Hi Yield 11.3-11.9

mhewett's version from 2016-06-25 21:29

Section 11.3 Polyps & Cancer of the Intestine

Section 11.3.1 Intestinal Polyps

Question Answer
Major types of intestinal polyps1. hyperplastic
2. hamartomatous
3. inflammatory
4. lymphoid
5. adenomatous
hyperplastic polypsmost common colonic polyp
50s & 60s
d/t dec epithelial cell turnover in the bowel, resulting in the accumulation of mature cells on the surface
little to no risk for malignant transformation
Hamartomatous Polyps-represent malformations of the glands and stroma of the epithelium, causing overgrowth of mature tissue natural to the area
-have little to no risk for malignant transformation
-can occur sporadically or in association with Peutz-Jeghers Syndrome
Inflammatory polyps (pseudopolyps)-represent inflamed regenerating tissue surrounded by ulceration
- most associated with those who have inflammatory bowel disease
Lymphoid Polypsthese are a large but normal variants of intramucosal lymphoid tissue
adenomatous polyps (adenomas)-are neoplastic - therefore, are premalignant, acting as a precursor lesion for invasive colorectal carcinoma
-all arise from proliferative dysplasia of epithelial cells lining the colon
-3 subtypes: tubular adenoma, villous adenoma, tubulovillous adenoma
tubular adenoma-comprised of tubular epithelial glands
villous adenoma-has villous (finger like projections); when these are >4cm in diameter, they are the polyps with the highest risk for malignant transformation
- they are most common to the rectum and rectosigmoid colon, and usually cause gross rectal bleeding, hypokalemia and hypoproteinemia
tubulovillous adenomahas both villous and tubular features
Peutz-Jeghers Syndrome-an inherited autosomal dominant hamartomatous polyp disorder that is familial polyposis syndrome of the entire bowel
-hamartomatous polyps + spotted melanin hyperpigmentation of lips, palms, and soles
-polyps have very low cancer potential
-however, the risk of colon cancer (and other cancers) not related to these polyps is greater than that of the general population

Section 11.3.2 Familial Polyposis Syndromes of the Colon

Question Answer
Familial adenomatous polyposis (FAP) -due to loss of the tumor suppressor gene, APC
- once polyps develop, there is almost a 100% chance of colon cancer development
- typically patients develop 500-2500 polyps that carpet the colon
-all polyps are adenomatous
-autosomal dominant
Gardeners Syndrome-a form of classic FAP
-classic FAP colon polyps + benign mandible and skull tumors + epidermal cysts + high risk for abnormal dentition
-nearly 100% chance of polyps developing into a colon cancer
-autosomal dominant
Turcot's Syndrome- a form of classic FAP
- classic FAP colon polyps + malignant brain tumors
-high risk of polyps becoming a colon cancer
- autosomal dominant

Section 11.3.3 Familial Cancer-Risk Syndromes of the Colon Without Polyps

Question Answer
How is hereditary nonpolyposis colorectal cancer (HNPCC aka LYNCH syndrome) inherited and what causes it?Auto dominant; d/t defective DNA mismatch repair genes
What type of cancer (besides colon) are pts suffering from Lynch syndrome at an especially high risk for developing?Endometrium and ovary

Section 11.3.4 Colon Cancer

Question Answer
From what do most colon cancers arise?Adenomas (adenomatous polyps)
What are the 2 molecular pathways responsible for the development of colon cancer?1) loss of tumor suppressor APC genes
2) Mutation of oncogene k-RAS and inactivation of tumor suppressor p53
Patients with right colonic cancers are more likely to have what symptoms?Iron-deficiency anemia, +hemoccult, - stool changes
Patients with left colonic cancers are more likely to have what symptoms?+ hemoccult stool, Change in bowel habits, Crampy LLQ discomfort/tenesmus (d/t stimulation of bowel by the tumor), Pencil stools
A 55 yo patient comes in with complaints of chronic fatigue. It is determined that he has iron deficiency anemia. What is your next thought?He's got colon cancer until it's ruled out with a further workup

Section 11.4 Diverticular Disease

Question Answer
What area of the colon is most at risk for developing diverticula?Sigmoid colon at the areas where blood vessels penetrate the full thickness of the bowel - this is the weakest spot in the bowel
What symptoms would diverticulosis cause?+ hemoccult, gross bleeding, painless
What is diverticulitis?An inflamed (d/t infection) diverticula that has been blocked off by a particle of food allowing the bacteria to proliferate
What are the symptoms of diverticulitis?LLQ pain, fever, increased PMNs, +/- diarrhea, - hemoccult (b/c b.v. is tamponaded by impacted debris)
What is the major concern with diverticulitis? How is it treated?Abscess formation, bowel perforation, and/or sepsis that is potentially life-threatening
Ciprofloxacin and Metronidazole

Section 11.5 Irritable Bowel Syndrome

Question Answer
What causes irritable bowel syndrome?dysregulation of the enteric nervous system where it activates and inhibits itself w/o regard to the autonomic nervous system

Section 11.6 Inflammatory Bowel Disease (IBD)

