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Gi Gallbladder & Pancreas
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Gi Gallbladder & Pancreas

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  • 1. Pascale Gehy-Andre PA-C Diseases of Gallbladder & Bile Ducts
  • 2. Anatomy of the Gallbladder
    • A. A pickle shaped sac that is 8-10 cm long c a capacity of about 50 ml.
    • B. Divided into:
      • Neck: (has a small pouch called Hartmann’s pouch. This is the location of most of the pathology)
      • Body
      • Fundus
    • C. Contracts after a fatty meal is ingested.
    Add a picture here.
  • 3. Biliary Anatomy
    • Hepatocytes  canaliculi  biliary ductules 
    • L & R hepatic ducts  common hepatic duct
    • Common hepatic ducts & Cystic Duct  Common Bile Duct (CBD)
  • 4. Bile Production
    • A. Bile is an isotonic mixture consisting of
      • 1. electrolytes
      • 2. Protein
      • 3. bile salts
      • 4. cholesterol
      • 5. phospholipids- (phospholipids: contain phos. & on hydrolysis yield fatty acids, glycerol, lethicin, & cephalins. Phospholipase is the enzyme found in liver & pancrease)
      • 6. bile pigment
  • 5. Bile Production
    • B. Cholate & chenodeoycholate which are bile salts are synthesized by hepatocytes from cholesterol in a multi-step procedure.
    • C. Cholecystokinin (pancreatic enzyme) is released from the small bowel after a fatty meal, stimulates the GB to contract & sphincter of oddi to relax
    • D. Bile acids aid in the absorption of fat forming micelles which are absorbed in the small bowel.
    • E. The bile salts are reabsorbed in the small bowel & transported back to the liver. Averaging 9x’s/day.
  • 6. Bile Acid Insufficiency
    • 1. Insufficient bile acids can result from a disorder at any step in enteropathic circulation
      • A. liver disease with decreased production of acids
      • B. obstruction of the duct
      • C. Bacterial overgrowth
        • (bile acids are conjugated before they can participate in fat absorption)
      • D. Disorders of the terminal ileum which decrease the absorption of the bile salts.
  • 7. Bile Acid Insufficiency (cont)
    • 2. Bile acids facilitate the absorption of dietary fat by the formation of intraluminal micelles.
    • Therefore if absent will result in malabsorption of fat.
    • Treatment
      • A. Tetracycline for small bowel overgrowth
      • B. Terminal ileum disorders should be treated
      • C. Use of medium chain triglycerides are helpful
      • Note: failure to correct allows bile acids to enter the large bowel producing diarrhea.
  • 8. Cholelithiasis (Gallstones)
    • Definition: presence of concretions in the gallbladder or bile ducts.
    • 1. Affects 20 million people/year
    • 2. Stone type
      • A. Cholesterol (70%) (most common)
        • All ages
        • Mostly women
        • Use of estrogen
        • Obesity
        • Diabetes
        • Disease of small bowel & sphincter
  • 9. GallStones (Cholelithiasis)
    • 2. Stone type (cont):
      • B. pigment 30%
        • (calcium bilirubinate)
        • Mostly bilirubin
        • Hemolytic states, cirrhosis & elderly
    • 3. Mixed
  • 10. Interrelation of gallbladder disease
    • 1. Cholecystitis is associated with cholelithiasis in 85%-90% of cases
    • 2. Regurgitation of pancreatic acid causes non-bacterial cholecystitis
    • 3. Bile stasis due to sphincter of oddi spasm or obstruction is a cause of inflammation
    • 4. Gangrene of GB is due to chronic cholecystitis
    • 5. A porcelain GB (heavily calcified) should be removed surgically because of increased risk of GB cancer
  • 11. Diagnostic Studies
    • A. Chemistry, CBC, LFT’s, amylase
      • 1. CBC elevated in cholecystitis c slight elevation of LFT’s
      • 2. Biliary obstruction: bilirubin, alk phos & amylase may be elvated.
    • B. Plain film of the abdomen is of poor value.
