Gastrointestinal Osmosis HY Pathology Notes ATF

GASTROINTESTINAL
SYSTEM
High-Yield
NOTES
by
AfraTafreeh.com
PATHOLOGY
Table of contents
Biliary Tract Diseases 2 Oral Cancer 56
Ascending Cholangitis 2 Pancreatic Cancer 58
Biliary Colic 4 Stomach (Gastric) Cancer 59
Cholecystitis (Acute) 5 Warthin’s Tumor 61
Cholecystitis (Chronic) 7
Summary of Biliary Tract Diseases 9 Inflammatory Bowel Disease 62
Gallstone 10 Crohn’s Disease 62
Primary Sclerosing Cholangitis (PSC) 12 Microscopic Colitis 65
Protein Losing Enteropathy 66
Colorectal Polyp Conditions 14 Ulcerative Colitis 67
Familial Adenomatous Polyposis (FAP) 16 Chrohn’s vs. UC 69
Gardner’s Syndrome (GS) 17
Juvenile Polyposis Syndrome 18 Intestinal Diseases 69
Peutz-Jeghers Syndrome (PJS) 20 Appendicitis 71
Diverticulitis 72
Esophageal Disease 22 Diverticulosis 73
Achalasia 22 Femoral Hernia 75
Barrett’s Esophagus 24 Gallstone Ileus 76
Boerhaave Syndrome 26 Gastroenteritis 77
Diffuse Esophageal Spasm 28 Inguinal Hernias 78
Gastroesophageal Reflux Disease (GERD) 29 Intestinal Adhesions 80
Mallory-Weiss Syndrome 31 Intussusception 81
Plummer-Vinson Syndrome 33 Irritable Bowel Syndrome (IBS) 82
Zenker’s Diverticulum 34 Ischemic Colitis 83
Necrotizing Enterocolitis (NEC) 85
Gastric Disease 35 Small Bowel Ischemia & Infarction 87
Cyclic Vomiting Syndrome 36 Volvulus 88
Gastric Dumping Syndrome 37
Gastritis 38 Liver & Gallbladder Congenital Conditions 90
Chronic Atrophic Gastritis Overview 41 Biliary Atresia 90
Gastroparesis 41 Crigler-Najjar Syndrome 92
Peptic Ulcer 42 Dubin-Johnson Syndrome 93
Gilbert’s Syndrome 94
Gastrointestinal Cancers 44 Rotor Syndrome 94
Carcinoid Tumor 45
Cholangiocarcinoma 46 Liver Diseases 96
Colorectal Cancer 49 Alcoholic Liver Disease 98
Esophageal Cancer 51 Autoimmune Hepatitis 100
Gallbladder Cancer 52 Budd-Chiari Syndrome 101
Hepatoblastoma 54 Cholestatic Liver Disease 103
Hepatocellular Carcinoma 55 Cirrhosis 104
Table of contents
Child-Pugh Grading of Cirrhosis 107 Pancreatitis 152
Fitz-Hugh-Curtis Syndrome 107 Pancreatic Pseudocyst 152
Hemochromatosis 109 Pancreatitis (Acute) 154
Hepatitis B 111 Pancreatitis (Chronic) 156
Hepatitis C 112
Hepatitis E 113 Peritoneal Pathology 158
Hepatocellular Adenoma 114 Peritonitis 159
Neonatal Hepatitis 115 Pneumoperitoneum 160
Non-Alcoholic Fatty Liver Disease (NAFLD) 116
Portal Hypertension 118 Rectal & Anal Pathology 162
Primary Biliary Cirrhosis 120 Anal Fissure 162
Wilson’s Disease 121 Anal Fistula 163
Hemorrhoid 164
Lower Gastrointestinal Congenital Rectal Prolapse 165
Malformations 123
Gastroschisis 123 Upper Gastrointestinal Congenital
Hirschprung’s Disease 125 Malformations 167
Imperforate Anus 126 Cleft Lip & Palate 167
Intestinal Atresia 127 Congenital Diaphragmatic Hernia (CDH) 169
Intestinal Malrotation 129 Esophageal Web 170
Meckel’s Diverticulum 130 Hypertrophic Pyloric Stenosis 171
Omphalocele 132 Thyroglossal Duct Cyst 172
Gastroschisis vs. Omphalocele 133 Tracheoesophageal Fistula 173
Malabsorption Conditions 134

Celiac Disease 135
Lactose Intolerance 136
Small Bowel Bacterial Overgrowth Syndrome 137
Tropical Sprue 138
Whipple’s Disease 139
Oral Disease 141

Aphthous Ulcers 141
Dental Caries Disease 143
Gingivitis 144
Ludwig’s Angina 145
Oral Candidiasis 146
Parotitis 147
Periodontitis 148
Sialadenitis 149
NOTES
• NOTES
~ BILIARY TRACT DISEASES
GENERALLY, WHAT ARE THEY?
Magnetic resonance
( PATHOLOGY & CAUSES ) cholangiopancreatograph
y (MRCP)
• MRI for detailed images of hepatobiliary,
• Diverse spectrum of diseases affecting pancreatic systems
biliary system (gallbladder, bile ducts, liver)
• Bile stored in gallbladder----> stasis/chemical Endoscopic retrograde cholangiopancrea-
constituents change ----> precipitate to tography (ERCP)
solid stone-« travel down biliary tract-« • Down esophagus, stomach, duodenum,
obstruction ----> decreased bile drainage----> ducts ----> contrast medium injected into
symptoms ducts ----> X-ray shows narrow areas/
blockages
n Complications: pancreatitis (most
(..___s,_G_Ns_&_sv_M_PT_O_M_s ) common); intraluminal/intraductal
bleeding, hematomas; perforation;
• Symptoms vary, based on location infection {cholangitis, cholecystitis);
OPain, jaundice, infection, inflammatory cardiopulmonary complications (cardiac
response, sepsis arrhythmia, hypoxemia, aspiration)
• Right upper quadrant (RUQ) epigastric pain
• Jaundice LAB RESULTS
• Nausea, vomiting • See table
• Fever, chills e- sepsis
C...____ T_R_EA_~_M_EN_T
)
(...____ D_IA_GN_o_s,_s )
MEDICATIONS
DIAGNOSTIC IMAGING • Antibiotics
CT scan/ultrasound
• Locations of stones, gallbladder wall SURGERY
thickening/inflammation • Cholecystectomy
X-ray
OTHER INTERVENTIONS
• Pigmented gallbladder stones (radiopaque)
• Sepsis management. biliary drainage,
ERCP
1
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ASCENDING CHOLANGITIS
osms.l"l/ o.seending-eholo.ngi"lis
• Common bacteria: E.coli, Klebsielfa,
( PATHOLOGY & CAUSES ) Enterobacter, Enterococcus
• Medical emergency
• Acute infection of bile duct caused
by intestinal bacteria ascending from
duodenum RISI( FACTORS
• Bacterial infection of bile duct • Gallstones (most common)
superimposed on obstruction of biliary tree; • Stenosis of bile duct due to neoplasm/injury
due to choledocholithiasis from laparoscopic procedure
• Gallstones form in gallbladder - slip out
- travel through cystic bile duct, lodge
in common bile duct - obstruction of
normal bile flow - bacteria ascend from
duodenum to bile duct - infect stagnant
bile, surrounding tissue
2
COMPLICATIONS LAB RESULTS
• Sepsis, septic shock • Assess infection, jaundice
OHigh pressure on bile duct - , Increased WBC
obstruction - cells lining ducts widen , Increased serum (-reactive protein
- bacteria, bile enter bloodstream (CRP)
• Multiorgan failure , Elevated LFTs: ALP, GGT, ALT, AST
(__ s,_G_NS_&_SY_M_PT_O_M_s_) ( T_R_EA_:l"_M_EN_T__ )

• Charcot's triad MEDICATIONS
O RUQ pain, jaundice, fever/chills • Antibiotics + IV fluids
• Reynold's pentad
° Charcot's triad + hypotension/shock, SURGERY
altered consciousness
• Cholecystectomy
O Associated with significant morbidity,
, Avoid future complications
mortality
OTHER INTERVENTIONS
( D_IA_GN_O_s,_s __ ) • ERCP
, Removes gallstones
DIAGNOSTIC IMAGING • Shockwave lithotripsy
Ultrasound, ERCP O High frequency sound waves break
• Biliary dilation down stone
• Bile duct wall thickening • Stent

O Widen bile ducts in areas of stricture
• Evidence of etiology (stricture/stone/stent)
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Figure 28.1 The pathophysiology of ascending cholangitis.
3
BILIARY COLIC
osmsJl/\,iliC1T1J-eolie
( PATHOLOGY & CAUSES ) (__ SI_G_NS_&_SY_M_PT_O_M_s_)

• AKA "gallbladder attack" • Pain
• Gallstones lodged in bile ducts - • Severe right upper quandrant pain;
temporary severe abdominal pain radiates to right shoulder/shoulder
• After meal, gallbladder contracts - blades
gallstone ejected into cystic duct, lodged • Intensity increases for 15 minutes,
- gallbladder contracts against lodged plateaus for few hours (< six), subsides
stone - severe abdominal pain • Starts hours after meal/at night/laying
• Pain subsides when gallstone dislodged flat
• Nausea, vomiting, anorexia
CAUSES
• Gallstones
( D_IA_GN_O_s,_s
__ )
• Narrow bile duct
• Pancreatitis • Recurrent symptoms
• Duodenitis
• Esophageal spasms
DIAGNOSTIC IMAGING
RISk FACTORS Ultrasound
• More common in individuals who are • Confirmation of obstruction

biologically female
X-ray, CT scan, MRI
• Obesity
• Pregnancy
•Age;;;: 40 ( T_R_EA_~_M_EN_T
__ )
SURGERY
COMPLICATIONS
• Cholecystectomy
• Acute cholecystitis
• Gallbladder removal
O Inflammation of gallbladder wall
• Definitive
O Gallstone doesn't dislodge from cystic
duct
OTHER INTERVENTIONS
• Pain, symptom management
4
CHOLECYSTITIS (ACUTE)
osmsJl/ o.eu-le-eholee14s-li"lis
Acalculous cholecystitis
( PATHOLOGY & CAUSES ) • Acute inflammation of gallbladder without
gallstones/cystic duct obstruction; high
• Stone lodged in cystic duct/common bile
morbidity, mortality rate
duct - acute inflammation - pain
• 5-10% of acute cholecystitis cases
0 90% of acute cholecystitis resolves
• Rare, difficult to diagnose
within month as stone dislodges
• Multifactorial etiology
• Fatty meal - small intestine
cholecystokinin (CCK) signals gallbladder • Often occurs in critically ill individuals/
to secrete bile - gallbladder contracts following major surgery
- stone lodged in cystic duct - blocks • Pathogenesis
bile flow - irritates mucosa - mucosa = Gallbladder ischemia, reperfusion injury
secretes mucus, inflammatory enzymes - = Bacterial invasion of ischemic tissue
inflammation, distention, pressure
• Cholesterol stones
COMPLICATIONS
O More potent ability to stimulate
• Biliary peritonitis (from rupture)
inflammation compared to pigment
gallstones • Gallbladder ischemia - rupture - sepsis
• Possible progressions • Acalculous cholecystitis
O Stone ejected out of cystic duct -
cholecystitis subsides, symptoms
subside
O Stone remains in place - pressure
builds - pushes down on blood vessels
supplying gallbladder - ischemia -
gangrenous cell death - gallbladder
walls weaken - perforation/rupture -
bacteria seeds to bloodstream - sepsis
- medical emergency
O Stone lodged in common bile duct -
blocks flow of bile out of liver
• Bacterial growth (cholangitis)
° Cholelithiasis - stone descends to
cystic duct - cholecystitis - stone
descends from cystic duct, lodges in
common bile duct - choledolithiasis -
secondary infection due to obstruction
- cholangitis Figure 28.2 A CT scan in the coronal plane
O Most commonly E.coli, Enterococci, demonstrating a thickened, oedematous
Bacterioides fragilis, Cfostridium gallbladder, indicative of acute cholecystitis.
5
( SIGNS & SYMPTOMS ) Diffusion-weighted MRI
• Differentiate between acute, chronic
cholecystitis
• Midepigastric pain ----> dull right upper
quadrant pain radiates to right scapula/ Ultrasound
shoulders (esp. after a meal in chronic • Gallstones/sludge
cholecystitis) O Gallbladder wall thickening, distention
• Hypoactive bowel sounds; nausea, O Air in gallbladder wall (gangrenous
vomiting, anorexia; jaundice; low grade
cholecystitis)
fever
O Pericholecystic fluid from perforation/
• Blumberg's sign/rebound tenderness
exudate
O RUQ pain when pressure rapidly
released from abdomen; peritonitis
(secondary to gallbladder perforation/ LAB RESULTS
rupture) • Elevated ALP
• Positive Murphy's sign ° Concentrated in liver, bile ducts
O Sudden cessation of inhalation due to O Bile backs up, pressure in ducts increase
pain when inflamed gallbladder reaches ----> cells damaged, die----> ALP released
examiner's fingers • Elevated leukocyte count
O Examiner asks individual to exhale ---->
places hand below right costal margin
in midclavicular line----> individual ( TR_E_AT_M_E_N_T__ )
instructed to breathe in ----> cessation due
to pain MEDICATIONS
O Differentiates cholecystitis from other • Antimicrobials
causes of right upper quadrant pain
SURGERY
• Cholecystectomy
(.____ D_IA_GN_O_SI_S
)
DIAGNOSTIC IMAGING
Cholescintigraphy/hepatic iminodiacetic
acid (HIDA) scan
• Radioactive tracer injected into individual
----> marked HIDA taken up by hepatocytes,
excreted in bile ----> drains down hepatic
ducts
• Location of blockage
6
CHOLECYSTITIS (CHRONIC)
osms.i"l/ ehTonie-eholee14s·tJlis
COMPLICATIONS
( PATHOLOGY & CAUSES ) • Biliary peritonitis (from rupture)
• Gallbladder ischemia - rupture - sepsis
• Obstruction of cystic duct (not infection) -
inflammation of gallbladder wall • Porcelain gallbladder (chronic cholecystitis)
• Constant state of inflammation due to , Chronic state of inflammation -
gallstones repeatedly blocking ducts epithelial fibrosis, calcification
° Changes gallbladder mucosa - deep , Bluish discoloration of gallbladder;

grooves (Rokatansky-Aschoff sinus) becomes hard, brittle
O Pain esp. after meal; gallbladder ' Bile stasis - calcium carbonate bile
attempts to secrete bile to small salts to precipitate out - deposit into
intestine for digestion walls
• Fatty meal - small intestine 'Increased risk of gallbladder cancer

cholecystokinin (CCK) signals gallbladder • Acalculous cholecystitis
to secrete bile - gallbladder contracts
- stone lodged in cystic duct - blocks
bile flow - irritates mucosa - mucosa (__ S_IG_N_S_&_S_Y_M_PT_O_M_s_)
secretes mucus, inflammatory enzymes -
inflammation, distention, pressure • Midepigastric pain - dull right upper
• Cholesterol stones quadrant pain radiates to right scapula/
shoulders (esp. after a meal in chronic
O More potent ability to stimulate
cholecystitis)
inflammation compared to pigment
gallstones • Hypoactive bowel sounds; nausea,
vomiting, anorexia; jaundice; low grade
• Possible progressions
fever
O Stone ejected out of cystic duct -
• Blumberg's sign/rebound tenderness
cholecystitis subsides, symptoms
subside ' Right upper quadrant pain when
pressure rapidly released from
O Stone remains in place - pressure
abdomen; peritonitis (secondary to
builds - pushes down on blood vessels
gallbladder perforation/rupture)
supplying gallbladder - ischemia -
gangrenous cell death - gallbladder • Positive Murphy's sign
walls weaken - perforation/rupture - • Sudden cessation of inhalation due to
bacteria seeds to bloodstream - sepsis pain when inflamed gallbladder reaches
- medical emergency examiner's fingers
O Stone lodged in common bile duct - O Examiner asks individual to exhale -
blocks flow of bile out of liver places hand below right costal margin
• Bacterial growth (cholangitis) in midclavicular line - individual
instructed to breathe in - cessation due
° Cholelithiasis - stone descends to
to pain
cystic duct - cholecystitis - stone
descends from cystic duct, lodges in O Differentiates cholecystitis from other
common bile duct - choledolithiasis - causes of right upper quadrant pain
secondary infection due to obstruction
- cholangitis
O Most commonly E.coli, Enterococci,
Bacterioides fragilis, Cfostridium
7
( D_IA_GN_O_SI_S )
DIAGNOSTIC IMAGING
Cholescintigraphy/hepatic iminodiacetic
acid (HIDA) scan
• Radioactive tracer injected into individual
- marked HIDA taken up by hepatocytes,
excreted in bile - drains down hepatic
ducts
• Location of blockage
Diffusion-weighted MRI
• Differentiate between acute, chronic
cholecystitis
Ultrasound
• Gallstones/sludge Figure 28.3 Endoscopic retrograde
cholangiopancreatography demonstrating
O Gallbladder wall thickening, distention
gallstones in the cystic duct.
O Air in gallbladder wall (gangrenous
cholecystitis)
O Pericholecystic fluid from perforation/
exudate
LAB RESULTS
• Elevated ALP: concentrated in liver, bile
ducts
O Bile backs up, pressure in ducts increase
- cells damaged, die - ALP released

• Elevated leukocyte count
( T_R_EA_:l"_M_EN_T ) Figure 28.4 Histological appearance of

cholestasis in the liver. There is build up of
MEDICATIONS bile pigment in the hepatic parenchyma.
• Antimicrobials
SURGERY
• Cholecystectomy
8
Cystic duct Gallbladder Common bile duct Biliary tree
Nausea, vomiting,
fever, RUQ pain, pain Elevations in liver
lasting > 6 hrs, Asymptomatic, sudden enzymes, WBC,
Abnormalities in liver
midepigastric pain, intense abdominal pain, pancreatic
enzymes, pain,
hypoactive bowel normal liver enzymes, enzymes, bilirubin,
no fever
sounds, Blumberg's nausea/vomiting, jaundice Charcot's triad,
sign, positive Reynold's pentad
Murphy's sign
Acalculous Choledocholithiasis,
cholecystitis, cholecystitis, ascending
blockage of bile cholangitis, blockage Cholangitis, Septic shock.
outflow. cholangitis, of common bile/pancreatic acute pancreatitis multiorgan failure
biliary peritonitis. duct increased risk
porcelain gallbladder of gallbladder cancer
Elevated ALP. HIDA

scan. ultrasound,
Ultrasound, CT, X-ray, Ultrasound, CT, X-ray, Labs (WBC count,
cholescintigraphy.
ERCP ERCP CRP, LFTs), ERCP
diffusion-weighted
MRI
Treatment only if Treatment only if

Antibiotics. IV
symptomatic, pain symptomatic. pain
fluids ..
reduction, reduction.
Cholecystectomy cholecystectomy,
cholecystectomy, cholecystectomy,
ERCP. shod<wave
ursodiol, shock wave ursodiol, shock wave
lithotripsy. stent
therapy, ERCP therapy, ERCP
9
GALLSTONE
osmsJl/ gC1lls-lone
( PATHOLOGY & CAUSES )

• Solid stones inside gallbladder composed
of bile components
• Form based on imbalance of chemical
constituents - precipitate out to form solid
stone
TYPES
• Categorized by location
(choledocholithiasis, cholelithiasis) or major
composition (cholesterol, bilirubin stones)
Choledocholithiasis
• Gallstones in common bile duct -
obstruction of outflow tract Figure 28.5 Cholesterol gallstones.
, Stasis, infection (primary cause)
, Affects liver function; may cause liver
damage • Radiopaque (visible on X-ray)
• Can be caused by excessive extravascular
Cholelithiasis
hemolysis
• Gallstones in gallbladder
= Extravascular hemolysis -
, Primary cause: imbalance of bile
macrophages consume RBCs -
components increased unconjugated bilirubin
, Bile flow out of liver not obstructed; liver production - too much unconjugated
function not affected bilirubin for liver to conjugate -
unconjugated bilirubin binds to calcium
Cholesterol stones
instead of bile salts - precipitate out to
• Most common, 80% form black pigmented stones
• Composed primarily of cholesterol • Brown pigmented gallstone: gallbladder/
• Cholesterol precipitation out of bile: biliary tract infection
supersaturation; inadequate salts/acids/ = Stones enter common bile duct
phospholipids; gallbladder stasis
= Brown pigment due to unconjugated/
• Radiolucent (not visible on X-ray) hydrolyzed bilirubin, phospholipids:
infectious organism brings hydrolytic
Bilirubin stones (pigmented stones)
enzymes - hydrolysis of conjugated
• Composed primarily of unconjugated bilirubin, phospholipids - combine with
bilirubin calcium ions - precipitate out to form
, Formed from nonbacterial, stones
nonenzymatic hydrolysis of conjugated , Common infections: E. coli, Ascaris
bilirubin lumbricoides, Clonorchis sinensis
• Occurs when too much bilirubin in bile (trematode endemic to China, Korea,
• Combines with calcium - solid calcium Vietnam)
bilirubinate , Commonly seen in Asian populations
10
RISI( FACTORS
• More common in individuals who (..____ D_IA_GN_O_SI_S _---)
are biologically female, who use oral
contraceptive
DIAGNOSTIC IMAGING
O t estrogen - t cholesterol in bile + bile Ultrasound, CT scan, X-ray, ERCP
hvpomotllitv -e t risk of gallstones • Visualize stones
• Obesity
• Rapid weight loss
LAB RESULTS
O Imbalance in bile composition - t risk • Elevated bilirubin levels
of calcium-bilirubin precipitation
• Liver function tests (LFTs)
• Total parenteral nutrition (prolonged)
, Elevated gamma-glutamyl transferase
(GGT), alkaline phosphatase (ALP).
COMPLICATIONS alanine aminotransferase (ALT),
• Cholecystitis (inflammation of gallbladder) aspartate transaminase (AST)
• Ascending cholangitis
• Blockage of common, pancreatic bile ducts
• Gallbladder cancer: history of gallstones -
t risk of gallbladder cancer
(....__s,_G_NS_&_SY_M_P_TO_M_s_)
• May be asymptomatic
• Sudden, intense abdominal epigastrid
substernal pain; radiates to right shoulder/
shoulder blades
• Nausea/vomiting; jaundice; abdominal
tenderness. distension; fever. chills;
flatulence, belching
• See mnemonic for summary
Figure 28.6 Abdominal ultrasound

MNEMONIC: G Fs
' Typical clinical presentation
demonstrating cholelithiasis. The gallstones
cast an acoustic shadow.
of an individual with
gallstones
Fat (.._____ T_R_EA_~_M_EN_T )
Female
Fertile • Necessary only if symptomatic
Forty
Fatty food intolerance MEDICATIONS
Flatulence • Bile salts
O Dissolve cholesterol stones
11
SURGERY
• Cholecystectomy
OTHER INTERVENTIONS
• Pain management
• Shock wave therapy (lithotripsy)
= 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
fibrotic, consistent with long-standing
disease.
PRIMARY SCLEROSING
CHOLANGITIS (PSC)
osms.i-l/ Timo.T14-seleTosing-eholo.ngi-lis
COMPLICATIONS
( PATHOLOGY & CAUSES ) • Portal hypertension
= Fibrosis builds around bile ducts -
• Autoimmune disorder in which T-cells
constricts portal veins - t pressure
attack, destroy bile duct epithelial cells
in genetically predisposed individuals • Hepatosplenomegaly
exposed to environmental stimuli = Portal hypertension - backup of fluid,
O HLA-88, HLA-DR3, HLA-DRw52a enlargement of spleen, liver
• Associated with ulcerative colitis, Crohn's • Cirrhosis

disease = Recurrent cycle of inflammation. healing
• Sclerosis, inflammation of intra-, - tissue scarring - fibrosis
extra hepatic ducts • l risk of cholangiocarcinoma, gallbladder
• Cells around bile ducts inflamed. die - cancer, hepatocellular carcinoma
fib rose
• Death of epithelial cells lining bile ducts
- bile leaks into interstitial space.
(__ SI_G_NS_&_S_Y_M_PT_O_M_s_)
bloodstream
• May remit, recur spontaneously
• "Beaded" appearance of bile ducts
• Jaundice, RUQ pain. weight loss, pruritus
O Stenosis of affected ducts, dilation of
(deposition of bile salts, acids in skin).
unaffected ducts
hepatosplenomegaly
• Severity depends on bilirubin levels. • Liver failure
encephalopathy, presence/absence of
O Ascites, muscle atrophy, spider
ascites, serum albumin level. prothrombin
angiomas, increased clotting time. dark
time
urine. pale stool
12
(..____ D_IA_GN_o_s,_s)
DIAGNOSTIC IMAGING
MRCP
• lntrahepatic and/or extra hepatic bile duct
dilation; multifocal or diffuse strictures
ERCP
• lntrahepatic and/or extra hepatic bile duct
dilation; multifocal or diffuse strictures
LAB RESULTS
• Liver function tests (LFTs)
O Elevated conjugated bilirubin, ALP, GGT
• Elevated serum lgM antibody, p-ANCA
(targets antigens in cytoplasm/nucleus of
neutrophils; 80% of individuals with PSC)
Figure 28.8 Cholangiogram demonstrating
• Bilirubinuria multiple biliary strictures in a case of primary
• Liver biopsy sclerosing cholangitis.
O Stage disease, predict prognosis
OTHER DIAGNOSTICS
• Histology
0 "Onion-skin fibrosis": concentric rings
of fibrosis around bile duct, resembles
onion skin
C..____ T_R_EA_:l"_M_EN_T
)
• No effective treatment
MEDICATIONS
• Treat symptoms, manage complications,
not curative (e.g. antibiotics) Figure 28.9 Histological appearance of
• lmmunosuppressants, chelators, steroids primary sclerosing cholangitis. There is
onion-skin fibrosis of the biliary ducts.
SURGERY
• Liver transplant
O Advanced liver disease
13
NOTES
GENERALLY,WHAT ARE THEY?

Inflammatory polyps
( PATHOLOGY & CAUSES ) • Caused by inflammatory bowel diseases
° Crohn's disease, ulcerative colitis
• Colorectal polyps: overgrowths of epithelial
cells lining colon/rectum • Not malignant
• Usually benign, can turn malignant
CAUSES
TYPES • Genetic mutations
• Inflammatory conditions (e.g. Crohn's
Adenomatous polyps/colonic adenomas disease)
• Gland-like polyps caused by tumor
suppressor gene mutation in adenomatous
polyposis coli (APC)
RISI( FACTORS
• Family history
• Characterized by accelerated division of
• Bowel wall injury (e.g. radiation exposure,
epithelial cells - epithelial dysplasia -
polyp formation smoking, inflammatory bowel disease)
• No malignant potential by itself; requires • Risk increases with age

mutations in other tumor suppressants (K-
RAS, p53) COMPLIC ATIONS
• Histologic classification • Malignancy
O Tubular: pedunculated polyp, protrudes O Depends on degree of dysplasia, size of
out in lumen polyp
O Villous: sessile. cauliflower-like
appearance; more often malignant
O Tubulovil/ous: characteristics of tubular. (__ s,_G_NS_&_SY_M_PT_O_M_s_)
villous polyps
• Often asymptomatic
Serrated polyps • If ulcerating
• Saw-tooth appearance microscopically O Rectal bleeding. anemia symptoms (e.g.
• Contain methylated CpG islands - fatigue)
silencing of DNA-repair genes, others - • If large
more mutations - malignancy O Obstruction - abdominal pain,
O Small polyps (most common): AKA constipation
hyperplastic polyps; rarely malignant
• Malabsorption - diarrhea
O Large polyps: often flat. sessile.
• Some polyposis syndromes
malignant
O Extracolonic symptoms
Hamartomatous polyps
• Mixture of tissues; disorganized mass
containing tissue found at site of polyp
• Occur sporadically/in genetically inherited
conditions (Juvenile polyposis. Peutz-
Jeghers syndrome)
14
(..____ D_IA_GN_O_SI_S) (..__ __ T_R_EA_~_M_EN_T
)
DIAGNOSTIC IMAGING SURGERY
CT scan, MRI Polyp removal (polypectomy)
• Hyperdense outpouchings of colonic wall
Colonic resection (colectomy)
into lumen; detection of metastases
• If multiple polyps associated with polyposis
Endoscopy (colonoscopy) with biopsy syndromes/polyps with high-grade
• Type of polyp, malignant potential (degree dysplasia
of dysplasia)
LAB RESULTS
• Iron-deficiency anernia=-s decreased
red blood cell (RBC) count, low mean
corpuscular volume (MCV) levels
• Iron-deficiency anernia -e low ferritin,
serum iron, transferrin saturation
• APC, RAS, etc. mutations
• Assess asymptomatic family members for
risk
OTHER DIAGNOSTICS Figure 29.1 The gross pathological

appearance of a sessile colorectal polyp.
Digital rectal examination
• 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.
15
FAMILIAL ADENOMATOUS
POLYPOSIS (FAP)
osms.i"l/fo.milio.l-o.denomo.tous-pol14posis
O Abdominal mesenchymal desmoid
( PATHOLOGY & CAUSES ) tumors: compress adjacent structures=-
obstruction/vascular impairment
• Inherited condition; hundreds/thousands O Other potential malignancies:
adenomatous polyps in colon
thyroid, pancreas, brain (glioma), liver
• Autosomal dominant inheritance; 100% (hepatoblastoma)
penetrance; de novo mutations may occur
TYPES ( s,_G_NS_&_SY_M_PT_O_M_s_)
Classic FAP • Usually asymptomatic until malignancy
• Most aggressive, frequent;> 100 polyps at • Colonic manifestations
diagnosis; early onset O Palpable abdominal mass;
hematochezia (rectal bleeding); pain
Attenuated FAP (AFAP)
(esp. abdomen); diarrhea
• < 100 polyps at diagnosis (oligopolyposis);
later onset
Autosomal recessive FAP

( D_IA_GN_O_s,_s __ )
DIAGNOSTIC IMAGING
CAUSES
• Germline mutation in APC gene (tumor Endoscopy with biopsy
suppressor) ---'> prevention of apoptosis ---'>
Colonoscopy, flexible sigmoidoscopy:
cell overgrowth---'> polyps
• Detection of 2: 100 polyps; -30 polys,
• APC gene nonfunctional in FAP; slightly
AFAP
impaired in AFAP
• Autosomal recessive FAP Esophagogastroduodenoscopy(EGO)
O Mutations of MUTYH gene on • Gastric, duodenal adenomas
chromosome 1
Barium enema (with double contrast)
• Filling defects
RISI( FACTORS
• Family history Abdominal CT scan
COMPLICATIONS into lumen
• Malignancy if untreated
• Extracolonic manifestations LAB RESULTS
° Congenital hypertrophy of retinal • Iron-deficiency anemia
pigment epithelium (CHRPE) • ! RBC, ! MCV
° Fundic gland polyps: sessile polyps in • ! ferritin, ! serum iron, ! transferrin
stomach, usually not malignant saturation
O Duodenal adenomas: malignant • APC mutations
potential
16
OTHER DIAGNOSTICS
(..__ __ T_R_EA_~_M_EN_T
)
Family history
• Cancers, gastrointestinal (GI) tract diseases MEDICATIONS
• Cyclooxygenase 2 inhibitors, other
Digital rectal examination nonsteroidal anti-inflammatory drugs
• Palpable mass (NSAIDs)
• Epidermal growth factor receptor inhibitor:
Ophthalmic examination
erlotinib
• CHRPE
• Chemotherapy, if colon cancer
SURGERY
• Frequent endoscopic check-ups to detect
onset of polyposis every 1-2 years
, If polyps detected - 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)

osmsJl/ go.TelneTs-s14ncJ.Tome
• Tumors outside colon
( PATHOLOGY & CAUSES ) , Fibromas, lipomas, epidermoid cysts,
thyroid neoplasms, osteomas, desmoid
• Variant of FAP with prominent extracolonic
• Extracolonic polyps can arise in stomach,
manifestations
duodenum, spleen, kidneys, liver,
• Inherited condition; numerous mesentery, small bowel; CHRPE lesions
adenomatous polyps in colon; extracolonic
polyps, tumors
17
CAUSES • Supernumerary impacted teeth
• APC, RAS, TP53 mutation; DCC deletion - • Multiple jaw osteomas, odontomas
furthers carcinogenesis
Digital rectal examination
• Autosomal dominant inheritance
• Palpable mass
COMPLICATIONS Ophthalmic examination

• Malignancy in colon, thyroid, liver, kidneys • CHRPE
ECG
(__ s,_G_NS_&_S_Y_M_PT_O_M_s_) • Stomach, duodenum for polyps
• Colonic manifestations
O Rectal bleeding, diarrhea ( TR_E_AT_M_E_N_T )
• Extracolonic manifestations
• No cure; palliative treatment
O Desmoid tumors (parietal bumps,
bleeding)
O Dental problems SURGERY
O Epidermoid cysts • Excision of tumors/polyps with wide (8mm)
margin
O Epigastric pain, bleeding, jaundice
• Colectomy
O Malnutrition - malaise, lethargy, fatigue
OTHER INTERVENTIONS
( D_IA_GN_O_s,_s __ ) • Radiotherapy, if recurrent
DIAGNOSTIC IMAGING
Endoscopy with biopsy
Colonoscopy, flexible sigmoidoscopy

• Direct visualization of adenomatous polyps
in colon
Abdominal CT scan
into lumen
Head/dental X-ray
• Dental abnormalities
LAB RESULTS
• Iron-deficiency anemia
o ! RBC, ! MCV
0 ! ferritin, ! serum iron, ! transferrin
saturation
• Tumoral markers (e.g. carcinoembryonic
antigen)
• APC, RAS, TP53 mutations; DCC deletion
OTHER DIAGNOSTICS
Physical examination
18
J"UVENILEPOLYPOSIS SYNDROME
osmsJl/ juvenile-poh4posis
( PATHOLOGY & CAUSES ) ( D_IA_GN_O_SI_S

