Mindanao State University

COLLEGE OFMEDICINE
Department of Surgery

CASE
PRESENTATIO
N
Surgery Clerk Danessa A. Jutba
General Objective

To discuss and understand the diseases presenting as right
upper quadrant pain.

Inclusive Dates:
Specific Objectives

1 To review the basic anatomy, histology and physiology of the gallbladder and
extrahepatic bile ducts.

2 To trace the pathophysiology of cholelithiasis, including its etiology, risk factors, and
clinical manifestations.

3 To correlate the histopathologic findings and other diagnostic results with regards to the
Inclusive
pathogenesis Dates:
of cholecystitis.
Specific Objectives

4 To tackle the differential diagnoses of cholelithiasis and its main considerations.

5 To differentiate the mechanism and characteristics of cholesterol stones from pigment

stones.

Inclusive Dates:
 CASE PRESENTATION
IDENTIFYING DATA
J.C.C.
35 yrs old
Female

Married
Filipino
Roman Catholic
Vocational graduate
Housewife
Currently residing at Purok 7, Brgy. Palao Iligan City

Admitted for the first time at GTLMH last July 18, 2016 2:40PM
under the care of Dr. Marquez.
 CASE PRESENTATION

Source and Reliability:

Patient, 95% 
 
Chief complaint:
Right upper quadrant pain
 CASE PRESENTATION
HISTORY OF PRESENT ILLNESS
sudden onset RUQ Persistence of the UTZ reveal

21 months PTA
22 months PTA

pain, colicky,
intermittent,
PS scale 5/10,

symptom
prompted consult
to a private
composite
gallstones inside
the gallbladder,
non-radiating, physician and was and was given PO
lasts for 5-10 ordered for labs, to meds for 3 months.
minutes, noted to include CBC, UA
occur after and ultrasound of
ingestion of fatty whole abdomen.
foods (i.e. lechon
baboy, balbacua, etc).
 CASE PRESENTATION
HISTORY OF PRESENT ILLNESS

Meds given:
Rowachol PO TID for 3 months

Udkacid PO OD for 1 month
unrecalled antibiotic for 7 days.

Patient was compliant with medications.

Patient remained asymptomatic for 16 months.
No follow up was done.
 CASE PRESENTATION
HISTORY OF PRESENT ILLNESS
RUQ pain RUQ pain Patient consulted
1 month PTA

8 days PTA
recurred, now
more severe with
pain scale of 8/10,

persisted, now
intolerable, PS
10/10, radiating to
at Iligan Medical
Center, was
admitted as a case
radiating to the the back up to the of gallstone
back, lasts for 5 to right shoulder, disease. After 4
10 minutes, noted triggered by days of
to occur after ingestion of pork hospitalization at
ingestion of fatty sisig when patient that institution,
foods (i.e. lechon attended a buffet patient went
baboy, pork chop, dinner. (+) SOB, HAMA.
etc). (+) fever
 CASE PRESENTATION
HISTORY OF PRESENT ILLNESS
RUQ pain persisted, Patient consulted at

6 hrs PTA
still intolerable with GTLMH ER, and was
pain scale of 10/10, subsequently
radiating to the back up admitted.
to the right shoulder,
lasting for 5-10 minutes,
associated with
shortness of breath and
loss of appetite.
 CASE PRESENTATION
HISTORY OF PAST ILLNESS


No known chronic diseases such as diabetes
mellitus, hypertension or asthma.
No history of infectious diseases.
No allergies to food or medications.
 CASE PRESENTATION
FAMILY HISTORY


There is no history of heredo-familial diseases such
as diabetes mellitus, hypertension and asthma.
 CASE PRESENTATION
MENSTRUAL HISTORY


Menarche at 12 years old. Menstrual cycle is regular, every
28 to 32 days, lasting for 3-5 days, consuming 2 to 3 napkins a
day, non-heavy menstrual flow. There is history of
dysmennorhea but very seldom.
 CASE PRESENTATION
OBSTETRIC HISTORY


Delivered a live, full-term baby girl via cephalic NSVD
at a birthing clinic in Tubod, IC last April 2001. No
complications were met prenatally and postnatally.
 CASE PRESENTATION
GYNECOLOGIC HISTORY


Patient is sexually active and is not using any
contraceptive methods now. However, she reports to have
used ORAL CONTRACEPTIVE PILLS for 5 years after
delivering her first born.

