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Maddy - GI II Exam I - some pharm > Path - Anus, Appendix, Gallbladder, Pancreas > Flashcards

Path - Anus, Appendix, Gallbladder, Pancreas Flashcards

1
Q

morphology of cholesterol stones

A
  • found only in the gall

- pale yellow, finely granular, hard, crystalline palisade

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2
Q

morphology of pancreas in acute pancreatitis

A

1) microvascular leak and edema
2) fat necrosis
3) acute inflammation
4) destruction of pancreatic parenchyma
5) destruction of blood vessels and interstitial hemorrhage

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3
Q

describe the CA19-9 antigen marker and its efficacy in early detection of pancreatic carcinoma

A

serum levels of CA19-9 are often elevated in pancreatic cancer pts, but are relatively nonspecific and lack sensitivity

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4
Q

significant lab values in acute pancreatitis

A
  • increased plasma amylase after 24 hours and increased lipase after 72-96 hours
  • hypocalcemia
  • glycosuria
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5
Q

how to diagnose chronic pancreatitis

A

visualization of calcifications within pancreas on CT or US

- acinar cell loss

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6
Q

what part of the pancreas is most often affected by pancreatic cancer

A

head (60%)

  • then body (15%)
  • then tail (5%)
  • 20% diffuse involvement
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7
Q

what is sclerosing retroperitonitis

A

dense fibrosis that may extend to involve the mesentery

- cause unknown, but most likely on spectrum of IgG4 related sclerosing dz

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8
Q

what is the most common primary benign or malignant soft tissue tumor that develops within peritoneum and retroperitoneum

A

desmoplastic round cell tumor

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9
Q

describe the congenital anomaly annular pancreas

A

band like ring of normal pancreatic tissue that encircles second portion of the duodenum –> can cause duodenal obstruction

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10
Q

what is the most frequently altered oncogene and what is the most frequently inactivated tumor suppressor gene in pancreatic cancer

A

altered oncogene: KRAS

inactivated tumor suppressor gene: CDKN2A

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11
Q

what cells line the middle 1/3 of the anal canal and what kind of cancer develops from it

A

transitional epithelium

cloacogenic carcinoma

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12
Q

pathogenesis of carcinoma of gallbladder

A

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
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13
Q

how are KRAS mutations related to pancreatic carcinomas and at what point are they involved in the progression from PanIN to invasive carcinoma

A

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
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14
Q

how are CDKN2A mutations related to pancreatic carcinomas and at what point are they involved in the progression from PanIN to invasive carcinoma

A

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
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15
Q

morphology of pigment stones

A

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

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16
Q

serous cystic neoplasms are associated with what genetic abnormality

A

inactivation of VHL tumor suppressor gene

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17
Q

morphology of pancreas in chronic pancreatitis

A

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

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18
Q

pathogenesis of cholesterol stones

A

too much cholesterol, accelerated cholesterol crystal nucleation, or mucus secretion –> cholesterol concentration increases above the capacity of bile –> cholesterol stone

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19
Q

morphology of acute cholecystitis

A

gall is enlarged and tense, may be green-black, bright red, or blotchy
- serosa covered in fibrous exudate

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20
Q

describe cloacogenic carcinomas

A

basaloid tumors with immature cells from the basal layer of the transitional epithelium of the middle 1/3 anal canal

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21
Q

describe how primary acinar cell injury causes acute pancreatitis

A

primary acinar cell injury –> release of digestive enzymes, inflammation, and autodigestion of pancreatic tissue

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22
Q

sx of chronic pancreatitis

A
  • 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
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23
Q

what genetic defect is associated with pancreatic carcinoma in Ashkenazi Jewish patients

A

BRCA2 mutation

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24
Q

pathogenesis and tx of autoimmune pancreatitis

A

associated with IgG4-secreting plasma cells in pancreas

- responds to steroids

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25
Q

what cells line the upper 1/3 of the anal canal and what kind of cancer develops from it

A

columnar rectal epithelial cells

glandular crcinoma

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26
Q

describe gallbladder empyema

A

wall is thickened, edematous, and hyperemic that may become green-black necrotic in severe cases (gangrene cholecystitis)

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27
Q

etiologies of pancreatic duct obstruction

A

1) gallstones
2) biliary sludge
3) periampullary neoplasms
4) choledochoceles
5) parasites
6) pancreas divisum

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28
Q

clinical features acute cholecystitis

A

acute attack: progressive pain in RUQ or epigastrium that lasts longer than 6 hours
- mild fever, anorexia, tachycardia, sweating, N/V

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29
Q

medications that trigger acute pancreatitis

A

1) furosemide
2) azathioprine
3) estrogens

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30
Q

describe mucinous cystic neoplasms

A

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
31
Q

pure squamous cell carcinoma of the lower 1/3 anal canal is most often associated with ______

A

HPV infection

32
Q

describe serous cystic neoplasms of the pancreas

A

multicystic neoplasms that occur in the tail of the pancreas

  • lined by glycogen rich cuboidal cells
  • contain clear, thin, straw colored fluid
33
Q

clinical features of carcinoma of gallbladder

A

insidious onset and typically indistinguishable from cholelithiasis: abd pain, jaundice, anorexia, nausea, and vomiting

