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Department of Pathology, Faculty of Veterinary Medicine, Zagazig University, Egypt.

Pathology of Digestive System BY

Prof. Dr. Mohamed Hamed Mohamed mohamedelariny@yahoo.com +20124067373

2011


THE DIGESTIVE SYSTEM Oral cavity Anomalies: Congenital disturbances in development involve one tissue or organs. Facial Clefts: Longitudinal fissure in the face. Harelip or Chelioschisis): (Cleft = schisis = fissure) fissure in the lip. Cleft palate or Palatoschisis): fissure in the palate. Glossoschisis: fissure in the tongue. Brachygnathia: (brachy = short gnathia = jaw). It is the short jaw. i-Superior: upper jaw. ii-Inferior: lower jaw. Prognathia: Protruded anteriorly jaw Agnathia: Absence of jaw. Polyodontia: Increase the number of the teeth than the normal.

Stomatitis Definition: It is the inflammation of the oral cavity. Classification or Types of Stomatitis: I-According to location: i-Diffuse Stomatitis: it is usually due to hot drench, chemicals. ii-Focal Stomatitis: due to infectious agents.


II-According to the cause: i-Primary Stomatitis: The cause affects directly on buccal cavity ii-Secondary Stomatitis: It occurs secondary to specific disease.

III-According to the Exudate IV-According to the lesions 1-Catarrhal Stomatitis 2-Suppurative Stomatitis 3-Fibrinous Stomatitis 1-Catarrhal Stomatitis

1-Vesicular Stomatitis 2-Ulcerative Stomatitis 3-Necrotic Stomatitis

It is a mild inflammation of oral mucosa. Causes: trauma, chemical irritants and infectious agents.

Microscopic Picture: 1-Dilatation of the submucosal blood vessels. 2-Leukocytic infiltration in the submucosa. 3-Hyperplasia and desquamation of the lining epithelium. 4-The mucosa is covered with mucus (basophilic material).

Macroscopic Picture: 1-Mucosa is covered by grayish or brownish mucus. 2-The buccal mucosa is red and swollen. 3-Small retention cysts due to obstruction of the duct of salivary glands 4-Fetid odor is present due to bacterial decomposition of food.


2-Vesicular Stomatitis: Causes: 1-Thermic and chemical agents. 2-Some specific infectious diseases as: Foot and mouth disease in cattle and sheep. Infectious vesicular stomatitis in horse, swine and cattle. Infectious vesicular exanthema in swine Herpes virus in cattle. Microscopic Picture: 1-The covering epithelium show vacuolar and hydropic degenerations. 2-Several cells may be ruptured on each others forming cavity containing fluid (vesicle or aphtha). 3-These vesicles may coalesced together to form large ones (bulla). 4-The vesicles may be ruptured leaving erosions with intact basal layer. NB: Erosion is loss of the superficial layer of the epithelium with intact basement membrane (heal by regeneration).


Macroscopic Picture: 1-Vesicles (1-25 mm or more) are seen on the mucosa of the gum, lips, tongue, dental pad and hard palate. 2-These vesicles filled with serous fluid. 3-Rupture of the vesicles leave eroded mucosa.

3-Suppurative Stomatitis: 1-It is produced as a result of trauma of the mouth and pyogenic m.o. complication (focal or diffuse). 2-The pus is usually removed by movement of food leaving ulcer (ulcerative stomatitis).

4-Ulcerative Stomatitis: Causes: 1-Trauma as foreign bodies and sharp teeth. 2-Complication of catarrhal type by pyogenic m.o. 3-Chemical agents, acids, alkalies and erosive salts. 4-Nicotinic acid deficiency in dogs (black tongue). 5-Vit. A deficiency in chicks and poults. 6-Some specific infectious diseases as cattle plague, mucosal disease and viral diarrhea.


NB: Ulcer is discontinuation of the epithelial lining, where the base lies in the lamina propria (epithelial lining). The ulcer is deep, red base, elevated edges, covered by epithelial shreds (ragged) and healed by scar formation. 5-Fibrinous, Fibrinonecrotic and Necrotic Stomatitis: A-Fibrinous (Croupous) Stomatitis: It is characterized by only deposition of fibrin threads on the mucosa.

B-Fibrinonecrotic (Diphtheritic) Stomatitis: It is characterized by more or less coagulative necrosis of the mucous membrane with marked fibrinous exudate. C-Necrotic Stomatitis: It is characterized by pure necrosis without fibrin formation.

Causes: i-Bacteria: as Coryne pyogenes and Spheropherous

(Fusobacterium) necropherus. ii-Viruses: as Fowl pox and cattle plague.


iii-Endotoxins: as uremia in dogs. iv-Nicotinic acid deficiency (black tongue) in dogs.

Microscopic Picture: 1-Dilation of the submucosal blood vessels. 2-Leukocytic infiltration in the submucosa. 3-Fibrin network (fibrinous), coagulative necrosis and fibrin (Fibrinonecrotic) or only coagulative necrosis (Necrotic).

