1.

Differential diagnosis for acute abdominal pain

Gastroenteritis
o non-focal, crampy abdominal pain, mild-moderate intensity progressing over
days before peaking and resolving.
o Low- grade fever, n/vomiting not associated with meals/d.
o Abdominal exam: generalized tenderness, w/o guarding or rebound.
o In severe cases: dehydration evident as sunken eyes, dry mucus
membranes, skin tinting, and orthostatic hTN.
Appendicitis
o vague periumbilical pain associated with n/v which progresses over 6-10
hours to a more intense and localized pain in the RLQ
o not usually associated with meals, low grade fever.
o involuntary guarding and rebound pain with high fever = Perforation.
Biliary colic
o d/t intermittent obstruction of cystic duct by calculi, dull pain, localized to
RUQ and epigastric region.
o Lasts 6-8 hours, sometimes after a fatty meal, n/v, occasional low-grade
fevers.
o Between episodes patient may be asymptomatic for years
Acute Cholecystitis
o d/t persistent obstruction of cystic duct by calculi,
o s/s similar to biliary colic but persist beyond 6-8 hours.
o Pain localized to epigastric area, RUQ, can radiate toward right scapular
region
Pancreatitis
o epigastric pain that progresses in severity over hours to days,
o initially vague, becomes more localized, constant and radiates to back.
o NV and fever, symptoms worsen with meals.
o Abdominal exam: hypoactive bowel sounds, guarding, rebound.
o Intra-abdominal bleeding into pancreatic bed may manifest with
periumbilical (Cullens) or flank (Gray-Turners) ecchymoses
Diverticulitis
o infection of colnic diverticula, elderly, in sigmoid colon,
o dull pain poorly localized to lower-mid abdomen, progresses over hours to
days localizing to LLQ
o NV and fever are common. Exam reveals tenderness, guarding and possible
palpable mass.
Small bowel obstruction
o most commonly the result of intra-abdominal adhesions from previous sx in
adults
o site dependent pain may be epigastric (upper small bowel) or periumbilical
(distal small bowel) both described as crampy, emesis of bilious or feculent
matter common.
o Exam reveals distension, diffuse tenderness, hyperactive bowel sounds, low
grade fever may be present
Perforated peptic ulcer
o most common in the proximal portion of duodenum,

o severe pain initially localized to the epigastric region, however gastric and
intestinal contents quickly spread down the right pericolic gutter leading to
diffuse peritonitis.
o Exam reveals hypotension, tachycardia, involuntary guarding, abdominal
rigidity and rebound.
o Flat plate reveals air under diaphragm
Mesenteric ischemia
o patients with compromised intestinal circulation (ie cardiac arrhythmias,
PVD, hypercoagulable states, & acute arterial and venus insufficiency.
o Pain is poorly localized to epigastric and periumbilical regions frequently
described as developing suddenly, initial milder pain that worsens with meals
is indicative of pre-existing ischemia.
o Exam reveals uncomfortable patient with benign findings seemingly out of
proportion to the severe, subjective complaints.
o Evidence of GI bleeding is common if bowel infarction has occurred; VS are
unstable with hypotension and tachycardia
Ruptured AAA rapidly occurring event present with acute mid-abdominal pain
that is described as tearing. Typically hemodynamically unstable with
hypotension and tachycardia, diminished to absent femoral pulses and skin
mottling present.

2. Describe the mechanisms involved in bile production.

Macrophages break down RBC Heme Unconjugated bilirubin
Bloodstream: Unconjugated bilirubin-albumin complex = indirect water-insoluble
bilirubin
Liver: UDP-glucuronyl transferase converts unconjugated (insoluble) bilirubin
conjugated (water soluble) bilirubin.
GI: Excreted in bile where gut bacteria act on it Urobilinogen
some gets reabsorbed, some excreted in urine as urobilin, and some excreted in
feces at stercobilin.
3. Risk factors for gall stone production
affects 10% of Americans, common cause of extrahepatic cholestasis, twice as common
in women, increasing incidence with age (30% of women over age 50 have gall stones),
genetic predisposition, if first degree relative 4.5 times more likely to develop, Native
American descent is a high-risk group. Also obesity, rapid weight loss, medications and
administration of total parenteral nutrition. Gall stone disease may manifest itself by
cholelithiasis, acute cholecystitis, choledocholithiasis or primary cholangitis.
Diabetes- complication would be polyneuropathy and angiopathy leading to lesser
motility of gallbladder and thus leading to stasis.
4. Describe the anatomy of the biliary tract

Bile canaliculi >> Canals of Hering >> bile ductules (in portal tracts) >>
intrahepatic bile ducts >> left and right hepatic ducts >>

merge to form >> common hepatic duct >>

exits liver and joins >> cystic duct (from gall bladder) >>

forming >> common bile duct >> joins with >> pancreatic duct >>

forming >> ampulla of Vater >> enters duodenum

Contraction of the gallbladder to secrete its stored bile is via CCK (fatty acids and AA).
Bile leaves through the cystic duct, where it meets the common hepatic duct and they
join to form the common bile duct. The Sphincter of Oddi is around the duct, and the
Ampulla of Vater is at the lumen of the duct. Tumors that arise in the head of the
pancreas can cause obstruction of the common bile duct. Gallstones that reach the
common channel at ampulla can block both the bile and pancreatic ducts.

