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A good eater must be a good man;

for a good eater must have good digestion,


and good digestion depends upon a good
conscience.
Benjamin Disraeli (1804-1881)

PDI
The
Abdomen
ADAPTED BY P. EDGAR MD
FROM TEXTBOOK OF PHYSICAL
DIAGNOSIS BY M.H.SWARTZ
BATES: PHYSICAL EXAMINATION

Abdomen: General Considerations


Diseases of abdomen are common
USA: ~10% adult males affected by peptic ulcer disease.
~5% persons >40years has diverticular disease.
~11% all malignancy is cancer large bowel (3rd most common neoplasm, ~10%
all deaths)

~6% lifetime probability for colorectal cancer (1/18 persons)

Risk colorectal cancer differs: African Americans (highest:


50/100,000)

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)

divide abdomen into


four quadrants
right upper
quadrant
right lower
quadrant

Abdomen:
Structure and
Physiology

Nine areas: epigastric, umbilical,


suprapubic, right/left
hypochondriac, right/left
lumbar, right/left inguinal.
costal
margi
n

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)

Chyme (semifluid, creamy material produced by gastric digestion)


intermittent stomach emptying when intragastric pressure
>pyloric sphincter resistance
Stomach emptying normally complete ~6 hours after eating.

Abdomen:
Structure and Physiology
chyme (stomachduodenum): stimulates pancreatic secretion,
gallbladder contraction

Pancreatic enzyme secretion (1-2L)


2hr post-prandial,
Enzymes: lipase: fat, amylase: starch, trysin: protein

Pancreatic insufficiency: bulky/pale stool with offensive


odor
Chyme: neutralizing effect for pancreatic enzymes pH duodenal
contents (acidity)
duodenal ulcer pain
Inflamed gallbladder/pancreas pain at this digestive phase

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

~600mL/d of fluid enters colon200mL/d excreted stool


Abnormal colonic function (diarrhea/constipation)
Colonic mucosal aneurysmal pouches (bleeding if infected, pain
results)

Abdomen: Review of Symptoms

Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice,
Abdominal Distention, Mass, Pruritus (itching)

Pain most important symptom of abdominal disease


calls for speedy diagnosis/therapy
most abdominal disease manifest some pain (abdominal neoplasia
painless).
result from mucosal irritation, smooth muscle spasm, peritoneal
"Where
is the pain?"
"Has the
pain changed
location since it started?"
irritation,
capsular swelling,
direct
nerveitsstimulation

"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?"

Abdomen: Review of Symptoms


Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding,
Jaundice, Abdominal Distention, Mass, Pruritus (itching)

Upper Abdominal Pain or Discomfort


Causes range from benign life-threatening (conduct careful history)
Timing of pain? Acute or chronic? Start suddenly or gradually? When did it
begin? How long does it last? What is pattern over 24-hour period? Weeks or
months? Acute illness or a chronic and recurring one?

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

Abdomen: Review of Symptoms

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.

sudden, severe pain awakening sleep: acute perforation, inflammation,


abdominal organ torsion, biliary/renal stone
Acuteness pain: acute fallopian tube rupture (ectopic pregnancy),
gastric ulcer perforation, pancreatitis (may cause fainting)

Location pain at onset, localization, character, radiation.


abdominal organ rupture: pain felt all over belly (no localization)
small intestine pain: umbilical/epigastric regions (acute
appendicitis)

pain may become localized to other areas (appendicitis pain:


umbilicusRLQ ~1-3hr)

dissecting aortic aneurysm: chest painabdominal pain

Abdomen: Review of Symptoms

Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice,
Abdominal Distention, Mass, Pruritus (itching)

Referred pain: pain originates internal organs but felt in abdominal/chest


wall, shoulder, jaw, other areas supplied by somatic nerves (entering spinal cord
at same segment as organs sensory nerves)

Abdomen: Review of Symptoms


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.

Abdomen: Review of Symptoms

Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice, Abdominal
Distention, Mass, Pruritus (itching)

Time of occurrence and factors that aggravate/alleviate


symptoms (meals or defecation) are particularly important.
Gastric/Peptic Ulcer: periodic epigastric pain (30-60min postprandial)
Duodenal ulcer: pain 2-3hr postprandial or before next meal; food
tends pain,
duodenal ulcer perforation (into pancreas): produce backache
(mimic orthopedic problem).

Nocturnal pain: classic symptom of duodenal ulcer disease.


Abdominal Angina: obstructive vascular disease celiac
axis/superior mesenteric artery in older patients

Abdomen: Review of Symptoms

Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice,
Abdominal Distention, Mass, Pruritus (itching)

Right lower quadrant pain


(RLQ pain) or pain that migrates
from the periumbilical region,
combined with abdominal wall
rigidity on palpation, is most
likely appendicitis.
In women other causes include:
pelvic inflammatory
disease,
ruptured ovarian follicle,
ectopic pregnancy

Abdomen: Review of Symptoms

Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice,
Abdominal Distention, Mass, Pruritus (itching)

Acute Left lower quadrant


pain (LLQ) or
diffuse abdominal pain:
requires
investigation associated
symptoms
(fever, loss of appetite)

LLQ pain with a palpable mass:


diverticulitis.
Diffuse abdominal pain, absent

Abdomen: Review of Symptoms

Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice,
Abdominal Distention, Mass, Pruritus (itching)

Chronic Lower Abdominal Pain


Colon cancer: change bowel habits
with mass lesion
Irritable Bowel Syndrome:
intermittent pain: >12 weeks
relieved by defecation
change frequency of bowel
movements,
change in form of stool (loose,
watery, pellet like),
no structural/biochemical

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

Abdomen: Review of Symptoms

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)

Vomiting complications: pulmonary aspiration into (debilitated,


elderly)

Anorexia: loss/lack of appetite


intolerance certain foods, reluctance due to anticipated
discomfort.
Gastroparesis: anticholinergic medications, gastric outlet

Abdomen: Review of Symptoms

Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice, Abdominal
Distention, Mass, Pruritus (itching)

"How long have you had nausea or vomiting?"


"What is the color of the
vomitus?"
"Is there any unusually foul odor to the vomitus?"
"How often do you
vomit?"
"Is vomiting related to eating?" If yes, "How soon after eating do you vomit?
Vomit only after eating certain foods?"
"Do you have nausea without vomiting?"
"Is nausea or vomiting associated with abdominal pain? Constipation?
Diarrhea? Loss of appetite? Change in stool color? Urine color? Fever? Chest
pain?"
"Have you noticed a change in your hearing ability?"
"Have you noticed ringing in your ears?"
If the patient is a woman, ask "When was your last period?"

Abdomen: Review of Symptoms

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);

obstruction (bile duct, ureter: episodic vomiting at height pain)


intestinal obstruction (contents cannot move distal);
toxins (persistent vomiting)
inflammation of intra-abdominal structures
extra-abdominal conditions (drug toxicity, CNS disorders, MI,
pregnancy)

Not all abdominal emergencies cause vomiting (intraperitoneal


bleeding).

Abdomen: Review of Symptoms

Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice, Abdominal
Distention, Mass, Pruritus (itching)

Pains relationship to vomiting is important and help provide


diagnosis.
acute appendicitis: pain precedes vomiting by a few hours.
Vomitus character aid in determining cause.
acute gastritis: vomit stomach contents.
biliary colic: vomit bilious, greenish-yellow
intestinal obstruction: vomit bilious followed by feculentsmelling fluid.
Feculent vomitus: intestinal obstruction.
Nausea without vomiting: hepatocellular disease, pregnancy,

Abdomen: Review of Symptoms

Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice,
Abdominal Distention, Mass, Pruritus (itching)

Gastric juice is clear, mucoid.

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,

Abdomen: Review of Symptoms

Pain, Nausea and Vomiting,, Rectal Bleeding,


Jaundice, Abdominal Distention, Mass,
Pruritus (itching) Change in Bowel Movements

Diarrhea: water content stool


stool volume
>200grams/24hr
Acute: <2 weeks (infection)
Chronic: >4 weeks (non-infectious)
inflammatory bowel disease (Crohns
Medications:
penicillins,
macrolides,
disease,
Ulcerative
Colitis)

magnesium based antacids, metformin, herbal,


alternative medicines.

Steatorrhea:
Malabsorption: oily residue,
floating, fatty diarrheal stools

(celiac sprue, pancreatic insufficiency,


bowel bacterial overgrowth)
frequentsmall
watery

Small intestine: high volume,


Rectal inflammatory: small volume , tenesmus, diarrhea with
mucus, pus, blood.

