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All the things > Last two sections of GI path (10.7 - 10.8) > Flashcards

Last two sections of GI path (10.7 - 10.8) Flashcards

1
Q

What disease is associated with an increased risk of Hirschsprung’s disease?

A

Down syndrome

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2
Q

What is Hirschsprung’s disease? What gene is mutated?

A

Denervation d/t loss of RET gene (which controls neural crest cell growth)

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3
Q

What is the nerve plexus between the inner circular layer, and outer longitudinal layer of the GI tract? What is the one in the submucosa? What is the function of each?

A
  • Myenteric plexus–peristalsis

- Submucosal plexus–secretion, absorption

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4
Q

What are the s/sx of Hirschsprung’s disease? (at birth, DRE findings, histological findings, and general)

A
  1. Failure to pass meconium
  2. Empty rectal vault on DRE
  3. Obstruction (with risk for rupture)
  4. Lack of ganglion cells on histology
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5
Q

What type of biopsy is needed to diagnose Hirschsprung? Why?

A

Rectal suction– need to grab the submucosa into the biopsy

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6
Q

What is the treatment for Hirschsprung’s disease?

A

Resection of the GI tract to tie together two areas that both have ganglion cells

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7
Q

Is a colonic diverticula a true or false diverticula? What does this mean?

A

It’s a false diverticula–only mucosa and submucosal involvement, not all layers as seen in true diverticula

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8
Q

What is the cause of colonic diverticula?

A

constipation and low fiber diet lead to increased pressure in the intestines, and thus weakening walls

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9
Q

What are the points in the colon that are particularly susceptible to diverticula formation?

A

Where the vasa recta traverse the muscularis mucosa

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10
Q

What is the most common part of the colon that has diverticula?

A

Sigmoid colon

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11
Q

What are the complications of of diverticulosis?

A
  • Diverticulitis
  • Hematochezia
  • Fistulas
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12
Q

What is the “classical” fistula that develops with colonic diverticula?

A

colovesical fistula

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13
Q

What is angiodysplasia? Where in the colon does this usually occur? Why?

A
  • Acquired malformation of mucosal and submucosal capillary beds
  • Usually arise in the cecum and right colon d/t high wall tension
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14
Q

What are the presenting symptoms of angiodysplasia?

A

Hematochezia in an older adult

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15
Q

What is the cause and inheritance pattern of hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu)?

A

AD disorder, resulting in thin-walled blood vessels, especially in the nasopharynx and GI tract

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16
Q

What is the most common site of damage in ischemic colitis? Why? What is the usual cause?

A
  • Splenic flexure (watershed area)

- Atherosclerosis of the SMA

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17
Q

Infarction of the bowel results in what s/sx?

A

Postprandial pain and bloody diarrhea

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18
Q

Why is there postprandial pain with ischemic colitis?

A

Increased energy demand of the intestines are not being met by increased blood flow

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19
Q

What irritable bowel syndrome (IBS)

A

Idiopathic relapsing abdominal pain with bloating, flatulence, and diarrhea / constipation

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20
Q

What are the s/sx of IBS? What classically improves the symptoms?

A
  • Relapsing abdominal pain with diarrhea/constipation.

- Pain is improved with defecation

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21
Q

In whom is IBS usually seen?

A

Middle aged females

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22
Q

What improves that symptoms of IBS? (2)

A
  • Defecation

- Increased dietary fiber

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23
Q

What are the pathological changes in IBS?

A

None seen

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24
Q

What are the two most common types of colonic polyps?

A

Hyperplastic and adenomatous

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25
Q

What are hyperplastic polyps? What are their histological characteristics?

A

Polyps that result from hyperplasia of the intestinal glands, characterized by ‘serrated’ appearance on microscopy

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26
Q

What is the potential for malignancy with hyperplastic polyps?

A

None–totally benign

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27
Q

Polyps with a “serrated” appearance on microscopy are of what type?

A

Hyperplastic polyps

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28
Q

What are adenomatous polyps? What is the malignancy potential for this?

A

-Neoplastic proliferation of glands that is benign, but has the potential to become malignant

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29
Q

What are the three steps of developing an adenocarcinoma polyp? (all genetic mutations)

A
  1. APC gene mutates
  2. KRAS gene mutates
  3. p53 damaged, with increased COX
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30
Q

What must happen to the APC gene for a polyp to develop? What chromosome is this gene on, and what does this do?

A
  • Both alleles must be knocked out
  • Chromosome 5
  • Tumor suppressor gene
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31
Q

What is the OTC drug that protects against carcinoma of the intestines? How?

A
  • ASA

- Inhibits COX, which is needed along with a p53 mutation to develop cancer

32
Q

What are the two tests that are done to screen for intestinal carcinoma?

A
  • Colonoscopy

- Fecal occult blood test (FOBT)

33
Q

What is the goal of colonoscopy?

A

Remove all the polyps and examine them microscopically

34
Q

What are the three factors that determine the risk of an adenoma becoming a adenocarcinoma? (size, growth pattern, histological pattern)

A
  • Size >2 cm
  • Sessile growth
  • Villous histology
35
Q

What is the sessile pattern of polyp growth? Pedunculated? Which has an increased risk for the development of CA?

A
  • Sessile = ball on epithelium (higher risk)

- Pedunculated = has a stalk

36
Q

What is the genetic cause of FAP? Signs? Natural history?

A
  • APC gene mutation (chr 5)
  • Tons on tons of polyps in the colon
  • Will develop CA by age 40
37
Q

What is the treatment for FAP?

A

Total colectomy

38
Q

What is Gardner syndrome?

A

FAP with fibromatosis and osteomas

39
Q

What is Turcot syndrome?

A

FAP with CNS tumors (medulloblastomas and glial tumors)

40
Q

What is a hamartoma?

A

Tumor of cells that are in the right place, but are disorganized

41
Q

What is Juvenile polyposis?

A

Sporadic hamartomatous polyps in children (benign), that presents as a solitary rectal polyp that prolapses and bleeds

42
Q

What can juvenile polyposis progress to? When would you worry about this?

A

Benign hamartomas in the intestines and stomach, that can progress to adenoCA

43
Q

—What is Peutz-Jeghers syndrome? How is this inherited?—-

A
  • –Hamartomatous polyps throughout the GI tract, as well as mucocutaneous hyperpigmentation on the lips.
  • AD—-
44
Q

What age does colorectal carcinomas usually present?

45
Q

What is the most common pathway through which colorectal carcinoma can arise? Second most common?

A
  1. Adenoma-carcinoma sequence

2. Microsatellite instability

46
Q

What are microsatellites? What causes instability?

A
  • Repeating, non-coding regions of DNA that are replicated in DNA replication
  • DNA repair mechanisms or copy mechanisms
47
Q

What is the cause of HNPCC? What are the increased cancer risks with this (3)?

A

Inherited mutation in the DNA mismatch repair enzymes, that leads to an increased risk for:

  • colorectal
  • ovarian
  • endometrial cancers
48
Q

What is unique about the development of carcinomas in HNPCC (hereditary non-polyposis colorectal carcinoma)?

A

No polyp forms, just CA over time

49
Q

What causes the increased risk for colorectal CA with UC?

A

Chronic inflammation

50
Q

What is the characteristic shape of colorectal CA in the left side of the colon? What causes this?

A

“Napkin ring” lesion caused by squeezing

51
Q

What are the s/sx of left sided carcinoma (3)

A
  • Pencil thin stools
  • Blood
  • LLQ pain
52
Q

How do right sided colorectal CA usually grow? S/sx (2)?

A

-Raised lesions

  • Fe deficiency anemia
  • Vague pain
53
Q

Why are obstructions less likely in the right side of the colon, as compared to the left?

A

More watery stools

Wider diameter

54
Q

Which side of the colon is usually associated with microsatellite instability? Adenoma-carcinoma pathway?

A 
Right = microsatellite
Left = adenoma-carcinoma
55
Q

There is an increased risk of endocarditis caused by what organism with colorectal CA?

A

Strep bovis (“bovis in the blood, cancer in the colon”)

56
Q

What are the parts of the TMN staging system of CA?

A 
T = depth of invasion
N = nodes
M = mets
57
Q

What is the most common site for mets from intestinal CA?

58
Q

What is the serum tumor marker for rectal CA? Is this useful for screening?

A
  • CEA

- Not useful for screening

59
Q

FAP with fibromatosis and osteomas = ?

A

Gardener’s syndrome

60
Q

FAP with CNS tumors (medulloblastomas and glial tumors) = ?

A

Turcot syndrome

61
Q

What are the 3 cancers that are associated with Peutz-Jueger’s syndrome?

A

-Colorectal, breast, and GYN CA

62
Q

What is the common suffix for H2 receptor antagonists?

A

“-dine” (e.g. ranitidine, cimetidine)

63
Q

What is the common suffix for PPIs?

A

“-prazole”, (e.g. omeprazole, lansoprazole)

64
Q

What is the MOA of bismuth?

A

Binds to ulcer base, provides physical protection and allowing HCO3 secretion to reestablish pH gradient in the mucous layer

65
Q

What is the MOA, use, and side effects of misoprostol?

A
  • PGE1 analog that increases production and secretion of gastric mucus barrier
  • Prevent NSAID-induced ulcers
  • Abortifacient
66
Q

What must always be screened for prior to administering misoprostol to a woman? Why?

A
  • Pregnancy

- Misoprostol is an abortifacient

67
Q

What is the MOA, use, and side effect of octreotide?

A
  • Somatostatin analog
  • Acute variceal bleeds, VIPomas, carcinoid tumors
  • Steatorrhea, n/v
68
Q

What abx should never be administered with CaCO3, or other antacids? Why?

A

Tetracyclines–these abx chelate metals

69
Q

What is MgOH used for?

70
Q

What metabolic abnormality can be caused by antacid use (hint: not alkalosis)

A

Hypokalemia

71
Q

What is the use of AlOH?

A

antidiarrheal

72
Q

What is the MOA, use, and side effect of infliximab?

A
  • Anti-TNF-alpha antibody
  • Crohn’s disease, ulcerative colitis, RA
  • Predisposes to infections
73
Q

What must always be screened for prior to administering infliximab? Why?

A
  • TB

- TNF-alpha needed to maintain granulomas. Thus infliximab will cause disseminated TB

74
Q

What is the MOA, use, and side effect of ondansetron (brand name zofran)?

A
  • 5HT3 inhibitor
  • Antiemetic
  • HA, constipation
75
Q

What is the MOA, use, and side effect of metoclopramide?

A
  • D2 receptor antagonist
  • Increases resting tone of intestinal muscle, and motility
  • Parkinsonian effects from blocking dopamine

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