__ )
• Numerous benign (AKA juvenile) polyps DIAGNOSTIC IMAGING
along GI tract
Endoscopic studies
• Majority non-neoplastic hamartomas
polyps, in colorectum • E.g. endoscopy, colonoscopy,
sigmoidoscopy
• Criteria for diagnosis
CAUSES 0 > five juvenile polyps in colon/rectum
• BMPRlA, SMAD4 mutations
O Multiple juvenile polyps in other areas of
• Autosomal dominant inheritance; GI tract
incomplete penetrance
nFamily history with any number of
• De novo mutations (25%)
polyps
• Biopsy, cytology
COMPLICATIONS
• Increased risk of colorectal/extracolonic LAB RESULTS
adenocarcinoma; intestinal obstruction
• Iron-deficiency anemia
, ! RBC, ! MCV
( SIGNS & SYMPTOMS ) , ! ferritin, ! serum iron, ! transferrin
saturation
• Hematochezia, anemia symptoms; • BMPRlA, SMAD4 mutations
abdominal pain; diarrhea/constipation;
rectal prolapse
( T_R_EA_~_M_EN_T
__ )
SURGERY
• Polypectomy
• Surgical colectomy, proctocolectomy
O
Malignant, ulcerating polyps
Figure 29.6 A juvenile retention polyp with

abundant edematous stroma and dilated
cystic spaces filled with mucin. The spaces
are lined by cuboidal epithelium.
19
PEUTZ-JEGHERSSYNDROME
(PJS)
osmsJl/peulz- jegheTs
( PATHOLOGY & CAUSES ) ( D_IA_GN_o_s,_s __ )

• Inherited condition; benign hamartomatous DIAGNOSTIC IMAGING
polyps, in small bowel; also in colon,
stomach Endoscopy, colonoscopy, with biopsy
• Associated with hyperpigmented (melanin- Capsule endoscopy

containing) macules on skin, mucosa
Abdominal CT scan
CAUSES • Hyperdense outpouchings of colonic wall

into lumen
• IV drug use
O Increases likelihood of infective
endocarditis LAB RESULTS
• Congenital bicuspid aortic valve • Fecal occult blood test
• Diabetes, high blood pressure, smoking • Iron-deficiency anemia
• ! RBC, ! MCV
COMPLICATIONS • ! ferritin, ! serum iron, ! transferrin
saturation
• Very high risk of extracolonic malignant
transformation • Tumor markers
O Breast, ovarian, cervical, testicular. • CEA, CA-19-9, CA-125
pancreatic, thyroid cancer • STKll (LKB1) mutations
• Mild malignant potential of polyps
OTHER DIAGNOSTICS
(__ s,_G_NS_&_S_Y_M_PT_O_M_s_)
Diagnostic criteria
• One of following
• GI • ~ two PJ polyps confirmed histologically
O Ulceration ----. GI bleeding •~one PJ polyp with family history
(hematochezia/melena) ----. symptoms of • PJS-associated mucocutaneous
anemia pigmentations
° Colicky abdominal pain
O lntussusception ----. bowel obstruction, Digital rectal examination
bowel infarction • Palpable mass
O Diarrhea. constipation
• Pigmented lesions around oral mucosa,
nostrils. perianal area of extremities; fade
( TR_E_AT_M_E_N_T __ )
after puberty
SURGERY
• Polypectomy
MEDICATIONS
• Cyclooxygenase 2 inhibitors (celecoxib)
20
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.
21
NOTES
GENERALLY.WHAT IS IT?
• Pathologies of the esophagus • Individual history/clinical features,
• Esophageal motility disorders esophagogastroduodenoscopy (EGO).
barium swallow X-ray, esophageal
O Diseases interfering with correct
manometry, endoscopic biopsy
function of esophagus' various muscular
components
( T_R_E~_~_M_EN_T__ )
CAUSES
• Infections, autoimmune disease, anatomical • See individual diseases
defects, irritative processes
• Difficulty/pain while swallowing, especially
spasm-type pain
• Difficulty with food regurgitation
ACHALASIA
osms.i"l/ o.eho.lo.slo.
• Affected individual lacks nonadrenergic,
( PATHOLOGY & CAUSES ) noncholinergic, inhibitory ganglion cells
---> imbalanced excitation and relaxation
• Esophageal smooth muscle fibres fail ---> incomplete lower esophageal sphincter
to relax-» lower esophageal sphincter relaxation, increased lower esophageal
remains closed/fails to open tone. lack of esophageal peristalsis
• AKA esophageal achalasia, achalasia
cardiae, cardiospasm, esophageal
a peristalsis
CAUSES
• Likely caused by underlying autoimmune
• Progressive degeneration of ganglion cells
process triggered by previous viral
in myenteric plexus within esophageal wall
infection/ genetic predisposition/
---> lower esophageal sphincter fails to relax
neurodegenerative disease/other infective
---> loss of peristalsis in distal esophagus
process
• Involves smooth muscle layer of
esophageal, lower esophageal sphincters
22
Primary achalasia (most common) Endoscopic biopsy
• No known underlying cause---'> failure of • Hypertrophic musculature
distal esophageal inhibitory neurons • Absence of specific nerve cells within
myenteric plexus
Secondary achalasia
• Esophageal cancer
• Chagas disease
OTHER DIAGNOSTICS
O Protozoan infection due to Trypanosoma Esophageal manometry
cruzl-« loss of intramural ganglion • Lower esophageal sphincter fails to relax
cells=- aperistalsis, incomplete lower upon wet swallow (< 75% relaxation)
esophageal sphincter relaxation
• Lower esophageal pressure
O Normal < 26mmHg
c SIGNS & SYMPTOMS ) O
O
Achalasia > lOOmmHg
Nutcracker achalasia > 200mmHg
• Dysphagia to solids/liquids, odynophagia • Aperistalsis in esophageal body
(rarely), heartburn unresponsive to proton • Relative increase in intraesophageal
pump inhibitor therapy, symptoms worsen pressure vs. intragastric pressure
progressivelys, regurgitation of undigested
food, substernal chest pain, hiccups
• Weight loss ( T_R_EA_~_M_EN_T__ )
• Coughing while lying horizontally,
aspiration of food ---'> recurrent pulmonary MEDICATIONS
complications • Calcium channel blockers for mild to
moderate disease
• Nitrates effective before dilatation occurs
( D_IA_GN_o_s,_s__ ) • Antimuscarinic agents (rarely effective)
• Proton pump inhibitors (after surgery/
DIAGNOSTIC IMAGING
pneumatic dilatation) to prevent reflux
Barium swallow X-ray and continuous damage
fluoroscopy
• Normal peristalsis not seen SURGERY
• Acute tapering at lower esophageal
sphincter Laparoscopic Heller myotomy
• Narrowing of gastroesophageal junction • Esophageal dilatation via surgical cleaving
(bird's beak/rat's tail appearance) of muscle
• Dilated esophagus above narrowing • Only cut through outer muscle layers (those
failing to relax), leaving inner mucosal layer
• Air-fluid margin over barium column due to
intact
lack of peristalsis
Endoscopic myotomy
Esophageal endoscopy with or without
endoscopic ultrasound • Peroral endoscopic myotomy, minimally
invasive e- incision made through
• May appear normal
esophageal mucosa, innermost circular
• Unusually increased resistance to passage muscle layer divided and extended through
of endoscope through esophagogastric
lower esophageal sphincter, 2cm/0.8in into
junction
gastric muscle
• Retained food in esophagus on upper
endoscopy
23
OTHER 1NTERVENT10NS
• 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)
• Avoid foods that aggravate reftux=-s
ketchup, citrus, chocolate, caffeine
Botox injection
• Paralyze muscle keeping lower esophageal
sphincter shut (causes scarring of sphincter
----. may complicate later myotomy)
Pneumatic dilatation
• Muscle fibres stretched/torn by forceful
inflation of balloon placed in lower
esophageal sphincter Figure 30.1 A barium swallow demonstrating
the bird's beak sign in achalasia. The proximal
• Lowers basal lower esophageal tone by
esophagus is dilated.
disruption of muscular ring
BARRETT'S ESOPHAGUS
osms.i-l/bo.TTe-Hs-esopho.gus
• Upright/supine reflux
( PATHOLOGY & CAUSES ) O Significantly more likely to develop
adenocarcinoma
• Premalignant condition; metaplasia of cells
lining lower esophagus Short-segment Barrett's
• Normal stratified squamous epithelium ----. • Distance between z-line and
simple columnar epithelium, goblet cells gastroesophageal junction < 3cm/1.2in
(usually native to lower gastrointestinal O Greater prevalence
tract) O Shorter history of heartburn
• Chronic acid exposure ----. reflux esophagitis O Usually asymptomatic
{chronic irritation) ----. metaplasia
O Predominantly upright reflux
• Bile aclds=- intestinal differentiation ----.
O Less mucosa involved ----. lower
promotes cancer growth
incidence of dysplasia
TYPES
R1S1( FACTORS
• If z-Iine and gastroesophageal junction
coincide e- intestinal metaplasia at • Bulimia
gastroesophageal junction • Central obesity
O Associated with Helicobacter pylori • Previous chemical damage to esophageal
epithelium (e.g. swallowing lye)
Long-segment Barrett's • Smoking
• Distance between z-line and • Hiatal hernia
gastroesophageal junction > 3cm/1.2in
O Associated with more severe reflux
24
COMPLICATIONS
• Esophageal adenocarcinoma
( T_R_EA_~_M_EN_T )
MEDICATIONS
(__ SI_G_NS_&_SY_M_PT_O_M_s_) Proton pump inhibitors
• E.g. omeprazole; manage acid reflux
• Same as reflux, not (initial) cancerous Chemoprevention
changes • Nondysplastidlow-grade lesion
• Frequent, prolonged heartburn, dysphagia, , Aspirin, NSAIDS----. inhibition of
hematemesis, epigastric pain, weight loss cyclooxygenase (COX-1 & 2) may
(due to painful eating) protect against progression of disease
( D_IA_GN_o_s,_s __ ) SURGERY
Treatment of dysplastic lesions
DIAGNOSTIC IMAGING • Endoscopic mucosal resection, surgical
Esophagogastroduodenoscopy removal of esophagus, radiation therapy,
systemic chemotherapy
• Fiber optic camera inserted via mouth ----.
examine and biopsy esophagus, stomach.
duodenum OTHER INTERVENTIONS
Annual endoscopic observation
LAB RESULTS • For nondysplastidlow-grade lesions
Biopsy
Management of acid reflux
• Specimen from
• Avoid/reduce intake of foods known to
esophagogastroduodenoscopy must
worsen reflux: chocolate, coffee, tea,
contain goblet cetts=- "intestinal
peppermint. alcohol, fatty/spicy/acidic foods
metaplasia" ----. marker for progression of
metaplasia to dysplasia ----. adenocarcinoma Treatment of dysplastic lesions
• lmmunohistochemical staining assists in • Radiofrequency ablation
diagnosis
, Electrical current used to destroy small
• Biopsy classification regions of tissue
O Nondysplastic • Spray cryotherapy
O Low-grade dysplasia , Liquid nitrogen spray applied to small
O High-grade dysplasia region of tissue ----. freezing ----. tissue
° Frank carcinoma death
• Photodynamic therapy
OTHER DIAGNOSTICS , Chemical photosensitizer=-. cytotoxicity
when stimulated by certain frequency
Screening of light
• Biological males, > 60 years old. long
standing reflux, life expectancy> five years
• Anyone with diagnosis of Barrett's
esophagus
Esophageal pH studies
• Establish efficacy of proton pump inhibitor
treatment
25
SQUAMOUS EPITHELIUM
Figure 30.2 Histological appearance of the squamocolumnar junction in a case of Barrett's

esophagus. The underlying glandular epithelium contains goblet cells, indicating intestinal
metaplasia.
BOERHAAVE SYNDROME
osmsJl:/\,oe,-hC1C1Ve-s14nd,-ome
• Chemical mediastinitis e- mediastinal
( PATHOLOGY & CAUSES ) necrosis ---'> rupture of overlying pleura
---'> contamination of pleural cavity---'>
• Rupture through esophagus caused by pleural effusion
increased intraesophageal pressure and
= Effort rupture of cervical esophagus ---'>
negative intrathoracic pressure
localized cervical perforation
• Vomiting I retching ---'> unrelaxed
= Spread of contamination slow due
esophagus. closed glottis ---'> increase
to attachments of esophagus to
in esophageal pressure. slight drop in
prevertebral fascia
intrathoracic pressure ---'> spontaneous
• Usually occurs in anatomically normal
rupture of esophageal wall ---'>
esophagi
contamination of mediastinum with gastric
contents - chemical mediastinitis
O Tears commonly occur at left RISI( FACTORS
posterolateral aspect (distal esophagus), • Caustic ingestion. pill/medication
just above esophageal hiatus of esophagitis, eosinophilic esophagitis,
diaphragm Barrett's esophagus. infectious ulcers,
° Can be fatal without treatrnent e- sepsis stricture dilatation
26
• Barium sulfate common contrast material,
(__ SI_G_NS_&_SY_M_PT_O_M_s
) but spillage into mediastinal and pleural
spaces - inflammatory response -
• Severe vomiting - profound retrosternal fibrosis
chest pain (may radiate to left shoulder) or
abdominal pain Endoscopy avoided
° Followed by painful swallowing • May extend tear, introduce air into
(odynophagia), tachypnea, dyspnea, mediastinum
cyanosis, fever, shock
• Mackler's triad: chest pain, vomiting, LAB RESULTS
subcutaneous emphysema
• Hemoglobin and hematocrit
• Hamman's sign: crunching/rasping sound,
• Assess severity of initial bleeding
synchronous with heartbeat:
• Pleural effusion fluid may be high in
O Heard over precordium, left lateral
amylase (saliva), low pH
position
• Leukocytosis
° Caused by mediastinal emphysema
• Cervical perforation: neck pain, difficulty
swallowing (dysphagia), difficulty
speaking (dysphonia), tenderness of
sternocleidomastoid
• Intra-abdominal perforation: epigastric
pain (may radiate to left shoulder), back
pain, inability to lie supine, acute abdomen
pain
(...____ D_IA_GN_o_s,_s)
• Non-specific symptoms - diagnostic delay,
poor outcome
• Physical examination often unhelpful;
history important
DIAGNOSTIC IMAGING
Chest X-ray
• Early: free mediastinal air
• 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
Chest CT scan contrast has leaked into and accumulated in
the thoracic cavity.
• Esophageal wall edema/thickening,
extraesophageal air, periesophageal fluid,
mediastinal widening, pneumothorax
Fluoroscopy
• Water soluble contrast (gastrografin)
esophagram - location and extent of
extravasation of contrast
27
SURGERY
C..____ T_R_EA_:T_M_EN_T
) • Debride infected/necrotic tissue, repair
defect/resection of defect/diversion
MEDICATIONS
• IV proton pump inhibitor - reduce acidity,
irritation OTHER INTERVENTIONS
• Prophylactic antibiotic therapy • Parenteral/enteral (jejunostomy/PEG tube)
nutritional support
DIFFUSE ESOPHAGEAL SPASM

osmsJl/ esopho.geo.1-spo.sm
( PATHOLOGY & CAUSES ) (..____ D_IA_GN_O_SI_S _~)

• Esophageal motility disorder characterized DIAGNOSTIC IMAGING
by repetitive, non-peristaltic. spontaneous
contractions of the distal esophageal Barium swallow x-ray (upper GI)
smooth muscle • "Corkscrew" appearance is characteristic
• Sphincter function = normal
Endoscopy
• Exclude heart disease, mechanical
CAUSES intraluminal obstruction
• Cause relatively unknown
• Uncontrolled brain signals and extremely OTHER DIAGNOSTICS
hot/cold beverages can trigger disease
24-hour esophageal manometry
COMPLICATIONS • Shows uncoordinated esophageal
contractions of normal amplitude
• Leads to difficulty swallowing. impaired
advancement of food and/or regurgitation
C..____ T_R_EA_:T_M_EN_T
)
( SIGNS & SYMPTOMS ) • No cure
• Intermittent dysphagia
• Atypical chest pain that mimics cardiac MEDICATIONS
chest pain; may radiate to jaw. arms. back • Nitrates. calcium channel blockers. and/
• Food regurgitation relatively uncommon or botulinum toxin injections to lower
esophageal muscle; used to decrease
spasms
• Antidepressants, anti-anxiety medications
SURGERY
• Surgical esophagomyotomy rarely
considered
28
GASTROESOPHAGEALREFLUX
DISEASE (GERD)
osms.i"l/ go.s-lToesopho.geo.1-Teflux
, Often felt shortly after eating meals
( PATHOLOGY & CAUSES ) (worse after large meals/when lying
down)
• AKA acid reflux
• Halitosis, tooth decay
• Failure of lower esophageal sphlncter e-
poor closure/inappropriate relaxation (poor
tone) of lower esophageal sphincter=-. ( D_IA_GN_O_s,_s
__ )
stomach contents re-enter esophagus
• Commonly associated with decreased • Can be diagnosed based on clinical
esophageal motility, gastric outlet symptoms, history alone
obstruction, hiatal hernia
DIAGNOSTIC IMAGING
RISI( FACTORS
• Obesity, pregnancy, smoking, hiatal hernia Endoscopy
• Medications • Used when therapeutic response poor/
concerning symptoms present (dysphagia,
, Antihistamines, calcium channel
anemia, blood in stool, wheezing, weight
blockers, antidepressants, hypnotics,
loss, voice changes)
glucocorticoids
• Zollinger-Ellison syndrome, high blood Upper GI series X-rays with barium con-
calcium (increased gastrin production), trast
scleroderma/systemic sclerosis (esophageal • Useful to identify complications
dysmotility)
• Early stages of reflux esophagitis: granular
• Visceroptosis nodular appearance of mucosa in distal
third of esophagus with numerous ill-
COMPLICATIONS defined 1-3mm lucencies
• Esophagitis, esophageal strictures, Barrett's • Shallow ulcers and erosions
esophagus (premalignant condition), n Collections of barium in distal
esophageal adenocarcinoma, laryngitis, esophagus near gastroesophageal
chronic cough, pulmonary fibrosis, earache, junction
asthma, recurrent pneumonia O Identify stricture (tapered area
of concentric narrowing in distal
esophagus)
(__ s,_G_NS_&_SY_M_PT_O_M_s_)
• Acid taste in mouth, heartburn, retrosternal
LAB RESULTS
chest pain, early satiety, regurgitation, • 24-hour esophageal pH monitoring in
odynophagia, increased salivation, lower esophagus
postprandial nausea and vomiting,
sore throat, sensation of lump in throat,
coughing, wheezing
29
Biopsy
• Edema, basal hyperplasia (non-specific
inflammation)
• Lymphocytic inflammation (non-specific)
• Neutrophilic inflammation (reflux/
Heficobacter gastritis)
• Eosinophilic inflammation (usually reflux.
if> 20 eosinophils per high-power field
extending beyond distal esophagus, more
like eosinophilic esophagitis)
• Elongation of papillae
• Goblet cell intestinal metaplasia
• Thinning of squamous cell layer
• Dysplasia
• Carcinoma Figure 30.4 The histological appearance of
the squamous-lined esophagus in a case of
OTHER DIAGNOSTICS reflux. The papillae become elongated and
• Esophageal manometry (excludes motility there is overgrowth of the basal cells (darker
disorder) blue) known as basal cell hyperplasia.
• Short term trial of proton-pump inhibitors
( T_R_EA_:T_M_EN_T__ )
MEDICATIONS
• Antacids neutralise acidity of gastric
secretions
• H2 receptor blockers decrease acidification
of gastric secretions
• Proton pump inhibitors decrease
acidification of gastric secretions
• Prokinetics strengthen lower esophageal
sphincter (LES). causing stomach contents
to empty faster
• Baclofen (GABAB agonist)
= Inhibits transient LES relaxations,
particularly in postprandial period
= Modestly effective, but rarely used due
to frequent dosing requirements
Surface agents and alginates

Figure 30.5 A contrast X-ray demonstrating • Sucralfate (aluminium sucrose sulfate)
gastroesophageal reflux. The contrast = Adheres to mucosal surface-«
medium was injected percutaneously into promotes healing, protects from peptic
the stomach and has migrated into the injury
esophagus.
• Sodium alginate
O Polysaccharide derived from seaweed
----. forms a viscous gum that floats
within stomach ----. reduced postprandial
acid pocket in proximal stomach
30
SURGERY
Nissen fundoplica
tion
• Upper part of stomach wrapped around
lower esophageal sphincter ----> strengthens
sphincter, prevents acid reflux
Transoral incisionless fundoplication

• Similar procedure to Nissen fundoplication,
performed transorally with endoscope
LINX reflux management system

• Titanium beads with magnetic cores
wrapped around weak native lower
esophageal sphlncter e- attractive force
between beads closing sphtncter=- force
of peristaltic wave of caused by swallowing Figure 30.6 An endoscopic view of
can transiently open beads an esophageal stricture, a potential
consequence of severe, long-standing reflux.
OTHER INTERVENTIONS
Lifestyle modifications
• Avoid lying down within three hours after
eating, wedge pillow when sleeping to
elevate head, weight loss, avoid certain
foods (coffee, alcohol, chocolate, fatty/
acidic/spicy foods), smoking cessation,
moderate exercise
MALLORY-WEISS SYNDROME
osms.i"l/ mo.lloT14-weiss
CAUSES
( PATHOLOGY & CAUSES ) • Vomiting, straining, coughing, seizures,
blunt abdominal injury, nasogastric tube
• Severe vomiting----> sudden increase
placement, gastroscopy
in intra-abdominal pressure----> partial
thickness laceration at gastroesophageal
junction ----> bleeding from mucosa RISI( FACTORS
• Also called gastroesophageal laceration • Alcoholism, bulimia, food poisoning, hiatal
syndrome hernia, NSAID abuse, biological male sex
• Laceration known as "Mallory-Weiss tear", (80%), hyperemesis gravidarum (severe
involves mucosa and submucosa, not morning sickness in pregnancy)
muscular layer
31
(
(__ SI_G_NS_&_S_Y_M_PT_O_M_s
) T_R_EA_:T_M_EN_T
)
• Hematemesis after episode of violent • In absence of comorbidities (esp. portal vein
retching/vomiting hypertension), significant healing occurs in
• Melena first 24-48 hours
• Bleeding associated symptoms may cease
after 24-48 hours MEDICATIONS
• Epigastric, back pain
Supportive (persistent bleeding uncom-
• Signs of hemodynamic instability
mon)
O Resting tachycardia, hypotension
• Acid suppression
O IV proton pump inhibitor
( D_IA_GN_O_SI_S
) • If nausea and vomiting persistent
O Antiemetics
DIAGNOSTIC IMAGING
Endoscopy SURGERY
• Tears appear as red longitudinal breaks in Endoscopy (for spurting/oozing tears)
mucosa, may be covered by clot
• Cauterization, hemoclips {hemostasis of
small defects), endoscopic band ligation
LAB RESULTS (with or without epinephrine injection),
• Hemoglobin, hematocrit (assess severity of arterial embolization
initial bleeding)
Figure 30.7 Endoscopic appearance of a

Mallory-Weiss tear.
32
PLUMMER-VINSON SYNDROME
osms.i"l/ plummeT-vinson
DIAGNOSTIC IMAGING
Barium esophagograph
y, videofluoroscopy,
• Triad of iron deficiency anemia, dysphagia, esophagogastroduodenoscopy
cervical esophageal web • Esophageal web
• AKA Paterson-Brown-Kelly syndrome,
sideropenic dysphagia
LAB RESULTS
• Premalignant disease
• Anemia
, Complete blood cell count, peripheral
CAUSES blood smear, iron study
• Exact cause unknown, likely connected to
genetic factors, nutritional deficiencies
( T_R_E~_;,-_M_EN_T__ )
RISI( FACTORS MEDICATIONS
• Postmenopause
• Iron supplementation, folate, vitamin 812
- correct iron deficiency anemia
COMPLICATIONS
• Esophageal/pharyngeal squamous cell SURGERY
carcinoma
• Mechanical widening of esophagus
( s,_G_NS_&_SY_M_PT_O_M_s_)
• Esophageal signs and symptoms
O Esophageal webs, difficult/painful
swallowing, Plummer-Vinson syndrome
at upper end of esophagus, Schatzki
ring lower end of esophagus
• Iron deficiency signs and symptoms
O Glossitis, cheilosis, angular stomatitis,
koilonychia, splenomegaly, dizziness,
pallor, dyspnea
( D_IA_GN_O_SI_S
__ )
• Presence of esophageal web in individual
with iron deficiency anemia Figure 30.8 An endoscopic view of an
esophageal web which is usually associated
with Plummer-Vinson syndrome.
33
ZENl(ER'S DIVERTICULUM
osms.i"l/zenkeTs
CT scan with oral contrast
• Distinct outpouching visible
• Diverticulum (outpouching) of pharyngeal
mucosa through Killian's triangle (area of
muscular weakness). between transverse
( T_R_EA_:T_M_EN_T
)
fibres of cricopharyngeus muscle and
• Small/asymptomatic diverticula do not
oblique fibres of lower inferior constrictor
require treatment
muscle
• AKA pharyngoesophageal diverticulum,
pharyngeal pouch, hypopharyngeal SURGERY
diverticulum • Neck surgery - cricopharyngeal myotomy,
• Pseudodiverticulum diverticulopexy
O Does not involve all layers of esophageal
wall - contains mucosa, submucosa OTHER INTERVENTIONS
• Non-surgical endoscopic technique
CAUSES • Endoscopic stapling
• Uncoordinated swallowing, impaired • Endoscopic laser
relaxation and swallowing, impaired
relaxation and spasm of cricopharyngeus
muscle - increased pressures in distal
pharynx - excessive lower pharyngeal
pressures - diverticulum formation
RISI( FACTORS
• Biological male > 60 years old
(__ s,_G_Ns_&_s_v_M_PT_O_M_s_)
• Difficulty swallowing. sense of lump in
throat, cervical webs
• Food trapping
O Regurgitation. cough, halitosis, infection
( 0_1A_GN_o_s1_s
__ )
DIAGNOSTIC IMAGING
Barium swallow
• Distinct outpouching visible
Figure 30.9 A barium swallow
Upper gastrointes
tinal endoscopy demonstrating a Zenker's diverticulum,
• Pouch visualized outlined on the right of the image.
34
NOTES
( PATHOLOGY & CAUSES ) C...____ T_R_EA_:l"_M_EN_T )
• Diseases affecting gastric mucosa, gastric MEDICATIONS
outlet, etc. • Proton pump inhibitor (PPI)
• Inflammation due to infection; ulceration • Correct fluid, electrolyte deficits
• Discontinue nonsteroidal anti-inflammatory
drugs (NSAIDs)
(..___s,_G_Ns_&_sv_M_PT_O_M_s
)
• May be asymptomatic SURGERY
• Epigastric pain, nausea, vomiting • Endoscopic ligation/coagulation
• Anemia; fecal, urinary incontinence; ulcers; • Surgical repair

bleeding
OTHER INTERVENTIONS
• Dietary modification; exercise
(...____ D_IA_GN_o_s,_s) • Avoid smoking
DIAGNOSTIC IMAGING
• Endoscopy
LAB RESULTS
• Biopsy
35
CYCLIC VOMITING SYNDROME
osms.i"l/e14elie-vomtling
• Autonomic: lethargy, pallor, excessive
( PATHOLOGY & CAUSES ) salivation, low grade fever
• Neurologic: headache, photophobia,
• An uncommon disorder characterized by
phonophobia, vertigo
recurrent episodes of vomiting separated
by asymptomatic periods • Social withdrawal
• Median onset age: 5-6 years old
( D_IA_GN_o_s,_s __ )
CAUSES
• Cause unknown; triggers may include OTHER DIAGNOSTICS
psychological stress (e.g. interpersonal • History and physical examination
conflict, holidays) or physical stress (e.g. • No identifiable organic cause
infections, exhaustion). certain foods (e.g. • Diagnostic criteria (Rome IV criteria)
cow's milk, chocolate, cheese, monosodium
• ~ three recurrent, discrete episodes
glutamate) menses
of vomiting in the prior year, with
two episodes in the past six months
RISI( FACTORS occurring at least one week apart
• Children > adults = Variable intervals between vomiting
O In children: mitochondrial DNA deletions episodes and asymptomatic baseline
and polymorphisms • Stereotypical characteristics regarding
• Females > males timing of onset, symptoms, and duration
• Family history of migraines
• Autonomic abnormalities (elevated
sympathetic tone)
( T_R_E~_~_M_EN_T__ )
• Hypothalamic-pituitary-adrenal activation
OTHER INTERVENTIONS
(Sato variant)
• During cyclic vomiting episodes
• Chronic cannabis use
• IV fluids, antiemetics, sedatives; comfort
care in dark, quiet room
COMPLICATIONS
Prevention
• Erosive esophagitis
• Mallory-Weiss tear • Prophylactic therapy
• Dehydration
O Hl-antagonists (e.g. cyproheptadine)
for children s five years old
• Electrolyte imbalance
• Tricyclic antidepressants (e.g.
• Unintended weight loss
amitriptyline) > years of age
• Abortive therapy
( SIGNS & SYMPTOMS ) • Triptans; neurokinin-1
antagonists
receptor
• Symptoms tend to develop at night, in the • Avoidance of triggers

early morning hours. or upon awakening
• Prodromal period is common
• Gastrointestinal: vomiting which may
include bile or blood; retching, abdominal
pain. diarrhea
36
GASTRIC DUMPING SYNDROME
osmsJl/ gas-l,-ie-dumping

__ )
• Iatrogenic post-gastric surgery syndrome; DIAGNOSTIC IMAGING
impaired gastric rnotilltv=-v rapid stomach • Endoscopy
emptying
• Surgical intervention ----. disruption in
LAB RESULTS
gastric anatomy, mucosal function, fundus
• Oral glucose challenge test elicits
tone, antropyloric regulatory mechanisms,
symptoms
duodenal feedback on mottlttv -« rapid
emptying of stomach contents into • Hydrogen breath test after glucose
duodenum ingestion
• 50% of individuals undergoing gastric
surgical procedures OTHER DIAGNOSTICS
• More common in individuals who are • Gastric emptying study
biologically female • Clinical indices
, Sigstad's diagnostic index: > 7
( SIGNS & SYMPTOMS ) , Visick classification: heart rate

variations after oral glucose challenge
• GI: early satiety; abdominal colic; nausea,

vomiting; explosive diarrhea; bloating;
malabsorption
( T_R_EA_:l"_M_EN_T
__ )
• Vasomotor: diaphoresis; palpitations; MEDICATIONS
vertigo
• Early dumping syndrome Acarbose
0 30-60 minutes post-meal • Interferes with carbohydrate reabsorption
O Accelerated stomach emptying ----.
Octreotide
hyperosmolar contents poured into
small bowel ----. osmotic activity----. bowel • Inhibits insulin release
distention, motility sttmulated=-. GI
symptoms OTHER INTERVENTIONS
• Late dumping syndrome
0 60-180
Dietary modification
minutes post-meal
• Avoid simple sugars, fluid intake during
O Accelerated stomach emptying ----. l
meals; low carbohydrate, high protein diet
carbohydrate concentration in proximal
irrtestine e- rapid glucose absorption
----. rapid, sustained insulin response----.
hypoglycemia ----. vasomotor symptoms
37
GASTRITIS
osmsJI:/ go.s-1:Ti-l:is
• Infectious
= Most common cause (80%)
• Inflammation of the lining of the stomach , H. pylori - chronic gastritis - gastric

• May occur as a short episode or may be of atrophy - metaplasia - dysplasia -
cancer (associated with intestinal-type
a long duration
gastric carcinoma)
= Cytotoxin-associated gene A (CagA);
TYPES carcinogenic virulence factor of H. pylori
= Normal gastrin levels, no hypochloridia,
Acute gastritis
no anti-parietal cell/anti-intrinsic factor
• Inflammation of gastric mucosa; compare to
antibodies (compare to autoimmune
gastropathy (without active inflammation)
atrophic gastritis; hypochloridia, anti-
• Gastritis, gastropathy parietal/anti- intrinsic factor antibodies)
O Clinically identical, histologically distinct = Gastric ulcers
Atrophic gastritis
• AKA chronic gastritis, metaplastic gastritis,
gastric atrophy
• Chronic inflammation of gastric mucosa
- epithelial metaplasia, mucosal atrophy,
gland loss
O Metaplasia: reversible change of one
epithelium into another, response to
stress
O Intestinal metaplasia: goblet cells
CAUSES
Acute gastritis
• Certain medications, alcohol,
corticosteroids, uremia
• NSAIDs block cyclooxygenase - !
prostaglandin E2, 12 production - !
gastric defense mechanisms (mucus, HC03 Figure 31.1 A high magnification image of
secretion) - mucosa! injury Helicobacter organisms within a gastric crypt.
• H. pylori infection - gastric mucosa Helicobacter are a common cause of gastritis.
infiltrates antrum, corpus - inflammation
involving neutrophil, mononuclear cells
• Alcohol, cigarette smoke, caffeine - • Autoimmune
O Most common cause in individuals
irritates, erodes stomach mucosa lining
• Extreme physiological stress (e.g. shock, without H. pylori
sepsis, burns) O Inherited autoimmunity against intrinsic
factor, H+/K- ATPase in parietal cells
Atrophic gastritis - inhibition of gastric acid secretion
• Two main causes: infectious and (hypochloridia). ! intrinsic factor -
autoimmune
38
cobalamin (812) malabsorption -
pernicious anemia (..__ __ D_IA_GN_O_s,_s
__ )
O Hypochloridia (impaired iron absorption
/G-cell hyperplasia, hypergastrinemia -
LAB RESULTS
t neuroendocrine tumor formation) Endoscopic biopsy
O t gastric adenocarcinoma, • Distinguish gastropathy from gastritis,
neuroendocrine tumors nonspecific; mucosal erosions, erythema,
O Damage limited to gastric fundus, body absence of rugae
• Infectious atrophic gastritis
RISI( FACTORS , Multifocal atrophy; gastridduodenal
ulcers; erythematous, nodular mucosa;
Atrophic gastritis thickened rugal folds in early disease,
• Infectious loss of rugal folds in late disease;
O Household crowding; rural areas; poor damage limited to gastric antrum
sanitation • Autoimmune atrophic gastritis
• Autoimmune , Diffuse atrophy, absent rugae, mucosal
O Associated with HLA-DR3, BS, other thinning, visible submucosal blood
autoimmune diseases; more common in vessels
biologically-female individuals
H. pylori detection
• Serology, stool antigen test, urease breath
( s,_G_NS_&_SY_M_PT_O_M_s_) test, biopsy
• Atrophic gastritis
• May be asymptomatic , H. pylori curved bacilli (hematoxylin,
• Epigastric pain, nausea, vomiting eosin; Giemsa; Warth in-Starry stain);
• Mucosal ulcers intraepithelial neutrophil, plasma cell
invasion
• Hemorrhage, hematemesis, melena
Other lab results
Autoimmune atrophic gastritis
• Autoimmune atrophic gastritis
• Iron deficiency anemia
, Anti-IF antibodies, anti-parietal cell
O Hypochlorhydria - dietary iron in
antibodies
ferric form - ! iron absorption - iron
deficiency , t serum gastrin: parietal cell loss -
achlorhydria - unrestricted gastrin
• Pernicious anemia (symmetrical neuropathy
secretion
predominantly affecting lower limbs)
, ! serum pepsinogen: gastric oxyntic
O Anti-intrinsic factor (IF) antibodies,
mucosa damaged - ! chief cells - !
! cobalamin (812) absorption -
serum pepsinogen
depletion of 5-methyl-tetrahydrofolate
- homocysteine cannot convert , Lymphocytosis, eosinophilia, plasma
into methionine - impaired myelin cell invasion; oxyntic gland destruction;
regeneration - subacute combined metaplasia (intestinal, pyloric,
degeneration of spinal cord posterior pancreatic)
columns
O Weakness, paraplegia, paresthesias,
ataxia, loss of position/vibration sense
O Spasticity, clonus; atrophic glossitis;
fecal/urinary incontinence; diarrhea;
dementia
39
( T_R_E~_~_M_EN_T
)
MEDICATIONS
Remove offending agents
• NSAIDs, acids/alkalis
Eradicate H. pylori
• Triple therapy
, PPI + clarithromycin + amoxicillin (2
weeks)
• Quadruple therapy
= PPI + bismuth + metronidazole +
tetracycline (1 week)
Correct vitamin deficiencies