Abdomen: Review of Symptoms

Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice, Abdominal
Distention, Mass, Pruritus (itching)

careful history of bowel habits: change in bowel movements


requires elaboration
Acute onset of diarrhea:
postprandial: acute infection/toxin.
watery stools: inflammatory processes small bowel/colon.
bloody diarrhea: shigellosis/amebiasis
"How long have you had the diarrhea?"
"How many bowel movements do you have a day?"
"Did the diarrhea start suddenly?"
"Did the diarrhea begin after a meal?" If yes, "What did you eat?"
"Are the stools watery? Bloody? Malodorous?"
"Is the diarrhea associated with abdominal pain? Loss of appetite?
Nausea? Vomiting?"

Abdomen: Review of Symptoms

Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice, Abdominal
Distention, Mass, Pruritus (itching)

Chronic diarrhea: alternating diarrhea/constipation (colon


cancer,diverticulitis)

loose bowel movements: left colon diseases,


"How
watery
movements:
inflammatory bowel/protein-losing
long have
you had diarrhea?"
"Doenteropathies.
you have periods of diarrhea alternating with constipation?"
"Are
the stools
watery?
Loose? Floating?
Malodorous?"
floating
stools:
malabsorption
syndromes

"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?"

ulcerative colitis: stool mixed with blood/mucus.


small bowel inflammatory disease (small bowel/colon):
blood-stool mix, undigested food.
irritable bowel syndrome: morning diarrhea

Abdomen: Review of Symptoms

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 and caliber of stool change is significant

anal/distal rectal carcinoma: pencil-diameter stools

color of stools change is important.


pale brown-gray stools (bile absence): bile flow obstruction, decreased bile
production

Constipation and weight changes are


important
weight increase: decreased metabolism
(hypothyroidism)
weight decrease: colon cancer, hypermetabolic

Abdomen: Review of Symptoms


Pain, Nausea and Vomiting,
Change in Bowel Movements,
Rectal Bleeding, Jaundice, Abdominal Distention,
Mass, Pruritus (itching)

Constipation:
>12 weeks (of prior 6mo with 2> following) :

<3 bowel movements/wk


>25% straining/sensation
(incomplete evacuation)

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,

Abdomen: Review of Symptoms

Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice, Abdominal
Distention, Mass, Pruritus (itching)

Rectal bleeding: bright red blood, blood-stool mixed, black, tarry


stools.
Hematochezia: bright red blood per rectum BRBPR: colonic
tumors, diverticular disease, ulcerative colitis
"How
long have mixed:
you noticed
bright red
blood diverticular
in your stools?"
Blood-stool
ulcerative
colitis,
disease,
"Istumors,
the bloodhemorrhoids
mixed with the stool?"
"Are there streaks of blood on the surface of the stool?"
"Have you noticed a change in your bowel habits?"
"Have you noticed a persistent sensation in your rectum that you have to
move your bowels but cannot?"

Tenesmus: painful, continued, ineffective straining at stool


inflammation, space-occupying lesion (distal rectum/anus tumor)
Hemorrhoidal bleeding: cause of hematochezia, stool streaked

Abdomen: Review of Symptoms

Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice,
Abdominal Distention, Mass, Pruritus (itching)

Melena: ~100mL UGI


bleeding

Hematochezia: >1000 mL LGI

Abdomen: Review of Symptoms

Pain, Nausea and Vomiting, Change in Bowel Movements,


Rectal Bleeding, Jaundice, Abdominal Distention, Mass, Pruritus (itching)

Inquire about Melena: black, tarry stool (bleeding above first


duodenal section) with partial hemoglobin digestion.

"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)

silver-colored stools: rare but pathognomonic: acholic stools


with melena

Jaundice (icterus): liver parenchymal


disease or bile flow obstruction
from decreased excretion of conjugated
bilirubin into bile

Intrahepatic biliary
obstruction (medical
jaundice)
Extrahepatic biliary
obstruction (surgical

Abdomen: Review of Symptoms

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?"

Abdomen: Review of Symptoms


Pain, Nausea and Vomiting, Change in Bowel Movements,
Rectal Bleeding, Jaundice, Abdominal Distention,
Mass, Pruritus (itching)
conjugated bilirubin
urine bilirubin (dark

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)

Abdomen: Review of Symptoms

Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice, Abdominal
Distention, Mass, Pruritus (itching)

Viral hepatitis: nausea, vomiting, loss of appetite, aversion to


smoking.
Hepatitis A: fecal-oral transmission route, incubation period 2-6wk

linked to ingestion of raw shellfish.

Hepatitis B: blood-borne, incubation period 1-6mo

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)

End-stage Liver Disease secondary to HCV infection: most common


indication for liver transplantation (<50yr) with progressive

Abdomen: Review of Symptoms

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

Abdomen: Review of Symptoms

Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice,
Abdominal Distention, Mass, Pruritus (itching)

Risk Categories for Hepatitis B


Sexual contacts:
sex partners those already
infected,
people >one sex partner in prior
6mo,
people evaluated for STDs
men having sex with men.
People with percutaneous/mucosal
exposure to blood:
IV drug users,
household contacts antigen positive
persons,

Abdomen: Review of Symptoms

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

Abdomen: Review of Symptoms


Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding, Jaundice,
Abdominal Distention, Mass, Pruritus (itching)

Obstructive Jaundice (intrahepatic/extrahepatic): slowly developing


jaundice, pale-colored stools, cola-colored urine
Cholangitis: Jaundice with fever/chills (until proved otherwise).
from bile stasis in bile duct (gallstone, cancer pancreatic head)
Determine if chemicals/toxins (patient's occupation/hobbies)
industrial chemicals/drugs have been associated with liver
disease (viral hepatitis-like illness, cholestasis, granulomas, hepatic
tumors).
Occupational exposure to carbon tetrachloride, vinyl chloride
cause liver disease.
Ask questions related to alcohol abuse.

Abdomen: Review of Symptoms

Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding,


Jaundice, Abdominal Distention, Mass, Pruritus (itching)

Abdominal Distention: related to increased GI gas or presence


of ascites.
from malabsorption, irritable colon, air swallowing (aerophagia)
Gaseous distention related to eating: intermittent, relieved by
flatus/belching.
"How long have you noticed your abdomen to be distended?"
"Is the distention
Ascites:
variety
of
causes
(cirrhosis,
congestive
heart
failure,
portal
intermittent?"
hypertension,
peritonitis,
neoplasia)
"Is distention related
to eating?"

"Is distention lessened by passing gas

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

Abdomen: Review of Symptoms

Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding,


Jaundice, Abdominal Distention, Mass, Pruritus (itching)

Abdominal Mass: neoplasm or hernia.


Abdominal Hernia (inguinal, femoral, umbilical, internal, depending on
location) : protrusion from peritoneal cavity into which peritoneal
contents (omentum, intestine, bladder wall) are extruded.
Most common complaint: swelling (may/may not be painful).
Inguinal hernia: mass in groin/scrotum
Major complications: blood supply interference (intestinal
obstruction/strangulation)

Reducible hernia: can empty contents by pressure/change


in posture.

Newborn with abdominal mass


and gaseous abdominal
distension

Abdomen: Review of Symptoms

Pain, Nausea and Vomiting, Change in Bowel Movements, Rectal Bleeding,


Jaundice, Abdominal Distention, Mass, Pruritus (itching)

Pruritus (itching): common symptom.


Generalized itching: diffuse skin disorder; manifestation of
chronic renal/hepatic disease.
Intense pruritus: lymphoma, Hodgkin's disease, GI
malignancies, dry skin (older persons)
Pruritus ani: localized anal skin itching (fistulas, fissures,
psoriasis, parasites, poor hygiene, diabetes)

Abdomen: Urinary and Renal Disorders

Suprapubic pain
Dysuria, urgency, frequency
Hesitancy, decreased stream
in males
Polyuria or nocturia
Urinary incontinence
Hematuria
Kidney or flank pain
Ureteral colic

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult
developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

patient lying flat in bed


abdomen fully
exposed(sternumknees)
arms at sides,
legs flat.
Frequently, patients place arms behind
head, which tightens abdominal
muscles makes examination more
difficult.

pillow beneath knees aid


relaxation

Examine painful areas last


touching area of maximal
paintightening abdominal
muscles
examination will be more

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

Evaluate General Appearance: valuable information re nature


of condition.
patients with renal/biliary colic writhe in bed (squirm constantly,
find no comfortable position).

patients with peritonitis have intense pain on movement

(remain still in bed, any slight motion worsens pain)

lying in bed, knees drawn

(relax abdominal muscles, reduce intra-abdominal pressure)

pale/sweating patient may be suffering from initial shock


(pancreatitis/perforated gastric ulcer)

Determine Respiratory Rate: RR increased with generalized


peritonitis, intra-abdominal hemorrhage, intestinal obstruction.

