ESOPHAGUS 4 Near gastroesophageal *acid hyposecretion

junction
Constrictures Level cm from incisors 5 Anywhere in the Medication induced
Cricopharengeal C6 Male- 15 stomach (NSAID)
muscle Female 14
Crossing of left m. T5/T4 24-26
bronchus and aortic
arch
Gastro esophageal T10 Male 40
sphincter Female - 38
(diaphragm)
*the esophagus is 23-25 cm long

Arterial Blood supply

Cervical portion Inf. Thyroid artery

Thoracic portion Bronchial arteries
Abdominal portion Ascending branch of left
gastric artery
Inferior phrenic artery

*The branch that the posterior vagus sends to the

Venous Drainage
Esophageal veins inf. Thyroid vein bronchial,
azygos or hemiazygous vein coronary vein
* the submucosal venous networks of the esophagus
is continuous with the stomach, and in portal venous
obstruction this communication functions as collateral
for portal blood to enter the SVC via azygos vein
STOMACH
Arterial Blood Supply
posterior fundus is termed the criminal nerve of
Grassi. This branch typically arises above the
esophageal hiatus and is easily missed during truncal
or highly selective vagotomy (HSV). Vagal fibers
originating in the brain synapse with neurons in
Auerbachs myenteric plexus and Meissners
submucosal plexus.
Gastric Hormone:
Notes
Gastrin produced by antral G cells and is
the major hormonal stimulant of
acid secretion during the gastric
phase

Luminal peptides and amino acids

are the most potent stimulants of
gastrin release, and luminal acid is
the most potent inhibitor of
gastrin secretion.

Blocked by H2 antagonists
Types of Peptic ulcer

Duodenal ulcer 1-2 cm of the pylorus Somatostatin produced by D cells located

throughout the gastric mucosa.
Gastric Ulcer (Modified Johnson Category):
inhibits acid secretion from parietal
Location *notes cells and gastrin release from G
1 Near angularis incisura Often due to acid cells.
on the lesser curvature hyposecretion
(most common) It also decreases histamine
2 Body of the stomach + Pyloric stenosis release from ECL cells
duodenal ulcer *acid Gastrin- mammalian equivalent of
hypersecretion Releasing bombesin, In the antrum, GRP
3 Prepyloric *acid hypersecrtion Peptide
 stimulates both gastrin and Hepatic Artery Carries O2 blood
somatostatin accounts for 25 %
hepatic blood flow
given peripherally, it stimulates acid
secretion, but when it is given The cystic artery feeding
centrally it inhibits acid secretion, the gallbladder usually
arises from the
mediator of gastroprotective right hepatic artery in
increased mucosal blood flow Calots triangle
in response to luminal irritants
Leptin primarily synthesized in adipocytes. Portal Vein formed by the
It is also made by chief cells in the confluence of the
stomach to decrease food intake in splenic vein
animals and the superior
mesenteric vein
leptin, a satiety signal hormone,
and ghrelin, a hunger Accounts for 75 % of
signal hormone hepatic blood flow and
Ghrelin Ghrelin is a potent secretagogue of drains the splanchnic
pituitary growth hormone circulation

orexigenic regulator of appetite The portal vein pressure

Resection of the primary source of in an individual with
this hormone (i.e., the stomach) normal physiology is
may partly account for the low
anorexia and weight loss at 3 to 5 mmHg. The
portal vein is valveless,
however, and in
the setting of portal
hypertension, the
pressure can be quite
high
(20 to 30 mmHg)

Pringle maneuver - to clamp the hepatoduodenal

ligament (free border of the lesser omentum)
interrupting the flow of blood through the hepatic
artery and the portal vein and thus helping to control
bleeding from the liver. If needed longer than 30
mins, do intermittent clamping:

15 mins of clamping

5 mins of reperfusion

Venous Drainage: Hepatic Veins and Inferior Vena

Cava

There are three hepatic veins (right, middle, and left)

that pass obliquely through the liver to drain the
blood to the suprahepatic IVC and eventually the right
atrium.
LIVER
Segment
Blood Supply Right hepatic V- VIII
Notes Middle hepatic IV and V- VIII
Left hepatic II - III
The caudate lobe is unique because its venous
drainage feeds directly into the IVC.
Liver Function Test
Measures: Circulatory system, biliary passages, RE
system, functioning hepatocytes
Function test Notes
Proteins Albumin half life 21 days
Carb and Lipids Hepatic dse more common
effect is hyperglycemia, dec
total cholesterol and %
esterified fraction
Enzymes Three enzymes: alkaline
phosphatase, AST (SGOT),
ALT (SGPT)- elevations
accompany acute liver
damage, obstruction
ALT- more liver specific
Alkaline- patency of bile
channel
Nucleotidase elevated in
hepatobiliary dse
Dye Excretion Presence of jaundice, fever,
shock, hemorrhage, or
cellular damage causes
disproportionate
indocyanine green or
bromsulphalein retention
Coagulation Factors Multiple coagulation
defects may occur. Two
mechanism:
1. Obstructive
jaundice dec bile
dec Vit K
2. Hepatocellular
dysfunction
Imaging of the Portal Venous System and
Measurement of Portal Venous Pressure
The patency of the portal vein and the nature of the
collateral
The simplest initial investigation is abdominal
ultrasonography. A large portal vein suggests portal
hypertension but is not diagnostic. Doppler
ultrasound also is useful in evaluating blood flow
through surgical shunts and TIPS.
Abdominal CT and magnetic resonance angiography
both are capable of revealing portal vein anatomy as
well as patency. Visceral angiography and portal
venography are reserved for cases that cannot be
evaluated satisfactorily by noninvasive methods and
require further clarification of portal patency or
anatomy.
The most accurate method of determining portal
hypertension is hepatic venography.
The hepatic venous pressure gradient (HVPG) is then
calculated by subtracting the free from the wedged
venous pressure (HVPG = WHVP FHVP). The HVPG
represents the pressure in the hepatic sinusoids and
portal vein and is a measure of portal venous
pressure. Clinically significant portal hypertension is
evident when HVPG exceeds 10 mmHg.
Portal HPN:
Portal Venous pressure > 5 mmHg than IVC
Splenic pressure > 15 mmHg
Portal venous pressure > 20 mmHg
Tumor Markers:
Notes
CEA Can be elevated with
liver cirrhosis
AFP Screening patients at
high risk for HCC,
especially those with
hepatitis B and hepatitis
C - related liver cirrhosis
CA 19-9 Pancreatic ca
GALLBLADDER
Ultrasound findings (acute /calculous cholecystitis):
The most useful radiologic test for diagnosing acute
cholecystitis. It has a sensitivity and specificity of 95%.
it will show the thickening of the gallbladder wall and
the pericholecystic fluid. There are several stones in
the gallbladder (arrows) throwing acoustic shadows.
Focal tenderness over the gallbladder when Once considered the diagnostic procedure of choice
compressed by the sonographic probe (sonographic for gallstones, oral cholecystography has largely been
Murphys sign) replaced by ultrasonography. It involves oral
administration of a radiopaque compound that is
Biliary radionuclide scanning (HIDA scan) may be of
absorbed, excreted by the liver, and passed into the
help in the atypical case. Lack of filling of the
gallbladder. Stones are noted on a film as filling
gallbladder after 4 hours indicates an obstructed
defects in a visualized, opacified gallbladder. Oral
cystic duct and, in the clinical setting of acute
cholecystography is of no value in patients with
cholecystitis,
intestinal malabsorption, vomiting,obstructive
A normal HIDA scan excludes acute cholecystitis. CT jaundice, and hepatic failure.
scan is frequently performed on patients with acute
APPENDIX
abdominal pain. It demonstrates thickening of the
gallbladder wall, pericholecystic fluid, and the Age Differential Notes
presence of gallstones as well as air in the gallbladder Pediatrics Acute mesenteric + URTI
wall, but is less sensitive than ultrasonography adenitis +Generalized
lymphadenopathy
(self limiting)
Elderly Diverticulitis or CT scan helpful
perforating CA of
the cecum or
portion of the
sigmoid
Female Female internal
repro organs:
PID, ruptured
Graafian follicle,
ruptured ectopic
pregnancy

