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ATOC 2009 RM

Accessory Organs
Anatomy and Physiology
1. Liver
- right diaphragm inferior surface
- located in RUQ (inside th rib cage) or abdomen weighting 1200-1600
- composed of 2 lobes: right and left (second largest organ)
- the right and left lobes are separated by the falciparum ligament which
anchors the liver and abdominal wall
- covered with a fibroelastic capsule that contains blood vessels, lymphatics
and nerves
- trauma (detrimental) > shock
- reddish brown organ
- inferior to the diaphragm and fills most of the right hypochondriac and
epigastric regions of the abdominal cavity.
- four lobes called the right, left, quadrate, and caudate lobes
- 1. liver is largest gland in body
2. overall function to “filter” and process nutrient-rich blood delivered to
3. receives nutrient-rich blood from SI via the hepatic portal vein
4. many functions to liver besides aiding in digestion
5. regulates carbohydrate metabolism
a. glucose secretion into blood/absorption from blood into glycogen
b. regulated by insulin & glucagon (endocrine review)
6. regulates many aspects of lipid metabolism
a. chemical digestion of fatty acids (B-oxidation) for entry into Krebs
i. release of ketones as metabolic waste product of fatty acid
b. cholesterol synthesis
7. detoxifies blood
a. ETOH detoxification
b. other dietary toxins neutralized by liver
8. bile synthesis (approx 1L/day)
a. bile salts (cholesterol derivatives) function to emulsify fats to aid
enzymatic digestion
i. bile salts are recycled (are not excreted) from colon back into liver
for reuse
b. main bile pigment is bilirubin – derived from RBC heme
i. bilirubin and other neutral fats in bile do not aid in digestion; they
are excreted
e. bile is synthesized in liver, stored in gall bladder
f. release of bile from gall bladder stimulated by CCK and vagus nerve
i. CCK also causes hepatopancreatic sphincter to relax – allows bile
to enter duodenum
ii. secretin also stimulates bile synthesis
iii. bile salts also act as positive feedback activator to enhance more
bile synthesis
g. “gallstones” are concentrated precipitates of cholesterol
i. gallstones form when bile is too rich in cholesterol or lacking bile
biliary tract
- composed of the gallbladder and associated ducts: cystic, hepatic, and
common bile ducts
- bile is synthesized in the liver and transported to the bile via the bile
canaliculi that surround each hepatic cell (1000ml /day)
- bilirubin → bile from the liver through hemolysis; pigment stores

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- bile canaliculi drain into the right or left hepatic duct which come together
to form the common hepatic duct
- bile emulsifies for which gives odor to the urine and skin
- the sphincter of oddi is at the distal end of the common hepatic duct and
controls the flow of bile into the duodenum → jaundice → flow of blood
- damaged sphincter of oddi → destruction of bile (→salt accumulation
→pruritis, itching) → jaundice
- the cystic duct connects the gall bladder to the hepatic duct and they
merge to form the common bile duct
2. gall bladder
- store and concentrate bile 5 – 10 x between meals
- sac like organ on the inferior surface of the liver
- its mucosa readily absorbs water and electrolytes , leaving a high
concentration of bile salts, bile pigment and cholesterol
- holds about 60-90 ml of bile
- small greenish sac semi-embedded in the inferior surface of the liver
- neck of the gallbladder is continuous with the cystic duct that joins with
the hepatic bile duct to become the common bile duct
- stores about 50 mL (1.7 US fluid ounces / 1.8 Imperial fluid ounces) of bile,
which is released when food containing fat enters the digestive tract,
stimulating the secretion of cholecystokinin (CCK). The bile, produced in
the liver, emulsifies fats and neutralizes acids in partly digested food.

3. pancreas

- Role Of The Pancreas In Digestion

1. approx 1.5L/day pancreatic secretions produced
2. secretions enter duodenum via two pancreatic ducts
3. many different components in these secretions
a. NaHCO3 – buffers pH of chyme
b. pancreatic amylase
c. trypsinogen, chymotrypsinogen, carboxypeptidase

ATOC 2009 RM
i. trypsinogen activated by enterokinase to become trypsin
ii. trypsin acts on other proteases to activate them
d. lipases
e. ribonucleases
- Regulation Of Pancreatic Secretions
1. neuronal regulation
a. initiated by parasympathetic activation (vagal innervation)
b. same stimuli as with cephalic and gastric phases
2. hormonal regulation
a. CCK stimulates pancreatic enzyme secretions
b. secretin stimulates bicarbonate secretions
- aprox. 20 cm long (head tucked into the curve of the duodenum; tail
touching the spleen; body lies deep in the abdomen, behind the stomach;
head and tail both secrete enzymes that left side has humerous nerve
endings- tail)
- soft, spongy, pink gland that is posterior to the greater curvature of the
stomach and outside the peritoneal cavity
- enzyme- producing gland of the digestive system (acts on all the things
you eat or digest) – it is important for break down of the things ingested
- endocrine pancreas secrete
o insulin: for sugar regulation ; protein hormone
o glucagons: converts carbohydrates to simple sugar (lactose, fructose,
glucose) stimulates glycogen in liver→ feeds the cell→converts the food
into [ATP] Adenosine triphosphate for energy
> from (insulin and glucagon) islets of langerhans; must come together; if not,
it may result to DM or AN
- if sugar is not controlled → clot formation ‘crystals’→ thrombus formation →
trauma → death
- purine(→coma) →uric acid →blood stream → joints →”osteoarthritis”
- glucogenesis → stored CHO are converted into sugar
- glycogenolysis→ breakdown sugar / glucose in the body with the help of
insulin through sweat and fecalysis
- produces alkaline fluid (1-1.5mL of pancreatic juice / day)
 the body is nourished by the HCl through stomach. To neutralize this acid chyme
as it empties into the duodenum, pancreas releases alkaline fluid
o lipase[lipids] neutralizes / breakdowns fats
o pancreatic alpha amylase [carbohydrates] / TAA promotes CHO
breakdown; starch / sugar
o trypsin, chymotrypsin & carboxypeptidase [amino acids] breakdown
proteins to energy

EXOCRINE PANCREAS- secretes enzymes coposed of secretory units called acini and
series of ducts that secrete enzymes and alkaline fluids into the pancreatic duct
(Wirsung duct), which empties into the common bile duct of the ampulla of vater

Protein→ ALT & AST free flowing is blood, necrosis, protein by product will retain –NH3
& ammonia → metabolic acidosis → brain → hepatic trauma
1. stores fat- soluble vitamins (ADEK)
o trauma→ release of ADEK
o liver cirrhosis [necrosis of the liver] → vitamin K (IM/ ampule)
2. metabolizes bilirubin, by- product of the destruction of old RBC
o RBC[ from bone marrow gets oxygen during inhalation then runs
through the body]

↓ ↓
heme globulin (CHON
content of RBC) ATOC 2009 RM
in the systems for tissue perfusion

kidney uses up the

matures 180
↓ ↓

some destroy/ death

MATS macrophage

breakdown globulin into smaller pieces

damaged liver

↓ Iron should be “ready made”

globulin→ bilirubin
goes to spleen o liver → bile (emulsifies fats → prevents thrombus & decrease tissue
(stored) o fats- minimal
heme→ ferretin → usually
3. stores stored in blood
and releases the liver
during hemorrhage
o blood loss → shock → death
4. synthesizes plasma proteins to maintain plasma oncotic pressure
o attracts water component (oncotic pressure) to retain; temporarily
stays in the body to avoid dehydration
o release (hydrostatic pressure)
o hemolyze (osmotic pressure)
5. synthesizes prothrombin, fibrinogen and clotting factors I, II, VII, IX, X
o prevents too much bleeding / hemorrhage
6. synthesizes phospholipids & cholesterol necessary for the production of bile
salts , steroid hormones and plasma membranes
o phospholipids → good cholesterol (concentrates bile) it gives salt to bile so
that it will not burn all our fats
o increase bile → burns fat→ thin → malnutrition
7. converts amino acids to carbohydrates through deamination
o converts protein to carbohydrates to energy; if necessary liver converts
amino acid → CHO → ATP during conditions of A.N. / underweight (there is
severe weakness & easy fatigability)
8. stores and release glucose
9. stores and release copper (immune builders)
10. stores iron as ferritin (gives color to the blood)
11. detoxification of alcohol and certain drugs
o Rho
o GIT digest alcohol→ if w/o liver → goes directly to brain →destroys/ shrinks
neuron→ altered level of consciousness → comatose
12. phagocytosis
13. produces bile , contains salt necessary for digestion of fat
Lab test
(bile formation and excretion)
1. serum bilirubin
o Van Den Bergh’s reaction
o Measure the ability of the liver to coagulate / excrete
Two types:

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a. conjugated (soluble in water)
 normal
 0.2-0.4
 0-5.1 umol/ L
b. unconjugated (insoluble in water)
 normal
 0.8
 0-14 umol/L

o increase with hepatocellular / obstruction

o increase with hemolysis
o total serum bilirubin 1.7- 20.5 umol/L
2. serum urine bilirubin
o increase with biliary obstruction
3. urobilinogen
o increase with hemolysis / shunting blood of portal flow
o normal urobilinogen 0.09-4023umol/ 24 hours
o normal fecal urobilinogen 0.068-0.34 umol/ 24 hours
Protein studies
1. albumin and globulin measurement
o redirect with hepatocellular injury with hepatitis
o albumin normal 3.5-5.5 g/ dL
o globulin normal: 15-30 g/ dL
o total serum protein: 60-80 g/ dL
2. prothrombin time (PT)
o need vit K (essential for synthesis and other clotting factors)
o normal 100% control (11.5-14s)
o prolonged during liver impairment
o can be corrected by vit K treatment
o increase in chronic liver disease / vit K deficiency
Fat metabolism
1. serum cholesterol
o normal: 3.90-6.50 mmol/ L
o measurement lipid metabs

Liver detoxification
1. serum alkaline phophatase
o disposed by the bile
o impairment in liver cell / excretory function will cause increase
o normal: 20-90 U/L at 30 hours (32-92 U/L)
o biliary obstruction / cholestatic hepatitis
Enzyme production
1. apartate aminotransferase / ACT (SGOT)
o normal < 1.8-19 u/ L (8-20 U/L)
o increase in liver impairment / hepatocellular injury
2. alanine aminotransferase / ALT (SGPT)
o normal: 2.4-7 U/L (10-35 U/L)
o approximately seven to 50 IU/L to be normal.
o Low levels of ALT (generally below 300 IU/L) may indicate any kind of
liver disease. Levels above 1,000 IU/L generally indicate extensive liver
damage from toxins or drugs, viral hepatitis, or a lack of oxygen
(usually resulting from very low blood pressure or a heart attack). A
briefly elevated ALT above 1,000 IU/L that resolves in 24-48 hours may
indicate a blockage of the bile duct. More moderate levels of ALT (300-
1,000IU/L) may support a diagnosis of acute or chronic hepatitis.
o increase with hepatocellular injury
3. lactic dehydrogenase (LDL)

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o normal 80-192 U/L (200-500 U/L)
o 45-90 U/L
o the range can be up to approximately 200 units/L
o It is responsible for converting muscle lactic acid into pyruvic acid, an
essential step in producing cellular energy.
o elevated with hypoxic and with liver injury
4. gamma glutamyl transpeptidase
o formed in heart, liver, lungs, spleen
o normal: 0-30 U/L at 30 hour
5. serum ammonia
o 35 to 65 mcg/dl
o Adults: 15-110 ug/dl (ug = micrograms)
o Children: 40-80 ug/dl
o Newborns: 90-150 ug/dl
Radiology and Imaging
1. hepatobiliary scan
o non-invasive with radiographic material to visualize / hepatobiliary disorder ,
o maintain nPO at least 4 hours before procedure
o no opiate 4 hours before procedure
o there will be an additional procedure after 24 hours
2. oral cholesystography
o use contrats medium → gallbladder
 gall stone
 ability of the gallbladder to contract / empty
 ability of the gall bladder to fill its content
o assess if patient is allergy to seafood / allergic rxn to contrast medium
o self administration of contrats medium 10-20 hours before x-ray (evening)
o NPO to prevent contraction and emptying of bladder
o May be repeated after 24 hours
o CT with jaundice patient cannot excrete, dye is a toxic waste
3. endoscopic retrograde cholangiopancreatography (ERCP)
o with flexible fiberoptic endoscope
o visualize common bile duct, pancreatic and hepatic duct for any obstruction
such as stones and tumors
o nursing responsibility
 assess patient for allergy / hypersensitivity to dye/ seafood
 NPO 4 hour prior to procedure , assess bilirubin level; if > 3 procedure is stopped
 Sign informed consent prior to procedure (sedation/ anesthesia)
 Get v/s- baseline data
 IV access
 Antibiotics for prophylaxis
 10-12 hours self administration
o post –op
 monitor v/s
 report any discomfort such as abdominal distention
 GI bleeding
 Pain
 Tachycardia
 NPO until reflex return
4. endoscopic ultrasound (EUS)
o high frequency UTZ palced at a tip of a endoscope to assess pancreas through
GI lumen
o for staging pancreatic tumors, site of tumors, blood vessels involved local &
regional involvement, size , extention
o same nsg resp. for ERCP
5. Magnetic resonance cholangiopancreatography (MRCP)

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o Non-invasive used to view pancreatic duct
o Used for patient with allergy to iodine based contrast material
o No contrast material used
o Similar to ERCP
o Nursing responsibility
 remove jewelries and other metals
 dentures if patient has pacemakers
 NPO 4 hours before procedure will take 10-15 minutes
6. percutaneous transhepatic cholangiography (PTC)
o flourascopic exam
o intrahepatic and extrahepatic biliary ducts after injection of contrats medium
into the biliary tree through percutaneous needle injection
o distinguish obstructive jaundice caused by disease from jaundice due to biliary
obstruction such as tumor , injury to common bile duct stones
o biliary catheter > drain biliary tree percutaneous transhepatic biliary drainage
(PTB) → relieve jaundice, itchiness, improve nutritional status, allow easy
access to the biliary tree for further procedure
o nursing responsibility
 preop: same with 4
 inject antihistamine for allergic reaction
 post-op: continue antibiotic
 PTBP – check drainage (amount 700-100mL/ 24hours)
 Presence of blood in drainage
 Check site for presence of blood after procedure
 Complications; fever, chills, jaundice, bleeding
 If with PTBP- be careful, it might dislodge
 v/s, bleeding
7. liver biopsy
o sample of liver tissue thru needle aspiration for disease of liver- histopath
o nursing responsibility
 instruct patient to breath for seconds
 normal v/s, informed consent
 bleeding (hgb/ Hct)
 cooperation
 patient should not move during procedure
 post-op
• position patient on right side with pillow supporting the rib cage
• for several (for pressure and to prevent bleeding)
• observe for bleeding on biopsy site
• check v/s
• report changes in bp
Salivary gland
- oral cavity (regulated by ANS) (98.7%)
- secretes saliva (viscous, colorless, contain water, mucoprotein,
immunoglobulin, Ca+, P+, NA+, MgCl+, Fe+, I+, ptyalin/ amylase (enzymes),
CHON/ starch metabs)
- three functions
 lubricates the food (coats it)
 protects → clears the mouth (contain lysosome: antimicrobial, anti bacterial)
 contains ptyalin/ amylase- digest starch
Three parts
1. parotid gland
- affected area during mumps
- ptyalin: active in breakdown process of starch
2. sublingual gland
- under the tongue
- mucin: attract starch without ptyalin

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3. submandibular gland
- forms the floor of the mouth
- ptyalin + mucin: fremulum of tongue
- weighs 1200-1600g
- biggest gland in the body
- below the diaphragm, occupies upper right hypochondrium
- left visceral organ of the body with 450 – 500 mL of blood reserve blood)
- storage extra for emergencies such as shock (compensation)
- store blood in the liver clearing CHF
- vital organ in metabolizing
a. hepatic artery : carries blood to IVC (25%)
b. portal vein: blood from , pancreas, spleen to liver 79%; 300 mL/ blood
enter to liver; 1900 mL/ blood portal vein
- hepatocytes
- lobules: functional unit of liver
- sinusoids
 supply blood to the liver
 absorp, release, excrete substance from blood
 special vein that store blood in the liver
a. kupfer cells: filter; removes and phagocyte old defective RBC blood
, bacteria and other foreign materials in the portal blood
b. typical endothelial cellls
- metabolic function of the liver
1. produce bile (700-1200 mL / day) emulsify fat
2. metabolizes hormones/ drug (detoxification)- clean foreign substance
3. synthesize CHON, sugar, glucose, CHO
4. blood clotting function for metabolism
5. stores nutrients (vitamin and minerals) fat soluble vitamin
6. converts ammonia – urea
7. converts fatty acids – ketones
8. produces prothrombin and other factors for coagulation
- alkaline, filter tasting, yellowish green fluid that contain bile salts,
cholesterol, bilirubin, electrolyte and water
- formed by hepatocytes and released to the canaliculi
Bile salts
- conjugated bile acids → intestinal emusifcation and absorption of fats
CHO, CHON, FAT metabolism
1. CHO metabolism (4 types), release glucose: hypoglycemia; stores glucose
a. gluconeogenesis: catabolism of amino acid (CHON) and glycerol (fat) into
glucose for energy
b. glucogenesis: anabolism of glucose into glycogen for storage
c. glycogenesis: anabolism of starch into glycogen for storage
d. glycogenolysis: catabolism of glucagons into glucose , CO2 and water
> liver converts fat excess into triglycerides for storage in the liver
2. CHON metabolism
- produces CHON for own cellular needs and secretory CHON release into
circulation → albumin
- plasma colloidal osmotic pressure, binding and transport of numerous
substance ( hormones, fatty acids, bilirubin and other anions)
- liver → other CHON substance: fibrinogen, blood clotting factors ( I, II VII,
IX, X)
Excretion of ammonia
Amino acids: repair of muscle tissue / energy
Ammonia: end product of CHON, toxic effect to body if it goes into circulation
Ammonia: → liver (converts to urea) → kidney→ urine