• 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

of intestinal metaplasia, characterized by
the presence of goblet cells in the gastric
mucosa.
40
CD4" cells vs. H"/K· ATPase
H. pylori infection
in gastric cells
Body, fundus Antrum
Hypochloridia Urease production by H. pylori

f gastrin
Mostly asymptomatic until severe
Symptoms of vitamin deficiencies Epigastric pain
Mal absorption
Lymphocytic infiltrate Neutrophilic infiltrate
Pernicious anemia
Peptic ulcers
Iron deficiency anemia
Mucosa-associated lymphoid
tissue lymphomas (MALTomas)
Carcinoid tumors
Autoimmune diseases low socioeconomic status
GASTROPARESIS
osms.tl/ go.s-lropo.resls
( PATHOLOGY & CAUSES ) (__ SI_G_NS_&_S_Y_M_PT_O_M_

)
• Delayed gastric emptying, no mechanical • Chronic nausea, vomiting
obstruction • Early satiety, bloating
• Abdominal pain
CAUSES
• Most common cause
, ldiopathiddiabetes
( D_IA_GN_O_SI_S
)
• Iatrogenic (post-surgical/medication side DIAGNOSTIC IMAGING
effect), post-viral
• More common among individuals with Endoscopy, CT scan, MRI
TlDM than T2DM secondary to neuropathy • Exclude mechanical obstruction
Gastric emptying scintigraphy
41
( T_R_E~_~_M_EN_T
) OTHER INTERVENTIONS
• Exercise; low fat diet
MEDICATIONS
• Metoclopramide (gastrointestinal prokinetic)
• Remove medications that may delay gastric
emptying
PEPTIC ULCER
osms.i"l/pep-lie-u leel9

• Chronic mucosal ulceration of stomach/
duodenum extends into muscularis mucosa.
• Most common cause of upper
gastrointestinal bleeding; proximal
duodenum/gastric antrum
• Associated with chronic gastritis
• j acid secretion, ! protective mechanisms
----> mucosal damage----> ulceration
RISI( FACTORS
• H. pylori infection (most common)
O l gastric acid secretion, ! duodenal
HC03 secretion
• NSAID Figure 31.4 An endoscopic view of the
O Particularly low dose aspirin gastric antrum which displays two discrete
corticosteroids ulcers.
• Physiologic stress
° Cushing's ulcer (intracranial
hypertension), Curling ulcer (severe
burns)
(__ SI_G_NS_&_SY_M_PT_O_M_s_)
• Psychological stress • Up to 70% asymptomatic
• Hyperchlorydia • Epigastric burning pain; may mimic
• Smoking myocardial infarction
• Chronic obstructive pulmonary disease = Usually occurs few hours after meal,
(COPD) worsens at night
• Hypergastrinemia (Zollinger-Ellison O Pain characteristically relieved by food/
syndrome) antacids
• Pain may radiate to back, chest, left/right
upper abdominal quadrants
• Nausea, vomiting, coffee-ground emesis,
bloating, weight loss
42
• Surgical emergency
O Hematemesis, melena, positive guaiac
test if slow bleed
O Acute abdomen; abdominal guarding,
peritonitis
O GI obstruction
• Gastric outlet obstruction, fistula formation
( D_IA_GN_O_s,_s __ )
DIAGNOSTIC IMAGING
Abdominal CT scan
Barium abdominal radiography
Endoscopy
• Diagnostic, therapeutic Figure 31.5 A barium study demonstrating
the bullseye sign in a case of a gastric ulcer.
( T_R_EA_:l"_M_EN_T__ )
MEDICATIONS
• Discontinue NSAIDs, avoid smoking
• PPI
SURGERY
• Endoscopic ligation/coagulation of bleeding
ulcers
43
NOTES
• NOTES
~ GASTROINTESTINALCANCERS

• Grading, TNM staging for treatment
( PATHOLOGY & CAUSES ) , T: characteristic of primary Tumor (e.g.
invasion of nearby tissue)
• Tumors arising from cells in gastrointestinal
n N: involvement of regional lymph Nodes
(GI) tract
n M: Metastasis; spread from primary
• Multifactorial etiology; generally result from
tumor to other body parts
aberrant cellular signaling, unregulated
cellular growth
O Genetic alterations (e.g. point mutations, LAB RESULTS
amplifications, rearrangements,
deletions) Biopsy
O Epigenetic influence (e.g. DNA • Histopathological diagnosis
methylation, chromatin remodeling)
O Environmental factors (e.g. exposure to
carcinogens, chronic inflammation)
(..____ T_R_E~_~_M_EN_T
__ )
• Risk increases with age MEDICATIONS
• Chemotherapy
SURGERY
• Highly variable clinical presentation; see • See individual disorders
individual disorders
• Fatigue, anorexia, weight loss
OTHER INTERVENTIONS
• Radiation therapy
(..____ D_IA_GN_O_s,_s
__ )
DIAGNOSTIC IMAGING
Imaging studies
• Localization, staging
44
CARCINOID TUMOR
osms.i"l/ eo.Teinoid--lumoT
cells
( PATHOLOGY & CAUSES ) , Commonly located in ileum; may arise
from Meckel's diverticulum
• Uncommon, well-differentiated, slow-
growing neuroendocrine tumor; originates , Potential for lymph node/hepatic
in tubular digestive tract; also found in metastasis
bronchopulmonary system, genitourinary • Appendix
tract , Originates from subepithelial endocrine
• Benign/malignant; tendency for liver cells
metastasis , Relatively low potential for metastasis
• Carcinoid: tumors of different
Hindgut tumors
morphology, less aggressive than GI tract
adenocarcinomas; low grade (proliferative • Rectum, colon, cecum (most common)
activity); low mitotic rate
COMPLICATIONS
TYPES • Depend on tumor's location, size, local
• Embryonic origin of GI tract (e.g. foregut, biochemical attributes
midgut, hindgut) , Local/distant metastasis
, Pain: obstruction, intussusception,
Foregut tumors (e.g. stomach) bowel ischemia, mechanical pressure
• Type I from tumor
O Most common , Desmoplasia: intense, local reaction
O Originates from enterochromaffin-like characterized by overproduction
(ECL) cells of extracellular matrix proteins+
O In association with high gastrin levels myofibroblast cell proliferation ----.
secondary to chronic atrophic gastritis fibrosis, obstruction
O Small, usually benign , Carcinoid syndrome: tumor-related
humoral factors (e.g. serotonin,
• Type II
histamine, etc.) ----. cutaneous flushing,
O Originates from ECL cells
pruritic rash; excessive lacrimation;
O 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 )
(MENl)
O Often large, indolent; low-grade • Often asymptomatic, discovered
malignancy incidentally (e.g. imaging, surgery,
• Type Ill endoscopy)
O Not associated with high gastrin levels • Vary according origin site
O Large, aggressive; local lymphatid , Nonspecific, vague abdominal pain
hepatic metastases; produce serotonin , Loss of appetite, vomiting, diarrhea,
(5-HT) con sti patio n
• Desmoplasia (with CT scan)
Midgut tumors
• Small bowel (most common)
O Originates from intraepithelial endocrine
45
( D_IA_GN_O_SI_S ) ( T_R_EA_:T"_M_EN_T
)
DIAGNOSITC IMAGING MEDICATIONS
• Somatostatin analogues suppress tumor
CT scan, MRI, labeled somatostat
in recep-
proliferation, decrease symptoms
tor-based diagnostic imaging
• Localization, TNM staging
• Presence of hepatic lesions SURGERY
• Surgical removal of tumor
Endoscopy with biopsy
• Tumor visualization
• Histopathological analysis, grading
LAB RESULTS
• 5-hydroxyindoleacetic acid, chromogranin
Figure 32.2 Gross pathology of carcinoid

tumor of the terminal ileum.

carcinoid tumor of the lung.
' MNEMONIC: CARCinoid.

Carcinoid syndrome
components
Cutaneous flushing
Asthmatic wheezing
Right-sided valvular heart
lesions
Cramping and diarrhea
46
CHOLANGIOCARCINOMA
osms.i"l/ eholo.ngioeo.Teinomo.
(IDH1)
( PATHOLOGY & CAUSES ) • Risk increases with age
• Slightly more common in individuals who
• Rare bile duct cancers; arise from epithelial
are biologically male
cells of intrahepatic, extrahepatic bile ducts
(not including gallbladder, ampulla of Vater)
• High fatality due to late diagnosis; highly COMPLICATIONS
proliferative • Metastasis
• Mostly adenocarcinomas; minority , Liver, lymph nodes, peritoneum, bone,
squamous cell carcinomas etc.
• Bowel perforation, bleeding
TYPES
• Determined by location (Bismuth-Corlette)
(__ SI_G_NS_&_S_Y_M_PT_O_M_
Type I
• Located below confluence of left, right • Often asymptomatic initially; malaise,
hepatic ducts weight loss, abdominal pain
• Extrahepatic disease (when bile drainage
Type II obstructed)
• Located at confluence , Right upper quadrant pain, jaundice,
pruritus, dark urine, clay-colored stools,
Type Illa
weight loss
• Occludes common hepatic duct • lntrahepatic disease
Type lllb = Dull right upper quadrant pain, malaise,
weight loss
• Occludes right/left hepatic duct
• Other findings
Type IV = Hepatomegaly, palpated mass
• Multicentric
RISI( FACTORS
• Primary
O Existing liver, gallbladder disease:
primary sclerosing cholangitis (PSC);
chronic liver disease (e.g. viral hepatitis,
cirrhosis)
• Congenital abnormalities of biliary tree
• Genetic disorders
O Lynch syndrome; multiple biliary
papillomatosis
• Obesity
• Liver fluke infection (undercooked fish)
a cholangiocarcinoma. There are normal
• lntrahepatic cholangiocarcinomas hepatocytes in the top left of the image, with
O Associated with mutations in gene the tumour occupying the bottom right of the
encoding isocitrate dehydrogenase 1 image.
47
( D_IA_GN_O_SI_S )
• History, physical examination
° Consistent with hepatobiliary disease
DIAGNOSTIC IMAGING
MRI, CT scan, PET, etc.
• Detailed evaluation of lesion TNM staging
Transabdominal/endoscopic ultrasound
(EUS) with biopsy
• Biliary obstruction, dilation of intrahepatic
ducts
• Histolopathological analysis, grading

LAB RESULTS cholangiocarcinoma. This image shows the
• Tumor markers tumor edge, with normal hepatocytes on the
° Carbohydrate antigen (CA) 19-9; right and tumor on the left. The tumor cells
carcinoembryonic antigen (CEA) form tubular structures and are surrounded
• Liver function tests by fibrosis.
° Consistent with biliary obstruction,
cholestasis
O Elevated transaminases,
glutamyl transpeptidase,
gamma-
alkaline
C T_R_E~_~_M_EN_T__ )
phosphatase
MEDICATIONS
O Prolonged prothrombin time/elevated
• Fluoropyrimidine-based chemoradiotherapy
INR
• Chemotherapy
O Elevated bilirubin
SURGERY
• Resection
OTHER INTERVENTIONS
• Radiation
48
COLORECTALCANCER
osms.i"l/ eoloree-lo.1-eo.neeT
• Black people of African descent
( PATHOLOGY & CAUSES ) ' Highest rates in United States
• More common in individuals who are
• Common malignancy of large bowel/rectum
biologically male
• Third most common cancer worldwide
• Risk increases with age
• Often arises from colonic epithelial tissue
• Protective factors
- adenomatous polyp formation -
adenocarcinoma O Physical activity; regular use of aspirin,
other nonsteroidal anti-inflammatory
• High metastatic potential after penetrating
drugs (NSAIDs)
muscularis mucosa
RISI( FACTORS COMPLICATIONS

• Iron-deficiency anemia (due to bleeding)
• Hereditary
• Local, distant metastasis
° Familial adenomatous polyposis;
Lynch syndrome, MUTYH-associated • Bowel obstruction
polyposis • Cachexia
• Inflammatory bowel disease • Bowel perforation - peritonitis
• Lifestyle
O Smoking, physical inactivity
• Dietary
( s,_G_NS_&_S_Y_M_PT_O_M_s_)
O High alcohol consumption; processed • May be asymptomatic initially
red meat; low consumption of fruits,
• Vague constitutional symptoms
vegetables
' Fatigue, anorexia, weight loss
• Obesity
• Change in bowel habits
• Diabetes mellitus, insulin resistance
O Narrowing of stool, constipation,
• Low socioeconomic status
diarrhea
• History of abdominal radiation
• Rectal bleeding
• Lack of screening colonoscopy
n Frank/occult
• Rectal pain, tenesmus (feeling of

incomplete defecation)
• Nausea, vomiting
O Bowel obstruction from advanced
malignancy
(..__ __ D_IA_GN_o_s,_s __ )
DIAGNOSTIC IMAGING
Colonoscopy/flexible sigmoidoscopy;
biopsy, CT colonography
• Tumor visualization. histopathological
Figure 32.5 Gross pathology of an exophytic analysis. grading, TNM staging, potential
colorectal carcinoma. for resection
49
( T_R_E_AT_M_E_N_T
__ )
MEDICATIONS
• Chemotherapy
SURGERY
• Polypectomy with clear margins
• Surgical resection
• Sessile polyps: colectomy

OTHER INTERVENTIONS
adenocarcinoma of the colon. The tumor is
• Chemoradiation therapy
composed of malignant cells which continue
to form glandular structure. The left side of
the image displays normal colonic mucosa.
LAB RESULTS
• Tumor marker: CEA
• Stool guaiac testing
O Positive for occult blood
OTHER DIAGNOSTICS
Digital rectal exam
• Palpable mass if distal rectal mass
Figure 32.8 Positron emission tomography

Figure 32.7 A CT scan in the axial plane
with high levels of tracer accumulation in the
demonstrating a tumor in the cecum.
pelvis (rectal tumor) as well as the liver and
kidneys (metastases).
50
ESOPHAGEAL CANCER
osms.i"l/ esopho.geo.1-eo.neeT

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

• Chronic exposure to lrrltants c- metaplasia
----. dysplasia ----. malignant transformation DIAGNOSTIC IMAGING
EUS guided biopsy, CT scan, PET, integrat-
RISI( FACTORS ed fluorodeoxyglucose(FOG)
• Smoking
• Tumor visualization, histopathological
• Alcohol (esp. combined with smoking) analysis, grading, TNM staging, potential
• Gastroesophageal reflux disease (GERD); for resection
reflux esophagitis, Barrett esophagus
• Hiatal hernia Bronchoscopy
• More common in individuals who are • In carina identifies potential lung
biologically male involvement
OTHER DIAGNOSTICS
• Palpable supraclavicular lymphadenopathy
\ MNEMONIC: ASCOEF
Esophageal cancer risk
factors
Achalasia
Barret's esophagus
Corrosive esophagitis
Diverticulitis
Esophageal web
Familial
COMPLICATIONS
• Esophageal obstruction; regurgitation Figure 32.9 Endoscopic appearance of an
- aspiration ----. aspiration pneumonia; esophageal tumor. The tumor sits at the
metastasis gastroesophageal junction and is viewed
from above.
51
( T_R_EA_:T_M_EN_T
__ )
MEDICATIONS
• Chemotherapy
SURGERY
• Resection of primary tumor, associated
nodes
OTHER INTERVENTIONS
• Radiation
Esophageal stenting
• Therapeutically enlarges esophageal lumen,
reduces dysphagia
Figure 32.10 A barium swallow

demonstrating a tumor distorting the normal
outline of the esophagus.
GALLBLADDER CANCER
osmsJl/ ge1ll\>lcuideT-ee1neeT
= Cholelithiasis(gallstones), primary
( PATHOLOGY & CAUSES ) sclerosing cholangitis, porcelain
gallbladder. gallbladder polyps. biliary
• Uncommon malignancy; most frequently cysts; chronic infection (e.g. Salmonella
diagnosed cancer of biliary tract typhi, Heficobacter bilis)
• High fatality rate due to typically late • More common in individuals who are
diagnosis biologically female
• Most gallbladder cancers arise within • Obesity
fund us
• Cigarette smoking
• May obstruct bile flow at common bile duct/
• Occupational exposure to carcinogens:
duodenum
textile, oil. paper, chemical industries. radon
(mining)
RISk FACTORS • Genetic predisposition
• Chronic gallbladder inflammation
52
COMPLICATIONS
• Biliary fistula
• Local/nodal/distant metastases
• Often asymptomatic in early stages;
malignancy discovered incidentally after
symptoms mimic benign gallbladder
disease
• Non-specific symptoms Figure 32.11 Histological appearance of
O Malaise, pain, anorexia, nausea, gallbladder adenocarcinoma. The tumor
vomiting, weight loss cells show increased nuclear size, prominent
• Clinical manifestations (when bile drainage nucleoli and are forming tubular structures.
obstructed)
O Jaundice, dark urine
• Palpable gallbladder
( T_R_EA_~_M_EN_T__ )
MEDICATIONS
( D_IA_GN_o_s,_s __ ) • Chemotherapy
DIAGNOSTIC IMAGING
SURGERY
EUS guided/percutaneous biopsy, CT scan,
• Simple/radical cholecystectomy
MRI, PET, MRCP
analysis, grading, TNM staging, potential OTHER INTERVENTIONS
for resection • Radiation
LAB RESULTS
• Tumor markers: CA 19-9; CEA
• Liver function tests
° Consistent with biliary obstruction,
cholestasis
O Elevated transaminases, gamma-
glutamyl transpeptidase, alkaline
phosphatase
O Elevated bilirubin
53
HEPATOBLASTOMA
osms.i"l/hepa-lo\,las-loma
( PATHOLOGY & CAUSES ) (..____ D_IA_GN_O_s,_s

__ )
• Common primary childhood hepatic DIAGNOSTIC IMAGING
malignancy; arises from primitive hepatic
cells Ultrasound, percutaneous biopsy, CT scan
with/without contrast, MRI
• Usually occurs in right lobe of liver
• Diagnostic workup for tumor visualization,
• Morphologically diverse tumor: composed
histopathological analysis, grading,
of many cell types including embryonal
pretreatment staging system (PRETEXT);
hepatocytes, tissues (e.g. bone, striated
potential for resection
muscle)
• Extramedullary hematopoiesis may occur in
sinusoids LAB RESULTS
• Usually present during first two years of life • Elevated alpha-fetoprotein (AFP)
• Genetic testing
RISI( FACTORS
• Beckwith Wiedemann syndrome
• Trisomies 18, 21
• Familial adenomatous polyposis
• Type la glycogen storage disease
• Li-Fraumeni syndrome
biologically male
COMPLICATIONS
• Ectopic gonadotropin ----> precocious
puberty (uncommon)
• Fatal hepatic hemorrhage, rupture Figure 32.12 Histological appearance of
a hepatoblastoma, a tumor of immature
• Metastasis: commonly lungs
hepatocytes.
( SIGNS & SYMPTOMS )

(..____ T_R_E~_~_M_EN_T__ )
• Children
O Abdominal mass: discomfort MEDICATIONS
• Anorexia, weight loss, precocious puberty • Chemotherapy
SURGERY
• Resection
54
HEPATOCELLULARCARCINOMA
osms.i-l/hepo.-loeellulo.T-eo.Teinomo.

)
• Hepatic malignancy commonly diagnosed • Often no symptoms aside from those of
in presence of chronic liver disease chronic liver disease
• Epigastric pain; appetite, weight loss
RISI( FACTORS • Palpable abdominal mass; manifestations
• Hepatitis B/C infection, coinfection with of decompensated cirrhosis (e.g.
hepatitis D splenomegaly, ascites, jaundice); hepatic
bruit
• Hereditary hemochromatosis
• Cirrhosis
• Smoking; frequent alcohol consumption
• Obesity
• Alpha-1 antitrypsin deficiency
• Gallstones
• Chronic exposure to aflatoxin (mycotoxin
found in peanuts, soybeans, corn)
biologically male
COMPLICATIONS
• Paraneoplastic syndrome: watery
diarrhea, hypoglycemia, hypercalcemia,
erythrocytosis; cutaneous lesions (e.g.
pemphigus foliaceus)
• 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 ( D_IA_GN_O_SI_S )
etiology
Aflatoxins DIAGNOSTIC IMAGING
HepB
Ultrasound with biopsy, CT scan, MDCT,
Cirrhosis
arteriography
, portography , MRI
Hepatocellular carcinoma
analysis, grading, TNM staging, potential
features
for resection
AFP increased: classic marker
Bile-producing: DDx from MRI angiography
cholangiocarcinoma • 30 characterization of lesion, hepatic
Most Common primary liver circulation
tumor
55
LAS RESULTS
• Elevated aminotransferases, alkaline
phosphatase, gamma-glutamyl
transpeptidase; hyperbilirubinemia;
hypoalbuminemia
• Elevated alpha-fetoprotein (most common
serum marker)
Figure 32.14 Gross pathology of

hepatocellular carcinoma.
( T_R_EA_:l'_M_EN_T__ )
MEDICATIONS
• Chemotherapy
• Systemic molecularly targeted therapy;
sorafenib, nivolumab
hepatocellular carcinima. The cells show
high nuclear variation, thickened nuclear SURGERY
envelopes and occasional prominent nucleoli. • Partial hepatectomy
The cells also have abundant eosinophilic • Liver transplant
cytoplasm.
OTHER INTERVENTIONS
• Radiofrequency ablation
• Percutaneous ablation with ethanol/acetic
acid
• Transarterial chemoembolization
• Cryoablation
• Radiation therapy; stereotactic body
radiation therapy
56
ORAL CANCER
osmsJl/ erel-ceneer
COMPLICATIONS
( PATHOLOGY & CAUSES ) • Surgical resection - airway, speech,
mastication, cosmetic complications
• Oral cavity malignancy; arises from mucosal
• Metastasis
surfaces
O Lips, buccal mucosa, anterior tongue,
mouth floor, hard palate, gingiva,
retromolar trigone
O Most often: squamous cell carcinoma • Asymptomatic initially
• May arise from normal mucosa/ • Pain/burning sensation
premalignant lesions (e.g. erythroplakia,
• Lump/ulcer visualized, palpated
leukoplakia); undergo malignant
• Hard, fixed lymph nodes
transformation
RISI( FACTORS ( D_IA_GN_O_s,_s __ )

• Tobacco (esp. with alcohol)
• Alcohol DIAGNOSTIC IMAGING
• Human papillomavirus (HPV) infection:
CT scan/MRI
oropharynx
• Local spread/location of additional primary
• Periodontal disease
tumors
• Chronic oral candidiasis
• Betel quid chewing
LAB RESULTS
• lmmunosuppression
• Fine needle biopsy; histopathological
• Hepatitis C infection
diagnosis
• Genetic polymorphisms: cytochrome P450
1A1 (CYPIA 1); glutathione S-transferase
mu 1 (GSTM1); alcohol dehydrogenase 3 OTHER DIAGNOSTICS
genotype - oropharyngeal cancers • Palpation and visualization
• More common in individuals who are , Of mucous membranes, oral cavity,
biologically male lymph nodes
• Flexible laryngoscopy
O Back of throat, vocal cords
MNEMONIC: PATH LAS
Oral cancer risks ( T_R_EA_~_M_EN_T )
Plummer-vinson syndrome
Alcohol MEDICATIONS
Tobacco • Chemotherapy
Human papilloma virus
Leukoplakia SURGERY
Asbestos • Resection
Bad oral hygiene
OTHER INTERVENTIONS
• Radiation
57
PANCREATIC CANCER
osms.it/ po.neY-eo.tie-eo.Y-einomo.

)
• Highly lethal malignancy of exocrine DIAGNOSTIC IMAGING
pancreas
Transabdomina
l ultrasound
• Usually unresectable at presentation
• Detects degree of biliary tract dilation,
obstruction
RISI( FACTORS
• Chronic pancreatitis ERCP
• Malignant transformation of pancreatic • Increased visibility of pancreaticobiliary tree
intraductal papillary mucinous neoplasm
MRCP
(IPMN)
• Visualization of liver parenchyma, vascular
• Genetic mutations (e.g. BRCA-1, BRCA-2,
structures
ATM, PALB2, CDKN2A, MLHl)
• Smoking; obesity; sedentary lifestyle Laparoscopy
• Determines resectability
COMPLICATIONS Abdominal CT scan; contrast-enhanced CT
• Hypercoagulability with possible venous/ scan, EUS guided/percutaneous biopsy
arterial thromboembolism
• Paraneoplastic manifestations analysis, grading, TNM staging
O Bullous pemphigoid; nodular fat necrosis
(pancreatic panniculitis)
• Metastasis
LAB RESULTS
• Tumor marker: CA 9-19
• Hyperbilirubinemia (mostly conjugated);
(__ s,_G_Ns_&_s_v_M_PT_O_M_s_) elevated alkaline phosphatase
• Recent onset of diabetes mellitus OTHER DIAGNOSITCS

• Clinical presentation
O Tumor location Cardiac catheterization
• Pain • Measure pressure in right side of heart
O Epigastric, abdominal, may radiate to
the back, may worsen after eating/when
lying down; asthenia:
( T_R_EA_:t"_M_EN_T
)
• Physical weakness, loss of strength;
MEDICATIONS
anorexia, nausea; weight loss; jaundice,
• Chemotherapy with/without
dark urine
chemoradiotherapy
• Hepatomegaly; right upper quadrant mass;
Courvoisier's sign (nontender, palpable
gallbladder at right costal margin); cachexia; SURGERY
metastasis: left supraclavicular/periumbilical • Resection (e.g. pancreaticoduodenectomy)
lymphadenopathy, ascites, abdominal mass O Only curative treatment
58
pancreatic adenocarcinoma. The tumor cells
form acini, small sack like spaces surrounded
Figure 32.16 Cytological preparation of
by malignant glandular cells.
a pancreatic fine needle aspirate which
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.i-1:/s-1:omo.eh-eo.neeT
common in high-risk populations
( PATHOLOGY & CAUSES ) • lntercellular adhesion molecules -
adherence of tumor eel Is - arrangement in
• Aggressive adenocarcinoma arising from
glandular formations
gastric mucosa
RISI( FACTORS
TYPES
• Primary cause (G-INT)
Diffuse type (G-DIF): undifferentiated , H. pylori infection
• Impairment/lack of adhesion molecule • Family history of gastric cancer
E-cadherin • Autoimmune atrophic gastritis
• Genetic mutation (germline, somatic, • Lifestyle
epigenetic methylation) of CDH 1 gene O Smoking. alcohol consumption
- inactivation of CDHl - nonfunctional
• Diet
E-cadherin - unregulated division
O Nitrates, nitrosamines, highly-salted
(impaired tumor suppressor function);
increased ability to spread. invade adjacent foods; pickled/smoked foods
structures • Obesity
O Autosomal dominant inheritance pattern • Risk increases with age
O More aggressive than G-INT • More common in individuals who are
biologically male
Intestinal type (G-INT): well-differentiated
• Due to environmental factors; more
59
• Protective factors
O Intake of fruit, vegetables, fiber, folate
( D_IA_GN_O_s,_s __ )
DIAGNOSTIC IMAGING
COMPLICATIONS
Esophagogastroduodenoscopy with biop-
• Metastasis to liver, peritoneum, lymph
sy, barium studies, abdominopelvic CT scan
nodes, etc.
• Paraneoplastic manifestations
analysis, grading, TNM staging, potential
O Seborrheic keratoses, polyarteritis
for resection
nodosa, Trousseau's syndrome
(spontaneous, recurrent, migratory
venous thrombosis) OTHER DIAGNOSTICS
Physical examination
• Enlarged supraclavicular, anterior axillary,
periumbilical lymph nodes
• Palpable abdominal mass
Figure 32.18 Gross pathology of gastric

carcinoma. The stomach has been pinned
flat. The tumor is found in the antrum.
• Asymptomatic initially
• Early symptoms
O Vague constitutional symptoms (e.g.
malaise, loss of appetite, dyspepsia)
• With disease progression
O Epigastric pain, nausea, vomiting,
dysphagia, weight loss
Figure 32.19 The histological appearance of
• If GI bleeding a well-differentiated gastric adenocarcinoma
O Anemia, melena, coffee-ground of intestinal type. The tumor is composed of
hematemesis disordered glands, the cells of which have
• Pseudoachalasia syndrome (difficulty large, hyperchromatic nuclei.
moving food, liquids from esophagus to
stomach)
O If tumor extends to Auerbach's
plexus/obstruction occurs near
gastroesophageal junction
60
SURGERY
(..__ __ T_R_EA_:T_M_EN_T
) • Resection
MEDICATIONS
OTHER INTERVENTIONS
Chemotherapy • Chemoradiotherapy
• G-INT, G-DIF differ in susceptibility to
chemotherapeutic agents
• Eradication of H pylori infection
WARTHIN'S TUMOR
osms.i-1:/wo:r-lhins--1:umoT

)
• Uncommon benign tumor; arises from • Development of painless nodular mass,
salivary gland usually near mandible angle
• AKA papillary cystadenoma
lymphomatosum
• May involve submandibular/sublingual/ (..____ D_IA_GN_O_SI_S
)
parotid gland (most common)
• Unilateral/bilateral, slow-growing
OTHER DIAGNOSTICS
• Easily palpable tumor
RISI( FACTORS Fine needle aspiration

• Smoking • Histopathological diagnosis
biologically male
( T_R_EA_:T_M_EN_T
)
SURGERY
COMPLICATIONS • Local resection/parotidectomy
• Malignant transformation (rare)
61
NOTES
• NOTES
~ INFLAMMATORY BOWEL DISEASE
( PATHOLOGY & CAUSES ) (.____ D_IA_GN_O_s,_s
)
• Immune-mediated inflammatory bowel DIAGNOSTIC IMAGING
conditions • Endoscopy
• More common in White people of Jewish
descent
LAB RESULTS
• Usually presents in young people, 15-35
• Biopsy
• Up to 25% of people with inflammatory
bowel disease have affected first-degree
relative (.____ T_R_E~_~_M_EN_T
)
CAUSES MEDICATIONS
• Gut microbiome alterations • Anti-inflammatory medications; antibiotics;
immunosuppressants
• "Western" style diet: high processing/
sugar/fat content
SURGERY
RISI( FACTORS • Surgical resection
• Crohn's disease: smoking
O Smoking may be protective for OTHER INTERVENTIONS
Ulcerative colitis • Dietary changes
• Chronic diarrhea, frequently bloody/mucous
• Abdominal pain
• Fever, weight loss, anemia
• Extraintestinal manifestations
O Arthritis, uveitis
62
CROHN'S DISEASE
osms.i"l/ eY-ohns-disee1se
( PATHOLOGY & CAUSES ) CAUSES

