• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/8

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

8 Cards in this Set

  • Front
  • Back
Normal SI histology
Villi prominent with smaller crypt component
Normal villous-crypt ratio is 3-5:1
Surface cells mostly columnar absorptive cells with brush border
Goblet cells present
Less than 10 IEL/100 epithelial cells
Brunner’s glands in duodenum
Peyer’s patches in ileum
Celiac Disease-sprue aka non tropical sprue?
An immune – mediated disorder in genetically susceptible hosts (HLA genotype) with damage to SI mucosa & malabsorption.
Worldwide in distribution
Occurs mostly in European whites
Clinical onset anytime from infancy to late adulthood
Abdominal pain, diarrhea, steatorrhea, dermatitis herpetiformis*, fatigue
Pathogenesis of Celiac Disease
2 or more genes involved: class I HLA-B8 & class II HLA-DR3 & DQW2
Exposure to gliadin results in humoral & cell mediated injury
Possible relationship to prior infection with adenovirus I2
E1B viral protein homologous with gliadin possibly resulting in cross reactivity
Serum endomysial and tissue transglutaminase autoantibodies
Refractory Sprue-
Absent or incomplete clinical response to gluten free diet
Abnormalities in T cells in many patients with loss of CD4 & CD8 & with monoclonal rearrangements in TCR gamma gene
? Early T cell lymphoma
Some develop collagenous sprue
Giardiasis
most common parasite in US
More comon in children
infects via ingestion of water or food contaminated by cysts.
Abrubt or gradual onset diarrhea
More severe if underlying malnutrition or disease.
Non invasive, provides mechanical blockade
Crohn's Disease
An idiopathic chronic inflammatory disorder involving any part of the GIT
Worldwide distribution
More common in western nations
In US, incidence is rising; 8/100,000
Genetic susceptibility
Most often presents in 2nd decade
2nd smaller peak in 8th decade
Gross Pathology of Crohn's Disease
Thickened** wall with firm, stiff consistency due to fibrosis in submucosa, muscular hypertrophy & fat wrapping
Strictures- from thickened walls
Fistulas- from fissures going all the way thru walls.
In early or mild disease, mucosa has aphthous ulcers
With progression, fissures or wide based longitudinal ulcers; cobblestone mucosa
Skip areas**
Histopathology of Crohns Disease
Transmural chronic inflammation with lymphoid nodules (string of beads)**
Fibrosis**
Muscular & neuronal hypertrophy
Basilar plasmacytosis
PMNs in LP & epithelium (cryptitis)
Ulcers, including fissures
Pseudopyloric metaplasia
Non-necrotizing granulomas**
(biopsies 30%; resections 60%)
Vasculitis
Variability in changes