1. Pancreas
It had both endocrine( like insulin and glucagon secretions) and exocrine fuction. The principal inorganic components of exocrine pancreatic secretions are water, sodium, potassium, chloride, and bicarbonate. The purposes of the water and ion secretions are to deliver digestive enzymes to the intestinal lumen and to help neutralize gastric acid emptied into the duodenum. Pancreatic juice secreted during stimulation with secretin is clear, colorless, alkaline, and isotonic with plasma. The human pancreas has a large capacity for synthesizing protein (mostly digestive enzymes). Enzymes that could digest the pancreas are stored in the pancreas and secreted into the pancreatic duct as inactive precursor forms. activation of these enzymes takes place in the intestinal lumen, where a brush-border glycoprotein peptidase, enterokinase, activates trypsinogen . The active form, trypsin, then catalyzes the activation of the other inactive proenzymes( e.g. amylase and lipase).

2. Acute pancreatitis
Acute pancreatitis is best defined clinically by a patient presenting with two of the following criteria: (1) symptoms, such as epigastric pain, consistent with the disease; (2) a serum amylase or lipase greater than three times the upper limit of normal; or (3) radiologic imaging consistent with the diagnosis, usually using computed tomograph.y (CT) or magnetic resonance imaging (MRI).
Once the diagnosis is established, patients are classified as having mild or severe pancreatitis. Mild acute pancreatitis consists of interstitial (edematous) pancreatitis on imaging, minimal or no extrapancreatic organ dysfunction, and typically an uneventful recovery. Severe pancreatitis manifests as organ failure or local complications such as necrosis, abscess, or pseudocyst.
PREDISPOSING CONDITIONS :Many conditions predispose to acute pancreatitis to varying degrees . This list will undoubtedly continue to grow, and the number of cases diagnosed as “idiopathic” will decrease as our understanding of the disease improves. Gallstones and chronic alcohol abuse account for 70% of acute pancreatitis.other causes are metabolic( like hypertriglyceridemia and hypercacemia), traumatic , vascular and infectious.
CLINICAL FEATURES:Abdominal pain is present at the onset of most attacks of acute pancreatitis. Ninety percent of patients have nausea and vomiting. Abdominal tenderness may be present. Additional abdominal findings may include ecchymosis in one or both flanks (Grey Turner's sign) or about the periumbilical area (Cullen's sign), owing to extravasation of hemorrhagic pancreatic exudate to these areas. These signs occur in less than 1% of cases and are associated with a poor prognosis. A palpable epigastric mass may appear during the disease from a pseudocyst or a large inflammatory mass.

3. LABORATORY DIAGNOSIS :
PANCREATIC ENZYMES :In general, the diagnosis of acute pancreatitis relies on at least a three-fold elevation of amylase or lipase in the blood.lipase is more specific and durable than amylase.
STANDARD BLOOD TESTS :The white blood cell count frequently is elevated, often markedly so in severe pancreatitis. The blood glucose also may be high and associated with high levels of serum glucagon. Serum aspartate transaminase (AST), alanine aminotransferase (ALT), alkaline phosphatase, and bilirubin also may increase, particularly in gallstone pancreatitis.
DIAGNOSTIC IMAGING
ABDOMINAL PLAIN FILM :Findings on a plain radiograph range from no abnormalities in mild disease to localized ileus of a segment of small intestine (“sentinel loop”) or the colon cut-off sign in more severe disease. In addition, an abdominal plain film helps exclude other causes of abdominal pain, such as bowel obstruction and perforation.
ABDOMINAL ULTRASONOGRAPHY :Abdominal ultrasonography is used during the first 24 hours of hospitalization to search for gallstones, dilation of the bile duct due to choledocholithiasis, and ascites. If the pancreas is seen (bowel gas obscures the pancreas 25% to 35% of the time), it is usually diffusely enlarged and hypoechoic.
COMPUTED TOMOGRAPHY :CT is the most important imaging test for the diagnosis of acute pancreatitis and its intra-abdominal complications. It can detect pancreatic enlargement , necrosis,gas,pseudocyst and abscess.

4. PREDICTORS OF SEVERITY:Initially at presentation and over the first 48 hours, patients should be classified temporarily as having severe acute pancreatitis (and managed as such initially) based on the presence of SIRS or organ failure. SIRS is defined by two or more of the following four criteria: pulse greater than 90 beats/minute; rectal temperature less than 36?C or more than 38?C; white blood count less than 4000 or more than 12,000/mm3; and respirations greater than 20/minute or Pco2 less than 32 mm Hg. The presence of SIRS at admission and persistence of SIRS to 48 hours increases the morbidity and mortality rate. Ranson's criteria include 11 signs that had prognostic significance during the first 48 hours. Higher Ranson's scores predict more severe disease. In mild pancreatitis (scores < 2), the mortality is 2.5% and in severe pancreatitis (scores > 3) the mortality is 62%. Also, the higher the Ranson's score the higher the incidence of systemic complications, necrosis, and infected necrosis.
RX:
1-FLUID RESUSCITATION
2-RESPIRATORY CARE (Hypoxemia (oxygen saturation <90%) requires supplemental oxygen, ideally by nasal prongs or by face mask if needed)
3-CARDIOVASCULAR CARE(If hypotension persists even with appropriate fluid resuscitation, intravenous dopamine may help maintain the systemic blood pressure)
4-RX of METABOLIC COMPLICATIONS
5-ANTIBIOTICS :Antibiotics are not indicated in mild pancreatitis. However, pancreatic sepsis (infected necrosis and, less often, abscess) and nonpancreatic sepsis (line sepsis, urosepsis, or pneumonia) are major sources of morbidity and mortality in severe acute pancreatitis. Thus, it would seem logical to consider antibiotic prophylaxis to improve the outcome.
6- NUTRITIONAL: In general, intravenous feedings are continued until patients are able to tolerate liquids or solids.