• Unclear; mycobacterium paratuberculosis,
pseudomonas, listeria implicated
• AKA Crohn disease, regional enteritis
• Chronic, immune-related disorder -
excessive immune response to unknown ( s,_G_NS_&_SY_M_PT_O_M_s_)
trigger - transmural inflammation
anywhere along gastrointestinal (GI) tract,
• Unpredictable patterns of flares, remissions
mouth to anus
• Abdominal pain; most common in right
• Compare to ulcerative colitis
lower quadrant (ileal inflammation)
O Only affects colon, rectum; superficial
• Fatigue, fever, nausea, vomiting
lesions; autoimmune disorder where
• Chronic diarrhea; may/may not be bloody
tissue is directly attacked by immune
system , Gross bleeding rare; upon microscopy,
bleeding common
• Frameshift mutation in nucleotide-binding
oligomerization domain-containing protein • Malabsorption, weight loss, vitamin
2 (NOD2)/ caspase recruitment domain- deficiencies
containing protein 15(CARD15) • Up to 20% of cases present with
O Excessive inflammatory response - inflammatory eye, skin, joint lesions
tissue damage O Uveitis, erythema nodosum, pyoderma
• Unknown immune response trigger - T gangrenosum, cholelithiasis (impaired
helper (Th) 1 cells release inflammatory bile reabsorption), arthritis
cytokines • Perianal abscesses, phlegmon, fistulae
O Interferon (IFN) gamma, tumor necrosis O Perianal fistulas (up to 30%)
factor (TNF) alpha - inflammatory O Enterovesical fistulae - recurrent UTI,
response - cytokines recruit pneumaturia
macrophages - further inflammatory O Enteroenteric fistulae - asymptomatic
mediators released (proteases, platelet O Enterovaginal fistulae - passage of
activating factor, free radicals) - fecal matter through vagina
further inflammation - healthy tissue
O Enterocutaneous fistulae - draining of
destroyed - inflammatory cells invade
bowel contents unto skin
intestinal mucosa - ulcer, granuloma
form - transmural inflammation - • Intestinal obstruction (up to 30%)
intestinal lumen; fistula formation,
narrowing
• Fistula, stricture formation
O Serosal layer involvement - fistula
O Most common: enterovesical,
enterocutaneous, enterovaginal,
enteroenteric fistulae
• Scattered inflammation - cobblestone
appearance
• Most commonly affects terminal ileum,
colon
Figure 33.1 Pyoderma gangrenosum on the
leg of an individual with Crohn's disease.
63
\ MNEMONIC: CHRISTMAS
Features of Crohn's disease
Cobblestones
High temperature
Reduced lumen
Intestinal fistulae
Skip lesions
Transmural: all layers, may
ulcerate
Figure 33.3 Gross pathology of a resected
Malabsorption
colon involved by Crohn's disease. The
Abdominal pain severe and prolonged inflammation has led
Submucosal fibrosis to a cobblestone appearance of the colonic
mucosa.
( D_IA_GN_O_s,_s)
( T_R_E~_~_M_EN_T
)
DIAGNOSTIC IMAGING
• Endoscopy MEDICATIONS
• Anti-inflammatory medications ---->
sulfasalazine
LAB RESULTS
° For colonic symptom management
• Biopsy
• Antibiotics----> metronidazole
° Cobblestone appearance, intermittent
lesion pattern, pseudopolyps, aphthous O Reduce bacterial overgrowth, anti-
ulcers inflammatory effect
• lmmunosuppressants----> prednisone,
azathioprine
OTHER DIAGNOSTICS O Only if no response to antibiotics
• Barium enema
• Antidiarrheals
• Methotrexate, anti-TNF agents
O Refractory disease
SURGERY
• Surgical removal of affected tissue
O
High relapse rate
O Short bowel syndrome: complication of
resection
OTHER INTERVENTIONS
• Nutritional supplementation, support

Crohn's disease. The lamina propria is
expanded by chronic inflammatory cells and
there is a non-caseating granuloma present.
64
MICROSCOPIC COLITIS
osms.i"l/ mieroseopie-eoli-lis
( PATHOLOGY & CAUSES ) (..__ __ D_IA_GN_O_s,_s __ )

• Idiopathic chronic inflammation of colon - DIAGNOSTIC IMAGING
watery diarrhea
Endoscopy
• Associated with celiac disease,
autoimmune diseases, NSAIDs, smoking • Non-specific findings, normal mucosa

biologically female LAB RESULTS
• Unknown trigger - abnormal collagen • Biopsy of colonic mucosa
metabolism - dysfunctional epithelium , Inflammatory changes in lamina propria,
- alteration in barrier function - mucosal intraepithelial lymphocytic infiltration,
inflammation - decreased sodium dense subepithelial collagenous layer
absorption, increased chloride secretion - • Elevated inflammatory markers
secretory diarrhea (nonspecific)
O Erythrocyte sedimentation rate,
TYPES myeloperoxidase
• Autoantibodies
Collagenous
O Anti-thyroid peroxidase (TPO),
• More common in older individuals who are
antinuclear (ANA), antineutrophil
biologically female
cytoplasmic (ANCA). anti
• Dense subepithelial collagenous layer; Saccharomyces cerevisiae (ASCA).
increased intraepithelial lymphocytes, rheumatoid factor (RF)
inflammatory infiltrate in lamina propria
Lymphocytic
(..____ T_R_EA_~_M_EN_T )
• Increased intraepithelial lymphocytes,
inflammatory infiltrate in lamina propria MEDICATIONS
• Avoid NSAIDs. other medications
associated with microscopic colitis
(_~s,_G_NS_&~SY_M_P_TO_M_s_) • Antidiarrheals
• Abdominal pain , Loperamide, bismuth salicylate
• Chronic watery diarrhea • Corticosteroids
• No weight loss O Budesonide, prednisone
• Fecal urgency, incontinence • Bile acid sequestrants
n Cholestyramine
• Anemia
SURGERY
• Surgical resection (ileostomy)
65
BASEMENT MEMBRANE j
\

Figure 33.4 Histological appearance
lymphocytic colitis. There is an increase in
of collagenous colitis. The subepithelial
the number of intraepithelial lymphocytes
basement membrane is markedly thickened.
(>20/100 epithelial cells).
PROTEIN LOSING ENTEROPATHY

osmsJl/ pro-lein-losing-en-leropo.-lh14
( PATHOLOGY & CAUSES ) (__ s,_G_NS_&_SY_M_P_TO_M_s )

• Inflammatory GI conditions - loss of serum • Hyponatremia. peripheral edema, ascites
proteins into GI tract • Serosal effusions (pleural and pericardia!)
• Mucosal injury- epithelial inflammation, O Dyspnea, cough, chest pain
- mucosal permeability - protein • Steatorrhea, bloating, flatulence, abdominal
exudates across epithelium - proteins in pain
GI tract degraded into amino acids (AA)
• Weight loss. chronic diarrhea
• Lymphatic obstruction/venous stasis
- increased hydrostatic pressure in
lymphatics - lymph leaks into intestinal (..____ D_IA_GN_O_s,_s )
lumen - reduced chylomicron reabsorption
- decrease in fat soluble vitamins - LAB RESULTS
protein deficiency
• Consider in individuals with edema,
hypoalbuminemia
CAUSES • Increase in alpha-1 antitrypsin clearance
• Inflammatory bowel disease • Exclude other causes of hypoproteinemia
° Crohn's disease, ulcerative colitis = Renal disease - proteinuria
• Malabsorptive diseases • Hepatic disease - impaired protein
O Tropical sprue, celiac sprue synthesis
• Infectious diseases O Malnutrition
O C. difficile - pseudomembranous colitis
• GI malignancies
( T_R_E~_~_M_EN_T )
OTHER INTERVENTIONS
• Low fat, high protein diet; supplement
medium chain triglycerides (MCT)
66
ULCERATIVE COLITIS
osms.i"l/ u leel9o..live-eoli-lis
I MNEMONIC: ULCERATIONS
i
Features of Ulcerative colitis
Ulcers
• Autoimmune disease-« superficial ulcer
formation; continuous, circumferential Large intestine
inflammation in colonic, rectal mucosa Carcinoma (risk of)
• Most common inflammatory bowel disease; Extraintestinal manifestations
may present at any age Remnants of old ulcers
• Compare to Crohn's disease (pseudopolyps)
O Usually affects young people, affects Abscesses in crypts
entire GI tract; causes transmural Toxic megacolon (risk of)
inflammation; patches of inflamed Inflamed, red, granular mucosa
mucosa, cobblestone appearance Originates at rectum
• CD8+ cell activation ----. destruction of cells Neutrophil invasion
in mucosal, submucosal colonic layers
Stool is bloody
O Associated with perinuclear anti-
neutrophil cytoplasmic antibodies
(p-ANCAs)
• Multifactorial origin ( SIGNS & SYMPTOMS )
O Environmental stimuli + excessive
sulfide-producing bacteria + genetic • Acute flares, remissions; gradual onset
predisposition , Risk of relapse related to person's age at
• More common among white people, diagnosis
especially of Eastern European descent • Severity determined by frequency of bowel
• More common in young individuals who are movements, degree of inflammation,
biologically female systemic symptoms
• Colicky, left lower quadrant pain
CAUSES • Diarrhea; frequently grossly bloody, mucous
• Unclear; autoimmune reaction against • Rectal tenesmus, incontinence, urgency,

colonic flora. molecular mimicry, increased bleeding
O Tenesmus: Latin teinesmos; to strain
sulfide production implicated
• Environmental factors contribute to acute • Fever. fatigue. weight loss. anemia,
flares dehydration
• Extraintestinal manifestations
O Arthritis (most common); uveitis;
COMPLICATIONS
erythema nodosum; pyoderma
• Toxic megacolon, anal fissures, perirectal
gangrenosum; primary sclerosing
abscess
cholangitis; arterial. venous
thromboembolisms
67
( D_IA_GN_O_SI_S )
• > four weeks active diarrhea +
inflammatory findings on endoscopy+
chronic inflammatory changes on biopsy
• Biopsy
o Crypt abscesses
LAB RESULTS
• Anemia
• Elevated inflammatory markers
Figure 33.6 A pancolectomy specimen from
O Erythrocyte sedimentation rate (ESR),
an individual with ulcerative colitis.
C-reactive protein (CRP)
OTHER DIAGNOSTICS
• Clinical diagnosis; exclude other causes of
colitis
O Infections (e.g. parasites, Clostridium
difficile), STls, radiation, medications
( T_R_E~_;,-_M_EN_T
)
MEDICATIONS
• Anti-inflammatory medications
O Sulfasalazine, mesalamine
• lmmunosuppressors
° Corticosteroids, azathioprine,
cyclosporine
• TNF blocking agent
SURGERY
• Colectomy only if disease localized Figure 33.7 Abdominal radiograph
demonstrating toxic megacolon, a
complication of ulcerative colitis.
Figure 33.8 The clinical appearance

of erythema nodosum; a cutaneous
manifestation of inflammatory bowel disease.
68
active ulcerative colitis in a colonic biopsy.
There is active inflammation causing crypt
destruction. Cryptitis and crypt abscesses are
also present.
15-35 Throughout lifespan
Mouth to anus Colonic, rectal mucosa
Transmural inflammation Superficial ulcers
Non-c.:isc.:iting gr.:inulom.:is Crypt ulcers, abscesses
Skip lesions Continuous lesions
Cobblestone pattern, creeping fat. string Loss of haustra on imaging

sign on barium x-rays (lead pipe appearance), friable mucosa
Right lower quadrant pain Left lower quadrant pain

fistulas. phlegmon Gross bleeding
Destruction of colonic mucosa,

Transmural inflammation along GI tract
submucosa
Corticosteroids. azathioprine. Mesalamine. infliximab.

metronidazol, infliximab, adalimumab surgical resection
69
NOTES

( PATHOLOGY & CAUSES ) ( T_R_E~_~_M_EN_T )
• Diseases preventing adequate digestive • See individual diseases
system function
O Often involve inflammation, stasis,
obstruction, necrosis MNEMONIC: APPENDICITIS
• Various structural, functional etiologies Right lower-quadrant pain
common differential
Appendicitis/ Abscess
( SIGNS & SYMPTOMS ) Pelvic inflammatory disease
(PIO)/ Period pancreatitis
• Abdominal symptoms etiologically- Ectopid Endometriosis
dependent Neoplasia
• Abdominal pain, distension, constipation, Diverticulitis
bowel-habit change, hematochezia,
lntussusception
nausea, vomiting
Crohn's Disease/ Cyst (ovarian)
• Bulging abdominal mass (in hernia)
180
Torsion (ovary)
( D_IA_GN_O_s,_s) Irritable Bowel Syndrome
Stones
DIAGNOSTIC IMAGING
• CT scan, MRI, ultrasound
OTHER DIAGNOSTICS
• Right lower-quadrant pain common
differential (see mnemonic)
70
APPENDICITIS
osms.i"l/ o.ppendiei-lis
( PATHOLOGY & CAUSES ) (__ s,_G_NS_&_S_Y_M_PT_O_M_

• Lumen obstruction - vestigial vermiform • Abdominal pain
appendix inflammation , Often begins in umbilical area -
• Located at cecum base (near ileocecal McBurney's point (abdomen's right
valve) lower-quadrant; one-third distance from
• Obstruction - intraluminal content anterior superior iliac spine, umbilicus)
stasis - r
luminal, intramural pressure - progressive inflammation
- thrombosis, occlusion small vessels, , Rovsing's sign: left lower-quadrant
lymphatic flow stasis - ischemia, necrosis palpated - right lower-quadrant pain
• Excessive multiplication (gut flora) behind , Psoas sign: right leg extended in left-
obstruction - immune system response side position - retrocecal appendix
- fibropurulent reaction - parietal , Obturator sign: right leg internally
peritoneum irritation rotated in supine position - pelvic
• Visceral nerve fiber stimulation - appendix
abdominal pain • Fever, anorexia, nausea, vomiting, diarrhea/
constipation
CAUSES • In case of peritonitis
• Obstruction O Rebound tenderness at McBurney's
O Lymphoid
point
hyperplasia (adolescence,
viral infection), fecalith, foreign body O Abdominal guarding (peritoneal
(e.g. undigested seeds), pinworm irritation)
infection, tumor (benign, malignant)
( D_IA_GN_o_s,_s
__ )
RISI( FACTORS
• 10-30 years old, family history, biologically- DIAGNOSTIC IMAGING
male, cystic fibrosis comorbidity (children)
CT scan with IV contrast
• Increased appendix diameter
COMPLICATIONS
• Increased wall enhancement
• Appendix-supplying vessel compression
- ischemia - appendix wall necrosis • Severe
- bacterial invasion (wall) - appendix O Visible abscess, pus spillage
rupture - bacterial invasion (peritoneum)
Ultrasound (pregnancy, children)
- peritonitis
• Periappendiceal abscess, subphrenic • Visible, noncompressible, dilated appendix
abscess, pylephlebitis, portal venous • j blood flow in appendix wall
thrombosis, sepsis • Visible appendicolith
• Right iliac fossa fluid collection
71
LAS RESULTS
• Neutrophilic leukocytosis
O I with progression
• Mildly elevated serum bilirubin
O Perforation marker
( T_R_E~_~_M_EN_T__ )
MEDICATIONS
• Antibiotics
• IV fluids, no food/water orally (NPO)
Figure 34.1 Camera view of a laparoscopic
appendicectomy being performed. The
SURGERY
appendicectomy has been performed and
• Removal (appendectomy)
the stump is visible on the right of the image,
• Abscess drainage with the severed appendix reflected laterally.
DIVERTICULITIS
osmsJI:/ diveT-lieuli-1:is
( PATHOLOGY & CAUSES ) (__ s,_G_NS_&_S_Y_M_PT_O_M_s_)

• Inflamed diverticula; microperforation of • Left lower-quadrant pain (often sigmoid
diverticulum colon); palpable abdominal mass; diarrhea/
constipation; nausea; vomiting; fever;
urinary urgency/frequency/dysuria (inflamed
CAUSES sigmoid colon - bladder irritation)
• Increased intraluminal pressure - erosion
- inflammation, focal necrosis - micro/
macro perforation ( D_IA_GN_o_s,_s __ )
RISI( FACTORS DIAGNOSTIC IMAGING
• Diverticula present
CT scan with contrast
• Inflammation - hyperdense tissue
COMPLICATIONS
• Stricture, intestinal obstruction Abdominal X-ray
• Diverticulum perforation • Bowel obstruction

O Abscess, peritonitis • Bowel perforation
° Free air
• Fistula formation
O Bladder communication
O Other organ communication (vagina, LAS RESULTS
skin, other parts of bowel) • Leukocytosis
O Vesicoenteric fistula: pneumaturia (air in
urine), fecaluria (stool in urine)
72
(~~~TR_E_AT_M_E_N_T~
__ )
MEDICATIONS
• Uncomplicated
o Antibiotics, fluids, no food/water orally
(NPO)
SURGERY
• Resection
o Severe case/recurrence/complication
Figure 34.2 Gross pathology of sigmoid
diverticulosis. Notice how the diverticula
OTHER INTERVENTIONS appear either side of the longitudinal muscle.
• High-fiber diet
o Prevents recurrence
DIVERTICULOSIS
osms.i"l/ diver-lieu losis
(some areas) ---" mucosa/submucosa
( PATHOLOGY & CAUSES ) herniation predisposed ---" diverticulum
formation
• Diverticulum (plural diverticula): , Sigmoid colon: smallest diarneter e-
outpouching of hollow anatomical structure highest pressure (Laplace's Law:
wall Pcxl/0), most common location
o Most frequent in large intestine • Outpouching: tend to form where intestinal
(particularly sigmoid colon) wall-supplying blood vessels (i.e. vasa
• Diverticulosis: multiple diverticula present recta) traverse muscle layer
TYPES RISI( FACTORS

• Lifestyle: low-fiber diet, constipation; fatty
True diverticu
lum
food, red meat-rich diet; inactivity; smoking
• All organ wall layers included (e.g. Meckel's
• j age j risk
diverticulum)
• Biologically-male
False (pseudo-) diverticulum • Family history
• Only mucosa, submucosa layers included • Obesity
o Most common • Connective tissue disorders
o Colonic diverticula , Marfan syndrome
, Ehlers-Danlos syndrome
CAUSES , Autosomal dominant polycystic kidney
• Multifactorial pathogenesis from abnormal disease
colonic motility
• Abnormal/exaggerated smooth muscle
corrtractlons=- unequal intraluminal
pressure distribution ---" high pressure
73
COMPLICATIONS
• Blood vessel surrounding weakened (..____ T_R_EA_~_M_EN_T
__ )
outpouching ruptures----. large intestine
blood loss ----. bloody stool SURGERY
• Resection (if complications develop)
• Inflammation (diverticulitis)
• Segmental colitis
OTHER INTERVENTIONS
• Lifestyle changes
( s,_G_NS_&_SY_M_PT_O_M_s_) , Diet (i fiber intake), avoid constipation, I
physical activity, smoking cessation
• Vague abdominal pain, tenderness, bloating
• Occasional cramping
• Altered bowel habit (diarrhea/constipation)
• Rectal bleeding (hematochezia-fresh
blood in stool)
(..____ D_IA_GN_o_s,_s __ )
• Often found incidentally
DIAGNOSTIC IMAGING
X-ray with barium enema
• Lower gastrointestinal series
• Directly shows pouches
CT scan Figure 34.3 Barium study demonstrating

• Visualization of colonic diverticula, multiple diverticula.
thickening of the bowel wall thickening (>
4mm), an increase in soft tissue density
within pericolonic
OTHER DIAGNOSTICS
Colonoscopy
, sigmoidoscopy
• Visible outpouching
74
FEMORAL HERNIA
osms.i"l/femoro.1-hernio.
• Abdominal contents enter hernia - may
( PATHOLOGY & CAUSES ) precipitate intestinal obstruction
, Most common cause worldwide
• Intestinal projection across femoral canal
associated with femoral artery, vein; below , Incarcerated/strangulated; severe
inguinal ligament, lateral to pubic tubercle abdominal pain, tenderness, erythema,
fever, nausea, vomiting
CAUSES
• Congenital, acquired (..____ D_IA_GN_O_s,_s )
• Weakness/abnormal fascial opening in
abdominal wall DIAGNOSTIC IMAGING
• Usually includes properitoneal fat/omentum
Ultrasound
edge/small bowel loop
• Variable echogenicity of tissue; movement
of intra-abdominal structures in an inferior
RISI( FACTORS direction through the femoral canal
• Biologically-female, congenital disorder
(embryological development - processus CT scan
vaginalis obliteration failure), hernia (family • Visualization of characteristic funnel-
history), obesity, pregnancy, frequent heavy shaped neck; protrusion through femoral
lifting ring
COMPLICATIONS ( T_R_EA_~_M_EN_T )
• Narrow femoral canal
j incarceration/strangulation
O risk SURGERY
• Compression of femoral vein • Repair
• Bowel obstruction ' Open/laparoscopic (case-dependent)
• Early/elective repair
( SIGNS & SYMPTOMS ) O Uncomplicated,
• Urgent repair
asymptomatic hernia
n Complicated hernia (may require bowel

• Asymptomatic (commonly)
resection)
• Can manifest intestinal obstruction
symptoms
O Bulging mass, pain, discomfort
O Supine: may resolve
O Valsalva maneuver (coughing/straining):
worsens
75
GALLSTONEILEUS
osms.i"l/ gC1lls-lone-ileus
Effect on intestinal wall
( PATHOLOGY & CAUSES ) • Simple: no blood supply impairment
• Gastrointestinal motility (peristalsis) • Strangulated: blood supply cut off to bowel

section
disruption - impaired bowel content
propulsion • Closed loop: obstruction occurs at each end
of bowel section
• Blockage - progressive intestine dilation
blockage-proximal, decompression
Type of factor
blockage-distal
• Mechanical: obstruction caused by
• Gas accumulation (swallowed air, bacterial
gallstone, neoplasm, adhesion, stricture,
fermentation) - j bowel distention hematoma, meconium (in cystic fibrosis),
• Bowel wall edema - I bowel content medical device migration (PEG tube)
absorption - luminal fluid sequestration • Functional: intestinal musculature
• j capillary permeability - transudative fluid paralysis caused by trauma (surgery, blunt
loss from intestinal lumen into peritoneal abdominal trauma), peritonitis, medication
cavity (opiates, anticholinergics)
• Emesis - fluid, electrolyte (Na, K, H, Cl)
loss - metabolic alkalosis, hypovolemia
RISI( FACTORS
• Bowel dilation continues - ! intestinal
• Surgery; bowel manipulation, anesthesia,
wall tissue perfusion - ischemia, necrosis,
postoperative opioids
bowel perforation
• Hernia, neoplasm history, abdominal/pelvic
irradiation, chronic inflammation, abdominal
TYPES trauma
Onset
• Acute: factors such as torsion, COMPLICATIONS
intussusception - sudden onset • Fluid/electrolyte/acid-base imbalance;
• Chronic: factors such as tumor growth - bowel strangulation, necrosis; perforation;
prolonged onset sepsis
• Recurrent: often caused by adhesions -
intermittent obstructions
Extent
• Partial: some of intestinal lumen remains • Abdominal distension, cramping pain,
open constipation, nausea, vomiting
• Complete: total lumen obstruction • Dehydration: tachycardia, dry mucous
membranes, ! urine output
Location • Bowel sounds
• Intrinsic: obstruction within bowel O High-pitched "tinkling" sound
wall-e.g. inflammatory stricture, edema, auscultated: acute mechanical bowel
hemorrhage, foreign body (ingested, obstruction
parasite accumulation, large biliary calculus) O Muffled, hypoactive bowel sounds:
• Extrinsic: obstruction outside bowel wall- significant bowel distention association
e.g. torsion, compression (hernia)
• Abdominal percussion: hyperresonance/
tympany
76
(..__ __ D_IA_GN_O_SI_S )
DIAGNOSTIC IMAGING
X-ray
• Small intestine, colon distension
( T_R_EA_:l'_M_EN_T
)
SURGERY
• Surgical intervention: e.g. release
adhesions, complete obstructions, repair
bowel
OTHER INTERVENTIONS
Figure 34.4 A CT scan of the abdomen and
• No food/water orally (NPO)
pelvis in the coronal plane demonstrating
• Fluid, electrolyte replacement a gallstone in the terminal ileum. If so large
• Parenteral feeding - nasogastric that it is unable to pass through the ileocecal
decompression valve, the gallstone will cause small bowel
obstruction.
GASTROENTERITIS
osms.i"l/ viTe1l-ge1s-lToen-leTi-lis
• Viral contact
( PATHOLOGY & CAUSES ) , E.g. daycare center, cruise ship, closed
community outbreak; contaminated
• Gastrointestinal tract viral infection (lasts
food/water
12 hours-3 days)
• Primary transmission
O Oral-fecal route
COMPLICATIONS
• Severe dehydration - altered mental
• Viruses - epithelium damage - osmotic
status, weight loss
diarrhea (> three stools daily), vomiting
CAUSES (__ s,_G_NS_&_S_Y_M_PT_O_M_

)
• Children: rotavirus (most common)
• Adult norovirus (most common), astrovirus, • Watery diarrhea; nausea; vomiting;
adenoviruses abdominal cramps, pain; fever; malaise;
dehydration (dry lips, skin turgor,
tachycardia)
RISI( FACTORS
• j morbidity
° Children, elderly, immunocompromised
individuals
77
( D_IA_GN_O_SI_S )
LAB RESULTS
• Stool sample
, Excludes bacterial/parasitic etiology
• f C-reactive protein (CRP), f leukocytes
• Polymerase chain reaction (PCR)
= Stool, vomit: enzyme-linked
immunosorbent assay (ELISA)
performed for rotavirus
( T_R_E~_~_M_EN_T__ )
Figure 34.5 A scanning electron micrograph
of a cluster of Norwalk virus capsids. OTHER INTERVENTIONS
• Fluid replacement
Prevention
• Hygiene practices, rotavirus vaccine
INGUINAL HERNIAS
osms.i"l/inguino.1-he,-nio.s
= Testicular descent path: covered
( PATHOLOGY & CAUSES ) by three layers of spermatic fascia
(three layers); external spermatic
Direct inguinal hernia fascia (external oblique muscle fascia
• Peritoneal sac; projects directly through continuation); cremasteric muscle
inguinal triangle (AKA Hesselbach's fascia; internal spermatic fascia (internal
triangle) oblique muscle fascia continuation)
• Projects medially to inferior epigastric
vessels, lateral to rectus abdominis, pierces CAUSES
parietal peritoneum
• Hesselbach's triangle composition: inguinal Indirect inguinal hernia
ligament (AKA Poupart's ligament). rectus • Processus vaginalis closure failure (i.e.
abdominis muscle (lateral border). inferior internal inguinal ring and processus
epigastric vessels vaginalis obliteration failure)
• Covered by external spermatic fascia
Indirect inguinal hernia RISI( FACTORS

• Most common hernia Direct inguinal hernia
• Intestinal projection through internal • Acquired, affects transversalis fascia
inguinal ring ° Chronic intra-abdominal pressure j (e.g.
O Location: spermatic cord (biologically- obesity, chronic cough, constipation,
male). round ligament (biologically- heavy lifting-occupational/recreational)
female) exit the abdomen
• Abdominal wall musculature atrophy
78
(aging)
• Older, biologically-male individuals
( D_IA_G_N_O_s,_s )
Indirect inguinal hernia DIAGNOSTIC IMAGING
• Biologically-male individuals> biologically- Ultrasound
female individuals
• Direct inguinal hernia
o Biologically male: late right testicle
, Variable echogenicity of tissue;
descent
movement of intra-abdominal structures
o Biologically female: asymmetric pelvis in an anterior direction through the
Hesselbach triangle
COMPLICATIONS • Indirect inguinal hernia
= Visualization through abdominal wall in
Direct inguinal hernia
• Incarceration/strangulation potential
CT scan
Indirect inguinal hernia
• Direct inguinal hernia
• Can form hydrocele
= Visualization of a protrusion with
• May precipitate intestinal obstruction compressing inguinal canal contents;
• Most common cause worldwide inguinal canal pushed into a semicircle
of tissue that resembles a moon
crescent
( s,_G_NS_&
__SY_M_PT_O_M_s_)
• Indirect inguinal hernia
= Identifies occult hernia/complications;
• May be asymptomatic hernia neck visualized superolateral to
• Bulging mass (indirect inguinal hernia, the inferior epigastric vessels
mass in groin), pain, discomfort
o Valsalva maneuver cessation/prone: may
resolve
OTHER DIAGNOSTICS
• Indirect inguinal hernia
• Valsalva maneuver: worsens projection
, History, clinical exam; sufficient for
o Coughing/straining
majority of suspected inguinal hernias
Direct inguinal hernia
• May precipitate intestinal obstruction
o Most common cause worldwide
o Incarcerated/strangulated: severe
abdominal pain, tenderness, erythema,
fever, nausea, vomiting
Indirect inguinal hernia

• Visible bulge
o May be unapparent in biologically-
female individuals
• Incarcerated/strangulated
o Severe abdominal pain, tenderness,
erythema, fever, nausea, vomiting
Figure 34.6 Intra peritoneal view of an

inguinal hernia during a laparoscopic hernia
repair. The peritoneal cavity extends into the
inginal canal, lateral to the epigastric vessels,
making this an indirect hernia.
79
(..__ __ TR_E_~_~M_E_N_T
)
SURGERY
Repair
• Open/laparoscopic (case-dependent)
• Elective repair
O Symptomatic hernias
• Direct inguinal hernia (asymptomatic)
O Monitor, surgical repair preferred
Figure 34.8 A CT scan in the coronal plane

demonstrating an indirect inguinal hernia.
Figure 34.7 Clinical appearance of a hernia
The proximal bowel is dilated, indicating a
in the groin. It is often not possible to
strangulated hernia causing obstruction.
distinguish between a direct and indirect
hernia on clinical examination alone.
INTESTINAL ADHESIONS
osms.i-l/in-les-lino.1-o.dhesions
• Injury prevents enzyme secretion -
( PATHOLOGY & CAUSES ) macrophages. fibroblasts deposit collagen
into adhesion - permanent
• Fibrous tissue bands form physical
attachment between intestines - !
intestinal motility CAUSES
• Formed from scarred, post-trauma tissue • Surgery (most common), inflammation
(cholecystitis, pancreatitis, peritonitis),
• Tissue injury - inflammation - fibrin
endometriosis, pelvic inflammatory disease
deposits - fibrin connects parts left (similar
to reconstructive "glue")
• Adhesions extend between tissue if both COMPLICATIONS
parts have been injured, close proximity • Bowel obstruction, intestinal wall volvulus/
• Initial fibrous adhesions dissolved by ischemia
fibrinolytic enzymes
80
)
• Abdominal pain, vomiting, bloating,
constipation
(..____ D_IA_GN_O_SI_S
)
DIAGNOSTIC IMAGING
X-ray
• Detect obstruction; small intestine dilation
CT scan, ultrasound Figure 34.9 lntraoperative view of abdominal

• Exclude other obstructive causes adhesions.
( T_R_EA_:l"_M_EN_T
)
SURGERY
• Surgical/laparoscopic adhesion excision
INTUSSUSCEPTION
osms.l-l/ln-lussuseep-llon
RISI( FACTORS
( PATHOLOGY & CAUSES ) • Most common < 24 months old,
intestinal malrotation history, previous
• Condition that occurs when part of intussusception, intussusception in sibling,
intestine folds into adjacent section - biologically male
obstruction
• lleocecal region most commonly affected
• May be idiopathidcaused by abnormal
COMPLICATIONS
structure (causes pathological lead point) • Peritonitis, sepsis
- peristalsis causes one part of bowel
to move ahead of adjacent section -
bowel telescoping - j pressure, impaired (__ SI_G_NS_&_S_Y_M_PT_O_M_
)
venous return - bleeding, bowel ischemia,
infarction • Intermittent abdominal pain (worsens with
peristalsis)
• Guarding
CAUSES
• Straining efforts, draw knees toward chest
• Adults: abnormal growth (e.g. polyp, tumor)
• Vomiting
• Infants: post-infection lymphoid hyperplasia
• Sausage-like abdominal mass
(Peyer's patches), Meckel's diverticulum
• "Red currant jelly" stool (blood, mucus)
81
( D_IA_GN_O_SI_S ) ( T_R_E~_~_M_EN_T
)
DIAGNOSTIC IMAGING SURGERY
• Free telescoped intestine portion ---'> clear
Ultrasound, X-ray, CT scan
obstruction ---'> remove necrotic tissue
• Telescoped intestine: visualized as classic
bull's-eye image
• Intestinal obstruction signs
OTHER INTERVENTIONS
• Reduction by air/hydrostatic contrast
material enema (e.g. saline, barium)
OTHER DIAGNOSTICS
• May be felt during digital rectal examination
(children)
IRRITABLE BOWEL SYNDROME

(IBS)
osmsJl/lBS
previous gastroenteritis, stress
• Chronic functional gastrointestinal system
disorder; recurrent abdominal pain,
impaired bowel motility • Impaired bowel motllitv-« diarrhea/
O No microscopic, macroscopic constipation
irregularities • Recurrent abdominal pain
° Constipation/diarrhea • Bowel movement ---'> improvement
• Bloating, nausea, mucus in stool
CAUSES
• Pathology not completely understood; likely
multifactorial ( D_IA_GN_o_s,_s)
O Visceral hypersensitivity: altered stimuli
response OTHER DIAGNOSTICS
° Fecal flora alterations; bacterial • Based on predominant consistency of stool
overgrowth O Diarrhea predominant, constipation
° Food sensitivity: short-chain predominant, mixed stool pattern,
carbohydrates; j water in bowel-» unclassified
smooth muscle spasm, diarrhea; • Organic disease exclusion
metabolized by bacteria ---'> gas ---'>
"Rome IV" diagnostic criteria
bloating, spasm, pain
O Psychosocial influence • Abdominal pain ~ one day weekly in last
three months, associated with two/more of
O Genetic factor
following
O Oefecatlon-» lessened pain
RISK FACTORS ° Change in stool frequency
• Biologically-female (region-dependent), ° Change in stool consistency
82
OTHER INTERVENTIONS
(..__ __ T_R_EA_:T_M_EN_T
__ ) • Stress management
• Diet modification
• No definitive cure
, Low fermentable oligo-, di-,
monosaccharides/polyols diet (low
MEDICATIONS FODMAPs diet)
• Symptom-guided therapy , Avoid gas-producing food (caffeine,
O Diarrhea predominant: drugs (e.g. alcohol)
loperamide) , Probiotics
° Constipation predominant: fiber , Physical activity
supplementation, adequate fluid intake,
osmotic laxatives
O Spasm, pain: antispasmodics
ISCHEMIC COLITIS
osms.i"l/isehe mie-eoli-lis
, Hypercoagulable states (e.g. factor V
( PATHOLOGY & CAUSES ) Leiden)
, Biologically-female individuals
• Inflammatory, ischemic condition; , Impaired perfusion (e.g. aortic surgery,
affects colon, most often splenic flexure, myocardial infarction, hemodialysis)
rectosigmoid junction
, Vasculopathy
• Sudden blood flow ! - insufficient
, Certain drugs (e.g. vasopressors)
perfusion, oxygen/nutrient delivery to
bowel - compromised cellular metabolism
- ischemia, inflammation, infarction, COMPLICATIONS
necrosis - possible perforation • Gangrenous bowel, stricture, pancolitis,
• Damaged, gangrenous mucosa promotes colonic perforation, peritonitis, sepsis,
fluid/electrolyte loss - dehydration, shock, shock, metabolic acidosis, multisystem
metabolic acidosis organ failure, reperfusion injury, potentially
fatal
CAUSES
• lschemia causes may be occlusive (embolic,
thrombotic)/nonocclusive (! mesenteric
( SI_G_NS_&_S_Y_M_PT_O_M_
circulation - severe hypotension,
• Symptomatology may be self-limiting
vasospasm)
• Localized abdominal cramping, tenderness
O Usually acute, may be chronic disorder
(usually left side)
for marathon runners
• Loose, bloody stools, hematochezia
• ! bowel sounds
RISI( FACTORS • Guarding, rebound tenderness
• Any cause of ! perfusion/mesenteric arterial
• Fever
embolism, thrombosis/vasoconstriction
• May develop shock signs (e.g. hypotension)
O Risk j with age/comorbidities
83
CHARACTERISTICS OF ACUTE BOWEL ISCMEMIA
IV LOCATION
SMAll 80WEl
C.OlONIC. ISC.MEMIA
(MESENTERIC. ISC.MEMIA)
AGE Presentation age varies with cause Risk j with age (> 60 years)
Superior. inferior mesenteric arteries:

