Disorders of the Small Bowel and Colon Flashcards
If there’s Chronic Diarrhea, is it likely to be infectious?
no
-it’s gonna be something like IBD or something like that
What are the most common infectious causes of bloody diarrhea?
- salmonella
- shigella
- E. coli (0157 H7)
- Campylobacter
- Yersinia enterocolitica (sometimes)… that one is psuedo appendicits
Salmonella Typhi
- Gram - enteric bacillus
- fever
- Endotoxin like the rest of gram negative things AND Vi antigen
- Relative bradycardia
- Rose spots
What can be a chronic reservoir for Salmonella Typhi?
Gallbladder
-healthy asymptomatic carrier
What does MEN1 have?
- pituitary adenoma*
- parathyroid hyperplasia
- pancreatic tumors
What does MEN2a have?
- parathyroid hyperplasia
- Medullary thyroid carcinoma
- Pheochromocytoma
What doe MEN2b have ?
- mucosal neuromas*
- MArfanoid body habitus*
- Medullary thyroid carcinoma
- Pheochromocytoma
If the diarrhea is osmotic, what will decrease the stool volume?
fasting
-there will be a high osmotic gap
If the diarrhea is secretory, what will it be like?
- large volume (>1L a day)
- normal osmotic gap
- stool sodium will be high
- little change with fasting
- hyponatremia and nonanion gap metabolic acidosis
- Villous adneoma
- Bile salt malabsorption
What should we think if we see fecal calprotectin?
IBD
What are the most common causes of Chronic diarrhea?
- meds
- IBS
- Lactose intolerance
What is the stool osmotic gap?
difference between measured osmolality of the stool and the estimated stool osmolality
-Normal is <50 mOsm/kg
if chromogranin A is positive, what is it?
VIPoma
If calcitonin is high, what’s up?
Medullary thyroid cancer
If gastrin is high, what’s up?
ZE syndrome
If we see fecal calprotectin, what’s up?
IBD
What do we think of if we see 5-HIAA in the urine?
Carcinoid tumor
What is IBS?
- chronic functional disorder
- Not expleained by the presence of structural or biochemical abnormalities
- Dx: based on the presence of a compatible profile (ROME III)
- it’s idiopathic
What is the ROME II criteria for IBS Dx?
-abdominal discomfort or pain at least 3 days/month for the past 3 months, with symptom onset>6 months before diagnosis and at least 2/3: relieved with defecation, onset associated with a change in frequency of stool, onset associated with a change in form of stool
What is FODMAPS?
Fermentable monosaccharides and short chain carbohydrates
-exacerbate bloating, flatulence, and diarrhea in some patients
Is high fiber a good thing in IBS patients?
“appears to be of little value in helping IBS patients”
What do we use to treat C diff?
Metronidazole
-harry potter and voldemort
What is colitis from antibiotics caused by?
C diff
What are most cases of antibiotic associated diarrhea from?
adverse effects of antibiotics
- NOT c diff
- mild and self limited
What two toxins does C diff form?
TcdA (enterotoxin)
TcdB (cytotoxin)
So, what do we need to check if we suspect C diff?
check stool for toxin assay
- flex sig used if atypical symptoms and positive toxins
- CT or Abd Xray if severe or fulminant symptoms to look for megacolon or perforation
What antibiotics will we usually see used in a question stem if C diff is cookin?
ampicillin
clindamycin
3rd gen cephalosporins and fluoroquinolones
-hospitalizations
What’s a weird thing that can happen with fecal impaction?
paradoxical or “overflow” diarrhea
-the only thing that can get past is liquid
How do you treat constipation/fecal impaction?
enemas
digital disruption
-long term- good bowel regimen
What is Microscopic colitis?
- idiopathic
- sometimes medications can cause it
- R/o celiac
- chronic or intermittent watery diarrhea
- *normal mucosa on endoscopy
How do you treat microscopic colitis?
stop offending medication
-loperamide, budesonide, bile-slat binding agents, or 5-ASA’s
What are some risk factors for diverticular disease of the colon?
- old
- CT disease: Ehlers-Danlos, Marfan syndrome, Scleroderma
What is diverticulosis?
- Asymptomatic, Dx on colonoscopy or barium enema
- usually sigmoid and descending colon, can be anywhere in the colon
- symptomatic complications: GI bleed, Diverticulitis
What is diverticulitis?
