Non-neoplastic bowel diseases

Question 1

Aside from IBD, what are 4 causes of colitis ?

Answer 1

Diversion Colitis, collagenous colitis, lymphocytic colitis, Graft versus host disease.

Question 2

When does diversion colitis occur? How? What is the gross and microscopic pathology? What are some possible pathogeneses? Treatment?

Answer 2

 Occurs post surgical intervention and when the normal fecal flow is diverted

 Colitis develops within the diverted segment

 Gross: mucosal erythema and friability

 Microscopic:

o numerous mucosal lymphoid follicles

o increased numbers of lamina propria lymphocytes, monocytes, macrophages, and plasma

o resemble IBD in servere case (cryptitis, crypt abscesses, mucosal architectural distortion, or, rarely, granulomas).

 Possible pathogenesis:

o changes in the luminal microbiota

o lack of nutrients from the fecal stream to colonic epithelial cells.

 Treatment:

o enemas containing short-chain fatty acids

o restoration of fecal flow.

Question 3

What is collagenous colitis? In which pts. does it occur? What will colonoscopy be like? What will the microscopic pathology be like?

Answer 3

Collagenous colitis

 AKA microscopic colitis together with lymphocytic colitis

 Middle-aged and older women with chronic watery diarrhea

 Normal colonoscopy

 Microscopic:

o characterized by the presence of a dense subepithelial collagen layer (referred to as “ irregularly thickened collagen table”)

o increased numbers of intraepithelial lymphocytes, and a mixed inflammatory infiltrate within the lamina propria

o surface epithelial injury and regeneration.

Question 4

How will lymphoctyic colitis present? How does it compare/contrast to collagenous colitis? What is it associated with?

Answer 4

 AKA microscopic colitis together with collagenous colitis

 Men or women with chronic diarrhea

 Microscopic:

o no thickened collagen table

o increased numbers of intraepithelial lymphocytes, frequently exceeding one T lymphocyte per five colonocytes

o increased numbers of intraepithelial lymphocytes, and a mixed inflammatory infiltrate within the lamina propria

o surface epithelial injury and regeneration.

 Strong association with celiac disease and autoimmune diseases, including thyroiditis, arthritis, and autoimmune or lymphocytic gastritis.

Question 5

When does GVHD colitis occur? Which parts of the GI are affected? What causes it? Presentation? microscopic histology?

Answer 5

 Occurs following allogeneic bone marrow transplantation

 Involvement of small bowel and colon in most cases

 Secondary to donor T cells targeting antigens on the recipient’s GI epithelial cells

 Clinical presentation: commonly watery diarrhea

 Microscopic:

o sparse the lamina propria lymphocytic infiltrate

o epithelial apoptosis (particularly of crypt cells) with or without resultant total crypt destruction is the most common histologic finding.

Question 6

What are the two watershed zones for Ischemic bowel disease? What are the two types of intestinal ischemia? What is the pathogenesis? What are the gross and microscopic pathologies?

Answer 6

• the splenic flexure (SMA, IMA)
• the sigmoid colon and rectum (IMA, pudendal, and iliac arterial circulations end)

 Two types: mesenteric (superior mesenteric) or colonic (ischemic colitis).

 Pathogenesis:
o initial hypoxic injury
o followed up by reperfusion injury which is more extensive and hemorrhagic.

 Gross:
o infarct starting from mucosal surface extending to mural infarct or transmural infarct in more severe cases
o patchy or segmental with sharp demarcation from non-involved areas

 Microscopic:
o acute: necrosis or sloughing of mucosa, inflammatory cells absent initially, neutrophils recruited within hours of reperfusion, pseudomembrane formation in some cases
o chronic: fibrous scarring of the lamina propria (hyalinization) and mucosal atrophy (withering of crypts).

Question 7

Clinically, what does mesenteric ischemia require? What is it like? What are some etiologies? How does it present? How is it diagnosed? What happens if it is diagnosed late? How is it treated?

