L6- GIT Pathology III (intestines) Flashcards
Meckel’s Diverticulum:
- (1) definition
- (2) explain the rule of 2’s
- found on (anti-/mesenteric) border
- (4) types
1- incomplete involution of vitelline duct
2- 2% of normal population (x2 in males), 2in (5cm) in length, 2ft from ileocecal valve
3- anti-mesenteric border
4- True Diverticulum (all GIT layers) or Heterotopia (gastric mucosa or pancreatic tissue)
Meckel’s Diverticulum:
- (1) common Sxs
- (2) potential complications
1- asymptomatic
2- hemorrhage / peptic ulcer, intestinal obstruction, diverticulitis, perforation, fistula
Malabsorption syndromes:
- (1) definition
- (2) clinical presentation
- (3) are impaired
1- defective absorption in fats, fat soluble / other vitamins, proteins, carbs, electrolytes, minerals, water
2- chronic diarrhea, steatorrhea
3- digestion, absorption
Celiac Sprue:
- (1) alternate names
- mostly presents in (2- race/age) population
- in atypical presentations in adults, (3) maybe noted
- all intestinal changes are reversible upon (4)
- (5) is a important long-term risk
1- gluten-sensitive enteropathy, non-tropical sprue 2- whites, 1-10 y/o 3- Fe deficient anemia 4- gluten free diet 5- T-cell lymphomas
Celiac Sprue mostly affects (1) segment with (2) changes
Proximal Intestine:
- villous atrophy (typical)
- inc intraepithelial lymphocytes
- inc lymphocytes, macrophages, plasma cells in lamina propria
- elongated, hyperplastic crypts
Celiac Sprue pathogenesis
1) gluten –> gliadin upon contact with brush border
2) gliadin converted to deamidated gliadin by tTG
3) APC attaches to deamidated gliadin via HLA-DQ2/DQ8
4) APC complex activates T cell
5) IFN-γ production
6) activation of B-cell to create Anti-gliadin Anti-endomysium, Anti-tTG Igs
Celiac sprue:
- Ig’s against (1)
- HLA-(2) are heavily involved
- (3) is an important component for pathogenesis and diagnosis
1- (anti-) gliadin, tTG, endomysium
2- HLA-DQ2, HLA-DQ8
3- tTG = tissue transglutaminase
Celiac Sprue histology:
include all changes
- villous blunting
- inc lamina propria in chronic inflammation
- crypt hyperplasia
- intraepithelial lymphocytosis = >30 lymphocytes per 100 enterocytes (normally <20)
Celiac sprue diagnosis investigations
- malabsorption documentation (IDA)
- SI biopsy
- reversal of changes after gluten-free diet
- Serology: Anti-gliadin, Anti-endomysial, Anti-tTG
- HLA genotyping: majority DQ2, sometimes DQ8
Tropical Sprue:
- occurs to people living or after visiting (1) in a (2) time-frame
- involves (3) part of SI in comparison to celiac sprue
- (4) SI appearance
1- Puerto Rico, Caribbean
2- mos-yrs after visit
3- entire SI, mainly proximal SI in celiac’s
4- may appear normal, can appear like celiac’s
Tropical sprue, aka (1):
-pathogenesis is related to (2), therefore (3) are effective in treatment, which is one distinguishing factor from (4)
1- post-infectious sprue
2- superimposed bacterial infection on pre-existing SI injury (although unknown cause)
3- antibiotics
4- celiac’s
Whipple disease:
- caused by (1), described as (2)
- affects (3) parts of the body
- affects (males/females) more
1- Tropheryma whippelii
2- Gram+ sickle shaped bacteria
3- (systemic disease) intestines, joints, CNS
4- males (10:1)
Whipple disease:
- (1) is seen in H&E, PAS stain
- (2) is seen on EM
- (3) may be present in affected areas
- (4) Tx
1- mucosa laden with distended macrophages (a sheet on macrophages) in lamina propria PAS-positive granules
2- rod shaped bacilli
3- granulomatous inflammation
4- antibiotics
Giardia (lamblia):
- described as (1) with (2) forms present in the GIT
- usually acquired due to (3), where (4) and (5) are big risk factors for getting the disease
1- protozoa gut pathogen with flagellum
2- trophozoites, cysts (shed in the GIT)
3- drinking contaminated water with cysts
4- areas of poor sanitation, crowded areas
5- immunosuppression
Cryptosporidium:
- causes (1) in a normal host
- causes (2) in a (3) patient
- (4) appearance on histology
1- self-limiting infection
2- chronic diarrhea
3- AIDS
4- small blue intracellular spheres lying at the top of brush border cells (enveloped by thin layer of host cytoplasm)
obstructional bowel disease is most common in (1) area GIT with either a (2) or (3) cause
1- SI
2- Mechanical: hernias, intestinal adhesions, intussusception, volvulus
3- Non-mechanical / pseudo-obstruction: failure of propulsion due to SM disorder or paralysis or local nerve dysfunction
list the mechanical causes of intestinal obstruction
- herniation
- adhesion
- intussesception
- volvulus
(1) is the most common cause of intestinal obstruction in children, even though there is no (2). If left untreated, (3) may occur.
1- intussusception
2- underlying anatomic defect
3- obstruction and infarction
Intestinal Obstruction:
- (1) clinical features
- (2) clinical complications
- (3) investigations / lab testing
1- abdominal pain, abdominal distension, vomiting, constipation
2- infarction, peritonitis, electrolyte derangement
3- X-Ray, US, electrolytes
list the types of Ischemic Bowel diseases
- mucosal infarction: up to muscularis mucosa
- mural infarction: mucosa and submucosa
- transmural infarction: all 3 wall layers involved
list the causes for Ischemic Bowel disease
Hypoperfusion: acute or chronic
Acute vascular obstruction:
- severe atherosclerosis
- AAA
- hypercoaguable states / oral contraception
- embolizations of cardiac vegetations / aortic atheromas
Ischemic Bowel disease:
- (1) first phase, (2) second phase of pathogenesis
- (3) and (4) aspects of intestinal vascular anatomy also contribute to distribution of ischemic changes
1- initial hypoxic injury
2- reperfusion injury
3- watershed zones (spleni flexure, sigmoid-rectal junction)
4- patterns of intestinal microvessels
Ischemic Bowel disease:
- mainly affects (1) part of the GIT in a (diffuse/discontinuous) fashion
- mucosa often appears (3), and he bowel wall has markedly (4)
1- any level of the gut
2- discontinuous / segmental and patchy
3- hemorrhagic and ulcerated
4- thickening due to edema
Ischemic Bowel disease:
- damage is most pronounced in (1) or (2) events
- (3) of the muscularis propria occurs in days 1-4 and may be associated with (4)
1- acute arterial thrombosis
2- transmural infarction
3- coagulative necrosis
4- purulent serositis and perforation
