pancreatic disease

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Pancreatic Disorders:

Pancreatic Disorders

Etiologies:

Etiologies Alcohol abuse Biliary tract diseases Drugs Trauma Viral infections Metabolic disorders Connective tissue diseases

Etiologies:

Etiologies Idiopathic in 30% of acute pancreatitis 25 – 40% of chronic pancreatitis

Clinical Features:

Clinical Features Severe constant epigastric pain  back Elevated serum Amylase, Lipase levels Ascites, pleural effusion Hypercalcemia, hypocalcemia Hypertriglyceridemia (Serum amylase maybe normal) Chronic pancreatitis: Normal enzyme levels

Laboratory Exams:

Laboratory Exams Serum Amylase: rises within 24 hrs; remains elevated 1-3 days; 3x ULN; 85% of patients will have elevated amylase levels Amylase also found in salivary glands, liver, small intestines, kidneys and fallopian tubes Amylase elevated in CA of lungs, esophagus, breast, and ovary Lipase: single best enzyme

Radiologic Tests:

Radiologic Tests Plain radiography: 1. sentinel loop (localized ileus of jejunum) 2. air fluid levels 3. colon cut off sign (distension of transverse colon) 4. duodenal distension 5. mass (pseudocyst)

Radiologic Tests:

Radiologic Tests UGIS: widened C loop Ultrasonography: edema, inflammation, calcifications, cysts, mass lesions CT Scan EUS (Endoscopic Ultrasound) MRCP ERCP

Acute Pancreatitis:

Acute Pancreatitis Interstitial: mild and self-limiting Necrotizing: degree of necrosis correlates with the severity of clinical manifestations

Etiologies:

Etiologies Gallstones: 30-60% Alcohol: 15-30% Others

Pathogenesis:

Pathogenesis Initial Phase: Intrapancreatic digestive enzyme activation andacina cell injury Second phase: activation, chemoattraction, sequestration of neutrophils  intrapancreatic inflammation Third phase: due to the effects on the distant organs of activated proteolytic enzymes and cytokines  proteolysis, edema, insterstitial hemorrhage, vasgular damage, coag necrosis

Pathogenesis…cont:

Pathogenesis…cont Cellular necrosis  liberation of bradykinin, histamine and vasoactive substances  vasodilation, increased vascular permeability and edema  lungs (ARDS , SIRS), multiorgan failure

Clinical Features:

Clinical Features Pain: constant, severe, boring; epigastrium  back, chest, flanks: supine and relieved by trunk flexing and knees drawn up. Nausea, vomiting, abdominal distention Fever, tachycardia, hypotension Hypovolemia; shock Cullen’s sign Turner’s sign

Laboratory Exams:

Laboratory Exams Amylase: 3x ULN; return to N in 72 hrs; higher in gall stones Lipase: elevated for 7-14 days; higher in alcohol-related Leukocytosis Hyperglycemia Hypocalcemia Hyperbilirubinemia

Lab Exams….cont:

Lab Exams….cont Hypertriglyceridemia LDH, AST Alkaline phosphatase Hypoxemia

Treatment:

Treatment Self-limited in 85-90% Conventional measures: IV fluids, analgesics, colloids, no oral alimentation Role of antibiotics – controversial Somatostatin, H2 blockers, glucagon, steroids Resumption of feeding: decrease/resolution of pain, resolution of organ dysfunction, patient feels hungry

Chronic Pancreatitis:

Chronic Pancreatitis Chronic inflammation, fibrosis, progressive destruction of exocrine, and later endocrine function Complications: chronic pain, steatorrhea, DM

Etiologies:

Etiologies Alcohol: as little as <50g/d prolonged consumption Idiopathic: 15% genetic defects Clinical Features: 1. pain – related to food intake 2. maldigestion – diarrhea, steatorrhea, weight loss

Diagnostic Tests:

Diagnostic Tests Amylase and Lipase not usually elevated Secretin test: best sensitivity/specificity; abN when 60% of exocrine function is lost Radiography: calcifications Ultrasonography CT scans MRCP ERCP

Treatment:

Treatment Enzyme therapy to control diarrhea Octreotide – somatostatin analogue that inhibits pancreatic secretion; decrease pain in large-duct disease Endoscopic treatment: sphincterotomy, stenting, stone extraction, drainage of pseudocyst

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