Pathology of Digestive Systems

Dr. Bikash Puri

MVSc (Veterinary Pathology)

Dr. Bikash Puri

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Introduction

• Oral cavity & pharynx
• Oral mucous membranes
• Teeth
• Tonsils
• Salivary glands
• Tongue
• Esophagus
• Stomach (simple or complex)
• Intestines
• Peritoneum
• Liver & pancreas

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Oral Cavity

CONGENITAL DEFORMITIES

1. Palatoschisis (Cleft palate) and Cheiloschisis (Cleft lip)

• Most common abnormalities of the oral cavity.
• failure of fusion of the upper lip along the midline or philtrum ……..Palatoschisis

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• Failure of fusion of lateral palatine processes…….Cheiloschisis.

Causes:

• Genetic
• Sterioid administration (Primates) during pregnancy
• Toxic eg. Ingestion of toxic plants in cattle , sheep and pigs.

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May lead to starvation and aspiratory pneumonia.

No clinical significance

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Figure: Cleft palate exposing the nasal cavity in a calf. (Courtesy J. Caswell.)

Anomalies in the growth of jaws

Brachygnathia superior, shortness of the maxillae,

• is an inherited breed characteristic among dogs and swine.
• The condition is progressive with age, resulting in malapposition of the incisor and cheek teeth, which interferes with prehension and mastication.

Brachygnathia inferior or micrognathia, shortness of the mandibles

• may be a mild to lethal defect in cattle and sheep
• common defect in calves and males are more susceptible.
• This condition in calves has been associated with cerebellar hypoplasia

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Prognathism refers to abnormal prolongation of the mandibles

• rather common, especially in sheep

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Agnathia is a mandibulofacial malformation characterized by absence of the lower jaw,

• caused by failure of development of the first branchial arch and associated structures.
• Common anamolies in lambs and is rare in calves.
• Associated malformations in lambs may include ateloprosopia (incomplete development of the face), microglossia or aglossia, and atresia of the oropharynx.

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Stomatitis

• It is the inflammation of buccal mucosa characterized by red, inflamed gums, and infiltration of inflammatory cells with in buccal mucosa
• An important indicator of some systemic disease

Etio-pathogenesis:

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Bacterial invasion

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Etiology

• Infectious
• Chemical
• Autoimmune disease
• Mechanical Injury

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Irritation

Acute inflammation

Necrosis and gangrene formation

Types of stomatitis

• Catarrhal stomatitis: Mucous exudation in oral cavity
• Vesicular stomatitis: Vesicles in oral mucosa. Eg. FMD
• Erosive stomatitis: Erosions in oral mucosa e.g: Rinderpest
• Fibrinous stomatitis: False membrane in oral mucosa
• Ulcerative stomatitis: Presence of ulcers in oral mucosa e.g: mucosal disease.

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• Trauma due to foreign bodies
• Chemicals- Acids, alkalies
• Infection- Mucosal disease virus
• Parasite- Spirocerca lupi. Oesophagostomum
• Nutritional- Vitamine A deficiency
• REFLEX OF STOMACH ACID

Etiology

Vesicular stomatitis

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Vesicle: Fluid-filled raised lesion 1 cm or less across (Bullais greater than 1 cm. Blisteris the common term for either)

A fluid filled space above the basal stratum (b). The rest of the epidermis (e), including the stratum corneum (c) forms the roof

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PATHOLOGY OF ORAL CAVITY

• TEETH
• GUM
• TONGUE

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PATHOLOGY TEETH

Malocclusions

• Failure of the upper and lower incisor to inter- digitate properly.
• Normal in dogs
• Two types depending on position of the mandible.
• Prognathia: Protrusion of the lower jaw.
• Brachygnathia: Protrusion of the upper jaw.
• It results from poor jaw conformation or from abnormal tooth eruption patterns.
• lead to difficulty in the prehension and mastication of food.

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PATHOLOGY OF TEETH

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ANOMALIES OF TOOTH DEVELOPMENT

Tooth agenesis

• Absence or incomplete development of teeth.
• No clinical significance in animal

Dentigerous cyst

• Result from dental dysgenesis
• Dental dysgenesis may primarily due dysplasias of the enamel forming organ or secondary to trauma, infection and hyperthermia
• Although rare, dentigerous cysts are often painful and although not usually neoplastic , they can destroy the jaw.
• Dentigerous cysts are epithelial lined and may become impacted with keratin.
• Rudimentary, malformed teeth may be found within these cysts and painful fistulas may develop, especially in horses

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Segmental Enamel Hypoplasia

• This condition arises due to temporal lack of enamel formation
• Occurs in the permanent teeth of dogs infected with the canine distemper virus during odontogenesis (development of teeth)
• During viral infection the enamel organ get necrotized and disorgnized and after recovery, the function an organization of the enamel organ return and this is followed by re-establishment of normal enamel formation..

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Abnormal coloration of teeth

• Abnormal coloration of teeth can result from the incorporation of chemical agents, typically tetracyclines, during mineralization.
• In corporation of porphyrins into dentin in animals with congenital porphyria can cause pink discoloration of the teeth.
• Excessive fluoride incorporation into enamel and dentine leads to yellow, dark brown or black discoloration of enamel.

