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31 Cards in this Set
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pancreatitis,epidemiology :
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* men 40 to 45 years of age with a history of alcoholism
* women 50 to 55 years of age with a history of biliary disease |
3:2 (men>women)
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pancreatitis,etiology :
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* unknown
Generally, it is believed that the pancreatic duct becomes obstructed, accompanied by hypersecretion of the exocrine enzymes of the pancreas. These enzymes enter the bile duct, where they are activated and, together with bile, back up (reflux)into the pancreatic duct, causing pancreatitis. |
not acute/chronic as a whole
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what is the major symptom of acute pancreatitis ?
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Severe abdominal pain
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etiology and pathophysiology of abdominaland back pain in acute pancreatitis ?
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irritation and edema of the inflamed pancreas that stimulate the nerve endings
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Diagnostic assessment of acute pancreatitis ?
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US and contrast-enhanced CT
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etiology of acute pancreatitis :
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1.Alcohol abuse
2.bacterial/viral infection 3.duodenitis spasm of ampulla of Vatter 4.blunt abdominal trauma 5.peptic ulcer disease 5.ischemic vascular disease 6.drugs |
6 major etiologies
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pathophysiology of the pain in acute pancreatitis :
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* acute in onset
* more severe after meals 24-48 hrs after a heavy meal/alcoholic ingestion * occurs in midepigastrium * unrelieved by antacids * may be accompanied by abdominal distension * decreased peristalsis * is accompanied with vomiting that does not releive the pain |
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lab findings :
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* amylase (norm.60-160)
returns to normal within 48-72 hrs * urinary amylase * lipase (norm.0-120) may remain elevated 7-14 days may remain elevated *WBS elevated (left shift) * hypocalcemia * hyperglycemia * bilirubinamia |
amylase & lipase are elevated 3 times their normal upper limit
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treatment in acute pancreatitis :
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1.parenteral nutrition
2. nasogastric suctioning 3. H2antagonists(Cimetidine,Ranitidine) 4.PPI 5.Antibiotics 6.Insulin |
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pain management in acute pancreatitis :
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1.MO
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לא לבלבל עם כאבים בעקבות אבנים בכיס מרה!
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chronic pancreatitis , etiology:
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1.alcohol consumption
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1 major cause
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what is the major problem in chronic panreatitis ?
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weight loss
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in more than 75%of patients
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assessment of chronic pancreatitis :
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1.ERCP
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the most useful study
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surgical treatment in chronic panceatitis ?
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1.Pancreaticojejunostomy
2.stent 3.pancreatectomy |
1.to reduce pain
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Ranson's criteria in acute pancreatitis :
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Criteria on Admission to Hospital
* Age >55 years * WBC >16,000 mm3 * Serum glucose >200 mg/dL (>11.1 mmol/L) * Serum LDH >350 IU/L (>350 U/L) * AST >250 U/mL (120 U/L) Criteria Within 48 Hours of Hospital Admission * Fall in hematocrit >10% (>0.10) * BUN increase >5 mg/dL (>1.7 mmol/L) * Serum calcium <8 mg/dL (<2.0 mmo/L) * Base deficit >4 mEq/L (>4 mmol/L) * Fluid retention or sequestration >6 L PO2 <60 mm Hg |
acute not chrinic
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Acute pancreatitis , complications:
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1.in mild :
*hypovolemic shock *electrolyte disturbances *sepsis 2.severe acute: *panceatic cysts *abscess *shock *pleural effusion |
1.mild
2.severe *local *systemic |
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what is gangrenous appendicitis?
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Gangrenous appendicitis is recognized as enlargement of the appendix with associated fluid and loculated air within the lumen
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complication of acute pancreatitis
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what is the complication of gangrenous pancreatitis ?
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peritonitis
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what are an indications of somatostatin treatment in acute pancreatitis?
