PART 2 GI PATHOLOGY: LIVER, PANCREAS, & BILIARY SYSTEM

FUNCTIONS OF THE LIVER:

Dr. ROXAS – September 28, 2010

- Has cells called HEPATOCYTE

a. Necessary for metabolism stuff
b. Erythropoiesis
- During Intra-utero (2nd trimester)  the liver & spleen is capable of
producing RBC. (Yolk sac  1st trimester, 3rd trimester-birth (Bones) )
- During CHRONIC ANEMIA ex:
1. Cancer elevation of TNF alpha that my inhibit erythropoietin release
2. Hemoglobinopathies (thalasemia)
- The liver & spleen hyperplasia  HEPATOSPLENOMEGALY these
organs has capability of producing RBC.

c. Storage

1. Blood supply stores - Acute blood loss  Liver & Spleen contracts 
stored blood adds on the blood volume that has been during the
hemorrhage. Therefore there no change in the serum of RBC, Hct level but
there is loss in the blood volume.
2. Glycogen stores – Excess glucose or energy derived from amino acids
or fats stored energy in the liver. During of starvation these glycogen can
be converted to Glucose as a source of energy.
3. Adipose/Fats  Pathological changes (fatty change), alcoholism &
hyperlpedemia.

d. Synthesis of Bile. Cholesterol, energy etc

.
Macrophages (Kupper Cells) 

RBC sequestrated by the spleen  HEME + GLOBIN

HEME  BILIVERDIN (Will further synthesized by liver) + Fe++ (Transported
back by iron binding CHON / Transfferin to the Bone marrow)
 ROLES LIVER
1. Heme Oxygenase (HEME  BILIVERDIN)
1. Biliverdin reductase (BILIVERDIN  BILIRUBIN unconjugated)
2. UDP Glucoronide transferase (Unconjugated lipid solube (not readily
excreted  Conjugated water solute not easily absorb readily excreted in the
urine, feces)
a. Immunogenic actions to immunogens (bacteria/virus/fungal/parasites)
b. Degradation of HEME or damaged RBC (SPLEEN) reticuloendothelial
system  (is already the job of hepatocyte) Biliverdin (Bilivervin
reductase  BILIRUBIN unconjugated)
c. Enzymes that induce apoptosis to the hepatocyte

Bilirubin > 300mg in times of hyperbilirubinemia  KERNICTERUS (CNS

Damage), Jaundice

1. Massive RBC Destruction

2. Liver disease obstruction in the portal tracts
General functions of the Liver:

1. Involved in Major Metabolic Processes.

a. Cytochrome p450 system necessary for drug metabolism
b. Carbohydrate Metabolism
- Glycolysis  Storage Glycogen (major site)  glucose
- Gluconeogenesis  Using non-glucose source (CHON amino acids & FFA) can
be used to form Acetyl-CoA (for Kreb Cycle)
- Conversion of Fructose to glucose (Pentose Phosphate Pathway)

2. ALBUMIN PRODUCTION  Proteins is a complex type amino acids (LIVER)

a. Osmotic Pressure Regulation (Intracellulary)  Resist Hydrostatic pressure

so that fluids in the extracellular will not move inside cell  PREVENT 3rd spacing or edema.
b. Drug Binding  bound drugs to protein are inactive form (high protein bound
drugs)  NO PHYSIOLOGICAL ACTION

Neonates  IMMATURE LIVER  Less or no albumin

ELDERLY  LIVER DEGENERATED/ damage  Less albumin

Drugs  should not be same dosage as in normal functioning liver adult 

OVERDOSAGE OR POISONING

c. Can serve as energy reserve in times starvation  NET PRODUCT KETO ACIDS

c. Protein Metabolism

ALL PARTS IN YOUR BODY  contain the following enzymes: Found inside
the cytoplasm of the cell, actions is deaminating the amino acids
(PROTEINS)
1. Aspartate aminotransferase/ SGOT/AST  GLUTAMINE  alpha
KETOGLUTARATE (PART OF THE KREB CYCLE  ATP production)
2. Alanine aminotransferase/SGPT/ALT  PYRUVATE (KREB CYCLE ) 
ENERGY

Deamination of CHONs  NH3+ (AMMONIA)

