƎNjɒ
biopsy, CT colonography
ƒ Tumor visualization, histopathological
Figure 32.5 Gross pathology of an exophytic analysis, grading, TNM staging, potential
colorectal carcinoma. for resection

242 OSMOSIS.ORG
 Chapter 32 Gastrointestinal Cancers

TREATMENT
MEDICATIONS
ƒ Chemotherapy

SURGERY
ƒ Polypectomy with clear margins
ƒ Surgical resection
ƒ Sessile polyps: colectomy

Figure 32.6 Histological appearance of

OTHER INTERVENTIONS
adenocarcinoma of the colon. The tumor is
composed of malignant cells which continue ƒ Chemoradiation therapy
to form glandular structure. The left side of
the image displays normal colonic mucosa.

LAB RESULTS
ƒ ¹ƭŞūƑŞîƑŒĚƑɇ CEA
ƒ Stool guaiac testing
Ɠ Positive for occult blood

OTHER DIAGNOSTICS
'ĿijĿƥîŕƑĚČƥîŕĚNJîŞ
ƒ Palpable mass if distal rectal mass

Figure 32.7 A CT scan in the axial plane Figure 32.8 Positron emission tomography
demonstrating a tumor in the cecum. with high levels of tracer accumulation in the
pelvis (rectal tumor) as well as the liver and
kidneys (metastases).

OSMOSIS.ORG 243
 ESOPHAGEAL CANCER
osms.it/esophageal-cancer

PATHOLOGY & CAUSES SIGNS & SYMPTOMS

ƒ Rare malignancy of esophageal epithelium ƒ Asymptomatic initially; dysphagia; pyrosis;
ƒ Squamous cell carcinoma (most common)/ retrosternal pain; weight loss
adenocarcinoma ƒ Late symptoms
ƒ Commonly diagnosed when disease Ɠ Coughing, chest discomfort when
advanced swallowing; hiccups if spread to
ƒ Tendency for rapid metastasis diaphragm

CAUSES DIAGNOSIS
ƒ Chronic exposure to irritants ĺ metaplasia
ĺ dysplasia ĺ malignant transformation DIAGNOSTIC IMAGING
EUS guided biopsy, CT scan, PET, integrat-
RISK FACTORS ĚēǷƭūƑūēĚūNJNjijŕƭČūƙĚɚG'Hɛ
ƒ Smoking
ƒ Tumor visualization, histopathological
ƒ Alcohol (esp. combined with smoking) analysis, grading, TNM staging, potential
ƒ HîƙƥƑūĚƙūƎĺîijĚîŕƑĚǷƭNJēĿƙĚîƙĚɚH/¤'ɛɒ for resection
ƑĚǷƭNJĚƙūƎĺîijĿƥĿƙɈîƑƑĚƥƥĚƙūƎĺîijƭƙ
ƒ Hiatal hernia Bronchoscopy
ƒ More common in individuals who are ƒ TŠČîƑĿŠîĿēĚŠƥĿǶĚƙƎūƥĚŠƥĿîŕŕƭŠij
biologically male involvement
ƒ Risk increases with age
OTHER DIAGNOSTICS
ƒ Palpable supraclavicular lymphadenopathy
MNEMONIC: ABCDEF
Esophageal cancer risk
factors
Achalasia
Barret’s esophagus
Corrosive esophagitis
Diverticulitis
Esophageal web
Familial

COMPLICATIONS
ƒ Esophageal obstruction; regurgitation Figure 32.9 Endoscopic appearance of an
ĺ aspiration ĺ aspiration pneumonia; esophageal tumor. The tumor sits at the
metastasis gastroesophageal junction and is viewed
from above.

244 OSMOSIS.ORG
 Chapter 32 Gastrointestinal Cancers

TREATMENT
MEDICATIONS
ƒ Chemotherapy

SURGERY
ƒ Resection of primary tumor, associated
nodes

OTHER INTERVENTIONS
ƒ Radiation

Esophageal stenting
ƒ Therapeutically enlarges esophageal lumen,
reduces dysphagia

Figure 32.10 A barium swallow

demonstrating a tumor distorting the normal
outline of the esophagus.

GALLBLADDER CANCER
osms.it/gallbladder-cancer
Ɠ Cholelithiasis (gallstones), primary
PATHOLOGY & CAUSES sclerosing cholangitis, porcelain
gallbladder, gallbladder polyps, biliary
ƒ Uncommon malignancy; most frequently cysts; chronic infection (e.g. Salmonella
diagnosed cancer of biliary tract typhi, Helicobacter bilis)
ƒ High fatality rate due to typically late ƒ More common in individuals who are
diagnosis biologically female
ƒ Most gallbladder cancers arise within ƒ Obesity
fundus ƒ Cigarette smoking
ƒ qîNjūċƙƥƑƭČƥċĿŕĚǷūDžîƥČūŞŞūŠċĿŕĚēƭČƥɓ ƒ Occupational exposure to carcinogens:
duodenum textile, oil, paper, chemical industries, radon
(mining)
RISK FACTORS ƒ Genetic predisposition
ƒ ĺƑūŠĿČijîŕŕċŕîēēĚƑĿŠǷîƥĿūŠ

OSMOSIS.ORG 245
 COMPLICATIONS
ƒ ĿŕĿîƑNjǶƙƥƭŕî
ƒ Local/nodal/distant metastases

SIGNS & SYMPTOMS

ƒ Often asymptomatic in early stages;
malignancy discovered incidentally after
symptoms mimic benign gallbladder
disease
ƒ sūŠɠƙƎĚČĿǶČƙNjŞƎƥūŞƙ Figure 32.11 Histological appearance of
Ɠ Malaise, pain, anorexia, nausea, gallbladder adenocarcinoma. The tumor
vomiting, weight loss cells show increased nuclear size, prominent
ƒ Clinical manifestations (when bile drainage nucleoli and are forming tubular structures.
obstructed)
Ɠ Jaundice, dark urine
ƒ Palpable gallbladder
TREATMENT

DIAGNOSIS MEDICATIONS
ƒ Chemotherapy
DIAGNOSTIC IMAGING
SURGERY
EUS guided/percutaneous biopsy, CT scan,
ƒ Simple/radical cholecystectomy
MRI, PET, MRCP
ƒ Tumor visualization, histopathological
analysis, grading, TNM staging, potential OTHER INTERVENTIONS
for resection ƒ Radiation

LAB RESULTS
ƒ ¹ƭŞūƑŞîƑŒĚƑƙɇ CA 19-9; CEA
ƒ Liver function tests
Ɠ Consistent with biliary obstruction,
cholestasis
Ɠ Elevated transaminases, gamma-
glutamyl transpeptidase, alkaline
phosphatase
Ɠ Elevated bilirubin

246 OSMOSIS.ORG
 Chapter 32 Gastrointestinal Cancers

HEPATOBLASTOMA
osms.it/hepatoblastoma

PATHOLOGY & CAUSES DIAGNOSIS

ƒ Common primary childhood hepatic DIAGNOSTIC IMAGING
malignancy; arises from primitive hepatic
cells Ultrasound, percutaneous biopsy, CT scan
with/without contrast, MRI
ƒ Usually occurs in right lobe of liver
ƒ Diagnostic workup for tumor visualization,
ƒ qūƑƎĺūŕūijĿČîŕŕNjēĿDŽĚƑƙĚƥƭŞūƑɇcomposed
histopathological analysis, grading,
of many cell types including embryonal
pretreatment staging system (PRETEXT);
hepatocytes, tissues (e.g. bone, striated
potential for resection
muscle)
ƒ Extramedullary hematopoiesis may occur in
sinusoids LAB RESULTS
ƒ ÀƙƭîŕŕNjƎƑĚƙĚŠƥēƭƑĿŠijǶƑƙƥƥDžūNjĚîƑƙūIJŕĿIJĚ ƒ Elevated alpha-fetoprotein (AFP)
ƒ Genetic testing
RISK FACTORS
ƒ Beckwith Wiedemann syndrome
ƒ Trisomies 18, 21
ƒ Familial adenomatous polyposis
ƒ Type Ia glycogen storage disease
ƒ Li–Fraumeni syndrome
ƒ More common in individuals who are
biologically male

COMPLICATIONS
ƒ Ectopic gonadotropin ĺprecocious
puberty (uncommon)
ƒ Fatal hepatic hemorrhage, rupture Figure 32.12 Histological appearance of
a hepatoblastoma, a tumor of immature
ƒ Metastasis: commonly lungs
hepatocytes.

SIGNS & SYMPTOMS

TREATMENT
ƒ Children
Ɠ Abdominal mass; discomfort MEDICATIONS
ƒ Anorexia, weight loss, precocious puberty ƒ Chemotherapy

SURGERY
ƒ Resection

OSMOSIS.ORG 247
 HEPATOCELLULAR CARCINOMA
osms.it/hepatocellular-carcinoma

PATHOLOGY & CAUSES SIGNS & SYMPTOMS

ƒ Hepatic malignancy commonly diagnosed ƒ Often no symptoms aside from those of
in presence of chronic liver disease chronic liver disease
ƒ Epigastric pain; appetite, weight loss
RISK FACTORS ƒ Palpable abdominal mass; manifestations
ƒ Hepatitis B/C infection, coinfection with of decompensated cirrhosis (e.g.
hepatitis D splenomegaly, ascites, jaundice); hepatic
bruit
ƒ Hereditary hemochromatosis
ƒ Cirrhosis
ƒ Smoking; frequent alcohol consumption
ƒ Obesity
ƒ ŕƎĺîɠȂîŠƥĿƥƑNjƎƙĿŠēĚǶČĿĚŠČNj
ƒ Gallstones
ƒ ĺƑūŠĿČĚNJƎūƙƭƑĚƥūîǷîƥūNJĿŠ (mycotoxin
found in peanuts, soybeans, corn)
ƒ More common in individuals who are
biologically male

COMPLICATIONS
ƒ Paraneoplastic syndrome: watery
diarrhea, hypoglycemia, hypercalcemia,
erythrocytosis; cutaneous lesions (e.g.
pemphigus foliaceus)
ƒ Extrahepatic metastasis: commonly lymph Figure 32.13 An abdominal CT scan in
nodes, lungs, adrenal gland the axial plane demonstrating a massive
hepatocellular carcinoma.

MNEMONIC: ABC
Hepatocellular carcinoma DIAGNOSIS
etiology
AǷîƥūNJĿŠƙ DIAGNOSTIC IMAGING
Hep B
Cirrhosis Ultrasound with biopsy, CT scan, MDCT,
arteriography, portography, MRI
ƒ Tumor visualization, histopathological
Hepatocellular carcinoma
analysis, grading, TNM staging, potential
features
for resection
AFP increased: classic marker
Bile-producing: DDx from MRI angiography
cholangiocarcinoma ƒ 3D characterization of lesion, hepatic
Most Common primary liver circulation
tumor

248 OSMOSIS.ORG
 Chapter 32 Gastrointestinal Cancers

LAB RESULTS
ƒ Elevated aminotransferases, alkaline
phosphatase, gamma-glutamyl
transpeptidase; hyperbilirubinemia;
hypoalbuminemia
ƒ Elevated alpha-fetoprotein (most common
serum marker)

Figure 32.14 Gross pathology of

hepatocellular carcinoma.

TREATMENT
MEDICATIONS
ƒ Chemotherapy
ƒ Systemic molecularly targeted therapy;
sorafenib, nivolumab
Figure 32.15 Histological appearance of a
hepatocellular carcinima. The cells show
high nuclear variation, thickened nuclear SURGERY
envelopes and occasional prominent nucleoli. ƒ Partial hepatectomy
The cells also have abundant eosinophilic ƒ Liver transplant
cytoplasm.
OTHER INTERVENTIONS
ƒ Radiofrequency ablation
ƒ Percutaneous ablation with ethanol/acetic
acid
ƒ Transarterial chemoembolization
ƒ Cryoablation
ƒ Radiation therapy; stereotactic body
radiation therapy

OSMOSIS.ORG 249
 ORAL CANCER
osms.it/oral-cancer
COMPLICATIONS
PATHOLOGY & CAUSES ƒ Surgical resection ĺ airway, speech,
mastication, cosmetic complications
ƒ Oral cavity malignancy; arises from mucosal
ƒ Metastasis
surfaces
Ɠ Lips, buccal mucosa, anterior tongue,
ŞūƭƥĺǷūūƑɈĺîƑēƎîŕîƥĚɈijĿŠijĿDŽîɈ SIGNS & SYMPTOMS
retromolar trigone
Ɠ Most often: squamous cell carcinoma ƒ Asymptomatic initially
ƒ May arise from normal mucosa/ ƒ Pain/burning sensation
premalignant lesions (e.g. erythroplakia,
ƒ Lump/ulcer visualized, palpated
leukoplakia); undergo malignant
transformation ƒ OîƑēɈǶNJĚēŕNjŞƎĺŠūēĚƙ

RISK FACTORS DIAGNOSIS

ƒ Tobacco (esp. with alcohol)
ƒ Alcohol DIAGNOSTIC IMAGING
ƒ Human papillomavirus (HPV) infection: CT scan/MRI
oropharynx
ƒ Local spread/location of additional primary
ƒ Periodontal disease tumors
ƒ Chronic oral candidiasis
ƒ Betel quid chewing
LAB RESULTS
ƒ Immunosuppression
ƒ Fine needle biopsy; histopathological
ƒ Hepatitis C infection diagnosis
ƒ Genetic polymorphisms: cytochrome P450
1A1 (CYPIA 1); glutathione S-transferase
mu 1 (GSTM1); alcohol dehydrogenase 3 OTHER DIAGNOSTICS
genotype ĺoropharyngeal cancers ƒ Palpation and visualization
ƒ More common in individuals who are Ɠ Of mucous membranes, oral cavity,
biologically male lymph nodes
ƒ Flexible laryngoscopy
Ɠ Back of throat, vocal cords
MNEMONIC: PATH LAB
Oral cancer risks TREATMENT
Plummer-vinson syndrome
Alcohol MEDICATIONS
Tobacco ƒ Chemotherapy
Human papilloma virus
Leukoplakia SURGERY
Asbestos ƒ Resection
Bad oral hygiene
OTHER INTERVENTIONS
ƒ Radiation

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 Chapter 32 Gastrointestinal Cancers

PANCREATIC CANCER
osms.it/pancreatic-carcinoma

PATHOLOGY & CAUSES DIAGNOSIS

ƒ Highly lethal malignancy of exocrine DIAGNOSTIC IMAGING
pancreas
Transabdominal ultrasound
ƒ Usually unresectable at presentation
ƒ Detects degree of biliary tract dilation,
obstruction
RISK FACTORS
ƒ Chronic pancreatitis ERCP
ƒ Malignant transformation of pancreatic ƒ Increased visibility of pancreaticobiliary tree
intraductal papillary mucinous neoplasm
MRCP
(IPMN)
ƒ Visualization of liver parenchyma, vascular
ƒ Genetic mutations (e.g. BRCA-1, BRCA-2,
structures
ATM, PALB2, CDKN2A, MLH1)
ƒ Smoking; obesity; sedentary lifestyle Laparoscopy
ƒ Determines resectability
COMPLICATIONS
ċēūŞĿŠîŕ ¹ƙČîŠɒČūŠƥƑîƙƥɠĚŠĺîŠČĚē ¹
ƒ Hypercoagulability with possible venous/ scan, EUS guided/percutaneous biopsy
arterial thromboembolism
ƒ Tumor visualization, histopathological
ƒ Paraneoplastic manifestations analysis, grading, TNM staging
Ɠ Bullous pemphigoid; nodular fat necrosis
(pancreatic panniculitis)
ƒ Metastasis
LAB RESULTS
ƒ ¹ƭŞūƑŞîƑŒĚƑɇ CA 9-19
ƒ Hyperbilirubinemia (mostly conjugated);
SIGNS & SYMPTOMS elevated alkaline phosphatase

ƒ Recent onset of diabetes mellitus OTHER DIAGNOSITCS

ƒ Clinical presentation
Ɠ Tumor location Cardiac catheterization
ƒ Pain ƒ Measure pressure in right side of heart
Ɠ Epigastric, abdominal, may radiate to
the back, may worsen after eating/when
lying down; asthenia:
TREATMENT
ƒ Physical weakness, loss of strength; MEDICATIONS
anorexia, nausea; weight loss; jaundice,
ƒ Chemotherapy with/without
dark urine
chemoradiotherapy
ƒ Hepatomegaly; right upper quadrant mass;
Courvoisier’s sign (nontender, palpable
gallbladder at right costal margin); cachexia; SURGERY
metastasis: left supraclavicular/periumbilical ƒ Resection (e.g. pancreaticoduodenectomy)
lymphadenopathy, ascites, abdominal mass Ɠ Only curative treatment

OSMOSIS.ORG 251
 Figure 32.17 Histological appearance of
pancreatic adenocarcinoma. The tumor cells
Figure 32.16 Cytological preparation of form acini, small sack like spaces surrounded
îƎîŠČƑĚîƥĿČǶŠĚŠĚĚēŕĚîƙƎĿƑîƥĚDžĺĿČĺ by malignant glandular cells.
demonstrates pancreatic adenocarcinoma.
The group on the left is the cancer, with large,
pleomorphic nuclei, which overlap with one
another. Contrast these with the smaller,
regularly spaced pancreatic ductal epithelial
cells on the right.

STOMACH (GASTRIC) CANCER

osms.it/stomach-cancer
common in high-risk populations
PATHOLOGY & CAUSES ƒ Intercellular adhesion molecules ĺ
adherence of tumor cells ĺ arrangement in
ƒ Aggressive adenocarcinoma arising from glandular formations
gastric mucosa

RISK FACTORS
TYPES
ƒ Primary cause (G-INT)
'ĿIJIJƭƙĚƥNjƎĚɚHɠ'TGɛɇƭŠēĿIJIJĚƑĚŠƥĿîƥĚē Ɠ H. pylori infection
ƒ Impairment/lack of adhesion molecule ƒ Family history of gastric cancer
E-cadherin ƒ Autoimmune atrophic gastritis
ƒ Genetic mutation (germline, somatic, ƒ Lifestyle
epigenetic methylation) of CDH1 gene Ɠ Smoking, alcohol consumption
ĺ inactivation of CDH1 ĺ nonfunctional
ƒ Diet
E-cadherin ĺ unregulated division
(impaired tumor suppressor function); Ɠ Nitrates, nitrosamines, highly-salted
increased ability to spread, invade adjacent foods; pickled/smoked foods
structures ƒ Obesity
Ɠ Autosomal dominant inheritance pattern ƒ Risk increases with age
Ɠ More aggressive than G-INT ƒ More common in individuals who are
biologically male
TŠƥĚƙƥĿŠîŕƥNjƎĚɚHɠTs¹ɛɇDžĚŕŕɠēĿIJIJĚƑĚŠƥĿîƥĚē
ƒ Due to environmental factors; more

252 OSMOSIS.ORG
 Chapter 32 Gastrointestinal Cancers

ƒ Protective factors
Ɠ TŠƥîŒĚūIJIJƑƭĿƥɈDŽĚijĚƥîċŕĚƙɈǶċĚƑɈIJūŕîƥĚ
DIAGNOSIS
DIAGNOSTIC IMAGING
COMPLICATIONS
ƒ Metastasis to liver, peritoneum, lymph Esophagogastroduodenoscopy with biop-
nodes, etc. sy, barium studies, abdominopelvic CT scan
ƒ Paraneoplastic manifestations ƒ Tumor visualization, histopathological
analysis, grading, TNM staging, potential
Ɠ Seborrheic keratoses, polyarteritis
for resection
nodosa, Trousseau’s syndrome
(spontaneous, recurrent, migratory
venous thrombosis) OTHER DIAGNOSTICS
¡ĺNjƙĿČîŕĚNJîŞĿŠîƥĿūŠ
ƒ Enlarged supraclavicular, anterior axillary,
periumbilical lymph nodes
ƒ Palpable abdominal mass

Figure 32.18 Gross pathology of gastric

carcinoma. The stomach has been pinned
Ƿîƥɍ¹ĺĚƥƭŞūƑĿƙIJūƭŠēĿŠƥĺĚîŠƥƑƭŞɍ

SIGNS & SYMPTOMS

ƒ Asymptomatic initially
ƒ Early symptoms
Ɠ Vague constitutional symptoms (e.g.
malaise, loss of appetite, dyspepsia)
ƒ With disease progression
Ɠ Epigastric pain, nausea, vomiting,
dysphagia, weight loss Figure 32.19 The histological appearance of
ƒ If GI bleeding a well-differentiated gastric adenocarcinoma
Ɠ Anemia, melena, coffee-ground of intestinal type. The tumor is composed of
hematemesis disordered glands, the cells of which have
ƒ ¡ƙĚƭēūîČĺîŕîƙĿîƙNjŠēƑūŞĚɚēĿIJǶČƭŕƥNj large, hyperchromatic nuclei.
moving food, liquids from esophagus to
stomach)
Ɠ If tumor extends to Auerbach’s
plexus/obstruction occurs near
gastroesophageal junction

OSMOSIS.ORG 253
 SURGERY
TREATMENT ƒ Resection
MEDICATIONS
OTHER INTERVENTIONS
Chemotherapy ƒ Chemoradiotherapy
ƒ G-INT, G-DIF differ in susceptibility to
chemotherapeutic agents
ƒ Eradication of H pylori infection

WARTHIN'S TUMOR
osms.it/warthins-tumor

PATHOLOGY & CAUSES SIGNS & SYMPTOMS

ƒ Uncommon benign tumor; arises from ƒ Development of painless nodular mass,
salivary gland usually near mandible angle
ƒ AKA papillary cystadenoma
lymphomatosum
ƒ May involve submandibular/sublingual/ DIAGNOSIS
parotid gland (most common)
ƒ Unilateral/bilateral, slow-growing
OTHER DIAGNOSTICS
ƒ Easily palpable tumor

RISK FACTORS Fine needle aspiration

ƒ Smoking ƒ Histopathological diagnosis
ƒ Risk increases with age
ƒ More common in individuals who are
biologically male
TREATMENT
SURGERY
COMPLICATIONS ƒ Local resection/parotidectomy
ƒ Malignant transformation (rare)

254 OSMOSIS.ORG
 NOTES

NOTES
INFLAMMATORY BOWEL DISEASE

GENERALLY, WHAT IS IT?

PATHOLOGY & CAUSES DIAGNOSIS
ƒ TŞŞƭŠĚɠŞĚēĿîƥĚēĿŠǷîƥūƑNjċūDžĚŕ DIAGNOSTIC IMAGING
ČūŠēĿƥĿūŠƙ ƒ /ŠēūƙČūƎNj
ƒ qūƑĚČūŞŞūŠĿŠØĺĿƥĚƎĚūƎŕĚūIJcĚDžĿƙĺ
ēĚƙČĚŠƥ LAB RESULTS
ƒ ÀƙƭîŕŕNjƎƑĚƙĚŠƥƙĿŠNjūƭŠijƎĚūƎŕĚɈȂȆɝȄȆ ƒ ĿūƎƙNj
ƒ ÀƎƥūȃȆʣūIJƎĚūƎŕĚDžĿƥĺĿŠǷîƥūƑNj
ċūDžĚŕēĿƙĚîƙĚĺîDŽĚîIJIJĚČƥĚēǶƑƙƥɠēĚijƑĚĚ
ƑĚŕîƥĿDŽĚ TREATMENT
CAUSES MEDICATIONS
ƒ HƭƥŞĿČƑūċĿūŞĚîŕƥĚƑîƥĿūŠƙ ƒ ŠƥĿɠĿŠǷîƥūƑNjŞĚēĿČîƥĿūŠƙɒîŠƥĿċĿūƥĿČƙɒ
ƒ “Western” style diet: ĺĿijĺƎƑūČĚƙƙĿŠijɓ ĿŞŞƭŠūƙƭƎƎƑĚƙƙîŠƥƙ
ƙƭijîƑɓIJîƥČūŠƥĚŠƥ
SURGERY
RISK FACTORS ƒ ¬ƭƑijĿČîŕƑĚƙĚČƥĿūŠ
ƒ Crohn’s disease: ƙŞūŒĿŠij
Ɠ ¬ŞūŒĿŠijŞîNjċĚƎƑūƥĚČƥĿDŽĚIJūƑ OTHER INTERVENTIONS
ÀŕČĚƑîƥĿDŽĚČūŕĿƥĿƙ ƒ 'ĿĚƥîƑNjČĺîŠijĚƙ

SIGNS & SYMPTOMS

ƒ ĺƑūŠĿČēĿîƑƑĺĚîɈIJƑĚƐƭĚŠƥŕNjċŕūūēNjɓŞƭČūƭƙ
ƒ ċēūŞĿŠîŕƎîĿŠ
ƒ GĚDŽĚƑɈDžĚĿijĺƥŕūƙƙɈîŠĚŞĿî
ƒ /NJƥƑîĿŠƥĚƙƥĿŠîŕŞîŠĿIJĚƙƥîƥĿūŠƙ
Ɠ ƑƥĺƑĿƥĿƙɈƭDŽĚĿƥĿƙ

OSMOSIS.ORG 255
 CROHN'S DISEASE
osms.it/crohns-disease
CAUSES
PATHOLOGY & CAUSES
ƒ ÀŠČŕĚîƑɒŞNjČūċîČƥĚƑĿƭŞƎîƑîƥƭċĚƑČƭŕūƙĿƙɈ
ƎƙĚƭēūŞūŠîƙɈŕĿƙƥĚƑĿîĿŞƎŕĿČîƥĚē
ƒ e ƑūĺŠēĿƙĚîƙĚɈƑĚijĿūŠîŕĚŠƥĚƑĿƥĿƙ
ƒ ĺƑūŠĿČɈĿŞŞƭŠĚɠƑĚŕîƥĚēēĿƙūƑēĚƑĺ
ĚNJČĚƙƙĿDŽĚĿŞŞƭŠĚƑĚƙƎūŠƙĚƥūƭŠŒŠūDžŠ SIGNS & SYMPTOMS
ƥƑĿijijĚƑĺƥƑîŠƙŞƭƑîŕĿŠǷîƥĿūŠ
îŠNjDžĺĚƑĚîŕūŠijijîƙƥƑūĿŠƥĚƙƥĿŠîŕɚHTɛƥƑîČƥɈ ƒ ÀŠƎƑĚēĿČƥîċŕĚƎîƥƥĚƑŠƙūIJǷîƑĚƙɈƑĚŞĿƙƙĿūŠƙ
ŞūƭƥĺƥūîŠƭƙ
ƒ ċēūŞĿŠîŕƎîĿŠɒŞūƙƥČūŞŞūŠĿŠƑĿijĺƥ
ƒ ūŞƎîƑĚƥūƭŕČĚƑîƥĿDŽĚČūŕĿƥĿƙ ŕūDžĚƑƐƭîēƑîŠƥɚĿŕĚîŕĿŠǷîƥĿūŠɛ
Ɠ ~ŠŕNjîIJIJĚČƥƙČūŕūŠɈƑĚČƥƭŞɒƙƭƎĚƑǶČĿîŕ ƒ GîƥĿijƭĚɈIJĚDŽĚƑɈŠîƭƙĚîɈDŽūŞĿƥĿŠij
ŕĚƙĿūŠƙɒîƭƥūĿŞŞƭŠĚēĿƙūƑēĚƑDžĺĚƑĚ
ƒ ĺƑūŠĿČēĿîƑƑĺĚîɒŞîNjɓŞîNjŠūƥċĚċŕūūēNj
ƥĿƙƙƭĚĿƙēĿƑĚČƥŕNjîƥƥîČŒĚēċNjĿŞŞƭŠĚ
ƙNjƙƥĚŞ Ɠ HƑūƙƙċŕĚĚēĿŠijƑîƑĚɒƭƎūŠŞĿČƑūƙČūƎNjɈ
ċŕĚĚēĿŠijČūŞŞūŠ
ƒ GƑîŞĚƙĺĿIJƥŞƭƥîƥĿūŠĿŠŠƭČŕĚūƥĿēĚɠċĿŠēĿŠij
ūŕĿijūŞĚƑĿǕîƥĿūŠēūŞîĿŠɠČūŠƥîĿŠĿŠijƎƑūƥĚĿŠ ƒ qîŕîċƙūƑƎƥĿūŠɈDžĚĿijĺƥŕūƙƙɈDŽĿƥîŞĿŠ
ȃɚs~'ȃɛɓČîƙƎîƙĚƑĚČƑƭĿƥŞĚŠƥēūŞîĿŠɠ ēĚǶČĿĚŠČĿĚƙ
ČūŠƥîĿŠĿŠijƎƑūƥĚĿŠȂȆɚ ¤'ȂȆɛ ƒ ÀƎƥūȃȁʣūIJČîƙĚƙƎƑĚƙĚŠƥDžĿƥĺ
Ɠ /NJČĚƙƙĿDŽĚĿŠǷîƥūƑNjƑĚƙƎūŠƙĚĺ ĿŠǷîƥūƑNjĚNjĚɈƙŒĿŠɈŏūĿŠƥŕĚƙĿūŠƙ
ƥĿƙƙƭĚēîŞîijĚ Ɠ ÀDŽĚĿƥĿƙɈĚƑNjƥĺĚŞîŠūēūƙƭŞɈƎNjūēĚƑŞî
ƒ ÀŠŒŠūDžŠĿŞŞƭŠĚƑĚƙƎūŠƙĚƥƑĿijijĚƑĺ¹ ijîŠijƑĚŠūƙƭŞɈČĺūŕĚŕĿƥĺĿîƙĿƙɚĿŞƎîĿƑĚē
ĺĚŕƎĚƑɚ¹ĺɛȂČĚŕŕƙƑĚŕĚîƙĚĿŠǷîƥūƑNj ċĿŕĚƑĚîċƙūƑƎƥĿūŠɛɈîƑƥĺƑĿƥĿƙ
ČNjƥūŒĿŠĚƙ ƒ ¡ĚƑĿîŠîŕîċƙČĚƙƙĚƙɈƎĺŕĚijŞūŠɈǶƙƥƭŕîĚ
Ɠ TŠƥĚƑIJĚƑūŠɚTGsɛijîɈƥƭŞūƑŠĚČƑūƙĿƙ Ɠ ¡ĚƑĿîŠîŕǶƙƥƭŕîƙɚƭƎƥūȄȁʣɛ
IJîČƥūƑɚ¹sGɛîŕƎĺîĺĿŠǷîƥūƑNj Ɠ /ŠƥĚƑūDŽĚƙĿČîŕǶƙƥƭŕîĚĺƑĚČƭƑƑĚŠƥÀ¹TɈ
ƑĚƙƎūŠƙĚĺČNjƥūŒĿŠĚƙƑĚČƑƭĿƥ ƎŠĚƭŞîƥƭƑĿî
ŞîČƑūƎĺîijĚƙĺIJƭƑƥĺĚƑĿŠǷîƥūƑNj Ɠ /ŠƥĚƑūĚŠƥĚƑĿČǶƙƥƭŕîĚĺîƙNjŞƎƥūŞîƥĿČ
ŞĚēĿîƥūƑƙƑĚŕĚîƙĚēɚƎƑūƥĚîƙĚƙɈƎŕîƥĚŕĚƥ Ɠ /ŠƥĚƑūDŽîijĿŠîŕǶƙƥƭŕîĚĺƎîƙƙîijĚūIJ
îČƥĿDŽîƥĿŠijIJîČƥūƑɈIJƑĚĚƑîēĿČîŕƙɛĺ IJĚČîŕŞîƥƥĚƑƥĺƑūƭijĺDŽîijĿŠî
IJƭƑƥĺĚƑĿŠǷîƥĿūŠĺĺĚîŕƥĺNjƥĿƙƙƭĚ
Ɠ /ŠƥĚƑūČƭƥîŠĚūƭƙǶƙƥƭŕîĚĺēƑîĿŠĿŠijūIJ
ēĚƙƥƑūNjĚēĺ ĿŠǷîƥūƑNjČĚŕŕƙĿŠDŽîēĚ
ċūDžĚŕČūŠƥĚŠƥƙƭŠƥūƙŒĿŠ
ĿŠƥĚƙƥĿŠîŕŞƭČūƙîĺƭŕČĚƑɈijƑîŠƭŕūŞî
IJūƑŞĺƥƑîŠƙŞƭƑîŕĿŠǷîƥĿūŠĺ ƒ TŠƥĚƙƥĿŠîŕūċƙƥƑƭČƥĿūŠɚƭƎƥūȄȁʣɛ
ĿŠƥĚƙƥĿŠîŕŕƭŞĚŠɒǶƙƥƭŕîIJūƑŞîƥĿūŠɈ
ŠîƑƑūDžĿŠij
ƒ GĿƙƥƭŕîɈƙƥƑĿČƥƭƑĚIJūƑŞîƥĿūŠ
Ɠ ¬ĚƑūƙîŕŕîNjĚƑĿŠDŽūŕDŽĚŞĚŠƥĺǶƙƥƭŕî
Ɠ Most common: ĚŠƥĚƑūDŽĚƙĿČîŕɈ
ĚŠƥĚƑūČƭƥîŠĚūƭƙɈĚŠƥĚƑūDŽîijĿŠîŕɈ
ĚŠƥĚƑūĚŠƥĚƑĿČǶƙƥƭŕîĚ
ƒ ¬ČîƥƥĚƑĚēĿŠǷîƥĿūŠĺ ČūċċŕĚƙƥūŠĚ
îƎƎĚîƑîŠČĚ
ƒ qūƙƥČūŞŞūŠŕNjîIJIJĚČƥƙƥĚƑŞĿŠîŕĿŕĚƭŞɈ
ČūŕūŠ
Figure 33.1¡NjūēĚƑŞîijîŠijƑĚŠūƙƭŞūŠƥĺĚ
ŕĚijūIJîŠĿŠēĿDŽĿēƭîŕDžĿƥĺ ƑūĺŠɫƙēĿƙĚîƙĚɍ

256 OSMOSIS.ORG
 Chapter 33 TŠǷîƥūƑNjūDžĚŕ'ĿƙĚîƙĚ

MNEMONIC: CHRISTMAS
Features of Crohn’s disease
CūċċŕĚƙƥūŠĚƙ
HĿijĺƥĚŞƎĚƑîƥƭƑĚ
RĚēƭČĚēŕƭŞĚŠ
IŠƥĚƙƥĿŠîŕǶƙƥƭŕîĚ
SŒĿƎŕĚƙĿūŠƙ
TƑîŠƙŞƭƑîŕɇîŕŕŕîNjĚƑƙɈŞîNj
ƭŕČĚƑîƥĚ
Figure 33.3HƑūƙƙƎîƥĺūŕūijNjūIJîƑĚƙĚČƥĚē
MîŕîċƙūƑƎƥĿūŠ
ČūŕūŠĿŠDŽūŕDŽĚēċNj ƑūĺŠɫƙēĿƙĚîƙĚɍ¹ĺĚ
AċēūŞĿŠîŕƎîĿŠ ƙĚDŽĚƑĚîŠēƎƑūŕūŠijĚēĿŠǷîƥĿūŠĺîƙŕĚē
SƭċŞƭČūƙîŕǶċƑūƙĿƙ ƥūîČūċċŕĚƙƥūŠĚîƎƎĚîƑîŠČĚūIJƥĺĚČūŕūŠĿČ
ŞƭČūƙîɍ

DIAGNOSIS
TREATMENT
DIAGNOSTIC IMAGING
ƒ /ŠēūƙČūƎNj MEDICATIONS
ƒ ŠƥĿɠĿŠǷîƥūƑNjŞĚēĿČîƥĿūŠƙĺ
LAB RESULTS ƙƭŕIJîƙîŕîǕĿŠĚ
ƒ ĿūƎƙNj Ɠ GūƑČūŕūŠĿČƙNjŞƎƥūŞŞîŠîijĚŞĚŠƥ
Ɠ ūċċŕĚƙƥūŠĚîƎƎĚîƑîŠČĚɈĿŠƥĚƑŞĿƥƥĚŠƥ ƒ ŠƥĿċĿūƥĿČƙĺŞĚƥƑūŠĿēîǕūŕĚ
ŕĚƙĿūŠƎîƥƥĚƑŠɈƎƙĚƭēūƎūŕNjƎƙɈîƎĺƥĺūƭƙ Ɠ ¤ĚēƭČĚċîČƥĚƑĿîŕūDŽĚƑijƑūDžƥĺɈîŠƥĿɠ
ƭŕČĚƑƙ ĿŠǷîƥūƑNjĚIJIJĚČƥ
ƒ TŞŞƭŠūƙƭƎƎƑĚƙƙîŠƥƙ ĺƎƑĚēŠĿƙūŠĚɈ
îǕîƥĺĿūƎƑĿŠĚ
OTHER DIAGNOSTICS
Ɠ ~ŠŕNjĿIJŠūƑĚƙƎūŠƙĚƥūîŠƥĿċĿūƥĿČƙ
ƒ îƑĿƭŞĚŠĚŞî
ƒ ŠƥĿēĿîƑƑĺĚîŕƙ
ƒ qĚƥĺūƥƑĚNJîƥĚɈîŠƥĿɠ¹sGîijĚŠƥƙ
Ɠ ¤ĚIJƑîČƥūƑNjēĿƙĚîƙĚ

SURGERY
ƒ ¬ƭƑijĿČîŕƑĚŞūDŽîŕūIJîIJIJĚČƥĚēƥĿƙƙƭĚ
Ɠ OĿijĺƑĚŕîƎƙĚƑîƥĚ
Ɠ Short bowel syndrome: ČūŞƎŕĿČîƥĿūŠūIJ
ƑĚƙĚČƥĿūŠ

OTHER INTERVENTIONS
ƒ sƭƥƑĿƥĿūŠîŕƙƭƎƎŕĚŞĚŠƥîƥĿūŠɈƙƭƎƎūƑƥ

Figure 33.2OĿƙƥūŕūijĿČîŕîƎƎĚîƑîŠČĚūIJ
ƑūĺŠɫƙēĿƙĚîƙĚɍ¹ĺĚŕîŞĿŠîƎƑūƎƑĿîĿƙ
ĚNJƎîŠēĚēċNjČĺƑūŠĿČĿŠǷîƥūƑNjČĚŕŕƙîŠē
ƥĺĚƑĚĿƙîŠūŠɠČîƙĚîƥĿŠijijƑîŠƭŕūŞîƎƑĚƙĚŠƥɍ

OSMOSIS.ORG 257
 MICROSCOPIC COLITIS
osms.it/microscopic-colitis

PATHOLOGY & CAUSES DIAGNOSIS

ƒ TēĿūƎîƥĺĿČČĺƑūŠĿČĿŠǷîƥĿūŠūIJČūŕūŠ ĺ DIAGNOSTIC IMAGING
DžîƥĚƑNjēĿîƑƑĺĚî
Endoscopy
ƒ ƙƙūČĿîƥĚēDžĿƥĺČĚŕĿîČēĿƙĚîƙĚɈ
îƭƥūĿŞŞƭŠĚēĿƙĚîƙĚƙɈs¬T'ƙɈƙŞūŒĿŠij ƒ sūŠɠƙƎĚČĿǶČǶŠēĿŠijƙɈŠūƑŞîŕŞƭČūƙî
ƒ qūƑĚČūŞŞūŠĿŠĿŠēĿDŽĿēƭîŕƙDžĺūîƑĚ
ċĿūŕūijĿČîŕŕNjIJĚŞîŕĚ LAB RESULTS
ƒ ÀŠŒŠūDžŠƥƑĿijijĚƑĺ îċŠūƑŞîŕČūŕŕîijĚŠ ƒ ĿūƎƙNjūIJČūŕūŠĿČŞƭČūƙî
ŞĚƥîċūŕĿƙŞ ĺēNjƙIJƭŠČƥĿūŠîŕĚƎĿƥĺĚŕĿƭŞ Ɠ TŠǷîƥūƑNjČĺîŠijĚƙĿŠŕîŞĿŠîƎƑūƎƑĿîɈ
ĺîŕƥĚƑîƥĿūŠĿŠċîƑƑĿĚƑIJƭŠČƥĿūŠĺŞƭČūƙîŕ ĿŠƥƑîĚƎĿƥĺĚŕĿîŕŕNjŞƎĺūČNjƥĿČĿŠǶŕƥƑîƥĿūŠɈ
ĿŠǷîƥĿūŠĺēĚČƑĚîƙĚēƙūēĿƭŞ ēĚŠƙĚƙƭċĚƎĿƥĺĚŕĿîŕČūŕŕîijĚŠūƭƙŕîNjĚƑ
îċƙūƑƎƥĿūŠɈĿŠČƑĚîƙĚēČĺŕūƑĿēĚƙĚČƑĚƥĿūŠĺ ƒ /ŕĚDŽîƥĚēĿŠǷîƥūƑNjŞîƑŒĚƑƙ
ƙĚČƑĚƥūƑNjēĿîƑƑĺĚî ɚŠūŠƙƎĚČĿǶČɛ
Ɠ /ƑNjƥĺƑūČNjƥĚƙĚēĿŞĚŠƥîƥĿūŠƑîƥĚɈ
TYPES ŞNjĚŕūƎĚƑūNJĿēîƙĚ
ƒ ƭƥūîŠƥĿċūēĿĚƙ
Collagenous
Ɠ ŠƥĿɠƥĺNjƑūĿēƎĚƑūNJĿēîƙĚɚ¹¡~ɛɈ
ƒ qūƑĚČūŞŞūŠĿŠūŕēĚƑĿŠēĿDŽĿēƭîŕƙDžĺūîƑĚ
îŠƥĿŠƭČŕĚîƑɚsɛɈîŠƥĿŠĚƭƥƑūƎĺĿŕ
ċĿūŕūijĿČîŕŕNjIJĚŞîŕĚ
ČNjƥūƎŕîƙŞĿČɚs ɛɈîŠƥĿ
ƒ 'ĚŠƙĚƙƭċĚƎĿƥĺĚŕĿîŕČūŕŕîijĚŠūƭƙŕîNjĚƑɒ ¬îČČĺîƑūŞNjČĚƙČĚƑĚDŽĿƙĿîĚɚ¬ ɛɈ
ĿŠČƑĚîƙĚēĿŠƥƑîĚƎĿƥĺĚŕĿîŕŕNjŞƎĺūČNjƥĚƙɈ ƑĺĚƭŞîƥūĿēIJîČƥūƑɚ¤Gɛ
ĿŠǷîƥūƑNjĿŠǶŕƥƑîƥĚĿŠŕîŞĿŠîƎƑūƎƑĿî

