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GI 1 > Patho - GI Neoplasia > Flashcards

Patho - GI Neoplasia Flashcards

1
Q

What are the screening methods of detection for GI neoplasia?

A
  • hemoccult
  • InSure FIT test
  • cologuard
  • colonoscopy (definitive)
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2
Q

Hemoccult sensitivity

A
  • sensitivity as low as 4.9% if using a single card
  • sensitivity increases if multiple samples used on 3 cards
  • does not distinguish b/w human and animal hgb
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3
Q

Where does a hemoccult detect blood from?

A
  • the entire length of GI tract

- can detect from the esophagus

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4
Q

reasons for doing a hemoccult

A
  • colon cancer screening

- detect bleeding from peptic ulcer dz

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5
Q

When would you do a hemoccult?

A
  • complete PE

- abdominal/pelvic complaint

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6
Q

What would cause a false positive in a hemoccult?

A
  • dietary animal blood in meat (avoid 3 days prior)
  • hemorrhoids
  • menstruation
  • vit. C and other antioxidants that interfere w/ peroxidase rxn
  • intermittent bleeding
  • sampling error
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7
Q

hemoccult cost

A

about $14

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8
Q

what does FIT stand for?

A

fecal immunochemical test

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9
Q

FIT test sensitivity and specificity

A
  • 78% sensitive for colorectal CA (33% more than guaiac/hemoccult)
  • 98% specific
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10
Q

How does an immunochemical test (FIT) work?

A
  • involves monoclonal antibody coated chromatography test strip
  • specific to the globin portion of human** hgb
  • can be done at home on 2 different stool test
  • uses a brush to skim the surface of the stool
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11
Q

Why is a FIT test only specific to colonic bleeds?

A

hgb won’t survive the path through the GI tract if it comes from higher up

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12
Q

what is the false positive rate for colon CA w/ a FIT test?

A

2%

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13
Q

Cologuard sensitivity and specificity

A
  • 92% sensitive

- 87% specific

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14
Q

how does the cologuard test work?

A
  • DNA testing
  • stool is lab tested for mutated DNA
  • looks for DNA mutations that are suggestive of a tumor
  • doesn’t telly you what or where - just that there is mutated DNA present
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15
Q

Research comparing FIT and DNA testing

A
  • sensitivity for detecting colorectal CA was 92.3% with DNA testing and 73.8% with FIT
  • similar comparison for detecting advanced precancerous lesions
  • DNA testing also was better at detecting polyps
  • FIT had better specificity
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16
Q

What are the symptoms used as methods of detection?

A
  • pain
  • mass effect
  • achalasia
  • dysphagia
  • painless jaundice
  • weight loss
  • change in character of stool
  • hematochezia
  • obstruction

-can be incidental finding

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17
Q

When does visceral pain arise?

A
  • when there is ischemia

- or when there is a tumor pressing against a capsule

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18
Q

Why is painless** jaundice an important symptom?

A
  • painless jaundice is pancreatic cancer until proven other wise
  • painful** jaundice is likely caused by something like a stone
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19
Q

What is the #1 cause of bowel obstruction in someone who has, and has not, had abdominal surgery?

A
  • someone who HAS: adhesions

- has NOT: neoplasia

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20
Q

What are the modalities for detection?

A
  • KUB (won’t really use)
  • CT - contrast
  • Ultrasound
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21
Q

once a tumor is detected, what are the modalities used?

A
  • PET scan (initially and serially)
  • Bone scan
  • Tumor board for best option
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22
Q

if pt is too sick to get a colonoscopy, what can be done?

A
  • barium enema (or swallow) xray

- would show as a filling defect

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23
Q

What are the two cellular origins of neoplasia in the GI tract?

A
  1. Squamous: top and bottom of the tract, where mucosa meets the skin (i.e oral mucosa)
  2. Adenomatous: arising from glandular cells, GI epi
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24
Q

What is the first step when considering treatment options?

A

biopsy and staging

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25
Q

TNM staging

A
  • T: size or direct extent of primary tumor
  • N: degree of spread to regional lymph nodes
  • M: presence of mets
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26
Q

What are the following treatment options once the tumor has been biopsied and staged?