- macroscopic inflammation of diverticulum
- may have microperforation with localized paracolic inflammation
- may have macroperforation with abscess or peritonitis
How do you treat Diverticulitis?
- maybe Abx
- NPO/clear liquid diet
What should people with diverticulitis do after symptom resolution?
undergo diagnositc imaging to exclude colonic neoplasms
-CT with contrast
What is the most common type of polyp?
Mucosal adenomatous polyps (70%)
- tubular
- tubulovillous
- villous
What do mucosal serrated polyps look like?
- hyperplastic
- sessile serrated polyps
- traditional serrated adenoma
What are some mucosal nonneoplastic polyps?
Juvenile
hamartomas
inflammatory
What are some submucosal lesions that can happen in the colon?
Lipomas
Lymphoid aggregates
Carcinoids
Pneumatosis cystoides intestinalis
What do 95% of cases of Colon adenocarcinoma come from?
Adenomas and serrated polyps
-high risk of prgressing to malignancy if they are: >1 cm, contain villous features, have high grade dysplasia
What will we see in a patient who has asymptomatic colon cancer?
FOBT positive
Iron deficiency anemia
What is the Gold standard for detecting polyps?
Colonoscopy
What are potential complications of colonoscopy?
Bleeding and perforation
FOBT
Fecal occult blood testing -Guaiac based -detect pseudoperoxidase activity of heme or hemogloblin -need predietary restrictions -
FIT
Fecal immunochemical test -Tests for hgb -no predietary restrictions preferred over FOBT -more sensitive than Guaiac based tests -Screening for CRC and advanced adenomas
Fecal DNA
Tests for stool Hgb
-measures a variety of mutated genes and methylated gene markers from exfoliated tumor cells
Does intussusception happen more in adults or kids?
kids!
-more common in kids, rare in adults
FAP
Familial adenomatous polyposis
- eraly development of a shit ton of polyps and adenocarnicoma
- Extracolonic: dudoenal adenomas, desmoid tumors, osteomas
What gene is associates with FAP?
-APC gene (90%) or MUTYH gene mutation
Tx of FAP
- prophylactic colectomy (CRC inevitable by age 50)
- family needs to be testing and genetic counseling
Peutz Jeghers Syndrome
- Hamartomatous polyposis syndrom
- auto dominant
- Hamartomatous polyps thorughout GI tract, mostly small intestine
- Mucocutanious pigmented macules on the lips, buccal mucosa, or skin
Are Hamartomas malignant?
NO!
What kinds of cancer can develop in Peutz Jeghers?
GI malignancy in 40-60%
- Breast CA in 30-50%
- Gonadal or pancreatic CA
What gene is there a defect in in Puetz Jeghers?
Threonine kinase II gene
Familial Juvenile polyposis
- Hamartomatous polyposis syndrome
- auto dominant
- > 10 juvenile hamartomataus polyps (mostly in colon)
What genetic defects are in Familial Juvenile polyposis?
Loci on 18q and 10q
-MADH4 and BMPR I A
Cowden disease
- PTEN multiple hamartoma syndrome
- hamartomatous polyps and lipomas throughout the GI tract
- Trichilemmomomas: benign tumor at the root of the hair follicle
- Cerebellar lesions
- Increased rate of malignancy (thyroid, breast, and urogenital tract)
Lynch syndrome
- aka: Hereditary nonpolyposis colon cancer (HNPCC)
- autosomal dominant
- Gene mutation: MLH1, MSH2
- increased risk of CRC, endometrial CA, and others at a young age
- Rapid poly transformation benign to malignant in 1-2 years
When should we suspect Lynch syndrome?
person early onset CRC
-FH of CRC, edonmetrial CA, or lynch syndrome
Dx of Lynch syndrome?
- Besthesda criteria
- tumor tissue immunohistochemcial staining for mismatch repair proteins
- testing for microsatellite instability
- confirmed by genetic testing
Screening for lynch syndrome
- colonoscopy every 1-2 yrs begin age 25, or 5 yrs younger than age of youngest affected family member at diagnosis
- pelvic exam, transvaginal US, and endometrial sampling for Women starting at age 30-35
- upper endoscopy every 2-3 years beginning at age 30-35 to look for gastric cancer
- prophylactic hysterectomy with oophorectomy age 40 or once done childbearing
Besthesda Criteria?
