Special slides - Everything Flashcards
248
Post traumatic focal inflammatory reaction of myocardium
Description
* Round hole surrounded expressive reaction tissue, includes neutrophils, macrophages and lymphocytes
* Process locally intrudes to deeper areas as a result of foreign body
Etiology
* Due to a foreign body, it produces the inflammatory reaction/immune response
Pathogenesis
* Neutrophils are present for foreign body phagocytosis
* Continuation of repair process, granulation tissue forms with macrophages and lymphocytes
* Fibrocytes are also seen (spindle shaped cells) in the same direcion as the normal myocytes (more mature scar tissue)
261
Vasculitis chronica/Mediocalcinosis
Description
* Tunica media of aorta has increased in thickness as native fibrous tissue proliferates
* Seen by increased fibroblasts (producing intercellular collagen fibres), lymphocytes and macrophage infiltration (due to chronic inflammation)
Etiology
* Seen during uraemia/uremic syndrome
* White yellow plaques present in arteries (arteriosclerosis)
Pathogenesis
* During uraemia there is deposititon of calcia salts occurs
* Chronic inflammatory processes in the arteries tunica mediae
262
Vasculitis chronica/Mediocalcinosis (van Kossa)
Description
* The van Kossa staining is used to prove the presence of calcium (calcia salt deposition)
* Between tunica intima and tunica media among the cells and also in the intercellular mass there are bown diffuse staining as the evidence of calcium salts
Etiology
* Seen during uraemia/uremic syndrome
* White yellow plaques present in arteries (arteriosclerosis)
Pathogenesis
* During uraemia there is deposititon of calcia salts occurs
* Chronic inflammatory processes in the arteries tunica mediae
6
Emphysema alveolare chronicum
Description
* Alveoli are too large and either have wide openings into each other or common space due to rupture
* Blunt broken ends of walls may persist and thicken, becoing inelastic, but other walls may be streached and thin
* Blood filled capillaries are scarce
Etiology
* One of the two conditions under the umbrella term “chronic obstructive pulmonary disease”, due to long term exposure to inhaled irritants
* Other causes include allergic respiratory diseases, asthma conditions (end stage in cats) and in cerain viral infections (bovine respiratory syncytial virus infection)
Pathogenesis
* Most important is the loss of bronchus wall elasticity causing poorer expirium than inspiriu
* Air accumulates in the lungs (long inhales and short fast exhales) leading to distention of alveoli and lung inflation ending in rupture
200
Endobronchiolotis obliterans et peribronchiolitis nodosa
Description
* Bronchioles with obstructed lumina, filled with fibroelastic granulation tissue, proliferating into the alveoli (endobronchiolitis)
* Granulation tissue can also be seen on the periphery of the bronchioles (peribrochiolitis)
Etiology
* Common in cattle with atypical interstitial pneumonia but also seen under various conditions in other species
Pathogenesis
* Obstructive atelectasis areas of round-irregular shape occur and bronchioles become obstructed, filling with granulation tissue
* This may proliferate into the alveoli causing carnification of the lung
228
Crupous (fibrinous, lobar) pneumonia and chronic interstitial pneumonia
Description
* Basophilic margin created by polymorphus leukocytes inside alveoli
* Beginning stage of grey hepatisation
* Other alveoli are filled with pinkish mass containing fine fibrinous fibres
* Dilated lymph vessels and foci of fungal hyphae
* At one margin there is a cord, created by mature fibrous tissue, the alveolar walls and broncholes are thickened by fibrous hyperplasia due to chronic process (chronic perilobular, intralobular and peribronchial interstitial pneumonia)
Etiology
* Due to visualisation of fungal hyphae, the crupous pneumonia was caused by mycotic infection
Pathogenesis
* The pink colour inside alveoli is due to fibrin and exudate, walls are slightly thickend
* Darkened margin surrounds the pathology and coagulation necrosis also occurs
* The stages of interstitial pneumonia: congestive stage, red hepatization, and resolution (repair or carnification)
270
Epulis fibromatosa
Description
* Islands of conspicuous proliferated gingival squamous epithelum separated by maturated dense fibrous stroma with blood vessels
* Dense fibrillar collagen is present with stellate cells and a regular, open vascular pattern
Etiology
* Tumour like masses on the gingiva, often referring to epulides of periodontal origin
Pathogenesis
* Occur in gingiva near teeth as covered, soft, nodular masses with three potential forms: fibromatous, osseous and acanthomatous.
