Adv Pathophysiology Unit 9: GI Page 1 of 10

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1 Adv Pathophysiology Unit 9: GI Page 1 of 10 Learning objectives for this file: 1. Recognize positive physical and lab findings that point to the diagnosis 2. Appreciate the appearance of the affected organ on CT 3. Recognize abnormal findings on KUB from ileus 4. Recognize histological changes in inflammation 5. Review lab findings in jaundice and types of bilirubinemia 6. Review diagnostic GI lab tests

2 Adv Pathophysiology Unit 9: GI Page 2 of 10 CASE STUDY: a 73 YO MAN WITH SEVERE ABDOMINAL PAIN INITIAL PRESENTATION: (CC, HPI, FH/SH) This 73 yo WM is brought to your office by his family c/o severe abdominal pain. It began 2 days ago, with N&V, and has worsened over the past 2 days. Location of the pain is in the epigastrium, with some radiation to his back, but no radiation to the chest. No BM yesterday or today, appetite is gone. Denies fever, some "chills" last night and today. Denies recent weight loss or dark stools. No prior h/o PUD, gallstones. SH: nondrinker, nonsmoker. PMH: HTN and dyslipidemia, controlled with beta-blocker and statin drug. FH: noncontrib. PE: VS BP 115/85, P 92, RR 20, T 99 F. Positive findings: scleral icterus bilaterally, abdomen tender to superficial and deep palpation, positive rebound tenderness, bowel sounds diminished. Negative findings: Rectal exam with normal sphincter tone, nontender, guiaic neg stool (brown/yellow). INITIAL EVALUATION (WORKUP): CBC: W 13.7 (92% neut, 3% lymp, 5% mono). H/H & RBC wnl. Plt wnl. U/A: ph 5.0, sg 1.020, hazy, orange, bilirubin pos, glucose 1+, wbc 20/hpf (0-2). Chemistry: Elevated: o glucose 184 o LDH 450 ( ) o Alk Phos 238 (30-120) o GGTP 242 (0-50) o Total bili 3.7 (0-1.5) & direct bili 2.85 ( ). Special Chemistry: amylase 3429 (23-85), lipase 216 (4-24).

3 Adv Pathophysiology Unit 9: GI Page 3 of 10 Abdominal CT: diffusely enlarged pancreas with hazy outline due to inflammation (see arrows) consistent with acute pancreatitis. Normal Abdominal CT (note clear borders of organs) Pancreatitis: note fuzzy borders and enlarged size of organ (arrows)

4 Adv Pathophysiology Unit 9: GI Page 4 of 10 Flat plat Abdomen (Xray)(KUB): o this was done looking for free air to evaluate for perforated viscus o no opacifications seen in gallbladder area, no masses seen o bowel is more air-filled (report stated dilated small bowel with minor ileus )

5 Adv Pathophysiology Unit 9: GI Page 5 of 10 INITIAL PRESENTATION & EVALUATION: "Left shift" on CBC from bacterial infection (although left & right shift on CBC are not conclusive for bacterial vs. viral diagnosis) Elevated glucose is he diabetic? OR, is this stress hyperglycemia from counterregulatory hormone release Elevated LFTs suggest acute hepatic inflammation. o Increased bilirubin that is mostly direct bilirubin (conjugated) suggests normal liver function is preserved, but unable to excrete the conjugated bilirubin into the gut. o Suggests blockage of CBD such as from biliary disease (stones). o Urinary urobilinogen is negative (the bilirubin isn't reaching the bacteria in the gut to make it). Elevated serum amylase, lipase and positive CT make a diagnosis of acute pancreatitis. o Concern here are major fluid shifts, acid-base disorders, calcium-phosphorus metabolic derangements, and electrolyte abnormalities. o Even DIC, renal failure, shock and adult respiratory distress syndrome are concerns during the course of this disease. Ileus may result o bowel function slowed due to any inflammation in the abdominal organs o imaging showing dilated bowel o clinically, nausea & vomiting may result to to reverse peristalsis from distal blockage (poor distal bowel motility) Direct bilirubinemia & scleral icterus (jaundice) from hepatic obstruction (see below for discussion)

6 Adv Pathophysiology Unit 9: GI Page 6 of 10 CLINICAL COURSE: Management: monitoring electrolytes and fluid balance managing pain continue workup to determine etiology of acute pancreatitis. Workup: Abdominal Ultrasound: multiple gallstones (cholelithiasis). These are radiolucent. Appreciate where the gallbladder is located in relation to intestine & liver & pancreas. Ultrasound showing gallstones -- 85% of gallstones are radiolucent (not seen on plain Xrays) but can be seen using radar -- ultrasound!! SURGICAL TREATMENT: taken to the OR for cholecystectomy on day 6 of hospital stay (once stabilized) Uneventful recovery ensues. At the same time, biopsy of pancreas is obtained.

