Pathomorph. II - special pathology on microscopy Flashcards

1
Q

What is Enteritis haemorrhagica?

A

Hemorrhagic enteritis is a more severe form of acute catarrhal enteritis (outpouring of protein rich fluid and low absorption produces rapid dehydration and often death).

distribution is patchy because if it was diffuse the animal would not survive.

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2
Q

Hemorrhagic enteritis is usually caused by

A

a locally destructive endo- or exotoxin in concentrated form, or by a highly virulent infection, such as anthrax.

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3
Q

The predominant histological features of hemorrhagic enteritis are (3)

A
  1. severe necrosis of epithelial cells of the intestine,
  2. distension of the crypts lumen with hemorrhagic exudates and
  3. degenerative changes of crypt epithelium.
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4
Q

another term for cecal inflammation

A

typhlitis

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5
Q

inflammation of the lining of the rectum is called

A

proctitis

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6
Q

identify

A

hemorrhagic enteritis

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7
Q

Suppurative pericarditis is seen in what animal due to what?

A

mainly in cattle as a complication of traumatic reticuloperitonitis („hardware disease“).

Fibrinopurulent subacute pericarditis
or Purulent fibrinous pericarditis

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8
Q

What might you diagnose in the case of Pericardial surface thickened with white, rough and shaggy masses of fibrous connective tissue with white to grey, thick, purulent exudate.

A

Fibrinopurulent subacute pericarditis
(Purulent fibrinous pericarditis)

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9
Q

increased cellularity implies what?

A

inflammatory infiltration so inflammation

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10
Q

What is the top arrow pointing to?
middle?
bottom arrow pointing to?

A

Top: myocardium so cardiac myocytes (they have nuclei and an arrangement)
middle: inflammatory cells
bottom: the pink/red mass is accumulated fibrin, note the lack of nuclei

the empty looking pockets/vacuoles are adipocytes

image is of Fibrinopurulent subacute pericarditis (Purulent fibrinous pericarditis)

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11
Q

What is found under the epicardium in general?

A

adipose tissue so adipocytes

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12
Q

The term fibrinous pneumonia is often used synonymously with

A

lobar pneumonia, but fibrinous describes the character of the exudate rather than the anatomical distribution, and should not be considered as a substitute for the term lobar.

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13
Q

Most pneumonias in animals are

A

lobular.

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14
Q

What is red hepatization?

A

Stage 2 of pneumonia progression, occurs after 48 to 72 hours and lasts for about 2 to 4 days.

During this stage, red blood cells and immune cells travel to the alveoli to prepare to fight the infection.

Since there are more red blood cells, the lungs may appear red. The lungs also become dry, airless, and firm, often resembling the liver.

Stage 1: Congestion
Stage 2: Red hepatization
Stage 3: Grey hepatization
Stage 4: Resolution

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15
Q

What is xanthomatosis?

A

Xanthelasma.

Xanthoma is a skin condition in which certain fats build up under the surface of the skin. Xanthomas are raised, waxy-appearing, frequently yellowish-colored skin lesions. They may be associated with an underlying lipid (cholesterol/triglyceride) abnormality.

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16
Q

Fibrinous pneumonia – red hepatization, 4 main observations on histology

A
  1. intra-alveolar fibrin accumulation in the form of solid blocks,

interstitial inflammatory infiltrate,

alveolar septal edema and congestion

pneumocytes hyperplasia

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17
Q

Identify what the arrows are all point at.
What is the condition?

A

Fibrinous pneumonia - red hepatization

thrombotic vessels potentially visible too.

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18
Q

What is gray hepatization?

A

Stage 3 of pneumonia progression, occurs on day 4 to 6 and continues for 4 to 8 days. The lung looks grey or yellow in color but still has the consistency of liver.

Alveolar lumens are filled with leukocytic (suppurative) exudate (neutrophils and macrophages, in order to remove the fibrin).

Fibrin, hemosiderin and red blood cells break down and lead to a more fluid-like exudate. Macrophages, a type of large white blood cell, start to appear.