Lymphocytic
TREATMENT
ƒ TŠČƑĚîƙĚēĿŠƥƑîĚƎĿƥĺĚŕĿîŕŕNjŞƎĺūČNjƥĚƙɈ
ĿŠǷîƥūƑNjĿŠǶŕƥƑîƥĚĿŠŕîŞĿŠîƎƑūƎƑĿî MEDICATIONS
ƒ DŽūĿēs¬T'ƙɈūƥĺĚƑŞĚēĿČîƥĿūŠƙ
SIGNS & SYMPTOMS îƙƙūČĿîƥĚēDžĿƥĺŞĿČƑūƙČūƎĿČČūŕĿƥĿƙ
ƒ ŠƥĿēĿîƑƑĺĚîŕƙ
ƒ ċēūŞĿŠîŕƎîĿŠ Ɠ gūƎĚƑîŞĿēĚɈċĿƙŞƭƥĺƙîŕĿČNjŕîƥĚ
ƒ ĺƑūŠĿČDžîƥĚƑNjēĿîƑƑĺĚî ƒ ūƑƥĿČūƙƥĚƑūĿēƙ
ƒ sūDžĚĿijĺƥŕūƙƙ Ɠ ƭēĚƙūŠĿēĚɈƎƑĚēŠĿƙūŠĚ
ƒ GĚČîŕƭƑijĚŠČNjɈĿŠČūŠƥĿŠĚŠČĚ ƒ ĿŕĚîČĿēƙĚƐƭĚƙƥƑîŠƥƙ
ƒ Anemia Ɠ ĺūŕĚƙƥNjƑîŞĿŠĚ

SURGERY
ƒ ¬ƭƑijĿČîŕƑĚƙĚČƥĿūŠɚĿŕĚūƙƥūŞNjɛ

258 OSMOSIS.ORG
 Chapter 33 TŠǷîƥūƑNjūDžĚŕ'ĿƙĚîƙĚ

Figure 33.4OĿƙƥūŕūijĿČîŕîƎƎĚîƑîŠČĚ Figure 33.5OĿƙƥūŕūijĿČîŕîƎƎĚîƑîŠČĚūIJ

ūIJČūŕŕîijĚŠūƭƙČūŕĿƥĿƙɍ¹ĺĚƙƭċĚƎĿƥĺĚŕĿîŕ ŕNjŞƎĺūČNjƥĿČČūŕĿƥĿƙɍ¹ĺĚƑĚĿƙîŠĿŠČƑĚîƙĚĿŠ
ċîƙĚŞĚŠƥŞĚŞċƑîŠĚĿƙŞîƑŒĚēŕNjƥĺĿČŒĚŠĚēɍ ƥĺĚŠƭŞċĚƑūIJĿŠƥƑîĚƎĿƥĺĚŕĿîŕŕNjŞƎĺūČNjƥĚƙ
ɚʑȃȁɓȂȁȁĚƎĿƥĺĚŕĿîŕČĚŕŕƙɛɍ

PROTEIN LOSING ENTEROPATHY

osms.it/protein-losing-enteropathy

PATHOLOGY & CAUSES SIGNS & SYMPTOMS

ƒ TŠǷîƥūƑNjHTČūŠēĿƥĿūŠƙĺ ŕūƙƙūIJƙĚƑƭŞ ƒ ONjƎūŠîƥƑĚŞĿîɈƎĚƑĿƎĺĚƑîŕĚēĚŞîɈîƙČĿƥĚƙ
ƎƑūƥĚĿŠƙĿŠƥūHTƥƑîČƥ ƒ ¬ĚƑūƙîŕĚIJIJƭƙĿūŠƙɚƎŕĚƭƑîŕîŠēƎĚƑĿČîƑēĿîŕɛ
ƒ qƭČūƙîŕĿŠŏƭƑNjĺĚƎĿƥĺĚŕĿîŕĿŠǷîƥĿūŠɈ Ɠ 'NjƙƎŠĚîɈČūƭijĺɈČĺĚƙƥƎîĿŠ
ĺ ŞƭČūƙîŕƎĚƑŞĚîċĿŕĿƥNj ĺƎƑūƥĚĿŠ ƒ ¬ƥĚîƥūƑƑĺĚîɈċŕūîƥĿŠijɈǷîƥƭŕĚŠČĚɈîċēūŞĿŠîŕ
ĚNJƭēîƥĚƙîČƑūƙƙĚƎĿƥĺĚŕĿƭŞĺƎƑūƥĚĿŠƙĿŠ ƎîĿŠ
HTƥƑîČƥēĚijƑîēĚēĿŠƥūîŞĿŠūîČĿēƙɚɛ
ƒ ØĚĿijĺƥŕūƙƙɈČĺƑūŠĿČēĿîƑƑĺĚî
ƒ gNjŞƎĺîƥĿČūċƙƥƑƭČƥĿūŠɓDŽĚŠūƭƙƙƥîƙĿƙ
ĺĿŠČƑĚîƙĚēĺNjēƑūƙƥîƥĿČƎƑĚƙƙƭƑĚĿŠ
ŕNjŞƎĺîƥĿČƙĺŕNjŞƎĺŕĚîŒƙĿŠƥūĿŠƥĚƙƥĿŠîŕ DIAGNOSIS
ŕƭŞĚŠ ĺƑĚēƭČĚēČĺNjŕūŞĿČƑūŠƑĚîċƙūƑƎƥĿūŠ
ĺēĚČƑĚîƙĚĿŠIJîƥƙūŕƭċŕĚDŽĿƥîŞĿŠƙĺ LAB RESULTS
ƎƑūƥĚĿŠēĚǶČĿĚŠČNj
ƒ ūŠƙĿēĚƑĿŠĿŠēĿDŽĿēƭîŕƙDžĿƥĺĚēĚŞîɈ
ĺNjƎūîŕċƭŞĿŠĚŞĿî
CAUSES ƒ TŠČƑĚîƙĚĿŠîŕƎĺîɠȂîŠƥĿƥƑNjƎƙĿŠČŕĚîƑîŠČĚ
ƒ TŠǷîƥūƑNjċūDžĚŕēĿƙĚîƙĚ ƒ /NJČŕƭēĚūƥĺĚƑČîƭƙĚƙūIJĺNjƎūƎƑūƥĚĿŠĚŞĿî
Ɠ ƑūĺŠɫƙēĿƙĚîƙĚɈƭŕČĚƑîƥĿDŽĚČūŕĿƥĿƙ Ɠ ¤ĚŠîŕēĿƙĚîƙĚĺƎƑūƥĚĿŠƭƑĿî
ƒ qîŕîċƙūƑƎƥĿDŽĚēĿƙĚîƙĚƙ Ɠ OĚƎîƥĿČēĿƙĚîƙĚĺĿŞƎîĿƑĚēƎƑūƥĚĿŠ
Ɠ ¹ƑūƎĿČîŕƙƎƑƭĚɈČĚŕĿîČƙƎƑƭĚ ƙNjŠƥĺĚƙĿƙ
ƒ TŠIJĚČƥĿūƭƙēĿƙĚîƙĚƙ Ɠ qîŕŠƭƥƑĿƥĿūŠ
Ɠ ɍēĿIJǶČĿŕĚĺƎƙĚƭēūŞĚŞċƑîŠūƭƙČūŕĿƥĿƙ
ƒ HTŞîŕĿijŠîŠČĿĚƙ
TREATMENT
OTHER INTERVENTIONS
ƒ gūDžIJîƥɈĺĿijĺƎƑūƥĚĿŠēĿĚƥɒƙƭƎƎŕĚŞĚŠƥ
ŞĚēĿƭŞČĺîĿŠƥƑĿijŕNjČĚƑĿēĚƙɚq ¹ɛ

OSMOSIS.ORG 259
 ULCERATIVE COLITIS
osms.it/ulcerative-colitis
MNEMONIC: ULCERATIONS
PATHOLOGY & CAUSES Features of Ulcerative colitis
UŕČĚƑƙ
ƒ ƭƥūĿŞŞƭŠĚēĿƙĚîƙĚĺ ƙƭƎĚƑǶČĿîŕƭŕČĚƑ
IJūƑŞîƥĿūŠɒČūŠƥĿŠƭūƭƙɈČĿƑČƭŞIJĚƑĚŠƥĿîŕ LîƑijĚĿŠƥĚƙƥĿŠĚ
ĿŠǷîƥĿūŠĿŠČūŕūŠĿČɈƑĚČƥîŕŞƭČūƙî CîƑČĿŠūŞîɚƑĿƙŒūIJɛ
ƒ qūƙƥČūŞŞūŠĿŠǷîƥūƑNjċūDžĚŕēĿƙĚîƙĚɒ ENJƥƑîĿŠƥĚƙƥĿŠîŕŞîŠĿIJĚƙƥîƥĿūŠƙ
ŞîNjƎƑĚƙĚŠƥîƥîŠNjîijĚ RĚŞŠîŠƥƙūIJūŕēƭŕČĚƑƙ
ƒ ūŞƎîƑĚƥū ƑūĺŠɫƙēĿƙĚîƙĚ ɚƎƙĚƭēūƎūŕNjƎƙɛ
Ɠ ÀƙƭîŕŕNjîIJIJĚČƥƙNjūƭŠijƎĚūƎŕĚɈîIJIJĚČƥƙ AċƙČĚƙƙĚƙĿŠČƑNjƎƥƙ
ĚŠƥĿƑĚHTƥƑîČƥɒČîƭƙĚƙƥƑîŠƙŞƭƑîŕ TūNJĿČŞĚijîČūŕūŠɚƑĿƙŒūIJɛ
ĿŠǷîƥĿūŠɒƎîƥČĺĚƙūIJĿŠǷîŞĚē IŠǷîŞĚēɈƑĚēɈijƑîŠƭŕîƑŞƭČūƙî
ŞƭČūƙîɈČūċċŕĚƙƥūŠĚîƎƎĚîƑîŠČĚ OƑĿijĿŠîƥĚƙîƥƑĚČƥƭŞ
ƒ 'ȉʋČĚŕŕîČƥĿDŽîƥĿūŠĺēĚƙƥƑƭČƥĿūŠūIJČĚŕŕƙ NĚƭƥƑūƎĺĿŕĿŠDŽîƙĿūŠ
ĿŠŞƭČūƙîŕɈƙƭċŞƭČūƙîŕČūŕūŠĿČŕîNjĚƑƙ
SƥūūŕĿƙċŕūūēNj
Ɠ ƙƙūČĿîƥĚēDžĿƥĺƎĚƑĿŠƭČŕĚîƑîŠƥĿɠ
ŠĚƭƥƑūƎĺĿŕČNjƥūƎŕîƙŞĿČîŠƥĿċūēĿĚƙ
ɚƎɠs ƙɛ
ƒ qƭŕƥĿIJîČƥūƑĿîŕūƑĿijĿŠ SIGNS & SYMPTOMS
Ɠ /ŠDŽĿƑūŠŞĚŠƥîŕƙƥĿŞƭŕĿʋĚNJČĚƙƙĿDŽĚ
ƙƭŕǶēĚɠƎƑūēƭČĿŠijċîČƥĚƑĿîʋijĚŠĚƥĿČ ƒ ČƭƥĚǷîƑĚƙɈƑĚŞĿƙƙĿūŠƙɒijƑîēƭîŕūŠƙĚƥ
ƎƑĚēĿƙƎūƙĿƥĿūŠ Ɠ ¤ĿƙŒūIJƑĚŕîƎƙĚƑĚŕîƥĚēƥūƎĚƑƙūŠɫƙîijĚîƥ
ƒ qūƑĚČūŞŞūŠîŞūŠijDžĺĿƥĚƎĚūƎŕĚɈ ēĿîijŠūƙĿƙ
ĚƙƎĚČĿîŕŕNjūIJ/îƙƥĚƑŠ/ƭƑūƎĚîŠēĚƙČĚŠƥ ƒ ¬ĚDŽĚƑĿƥNjēĚƥĚƑŞĿŠĚēċNjIJƑĚƐƭĚŠČNjūIJċūDžĚŕ
ƒ qūƑĚČūŞŞūŠĿŠNjūƭŠijĿŠēĿDŽĿēƭîŕƙDžĺūîƑĚ ŞūDŽĚŞĚŠƥƙɈēĚijƑĚĚūIJĿŠǷîƥĿūŠɈ
ċĿūŕūijĿČîŕŕNjIJĚŞîŕĚ ƙNjƙƥĚŞĿČƙNjŞƎƥūŞƙ
ƒ ūŕĿČŒNjɈŕĚIJƥŕūDžĚƑƐƭîēƑîŠƥƎîĿŠ
CAUSES ƒ 'ĿîƑƑĺĚîɒIJƑĚƐƭĚŠƥŕNjijƑūƙƙŕNjċŕūūēNjɈŞƭČūƭƙ
ƒ ÀŠČŕĚîƑɒîƭƥūĿŞŞƭŠĚƑĚîČƥĿūŠîijîĿŠƙƥ ƒ ¤ĚČƥîŕƥĚŠĚƙŞƭƙɈĿŠČūŠƥĿŠĚŠČĚɈƭƑijĚŠČNjɈ
ČūŕūŠĿČǷūƑîɈŞūŕĚČƭŕîƑŞĿŞĿČƑNjɈĿŠČƑĚîƙĚē ċŕĚĚēĿŠij
ƙƭŕǶēĚƎƑūēƭČƥĿūŠĿŞƎŕĿČîƥĚē Ɠ Tenesmus: gîƥĿŠƥĚĿŠĚƙŞūƙɒƥūƙƥƑîĿŠ
ƒ /ŠDŽĿƑūŠŞĚŠƥîŕIJîČƥūƑƙČūŠƥƑĿċƭƥĚƥūîČƭƥĚ ƒ GĚDŽĚƑɈIJîƥĿijƭĚɈDžĚĿijĺƥŕūƙƙɈîŠĚŞĿîɈ
ǷîƑĚƙ ēĚĺNjēƑîƥĿūŠ
ƒ /NJƥƑîĿŠƥĚƙƥĿŠîŕŞîŠĿIJĚƙƥîƥĿūŠƙ
COMPLICATIONS Ɠ ƑƥĺƑĿƥĿƙɚŞūƙƥČūŞŞūŠɛɒƭDŽĚĿƥĿƙɒ
ĚƑNjƥĺĚŞîŠūēūƙƭŞɒƎNjūēĚƑŞî
ƒ ¹ūNJĿČŞĚijîČūŕūŠɈîŠîŕǶƙƙƭƑĚƙɈƎĚƑĿƑĚČƥîŕ
ijîŠijƑĚŠūƙƭŞɒƎƑĿŞîƑNjƙČŕĚƑūƙĿŠij
îċƙČĚƙƙ
ČĺūŕîŠijĿƥĿƙɒîƑƥĚƑĿîŕɈDŽĚŠūƭƙ
ƥĺƑūŞċūĚŞċūŕĿƙŞƙ

260 OSMOSIS.ORG
 Chapter 33 TŠǷîƥūƑNjūDžĚŕ'ĿƙĚîƙĚ

DIAGNOSIS
ƒ ʑIJūƭƑDžĚĚŒƙîČƥĿDŽĚēĿîƑƑĺĚîʋ
ĿŠǷîƥūƑNjǶŠēĿŠijƙūŠĚŠēūƙČūƎNjʋ
ČĺƑūŠĿČĿŠǷîƥūƑNjČĺîŠijĚƙūŠċĿūƎƙNj
ƒ ĿūƎƙNj
Ɠ ƑNjƎƥîċƙČĚƙƙĚƙ

LAB RESULTS
ƒ Anemia
ƒ /ŕĚDŽîƥĚēĿŠǷîƥūƑNjŞîƑŒĚƑƙ
Figure 33.6ƎîŠČūŕĚČƥūŞNjƙƎĚČĿŞĚŠIJƑūŞ
Ɠ /ƑNjƥĺƑūČNjƥĚƙĚēĿŞĚŠƥîƥĿūŠƑîƥĚɚ/¬¤ɛɈ îŠĿŠēĿDŽĿēƭîŕDžĿƥĺƭŕČĚƑîƥĿDŽĚČūŕĿƥĿƙɍ
ɠƑĚîČƥĿDŽĚƎƑūƥĚĿŠɚ ¤¡ɛ

OTHER DIAGNOSTICS
ƒ ŕĿŠĿČîŕēĿîijŠūƙĿƙɒĚNJČŕƭēĚūƥĺĚƑČîƭƙĚƙūIJ
ČūŕĿƥĿƙ
Ɠ TŠIJĚČƥĿūŠƙɚĚɍijɍƎîƑîƙĿƥĚƙɈClostridium
ēĿIJǶČĿŕĚɛɈ¬¹TƙɈƑîēĿîƥĿūŠɈŞĚēĿČîƥĿūŠƙ

TREATMENT
MEDICATIONS
ƒ ŠƥĿɠĿŠǷîƥūƑNjŞĚēĿČîƥĿūŠƙ
Ɠ ¬ƭŕIJîƙîŕîǕĿŠĚɈŞĚƙîŕîŞĿŠĚ
ƒ TŞŞƭŠūƙƭƎƎƑĚƙƙūƑƙ
Ɠ ūƑƥĿČūƙƥĚƑūĿēƙɈîǕîƥĺĿūƎƑĿŠĚɈ
ČNjČŕūƙƎūƑĿŠĚ
ƒ ¹sGċŕūČŒĿŠijîijĚŠƥ

SURGERY
ƒ ūŕĚČƥūŞNjūŠŕNjĿIJēĿƙĚîƙĚŕūČîŕĿǕĚē Figure 33.7ċēūŞĿŠîŕƑîēĿūijƑîƎĺ
ēĚŞūŠƙƥƑîƥĿŠijƥūNJĿČŞĚijîČūŕūŠɈî
ČūŞƎŕĿČîƥĿūŠūIJƭŕČĚƑîƥĿDŽĚČūŕĿƥĿƙɍ

Figure 33.8¹ĺĚČŕĿŠĿČîŕîƎƎĚîƑîŠČĚ
ūIJĚƑNjƥĺĚŞîŠūēūƙƭŞɒîČƭƥîŠĚūƭƙ
ŞîŠĿIJĚƙƥîƥĿūŠūIJĿŠǷîƥūƑNjċūDžĚŕēĿƙĚîƙĚɍ

OSMOSIS.ORG 261
 Figure 33.9OĿƙƥūŕūijĿČîŕîƎƎĚîƑîŠČĚūIJ
îČƥĿDŽĚƭŕČĚƑîƥĿDŽĚČūŕĿƥĿƙĿŠîČūŕūŠĿČċĿūƎƙNjɍ
¹ĺĚƑĚĿƙîČƥĿDŽĚĿŠǷîƥĿūŠČîƭƙĿŠijČƑNjƎƥ
ēĚƙƥƑƭČƥĿūŠɍ ƑNjƎƥĿƥĿƙîŠēČƑNjƎƥîċƙČĚƙƙĚƙîƑĚ
îŕƙūƎƑĚƙĚŠƥɍ

262 OSMOSIS.ORG
 NOTES

NOTES
INTESTINAL DISEASES

GENERALLY, WHAT ARE THEY?

PATHOLOGY & CAUSES TREATMENT
ƒ Diseases preventing adequate digestive ƒ See individual diseases
system function
Ɠ ~IJƥĚŠĿŠDŽūŕDŽĚĿŠǷîƥĿūŠɈƙƥîƙĿƙɈ
ūċƙƥƑƭČƥĿūŠɈŠĚČƑūƙĿƙ MNEMONIC: APPENDICITIS
ƒ ×îƑĿūƭƙƙƥƑƭČƥƭƑîŕɈIJƭŠČƥĿūŠîŕĚƥĿūŕūijĿĚƙ Right lower-quadrant pain
common differential
Appendicitis/ Abscess
SIGNS & SYMPTOMS PĚŕDŽĿČĿŠǷîƥūƑNjēĿƙĚîƙĚ
(PID)/ Period pancreatitis
ƒ Abdominal symptoms etiologically- Ectopic/ Endometriosis
dependent Neoplasia
ƒ ċēūŞĿŠîŕƎîĿŠɈēĿƙƥĚŠƙĿūŠɈČūŠƙƥĿƎîƥĿūŠɈ Diverticulitis
ċūDžĚŕɠĺîċĿƥČĺîŠijĚɈĺĚŞîƥūČĺĚǕĿîɈ
Intussusception
ŠîƭƙĚîɈDŽūŞĿƥĿŠij
Crohn’s Disease/ Cyst (ovarian)
ƒ Bulging abdominal mass (in hernia)
IBD
Torsion (ovary)
DIAGNOSIS Irritable Bowel Syndrome
Stones
DIAGNOSTIC IMAGING
ƒ ¹ƙČîŠɈq¤TɈƭŕƥƑîƙūƭŠē

OTHER DIAGNOSTICS
ƒ Right lower-quadrant pain common
differential (see mnemonic)

OSMOSIS.ORG 263
 APPENDICITIS
osms.it/appendicitis

PATHOLOGY & CAUSES SIGNS & SYMPTOMS

ƒ Lumen obstruction ĺ vestigial vermiform ƒ Abdominal pain
îƎƎĚŠēĿNJĿŠǷîƥĿūŠ Ɠ Often begins in umbilical area ĺ
ƒ Located at cecum base (near ileocecal McBurney’s point (abdomen’s right
valve) lower-quadrant; one-third distance from
ƒ Obstruction ĺ intraluminal content îŠƥĚƑĿūƑƙƭƎĚƑĿūƑĿŕĿîČƙƎĿŠĚɈƭŞċĿŕĿČƭƙ)
stasis ĺ ĹŕƭŞĿŠîŕɈĿŠƥƑîŞƭƑîŕƎƑĚƙƙƭƑĚ ĺƎƑūijƑĚƙƙĿDŽĚĿŠǷîƥĿūŠ
ĺƥĺƑūŞċūƙĿƙɈūČČŕƭƙĿūŠƙŞîŕŕDŽĚƙƙĚŕƙɈ Ɠ Rovsing’s sign: left lower-quadrant
ŕNjŞƎĺîƥĿČǷūDžƙƥîƙĿƙĺĿƙČĺĚŞĿîɈŠĚČƑūƙĿƙ palpated ĺ right lower-quadrant pain
ƒ /NJČĚƙƙĿDŽĚŞƭŕƥĿƎŕĿČîƥĿūŠɚijƭƥǷūƑîɛċĚĺĿŠē Ɠ Psoas sign: right leg extended in left-
obstruction ĺ immune system response side position ĺ retrocecal appendix
ĺǶċƑūƎƭƑƭŕĚŠƥƑĚîČƥĿūŠĺ parietal Ɠ Obturator sign: right leg internally
peritoneum irritation rotated in supine position ĺ pelvic
ƒ ×ĿƙČĚƑîŕŠĚƑDŽĚǶċĚƑƙƥĿŞƭŕîƥĿūŠĺ appendix
abdominal pain ƒ FeverɈîŠūƑĚNJĿîɈnauseaɈDŽūŞĿƥĿŠijɈēĿîƑƑĺĚîɓ
constipation
CAUSES ƒ In case of peritonitis
ƒ Obstruction Ɠ Rebound tenderness at McBurney’s
Ɠ Lymphoid hyperplasiaɚîēūŕĚƙČĚŠČĚɈ point
DŽĿƑîŕĿŠIJĚČƥĿūŠɛɈfecalithɈIJūƑĚĿijŠċūēNj Ɠ Abdominal guarding (peritoneal
ɚĚɍijɍƭŠēĿijĚƙƥĚēƙĚĚēƙɛɈƎĿŠDžūƑŞ irritation)
ĿŠIJĚČƥĿūŠɈƥƭŞūƑɚċĚŠĿijŠɈŞîŕĿijŠîŠƥɛ

DIAGNOSIS
RISK FACTORS
ƒ ȂȁɝȄȁNjĚîƑƙūŕēɈIJîŞĿŕNjĺĿƙƥūƑNjɈċĿūŕūijĿČîŕŕNjɠ DIAGNOSTIC IMAGING
ŞîŕĚɈČNjƙƥĿČǶċƑūƙĿƙČūŞūƑċĿēĿƥNjɚČĺĿŕēƑĚŠɛ
CT scan with IV contrast
COMPLICATIONS ƒ Increased appendix diameter
ƒ Appendix-supplying vessel compression ƒ Increased wall enhancement
ĺ ischemia ĺ appendix wall necrosis ƒ Severe
ĺ bacterial invasion (wall) ĺ appendix Ɠ ×ĿƙĿċŕĚîċƙČĚƙƙɈƎƭƙƙƎĿŕŕîijĚ
rupture ĺ bacterial invasion (peritoneum)
ĺ peritonitis Ultrasound (pregnancy, children)
ƒ ¡ĚƑĿîƎƎĚŠēĿČĚîŕîċƙČĚƙƙɈƙƭċƎĺƑĚŠĿČ ƒ ×ĿƙĿċŕĚɈŠūŠČūŞƎƑĚƙƙĿċŕĚɈēĿŕîƥĚēîƎƎĚŠēĿNJ
îċƙČĚƙƙɈƎNjŕĚƎĺŕĚċĿƥĿƙɈƎūƑƥîŕDŽĚŠūƭƙ ƒ ĹċŕūūēǷūDžĿŠîƎƎĚŠēĿNJDžîŕŕ
ƥĺƑūŞċūƙĿƙɈƙĚƎƙĿƙ ƒ Visible appendicolith
ƒ ¤ĿijĺƥĿŕĿîČIJūƙƙîǷƭĿēČūŕŕĚČƥĿūŠ

264 OSMOSIS.ORG
 Chapter 34 Intestinal Diseases

LAB RESULTS
ƒ sĚƭƥƑūƎĺĿŕĿČŕĚƭŒūČNjƥūƙĿƙ
Ɠ Ĺ with progression
ƒ Mildly elevated serum bilirubin
Ɠ ¡ĚƑIJūƑîƥĿūŠŞîƑŒĚƑ

TREATMENT
MEDICATIONS
ƒ Antibiotics
ƒ T×ǷƭĿēƙɈŠūIJūūēɓDžîƥĚƑūƑîŕŕNjɚs¡~ɛ
Figure 34.1 Camera view of a laparoscopic
SURGERY appendicectomy being performed. The
appendicectomy has been performed and
ƒ Removal (appendectomy)
ƥĺĚƙƥƭŞƎĿƙDŽĿƙĿċŕĚūŠƥĺĚƑĿijĺƥūIJƥĺĚĿŞîijĚɈ
ƒ Abscess drainage DžĿƥĺƥĺĚƙĚDŽĚƑĚēîƎƎĚŠēĿNJƑĚǷĚČƥĚēŕîƥĚƑîŕŕNjɍ

DIVERTICULITIS
osms.it/diverticulitis

PATHOLOGY & CAUSES SIGNS & SYMPTOMS

ƒ TŠǷîŞĚēēĿDŽĚƑƥĿČƭŕîɒŞĿČƑūƎĚƑIJūƑîƥĿūŠūIJ ƒ Left lower-quadrant pain (often sigmoid
diverticulum colon); palpable abdominal mass; diarrhea/
constipation; nausea; vomiting; fever;
ƭƑĿŠîƑNjƭƑijĚŠČNjɓIJƑĚƐƭĚŠČNjɓēNjƙƭƑĿîɚĿŠǷîŞĚē
CAUSES sigmoid colon ĺ bladder irritation)
ƒ Increased intraluminal pressure ĺ erosion
ĺĿŠǷîƥĿūŠɈIJūČîŕŠĚČƑūƙĿƙĺ micro/
macro perforation DIAGNOSIS
RISK FACTORS DIAGNOSTIC IMAGING
ƒ Diverticula present
CT scan with contrast
ƒ TŠǷîƥĿūŠĺ hyperdense tissue
COMPLICATIONS
ƒ ¬ƥƑĿČƥƭƑĚɈĿŠƥĚƙƥĿŠîŕobstruction Abdominal X-ray
ƒ Diverticulum perforation ƒ Bowel obstruction
Ɠ ċƙČĚƙƙɈƎĚƑĿƥūŠĿƥĿƙ ƒ Bowel perforation
ƒ Fistula formation Ɠ Free air
Ɠ Bladder communication
Ɠ ~ƥĺĚƑūƑijîŠČūŞŞƭŠĿČîƥĿūŠɚDŽîijĿŠîɈ LAB RESULTS
ƙŒĿŠɈūƥĺĚƑƎîƑƥƙūIJċūDžĚŕɛ ƒ gĚƭŒūČNjƥūƙĿƙ
Ɠ ×ĚƙĿČūĚŠƥĚƑĿČǶƙƥƭŕîɇ pneumaturia (air in
ƭƑĿŠĚɛɈIJĚČîŕƭƑĿîɚƙƥūūŕĿŠƭƑĿŠĚɛ

OSMOSIS.ORG 265
 TREATMENT
MEDICATIONS
ƒ Uncomplicated
Ɠ AntibioticsɈǷƭĿēƙɈŠūIJūūēɓDžîƥĚƑūƑîŕŕNj
ɚs¡~ɛ

SURGERY
ƒ Resection
Ɠ Severe case/recurrence/complication
Figure 34.2 Gross pathology of sigmoid
ēĿDŽĚƑƥĿČƭŕūƙĿƙɍsūƥĿČĚĺūDžƥĺĚēĿDŽĚƑƥĿČƭŕî
OTHER INTERVENTIONS appear either side of the longitudinal muscle.
ƒ OĿijĺɠǶċĚƑēĿĚƥ
Ɠ Prevents recurrence

DIVERTICULOSIS
osms.it/diverticulosis
(some areas) ĺ mucosa/submucosa
PATHOLOGY & CAUSES herniation predisposed ĺ diverticulum
formation
ƒ 'ĿDŽĚƑƥĿČƭŕƭŞɚƎŕƭƑîŕēĿDŽĚƑƥĿČƭŕîɛɇ Ɠ ¬ĿijŞūĿēČūŕūŠɇsmallest diameter ĺ
outpouching of hollow anatomical structure highest pressure (Laplace’s Law:
wall P∝Ȃɓ'ɛɈŞūƙƥČūŞŞūŠŕūČîƥĿūŠ
Ɠ Most frequent in large intestine ƒ ~ƭƥƎūƭČĺĿŠijɇ tend to form where intestinal
(particularly sigmoid colon) wall-supplying blood vessels (i.e. vasa
ƒ 'ĿDŽĚƑƥĿČƭŕūƙĿƙɇmultiple diverticula present recta) traverse muscle layer

TYPES RISK FACTORS

True diverticulum ƒ gĿIJĚƙƥNjŕĚɇ ŕūDžɠǶċĚƑēĿĚƥɈ constipation; fatty
IJūūēɈƑĚēŞĚîƥɠƑĿČĺēĿĚƥɒĿŠîČƥĿDŽĿƥNjɒƙŞūŒĿŠij
ƒ ŕŕūƑijîŠDžîŕŕŕîNjĚƑƙĿŠČŕƭēĚēɚĚɍijɍqĚČŒĚŕɫƙ
diverticulum) ƒ Ĺ age ĹƑĿƙŒ
ƒ Biologically-male
False (pseudo-) diverticulum ƒ Family history
ƒ ~ŠŕNjŞƭČūƙîɈƙƭċŞƭČūƙîŕîNjĚƑƙĿŠČŕƭēĚē ƒ Obesity
Ɠ Most common ƒ Connective tissue disorders
Ɠ Colonic diverticula Ɠ Marfan syndrome
Ɠ Ehlers–Danlos syndrome
CAUSES Ɠ ƭƥūƙūŞîŕēūŞĿŠîŠƥƎūŕNjČNjƙƥĿČŒĿēŠĚNj
ƒ Multifactorial pathogenesis from abnormal disease
colonic motility
ƒ Abnormal/exaggerated smooth muscle
contractions ĺ unequal intraluminal
pressure distribution ĺ high pressure

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COMPLICATIONS
ƒ ŕūūēDŽĚƙƙĚŕƙƭƑƑūƭŠēĿŠijDžĚîŒĚŠĚē
TREATMENT
outpouching ruptures ĺlarge intestine
blood loss ĺbloody stool
SURGERY
ƒ Resection (if complications develop)
ƒ TŠǷîƥĿūŠɚēĿDŽĚƑƥĿČƭŕĿƥĿƙɛ
ƒ Segmental colitis
OTHER INTERVENTIONS
ƒ Lifestyle changes
SIGNS & SYMPTOMS Ɠ Diet (ĹǶċĚƑĿŠƥîŒĚɛɈîDŽūĿēČūŠƙƥĿƎîƥĿūŠɈĹ
ƎĺNjƙĿČîŕîČƥĿDŽĿƥNjɈƙŞūŒĿŠijČĚƙƙîƥĿūŠ
ƒ Often asymptomatic
ƒ ×îijƭĚîċēūŞĿŠîŕƎîĿŠɈƥĚŠēĚƑŠĚƙƙɈċŕūîƥĿŠij
ƒ Occasional cramping
ƒ Altered bowel habit (diarrhea/constipation)
ƒ ¤ĚČƥîŕċŕĚĚēĿŠijɚĺĚŞîƥūČĺĚǕĿîɜIJƑĚƙĺ
blood in stool)

DIAGNOSIS
ƒ Often found incidentally

DIAGNOSTIC IMAGING
X-ray with barium enema
ƒ Lower gastrointestinal series
ƒ Directly shows pouches

CT scan Figure 34.3 Barium study demonstrating

ƒ ×ĿƙƭîŕĿǕîƥĿūŠūIJČūŕūŠĿČēĿDŽĚƑƥĿČƭŕîɈ multiple diverticula.
ƥĺĿČŒĚŠĿŠijūIJƥĺĚċūDžĚŕDžîŕŕƥĺĿČŒĚŠĿŠijɚʑ
ȅŞŞɛɈîŠĿŠČƑĚîƙĚĿŠƙūIJƥƥĿƙƙƭĚēĚŠƙĿƥNj
within pericolonic

OTHER DIAGNOSTICS
Colonoscopy, sigmoidoscopy
ƒ Visible outpouching

OSMOSIS.ORG 267
 FEMORAL HERNIA
osms.it/femoral-hernia
ƒ Abdominal contents enter hernia ĺ may
PATHOLOGY & CAUSES precipitate intestinal obstruction
Ɠ Most common cause worldwide
ƒ Intestinal projection across femoral canal
îƙƙūČĿîƥĚēDžĿƥĺIJĚŞūƑîŕîƑƥĚƑNjɈDŽĚĿŠɒbelow Ɠ Incarcerated/strangulated; severe
ĿŠijƭĿŠîŕŕĿijîŞĚŠƥɈŕîƥĚƑîŕƥūƎƭċĿČƥƭċĚƑČŕĚ îċēūŞĿŠîŕƎîĿŠɈƥĚŠēĚƑŠĚƙƙɈĚƑNjƥĺĚŞîɈ
IJĚDŽĚƑɈŠîƭƙĚîɈDŽūŞĿƥĿŠij

CAUSES
ƒ ūŠijĚŠĿƥîŕɈîČƐƭĿƑĚē DIAGNOSIS
ƒ ØĚĚƙƙɓîċŠūƑŞîŕIJîƙČĿîŕūƎĚŠĿŠijĿŠ
abdominal wall DIAGNOSTIC IMAGING
ƒ Usually includes properitoneal fat/omentum
Ultrasound
edge/small bowel loop
ƒ Variable echogenicity of tissue; movement
of intra-abdominal structures in an inferior
RISK FACTORS direction through the femoral canal
ƒ ĿūŕūijĿČîŕŕNjɠIJĚŞîŕĚɈ congenital disorder
(embryological development ĺ processus CT scan
DŽîijĿŠîŕĿƙūċŕĿƥĚƑîƥĿūŠIJîĿŕƭƑĚɛɈĺĚƑŠĿîɚIJîŞĿŕNj ƒ ×ĿƙƭîŕĿǕîƥĿūŠūIJČĺîƑîČƥĚƑĿƙƥĿČIJƭŠŠĚŕɠ
ĺĿƙƥūƑNjɛɈūċĚƙĿƥNjɈƎƑĚijŠîŠČNjɈIJƑĚƐƭĚŠƥĺĚîDŽNj ƙĺîƎĚēŠĚČŒɒƎƑūƥƑƭƙĿūŠƥĺƑūƭijĺIJĚŞūƑîŕ
lifting ring

COMPLICATIONS TREATMENT
ƒ sîƑƑūDžIJĚŞūƑîŕČîŠîŕ
Ɠ ĹĿŠČîƑČĚƑîƥĿūŠɓƙƥƑîŠijƭŕîƥĿūŠƑĿƙŒ SURGERY
ƒ Compression of femoral vein ƒ Repair
ƒ Bowel obstruction Ɠ Open/laparoscopic (case-dependent)
ƒ Early/elective repair
Ɠ ÀŠČūŞƎŕĿČîƥĚēɈîƙNjŞƎƥūŞîƥĿČĺĚƑŠĿî
SIGNS & SYMPTOMS
ƒ Urgent repair
ƒ Asymptomatic (commonly) Ɠ Complicated hernia (may require bowel
resection)
ƒ Can manifest intestinal obstruction
symptoms
Ɠ ƭŕijĿŠijŞîƙƙɈƎîĿŠɈēĿƙČūŞIJūƑƥ
Ɠ ¬ƭƎĿŠĚɇmay resolve
Ɠ ×îŕƙîŕDŽîŞîŠĚƭDŽĚƑɚČūƭijĺĿŠijɓƙƥƑîĿŠĿŠijɛɇ
worsens

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GALLSTONE ILEUS
osms.it/gallstone-ileus
Effect on intestinal wall
PATHOLOGY & CAUSES
ƒ ¬ĿŞƎŕĚɇno blood supply impairment
ƒ Gastrointestinal motility (peristalsis) ƒ ¬ƥƑîŠijƭŕîƥĚēɇ blood supply cut off to bowel
disruption ĺ impaired bowel content section
propulsion ƒ ŕūƙĚēŕūūƎɇobstruction occurs at each end
ƒ ŕūČŒîijĚĺ progressive intestine dilation of bowel section
ċŕūČŒîijĚɠƎƑūNJĿŞîŕɈēĚČūŞƎƑĚƙƙĿūŠ Type of factor
ċŕūČŒîijĚɠēĿƙƥîŕ
ƒ qĚČĺîŠĿČîŕɇobstruction caused by
ƒ Gas accumulation ɚƙDžîŕŕūDžĚēîĿƑɈċîČƥĚƑĿîŕ ijîŕŕƙƥūŠĚɈŠĚūƎŕîƙŞɈîēĺĚƙĿūŠɈƙƥƑĿČƥƭƑĚɈ
fermentation) ĺĹ bowel distention ĺĚŞîƥūŞîɈŞĚČūŠĿƭŞɚĿŠČNjƙƥĿČǶċƑūƙĿƙɛɈ
ƒ Bowel wall edema ĺĻ bowel content medical device migration (PEG tube)
absorption ĺŕƭŞĿŠîŕǷƭĿēƙĚƐƭĚƙƥƑîƥĿūŠ ƒ GƭŠČƥĿūŠîŕɇ intestinal musculature
ƒ Ĺ capillary permeability ĺƥƑîŠƙƭēîƥĿDŽĚǷƭĿē ƎîƑîŕNjƙĿƙČîƭƙĚēċNjƥƑîƭŞîɚƙƭƑijĚƑNjɈċŕƭŠƥ
loss from intestinal lumen into peritoneal îċēūŞĿŠîŕƥƑîƭŞîɛɈƎĚƑĿƥūŠĿƥĿƙɈŞĚēĿČîƥĿūŠ
cavity ɚūƎĿîƥĚƙɈîŠƥĿČĺūŕĿŠĚƑijĿČƙɛ
ƒ Emesis ĺǷƭĿēɈĚŕĚČƥƑūŕNjƥĚɚsîɈeɈOɈ ŕɛ
loss ĺŞĚƥîċūŕĿČîŕŒîŕūƙĿƙɈĺNjƎūDŽūŕĚŞĿî
RISK FACTORS
ƒ Bowel dilation continues ĺĻ intestinal
ƒ SurgeryɒċūDžĚŕŞîŠĿƎƭŕîƥĿūŠɈîŠĚƙƥĺĚƙĿîɈ
wall tissue perfusion ĺĿƙČĺĚŞĿîɈŠĚČƑūƙĿƙɈ
postoperative opioids
bowel perforation
ƒ OĚƑŠĿîɈŠĚūƎŕîƙŞĺĿƙƥūƑNjɈîċēūŞĿŠîŕɓƎĚŕDŽĿČ
ĿƑƑîēĿîƥĿūŠɈČĺƑūŠĿČĿŠǷîƥĿūŠɈîċēūŞĿŠîŕ
TYPES trauma
Onset
ƒ Acute:IJîČƥūƑƙƙƭČĺîƙƥūƑƙĿūŠɈ COMPLICATIONS
intussusception ĺ sudden onset ƒ Fluid/electrolyte/acid-base imbalance;
ƒ ĺƑūŠĿČɇfactors such as tumor growth ĺ ċūDžĚŕƙƥƑîŠijƭŕîƥĿūŠɈŠĚČƑūƙĿƙɒƎĚƑIJūƑîƥĿūŠɒ
prolonged onset sepsis
ƒ Recurrent: often caused by adhesions ĺ
intermittent obstructions
SIGNS & SYMPTOMS
Extent
ƒ ¡îƑƥĿîŕɇsome of intestinal lumen remains ƒ ċēūŞĿŠîŕēĿƙƥĚŠƙĿūŠɈČƑîŞƎĿŠijƎîĿŠɈ
open constipationɈŠîƭƙĚîɈDŽūŞĿƥĿŠij
ƒ ūŞƎŕĚƥĚɇ total lumen obstruction ƒ 'ĚĺNjēƑîƥĿūŠɇƥîČĺNjČîƑēĿîɈēƑNjŞƭČūƭƙ
ŞĚŞċƑîŠĚƙɈĻ urine output
Location ƒ Bowel sounds
ƒ Intrinsic: obstruction within bowel Ɠ OĿijĺɠƎĿƥČĺĚēɨƥĿŠŒŕĿŠijɩƙūƭŠē
DžîŕŕɜĚɍijɍĿŠǷîƥūƑNjƙƥƑĿČƥƭƑĚɈĚēĚŞîɈ îƭƙČƭŕƥîƥĚēɇacute mechanical bowel
ĺĚŞūƑƑĺîijĚɈIJūƑĚĿijŠċūēNjɚĿŠijĚƙƥĚēɈ obstruction
ƎîƑîƙĿƥĚîČČƭŞƭŕîƥĿūŠɈŕîƑijĚċĿŕĿîƑNjČîŕČƭŕƭƙɛ Ɠ qƭIJǷĚēɈĺNjƎūîČƥĿDŽĚċūDžĚŕƙūƭŠēƙɇ
ƒ Extrinsic:ūċƙƥƑƭČƥĿūŠūƭƥƙĿēĚċūDžĚŕDžîŕŕɜ ƙĿijŠĿǶČîŠƥċūDžĚŕēĿƙƥĚŠƥĿūŠîƙƙūČĿîƥĿūŠ
ĚɍijɍƥūƑƙĿūŠɈČūŞƎƑĚƙƙĿūŠɚĺĚƑŠĿîɛ ƒ ċēūŞĿŠîŕƎĚƑČƭƙƙĿūŠɇ hyperresonance/
tympany

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 DIAGNOSIS
DIAGNOSTIC IMAGING
X-ray
ƒ ¬ŞîŕŕĿŠƥĚƙƥĿŠĚɈČūŕūŠēĿƙƥĚŠƙĿūŠ

TREATMENT
SURGERY
ƒ Surgical intervention: e.g. release
îēĺĚƙĿūŠƙɈČūŞƎŕĚƥĚūċƙƥƑƭČƥĿūŠƙɈƑĚƎîĿƑ
bowel

OTHER INTERVENTIONS
Figure 34.4 A CT scan of the abdomen and
ƒ sūIJūūēɓDžîƥĚƑūƑîŕŕNjɚs¡~ɛ
pelvis in the coronal plane demonstrating
ƒ GŕƭĿēɈelectrolyte replacement a gallstone in the terminal ileum. If so large
ƒ Parenteral feeding ĺ nasogastric that it is unable to pass through the ileocecal
decompression DŽîŕDŽĚɈƥĺĚijîŕŕƙƥūŠĚDžĿŕŕČîƭƙĚƙŞîŕŕċūDžĚŕ
obstruction.

