The Digestive System

THE DIGESTIVE SYSTEM

Oral cavity

Developmental anomalies

Anomalies occur infrequently in domestic animals.

Cleft lip (chelioschisis): affects the upper lip.

Cleft palate (palatoschisis): is an open cleft between the oral and nasal cavities. The new-born animals with cleft palate drip milk from their nostrils during nursing, whereas older animals develops respiratory affection and pneumonia.

Inflammatory processes

The inflammation of oral cavity may be diffuse (stomatitis) or localized inflammation of gingival (gingivitis), tissue surrounded the teeth (periodontitis), pharynx (pharyngitis), tongue (glossitis), tonsils (tonsillitis) or lips (chelitis).

GingivitisMost cases result from bacterial infection follow either trauma, poor oral hygiene or various immunodeficient states.Macroscopic pictureThe gingiva bleeds easily, erythematous and edematous.Microscopic picture• The gingival connective tissue shows congested blood vessels and infiltrated with neutrophils and lymphocytes.•The overlying gingivial epithelium may be ulcerated or hyperplastic.

Stomatitis1- Catarrhal stomatitisIt is a mild inflammation of oral mucosa. It is caused by mild irritant as trauma, chemical and infectious agents.Macroscopic picture•The buccal mucosa shows redness, swelling and covered with grayish or brownish gray mucus.•Bacterial decomposition of food results in a fetid odor.Microscopic picture•Dilatation of the submucosal blood vessels beside infiltration of the submucosa by inflammatory cells.•Desquamation of the epithelial lining which covered with mucus and bacteria.

2 -Vesicular stomatitisCauses1- Viral diseases as foot and mouth disease, infectious

vesicular stomatitis and herpes virus.2- Thermal and chemical agents.Macroscopic picture•Vesicles containing clean fluid are seen on oral mucosa.

Rupture of vesicles leaving an erosion or ulcer.Microscopic picture•The affected epithelial cells show vacuolar and hydropic

degenerations. The degenerated cells coalesce with each other to form vesicles.•Some vesicles may be rupture leaving erosions with intact

germinal basal layer.

3 -Suppurative stomatitis•It occurs associated with wound infected with pyogenic

microorganisms.•The inflammation may be focal or diffuse. The inflamed oral tissue

shows redness and swelling. The pus are usually removed by movement of food leaving erosion or ulcer.4- Fibrinous stomatitis•It occurs with severe irritation where the principle constituent of

exudate is fibrin.•It is usually associated with necrosis and ulceration of oral

epithelium.5- Necrotic stomatitis•It may be diffuse associated with chemical and thermal agent or

focal associated with foreign bodies, sharp teeth and bacterial infection as Fusiform necrophorum.

•It is usually associated with necrosis and ulceration of oral epithelium. Macroscopically, focally slight swollen gray, yellow or brown oral mucosa surrounded by red zone. The necrotic areas may removed leaving ulcer.

•Microscopically, the oral mucosa shows coagulative necrosis infiltrated and separated by inflammatory cells

Neoplasm of the oral cavityViral papilloma occurs in dogs, cattle and rabbit. Oral and

labial mucosa.Epulis is a benign neoplasm derived from connective tissue or

periodontal ligament.Classification1-Fibromatous epulisIt consists of mass of stellate fibroblasts surrounded by dense

fibrillar collagen and covered by intact gingival epithelium.2-Acanthomatous epulisIt similar to fibromatous epulis but, contain sheets or cords of

stratified squamous epithelium.3-Ossification epulisIt similar to fibromatous epulis, but in addition contains either

irregular island of osteoid or mineralized bone or acellular eosinophilic cemmentum or dentin-like structure

Squamaous cell carcinoma occurs in any species. It is the most common malignancy of the oral cavity of cats and dogs.Malignant melanoma is common in dog and rare in others.Fibrosarcoma is common in dog and cat.Osteosarcoma occurs in bone of upper and lower jaws.Lymphosarcoma, Mast cell tumors and granular cell tumor are observed.

TonsillitisCausesIt occurs when pathogenic bacteria as staphylococci colonize the tonsillar crypts and induce an acute inflammation.Macroscopic picture • Tonsils appear swollen and hyperemic.• The crypt will exude a purulent white yellow exudate. Also the surface of tonsils may covered by some exudate.• Painful swelling of mandibular lymph nodes.Microscopic picture • Tonsils show follicular hyperplasia.• Tonsils crypts are filled with desquamated epithelium, bacteria and inflammatory cells mainly neutrophils is suppurative

Dental pathologyDental anomaliesDentigerous cystsIt is epithelial lined cystic structures in bone or soft tissue of jaw.

Usually, the cysts are lined by stratified squamous epithelium and they often filled with keratin. Occasionally fragments of poorly formed tooth within dentigerous cyst.Segmental enamel hypoplasiaNB: The enamel of tooth is produced by specialized cells called

ameloblasts. The ameloblasts are susceptible to injury by poisons as fluorine, drugs as tetracycline and viruses as canine distemper.Causes Exposure to poisons or viruses prior to or during enamel

development.Macroscopically, affected teeth have defects in enamel that result

in exposure of underlying dentin giving the teeth a mottled appearance. Anodontia is lack of tooth development.Oligodontia is development of fewer teeth than normal.Polydontia is the presence of supernumerary

Degenerative dental diseases1- Dental attritionIt is the wearing away of dental structure as a result of poor

masticatory function, or oral cavity conformation.2- Dental cariesIt is characterized by digestion of the inorganic matrix of enamel

and dentin dermineralization. Dental caries results from bacterial metabolites with production of acids and enzymes, which lead to demineralization and destruction of dental matrices.