Question Answer
What type of lesions are seen in Crohn's dz?Skip lesions
What are the complications of Crohn's dz?Fistula, fissures, strictures
If you have a patient do a barium swallow and see a + string sign on x-ray, what type of bowel dz do they have?Crohn's dz d/t strictures
Where do the lesions for ulcerative colitis begin?At the rectum and progresses proximally to the ileocecal jxn
What can be seen in UC where an area of regenerating mucous membrane is encircled by ulcer?Pseudopolyps
Which dz has the lead pipe colon?UC (d/t fibrosis from long standing dz resulting in loss of haustra)
Risk for which dz is decreased by smoking (Crohn's or UC)?UC
What are the major concerns for UC?Toxic megacolon and high risk of colon cancer (vs. mod risk of colon cancer in Crohn's)
Describe Crohn's and UC in terms of pain and bleedingCrohn's: less bleeding, more pain (d/t transmural lesions irritating nerves)
UC: more bleeding, less pain (lesions are superficial)

Section 11.7 Malabsorption

Question Answer
What are the most common universal symptoms for malabsorption?Steatorrhea +/- diarrhea
What is the Sudan III test and what is its purpose?Qualitative test to screen for whether or not there is an increased amount of fat in stool
What is the gold standard test for malabsorption?Stool fat analysis: measures amount of fat in stool after being fed a measured quantity of fat
High amount in stool indicates malabsorption
How does the D-xylose absorption test work?D-xylose is non-digestible so in healthy pts it's absorbed from the intestines into the blood and then excreted into the urine. In malabsorption pts there will be no D-xylose in the urine as it was not absorbed in the intestines.
What is the purpose of the Schilling test?Identifies the cause of vitamin B12 (cobalamin) deficiency.
How does the Schilling test work?Cobalt-labeled B12 is administered and then excretion is measured with a 24h urine. Neg test means there's a B12 deficiency. On 2nd test, IF is administered with the labeled B12. If the urine is + for B12 after having IF co-administered it indicates pernicious anemia. If the test is neg it indicates chronic pancreatitis, bacterial overgrowth, or dz of ileum
What happens in celiac sprue?Flattened villi d/t deposition of Ab-gliadin ag on the villi resulting in MAC damage and decapitation of the villi.
What type of lymphoma are pts with celiac sprue at an increased risk for?MALToma (mucosa-associated lymphoid tissue lymphoma)
What are the primary sites affected by Whipple dz?Intestine, CNS, and joints
What are the symptoms of Whipple dz?Arthralgia, Steatorrhea, Fever
What causes Whipple dz and what is seen on biopsy?Tropheryma whippelii
PAS + macs in the mucosa d/t gram + Actinomyces
How long does Whipple dz need to be treated and what are some examples of preferred abx?4-6 months minimum; 1y preferred
1st line: PCN G or ceftriaxone
2nd line: TMP-SMX

Section 11.8 Cholelithiasis

Question Answer
Who is most at risk for cholesterol stones?Fat, Female, (over) 40, Fertile; MC stone in US
What are mixed stones?combo of cholesterol & bilirubin precipitant; most common type of stone worldwide
What could potentially lead to excess bilirubin thus increasing a pt's risk for pigment stones?Hemolysis

Section 11.9 A Synopsis of Biliary Disorders

Question Answer
How is cholelithiasis treated?Generally it's asymptomatic so no tx is needed but it's surgically removed in those with a porcelain GB (calcium deposits in GB) and in Native Americans it's removed d/t their increased risk of GB cancer
What is the difference between cholelithiasis and cholecystitis?Cholelithiasis: gallstones in GB
Cholecystitis: infection of GB (presents with f/RUQ pain/ + Murphy's sign/n/v d/t blockage of GB resulting in rapid proliferation of bacteria trapped in GB)
What lab results would you expect to find in cholecystitis?Increased PMNs d/t infxn
Increased alk phos d/t damage to the cells in the biliary tree
Pericholecystic fluid w/ thickened GB wall on ultrasound
What happens in choledocolithiasis?Common bile duct is obstructed resulting in RUQ pain, jaundice (d/t back up of conjugated bili), acholic stool, tea-colored urine (stool has no pigment from bili and urine is dark b/c all the conjugated bili is exiting through the urine)
Why is ascending cholangitis a serious condition?Infection of common bile duct which can quickly ascend to the liver and cause life-threatening sepsis
What is Charcot's triad?RUQ pain + Jaundice + Fever
Indicates ascending cholangitis when in the context of increased PMNs, elevated conjugated bili, and increased alk phos
What is primary sclerosing cholangitis (PSC)?non-infectious inflammation and sclerosis of bile ducts with eventual obliteration of all biliary ducts
What labs do you expect with PSC?elevated conjugated bilirubin and alkaline phosphatase
What is primary biliary cirrhosis (PBC)?autoimmune destruction of intrahepatic bile ducts
What is the difference between Primary Sclerosing Cholangitis and Primary Biliary Cirrhosis?PSC: unknown cause results in sclerosis and eventual obliteration of biliary ducts - highest risk for development is IBD (esp UC)
PBC: d/t autoimmune destruction of biliary system, will have a +AMA and is more common in CREST, Sjogren's, and T1DM