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Fig: Pink tooth in adult ox resulting from accumulation ofporphyrins in the dentin

Fluorosis, cheek teeth, cow. The enamel is chalky and weak, and the teeth are usually rapidly worn

down.

Periodontal disease

• Most common disease of dogs and sheep (also important in ruminants, horses and cat)
• Begins as gingivitis associated with subgingival plaque and may progress through gingival creviceand loss of alveolar bone to chronic periodontitis and exfoliation of teeth.
• Bacterial films resident on the tooth surface and the acids and enzymes they produce may damage their enamel substrate (cavities) and also destroy the subjacent gingival tissue and periodontal ligament.
• More than 200 species of bacteria and fungi have been associated with dental plaque.
• Dental plaque is a film of an organic matrix, food particles and bacteria on the tooth surface.
• This plaque often becomes mineralized.

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• The mineralized material contributes to atrophy and inflammation of the gingival epithelium and supporting stroma by acting as a nidus for additional plaque accumulation.
• The initial site for destructive inflammation is in the gingival crevice forming pockets.
• With time, this inflammation spread distally along the tooth, resulting in gingival epithelial attachment only on the root of the tooth, deep in the alveolar socket.
• Progression of inflammation destroys the connective tissue of the periodontal ligament, resulting in loosening of the tooth.

• Severe dental caliculus

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Marked gingival recession with exposure of roots of the molar teeth in advanced periodontal disease in a dog.

SIALOADENITIS

• It is the inflammation of a salivary gland
• Rabies and canine distemper are two very important diseases that cause inflammation of a slivary gland.

Gross findings:

• Swelling and edema of salivary gland
• Occasionally, abscess formation.

Microscopic findings:

• Focal lysis of glandular linning in case of rabies
• Mononuclear infiltration

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Sialoliths

• Present of salivary calculi are present in the ducts of salivary glands.
• Mainly composed of largely calcium carbonate, and the nidus may be of dead cells.
• Most of the sialoliths are single and cylindrical in shape an may be quite large.
• Most of them lodge at the orifice and cause some degree of salivary retention, glandular atrophy and sialoadenitis.

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Mucoceles (Salivary cysts)

• Salivary mucocele (or sialocele) is an accumulation of saliva in the submucosal or subcutaneous tissues after damage to the salivary duct or gland capsule.
• This is the most common salivary gland disorder of dogs.
• Although any of the salivary glands may be affected, the ducts of the sublingual and mandibular glands are involved most commonly.
• Saliva often collects in the intermandibular or cranial cervical area (cervical mucocele).
• It can also collect in the sublingual tissues on the floor of the mouth (sublingual mucocele or ranula).
• A less common site is in the pharyngeal wall (pharyngeal mucocele) or lower eyelid (zygomatic mucocele).

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Cervical mucocele

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Ranula

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 A ranula is a thin walled linear swelling that results from ruptured sublingual or mandibular salivary ducts below the oral mucosa next to the tongue or rupture of the polystomatic portion of the sublingual gland.. Rannulas have been reported in cats.

Causes

• Usually, the exact cause is not determined, but a developmental predisposition in dogs has been suggested
• Traumatic injury
• Blockage
• Rupture of the duct or capsule (with damage of parenchyma) of the sublingual, mandibular, parotid, or zygomatic salivary gland.

Note: the leakage of the salia into the surrounding tissue and their reaction with local tissue may lead to development of salivary cyst or ranula.

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Signs

• A mucocele is detectable as a soft, fluctuant, painless mass
• Pain or fever may be present if the mucocele becomes infected.
• On aspiration of light brown or blood-tinged, viscous saliva can be detected.
• Usually, careful palpation with the animal in dorsal recumbency can determine the affected side;
• if not, sialography may be helpful.
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PATHOLOGY OF TONGUE

Actinobacillosis “Wooden tongue disease”

• Primarly affect the tongue

Etiology:

• Actinobacillus lignieresii, a gram-negative bacillus

Gross findings:

• Swelling, inflammation, and fibrosis that causes increased firmness of the tongue and linguomegaly

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Microscopic findings

• Centrally located actinobacilli rimmed by radiating amorphic eosinophilic, clublike structures composed of immunoglobulin molecules from lesion plasmacytes
• Mixed mononuclear inflammatory cells, including multinucleated Langhans’ giant cells, often surround these foci (Splendore-Hoeppli phenomenon)

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Thrush

• Thrush is the fungal infection of the tongue and oesophagus
• Occur in hoofed animals but has also been observed in carnivores

Etiology:

• Candida albicans
• Prolonged antibiotic threapy.

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Gross findings:

• Presence of grey-green pseudomembrane that is easily peeled off from the intact underlying mucosal surface

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Epitheliogenesis imperfecta

• Is an anomaly that causes wide spread defects in cutaneous epithelium, and also affects the epithelial lining of the oral cavity, especially the tongue.
• Characterized by irregular, well demarcated, red areas from which the epithelium of the oral mucosa is absent.
• Histologically: consist of abruptly defective areas in the squamous mucosa with inflammation of the sub mucosal connective tissues.