BLOOD SUPPLY Superior mesenteric artery
internal iliac arteries
Pain: severe: tenderness develops

Mild. crampy pain; tenderness present
late in course
SIGNS & SYMPTOMS
Prominent bloody diarrhea. hematochezia
Bleeding occurs late
DIAGNOSIS Imaging, angiography, laparotomy Imaging, colonoscopy
• Stool culture
( D_IA_GN_O_SI_S
__ ) • Identifies infectious etiology
DIAGNOSTIC IMAGING
X-ray/CT scan ( T_R_E~_~_M_EN_T
__ )
• Abdominal; visualizes obstruction,
perforation. pneumonitis
MEDICATIONS
O Thumbprinting:
• Antibiotics
segmented bowel
edema/thickening pattern
O Perforation/infection
O Double-halo pattern: mucosa.
muscularis hyperdensity SURGERY
O Pneumatosis coli, pneumoperitoneum • Bowel resection
indicates perforation O Necrotic tissue
Colonoscopy
• Visualizes ischemia: edema, erythema.
friable mucosa
• Single-stripe sign: linear ulcer seen along
longitudinal axis
• Submucosal hemorrhage: bluish nodules
• Biopsy: transmural fibrosis, mucosa I
atrophy
LAB RESULTS
• Leukocytosis, thrombocytopenia, !
hemoglobin
• j serum lactate, lactate dehydrogenase Figure 34.10 The endoscopic appearance of
(LDH). creatine phosphokinase (CPK). the colon in a case of ischemic colitis. There is
amylase indicates tissue damage mucosal edema and patchy erythema.
84
OTHER INTERVENTIONS
• Circulatory support
, IV fluids, electrolytes
• Supplemental oxygen
• Bowel rest
Figure 34.11 Histological appearance of the

colon in an individual with ischemic colitis.
There is mucosa I necrosis, a sign that the
condition is in its early stages at the time of
biopsy.
NECROTIZING ENTEROCOLITIS
(NEC)
osms.i"l/ neeTo-lizing-e n-leToeoli-lis
RISI( FACTORS
( PATHOLOGY & CAUSES ) • Gestational age< 32 weeks
• Low birth weight< 2kg/4.4llbs
• Severe intestinal disorder: inflammation,
ischemic necrosis • Dysbiosis-contributing interventions
O Terminal ileum. colon (most often , Antibiotics. acid-reducing agents.
affected) feeding bovine milk formula
• Multifactorial pathology • Human milk promotes commensal bacteria
growth, supports mucosal integrity
• Preterm infants
• Infections. gas-forming organism presence
, Immature gastrointestinal tract
characterized by ! intercellular junction • Underlying conditions
O Term infants (e.g. fetal growth
integrity+ ! mucosa I barrier -
triggering event - normal intestinal restriction. perinatal hypoxia, congenital
microbiome dysbiosis - j pathogenic heart disease. gastrointestinal disorders.
bacterial growth - exaggerated sepsis)
immune system response - release of
host cytokines, chemokines - tissue COMPLICATIONS
injury - necrosis
• Bowel perforation. ileus, septic shock,
• Term infants metabolic acidosis. coagulopathy,
, Usually underlying condition adversely respiratory failure
affecting intestinal perfusion
• Surgical complications
85
O Strictures, short bowel syndrome OTHER DIAGNOSTICS
• j impaired neurodevelopmental
Surgery
development risk
• Through surgical/postmortem specimens
• High mortality rate
, Gross examination: gangrenous
necrosis, hemorrhage, subserosal gas
( SIGNS & SYMPTOMS ) collection
= Histological examination: edema,
• Abrupt feeding tolerance change hemorrhage, transmural necrosis,
bacterial infiltration
• Abdominal distension, tenderness
• Erythema, crepitus, induration may also be
present
( T_R_E~_~_M_EN_T__ )
• j gastric residuals
• Vomiting (often bilious), bilious drainage MEDICATIONS
from enteral feeding tubes • Empirical antimicrobial therapy
• Hematochezia
• Nonspecific findings
SURGERY
O Temperature instability, lethargy, apnea
• Exploratory laparotomy, bowel resection
• Primary peritoneal drainage (PPD) ----. !
intra-abdominal pressure
OTHER INTERVENTIONS
• Address complications (e.g. metabolic
correction/hematologic abnormalities)
• Bowel rest with nasogastric intubation
decompression
• Supplemental oxygen/mechanical
ventilation
• Fluid replacement
• lnotropic support
Figure 34.12 Gross pathology of necrotizing • Total parenteral nutrition (TPN)
enterocolitis.
( D_IA_GN_O_s,_s
__ )
DIAGNOSTIC IMAGING
Abdominal radiography, ultrasound
• Pneumatosis intestinalis,
pneumoperitoneum/hepatobiliary gas
LAB RESULTS
• Positive blood culture, ! platelets, ! red
blood cells, disseminated intravascular
coagulopathy evidence, l serum lactate
86
SMALL BOWEL ISCHEMIA &
INFARCTION
osmsJl/isehe mici-cind-infcil'"elion
cardiopulmonary bypass surgery,

( PATHOLOGY & CAUSES ) hemodialysis - ! intestinal perfusion)
• Coagulative disorders
• Serious small bowel condition; reduced
• Atherosclerotic occlusive disease
blood flow, subsequent infarction; AKA
mesenteric ischemia • Hypovolemia (e.g. dehydration,
hemorrhage)
° Collateral circulation network -
small bowel especially vulnerable to • Bowel strangulation (e.g. volvulus,
widespread ischemic injury incarcerated hernia)
O Hypoxia, subsequent reperfusion - • Vasoconstriction medications
tissue injury
• ! blood flow may be acute/chronic COMPLICATIONS
O Acute: sudden ! small intestine • lieus, shock, metabolic acidosis,
perfusion multisystem organ failure, high mortality
° Chronic: episodic ! digestion
perfusion (often related to mesenteric
atherosclerosis) (.___S_IG_N_S_&_S_YM_P_T_O_M_s )
• Insufficient perfusion, oxygen/nutrient
delivery to bowel - compromised cellular • Severe abdominal pain (often postprandial);
metabolism - ischemia, inflammation, nausea, vomiting; distended abdomen;
transmural infarction, necrosis - bacterial guarding, rebound tenderness (develops
transmigration+ possible perforation later); ! bowel sounds; fever; feculent
breath odor; rectal bleeding; may exhibit
• Damaged, gangrenous mucosa promotes
shock signs (e.g. hypotension)
fluid/electrolyte loss - dehydration, shock,
metabolic acidosis
( D_IA_GN_O_s,_s )
CAUSES
• lschemia causes DIAGNOSTIC IMAGING
O Occlusive (arterial/venous): embolic,
CT/magnetic resonance (MR) angiography
thrombotic, tumor, volvulus,
intussusception, hernia, atherosclerosis • Detects acute mesenteric ischemia
O Nonocclusive: severe hypotension, Abdominal X-ray/CT scan
vasospasm - ! mesenteric circulation
• Dilated bowel loops, bowel wall thickening,
thumbprinting, intestinal pneumatosis, free
RISI( FACTORS intraperitoneal air
• Any cause of! perfusion/mesenteric arterial
embolism, thrombosis/vasoconstriction LAB RESULTS
• Cardiac disorders (e.g. arrhythmia, valvular
• Leukocytosis with left shift, j hematocrit
disease - arterial emboli formation (dehydration, hemoconcentration)
from heart; ! cardiac output, peripheral
• l serum lactate, amylase, alkaline
hypoperfusion)
phosphatase
• Procedures (e.g. cardiac catheterization,
87
OTHER DIAGNOSTICS SURGERY
• Laparotomy • Resection
O Abdominal exploration
OTHER INTERVENTIONS
• Pain management
( T_R_E~_~_M_EN_T__ )
• Bowel rest with decompression
MEDICATIONS
• Antibiotics
• Circulatory support
O IV fluids, electrolytes, inotropic
medications
VOLVULUS
osmsJl/ volvulus

• Intestinal obstruction • Abdominal tenderness, pain, distension,
O Intestinal twisting/looping bilious vomiting, constipation, fever,
auscultation (abnormal bowel sounds,
often decreased), percussion (tympany),
TYPES hematochezia (may indicate bowel
• Classified by location ischemia, necrosis)
Sigmoid volvulus (most common)

• Usually middle-aged/elderly individuals ( D_IA_GN_o_s,_s __ )
• Causes include pregnancy, chronic
constipation (e.g. Hirschsprung's disease), DIAGNOSTIC IMAGING
intestinal adhesions
X-ray
Cecal volvulus • Asses volvulus shape
• Causes include impaired abdominal O Bent inner tube sign ("coffee bean" sign)
mesentery development. pregnancy,
chronic constipation Barium enema
• May show "bird's beak" shape (point of
Midgut volvulus
twisted bowel)
• Usually infants/young children • Perforation suspected ----. barium contrast
• Caused by anomalous intestinal contraindicated
development (e.g. intestinal malrotation)
CT scan
COMPLI CATIONS • Twisted mesentery ("whirlpool" sign)
• Mesenteric artery compression ----. intestinal

wall ischemia, infarction
• Intestinal wall perforation, infection (e.g.
diffuse peritonitis)
88
(..__ __ T_R_EA_~_M_EN_T
)
SURGERY
• In case of midgut volvulus/ischemia/
necrosis; surgical resection if necessary
OTHER INTERVENTIONS
• IV fluid replacement
• Bowel decompression
, Sigmoid volvulus: sigmoidoscopy
, Cecal volvulus: colonoscopy
Figure 34.13 Abdominal radiograph

demonstrating a massively dilated sigmoid
colon in a case of sigmoid volvulus.
Figure 34.14 30 CT virtual colonoscopy

demonstrating sigmoid volvulus.
89
NOTES

• Inherited metabolidcongenital structural DIAGNOSTIC IMAGING
anomalies, affect hepatobiliary system ----> • Ultrasound
hyperbilirubinemia • Oral cholecystogram
COMPLICATIONS LAB RESULTS

• Kernicterus • Conjugated vs. unconjugated bilirubin, liver
• Recurrent cholangitis, cirrhosis function tests
• Portal hypertension • Biopsy
• Metabolic problems, impaired growth
( T_R_E~_~_M_EN_T__ )
• See individual disorders
• Jaundice, dark urine, light stools
• Impaired liver function
• Neurologic alterations
BILIARY ATRESIA
osms.i"l/\,ilio.T14-o.-lTesio.
TYPES
( PATHOLOGY & CAUSES ) • Biliary atresia only; not accompanied by
other anomalies (most common)
• Congenital anomaly of extrahepatic duct
• Biliary atresia + laterality malformations
fibrosis, obstruction of bile flow
(left-right axis patterning/malpositioning of
• Infections. environmental toxins. immune organs)
dysregulation, genetic mutations ----> O Dextrocardia, situs inversus, asplenia/
perinatal injury to biliary system
polysplenia, interrupted inferior vena
• Bile prevented from entering duodenum cava
----> impaired fat digestion. absorption+
O Related CFCl gene mutation
cholestasis, distension of gallbladder, ducts
• Biliary atresia + intestinal atresia,
imperforate anus. kidney anomalies
90
COMPLICATIONS
• Liver cirrhosis, portal hypertension, hepatic
encephalopathy
• Recurrent cholangitis, cirrhosis
• Metabolic problems, impaired growth
(associated with malabsorption)
• Neonates asymptomatic at birth; stools
Figure 35.1 lntraoperative photography of
gradually become acholic, clay-colored
extra-hepatic biliary atresia. The underside of
• Persistent jaundice the liver displays only connective tissue in the
O Skin gradually turns yellow, greenish- gallbladder fossa.
bronze
• Dark urine
O Increased bilirubin concentration
• Portal hypertension
( T_R_EA_~_M_EN_T
__ )
O Splenomegaly, ascites, enlarged MEDICATIONS
abdominal veins
• Ursodeoxycholic acid (hydrophilic bile acid)
• Impaired liver function - decreased
coagulation factors, bleeding tendencies
O Impaired coagulation also related to SURGERY
decreased vitamin K absorption • Type indicated by blood chemistry, imaging,
biopsy
lntraoperative cholangiogram
( D_IA_GN_O_s,_s __ )
• Gold standard for confirming obstruction,
DIAGNOSTIC IMAGING diagnosis
Ultrasound Hepatoportoenterostomy (Kasai HPE)
• Abnormal gallbladder size, shape, • Restores bile flow from liver; may need
contractility; absent common bile duct; subsequent revision
"triangular cord" sign (triangle-shaped
Liver transplant
echogenic density above porta hepatis)
• If Kasai procedure unsuccessful
Hepatobiliary scintigraphy
• Decreased/absent patency of extra hepatic OTHER INTERVENTIONS
biliary tree
Diet
• Fat-soluble vitamin supplements; high
LAB RESULTS
protein diet, medium-chain triglyceride
• Increased conjugated serum bilirubin,
supplements
aminotransferases
Liver biopsy
• Identifies obstruction-related histological
changes
91
BILIARY ATRESIA ~
HEPATIC, DUCT
~0
CYSTIC, DUCT
COMMON SILE
DUCT
CRIGLER-NAJJAR SYNDROME
osms.i"l/ eTigleT-nojje1T-s14nd
Tome
COMPLICATIONS
( PATHOLOGY & CAUSES ) • Kernicterus (Type 1), if not promptly
addressed
• Rare inherited metabolic disorder;
nonhemolytic hyperbilirubinemia
• Autosomal recessive inheritance pattern
• AKA congenital nonhemolytic jaundice with
glucuronosyltransferase deficiency • Persistent jaundice in first few days of life
• Neurological symptoms as kernicterus
TYPES develops
Type I
• Severe jaundice, bilirubin encephalopathy, ( D_IA_G_N_os_,s )
possible kernicterus-associated neurologic
impairment LAB RESULTS
Type II Unconjugated hyperbilirubinemia
• Lower serum bilirubin concentration; no • Type I: 20-50 mg/dl
neurologic impairment • Type II: < 20 mg/dl
Stool color
CAUSES • Type I: pale yellow, low fecal urobilinogen
• Mutation in coding area of UGT gene, (significantly decreased bilirubin
encodes for bilirubin-conjugating enzyme conjugation)
UGTlAl (bilirubin-uridine diphosphate
• Type II: normal
glucuronosyltransferase) ----. structurally
abnormal enzyme----. decreased/absent Normal liver histology
, liver function tests
conjugation of bilirubin
RISI( FACTORS
• Consanguinity
92
OTHER INTERVENTIONS
C..__ __ T_R_EA_:T_M_EN_T
)
Phototherapy
MEDICATIONS • In first years of life; effectiveness decreases
overtime
Phenobarbital
• Useful in Type 11, induces residual UGT Exchange transfusion
activity
Plasmapheresis + albumin infusions
• Removes bilirubin tightly bound to serum
SURGERY albumin
Liver transplant
• Definitive treatment for Crigler-Najjar
syndrome Type I
DUBIN-J"OHNSON SYNDROME
osmsJl/ du \>in-johnson-s14ndTome
( PATHOLOGY & CAUSES ) (..____ D_IA_GN_o_s,_s)

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

(__ SI_G_NS_&_SY_M_PT_O_M_s ) • Brown, black discoloration
O Pigment accumulates in lysosomes
• Mild jaundice; evident during physiological
stress (e.g. illness)/hormonal fluctuations
(e.g. pregnancy, oral contraceptives) ( TREATMENT )
• Constitutional
O Vague abdominal pains, weakness • None required
• Occasional hepatosplenomegaly
93
GILBERT'S SYNDROME
osmsJl/ gil\>eT-ls-s14ndTome
( PATHOLOGY & CAUSES ) (__ SI_G_NS_&_SY_M_PT_O_M_s

)
• Benign, inherited metabolic disorder; • Asymptomatic between episodes, jaundice
recurring unconjugated hyperbilirubinemia, evident during physiological stress
jaundice • Clinical manifestations
• Autosomal recessive inheritance pattern O During adolescence, with effects of sex
• AKA Meulengracht disease, familial steroids on bilirubin metabolism
nonhemolytic jaundice
• Serum bilirubin increases during
physiologic stress (e.g. illness, dehydration, ( D_IA_GN_O_s,_s)
fasting, overexertion, menses)
• Differs from other forms of non-hemolytic • Exclude other causes of unconjugated
hyperbilirubinemia hyperbilirubinemia
, Genetic mutation in promoter region
of UGT gene - structurally normal
enzyme - impaired genetic expression
( T_R_EA_:T_M_EN_T
)
of hepatic UGT with decreased activity
• None required
- decreased conjugation of bilirubin
ROTOR SYNDROME
osms.i-l/To-loT-s14ndTome
( PATHOLOGY & CAUSES ) (__ SI_G_NS_&_S_Y_M_PT_O_M_s

)
• Rare benign inherited disorder; • Mild jaundice; during physiological
chronic conjugated, unconjugated hormonal fluctuations (e.g. pregnancy, oral
hyperbilirubinemia; no hemolysis contraceptive use)
• SLC0181, SLC0183 gene mutations
(code for transporter proteins lBl, 183
responsible for bilirubin re-uptake by ( D_IA_G_N_OS_IS)
hepatocytes) - alters bilirubin re-uptake -
increases bilirubin in plasma DIAGNOSTIC IMAGING
Oral cholecystogram
COMPLICATIONS • Normal gallbladder opacification
• Impaired lBl activity - significant drug
toxicities (e.g. statin-associated myopathy)
LAB RESULTS
• Hyperbilirubinemia, normal liver function
tests
94
• Total urinary coproporphyrin markedly
increased; majority coproporphyrin I
Liver biopsy, histologica

l exam
• Normal
(.____ T_R_EA_~_M_EN_T__ )
• None required
95
NOTES

(e.g. increase in free calcium)
( PATHOLOGY & CAUSES ) • Decreased hepatic metabolism of
circulating estroqens v- hyperestrogenism
• Diseases affecting hepatic parenchymal
= Spider nevi: vascular lesions, central
tissue or vasculature
arteriole surrounded by smaller vessels
• Variable insults
• Pal mar erythema
O Impairment in function of/destruction
• Gynecomastia
of liver parenchyma ---'> inflammation ---'>
scarring (cirrhosis) ---'> liver failure • Fetor hepaticus (breath odor due to
increased dimethyl sulfide levels)
O Obstruction or restriction of blood flow
through liver---'> hypertension in portal • Jaundice (cellular necrosts=- reduced
circuit producing secondary systemic hepatic ability to metabolize, excrete
effects bilirubin ---'> buildup of unconjugated
bilirubin in the blood)
O Diseases caused by anomalies in
absorbing, storing, converting or • Decreased production of coagulation
detoxification ---'> accumulation of tactors e- easy bruising, bleeding
substances in the liver and other tissues • Hepatic encephalopathy
causing damage • Ammonia, related nitrogenous
substances not cleared from blood ---'>
accumulate in brain c- impaired cerebral
) function
• Early stages generally asymptomatic

• Non-specific symptoms MNEMONIC: ASCDEFGHIJ"
O Weakness, weight loss, fatigue Common signs of liver
disease
Portal hypertension Asterixis, Ascites, Ankle
• Abdominal distension (ascites) edema, Atrophy of testicles
• Splenomegaly Bruising
• Esophageal varices ---'> trouble swallowing, Clubbing/ Color change of nails
hematemesis, dark stools (leukonychia)
• Caput medusae Dupuytren's contracture
ODilated periumbilical collateral veins Encephalopathy I palmar
• Cruveilhier-Baumgarten murmur Erythema
O Venous hum heard in epigastric region Fetor hepaticus
with stethoscope Gynecomastia
Hepatomegaly
Liver cellular dysfunction
Increase size of parotids
• Decreased hepatic albumin production
Jaundice
O Decreased osmotic pressure - edema
O Increase in levels of free circulating
compounds normally bound to albumin
96
O Neglect of personal appearance MNEMONIC: 3Cs & 3Cs
O Unresponsive, forgetful, trouble Hepatomegaly common
concentrating causes
° Changes in sleeping habits Cirrhosis
o Psychosis Carcinoma
O Asterixis (bilateral asynchronous Cardiac failure
flapping of outstretches, dorsiflexed
hands) Hepatomegaly rare causes
• Decreased metabolism of active Cholestasis
compounds - increased sensitivity to
Cysts
certain medications
Cellular infiltration
• Pruritus
anti-hepatitis B core lgM

( D_IA_GN_O_s,_s __ )
, Hepatitis C: hepatitis C antibody,
hepatitis C RNA
DIAGNOSTIC IMAGING
, Hepatitis D & E: lgM, lgG antibodies
• CT scan with contrast, MRI, ultrasound,
radionuclide imaging • Autoimmune panel
O Rheumatoid factor (RF), anti-cyclic
citrullinated peptide antibody (CCP),
LAB RESULTS anti-nuclear antibody (ANA), anti-
• Complete blood count (CBC) double stranded DNA (anti-dsDNA),
• Liver function tests anti-extractable nuclear antigen (anti-
O Tests of synthetic function: serum ENA), antineutrophil cytoplasmic
albumin level, international normalized antibody (ANCA)
ratio (INR) • Liver biopsy
O Hepatocellular enzymes: aspartate
transaminase (AST), alanine
transaminase (ALT), total bilirubin, direct ( T_R_EA_~_M_EN_T
__ )
bilirubin
O Ductal enzymes: alkaline phosphatase • Initially disease-specific; see individual
(ALP), gamma glutamyl transpeptidase disorders
(GGT)
• Hepatitis virus serology SURGERY
O Hepatitis A: anti-hepatitis A lgM, anti- • Advanced disease - liver transplant
hepatitis A lgG
O Hepatitis 8: hepatitis B surface antigen,
anti-hepatitis B core/surface antibodies,
97
ALCOHOLIC LIVER DISEASE
osmsJl/ e1leoholie-liver-disee1se
• Large vacuoles coalesce - fatty cysts -
( PATHOLOGY & CAUSES ) irreversible lesions
• Macrovesicular steatosis most commonly
• Abnormal lipid retention in hepatocytes
associated with alcohol, diabetes, obesity.
(steatosis) - large triglyceride fat vacuoles
corticosteroids
accumulate in liver cells - fatty liver
• Severe fatty liver may be accompanied by
• Fat content of liver exceeds 5-10% by
inflammation. steatosis - steatohepatitis
weight
O Steatohepatitis - hepatocyte
• Can be accompanied by progressive
ballooning, necrosis - liver cell death,
inflammation (hepatitis) - steatohepatitis
inflammatory response - hepatic
stellate cell activation - fibrosis -
RISI( FACTORS cirrhosis
• Glycogen storage diseases, acute fatty liver
during pregnancy, malnutrition, obesity, COMPLICATIONS
HIV. hepatitis C
• Hepatocellular carcinoma
Alcohol
• Most common cause
• Chronic alcohol use - production of toxic
metabolites (e.g. aldehydes)
• Fatigue, malaise, dull right-upper-quadrant
O Damages mitochondria, cellular pain, mild jaundice (rare), significant
structures - impaired cellular energy damage - hepatomegaly, ascites
mechanisms
O Alcohol metabolised to aldehyde hepatic
enzymes (reaction facilitates conversion ( D_IA_GN_o_s,_s __ )
of NAO+ - NADH; lower NAO+
concentration - less fatty acid oxidation DIAGNOSTIC IMAGING
- fatty acids accumulate - steatosis)
Ultrasound
• Steatosis - bright liver with increased
STAGING echogenicity
• Stages of intracytoplasmic accumulation of
• Fibrosis - coarse echo pattern
triglycerides - fatty change
• Cirrhosis - nodules - irregular outline of
Initial stage liver surface
• Hepatocytes contain small fat vacuoles
CT scan
(liposomes) around nucleus (microvesicular
fatty change) • Lower density than spleen on CT scan
Late stage MRI

• Vacuoles enlarge - nucleus pushed to • Fat - bright on Tl and T2-weighted
cell periphery - signet ring appearance images
(macrovesicular fatty change)
• Vesicles well-delineated, optically empty LAB RESULTS
° Fats dissolve during tissue processing
Liver function tests
• Serum aminotransferases normal/
98
moderately elevated
O AST usually more elevated than ALT in
(..__ __ T_R_EA_~_M_EN_T
)
alcoholic fatty liver disease
• Hepatic steatosis reversible, non-
O GGT often elevated in alcoholic fatty
progressive if underlying cause controlled
liver disease
(e.g. cease alcohol use)
Secondary causes of steatosis
• Hepatitis C virus antibodies
• Hepatitis A lgG
• Hepatitis B surface antigen, surface
antibody, core antibody
• Plasma iron, ferritin, total iron-binding
capacity
Biopsy
• Early changes
O Accumulation of membrane bound large
droplet steatosis (Large macrovesicular
drops----. alcoholic steatosis; small
microvesicular droprets=- 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.
O Proliferation of smooth endoplasmic
reticulum
O Gradual distortion of mitochondria
• Steatohepatitis
O Presence of neutrophtts=- alcoholic
steatohepatitis, unusual in chronic viral
hepatitis
OMallory-Denk bodies (clusters of
intracellular cytoskeletal protein
aggregates)
• Advanced changes
° 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 liver. The numerous white spaces represent
by presence of regenerative nodules the accumulation of lipid.
(irreversible)
99
AUTOIMMUNE HEPATITIS
osms.i"l/ o.uloimmune-hepo.-li"lis

)
• Inflammation of the liver tissue caused by LAB RESULTS
autoimmunity • HALT, t AST,! albumin, I prothrombin
time
TYPES • Type 1
O Antinuclear antibodies (ANAs),
• Type 1: 80% of cases
antibodies against smooth muscle
• Type 2: most common in young
proteins, or (ASMAs)
• Type 2
• Type 3: different antibodies but presents as
O Antibodies to the microsomes of the
Type 1
liver or kidney (ALKM-1), liver cytosol
• Type 4: no detectable antibodies
antigen (ALC-1)
• Type 3
CAUSES O Soluble liver antigen positive
• Combination of environmental triggers and
genetic predisposition
( T_R_E~_~_M_EN_T
)
RISk FACTORS
• Young biologically-female individuals; MEDICATIONS
presence of HLA-DR3.DR4 lmmunosuppressants
• Corticosteroids, azathioprine
COMPLICATIONS
• Acute liver failure, chronic liver failure,
SURGERY
hepatocellular carcinoma, long term
immunosuppression can lead to Liver transplantation
malignancies • If resistant to drug therapies
( SI_G_NS_&_S_Y_M_PT_O_M_s
)
• Wide spectrum of presentation, from
asymptomatic to cirrhosis and liver failure
• Common moderate symptoms
° Fever, jaundice, and
hepatosplenomegaly
• Chronic disease symptoms
° Coagulation disturbance, impaired
immunity
• Type 2 is associated with other diseases
(Hashimoto's thyroiditis, Grave's disease)
100
autoimmune hepatitis. There is an infiltration
of lymphocytes and plasma cells at the
interface between the hepatic lobule and the
portal tract i.e. lymphoplasmacytic interface
hepatitis.
BUDD-CHIARI SYNDROME
osms.i-l/\>ucJ.cJ.-ehio.Ti-s14ncJ.Tome
• Trauma
( PATHOLOGY & CAUSES ) • Pregnancy
• Contraceptive therapy
• Congestive hepatic disease caused by
obstruction of hepatic venous outflow
• Usually> one hepatic vein or hepatic COMPLICATIONS
section of vena cava • Cirrhosis and liver failure
• Venous congestion leads to • Esophageal, gastric and rectal varices
O lschemia and centrilobular necrosis • Kidney dysfunction (hepatorenal syndrome)
O Increased pressure in portal system -
portal hypertension
(__ s,_G_NS_&_SY_M_P_TO_M_s_)
CAUSES • Can present acutely or chronically
• Occlusion (primary)
• Classic triad
O Thrombosis (most common)
, Hepatomegaly
• Compression (secondary)
, Abdominal pain
O Tumor mass, granuloma
, Ascites
• Jaundice
RISI( FACTORS • Fever
• Myeloproliferative and hematologic • Other signs and symptoms of portal
disorders (e.g. polycythemia vera) hypertension (e.g. splenomegaly,
• Hypocoagulative disorders encephalopathy)
• Tumors
• Infections (e.g. tuberculosis)
• Inflammatory diseases
101
( D_IA_GN_O_SI_S ) ( T_R_EA_~_M_EN_T )
DIAGNOSTIC IMAGING • Treat the underlying cause
Doppler ultrasound
• Thrombus MEDICATIONS
• Usually insufficient
• Alteration of hepatic venous outflow
• Anticoagulants
• 'Spider web' formation around the
obstruction duto collateral vessels • Diuretics
proliferation
Venography
SURGERY
Liver transplantation
CT scan, MRI
• In case offulminant liver failure
LAB RESULTS Portosystemic shunt

