General Slides - Everything Flashcards
285
Dystrophic calcification (Infarctus renis anemicus)
Description
* Irregular oval focus
* Red-violet stained centre = Calcification (dystrophic calcium salt deposition)
* Focus is limited by granulation tissue (fibrocytes and collagenous fibres)
* At margin lymphocytes and histiocytes infiltration is seen
Etiology
* Infract is a circulatory disturbance caused by obstruction of tissue’s blood supply
Pathogenesis
* Infract causes tissue damage causing inflammation, degeneration, cell death and protein denaturation
* This causes calcification
* Granulation tissue prevents further infiltration of the pathological process
225
Hemosiderosis of spleen (Liesegang)
Description
* Liesegang staining is used to prove presence of haemosiderin
* Haemosiderins appear as BLUE stained granules in the red pulp of the spleen (nuclei are stained red)
* Present as lumps in macrophages (siderophages, siderocytes) or encrusted on fibers of the connective tissue
Etiology
* Diffuse hemosiderosis occurs during excess intravascular destruction of erythrocytes
* Example: haemolytic infection, parasitic diseases and blood poisoing
Pathogenesis
* Haemosiderin is an endogenous (yellow, beown) pigmentation
* They are released from erythrocyte breakdown
* Occurs in the spleen and other organs of monocyte-macrophage system (lymph nodes, liver, kidneys)
33
Necrosis hepatis centrolobularis
Description
* All lobules show alteration
* Branching plates are normal only at the periphery of lobules
* Center of lobules is filled with erythrocytes so the necrosis is not seen
* We can seem remenents of the hepatocytes as the undergo necrosis
* Affected zone appears red
Etiology
* Most common form of zonal necrosis in domestic animals
* Hepatocytes in this area are vulnerable to necrosis due to being farthest away from incoming arterial and portal venous blood (oxygen, essential vitamins)
* Viral infections, tissue hypoxia, passive venous congestion can all lead to centrolobular necrosis of liver
Pathogenesis
* Seen under conditions of viral infection, hypoxia or anaemia from failing circulation
* Causing necrosis of the hepatocytes in a particular zone of the tubules results in dilation and congestion of the sunusoid
* Necrosis is the death of tissue in a living organism
180
Necrosis hepatis focalis
Description
* Eosinophilically stainded focus, without nuclei due to karyolysis, with trabecular structure still present and simple coagulative necrosis
* Inflammatory cells on the edge line the nodule, they undergo necrobiosis. Separate the dead/necrotic tissue from the healthy
* Intact hepatocytes observed on the other side of the line of inflammatory cells
Etiology
* Caused by bacteria, infectious processs, vascular ischaemia, toxicities, metabolic disorders or neoplastic causes
Pathogenesis
* Simple coagulative necrosis occurs when trabecular structure of the tissue is preserved through the necrotic process
* Heterolysis occurs when cells are degraded by other cells
187
Infarctus renis anemicus
Description
* Necrotic tissue stains bright pink, coagulative necrosis, cellular outlines and tissue structure are still present
* Necrotic area is surrounded by inflammatory zone (darker/hyperaemia) with neutrophilic granulocytes and erythrocytes (red line)
Etiology
* Infract is a circulatory disturbance caused by obstruction of tissue’s blood supply
* Microthrombus leading to widespread ischaemia, necrosis and haemorrhage
Pathogenesis
* Infract (obstruction of blood supply) causes tissue damage leading to necrosis, nuclear karyolysis is present in coagulative necrosis
* Affected areas of kidney are surounded by normal structures and function
223
Chronic passive hyperemia of liver
Description
* Congestion and dilation of the blood vessels is seen
* Sinusoids of the liver parenchyma are widened and filled with erythrocytes
* Hemosiderin in macrophages can be found if process is chronic
Etiology
* Occurs with prolonged impairment of blood outflow from the liver
* Common causes are right-sided heart failure and cirrhosis
Pathogenesis
* Any cause of increase of pressure within the hepatic beins and sinusoids, disturbes blood drainage causing congestion
* Leading to hepatocellular hypoxia, kupffer cell activation and collagen deposition = liver fibrosis
* Eventually the reduced blood flow exacerbates heparic dysfunction
25
Pleuritis fibrinosa (repair by organistation)
Description
* Pink stained fibrin, locally infiltrated by macrophages, lymphocytes and neutrophils
* Beneath the fibrin is young granulation tissue, it proliferates into fibrin
* Deeper the maturition to fibrous connective tissue can be seen
* The spaces between the capillarie are filled with macrophages, lymphocytes and spindle shaped fibroblasts
Etiology
* Often part of pleural changes in response to various insults, and presentation can vary based on the underlying cause
* Example: infections, pulmonary embolism, trauma, neoplasia etc.
