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29 Cards in this Set

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GI System- Path of the colon, anus, by Leonard
GI System- Path of the colon, anus, by Leonard
Anorectal Malformations
Relatively common; 1 : 5,000 live births

Maldevelopment of dorsal portion of hindgut (cloacal cavity) and urorectal septum

Anorectal agenesis and rectal atresia

Imperforate anus (common): Opening to the anus absent or structurally obstructed
Rectum may end in blind sac or connect to urethra, urinary bladder, vagina, scrotum

Anal stenosis

Fistulas: Aberrant connections between urinary bladder, urethra, vagina, skin
Hirschsprung’s Disease is also called what? it's common in what other disorder? what causes it?
Congenital aganglionosis; congenital megacolon
-Absence of parasympathetic neuronal cell bodies (ganglion cells) of the enteric ganglia
--Neurons of the submucosal (Meissner’s) and *myenteric (Auerbach’s) plexus
--Failure of normal caudal migration of enteric neurons produces aganglionic segment
--Familial and sporadic cases related to *RET gene loss-of-function mutations
---RET gene: receptor tyrosine kinase, plays crucial role in neural crest development
--Common in Trisomy 21
What is the most common congenital cause of intestinal obstruction?
Hirschspring's Disease:
-Results in chronically contracted muscularis
--Stenosis and constipation: newborns with failure to pass meconium and vomiting
--Dilation of proximal (“upstream”) uninvolved segment of bowel
Involves variable lengths of the bowel
--Rectum, left colon, entire colon
Diagnosis based upon (suction) rectal biopsy
--Absence of submucosal enteric ganglion cells with compensatory hypertrophy of non-enteric parasympathetic nerve fibers that normally innervate the enteric ganglion cells

**want to see absence of ganglion cells and hypertrophy of nerve fibers
What is the most common functional GI disorder?
Irritable bowel syndrome (IBS)

-Most common functional GI disorder (~ 12% of primary care clinic visits)
-Dx “criteria”
--Absence of identifiable structural abnormalities on Dx evaluation
--Rome III Diagnostic Criteria
--Rule out “alarm symptoms” (e.g., anemia, + FOB, wt. loss)

-Chronic episodic abdominal discomfort with altered bowel function
--Abnormal stool frequency +/or form/composition (Bristol Stool Chart)
Pathology of IBS,
Pathophysiology remains unclear
-Altered GI sensation (visceral hypersensitivity)
-Altered GI motility (motor function)
-Dysregulation of brain-gut interactions
--Autonomic nervous system dysfunction
--Hypothalamic-pituitary-adrenal axis
-Multifactorial

OMT and IBS
“Ripe” for clinical studies and treatment approaches
This article is interesting and compelling
Name the Inflammatory and Infectious Disorders
1. Diverticular disease (Diverticulosis → diverticulitis)
2. Pseudomembranous colitis
3. Inflammatory bowel disease (IBD) **we see lots of neutrophils in CD, UC
--Crohn’s disease (CD)
--Ulcerative colitis (UC)
--Microscopic colitis (Collagenous colitis, Lymphocytic colitis)
Where do you find diverticulosis? what is the pathology? where does it happen most often? is it always symptomatic?
Diverticulosis
-Acquired herniations of mucosa/submucosa into muscularis propria (muscularis externa)
--Actually are pseudodiverticula
--Located between taenia coli (outer longitudinal layer of muscularis propria)
---Sites of penetrating nutrient blood vessels surrounded by collagen
-Surrounding muscular wall is hypertrophied

Pathogenesis: Prolonged increased intraluminal pressure (Lack of adequate fiber)
-Most often affects sigmoid colon
-Asymptomatic in majority of cases (~ 80%)
--Flatulence; Inflammation from retained fecal material (~ 10-20%)
Diverticulitis..what is happening? sxs, and tx?
Inflammation of diverticula:
-Inflammatory infiltrate is destructive and weakens wall
--Abscess
--Perforation → peritonitis and possibly sepsis
--Fistulas between colon and adjacent structures(e.g., urinary bladder, segment of bowel, vagina, skin)

Sx’s and signs: abdominal pain, ∆ in bowel habits, dysuria, fever, blood per rectum; leukocytosis, palpable mass, + FOB

Tx: Abx, supportive care, surgery
Pseudomembranous Colitis key feature? pathogenesis?
Inflammatory process characterized by “paper-like” (plaque) exudate coating the mucosal surface

Pathogenesis:
*Clostridium difficile
Neonatal enterocolitis or in older adults following antibiotic therapy that disrupts normal colonic flora
Toxins damage mucosa (can detect C. diff. toxins in stool sample)