    • Only 15-20% of stones are radiopaque.
    • C. Oral Cholecystogram:
      • Requires patient to take pills
  • 12. Diagnostic Studies (cont)
    • D. Ultrasound:
      • Most sensitive and specific test for the detection of gallstones
      • Limited in obese patients
      • Simple to do & safe
      • No preparation needed
      • May show thinkened wall in acute cholecystitis
    • E. HIDA scan:
      • Used if acute cholecystitis is suspected. The nuclear material is normally taken up in the GB. If obstructed no GB will be seen.
    • F. CT scan
  • 13. Treatment of Cholelithiasis (Gallstones)
    • 1. Pain relief
    • 2. Cholecystectomy
      • Emergent for cholecystitis
      • Scheduled if symptomatic cholelithiasis s/ cholecystitis
    • 3. Dissolution with
      • Ursidiol,
      • chenodeoxycholic acid (actigall)
      • Contraindicated in:
        • Liver ds
        • large stones
        • Pregnant women
        • Severe sx
        • **It takes 2 yrs to work
      • Indications: elderly?
    • 4. Lithotripsy
  • 14. Complications of Cholelithiasis (Gallstones)
    • Colic
    • Acute cholecystitis
    • Cholangitis
    • Perforation
    • Fistulization
    • Gallstone ileus
  • 15. Acute Cholecystitis
    • Types:
      • 1. Acute calculus cholecystitis
        • Inflammation of GB in association with stones
        • Stones are in the GB, cystic duct, or in CBD
      • 2. Acute Acalculus cholecystitis
        • Acute inflammation of the GB without the presence of stones
        • High incidence of gangrene, necrosis, & perforation
        • High mortality rate because more common in elderly & debilitated c absence of oral intake & GB stasis
        • Early intervention (consider drainage first)
        • Large doses of IV antibiotics
  • 16. Acute Cholecystitis
    • 1. Key Symptoms:
      • Pain in RUQ or epigastric area
      • Possible radiation to shoulder, back, tip of R scapula, or flank
      • Nausea & vomiting
      • Fever, tachycardia, tachypnea
      • Jaundice (represents obstruction)
        • Urine turns dark (acolic stool-Bilirubin)
    • 2. Key Signs:
      • RUQ (or epigastric) tenderness
      • +Murphy’s sign
    • 3. Laboratory:
      • Leukocytosis
      • Alk Phos & bilirubin
        • (c obstruction & pathology of GB)
      • SGOT ^, SGPT ^ (if cholangitis present)
  • 17. Acute Cholecystitis (cont)
    • 4. Common in:
      • Fat
      • Fertile
        • (OCP use)
      • Forty
      • Females
    • 5. Differential Diagnosis:
      • Peptic ulcer
      • Appendicitis
      • Hepatitis
      • Pyelonephritis
      • Pneumonia
      • MI
      • Renal colic
      • Pancreatitis
      • Cholangitis
  • 18. Acute Cholecystitis
    • 6. Key Diagnostic Tests:
      • Ultrasound
        • Most sensitive and specific test for the detection of gallstones
        • GB wall thickening and the presence of pericholecystic fluid are radiographic signs of acute cholecystitis
      • HIDA Scan (dimethyl iminodiacetic acid)
        • great when bilirubin elevated
        • Does not detect gallstones
        • Identifies an obstructed GB
        • The most sensitive and specific test for cholecystitis (especially acalculus cholecystitis)
  • 19. Acute Cholecystitis
    • Key Diagnostic Tests: (continued)
      • Oral cholecystogram (limited)
      • CT scan
        • most accurate for differential of intra- & extrahepatic obstruction with 95% accuracy.
        • Often used in the workup of abdominal pain without specific localizing signs & symptoms
        • CT scan is not a first line study for detection of gallstones because of greater cost & invasive nature of the test
        • When present gallstones usually are observed on CT
  • 20.  