Macroscopically, the enamel becomes dull, white and pocked. The exposed dentine becomes brownish black.

Dental plaqueIt is accumulated non mineralized bacterial mass, food particles,

desquamated epithelium adhered to tooth surface.Dental calculus (Dental tartar)It is the mineralization of dental plaque by utilizing calcium of

saliva. It consists of calcium phosphate in dog and calcium carbonate in horse.

It causes mechanical irritation and persistent inflammation of gums.

Inflammation of teeth and periodentiumPulpitis•It is the inflammation of vascular part of the tooth (pulp).•The cause is usually bacteria and enter through enamel

defect or via blood.•It may lead to osteomyelitisPeriodontitis•It is the inflammation of tissue around teeth.•It may be superficial (gingivitis) or deep (pyorrhea).Salivary glandsSialoadenitisIt is the inflammation of salivary glands. Causes-Bacterial as in strangles.-Viral infections as rabies, distemper and malignant

catarrhal fever.-Trauma and vitamin A deficiency.-The infections occur through salivary ducts by extension

or through blood.-Ptylism is the increased salivary secretion. The caseous

may be poisoning or associated with stomatitis

Cysts•It occurs due to obstruction of the salivary ducts by foreign

bodies. The fluid content is odorless, grayish white or brownish and clear or turbid.

• In dog and cow a cyst frequently observed in sublingual duct, located in frenulum of tongue is referred to as a ranula.

Sialoliths (salivary calculi)•It is a rare disorder of cattle, horse and dog.• It is a calcium concretions which formed either in duct or in the

gland itself as a result of chronic inflammation which provides desquamated cells as a minute nidus upon which calcium salts precipitate.

• When the duct is occluded for long periods, a cyst may be formed in salivary duct and followed by gland atrophy.

Neoplasm of salivary glandThe neoplasm of salivary glands are uncommon in domestic

animals. Adenoma and adenocarcinoma

PharynxPharyngitis usually accompanies stomatitis. Pharyngitis are seen in the course of several diseases including Anthrax in pig and dog and calf diphtheria.EsophagusEsophagus is a muscular tube that extend from pharynx down ad through diaphragm to the stomach. The esophagus has physiologic high pressure zones at either end that act as sphincters. The upper cricopharyngeal sphincter prevent entry of air and pharyngeal contents in the esophagus except during swallowing and the lower esophageal (cardiac sphincter) prevents reflex into the esophagus of acidic cardiac juice.Disorders of esophagus can be categorized into one of three types; inflammatory degenerative lesions, obstructive lesions or motility disorders.

Obstructive and functional disorders1- Cricopharyngeal achalasia(sphincter spasm)It is a disorder due to inadequate relaxation of the upper esophageal

sphincter recognized infrequency in canine and characterized by dysphagia and regurgitation of food. Grossly, deformity of cricopharyngeal muscle is seen. Microscopically, fibrosis, atrophy, regeneration and phagocytosis are recorded.Cardiac achalasia is spasm of the cardiac oesophageal sphincter which treated surgically (cardiomyotomy) or by injection of Botuline toxins in oesopgagial muscle

2- Megaesophagus (esophageal achalasia)Generalized or segmental dilatation of the esophagus results from

neuromuscular disorders that impair esophageal motility.Megaesophagus has been described in dogs, cats, foal and human

and can be congenital or acquired.a- Congenital megaesophagusIt is an inherited disorder in several breeds of dogs. It has also been

described in cats.Affected puppies and kittens usually suckle normally but after

weaning regurgitate solid food shortly after swallowing.The pathogenesis of this condition is poorly understood, but it has

been speculated that there is a delay in the maturation of esophagus nervous innervation.

Macroscopic picture•Prominently dilated and flaccid esophagus, two to three time

normal is seen.•Sometimes the dilatation is uniform, but in other is quite to

eccentric.• The dilated portion usually contain fetid fluid.Microscopic picture •There is no reduction in the number of myenteric ganglial cells in

the wall of esophagus.b- Acquired megaesophagusCauses• It occurs in adult dogs secondary to any defect in neural reflex

involved in swallowing and normal function of esophagus musculature.

•A variety of central and peripheral nervous system disorders include canine distemper, other viral encephalitis, neoplasms, peripheral neuritis, bilateral vagus nerve damage, lead poisoning, botulism and myasthenia gravis.

Myasthenia gravisIt is reported in dogs and cats.

The pathogenesis of this condition is due to develop autoantibodies to nicotinic acetylcholine receptors, which interfere with neuromuscular

innervation.The affected dogs develop generalized muscular weakness followed

by signs of megaesophagus.3- Choke

It is complete or partial obstruction of the esophagus.Causes

1- Enlarged lymph nodes, tumor ad abscess.2- Congenital vascular ring anomalies and esophageal hypoplasia.

3- Potato, turnips or small ears of corn in ruminants and accumulation and germination of grains in horse.

4- Sharp pieces of bones in dog and cat.Macroscopically, the esophagus shows distention of the

esophageal portion above the obstruction. Sequalae

1- Local gangrene with sapremia and toxemia which kill the animal.2- Tympany in ruminant due to prevent regurgitation of gas.

3-Partial obstruction lead to formation of esophageal diverticulum ectasia or perforation.

Diverticulum is a symmetrical and unilateral sac like dilatation.Ectasia is a uniform spindle or clyndrical shaped dilatation.

EsophagitisThe inflammation of esophagus is infrequent due to the strong stratified squamous epithelial lining.

Causes1- Trauma.

