Path - Anus, Appendix, Gallbladder, Pancreas Flashcards
morphology of cholesterol stones
- found only in the gall
- pale yellow, finely granular, hard, crystalline palisade
morphology of pancreas in acute pancreatitis
1) microvascular leak and edema
2) fat necrosis
3) acute inflammation
4) destruction of pancreatic parenchyma
5) destruction of blood vessels and interstitial hemorrhage
describe the CA19-9 antigen marker and its efficacy in early detection of pancreatic carcinoma
serum levels of CA19-9 are often elevated in pancreatic cancer pts, but are relatively nonspecific and lack sensitivity
significant lab values in acute pancreatitis
- increased plasma amylase after 24 hours and increased lipase after 72-96 hours
- hypocalcemia
- glycosuria
how to diagnose chronic pancreatitis
visualization of calcifications within pancreas on CT or US
- acinar cell loss
what part of the pancreas is most often affected by pancreatic cancer
head (60%)
- then body (15%)
- then tail (5%)
- 20% diffuse involvement
what is sclerosing retroperitonitis
dense fibrosis that may extend to involve the mesentery
- cause unknown, but most likely on spectrum of IgG4 related sclerosing dz
what is the most common primary benign or malignant soft tissue tumor that develops within peritoneum and retroperitoneum
desmoplastic round cell tumor
describe the congenital anomaly annular pancreas
band like ring of normal pancreatic tissue that encircles second portion of the duodenum –> can cause duodenal obstruction
what is the most frequently altered oncogene and what is the most frequently inactivated tumor suppressor gene in pancreatic cancer
altered oncogene: KRAS
inactivated tumor suppressor gene: CDKN2A
what cells line the middle 1/3 of the anal canal and what kind of cancer develops from it
transitional epithelium
cloacogenic carcinoma
pathogenesis of carcinoma of gallbladder
chronic inflammation
- biggest risk factor is gallstones (1-2% stone patients get CA)
- 2/3 cases express oncoprotein ERBB2
- 1/4 cases express chromatin remodeling genes PBRM1 and MLL3
how are KRAS mutations related to pancreatic carcinomas and at what point are they involved in the progression from PanIN to invasive carcinoma
constitutive KRAS signaling augments cell growth and survival via the MAPK and P13K/AKT pathways
- mutations occur early in progression from PanIN to carcinoma in PanIN 1A and 1B stages
how are CDKN2A mutations related to pancreatic carcinomas and at what point are they involved in the progression from PanIN to invasive carcinoma
it encodes p16/INK4a which normally inhibits cell cycle progression, and encodes ARF which normally augments p53
(the mutation blocks both of these things)
- mutations occur in intermediate grade lesions in the PanIN-2 stage
morphology of pigment stones
1) black stones:
- found in sterile bile ducts
- made of bilirubin, salts, and mucin
- friable, spiculated and molded contours
2) brown stones:
- found in infected ducts
- made of bilirubin, salts, mucin, and some cholesterol
- soap-like, greasy, soft, laminated
serous cystic neoplasms are associated with what genetic abnormality
inactivation of VHL tumor suppressor gene
morphology of pancreas in chronic pancreatitis
1) fibrosis
2) atrophy and loss of acini
3) variable dilation of pancreatic ducts
4) gland is hard with calcification
5) sparing of islets of Langerhans
pathogenesis of cholesterol stones
too much cholesterol, accelerated cholesterol crystal nucleation, or mucus secretion –> cholesterol concentration increases above the capacity of bile –> cholesterol stone
morphology of acute cholecystitis
gall is enlarged and tense, may be green-black, bright red, or blotchy
- serosa covered in fibrous exudate
describe cloacogenic carcinomas
basaloid tumors with immature cells from the basal layer of the transitional epithelium of the middle 1/3 anal canal
describe how primary acinar cell injury causes acute pancreatitis
primary acinar cell injury –> release of digestive enzymes, inflammation, and autodigestion of pancreatic tissue
sx of chronic pancreatitis
