TRANS #16, EXAM #1

SGD 1: Acute Cholecystitis

VARIOUS PRECEPTORS
01/23/2018

OUTLINE 9. After cholecystectomy, what will happen to bile secretion?

V. Diagnosis
I. Case Presentation
A. Murphy’s Sign
A. Learning Objectives
B. Sonography
II. REVIEW OF THE GALLBLADDER
B. Case Scenario A. ANATOMY
C. Ultrasound
C. Guide Questions
D. Plain Radiograph/CT Scan • Location: junction of right 9th costal cartilage and lateral border of
II. Review of the Gallbladder
VI. Treatment the rectus abdominis
A. Anatomy
A. Symptomatic Cholecystitis
B. Functions
B. Asymptomatic Cholecystitis
® Lies along the visceral surface of liver, in the fossa of
III. Biliary Physiology gallbladder
VII. Patient Education
A. Bile Composition • Shape: piriform or pear-shaped
A. Post-Operative Biliary
B. Gallbladder Stimulation
C. Biliary Flow
Physiology • Size: 7-10 cm long; capacity of 30-50mL (bile) and can store up to
B. Gallbladder Flush 12 hours of secretion
D. Biliary Secretion
C. Public Health
E. Gallstone Formation • Parts:
Quick Review
IV. Clinical Correlations
Review Questions ® Fundus – part of the gallbladder that can be palpated
A. Cholelithiasis ® Body – main part
References
B. Cholecystitis
Appendix ® Neck – narrowing tapering which leads to the biliary tree
§ Hartmann’s Pouch – mucosal folds forming a pouch at the
I. CASE PRESENTATION junction of the neck and cystic duct
A. LEARNING OBJECTIVES - Common location for gallstones to become lodged
At the end of the learning session, the learner must be able to: • Biliary Tree:
1. Describe the normal anatomy and function of the gallbladder. ® L/R hepatic duct à common hepatic duct + cystic duct à
2. Discuss normal biliary secretion. common bile duct + pancreatic duct à sphincter of Oddi à
3. Discuss how gallstones are formed. Ampulla of Vater à D2 of duodenum
4. Discuss biliary secretion after cholecystectomy.

B. CASE SCENARIO
Gallstones affect 10-20% of the world’s population. About 500,000
people undergo removal of their gallbladder mostly for gallstones in the
U.S. This session will discuss biliary secretion in health and disease
(gallstone disease).

Your mother, a 50-year old obese female, complained of severe

abdominal pain that began approximately 2 hours after a heavy
meal. The pain began as a dull ache in the epigastric area but later
localized to the right upper quadrant and radiated between her
scapulae. She had nausea but no vomiting. She had similar, but mild,
episodes in the past. She was rushed to the Emergency Room of the
nearby hospital. You observed the ER physician during the
examination of your mother. Her temperature was 38.50C with normal
heart rate and BP. Examination of her abdomen revealed tenderness
in the RUQ. The Physician talked to you and informed you that your
mother had probable biliary tract disease based on her history and
PE finding of positive Murphy’s sign. A subsequent ultrasound
examination of the abdomen showed cholecystolithiases with acute
cholecystitis. In the ultrasound report you also noted the finding of
positive Sonographic Murphy sign.
Your mother is being advised to have surgical removal of her
gallbladder (cholecystectomy) but she is hesitating. She asks you
several questions regarding her condition. She wants to know what is
the gallbladder and why must it be removed. She is wondering why
not just remove the stones. She is also concerned about what will
happen to her after her cholecystectomy. You decided to review your
biliary anatomy and physiology so you can answer all her questions.
C. GUIDE QUESTIONS
1. What is the gallbladder and what is its function?
2. Differentiate cholelithiasis and cholecystitis.
3. Discuss normal biliary secretion.
4. What is the difference between Murphy’s sign and sonographic
Murphy sign.
5. During cholecystectomy, what blood vessels must be ligated?
6. How are gallstones (cholesterol) produced and how is obesity
related to gallstones?
7. A friend of your mother advised “gallbladder flush” of olive oil and
lemon instead of cholecystectomy. What is “gallbladder flush” and
will you recommend that instead?
8. Can removal of stones be the primary treatment for asymptomatic
and symptomatic gallstones?
Figure 1. Parts of the gallbladder include the head, body, and neck. The
gallbladder is connected to the bile duct via the cystic duck attached to its neck
B. FUNCTIONS
• Releases stored bile during fat/lipid digestion
• Stores bile synthesized by the liver
• Concentrates bile through absorbent lining of the gallbladder
III. BILIARY PHYSIOLOGY
A. BILE COMPOSITION
• Bile is normally composed of bile acids, cholesterol, phospholipids,
lecithin, ions including sodium and chloride, and bilirubin.
• The normal ratio of bile acids to phosphatidylcholine to cholesterol
is 10:3:1.
B. GALLBLADDER STIMULATION
• When chyme (gastric juices + food) from the stomach enters the
small intestine, acid and partially digested fats stimulate the
duodenum to secrete cholecystokinin (CCK) and secretin.
® Fat is the most potent stimulus for CCK secretion which
stimulates gallbladder contraction, resulting in the release of
stored bile.
® Acid, on the other hand, results in the release of secretin in the
duodenum. Its effect on the biliary system is similar to what is
seen in the pancreas. The biliary duct secretes bicarbonate
and water, increasing the flow of bile into the intestine.

