Académique Documents
Professionnel Documents
Culture Documents
PDI
The
Abdomen
ADAPTED BY P. EDGAR MD
FROM TEXTBOOK OF PHYSICAL
DIAGNOSIS BY M.H.SWARTZ
BATES: PHYSICAL EXAMINATION
Caucasian (44/100,000)
Native American (lowest:
16/100,000)
congenital polyposis (1/7000-1000 live births) increased colon cancer risk
Abdomen:
Structure and
Physiology
four quadrants
two perpendicular
lines (sternumpubic bone
through umbilicus;
2nd right-angles to 1st at
umbilicus)
Abdomen:
Structure and
Physiology
Ant-sup
iliac
spines
midclaviclaringuinal
Lateral extent rectus
Abdomen:
Structure and Physiology
Posterior organs:
kidneys, duodenum,
pancreas
Adults unlikely that
abnormalities in these
organs felt
Children
abdominal muscles less
developed
renal masses (especially right)
Abdomen:
Structure and Physiology
Food passes mouth esophagus
obstructing lesion produce dysphagia (difficulty swallowing).
gastroesophageal refluxheartburn
Partially digested food stomach (food reservoir, secrete gastric juice,
muscular peristaltic activity)stomach relaxation
failure stomach relaxation lead early satiety/pain.
2-3L/d gastric juice affecting protein digestion (pain with gastric
ulcer)
Abdomen:
Structure and Physiology
chyme (stomachduodenum): stimulates pancreatic secretion,
gallbladder contraction
Abdomen:
Structure and Physiology
Liver: produces bile (1L/d), detoxifies digestion by-products,
metabolizes proteins, lipids, carbohydrates.
absence normal liver function: jaundice, ascites, coma
Jejunum and ileum (absorb bile acids/vit B12) further digest/absorb
nutrients
Stercobilin (bilirubin metabolite from bile): dark color of stool
Acholic: bile small intestine, stools (pale brown, gray)
Colon removes remaining water/electrolytes from chyme
Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice,
Abdominal Distention, Mass, Pruritus (itching)
"Do you feel the pain in any other part of your body?"
"How long have you had the pain?"
"Have you had recurrent episodes of abdominal pain?" "Did the pain start suddenly?"
"Can you describe pain? Sharp? Dull? Burning? Cramping?" "Is the pain continuous? Waves?"
"Has there been any change in the severity or nature of the pain since it began?"
"What makes it worse?" Better?"
"Is the pain associated with nausea? Vomiting? Sweating? Constipation? Diarrhea? Bloody
stools? Abdominal distention? Fever? Chills? Eating?"
"Have you ever had gallstones? Kidney stones?"
"When was your last period?"
Emergency rooms 40-45% present with nonspecific pain, but 1530% need surgery, usually for appendicitis, intestinal
obstruction, cholecystitis
Doubling over with cramping colicky pain: renal lithiasis
Sudden knifelike epigastric pain: gallstone pancreatitis.
Epigastric pain: gastritis or GERD.
Right upper quadrant and upper abdominal pain: cholecystitis.
Indigestion: angina from inferior wall coronary artery disease
precipitated by exertion and relieved by rest
Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice, Abdominal
Distention, Mass, Pruritus (itching)
Time (exact) pain started, what was patient doing at that time.
Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice,
Abdominal Distention, Mass, Pruritus (itching)
Parietal Pain:
Inflammation in parietal
peritoneum
steady, aching pain
usually more severe than visceral
pain
more precisely localized over
involved structure.
typically aggravated by
movement or coughing.
Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice, Abdominal
Distention, Mass, Pruritus (itching)
Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice,
Abdominal Distention, Mass, Pruritus (itching)
Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice,
Abdominal Distention, Mass, Pruritus (itching)
Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice,
Abdominal Distention, Mass, Pruritus (itching)
Area of Pain
Substernal
Affected Organ
Esophagus
Clinical Example
Esophagitis
Shoulder
Diaphragm
Epigastric
Stomach
Duodenum
Gallbladder
Subphrenic
abscess
Peptic gastric
ulcer
Peptic duodenal
ulcer
Cholecystitis
Liver
Hepatitis
Bile ducts
Cholangitis
Pancreas
Pancreatitis
Right scapula
Biliary tract
Midback
Location of Pain in
Abdominal Disease
Maneuvers for Ameliorating
Abdominal Pain
Affected
Clinical
Maneuver
Belching
Organ
Stomach
Example
Gastric
distention
Eating
Stomach,
duodenum
Peptic ulcer
Vomiting
Stomach,
duodenum
Pyloric
obstruction
Biliary colic
Leaning
forward
Retroperitonea Pancreatic
l structures
cancer
Aorta
Aortic dissection
Pancreas
Pancreatitis
Periumbilical
Small intestine
Obstruction
Hypogastrium
Colon
Ulcerative colitis
Diverticulitis
Sacrum
Rectum
Proctitis
Perirectal abscess
Pancreatitis
Flexion of
Peritoneum
knees
Flexion of right Right psoas
thigh
muscle
Peritonitis
Flexion of left
thigh
Diverticulitis
Left psoas
muscle
Appendicitis
Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice,
Abdominal Distention, Mass, Pruritus (itching)
Dehydration/Electrolyte imbalance:
prolonged vomiting
significant (>500mL) blood loss (lightheadedness, syncope: dependent
on rate/volume)
Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice, Abdominal
Distention, Mass, Pruritus (itching)
Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice, Abdominal
Distention, Mass, Pruritus (itching)
Causes Vomiting:
severe peritoneal irritation (organ perforation: not massive
vomiting);
Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice, Abdominal
Distention, Mass, Pruritus (itching)
Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice,
Abdominal Distention, Mass, Pruritus (itching)
small amounts of
yellowish/greenish bile common
(no special significance)
Hematemesis: vomitus
contains blood (Amount? Bright
red?)
brownish/blackish vomit
coffee ground
appearance
blood altered by gastric acid
esophageal, gastric varices,
Steatorrhea:
Malabsorption: oily residue,
floating, fatty diarrheal stools
Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice, Abdominal
Distention, Mass, Pruritus (itching)
Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice, Abdominal
Distention, Mass, Pruritus (itching)
"Have you noticed blood in stools? Mucus? Undigested food?" "What is the
color of the stools?"
"How many bowel movements do you have a day?"
"Does the diarrhea
occur after eating?"
"What happens when you fast? Do you still have diarrhea?"
"Is the diarrhea associated with abdominal pain? Abdominal distention?
Nausea? Vomiting?"
"Have you noticed that the diarrhea is worse at certain times of the day?"
Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice, Abdominal
Distention, Mass, Pruritus (itching)
"How long have you been constipated?" "How often do you have a
bowel movement?"
"What is the size of your stools?"
"What is the color of your stools?"
"Is the stool ever mixed with blood? Mucus?"
"Have you noticed periods of constipation alternating with periods of
diarrhea?"
"Have you noticed a change in the caliber of the stool?" "Do you have
much gas?"
"How's your appetite?"
"Has there been any change in your weight?"
Constipation:
>12 weeks (of prior 6mo with 2> following) :
lumpy/hard stool.
manual facilitation.
Obstructing lesion Sigmoid Colon apple core: thin, pencil-like stool
Medications: anticholinergic agents, calcium channel blockers, iron
supplements, opiates.