7 Adv Pathophysiology Unit 9: GI Page 7 of 10 CONTINUED CLINICAL COURSE & CLINICAL EVALUATION: Serial monitors: o CBC: WBC drops to 12.8 by day 6, then to 9.2 by day 12. o Chemistry: glucose back to normal by day 3, LFTS tending towards normal and only 1.5x normal by day 12, bilirubin drops to 0.6 by day 12 (direct 0.26). o Amylase and lipase are almost normal by day 12. Histology of pancreas biopsy: o fat necrosis, destruction of acinar cells, inflammatory infiltrate. o Consistent with acute pancreatitis. Note inflammatory cells (darker staining cells) and fat necrosis (large holes ) Appreciate the anatomy of the pancreas & gross relationship to other abdominal structures as well as parenchymal organization Histology of gallbladder resection: o thickening of gallbladder wall due to fibrosis and inflammation, with focal hemorrhage. Inflammatory cells are present. o Consistent with acute and chronic cholecystitis. Note again the darker staining cells that are inflammatory and the dilated ducts

8 Adv Pathophysiology Unit 9: GI Page 8 of 10 CLINICAL COURSE & REPEAT EVALUATION: Acute considerations are preparing patient for surgery Keeping vascular compartment expanded with fluid -- remember fluid shifts in the face of inflammation that allows fluid to leave the more permeable capillaries Monitoring urine output -- renal perfusion must be maintained to preserve the nephrons Monitoring lab markers for acute illness (LFTs, bilirubin, amylase/lipase). DDX includes the reasons for acute pancreatitis: o initial symptom suggestive of this is pain radiating to the back ( like a knife in my back like a knife going from my upper abdomen straight through to my back ) o Worry about cardiac causes of similar presentations -- abdominal pain can be angina o Etiology of acute pancreatitis is 80% from either alcohol or biliary tract disease in North America. o In those with gallstones, 5% will develop acute pancreatitis as a secondary complication o Not all gallstones are radio-opaque -- most are radiolucent (85%) Any GI condition resulting in inflammation can cause peritonitis: o abdominal tenderness o rebound tenderness o diminished bowel activity. Late complications of pancreatitis include pancreatic pseudocyst. (Pseudo because it is a cyst that is not lined by epithelial cells) Big hole -- pseudocyst Remember his scleral icterus and bilirubinemia? see below

9 Adv Pathophysiology Unit 9: GI Page 9 of 10 CHOLECYSTITIS FROM GALLSTONES (CHOLELITHIASIS): Cholecystitis can be ACUTE or CHRONIC Gallstones can form in the gallbladder AND in the bile ducts Complications: o obstruction of the gallbladder and resulting inflammation acute cholecystitis o obstruction of the liver jaundice (with direct hyperbilirubinemia) o obstruction of the pancreatic ducts acute pancreatitis o chronic cholecystitis and loss of gallbladder function o gallbladder neoplasm (cancer can develop due to chronic irritation??) Symptoms: o Pain (biliary colic) due to smooth muscle contraction on the actual stone o Pain from inflammation of accessory structures (gallbladder, bile ducts, pancreas) o May be asymptomatic for years and only cause symptoms when stones migrate or cause obstruction Types of stones: o Most are cholesterol stones due to an imbalance of cholesterol and bile salts o Other types of stones are calcium, pigment, and bilirubin gallstones Risk factors for development: o Female gender and estrogen hormone and pregnancy o DM (see stones at an early age, and a white gallbladder) o Large amount of weight lost suddenly (e.g. crash diets) due to cholestasis (gallbladder function is not normal due to lack of stimulation by fats in diet) o Hereditary disposition o Obesity o Advancing age o Hepatic cirrhosis o The uncommon types of stones may result from hemolytic anemias, portal hypertension, and bacterial colonization of the bile ducts Management: o For symptomatic, calcified stones cholecystectomy o For prevention ursodeoxycholic acid to have a detergent action on the cholesterol stones to dissolve them o For treatment of radiolucent (non-calcified) stones ursodeoxycholic acid (to dissolve the stones) o Lithotripsy (ultrasound applied to the body to break down the stones) ACALCULUS CHOLECYSTITIS: (without stones) sometimes there are NOT any gallstones yet cholecystitis occurs and is sometimes hard to diagnose usually sudden severe upper abdominal pain may include gangrene & rupture of the gallbladder

10 Adv Pathophysiology Unit 9: GI Page 10 of 10 JAUNDICE & BILIRUBINEMIA: enormously simplistic way MANY clinicians think of this situation Pre-hepatic, such as hemolytic anemia: increased total bili and unconjugated bilirubin liver is healthy, there is some other process causing the problem excretion of bilirubin to intestine creates more urobilinogen, urine may have more urobilinogen Hepatic, such as any intrinsic liver disease (hepatitis, even heart failure): increase in total bilirubin (mostly unconjugated) diseased liver is unable to reabsorb urobilinogen from the entero-hepatic circulation urobilinogen stays in the portal blood systemic blood kidneys urine urobilinogen Post-hepatic (obstructive): increased total bili & conjugated bilirubin conditions such as cholelithiasis, pancreatic neoplasm ( painless jaundice ) urobilinogen amounts decrease, and urinary urobilinogen amounts decrease in urine bilirubin increases in urine (conjugated bilirubin into systemic bloodstream) LAB PEARLS: AMYLASE AND LIPASE Increased amylase: amylase rises in other conditions (than pancreatitis) These include PID ruptured ectopic pregnancy (the inflamed fallopian tubes make amylase) appendicitis viral hepatitis diabetic ketoacidosis (DKA) mumps dissecting aortic aneurysm cancer of lung and ovary. Decreased amylase: late pregnancy pleurisy HF chronic pancreatitis. Lipase: very specific marker for pancreatitis. Always order the two tests together to narrow down your diagnosis If both are elevated, you are almost 100% sure it is from acute pancreatitis CASE STUDY IN CHOLECYSTITIS: