Special pathology (2nd slide test) Flashcards
Hemorrhagic enteritis:
-More acute form of acute catarrhal enteritis
-Distribution is “patchy”, not diffuse (if it was widespread, animal would not survive)
-Caused by destructive endo-or exotoxin in concentrated form or highly virulent infection (anthrax)
-Severe necrosis of epithelial cells
Fibrinopurulent subacute pericarditis:
-In cattle as a complication of traumatic reticuloperitonitis (hardware disease)
-Pericardium is thickened with fibrous connective tissue with exudate
In the slide:
-Fibrin and leukocytes, inflammation, erythrocytes in pericardium
Fibrinous pneumonia - grey hepatization:
-3rd stage (5-7 days)
-Affected lobular has a liver-like consistency, uniform grey color
-Alveolar lumens are filled with suppurative exudate and possibly fibrin
-Not that many erythrocytes
-Congestion and edema, thick alveolar walls
Fibrinous pneumonia - red hepatization:
-Usually lobular
-Red hepatization happens in the 2nd stage (3-4 days)
-Pneumonic lobe gets a liver-like consistency and sinks in water, is red-brown, dry and granular
-No air inside
-Alveolar spaces are filled with exudate rich fibrin, bacteria, leukocytes, erythrocytes = solid blocks
-Alveolar walls are thickened (capillary congestion and edema)
-Necrotic areas and thrombosed interstitial tissue
-Hemorrhaging –> red
Fibrinous pneumonia - grey hepatization:
-3rd stage (5-7 days)
-Affected lobular has a liver-like consistency, uniform grey color
-Alveolar lumens are filled with suppurative exudate and possibly fibrin
-Not that many erythrocytes
-Congestion and edema, thick alveolar walls
Fibrinous pneumonia - grey hepatization:
-3rd stage (5-7 days)
-Affected lobular has a liver-like consistency, uniform grey color
-Alveolar lumens are filled with suppurative exudate and possibly fibrin
-Not that many erythrocytes
-Congestion and edema, thick alveolar walls
Diphteritic enteritis:
-Acute fibrinous enteritis
-Fibrinous exudate
In the slide:
-Layer of fibrinocellular exudate on short and blunt villi
-Necrosis and ulceration of mucosa
-Fibrin and neutrophils from ulcerated areas into lumen
Diphteritic enteritis:
-Acute fibrinous enteritis
-Fibrinous exudate
In the slide:
-Layer of fibrinocellular exudate on short and blunt villi
-Necrosis and ulceration of mucosa
-Fibrin and neutrophils from ulcerated areas into lumen
Diphteric esophagitis:
-Necrotic ulcers on mucosa of pharynx, esophagus and crop
-Fibrin
-Exudate accumulates on surface and forms a film “pseudomembrane”
Diphteric esophagitis:
-Necrotic ulcers on mucosa of pharynx, esophagus and crop
-Fibrin
-Exudate accumulates on surface and forms a film “pseudomembrane”
Acute purulent myositis:
-Serous inflammation of muscle tissue
-Edema, leukocyte infiltration, necrosis of muscle fibers
-Yellow/grey waxy degeneration (exudate)
-Sometimes exudate might be hemorrhagic
-Cellular infiltration!
Acute purulent myositis:
-Serous inflammation of muscle tissue
-Edema, leukocyte infiltration, necrosis of muscle fibers
-Yellow/grey waxy degeneration (exudate)
-Sometimes exudate might be hemorrhagic
-Cellular infiltration!