Systemic: hypothyroidism, hypercalcemia, MS, Parkinsons,
Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice, Abdominal
Distention, Mass, Pruritus (itching)
Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice,
Abdominal Distention, Mass, Pruritus (itching)
"Have your bowel movements ever been this color (point at black)?"
"Have you passed more than one black, tarry stool?"
If yes, "When?"
"How long have you been having black, tarry stools?" "Have you noticed feeling
lightheaded?"
"Have you had any nausea associated with these stools?
Vomiting? Diarrhea? Abdominal pain? Sweating?"
acuteness/amount of hemorrhage
lightheadedness, nausea, diaphoresis (rapid GI bleeding,
hypotension)
Intrahepatic biliary
obstruction (medical
jaundice)
Extrahepatic biliary
obstruction (surgical
Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice, Abdominal
Distention, Mass, Pruritus (itching)
"How long have you been jaundiced?" "Did the jaundice develop rapidly?
" Distaste for cigarettes?"
"Is jaundice associated with abdominal pain? Loss of appetite? Nausea? Vomiting?
"Is the jaundice associated with chills? Fever? Itching? Weight loss?"
"In the past year have you had any transfusions? Tattooing? Inoculations?"
"Do you use any recreational drugs?" If yes, "Do you use any drugs
intravenously?"
"Do you eat raw shellfish? oysters?"
"Have you traveled abroad in past year?" If yes, "Where? Were you aware you may
consumed unclean water?"
"Have you been jaundiced before?"
"Has your urine changed color since you noticed that you jaundiced?"
"What is color of your stools?"
"Do you have any friends or relations who are also jaundiced?"
"What type of work do you do? have you done?" "What are your hobbies?"
Mechanisms jaundice:
yellowish/tea colored)
bilirubin production
Unconjugated bilirubin
bilirubin uptake by hepatocytes
(not water soluble): not
ability (liver) to conjugate bilirubin
excreted into urine.
bilirubin excretion into bile
absorption conjugated bilirubin into
Intrahepatic jaundice:
blood
hepatocellular
damage hepatocytes or
intrahepatic bile ducts.
Extrahepatic jaundice:
obstruction extrahepatic bile
ducts (cystic and
common bile ducts)
Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice, Abdominal
Distention, Mass, Pruritus (itching)
Health professionals at increased risk (contact with infected person increases risk)
Hepatitis C virus (HCV): most common chronic blood-borne infection
(>3.9million USA have antibody to HCV currently asymptomatic but at risk for
chronic liver disease, 10th leading cause of death)
40% Chronic Liver Disease is HCV related (8000-10,000 deaths/yr)
Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice,
Abdominal Distention, Mass, Pruritus (itching)
Hepatitis A vaccination
immediate
protection/prophylaxis
household
contacts/travelers: immune
serum globulin administered
<2 weeks (before) hepatitis A
contact
Advise hand washing with
soap/ water before
bathroom use, changing
diapers, preparing/eating
Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice,
Abdominal Distention, Mass, Pruritus (itching)
Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice,
Abdominal Distention, Mass, Pruritus (itching)
Hepatitis C:
repeated percutaneous exposure to blood
~2% of U.S. adults. (prevalence 50-90% high risk groups)
Strongest risk factors: IV drug use, transfusion with clotting factors
prior 1987.
Other risk factors: hemodialysis, sex partners using IV drugs, organ
transplant before 1992, undiagnosed liver disease, infants born to
infected mothers, occupational exposure, multiple sex partners,
infected sex partner, tattoos
Sexual transmission is rare.
no vaccine for prevention, so screening for risk factors an
above
insidious
development abdominal girth (progressive increase
from
or below?"
"Is distention
associated with vomiting? Loss appetite? Weight loss? Change in bowel
belt size)
habits?
Loss
of of
appetite:
cirrhosis, malignancy, end-stage congestive
Shortness
breath?"
heart failure
shortness of breath: decrease in pulmonary capacity
Suprapubic pain
Dysuria, urgency, frequency
Hesitancy, decreased stream
in males
Polyuria or nocturia
Urinary incontinence
Hematuria
Kidney or flank pain
Ureteral colic
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult
developer
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
Jaundice
apparent: serum
bilirubin
>2.5mg/dL
(adults)
6mg/dL
(neonates)
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
Spider angiomas:
sensitivity (alcoholic cirrhosis)
nonspecific (pregnancy, collagen vascular
disorders)
Pyoderma gangrenosum
necrotic, undermined tender ulceration
with pus.
commonly lower extremities
associated with inflammatory bowel
disease (ulcerative colitis)
Generally clinical course follows bowel
disease.
equipment: stethoscope, gloves , lubricant, tiss ues, occult blood tes ting card, Hemoccult developer
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
Osler-Weber-Rendu
syndrome:
Hypercortisolism (Cushing's
syndrome):
obesity (90%),
facial plethora (moon facies),
hirsutism,
hypertension.
prominent fat deposits
supraclavicular/retrocervical areas
(buffalo hump)
Telangiectases: lips/tongue
(throughout GIT)
autosomal dominant
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
pinkish-purple striae
(classic adrenocortical excess)
Everted Umbilicus: abdominal pressure
(ascites ,large mass)
Umbilical hernia: umbilicus to be everted.
Grey Turners sign: abdomen/flank
ecchymoses (hemorrhagic pancreatitis or
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
Auscultation abdomen
before
percussion/palpation:
more accurate assessment
existing BS (percussion/palpation may
change intestinal motility)
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
Spleen:
Percussion is moderately
accurate in detecting
splenomegaly
sensitivity, 60-80%
specificity, 72-94%
Semilunar shaped
Traubes Space
Line passing though
9th rib midaxillary line
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
Percuss
lowest interspace in
Spleen:Check for a splenic percussion sign
.
left anterior axillary line
(usually tympanitic) patient
takes deep breath (percuss
again).
Normal spleen size remains
tympanitic.
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
Ticklish: useful have patient hold their hand over examiner's hand
Expiration: normally rectus muscles relax/soften
Rigidity: little change, involuntary muscle spasm (peritoneal irritation)
Diffuse: diffuse (peritonitis: boardlike), or localized (over inflamed
appendix/gallbladder)
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
Liver palpation:
left hand posteriorly: right 12thrib iliac crest, lateral paraspinal muscles.
right hand in RUQ parallel/lateral rectus muscles below liver dullness.
patient deep breath, press right hand in/up left hand pulls up
liver edge felt slip over right fingertips as patient breathes.
start low (pelvic brim) gradually work up (otherwise miss enlarged liver edge)
not felt readjusting right hand closer CCM.
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
Liver palpation:
On inspiration, liver is
palpable about 3 cm
below RCCM in
midclavicular line.
obstructed, distended
gallbladder may form
an oval mass below
edge of liver and
merge with it.
It is dull to
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
Splenomegaly (splenic
enlargement): hyperplasia,
congestion, infection, tumor,
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
Spleen palpation:
Enlarged spleen expands anteriorly,
downward and
medially, replacing tympany of stomach
and colon with dullness of a solid organ
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
Bladder
Normally bladder cannot be examined
unless distended above symphysis pubis.
Check for suprapubic tenderness: bladder
infection
Percussion: dullness (how high bladder rises
above symphysis pubis)
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
Aorta:
press firmly deep in upper
abdomen,
slightly to left of midline,
identify aortic pulsations.
