ATOC 2009 RMACCESSORY ORGANS

LIVER, GALL BLADDER, PANCREAS

Accessory Organs Anatomy and Physiology

1. Liver - right diaphragm inferior surface- located in RUQ (inside th rib cage) or abdomen weighting 1200-1600 grams- 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 it 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 storage 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 cycle i. release of ketones as metabolic waste product of fatty acid metabolism 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 salts

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 - 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.

1

ATOC 2009 RMACCESSORY ORGANS

LIVER, GALL BLADDER, PANCREAS

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 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 secreteo insulin: for sugar regulation ; protein hormoneo 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

2

ATOC 2009 RMACCESSORY ORGANS

LIVER, GALL BLADDER, PANCREAS

- 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 fluido lipase[lipids] neutralizes / breakdowns fatso pancreatic alpha amylase [carbohydrates] / TAA promotes CHO breakdown; starch / sugaro 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 FUNCTIONS OF THE LIVER

1. stores fat- soluble vitamins (ADEK)o trauma→ release of ADEKo liver cirrhosis [necrosis of the liver] → vitamin K (IM/ ampule)

2. metabolizes bilirubin, by- product of the destruction of old RBCo RBC[ from bone marrow gets oxygen during inhalation then runs through the body]

o Iron should be “ready made”o globulin→ bilirubino liver → bile (emulsifies fats → prevents thrombus & decrease tissue perfusion o fats- minimal

3. stores and releases blood during hemorrhageo 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

dehydrationo release (hydrostatic pressure)o hemolyze (osmotic pressure)

5. synthesizes prothrombin, fibrinogen and clotting factors I, II, VII, IX, Xo prevents too much bleeding / hemorrhage

6. synthesizes phospholipids & cholesterol necessary for the production of bile salts , steroid hormones and plasma membraneso phospholipids → good cholesterol (concentrates bile) it gives salt to bile so that it will not burn all our

fatso 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 glucose9. stores and release copper (immune builders)

Hgb ↓ ↓ heme globulin (CHON content of RBC) ↓ transports oxygen in the systems for tissue perfusion ↓ kidney uses up the globin ↓ matures 180 days ↓ ↓ some destroy/ death MATS macrophage ↓ breakdown globulin into smaller pieces ↓ damaged liver ↓ goes to spleen (stored)heme→ ferretin → usually stored in the liver

3

ATOC 2009 RMACCESSORY ORGANS

LIVER, GALL BLADDER, PANCREAS

10. stores iron as ferritin (gives color to the blood)11. detoxification of alcohol and certain drugs

o Rhoo GIT digest alcohol→ if w/o liver → goes directly to brain →destroys/ shrinks neuron→ altered level of

consciousness → comatose12. phagocytosis 13. produces bile , contains salt necessary for digestion of fat

DIAGNOSTIC EVALUATION 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: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 / obstructiono increase with hemolysiso total serum bilirubin 1.7- 20.5 umol/L

2. serum urine bilirubino increase with biliary obstruction

3. urobilinogen o increase with hemolysis / shunting blood of portal flowo normal urobilinogen 0.09-4023umol/ 24 hourso normal fecal urobilinogen 0.068-0.34 umol/ 24 hours

Protein studies1. albumin and globulin measurement

o redirect with hepatocellular injury with hepatitiso albumin normal 3.5-5.5 g/ dLo 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 treatmento increase in chronic liver disease / vit K deficiency

Fat metabolism1. serum cholesterol

o normal: 3.90-6.50 mmol/ Lo measurement lipid metabs

Liver detoxification1. serum alkaline phophatase

o disposed by the bileo 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

4

ATOC 2009 RMACCESSORY ORGANS

LIVER, GALL BLADDER, PANCREAS

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 injury3. lactic dehydrogenase (LDL)

o normal 80-192 U/L (200-500 U/L)o 45-90 U/Lo the range can be up to approximately 200 units/Lo 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 transpeptidaseo formed in heart, liver, lungs, spleeno normal: 0-30 U/L at 30 hour

5. serum ammonia o 35 to 65 mcg/dlo Adults: 15-110 ug/dl (ug = micrograms) o Children: 40-80 ug/dl o Newborns: 90-150 ug/dl

Radiology and Imaging1. hepatobiliary scan

o non-invasive with radiographic material to visualize / hepatobiliary disorder , cholelithiasis]o maintain nPO at least 4 hours before procedureo no opiate 4 hours before procedure o there will be an additional procedure after 24 hours

