Flashcards in Colonic Diseases Deck (53)
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1
What is the anatomical division of the colon from proximal to distal?
• Ileocecal valve
• Cecum
• Ascending colon
• Hepatic flexure
• Transverse colon
• Splenic flexure
• Descending colon
• Sigmoid colon
• Rectum
• anus
2
Why are the splenic flexure and rectum considered watershed areas of the large bowel?
• The receive blood from terminal branches of their respective arteries
• IMA for the most of the descending colon
• Rectum gets terminal branches from exterinal and internal iliac arteries, the inferior rectal and hemorrhoidal arteries
• These are somewhat easily "shut off" in cases of global hypo-perfusion and thus the splenic flexure and rectum can experience ischemic injury in septic cases or anything else that really drops blood pressure or volume
3
Even though the colon's main job is water reabsorption, does it do a lot of it?
• Normally, it doesn't need to
• The small intestine does the majority of absorption, and usually the colon plays a minor physiological role
• It's when small intestine motility or volume is ramped up that the colon has to suck back some water before it's too late
4
What are the bacterial colonies of normal flora in the colon supposed to do?
• They ferment non-absorbed nutrients and produce trophic factors that maintain a healthy mucosa and motility
5
How does the colon reabsorb water?
• Na, Cl and K are reabsorbed through trasport systems
○ Very similar to kidney
• Water follows passively
6
What is meant by indeterminant colitis?
• In 20% of cases the presenting colitis will have features of both chron disease and ulcerative colitis and you can't further differentiate
• At this point you call it indeterminant colitis
7
Is there a cause, or at least some risk factors for IBD?
• There is a genetic component because risk goes up in a family of cases
○ HLA-B27 is a genetic risk factor
• No real good cause yet
• Risk factors ("environmental triggers")
○ Bacterial infection
○ Tobacco exposure
○ Diet
○ climate
8
Compare and contrast the two IBDs in terms of where they affect the GI tract
• UC is limited to the colon
• Crohn's disease is "tongue to bung" or anywhere in GI tract
• UC usually involves rectosigmoid
○ 50% of cases are pan-colonic
• UC can be fully managed by colectomy but CD may be only modified by it
• CD is usually in terminal ileum and right colon
○ Jejunal invlolvment is infrequent
○ Anything above jejunum is downright RARE
• Smoking is protective in UC and a risk factor for CD
9
Why might Crohn's patients have a bowel obstruction?
• Because the disease is transmural it carries a greater risk of fibrotic strictures in the small bowel
• These focal strictures may cause obstruction
10
What is different between the IBD's in terms of mucosal penetration of inflammation?
• CD can be completely transmural
• UC is limited to mucosa, and in severe cases can be in submucosa
• CD is transmural enough to spread beyond strict GI tract
• CD can cause fistula formation due to complete transmural inflammatory injury
11
Describe the landscape of the affected bowel as seen endoscopically in CD vs. UC.
• CD has skip lesions
○ Relative sparing of mucosa in between lesions
○ Less mucosa affected, but deeper inflammation
• UC has linear or focal ulceration
○ Diffuse inflammation that is friable, edematous, and bloody
○ Punctate ulcerations
○ Sometimes Has pseudopolyps, which are islands of spared mucosa
12
What are the intestinal signs and symptoms (clinical manifestations) of crohn's disease vs. ulcerative colitis?
• Both - diarrhea or abdominal pain
○ Usually small-volume, 4-6 times per day
○ Often tenesmus = extreme urgency to defecate
○ Often sense of incomplete evacuation
○ Weight loss
§ Increased catolism, loss of nutrients in stool or decreased PO intake
○ Hematochezia and anemia in severe disease
• Crohn's
○ Lower abdominal pain consistent with colitis or mid-abdominal (perumbilical) pain more consistent with small bowel disease
○ Ileitis or jejunitis - diarrhea may occasionally be large-volume, foul smelling and/or associated with steatorrhea (might indicate malabsorption)
○ Nausea and vomiting more common here but still a bit on the rare side
○ Small bowl obstruction
○ Fistula formation
• UC
○ Almost always localized to the lower quadrants, LLQ more frequently than RLQ
§ Consistent with sigmoid and rectal involvement
○ Visible mucus in stool
13
What are the extra-intestinal clinical manifestations of crohn's vs. ulcerative colitis?
• More common in UC than crohn's but rare overall
• Eye, skin, bile ducts and joint inflammatory symptoms
• Don't follow the course of IBD, meaning IBD may be well controlled but these pop up anyway
○ Except erythema nodosum
• Uveitis
• Pyoderma gangrenosum
• Erythema noddosum
• Ankylosing spondylitis
• Primary sclerosing cholangitis
14
What is up with primary sclerosing coholangitis in IBD?