Persons >50yr:
assess aortic width by pressing
deeply in upper abdomen with
one
hand on
side of
aorta.
Risk factors
for each
abdominal
aortic
aneurysm (AAA)
normal aorta <3 cm
>65yr male
history of smoking
wide.
first degree relative with a history of AAA repair.
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
Bimanual: right hand under right thigh, right index finger in rectum
left hand on abdomen
Supine (modified lithotomy): knees flexed if detailed anal exam not
required
Sims position: left lateral supine (right leg flexed, left leg semiextended) for those weak, confined to bed
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
Prolapsed Internal
Palpate areas of
tenderness
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
DRE Technique:
patient advised
rectal examination
now be performed.
advise patient
lubricant will feel
cool followed by
sensation to
move bowels
patient advised
to relax and
reassured will
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
DRE Technique: lubricate right gloved index finger, place left hand patient's
buttocks as left hand spreads patient's buttocks, right index finger is gently
placed on anal verge.
Anal sphincter should be relaxed by gentle pressure with palmar surface
right index finger
patient take deep breath, right index finger inserted into anal canal as anal
sphincter relaxes.
sphincter closes completely around examining digit (assess sphincter
finger inserted as far as
tone).
possible into rectum (~10cm
probable limit)
left hand moved to patient's
left buttock, while right index
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
Special Techniques
Iliopsoas sign: Intra-abdominal inflammation
irritating psoas muscle.
patient lies on unaffected side, extend other
leg at hip against resisting examiners hand
positive psoas sign: abdominal pain with
maneuver.
Appendicitis: Irritation of right psoas
muscle
Obturator sign: inflammatory process
adjacent to obturator muscle, causes pain
patient supine examiner flexes patient's thigh
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
Abdomen:
Clinicopathologic Correlations
Double Contrast Barium
Enema (DCBE):
indirect evidence supporting
screening use
image entire colon: detect
cancers/large polyps
Abdomen:
Clinicopathologic Correlations
Screening colonoscopy:
identify/remove
cancers/premalignant
lesions throughout
colon/rectum
Abdomen:
Clinicopathologic Correlations
Dysphagia: difficulty
swallowing
impaired passage of
solid/liquids
from mouthstomach
Solid foods: structural
(mechanical) esophageal
conditions (esophageal stricture,
neoplasm)
Oropharyngeal
Abdomen:
Clinicopathologic Correlations
Dysphagia: Esophageal Diverticula
Saccular ontpouchings found in esophagus/colon.
False (pulsion) diverticula: mucosal layers protrude through
muscularis (most common type).
True (traction) diverticula: contains all layers of esophageal wall
(less common type)
Abdomen:
Clinicopathologic Correlations
Dysphagia: Esophageal
Diverticula
Zenker's and Epiphrenic Diverticula
motor abnormalities of esophagus
(spasm, achalasia, UES/LES
hyperactivity)
Abdomen:
Clinicopathologic Correlations
Esophageal Varices: due to portal
hypertension
venous dilation due portal venous
pressure (>12mmHg).
distal esophageal veins thinner
walled
Abdomen:
Clinicopathologic Correlations
Esophageal Varices: Treatment:
Vasopressin (ADH): vasoconstriction
mesenteric vesselsportal venous
flow (initial management).
Somatostatin (octreotide) : inhibits
Abdomen:
Clinicopathologic Correlations
Achalasia: failure to relax
characterized by aperistalsis (required for diagnosis)
incomplete relaxation LES with difficulty swallowing (often associated, but not
Abdomen:
Clinicopathologic Correlations
Achalasia continued..
Clinical presentation: (progressive dysphagia)
young adults (infants, children): progressive dysphagia,
nocturnal regurgitation/aspiration undigested food
Manometry: normal/elevated resting LES pressure, decreased LES
pressure
absence of peristalsis
Classic imaging findings:
Barium swallow: dilated esophagus with distal bird-beak
narrowing
Differential diagnosis distal esophageal
Fluoroscopy: disorganized tertiary
contractions esophagus.
narrowing: includes esophageal cancer
Patients+/with partial
difficulty swallowing
Treatment: distal esophageal myotomy
gastric(> 50 years):
endoscopy to rule out cancer
Abdomen:
Clinicopathologic Correlations
Heartburn:
retrosternal burning
pain/discomfort,
Weekly (>often)
Aggravated:
food (alcohol,
chocolate, citrus fruits,
coffee onions,
peppermint)
positions (bending
over, exercising,
Abdomen:
Clinicopathologic Correlations
Chronic upper abdominal pain
complain of heartburn, acid
reflux, regurgitation.
if these symptoms are reported >
alarm symptoms:
likely have GERD (until proven
difficulty swallowing
otherwise)
atypical respiratory symptoms:
(dysphagia),
cough, wheezing, aspiration
pain with swallowing
(odynophagia),
pneumonia, adult-onset asthma
pharyngeal symptoms: hoarseness, recurrent vomiting, GI
bleeding, weight loss,
chronic sore throat.
anemia,
Risk factors: reduced salivary flow,
risk factors for gastric
delayed gastric emptying, hiatal hernia. cancer.
Abdomen:
Clinicopathologic Correlations
GERD continued
OTC H2 blockers
Abdomen:
Clinicopathologic Correlations
Barrett' s esophagus: precancerous lesion distal esophagus
complication long-standing GERD
GERD.
Abdomen:
Clinicopathologic Correlations
Esophageal Cancer: incidence varies: geographic region (?
environmental), male, low socioeconomic status, blacks>whites
Two major types: Squamous Cell Carcinoma and
Adenocarcinoma
SCC: smoking, alcohol (spirits>beer), nitrites,
smoked opiates, fungal toxins, radiation, lye
upper/middle esophagus
Abdomen:
Clinicopathologic Correlations
Esophageal Cancer: continued
circumference involved)
Cancer typically spreads locally: surrounding tissue, lymph nodes, lungs,
liver, pleura
Abdomen:
Clinicopathologic Correlations
Gastritis: inflammation gastric
mucosa (acute/chronic)
Acute Gastritis: acute, transient
mucosal damage (edema, inflammation)
erode underlying mucosa and affect
epithelium (hemorrhagic gastritis)
Causes: NSAIDs, alcohol consumption,
Cushings ulcer (head trauma), Curlings
ulcers (burns), uremia stress-induced
ulcers
Investigation: Hemoccult positive
Abdomen:
Clinicopathologic Correlations
Chronic (Atrophic) Gastritis
(Types A and B): continuous
inflammation gastric mucosa
mucosal atrophy/epithelial
metaplasia
Type A: fundus/body stomach
(spares antrum)
achlorhydria,
hypergastrinemia.
Autoimmunue gastritis:
IF leads to pernicious
anemia.
(megaloblastic anemia,
neurologic changes,
abnormalChronic
Schillinggastritis
test.
risk gastric
adenocarcino
ma.
