GIT

Gastrointestinal system

د –قاسم سعيد المختار

Objectives

To know the lesions affecting the GIT Their gross & microscopical picture Their diagnosis Some of the clinical effects

The lips and mouth

Histology: The lips, Tongue, are lined by stratified squamous epithelium. contain scattered minor salivary glands and some lymphoid follicles.

Lesions of lips and mouth

1.Congenital anomalies :e.g. cleft lips &/or cleft palate ,macroglossia, microglossia etc 2.Inflammatory lesions :e.g. stomatitis, glossitis, thrush(monilial infection),Herpes ,measles, syphilis,Tuberculosis,aphthus ulcer. Pigmentaion, leukoplakia. etc. 3.Tumours: benign and malignant tumors

Tumours of the lips and mouth

Benign tumours : e.g.haemangioma, pleomorphic adenoma ,squamous cell papillom Malignant tumours: e.g.Squamous cell carcinoma and other rare tumours like lymphoma, rhabdomyosarcoma.

The salivary glands

1.Major salivary glands: parotid, submandibular, & sublingual. 2.Minor salivary gland, scattered throughout the mucus membrane

Lesions of salivary glands

1.Cysts of salivary glands: Ranula. 2.Salivary calculi. 3.Viral infections e.g. Mumps 4.Bacterial infections 5.Sjogrens syndrome and Mikulicks syndrome 6.Tumours of salivary gland:Benign &Malignant tumors

Tumors of Salivary glands

1.Benign tumors: Adenoma e.g. Pleomorphic adenoma, Adenolymphoma (Warthins tumor). 2. Malignant tumors: Mucoepidermoid carcinoma , Adenoid cystic carcinoma and malignant changes in pleomorphic adenoma

Pleomorphic adenoma(Mixed parotid tumour)

Most common benign tumor of salivary gland ,epithelial in origin grow slowly over years, painless Grossly rubbery well circumscribed,bosselated mass, encapsulated with projections from capsule, grayish white in color, microscopically consist of glandular element , groups of epithelial cells& myoepithelial cells and myxoid, chondroid stroma

Adenolymphoma (Warthins tumor)

Benign tumor Affect almost exclusively parotid gland. bilateral in 10-15% ,male 60s years Cystic in nature with papillary growth The epithelial cells are in double layer, has granular eosinophilic cytoplasm. The stroma is infiltrated by lymphoid tissue.

Adenoid cystic carcinoma

It may affect any salivary gland Consist of malignant cells arranged in cribriform pattern and ducts like structure. Local recurrence is common but distal metastasis is rare

Mucoepidermoid carcinoma

Affect all age groups even children Consist of Mucus secreting cells and epidermoid cells in various proportions may affect any salivary gland

Other carcinoma

Example: Adenocarcinoma, squamous cell carcinoma, Clear cell carcinoma etc.

The tonsils

Tonsillitis: mean inflammation of the tonsils due to streptococci, staph., diphtheria etc

Diphtheria

Infection by c.bacterium diphtheria, can affect tonsils, pharynx nose etc and cause pseudomembranous inflammation

The Esophagus

A muscular tube extend from the epiglottis to the gastro-esophageal junction

Histology of esophagus

1.Mucosa: non keratinised stratified squamous epithelium. 2.Submucosa 3..Muscular layer 4.Adventitia

Functions of Esophagus

1.Conduct food and fluid. 2.Prevent reflux of acid gastric juice What is dysphagia? What will happen if gastric juice return to the esophagus?

Symptoms related to the esophagus

1.Heartburn: retrosternal burning pain. due to reflux of gastric acid juice 2.Dysphagia:Difficulty of swallowing, due to obstruction ,or deranged function

Congenital Anomalies of Esophagus

1.Ectopic glands : ectopic gastric glands at distal esophagus 2.Achalasia of esophagus 3.Tracheo-Esophageal fistula TE-fistula

Achalasia of esophagus

Failure of distal few cm of the esophagus to dilate leading to obstruction and marked dilatation of the esophagus above the obstruction. The cause is unknown possibly due to absence of nerve fibers and ganglia of Auerbach plexus.

