Digestive system Structure and function: - Structure: mucosa and serosa of gastrointestinal tract (G.I.T.

) must be smooth and shiny except in compound stomach of ruminant. - Function: digestion and absorption of ingested food. Portals of entry in the alimentary system: 1- Ingestion. 2- Coughed up by lung and swallowed. 3- Blood. 4- Parasitic migration. Defense mechanism: 1- Saliva. 2- Flora and fauna. 3- Gastric acidic pH. 4- IG. 5- Vomition. 6- Diarrhea. 7- Liver and pancreatic secretion. 8- High rate of epithelial turnover. 9- Normal gastrointestinal motility.

Digestive system affections 1- Oral cavity I-Congenital anomalies: -palatoschesis (cleft palate), it may be genetic or toxic (Fig. 1). - cheiloschesis (hare lip, cleft lip) (Fig. 2). Fate: animal unable to suckle, aspiration pneumonia and suffocation. II-Stomatitis: -Definition: It is an inflammation of oral mucus membrane. Cheilitis (lampas): inflammation of lips Gingivitis: inflammation of gum Glossitis: inflammation of tongue Palatitis: inflammation of hard palate Angina: inflammation of soft palate Tonsilitis: inflammation of tonsils Pharyngitis: inflammation of pharynx -Causes: 1- Physical: trauma, hot and cold materials 2-Cemical: toxins, caustic alkali and corrosive acids.

3-Biological:

viruses

(F.M.D.,

R.P.,

B.V.D.),

bacteria

(Fusobacterium

necrophorum, Actinomyces, Actinobacillus), fungus (Monilia). 4- Vitamin A deficiency in poultry and niacin deficiency in dog (black tongue or necrotic stomatitis). -Types of stomatitis: a- Catarrhal stomatitis: - It is the mildest type of stomatitis. - Gross lesion: congested and thickened mucosa which covered with mucus exudate and cell debris. - Microscopic appearance: submucosa infiltrated by inflammatory edema and inflammatory cells and their blood vessels are hyperemic, surface epithelium covered with cell debris and bluish mucus exudate and inflammatory cells, degeneration and desquamation of epithelial cells, hyperplasia of mucus secreting cells. b- Vesicular stomatitis: - Causes: viral (as F.M.D., vesicular exanthema and vesicular stomatitis) and thermal. -virus is cytolytic, so released from cell to another and form vesicle - Gross lesion: fluid filled vesicle in oral cavity, vesicle coalesce and form bullae, then ruptured and form erosions and ulcers which are hyperemic. - microscopic appearance: intracellular edema of stratum spongiosum, cell lysis and intercellular edema occurred, the epithelium serve as a roof of vesicle, vesicle

then form bullae and ruptured and ulceration occurred, ulcerated area is covered with fibrin then granulation tissue. submucosa as in catarrhal. c- Erosive and ulcerative stomatitis: - Causes: viral (B.V.D, R.P., B.T.), toxic (uremia), foreign body, vit. C deficiency in Guinea pig. d- Necrotic and fibrinonecrotic: - Cause: Fusobacterium necrophorum (calf diphtheria in cattle). - Gross lesion: yellow grey round foci surrounded by hyperemic zone and covered with fibrin and cell debris. - Microscopic appearance: well demarcated foci of coagulative necrosis surrounded by hyperemic blood vessels and inflammatory cells and covered with fibrin and inflammatory cells. e- Esinophilic stomatitis: Immune-mediated disease occurred in cat and characterized by oral granulome. f- Lymphoplasmocytic stomatitis: Idiopathic condition of cat, it is a chronic condition. - Thrush: fungal infection of tongue and esophageal mucus membrane and occurred in birds, the lesion appeared as a grey-green pseudomembrane covered healthy epithelium. III- Neoplasms: - Squamous cell papilloma (infectious).

- Squamous cell carcinoma - Epulis: fibroblastic tumor.

2- Salivary glands -Major salivary glands: Parotid, mandibular and sublingual. -Minor salivary glands: buccal, labial, lingual and palatine. -salivary glands are aggregates of compound tubuloalveolar tissue. -saliva is a mixture of serous and mucoid secretion and its function is to lubricate mouth and esophagus and moistens the ingesta and dissolve water soluble component of food and its mucus content form food bolus to be easily swallowed, also mucus coat lining of mouth, has a flushing and buffer action. -Rarely to be affected due to: salivary secretion has antimicrobial effect, flushing and buffer action of saliva and protected situation of glands. I- Inflammation: (sialoadenitis, parotiditis): - Rare in animals. - Causes: infection (rabies, canine distemper) or traumatic. - Gross lesion: edema, swelling, pain in palpation and abscessiation may be occurred. II- Salivary calculi (sialolith): - Rare in animals. - Cause: inflammation of salivary glands. - Sloughed epithelium and inflammatory exudate form nidus for mineral ppt. - Sequellae: stasis of saliva and distention of duct and atrophy of gland.