Type B: risk
mucosaassociated
lymphoid tissue
(MALT)
Abdomen:
Clinicopathologic Correlations
Gastritis continued
Presentation: abdominal
pain, dyspepsia
Endoscopy: not reliably correlate
with histopathologic gastritis
diagnosis
Diagnosis: histologically (biopsy)
H . Pylori: biopsy (gramnegative rods), urease breath test ,
stool/serum antigen
Abdomen:
Clinicopathologic Correlations
Peptic Ulcer Disease: Ulcer formation: stomach/1st part
duodenum secondary to mucosal disruption
Gastric mucosal cells: secrete mucus bicarbonate (pH ~6-7 near
epithelial cells) yet pH 1-2 in gastric lumen
breaching mucus layer (drugs, bacteria, systemic disorder): epithelial
injury/ulcer
Gastric Ulcers: less common, older persons, lesser curvature,
antral, prepyloric regions, malignant potential, basal/nocturnal acid
secretion normal/decreased
Cause: H. pylori.
Duodenal Ulcers: >95% 1st portion duodenum, >1cm diameter,
Abdomen:
Clinicopathologic Correlations
Peptic Ulcer Disease: continued
Abdomen:
Clinicopathologic Correlations
Peptic Ulcer Disease: continued
Diagnosis: nonspecific
history/physical,
contrast radiography
(defects/ulcers gastric/duodenal
epithelium although small erosions
missed),
exclude H.pylori (serum
antibodies not helpful in
confirming treatment) stool H.
pylori antibodies (useful in
Abdomen:
Clinicopathologic Correlations
Gastric Cancer: 2nd most common cause cancer-related death
worldwide
Linitis
plastica
~85% adenocarcinomas, 15% lymphomas, leiomyosarcomas.
Adenocarcinoma: two types
Intestinal type: intestinal metaplasia gastric mucosal cells .
lesions ulcerative (antrum, lesser curvature)
risk factors are high salt/nitrates diet, H.pylori colonization,
chronic gastritis.
Diffuse type: cells lack normal cohesion (infiltrating , discrete mass
stomach wall), younger age, all parts stomach, decreased motility
Abdomen:
Clinicopathologic Correlations
Gastric Cancer continued
Abdomen:
Clinicopathologic Correlations
Gastric Cancer continued
Abdomen:
Clinicopathologic Correlations
Gastric Cancer continued
Diagnosis: double-contrast radiography, CT imaging (very small
lesions)
Abdomen:
Clinicopathologic Correlations
Malabsorption Syndromes: decreased intestinal absorption
essential nutrients and chronic diarrhea (secretory, osmotic) with
steatorrhea (stool fat content >6% dietary fat intake: not seen with
lactate deficiency or pernicious anemia), weight loss, vitamin (ADEK),
mineral deficiencies,
Underlying disorders:
Pancreatic deficiency:
Damage/loss intestinal mucosal surface (surgery, damage to
intestinal villi)
Abdomen:
Clinicopathologic Correlations
Malabsorption Syndromes continued.
Abdomen:
Clinicopathologic Correlations
Malabsorption Syndromes continued.
Celiac Sprue (Gluten-sensitive enteropathy): autoimmune disease
with antibodies against water-insoluble gliadin (part of gluten: protein
wheat, barley, rye, oats)
Presentation:
Symptoms: varies, classically occurs in infants
introduction
Mild: single vitamin deficiency, chronic
diarrhea Severe: chronic diarrhea with
steatorrhea (pale, bulky, foul-smelling stools),
multiple
vitamin/mineral deficiency, growth
retardation, failure to thrive, dermatitis
herpetiformis, human leukocyte antigen
(HLA B8, HLA DW3)
anti-gliadin, antiat
time of antibodies
cereal
endomysial
(90- 95%
sensitivity/specificity)
along with resolution of
symptoms with
elimination diet
diagnosis can be made
without mucosal biopsy
Abdomen:
Clinicopathologic Correlations
Malabsorption Syndromes continued.
Disaccharidase Deficiency: lactase (brush border enzyme): dairy intolerance
rare inborn error, common during adulthood as lactase in immature
brush border disappears (acquired lactose intolerance)
no intestinal changes
less common disaccharidase deficiencies are sucrase (table sugar),
trehalase (mushrooms)
Whipples Malabsorption Syndrome: Tropheryma whippelii (gram-positive
electron microscopy)
Abdomen:
Clinicopathologic Correlations
Diverticular Disease
Diverticula: congenital (entire thickness involved segment) or acquired
(mucosal herniation through muscular laver).
Abdomen:
Clinicopathologic
Correlations
Meckels Diverticulum:
Congenital, true diverticulum
terminal ileum
(incomplete closure
omphalomesenteric duct),
Abdomen:
Clinicopathologic
Correlations
Meckels Diverticulum: Mucosa: ileal (50%
cases), gastric, pancreatic, duodenal, colonic.
Typically asymptomatic and discovered
incidentally (typically <5yr old)
Abdominal pain: intussusception, volvulus
Bleeding: ileal peptic ulcer formation (gastric
mucosa: Meckels scan IV technetium-99 taken
up by ectopic gastric mucosal parietal cells).
Meckel's diverticulum: complicated by Meckel's
diverticulitis
(lower Gl bleeding in children)
Abdomen:
Clinicopathologic Correlations
Diverticulosis: acquired (pulsion) multiple diverticula at origin
mesenchymal feeder artery (typically sigmoid colon), secondary to
increased luminal pressure (low-fiber dietcolonic muscular
contractions to move stool).
Abdomen:
Clinicopathologic Correlations
Diverticulosis:
Treatment: unnecessary unless
bleeding
High-fiber diets suggested
(increase stool bulkcolonic
intraluminal pressure).
Severe: vessel
Abdomen:
Clinicopathologic Correlations
Diverticulosis:
Mesenteric angiography:
diagnostic/therapeutic
(vasoconstriction, artificial blood
clot formation induced)
Abdomen:
Clinicopathologic Correlations
Diverticulitis:
Most common
complication
diverticulosis (infection
secondary impacted
fecalithlymphatic
obstructionlocalized
ischemiabacterial
overgrowth)
Abdomen:
Clinicopathologic Correlations
Diverticulitis:
Diverticular rupture
contained: abscess
uncontained: generalized
peritonitis
Presentation: LLQ pain, guarding,
peritoneal signs (rebound tenderness),
leukocytosis, fecal leukocytes, fever
(constipation secondary to localized
swelling)
Abdomen:
Clinicopathologic Correlations
Diverticulitis:
Investigation:
Abdominal CT scan
(diverticular inflammation,
pericolic abscess)
acute diverticulitis: risk
perforation during
imaging (barium
enema, colonoscopy
contraindicated)
Treatment: no signs
perforation: bowel rest,
pain control, fluids, broad
Abdomen:
Clinicopathologic Correlations
Intussuscepti
on:
Investigation:
Abdominal
ultrasound:
birds-eye or
coiled-spring
pattern
(invagination
proximal
segment).
Abdomen:
Clinicopathologic Correlations
Intussusception:
Investigation:
Air/barium enemas
diagnostic/therape
utic (most cases).
Abdominal plain
film: filling defect
Treatment:
large
colon
Nonsurgical means: 1st
attempted (air/barium
enema)
Surgery indicated if
air/barium enema fails or
Abdomen:
Clinicopathologic Correlations
Hirschsprung's disease: complete functional obstruction large
bowel (absence ganglion cells both submucosa, myenteric neural plexuses)
Aganglionic bowel always involves anus progresses proximally to
varying degrees (severe disease: entire colon, some small intestine)
Obstruction results in characteristic dilation bowel proximal
aganglionic segment (congenital megacolon)
Several genetic mutations: most common RET proto-oncogenic,
Down's syndrome , Waardenburg's syndrome, cardiac defects
(~1:5000 live births, male/female ratio 3-4:1)
Abdomen:
Clinicopathologic Correlations
Hirschsprung's disease:
Diagnosis:
Rectal biopsy (gold standard) reveal
absence of ganglion cells rectal
tissue.
