Colonic Diseases Flashcards

1
Q

What is the anatomical division of the colon from proximal to distal?

A
  • Ileocecal valve
    • Cecum
    • Ascending colon
    • Hepatic flexure
    • Transverse colon
    • Splenic flexure
    • Descending colon
    • Sigmoid colon
    • Rectum
    • anus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Why are the splenic flexure and rectum considered watershed areas of the large bowel?

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Even though the colon’s main job is water reabsorption, does it do a lot of it?

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the bacterial colonies of normal flora in the colon supposed to do?

A

• They ferment non-absorbed nutrients and produce trophic factors that maintain a healthy mucosa and motility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How does the colon reabsorb water?

A

• Na, Cl and K are reabsorbed through trasport systems
○ Very similar to kidney
• Water follows passively

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is meant by indeterminant colitis?

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Is there a cause, or at least some risk factors for IBD?

A
• 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Compare and contrast the two IBDs in terms of where they affect the GI tract

A

• 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Why might Crohn’s patients have a bowel obstruction?

A
  • Because the disease is transmural it carries a greater risk of fibrotic strictures in the small bowel
    • These focal strictures may cause obstruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is different between the IBD’s in terms of mucosal penetration of inflammation?

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the landscape of the affected bowel as seen endoscopically in CD vs. UC.

A

• 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the intestinal signs and symptoms (clinical manifestations) of crohn’s disease vs. ulcerative colitis?

A

• 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the extra-intestinal clinical manifestations of crohn’s vs. ulcerative colitis?

A

• 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is up with primary sclerosing coholangitis in IBD?

A

• 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is up with ankylosing spondylitis in IBD?

A
  • Stiffness and pain in the lumbar spine
    • Typically in young males
    • May be severe and disabling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is up with erythema nodosum in IBD?

A
  • Characterized by painful nodules arising within an erythodermous patch
    • Dermatologic condition
    • Usually follows course of IBD and goes away with well controlled IBD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is up with pyoderma gangrenosum in IBD?

A

• Large, painful, impressive ulcerative condition that usually occurs all over the lower extremities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is up with Uveitis in IBD?

A
  • Also scleritis or episcleritis
    • Eye pain and redness, can be severe
    • Opth consultation is usually necessary
    • Use topical steroids to provide relief
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe the treatment paradigm for inflammatory bowel disease

A

• 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the long-term management issues of IBD patients?

A

• 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is microscopic colitis?

A

• 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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How is microscopic colitis treated?

A
• 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
Q

What tests are done to dx microscopic colitis?

A

• 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
Q

What are the clinical manifestations of microscopic colitis?

A
  • 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
Q

Who gets microscopic colitis?

A
  • 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
Q

What predisposes a patient to ischemic colitis?

A

• 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
Q

What are the clinical manifestations of ichemic bowel disease

A

• 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
Q

What is intestinal gangrene?

A
• 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
Q

How do you treat ischemic bowel?

A

• Supportive - IV hydration and correction of any predisposing factors
○ Arrhythmia, CHF, myocardial infarction
• Most recover spontaneously within 5-10 days

30
Q

What are the common presenting symptoms of infectious colitis?

A
  • 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
Q

How can you test for the presence of infectious colitis?

A

• 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
Q

What drugs may cause colitis?

A
• 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
Q

What’s up with radiation colitis?

A

• 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
Q

What is up with diverticulosis?

A

• 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
Q

How does LGIB present?

A
  • 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
Q

What is the differential for LGIB?

A
  • Decreasing order of prevalance
    • Diverticulosis
    • Atertiovenous malformations
    • Neoplasia
    • Colitis
    • Iatrogentic (post polypectomy is common)
    • Anorectal disease
    • misc
37
Q

What causes the vast majority of colonic obstruction cases?

A

• 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
Q

How do you get dx of colonic obstruction?

A
  • 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
Q

What are the presenting signs and symptoms of colonic obstruction?

A
  • Diffuse or upper abdominal discomfort, distension, and nausea/vomiting
    • Emesis may be feculent
40
Q

What is giardiasis?

A

• 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
Q

What are the campylobacter species that cause colitis and what do these infections look like?

A
  • 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
Q

How does salmonella infection lead to diarrhea?

A

• 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
Q

What is the presentation of Enterohemorrhagic E coli infection?

A
• 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
Q

What are the different types of enterocolitis caused by E. coli?

A
  • Enteroadherent E coli
    • Enterotoxigenic E coli
    • Enteroinvasive E coli
    • Enterohemorrhagic E coli
45
Q

What does enteroadherent E coli infection look like?

A
• 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
Q

What does enterotoxigenic e coli infection look like?

A
  • Noninvasive
    • Nonbloody diarrhea
    • Enterotoxigenic e coli is major cause of traveler’s diarrhea
    • Enteropathogenic e coli is infection of infants and neonates
47
Q

What does enteroinvasive e coli infection look like?

A
  • 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
Q

Describe pathogenesis of C difficile caused pseudomembranous colitis

A
  • 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
Q

What is a pseudomembrane in pseudomembranous colitis?

A
  • Adherent layer of inflammatory cells and mucinous debris at sites of colonic mucoasl injury
    • Surface epithelium denuded, mucopurulent exudates
50
Q

What are the viral infections that can cause enterocolitis?

A
• Cytomegalovirus
		○ Anywhere in tract
	• Herpesvirus
		○ Typically esophagus and/or anorectum
	• Enteric viruses
		○ Rotavirus
51
Q

What does a rotavirus infection look like?

A

• 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
Q

What infection causes a “flask shaped ulcer”?

A
  • Entamoeba histolytica infection
    • Severe dysentery-like fulminant colitis
    • Can go to liver
53
Q

Ascaris lumbricoides is an example of what?

A
  • Helminth. Common delevloping country and immigrant disease
    • Common in tropics
    • Ingested from soil contaminated with ova from feces
    • Obstruction, perforation, growth retardation
    • Big, macroscopic worms