  • 21. Acute Cholecystitis (cont)
    • Treatment:
      • IV fluids
      • Antibiotics
      • Analgesics
        • ( No morphine- theories of sphincter of Oddi spasm)
      • Cholecystectomy
        • Open vs. laparoscopic surgery
  • 22. Acute Cholecystitis (cont)
    • Complications:
      • Perforation
      • GB ileus
      • Biliary colic
      • Biliary Dyskinesia
      • Choledocholithiasis
      • Chronic Cholecystitis
      • Tumors of GB
  • 23. Gallbladder disease (cont)
    • Biliary colic:
      • Usually due to stones
      • Pain due to GB distention
      • Nausea/ Vomiting
      • Relief of pain suddenly
    • Biliary Dyskinesia:
      • Symptoms without stones
      • GB doesn’t empty properly
  • 24. Choledocholithiasis
    • Stones in the common duct which may cause the following symptoms:
      • Biliary colic
      • Obstructive jaundice
      • Intermittent jaundice
      • Pancreatitis
      • Cholangitis (inflammation of CBD)
      • Hemobilia
        • Fever
        • Pain
        • Blood (in the intrahepatic system)
  • 25. Cholangitis
    • inflammation of CBD
    • Charcot’sTriad:
          • RUQ pain (biliary pain)
          • Jaundice
          • Fever
  • 26. Cholangitis Mneumonic
    • C harcot's triad/ C onjugated bilirubin increase H epatic abscesses/ H epatic (intra/extra) bile ducts O bstruction L eukocytosis A lkaline phosphatase increase N eoplasms G allstones I nflammatory bowel disease (ulcerative colitis) T ransaminase increase I nfection S clerosing
  • 27. Chronic Cholecystitis
    • Associated c GB stones in 95% of cases
    • Frequent attacks & GB empties poorly
    • Fever unusual
    • Pain usually several hrs after eating
    • Bloating, belching, and flatus
    • Murphy’s sign absent
    • Labs : CBC, Amylase, bilirubin, enzymes normal
    • HIDA scan positive
  • 28. Tumors of the Gallbladder
    • Polyps: are rare
    • Carcinoma of GB:
      • Uncommon
      • Mostly women
      • Usually diagnosed too late
      • Spread by direct invasion
      • Adenocarcinoma
      • Courvoisier’s sign (palpable GB)
    • Carcinoma of Bile Duct:
      • Usually adenocarcinoma
      • Symptoms:
        • Painless jaundice
        • Mass palpable
  • 29. Review Gallbladder
    • Gallstones ~ 70% cholesterol & 30% pigment stones
      • May be asymptomatic (70%)
      • May cause biliary colic (20%)
      • May cause cholecystitis (10%)
    • Biliary colic- steady cramplike pain in epigastrium (RUQ)
      • Pain subsides over 30-60 min
    • Cholecystitis - steady cramplike pain in epigastrium (RUQ) & + Murphy’s sign
      • Pain does not subside spontaneously
    • Cholangitis - triad=
      • 1. biliary pain (RUQ) 2. jaundice 3. fever
      • Sclerosing cholangitis- autoimmune inflammation of the bile ducts. A rare complication of ulcerative colitis
  • 30. Pancreas
    • Anatomy
      • Head: embraces the duodenal curve
      • Body: crosses the vertebral column
      • Tail: in the hilum of the spleen
  • 31.  
  • 32.  
  • 33.  
  • 34. Pancreas Physiology
    • 1. Islets of Langerhans: responsible for the production of:
      • A. Insulin
      • B. Glucagon:
        • A hormone that is produced by the alpha cells of langerhan that produces glucose from glycogen.
      • C. Gastrin
      • D. Somatostatin
        • Gastrin and somatostatin are mostly in stomach, but also in pancreas, stimulates HCL stopping agents.