Stage 1: Congestion
Stage 2: Red hepatization
Stage 3: Grey hepatization
Stage 4: Resolution

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19
Q

The 4 stages of untreated lobar pneumonia are:

A

Stage 1: Congestion
Stage 2: Red hepatization
Stage 3: Grey hepatization
Stage 4: Resolution

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20
Q

identify what the arrows are pointing to and what the condition might be

A

Slide is of Fibrinous pneumonia -grey hepatization

top arrows: alveoli filled with fibrin and inflammatory cells. the fibrin is not as visible due to the cellularity.

erythrocytes are no longer as visible.

bottom arrow: bronchiole filled with fibrinous exudate

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21
Q

Diphtheritic enteritis can also be termed what?

A

Acute fibrinous enteritis due to the main component of the exudate being fibrinous which causes it to become pseudomembranous.

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22
Q

Diphtheritic enteritis histologically (4)

A

Fibrinous exudate (pseudomembraneous) so layer of fibrinocellular exudate on short and blunt villi.

Necrosis and ulceration of mucosa

fibrin and neutrophils from ulcerated areas exude into lumen

Mononuclear cells in lamina propria

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23
Q

identify

A

image is of Diphtheritic enteritis

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24
Q

If fibrinous exudate can be removed, leaving an intact underlying mucosa, the disease is termed

A

a croupous or pseudo diphtheritic (location)-itis

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25
Q

if removal of pseudomembrane leaves an ulcerated mucosa, it is referred to as

A

diphtheritic or fibrinonecrotic esophagitis.

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26
Q

A specific example of suppurative nephritis in foals is

A

actinobacillosis of foals.

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27
Q

identify

A

Acute purulent nephritis

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28
Q

Acute suppurative inflammation of the kidney can be termed?

A

Acute purulent nephritis

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29
Q

most common causes of tracheitis are

A

viral infections, such as those causing infectious bovine rhinotracheitis (IBR), equine viral rhinopneumonitis (EVR), canine distemper and feline rhinotracheitis.

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30
Q

tracheitis in all animal species is classified as 1 or a combination of the following 4:

A

fibrinous, catarrhal, purulent, or granulomatous.

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31
Q

Catarrhal inflammation, or called

A

or mucoid inflammation

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32
Q

Catarrhal inflammation, or mucoid inflammation, is the term used to describe a pattern of

A

acute inflammation in which the tissue response consists of the secretion or accumulation of a thick gelatinous fluid containing abundant mucus and mucins from a mucous membrane.

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33
Q

Acute catarrhal enteritis is a common finding in

A

many infectious diseases, as well as chemical intoxications.

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34
Q

Chronic catarrhal enteritis accompanies such disease as (2)

A

intestinal helminthiasis and chronic visceral congestion.

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35
Q

corrugated surace of intestinal mucosa could be a sign of

A

chronic inflammation
(e.g. chronic catarrhal enteritis)

the chronic nature causes thickening of the mucosa over time (hyperplastic connective tissue)

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36
Q

Bronchopneumonia refers to a particular type of pneumonia in which

A

injury and the inflammatory process take place primarily in the bronchial, bronchiolar and alveolar lumens.

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37
Q

What part of the lungs are typically affected in bronchopneumonia?

A

Distribution of lesions is generally cranioventral.

Filling of alveoli, bronchioles, and small bronchi with inflammatory exudate progressively obliterates airspaces.

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38
Q

Bronchopneumonia is generally caused by

A

bacteria and mycoplasmas, by bronchoaspiration of feed or gastric contents, or by improper tubing.

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39
Q

Atrophic cirrhosis of the liver grossly

A

the liver is small, contracted but is very hard and dense (weighty).

the surface irregular, the color varying greatly; grey/yellow/brown depending on bile and fatty degeneration.

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40
Q

identify

A

Atrophic cirrhosis of the liver

proliferation of connective tissue with the formation of new fibers.

marked fatty degeneration.

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41
Q

Cirrhosis is not a primary disorder, but rather represents

A

end stage liver disease from any of several causes.

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42
Q

Cirrhosis is characterized by

A

diffuse hepatic fibrosis.

