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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetic ketoacidosis (DKA) is the commonest endocrine emergency encountered in clinical practice. Although in the last 3 decades the average worldwide immediate mortality has decreased from 10% to 5%, survival has not improved strikingly. The pathogenesis of DKA is currently attributed to a combination of two hormonal abnormalities--a relative insulin insufficiency and stress hormone excess (glucagon, catecholamines, cortisol and growth hormone). Withdrawal of exogenous insulin, pancreatic beta cell failure and insulin resistance are factors leading to relative insulin insufficiency. Factors leading to stress hormone excess include fasting, stress and dehydration. The combination of these two hormonal abnormalities leads to impaired carbohydrate utilization and ketonaemia which in turn results in metabolic acidosis with loss of water through acidotic breaths, rise in plasma lipids, hyperglycaemia and glycosuria leading to osmotic diuresis and further loss of water, excretion of partly neutralised ketoacids via the kidney with loss of cations (Na+ and K+). A net increase in protein catabolism which leads to an increased amino acid flux from muscle and an enhanced load of gluconeogenic precursor to the liver and a rise in blood pyruvate and lactate concentration. The prevention of either of these hormonal abnormalities will prevent the development of DKA. The successful outcome in the treatment of DKA is clearly related to the prompt recognition of the diagnosis and the precipitation factors, the severity of the initial metabolic derangements, the judicious use of fluid and electrolyte replacement, the choice, route and dosage of the insulin therapy and above all the close monitoring and meticulous clinical care of the patient throughout the entire course of the treatment. Current acceptable treatment of DKA include the following: adequate fluid replacement: low dose insulin therapy at frequent intervals; adequate potassium replacement from time of first insulin therapy with ECG monitoring; bicarbonate replacement if pH less than 7.1; broad spectrum antibiotics if infections is suspected and other supportive measures. The role of phosphate and magnesium replacement is still controversial. An awareness of the complications during the treatment of DKA including cerebral edema (paradoxical acidosis), altered central nervous system oxygenation, vascular thrombosis, shock, myocardial infarction, pancreatitis, infection, inhalation of vomitus , overhydration, underhydration , hypoglycaemia, hyperkalemia and hypokalemia all certainly help improve the morbidity and mortality of DKA.
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PMID:Current concepts of the pathogenesis and management of diabetic ketoacidosis (DKA). 633 Dec 71

The aetiology of acute pancreatitis in dogs is rather obscure. Although experimental studies may reveal a number of causative factors, an aetiological diagnosis is rarely established in 'spontaneous' pancreatitis. The pathogenesis and pathophysiology are reviewed. Activated trypsin plays a leading role in the injury to the pancreas, the ischaemia of the tissues and the disseminated intravascular coagulation. Vomiting, abdominal pain and general malaise are prominent features in the externally perceptible symptoms. Examination of the blood is of importance both in establishing the diagnosis and in determining the course of the disease. Great caution is indicated in setting store by individual results of haematological studies. There is neither a biochemical nor a haematological method of estimation today, by which acute haemorrhagic necrotic pancreatitis can be shown to be present or ruled out with one hundred per cent certainty. Treatment of the disease is mainly symptomatic. Complete withdrawal of food and water is the most important factor. Intravenous fluid therapy, anti-emetics, analgesics and possibly antibiotics are the main adjuncts to treatment. The prognosis will largely depend on the stage of the disease and the extent to which complications have occurred at the time.
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PMID:[Acute pancreatitis in dogs. A literature study]. 636 36

The computed tomographic (CT) findings in 13 consecutive patients with proven gastric varices were analyzed and correlated with the radiographic, angiographic, and gastroscopic evaluations. In 11 patients, CT clearly identified large (five) or smaller (six) varices located mainly along the posteromedial wall of the gastric fundus and proximal body of the stomach. Well defined rounded or tubular densities that enhanced during intravenous administration of contrast material and could not be distinguished from the gastric wall were identified. Dense, enhancing, round or tubular, intraluminal filling defects were seen in the cases where the stomach was distended with water. In two patients, the CT diagnosis of gastric varices could not be confidently made. All patients had associated intraabdominal collateral circulation, situated medial to the stomach within the lesser omentum, along the distribution of the coronary venous system. In seven patients, the CT examination correctly diagnosed the pathogenesis of gastric varices by identifying hepatic cirrhosis, calcific pancreatitis, and carcinoma of the pancreas.
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PMID:Computed tomographic recognition of gastric varices. 660 94