Macroscopic Picture: 1-Dirty grayish and dry fibrinous membrane on the mucosa. 2-The affected mucosa is congested and swollen. 3-In necrotic stomatitis: it varies according to the cause. a-Acids or alkalies show deep irregular necrotic areas (diffuse) in the mucosa, which slough leaving ulcers. b-Spheropherous necropherus produce single or rarely multiple sharply circumscribed dirty grayish red foci (focal).


Inflammation of Stomatitis Cheilitis Glossitis Gengivitis Pulpitis Pharyngitis Tonsilitis Sialoadenitis Esophagitis Ingluvitis Gastritis Abomasitis Ruminitis

The affected organs The oral cavity The lips The tongue The gum The tooth The pharynx The tonsils The salivary gland The Esophagus The Crop in birds The stomach The abomasum The rumen

Inflammation of Enteritis Duodenitis Jejunitis Ileitis Colitis Typhlitis, cecitis Proctitis Hepatitis Cholangitis Cholecystitis Pancreatitis Omasititis Reticulitis

The affected organs The intestine The duodenum The jejunum The ileum The colon The cecum The rectum The liver The bile duct The gallbladder The pancreas The omasum The reticulum

Epulis: It is a benign neoplasm derived from connective tissue or periodontal ligament.

It is classified into: 1- Fibromatous epulis (collagen ) 2- Acanthomatous epulis (stratified sq. ep.) 3- Ossification epulis (osteoid bone).


Tonsilitis: It is inflammation of tonsils, particularly in dog and cats. Causes: (either primary or secondary). i-Bacteria as staphylococci (primary) ii-Virus as Canine infectious hepatitis (secondary).

Types of Tonsilitis: i-Catarrhal tonsilitis iii-Serous tonsilitis

ii-Suppurative tonsilitis iv-Diphtheritic tonsilitis

Microscopic Picture: 1-Dilation of blood vessels. 2-Leukocytic infiltrations. 3-Hyperplasia of lymphoid follicles. 4-Desquamation of the epithelial lining and mucus in the crypts (catarrhal), large number of neutrophils and pus (suppurative), eosinophilic granular material in lamina propria (serous) or fibrin threads and coagulative necrosis (diphtheritic).

Microscopic Picture: 1-Tonsils appear swollen and hyperemic. 2-The crypts will exude a purulent white yellow exudate on the surface.

3-Painful swelling of mandibular lymph nodes.


In case of Strept infection: Glomerulonephritis and renal failure occur. The strept has an antigen similar to the glomerular tufts. So when the body produce antibody against the strept, it could react specifically with the glomerular tufts (Ag-Ab complex) with production of glomerulonephritis.

Hyperplasia and Hyperkeratosis: They occur in buccal cavity of cattle due to chlorinated naphthalene poisoning. This poison kills the microflora in rumen (produce diesterase enzyme that acts on carotene to give 2 molecules of vit. A) and induce vit. A deficiency. The vit A deficiency leads to hyperplasia and hyperkeratosis on the mucosa of the tongue, lips, gum,…

Lead Toxicosis: Its lesion is “blue line” on the gum of dog, horse and human. It is produced by lead salts with H2S released by m.o. in the buccal cavity.


NB Definitions: Blue tongue: viral disease affecting sheep. Blue line: appears on the gum in lead toxicosis. Blue bag: gangrenous mastitis. Kock’s blue bodies: theileria in the lymphocytes and histiocytes of lymphoid tissue (Lns and spleen) in cattle.

Salivary glands Ptylism: It is excessive salivations, which occur in some specific diseases as: 1-Foot and mouth disease. 2-Infectious vesicular stomatitis. 3-Infectious vesicular exanthema. 4-Toxicosis with salts of heavy metals. Sialoadenitis: It is the inflammation of salivary glands.


Types Sialoadenitis : 1-Catarrhal Sialoadenitis (primary or secondary). 2-Suppurative Sialoadenitis: it is usually with pyogenic m.o. such as strangles in equine (Strept equi) or foreign bodies with Coryne infection.

Sequellae: i-It return to the normal after removal the cause. ii-Produce abscesses, which rupture either in the oral cavity (fistula) or on the surface (sinus).

NB: Sinus: It is the formation of tract lined by FCT connects

between cavity and surface.

Fistula: It is a tract between 2 cavities. Cysts: These cysts are formed due to obstruction of the salivary ducts, particularly in sublingual salivary gland of dog and cow. It is called

“Ranula�


Ranula: It is a large salivary cyst (up to 8 cm in diameter) formed due to occlusion of its duct. It lies under the tongue, fluctuating and contains viscid odorless, grayish white or brownish and clear or turbid fluid. The cyst lined by cylindrical epithelium. NB: The cysts are either a-True cysts: If the content is produced by its wall (Ranula). b-False cysts: Its content is not produced from its wall (Hematoma).

Sialoliths (salivary calculi): It is a calcium concretion formed either in the duct or in the gland itself as a result of chronic inflammation. Liths (Concretion)

Affected organ

Liths (Concretion)

Affected organ

Pancreatolith

Pancreatic ducts

Enterolith

Intestine

Urolith

Urinary bladder

Phlebolith

Vein

Cholelith

Gallbladder

Coprolith

Fecal concretion


Anodontia: Absence of teeth. Oligodontia: Fewer teeth than normal. Polydontia: Supernumerary teeth (increase the number of teeth). Degenerative dental diseases: 1-Dental attrition: It is the wearing of the substance of teeth under the stress of mastication (form sharp teeth). NB: Enamel does not regenerate while the cement can be regenerated. 2-Dental tartar(calculus): It is precipitation of the salts between gum and teeth (calcium carbonate in horse and calcium phosphate in dog). It causes mechanical irritation and persistent inflammation of gum. 3-Dental caries: It is destructive decalcification of dental enamel, followed by enzymatic lysis of the exposed matrix. The affected teeth show brownish-black dentin.