- normally clinically silent but may have recurrent attacks of pain and/or jaundice triggered by ETOH, overeating, or opiates
- can have constant abd and back pain
what genetic defect is associated with pancreatic carcinoma in Ashkenazi Jewish patients
BRCA2 mutation
pathogenesis and tx of autoimmune pancreatitis
associated with IgG4-secreting plasma cells in pancreas
- responds to steroids
what cells line the upper 1/3 of the anal canal and what kind of cancer develops from it
columnar rectal epithelial cells
glandular crcinoma
describe gallbladder empyema
wall is thickened, edematous, and hyperemic that may become green-black necrotic in severe cases (gangrene cholecystitis)
etiologies of pancreatic duct obstruction
1) gallstones
2) biliary sludge
3) periampullary neoplasms
4) choledochoceles
5) parasites
6) pancreas divisum
clinical features acute cholecystitis
acute attack: progressive pain in RUQ or epigastrium that lasts longer than 6 hours
- mild fever, anorexia, tachycardia, sweating, N/V
medications that trigger acute pancreatitis
1) furosemide
2) azathioprine
3) estrogens
describe mucinous cystic neoplasms
painless, slow growing masses arising in tail of pancreas
- lined by columnar mucin-producing epithelium
- filled with thick mucin
- can be precursors to invasive carcinomas
pure squamous cell carcinoma of the lower 1/3 anal canal is most often associated with ______
HPV infection
describe serous cystic neoplasms of the pancreas
multicystic neoplasms that occur in the tail of the pancreas
- lined by glycogen rich cuboidal cells
- contain clear, thin, straw colored fluid
clinical features of carcinoma of gallbladder
insidious onset and typically indistinguishable from cholelithiasis: abd pain, jaundice, anorexia, nausea, and vomiting
what are PanIN lesions
well-defined, noninvasive precursor lesions in small ducts that lead to invasive pancreatic cancers
risk factors for hemorrhoids
- constipation (straining)
- venous stasis in pregnancy
- cirrhosis from portal HTN
morphology of carcinoma of gallbladder
show two patterns of growth:
1) infiltrating
- more common, poorly defined area of diffuse mural thickening and induration
2) exophytic
- grow in lumen as irregular, cauliflower mass and invades underlying wall
how are acinar cells of the pancreas damaged
1) oxidative stress can generate free radicals
2) increased Ca2+ triggers inappropriate activation of digestive enzymes (trypsin)
what is peritonitis and what causes it
inflammation of the membrane lining the abdominal wall
- due to bacterial infection or chemical irritation or perforation of the abdominal viscera
where does pancreatic CA metastasize to
liver and lungs
metabolic triggers for acute pancreatitis
1) hypertriglyceridemia
2) hypercalemia
3) hyper PTH
infections that trigger acute pancreatitis
mumps –> direct acinar cell injury leading to pancreatitis
risk factors for pancreatic carcinoma
1) smoking
2) high fat diet
3) FMHx of chronic pancreatitis
4) DM
sx acute pancreatitis
constant abd pain that may refer to upper back or L shoulder
- anorexia, N/V
describe xanthogranulomatous cholecystitis
feature of chronic cholecystitis:
- very thick wall and a shrunken gall, nodular with foci of necrosis and hemorrhage
- triggered by rupture of rokitansky-aschoff sinuses
lab values in acute cholecystitis
elevated serum bilirubin and alk phos
causes of acute cholecystitis
chemical irritation and inflammation from a gallstone
most often a stone obstructing the neck of gallbladder
clinical features pancreatic CA
1) pain
2) obstructive jaundice
3) weight loss, anorexia
4) general malaise, weakness
6) trousseau sign in 10% pts
rupture of rokitansky-aschoff sinuses causes _____
xanthogranulomatous cholecystitis
what inherited disorders predispose patients to pancreatic cancer
1) Peutz-Jeghers
2) hereditary pancreatitis
3) familial atypical multiple-mole malenoma syndrome
4) strong FMHX pancreatic CA
5) hereditary breast cancer (BRCA)
6) HNPCC
what cells line the lower 1/3 of the anal canal and what kind of cancer develops from it
stratified squamous epithelium