2- Caustic chemical and reflex gastric acid.3- Infection with parasites (tricmoniasis, Congylonemiasis and Spirocercosis), mycotic as (candidiasis) and

viral (bovine viral diarrhea).Esophagitis may be catarrhal, fibrinous, suppurative and necrotic. Eosinophilic esophagitis is an inflammatory

condition in which the wall of the esophagus becomes filled with large numbers of eosinophilsEosinophilic esophagitis affects both children and adults. For unknown reasons, men are more commonly

affected than women, and it is most commonly found among young boys and menReflux esophagitis

It is a form of chemical esophagitis due to reflex of gastric acid and pepsin from stomach into the lower portion of esophagus.

Macroscopic picture • The affected part is hyperemic and contain linear erosion and ulceration.

Microscopic picture 1- Epithelial erosion or ulceration and proliferation of adjacent epithelial lining to repithelization of damaged

area.2- Capillary dilatation and polymorphonuclear leukocytes in lamina propria beside fibroblasts proliferation.

3-In chronic cases fibrosis is a sequelea.Sequalae

Fibrosis which contract and lead to stenosis of esophagus and esophageal chock and diverticulum.Neoplasm of esophagus

Papilloma, squamous cell carcinoma, and fibrosarcoma are recorded. Crop of birds

Impaction, necrosis and inflammation (ingluvitis) occur.

Forestomach of ruminantsThe rumen, reticulum and omasum are called forestomach. They have

no secretory function. They are lined by keratinized stratified squamous epithelium and function as a large fermentation chamber where digestion

of plant material occur by some bacteria and protozoa.Physical influence

1- Perforation occurs usually in reticulum but infrequently in rumen. It may be:

1) External perforationIt is most commonly in rumen as result of insertion of trocars and knives

to relieve tympany.2) Internal perforation (Traumatic reticulitis)

It occurs in bovine species due to they doesn’t have highly sensitive prehensile organ as lips and tongue nor a discriminating sense of taste.

Cattle swallow metallic objects such as nails, screws, and pieces of wire that have been carelessly left in their feeding areas. Most foreign bodies

always remain in the reticulum by the folds of its mucosa. The foreign body penetrate the reticulum by the help of its movement, abdominal

pressure, pressure of uterus and during paruration. At the point of penetration at first there is hemorrhage. After that the migration of foreign body through the wall of reticulum causes an inflammatory tract filled with

pus and food and surrounded by granulation tissue.

When the foreign body reachs the serosa, a local fibrinous peritonitis is produced and adhesion occurs between reticulum and other viscera.After leaving the reticulum the foreign body penetrate the diaphragm, pericardial sac, heart,

lung or spleen lead to abscess formation.Atony of rumen may result from serious nerve involvement or by pressure on nerve by abscess.2- Rupture of rumen may occurs due to mechanical injury from outside or over distention from

inside. 3- Dilatation of forestomach (Tympany,tympanites or Bloat) it is the excessive quantities of

gas in the lumen of rumen.Causes1- Interference with normal eructation as by chock.2-Over production of gas during fermentation process.Classification of tympanya) Frothy or primary tympanyIn this case the gas is dispersed in the form of small bubbles in rumenal fluid.It is acute ,occure

suddenly and mostly fatal.It is due to either feeding on large quantity of green succulent legumes as clover or alfilfa or sudden change from dry ration to green ration.The pathogenesis depend on excessive gas production due to colonization of ruminal bacteria on the chloroplast of the green legumes,denaturation of the soluble protein of the chloroplast by the ruminal acidity,such denaturated protein act as foam-stabilizer.morovere plant pectines increase the surface tension of the ruminal fluid.additionally,the green plants lacke the stacks or stems which enhance the ruminal expulsive movement.in contrast plant lipids act as anti-foamingb) Secondary tympany or free gas tympanyIt results from physical obstruction of esophageal or pharyngeal passage ways or pressure

upon the esophagus by tumor, abscess and swollen lymph node.

It is develop gradually and often are chronic or intermittent.Death which is common in primry type or in the secondry type of complete obstruction,results from forward displacement of the diaphragm which limit the respiratory capacity and also the expanded rumen compress the abdominal viscera and occlude the caudal vena cava, which result in anoxia. Moreover, absorption of toxic gases as carbon monoxide, carbon dioxide and hydrogen sulfide is another cause of death.Lesions1-Distended rumen and marked forward displacement of diaphragm that compress the lungs into the anterior portion of thorax.2- The abdominal viscera appear pale.3- The ruminal content will contain small bubbles of gas, clotted blood or free gas.4- Numerous hemorrhages are present on the serosa, trachea, heart and bronchial lymph nodes.4- Atony or rumen impaction it is the tightly impacted rumen with undigested food.After few hors ruminal contraction becomes weak or stops. There is a little or no gas in rumen.Lesions1- Thin easily folded wall of the rumen.2-The ruminal content has fetid odor.3-Atrophy of the ruminal muscles.4-Acute toxic hepatitis is seen (cause of death).

5 -Ruminal acidosis, rumenitis and ulcer These condition represent successive stages often associated with sudden

changes of diet from a low energy ration to highly fermentable carbohydrates as grain and bread.

Pathogenesis•Ingestion of excessive quantities of highly fermentable carbohydrate which

fermented by normal ruminal flora and bound with production of volatile fatty acids which lead to decrease ruminal pH.