GASTROENTERITIS
osms.it/viral-gastroenteritis
ƒ Viral contact
PATHOLOGY & CAUSES Ɠ /ɍijɍēîNjČîƑĚČĚŠƥĚƑɈČƑƭĿƙĚƙĺĿƎɈČŕūƙĚē
ČūŞŞƭŠĿƥNjūƭƥċƑĚîŒɒČūŠƥîŞĿŠîƥĚē
ƒ Gastrointestinal tract viral infection (lasts food/water
12 hours–3 days)
ƒ Primary transmission
Ɠ Oral–fecal route
COMPLICATIONS
ƒ Severe dehydrationĺ altered mental
ƒ Viruses ĺ epithelium damage ĺosmotic
ƙƥîƥƭƙɈDžĚĿijĺƥŕūƙƙ
ēĿîƑƑĺĚîɚʑƥĺƑĚĚƙƥūūŕƙēîĿŕNjɛɈDŽūŞĿƥĿŠij

CAUSES SIGNS & SYMPTOMS

ƒ ĺĿŕēƑĚŠɇ rotavirus (most common)
ƒ ēƭŕƥɇŠūƑūDŽĿƑƭƙɚŞūƙƥČūŞŞūŠɛɈîƙƥƑūDŽĿƑƭƙɈ ƒ Watery diarrhea; nausea; vomiting;
adenoviruses îċēūŞĿŠîŕČƑîŞƎƙɈƎîĿŠɒIJĚDŽĚƑɒŞîŕîĿƙĚɒ
ēĚĺNjēƑîƥĿūŠɚēƑNjŕĿƎƙɈƙŒĿŠƥƭƑijūƑɈ
tachycardia)
RISK FACTORS
ƒ Ĺ morbidity
Ɠ ĺĿŕēƑĚŠɈĚŕēĚƑŕNjɈĿŞŞƭŠūČūŞƎƑūŞĿƙĚē
individuals

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 Chapter 34 Intestinal Diseases

DIAGNOSIS
LAB RESULTS
ƒ Stool sample
Ɠ Excludes bacterial/parasitic etiology
ƒ Ĺ ɠƑĚîČƥĿDŽĚƎƑūƥĚĿŠɚ ¤¡ɛɈĹŕĚƭŒūČNjƥĚƙ
ƒ Polymerase chain reaction (PCR)
Ɠ ¬ƥūūŕɈDŽūŞĿƥɇĚŠǕNjŞĚɠŕĿŠŒĚē
immunosorbent assay (ELISA)
performed for rotavirus

TREATMENT
Figure 34.5 A scanning electron micrograph
ūIJîČŕƭƙƥĚƑūIJsūƑDžîŕŒDŽĿƑƭƙČîƎƙĿēƙɍ OTHER INTERVENTIONS
ƒ Fluid replacement

Prevention
ƒ ONjijĿĚŠĚƎƑîČƥĿČĚƙɈƑūƥîDŽĿƑƭƙDŽîČČĿŠĚ

INGUINAL HERNIAS
osms.it/inguinal-hernias
Ɠ ¹ĚƙƥĿČƭŕîƑēĚƙČĚŠƥƎîƥĺɇcovered
PATHOLOGY & CAUSES by three layers of spermatic fascia
(three layers); external spermatic
Direct inguinal hernia fascia (external oblique muscle fascia
ƒ Peritoneal sac; projects directly through continuation); cremasteric muscle
inguinal triangle ɚeHesselbach’s fascia; internal spermatic fascia (internal
triangle) oblique muscle fascia continuation)
ƒ Projects medially to inferior epigastric
DŽĚƙƙĚŕƙɈŕîƥĚƑîŕƥūƑĚČƥƭƙîċēūŞĿŠĿƙɈƎĿĚƑČĚƙ CAUSES
parietal peritoneum
ƒ OĚƙƙĚŕċîČĺɫƙƥƑĿîŠijŕĚČūŞƎūƙĿƥĿūŠɇ inguinal Indirect inguinal hernia
ŕĿijîŞĚŠƥɚe¡ūƭƎîƑƥɫƙŕĿijîŞĚŠƥɛɈƑĚČƥƭƙ ƒ Processus vaginalis closure failure (i.e.
îċēūŞĿŠĿƙŞƭƙČŕĚɚŕîƥĚƑîŕċūƑēĚƑɛɈĿŠIJĚƑĿūƑ internal inguinal ring and processus
epigastric vessels vaginalis obliteration failure)
ƒ Covered by external spermatic fascia

Indirect inguinal hernia RISK FACTORS

ƒ Most common hernia Direct inguinal hernia
ƒ Intestinal projection through internal ƒ ČƐƭĿƑĚēɈîIJIJĚČƥƙtransversalis fascia
inguinal ring
Ɠ Chronic intra-abdominal pressure Ĺ (e.g.
Ɠ Location: spermatic cord (biologically- ūċĚƙĿƥNjɈČĺƑūŠĿČČūƭijĺɈČūŠƙƥĿƎîƥĿūŠɈ
ŞîŕĚɛɈƑūƭŠēŕĿijîŞĚŠƥɚċĿūŕūijĿČîŕŕNjɠ ĺĚîDŽNjŕĿIJƥĿŠijɜūČČƭƎîƥĿūŠîŕɓƑĚČƑĚîƥĿūŠîŕɛ
female) exit the abdomen
ƒ Abdominal wall musculature atrophy

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 (aging)
ƒ ~ŕēĚƑɈ biologically-male individuals
DIAGNOSIS
Indirect inguinal hernia DIAGNOSTIC IMAGING
ƒ Biologically-maleĿŠēĿDŽĿēƭîŕƙʑċĿūŕūijĿČîŕŕNjɠ Ultrasound
female individuals
ƒ Direct inguinal hernia
Ɠ ĿūŕūijĿČîŕŕNjŞîŕĚɇ late right testicle
Ɠ Variable echogenicity of tissue;
descent
movement of intra-abdominal structures
Ɠ ĿūŕūijĿČîŕŕNjIJĚŞîŕĚɇasymmetric pelvis in an anterior direction through the
Hesselbach triangle
COMPLICATIONS ƒ Indirect inguinal hernia
Ɠ ×ĿƙƭîŕĿǕîƥĿūŠƥĺƑūƭijĺîċēūŞĿŠîŕDžîŕŕĿŠ
Direct inguinal hernia
biologically-female individuals
ƒ Incarceration/strangulation potential
CT scan
Indirect inguinal hernia
ƒ Direct inguinal hernia
ƒ Can form hydrocele
Ɠ ×ĿƙƭîŕĿǕîƥĿūŠūIJîƎƑūƥƑƭƙĿūŠDžĿƥĺ
ƒ May precipitate intestinal obstruction compressing inguinal canal contents;
ƒ Most common cause worldwide inguinal canal pushed into a semicircle
of tissue that resembles a moon
crescent
SIGNS & SYMPTOMS ƒ Indirect inguinal hernia
Ɠ TēĚŠƥĿǶĚƙūČČƭŕƥĺĚƑŠĿîɓČūŞƎŕĿČîƥĿūŠƙɒ
ƒ May be asymptomatic ĺĚƑŠĿîŠĚČŒDŽĿƙƭîŕĿǕĚēƙƭƎĚƑūŕîƥĚƑîŕƥū
ƒ ƭŕijĿŠijŞîƙƙɚĿŠēĿƑĚČƥĿŠijƭĿŠîŕĺĚƑŠĿîɈ the inferior epigastric vessels
ŞîƙƙĿŠijƑūĿŠɛɈƎîĿŠɈēĿƙČūŞIJūƑƥ
Ɠ Valsalva maneuver cessation/prone: may
resolve
OTHER DIAGNOSTICS
ƒ Indirect inguinal hernia
ƒ Valsalva maneuver: worsens projection
Ɠ OĿƙƥūƑNjɈČŕĿŠĿČîŕĚNJîŞɒƙƭIJǶČĿĚŠƥIJūƑ
Ɠ Coughing/straining
majority of suspected inguinal hernias
Direct inguinal hernia
ƒ May precipitate intestinal obstruction
Ɠ Most common cause worldwide
Ɠ Incarcerated/strangulated: severe
îċēūŞĿŠîŕƎîĿŠɈƥĚŠēĚƑŠĚƙƙɈĚƑNjƥĺĚŞîɈ
IJĚDŽĚƑɈŠîƭƙĚîɈDŽūŞĿƥĿŠij

Indirect inguinal hernia

ƒ Visible bulge
Ɠ May be unapparent in biologically-
female individuals
ƒ Incarcerated/strangulated
Ɠ ¬ĚDŽĚƑĚîċēūŞĿŠîŕƎîĿŠɈƥĚŠēĚƑŠĚƙƙɈ
ĚƑNjƥĺĚŞîɈIJĚDŽĚƑɈŠîƭƙĚîɈDŽūŞĿƥĿŠij

Figure 34.6 Intraperitoneal view of an

inguinal hernia during a laparoscopic hernia
repair. The peritoneal cavity extends into the
ĿŠijĿŠîŕČîŠîŕɈŕîƥĚƑîŕƥūƥĺĚĚƎĿijîƙƥƑĿČDŽĚƙƙĚŕƙɈ
ŞîŒĿŠijƥĺĿƙîŠĿŠēĿƑĚČƥĺĚƑŠĿîɍ

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TREATMENT
SURGERY
Repair
ƒ Open/laparoscopic (case-dependent)
ƒ Elective repair
Ɠ Symptomatic hernias
ƒ Direct inguinal hernia (asymptomatic)
Ɠ qūŠĿƥūƑɈƙƭƑijĿČîŕƑĚƎîĿƑƎƑĚIJĚƑƑĚē

Figure 34.8 A CT scan in the coronal plane

Figure 34.7 Clinical appearance of a hernia demonstrating an indirect inguinal hernia.
in the groin. It is often not possible to ¹ĺĚƎƑūNJĿŞîŕċūDžĚŕĿƙēĿŕîƥĚēɈĿŠēĿČîƥĿŠijî
distinguish between a direct and indirect strangulated hernia causing obstruction.
hernia on clinical examination alone.

INTESTINAL ADHESIONS
osms.it/intestinal-adhesions
ƒ TŠŏƭƑNjƎƑĚDŽĚŠƥƙĚŠǕNjŞĚƙĚČƑĚƥĿūŠĺ
PATHOLOGY & CAUSES ŞîČƑūƎĺîijĚƙɈǶċƑūċŕîƙƥƙēĚƎūƙĿƥČūŕŕîijĚŠ
into adhesion ĺ permanent
ƒ Fibrous tissue bands form physical
attachment between intestines ĺĻ
intestinal motility CAUSES
ƒ Formed from ƙČîƑƑĚēɈƎūƙƥɠƥƑîƭŞîƥĿƙƙƭĚ ƒ Surgery (most common)ɈĿŠǷîƥĿūŠ
ɚČĺūŕĚČNjƙƥĿƥĿƙɈƎîŠČƑĚîƥĿƥĿƙɈƎĚƑĿƥūŠĿƥĿƙɛɈ
ƒ Tissue injury ĺĿŠǷîƥĿūŠĺǶċƑĿŠ
ĚŠēūŞĚƥƑĿūƙĿƙɈƎĚŕDŽĿČĿŠǷîƥūƑNjēĿƙĚîƙĚ
deposits ĺǶċƑĿŠČūŠŠĚČƥƙƎîƑƥƙŕĚIJƥɚƙĿŞĿŕîƑ
to reconstructive “glue”)
ƒ Adhesions extend between tissue if both COMPLICATIONS
ƎîƑƥƙĺîDŽĚċĚĚŠĿŠŏƭƑĚēɈČŕūƙĚƎƑūNJĿŞĿƥNj ƒ ūDžĚŕūċƙƥƑƭČƥĿūŠɈĿŠƥĚƙƥĿŠîŕDžîŕŕDŽūŕDŽƭŕƭƙɓ
ƒ TŠĿƥĿîŕǶċƑūƭƙîēĺĚƙĿūŠƙēĿƙƙūŕDŽĚēċNj ischemia
ǶċƑĿŠūŕNjƥĿČĚŠǕNjŞĚƙ

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 SIGNS & SYMPTOMS
ƒ ċēūŞĿŠîŕƎîĿŠɈDŽūŞĿƥĿŠijɈċŕūîƥĿŠijɈ
constipation

DIAGNOSIS
DIAGNOSTIC IMAGING
X-ray
ƒ Detect obstruction; small intestine dilation

CT scan, ultrasound Figure 34.9 Intraoperative view of abdominal

ƒ Exclude other obstructive causes adhesions.

TREATMENT
SURGERY
ƒ Surgical/laparoscopic adhesion excision

INTUSSUSCEPTION
osms.it/intussusception
RISK FACTORS
PATHOLOGY & CAUSES ƒ Most common < 24 months oldɈ
ĿŠƥĚƙƥĿŠîŕŞîŕƑūƥîƥĿūŠĺĿƙƥūƑNjɈƎƑĚDŽĿūƭƙ
ƒ Condition that occurs when part of ĿŠƥƭƙƙƭƙČĚƎƥĿūŠɈĿŠƥƭƙƙƭƙČĚƎƥĿūŠĿŠƙĿċŕĿŠijɈ
intestine folds into adjacent section ĺ biologically male
obstruction
ƒ Ileocecal region most commonly affected
ƒ May be idiopathic/caused by abnormal
COMPLICATIONS
structure (causes pathological lead point) ƒ ¡ĚƑĿƥūŠĿƥĿƙɈƙĚƎƙĿƙ
ĺ peristalsis causes one part of bowel
to move ahead of adjacent section ĺ
bowel telescoping ĺĹƎƑĚƙƙƭƑĚɈĿŞƎîĿƑĚē SIGNS & SYMPTOMS
venous return ĺċŕĚĚēĿŠijɈċūDžĚŕĿƙČĺĚŞĿîɈ
infarction ƒ Intermittent abdominal pain (worsens with
peristalsis)
ƒ Guarding
CAUSES
ƒ ¬ƥƑîĿŠĿŠijĚIJIJūƑƥƙɈēƑîDžŒŠĚĚƙƥūDžîƑēČĺĚƙƥ
ƒ ēƭŕƥƙɇîċŠūƑŞîŕijƑūDžƥĺɚĚɍijɍƎūŕNjƎɈtumor)
ƒ Vomiting
ƒ Infants: post-infection lymphoid hyperplasia
(Peyer’s patchesɛɈqĚČŒĚŕɫƙēĿDŽĚƑƥĿČƭŕƭŞ ƒ ¬îƭƙîijĚɠŕĿŒĚîċēūŞĿŠîŕŞîƙƙ
ƒ “Red currant jelly” stoolɚċŕūūēɈŞƭČƭƙɛ

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DIAGNOSIS TREATMENT
DIAGNOSTIC IMAGING SURGERY
ƒ Free telescoped intestine portion ĺ clear
Ultrasound, X-ray, CT scan
obstruction ĺ remove necrotic tissue
ƒ ¹ĚŕĚƙČūƎĚēĿŠƥĚƙƥĿŠĚɇDŽĿƙƭîŕĿǕĚēîƙclassic
bull’s-eye image
ƒ Intestinal obstruction signs OTHER INTERVENTIONS
ƒ Reduction by air/hydrostatic contrast
ŞîƥĚƑĿîŕĚŠĚŞîɚĚɍijɍƙîŕĿŠĚɈċîƑĿƭŞɛ
OTHER DIAGNOSTICS
ƒ May be felt during digital rectal examination
(children)

IRRITABLE BOWEL SYNDROME

(IBS)
osms.it/IBS
ƎƑĚDŽĿūƭƙijîƙƥƑūĚŠƥĚƑĿƥĿƙɈƙƥƑĚƙƙ
PATHOLOGY & CAUSES
ƒ Chronic functional gastrointestinal system SIGNS & SYMPTOMS
disorder; recurrent abdominal painɈ
impaired bowel motility ƒ Impaired bowel motility ĺ diarrhea/
Ɠ sūŞĿČƑūƙČūƎĿČɈŞîČƑūƙČūƎĿČ constipation
irregularities ƒ Recurrent abdominal pain
Ɠ Constipation/diarrhea Ɠ Bowel movement ĺ improvement
ƒ ŕūîƥĿŠijɈŠîƭƙĚîɈŞƭČƭƙĿŠƙƥūūŕ
CAUSES
ƒ ¡îƥĺūŕūijNjŠūƥČūŞƎŕĚƥĚŕNjƭŠēĚƑƙƥūūēɒŕĿŒĚŕNj
multifactorial DIAGNOSIS
Ɠ ×ĿƙČĚƑîŕĺNjƎĚƑƙĚŠƙĿƥĿDŽĿƥNjɇaltered stimuli
response OTHER DIAGNOSTICS
Ɠ GĚČîŕǷūƑîîŕƥĚƑîƥĿūŠƙɒċîČƥĚƑĿîŕ ƒ Based on predominant consistency of stool
overgrowth Ɠ 'ĿîƑƑĺĚîƎƑĚēūŞĿŠîŠƥɈČūŠƙƥĿƎîƥĿūŠ
Ɠ GūūēƙĚŠƙĿƥĿDŽĿƥNjɇ short-chain ƎƑĚēūŞĿŠîŠƥɈŞĿNJĚēƙƥūūŕƎîƥƥĚƑŠɈ
carbohydrates;Ĺwater in bowel ĺ ƭŠČŕîƙƙĿǶĚē
ƙŞūūƥĺŞƭƙČŕĚƙƎîƙŞɈēĿîƑƑĺĚîɒ ƒ Organic disease exclusion
ŞĚƥîċūŕĿǕĚēċNjċîČƥĚƑĿîĺ gas ĺ
ċŕūîƥĿŠijɈƙƎîƙŞɈƎîĿŠ “Rome IV” diagnostic criteria
Ɠ ¡ƙNjČĺūƙūČĿîŕĿŠǷƭĚŠČĚ ƒ ċēūŞĿŠîŕƎîĿŠʓūŠĚēîNjDžĚĚŒŕNjĿŠŕîƙƥ
ƥĺƑĚĚŞūŠƥĺƙɈîƙƙūČĿîƥĚēDžĿƥĺƥDžūɓŞūƑĚūIJ
Ɠ Genetic factor
following
Ɠ Defecation ĺ lessened pain
RISK FACTORS Ɠ Change in stool frequency
ƒ Biologically-femaleɚƑĚijĿūŠɠēĚƎĚŠēĚŠƥɛɈ Ɠ Change in stool consistency

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 OTHER INTERVENTIONS
TREATMENT ƒ Stress management
ƒ 'ĿĚƥŞūēĿǶČîƥĿūŠ
ƒ sūēĚǶŠĿƥĿDŽĚČƭƑĚ
Ɠ gūDžIJĚƑŞĚŠƥîċŕĚūŕĿijūɠɈēĿɠɈ
monosaccharides/polyols diet (low
MEDICATIONS FODMAPs diet)
ƒ Symptom-guided therapy Ɠ DŽūĿēijîƙɠƎƑūēƭČĿŠijIJūūēɚČîIJIJĚĿŠĚɈ
Ɠ 'ĿîƑƑĺĚîƎƑĚēūŞĿŠîŠƥɇ drugs (e.g. alcohol)
loperamide) Ɠ Probiotics
Ɠ ūŠƙƥĿƎîƥĿūŠƎƑĚēūŞĿŠîŠƥɇǶċĚƑ Ɠ Physical activity
ƙƭƎƎŕĚŞĚŠƥîƥĿūŠɈîēĚƐƭîƥĚǷƭĿēĿŠƥîŒĚɈ
osmotic laxatives
Ɠ ¬ƎîƙŞɈƎîĿŠɇantispasmodics

ISCHEMIC COLITIS
osms.it/ischemic-colitis
Ɠ Hypercoagulable states (e.g. factor V
PATHOLOGY & CAUSES Leiden)
Ɠ Biologically-female individuals
ƒ TŠǷîƥūƑNjɈĿƙČĺĚŞĿČČūŠēĿƥĿūŠɒ Ɠ TŞƎîĿƑĚēƎĚƑIJƭƙĿūŠɚĚɍijɍîūƑƥĿČƙƭƑijĚƑNjɈ
îIJIJĚČƥƙČūŕūŠɈŞūƙƥūIJƥĚŠƙƎŕĚŠĿČǷĚNJƭƑĚɈ ŞNjūČîƑēĿîŕĿŠIJîƑČƥĿūŠɈĺĚŞūēĿîŕNjƙĿƙɛ
rectosigmoid junction
Ɠ Vasculopathy
ƒ ¬ƭēēĚŠċŕūūēǷūDžĻĺĿŠƙƭIJǶČĿĚŠƥ
Ɠ Certain drugs (e.g. vasopressors)
ƎĚƑIJƭƙĿūŠɈūNJNjijĚŠɓŠƭƥƑĿĚŠƥēĚŕĿDŽĚƑNjƥū
bowel ĺ compromised cellular metabolism
ĺĿƙČĺĚŞĿîɈĿŠǷîƥĿūŠɈĿŠIJîƑČƥĿūŠɈ COMPLICATIONS
necrosis ĺ possible perforation ƒ HîŠijƑĚŠūƭƙċūDžĚŕɈƙƥƑĿČƥƭƑĚɈƎîŠČūŕĿƥĿƙɈ
ƒ 'îŞîijĚēɈijîŠijƑĚŠūƭƙŞƭČūƙîƎƑūŞūƥĚƙ ČūŕūŠĿČƎĚƑIJūƑîƥĿūŠɈƎĚƑĿƥūŠĿƥĿƙɈƙĚƎƙĿƙɈ
ǷƭĿēɓĚŕĚČƥƑūŕNjƥĚŕūƙƙĺēĚĺNjēƑîƥĿūŠɈƙĺūČŒɈ ƙĺūČŒɈŞĚƥîċūŕĿČîČĿēūƙĿƙɈŞƭŕƥĿƙNjƙƥĚŞ
metabolic acidosis ūƑijîŠIJîĿŕƭƑĚɈƑĚƎĚƑIJƭƙĿūŠĿŠŏƭƑNjɈƎūƥĚŠƥĿîŕŕNj
fatal
CAUSES
ƒ TƙČĺĚŞĿîČîƭƙĚƙŞîNjċĚūČČŕƭƙĿDŽĚɚĚŞċūŕĿČɈ SIGNS & SYMPTOMS
thrombotic)/nonocclusive (Ļ mesenteric
circulation ĺƙĚDŽĚƑĚĺNjƎūƥĚŠƙĿūŠɈ
ƒ Symptomatology may be self-limiting
vasospasm)
ƒ gūČîŕĿǕĚēîċēūŞĿŠîŕČƑîŞƎĿŠijɈƥĚŠēĚƑŠĚƙƙ
Ɠ ÀƙƭîŕŕNjîČƭƥĚɈŞîNjċĚČĺƑūŠĿČēĿƙūƑēĚƑ
(usually left side)
for marathon runners
ƒ gūūƙĚɈċŕūūēNjƙƥūūŕƙɈĺĚŞîƥūČĺĚǕĿî
ƒ Ļ bowel sounds
RISK FACTORS ƒ HƭîƑēĿŠijɈƑĚċūƭŠēƥĚŠēĚƑŠĚƙƙ
ƒ Any cause of Ļperfusion/mesenteric arterial
ƒ Fever
ĚŞċūŕĿƙŞɈƥĺƑūŞċūƙĿƙɓDŽîƙūČūŠƙƥƑĿČƥĿūŠ
ƒ qîNjēĚDŽĚŕūƎƙĺūČŒƙĿijŠƙɚĚɍijɍĺNjƎūƥĚŠƙĿūŠɛ
Ɠ ¤ĿƙŒĹ with age/comorbidities

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ƒ Stool culture
DIAGNOSIS ƒ TēĚŠƥĿǶĚƙĿŠIJĚČƥĿūƭƙĚƥĿūŕūijNj
DIAGNOSTIC IMAGING
X-ray/CT scan TREATMENT
ƒ ċēūŞĿŠîŕɒDŽĿƙƭîŕĿǕĚƙūċƙƥƑƭČƥĿūŠɈ
ƎĚƑIJūƑîƥĿūŠɈƎŠĚƭŞūŠĿƥĿƙ MEDICATIONS
Ɠ ¹ĺƭŞċƎƑĿŠƥĿŠijɇsegmented bowel ƒ Antibiotics
ĚēĚŞîɓƥĺĿČŒĚŠĿŠijƎîƥƥĚƑŠ Ɠ Perforation/infection
Ɠ 'ūƭċŕĚɠĺîŕūƎîƥƥĚƑŠɇŞƭČūƙîɈ
muscularis hyperdensity SURGERY
Ɠ ¡ŠĚƭŞîƥūƙĿƙČūŕĿɈƎŠĚƭŞūƎĚƑĿƥūŠĚƭŞ ƒ Bowel resection
indicates perforation Ɠ sĚČƑūƥĿČƥĿƙƙƭĚ
Colonoscopy
ƒ ×ĿƙƭîŕĿǕĚƙĿƙČĺĚŞĿîɇĚēĚŞîɈĚƑNjƥĺĚŞîɈ
friable mucosa
ƒ ¬ĿŠijŕĚɠƙƥƑĿƎĚƙĿijŠɇ linear ulcer seen along
longitudinal axis
ƒ ¬ƭċŞƭČūƙîŕĺĚŞūƑƑĺîijĚɇ bluish nodules
ƒ ĿūƎƙNjɇƥƑîŠƙŞƭƑîŕǶċƑūƙĿƙɈŞƭČūƙîŕ
atrophy

LAB RESULTS
ƒ gĚƭŒūČNjƥūƙĿƙɈƥĺƑūŞċūČNjƥūƎĚŠĿîɈĻ
hemoglobin
ƒ ĹƙĚƑƭŞŕîČƥîƥĚɈŕîČƥîƥĚēĚĺNjēƑūijĚŠîƙĚ Figure 34.10 The endoscopic appearance of
ɚg'OɛɈČƑĚîƥĿŠĚƎĺūƙƎĺūŒĿŠîƙĚɚ ¡eɛɈ the colon in a case of ischemic colitis. There is
amylase indicates tissue damage mucosal edema and patchy erythema.

OSMOSIS.ORG 277
 OTHER INTERVENTIONS
ƒ Circulatory support
Ɠ T×ǷƭĿēƙɈĚŕĚČƥƑūŕNjƥĚƙ
ƒ Supplemental oxygen
ƒ Bowel rest

Figure 34.11 Histological appearance of the

colon in an individual with ischemic colitis.
¹ĺĚƑĚĿƙŞƭČūƙîŕŠĚČƑūƙĿƙɈîƙĿijŠƥĺîƥƥĺĚ
condition is in its early stages at the time of
biopsy.

NECROTIZING ENTEROCOLITIS
(NEC)
osms.it/necrotizing-enterocolitis
RISK FACTORS
PATHOLOGY & CAUSES ƒ HĚƙƥîƥĿūŠîŕîijĚʒȄȃDžĚĚŒƙ
ƒ gūDžċĿƑƥĺDžĚĿijĺƥʒȃŒijɓȅɍȅȂŕċƙ
ƒ ¬ĚDŽĚƑĚĿŠƥĚƙƥĿŠîŕēĿƙūƑēĚƑɇĿŠǷîƥĿūŠɈ
ischemic necrosis ƒ Dysbiosis-contributing interventions
Ɠ ¹ĚƑŞĿŠîŕĿŕĚƭŞɈČūŕūŠɚŞūƙƥūIJƥĚŠ Ɠ ŠƥĿċĿūƥĿČƙɈîČĿēɠƑĚēƭČĿŠijîijĚŠƥƙɈ
affected) IJĚĚēĿŠijċūDŽĿŠĚŞĿŕŒIJūƑŞƭŕî
ƒ Multifactorial pathology ƒ OƭŞîŠŞĿŕŒƎƑūŞūƥĚƙČūŞŞĚŠƙîŕċîČƥĚƑĿî
ijƑūDžƥĺɈƙƭƎƎūƑƥƙŞƭČūƙîŕĿŠƥĚijƑĿƥNj
ƒ Preterm infants
ƒ TŠIJĚČƥĿūŠƙɈijîƙɠIJūƑŞĿŠijūƑijîŠĿƙŞƎƑĚƙĚŠČĚ
Ɠ Immature gastrointestinal tract
ČĺîƑîČƥĚƑĿǕĚēċNjĻ intercellular junction ƒ Underlying conditions
integrity + Ļ mucosal barrier ĺ Ɠ Term infants (e.g. fetal growth
triggering event ĺ normal intestinal ƑĚƙƥƑĿČƥĿūŠɈƎĚƑĿŠîƥîŕĺNjƎūNJĿîɈČūŠijĚŠĿƥîŕ
microbiome dysbiosis ĺĹ pathogenic ĺĚîƑƥēĿƙĚîƙĚɈijîƙƥƑūĿŠƥĚƙƥĿŠîŕēĿƙūƑēĚƑƙɈ
bacterial growth ĺ exaggerated sepsis)
immune system response ĺ release of
ĺūƙƥČNjƥūŒĿŠĚƙɈČĺĚŞūŒĿŠĚƙĺ tissue COMPLICATIONS
injury ĺ necrosis
ƒ Bowel perforationɈĿŕĚƭƙɈƙĚƎƥĿČƙĺūČŒɈ
ƒ Term infants ŞĚƥîċūŕĿČîČĿēūƙĿƙɈČūîijƭŕūƎîƥĺNjɈ
Ɠ Usually underlying condition adversely respiratory failure
affecting intestinal perfusion ƒ Surgical complications

278 OSMOSIS.ORG
 Chapter 34 Intestinal Diseases

Ɠ ¬ƥƑĿČƥƭƑĚƙɈƙĺūƑƥċūDžĚŕƙNjŠēƑūŞĚ OTHER DIAGNOSTICS

ƒ Ĺ impaired neurodevelopmental
Surgery
ēĚDŽĚŕūƎŞĚŠƥƑĿƙŒ
ƒ Through surgical/postmortem specimens
ƒ High mortality rate
Ɠ HƑūƙƙĚNJîŞĿŠîƥĿūŠɇgangrenous
ŠĚČƑūƙĿƙɈĺĚŞūƑƑĺîijĚɈƙƭċƙĚƑūƙîŕijîƙ
SIGNS & SYMPTOMS collection
Ɠ OĿƙƥūŕūijĿČîŕĚNJîŞĿŠîƥĿūŠɇĚēĚŞîɈ
ƒ Abrupt feeding tolerance change ĺĚŞūƑƑĺîijĚɈƥƑîŠƙŞƭƑîŕŠĚČƑūƙĿƙɈ
ƒ ċēūŞĿŠîŕēĿƙƥĚŠƙĿūŠɈƥĚŠēĚƑŠĚƙƙ ċîČƥĚƑĿîŕĿŠǶŕƥƑîƥĿūŠ
ƒ /ƑNjƥĺĚŞîɈČƑĚƎĿƥƭƙɈĿŠēƭƑîƥĿūŠŞîNjîŕƙūċĚ
present
TREATMENT
ƒ Ĺ gastric residuals
ƒ ×ūŞĿƥĿŠijɚūIJƥĚŠċĿŕĿūƭƙɛɈċĿŕĿūƭƙēƑîĿŠîijĚ MEDICATIONS
from enteral feeding tubes ƒ Empirical antimicrobial therapy
ƒ OĚŞîƥūČĺĚǕĿî
ƒ sūŠƙƎĚČĿǶČǶŠēĿŠijƙ
SURGERY
Ɠ ¹ĚŞƎĚƑîƥƭƑĚĿŠƙƥîċĿŕĿƥNjɈŕĚƥĺîƑijNjɈîƎŠĚî
ƒ /NJƎŕūƑîƥūƑNjŕîƎîƑūƥūŞNjɈċūDžĚŕƑĚƙĚČƥĿūŠ
ƒ Primary peritoneal drainage (PPD) ĺĻ
intra-abdominal pressure

OTHER INTERVENTIONS
ƒ Address complications (e.g. metabolic
correction/hematologic abnormalities)
ƒ Bowel rest with nasogastric intubation
decompression
ƒ Supplemental oxygen/mechanical
ventilation
ƒ Fluid replacement
ƒ Inotropic support
Figure 34.12HƑūƙƙƎîƥĺūŕūijNjūIJŠĚČƑūƥĿǕĿŠij ƒ ¹ūƥîŕƎîƑĚŠƥĚƑîŕŠƭƥƑĿƥĿūŠɚ¹¡sɛ
enterocolitis.

DIAGNOSIS
DIAGNOSTIC IMAGING
Abdominal radiography, ultrasound
ƒ ¡ŠĚƭŞîƥūƙĿƙĿŠƥĚƙƥĿŠîŕĿƙɈ
pneumoperitoneum/hepatobiliary gas

LAB RESULTS
ƒ ¡ūƙĿƥĿDŽĚċŕūūēČƭŕƥƭƑĚɈĻƎŕîƥĚŕĚƥƙɈĻ red
ċŕūūēČĚŕŕƙɈēĿƙƙĚŞĿŠîƥĚēĿŠƥƑîDŽîƙČƭŕîƑ
ČūîijƭŕūƎîƥĺNjĚDŽĿēĚŠČĚɈĹserum lactate

OSMOSIS.ORG 279
 SMALL BOWEL ISCHEMIA &
INFARCTION
osms.it/ischemia-and-infarction

ČîƑēĿūƎƭŕŞūŠîƑNjċNjƎîƙƙƙƭƑijĚƑNjɈ
PATHOLOGY & CAUSES hemodialysis ĺĻ intestinal perfusion)
ƒ Coagulative disorders
ƒ Serious small bowel condition; reduced
ƒ Atherosclerotic occlusive disease
ċŕūūēǷūDžɈƙƭċƙĚƐƭĚŠƥĿŠIJîƑČƥĿūŠɒe
mesenteric ischemia ƒ ONjƎūDŽūŕĚŞĿîɚĚɍijɍēĚĺNjēƑîƥĿūŠɈ
hemorrhage)
Ɠ ūŕŕîƥĚƑîŕČĿƑČƭŕîƥĿūŠŠĚƥDžūƑŒĺ
small bowel especially vulnerable to ƒ ūDžĚŕƙƥƑîŠijƭŕîƥĿūŠɚĚɍijɍDŽūŕDŽƭŕƭƙɈ
widespread ischemic injury incarcerated hernia)
Ɠ ONjƎūNJĿîɈƙƭċƙĚƐƭĚŠƥƑĚƎĚƑIJƭƙĿūŠĺ ƒ Vasoconstriction medications
tissue injury
ƒ ĻċŕūūēǷūDžŞîNjċĚîČƭƥĚɓČĺƑūŠĿČ COMPLICATIONS
Ɠ Acute: sudden Ļ small intestine ƒ TŕĚƭƙɈƙĺūČŒɈŞĚƥîċūŕĿČîČĿēūƙĿƙɈ
perfusion ŞƭŕƥĿƙNjƙƥĚŞūƑijîŠIJîĿŕƭƑĚɈĺĿijĺŞūƑƥîŕĿƥNj
Ɠ ĺƑūŠĿČɇepisodic Ļ digestion
perfusion (often related to mesenteric
atherosclerosis) SIGNS & SYMPTOMS
ƒ TŠƙƭIJǶČĿĚŠƥƎĚƑIJƭƙĿūŠɈūNJNjijĚŠɓŠƭƥƑĿĚŠƥ
delivery to bowel ĺ compromised cellular ƒ Severe abdominal pain (often postprandial);
metabolism ĺĿƙČĺĚŞĿîɈĿŠǷîƥĿūŠɈ ŠîƭƙĚîɈDŽūŞĿƥĿŠijɒēĿƙƥĚŠēĚēîċēūŞĚŠɒ
ƥƑîŠƙŞƭƑîŕĿŠIJîƑČƥĿūŠɈŠĚČƑūƙĿƙĺ bacterial ijƭîƑēĿŠijɈƑĚċūƭŠēƥĚŠēĚƑŠĚƙƙɚēĚDŽĚŕūƎƙ
transmigration + possible perforation later); Ļ bowel sounds; fever; feculent
ƒ 'îŞîijĚēɈijîŠijƑĚŠūƭƙŞƭČūƙîƎƑūŞūƥĚƙ breath odor; rectal bleeding; may exhibit
ǷƭĿēɓĚŕĚČƥƑūŕNjƥĚŕūƙƙĺēĚĺNjēƑîƥĿūŠɈƙĺūČŒɈ ƙĺūČŒƙĿijŠƙɚĚɍijɍĺNjƎūƥĚŠƙĿūŠɛ
metabolic acidosis
DIAGNOSIS
CAUSES
ƒ Ischemia causes DIAGNOSTIC IMAGING
Ɠ ~ČČŕƭƙĿDŽĚɚîƑƥĚƑĿîŕɓDŽĚŠūƭƙɛɇĚŞċūŕĿČɈ
ƥĺƑūŞċūƥĿČɈƥƭŞūƑɈDŽūŕDŽƭŕƭƙɈ CT/magnetic resonance (MR) angiography
ĿŠƥƭƙƙƭƙČĚƎƥĿūŠɈĺĚƑŠĿîɈîƥĺĚƑūƙČŕĚƑūƙĿƙ ƒ Detects acute mesenteric ischemia
Ɠ sūŠūČČŕƭƙĿDŽĚɇƙĚDŽĚƑĚĺNjƎūƥĚŠƙĿūŠɈ Abdominal X-ray/CT scan
vasospasm ĺĻ mesenteric circulation
ƒ 'ĿŕîƥĚēċūDžĚŕŕūūƎƙɈċūDžĚŕDžîŕŕƥĺĿČŒĚŠĿŠijɈ
ƥĺƭŞċƎƑĿŠƥĿŠijɈĿŠƥĚƙƥĿŠîŕƎŠĚƭŞîƥūƙĿƙɈIJƑĚĚ
RISK FACTORS intraperitoneal air
ƒ Any cause of Ļ perfusion/mesenteric arterial
ĚŞċūŕĿƙŞɈƥĺƑūŞċūƙĿƙɓDŽîƙūČūŠƙƥƑĿČƥĿūŠ LAB RESULTS
ƒ îƑēĿîČēĿƙūƑēĚƑƙɚĚɍijɍîƑƑĺNjƥĺŞĿîɈDŽîŕDŽƭŕîƑ ƒ gĚƭŒūČNjƥūƙĿƙDžĿƥĺŕĚIJƥƙĺĿIJƥɈĹ hematocrit
disease ĺ arterial emboli formation ɚēĚĺNjēƑîƥĿūŠɈĺĚŞūČūŠČĚŠƥƑîƥĿūŠɛ
from heart; ĻČîƑēĿîČūƭƥƎƭƥɈƎĚƑĿƎĺĚƑîŕ
ƒ ĹƙĚƑƭŞŕîČƥîƥĚɈîŞNjŕîƙĚɈîŕŒîŕĿŠĚ
hypoperfusion)
phosphatase
ƒ ¡ƑūČĚēƭƑĚƙɚĚɍijɍČîƑēĿîČČîƥĺĚƥĚƑĿǕîƥĿūŠɈ

280 OSMOSIS.ORG
 Chapter 34 Intestinal Diseases

OTHER DIAGNOSTICS SURGERY

ƒ Laparotomy ƒ Resection
Ɠ Abdominal exploration
OTHER INTERVENTIONS
TREATMENT ƒ Pain management
ƒ Bowel rest with decompression
MEDICATIONS
ƒ Antibiotics
ƒ Circulatory support
Ɠ T×ǷƭĿēƙɈĚŕĚČƥƑūŕNjƥĚƙɈĿŠūƥƑūƎĿČ
medications

VOLVULUS
osms.it/volvulus

PATHOLOGY & CAUSES SIGNS & SYMPTOMS

ƒ Intestinal obstruction ƒ ċēūŞĿŠîŕƥĚŠēĚƑŠĚƙƙɈƎîĿŠɈēĿƙƥĚŠƙĿūŠɈ
Ɠ Intestinal twisting/looping ċĿŕĿūƭƙDŽūŞĿƥĿŠijɈČūŠƙƥĿƎîƥĿūŠɈIJĚDŽĚƑɈ
îƭƙČƭŕƥîƥĿūŠɚîċŠūƑŞîŕċūDžĚŕƙūƭŠēƙɈ
ūIJƥĚŠēĚČƑĚîƙĚēɛɈƎĚƑČƭƙƙĿūŠɚƥNjŞƎîŠNjɛɈ
TYPES ĺĚŞîƥūČĺĚǕĿîɚŞîNjĿŠēĿČîƥĚċūDžĚŕ
ƒ ŕîƙƙĿǶĚēċNjŕūČîƥĿūŠ ĿƙČĺĚŞĿîɈŠĚČƑūƙĿƙɛ
Sigmoid volvulus (most common)
ƒ Usually middle-aged/elderly individuals DIAGNOSIS
ƒ îƭƙĚƙĿŠČŕƭēĚƎƑĚijŠîŠČNjɈČĺƑūŠĿČ
ČūŠƙƥĿƎîƥĿūŠɚĚɍijɍOĿƑƙČĺƙƎƑƭŠijɫƙēĿƙĚîƙĚɛɈ DIAGNOSTIC IMAGING
intestinal adhesions
X-ray
Cecal volvulus ƒ Asses volvulus shape
ƒ Causes include impaired abdominal Ɠ Bent inner tube sign (“coffee bean” sign)
ŞĚƙĚŠƥĚƑNjēĚDŽĚŕūƎŞĚŠƥɈƎƑĚijŠîŠČNjɈ
chronic constipation Barium enema
ƒ qîNjƙĺūDžɨċĿƑēɫƙċĚîŒɩƙĺîƎĚɚƎūĿŠƥūIJ
Midgut volvulus
twisted bowel)
ƒ Usually infants/young children
ƒ Perforation suspected ĺ barium contrast
ƒ Caused by anomalous intestinal contraindicated
development (e.g. intestinal malrotation)
CT scan
COMPLICATIONS ƒ Twisted mesentery (“whirlpool” sign)
ƒ Mesenteric artery compression ĺ intestinal
DžîŕŕĿƙČĺĚŞĿîɈinfarction
ƒ TŠƥĚƙƥĿŠîŕDžîŕŕƎĚƑIJūƑîƥĿūŠɈĿŠIJĚČƥĿūŠɚĚɍijɍ
diffuse peritonitis)

OSMOSIS.ORG 281
 TREATMENT
SURGERY
ƒ In case of midgut volvulus/ischemia/
necrosis; surgical resection if necessary

OTHER INTERVENTIONS
ƒ T×ǷƭĿēƑĚƎŕîČĚŞĚŠƥ
ƒ Bowel decompression
Ɠ ¬ĿijŞūĿēDŽūŕDŽƭŕƭƙɇsigmoidoscopy
Ɠ ĚČîŕDŽūŕDŽƭŕƭƙɇ colonoscopy

Figure 34.13 Abdominal radiograph

demonstrating a massively dilated sigmoid
colon in a case of sigmoid volvulus.