• Elevated aminotransferases • Divert the flow away from the obstruction
• Liver biopsy • Transjugular intrahepatic portosystemic
shunt (TIPS)
• Surgical shunt
OTHER INTERVENTIONS
Thrombolytic therapy
• Dissolve clots
• 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.
102
CHOLESTATIC LIVER DISEASE
osms.i"l/ eholes-1:a-lie-live,--disease
malignancy (biliary tree/head of
( PATHOLOGY & CAUSES ) pancreas), strictures, cystic fibrosis
(impaired secretory function of biliary
• Cholestasis: decrease in bile flow through epithelium), primary sclerosing
bile ducts into duodenum cholangitis (immune system attacks
• Hepatic retention, spillage into systemic bile ducts=- inflammation, scar tissue),
circulation of cholesterol, bile salts ---'> biliary atresia (2:: one newborn infant's
incorporation into biological membranes bile ducts narrow/blocked/absent)
---'> altered membrane fluidity---'> injury to , Complications: prolonged obstruction
biological membranes, impaired function ---'> biliary cirrhosis; subtotal/intermittent
of membrane channels=-s bile secretion obstruction ---'> ascending cholangitis
impaired in liver (secondary bacterial infection of biliary
• No bile reaches small tntestlne s- intestinal tree) ---'> sepsis, if untreated
malabsorption-» nutritional deficiencies of
c
fat soluble vitamins (A, D, E, K)
SIGNS & SYMPTOMS )
CAUSES
• Jaundice
Hepatocellular cholestasis , Individual components of bile enter
• Impaired secretion of bile by hepatocytes serum (e.g. conjugated bilirubin)
O Intracellular accumulation of bile • Pain
acids ---'> ! regulation of bile synthesis , Right upper quadrant (RUQ) pain,
---'> ! total bile production/secretion radiates to right shoulder, minutes to
---'> accumulation of bile components hours in duration (often after fatty meal)
(e.g. conjugated bilirubin) ---'> diffuse/ • Pruritus
exocytose into interstitium ---'> diffuse
, Systemic accumulation of bile salts/
into blood
endogenous opioids/lysophosphatidic
Elevated levels of estrogen acid
• Breakdown of cholesterol ---'> cholic acid • Skin xanthomas
(bile acid) , Focal accumulations of cholesterol
• j estrogen ---'> inhibition of export pump---'> (common in obstructive jaundice)
estrogen-induced cholestasis • Pale stools/dark urine
• Risk factors O Absence of bile in gut ---'> conjugated
O Oral contraceptives (increase estrogen bilirubin (water soluble) not excreted
exposure), pregnancy (pregnancy- with bile, excreted via kidneys
induced cholestasis), anabolic steroids
(similar in structure to estrogen)
• Extra hepatic cholestasis
O Physical obstruction blocks bile flow
O Ductal obstruction-« bile accumulates
in liver e- j pressure in bile ducts ---'> bile
leaks through tight junctions between
hepatocvtes=- enters serum, interstitial
space
° Causes: cholelithiasis (gallstones),
103
__) (~~~T_RE_A_~M_E_N_T~~)
(-~~D_IA_G_N_O_Sl~S~
LAB RESULTS MEDICATIONS
• Associated vitamin deficiency
Liver function tests (LFTs)
, Fat-soluble vitamin supplementation
• Elevated membrane-bound enzymes
• Children
(sensitive to hepatocyte damage) ----> t
serum alkaline phosphatase (ALP), gamma- , Ursodeoxycholic acid ----> increased bile
glutamyl transpeptidase (GGT) formation
Histology
SURGERY
• Individual hepatocytes take on brownish-
• Extrahepatic obstruction
green stippled appearance (due to
, Surgical correction of obstruction
trapped bile), canalicular bile plugs form
(e.g. cholecystectomy; if gallstone
between individual hepatocytes/bile ducts
obstructing common bile duct, removal
(excreted bile cannot travel further due to
of gallbladder)
obstruction)
o Under sufficient pressure, canalicular
plugs may rupture ----> spillage of bile into OTHER INTERVENTIONS
surrounding tissue-» hepatic necrosis • Pregnancy-induced cholestasis
, Early delivery (around week 36 of
gestation)
CIRRHOSIS
osms.i"l/etrrhests
fibrotic material in extracellular matrix
( PATHOLOGY & CAUSES ) • Fibrotic cascade-» formation of fibrous
septa ----> separation of hepatocyte nodules
• Hepatic parenchyma replaced by scar ----> distortion of liver architecture ---->
tissue e- scar tissue blocks portal flow of
decrease blood flow throughout ----> splenic
blood through liver ----> raised blood pressure
congestion ----> hypersplenism. splenic
and disturbance of function
sequestration of platelets
• Reversible phase ----> hepatitis/fatty liver
• Injured liver cells group together---->
(steatosis) often precedes cirrhosis regenerative nodules (clumps of cells
• Long term accumulation of liver damage ----> between fibrotic tissue, collagen) ----> bumpy
disruption of liver archltecture-» functional cirrhotic liver
impairment
• Develops over months to years
RISI( FACTORS
• Damage to parenchyma ----> activation of
• Chronic alcohol use, chronic hepatitis C
stellate cells (sit between sinusoids and
infection, chronic hepatitis B (+/- hepatitis
hepatocytes in perisinusoidal space) ---->
DJ infection. autoimmune hepatitis,
secretion of
hereditary hemochromatosis, Wilson
o TGF-~1----> production of myofibroblasts
disease. alpha 1-antitrypsin deficiency,
----> increased fibrosis, proliferation of
medications
connective tissue
o TIMP 1 & 2 (matrix metalloproteinase
inhibitors) ----> prevents breakdown of
104
COMPLICATIONS (ERCP) /magnetic resonance
• Portal hypertension, hepatic cholangiopancreatography (MRCP))
encephalopathy, increased blood levels of
Diagnostic paracentesis
estrogens, hepatocellular carcinoma
• Determine ascitic fluid origin
• Portal hypertension
\ MNEMONIC: HEPATIC • Suspected spontaneous bacterial peritonitis
Causes of Cirrhosis , Cell count, gram stain, culture
Hemochromatosis (primary) , Serum: ascites albumin gradient (SAAG)
Enzyme deficiency (alpha-1- > 1.1 g/dL - portal HTN
anti-trypsin)
Post hepatic (infection + drug LAB RESULTS
induced) • AST, ALT moderately elevated, AST > ALT
Alcoholic • ALP 2-3x normal
Tyrosinosis • GGT very high in chronic alcoholic liver
Indigenous people in America disease
(galactosemia) • Bilirubin increases as cirrhosis worsens
Cardiad Cholestatic (biliary)/ • Albumin decreases as synthetic function
Cancer/ Copper (Wilson's) declines
• Prothrombin time increases as synthetic
function declines
( SIGNS & SYMPTOMS ) • Hyponatremia from inability to excrete free
water (high levels of antidiuretic hormone,
• Early stages generally asymptomatic aldosterone)
O Liver may be enlarged, shrinks as • Serum biomarkers correlate with degree of
cirrhosis progresses liver damage in variety of liver diseases
O Non-specific symptoms: weakness, • A2-macroglobulin, haptoglobin,
weight loss, fatigue apolipoprotein Al, bilirubin, GGT, age,
• Portal hypertension biological sex
• Liver cellular dysfunction Histology
• Nail changes (Muehrcke's lines, Terry's • Macroscopic appearance
nails, clubbing) O Surface irregular, consistency firm
• Hypertrophic osteoarthropathy O Yellow color (in steatosis)
• Dupuytren's contracture O Nodular
• Liver biopsy
( D_IA_GN_O_s,_s
__ ) O Microscopic appearance of hepatocytes
(regenerating nodules) and fibrosis/
DIAGNOSTIC IMAGING connective tissue deposits between
nodules
Ultrasound • Cause specific abnormalities
• Small nodular liver (advanced cirrhosis), n Chronic hepatitis B: infiltration of liver
increased echogenicity, irregular- looking parenchyma with lymphocytes
areas, widening fissures, splenomegaly, n Cardiac cirrhosis: erythrocytes, greater
imaging of blood flow in portal vein amount of fibrosis in tissue surrounding
hepatic vein
Endoscopy
, Primary biliary cholangitis: fibrosis
• Esophagogastroduodenoscopy (EGO)
around bile duct, presence of
O Exclude esophageal varices granulomas, pooling of bile
• Imaging of bile ducts (endoscopic O Alcoholic cirrhosis: neutrophilic
retrograde cholangiopancreatography
infiltration
105
OTHER DIAGNOSTICS
Child-Pugh score
• Grading of cirrhosis
° Class A (5-6 points): one year survival
100%, two year survival 85%
° Class B (7-9 points): one year survival
81 %, two year survival 57%
° Class C (10-15 points): one year
survival 45%, two year survival 35%
Figure 36.5 Gross pathology of micronodular

( T_R_E~_;,-_M_EN_T__ ) liver cirrhosis.
MEDICATIONS
• Antiviral medication (e.g. interferon)
o For hepatitis B, C
• Corticosteroids
° For autoimmune hepatitis
• Diuretics, antibiotics, laxatives, enemas,
thiamine, steroids, acetylcysteine,
pentoxifylline
° For decompensation (compensated
cirrhosis-no jaundice, ascites, variceal
bleeding, hepatic encephalopathy;
development of any of above ---->
decompensated)
Figure 36.6 Histological appearance of liver
cirrhosis (trichrome stain). The blue highlights
OTHER INTERVENTIONS the bands of fibrosis between islands of
• Abstain from alcohol hepatocytes.
° For alcoholic hepatitis
• Chelation therapy (e.g. penicillamine)
° For Wilson disease
• Dissolve gallstones
O Blockage of bile ducts
106
< 34 (< 2) 34-50 (2-3) > 50 (> 3)
> 3.5 2.8-3.5 <2.8
< 4.0 4.0-6.0 >6.0

< 1.7 1.7-2.3 > 2.3
Mild (or suppressed Moderate to severe

None
with medication) (or refractory)
None Grade 1-11 Grade Ill-IV
FITZ-HUGH-CURTIS SYNDROME
osms.i"l/fi"l2-hugh-euT-lis-s14nd Tome
• Causative organisms
( PATHOLOGY & CAUSES ) , Commonly: Chlamydia trachomatis,
Neisseria gonorrhoeae, Mycobacterium
• Pelvic inflammatory disease (PIO) - tuberculosis (endemic areas)
inflammation of local structures - anterior
, Reported: Trichomonas vaginalis,
liver capsule inflammation (perihepatitis)
Ureaplasma urealyticum, Mycoplasma
- patchy purulent, fibrinous exudate -
hominis, Bacteroides spp., Gardnerella
adhesions form
vaginalis, E. coli and Streptococcus spp.
CAUSES RISI( FACTORS

• Etiology of inflammation poorly understood
• Biological females of reproductive age
• Thinning of cervical mucus - bacteria
colonizing vagina enters uterus, fallopian
tubes - infection, inflammation - possibly
spreads via
O Direct intraperitoneal spread from initial • Vomiting, nausea, hiccupping, headaches
pelvic inflammation and infection
• Acute onset right upper quadrant
O Bacterial seeding via lymphatic abdominal pain; aggravated by breathing,
bloodstream coughing, laughing (pleuritic pain), may
O Autoimmune response to PID refer to right shoulder, tenderness to
107
palpation, tenderness to percussion of
overlying ribs (.____ T_R_E~_~_M_EN_T
)
• Fever, chills, night sweats, malaise, vaginal
discharge, lower abdominal pain, cervical
MEDICATIONS
motion tenderness • Organism-specific antibiotics
• Pain management
= Appropriate analgesia
(.____ D_IA_GN_O_s,_s __ ) , Laparoscopy for lysis of adhesions for
refractory pain
• History of pelvic inflammatory disease
DIAGNOSTIC IMAGING
Abdominal ultrasound
• Typically normal
Abdominal CT scan with contrast

• Perihepatic
O Subtle enhancement of liver capsule,
inflammatory stranding and fluid along
right paracolic gutter and perihepatic
region, gallbladder wall thickening,
pericholecystic inflammatory change
• Pelvic Figure 36.7 A laparoscopic view of intra
O Possible tubo-ovarian abscess abdominal adhesions caused by Fitz-Hugh-
Curtis syndrome.
LAB RESULTS
• Liver function tests
o Typically normal
• 0-dimer
O Markedly raised
O Often ordered due to pleuritic chest pain
• Endocervical/low vaginal swab
° Culture causative organism
OTHER DIAGNOSTICS
Laparoscopy
• "Violin string" adhesions of parietal
peritoneum to liver/diaphragm
108
HEMOCHROMATOSIS
osms.i"l/hemoehTomolosis

• Excessive iron absorption in the intestine - • Initially asymptomatic
iron deposited in organs and tissues - free , Biogically male: symptoms appear
radical generation - cellular damage - around age 50
cell death - tissue fibrosis , Biologically female: eliminate iron
through menstrual bleeding -
TYPES symptoms appear 10-20 years after
menopause
Primary (hereditary: autosomal recessive) • Signs and symptoms of liver disease
• Variety of possible mutations (C282Y • Altered glucose homeostasis (hyper/
being the most common) in HFE gene on hypoglycemia)
chromosome 6 regulating iron absorption
• Fatigue
from food - most of the iron in the food
• Arthralgia
is absorbed by enterocytes in the gut and
pass into the bloodstream - iron overload • Sexual dysfunction
• Abdominal pain
Secondary (not genetic) • Cardiac arrhythmias
• Multiple blood transfusions - erythrocytes
contain iron bound to the hemoglobin -
heme is released in bloodstream when (..____ D_IA_GN_O_s,_s
__ )
erythrocytes die after 120 days
• Chronic hemolytic anemias LAB RESULTS
• Excessive iron intake (very rare) • High levels of serum iron
• Elevated ferritin
COMPLICATIONS • High transferrin saturation
• Caused by deposition of iron in tissues • Decreased total iron binding capacity
O Liver: cirrhosis, cancer
Liver biopsy
O Pancreas: altered endocrine and
• Iron can be seen as brown spots inside
exocrine function
hepatocytes - it becomes blue with a
O Skin: bronze pigmentation Prussian blue stain
O Heart: cardiomyopathy, arrhythmias
O Gonads (related to impaired pituitary
OTHER DIAGNOSTICS
function): amenorrhea in biologically-
female individuals, testicular atrophy in • Genetic analysis and screening of family
biologically-male individuals members
O Adrenal gland: gland insufficiency
O Joints: degenerative joint disease
109
(..__ __ T_R_E~_~_M_EN_T
__ )
MEDICATIONS
Deferoxamine
• Chelating agent binds iron molecules -
deferoxamine excreted by kidneys - urine
excretion - decreases iron load
SURGERY
• Advanced liver damage - transplantation
Figure 36.8 Iron deposition (hemosiderosis)
in the liver parenchyma in a case
hemochromatosis. There is associated OTHER INTERVENTIONS
hepatocyte damage. • Phlebotomy
• Dietary changes to reduce iron absorption
Figure 36.9 Prussian blue stain on a liver

biopsy highlights iron deposits in a case of
hemochromatosis.
110
HEPATITIS B
osms.i-l/hepo.·tJlis

)
• Infection of the liver caused by hepatitis B LAB RESULTS
virus (HBV) • HBVvirions found in blood serum, proves
• DNA virus from the hepadna group viral replication
• Incubation is 1-6 months, long term carrier • l ALT, i AST
state established after, transmitted through • l CRP, l ESR, i WBC
blood or semen • HBsAg (surface antigen); present in acute
• Immune system attacks infected infection then cleared in recovery; if present
hepatocytes over six months - chronic infection; used
to create vaccine
RISI( FACTORS • Anti-HBc lgM (core antigen); present in
active infection for six months; if present
• Intravenous drug users, unprotected
longer individual is carrier; used for
sexual intercourse, blood transfusions;
screening because present most of the time
hemodialysis
• Anti-HBc lgG develop after lgM, lifelong
secretion indicates individual is immune
COMPLICATIONS • Anti-HBe secreted core antigen, appears
• Liver cirrhosis, hepatocellular carcinoma during viral replication, indicates active
infection
C__s,_G_Ns_&_sv_M_PT_O_M_s_) • Bilirubin normal to increased
• General infection OTHER DIAGNOSTICS

O Low grade fever, malaise, lethargy, • Physical exams shows hepatomegaly
anorexia
• Liver related
° Fatty stool, dark urine, jaundice,
( T_R_EA_~_M_EN_T
__ )
hepatomegaly, scleral icterus, pruritus,
right upper quadrant tenderness
MEDICATIONS
• Interferon alpha. nucleoside reverse
transcriptase inhibitors (NRTI)
• Post exposure prophylaxis available with
HBV immunoglobulins
• Vaccine available
111
HEPATITIS C,
osms.i-l/hepe1·tJlis
( PATHOLOGY & CAUSES ) ( D_IA_GN_O_s,_s)

• Viral hepatitis caused by hepatitis C virus LAB RESULTS
(HCV) • Enzyme-linked immunosorbent assay
• RNA virus from the class of flaviviridae (ELISA) used to detect antibodies in
• Incubation is 6-7 weeks, lifelong infectious chronic cases, may be false negative in
carrier state immunosuppressed
• Virus mutates often to bypass the host • Specific hepatitis C antigens immunoassay
immune system • HCV RNA test with PCR
• Minority of individuals develop acute • t ALT
hepatitis symptoms, due to this majority • l CRP, l ESR, i WBC
progress to chronic infection
OTHER DIAGNOSTICS
RISI( FACTORS • Physical exam shows enlarged liver
• Intravenous drug use, sexual contact, from
mother to child in neonatal period (vertical
transmission); chronic hemodialysis C T_R_E_AT_M_EN_T
)
COMPLICATIONS MEDICATIONS
• Interferon alfa, ribavirin
• Cirrhosis, hepatocellular carcinoma, renal
dysfunction (HCV immune complexes • Screen for HBV, HIV and HAV; vaccinate
involved in pathogenesis) against HBV and HAV if tests are negative
• No HCV vaccine available
( s,_G_NS_&_SY_M_PT_O_M_s_) SURGERY
• Liver transplant in case of liver failure
• General infection
O Low grade fever. malaise, lethargy,
anorexia
• Liver related
° Fatty stool, dark urine (iron), jaundice,
hepatomegaly, icterus. pruritus
112
HEPATITIS E
osms.tl/hepo.-1:i-l:is

__ )
• Viral hepatitis caused by hepatitis E virus LAB RESULTS
(HEV) • Anti - HEV lgM assay in acute infection,
• RNA virus from the class hepeviridae PCR in chronic cases
• Transmitted via fecal-oral route • i ALT
• i CRP, i ESR, i WBC
RISI( FACTORS
• Consuming contaminated food and water OTHER DIAGNOSTICS
in endemic areas, blood transfusions, from • Physical exam shows enlarged liver
mother to child in neonatal period
COMPLICATIONS ( T_R_E~_~_M_EN_T
__ )
• Rare but if present then cholestatic
MEDICATIONS
hepatitis, chronic infection in
• Ribavirin used in immunosuppressed
immunosuppressed individuals, liver failure,
individuals
high mortality rate in pregnant individuals
SURGERY
(__ SI_G_NS_&_SY_M_PT_O_M_s_) • Liver transplant in case of liver failure
• General infection
, Low grade fever, malaise, lethargy,
anorexia
• Liver related
, Fatty stool, dark urine (iron), jaundice,
hepatomegaly, icterus, pruritus
• Other
, Diarrhea, arthralgia, urticaria! rash
113
HEPATOCELLULARADENOMA
osms.i"l/hepo.-loeellulo.,--o.denomo.
( PATHOLOGY & CAUSES ) ( D_IA_GN_O_s,_s

__ )
• Rare, benign liver tumor DIAGNOSTIC IMAGING
• Formed from hepatic epithelial cells, often • Often incidental finding on abdominal
in healthy liver imaging
O Enlarged, nonfunctional epithelial cells
Ultrasound
O More glycogen, lipids than expected
• Solitary well-demarcated heterogeneous
O Surrounding tissue highly vascularized mass with variable echogenicity
O Bile ducts, portal triads absent
CT scan
• Well-marginated isoattenuating hepatic
CAUSES
lesions; fat content ----. hypoattenuation
• Exact mechanisms unknown; associated
with estrogen-based drugs: oral
contraceptives, anabolic steroids LAB RESULTS
• Genetic diseases
Histology (definitive)
O Glycogen storage disease type I (von
• Well-circumscribed nodules
Gierke's disease): glucose cannot
be generated from glycogen via = Sheets of hepatocytes with bubbly
gluconeogenesis vacuolated cytoplasm
• Lack portal tracts/central veins
RISI( FACTORS
• Diabetes, metabolic syndrome, obesity ( T_R_E~_~_M_EN_T
__ )
COMPLICATIONS SURGERY
• Rupture, bleeding; malignant • Surgical resection
transformation (rare)
OTHER INTERVENTIONS
( SIGNS & SYMPTOMS ) • Estrogen-associated
• Cessation of estrogen-based medication
----. adenoma regression
• Usually asymptomatic • Von Gierke's disease
• Abdominal pain (esp. epigastric/RUQ), • Strict dietary manaqement e- adenoma
palpable mass
regression
• If adenoma ruptures, bleeds
O Hypotension, tachycardia, diaphoresis
114
Figure 36.10 lntraoperative photograph of
a large, well-circumscribed hepatocellular
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.i"l/neonatal-hepa-lrlis
COMPLI CATIONS
( PATHOLOGY & CAUSES ) • If untreated > six months
° Chronic liver disease---> hepatic cirrhosis
• Inflammation of liver in newborns (usually
---> liver failure
1-2 months after birth)
CAUSES ( SI_G_NS_&_SY_M_P_TO_M_
• Viruses (20%)
, Infect mother during pregnancy/baby • Jaundice, pruritus, rashes, dark urine,
shortly after birth pale stools, hepatomegaly (due to liver
inflammation)
, Rubella; Cytomegafovirus (CMV);
hepatitis A,B,C • Decreased intestinal bile ftow -» impaired
fat digestion, vitamin absorption ---> failure
• Idiopathic (80%)
to grow
, Unknown origin
, Viral
, Neonatal cholestasis (..____ D_IA_GN_O_s,_s)
, Newborn bile production irnrnature e- !
bile production DIAGNOSTIC IMAGING
, Developing liver more sensitive to injury
---> ! bile synthesis, flow
Ultrasound
• Genetic • Check bile ducts for obstruction, correct

development
, Alpha 1-antitrypsin deficiency:
malformation ---> cannot be transported
out of hepatocytes ---> accumulation
within cells ---> cell death ---> hepatitis
115
LAS RESULTS
(..____ T_R_EA_:T_M_EN_T
__ )
Liver biopsy
• Multi nucleated giant cells MEDICATIONS
O Arise from combination of neighboring • Ursodeoxycholic acid
cells (hepatocytes) O Increase bile formation
O Signs of cholestatic liver disease
Blood tests SURGERY

• Cirrhotic liver disease/liver failure requires
• i serum bilirubin
liver transplant
OTHER INTERVENTIONS
• Optimize nutrition/vitamin supplementation
NON-ALCOHOLIC FATTY LIVER

DISEASE
osmsJl/ non-aleoholie-fa-H:14-live,-
NAFL- NASH
( PATHOLOGY & CAUSES ) • Second hit hypothesis
• Disease due to fat accumulation in liver,

OInitial fatty change benign - oxidative
stress, hormonal imbalances,
associated inflammation
mitochondrial abnormalities -
progression
TYPES • Hepatocytic fat vulnerable to degradation
Non-alcoholic fatty liver (NAFL)
O Unsaturated fatty acids: ::::: one double
bond, hydrogen atoms vulnerable to
• Steatosis without inflammation
initiators (e.g. reactive oxygen species)
Non-alcoholic steatohepatitis (NASH) O Process damages cell lipid membranes
• Steatosis with hepatic inflammation, - mitochondrial dysfunction - cell
indistinguishable from alcoholic death - inflammation - steatohepatitis
steatohepatitis (NASH)
Subtype
RISI( FACTORS
• Liver steatosis without evident secondary
• NAFL- NASH
cause (e.g. chronic alcohol use/persistent
viral infection)
O Age> 50
O Liver large, soft, yellow greasy
O BMI ::::: 28kg/m2 (5.71bs/ft2)
O Bloating, hepatocyte necrosis
O Diabetes mellitus
O Mallory-Denk bodies
O Elevated serum aminotransferases
O Damage attracts neutrophils - more
O Ballooning degeneration, Mallory-Denk
inflammation bodies or fibrosis on biopsy
O Inflammation - hepatic stellate cells • NAFL (general)
O Insulin resistance, metabolic syndrome,
activate - fibrosis - cirrhosis
, z Three of: obesity, hypertension,
116
diabetes, hypertriglyceridem ia, Liver biopsy
hyperlipidemia, excessive soft drink • > 5% fat content ---'> NAFL
consumption (high concentration of • Iron deposits
fructose), diet rich in saturated fats,
• NAFL
medications (corticosteroids)
O Steatosis alone
n Steatosis with lobular/portal
COMPLICATIONS inflammation without hepatocyte
• Liver cirrhosis, hepatocellular carcinoma ballooning
n Steatosis with hepatocyte ballooning
( SIGNS & SYMPTOMS ) • NASH

but without inflammation
, Hepatocyte ballooning degeneration,

• Usually asymptomatic
hepatic lobular inflammation,
• Fatigue, malaise, dull right upper quadrant
apoptotic bodies, mild chronic portal
pain, mild jaundice (rare), significant liver
inflammation, perisinusoidal collagen
damage ---'> hepatomegaly, ascites
deposition ---'> zone 3 accentuation
(chicken wire pattern), portal fibrosis
without perisinusoidal or pericellular
(..____ D_IA_GN_O_s,_s __ ) fibrosis, cirrhosis (macronodular
or mixed), Mallory-Denk bodies,
• Typically diagnosed as incidental finding on megamitochondria, vacuolated nuclei in
liver function panel periportal hepatocytes
DIAGNOSTIC IMAGING OTHER DIAGNOSTICS

• Identify fatty infiltrates • Alcohol consumption> 25 ml/day pure
ethanol excludes diagnosis
Ultrasound
• Increased echoqenicitv -e bright appearing
liver e- diffuse fatty infiltration
(..__ TR_E_AT_M_E_N_T__ )
CT scan
• Decreased hepatic attenuation
OTHER INTERVENTIONS
Dietary changes
MRI
• Avoid high fructose-corn syrup, trans-fats
• Increased fat signal
• Omega 3 fatty acid supplementation ---'>
improvement in liver fat deposition
LAB RESULTS • Coffee and olive oil consumption may be
• Destruction of hepatocytes ---'> increase in protective
liver enzymes AST/ALT
• Serum ALT> AST level= NAFL Treat insulin resistance
• Weight-loss
• Insulin sensitizers
Treat hyperlipidemia
• Statins
117
PORTAL HYPERTENSION
osms.i"l/po,--lo.l-h14pe,--lension
( PATHOLOGY & CAUSES ) (__ SI_G_NS_&_SY_M_PT_O_M_s_)

• Elevation of blood pressure in the portal • GI bleeding (secondary to esophagogastric
venous system above 5mmHg varices) - most life-threatening
complication
= Hematemesis
CAUSES
= Melena
Prehepatic causes • Jaundice
• Portal vein obstruction (e.g. thrombosis) • Ascites
• Periumbilical caput medusae
lntrahepatic causes
• Signs and symptoms of encephalopathy
• Cirrhosis (most common of all causes)
• Altered level of consciousness
• Schistosomiasis
• Sarcoidosis • Lethargy
• Hand tremor when the wrist is extended
Posthepatic causes (aka asterixis)
• Right-sided heart failure • Seizure, coma and death
• Constrictive pericarditis
• Budd-Chiari syndrome
( D_IA_GN_O_s,_s
__ )
COMPLICATIONS DIAGNOSITC IMAGING
• Portosystemic shunts and development of
collateral channels Liver ultrasound
O Esophageal varices • Nodules in case of cirrhosis
O Hemorrhoids
CT scan, MRI
° Caput medusae (distension of
• Ascites
abdominal wall veins)
• Cirrhosis
• Increased hydrostatic pressure and
• Splenomegaly
hypoalbuminemia - ascites
• Vascular alteration such as inferior vena
• Splenomegaly (blood drainage backs up to
cava dilatation
spleen due to high pressure portal system)
- sequestration of blood elements -
anemia, thrombocytopenia, leukopenia LAB RESULTS
• Liver disease and blood shunting away • Full blood count
from liver - decreased blood detoxification • Liver enzymes and serology
- increased ammonia in the blood - • Perform emergent upper GI endoscopy, to
encephalopathy
diagnose/treat varices
• Spontaneous bacterial peritonitis
118
OTHER DIAGNOSTICS
(..__ __ T_R_EA_:T_M_EN_T
)
Diagnostic paracentesis
• Will determine if ascites is due to portal • Prevent and treat the complications
HTN or other etiology
• Serum ascites albumin gradient (SAAG) > MEDICATIONS
1.1 mg/dl • Beta-blockers
O Portal HTN is likely , ----> decrease portal venous pressure
• IV octreotide
O If bleeding, non-selective beta blockers
(prophylaxis), antibiotics (prophylaxis for
spontaneous bacterial peritonitis)
n For esophageal varices
• Diuretics and sodium restriction
n For ascites
SURGERY
• Transjugular intrahepatic portosystemic
shunt
, Communication between portal vein
and hepatic vein=-s blood bypasses the
liver circulation ----> reduced intrahepatic
pressure
• Balloon tamponade, sclerotherapy, variceal
ligation/banding
Figure 36.11 Ascites as a consequence of
n For esophageal varices
portal hypertension caused by cirrhosis of
the liver.
MNEMONIC: ASCOE
Features of Portal
hypertension
Ascites
Bleeding (haematemesis, piles)
Caput medusae
Diminished liver
Enlarged spleen
Figure 36.12 Barium swallow demonstrating

esophageal varices.
119
Figure 36.13 Endoscopic appearance of

esophageal varices.
PRIMARY BILIARY CIRRHOSIS
COMPLICATIONS
( PATHOLOGY & CAUSES ) • Osteoporosis, hyperlipidemia, fat soluble
vitamin deficiencies
• Autoimmune disease of liver - progressive
destruction of cells lining small intrahepatic
bile ducts - leakage of bile, toxins into
liver parenchyma, blood - inflammation,
fibrosis - cirrhosis • Fatigue, pruritus, jaundice, right upper
• AKA primary biliary cholangitis quadrant pain
• Loss of bone density - fractures
CAUSES • Hypercholesterolemia - xanthelasma,
• Failure of immune tolerance against xanthoma
mitochondrial pyruvate dehydrogenase • Liver cirrhosis - ascites, splenomegaly,
complex (PDC-E2). other hepatic proteins esophageal varices. hepatic
- destruction of cells lining bile ducts - encephalopathy
autoimmunity
RISI( FACTORS ( 0_1A_GN_o_s1_s __ )

• Biological female, family history of disease,
DIAGNOSTIC IMAGING
extra hepatic autoimmune disease
O Previous infection with environmental Abdominal ultrasound
/MRCP/CT scan
gram-negative Novosphingobium • Rule out bile duct obstruction
aromaticivorans - cross-reaction
between bacterial antigens, hepatic
mitochondrial proteins LAB RESULTS
• Antimitochondrial antibodies (most
individuals)
120
• Other autoantibodies may be present
O Antinuclear antibody, anti-
(..__ __ T_R_EA_~_M_EN_T
)
glycoprotein-210 antibodies, anti-p62
antibodies (suggests more severe
MEDICATIONS
disease - liver failure), anticentromere • Ursodeoxycholic acid
antibodies (correlates with developing , Reduces intestinal absorption of
portal hypertension). anti-np62 and cholesterol - reduces cholestasis,
anti-splOO improves liver function tests
• Elevated lgM. total cholesterol. HDL. GGT. • Cholestyramine
ALP (released from damaged bile ducts), , Bile acid sequestrant - reduces bile
bilirubin = advanced disease acid absorption in gut - relieves itching
due to bile acids in circulation
Liver biopsy (percutaneous
/laparoscopic)
• Modafinil
• Interlobular bile duct destruction, bile duct
= For fatigue
inflammation (intraepithelial lymphocytes).
periductal epithelioid granulomas
OTHER INTERVENTIONS
• Cease all alcohol intake

of primary biliary cirrhosis. The bile duct
is surrounded by epithelioid macrophages
which in turn are surrounded by a rim of
lymphocytes, indicative of granulomatous
inflammation.
WILSON'S DISEASE
osmsJl/ wilsons-diseo.se
• Reduced copper elimination in the bile

( PATHOLOGY & CAUSES ) • Copper accumulation in hepatocytes - free
radical generation - hepatocyte damage
• Autosomal recessive mutation in ATP78
- spilling of free copper into the blood
gene - defect in ATP7B transport protein - copper accumulation in organs and
action in the hepatocyte tissues - free radical generation - tissues
• AKA hepatolenticular degeneration damage
• Reduced copper incorporation into
apoceruloplasmin and reduction of its
copper-bound form (ceruloplasmin)
121
COMPLICATIONS
• Liver: cirrhosis, liver failure
(..____ D_IA_G_N_O_s,_s
__ )
• Brain: movement disorders, dementia, and
LAB RESULTS
psychiatric issues
• Signs of liver dysfunction (e.g. high liver
• Kidney: renal disease
enzymes)
• Eye: Kayser-Fleischer's ring, sunflower
• Low serum ceruloplasmin
cataract
• High 24-hour copper excretion
• Blood: hemolytic anemia
(__ s,_G_NS_&_SY_M_PT_O_M_s_) (..__ __ TR_E_~_~M_E_N_T

__ )
MEDICATIONS
• Presents at a young age (< 30 years old)
• Chelating agents ----> make it easier to
• Signs and symptoms of cirrhosis and portal excrete copper
hypertension (e.g. hepatosplenomegaly,
n Penicillamine (penicillin metabolite
jaundice, ascites, esophageal varices)
without antibiotic properties)
• Signs of renal dysfunction
n Trientine hydrochloride
• Parkinsonian-like movement disorders
• Agents that block intestinal absorption of
o Tremors copper
o Rigidity n Ammonium tetrathiomolybdate
• Psychiatric illness n Zinc
o Depression
o Personality changes
SURGERY
o Psychosis
• Advanced liver damage----> transplantation
o Cognitive dysfunctions
• Kayser-Fleischer ring
o Ring of copper deposition in the cornea
OTHER INTERVENTIONS
(Descernet's membrane) • Eliminate copper-rich food (e.g.
mushrooms, nuts, shellfish)
o Appears to encircle the iris
Figure 36.15 Copper deposition in

Descemet's membrane of the sclera results in
a Kayser-Fleischer ring.
122
NOTES
GENERALLY, WHAT ARE THEY?