ATOC 2009 RM
3. Fat metabolism
- formation of triglycerides, fro starch and CHON
- fat soluble vitamin A vision, Ca+ absorption, E antioxidant/ regulation of
cells, K blood coagulation, Fe+
- (excess CHO) triglycerides (neutral fats) adipose fats→ split into (to be
used) → glycerol

fatty acids → acetyl- coenzymes A (acetyl-CoA)
- used by liver to produce ATP energy
- convert into aceto acetic acid used to synthesize cholesterol and bile acid
- release into blood stream and tissue for energy

Figure 1. Metabolism Fat Diagram

4. drug/ metabolic detoxification (hormone metab)

- hepatic detoxification and metabs of drugs (chemical)
- 2 types
• Phase I reaction: chemical modification/ inactivation of substance
• Phase II: non- convert lipid soluble substance to water soluble
- Complication drug toxicity
5. bile production / chole statsis
- 600-1000 yellow green daily
Bile: digestion of dietary fats, absorbs fat/fat soluble vitamin from intestine
Cholecystokinin: stimulate (hormone) gallbladder to contract during ingestion of fat
Significance of Bile:
1. important function in digestion
2. emulsify fat
3. transport fatty acids and fat soluble vitamin in intestine for proper absorption
Blood supply
Abdominal aorta → hepatic artery
Oxygen blood → 400-500 mL/ min/ 25 % CO
Inferior & superior → hepatic portal vein
Mesenteric vein → hepatic portal vein
Splenic vein → hepatic portal vein

deoxygenated blood (100-1200mL / min to liver)
Portal venous blood- 70% of blood supply to the liver
Bilirubin: by product of the destruction of aged RBC
: gives bile a greenish black color & produces yellow tinge of jaundice

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1. absorbed in the portal circulation
↓ ↓
2. excreted in the feces
heme Bilirubin metabolism globin
↓ ↓
Fe+ Biliverdin
↓ ↓
Fe + pool unconjugated bilirubin (free bilirubin) (lipid soluble)

unconjugated bilirubin (free bilirubin) + albumin
(….. bilirubin soluble in blood )

unconjugated bilirubin + glucoronic acid

(conjugated bilirubin – water soluble)

conjugated bilirubin excreted
with bile

conjugated bilirubin stools
→ urobilinogen
↓ ↓

urobilinogen→urobilin→ urine

stercobilinogen → stercobilin
- ½ of the bilirubin is converted into urobilinogen , a highly soluble
substance with intestinal flora ↓
- most of the urobilinogen that is absorbed is returned
fecesto the liver to be re-
excreted into the bile . a small amount of urobilinogen , approximately 5%
is absorbed into the general circulation
- viral infection of the liver
1. Hepa A
- fecal – oral
- caused by RNA virus , disease with presence of anti- HAV
- fecal- oral transmissions, parenteral, sexual
- 30 days incubation pd (4-6 weeks)
- onset= acute with fever
- avoid crowdede unsanitary condition
- close contact between patient and caregiver
- poor hygiene
- contaminated food, drinks
2. Hepa B
- parenteral route
- caused by DNA virus
- parenteral/ sexual transmission
- thru contaminated needle, blood products, coitus, exchange of body fluids,
- incubation period 60-180 days
- (syphilis – male, gonorrhea- Female)
3. Hepa C
- IV drug user, multiple blood transfusion
- Caused by RNA virus, disease with presence of anti HCV
- Parenteral to sexual route
- Blood contact/ multiple blood transfusion
- Incubation period 35-60 days
4. Hepa D
- severe than hepa B

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- caused by RNA virus
- parenteral, fecal- oral, sexual
- individual with hepa B
- severe or rare
- incubation period 30-180 days
5. Hepa E
- caused by RNA virus (resembles hepa A)
- fecal- oral route (contaminated food / fluid water)
- incubation period 15-60 days
- severe in pregnant woman
Clinical manifestations
1. prodromal phase
o 2 weeks after exposure to appearance of jaundice
o fatigue, anorexia, malaise, n/v, h/a, hyperalgia, cough, low grade fever
o infection is highly transmissible during this phase
2. icteric phase
o 1-2 weeks after prodromal phase 2-6 weeks
o jaundice ( very evident), dark urine & clay colored stool
o enlarged liver, smooth and tender > percussion causes pain
o actual phase of illness
3. recovery phase
o resolution of jaundice 6-8 weeks after experience
o sx diminish but liver remains enlarged & tender
o liver function returns to normal 2-12 weeks after onset of jaundice
o persistence of clinical manifestation and liver inflammation after acute hepa B,
o liver function test remain abnormal > 6 months
o chronic, active hepa B – predisposition to cirrhosis and primary hepatocellular
Nursing intervention:
1. maintain adequate nutrition
2. maintain adequate fluid intake
3. ensuring of disease transmission
4. preventing and controlling bleeding
5. patient education and health maintenance
Management / evaluation Treatment:
Serological analysis for HBsAg> marker for HBV ; most specific diagnosis for
1. encourage patient to rest, gradual increase in activity
2. low fat, high carbohydrate diet > if bile flow is obstructed
3. if with fever (antipyretic drug), nauseated (antiemetic)
4. therapeutic measures control dyspeptic sx & malaise
5. if sever n/v, advise patient to go to hospital (life threatening) if more than 2
episodes do IVF treatment (plazil/ metoclopromide)- antiemetic
6. hand washing & use of gloves
7. small frequent feeding ( high cal, low fat, no CHON)
8. administration vitamin K for bleeding tendencies
9. IVF & electrolyte replacement
- gradual increase in activity after jaundice is diminished
- mannitol- diuretics
complication: dehydration, hypokalemia (prolonged vomiting), hepatic
encephalopathy, hepatocellular
carcinoma, chronic active hepatitis- develop
hepatocellular cancer
o obtain HPI, IV drug, sexual activity, trvel, ingestion of contaminated food,
alteration in bowel function
o systemic related s/sx= size and shape of liver
Nursing intervention

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o adequate fluid- IVF, measure I/O
o rest/ activity, emotional support
o health teaching
- dse-dse transmission, prevention
- report complication, bleeding
- sx of encelopathy (aggressive, unruly behavior)
Nx Dx
o Hypothermia
o Activity intolerance
o Risk for infection
o Risk for injury
- end stage of chronic liver disease
- irreversible inflammatory disease that disrupts liver structure and function
- liver may be unusually firm/ hard when palpated
Table 1: Forms of Alcoholic Liver Disease
Parameter Fatty Liver Alcoholic Hepatitis Cirrhosis
Histologic specificity for alcoholic
No Yes No
Prognosis Excellent Variable Guarded
Reversible Yes Variable Generally, no
1. Alcoholic cirrhosis: caused by toxic effects of alcohol on the liver, immunological
and oxidative stress from lipid
• alcohol is transformed into acetaldehyde → inhibits export of CHON from the
liver, alters metabolism of vitamin and minerals and induces malnutrition
2. Fatty Liver (Steatosis)
• mildest form of alcoholic liver disease
• may be caused by relatively small amount of alcohol may asymptomatic and is
reversible with cessation of drinking
3. Alcoholic hepatitis
• precursor of cirrhosis characterized by inflammation degeneration and
necrosis of hepatocytes & infiltration of polymorphonuclear leukocytes and

They include:

o Chronic Hepatitis C, B and D are viral infections affecting the liver. The
inflammation caused by the different hepatitis viruses causes damage and
scarring over a number of years and decades. This scaring can lead to
o Cirrhosis of the liver develops over a number of years of heavy drinking.
Currently more men that women are affected but this picture is changing along
with the social roles of women. Women are more susceptible to liver damage
from drinking alcohol.
o Autoimmune hepatitis appears to be caused by the immune system attacking
the liver and causing inflammation, damage, and scarring that can lead to
o Toxins can cause cirrhosis. These toxins include prescription and non
prescription drugs and environmental toxins and a parasitic infection called
o Inherited diseases such as hemochromatosis, a condition where too much iron
is present in the body, and Wilson's disease a rare disease of copper
metabolism. Also, in Alpha-1 antitrypsin deficiency, galactosemia, and
glycogen storage diseases.