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

Inspect Skin: Inspect skin/sclera for jaundice.


evaluated jaundice in natural light
incandescent light masks icterus

Jaundice
apparent: serum
bilirubin
>2.5mg/dL
(adults)

6mg/dL
(neonates)

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

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.

Abdomen: Physical Ex amination

equipment: stethoscope, gloves , lubricant, tiss ues, occult blood tes ting card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

Inspect Hands: wasting (loss of small


muscles hand)?
changes in nail bed (lunula size)
cirrhosis showing Lindsay nails (halfand-halfnails)

Inspect Facies: wasting, poor nutrition


(sunken eyes? temporal wasting?)

Peutz-Jeghers sundrome: perioral skin


melanin deposition (buccal mucoa) of GI
disorders

autosomal dominant disorder

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

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)

lesions may bleed insidiously


(anemia)

autosomal dominant

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

Inspect Abdomen: abdominal contour assessed.


scaphoid (concave): cachexia
protuberant: gaseous intestinal distention, ascites,
organomegaly, obesity.
Standing ascites patient: fluid sinks into lower abdomen;
Supine ascites patient: fluid bulges in flanks. If a patient with
Lateral decubitus ascites patient: fluid flows to dependent lower side .

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

Any asymmetry, distention, masses,


visible peristaltic waves?

observe abdomen from above (for same


signs)

Striae/Scars: silver striae (stretch marks:


weight loss),

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

Common surgical scar locations

Patient asked to cough: inspect


inguinal, umbilical, femoral
areas.
increasing intra-abdominal
pressure (produce sudden bulging)
related to hernia.
If patient had surgery, coughing
may show bulging along previous
incision.
coughing may elicit pain

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

Inspect superficial veins: abdominal venous pattern usually


barely perceptible.
if visible in normal individual: drainage of lower 2/3 rd downward
(caudad)
Distended superficial evaluate
Vena caval obstruction: superficial veins
dilate,
drain cephalad
direction
of drainage:
place tips
index fingers on vein oriented
(toward head)
(not transverse),
Portal hypertension: caput medusacephalad-caudad
dilated
veins
radiate from
compress it using continuous
umbilicus (backflow through collateral veins within
falciform ligament)
pressure
(slide index fingers apart for~3-4in).

Remove one finger; observe refilling


flow direction
Repeat procedure, but this time
remove other finger (observe direction

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

Auscultation of bowel sounds


provides information about motion of
air/liquid in GIT.

Auscultation abdomen
before
percussion/palpation:
more accurate assessment
existing BS (percussion/palpation may
change intestinal motility)

Auscultate (supine position) 1st


over umbilicus then four
quadrants with diaphragm

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

Normal bowel sounds: ~5-10 seconds (high-pitched)


>2 minutes no bowel sounds (absent bowel sounds)
paralytic ileus (diffuse peritoneal irritation).
Borborygmi: rushes low-pitched rumbling (hyperperistalsis)
early acute intestinal obstruction

Rule-Out Obstructed Viscus: succussion


splash (distended abdomen) presence gas/fluid in
obstructed organ.
apply stethoscope over abdomen while shaking
abdomen from sideside.
Rule
presence
of sloshingRubs
sound
indicates distention
Out Peritoneal
: peritoneal
friction
stomach/colon
rub (like pleural/pericardial rub) sound heard during
respiration (inflammation)

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

Percussion: demonstrate presence of gaseous distention, fluid,


solid masses
size/location liver/spleen determined (correct to palpate before
Percuss:
percussion if abdominal pain complaints)
Abdomen
Liver
Spleen
Rule-Out
Ascites

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

Abdomen: (supine) all four quadrants


tympanic: percussion note in abdomen (gas stomach, small bowel, colon)

suprapubic area percussed: dull (distended urinary bladder, enlarged uterus)


Liver: upper liver border percussed right midclavicular line (begin midchest)
percuss downward, chests resonant note becomes liver dull
continues further dull note becomes tympanic over colon
upper/lower liver borders ~10cm apart
Problems predicting liver (percussion):
Ascites: only speculate correct liver size
overestimating liver size (false-positive measurement) percussion upper liver
border difficult
Obesity: problems in percussion/palpation.
Underestimating liver size (false-negative measurement)

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

Spleen: size difficult to determine


begin with percussion (size) normally spleen hidden within rib
cage (Traubes space) against posterolateral wall abdomen (6thrib
superiorly, left anterior axillary line laterally, costal margin inferiorly).

Spleen enlarges: remains close


abdominal wall, tip moves down/toward
midline (anteroposterior)
considerable enlargement occur
without becoming palpable below
CCM
dullness to percussion in

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

Spleen:
Percussion is moderately
accurate in detecting
splenomegaly
sensitivity, 60-80%
specificity, 72-94%

Line passing through


6th rib midclavicular
line

Semilunar shaped
Traubes Space
Line passing though
9th rib midaxillary line

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

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.

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

Ascites: percussion test for shifting dullness

Supine: determine borders tympany/dullness (tympany above dullness: bowel


gas above ascites).

Lateral decubitus: determine borders percussion notes


Shifting dullness: sensitivity 83-88% specificity 56%.
Ascites present: dullness shifts more dependent position; area around
the umbilicus area (initially tympanic) becomes dull (most sensitive sign ascites)
fluid wave: hand in middle abdomen indenting abdomen stop transmission of impulse
by subcutaneous adipose tissue then tap one flank while palpating other side (prominent
fluid wave: positive ascites)

most specific physical diagnostic tests for ascites


specificity 82-92% (false-positive: obese) false-negative (smallmoderate ascites)
bulging flanks: weight free abdominal fluid sufficient push flanks outward

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

common historical items perceived by patients (highest positive


correlation ascites):

abdominal girth: +likelihood ratio (LR+) 4.16 (absence: LR0.17)

weight: +likelihood ratio (LR+) 3.20 (absence ankle swelling LR0.10)

fluid wave presence (LR+ 9.6) or shifting dullness (LR+ 5.76)


absence ascites: absence bulging flanks (LR- 0.12) or edema
(LR- 0.17)

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

Abdominal Palpation: supine, begin palpation in area farthest


from pain location
Light
palpation,systematically
Deep palpation,
Liverabdomen,
palpation,flat
Spleen
palpation,
Light
palpation:
entire
part right
Kidneypads
palpation
hand/finger
(not fingertips), fingers together (sudden jabs avoided), hand
lifted from area to area (not slid over abdomen)

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)

Abdominal Pain: perform gently


Hyperesthesia: lightly stroking pin reveals increased sensation due

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

Deep palpation: determine organ size, abnormal abdominal


masses
Abdominal
flat portion
hand
placed
abdomen, left hand over it, left fingertips
massesright
may be
categorized
in on
several
ways:
exert pressure (gently, steadily), right hand appreciates tactile stimulation
Physiologic: Pregnant uterus
(tender
areas)
Inflammatory: Diverticulitis of the colon
Vascular: An abdominal aortic aneurysm
Neoplastic: Carcinoma of the colon
Obstructive: A distended bladder or dilated loop
of bowel

During deep palpation:


quietly open-mouth breathe (muscular relaxation)
arms at sides.

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

Rule-Out Rebound Tenderness: sign of peritoneal irritation

elicited by palpating (hand 90angle) deeply/slowly remote from suspected


local inflammation; palpating hand is then quickly removed

Rebound tenderness: pain sensation


with pressure release on inflammation
side

generalized peritonitis: ilicit generalized


pain "Which hurts more, now
(while pressing)
or now? (during release)

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

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.

normal liver edge: firm, regular ridge, smooth surface


Liver enlargement: vascular congestion, hepatitis, neoplasm, cirrhosis
hooking technique: another liver palpation method.
stand at patient's head, place both hands below RCCM (dullness area),
press in/up hook liver edge (patient inhales deeply)

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

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

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

Scratch test: difficult to discern enlarged liver edge


stethscope diaphragm (left hand) below RCCM listen while right
index finger scratches abdomen in a semicircle equidistant
from stethoscope.
marked increase sound intensity over liver
palpable liver (not necessarily enlarged/diseased): risk hepatomegaly
(LR+2.5)

non-palpable liver (not rule-out hepatomegaly): likelihood enlarged


liver (LR- 0.45)
enlarged liver detected by scintigraphic
scanning

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

Rule-Out Hepatic Tenderness: tenderness elicited by placing left


palm over RUQ
gently hitting with right ulnar surface
Inflammatory processes liver/gallbladder produce tenderness
on fist palpation
Murphys
sign: during liver
palpation: pain elicited during
inspiration (patient suddenly stops
inspiratory efforts)

suggestive of acute cholecystitis


(inflamed gallbladder descends against
palpating hand producing pain
inspiratory arrest)