•At pH 5.0 the normal Gram-negative bacteria and protozoa of rumen die, with overgrowth of streptococcus whch produce large quantities of lactic acid leading

to decrease of ruminal pH to level than so which in turn kill off streptococcus.•At this point, the acid loving lactobacillus acidophilus rapidly proliferate with the

ruminal contents and death occurs when pH drops below 4.5. •During the sequence of chemical changes described above, the musculature of

rumen and reticulum lose their tone and ability to contract due to effect of increased level of volatile fatty acids which interact epithelial receptors in ruminal

and reticulum mucosa and inhibit contraction through vagovagal reflex.•The over production of lactic acid by streptococci lead to chemical rumenitis and

reticulitis with damage and loss of epithelial.•Moreover, increase lactic acid concentration lead to increase osmotic pressure of the ingesta, which attract water and electrolytes from blood leading to clinical

dehydraton, hemoconcentration, anuria and shock.

Postmortem findings1-The ruminal content is thick in consistency with

fetid odor.2-Swollen ruminal papillae, cytoplasmic vacuolization,

erosion or ulcer are seen.3-The lamina propria shows infiltration with

neutrophils.4-The necrotic areas slough and showed re-

epithelization which is usually white in contrast to the normal black epithelium.

OmasumThe omasum and esophageal groove are seldom the

site of important pathologic processes.Pyogranulom caused actinobacillosis may be seen.Neoplasms of the forestomachPapilloma and squamous cell carcinoma and

lymphosaroma are recorded

StomachThe abomasum of ruminants is essentially similar in anatomic structure and physiologic function to the glandular stomach of monogastric animals.Pyloric stenosis and hypertrophyFunctional pyloric stenosis occurs sometimes in young dogs and characterized clinically by delayed gastric emptying which lead to vomiting and poor growth.In some cases, there is grossly hypertrophy of pyloric muscle, but in other cases is only function disorder of the gastric sphincter.Gastric dilatation and torsionAcute distension of stomach with gas occurs in several species mainly in dog.Acute dilatation characterized clinically by discomfort, abdominal pain, marked distension of abdomen and reluctance to move.CauseThe cause is generally unknown but predisposing causes may be parturation, overeating, pica, abdominal surgery and trauma.SequelaeIt lead to torsion.•Mechanical obstruction of caudal vena cava and portal vein.•Cardiac output is decreased lead to arterial hypotension, cellular catabolism increase and decrease renal function.Macroscopic picture1- Greatly enlarged stomach, distended with gas and ingesta.2- Torsion may be result in twisting of the gastrosplenic omintum.3- Severe congestion of veins and organs of caudal aspect of the body.4- Stomach may be ruptured and spilling its content into the peritoneal cavity.5- The cranial aspect of the body is ischemic.6- Liver is pale and spleen in congested.7- Petechae and ecchymosis may be seen in serous membrane.-Acute dilatation in horse lead to stomach rupture. Rabbit may also affected. The disorders has been reported in swine.

Displacement of abomasumIt is the displacement of abomasum from its ventral and right sided position in the anterior abdomen to the left side displacing the rumen to the right.Cause• It may be due to atony and gaseous distension of abomasum associated with feeding ration containing high proportions of concentrates rather than roughage.• Also following recent parturation.• Clinical signs include anorexia, depression, dehydration and distended abdomen particularly protrusion of left paralumber fossa.• If the displacement isn’t corrected immediately, the condition is fetal.ImpactionIt occurs in stomach as the result of rapid ingestion of an excessive amount of ground feed, grains without adequate water consumption.It is especially serious in horse even without gaseous fermentation, which is usually absorbed. Circulatory disturbances and shock may be fatal in few hours.Parasites• A wide variety of parasites may infest the stomach.• Gastrophilus spp. larvae, Habroonema spp., and Draschia spp. are seen in horse.• Haemonchus spp., Ostertagia spp. and Trichostrongylus spp. are recorded in ruminant.• Physaloptera spp. and Ganthostoma are seen in dog and cat

Gastritis• It is the inflammation of stomach.

• It may be primary mostly due to ingestion of toxic substances or secondary to an infection as canine distemper, hog cholera and viral diarrhea.

• Clinically, it is characterized by pain, anorexia and vomiting.• It is usually catarrhal or hemorrhagic.

1) Acute catarrhal gastritisCauses

1- Physical or chemical agents.2- Infectious agents as in case of canine distemper, feline enteritis and parasitic

gastritis.Macroscopic picture

1- Reddening and thickening of gastric mucosa.2- Increase in mucus secretion.

Microscopic picture1- Hyperemia, desquamated epithelium beside leukocytic infiltration are seen.

2- Hyperplasia of minute mucosal lymphoid nodules.2) Chronic catarrhal gastritis

• It reported with Haemonchus contortus.• The hyperplastic lymphoid tissue seen grossly as small white mucosal

nodules.

3 (Acute hemorrhagic gastritisCauses

1-Infectious agent as leptospirosis in dog and Clostridium septicum (Braxy) in sheep.

2- Uremia and arsenic poison.Macroscopic picture

1- Deep reddening of gastric mucosa.2- Presence of blood on the surface of mucosa and mix with content

which turned to brown black due to effect of gastric acid.Microscopic picture

• The predominant type of exudate is erythrocytes beside congested capillaries, leukocytic infiltration and desquamated epithelium.

• Inflammatory edema and fibrinous exudate may be seen.4) Lymphocytic gastritis

It is seen in dog and cats associated with infection by Heliobacter and H. pylori.

5) Eosinophilic gastritisIt is characterized by the predominant type of exudate is eosinophils.

Moreover, it cause chronic fibrotic gastritis. Mostly it associated with larva migrans in dog.

HemorrhagesLarge and small hemorrhages may occur in the gastric

mucosa. Hemorrhage producing infection involve the gastric mucosa are hog cholera, anthrax and leptospirosis.