Esophageal varieces

Dilatation of the veins of the submucous plexus at the lower end of the esophagus due to portal hypertension. They are liable to rupture causing fatal bleeding

Inflammation of esophagus

Rare include Diphtheria, Herpes, Monilia

Reflux esophagitis

Inflammation and ulceration at the lower part of the esophagus due to reflux of the acid gastric juice .

Causes of Reflux esophagitis

1.Hiatus hernia 2.Persistant vomiting 3.Increased intra-abdominal pressure e.g. pregnancy, obesity etc.

Pathology of reflux esophagitis

Macroscopically: The lower part of the esophageal mucosa show patchy ulceration, inflammation and in chronic cases fibrosis and stricture Microscopically: Chronic inflammation and fibrosis

(Barretts metaplasia)

Conversion of the stratified squamous epith. To columnar epith. In the lower portion of esophagus . It may lead to ulceration , stricture &adenocarcinoma ,perforation

Obstruction of esophagus

1. Organic obstruction: e.g. tumor, foreign body, webs & rings , fibrosis ,Systemic sclerosis 2. Functional obstruction: e.g. Achalasia --- Plummer Vinson syndrome (diaphragm at upper end of esophagus (esophageal webs) in association with iron deficiency anemia).

Tumors of Esophagus

1.Benign tumors :Rare e.g. Leiomyoma, 2.Malignant tumors: e.g. squamous cell carcinoma, adenocarcinoma and others.

squamous cell carcinoma

80-85% of esophageal carcinomaMore common in blacks& malesRisk factors-----plummer-vinson syndrom, esophagitis alcohol, smoking, achalasia .50%mid third 30%lower third 20%upper thirdDysphagia, Hemorrhage—sepsis—fistula--


squamous cell carcinoma
Gross: Form a mass which may ulcerate, bleed or perforate Microscopical : Squamous cell carcinoma. Less common adenocarcinoma.

The stomach

Anatomy: Histology:

Congenital pyloric stenosis

Hypertrophy of circular muscle of pyloric sphincter resulting in narrowing of the pyloric canal and pyloric obstruction Affects children at first 3 wk Present with vomiting Microscopically:Hypertrophy of smooth muscle and degeneration of ganglia of Auerbach plexus

Bezoar

Collection of indigestible substance that take the shape of the stomach and causes dyspepsia and palpable massHair……. TrichobezoarPlant …….Phytobezoar

Acute gastritis

Acute inflammation of the gastric mucosa Etiology: drugs (NSAID), alcohol, bacterial toxins Bacterial infection is not important Macro: the mucosa red edematous with focal hemorrhages ,ulceration ,perforation Micro: Congestion and acute inflammation

Chronic gastritis

Chronic inflammatory changes of gastric mucosa with variable degree of loss of specialized glandular epithelium & metaplasia that may lead to achlorhydria and loss of intrinsic factor which lead to pernicious anemia. It is usually associated with chronic gastric ulcer and gastric cancer



Chronic gastritis
Etiology: 1. It is considered as organ specific autoimmune disease. Due to presence of autoantibody in the serum against cell membrane of parietal cells and against intrinsic factor. It has familial tendency and associated with other autoimmune diseases e.g thyroiditis

Etiology (cont)

2.H.pylori (Helicobacterium pylori) an extracellular bacilli live of surface mucosa of the stomach 3.Drugs,alcohol smoking

Pathology of chronic gastritis

Macroscopically: There is little correlation between gross, microscopic appearance and symptom of the patient So the classification of chronic gastritis depends on the microscopical appearance

Pathology of chronic gastritis (cont)