Barium enema: suggestive, severe
dilation proximal colon abruptly
narrowing into aganglionic distal
colon.
Aganglionic section corresponds to narrowed
Treatment:
Surgical (aganglionic section
segment;
resected,
normal
bowel
connect
anus)
dilated portion
bowel
structurally
normal
Abdomen:
Clinicopathologic Correlations
Colitis: inflammation colon .
Based on etiology, several types of idiopathic colitis, Crohn's
Disease (CD) and Ulcerative Colitis (UC)
UC and CD share many features resulting
from isbowel
inflammation
Sulfasalazine
not absorbed
by small
It is hydrolyzed
by colon flora
(diarrhea, pain, fever, blood loss) but differ intestine.
in important
ways
into 5-aminosalicylate acid (5-ASA)
(mesalazine) and sulfapyridine.
5-ASA acts as local antiinflammatory agent
in colon.
Treatment:
Medical treatment: both IBDs similar: includes antiinflammatory
(sulfasalazine: milder forms; corticosteroids, azathioprine: severe cases) ,
antidiarrheal, antibiotics
Surgical therapy (colectomy): uncontrolled UC , colectomy is
curative.
Abdomen:
Abdomen:
to the disease
emotional factors are important in maintaining/prolonging
existing attack. Schoolwork deteriorates as miss more/more
Abdomen:
Abdomen:
Clinicopathologic Correlations
Diarrhea
Ulcerative Colitis
Present
Crohn's Disease
Present
Hematochezia
Common
Rare
Extraintestinal
manifestations
Common
Common
Perirectal disease
Fissures
Fistulas
Abscesses
Rectal disease
Present
Absent
Anal disease
Absent
Present
Abdomen:
Clinicopathologic Correlations
Pseudomembranous colitis:
acute inflammation colon precipitated by course of antibiotics
(ampicillin, clindamycin, cephalosporin) normal colonic bacterial flora
(E. Coli, Bacteroides fragilis) enabling Clostridium difficile overgrowth.
C difficile: gram-positive, spore- forming anaerobic rod.
Antibiotic therapy decreases protective flora allowing C difficile
become pathogenic
Symptoms: due C. difficile toxins.
A,B toxins attack colonic mucosa (hypermotility, inflammation,
capillary permeability).
Abdomen:
Clinicopathologic Correlations
Pseudomembranous colitis continued.
severe cases: colonic mucosa covered with yellow/gray
exudates (pseudomembranous colitis) toxic megacolon,
volvulus, colonic perforation (life-threatening)
Diagnosis: stool sample tested for A, B toxins of C.difficile
Colonoscopy: rarely indicated (confluent patches yellow/gray
exudates obscuring normal colonic mucosa)
Amebic
liver
abscess
Abdomen:
Clinicopathologic Correlations
Infectious Colitis: viral, bacterial, parasitic
Patient: severe diarrhea, fever, WBC, abdominal pain
Clues: travel, recent antibiotic use, specific food consumption,
person with severe
immunodeficiency
dehydration due to
Pathogens:
cholera.
Note the sunken eyes and
Entamoeba histolytica: amebic colitis:
asymptomaticsevere bloody diarrhea, liver abscesses, decreased skin turgor
which produces wrinkled
bowel necrosis/perforation, fulminant peritonitis
hands and skin
Vibrio cholerae: gram-negative bacterium (toxin):
watery diarrhea, loss fluid, electrolytesdehydration
(deadly within days)
Treatment: dependent on
underlying microorganism
(appropriate antimicrobial/antiparasitic
therapy and supportive care)
Abdomen:
Clinicopathologic Correlations
Benign Polyps: extremely common >40 (possible precursors to
colorectal cancer)
Abdomen:
Clinicopathologic Correlations
Multiple Polyposis Syndromes: several genetic disorders (young
ages)
Abdomen:
Clinicopathologic Correlations
Multiple Polyposis Syndromes continued.
Turcots syndrome: autosomal recessive: colonic polyps, CNS
tumors (glioblastoma multiforme, medulloblastoma)
Hereditary Nonpolyposis Colorectal Cancer (HNPCC):
autosomal dominant: colorectal adenomas, colorectal cancer.
mutation DNA mismatch repair gene (hMLH1, hMSH2) part of
Lynch1, Lynch2 (extracolonic tumors: endometrium, ovary, pancreas)
Peutz-Jeghers syndrome: autosomal dominant:
hamartomatous colon polyps, mucocutaneous hyperpigmentation
(lips, oral mucosa, hands, genitals).
Cancer of Stomach
Major Symptoms
Cancer of Pancreas
Cancer of Colon
Occult bleeding
Back pain
Gastrointestinal bleeding
Weight loss
Weight loss
Vomiting
Jaundice
Anorexia
Dysphagia
Adenomatous polyps
Smoking
Adenomatous polyps
Pernicious anemia
Alcoholism (?)
Ulcerative colitis
Family history
Familial polyposis
Gardner's syndrome
Villous adenomas
Risk Factors
Abdomen:
Clinicopathologic Correlations
Colorectal Cancer: adenocarcinoma large intestine/rectum
Abdomen:
Clinicopathologic Correlations
Colorectal Cancer:
>50yr presenting with stool
changes (melena, hematochezia,
pencil-thin caliber), abdominal
discomfort, constitutional
symptoms (weight loss),
unexplained anemia
Left-sided (sigmoid)
colon cancer: early symptoms obstruction
(men/postmenopausal
women)
(narrower lumen).
tumors produce napkin-ring, apple-core constriction
(encircling annular growth)
stool solid.
Right-sided colon cancer: anemia, weight loss, abdominal pain.
Symptom
Pain
Cancer Right
Colon
Ill defined
Cancer Left
Colon
Colicky
Cancer
Rectum
Steady, gnawing
Obstruction
Infrequent
Common
Infrequent
Bleeding
Brick-red
Weakness
Common
Infrequent
Infrequent
Abdomen:
Clinicopathologic Correlations
Colorectal Cancer continued.
Abdomen:
Clinicopathologic Correlations
Colorectal Cancer continued
Diagnosis: colonoscopy with tissue biopsy (adenocarcinoma gold
standard).
Abdomen:
Clinicopathologic Correlations
Appendicitis: most common
indication emergency
abdominal surgery children,
(can occur all age groups, peak 1530yrs)
Abdomen:
Clinicopathologic Correlations
Appendicitis continued
Diagnosis: lab: leukocytosis, pyuria, fecal
leukocytes
Abdominal X-ray: 2/3rd cases:
radiopaque fecaliths (impacted in
appendix)
Abdomen:
Clinicopathologic Correlations
Hernias: protrusion abdominal
contents through defect in abdominal
wall
Hernial mass: three parts: covering
tissues (layers abdominal wall),
peritoneal sac, structure contained
inside (including viscera)
Groin hernias 75%: direct inguinal,
indirect inguinal, femoral
Incisional and Ventral hernias 10%
Umbilical hernias 3%: infants
Rare hernias: Spigelian, Petit's (lumbar
Abdomen:
Clinicopathologic
Correlations
Hernia continued
Spigelian: through
spigelian fascia
(aponeurotic layer between
rectus abdominus and
semilunar line above arcuate
line) interparietal (below
not
protruding, small, high
risk stangulation
subcutaneous fat)
Diagnosis:
Reducible: common, painless, abdominal contents easily
returned to abdomen
Irreducible (incarcerated): difficult return contents to abdominal
cavity, painful if obstructed
Strangulated: entrapped organ (bowel, fat) incarcerated in
Abdomen:
Clinicopathologic Correlations
Hernias continued.
Children/young adults or uncovered by comorbid medical
conditions (intraabdominal pressure older patients: chronic cough, COPD,
constipation)
Abdomen:
Clinicopathologic Correlations
Hernias continued
Umbilical hernias (infants,
children): congenital defect
abdominal wall at umbilicus.
Adults: comorbid conditions
(pregnancy) that increase
intraabdominal pressure (cough,
COPD, ascites),
complain of umbilical bulge
worsens with Valsalva
maneuver, pain
(incarceration/strangulation),
Abdomen:
Clinicopathologic Correlations
Hernias continued
Abdomen:
Clinicopathologic Correlations
Hernias continued
Femoral hernias: palpated medial
femoral pulse, inferior inguinal ring.
CT scan, ultrasound: those difficult
to palpate (obese)
Treatment: surgical repair
(herniorrhaphy)
Abdomen:
Clinicopathologic Correlations
Alcoholic Hepatitis: reversible inflammatory liver damage
(alcohol consumption over time), genetic, environmental factor,
direct toxicity ethanol/metabolites: oxidative damage disrupting
mitochondrial and cell membranes (lipid accumulation)
Asymptomatic (mildest)fulminant hepatic failure/death (most
severe)
Abdomen:
Clinicopathologic Correlations
Abdomen:
Clinicopathologic Correlations
Alcoholic Hepatitis continued
Lab test: elevated aspartate aminotransferase (AST), alanine
aminotransferase (ALT), AST:ALT ratio of 2:1, elevated alkaline
phosphatase (ALP), prolonged prothrombin time (PT)
mildly elevated AST may be only laboratory abnormality in mild
cases.
Mneumonic: A Scotch and Tonic:
Alcoholic hepatitis; AST>>ALT
Viral hepatitis: AST<<ALT
Abdomen:
Clinicopathologic Correlations
Alcoholic Hepatitis continued
Abdomen:
Clinicopathologic Correlations
Cirrhosis and Portal Hypertension:
Cirrhosis: irreversible scarring liver after years chronic insult
Characterized: complete disarray hepatic architecture (progressive
scarring: generalized fibrosis), regenerative nodule
Morphologically:
Micronodular cirrhosis: nodules <3mm, uniform in size.
Macronodular cirrhosis: nodules >3mm, increased risk
hepatocellular carcinoma (HCC) due significant liver injury (hepatic
necrosis: postinfectious, drug-induced).
Mixed: Macromicronodnlar
form.
many etiologic divided into four major groups: Infectious,
Hepatocellular Failure
Spider angiomata
Gynecomastia
Palmar erythema
Ascites
Jaundice
Testicular atrophy
Erectile dysfunction
Bleeding problems
Changes in mental function
Portal Hypertension
Ascites
Varices: esophageal
Hemorrhoids
Caput medusae
Splenomegaly
Abdomen:
Clinicopathologic Correlations
Alcoholic Cirrhosis: Alcoholism most
common cause cirrhosis USA (Variety
manifestations):
Abdomen:
Clinicopathologic Correlations
Alcoholic Cirrhosis continued.
Consequences Diffuse Hepatic Tissue Scarring with Portal
Hypertension:
Clinical features portal hypertension: establishment
portosystemic collaterals
gastroesophageal varices (potential for significant bleeding),
hemorrhoids
periumbilical venous collaterals (caputmedusae), splenomegaly
(thrombocyopenia), peripheral edema, hydrothorax,
hypoalbuminemia (oncotic pressure), portal hypertension
>10mmHg (ascites: become infected, spontaneous bacterial peritonitis),
Hepatic encephalopathy .
Abdomen:
Clinicopathologic Correlations
Alcoholic Cirrhosis continued.
Cirrhosis complete disarray liver function ALP, bilirubin, yglutamyl transferase, PTanemia, thrombocytopenia,
hypoalbuminemia, hyponatremia.
AST:ALT ratio > 2.0 (cutoff > 1.5) suggestive of alcoholic cirrhosis.
intrasinusoidal pressure (intrasinusoidal hypertension).
Physical exam: signs/symptoms: cirrhotic liver shrunken, firm,
nodular (damaged liver enlarged/tender)
Lab tests: AST, ALT (normal values do not rule out cirrhosis, as these
values return normal as hepalocytes burn out).
Abdomen:
Clinicopathologic Correlations
Alcoholic Cirrhosis continued.
Complications cirrhosis:
Sclerotherapy/banding (symptomatic
esophageal varices), drainage excess
peritoneal fluid (paracentesis), nutritional
support
Treatment: hepatic encephalopathy:
lactulose (ammonia production colonic
bacteria),
neomycin (ammoniaogenic bacterial load)
Procedures: allow blood bypass portal
venous system (symptoms/signs portal
TIPS
Abdomen:
Clinicopathologic Correlations
Hemochromatosis: inherited,
autosomal recessive
(HFE gene: affinity transferrin receptor bind
transferrinserum iron iron deposition/damage to liver,
pancreas, heart, joints, pituitary), male-predominant
metabolic iron storage (intestinal iron absorption)
Abdomen:
Clinicopathologic Correlations
Hemochromatosis continued.
Clinical presentation: %
transferrin saturation (>50%),
Urinary iron,
serum iron/ferritin(iron:total iron
binding capacity Fe:TIBC) >50%,
Confirm with liver biopsy
Treatment: recurrent phlebotomy
to remove excess iron, chelating
agents (deferoxamine), abstain
alcohol (increases iron absorption).
Abdomen:
Clinicopathologic Correlations
Wilson's Disease (Hepatolenticular Degeneration):
inherited (autosomal recessive: ATP7B gene chromosome 13: 13q14.3 codes
for P-type ATPase that transports copper into bile and incorporates it into
ceruloplasmin)
metabolic disorder (inhibits release copper into bile)
excessive serum copper (deposition organs liver, brain, kidneys, corneas)
Wilsons
Disease
continued
Presentation:
young adult stigma
liver disease
(hepatitis, cirrhosis,
failure),
neurologic changes
(accumulation copper
CNS),
Kayser-Fleisher
rings (slit lamp
exam: copper deposits
Abdomen:
Clinicopathologic Correlations
Cholelithiasis: Gallstones common cause RUQ pain (fair, fat,
female, fertile, forty)
Abdomen:
Clinicopathologic Correlations
Cholelithiasis:
Clincially: RUQ pain (worse postprandial), nausea,
vomiting, food intolerance
Diagnosis: Ultrasound, XR
(gallstones radiolucent: except pigmented stones),
Endoscopic retrograde
cholangiopancreatography
(ERCP: visualize stone common bile duct)
Abdomen:
Clinicopathologic Correlations
Cholecystitis: common complication of cholelithiasis (similar
cholelithiasis) Postprandial colicky RUQ pain radiating to right
scapula (intermittent blockage common bile duct),
nausea/vomiting, bloating, jaundice (complete blockage CBD--:
Charcot's triad: epigastric/RUQ pain, fever, jaundice (cholangitis)
Reynolds' pentad: Charcot's triad + Shock + altered mental
Classic physical exam feature:
status
Murphy's sign:
Elicitation: palpate right subcostal (GB
fossa) while patient inhales (deeply),GB
descends toward fingers.