UlcerIt is a result of deep necrosis and usually acute. It is now

recognized in most domestic species.Foreign bodies

Rubber ball in dog stomach, hair balls in cat stomach are seen. Sand in horse, cattle and sheep raised on sandy land.

Neoplasm of stomachAdenocarcinoma, adenomatous polyps, undifferentiated

carcinoma, squamous cell carcinoma and leiomyoma and leiomyosarcoma are recorded.

Small intestineEnteritis

It is inflammation of any part of intestinal tract. Gastroenteritis is the inflammation involve the entire tract. Other terminology may be used when

inflammation more than one part as duodenitis, jejunitis, typhlitis or cectis and proctitis.

Acute enteritis may confirm to any one of the five types of exudative acute inflammation.

Subacute and chronic inflammation are by no mean rare.The whole small intestine and large intestine may be uniformly inflamed or

perhaps localized.1) Catarrhal enteritis

Causes1- Chemical intoxication.

2- Many infectious agent and parasites.3- Physical agent as coarse food.

Macroscopic picture1- The intestinal content contain mucus.

2- The intestinal wall become swollen, red and thick.Microscopic picture

Numerous goblet cells, congested blood vessels and leukocytic infiltration are seen.

2 (Hemorrhagic enteritisCauses

Locally destructive endo or exotoxin or by highly virulent infection as anthrax, S. typhimurium and Shigella. Also virus as canine and feline

parvo virus.Macroscopic picture

• The intestinal content is mixed with blood (brownish in anterior portion and bright red in posterior portion).

• The intestinal wall are hemorrhagic and thickened.Microscopic picture

• Extravasated erythrocytes and inflammatory cells in intestinal wall.3) Purulent inflammation

CausesIt is due to pyogenic microorganisms associated with mechanical injuries

as foreign body or helminth parasite as hook worms.Macroscopic picture

• It is characterized by presence of pus mixed with ingesta beside congestion and swollen mucosa.

Microscopic picture• The intestinal mucosa infiltrated with dead and life neutrophils beside

congested blood vessels.

4 (Acute fibrinous enteritisCauses 1- Severe chemical agent as mercuric chloride and arsenic.2- Infectious agents as Salmonella enteritidis, Escherichia coli and Salmonella cholera suis.Macroscopic picture• The intestinal mucosa is covered by yellowish gray fibrinous membrane.• The intestinal mucosa is usually eroded, congested and edematous.Microscopic picture1- The intestinal mucosa covered with fibrin mixed with inflammatory cells and necrotic epithelium.2- The intestinal mucosa shows, necrotic epithelium, congested blood vessels and infiltration with neutrophils.5) Lymphocytic-plasmocytic enteritisIt is the most common idiopathic inflammatory bowel disease of dog and cat and associated with chronic diarrhea and vomiting.Progressive weight loss, hypoproteinemia, ascitis and peripheral edema are noticed in severely affected animal.Microscopically, extensive infiltration of lamina propria by lymphocytes and plasma cells are noticed beside fusion and atrophy of intestinal villi.Crypt may be hypertrophied and filled with mucus

6 (Eosinophilic enteritisChronic gastroenteritis occurs in dog and cat and associated with repeated

episodes of diarrhea and peripheral eosinophilia.Causes

The cause is unknown but it may be an immune reaction to some antigen.Microscopically, the mucosa, submucosa and tunica muscularis are infiltrated by

eosinophils, mast cells and macrophages.Caseous necrosis surrounded by eosinophils is noticed.

7) Chronic proliferaive enteritisIt is seen with those granulomatous diseases involving intestine as

partuberculosis (Johne’s disease, tuberculosis, Hjarre’s disease in fowl). Macroscopic picture

• The intestinal wall is thickened and covered with mucus.• The intestinal content is watery.

Microscopic picture• It is varies and characteristic for each disease.

•Mucinous degeneration of intestinal epithelium and infiltration of tunica propria with macrophages, lymphocytes, plasma cells and fibroblasts are seen.

•The crypt become atrophied or cystic.

PerforationIt may be caused by gunshot, parasites and ulcers.

Sequelae1- Rapid perforation causes acute peritonitis and death.

2- Slow perforation causes localized peritonitis, adhesion and abscess.Rupture

It occurs due to trauma and lead to death.Intestinal obstruction

The small intestine becomes completely obstructed by foreign bodies such as rubber balls, nipples or nuts in dogs or hair ball (piliconcretion) in cats and

phytolith in hores and ruminents. Strangulated hernias intussusception portion, volvulus and torsion cause complete obstruction in any species.

VolvulusIt is twisting of intestine ,may be due to passing of loop of intestine through a tear

in the mesentry.Torsion

It is the rotation of intestine around its long axis.Intussusception

It occurs due to excessive peristaltic motility forces a segment of intestine inside the segment just below it.

The result of volvulus, torsion, intussusception are passive congestion, hemorrhage, necrosis and gangrene.

The animal die from toxemia.

HerniaIt is the abnormal protrusion of the viscera or its covering through

an abnormal opening in the wall of body cavity.Hernia consist of hernial sac consists of peritoneum covered by

skin, hernial ring and hernieal contents.Types

Several types depend upon their location as inguinal, umbilical and diaphragmatic hernia(hiatus) are observed.

Eversion(prolaps)It is turning outward of the rectum through anal canal opening.

Intestinal emphysemaNumerous gas vesicles are seen in the wall of small intestine, mesentry and esentirc lymph nodes is slaughtered swine and

sheepNeoplasm of small intestine

Adenoma, adenocarcinomal ,leiomyoma and leiomyosarcoma, lipoma, lymphosarcoma and mast cell tumors are recorded.