Answer 7

o Requires a high index of suspicion for early diagnosis and treatment.

o Acute form more common than chronic.

o Etiologies: SMA Embolus, non-occlusive mesenteric ischemia, SMA thrombus, SMV thrombus

o Presentation: patient with CV risk factors presenting with severe unexplained abdominal pain. Initially with few physical findings.
Later: peritoneal signs, bleeding.

o Diagnosis: CT scan, CT or MR angiography, regular angiography, surgery.

o Late diagnosis leads to infarction, need for extensive resections.

o Treatment: IVF’s, antibiotics, early revascularization, surgery.

Question 8

What does colonic ischemia involve? What is the main etiology with examples? What are some other etiologies? How does it present? How is it diagnosed? How is it treated/approached?

Answer 8

Colonic ischemia: Involves mostly the left colon (IMA)

o Non-occlusive in most cases (hypoperfusion related to decrease in cardiac

output, drugs, hypovolemia, etc.)

o Other causes: post aneurysm repair, vasculitis, emboli, thrombosis.

o Presentation: LLQ pain, bloody diarrhea, low grade fever, anorexia, nausea, Leukocytosis (“diverticulitis with bleeding”).

o Diagnosis: CT scan, colonoscopy.

o Treatment: self-limited in most cases. Supportive treatment (IVF’s, antibiotics, bowel rest).

o Evaluate for underlying factors (medications, cardiac causes, etc.).

Question 9

How is a diagnosis made for a bacterial infectious colitis? What is the most common pattern? What is seen on biopsy? What are some organisms that cause it?

Answer 9

Bacterial infection – stool culture for the diagnosis

 Acute self-limiting enterocolitis

o Most common pattern of bacterial infectious colitis

o Cryptitis and crypt abscesses

o No crypt architectural distortion

o Diagnosis made on stool culture

o Campylobacter

o Salmonellosis (non-typhoid)

o Shigellosis: also aphthous ulcer

Question 10

What are two bacteria that cause granulomatous enterocolitis? What are the clinical/pathological features of each?

Answer 10

 Granulomatous enterocolitis

o Yersinia:

o Multiply extracellulary in lymphoid tissue
o Lymph node and Peyer’s patch hyperplasia
o Aphthous ulcers
o Neutrophilic infiltrate

o Mycobacterium tuberculosis
o Caseating granulomas
o Organism (acid fast bacilli) demonstrable by acid fast
staining (AFB stain).

Question 11

What is pseudomembranous colitis? What causes it? What is the gross/microscopic pathology?

Answer 11

o Caused by Clostridium difficile toxin

o Associated with antibiotic use

o Gross: pseudomembrane

o Microscopic: damaged crypts distended by mucopurulent exudates (forms eruption reminiscent of a volcano), pseudomembrane (coalesce of exudates).

Question 12

What is whipple’s disease? What organism causes it? What is the clinical presentation? What is the LM pathology? What is the EM pathology? What is seen in mycobacteria colitis? What kind of colitis are whipple disease and mycobacteria? What causes an ischemic enterocolitis?

Answer 12

 Diffuse histiocytic enterocolitis

o Whipple disease

o Rare, multivisceral chronic disease
o Clinical presentation: malabsorption, lymphadenopathy,
and arthritis
o Caused by gram-positive actinomycete, Tropheryma
whippelii
o Dense accumulation of distended, foamy macrophages
containing periodic acid-Schiff (PAS) positive, diastase-resistent granules that represent lysosomes stuffed with partially digested bacteria in the small intestinal lamina propria
o EM: rod-shaped bacilli

o Mycobacteria (especially atypical mycobacterial infection in immunocompromised patients)
o Foamy macrophages in the lamina propria that are PAS-positive
o Also AFB stain positive

 Ischmic pattern

o Enterohemorrhagic E coli (O157:H7)

Question 13

What are 3 causes of parasitic enterocolitis? For each, describe the organism, how it is diagnosed, where they are found, and what the resulting intestinal morphology is.