34
Q

what are PanIN lesions

A

well-defined, noninvasive precursor lesions in small ducts that lead to invasive pancreatic cancers

35
Q

risk factors for hemorrhoids

A
  • constipation (straining)
  • venous stasis in pregnancy
  • cirrhosis from portal HTN
36
Q

morphology of carcinoma of gallbladder

A

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

37
Q

how are acinar cells of the pancreas damaged

A

1) oxidative stress can generate free radicals

2) increased Ca2+ triggers inappropriate activation of digestive enzymes (trypsin)

38
Q

what is peritonitis and what causes it

A

inflammation of the membrane lining the abdominal wall

- due to bacterial infection or chemical irritation or perforation of the abdominal viscera

39
Q

where does pancreatic CA metastasize to

A

liver and lungs

40
Q

metabolic triggers for acute pancreatitis

A

1) hypertriglyceridemia
2) hypercalemia
3) hyper PTH

41
Q

infections that trigger acute pancreatitis

A

mumps –> direct acinar cell injury leading to pancreatitis

42
Q

risk factors for pancreatic carcinoma

A

1) smoking
2) high fat diet
3) FMHx of chronic pancreatitis
4) DM

43
Q

sx acute pancreatitis

A

constant abd pain that may refer to upper back or L shoulder

- anorexia, N/V

44
Q

describe xanthogranulomatous cholecystitis

A

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
45
Q

lab values in acute cholecystitis

A

elevated serum bilirubin and alk phos

46
Q

causes of acute cholecystitis

A

chemical irritation and inflammation from a gallstone

most often a stone obstructing the neck of gallbladder

47
Q

clinical features pancreatic CA

A

1) pain
2) obstructive jaundice
3) weight loss, anorexia
4) general malaise, weakness
6) trousseau sign in 10% pts

48
Q

rupture of rokitansky-aschoff sinuses causes _____

A

xanthogranulomatous cholecystitis

49
Q

what inherited disorders predispose patients to pancreatic cancer

A

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

50
Q

what cells line the lower 1/3 of the anal canal and what kind of cancer develops from it

A

stratified squamous epithelium

squamous cell carcinoma

51
Q

what is the most common congenital anomaly of the gallbladder

A

a folded fundus that creates a phrygian cap

52
Q

demographic for pancreatic carcinoma

A
  • older adults (60s-80s)
  • blacks > whites
  • Ashkenazi Jewish decent
53
Q

most carcinomas of the gallbladder are ______

A

adenocarcinomas

54
Q

mucinous cystic neoplasms are associated with what genetic abnormality

A

KRAS oncogene and mutations in TP53 and RNF43 tumor suppressor genes

55
Q

describe how pancreatic duct obstruction causes acute pancreatitis

A

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

56
Q

describe pseudocysts of the pancreas

A

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
57
Q

risk factors for acute cholecystitis

A
  • sepsis w/ hypotension and multiorgan failure
  • immunosuppression
  • major trauma and burns
  • DM
  • infections
58
Q

morphology of chronic cholecystitis

A
  • dulled serosa
  • thickened wall, grey-white apperance
  • fusion of mucosal folds
  • rokitansky-aschoff sinuses
  • porcelain gall
  • xanthogranulomatous cholecystitis
59
Q

how are SMAD4 mutations related to pancreatic carcinomas and at what point are they involved in the progression from PanIN to invasive carcinoma

A

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
60
Q

clinical features of appendicitis

A
  • periumbilical pain migrating to RLQ
  • N/V
  • McBurney’s point
  • mild fever
  • leukocytosis
61
Q

list the 6 genes associated with predisposition to pancreatitis

A

1) CFTR
2) PRSS1
3) SPINK1
4) CASR
5) CTRC
6) CPA1

62
Q

pathogenesis of chronic pancreatitis

A

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

63
Q

describe congenital cysts of the pancreas

A
  • 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
64
Q

how are TP53 mutations related to pancreatic carcinomas and at what point are they involved in the progression from PanIN to invasive carcinoma

A

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
65
Q

clinical features of gallstones

A

pain in RUQ that radiates into right upper shoulder or back that occurs after a fatty meal

66
Q

what are primary peritoneal tumors and what causes them

A

they are mesotheliomas due to asbestos exposure

67
Q

describe the congenital anomaly pancreas divisum

A

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

68
Q

complications of acute pancreatitis

A

1) pancreatic abscess
2) pancreatic pseudocyst
3) gram (-) infections of necrotic debris

69
Q

compare internal and external hemorrhoids

A

internal: above anorectal line, generally painless
external: below anorectal line, extremely painful

70
Q

causes of chronic cholecystitis

A

chronic inflammation due to stones 90% of the time

71
Q

morphology/histology of pancreatic cancer

A

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

72
Q

clinical features of chronic cholecystitis

A

recurrent acute symptoms with intolerance for fatty foods

73
Q

pathogenesis of pigment stones

A

infections of biliary tract –> elevated levels of unconjugated bilirubin in the bile –> stones of bilirubin and salts

74
Q

prognosis of chronic pancreatitis

A

20-25 year mortality rate of 50%

Maddy - GI II Exam I - some pharm (23 decks)

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