Figure 34.14 3D CT virtual colonoscopy

demonstrating sigmoid volvulus.

282 OSMOSIS.ORG
 NOTES

NOTES
LIVER & GALLBLADDER
CONGENITAL CONDITIONS

GENERALLY, WHAT ARE THEY?

PATHOLOGY & CAUSES DIAGNOSIS
ƒ Inherited metabolic/congenital structural DIAGNOSTIC IMAGING
anomalies, affect hepatobiliary system ĺ ƒ Ultrasound
hyperbilirubinemia ƒ Oral cholecystogram

COMPLICATIONS LAB RESULTS

ƒ Kernicterus ƒ Conjugated vs. unconjugated bilirubin, liver
ƒ Recurrent cholangitis, cirrhosis function tests
ƒ Portal hypertension ƒ Biopsy
ƒ Metabolic problems, impaired growth

TREATMENT
SIGNS & SYMPTOMS
ƒ See individual disorders
ƒ Jaundice, dark urine, light stools
ƒ Impaired liver function
ƒ Neurologic alterations

BILIARY ATRESIA
osms.it/biliary-atresia
TYPES
PATHOLOGY & CAUSES ƒ Biliary atresia only; not accompanied by
other anomalies (most common)
ƒ Congenital anomaly of extrahepatic duct
ƒ Biliary atresia + laterality malformations
ǶċƑūƙĿƙɈūċƙƥƑƭČƥĿūŠūIJċĿŕĚǷūDž
(left-right axis patterning/malpositioning of
ƒ Infections, environmental toxins, immune organs)
dysregulation, genetic mutations ĺ
Ɠ Dextrocardia, situs inversus, asplenia/
perinatal injury to biliary system
polysplenia, interrupted inferior vena
ƒ Bile prevented from entering duodenum cava
ĺ impaired fat digestion, absorption +
Ɠ Related CFC1 gene mutation
cholestasis, distension of gallbladder, ducts
ƒ Biliary atresia + intestinal atresia,
imperforate anus, kidney anomalies

OSMOSIS.ORG 283
 COMPLICATIONS
ƒ Liver cirrhosis, portal hypertension, hepatic
encephalopathy
ƒ Recurrent cholangitis, cirrhosis
ƒ Metabolic problems, impaired growth
(associated with malabsorption)

SIGNS & SYMPTOMS

ƒ Neonates asymptomatic at birth; stools
Figure 35.1 Intraoperative photography of
gradually become acholic, clay-colored
extra-hepatic biliary atresia. The underside of
ƒ Persistent jaundice the liver displays only connective tissue in the
Ɠ Skin gradually turns yellow, greenish- gallbladder fossa.
bronze
ƒ Dark urine
Ɠ Increased bilirubin concentration
TREATMENT
ƒ Portal hypertension
Ɠ Splenomegaly, ascites, enlarged MEDICATIONS
abdominal veins
ƒ Ursodeoxycholic acid (hydrophilic bile acid)
ƒ Impaired liver function ĺ decreased
coagulation factors, bleeding tendencies
Ɠ Impaired coagulation also related to SURGERY
decreased vitamin K absorption ƒ Type indicated by blood chemistry, imaging,
biopsy

DIAGNOSIS Intraoperative cholangiogram

ƒ HūŕēƙƥîŠēîƑēIJūƑČūŠǶƑŞĿŠijūċƙƥƑƭČƥĿūŠɈ
DIAGNOSTIC IMAGING diagnosis

Ultrasound Hepatoportoenterostomy (Kasai HPE)

ƒ Abnormal gallbladder size, shape, ƒ ¤ĚƙƥūƑĚƙċĿŕĚǷūDžIJƑūŞŕĿDŽĚƑɒŞîNjŠĚĚē
contractility; absent common bile duct; subsequent revision
“triangular cord” sign (triangle-shaped
Liver transplant
echogenic density above porta hepatis)
ƒ If Kasai procedure unsuccessful
Hepatobiliary scintigraphy
ƒ Decreased/absent patency of extrahepatic OTHER INTERVENTIONS
biliary tree
Diet
LAB RESULTS ƒ Fat-soluble vitamin supplements; high
protein diet, medium-chain triglyceride
ƒ Increased conjugated serum bilirubin,
supplements
aminotransferases

Liver biopsy
ƒ TēĚŠƥĿǶĚƙūċƙƥƑƭČƥĿūŠɠƑĚŕîƥĚēĺĿƙƥūŕūijĿČîŕ
changes

284 OSMOSIS.ORG
 Chapter 35 Liver & Gallbladder Congenital Conditions

CRIGLER–NAJJAR SYNDROME
osms.it/crigler-najjar-syndrome
COMPLICATIONS
PATHOLOGY & CAUSES ƒ Kernicterus (Type I), if not promptly
addressed
ƒ Rare inherited metabolic disorder;
nonhemolytic hyperbilirubinemia
ƒ Autosomal recessive inheritance pattern SIGNS & SYMPTOMS
ƒ AKA congenital nonhemolytic jaundice with
ijŕƭČƭƑūŠūƙNjŕƥƑîŠƙIJĚƑîƙĚēĚǶČĿĚŠČNj ƒ Persistent jaundiceĿŠǶƑƙƥIJĚDžēîNjƙūIJŕĿIJĚ
ƒ Neurological symptoms as kernicterus
TYPES develops

Type I
ƒ Severe jaundice, bilirubin encephalopathy, DIAGNOSIS
possible kernicterus-associated neurologic
impairment LAB RESULTS
Type II Unconjugated hyperbilirubinemia
ƒ Lower serum bilirubin concentration; no ƒ Type I: 20–50 mg/dL
neurologic impairment ƒ Type II: < 20 mg/dL

Stool color
CAUSES ƒ Type I: pale yellow, low fecal urobilinogen
ƒ Mutation in coding area of UGT gene, ɚƙĿijŠĿǶČîŠƥŕNjēĚČƑĚîƙĚēċĿŕĿƑƭċĿŠ
encodes for bilirubin-conjugating enzyme conjugation)
UGT1A1 (bilirubin-uridine diphosphate
ƒ Type II: normal
glucuronosyltransferase) ĺ structurally
abnormal enzyme ĺ decreased/absent Normal liver histology, liver function tests
conjugation of bilirubin

RISK FACTORS
ƒ Consanguinity

OSMOSIS.ORG 285
 OTHER INTERVENTIONS
TREATMENT
Phototherapy
MEDICATIONS ƒ TŠǶƑƙƥNjĚîƑƙūIJŕĿIJĚɒeffectiveness decreases
over time
Phenobarbital
ƒ Useful in Type II, induces residual UGT Exchange transfusion
activity
Plasmapheresis + albumin infusions
ƒ Removes bilirubin tightly bound to serum
SURGERY albumin
Liver transplant
ƒ 'ĚǶŠĿƥĿDŽĚƥƑĚîƥŞĚŠƥIJūƑ ƑĿijŕĚƑɠsîŏŏîƑ
syndrome Type I

DUBIN–JOHNSON SYNDROME
osms.it/dubin-johnson-syndrome

PATHOLOGY & CAUSES DIAGNOSIS

ƒ Inherited metabolic disorder; mild, DIAGNOSTIC IMAGING
ǷƭČƥƭîƥĿŠijĚŕĚDŽîƥĿūŠƙ in conjugated
(predominantly), unconjugated bilirubin, no Oral cholecystogram
evidence of hemolysis ƒ Gallbladder may not be visualized
ƒ Autosomal inheritance pattern
ƒ MRP2 (ABCC) gene mutation ĺ LAB RESULTS
impaired hepatic excretion of non-bile- ƒ Hyperbilirubinemia, normal liver function
salt organic anions, bilirubin into bile via tests
canalicular membrane ĺ cholestasis ĺ ƒ Total urinary coproporphyrin normal;
hyperbilirubinemia majority, coproporphyrin I

Liver biopsy, histological exam

SIGNS & SYMPTOMS ƒ Brown, black discoloration
Ɠ Pigment accumulates in lysosomes
ƒ Mild jaundice; evident during physiological
ƙƥƑĚƙƙɚĚɍijɍĿŕŕŠĚƙƙɛɓĺūƑŞūŠîŕǷƭČƥƭîƥĿūŠƙ
(e.g. pregnancy, oral contraceptives) TREATMENT
ƒ Constitutional
Ɠ Vague abdominal pains, weakness ƒ None required
ƒ Occasional hepatosplenomegaly

286 OSMOSIS.ORG
 Chapter 35 Liver & Gallbladder Congenital Conditions

GILBERT'S SYNDROME
osms.it/gilberts-syndrome

PATHOLOGY & CAUSES SIGNS & SYMPTOMS

ƒ Benign, inherited metabolic disorder; ƒ Asymptomatic between episodes, jaundice
recurring unconjugated hyperbilirubinemia, evident during physiological stress
jaundice ƒ Clinical manifestations
ƒ Autosomal recessive inheritance pattern Ɠ During adolescence, with effects of sex
ƒ AKA Meulengracht disease, familial steroids on bilirubin metabolism
nonhemolytic jaundice
ƒ Serum bilirubin increases during
physiologic stress (e.g. illness, dehydration, DIAGNOSIS
fasting, overexertion, menses)
ƒ Differs from other forms of non-hemolytic ƒ Exclude other causes of unconjugated
hyperbilirubinemia hyperbilirubinemia
Ɠ Genetic mutation in promoter region
of UGT gene ĺ structurally normal
enzyme ĺ impaired genetic expression
TREATMENT
of hepatic UGT with decreased activity
ĺ decreased conjugation of bilirubin ƒ None required

ROTOR SYNDROME
osms.it/rotor-syndrome

PATHOLOGY & CAUSES SIGNS & SYMPTOMS

ƒ Rare benign inherited disorder; ƒ Mild jaundice; during physiological
chronic conjugated, unconjugated ĺūƑŞūŠîŕǷƭČƥƭîƥĿūŠƙɚĚɍijɍƎƑĚijŠîŠČNjɈūƑîŕ
hyperbilirubinemia; no hemolysis contraceptive use)
ƒ SLCO1B1, SLCO1B3 gene mutations
(code for transporter proteins 1B1, 1B3
responsible for bilirubin re-uptake by DIAGNOSIS
hepatocytes) ĺ alters bilirubin re-uptake ĺ
increases bilirubin in plasma DIAGNOSTIC IMAGING
Oral cholecystogram
COMPLICATIONS ƒ sūƑŞîŕijîŕŕċŕîēēĚƑūƎîČĿǶČîƥĿūŠ
ƒ Impaired 1B1 activity ĺƙĿijŠĿǶČîŠƥēƑƭij
toxicities (e.g. statin-associated myopathy)
LAB RESULTS
ƒ Hyperbilirubinemia, normal liver function
tests

OSMOSIS.ORG 287
 ƒ Total urinary coproporphyrin markedly
increased; majority coproporphyrin I

Liver biopsy, histological exam

ƒ Normal

TREATMENT
ƒ None required

288 OSMOSIS.ORG
 NOTES

NOTES
LIVER DISEASES

GENERALLY, WHAT ARE THEY?

(e.g. increase in free calcium)
PATHOLOGY & CAUSES ƒ Decreased hepatic metabolism of
circulating estrogens ĺ hyperestrogenism
ƒ Diseases affecting hepatic parenchymal
Ɠ Spider nevi: vascular lesions, central
tissue or vasculature
arteriole surrounded by smaller vessels
ƒ Variable insults
Ɠ Palmar erythema
Ɠ Impairment in function of/destruction
Ɠ Gynecomastia
of liver parenchyma ĺĿŠǷîƥĿūŠĺ
scarring (cirrhosis) ĺ liver failure ƒ Fetor hepaticus (breath odor due to
ĿŠČƑĚîƙĚēēĿŞĚƥĺNjŕƙƭŕǶēĚŕĚDŽĚŕƙɛ
Ɠ ~ċƙƥƑƭČƥĿūŠūƑƑĚƙƥƑĿČƥĿūŠūIJċŕūūēǷūDž
through liver ĺ hypertension in portal ƒ Jaundice (cellular necrosis ĺ reduced
circuit producing secondary systemic hepatic ability to metabolize, excrete
effects bilirubin ĺ buildup of unconjugated
bilirubin in the blood)
Ɠ Diseases caused by anomalies in
absorbing, storing, converting or ƒ Decreased production of coagulation
ēĚƥūNJĿǶČîƥĿūŠĺ accumulation of factors ĺ easy bruising, bleeding
substances in the liver and other tissues ƒ Hepatic encephalopathy
causing damage Ɠ Ammonia, related nitrogenous
substances not cleared from blood ĺ
accumulate in brain ĺ impaired cerebral
SIGNS & SYMPTOMS function

ƒ Early stages generally asymptomatic

ƒ sūŠɠƙƎĚČĿǶČƙNjŞƎƥūŞƙ MNEMONIC: ABCDEFGHIJ
Ɠ ØĚĚƙƙɈDžĚĿijĺƥŕūƙƙɈIJîƥĿijƭĚ Common signs of liver
disease
Portal hypertension Asterixis, Ascites, Ankle
ƒ Abdominal distension (ascites) edema, Atrophy of testicles
ƒ Splenomegaly Bruising
ƒ Esophageal varices ĺƥƑūƭċŕĚƙDžîŕŕūDžĿŠijɈ Clubbing/ Color change of nails
hematemesis, dark stools (leukonychia)
ƒ Caput medusae Dupuytren’s contracture
Ɠ Dilated periumbilical collateral veins Encephalopathy / palmar
ƒ Cruveilhier–Baumgarten murmur Erythema
Ɠ Venous hum heard in epigastric region Fetor hepaticus
DžĿƥĺƙƥĚƥĺūƙČūƎĚ Gynecomastia
Liver cellular dysfunction Hepatomegaly
ƒ Decreased hepatic albumin production Increase size of parotids
Ɠ Decreased osmotic pressure ĺ edema Jaundice
Ɠ Increase in levels of free circulating
compounds normally bound to albumin

OSMOSIS.ORG 289
 Ɠ Neglect of personal appearance MNEMONIC: 3Cs & 3Cs
Ɠ Unresponsive, forgetful, trouble Hepatomegaly common
concentrating causes
Ɠ Changes in sleeping habits Cirrhosis
Ɠ Psychosis Carcinoma
Ɠ Asterixis (bilateral asynchronous Cardiac failure
ǷîƎƎĿŠijūIJūƭƥƙƥƑĚƥČĺĚƙɈēūƑƙĿǷĚNJĚē
hands) Hepatomegaly rare causes
ƒ Decreased metabolism of active Cholestasis
compounds ĺ increased sensitivity to Cysts
certain medications
CĚŕŕƭŕîƑĿŠǶŕƥƑîƥĿūŠ
ƒ Pruritus

anti-hepatitis B core IgM

DIAGNOSIS
Ɠ Hepatitis C: hepatitis C antibody,
DIAGNOSTIC IMAGING hepatitis C RNA
ƒ ¹ƙČîŠDžĿƥĺČūŠƥƑîƙƥɈq¤TɈƭŕƥƑîƙūƭŠēɈ Ɠ Hepatitis D & E: IgM, IgG antibodies
radionuclide imaging ƒ Autoimmune panel
Ɠ Rheumatoid factor (RF), anti-cyclic
citrullinated peptide antibody (CCP),
LAB RESULTS anti-nuclear antibody (ANA), anti-
ƒ Complete blood count (CBC) double stranded DNA (anti-dsDNA),
ƒ Liver function tests anti-extractable nuclear antigen (anti-
Ɠ Tests of synthetic function: serum ENA), antineutrophil cytoplasmic
albumin level, international normalized antibody (ANCA)
ratio (INR) ƒ Liver biopsy
Ɠ Hepatocellular enzymes: aspartate
transaminase (AST), alanine
transaminase (ALT), total bilirubin, direct TREATMENT
bilirubin
Ɠ Ductal enzymes: alkaline phosphatase ƒ TŠĿƥĿîŕŕNjēĿƙĚîƙĚɠƙƎĚČĿǶČɒƙĚĚĿŠēĿDŽĿēƭîŕ
(ALP), gamma glutamyl transpeptidase disorders
(GGT)
ƒ Hepatitis virus serology SURGERY
Ɠ Hepatitis A: anti-hepatitis A IgM, anti- ƒ Advanced disease ĺ liver transplant
hepatitis A IgG
Ɠ Hepatitis B: hepatitis B surface antigen,
anti-hepatitis B core/surface antibodies,

290 OSMOSIS.ORG
 Chapter 36 Liver Diseases

ALCOHOLIC LIVER DISEASE

osms.it/alcoholic-liver-disease
ƒ Large vacuoles coalesce ĺ fatty cysts ĺ
PATHOLOGY & CAUSES irreversible lesions
ƒ Macrovesicular steatosis most commonly
ƒ Abnormal lipid retention in hepatocytes
îƙƙūČĿîƥĚēDžĿƥĺalcohol, diabetes, obesity,
(steatosis) ĺ large triglyceride fat vacuoles
corticosteroids
accumulate in liver cells ĺ fatty liver
ƒ Severe fatty liver may be accompanied by
ƒ Fat content of liver exceeds 5–10% by
ĿŠǷîƥĿūŠɈƙƥĚîƥūƙĿƙ ĺ steatohepatitis
DžĚĿijĺƥ
Ɠ Steatohepatitis ĺ hepatocyte
ƒ Can be accompanied by progressive
ballooning, necrosis ĺ liver cell death,
ĿŠǷîƥĿūŠɚĺĚƎîƥĿƥĿƙɛĺ steatohepatitis
ĿŠǷîƥūƑNjƑĚƙƎūŠƙĚĺ hepatic
stellate cell activation ĺǶċƑūƙĿƙĺ
RISK FACTORS cirrhosis
ƒ Glycogen storage diseases, acute fatty liver
during pregnancy, malnutrition, obesity, COMPLICATIONS
HIV, hepatitis C
ƒ Hepatocellular carcinoma
Alcohol
ƒ Most common cause
SIGNS & SYMPTOMS
ƒ Chronic alcohol use ĺ production of toxic
metabolites (e.g. aldehydes)
ƒ Fatigue, malaise, dull right-upper-quadrant
Ɠ Damages mitochondria, cellular ƎîĿŠɈŞĿŕēŏîƭŠēĿČĚɚƑîƑĚɛɈƙĿijŠĿǶČîŠƥ
structures ĺ impaired cellular energy damageĺ hepatomegaly, ascites
mechanisms
Ɠ Alcohol metabolised to aldehyde hepatic
enzymes (reaction facilitates conversion DIAGNOSIS
of NAD+ ĺs'OɒŕūDžĚƑs'ʋ
concentration ĺ less fatty acid oxidation DIAGNOSTIC IMAGING
ĺ fatty acids accumulate ĺ steatosis)
Ultrasound
STAGING ƒ Steatosis ĺċƑĿijĺƥŕĿDŽĚƑDžĿƥĺĿŠČƑĚîƙĚē
echogenicity
ƒ Stages of intracytoplasmic accumulation of
triglycerides ĺ fatty change ƒ Fibrosis ĺ coarse echo pattern
ƒ Cirrhosis ĺ nodules ĺ irregular outline of
Initial stage liver surface
ƒ Hepatocytes contain small fat vacuoles
(liposomes) around nucleus (microvesicular CT scan
fatty change) ƒ gūDžĚƑēĚŠƙĿƥNjƥĺîŠƙƎŕĚĚŠūŠ ¹ƙČîŠ

Late stage MRI

ƒ Vacuoles enlarge ĺ nucleus pushed to ƒ Fat ĺċƑĿijĺƥūŠ¹ȂîŠē¹ȃɠDžĚĿijĺƥĚē
cell periphery ĺ signet ring appearance images
(macrovesicular fatty change)
ƒ ×ĚƙĿČŕĚƙDžĚŕŕɠēĚŕĿŠĚîƥĚēɈūƎƥĿČîŕŕNjĚŞƎƥNj LAB RESULTS
Ɠ Fats dissolve during tissue processing
Liver function tests
ƒ Serum aminotransferases normal/

OSMOSIS.ORG 291
 moderately elevated
Ɠ AST usually more elevated than ALT in
TREATMENT
alcoholic fatty liver disease
ƒ Hepatic steatosis reversible, non-
Ɠ GGT often elevated in alcoholic fatty progressive if underlying cause controlled
liver disease (e.g. cease alcohol use)
Secondary causes of steatosis
ƒ Hepatitis C virus antibodies
ƒ Hepatitis A IgG
ƒ Hepatitis B surface antigen, surface
antibody, core antibody
ƒ Plasma iron, ferritin, total iron-binding
capacity

Biopsy
ƒ Early changes
Ɠ Accumulation of membrane bound large
droplet steatosis (Large macrovesicular
drops ĺîŕČūĺūŕĿČƙƥĚîƥūƙĿƙɒƙŞîŕŕ
microvesicular droplets ĺ acute fatty Figure 36.1 A Mallory–Denk body is a feature
liver of pregnancy, tetracycline toxicity, of many liver pathologies including alcoholic
Reye’s syndrome) hepatitis and alcoholic cirrhosis.
Ɠ Proliferation of smooth endoplasmic
reticulum
Ɠ Gradual distortion of mitochondria
ƒ Steatohepatitis
Ɠ Presence of neutrophils ĺ alcoholic
steatohepatitis, unusual in chronic viral
hepatitis
Ɠ Mallory-Denk bodies (clusters of
intracellular cytoskeletal protein
aggregates)
ƒ Advanced changes
Ɠ Fibrosis: accumulation of scar tissue
or extracellular matrix, potentially
reversible if individual stops drinking Figure 36.2 Histological appearance of fatty
alcohol, not true cirrhosis characterized ŕĿDŽĚƑɍ¹ĺĚŠƭŞĚƑūƭƙDžĺĿƥĚƙƎîČĚƙƑĚƎƑĚƙĚŠƥ
by presence of regenerative nodules the accumulation of lipid.
(irreversible)

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 Chapter 36 Liver Diseases

AUTOIMMUNE HEPATITIS
osms.it/autoimmune-hepatitis

PATHOLOGY & CAUSES DIAGNOSIS

ƒ TŠǷîƥĿūŠūIJƥĺĚŕĿDŽĚƑƥĿƙƙƭĚcaused by LAB RESULTS
autoimmunity ƒ ĹĹALT, Ĺ AST, Ļalbumin, Ĺ prothrombin
time
TYPES ƒ Type 1
ƒ Type 1: 80% of cases Ɠ Antinuclear antibodies (ANAs),
ƒ Type 2: most common in young antibodies against smooth muscle
biologically-female individuals proteins, or (ASMAs)
ƒ Type 3: different antibodies but presents as ƒ Type 2
Type 1 Ɠ Antibodies to the microsomes of the
ƒ Type 4: no detectable antibodies liver or kidney (ALKM-1), liver cytosol
antigen (ALC-1)
ƒ Type 3
CAUSES Ɠ Soluble liver antigen positive
ƒ Combination of environmental triggers and
genetic predisposition
TREATMENT
RISK FACTORS
ƒ ÞūƭŠijċĿūŕūijĿČîŕŕNjɠIJĚŞîŕĚĿŠēĿDŽĿēƭîŕƙɒ MEDICATIONS
presence of HLA-DR3.DR4 Immunosuppressants
ƒ Corticosteroids, azathioprine
COMPLICATIONS
ƒ Acute liver failure, chronic liver failure, SURGERY
hepatocellular carcinoma, long term
immunosuppression can lead to Liver transplantation
malignancies ƒ If resistant to drug therapies

SIGNS & SYMPTOMS

ƒ Wide spectrum of presentation, from
asymptomatic to cirrhosis and liver failure
ƒ Common moderate symptoms
Ɠ Fever, jaundice, and
hepatosplenomegaly
ƒ Chronic disease symptoms
Ɠ Coagulation disturbance, impaired
immunity
ƒ ¹NjƎĚȃĿƙîƙƙūČĿîƥĚēDžĿƥĺūƥĺĚƑēĿƙĚîƙĚƙ
(Hashimoto’s thyroiditis, Grave’s disease)

OSMOSIS.ORG 293
 Figure 36.3 The histological appearance of
îƭƥūĿŞŞƭŠĚĺĚƎîƥĿƥĿƙɍ¹ĺĚƑĚĿƙîŠĿŠǶŕƥƑîƥĿūŠ
of lymphocytes and plasma cells at the
ĿŠƥĚƑIJîČĚċĚƥDžĚĚŠƥĺĚĺĚƎîƥĿČŕūċƭŕĚîŠēƥĺĚ
portal tract i.e. lymphoplasmacytic interface
hepatitis.

BUDD–CHIARI SYNDROME
osms.it/budd-chiari-syndrome
ƒ Trauma
PATHOLOGY & CAUSES ƒ Pregnancy
ƒ Contraceptive therapy
ƒ Congestive hepatic disease caused by
ūċƙƥƑƭČƥĿūŠūIJĺĚƎîƥĿČDŽĚŠūƭƙūƭƥǷūDž
ƒ Usually > one hepatic vein or hepatic COMPLICATIONS
section of vena cava ƒ Cirrhosis and liver failure
ƒ Venous congestion leads to ƒ Esophageal, gastric and rectal varices
Ɠ Ischemia and centrilobular necrosis ƒ Kidney dysfunction (hepatorenal syndrome)
Ɠ Increased pressure in portal system ĺ
portal hypertension
SIGNS & SYMPTOMS
CAUSES ƒ Can present acutely or chronically
ƒ Occlusion (primary)
ƒ Classic triad
Ɠ Thrombosis (most common)
Ɠ Hepatomegaly
ƒ Compression (secondary)
Ɠ Abdominal pain
Ɠ Tumor mass, granuloma
Ɠ Ascites
ƒ Jaundice
RISK FACTORS ƒ Fever
ƒ Myeloproliferative and hematologic ƒ Other signs and symptoms of portal
disorders (e.g. polycythemia vera) hypertension (e.g. splenomegaly,
ƒ Hypocoagulative disorders encephalopathy)
ƒ Tumors
ƒ Infections (e.g. tuberculosis)
ƒ TŠǷîƥūƑNjēĿƙĚîƙĚƙ

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 Chapter 36 Liver Diseases

DIAGNOSIS TREATMENT
DIAGNOSTIC IMAGING ƒ Treat the underlying cause

Doppler ultrasound
ƒ Thrombus MEDICATIONS
ƒ ŕƥĚƑîƥĿūŠūIJĺĚƎîƥĿČDŽĚŠūƭƙūƭƥǷūDž ƒ ÀƙƭîŕŕNjĿŠƙƭIJǶČĿĚŠƥ
ƒ ɪ¬ƎĿēĚƑDžĚċɫIJūƑŞîƥĿūŠîƑūƭŠēƥĺĚ ƒ Anticoagulants
obstruction duto collateral vessels ƒ Diuretics
proliferation

Venography
SURGERY
Liver transplantation
CT scan, MRI
ƒ In case of fulminant liver failure

LAB RESULTS Portosystemic shunt

ƒ Elevated aminotransferases ƒ 'ĿDŽĚƑƥƥĺĚǷūDžîDžîNjIJƑūŞƥĺĚūċƙƥƑƭČƥĿūŠ
ƒ Liver biopsy ƒ Transjugular intrahepatic portosystemic
shunt (TIPS)
ƒ Surgical shunt

OTHER INTERVENTIONS
Thrombolytic therapy
ƒ Dissolve clots
ƒ Balloon angioplasty

Figure 36.4 An abdominal CT scan in the

axial plane demonstrating hypoperfusion of
the right lobe of the liver secondary to Budd-
Chiari syndrome.

OSMOSIS.ORG 295
 CHOLESTATIC LIVER DISEASE
osms.it/cholestatic-liver-disease
malignancy (biliary tree/head of
PATHOLOGY & CAUSES ƎîŠČƑĚîƙɛɈƙƥƑĿČƥƭƑĚƙɈČNjƙƥĿČǶċƑūƙĿƙ
(impaired secretory function of biliary
ƒ Cholestasis: decrease in ċĿŕĚǷūDž through epithelium), primary sclerosing
bile ducts into duodenum cholangitis (immune system attacks
ƒ Hepatic retention, spillage into systemic bile ducts ĺĿŠǷîƥĿūŠɈƙČîƑƥĿƙƙƭĚɛɈ
circulation of cholesterol, bile salts ĺ ċĿŕĿîƑNjîƥƑĚƙĿîɚʓūŠĚŠĚDžċūƑŠĿŠIJîŠƥɫƙ
incorporation into biological membranes ċĿŕĚēƭČƥƙŠîƑƑūDžɓċŕūČŒĚēɓîċƙĚŠƥɛ
ĺîŕƥĚƑĚēŞĚŞċƑîŠĚǷƭĿēĿƥNjĺ injury to Ɠ Complications: prolonged obstruction
biological membranes, impaired function ĺċĿŕĿîƑNjČĿƑƑĺūƙĿƙɒƙƭċƥūƥîŕɓĿŠƥĚƑŞĿƥƥĚŠƥ
of membrane channels ĺbile secretion obstruction ĺ ascending cholangitis
impaired in liver (secondary bacterial infection of biliary
ƒ No bile reaches small intestine ĺ intestinal tree) ĺ sepsis, if untreated
malabsorption ĺŠƭƥƑĿƥĿūŠîŕēĚǶČĿĚŠČĿĚƙūIJ
fat soluble vitamins (A, D, E, K)
SIGNS & SYMPTOMS
CAUSES
ƒ Jaundice
Hepatocellular cholestasis Ɠ Individual components of bile enter
ƒ Impaired secretion of bile by hepatocytes serum (e.g. conjugated bilirubin)
Ɠ Intracellular accumulation of bile ƒ Pain
acids ĺ Ļ regulation of bile synthesis Ɠ Right upper quadrant (RUQ) pain,
ĺĻ total bile production/secretion radiates to right shoulder, minutes to
ĺ accumulation of bile components hours in duration (often after fatty meal)
(e.g. conjugated bilirubin) ĺ diffuse/ ƒ Pruritus
exocytose into interstitium ĺ diffuse
Ɠ Systemic accumulation of bile salts/
into blood
endogenous opioids/lysophosphatidic
Elevated levels of estrogen acid
ƒ ƑĚîŒēūDžŠūIJČĺūŕĚƙƥĚƑūŕ ĺcholic acid ƒ Skin xanthomas
(bile acid) Ɠ Focal accumulations of cholesterol
ƒ Ĺestrogen ĺ inhibition of export pump ĺ (common in obstructive jaundice)
estrogen-induced cholestasis ƒ Pale stools/dark urine
ƒ Risk factors Ɠ Absence of bile in gut ĺ conjugated
Ɠ Oral contraceptives (increase estrogen ċĿŕĿƑƭċĿŠɚDžîƥĚƑƙūŕƭċŕĚɛŠūƥĚNJČƑĚƥĚē
exposure), pregnancy (pregnancy- DžĿƥĺċĿŕĚɈĚNJČƑĚƥĚēDŽĿîŒĿēŠĚNjƙ
induced cholestasis), anabolic steroids
(similar in structure to estrogen)
ƒ Extrahepatic cholestasis
Ɠ ¡ĺNjƙĿČîŕūċƙƥƑƭČƥĿūŠċŕūČŒƙċĿŕĚǷūDž
Ɠ Ductal obstruction ĺ bile accumulates
in liver ĺĹ pressure in bile ducts ĺ bile
ŕĚîŒƙƥĺƑūƭijĺƥĿijĺƥŏƭŠČƥĿūŠƙċĚƥDžĚĚŠ
hepatocytes ĺ enters serum, interstitial
space
Ɠ Causes: cholelithiasis (gallstones),

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 Chapter 36 Liver Diseases

DIAGNOSIS TREATMENT
LAB RESULTS MEDICATIONS
ƒ ƙƙūČĿîƥĚēDŽĿƥîŞĿŠēĚǶČĿĚŠČNj
Liver function tests (LFTs)
Ɠ Fat-soluble vitamin supplementation
ƒ Elevated membrane-bound enzymes
ƒ Children
(sensitive to hepatocyte damage) ĺĹ
serum alkaline phosphatase (ALP), gamma- Ɠ Ursodeoxycholic acid ĺ increased bile
glutamyl transpeptidase (GGT) formation

Histology
SURGERY
ƒ Individual hepatocytes take on ċƑūDžŠĿƙĺɠ
ƒ Extrahepatic obstruction
green stippled appearance (due to
trapped bile), canalicular bile plugs form Ɠ Surgical correction of obstruction
ċĚƥDžĚĚŠĿŠēĿDŽĿēƭîŕĺĚƎîƥūČNjƥĚƙɓċĿŕĚēƭČƥƙ ɚĚɍijɍČĺūŕĚČNjƙƥĚČƥūŞNjɒĿIJijîŕŕƙƥūŠĚ
(excreted bile cannot travel further due to obstructing common bile duct, removal
obstruction) of gallbladder)
Ɠ ÀŠēĚƑƙƭIJǶČĿĚŠƥƎƑĚƙƙƭƑĚɈČîŠîŕĿČƭŕîƑ
plugs may rupture ĺ spillage of bile into OTHER INTERVENTIONS
surrounding tissue ĺ hepatic necrosis ƒ Pregnancy-induced cholestasis
Ɠ /îƑŕNjēĚŕĿDŽĚƑNjɚîƑūƭŠēDžĚĚŒȄȇūIJ
gestation)

CIRRHOSIS
osms.it/cirrhosis
ǶċƑūƥĿČŞîƥĚƑĿîŕĿŠĚNJƥƑîČĚŕŕƭŕîƑŞîƥƑĿNJ
PATHOLOGY & CAUSES ƒ Fibrotic cascade ĺIJūƑŞîƥĿūŠūIJǶċƑūƭƙ
septa ĺ separation of hepatocyte nodules
ƒ Hepatic parenchyma replaced by scar ĺ distortion of liver architecture ĺ
tissue ĺƙČîƑƥĿƙƙƭĚċŕūČŒƙƎūƑƥîŕǷūDžūIJ ēĚČƑĚîƙĚċŕūūēǷūDžƥĺƑūƭijĺūƭƥĺ splenic
blood through liver ĺ raised blood pressure congestion ĺ hypersplenism, splenic
and disturbance of function sequestration of platelets
ƒ Reversible phase ĺ hepatitis/fatty liver ƒ Injured liver cells group together ĺ
(steatosis) often precedes cirrhosis regenerative nodules (clumps of cells
ƒ Long term accumulation of liver damage ĺ ċĚƥDžĚĚŠǶċƑūƥĿČƥĿƙƙƭĚɈČūŕŕîijĚŠɛĺ bumpy
disruption of liver architecture ĺ functional cirrhotic liver
impairment
ƒ Develops over months to years
RISK FACTORS
ƒ Damage to parenchyma ĺ activation of
ƒ Chronic alcohol use, chronic hepatitis C
ƙƥĚŕŕîƥĚČĚŕŕƙɚƙĿƥċĚƥDžĚĚŠƙĿŠƭƙūĿēƙîŠē
infection, chronic hepatitis B (+/- hepatitis
hepatocytes in perisinusoidal space) ĺ
D) infection, autoimmune hepatitis,
secretion of
hereditary hemochromatosis, Wilson
Ɠ TGF-ȕ1 ĺƎƑūēƭČƥĿūŠūIJŞNjūǶċƑūċŕîƙƥƙ ēĿƙĚîƙĚɈîŕƎĺîȂɠîŠƥĿƥƑNjƎƙĿŠēĚǶČĿĚŠČNjɈ
ĺĿŠČƑĚîƙĚēǶċƑūƙĿƙɈƎƑūŕĿIJĚƑîƥĿūŠūIJ medications
connective tissue
Ɠ TIMP 1 & 2 (matrix metalloproteinase
inhibitors) ĺƎƑĚDŽĚŠƥƙċƑĚîŒēūDžŠūIJ

OSMOSIS.ORG 297
 COMPLICATIONS (ERCP) /magnetic resonance
ƒ Portal hypertension, hepatic cholangiopancreatography (MRCP))
encephalopathy, increased blood levels of
Diagnostic paracentesis
estrogens, hepatocellular carcinoma
ƒ 'ĚƥĚƑŞĿŠĚîƙČĿƥĿČǷƭĿēūƑĿijĿŠ
ƒ Portal hypertension
MNEMONIC: HEPATIC ƒ Suspected spontaneous bacterial peritonitis
Causes of Cirrhosis Ɠ Cell count, gram stain, culture
Hemochromatosis (primary) Ɠ Serum: ascites albumin gradient (SAAG)
EŠǕNjŞĚēĚǶČĿĚŠČNjɚîŕƎĺîɠȂɠ > 1.1 g/dL ĺ portal HTN
anti-trypsin)
Post hepatic (infection + drug LAB RESULTS
induced) ƒ AST, ALT moderately elevated, AST > ALT
Alcoholic ƒ ALP 2–3x normal
Tyrosinosis ƒ GGT very high in chronic alcoholic liver
Indigenous people in America disease
(galactosemia) ƒ ĿŕĿƑƭċĿŠĿŠČƑĚîƙĚƙîƙČĿƑƑĺūƙĿƙDžūƑƙĚŠƙ
Cardiac/ Cholestatic (biliary)/ ƒ Albumin decreases as synthetic function
Cancer/ Copper (Wilson’s) declines
ƒ Prothrombin time increases as synthetic
function declines
SIGNS & SYMPTOMS ƒ Hyponatremia from inability to excrete free
DžîƥĚƑɚĺĿijĺŕĚDŽĚŕƙūIJîŠƥĿēĿƭƑĚƥĿČĺūƑŞūŠĚɈ
ƒ Early stages generally asymptomatic aldosterone)
Ɠ Liver may be enlarged, shrinks as ƒ ¬ĚƑƭŞċĿūŞîƑŒĚƑƙČūƑƑĚŕîƥĚDžĿƥĺēĚijƑĚĚūIJ
cirrhosis progresses liver damage in variety of liver diseases
Ɠ sūŠɠƙƎĚČĿǶČƙNjŞƎƥūŞƙɇDžĚĚƙƙɈ ƒ A2-macroglobulin, haptoglobin,
DžĚĿijĺƥŕūƙƙɈIJîƥĿijƭĚ apolipoprotein A1, bilirubin, GGT, age,
ƒ Portal hypertension biological sex
ƒ Liver cellular dysfunction Histology
ƒ Nail changes (Muehrcke’s lines, Terry’s ƒ Macroscopic appearance
nails, clubbing)
Ɠ ¬ƭƑIJîČĚĿƑƑĚijƭŕîƑɈČūŠƙĿƙƥĚŠČNjǶƑŞ
ƒ Hypertrophic osteoarthropathy
Ɠ ÞĚŕŕūDžČūŕūƑɚĿŠƙƥĚîƥūƙĿƙɛ
ƒ Dupuytren’s contracture
Ɠ Nodular
ƒ Liver biopsy
DIAGNOSIS Ɠ Microscopic appearance of hepatocytes
ɚƑĚijĚŠĚƑîƥĿŠijŠūēƭŕĚƙɛîŠēǶċƑūƙĿƙɓ
DIAGNOSTIC IMAGING ČūŠŠĚČƥĿDŽĚƥĿƙƙƭĚēĚƎūƙĿƥƙċĚƥDžĚĚŠ
nodules
Ultrasound ƒ îƭƙĚƙƎĚČĿǶČîċŠūƑŞîŕĿƥĿĚƙ
ƒ Small nodular liver (advanced cirrhosis), Ɠ Chronic hepatitis B: ĿŠǶŕƥƑîƥĿūŠūIJŕĿDŽĚƑ
increased echogenicity, irregular- looking ƎîƑĚŠČĺNjŞîDžĿƥĺŕNjŞƎĺūČNjƥĚƙ
îƑĚîƙɈDžĿēĚŠĿŠijǶƙƙƭƑĚƙɈƙƎŕĚŠūŞĚijîŕNjɈ Ɠ Cardiac cirrhosis: erythrocytes, greater
ĿŞîijĿŠijūIJċŕūūēǷūDžĿŠƎūƑƥîŕDŽĚĿŠ îŞūƭŠƥūIJǶċƑūƙĿƙĿŠƥĿƙƙƭĚƙƭƑƑūƭŠēĿŠij
Endoscopy hepatic vein
ƒ Esophagogastroduodenoscopy (EGD) Ɠ Primary biliary cholangitis:ǶċƑūƙĿƙ
around bile duct, presence of
Ɠ Exclude esophageal varices
granulomas, pooling of bile
ƒ Imaging of bile ducts (endoscopic
Ɠ Alcoholic cirrhosis: neutrophilic
retrograde cholangiopancreatography
ĿŠǶŕƥƑîƥĿūŠ

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OTHER DIAGNOSTICS
Child-Pugh score
ƒ Grading of cirrhosis
Ɠ Class A (5–6 points): one year survival
ȂȁȁʣɈƥDžūNjĚîƑƙƭƑDŽĿDŽîŕȉȆʣ
Ɠ Class B (7–9 points): one year survival
ȉȂʣɈƥDžūNjĚîƑƙƭƑDŽĿDŽîŕȆȈʣ
Ɠ Class C (10–15 points): one year
ƙƭƑDŽĿDŽîŕȅȆʣɈƥDžūNjĚîƑƙƭƑDŽĿDŽîŕȄȆʣ

Figure 36.5 Gross pathology of micronodular

TREATMENT liver cirrhosis.
MEDICATIONS
ƒ Antiviral medication (e.g. interferon)
Ɠ For hepatitis B, C
ƒ Corticosteroids
Ɠ For autoimmune hepatitis
ƒ Diuretics, antibiotics, laxatives, enemas,
thiamine, steroids, acetylcysteine,
pentoxifylline
Ɠ For decompensation (compensated
cirrhosis—no jaundice, ascites, variceal
ċŕĚĚēĿŠijɈĺĚƎîƥĿČĚŠČĚƎĺîŕūƎîƥĺNjɒ
development of any of above ĺ
decompensated)
Figure 36.6 Histological appearance of liver
cirrhosis (trichrome stain). The blue highlights
OTHER INTERVENTIONS ƥĺĚċîŠēƙūIJǶċƑūƙĿƙċĚƥDžĚĚŠĿƙŕîŠēƙūIJ
ƒ Abstain from alcohol hepatocytes.
Ɠ For alcoholic hepatitis
ƒ Chelation therapy (e.g. penicillamine)
Ɠ For Wilson disease
ƒ Dissolve gallstones
Ɠ Blockage of bile ducts

OSMOSIS.ORG 299
 FITZ–HUGH–CURTIS SYNDROME
osms.it/fitz-hugh-curtis-syndrome
ƒ Causative organisms
PATHOLOGY & CAUSES Ɠ Commonly: Chlamydia trachomatis,
Neisseria gonorrhoeae, Mycobacterium
ƒ ¡ĚŕDŽĿČĿŠǷîƥūƑNjēĿƙĚîƙĚɚ¡T'ɛĺ tuberculosis (endemic areas)
ĿŠǷîƥĿūŠūIJŕūČîŕƙƥƑƭČƥƭƑĚƙĺ anterior
Ɠ Reported: Trichomonas vaginalis,
ŕĿDŽĚƑČîƎƙƭŕĚĿŠǷîƥĿūŠɚƎĚƑĿĺĚƎîƥĿƥĿƙɛ
Ureaplasma urealyticum, Mycoplasma
ĺƎîƥČĺNjƎƭƑƭŕĚŠƥɈǶċƑĿŠūƭƙĚNJƭēîƥĚĺ
hominis, Bacteroides spp., Gardnerella
adhesions form
vaginalis, E. coli and Streptococcus spp.