Microscopically: there are three types: 1.Chronic superficial gastritis. characterized by: Normal thickness of the mucosa The inflammatory changes is limited to the superficial zone only

Pathology of chronic gastritis (cont)

2. Chronic atrophic gastritis: Follow chronic superficial gastritis. The inflammatory changes involve the entire thickness of the mucosa The thickness of the mucosa reduced There is atrophy of the specialized cells(chief &parietal cells) which are replaced by mucus secreting cells(pyloric metaplasia) Intestinal metaplasia :presence of goblet cells, paneth cells and prominent striated border

Pathology of chronic gastritis (cont)

3-Gastric atrophy: Thickness of mucosa markedly reduced Complete atrophy of specialized cells Intestinal metaplasia , cystic changes and presence of lymphoid follicles

Menetrier disease

Rare condition characterized by giant mucosal folds, hypertrophyed ruge Involve fundus spare antrum Foveolar hyperplasia; cystic dilatation of the gland ,hypochlorhydria

Peptic ulcer

Digestion of the mucosa of the affected part (stomach, esophagus, meckles diverticulum) by acid and pepsin

Etiology of peptic ulcer

1.Acid and pepsin secretion 2. Infection by H-pylori 3.Alteration of mucus secretion 4.Others: dietary, genetics, vascular trauma, gastritis, smoking, psychsomatic etc.

Types of gastric ulcer

According to the duration, degree of penetration and degree of healing , peptic ulcer is divided in to: 1.Acute peptic ulcer. 2.Chronic peptic ulcer

Acute gastric ulcer

Gross: small less than 1 cm ,multiple , affect any part of the stomach, involve mucosa and submucosa and heal without fibrosis Rarely it may perforate and bleed

Chronic gastric ulcer

Usually single rarely two ,The lesser curvature is most commonly affected .Large in size up to 5 cm rounded or oval , its surface is covered by necrotic materials and has an indurated base.The indurations involve the entire thickness of the wall of the stomach, it may be adherent to surrounding organ and may form fistula.

Chronic gastric ulcer (cont)

Microscopically: the surface is covered by fibrinoid materials. Layer of granulation tissue Layer of fibrous tissue Interruption of muscular layer Endarteritis of affected vessels

Complications of chronic gastric ulcer

1. Heamorrhage; leading to haematemesis and malena .Chronic oozing lead to anemia 2.Perforation: result in passage of food, gastric juice , bacteria to peritoneal cavity leading to peritonitis 3.Fibrosis: fibrosis lead to pyloric obstruction , hour glass stomach 4.Malignant changes: Rare less than 1%

Duodenal ulcer

Usually affect the first part of the duodenum Grossly and microscopically the same as chronic gastric ulcer The complications are similar except that malignant changes is extremely rare

Tumors of the stomach

1. Benign tumors: polyps, leiomyoma all rare.2. Malignant tumors:Epithelial…. Carcinoma (Adenocarcinoma)Smooth muscle…..LeiomyosarcomaLymphoid tissue….Lymphoma

Carcinoma of the stomach

Etiology: Unknown but the following play a role: 1.Genetics: through blood group A, pernicious anemia 2.Dietary factor: Factors in soil ,cooking etc 3.Racial factors e.g. japanese 4.Precancerous lesions: chronic gastritis, Intestinal metaplasia, G.U.

Pathology of carcinoma of stomach

Macroscopical: commonly affect pylorus and pyloric antrum. It may be: Ulcerative Fungating Mucoid Diffuse scirrhous Superfecial spreading


Pathology of carcinoma stomach (cont)
Microscopically: adenocarcinoma of variable differentiation. Mucus secretion is common The tumor cell infiltrate the wall with ulceration. In diffuse type the mucus membrane may be intact but the wall is extensively involved by signet ring cells .

Spread of gastric cancer

1.Local spread: through the wall to pancreas ,liver, Esophagus ,pylorus. 2.Transcoelamic:peritoneum,Ovary (Krukenberg tumor). 3.Lymphatic: To regional L.N. 4.Haematogenous spread :(by blood) to lung, liver brain etc.