Trans #16 Group #12: Arriola, Oblepias, Que, Racela, Sangil, Yamsuan 1 of 5
 C. BILIARY FLOW
• Pathway of biliary flow in a non-fasting state
® Production and secretion by hepatocytes
® Bile canaliculi (located in the hepatocytes)
® Canals of Herring and intrahepatic bile duct (portal triad)
® Interlobular biliary ducts (in the interlobular septa)
® L/R hepatic ducts
® Common hepatic duct
® Common bile duct (joins with pancreatic juices via pancreatic
duct)
® Duodenum (via ampulla of Vater through sphincter of Oddi)
• Pathway of biliary flow in a fasting state
® first 6 steps are similar to non-fasting state but after entering the
common hepatic duct, it enters:
® Cystic duct
® Gallbladder (for storage and concentration)
NICE TO KNOW:
• The gallbladder can empty its stored bile in 1 hour
• It takes 30 mins for ingested fatty food to reach the duodenum.
E. GALLSTONE FORMATION
Process
• Concentrated bile can be supersaturated with cholesterol and
calcium bilirubinate
• These can precipitate into microscopic crystals
• Crystals can get trapped in the gallbladder mucus forming a sludge
• Overtime, the sludge can grow, aggregate, and fuse to form
macroscopic stones

D. BILE SECRETION

Overview of Biliary Secretion

• The initial portion is secreted by the principal functional cells of the
liver, the hepatocytes.
® This initial secretion contains large amounts of bile acids,
cholesterol, and other organic constituents
® It is secreted into minute bile canaliculi that originate between
hepatic cells
• Next, the bile follows in the canaliculi toward the interlobular septa,
where the canaliculi empty into terminal bile ducts and then into
progressively larger ducts, finally reaching the hepatic duct and
common bile duct
® From here, the bile empties directly into the duodenum or is
diverted for minutes up to hours through the cystic duct into the
gallbladder.
• In its course through the bile ducts, an additional secretion is
added to the bile – a watery solution of sodium and
bicarbonate ions
® This second secretion sometimes increases the total quantity of
bile by as much as an additional 100%
® The second secretion is stimulated especially by secretin and
it functions for neutralizing acid that empties into the duodenum
from the stomach
• Bile is then reabsorbed in the small intestines, proximally via Figure 2. Any change in the normal amount of constituents found in bile can
cause supersaturation and ultimately lead to the formation of gallstones
diffusion and distally via active transport, and back to the liver

