Pancreatitis, chronic 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. 

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... 

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 ... 

Patients with alcoholic CP usually present with an initial acute attack followed by successive attacks that are slower to resolve. Continued alcohol use leads to chronic abdominal pain and progressive exocrine and endocrine insufficiency. In about 50% of patients, the pain diminishes 5 to 10 years after the onset of symptoms. Steatorrhea, calcification, and diabetes usually develop after 10 to 20 years of heavy ethanol ingestion. Most patients present with varying degrees of pain, malnutrition, and glucose intolerance. The mortality rate of CP is approximately 50% within 20 to 25 years of the diagnosis. About 15% to 20% actually die of complications associated with acute attacks. Most deaths occur as a consequence of malnutrition, infection, or ethanol, narcotic, and tobacco nse. The clinical course of idiopathic CP is more favorable than that of alcoholic pancreatitis. ... 

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