  • 35. Pancreas Physiology (cont)
    • 2. Enzymes secreted from ducts:
      • Amylase (CHO)
      • Lipase (Fats)
      • Trypsinogen (Protein)
        • Is converted to trypsin in the duodenum so as not to cause autodigestion
        • NOTE: Liver produces alpha trypsin to protect against autodigestion
  • 36. Pancreas Physiology (cont)
    • 3. Pancreatic secretion stimulated by two hormones:
      • Secretin :
        • Produced in the duodenum & stimulated by acid
        • Inhibits gastric acid
        • Stimulates pancreas to produce bicarb & chloride
      • Cholecystokinin :
        • A pancreozymin which is released in response to fat & amino acids in the duodenum
        • Stimulates pancreas to produce amylase, lipase, & trypsin
  • 37. Pancreas Physiology (cont)
    • 4. The pancreas secrets 1-4 Liters of fluid per day
    • 5. The pancreatic juice is usually alkaline.
      • Food in duodenum causes secretion of secretin (due to high acid content). Secretin releases H2O & bicarb.
    • 6. In pancreatitis we use foods low in fat & protein because they stimulate secretion from the pancreas. CHO is a weaker stimulant.
    • 7. Pancreatic enzymes inhibit gastric secretion of its enzymes.
  • 38. Acute Pancreatitis
    • Etiology: Alcohol & Gallstones = 80-90%
      • Other causes:
        • Complications of ERCP (endoscopic retrograde cholangiopancreatography)
        • Trauma
        • Infections (mumps/ viral)
        • Hyperlipidemia: TG > 1000 mg
        • Hypercalemia
        • Drugs (thiazides, lasix)
        • Idiopathic
  • 39. Pancreatitis Causes Mneumonic
    • I GET SMASHED :
    • I diopathitic G allstones E thanol T rauma S teroids M umps A utoimmune (PAN) S corpion stings H yperlipidemia/ H ypercalcemia E RCP D rugs (including azathioprine and diuretics)
    • Note: 'Get Smashed' is slang in some countries for drinking, and ethanol is an important pancreatitis cause.
    • Note: Shortest answer is gallstones for women, and ethanol for men.
  • 40.  
  • 41.  
  • 42.  
  • 43.  
  • 44. Acute Pancreatitis
    • Symptoms:
      • Epigastric pain severe, boring in nature
      • Radiation to back
      • Nausea & vomiting
      • Aggravated by eating
      • Feels better leaning forward
      • Possible + peritoneal signs
  • 45. Acute Pancreatitis
    • Key Signs:
      • Low grade fever, tachycardia, tachypnea
      • Pleural effusions or basal consolidation of lung (left)
      • Bowel sounds are feeble or absent
      • Low blood pressure, thready pulse, diaphoretic (shock)
      • Rare findings are:
        • Jaundice due to common bile duct compression
        • Cullen sign : discoloration of the periumbilical area
        • Grey turner sign : flank discoloration
          • These two are specific for pancreatitis
  • 46. Acute pancreatitis
    • Laboratory tests:
      • Elevated serum amylase (>4x’s normal)
        • Goes down within 48 hrs
        • Urine amylase neither specific nor sensitive
        • If normal needs to be confirmed by CT
      • Serum lipase
        • delayed but more specific
      • CBC usually abnormal
        • Elevated WBC
        • If hgb/hct fall means poor prognosis
      • Chemistry
        • Hyperglycemia
        • hypocalcemia
      • LFT’s
        • Abnormal if biliary tree involved
      • **Excessive fluid loss
  • 47. Ranson’s criteria on admission
    • 1. Age greater than 55 on admission? Yes (1 points) No (0 points)
    • 2. WBC greater than 16K on admission? Yes (1 points) No (0 points)
    • 3. Blood glucose greater than 200 mg% on admission? Yes (1 points) No (0 points)
    • 4. Serum LDH greater than 350 IU/L on admission? Yes (1 points) No (0 points)
    • 5. Serum SGOT (AST) greater than 250 SF units on admission? Yes (1 points) No (0 points)
  • 48. Ranson’s criteria within 48 hrs
    • 1. Hematocrit fall more than 10% within 48 hrs of admission? Yes (1 points) No (0 points)
    • 2. BUN rise more than 5 mg/dl within 48 hrs of admission? Yes (1 points) No (0 points)
    • 3. Serum calcium less than 8 mg% within 48 hrs of admission? Yes (1 points) No (0 points)
    • 4. Arterial pO2 less than 60 mmHg within 48 hrs of admission? Yes (1 points) No (0 points)
    • 5. Base deficit less than 4 mEq/L within 48 hrs of admission? Yes (1 points) No (0 points)
    • 6. Fluid sequestration more than 6L within 48 hrs of admission? Yes (1 points) No (0 points)
  • 49. Ranson's criteria for pancreatitis mortality prediction
    • Score Interpretation
    • under 3 Predicted mortality about 1%
    • 3-4 Predicted mortality of 15%
    • 5-6 Predicted mortality of 40%
    • > 6 Predicted mortality of 100%
  • 50.  