5. 4-Abscess 5-Gastrointestinal bleeding
LOCAL COMPLICATIONS:
1-Pseudocyst
2-Sterile necrosis
3-Infected necrosis
4-Abscess 5-Gastrointestinal bleeding
SYSTEMIC COMPLICATIONS:
1-Respiratory failure 2-Renal failure 3-Shock
4-Hyperglycemia 5-Hypocalcemia
6-Disseminated intravascular coagulation
7-Fat necrosis (subcutaneous nodules)

6. PSEUDOCYST :
A pseudocyst may occur secondary to acute pancreatitis, pancreatic trauma, or chronic pancreatitis. It usually contains a high concentration of pancreatic enzymes and variable amounts of tissue debris. Most are sterile. Regardless of size, an asymptomatic pseudocyst does not require treatment. It is satisfactory to monitor the pseudocyst with abdominal ultrasonography. Pseudocysts can be complicated by infection, intracystic hemorrhage , or rupture leading to pancreatic ascites. Further, pseudocysts can migrate into the chest or other unusual locations. In patients with known pseudocysts, new symptoms, such as abdominal pain, chills, or fever, should alert the clinician to the emergence of an infected pseudocyst or abscess. Treatment choices include surgical, radiologic, and endoscopic drainage.

7. Chronic Pancreatitis
The traditional definition of chronic pancreatitis has been permanent and irreversible damage to the pancreas, with histologic evidence of chronic inflammation, fibrosis, and destruction of exocrine (acinar cell) and endocrine (islets of Langerhans) tissue. In Western countries, alcohol is the cause of at least 70% of all cases of chronic pancreatitis.
CLINICAL FEATURES
1-ABDOMINAL PAIN :Abdominal pain is the most common clinical problem in patients with chronic pancreatitis, and the symptom that most detracts from quality of life. Severe pain decreases appetite and limits food consumption, contributing to weight loss and malnutrition. Chronic severe pain leads to a dramatic reduction in quality of life.
2-STEATORRHEA :The human pancreas has substantial exocrine reserve. Steatorrhea does not occur until pancreatic lipase secretion is reduced to less than 10% of the maximum output.[152] Steatorrhea is therefore a feature of far-advanced chronic pancreatitis.
3-DIABETES MELLITUS :Like exocrine insufficiency, endocrine insufficiency is a consequence of long-standing chronic pancreatitis. Diabetes mellitus appears to be nearly as common as steatorrhea in patients with far-advanced chronic pancreatitis.

8. TESTS OF PANCREATIC FUNCTION:
1-Serum Trypsinogen: Serum trypsinogen (often called serum trypsin) can be measured in blood and provides a rough estimation of pancreatic function. Very low levels of serum trypsinogen (<20 ng/mL) can be seen in patients with advanced chronic pancreatitis with steatorrhea.
2-Pancreatic Enzymes in Stool :Low concentrations of chymotrypsin or elastase in stool can reflect inadequate delivery of these pancreatic enzymes to the duodenum.
3-Fecal Fat Excretion :Maldigestion of fat occurs after 90% of pancreatic lipase secretory capacity is lost. The simplest evaluation of pancreatic lipase action is the measurement of fecal fat excretion during a 72-hour collection of stool. In health, less than 7 g of fat (7% of the ingested dose) should be present in stool.
TESTS OF PANCREATIC STRUCTURE (IMAGING)
1-Plain Abdominal Radiography :The finding of diffuse (but not focal) pancreatic calcifications on plain abdominal films is quite specific for chronic pancreatitis.
2-Endoscopic Ultrasonography :EUS allows a highly detailed examination of pancreatic parenchyma and the pancreatic duct by overcoming the imaging problems in transabdominal ultrasonography (such as intervening gas in the bowel lumen). The diagnosis of chronic pancreatitis on EUS is based on the presence of abnormalities in the pancreatic duct and the parenchyma .
3-Computed Tomography and Magnetic Resonance Imaging.

9. Simply to DX chronic pancreatitis , 2 OUT OF 3 :
1- chronic abdominal pain.
2- chronic exocrine (diarrhea, steatorrhea, weight loss) or endocrine insufficiency (diabetes mellitus).
3- pancreatic calcification on radiology.
RX :
1- Analgesics
2-Pancreatic Enzyme Therapy
3-management of DIABETES MELLITUS :Some patients show response to the use of an oral hypoglycemic, such as a sulfonylurea, a thiazolidinedione, or metformin. Insulin is often needed, however, and patients with chronic pancreatitis tend to have lower insulin requirements than patients with type 1 diabetes mellitus.