There is no history of multiple sexual partners, or

sexually-transmitted diseases.
 CASE PRESENTATION
PERSONAL AND SOCIAL HISTORY


Patient JCC is the only child of Mr RC and Mrs JC.
She graduated a vocational course in ICI (housekeeping)
but was not able to work due to unplanned pregnancy
when she was 20 years old.
 CASE PRESENTATION
PERSONAL AND SOCIAL HISTORY


She is married to Mr PC, 37-year old construction
worker, who also resides in Palao, IC. They have one child,
JC, 15 year old female, who is currently a grade 9 student
at St Michael’s High School, San Miguel, IC.
 CASE PRESENTATION
REVIEW OF SYSTEMS
General: (+) for fever and loss of appetite; (-) for body weakness,

loss of consciousness, and weight loss.

Skin: (-) for dryness, discoloration and rashes.

HEENT: (-) for dizziness, visual disturbances, yellowing of eyes,

eye/ear pain, and ear/nasal discharges.

Neck: (-) for swollen glands and stiffness.

Respiratory: (+) for shortness of breath, (-) for difficulty

breathing and cough.
 CASE PRESENTATION
PHYSICAL EXAMINATION


General: conscious, coherent, ambulatory, not in respiratory
distress, in pain

Vital Signs:
Temp (axilla) 36.7 degree Celsius.
Heart rate 90 and regular.
Respiratory rate 26.
Blood pressure 120/80 mmHg.
 CASE PRESENTATION
PHYSICAL EXAMINATION
Anthropometric:
Weight: 58.4kg Height: 4’8” 
BMI: 29 (overweight)

Skin: Skin is dry, warm to touch, no discoloration, with good

turgor.
 CASE PRESENTATION
PHYSICAL EXAMINATION


Head, Eyes, Ears, Nose, Throat (HEENT):

Head: Scalp without lesions and atraumatic.

Eyes: PERLA. Pinkish palpebral conjunctivae, anicteric
sclerae.
Ears: Good acuity to whispered voice.
Nose: Septum at midline.
Mouth: Oral mucosa is pinkish and moist.
Throat: Non erythematous tonsillopharyngeal mucosa.
No exudates.
 CASE PRESENTATION
PHYSICAL EXAMINATION


Neck: Supple. Trachea at midline. No thyroid enlargement. No
lympahadenpathies.

Chest and Lungs: Equal chest expansion with shallow breathing,

tachypneic at rate of 26cpm. Equal tactile fremitus. Lung fields are
equally resonant. Clear breath sounds heard upon auscultation.
 CASE PRESENTATION
PHYSICAL EXAMINATION
Cardiovascular: PMI at 5th ICS MCL. No heaves or thrills. No
murmurs. 
Abdomen: Flabby. No scars. No dilated veins. Normoactive bowel
sounds. Soft, but (+) direct tenderness at RUQ. (+) for murphy’s
sign. (-) for obturator, psoas, rovsing sign, direct tenderness,
RLQ.
 CASE PRESENTATION
PHYSICAL EXAMINATION


Genitalia: Grossly female. Non-erythematous. No discharges.

Peripheral Vascular: No edema or varicosities.

Extremities: Equal and palpable peripheral pulses such as brachial,

radial, popliteal, and dorsalis pedis pulses. No edema. CRT <2 secs.
 CASE PRESENTATION
ADMITTING DIAGNOSIS
Acute on Chronic Cholecystitis

with Cholecystolithiasis
RUQ COLICKY PAIN, radiates to the back and shoulder region

TIMING OF RUQ PAIN: after ingestion of food

(+) fever, undocumented Tmax

UTZ findings in 2014 reveal gallstones

PE: (+) murphy’s sign, shallow breathing

Obesity, Hx of Pregnancy

Use of oral contraceptive pills (for 5 years duration)

 GALLBLADDER
INNERVATION


The nerves of the
gallbladder arise
from the vagus and
from sympathetic
branches that pass
through the celiac
plexus.