4-Dental plaque: It is accumulated non-mineralized bacterial mass, food particles or desquamated epithelium adhered to the tooth surface. NB: Pulpitis: It is the inflammation of the tooth (pulp). It is either suppurative or gangrenous. It may lead to osteomyelitis. Periodontitis: It is the inflammation of tissue around teeth. Gingivitis: It is the inflammation of the gum (superficial). Pyorrhea: It is deep suppurative inflammation in the gum (abscesses). Gingival hypertrophy: It is chronic painless focal or diffuse enlargement of the gum.

Pigmentation of the teeth: Yellowish white Reddish brown Greenish or black Yellowish Red (pink)

Normal teeth (no pigmentation). Pulpal hemorrhages or pulpitis. Gangrene. Icterus. Congenital porphyria (pink tooth)

Pharyngitis It is the inflammation of the pharynx (catarrhal, suppurative, fibrinous types).


Esophagus Anomalies of Esophagus: Agenesis: It is absence of the esophagus due to absence of primordium during embryogenesis. Aplasia: It is a local failure of development of esophagus with presence of primordium. Hypoplasia: Incomplete development of esophagus.

Obstructive and functional disorders: Achalasia: It is a failure of the esophageal sphincter (cardiac) to relax and allow food to enter the stomach. It is either:

1-Cricopharyngeal Achalasia: in the upper esophageal sphincter of dogs and characterized by dysphagia and regurgitation of food. 2-Esophageal achalasia (Megaesophagus): It is generalized or segmental dilation of the esophagus. It includes: i-Congenital megaesophagus: It is prominently dilated and flaccid esophagus (in puppies due to persistent right aortic arch). The dilation is uniform and bilateral (cylindrical) or unilateral (sac-like). ii-Acquired megaesophagus: It is secondary to any defect in neural reflex involved in swallowing and normal function of esophagus musculature.


3-Choke: It is complete or partial obstruction of the esophagus. It is either:

From Inside: by any foreign body Potato, turnips or small ears of corn in ruminants and accumulation and germination of grains in horse. From Outside: by enlarged lymph nodes, tumor ad abscess.

Sequellae: 1- Local gangrene with sapremia and toxemia which kill the animal. 2- Tympany in ruminant due to prevent regurgitation of gas. 3-Partial obstruction leads to formation of esophageal diverticulum ectasia or perforation. Diverticulum: It is a symmetrical and unilateral sac like dilatation. Ectasia: It is a uniform spindle or clyndrical shaped dilatation. Esophagitis: It is the inflammation of esophagus (rare due to strong epithelial mechanical barrier).

Esophageal Parasites: 1-Spirocerca lupi in dogs forming nodules in the wall. 2-Hypoderma bovis and Lineatum larvae in cattle. 3-Gastrophilus larvae in horse 4-Gongylonema pulchrum in ruminants. Ingluvitis: It is the inflammation of crop (catarrhal or ulcerative types).


Esophageal or nutritional roup: This condition occurs in poultry due to deficiency of vit. A. In which the cuboidal epithelium of esophageal glands change into stratified squamous epithelium with hyperkeratosis (metaplasia). The latter could obstruct the ducts of the glands and protruded in the lumen of the esophagus as pin headed spots (esophageal roup).

Forestomachs (Rumen, Reticulum and Omasum) Dilatation of forestomachs: It is classified according to the cause into:

i-Tympanic Dilation: (Tympany or Bloat). ii-Alimental dilation: (Impaction). Tympany (Bloat): it is overdistention of rumen and reticulum with gasses. It is either acute or chronic (recurrent tympany).

Classification of tympany: a) Frothy or primary tympany: Small bubbles with the ruminal fluid.

b) Secondary tympany or free gas tympany: With obstruction of esophageal or pharyngeal passages. Causes: 1-Excessive fermentation of the ingesta due to. i-Sudden changes from dry to green ration. ii-Fed on large amount of cereal grains.


2-Prevention of eructation due to obstruction of the esophageal lumen (chock) 3-Poisonus plants containing saponin. 4-Any conditions interfere with the normal contraction of the rumen as atony (muscular weakness of the rumen due to toxic production).

NB: The death is usually occurs from: i-Asphyxia (suffocation) ii-Toxemia

Pushing the diaphragm. due to absorption of toxic gases.

Pathognomonic Lesions: 1-The rumen is overdistended with gasses. 2-Severe congestion in all organs. 3-Cyanosis of mucous membranes. 4-Petechial hemorrhages on serous membranes. 5-Dark unclotted blood.

Impaction: Overdistention of the rumen with indigestible food and without or with little gas production. Death occurs due to toxemia (acute toxic hepatitis).