Postive response: increased
MRCP
Abdomen:
Clinicopathologic Correlations
EUS demonstrating a
small stone (arrowed)
within the common bile
duct
thickening of
gallbladder
wall, a fixed
(immobile)
intraluminal
gallbladder
mass,
gallstones,
biliary
obstruction,
(magnetic resonance
cholangiopancreatography)
and
intraoperative
cholangiography in this 65
year male with clinical signs
of biliary obstruction
Abdomen:
Clinicopathologic Correlations
Cholecystitis:
Ultrasound: GB stones, thickening GB
wall, edema
Sonographic Murphy's sign occurs
during ultrasound examination
HIDA scan (cholescintography): most
sensitive cholecystitis (makes diagnosis)
hepatobiliary iminodiacetic acidscan
(nuclear scan)
Abdomen:
Clinicopathologic Correlations
Acute Pancreatitis: activation
pancreatic enzymes (pancreatic
autodigestion, hemorrhagic fat necrosis)
Abdomen:
Clinicopathologic Correlations
Acute Pancreatitis continued.
Contrast-enhanced CT: severe
pancreatitis
(r/o pseudocyst, fully visualize extent
disease)
Abdomen:
Clinicopathologic Correlations
Chronic Pancreatitis: present as:
episodes of acute inflammation in previously injured pancreas
chronic damage with persistent pain or malabsorption
Causes: similar to acute pancreatitis (alcoholism, cystic fibrosis in
children)
Abdomen:
Clinicopathologic Correlations
Chronic Pancreatitis continued.
Radiology: presence scattered
calcifications
Treatment: address pain and
malabsorption
Morphine: spasm sphincter of
Oddi (worsen pain).
Meperidine: preferred analgesic not
cause spasm of sphincter of Oddi.
Cystic fibrosis: primary defect:
inspissated enzymes in ducts
ductal obstruction ductal dilation
Abdomen:
Clinicopathologic Correlations
Pancreatitis continued.
Enzyme Markers Commonly used laboratory assays serum AST,
ALT, GGT, bilirubin, ALP, amylase, lipase, PT
many enzyme markers affected by pathologies outside gut.
differential diagnosis include both extrinsic (outside GI tract),
intrinsic (within Gl tract) pathologies.
Aspartate Aminotransferase (AST)
Intracellular (cytosol, mitochondria) enzyme found in liver cells,
skeletal muscle, heart, brain, RBCs.
Calalyze transfer amino groups to form pyruvate.
Lab test interpretation: concentration blood with liver damage,
cor pulmonale (RHF), myocardial ischemia, extensive trauma
Abdomen:
Clinicopathologic Correlations
Alanine Aminotransferase (ALT)
intracellular (cytosol) enzyme, relatively specific to liver (also
kidney cells, skeletal muscle, cardiac tissue)
Abdomen:
Clinicopathologic Correlations
Alkaline Phosphatase (AlkP, ALP)
synthesized: liver, bone, intestine, placenta.
nonspecific indicator tissue damage (liver, bone, intestine,
placenta).
Amylase
synthesized: pancreas, salivary glands (also ovaries, intestines,
skeletal muscle)
Abdomen:
Clinicopathologic Correlations
Lipase
synthesized: pancreas, liver, intestine, stomach, tongue, others
Prostate
Cancer
PSA blood test and DRE yearly: beginning 50yr (at least 10-year
life expectancy)
Men at high risk (45y): African-Americans, men with first-degree
relative (father, brother, son) diagnosed with early age diagnosis
prostate cancer
Abdomen:
Renal Ectopy
Clinicopathologic Correlations
Pelvic and Horsehoe
Kidneys
Abdomen:
Clinicopathologic Correlations
Renal
Pelvic Kidney: 1/9110 births
embryologic kidneys ascend from pelvis to
their adult position along posterior abdominal
wall pass under umbilical arteries (if unable
pass beneath umbilical artery remain in pelvis)
Abdomen:
Clinicopathologic Correlations
Horseshoe Kidney: while ascending
from pelvis under umbilical arteries,
kidneys may be pushed close
together (lower poles fuse: fusion
anomaly: horseshoe kidney) continues
ascend until trapped under inferior
mesenteric artery (rare females,
prompt workup for Turners syndrome)
90% asymptomatic, found incidentally
Clinical presentation: UTI, symptoms
obstruction, hematuria, abdominal pain,
predisposes nephrolithiasis
Diagnosis: CT, IVP shows rotated calyces
Abdomen:
Clinicopathologic Correlations
Retroperitoneal Structures: renal, pancreas (except tail)
duodenum (2nd, 3rd, 4th parts), ascending colon, descending colon,
aorta, IVC, rectum, adrenal glands
Ureters: Descend from renal pelvis along psoas muscle, cross
bifurcation common iliac artery, pass under uterine artery, vas
deferens, join bladder in posterior-inferior portion.
Kidney: retroperitoneal organ (mediolateral aspect posterior abdominal
wall) .
Point maximal concavity (hilum) site renal arteries/veins,
ureters, adjoin kidney.
Abdomen:
Clinicopathologic Correlations
Kidney continued.
Arterial supply: Renal arteries
branches abdominal aorta
Venous return:
Renal veins drain to IVC
Left renal vein: also drains
left gonad, longer than right
renal vein (must cross aorta joint
IVC)
Abdomen:
Clinicopathologic Correlations
Kidney continued.
Urinary Casts (protein matrix: TammHorsfall mucoprotein)
Abdomen:
Clinicopathologic Correlations
Kidney continued.
Glomerulopathy: applies group conditions affecting glomeruli.
Divided into two major groups based on pathogenesis and clinical
manifestations.
Type III hypersensitivity: Granular deposits IgG- antibodycomplement; (Poststreptococcal, Type II RPGN, Membranous glomerulopathy
Abdomen:
Clinicopathologic Correlations
Glomerulopathy continued
Nephrotic Syndrome: complex secondary/metabolic changes
increased permeability GBM, secondary intra/extrarenal insults
Abdomen:
Clinicopathologic Correlations
Nephrotic Syndrome continued..
Hypercoagulability: secondary loss anticoagulant factors through
damaged glomeruli
different pathologies result in nephrotic syndrome (diagnosis:
renal biopsy)
Abdomen:
Clinicopathologic
Correlations
Abdomen:
Clinicopathologic Correlations
Glomerulopathy continued
Nephrotic Syndrome:
Important points:
1. Distinguish nephrotic syndrome (bland sediment, isolated heavy
proteinuria,
> 3.5 g/day) from nephritic syndrome (dysmorphic RBCs, RBC casts,
active sediment, proteinuria < 3 g/day)
Abdomen:
Clinicopathologic Correlations
Minimal Change Disease: most
frequent cause (>80%) childhood (23yr) nephrotic syndrome
normal appearance glomeruli (light
microscopy) electron microscopy
(effacement visceral epithelial fool
processes) causing increased
glomerular permeability.