Role of Gallbladder in Biliary Secretion Relation to Obesity

• Obese individuals have higher levels of HMG-CoA reductase
• Bile is stored and concentrated within the gallbladder that is
activity
why it can store as much as 12 hours of bile secretion
• 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase is the
• This gall bladder absorption is caused by the active transport of
rate limiting enzyme in the mevalonate pathway, the metabolic
sodium through the gallbladder epithelium
pathway that produces cholesterol
• Followed by the secondary absorption of chloride ions, water, and
® Principal enzyme for cholesterol synthesis
most other diffusible constituents
® Normally targeted by drugs (e.g. statin, simvastatin)
• The remaining bile constituents (e.g. bile salts, cholesterol, lecithin,
and bilirubin) are thus concentrated. • High level of HMG-CoA activity leads to increased cholesterol
in bile and reduced bile salts
• The gallbladder concentrates bile five to twenty-fold.
Triangle of Gallstone Formation
Emptying of Gallbladder • Components
• Mechanism of gallbladder emptying is rhythmical contractions of ® Hypersaturation
the wall of the gallbladder, but effective emptying also requires ® Nucleation
the simultaneous relaxation of the Sphincter of Oddi, which ® Stasis
guards the exit of the common bile duct into the duodenum • Any imbalance in these components could contribute to the
• The most potent stimulus for causing gallbladder contractions formation of gallstones (Siy, 2016)
is cholecystokinin (CCK) ® High cholesterol contributes to hypersaturation
• The stimulus for CCK entry into the blood from the duodenal ® Most risk factors relating to females (gender, fertility, and age)
mucosa is mainly the presence of fatty foods in the duodenum are all due to estrogen, which is mainly related to stasis
• The gallbladder is also stimulated less strongly by acetylcholine-
secreting nerve fibers from both the vagi and the intestinal
enteric nervous system
• Prolonged storage of bile increases the chance that nucleation can
occur

Gastrointestinal & Nutrition 09.16: SGD 1: ACUTE CHOLECYSTITIS 2 of 5

 Chronic Cholecystitis
• Damage caused by repeated attacks of acute inflammation
• Pain is generalized and cannot be localized or isolated
• Usually present with GI symptoms (jaundice, pruritus secondary to
jaundice, alcoholic stools, nausea, vomiting, bloating, etc.)
® Obstruction of biliary flow
® Increased bilirubin diglucuronide (conjugated hyperbilirubinemia)
® Elevated levels of nonpolar bilirubin (unconjugated
hyperbilirubinemia)
• Alcoholic stools
Figure 3. Hypersaturation, nucleation, and stasis make up the triangle of ® Colorless stools
gallstone formation and any imbalance in one of the them can contribute to ® Bilirubin is not conjugated and excreted as stercobilin in feces
gallstone formation • Previous episodes of biliary pain may indicate chronicity of
cholecystitis
NICE TO KNOW: Fibrates
• Lipid-reducing agent/ drug (decreased VLDL and IDL) that may V. DIAGNOSIS
increase incidence of cholesterol gallstones
• Activates peroxisome proliferator-activated receptors (PPARs) A. MURPHY’S SIGN
during lipid metabolism
Elicitation
• May cause changes in biliary lipid composition and reduce bile acid
1. Let the patient lie in supine position
excretion
2. Palpate the right subcostal area, approximately along the
midclavicular line, while the patient inspires deeply
IV. CLINICAL CORRELATIONS • It is important that the examiner looks at the patient’s face rather
A. CHOLELITHIASIS than abdomen to check if there is inspiratory arrest
• Bile stones or gallstones
• Cholesterol stones (~80%) Responses
® Common among Caucasians Positive Response
® Yellow-green, primarily made of hardened cholesterol • The patient feels pain upon maneuver and may have an associated
® Seen as sonic shadowing in ultrasound, with absent echoes involuntary inspiratory arrest due to the movement of the diaphragm
® Commonly involved in obstruction and inflammation against the inflamed gallbladder.
• Pigment stones (~20%)
® Common among Asians Negative Response
® Black or brown stones • No inspiratory arrest
® Composed of pure calcium bilirubinate or complexes of
calcium, copper, and mucin glycoproteins NICE TO KNOW:
® Typically form in conditions of stasis or excess unconjugated • May result to false negative due to:
bilirubin (unconjugated hyperbilirubinemia) ® Mispositioned fingers of the examining physician
® Hemolytic anemia is a risk factor for the formation of pigment ® Patient intake of painkillers before the physical examination
stones ® Patients with chronic diseases such as diabetes because they
• Asymptomatic until dislodged in: may have polyneuropathy. This means that their ability to sense
® Hartmann’s pouch pain is not as good which means Internal organs can be inflamed
® Cystic duct and they might not show you pain at all in a murphy’s sign test.
® Common bile duct Thus, you might be pressing on the expected location and they
don’t feel any pain at all despite them patients might show other
Cholecystolithiasis symptoms like vomiting or abdominal tenderness.
• Bile stones located within the gallbladder that may/may not cause
obstruction (symptomatic/ asymptomatic) B. SONOGRAPHIC MURPHY’S SIGN
Choledocholithiasis Elicitation
• Bile stones located in the common bile duct 1. Let the patient lie in supine position
2. Probe the right subcostal area, approximately along the
B. CHOLECYSTITIS midclavicular line, using an ultrasound transducer while the
• Inflammation of the gallbladder patient inspires deeply.
® Obstruction in the cystic duct or common bile duct results in the
accumulation of bile, which then results in inflammation Responses
• ·Usually follows/common complication after cholelithiasis Positive Response
® 90% of cases are caused by cholelithiasis • The patient feels pain upon maneuver or deep probing, and the
® 10% develop as a result of injury/illness causing damage to the ultrasound transducer can confirm that the gallbladder is being
gallbladder pushed when the patient experiences inspiratory arrest.
• Acalculous cholecystitis – More serious morbidity/mortality rates
• A disease not caused neither by gallstones or duct obstruction Negative Response
• May be acute or chronic • No inspiratory arrest