- CO2, Alcohol, NH3+  PASS THROUGH cell membrane freely  EASILY
ABSORB.
- AMMONIA is converted by the liver via ORNITINE CYCLE/ UREA CYCLE
 UREA (Excreted in the feces & urine)
1. Can produced conversion of UREA into ammonia by Intestinal bacteria
(UREASE)
- can be prevented by NEOMYCIN (Kills microorganism), LACTULOSE
(Osmotic Diarrhea)  MAITAE and lactic acid that formed prevents urease
activity.
 - Remember if the PORTAL CIRCULATION is obstructed/ PORTAL
HYPERTENSION  Formation of collateral venous system  by pass the
liver  Ammonia cannot go directly and covert to urea  level of ammonia
rises in the blood  HYPERAMMONEMIA

- Degradation of Purine & Pyrimidine Amino Acids  UREA  NH3 (INTESTINE)

- Remember: NH3 is highly lipophillic it can pass through cell membranes, this can
be reabsorbed & also can penetrate the Blood Brain Barrier  CNS
- If you have too much NH3

1. Encephalopathy (Hepatic)  Damages the cell membranes of the nerves that

Impedes the synaptic homeostasis (Electrical & Chemical) (RELATED IN LIVER
FAILURE)

RATIONALE: HYPERAMMONEMIA there conversion of direction reaction to

GLUTAMATE FORMATION  INHIBITS FORMATION OF alpha KETOGLUTARATE
 KREBS CYCLE REDUCED  LACK ATP  LACTIC ACIDOSIS  ISCHEMIA
death cell CNS.  COMATOSE

1.b Can cause bubbles (this is not related to LIVER FAILURE  DEEP SEA diving
(Barotrauma  BENDS can cause embolism & Stroke) if very fast ascending from the
deep sea. (DIFFERENT STORY)

- Transamination of Proteins
d. FAT Metabolism
- Cholesterol Synthesis of (VLDL & HDL)
- Bile is formed  Emulsify Fats in the Ileum area  To form Micelles  bind in
the lacteals  Thoracic or Lympathic duct in the circulation.
- Bile  Fat Soluble Vitamins absorption (ADEK)
e. For the conversion of ANGIOTENSINOGEN  AGIOTENSIN 1 (aided with
RENNIN release by JG CELLS of the afferent arteriole of the Kidney)
2. Synthesis of Proteins:
Albumin Production Characteristic Action:
- Regulation of Osmotic Pressure ( Resistance to the Hydrostatic Pressure)
- Drug Binding (Protein Bound Drugs  NO PHYSIOLOGIC EFFECT)
a. Drugs
b. Fe (Iron Binding Protein)
c. T3 & T4 (Thyroxine Binding Protein)
Therefore all unbound drugs  these participates on Physiologic Actions.
- The albumin is also the measure for (Nutrition in the body specially in patients
with PEM)
3. Synthesis of Clotting Factors for Control of Bleeding: (II, VII, IX, X  1972) with
the action of the Vitamin K
4. Synthesis of Fat Soluble Vitamins
 a. (EXAMPLE) Step in initial activation of Vitamin D2  Vitamin D3 (KIDNEY)
5. For the Synthesis of Globin Molecule  Immune-response ( Immunoglobulin in
Humural Immunity *(IgG, IgA) IMMUNO+GLOBIN

Unconjugated Bilirubin Increase

1. INBORN ERRORS of Metabolism ( NO BILIVERDIN REDUCTASE or NO

UDP-GT)
2. SUPER DAMI ng HEMOLYSIS (destruction of RBC)
- BLOOD TRANSFUSION RXN
- IMMUNE RESPONSE (AUTOIMMUNITY) SELF DESTRUCT
- INFECTION (MALARIA)
- ANIMAL TOXIN (VIBURA  LOYAL SERPENT OF VALENTINA  COBRA)
- SPLENOMEGALY (LUMAKI ang SPLEEN)  Increases the size, enzymatic
activity of the Reticulo endothelial cells  HIGHER FUNCTION 
DESTRUCTION RBC
- GENETIC (Thallasemia, Membrane Defect)
- Mechanical ( Prosthesis  MITRAL VALVE ARTIFICIAL ) cause damage directly
in the RBC  HEMOLYSE
- Mechanical FORCE or COMPRESSION  SINAPAK, INIPET, NECROSIS,
decrease blood flow
a. Conjugated Bilurubin Increased
- VERY COMMON (LIVER CIRRHOSIS) specially if (+) FIBROSIS of the
Hepatocyte (OBSTRUCTION OF THE BILIARY SYSTEM)
- STONE in the Biliary Tract
- Strictures ( kumipot ung BLOOD VESSEL NG PORTAL CIRCULATION 
atherosclerosis)
- TUMOR Compression
- GENETIC