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

Spleen palpation: >difficult than liver palpation (not normally


palpable)
Supine (examiner on right) left hand over chest, elevate left rib cage.
right hand flat below LCCM press in/up toward anterior axillary line
left hand exerts anterior force to displace spleen anteriorly.
deep breath, press in (right hand) feel spleen tip as descends during
inspiration.
enlarged spleen tip will
lift right
fingers
upward.
spleen
enlarges
diagonally
repeat right side lateral
decubitus (gravity to bring spleen anterior/downward for
LUQ umbilicus
palpation)

right hand start near umbilicus,


gradually move to LUQ (important

left hand on LCCM while


rightenlarged
handspleen:
palpates
LUQ
if massively
miss
splenic border)

Splenomegaly (splenic
enlargement): hyperplasia,
congestion, infection, tumor,

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

Spleen palpation:
Enlarged spleen expands anteriorly,
downward and
medially, replacing tympany of stomach
and colon with dullness of a solid organ

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

Kidney Palpation: normally neither kidney palpated in adult


(important in young child)

right kidney: deep palpation below RCCM (examiner on right)


left hand behind right flank (between RCCM and iliac crest)
right hand below RCCM, right fingertips pointing to left hand
deep palpation reveals lower pole right kidney (during
inspiration)
smooth, rounded mass
left kidney (examiner on left) left kidney more superior (than right),
may
be normally
mistaken for
Spleen
lower
pole
not palpable.
enlarged left kidney (medial
splenic notch) aids
differentiation

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

Rule Out Renal


Tenderness: upright
patient
make fist,
gently hit
costovertebral angle on
each side
Pyelonephritis: extreme
pain on slight percussion
(digital pressure used)

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

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)

Bladder distention from obstruction:


urethral stricture, prostatic hyperplasia;
neurologic disorders (stroke, multiple
sclerosis)

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

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.

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

Digital Rectal Examination DRE Male: concludes routine


abdominal examination
anterior rectum has peritoneal surface
DRE reveal tenderness if peritoneal inflammation present.

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

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

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

Standing DRE: standing position most commonly used for men


Standing: bent over exam table (common)
examine anus/surrounding tissue
asked to strain: inspect anus for hemorrhoids/fissures
allows for thorough anal inspection and rectum palpation
inflammation, fissures
excoriation, nodules,
fistulas, scars, tumors,
hemorrhoids

Prolapsed Internal

Palpate areas of
tenderness

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

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

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

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

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

Palpate Rectal Walls: lateral, posterior, anterior rectal walls


palpated.
lateral walls: rotate digit along rectal sides,
palpate for polyps: sessile (attached by base), pedunculated
(attached by stalk)

Irregularities, undue tenderness noted


ischial spines,
coccyx,
lower sacrum:
easily palpated

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

only way to examine entire


circumference rectal wall
fully is to turn your back to
patient, allowing you to
hyperpronate your hand
(otherwise unable examine rectal
wall between 12 -3 o'clock
quadrant and small lesion could
go undetected)

Intraperitoneal metastases: anterior to rectum


hard, shelflike (Blumers shelf) structure projects into rectum
(neoplastic infiltration Douglas' pouch)

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

Prostate Gland: anterior to rectal wall


size, surface, consistency, sensitivity,
Shape : bi-lobed, heart-shaped apex heartshape
points toward anus.
Identify median sulcus and lateral lobes.
Size: ~4cm diameter
Surface: smooth, firm
only lower apex portion is palpable.
superior margin too high to reach
Note any masses, tenderness, nodules
Consistency: hard rubber ball.

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

Fecal Occult Blood Test:


examining digit inspected and color of fecal material noted.
fecal material on fecal occult blood test (FOBT) card; use Hemoccult
developer.

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

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

Abdomen: Physical Examination

equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer

Inspection, Auscultation, Percussion, Palpation, Rectal examination, Special techniques

Abdomen: Clinicopathologic Correlations


Evidence that detecting and removing polyps reduces incidence of
colorectal cancer
detecting early cancers lowers mortality rate from colorectal
cancer.
Following guidelines for early detection colorectal cancer (without
increased risk)

age 50yrs, men/women should:


FOBT (fecal occult blood test):
yearly
Flexible sigmoidoscopy:
every 5 years
Annual FOBT and flexible sigmoidoscopy:
every 5 years
Double-contrast barium enema (DCBE):
every 5 years

Abdomen: Clinicopathologic Correlations


Colorectal Cancer: mortality rate
15% (to 33%) by Fecal Occult
Blood Test (FOBT) and diagnostic
evaluation/treatment for positive
tests.
Annual FOBT (rather than
biennial) screening: greater
colorectal cancer mortality
Flexible sigmoidoscopy:
identifies nearly all cancers/polyps
>1cm diameter ;
75-80% small polyps located in

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)

Solids and Liquids: indicates


motility (neuromuscular)
problem.
.

Oropharyngeal

What type of foods provoke symptoms?


Solid foods? Solids and Liquids?
When does dysphagia start?
Are there any associated symptoms?

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)

Three characteristic locations:


Pharyngoesophageal (Zenker's;
pulsion) diverticulum above UES
cricopharyngeus
Midesophagcal (traction) diverticula:
middle third esophagus, inflammatory
conditions (TB)

Abdomen:
Clinicopathologic Correlations
Dysphagia: Esophageal
Diverticula
Zenker's and Epiphrenic Diverticula
motor abnormalities of esophagus
(spasm, achalasia, UES/LES
hyperactivity)

Patients typicallv present in 60s


earliest sign is transient
dysphagia.
as pouch enlarges, more debris
Lateral:
is retained
Zenkers
diverticulum

Abdomen:
Clinicopathologic Correlations
Esophageal Varices: due to portal
hypertension
venous dilation due portal venous
pressure (>12mmHg).
distal esophageal veins thinner
walled

(more prone to bleeding)

Variceal bleeding important cause


UGI bleed (alcoholics, liver cirrhosis)
Portal hypertension leads to stasis

Abdomen:
Clinicopathologic Correlations
Esophageal Varices: Treatment:
Vasopressin (ADH): vasoconstriction
mesenteric vesselsportal venous
flow (initial management).
Somatostatin (octreotide) : inhibits

release vasodilating hormones


(glucagon) indirectly causing
vasoconstriction.
Endoscopy: Definitive treatment:
sclerotherapy or variceal band
ligation.
Balloon tamponade (short-term)

Abdomen:
Clinicopathologic Correlations
Achalasia: failure to relax
characterized by aperistalsis (required for diagnosis)

incomplete relaxation LES with difficulty swallowing (often associated, but not

required for diagnosis).


resting LES tone (associated, not required for diagnosis).

Primary achalasia (most common): absence ganglionic cells in


myenteric plexus (persistent contraction LES) progressive dilation
distal esophagus
Secondary achalasia: impairment esophageal motility.
Chagas' disease (principal cause South America): infestation Tryanosoma cruzi
destroys myenteric plexus (esophagus , duodenum, colon, ureter)

Achalasia-like conditions: amyloidosis, sarcoidosis, carcinoma

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

Symptoms: heartburn, water brash (acidic taste in mouth), dysphagia,


hoarseness, globus sensation (lump in throat), chronic cough (night),
regurgitation .
Definitive diagnosis: endoscopic observation mucosal changes, pH
Longstanding GERD:
monitoring
predispose to Barrett' s
Triad of histologic features keyesophagus
to GERDesophageal
diagnosis: mucosal
adenocarcinoma
inflammation

Eosinophils (advanced cases show neutrophils)


Basal zone hyperplasia
Elongation lamina propria papillae
Treatment: lifestyle, diet changes (smoking cessation, alcohol/caffeine
avoidance (alcohol, caffeine, fatty/acidic/spicy foods, chocolate) antacids,

OTC H2 blockers

Abdomen:
Clinicopathologic Correlations
Barrett' s esophagus: precancerous lesion distal esophagus
complication long-standing GERD

esophageal mucosa undergoes melaplasia (squamousspecialized columnar


epithelial cells containing goblet cells)

gastric-type columnar cells not diagnostic of Barrett' s esophagus .


Incidence: highest in white males (40-60yr) years of symptomatic

GERD.

advanced disease: progressive (weeks-months) solids dysphagia, weight loss,


cough, regurgitation, aspiration (worse at night)

Endoscopic findings: red, velvety Gl mucosa extending upward


from GE junction (contrast to normal pale pink squamous epithelial
mucosa esophagus).

