Flashcards in GI 4 Deck (47):
Injury to _____ cells in the _______ portion of the pancreas leads to an inflammatory condition known as pancreatitis.
injury to acini cells in the exocrine portion --> pancreatitis
Acute pancreatitis varies from a mild, self-limited condition with acute inflammation and stromal _______ to a severe, acute _________ disorder with massive necrosis and may be fatal.
acute hemorrhagic disorder that can be fatal
What can repeated episodes of acute pancreatitis lead to?
Describe three characteristics of chronic pancreatitis.
1. Recurrent severe abdominal pain.
2. Progressive fibrosis.
3. Pancreatic insufficiency (eventually).
Are either acute or chronic pancreatitis reversible?
Acute is if underlying cause is removed. Chronic is not - there is irreversible destruction of the parenchyma, especially the exocrine portion.
Name six causes of pancreatitis.
1. Inappropriate activation of pancreatic enzymes.
2. Duct obstruction.
4. Alcohol abuse.
5. Other: Viral infections, drugs, trauma, hyperlipidemia or calcemia.
6. Idiopathic (unknown) - makes up 10-20% of cases.
What type of necrosis would be seen in a case of pancreatitis caused by inappropriate activation of enzymes?
Name some plasma protease inhibitors that are supposed to provide protection against pancreatic enzyme activation.
3. C1 esterase inhibitor
4. Pancreatic secretory trypsin inhibitor.
Injury to acinar cells in the pancreas leads to ________ activation, which starts a cascade of proteolytic _________ activations.
Leads to trypsin activation, trypsin activates a bunch of other enzymes (biochem)
___% of patients with acute pancreatitis have gallstones, while only ____% of people with gallstones develop acute pancreatitis.
45% with acute pancreatitis have gallstones but only 5% of people with gallstones get acute pancreatitis.
Having gallstone(s) increases risk for development of acute pancreatitis by ____ times.
What proportion of acute pancreatitis cases are associated with alcohol abuse? What percentage of alcoholics develop acute pancreatitis?
1/3 are associated with alcohol abuse.
5% of alcoholics develop acute pancreatitis.
Ethanol causes spasm or acute edema of the ______ of _____. Ethanol is also thought to stimulate the pancreas to release ________ without concomitantly increased fluid.
sphincter of Oddi.
Ethanol triggers release of pancreatic enzymes without concomitantly increased fluid.
Describe the macroscopic changes associated with acute pancreatitis.
Edema, hyperemia at first, leading to hemorrhagic foci.
Severe cases: Organ is destroyed and converted into a retroperitoneal hematoma.
Describe the 5 microscopic changes associated with acute pancreatitis.
2. Fat necrosis with calcium deposits, saponification, involvement of extrapancreatic fat.
3. Acini cell necrosis.
4. Intense acute inflammation.
5. Destruction of blood vessels with extravasation of RBCs.
List 5 clinical features of acute pancreatitis. What percentage are mild, and what percentage are severe/life-threatening?
1. Severe epigastric (upper abdominal) and upper back pain.
2. Nausea and vomiting
3. Vascular collapse/shock from hemorrage of destroyed vessels.
4. Elevated serum amylase/lipase.
5. Gram-negative bacteria infection.
Usually mild/self limiting, but 20% severe and a medical emergency
___% of patients experience repeat episodes of acute pancreatitis, leading to chronic pancreatitis. This disease is characterized by abdominal/back pain, weight loss, and jaundice. ________ is visible in radiographs. In ___% of cases it is fatal.
5% get chronic pancreatitis.
Calcification is visible in radiographs.
20% die from it.
____% of patients who survive acute pancreatitis, especially alcoholic pancreatitis, go on to develop a pancreatic _________
50% develop a pancreatic pseudocyst
What is a pancreatic pseudocyst?
Complication of acute pancreatitis: A circumscribed collection of fluid rich in pancreatic enzymes, blood, and necrotic tissue, typically located in the lesser sac of the abdomen.
Do pancreatic pseudocysts have epithelial linings? How big are they? Can they become infected?
No epithelial lining. 2-30 cm. Can become infected and form an abscess.
Name the three major causes of acute pancreatitis.
1. Alcohol in 2/3 of adult cases.
2. Pancreatic duct obstruction.
3. Chronic injury to acinar cells as in hemochromatosis.
Describe two microscopic changes seen in chronic pancreatitis.