5. Compare and contrast the clinical presentation (signs, symptoms and lab
values) of biliary colic and acute cholecystitis.
General overview of the two:
Acute cholecystitis is not fully explained by cystic duct obstruction alone. It is usually
due to this combined with irritation of the gallbladder mucosa. This irritation could
mechanical, chemical (lysolecithin, normally absent in bile is found in the bile of those
with acute cholecystitis) or due to an infection being present within the biliary system.
The irritation is further promoted by the immune response, namely prostaglandins.
This inflammation will explain many of the differences in findings of signs, symptoms and
lab values between biliary colic and acute cholecysitis.
In contrast to acute cholecystitis, biliary colic is usually caused by the gallbladder
contracting in response to hormonal or neural stimulation usually due to a fatty meal,
forcing a stone against the gallbladder outlet or cystic duct opening, and leading to
increased intragallbladder pressure and pain. The stones often fall back from the cystic
duct as the gallbladder relaxes.
According to Uptodate: Biliary colic must be distinguished from the more serious
complication of acute cholecystitis, which is associated with gallbladder wall
inflammation, fever and an elevated white cell blood count. Prolonged/recurrent cystic
duct blockage can progress to total obstruction causing acute cholecystitis. An episode of
prolonged right upper quadrant pain (greater than four to six hours), especially if
associated with fever, should arouse suspicion for acute cholecystitis as opposed to an
attack of simple biliary colic.
Physical Exam Differences:
Major: Physical examination can help distinguish patients with acute cholecystitis. While
biliary-type pain is present in both uncomplicated biliary colic and in acute cholecystitis,
the pain in uncomplicated biliary colic is entirely visceral in origin since the gallbladder
wall is not inflamed. Thus, it is generally less well localized and patients do not exhibit a
positive "Murphy" sign on physical examination.
Biliary colic: Often the stone lodges and then eventually dislodges. As a result, the
discomfort progresses in less than an hour to a steady plateau that ranges from

moderate to excruciating and remains constant for more than an hour, then slowly
subsides over several hours. The pain is often associated with diaphoresis (sweating),
nausea and vomiting. It is not exacerbated by movement and not relieved by squatting,
bowel movements, or flatus.
Acute Cholecystitis: Patients with acute cholecystitis are usually ill appearing, febrile, and
tachycardic, and lie still on the examining table because cholecystitis is associated with
true local parietal peritoneal inflammation that is aggravated by movement. Abdominal
examination usually demonstrates voluntary and involuntary guarding.
Lab Values Differences:
Biliary Colic: Laboratory studies should be normal in patients with uncomplicated biliary
colic both during asymptomatic periods and during attacks of symptoms.
Acute Cholecystitis: Initial evaluation should include a white blood cell count with
differential, which often shows leukocytosis with an increased number of band forms (ie,
a left shift). Elevation in the serum total bilirubin and alkaline phosphatase
concentrations are not common in uncomplicated cholecystitis, since biliary obstruction
is limited to the gallbladder.
Ultrasound should also be used in both to confirm gallstones and Murphys
Sign in acute cholecystitis.
6. Identify the causes of pancreatitis
-Biliary tract Disease / Gall stones - causes 35 to 60 % of pancreatitis. F:M ratio is 3:1
-Alcoholism causes up to 65% of pancreatitis in the US. M:F ratio is 6:1
-Obstruction of pancreatic duct system: periampullary tumors, pancreas divisum,
choledochoceles, biliary sludge, parasites (Ascaris, Clonorchis).
-Medications thiazide diuretics, azothioprine, estrogen, sulfonamide, furosemide,
methyldopa, pentamidine, procainamide.
-Infections mumps, coxsackie, mycoplasma.
-Metabolic disorders with hypercalcemia hyperparathyroidism, hypertriglyceridemia.
-Acute ischemia induced by vascular thromboembolism, vasulitis, shock.
-Trauma, iatrogenic injury.
-Genetic mutations in pancreatic (inhibitors of) enzymes PRSS1, SPINK1. Also cystic
fibrosis.
-Autoimmune disorder
-Scorpion sting
-Endoscopy

G - gallstone. Gallstones that travel down the common bile duct and which
subsequently get stuck in the Ampulla of Vater can cause obstruction in the
outflow of pancreatic juices from the pancreas into the duodenum. The backflow of
these digestive juices causes lysis (dissolving) of pancreatic cells and subsequent
pancreatitis.