The preganglionic
sympathetic level is
T8 and T9.
 GALLBLADDER
PHYSIOLOGY


 CASE PRESENTATION
DIFFERENTIAL DIAGNOSIS
Gallbladder polyp

BASIS:
May mimic the symptoms of cholecystolithiasis

TO RULE OUT:
Note: Sensitivity of Ultrasonography is only 50% in the
presence of gallstones
Cholecystectomy is the treatment of choice (esp to identify
benign from malignant type)
 CASE PRESENTATION
DIFFERENTIAL DIAGNOSIS
Acute Hepatitis

BASIS:
RUQ pain
Fever
Loss of appetite

RULE OUT:
HBSAg - nonreactive
Ultrasound – whole abdomen shows normal sized liver
 CASE PRESENTATION
DIFFERENTIAL DIAGNOSIS
Acute Hemorrhagic Pancreatitis

BASIS:
RUQ pain
Loss of appetite

RULE OUT:
RUQ pain radiates to the back in a girdle-ike fashion,
not directly to the back
No history of alcohol intake or binge eating
(-) signs of peritonitis (i.e. abdominal ridigidity)
 CASE PRESENTATION
DIFFERENTIAL DIAGNOSIS
Sphincter dyskinesia

BASIS:
Chronic RUQ pain
Prior ultrasound shows gallstones

TO RULE OUT:
HIDA
 GALLBLADDER
PHYSIOLOGY

CCK-HIDA or Hepatobiliary scintigraphy

 assesses gallbladder contractile function
 diagnose bile leaks arising from fistulas and cystic duct obstruction
 CASE PRESENTATION
DIFFERENTIAL DIAGNOSIS
Peptic Ulcer Diseases

BASIS:
Abdominal pain may mimic extreme stabbing pain and loss of
appetite

RULE OUT:
Pain is usually correlated to meal times and characterized as
burning sensation.
No history of GERD or heartburn.
 CASE PRESENTATION
DIFFERENTIAL DIAGNOSIS
Hepatic Abscess

BASIS:
RUQ pain
(+) direct tenderness, RUQ

RULE OUT:
Ultrasound – whole abdomen
 CASE PRESENTATION
AT THE EMERGENCY ROOM

7/18/16 2:40pm 
>Please
>Please schedule patient
admit patient for openward
to surgery cholecystectomy
>Secure
>Secure consent
consent for contemplated surgery
to care
>Notify
>NPO OR staff and Anesthesiologist
>Monitor intake and
>Start venoclysis withoutput q shift
#1 D5LR; L regulate at KVO
>Monitor vital signs q 4hrs, and plot on chart
>Attach all lab results
>Meds: Tramadol 50mg cap TID PO PRN for pain
>Labs: CBC, platelet, blood typing
>Refer for any abnormal findings
>For CP clearance
 CASE PRESENTATION
COURSE IN THE WARD
7/19/16 9:00am
Hospital Day 2 
S:
(-) for pain on RUQ
(-) for headache, nausea, vomiting, and fever

Intake: 0.71cc/kg/hr (625cc in 15 hrs)

Urine output: 0.69cc/kg/hr (300cc + 300cc within 15 hrs)
Bowel output: none
 CASE PRESENTATION
COURSE IN THE WARD
7/19/16 9:00am
Hospital Day 2 
O:
Vital signs: 120/80mmHg, 37.0oC, 18cpm, 88bpm
Abdomen: flabby, soft, (+) normoactive bowel sounds. (+) direct tenderness at
RUQ. (+) for murphy’s sign. (-) for obturator, psoas, rovsing sign.

A:
Acute on chronic cholecystitis with cholelcystoithiasis
 CASE PRESENTATION
COURSE IN THE WARD
7/19/16 9:00am
Hospital Day 2 
P:
>NPO
>IVF to ff with ii ; L D5LR at 83cc/hr (regulate at 20gtts/min)
>Follow up CBC, platelet, blood typing - done
>CP clearance – done
>Meds: Tramadol 50mg cap TID PO PRN for pain
>Monitor intake and output q shift
>Monitor vital signs q 4hrs
>Refer for any abnormal findings
 CASE PRESENTATION
COURSE IN THE WARD
7/20/2016 9:00AM
Hospital Day 3
 

S:
(-) for pain on RUQ
(-) for headache, nausea, vomiting, and fever
Intake: 1.2cc/kg/hr (1800cc in 24 hrs)
Urine output: 1.14cc/kg/hr (650cc + 550cc + 400cc within 24 hrs)
Bowel output: once
 CASE PRESENTATION
COURSE IN THE WARD
7/20/2016 9:00AM
Hospital Day 3
 

