Pancreas Pathology Flashcards
Pancreatitis
Pancreas inflammation
Types of pancreatitis
Acute pancreatitis
Acute hemorrhagic pancreatitis
Chronic pancreatitis
Presentation of acute pancreatitis
Enzymatic necrosis and inflammation of pancreas with abdominal pain
Acute pancreatitis biochemistry
Raised level of pancreatic enzymes, amylase and lipase in urine and in blood
Is acute pancreatitis mild and self limiting ?
Yes
Pancreas gross morphology In acute pancreatitis
Edema
Inflammation
Limited tissue necrosis
Acute hemorrhagic pancreatitis
Around pancreas :
Extensive necrosis and hemorrhage
Extensive fat necrosis
In tissue cells :
Fat deposits with hemorrhage
Acute hemorrhagic pancreatitis incidence
5% of cases
What population has acute pancreatitis associated with alcoholism
Middle aged man (6:1)
What population has acute pancreatitis associated with biliary dx
Middle aged Female (3:1)
Etiology of acute pancreatitis
Cholelithiasis (30-35%) Alcoholism (60-65%) Abdominal procedures Infections (mumps, cocksackie,mycoplasma, ascaris, clonorchis sinensis) Vasculitiz Ischemia Trauma Drugs (thiazides diuretics) Hereditary hyperlipidemias Hypercalcemia Uremia Hemochromatosis Idiopathic
Pathogenesis of acute pancreatitis
Enzymes released from pancreatic acinar
Enzymes cause Proteolysis, lipolysis, hemorrhage
Lipids digested by trypsin, chimotrypsin, lipase, phospholipase etc
Vessel walls destroyed by elastase
3 hypothesis of release of enzymes in acute pancreatitis
1st
Direct obstruction by stone -> rupture of ductules ->release of enzymes
Obstruction could be caused by alcohol
2nd
Acinar cell injury by direct effect, (alcohol, viruses, trauma, shock)
3rd
Deranged intracellular transport of pancreatic enzymes
Acute pancreatitis morphology
Proteolytic destruction of pancreatic substance
Necrosis of blood vessels
May have Hemorrhage
Necrosis of fat
Early Inflammation (edema)
Late inflammation (edema, necrosis, neutrophil infiltration, hemorrhage, focal fat necrosis, amorphous basophilic deposits of calcium)
Hemorrhagic pancreatitis morphology
Blue black hemorrhage
Grey white necrosis
Chalky white areas of fat necrosis
Clinical presentation of acute pancreatitis
Abdominal pain (epigastric, constant, severe, radiating to the back)
Elevation of serum amylase (24h) and lipase (72-96h)
Leucocytosis
Hemolysis
DIC
ARDS
diffuse fat necrosis
Shock ( bradykinin, pgs, pancreatic cardiac depressant agents released. Vasodilation. )
ARF
Glycosuria
Hypocalcemia
Differential of serum amylase and lipase to test before
Ruptured appendicitis
Perforated duodenal ulcer
Acute cholecystitis
Mesenteric vein thrombosis with bowel infarction
X ray of acute pancreatitis
Large pancreas shadow
Prognosis of acute pancreatitis
5% die from shock
Complications of acute pancreatitis
Shock ARDS ARF (acute renal failure) Abscess Pseudocyst Duodenal obstruction from inflammation of pancreas
Chronic pancreatitis
Chronic relapsing inflammation of pancreas
Leading to progressive destruction of pancreas
Repeated flare ups of silent or mildly symptomatic pancreatitis
Patient at risk of chronic pancreatitis
Middle age
Male over female
Alcoholics
Biliary disease
Causes of chronic pancreatitis
Alcoholism Biliary disease Hypercalcemia Hyperlipidemia Familial Idiopathic (40%)
Chronic pancreatitis pathogenesis
Ductal obstruction by concretions (alcohol induced abnormal secretion)
Interstitial fat necrosis and hemorrhage -> fibrosis, duct distortion, altered pancreatic secretions, flow
PCM (protein calorie malnutrition) especially