2. oral cholesystographyo use contrats medium → gallbladder

gall stone ability of the gallbladder to contract / empty ability of the gall bladder to fill its contento assess if patient is allergy to seafood / allergic rxn to contrast mediumo self administration of contrats medium 10-20 hours before x-ray (evening)o NPO to prevent contraction and emptying of bladdero May be repeated after 24 hourso CT with jaundice patient cannot excrete, dye is a toxic waste

3. endoscopic retrograde cholangiopancreatography (ERCP)o with flexible fiberoptic endoscopeo 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 administrationo 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 lumeno for staging pancreatic tumors, site of tumors, blood vessels involved local & regional involvement, size ,

extentiono same nsg resp. for ERCP

5. Magnetic resonance cholangiopancreatography (MRCP)o Non-invasive used to view pancreatic ducto Used for patient with allergy to iodine based contrast materialo No contrast material used o Similar to ERCP

5

ATOC 2009 RMACCESSORY ORGANS

LIVER, GALL BLADDER, PANCREAS

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 examo 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 stoneso 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- histopatho 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

3. submandibular gland- forms the floor of the mouth - ptyalin + mucin: fremulum of tongue

LIVER - 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

6

ATOC 2009 RMACCESSORY ORGANS

LIVER, GALL BLADDER, PANCREAS

- 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 fat2. metabolizes hormones/ drug (detoxification)- clean foreign substance3. synthesize CHON, sugar, glucose, CHO4. blood clotting function for metabolism5. stores nutrients (vitamin and minerals) fat soluble vitamin 6. converts ammonia – urea7. converts fatty acids – ketones 8. produces prothrombin and other factors for coagulation

BILE - 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 metabolism1. CHO metabolism (4 types), release glucose: hypoglycemia; stores glucose hyperglycemic

a. gluconeogenesis: catabolism of amino acid (CHON) and glycerol (fat) into glucose for energyb. glucogenesis: anabolism of glucose into glycogen for storagec. glycogenesis: anabolism of starch into glycogen for storaged. 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 ammoniaAmino acids: repair of muscle tissue / energyAmmonia: end product of CHON, toxic effect to body if it goes into circulationAmmonia: → liver (converts to urea) → kidney→ urine

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

7

ATOC 2009 RMACCESSORY ORGANS

LIVER, GALL BLADDER, PANCREAS

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 intestineCholecystokinin: stimulate (hormone) gallbladder to contract during ingestion of fat Significance of Bile:

1. important function in digestion2. 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 % COInferior & superior → hepatic portal veinMesenteric vein → hepatic portal veinSplenic vein → hepatic portal vein ↓deoxygenated blood (100-1200mL / min to liver)Portal venous blood- 70% of blood supply to the liverBilirubin: by product of the destruction of aged RBC

: gives bile a greenish black color & produces yellow tinge of jaundiceUrobilinogen:

1. absorbed in the portal circulation2. excreted in the feces

Bilirubin metabolism

8

ATOC 2009 RMACCESSORY ORGANS

LIVER, GALL BLADDER, PANCREAS

- ½ of the bilirubin is converted into urobilinogen , a highly soluble substance with intestinal flora - most of the urobilinogen that is absorbed is returned to the liver to be re-excreted into the bile . a small

amount of urobilinogen , approximately 5% is absorbed into the general circulationHEPATIC DISORDER

Hepatitis- 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, kissing- 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- 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

Hgb ↓ ↓ heme 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 urobilinogen→urobilin→ urine ↓ stercobilinogen → stercobilin ↓ feces

9

ATOC 2009 RMACCESSORY ORGANS

LIVER, GALL BLADDER, PANCREAS

- severe in pregnant womanClinical manifestations

1. prodromal phaseo 2 weeks after exposure to appearance of jaundiceo fatigue, anorexia, malaise, n/v, h/a, hyperalgia, cough, low grade fevero 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 paino actual phase of illness

3. recovery phase o resolution of jaundice 6-8 weeks after experienceo sx diminish but liver remains enlarged & tendero liver function returns to normal 2-12 weeks after onset of jaundice

Complications:o persistence of clinical manifestation and liver inflammation after acute hepa B, C & Do liver function test remain abnormal > 6 monthso chronic, active hepa B – predisposition to cirrhosis and primary hepatocellular carcinoma

Nursing intervention:1. maintain adequate nutrition2. maintain adequate fluid intake3. ensuring of disease transmission4. preventing and controlling bleeding5. patient education and health maintenance

