Chapter 17 part 8 Flashcards

1
Q

Crohn Disease Morphology–areas involved

A
  • involves small intestine alone in 40% of cases
  • small intestine and colon in 30%
  • other areas uncommon
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2
Q

Crohns disease–Gross Morphology

A
  • Skip lesions
  • Punched out mucosal aphthous ulcers
  • cobblestone appearance
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3
Q

Skip lesions in Crohns Disease

A

-separate, sharply delineated disease areas with granular and inflamed serosa and adherent “creeping” mesenteric fat; the bowel wall is thick and rubbery and often strictured

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4
Q

Punched out mucosal pathos ulcers in Crohn’s disease

A

-coalescing into axially oriented serpentine ulcers

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5
Q

Cobblestone appearance in Crohn’s disease

A
  • Sparing of interspersed mucosa gives a cobblestone appearance with diseased tissue depressed relative to normal mucosa
  • fissures and fistula tracts are also common
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6
Q

Microscopic morphology of Crohn’s Disease

A
  • Mucosal inflammation and ulceration with intraepithelial neutrophils and crypt abscesses
  • Chronic mucosal damage with villus blunting, atrophy, pseudopyloric or Paneth cell metaplasia and architectural disarray
  • Transmural inflammation with lymphoid aggregates in submucosa, muscle wall, and subserosal fat
  • Noncaseating granulomas throughout the gut, even in uninvolved segments (but only seen in 35% of patients)
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7
Q

S/S of CD

A
  • intermittent attacks of diarrhea, fever, and abdominal pain
  • asymptomatic periods last for weeks to months
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8
Q

Extensive CD can lead to?

A

-malabsorption and malnutrition, loss of albumin (protein-losing enteropathy), iron-losing enteropathy, iron deficiency anemia and/or vitamin B12 deficiency

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9
Q

Tx for Crohn’s Disease

A
  • Fibrotic strictures or fistulas to adjacent viscera, abdominal and perineal skin, bladder or vagina require surgical resection
  • disease often recurs at the anastomosis with 40% of patients requiring additional surgery within a decade
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10
Q

Extra intestinal manifestation for Crohn’s Disease

A
  • migratory polyarthritis
  • sacroilitis
  • ankylosing spondylitis
  • erythema nodosum
  • uveitis
  • cholangitis
  • amyloidosis
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11
Q

Crohn’s disease increases the risk for?

A

-colonic adenocarcinoma in patients with long-standing colon involvement

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12
Q

Potent therapeutic option for Crohn’s disease

A

-Anti-TNF Abs!!

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13
Q

Ulcerative Colitis

A
  • disease of continuity with no skip lesions
  • involves rectum and extending proximally in retrograde fashion to involve the entire colon (pan colitis)
  • distal ileum may also show some inflammation (backwash ileitis)
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14
Q

Gross morphology of Ulcerative colitis

A
  • Mucosa is reddened, granular, and friable with inflammatory pseudo polyps and easy bleeding
  • can be extensive ulceration or atrophic and flattened mucosa
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15
Q

Microscopic morphology of Ulcerative colitis

A
  • Mucosal inflammation is similar to CD but generally limited to mucosa
  • crypt abscesses, ulceration, chronic mucosal damage, glandular architectural distortion, and atrophy but no fissures, aphthous ulcers, or granulomas
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16
Q

Clinical features of Ulcerative colitis

A
  • present with intermittent attacks of blood mucoid diarrhea and abdominal pain that can persist for days to months before subsiding
  • half have mild disease, but most will relapse within 10 years and up to 30% require colectomy within 3 years to control symptoms
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17
Q

Extra intestinal manifestations of Ulcerative colitis

A
  • migratory polyarthritis
  • sacroiliitis
  • ankylosing spondylitis
  • uveitis
  • cholangitis (up to 7.5% of patients) and skin lesions
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18
Q

UC increases the risk for?

A

-colonic adenocarcinoma

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19
Q

Colitis associated Neoplasia–risk of malignancy in IBD

A
  • Increases sharply 8-10 yrs after disease onset
  • greater with pan colitis vs. left sided only disease
  • Increases with severity and duration of active inflammation
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20
Q

Patients with long standing disease of UC are followed by

A
  • biopsy surveillance

- dysplasia is classified histologically as low or high grade and can be multifocal

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21
Q

Other causes of chronic colitis

A
  • Diversion colitis

- Microscopic colitis

22
Q

Diversion colitis

A
  • occurs in blind distal colonic segment created after surgery diverts fecal stream to an ostomy site
  • lack of short-chain fatty acids and other nutrients, and changes in the flora
  • mucosal erythema and friability with lymphoplasmacytic inflammation and a characteristic lymphoid follicular hyperplasia
23
Q

Microscopic Colitis

A
  • middle aged women
  • present as chronic watery diarrhea with abdominal pain
  • Endoscopic findings are grossly normal (“microscopic”)
  • 2 forms: Collagenous colitis and Lymphocytic colitis
24
Q

Microscopic Colitis–Collagenous colitis

A

-dense submucosal bandlike collagen with mixed inflammation in lamina propria

25
Q

Microscopic Colitis–Lymphocytic colitis

A
  • prominent intraepithelial infiltrate of lymphocytes without the sandlike collagen
  • associated with autoimmune diseases and sprue
26
Q

Graft vs. Host Disease

A

-occurs following hematopoietic stem cell transplantation due to donor T cells targeting Ags on the recipient’s GI epithelial cells