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o Nonalcoholic steatohepatitis (NASH) where fat builds up in the liver that
eventually cause scar tissue. Although it is not fully understood NASH appears
to be associated with diabetes, obesity, treatment using corticosteroid
medications and coronary artery disease.
o Blocked absent or injured bile ducts can cause cirrhosis. Biliary atresia in
babies and biliary cirrhosis are examples of such conditions.
1. weight loss, weakness, anorexia, (no proper CHON metabolism muscle wasting)
2. fatigue/ malaise
3. mild to severe jaundice, late sign
4. frequent diarrhea/ constipation
5. abdominal pain (liver enlargement) epigastric, RUQ pain with dull aching,
sensation of fullness

Sign and symptom

1. Fatigue
2. Itching
3. Jaundice caused by high levels of bilirubin that are not able to be excreted
from the body
4. Enlarged liver
5. Abdominal pain
6. Fatty deposits under the skin caused by cholesterol deposits
7. Soft yellow spots on the eyelid
8. Fatty stools
9. Dry eyes and mouth
10. Digestive problems
Box 1: Physical Examination and Laboratory
Findings in Alcoholic Liver Disease
Physical Examination
• Constitutional—fever
• Skin—spider angioma
• Parotid and lacrimal gland enlargement
• Palmer erythema
• Jaundice
• Decreased body hair
• Gynecomastia
• Musculoskeletal—Dupuytren's contracture
• Clubbing
• Muscle wasting
• Genitourinary—testicular atrophy
• Abdomen—hepatomegaly or small shrunken liver
• Splenomegaly
• Ascites
• Hepatic tenderness
• Neurologic—asterixis
• Confusion, stupor
Laboratory Findings
• Liver synthetic function—hyperbilirubinemia
(usually conjugated)
• Prolonged prothrombin time
• Hypoalbuminemia
• Liver enzyme levels—aspartate
aminotransferase (AST) and alanine
aminotransferase (ALT) levels elevated,
usually < 300 U/L; AST/ALT ratio ~2:1
• Hematologic—anemia

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• Leukocytosis or leukopenia
• Thrombocytopenia
• Increased serum globulin levels
• Metabolic—elevated blood ammonia level
• Hyperglycemia
• Respiratory alkalosis
• Hypomagnesemia
• Hypophosphatemia
• Hyponatremia
• Hypokalemia
Late stage
o Portal hypertension→ esophageal varices, hemorrhoids; increase in portal vein
> collateral channels to supply blood to other parts
o Spleenomegaly, liver failure
o Ascites
• portal systemic shunt = increase pressure
• bleeding
• thrombocytopenia & spleenomegaly
Loss of liver function affects the body in many ways. Following are common problems, or
complications, caused by cirrhosis.
- Edema and ascites. When the liver loses its ability to make the protein albumin,
water accumulates in the leg (edema) and abdomen (ascites).
- Bruising and bleeding. When the liver slows or stops production of the
proteins needed for blood clotting, a person will bruise or bleed easily.
- Jaundice. Jaundice is a yellowing of the skin and eyes that occurs when
the diseased liver does not absorb enough bilirubin.
- Itching. Bile products deposited in the skin may cause intense itching.
- [link url=/library/basics/blgallstns.htm]Gallstones[/a]. If cirrhosis prevents bile
from reaching the gallbladder, a person may develop gallstones.
- Toxins in the blood or brain. A damaged liver cannot remove toxins from the
blood, causing them to accumulate in the blood and eventually the brain. There,
toxins can dull mental functioning and cause personality changes, coma, and
even death. Signs of the buildup of toxins in the brain include neglect of personal
appearance, unresponsiveness, forgetfulness, trouble concentrating, or changes
in sleep habits.
- Sensitivity to medication. Cirrhosis slows the liver's ability to filter medications
from the blood. Because the liver does not remove drugs from the blood at the
usual rate, they act longer than expected and build up in the body. This causes a
person to be more sensitive to medications and their side effects.
- Portal hypertension. Normally, blood from the intestines and spleen is carried to
the liver through the portal vein. But cirrhosis slows the normal flow of blood
through the portal vein, which increases the pressure inside it. This condition is
called portal hypertension.
- Varices. When blood flow through the portal vein slows, blood from the intestines
and spleen backs up into blood vessels in the stomach and esophagus. These
blood vessels may become enlarged because they are not meant to carry this
much blood. The enlarged blood vessels, called varices, have thin walls and carry
high pressure, and thus are more likely to burst. If they do burst, the result is a
serious bleeding problem in the upper stomach or esophagus that requires
immediate medical attention.
- Problems in other organs. Cirrhosis can cause immune system dysfunction,
leading to infection. Ascites (fluid) in the abdomen may become infected with
bacteria normally present in the intestines, and cirrhosis can also lead to kidney
dysfunction and failure.

ATOC 2009 RM

 rest, vitamin supplements
 nutritious disease and management of complications
 cessation of drinking → slows progression of liver damage, improves clinical sx
& prolongs life
 individual with severe → treatment with corticosteroids
Treatment of cirrhosis includes
1) preventing further damage to the liver,
2) treating the complications of cirrhosis,
3) preventing liver cancer or detecting it early, and
4) liver transplantation.
Preventing further damage to the liver
o Consume a balanced diet and one multivitamin daily. Patients with PBC with
impaired absorption of fat soluble vitamins may need additional vitamins D and K.
o Avoid drugs (including alcohol) that cause liver damage. All patients with cirrhosis
should avoid alcohol. Most patients with alcohol induced cirrhosis experience an
improvement in liver function with abstinence from alcohol. Even patients with
chronic hepatitis B and C can substantially reduce liver damage and slow the
progression towards cirrhosis with abstinence from alcohol.
o Avoid nonsteroidal antiinflammatory drugs (NSAIDs, e.g., ibuprofen). Patients with
cirrhosis can experience worsening of liver and kidney function with NSAIDs.
o Eradicate hepatitis B and hepatitis C virus by using anti-viral medications. Not all
patients with cirrhosis due to chronic viral hepatitis are candidates for drug
treatment. Some patients may experience serious deterioration in liver function
and/or intolerable side effects during treatment. Thus, decisions to treat viral
hepatitis have to be individualized, after consulting with doctors experienced in
treating liver diseases (hepatologists).
o Remove blood from patients with hemochromatosis to reduce the levels of iron and
prevent further damage to the liver. In Wilson's disease, medications can be used
to increase the excretion of copper in the urine to reduce the levels of copper in
the body and prevent further damage to the liver.
o Suppress the immune system with drugs such as prednisone and azathioprine
(Imuran) to decrease inflammation of the liver in autoimmune hepatitis.
o Treat patients with PBC with a bile acid preparation, ursodeoxycholic acid (UDCA),
also called ursodiol (Actigall). Results of an analysis that combined the results from
several clinical trials showed that UDCA increased survival among PBC patients
during 4 years of therapy. The development of portal hypertension also was
reduced by the UDCA. It is important to note that despite producing clear benefits,
UDCA treatment primarily retards progression and does not cure PBC. Other
medications such as colchicine and methotrexate also may have benefit in subsets
of patients with PBC.
o Immunize patients with cirrhosis against infection with hepatitis A and B to prevent
a serious deterioration in liver function. There are currently no vaccines available
for immunizing against hepatitis C.
 abnormal high blood pressure in the portal venous system
 > 10 mmHg ( normal 3 mmHg)
 caused by disorders that obstruct / impede blood flow thru any component of the
 common cause → liver cirrhosis
Pre-hepatic obstruction – obstruction of portal vein before entering the liver
Post-hepatic obstruction- obstruction distal to the liver
a. “bold –chain syndrome”
 congestive disease of the liver caused by occlusion of the portal vein
and their tributaries
 associated with polycythemia vera, hypercoagulability states,
associated with malignant tumor, pregnancy

ATOC 2009 RM
b. hepatic veno occlusive disease
 variant of “BCS” in patient with certain chemotherapeutic drug, hepatic
irradiation of bone marrow transplant
Intra hepatic obstruction- portal hypertension with in the l;iver
1. Varices (distended, collateral veins)
o Prolonged elevation of pressure in collateral veins → lower
esophagus , stomach & rectum
2. splenomegaly (enlargement of spleen)
o caused by increase pressure in the splenic vein which branches from
the portal vein
3. ascites ( accumulation of fluid in the peritoneal cavity)
o increase in pressure in the mesenteric tributaries of the portal vein
o high pressure forces the water out of the vessels into the peritoneal
4. hepatic encelopathy
o “portal systemic encelopathy”Portal Hypertension

o characterized by CNS disturbances,↓particularly reversible alterations
↓ of consciousness
o results from presence of ammonia in the brain
increase pressure in capillaries port systemic with shunting of blood
↓ ↓ ↓
↓ ↓ ↓
ascites development of collateral channels shunting of ammonia and toxins
anemia thrombocytopenia kalemic
↓ ↓ ↓ from intestines to the general

caput medullae hemorrhoids esophageal varices ↓
Manifestation: hepatic encelopathy
1. vomiting of blood from bleeding esophageal varices – common sx of portal
2. anemia, blood in stool, abdominal discomfort, insomnia, dyspepsia
3. hemorrhage, edema formation, increase BP, decrease CO
- portal hypertension → disease at the time varice .. bleeding and confirmed by
endoscopy and evaluation of portal venous pressure
1. withdraw from drinking alcohol
2. nutritional or vitamin supplement ( high cal, moderate CHON)
3. treatment for ascites / F&E imbalance
o Na+ restriction
o Water restriction
o Oral supplement K+
o Paracentesis: to relieve abdominal pressure from ascites
o Pain for algesia
o Albumin administration
o Bed rest
o Diuretics → spironolactone (K+ sparring), lasix (loop diuretics)
1. hyper Na+, water retention
2. bleeding
3. esophageal varices
4. coagulopathy
5. spontaneous bacterial peritonitis
6. hepatic encelopathy

ATOC 2009 RM
7. caput medusae: is the appearance of distended and engorged paraumbilical
veins which are seen radiating from the umbilicus across the abdomen to join
systemic veins.