  • 51. Pancreatitis Ranson’s Criteria On Admission Mneumonic
    • " GA LAW " (GA is abbreviation for Georgia): G lucose >200 A ST >250 L DH >350 A ge >55 y.o. W BC >16000
    • Or
    • LEGAL : L eukocytes > 16.000 E nzyme AST > 250 G lucose > 200 A ge > 55 L DH > 350
  • 52. Pancreatitis Ranson’s Criteria Initial 48 hrs Mneumonic
    • &quot; C & HOBBS &quot; ( C alvin and Hobb e s ): C alcium < 8 H ct drop > 10% O xygen < 60 mm B UN rise > 5 B ase deficit > 4 S equestration of fluid > 6L
  • 53. Acute Pancreatitis
    • Radiology studies:
      • Plain films of abdomen (upright)
        • Helps r/o perforation (free air) or intestinal obstruction
      • Abdominal sonogram identifies:
        • GB, CBD size, stones
      • CT scan
        • Size of pancreas
        • Extent of necrosis
        • Fluid collection
    • Prognosis: most recover within 48-72 hrs
      • Mortality average is about 10%
  • 54. Acute Pancreatitis
    • Treatment:
      • NPO
      • Nasogastric tube (rids acid)
      • IV fluids (electrolytes, calcium)
      • Parenteral analgesics (Demerol)
      • Antibiotics in severe biliary pancreatitis
      • Removal of stones from ampulla if needed.
      • High CHO, low fat & protein
  • 55. Pancreatitis: Treatment Mneumonic
    • MACHINES : M onitor vital signs A nalgesia/ A ntibiotics C alcium gluconate (if necessary) H 2 blockers I V access/ I V fluids N il by mouth E mpty gastric contents S urgery if required/ S enior review
  • 56. Acute pancreatitis
    • Complications of pancreatitis
      • 1. Pseudocysts
        • Due to necrosis of cells causing accumulation of blood, pancreatic juices, fat
        • Resolve spontaneously
      • 2. Pancreatic Abscess
        • Infected cysts
      • 3. Others
        • Fat necrosis
        • ARDS (respiratory distress syndrome)
        • Acute tubular necrosis
        • DIC, hemorrhage
        • Pancreatic insufficiency
  • 57. Acute Pancreatitis
    • Differential diagnosis
      • Acute cholecystitis
      • Biliary colic
      • Cholangitis
      • Peptic ulcer
      • Hepatitis
      • Intestinal obstruction
      • MI
      • Pneumonia
  • 58. Chronic Pancreatitis
    • Defined:
      • Episodes of acute inflammation in a previously injured pancreas
    • Causes:
      • Alcoholic abuse
      • Trauma
      • Pancreas divisum: failure of the ventral & dorsal pancreatic ducts to fuse
      • Most common cause in children is cystic fibrosis
  • 59.  
  • 60. Chronic Pancreatitis
    • Key Symptoms:
      • 1. Recurrent abdominal pain radiating to back, lasting hrs to days, precipitated by alcohol.
      • 2. Steatorrhea when 90% of pancreas is destroyed. Increase protein in diet without complications. Increased fat intake will cause further increase in diarrhea.