A
  • debulking (just a delay, not cure)
  • chemo/radiation therapy
  • surgery
  • palliative care
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27
Q

when is targeted therapy used?

A

-usually when everything else has failed

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28
Q

targeted therapy examples

A
  • drugs that target blood vessel growth (sorafenib, bevacizumab, paxopanib, regorafenif)
  • drugs that target epidermal growth factor receptor (cetuximab, panitumumab)
  • mitogen-activated protein kinase enzyme inhibitors (trametinib)
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29
Q

What is the cellular origin of cancer of the oral cavity?

A
  • 90% are of squamous in origin (from the lip to the hypopharynx)
  • could be adeno (salivary), lymphoid (always an option) or melanoma
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30
Q

what are the precancerous forms in the oral cavity?

A
  • leukoplakia
  • erythroplakia (worse)
  • usually on lateral margins of the tongue - all non keratinized stratified squamous epi
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31
Q

What is the downfall of most oral cancers located on the posterior tongue or hypopharynx?

A

they are often only detected after mets to neck nodes

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32
Q

risk factors for oral cavity cancer

A
  • male (2X)
  • > 40
  • tobacco/ETOH
  • sun exposure (lower lip)
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33
Q

prognosis of oral cavity cancer

A

5 yr survival rate: 57%

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34
Q

What is the relationship of oral cavity cancer with HPV?

A
  • most squamou cell carcinomas of the oral cavity are induced into caner by HPV
  • if the tumor is HPV positive, there is a better outcome
  • in US, mostly HPV derived
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35
Q

Treatment options of oral cavity cancer

A
  • after the routine biopsy, CT, PET:
  • surgery
  • PEG tube
  • radiation
  • cooling
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36
Q

what are the side effects of radiation in oral cavity cancer?

A
  • loss of taste
  • loss of salivation (xerostomia)
  • can take amifostine prophylactically to help prevent damaging salivary glands
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37
Q

Why do some people have molar extracted before beginning oral cancer treatments?

A

-the radiation damages the gingiva and causes pts to lose teeth

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38
Q

esophageal cancer cellular origins

A
  • Upper 2/3: squamous (somatic control)

- Bottom 1/3: adeno (autonomic control)

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39
Q

Which type of esophageal cancer is most common?

A
  • in US: adeno

- worldwide: squamous

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40
Q

outcome of esophageal cancer

A

overall 5 yr survival: 18%

41
Q

Tx options for esophageal cancer

A
  • surgery, radiation/chemo, palliative
  • dilation (increasing diameter of esophagus b/c has a tendency to scar down)
  • stent placement
42
Q

risk factors for esophageal cancer

A
  • tabacco/ETOH**
  • obesity
  • GERD
  • Barrett’s esophagus
  • esophageal web
  • achalasia
  • tylosis: excess skin on palms/soles
43
Q

What is significant about GERD as a risk factor to esophageal cancer?

A
  • don’t take heartburn lightly
  • if it doesn’t respond to prilosec, be very cautious
  • all long term reflux needs to be worked up
  • irritant to lower esophagus just like tobacco/ETOH
44
Q

signs and symptoms side note

A

all of the signs and symptoms are intuitive and we won’t be asked specific questions about them - review to have general understanding

45
Q

cellular origins of gastric cancer

A
  • 95% are adenocarinoma
  • others include:
  • lymphoma
  • leiomyomas
  • squamous cell
  • carcinoid
46
Q

What is a carcinoid tumor?

A
  • a specific tumor type that produces neuroendocrine secretory products (like serotonin)
  • mostly found in GI tract and lungs
47
Q

carcinoid syndrome

A
  • facial flushing
  • facial purpleish spider viens on nose/face
  • tachy
  • diarrhea
  • asthma-like SOB
48
Q

Why do carcinoid tumors in the lungs cause carcinoid syndrome but ones in the GI tract do not?