Answer 13

 Giardia
o Most common pathogenic parasitic infection in humans
o Flagellated protozoans
o Trophozoites can be identified in duodenal biopsies
 Pear shape with two nuclei of equal size like “falling leaves”
 Large numbers of organisms show sickle shape
o small intestinal morphology normal to villous blunting with intraepithelial lymphocytosis and lamina propria inflammatory infiltrate in patients with heavy infection

 Cryptosporidium
o Minimally altered mucosal histology
o Villous atrophy, crypt hyperplasia and variable inflammatory infiltrates in heavy infection in immunosuppressed individuals
o Microscopic: intracellular sporozoites appear sitting on top of the epithelial apical membrane
o More concentrated in the terminal ileum and proximal colon
o Diagnosis: oocysts in the stool

 Entamoeba histolytica
o Flask-shaped ulcer with a narrow neck and broad base
o Also cause amebic liver abscesses

Question 14

What is a diverticula? What is diverticulosis? What is diverticulitis? What complicates it?

Answer 14

 Acquired pseudodiverticular outpouchings of the colonic mucosa and submucosa

 Multiple – diverticulosis

 More commonly sigmoid colon

 Diverticulitis: obstruction of diverticulae leads to inflammatory changes, producing diverticulitis and peri-diverticulitis.

 Complication: perforation and segmental diverticular disease-associated colitis.

Question 15

How common is colonic diverticulosis? What causes it? Where does it often arise? How often is it symptomatic? What are some symptoms? How is it diagnosed? How is it treated? What is the presentation of diverticular bleeding? How is it managed?

Answer 15

o Very common: >50% prevalence in persons aged >60.
o Increasing incidence in younger individuals.
o Higher incidence in developed countries.
o 80% remain asymptomatic.

B. Related to wall stress
1 . Associated with constipation, straining, and low-fiber diet; commonl y seen in
older adults (risk increases with age)
2. Arise where the vasa recLa traverse the muscularis propria (weak point in colonicwall); sigmoid colon is the most commo n location.

C. Usually asymptomatic; complications include
1 . Rectal bleeding (hematochezial
2. Diverticulitis—due to obstructing fecal material; presents with appendicitis-like symptoms in the left lower quadrant
4. Anorexia, nausea, constipation or diarrhea,
3 . Fistula—Inflamed diverticulum rupture s and attaches to a local structure.
Colovesicular fistula presents with air (or stool) in urine.

o Diagnosis: CT scan (inflammation, micro- or macro-abscess,peritonitis). Previously: gastrograffin enema. Possible “gentle” limited endoscopy to exclude other diseases (ischemia, colitis, etc.).

o Treatment: NPO, antibiotics, CT drainage (abscess),+/- surgery.

DIVERTICULAR BLEEDING
o Clinical presentation: acute, sudden hemorrhage with or without symptoms of hypovolemia.
o Red or maroon stools depending on location and severity. Melena very rare.
o Not a cause of chronic GI blood loss (iron deficiency).
o Management: volume replacement essential. Correct
coagulopathy if present. If massive perform EGD first to rule out UGI source, otherwise colonoscopy as soon as prep feasible. If lesion identified can be treated endoscopically. If specific site not identified: Angiography or tagged RBC scan.

Question 16

What is Celiac disease? Which HLA types is it associated with? Describe the pathogenesis of it. How do children present? How do adults present? What is an associated clinical sign? What causes it? What lab findings will there be? Which part of the GI system is most effected ? What is the microscopic pathology? How is it treated? What are some late complications?

Answer 16

A. Immune-mediate d damage of small bowel villi due to gluten exposure; associated with HLA-DQ 2 and D Q 8

B. Gluten is present in wheat and grains; its most pathogenic component is gliadin.
1 . Once absorbed, gliadin is deamidate d by tissue transglutaminas e (tTG).
2. Deamidated gliadin is presented by antigen presenting cells via MHC class II.
3 . Helper T cells mediate tissue damage .

