Diseases of the lower GI path

Question 1

1. Define Gluten Sensitive Enteropathy and describe the diagnostic histologic features.

Answer 1

exposure to α-gliadin peptide results in autoantibody formation → inflammation ( ↑ T-lymphocytes) → villous atrophy → tissue damage → loss of mucosal and brush-border surface area → malabsorption, diarrhea

villous blunting (atrophy)
increased intraepithelial lymphocytes
lymphoplasmacytosis of the lamina propria
Scalooped mucosa in duodenum

Associated with dermatitis herpetiformis blistering skin disease
Celiac-disease associated malignancies include enteropathy-associated T-cell lymphoma (EAT Lymphoma), and small intestinal adenocarcinoma

Question 2

2. Describe the etiology and clinical presentation of Whipple’s disease.

Answer 2

Pathogenesis-
Caused by gram-positive bacilli Tropheryma whippelii
Bacilli absorbed by lamina propria MO’s
Organism-laden macrophages accumulate within the small intestinal lamina propria and mesenteric lymph nodes → lymphatic obstruction→ Impaired lymphatic transport causes malabsorptive diarrhea

Presentation-
Triad of diarrhea, weight loss, malabsorption
Other common symptoms: arthritis, lymphadenopathy, neurologic disease
Typically presents in middle-aged or elderly white males

Question 3

4. Describe acute and chronic ischemic colitis and its complications.

Answer 3

Clinical Features
Older individuals with co-existing cardiac or vascular disease
Young patients: long-distance runners, women on oral contraceptives
Mechanical Obstruction: hernias, volvulus

Pathogenesis
Lack of blood flow due to:
Low cardiac output
Occlusive disease of vascular supply to bowel
most often splenic flexure or recto sigmoid

Diagnosis
Clinical presentation:
Acute transmural infarction: severe abdominal pain, tenderness, nausea and vomiting, bloody diarrhea and blood in stool
Peristaltic sounds disappear, rigid abdomen, shock, sepsis

Histologic Findings
Varies from focal acute mucosal necrosis to full-thickness necrosis

Question 4

5. Define pseudomembranous colitis, and describe the “pseudomembrane” and the etiology of this form of colitis.

Answer 4

most common C Diff. most implicated with ceftriaxone. bug found on fomites, like stethoscopes–> releases toxin, breaks epithelial brrier–> diarrhea cell death and creates psuedo membranes- thick layer of all types of stuff

no crypts, volcano like eruption of debris

Question 5

6. Describe the two histologic patterns associated with the clinical entity of microscopic colitis and explain why it is called “microscopic” colitis.

Answer 5

can only be identified on microscopy.

Collagenous collitis-Thickened subepithelial collagen layer

Lymphocytic colitis-Increased intraepithelial lymphocytes

Question 6

7. Compare and contrast the gross and microscopic features of Crohns Disease and Ulcerative Colitis.

Answer 6

Crohns-
Skip lesions, Ileal involvement (“regional enteritis”)
Transmural chronic inflammation, Inflammatory strictures
Fissuring ulcers, sinus tracts, fistulae. *can affect u from mouth to anus spares rectum
wall appearance thickened (fibrotic)
ulcers- deep knife like
lymphocytes- high
fibrosis- high
serositis- high
*granulomoas- yes
fistuylae- yea

crypt architectural distortion, Cryptitis (PMNs), crypt absesess

UC-
always *Rectal involvement with retrograde continuous diffuse disease up colon, No ileal involvement (except “backwash ileitis”)
Disease worse distally, Mucosal inflammation only – no transmural disease, No fissures, sinuses, fistula tracts
* extra GI issues- primary sclerosing cholangitis
wall appearance thinned–>megacolon
ulcers-superficial broad based
lymphocytes moderate
fibrosis- none
serositis- none
*granulomas- no
fistulae-nope

crypt architectural distortion,Cryptitis (PMNs), crypt absesess

Question 7

8. Describe the anatomic process underlying diverticulosis, list the clinical factors that predispose to this illness, and explain a diverticulum.

Answer 7

Pathogenesis
Results from decreased dietary fiber → decreased stool bulk → elevated intraluminal pressure → mucosal herniation through focal defects in the bowel wall

Question 8

9. Describe the histologic features of appendicitis.

Answer 8

Mucosal ulceration
Transmural acute and chronic inflammation
Extension of inflammation into the mesoappendix

Question 9

Giardia

Answer 9

7-14 day incubation period, cysts are resistant to chlorine, wt loss chronic diarrhea, malabsorption, flatulence, protozoa, treat with flagol

looks like schools of fish in the lamina propria

Question 10

campylobacter

Answer 10

watery diarrhea, found in contaminated meat poultry dairy

Question 11

salmonella

Answer 11

gram - bacillus transmitted through food and water
typhoid-bloody diarrhea, abd pain, characteristic abdominal rash, headache fever.
non-typhoid- mild self limited

Question 12

E.Coli (0157:H7)

Answer 12

non invasive, toxin prodcuing contaiminated hamburger
bloody diarrhea, severe cramps, mild or no fever, sometimes renal failure, can be deadly
edema erosions ulcers hemorrhage

Question 13

viral

Answer 13

most self limited infectious diarrhea

Question 14

rotovirus

Answer 14

causes extreme watery diarrhea, babies most vulnerable, osmotic diarrhea.

Question 15

parasitic- entamoeba histolytica

Answer 15

10% of world has it
severe dysentric like fulminant colitis
can disseminate to liver
cecum most common
flask shaped ulcers

Question 16

parasitic- helmynths (ascaris lumbricoides)

Answer 16

look at stool for ova and worms
nutritional problems can be severe
tropics
soil contaminated with feces
obstruction perforation growth retardation
worms can be giant