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MDCN 350.3- Course 1 Pathology > CPC: Stomach and Colon > Flashcards

CPC: Stomach and Colon Flashcards

1
Q
A

gastritis : inflammation of the stomach

  • features of inflammatino: erythema, edema, punctate hemorrhages.
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2
Q
A

gastritis

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3
Q
A

flat base ulcer

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4
Q
A

duodenal ulver. can erode into the submucosa

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5
Q
A

gastric ulcer: full thickness defect in mucosa. extends into the submucosa.

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6
Q

Picture of an ulcer bed: what cells are persent

A

fibrin (scarring)

neutrophils– sign of acute inflammation

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7
Q

gross and micropscopic features of a benign peptic ulcer?

A

gross: sharp, punched out border, mucosal margin level with surrounding margin.
microscopic: inflammation (neutrophils), sharp border, no malignant/premature cells.

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8
Q

gross and micropscopic features of a malignant peptic ulcer?

A

gross: heaped up margins

microscopic; malignant cells

can be diffuse (signet ring cells), or intestinal (glands present)

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9
Q

is this ulcer benign or malignant?

A

benign, has flat edge.

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10
Q

is this ulcer benign or malignant?

A

malignant: heaped up edges.

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11
Q

is this ulcer benign or malignant?

A

malignant– has heaped up edges.

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12
Q

is this ulcer benign or malignant?

A

malignant–has heaped up edges

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13
Q

is this ulcer benign or malignant?

A

benign–it has level margins

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14
Q

intestinal gastric adenocarcinoma featurs

A

tumor cells form glands, as well as mass/ulceration.

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15
Q

diffuse gastric adenocarcinoma features

A
  • signet ring cells because body forms an immune response, preventing stromal flexibility
  • becomes thick nad rigid stomach wall.
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16
Q

diffuse or intestinal gastric adenocarcinoma?

A

intestinal. lots of gland formation.

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17
Q

diffuse or intestinal gastric adenocarcinoma?

A

diffuse. intense immune/desmoplastic response. lack of glands indicates it’s not intestinal gastric adenocarcinoma.

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18
Q

diffuse or intestinal gastric adenocarcinoma?

A

gastric intestinal

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19
Q
A
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20
Q

diffuse or intestinal gastric adenocarcinoma?

A

diffuse type– firm rubbery gastri wall. prevents inflation in endoscopy– lots of inflammation.

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21
Q

diffuse or intestinal gastric adenocarcinoma?

A

diffuse. Dysmoplastic repair causes inflammation. There’s a reduced muscle layer

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22
Q

diffuse or intestinal gastric adenocarcinoma?

A

diffuse. expanded layers. dense layers are expanding

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23
Q

diffuse or intestinal gastric adenocarcinoma?

A

diffuse. there is desmoplastic strome (very fibrous and dense)– reaction to the cancer cells. There are discohexive malignant cells percolating through the stroma which causes an immune esponse.

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24
Q

diffuse or intestinal gastric adenocarcinoma?

A

diffuse type

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25
Q

benign or malignant ulcer?

A

malignant–heaped up edges. probably creates glands that are secreting.

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26
Q

benign or malignant ulcer?

A

malignant

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27
Q

what causes chronic gastritis

A

GERD, helicobacter pylori etc. PUD

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28
Q

how is H.Pylori linked to causing duodenal ulcers? (mechanisms of virulence)

A
  1. urease: elevates local gastric PH
  2. adhesins: allow adherence to gastric epithelium
  3. Toxins: may be involved in ulcer or cancer development
  4. flagella: provides motility in viscous mucus.
29
Q

histologic features of H. Pylori Gastritis

A
  1. H.pylori organisms present
  2. acute inflammation with intraepithelial neutrophils
  3. chronic inflammation (subepithelial plasma cells wtih lymphoid aggregates)
30
Q

IBD –> _____—> colonic _____

(inflammation-dysplasia-carcinoma sequence)

A

IBD –> DYSPLASIA—> colonic ADENOCARCINOMA

31
Q

Two immune mediated diseases that make up IBD

A

crohns and ulcerative colitis.

32
Q

which one illustrates crohns vs ulcerative colitis

A
33
Q

which IBD?

A

crohns– ileum is affected. crohns can start anywhere in the GI whereas UC starts at the rectum and progresses upwards.

34
Q

picture of terminal ileum. which IBD?

A

Crohns.

35
Q
A

crohns disease with ileal ulcers.

36
Q

what lesion pattern is this called

A

skip lesions seen in crohns disease.

37
Q

which IBD? what is the characteristic feature?

A

cobblestone appearance of mucosa in Crohns.

38
Q

what is the instrument poking out of?

A

a fistula-seen in crohns disease. fistula is an abnormal connection between two epithelialized surfaces (colon-bladder), (colon-colon), (colon-small intestine) (colon-uterus)

39
Q
A

transmural inflammation causing a fistula (between colon and bladder) seen in crohns disease.

40
Q
A

fistula. seen in crohns disease.

41
Q

which IBD? what is the characteristic feature?

A

ulcerative colitis. there is continuous involvement without skip areas.

42
Q

Which IBD? Is there transmural inflammation occuring in this speciman?

A

UC. no transmural inflammation– continous mucosal erosion.

43
Q
A

the intact portions of the colonic mucosa creates a pseudopolyp appearance.

44
Q

fill out this table for crohns an UC

A
45
Q

wall appearance for UC vs Crohns

A

crohns can cause transmural inflammation and breakdown so crohns causes thickened walls, where as UC still has thin walls because it only affects the mucosa.

46
Q

Why Does UC not cause fat malabsorption

A

because it usually affects hte lower colon which isn’t involved in nutrient absorption. Crohns can cause marked malabsorption because it can involve the small bowel.

47
Q

meaning for dysplasia

A

disordered growth. can be pre-malignant, althouhgh doens’t always progress to acncer.

48
Q

If UC is occuring in someone with ____, it increases the risk of maliganncy. It requires endoscopic surveillance with mucosal biopsies.

A

if co-existing with primary sclerosing cholangitis (PSC), colitis associated neoplasia risks are increased.

49
Q

what is happening to the colon?

A

low-grade dysplasia. Ducts are still apparent but there is extensive nuclear crowing, stratification and marked nuclear hyperchromasia.

this pic below is normal

50
Q

what is happening to the colon?

A

high -grade dysplasia. more complex architecture is happening and the normal organization of the ducts is disappearing. htere is a loss of nuclear polarity, and increased nuclear pleomorphism

51
Q

metaplasia vs dysplasia.

A

metaplasia is a change in structure but still normal (ex/ squamous to columnar), but dysplasia is irregular growth.

52
Q

polyp-cancer sequence is aka

A

adenoma-carcinoma seuqence.

  • differs from inflammation sequence (ex/ IBD–> dysplasia–>adenocarcinoma, or hepatitis –> HCC) because inciting factor is genetic rather than inflammation.
53
Q

two types of neoplastic polyps

A
  1. conventional adenomas (tubular and villous)
  2. serrated adenoma
54
Q

T/F hyperplastic polyps can become dysplastic and then malignant

A

false. hyperplastic polyps to not have dysplasia ever.

55
Q

villous or tubular adenomatous polyp?

A

tubular

56
Q

villous or tubular adenomatous polyp?

A

villous

57
Q

what type of adenomatous polyps is associated with more advanced lesions

A

villous polyps

58
Q
A
59
Q

type of adenoma/polyp

A

tubular

60
Q
A

tubular adenoma

61
Q

where are you most likely to see this type of polyp?

A

this is a sessile serrated adenoma (SSA)

  • more common on the right colon
  • they lack histological features of dysplasia, but still have malignant potential. they do not follow traditional adenoma-carcinoma sequence previously described.
62
Q

what type of adenoma/polyp and where is it usually found?

A

hyperplastic polyp– usually sigmoid/rectum (left colon)

  • no malignent potential.

serrated morphology but only on the surface. (SSA extends to the base)

63
Q

T/F p53 tumor suppressor gene is mutated in adenomas

A

false. it is mutated in 75% of colon cancer, but isn’t mutated in adenomas (therefore a late step in the sequence)

Loss of function of p53 causes a lack of tumor suppression, and the polyp advances into a carcinoma.

64
Q
A

colon cancer

65
Q
A
66
Q
A
67
Q

histological features of colon cancer:

• Composed of varying complexity of glands (differentiation)
– Lots of glands – ____ differentiated
– Few glands – ____ differentiated

• Glands often filled with debris (“___ ____”)

• Invasive component causes ____ response (scarring and reaction to the
malignant cells)

• Many different morphologies make many different subtypes, not necessary to know at
this point

A

• Composed of varying complexity of glands (differentiation)
– Lots of glands – well differentiated
– Few glands – poorly differentiated

• Glands often filled with debris (“dirty necrosis”)

• Invasive component causes desmoplastic response (scarring and reaction to the
malignant cells)

• Many different morphologies make many different subtypes, not necessary to know at
this point

68
Q
A

invasice adenocarcinoma

69
Q
A

MDCN 350.3- Course 1 Pathology (13 decks)

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