C. Clinical presentation
1 . Children classically present with abdominal distension, diarrhea, and failure tothrive.
2. Adults classically present with chronic diarrhe a and bloating.
3 . Small, herpes-like vesicles may arise on skin (dermatitis herpetiformis) . Due to
IgA deposition at the lips of dermal papillae; resolves with gluten-free diet

D. Laboratory findings
1 . IgA antibodies against endomysium, tTG, or gliadin; IgG antibodies are also present and are useful for diagnosis in individuals with IgA deficiency (increased
incidence of IgA deficiency is seen in celiac disease).
2, Duodenal biopsy reveals flattening of villi, hyperplasia of crypts, and increased intraepithelial lymphocytes (Fig. 10.18). Damage is most prominent In the duodenum; jejunum and ileum are less involved,

E. Symptoms resolve with gluten-free diet.
1 . Small bowel carcinoma and T-cell lymphoma are late complications that presentas refractory disease despite good dietary control.

Question 17

What are hemorrhoids? How common are they? What causes them? What is the difference between external and internal hemorrhoids? What do they look like histologically? Why are they troublesome? What is the bleeding like? What are they commonly associated with? Commonly confused with? How are they diagnosed? Treated?

Answer 17

 Hemorrhoids affect about 5% of the general population and develop secondary to persistently elevated venous pressure within the hemorrhoidal plexus.

 Collateral vessels within the inferior hemorrhoidal plexus are located below the anorectal line and are termed external hemorrhoids, while those that result from dilation of the superior hemorrhoidal plexus within the distal rectum are referred to as internal hemorrhoids.

 Histologically, hemorrhoids consist of thin-walled, dilated, submucosal vessels that protrude beneath the anal or rectal mucosa.

In their exposed position, they are
subject to trauma and tend to become inflamed, thrombosed, and, in the course of time, recanalized. Superficial ulceration may occur.

 Normal vascular channels of the anal region.
 Abnormal if prolapsed, bleeding or thrombosed (pain).
 “Rectal outlet bleeding” vs. LGI bleeding:
BRB on toilet paper, around stool, in toilet bowl (in small amounts) or on underwear.
 May be internal or external.
 Common with constipation, straining, hard stools.
 Frequently confused with pruritus ani, fissures, tears, cancer.
 Diagnosis: inspection, anuscopy, flexible sigmoidoscopy with retroflexion.

 Treatment: patient education, sitz baths, stool softeners, suppositories, fiber.

 If persistent: endoscopic banding or surgical resection.

Question 18

What is angiodysplasia? What causes it? What does it result in? How is it diagnosed? Treated?

Answer 18

A. Acquired malformatio n of mucosal and submucosal capillary beds
R. Usually arises in the cecum and right colon due to high wall tension
C. Rupture classically presents as hematochezia in an older adult.

o Diagnosis: colonoscopy, endoscopy, angiography.
o Treatment: observation, iron replacement, cautery.

Question 19

What is the morphology of acute appendicitis? What does diagnosis require? What can it lead to? What causes it? What are some clinical features? What are some complications? How is it diagnosed? Treated?

Answer 19

Morphology. In early acute appendicitis subserosal vessels are congested and there is a modest perivascular neutrophilic infiltrate within all layers of the wall. The inflammatory reaction transforms the normal glistening serosa into a dull, granular, erythematous surface. Diagnosis of acute appendicitis requires neutrophilic infiltration of the muscularis propria. Although mucosal neutrophils and focal superficial ulceration are often present, these are not specific markers of acute appendicitis. In more severe cases a prominent neutrophilic exudate generates a serosal fibrinopurulent reaction. As the process continues, focal abscesses may form within the wall (acute suppurative appendicitis). Further appendiceal compromise leads to large areas of hemorrhagic ulceration and gangrenous necrosis that extends to the serosa creating acute gangrenous
appendicitis, which is often followed by rupture and suppurative peritonitis.

A. Acute inflammation of the appendix; most common cause of acute abdomen
B. Related to obstruction of the appendix by lymphoid hyperplasia (children) or a fecalith (adults)
C. Clinical features include
1 . Periumbilical pain, fever, and nausea; pain eventually localizes to right lower quadrant (McBurney point).
2. Rupture results in peritonitis that presents with guarding and rebound tenderness.
o Complications: perforation (10-15%), peritonitis, abscess, septic thrombophlebitis (portal vein), sepsis.

