GIT Dz.
Gastritis Type A
(Also known as
Biermer's anemia,
Addison's anemia,
Pernicious
Anemia)
Gastritis Type B
Site of Dz.
Stomach
Pathogenicity (I.M.)
Autoimmune mediated Dz due
to Anti-Parietal cell (Atrophic
gastritis), Anti-intrinsic factor
results in inhibition of Vitamin
B12 absorption
H.pylori mediated Dz. Results in
peptic ulcer due to Cytotoxin A [
vacuolating toxin A (vac A)] or
genetic virulent strain [(CagA
protein (CagA+)]: gastric
Corpus inflammation results in
, parietal cells inhibition leading
to reduced acid secretion.
Continued inflammation results
in loss of parietal cells while
Antral inflammation alters
gastrin and somatostatin
secretion, affecting G cells
(gastrin-secreting cells) and D
cells (somatostatin-secreting
cells)
Main Clin. Feature
Severe gastric parietal cell
atrophy. The disease has an
insidious
onset
and
progresses
slowly.
Cobalamin deficiency affects
the
hematologic,
gastrointestinal,
and
neurologic systems.
Many signs and symptoms
are attributed to anemia:
Fatigue, low blood pressure,
rapid heart rate, pallor, and
shortness of breath, Neuropathic pain, diarrhea, Paresthesias, such as pins and
needles
sensations
or
numbness in fingers or toes,
due to B12 deficiency
affecting nerve function
Bad breath (ie, halitosis)
and abdominal pain or
discomfort may occur, with
bloating associated with
bacterial overgrowth syndrome. Persistence of the
organism causes H pylori
chronic gastritis, with development of complications
which include peptic ulcers,
gastric adenocarcinoma, and
MALT lymphoma.
Main Diagnostic Lab. Test
Lab. Tests: 1.CBP, 2.Bone
marrow
examination
(MCV,MCHC, 3.serum holotranscobalamin II, 4.serum
LDH,
5.Schilling Test,
corrected with (IF) 6.TIBC,
7.Serum methylmalonic acid
(MMA) level , 8.serum Vitamin
B12 level measurement
9.Anti-parietal and anti-IF
antibodies in the serum &
10.Gastrin estimation.
Endoscopy:
To
detect
inflammatory areas (spares
Antrum in Type A Gastritis)
Endoscopy & Invasive
methods:
1. Micro-Culture of biopsy
2. Rapid urease test from
gastric biopsy tissue
Non-invasive:
1.Breathe test, ELISA serum
test for Anti-H. pylori IgG
Detection.
2.Estimation of Gastrin,
3.Pepsinogen I to pepsinogen
II ratio
GSE (Glutin
Sensitive
Enteropathy)
Small Intestine The inflammatory lesions are
Mainly children found at the area in great contact
affected
the ingested gliadin. After
endocytosis,
gliadin
will
presented results in an increased
No. of lamina propria (LP)
mononuclear cells underlying
normal intestinal crypts & villi,
which leads to TH1 activation
and release of TNF- α, IFN-γ & Il1β; that induce fibroblast to
produce
metallo-proteinases
ended with the proximal injury to
the LP matrix supporting the villi.
These events progress to further
increased in cellular filtrate &
development of hypertrophic
crypts and elaborate crypt
epithelial cells at a rate that
compensates for the loss of
epithelial villous cells. Further
inflammatory progression due to
B cells activation and production
of s-IgA antigliadin Ab. & Ab
Malabsorption of nutrients
results in diarrhea and loss
of many factors responsible
for functioning of organs like
fatigue, malaise, bone pain,
wt. loss diarrhea , abdominal
pain, infertility Gas, flatus,
borborygmus and others.
Endoscopy to detect villus
atrophy in intestine and
biopsy.
Serological Tests: For
detection of Antis-IgA
antigliadin Ab, Anti-tTG and
Anti-endomysial Ab (EMA) are
the most sensitive specific
tests for GSE and indicators
for tissue damage in LP and
Crypt.
Crohn’s’ Dz.
Dermatitis
herpetiformis
is
intensely
pruritic lesions
f skin typically
occurs on the
back, buttocks,
knees,
and
elbows
against an endogenous enzyme
[transglutaminase (tTG)]. These
entire Ab act to activate
complement and subsequently
amplify-ing the inflammatory
process to reach a destructive
stage by intense mono-nuclear
infiltrate associated with crypt
hyperplasia that can no longer
keep pace with the loss of villous
cells ; as a result, the villi become
shortened or even flattened &
the Pt. now develop the
characteristic malabsorption of
GSE. Prolonged inflammation,
the mature lesion may progress
to the fibrotic or burned
permanent stage and the Pt no
longer fully recovers when
placed on a gluten-free diet.
From the
mouth till the
anus
Cell-mediated I.R. due to TH1
activation and release of IL-17,
INF-γ results granuloma
formation
Stricturing disease causes
narrowing of the bowel which
may lead to bowel
obstruction or changes in the
caliber of the feces.
Penetrating disease creates
abnormal passageways
(fistulae) between the bowel
and other structures such as
the skin. The nature of the
diarrhea in Crohn's disease
depends on the part of the
small intestine or colon that
is involved. Ileitis typically
results in large-volume
watery feces. Colitis may
Endoscopy for detection the
site or locus of inflammatory
pouch, types of lesions
(continuous or noncontinuous) and biopsy for
detection of inflammatory
lesion if they are superficial
(shallow) or deep in the bowel
wall [transmural].
Blood Tests: CBC & ESR.
Serological: Anti-Neutrophil
Cytoplasmic Antibody
(ANCA) & antiSaccharomyces cerevisiae
antibodies (ASCA)
CRP, GSE
Ulcerative Colitis
Restricted to
colon
Genetic susceptibility may be
triggered in a susceptible person
by environmental factors.
Although dietary modification
may reduce the discomfort of a
person with the disease which
leads to TH2 cell activation and
release of IL-4, IL-5 and Levels
of sulfate-reducing bacteria tend
to be higher in persons with
ulcerative colitis. This could
mean that there are higher
levels of hydrogen sulfide in the
intestine
result in a smaller volume of
feces of higher frequency.
Fecal consistency may
range from solid to watery. In
severe cases, an individual
may have more than 20
bowel movements per day
and may need to awaken at
night to defecate. Visible
bleeding in the feces is less
common in Crohn's disease
than in ulcerative colitis.
Flatulence and bloating
None intestinal features
include Arthritis, eye
problem, & skin lesions
Intestinal Manifestation:
Pseudo polyps formation as
a result of superficial shallow
inflatiomatory lesion which
extended in continuous
fashion results in tenesmus
pain due to proctitis then
Proctosigmoiditis ,
Extensive colitis to
Pancolitis (i.e. megacolon)
from rectum to cecum.
Extra intestinal
manifestation: aphthous
ulcers involving the
tongue, lips, palate and
pharynx
Pyoderma gangrenosum
on the skin
Musculoskeletal
involvement,
CBC& ESR.
Electrolyte studies and renal
function tests. Liver function
test, Urine analysis, Stool
culture, CRP & Serological
tests (ANCA & ASCA Tests)
Sigmoidoscopy & Biopsy