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Gi Gallbladder & Pancreas
 

Gi Gallbladder & Pancreas

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    Gi Gallbladder & Pancreas Gi Gallbladder & Pancreas Presentation Transcript

    • Pascale Gehy-Andre PA-C Diseases of Gallbladder & Bile Ducts
    • 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.
    • Biliary Anatomy
      • Hepatocytes  canaliculi  biliary ductules 
      • L & R hepatic ducts  common hepatic duct
      • Common hepatic ducts & Cystic Duct  Common Bile Duct (CBD)
    • 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
    • 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.
    • 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.
    • 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.
    • 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
    • GallStones (Cholelithiasis)
      • 2. Stone type (cont):
        • B. pigment 30%
          • (calcium bilirubinate)
          • Mostly bilirubin
          • Hemolytic states, cirrhosis & elderly
      • 3. Mixed
    • 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
    • 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
    • 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
    • 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
    • Complications of Cholelithiasis (Gallstones)
      • Colic
      • Acute cholecystitis
      • Cholangitis
      • Perforation
      • Fistulization
      • Gallstone ileus
    • 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
    • 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)
    • 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
    • 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)
    • 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
    •  
    • Acute Cholecystitis (cont)
      • Treatment:
        • IV fluids
        • Antibiotics
        • Analgesics
          • ( No morphine- theories of sphincter of Oddi spasm)
        • Cholecystectomy
          • Open vs. laparoscopic surgery
    • Acute Cholecystitis (cont)
      • Complications:
        • Perforation
        • GB ileus
        • Biliary colic
        • Biliary Dyskinesia
        • Choledocholithiasis
        • Chronic Cholecystitis
        • Tumors of GB
    • 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
    • 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)
    • Cholangitis
      • inflammation of CBD
      • Charcot’sTriad:
            • RUQ pain (biliary pain)
            • Jaundice
            • Fever
    • 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
    • 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
    • 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
    • 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
    • Pancreas
      • Anatomy
        • Head: embraces the duodenal curve
        • Body: crosses the vertebral column
        • Tail: in the hilum of the spleen
    •  
    •  
    •  
    • 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.
    • 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
    • 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
    • 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.
    • 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
    • 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.
    •  
    •  
    •  
    •  
    • Acute Pancreatitis
      • Symptoms:
        • Epigastric pain severe, boring in nature
        • Radiation to back
        • Nausea & vomiting
        • Aggravated by eating
        • Feels better leaning forward
        • Possible + peritoneal signs
    • 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
    • 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
    • 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)
    • 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)
    • 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%
    •  
    • 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
    • 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
    • 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%
    • 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
    • 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
    • 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
    • Acute Pancreatitis
      • Differential diagnosis
        • Acute cholecystitis
        • Biliary colic
        • Cholangitis
        • Peptic ulcer
        • Hepatitis
        • Intestinal obstruction
        • MI
        • Pneumonia
    • 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
    •  
    • 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
    • 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
    •  
    •  
    • 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
    • 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
    • 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)
    • 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
    • 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.
    • 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
    •  
    • 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
    • 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