* Fibromatous and osseous types are benign tumours
* Acanthomatous type infiltrates and destroys periodontal apparatus
177
Colitis fibrinosa/Treponema dysentery (Levaditi)
Description
* Staining by Levaditi
* Masses of fibrin seen on yellow floor base of large intestine
* Black round curve and distinct undulating sticks (causative agents) often observed in exudate
Etiology
* Serpulina hyodysenteriae, now Brachyspira hyodysenteriae
* Observable in exudae when over 10 micrometers in length
Pathogenesis
* Bacteria colonise large intestine and releases toxins that damage the intestinal lining
* May penetrate deeper into mucous membrane at the base ofcrypts
* Transmission primarily occurs through the fecal-oral route
9
Lymphadenitis acuta simplex
Description
* Follicular structure of lymph node is obscured due to follicular hyperplasia and oedema
* Blood vessels are dilated and filled with blood
* Subscapular siunuses are also dilated and filled with leukocytes and neutrophils (mainly)
Etiology
* Most common form of lymphnode inflammation
* Commonly caused by bacerial infection
* Often arising from local skin lesions or mucous membranes
Pathogenesis
* An infection at a nearby site, bacteria or their products drain into regional lymph nodes, triggering an inflammatory response
* Leading to lymph node enlargement, as immune cells are recruited to the site of infection
238
Infectious bursal disease
Description
* Desquamation of epithelial cells in the folds is seen
* Extensice hyperaemia and edema of interstitial tissue
* Liquefactive necrosis, lack of lymphocytes in lymph follicles due to apoptosis is seen
* Proliferation of stroma and fibrinous exudate leakage from the bursa
Etiology
* Gumboro, birnavirus
Pathogenesis
* Virus is shed in feces, it is highly contagious an the results depend on age and breed of the chicken
* Subclinical and clinical infection occur
* Cloacal bursa is swollen, edematous, yellowish/haemorrhagic and muscular haemorrhage in legs is common
27
Cholangitis et pericholangitis chronica hyperplastica
Description
* Irregularly shaped areas bordered by fibrous tissue are seen indicating bile duct wall hyperplasia
* Epithelium proliferates and forced up into papillary folds, simulating adenomatous hyperplasia
Etiology
* Coccidea hepatis cuniculorum
Pathogenesis
* The coccidea hepatis cuniculorum are intracellular parasites, develop within the cytoplasm of epithelial cells, resultins in death of each cell affected
268
Hepatitis purulenta acuta
Description
* Cross section of bovine liver with advanced traumatic reticuloperitonitis
* A conspicuous extravasation and increased infiltration of parenchyma by neutrophils in some lobules between branches of hepatocytes
Etiology
* Originated by haematogenous transfer (metastatic) or purulent bacteria from the reticulum
Pathogenesis
* Early stadium of purulent inflammation occurs in hepatic parenchyma
* Later stadium form neutrophilic granulocyte accumulations (abscesses)
196
Leucosis lymphadenoidea hepatis
Description
* One end of the liver there is basophilic stained tumour tissue formed by slightly differentiated lymphocytes
Etiology
* Cause by bovine leukemia virus by transmission through exchange of bodily fluids
* And parasites
Pathogenesis
* Virus infects, leading to proliferatio of B lymphocytes and the development of lymphosarcoma, affecting various organs, like liver
* Tumour tissue arises from portal and bile tracts and gradually invades the center of the lobules and may even substitue them
* After parasitic larvae migration, haemorrhagi tracts may arise in normal liver tissue
164
Glomerulonepritis chronica
Description
* Nearly all glomeruli are morphologocally changed
* Many show thickened Bowman’s capsule, which press on the glomeruli causing atrophy (periglomerulitis chronica)
* Many vessels of the glomeruli are hyalinized, some are fibrotic (sclerosis)
* Large number of tubules atrophy and others dilated and become filled with eosinophilic casts
* The interstitium is dilated and infiltrated by chronic inflammatory cells – lymphocytes, plasma cells, macrophages and neutrophils (rare)
* Proliferate (dark purple brain), Membranous (pink brain), Membranoproliferative (purple flower smudge) and Glomerulosclerosis (pink smudge circle/ring)
Etiology
* Inflammation is divided by: Localisation, process starting point, pathogenesis into immune mediated GN, suppurative glomerulitis to GN and viral glomerulitis
* Most commonly seen in carnivors, associated with persistent infections and prolonged antigenaemia
Pathogenesis
* Kidney fibrosis occurs in the chronic process of periglomerulitis chronica
* End stage healing of damaged tissue leading to glomerulosclerosis