1. alcohol abuse
2. history of jaundice
3. hepa
4. alcoholism
5. biliary stasis
6. abdominal observation
7. daily weight

Nursing intervention:
1. jaundice/ icterus: At least one medical dictionary defines icterus as the presence
of jaundice seen in the sclera of the eye. This is incorrect. Icterus is synonymous
with jaundice. They are one and the same thing.
a. hemolytic jaundice – normal liver with rapid RBC destruction
b. hepato cellular – defective liver
c. obstructive jaundice
a) itchiness- give antipruritic lotions/ starch bath
b) altered body image- isolation , support system
2. edema/ ascites
- diet
- low Na+, high CHON, high calories with small frequent feeding
- n/v- teach self administration of supplementary feedings
- measure abdominal girth
- paracentesis
 aspiration of fluid from peritoneal cavity
 between umbilicus and symphisis pubis 2 finger breath
 position patient in fowler’s/ upright position, feet should not dangle
3. hepatic encelopathy (portal systemic encelopathy problem)
- low CHON diet with laxative
- low pH favors conversion ….
- Drug treatment (intestinal antibiotics – neomycin sulfate)
4. malnutrition
- high calories, moderate to high CHON
- multivitamins
5. bleeding
- avoid all form of trauma, blow nose gently, use soft bristle toothbrush
- avoid internal bleeding
- monitor v/s and for sign of epigastric fullness, restlessness > shock!!
- Administer vitamin K (aqua mephyton)
If still + for bleeding : sengstaken- Blakemore tube method
3 lumen
- esophageal balloon = dilates and compresses vein prevents bleeding
- gastric balloon – anchors the tube in place
- suction
Nursing responsibility:
a) observe oral hygiene and nasal care
b) check if gastric balloon is always in place
c) keep balloon pressure at required level
d) check/ monitor v/s for shock or bleeding
e) F/e
Patient care!
• if bleeding still persist: sclerotherapy/ variceal ligation
 from mouth to esophagus

ATOC 2009 RM
 sclerosing agent is injected directly into the vein with a flexible fiber optic
endoscope > thrombosis
* decrease pressure by shunting blood around liver
a) portal systemic shunt (portal canal): portal vein is anastomosed the inferior vena
cava to reduce variceal blood flow and pressure
b) spleno renal shunt: splenic vein and left renal vein after splenectomy ; portal
vein can’t be used d/t thrombosis
c) internal position renocaval vein: superior mesenteric vein is grafted to IVC
Diagnostic test:
1. liver biopsy: obstruction/ fibrosis of liver tissue
2. liver scan: abdominal thickening/ liver mass
3. computed tomography scan: size of the liver
4. esophagoscopy: view esophageal varices
5. paracentesis: to remove fluid (ascites)
6. percutaneous transhepatic cholangiography: (PTC) differentiate between
extraobstructive/ intraobstructive type of jaundice
7. laparoscopy & liver biopsy – direct visualization
8. serum liver function test: elevated SGPT
Common bile duct- hepatic duct & cystic duct
s/sx of decrease liver function:
1. weight loss/ decrease body mass
2. steatorrhea : is the presence of excess fat in faeces
3. gastric fullness/ dyspepsia: popularly known as indigestion, meaning hard or
difficult digestion, is a medical condition characterized by chronic or recurrent
pain in the upper abdomen, upper abdominal fullness and feeling full earlier
than expected when eating.
4. palmar erythema: is reddening of the palms at the thenar and hypothenar
5. spider angioma: (also known as a nevus araneus, spider nevus, or vascular
spider) is a type of angioma found slightly beneath the skin surface, often
containing a central red spot and reddish extensions which radiate outwards
like a spider's web
6. jaundice
7. bleeding gums, epistaxis
8. hepatic encelopathy
9. fatigue, weakness, anorexia
- gradual obstruction of venous blood flow to liver
- pressure in the portal vein increase → left collateral channel develop between
the portal systemic vein that supply lower rectum , esophagus and umbilical
- collateral between inferior & internal hemorrhoids
Gall bladder
 distensible pear shaped muscular sac at the ventral (inferior surface) of the liver
Function: store and concentrate bile bet. Meals (90mL of bile)
Fat ingestion stimulate the release of GI hormone stimulate contraction of gall
bladder and relax sphincter of oddi
Release bile (sphincter of oddi)
Bile flows through the cystic duct into the gall bladder
Bile is concentrated and stored
Common bile duct
Small intestine (ampulla of vater)
Aid in digestion of fats and excretion of conjugated bilirubin from liver
40 y/o

ATOC 2009 RM
multiparity stone formation ( cholesterol, Ca+ pigment)
oral contraceptive
liver problem
increase hemolysis
biliary tree infection
- oral cholecystography
- Hepatic biliary scar
1. conservative (symptomatic): relieve pain
2. surgicall management
- Cholecystectomy ( open/ laparoscopic)
- Choledoclostomy ???

Acute cholecystitis
• This should be suspected whenever there is acute right upper quadrant or epigastric
o Other possible causes include:
 Perforated peptic ulcer
 Acute peptic ulcer exacerbation
 Amoebic liver abscess
 Acute amoebic liver colitis
 Acute pancreatitis
 Acute intestinal obstruction
 Renal colic
 Acute retrocolic appendicitis
Chronic cholecystitis
• The symptoms of chronic cholecystitis are non-specific, thus chronic cholecystitis may
be mistaken for other common disorders:
o Peptic ulcer
o Hiatus hernia
o Colitis
o Functional bowel syndrome
Quick Differential
• Biliary colic - Cystic duct blocked. Sharp and constant pain without fever. Negative
Murphy's sign. LFT WNL. Ultrasound scan.
• Cholecystitis - Cystic duct blocked with infection. Colicky brief pain at first, then
constant pain in RUQ with fever caused by E coli, klebsiella, pseudomonas, B fragilis,
enterococcus. Murphy's sign positive. Increased AST, ALT, AP, WBC. Ultrasound scan.
• Choledocholithiasis - Common bile duct blocked. Colicky pain. Jaundice. Increased
bilirubin. Cholangiogram.
• Cholangitis - Infection of entire biliary tract. Charcot's triad. Jaundice and fever.
Increased AST, ALT, AP, bilirubin. Cholangiogram.
Laboratory values may be notable for an elevated alkaline phosphatase,
possibly an elevated bilirubin (although this may indicate
choledocholithiasis), and possibly an elevation of the WBC count. CRP (C-reactive
protein) is often elevated. The degree of elevation of these laboratory values may
depend on the degree of inflammation of the gallbladder. Patients with
acute cholecystitis are much more likely to manifest abnormal laboratory
values, while in chronic cholecystitis the laboratory values are frequently normal.
Sonography is a sensitive and specific modality for diagnosis of acute
cholecystitis; adjusted sensitivity and specificity for diagnosis of acute
cholecystitis are 88% and 80%, respectively. The 2 major diagnostic criteria
are cholelithiasis and sonographic Murphy's sign. Minor criteria include gallbladder wall

ATOC 2009 RM
thickening greater than 3mm, pericholecystic fluid, and gallbladder
The reported sensitivity and specificity of CT scan findings are in the range of
90-95%. CT is more sensitive than ultrasonography in the depiction of
pericholecystic inflammatory response and in localizing
pericholecystic abscesses, pericholecystic gas, and calculi outside the lumen of the
gallbladder. CT cannot see noncalcified gallbladder calculi, and cannot assess
for a Murphy's sign.
Hepatobiliary scintigraphy with technetium-99m DISIDA (bilirubin) analog is
also sensitive and accurate for diagnosis of chronic and acute cholecystitis. It
can also assess the ability of the gall bladder to expel bile (gall bladder
ejection fraction), and low gall bladder ejection fraction has been linked to chronic
cholecystitis. However, since most patients with right upper quadrant pain
do not have cholecystitis, primary evaluation is usually accomplished
with a modality that can diagnose other causes, as well.
1. RUQ pain, guarding
2. murphy’s sign: inability to take a deep breath (inspiration) when examiner’s
fingers are pressed below the hepatic margin
3. biliary colic: steady severe, aching pain may radiate in epigastric RUQ radiating
to right scapular area
4. obstruction : increase pressure > pain> vagal stimulation> n/v
5. chemical irritation> inflammation> low grade fever
6. swelling and rebound tenderness
7. pain perceived every after eating begins and persist 1-3 hours
8. decrease release of bile and pancreatic juice
• decrease gastric emptying: nausea, increase content and pressure in GIT>
vomiting, heartburn, dyspepsia
• decrease amount of bile in fecal material > light to clay colored stool
• circulatory retention of bile- jaundice, increase serum conjugated bilirubiin
Diagnostic: visualization of stones/ inflammation → oral cholecystography
ultrasonography, hepatobiliary scan
Diagnostic test:
1. cholecystography GI series: visualize bladder with contrast media (oral)→ to detect
gall stones
telepaque (6-8 tablets) , biloptin (5-6 cups)
Nursing responsibility:
- Taken at night, low fat meal, NPO except fluid
- Taken at bed time , 1 every 5 hours with minimal sips of water
- Prior to procedure x- ray gall bladder (calm / quiet)
- After 30 min, do x-ray again gall bladder (active/ contracting): quiet and calm –
expected outcome > increase fat- morning???
2. cholangiography: visualization of bile duct by use of radio opaque dye given by use
of t- tube
• if there is inflammation of bile duct, there will be low bile circulation to the
intestine, destruction is drained by t-tube
1. fever (antipyretic), fatigue (test)
2. pain ( low fat diet, maintain NPO, give analgesic [Demerol])
3. f/e balance – IVF treatment
4. n/v –antiemetic drug (placil / metoclopramide)
a) cholecystectomy- open/ laparascopic; removal of gall bladder
b) choledochostomy- exploration of common bile duct
• t-tube decompress kidney tree and allow access to biliary tree

