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T2 GI > MOD (more IBS/IBD etc stuff) > Flashcards

MOD (more IBS/IBD etc stuff) Flashcards

1
Q

Diff between acute and chronic colitis in terms of histo?

A

acute (NOT IBD)–straight crypts, normal bowel with neutros
chronic–distortion of normal architecture (not straight crypts), paneth cell dysplasia (usu only SI) and pseudopyloric metaplasia (int starts to look like stomach with branching crypts and mucinous glands), fibrosis

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2
Q

Cx of Chron’s?

site, what site is spared, what happens after resection, gross appearance, wall etc

A
  • commonly occurs at terminal ileum (w/ prox colon), spares rectum, but can affect any part of GI tract
  • can easily recur after resection
  • skip areas of inflammation, and transmural (entire wall) inflam
  • CHRONIC
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3
Q

Chron’s sx/complications

A

Pain, diarrhea or constipation, obstruction, dysplasia, carcinoma, perianal disease, and fistulas from transmural inflam
-can also lead to pydoerma gangrenosum, toxic megacolon, arthritis, spondy, oral ulcers, erythema nodosum

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4
Q

Chron’s pop?

A

teens-20s, and 50s-60s (same w/ UC!)

caucasian (same w/ UC)

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5
Q

More chron’s path/ histo/ gross/ complications

A
  • transmural inflammation with skip areas
  • mucosal crypt distortion and metaplasia
  • COULD have noncaseating granulomas
  • could have fissures and fistulas
  • fibrosis
  • creeping fat, neuronal hyperplasia
  • COBBLESTONING is common
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6
Q

Which cancer can occur from chron’s

A

adenocarcinoma of intestine (more likely to occur when more bowel is involved)

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7
Q

UC site involved?

A

COLON ONLY! (mucosa) (starts at rectum and moves up)

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8
Q

UC complications?

A

can have bloody diarrhea

-stricture and toxic megacolon

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9
Q

UC path/gross

A

continuous inflammation and diffuse discoloration and flattening of mucosa (ONLY inv mucosa!)

  • can also get basal plasmacytosis w branching crypts, and inflam pseudopolyps (continuous)
  • architectural distortion (sign of CHRONIC colitis)
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10
Q

What type of cancer is commonly involved in UC and what does it look like?

A

SIgnet ring cell adenocarcinoma

and mucinous

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11
Q

Chron’s vs UC anatomy

A

Chron’s: ileum and colon, skip lesions, thicc wall

UC: COLON ONLY, diffuse spread, thin wall

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12
Q

Chron’s vs UC histo

A

Chron’s: transmural inflam, deep ulcers/fissures, can have granulomas, can have fistulas, marked fibrosis

UC: mucasal inflam only, superficial ulcers, NO granulomas or fistulas, MILD fibrosis

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13
Q

IBS hallmarks?

A

abdominal pain and alterations of bowel fxn (const or diarr)

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14
Q

Rome III criteria

A

for IBS:
pain for at least 3 days a month in last 2 months, sx for 6 months total
-must have 2 of following: improve pain with defecation, change in freq of stool, change in appearance of stool
-v common!

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15
Q

IBS pop?
What plays a major role in IBS?
more ibs hallmarks?

A

v common in US, west europe. east asia, no socioeconomic assoc

  • often younger women
  • gut brain axis plays major role (enhanced perception of pain, hypersensitivity, altered motility)
  • prolonged gastrocolic reflex (takes longer to expel after eating)
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16
Q

What other dis is IBS linked to

A

noncardiac chest pain, fatigue, fibro etc

-may also have sx that mimic IBD, psychosocial issues

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17
Q

Role of serotonin in IBS?

A

enterochrom cells rel serotonin, goes to myenteric plexus and stim peristalsis, leaky gut, microbiome
-ACh and NO may also mediate motility, tachys and bradys may also mediate visceral sensitivity

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18
Q

red flags that may be alternative to IBS?

A

anemia, weight loss, lots of blood (eg test for celiacs etc)

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19
Q

IBS tx?

A

biofeedback, therapy, diet, tricyclics and antispasmotics to relax GI, antiflat/dig enz, antidiarrh, probiots, fiber, lax, cl channel agents

20
Q

Ischemic bowel disease and sx?

A

decreased blood flow to intestine, an cause occulsion of mesenteric aa resulting in acute onset abd pain and ELEVATED LACTIC ACID

21
Q

levels of ischemic dmg?

A

mucosal, mural (mucosal/submucosa), and transmural

as size of bv gets larger, injury goes deeper

22
Q

what is chronic ischemia often due to?

acute?

A

atherosclerosis, 2+ major arteries injured

-acute: thrombus or clot, quick onset and high lactic acid/ bloody stool, transmural

23
Q

How does vascular ischemia progression appear gross/histo?

A

congested dusky red tissue
micro-submuc edema, ecchymosis, hemorr, thickening, then lose distinctino of muscle layers and get blood in lumen (maybe gangrene), erosion of mucosa, ischemic dmg with crypts reduced, lots of red
-may see black/purple tissue from infarct among scope examination (dont want to risk perforation)

24
Q

Histo of ischemic dmg

A

erosion of mucosa, fibrosis, ischemic dmg, cr

25
Q

3 main categories of causes of malabsorption?

A

Secretory insufficiency, imparied motility, and impaired mucosal function!

26
Q

causes of secretory insuff in malabs?

A

biliary obstruction, and pancreatic enz insuff (eg alc, CF)

27
Q

causes of impaired motility in malabs?

A

diab neurop, amyloidosis and scleroderma, also BLIND LOOP sydnrome (section of SI doesnt have normal digestive flow usu from surgery)

28
Q

causes of impaired mucosal fxn in malabs?

A

from short bowel syndrome, sprue (blunting of villi), lymphomas, inflamm disease eg chrons, whipple dis

29
Q

Which dis result in villous atrophy?

A 
celiac sprue (diffuse atrophy)
bacterial overgrowth (patchy atrophy)
infectious gastroenteritis (patchy)
tropical sprue (usu bacterial) (entire SI)
kwashiorkor (protein deficiency)
30
Q

Celiac

  • what can it lead to
  • histo
  • dx
A

ANEMIA, FLAT VILLI, IgA/HLA dx

  • can lead to anemia and iron/folate/b12 def, compl include primary T cell lympoma, ulceration of SI, collagenous sprue
  • flat villi and more lymphos, elong crypts
  • serology for IgA, gen test for HLA markers etc
31
Q 
Whipples disease
cause?
sx?
pop?
histo?
A

rare bacterial sys infxn that affects intestine, cns and joints

  • eg middle aged white male with fever, malabs, weight loss, arthirits, and lymphadenopathy (from tropheryma whippelii)
  • histo: extension of lamina propria by foamy macros, PAS positive granules, rod shaped bacilli
32
Q

What genetic changes can change adenomas to adenocarcinomas in SI?

A

multi hit theory

ras, 5q21, los of 18q or tsg p53 etc

33
Q

Adenomatous polyps (adenoma)

A

benign but can become cancer

slow, can be tubular or villous (fingerlike projections, but rare) or both

34
Q

Serrated polyps?

A

adenoma with sawtooth pattern due to infolding/shark tooth, crypts lined w goblet cells, uniform glands mostly parallel)
-serrated polyps can be hyperplastic polyps (no malig) or serrated adenomas (with epith dysreg, can lead to microsatellite instability which can be seen in Lynch synd) (disorg nonuniform glands w pinkish mucus)

35
Q

when is a tumor considered malig?

A

when it goes into submucosa (past mucosa) and penetrates BM

36
Q

carcinoma in situ?

A

not malig, high grade dysplasia, stays in epith or extends into lamina prop (in mucus)

37
Q

colon risks prevention

A

smoking, alc, red meat maybe, obesity and sendentary, AA, IBD, fHx
-prevent wiht fruits/veg, Ca/dairy, high fiber, whole grains etc, colonoscopy at 45 yo

38
Q

screening/testing for colon cancer>

A

AA age 45

  • fecal IHC test to detect abs to hb (better than fecal guiac)
  • colonoscopy and snip out polyp
39
Q

how do colon adenocarcinomas appear in right vs left colon

A

right (cecum etc)–polypoid, fungating lesion w raised edge (fewer sx than left)
-left: annular napkin ring lesion with heaped up edge (can have iron def anemia from GI bleeding)

40
Q

adenocarcinoma general appearance? sx? results? assoc with Lynch synd?

A

-both can get central necrosis, usu well-diff, but CAN be poorly sometimes (mucinous, signet ring tumors, of which are assoc with Lynch synd)

41
Q

What are ~6 sx assoc with colon cancers? Which one is AR?

A 
Lynch syndrome
FAP (fam adenoma polyposis)
MYH polyposis [AR!]
Puetz-Jegher's syndrome
Juvenile polyposis syndrome
Appendicular tumors
42
Q 
Lynch syndrome 
genetics/dysfxnl genes?
MSI?
appearance?
site?
assocs?
Tx?
best testing/prevention?
A
  • AD, dysfxn with mismatch repair prot, allowing small errors to accum (microsat instability, most occur in MSH2 and MLH1 genes, some others)
  • RIGHT colon
  • signet ring or mucinous (atypical adenocarc)
  • avg age dx 45
  • MSI testing, but IHC best bc dir tests for MMR expression, colonoscopy 10 yr earlier than age of dx of family hx, may req SUBTOTAL colonectomy maybe hysterect
43
Q 
FAP
genetics
assoc
attenuated FAP
tx/prevention?
A

thousands of small polyps throughout colon

  • mutation of APC gene
  • assoc with duod adenocarc and congen hypertrophy of retinal pigmented epith, duod/periamp/amp adenomas
  • Attenuated FAB if mtuation on side of gene, toned down with <100
  • polyps, later in life but colon cancer still likely
  • kids should get sigmoidoscopy, thyroid ultrasounds bc risk of thyroid dis, may req total proctoectomy (w rectum) (atten is subtotal)
44
Q

Puetz Jegher

A

mutation STK11, pigmented spots on lips/buccal mucosa (hallmark!)

45
Q

Juvenile polyposis sydnrome

A

AD, germline mutations in transformaing growth factor beta signaling path

46
Q

appendicular tumors

A

v rare, mostly carcinoid which can lead to carcinoid (serotonin) syndrome, which looks like red sweaty asthmatic

47
Q

Size of appendicular tumors that have risk of metastasis

A

2 cm

T2 GI (6 decks)

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