The document discusses gallstones and cholelithiasis. It begins with an outline of the biliary system anatomy and physiology. It then describes that gallstones form when there is too much cholesterol or bilirubin in the bile stored in the gallbladder. Risk factors for developing gallstones include being fair-skinned, female, overweight, pregnant, or over 40 years old. Gallstones can cause symptoms like pain in the upper right abdomen. Treatment may involve surgery to remove the gallbladder if symptoms persist or worsen. Repeated pregnancies are associated with an increased risk of gallstone formation due to changes in gallbladder function.

1. CHOLELITHIASIS
Jessa Reomales Goyena, RN

2. FAT, FEMALE, FORTY AND
FERTILE:
A Recipe for Gallstones (Dr. Daemon
Jones)

3. OUTLINE
 Brief Anatomy and Physiology of Biliary
System
 Description of Gallstones
 Overview of Cholelithasis
 Sign and Symptoms
 Pathology
 Treatment
 Prevention

4. GALLSTONES
 Small gravel or pebble –like substance that
are found in GB
 Where does it came from? : Liver that
produces the so called bile (which is by
digestive system it emulsify fats) 700ml of
bile/day, it does not have digestive enzyme but
it plays a role in digestion by diluting and
neutralizing stomach acid by increasing
efficiency of fat digestion and absorption.
 GB acts as the bank unit of bile until we need it
for digestion

5. Maximize BILE
 Composition: group of electrolytes (Chloride
and Ca), lecithin, fatty acids, cholesterol,
bilirubin and bile salts
 BILE SALTS : are synthesized by the liver cells
from the cholesterol. Also it undergo
conjugation to taurine and glycine (Amino
Acids)
 BILIRUBIN/ BILE PIGMENTS: found in the
breakdown of hemoglobin

6. BILIRUBIN
Urine : 0.5 – 2.5mg/24hrs or 0.09 umol/24 hours
Feces: 40 – 200mg/24 hours or 0.068umol/24 hours
 Removed b the hepatocytes from the blood by
chemically modifying through CONJUGATION
 Glucoronic acid – bilirubin becomes more
soluble
 Secreted by the hepatocytes in canaliculi
 “It represents that bile is the major route of
elimination of bilirubin”
 ONCE it is used, it can be found in the GIT
(feces), and Circulatory System (Portal blood),
GUT (urine)
 In GIT : intestinal flora convert it to
UROBILINOGEN

7. ENTEROHEPATIC Circulation
 Hepatocytes forms the bile which is collected by
 Canaliculi and hepatic ducts
 Cystic duct
 Collected and stored in GB – bile is stored and
concentrated 5 to 10 times that the bile originally
made by the liver
 RELEASE of BILE: Increase in PH in the
duodenum
 Release of secretin from the duodenum
 Signals the PARASYMPATHETIC NERVOUS
SYSTEM (vagus nerve) by the aid of
CHOLECYTOKININ

8.  Contract to release Bile to the duodenum
 Pass through the duodenal papilla by the
relaxation of Sphincter of Oddi
 Furthermore, it is mediated by the secretion of
hormone, chlecytokinin – pancreozymin (CCK-
PZ) from the intestinal wall

9. EMULSIFICATION OF FATS
OCCUR?
 Bile salts + Cholesterol + Lecithin
 WHERE DOES REABSORPTION OCCURS?
 Small amount of bile salts is reabsorbed in the
distal ileum, going to the portal blood and back
to the liver.

10. OVERVIEW OF
CHOLELITHIASIS
 According tot he National Digestive Disease
information Clearinghouse (NDDIC), BILE
contains: water, cholesterol, fats, bile salts,
proteins, and bilirubin.
 Types of gallstones:
 Cholesterol – created if there is too much
chlesterol in the body
 Pigment – too much bilirubin which is a waste
product of RBC destruction

11. HEREDITARY BILIRUBINEMIA
 Gilbert Syndrome – Increase level of
uconjugated bilirubin which causes jaundice.
Serum bilirubin level is high, liver histology and
liver function is normal in result and there is
no hemolysis : Familial Disorder
 IN BORN ERROR OF BILIARY
METABOLISM:
 Dubin – Johnson Syndrome – Chronic
idiopathic jaundice with pigment in the liver
 Rotor’s Syndrome – chronic familial
conjugated hyperbilirubenemia without