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Epitheliogenesis imperfecta of the tongue of a pig.

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Epitheliogenesis imperfecta

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May lead to starvation and aspiratory pneumonia.

No clinical significance

ESOPHAGITIS�

• Inflammation of esophagus characterized by catarrhal inflammation, ulceration or stenosis due to fibrosis.

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• Trauma due to foreign bodies
• Chemicals- Acids, alkalies
• Infection- Mucosal disease virus
• Parasite- Spirocerca lupi. Oesophagostomum
• Nutritional- Vitamine A deficiency
• REFLEX OF STOMACH ACID

Etiology

Macroscopic features�

• Congestion and hemorrhage of mucosa
• Ulcer formation.
• Red streaks of catarrhal inflammation.
• Stenosis due to fibrous nodules or inflammatory exudate.

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Microscopic features�

• Enlargement of glands.
• Infiltration of neutrophils, lymphocytes
• Sub-epithelial fibrosis/ nodules by Spirocerea lupi.
• the stratum germinativum and prickly cell layers are notably thickened,and the surface cells have pyknotic nuclei and some parakeratosis

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• Megaesophagus is dilation of the esophagus because of insufficient or uncoordinated peristalsis in the mid and cervical esophagus.
• Reported in dogs, cats, cows, ferrets, horses, and new world camelids.

Causes

• include motility problems related to innervation or denervation disorders and to partial
• physical obstructions and stenosis,
• secondary to inflammatory diseases of esophageal musculature or
• persistence of the right aortic arch.

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Megaesophagus

Megaesophagus

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Types:

• Congenital megaoesophagus
• is due to partial blockage of th lumen of the oesophagus by persistent right fourth aortic arch.
• Has been described in dog and siamese cats.
• Acquired megaoesophagus
• is due to failure of relaxation of the cardiac sphincter.

Clinical findings:

• Recognized by regurgitation after ingestion of solid food and weight loss.
• Sometime aspiratory pneumonia can be manifested in affected animals

Grossly:

• Oesophagus is greatly dilated, about tow to three times its normal diameter
• Dilated portion usually contain a foul smelling fluid residue of ingesta

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Oesophageal obstruction

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Normal stratified epithelium of the lower esophagus may undergo metaplastic transformation to gastric or intestinal-type columnar epithelium

Parasitic Lesion in oesophagus

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Spirocera lupi

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INGLUVITIS�

• Inflammation of crop caused by fungi and characterized by ulcerative or diphtheritic lesions.

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Etiology

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• Candida albicans
• Monilia albicans

Macroscopic�

• Turkish towel like appearance in crop mucosa.
• Round and raised ulcers.
• In moniliasis, formation of diphtheritic membrane

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Microscopic features

• Necrotic and ulcerative lesions
• Fibrinous inflammation with infiltration of mononuclear cells

RUMENITIS�

• Rumenitis is the inflammation of rumen in ruminant characterized by seropurulent exudate or ulcer formation with or without parakeratosis. Also called lactic acidosis or grain overload.

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Etiology

• Accidental ingestion of excessive carbohydrate containing foods like, wheat , potaotoes, grains, over-night kept boiled rice, etc.
• Sudden change in diet containing higher percentage of concentrate to roughage ratio.

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Pathogenesis�

• Ruminal microflora is generally rich in cellulolytic gram-negative bacteria necessary for the digestion of hay.
• A sudden change to a highly fermentable, carbohydrate- rich feed promotes the growth of gram-positive bacteria, Streptococcus bovis, and Lactobacillus spp.
• The lactic acid produced by the fermentation of ingested carbohydrates
• decreases the ruminal pH below 5 (normal = 5.5 to 7.5).
• This acidic pH damages ruminal mucosa.

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Con……

• Increased concentrations of dissociated fatty acids lead to ruminal atony.
• Death, when it occurs, is due to dehydration secondary to the increased osmotic effect of ruminal solutes (organic acids) causing movement of fluids across the damaged ruminal mucosa into the rumen, acidosis (from absorption of lactate from the rumen), and circulatory collapse. Mortality among animals with lactic acidosis ranges from 25% to 90% and usually occurs within 24 hours. 

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Macroscopic features�

• Ruminal and intestinal contents are watery and acidic. Often abundant grain is found in the rumen.
• Mucosa of the ruminal papillae is brown and friable and detaches easily, especially from the ventral ruminal sac.
• Animals surviving lactic acidosis have stellate scars develop, visible because of their color difference from the unaffected surrounding mucosa. Scars are pale; unaffected mucosa is dark brown to black

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Microscopic features�

• Hydropic change and coagulative necrosis of the ruminal epithelium followed by an influx of neutrophils
• The affected villi die, become detached and disapper, leaving a smooth, raw surface.
• Parakeratosis of rumen
• Fibrous nodules due to hyperplasia of fibroblast

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Tympanites (Bloat)�

• Tympany or bloat is a clinical condition where rumen is filled with gases of fermentation due to excessive intake of easily fermentable foods.
• If the gas bubbles remain intimately adhered with the ingesta the condition is referred as frothy bloat as there is lot of production of foam within the rumen.