Signs & Sx’s: Diarrhea, fever, leukocytosis, abdominal cramps
Irritable Bowel Disease is due to what?
Spectrum of chronic inflammatory intestinal diseases, the etiology of which remains unclear
-*Persistent inappropriate immunologic response to GI luminal antigens … BUT
--Exclude TB, Yersinia infection, NSAID use in CD
--Exclude C. difficile, Campylobacter, Shigella, Salmonella infection, NSAID use, and ischemia in UC

Relatively common
~ 7: 100,000 CD (incidence)
~ 11: 100,000 UC (incidence)
Crohn's Disease... where does it affect you? continuous?

what do you see on radiography?

what type of inflammations? full thickness?
-Mouth-to-anus; discontinuous (skip lesions); strictures (thickened bowel wall/fibrosis); linear ulcers & “cobblestoning”; “creeping fat”

Radiography: “string sign” from narrowed lumen

Granulomatous inflammation:
-~ 50% have **noncaseating granulomas with multinucleated giant cells (pathognomonic); crypt abscesses (more common in UC)
-Transmural inflammation (full-thickness); Paneth cell metaplasia in left colon; mucosal aphthous ulcers
Ulcerative Colitis.. continuous? where does it happen? what does the mucosa look like? full thickness? radiography appearance?
Continuous lesions (ulcers, hemorrhagic inflammation) affecting the colon
-Rectum and extends proximally
-Mucosa and submucosa (NOT full-thickness)
---Lack granulomas
---Mucosa is “friable” (easily falls apart) and hemorrhagic

Flattened mucosa (absence of colonic haustra); wall is thin
--Radiography: “lead pipe” appearance; megacolon (toxic)

With prolonged inflammation, develop inflammatory *pseudopolyps; crypt abscesses

**primary sclerosing cholangitis involving intrahepatic biliary tree
smoking and CD vs UC...labs...complications
increases the risk of crohn's disease but protects for ulcerative colitis


also, in labs, the CRP is elevated in both CD and UC, but it's elevated more in CD

p-ANCA: neg in CD, pos in UC
ASCA: post in CD, neg in ASCA

UC: Epithelial dysplasia and adenocarcinoma (signif risk of development)
When you cannot distinguish CD and UC, you can call this IBD...
Indeterminate Colitis

~ 10-15% of cases of IBD
Cannot distinguish between CD and UC
CD and UC may likely represent distinct disorders along a spectrum of IBD
What are polyps?
Aberrant cellular proliferations that form mucosal outgrowths, often with a stalk (like a little tree)

Hamartomatous:
-Abnormal proliferations/arrangements of normal tissue constituents (epithelium, smooth muscle)

Epithelial proliferations:
-Non-neoplastic (Hyperplastic)
-Neoplastic (Dysplastic; Malignant (adenocarcinoma))
Hamartomatous Polyps

which have risk for malignancy?

what is the most common childhood polyp?
Typically part of a syndrome
-Constellation of structural and functional abnormalities
--Incorporate both epithelial and stromal components
-Most often are isolated, but can occur as part of a polyposis syndrome (multiple polyps)

Juvenile polyposis syndromeS:
-Variable inheritance
-Mixture of adenomatous and nonadenomatous features
-Increased risk of GI carcinoma

Juvenile (retention) polyp:
-usually sporadic and single or few (not part of a syndrome) – most common childhood polyp; not thought to have malignant potential
Cowden’s syndrome

vs

Peutz-Jeghers polyposis
Cowden’s syndrome:
-Autosomal dominant
--Colorectal polyps, but hamartomas of all three germ layers
--Mucocutaneous lesions: tricholemmomas, oral mucosal papillomas, acral keratoses
-*Increased risk of malignancy (thyroid, breast), but NOT in colorectal polyps (these are benign)

Peutz-Jeghers polyposis:
-Autosomal dominant, usually Dx’d in 20’s
-Polyps throughout GI tract: Small bowel > colon or stomach
-Mucosal pigmentation: buccal mucosa, lips
-Increased risk of malignancies: gastric, small bowel, colorectal, pancreas, breast, lung, ovary
adenoma, by definition, is neoplastic
there's at least low grade dysplasia
Describe Non-neoplastic vs neoplastic (benign vs invasive) proliferations
Non-neoplastic: Hyperplastic (hyperplastic polyps)
Neoplastic:
Benign, pre-invasive
-Adenomas (Tubular, Villous, Tubulovillous)
-Grade the dysplasia: low-grade or high-grade