      • 3. CHO malabsorption is rare
      • 4. Vitamin B12 malabsorption: due to decreased secretion of trypsin. B12 combines with a R-protein in the stomach. If not cleaved by trypsin, it will not bind with IF. Then can not be absorbed in the terminal ileum
      • 5. Diabetes mellitus
  • 61. Chronic Pancreatitis
    • Key Sign:
      • Epigastric tenderness
    • Laboratory:
      • Blood tests not useful: serum amylase often normal ; amylase & lipase only ^ in acute states
      • Secretin test: to estimate the volume of fluid & bicarb.
      • Radiology tests:
        • Flat plate (AXR) may reveal calcifications
        • ERCP showing a dilated CBD
        • CT scan showing calcifications , pseudocysts, ductal abnormalities
  • 62.  
  • 63.  
  • 64. Chronic Pancreatitis
    • Treatment:
      • 1. pain relief:
        • No alcohol
        • Analgesics (narcotics- careful c addicts)
        • Pancreatic extracts
      • 2. Steatorrhea:
        • use of oral enzymes with meals, low fat diet, low protein, medium chain triglycerides.
      • Diabetes:
        • Calorie restriction
        • Small doses of insulin
  • 65. Pancreatic Carcinoma
    • Most common is Ductal carcinoma accounts for more than 90% of all pancreatic carcinomas. This is exocrine.
    • Most are adenocarcinoma of ampulla area = no cure
    • More frequent in males over 40 yo
    • Smoking increases incidence
    • Top ranked cancers:
      • Men Women
      • Lung breast
      • Colon colon
      • Prostate lung
      • Pancreas ovary
      • pancreas
  • 66. Pancreatic Carcinoma
    • Less common: Endocrine causes
      • 1. insulinoma
      • 2. gastrinoma
      • 3. glucagonoma
      • 4. somatostatinoma inhibits all islet cell fxn
      • 5. VIPoma (pancreatic polypeptide) causes severe diarrhea & hypokalemia (pancreatic diarrhea)
  • 67. Pancreatic Carcinoma
    • About 2/3 occur in the head & usually spreads to the contiguous structures
    • Symptoms:
      • Vague discomfort
      • More toward back
      • Worse on lying down
      • Weight loss
      • Jaundice is characteristic
      • Glucose intolerance can be an early sign
      • N/V weakness on occasion
      • Pruritis
      • Pain can be early if the tail is involved because of splanchnic nerve
      • Note: painless, non-pruritic, jaundice if head involved
      • but painful if tail is involved
  • 68. Pancreatic Carcinoma
    • Classic findings:
      • None in early stages
      • If common duct obstructed due to head tumor = jaundice & icterus
      • GB can be palpable (Courvoisier’s sign)
      • Ascites & peripheral edema may be a sign of portal hypertension
      • Superficial thrombophlebitis (Trousseau’s sign) occurs.
  • 69. Pancreatic Carcinoma
    • Laboratory Tests:
      • Routine tests in early stages normal
      • Alk phos & transaminases (AST/ALT) are slightly elevated
      • Ultrasound: the best in the initial diagnosis
      • CT scan is better at staging the tumor
      • Angiography (helpful if tumor is resectable)
        • Stages:
          • I. Confined to pancreas
          • II. Involving only the neighboring structures
          • III. Involving regional lymph nodes
          • IV. Metastatic to liver & distant spread
  • 70.  
  • 71. Pancreatic Carcinoma
    • Differential Diagnosis:
      • Chronic pancreatitis
      • Cholecystitis
      • Causes of jaundice: hepatitis
      • Irritable bowel syndrome
      • Carcinoma of duodenum
      • Common bile duct stones
      • Peptic ulcer disease
      • Depression
      • Ampulla carcinoma
      • Metastatic disease to the pancreas
  • 72. Pancreatic Carcinoma
    • Treatment:
      • Prognosis is poor, with no survivors to 5 yrs
      • 10-15% are resectable
      • If resectable 30% survive less than 2 yrs
      • Chemotherapy gives poor response
      • A whipple procedure for temporary relief
        • Includes removal of small portion of duodenum, distal stomach, GB, CBD, regional nodes, some jejunum & pancreas