We investigated changes of alveolar stability and phospholipids in the pulmonary surfactant in case of acute pancreatitis induced in rats. Alveolar stability was examined by recording the pressure-volume relationship. The lung volumes during deflation decreased significantly at equivalent transpulmonary pressures, particularly when the pressure was lower than 6 cm H2O. Bubble stability ratio and surface tension indicated that the surface activity of the pulmonary surfactant did decrease in the rats with acute pancreatitis. The alveolar phospholipid content decreased, and the lecithin fraction also decreased significantly, as compared to the control groups. The metabolism of alveolar lecithin was examined following intravenous administration of 14C-labeled palmitate. The biological half-life of the radioactivity of alveolar lecithin was approximately 6 hours in the pancreatitis group, 12 hours in the hepatic ducts ligated group and 14 hours in the simple laparotomy group. The degradation of alveolar lecithin, as well as its synthesis, was accelerated in the rats with acute pancreatitis. However, a decrease in alveolar phospholipid, mainly in lecithin fraction, indicated that the synthesis was inadequate to maintain normal levels and the impairment in pulmonary surfactant may result in a respiratory insufficiency.
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PMID:Changes of alveolar stability and phospholipids in pulmonary surfactant in acute pancreatitis. 668 35

Biliary tract disease is a major cause of acute pancreatitis. However, with traditionally employed Telepaque, radiographic visualization of the gallbladder during acute pancreatitis remains unreliable, even in patients with apparently normal gallbladders. Therefore, oral cholecystography has customarily been deferred for such patients for several weeks. Recently, successful oral cholecystography has been described during the acute episode of pancreatitis, using Bilopaque, a more water-soluble cholecystopaque. The relative intestinal absorption of Telepaque and Bilopaque and the ability of these agents to produce diagnostic oral cholecystograms of fasting patients with acute alcoholic pancreatitis were compared. Forty-five hospitalized patients were studied within 96 hours of admission. Mean peak plasma contrast concentrations for Bilopaque exceeded those for Telepaque. Thirty-one percent of the Bilopaque group achieved diagnostic single-dose oral cholecystograms, compared with to 11% of the Telepaque group (P less than 0.05).
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PMID:Oral cholecystography in the early phase of acute alcoholic pancreatitis. A prospective, randomized comparison of Telepaque and Bilopaque. 675 57

One hundred twenty-seven artificially ventilated patients with acute respiratory insufficiency (ARI) were investigated. In 61 patients positive endexpiratory pressure (PEEP) was used when ventilation with ZEEP proved to be insufficient for one or more of the following reasons: increasing I-aDO2m PaO3 below 60 Torr at FiO2 greater than or equal to 0.5, deterioration of clinical status (group = secondary PEEP). The time elapse between beginning of artificial ventilation and institution of PEEP was 46 +/- 47 h (median 33 h). In 66 patients PEEP was used from the beginning of artificial ventilation (group II = primary PEEP). The distribution of underlying diseases (severe poisoning, pancreatitis, polytrauma or major surgery, pneumonia, cardiovascular failure, sepsis) as well as the frequency of additional vital function failure (circulatory shock, acute renal failure) were comparable in both groups (p greater than 0.05). At the beginning of artificial ventilation both groups were comparable in respect to respiratory insufficiency. PaO2 was 75 +/- 26 Torr in group I and 70 +/- 29 Torr in group II at comparable levels of FiO2 (p greater than 0.05). PaCO2 was 34.7 +/- 8.2 Torr in group I and 37.4 +/- 10.5 Torr in group II. Significantly more patients in group II received corticosteroids (greater than 1 gr/die). Mortality was 48/61 (79%) in group I and 37/66 (56%) in group II (p less than 0.01). End-inspiratory pressure exceeding 35 cm H2O was necessary in 42/61 patients in group I and 28/66 patients in group II (p less than 0.01) and FiO2 greater than 0.5 was necessary to keep PaO2 above 60 Torr in 39/61 patients in group I and 27/66 patients in group II (p less than 0.01). It is concluded that early institution of PEEP improves the course and outcome of patients with ARI.
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PMID:[Early PEEP for improvement of prognosis in patients with acute respiratory insufficiency (author's transl)]. 678