squamous cell carcinoma
what is the most common congenital anomaly of the gallbladder
a folded fundus that creates a phrygian cap
demographic for pancreatic carcinoma
- older adults (60s-80s)
- blacks > whites
- Ashkenazi Jewish decent
most carcinomas of the gallbladder are ______
adenocarcinomas
mucinous cystic neoplasms are associated with what genetic abnormality
KRAS oncogene and mutations in TP53 and RNF43 tumor suppressor genes
describe how pancreatic duct obstruction causes acute pancreatitis
obstruction –> rise in intrapancreatic ductal pressure –> accumulation of enzyme-rich fluid in the interstitium –> lipase is produced in its active form and its accumulation can cause fat necrosis –> initiation inflammation
describe pseudocysts of the pancreas
localized collections of necrotic and hemorrhagic material that are rich in pancreatic enzymes
- lack an epithelial lining (hence “pseudo”)
- walled off areas of fat necrosis encircled by fibrosed granulation tissue
risk factors for acute cholecystitis
- sepsis w/ hypotension and multiorgan failure
- immunosuppression
- major trauma and burns
- DM
- infections
morphology of chronic cholecystitis
- dulled serosa
- thickened wall, grey-white apperance
- fusion of mucosal folds
- rokitansky-aschoff sinuses
- porcelain gall
- xanthogranulomatous cholecystitis
how are SMAD4 mutations related to pancreatic carcinomas and at what point are they involved in the progression from PanIN to invasive carcinoma
SMAD4 normally plays a role in signal transduction from the TGF-B family (anti-inflammatory - mutation blocks this)
- mutations occur in higher grade lesions in the PanIN-3 stage
clinical features of appendicitis
- periumbilical pain migrating to RLQ
- N/V
- McBurney’s point
- mild fever
- leukocytosis
list the 6 genes associated with predisposition to pancreatitis
1) CFTR
2) PRSS1
3) SPINK1
4) CASR
5) CTRC
6) CPA1
pathogenesis of chronic pancreatitis
repeated episodes of acute pancreatitis –> initiates sequence of perilobar fibrosis, duct distortion, and altered pancreatic secretions –> loss of pancreatic parenchyma and deposition of collagen and fibrosis
describe congenital cysts of the pancreas
- unilocular, thin walled cysts that are the result from anomalous development of the pancreatic ducts
- lined w/ cuboidal epithelium
- enclosed by thin, fibrous capsule
- filled with clear serous fluid
how are TP53 mutations related to pancreatic carcinomas and at what point are they involved in the progression from PanIN to invasive carcinoma
p53 is the guardian of the genome and responds to DNA damage by arresting cell growth and inducing apoptosis
- mutations occur in higher grade lesions in the PanIN-3 stage
clinical features of gallstones
pain in RUQ that radiates into right upper shoulder or back that occurs after a fatty meal
what are primary peritoneal tumors and what causes them
they are mesotheliomas due to asbestos exposure
describe the congenital anomaly pancreas divisum
failure of the ventral and dorsal fetal duct to fuse, causing the majority of pancreatic secretions to drain via the small, minor papilla rather than the papilla of vater –> predisposes patients to chronic pancreatitis
complications of acute pancreatitis
1) pancreatic abscess
2) pancreatic pseudocyst
3) gram (-) infections of necrotic debris
compare internal and external hemorrhoids
internal: above anorectal line, generally painless
external: below anorectal line, extremely painful
causes of chronic cholecystitis
chronic inflammation due to stones 90% of the time
morphology/histology of pancreatic cancer
1) glands lined w/ pleomorphic cuboidal columnar epithelium
2) abortive tubular structures
3) dense stromal fibrosis
4) often grows along nerves or invades blood vessles
clinical features of chronic cholecystitis
recurrent acute symptoms with intolerance for fatty foods
pathogenesis of pigment stones
infections of biliary tract –> elevated levels of unconjugated bilirubin in the bile –> stones of bilirubin and salts
prognosis of chronic pancreatitis
20-25 year mortality rate of 50%