* Neutrophil aggregation occurs as they move by chemotacis to the site of Ag-Ab complex
259
Nephrocirrhosis/Nephrocalcinosis
Description
* In some parts there is differentiated granulation tissue that causes atrophy of the parenchyma
* Tubular epithelium and glomeruli undergo atrophy and necrosis, interstitium is infiltrated with lymphocytes
* Lumen of some tubules and glomeruli are filled with hyaline
* Walls of the vessels show fibrotic thickening
* Thickening wall of the Bowman’s capsule is seen as a finely basophilic stained amorphous mass
*Calcium deposition is seen
Etiology
* Can occur due to various factors: hypercalcemia, hypercalciuria, renal tubular acidosis, uremic syndrome and metabolic disorders
Pathogenesis
* Deposition of calcium salts, primarily calcium oxalate or calcium phosphate, within the renal parenchyma
* Formation of crystals within the renal tubules impairs normal renal function
260
Nephrocirrhosis/Nephrocalcinosis (von Koss)
Description
* Staining with van Kossa to prove presence of calcium salts
* Finely basophilic stained amorphous mass of bowman’s capsule causes thickening, dark brown stain shows positive reaciton for calcium salts
Etiology
* Can occur due to various factors: hypercalcemia, hypercalciuria, renal tubular acidosis, uremic syndrome and metabolic disorders
Pathogenesis
* Deposition of calcium salts, primarily calcium oxalate or calcium phosphate, within the renal parenchyma
* Formation of crystals within the renal tubules impairs normal renal function
206
Meningitis spinalis purulenta
Description
* The meningies (dura mater, arachnoidea and pia mater) are dilated and infiltrated by cells, mainly neutrophils
* White matter of spinal cord is not seriously damaged
* Dilation of lymp cessels and blood vessels may be seen, filled with edema and inflammatory infiltrate
Etiology
* Abscess usually transfers haematogenously, by direct contact or iatrogenic spread to meninges
Pathogenesis
* The infectious agents trigger an intense inflamatory response in the meninges, leading to accumulation of pus
* This inflammation can result in spinal cord compression, vascular compromise and neurological symptoms
159
Cysticercus ovis (brain)
Description
* At the peripehry of the section under the meninges, ther is a cyst that intrudes into the brain
* In the center there is necrosis, mostlu infiltrated by eosinophils
* Surroundings of the necrosis filled with granulation tissue (with giant cells) forming a capsule
Etiology
* Cysticercus ovis, infective larval stage of oestrus ovis
Pathogenesis
* The death of the parasite result from development of an immune response
* The necrotizing larvocst is surrounded by giant cells and is accompanied by necrosis and meningiis with eosinophils, lymphocytes and macrophages
* Anaohylactic reaction may occur as well
207
Fibrosarcoma uteri
Description
* Tumour tissue composed of bundles of fibrous cells in different orientations and directions
* There is abundant capillary framework in the tissue
* Cells are slender, prolonged and typical spindled with large oval, bright nuclei
* Ratio of mitotic figures in the nuclei is high and tissue is poor for collagen fibres
* At the margin there is an extensive necrosis borderde mainly by neutrophils with nreaking nuclei
Etiology
* Malignant mesencymal tumour derived from fibrous connective tissue, tumour of fibrocytes
Pathogenesis
* Cells have different size and shape of nuclei, and general pleomorphism, malignacy is clear
* Pathological mitosis signifies rapid tumour growth and increases metastatic potential
242
Hypertrophy of prostata
Description
* Fibroelastic capsule at one margin with smooth muscle cell bundles
* Fibrotic septae divide the parenchyma into lobules
* Glandular epithelium is papillomatous proliferated
* Cysts with fluid arise under the capsule due to enlarged prostatic gland lumens
* Opposite side there is proliferation of fibromuscular stroma and different large cysts with atrophic epithelium
Etiology
* Due to hormonal imbalances
Pathogenesis
* Division: Acinar with cyst formation due to overproduction of androgens or Fibromuscular due to estrogen overproduction
* Consequences include infections, urinary bladder obstruction, hydronephrosis and constipation
163
Dystrophia musculorum
Description
* Normal and degenerated myofibres can be seen
* Sarcoplasm of degenerated fibres is homogenized (hyaline dystrophy) and damaged by large shreds or tiny granules
* Sarcolemma may also be rupturedin the process of Zenker’s necrosis
* Surroundings infiltrated by leukocytes and lymphatic capillaries are dilated
Etiology
* Nutritional myopathy: Selenium and Vit E deficiency, increase in PUFA in the diet (white muscle disease).