Early gastric cancer

This term is used for carcinoma of the stomach limited to the mucosa and submucosa without invasion of muscular layer. Irrespective of the L.N. involvement.

Malabsorption

A condition arising from abnormality in absorption of food nutrient across the GIT affecting single or multiple nutrients depending on the cause This abnormality may be in: Digestion (Intraluminal) Absorption (Mucosa) Transport (postmucosal)

Malabsorption syndrom

Clinically : it lead to : 1. Deficiency state:e.g. Anaemia hypoprotenaemia etc. 2. Gastrointestinal symptom: e.g. Abdominal discomfort, diarrhea, bulky pale stool (Steatorrhea)

Malabsorption syndrome

Classification: 1.Primary malabsorption syndrome: A.Celiac disease (gluten sensitive enteropathy) B.Idiopathic steatorrhea C.Tropical spru.

Malabsorption syndrome

Secondary malabsorption syndrome: A. Chronic intestinal disease B. Abnormal bacterial proliferation C. Inadequate digestion D. Others

Malabsorption: Investigation

Investigations are guided by symptom & signs: Stool exam Blood tests Radiological tests (Barium meal , Ct, MRI) Small intestinal biopsy.

Villous atrophy

It is the most important pathological changes in malabsorption syndrome and can be classified in to : 1. Partial villous atrophy (P.V.A) 2. Subtotal villous atrophy (S.V.A.)

Partial villous atrophy (P.V.A)

The villi are shorter and broader than normal. The crypts are enlarged and hyperplastic.The epithelium show degenerative changes and the lamina propria is infiltrated by plasma cells and lymphocytes.

Subtotal villous atrophy (S.V.A)

It is more severe than P.V.A, There is sever shortening of the villi .The mucosa looks flat.

Celiac disease (Gluten sensitive enteropathy)

A genetically determined abnormal immune response to gluten Affect children Characterized by severe steatorrhea The mucosal lesion is S.V.A at the proximal jejunum become less severe i.e P.V.A. distally Withdrawal of gluten from diet result in clinical and morphological remission


Complication of celiac disease
Failure to thrive Increased incidence of intesinal lymphoma and adenocarcinoma Associated with skin lesions e.g dermatitis hepitiformis, rosacia etc.

Idiopathic steatorrhea (Adult form of celiac disease)

Affects adult patients The mucosal lesion is P.V.A. But it is more extensive The response to gluten free diet is less satisfactory

Tropical spru

This type of malabsorption is common in tropical and subtropical area Affects children and adults Characterized by chronic diarrhea, severe anemia and folic acid deficiency The mucosal lesion is P.V.A. rarely S.V.A. Broad spectrum antibiotics and removal from tropical area is helpful Gluten free diet has no effects

Whipple disease

Rare disease present as: Malabsorption Lymphadenopathy Arthropathy Skin pigmentaion Jujenal biopsy show infiltration of lamina propria by granular macrophages

Secondary malabsorption

1.Chronic intestinal diseases e.g. T.B, Amyloidosis. Crohns disease etc. 2. Abnormal bacterial proliferation: e.g. in blind loop syndrome, Giardia infestation 3.Inadequate digestion: e.g. liver diseases, billiary diseases etc 4. Others e.g. enzyme deficiency drugs , radiotherapy etc.

Tumors of Small Intestine

1.Benign tumors: Epithelial tumors: Rare e.g polyp Stromal tumors: Common e.g, leiomyoma, neuroendocrine tumors 2-Malignant tumors: Carcinoma, lymphoma.