E - ethanol

T - trauma

S - steroids

M - mumps (paramyxovirus) and other viruses (Epstein-Barr virus,

Cytomegalovirus)

A - autoimmune disease (Polyarteritis nodosa, Systemic lupus erythematosus)

S - scorpion sting

H - hypercalcemia, hyperlipidemia/hypertriglyceridemia

E - ERCP (Endoscopic Retrograde Cholangio-Pancreatography - a procedure that

combines endoscopy and fluoroscopy)

D - drugs (SAND - steroids & sulfonamides, azathioprine, NSAIDS, diuretics)

7. Describe the signs and symptoms of pancreatitis

Acute pancreatitis signs and symptoms include:
- Upper abdominal pain in the epigastric region that radiates to the back or
below the left scapula
- The pain may be worse when lying flat on the back and somewhat relieved by
leaning forward or curling into a ball
- Abdominal pain that feels worse after drinking alcohol or eating, especially
foods with a high fat content
- Nausea, vomiting
- Tenderness when touching the abdomen
- Fever
- Tachycardia
- Mild jaundice
Chronic pancreatitis signs and symptoms include:
- The symptoms of chronic pancreatitis are similar to those of acute pancreatitis.
In addition:
- Losing weight without trying
- Steatorrhea
- Diabetes may develop if the islet cells become damaged (mayo, web md, medline
plus)
- CAUSE: symptoms are more due to the loss exocrine and endocrine functions (such
as vasculitis, alcoholic, autoimmune system)
- Signs: cachexia, tenderness
- Lab test: amylase and lipase can be up or normal, imaging can see calcification
8. Compare and contrast acute vs chronic pancreatitis
Acute pancreatitis is a sudden inflammation that occurs over a short period of time,
causing sudden and severe abdominal pain. In the majority of cases, acute
pancreatitis is caused by gallstones or heavy alcohol use. The severity of acute
pancreatitis may range from mild abdominal discomfort to a severe, lifethreatening illness. However, the majority of people with acute pancreatitis
(more than 80%) recover completely after receiving the appropriate treatment.

Acute pancreatitis can occur 2ry to surgeries that involve the common bile duct.
Parasites like C.sinensis, Ascaris. Viruses like paramyxovirus (mumps, most common),
hepatitis virus, HIV, HSV, EBV, CMV. Drugs can also cause acute pancreatitis.
Chronic pancreatitis occurs most commonly after an episode of acute pancreatitis
and is the result of ongoing inflammation. If the pancreas becomes scarred during
the attack of acute pancreatitis, it cannot return to its normal state. Chronic pancreatitis
does not resolve itself and results in a slow destruction of the pancreas. In more
than 70% of the cases, chronic pancreatitis is caused by prolonged alcohol use.
Damage to the pancreas from excessive alcohol use may not cause symptoms for
many years, but then the person may suddenly develop severe pancreatitis
symptoms. (medline plus, webmd)
ALCOHOL, primary hyperparathyroidism (rare), hyperlipidemic conditions (high
triglycerides), CF,
9. Laboratory values in the evaluation of epigastric pain.
Laboratory values revealing leukocytosis with a left shift are common for many causes
of epigastric pain. Gastroenteritis, appendicitis, acute cholcystitis, pancreatitis,
diverticulitis, small bowel obstruction, perforated peptic ulcer and mesenteric ischemia
all present with leukocytosis. Some values are specific to certain diseases.
Gastroenteritis (due to diarrhea and vomit) will also present with hypokalemia, and
prerenal azotemia. Appendicitis frequently reveals acidosis, multiple electrolyte
disorders, and renal dysfunction (inflammation,, local inflammation, dehydration); and
urinalysis to evaluate for a urinary tract process. Acute cholecystitis frequently reveals
mild transaminase, alkaline phosphatase, and bilirubin elevation. Pancreatitis is
evaluated with amylase and lipase testing and a liver panel. Perforated peptic
ulcer and mesenteric ischemia both also present with mild acidosis.
10. Discuss the role of radiological studies in the evaluation of abdominal pain.
Radiology can be used to diagnose many abdominal issues. For one, some gallstones
have calcifications that can be seen on an X-ray. Also, in chronic pancreatitis,
calcifications can be seen. With the help of contrast dyes, blockages or narrowing can
be seen like in achalasia or intestinal blockage.
Can use endoscopy retrograde cholaniopancratography (ERCP) to get image of the biliary
tree
X-RAY: flat plate and upright. Sentinel loop = localized paralytic ileus; colonic cut-off sign
look up!!
Advantages of X-RAY: easy, fast, and cheap
Disadvantages: limited to obstruction and ileus (decrease in motility lead to dilated
bowel loop) and can also see Calcification
Ultrasound: cheap, easy, good to see stone, dilation, and good visualization but cant see
retroperitoneal and amount of abdominal gas
CT: fast and good visualization but expensive and limited contrast, and radiation. CT will
help us distinguish b/w edematous pancreatitis and necrotic pancreatitis. Do contrast
enhanced. Have to ask about allergies to contrast media and kidney function.
Outpatients: ultrasound, x-ray, CT (after 48hours)
FIRST IMAGING FOR ACUTE PANCREATITIS IS ULTRASOUND
11. Describe the initial evaluation for a patient with pancreatitis including
methods used to predict prognosis.