III- Ranula: - Salivary cyst on mouth floor which is smooth and round, contain clear fluid (Fig. 3) and lined with epithelium. - Cause: occlusion of salivary ducts by salivary calculi or inflammatory exudate. IV- Salivary mucocele: - Pseudocyst, filled with saliva. - Not lined with epithelium. - Caused by traumatic rupture of salivary ducts with leakage of saliva which encapsulated with c.t. 3- Esophagus - Lined by stratified squamous keratinized or non- keratinized epithelium according to animal spp. I- Developmental anomalies: - Achalasia: -It is a motility disorder in which there is contraction defect. -Cause: congenital neurogenic disorders. -it causes regurgitation and weight loss. II- Megaesophagus (ectasia): -it is a dilatation of esophagus (Fig.4).

-Cause: nervous disorders, stenosis and obstruction, inflammatory process in muscular layer of esophagus, myopathy and blockage from persistent right aortic arch. III- Ulcer: -Causes: acid reflux, trauma from stomach tube, infectious (B.V.D.). IV- Choke: -it is an esophageal obstruction (Fig.5). -Cause: ingestion of large foreign body, poor dentition in horse which causes poor mastication, neoplasm or inflammation of esophageal wall or pressure from outside and persistent right aortic arch. -Fate: *Partial obstruction: dilatation of esophagus above obstructed area (diverticulum) *complete obstruction: tympany, pressure necrosis, gangrene and gangrenous pneumonia. V- Esophagitis: - Rare due to thick and resistant mucosa. - Causes: trauma, foreign body, chemicals, parasites, persistant vomiting. - Types: as stomatitis. 4- Rumen, reticulum and omasum (Ruminant forestomach) - Structure and function: stratified squamous non- glandular epithelium (protective barrier).

- Reticulo-omasal orifice is more dorsal than floor of compartments, so reticulum can trap foreign body (traumatic reticulitis). Affections of forestomach I-bloat (ruminal tympany): - It is overdistension of rumen and reticulum by gases produced during fermentation. - Classification: Primary and secondary. A- Primary (legume, dietary or frothy bloat): the most severe type. Causes: change of diet, feed on legumes and grain concentrates. Pathogenesis: feed on legumes and grain concentrates promotes formation of stable foam and formation of non- volatile acids which lowered pH to 5-6 and this pH is optimum for formation of bloat, foam mixed with ruminal content and this factors block cardiac sphincter and prevent gas eructation. Absence of fibers in food prevent stimulation of ruminal mucosa to be contracted to eructate gases. - Death occurred from respiratory failure due to distension of abdomen and compression of diaphragm. P.M. lesions: sharp line of demarcation between pale distal esophagus and congested proximal one at thoracic inlet and this line called ( bloat line) (Fig.6). Also there is congestion of abdominal viscera and hemorrhage, pale liver, ruminal mucosa is friable and detached easily. B- Secondary (obstructive) bloat: Causes: physical or functional obstruction of esophagus (vagal indigestion, esophageal neoplasms and esophageal foreign body) result in failure of eructation.Accumulation of non frowthy gases my lead to pressure on diaphragm or rupture of rumen.

II-Impaction (ruminal atony, lactic acidosis, CHO engorgement, rumen overload, grain overload and chemical rumenitis, engorgement toxemia). Causes: change of diet to easily fermentable food (CHO rich food) or change of food quantity with insufficient water intake, vagal indigestion, ruminal atony. Pathogenesis: change of diet to easily fermented food (CHO rich food) or change of food quantity with insufficient water intake promotes growth of gram negative cellulolytic microflora, these bacteria ferment CHO to lactic acid and lower ruminal pH, acidic pH eliminate normal flora and fauna and these factors lead to damage to mucosal surface of rumen, death occurr from dehydration (increased osmotic pressure of ruminal content) and circulatory collapse and also from acidosis and toxaemia. P.M. lesion: ruminal and intestinal content are watery and acidic and abundant grains are found, ruminal mucosa is brown, friable and detached easily, animal which survive has stellate scars. III-Foreign body: 1-Trichobezoara (hair ball): calves licking each other or irritabe skin lesions. 2-Phytobezoara (plant ball): excess of indigestible roughages. 3-Nails and wires, cause traumatic reticulitis, peritonitis and pericarditis (hardware disease). IV- Rumenitis: Causes: lactic acidosis, bacterial (as Fusobacterium necrophorum which invade rumen after lactic acidosis or traumatic injury and cause ruminal and liver

affections), mycotic (as asperigellosis after lactic acidosis, traumatic injury or antibiotic treatment).