Incidence:
Acute Cholecystitis 1. Sudden RUQ pain
Fecaliths and calculi are found in 40% of cases of
2. Fever
simple acute appendicitis,23 in 65% of cases of
3. Leukocytosis
Charcots triad of 1. Biliary RUQ pain gangrenous appendicitis without rupture, and in
Acute Cholangitis 2. Jaundice nearly 90% of cases of gangrenous appendicitis with
3. Spiking fever with rupture.
chills
2nd to 4th decade of life (mean: 31.3y)
Reynolds Pentad Charcots triad +
of acute Shock and Altered Mental 40% - 10 to 29 yrs old
Cholangitis status
Murphys sign Usually in acute cholecystitis 67% mortality rate if not treated surgically
Deep inspiration or cough Lifetime rate: M:F ratio = 1.2-1.3 : 1
during subcostal palpation of
the RUQ produces inc pain or - male: 12%
inspiratory arrest
- female: 25%

Biliary obstruction due to cholecystolithiasis (Mirizzis Misdiagnosis:

syndrome). Gallstone becomes impacted in the cystic
duct or neck of the gallbladder causing compression
of the common bile duct (CBD) or common hepatic
duct, resulting in obstruction and jaundice
Oral Cholecystography
male 9.3%
Female 22.2% (highest among >80y)
Overall perforated appendicitis is 25.8%, Children
younger than 5 (45%) and patients older than 65
(51%) have the highest rate
Neoplasia
Notes
Carcinoid The appendix is the most
common site of gastrointestinal
carcinoid,
followed by the small bowel and
rectum.
The majority of carcinoids are
located in the tip of the
appendix.
Carcinoid tumors usually
present with localized disease
(64%). Treatment for tumors 1
cm is appendectomy.
Adenocarcinoma three major histologic subtypes:
mucinous adenocarcinoma,
colonic adenocarcinoma, and
adenocarcinoid.
The most common mode of
presentation for appendiceal
carcinoma is that of acute
appendicitis.
Patients also may present with
ascites or a palpable mass, or
the neoplasm may be
discovered during an
operative procedure for an
unrelated cause.
significant risk for both
synchronous and metachronous
neoplasms, approximately half
of which will originate from the
gastrointestinal tract
Mucocele A an obstructive dilatation by
intraluminal accumulation of
mucoid material. Mucoceles
maybe caused by one of four
processes: retention cysts,
mucosal hyperplasia,
cystadenomas, and
cystadenocarcinomas.
COLORECTAL
Modality Indication
Flexible Video or fiberoptic flexible
Sigmoidoscopy sigmoidoscopy and colonoscopy
and provide excellent visualization of
Colonoscopy the colon and rectum.
procedure without sedation.
Both sigmoidoscopy and
colonoscopy can be used
diagnostically and
therapeutically.
Barium enema perforation or leak is suspected.
Double-contrast
barium enema (use of barium
followed by the insufflation of
air
into the colon) has been
reported to be 70% to 90%
sensitive
for the detection of mass lesions
greater than 1 cm in diameter
angiography used for the detection of
bleeding within the colon or
small bowel.
Anoscopy The anoscope is a useful
instrument for examination of
the anal canal.
A larger anoscope provides
better exposure for anal
procedures such as rubber
band ligation or sclerotherapy of
hemorrhoids.
Endorectal is primarily used to evaluate the
ultrasound depth of invasion of
neoplastic lesions in the rectum.
Ultrasound can reliably
differentiate most benign polyps
from invasive tumors based on
the integrity of the submucosal
layer.
This modality also can detect
enlarged perirectal lymph nodes,
which may suggest nodal
metastases.
Fecal Occult Blood Testing.
used as a screening test for colonic neoplasms in
asymptomatic, average-risk individuals. FOBT has
been a nonspecific test for peroxidase contained in
hemoglobin; consequently, occult bleeding from any
gastrointestinal source will produce a positive result.
Similarly, many foods (red meat, some fruits and
vegetables, and vitamin C) will produce a false-
positive result. Any positive FOBT mandates further
investigation, usually by colonoscopy
Carcinoembryonic antigen (CEA) may be elevated in
60% to 90% of patients with colorectal cancer. is not
an effective screening tool for this malignancy. Many
practitioners follow serial CEA levels after
curative-intent surgery in order to detect early
recurrence ofcolorectal cancer. However, this tumor