• Lower gastrointestinal tract structural/ DIAGNOSTIC IMAGING
functional anomalies during embryonic • Prenatal ultrasound, MRI, CT scan/
development; present at birth radiography
• Malformations from duodenum to anus • Avoid X-ray due to teratogenicity
CAUSES
• Genetic, environmental factors
( T_R_EA_~_M_EN_T__ )
SURGERY
• At birth: may be asymptomatic
• Malformations: relatively benign (nausea,
vomiting, difficulty passing stool) to life
incompatibility
GASTROSCHISIS
osmsJl/ge1s-lY-osehisis
CAUSES
( PATHOLOGY & CAUSES ) • Genetic, environmental factors
• Extrasomatic protrusion of intestines

through hole in abdominal wall near RISI( FACTORS
umbilicus • Mother's young age
• Hernia: affected organs exit cavity • Exposure to teratogenic substances
• Week 4 of gestation: lateral folds fail to (alcohol, tobacco)
fuse-« hole in abdominal wall ----. organs
protrude COMPLICATIONS
• Most common on right side • Intestinal inflammation due to intrauterine
• Usually small intestine exposure to amniotic fluid, malabsorption,
• Stomach, liver may also protrude (rare) infarction of intestinal tube due to
compressed blood vessels, infection
123
(__ SI_G_NS_&_S_Y_M_PT_O_M_s )
• During fetal life: asymptomatic
• At birth: difficulty feeding/passing stool
C D_IA_GN_O_SI_S
__ )
DIAGNOSTIC IMAGING
Intrauterine ultrasound
, MRI
X-ray, CT scan
• Post-op evaluation
LAB RESULTS
• Increased maternal serum alpha-
fetoprotein (MSAFP) Figure 37.1 An abdominal X-ray of a newborn
with gastroschisis. The abdominal contents
OTHER DIAGNOSTICS are clearly visible outside the abdominal wall.
• Defect visible at birth
( T_R_E~_;i-_M_EN_T
)
• Fatal if untreated
MEDICATIONS
• Antibiotics for existing/potential infection
• IV fluid/nutrients
SURGERY
• Surgical repositioning of organs back into
abdominal cavity, closure of abdominal wall
defect
• Usually requires multiple surgeries
124
HIRSCHSPRUNG'S DISEASE
osms.i"l/hiTsehspTungs-disee1se
( PATHOLOGY & CAUSES ) ( D_IA_GN_o_s,_s

__ )
• Myenteric (Auerbach). submucosal DIAGNOSTIC IMAGING
(Meissner) plexuses absent from intestinal • Barium assisted radiography
wall in distal bowel
• AKA congenital aganglionic megacolon
LAB RESULTS
• Absent plexuses (regulate bowel function)
• Rectal suction biopsy
- intestine muscles permanently
constricted - passing stool difficult,
impossible OTHER DIAGNOSTICS
• Digital rectal exam
CAUSES
• Failure of neuroblasts to migrate from
neural crest to intestine, form plexuses
( T_R_E~_~_M_EN_T
_ _____.)
• Genetic: RET proto-oncogene, EDNRB, etc.
SURGERY
• RET proto-oncogene: sporadidautosomal
• Surgical resection of intestine, subsequent
dominant (familial) cases; associated with
fusion of remaining healthy tissue (pull-
Down syndrome
through technique)
• Isolated: sporadidautosomal dominant
• Present within syndrome: Down syndrome,
multiple endocrine neoplasia II, etc.
COMPLICATIONS
• Constipation/obstipation, malnutrition,
enterocolitis, intestinal perforation,
megacolon
• At birth: asymptomatic
• Can be diagnosed in adulthood
• First sign: baby's inability to pass Figure 37.2 lmmunohistochemical
meconium, 48 hours postpartum staining for acetylcholinesterase in the
• 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.
125
IMPERFORATE ANUS
osms.i"l/impeTfoTate-anus

• Narrowed anal opening (anal stenosis)/ DIAGNOSTIC IMAGING
complete atresia
MRI, ultrasound
, X-ray/CT scan
• AKA anal atresia
• Determine internal extent of defect, plan
• Anus completely closed - colon ends in
corrective surgery
blind pouch in pelvis/opens into other pelvic
structures (bladder, vagina) via fistulae
• All pelvic structures open into same OTHER DIAGNOSTICS
channel - persistent cloaca • Physical exam at birth, defect visible
• Nerve, muscle tissue of missing parts of
anus, rectum missing/malformed
C T_R_E~_~_M_EN_T
__ )
CAUSES SURGERY
• Mostly unknown genetic cause • Anoplasty if possible, colostomy if not
• HLXB9 gene: only when imperforate anus
is present within Currarino syndrome
COMPLICATIONS
• Megacolon, intestinal rupture, septic shock,
incontinence/constipation (even after
surgery)
\ MNEMONIC: VACTERL
Group of malformations with
common, unknown cause
Vertebral anomalies
Anal atresia
Cardiovascular anomalies
Tracheoesophageal fistula
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.
(__ s,_G_NS_&_S_Y_M_PT_O_M_s
)
• Constipation (if anus narrowed), obstipation
(if anus non-existent)
• Vomiting, abdominal distension
126
INTESTINAL ATRESIA
osms.i-l/in-les-lino.l-o.-ll9esio.
CAUSES
( PATHOLOGY & CAUSES ) • Duodenal intestinal atresia
O Strongly associated with trisomy 21
• Congenital malformation resulting in closed/
(Down syndrome)
absent part of small/large intestine
• Non-duodenal intestinal atresias
• Different from intestinal stenosis; in
stenosis the passageway exists, and is just
O Intrauterine ischemic injury (small part
narrowed of duodenum, entire jejunum, ileum,
colon receive vascularization from
superior mesenteric artery)
TYPES
• Named according to affected portion of
intestine: duodenal, jejunal, ileal, colonic
COMPLICATIONS
• Distension of stomach and duodenum
• Divided into duodenal/non-duodenal
caused by accumulated amniotic fluid
intestinal atresia due to different
which has nowhere to go
mechanism of origin
• Polyhydramnios (accumulation of amniotic
• Duodenal intestinal atresia is caused by
fluid in amniotic sac)
failure in duodenal vacuolization
° Fetus swallows less fluid due to
O During fetal development duodenal
intestinal obstruction ---'> more fluid
epithelium proliferates rapidly---'>
accumulates in amniotic sac
complete duodenal obstruction
(AKA solid phase of vacuolizationl-« • Intestinal perforation and
apoptosis of excess cells ---'> formation pneumoperitoneum/meconium peritonitis
of small vacuoles which fuse-« re-
establish duodenal passageway (AKA
recanalization phase) (__ s,_G_NS_&_SY_M_PT_O_M_
• Bilious vomiting, abdominal pain,
malnutrition
Error in vacuolization Decreased perfusion -• ischemic necrosis
Genetic Unknown
127
( D_IA_GN_O_SI_S )
DIAGNOSTIC IMAGING
Prenatal ultrasound
• To assess signs of obstruction; detectable
in the third trimester
O Duodenal atresia: dilated fluid-filled
stomach adjacent to dilated duodenum
O Non-duodenal intestinal atresia: Dilated
fluid-filled bowel loops
o Polyhydramnios
Postnatal X-ray
• Duodenal atresia: Double bubble sign
(dilated stomach adjacent to dilated
duodenum) Figure 37.5 A plain abdominal radiograph of
• Non-duodenal intestinal atresia: dilated a neonate demonstrating the double bubble
bowel loops with air-fluid levels proximal to sign of duodenal atresia.
the obstruction
OTHER DIAGNOSTICS
• Physical examination
= Apple peel (spiral) shape of intestines
upon visual examination during surgery
• Amniocentesis to determine possible
trisomy 21
( T_R_E~_~_M_EN_T
__ )
SURGERY
• Gastric decompression: removal of fluid
from stomach
• IV fluid compensation
• Surgical reattachment of functional portions
of intestines
O
In case of duodenal intestinal atresia -
duodenoduodenostomy
Figure 37.4 A plain abdominal radiograph of

a neonate demonstrating the triple bubble
sign of jejuna I atresia.
128
INTESTINAL MALROTATION
osms.i-l/in-les-lino.1-mo.h·o-lo.-lion
( PATHOLOGY & CAUSES ) ( D_IA_GN_O_s,_s __ )

• Improper rotation of midgut during DIAGNOSTIC IMAGING
em bryogenesis
MRI/CT scan/barium-assisted radiography
• Rapid midgut growth in restricted space---->
herniation into umbilical coelum ----> rotation • Detect improper organ position
270° around SMA----> error occurs= final
anatomy description
O Small intestine lodges into left (...____ T_R_EA_~_M_EN_T__ )
abdominal cavity----> cecum in lower
right quadrant, first two thirds of colon SURGERY
lodge into right side over small intestine • Surgical repositioning of intestines,
• Due to error, several organs in incorrect resection of Ladd's bands to remove
anatomical position duodenal obstruction
O Small intestine in right side • Preventive appendectomy
° Coecum in epigastrium
O Appendix follows coecum
O Ladd's bands span over vertical
duodenum, compressing from outside
O Suspensory muscle of duodenum
further right
O Mesentery of small intestine narrower
root
COMPLICATIONS
• Omphalocele, volvulus (part of intestine
rotates around itself/part of mesenterium
----> blocks passage of intestinal content-«
compresses blood vessels=- obstructs
blood flow), ileus, ischemic bowel,
malnutrition, hernias
Figure 37.6 An abdominal X-ray with bowel
contrast demonstrating intestinal malrotation.
• Colic, bilous regurgitation, abdominal The entire small bowel is situated on the right
distension side of the abdomen.
129
MECl(EL'S DIVERTICULUM
osms.i"l/meekels-dive,--lieulum
( PATHOLOGY & CAUSES ) ( D_IA_GN_O_s,_s )

• Abnormal pouch on antimesenteric side of DIAGNOSTIC IMAGING
ileum
Abdominal ultrasound
/CT scan
• True diverticulum (contains all three layers
of intestinal wall) • Incidental finding
• Early fetal lite: nutrients received from yolk Angiograph

y
sac into ileum via omphalomesenteric duct
until it obliterates (week 5-6 of pregnancy)
• If omphalomesenteric duct obliterates OTHER DIAGNOSTICS
improperly: Meckel's diverticulum Meckel's scan
• May contain ectopic epithelia, • In children; technetium-99m procedure,
omphalomesenteric duct lined with detects gastric mucosa in diverticulum
pluripotent cells
Surgery
COMPLICATIONS • Incidental finding
• Diverticulitis, ulcers from HCI secretion
if gastric mucosa present, perforation of
diverticulum, food impaction, lithiasis, ( T_R_E~_~_M_EN_T__ )
peritonitis, peritoneal adhesions,
intussusception, volvulus, neoplasms SURGERY
• Uncomplicated: resection of diverticulum
• 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
(pancreatic, gastric)
• Usually asymptomatic
• Abdominal pain/distension, melena,
vomiting, constipation
Figure 37.7 lntraoperative photograph of a
Meckel's diverticulum.
130
demonstrating a Meckel's diverticulum.
Figure 37.9 Histological appearance of a Meckel's diverticulum containing ectopic gastric

mucosa.
131
OMPHALOCELE
osmsJl/ ompho.loeele
( PATHOLOGY & CAUSES ) ( D_IA_GN_O_s,_s )

• Persistent, pathological, herniation of DIAGNOSTIC IMAGING
intestines into umbilical cord
Intrauterine ultrasound
• Midgut herniates through urnblllcus=- pulls
layer of peritoneum into umbilical cord in MRI
order to properly develop (grow, rotate) due
to insufficient space in abdominal cavity---->
returns into abdomen LAB RESULTS
• Midgut doesn't return: omphalocele • Blood test for MSAFP
• High mortality rate • Amniocentesis
CAUSES
C T_R_E~_~_M_EN_T )
• Associated with: trisomy 13 (Patau SURGERY
syndrome), trisomy 18 (Edward's • Surgical repositioning of protruding organs
syndrome), trisomy 21 (Down syndrome),
Beckwith-Wiedemann syndrome
RISI( FACTORS
• Consumption of alcohol/tobacco during
pregnancy, certain medications (SSRls),
obesity
COMPLICATIONS
• Abdominal cavity malformation, volvulus,
ischemic bowel
• Intrauterine: asymptomatic
• 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.
132
GASTROSCHISIS
VS OMPHAlOCElE
GASTROSC.HISIS OMPHA\.OC.E\.E
Herniated organs
Herniated organs
covered by
exposed to air
peritoneum
Organs protrude
through lateral
Organs protrude
opening in
through umbilicus
abdominal
wall
Small defect in Large defect in

abdominal wall abdominal wall
133
NOTES
• NOTES
~ MALABSORPTION CONDITIONS

( PATHOLOGY & CAUSES ) c DIAGNOSIS )
• Impaired ability of gastrointestinal tract to DIAGNOSTIC IMAGING
absorb nutrients • Abdominal ultrasound, colonoscopy,
• Malabsorption may be intestinal biopsy, serological markers
O Global ----. impaired function of intestinal
cells LAB RESULTS
O Partial ----. external agent interferes with • 0-xylose test
absorption O Test for carbohydrate malabsorption
• Manifestation of underlying illness; may be
• Fecal fattesting
congenital/acquired/infectious
• Complete blood count (CBC)
O Look for for infection, anemia
CAUSES
• Defects in absorption process of intestinal
cells (e.g. change to bowel surface area)
OTHER DIAGNOSTICS
• Individual history
• Impaired nutrient digestion (e.g. altered
digestive enzymes) O Pancreatitis
O Recent surgeries
O Symptoms of vitamin deficiency
) Family history °
• Abdominal distention, pain

• Chronic diarrhea,
dehydration
malabsorption,
c TREATMENT )
• Weight loss • See individual disorders
• Clinical manifestations of nutritional
deficiencies (e.g. paresthesias from
cobalamin deficiency)
134
CELIAC DISEASE
osmsJl/eelio.e-diseo.se
( PATHOLOGY & CAUSES ) (__ s,_G_NS_&_SY_M_PT_O_M_

• Autoimmune disorder of small intestine • Abdominal distention, chronic diarrhea
• AKA gluten-sensitive enteropathy/ (steatorrhea)
nontropical sprue • Failure to thrive (children)
• Dermatitis herpetiformis
CAUSES n Circulating lgA antibodies attack dermal
• Triggered by foods containing gliadin, a papillae - generalized rash
peptide found in foods containing gluten
(e.g. grains: wheat, barley, rye, oats)
O Gluten consumption - degradation into
(..____ D_IA_GN_o_s,_s
__ )
peptides in small intestine - secretory
lgA binds to gliadin in duodenum -
LAB RESULTS
lgA-gliadin complex binds to transferrin • Anti-gliadin lgA/lgG
receptor - lgA-gliadin complex travels • Anti-endomysium lgA
across enterocyte into lamina propria • Anti-tissue transglutaminase lgA
- tissue transglutaminase deaminates , Tissue transglutaminase: endomysial
gliadin - macrophages uptake, present enzyme released in response to cellular
deaminated gliadin in MHC-2 molecules stress
HLA-DQ 2, 8 - CD4+ activation , More sensitive, specific
- inflammatory cytokines released
(interferon gamma, tumor necrosis Duodenal biopsy
factor) - damage/destruction of • Showing lymphocytic infiltration, villous
intestinal villi - B cell activation - anti- atrophy, crypt hyperplasia
gliadin, anti-tissue transglutaminase,
antiendomysial antibodies released
- CDS+ cell activation - tissue C..____ T_R_EA_~_M_EN_T
__ )
destruction
• On microscopy OTHER INTERVENTIONS
O Villous atrophy, mucosa I inflammation, • Correct nutritional deficiencies related to
intestinal crypt hyperplasia malabsorption
• Presence of anti-gliadin, anti-endomysium
lgA = pathognomonic Preventative
• Gluten-free diet
RISI( FACTORS
• Northern European ancestry, genetic I MNEMONIC: Grains are
component BROWn
i Grains to avoid with Celiac

disease
Barley
Rye
Oats
Wheat
135
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
inflammatory cells and an increase in crypt
length. A higher magnification would reveal
an increase in lymphocyte count in the
surface epithelium.
LACTOSE INTOLERANCE
osms.i"l/lo.etose-intoleY-o.nee
( PATHOLOGY & CAUSES ) (__ SI_G_NS_&_SY_M_PT_O_M_s

)
• Decreased ability to digest lactose • Occur after consuming lactose (e.g. milk,
• Lactose consurnption-» lactase deficiency/ cheese)
inactivity----> I undigested lactose ----> • Abdominal pain, cramping in lower
fermentation by colonic flora ----> gas. quadrants
osmotically active substances produced ----> • Abdominal distention. flatulence, vomiting,
bloating. diarrhea diarrhea (more common in children)
CAUSES
• Most often acquired due to physiologic
( D_IA_GN_O_s,_s)
weaning off of milk
• Based on above symptoms
RISK FACTORS
LAB RESULTS
• Non-European ancestry (most common)
• Unabsorbed carbohydrates ----> high stool
• Increases with age
osmotic gap
• May be congenital
• Bacterial lactose fermentation ----> acidic
O Rare, autosomal recessive disorder stool pH
• May be developmental
O Most common among premature infants
• Underlying intestinal disease
136
Preventative
(..____ T_R_EA_:T_M_EN_T
) • Lactose-free diet
, Compensate with lactase
OTHER INTERVENTIONS
• Optimize calcium, vitamin D intake
SMALL BOWEL BACTERIAL

OVERGROWTH SYNDROME
osmsJl/s\, \Jos
• Altered mental status after high

( PATHOLOGY & CAUSES ) carbohydrate meal
• Failure to thrive (children)
• Excessive colonic bacteria colonizing small
intestine
• Often occurs secondary to conditions (..__ __ D_IA_GN_O_SI_S )
limiting intestinal motility, gastric acid and
bile secretion and lgA deficiencies LAB RESULTS
• Signs/symptoms of vitamin, electrolyte
CAUSES abnormalities
• Alteration of factors regulating intestinal , Weakness, ataxia, paresthesias ----. 812
flora ----. aerobic bacteria proliferation ----. deficiency
changes in aerobic microclimate of small , Perioral numbness, feet paresthesias,
intestine e- migration of colonic anaerobic muscle crampinq-» calcium deficiency
bacteria ----. damage to intestinal surface e- • Anemia
maldigestion, malabsorption ----. symptoms
= Macrocytic----. 812 deficiency
, j bacteria ----. j carbohydrate metabolism
, Microcvtic=-. chronic bleeding
----. I gas production ----. bloating
• Fecal fat testing
, i bacteria ----. bile acid inactivation ----.r • Lactulose/glucose breath testing
fat in colon ----. osmotic effect ----. diarrhea
• Jejunal aspirate, culture
, j bacteria ----. intrinsic factor degradation
----. impaired 812 absorption=-. 812 , > 103 colony forming units
deficiency
OTHER DIAGNOSTICS
RISI( FACTORS • Individual history
• Increases with age , Chronic pancreatitis, intestinal surgery,
GI neuropathy
C__s,_G_Ns_&_sv_M_PT_O_M_s_)
( T_R_EA_:T_M_EN_T )
• Abdominal pain/distention, chronic diarrhea,
flatulence MEDICATIONS
• Tympanitic abdomen upon percussion • Antibiotics
137
TROPICAL SPRUE
osms.i"l/-lTopieo.1-spTue
( PATHOLOGY & CAUSES ) ( D_IA_GN_O_s,_s

__ )
• Gastrointestinal disease of uncertain DIAGNOSTIC IMAGING
etiology resulting in nutrient malabsorption
Endoscopy
CAUSES Barium swallow

• Acute intestinal infection (viral/bacterial/ • Shows intestinal wall thickening
protozoan) ---'> damaged intestinal lining ---'>
inflammation ---'> enteroglucagon secretion LAB RESULTS
---'> decreased intestinal motility---'> increased
• Fecal fat test
intestinal transit time v- overgrowth
• 0-xylose test
of Klebsielfa, E. coli, Eoterobacter e-
production of toxic fermentation byproducts • Jejunal biopsy
---'> further inflammation ---'> villous atrophy O Shows villous atrophy, inflammation
---'> malabsorption ---'> depletion of folate,
812---'> intestinal villi can't function normally
---'> further intestinal injury, megaloblastic ( T_R_E_AT_M_E_NT
__ )
anemia
MEDICATIONS
• Antibiotics ---'> reduce bacterial overgrowth
RISk FACTORS
• Replace folate, 812
• Most common in individuals living in
tropical regions
(__ s,_G_NS_&_SY_M_P_TO_M_s_)
• Diarrhea, weight loss, dehydration,
abdominal pain, fatigue, megaloblastic
anemia
138
WHIPPLE'S DISEASE
osms.i"l/whipples-diseo.se

• Rare, malabsorptive infectious disease • Four cardinal signs
caused by Tropheryma whipplei , Diarrhea, weight loss, abdominal pain,
• Pathognomonic finding ----> lamina propria a rthralgias
displays numerous macrophages with • Endocarditis, pericarditis, myocarditis
periodic acid-Schiff (PAS) positive • Skin hyperpigmentation
intracellular material
• Pleural disease
CAUSES
• Tropheryma whipplei ( D_IA_GN_O_s,_s __ )
O Gram-positive, non-acid fast, PAS
positive bacillus; ubiquitous in LAB RESULTS
environment • Biopsy
° Fecal-oral transmission , Shows copious PAS positive
• Readily spreads throughout body, causing macrophages invading lamina propria in
multisystem effects intestine
O Evades immune response----> allows for • ;;;: two positive PCR/PAS tests
accumulation of bacilli in tissues • lmmunohistochemistry for T. whipplei
• Current hypothesis suggests host • Laboratory findings suggesting chronic
immunodeficiency as predisposing factor inflammation, nutritional deficits
RISk FACTORS ( T_R_EA_~_M_EN_T__ )

• Middle-aged biological males of European
ancestry; exposure to fecal matter (sewage MEDICATIONS
workers, farmers)
• Start with IV antibiotics ----> ceftriaxone/
penicillin G
\ MNEMONIC: WHIPPLES • 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
139
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.

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.
140
NOTES
( PATHOLOGY & CAUSES ) ( D_IA_GN_O_SI_S )
• Infectious, inflammatory diseases; affect DIAGNOSTIC IMAGING
oral cavity, associated structures
X-ray
• See individual diseases
RISI( FACTORS
• Poor oral hygiene, dehydration, CT scan
concomitant illness, malnutrition • Soft tissue inflammation extension
(..___s,_G_Ns_&_sY_M_PT_O_M_s ) C T_R_EA_~_M_EN_T__ )
• Inflammation MEDICATIONS
O Redness, swelling, pain, loss of function, • Nonsteroidal anti-inflammatory drugs
warmth (NSAIDs) for pain
• Infection , For inflammation
° Fever, malaise, localized pain • Antibiotics, antifungal medications
, For infection
APHTHOUS ULCERS
osmsJl/ o.ph-lhous-ulee,-s
Herpetiform
( PATHOLOGY & CAUSES ) • Coalesce, recur frequently
• Painful lesions inside mouth; benign, non-

infectious; AKA canker sores CAUSES
• Idiopathic; likely multifactorial; may be part
of TH 1 autoimmune response, hormonal
TYPES
factors influence epithelium thickness,
Minor connected to vitamin 812 deficiencies
• Small (3-4mm), last 7-10 days, recur 3-4
times/year; if recurrent, > 4 times/year RISI( FACTORS
• Stress, systemic autoimmune disorders (e.g.
Major
celiac), nutritional deficiencies, stopping
• Lesions > lcm, last 10-30 days smoking, oral cavity trauma (e.g. biting lips,
dentures)
141
COMPLICATIONS
• Recurrent aphthous stomatitis (Mikulicz
( D_IA_GN_O_s,_s
__ )
ulcers), infection; may interfere with eating/
drinking
OTHER DIAGNOSTICS
• Recurrence of ulcers
( T_R_E~_~_M_EN_T
__ )
• Round/oval ulcerations in oral mucosa,
white/yellow sharply demarcated center MEDICATIONS
covered with fibrous membrane cap, • Vitamin 812 supplementation
surrounded by red erythematous margins; • Topical analgesics, corticosteroids,
yellowish exudate sucralfate suspension
• Inside of cheeks, lips; under tongue; painful • Anti-tumor necrosis factor (TNF)-alpha
swallowing, if in back of throat agents
O Recalcitrant, recurrent ulcers
Minor
• Small, mildly painful, annoying, round/
oval, disappear within seven days, resolve OTHER INTERVENTIONS
spontaneously, no scarring; more common • Avoid triggers
on non-keratinized epithelium
Major
• Larger, painful, recur more often, may scar
Herpetiform
• Not herpes virus connected, vesicles
coalesce into patches
Figure 39.1 The clinical appearance of

aphthous ulcers.
142
DENTAL CARIES DISEASE
osms.i"l/ den-le1l-ee1,-ies

• Odontogenic infections; tooth decay caused DIAGNOSTIC IMAGING
by acids produced by bacteria.
Odontogram (jaw X-ray)
• Bacteria - plaque - ! pH -
• Examine depth of lesions
demineralization - caries
CT scan
CAUSES • If widespread, soft tissue infection
• Streptococcus mutans, Streptococcus
sabrinus, Lactobaciflus spp.
OTHER DIAGNOSTICS
O Metabolically produce acids
Clinical presentation
RISk FACTORS • Teeth discoloration, changes
• Prolonged bottle use (baby bottle tooth

decay), poor oral hygiene, sugar-rich foods,
diabetes mellitus (DM). salivary gland
( T_R_EA_:l"_M_EN_T
)
disorders (e.g. Sjogren's), medications that
decrease salivation
MEDICATIONS
• Topical/systemic antibiotics
COMPLICATIONS
• Hematogenous spread of bacteria to heart
SURGERY
valves, joints, implanted prosthetics • Extraction of infected material, replacement
with fillings
• Spread from enamel to tooth pulp, alveolar
bone
• Abscesses OTHER INTERVENTIONS
• Soft tissue infections in extraoral • Dietary counselling, hygiene improvement
perforation
• Deep head, neck infections
• Jaw osteomyelitis
• Tooth loss
)
• Yellow/black teeth staining, enamel
softening; appearance of pits, cracks
• If severe: tooth collapse
• If pulp affected: dull pain exacerbated by
cold, soft food
• If root caries: lower, where teeth close
together, food difficult to extract; more Figure 39.2 A dental cavity in the tooth of a
difficult to diagnose ten-year-old boy.
143
Figure 39.3 An orthopantomogram
demonstrating dental cavities of the left
mandibular second and third molar teeth.
GINGIVITIS
osmsJI:/ gingivi-1:is
COMPLICATIONS
( PATHOLOGY & CAUSES ) • Periodontitis, tooth loss. receding gums
• Type of periodontal disease; inflammation

of gums
)
• Pathogenic bacteria tunnel between
microcolonies on tooth to surface in order • Redness, swelling, bleeding after brushing/
to bring in steady supply of food - form flossing
hard mass (dental calculus) - bacterial
• May be asymptomatic in early infection
plaque formation - enter gingival sulcus -
gingivitis
• Immune response delivers blood to ( D_IA_GN_O_s,_s)
damaged tissue - provides nutrients for
bacteria - immune response activates DIAGNOSTIC IMAGING
osteoclasts - dissolves bone - tooth
loosening X-ray
• Non-infectious systemic factors - gingival • Evaluate bone level, sulcus becomes
overgrowth, inflammation deeperaspeModontal pocket expands
O Hormonal shifts (e.g. during pregnancy)
O Drug-induced (e.g. phenytoin, calcium OTHER DIAGNOSTICS
channel blockers)
O Malnutrition-induced (e.g. vitamin C Physical exam
deficiency) • Swollen/bleeding gums. probe gingival
O Non-plaque-induced (rare, associated sulcus to determine depth
with genetics, allergy, trauma)
RISI( FACTORS
• Poor dental hygiene, older age
144
(..____ T_R_EA_~_M_EN_T
)
MEDICATIONS
• Antibiotics for severe infections
SURGERY
• Removal of infected tissue if severe
Figure 39.4 An individual with a severe

case of gingivitis. The gums are swollen and
hemorrhagic. There is visible plaque covering
the free gingival margin of both maxillary
incisors.
LUDWIG'S ANGINA
osms.i"l/lucJ.wigs-o.ngino.

)
• Bilateral infection of submandibular space • Infection
(sublingual, submylohoid) , Fever, chills, malaise, pain
• Stiff neck, dysphagia, individual
CAUSES leans forward to expand airway, no
lymphadenopathy, bilateral, sudden
• Spread from infection of 2"d/3'd mandibular
aggressive spread, enlarged tongue,
molars. pericoronitis, parotitis, peritonsillar
drooling
abscess
• Critical symptoms
• Mandibular fracture, piercings
O Stridor. cyanosis
• Causative agents polymicrobial from mouth
flora. dominated by Streptococcus viridans; • No abscess formation
staphylococci, bacteroides also common
(..____ D_IA_GN_O_s,_s)
RISk FACTORS
• DM. hypertension, HIV infection, DIAGNOSTIC IMAGING
immunosuppression
CT scan
• Rule out abscess formation (occurs late in
COMPLICATIONS
disease)
• Airway obstruction, mediastinitis,
• Chest CT scan
necrotizing cellulitis, sepsis, asphyxia
O Mediastinitis
145
LAS RESULTS
• Blood culture
( T_R_E~_~_M_EN_T
)
MEDICATIONS
OTHER DIAGNOSTICS • Empiric broad-spectrum antibiotics with
• Ultrasound-guided needle aspiration beta-lactamase activity
SURGERY
• Surgical drainage, if abscess identified on
CT scan
OTHER INTERVENTIONS
Airway management
• Fiberoptic nasal intubation, emergent
tracheostomy may be necessary
ORAL CANDIDIASIS
osms.i"l/ o,-o.1-eo.ndidio.sis
COMPLIC ATIONS
( PATHOLOGY & CAUSES ) • Spread into pharynx, disseminated
candidiasis
• Opportunistic infection of oral mucosal
membranes by Candida spp. (e.g. Candida
albicans)
• AKA thrush
TYPES • Cottony feeling in mouth; lesions
• Pain/tenderness in oral cavity
Pseudomembrano
us
• Painful swallowing (odynophagia)
• Whitish plaques on oral mucosa (most
common); can be scraped off to reveal • Decreased sense of taste
erythematous surface • Angular cheilitis
Atrophic (denture stomatitis)

• Red lesions without plaques ( D_IA_GN_O_SI_S __ )
Hyperplastic (rare) LAS RESULTS
• Non-scrapable plaques • Microbiological analysis of scrapings; Gram
stain; KOH preparation; biopsy
RISI( FACTORS
• Young age, dentures, xerostomia,
antibiotics, OM, malnutrition
• lmmunosuppression due to corticosteroids,
chemotherapy, HIV/AIDS
146
C.._____ T_R_EA_:T_M_EN_T
)
MEDICATIONS
• Topical antifungal agents (e.g. nystatin
suspension, clotrimazole troches, systemic
fluconazole)
Figure 39.5 Oral candidiasis in a child who

had taken antibiotics.
PAROTITIS
osms.i"l/ po.To·tJlis
sympathom imetics)
• Parotid gland inflammation COMPLICATIONS
• Salivary stasis - seeding of parotid • Spread to deep head, neck structures;
(Stensen) duct by microorganisms - septic jugular thrombophlebitis; septic
infection. inflammation osteomyelitis; sepsis; respiratory
obstruction; facial nerve palsy
CAUSES
• Bacterial: S. aureus, most common ( SIGNS & SYMPTOMS )
• Viral: mumps, influenza. coxsackie, Epstein-
Barr virus (EBV) • Systemic manifestations
• Autoinflammatory: sarcoidosis as part of , Fever, chills
Mikulicz syndrome • Periauricular, mandibular pain, swelling;
trismus, dysphagia; purulent drainage
RISk FACTORS • Viral
O No discharge, prodrome followed by
• Surgery, dehydration, salivary gland
stones. poor oral hygiene, medications that swelling lasting 5-10 days
decrease salivation (e.g. anticholinergic,
147
( D_IA_G_N_OS_IS )
DIAGNOSTIC IMAGING
• Sample purulent exudate, ultrasound
guided needle aspiration; culture, Gram
stain
Ultrasound
• Increased blood flow through gland,
enlargement, nodules
CT scan
• Extension of inflammation to surrounding
tissues
LAS RESULTS
• Complete blood count (CBC) Figure 39.6 The clinical appearance of
• Increased amylase without underlying parotitis of the left parotid gland. There is a
pancreatitis marked swelling just anterior to the left ear.
• Viral shows leukocytosis, increased lgM
against mumps
( T_R_E_AT_M_E_N_T _ __,,)
MEDICATIONS
• Hydration; IV antibiotics
• Vaccination
= Mumps prevention
PER IODONTITIS
osms.i"l/ peTiodon-ll-lls
----> tooth loosening
( PATHOLOGY & CAUSES ) • Severity based on ligament loss
• Porphyromonas gingivafis impairs immune
• Inflammation, destruction of supporting
cells, kills bacteria ----> pathogenic bacteria
structures around teeth, wasting of bone
overgrow
• Dysbiosis (disturbed bacterial symbiosis)
• Necrotizing ulcerative periodontitis (NUP)
more extreme than in gingivitis
= Extreme loss of periodontal attachment,
• Orange-complex of bacteria
alveolar bone; associated with
(Fusobacterium nucfeatum, Prevotefla
immunosuppression (e.g. HIV/AIDS;
intermedia), red-complex of bacteria
chemotherapy, severe malnutrition);
(Tannerefla forsythia, Treponema denticola,
may be associated with enteric bacteria,
Porphyromonas gingivalis) ----> immune
yeast
response----> more blood flow to damaged
tissue ----> provides nutrients for bacteria
----> more damage to gingiva, periodontal
ligament----> activated osteoclasts in bone
148
CAUSES OTHER DIAGNOSTICS
• Poor oral hygiene; red-, orange-complex • Clinical exam
bacteria , Probe teeth pockets, test for bleeding,
depth
RISI( FACTORS
• OM, smoking, Ehler-Danlos syndrome
( T_R_EA_:-t"_M_EN_T__ )
COMPLICATIONS MEDICATIONS
• Tooth loss, infection spread to soft tissues • Systemic antibiotics (if severe)
of head, neck, sinusitis; hematogenous
dissemination to heart valves (prosthetic/
native), joints, etc.
SURGERY
• Removal of infected tissue (if severe)
(__ s,_G_NS_&_SY_M_PT_O_M_s_) OTHER INTERVENTIONS

• Prevent plaque formation
• Redness, swelling, tender to palpation
, Daily brushing, flossing; antimicrobial
• Halitosis agents (e.g. mouthwash)
• Bleeding during teeth brushing • Scaling, root planing
• Teeth loosening Remove plaque
O
• Periodontal pockets widen • Topical fluoride
( D_IA_GN_o_s,_s __ )
DIAGNOSTIC IMAGING
Panoramic dental X-ray
• Bone loss around tooth
SIALADENITIS
osms.i"l/ sio.lo.cJ.eni-lis
inflammation, tissue swelling
• Inflammation of salivary glands CAUSES
O Parotid (most common), sublingual, • Bacterial: Staphylococcus aureus (most
submandibular; unilateral common), Streptococcus viridans,
Haemophilus influenzae
• Decreased flow of saliva - deposits settle
in walls of salivary duct - duct blocked • Viral: mumps, HIV
- flow of saliva slowed - deposits of
calcium, phosphorous, etc. precipitate - RISI( FACTORS
form small concretions (microsialoliths) • Decreased salivary flow (dehydration,
- grow into sialoliths - stones block illness, anticholinergic medications,
duct - bacteria moves from mouth up, Sjogren's syndrome)
around blockage, into salivary duct -
149
LAB RESULTS
• Lab culture of pus
= Gentle compression of gland
OTHER DIAGNOSTICS
• Clinical presentation
( T_R_E~_~_M_EN_T__ )
MEDICATIONS
• Antibiotics
SURGERY
• Surgical gland removal
= If disease recurrent
Figure 39.7 An individual holding their
own salivary duct stone following surgical
removal. Salivary duct stones predispose OTHER INTERVENTIONS
individuals to sialadenitis. • Hydration, warm compress. glandular
massage, sialogogues
• Acute sialadenitis
° Fever, chills, abscess formation
O Pain, swelling, redness of skin overlying
affected gland
O
Less saliva - dry mouth - bad taste
(pus leaking out of affected duct)
O Severe: painful to open mouth
• Chronic sialadenitis
O Less painful, gland enlarges following
meals, no overlying redness of the skin
O Associated with conditions linked
to chronic decreased salivary flow
(e.g. Sjogren's syndrome), due to
inflammation, salivary duct fibrosis,
altering glandular tissue, composition of
saliva Figure 39.8 A submandibular sialogram
demonstrating a salivary duct stone; a risk
factor for sialadenitis.
( D_IA_G_N_os_,s )
DIAGNOSTIC IMAGING
Ultrasound
• Abscess. salivary stone, tumor
150
of sialadenitis at low power. The acini are
surrounded by dense fibrosis and display
patchy lymphocytic infiltrates.
151
NOTES
• Inflammation of pancreas • Upper abdominal pain radiating to back;
nausea; vomiting
TYPES
• Acute, chronic ( D_IA_GN_o_s,_s __ )
CAUSES DIAGNOSTIC IMAGING
• Acute • Abdominal CT scan; ultrasound
O Gallstones, alcoholism, direct trauma,
infections (mumps) LAB RESULTS
• Chronic • Clinical, lab findings; see individual
O Recurrent acute pancreatitis, chronic disorders
alcoholism, cystic fibrosis
RISI( FACTORS ( T_R_E~_~_M_EN_T__ )

