MALABSOROPTION It is characterized by sub-optimal obsoption of fat, fat soluble and other vitamines, protein, CBH, electrolytes and minerals and water.
Abnormal fecal defecation of fat (steatorrhae) with variable inappropriate absorption of fat, fat-soluble vits, other vits, proteins, CBH, minerals, water. This can be due to 1.
2. 3.
Indigestion of nutrient to small molecules to be absorbed and transported across intestinal mucosal cells. ↓ absorptive capacity of the bowel mainly small bowel. abnormal transport of absorbed product.
Classification include: 1.
of
the
cause
of
malabsorption
Defective intraluminal hydrolysis or solubility came by secondary or primary pancreatic insufficiency, ↓ conjugated bilirubin and bacterial over growth due to fistula, mild loop, post gastrectomy, and scleroderma or amyloidosis.
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2.
Mucosal surface.
cell
abnormality
and
inadequate
This can be mucosal cell disorder as abetalipoproteinemia, and Vit B12 malabsorption. It could be due to small bowel disease as celiac disease, whipple’s disease, allergic or eosinophilic gastroenteritis and Crohn’s disease. 3.
Lymphatic obstruction, as in lymphoma, TB, and lymphangiectasis.
4.
Multiple defects as subtotal gastrectomy, radiation enteritis and distal ileal resection.
5.
Unexplained: Carcinoid syndrome, D.M., mastocytosis, hypothyroidism hyperthyroidosim.
6.
Infection: Tropical sprue, parasite and acute infectious enteritis.
7.
Drug-induced malabsorption colehicine, irritant laxative neomycin in and phenidione.
From all the above the most common are celiac sprue, regional entity and chronic pancreatitis. Mucosal abnormalities of small intestine in malabsorption syndrome.
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A.
CHARACTERISTIC FINDINGS: 1.
2.
3. 4. 5. 6. 7. 8.
Coeliac and tropical sprue – villi blunted or absent, mucosal epithelium abnormal, crypts lengthened. ↑ mononuclear infiltrate. Whipple – lamina propria filled in glycoprotein containing macrophages, villous abnormality with variable severity Bacilli in macrophages. Abetalipoproteinaemia: vacuolated mucosal cells by lipid inclusion. Villi normal. Agammaglobulinemia: flattened or absent villi, absence of plasma cells, ↑ lymphocytes. Amyloidosis: Regional enteritis: Non-caseating granuloma. Parasitic infection as giardiasis, schistosoma, strongyloidiasis, histoplasma. Mastocytosis – mast cells.
Allergic or eosinophilic enteritis, normal villi, ↑ eosinophils. 10. Lymphoma. 11. TB, mainly the ones involving small intestine
9.
Typhoid Fever Due to salmonella typhi Three phases 1.
Invasion of intestinal lymphoid tissue and proliferation of bacteria – last for 2 weeks and usually asymptomatic.
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2.
Invasion of blood stream bacteraimia general toxaemia ↑ temperature positive widal test at the end of the phase.
3.
Localization of bacteria in intestinal lymphoid tissue. Mesenteric lymph nodes, gall bladder, liver, spleen, bone local necrosis secondary to AgAb reaction.
The ileum is most affected but may be found in the jejunum and colon. Coeliac sprue:sprue:- Rare chronic desease, characteristic muscosal lesion of the small intestine and impaired nutrient absorption. Glutean – sensitive enteropathy due to immune reaction to gliadin loss of villi ↓ absorption surface. 80% - HLA B8. 90%- D/DR3 or D/DR7. 90-95% express DQ a/B on chromosomes 6. linked to HLA-B8.
DQ is
Circulating Abs to Gliadin are present in all patient. Long term celiac disease have 10-15% chance of developing Ca. in 8-10 yrs i.e. malignant lymphoma and adenocarcinoma – pathogenesis.
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TROPICAL SPRUE: Celiac like – occur in people living in the tropic, except Africa. Unknown etiology but E. coli is suspected. Can occur as endemic, Intestinal changes are variable. Malabsorption is only one Whipple’s disease:disease: manifestation combined to middle aged male. Uncommon, multisystem. Rod-shaped bacilli in macrophages within the body and mainly in the small bowel. Micro biologic studies revealed rod shaped and non-rod shaped bacteria as streptococci, Shigella flexnerini It is thought before to be intestinal but now can be everywhere. The presenting symptoms can be migrating polyarthritis with neurologic manifestation, skin pigmentation. Diarrhea, malabsorption, weight loss fever M:F = 10:1. The macrophages contain mucopolysacharide staining strongly with P.A.S. Sinilo cells can be seen with lymphnode and other organs. Fat accumulate in lymphatics possibly due to obstruction by the macrophages.