Acute purulent nephritis:
-Entire kidney is infiltrated, esp. cortex
-Acute embolic nephritis (suppurative glomerulitis)
-Result from bacteremia: bacteria lodge in glomeruli and capillaries and form multiple inflammation loci
-Can result in necrosis, neutrophil infiltration, glomerular or interstitial hemorrhages –> glomerular destruction
Acute purulent nephritis:
-Entire kidney is infiltrated, esp. cortex
-Acute embolic nephritis (suppurative glomerulitis)
-Result from bacteremia: bacteria lodge in glomeruli and capillaries and form multiple inflammation loci
-Can result in necrosis, neutrophil infiltration, glomerular or interstitial hemorrhages –> glomerular destruction
Acute catarrhal tracheitis:
-Usually caused by viral infections, become severe with secondary bacterial infection
-Early stage is hyperemic, can find white foci of necrosis
-Severe case can cause ulceration
-Fibers are separated, hyperemia, endothelial cells can be flattened to hypertrophied, mucosal epithelium is thickened, has clear layer of mucus and nodular appearance (by catarrhal exudate)
Acute catarrhal tracheitis:
-Usually caused by viral infections, become severe with secondary bacterial infection
-Early stage is hyperemic, can find white foci of necrosis
-Severe case can cause ulceration
-Fibers are separated, hyperemia, endothelial cells can be flattened to hypertrophied, mucosal epithelium is thickened, has clear layer of mucus and nodular appearance (by catarrhal exudate)
Acute catarrhal enteritis:
-Mucoid inflammation –> usually thick gelatinous fluid from mucous membrane
-Hyperplastic epithelial cells of mucus glands and goblet cells connective tissue fibers separated by mucins
-Epithelial cell death, hyperemia, lymphocytic infiltration
-Some degeneration might be found
-Eosinophils are also found
Acute catarrhal enteritis:
-Mucoid inflammation –> usually thick gelatinous fluid from mucous membrane
-Hyperplastic epithelial cells of mucus glands and goblet cells connective tissue fibers separated by mucins
-Epithelial cell death, hyperemia, lymphocytic infiltration
-Some degeneration might be found
-Eosinophils are also found
Hemorrhagic enteritis:
-More acute form of acute catarrhal enteritis
-Distribution is “patchy”, not diffuse (if it was widespread, animal would not survive)
-Caused by destructive endo-or exotoxin in concentrated form or highly virulent infection (anthrax)
-Severe necrosis of epithelial cells
Fibrinopurulent subacute pericarditis:
-In cattle as a complication of traumatic reticuloperitonitis (hardware disease)
-Pericardium is thickened with fibrous connective tissue with exudate
In the slide:
-Fibrin and leukocytes, inflammation, erythrocytes in pericardium
Fibrinous pneumonia - red hepatization:
-Usually lobular
-Red hepatization happens in the 2nd stage (3-4 days)
-Pneumonic lobe gets a liver-like consistency and sinks in water, is red-brown, dry and granular
-No air inside
-Alveolar spaces are filled with exudate rich fibrin, bacteria, leukocytes, erythrocytes = solid blocks
-Alveolar walls are thickened (capillary congestion and edema)
-Necrotic areas and thrombosed interstitial tissue
-Hemorrhaging –> red
Diphteritic enteritis:
-Acute fibrinous enteritis
-Fibrinous exudate
In the slide:
-Layer of fibrinocellular exudate on short and blunt villi
-Necrosis and ulceration of mucosa
-Fibrin and neutrophils from ulcerated areas into lumen
Diphteric esophagitis:
-Necrotic ulcers on mucosa of pharynx, esophagus and crop
-Fibrin
-Exudate accumulates on surface and forms a film “pseudomembrane”
Acute purulent myositis:
-Serous inflammation of muscle tissue
-Edema, leukocyte infiltration, necrosis of muscle fibers
-Yellow/grey waxy degeneration (exudate)
-Sometimes exudate might be hemorrhagic
-Cellular infiltration!