Causes: 1-Overfeeding on concentrates. 2-Atony of the musculature of the forestomach (atony rumen impaction). 3-Insuffient water supply.


Pathognomonic Lesions 1-Overdistention of the rumen with indigestible food. 2-The ruminal content has fetid odor. 3- Weakness of the ruminal wall (thin) and easily folded. 4-Severe congestion in all organs. 5-Petechial hemorrhages on serous membranes.

Abomasum (True stomach)

Gastritis: It is the inflammation of stomach or abomasum in ruminants. Types of gastritis (Abomasitis):

A-Acute gastritis

B-Chronic Gastritis

1-Acute Catarrhal Gastritis 2- Acute Hemorrhagic Gastritis 3- Acute Fibrinous Gastritis 4- Acute Suppurative Gastritis 5- Acute Necrotic Gastritis

Acute Catarrhal Gastritis: Causes: 1- Physical (cold or hot) or chemical agents. 2-Parasitic gastritis 3-Canine distemper and feline enteritis. 4-Nutritional deficiency.


Macroscopic picture: 1- Reddens and thickening of gastric mucosa. 2- Increase in mucus secretion.

Microscopic picture: 1-Dilation of the gastric blood vessels. 2-Leukocytic infiltration. 3-Hyperplasia and desquamated of the lining. 4-Presence of basophilic material (mucus). 5-Hyperplasia of the mucosal lymphoid nodules.

Acute hemorrhagic gastritis: Causes: 1-Infectious diseases as cattle plague, H.S., leptospirosis and Clostridium septicum (Braxy) in sheep. 2- Uremia and Arsenic poison.

Macroscopic picture: 1-Deep reddening of gastric mucosa. 2-The blood in hemorrhagic gastritis appear black due to formation of acid hematin.

Microscopic picture: 1-Dilation of the gastric blood vessels. 2-Leukocytic infiltration. 3-The predominant type of exudate is erythrocytes.


B-Chronic catarrhal gastritis Causes: 1-Fellow the acute type. 2-Habronema megastoma in horse and Haemonchus contortus. 3-Secondary to chronic gastric dilation and hepatic cirrhosis.

Microscopic Picture: 1-Focal or diffuse hyperplasia and desquamation of the lining epithelium 2-Metaplasia of the lining epithelium into goblet cells. 3-The mucosa infiltrated with chronic inflammatory cells and fibroblasts. 4-Hypertrophy of the smooth muscle fibers. Gastric Ulcer: It is usually acute and caused by 1-Necrotic or suppurative gastritis. 2-Submucosal hemorrhages leading to necrosis and ulceration of the mucosa. 3-Some specific infectious diseases as Hog cholera, cattle plague and mucormyces bovis.

Foreign Bodies in Stomachs: Rubber ball (in dog), hair balls (in cat), sand (in horse, cattle and sheep).


The parasites in the stomachs: 1-Gastrophilus spp larvae (horse). 2-Habroonema spp (horse). 3-Haemonchus spp, Ostertagia spp and Trichostrongylus spp. 4-Physaloptera spp and Ganthostoma (dogs and cats).

Small intestine Torsion: It is the rotation of intestine around its long axis. Volvulus (Strangulation): It is the rotation of the intestine around its mesentery or loop of the intestine passes through a teared mesentery. Intussusception (Telescoping): It is invagination of one portion of the intestine in the next segment. Hernia: It is abnormal protrusion of the viscera (hernia contents) through natural or artificial opening (hernia ring) into a cavity (hernia sac).

According to locations or sites: A-External Hernia: Visible on the body surface as umbilical, scrotal and inguinal B- Internal Hernia: Not visible on the surface as diaphragmatic or pelvic.

According to statement of the content: 1-Reduciable hernia: The content easily retuned into the normal site. 2-Irreducible hernia: The content is not returned to the normal site due to narrowing of its opening with strangulation or adhesion.


Eversion: Extrusion of the rectum through the anal opening (normal in equine).

Sequelae of these changes: i-Passive hyperemia ii-necrosis moist gangrene iii-toxemia and death

Perforation: It is deep wound with narrow inlet and caused by gunshot, parasites and ulcers.

Rupture: It is discontinuation in the wall of hollow organs. Atresia Ani: It is a failure of development of the anal opening (a blind ending of the gut) results in ballooning and devitalisation of the proximal gut. Stenosis and obstruction (ileus) of the intestine: It is due to

1-Factors on the outside of intestine e.g. tumor, enlarged Lns. 2-Factors located within the lumen e.g. concretions (Enterolith or bezoars), foreign bodies or mass of parasite. 3-Strangulation resulting from torsion, volvulus, intussusceptions, ‌‌


Bezoars (concretions or lith): They are seen in the stomach or intestine. Types of bezoars or concretions: i-Piliconcretions: ball of hair and salts precipitation in the intestine. ii-Phytoconcretions: plant fibers and salts precipitation in the intestine. iii-Coproconcretion (coprolith): Fecal type (dryness and mineralization) Paralytic ileus: It is obstruction of the intestinal lumen (due to paralysis in the wall of the intestine due to long manipulation during surgical operation).