ATOC 2009 RM
Liver (hepatic duct) gall bladder
(cystic duct)
↓ ↓
common bile duct ( inflamed )

lumen of common bile duct

minimal bile to sf → bile
to peritoneum

Post-op peritonitis
- semi-fowler’s 6-8 hours > lessened diaphragm – dyspnea
- assess bile 23- 34 hours (500-700mL/ day)
Pancreatic secretions contain:
1) proteolytic enzy,es- trypsin, ribonucleic, deoxyribonucleic, carboxypeptidase;
breakdown of CHON
2) pancreatic amylase- breakdown starch & amylase; hydrolyze neutral fats into
glycerol & fatty acids
3) lipase (fats)
Trypsin inhibitor- inhibits trypsin > stimulate other enzymes

inhibits release of other enzymes like deoxyribonucleic
organs liver; skeletal muscles food in stomach
↓ ↓
lobules ( acinar cells) stimulate pancreas
↓ ↓
release digestive enzymes pancreatic enzymes
(pancreatic duct)
↓ ↓
release pancreatic enzymes SI

trypsin (CHON)

A. pancreatitis
1. interstitial pancreatitis
- severe and life threatening with cause of fat necrosis
- scope on enzymes to tissues
- assessment :
a) pain ( severe, supine relieved by upright & leaning forward)
b) n/v ( f/e imbalance – IV therapy)
c) fever, chills
2. hemorrhagic pancreatitis
- blood vessels
- manifestation
(Cullen’s sign) coolish sign- bluish color in umbilical area
turner’s sign- flush area; bluish discoloration, grayish

increase glucose> release insulin in blood> B cells

decrease glucose> release glucagons> …. Cells

liver stimulated to produce glucose

ATOC 2009 RM
increase blood glucose

release of insulin

glucose brought to cells

cells utilize glucose
Cholelithiasis (disease by laparoscopic cholecystectomy)
- gall stone formation > cholesterol/ pigmented
- obesity
- middle age
- ……
- gall bladder, pancreatic/ ileac disease
cholesterol – supersaturated with cholesterol …by the liver
pigmented gall stones- increase levels of unconjugated bilirubin w/c binds with
Post-op care
- diaphragm relax compress lung
- 24-36 hours semi fowler’s after cause 6-8 hours (dyspnea)
T-tube care
- 500-700 mL / day
- decrease 200 mL / day
- if after 3 days discharge bile increase in amount
- clamp tube 15-20 minutes
- remove…
- low fat diet
- steatorrhea
- 20 cm long
- curve of the duodenum
- tail touching the spleen

a. alpha cells: glucagons (increase glucose)

b. beta cell: insulin ( decrease glucose)
c. delta cells: pancreatic polypeptide
serum amylase > 400 u- pancreatitis
serum lipase – sensitive marker of pancreatic injury – acute alcoholic pancreatitis
Plan of care
1. relieve pain: upright/ leaning forward
2. narcotic meds (analgesic)> demerol
3. decrease pancreatic stimulation > oral food / fluids
4. maintain f/e> IVF treatment
5. antiemetic for n/v
6. decrease alcoholic intake > stimulate pancreatic juice
7. low fat, caffeine, moderate CHON


• The pancreas is an elongated organ that lies in the back of the mid-abdomen. It is
responsible for producing digestive juices and certain hormones, including insulin, the
main hormone responsible for regulating blood sugar.
• Acute pancreatitis refers to inflammation of the pancreas and is associated with sudden
onset of severe abdominal pain.
• It usually develops as a result of passage of gallstones through the common bile duct or
after regular consumption of alcohol for a number of years.
• Several additional causes of acute pancreatitis have been described due to a variety of
medications, genetic diseases, infectious agents, postoperative states, endoscopic

ATOC 2009 RM
procedures involving the pancreatic and bile ducts, and other types of injury to the
• Most attacks of acute pancreatitis do not lead to complications, and most people recover
uneventfully with supportive medical care.
• However, in a small proportion of people, acute pancreatitis takes a more serious course
that requires intensive medical care. In all cases, it is essential to determine the underlying
cause of acute pancreatitis and, if possible, to treat this condition to prevent a recurrence.
• Because the severity and course of acute pancreatitis can vary widely from person to
person, the treatment of this condition is individualized.


• There are many possible underlying causes of acute pancreatitis, but 60 to 75 percent of
all cases are caused by gallstones or alcohol abuse.
• Gallstone pancreatitis — Because the gallbladder and pancreas share a drainage duct,
gallstones that lodge in this duct can prevent the normal flow of pancreatic enzymes and
trigger acute pancreatitis.
• Gallstone pancreatitis is more common in women than in men.
• Alcoholic pancreatitis — Alcohol is also a common cause of acute pancreatitis.
• Alcoholic pancreatitis is more common in men, and usually occurs in individuals with long-
standing alcohol abuse.
• Drug-induced pancreatitis — A large number of drugs used to treat medical conditions
can trigger acute pancreatitis; for example, dideoxyinosine, DDI (used for treating AIDS), 6-
mercaptopurine, 6-MP (an immunosuppressant drug), and angiotensin-converting enzyme
(ACE) inhibitors (used for treating high blood pressure).
• Post-ERCP — Endoscopic retrograde cholangiopancreatography (ERCP) is an endoscopic
test that involves the injection of dye into the bile duct and pancreatic duct.
• Acute pancreatitis develops in about 3 to 5 percent of people who undergo ERCP.
• Certain characteristics of the patients, such as female sex and younger age, make them
more prone to develop this complication.
• Certain types of procedures also may increase the risk, particularly complicated
procedures that can cause trauma to the pancreatic duct. Most cases of ERCP-induced
pancreatitis are mild.
• Hereditary conditions — Acute pancreatitis can be caused by hereditary conditions, for
example, familial hypertriglyceridemia (high blood triglyceride levels) and hereditary
• The genetic basis for hereditary pancreatitis is rapidly being uncovered, and some specific
tests are already available. These conditions may cause acute pancreatitis in children.
• Idiopathic — No underlying cause can be identified in about 20 percent of people with
acute pancreatitis. This condition is called idiopathic pancreatitis.
• Only about 3 percent of people will experience additional attacks over time, a condition
called idiopathic recurrent pancreatitis.
• Other causes — In rare cases, acute pancreatitis is caused by infections, such as mumps
or viral hepatitis, or by abdominal injury.

• Sudden, constant pain in the upper part of the abdomen is a hallmark of acute
pancreatitis, although other medical conditions can also cause this pain pattern.
• In about half of all people who experience pain during acute pancreatitis, the pain wraps
around the trunk and also involves the back in a band-like pattern.
• The pain typically lasts days and is often relieved by leaning forward. In mild cases of
acute pancreatitis, the pain may be limited to slight abdominal tenderness, and about 5 to
10 percent of people with acute pancreatitis do not experience any pain at all.
• In people with gallstone pancreatitis, gallbladder pain may occur before pancreatic pain.
• Gallbladder pain (referred to as biliary colic) is typically described as a moderately severe
pain in the right upper region of the abdomen extending to the back and right shoulder.
• The pain gradually rises in intensity and may be accompanied by nausea and vomiting.
• Although the term "colic" implies that the pain is intermittent, it typically is steady.

ATOC 2009 RM
• Gallbladder pain lasts six or eight hours at most and often follows a meal.
• In people with alcoholic pancreatitis, the symptoms of acute pancreatitis often occur one
to three days after an alcohol binge or after stopping drinking.
• The pain of acute pancreatitis is accompanied by nausea and vomiting in about 90 percent
of people. In severe cases of acute pancreatitis, the initial symptom may be shock or

• The diagnosis of acute pancreatitis can be challenging because the signs and symptoms of
other medical conditions can mimic those of pancreatitis.
• The diagnosis is usually based upon careful consideration of a person's medical history, the
signs and symptoms noted during a physical examination, and the results of specific
diagnostic tests.
• Once a diagnosis of acute pancreatitis is made, additional tests are used to determine the
underlying cause.
• This step ensures that a person will receive the correct treatment to prevent pancreatitis
from recurring.
• Additional tests also help predict the likely course of pancreatitis over time. This step is
important because in a small percentage of people with acute pancreatitis, the condition
will progress to a more serious condition called severe acute pancreatitis, often referred to
as "necrotizing pancreatitis".
• If tests suggest that necrotizing pancreatitis is likely, early intensive medical treatment
may help improve the prognosis.
• Medical history — A medical history often provides clues about the underlying cause of
acute pancreatitis.
• Your doctor will ask about any previous symptoms of gallstones and about your alcohol
intake because these two factors account for the majority of cases of acute pancreatitis.
• Your doctor will also ask if you have other medical conditions, if you take any medications,
and if any family members have experienced similar symptoms.
• Physical examination — Your doctor will perform a physical examination to check for the
signs and symptoms of acute pancreatitis.
• These signs and symptoms vary with the severity of the attack, and their number and
extent can help predict the course of pancreatitis.
• Your doctor will ask about abdominal pain, nausea, and vomiting, and will check for other
signs and symptoms of acute pancreatitis, including fever, rapid heart rate, and shallow
breathing or difficulty breathing. You will also be checked for less common signs and
symptoms, including bruise-like areas on the stomach or back, jaundice (yellowish
discoloration of the skin), red nodules under the skin, inflammation of the leg veins, and
pain and inflammation of the joints.