5. STORAGE of BLOOD: MAJOR (400ml?)

6. STORAGE of MINERALS & VITAMINS (IRON)
7. PORTAL SYSTEM  MAJOR BLOOD FLOW & Control of Pressure

CONSEQUENCES IF THERE IS (+) LIVER DAMAGE

1. Impaired Metabolism
2. Bleeding  10,9,7,2 inhibition
3. Obstruction to flow  PORATL CIRCULATION
v
4. PORTAL HYPERTENSION
- Obstruction Portal Tracts  COLLATERAL CIRCULATION
 a. Esophageal Varices (Block L gastric Artery)
- This can generate the following symptoms:
1. Odynophagia usually after swallowing specifically solid bolus
2. Dysphagia with solid foods can be relieved significantly with water/liquids
3. Angina Pectoris but non cardiac origin
4. Vomiting can cause pressure in the esophagus that can mimic esophageal
venal rupture.
b. Gastric Ulcer  Blockage to the blood flow and reflux may complicate
symptoms including esophageal damage
c. Rectal Varices  notable blood in the anal area or after defecating. Must
institute laxatives to prevent straining or valsalva maneuver
d. Umbilical Varices  Caput medusa
e. Peritonitis or enlargement of the abdomen

5. Hypoalbuminemia  EDEMA (3rd Spacing), due to osmotic pressure reduction

vs. hydrostatic pressure
- Important to modify salt, NSS, water intake may retain cause hypervolemia
6. Vitamin Deficiency – ADEK
- Vitamin A  May precipitate vision complaints, and reduction of growth of
mucous membranes
- Vitamin D  May rise serum levels of calcium in the blood due to leaking out of
calcium in the bone and may be excreted in urine and feces
- Vitamin K  Complicates bleeding

7. Immunosuppression
8. Hypertension  PORTAL CIRCULATION & Collateral circulation, back-flow
-must remember that portal obstruction mediated by fibrosis of liver may impede
ammonia flow from the blood preventing ammonia (usually from intestines due
urease mediated bacterias) to proceed ornithine cycle/urea conversion
9. Accumulate NH3  CNS inflammation (increase cell membrane permeability 
damage  Decrease neurotransmitter release, impaired synapsis  HEPATIC
ENCEPHALOPATHY (Coma  Late & very high ammonia in blood), Hepatic
Flap & Apraxia, even behavioral changes  early)
- Remember that alpha ketoglutarate may not give the CNS enough energy ATP,
that may activate lactic acidosis and damage.
10. Metabolic Acidosis  Lactic acid buildup.
11. FATS  Cholesterol  REQUIREMENT in steroid synthesis (affect
ESTROGEN  GYNECOSMASTIA (FOR MALES only, estrogen fails to
converted to testosterone), CAPUT MEDUSAE
12. HEPATO-RENAL syndrome  Renal failure in Liver Failure (Remember this is
transient if LIVER failure becomes compensated this can be recovered)
Related to decreased renal blood flow  RENNIN RELEASE 
 VASOCONSTRICON  Reduction in blood flow in the kidney that may damage
kidney.
- Check the urine output is very critical (0.5cc/kg/hr)

CAUSATIVE AGENTS:

1. CHEMICAL (Drugs hepatotoxic, Alcohol, AFLATOXIN (Nuts)  fatty liver,

Benzene)
2. BIOLOGICAL (Atherosclerosis in the portal tracts, Hyopercholesteremia,
Obstruction  stones, Parasite, Strictures, Viral hepatitis, Parasites, Bacterial)
3. IMMUNOLOGICAL (Autoimmunity)
4. DEGENERATIVE (old age, senescence cells  apoptosis  reduce number of
hepatocytes  reduction function)
5. CONGENITAL (Inborn errors, Atresia)
6. MECHANICAL (Gunshot, Bugbug, Tumor, etc)
7. GENETIC
8. PARASITES (Liver Fluke & Amoebiasis)
9. INFECTION: Hepatitis B (10-20 Years), & C (faster)

LIVER CIRRHOSIS: Irreversible liver damage (accumulation of regenerative

cells, inflammatory substrates , collagen type 1 & FIBROSIS), last stage of
changes in the liver.