O:
Abdomen: flabby, soft, (+) normoactive bowel sounds. (+) direct
tenderness at RUQ. (+) for murphy’s sign. (-) for obturator,
psoas, rovsing sign.
Extremities: EPPP, no edema, CRT<2sec

A: Acute on Chronic Cholecystitis with Cholecystolithiasis

 CASE PRESENTATION
COURSE IN THE WARD
 
P: 
>NPO post midnight Wednesday, for open
cholecystectomy tomorrow 7/21/2016 8AM
>IVF to ff with iii ; L D5LR at 125cc/hr (regulate at
30gtts/min)
>Meds:
Cefuroxime 1.5gm IVTT ANST by 8AM tomoro,
then 750mg IVTT q 8hrs
Ranitidine 50mg IVTT q 8hrs, start once on NPO
 GALLBLADDER
SPECIMEN FOR BIOPSY


 GALLBLADDER
SPECIMEN FOR BIOPSY


 GALLBLADDER
HISTOPATHOLOGIC
FINDINGS
GROSS 
DESCRIPTION
:

Size:
8.1 X 2.6 X 1.7cm

Mucosa:
velvety

Wall thickness:
0.3cm
 GALLBLADDER
HISTOPATHOLOGIC
FINDINGS
SCANNING
VIEW:

thickening
and fibrosis of
wall
 GALLBLADDER
HISTOPATHOLOGIC
FINDINGS
SCANNING 
VIEW:

invagination of
mucosal glands
through
muscular layer
(Rokitansky-
Aschoff sinuses)
 GALLBLADDER
HISTOPATHOLOGIC
FINDINGS


Rokitansky- Aschoff sinuses

 GALLBLADDER
HISTOPATHOLOGIC
FINDINGS
HIGH POWER
MAGNIFICATION
:

Subserosal
fibrosis with
infilitration of
neutrophils
 GALLBLADDER
HISTOPATHOLOGIC
FINDINGS

 CASE PRESENTATION
COURSE IN THE WARD
7/21/2016 3:00PM
Hospital Day 4 
3 hours Post-Op
S:
(+) for pain at post-op site
(-) for headache, nausea, vomiting, and fever
Intake: 1.9cc/kg/hr (2700cc in 24 hrs)
Urine output: 1.1cc/kg/hr (480cc + 550cc + 640cc within 24 hrs)
Bowel output: none
 CASE PRESENTATION
COURSE IN THE WARD
7/21/2016 3:00PM
Hospital Day 4
3 hours Post-Op

O:
Abdomen: flabby, soft, (+) normoactive bowel sounds. With dry
dressing on post-op site. Post-op site is nonleaky, with dry and
nonerythematous borders.

A: Acute Cholecystitis with Cholecystolithiasis

s/p cholecystectomy
 CASE PRESENTATION
COURSE IN THE WARD
7/21/2016 3:00PM
Hospital Day 4 
3 hours Post-Op
P:
NPO temporarily
>IVF to ff with iii ; L D5LR at 125cc/hr (regulate at 30gtts/min)
>Meds:
Cefuroxime 750mg IVTT q 8hrs
Ranitidine 50mg IVTT q 8hrs
Pancoxib 400mg IVTT q 4hrs for 3 doses
 CASE PRESENTATION
COURSE IN THE WARD

7/22/2016 8:00AM 
Hospital Day 5
Post Op Day 1
S:
(+) for mild pain at post-op site
(-) for headache, nausea, vomiting, and fever
Intake: 2.03cc/kg/hr (2850cc in 24 hrs)
Urine output: 1.7cc/kg/hr (820cc + 880cc + 740cc within 24 hrs)
Bowel output: none, (+)flatus, more than 6x
 CASE PRESENTATION
COURSE IN THE WARD
7/22/2016 8:00AM
Hospital Day 5 
Post Op Day 1
O:
Vital signs: 100/60mmHg, 36.4oC, 16cpm, 84bpm
Abdomen: flabby, soft, (+) normoactive bowel sounds. With
dry dressing on post-op site. Post-op site is nonleaky, with
dry and nonerythematous borders.