• Diagnostic tests help confirm the presence of acute pancreatitis and predict the likely
course of the condition. It is important to discuss the timing, usefulness, and risks of
various tests with your doctor.
• The extent of testing is usually tailored to the severity of acute pancreatitis and the most
likely underlying causes.
• Pancreatic enzymes — During acute pancreatitis, enzymes that normally flow from the
pancreas into the digestive tract leak out of the pancreas and into the bloodstream. Tests
can detect two of these enzymes—amylase and lipase—in the blood.
• Serum amylase — A serum amylase test determines levels of amylase in a blood sample.
Marked increase (more than three times the upper limit of normal) in the levels of amylase
strongly suggest the diagnosis of acute pancreatitis. This is the most commonly used test
to aid the diagnosis of acute pancreatitis. Levels of amylase in the blood rise within 6 to 12
hours after acute pancreatitis begins and remain elevated for three to five days in
uncomplicated attacks.
• Tissues other than the pancreas also produce amylase. However, during acute
pancreatitis, blood levels of this enzyme are often more than three times the upper limit of

ATOC 2009 RM
normal, and this pattern helps differentiate most cases of acute pancreatitis from other
conditions that increase blood amylase levels.
• Concomitant elevation of the serum lipase also helps to confirm the diagnosis.
Occasionally, markedly elevated levels of amylase can occur in the absence of pancreatitis
due to the combination of amylase with another protein in the blood.
• This combined amylase-protein complex cannot be eliminated by the kidneys and leads to
elevated amylase levels in the blood. This condition, macroamylasemia, is benign and can
be diagnosed by a blood test or a urine test; the absence of amylase in the urine in the
presence of high levels in the blood suggests macroamylasemia.
• Unnecessary and costly testing for pancreatitis can be avoided if this condition is
• Serum lipase — The serum lipase test determines levels of lipase in a blood sample.
Elevated serum lipase levels help to confirm the pancreatic origin of elevated serum
amylase levels.
• Markers of inflammation — Rising blood levels of some substances signal inflammation,
although these markers are non-specific because they do not point to the source of
• These markers include C-reactive protein (CRP), neutrophil elastase, procalcitonin, tumor
necrosis factor, and interleukin-6 (IL-6). Ongoing studies are determining if levels of
inflammatory markers help predict the course of acute pancreatitis. At the present time,
these markers are not routinely used.
• Liver enzymes — Liver enzymes can sometimes be helpful for determining the cause of
pancreatitis. For example, elevated levels of alanine aminotransferase (ALT) at the onset
of symptoms suggest that a person has gallstone pancreatitis. Although often referred to
as liver function tests, these enzymes are not true indicators of the status of liver function.
• Imaging tests — Imaging tests provide information about the structure of the pancreas,
the ducts that drain the pancreas and gallbladder, and the tissues surrounding the
• Abdominal X-ray — In acute pancreatitis, an x-ray of the abdomen may reveal a normal
appearance of the digestive tract or abnormalities that are characteristic of acute
pancreatitis. These abnormalities include paralysis of regions of the small intestine and
spasm of part of the colon. In severe cases, both the small intestine and colon may cease
to function. An abdominal x-ray may also point to other conditions that mimic acute
pancreatitis, such as blockage of the intestine and a tear in the intestinal wall.
• Chest X-ray — About one-third of people with acute pancreatitis have abnormalities on a
chest x-ray. These abnormalities may include elevation of the diaphragm (the large muscle
that separates the abdomen and the chest), collection of fluid in the chest cavity, collapse
of the base of the lungs, and inflammation of the lungs.
• Abdominal ultrasound — An abdominal ultrasound test can also aid the diagnosis of
acute pancreatitis. This test is particularly useful for identifying gallstones in the
gallbladder or in the ducts that drain the gallbladder as the cause of acute pancreatitis.
• However, this test cannot identify the more serious abnormalities associated with
moderate and severe pancreatitis.
• Computerized tomography scan — The computerized tomography (CT) scan is the
most useful radiology test for diagnosing acute pancreatitis. This test is often done if
conditions other than pancreatitis are suspected, if conservative medical care fails to
relieve the symptoms of acute pancreatitis, or if complications such as necrotizing
pancreatitis are suspected.
• The CT scan is especially useful for determining the extent of pancreatitis. It can identify
enlargement or abnormal contours of the pancreas, inflammation of the tissues
surrounding the pancreas, collection of fluid around the pancreas, and collection of gas in
the pancreas or in the tissues behind the pancreas. The type and number of these
abnormalities have been found to correspond to the severity of pancreatitis.
• Magnetic Resonance Imaging Scan (MRI) — MRI may be used to diagnose acute
pancreatitis, to assess the severity of disease, to identify complications of pancreatitis
such as fluid collections and areas of necrosis or dead tissue.

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• An MRCP (magnetic resonance cholangiopancreatography), which can be performed along
with an MRI, can identify the bile duct and pancreatic duct as well as small gall stones
within the bile duct. This information can help guide further treatment.
• However, MRI may not be easily available in all the centers and sick patients sometimes
find it difficult to undergo this procedure as it is time-consuming (>30 minutes).
• Endoscopic retrograde cholangiopancreatography — As mentioned above, ERCP can
cause acute pancreatitis. However, it may also provide helpful information in people who
are suspected of having pancreatitis due to gallstones or other problems with the bile or
pancreatic ducts.
• In addition, ERCP permits treatment of some causes of pancreatitis. An example is removal
of a gallstone that has become impacted in the common bile duct.
• Fine needle aspiration — In this procedure, a thin needle is used to collect tissue/fluid in
and around the pancreas, usually under CT guidance. This is recommended if the patient
has a persistent fever or necrotizing pancreatitis fails to improve or worsens despite
• The small sample of pancreatic tissue/fluid that is removed is sent for laboratory analysis,
including staining for bacteria and culture.
• This analysis can help determine if the damaged pancreatic tissue has become infected. If
infection is present in dead pancreatic tissue, further treatment may involve removal of
the dead tissue by surgery.
• Serum triglyceride levels — A serum triglyceride test determines blood levels of the fat-
like triglycerides. This test is useful for diagnosing familial hypertriglyceridemia or simple
hypertriglyceridemia in adults. In patients with pancreatitis due to hypertriglyceridemia,
the triglyceride levels are usually very high (>1000 mg/dL with upper limit of normal being
150 mg/dL).
• Genetic tests — Genetic tests are useful for diagnosing hereditary forms of pancreatitis.
Examples include genetic tests for mutations of the hereditary pancreatitis gene.

• The goals of treatment of acute pancreatitis are to alleviate pancreatic inflammation and
to correct the underlying cause.
• Treatment usually requires hospitalization for at least a few days.
• The specific treatment measures used depend upon whether a person has mild or
moderate to severe pancreatitis.
• Mild pancreatitis — Mild pancreatitis is typically self-limited, and the symptoms usually
resolve with simple supportive care, which entails monitoring, drugs to control the pain,
and intravenous fluids. Although doctors typically discourage eating during the first few
days, most people with mild pancreatitis are able to gradually resume eating within three
to seven days.
• Moderate to severe pancreatitis — Moderate to severe pancreatitis requires more
extensive monitoring and supportive care. In cases of necrotizing pancreatitis, treatment
may also entail antibiotics and surgery.
• Monitoring — Moderate to severe pancreatitis can lead to potentially life-threatening
complications, including damage of the heart, lung, and kidneys. Patients who develop
kidney failure may need dialysis until kidney function returns. Those who have severe lung
injury may need to be on a ventilator (a machine that facilitates breathing).
• People with pancreatitis of this severity may be closely monitored in an intensive care unit
where advanced supportive care is available if needed.
• Intravenous fluids — Intravenous fluids can help prevent the dehydration that often
results from moderate to severe pancreatitis.
• Feeding and eating — Studies suggest that early enteral feeding (feeding through a tube
advanced into the middle part of the small intestine) may actually help prevent infections,
reduce the likelihood of complications, and lessen the severity of pancreatitis.