Results or sequelae of the intestinal obstruction:

I-Stenosis (partial obstruction): 1-Accumulation of ingesta anteriorly to the narrowing with dilation of the intestine. 2-Compensatory hypertrophy of musculature of anterior part. 3-Bactrial invasions leads to necrosis or ulceration then gangrene

II-Obstruction (complete obstruction): 1-Accumulation of ingesta anteriorly with severe dilation and muscular paralysis leads to rupture of the intestine and diffuse peritonitis 2-Return the food to stomach leads to gastric dilation. 3-Fermentation of ingesta production of toxic gases and tympany then toxemia and death. 4-Necrosis and gangrene.


Enteritis It is inflammation of the intestinal mucosa (as duodenitis, jejunitis, ileitis, typhlitis or cectis and proctitis). I-Acute Type: II-Chronic Type: Types

Catarrhal

Suppurative

Causes

Mild irritant pyogenic Sands M.O. Parasites moldy food

Hemorrhagic

Fibrinous

Necrotic

Pasteurellosis Clostridial disease Coccidiosis Arsenic poisons Cattle plague

Salmonellosis E. coli Mercuric chloride toxicosis

S. necropherus Arsenic Histomoniasis Cattle plague Coccidiosis

Catarrhal enteritis small dose 1-The arsenic poisons cause Hemorrhagic enteritis medium dose Necrotic enteritis large dose 2-Salmonellosis: could induce catarrhal, suppurative, hemorrhagic, fibrinous and necrotic enteritis; but depend on the degree of resistance of the host and virulence of the organisms.

II-Chronic Type: Causes: 1-Extentsion from acute one. 2-Chronic Passive hyperemia 3-Johne’s disease, TB, Hajerr’s disease 4-Some parasitic infestation.


Acute enteritis: Microscopic Pictures: 1-Dilation of the blood vessels (active hyperemia). 2-Leukocytic infiltrations. 3-Hyperplasia of the lymphoid follicles 4-Hypeplasia and desquamation of the lining epithelium, metaplasia into goblet cells and mucus (catarrhal). -Large number of neutrophils (suppurative). -Extravasated erythrocytes in the lumen (hemorrhagic). -Fibrinous exudate (Croupous) or fibrin + necrosis (diphtheritic). -Deep or superficial coagulative necrosis with line of defense (necrotic)

Macroscopic Pictures: 1-The intestinal mucosa is congested, swollen or thickened. 2-Diarrhea (watery content) with abundant mucus (catarrhal). -Bloody contents (hemorrhagic). -yellowish or yellowish gray pseudomembane (fibrinous). -Dull gray or yellow necrotic areas (necrotic).

Sequellae: 1-Malabsorption (emaciation) appeared as i-The animal become thin. ii-Bony prominence. iii-Wrinkled or folded skin and sunken eye.


iv-The muscles are congested. v-Serous atrophy of fat (gelatinous appearance). vi-Atrophy in the parenchymatous organs.

2-Dehydration: (due to profuse watery diarrhea).

Diarrhea: It is the net failure of water and electrolyte (sodium) uptake in the small intestine so the absorption capability of the colon is exceeded i.e. secretion and absorption mismatch.

It includes 2 types: 1-Hypersecretoty diarrhea: It occurs when increase in net fluid flow out of body compartment and into the lumen (caused by vascular leakage due to toxin induced inflammation and increased hydrostatic pressure). Enterocytes remain normal.

2-Malabsorptive diarrhea: It occurs when the enterocytes of small intestines cannot absorb water and ingesta (caused by lack of enzymes (pancreatic/liver disease) and destruction of villi/surface area).

Chronic enteritis: Macroscopic picture: 1-The intestinal wall is thickened and covered with mucus. 2-The intestinal content is watery.

Microscopic picture: 1-It is varies and characteristic for each disease.


2-Mucinous degeneration and infiltration of lamina propria with macrophages, lymphocytes, plasma cells and fibroblasts. 3-The crypt become atrophied or cystic. Atresia coli: It is the absence of colon.

Peritoneum It is consisted of 2 layers of mesothelium cells (simple squamous cells). Hematoperitoneum: Abnormal accumulation of blood in the peritoneal cavity. Hydroperitoneum: Abnormal accumulation of fluid in the peritoneal cavity. Ascites: Abnormal accumulation of transudate in the peritoneal cavity. Chylous ascites: Abnormal accumulation of lymph in the peritoneal cavity. Peritonitis: inflammation of the peritoneum (acute or chronic).

Types of acute: Serous, fibrinous, serofibrinous, suppurative and hemorrhagic Parasites in the peritoneal cavity: 1-Migrating Fasciola or larva migrans. 2-Parasitic cysts as Cysticercus tenuicollis Cysticercus pisiformis

in sheep. in rabbits.


Liver It is consisted of several hexagonal lobules. Each is represented by central vein, cords, sinusoids and portal tracts containing artery, portal vein, bile duct and lymphatic. The hepatocytes are separated from sinusoids by space of disse. Kupffer cells are present in the sinusoids scattered among endothelial cells.

The zones of hepatic Lobule: 1-Centrolobular (centrilobular) zone. 2-Mid-zonal zone. 3-Peripherolbular or periportal zone. 4-Paracentrolobular zone.