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Etiology

1. Any interference with the normal eructations. Example: Choke of esophagus
2. Production of gas at a rate beyond the capacity of esophageal eructations to discharge it. Example: Sudden change in animal feed with high content of legumes, feeding excessive lush green fodder or excessive intake of soluble carbohydrates.

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Pathogenesis:�

1. One of the effects of severe bloating is to push the diaphragm forward, seriously limiting the respiratory capacity.
2. The increase of pressure within the rumen causes it to expand and thereby compress the abdominal viscera and occlude the caudal vena cava.
3. This shunts the blood from caudal to cephalic parts of the body.
4. Theses mechanism result in anoxia, which is the immediate cause of death in thoses cases which are fatal.

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 Production of gases

Formed gas are eliminated by eructation

Obstruction of oesophagus

Gaseous bloat

Microbial fermentation in rumen

Ingestion of forage (Legumes)

Prevent eructation

Excessive ingestion of leguminous plant

Presence of saponin, pectin&hemicellulose in plant cytoplasm

Pectin on hydrolysis yield acid pectin and poly-glacturonic acid

Acid pectin have got gellatining property

At acidic Ph the gel become stable

Block cardia

Postmortem Findings

• Rumen is distended . On rupture of rumen gas comes out (dry tympany).
• Tarry colour blood, pale liver and rupture of diaphragm.
• Sharp line of demarcation between the pale, bloodless distal esophagus and the congested proximal esophagus at the thoracic inlet (Bloat line).
• Tracheal mucosa is hemorrhagic especially anterior to the thoracic inlet
• Oedema, congestion and heaemorrhages of cervical muscles and lymph nodes of head and neck.
• Atelectasis in lungs. Haemorrhage in lungs, pericardium, trachea and lymphnodes

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Reticulitis�

• Inflammation of reticulum in ruminant animals caused by trauma/ perforation by foreign body including sharp object like needles, wires, etc.
• Characterized by abscess formation, adhesions, peritonitis and pericarditis.

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Etiology

• Consumption of foreign body- sharp objects like needles, wires etc.

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Pathogenesis�

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Most perforation occur in the lower part of the anterior wall but some occur laterally in the direction of the spleen and medially towards the liver.

Lack of oral discrimination in cattles leads to ingestion of foreign bodies like needle, wire etc at the time of grazing

In most instance foreign bodies passes to the reticulum and lie there without causing harm.

But the honey comb like structure of the reticulum provides many spots for fixation of the foreign body which stimulate the stretch receptors of the reticulum causing contraction of reticulum.

This vigorous contraction of the reticulum pushes the sharp object through the wall of reticulum

Macroscopic

• Presences of dense fibrous encapsulation mass of highly variable size and shape, but with a slender, blackened tract usually demonstrable along the path taken by the penetrating body.
• Perforation of reticulum by foreign body forming white scarred areas at point of perforation.
• Abscessation/ suppuration
• Peritonitis, adhesions of reticulum with diaphragm
• Pericarditis due to foreign body (traumatic reticulo pericarditis).

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Microscopic

• Infiltration of neutrophils, macrophages, lymphocytes
• Proliferation of fibroblasts producing adhesions.
• Liquefactive necrosis.

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IMPACTION OF RUMEN AND RETICULUM�

• Impaction of rumen and reticulum is common in cattle and buffaloes caused by heavy carbohydrate diet and characterized by atony of rumen, indigestion, acidosis and haemorrhage on serous membranes.

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Etiology

• Overfeeding of carbohydrate feed.
• Lack of water..
• Paralysis of rumen.

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Macroscopic and microscopic features�

• Atony of rumen due to lactic acid production.
• Rumen is filled with hard, caked undigested food with foul odour.
• Hemoconcentration, anuria, blood becomes dark in colour.
• Hemorrhage in lungs.
• Desquamation of ruminal epithelium.
• A Lesions of acidosis/ toxicosis.

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• STOMACH AND ABOMASAM

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Gastric dilatation�

• Acute distension of the stomach with gas is life threatening condition. It occurs in several species including man, dog, horse, swine, rabbit, cat and monkey.

Etiology:

• Obstruction of cardia that prevents eructation and emesis
• Obstruction of pylorus that prevents passage of gastric ontents into the small intestine
• Torsion of stomach ,
• Overeating
• Abdominal surgery
• Lymphoma of gastric wall

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Gross findings�

• Greatly enlarged stomach, distended with gas and some ingesta
• Repeated episodes of gastric dilation results in stretching and relaxation of the gastrohepatic ligament.
• Recurrent dilation combined with overfeeding and perhaps herediatary predisposition results in gastric rotation (Torsion). The stomach generally is rotated clockwise on the ventrodorsal axis when the abdomen is viewed from the ventral surface.`
• Torsion may result in twisting of the gastrosplenic omentum
• Veins in the caudal aspect of the body are usually intensely engorged and the associated tissues congested
• The stomach may ruptured, spilling its contents into the peritoneal cavity.
• Liver become pale and friable
• Spleenic vein is compressed , resulting in congested spleen

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GASTRITIS/ABOMASAITIS�

• Inflammation of the simple stomach is called gastritis and abomasums as abomastitis
• Characterized by pain, anorexia and vomiting.
• It may be primary consequent to irritants or may be secondary bacterial, viral and parasitic infections.