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Celiac sprue: sprue: Fundamental disorder in celiac sprue is sensitivity to glutaryl, which is the alcohol soluble water-insoluble protein component (gliadin) of wheat and closely related grain as Oat, Barley, ad rye). Cell mediated immunity appear to be an important pathogenesis where when small intestine mucosa is exposed to gluten, T-cytotoxic lymphocytes will accumulate in the intraepithelial region while the helper T-lymphocytes will be in the lamina propria which is sensitized to gliadin cytokinine release damage to the intestinal enterocytes. Morphology:Morphology:- The mucosa can be visually normal but biopsy will demonstrate diffuse enteritis with marked atrophy or total loss of the villi. The epithelium will show vacuolar degeneration, loss of micro-villi and ↑ number of epithelial lymphocytes. The crypt exhibit ↑ mitotic atrophy and are elongated, hyperplastic and tortuous but still the mucosal thickness remain the same. Lamina propria with few lymphocytes, plasma cells, macrophages and eosinophils and mast cells, more marked in proximal than in distal because duodenum and 1st part of the Jejunum are exposed to the highest concentration of dietary gluten. These can be also noted in tropical sprue.
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Clinical feature: feature It is variable from patient to patient. Diarrhea, failure to thrive, may be evident during infancy. Tuberculous Enteritis. Three main pathological forms are recognized: 1.
Primary infection
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This is due to ingestion of infected mild, usually containing bovine tubercle bacilli, and affects the small bowel.
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The reaction is similar to that seen in primary tuberculosis of the lung.
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A tiny lesion, often undiscovered, occurs in the bowel mucosa. This is a equivalent to the Ghon focus. The infection spreads to the local lymph nodes which are greatly enlarged and caseous (sometimes called tabes mesenterica).
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Usually the condition subsides and the caseous nodes undergo calcification. Infrequently the disease spreads and causes tuberculous peritonitis.
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2.
Secondary infection:
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Swallowing of sputum containing large numbers of tubercle bacilli in cases of open pulmonary tuberculosis gives rise to tuberculous lesions in the intestine. Again the small intestine is affected
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As in secondary tuberculosis of the lung, the local lesion is prominent and the lymph nodes are less affected. The lesions start in the Peyer’s patches and solitary lymphoid follicles.
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As in the lung, there is a good deal of fibrous granulation tissue surrounding the caseous lesions and the vessels undergo obliteration. For this reason, perforation and haemorrhage are uncommon.
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Adhesions to other loops of bowel are common and the caseating process may erode through the walls and cause fistula formation with short circuiting and resulting malabsorption. If the fibrous adhesions are dense, obstruction may arise. Hyperplastic caecal tuberculosis: tuberculosis:
3. -
This rare affection of the caecum involves great fibro-caseous thickening of the bowel wall and numerous pericaecal adhesions.
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CROHN’S Disease Disease:: -
chronic condition affecting young adult usually affect the terminal 10-20cm of the ileum and colon.
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Idiopathic, chronic, ulcerato-constrictive bowel disease sharply delimited and typical transmural with non-caseating granuloma.
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Any segment of G.I.T can be involved. However, most commonly affect terminal ileum, and/or colon.
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It is recognized by Burnil Bernard Crohn at 1932. it was confused by T.B.
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It is most frequently segmental, early lesion is small ulcer, discrete with hgic rim longitudinal ulcer deep tissue. All the wall is affected with fibrosis narrowing constriction (string sign). The wall is thickened, especially in the submucosa white is oedematous and have gelatinous appearance.
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cobble stone appearance. Lymph node will show reactive hyperplasia which may contain granuloma. Light microscope show
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lymphocytes, plasma cells (transmural) noncaseating granuloma found in 60% of cases. Adhesion to other structures occur and the ulcer penetrate the bowel wall fistule channels.
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Complication include malabsorption due to short bowel syndrome, fistula formation, anal skin tag, fistula, fissue, perforation, huge, toxic dilatation. Malignancy is rare and systemic amyloidosis is rare.
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The ulcer is narrow and linear (Figure 5).
Etiology: Unknown. Unclassified mycobacteria immunological disorder stress. It is a disease of developed countries. Food preservating may be potentiating factor. Microscopic changes: changes The inflammatory reaction extend through whole wall of the intestine. Granulation reaction occur resembling sarcoidosis lesions. Occur in assuration with lymphatic channels causing lymphatic obstruction. Subsequently fibrosis occur mucosa metaplasia to simple mucus seneting type resembling that of the mucus. Secondary infection is common and is responsible for ulcerative of fissure formatioin.