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Somatostatin and its long-acting analogue, octreotide, are potent inhibitors of exocrine secretion of the pancreas, which plays an important role in the pathogenesis of acute pancreatitis. In addition, somatostatin and octreotide have direct anti-inflammatory and cytoprotective effects. It has therefore been suggested that somatostatin and octreotide be used in the treatment and prevention of acute pancreatitis, and this concept has been studied extensively over the past 2 decades
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2 major indications
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Follow up of patient with chronic pancreatitis :
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*US
*X-Ray studies/ERCP |
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nasogastric tube indication in pancreatitis ?
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לאפשר ריקון המערכת ומתן מנוחה
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כאשר חולה עם זונדה מתחיל
להקיא מה על האחות לעשות |
לפתוח את הזונדה לניקוז
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A 44 year old alcoholic male presents with severe epigastric pain that began shortly after a heavy bout of alcoholic intake, and reached maximum intensity over a period of two hours. The pain is constant, radiates straight through to the back and is accompanied by nausea, vomiting and retching. He had a similar episode two years ago, for which he required hospitalization.
Dx? Diagnostic test? If Dx is unclear? Management? |
Dx: Acute pancreatitis
Diagnostic test: Serum and Urinary Amylase and Lipase If unclear: CT scan (or in a day or two if there is no improvement) Management: NPO, NG suction, IV fluids |
3 together
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A disheveled, malnourished individual shows up in the emergency room requesting medication for pain. He smells of alcohol and complains bitterly of constant epigastric pain, radiating straight through to the back that he says he has had for several years. He has diabetes, steatorrhea and calcifications in the upper abdomen in a plain X-Ray.
Dx? Diagnostic test? Management? |
Dx: Chronic pancreatitis
Diagnostic test: AXR visualizing calcifications Management: Stop alcohol, replacement of pancreatic enzymes and control of the diabetes; ERCP |
3
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A 56 year old man presents with progressive jaundice which he first noticed six weeks ago. He has a total bilirubin of 22, with 16 direct and 6 indirect, and minimally elevated SGOT. He alkaline phosphatase is about eight times the upper limit of normal. He has lost 20 pounds over the past two months, and has a persistent, nagging mild pain deep into his epigastrium and in the upper back. His sister died at age 44 from a cancer of the pancreas. A sonogram shows dilated intrahepatic ducts, dilated extrahepatic ducts and a very distended, thin walled gallbladder.
Dx? Diagnostic test? |
Dx: Cancer of the head of the pancreas
(Terrible prognosis) Diagnostic test: CAT scan –which may show the mass in the head of the pancreas; then ERCP –which will probably show obstruction of both common duct and pancreatic duct |
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A 56 year old alcoholic male is admitted with a clinical picture of acute upper abdominal pain. The pain is constant, radiates straight through to the back, and is extremely severe. He has a serum amylase of 800, WBC of 18,000 blood glucose of 150, serum calcium of 6.5 and a hematocrit of 40. He is given IV fluids and kept NPO with NG suction. By the next morning, his hematocrit has dropped to 30 the serum calcium has remained below 7 in spite of calcium administration, his BUN has gone up to 32 and he has developed metabolic acidosis and a low arterial PO2.
Dx? Management/test? |
Dx: Hemorrhagic Pancreatitis
(In fact, he is in deep trouble, with at least eight of Ranson’s criteria predicting 80 to 100% mortality) Management/test: Very intensive support will be needed, but the common pathway to death from complication of hemorrhagic pancreatitis frequently is by way of pancreatic abscesses that need to be drained as soon as they appear. Thus serial CT scans will be required. |
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ERCP complications
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*cholangitis
*pancreatitis |
2
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what does whipple procedure include :
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the removal of :
-antrum of the stomack -1-st + 2-nd portion of duodenum -head of pancrease -the common bile duct -gallblader |
pancreaticoduodenectomy(5)
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somatostatine is prodused in
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hypothalamus
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A 56-year-old alcoholic presents complaining of 6 months of worsening midepigastric pain radiating to his back. The pain is exacerbated by eating and continued alcohol use. One month ago he was told that he had developed diabetes. He has also noted that, over the past 2 months, he has had greasy, foul-smelling, large-volume stools. Which is of the following is the most likely cause of this man's steatorrhea?