Etiology:

Physical causes:

• Overfeeding and feeding inferior quality of foods
• Ingestion of foreign bodies
• Consumption of too cold or too hot food and water
• Ingestion of irritant chemicals eg. Acid and alkali, aspirin, steroids, cupper poisioning, lead poisioning etc

Infective causes

• Virus (Rinderpest, FMD, Swine fever, transmissible gastroenteritis, Canine distemper, etc)
• Bacteria (E-coli, Salmonella sps., leptospira sps., Clostridium perfringens, etc)
• Fungus (Aspergillus spp., monilia Sps., Mucor sps., etc)
• Parasities ( Haemonchus, Spirocera lupi, Gastrothylax sps, Oesosphagastomum sps., Trihostrongylus sps., etc)
• Allergy

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Types of Gastritis�

1. Acute catarrhal gastritis:

Grossly:

• The stomach is dilated and has thickened walls
• Congestion, oedema and haemorrhage of mucosal surface
• Thick mucous exudate in stomach
• Presence of vesicles/ ulcers on gastric mucosa

Microscopically:

• Desquamation of the epithelium
• Neutrophilic infiltration of the mucosa and submucosa
• Hyperplasia of minute lymphocytic foci in the gastric mucous membrane

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2. Acute hemorrhagic gastritis:�

Grossly:

• Deeper reddening and hemorrhage on the surface of gastric mucosa or gastric contents.
• Congestion and haemorrhage of gastric mucosa.
• Presence of ulcers/ necrosis.

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3. Chronic hypertrophic gastritis:�

Grossly:

• Elevation and folding of the mucosa especially in the fundus around greater curvature due to severe local epithelial hyperplasia.

Microscopic:

• Severe local epithelial hyperplasia
• Infiltration of inflammatory cells in the superficial parts of the lamina propria
• Cystic glands are seen at the base of the crypts.

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Mass of hyperplastic glandular tissue at the pylorus

4. Eosinophilic gastritis:�

Grossly:

• Presence of nodular mass on the gastric mucosa consisting of an embedded parasite surrounded by eosinophils.

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Microscopically:

• Infiltration of eosinophils in the mucosa, sub-mucosa and muscle layers of stomach
• In dog, sometime necroproliferative eosinophilic perivasculitis and eosinophilic lymphadenopathy.

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Intestine

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Enteritis�

• It is the inflammation of the intestinal mucosa characterized by frequent passing of loose feces, flatulence, abdominal distension and borborygmus.
• It may accompany with gastritis leading to a syndrome known as gastro enteritis.

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Etiology

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Physical causes:

• Overfeeding and feeding inferior quality of foods
• Ingestion of foreign bodies
• Consumption of too cold or too hot food and water
• Ingestion of irritant chemicals eg. Acid and alkali, aspirin, steroids,

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Infective causes

• Virus (Rinderpest, FMD, Swine fever, transmissible gastroenteritis, etc)
• Bacteria (E-coli, Salmonella sps., leptospira sps., Clostridium perfringens, etc)
• Fungus (Aspergillus spp., monilia Sps., Mucor sps., etc)
• Parasities
• Allergy

Types of enteritis

1. Catarrhal enteritis

Macroscopic

• Presence of catarrhal exudates in lumen of intestine
• Congestion & thickening of the wall of intestine
• Intestinal wall is usually flaccid and lumen may be dilated

Microscopic

• Increase number of globlet cells
• Reduce length of villi
• Desquamation of epithelial cells of intestine
• Infiltration of neutrophils in intestinal mucosa

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2. Hemorrhagic Enteritis

• Macroscopic
• Blood mixed content in the intestine
• Petechial or ecchymotic haemorrhage in intestinal mucosa
• Presence of erosion or ulcer in intestinal mucosa

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• Microscopic
• Presence of coccidial oocysts in intestinal scrapping
• Infiltration of neutrophils and mononuclear cells

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3. Chronic Enteritis

• Macroscopic
• Thickening of the wall of intestine. Example: Corrugations in Johne’s disease
• Granulomatous nodules in duodenum
• Small, round, raised necrotic foci on serosal surface of intestine covering whole length of intestine
• Thick mucous cover over mucosa of intestine
• Microscopic
• Proliferation of fibrous tissue in lamina propria
• Infiltration of macrophages, lymphocytes and plasma cells
• Atrophy of intestinal glands