Invasive carcinoma
-Determine depth of invasion
--Intramucosal (Tis: a form of carcinoma in situ – invades only into lamina propria, not beyond the muscularis mucosa)
--Deeper invasion: submucosa (T1); into muscularis propria (T2); through muscularis propria into subserosa (T3); invades adjacent structures or penetrates visceral peritoneum (T4)
Hyperplastic Polyps. who gets them? from where? what do they look like? high malignant potential?
Typically in people > 50 yo
-Present in 30-85% normal individuals (Much more common in “Western world”)
-Asymptomatic; Typically do not enlarge;

Minimal malignant potential:
-Presence does not suggest need for closer surveillance
-BUT: hyperplastic features may be combined with adenomatous features → **serrated adenoma
Hyperplastic polyps > 1 cm MAY develop into sessile serrated adenomas that could progress to carcinoma
Neoplastic Polyps: Adenomas
-**All adenomas, by definition, exhibit at least low-grade dysplasia and are neoplastic

-Adenomas are common and typically asymptomatic
--Prevalence increases with age
---By 50 yo, ~ 12% of people have adenomas
---~ 25% of these are considered high-risk lesions (Large adenomas, high-grade dysplasia)
---Strongly influenced by family history and “nutritional factors”
Tubular vs Villous Adenoma
Villous adenomas, compared to tubular adenomas, pose a greater risk of developing adenocarcinoma.

Large villous adenomas can be associated with watery (secretory) diarrhea.
Familial Adenomatous Polyposis (FAP): this is not hamartomatous.

pathogenesis

Gardner's syndrome and Turcot's syndrome
Autosomal dominant
Polyps can be Dx’d in 1st or 2nd decade of life

Pathogenesis: inactivation of adenomatous polyposis coli (*APC) tumor suppressor gene
-Hundreds of adenomas, with malignant transformation in 30’s or 40’s (Prophylactic colectomy)

Gardner’s syndrome (AD) polyposis with osteomas and desmoid tumors

Turcot’s syndrome (AR) polyposis with CNS tumors
Colorectal Carcinoma (CRC). vast majority are what?

how does it rank as a form of cancer and cause of death?
-98% are adenocarcinoma
-3rd leading form of cancer and 3rd leading cause of cancer death
-Vast majority thought to arise from pre-existing adenomatous lesions
--Adenocarcinoma sequence (“Vogelgram”)
---APC → RAS → p53

~ 5-15% due to mutations in or loss of expression of DNA mismatch repair genes
~ 1% due to FAP
Hereditary Nonpolyposis Colon Cancer (HNPCC) aka Lynch Syndrome
-~ 5% of all CRC
-Dx based on Amsterdam Criteria (see notes on slide)
-Germline mutations in DNA mismatch repair genes: microsatellite instability (MSI)
--Seen in almost all cases of HNPCC but only ~ 15% of sporadic cases
--If MSI is present, strongly suggestive of hereditary cancer syndrome
--MLH1, MSH2
Compare left-sided and right-sided CRC.

where are there metastases?
Left-sided CRC:
-Bowel diameter smaller: tend to obstruct
--Change in bowel habits +/- bleeding
-Streptococcus bovis endocarditis (in UC as well)

Right-sided CRC:
-Tumors tend to be larger (larger diameter bowel), more polypoid
--Greater tendency for more substantial bleeding (Iron-deficiency anemia)

Metastases:
Liver, lungs, brain, bone
Anorectal Diseases: hemorrhoids and neoplasms
Hemorrhoids:
-Internal (superior plexus, above pectinate line):Bleeding, painless
-External (inferior plexus, below pectinate line): Painful thrombosis

Neoplasms (anus has squamous, transitional, and glandular epithelium)
-More common above the pectinate line
--Basaloid carcinoma (cloacogenic, epidermoid)
--Adenocarcinoma
-Squamous cell carcinoma (HPV 16 & 18 association)
-Verrucous carcinoma; giant condylmona acuminatum
Appendix things...

carcinoid tumor is a___

mucoceles are neoplastic? can be associated with what?
Appendicitis:
-Complications: peritonitis

Neoplasms:
1. *Carcinoid (neuroendocrine tumor, NET)
--Most often incidental findings at time of appendectomy for presumed appendicitis
--Located at the tip; typically good prognosis
2. *Mucocele: dilate, mucin-filled appendix
--*Non-neoplastic, obstructed appendix
--Mucinous *cystadenoma or *cystadenocarcinoma
3. *Pseudomyxoma peritonei
--Mucinous neoplasm erodes through the appendiceal wall and mucinous tumor implants throughout peritoneum – ovaries
---Confused with primary ovarian mucinous neoplasm