Changes on how the liver adapt on the insults:

1. Fatty Changes Phase
2. Hepatitis/Inflammatory Phase
3. Cirrhosis of the Liver Phase
4. Liver Failure
5. Hepatocellular Carcinoma (Cancer)

Etiology:
A. Alcoholic (common) or Laennecks Cirrhosis
B. Cryptogenic (Unknown cause) Cirrhosis
C. Drug-Induced Cirrhosis (Chemotherapy)
D. Cardiac Cirrhosis  R Sided Heart Failure
E. Posthepatitic (portal tracts)
- Presinusodal  Portal Tracts (SVC/IVC) – problems Strictures or damage in
the blood vessel, Shock or loss blood)
- Sinusodal  Within the hepatocyte (Viral (Hepatitis C & B), Enzymatic Free
Radical Damage, Parasitic, Alcoholism etc)
- Postsinusodal  Biliary Tracts (Gallstones, Pancreatitis etc)
F. Inherited
G. Parasities
Insult in the hepatocyte  damage in cell membrane  Inflammation released
(Pholipase A2, Leukotrine Synthesis, Arcachidonic Synthesis, PGE1, etc) 
Leukocyte migration and Differentiation (KUPPER CELLS) releases Cytokines
(TNF alpha Leukocyte differentiation, damage, TGF B  (Collagen Type1),
IL1(FEVER), IL6)  Changes in the structure FIBROSIS  LOSS FUNCTION

Dysfunctional Changes in Liver Cirrhosis:

a. Anorexia
- (TNF-alpha) (controls the satiety center)
- Accompanied with Hepatomegaly or Ascites  can cause compresses the
stomach  fullness feeling (BUSOG)
- Dysphagia ( related to the Esophageal Varices  Obstruction on the bolus
flow)
b. Malnutrition (loss of albumin formation, Loss of synthesis & storage of Fat
soluble vitamin (ADEK) & Carbohydrate Metabolism (Hexokinase,
Glucokinase etc. are affected)
c. Easy Bruising (Loss synthesis of Vitamin K  Coagulative problems X, IX,
VII, II synthesis)
d. Easy Fatigability  Carbohydrate Metabolism is affected( production of
ATP, doesn’t satisfy the need body  weakness)
e. MALE Hormonal Imbalance  Gynecomastia (breast enlargement), Palmar
Erythema, Caput Medusa, Testicular Atrophy ( PERIPHERAL ESTROGEN
CONVERSION  accumulation ANDROSTENEDIONE) (because unable
degrade

f. PORTAL HYPERTENSION  Obstruction in the tracts that govern the portal

system ( Because of compression, obstruction of fibrosed hepatocyte)
 Effects of PORTAL HPN: is not HIGH BLOOD focus
NORMAL  5-10mmHg
ABNORMAL  >10mmHg
Obstruction to flow (because of the fibrosed hepatocyte due to compression)
 Generates pressure > 12mmHg  Reduction in the portal blood flow 
a. (some areas of the hepatocyte can be ischemic)
b. Porto-Fugal Flow  Formation of Collateral Circulation ( Back Flow in
areas has less pressure VEINS)
1. Gastrioesophageal Varices (Cardiac-Esophageal Junction) 
Bleeding (ulcer, rupture) Risk
2. DANGER  RUPTURE  BLOOD LOSS SHOCK
3. Esophageal Varices  precipitate Dysphagia (obstruction & decrease
in the diameter of the esophagus)

ESOPHAGEAL VARICES Treatment:

a. Vasoconstrictors (VASOPRESSION/IV) Vasoconstrict the blood

vessels  RISK Ischemia & HPN
b. REPLACEMENT  BLOOD (if (+) Blood Loss), Lactate Ringers

INVASIVE PROCEDURES  CONSENT: REQUIRES SEDATION

c. Endoscopic Banding
d. Endoscopic Sclerotherapy  injects (?)
e. Baloon Tamponade
- SENGSTAKEN BLAKEMORE (3 LUMEN)
- MINNESOTA (4 LUMEN)
- Endotrachial tube should be inserted  risk aspiration (saliva)
- Side Effects: Esophageal Ischemia or Necrosis  REDUCED BLOOD FLOW in
the Esphageal Mucosa (Arterial Compression)  Perforation or Damage in
Esopgaus
- If survived , Risk for Esophageal Strictures & Fibrosis

- ACTIVE ESOPHAGEAL BLEEDING: EMERGENCY & DEADLY

a. Reduce of Blood Pressure  SHOCK
b. CNS signs: Dizziness, Seizure, Delerium  Reduction of Cerebral Blood
Flow
c. Tachycardia  Arrhythmia ( Baroreceptor Reflex)