CAUSES
RISK FACTORS
ƒ /ƥĿūŕūijNjūIJĿŠǷîƥĿūŠƎūūƑŕNjƭŠēĚƑƙƥūūē
ƒ Biological females of reproductive age
ƒ Thinning of cervical mucus ĺ bacteria
colonizing vagina enters uterus, fallopian
tubes ĺĿŠIJĚČƥĿūŠɈĿŠǷîƥĿūŠĺ possibly SIGNS & SYMPTOMS
spreads via
Ɠ Direct intraperitoneal spread from initial ƒ Vomiting, nausea, hiccupping, headaches
ƎĚŕDŽĿČĿŠǷîƥĿūŠîŠēĿŠIJĚČƥĿūŠ
ƒ Acute onset right upper quadrant
Ɠ Bacterial seeding via lymphatic îċēūŞĿŠîŕƎîĿŠɒîijijƑîDŽîƥĚēċNjċƑĚîƥĺĿŠijɈ
bloodstream coughing, laughing (pleuritic pain), may
Ɠ Autoimmune response to PID refer to right shoulder, tenderness to

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palpation, tenderness to percussion of

overlying ribs TREATMENT
ƒ GĚDŽĚƑɈČĺĿŕŕƙɈŠĿijĺƥƙDžĚîƥƙɈŞîŕîĿƙĚɈDŽîijĿŠîŕ
ēĿƙČĺîƑijĚɈŕūDžĚƑîċēūŞĿŠîŕƎîĿŠɈČĚƑDŽĿČîŕ
MEDICATIONS
motion tenderness ƒ ~ƑijîŠĿƙŞɠƙƎĚČĿǶČîŠƥĿċĿūƥĿČƙ
ƒ Pain management
Ɠ Appropriate analgesia
DIAGNOSIS Ɠ Laparoscopy for lysis of adhesions for
refractory pain
ƒ OĿƙƥūƑNjūIJƎĚŕDŽĿČĿŠǷîƥūƑNjēĿƙĚîƙĚ

DIAGNOSTIC IMAGING
Abdominal ultrasound
ƒ Typically normal

Abdominal CT scan with contrast

ƒ Perihepatic
Ɠ Subtle enhancement of liver capsule,
ĿŠǷîƥūƑNjƙƥƑîŠēĿŠijîŠēǷƭĿēîŕūŠij
right paracolic gutter and perihepatic
ƑĚijĿūŠɈijîŕŕċŕîēēĚƑDžîŕŕƥĺĿČŒĚŠĿŠijɈ
ƎĚƑĿČĺūŕĚČNjƙƥĿČĿŠǷîƥūƑNjČĺîŠijĚ
ƒ Pelvic Figure 36.7ŕîƎîƑūƙČūƎĿČDŽĿĚDžūIJĿŠƥƑî
Ɠ Possible tubo-ovarian abscess abdominal adhesions caused by Fitz-Hugh-
Curtis syndrome.

LAB RESULTS
ƒ Liver function tests
Ɠ Typically normal
ƒ D-dimer
Ɠ Markedly raised
Ɠ Often ordered due to pleuritic chest pain
ƒ /ŠēūČĚƑDŽĿČîŕɓŕūDžDŽîijĿŠîŕƙDžîċ
Ɠ Culture causative organism

OTHER DIAGNOSTICS
Laparoscopy
ƒ “Violin string” adhesions of parietal
peritoneum to liver/diaphragm

OSMOSIS.ORG 301
 HEMOCHROMATOSIS
osms.it/hemochromatosis

PATHOLOGY & CAUSES SIGNS & SYMPTOMS

ƒ Excessive iron absorption in the intestine ĺ ƒ Initially asymptomatic
iron deposited in organs and tissues ĺ free Ɠ Biogically male: symptoms appear
radical generation ĺ cellular damage ĺ around age 50
cell death ĺ ƥĿƙƙƭĚǶċƑūƙĿƙ Ɠ Biologically female: eliminate iron
through menstrual bleeding ĺ
TYPES symptoms appear 10-20 years after
menopause
Primary (hereditary: autosomal recessive) ƒ Signs and symptoms of liver disease
ƒ Variety of possible mutations (C282Y ƒ Altered glucose homeostasis (hyper/
being the most common) in HFE gene on hypoglycemia)
ČĺƑūŞūƙūŞĚȇƑĚijƭŕîƥĿŠijĿƑūŠîċƙūƑƎƥĿūŠ ƒ Fatigue
from food ĺ most of the iron in the food
ƒ Arthralgia
is absorbed by enterocytes in the gut and
pass into the bloodstream ĺ iron overload ƒ Sexual dysfunction
ƒ Abdominal pain
Secondary (not genetic) ƒ Cardiac arrhythmias
ƒ Multiple blood transfusions ĺ erythrocytes
contain iron bound to the hemoglobin ĺ
ĺĚŞĚĿƙƑĚŕĚîƙĚēĿŠċŕūūēƙƥƑĚîŞDžĺĚŠ DIAGNOSIS
erythrocytes die after 120 days
ƒ Chronic hemolytic anemias LAB RESULTS
ƒ Excessive iron intake (very rare) ƒ High levels of serum iron
ƒ Elevated ferritin
COMPLICATIONS ƒ High transferrin saturation
ƒ Caused by deposition of iron in tissues ƒ Decreased total iron binding capacity
Ɠ Liver: cirrhosis, cancer
Liver biopsy
Ɠ Pancreas: altered endocrine and
ƒ TƑūŠČîŠċĚƙĚĚŠîƙċƑūDžŠƙƎūƥƙĿŠƙĿēĚ
exocrine function
hepatocytes ĺĿƥċĚČūŞĚƙċŕƭĚDžĿƥĺî
Ɠ Skin: bronze pigmentation Prussian blue stain
Ɠ Heart: cardiomyopathy, arrhythmias
Ɠ Gonads (related to impaired pituitary
OTHER DIAGNOSTICS
function): amenorrhea in biologically-
female individuals, testicular atrophy in ƒ Genetic analysis and screening of family
biologically-male individuals members
Ɠ Adrenal gland: ijŕîŠēĿŠƙƭIJǶČĿĚŠČNj
Ɠ Joints: degenerative joint disease

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 Chapter 36 Liver Diseases

TREATMENT
MEDICATIONS
Deferoxamine
ƒ Chelating agent binds iron molecules ĺ
deferoxamine excreted by kidneys ĺ urine
excretion ĺ decreases iron load

SURGERY
ƒ Advanced liver damage ĺ transplantation
Figure 36.8 Iron deposition (hemosiderosis)
in the liver parenchyma in a case
hemochromatosis. There is associated OTHER INTERVENTIONS
hepatocyte damage. ƒ Phlebotomy
ƒ Dietary changes to reduce iron absorption

Figure 36.9 Prussian blue stain on a liver

biopsy highlights iron deposits in a case of
hemochromatosis.

OSMOSIS.ORG 303
 HEPATITIS B
osms.it/hepatitis

PATHOLOGY & CAUSES DIAGNOSIS

ƒ Infection of the liver caused by hepatitis B LAB RESULTS
virus (HBV) ƒ HBV virions found in blood serum, proves
ƒ DNA virus from the hepadna group viral replication
ƒ Incubation is ȂɝȇŞūŠƥĺƙ, long term carrier ƒ ĹALT, ĹAST
state established after, transmitted through ƒ ĹCRP, ĹESR, ĹWBC
blood or semen ƒ OƙijɚƙƭƑIJîČĚîŠƥĿijĚŠɛɒƎƑĚƙĚŠƥĿŠîČƭƥĚ
ƒ Immune system attacks infected ĿŠIJĚČƥĿūŠƥĺĚŠČŕĚîƑĚēĿŠƑĚČūDŽĚƑNjɒĿIJƎƑĚƙĚŠƥ
hepatocytes over six months ĺČĺƑūŠĿČĿŠIJĚČƥĿūŠɒƭƙĚē
to create vaccine
RISK FACTORS ƒ ŠƥĿɠOČTijqɚČūƑĚîŠƥĿijĚŠɛɒƎƑĚƙĚŠƥĿŠ
ƒ Intravenous drug users, unprotected îČƥĿDŽĚĿŠIJĚČƥĿūŠIJūƑƙĿNJŞūŠƥĺƙɒĿIJƎƑĚƙĚŠƥ
ƙĚNJƭîŕĿŠƥĚƑČūƭƑƙĚɈċŕūūēƥƑîŠƙIJƭƙĿūŠƙɒ ŕūŠijĚƑĿŠēĿDŽĿēƭîŕĿƙČîƑƑĿĚƑɒƭƙĚēIJūƑ
hemodialysis screening because present most of the time
ƒ Anti-HBc IgG develop after IgM, lifelong
secretion indicates individual is immune
COMPLICATIONS ƒ Anti-HBe secreted core antigen, appears
ƒ Liver cirrhosis, hepatocellular carcinoma during viral replication, indicates active
infection
ƒ Bilirubin normal to increased
SIGNS & SYMPTOMS
ƒ General infection OTHER DIAGNOSTICS
Ɠ gūDžijƑîēĚIJĚDŽĚƑɈŞîŕîĿƙĚɈŕĚƥĺîƑijNjɈ ƒ ¡ĺNjƙĿČîŕĚNJîŞƙƙĺūDžƙĺĚƎîƥūŞĚijîŕNj
anorexia
ƒ Liver related
Ɠ Fatty stool, dark urine, jaundice,
TREATMENT
hepatomegaly, scleral icterus, pruritus,
right upper quadrant tenderness
MEDICATIONS
ƒ Interferon alpha, nucleoside reverse
transcriptase inhibitors (NRTI)
ƒ ¡ūƙƥĚNJƎūƙƭƑĚƎƑūƎĺNjŕîNJĿƙîDŽîĿŕîċŕĚDžĿƥĺ
HBV immunoglobulins
ƒ Vaccine available

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 Chapter 36 Liver Diseases

HEPATITIS C
osms.it/hepatitis

PATHOLOGY & CAUSES DIAGNOSIS

ƒ Viral hepatitis caused by hepatitis C virus LAB RESULTS
(HCV) ƒ Enzyme-linked immunosorbent assay
ƒ RNA virus from the class of ǷîDŽĿDŽĿƑĿēîĚ (ELISA) used to detect antibodies in
ƒ TŠČƭċîƥĿūŠĿƙȇɝȈDžĚĚŒƙ, lifelong infectious chronic cases, may be false negative in
carrier state immunosuppressed
ƒ Virus mutates often to bypass the host ƒ ¬ƎĚČĿǶČĺĚƎîƥĿƥĿƙ îŠƥĿijĚŠƙĿŞŞƭŠūîƙƙîNj
immune system ƒ O פsƥĚƙƥDžĿƥĺ¡ ¤
ƒ Minority of individuals develop acute ƒ ĹALT
hepatitis symptoms, due to this majority ƒ ĹCRP, ĹESR, ĹWBC
progress to chronic infection
OTHER DIAGNOSTICS
RISK FACTORS ƒ ¡ĺNjƙĿČîŕĚNJîŞƙĺūDžƙĚŠŕîƑijĚēŕĿDŽĚƑ
ƒ Intravenous drug use, sexual contact, from
mother to child in neonatal period (vertical
ƥƑîŠƙŞĿƙƙĿūŠɛɒČĺƑūŠĿČĺĚŞūēĿîŕNjƙĿƙ TREATMENT

COMPLICATIONS MEDICATIONS
ƒ Cirrhosis, hepatocellular carcinoma, renal ƒ Interferon alfa, ribavirin
dysfunction (HCV immune complexes ƒ ¬ČƑĚĚŠIJūƑO×ɈOT×îŠēO×ɒDŽîČČĿŠîƥĚ
involved in pathogenesis) against HBV and HAV if tests are negative
ƒ No HCV vaccine available

SIGNS & SYMPTOMS SURGERY

ƒ Liver transplant in case of liver failure
ƒ General infection
Ɠ gūDžijƑîēĚIJĚDŽĚƑɈŞîŕîĿƙĚɈŕĚƥĺîƑijNjɈ
anorexia
ƒ Liver related
Ɠ Fatty stool, dark urine (iron), jaundice,
hepatomegaly, icterus, pruritus

OSMOSIS.ORG 305
 HEPATITIS E
osms.it/hepatitis

PATHOLOGY & CAUSES DIAGNOSIS

ƒ Viral hepatitis caused by hepatitis E virus LAB RESULTS
(HEV) ƒ Anti - HEV IgM assay in acute infection,
ƒ RNA virus from the class hepeviridae PCR in chronic cases
ƒ Transmitted via fecal-oral route ƒ ĹALT
ƒ ĹCRP, ĹESR, ĹWBC
RISK FACTORS
ƒ ūŠƙƭŞĿŠijČūŠƥîŞĿŠîƥĚēIJūūēîŠēDžîƥĚƑ OTHER DIAGNOSTICS
in endemic areas, blood transfusions, from ƒ ¡ĺNjƙĿČîŕĚNJîŞƙĺūDžƙĚŠŕîƑijĚēŕĿDŽĚƑ
mother to child in neonatal period

COMPLICATIONS TREATMENT
ƒ Rare but if present then cholestatic
MEDICATIONS
hepatitis, chronic infection in
immunosuppressed individuals, liver failure, ƒ Ribavirin used in immunosuppressed
high mortality rate in pregnant individuals individuals

SURGERY
SIGNS & SYMPTOMS ƒ Liver transplant in case of liver failure

ƒ General infection
Ɠ gūDžijƑîēĚIJĚDŽĚƑɈŞîŕîĿƙĚɈŕĚƥĺîƑijNjɈ
anorexia
ƒ Liver related
Ɠ Fatty stool, dark urine (iron), jaundice,
hepatomegaly, icterus, pruritus
ƒ Other
Ɠ Diarrhea, arthralgia, urticarial rash

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HEPATOCELLULAR ADENOMA
osms.it/hepatocellular-adenoma

PATHOLOGY & CAUSES DIAGNOSIS

ƒ Rare, benign liver tumor DIAGNOSTIC IMAGING
ƒ Formed from hepatic epithelial cells, often ƒ ~IJƥĚŠĿŠČĿēĚŠƥîŕǶŠēĿŠijūŠîċēūŞĿŠîŕ
in healthy liver imaging
Ɠ Enlarged, nonfunctional epithelial cells
Ultrasound
Ɠ More glycogen, lipids than expected
ƒ ¬ūŕĿƥîƑNjDžĚŕŕɠēĚŞîƑČîƥĚēĺĚƥĚƑūijĚŠĚūƭƙ
Ɠ Surrounding tissue highly vascularized ŞîƙƙDžĿƥĺ variable echogenicity
Ɠ Bile ducts, portal triads absent
CT scan
CAUSES ƒ Well-marginated isoattenuating hepatic
lesionsɒIJîƥČūŠƥĚŠƥĺ hypoattenuation
ƒ /NJîČƥŞĚČĺîŠĿƙŞƙƭŠŒŠūDžŠɒîƙƙūČĿîƥĚē
DžĿƥĺĚƙƥƑūijĚŠɠċîƙĚēēƑƭijƙɇūƑîŕ
contraceptives, anabolic steroids LAB RESULTS
ƒ Genetic diseases
OĿƙƥūŕūijNjɚēĚǶŠĿƥĿDŽĚɛ
Ɠ Glycogen storage disease type I (von
ƒ Well-circumscribed nodules
Gierke’s disease): glucose cannot
be generated from glycogen via Ɠ ¬ĺĚĚƥƙūIJĺĚƎîƥūČNjƥĚƙDžĿƥĺċƭċċŕNj
gluconeogenesis vacuolated cytoplasm
ƒ Lack portal tracts/central veins
RISK FACTORS
ƒ Diabetes, metabolic syndrome, obesity TREATMENT

COMPLICATIONS SURGERY
ƒ ¤ƭƎƥƭƑĚɈċŕĚĚēĿŠijɒŞîŕĿijŠîŠƥ ƒ Surgical resection
transformation (rare)
OTHER INTERVENTIONS
ƒ Estrogen-associated
SIGNS & SYMPTOMS Ɠ Cessation of estrogen-based medication
ĺ adenoma regression
ƒ Usually asymptomatic
ƒ Von Gierke’s disease
ƒ Abdominal pain (esp. epigastric/RUQ),
Ɠ Strict dietary management ĺ adenoma
palpable mass
regression
ƒ If adenoma ruptures, bleeds
Ɠ Hypotension, tachycardia, diaphoresis

OSMOSIS.ORG 307
 Figure 36.10 Intraoperative photograph of
îŕîƑijĚɈDžĚŕŕɠČĿƑČƭŞƙČƑĿċĚēĺĚƎîƥūČĚŕŕƭŕîƑ
adenoma of the left lobe of the liver. There
is a rim of normal liver surrounding the
adenoma. The right lobe of the liver is just
visible to the left of the image.

NEONATAL HEPATITIS
osms.it/neonatal-hepatitis
COMPLICATIONS
PATHOLOGY & CAUSES ƒ If untreated > six months
Ɠ Chronic liver disease ĺ hepatic cirrhosis
ƒ TŠǷîƥĿūŠūIJŕĿDŽĚƑĿŠŠĚDžċūƑŠƙ (usually
ĺliver failure
1–2 months after birth)

CAUSES SIGNS & SYMPTOMS

ƒ Viruses (20%)
Ɠ Infect mother during pregnancy/baby ƒ Jaundice, pruritus, rashes, dark urine,
shortly after birth pale stools, hepatomegaly (due to liver
Ɠ ¤ƭċĚŕŕîɒCytomegalovirusɚ q×ɛɒ ĿŠǷîƥĿūŠɛ
hepatitis A,B,C ƒ 'ĚČƑĚîƙĚēĿŠƥĚƙƥĿŠîŕċĿŕĚǷūDžĺ impaired
ƒ Idiopathic (80%) fat digestion, vitamin absorption ĺ failure
ƥūijƑūDž
Ɠ ÀŠŒŠūDžŠūƑĿijĿŠ
Ɠ Viral
Ɠ Neonatal cholestasis DIAGNOSIS
Ɠ sĚDžċūƑŠċĿŕĚƎƑūēƭČƥĿūŠĿŞŞîƥƭƑĚĺĻ
bile production DIAGNOSTIC IMAGING
Ɠ Developing liver more sensitive to injury
ĺĻċĿŕĚƙNjŠƥĺĚƙĿƙɈǷūDž Ultrasound
ƒ Genetic ƒ Check bile ducts for obstruction, correct
development
Ɠ ŕƎĺîȂɠîŠƥĿƥƑNjƎƙĿŠēĚǶČĿĚŠČNjɇ
malformation ĺ cannot be transported
out of hepatocytes ĺ accumulation
DžĿƥĺĿŠČĚŕŕƙĺ cell death ĺ hepatitis

308 OSMOSIS.ORG
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LAB RESULTS
TREATMENT
Liver biopsy
ƒ Multinucleated giant cells MEDICATIONS
Ɠ Arise from combination of neighboring ƒ Ursodeoxycholic acid
cells (hepatocytes) Ɠ Increase bile formation
Ɠ Signs of cholestatic liver disease

Blood tests
SURGERY
ƒ Cirrhotic liver disease/liver failure requires
ƒ Ĺ serum bilirubin
liver transplant

OTHER INTERVENTIONS
ƒ Optimize nutrition/vitamin supplementation

NON-ALCOHOLIC FATTY LIVER

DISEASE
osms.it/non-alcoholic-fatty-liver

NAFL ĺ NASH
PATHOLOGY & CAUSES
ƒ Second hit hypothesis
ƒ Disease due to fat accumulation in liver, Ɠ Initial fatty change benign ĺ oxidative
îƙƙūČĿîƥĚēĿŠǷîƥĿūŠ stress, hormonal imbalances,
mitochondrial abnormalities ĺ
progression
TYPES ƒ Hepatocytic fat vulnerable to degradation
Non-alcoholic fatty liver (NAFL) Ɠ Unsaturated fatty acids:ʓūŠĚēūƭċŕĚ
bond, hydrogen atoms vulnerable to
ƒ ¬ƥĚîƥūƙĿƙDžĿƥĺūƭƥĿŠǷîƥĿūŠ
initiators (e.g. reactive oxygen species)
Non-alcoholic steatohepatitis (NASH) Ɠ Process damages cell lipid membranes
ƒ ¬ƥĚîƥūƙĿƙDžĿƥĺĺĚƎîƥĿČĿŠǷîƥĿūŠɈ ĺ mitochondrial dysfunction ĺ cell
indistinguishable from alcoholic death ĺĿŠǷîƥĿūŠĺ steatohepatitis
steatohepatitis (NASH)

Subtype
RISK FACTORS
ƒ gĿDŽĚƑƙƥĚîƥūƙĿƙDžĿƥĺūƭƥĚDŽĿēĚŠƥƙĚČūŠēîƑNj
ƒ NAFL ĺ NASH
cause (e.g. chronic alcohol use/persistent
viral infection) Ɠ Age > 50
Ɠ gĿDŽĚƑŕîƑijĚɈƙūIJƥɈNjĚŕŕūDžijƑĚîƙNj Ɠ qTʓȃȉŒijɓŞ2ɚȆɍȈŕċƙɓIJƥ2)
Ɠ Bloating, hepatocyte necrosis Ɠ Diabetes mellitus
Ɠ Mallory–Denk bodies Ɠ Elevated serum aminotransferases
Ɠ Damage attracts neutrophils ĺ more Ɠ Ballooning degeneration, Mallory–Denk
ĿŠǷîƥĿūŠ ċūēĿĚƙūƑǶċƑūƙĿƙūŠċĿūƎƙNj
Ɠ TŠǷîƥĿūŠĺ hepatic stellate cells ƒ NAFL (general)
activate ĺǶċƑūƙĿƙĺ cirrhosis Ɠ Insulin resistance, metabolic syndrome,
Ɠ ʓ¹ĺƑĚĚūIJɇobesity, hypertension,

OSMOSIS.ORG 309
 diabetes, hypertriglyceridemia, Liver biopsy
hyperlipidemia, excessive soft drink ƒ > 5% fat content ĺ NAFL
consumption (high concentration of ƒ Iron deposits
fructose), diet rich in saturated fats,
ƒ NAFL
medications (corticosteroids)
Ɠ Steatosis alone
Ɠ ¬ƥĚîƥūƙĿƙDžĿƥĺŕūċƭŕîƑɓƎūƑƥîŕ
COMPLICATIONS ĿŠǷîƥĿūŠDžĿƥĺūƭƥĺĚƎîƥūČNjƥĚ
ƒ Liver cirrhosis, hepatocellular carcinoma ballooning
Ɠ ¬ƥĚîƥūƙĿƙDžĿƥĺĺĚƎîƥūČNjƥĚċîŕŕūūŠĿŠij
ċƭƥDžĿƥĺūƭƥĿŠǷîƥĿūŠ
SIGNS & SYMPTOMS ƒ NASH
ƒ Usually asymptomatic Ɠ Hepatocyte ballooning degeneration,
ĺĚƎîƥĿČŕūċƭŕîƑĿŠǷîƥĿūŠɈ
ƒ Fatigue, malaise, dull right upper quadrant
apoptotic bodies, mild chronic portal
ƎîĿŠɈŞĿŕēŏîƭŠēĿČĚɚƑîƑĚɛɈƙĿijŠĿǶČîŠƥŕĿDŽĚƑ
ĿŠǷîƥĿūŠɈƎĚƑĿƙĿŠƭƙūĿēîŕČūŕŕîijĚŠ
damage ĺ hepatomegaly, ascites
deposition ĺ zone 3 accentuation
ɚČĺĿČŒĚŠDžĿƑĚƎîƥƥĚƑŠɛɈƎūƑƥîŕǶċƑūƙĿƙ
DžĿƥĺūƭƥƎĚƑĿƙĿŠƭƙūĿēîŕūƑƎĚƑĿČĚŕŕƭŕîƑ
DIAGNOSIS ǶċƑūƙĿƙɈČĿƑƑĺūƙĿƙɚŞîČƑūŠūēƭŕîƑ
or mixed), Mallory–Denk bodies,
ƒ ¹NjƎĿČîŕŕNjēĿîijŠūƙĚēîƙĿŠČĿēĚŠƥîŕǶŠēĿŠijūŠ megamitochondria, vacuolated nuclei in
liver function panel periportal hepatocytes

DIAGNOSTIC IMAGING OTHER DIAGNOSTICS

ƒ TēĚŠƥĿIJNjIJîƥƥNjĿŠǶŕƥƑîƥĚƙ ƒ Alcohol consumption > 25 ml/day pure
Ultrasound ethanol excludes diagnosis
ƒ Increased echogenicity ĺ bright appearing
liver ĺēĿIJIJƭƙĚIJîƥƥNjĿŠǶŕƥƑîƥĿūŠ TREATMENT
CT scan
ƒ Decreased hepatic attenuation
OTHER INTERVENTIONS
Dietary changes
MRI
ƒ Avoid high fructose-corn syrup, trans-fats
ƒ Increased fat signal
ƒ Omega 3 fatty acid supplementation ĺ
improvement in liver fat deposition
LAB RESULTS ƒ Coffee and olive oil consumption may be
ƒ Destruction of hepatocytes ĺ increase in protective
liver enzymes AST/ALT
ƒ Serum ALT > AST level = NAFL Treat insulin resistance
ƒ Weight-loss
ƒ Insulin sensitizers

Treat hyperlipidemia
ƒ Statins

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PORTAL HYPERTENSION
osms.it/portal-hypertension

PATHOLOGY & CAUSES SIGNS & SYMPTOMS

ƒ Elevation of blood pressure in the portal ƒ GI bleeding (secondary to esophagogastric
venous system above 5mmHg varices) ĺ most life-threatening
complication
CAUSES Ɠ Hematemesis
Ɠ Melena
Prehepatic causes ƒ Jaundice
ƒ Portal vein obstruction (e.g. thrombosis) ƒ Ascites
Intrahepatic causes ƒ Periumbilical caput medusae
ƒ Cirrhosis (most common of all causes) ƒ Signs and symptoms of encephalopathy
ƒ Schistosomiasis Ɠ Altered level of consciousness
ƒ Sarcoidosis Ɠ Lethargy
Ɠ OîŠēƥƑĚŞūƑDžĺĚŠƥĺĚDžƑĿƙƥĿƙĚNJƥĚŠēĚē
Posthepatic causes (aka asterixis)
ƒ Right-sided heart failure Ɠ Seizure, coma and death
ƒ Constrictive pericarditis
ƒ Budd–Chiari syndrome
DIAGNOSIS
COMPLICATIONS DIAGNOSITC IMAGING
ƒ Portosystemic shunts and development of
collateral channels Liver ultrasound
Ɠ Esophageal varices ƒ Nodules in case of cirrhosis
Ɠ Hemorrhoids CT scan, MRI
Ɠ Caput medusae (distension of ƒ Ascites
îċēūŞĿŠîŕDžîŕŕDŽĚĿŠƙɛ
ƒ Cirrhosis
ƒ Increased hydrostatic pressure and
ƒ Splenomegaly
hypoalbuminemia ĺ ascites
ƒ Vascular alteration such as inferior vena
ƒ Splenomegaly (blood drainage backs up to
cava dilatation
spleen due to high pressure portal system)
ĺ sequestration of blood elements ĺ
anemia, thrombocytopenia, leukopenia LAB RESULTS
ƒ gĿDŽĚƑēĿƙĚîƙĚîŠēċŕūūēƙĺƭŠƥĿŠijîDžîNj ƒ Full blood count
from liver ĺēĚČƑĚîƙĚēċŕūūēēĚƥūNJĿǶČîƥĿūŠ ƒ Liver enzymes and serology
ĺ increased ammonia in the blood ĺ ƒ Perform emergent upper GI endoscopy, to
encephalopathy diagnose/treat varices
ƒ Spontaneous bacterial peritonitis

OSMOSIS.ORG 311
 OTHER DIAGNOSTICS
TREATMENT
Diagnostic paracentesis
ƒ Will determine if ascites is due to portal ƒ Prevent and treat the complications
HTN or other etiology
ƒ Serum ascites albumin gradient (SAAG) > MEDICATIONS
1.1 mg/dL ƒ Beta-blockers
Ɠ Portal HTN is likely Ɠ ĺ decrease portal venous pressure
ƒ IV octreotide
Ɠ If bleeding, non-selective beta blockers
(prophylaxis), antibiotics (prophylaxis for
spontaneous bacterial peritonitis)
Ɠ For esophageal varices
ƒ Diuretics and sodium restriction
Ɠ For ascites

SURGERY
ƒ Transjugular intrahepatic portosystemic
shunt
Ɠ ūŞŞƭŠĿČîƥĿūŠċĚƥDžĚĚŠƎūƑƥîŕDŽĚĿŠ
and hepatic vein ĺ blood bypasses the
liver circulation ĺ reduced intrahepatic
pressure
ƒ Balloon tamponade, sclerotherapy, variceal
ligation/banding
Figure 36.11 Ascites as a consequence of
Ɠ For esophageal varices
portal hypertension caused by cirrhosis of
the liver.

MNEMONIC: ABCDE
Features of Portal
hypertension
Ascites
Bleeding (haematemesis, piles)
Caput medusae
Diminished liver
Enlarged spleen

Figure 36.12îƑĿƭŞƙDžîŕŕūDžēĚŞūŠƙƥƑîƥĿŠij
esophageal varices.

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 Chapter 36 Liver Diseases

Figure 36.13 Endoscopic appearance of

esophageal varices.

PRIMARY BILIARY CIRRHOSIS

osms.it/primary-biliary-cirrhosis
COMPLICATIONS
PATHOLOGY & CAUSES ƒ Osteoporosis, hyperlipidemia, fat soluble
DŽĿƥîŞĿŠēĚǶČĿĚŠČĿĚƙ
ƒ Autoimmune disease of liver ĺ progressive
destruction of cells lining small intrahepatic
bile ducts ĺ leakage of bile, toxins into SIGNS & SYMPTOMS
liver parenchyma, blood ĺĿŠǷîƥĿūŠɈ
ǶċƑūƙĿƙĺ cirrhosis
ƒ Fatigue, pruritus, jaundice, right upper
ƒ AKA primary biliary cholangitis quadrant pain
ƒ Loss of bone density ĺ fractures
CAUSES ƒ Hypercholesterolemia ĺ xanthelasma,
ƒ Failure of immune tolerance against xanthoma
mitochondrial pyruvate dehydrogenase ƒ Liver cirrhosis ĺ ascites, splenomegaly,
complex (PDC-E2), other hepatic proteins esophageal varices, hepatic
ĺ destruction of cells lining bile ducts ĺ encephalopathy
autoimmunity

RISK FACTORS DIAGNOSIS

ƒ Biological female, family history of disease,
DIAGNOSTIC IMAGING
extrahepatic autoimmune disease
Ɠ ¡ƑĚDŽĿūƭƙĿŠIJĚČƥĿūŠDžĿƥĺĚŠDŽĿƑūŠŞĚŠƥîŕ Abdominal ultrasound/MRCP/CT scan
gram-negative Novosphingobium ƒ Rule out bile duct obstruction
aromaticivorans ĺ cross-reaction
ċĚƥDžĚĚŠċîČƥĚƑĿîŕîŠƥĿijĚŠƙɈĺĚƎîƥĿČ
mitochondrial proteins LAB RESULTS
ƒ Antimitochondrial antibodies (most
individuals)

OSMOSIS.ORG 313
 ƒ Other autoantibodies may be present
Ɠ Antinuclear antibody, anti-
TREATMENT
ijŕNjČūƎƑūƥĚĿŠɠȃȂȁîŠƥĿċūēĿĚƙɈîŠƥĿɠƎȇȃ
antibodies (suggests more severe
MEDICATIONS
disease ĺ liver failure), anticentromere ƒ Ursodeoxycholic acid
îŠƥĿċūēĿĚƙɚČūƑƑĚŕîƥĚƙDžĿƥĺēĚDŽĚŕūƎĿŠij Ɠ Reduces intestinal absorption of
ƎūƑƥîŕĺNjƎĚƑƥĚŠƙĿūŠɛɈîŠƥĿɠŠƎȇȃîŠē cholesterol ĺ reduces cholestasis,
anti-sp100 improves liver function tests
ƒ Elevated IgM, total cholesterol, HDL, GGT, ƒ Cholestyramine
ALP (released from damaged bile ducts), Ɠ Bile acid sequestrant ĺ reduces bile
bilirubin = advanced disease acid absorption in gut ĺ relieves itching
due to bile acids in circulation
Liver biopsy (percutaneous/laparoscopic)
ƒ qūēîǶŠĿŕ
ƒ Interlobular bile duct destruction, bile duct
Ɠ For fatigue
ĿŠǷîƥĿūŠɚĿŠƥƑîĚƎĿƥĺĚŕĿîŕŕNjŞƎĺūČNjƥĚƙɛɈ
periductal epithelioid granulomas
OTHER INTERVENTIONS
ƒ Cease all alcohol intake

Figure 36.14 The histological appearance

of primary biliary cirrhosis. The bile duct
is surrounded by epithelioid macrophages
DžĺĿČĺĿŠƥƭƑŠîƑĚƙƭƑƑūƭŠēĚēċNjîƑĿŞūIJ
lymphocytes, indicative of granulomatous
ĿŠǷîƥĿūŠɍ

WILSON'S DISEASE
osms.it/wilsons-disease
ƒ Reduced copper elimination in the bile
PATHOLOGY & CAUSES ƒ Copper accumulation in hepatocytes ĺ free
radical generation ĺ hepatocyte damage
ƒ Autosomal recessive mutation in ATP7B ĺ spilling of free copper into the blood
gene ĺēĚIJĚČƥĿŠ¹¡ȈƥƑîŠƙƎūƑƥƎƑūƥĚĿŠ ĺ copper accumulation in organs and
action in the hepatocyte tissues ĺ free radical generation ĺ tissues
ƒ AKA hepatolenticular degeneration damage
ƒ Reduced copper incorporation into
apoceruloplasmin and reduction of its
copper-bound form (ceruloplasmin)

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COMPLICATIONS
ƒ Liver: cirrhosis, liver failure
DIAGNOSIS
ƒ Brain: movement disorders, dementia, and LAB RESULTS
psychiatric issues
ƒ Signs of liver dysfunction (e.g. high liver
ƒ Kidney: renal disease enzymes)
ƒ Eye: Kayser–Fleischer’s ring,ƙƭŠǷūDžĚƑ ƒ gūDžƙĚƑƭŞČĚƑƭŕūƎŕîƙŞĿŠ
cataract
ƒ High 24-hour copper excretion
ƒ Blood: hemolytic anemia

TREATMENT
SIGNS & SYMPTOMS
MEDICATIONS
ƒ Presents at a young age (< 30 years old)
ƒ Chelating agents ĺ make it easier to
ƒ Signs and symptoms of cirrhosis and portal excrete copper
hypertension (e.g. hepatosplenomegaly,
Ɠ Penicillamine (penicillin metabolite
jaundice, ascites, esophageal varices)
DžĿƥĺūƭƥîŠƥĿċĿūƥĿČƎƑūƎĚƑƥĿĚƙɛ
ƒ Signs of renal dysfunction
Ɠ Trientine hydrochloride
ƒ Parkinsonian-like movement disorders
ƒ Agents that block intestinal absorption of
Ɠ Tremors copper
Ɠ Rigidity Ɠ Ammonium tetrathiomolybdate
ƒ Psychiatric illness Ɠ Zinc
Ɠ Depression
Ɠ Personality changes
SURGERY
Ɠ Psychosis
ƒ Advanced liver damage ĺ transplantation
Ɠ Cognitive dysfunctions
ƒ Kayser–Fleischer ring
Ɠ Ring of copper deposition in the cornea
OTHER INTERVENTIONS
(Descemet’s membrane) ƒ Eliminate copper-rich food (e.g.
ŞƭƙĺƑūūŞƙɈŠƭƥƙɈƙĺĚŕŕǶƙĺɛ
Ɠ Appears to encircle the iris

Figure 36.15 Copper deposition in

Descemet’s membrane of the sclera results in
a Kayser–Fleischer ring.

OSMOSIS.ORG 315
 NOTES

NOTES
LOWER GASTROINTESTINAL
CONGENITAL MALFORMATIONS

GENERALLY, WHAT ARE THEY?

PATHOLOGY & CAUSES DIAGNOSIS
ƒ Lower gastrointestinal tract structural/ DIAGNOSTIC IMAGING
functional anomalies during embryonic ƒ Prenatal ultrasound, MRI, CT scan/
development; present at birth radiography
ƒ Malformations from duodenum to anus ƒ Avoid X-ray due to teratogenicity

CAUSES
TREATMENT
ƒ Genetic, environmental factors
SURGERY
ƒ See individual disorders
SIGNS & SYMPTOMS
ƒ At birth: may be asymptomatic
ƒ Malformations: relatively benign (nausea,
DŽūŞĿƥĿŠijɈēĿIJǶČƭŕƥNjƎîƙƙĿŠijƙƥūūŕɛƥūŕĿIJĚ
incompatibility

GASTROSCHISIS
osms.it/gastroschisis
CAUSES
PATHOLOGY & CAUSES ƒ Genetic, environmental factors
ƒ Extrasomatic protrusion of intestines
through hole in abdominal wall near RISK FACTORS
umbilicus ƒ Mother’s young age
ƒ Hernia: affected organs exit cavity ƒ Exposure to teratogenic substances
ƒ Week 4 of gestation: lateral folds fail to ɚîŕČūĺūŕɈƥūċîČČūɛ
fuse ĺ hole in abdominal wall ĺ organs
protrude COMPLICATIONS
ƒ Most common on right side ƒ TŠƥĚƙƥĿŠîŕĿŠǷîƥĿūŠēƭĚƥūĿŠƥƑîƭƥĚƑĿŠĚ
ƒ Usually small intestine ĚNJƎūƙƭƑĚƥūĿūƥĿČǷƭĿēɈŞîŕîċƙūƑƎƥĿūŠɈ
ƒ ¬ƥūŞîČĺɈŕĿDŽĚƑŞîNjîŕƙūƎƑūƥƑƭēĚɚƑîƑĚɛ infarction of intestinal tube due to
compressed blood vessels, infection

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 Chapter 37 Lower Gastrointestinal Congenital Malformations

SIGNS & SYMPTOMS

ƒ During fetal life: asymptomatic
ƒ At birth: ēĿIJǶČƭŕƥNjIJĚĚēĿŠijɓƎîƙƙĿŠijƙƥūūŕ

DIAGNOSIS
DIAGNOSTIC IMAGING
Intrauterine ultrasound, MRI

X-ray, CT scan
ƒ Post-op evaluation

LAB RESULTS
ƒ Increased maternal serum alpha-
IJĚƥūƎƑūƥĚĿŠɚq¬G¡ɛ Figure 37.1 An abdominal X-ray of a newborn
with gastroschisis. The abdominal contents
OTHER DIAGNOSTICS are clearly visible outside the abdominal wall.
ƒ Defect visible at birth

TREATMENT
ƒ Fatal if untreated

MEDICATIONS
ƒ Antibiotics for existing/potential infection
ƒ T×ǷƭĿēɓŠƭƥƑĿĚŠƥƙ

SURGERY
ƒ Surgical repositioning of organs back into
abdominal cavity, closure of abdominal wall
defect
ƒ Usually requires multiple surgeries

OSMOSIS.ORG 317
 HIRSCHSPRUNG'S DISEASE
osms.it/hirschsprungs-disease

PATHOLOGY & CAUSES DIAGNOSIS

ƒ qNjĚŠƥĚƑĿČɚƭĚƑċîČĺɛɈƙƭċŞƭČūƙîŕ DIAGNOSTIC IMAGING
ɚqĚĿƙƙŠĚƑɛƎŕĚNJƭƙĚƙîċƙĚŠƥ from intestinal ƒ Barium assisted radiography
wall in distal bowel
ƒ AKA congenital aganglionic megacolon
LAB RESULTS
ƒ ċƙĚŠƥƎŕĚNJƭƙĚƙɚƑĚijƭŕîƥĚċūDžĚŕIJƭŠČƥĿūŠɛ
ƒ Rectal suction biopsy
ĺ intestine muscles permanently
constricted ĺƎîƙƙĿŠijƙƥūūŕēĿIJǶČƭŕƥɈ
impossible OTHER DIAGNOSTICS
ƒ Digital rectal exam
CAUSES
ƒ Failure of neuroblasts to migrate from
neural crest to intestine, form plexuses
TREATMENT
ƒ Genetic: RET proto-oncogene, EDNRB, etc. SURGERY
ƒ RET proto-oncogene: sporadic/autosomal ƒ Surgical resection of intestine, subsequent
ēūŞĿŠîŠƥɚIJîŞĿŕĿîŕɛČîƙĚƙɒ associated with fusion of remaining healthy tissue (pull-
Down syndrome ƥĺƑūƭijĺƥĚČĺŠĿƐƭĚɛ
ƒ Isolated: sporadic/autosomal dominant
ƒ Present within syndrome: Down syndrome,
multiple endocrine neoplasia II, etc.

COMPLICATIONS
ƒ Constipation/obstipation, malnutrition,
enterocolitis, intestinal perforation,
megacolon

SIGNS & SYMPTOMS

ƒ At birth: asymptomatic
ƒ Can be diagnosed in adulthood
ƒ First sign: baby’s inability to pass Figure 37.2 Immunohistochemical
meconium, 48 hours postpartum staining for acetylcholinesterase in the
ƒ Vomiting, abdominal distension, colics colon of an individual with Hirschprung’s
disease. Ganglia are absent resulting in
overstimulation of nerves and increased
levels of acetylcholinesterase.