• PSC - fibrosing condition of the intra and extra hepatic bile dcuts
• Can progress to cirrhosis or cause cholestasis alone
• ERCP is usually required for dx and treatment
• Liver transplant may be necessary
○ Also a risk factor for neoplasm
15
What is up with ankylosing spondylitis in IBD?
• Stiffness and pain in the lumbar spine
• Typically in young males
• May be severe and disabling
16
What is up with erythema nodosum in IBD?
• Characterized by painful nodules arising within an erythodermous patch
• Dermatologic condition
• Usually follows course of IBD and goes away with well controlled IBD
17
What is up with pyoderma gangrenosum in IBD?
• Large, painful, impressive ulcerative condition that usually occurs all over the lower extremities
18
What is up with Uveitis in IBD?
• Also scleritis or episcleritis
• Eye pain and redness, can be severe
• Opth consultation is usually necessary
• Use topical steroids to provide relief
19
Describe the treatment paradigm for inflammatory bowel disease
• Complex - depends on type, severity, location of disease and the type of previous therapy used
• Glucocorticoids may help induce remission
○ New disease or acute flare
○ Don't use for chronic management
• Chronic treatments
○ Sulfasalazine
○ 5-aminosalicylates
○ Topical steroids - budenoside
○ Immunomodulators - azathioprine and 6-mercaptopurine
○ TNF-alpha antagonists - infliximab, adalimumab, certolizumab
• Surgery
○ Fistula treatment
○ Subtotal colectomy
○ Partial small bowel or colon resection
○ Structuroplasty
○ UC - may be curative
20
What are the long-term management issues of IBD patients?
• Carry a higher risk of colorectal cancer
○ 5-7 fold higher risk
○ Associated with disease duration and severity
○ Surgical indications more radical with biopsy results showing dysplasia
• Screen for osteoporosis
○ IBD even without steroid use can cause osteopenia and osteoporosis
• Malabsorption? Screen for fat-soluble vitamin deficiency
○ ADEK and B12
• Immunomodulators or immunosupression? Think infection
○ Lymphoma, fungal and mycoplastic infections
○ Also CNS disease
○ Need TB test before starting therapy
• Pregnancy considerations
○ Higher risk of flare up during pregnancy, and immunomodulators might be terotogenic
○ Patients should probably reconsider pregancy during treatment
21
What is microscopic colitis?
• Autoimmune, inflammatory condition of the colon associated with mild to moderate diarrhea
• Presumed cause is inflammation to colonic mucosa with associated malabsorption of water and sodium
• 2 major variants only differentiated by histology
○ Lymphocytic colitis
○ Collagenous colitis
• Intraluminal bacteria or dietary components are presumed to TRIGGER
○ Etiology is unknown
• Could also be associated with bile acid-related irritation of the colon (in sensitized individuals)
22
How is microscopic colitis treated?
• Both variants are treated the same
• Antidiarrheals for initial symptom control
○ Imodium, lomotil
○ Bismuth subsalicylate
• Topical steroids
○ Budensoide
• Aminosalicylates or bile acid binders (cholestyramine)
• Sometimes immunomodulators
23
What tests are done to dx microscopic colitis?
• Imaging
○ Almost always normal even by endoscopy
• Fecal leukocytes may be present on stool analysis
• Dx is made by endoscopic biopsy
• Association with celiac disease so test for that
24
What are the clinical manifestations of microscopic colitis?
• Symptoms - chronic, watery, non-bloody diarrhea
• Diarrhea generally mild, occsionally moderate
• Rarely causes dehydration or requires hospitalization
• Fasting diarrhea usually, suggesting it relates to colonic salt and malabsorption of NaCl/water
• Weight loss, constipation, bleeding, non-GI symptoms ALL RARE
25
Who gets microscopic colitis?
• More common in females than males
• Usually after age 50
• Symptoms - chronic, watery, non-bloody diarrhea
• Diarrhea generally mild, occsionally moderate
• Rarely causes dehydration or requires hospitalization
• Fasting diarrhea usually, suggesting it relates to colonic salt and malabsorption of NaCl/water
• Weight loss, constipation, bleeding, non-GI symptoms ALL RARE
26
What predisposes a patient to ischemic colitis?