The cecumImpaction of the cecum

It is often fetal in horse. It occurs when old animal switch from soft food to coarse ration (dry roughage).

Grossly, the cecum become atonic and distended to unbelievable dimensinon with undigested food.

Tympanites of cecum is the form of alimentary bloating in horse.Intussusception rarely occurs in dog and cats.

The colonCongenital and hereditary anomalies

MegacolonIt occurs in dog and mice due to absence of myenteric ganglia distal to the dilated portion.

Duplication of colonIt occurs in dogs where the colon was equally duplicated from the cecum to colon.

Atrasia coliIt is the absence of colon.

The rectum and anusAtrasia ani: It is the failure of development of anal opening.

Prolapse of rectum: it occurs in all species but more in swine and cattle.Peritoneum

Peritonitis• Most cases of peritonitis result from infectious agents. It may be localized in dogs and

ruminant or generalized in equine.• The principle routes by which infectious agants enter to the peritoneal cavity are:

1) Surgical incision through abdomen.2) Rupture or perforation of stomach, intestine and uterus.

3) Via blood stream in certain specific infection as feline infectious peritonitis.

Acute peritonitisIt is characterized by great amount of fluid in abdominal cavity. The

exudate may be fibrinous, suppurative or hemorrhagicChronic peritonitisIt is characterized by diffuse of localized thickening of peritoneum.Hydroperitoneum, ascitisAccumulation of watery fluid in peritoneal cavity is called

hydroperitoneum but in non inflammatory fluid is called Ascitis. Ascitis occurs as a part of generalized edema. Ascitis morphologically results from chronic passive congestion of portal venous system especially with hepatic cirrhosis.Chylous ascitisIt occurs due to injury of thoracic duct and accumulation of chyle in

abdominal cavity.NeoplasmMesotheloma and lipoma are recorded.

Liver and biliary tractLiver is seen by light microscope or even by necked eye to be divided into many lobule with the shape of an irregular pyramidal hexahedron (classic anatomic lobules). At the center of anatomic lobules is the central vein (smallest branch of hepatic vein). The lobule is made of interconnecting plate of hepatocytes separated by endothelium lined sinusoids. Individual hepatocytes are large, with a central round nucleus and abundant cytoplasm.

The liver cells are separated from sinusoids by a narrow space (space of disse). Kupffer cells are present in the sinusoids scattered among endothelial

cells. The biliary system begins at the biliary canaliculi (which are small channels lined by the complex microvilli of hepatocytes), which drain into

interlobular bile duct (canals of hering), which drain into bile duct in the portal tract. Around the periphery of each lobule are four to five portal tracts,

composed of terminal branches of hepatic artery, portal vein and bile ducts which embedded in connective tissue. The blood supply to the liver

parenchyma flows from the portal triads to the central veins. About 30 to 40% is provide by terminal branch of hepatic artery, and the remainder by the portal

vein branch. The bile in canaliculi flows from the center of hepatic lobule towards periphery.

Liver is characterized by its great ability to regenerate. If three quarters of dog’s liver is removed the original mass will be restored with six to eight weeks.

Normal Liver

Hepatic failureThe liver failure occurs only when there is extensive liver destruction ,over 80%

of the organ.Acute liver failure

It results from acute liver necrosis caused by viral hepatitis, toxic drugs and chemicals, and characterized by:

(1) Jaundice. (2) Hypoglycemia.

(3) Bleeding tendency. (4) Electrolyte and acid base disturbance.

(5) Hepatic encephalopathy. (6) Elevation of serum enzymes (LDH, AST, ALT).

Chronic liver failureIt usually result from cirrhosis, which associated with progressive necrosis of

liver cells fibrosis, and nodular regeneration and it characterized by:(1) Edema.

(2) Bleeding. (3) Portal hyperplasia.and portal hypertension

(4) Hepatic encephalopathy.(5) Hepatorenal syndrome.

(6) Endocrine changes caused by disorder metabolism of certain hormones.

Hepatic encephalopathyIt is clear that there are association between the hepatic diseases and nervous signs

or symptoms. Pathogenesis

Impaired hepatic function allows various exogenous and endogenous metabolites to enter circulation, which are responsible for signs and lesions of

hepatoencephalopathy. Elevated level of amonia is considered the principle offending metabolites (liver converts ammonia to urea).

Causes1- It associated with acute or chronic hepatic failure.

2- Porto-systemic shunt which allow the portal blood to by-pass the liver.Signs

Blindness, abdominal movement, convulsion, coma and death.Lesions

-The liver shows massive necrosis or fibrosis.-The brain shows edema, neuronal necrosis and swelling, astrocytes degeneration.

Hepatorenal syndromeIt is appearance of renal failure in patients with severe liver diseases.

Congenital defectsCongenital defects aren’t common.

Intrahepatic congenital cystIt observed in liver due to lack of outlet of primitive bile duct or connection with the

main biliary system.

Atrasia of extrahepatic bile ductIt will lead to biliary cirrhosis.

Congenital portal- systemic vascular shuntsIt occurs due to persistence of ducts venosus or connection between portal vein and

caudal vena cava.Circulatory disorders

Passive congestionIt may be either acute or chronic. Passive congestion is due to reduction in blood flow

through hepatic vein or vena cava, heart or lungs. The liver is cyanotic in acute form and nutmeg appearance in chronic cases.

Acquired porto-systemic shuntIt follow chronic liver diseases leading to portal hypertension. The liver shows numerous

tortuous connection between the poral vein and systemic veins. Telangiectasis

It is greatly dilated sinusoids within any part of hepatic lobules.The hepatic cells between lobules are partially or completely disappeared. Telangiectasis

is observed in cattle without clinical significance.Telangiectasis may results from foci of necrosis termed saw dust.