Circulation of the blood: It is from the periphery to the center i.e. from the portal vein and hepatic artery (oxygenated blood) then to the hepatic sinusoids (to supply the blood to the hepatic cells) then to central vein (nonoxygenated blood) then to hepatic vein and posterior venacava in the right auricle. Circulation of bile: The bile secreted from the hepatic cells to the bile canaliculi then to interlobular bile duct (canal of hering) common bile ducts then to gallbladder.


Function of the liver: 1-It is responsible for the metabolism of inorganic matter (ammonia) 2-It acts as storage for glycogen, vit A and iron. 3-Detoxication of hormones as ADH, estrogen and aldosterone. 4-Manifacturing the plasma protein, albumen, fibrinogen and globins 5-Manifacturing of the thrombin from vit k. 6-Secret the bile, which helps in absorption of fat, calcium and fat soluble vitamins. 7-Extramedullary hematopoiesis during fetal life and severe anemia in adults.

Circulatory disorders: Passive congestion (Nut meg liver): CVC Telangiectasis: It is a focal dilation of the hepatic sinusoids. Peliosis: is irregular blood spaces with no evidence of lining epithelium (post necrotic)

Anemia: It is local ischemia and lead to various retrogressive changes. Hemorrhage: It is observed in dog and cats due to hepatic rupture. Thrombosis: It is common with hepatitis. Infarction: It is due to impaired portal and hepatic circulation as caused by bacillary hemoglobinuria in cattle and sheep.


Disturbances in Metabolism: Fatty liver: in excessive fat or carbohydrate diet Glycogen infiltration: in diabetes mellitus and glycogen storage diseases Amyloid: in the liver either primary or secondary. Cloudy swelling: vacuolar and hydropic degenerations: Pigment deposition: bile pigments (cholestasis), Lipofuscin (in old animals), Hemosiderin and Melanin. Hepatomegalocytes: It is the hypertrophy of the hepatic cells which appeared in some poisons. Saw dust liver: It is local areas of coagulative necrosis in the liver of well fattening animals. It is caused by overfeeding on concentrates leads to excessive H2S production then absorbed from the intestine to the liver inducing coagulative necrosis (saw dust in appearance).


Hepatic necrosis: It is either: 1-Focal Necrosis: It is usually infectious (caused by bacteria, virus, fungus and parasites).

2-Diffuse Necrosis (massive): It is usually toxic as in case of Poisonous agents (chemical or plant). Severe anemia and CVC. Nutritional deficiency as vit E and selenium. NB: Hepatosis dietetica: It is hepatic necrosis in young growing pigs due to deficiency of vit E and selenium.

Types of Hepatic necrosis: I-According to gross and microscopic appearance: 1-Coagulative necrosis. 2-Caseous necrosis. 3-Liquefactive necrosis.

II-According to the predominant portion of hepatic lobule: 1-Centrolobular (centrilobular or periacinar) necrosis. 2-Peripherolobular (periportal) necrosis. 3-Mid-zonal necrosis. 4-Parcentrolobular necrosis. 5-Massive necrosis (involve the whole lobule).


Centrolobular necrosis: It is seen in hypoxic condition (CVC and anemia). Mid-zonal necrosis: It is usual form of necrosis. Periportal necrosis: It is seen associated with blood borne toxins. Paracentral necrosis: It 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. Massive necrosis: It involves the whole hepatic lobule. The necrotic lobule is replaced by hemorrhage, and then followed by granulation tissue and scar as in case of nutritional deficiencies.

NB: Aflatoxins cause necrosis in various portions according to the species: 1-Peripherolobular necrosis: (duck, turkey, cat, adult rats and chickens). 2-Mid-zonal necrosis: in rabbits. 3-Centrolobular necrosis: in dogs, pigs, sheep, cattle and guinea pigs. 4-Diffuse necrosis: in neonatal rats and trout.

Disassociation of liver cells: The liver cells detached from one to another (individualized) and somewhat rounded and the cytoplasm become acidophilic (in leptospirosis).

Causes of Necrosis: Coagulative necrosis: 1-Clostridial diseases as Cl hemolyticum and Cl novyi in sheep and cattle. 2-All viruses affect the liver 3-Fusobacterium necropherus in cattle. 4-Salmonellosis and acute fowl cholera in poultry.


Caseous necrosis: 1-TB 2-Aspergillosis in chickens. 3-Histomoniasis in turkeys. 4-Degenerated parasitic cysts.

Liquefactive necrosis: It is usually caused by pyogenic bacteria as Coryne, staph strept Hepatitis: It is the inflammation of the liver.

Types of hepatitis: I-According to the cause: 1-Infectious hepatitis (focal inflammation). 2-Toxic hepatitis (diffuse inflammation).

II-According to exudate: 1-Suppurative hepatitis. 2-Non-suppurativ hepatitis.

A-Infectious Hepatitis: Causes: 1-Viral causes: as Rift valley fever and infectious canine hepatitis. 2-Bacterial causes: Coryne, E coli, staph, strept, salmonella, and clostridium.

3-Parasitic causes: Fasciola, ascaris, hydatid cysts, Cysticercosis. 4-Mycotic causes: Aspergillosis.