A. Acid inactivation of pancreatic enzymes B. Bacterial overgrowth C. Biliary insufficiency D. Excess secretion of glucagon E. Insufficient lipase available for normal fat digestion |
The correct answer is E. Midepigastric pain radiating to the back and exacerbated by eating and continued alcohol use should suggest the diagnosis of pancreatitis. Significant risk factors for pancreatitis include alcoholism (as this patient has) and biliary tract disease (for which there is no evidence in this patient). It is a little unclear from the history whether the patient is experiencing recurrent episodes of acute pancreatitis or is developing the onset of chronic pancreatitis. Whichever is the case, both processes are capable of destroying enough exocrine pancreatic tissue to predispose for exocrine pancreatic insufficiency with resultant insufficient production of pancreatic enzymes, such as lipase, which normally facilitates fat usage, to allow for normal digestion. Steatorrhea, or excess fat in stool, is seen clinically as greasy, foul-smelling (because of bacterial action on the fat), large-volume (in part due to gas production by bacteria and in part due to failure to digest most of the food) stools.
There is no evidence that there is hyperacidity to account for inactivation of pancreatic enzymes (choice A). This phenomenon can occur, but it would be more likely to be seen in settings such as Zollinger-Ellison syndrome, in which a gastrin-producing tumor of the pancreas or small intestine stimulates excess acid production by the stomach. Bacterial overgrowth (choice B) can produce steatorrhea by deconjugating bile salts and making them unavailable to form micelles. However, this patient has no underlying etiology for bacterial overgrowth, such as blind loop syndrome or hypomotility. Biliary insufficiency (choice C) can cause steatorrhea; however, although biliary tract disease can predispose for pancreatitis, pancreatitis does not predispose for biliary insufficiency. The pain of biliary tract disease is usually localized to the left upper quadrant and may radiate to the left shoulder. Excess glucagon (choice D) is rarely noted in the absence of the very rare neuroendocrine tumor known as glucagonoma. It does not produce fat maldigestion or malabsorption. |
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A 57-year-old alcoholic man is being treated for acute hemorrhagic pancreatitis. He was in the intensive care unit for 1 week, where he required chest tubes for pleural effusions and was on a respirator for several days. Eventually, he improved sufficiently to be transferred to the floor. Three days after leaving the unit, and about 2 weeks after the onset of the disease, he spikes a fever and develops leukocytosis. Which of the following developments do these recent findings most likely suggest?
A. Chronic pancreatitis B. Pancreatic abscess C. Pancreatic pseudocyst D. Pelvic abscess E. Subphrenic abscess |
The correct answer is B. A very common complication of hemorrhagic pancreatitis, and often the reason for the demise of the patient, is the development of a pancreatic abscess. The timetable is usually about 10-14 days from the onset of the disease, and the initial manifestations are fever and leukocytosis.
Chronic pancreatitis (choice A) develops after several years of recurrent attacks of pancreatitis, and is characterized by steatorrhea, diabetes, and constant pain. Pancreatic pseudocyst (choice C) is another potential complication of pancreatitis, but the manifestations are related to pressure symptoms from the fluid collection, there is no fever or leukocytosis, and the timetable for development is about 6 weeks from the onset of the disease. Pelvic abscess (choice D) and subphrenic abscess (choice E) are indeed in the differential diagnosis, as they also show up with fever and leukocytosis some 10-14 days from the original problem. But, the original problem for these patients is usually an infectious process in the abdomen, e.g., a ruptured appendix or a perforated viscus. If the problem began with pancreatitis, and then there are signs of sepsis, the pancreas is the logical place to harbor the pus. |
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