A

the liver metabolizes he secretory products if they come from the GI tracts

49
Q

outcome of gastric cancer

A

5 yr survival: 29%

50
Q

diagnosis of gastric cancer

A
  • CBC (30% are anemic)
  • hemoccult
  • EGD
  • CMP (for liver enzymes)
  • CEA (carcinoembryonic ag)
51
Q

CEA testing in gastric cancer

A
  • it is an antigen that will be elevated in about 50% of cases
  • also used for serial testing after surgery
  • CA 19-9 is another antigen used
52
Q

how is gastric cancer staged?

A

-endoscopic US

53
Q

How common is gastric cancer?

A

15th most common malignancy

54
Q

What is the relationship between the area in the stomach of the cancer and outcome?

A

-arising near the pylorus has better outcome than in cardia -probably b/c of better detection

55
Q

tx of gastric cancer

A
  • surgery: partial/total gastrectomy, esophagogastrectomy

- chemo/radiation

56
Q

risk factors for gastric cancer

A

-diet low in fruits/veggies
-fam hx
-infection by h. pylori
hx of stomach polyp > 2cm
-chronic atrophic gastritis
-pernicious anemia
-smoke

57
Q

sister mary joseph’s nodule

A

a nodule in the umbilicus that is often associated w/ advanced malignancy

58
Q

common cancer types of the liver, GB, and biliary tract

A
  • primary liver CA: hepatocellular carcinoma

- biliary tract: cholangiocarcinoma

59
Q

releationship b/w hepatocellular cancer and hepatitis

A
  • 2% d/t hepatitis

- up to 50% of all cancers in undeveloped countried d/t hepatitis

60
Q

tx of cancer of the liver, GB, and biliary tract

A
  • resection

- Nexavar if unresectable (increases overall survival)

61
Q

5 yr survival of cancer of the liver, GB, and biliary tract

A
  • early stage w/ transplantation: 60-70%
  • small resectable w/o cirrhosis: 50%
  • localized stages: 30%
  • regional mets: 10%
  • distant mets: 3%
62
Q

liver cancer screening

A
  • US
  • LFTs
  • serial testing (AFP) q. 6 mo
63
Q

benign hepatic tumors

A
  • hemangioma
  • hepatic adenoma
  • focal nodular hyperplasia
  • cysts
  • lipoma
  • fibroma
  • leiomyoma
64
Q

what is significant of cysts of liver or pancreas?

A

you might think it is just a benign cyst, but it could be a cyst d/t necrotic tissue surrounding cancerous cells

65
Q

risk factors stats for hepatic CA

A
  • men (behavior)
  • asian americans and pacific islanders
  • hep C (<5% progress to CA)
  • hep B - MC cause worldwide
66
Q

risk factors for HCCA

A
  • cirrhosis
  • hep B and C
  • fatty liver
  • obesity
  • hemochromatosis
  • environmental: vinyl chloride, arsenic
  • anabolic steroid** board
67
Q

sites of cholangiocarcinoma

A
  • perihilar: 50% (where right and left hepatic ducts join, aka Klatskin tumors)
  • distal: 30%
  • intrahepatic: 10%
68
Q

cellular types of cholangiocarcinoma

A
  • almost all are adenocarcinoma
  • few are lymphomas, sarcomas, and small cell
  • benign: hamartomas and adenomas
69
Q

what population is cholangiocarcinoma most common in?

A

-hispanic americans and native americans

70
Q

Modalities for cholangiocarcinoma

A
  • CT

- ERCP (endoscopic retrograde cholangiopancreatography

71
Q

risk factors for cholangiocarcinoma

A
  • family hx
  • hep B and C if intrahepatic
  • cirrhosis - ETOH
  • inflammatory bowel dz
  • long standing inflammation of the duct system: primary sclerosing cholangitis, duct stones, choledochal cysts
  • obesity
72
Q

outcome of cholangiocarcinoma

A

if untreated: 50% at 1 yr, 20% at 2 yrs and 10% at 3 yrs

73
Q

what are the 5 types of cancer of the small intestine?