The lesions of some specific infectious diseases in the livers: Infectious canine hepatitis: 1-The liver enlarged and mottled. 2-Coagulative necrosis. 3-Basophilic IN/IB in the hepatocytes

Rift Valley Fever: 1-Parcentrolobular coagulative necrosis. 2-Eosinophilic IN/IB.

NB: All viruses cause: 1-Lymphocytic infiltration. 2-Seous inflammation 3-Coagulative necrosis. 4-Hydropic degeneration. Corynebacterium pyogenes: It causes focal abscesses in the liver of cattle, which characterized by thick greenish viscid pus (suppurative hepatitis). Salmonellosis: It causes focal granulomatous reaction (macrophages) and coagulative necrosis.

Bacillary Hb-urea (Clostridium hemolyticum): It is characterized by formation of several thrombi and infarctions. The urinary bladder contained Hb-urea (not precipitated).

Spheropherous (Fusobacterium) necropherus: Multiple grayish foci on the hepatic surface which represented by coagulative necrosis.


Leptospirosis: It causes acute hepatitis with multiple focal coagulative necrosis and individualization of the hepatic cells. Fascioliasis (rot-liver): It causes several migratory tracks (hemorrhagic or yellow types) besides biliary cirrhosis (proliferation of the bile ducts with thick and calcified wall).

Ascariasis (larva migrans): The liver shows multiple white spots on the hepatic surface particularly in pigs (milky spot liver). These spots are represented by caseous necrosis, inflammatory cells and larvae (migratory tracks).

B-Non-Infectious or Toxic Hepatitis: Causes: 1-Plant poisons. 2-Chemical poisons (arsenic or organophosphrus compound). 3-Mycotoxins (products of fungi) as aflatoxins.

The lesions and fate of toxic hepatitis: 1-The toxic hepatitis is firstly characterized by diffuse retrogressive changes as cloudy swelling and fatty change (Yellow Atrophy). 2-Later on, the hepatic cells suffer coagulative necrosis then they replaced by hemorrhages and the liver become atrophied and red (Red Atrophy). 3-The necrotic cells and the remnant of hemorrhage are replaced by fibrous connective tissue (Fibrosis or Cirrhosis). 4-Some hepatic cells are enlarged (Megalohepatocytes).


Cirrhosis (End stage liver) It is extensive replacement of the hepatic parenchyma by fibrous connective tissue, which leads to hepatic failure. Fibrosis: It is local replacement of the necrosed hepatic cells by fibrous connective tissue with maintenance of the hepatic function.

Types of Cirrhosis: 1-Lobular or Portal Cirrhosis. 2-Biliary Cirrhosis.

Lobular or Portal cirrhosis: It is characterized by periportal necrosis and fibrous connective tissue proliferations around the lobules without hyperplasia of the bile ducts. The fibrous tissue is contracted and the liver becomes small (atrophied) and nodular. In some cases, the liver cells are regenerated in the form of solid nodules without the normal histological arrangement of hepatic lobules i.e. without central vein, sinusoids and cords.

Microscopic picture: 1-Fibrous connective tissue proliferation infiltrated with lymphocytes and plasma cells. 2-Hepatic nodules formed from regenerating hepatocytes without the normal histological arrangement of hepatic lobules.


3-These nodules are usually surrounded by a basket-like arrangement of small branches from the portal vein the hepatic artery forming arterio-venous shunts which leads to ischemia. 4-In the interlobular cirrhosis, the fibrous invade the hepatic parenchyma and may obstruct some blood vessels.

Macroscopic picture: 1-The affected liver is small, hard and nodular (irregular surface). 2-Ascites is usually present. 3-Jaundice is seen at the terminal stage.

Biliary Cirrhosis: It is a type of cirrhosis where the hepatic cells replaced by numerous bile ducts with thick calcified wall and fibrous connective tissue proliferation. Pathogenesis: Firstly, there is hyperplasia of bile ducts leads to pressure atrophy of the adjacent hepatic cells followed by necrosis then secondary fibrous connective tissue proliferation. Microscopic picture: 1-Hyperplasia of bile ducts with newly formed bile ductules (adenoma or adenocarcinoma may present). 2-The wall of these bile ducts is surrounded by thick fibrous tissue and show dystrophic calcified.


3-Extensive fibrous connective tissue proliferation. 4-Chronic inflammatory cells infiltration (macrophages, plasma cells and lymphocytes) Macroscopic picture: 1-Liver is hard, firm and enlarged (hypertrophied) with smooth surface. 2-Bile ducts are prominent with thick, white and calcified wall on the cut sections (give gritty sound). 3-The hepatic tissue is yellowish green (jaundice appear early).


The differences between biliary and portal cirrhosis Criteria

Biliary Cirrhosis

Portal Cirrhosis

1-Size

Enlarged (Hypertrophied Cirrhosis) Small (Atrophied Cirrhosis)

2-Surface

Smooth

Nodular or irregular

3-Consistency

Firm

Hard

4-Cut sections

Thick, prominent bile ducts and Fibrosis calcified with gritty sound. bands.

5-Ascites

Absent or in late stage

Present

6-Juandice

Present in early stage

Absent or in late stage

with

thick white

The cirrhosis can be classified according to the distribution of the fibrous tissue into: 1-Multilobular Cirrhosis: The fibrous tissue around groups of lobules. 2-Monolobular Cirrhosis: The fibrous tissue around one lobule (biliary type). 3-Pericellular Cirrhosis: The fibrous tissue encircled around the individual cells.