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Possible mechanism: Focal vascular damage due to an immune reaction inflammation and granulomatous lesion lymphatic obstruction. Healing with fibrous Gross oedema Ulcerative Fissures Fistula
← Secondary infection
Cmplication:Cmplication:1.
Intestinal obstruction. Spontaneous
2.
Fistula formation Following operation.
3.
Perianal fistulae are common.
4.
Hypochromic anaemia due to age.
5.
Macrocytic anaemia caused by interferon in obsorption.
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6.
Sign of immunological diseases – arthritis, ureitis and dermatitis.
Ulcerative colitis colitis:: -
Chronic but presentation.
can
have
acute
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It is the commonest associated with blood.
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It is confined to large bowel commencing from the rectum.
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The ileum is occasionally backwash ileitis.
cause
fulminating
of
diarrhea
involved
by
Etiology: Still unknown but three theories have been proposed. A.
Infection. Shigella due to high titre of agglutinin are found in pt. With U.C. E. coli also is under investigation.
B.
Psycogenic factors:
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Stressful events. C.
Immunological factors: Many immunological phenomena have been described. This can be categorized in the following. 1.
Mucosal response: T cell and plasma cells are seen in lamina propria to recognized intraluminal Ag humoral and cell mediated reaction. Presence of eosinophils of most cell suggest IgE mediated reaction.
2.
Gut associated Ags: some patients have this Ag in their sera however there is no definitive correlation between their presence and severity of the disease nevertheless pts with U.C are known to have raised Abs to E-coli 014.
3.
Immune complex: These are found in-patient with active disease but not correlate with the extent of the disease. These high of immune complex in patient (are seen) with lesions in the skin, eye, and joint.
4.
Steroid treatment, pt with U.C. shows successful treatment remission following by steroids. ∴ The most likely for etiology are pathogenic and immunological pathology.
Pathology
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It shows continuous distribution which is maximally in the rectum and extend proximally to involve the entire colon.
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Some cases can be confined to the rectum (Proctitis, other to rectosigmoid (distal colitis). It does not involve the mucosa of anal transitional zone or the anal canal but small proportion exhibits skin tag and anal fissures. Ulcers are irregular in outline and orientations, which become later confluent extend horizontally. Ulceration is superficial to mucosa and submucosa. But severe form can extend to the muscle layer and perforate.
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Intact mucosa will be hyperemic and ulcer will show haemorrhage.
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Microscopically there is diffuse infiltrate of acute and chronic inflammatory cells with crypt abscess with degenerative changes in the epithelium of the crypts and mucosal surface.
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There will be reduction of goblet cells and dysplastic changes.
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Complication 1.
malignancy – 2-10% in patient who had the disease for 25 yrs i.e. the onset is at childhood with severe first attack, involvement of the colon and continuous rather than intermittent symptoms.
2.
Local complication: hge which can be life threatening diarrhea with severe loss of electrolyte, toxic dilatation due to ulceration affect layers of muscle areas disturbing their viability and contractile strength Dilatation thinning of the wall and perforation peritonitis.
3.
systemic complication: a. skin – hyper pigmentation, erythema nodosum, and pyoderma gangrenosum. (sterile dermal abscess). b. Liver: fatty change due to infection anaemia, protein deficiency. Chronic pericholangitis, chronic active hepatitis.
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c. joints: ankylosing spondylitis specially ankle and knee joints.
arthritis
Amaebic colitis: colitis -
Amaebiesis is primarily an infection of the colon, which can spread to the liver, lung and brain. It is limited to human.
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E. histolytic is the responsible pathogen. The caecum, ascending colon are commonly affected, followed by sigmoid, rectum and appendix.
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In severe all cell the colon will be involved. It invades the crypts lamina propria muscularis mucosa ulcer flask shaped abscess i.e. narrow neck and broad base larger ulceration due to liguefactive necrosis. Inflammatory process is limited. Mucosa between the ulcer will be either normal or mildly inflamed in contrast to U.C.
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Penetratic of the wall is rare but may occur specially in children or immune-suppressed pts.
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Amoebana – Napkin – like constrictive lesion that might be confused with tumor due to profuse granulation tissue response.
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40% of case can penetrate the BVS liver abscess solitary but less often multiple.
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Bacillary dysentery dysentery:: -
This is reserved for four species of shigella. They usually invade the colonic mucosa and multiply in lamina propria. LNs they don’t lead to bacterimia as salmonella.
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The mucosa will be hyperemic and edematous with enlargement of lymphoid follicles projecting nodules. Fibrinopurulent exudates will be seen.
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Superficial ulceration can develop and rarely extend below the mucosal level. Perforation is common. Incubation period is < 48 hours watery diarrhea, nausea, vomiting crampy abdominal pain dehydration and neck stiffness.
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