Small/Large Intestine 2 Flashcards
(33 cards)
True vs pseudo diverticulum
true-all three wall layers (meckel’s)
false-only mucosa and submucosa
Diverticulosis
- many diverticuli, usually in the sigmoid colon where vasa recta perforate colon
- 50% >60 y.o
- associated with low fiber diet
- symptoms: vague discomfort, feeling of incomplete emptying
Diverticulitis
Inflammation of diverticula
- LLQ pain, fever, leukocytosis
- may perforate-peritonitis, abscess formation, pneumaturia
Hernias
serosal lined outpouching of peritoneum
- loop of intestines becomes trapped within hernia sac
- bowel compressed twisted in the mouth of heria, compromising blood supply-infarction-strangulation
Ischemic bowel disease
Symptoms: -sudden severe abdominal pain -tenderness -bloody diarrhea, melanotic stools More severe injury: shock, sepsis, death
Causes: Acute arterial occlusion -Atherosclerosis -Aortic aneurysm -Hypercoagulable state -Oral Contraceptive use -Embolization of cardiac vegetations Other intestinal hypoperfusion: -cardiac failure -shock dehydration -vasoconstrictive drugs
Pathogenesis:
hypoxic injury
reperfusion injury
Variable degree of injury
-severity of vascular compromise
length of time of injury
-vessels affected
Watershed zones:
splenic flexure**
-ranges from mucosal hemorrhage to transmural necrosis of bowel wall
Histology:
necrotic mucosa, hemorrhage
Internal Hemorrhoids
Above pectinate line
- receive visceral innervation =NOT painful
- rectal bleeding, pain, worse with defecation
External Hemorrhoids
Below pectinate line
- receive somatic innervation=PAINFUL
- rectal bleeding, worse with defecation
4 Non-neoplastic polyps of the intestine
- Inflammatory Polyp
- Hamartomatous (Peutz-Jeghers Syndrome)
- Juvenile Polyp
- Hyperplastic Polyp
Inflammatory Polyp
Solitary Rectal ulcer syndrome (rectal prolapse syndrome)
- impaired relaxation of anorectal sphincter creates a sharp angle at anterior rectal shelf which leads to abrasion and ulceration of overlying rectal mucosa
- polyp forms as a result of chronic cycles or injury
- pulled into fecal stream this leads to mucosa prolapse
Histology:
-lamina propria fibromuscular hyperplasia, inflammation and erosion of epithelial hyperplasia
Juvenile Polyp
mostly sporadic in children
Hamartomatous (peutz-Jeghers syndrome)
AD syndrome
multiple non malignant hartomas throughout GI tract
-hyperpigmented melanotic macules of mouth, lips, gentalia, hands
-polyps have no malignant potential
-but patients are at an increased risk of CRC and other malignancies (pancreas, breast, ovary, uterus, testicle)
Hyperplastic polyp
prevalence: up to 30% of people>50
- asymptomatic
- endoscopically looks similar to adenomas
- majority 50% in rectosigmoid colon
- proliferation of mature goblet cells
Neoplasm small and large intestine
- adenomatous
- sessile serrated adenoma
- adenomatous dysplasia
Adenomatous
- Benign polps that are precursors to majority of colorectal adenocarcinomas
- 50% of people older than 50 in western world
- most clinically silent
- .3-10cm
Gross:
pedunculated or sessile(bad)
Histology:
Tubular or villous (bad)
Risk of cancer:
- size
- presence of high grade dysplasia
sessile serrated adenoma
type of adenomatous polyp occurring predominantly in the right colon
Adenomatous dysplasia
neoplastic dysplastic epithelium
-lines the glands as hyperchromic somewhat disordered cells with or without mucin production
Familial adenomatous polyposis
- AD
- defect: APC
- 100-thousands polyps
- 100% develop colorectal adenocarcinoma
- prophylactic colectomy-but may still develop adenomas at other sites (ampulla of vater, stomach)
Gardner Syndrome
- AD
- polyps similar to FAP but with osteomas of the mandible, skull, and long bon, epidermal cysts, desmoid tumors, thyroid tumors, and dental abnormalities
Turcots Syndrome
- Intestinal adenomas
- tumors of the CNS
- 2/3 have APC mutations and develop medulloblastoma
- 1/3 have other DNA repair mutations and develop gliobasotmas
Hereditary nonpolyposis colorectal cancer (HNPCC)
Lynch syndrome
- AD
- lower number of polyps but cancer occurs at younger ages than sporadic colon cancer
- increase risk of cancers of endometrium, stomach, ureter, renal pelvis, bladder, pancreas, and biliary tract
- *caused by mutation in DNA mismatch repair gene
What pathway do is irregular in FAP and sportic CRC? What is the pathway? What side of the colon is affected?
APC/WNT pathway
APC is negative regulator of Beta catenin-loss of APC–>B catenin translocates to nucleus and activates genes encoding MYC and cyclin D1 which promote proliferation
1. Germline or somatic mutation of APC Normal colon 2. Second hit Mucosa at risk 3. Proto Oncogene mutation (K-RAS) 4. Homozygous loss of additional cancer suppressor genes ( p53) adenomas 5. additional mutations, gross chromosome alteration (telomerase) carcinoma
What pathway do is irregular in HNPCC and SSA? What is the pathway? What side of the colon is affected?
DNA mismatch repair
(about 10% are Sporadic and FAP)
-microsatellite instability in coding area or promoter region
1. germline or somatic mutation of mismatch repair gene
(MLH1, MSH2)
2. alteration of second allele
3. microsatellite instability/mutator phenotype
(sessile serrated adenoma)
4. accumulation of mutations in genes that regulate differentiation and growth and apoptosis
carcinoma
CRC presentation
retrosigmoid>ascending>descending -apple core lesion barium x-ray -CEA for monitoring not screening peak incidence 60-79 25% have family history
right sided CRC
usually asymptomatic for long period of time
-iron deficiency anemia due to surface ulceration and blood loss