Anemia: It is associated with general anemia and lead to various retrogressive changes.Hemorrhage: It is observed in dog and cats due to hepatic rupture.

Thrombosis of hepatic vessels is common with hepatitis.Infarction of the liver is usually caused by hepatitis which impaired portal and hepatic

circulation as caused by bacillary hemoglobinuria in cattle and sheep.

Degeneration and depositionFatty liverThe accumulation of fat or triglycerides in cytoplasm of hepatocytes known as fatty liver. Hepatic lipidosis or fatty change is one of the most common lesions encountered.GlycogenHepatocytes normal contain glycogen. Abnormal accumulation of glycogen is seen in diabetes mellitus and glycogen storage diseases.Amyloid Amyloid infiltration are seen in liver either primary or secondary.PigmentBile pigments are seen in association with cholestasis.Lipofuscin is common in liver of old animal.Hemosiderin is accumulated in kupffer’s cell and hepatocytes in case of increase destruction of erythrocytes.Melanosis is occasionally seen in liver.Hepatic necrosisThe liver responds to injury takes so many ways. One feature of responds to many diseases is necrosis.The hepatic necrosis is usually coagulative in type and recognized microscopically by pyknosis and acidophilic cytoplasm follow by disappearance of cells.Caseous or liquifactive necrosis may seen in liver with granulomatous diseases and abscess.According to location, necrosis may take several forms.

a) Focal necrosis Where small necrotic area or foci of sublobular size appear here and there as saw

dust liver of cattle which seen frequently by meat inspectors. It occurs in well fattened young cattle which appear in perfect health. Macroscopically, the liver shows several or many yellowish foci of necrosis as granules of saw dust scattered over the liver. Microscopically, they consist of collection of hepatic cells in state of coagulative necrosis surrounded and mixed with neutrophils and lymphocytes.b) Zonal necrosisIt is characterized by necrosis of hepatocytes restricted to a particular part of

lobules.1-Centrolobular necrosis characterized by necrosis of hepatocytes nearest or

entirely circle the central vein. It is usually seen in hypoxic condition such as passive congestion and anemia.2- Midzonal necrosis affects the hepatocytes half ways between the periphery and

center of lobule. It is usual form of necrosis.3- Periportal necrosis is characterized by necrosis of hepatocytes surrounding the

portal areas. It is seen associated with blood borne poison as phosphorus poisoning.4 -Paracentral necrosis is characterized by wedge-shaped with apex at central vein

and base at the portal area. It is seen associated with occlusion of terminal branches of portal vein as Rift valley fever. Disassociation of liver cellsIt is one of characteristic feature of certain diseases (particularly leptospirosis) where the liver cells detached from one to another (individualized) and somewhat rounded and the cytoplasm become more acidophilic.

HepatitisIt is the inflammation of the liver parenchyma.N.B.: •The inflammation of bile duct is called cholangitis while cholangiohepatitis ,inflammation of the the bilary system which extend into liver parenchyma.•Portal hepatitis, which refer to inflammation of hepatic parenchyma around the portal area and infiltrate the portal area with inflammatory cells.Acute hepatitis• In acute hepatitis, vascular feature of inflammation (dilatation of arterioles, venules and lymphatics may be present in portal areas).•Leukocytes present in portal areas and sinusoid (neutrophils in bacterial, lymphocytes and plasma cells in viral) •Degenerative changes in hepatocytes including swelling, apoptosis, and necrosis are seen.•If the animal survives, necrotic tissue is removed by phagocytic cells and replaced by regenerating parenchyma or fibrous scar, but if the antigen persists an abscess or granuloma form.

Chronic hepatitis•It is characterized by infiltration of the hepatic parenchyma and mainly

portal areas by lymphocytes and plasma cells (portal hepatitis).• Increased fibrous connective tissue in portal areas with proliferation of bile

ducts.• With progression, the fibrosis extend from the portal area to the central

vein (pseudolobulation).•Chronic hepatitis may include focal necrosis with association of

macrophages and few neutrophils along with fibrous tissue (chronic active hepatitis) which is progressive and lead to cirrhosis.•Certain species of bacteria and fungi are particularly resistant to killing by

phagocytic cells and are capable of inducing chronic inflammation and granuloma.Causes and forms of hepatitis• The causes usually blood borne infection, because the liver receives both

arterial blood via hepatic artery and venous blood from gastrointestinal tract via portal vein.•It can either primary or part of systemic process. •Infection also can gain access to the liver by ascending through biliary

system or by direct extension through the peritoneal cavity.

1 -Infectious hepatitisIt caused by infectious agents as bacteria, virus or parasitic.

Bacterial causes of hepatitis include Clostridium novyi (black disease), Clostridium hemolyticum (bacillary hemoglobinurea). Also, it associated with leptpspirosis, salmonellosis and necrobacillosis. Corynebacterium

pyogenes is a common cause of suppurative hepatitis in cattle.Viral causes of hepatitis including infectious canine hepatitis, rift valley

fever, yellow fever and generalized herpesvirus infection. And HVCandB in human

Protozoal infections include coccidiosis, leishmaniasis and amoebiasis.Metazoan parasites due to migration of larvae which lead to necrosis,

inflammation and fibrosis as Ascaris sum. Strongylus in horse and Cysticercus tenuicollis in sheep and cattle.

Capilari hepatica and Echinococcus replaced the hepatic parenchyma.Liver flukes including Fasciola hepatica, F. gigantica, Dicrocoelium

dendriticum damage the liver through larval migration and the presence of adults within the bile ducts and hepatic parenchyma.