- CRC under age 50
- Synchronous CRC or lynch syndrome-associated tumor regardless of age (enometrial, stomach, ovary, pancreas, ureter, renal, biliary, brain)
- CRC with one or more first degree relations with CRC or lynch syndrom erelated cancer with one of the cancers occurring before age 50
- CRC with two or more second degree relative with CRC or LS
- Tumors with infiltrating lymphocytes, mucinous/signet ring differentiation or medullary growth pattern in patients younger than 60 yo
Gardner’s syndrome
- adenomatous colon polyps
- 95% develop cr polpyps
- Osteomas of mandible, skull and long bones
- supernumerary teeth, epidermoid and sebaceous teeth, thyroid and adrenal tumors. desmoid (fibrous) tumors
- Autosomal dominant
Turcot’s syndrome
- Adenomatous colon polyps
- brain tumors
- colorectal cancer–100% over 40 years of age
- Auto dominant
Pernicious anemia/ Autoimmune Gastritis
- Autoimmune destruction of fundic glands
- loss of them
- achlorhydria… pronounced hypergastrinemia (kinda like ZE)
- induce hyperplasia of gastric enterochromaffin-like cells
- development of small, multicentric carcinoid tumors (5% of patients)
in Autoimmune gastritis, what is the result of the loss of fundic glands?
achlorhydria
decreased IF secretion
Vitamin B12 malabsorption
Celiac disease
IgA tissue tansglutaminase
- if IgA deficiency, check IgG to deamidated gliadin peptide (anti-DGP)
- Wgt loss, chronic diarrhea, abdominal distention, growth retardation
- Dermatitis herpetiformis, iron deficiency anemia, osteoporosis
What part of the GI tract does Celiac disease damage most?
proximal small intestinal mucosa
What is the weird gene that is with celiac disease?
HLA-DQ2 or DQ8
Whipple disease
- rare multi system disease
- fever, LAD, Arthralgias, Wgt loss, malabsorption, chronic diarrhea
- Encephalitis, ocular abnormalities
Dx Whipple disease
Duodenal bx with PAS + periodic acid schiff macrophages with characteristic bacillus
What is the characteristic bacillus in Whipple disease?
Tropheryma whippelli
-gram positive bacilli (not acid fast
Tx of whipple disease
Abx
Bacterial overgrowth
- distention, flatulence, diarrhea, weight loss
- increased qualitative and quantitative fecal fat
- reduced absorption of B12 and carbs
- need to check serum iron
- osmotic and secretory diarrhea
When should we think of bacterial overgrowth?
in the elderly with malabsorption
Dx of bacterial overgrowth
Breath tests (hydrogen, methane, glucose, lactulose, or C-xylose)
Tx of bacterial overgrowth
Abx duh!
Short bowel syndrome
- removal of significant segments of small intestine
- crohn, volvulus, tumor resection, trauma…
Terminal ileum resection
- bile salts and vit B12 malabsorption
- Increased chance of oxylate kidney stones
- Increased chance of cholesterol gallstones
how do you treat that B12 malabsorption?
B12 injections, bile salt binding resins, low fat diet, fat soluble vitamin replacements
what to do about the oxylate kidney stones in short bowel syndrome?
Give calcium supplementation
How much of the proximal jejunum is required to maintain oral nutrition?
at least 200cm
-if there’s no colon and less than 100-200 cm of proximal jejunum, they require parenteral nutrition (TPN)
Lacatase deficiency
diarrhea, bloating, flatulence, abdominal pain AFTER ingestion of milk-containing product
- Dx: symptomatic improvement with lactose free diet (confirm by hydrogen breath test)
- Lactase-brush border enzyme hydroyzes disaccharide lactose into glucose and galactose
Urea breath test
H. pylori
Hydrogen breath test
Lactose intolerance
-can also do for bacterial overgrowth
Glucose, lactulose, or 14C-xylose breath test
-bacterial overgrowth
Pernicious anemia
- rare
- AI destruction of gastric fundic glands
- loss of inhibition to gastrin G cells
- may cause hyperplasia of gastric enterochromaffin-like cells (can lead to small carcioid tumors)
- decreased intrinsic factor secretion
- B12 malabsorption
What does the histology look like on pernicious anemia?
severe gland atrophy and intestinal metaplasia
What is the big risk that was bolded on the pernicious anemia slide?
3 FOLD INCREASED RISK OF GASTRIC ADENOCARCINOMA