History- alcoholism, gall stone risk factors

Exam- hunched over, not moving, epigastric pain, rebound tenderness
Blood tests- amylase, lipase, inflammatory cytokines,
RadiologicalPlain film of abdomen- colon cut-off sign (sentinel sign, in severeinflammation spread to colon resulting in vasospasm- see air in splenic
flexure ), R/O obstruction and bowel perforation
Chest film- Approximately one-third of patients with acute pancreatitis have
abnormalities visible on the chest film such as elevation of a
hemidiaphragm, pleural effusions, basal atelectasis, pulmonary
infiltrates, or acute respiratory distress syndrome. Left-sided or
bilateral pleural effusions suggest increased risk of complications
CT scan- bad prognosis associated with collection of fluid or gas
retroperitoneally
Risk factors for severe, necrolytic pancreatitis
Age >75, Obesity, Alcohol
Ransons and APACHE II staging criteria
12. Discuss initial therapeutic intervention for pancreatitis.
Supportive- Fluids (Saline) to prevent dehydration, Pulmonary, renal, circulatory,
and hepatobiliary support as needed, Oxygen therapy if needed. Should monitor
K+ levels and should also give K+ if needed.
Nutrition- Parenteral nutrition for 3 days for mild wait for symptoms to
subside, NG or tube into jejunum for severe cases- decreases incidence of
ascending infection. Give NPO (nothing PE Os by mouth)
Pain management- Usually opioids (morphine causes spasms in the
sphincter of Oddi they used to think that but not true. Alternative would
be Fentanyl)
Broad spectrum antibiotics if there is necrosis- Meropenem/impenem (If patient
doesnt get better within several days do cultures and sensitivity)
Necrosectomy if necessary major complication in pts w/ necrotizing pancreatitis
Anti-emetic- dimenhydrirate, metoclopramide
If gall stone related- must remove the stone
Cholecystectomy- high rate of recurrence if not removed. Surgery is
to be performed after pancreatitis settle down usually takes around
6 weeks)
DAVID = (Diet, Activity, Vital signs, Investigations, Drugs)

S/S of chronic vs. acute:

Less pain in chronic,
Complications: fat necrosis seen in subQ fat (chronic)

Pancreatitis and Diabetes: need > 90% pancreatic destruction for diabetes to manifest.
Difference b/w Type I DM and DM 2ry to pancreatitis is that in the latter you have
destruction of alpha cells as well and therefore NO GLUCAGON hypoglycemia.
You can also have malabsorption - deficiency of fat soluble vitamins = steatorrhea.
If ALT levels are elevated then more likely to be pancreatitis 2ry to gallstones.
ERCP: Endoscopic retrograde cholangiopancreatography is a procedure that combines
upper gastrointestinal (GI) endoscopy and x rays to treat problems of the bile and
pancreatic ducts. ERCP is also used to diagnose problems, but the availability of noninvasive tests such as magnetic resonance cholangiography has allowed ERCP to be used
primarily for cases in which it is expected that treatment will be delivered during the
procedure
This is the gold standard for diagnosing chronic pancreatitis.
Secretin test: secretin stimulates HCO3 production from the pancreas.
Morphologically If you take a bx from pancreas - is there a difference b/w acute and
chronic?
Acute = PMNs
Chronic = lymphocytes
Sentinel loop: It is a feature due to body's efforts to localize traumatic or inflammatory
lesions. The local distention of intestinal loop is due to local paralysis and accumulation
of gas in the intestinal loop.
In acute pancreatitis, the sentinel loop is usually seen in left hypochondrium while in
acute appendicitis, the sentinel loop is seen in right iliac fossa. The sentinel loop is seen
in right hypochondrium in acute cholecystitis.