Special Forms of Cirrhosis: Glissonian cirrhosis: It resembles the portal cirrhosis but restricted to short area under the capsule. Central Cardiac Cirrhosis: It is characterized by increase amount of fibrous tissue around the central vein in chronic venous congestion. Pigment Cirrhosis: It occurs with hemochromatosis. Parasitic cirrhosis: It occurs in association with parasites as fascioliasis and schistosomiasis

Fate or Sequellae of Cirrhosis: A-Hepatic failure which causes the following 1-Cholestasis and jaundice (in the biliary type). 2-Prolongation of blood clotting 3-Fail to store the vit A

4-Ascites (portal type) due to several mechanisms: i-Decrease the COP (decrease the albumin). ii-Hormonal factors (liver fail to detoxify the ADH and aldosterone so they persist in the blood for long time and reduce the renal function (retention of the urine) leading to increase HP).


iii-Disturbances in the electrolyte metabolism: inhibition of the renal function leads to decrease the salt excretion (increase the reabsorption of the electrolytes by renal tubules) leading to retention of salts in the body and increase the escape or exudation of the water from the blood to the tissue inducing ascites. iv-Mechanical Factors (interfere with the portal circulation that leads to passive hyperemia and increase HP). B-Splenomegaly, esophageal and rectal vericoses and hemorrhages: due to interference with portal circulation

C-Hepatic encephalopathy: It is a common condition in dogs and horses caused by : ingestion of plant toxins. It causes profound CNS neurotransmitter defects (vacuolations of white matter) and neuromuscular dysfunction and is also associated with severe, chronic liver disease. The pathogenesis is uncertain, but appears related to high concentrations of ammonia derived from amines absorbed in the gastrointestinal tract. The liver normally rapidly processes amines, but if liver disease is severe amines may not be removed by hepatocytes and so quickly cross the blood-brain barrier resulting in severe CNS defects. Alternatively, acquired or congenital shunts may pass portal blood directly to the venous system.

D-Death.


Gall bladder and bile duct Cholangitis: It is inflammation of bile ducts. Cholecystitis: It is inflammation of gall bladder. Cholelith: Stones in the bile ducts or gallbladder. Lipidosis: Fatty change Lipomatosis: Obesity. Steatosis: Replacement of the tissue by fat. Steatorrhea: Presence of indigestible fat in stool.

Pancreas Hypoplasia of pancreas: The pancreas fail to reach its mature size and appear small, pale, thin and a lace-like texture. The acinar cells appear small and few with less zymogene granules. Pancreatitis: It is inflammation of the pancreas (interfere with the exocrine function). Causes: 1-It is not clear but may be due to increase the fat-content in diet and low protein. 2-Increase the intraductal pressure.

Microscopic Picture: 1-Necrosis of acini (exocrine part). 2-Leukocytes infiltrations. 3-Thrombi inside the pancreatic blood vessels. 4-Internal fat necrosis.


Macroscopic Picture: 1-The pancreas is enlarged. 2-Grayish-white foci on the surface. 3-Hemorrhagic patches

Sequellae: 1-Fat necrosis due to escape of lipase enzyme. 2-Necrosis of the β cells leads to diabetes (decrease of insulin 3-Necrosis of the ι cells leads to decrease of glucagon. NB: Carotenosis: Yellow pigmentation of the liver due to increase the consumption of carotene.

Diabetes mellitus It is the reduced availability of insulin due to the destruction or degeneration of the islets, exhaustion secondary to prolonged antagonism or the presence of anti-insulin antibodies. Liver: Enlarged, yellow, fatty, friable and hyperglycemia (inhibited phosphorylation). Pancreas: Islets may show degranulation of cells or degeneration. Blood: Increased ketone bodies and lipemia Eyes: Cataracts (bilateral opacity) Muscle: Muscle atrophy due to inhibition of amino-acid entry into muscle Kidney: Glucosuria, polyuria and polydypsia.


Remember the following questions: 1-Describe the essential differences between secretory and malabsorptive diarrhea. 2-Which are the 3 most common sites for hernias in most animals. Describe structure and sequellae of it 3-How does fibrosis or cirrhosis of the liver lead to ascites. 4-What is the significance of erosive, ulcerated lesions in the mouth of: i- An old dog ii-An 8-month old heifer 5-During necropsy of a ruminant, you note that the mucosa of the rumen sloughs away at the slightest pressure. What is the significance of this 6-Explain the terms: 1-Chronic Catarrhal gastritis ii-Diphtheritic stomatitis iii-Necrotic enteritis 7-What are the causes and potential significance of ulcers in the mucosa of the stomach. 8-What factors can cause the liver to increase in size and decrease in size. 9-What is hepatic encephalopathy, and what is thought to be the pathogenesis of it. 10-What situations of necrosis in liver toxicated with aflatoxins 11-Discuss hepatic cirrhosis its causes, classification and sequelae. 12-Compare between lobular and biliary cirrhosis 13-Pathology of diabetes mellitus.



Pathology of Digestive System