• Smoking OTHER INTERVENTIONS
• Dietary modifications, symptomatic
treatment
PANCREATIC PSEUDOCYST
osms.i"l/ pe1neTee1-l:ie-pseucJ.oe14st
hemorrhagic fat necrosts=- inflammatory
( PATHOLOGY & CAUSES ) reaction ----> encapsulation of fluid by fibrous
and granulation tissue
• Localized fluid collection of pancreatic
enzymes, necrotic debris and blood
encapsulated by non-epithelialized wall CAUSES
(hence the name pseudocyst) composed of • Arises as complication of acute/chronic
fibrous and granulation tissue pancreatitis/abdominal trauma
• Usually take up to 4-6 weeks to develop,
unlike acute fluid collections COMPLICATIONS
• Occurs due to disruption of pancreatic • Infection; hemorrhage
duct-» accumulation of pancreatic fluid ---->
• Compression of the gastrointestinal/urinary/
152
biliary tract
• Rupture - spilling of enzymes and debris
into abdominal cavity - diffuse peritonitis
(....___s,_G_NS_&_SY_M_P_TO_M_s_)
• Abdominal discomfort, indigestion,
anorexia, abdominal mass
( D_IA_GN_o_s,_s __ )
DIAGNOSTIC IMAGING
CT scan
• Large cyst cavity of low attenuation
surrounded by well-defined enhancing wall Figure 40.1 A CT scan in the axial plane
within, around pancreas demonstrating a pancreatic pseudocyst.
• Calcifications
• If present, complications may be visualized
Ultrasound (..____ T_R_EA_:l"_M_EN_T__ )

• Visualization of hypoechoidanechoic cystic
fluid collections • Initially
, Bowel rest, total parenteral nutrition
MRI (TPN), observation
• Not necessary, but useful for distinguishing
from organized necrosis
SURGERY
• If symptoms do not improve
LAB RESULTS , Surgical drainage to establish
connection which drains
Cyst fluid analysis
pseudocystic fluid into small intestine
• To distinguish from tumor
(cystojejunostomy), stomach
0 ! carcinoembryonic antigen (CEA) (cystogastrostomy), or duodenum
O j cmylase (cystoduodenostomy)
o ! cluid viscosity • Endoscopic drainage
153
PANCREATITIS (ACUTE)
osmsJl/e1eule-pe1neTee1·(Jlis
Alcohol
( PATHOLOGY & CAUSES ) • Increases zymogen secretion; decreases
fluid, bicarbonate production - pancreatic
• Sudden inflammation of pancreas due
juices become thick, viscous - pancreatic
to autodigestion - reversible pancreatic duct blocked
injury.
• Stimulates release of inflammatory
cytokines
TYPES • Oxidative metabolism produces free
radicals
Mild
• Inflammation, parenchymal edema, Gallstones
peripancreatic fat necrosis • Lodge at Oddi sphincter - pancreatic duct
blocked
Severe
• Parenchymal necrosis, hemorrhage Alcohol and gallstones
• Pancreatic duct blocked - pancreatic
CAUSES juices back up - pressure increases -
zymogen granules fuse with lysosomes
• See mnemonic for summary of causes
- trypsinogen transforms into activated
trypsin - digestive enzyme activation,
autodigestion
MNEMONIC: I GET
' SMASHED
i
RISI( FACTORS
Causes of Acute pancreatitis • Biologically male to biologically female, 1:3
Idiopathic • Smoking
Gallstones
Ethanol abuse COMPLICATIONS
Trauma • Most often
Steroids • Acute pseudocyst, intra-abdominal
Mumps infection infection. pancreatic abscess,
Alcohol abuse disseminated intravascular coagulation
Scorpion sting (DIC), internal pancreatic fistula
Hypertriglyceridemia, • Severe manifestations
hypercalcemia • Acute respiratory distress syndrome
Endoscopic retrograde (ARDS), acute renal failure, hemorrhage,
cholangiopancreatography hypotensive shock
Drugs: sulfa drugs, reverse-
transcriptase inhibitors,
protease inhibitors
154
) C..____ T_R_EA_~_M_EN_T
)
• Abdominal pain; loss of appetite; palpable, MEDICATIONS
tender mass • Pain management, hydration, electrolytes
• Cullen's sign • Hyperbaric oxygen therapy, antibiotics
O Periumbilical region bruising
• Grey Turner's sign SURGERY
O Bruising along flank • Necrosectomy
OTHER INTERVENTIONS
• Total restriction of food intake, alcohol
cessation
• Endoscopic retrograde
cholangiopancreatography (ERCP)
Figure 40.2 Cullen's sign. Individual

presented with a four-day history of
abdominal pain following an alcohol binge.
( D_IA_GN_O_s,_s
__ )
DIAGNOSTIC IMAGING
CT scan
• Visualization of inflammation, necrosis,
abscess, pancreatic pseudocysts
Ultrasound Figure 40.3 A CT scan in the axial plane

• Gallstones demonstrating acute pancreatitis. There
is diffuse enlargement of the pancreas
associated with peripancreatic fluid.
LAB RESULTS
• Elevated serum amylase, lipase, bilirubin
OTHER DIAGNOSTICS
Histology
• Microvascular edema; fat tissue necrosis;
acute inflammation; destruction of
parenchyma, blood vessels; interstitial
hemorrhage
155
PANCREATITIS (CHRONIC)
osms.i-1:/ehronie-po.neTeo.·tJl:is
MNEMONIC: TIGAR-0
( PATHOLOGY & CAUSES ) Causes of Chronic
pancreatitis
• Persistent, chronic inflammation of
Toxins: chronic alcoholism
pancreas due to autodigestion -
Idiopathic
irreversible injury of exocrine, endocrine
pancreas Genetic
• Fibrosis, calcification Autoimmune
O Prolonged inflammation produces Recurrent acute pancreatitis
fibrogenic cytokines, transforming Obstruction: gallstones,
growth factor beta (TGF-beta), platelet- pancreatic head tumor
derived growth factor (PDGF) -
activates myofibroblasts - collagen
O
production, fibrosis
Early stages: Langerhans
affected
islets not c SIGNS & SYMPTOMS )
• Severe abdominal pain radiates to back;
O Advanced: atrophy, fibrosis of islets
nausea; vomiting; steatorrhea; weight loss;
edema due to malabsorption
CAUSES
• See mnemonic for summary of causes
• Genetic
( D_IA_GN_o_s,_s __ )
O Hereditary chronic pancreatitis:
autosomal-dominant disease due to
DIAGNOSTIC IMAGING
mutations in cationic trypsinogen gene CT scan
° Cystic fibrosis: cystic fibrosis • Visualization of pancreatic ducts dilatation,
transmembrane conductance regulator calcifications. atrophy, pseudocysts
(CFTR) mutation - decreased
bicarbonate secretion - pancreatic duct Ultrasound
plugged, obstructed • Hyperechogenicity (fibrosis). pseudocysts,
• Autoimmune pseudoaneurysms, ascites
O Distinct form of chronic pancreatitis -
ERCP/magnetic resonance cholangiopan-
manifestation of immunoglobulin G (lgG)
creatography (MRCP)
related disease
• Visualization of pancreatic ducts; chain-of-
lakes pattern due to alternating stenosis,
COMPLICATIONS dilation
• Pancreatic pseudocyst; ascites; pancreatic
insufficiency; diabetes mellitus; vitamins A,
D, E. K deficiency; pancreatic cancer
LAB RESULTS
• Mildly elevated serum amylase, alkaline
phosphatase, bilirubin
156
OTHER DIAGNOSTICS
Histology
• Dilatation of pancreatic ducts; acinar cell
atrophy; fibrosis; chronic inflammatory
infiltrate; protein plugs, calcifications
( T_R_EA_:l'__
_M_EN_T
)
MEDICATIONS pancreatic fat necrosis in a case of severe
• Pain management pa ncreatitis.
• Pancreatic enzyme replacement
SURGERY
Endoscopy, surgery
• Resectional/drainage procedures for
pseudocyst, fistula, ascites
OTHER INTERVENTIONS
• Alcohol cessation, dietary modifications
(low-fat)
157
NOTES
• Conditions affecting peritoneal cavity (e.g. DIAGNOSTIC IMAGING
serosal membrane inflammation, gas)
X-ray
• Peritonitis
CAUSES O Supine, upright abdominal films
Peritonitis • Pneumoperitoneum
• Spontaneous bacterial peritonitis O Upright chest radiography
• Leakage of gastrointestinal (GI) contents O Subdiaphragmatic free gas; cupola sign
• Presence of foreign material O Rigler's sign, football sign
O Bile, blood, contrast material O Lateral decubitus X-ray
• Endometriosis
CT scan
• Peritoneal dialysis
• Pneumoperitoneum
Pneumoperitoneum O Small quantities of air
• Perforation of anterior duodenal ulcer
• Iatrogenic LAB RESULTS
• Increased intrathoracic pressure
Paracentesis
• Peritonitis
(__ s,_G_NS_&_SY_M_PT_O_M_s
) If ascites O present
Peritonitis Complete blood count (CBC)
• Fever. chills. tachycardia Blood chemistry

• Ascites, abdominal distention, abdominal
rigidity, spider angiomata, jaundice
• Anorexia. nausea, vomiting. diarrhea ( T_R_EA_~_M_EN_T__ )
• Encephalopathy; delirium. confusion,
cognitive decline MEDICATIONS
• Absent bowel sounds, ileus • Systemic antibiotics
Pneumoperitoneum
SURGERY
• Abdominal pain, rigidity
• Exploratory laparotomy
• Absent bowel sounds, ileus
158
PERITONITIS
osms.i"l/ peTi-loni"lis
( PATHOLOGY & CAUSES ) ( D_IA_GN_O_SI_S)

• Inflammation of serosal membrane DIAGNOSTIC IMAGING
lining abdominal cavity, organs (AKA
peritoneum). Supine, upright abdominal films
• Neutrophilic infiltration, formation of • Subhepatic/subdiaphragmatic free air,
fibrinopurulent exudate abscesses in case of perforated viscus
CAUSES LAB RESULTS

• Spontaneous bacterial peritonitis • Leukocytosis, acidosis
O Bacterial migration from GI lumen; more Paracentesis
common in people with ascites/cirrhosis
• If ascites present
O E. coli, Klebsiella, Pseudomonas,
• Serum ascites albumin gradient (SAAG)
Proteus, Gram-negatives
= > 1.1 in spontaneous bacterial
• Leakage of GI contents; most common;
peritonitis
perforated viscera
• Neutrophil count > 250 cells/microliter
O Proximal GI tract perforation-» Gram-
positive bacteria
O Distal GI tract perforation ---> Gram- ( T_R_EA_~_M_EN_T
__ )
negative bacteria
• Foreign material MEDICATIONS
O Bile, blood, contrast material
Systemic antibiotics
• Endometriosis
• Third generation cephalosporins/quinolones
• Peritoneal dialysis
C__s,_G_Ns_&_sv_M_PT_O_M_s_)
• Fever, chills, tachycardia
• Ascites, abdominal distention, abdominal
rigidity, spider angiomata. jaundice
• Anorexia. nausea, vomiting. diarrhea --->
hypovolemia, renal failure
• Early stages
O Dull. poorly localized abdominal pain
• Late stages
O Severe. localized abdominal pain; acute
abdomen Figure 41.1 The histological appearance
• Encephalopathy; delirium. confusion, of tuberculous peritonitis, a rare kind of
cognitive decline peritonitis. There are numerous epithelioid
macrophages and giant cells infiltrating the
peritoneal biopsy.
159
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
fluid. On laparotomy this was discovered to
be pus.
PNEUMOPERITONEUM
osmsJl/ pneumope,-l-loneum

• Abnormal collection of gas within DIAGNOSTIC IMAGING
peritoneal cavity.
CT scan
• Small quantities of air
CAUSES
• Most common Upright chest radiography
O Perforation of anterior duodenal ulcer • Subdiaphragmatic free gas; Cupola sign
secondary to peptic ulcer disease (free intraperitoneal air. well-defined
• Iatrogenic superior border formed by diaphragm)
O Abdominal surgery; resolves Supine abdominal X-ray
spontaneously
• Rigler's sign (double wall sign): both sides
• Increased intrathoracic pressure of abdominal wall visible
(mechanical ventilation, chest
• Football sign (massive pneumoperitoneum):
compressions)
ellipsoid shape of abdominal cavity outlined
by gas
( SIGNS & SYMPTOMS ) Lateral decubitus X-ray
• Free gas between liver. abdominal wall
• Abdominal pain, rigidity
160
(..____ T_R_EA_:T_M_EN_T
)
SURGERY
Exploratory laparotomy
• Repair perforated viscus

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
bubble, diagnostic of pneumoperitoneum.
161
NOTES
• NOTES
~ RECTAL & ANAL PATHOLOGY
• Diseases affecting rectum and anal region • History, physical examination
COMPLICATIONS ( T_R_E~_~_M_EN_T__ )
• Discomfort during defecation, itching, pain,
bleeding • Change dietary/defecation habits,
pharmacological, surgical
)
• Visible abnormalities
ANAL FISSURE
osmsJl/a.no.I-fissure
COMPLICATIONS
( PATHOLOGY & CAUSES ) • Fecal bacteria infection
• Anal mucosa linear fissure

• Hard bowel movement - anal mucosa (__ s,_G_NS_&_SY_M_PT_O_M_s )
stretches - acute fissure - internal anal
sphincter spasms - blood flow reduces - • Midline tear
difficult healing - chronic fissure
• Pain during bowel movements - fear of
• Midline, anteriorly/posteriorly defecation - constipation - harder stool
- more pain
RISI( FACTORS • Blood on toilet paper/stool
• Low fiber diet
• Diarrhea
• Previous anal surgery
( D_IA_GN_o_s,_s__ )
• Anal trauma • History, examination of anal region/rectum
• Abnormalities in internal anal sphincter
• Sexually transmitted infections (STls)
O Human papillomavirus (HPV), herpes,
chlamydia
• Inflammatory bowel disease (IBD)
162
(..__ __ T_R_EA_:T_M_EN_T )
MEDICATIONS
• Stool softeners
• Topical nitrates/calcium channel blocker (e.g
diltiazem)
SURGERY
• Sphincterotomy
OTHER INTERVENTIONS
• Proper anal hygiene Figure 42.1 The clinical appearance of an anal
• Warm bath (AKA sitz bath) fissure affecting the posterior anal mucosa.
• Muscle relaxation - increase healing
mechanisms
• Fiber supplementation
ANAL FISTULA
osmsJl/ a.no.I-fistula.
Extrasphincteric
( PATHOLOGY & CAUSES ) • Rectum/sigmoid colon - levator muscle ani
-v skin
• Abnormal communication between anal
canal, perianal skin
° Fistula: Latin (pipe, catheter), from findo ( SI_G_NS_&_S_Y_M_PT_O_M_
__ )
(cleave, divide, split)
• Foreign material in anal crypts - anal • Skin excoriations, pus/serous fluid/feces
glands ducts blocked - anal abscess - draining from skin-opening, bleeding,
pus travels to skin through tract itching, pain, redness, swelling
TYPES
(..____ D_IA_GN_O_SI_S
)
lntersphin
cteric
• Internal anal sphincter - space between OTHER DIAGNOSTICS
internal, external anal sphincters (AKA • Anal examination - delineate course of
intersphincteric plane) - skin fistula
Transsphincteric (U-shaped fistula)

• Internal anal sphincter - intersphincteric C T_R_EA_:T_M_EN_T
__ )
plane - external anal sphincter - skin
SURGERY
Suprasphincteric
• Drain infection - eradicate fistulous tract
• Internal anal sphincter - puborectalis - preserve anal sphincter function - avoid
muscle - space between puborectalis, recurrences
levator ani muscle - skin
163
Figure 42.2 Surgical wound following
removal of an anal fistula.
HEMORRHOID
osmsJl/hemoTThoid
COMPLICATIONS
Internal hemorrhoids
• Anal cushions hypertrophy due to • Bleeding with bowel movements
supportive tissue deterioration • Prolapsing
• Incarceration, strangulation - pain
TYPES • Mucus deposits on perianal tissue -
itching
Internal
• Affecting hemorrhoidal venous cushions External hemorrhoids
above dentate line • Bleeding
O Grade I: bleed but not prolapse • Acute thrombosis - acute pain
O Grade II: prolapse on straining but • Itching
reduce spontaneously • Hygiene difficulties
O Grade Ill: prolapse on straining, require
manual reduction
O Grade IV: spontaneous, irreducible ( SIGNS & SYMPTOMS )
prolapse
• Itching
External
• Bleeding associated with bowel movement
• Affecting hemorrhoidal venous cushions - bright red blood on toilet paper
below dentate line
• Pain
• Mucous discharge
RISI( FACTORS • Perianal mass in case of prolapse
• Constipation (low fiber diet). strenuous
defecation. diarrhea, prolonged sitting,
aging, increased intra-abdominal pressure,
pregnancy, intra-abdominal mass, ascites,
portal hypertension
164
(..__ __ D_IA_GN_O_SI_S ) (..____ T_R_EA_~_M_EN_T
)
DIAGNOSTIC IMAGING MEDICATIONS
• Anoscopy for internal hemorrhoids • Stool softeners
• Topical, systemic analgesics
OTHER DIAGNOSTICS
• Anal, perianal inspection SURGERY
• Digital rectal examination • Sclerotherapy, rubber band ligation, infrared
coagulation
OTHER INTERVENTIONS
• Increase fiber, fluid intake

of an excised hemorrhoid. There is
fibromuscular hyperplasia and numerous
dilated vascular spaces.
Figure 42.4 External appearance of grade 2

hemorrhoids.
RECTAL PROLAPSE
osms.i"l/Tee-lo.I-prolo.pse

• Partial/total slip of rectal tissue through anal • Mass protruding through anus
orifice , After defecation; when sneezing/
coughing; when walking ----> pain, rectal
bleeding, incontinence
RISI( FACTORS
• Constipation, diarrhea, pregnancy, pelvic
floor damage
COMPLICATIONS
• Mucous discharge, bleeding. fecal
incontinence, constipation, rectal ulceration
165
( D_IA_GN_O_SI_S ) ( T_R_E~_~_M_EN_T
)
OTHER DIAGNOSTICS SURGERY
• Physical examination • Sutures/mesh slings to anchor rectum to
O Prolapse clearly evident posterior wall of pelvis (sacrum)
, Open or laparoscopic
• Rectosigmoidectomy
= Part of rectum and sigmoidpulled
through anus and removed,
reanastomosis of remaining rectum to
colon
• Usually reserved for severe prolapse/
non-candidates for open/laparoscopic
procedure
OTHER INTERVENTIONS
• High fiber diet, enemas, suppositories (to
avoid constipation/straining)
Figure 42.5 A complete rectal prolapse. • Kegel exercises may help limit progression
166
NOTES

( PATHOLOGY & CAUSES ) ( D_IA_GN_o_s,_s
__ )
• Upper gastrointestinal tract structural/ DIAGNOSTIC IMAGING
functional anomalies during embryonic • Prenatal ultrasound; MRI
development; present at birth • X-ray/CT scan
O Avoid if possible due to teratogenicity
CAUSES
(..____ TR_E_AT_M_E_N_T
)
SURGERY
• May be asymptomatic/complete
dysfunction of gastrointestinal (GI), life OTHER INTERVENTIONS
incompatibility
• Nasogastric intubation
CLEFT LIP & PALATE

osmsJl:/elef-l:-lip-C1nd-pC1IC1-l:e
Combination (CLP, cheilopalatoschisis)
( PATHOLOGY & CAUSES ) • Most severe forms; split alveolar ridge,
uvula (cheilognathopalatoschisis)
• Group of congenital malformations in upper
lip, oral cavity roof
• Result of improper fusion of facial bones, RISI( FACTORS
associated tissues • Other inherited genetic disorders (e.g.
Patau syndrome, Stickler syndrome)
• Environmental teratogenic factors
TYPES
(e.g. intrauterine hypoxia, pesticides.
• Based on severity anticonvulsant medication, folate
deficiency)
Cleft lip (CL, cheiloschisis)
• Unilateral, bilateral "hare lip"
COMPLICATIONS
Cleft palate (CP, palatoschisis)
• Speech impediments, hearing issues/
• Commonly uvula also split recurrent otitis media, difficulty eating
167
OTHER INTERVENTIONS
(__ SI_G_NS_&_S_Y_M_PT_O_M_s ) • Temporary prosthetic implants, until
surgery
• Velopharyngeal insufficiency
• Speech-language therapy
O Inability to temporarily stop physical
• Folate supplementation during pregnancy
communication between oral, nasal
decreases risk
cavities
• Dysphonia
O Air leaks to nasal cavity - hypernasal
vocalization
• Dysarthria
OAbnormal structure increases speech
difficulty - distorted word structure
• Nasal cavity infection
° Food trapped in nasal cavity -
predisposes infection
( D_IA_GN_O_SI_S )
DIAGNOSTIC IMAGING Figure 43.1 A cleft hard palate in an infant.
Prenatal ultrasound
• Evaluation of integrity of nares, upper lip,
hard and soft palate
• 30 reconstruction and surface rendering
allow for better diagnosis and help parents
prepare psychologically
MRI
• Evaluation of associated extra/intracranial
abnormalities
• Prenatal MRI aids in confirmation and
characterization/integrity of maxillary arch
CT scan/X-ray
• Not typically used; 30 reconstructions can
aid in surgical planning
OTHER DIAGNOSTICS
• Clinically evident at birth
( T_R_E~_;-r_M_EN_T )
SURGERY Figure 43.2 A child with a unilateral,
• Surgical closure of cleft lip by three months incomplete cleft lip.
of age
• Timing for surgical closure of palate is
variable; usually done by one year of age
168
CONGENITAL DIAPHRAGMATIC
HERNIA ( CDH)
osms.i"l/ eongeni-le1l-die1phTe1gme1-lie-heTnie1
MNEMONIC: 5Ss
i
Bochdalek hernia features
Bochdalek hernia
• Protrusion of abdominal viscera into chest
Big
cavity
Back and medial, usually left
• Results from abnormal development of
side
diaphragm in utero
• High mortality rate Baby
Bad: associated with
• Incomplete diaphragm forrnatlon=-.
pulmonary hypoplasia
abdominal organs protrude into chest
cavity----> physical obstruction of heart,
lung formation/function ----> pulmonary
hypoplasia, surfactant deficiency,
pulmonary hypertension, arrhythmia
( DIAGNOSIS )
DIAGNOSTIC IMAGING
TYPES
Prenatal ultrasound
Bochdalek hernia • Polyhydramnios
• Posterolateral diaphragmatic hernia; most • Cardiomediastinal shift with possible
common CDH abnormal cardiac axis
O Viscera protrude through posterolateral • Lack of visualization of normal stomach
segment of diaphragm bubble
O Left kidney, perinephric fat, stomach, • Absent bowel loops in abdomen; stomach
small intestine and small bowel in thorax
• lntrathoracic herniation of liver (seen in
Morgagni hernia
85%, poor prognosis)
• Retrosternal, parasternal diaphragmatic
• Peristaltic bowel movements in thorax
hernia
• Reduced abdominal circumference
O Viscera protrude through foramina of
Morgagni (form sternocostal angle) X-ray
• indistinct diaphragm, opacification of
CAUSES hemithorax (typically left-sided)
MRI
• Helpful in further assessment of pulmonary
C__s1_G_Ns_&_sv_M_PT_O_M_s_) hypoplasia
• Measurement of fetal lung volumes
• Dyspnea, tachypnea, central cyanosis,
tachycardia, retractions, nasal flaring,
decreased/absent breath sounds on
affected side, scaphoid abdomen
169
C..____ T_R_EA_~_M_EN_T
)
SURGERY
• Surgical repair of hernia
OTHER INTERVENTIONS
• Planned delivery after week 37 of gestation
----. immediate intubation, mechanical
ventilation
• Inhaled nitric oxide for severe pulmonary
hypertension
• Nasogastric, pulmonary intubation
Figure 43.3 A plain X-ray of a newborn

demonstrating visible bowel loops in the
thoracic cavity.
ESOPHAGEALWEB
osms.i"l/ esopho.geo.1-we\,
( PATHOLOGY & CAUSES ) (__ SI_G_NS_&_S_Y_M_PT_O_M_s_)

• Rare narrowing of esophagus due to thin • May be asymptomatic (if small)
membrane of esophageal tissues (mucosa, • Dysphagia: difficulty in swallowing
submucosa) • Odynophagia: painful swallowing
• Most commonly appear in lower third of • Retrosternal pain: can be mistaken for
esophagus angina pectoris
• Can be congenital/acquired
• May occur as solitary disease
( D_IA_GN_o_s,_s __ )
RISI( FACTORS OTHER DIAGNOSTICS
• Plummer-Vinson syndrome
O Sideropenic dysphagia. iron-deficiency Fluoroscopy /barium swallow
anemia, glossitis. cheilosis. esophageal • Visualized when esophagus is fully
webs distended with contrast
• "Jet effect" of contrast being ejected distally
COMPLICATIONS from web
• Food impaction, perforation by solid food/
esophageal probe insertion
( T_R_EA_~_M_EN_T__ )
OTHER INTERVENTIONS
• Endoscopic dilation via inflated balloon
170
HYPERTROPHIC PYLORIC STENOSIS
osms.tl/h14peT-lTophie-p14loTie-s-lenosis
Fluoroscopy
( PATHOLOGY & CAUSES ) • Delayed gastric emptying
• Elongated pylorus with narrow lumen
• Constriction of pylorus due to pyloric
sphincter hypertrophy - gastric outflow • Entrance to pylorus may be beak shaped
obstructed
• Autosomal dominant/multifactorial
( T_R_EA_:l"_M_EN_T__ )
RISI( FACTORS SURGERY
• Firstborn, biologically male, parents had • Pyloromyotomy
hypertrophic pyloric stenosis, macrolide
exposure
OTHER INTERVENTIONS
• Rehydration
COMPLICATIONS • Regulate acid-base status, correct
• Dehydration, malnourishment, acid-base electrolyte abnormalities
imbalance
C__ s,_G_Ns_&_sv_M_PT_O_M_s_)
• Projectile nonbilious vomiting at/soon after
birth
• Visible peristalsis
• Dehydrated, undernourished
( 0_1A_GN_o_s1_s __ )
DIAGNOSTIC IMAGING
X-ray
• Distended stomach, minimal intestinal gas
Ultrasound
• Modality of choice; but cannot exclude
midgut volvulus
• Pyloric muscle thickness Figure 43.4 An abdominal radiograph
demonstrating a grossly dilated stomach,
OTHER DIAGNOSITCS secondary to obstructive pyloric stenosis.
• Abdominal olive palpable on physical
examination
171
THYROGLOSSAL DUCT CYST
osms.i"l/-lh14Toglosse1l-due-l-e14s-l
OTHER DIAGNOSTICS
( PATHOLOGY & CAUSES ) • Fluctuant mass palpable at a anterior
midline/paramedian location
• Benign cyst; epithelium of unclosed
• Draining sinus may be visible
thyroglossal duct
• Thyroid cells migrate from fora men cecum
downward - leave thyroglossal duct - ( T_R_EA_:l"_M_EN_T__ )
thyroid duct stays open - fills with mucus
- cyst forms SURGERY
• Surgical excision (Sistrunk procedure)
COMPLICATIONS
• Infection (spread from respiratory system),
inflammation, discharging sinus with skin
(secondary to inflammation/trauma), thyroid
gland malformation (if thyroid cells remain
in thyroglossal duct/cyst), extrathyroid
thyroid carcinoma (from leftover thyroid
cells)
• Painless mass in front of neck, moves when Figure 43.5 The clinical appearance of a
swallowing; inflammation, pain; dysphagia; thyroglossal duct cyst. There is a vague,
dyspnea fluctuant swelling in the mid line of the neck.
( D_IA_GN_O_SI_S
__ )
DIAGNOSTIC IMAGING
Ultrasound
• Fluctuant mass filled with anechoic fluid,
thin walled, without vascularity
CT scan
• Thin-walled, well-defined homogeneous,
fluid dense lesions, anterior midline/
paramedian location
• May demonstrate capsular enhancement
• Sternocleidomastoid muscle may be
displaced posteriorly/posterolaterally
Figure 43.6 A CT scan of the head and
• May be embedded in infrahyoid muscles neck in the sagittal plane demonstrating a
thyroglossal duct cyst adjacent to the hyoid
bone.
172
TRACHEOESOPHAGEALFISTULA
osmsJl/ -1:To.eheoesopho.geo.l-fis-lulo.
COMPLIC ATIONS
( PATHOLOGY & CAUSES ) • Atresia {due to hydrochloric acid
accumulation), gastroesophageal reflux,
• Pathologic communication between dysphagia, frequent respiratory infections
trachea.esophagus
• Results from tracheoesophageal ridge
fusion failure ( SI_G_NS_&_S_Y_M_PT_O_M_
)
• Occurs as congenital malformation/surgery
complication (later in life) • Hypersalivation/drooling, choking, vomiting,
• VACTERL association; see mnemonic central cyanosis upon feeding
\ MNEMONIC: VACTERL ( D_IA_GN_O_s,_s)

Group of malformations with
common, unknown cause DIAGNOSTIC IMAGING
Vertebral anomalies Chest X-ray
Anal atresia • Nasogastric tube coiled in proximal
Cardiovascular anomalies esophagus (usually sufficient for diagnosis)
Tracheoesophageal fistula
Fluoroscopy
/Barium swallow
Esophageal atresia
• If difficult to diagnose, may require contrast
Renal anomalies
swallow study to visualize contrast passing
Limb defects
into tracheobronchial tree
= Barium is contrast medium of choice
(ionic iodinated medium can cause
TYPES chemical pneumonitis)
Type A
CT scan
• Middle esophageal segment missing
• Useful for preoperative planning
Type B
• Proximal esophagus communicates with OTHER DIAGNOSTICS
trachea • Inability to pass gastric tube
Type C (most common) • Neonates drool, choke, vomit during first
feeding
• Distal esophagus communicates with
trachea, proximal esophagus atresia
Type D ( T_R_EA_~_M_EN_T
__ )
• Proximal, distal esophageal segments
communicate with trachea, middle segment SURGERY
atresia • Surgical closing of pathologic
communication, fusion of esophageal buds
Type E (AKA Type H)
• Complete esophagus, additional part
communicates with trachea
173
Figure 43.7 An acquired trachea-esophageal
fistula.
174

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Gastrointestinal Osmosis HY Pathology Notes ATF

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GASTROINTESTINAL

Malabsorption Conditions 134

Oral Disease 141

Normal Normal Normal

(__ s,_G_NS_&_SY_M_PT_O_M_s_) ( T_R_EA_:l"_M_EN_T__ )

• Bile duct wall thickening • Stent

Figure 28.1 The pathophysiology of ascending cholangitis.

( PATHOLOGY & CAUSES ) (__ SI_G_NS_&_SY_M_PT_O_M_s_)

• More common in individuals who are • Confirmation of obstruction

° Changes gallbladder mucosa - deep , Bluish discoloration of gallbladder;

• Fatty meal - small intestine 'Increased risk of gallbladder cancer

- cells damaged, die - ALP released

( T_R_EA_:l"_M_EN_T ) Figure 28.4 Histological appearance of

Elevated ALP. HIDA

Treatment only if Treatment only if

( PATHOLOGY & CAUSES )

Figure 28.6 Abdominal ultrasound

Figure 28.7 Numerous gallstones, of mixed-

• Associated with ulcerative colitis, Crohn's • Cirrhosis

GENERALLY,WHAT ARE THEY?

• No malignant potential by itself; requires • Risk increases with age

OTHER DIAGNOSTICS Figure 29.1 The gross pathological

Figure 29.2 Histological appearance of a

Autosomal recessive FAP

Figure 29.4 Endoscopic appearannce of

Figure 29.5 A retinal photograph

GARDNER'S SYNDROME (GS)

COMPLICATIONS Ophthalmic examination

Colonoscopy, flexible sigmoidoscopy

( PATHOLOGY & CAUSES ) ( D_IA_GN_O_SI_S

Figure 29.6 A juvenile retention polyp with

( PATHOLOGY & CAUSES ) ( D_IA_GN_o_s,_s __ )

• Associated with hyperpigmented (melanin- Capsule endoscopy

CAUSES • Hyperdense outpouchings of colonic wall

c SIGNS & SYMPTOMS ) O

Figure 30.2 Histological appearance of the squamocolumnar junction in a case of Barrett's

DIFFUSE ESOPHAGEAL SPASM

( PATHOLOGY & CAUSES ) (..____ D_IA_GN_O_SI_S _~)

• Short term trial of proton-pump inhibitors

Surface agents and alginates

Transoral incisionless fundoplication

LINX reflux management system

Figure 30.7 Endoscopic appearance of a

• Anemia; fecal, urinary incontinence; ulcers; • Surgical repair

• Median onset age: 5-6 years old

• Symptoms tend to develop at night, in the • Avoidance of triggers

( PATHOLOGY & CAUSES ) ( D_IA_GN_O_SI_S

( SIGNS & SYMPTOMS ) , Visick classification: heart rate

• GI: early satiety; abdominal colic; nausea,

• Inflammation of the lining of the stomach , H. pylori - chronic gastritis - gastric

Correct vitamin deficiencies

Figure 31.3 The histological appearance

Body, fundus Antrum

Hypochloridia Urease production by H. pylori

Mostly asymptomatic until severe

Symptoms of vitamin deficiencies Epigastric pain

Lymphocytic infiltrate Neutrophilic infiltrate

Autoimmune diseases low socioeconomic status

( PATHOLOGY & CAUSES ) (__ SI_G_NS_&_S_Y_M_PT_O_M_

Gastric emptying scintigraphy

( PATHOLOGY & CAUSES )

Barium abdominal radiography

GENERALLY,WHAT ARE THEY?

Figure 32.2 Gross pathology of carcinoid

( PATHOLOGY & CAUSES ) (.. D_IA_GN_O_s,_s __ )