Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
29 Cards in this Set
- Front
- Back
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 |