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43
Q

Main features of Hypertrophic cirrhosis of the liver microscopically

A

diffuse hepatic fibrosis.

connective tissue proliferates in diffuse arrangement, is seen to extend into the lobules between the columns of cells as well as in the interlobular areas.

excessive formation of new biliary ducts.

hepatocyte necrosis

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44
Q

define periangiocholitis

A

Inflammation of the tissues around the bile ducts.

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45
Q

Cirrhosis is generally considered progressive, non-reversible, and ultimately fatal.

The architecture of the liver is altered by …?

A

loss of hepatic parenchyma, condensation of reticulin framework, and formation of tracts of fibrous connective tissue.

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46
Q

Acute encephalitis is typically caused by

A

a viral infection.

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47
Q

Acute encephallitis microscopic lesions are usually

A

nonsuppurative (lymphomonocytic)

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48
Q

identify

A

Acute encephalitis

Gross lesions often absent.

brain tissue is not very cellular.

typically lymphomonocytic (nonsuppurative), perivascular cuffing (lymphocytes, macrophages, plasma cells)

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49
Q

define leptomeningitis

A

is more commonly referred to as meningitis, represents inflammation of the subarachnoid space (i.e. arachnoid mater and pia mater) caused by an infectious or noninfectious process.

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50
Q

define Verrucous

A

wart-like, resembling a verruca (wart)

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51
Q

Endocarditis is commonly found in what species, and results from what?

A

Endocarditis is commonly found in pigs and results from a bacterial septicemia.

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52
Q

describe verrucous endocarditis

A

affected valves have large, yellow-to-gray masses of fibrin (“vegetations”), can
occlude the valvular orifice.

in chronic cases, fibrin deposits produce nodular masses termed “verrucae” (wart-like
lesions).

lesions are large by time of death and pressent on valves and extend to adjacent wall (mural).

microscopically lesions consist of accumulated layers of fibrin and bacterial
colonies underlain by a zone of infiltrated lymphocytes and granular tissue.

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53
Q

In both cytologic and histologic preparations, lymphoma is characterized by

A

a monomorphic population of morphologically atypical lymphocytes. Histologically, lymphoma is also characterized by disruption of normal tissue architecture.

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54
Q

how do you differentiate low-grade vs high-grade lymphomas histologically?

A

In general, lymphomas of small, well-differentiated cells with low mitotic rates are low-grade (indolent, slowly progressive) diseases,

whereas lymphomas of large, poorly differentiated cells with high mitotic rates are high-grade (aggressive, rapidly progressive) diseases.

55
Q

Leukemias are conventionally classified according to two criteria:

A

as lymphocytic (lymphoid) or myelogenous (myeloid), based on the cell of origin,

and as acute or chronic, based on the degree of differentiation of the neoplastic cells and their biologic behavior.

(and subcategories inside these groups)

56
Q

identify

A

Lymphosarcoma in the lung; the dense, darker lymphocytic area of cells is tumor.

57
Q

What is pictured?

A

mitoses

increased mitotic activity is a feature of malignancy

“Cancerous tissue generally has more mitotic activity than normal tissues.”

58
Q

the most common form of leukemia

A

Lymphoid leukemia (leucosis)

59
Q

Lymphoid leukemia (leucosis) Gross pathological changes are

A

significant enlargement of the liver with miliary, diffuse or nodular tumor foci

nodular tumors in the bursa of Fabricius of birds

tumorous enlargement of the spleen and other organs too.

60
Q

Lymphoid leukemia (leucosis) microscopic pathological changes are

A

the lesions consist of coalescing foci of extravascular, uniformly immature lymphoid cells (lymphoblasts).

The tumor cells are B-cells, expressing immunoglobulin M (IgM) and other B-cell markers, which originate in the bursa and metastasize to other organs.

61
Q

Chronic myeloid leukemias (CMLs) are rare in animals, with most reported cases occurring in dogs and cats.

Types of CML reported in animals include (2)

A

chronic granulocytic leukemias of neutrophils, eosinophils, and basophils;

chronic myelomonocytic leukemias.

62
Q

Chronic myeloid leukemias (CMLs) microscopically:

A

the liver shows intravascular, sinusoidal accumulations of immature myeloid cells (myeloblasts and myelocytes = neutrophil precursor),

and extravascular accumulations and perivascular cuffing, by these cells.

