Small intestinal diseases

and malabsorption
By
ESSAM .M.B.HELAL
Assist.prof intern med.
Ain Shams Univ.
 Small intestinal function
Assimilation of nutrients : digestion and absorption
Three phases:
-intraluminal phase:hydrolysis of fats ,protiens
,&carbohydrates.
-biliary&pancreatic juice are needed.
Fats:by pancreatic lipase into monoglycerides and
fatty acids---form micelles with bile salts ---
important for absorption of fat soluble
vitamins(A,D,E,K)
 Small intestinal function
-protiens by pancreatic proteases ---- di
&tripeptides&aminoacids.
-impaired intraluminal phase :insufficient
concentrations of biliary or pancreatic
secretions
Small intestinal function
 mucosal phase:
-it needs sufficient surface area of intestinal
epithelium
Brush border enzymes :important for
hydrolysis of disaccharides and di&
tripeptides
-deficiency of isolated brush border enzymes--
---malabsorption of specific nutrients
-primary mucosal disease<extensive
resection,infilteration of intestina wall.
 Absorptive phase
Obstruction of lymphatic system results in
impaired absorption of chylomicrons and
lipoprotiens----steatorhea&excessive protien
losses (protien losing enteropthy)
 Clinical and laboratory
manifestations of malabsorption
-steatorrhea(bulky ,light-colored,greasy stools)---lab:
increased fecal fat (>6gm/24 h.stools)----fat
malabsorption.
-diarrhea(increased fecal water)lab:increased frcal
fat ,positive bile salt breath test.---fatty acids or
bile salts.
-weight loss,malnutrition(muscle wasting ),fatigue
,weakness.abd.distention---lab:incresed fecal fat
content,decreased glucose &xylose absorption----
calories(fat,protien ,carbohydrates).
 Contin.
-iron deficiency anemia:---lab:hypochromic
anemia,low seum iron-----iron malabsorption.
-megaloblastic anemialab:macrocytosis,impaired
vit, B12 absorption,decreased serum B12 and red
cell folate.----vit.B12 or folic acid malabsorption
-parasthesia,tetanylab:decreased serum calcium
,magnesium &potassium.---malabsorption of
calcium ,vit D,magnesium,potassium.
 Contin.
-bone pain,pathologic fractures ,skeletal deformities-
---- osteoporosis on x-ray,osteomalacia on bone
biopsy.-----calcium ,protien malabsorption.
-bleeding tendency.----lab:prolonged prothrombin
time----- vit.k deficiency
-edema:----lab:decreased serum albumin,increased
fecal loss of protien.---protien malabsorption or
protien losing enteropathy.
-milk intolerance___lab:flat lactose tolerance
test,decreased mucosal lactase levels----lactose
malabsorption
 Celiac disease
-immune mediated disease in genetically
predisposed patients.
-celiac diseaseceliac spruegluten sensitive
enteropathy.
It results from intolerance to wheat gluten and
similar protiens found in rye,barley,and oats.
-it responds to gluten free diet.
-world wide distribution but more common in
northern europe.
 Celiac disease
Pathogenesis :immune reaction to gluten-----
inflammationin intestinal mucosa----
subtotal villus atrophy---malabsorption.
-it may be manifest ,silent,latent.
Celiac disease:pathogenesis
Celiac disease:pathology
Celiac disease:pathology
Celiac disease:pathology
Celiac disease:pathology
 Celiac disease:c/p
In infancy:after weaning and addition of
cereals in food :diarrhea,bloating ,abd .pain
,failure to thrive,retarded growth.
In adults:variable from marked malabsorption
to fatigue,wt, loss anemia.
-associated with other immune
disorders:DM,SARCOIDOSIS THYROID
DISEASE,IBD,DERMATITIS HERPETIFORMIS
 CELIAC DISEASE:diagnosis
-c/p
-endoscopic small intestinal biopsy &histopathology is the
gold standard for diagnosis----subtotal villous
atrophy.(DD).
-SEROLOGY:-serum antigliadine antibodies(igA)-serum anti
endomysial antibodies(igA)----SENSITIVESPECIFIC
-the autoantigen for antiendomysial antibodies is tissue
transglutaminase.
-serum assay of TTGis better than other abs.specially if there
is igA defeciency.
-CBC and biochemical profile to evaluate malabsorption.
 Celiac disease:management
-ensure gluten free diet :exclude wheat, rye
,barley,oats.
-rice,maize,potatoes are satisfactory sources of
complex cabohydrates
-minerals and vitamins supplements to correct
existing deficiencies.
-in refractory pts. Steroids and immunosupp ressives
are needed.
-prognosis:increased risk of lymphoma small
intestinal carcinoma and esophageal carcinoma.
 Dermatitis Herpetiformis
-crops of itchy blisters over the skin of elbows
,back,buttocks,knees.
-igA deposits in dermo epidermal junction.
-associated with subtotal villous atrophy.
Associated with celiac disease in10% of pts.
-symptomatic pts .respond to gluten free diet
And may need DAPSON for their skin lesions.
 Tropical sprue
It is a state of chronic progressive malabsorption in a patient
in or from tropics.