Acute Cholecystitis NICE TO KNOW:

• Generally caused by gallstones • Accuracy – 87.2%
• More localized, sharp pain • Sensitivity – 63%
® Pain is usually epigastric with radiating to the RUQ but can also • Specificity (if present) – 96%
reach the back in between the scapulae
• May or may not present with GI symptoms
C. ULTRASOUND
• Usually indicated by a positive Murphy’s sign and Sonographic
• Sonic shadowing
Murphy’s sign
® Normal wall thickness: 3mm or less
® Wall thickness >3mm = cholecystitis

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• Inflamed gallbladder due to a liver disease = reactive cholecystitis
® There is no need to operate a reactive cholecystitis
• A thickened gallbladder wall has a layered appearance in sonography.
• At CT, frequently contains a hypodense layer of subserosal edema that
mimics pericholecystic fluid.
D. PLAIN RADIOGRAPH/CT SCAN
• Plain radiographs are usually not used to assess for gallstones (it can’t
be seen) but can be used to evaluate for porcelain
gallbladders/calcifying cholecystitis
® porcelain gallbladder is the calcification of the mucosa of the
gallbladder
• CT scan can be used for better sensitivity and definition
VI. TREATMENT OPTIONS
A. SYMPTOMATIC CHOLELITHIASIS
• Usually warrants removal of the gallbladder to prevent further
complications and recurrence
® Ex. In cases where the gallbladder is already inflamed due to
infection caused by the damage of the gallstones
• 10-20% of cases present symptomatic cholelithiasis
• Cholecystectomy: removal of the gallbladder through surgical
procedure
® Inspect Triangle of Calot prior to procedure in case there
should be any anatomical variation
® Borders: cystic duct, hepatic duct, inferior surface of liver
® Contents: right hepatic artery, hepatic veins, cystic artery, cystic
lymph node (of Lund)
§ These components must be carefully identified and then
ligated to prevent massive bleeding during the surgery
Laparoscopic Cholecystectomy
• Treatment of choice for symptomatic cholelithiasis
• Produce less scars (only 2 to 3 small incisions)
• Heals quickly à less hospital stay
• Few complications
Open Cholecystectomy
• 5 to 7 inch incisions
• Better option for those who have had previous surgery
® Adhesions can form after any abdominal surgical procedures. An
accumulation of these scars may cause the problem. One will not be
able to fix this through laparoscopic cholecystectomy because you
don’t have a good visual scope.)
• Done during emergency procedures or complications (i.e. gallstone
prone to rupture)
Percutaneous Cholecystectomy
• Involves draining of the gallbladder
• Invasive (surgical)
® Catheter is inserted under ultrasound or CT guidance to drain bile
or pus in the gallbladder
• Decompression controls the acute disease, including any local infection,
but the gallstones cannot be removed
• A cholecystectomy is still advised after performing the procedure
since the operation only treats the symptoms and not the cause
Endoscopic Retrograde Cholangiopancreatography (ERCP)
• Uses endoscopy and fluoroscopy to diagnose and treat certain problems
of the biliary or pancreatic ductal systems
• Done to patients who are severely ill and at high risk of getting post
cholecystectomy complications
• ERCP is more specific to the part of the cystic duct that will be cut
(depending on area of ductal obstruction) vs. cholecystectomy (non-
specific)
B. ASYMPTOMATIC CHOLELITHIASIS
• Usually warrants for non-invasive procedures
• 80-90% of cases present asymptomatic cholelithiasis
Oral Dissolution Therapy
• Ursodiol and chenodiol are medications that contain bile acids that can
dissolve gallstones.
® Most effective medication in dissolving small cholesterol stones.
• Months or years of treatment may be needed to dissolve all stones.