63
Q

what are:
myelocytes
myeloblasts

A

neutrophil granulocytic differentiation:
The most immature stage, the myeloblast, is characterized by a large nucleus with several nucleoli and a nongranular cytoplasm.

Cell division ceases during the myelocyte stage and specific granules appear in the cytoplasm.

64
Q

identify

A

Myeloid leukemia in liver.

Intravascular, sinusoidal accumulations of immature myeloid cells (myeloblasts and
myelocytes) and extravascular accumulations and perivascular cuffing.

65
Q

Emphysema is strictly defined as

A

an abnormal permanent enlargement of airspaces distal to the terminal bronchiole, accompanied by destruction of alveolar walls (alveolar emphysema).

66
Q

Secondary pulmonary emphysema occurs frequently in animals with

A

bronchopneumonia, in which exudate plugging bronchi and bronchioles causes an airflow imbalance where the volume of air entering exceeds the volume leaving the lung.

67
Q

Depending on the localization in the lung, emphysema can be classified as

A

alveolar or interstitial.

Note: Emphysemas possible after death (bacterial gas producing) differentiate from
actual emphysemas

68
Q

Interstitial emphysema occurs mainly in

A

cattle, presumably because of their wide interlobular septa, and lack of collateral ventilation in these species does not permit air to move freely into adjacent pulmonary lobules.

As a result, accumulated air penetrates the alveolar and bronchiolar walls and forces its way into the interlobular connective tissue, causing notable distention of the interlobular septa.

69
Q

bullous emphysema is

A

Sometimes these bubbles of trapped air in alveolar or interstitial emphysema become confluent, forming large (several centimeters in diameter) pockets of air that are referred to as bullae (singular: bulla);
the lesion is then called bullous emphysema.

70
Q

microscopic difference between myeloid and lymphoid leukemias in e.g. the liver

A

in lymphoid leukemias, the accumulations of lymphoblasts are better demarcated.

In Myeloid leukemias, the accumulations of myeloid/myeloblasts cells are pretty diffuse, all through the liver parenchyma.

71
Q

identify

A

bullous emphysema

72
Q

define Rachitis

A

old-fashioned medical term for rickets.

Rickets is a disease of bone and epiphyseal (growth) cartilage in immature animals,

whereas osteomalacia is a disease where the lesions are confined to bone and only occurs in adults.

73
Q

define osteomalacia

A

softening of the bones/ bone lesions

only occurs in adults.

74
Q

define kyphosis

A

Kyphosis is an exaggerated, forward rounding of the upper back.

75
Q

identify

A

rickets shown at the epiphysis of growing bone

“Microscopically, the columns of chondrocytes in the plate are somewhat disorganized, and in mammals, there is a marked increase in the number of chondrocytes in the zone of hypertrophy compared with normal.”

“the surfaces of trabecular bone in rickets and osteomalacia contain excessive amounts of osteoid (unmineralized matrix).”

76
Q

identify

A

alveolar emphysema: broken walled alveoli are seen.

the funny looking buttholes are bronchioles

77
Q

Tuberculosis Respiratory infection usually starts when

A

inhaled bacilli reach the alveoli and are phagocytosed by pulmonary alveolar macrophages.

78
Q

Bovine tuberculosis (the prototype for granulomatous pneumonia), is characterized by

A

the presence of a few or many caseating granulomas.

The early gross changes are small foci (tubercles) most frequently seen in the dorsocaudal, subpleural areas.

With progression, the lesions enlarge and become confluent with the formation of large areas of caseous necrosis.

Calcification of the granulomas is a typical finding in bovine tuberculosis.

79
Q

identify

A

grossly, Miliary tuberculous pneumonia

“these lesions resemble a sprinkling of millet seeds to early observers, they gave the name miliary tuberculosis to infection of this rapidly fatal type.”

80
Q

identify

A

Miliary tuberculous pneumonia.

-Starts with small foci called tubercles (microscopic in this case)

-Tubercles have mononuclear cells of various types: young cells: noncaseous, epithelioid and Langhans giant cells are in center,
surrounded by lymphocytes, plasma cells, and macrophages

older: caseous necrosis develops at the center, fibrosis at periphery

81
Q

Tip from Tonu Järveots for studying a rickets slide:

A

be sure to study the entire slide (move around) due to the different layers observed in epiphyseal growth plates.