Fungal diseases as histoplasmosis.2-Toxic or non infectious hepatitis

•It is inflammation of liver due to exposure to many drugs and toxins.•In some cases it characterized by cell death after suffering cloudy

swelling and fatty changes. In other types, it is accompanied by acute or chronic inflammation.

PathogenesisBy the way of portal vein, the liver is the first organ to receive substance from the gastrointestinal tract so, it is the first organ expose to ingested

toxins or toxins formed in intestinal tract.In liver there are two principle mechanisms

a) Direct toxicity to hepatic cells during detoxify and removal of toxic substances.

b) Conversion of xenobiotic(chemicals that are forign to the biological system) to toxin as in aflatoxins and carbon tetrachloride.

Causes1- Chemical poisons as copper, arsenic and phosphorus ccl4 and others.

2-Mycotoxins as aflatoxin.3- Plant poisons as snecio.

4-Metabolic poisons are those produced during disease as gastroenteritis, metritis.

Macroscopically,The picture is vary according to the affected toxins.The liver is usually mottled, congested and enlarged first.

Later on the liver appears small in size and yellow in colour due to necrosis and fatty change (acute yellow atrophy) or become red and small due to

necrosis and congestion and hemorrhage (acute red atrophy).Finally, fibrosis, biliary hyperplasia and paranchymal regeneration are

noticed.

Microscopic picture1-Degenerative changes and necrosis of hepatocytes are seen.

2- Congestion of central veins, hepatic sinusoids and portal blood vessels in addition to fibroblast proliferation.

3- Inflammatory cells usually absent, but in some cases lymphocytic infiltration are seen in portal areas.

4-In chronic hepatitis, hepatocytes regeneration, fibrosis and cirrhosis are seen.

Response of liver to injury1- Regeneration

•The liver has regenerative capacity, so if the animal survive massive necrosis, parenchymal regeneration without scaring are noticed as long

as the reticulin frame-work of the affected portion remain intact.•The liver regenerate as much as 80% of its mass without apparent ill.

•A prolonged regeneration often results in nodular proliferation with architecturally distorted liver.

2-Fibrosis•It occurs with necrosis and destruction of hepatocytes and Reticulin fram. Also when necrosis is more than regenerative capacity of liver.•Chronic cholangitis can produce fibrosis that is most pronounced in

portal area.•Also, it observe in chronic hypoxia usually in centrolobular area.

3- Biliary hyperplasiaA variety of causes can results in proliferation of new bile ducts within the portal areas usually accompanied by fibrosis which is extended to

the hepatic lobules.

Cirrhosis (End stage liver)It is a serious disease of the liver characterized by massive replacement of the hepatic parenchyma by fibrous tissue and nodules of regenerating hepatocytes which lead to hepatic failure. Cirrhosis may be:1-Portal cirrhosis•It occurs following massive destruction of hepatic parenchyma and Reticulin network.•All the liver elements showed regeneration which lead to nodular hepatocytes, distortion of organs with fibrous tissue and anastomosis between hepatic artery and central vein with more necrosis and cirrhosis(no energy to cells).Macroscopic picture•The affected liver is small, firm nodular.•Ascites is usually present. Jaundice is seen at the terminal stage.Microscopic picture1- Hepatic nodules formed from regenerating hepatocytes without central vein and surrounded by small branches of central vein and hepatic artery (arteriovenous shunt) which lead to ischemia and necrosis.2- Fibrous connective tissue proliferation which start from the portal areas and extend between the lobules (interlobular cirrhosis.monolobular or multilobular).3- Moreover, the fibrous tissue enter the lobule and surrounded group of hepatocytes (intralobular cirrhosis or pericelular cirrhosis.4- The fibrous tissue is infiltrated with lymphocytes and plasma cells. Blood vessels may accompany those fibrous strands and connect the portal and central vein

2 -Biliary cirrhosisMacroscopic picture

1- Liver is hard, enlarged with smooth surface.2-Hepatic tissue is yellowish green (jaundice appear early).

3- Bile duct may be thicked white and calcified.Microscopic picture

1- Numerous newly formed bile ductules with thickened wall. Compressing the surrounding hepatocytes

2- The bile ducts surrounded by thick bands of fibrous tissue which extend between lobules and cause pressure atrophy of hepatocytes.

Special forms of cirrhosisGlissonian cirrhosis

It resemble portal cirrhosis but restricted to short area under the capsule.Central cardiac cirrhosis

It characterized by increase amount of fibrin tissue around central vein in chronic venous congestion.

Pigmentary cirrhosisIt occurs with hemochromatosis.

Parasitic cirrhosisIt occurs in association with parasites as fasioliasis and schistosomiasis

Effect of cirrhosis1- Ascites with portal cirrhosis due to increase portal hypertension.

2- Hepatic failure of synthesis prothrombin (defect in clotting) or protein (edema).3-Failure to detoxify toxins and hormones as estrogen which lead to atrophy of testes

and disappearance of secondary sexual characters of male.(feminization)The presence of fibrous tissue in liver is progressive process that means stimulate

proliferation of a new fibrous tissue even with cause removal4-anemia due to lack of erythropiotien and toxic depression of bon marrow

Neoplasm of liverHepatoma, hepatocellular carcinoma, cavernous

hemangioma and hemangiosarcoma are primary hepatic tumors.

Gall bladder and bile duct•Cholangitis is inflammation of bile ducts.

• Cholecystitis is inflammation of gall bladder.• Cholangitis and cholecystitis are usually

catarrhal or serous.Cholelithiasis

It is the formation of cholelith or gall-stone. It is rare in domestic animals.