Path - Small Intestine and Colon Flashcards
extraintestinal manifestations of juvenile polyposis
congenital malformations and digital clubbing
diffusely flattened (atrophic) villi w/ intraepithelial CD8 T cells and loss of mucosal and brush border surface
celiac dz
pathogenesis of graft vs host dz
donor T cells target antigens on recipient’s GI epithelial cells
sporadic colon cancer: typical or mucinous adenocarcinoma?
- 70-80% of cases
- 10-15% of cases
- 5-10% of cases
70-80%: typical
10-15%: mucinous
5-10%: mucinous
sx of adult celiac dz vs pediatric celiac dz vs non-classic pediatric celiac dz
adult: chronic diarrhea, bloating, fatigue, anemia
pediatric: chronic diarrhea, irritability, abd distension, anorexia, weight loss
non-classic pediatric: abd pain, n/v, bloating, constipation
target gene of familial adenomatous polyposis
APC
acanthocytic red cells (burr cells)
abetalipoproteinemia
presence of dense subepithelial collagen later, increased intraepithelial lymphocytes, and mixed inflammatory infiltrate
collagenous colitis
what is the defect(s) of nutrient absorption in chronic pancreatitis
intraluminal digestion
demographic IBS
b/w ages 20-40
strong female predominance
extraintestinal manifestations of classic familial adenomatous polyposis
congenital retinal pigmented epithelium hypertrophy
compare genetic factor contribution b/w crohn dz and ulcerative colitis
crohn dz: genetic factors are more dominant, 50% in monozygotic twins
UC: 15% in monozygotic twins
how does ulcerative colitis begin in the GI tract and subsequently travel
begins in the rectum and extends proximally in a continuous fashion to involve all or part of the colon
extraintestinal manifestations of gardner syndrome (familial adenomatous polyposis)
osteomas, thyroid and desmoid tumors, skin cysts
fibrous bridge b/w viscera of the intestines
adhesion
development of numerous mucosal lymphoid follicles
diversion colitis
when does abetalipoproteinemia present
in infancy
where are colonic adenocarcinomas distributed in the colon
approximately equal length over the entire length of colon
compare clinical features b/w right sided and left sided colorectal adnocarcinomas
right sided: fatigue and weakness due to iron deficiency anemia
left sided: occult bleeding, changes in bowel habits, cramping and LLQ abd pain
mesenteric fat extending around serosal surface (creeping fat)
crohn disease
diagnostic criteria for IBS
abd pain or discomfort at least 3 days per month over 3 months with improvement following defecation and change in stool frequency or form
inheritance pattern of MYH-associated polyposis
AR
sx of autoimmune enteropathy
severe, persistent diarrhea and autoimmune dz
age of presentation of juvenile polyposis
less than 5 y/o
two most important prognostic factors for colonic adenocarcinoma
- depth of invasion
2. presence of LN mets
hereditary nonpolyposis colorectal cancer: typical or mucinous adenocarcinoma?
mucinous
two types of microscopic colitis
collagenous colitis and lymphocytic colitis
familial adenomatous polyposis: typical or mucinous adenocarcinoma?
typical
inheritance pattern of hereditary nonpolyposis colorectal cancer
AD
compare location in the GI tract b/w crohn disease and ulcerative colitis
crohn: any area of GI tract, transmural
UC: limited to colon and rectum, only into mucosa and submucosa
physical effects to the intestine from crohn disease
fibrosing strictures, fistulae, perforations
diarrhea due to failure of nutrient absorption that is relieved by fasting
malabsorptive diarrhea
target gene of sporadic colon cancer
- 70-80% of cases
- 10-15% of cases
- 5-10% of cases
70-80%: APC
10-15%: MSH2, MLH1
5-10%: MLH1, BRAF
clinical features of microscopic colitis (both collagenous and lymphocytic)
chronic, nonbloody, watery diarrhea without weight loss
what is the defect(s) of nutrient absorption in disaccharidase deficiency
terminal digestion
describe the gliadin induced damage that occurs in celiac dz
gliadin peptides induce IL-15 expression –> activates CD8T cells that express NKG2D –> attack MIC-A receptor on enterocytes –> cause epithelial damage –> enhances passage of gliadin peptides into lamina propria –> peptides interact w/ HLA-DQ2 or D8 on APCs –> stimulates CD4 T cells –> more tissue damage
what is the defect(s) of nutrient absorption in whipple dz
lymphatic transport
NOD2 polymorphism
crohn disease
predominant site of familial adenomatous polyposis
none
permanent entrapment of bowel segment due to venous stasis and edema
incarcerated hernia
GI lesions in peutz-jeghers syndrome
arborizing polyps most commonly in the small intestine
define Tis, T1, T2, T3, and T4 in regards to classification of colorectal carcinomas
Tis: in situ dysplasia or intramucosal carcinoma
T1: invades submucosa
T2: invades into, but not through, muscularis propria
T3: invades through muscularis propria
T4: penetrates visceral peritoneum or invades adjacent organs
two types of IBD
crohn disease and ulcerative colitis
clinical sx of intestinal obstruction
abd distension, vomiting, pain, constipation, tympanic by percussion
define MX, M0, M1 in regards to classification of colorectal carcinoma distant mets
MX: distant mets cannot be assessed
M0: no distant mets
M1: distant mets
describe how fasting affects each type of diarrhea
secretory: persists
exudative: persists
osmotic: lessens (abates)
malabsorptive: stops
genetic defect:
SMAD4, BMPR1A, TGF-B signaling pathway
juvenile polyposis
genetic defect:
APC/WNT pathway
familial adenomatous polyposis (FAP)
pathogenesis of IBD
combined effects of:
- alterations in host interactions with intestinal microbiotica
- intestinal epithelial dysfunction
- aberrant mucosa immune responses
- altered composition of gut microbiome
extraintestinal manifestations of peutz-jeghers syndrome
pigmented macules, risk of colon, breast, lung, pancreatic, and thyroid CA
skip lesions
crohn disease