4. Rectal Varices  Hemorrhoids & Bleeding

- AVOID (VALSALVA MANEUVER or Straining)  rupture
- GIVE Laxatives Lactulose  Easy Defecation
- DO NOT LABATIBA  BAKA MATUSOK AT PUTOK ANG UGAT RECTUM
5. Jaundice 
- Due obstruction portal tracts
- Failure to convert conjugated bilirubin  DAMAGED HEPATOCYTE
- Accumulate conjugated bilirubin  OBSTRUCTION
- HEMOLYSIS  Toxins etc.
 EFFECTS:

a. Itchiness or Skin irritation  ACCUMULATION of BILE PIGMENTS

b. Eyes Irritated  in some cases (Inflammation by inflammatory
cytokines) FOREIGN BODY Bile pigments
c. DANGER if the Bile is severe sp. Unconjugated  KERNICTERUS
- Monitor serum levels of Bilirubin, dialysis might be an option
6. Ascites 
a. No albumin (lack of production) Loss of Oncotic Pressure
b. Increase in Intra-hepatic Pressure (obstructed portal tracts) 
pushes the fluid towards peritoneal area
c. Aldosterone Release (Adrenal Cotex)(Decrease Renal Blood Flow
 ANGIOTENSIN 2 activation to AT1 receptor)  Na & water
retention (Collecting Tubles)

Effects:

a. Anorexia  Mechanical Compression to the Stomach

b. Dyspnea  Compressive Effects that obstructs the ventilation
process (Compressive Type Atelectasis Risk Collapse Lung) 
affect CO2  Risk for acidosis
 3types: Compressive (Ito ang sa ascites okay), Obstructive,
Contractive
c. Mobility Deficit  Daily chores are affected
d. Bain Bridge Reflex Activation (increased water retention 
increasing blood volume) Tachycardia (Increasing work load on
the heart) Cardiac Remodeling (Hypertrophy or ACS  Acute
Coronary Syndrome)
e. Increase work load kidney  Release of RENNIN 
Vasoconstriction by (ANGIOTENSIN II)  RENAL BLOOD BLOW
 decrease U/O or ARF (HEPATO-RENAL-FAILURE or
SYNDROME)
Treatment:
1. Glucorticoids  Reduces Inflammation
2. Furosemide (LASIX) (LOOP) or Spironolactone (K-sparing
diuretic)
3. NaCl restriction & water intake(modify) Aldosterone release)
4. Monitor the weight & size of the abdominal girth
- With the use of Furosemide  enhancing K loss  pH rises (risk NH3 formation
 HEPATIC ENCEPHALOPATHY)
- So K-sparer prevents K loss  lowers the pH  Reduces the risk rising the NH4
7. Encephalopathy  Entry of ammonia in the cell membrane (CNS)
this damages the depolarization that impedes synaptic response.
AMMONIA  LIPOPHILLIC  it can pass through the cell membranes , and readily
reabsorbed.

What are the incidences to Rise your NH4:

1. Protein Intake (monitor diet)  Came from CHON degradation forms NH4
2. Colonic Bacteria  produces NH4 specially in the presence of CHON
Treat:
- Providing ANTIBIOTIC : NEOMYCIN (non absorptive antibiotic)  reduce the
number of colony of bacteria
- Providing use of Osmotic Laxative: LACTULOSE (Colonic bacteria will not
produce NH4 because this decreases GI pH (LACTIC ACID)
- Providing BENZODIAZEPINE (Flumazepine)  GABAmimetic (UMAYOS ANG
UTAK wag mo inumin please)
3. Bleeding  GI tract (amino acids/CHON in RBC or blood  rises NH4)
4. Rise pH
5. Loss Potassium or Hypokalemia ( using LOOP diuretics)
- ABG should be monitored for pH (rise pH indicates NH4 formation)
- Pulse oximeter check PaO2 & PaCO2
Stages Encephalopathy: (+) ASTEREXIS  FLAPPING TREMOR 
because un-synchronous depolarization nerve fiber)
STAGE 1: Euphoria
STAGE 2: Lethargy
STAGE 3: Confusion
STAGE 4: COMA  permanent damage (-) ASTEREXIS
6. HEPATOMEGALY
7. SPLENOMEGALY (Splenic vein Collateral) RAS activation by kupper cell 
Destroys the RBC  HEMOLYTIC ANEMIA
8. ANEMIA cause:
a. SPLENOMEGALY  Destruction of the MORE RBC
b. VARICES RUPTURE
c. ULCER  STRESS
d. LOSS CLOTTING FACTORS (Vitamin K synthesis)  RISES prothrombin
time
e. Loss of Vitamin (Folic Acid metabolism, ADEK)
f. TNF alpha inhibition of Erythropoietin release (KIDNEY)  ANEMIA of
CHRONIC DISEASE