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 Chapter 37 Lower Gastrointestinal Congenital Malformations

IMPERFORATE ANUS
osms.it/imperforate-anus

PATHOLOGY & CAUSES DIAGNOSIS

ƒ Narrowed anal opening ɚîŠîŕƙƥĚŠūƙĿƙɛɓ DIAGNOSTIC IMAGING
complete atresia
MRI, ultrasound, X-ray/CT scan
ƒ AKA anal atresia
ƒ Determine internal extent of defect, plan
ƒ Anus completely closed ĺ colon ends in
corrective surgery
blind pouch in pelvis/opens into other pelvic
ƙƥƑƭČƥƭƑĚƙɚċŕîēēĚƑɈDŽîijĿŠîɛDŽĿîǶƙƥƭŕîĚ
ƒ All pelvic structures open into same OTHER DIAGNOSTICS
channel ĺ persistent cloaca ƒ Physical exam at birth, defect visible
ƒ Nerve, muscle tissue of missing parts of
anus, rectum missing/malformed
TREATMENT
CAUSES SURGERY
ƒ Mostly unknown genetic cause ƒ Anoplasty if possible, colostomy if not
ƒ HLXB9 gene: only when imperforate anus
is present within Currarino syndrome

COMPLICATIONS
ƒ Megacolon, intestinal rupture, septic shock,
incontinence/constipation (even after
ƙƭƑijĚƑNjɛ

MNEMONIC: VACTERL
Group of malformations with
common, unknown cause
Vertebral anomalies
Anal atresia
Cardiovascular anomalies
TƑîČĺĚūĚƙūƎĺîijĚîŕǶƙƥƭŕî
Esophageal atresia
Renal anomalies
Figure 37.3 A lateral X-ray of a neonate
Limb defects
demonstrating an imperforate anus. The
rectum is dilated and the anal canal is absent.

SIGNS & SYMPTOMS

ƒ ūŠƙƥĿƎîƥĿūŠɚĿIJîŠƭƙŠîƑƑūDžĚēɛɈūċƙƥĿƎîƥĿūŠ
ɚĿIJîŠƭƙŠūŠɠĚNJĿƙƥĚŠƥɛ
ƒ Vomiting, abdominal distension

OSMOSIS.ORG 319
 INTESTINAL ATRESIA
osms.it/intestinal-atresia
CAUSES
PATHOLOGY & CAUSES ƒ Duodenal intestinal atresia
Ɠ Strongly associated with trisomy 21
ƒ Congenital malformation resulting in closed/
ɚ'ūDžŠƙNjŠēƑūŞĚɛ
absent part of small/large intestine
ƒ Non-duodenal intestinal atresias
ƒ Different from intestinal stenosis; in
stenosis the passageway exists, and is just Ɠ Intrauterine ischemic injury (small part
narrowed of duodenum, entire jejunum, ileum,
colon receive vascularization from
ƙƭƎĚƑĿūƑŞĚƙĚŠƥĚƑĿČîƑƥĚƑNjɛ
TYPES
ƒ Named according to affected portion of
intestine: duodenal, jejunal, ileal, colonic
COMPLICATIONS
ƒ Distension of stomach and duodenum
ƒ Divided into duodenal/non-duodenal
ČîƭƙĚēċNjîČČƭŞƭŕîƥĚēĿūƥĿČǷƭĿē
intestinal atresia due to different
which has nowhere to go
mechanism of origin
ƒ Polyhydramnios (accumulation of amniotic
ƒ Duodenal intestinal atresia is caused by
ǷƭĿēĿŠĿūƥĿČƙîČɛ
failure in duodenal vacuolization
Ɠ GĚƥƭƙƙDžîŕŕūDžƙŕĚƙƙǷƭĿēēƭĚƥū
Ɠ During fetal development duodenal
intestinal obstruction ĺŞūƑĚǷƭĿē
epithelium proliferates rapidly ĺ
accumulates in amniotic sac
complete duodenal obstruction
ɚeƙūŕĿēƎĺîƙĚūIJDŽîČƭūŕĿǕîƥĿūŠɛĺ ƒ Intestinal perforation and
apoptosis of excess cells ĺformation pneumoperitoneum/meconium peritonitis
of small vacuoles which fuse ĺre-
establish duodenal passageway (AKA
ƑĚČîŠîŕĿǕîƥĿūŠƎĺîƙĚɛ SIGNS & SYMPTOMS
ƒ Bilious vomiting, abdominal pain,
malnutrition

320 OSMOSIS.ORG
 Chapter 37 Lower Gastrointestinal Congenital Malformations

DIAGNOSIS
DIAGNOSTIC IMAGING
Prenatal ultrasound
ƒ To assess signs of obstruction; detectable
in the third trimester
Ɠ Duodenal atresia:ēĿŕîƥĚēǷƭĿēɠǶŕŕĚē
stomach adjacent to dilated duodenum
Ɠ Non-duodenal intestinal atresia: Dilated
ǷƭĿēɠǶŕŕĚēċūDžĚŕŕūūƎƙ
Ɠ Polyhydramnios

Postnatal X-ray
ƒ Duodenal atresia: Double bubble sign
(dilated stomach adjacent to dilated
ēƭūēĚŠƭŞɛ Figure 37.5 A plain abdominal radiograph of
ƒ Non-duodenal intestinal atresia: dilated a neonate demonstrating the double bubble
ċūDžĚŕŕūūƎƙDžĿƥĺîĿƑɠǷƭĿēŕĚDŽĚŕƙƎƑūNJĿŞîŕƥū sign of duodenal atresia.
the obstruction

OTHER DIAGNOSTICS
ƒ Physical examination
Ɠ ƎƎŕĚƎĚĚŕɚƙƎĿƑîŕɛƙĺîƎĚūIJĿŠƥĚƙƥĿŠĚƙ
upon visual examination during surgery
ƒ Amniocentesis to determine possible
trisomy 21

TREATMENT
SURGERY
ƒ Gastric decompression: ƑĚŞūDŽîŕūIJǷƭĿē
from stomach
ƒ T×ǷƭĿēČūŞƎĚŠƙîƥĿūŠ
ƒ Surgical reattachment of functional portions
of intestines
Ɠ In case of duodenal intestinal atresia ĺ
duodenoduodenostomy

Figure 37.4 A plain abdominal radiograph of

a neonate demonstrating the triple bubble
sign of jejunal atresia.

OSMOSIS.ORG 321
 INTESTINAL MALROTATION
osms.it/intestinal-malrotation

PATHOLOGY & CAUSES DIAGNOSIS

ƒ Improper rotation of midgut during DIAGNOSTIC IMAGING
embryogenesis
MRI/CT scan/barium-assisted radiography
ƒ Rapid midgut growth in restricted space ĺ
herniation into umbilical coelum ĺ rotation ƒ Detect improper organ position
270° around SMA ĺĚƑƑūƑūČČƭƑƙʏǶŠîŕ
anatomy description
Ɠ Small intestine lodges into left TREATMENT
abdominal cavity ĺ cecum in lower
ƑĿijĺƥƐƭîēƑîŠƥɈǶƑƙƥƥDžūƥĺĿƑēƙūIJČūŕūŠ SURGERY
lodge into right side over small intestine ƒ Surgical repositioning of intestines,
ƒ Due to error, several organs in incorrect resection of Ladd’s bands to remove
anatomical position duodenal obstruction
Ɠ Small intestine in right side ƒ Preventive appendectomy
Ɠ Coecum in epigastrium
Ɠ Appendix follows coecum
Ɠ Ladd’s bands span over vertical
duodenum, compressing from outside
Ɠ Suspensory muscle of duodenum
further right
Ɠ Mesentery of small intestine narrower
root

COMPLICATIONS
ƒ Omphalocele, volvulus (part of intestine
rotates around itself/part of mesenterium
ĺ blocks passage of intestinal content ĺ
compresses blood vessels ĺ obstructs
ċŕūūēǷūDžɛɈĿŕĚƭƙɈĿƙČĺĚŞĿČċūDžĚŕɈ
malnutrition, hernias

SIGNS & SYMPTOMS

Figure 37.6 An abdominal X-ray with bowel
ƒ May be asymptomatic
contrast demonstrating intestinal malrotation.
ƒ Colic, bilous regurgitation, abdominal The entire small bowel is situated on the right
distension side of the abdomen.

322 OSMOSIS.ORG
 Chapter 37 Lower Gastrointestinal Congenital Malformations

MECKEL'S DIVERTICULUM
osms.it/meckels-diverticulum

PATHOLOGY & CAUSES DIAGNOSIS

ƒ Abnormal pouch on antimesenteric side of DIAGNOSTIC IMAGING
ileum
Abdominal ultrasound/CT scan
ƒ True diverticulum (contains all three layers
ūIJĿŠƥĚƙƥĿŠîŕDžîŕŕɛ ƒ TŠČĿēĚŠƥîŕǶŠēĿŠij
ƒ Early fetal life: nutrients received from yolk Angiography
sac into ileum via omphalomesenteric duct
ƭŠƥĿŕĿƥūċŕĿƥĚƑîƥĚƙɚDžĚĚŒȆɝȇūIJƎƑĚijŠîŠČNjɛ
ƒ If omphalomesenteric duct obliterates OTHER DIAGNOSTICS
improperly: Meckel’s diverticulum Meckel’s scan
ƒ May contain ectopic epithelia, ƒ In children; technetium-99m procedure,
omphalomesenteric duct lined with detects gastric mucosa in diverticulum
pluripotent cells
Surgery
COMPLICATIONS ƒ TŠČĿēĚŠƥîŕǶŠēĿŠij
ƒ Diverticulitis, ulcers from HCl secretion
if gastric mucosa present, perforation of
diverticulum, food impaction, lithiasis,
TREATMENT
peritonitis, peritoneal adhesions,
intussusception, volvulus, neoplasms SURGERY
ƒ Uncomplicated: resection of diverticulum
ƒ Complicated: resection of diverticulum,
MNEMONIC intestine
Meckel's Rule of 2s
Symptomatic presentation
before 2 years of age
2% of population
Approximately 2 feet from
ileocecal valve
2 inches in length
2 types of ectopic mucosa
ɚƎîŠČƑĚîƥĿČɈijîƙƥƑĿČɛ

SIGNS & SYMPTOMS

ƒ Usually asymptomatic
ƒ Abdominal pain/distension, melena,
vomiting, constipation
Figure 37.7 Intraoperative photograph of a
Meckel’s diverticulum.

OSMOSIS.ORG 323
 Figure 37.8 A CT scan in the axial plane
demonstrating a Meckel’s diverticulum.

Figure 37.9 Histological appearance of a Meckel’s diverticulum containing ectopic gastric

mucosa.

324 OSMOSIS.ORG
 Chapter 37 Lower Gastrointestinal Congenital Malformations

OMPHALOCELE
osms.it/omphalocele

PATHOLOGY & CAUSES DIAGNOSIS

ƒ Persistent, pathological, herniation of DIAGNOSTIC IMAGING
intestines into umbilical cord
Intrauterine ultrasound
ƒ Midgut herniates through umbilicus ĺ pulls
layer of peritoneum into umbilical cord in MRI
ūƑēĚƑƥūƎƑūƎĚƑŕNjēĚDŽĚŕūƎɚijƑūDžɈƑūƥîƥĚɛēƭĚ
ƥūĿŠƙƭIJǶČĿĚŠƥƙƎîČĚĿŠîċēūŞĿŠîŕČîDŽĿƥNjĺ
returns into abdomen LAB RESULTS
ƒ Midgut doesn’t return: omphalocele ƒ Blood test for MSAFP
ƒ High mortality rate ƒ Amniocentesis

CAUSES TREATMENT
ƒ Genetic, environmental factors
ƒ Associated with: trisomy 13 (Patau SURGERY
ƙNjŠēƑūŞĚɛɈƥƑĿƙūŞNjȂȉɚEdward’s ƒ Surgical repositioning of protruding organs
ƙNjŠēƑūŞĚɛɈƥƑĿƙūŞNjȃȂɚ'ūDžŠƙNjŠēƑūŞĚɛɈ
Beckwith–Wiedemann syndrome

RISK FACTORS
ƒ Consumption of alcohol/tobacco during
ƎƑĚijŠîŠČNjɈČĚƑƥîĿŠŞĚēĿČîƥĿūŠƙɚ¬¬¤TƙɛɈ
obesity

COMPLICATIONS
ƒ Abdominal cavity malformation, volvulus,
ischemic bowel

SIGNS & SYMPTOMS

ƒ Intrauterine: asymptomatic
ƒ At birth: visible defect
Figure 37.10 An MRI scan in the sagittal plane
demonstrating a large omphalocele. The
abdominal organs are clearly visible outside
the abdominal wall.

OSMOSIS.ORG 325
326 OSMOSIS.ORG
 NOTES

NOTES
MALABSORPTION CONDITIONS

GENERALLY, WHAT ARE THEY?

PATHOLOGY & CAUSES DIAGNOSIS
ƒ Impaired ability of gastrointestinal tract to DIAGNOSTIC IMAGING
absorb nutrients ƒ Abdominal ultrasound, colonoscopy,
ƒ Malabsorption may be intestinal biopsy, serological markers
Ɠ Global ĺ impaired function of intestinal
cells LAB RESULTS
Ɠ Partial ĺ external agent interferes with ƒ D-xylose test
absorption
Ɠ Test for carbohydrate malabsorption
ƒ Manifestation of underlying illness; may be
ƒ Fecal fat testing
congenital/acquired/infectious
ƒ Complete blood count (CBC)
Ɠ Look for for infection, anemia
CAUSES
ƒ Defects in absorption process of intestinal
cells (e.g. change to bowel surface area) OTHER DIAGNOSTICS
ƒ Impaired nutrient digestion (e.g. altered ƒ Individual history
digestive enzymes) Ɠ Pancreatitis
Ɠ Recent surgeries
Ɠ ¬NjŞƎƥūŞƙūIJDŽĿƥîŞĿŠēĚǶČĿĚŠČNj
SIGNS & SYMPTOMS Ɠ Family history

ƒ Abdominal distention, pain

ƒ Chronic diarrhea, malabsorption, TREATMENT
dehydration
ƒ Weight loss ƒ See individual disorders
ƒ Clinical manifestations of nutritional
ēĚǶČĿĚŠČĿĚƙɚĚɍijɍƎîƑĚƙƥĺĚƙĿîƙIJƑūŞ
ČūċîŕîŞĿŠēĚǶČĿĚŠČNjɛ

OSMOSIS.ORG 327
 CELIAC DISEASE
osms.it/celiac-disease

PATHOLOGY & CAUSES SIGNS & SYMPTOMS

ƒ Autoimmune disorder of small intestine ƒ Abdominal distention, chronic diarrhea
ƒ AKA gluten-sensitive enteropathy/ (steatorrhea)
nontropical sprue ƒ Failure to thrive (children)
ƒ Dermatitis herpetiformis
CAUSES Ɠ Circulating IgA antibodies attack dermal
ƒ Triggered by foods containing gliadin, a papillae ĺ generalized rash
peptide found in foods containing gluten
(e.g. grains: wheat, barley, rye, oats)
Ɠ Gluten consumption ĺ degradation into
DIAGNOSIS
peptides in small intestine ĺ secretory
IgA binds to gliadin in duodenum ĺ LAB RESULTS
IgA-gliadin complex binds to transferrin ƒ Anti-gliadin IgA/IgG
receptor ĺ IgA-gliadin complex travels ƒ Anti-endomysium IgA
across enterocyte into lamina propria ƒ Anti-tissue transglutaminase IgA
ĺ tissue transglutaminase deaminates Ɠ Tissue transglutaminase: endomysial
gliadin ĺ macrophages uptake, present enzyme released in response to cellular
deaminated gliadin in MHC-2 molecules stress
HLA-DQ 2, 8 ĺ CD4+ activation
Ɠ qūƑĚƙĚŠƙĿƥĿDŽĚɈƙƎĚČĿǶČ
ĺĿŠǷîƥūƑNjČNjƥūŒĿŠĚƙƑĚŕĚîƙĚē
(interferon gamma, tumor necrosis Duodenal biopsy
factor) ĺ damage/destruction of ƒ ¬ĺūDžĿŠijŕNjŞƎĺūČNjƥĿČĿŠǶŕƥƑîƥĿūŠɈDŽĿŕŕūƭƙ
intestinal villi ĺB cell activation ĺ anti- atrophy, crypt hyperplasia
gliadin, anti-tissue transglutaminase,
antiendomysial antibodies released
ĺ CD8+ cell activation ĺ tissue TREATMENT
destruction
ƒ On microscopy OTHER INTERVENTIONS
Ɠ ×ĿŕŕūƭƙîƥƑūƎĺNjɈŞƭČūƙîŕĿŠǷîƥĿūŠɈ ƒ ūƑƑĚČƥŠƭƥƑĿƥĿūŠîŕēĚǶČĿĚŠČĿĚƙƑĚŕîƥĚēƥū
intestinal crypt hyperplasia malabsorption
ƒ Presence of anti-gliadin, anti-endomysium
IgA = pathognomonic Preventative
ƒ Gluten-free diet
RISK FACTORS
ƒ Northern European ancestry, genetic MNEMONIC: Grains are
component
BROWn
Grains to avoid with Celiac
disease
Barley
Rye
Oats
Wheat

328 OSMOSIS.ORG
 Chapter 38 Malabsorption Conditions

Figure 38.1 Histological appearance of Figure 38.2 Clinical appearance of dermatitis

a duodenal biopsy in an individual with herpetiformis. Individual with celiac disease
celiac disease. There is villous blunting, an are at increased risk of this condition.
expansion of the lamina propria by chronic
ĿŠǷîƥūƑNjČĚŕŕƙîŠēîŠĿŠČƑĚîƙĚĿŠČƑNjƎƥ
ŕĚŠijƥĺɍĺĿijĺĚƑŞîijŠĿǶČîƥĿūŠDžūƭŕēƑĚDŽĚîŕ
an increase in lymphocyte count in the
surface epithelium.

LACTOSE INTOLERANCE
osms.it/lactose-intolerance

PATHOLOGY & CAUSES SIGNS & SYMPTOMS

ƒ Decreased ability to digest lactose ƒ Occur after consuming lactose (e.g. milk,
ƒ Lactose consumption ĺŕîČƥîƙĚēĚǶČĿĚŠČNjɓ cheese)
inactivity ĺĹ undigested lactose ĺ ƒ Abdominal pain, cramping in lower
IJĚƑŞĚŠƥîƥĿūŠċNjČūŕūŠĿČǷūƑîĺ gas, quadrants
osmotically active substances produced ĺ ƒ Abdominal distentionɈǷîƥƭŕĚŠČĚɈDŽūŞĿƥĿŠijɈ
bloating, diarrhea diarrhea (more common in children)

CAUSES
ƒ Most often acquired due to physiologic
DIAGNOSIS
weaning off of milk
ƒ Based on above symptoms

RISK FACTORS
LAB RESULTS
ƒ Non-European ancestry (most common)
ƒ Unabsorbed carbohydrates ĺ high stool
ƒ Increases with age
osmotic gap
ƒ May be congenital
ƒ Bacterial lactose fermentation ĺ acidic
Ɠ Rare, autosomal recessive disorder stool pH
ƒ May be developmental
Ɠ Most common among premature infants
ƒ Underlying intestinal disease

OSMOSIS.ORG 329
 Preventative
TREATMENT ƒ Lactose-free diet
OTHER INTERVENTIONS Ɠ Compensate with lactase
ƒ Optimize calcium, vitamin D intake

SMALL BOWEL BACTERIAL

OVERGROWTH SYNDROME
osms.it/sbbos

ƒ Altered mental status after high

PATHOLOGY & CAUSES carbohydrate meal
ƒ Failure to thrive (children)
ƒ Excessive colonic bacteria colonizing small
intestine
ƒ Often occurs secondary to conditions DIAGNOSIS
limiting intestinal motility, gastric acid and
ċĿŕĚƙĚČƑĚƥĿūŠîŠēTijēĚǶČĿĚŠČĿĚƙ LAB RESULTS
ƒ Signs/symptoms of vitamin, electrolyte
CAUSES abnormalities
ƒ Alteration of factors regulating intestinal Ɠ Weakness, ataxia, paresthesias ĺ B12
ǷūƑîĺ aerobic bacteria proliferation ĺ ēĚǶČĿĚŠČNj
changes in aerobic microclimate of small Ɠ Perioral numbness, feet paresthesias,
intestine ĺ migration of colonic anaerobic muscle cramping ĺČîŕČĿƭŞēĚǶČĿĚŠČNj
bacteria ĺ damage to intestinal surface ĺ ƒ Anemia
maldigestion, malabsorption ĺ symptoms
Ɠ Macrocytic ĺ B12ēĚǶČĿĚŠČNj
ƓĹ bacteria ĺĹ carbohydrate metabolism
Ɠ Microcytic ĺ chronic bleeding
ĺĹgas production ĺ bloating
ƒ Fecal fat testing
ƓĹ bacteria ĺ bile acid inactivation ĺĹ
fat in colon ĺ osmotic effect ĺ diarrhea ƒ Lactulose/glucose breath testing
ƓĹ bacteria ĺ intrinsic factor degradation ƒ Jejunal aspirate, culture
ĺ impaired B12 absorption ĺ B12 Ɠ > 103 colony forming units
ēĚǶČĿĚŠČNj
OTHER DIAGNOSTICS
RISK FACTORS ƒ Individual history
ƒ Increases with age Ɠ Chronic pancreatitis, intestinal surgery,
GI neuropathy

SIGNS & SYMPTOMS

TREATMENT
ƒ Abdominal pain/distention, chronic diarrhea,
ǷîƥƭŕĚŠČĚ MEDICATIONS
ƒ Tympanitic abdomen upon percussion ƒ Antibiotics

330 OSMOSIS.ORG
 Chapter 38 Malabsorption Conditions

TROPICAL SPRUE
osms.it/tropical-sprue

PATHOLOGY & CAUSES DIAGNOSIS

ƒ Gastrointestinal disease of uncertain DIAGNOSTIC IMAGING
etiology resulting in nutrient malabsorption
Endoscopy

CAUSES Barium swallow

ƒ Acute intestinal infection (viral/bacterial/ ƒ Shows intestinal wall thickening
protozoan) ĺ damaged intestinal lining ĺ
ĿŠǷîƥĿūŠĺ enteroglucagon secretion LAB RESULTS
ĺ decreased intestinal motility ĺ increased ƒ Fecal fat test
intestinal transit time ĺ overgrowth
ƒ D-xylose test
of Klebsiella, E. coli, Enterobacter ĺ
production of toxic fermentation byproducts ƒ Jejunal biopsy
ĺIJƭƑƥĺĚƑĿŠǷîƥĿūŠĺ villous atrophy Ɠ ¬ĺūDžƙDŽĿŕŕūƭƙîƥƑūƎĺNjɈĿŠǷîƥĿūŠ
ĺ malabsorption ĺ depletion of folate,
B12 ĺ intestinal villi can’t function normally
ĺ further intestinal injury, megaloblastic TREATMENT
anemia
MEDICATIONS
RISK FACTORS ƒ Antibiotics ĺ reduce bacterial overgrowth
ƒ Most common in individuals living in ƒ Replace folate, B12
tropical regions

SIGNS & SYMPTOMS

ƒ Diarrhea, weight loss, dehydration,
abdominal pain, fatigue, megaloblastic
anemia

OSMOSIS.ORG 331
 WHIPPLE'S DISEASE
osms.it/whipples-disease

PATHOLOGY & CAUSES SIGNS & SYMPTOMS

ƒ Rare, malabsorptive infectious disease ƒ Four cardinal signs
caused by Tropheryma whipplei Ɠ Diarrhea, weight loss, abdominal pain,
ƒ ¡îƥĺūijŠūŞūŠĿČǶŠēĿŠijĺ lamina propria arthralgias
displays numerous macrophages with ƒ Endocarditis, pericarditis, myocarditis
periodic acid-Schiff (PAS) positive ƒ Skin hyperpigmentation
intracellular material
ƒ Pleural disease

CAUSES
ƒ Tropheryma whipplei DIAGNOSIS
Ɠ Gram-positive, non-acid fast, PAS
positive bacillus; ubiquitous in LAB RESULTS
environment ƒ Biopsy
Ɠ Fecal-oral transmission Ɠ Shows copious PAS positive
ƒ Readily spreads throughout body, causing macrophages invading lamina propria in
multisystem effects intestine
Ɠ Evades immune response ĺ allows for ƒ ʓƥDžūƎūƙĿƥĿDŽĚ¡ ¤ɓ¡¬ƥĚƙƥƙ
accumulation of bacilli in tissues ƒ Immunohistochemistry for T. whipplei
ƒ Current hypothesis suggests host ƒ gîċūƑîƥūƑNjǶŠēĿŠijƙƙƭijijĚƙƥĿŠijČĺƑūŠĿČ
ĿŞŞƭŠūēĚǶČĿĚŠČNjîƙƎƑĚēĿƙƎūƙĿŠijIJîČƥūƑ ĿŠǷîƥĿūŠɈŠƭƥƑĿƥĿūŠîŕēĚǶČĿƥƙ

RISK FACTORS TREATMENT

ƒ Middle-aged biological males of European
ancestry; exposure to fecal matter (sewage MEDICATIONS
workers, farmers)
ƒ Start with IV antibiotics ĺ ceftriaxone/
penicillin G
MNEMONIC: WHIPPLES ƒ Trimethoprim-sulfamethoxazole (1 year)
Features of Whipple’s
disease
Weight loss
Hyperpigmentation of skin
Infection with tropheryma
whippelii
PAS positive granules in
macrophage
Polyarthritis
Lymphadenopathy
Enteric involvement
Steatorrhea

332 OSMOSIS.ORG
 Chapter 38 Malabsorption Conditions

Figure 38.3 Histological appearance of the

duodenum in a case of Whipple’s disease.
The lamina propria is occupied by numerous
foamy macrophages. Electron microscopy
would reveal numerous membrane bound
bacilli.

Figure 38.4 Histological appearance of a

duodenal biopsy with the special stain DPAS
(diastase periodic acid-Schiff). This stain
highlights diastase resistant mucin within the
foamy macrophages residing in the lamina
propria. The mucin within goblet cells is also
positively stained.

OSMOSIS.ORG 333
 NOTES

NOTES
ORAL DISEASE

GENERALLY, WHAT IS IT?

PATHOLOGY & CAUSES DIAGNOSIS
ƒ TŠIJĚČƥĿūƭƙɈĿŠǷîƥūƑNjēĿƙĚîƙĚƙɒîIJIJĚČƥ DIAGNOSTIC IMAGING
ūƑîŕČîDŽĿƥNjɈîƙƙūČĿîƥĚēƙƥƑƭČƥƭƑĚƙ
X-ray
ƒ ¬ĚĚĿŠēĿDŽĿēƭîŕēĿƙĚîƙĚƙ
RISK FACTORS
ƒ ¡ūūƑūƑîŕĺNjijĿĚŠĚɈēĚĺNjēƑîƥĿūŠɈ CT scan
ČūŠČūŞĿƥîŠƥĿŕŕŠĚƙƙɈŞîŕŠƭƥƑĿƥĿūŠ ƒ ¬ūIJƥƥĿƙƙƭĚĿŠǷîƥĿūŠĚNJƥĚŠƙĿūŠ

SIGNS & SYMPTOMS TREATMENT

ƒ TŠǷîƥĿūŠ MEDICATIONS
Ɠ ¤ĚēŠĚƙƙɈƙDžĚŕŕĿŠijɈƎîĿŠɈŕūƙƙūIJIJƭŠČƥĿūŠɈ ƒ sūŠƙƥĚƑūĿēîŕîŠƥĿɠĿŠǷîƥūƑNjēƑƭijƙ
DžîƑŞƥĺ ɚs¬T'ƙɛIJūƑƎîĿŠ
ƒ Infection Ɠ GūƑĿŠǷîƥĿūŠ
Ɠ GĚDŽĚƑɈŞîŕîĿƙĚɈŕūČîŕĿǕĚēƎîĿŠ ƒ ŠƥĿċĿūƥĿČƙɈîŠƥĿIJƭŠijîŕŞĚēĿČîƥĿūŠƙ
Ɠ GūƑĿŠIJĚČƥĿūŠ

APHTHOUS ULCERS
osms.it/aphthous-ulcers
Herpetiform
PATHOLOGY & CAUSES ƒ ūîŕĚƙČĚɈƑĚČƭƑIJƑĚƐƭĚŠƥŕNj
ƒ ¡îĿŠIJƭŕŕĚƙĿūŠƙĿŠƙĿēĚŞūƭƥĺɒċĚŠĿijŠɈŠūŠɠ
infectiousɒeČĚƑƙūƑĚƙ CAUSES
ƒ TēĿūƎîƥĺĿČɒŕĿŒĚŕNjŞƭŕƥĿIJîČƥūƑĿîŕɒŞîNjċĚƎîƑƥ
ūIJ¹OȂîƭƥūĿŞŞƭŠĚƑĚƙƎūŠƙĚɈĺūƑŞūŠîŕ
TYPES
IJîČƥūƑƙĿŠǷƭĚŠČĚĚƎĿƥĺĚŕĿƭŞƥĺĿČŒŠĚƙƙɈ
Minor ČūŠŠĚČƥĚēƥūDŽĿƥîŞĿŠȂȃēĚǶČĿĚŠČĿĚƙ
ƒ ¬ŞîŕŕɚȄɝȅŞŞɛɈŕîƙƥȈɝȂȁēîNjƙɈƑĚČƭƑȄɝȅ
ƥĿŞĚƙɓNjĚîƑɒĿIJƑĚČƭƑƑĚŠƥɈʑȅƥĿŞĚƙɓNjĚîƑ RISK FACTORS
ƒ ¬ƥƑĚƙƙɈƙNjƙƥĚŞĿČîƭƥūĿŞŞƭŠĚēĿƙūƑēĚƑƙɚĚɍijɍ
Major
ČĚŕĿîČɛɈŠƭƥƑĿƥĿūŠîŕēĚǶČĿĚŠČĿĚƙɈƙƥūƎƎĿŠij
ƒ gĚƙĿūŠƙʑȂČŞɈŕîƙƥȂȁɝȄȁēîNjƙ ƙŞūŒĿŠijɈūƑîŕČîDŽĿƥNjƥƑîƭŞîɚĚɍijɍċĿƥĿŠijŕĿƎƙɈ
ēĚŠƥƭƑĚƙɛ

334 OSMOSIS.ORG
 Chapter 39 ~Ƒîŕ'ĿƙĚîƙĚ

COMPLICATIONS
ƒ ¤ĚČƭƑƑĚŠƥîƎĺƥĺūƭƙƙƥūŞîƥĿƥĿƙɚqĿŒƭŕĿČǕ
DIAGNOSIS
ƭŕČĚƑƙɛɈĿŠIJĚČƥĿūŠɒŞîNjĿŠƥĚƑIJĚƑĚDžĿƥĺĚîƥĿŠijɓ
ēƑĿŠŒĿŠij
OTHER DIAGNOSTICS
ƒ ¤ĚČƭƑƑĚŠČĚūIJƭŕČĚƑƙ

SIGNS & SYMPTOMS

TREATMENT
ƒ ¤ūƭŠēɓūDŽîŕƭŕČĚƑîƥĿūŠƙĿŠūƑîŕŞƭČūƙîɈ
DžĺĿƥĚɓNjĚŕŕūDžƙĺîƑƎŕNjēĚŞîƑČîƥĚēČĚŠƥĚƑ MEDICATIONS
ČūDŽĚƑĚēDžĿƥĺǶċƑūƭƙŞĚŞċƑîŠĚČîƎɈ ƒ ×ĿƥîŞĿŠȂȃƙƭƎƎŕĚŞĚŠƥîƥĿūŠ
ƙƭƑƑūƭŠēĚēċNjƑĚēĚƑNjƥĺĚŞîƥūƭƙŞîƑijĿŠƙɒ ƒ ¹ūƎĿČîŕîŠîŕijĚƙĿČƙɈČūƑƥĿČūƙƥĚƑūĿēƙɈ
NjĚŕŕūDžĿƙĺĚNJƭēîƥĚ ƙƭČƑîŕIJîƥĚƙƭƙƎĚŠƙĿūŠ
ƒ TŠƙĿēĚūIJČĺĚĚŒƙɈŕĿƎƙɒƭŠēĚƑƥūŠijƭĚɒƎîĿŠIJƭŕ ƒ ŠƥĿɠƥƭŞūƑŠĚČƑūƙĿƙIJîČƥūƑɚ¹sGɛɠîŕƎĺî
ƙDžîŕŕūDžĿŠijɈĿIJĿŠċîČŒūIJƥĺƑūîƥ îijĚŠƥƙ
Ɠ ¤ĚČîŕČĿƥƑîŠƥɈƑĚČƭƑƑĚŠƥƭŕČĚƑƙ
Minor
ƒ ¬ŞîŕŕɈŞĿŕēŕNjƎîĿŠIJƭŕɈūNjĿŠijɈƑūƭŠēɓ
ūDŽîŕɈēĿƙîƎƎĚîƑDžĿƥĺĿŠƙĚDŽĚŠēîNjƙɈƑĚƙūŕDŽĚ OTHER INTERVENTIONS
ƙƎūŠƥîŠĚūƭƙŕNjɈŠūƙČîƑƑĿŠijɒŞūƑĚČūŞŞūŠ ƒ DŽūĿēƥƑĿijijĚƑƙ
ūŠŠūŠɠŒĚƑîƥĿŠĿǕĚēĚƎĿƥĺĚŕĿƭŞ

Major
ƒ gîƑijĚƑɈƎîĿŠIJƭŕɈƑĚČƭƑŞūƑĚūIJƥĚŠɈŞîNjƙČîƑ

Herpetiform
ƒ sūƥĺĚƑƎĚƙDŽĿƑƭƙČūŠŠĚČƥĚēɈDŽĚƙĿČŕĚƙ
ČūîŕĚƙČĚĿŠƥūƎîƥČĺĚƙ

Figure 39.1¹ĺĚČŕĿŠĿČîŕîƎƎĚîƑîŠČĚūIJ
îƎĺƥĺūƭƙƭŕČĚƑƙɍ

OSMOSIS.ORG 335
 DENTAL CARIES DISEASE
osms.it/dental-caries

PATHOLOGY & CAUSES DIAGNOSIS

ƒ ~ēūŠƥūijĚŠĿČĿŠIJĚČƥĿūŠƙɒƥūūƥĺēĚČîNjČîƭƙĚē DIAGNOSTIC IMAGING
ċNjîČĿēƙƎƑūēƭČĚēċNjċîČƥĚƑĿîɍ
Odontogram ( jaw X-ray)
ƒ îČƥĚƑĿîĺƎŕîƐƭĚĺĻƎOĺ
ēĚŞĿŠĚƑîŕĿǕîƥĿūŠĺČîƑĿĚƙ ƒ /NJîŞĿŠĚēĚƎƥĺūIJŕĚƙĿūŠƙ

CT scan
CAUSES ƒ TIJDžĿēĚƙƎƑĚîēɈƙūIJƥƥĿƙƙƭĚĿŠIJĚČƥĿūŠ
ƒ Streptococcus mutans, Streptococcus
sabrinus, Lactobacillus spp.
OTHER DIAGNOSTICS
Ɠ qĚƥîċūŕĿČîŕŕNjƎƑūēƭČĚîČĿēƙ
Clinical presentation
RISK FACTORS ƒ ¹ĚĚƥĺēĿƙČūŕūƑîƥĿūŠɈČĺîŠijĚƙ
ƒ ¡ƑūŕūŠijĚēċūƥƥŕĚƭƙĚɚċîċNjċūƥƥŕĚƥūūƥĺ
ēĚČîNjɛɈƎūūƑūƑîŕĺNjijĿĚŠĚɈƙƭijîƑɠƑĿČĺIJūūēƙɈ
ēĿîċĚƥĚƙŞĚŕŕĿƥƭƙɚ'qɛɈƙîŕĿDŽîƑNjijŕîŠē
TREATMENT
ēĿƙūƑēĚƑƙɚĚɍijɍ¬ŏūijƑĚŠɫƙɛɈŞĚēĿČîƥĿūŠƙƥĺîƥ
ēĚČƑĚîƙĚƙîŕĿDŽîƥĿūŠ
MEDICATIONS
ƒ ¹ūƎĿČîŕɓƙNjƙƥĚŞĿČîŠƥĿċĿūƥĿČƙ

COMPLICATIONS
ƒ OĚŞîƥūijĚŠūƭƙƙƎƑĚîēūIJċîČƥĚƑĿîƥūĺĚîƑƥ
SURGERY
DŽîŕDŽĚƙɈŏūĿŠƥƙɈĿŞƎŕîŠƥĚēƎƑūƙƥĺĚƥĿČƙ ƒ /NJƥƑîČƥĿūŠūIJĿŠIJĚČƥĚēŞîƥĚƑĿîŕɈƑĚƎŕîČĚŞĚŠƥ
DžĿƥĺǶŕŕĿŠijƙ
ƒ ¬ƎƑĚîēIJƑūŞĚŠîŞĚŕƥūƥūūƥĺƎƭŕƎɈîŕDŽĚūŕîƑ
bone
ƒ Abscesses OTHER INTERVENTIONS
ƒ ¬ūIJƥƥĿƙƙƭĚĿŠIJĚČƥĿūŠƙĿŠĚNJƥƑîūƑîŕ ƒ 'ĿĚƥîƑNjČūƭŠƙĚŕŕĿŠijɈĺNjijĿĚŠĚĿŞƎƑūDŽĚŞĚŠƥ
ƎĚƑIJūƑîƥĿūŠ
ƒ 'ĚĚƎĺĚîēɈŠĚČŒĿŠIJĚČƥĿūŠƙ
ƒ cîDžūƙƥĚūŞNjĚŕĿƥĿƙ
ƒ ¹ūūƥĺŕūƙƙ

SIGNS & SYMPTOMS

ƒ ÞĚŕŕūDžɓċŕîČŒƥĚĚƥĺƙƥîĿŠĿŠijɈĚŠîŞĚŕ
ƙūIJƥĚŠĿŠijɒîƎƎĚîƑîŠČĚūIJƎĿƥƙɈČƑîČŒƙ
ƒ If severe: ƥūūƥĺČūŕŕîƎƙĚ
ƒ If pulp affected: ēƭŕŕƎîĿŠĚNJîČĚƑċîƥĚēċNj
ČūŕēɈƙūIJƥIJūūē
ƒ If root caries: ŕūDžĚƑɈDžĺĚƑĚƥĚĚƥĺČŕūƙĚ
ƥūijĚƥĺĚƑɈIJūūēēĿIJǶČƭŕƥƥūĚNJƥƑîČƥɒŞūƑĚ Figure 39.2ēĚŠƥîŕČîDŽĿƥNjĿŠƥĺĚƥūūƥĺūIJî
ēĿIJǶČƭŕƥƥūēĿîijŠūƙĚ ƥĚŠɠNjĚîƑɠūŕēċūNjɍ

336 OSMOSIS.ORG
 Chapter 39 ~Ƒîŕ'ĿƙĚîƙĚ

Figure 39.3ŠūƑƥĺūƎîŠƥūŞūijƑîŞ
ēĚŞūŠƙƥƑîƥĿŠijēĚŠƥîŕČîDŽĿƥĿĚƙūIJƥĺĚŕĚIJƥ
ŞîŠēĿċƭŕîƑƙĚČūŠēîŠēƥĺĿƑēŞūŕîƑƥĚĚƥĺɍ

GINGIVITIS
osms.it/gingivitis
COMPLICATIONS
PATHOLOGY & CAUSES
ƒ ¡ĚƑĿūēūŠƥĿƥĿƙɈƥūūƥĺŕūƙƙɈƑĚČĚēĿŠijijƭŞƙ
ƒ ¹NjƎĚūIJƎĚƑĿūēūŠƥîŕēĿƙĚîƙĚɒĿŠǷîƥĿūŠ
ūIJijƭŞƙ SIGNS & SYMPTOMS
ƒ ¡îƥĺūijĚŠĿČċîČƥĚƑĿîƥƭŠŠĚŕċĚƥDžĚĚŠ
ŞĿČƑūČūŕūŠĿĚƙūŠƥūūƥĺƥūƙƭƑIJîČĚĿŠūƑēĚƑ ƒ ¤ĚēŠĚƙƙɈƙDžĚŕŕĿŠijɈċŕĚĚēĿŠijîIJƥĚƑċƑƭƙĺĿŠijɓ
ƥūċƑĿŠijĿŠƙƥĚîēNjƙƭƎƎŕNjūIJIJūūēĺIJūƑŞ ǷūƙƙĿŠij
ĺîƑēŞîƙƙɚēĚŠƥîŕČîŕČƭŕƭƙɛĺċîČƥĚƑĿîŕ
ƒ qîNjċĚîƙNjŞƎƥūŞîƥĿČĿŠĚîƑŕNjĿŠIJĚČƥĿūŠ
ƎŕîƐƭĚIJūƑŞîƥĿūŠĺĚŠƥĚƑijĿŠijĿDŽîŕƙƭŕČƭƙĺ
ijĿŠijĿDŽĿƥĿƙ
ƒ TŞŞƭŠĚƑĚƙƎūŠƙĚēĚŕĿDŽĚƑƙċŕūūēƥū DIAGNOSIS
ēîŞîijĚēƥĿƙƙƭĚĺƎƑūDŽĿēĚƙŠƭƥƑĿĚŠƥƙIJūƑ
ċîČƥĚƑĿîĺĿŞŞƭŠĚƑĚƙƎūŠƙĚîČƥĿDŽîƥĚƙ DIAGNOSTIC IMAGING
ūƙƥĚūČŕîƙƥƙĺēĿƙƙūŕDŽĚƙċūŠĚĺƥūūƥĺ
ŕūūƙĚŠĿŠij X-ray
ƒ sūŠɠĿŠIJĚČƥĿūƭƙƙNjƙƥĚŞĿČIJîČƥūƑƙĺijĿŠijĿDŽîŕ ƒ /DŽîŕƭîƥĚċūŠĚŕĚDŽĚŕɈƙƭŕČƭƙċĚČūŞĚƙ
ūDŽĚƑijƑūDžƥĺɈĿŠǷîƥĿūŠ ēĚĚƎĚƑîƙƎĚƑĿūēūŠƥîŕƎūČŒĚƥĚNJƎîŠēƙ
Ɠ OūƑŞūŠîŕƙĺĿIJƥƙɚĚɍijɍēƭƑĿŠijƎƑĚijŠîŠČNjɛ
Ɠ 'ƑƭijɠĿŠēƭČĚēɚĚɍijɍƎĺĚŠNjƥūĿŠɈČîŕČĿƭŞ OTHER DIAGNOSTICS
ČĺĚŕċŕūČŒĚƑƙɛ
Ɠ qîŕŠƭƥƑĿƥĿūŠɠĿŠēƭČĚēɚĚɍijɍDŽĿƥîŞĿŠ  Physical exam
ēĚǶČĿĚŠČNjɛ ƒ ¬DžūŕŕĚŠɓċŕĚĚēĿŠijijƭŞƙɈƎƑūċĚijĿŠijĿDŽîŕ
Ɠ sūŠɠƎŕîƐƭĚɠĿŠēƭČĚēɚƑîƑĚɈîƙƙūČĿîƥĚē ƙƭŕČƭƙƥūēĚƥĚƑŞĿŠĚēĚƎƥĺ
DžĿƥĺijĚŠĚƥĿČƙɈîŕŕĚƑijNjɈƥƑîƭŞîɛ