1. Fibrosis - reduction in functional parenchyma (acinar and islet cell loss).
2. Dilation of ducts.
What are the two types of pancreatic cystic neoplasms?
Serous cystadenomas and mucinous cystic neoplasms.
What percentage of pancreatic cysts are neoplastic?
5 to 15%
Describe four characteristics of serous cystadenomas of the pancreas.
1. Glycogen-rich cuboidal cells surrounding cysts with clear, straw-colored (yellowish) fluid.
2. Begins in 7th decade of life.
3. Female/male ratio 2:1
Describe five characteristics of a mucinous cystic neoplasm of the pancreas.
1. Almost always in women.
2. In body or tail of pancreas.
3. Cystic space filled with thick, tenacious mucin.
4. Lined by columnar mucinous epithelium with dense cellular stroma.
5. Can be benign, borderline malignant, or malignant.
Has the five year survival rate from pancreatic cancer increased over the last 40 years?
Not really (from 3% in 1975 to 5% in 2004)
Pancreatic cancer is the ___th most common cause of cancer death in men and women in the U.S.
What is the five year survival rate of pancreatic cancer?
What type of pancreatic cancer makes up 90% of cases?
At what age is pancreatic cancer most commonly seen?
>60 years of age.
What two conditions/habits are thought to be associated with the development of pancreatic cancer?
1. Smoking associated in 25% of cases.
2. DM seen in 80% of cases.
___% of pancreatic cancers are found in the head of the pancreas, ___% are found in the body, and ___% are found in the tail. Cancers of the body and tail ______ (do or do not) impinge on the biliary tract and therefore may remain silent for a while.
60% in head
10% in body
5% in tail
the rest are diffused
cancers of body or tail do not impinge on biliary tract
There are four mutations that are often seen in pancreatic cancer cases. List them and briefly describe each.
1. K-RAS – early event; most frequently altered oncogene.
2. p16 – most frequently inactivated tumor suppressor gene.
3. SMAD4 – tumor suppressor gene inactivated in 55% of cases.
4. p53 – tumor suppressor gene inactivated in 50-70% of cases; late event.
Where does pancreatic cancer most often metastasize to (2)?
Regional lymph nodes and liver.
Is the order of occurrence of mutations important in the development of pancreatic cancer?
No, just the accumulation is what is needed for development of the disease.
Describe clinical features of pancreatic cancer.
1. Weight loss/anorexia.
2. Epigastric pain, often radiating to the back.
3. Jaundice in 50% of patients with cancer in the pancreatic head.
4. Courvorier sign: Acute, painless gallbladder dilation accompanied by jaundice as a result of comomon bile duct obstruction by the tumor.
5. Migratory thrombophlebitis: Deep venous thrombosis or Trosseau syndrome seen in 10% of pts, especially with body and tail cancers.
Pancreatic endocrine tumors (PETS) account for ___% of all pancreatic neoplasms.
What is the most common islet cell neoplasm?
Insulinoma (beta cell tumors) account for 75% of islet cell neoplasms.
Describe the morphological changes of an insulinoma.
They resemble normal beta cells but form trabecular and solid patterns. Amyloid found in stroma.
Most insulinomas are benign lesions in the _____ or _____ of the pancreas.
body or tail
What clinical features are associated with insulinoma?
1. Severe hypoglycemia.
2. Sweating, nervousness, hunger, confusion, lethargy, coma.
3. High levels of insulin in blood and in tumor cells.
Other than insulinoma (beta cells), name four other islet cell tumors.
1. Gastrinomas (G cell tumor)
2. Glucagonomas (alpha cell tumor)
3. Somatostatinoma (delta cell tumor)
4. Vasointestinal polypeptide-secreting tumors (VIPomas)
Describe clinical features of gastrinomas.
G cell tumor, hypersecretion of gastrin which triggers release of gastric acid from parietal cells leading to peptic ulceration of duodenum and jejunum. Most are malignant.
Describe clinical features of glucagonomas.
Alpha cell tumor. Mild diabetes, necrotizing migratory & erythematous rash, anemia, venous thrombosis. Glucagon levels 30x higher than normal. 2/3 are malignant.
Describe clinical features of somatostatinomas.
Delta cell tumor - excess somatostatin (normally functions to inhibit insulin and glucagon release). Mild diabetes, gallstones, steatorrhea. Most are malignant.