Acute purulent nephritis:
-Entire kidney is infiltrated, esp. cortex
-Acute embolic nephritis (suppurative glomerulitis)
-Result from bacteremia: bacteria lodge in glomeruli and capillaries and form multiple inflammation loci
-Can result in necrosis, neutrophil infiltration, glomerular or interstitial hemorrhages –> glomerular destruction
Acute catarrhal tracheitis:
-Usually caused by viral infections, become severe with secondary bacterial infection
-Early stage is hyperemic, can find white foci of necrosis
-Severe case can cause ulceration
-Fibers are separated, hyperemia, endothelial cells can be flattened to hypertrophied, mucosal epithelium is thickened, has clear layer of mucus and nodular appearance (by catarrhal exudate)
Acute catarrhal enteritis:
-Mucoid inflammation –> usually thick gelatinous fluid from mucous membrane
-Hyperplastic epithelial cells of mucus glands and goblet cells connective tissue fibers separated by mucins
-Epithelial cell death, hyperemia, lymphocytic infiltration
-Some degeneration might be found
-Eosinophils are also found
Chronic catarrhal enteritis
-Inflammation of intestinal tract with vascular congestion, mucosal edema, and increased mucus in intestinal lumen
-Can be caused by helminthiasis, chronic visceral congestion
-Thickened mucosa, lymphocyte infiltration, regenerative hyperplasia of epithelium
-Mucosa is more corrugated/folded, not as smooth as normal
Chronic catarrhal enteritis
-Inflammation of intestinal tract with vascular congestion, mucosal edema, and increased mucus in intestinal lumen
-Can be caused by helminthiasis, chronic visceral congestion
-Thickened mucosa, lymphocyte infiltration, regenerative hyperplasia of epithelium
-Mucosa is more corrugated/folded, not as smooth as normal
Chronic catarrhal enteritis
-Inflammation of intestinal tract with vascular congestion, mucosal edema, and increased mucus in intestinal lumen
-Can be caused by helminthiasis, chronic visceral congestion
-Thickened mucosa, lymphocyte infiltration, regenerative hyperplasia of epithelium
-Mucosa is more corrugated/folded, not as smooth as normal
Chronic catarrhal gastritis
-Stomach is dilated, thickened walls, white mucosal nodules
-Edematous submucosa
-Mucosa is hypertrophic and hyperplastic
-Glands are atrophied
-Possible to find hypertrophied lymphoid follicles
Chronic catarrhal gastritis
-Stomach is dilated, thickened walls, white mucosal nodules
-Edematous submucosa
-Mucosa is hypertrophic and hyperplastic
-Glands are atrophied
-Possible to find hypertrophied lymphoid follicles
Acute catarrhal bronchopneumonia
-Caused by bacteria and mycoplasmas, aspiration or improper tubing
-Pulmonary vessels hyperemic
-Edema in bronchi, bronchioles, and alveoles
-Airspaces filled with inflammatory exudate
Acute catarrhal bronchopneumonia
-Caused by bacteria and mycoplasmas, aspiration or improper tubing
-Pulmonary vessels hyperemic
-Edema in bronchi, bronchioles, and alveoles
-Airspaces filled with inflammatory exudate
Atrophic cirrhosis of the liver
-Bands of connective tissue. Gray, yellow or brown depending on fatty degeneration and bile
-Liver will be small and contracted, increased density
-Irreversible
Atrophic cirrhosis of the liver
-Bands of connective tissue. Gray, yellow or brown depending on fatty degeneration and bile
-Liver will be small and contracted, increased density
-Irreversible
Hypertrophic cirrhosis of the liver
-Diffuse hepatic fibrosis
-End-stage liver disease
-Larger that normal, smooth or finely granular. Dense and firm, mottled appearance.
-Loss of hepatic parenchyma, condensation of reticulin framework, formation of fibrous connective tissue
Hypertrophic cirrhosis of the liver
-Diffuse hepatic fibrosis
-End-stage liver disease
-Larger that normal, smooth or finely granular. Dense and firm, mottled appearance.
-Loss of hepatic parenchyma, condensation of reticulin framework, formation of fibrous connective tissue
Hypertrophic cirrhosis of the liver
-Diffuse hepatic fibrosis
-End-stage liver disease
-Larger that normal, smooth or finely granular. Dense and firm, mottled appearance.
-Loss of hepatic parenchyma, condensation of reticulin framework, formation of fibrous connective tissue
Acute encephalitis
-Microscopic lesions usually nonsuppurative (lymphomonocytic)
-Leptomeningitis, perivascular cuffing (lymphocytes, macrophages, plasma cells)
-Typically viral cause
Verrucous endocarditis
-Common in bacterial septicemia
-Lesions are large by time of death, present in valves and adjacent wall
-Valves have large, yellow-grayish masses of fibrin (“vegetations”) which can occlude valvular orifice
-In chronic version, fibrin can make nodular masses (wartlike lesions)
-Microscopical lesions have layers of fibrin and bacterial colonies, infiltrated lymphocytes and granular tissue
-Possible to find thrombotic masses