Biopsy: Intestinal-type goblet cells in esophageal columnar

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

Adenocarcinoma: chronic GERDintestinal metaplasia stratified

nonkeratinized esophageal epithelium (Barretts esophagus)dysplasic

Abdomen:
Clinicopathologic Correlations
Esophageal Cancer: continued

Symptoms: dysphagia, weight loss, odynophagia, emesis,


aspiration (secondary TE fistula formation)
incurable once dysphagia is present (>60% esophageal

circumference involved)
Cancer typically spreads locally: surrounding tissue, lymph nodes, lungs,
liver, pleura

Treatment: Periodic screening endoscopy (suspicious lesions);


Contrast radiography (esophageal strictures, ulcerations, ulcerated

mucosal appearance although only high-grade lesions seen)


Esophagectomy: potentially curable lesions
+/- preoperative chemotherapy radiotherapy (5yr survival 25%)

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

Acute Gastritis Stomach


Antrum
Acute
erosive gastritis is a
major cause of
hematemesis.

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)

secondary pernicious anemia


(autoimmune gastritis: antibodies
to parietal cells specifically targeting
H+ , K+-ATPase, IF)

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

Mucosal damage: erosive


ammonia (urea degraded by
H.pylori urease)

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

Presentation: burning, gnawing


epigastric pain (typical, not
specific)
Duodenal ulcers: pain 2-3
hours postprandial, by food
Gastric ulcers: pain with
food, nausea, weight loss

Physical exam: tenderness


epigastric region.
Perforation (DU), peritonitis:
abdominal rigidity/peritoneal
sign

Abdomen:
Clinicopathologic Correlations
Peptic Ulcer Disease: continued

Complication: UGI bleed (melena


or hematemesis)

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

Primary Gastric Lymphoma: stomach most common extranodal


site lymphoma formation (associated H.pylori infection)
Histology: low-grade (MALT lymphomas) to high-grade large-cell nonHodgkins lymphomas
Presentation: asymptomatic until metastases or incurable
extensive growth.
advanced cases present with insidious upper abdominal
pain, post-prandial fullness, early satiety, weight loss,
nausea
Local spread to adjacent organs (direct extension to porta hepatis,

Abdomen:
Clinicopathologic Correlations
Gastric Cancer continued

Metastases to left supraclavicular lymph node (Virchow's node palpable).


Hematogenous spread to ovaries (Krukenberg's tumor: signet ring)
Metastases to umbilicus: produce Sister Mary Joseph's sign.
Suspect: acanthosis nigricans, multiple outcroppings seborrheic keratosis,
(Leser-Trelat sign)

Abdomen:
Clinicopathologic Correlations
Gastric Cancer continued
Diagnosis: double-contrast radiography, CT imaging (very small
lesions)

Lack of distension clue to diffuse-type gastric carcinoma


Definitive diagnosis: biopsy
Treatment: Surgical resection involved gastric tissue/adjacent
lymph nodes,
radiation, chemotherapy
H. pylori antibiotic therapy: treat MALT lymphomas,
subtotal gastrectomy (chemotherapy, radiation): high-grade
lymphomas

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)

Liver deficiencies (inadequate bile salt production,


abetalipoproteinemia)

Decreased intestinal transit time

Abdomen:
Clinicopathologic Correlations
Malabsorption Syndromes continued.

Presentation: Slightly different for each disorder.


generally either chronic diarrhea or
steatorrhea with increased osmotic gap
Diarrhea: differentiate between two types:
24hr fast: secretory diarrhea continues
malabsorptive diarrhea stops
Calculate stool osmotic gap:
[ (2*Na stool + K stool) calculated stool
osmolality]
Osmotic gap >50 (with steatorrhea) indicates
malabsorption

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)

Pathologic findings: mucosal

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)

Symptoms: malabsorptive symptoms with systemic signs infection (fever,


polyarthralgias, generalized pain), multiple organ systems.
Pathohistologic findings: distended lamina propria (small intestine) distinctive
periodic acid-Schiff (PAS)-positive macrophages with pale, foamy
cytoplasm.

Abdomen:
Clinicopathologic Correlations
Diverticular Disease
Diverticula: congenital (entire thickness involved segment) or acquired
(mucosal herniation through muscular laver).

can occur anywhere in Gl tract:


esophagus (Zenker's diverticulum)
small bowel (Meckel's diverticulum)
colon.
Diverticulosis: having diverticula, typically implied as being
colonic.
Diverticulitis: diverticula become infected.

Abdomen:
Clinicopathologic
Correlations
Meckels Diverticulum:
Congenital, true diverticulum
terminal ileum
(incomplete closure
omphalomesenteric duct),

Rule of 2s: ~2% population,


~2ft (60cm) from ileocecal
valve, ~2 inches long, 2%
symptomatic

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).

Incidence: increases with age in Western populations (~50%adults


>50yr),

Typically asymptomatic, discovered incidentally on


colonoscopy , abdominal CT scan, barium enema .
Massive bleeding can occur secondary to vessel erosion in
diverticula.
Diverticulosis: most common cause of painless

Abdomen:
Clinicopathologic Correlations
Diverticulosis:
Treatment: unnecessary unless
bleeding
High-fiber diets suggested
(increase stool bulkcolonic
intraluminal pressure).

Diverticular bleeding managed with


fluids/transfusion (mild-moderate 80%
resolve spontaneously).

Severe: vessel

Abdomen:
Clinicopathologic Correlations
Diverticulosis:
Mesenteric angiography:
diagnostic/therapeutic
(vasoconstriction, artificial blood
clot formation induced)

Diverticulosis may lead to


formation of colonovesical
fistula (pneumaturia: air in urine).

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)

similar to left- sided appendicitis


Investigation:

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

CT scan of the abdomen showing acute


diverticulitis.

Classic triad: pain, palpable


sausage-shaped mass, currantAbdomen:
Clinicopathologic Correlations jelly stools

Intussusception: result telescoping portion proximal bowel into


more distal one (ileocecal junction: <2yr 80%)
most common abdominal emergency in infants, 2nd most
common cause of obstruction (1st pyloric stenosis)
Idiopathic (majority), although seasonal/clinical relationship to
viremia (rotovirus)
Secondary: proximal lead point invaginates into distal segment
an attached mesentery by peristaltic contractions (adults: r/o
cancer) lymphatic obstruction, swelling, perfusion affected
bowel. (Meckels diverticulum, vascular malformations, intestinal
polyps/lymphomas)

Symptoms: sudden onset episodic, crampy, severe abdominal pain

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)

Presentation: Newborn: failure to pass meconium within 1st 48hr,


other bowel obstruction symptoms (bilious vomiting, abdominal
distension)

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

Achalasia: dilated esophageal portion lacks ganglia;

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: Impact of Inflammatory Disease on


Patient
Inflammatory Bowel Disease: group of diseases of unknown
cause
Symptoms: depend on location, extent, acuteness of lesion
Presenting features: fever, anorexia, weight loss, abdominal
discomfort, diarrhea, rectal urgency, rectal bleeding.
chronic, potentially disabling illness (multiple surgeries, fistula
formation, cancer)

Long absences from school/work, disruption of family life,


malabsorption, malnutrition, multiple hospitalizations.
10-30 watery/bloody bowel movements/day.
psychological problems (particularly young adults)

Abdomen:

Impact of Inflammatory Disease on Patient


Sexual development: delayed due malnutrition.
Social development: delayed (constantly remaining near bathroom
inhibits ability develop normal dating patterns), socially immature (social
introversion), remain at home (lives revolve around bowel habits)
Emotional disturbance: positive correlation between disease physical
severity and emotional disturbance extent

Dependency: most reported characteristic, also repressed rage,


feelings suppression, anxieties, constant desire to rid themselves
of life events (diarrhea)
Obsessive-compulsive particularly when ill (worry incessantly about

Abdomen:

Impact of Inflammatory Disease on Patient


Sexual problems are common: interest/participation sexual activity
tend low level (prefer fondled like child, reject any genital contact)
prone to regard sexual activity in anal terms (dirty unclean soiling)
squeamish about body contact, odors, secretions.
loss of libido/decreased sexual drive: fear of bowel action during
intercourse, perineal pain, sexual intercourse may further damage the
bowel
frequent hospitalizations cause anxiety/depression (exacerbate
disease)
fear of cancer (basis of depression), which is a common response

to the disease
emotional factors are important in maintaining/prolonging
existing attack. Schoolwork deteriorates as miss more/more

Abdomen:

Impact of Inflammatory Disease on Patient


Ileostomy: fear disfigurement, loss self-confidence,
potential lack cleanliness, dread unexpected spillage
Time for listening/interest in patient's problem are important
in gaining the patient's confidence.
Listening reveals/aids unravelling emotional problems (source of
exacerbations)

Talking to patient more efficacious than prescribing antiinflammatory agents or tranquilizers.


Careful/thoughtful discussion of illness strengthens doctor-patient
relationship and produces immeasurable therapeutic benefits.