27
Q

GVHD presentation and hits

A
  • watery diarrhea but may become bloody in severe cases
  • small bowel and colon are involved in most cases
  • most common histo finding: Epithelial apoptosis, particularly of crypt cells!!!
28
Q

Sigmoid Diverticular Disease

A

-acquired colonic pseudodiverticular outpouchings (diverticulosis)=uncommon in pts younger than age 30 but occur in 50% of Western population older than 60

29
Q

Pathogenesis of Sigmoid Diverticular Disease

A

-Focal bowel wall weakness (at sites of penetrating blood vessels) allows mucosal out pouching when there is increased intraluminal pressure (e.g., with constipation and exaggerated peristaltic contractions)

30
Q

Morphology of Sigmoid Diverticular disease

A
  • Multiple flashlike outpouchings, 0.5 to 1 cm in diameter=more common in distal colon
  • occur where vasculature penetrates the inner circular layer of muscular propria at taeniae coli
  • diverticulum wall is lined by mucosa and submucosa without significant muscular propria, although muscular bw diverticula is hypertrophic
  • Obstruction of diverticula leads to inflammation producing DIVERTICULITIS–can perforate with tissue damage and increased pressure
31
Q

Clinical features of Sigmoid Diverticular Disease

A
  • Usually asymptomatic but associated with cramping, abdominal discomfort, and constipation
  • can result in pericolic abscesses, sinus tracts and peritonitis
  • Even without perforation, can cause fibrotic thickening and stricture formation
32
Q

Polyps

A

-Masses that protrude into the gut lumen can be pedunculated or sessile and can be non-neoplastic or neoplastic

33
Q

Types of polyps

A
  • Hyperplastic polyps
  • Inflammatory Polyps
  • Hamartomatous polyps
  • Neoplastic polyps
  • Adenomatous polyposis
34
Q

Hyperplastic polyps

A
  • result from decreased epithelial turnover with delayed shedding
  • have no malignant potential
  • usually less than 5mm and are composed of well-formed mature, albeit crowded, glands
35
Q

Inflammatory polyps

A
  • result from recurrent cycles of injury and healing
  • see lamina propria fibromuscular hyperplasia, mixed inflammatory cell infiltrates, and mucosal erosion and/or hyperplasia
36
Q

Hamartomatous polyps

A
  • tumorlike growths of tissues normally present at the site
  • occur in setting of many genetic or acquired syndromes:
  • Juvenile polyps
  • Juvenile polyposis syndrome
  • Peutz-Jeghers syndrome
37
Q

Juvenile polyps

A
  • focal hamartomatous malformations of small intestine and colon mucosa
  • most occur in children<5 years and involve rectum
  • SINGLE, large (1-3 cm) rounded and pedunculated with mystically dilated glands and abundant lamina propria
38
Q

Mutations associated with juvenile polyps

A

-SMAD4 and BMPR1A genes involved in TGF-B signaling

39
Q

Juvenile polyposis syndrome

A
  • rare autosomal dominant disorder–up to 100 hamartomatous polyps
  • may require colectomy to limit bleeding due to polyp ulceration and pulmonary arteriovenous malformations are known extra intestinal manifestations
  • also an increased risk o bowel malignancy–30% to 50% will develop adenocarcinoma by age 45
40
Q

Peutz-Jeghers syndrome

A
  • rare autosomal dominant syndrome
  • median age of onset=11
  • associated with multiple GI hamartomatous polyps and mucocutaneous hyperpigmentation
41
Q

Peutz-Jeghers syndrome–genetic associations

A

-In half of patients, there is a heterozygous LoF mutation in the LKB1/STK11 gene encoding a kinase that regulates cell polarization and growth

42
Q

What are the polyps like in Peutz-Jeghers syndrome?

A
  • order=small bowel>colon and stomach
  • large, pedunculated and lobulated with arborizing smooth muscle surrounding normal abundant glands
  • can initiate intussusception
  • Hyperpigmentation takes the form of molecules around mouth, eyes, nostrils, buccal mucosa, palms, and genital and perianal regions
43
Q

Peutz-Jeghers syndrome–pt has increased risk for what?

A

-several cancers including colon, pancreas, breast, lung, gonads, and uterus

44
Q

Neoplastic polyps–colonic adenomas

A
  • benign polyp precursors to majority of colorectal carcinomas
  • Epithelial dysplasia!!
  • 50% incidence by age 50 but majority do NOT progress to malignancy
  • Most are clinically silent but large ones can cause anemia and potassium loss causes hypoproteinemic hypokalemia
45
Q

Neoplastic lesions–risk of malignancy

A
  • correlated to size

- polyps >4cm have 40% risk harboring cancer and severity of dysplasia

46
Q

Morphology of adenomas

A
  • range from 0.3 to 10 cm
  • can be pedunculated or sessile
  • Dysplastic changes include hyperplasia, nuclear hyperchromasia and loss of polarity
47
Q

Adenomas–classification

A
  • classified based on architecture
  • tubular, tubulovillous and villous
  • have little clinical significance though
48
Q

Sessile serrated adenomas

A
  • full gland length exhibits serrated architecture; despite malignant potential
  • do not have typical dysplastic changes seen in other adenomas
49
Q

Intramucosal carcinoma

A
  • occurs when dysplastic cells invade lamina propria or muscluaris mucosa
  • little metastatic potential because colonic mucosa lacks lymphatic channels
50
Q

Polyps with invasive adenocarcinoma

A

-malignant with metastatic potential bc have crossed into submucosa and can access lymphatics