A: Acute Cholecystitis with Cholecystolithiasis

s/p cholecystectomy
 CASE PRESENTATION
COURSE IN THE WARD
7/22/2016 8:00AM
Hospital Day 5 
Post Op Day 1
P: >start with general liquids
>Meds:
Celecoxib 200mg BID PO
Cefuroxime 750mg IVTT q 8hrs
D/C Ranitidine
>IVF to ff with iii ; L PNSS at 125cc/hr (regulate
at 30gtts/min)
 CASE PRESENTATION
COURSE IN THE WARD
7/24/2016 7:00AM
Hospital Day 7 
Post Op Day 3
>MGH
>Remove IV, IVF
>Low fat diet
>Home Meds:
Celecoxib 200mg 1 cap BID PO for pain
Ciprofloxacin 500mg 1 tab BID for 7 days
>Advised daily dressing
>Follow-up check-up at OPD clinic on 8/1/2016
 Mindanao State University
COLLEGE OFMEDICINE
Department of Surgery

CASE
DISCUSSION
Surgery Clerk Danessa A. Jutba
 GALLBLADDER
GENERAL
DESCRIPTION

vesica fellae; hollow, piriform (pear-shaped)

lying on the inferior surface of the liver, attached via

loose areolar connective tissue
situated on a fossa between right and quadrate lobes of
the liver
 GALLBLADDER
EMBRYOLOGY


5 weeks gestation
Human embryo develops a
hepatic diverticulum within
the foregut

8 weeks gestation
Gallbladder is closely
associated with liver (fossa)
 GALLBLADDER
EMBRYOLOGY

12 weeks gestation
Bile is formed by hepatic cells and
may enter GI tract.
 GALLBLADDER
CONGENITAL ANOMALIES

Biliary

Gallbladder Double
Atresia Agenesis Gallbladder

Congenital
Septate Absence of
choledochal
Gallbladder cystic duct
cyst

Floating Intrahepatic Left-sided

gallbladder gallbladder gallbladder
 GALLBLADDER
ANATOMICAL
DESCRIPTION

length (saggital): 7-10cm
width (transverse): 3-5cm
wall thickness: up to 3mm
capacity: 30-50 cc
 GALLBLADDER
ANATOMICAL DIVISION


Fundus may be kinked or notched forming the
phrygian cap.

The fundus is a rounded, blind end which

may project 1– 2cm from the inferior
border of the liver. It contains most of the
smooth muscles.
 GALLBLADDER
ANATOMICAL DIVISION

The body is in contact with the 2nd

portion of duodenum. It contains the
Ductules of Luschka.
 GALLBLADDER
ANATOMICAL DIVISION

The neck lies deep in the gallbladder

fossa. Mucous glands are found only on
the neck.
 GALLBLADDER
ANATOMICAL DIVISION


Narrow angulated bulbous
portion of the neck forms the
infundibulum.

It is located at the free edge of

peritoneum, and serves as
landmark to identify cystic duct.
 GALLBLADDER
ANATOMICAL DIVISION

The spiral valves of Heister is an infolding

of the wall of the cystic duct. It has spiral
and smooth parts.
 GALLBLADDER
BLOOD SUPPLY
Abdominal aorta

Celiac trunk

Proper hepatic artery

Right hepatic artery

Cystic artery
 GALLBLADDER
HEPATOCYSTIC
TRIANGLE


Contents of
Calot’s triangle:
 Cystic artery
 Right hepatic
artery
 Cystic lymph
nodes
 GALLBLADDER
ANOMALOUS ORIGIN OF CYSTIC
ARTERY

 GALLBLADDER
VENOUS DRAINAGE

Venous return is carried through small veins that enter directly

into the liver or, rarely, to a large cystic vein that carries blood
back to the portal vein.
 GALLBLADDER
LYMPH NODES

Gallbladder lymphatics drain into nodes at the

neck of the gallbladder.
 GALLBLADDER
INNERVATION


The nerves of the
gallbladder arise
from the vagus and
from sympathetic
branches that pass
through the celiac
plexus.

The preganglionic
sympathetic level is
T8 and T9.
 HEPATOBILIARY DUCT
SYSTEM
The extrahepatic bile ducts consist of:


 HEPATOBILIARY DUCT
SYSTEM
Bile canaliculi

Intrahepatic ducts

Right and Left
hepatic duct

Common hepatic
duct

Joined by cystic
duct

Common bile duct

Joined by
pancreatic duct
 HEPATOBILIARY DUCT
SYSTEM

The common bile

duct is about 7 to 11 
cm in length and 5 to
10 mm in diameter.

