new_n_lost
Politically InCorrect
Topics: 650
Posts: 6,058
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Simple.
Pancreas is an enzyme production house. These enzymes are usually kept in a pro form in the zymogen granules. Any form of cellular injury leads to the premature activation of these enzymes. The zymogen release enzymes which get picked up by lysosomes and start releasing activated products which are chemo-attractants from PMNs. The second insult comes from the PMNs by their respiratory bursts release superoxide which is more harmful and then lasxtly macrophage drive the final assualt on tissues.
This causes massive hemorrhage and edema. As the mediators of inflammation reach systemic circulation they cause bacteremia by gut flora translocation which occurs due to the rapid infusion of inflammatory products and starting a localized response. The bacteremia itself causes further damage and also the inflammoty products launched into the blood stream wreak havoc on the body where ever they go.
It a pretty unpredictable cascade ot events which occurs in 30% of the cases of acute pancreatitis. The body is overwhelmed by the massive number of inflammatory mediators that hemodynamics change and if you can survive that the infection does a bang up jop of making sure that your family gets the life insurance you bought.
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| Tiff
Forum Guru
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DIC - Palpable pseudocysts can be formed blocking the bile duct causing obstructive jaundice hindering vitamin K transport hence decreased production of Vitamin K dependent factors affecting PT and PTT. Increased pressure from the obstruction causes a decreased functioning liver and the liver is unable to clear products from fibrinolysis.
ARDS - Several processes may contribute to ARDS. 1) Lecithinase breaks down surfactant and phospholipid layer of cell membranes. Cell membrane destruction by lecithinase produces arachidonic acid which can form thromboxane A2 increasing leukocyte adherence and injury to lung. 2) Proteases such as trypsin, chymotrypsin, and elastase are released, circulate, and breakdown surfactant and elastic tissue of the lung. 3) Activation of complement has been implicated where that complement causes the lung to trap leukocytes leading to destruction by the lysosomal enzymes and/or free radicals.
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| antidepressant
Forum Guru
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Thanks a lot NNL and Tiff!!!!!!!!!!!!!!
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| antidepressant
Forum Guru
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I was going through a pulmonlogy patho part of uw, i saw a question, thought i will add here,
A 55 year old guy with acute pancreatitis developed ARDS ( they didnt say like that, i made it short,) he died, what will you see in the autopsy:
a. Lung hyperinflation
b. alveolar hyaline membrane
c. interalveolar wall destruction
d. intraalveolar hemorrhage
e. cardiomegaly.
i picked b, that is right answer but i wondered why d is not correct, here is their explanation:
Acute necrotizing pancreatitis is a major risk factor for progression to ARDS. Diffuse injury to alveolocapillary membrane results in interstitial and intraalveolar edema, acute inflammation, and alveolar hyaline membrane. Hyaline membranes result from alveolocapillary membrane leakage and consist of fibrin exudate and plasma protein-rich edema fluid mixed with the cytoplasmic and lipid remnants of necrotic epithelial cells. (Hyaline membranes are produced by a different mechanism of alveolocapillary injury in neonatal respiratory distress syndrome).
(choice c) destruction of intraalveolar septae would be expected in a patient with emphysema.
(choice d) Frank intraalveolar hemorrhage could impair gas exchange and cause dyspnea if widespread, but would also tend to produce hemoptysis as a clinical sign. Widespread intra alveolar hemorrhage may occur in pulmonary hemorrhage syndromes, including Goddpastures syndrome, wegeners granulomatosis, and lupus erythomatosus. However, none of these conditions are associated with acute pancreatitis.
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Step 1 can not defeat me!!!!!!!!
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