Pancreatitis clinical presentation

Differentiating an episode of acute pancreatitis from chronic pancreatitis maybe difficult because the clinical presentations can be similar. The diagnosis of chronic pancreatitis is made by looking for the effects of chronic pancreatic inflammation and scarring on the pancreas and the patient as a whole. Computed tomography or ERCP will allow visualization of chronic calcified lesions in the pancreas when present.37... 

Pathogenesis of Type 1 Diabetes Mellitus Type 1 diabetes mellitus results from a cellular-mediated autoimmune destruction of the insuhn-secreting cells of pancreatic p-cells. In the vast majority of patients, the destruction is mediated by T cells. This is termed type lA or immune-mediated diabetes (Box 25-2). The a-, 8-, and other islet cells are preserved. The islet cells have a chronic mononuclear cell infiltrate, called insulitis. The autoimmune process leading to type 1 diabetes begins months or years before the clinical presentation, and an 80% to 90% reduction in the volume of the j3-cells is required to induce symptomatic type 1 diabetes. The rate of islet cell destruction is variable and is usually more rapid in children than in adults. 

Although this disorder is not usually expressed in childhood, several affected preadolescents have been described. Clinical presentations in adult patients include eruptive xanthomas, lipemia retinalis, pancreatitis, and abnormal glucose tolerance with hyperinsulinism. Premature atherosclerotic complications are not as commonly seen as with FH. This heterogeneous syndrome appears to be inherited in an autosomal dominant mode, but its genetic basis is yet to be elucidated. 

The clinical presentation of CP varies depending on the etiology of the disease, the severity of the inflammatory process, and the extent of irreversible damage to the pancreas (Table 39-6). " The classic features of CP are abdominal pain, malabsorption, weight loss, and diabetes. Most alcoholic patients have chronic pain, while others have intermittent attacks or painless pancreatitis. Abstinence from ethanol may provide relief from pain, but does not prevent exocrine... 

The clinical presentation of patients with endocrine pancreatic tumors will vary according to the type of hormone released. Hyperinsulinism manifested with diarrhea, abdominal pain, and low levels of glucose will be found in the majority of patients. Nesidioblastosis is a primitive pancreatic B cells hyperplasia. Approximately 5% of patients with hyperinsulinism may have this type of tumor. Hunger, jitteriness, lethargy, apnea, and seizures are common manifestations in newborns with nesidioblastosis, while older children may show diaphoresis, confusion, or unusual behavior. Zollinger-Elli-son syndrome will present with intractable peptic ulcers. Patients with vipomas will have watery diarrhea, hypokalemia, and achlorhydria, while multiple endocrine neoplasias have been reported with multiple endocrine neoplasia type 1 (MEN 1). 

Kaiser MH, Barkin J, MacIntyre JM (1985) Pancreatic cancer. Assessment of prognosis by clinical presentation. Cancer 56 397-402... 

Amylase enters the blood largely via the lymphatics. An increase in hydrostatic pressure in the pancreatic ducts leads to a fairly prompt rise in the amylase concentration of the blood. Neither an increase in volume flow of pancreatic juice nor stimulation of pancreatic enzyme production will cause an increase in senm enzyme concentration. Elevation of intraductal pressure is the important determinant. Stimulation of flow in the face of obstruction can, however, augment the entry of amylase into the blood, as can disruption of acinar cells and ducts. A functional pancreas must be present for the serum amylase to rise. Serum amylase determination is indicated in acute pancreatitis in patients with acute abdominal pain where the clinical findings are not typical of other diseases such as appendicitis, cholecystitis, peptic ulcer, vascular disease or intestinal obstruction. In acute pancreatitis, the serum amylase starts to rise within a few hours simultaneously with the onset of symptoms and remains elevated for 2 to 3 days after which it returns to normal. The peak level is reached within 24 hours. Absence of increase in serum amylase in first 24 hours after the onset of symptoms is evidence against a diagnosis of acute pancreatitis (76). 

As previously discussed, food effects are an important parameter for enteric-coated systems, especially for drugs, that are sensitive to food. Pancreatic enzyme-containing products fail when they come in contact too early with lipids, proteins, and carbohydrates present in food. The clinical efficacy of pancreatic enzymes formulated as enteric-coated tablets was investigated in man and dog [44], The enteric materials examined were hydroxypropyl methylcellulose phthal-ate (HPMCP), cellulose acetate phthalate (CAP), and the methacrylic acid copolymer USP/NF Type C. In vivo behavior monitored by x-ray scintigraphy showed clear differences between the three coating formulations. HPMCP-coated products adhered to the gastric mucosa, whereas CAP and methacrylate copolymer... 

In this charter, wc will focus on the present insights into the structure-activity relationship and the clinical situation of this enzyme without attempting to iiuaiuic U relevant studies. For reviews on the biochemistry up to l9W, largely refer to the work of M. Laskowsfci [1], who was closely Involved in early studies on DNase I, and of S. Moore [9]. Moore shared with W. Stein Nobel Prize in Chemistry in 1972 fra their work on the chemical structures of pancreatic ribanudesae and deoxyribonuclease [ID]. 

Steatorrhea, the clinical result of insufficient intraluminal lipid hydrolysis, is the most important digestive malfunction in pancreatic exocrine insufficiency. As a rule, concomitant malabsorption of the lipid-soluble vitamins A, D, E, and K must be suspected in these patients. Naturally, potential differential diagnoses have to be considered in patients who present with steatorrhea (Table 26-1). The pivotal role of fat malabsorption in chronic pancreatitis is due to several interacting mechanisms ... 

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