Carcinoid tumour (Neuroendocrine)

ٍSite: The most common site is the tip of appendix &terminal ileum though any part of the GIT can be affectedGrossly small nodule yellowish brown in color Micro: Consist of uniform bland looking cells arranges in sheets or alveolar pattern .contan argyrophil granules

Carcinoid syndrome

Consists of attack of flushing, diarrhea, bronchospasm and subendocardial fibrosis. Due to secretion of 5HT,and other vasoactive hormones It develop when these substances escape detoxication by amino-oxidase enzymes in the liver and lungs

Peutz Jeghers syndrome

Hereditary disease inherited as mendelian dominant and characterized by multiple hamartomatous polyps in the jujenum and colon associated with melanotic pigmentation of the lips and oral mucosa. Present as bleeding , may cause intuscusseption

Adenocarcinoma of small intestine

Rare. the common site is the ampulla of vater. Grossly and microscopically like other adenocarcinoma

Lymphoma of the intestine

It is common condition present as mass, intestinal obstruction, malabsorption. Gross: thickening of the wall, narrowing of lumen , ulceration. Micro:The entire wall is infiltrated by neoplastic lymphoid cells Burkitts lymphoma commonly affects the intestine in children.

Results from : 1. Complete obstruction of the mesenteric artery e.g.emboli, twisting , volvulus etc. 2.Partial obstruction e.g. atherosclerosis The effect depends on severity and duration of the ischemia
Ischemia of the intestine:

Pseudomembranous

This is a special type of enterocolitis associated with use of certain drugs like clindamycine, lincomycine.etc. Clinically present with bloody diarrhea and abdominal pain . Grossly : Pseuomembrane cover the mucosa Microscopically there is necrosis of superficial mucosa incorporated with fibrinopurulent exudates

Acute appendicitis

Etiology Obstruction: by fecolith, oedema, lymphoid hyperplasia. Bacterial invasion: e.g.E-coli. Sterpt, Yersinia etc.

Acute Appendicitis

Macroscopical:vary according to severity and duration. Edema, congestion, suppuration ,perforation and gangrene. Microscopical :Depend on duration and severity. Lumen full of pus, surface epithelium ulcerated, the wall infiltrated by neutrophils

Acute appendicitis

Clinically: Abdominal pain, radiate to RIF,nausia, vomiting,mild fever,high pulse rate, latter peritonitis

Acute appendicitis

Complications: 1.Perforation 2.Peritonitis 3.Appendicular abscess 4.pyelitis and pyelphlebitis 5.Mucocele and pseudomyxoma peritoni

Inflammatory bowel disease of unknown etiology

1.Crohns disease 2.Ulcerative colitis

Crohns disease

I.B.D . Of unknown etiology but diet smoking, infection , defective inflammatory response and immune mechanism has been suspected. Affect any age but 3rd and 4th decade Clinically: abdominal pain, intestinal obstruction.it has prolonged coarse with remission and relaps attacks

Pathology of Crohns disease

Gross 1.Affect any part of GIT specially terminal ileum, with skip lesion (Regional ileitis). 2.The affected part is thick ,edematous, and hard. The lumen is narrowed, the mucosa ulcerated, nodular and have cobble stone appearance with fissure in its wall, leading to fistula. The serosa is thick and edematous. The regional L.N. is enlarged.

Pathology of crohns disease

Microscopically: Chronic inflammatory changes involving the entire thickness of the wall i.e transmural with formation of noncaseating epitheloid granuloma. Lymphatic obstruction explain the edema , goblet cell hyperplasia with increased mucus secretion. The L.N. show epitheloid granuloma

Complication of Crohns disease

Malabsorption specially Vit.B12 Fistula formation Intestinal obstruction Carcinoma may complicate crohns dis.