It is divided into:
 Supraduodenal
 Retroduodenal
 Infraduodenal
 Intraduodenal
 Pancreatic
 HEPATOBILIARY DUCT
SYSTEM
The common bile duct runs obliquely downward within the
wall of the duodenum for 1 to 2 cm before opening on a
papilla of mucous membrane (ampulla of Vater) about 10
cm distal to the pylorus.
 HEPATOBILIARY DUCT
SYSTEM
The union of the common bile duct and the main
pancreatic duct:

 HEPATOBILIARY DUCT
SYSTEM


The sphincter of
Oddi, a thick coat
of circular
smooth muscle,
surrounds the
common bile duct
at the ampulla of
Vater.
 HEPATOBILIARY DUCT
SYSTEM
CHOLEDOCHODUODENAL
SPHINCTER

The sphincter of
Oddi, a thick coat
of circular
smooth muscle,
surrounds the
common bile duct
at the ampulla of
Vater.
 HEPATOBILIARY DUCT SYSTEM
ANATOMICAL VARIATIONS


 HEPATOBILIARY DUCT SYSTEM
ANATOMICAL VARIATIONS


 HEPATOBILIARY DUCT SYSTEM
ANATOMICAL VARIATIONS


 GALLBLADDER
HISTOLOGICAL
STRUCTURE

The hepatic, cystic and
common bile ducts are lined
by a single, highly folded,
tall columnar epithelium of
cholangiocytes.
 GALLBLADDER
HISTOLOGICAL
STRUCTURE


The epithelial lining of the gallbladder is supported by

a lamina propria. Normal findings show lining to be
quite uniform in appearance.
 GALLBLADDER
HISTOLOGICAL
STRUCTURE

For the biliary tract,
there is significant
muscularis externa
however, they are not
arranged
longitudinally or
circularly.
 GALLBLADDER
HISTOLOGICAL
STRUCTURE


There is an external adventitia (subserous layer) where it is

against the liver.

There is serosa (serosal layer)where it is exposed.

 GALLBLADDER
HISTOLOGICAL
STRUCTURE


The mucosa has abundant folds that are

particularly evident when the gallbladder is empty.
 GALLBLADDER
HISTOLOGICAL
STRUCTURE


The mucosa has abundant folds that are

particularly evident when the gallbladder is empty.
 GALLBLADDER
PHYSIOLOGY


 GALLBLADDER
PHYSIOLOGY

CCK-HIDA or Hepatobiliary scintigraphy

 assesses gallbladder contractile function
 diagnose bile leaks arising from fistulas and cystic duct obstruction
 GALLBLADDER
PHYSIOLOGY


Normal adult produces within the liver 500-1000 mL of bile
per day; yellow, brownish or olive-green in color

Secretion of bile is responsive to

Neurogenic
Vagal stimulation
Humoral
Chemical
Secretin
Cholecystokinin
 GALLBLADDER
PHYSIOLOGY
Composition of bile
1. Water

2. Electrolytes
3. Bile salts
4. Proteins
5. Lipids
6. Bile pigments
 GALLBLADDER
PHYSIOLOGY
Roles of bile
1. Excretion of toxins 
2. Absorption of most lipids

Primary bile salts are synthesized

in the liver from cholesterol
3. Cholate
4. Chenodeoxycholate
 PHYSIOLOGY
Metabolism of Bilirubin
Catabolism of RBC
 Ineffective erythropoiesis

Biliverdin reductase Biliverdin Bilirubin Albumin

Smooth endoplasmic reticulum Ligandin

Uridine diphosphogluconurate glucuronosyltransferase (UGT)

Conjugated bilirubin
B-glucoronidase
Intestines: Unconjugated bilirubin

Stercobilinogen
Urobilinogen
 PHYSIOLOGY
Metabolism of Bilirubin
Catabolism of RBC
 Ineffective erythropoiesis

Biliverdin reductase Biliverdin Bilirubin Albumin

Smooth endoplasmic reticulum Ligandin

Uridine diphosphogluconurate glucuronosyltransferase (UGT)

