zergling8

My friend was admitted recently due to billiary pancreatitis, just wondering how did it happen. I read the textbook, it says the most common pathogenic mechanism is believed to be autodigestion of the pancreas. the aetiological factors cause injury to pancreatic cells or activation of the pancreatic enzymes in the pancreas rather than in the intestine. It is not clear how the activation of pancreatic enzyme occurs. one possible cause could be reflux of bile acids into the pancreatic ducts through an open or distended sphincter of oddi. I have read the anatomy picture of the bile ducts/common bile duct/biliary tree. the cyctic duct or common bile duct might be obstructed if gallstone formated. But I just dont understand in the textbook how gallstones cause the reflux of bile acit into pancreas and cause pancreatitis.............

Hi everyone, I have read that gallstone formation causes the obstruction of bile flow from gallbladder, then when the gallbladder and its duct contracts, the colic causes agonizing pain that radiates to right epigastrium. And pancretitis is commonly believed to be caused by autodigestion and alcohol abuse, which the pancreatic enzymes are activated in pancreas rather than in intestine, therefore causes the digestion of pancreas. could anyone explain to me how gallstones contribute to acute pancreatitis, what's the physiology of acute billiary pancreatitis???? Thank you

I II: ST elevation III: ST depression V1: seems ok V2: ST elevation V3: ST elevation V4: ST elevation V5 V6: ST elevation aVL aVF: seems ok aVR: seems not P wave?? ...........I am not sure if my interpreting is right...........and I dont know what happened with Lead I, V, aVL and aVR.... um..........the function of left ventricle is to fill rapidly with oxygenated blood flowing from the lung veins, contract rapidly and forcibly to force the majority of this blood into the aorta. The V2,3,4 ST elevation on ECG indicates anferior wall infarction, so the left anterior descending artery might be blocked completely?? less blood supply to subendocardial ? transmural..? then the contractility of left ventricle decrease and same with the function of dialation------less oxygenated blood being delivered to the body --- pump failure?? (Patient is pale), it also causes the decrease of gas exchange and pulmonary ventilation----> hypoxia??--- increase RR and decrease O2 sats? The repolarization phase of the T wave and ST segment is usually the first to be involved during myocardial ischemia and injury. As the involved area becomes ischemic, myocardial repolarization is altered, causeing changes in T wave. Acute severe ischemia reduces the resting membrane potential and shortens the duration of the action potential in the ischemic area. these changes create a voltage difference between the mornal and ischemic areas of the myocardium that leads to a current of inury between these regions it says that anterior wall infarction causes tachycardia and hypotension but why this patient's HR is normal and BP is slightly high??? and with regard to the ECG, is there any other problems, I cant read Lead I, V, aVL and aVR........and does he also have a lateral infarction???? Thank you

Hi everyone, I have got a case study about myocardial infarction but I dont know much about ECG interpreting and MI related physiological changes. Scenario: Mr Ronald Bates is a 68 year-old retired school teacher. His wife drives him to the hospital after a three-hour history of increasing shortness of breath. History on presentation: On arrival Mr Bates states he has been experiencing episodes of shortness of breath all morning. It started when he was making breakfast, but became very uncomfortable when walking the dogs after breakfast. He denies chest pain but describes the sensation as a general discomfort. He is a smoker, is not on any regular medications. He is approximately 160cm tall and weighs 70kg. Mr Bates is pale and anxious. Vital signs: HR 78 beats/min BP 140/80 mmHg RR 24 breaths/min SpO2 94% on room air Pain score 4/10 - but more of a discomfort. ECG: http://i62.tinypic.com/24yr59t.jpg Lead III and aVR ST depression ? ---- inferior wall ischemic?? V2,V3,V4, Lead II and aVL ST elevation???----anferior and left high anterior wall infarction?? could anyone please explain to me the ECG and the changes in vital signs in relation to his ECG. Thanks