Abdomen:
Clinicopathologic Correlations

Inflammatory Bowel Disease


Mneumonic: Crohn's: think of a
fat granny and an old crone
skipping down a cobblestone
road away from the wreck
(rectal sparing).
Characteristic history
coupled with typical
radiographic and endoscopic
(gross ) appearance mucosa in
addition to confirmatory
histology (colonic biopsy)
IBDs should be differentiated
from: irritable bowel syndrome,
radiation colitis, ischemic

Abdomen: Clinicopathologic Correlations


Clinical Comparison of Ulcerative Colitis and Crohn's Disease

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).

frequent watery diarrhea, abdominal pain/cramping, fever,

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)

Treatment: stop antibiotics, supportive therapy, severe disease


(1st metronidazole, 2nd oral vancomycin)
Antidiarrheals (loperamide): contraindicated: prolong

introduction toxins in colon worsening condition

25yr female Caucasian with


complaints of two weeks
right fossa pain
Residual contrast (from the CT
scan performed the previous
day) is seen in colon and

outlines very prominent


mucosal thickening / edema
(thumb-printing). No
evidence of colonic
dilatation or free gas.
Pancolitis: marked mucosal
edema resulting in
thumbprinting. Diagnosis

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)

Hyperplastic polyps: most common benign polyp.


Other types: submucosal polyps, inflammatory pseudopolyps,
hamartomatuos polyps.
Low rate malignant conversion except in hereditary polyposes
Adenomatous Polyps: dysplastic (malignant potential):
three subtypes: tubular (most common), villous (cauliflower
appearance: highest rate malignant conversion), tubovillous
(intermediate neoplastic rate)

Abdomen:
Clinicopathologic Correlations
Multiple Polyposis Syndromes: several genetic disorders (young
ages)

Polyps and tumors typically arise in proximal (right-sided) colon.


Family adenomatous polyposis (FAP): autosomal dominant
(mutation adenomatosis polyposis coli gene APC), numerous
precancerous colonic polyps (2nd-3rd decade)
diagnoses confirmed if >100 colorectal polyps found.
100% patients develop colorectal cancer
associated periampullary tumors (2nd cause death in patients with
FAP)

Prophylactic colectomy indicated (childhood-early adulthood).

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).

Rarely polyps become cancerous but cause obstruction, pain,

Cancer of Stomach
Major Symptoms

Cancer of Pancreas

Cancer of Colon

Upper abdominal pain

Upper abdominal pain

Change in bowel habits

Occult bleeding

Back pain

Gastrointestinal bleeding

Weight loss

Weight loss

Lower abdominal pain

Vomiting

Jaundice

Anorexia

Dysphagia

Adenomatous polyps

Smoking

Adenomatous polyps

Pernicious anemia

Alcoholism (?)

Ulcerative colitis

Family history

Familial polyposis

Immigrants from Japan

Gardner's syndrome

Villous adenomas

Risk Factors

Abdomen:
Clinicopathologic Correlations
Colorectal Cancer: adenocarcinoma large intestine/rectum

3rd most common cancer,


2nd leading cause cancer related death USA

Risk factors: advanced age, family history, low-fiber diet, villous


adenomas, IBD (especially UC), FAP, Peutz-Jeghers, juvenile
nonpolyposis, HNPCC .
Screening: >50yr: colonoscopy, barium enema, flexible
sigmoidoscopy, fecal occult blood testing.
Colon cancer arising from dysplastic colon adenomas (two hit

hypothesis: genetic mutation with environmental influences stepwise


conversion normal colonic epithelium dysplastic adenomas malignant
adenocarcinoma)
APC gene (early development colon cancer), P53 (later), K-RAS gene

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.

Abdomen: Clinicopathologic Correlations

Symptom
Pain

Cancer Right
Colon
Ill defined

Cancer Left
Colon
Colicky

Cancer
Rectum
Steady, gnawing

Obstruction

Infrequent

Common

Infrequent

Bleeding

Brick-red

Red mixed with Bright red


stool
coating stool

Weakness

Common

Infrequent

Infrequent

Variation of Symptoms of Cancer of the Right Colon, Left


Colon, and Rectum

Abdomen:
Clinicopathologic Correlations
Colorectal Cancer continued.

Abdomen:
Clinicopathologic Correlations
Colorectal Cancer continued
Diagnosis: colonoscopy with tissue biopsy (adenocarcinoma gold
standard).

CT scan look for metastases.


Screening recommended (>50yr): colonoscopy, fecal occult blood
testing, flexible sigmoidoscopy, barium enema, digital rectal exam)
Carcinomaembryonic antigen (CEA) not recommended: useful for
evaluating surgical success and monitoring growth/recurrence of cancer

Treatment: surgical resection, chemotherapy (fluorouracil)


metastasize hematogenously, lymphatics (region lymph nodes, liver,
lungs, peritoneum, bone, brain)
Prognosis: stage tumor (favorable if detected early before metastases).

Widespread: 5yr survival <10%

Abdomen:
Clinicopathologic Correlations
Appendicitis: most common
indication emergency
abdominal surgery children,
(can occur all age groups, peak 1530yrs)

Presentation: classic: fever,


periumbilical abdominal pain
localizing to RLQ (McBurneys
point), peritoneal irritation
(anorexia, vomiting, constipation,
diarrhea)

McBurneys point: 2/3rd distance


umbilicus to anterior superior iliac
spine.

Abdomen:
Clinicopathologic Correlations
Appendicitis continued
Diagnosis: lab: leukocytosis, pyuria, fecal
leukocytes
Abdominal X-ray: 2/3rd cases:
radiopaque fecaliths (impacted in
appendix)

Abdominal CT: diagnostic (particularly


equivocal cases)

Differential diagnosis: diverticulitis


(elderly), ectopic pregnancy (r/o hCG)
Treatment: surgical appendectomy
(necessary/curative)

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)

Inguinal hernias: male (direct, indirect) present identically,


treated same
Patient complaints: inguinal bulge, exacerbated by
intraabdominal pressure (coughing, straining, defecation, lifting
weight), feeling of heaviness groin.
Femoral hernias: women: present with palpable lump medial

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

Inguinal hernia (male):


push finger into skin scrotum,
directing laterally, up toward
internal inguinal ring
Valsalva maneuver (coughing)
pushes hernia against finger
Women: hernia palpated directly
over internal inguinal ring on
Valsalva maneuver.

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)

Clinical diagnosis: presentation, history of alcohol abuse.


Classic: nausea, malaise, tachycardia, low-grade fever
Portal hypertension: ascites, hematemesis (esophageal varies)
encephalopathy (asterixes, altered mental status)

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

Tissue exam: steatosis, neutrophilic infiltrate , centrilobular


ballooning necrosis hepatocytes , Mallory's hyaline inclusion
bodies.
Treatment: completely reversible (alcohol abstinence), nutritional

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,

Abdomen: Clinicopathologic Correlations


Signs and Symptoms of Cirrhosis

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):

Clinical presentation: complex,


hepatocellular damage, diffuse hepatic
tissue scarring with portal hypertension
Impaired Liver
(Hepatocellular
(combination
ofFunction
both)
Damage)
Jaundice, Pruritis: inability liver conjugate
bilirubin,
Hypoalbuminemia: impaired albumin
synthesis
Hyperestrogenism: spider hemangiomas,
palmar erythema, gynecomastia,

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).

Ultrasound: evaluate splenomegaly, ascites, portal vein


thrombosis, HCC.

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

4 points of anastomosis between portal system


Venal caval system. Portocaval anastomosis.
1.Paraumbilical veins: superficial/inferior
epigastric
veins
2.Superior rectal veins: inferior/middle
rectal veins
3.Colic twigs: lumbar segmental/renal
venous
branches
4.Esophageal veins of abdomen:

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)

>40yr: weakness, weight loss, abdominal pain,


loss libido, cirrhosis (iron deposits affecting
hepatocyteshepatomegaly, stigmata chronic liver
disease), type 1 diabetes: bronze diabetes (iron
deposition pancreatic islet cells and deposition in
skinmelanin production/darker skin), heart failure

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)

Chronic disease: fatal without treatment


Diagnosis: serum ceruloplasmin levels, serum/urine copper
levels.
Confirm with liver biopsy

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)

20% Americans have gallstones (~50% become symptomatic)


Three types: cholesterol stones,
mixed stones, pigmented
(bilirubin) stones
Stones form:
Disruption Cholesterol transport from
liver into bile (coupled with simultaneous
secretion phospholipid/bile salts) cholesterol
gallbladder precipitation (stone formation)
Cholestrol load > bile salts: bile salts,
lecithin unable to solubilize cholesterol.
Disrupted bile salt production (bile acid

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)

Treatment: elective cholecystectomy, modified diet


Prognosis:
goodRecurrent biliary colic (intermittent pain from blockage
Complications:
cystic duct), acute cholecystitis (inflammation/infection gallbladder),
choledocholithiasis (stone common bile duct), gallstone ileus, acute