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• Parenteral feeding (feeding through an intravenous line placed in the upper chest) is an
alternative for people who cannot tolerate enteral feeding or who cannot get enough
nutrients with enteral feeding.
• People with moderate to severe pancreatitis can resume eating gradually once the pain
resolves and bowel functions return to normal.
• Antibiotics — About 30 percent of people with severe acute pancreatitis will develop an
infection of the damaged pancreatic tissue. Antibiotics can prevent this infection and
control infections that are already present. Studies have shown that antibiotics reduce the
likelihood of infection and death in people with severe necrotizing pancreatitis.
• This treatment may entail intravenous antibiotics and oral antibiotics. Because these
antibiotics increase the risk of fungal infection, treatment may also include antifungal
• Necrosectomy — Acute pancreatitis is sometimes complicated by extensive damage to
the pancreatic tissue and/or infection. In these cases, doctors usually recommend removal
of the damaged and/or infected tissue, a procedure referred to as a "necrosectomy." It can
be performed by open surgical procedure or at times by less invasive procedures, e.g.,
endoscopic or radiologic placement of drainage tubes into the area. Whether the
procedure should be done surgically or by a non-surgical procedure depends upon the
clinical condition of the patient and the expertise available in the hospital.
• Specific treatments of gallstone pancreatitis — In people who have gallstone
pancreatitis, the treatment of pancreatitis is usually coupled with the treatment of
• Endoscopic papillotomy — Most gallstones that cause attacks of acute pancreatitis clear
on their own, but some stones cause prolonged blockage that leads to complications. In
people with gallstone pancreatitis who also have jaundice (yellowing of the skin) or a
gallbladder infection, a procedure called endoscopic papillotomy can be used to quickly
relieve the obstruction.
• In contrast, this procedure is not necessary for people who have already passed their
gallstones. Because many patients are very ill, doctors sometimes place a stent (a thin
plastic tube) to drain the obstructed bile duct rather than attempting to remove the stone.
Placement of a stent is usually faster and safer than endoscopic papillotomy.
• Surgery — Gallstone pancreatitis recurs in 30 to 50 percent of people after an initial
attack of pancreatitis.
• Doctors usually recommend cholecystectomy (surgical removal of the gallbladder) to
prevent this recurrence. This surgery can now be performed through a tiny incision in the
abdominal wall, a procedure called laparoscopic cholecystectomy.
• During surgery, the ducts joining the gallbladder, pancreas, and small intestine are
examined for residual gallstones.
• If any stones remain after surgery, they can be detected and removed during endoscopic
retrograde cholangiopancreatography (ERCP).
CT Severity Index (Balthazar Score) in Acute Pancreatitis
On computed tomographic (CT) scanning of the abdomen can be used to determine the
severity of acute pancreatitis and to determine a patient's prognosis. Contrast enhanced CT
scans can be used to assess pancreatic necrosis, since loss of perfusion consequent to necrosis
results in reduce enhancement.

Element Finding Points

grade of acute pancreatitis normal pancreas 0
pancreatic enlargement 1
inflammation involving pancreas and 2
peripancreatic fat
single fluid collection or phlegmon 3
two or more fluid collections or phlegmons 4
degree of pancreatic necrosis no necrosis 0
necrosis of one third of pancreas 2
necrosis of one half of the pancreas 4
necrosis of more than one half of the 6

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CT severity index =
= (points for grade of acute pancreatitis) + (points for degree of pancreatic necrosis)

• minimum score 0
• maximum score 10

severity index mortality complications

0-1 0% 0%
2-3 3% 8%
4-6 6% 35%
7-10 17% 92%
Chronic Pancreatitis – Fibrosis + destruction of exocrine pancreatic tissue. DM occurs in
advanced cases because islets of Langerhans involved.

Protein rich, viscous pancreatic juice
Precipitation to form plugs
Alcohol |
| Obstruction of ductules
Decrease secretion of lithostatin  Calcification + glandular ischaemia
Progressive acinar ectasia and atrophy  Pancreatic
• Southern India – Non alcoholics. Possibly result of malnutrition + cassava consumption.
Other causes : 1. Calcific – Alcoholism, Tropical (India)
2. Obstructive – Stenosis of ampulla of Vater.
3. Pancreas divisum, CF, Hereditary, Idiopathic.
Clinical Features: (middle aged alcoholic men)
1. Abdominal pain – combination of increased pressure of duct + involvement of nerves
by the inflammatory process. Relieved by leaning forward/drinking alcohol. May
present as acute pancreatitis (50%), slowly progressive chronic pain without acute
exacerbation (30%), no pain and just diarrhoea. 1/5 chronically consume opiate
2. Weight loss  Anorexia, avoidance of food (post-prandial pain), malabsorption, and/or
3. Steatorrhoea – if > 90% exocrine tissue destroyed
4. Protein malabsorption – only in most advanced cases
* overall, 30% diabetic  70% having chronic calcific pancreatitis.
Physical exam:
1. Thin, malnourished with epigastric tenderness
2. Skin pigmentation over abdomen & back. Chronic use of hot H2O bottle
3. Features of alcoholism & smoking.
1. Pseudocysts & pancreatic ascites
2. Extrahepatic obstructive jaundice
3. Duodenal stenosis
4. Portal/ splenic vein thrombosis leading to segmental portal HTN + gastric varices
5. Peptic ulcer
1. Alcohol misuse
2. Pain relief
3. Steatorrhoea
4. Complications – Surgical/endoscopic therapy

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CHOLELITHIASIS [gall bladder]
- in medicine, gall stones (choletitus) are crystalline bodies form within the body
by secretion or concecration of normal or abnormal bile components ;
formation of bile , relieved by food
- because of the bile → stores in the bladder → increase bile increase
consistency increase cholesterol →unable to emulsify →sticks to bile → hardens
→ gallstones
- obstruction of the common bile duct is choledocholithesis (choledo- common
bile duct)
- obstruction of the biliary tree can cause jaundice
- obstruction of the outlet of the pancreatic exocrine system can cause
- cholelithias> presence of stone in the gall bladder “chole” bile, “Lithia” stone,
“sis” process
- size gall stone varies and maybe as small as sand grain or as large as golf ball.
The gall bladder may develop a single, often large , stone or maybe smaller
ones , even several thousands

Biliary sludge is often a precursor of gallstones. It consists of Ca bilirubinate (a
polymer of bilirubin), cholesterol microcrystals, and mucin. Sludge develops during
gallbladder stasis, as occurs during pregnancy or while receiving TPN. Most sludge is
asymptomatic and disappears when the primary condition resolves. Alternatively, sludge can

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evolve into gallstones or migrate into the biliary tract, obstructing the ducts and leading to
biliary colic, cholangitis, or pancreatitis.
There are several types of gallstones.
1. Cholesterol stones account for > 85% of gallstones in the Western world. For
cholesterol gallstones to form, the following is required:
o Bile must be supersaturated with cholesterol. Normally, water-insoluble
cholesterol is made water-soluble by combining with bile salts and lecithin to
form mixed micelles. Supersaturation of bile with cholesterol most commonly
results from excessive cholesterol secretion (as occurs in obesity or diabetes) but
may result from a decrease in bile salt secretion (eg, in cystic fibrosis because of
bile salt malabsorption) or in lecithin secretion (eg, in a rare genetic disorder that
causes a form of progressive intrahepatic familial cholestasis).
o The excess cholesterol must precipitate from solution as solid microcrystals.
Such precipitation in the gallbladder is accelerated by mucin, a glycoprotein, or
other proteins in bile.
o The microcrystals must aggregate and grow. This is facilitated by the binding
effect of mucin forming a scaffold and retention in the gallbladder (impaired
contractility from the excess cholesterol in bile).
2. Black pigment stones are small, hard gallstones composed of Ca
bilirubinate and inorganic Ca salts (eg, Ca carbonate, Ca phosphate).
Factors that accelerate their development include alcoholic liver disease, chronic hemolysis,
and older age.
3. Brown pigment stones are soft and greasy, consisting of bilirubinate and fatty
acids (Ca palmitate or stearate). They form during infection, inflammation, and parasitic
infestation (eg, liver flukes in Asia).
Gallstones grow at about 1 to 2 mm/yr, taking 5 to 20 yr before becoming large enough to
cause problems. Most gallstones form within the gallbladder, but brown pigment stones form
in the ducts. Gallstones may migrate to the bile duct after cholecystectomy or, particularly in
the case of brown pigment stones, develop behind strictures as a result of stasis and infection.
- cholesterol
- estrogen
- low fiber, high cholesterol diets high in starchy foods have been suggested as
containing to gall stone formation
- eating fewer meal per day, eating less fish , and low intakes of nutrients folate,
magnesium, calcium and vitamin C stored energy > converted by liver>
- wine and whole grain bread may decrease the risk of gall stone
- Ultrasonography

- Laparoscopic cholecystectomy for symptomatic stones
- Expectant for asymptomatic stones; sometimes stone dissolution
Surgery: Surgery can be done with an open or laparoscopic technique.
- gall stones are asymptomatic initially
- intense pain in RUQ, abdominal region that steadily increase for approximately
30 minutes to several hours ( lost when eating> bile goes to the food we eat
and acts there) pain due to obstruction of gall stones from bile ; gall bladder
propels harder to push those crystals , thus results to pain
- may also encounter pain in back , ordinarily between the shoulder blades or
pain under the right shoulder
- increase satiety , n/v
- abdominal bloating
- intolerance of fatty foods, belching, gas, indigestion
Complications of gallbladder disease include
- cholangitis;
- necrosis,

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- empyema, and
- perforation of gallbladder;
- biliary fistula through duodenum; gallstone ileus; and
- adenocarcinoma of the gallbladder