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Gastrointestinal II Exam #1 > GI Pathology - Colon > Flashcards

GI Pathology - Colon Flashcards

1
Q

What symptoms characterize IBS?

How is IBS diagnosed?

What is used to divide it into sub-types?

A

Chronic, relapsing abdominal pain, bloating and changed in bowel habits.

It is a clinical and functional diagnosis (the gross and microscopic eval. is normal).

The Rome criteria

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2
Q

What is the pathogenesis of IBS?

A

It is poorly defined, but there is clear interplay between psychologic stressors, diet, perturbation of gut biome, increased enteric response to gut stimuli and abnormal GI motility.

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3
Q

What is the prevalence of IBS?

What age/sex is most common?

A

5-10%

F>M; 20-40

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4
Q

Crohn disease vs. Ulcerative colitis macroscopic features

Location and distrubution
Strictures?
Wall appearance

A

CD - ileum and colon; skip lesions

  • yes strictures
  • thick wall

UC - colon only; diffuse

  • rarely strictures
  • thin wall
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5
Q

Crohn disease microscopic features

Inflammation
Pseudopolyps
Ulcers
Lymphoid reaction
Fibrosis
Serositis
Granulomas
Fistulae/sinuses
A 
Inflammation - transmural
Pseudopolyps - moderate
Ulcers - deep (knife-like)
Lymphoid reaction - marked
Fibrosis - marked
Serositis - marked
Granulomas - yes (approx. 35%)
Fistulae/sinuses - yes
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6
Q

Ulcerative colitis microscopic features

Inflammation
Pseudopolyps
Ulcers
Lymphoid reaction
Fibrosis
Serositis
Granulomas
Fistulae/sinuses
A 
Inflammation - limited to mucosa
Pseudopolyps - marked
Ulcers - superficial, broad-based
Lymphoid reaction - moderate
Fibrosis - mild to none
Serositis - mild to none
Granulomas - none
Fistulae/sinuses - none
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7
Q

Crohn disease

Perianal fistula
Fat/vitamin malabsorption
Malignant potential
Recurrence after surgery
Toxic megacolon
A 
Perianal fistula - yes (in colonic dz)
Fat/vitamin malabsorption - yes
Malignant potential - yes (if colonic involvement)
Recurrence after surgery - commonly
Toxic megacolon - no
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8
Q

Ulcerative colitis

Perianal fistula
Fat/vitamin malabsorption
Malignant potential
Recurrence after surgery
Toxic megacolon
A 
Perianal fistula - no
Fat/vitamin malabsorption - no
Malignant potential - yes
Recurrence after surgery - no
Toxic megacolon - yes
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9
Q

In which IBD is smoking protective vs. a risk factor?

A

Protective: UC

Risk factor: CD

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10
Q

In which IBD is perianal disease common?

In which IBD is rectal involvement common?

A

Perianal: CD

Rectal involvement: UC

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11
Q

What are the symptoms of Crohn disease?

A

Abdominal pain, diarrhea, nausea, vomiting and weight loss; rarely there are perforating/obstructive symptoms

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12
Q

What are the symptoms of Ulcerative colitis?

A

Abdominal pain, rectal bleeding, and bloody diarrhea. Can be relasping.

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13
Q

What age is most common to develop IBD? Which form is more common in females?

What race is most common?

What countries are most common?

A

Teens/early 20s; UC more common infemales, wit a second peak in 6-7th decade

Caucasians (3-5x more common in Ashkenazi Jews in US)

North America, Europe, Australia

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14
Q

Which systems/organs have some extra-intestinal manifestations of IBD? (8)

A 
Eyes
Kidneys
Skin
Mouth
Liver
Biliary tree
Joints
Circulation
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15
Q

What are the histologic features of colonic mucosa of UC?

A

Red and granular, or have broad-based ulcers.

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16
Q

What are pseudopolyps and mucosal bridges in UC?

A

Pseudopolyps are isolated islands of regenrating mucosa that bulge into the lumen. The tips of the pseudopolyps may fuse to create mucosal bridges.

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17
Q

As opposed to CD, what is the appearance of the mucosa in UC?

A

There is no mucosal thickening in UC; the serosal surface is normal and strictures don’t occur.

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18
Q

What is the most feared long-term complication of UC or colonic CD?

A

Development of neoplasia

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19
Q

What are 3 factors that increase the risk (in UC or colonic CD) of developing neoplasia?

A

Duration of disease: risk increases 8-10 years after disease onset.

Extent of disease: pts. with pancolitis are at greater risk than those with only left-sided disease.

Nature of the inflammatory response: presence of neutrophils increases risk.

20
Q

What are 3 acquired conditions that predispose patients to cancer (in UC or colonic CD)?

A

Chronic inflammation
Precursor lesions
Immune defiency

21
Q

What is the goal of surveillance of colitis-associated neoplasia?

A

To identify dysplastic epithelium, which is the precursor to colitis-associated carcinoma.

22
Q

What is the clinical setting where you might see diversion colitis?

What is the most striking feature microscopically?

What cell-types might be abundant? (4)

What may promote mucosal recovery?

A

It may develop post-op due to diversion - most commonly in patients with UC.

Numerous mucosal lymphoid follicles

Increased numbers of:

  • lamina propria lymphocytes
  • monocytes
  • macrophages
  • plasma cells

Enemas containing SCFA can promote mucosal recovery

23
Q

What 2 entities are included in microscopic colitis?

What is the cause?

What is the presentation?

What age/sex is most common?

What are the histological features? (3)

A

Collagenous colitis and lymphocytic colitis

Idiopathic

Chronic, non-bloody diarrhea without weight loss

Middle-aged to older women

Dense subepithelial collagen layer
Increased numbers of intraepithelial lymphocytes
Mixed inflammatory infiltrate within the lamina propria

24
Q

Lymphocytic colitis shows a strong association with what other disease?

A

Celiac disease

AI dz - Graves dz, RA, autoimmune gastritis, etc.

25
Q

When does graft vs. host disease colitis occur?

What is the most common histological finding?

What is the presentation?

A

Post hematopoeitc stem cell transplantation

Epithelial apoptosis of crypt cells

Watery diarrhea, which may become bloody in severe cases

26
Q

Colonic diverticular disease is most common from what ages?

What is the prevalence vs. the percent that manifest symptoms?

What are the symptoms?

A

30-60 y/o

50% prevalence, but only 20% of those manifest symptoms

Intermittent cramping, lower abdominal discomfort, constipation, distension or sensation of being unable to clear rectum.

27
Q

What type of polyp is most common?

Where are they found?

At what age?

What must be ruled-out?

A

Hyperplastic polyps

Left colon

6-7th decade

R/O sessile serrated adenoma

28
Q

Inflammatory polyps are part of what syndrome?

This syndrome has what triad?

A

Solitary rectal ulcer syndrome (SRUS)

Rectal bleeding, mucus discharge and naterior rectal wall location

29
Q

Hamartomatous polyps occur how?

What are the 2 types/syndromes?

Germline mutations in what kinds of genes may be associated?

These polyps are associated with an increased risk for…

What may suggest presence of these polyps?

A

Sporadically or as components of various genetically determined or acquired syndromes.

Juvenile polyps and Peutz-Jeghers syndrome

TSGs or proto-oncogenes

Cancer - either within the polyps or at other sites

Extra-intestinal manifestations or family members also affected

30
Q

Juvenile polyps occur how?

What age?

What is the location they appear?

Is dysplasia common?

What cancers may ensue as a result?

What are prominent extra-GI manifestations?

A

Sporadically (retention polyps) or syndromic (AD - 1/100K)

Under 5 y/o (infantile form is severe)

Rectum (SI and stomach in syndromic)

It is rare in sporadic, but common in syndromic

Gastric, SI, colonic, pancreatic adenocarcinoma

Congenital anomalies, digital clubbing

31
Q

Peutz-Jeghers syndrome is what kind of inheritance?

At what age does it present?

What GI lesions may ensue?

What are extra-GI manifestations?

What gene pathway is mutated?

A

AD (rare - 1/25-100K)

10-15 y/o (approx 11 y/o)

Multiple hamartomatous polyps (intussusception)

Pigmented macules: increase risk for cancer in colon, breast, lung, pancreas and thyroid

LOF mutations in STK11 (in 50% of pts.)

32
Q

Adenomatous polyps definition:

How many people have them? Which sex is more common?

What are the 3 morphologic types?

A

Adenomas that are intraepithelial neoplasms that range from small (ofte pedunculated) polyps to large sessile lesions.

30% of pts. by age 60 y/o; M>F

Tubular
Tubulovillous
Villous

33
Q

Familial adenomatous polyposis is associated with which gene?

How many polyps exist as a teen?

What is the risk of cancer?

What is detected at birth that may cue a diagnosis?

A

APC gene

100-1000 polyps by teenage

Colorectal adenocarcinoma develops in 100% of cases that are untreated, often prior to 30 y/o, but always by age 50 y/o

Congenital hypertrophy of retinal pigment epithelium

34
Q

What is the peak age associated with colonic adenocarcinoma? In what case would diagnosis at a younger age be possible?

A

60-70 y/o. It is rare under 50 y/o unless HNPCC.

35
Q

What diet is associated with an increased rick for colon adenocarcinoma?

A

Low fiber
High refined carbs
High fat

36
Q

What has a protective effect in the development of colon adenocarcinoma?

A

NSAIDs or aspirin

37
Q

What are the 2 major pathways of colon adenocarcinoma development and how common is each?

A

Adenoma-carcinoma pathway (70-80%)

Microsatellite instability pathway - MSI (10-15%)

38
Q

What variant of FAP/polyposis syndrome is associated with congenital RPE hypertrophy?

Which variant is associated with osteomas, thyroid and desmoid tumors, skin cysts?

Which variant is associated with medulloblastoma and glioblastoma?

A

Congenital RPE hypertrophy - classic FAP

Osteomas, thyroid and desmoid tumors, skin cysts - Gardner syndrome

Medulloblastoma and glioblastoma - Turcot syndrome

39
Q

What are the age of presentation of the following:

Classic FAP
Attenuated FAP
Gardner syndrome
Turcot syndrome
MYH-associated
A 
Classic FAP: 10-15 y/o
Attenuated FAP: 40-50 y/o
Gardner syndrome: 10-15 y/o
Turcot syndrome: 10-15 y/o
MYH-associated: 30-50 y/o
40
Q

Familial adenomatous polyposis

Molecular defect
Target gene
Transmission (heredity)
Predominant sites
Histology
A 
Molecular defect: APC/Wnt pathway
Target gene: APC
Transmission (heredity): AD
Predominant sites: none
Histology: tubular and villous; typical adenocarcinoma
41
Q

Hereditary non-polyposis colorectal cancer (HNPCC)

Molecular defect
Target gene
Transmission (heredity)
Predominant sites
Histology
A 
Molecular defect; DNA mismatch repair
Target gene: MSH2, MSH1
Transmission (heredity): AD
Predominant sites: right side
Histology: sessile serrated; mucinous adenocarcinoma
42
Q

Sporadic colon cancer (70-80%)

Molecular defect
Target gene
Transmission (heredity)
Predominant sites
Histology
A 
Molecular defect: APC/Wnt pathway
Target gene: APC
Transmission (heredity): none
Predominant sites: left side
Histology: tubular, villous; typical adenocarcinoma
43
Q

What is = to Lynch syndrome?

It is the most common…

When do patients present?

A

HNPCC

Most common syndromic form of colorectal cancer (2-4% of all colorectal cancers)

Earlier than other forms

44
Q

What is the morphology of tumors in the proximal colon?

What is the morphology in the distal colon?

A

Proximal colon - polypoid, exophytic masses

Distal colon - tend to annular lesions

45
Q

What are symptoms of right-sided vs. left-sided colon cancers?

A

Right-sided: fatigue and weakness due to iron deficiency anemia

Left-sided: occult bleeding, changes in bowel habits, cramping, LLQ discomfort

46
Q

Is a screening colonoscopy useful for staging?

What are the 2 most important factors of colorectal cancers?

What is the survival rate at 5 years?

A

No

Depth of invasion and presence of LN mets

65% at 5 yrs

Gastrointestinal II Exam #1 (19 decks)

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