Gastrointestinal & Nutrition 09.16: SGD 1: ACUTE CHOLECYSTITIS
Shockwave Lithotripsy
• A lithotripter machine is used to generate shockwaves which pass
through the person’s body to break the gallstones into smaller pieces.
® This procedure is rarely done may be used along with ursodiol.
Cholecystectomy
• Asymptomatic gallstones may be indicated with cholecystectomy if:
® Patients with large gallstones >2cm in diameter
® Patients with nonfunctional or calcified (porcelain) gallbladder
observed on imaging studies and who are at high risk of
gallbladder carcinoma
® Patients with spinal cord injuries or sensory neuropathies which
affects the abdomen
® Patients with sickle cell anemia in whom the distinction between
painful crisis and cholecystitis may be difficult
VIII. PATIENT EDUCATION
A. POST-CHOLECYSTECTOMY
• There is a continued production of bile by the liver. Fat digestion
and absorption occur.
® Bile becomes less concentrated.
® Drains more continuously into the intestine
• Bile secretion and fat intake will no longer be coupled. Fatty meals
will be harder to digest because of the absence of a large pool of
bile normally stored and released from the gallbladder à diarrhea
® Patients should be advised to adhere to a diet that is low in fat
content; otherwise, there may be occurrence of diarrhea
B. GALLBLADDER FLUSH
• Ingestion of olive oil (as lubricant) and lemon juice (for softening of
the cholesterol stones)
• Intended effect
® Elicit intense gallbladder contraction à flush gallstones
• No evidence of effectiveness
® The “stones” seen in stool after the flush are not of gallstone
origin, but more of saponified salts of olive oil and citric acid.
C. PUBLIC HEALTH
• The knowledge or risk factors of cholelithiasis in our population is
the essence of health-promoting actions.
• Obesity is the major risk factor in women.
® Promotion of appropriate eating habits can result in body mass
reduction, and may thus indirectly decrease other risk factors.
4F’s Risk Factors
• Female – high levels of estrogen
• Forty – cholesterol metabolism becomes less efficient with age
• Fat – more cholesterol deposited in bile and more HMG-CoAR
• Fertile – high levels of hormones or estrogen
Charcot’s triad for ascending cholangitis
• Charcot’s triad for ascending cholangitis is a result of ascending
cholangitis (an infection of the bile duct usually caused by bacteria
ascending from its junction with the duodenum)
1. Jaundice
2. Fever, usually with rigors
3. Right upper quadrant abdominal pain
QUICK REVIEW
SUMMARY OF TERMS
• Gallbladder
® Fundus – palpable area of the gallbladder
® Body – Main part
® Neck – leads to the biliary tree
® Hartmann’s pouch – where gallstones are commonly found
• Biliary Tree
® L/R hepatic duct à common hepatic duct + cystic duct à
common bile duct + pancreatic duct à sphincter of Oddi à D2
of duodenum
• Functions of the gallbladder
® Release of stored bile to aid in digestion
4 of 5
 ® Storage of bile ® Fertile – high levels of hormones or estrogen
® Concentrates bile
• CCK REVIEW QUESTIONS
® Secreted by I cells in the duodenum 1. Which of the following describes gallstones found in the common
® Aids in the first stage of bile secretion bile duct?
® Responds to presence lipids in the duodenum a. Cholestasis
® Stimulates contraction of the gallbladder and relaxation of the b. Cholelithiasis
sphincter of Oddi c. Choledocholithiasis
• Secretin d. Cholecystolithiasis
® Secreted by S cells in the duodenum
® Aids in the second stage of bile secretion 2. Which of the following statements is false?
® Responds to the presence of acid in the duodenum a. The health professional must palpate the right subcostal area,
® Stimulates secretion of water and bicarbonate from biliary approximately along the midclavicular line when doing the
ducts Murphy’s sign test.