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)

Positive HIDA scan=Obstruction


passage
=Nonvisualization GB: confirms

Abdomen:
Clinicopathologic Correlations
Acute Pancreatitis: activation
pancreatic enzymes (pancreatic
autodigestion, hemorrhagic fat necrosis)

Classically presents: sudden onset boring


epigastric abdominal pain radiating to
back/flanks, anorexia, nausea (after large
meal, drinking binge)

Diagnosis: clinical symptoms, imaging,


leukocytosis, serum amylase (>5*upper
limit normal), lipase (>specificity, longer
persistence)

Histology: fat necrosis, pale basophilic

Abdomen:
Clinicopathologic Correlations
Acute Pancreatitis continued.
Contrast-enhanced CT: severe
pancreatitis
(r/o pseudocyst, fully visualize extent
disease)

Treatment: rest, gastric suction,


fluid/electrolyte replacement, pain
control (opioids: meperidine).
Surgical treatment (trauma, ductal stones,
obstructive lesions, infected pancreatic
necrosis)

Prognosis: ~20% patients have

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)

Clinically: pain persistent, deep-seated, unresponsive to antacid,


worsened by ingestion fatty foods/alcohol
Symptoms: pancreatic insufficiency (steatorrhea, weight loss, deficiencies
fat soluble vitamins: ADEK)

Diagnosis: serum amylase, lipase not elevated


Classic triad: progressive parenchymal fibrosis with pancreatic

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)

catalyzes transfer amino groups to form oxaloacetate


Lab test interpretation: along with AST in blood with liver
damage.
Levels ~magnitude liver damage. (with RHF, myocardial ischemia,
extensive trauma)

AST: ALT ratio: relatively nonspecific measures liver damage


y-Glutamyl Transferase (GGT)
present in hepatic, biliary epithelial cells,
induced by alcoholic intake

Abdomen:
Clinicopathologic Correlations
Alkaline Phosphatase (AlkP, ALP)
synthesized: liver, bone, intestine, placenta.
nonspecific indicator tissue damage (liver, bone, intestine,
placenta).

: obstructive hepatobiliary disease, bone disease (Paget' s


disease , bone metastases)

hyperparathyroidism, pregnancy (third trimester), Gl disease


(perforated ulcer,
Best tool for recent alcohol use is alkaline phosphatase)

Amylase
synthesized: pancreas, salivary glands (also ovaries, intestines,
skeletal muscle)

Abdomen:
Clinicopathologic Correlations
Lipase
synthesized: pancreas, liver, intestine, stomach, tongue, others

hydrolysis glycerol esters, long-chain fatty acids.

Lab Test interpretation: pancreatic pathologies (acute/chronic


pancreatitis, pseudocyst, malignancy) cystic fibrosis, intestinal
malignancy, IBD, peritonitis, biliary disease, liver disease
Prothrombin Time
synthesized in liver
Screening test: extrinsic coagulation pathway, monitor
warfarin therapy
relatively rapid/sensitive indicator hepatic capacity for protein

Abdomen: Clinicopathologic Correlations


Carcinoma of Prostate: often posterior lobe (easily identified DRE)
second leading cause of male death USA
hard, irregular nodule (asymmetry) suggestive of cancer.
early detection usually limited to detection of abnormality on
DRE.
Benign Prostatic Hyperplasia: symmetrically/diffuse enlarged,
soft gland
protrudes into rectal lumen.
common among men>60yr
Acute
rectal
examination
is concluded
Prostatitis:
boggy,
fluctuant, tender prostate
Seminal
inform patient
yousuperior
are withdrawing
your
finger.
Vesicles:
to prostate
gland
(rarely felt, unless
enlarged)
gently remove examining finger, and give patient tissues to

Prostate
Cancer

Abdomen: Clinicopathologic Correlations


Prostate cancer: leading cancer diagnosed among men USA (33%
all male cancers) racial/ethnic variations in Surveillance
Epidemiology End Results (SEER) Study:
incidence rate African-American men (highest in world: 181/100,000)
>7x Koreans (24/100,000: most recent Asian immigrants).
Caucasian quite high <African-Americans. (Asian, Native American
lowest rates)

~9/10 prostate cancers (86%) diagnosed at localized stage (5-yr


survival rate 100%)

Incidence rates continue to increase (increased screening tests).


found early by DRE and testing blood prostate-specific antigen
(PSA)

Abdomen: Clinicopathologic Correlations


PSA (Prostate Specific Antigen): made by normal prostate gland (most
semen, small amount blood)

PSA two major forms in the blood.


bound (attached) to blood proteins (total)
circulates free (unattached).
percent-free PSA test: indicates amount PSA circulating free vs
total PSA level
Normal: >0.25 (cancer incidence 9-16%)
percentage of free PSA: prostate cancer < than in
normal men
Most men have PSA levels <4ng/mL

Prostate cancer 25%: >4ng/mL but <10 ng/mL

Abdomen: Clinicopathologic Correlations


PSA continued
PSA level can be affected by many factors:
noncancerous enlargement of the prostate (benign prostatic
hyperplasia BPH); prostatitis.
rise slowly with aging.
Ejaculation: temporary PSA levels (abstain from ejaculation for 2
days before testing)

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

Intravenous urography showing an


ectopic left pelvic kidney with the
stone lying in pelvis

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)

Presentation renal ectopy: obstructive


hydronephrosis, vesicoureteric reflux. Present
with pain/infection (pyelonephritis, renal stones) or
silent (discovered incidentally)
Diagnosis: incidental, or investigating for
symptoms of associated anomalies.
Treatment: surgical (challenging due to aberrant

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

Ectopic fused kidney and ectopic ovaries


(arrows)

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)

Lymphatic drainage: lumbar


nodes

Abdomen:
Clinicopathologic Correlations
Kidney continued.
Urinary Casts (protein matrix: TammHorsfall mucoprotein)

Casts seen on urinalysis may be


an indication of tubular pathology
Cells within casts reveal
intrarenal source
Casts indicate hematuria/pyuria
is of renal origin.
Other casts (hyaline casts) seen
normal individuals, lowintravascular states

Abdomen:
Clinicopathologic Correlations
Kidney continued.
Glomerulopathy: applies group conditions affecting glomeruli.
Divided into two major groups based on pathogenesis and clinical
manifestations.

Type II hypersensitivity: Anti- GBM diseases; linear deposits IgG


along the GBM; (Goodpasture's, Type I rapidly progressive glomerulonephritis
RPGN).

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

intact GBM negatively charged, preventing filtration proteins in urine


negative charge lost loss plasma proteins (predominantly lowmolecular-weight albumin) in urine.
Massive proteinuria (>5.5 g/24h): oncotic pressure edema (fluid into
interstitial space)

intravascular volume RAAS, sympathetic activation, release


vasopressin, atrial natriuretic peptide renal electrolyte/water retention
edema

Hypoalbmninemia (plasma albumin level <5 g/dl,) secondary to


proteinuria

Abdomen:
Clinicopathologic Correlations
Nephrotic Syndrome continued..
Hypercoagulability: secondary loss anticoagulant factors through
damaged glomeruli
different pathologies result in nephrotic syndrome (diagnosis:
renal biopsy)

High ratio of low- to high-MW proteins (albumin to globulin) indicates


highly selective proteinuria, with albumin and transferrin in urine.
Hallmarks Nephrotic Syndrome: edema (excessive fluid):
periorbital puffiness (morning), pitting edema legs, pleural effusion,
ascites proteinuria (> 3.5 g/24 h), hypoalbuminemia, edema,
hyperlipidemia,

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)

2. The spot urine protein:creatinine ratio can be a quick tool to


look for nephrotic range proteinuria
3. The secondary causes of nephrotic range proteinuria: think of
tumor, drugs, infections, and systemic causes

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%)

Diagnosis: dependent on renal biopsy (made with electron microscopy)


Treatment: high dose corticosteroids*8wk (prednisone)
Treatment failure: failure to achieve lasting remission (relapse during
steroid therapy, recurrence >3*yr after steroid taper): alkylating agents
(cyclophosphamide, chlorambucil)

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)

common cause of nephrotic syndrome in adults; nonselective


proteinuria
Cause: unknown: 33% adult nephrotic syndrome (50% AfricanAmericans)

Presentation: nephrotic syndrome, nonselective proteinuria,


hypertension, mild hematuria, mild renal function (associated
with IV abuse: heroin)

Diagnosis: renal biopsy (light microscopy: focal/hyaline masses,

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)

association with systemic lupus


erythematosus, rheumatoid arthritis,
hepatitis B/C, syphilis, schistosomiasis,
malaria, leprosy,
previous use gold/penicillamine