12.  PREDISPOSING FACTORS
 Liver Cirrhosis
 Hemolysis
 Infection in the Biliary System
 Infection in the Biliary Tract
 Geriatrics
 GI Disease/ T-Tube Fistula
 DM – insulin increasethe ablity to take up glucose
 Cystic Fibrosis – defective chloride channels which causes
cells to produce thich, viscous, mucous secretion – Prevents
pancreatic enzymes in reaching the duodenum – Results to
slowed fat digestion
 5 F’s – Fair, Fat, Fertile, Female, Fourty

13.  FAT /FEMALE: decrease bile salts in the bile and
excess estrogen is prevalent
 FERTILE: Hormonal Replacement Therapy, intake
of oral contraceptives which increases the
saturation of cholesterol ; CLOFIBRATE
 FAIR : Genetically speaking is candidate for
gallstone formation
 FORTY: DEGENERATIVE PROCESS - Increase
in risk of stone formation as there is an increase in
age because hepatic secretion of cholesterol is
increasing and there is a decrease bile acid
synthesis

14.  MULTIPARITY
 Benign Cholestatic jaundice of Pregnancy, with
retention of conjugated bilirubin probably
secondary to unusual sensitivity to the
hormones of pregnancy
 Repeated pregnancy causes increased
gallstone formation due to changes in
gallbladder kinetics leading to stasis and stone
formation

15. GALLSTONE IN PREGNANCY
US National Library of Medicine National Institute of Health
ABSTRACT
Gallbladder disease is four times as common in women as in men, and
pregnancy appears to contribute to the development of gallstones.
During pregnancy, most women receive ultrasound scans, which
are highly sensitive in detecting gallstones. The study was
undertaken to evaluate the prevalence of gallstones among the
pregnant woman. The aim was to determine any significant
difference in the prevalence of gallstone among the pregnant
woman compared to the generalized prevalence of gallstone in our
community.
METHODS The maternal gallbladder was examined in 1336
consecutive obstetric ultrasound scans performed for medical
indications at 3rd trimester of pregnancy. The study was conducted
in Centre for Nuclear Medicine and Ultrasond (CNMU) Mymensingh
on randomly selected subjects, among those who came here for
ultrasound evaluation of pregnancy. 500 control were taken from
age group between 20-30 yrs who came here for ultrasound
examination of lower abdomen other than pregnancy.

16. GALLSTONE IN PREGNANCY
US National Library of Medicine National Institute of Health
RESULT:
Gallstone were found in total one hundred eight cases.
Prevalence of gallstone in pregnant woman was
8.08% (n=108). The age ranges were 20 to 45 yrs
with mean age of 28.21 +/- 4.95 (mean +/- SD) yrs.
The highest prevalence (12.71%) were seen in 3rd or
higher gravida group with mean age of 30.32 +/- 4.74
yrs. Significantly higher cases of gallstone were found
in multiparity compared to control population of same
age group.
CONCLUSION:
Repeated pregnancy causes increased gallstone
formation due to changes in gallbladder kinetics
leading to stasis and stone formation.
Hossain GA1, Islam SM, Mahmood S, Chakrabarty
RK, Akhter N.

17. PATHOLOGY
 4 theory
 1. Changes in composition: BILE : SATURATED BILE WITH
CHOLESTEROL INCREASES BILE VISCOSITY
 2. Gallbladder Stasis – LACK OF GB CONTRACTION
:CAUSED BY SEVERE TRAUMA
 3. Biliary Tract Infection - debris caused by inflamaroty
response may form a nidus for ftone formation
 E.coli – can increase the amount of bilirubin
 Streptococus faecalis reduces bile salts
 4. Genetic and demography
 Native Americans- 75% cholesterol gallstones
 Northern Europeans
 South Americans

18. SIGN and SYMPTOMS

19. PANCREATITIS
Jessa Reomales Goyena, RN