marker is nonspecific, and no survival benefit has yet
been proven. It is also important to note that CEA may
be mildly elevated in patients who smoke tobacco.
Total mesorectal excision (TME) is a technique that
uses sharp dissection along anatomic planes to
ensure complete resection of the rectal mesentery
during low and extended low anterior resections. For
upper rectal or rectosigmoid resections, a partial
mesorectal excision of at least 5 cm distal to the
tumor appears adequate. TME both decreases local
recurrence rates and improves long-term survival
rates. Moreover, this technique is associated with less
blood loss and less risk to the pelvic nerves and
presacral plexus than is blunt dissection. The
principles of TME should be applied to all radical
resections for rectal cancer
Hartmann's operation. A proctosigmoidectomy or
Hartmann's procedure is the surgical resection of the
rectosigmoid colon with closure of the anorectal
stump and formation of an end colostomy. It was
used to treat colon cancer or inflammation
(proctosigmoiditis, proctitis, diverticulitis, etc.). If
dead bowel is present at laparotomy, a sigmoid
colectomywith end colostomy (Hartmanns
procedure) may be the safest operation to perform
Bowel Preparation
The rationale for bowel preparation isthat decreasing
the bacterial load in the colon and rectum will
decrease the incidence of postoperative infection.
Mechanical bowel preparation uses cathartics to rid
the colon of solid stool the night before surgery.28,29
The most commonly used regimens include
polyethylene glycol (PEG) solutions or magnesium
citrate. PEG solutions require patients to drink a large
volume of fluid and may cause bloating and nausea.
Magnesium citrate solutions are generally better
tolerated but are more likely to cause fluid and
electrolyte abnormalities.
Antibiotic prophylaxis also is recommended. The
addition of oral antibiotics to the preoperative
mechanical bowel preparation has been thought
todecrease postoperative infection by further
decreasing the bacterial load of the colon.
Broadspectrum parenteral antibiotic(s) with activity
against aerobic
Polyp management:
Benign polyps are asymptomatic, can be removed by
colonoscopic snaring, usually in one peace. Large or
sessile polypectomy, may require colectomy
Malignant polyp (Adenomatous)- polypectomy if:
1. Polyp pedunculated
2. Stalk not involved, margins of resection free
3. No invasion and not poorly differentiated
Internal hemorrhoids are located proximal to the dentate
line and covered by insensate anorectal mucosa. Internal
hemorrhoids may prolapse or bleed, but rarely become
painful unless
they develop thrombosis and necrosis (usually related to
severe
prolapse, incarceration, and/or strangulation). Internal
hemorrhoids are graded according to the extent of prolapse.
Firstdegree hemorrhoids bulge into the anal canal and may
prolapse
beyond the dentate line on straining. Second-degree
hemorrhoids prolapse through the anus but reduce
spontaneously.
Third-degree hemorrhoids prolapse through the anal canal
and
require manual reduction. Fourth-degree hemorrhoids
prolapse
but cannot be reduced and are at risk for strangulation.
Perianal Abscess
Most perianal abscesses can be drained under local
anesthesia in
the office, clinic, or emergency room. Larger, more
complicated
abscesses may require drainage in the operating room. A
skin
incision is created, and a disk of skin excised to prevent
premature closure. No packing is necessary, and sitz baths
are started
the next day (Fig. 29-37)
Fistula In Ano
Drainage of an anorectal abscess results in cure for about
50%
of patients. The remaining 50% develop a persistent fistula
in
ano. The fistula usually originates in the infected crypt
(internal
opening) and tracks to the external opening, usually the site
of
prior drainage. The course of the fistula can often be
predicted
by the anatomy of the previous abscess.
While the majority of fistulas are cryptoglandular in origin,
trauma, Crohns disease, malignancy, radiation, or unusual
infections (tuberculosis, actinomycosis, and chlamydia) may
also produce fistulas. A complex, recurrent, or nonhealing
fistula should raise the suspicion of one of these diagnoses