A
  • adenocarcinoma
  • sarcoma
  • lymphoma
  • carcinoid
  • gastrointestinal stromal tumor (GIST)
74
Q

adenocarcinoma of the SI

A
  • mucus secreting cells of the epithelial lining

- usually of the duodenum and jejunum

75
Q

sarcoma of the SI

A
  • muscularis layer

- usually in ileum

76
Q

lymphoma of the SI

A

-usually non-Hodgkin’s

77
Q

carcinoid tumor of the SI

A

usually ileum

78
Q

GIST of SI

A

rare, soft tissue sarcome

79
Q

What is a specific cancer of the small bowel?

A
  • gastrinoma

- gastrin secreting tumor from duodenum/pancreas/stomach

80
Q

what does a gastrinoma cause?

A

Zollinger-Ellison syndrome

81
Q

Zollinger-Ellison syndrome

A
  • characterized by ulcerations in stomach/duodenum/pancreas

- pancreas has greater malignant potential

82
Q

risk factors for small bowel cancers

A
  • Crohn’s dz*** not ulcerative colitis (boards)
  • diet: high fat, smoke/cured meats
  • familial adenomatous polyposis
  • Peutz-Jeghers - inherited polyposis
  • celiac dz (true dz, not gluten intolerance)
83
Q

What is a whipple procedure?

A
  • last option for surgical correction
  • removes the head of pancreas, duodenum, GB, and bile duct
  • can be curative if all CA was removed, but terrible quality of life after
84
Q

What is the only risk factor for tumors of the appendix?

A

age

85
Q

possible types of appendix tumors

A
  • colonic type adenocarcinoma - only about 10%
  • lymphoma
  • carcinoid
  • mucinous cystadenocarcinoma
  • signet ring cell adenocarcinoma - aggressive
  • goblet cell adenoma
  • paraganglioma
86
Q

prognosis of appendix tumors

A
  • less than 3 cm, not spread: 5 yr survival close to 100%
  • less than 3 cm and spread to regional nodes: 78%
  • larger than 3 cm, not spread: 78%
  • if spread to other parts of body: 32%
87
Q

where do most pancreatic cancers arise?

A

-within the duct of the exocrine pancreas
= adenocarcinoma (95%)
-about 5% arise from neuroendrocrine tumor from islets

88
Q

prognosis of pancreatic cancer

A
  • w/ mets: 3-6mos: highest mortality of all CAs
  • 1 yr: 26%
  • 5 yr: 8% (generous)
  • 3rd leading cause of cancer-related deaths in US
89
Q

What are the types of neuroendocrine tumors?

A
  • gastrinomas - 1/2 are CA
  • insulinomas - most benign; dont call everything reactive hypoglycemia
  • glucagonomas: most CA
  • somatostatinomas: most CA
  • VIPomas: most CA
  • PPomas: most CA
90
Q

what are the risk factors for pancreatic CA

A
  • African american
  • excess body weight
  • chronic pancreatitis
  • DM
  • fam hx of genetic syndromes: BRCA2 mutation, Lynch, FAMMM
  • personal or fam hx of pancreatic CA
  • smoking
91
Q

tx option for pancreatic CA

A
  • surgery - only 20% of the time
  • radiation
  • chemo
  • targeted therapy
92
Q

key consideration for pancreatic CA

A
  • always keep this in the back of your mind
  • chronic GI compliant, vague abdomen discomfort w/ no relief by PPIs or middle aged woman quickly losing 20 pounds no diet = WORK UP
93
Q

how do most colon cancers begin?

A

non-cancerous polyps

94
Q

when should colon CA screening begin?

A
  • 50

- 40 if high risk

95
Q

what are the different types of polyps

A
  • adenomatous: MC
  • tubular: <1cm
  • tubulovillus adenoma
  • villous: increased incidence of CA
  • hyperplastic: benign
96
Q

survival stats of colon and rectal CA

A
  • similar

- stage 1 87-92%

97
Q

anal cancer cell types

A
  • most are squamous

- some adenocarcinoma (if higher up)

98
Q

risk factors for anal CA

A
  • HPV (HPV-16 specifically)
  • anal warts
  • HIV
  • multiple partners
  • smoking
  • more common in women and african american men

GI 1 (16 decks)

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