b. Sonographic Murphy’s Sign is known to have an accuracy rate
• Biliary Flow
of 87.2% and sensitivity rate of 63%.
® Production and secretion by hepatocytes
c. The Murphy’s sign test requires the patient to take a breath and
® Bile canaliculi hold it while the Sonographic Murphy’s Sign test is elicited while
® Canals of Herring and intrahepatic duct (portal triad) inhaling.
® Interlobular biliary ducts (in the interlobular septa) d. None of the above
® L/R hepatic ducts
® Common hepatic duct 3. What is the effect of increased levels of HMG-CoA reductase
® Common bile duct (non-fasting state) / cystic duct (fasting state) activity seen in obese patients?
® Duodenum (non-fasting state) / gallbladder (fasting state) a. Decreased cholesterol in bile
• Gallstone formation – concentrated bile supersaturated with b. Increased cholesterol in bile
cholesterol and calcium bilirubinate à precipitation into microscopic c. Increased bile salts
crystals à crystals trapped in the gallbladder mucus forming a d. None of the above
sludge à sludge grow, aggregate and fuse forming macroscopic
stones 4. Which of the following is the correctly arranged bile flow in non-
• Obesity – high levels of HMG-CoA reductase activity, principal fasting state?
enzyme for cholesterol synthesis I. Hepatocytes
• Triangle of gallstone formation II. Common hepatic duct
® Hypersaturation III. Interlobular biliary duct
® Nucleation IV. Cystic duct
® Stasis V. Duodenum
• Cholelithiasis – bile stone or gallstones a. I à II à III à IV
® Cholesterol stones – made up of hardened cholesterol b. I à II à III à V
c. I à III à II à IV
® Pigment stones – pure calcium bilirubinate or complexes of
d. I à III à II à V
calcium, copper, and mucin glycoproteins
• Cholecystolithiasis – bile stones located within the gallbladder
5. What blood vessel is not ligated during cholecystectomy?
• Choledocholithiasis – bile stones located in the common bile duct a. Cystic artery
• Cholecystitis – inflammation of the gallbladder b. Cystic duct
® Acute – generally caused by gallstones c. Hepatic artery
® Chronic – caused by repeated attacks of acute inflammation d. None of the above
§ Jaundice
§ Pruritus secondary to jaundice Answers: 1C, 2C, 3B, 4D, 5C
§ Alcoholic stools
§ Nausea and vomiting
REFERENCES
§ Bloating
(1) Michele Rivera-Nuez, MD. 17 January 2018. Gross Anatomy of the
Table 1. Difference Between Murphy’s Sign and Sonographic Murphy’s Sign
Gallbladder [Lecture slides].
Sonographic Murphy’s (2) Guyton, A.C., and Hall, J.E. 2006. Textbook of medical physiology,
Murphy’s Sign 11th edition.
Sign
Instrument (3) Moore, K.L., Dailey, A.F., and Agur, A.M.R. 2014. Clinically oriented
None Ultrasound Transducer anatomy, 7th edition.
Used
Location of Examiner palpates at Sonographer can see (4) Rockwell, V.W., Bender, D.A., Botham, K.M., Kenelly, P.J., and
Gallbladder the expected location the exact location Weil, P.A. 2015. Harper’s illustrated biochemistry, 30th edition.
Timing of Test is elicited while Patient takes a breath (5) ASMPH Batch 2021. 2017. SGD 1: Acute Cholecystitis.
Breathing inhaling and holds it (6) ASMPH Batch 2020. 2016. SGD 1: Cholelithiasis, Cholecystitis, and
Examiner can tell if Sonographer asks the Cholecystectomy.
Pain
pain is elicited patient about the pain

• Symptomatic cholelithiasis
® Laparoscopic cholecystectomy – treatment of choice
® Open cholecystectomy – done during emergency procedures
or complication
® Endoscopic retrograde cholangiopancreatography (ERCP)
• Asymptomatic cholelithiasis
® Oral dissolution therapy – ursodiol and chenodiol
® Shockwave lithotripsy
• 4F’s Risk Factors
® Female – high levels of estrogen
® Forty – cholesterol metabolism becomes less efficient with age
® Fat – more cholesterol deposited in bile

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