• IC is an inflammatory condition of the bowel caused by lack of blood flow to the region
• Risk factors
○ Peripheral vascular disease
○ Congestive heart failure
○ Recent dehydration
○ Cocaine use
○ Abdominal surgery with cross-clamping of aorta
• 50% have no triggers or risk factors. Likely vasospasm in these cases
• Likely see the effects first in watershed areas
○ Splenic flexure, sigmoid, rectum
27
What are the clinical manifestations of ichemic bowel disease
• Sudden onset
○ Crampy lower abdominal pain, diarrhea, hematochezia
○ Patients over 60 years old in particular
• May have tenesmus
• Weight loss or severe bleeding suggests SOMETHING ELSE
• Dx is on strong suspicion from hisory and physical
• Contrast CT - could show colonic wall thickening or pericolonic inflammation
○ Fat stranding
• Could also show decreased perfusion
• GOLD STANDARD
○ Colonoscopy or flexible sigmoidoscopy with biopsy
○ Mucosal edema, friability, ulceration or hemorrhage is seen
○ Biopsy shows acute inflammation and intravascular thrombi or mucosal necrosis
28
What is intestinal gangrene?
• The most severe case of ischemic bowel. The tissue has no blood flow, is dead and being eaten by bacteria
• Positive peritoneal signs
• Often hemodynamic instability
• Medical emergency
• If found in a young patient, you need to look for a cause
○ Pro-coag?
○ Vasculitis?
○ Autoimmune like lupus?
29
How do you treat ischemic bowel?
• Supportive - IV hydration and correction of any predisposing factors
○ Arrhythmia, CHF, myocardial infarction
• Most recover spontaneously within 5-10 days
30
What are the common presenting symptoms of infectious colitis?
• Inflammatory diarrhea caused by invasion or destruction of mucosa
• Crampy lower abdominal pain and diarrhea
• Small-volume, frequent, may be bloody or mucoid
• Without caloric malabsorption
• Diarrhea can be frequent and severe, causing dehydration or anemia
31
How can you test for the presence of infectious colitis?
• Positive leukocyte stain of stool is suggestive, not definitive
• Stool cultures are over 90% sensitive for most bacterial pathogens
○ E coli, shigella, slmonella, yersinia
• Stool toxin assays are over 90% sensitive for C diff when repeated 2-3 times
• Amebiasis may be ruled out with negative serology (non-specific)
• If tests are negative but symptoms fit, endoscopy and biopsy is very sensitive
○ Specific for C diff and entamoeba histolitica as well
• Venerial proctitis can be assessed by tissue gram stain, culture, PCR or IF of a rectal ulcer specimen
○ Gonorrhea
○ Syphilis
○ Chlamydia
○ herpes
32
What drugs may cause colitis?
• Drug-induced colitis
○ NSAIDs are most commong
○ Gold salts
○ Penicillamine
• Findings and presentation usually mimic UC but may have more scattered and focal lesions
33
What's up with radiation colitis?
• Think of this in rectum problems in people treated for prostate, cervical or bladder cancer
• Painless rectal bleeding
• Tenesmus and mild diarrhea may also occur
• Endoscopic findings
○ Mucosal cobblestone-like edema and scattered telangiectasias
○ May be actively oozing
34
What is up with diverticulosis?
• Outpouchigns of colon wall
• Mucosa and submucosa, contained by serosa
• Grow into the gaps created by vasa recta
• Low fiber western diet is risk factor
○ Increases peristaltic squeeze pressure and intra-colonic pressure
• Common in older patients
• Often silent clinically until diverticulitis (fecalith)
*fever, nausea, vomiting, peritonism, mass (abcess), all in a fast onset
*Diverticular hemmorhage - mucosa of diverticulum erodes into adjacent, penetrating vasa recta
• From pressure necrosis
• Intraluminal bleeding ensues
35
How does LGIB present?
• LGIB = lower GI bleeding
• Most commonly from colon
• HEMATOCHEZIA = Red or marroon blood per rectum
• Less common - MELENA - black, foul-smelling, partially digested blood
• Severe is anemia, hemodynamic compromise, orthostatic hypotension, dizziness, syncope
36
What is the differential for LGIB?
• Decreasing order of prevalance
• Diverticulosis
• Atertiovenous malformations
• Neoplasia
• Colitis
• Iatrogentic (post polypectomy is common)
• Anorectal disease
• misc
37
What causes the vast majority of colonic obstruction cases?
• 90% of colonic obstruction are from adenocarcinoma of the colon or rectum
• OR these other problems
○ Volvulus
○ Benign strictures from acute diverticulitis
• Volvulus is usually elderly
• Cancer usually left colon and has a prodrome associated with it, with changes in stool over time
• More rare
○ Surgical adhesions, foregin bodies
§ More common in abuse, homosexual patients, rape victims, drug smugglers, prisoners
38
How do you get dx of colonic obstruction?