Management / evaluation Treatment:Serological analysis for HBsAg> marker for HBV ; most specific diagnosis for hepa

1. encourage patient to rest, gradual increase in activity2. low fat, high carbohydrate diet > if bile flow is obstructed 3. if with fever (antipyretic drug), nauseated (antiemetic)4. therapeutic measures control dyspeptic sx & malaise5. if sever n/v, advise patient to go to hospital (life threatening) if more than 2 episodes do IVF treatment (plazil/

metoclopromide)- antiemetic6. 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- diureticscomplication: dehydration, hypokalemia (prolonged vomiting), hepatic encephalopathy, hepatocellular

carcinoma, chronic active hepatitis- develop hepatocellular cancer Assessment:

o obtain HPI, IV drug, sexual activity, trvel, ingestion of contaminated food, alteration in bowel functiono systemic related s/sx= size and shape of liver

Nursing interventiono adequate fluid- IVF, measure I/Oo rest/ activity, emotional supporto health teaching

- dse-dse transmission, prevention- report complication, bleeding- sx of encelopathy (aggressive, unruly behavior)

Nx Dxo Hypothermia o FVDo Activity intoleranceo Risk for infectiono Risk for injury

CIRRHOSIS- 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 DiseaseParameter Fatty Liver Alcoholic Hepatitis Cirrhosis

Histologic specificity for alcoholic cause No Yes No

10

ATOC 2009 RMACCESSORY ORGANS

LIVER, GALL BLADDER, PANCREAS

Prognosis Excellent Variable GuardedReversible Yes Variable Generally, no

Types:1. Alcoholic cirrhosis: caused by toxic effects of alcohol on the liver, immunological and oxidative stress from lipid

production 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 lymphocytes

Causes:

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 cirrhosis.

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 cirrhosis.

o Toxins can cause cirrhosis. These toxins include prescription and non prescription drugs and environmental toxins and a parasitic infection called schistosomiasis.

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.

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.

Manifestations: 1. weight loss, weakness, anorexia, (no proper CHON metabolism muscle wasting)2. fatigue/ malaise3. mild to severe jaundice, late sign4. frequent diarrhea/ constipation5. abdominal pain (liver enlargement) epigastric, RUQ pain with dull aching, sensation of fullness

Sign and symptom 1. Fatigue2. Itching3. Jaundice caused by high levels of bilirubin that are not able to be excreted from the body4. Enlarged liver5. Abdominal pain6. Fatty deposits under the skin caused by cholesterol deposits7. Soft yellow spots on the eyelid8. Fatty stools9. Dry eyes and mouth10. 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

11

ATOC 2009 RMACCESSORY ORGANS

LIVER, GALL BLADDER, PANCREAS

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 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 partso Spleenomegaly, liver failure o Ascites

portal systemic shunt = increase pressure bleeding thrombocytopenia & spleenomegaly

Complications 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.

12

ATOC 2009 RMACCESSORY ORGANS

LIVER, GALL BLADDER, PANCREAS

- 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.

Management 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 livero 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.

PORTAL HYPERTENSION 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 VC 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,

pregnancyb. 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;iverComplications:

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 cavity

4. hepatic encelopathyo “portal systemic encelopathy”

13

ATOC 2009 RMACCESSORY ORGANS

LIVER, GALL BLADDER, PANCREAS

o characterized by CNS disturbances, particularly reversible alterations of consciousness o results from presence of ammonia in the brain

Pathophysiology

Manifestation:1. vomiting of blood from bleeding esophageal varices – common sx of portal hypertension2. anemia, blood in stool, abdominal discomfort, insomnia, dyspepsia3. hemorrhage, edema formation, increase BP, decrease CO

Management:- portal hypertension → disease at the time varice .. bleeding and confirmed by endoscopy and evaluation of

portal venous pressure1. withdraw from drinking alcohol 2. nutritional or vitamin supplement ( high cal, moderate CHON)3. treatment for ascites / F&E imbalance

o Na+ restrictiono Water restrictiono Oral supplement K+

o Paracentesis: to relieve abdominal pressure from asciteso Pain for algesia o Albumin administrationo Bed rest o Diuretics → spironolactone (K+ sparring), lasix (loop diuretics)

Complication: 1. hyper Na+, water retention2. bleeding3. esophageal varices4. coagulopathy5. spontaneous bacterial peritonitis6. hepatic encelopathy7. 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.

Assess1. alcohol abuse2. history of jaundice3. hepa4. alcoholism5. biliary stasis6. abdominal observation7. 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 destructionb. hepato cellular – defective liverc. obstructive jaundicea) itchiness- give antipruritic lotions/ starch bathb) 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

Portal Hypertension ↓ ↓ ↓ increase pressure in capillaries port systemic with shunting of blood splenomegaly ↓ ↓ ↓ ↓ ↓ ↓ascites development of collateral channels shunting of ammonia and toxins anemia thrombocytopenia kalemic ↓ ↓ ↓ from intestines to the general ↓ circulation bleedingcaput medullae hemorrhoids esophageal varices ↓ hepatic encelopathy

14

ATOC 2009 RMACCESSORY ORGANS

LIVER, GALL BLADDER, PANCREAS

- 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 careb) check if gastric balloon is always in placec) keep balloon pressure at required level d) check/ monitor v/s for shock or bleedinge) F/e

Patient care! if bleeding still persist: sclerotherapy/ variceal ligation

from mouth to esophagus sclerosing agent is injected directly into the vein with a flexible fiber optic endoscope > thrombosis

* decrease pressure by shunting blood around livera) portal systemic shunt (portal canal): portal vein is anastomosed the inferior vena cava to reduce variceal blood

flow and pressureb) spleno renal shunt: splenic vein and left renal vein after splenectomy ; portal vein can’t be used d/t thrombosisc) internal position renocaval vein: superior mesenteric vein is grafted to IVC Diagnostic test:

1. liver biopsy: obstruction/ fibrosis of liver tissue2. liver scan: abdominal thickening/ liver mass3. computed tomography scan: size of the liver4. esophagoscopy: view esophageal varices5. paracentesis: to remove fluid (ascites)6. percutaneous transhepatic cholangiography: (PTC) differentiate between extraobstructive/ intraobstructive type

of jaundice7. laparoscopy & liver biopsy – direct visualization8. serum liver function test: elevated SGPT

Common bile duct- hepatic duct & cystic duct s/sx of decrease liver function:

1. weight loss/ decrease body mass2. steatorrhea : is the presence of excess fat in faeces3. 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 eminences5. 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. jaundice7. bleeding gums, epistaxis 8. hepatic encelopathy9. fatigue, weakness, anorexia

PORTAL SYTEMIC SHUNT- 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 vein - collateral between inferior & internal hemorrhoids

15

ATOC 2009 RMACCESSORY ORGANS

LIVER, GALL BLADDER, PANCREAS

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)Pathophysiology

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)

(cholecystokinin) Aid in digestion of fats and excretion of conjugated bilirubin from liver 1. CHOLECYSTITIS 40 y/o obesityfemalemultiparity stone formation ( cholesterol, Ca+ pigment) oral contraceptiveliver problem increase hemolysis biliary tree infection

- oral cholecystography- UTI- Hepatic biliary scar

Management 1. conservative (symptomatic): relieve pain2. surgicall management- Cholecystectomy ( open/ laparoscopic)- Choledoclostomy ???

Acute cholecystitis This should be suspected whenever there is acute right upper quadrant or epigastric pain.

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. InvestigationsBlood

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

16

ATOC 2009 RMACCESSORY ORGANS

LIVER, GALL BLADDER, PANCREAS

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.

RadiologySonography 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 thickening greater than 3mm, pericholecystic fluid, and gallbladder dilatation.

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.

s/sx1. RUQ pain, guarding2. 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/v5. chemical irritation> inflammation> low grade fever6. swelling and rebound tenderness 7. pain perceived every after eating begins and persist 1-3 hours8. 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

Management: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)

Surgical 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

Post-op- semi-fowler’s 6-8 hours > lessened diaphragm – dyspnea- assess bile 23- 34 hours (500-700mL/ day)

17

Liver (hepatic duct) gall bladder (cystic duct) ↓ ↓ common bile duct ( inflamed ) ↓ lumen of common bile duct narrows ↓ minimal bile to sf → bile to peritoneum ↓ peritonitis

ATOC 2009 RMACCESSORY ORGANS

LIVER, GALL BLADDER, PANCREAS

Pancreatic secretions contain:1) proteolytic enzy,es- trypsin, ribonucleic, deoxyribonucleic, carboxypeptidase; breakdown of CHON2) 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 glycogen- liver; skeletal muscles

A. pancreatitisTypes

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 areaturner’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 ↓increase blood glucose ↓release of insulin ↓glucose brought to cells↓cells utilize glucoseCholelithiasis (disease by laparoscopic cholecystectomy)

- gall stone formation > cholesterol/ pigmentedetiology:

- 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 calcium

CholecystitisPost-op care

- diaphragm relax compress lung- 24-36 hours semi fowler’s after cause 6-8 hours (dyspnea)

T-tube care

Exocrine organs food in stomach↓ ↓lobules ( acinar cells) stimulate pancreas ↓ ↓release digestive enzymes pancreatic enzymes (pancreatic duct)↓ ↓release pancreatic enzymes SI

↓ amylase (CHO) lipase (fats)

trypsin (CHON)

18

ATOC 2009 RMACCESSORY ORGANS

LIVER, GALL BLADDER, PANCREAS

- 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

Pancreas - 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- pancreatitisserum lipase – sensitive marker of pancreatic injury – acute alcoholic pancreatitis Plan of care

1. relieve pain: upright/ leaning forward2. narcotic meds (analgesic)> demerol3. decrease pancreatic stimulation > oral food / fluids4. maintain f/e> IVF treatment5. antiemetic for n/v6. decrease alcoholic intake > stimulate pancreatic juice7. low fat, caffeine, moderate CHON

ACUTE PANCREATITIS

INTRODUCTION 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 procedures involving the pancreatic and bile ducts, and other types of injury to the pancreas.

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.

CAUSES OF ACUTE PANCREATITIS 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 pancreatitis.

19

ATOC 2009 RMACCESSORY ORGANS

LIVER, GALL BLADDER, PANCREAS

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.

SYMPTOMS 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. 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 coma.

DIAGNOSIS 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 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 normal, and this pattern helps differentiate most cases of acute pancreatitis from other conditions that increase blood amylase levels.

20

ATOC 2009 RMACCESSORY ORGANS

LIVER, GALL BLADDER, PANCREAS

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 diagnosed. 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 inflammation. 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 pancreas.

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.

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 treatment.

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.

TREATMENT 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.

21

ATOC 2009 RMACCESSORY ORGANS

LIVER, GALL BLADDER, PANCREAS

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.

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 drugs.

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 gallstones.

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 PancreatitisOn 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 Pointsgrade of acute pancreatitis normal pancreas 0 pancreatic enlargement 1 inflammation involving pancreas and peripancreatic fat 2 single fluid collection or phlegmon 3 two or more fluid collections or phlegmons 4degree 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 pancreas 6 CT severity index == (points for grade of acute pancreatitis) + (points for degree of pancreatic necrosis) Interpretation:• minimum score 0• maximum score 10

22

ATOC 2009 RMACCESSORY ORGANS

LIVER, GALL BLADDER, PANCREAS

 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.

PathophysiologyAlcohol |

Protein rich, viscous pancreatic juice |

Precipitation to form plugsAlcohol | | Obstruction of ductules

Decrease secretion of lithostatin Calcification + glandular ischaemia |

Progressive acinar ectasia and atrophy Pancreatic insufficiency 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 analgesics.

2. Weight loss Anorexia, avoidance of food (post-prandial pain), malabsorption, and/or diabetes.3. Steatorrhoea – if > 90% exocrine tissue destroyed4. Protein malabsorption – only in most advanced cases

* overall, 30% diabetic 70% having chronic calcific pancreatitis.Physical exam:

1. Thin, malnourished with epigastric tenderness2. Skin pigmentation over abdomen & back. Chronic use of hot H2O bottle3. Features of alcoholism & smoking.

Complications:1. Pseudocysts & pancreatic ascites2. Extrahepatic obstructive jaundice3. Duodenal stenosis4. Portal/ splenic vein thrombosis leading to segmental portal HTN + gastric varices5. Peptic ulcer

Management:1. Alcohol misuse2. Pain relief3. Steatorrhoea4. Complications – Surgical/endoscopic therapy

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 pancreatitis - cholelithias> presence of stone in the gall bladder “chole” bile, “Lithia” stone, “sis” processcharacteristic - 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

23

ATOC 2009 RMACCESSORY ORGANS

LIVER, GALL BLADDER, PANCREAS

PathophysiologyBiliary 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 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.

Causes- cholesterol- estrogen

24

ATOC 2009 RMACCESSORY ORGANS

LIVER, GALL BLADDER, PANCREAS

- 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> cholesterol

- wine and whole grain bread may decrease the risk of gall stone

Diagnosis- Ultrasonography

Treatment- Laparoscopic cholecystectomy for symptomatic stones

- Expectant for asymptomatic stones; sometimes stone dissolution

Surgery: Surgery can be done with an open or laparoscopic technique.Symptoms

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

25