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4. Necrotic enteritis

• Etiology: Bacteria (Salmonella, Clostridium), Virus (Rinderpest, corona virus, rota virus etc), Protozoa (Coccidia), Niacin deficiency
• Macroscopic:
• Necrotic patches in intestine
• Fibrinous deposits over necrotic patches like bran deposits
• Swelling of mesentric lymphnodes
• Ulcer in intestine
• Microscopic
• Necrosis and desquamation of intestinal villus epithelium
• Proliferation of crypt epithelium
• Congestion and infiltration of monomuclear cells in mucosa

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5. Parasitic Enteritis

• Etiology: Helminths (Roundworm, tapeworm), Protozoa (Coccidia, Histoplasma)
• Macroscopic
• Presence of parasite helminths in the lumen of intestine
• Thickening of the wall of intestine
• Catarrhal or haemorrhagic exudate in intestine
• Microscopic
• Infiltration of eosinophils in mucosa and submucosa of the intestine
• Coccidial oocysts in intestinal scrapping
• Increase number of globlet cells

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6. Fibrinous Enteritis

• Etiology: Salmonella, Cholera, Spherophorus sps
• Macroscopic
• Presence of diphtheritic membrane over mucosa of intestine
• Thickening of intestinal wall
• Microscopic
• Congestion and haemorrhage in intestine
• Fibrin network in mucosa

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7. Granulomatous enteritis

• Etiology: Mycobacterium tuberculosis, coli granuloma, Candidiasis
• Macroscopic
• Presence of elevated/raised granulomatous lesion on serous surface of intestine
• Thickening of wall of intestine
• Microscopic
• Granuloma formation consisting of central necrosed area covered by lymphocytes , macrophages, epithelioid cells, gaint cells and fibrous connective tissue

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Intestinal Obstruction

• Refer to the partial or complete occlusion of the lumen of the bowel. This result in interference with peristaltic contractions and the passage of intestinal contents.
• Etiology:
• Congenital or acquired
• Obstruction (Form within by foreign bodies, piliconcretions, phytobezoars, etc),
• Compression (From outside) or
• due to hypermotility of intestines leading to intussusception, volvulus or torsion.
• Hernia
• Embolism and thrombosis

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Piliconcretions

• Are the hair balls mostly found in the stomach or intestine of animals having habit of licking.
• Common in suckling calves, and in animal with pica
• Hair are accumulated in stomach which become rounded in shape due to movements of stomach and look like balls
• These are not degradable by digestive enzymes and can lead to obstruction

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Phytobezoars

• Are the fiber ball , made up of plant fibers intermixed with phosphate salts, found especially in colon of horses
• not heavy, usually round, smooth and moist with avelvety and occasionally convoluted surface.

Hairballs (trichobezoars)

• Hernia
• Hernia is presence of intestinal loop in umbilical area, scrotum or inguinal cavity which causes passive congestion, oedema and obstruction in intesines
• Intussusception
• A segment of the intestine is forced inside the segment just posterior to it. Intussusception is most common in the jejunum, proximal ileum and at the ileocecal junction. This interfere with venous drainage and /or arterial blood flow to the affected part result in congestion, hemorrhage and gangrene.
• Grossly: segments of the intestine feels swollen and doughy. They resemble the folds of an accordion. Red to black discoloration depends on the degree of vascular compromise, ranging from congestion to hemorrhage and necrosis. The mesenteric attachment of the intussusceptum may be seen extending from the lesion. Ischemic necrosis, congestion, and edema may occur in both the intussusceptum and intussuscipiens.

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Accordion-folded intestines.

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Volvulus�

• Rotation of a loop of intestine around its mesenteric base of attachment.
• The twist is usually more than 180 degree which leads to acute intestinal obstruction and strangulation.
• Thus, severe congestion, hemorrhage and gangrene develop rapidly.

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Grossly

• The affected loops of intestine are dark red,
• Veins are engorged and intestinal wall and mesentery are edematous.
• Segment of intestine anterior to the point of obstruction becomes distended with fluid and gas
• If animal lives long infarction gives develop into gangrene and finally death of animal
• Increase peristalsis both proximal and distal to the point of obstruction which is the cause of acute pain.

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Typhilitis

• It is the inflammation of caecum
• Particularly important in poultry

Etiology:

• Eimeria tenella
• Histomonas meleagridis

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Macroscopic Findings

• Haemorrhage in caecum
• Thickening of the wall of caecum
• Presence of necrotic ulcers in caecum in case of Histomoniasis which is further supported by round depressed, yellowish green area of necrosis in liver. Necrotic lesions in liver are circular, yellowish green and depressed.

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Peritoneum

• Abnormal content in the peritoneal cavity
• Inflammatory conditions

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Abnormal content in the peritoneal cavity

Peritonitis

• It is the inflammation of peritoneum.
• Very common in large animals
• Usually bacterial, less often viral, parasitic and chemical.

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Etiology:

• Operative incision through abdominal wall
• Rupture or perforation of stomach, intestine or uterus
• Direct extension of infection from the surrounding structures
• Through the infected umbilicus in young ones.
• Intra peritoneal administration of irritant drugs

Fig: Normal peritoneum: Normally peritoneum is smooth and shiny membrane.)