• Plain film x rays
• Dilated loops of colon or small intestine proximal to obstructing lesion
• Decompression and/or absence of gas distally
• CT is not necessary for dx but helpful in clarifying exact location and extent of obstructing lesion
39
What are the presenting signs and symptoms of colonic obstruction?
• Diffuse or upper abdominal discomfort, distension, and nausea/vomiting
• Emesis may be feculent
40
What is giardiasis?
• Giardia lamblia
○ Parasitic enterocolotis
• Protoxoan parasite causing sporadic or epidemic diarrhea
• Waterborne and boodborne
• Cysts are resitstant to chlorine, need a filter
• 7-14 day incubation period
• Chronic diarrhea, malabsorption, flatulence, weight loss, may cuase intermittent symptoms
41
What are the campylobacter species that cause colitis and what do these infections look like?
• C jejuni and C fetus, gram negative, worldwide leader in diarrhea
• Jejuni is commonly associated with food-borne gastroenteritis
• C. fetus is more often seen in immunosuppressed patients
• These are a leading cause of bacterial foodborne illness in US
• Watery diarrhea +/- blood
• Found in contaminated meat, water and unpasteurized dairy
42
How does salmonella infection lead to diarrhea?
• Gram negative bacilli
• Through food and water
• Traveler's diarrhea agent
• Typhoid fever
○ S typhimurium
○ Abdominal pain, headache, fever
○ Abdominal rash and leukopenia
○ Diarrhea (2nd week), initally watery then bloody
○ Pathology seen in ileum, colon, appendix and peyer's patches
○ Perforation and toxic megacolon possible
• Non-typhoid species
○ Mild, self-limited gastroenteritis
○ See mucosal redness, ulceration and exudates on endoscopy
43
What is the presentation of Enterohemorrhagic E coli infection?
• Enterohemorrhagic E coli
○ O157:H7 most common strain
○ Non-invasive, toxin-producing,
○ contaminated hamburger common source
○ Bloody diarrhea, severe cramps, mild or no fever
○ Sometimes renal failure (HUS)
○ Endoscopic findings - edema, erosions, ulcers, hemorrhage (right colon)
○ Deadly outbreaks
44
What are the different types of enterocolitis caused by E. coli?
• Enteroadherent E coli
• Enterotoxigenic E coli
• Enteroinvasive E coli
• Enterohemorrhagic E coli
45
What does enteroadherent E coli infection look like?
• Non-invasive
• Nonbloddy diarrhea
• Similar ot enteropathogenic E coli
○ Chronic diarrhea, wasting in AIDS
○ Forms a coating of adherent bacteria on surface epithelium of enterocytes
46
What does enterotoxigenic e coli infection look like?
• Noninvasive
• Nonbloody diarrhea
• Enterotoxigenic e coli is major cause of traveler's diarrhea
• Enteropathogenic e coli is infection of infants and neonates
47
What does enteroinvasive e coli infection look like?
• Invasive bacterial infection
• Similar course and pathophys to shigella
• Nonbloody diarrhea
• Dysentery-like illness
• Bactermia!
• Trasmitted in contaminated cheese, water, person to person
• Traveler's diarrhea differential
48
Describe pathogenesis of C difficile caused pseudomembranous colitis
• Disruption of normal flora allows C diff overgrowth
• Toxins produced by bacterial colonies cause disruption of epithelial cytoskelaton
• Tight junctions get leaky
• Cytokine release
• Inflammation and apoptosis
49
What is a pseudomembrane in pseudomembranous colitis?
• Adherent layer of inflammatory cells and mucinous debris at sites of colonic mucoasl injury
• Surface epithelium denuded, mucopurulent exudates
50
What are the viral infections that can cause enterocolitis?
• Cytomegalovirus
○ Anywhere in tract
• Herpesvirus
○ Typically esophagus and/or anorectum
• Enteric viruses
○ Rotavirus
51
What does a rotavirus infection look like?
• Most common cause of severe childhood diarrhea and diarrheal mortality worldwide
• Children between 6-24mo most vulnerable
• Selectively infects and destroys mature enterocytes
○ Villus surface repopulated by immature secretory cells
○ Loss of absorptive function
○ Net secretion of water and electrolytes
○ Osmotic diarrhea
• All these can lead to severe dehydration and death
• Remember previous vaccine increased intussusception risk
52
What infection causes a "flask shaped ulcer"?
• Entamoeba histolytica infection
• Severe dysentery-like fulminant colitis
• Can go to liver
53