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)

Treatment: oral glucocorticoids,


cyclophosphamide, cyclosporine
(proteinuria, slow decrease GFR),

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)

Type 2 (33%): Unknown pathogenesis: C3 nephritic factor (G3NeF:


dense deposit disease: dense deposition unknown substance between lamina
densa-GBM subendolhelial space)

C3: convertase-specific autoantibody preventing degradation

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)

Diagnosis: clinical presentation and renal biopsv (thickening


GBM,proliferation mesangial cells). Electron microscopy:
GBM divided by electron-dense material.
Type I: subendothilial, electron-dense deposits IgG/C3.
Type 2: inramembranous deposits, increased size glomeruli,
increased cellularity mesangial cells, capillary wall (double contour)
tram-track appearance (GBM splitting)

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)

Treatment: started before symptoms


progress to overt nephrotic syndrome
Microalbuminuria: start ACE inhibitiors
(delay progression nephropathy in diabetic

Abdomen:
Clinicopathologic Correlations
Renal Amyloidosis: deposition fibrous, insoluble proteins in
extracellular space (glomerulus)
Amyloidosis: multisystemic disorder of protein folding (acquired,
hereditary)

Two renal types:

Amyloid L (AL): immunoglobulin light chains (multiple myeloma)


Amyloid A (AA): chronic inflammatory conditons (inflammatory bowel)

Presentation: nephrotic-range proteinuria correlates to renal


involvement
Diagnosis: biopsy (renal, abdominal fat pad, rectal) stained Congo red
(amyloid apple-green birefringence under polarized light) mesangial
expansion, amorphous hyaline material, thickening of GBM

Proper diagnosis: detailed


history, serum chemistry,
Abdomen:
Clinicopathologic Correlationsurinalysis, pathology.
Nephritic Syndrome: inflammation glomerulus.
Hematuria, oliguria, azotemia, hypertension are hallmarks of
nephritic syndrome.
Complex of symptoms (different types but all display following core
symptoms):
Hematuria: destruction glomerular capillaries, loss RBCs into Bowmans
space urinalysis: dysmorphic RBCs, RBC casts
Oliguria: infiltration inflammatory cells, immune complex
depositionobstruction glomerular capillary lumenGFR oliguria
<400mL/d and azotemia BUN creatinine
Hypertension: renal fluid retention: GFR
Mild proteinuria: glomerular capillary injury
Presumptive diagnosis: clinical suspicion (definitive diagnosis renal
biopsy)

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

Presentation: nephritic syndrome


10d post pharyngeal infection,
14-21d post skin infection

Diagnosis: history, clinical findings (nephritic syndrome),


Serum chemistry (ASO antistreptolysin-O titers; streptococcal antibodies:
anti-DNAse B 90% patients; C3 levels, negative ANCA, negative anti-

Abdomen:
Clinicopathologic Correlations
Acute Proliferative Glomerulonephritis (Poststreptoccocal,
lnfectious):

Pathology: renal biopsy,


light microscopy (hypercellular, enlarged glomeruli)
electron microscopy (subepithelial electron-dense deposits)
immunofluorescence lumpy-bumpy appearance (IgG, C3 coarse
Treatment:
conservative, maintain
granular deposits)
proper water/electrolyte balance
(diuretic, antihypertensive), penicillin (rarely)
Prognosis: excellent (children recover
completely when adequately treated)

Abdomen:
Clinicopathologic Correlations
Rapidly Progressive Glomerulonephritis RPGN: malignant
nephritic syndrome with progressive loss kidney function (adults 3060yr, male>female, weeks-months after primary insult)

Presentation: classic nephritic syndrome varies on underlying


cause.
Three types:
Type I: Goodpastures syndrome: ANCA-negative, linear IgG, C3
deposits GBM.
Type II: Post-streptococcal GN, SLE, IgA nephropathy, HenochSchonlein purpura:
ANCA-negative , granular lumpy-bumpy

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:

Calcium oxalate/phosphate (most common):


absorb more calcium gut than excrete in urine; primary renal
defect calcium reabsorption, hypercalcemia (secondary

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)

Tumor lysis syndromes (alkalinisation urine, allopurinol, hydration)


more likely form in acidic urine

Cystine: genetic defects metabolism cystine, ornithine,


Iysine, arginine.

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)

no value uric acid, cysteine (radiolucent)


Non-contrast CT
Urinalysis: hematuria
Treatment: depends on size stones, increased fluid intake, pain
management (stones<9mm). Larger stones (noninvasive:
extracorporeal shockwave lithotripsy) surgical (nephrolithotomy)
Alkalinize urine in clinical conditions that trigger uric acid stone

X-ray KUB showing three opacities: calculi


right kidney and lower ureter.
Bilateral
staghorn renal calculi

Abdomen:
Clinicopathologic Correlations
Urinary Tract Infections: usually bacterial lower urinary tract
(treat antibiotics)

Outpatient: common young sexually active females (short female


urethra, small distance between urethra-anus)
Inpatient: Foley catheter use (asymptomatic: need high suspicion febrile
inpatient) Pregnancy: Asymptomatic bacteriuria (higher risk
pyelonephritis, preterm labor, low birth weight) always treated

Children: recurrent UTIs evaluate vesicoureteral reflux


Presentation: uncomplicated: dysuria, frequency, urgency,
suprapubic pain, hematuria (no fever, nausea, vomiting, costovertebral
tenderness)

Diagnosis: history alone, clean-catch urinalysis (pyuria: PMNs,


bacteriuria, leukocyte esterase, nitrites)

Abdomen:
Clinicopathologic Correlations
Acute Pyelonephritis: infection usually bacterial upper urinary
tract (kidney)
ascending infection from lower urinary tract (smaller numbers than
LUTI)

Presentation: fever, nausea, vomiting, flank pain, CVA tenderness


presence/absence LUTI: dysuria, frequency, urgency

Diagnosis: tenderness, history, physical examination (vital signs,


CVA tenderness),
UA, urine culture (antimicrobial sensitivities)
Urinalysis: pyuria, WBC casts (pathognomonic for acute pyelonephritis).
Microbiology: same pathogens as LUTI will demonstrate pyuria .

Abdomen:
Clinicopathologic Correlations
Chronic Pyelonephritis: recurrent/persistent renal infection
(irreversible pathologic changes corticomedullary renal region)
structural abnormalities (obstruction: stone, BPH; vesicoureteral reflux)

Presentation: asymptomatic pyuria, low-grade fever, flank pain,


nausea/vomiting, renal insufficiency (hypertension, proteinuria, failureto-thrive in children)

Diagnosis: renal ultrasound (evaluate renal damage) CT scan, voiding


cytourethrogram (vesicoureteral reflux)
Laboratory: pyuria, proteinuria, azotemia
Pathology: chronic inflammation, asymmetric corticomedullary
scarring, deformities renal pelvis/calyces, thyroidizaton kidney

Abdomen:
Clinicopathologic Correlations

Abdomen:
Clinicopathologic Correlations

Abdomen: Clinicopathologic Correlations


Useful Vocabulary
lapar( loin; flank
aerophagi Air
a
swallowingo)celi(o)- abdomen celiac
Pertaining
to
abdomen
eating
chol(e) bile
cholelith Gallstone phago
cyst- sac
cholecysti Inflammati
containing tis
on
liquid
gallbladde
-tripsy shock
r
waves
enter( intestines enteritis Inflammati
o)on small
intestines
aer(o)- air; gas

laparoto Surgical
my
incision
flank;
abd.
incision
phagocy cell
te
ingests
cells or
microorga
ni
lithotrips Noninvasi
y
ve
technique
for

Abdomen: Clinicopathologic Correlations


Abdomen is scaphoid without scars. Bowel sounds are
Abdomen has a scar in RUQ
present.
Liver felt 2 fingerbreadths below RCCM (total span 10cm). Bowel sounds are absent.
Marked tympany throughout
Neither spleen nor any masses felt.
abdomen. Rigidity is present
Kidneys are not palpable.
throughout.
Rectal examination reveals normal sphincter tone.
Marked tenderness present in
Prostate is soft, without any masses.
abdomen, especially LLQ
Rectal walls of the rectum are smooth, without masses.
Examination rectum reveals
Testing stool for blood is negative.
tenderness in same area (LLQ).
No
costovertebral
angle
tenderness
(CVAT)
is present.
Abdomen
is scaphoid
and
soft, without
guarding,
rigidity, or
Stool guaiac test is 4+.
tenderness.
Liver, spleen, kidneys not felt.
Bowel sounds are present.
No CVAT is present.
Liver measures 12cm in midclavicular line.
Spleen tip is felt below LCCM
No masses are present.
Rectal examination reveals 2cm hard, nontender nodule prostatic
posterior lobe

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