Classification

• Primary or secondary
• Acute or chronic
• Localized or diffuse
• Septic or nonseptic
• Type of predominant exudate
• Serous
• Fibrinous
• Suppurative
• Haemorrhagic
• Necrotic
• Gangrenous

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Pathological Alterations

• Thickening of peritoneum
• Adhesion of visceral organ with peritoneum due to fibrosis
• Presence of serofibrinous or fibrinous exudate which later become suppurative when invaded by pyogenic microorganism
• In case of tuberculous peritonitis presence of large number of shiny gray tubercules on the peritoneal surface or diaphragm “ so called pearly disease”

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Microscopic findings

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Microscopic findings:

• Infiltration of large no of neutrophils, macrophages and reactive mesothalial cells in peritoneum.

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Liver

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Hepatitis

• It is the inflammation of liver. It result form damage to the hepatic parenchymal cell of sufficient magnitude to cause abnormalities in clinical or biochemical findings.

Etiology:

• Infectious: Bacterial (E-coli, Salmonella,); Virus (Infectious canne hepatitis); Parasitic (Fasciola hepatica)
• Chemicals: Arsenic, leads, Alcohol, Drugs (Paracetamol, tetracycline)
• Passive venous congestion
• Miscellaneous: Ketosis, Pregnancy toxemia

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Gross findings

• Liver is enlarged and paler than normal.
• In severe cases the organ may be redder due to congestion
• The lobular marking are exaggerated. This is due to colour difference at the centre and periphery. When the congestion of central part is present, the periphery is paler due to degenerative changes in the cells. On other hand if necrosis of central part take place peripheral part will be paler.
• Presence of fibrinous diphtheritic membrane on liver
• Presence of necrotic patches in liver.

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Infectious canine hepatitis,

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A, The liver from a dog infected with infectious canine hepatitis (ICH) can be slightly enlarged and friable with a blotchy yellow discoloration. Sometimes fibrin is evident on the capsular surface. Note the petechiae on the serosal surface of the intestines caused by vascular damage from canine adenovirus type I infection.

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B, Infection of hepatocytes and endothelial cells with canine adenovirus type I produces characteristic basophilic intranuclear inclusions surrounded by a clear zone that separates them from the marginated chromatin (arrow).

Hepatic histoplasmosis, liver,

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Affected livers tend to be enlarged and pale mahogany from the diffuse hypertrophy and proliferation of Kupffer cells and macrophages.

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Microscopic findings

• Cloudy swelling and or fatty changes in liver
• Congestion of blood vessels and in sinusoidal area
• Infiltration of neutrophils, macrophages and lymphocytes
• Necrosis of hepatic parenchyma. Necrosis is most often coagulative type, recognized by pyknotic and acidiophilic cytoplasm.

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Hepatic Necrosis

• Necrosis of hepatic parenchyma is the most common and prominent feature of acute response of the liver to injurious agents.
• The term ‘hepatosis’ refer to necrotic or degenerative disease of liver.
• Based upon the anatomical location with in liver lobule liver necrosis can be classified as –

1. Focal necrosis:

• Refer to development of small area of necrosis with random distribution throughout the liver
• Charateristic of disseminated infection;
• Example: Listeriosis, Salmonellosis, Pseudotuberculosis in fetus, etc.

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Hepatic salmonellosis, liver

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Diaphragmatic surface, cow. Random 1- to 2-mm foci of focal necrosis in a cow with Salmonella septicemia. Multiple pale subcapsular foci of necrosis are evident.

Later in the disease process, the necrotic foci are infiltrated by macrophages and form discrete granulomas termed paratyphoid nodules.

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2. Centrilobular necrosis (Periacinar)

• Refer to necrosis of hepatic cell in zone around the central vein. Seen in case of Congestive heart failure
• Grossly, when the necrosis is mild, normal architectural marking of the lobules are exaggerated. However, in severe case, the necrotic tissue around central vein is replaced by blood and subsequently by fibrous tissue.

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3. Midzonal necrosis:

• Refer to necrosis of hepatocytes in a zone midway between the central vein and portal triads. Common in human eg. Eclampsia

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4. Periportal necrosis:

• Refer to necrosis of hepatocytes located along the peripherial zones of the lobules
• Seen when the blood stream brought strong toxic substance to the lobule. The peripheral cells receive the toxic blood first and suffer most from its effect.

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Centrilobular necrosis

5. Paracentral necrosis:

• Refer to the wedge shaped area of necrosis with apex located at the central vein and base of the wedge located at the portal area.
• Seen when occlusive lesion are present in branches of the portal vein

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6. Massive necrosis:

• Refer to necrosis that involves entire hepatic lobules
• Grossly, affected liver may be normal or abnormally small in size, with massive appearance of reddish grey or yellow areas intermingled with darker red areas. The grey or yellow areas represnts surviving tissue and the darker red areas represnet area of necrosis and hemorrhage.
• Leads to collapse of lobules and subsequent heavy connective tissue scarring “post necrotic cirrhosis”

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Massive necrosis, liver. A,

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Pig, cut surface. Massive

Necrosis

refers to a pattern of necrosis that involves an entire hepatic lobule, as seen here.