-structural and fuctional abnormalities in small intestine.
-an infectious agent(s) is incriminated.
-srarts as acute diarrhea-----small intestinal bacterial
overgrowth e.g.E.coli,Enterobacter,Klebsiella----chronic
intestinal mucosal damage(partial villous atrophy)-----
chronic diarrhea&malabsorption.
D.D:CAUSES OF INFECTIOUS DIARRHEA particularly in
visitors to tropical areas ttt:Tetracycline 250 mg /6h. For
4w. Or more .+supplementation by folic acid5mg /day.
 Small bowel bacterial
overgrowth(blind loop syndrome)
-Normal bacterial count in duodenum and
jejunum is <10000/ml(saliva).cliform
bacteria<1000.
In bacterial overgrowth syndrome, the count
is >1000000/ml
Disturbed mechanisms.bacterial overgrowth
:gastric acidity,intestinal motility,structural
abnormalities.,impairedimmune function.
 Bacterial overgrowth syndrome
c/p:watery diarrhea and/or steatorrhea,anemia due to B12
deficiency----due deconjugation of bile acids---impaires
micelles formation and due bacterial utilization of B12
-investigations:-serum B12 is low/folic acid normal or
high(bacterial formation)
-barium follow through /or small itestinal enema ---blind
loop/or fistula
-endoscopic duodenal biopsy to excludemucosal disease /and
to aspiratesmall intestinal contents for bacteriologic exam.
-
ttt:tetracycline250mg/6h,ciprofloxacine,metronidazole+sup
plements of B12 +ttt of the cause.
 Whipple,s disease
-infilteration of small intestinal mucosa by foamy
macrophages which stain +ve withPAS stain.
-multisystem disease,any other organ can be
affected ,even before GITaffection.
-middle aged men are most frequently affected----
c/p according to the pattern of organ system
affected
-usually :fever,joint manifestations neurologic
manifestations ,and GIT manfestations
(diarrhea,steatorrhea,wt.loss ,protien losing
enteropathy ..edema,ascites ,hepatosplenomegaly.
 Contin.
Musculoskletal:seronegative arthropathy of
large joints+sacroiliitis.
Cardiac:pericarditis,myocarditis ,endocarditis
,coronary arteritis.
Neurological:dementia,fits,abnormal
movements,meningitis.cranial nerve lesions.
Pulmonary:pulmonary infilterates pleurisy
chronic cough.
Hematological:anemia ,lymphadenopathy
 Whipple,s disease pathology
E/M:small gram +ve bacilli inside
macrophages---villi are widened and
flatteneddense infilteration of lamina
propria by macrophagesobstruct
lymphaticsfat malabsorption.
 management
Whipple disease is fatal if left untreated.
-antimicrobials are needed:co-trimoxazole---
tetracycline takes few weeks to respond.
 Ileal resection
-usually for ttt of Crohn,s disease
-B12 and bile salt malabsorption---fat
malabsorption,macrocytic anemia,secretory
diarrhea.
Decreased bile salt pool---lithogenic bile---
gallstones,
-renal stones rich in oxalates develops
(unabsorbed bile salts bind calcium in colon
oxalate hyper absorptionrenal stones)
 Short bowel syndrome
Causes:extensive surgical resction ,extensive
disease,radiation,congenital anomalies in
children.
-nearly most of digestion,absorption can be
completed in the first 100cm of
jejunum,most of water reabsorption (8
liters).
 Short bowel syndrome
c/p:large volume of jejunostomy fluid loss or
if colon is preserveddiarrhea or
steatorrhea.dehydration ,wt loss,muscle
wasting,mineral and vitamin deficiency.
-management: immediately,postoperatively
TPN---PPIS to reduce gastric secretions
Gradually enteral feeding is introduced as
tolerated.
 Radiation enteritis and colitis
-occures in 10-15% of pts receiving radiotherapy for
pelvic or abdominal malignancies.
Rectum ,sigmoid colon ,terminal ileum are most
frequently affected
-pathologically:acute effect:inflammation,shortening
of villi ,crypt abscess formation---may resolve,or
chronic lesionobliterative endarteritis affecting
submucosal arterioles2-12 monthes---
progressive ischemic fibrosis over years
adhesions,ulceration,strictures,obstruction.
 Radiation enteritis
c/p: acute:nausea,vomiting ,crampy abd
pain,diarrhea,tenesmus,recral bleeding.
--chronic:strictures,adhesions ,bleeding from
telagiectasia,malabsorption
-investigations:.colonoscopy to determine
extent of the lesion.
-ttt:symptomatic for diarrhea,cholysteramine
to chelate bile salt,endoscopic laser or argon
plasma coagulation for rectal bleeding
 Abetalipoproteinemia
-rare autosomal recessive disorder.
-deficiency of apolipoprotein B--- failure of formation
of chylomicrons---fat malabsorption ,+deficiency
of fat soluble vitamins
-jejunal biopsy:enterocytes distended with
resynthesized triglycerides+normal villi
-other organ system affection :retina ,nervous
system ,anemia
-it responds to low fat diet +supplemeted by
medium chain triglycerides and vit.A,D ,E,K.
 THANK YOU
THANK YOU.