Diagnostics:

Blood chemistry: AST, ALT, Cholestrol, NH3

Biopsy  Cirrhosis (beneficial for patients who deny alcoholism)
Ultrasound
MRI
 ALCOHOLIC LIVER CIRRHOSIS:
Ask  bottle/day, years, when is the last time?
- Considered to be malnourished (loss of Vitamin B6, & 12)
- Amount of Alcohol & Length EXPOSURE (years)
- Most common cause of liver damage (M>F common) but Females is most
affected has greater damage
- 1 BEER (330ml)  12g/dose of alcohol
- 60-80g/d for 10 years of exposure  CIRRHOSIS

Changes of Liver Hepatocyte Architecture with Exposure HEPATOTOXIN:

STAGES
a. Fatty Liver (REVERSIBLE)  accumulation of fatty lobules, 40-60g/d
b. Alcoholic Hepatitis  Inflammation
c. Liver Cirrhosis (IRREVERSIBLE)  Collagen type 1 substrates & Fibrosis +
Regenerative cells, if there is changes in the structure  function
changes,also (loss). (Cytokine release  TNF –alpha, Transforming Growth
Factor Beta (TGF Beta)  Collagen Type 1, IL1, IL6) , 80-160mg/d (alcohol)
d. LIVER CANCER (Hepatocellular Carcinoma)

(GALL BLADDER) Cholelithiasis  STONE

- OBESITY (Accumulation of FATS & Cholesterol)

- Weight Loss (* Anti-fat etc.) (Accumulation of Free Fatty acids in the Biliary
Tracts)
- FEMALE (Estrogen Surge  Retention of Cholesterol & FFA)
- PREGGY  Compression in the Gallbladder  HYPOMOTILITY ( loss of
peristaltic movement  SLUDGING)
- OLD AGE (HYPOMOTILITY  Stone sludging)

REMEMBER: Risk for Pancreatitis & Liver Damage

1. Pancreatic Damage is due when the stone obstructs the common biliary tract that
increase pressure in the pancreatic duct (Pancreas secretes zymogens, bicarbonate
and pancreatic amylases  May add build up pressure  May compress effect the
following:

1. Zymogen can be activated  AUTODIGESTION  Damage

2. Pressure can compress pancreatic arterial system that may decrease blood flow and pancreatal lactic
acidosis  Damage

2. Liver failure  May damage the liver due pressure.

STAGES STONE FORMATION

1. Supersaturation (Accumulate Cholesterol)

- Rises the nucleation ( MUCUS & Cholestrol)
- Lowers the nucleation (Lecithin, APO-1)
2. Nucleation
3. Microstoning formation
4. Stone Formation  BILE PIGMENT (CALCIUM)

CONSEQUENCES: STONE FORMATION

1. Stone generates pressure  Increase in the gallbladder Intra-luminal pressure

 dilatation
- Compress mucosa (dilation & stretch), and arteries that supports the gallbladder
 reducing cholecystal blood flow Ischemia  Inflammation  Necrosis
Perforation
2. Stretching the gall bladder induces reflex  contraction of gall bladder 
NOCICEPTOR activation  Biliary COLIC Pain
3. Obstruction in the Biliary Tracts  risk for damaging the liver (Posthepatitic),
Pancreas  Obstructs the enzymatic flow in the common bile duct area that lead
to autodigestion of enzymes due to pancreatic enzyme back flow( cause
inflammation to the pancreas)
4. Generates infection (stone)  Anaerobes

Symptom:

1. Cytokine Release : (non-specific)

TNF alpha Nausea & Vomiting CTZ activation
IL1  FEVER
 2. PGE2 release (Phospholipase A2 A.A), Bradykinin  NOCICEPTOR
ACTIVATION  VICERAL PAIN, Contraction Reflex  COLIC PAIN
(RUQ)
3. RARE Steatorrhea (FULL BLOWN OBSTRUCTION NO BILE RELEASE)
4. JAUNDICE (FULL BLOWN OBSTRUCTION)

Diagnostics:

ULTRASOUND

Abdominal Xray

TREATMENT: Surgery

1. Cholecystectomy
2. Laparoscopic Surgery

Non-invasive  Ultrasonic device

Cholecystitis  Inflammation

- Stone
- Parasites
- Viral
- Compression
- Immune Mediated
- Ischemia Reduction in the Blood flow