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B, Dog. The entire population of

hepatocytes within the lobule has undergone necrosis. P, Portal

area.

Cirrhosis

• It is the chronic liver disease characterized by concurrent hepatic cell necrosis, regeneration and diffuse fibrosis resulting in disorganization of the lobular architecture.

Etiology:

• Infectious: Bacterial (E-coli, Salmonella,); Virus (Infectious canne hepatitis); Parasitic (Fasciola hepatica)
• Chemicals: Arsenic, leads, Alcohol, Drugs (Paracetamol, tetracycline)
• Toxins: Aflatoxin
• Note: Once cirrhosis of liver starts, it is not checked even after removal of cause as the newly formed fibrosis tissue itself act as an irritant to cause further proliferation of fibroblast.

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Gross findings

• Loss of liver normal architecture.
• liver become hard and firm. On section, the liver cuts with difficulty due to dense fibrous tissue formed. While cutting a peculiar grating sound can be heard.
• Reduction in liver size due to atrophy.
• Colour of liver become yellowish grey.

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Chronic hepatic aflatoxicosis.

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Postnecrotic scarring, pig. Chronic aflatoxicosis produces a shrunken and fibrotic liver from collapse of areas of massive necrosis and condensation of the fibrous stroma.

Chronic active hepatitis.

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Liver, diaphragmatic surface, dog. The liver is characterized by scattered regenerative nodules of different sizes and extensive fibrosis that gives the liver an irregular surface.

Microscopic finding

• Proliferation of fibrous connective tissue, within and around the lobules.
• Infiltration of marcophages and lymphocyte
• Central vein is either absent or placed eccentrically.
• Hepatocytes show degenerative and necrotic changes
• Regenerative hyperplasia of hepatocyte result in rather bizarre cell with large hyperchromatic nuclei
• Presence of newly form bile duct.

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Histologic appearance.�Chronic aflatoxicosis is characterized by variable amounts of fatty change, biliary hyperplasia, and cellular atypia in hepatocytes. H&E stain.

Chronic hepatic aflatoxicosis

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Hepatic encephalopathy

• Refer to spectrum of central nervous system disturbances associated with chronic liver failure.
• Clinically manifested by changes ranging from reduced mental alertness, restlessness and confusion in the initial stages to loss of consciousness, convulsions and coma in the terminal stages.

Causes:

• Ammonia toxicity due to failure of damaged hepatic cells to convert ammonia to urea.
• Hepato toxic plant in horses eg. Senecio, crotalaria

Findings:

• Elevated level of ammonia in both blood and cerebrospinal fluid.
• There is hypertrophy and hyperplasia of protoplasmic astrocytes in the cerebral cortex and sub cortical nuclei.

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Cholecystitis

An inflammation of gall bladder characterized by congestion, thickening of wall and infilteration of mononuclear cells.Cholangitis I the inflammation of bile duct.

Etiology:

• Parasites: Fasciola sps
• Foreigh body- Stones
• Bacteria: E-coli

Macroscopic features

• Thickening of wall of gall bladder
• Presence of stones, parasites or foreign bodies
• Content of bile can be some time watery or thick oily.

Microscopic features

• Congestion
• Proliferationno f fibrous tissue I the wall of gall bladder
• Infiltration of mononuclear cells
• Increase number of mucus secreting cells.

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Pancreatitis

• It is the inflammation of pancreas characterized by necrosis of pancreatic tissue.

Etiology:

• Bacteria
• Virus
• Parasites

Macroscopic findings

• Pancreas become pale, swollen and oedematous
• In Chronic case, atrophy of pancreas
• Pancreas become hard, firm and fibrous

Microscopic findings

• Necrosis of pancreatic cells
• Oedema , infiltration of leucocytes, haemorrhage
• Proliferation of fibroblast.

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Acute pancreatitis

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The accumulation of fibrinous exudate and edema within the interlobular septa (S) and inflammatory cell infiltrate (I).

expansion of the pancreas by areas of hemorrhage and edema

Chronic pancreatitis,

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Lobules are more prominent due to fibrosis, and the pancreas is paler than normal. The white, raised, granular areas in the pancreas and mesentery are foci of fat necrosis that result from enzymatic digestion of lipids that then become mineralized

Remaining exocrine pancreatic cells are separated into small lobules by abundant fibrous connective tissue (F), which contains chronic inflammatory cells (arrow).

Practical

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Figure: Cirrhosis

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The liver is contracted, firm, tan and diffusely nodular. The nodularity is also readily observed on the capsular surface.

Gross Findings

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Microscopy

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Microscopy

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Microscopy

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Figure: Segment of Liver showing hepatic carcinoma

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Figure: The segment of oesophagus shows collapsed but previously engorged and tortuous submucosal veins (varices vein).

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The pancreas shows haemorrhagic foci mostly at the periphery. There is also parenchymal and fat necrosis accompanied by spotty deposits of chalky calcium soaps (fat saponification).

Fat necrosis appears bright orange-yellow in the fresh specimen

Viable pancreatic parenchyma

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Acute Hemorrhagic pancreatitis

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