Physical Examination Abdomen

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:
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:
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:
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?"

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
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
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)

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.
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
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
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
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
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
"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?"
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).
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,
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,
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.
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?"
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
"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

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,
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
Melena: ~100mL UGI

bleeding
Hematochezia: >1000 mL LGI

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
"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?"

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)
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
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
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,
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

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.

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

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

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
equipment: stethoscope, gloves, lubricant, tissues, occult blood testing card, Hemoccult developer
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.
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)
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
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
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
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 .
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
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
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
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)
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: (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)
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
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
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.
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
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)
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
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.
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)
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)
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
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
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)
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,
Spleen palpation:
Enlarged spleen expands anteriorly,
downward and
medially, replacing tympany of stomach
and colon with dullness of a solid organ
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
Rule Out Renal

Tenderness: upright
patient
make fist,
gently hit
costovertebral angle on
each side
Pyelonephritis: extreme
pain on slight percussion
(digital pressure used)
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)
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.
Digital Rectal Examination DRE Male: concludes routine

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

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:
Screening colonoscopy:
identify/remove
cancers/premalignant
lesions throughout
colon/rectum
Abdomen:
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:
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:
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:
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:
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:
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:
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:
Heartburn:
retrosternal burning
pain/discomfort,
Weekly (>often)
Aggravated:
food (alcohol,
chocolate, citrus fruits,
coffee onions,
peppermint)
positions (bending
over, exercising,
Abdomen:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
Diverticulosis:
Mesenteric angiography:
diagnostic/therapeutic
(vasoconstriction, artificial blood
clot formation induced)
Diverticulosis may lead to

formation of colonovesical
fistula (pneumaturia: air in urine).
Abdomen:
Diverticulitis:
Most common
complication
diverticulosis (infection
secondary impacted
fecalithlymphatic
obstructionlocalized
ischemiabacterial
overgrowth)
Abdomen:
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:
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:
Intussuscepti
on:
Investigation:
Abdominal
ultrasound:
birds-eye or
coiled-spring
pattern
(invagination
proximal
segment).
Abdomen:
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:
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:
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:
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:

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:

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:
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

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:
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:
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:
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:
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:
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:
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:
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:
Colorectal Cancer:
>50yr presenting with stool
changes (melena, hematochezia,
pencil-thin caliber), abdominal
discomfort, constitutional
symptoms (weight loss),
unexplained anemia
Left-sided (sigmoid)
colon cancer: early symptoms obstruction
(men/postmenopausal
women)
(narrower lumen).
tumors produce napkin-ring, apple-core constriction
(encircling annular growth)
stool solid.
Right-sided colon cancer: anemia, weight loss, abdominal pain.
Symptom
Pain
Cancer Right
Colon
Ill defined
Cancer Left
Colon
Colicky
Cancer
Rectum
Steady, gnawing
Obstruction
Infrequent
Common
Infrequent
Bleeding
Brick-red
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:
Colorectal Cancer continued.
Abdomen:
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:
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:
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:
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:
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:
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:
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:
Hernias continued
Femoral hernias: palpated medial
femoral pulse, inferior inguinal ring.
CT scan, ultrasound: those difficult
to palpate (obese)
Treatment: surgical repair
(herniorrhaphy)
Abdomen:
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:
Abdomen:
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:
Alcoholic Hepatitis continued
Abdomen:
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,

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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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

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

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)

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

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
Pelvic and Horsehoe
Kidneys
Intravenous urography showing an

ectopic left pelvic kidney with the
stone lying in pelvis
Abdomen:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
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:
Diabetic Nephropathy:
Abdomen:
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:
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:
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:
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:
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:
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:
Abdomen:
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:
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:
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:
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:
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:
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:
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:
Abdomen:

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 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

Physical Examination Abdomen

Enviado por

Dados do documento

Direitos autorais

Formatos disponíveis

Compartilhar este documento

Compartilhar ou incorporar documento

Opções de compartilhamento

Você considera este documento útil?

Este conteúdo é inapropriado?

Direitos autorais:

Formatos disponíveis

Physical Examination Abdomen

Enviado por

Direitos autorais:

Formatos disponíveis

A good eater must be a good man;

for a good eater must have good digestion,

Abdomen: General Considerations

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

Risk colorectal cancer differs: African Americans (highest:

divide abdomen into

Nine areas: epigastric, umbilical,

Chyme (semifluid, creamy material produced by gastric digestion)

Pancreatic enzyme secretion (1-2L)

Pancreatic insufficiency: bulky/pale stool with offensive

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

Abdomen: Review of Symptoms

Pain most important symptom of abdominal disease

Abdomen: Review of Symptoms

Upper Abdominal Pain or Discomfort

Abdomen: Review of Symptoms

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

Location pain at onset, localization, character, radiation.

pain may become localized to other areas (appendicitis pain:

dissecting aortic aneurysm: chest painabdominal pain

Abdomen: Review of Symptoms

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

Abdomen: Review of Symptoms

Abdomen: Review of Symptoms

Time of occurrence and factors that aggravate/alleviate

Nocturnal pain: classic symptom of duodenal ulcer disease.

Abdomen: Review of Symptoms

Right lower quadrant pain

Abdomen: Review of Symptoms

Acute Left lower quadrant

LLQ pain with a palpable mass:

Abdomen: Review of Symptoms

Chronic Lower Abdominal Pain

Abdomen: Review of Symptoms

Vomiting complications: pulmonary aspiration into (debilitated,

Anorexia: loss/lack of appetite

Abdomen: Review of Symptoms

"How long have you had nausea or vomiting?"

Abdomen: Review of Symptoms

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

Not all abdominal emergencies cause vomiting (intraperitoneal

Abdomen: Review of Symptoms

Pains relationship to vomiting is important and help provide

Abdomen: Review of Symptoms

Gastric juice is clear, mucoid.

Abdomen: Review of Symptoms

Pain, Nausea and Vomiting,, Rectal Bleeding,

Diarrhea: water content stool

magnesium based antacids, metformin, herbal,

(celiac sprue, pancreatic insufficiency,

Small intestine: high volume,

Abdomen: Review of Symptoms

careful history of bowel habits: change in bowel movements

Abdomen: Review of Symptoms

Chronic diarrhea: alternating diarrhea/constipation (colon

loose bowel movements: left colon diseases,

ulcerative colitis: stool mixed with blood/mucus.

Abdomen: Review of Symptoms

Constipation and caliber of stool change is significant

anal/distal rectal carcinoma: pencil-diameter stools

color of stools change is important.

Constipation and weight changes are

Abdomen: Review of Symptoms

<3 bowel movements/wk