DIAGNOSIS
o Very wide differential diagnosis: ileitis, ileo-colitis, mesenteric adenitis, Crohn’s disease, ovarian cystic pathology, etc.
o Leukocytosis in 80%.
o Clinical diagnosis can be made in 50-60% of cases.
o CT in non-classic cases.

Treatment:

o Surgical resection (laparoscopic whenever possible).
o Early diagnosis and intervention critical to avoid peritonitis and sepsis.
o Many unnecessary surgeries.

Question 20

What is intestinal obstruction? Where is it more common? What is the most common etiology in the small bowel? Less common? In the colon? What are some results of it (pathophys)?

Answer 20

 Obstruction: impaired intestinal transit due to a mechanical block.
 To be differentiated from ileus and pseudo-obstruction (failure of normal motility).
 More common in small bowel than colon.
 May be partial or complete.
 May occur with or without ischemia (strangulation).

Etiologies:

o Small Bowel Obstruction (SBO): Adhesions account for 75% of all cases.
o Other causes: strictures (Crohn’s disease, ischemia, radiation,), neoplasm, hernias, congenital causes (atresia, stenosis), extrinsic compression (abscess, neoplasm), intussusception, volvulus.
o Colon: cancer, diverticulitis and volvulus account for 90% of cases.

PATHOPHYS
o Increased fluid secretion and motility.
o Accumulation of fluid in the intestinal lumen.
o Systemic hypovolemia.
o Local ischemia.
o Translocation of intestinal bacteria, possible sepsis.

Question 21

What are some clinical manifestations of intestinal obstruction? How is it treated?

Answer 21

Clinical manifestations:

o Abdominal pain (crampy, waxing and waning), distention, nausea, vomiting, obstipation.
o Symptoms vary with duration and location.
o Physical exam: acutely ill. Hypovolemia. Abdominal distention. High pitched bowel sounds with periods of increased activity alternating with quiet exam (in contrast with pseudo-obstruction). Minimal tenderness.
o Obstructive series: distention and air-fluid levels.
o CT scan: distention, air-fluid levels, transition zone.
o In SBO: distended SB, decompressed colon.
o When colon is distended: distal obstruction vs. pseudo
obstruction.

Treatment:
o Volume replacement and naso-gastric suction alone may be sufficient in some cases (as many as >50% if due to adhesions).
o Surgical intervention frequently required (especially if
strangulation, incarcerated hernia, colon cancer).

Question 22

What is pseudo-obstruction? What is meant by ileus? What is meant by pseudo-obstruction? What is ogilvie’s syndrome? What causes pseudo obstruction? How does it present? How is it treated?

Answer 22

Pseudo-obstruction: failure of normal motility:

o Acute: “Ileus”. Small bowel +/- colon.

o Chronic pseudo-obstruction (“pseudo-obstruction” proper).

o Acute colonic pseudo-obstruction (Ogilvie’s syndrome).

o Many different causes: surgery (laparotomy), electrolyte
abnormalities, drugs, infection, inflammation, neuropathies, myopathies, mechanical ventilation, etc.

o Presentation: distention, some pain, nausea, decreased bowel sounds, obstipation.

o Treatment: identify and treat underlying condition. Prokinetic drugs.

Question 23

What is Meckel’s diverticulum? What causes it? What are the rules of 2? How does it present? How is it diagnosed? Treated?

Answer 23

A. Outpouching of all three layers of the bowel wall (true diverticulum, Fig. 10.16)
B. Arises due to failure of the vitelline duct to involute

C. ‘Rule of 2s’
1 . Seen in 2% of the population (most commo n congenital anomaly of the G) tract)
2. 2 inches long and located in the small bowel within 2 feet of the ileocecal valve
3 . Can present during the first 2 years oflife with bleeding (due to heterotopic gastric mucosa} , volvulus, intussusception, or obstruction (mimics appendicitis);
however, mos t cases are asymptomatic.
4. 2 types of ectopic GI mucosa (gastric and pancreatic, although others described).

 Diagnosis frequently made at the time of surgery.
 Technetium pertechnate nuclear medicine scan: uptake by gastric type mucosa (mucus secreting glands).

 Treatment: surgical resection (if necessary).