* Monday morning disease – Equine paralytic myoglobinuria
Pathogenesis
* Equine paralytic myoglobinuria = energy production in muscle cells is altered, causing severe myopathy, myoglobinuria (dark) and potentially fatal renal faiilure
* White muscle disease = increased oxidative damage due to a lack of suitable antioxidants (Se and Vit E) against FA oxidation, leading to degenerationof skeletal and cardiac muscle
151
Trichinellosis musculorum
Description
* Larva located in the tissue section, some are encapsulated and some are not
* Surroundings show a focal myositis, characterized by the presence of neutrophils, lymphocytes and eosinophils
Etiology
* Larvae of Trichinella spiralis, infection occurs by ingestion of encysted larvae in meat
Pathogenesis
* Larvae invade the interstital wall, enter the bloodstream and migrate to skeletal muscles, where they encapsulate as cysts and inflammatory response follows
109
Myositis sarcosporidica
Description
* Skeletal muscle with sarcocysts with sarcosporidia inside
* Some are stained by eosinophilic colour = dead parasites
* Some may be calcifided (dark red, violet)
* These cysts are bordered by inflammatoy cells – inflammatory cells, macrophages, lymphocytes, eosinophils and fibroblasts (rarely) form a capsul
Etiology
* Caused by protozoa Sarcocystis
Pathogenesis
* Ingestion of sporulated oocyst leads to sporozoite and cyst formation, causing an inflammatory response (myositis)
273
Mastitis apostematosa
Description
* Local necrotic reminants of native glandular structure (simple necrosis) remain
* Bordered by remnants of purulent exudate to the periphery, followed by formation of non-specific granulation tissue in a chronic process
* Macrophages , lymphocytes and fibroblasts are present
* Violet stained homogenous mass = corpora amylacea
Etiology
* Common causes include bacterial infection
* Other factors contributing to mastitis may include trauma, poor milking hygiene or systemic infections
Pathogenesis
* Corpora amylacea is normally present in milk of multiparous cows only, as a result of synthetic and secretory processes
* Has various staining properties
* Bacteria enter mammary glands and multiply an immune respone leads to inflammation
240
Tumor mixtus mammae
Description
* Proliferation by epithelial as well as fibrou tissue
* Epithelial proliferation preseves normal structure (glandular) with varying size and form of lumina
* Connective tissue proliferation is mottled with fibroid, myxoid and chondroid structures and mineral precipitatin
Etiology
* Typically arise from glandular tissue of mammae and exhibit a range of histological patterns
* Myltifactorial including genetc mutations, hormonal influences and environmental factors
Pathogenesis
* Slow growing tumour that may become malignant
* Characterized by the presence of both epithelial and stromal components
258
Dermatitis eosinophilica
Description
* Dermis and excessively hyperemic subcutis on the inner side if the ear are infiltrated by eosinophils
* erythrocytes observed free in the tissue (extravasation into the subcutis) and on the skin surface
Etiology
* Ectoparasite Psoroptes cuniculi, infesting rabbits (psoropic mange) and is highly contagious
Pathogenesis
* Mites burrow into the skin to feed, induce an inflammatory response
* Leading to the formation of crusts and debris within the ear
* Secondary bacterial infections may occur due to the compromised skin integrity
237
Fibropapiloma
Description
* Proliferation of fibrous tissue is as great or greater than epithelial tissue
* Forms whorls of fibres with plumb, stippled nuclei with few mitotic changes
* Epithelial rete pegs penetrate deep into the fibrous moiety
* On epidermis surface there is excessive hyperkeratosis ans parakeratosis
* epidermal cells below undergo dystrophy. The cytoplasm containing numerous smaller and larger basophilic clumps
Etiology
* Benign tumours usually induced by oncogenic viruses (BPV)
* Genetic factors can also play a role in their development
Pathogenesis
* Different type of viruses, various manifestations of papillomas
* Viral transmission occurs through direct contact or contaminates fomites