RISK FACTORS
ƒ ¡ūūƑēĚŠƥîŕĺNjijĿĚŠĚɈūŕēĚƑîijĚ

OSMOSIS.ORG 337
 TREATMENT
MEDICATIONS
ƒ ŠƥĿċĿūƥĿČƙIJūƑƙĚDŽĚƑĚĿŠIJĚČƥĿūŠƙ

SURGERY
ƒ ¤ĚŞūDŽîŕūIJĿŠIJĚČƥĚēƥĿƙƙƭĚĿIJƙĚDŽĚƑĚ

Figure 39.4ŠĿŠēĿDŽĿēƭîŕDžĿƥĺîƙĚDŽĚƑĚ
ČîƙĚūIJijĿŠijĿDŽĿƥĿƙɍ¹ĺĚijƭŞƙîƑĚƙDžūŕŕĚŠîŠē
ĺĚŞūƑƑĺîijĿČɍ¹ĺĚƑĚĿƙDŽĿƙĿċŕĚƎŕîƐƭĚČūDŽĚƑĿŠij
ƥĺĚIJƑĚĚijĿŠijĿDŽîŕŞîƑijĿŠūIJċūƥĺŞîNJĿŕŕîƑNj
ĿŠČĿƙūƑƙɍ

LUDWIG'S ANGINA
osms.it/ludwigs-angina

PATHOLOGY & CAUSES SIGNS & SYMPTOMS

ƒ ĿŕîƥĚƑîŕĿŠIJĚČƥĿūŠūIJƙƭċŞîŠēĿċƭŕîƑƙƎîČĚ ƒ Infection
ɚƙƭċŕĿŠijƭîŕɈƙƭċŞNjŕūĺūĿēɛ Ɠ GĚDŽĚƑɈČĺĿŕŕƙɈŞîŕîĿƙĚɈƎîĿŠ
ƒ ¬ƥĿIJIJŠĚČŒɈēNjƙƎĺîijĿîɈĿŠēĿDŽĿēƭîŕ
CAUSES ŕĚîŠƙIJūƑDžîƑēƥūĚNJƎîŠēîĿƑDžîNjɈŠū
ƒ ¬ƎƑĚîēIJƑūŞĿŠIJĚČƥĿūŠūIJȃŠēɓȄƑēŞîŠēĿċƭŕîƑ ŕNjŞƎĺîēĚŠūƎîƥĺNjɈċĿŕîƥĚƑîŕɈƙƭēēĚŠ
ŞūŕîƑƙɈƎĚƑĿČūƑūŠĿƥĿƙɈƎîƑūƥĿƥĿƙɈƎĚƑĿƥūŠƙĿŕŕîƑ îijijƑĚƙƙĿDŽĚƙƎƑĚîēɈĚŠŕîƑijĚēƥūŠijƭĚɈ
îċƙČĚƙƙ ēƑūūŕĿŠij
ƒ qîŠēĿċƭŕîƑIJƑîČƥƭƑĚɈƎĿĚƑČĿŠijƙ ƒ ƑĿƥĿČîŕƙNjŞƎƥūŞƙ
ƒ îƭƙîƥĿDŽĚîijĚŠƥƙƎūŕNjŞĿČƑūċĿîŕIJƑūŞŞūƭƥĺ Ɠ ¬ƥƑĿēūƑɈČNjîŠūƙĿƙ
ǷūƑîɈēūŞĿŠîƥĚēċNjStreptococcus viridans; ƒ sūîċƙČĚƙƙIJūƑŞîƥĿūŠ
staphylococci, bacteroidesîŕƙūČūŞŞūŠ

DIAGNOSIS
RISK FACTORS
ƒ 'qɈĺNjƎĚƑƥĚŠƙĿūŠɈOT×ĿŠIJĚČƥĿūŠɈ DIAGNOSTIC IMAGING
ĿŞŞƭŠūƙƭƎƎƑĚƙƙĿūŠ
CT scan
COMPLICATIONS ƒ ¤ƭŕĚūƭƥîċƙČĚƙƙIJūƑŞîƥĿūŠɚūČČƭƑƙŕîƥĚĿŠ
ēĿƙĚîƙĚɛ
ƒ ĿƑDžîNjūċƙƥƑƭČƥĿūŠɈŞĚēĿîƙƥĿŠĿƥĿƙɈ
ŠĚČƑūƥĿǕĿŠijČĚŕŕƭŕĿƥĿƙɈƙĚƎƙĿƙɈîƙƎĺNjNJĿî ƒ ĺĚƙƥ ¹ƙČîŠ
Ɠ qĚēĿîƙƥĿŠĿƥĿƙ

338 OSMOSIS.ORG
 Chapter 39 ~Ƒîŕ'ĿƙĚîƙĚ

LAB RESULTS
ƒ ŕūūēČƭŕƥƭƑĚ
TREATMENT
MEDICATIONS
OTHER DIAGNOSTICS ƒ /ŞƎĿƑĿČċƑūîēɠƙƎĚČƥƑƭŞîŠƥĿċĿūƥĿČƙDžĿƥĺ
ƒ ÀŕƥƑîƙūƭŠēɠijƭĿēĚēŠĚĚēŕĚîƙƎĿƑîƥĿūŠ ċĚƥîɠŕîČƥîŞîƙĚîČƥĿDŽĿƥNj

SURGERY
ƒ ¬ƭƑijĿČîŕēƑîĿŠîijĚɈĿIJîċƙČĚƙƙĿēĚŠƥĿǶĚēūŠ
¹ƙČîŠ

OTHER INTERVENTIONS
Airway management
ƒ GĿċĚƑūƎƥĿČŠîƙîŕĿŠƥƭċîƥĿūŠɈĚŞĚƑijĚŠƥ
ƥƑîČĺĚūƙƥūŞNjŞîNjċĚŠĚČĚƙƙîƑNj

ORAL CANDIDIASIS
osms.it/oral-candidiasis
COMPLICATIONS
PATHOLOGY & CAUSES
ƒ ¬ƎƑĚîēĿŠƥūƎĺîƑNjŠNJɈēĿƙƙĚŞĿŠîƥĚē
ČîŠēĿēĿîƙĿƙ
ƒ ~ƎƎūƑƥƭŠĿƙƥĿČĿŠIJĚČƥĿūŠūIJūƑîŕŞƭČūƙîŕ
ŞĚŞċƑîŠĚƙċNjCandida spp. ɚĚɍijɍCandida
albicans)
SIGNS & SYMPTOMS
ƒ eƥĺƑƭƙĺ
ƒ qîNjċĚîƙNjŞƎƥūŞîƥĿČ
TYPES ƒ ūƥƥūŠNjIJĚĚŕĿŠijĿŠŞūƭƥĺɒŕĚƙĿūŠƙ
ƒ ¡îĿŠɓƥĚŠēĚƑŠĚƙƙĿŠūƑîŕČîDŽĿƥNj
Pseudomembranous
ƒ ¡îĿŠIJƭŕƙDžîŕŕūDžĿŠijɚūēNjŠūƎĺîijĿîɛ
ƒ ØĺĿƥĿƙĺƎŕîƐƭĚƙūŠūƑîŕŞƭČūƙîɚŞūƙƥ
ČūŞŞūŠɛɒČîŠċĚƙČƑîƎĚēūIJIJƥūƑĚDŽĚîŕ ƒ 'ĚČƑĚîƙĚēƙĚŠƙĚūIJƥîƙƥĚ
ĚƑNjƥĺĚŞîƥūƭƙƙƭƑIJîČĚ ƒ ŠijƭŕîƑČĺĚĿŕĿƥĿƙ

Atrophic (denture stomatitis)

ƒ ¤ĚēŕĚƙĿūŠƙDžĿƥĺūƭƥƎŕîƐƭĚƙ DIAGNOSIS
Hyperplastic (rare) LAB RESULTS
ƒ sūŠɠƙČƑîƎîċŕĚƎŕîƐƭĚƙ ƒ qĿČƑūċĿūŕūijĿČîŕîŠîŕNjƙĿƙūIJƙČƑîƎĿŠijƙɒHƑîŞ
ƙƥîĿŠɒe~OƎƑĚƎîƑîƥĿūŠɒċĿūƎƙNj
RISK FACTORS
ƒ ÞūƭŠijîijĚɈēĚŠƥƭƑĚƙɈNJĚƑūƙƥūŞĿîɈ
îŠƥĿċĿūƥĿČƙɈ'qɈŞîŕŠƭƥƑĿƥĿūŠ
ƒ TŞŞƭŠūƙƭƎƎƑĚƙƙĿūŠēƭĚƥūČūƑƥĿČūƙƥĚƑūĿēƙɈ
ČĺĚŞūƥĺĚƑîƎNjɈOT×ɓT'¬

OSMOSIS.ORG 339
 TREATMENT
MEDICATIONS
ƒ ¹ūƎĿČîŕîŠƥĿIJƭŠijîŕîijĚŠƥƙɚĚɍijɍŠNjƙƥîƥĿŠ
ƙƭƙƎĚŠƙĿūŠɈČŕūƥƑĿŞîǕūŕĚƥƑūČĺĚƙɈƙNjƙƥĚŞĿČ
ǷƭČūŠîǕūŕĚɛ

Figure 39.5~ƑîŕČîŠēĿēĿîƙĿƙĿŠîČĺĿŕēDžĺū
ĺîēƥîŒĚŠîŠƥĿċĿūƥĿČƙɍ

PAROTITIS
osms.it/parotitis
ƙNjŞƎîƥĺūŞĿŞĚƥĿČƙɛ
PATHOLOGY & CAUSES
ƒ ¡îƑūƥĿēijŕîŠēĿŠǷîƥĿūŠ COMPLICATIONS
ƒ ¬îŕĿDŽîƑNjƙƥîƙĿƙĺƙĚĚēĿŠijūIJƎîƑūƥĿē ƒ ¬ƎƑĚîēƥūēĚĚƎĺĚîēɈŠĚČŒƙƥƑƭČƥƭƑĚƙɒ
ɚ¬ƥĚŠƙĚŠɛēƭČƥċNjŞĿČƑūūƑijîŠĿƙŞƙĺ ƙĚƎƥĿČŏƭijƭŕîƑƥĺƑūŞċūƎĺŕĚċĿƥĿƙɒƙĚƎƥĿČ
ĿŠIJĚČƥĿūŠɈĿŠǷîƥĿūŠ ūƙƥĚūŞNjĚŕĿƥĿƙɒƙĚƎƙĿƙɒƑĚƙƎĿƑîƥūƑNj
ūċƙƥƑƭČƥĿūŠɒIJîČĿîŕŠĚƑDŽĚƎîŕƙNj

CAUSES
ƒ Bacterial: S. aureusɈŞūƙƥČūŞŞūŠ SIGNS & SYMPTOMS
ƒ Viral: ŞƭŞƎƙɈĿŠǷƭĚŠǕîɈČūNJƙîČŒĿĚɈ/ƎƙƥĚĿŠɝ
îƑƑDŽĿƑƭƙɚ/×ɛ ƒ ¬NjƙƥĚŞĿČŞîŠĿIJĚƙƥîƥĿūŠƙ
ƒ ƭƥūĿŠǷîƥūƑNjɇƙîƑČūĿēūƙĿƙîƙƎîƑƥūIJ Ɠ GĚDŽĚƑɈČĺĿŕŕƙ
qĿŒƭŕĿČǕƙNjŠēƑūŞĚ ƒ ¡ĚƑĿîƭƑĿČƭŕîƑɈŞîŠēĿċƭŕîƑƎîĿŠɈƙDžĚŕŕĿŠijɒ
ƥƑĿƙŞƭƙɈēNjƙƎĺîijĿîɒƎƭƑƭŕĚŠƥēƑîĿŠîijĚ
RISK FACTORS ƒ ×ĿƑîŕ
ƒ ¬ƭƑijĚƑNjɈēĚĺNjēƑîƥĿūŠɈƙîŕĿDŽîƑNjijŕîŠē Ɠ sūēĿƙČĺîƑijĚɈƎƑūēƑūŞĚIJūŕŕūDžĚēċNj
ƙƥūŠĚƙɈƎūūƑūƑîŕĺNjijĿĚŠĚɈŞĚēĿČîƥĿūŠƙƥĺîƥ ƙDžĚŕŕĿŠijŕîƙƥĿŠijȆɝȂȁēîNjƙ
ēĚČƑĚîƙĚƙîŕĿDŽîƥĿūŠɚĚɍijɍîŠƥĿČĺūŕĿŠĚƑijĿČɈ

340 OSMOSIS.ORG
 Chapter 39 ~Ƒîŕ'ĿƙĚîƙĚ

DIAGNOSIS
DIAGNOSTIC IMAGING
ƒ ¬îŞƎŕĚƎƭƑƭŕĚŠƥĚNJƭēîƥĚɈƭŕƥƑîƙūƭŠē
ijƭĿēĚēŠĚĚēŕĚîƙƎĿƑîƥĿūŠɒČƭŕƥƭƑĚɈHƑîŞ
ƙƥîĿŠ

Ultrasound
ƒ TŠČƑĚîƙĚēċŕūūēǷūDžƥĺƑūƭijĺijŕîŠēɈ
ĚŠŕîƑijĚŞĚŠƥɈŠūēƭŕĚƙ

CT scan
ƒ /NJƥĚŠƙĿūŠūIJĿŠǷîƥĿūŠƥūƙƭƑƑūƭŠēĿŠij
tissues

LAB RESULTS
ƒ ūŞƎŕĚƥĚċŕūūēČūƭŠƥɚ  ɛ Figure 39.6¹ĺĚČŕĿŠĿČîŕîƎƎĚîƑîŠČĚūIJ
ƒ TŠČƑĚîƙĚēîŞNjŕîƙĚDžĿƥĺūƭƥƭŠēĚƑŕNjĿŠij ƎîƑūƥĿƥĿƙūIJƥĺĚŕĚIJƥƎîƑūƥĿēijŕîŠēɍ¹ĺĚƑĚĿƙî
ƎîŠČƑĚîƥĿƥĿƙ ŞîƑŒĚēƙDžĚŕŕĿŠijŏƭƙƥîŠƥĚƑĿūƑƥūƥĺĚŕĚIJƥĚîƑɍ
ƒ ×ĿƑîŕƙĺūDžƙŕĚƭŒūČNjƥūƙĿƙɈĿŠČƑĚîƙĚēTijq
îijîĿŠƙƥŞƭŞƎƙ
TREATMENT
MEDICATIONS
ƒ ONjēƑîƥĿūŠɒT×îŠƥĿċĿūƥĿČƙ
ƒ ×îČČĿŠîƥĿūŠ
Ɠ qƭŞƎƙƎƑĚDŽĚŠƥĿūŠ

PERIODONTITIS
osms.it/periodontitis
ĺƥūūƥĺŕūūƙĚŠĿŠij
PATHOLOGY & CAUSES ƒ ¬ĚDŽĚƑĿƥNjċîƙĚēūŠŕĿijîŞĚŠƥŕūƙƙ
ƒ Porphyromonas gingivalisĿŞƎîĿƑƙĿŞŞƭŠĚ
ƒ TŠǷîƥĿūŠɈēĚƙƥƑƭČƥĿūŠūIJƙƭƎƎūƑƥĿŠij
ČĚŕŕƙɈŒĿŕŕƙċîČƥĚƑĿîĺƎîƥĺūijĚŠĿČċîČƥĚƑĿî
ƙƥƑƭČƥƭƑĚƙîƑūƭŠēƥĚĚƥĺɈDžîƙƥĿŠijūIJċūŠĚ
ūDŽĚƑijƑūDž
ƒ 'NjƙċĿūƙĿƙɚēĿƙƥƭƑċĚēċîČƥĚƑĿîŕƙNjŞċĿūƙĿƙɛ
ƒ sĚČƑūƥĿǕĿŠijƭŕČĚƑîƥĿDŽĚƎĚƑĿūēūŠƥĿƥĿƙɚsÀ¡ɛ
ŞūƑĚĚNJƥƑĚŞĚƥĺîŠĿŠijĿŠijĿDŽĿƥĿƙ
Ɠ /NJƥƑĚŞĚŕūƙƙūIJƎĚƑĿūēūŠƥîŕîƥƥîČĺŞĚŠƥɈ
ƒ ~ƑîŠijĚɠČūŞƎŕĚNJūIJċîČƥĚƑĿî
îŕDŽĚūŕîƑċūŠĚɒîƙƙūČĿîƥĚēDžĿƥĺ
(Fusobacterium nucleatum, Prevotella
ĿŞŞƭŠūƙƭƎƎƑĚƙƙĿūŠɚĚɍijɍOT×ɓT'¬ɒ
intermediaɛɈƑĚēɠČūŞƎŕĚNJūIJċîČƥĚƑĿî
ČĺĚŞūƥĺĚƑîƎNjɈƙĚDŽĚƑĚŞîŕŠƭƥƑĿƥĿūŠɛɒ
(Tannerella forsythia, Treponema denticola,
ŞîNjċĚîƙƙūČĿîƥĚēDžĿƥĺĚŠƥĚƑĿČċîČƥĚƑĿîɈ
Porphyromonas gingivalis) ĺĿŞŞƭŠĚ
NjĚîƙƥ
ƑĚƙƎūŠƙĚĺŞūƑĚċŕūūēǷūDžƥūēîŞîijĚē
tissue ĺƎƑūDŽĿēĚƙŠƭƥƑĿĚŠƥƙIJūƑċîČƥĚƑĿî
ĺŞūƑĚēîŞîijĚƥūijĿŠijĿDŽîɈƎĚƑĿūēūŠƥîŕ
ŕĿijîŞĚŠƥĺîČƥĿDŽîƥĚēūƙƥĚūČŕîƙƥƙĿŠċūŠĚ

OSMOSIS.ORG 341
 CAUSES OTHER DIAGNOSTICS
ƒ ¡ūūƑūƑîŕĺNjijĿĚŠĚɒƑĚēɠɈūƑîŠijĚɠČūŞƎŕĚNJ ƒ ŕĿŠĿČîŕĚNJîŞ
ċîČƥĚƑĿî Ɠ ¡ƑūċĚƥĚĚƥĺƎūČŒĚƥƙɈƥĚƙƥIJūƑċŕĚĚēĿŠijɈ
ēĚƎƥĺ
RISK FACTORS
ƒ 'qɈƙŞūŒĿŠijɈ/ĺŕĚƑɝ'îŠŕūƙƙNjŠēƑūŞĚ
TREATMENT
COMPLICATIONS MEDICATIONS
ƒ ¹ūūƥĺŕūƙƙɈĿŠIJĚČƥĿūŠƙƎƑĚîēƥūƙūIJƥƥĿƙƙƭĚƙ ƒ ¬NjƙƥĚŞĿČîŠƥĿċĿūƥĿČƙɚĿIJƙĚDŽĚƑĚɛ
ūIJĺĚîēɈŠĚČŒɈƙĿŠƭƙĿƥĿƙɒĺĚŞîƥūijĚŠūƭƙ
ēĿƙƙĚŞĿŠîƥĿūŠƥūĺĚîƑƥDŽîŕDŽĚƙɚƎƑūƙƥĺĚƥĿČɓ
ŠîƥĿDŽĚɛɈŏūĿŠƥƙɈĚƥČɍ
SURGERY
ƒ ¤ĚŞūDŽîŕūIJĿŠIJĚČƥĚēƥĿƙƙƭĚɚĿIJƙĚDŽĚƑĚɛ

SIGNS & SYMPTOMS OTHER INTERVENTIONS

ƒ ¡ƑĚDŽĚŠƥƎŕîƐƭĚIJūƑŞîƥĿūŠ
ƒ ¤ĚēŠĚƙƙ, ƙDžĚŕŕĿŠij, ƥĚŠēĚƑƥūƎîŕƎîƥĿūŠ
Ɠ 'îĿŕNjċƑƭƙĺĿŠij, ǷūƙƙĿŠijɒîŠƥĿŞĿČƑūċĿîŕ
ƒ OîŕĿƥūƙĿƙ îijĚŠƥƙɚĚɍijɍŞūƭƥĺDžîƙĺɛ
ƒ ŕĚĚēĿŠijēƭƑĿŠijƥĚĚƥĺċƑƭƙĺĿŠij ƒ ¬ČîŕĿŠijɈƑūūƥƎŕîŠĿŠij
ƒ ¹ĚĚƥĺŕūūƙĚŠĿŠij Ɠ ¤ĚŞūDŽĚƎŕîƐƭĚ
ƒ ¡ĚƑĿūēūŠƥîŕƎūČŒĚƥƙDžĿēĚŠ ƒ ¹ūƎĿČîŕǷƭūƑĿēĚ

DIAGNOSIS
DIAGNOSTIC IMAGING
Panoramic dental X-ray
ƒ ūŠĚŕūƙƙîƑūƭŠēƥūūƥĺ

SIALADENITIS
osms.it/sialadenitis
ĿŠǷîƥĿūŠɈƥĿƙƙƭĚƙDžĚŕŕĿŠij
PATHOLOGY & CAUSES
ƒ TŠǷîƥĿūŠūIJƙîŕĿDŽîƑNjijŕîŠēƙ CAUSES
Ɠ ¡îƑūƥĿēɚŞūƙƥČūŞŞūŠɛɈƙƭċŕĿŠijƭîŕ, ƒ Bacterial: Staphylococcus aureusɚŞūƙƥ
ƙƭċŞîŠēĿċƭŕîƑɒƭŠĿŕîƥĚƑîŕ ČūŞŞūŠɛɈStreptococcus viridans,
OîĚŞūƎĺĿŕƭƙĿŠǷƭĚŠǕîĚ
ƒ 'ĚČƑĚîƙĚēǷūDžūIJƙîŕĿDŽîĺēĚƎūƙĿƥƙƙĚƥƥŕĚ
ĿŠDžîŕŕƙūIJƙîŕĿDŽîƑNjēƭČƥĺēƭČƥċŕūČŒĚē ƒ Viral:ŞƭŞƎƙɈOT×
ĺǷūDžūIJƙîŕĿDŽîƙŕūDžĚēĺēĚƎūƙĿƥƙūIJ
ČîŕČĿƭŞɈƎĺūƙƎĺūƑūƭƙɈĚƥČɍƎƑĚČĿƎĿƥîƥĚĺ RISK FACTORS
IJūƑŞƙŞîŕŕČūŠČƑĚƥĿūŠƙɚŞĿČƑūƙĿîŕūŕĿƥĺƙɛ ƒ 'ĚČƑĚîƙĚēƙîŕĿDŽîƑNjǷūDžɚēĚĺNjēƑîƥĿūŠɈ
ĺijƑūDžĿŠƥūƙĿîŕūŕĿƥĺƙĺƙƥūŠĚƙċŕūČŒ ĿŕŕŠĚƙƙɈîŠƥĿČĺūŕĿŠĚƑijĿČŞĚēĿČîƥĿūŠƙɈ
ēƭČƥĺċîČƥĚƑĿîŞūDŽĚƙIJƑūŞŞūƭƥĺƭƎɈ ¬ŏūijƑĚŠɫƙƙNjŠēƑūŞĚ)
îƑūƭŠēċŕūČŒîijĚɈĿŠƥūƙîŕĿDŽîƑNjēƭČƥĺ
ƒ ¤ĿƙŒĿŠČƑĚîƙĚƙDžĿƥĺîijĚ

342 OSMOSIS.ORG
 Chapter 39 ~Ƒîŕ'ĿƙĚîƙĚ

LAB RESULTS
ƒ gîċČƭŕƥƭƑĚūIJƎƭƙ
Ɠ HĚŠƥŕĚČūŞƎƑĚƙƙĿūŠūIJijŕîŠē

OTHER DIAGNOSTICS
ƒ ŕĿŠĿČîŕƎƑĚƙĚŠƥîƥĿūŠ

TREATMENT
MEDICATIONS
ƒ Antibiotics

SURGERY
ƒ ¬ƭƑijĿČîŕijŕîŠēƑĚŞūDŽîŕ
Ɠ TIJēĿƙĚîƙĚƑĚČƭƑƑĚŠƥ
Figure 39.7ŠĿŠēĿDŽĿēƭîŕĺūŕēĿŠijƥĺĚĿƑ
ūDžŠƙîŕĿDŽîƑNjēƭČƥƙƥūŠĚIJūŕŕūDžĿŠijƙƭƑijĿČîŕ
ƑĚŞūDŽîŕɍ¬îŕĿDŽîƑNjēƭČƥƙƥūŠĚƙƎƑĚēĿƙƎūƙĚ OTHER INTERVENTIONS
ĿŠēĿDŽĿēƭîŕƙƥūƙĿîŕîēĚŠĿƥĿƙɍ ƒ ONjēƑîƥĿūŠɈDžîƑŞČūŞƎƑĚƙƙɈijŕîŠēƭŕîƑ
ŞîƙƙîijĚɈƙĿîŕūijūijƭĚƙ

SIGNS & SYMPTOMS

ƒ ČƭƥĚƙĿîŕîēĚŠĿƥĿƙ
Ɠ GĚDŽĚƑɈČĺĿŕŕƙɈîċƙČĚƙƙIJūƑŞîƥĿūŠ
Ɠ ¡îĿŠɈƙDžĚŕŕĿŠijɈƑĚēŠĚƙƙūIJƙŒĿŠūDŽĚƑŕNjĿŠij
îIJIJĚČƥĚēijŕîŠē
Ɠ gĚƙƙƙîŕĿDŽîĺēƑNjŞūƭƥĺĺċîēƥîƙƥĚ
ɚƎƭƙŕĚîŒĿŠijūƭƥūIJîIJIJĚČƥĚēēƭČƥɛ
Ɠ Severe: ƎîĿŠIJƭŕƥūūƎĚŠŞūƭƥĺ
ƒ ĺƑūŠĿČƙĿîŕîēĚŠĿƥĿƙ
Ɠ gĚƙƙƎîĿŠIJƭŕɈijŕîŠēĚŠŕîƑijĚƙIJūŕŕūDžĿŠij
ŞĚîŕƙɈŠūūDŽĚƑŕNjĿŠijƑĚēŠĚƙƙūIJƥĺĚƙŒĿŠ
Ɠ ƙƙūČĿîƥĚēDžĿƥĺČūŠēĿƥĿūŠƙŕĿŠŒĚē
ƥūČĺƑūŠĿČēĚČƑĚîƙĚēƙîŕĿDŽîƑNjǷūDž
ɚĚɍijɍ¬ŏūijƑĚŠɫƙƙNjŠēƑūŞĚɛɈēƭĚƥū
ĿŠǷîƥĿūŠɈƙîŕĿDŽîƑNjēƭČƥǶċƑūƙĿƙɈ
îŕƥĚƑĿŠijijŕîŠēƭŕîƑƥĿƙƙƭĚɈČūŞƎūƙĿƥĿūŠūIJ
ƙîŕĿDŽî Figure 39.8ƙƭċŞîŠēĿċƭŕîƑƙĿîŕūijƑîŞ
ēĚŞūŠƙƥƑîƥĿŠijîƙîŕĿDŽîƑNjēƭČƥƙƥūŠĚɒîƑĿƙŒ
IJîČƥūƑIJūƑƙĿîŕîēĚŠĿƥĿƙɍ
DIAGNOSIS
DIAGNOSTIC IMAGING
Ultrasound
ƒ ċƙČĚƙƙɈƙîŕĿDŽîƑNjƙƥūŠĚɈƥƭŞūƑ

OSMOSIS.ORG 343
 Figure 39.9¹ĺĚĺĿƙƥūŕūijĿČîŕîƎƎĚîƑîŠČĚ
ūIJƙĿîŕîēĚŠĿƥĿƙîƥŕūDžƎūDžĚƑɍ¹ĺĚîČĿŠĿîƑĚ
ƙƭƑƑūƭŠēĚēċNjēĚŠƙĚǶċƑūƙĿƙîŠēēĿƙƎŕîNj
ƎîƥČĺNjŕNjŞƎĺūČNjƥĿČĿŠǶŕƥƑîƥĚƙɍ

344 OSMOSIS.ORG
 NOTES

NOTES
PANCREATITIS

GENERALLY, WHAT IS IT?

PATHOLOGY & CAUSES SIGNS & SYMPTOMS
ƒ TŠǷîƥĿūŠūIJƎîŠČƑĚîƙ ƒ ÀƎƎĚƑîċēūŞĿŠîŕƎîĿŠƑîēĿîƥĿŠijƥūċîČŒɒ
ŠîƭƙĚîɒDŽūŞĿƥĿŠij
TYPES
ƒ ČƭƥĚɈČĺƑūŠĿČ DIAGNOSIS
CAUSES DIAGNOSTIC IMAGING
ƒ ČƭƥĚ ƒ ċēūŞĿŠîŕ ¹ƙČîŠɒƭŕƥƑîƙūƭŠē
Ɠ HîŕŕƙƥūŠĚƙɈîŕČūĺūŕĿƙŞɈēĿƑĚČƥƥƑîƭŞîɈ
ĿŠIJĚČƥĿūŠƙɚŞƭŞƎƙɛ LAB RESULTS
ƒ ĺƑūŠĿČ ƒ ŕĿŠĿČîŕɈŕîċǶŠēĿŠijƙɒƙĚĚĿŠēĿDŽĿēƭîŕ
Ɠ ¤ĚČƭƑƑĚŠƥîČƭƥĚƎîŠČƑĚîƥĿƥĿƙɈČĺƑūŠĿČ ēĿƙūƑēĚƑƙ
îŕČūĺūŕĿƙŞɈČNjƙƥĿČǶċƑūƙĿƙ

RISK FACTORS
TREATMENT
ƒ ¬ŞūŒĿŠij OTHER INTERVENTIONS
ƒ 'ĿĚƥîƑNjŞūēĿǶČîƥĿūŠƙɈƙNjŞƎƥūŞîƥĿČ
ƥƑĚîƥŞĚŠƥ

PANCREATIC PSEUDOCYST
osms.it/pancreatic-pseudocyst
ĺĚŞūƑƑĺîijĿČIJîƥŠĚČƑūƙĿƙĺĿŠǷîƥūƑNj
PATHOLOGY & CAUSES ƑĚîČƥĿūŠĺĚŠČîƎƙƭŕîƥĿūŠūIJǷƭĿēċNjǶċƑūƭƙ
îŠēijƑîŠƭŕîƥĿūŠƥĿƙƙƭĚ
ƒ gūČîŕĿǕĚēǷƭĿēČūŕŕĚČƥĿūŠūIJƎîŠČƑĚîƥĿČ
ĚŠǕNjŞĚƙɈŠĚČƑūƥĿČēĚċƑĿƙîŠēċŕūūē
ĚŠČîƎƙƭŕîƥĚēċNjŠūŠɠĚƎĿƥĺĚŕĿîŕĿǕĚēDžîŕŕ CAUSES
ɚĺĚŠČĚƥĺĚŠîŞĚƎƙĚƭēūČNjƙƥɛČūŞƎūƙĚēūIJ ƒ ƑĿƙĚƙîƙČūŞƎŕĿČîƥĿūŠūIJîČƭƥĚɓČĺƑūŠĿČ
ǶċƑūƭƙîŠēijƑîŠƭŕîƥĿūŠƥĿƙƙƭĚ ƎîŠČƑĚîƥĿƥĿƙɓîċēūŞĿŠîŕƥƑîƭŞî
ƒ ÀƙƭîŕŕNjƥîŒĚƭƎƥūȅɝȇDžĚĚŒƙƥūēĚDŽĚŕūƎɈ
ƭŠŕĿŒĚîČƭƥĚǷƭĿēČūŕŕĚČƥĿūŠƙ COMPLICATIONS
ƒ ~ČČƭƑƙēƭĚƥūēĿƙƑƭƎƥĿūŠūIJƎîŠČƑĚîƥĿČ ƒ TŠIJĚČƥĿūŠɒĺĚŞūƑƑĺîijĚ
ēƭČƥĺîČČƭŞƭŕîƥĿūŠūIJƎîŠČƑĚîƥĿČǷƭĿēĺ ƒ ūŞƎƑĚƙƙĿūŠūIJƥĺĚijîƙƥƑūĿŠƥĚƙƥĿŠîŕɓƭƑĿŠîƑNjɓ

OSMOSIS.ORG 345
 ċĿŕĿîƑNjƥƑîČƥ
ƒ ¤ƭƎƥƭƑĚĺƙƎĿŕŕĿŠijūIJĚŠǕNjŞĚƙîŠēēĚċƑĿƙ
ĿŠƥūîċēūŞĿŠîŕČîDŽĿƥNjĺ ēĿIJIJƭƙĚƎĚƑĿƥūŠĿƥĿƙ

SIGNS & SYMPTOMS

ƒ ċēūŞĿŠîŕēĿƙČūŞIJūƑƥɈĿŠēĿijĚƙƥĿūŠɈ
îŠūƑĚNJĿîɈîċēūŞĿŠîŕŞîƙƙ

DIAGNOSIS
DIAGNOSTIC IMAGING
CT scan
ƒ gîƑijĚČNjƙƥČîDŽĿƥNjūIJŕūDžîƥƥĚŠƭîƥĿūŠ
ƙƭƑƑūƭŠēĚēċNjDžĚŕŕɠēĚǶŠĚēĚŠĺîŠČĿŠijDžîŕŕ Figure 40.1 ¹ƙČîŠĿŠƥĺĚîNJĿîŕƎŕîŠĚ
DžĿƥĺĿŠɈîƑūƭŠēƎîŠČƑĚîƙ ēĚŞūŠƙƥƑîƥĿŠijîƎîŠČƑĚîƥĿČƎƙĚƭēūČNjƙƥɍ
ƒ îŕČĿǶČîƥĿūŠƙ
ƒ TIJƎƑĚƙĚŠƥɈČūŞƎŕĿČîƥĿūŠƙŞîNjċĚDŽĿƙƭîŕĿǕĚē

Ultrasound TREATMENT
ƒ ×ĿƙƭîŕĿǕîƥĿūŠūIJĺNjƎūĚČĺūĿČɓîŠĚČĺūĿČČNjƙƥĿČ
ǷƭĿēČūŕŕĚČƥĿūŠƙ ƒ TŠĿƥĿîŕŕNj
Ɠ ūDžĚŕƑĚƙƥɈƥūƥîŕƎîƑĚŠƥĚƑîŕŠƭƥƑĿƥĿūŠ
MRI ɚ¹¡sɛɈūċƙĚƑDŽîƥĿūŠ
ƒ sūƥŠĚČĚƙƙîƑNjɈċƭƥƭƙĚIJƭŕIJūƑēĿƙƥĿŠijƭĿƙĺĿŠij
IJƑūŞūƑijîŠĿǕĚēŠĚČƑūƙĿƙ
SURGERY
ƒ TIJƙNjŞƎƥūŞƙēūŠūƥĿŞƎƑūDŽĚ
LAB RESULTS Ɠ ¬ƭƑijĿČîŕēƑîĿŠîijĚƥūĚƙƥîċŕĿƙĺ
ČūŠŠĚČƥĿūŠDžĺĿČĺēƑîĿŠƙ
NjƙƥǷƭĿēîŠîŕNjƙĿƙ
ƎƙĚƭēūČNjƙƥĿČǷƭĿēĿŠƥūƙŞîŕŕĿŠƥĚƙƥĿŠĚ
ƒ ¹ūēĿƙƥĿŠijƭĿƙĺIJƑūŞƥƭŞūƑ ɚČNjƙƥūŏĚŏƭŠūƙƥūŞNjɛɈƙƥūŞîČĺ
Ɠ ĻČîƑČĿŠūĚŞċƑNjūŠĿČîŠƥĿijĚŠɚ /ɛ ɚČNjƙƥūijîƙƥƑūƙƥūŞNjɛɈūƑēƭūēĚŠƭŞ
Ɠ ĹČŞNjŕîƙĚ ɚČNjƙƥūēƭūēĚŠūƙƥūŞNjɛ
Ɠ ĻČŕƭĿēDŽĿƙČūƙĿƥNj ƒ /ŠēūƙČūƎĿČēƑîĿŠîijĚ

346 OSMOSIS.ORG
 Chapter 40 ¡îŠČƑĚîƥĿƥĿƙ

PANCREATITIS (ACUTE)
osms.it/acute-pancreatitis
Alcohol
PATHOLOGY & CAUSES ƒ TŠČƑĚîƙĚƙǕNjŞūijĚŠƙĚČƑĚƥĿūŠɒēĚČƑĚîƙĚƙ
ǷƭĿēɈċĿČîƑċūŠîƥĚƎƑūēƭČƥĿūŠĺƎîŠČƑĚîƥĿČ
ƒ ¬ƭēēĚŠĿŠǷîƥĿūŠūIJƎîŠČƑĚîƙēƭĚ ŏƭĿČĚƙċĚČūŞĚƥĺĿČŒɈDŽĿƙČūƭƙĺƎîŠČƑĚîƥĿČ
ƥūîƭƥūēĿijĚƙƥĿūŠĺƑĚDŽĚƑƙĿċŕĚƎîŠČƑĚîƥĿČ ēƭČƥċŕūČŒĚē
ĿŠŏƭƑNjɍ
ƒ ¬ƥĿŞƭŕîƥĚƙƑĚŕĚîƙĚūIJĿŠǷîƥūƑNj
ČNjƥūŒĿŠĚƙ
TYPES ƒ ~NJĿēîƥĿDŽĚŞĚƥîċūŕĿƙŞƎƑūēƭČĚƙIJƑĚĚ
ƑîēĿČîŕƙ
qĿŕē
ƒ TŠǷîƥĿūŠɈƎîƑĚŠČĺNjŞîŕĚēĚŞîɈ Gallstones
ƎĚƑĿƎîŠČƑĚîƥĿČIJîƥŠĚČƑūƙĿƙ ƒ gūēijĚîƥ~ēēĿƙƎĺĿŠČƥĚƑĺƎîŠČƑĚîƥĿČēƭČƥ
ċŕūČŒĚē
Severe
ƒ ¡îƑĚŠČĺNjŞîŕŠĚČƑūƙĿƙɈĺĚŞūƑƑĺîijĚ Alcohol and gallstones
ƒ ¡îŠČƑĚîƥĿČēƭČƥċŕūČŒĚēĺƎîŠČƑĚîƥĿČ
CAUSES ŏƭĿČĚƙċîČŒƭƎĺƎƑĚƙƙƭƑĚĿŠČƑĚîƙĚƙĺ
ǕNjŞūijĚŠijƑîŠƭŕĚƙIJƭƙĚDžĿƥĺŕNjƙūƙūŞĚƙ
ƒ ¬ĚĚŞŠĚŞūŠĿČIJūƑƙƭŞŞîƑNjūIJČîƭƙĚƙ
ĺƥƑNjƎƙĿŠūijĚŠƥƑîŠƙIJūƑŞƙĿŠƥūîČƥĿDŽîƥĚē
ƥƑNjƎƙĿŠĺēĿijĚƙƥĿDŽĚĚŠǕNjŞĚîČƥĿDŽîƥĿūŠɈ
îƭƥūēĿijĚƙƥĿūŠ
MNEMONIC: I GET
SMASHED RISK FACTORS
îƭƙĚƙūIJČƭƥĚƎîŠČƑĚîƥĿƥĿƙ ƒ ĿūŕūijĿČîŕŕNjŞîŕĚƥūċĿūŕūijĿČîŕŕNjIJĚŞîŕĚɈȂɇȄ
IēĿūƎîƥĺĿČ ƒ ¬ŞūŒĿŠij
GîŕŕƙƥūŠĚƙ
EƥĺîŠūŕîċƭƙĚ COMPLICATIONS
TƑîƭŞî ƒ qūƙƥūIJƥĚŠ
SƥĚƑūĿēƙ Ɠ ČƭƥĚƎƙĚƭēūČNjƙƥɈĿŠƥƑîɠîċēūŞĿŠîŕ
MƭŞƎƙĿŠIJĚČƥĿūŠ ĿŠIJĚČƥĿūŠɈƎîŠČƑĚîƥĿČîċƙČĚƙƙɈ
AŕČūĺūŕîċƭƙĚ ēĿƙƙĚŞĿŠîƥĚēĿŠƥƑîDŽîƙČƭŕîƑČūîijƭŕîƥĿūŠ
SČūƑƎĿūŠƙƥĿŠij ɚ'T ɛɈĿŠƥĚƑŠîŕƎîŠČƑĚîƥĿČǶƙƥƭŕî
HNjƎĚƑƥƑĿijŕNjČĚƑĿēĚŞĿîɈ ƒ ¬ĚDŽĚƑĚŞîŠĿIJĚƙƥîƥĿūŠƙ
ĺNjƎĚƑČîŕČĚŞĿî Ɠ ČƭƥĚƑĚƙƎĿƑîƥūƑNjēĿƙƥƑĚƙƙƙNjŠēƑūŞĚ
EŠēūƙČūƎĿČƑĚƥƑūijƑîēĚ ɚ¤'¬ɛɈîČƭƥĚƑĚŠîŕIJîĿŕƭƑĚɈĺĚŞūƑƑĺîijĚɈ
ČĺūŕîŠijĿūƎîŠČƑĚîƥūijƑîƎĺNj ĺNjƎūƥĚŠƙĿDŽĚƙĺūČŒ
DƑƭijƙɇƙƭŕIJîēƑƭijƙɈƑĚDŽĚƑƙĚɠ
ƥƑîŠƙČƑĿƎƥîƙĚĿŠĺĿċĿƥūƑƙɈ
ƎƑūƥĚîƙĚĿŠĺĿċĿƥūƑƙ

OSMOSIS.ORG 347
 SIGNS & SYMPTOMS TREATMENT
ƒ ċēūŞĿŠîŕƎîĿŠɒŕūƙƙūIJîƎƎĚƥĿƥĚɒƎîŕƎîċŕĚɈ MEDICATIONS
ƥĚŠēĚƑŞîƙƙ ƒ ¡îĿŠŞîŠîijĚŞĚŠƥɈĺNjēƑîƥĿūŠɈĚŕĚČƥƑūŕNjƥĚƙ
ƒ ƭŕŕĚŠɫƙƙĿijŠ ƒ ONjƎĚƑċîƑĿČūNJNjijĚŠƥĺĚƑîƎNjɈîŠƥĿċĿūƥĿČƙ
Ɠ ¡ĚƑĿƭŞċĿŕĿČîŕƑĚijĿūŠċƑƭĿƙĿŠij
ƒ HƑĚNj¹ƭƑŠĚƑɫƙƙĿijŠ SURGERY
Ɠ ƑƭĿƙĿŠijîŕūŠijǷ ƒ sĚČƑūƙĚČƥūŞNj

OTHER INTERVENTIONS
ƒ ¹ūƥîŕƑĚƙƥƑĿČƥĿūŠūIJIJūūēĿŠƥîŒĚɈîŕČūĺūŕ
ČĚƙƙîƥĿūŠ
ƒ /ŠēūƙČūƎĿČƑĚƥƑūijƑîēĚ
ČĺūŕîŠijĿūƎîŠČƑĚîƥūijƑîƎĺNjɚ/¤ ¡ɛ