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I.B.D of unknown etiology . sensitivity to ingested substances, neuromuscular disorder and psychological factors has been suspected. Clinically : affect young adult Cause diarrhea, bleeding per rectum, toxic dilatation and perforation of the colon Has chronic coarse with relapse & remission

Pathology of Ulcerative Colitis

Gross It is an inflammatory condition of the mucus membrane of the large bowel start at the rectum and extend proximally to involve the whole colon and sometime the terminal ileum in continuity without skip lesion. The mucosa is congested ulcerated (The ulcer are long the tenia coli). covered by mucopurulent discharge and blood

Pathology of Ulcerative Colitis 

The surviving mucosa in between the ulcer are hyperplastic forming pseudopolyposis. Fibrosis is not a feature of U.C. but hypertonia of the muscle cause shortening and loss of normal haustration leading to pipe stem colon Toxic dilatation and perforation in sever cases

Pathology of U.C.

Microscopically: Congestion ,edema and infiltration of the mucosa by inflammatory cells Collection of mucus, neutrophils and M.O. in the lumen of the gland form crypt abscess. The surviving epithelium show hyperplasia and mucus depletion The pseudopolyp consist of granulation tissue and inflammatory cells

Complication of Ulcerative Colitis

Toxic megacolon Bleeding Perforation Carcinoma Involvment of other organs e.g arthritis, uveitis. skin lesions, liver lesions etc

Diverticular disease

False diverticulum: Protrusion of mucosa and submucosa through the muscular layer of the intestine. True diverticulum: has muscular layer in its wall e.g.Meckles diverticulum

Diverticulum of small intestine

It may affect duodenum,jejunum,ileum. Site: at entry of mesenteric vessel i.e at the mesenteric border Complications: hemorrhage, perforation, malabsorption (as it act as blind loop syndrome)

Diverticulum of large intestine

Site: affect any part but specially sigmoid colon. It develop at site of entry of blood vessels. so it arrange in two raw between mesenteric and ante mesenteric taenia within the appendices epiploicae Complication :inflammation, hemorrhage perforation

Meckles diverticulum

Represent remnant of the proximal end of vetello intestinal duct .At the antimeseneric border of ileum .About 80 cm from ileocaecal valve about 2-8 cm in length. It has muscular wall, its mucosa contain heterotropic gastric mucosa. Complications: Hemorrhage, inflammation perforation , intestinal obstruction ,fistula

Intestinal obstruction

Interference with passage of intestinal contents. It may be: Partial or complete Chronic (develops gradually) or Acute (develops suddenly) . Affects small intestine or large intestine

Causes of Intestinal obstruction

1.Mechanical : A. Causes in lumen e.g. Tumor ,F.B. B. Causes in the wall e.g. Tumor, Fibrosis C. Causes out side the wall e.g. Fibrous band. 2.Neural: e.g. Paralytic ileus . 3.Vascular:e.g. Emboli. Thromosis of mesenetric vessels.

Hernia

Protrusion of a viscus outside it anatomical site. e.g. inguinal , femoral, umbalical , diaphragmatic etc Reducable Obstructed Strangulated

Intussusception

Invagenation of portion of bowel in to the portion below. It usually affects children Causes: polyp, enlarged lympoid follicle etc Site: Ileocecal , ileocolic. Grossly: consist of three layers. Effects: Intestinal obstruction Gangrene of intestine

Hirschprungs disease (Congenital megacolon)

Absence of parasympathetic ganglia of aurbach and meissner plexus of the terminal 5-20 cm of rectum. Effects: Obstruction and marked dilatation of the colon above the obstruction


Volvulus
Twisting of a loop of intestine around its axis. Usually affects the sigmoid colon due to its long mesocolon. Effects: Intestinal obstruction Gangrene if not relieved.