Verrucous endocarditis
-Common in bacterial septicemia
-Lesions are large by time of death, present in valves and adjacent wall
-Valves have large, yellow-grayish masses of fibrin (“vegetations”) which can occlude valvular orifice
-In chronic version, fibrin can make nodular masses (wartlike lesions)
-Microscopical lesions have layers of fibrin and bacterial colonies, infiltrated lymphocytes and granular tissue
-Possible to find thrombotic masses
Chronic fibrous myocarditis
-Increase in interstitial connective tissue (due to inflammation)
-Might be obstruction of coronary artery
-Inflammation may extend to muscle substance
Chronic fibrous myocarditis
-Increase in interstitial connective tissue (due to inflammation)
-Might be obstruction of coronary artery
-Inflammation may extend to muscle substance
Lymphosarcoma
-Lots of morphologically atypical lymphocytes
-Disruption of normal tissue architecture
-Separated into low-grade (slowly progressive) and high-grade (aggressive)
Lymphosarcoma
-Lots of morphologically atypical lymphocytes
-Disruption of normal tissue architecture
-Separated into low-grade (slowly progressive) and high-grade (aggressive)
Lymphoid leukemia in liver
-Leukemia can be lymphocytic or myelogenous and acute or chronic
-Organs are lighter, nodules, tumorous masses
-Systemic tumorous processes also possible
-Abnormal hepatocytes
-Lots of lymphocytes, tumorous cells, lymphoblasts, giant cells
Lymphoid leukemia in liver
-Leukemia can be lymphocytic or myelogenous and acute or chronic
-Organs are lighter, nodules, tumorous masses
-Systemic tumorous processes also possible
-Abnormal hepatocytes
-Lots of lymphocytes, tumorous cells, lymphoblasts, giant cells
Lymphoid leukemia in liver
-Leukemia can be lymphocytic or myelogenous and acute or chronic
-Organs are lighter, nodules, tumorous masses
-Systemic tumorous processes also possible
-Abnormal hepatocytes
-Lots of lymphocytes, tumorous cells, lymphoblasts, giant cells
Myeloid leukemia in liver
-Chronic myeloid leukemias are rare
-Intravascular, sinusoidal accumulations of immature myeloid cells (myeloblasts and myelocytes) and extravascular accumulations of perivascular cuffing
-Myelocytes are larger than lymphocytes
Myeloid leukemia in liver
-Chronic myeloid leukemias are rare
-Intravascular, sinusoidal accumulations of immature myeloid cells (myeloblasts and myelocytes) and extravascular accumulations of perivascular cuffing
-Myelocytes are larger than lymphocytes
Chronic alveolar emphysema
-Enlargement of airspaces which will lead to destruction of alveolar walls
-No primary emphysema in animals
-Secondary emphysema is common with bronchopneumonia
-Alveolar or interstitial emphysema
-Bulla = bubbles of trapped air in alveolar or interstitial emphysema –> lesion of this bulla is called bullous emphysema
Chronic alveolar emphysema
-Enlargement of airspaces which will lead to destruction of alveolar walls
-No primary emphysema in animals
-Secondary emphysema is common with bronchopneumonia
-Alveolar or interstitial emphysema
-Bulla = bubbles of trapped air in alveolar or interstitial emphysema –> lesion of this bulla is called bullous emphysema
Rickets
-Disease of bone and cartilage of young animals
-Osteomalacia is in adults
-Leads to bone pain, fractures, deformities
-Growth plates are thickened
-Problem with vitamin D or calcium metabolite
-Surface of trabecular bone have excessive amount of osteid (unmineralized matrix)
-Chronic process
Rickets
-Disease of bone and cartilage of young animals
-Osteomalacia is in adults
-Leads to bone pain, fractures, deformities
-Growth plates are thickened
-Problem with vitamin D or calcium metabolite
-Surface of trabecular bone have excessive amount of osteid (unmineralized matrix)
-Chronic process
Miliary tuberculous pneumonia
-Tuberculosis - chronic bacterial disease
-Starts with small foci (tubercles), then lesions, caseous necrosis, calcification of granulomas, nodules or cluster in pleura and peritoneum
-Mononuclear cells of many types
Miliary tuberculous pneumonia
-Tuberculosis - chronic bacterial disease
-Starts with small foci (tubercles), then lesions, caseous necrosis, calcification of granulomas, nodules or cluster in pleura and peritoneum
-Mononuclear cells of many types
Caseous tuberculous pneumonia
-Distinct areas of pulmonary necrosis centered around bronchi or bronchioles
-Necrosis is formed by a core of eonisophilic granular debris surrounded by neutrophils, macrophages and fibroblasts
-In caseous necrosis tubercles are not so visible
Caseous tuberculous pneumonia
-Distinct areas of pulmonary necrosis centered around bronchi or bronchioles
-Necrosis is formed by a core of eonisophilic granular debris surrounded by neutrophils, macrophages and fibroblasts
-In caseous necrosis tubercles are not so visible