Conjugated bilirubin
B-glucoronidase
Intestines: Unconjugated bilirubin

Stercobilinogen
Urobilinogen
 GALLBLADDER
PATHOLOGY


 GALLBLADDER
PATHOLOGY
Prevalence and
Incidence 
Female

Obesity

Pregnancy

Dietary factors
 GALLBLADDER
PATHOLOGY

Natural history 
Most patients are
asymptomatic

Some progress to
symptomatic stage

Biliary colic
Jaundice
Fever – infection
 GALLBLADDER
PATHOLOGY

Bile stasis 
Bacterial inoculation
Infection
Inflammation
RUQ
Direct tenderness
(+) Murphy’s sign
Peritonitis
 GALLBLADDER
PATHOLOGY
CHOLELITHIASIS 
TYPES:
1. cholesterol gallstones
pure subtype
mixed subtype
2. pigment stones
brown subtype
black subtype
 GALLBLADDER
PATHOLOGY
CHOLESTEROL GALLSTONES
PURE  MIXED
90-100% cholesterol content 50-90% cholesterol content

Pale, whitish-yellow Various colors

Solitary Multiple

>2.5cm 0.5-2.5cm

Interior contains crystals that Smooth-faceted exterior,

radiate outwardly pigmented center, laminated with
layers of cholesterol crystals
 GALLBLADDER
PATHOLOGY
CHOLESTEROL GALLSTONES


Pure cholesterol gallstonesMixed cholesterol gallstones

 GALLBLADDER
PATHOLOGY
1. Supersaturation of bile with

cholesterol
 the result of hepatocellular
hypersecretion of cholesterol.
 primary defect, mediated by
abnormal regulation of hepatic
mechanisms for delivering
cholesterol to bile.[
 The abundant free cholesterol is
toxic to the gallbladder, penetrating
the wall and exceeding the ability of
the mucosa to detoxify it by
esterification.
 GALLBLADDER
PATHOLOGY
2. Gallbladder hypomotility ensues.

 Muscular stasis appears to result
both from intrinsic neuromuscular
dysmotility and from diminished
muscular responsiveness to
cholecystokinin, the hormone
secreted by the gut that promotes
gallbladder contraction.
 GALLBLADDER
PATHOLOGY
3. Accelerated nucleation of

cholesterol crystals

Nucleation is further promoted by the

presence of microprecipitates of
inorganic or organic calcium salts. As
a result of these events, supersaturated
bile is sequestered in a hypomotile
gallbladder under favorable nucleating
conditions.
 GALLBLADDER
PATHOLOGY
4. Hypersecretion of gallbladder
mucus
 cholesterol crystals are trapped for
sustained periods, enabling their
growth into macroscopic
concretions.
 GALLBLADDER
PATHOLOGY
PIGMENT GALLSTONES
BROWN  BLACK
Calcium bilirubinate in Calcium bilirubinate in monomeric
polymerized form form

10-40% calcium carbonate Little calcium carbonate

Little calcium palmitate 10-40% calcium palmitate

<10% cholesterol content <10% cholesterol content

Dull, orange-to-brown exterior Lustrous, amorphous shape

Greasy, laminated interior Homogenous, brittle interior

Multiple, 0.5-1.0cm diameter Multiple, 0.5-1.0cm diameter

 GALLBLADDER
PATHOLOGY
PIGMENT GALLSTONES


Brown pigment gallstones Black pigment gallstones

 GALLBLADDER
PATHOLOGY
PIGMENT GALLSTONES

Risk factors:
Asian
Chronic hemolytic syndromes
Biliary infection
Gastrointestinal disorders (i.e. ilieal
disease, crohn’s disease, ilieal
resection or bypass, cystic
fibrosis with pancreatic
insufficiency)
 GALLBLADDER
PATHOLOGY


 GALLBLADDER
PATHOLOGY


 GALLBLADDER
DIAGNOSIS


Standard: Abdominal Ultrasound
Occasionally, patients with typical attacks of biliary pain
have no evidence of stones on ultrasonography.

If the patient has recurrent attacks of typical biliary pain

and sludge is detected on two or more occasions,
cholecystectomy is warranted.
 GALLBLADDER
MANAGEMENT


Symptomatic gallstones - elective laparoscopic
cholecystectomy.

Avoid dietary fats and large meals.

Diabetic patients with symptomatic gallstones –

prompt cholecystectomy

About 90% of patients with typical biliary

symptoms and stones are rendered symptom free
after cholecystectomy.
 
Mindanao State University
COLLEGEOFMEDICINE
Department of Surgery

Thank You.
Inclusive Dates:
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Mindanao State University
COLLEGEOFMEDICINE
Department of Surgery

Thank You.
Inclusive Dates: