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42 Cards in this Set

  • Front
  • Back
Hematochezia
Bright Red Stool
Usually associated as Distal GI Bleed or bleeding too quickly to not be broken down
Melana
Dark Stool
Digestion/Oxidation of hemoglobin
Upper GI Bleed or small amounts of blood
Congenital Anorectal malformations
Anorectal Agenesis
Rectal Atresia
Imperforate Anus
Anal Stenosis
Fistulas
Hirschsprung's Disease
-'Congenital Megacolon' or 'Congenital Aganglionosis'
-intestinal obstruction
-Constipation/Stenosis
-Rectal Biopsy
-Absence of Submucosal Enteric Ganglion Cells
-Compensatory HYPERTROPHY of non-enteric PSNS nerve fibers
-RET gene loss-of-function mutations
What is the most common Functional GI tract disorder?
Irritable Bowel Syndrome
-ROME III criteria (must present >3 months with symptoms)
-Bristol Stool Chart
-Unknown pathophys
Diverticulosis vs Diverticulitis... etiology?
-osis: d/t prolonged intralumenal pressure (low dietary fiber)
-itis: inflammation of the diverticula
Complications of Diverticulitis?
-can destroy/weaken wall of colon
-Abscess formation (contains neutrophils)
Location of diverticular disease?
can be all through GI tract but occurs mostly in the distal colon d/t the reabsorption of water --> hard stool forms --> pressure on wall of colon
Pseudomembranous colitis..presentation on colonoscopy?
mucosal surface is hyperemic and partially covered by YELLOW-GREEN EXUDATE
Most likely pathogen for Pseudomembranous Colitis?
C difficile (post Abx therapy when normal colonic flora is inhibited and C difficile can grow rapidly)
Inflammatory Bowel Disease has one vague overlying cause ....
-pronounced inflammatory process is occurring (persistent inappropriate immunologic response to GI lumenal Ag's)
Name of IBD where you cannot distinguish between Crohn's disease and Ulcerative colitis...
Indeterminant colitis
Major characteristics of Crohn's disease..
-very high C reactive protein levels
-anywhere within GI tract (mouth --> anus)
-Skip lesions
-'cobblestoning' mucosal pattern
-'creeping fat'
-NON-caseating granuloma with multinucleated giant cells
-Transmural inflammation (Full thickness of the gut wall)
-Perianal Fistulas
-Th1 cells are active
-'string sign' found by radiologist
-Nephrolithiasis may occur (along with other extra-intestinal manifestations)
-Colonic carcinoma is less of a risk than UC
Major characteristics of Ulcerative colitis..
-elevated C reactive protein (less severe than CD though)
-Begins at the Rectum and moves proximally (more definite location --> can tx surgically)
-continuous lesions
-smoking PREVENTS UC
-Partial thickness of gut wall
-Crypt Abscesses
-'lead pipe' (radiology)
-inflammatory pseudopolyps
-higher risk of colonic carcinoma!!! compared to CD
Which is more apt to have systemic inflammatory processes - UC or CD?
UC
Important aspect to Microscopic colitis?
It appears normally but if you look at microscopically --> increase in inflammatory cells
-Collagenous colitis
-Lymphocytis colitis
Are Sporadic (isolated) Juvenile Polyps malignant?
NO!
-most common childhood polyp
Does Hereditary Juvenile Polyposis Syndrome have a risk for GI carcinoma?
Yes!
Extra-GI manifestations of Cowden's disease?
Mucocutaneous Lesions
Extra-GI manifestations of Peutz-Jeghers polyposis?
Mucosal Pigmentation (on buccal mucosa, lips)
What do Cowden's disease and Peutz-Jeghers Polyposis have in common?
-have increased risk of malignancy (Cowden = breast, thyroid; Peutz-Jeghers = gastric, small intestines, CRC, pancreas, breast, lung, ovary)
-Autosomal Dominant
-pt < 15 yo at presentation (Peutz-Jeghers is 10-15 yo; Cowden's is <15 yo)
Characteristics of Hyperplastic Polyps..
-pts > 50 yo
-Asymptomatic
-do NOT grow and get larger
-usually benign with little malignant potential
-Hyperplastic + Adenomatous features = Serrated Adenoma
Tubular Adenoma
Neoplastic (benign, pre-invasive)

ROUND!

Lower risk of dev into invasive Adenocarcinoma
Villous Adenoma
Higher risk of developing into Invasive Adenocarcinoma

Large Villous Adenomas = Watery, Secretory Diarrhea
What is the genetic component to Familial Adenomatous Polyposis?
APC gene is inactivated
When is FAP usually diagnosed or found (with colonoscopy)?
10-20 yo

NOTE: when younger and family hx of FAP --> genetic testing for APC gene
Important aspect to FAP...
hundreds --> thousands of polyps form

Polyps themselves have malignant potential

May develop into malignancy by 30s-40s

Tx: prophylactic colectomy

1% of Colorectal Carcinomas = d/t FAP
Gardner's Syndrome =
FAP + osteomas, desmoid tumors
Turcot's Syndrome =
FAP + CNS tumors
HNPCC =
Hereditary Non-Polyposis Colon Cancer

5-15% of Colorectal Carcinomas = d/t HNPCC

Genetics = DNA mismatch repaid genes with MSI (microsatellite instability); MSH2 and MLH1

Lynch Syndrome
Adenocarcinoma sequence
-The accumulation of mutations is more important than their actual sequence

-APC Gene is mutated FIRST (birth or later in life) --> K-RAS --> p53
Where else is K-RAS gene effected (beyond Adenocarcinoma sequence)?
Pancreatic Ductal Carcinoma
Left-sided colon cancer..location/size/shape?
-nearer to rectum

-SMALLER (d/t smaller diameter of bowel wall)

-usually develops as a ring
Rigth-sided colon cancer..size/shape?
-LARGER (d/t larger bowel diameter size)

-Polypod shape
Which has more bleeding..left or right sided colon cancer?
Right-sided colon cancer has MORE bleeding --> pt can have Melana in feces and may develop Iron Def Anemia
Where do Left-sided colon cancers and Right-sided colon cancers metastasize to?
LIVER, Lungs, Brain, Bone
Three common forms of Anorectal Neoplasms?
Basaloid Carcinoma
Adenocarcinoma
Squamous Cell Carcinoma (HPV 16 and 18)
External Hemorrhoids
PAINFUL!

-Inferior Rectal Vein
Internal Hemorrhoids
PainLESS!

-Superior Rectal Vein

-may lead to External Thrombosis
Appendiceal Mucocele.. characteristics?
Dilated, mucin-filled Appendix

May be Mucinous Cystadenoma or Mucinous Cystadenocarcinoma (difficult to tell the difference)
Appendiceal Carcinoids
Neuroendocrine Tumor

TIP if Appendix

Good Prognosis
What can develop between Taenia coli?
Diverticula