Pathogenesis
* Inflammatory stimulus leads to mediator release and the pleural blood vesel permeability increases
* Fibrin deposition occurs an accumulates in the pleural space, and eventually organises into fibrous scarring
* Often accompanied by crupous inflammation in the lungs
148
Fibrosis myocardii
Description
* Myocardium is locally substituted by mature fibous tissue, bright staining
* In some areas fatty tissue is present
Etiology
* This is a substitution of damaged myocardium caused by infract, necrosis, inflammaton etc.
Pathogenesis
* Repair of damaged myocardium, when arising granulation tissue mature to high differentiated connective tissue during healing
255
Bronchopneumonia purulenta
Description
* Enlargement of capillaries with blood is seen especially in itraalveolar septa
* Alveoli are filled with extensive infiltrate containing different cells, predominently neutrophils but also has leukocytes, lymphocytes, desquamated pneumocytes and alveolar macrophages
* Usually lies in blank amount of grey pinkish homogenous fluid exudate, neutrophils also fill the bronchial spaces
Etiology
* Occurs when damage is more severe and large number of neutrophils are present
Pathogenesis
* Infectious agent, usually bacteria, triggers inflammatory response
* Exudate then forms with neutriphils predominating as main cell population
* Accumulation causes consolidation of the lung tissue
253
Pericarditis fibrinosa
Description
* On myocardial surface is thickened layer of oedematous subepicardial tissue and endothelial reminants covered in fibrinous mass mixed with lymphocytes and neutrophils
Etiology
* Seen most often in in ruminants and swine
* Caused by infections, uremia, trauma, neoplasia, …
* Often part of the broader spectrum of pericardial diseases
Pathogenesis
* Small amount of fibrin leaves the vessels and settles in the pericardium, where it proliferates
* Demonstrates acute stadium of serosal fibrinous inflammation
* Production of fibrous tissue represents healing of fibrinous inflammation
166
Cirrhosis hepatis
Description
* Proliferated fibrous tissue
* Infiltrated by chronic inflammatory cells, lymphocytes, plasma cells and macrophages
Etiology
* Represents the final stage of severe hepatocyte damage after chronic disease processes of liver
Pathogenesis
* Fibrous tissue originates from interlobular spaces and moves into lobule centers, causing press atrophy of parenchyma
* Proliferation of interstitial tissue leads to fibroblasts forming fibrous connective tisue
* Biliary hyperplasia is associated with peribiliary fibrosis
201
Actionomycosis
Description
* Actinomycotic nodules are seen at lower magnification, with bacterial colonies in center
* Bacterial colonies consisting of intertwined radiating filaments (rays), capped by eosinofilic hyaline material (clubs) creating a sunburst pattern = Splendor-Hoeppli phenomen surrounded by disintegrated neutrophils (pus)
* Specific granulation tissue is the next layer (epithelioid and multinucleated giant macrophages)
* Non-specific granulation tissue may border the nodules (fibroblasts) forming the next to layers
Etiology
* Causative agent in bovine is Actinomyces bovis
Pathogenesis
* Affects one part of the jaw, in tisse and bone (“lumpy jaw”)
263
Pneumonia TBC miliaris - poultry
Description
* Pathological content fills most of the air fistulas
* Formed by round foci with central necrosis (pink), surrounded by specific granulation tissue
* Close to the necrotic centers are macrophages and lymphocytes, numerous to the periphery
* Giant cell may also form in some
Etiology
* Caused by Mycobacterium avium subsp. avium
Pathogenesis
* Formation of tiny granulomas in the lungs lead to respiratory signs after infection with Mycobacterium
264
Pneumonia TBC miliaris - poultry - ZN
Description