Proximal tubules: heavily laden with
lipids secondary to increased tubular
lipoprotein reabsorption through
effaceme
nt foot
processes
(double
arrows),
absence
deposits,
vacuoles
microvilli
Abdomen:
Clinicopathologic Correlations
Minimal Change Disease continued..
Symptoms: insidious nephrotic syndrome without obvious clinical
disease (no hypertension)
selective proteinuria: primarily albumin lost (renal function
maintained, slight GFR 10-30%)
Abdomen:
Clinicopathologic Correlations
Focal Segmental Glomerulosclerosis (FSGS): more severe form
minimal change disease (similar loss visceral epithelial foot processes),
sclerosis <50% glomeruli on tissue (focal) section (segmental: only
distinct portions affected glomeruli)
Abdomen:
Clinicopathologic Correlations
Membranous Glomerulopathy: pathogenesis not clearly
established.
immunofluorescent studies (hypothesis): immune complex
deposition (association infections/systemic diseases).
leading cause adult nephrotic syndrome (male:female 2:1, 30-50yr):
Presentation:
insidious
30-40% (<5%
children).nephrotic syndrome
(otherwise healthy)
Abdomen:
Clinicopathologic Correlations
Membranous Glomerulopathy continued
Diagnosis: renal biopsy:
Light microscopy(diffuse GBM thickening,
subepithelial deposits) Electron
microscopy (subepithelial deposits spike:
extension GBM
around deposits, immunofluorescence: IgG,
C3)
Transplantation effective
Prognosis: 40% spontaneous remission,
Abdomen:
Clinicopathologic Correlations
Membranoproliferative Glomerulonephritis (MPGN):
pathogenesis unknown.
Two distinct types:
Type I (66%): secondary to immune complex formation (type 3
hypersensitivity) certain infections (hepatitis B/C, some nephritic
presentation)
Abdomen:
Clinicopathologic Correlations
Membranoproliferative Glomerulonephritis (MPGN) continued..
Presentation:
Type 1: nephrotic syndrome, hepatitis B/C, SLE, systemic infections
(large amount immune complex formation: bacterial endocarditis, sepsis)
Type 2: nephrotic/nephritic syndrome (or mixed)
Abdomen:
Clinicopathologic Correlations
Membranoproliferative Glomerulonephritis (MPGN) continued.
Differentiation:
important due
difference prognosis.
Treatment: no effective
therapy
Prognosis:
Type 1 (benign 70-80% no
chronic decrease GFR)
Type 2 (deteriorating GFR
progressing to ESRD 10-
Abdomen:
Clinicopathologic Correlations
Diabetic Nephropathy: leading cause ESRD Western society,
secondary to glomerular hypertension/hyperfiltration .
first sign glomerular injury microalbuminuria (5-10yr before other
symptoms), untreated microalbuminuria progresses slowly to
nephrotic-range proteinuria, nephropathy (DM1: 30%, DM2: 20%)
Presentation: CRF aggravated by glomerulosclerosis, fluid filtration
abnormalities renal function disorder
Cardinal symptoms: hypertension, edema, arteriosclerosis (renal
artery, efferent arterioles) nephrotic-range proteinuria
Early course (no symptoms)
Late stage (full blown CRF)
Abdomen:
Clinicopathologic Correlations
Diabetic Nephropathy:
Abdomen:
Clinicopathologic Correlations
Diabetic Nephropathy continued.
Diagnosis: clinical, without need renal
biopsy.
Suspect in DM 1/2, with retinopathy,
neuropathy, dipstick-positive
proteinuria
Light microscopy (thickening GBM,
expansion mesangium, classic KimmelsteilWilson lesions, nodular glomerulosclerosis)
Abdomen:
Clinicopathologic Correlations
Renal Amyloidosis: deposition fibrous, insoluble proteins in
extracellular space (glomerulus)
Amyloidosis: multisystemic disorder of protein folding (acquired,
hereditary)
Abdomen:
Clinicopathologic Correlations
Acute Proliferative Glomerulonephritis
nephritic syndrome (2-6yr, occasionally adults) following infection
(group A -hemolytic streptococcus) secondary to immune-complex
deposition (glomerulus) causing complement
activation/inflammation.
effective immunity after infection
Abdomen:
Clinicopathologic Correlations
Acute Proliferative Glomerulonephritis (Poststreptoccocal,
lnfectious):
Abdomen:
Clinicopathologic Correlations
Rapidly Progressive Glomerulonephritis RPGN: malignant
nephritic syndrome with progressive loss kidney function (adults 3060yr, male>female, weeks-months after primary insult)
Abdomen:
Clinicopathologic Correlations
Rapidly Progressive Glomerulonephritis RPGN:
Diagnosis: history, histologic findings
Serum chemistry: rapid rise BUN, creatinine; positive anti-GBM
antibody (Goodpastures syndrome), ANCA (varies with underlying cause),
complement levels
Urinalysis: RBCs, protein, WBC (monocytes), casts
Pathology: Renal biopsy.
Light microscopy: crescent formation: proliferated glomerular
parietal cells, Bowman' s space filled with
monocytes/macrophages, large amounts fibrin accumulating
within crescent cellular layers
Abdomen:
Clinicopathologic Correlations
Abdomen:
Clinicopathologic Correlations
Urolithiasis
Stone formation can take place anywhere in urinary collecting
system (kidneys) depends on sex (male>female), age, diet ,
climate, genetic makeup .
Size: varies crystals-large stones.
Types:
Abdomen:
Clinicopathologic Correlations
Urolithiasis
Struvite: (magnesium
ammonium phosphate):
persistently alkaline
urine from UTIs caused
by urease-positive
organisms (proteus
vulgaris, staphylococci),
staghorn calculus
cast of renal pelvis
Abdomen:
Clinicopathologic Correlations
Urolithiasis continued
Uric acid: gout, rapid cell turnover (leukemia, myeloproliferative
diseases)
Abdomen:
Clinicopathologic
Correlations
Medullary
nephrocalcinosis and
renal calculi
Abdomen:
Clinicopathologic Correlations
Urolithiasis continued.
Presentation: severe flank pain radiating to groin, colicky nature
Hydronephrosis, infection proximal to obstruction
Diagnosis: Abdominal XR radiopaque (calcium oxalate, calcium
phosphate, struvite stones)
Abdomen:
Clinicopathologic Correlations
Urinary Tract Infections: usually bacterial lower urinary tract
(treat antibiotics)
Abdomen:
Clinicopathologic Correlations
Acute Pyelonephritis: infection usually bacterial upper urinary
tract (kidney)
ascending infection from lower urinary tract (smaller numbers than
LUTI)
Abdomen:
Clinicopathologic Correlations
Chronic Pyelonephritis: recurrent/persistent renal infection
(irreversible pathologic changes corticomedullary renal region)
structural abnormalities (obstruction: stone, BPH; vesicoureteral reflux)
Abdomen:
Clinicopathologic Correlations
Abdomen:
Clinicopathologic Correlations
laparoto Surgical
my
incision
flank;
abd.
incision
phagocy cell
te
ingests
cells or
microorga
ni
lithotrips Noninvasi
y
ve
technique
for