Figure 40.2 ƭŕŕĚŠɫƙƙĿijŠɍTŠēĿDŽĿēƭîŕ

ƎƑĚƙĚŠƥĚēDžĿƥĺîIJūƭƑɠēîNjĺĿƙƥūƑNjūIJ
îċēūŞĿŠîŕƎîĿŠIJūŕŕūDžĿŠijîŠîŕČūĺūŕċĿŠijĚɍ

DIAGNOSIS
DIAGNOSTIC IMAGING
CT scan
ƒ ×ĿƙƭîŕĿǕîƥĿūŠūIJĿŠǷîƥĿūŠɈŠĚČƑūƙĿƙɈ
îċƙČĚƙƙɈƎîŠČƑĚîƥĿČƎƙĚƭēūČNjƙƥƙ

Ultrasound Figure 40.3 ¹ƙČîŠĿŠƥĺĚîNJĿîŕƎŕîŠĚ

ƒ HîŕŕƙƥūŠĚƙ ēĚŞūŠƙƥƑîƥĿŠijîČƭƥĚƎîŠČƑĚîƥĿƥĿƙɍ¹ĺĚƑĚ
ĿƙēĿIJIJƭƙĚĚŠŕîƑijĚŞĚŠƥūIJƥĺĚƎîŠČƑĚîƙ
îƙƙūČĿîƥĚēDžĿƥĺƎĚƑĿƎîŠČƑĚîƥĿČǷƭĿēɍ
LAB RESULTS
ƒ /ŕĚDŽîƥĚēƙĚƑƭŞîŞNjŕîƙĚɈŕĿƎîƙĚɈċĿŕĿƑƭċĿŠ

OTHER DIAGNOSTICS
OĿƙƥūŕūijNj
ƒ qĿČƑūDŽîƙČƭŕîƑĚēĚŞîɒIJîƥƥĿƙƙƭĚŠĚČƑūƙĿƙɒ
îČƭƥĚĿŠǷîƥĿūŠɒēĚƙƥƑƭČƥĿūŠūIJ
ƎîƑĚŠČĺNjŞîɈċŕūūēDŽĚƙƙĚŕƙɒĿŠƥĚƑƙƥĿƥĿîŕ
ĺĚŞūƑƑĺîijĚ

348 OSMOSIS.ORG
 Chapter 40 ¡îŠČƑĚîƥĿƥĿƙ

PANCREATITIS (CHRONIC)
osms.it/chronic-pancreatitis
MNEMONIC: TIGAR-O
PATHOLOGY & CAUSES îƭƙĚƙūIJ ĺƑūŠĿČ
ƎîŠČƑĚîƥĿƥĿƙ
ƒ ¡ĚƑƙĿƙƥĚŠƥɈČĺƑūŠĿČĿŠǷîƥĿūŠūIJ
TūNJĿŠƙɇČĺƑūŠĿČîŕČūĺūŕĿƙŞ
ƎîŠČƑĚîƙēƭĚƥūîƭƥūēĿijĚƙƥĿūŠ ĺ
ĿƑƑĚDŽĚƑƙĿċŕĚĿŠŏƭƑNjūIJĚNJūČƑĿŠĚɈĚŠēūČƑĿŠĚ IēĿūƎîƥĺĿČ
ƎîŠČƑĚîƙ GĚŠĚƥĿČ
ƒ GĿċƑūƙĿƙɈČîŕČĿǶČîƥĿūŠ AƭƥūĿŞŞƭŠĚ
Ɠ ¡ƑūŕūŠijĚēĿŠǷîƥĿūŠƎƑūēƭČĚƙ RĚČƭƑƑĚŠƥîČƭƥĚƎîŠČƑĚîƥĿƥĿƙ
ǶċƑūijĚŠĿČČNjƥūŒĿŠĚƙɈƥƑîŠƙIJūƑŞĿŠij OċƙƥƑƭČƥĿūŠɇijîŕŕƙƥūŠĚƙɈ
ijƑūDžƥĺIJîČƥūƑċĚƥîɚ¹HGɠċĚƥîɛɈƎŕîƥĚŕĚƥɠ ƎîŠČƑĚîƥĿČĺĚîēƥƭŞūƑ
ēĚƑĿDŽĚēijƑūDžƥĺIJîČƥūƑɚ¡'HGɛĺ
îČƥĿDŽîƥĚƙŞNjūǶċƑūċŕîƙƥƙĺČūŕŕîijĚŠ
ƎƑūēƭČƥĿūŠɈǶċƑūƙĿƙ
Ɠ Early stages: gîŠijĚƑĺîŠƙĿƙŕĚƥƙŠūƥ
SIGNS & SYMPTOMS
îIJIJĚČƥĚē
ƒ ¬ĚDŽĚƑĚîċēūŞĿŠîŕƎîĿŠƑîēĿîƥĚƙƥūċîČŒɒ
Ɠ Advanced: îƥƑūƎĺNjɈǶċƑūƙĿƙūIJĿƙŕĚƥƙ
ŠîƭƙĚîɒDŽūŞĿƥĿŠijɒƙƥĚîƥūƑƑĺĚîɒDžĚĿijĺƥŕūƙƙɒ
ĚēĚŞîēƭĚƥūŞîŕîċƙūƑƎƥĿūŠ
CAUSES
ƒ ¬ĚĚŞŠĚŞūŠĿČIJūƑƙƭŞŞîƑNjūIJČîƭƙĚƙ
ƒ HĚŠĚƥĿČ DIAGNOSIS
Ɠ Hereditary chronic pancreatitis:
DIAGNOSTIC IMAGING
îƭƥūƙūŞîŕɠēūŞĿŠîŠƥēĿƙĚîƙĚēƭĚƥū
ŞƭƥîƥĿūŠƙĿŠČîƥĿūŠĿČƥƑNjƎƙĿŠūijĚŠijĚŠĚ CT scan
Ɠ NjƙƥĿČǶċƑūƙĿƙɇČNjƙƥĿČǶċƑūƙĿƙ ƒ ×ĿƙƭîŕĿǕîƥĿūŠūIJƎîŠČƑĚîƥĿČēƭČƥƙēĿŕîƥîƥĿūŠɈ
ƥƑîŠƙŞĚŞċƑîŠĚČūŠēƭČƥîŠČĚƑĚijƭŕîƥūƑ ČîŕČĿǶČîƥĿūŠƙɈîƥƑūƎĺNjɈƎƙĚƭēūČNjƙƥƙ
ɚ G¹¤ɛŞƭƥîƥĿūŠĺēĚČƑĚîƙĚē
ċĿČîƑċūŠîƥĚƙĚČƑĚƥĿūŠĺƎîŠČƑĚîƥĿČēƭČƥ Ultrasound
ƎŕƭijijĚēɈūċƙƥƑƭČƥĚē ƒ ONjƎĚƑĚČĺūijĚŠĿČĿƥNjɚǶċƑūƙĿƙɛɈƎƙĚƭēūČNjƙƥƙɈ
ƒ ƭƥūĿŞŞƭŠĚ ƎƙĚƭēūîŠĚƭƑNjƙŞƙɈîƙČĿƥĚƙ
Ɠ 'ĿƙƥĿŠČƥIJūƑŞūIJČĺƑūŠĿČƎîŠČƑĚîƥĿƥĿƙĺ
/¤ ¡ɓŞîijŠĚƥĿČƑĚƙūŠîŠČĚČĺūŕîŠijĿūƎîŠɠ
ŞîŠĿIJĚƙƥîƥĿūŠūIJĿŞŞƭŠūijŕūċƭŕĿŠHɚTijHɛ
creatography (MRCP)
ƑĚŕîƥĚēēĿƙĚîƙĚ
ƒ ×ĿƙƭîŕĿǕîƥĿūŠūIJƎîŠČƑĚîƥĿČēƭČƥƙɒČĺîĿŠɠūIJɠ
ŕîŒĚƙƎîƥƥĚƑŠēƭĚƥūîŕƥĚƑŠîƥĿŠijƙƥĚŠūƙĿƙɈ
COMPLICATIONS ēĿŕîƥĿūŠ
ƒ ¡îŠČƑĚîƥĿČƎƙĚƭēūČNjƙƥɒîƙČĿƥĚƙɒƎîŠČƑĚîƥĿČ
ĿŠƙƭIJǶČĿĚŠČNjɒēĿîċĚƥĚƙŞĚŕŕĿƥƭƙɒDŽĿƥîŞĿŠƙɈ
'Ɉ/ɈeēĚǶČĿĚŠČNjɒƎîŠČƑĚîƥĿČČîŠČĚƑ
LAB RESULTS
ƒ qĿŕēŕNjĚŕĚDŽîƥĚēƙĚƑƭŞîŞNjŕîƙĚɈîŕŒîŕĿŠĚ
ƎĺūƙƎĺîƥîƙĚɈċĿŕĿƑƭċĿŠ

OSMOSIS.ORG 349
 OTHER DIAGNOSTICS
OĿƙƥūŕūijNj
ƒ 'ĿŕîƥîƥĿūŠūIJƎîŠČƑĚîƥĿČēƭČƥƙɒîČĿŠîƑČĚŕŕ
îƥƑūƎĺNjɒǶċƑūƙĿƙɒČĺƑūŠĿČĿŠǷîƥūƑNj
ĿŠǶŕƥƑîƥĚɒƎƑūƥĚĿŠƎŕƭijƙɈČîŕČĿǶČîƥĿūŠƙ

TREATMENT
Figure 40.4¹ĺĚĺĿƙƥūŕūijĿČîŕîƎƎĚîƑîŠČĚūIJ
MEDICATIONS ƎîŠČƑĚîƥĿČIJîƥŠĚČƑūƙĿƙĿŠîČîƙĚūIJƙĚDŽĚƑĚ
ƒ ¡îĿŠŞîŠîijĚŞĚŠƥ ƎîŠČƑĚîƥĿƥĿƙɍ
ƒ ¡îŠČƑĚîƥĿČĚŠǕNjŞĚƑĚƎŕîČĚŞĚŠƥ

SURGERY
Endoscopy, surgery
ƒ ¤ĚƙĚČƥĿūŠîŕɓēƑîĿŠîijĚƎƑūČĚēƭƑĚƙIJūƑ
ƎƙĚƭēūČNjƙƥɈǶƙƥƭŕîɈîƙČĿƥĚƙ

OTHER INTERVENTIONS
ƒ ŕČūĺūŕČĚƙƙîƥĿūŠɈēĿĚƥîƑNjŞūēĿǶČîƥĿūŠƙ
ɚŕūDžɠIJîƥɛ

350 OSMOSIS.ORG
 NOTES

NOTES
PERITONEAL PATHOLOGY

GENERALLY, WHAT IS IT?

PATHOLOGY & CAUSES DIAGNOSIS
ƒ Conditions affecting peritoneal cavity (e.g. DIAGNOSTIC IMAGING
ƙĚƑūƙîŕŞĚŞċƑîŠĚĿŠǷîƥĿūŠɈijîƙɛ
X-ray
ƒ Peritonitis
CAUSES
Ɠ ¬ƭƎĿŠĚɈƭƎƑĿijĺƥîċēūŞĿŠîŕǶŕŞƙ
Peritonitis ƒ Pneumoperitoneum
ƒ Spontaneous bacterial peritonitis Ɠ Upright chest radiography
ƒ Leakage of gastrointestinalɚHTɛcontents Ɠ Subdiaphragmatic free gas; cupola sign
ƒ Presence of foreign material Ɠ ¤ĿijŕĚƑɫƙƙĿijŠɈIJūūƥċîŕŕƙĿijŠ
Ɠ ĿŕĚɈċŕūūēɈČūŠƥƑîƙƥŞîƥĚƑĿîŕ Ɠ Lateral decubitus X-ray
ƒ Endometriosis
CT scan
ƒ Peritoneal dialysis
ƒ Pneumoperitoneum
Pneumoperitoneum Ɠ Small quantities of air
ƒ Perforation of anterior duodenal ulcer
ƒ Iatrogenic LAB RESULTS
ƒ Increased intrathoracic pressure
Paracentesis
ƒ Peritonitis
SIGNS & SYMPTOMS Ɠ If ascites present

Peritonitis Complete blood count (CBC)

ƒ GĚDŽĚƑɈČĺĿŕŕƙɈƥîČĺNjČîƑēĿî Blood chemistry
ƒ AscitesɈîċēūŞĿŠîŕēĿƙƥĚŠƥĿūŠɈîċēūŞĿŠîŕ
ƑĿijĿēĿƥNjɈƙƎĿēĚƑîŠijĿūŞîƥîɈŏîƭŠēĿČĚ
ƒ ŠūƑĚNJĿîɈŠîƭƙĚîɈDŽūŞĿƥĿŠijɈēĿîƑƑĺĚî TREATMENT
ƒ /ŠČĚƎĺîŕūƎîƥĺNjɒēĚŕĿƑĿƭŞɈČūŠIJƭƙĿūŠɈ
cognitive decline MEDICATIONS
ƒ ċƙĚŠƥċūDžĚŕƙūƭŠēƙɈĿŕĚƭƙ ƒ Systemic antibiotics

Pneumoperitoneum
SURGERY
ƒ ċēūŞĿŠîŕƎîĿŠɈƑĿijĿēĿƥNj
ƒ Exploratory laparotomy
ƒ ċƙĚŠƥċūDžĚŕƙūƭŠēƙɈĿŕĚƭƙ

OSMOSIS.ORG 351
 PERITONITIS
osms.it/peritonitis

PATHOLOGY & CAUSES DIAGNOSIS

ƒ TŠǷîƥĿūŠ of serosal membrane DIAGNOSTIC IMAGING
liningîċēūŞĿŠîŕČîDŽĿƥNjɈūƑijîŠƙɚe
ƎĚƑĿƥūŠĚƭŞɛɍ ¬ƭƎĿŠĚɈƭƎƑĿijĺƥîċēūŞĿŠîŕǶŕŞƙ
ƒ sĚƭƥƑūƎĺĿŕĿČĿŠǶŕƥƑîƥĿūŠɈIJūƑŞîƥĿūŠūIJ ƒ ¬ƭċĺĚƎîƥĿČɓƙƭċēĿîƎĺƑîijŞîƥĿČIJƑĚĚîĿƑɈ
ǶċƑĿŠūƎƭƑƭŕĚŠƥĚNJƭēîƥĚ abscesses in case of perforated viscus

CAUSES LAB RESULTS

ƒ Spontaneous bacterial peritonitis ƒ gĚƭŒūČNjƥūƙĿƙɈîČĿēūƙĿƙ
Ɠ Bacterial migration from GI lumen; more Paracentesis
common in people with ascites/cirrhosis
ƒ If ascites present
Ɠ E. coli, Klebsiella, Pseudomonas,
ƒ ¬ĚƑƭŞîƙČĿƥĚƙîŕċƭŞĿŠijƑîēĿĚŠƥɚ¬Hɛ
ProteusɈHƑîŞɠŠĚijîƥĿDŽĚƙ
Ɠ > 1.1 in spontaneous bacterial
ƒ Leakage of GI contents; most common;
peritonitis
perforated viscera
ƒ Neutrophil count > 250 cells/microliter
Ɠ Proximal GI tract perforation ĺ Gram-
positive bacteria
Ɠ Distal GI tract perforation ĺ Gram- TREATMENT
negative bacteria
ƒ Foreign material MEDICATIONS
Ɠ ĿŕĚɈċŕūūēɈČūŠƥƑîƙƥŞîƥĚƑĿîŕ
Systemic antibiotics
ƒ Endometriosis
ƒ Third generation cephalosporins/quinolones
ƒ Peritoneal dialysis

SIGNS & SYMPTOMS

ƒ GĚDŽĚƑɈČĺĿŕŕƙɈƥîČĺNjČîƑēĿî
ƒ ƙČĿƥĚƙɈîċēūŞĿŠîŕēĿƙƥĚŠƥĿūŠɈîċēūŞĿŠîŕ
ƑĿijĿēĿƥNjɈƙƎĿēĚƑîŠijĿūŞîƥîɈŏîƭŠēĿČĚ
ƒ ŠūƑĚNJĿîɈŠîƭƙĚîɈDŽūŞĿƥĿŠijɈēĿîƑƑĺĚîĺ
ĺNjƎūDŽūŕĚŞĿîɈƑĚŠîŕIJîĿŕƭƑĚ
ƒ ċƙĚŠƥċūDžĚŕƙūƭŠēƙɈĿŕĚƭƙ
ƒ Early stages
Ɠ 'ƭŕŕɈƎūūƑŕNjŕūČîŕĿǕĚēîċēūŞĿŠîŕƎîĿŠ
ƒ Late stages
Ɠ ¬ĚDŽĚƑĚɈŕūČîŕĿǕĚēîċēūŞĿŠîŕƎîĿŠɒîČƭƥĚ
abdomen Figure 41.1 The histological appearance
ƒ /ŠČĚƎĺîŕūƎîƥĺNjɒēĚŕĿƑĿƭŞɈČūŠIJƭƙĿūŠɈ ūIJƥƭċĚƑČƭŕūƭƙƎĚƑĿƥūŠĿƥĿƙɈîƑîƑĚŒĿŠēūIJ
cognitive decline peritonitis. There are numerous epithelioid
ŞîČƑūƎĺîijĚƙîŠēijĿîŠƥČĚŕŕƙĿŠǶŕƥƑîƥĿŠijƥĺĚ
peritoneal biopsy.

352 OSMOSIS.ORG
 Chapter 41 Peritoneal Pathology

Figure 41.2 An abdominal CT scan with oral

contrast in the axial plane demonstrating
severe peritonitis. There is diffuse peritoneal
thickening and large amounts of radiodense
ǷƭĿēɍ~ŠŕîƎîƑūƥūŞNjƥĺĿƙDžîƙēĿƙČūDŽĚƑĚēƥū
be pus.

PNEUMOPERITONEUM
osms.it/pneumoperitoneum

PATHOLOGY & CAUSES DIAGNOSIS

ƒ Abnormal collection of gas within DIAGNOSTIC IMAGING
peritoneal cavity.
CT scan
ƒ Small quantities of air
CAUSES
ƒ Most common Upright chest radiography
Ɠ Perforation of anterior duodenal ulcer ƒ Subdiaphragmatic free gas; Cupola sign
secondary to peptic ulcer disease ɚIJƑĚĚĿŠƥƑîƎĚƑĿƥūŠĚîŕîĿƑɈDžĚŕŕɠēĚǶŠĚē
ƒ Iatrogenic ƙƭƎĚƑĿūƑċūƑēĚƑIJūƑŞĚēċNjēĿîƎĺƑîijŞɛ
Ɠ Abdominal surgery; resolves Supine abdominal X-ray
spontaneously
ƒ ¤ĿijŕĚƑɫƙƙĿijŠɚēūƭċŕĚDžîŕŕƙĿijŠɛɇċūƥĺƙĿēĚƙ
ƒ Increased intrathoracic pressure of abdominal wall visible
ɚŞĚČĺîŠĿČîŕDŽĚŠƥĿŕîƥĿūŠɈČĺĚƙƥ
ƒ GūūƥċîŕŕƙĿijŠɚŞîƙƙĿDŽĚƎŠĚƭŞūƎĚƑĿƥūŠĚƭŞɛɇ
ČūŞƎƑĚƙƙĿūŠƙɛ
ellipsoid shape of abdominal cavity outlined
by gas
SIGNS & SYMPTOMS Lateral decubitus X-ray
ƒ GƑĚĚijîƙċĚƥDžĚĚŠŕĿDŽĚƑɈîċēūŞĿŠîŕDžîŕŕ
ƒ ċēūŞĿŠîŕƎîĿŠɈƑĿijĿēĿƥNj
ƒ ċƙĚŠƥċūDžĚŕƙūƭŠēƙɈĿŕĚƭƙ

OSMOSIS.ORG 353
 TREATMENT
SURGERY
Exploratory laparotomy
ƒ Repair perforated viscus

Figure 41.3 A CT scan in the axial plane

demonstrating air in the peritoneal cavity.
The air has also tracked along an umbilical
hernia.

Figure 41.4 An erect chest radiograph

demonstrating a sub-diaphragmatic air
ċƭċċŕĚɈēĿîijŠūƙƥĿČūIJƎŠĚƭŞūƎĚƑĿƥūŠĚƭŞɍ

354 OSMOSIS.ORG
 NOTES

NOTES
RECTAL & ANAL PATHOLOGY

GENERALLY, WHAT IS IT?

PATHOLOGY & CAUSES DIAGNOSIS
ƒ Diseases affecting rectum and anal region ƒ History, physical examination

COMPLICATIONS TREATMENT
ƒ Discomfort during defecation, itching, pain,
bleeding ƒ Change dietary/defecation habits,
pharmacological, surgical
SIGNS & SYMPTOMS
ƒ Visible abnormalities

ANAL FISSURE
osms.it/anal-fissure
COMPLICATIONS
PATHOLOGY & CAUSES ƒ Fecal bacteria infection
ƒ ŠîŕŞƭČūƙîŕĿŠĚîƑǶƙƙƭƑĚ
ƒ Hard bowel movement ĺ anal mucosa SIGNS & SYMPTOMS
stretches ĺîČƭƥĚǶƙƙƭƑĚĺ internal anal
sphincter spasms ĺċŕūūēǷūDžƑĚēƭČĚƙĺ ƒ Midline tear
ēĿIJǶČƭŕƥĺĚîŕĿŠijĺČĺƑūŠĿČǶƙƙƭƑĚ
ƒ Pain during bowel movements ĺ fear of
ƒ Midline, anteriorly/posteriorly defecation ĺ constipation ĺ harder stool
ĺ more pain
RISK FACTORS ƒ ŕūūēon toilet paper/stool
ƒ gūDžǶċĚƑēĿĚƥ
ƒ Diarrhea
DIAGNOSIS
ƒ Previous anal surgery
ƒ Anal trauma ƒ History, examination of anal region/rectum
ƒ Abnormalities in internal anal sphincter
ƒ Sexually transmitted infections (STIs)
Ɠ Human papillomavirus (HPV), herpes,
chlamydia
ƒ TŠǷîƥūƑNjċūDžĚŕēĿƙĚîƙĚɚT'ɛ

OSMOSIS.ORG 355
 TREATMENT
MEDICATIONS
ƒ Stool softeners
ƒ Topical nitrates/calcium channel blocker (e.g
diltiazem)

SURGERY
ƒ Sphincterotomy

OTHER INTERVENTIONS
ƒ Proper anal hygiene Figure 42.1 The clinical appearance of an anal
ƒ Warm bath (AKA sitz bath) ǶƙƙƭƑĚîIJIJĚČƥĿŠijƥĺĚƎūƙƥĚƑĿūƑîŠîŕŞƭČūƙîɍ
ƒ Muscle relaxation ĺ increase healing
mechanisms
ƒ Fiber supplementation

ANAL FISTULA
osms.it/anal-fistula
Extrasphincteric
PATHOLOGY & CAUSES ƒ Rectum/sigmoid colon ĺ levator muscle ani
ĺ skin
ƒ Abnormal communication between anal
canal, perianal skin
Ɠ Fistula: Latin (pipe, catheter), from ǶŠēū SIGNS & SYMPTOMS
(cleave, divide, split)
ƒ Foreign material in anal crypts ĺ anal ƒ ¬ŒĿŠĚNJČūƑĿîƥĿūŠƙɈƎƭƙɓƙĚƑūƭƙǷƭĿēɓIJĚČĚƙ
glands ducts blocked ĺ anal abscess ĺ draining from skin-opening, bleeding,
pus travels to skin through tract itching, pain, redness, swelling

TYPES
DIAGNOSIS
Intersphincteric
ƒ Internal anal sphincter ĺ space between OTHER DIAGNOSTICS
internal, external anal sphincters (AKA ƒ Anal examination ĺ delineate course of
intersphincteric plane) ĺ skin Ƕƙƥƭŕî

¹ƑîŠƙƙƎĺĿŠČƥĚƑĿČɚÀɠƙĺîƎĚēǶƙƥƭŕîɛ
ƒ Internal anal sphincter ĺ intersphincteric TREATMENT
plane ĺ external anal sphincter ĺ skin
SURGERY
¬ƭƎƑîƙƎĺĿŠČƥĚƑĿČ
ƒ Drain infection ĺĚƑîēĿČîƥĚǶƙƥƭŕūƭƙƥƑîČƥ
ƒ Internal anal sphincter ĺ puborectalis ĺ preserve anal sphincter function ĺ avoid
muscle ĺ space between puborectalis, recurrences
levator ani muscle ĺ skin

356 OSMOSIS.ORG
 Chapter 42 Rectal & Anal Pathology

Figure 42.2 Surgical wound following

ƑĚŞūDŽîŕūIJîŠîŠîŕǶƙƥƭŕîɍ

HEMORRHOID
osms.it/hemorrhoid
COMPLICATIONS
PATHOLOGY & CAUSES
TŠƥĚƑŠîŕĺĚŞūƑƑĺūĿēƙ
ƒ Anal cushions hypertrophy due to ƒ ŕĚĚēĿŠijDžĿƥĺċūDžĚŕŞūDŽĚŞĚŠƥƙ
supportive tissue deterioration ƒ Prolapsing
ƒ Incarceration, strangulation ĺ pain
TYPES ƒ Mucus deposits on perianal tissue ĺ
itching
TŠƥĚƑŠîŕ
ƒ Affecting hemorrhoidal venous cushions /NJƥĚƑŠîŕĺĚŞūƑƑĺūĿēƙ
above dentate line ƒ ŕĚĚēĿŠij
Ɠ Grade I: bleed but not prolapse ƒ Acute thrombosis ĺ acute pain
Ɠ Grade II: prolapse on straining but ƒ Itching
reduce spontaneously ƒ ONjijĿĚŠĚēĿIJǶČƭŕƥĿĚƙ
Ɠ Grade III: prolapse on straining, require
manual reduction
Ɠ Grade IV: spontaneous, irreducible SIGNS & SYMPTOMS
prolapse
ƒ Itching
/NJƥĚƑŠîŕ
ƒ ŕĚĚēĿŠijîƙƙūČĿîƥĚēDžĿƥĺċūDžĚŕŞūDŽĚŞĚŠƥ
ƒ Affecting hemorrhoidal venous cushions ĺ bright red blood on toilet paper
below dentate line
ƒ Pain
ƒ Mucous discharge
RISK FACTORS ƒ Perianal mass in case of prolapse
ƒ ConstipationɚŕūDžǶċĚƑēĿĚƥɛɈƙƥƑĚŠƭūƭƙ
defecation, diarrhea, prolonged sitting,
aging, increased intra-abdominal pressure,
pregnancy, intra-abdominal mass, ascites,
portal hypertension

OSMOSIS.ORG 357
 DIAGNOSIS TREATMENT
DIAGNOSTIC IMAGING MEDICATIONS
ƒ Anoscopy for internal hemorrhoids ƒ Stool softeners
ƒ Topical, systemic analgesics
OTHER DIAGNOSTICS
ƒ Anal, perianal inspection SURGERY
ƒ Digital rectal examination ƒ Sclerotherapy, rubber band ligation, infrared
coagulation

OTHER INTERVENTIONS
ƒ TŠČƑĚîƙĚǶċĚƑɈǷƭĿēĿŠƥîŒĚ

Figure 42.3 The histological appearance

of an excised hemorrhoid. There is
ǶċƑūŞƭƙČƭŕîƑĺNjƎĚƑƎŕîƙĿîîŠēŠƭŞĚƑūƭƙ
dilated vascular spaces.

Figure 42.4 External appearance of grade 2

hemorrhoids.

RECTAL PROLAPSE
osms.it/rectal-prolapse

PATHOLOGY & CAUSES SIGNS & SYMPTOMS

ƒ Partial/total slip of rectal tissue through anal ƒ Mass protruding through anus
ūƑĿǶČĚ Ɠ After defecation; when sneezing/
coughing; when walking ĺ pain, rectal
RISK FACTORS bleeding, incontinence
ƒ Constipation, diarrhea, pregnancy, pelvic
ǷūūƑēîŞîijĚ

COMPLICATIONS
ƒ Mucous discharge, bleeding, fecal
incontinence, constipation, rectal ulceration

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DIAGNOSIS TREATMENT
OTHER DIAGNOSTICS SURGERY
ƒ Physical examination ƒ Sutures/mesh slings to anchor rectum to
Ɠ Prolapse clearly evident posterior wall of pelvis (sacrum)
Ɠ Open or laparoscopic
ƒ Rectosigmoidectomy
Ɠ Part of rectum and sigmoid pulled
through anus and removed,
reanastomosis of remaining rectum to
colon
Ɠ Usually reserved for severe prolapse/
non-candidates for open/laparoscopic
procedure

OTHER INTERVENTIONS
ƒ OĿijĺǶċĚƑēĿĚƥɈĚŠĚŞîƙɈƙƭƎƎūƙĿƥūƑĿĚƙɚƥū
avoid constipation/straining)
Figure 42.5 A complete rectal prolapse. ƒ Kegel exercises may help limit progression

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 NOTES

NOTES
UPPER GASTROINTESTINAL
CONGENITAL MALFORMATIONS

GENERALLY, WHAT ARE THEY?

PATHOLOGY & CAUSES DIAGNOSIS
ƒ Upper gastrointestinal tract structural/ DIAGNOSTIC IMAGING
functional anomalies during embryonic ƒ Prenatal ultrasound; MRI
development; present at birth ƒ X-ray/CT scan
Ɠ Avoid if possible due to teratogenicity
CAUSES
ƒ Genetic, environmental factors
TREATMENT
SIGNS & SYMPTOMS SURGERY
ƒ See individual disorders
ƒ May be asymptomatic/complete
dysfunction of gastrointestinal (GI), life OTHER INTERVENTIONS
incompatibility
ƒ Nasogastric intubation

CLEFT LIP & PALATE

osms.it/cleft-lip-and-palate
Combination (CLP, cheilopalatoschisis)
PATHOLOGY & CAUSES ƒ Most severe forms; split alveolar ridge,
uvula (cheilognathopalatoschisis)
ƒ Group of congenital malformations in upper
lip, oral cavity roof
ƒ Result of improper fusion of facial bones, RISK FACTORS
associated tissues ƒ Other inherited genetic disorders (e.g.
Patau syndrome, Stickler syndrome)
ƒ Environmental teratogenic factors
TYPES
(e.g. intrauterine hypoxia, pesticides,
ƒ Based on severity anticonvulsant medication, folate
Cleft lip (CL, cheiloschisis) ēĚǶČĿĚŠČNjɛ
ƒ Unilateral, bilateral “hare lip”
COMPLICATIONS
Cleft palate (CP, palatoschisis) ƒ Speech impediments, hearing issues/
ƒ Commonly uvula also split ƑĚČƭƑƑĚŠƥūƥĿƥĿƙŞĚēĿîɈēĿIJǶČƭŕƥNjĚîƥĿŠij

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 Chapter 43 Upper Gastrointestinal Congenital Malformations

OTHER INTERVENTIONS
SIGNS & SYMPTOMS ƒ Temporary prosthetic implants, until
surgery
ƒ ×ĚŕūƎĺîƑNjŠijĚîŕĿŠƙƭIJǶČĿĚŠČNj
ƒ Speech-language therapy
Ɠ Inability to temporarily stop physical
ƒ Folate supplementation during pregnancy
communication between oral, nasal
decreases risk
cavities
ƒ Dysphonia
Ɠ Air leaks to nasal cavity ĺ hypernasal
vocalization
ƒ Dysarthria
Ɠ Abnormal structure increases speech
ēĿIJǶČƭŕƥNjĺ distorted word structure
ƒ Nasal cavity infection
Ɠ Food trapped in nasal cavity ĺ
predisposes infection

DIAGNOSIS
DIAGNOSTIC IMAGING Figure 43.1 A cleft hard palate in an infant.

Prenatal ultrasound
ƒ Evaluation of integrity of nares, upper lip,
hard and soft palate
ƒ 3D reconstruction and surface rendering
allow for better diagnosis and help parents
prepare psychologically

MRI
ƒ Evaluation of associated extra/intracranial
abnormalities
ƒ ¡ƑĚŠîƥîŕq¤TîĿēƙĿŠČūŠǶƑŞîƥĿūŠîŠē
characterization/integrity of maxillary arch

CT scan/X-ray
ƒ Not typically used; 3D reconstructions can
aid in surgical planning

OTHER DIAGNOSTICS
ƒ Clinically evident at birth

TREATMENT
SURGERY Figure 43.2 A child with a unilateral,
ƒ Surgical closure of cleft lip by three months incomplete cleft lip.
of age
ƒ Timing for surgical closure of palate is
variable; usually done by one year of age

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 CONGENITAL DIAPHRAGMATIC
HERNIA (CDH)
osms.it/congenital-diaphragmatic-hernia
MNEMONIC: 5Bs
PATHOLOGY & CAUSES Bochdalek hernia features
Bochdalek hernia
ƒ Protrusion of abdominal viscera into chest
cavity Big
ƒ Results from abnormal development of Back and medial, usually left
diaphragm in utero side
ƒ High mortality rate Baby
ƒ Incomplete diaphragm formation ĺ Bad: associated with
abdominal organs protrude into chest pulmonary hypoplasia
cavity ĺ physical obstruction of heart,
lung formation/function ĺ pulmonary
ĺNjƎūƎŕîƙĿîɈƙƭƑIJîČƥîŠƥēĚǶČĿĚŠČNjɈ DIAGNOSIS
pulmonary hypertension, arrhythmia
DIAGNOSTIC IMAGING
TYPES
Prenatal ultrasound
Bochdalek hernia ƒ Polyhydramnios
ƒ Posterolateral diaphragmatic hernia; most ƒ Cardiomediastinal shift with possible
common CDH abnormal cardiac axis
Ɠ Viscera protrude through posterolateral ƒ Lack of visualization of normal stomach
segment of diaphragm bubble
Ɠ Left kidney, perinephric fat, stomach, ƒ Absent bowel loops in abdomen; stomach
small intestine and small bowel in thorax
ƒ Intrathoracic herniation of liver (seen in
Morgagni hernia
85%, poor prognosis)
ƒ Retrosternal, parasternal diaphragmatic
ƒ Peristaltic bowel movements in thorax
hernia
ƒ Reduced abdominal circumference
Ɠ Viscera protrude through foramina of
Morgagni (form sternocostal angle) X-ray
ƒ ĿŠēĿƙƥĿŠČƥēĿîƎĺƑîijŞɈūƎîČĿǶČîƥĿūŠūIJ
CAUSES hemithorax (typically left-sided)
ƒ Genetic, environmental factors
MRI
ƒ Helpful in further assessment of pulmonary
SIGNS & SYMPTOMS hypoplasia
ƒ Measurement of fetal lung volumes
ƒ Dyspnea, tachypnea, central cyanosis,
ƥîČĺNjČîƑēĿîɈƑĚƥƑîČƥĿūŠƙɈŠîƙîŕǷîƑĿŠijɈ
decreased/absent breath sounds on
affected side, scaphoid abdomen

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TREATMENT
SURGERY
ƒ Surgical repair of hernia

OTHER INTERVENTIONS
ƒ Planned delivery after week 37 of gestation
ĺ immediate intubation, mechanical
ventilation
ƒ Inhaled nitric oxide for severe pulmonary
hypertension
ƒ Nasogastric, pulmonary intubation

Figure 43.3 A plain X-ray of a newborn

demonstrating visible bowel loops in the
thoracic cavity.

ESOPHAGEAL WEB
osms.it/esophageal-web

PATHOLOGY & CAUSES SIGNS & SYMPTOMS

ƒ Rare narrowing of esophagus due to thin ƒ May be asymptomatic (if small)
membrane of esophageal tissues (mucosa, ƒ Dysphagia:ēĿIJǶČƭŕƥNjĿŠƙDžîŕŕūDžĿŠij
submucosa) ƒ Odynophagia: painful swallowing
ƒ Most commonly appear in lower third of ƒ Retrosternal pain: can be mistaken for
esophagus angina pectoris
ƒ Can be congenital/acquired
ƒ May occur as solitary disease
DIAGNOSIS
RISK FACTORS
OTHER DIAGNOSTICS
ƒ Plummer–Vinson syndrome
Ɠ ¬ĿēĚƑūƎĚŠĿČēNjƙƎĺîijĿîɈĿƑūŠɠēĚǶČĿĚŠČNj Fluoroscopy/barium swallow
anemia, glossitis, cheilosis, esophageal ƒ Visualized when esophagus is fully
webs distended with contrast
ƒ “Jet effect” of contrast being ejected distally
COMPLICATIONS from web
ƒ Food impaction, perforation by solid food/
esophageal probe insertion
TREATMENT
OTHER INTERVENTIONS
ƒ /ŠēūƙČūƎĿČēĿŕîƥĿūŠDŽĿîĿŠǷîƥĚēċîŕŕūūŠ

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 HYPERTROPHIC PYLORIC STENOSIS
osms.it/hypertrophic-pyloric-stenosis
Fluoroscopy
PATHOLOGY & CAUSES ƒ Delayed gastric emptying
ƒ Elongated pylorus with narrow lumen
ƒ Constriction of pylorus due to pyloric
sphincter hypertrophy ĺijîƙƥƑĿČūƭƥǷūDž ƒ Entrance to pylorus may be beak shaped
obstructed
ƒ Autosomal dominant/multifactorial
TREATMENT
RISK FACTORS SURGERY
ƒ Firstborn, biologically male, parents had ƒ Pyloromyotomy
hypertrophic pyloric stenosis, macrolide
exposure
OTHER INTERVENTIONS
ƒ Rehydration
COMPLICATIONS ƒ Regulate acid-base status, correct
ƒ Dehydration, malnourishment, acid-base electrolyte abnormalities
imbalance

SIGNS & SYMPTOMS

ƒ Projectile nonbilious vomiting at/soon after
birth
ƒ Visible peristalsis
ƒ Dehydrated, undernourished

DIAGNOSIS
DIAGNOSTIC IMAGING
X-ray
ƒ Distended stomach, minimal intestinal gas

Ultrasound
ƒ Modality of choice; but cannot exclude
midgut volvulus
ƒ Pyloric muscle thickness Figure 43.4 An abdominal radiograph
demonstrating a grossly dilated stomach,
OTHER DIAGNOSITCS secondary to obstructive pyloric stenosis.
ƒ Abdominal olive palpable on physical
examination

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THYROGLOSSAL DUCT CYST

osms.it/thyroglossal-duct-cyst
OTHER DIAGNOSTICS
PATHOLOGY & CAUSES ƒ Fluctuant mass palpable at a anterior
midline/paramedian location
ƒ Benign cyst; epithelium of unclosed
ƒ Draining sinus may be visible
thyroglossal duct
ƒ Thyroid cells migrate from foramen cecum
downward ĺ leave thyroglossal duct ĺ TREATMENT
thyroid duct stays open ĺǶŕŕƙDžĿƥĺŞƭČƭƙ
ĺ cyst forms SURGERY
ƒ Surgical excision (Sistrunk procedure)
COMPLICATIONS
ƒ Infection (spread from respiratory system),
ĿŠǷîƥĿūŠɈēĿƙČĺîƑijĿŠijƙĿŠƭƙDžĿƥĺƙŒĿŠ
ɚƙĚČūŠēîƑNjƥūĿŠǷîƥĿūŠɓƥƑîƭŞîɛɈƥĺNjƑūĿē
gland malformation (if thyroid cells remain
in thyroglossal duct/cyst), extrathyroid
thyroid carcinoma (from leftover thyroid
cells)

SIGNS & SYMPTOMS

ƒ Painless mass in front of neck, moves when Figure 43.5 The clinical appearance of a
ƙDžîŕŕūDžĿŠijɒĿŠǷîƥĿūŠɈƎîĿŠɒēNjƙƎĺîijĿîɒ thyroglossal duct cyst. There is a vague,
dyspnea ǷƭČƥƭîŠƥƙDžĚŕŕĿŠijĿŠƥĺĚŞĿēŕĿŠĚūIJƥĺĚŠĚČŒɍ

DIAGNOSIS
DIAGNOSTIC IMAGING
Ultrasound
ƒ GŕƭČƥƭîŠƥŞîƙƙǶŕŕĚēDžĿƥĺîŠĚČĺūĿČǷƭĿēɈ
thin walled, without vascularity

CT scan
ƒ ¹ĺĿŠɠDžîŕŕĚēɈDžĚŕŕɠēĚǶŠĚēĺūŞūijĚŠĚūƭƙɈ
ǷƭĿēēĚŠƙĚŕĚƙĿūŠƙɈîŠƥĚƑĿūƑŞĿēŕĿŠĚɓ
paramedian location
ƒ May demonstrate capsular enhancement
ƒ Sternocleidomastoid muscle may be
displaced posteriorly/posterolaterally
Figure 43.6 A CT scan of the head and
ƒ May be embedded in infrahyoid muscles neck in the sagittal plane demonstrating a
thyroglossal duct cyst adjacent to the hyoid
bone.

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 TRACHEOESOPHAGEAL FISTULA
osms.it/tracheoesophageal-fistula
COMPLICATIONS
PATHOLOGY & CAUSES ƒ Atresia (due to hydrochloric acid
accumulation),ijîƙƥƑūĚƙūƎĺîijĚîŕƑĚǷƭNJɈ
ƒ Pathologic communication between dysphagia, frequent respiratory infections
trachea, esophagus
ƒ Results from tracheoesophageal ridge
fusion failure SIGNS & SYMPTOMS
ƒ Occurs as congenital malformation/surgery
complication (later in life) ƒ Hypersalivation/drooling, choking, vomiting,
ƒ VACTERL association; see mnemonic central cyanosis upon feeding

MNEMONIC: VACTERL DIAGNOSIS

Group of malformations with
common, unknown cause DIAGNOSTIC IMAGING
Vertebral anomalies Chest X-ray
Anal atresia ƒ Nasogastric tube coiled in proximal
Cardiovascular anomalies esophagus ɚƭƙƭîŕŕNjƙƭIJǶČĿĚŠƥIJūƑēĿîijŠūƙĿƙɛ
TƑîČĺĚūĚƙūƎĺîijĚîŕǶƙƥƭŕî
Fluoroscopy/Barium swallow
Esophageal atresia
ƒ TIJēĿIJǶČƭŕƥƥūēĿîijŠūƙĚɈŞîNjƑĚƐƭĿƑĚČūŠƥƑîƙƥ
Renal anomalies
swallow study to visualize contrast passing
Limb defects into tracheobronchial tree
Ɠ Barium is contrast medium of choice
(ionic iodinated medium can cause
TYPES chemical pneumonitis)
Type A
CT scan
ƒ Middle esophageal segment missing
ƒ Useful for preoperative planning
Type B
ƒ Proximal esophagus communicates with OTHER DIAGNOSTICS
trachea ƒ Inability to pass gastric tube
Type C (most common) ƒ Neonates drool, choke, vomit ēƭƑĿŠijǶƑƙƥ
feeding
ƒ Distal esophagus communicates with
trachea, proximal esophagus atresia

Type D TREATMENT
ƒ Proximal, distal esophageal segments
communicate with trachea, middle segment SURGERY
atresia ƒ Surgical closing of pathologic
communication, fusion of esophageal buds
Type E (AKA Type H)
ƒ Complete esophagus, additional part
communicates with trachea

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 Chapter 43 Upper Gastrointestinal Congenital Malformations

Figure 43.7 An acquired tracheo-esophageal

Ƕƙƥƭŕîɍ

OSMOSIS.ORG 367