Acute hemorrhagic pancreatitis was induced in rats by injecting sodium taurocholate into the common biliopancreatic duct. The extent of pancreatic necrosis was quantified in histological sections during the course of the disease. The proportion of necrotic acini was low, although the amount of necrosis increased from 3.3% of pancreatic parenchyma at 15 min to 10.5% at 12 h. The degree of ischemia in the inflamed pancreas was estimated by extracting intravenously injected toluidine blue from the gland. The amount of the dye in the gland decreased progressively during 12 h to 58.8% of the amount in normal pancreas. The development of pancreatic edema was studied by recording the water content of the gland. The edema was maximal at 3 h and resolved partly in 12 h after the induction of the disease. Necrosis and ischemia become progressively more pronounced in the edematous pancreas during sodium taurocholate-induced acute hemorrhagic pancreatitis. This kind of pathophysiologic course is also thought to characterize human pancreatitis. The present simple model of acute hemorrhagic pancreatitis in the rat is suitable for quantitative observations on the development of pancreatic damage under various experimental conditions.
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PMID:Experimental pancreatitis in the rat. Development of pancreatic necrosis, ischemia and edema after intraductal sodium taurocholate injection. 684 Jan 52

Inhibition of pancreatic secretion is a widely accepted therapeutical principle of acute pancreatitis. However, stimulation of water and bicarbonate secretion may be beneficial by washing out the ductular system in pancreatitis. Secretin (2 and 16 CU/kg body weight) or saline were given to rats at different time intervals after induction of sodium taurocholate pancreatitis. Pancreatic necrosis and edema were slightly more marked after secretin but secretin had no influence on the survival time and rate or enzymatic parameters. It is concluded that in the rat secretin-induced pancreatic secretion does not alter the course of acute pancreatitis.
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PMID:Influence of secretin on the course of acute experimental pancreatitis in rats. 687 5

Eleven healthy volunteers (C) and nine patients affected by chronic relapsing pancreatitis (CP) were administered N-Benzoyl-L-Tyrosyl-PABA orally, at a dose of 150 mg combined, on different days, with: 1) water alone (schedule a); 2) Lundh meal (schedule b); 3) Secretin-Caerulein by i.v. infusion (0.5 CU/kg/hr and 75 ng/kg/hr respectively) (schedule c); 4) Caerulein by i.m. injection (300 ng/kg) (schedule d). The mean urinary PABA recovery in CP was lower than in C with all the schedules, but this was statistically significant only with schedules a and c (P less than 0.02 and P less than 0.05 respectively). With respect to b, c, and d, the mean urinary PABA recovery seemed to increase both in C and in CP as compared with schedule a, but only in the CP group with schedule b was the increase statistically significant (P less than 0.05). The present data show that the exocrine pancreatic stimulants do not improve the reliability of the PABA test.
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PMID:Urinary PABA recovery after oral N-benzoyl-L-tyrosyl-PABA administration combined with various exocrine pancreatic stimulants. 697 Jan 60

We used the anesthetized sheep lung lymph preparation to examine the effects of acute hemorrhagic pancreatitis on pulmonary transvascular fluid and protein exchange. Induction of acute pancreatitis by injection of trypsin and sodium taurocholate into the pancreatic duct caused significant increases (p less than 0.05) in lung lymph flow, ratio of lymph to plasma protein concentration (L/P ratio), and transvascular protein clearance. Pulmonary arterial and pulmonary arterial wedge pressures did not change significantly, but pulmonary blood flow decreased (p less than 0.05) and pulmonary vascular resistance increased (p less than 0.05). In contrast to the effects of acute pancreatitis, left atrial hypertension caused increases in lung lymph flow that were associated with decreases in the L/P ratio. Extravascular lung water content was increased after acute pancreatitis by 25% from the value obtained in sham-operated animals in which saline was injected into the pancreatic duct. These findings indicate that acute hemorrhagic pancreatitis causes an increase in pulmonary vascular permeability to proteins. Because pulmonary vascular pressures did not change, the increased permeability may be due to the cellular and humoral factors rather than hemodynamic mechanisms.
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PMID:Effect of acute pancreatitis on pulmonary transvascular fluid and protein exchange. 727 Oct 55


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