Tuberculosis Of The Intestine

Primary tuberculosis Secondary (Reinfection) tuberculosis Hyperplastic caecal tuberculosis

Primary tuberculosis

Acquired by ingestion of T.B. bacilli The small intestine specially the terminal ileum is the commonest site of infection Grossly & microscopiccally the same like other primary T.B. lesion else where

Secondary Tuberculosis

Develop in immunized person Gross & Micro is the same like other secondary T.B. The terminal ileum commonly affected and show ulceration of mucosa and submucosa. The ulcer is transverse to the long axis of the intestine. Its surface is covered by necrotic materials and has undermined edges

Typhoid fever

Result from infection by salmonella typhi through oral rout, infect the lymphoid follicles in peyers patches, to the blood were it multiply and excreted through the bile to the ileum were it re-infect the lymphoid follicle producing characteristic ulceration of the intestinal mucosa (typoid ulcers)

Intestinal lesion of Typhoid fever

Macroscopically: swelling of peyers patches at the ileum, then ulceration. Typhoid ulcer is an oval ulcer its long axis is along the long axis of the intestine( it takes the shape of peyers patches). Microscopically: congestion edema and infiltration by lymphocytes, plasma cells and macrphages with absence of neutrophils. The regional L.N. show similar reaction

Complications of intestinal lesion of typhoid fever

1.Perforation 2.Haemorrhage

Amoebic dysentry

Affect mainly the colon Produce flask shaped ulcer with undermined edges Microscopically: congestion, edema inflammatory cell infiltration with large number of amoeba Its main complication is liver abscess, bleeding , perforation , amoeboma

Tumors of Large Intestine

1.Benign tumors: A. Benign neoplastic polyps: I.Tubular adenoma II.Villous adenoma III.Mixed villo-tubular adenoma

Tubular adenoma

The most common, affect colon specially rectum. Single or multiple. Few mm to 2-3 cm Sessile or pedunculated, smooth surface. Consist of tubular glands lined by columnar cells with variable degree of dedifferentiation. malignant changes may develop

Villous adenoma

Least common but carry high risk of malignancy Affect colon commonly rectum Usually Single Few cm up to 10 cm Usually sessile covered by fronds like structure Microscopically: villi lined by columnar epithelium with variable degree of dedifferentiation mounting to carcinoma. Secret large amount of mucus--> K-deplesion

Mixed villotubular adenoma

Mixture of villous and tubular type Less common than tubular but more common than villous


Familial Polyposis coli
Rare disease transmitted as autosomal dominant gene Characterized by hundereds of adenomatous polyps develops at neonatal life and presents at early adult life as bleeding ulceration and then Malignant changes is inevitable.

Other non-neoplastic polyps

Metaplastic Hamartomatus, Juvenile Inflammatory

Carcinoma of large bowel (colon)

One of the most common tumor Etiology: Age: usually affects old age group. At younger age group as complication of preneoplastic lesions Preneoplastic lesions: Adenoma, Ulcerative colitis, Crohns disease.Diet: low rouphage diet, refined carbohydrate, high fatty diet

Carcinoma of colon

Gross: 1.Ulcerative 2.Polypoid 3.Annular 4.Colloid or mucoid

Carcinoma of colon

Microscopically: All carcinoma of the colon are adenocarcinoma with variable degree of differentiation. Well differentiated Moderately differentiated Poorly differentiated and undifferentiated and signet ring type

Spread of carcinoma of colon

1. Direct 2.Lymphatics 3.Haematogenous


Dukes staging of carcinoma of colon
Stage A tumor limited to wall 5 year/80% Stage B Penetrating the wall 5 Years 60% Stage C Involve the lymph node 5 Y. 30%

Malignant Tumors of anal canal

Adenocarcinoma Squamous cell carcinoma Malignant melanoma Cloacal tumor

Peritonitis

Inflammation of the peritoneum. It can be: Acute Peritonitis: As in perforated viscus e.g.Du,Gu Penetrating wound e.g. bullet injury Inflamed viscus: e.g.appenicitis, diverticulitis, cholecystitis etc Haematogenus

Chronic peritonitis

1.Tuberculosis 2.Malignant lesion 3.Nonbacterial causes : e.g. talk

Ascitis

Collection of fluid in peritoneal cavity

Causes of Ascitis

1.Generalised edema 2.Tuberculous peritonitis Portal hypertention Malignant lesion