* Ziehl-Nielson staining is used for special proof of mycobacterium
* Positive acid-fast rods bacilli and their clumps stain red, are localised mainly in necrotic centre
Etiology
* Caused by Mycobacterium avium subsp. avium
Pathogenesis
* Formation of tiny granulomas in the lungs lead to respiratory signs after infection with mycobacterium
* During gerneralised TBC process, the lungs tend to be the last organ receiving tubercule dissemination
219
Adenoma and Adenocarcinoma sebaceum
Description
* On the left side is Adenoma a benign tumour
* On the right side is Adenocarcinoma a malignant tumour
* In adenoma there are lighter cells more similar in size/shape/acinar structure
* In adenocarcinoma basophilic cells that rarely resemble normal acinar structure and cells, pathogenic mitosis is noted
* The tumour cells are relatively large, light ones with vacuolated foamy cytoplasm, and large light nuclei (some with necrotic changes)
Etiology
* Arise from glandular tissues
* Causes are multifactorial (genetics, environment, inflammation, viruses…)
Pathogenesis
* In adenomas there may be necrotic changes in the nuclei
* In adenocarcinoma the alveolar centers undergo regressive changes such as dystrophy and necrosis
235
SCC - Squamous Cell Carcinoma
Description
* Eosinophilic stained formation grow into the dermis with tumour cells spread as slender anastomotic cords, some cells fall off the cord and remain as isolated islands in the dermal stroma
* The tumour cells resemble the normal stratum spinosum epidermis but have vesicular nuclei with one or more prominent nucleoli
* Keratinization within such cords of islands result in laminated keratin “pearls” surrounded by tumour cells
* At the periphery of these islet cells resemble to basal ones following differentiated cells of stratum spinosum and keratinization in the center occurs
Etiology
* There is specific classification depending on proportion of parenchyma or stroma is present in the tumour
Pathogenesis
* Characterised by uncontrolled growth of abnormal cells arising from squamous cells in epidermis
283
Fibroma molle
Description
* Cells with fewer fibrils run aimlessly in all directions and mitosis are seldom.
* Tumour tissue is locally oedematous, permeated (no stained slots among individual cells) or infiltrated by heterophils, lymphocytes and macrophages (body reaction)
Etiology
* Exact etiology is not fully understood, can be due to friction, genetics, hormonal changes and age
Pathogenesis
* Benign tumour that arises from fibrous connective tissue, consisting of fibrous material predominating at the expense of nuclei and plumb cell bodies
* Slow growing and do not metastasize
* Can cause press atrophy or issues depending on their location
219
Adenoma et Adenocarcinoma sebaceum
Description
* Adenocarcinoma is a malignant tumour
* In adenocarcinoma basophilic cells that rarely resemble normal acinar structure and cells, pathogenic mitosis is noted
* The tumour cells are relatively large, light ones with vacuolated foamy cytoplasm, and large light nuclei (some with necrotic changes)
Etiology
* Arise from glandular tissues
* Causes are multifactorial (genetics, environment, inflammation, viruses…)
Pathogenesis
* In adenocarcinoma the alveolar centers undergo regressive changes such as dystrophy and necrosis
219
Adenoma and Adenocarcinoma sebaceum
Description
* Adenoma is a benign tumour
* In adenoma there are lighter cells more similar in size/shape/acinar structure
* The tumour cells are relatively large, light ones with vacuolated foamy cytoplasm, and large light nuclei (some with necrotic changes)
Etiology
* Arise from glandular tissues
* Causes are multifactorial (genetics, environment, inflammation, viruses…)
Pathogenesis
* In adenomas there may be necrotic changes in the nuclei