If you don’t move around and view all areas, you’ll likely misdiagnose and something else altogether.

82
Q

identify

A

Caseous tuberculous pneumonia.

Lesions consist of distinct areas of pulmonary necrosis centered around bronchi/
bronchioles, formed by a core of fine eosinophilic granular debris, surrounded by rim
of neutrohpils, macrophages and fibroblasts.

83
Q

identify

A

peritoneal tuberculosis

Characterized by tubercles: yellowish white, uniform sized (about 4-5mm) tubercles diffusely distributed on the parietal peritoneum.

tend to occur in clusters, frequently coalesce to form cauliflower-like nodes.

84
Q

identify

A

Peritoneal tuberculosis

85
Q

What is a tubercle and what cells are found in one?

A

An immunological granuloma or “tubercle”.

  • Epithelioid cells are involved (also called activated macrophages)
  • Multinuclear giant cells near the center (also called Langhans giant cells)

Important feature is necrotic center with eventual calcification (which makes it dry on the inside when cut, not wet like in an abscess).

86
Q

Do not mistake miliary tuberculous pneumonia for

A

alveolar emphysema. They can look similar as miliary tuberculous pneumonia also ivolves broken and enlarged alveoli.

Look around the slide for tubercles characteristic to tuebrculous pneumonia.

87
Q

What is pictured (other than the langhans cells)?

A

A tubercle (so an inflammatory granuloma) typical to tuberculosis.

88
Q

identify

A

Peritoneal tuberculosis

This diffes from miliary tuberculosis not only based on organ affected (lungs vs abdominal serosa) but also in that peritoneal develops calcifications.

89
Q

whats this

A

calcifications of calcium salts in serosa affected by peritoneal tuberculosis.

90
Q

identify

A

tuberculous leptomeningitis

91
Q

identify

A

tuberculous lymphadenitis

92
Q
A
93
Q

identify

A

Tuberculous leptomeningitis

94
Q

identify

A

Tuberculous lymphadenitis

95
Q

Degeneration and necrosis in heart muscle is characteristic of what viral animal disease?

A

The foot and mouth disease virus often causes severe myocardial necrosis in neonatal and young pigs. This often leads to sudden deaths from myocardial failure.

The mottled myocardial lesions sometimes are referred to as “tiger-heart” lesions and are useful in diagnosis.

96
Q

identify

A

Degeneration and necrosis in heart muscle such as in foot and mouth disease.

Grayish or yellowish streaking in myocardium -degeneration and necrosis. ”Tiger heart”

In Heart and skeletal muscle foci -> Segmental myofibral necrosis accompanied by intense lymphocytic and neutrophilic infiltration.

97
Q

Colloid goiter represents what phase of diffuse hyperplastic goiter in both young and adult animals.

A

the involutionary phase

98
Q

identify

A

Colloid goiter

  • more translucent and lighter than hyperplastic goiter.
    -follicles are distended with densely eosinophilic colloid
  • cell lining of macrofollicles atrophied and flattened
    -may be remains of papillary projections on follicular cells
    -colloid eosinophilic and vacuolated, there can also be collapsed follicles
99
Q

identify

A

Follicular goiter

-Goiter is non-neoplastic and non-inflammatory enlargement of thyroid gland

-This type of goiter may be darker than colloid goiter

100
Q

identify

A

follicular goiter

101
Q

identify

A

follicular goiter

102
Q

Chronic fibrosing nodular myositis of the tongue musculature in cattle describes what condition?

A

Actinomycosis/Actinobacillosis or “wooden tongue” caused by Actinobacillus lignieresii or Actinomyces bovis.

103
Q

identify

A

Actinomycosis

-Inflammatory lesions contain central focus of amorphous eosinophilic material, neutrophil mixed with macrophages (pyogranulomatous inflammation) can also be seen.

104
Q

identify

A

Fragmentation of the myocardium (fatal)

Cardiomyocytes that appeared clearly necrotic, as indicated by loss of cross-striations, cytoplasmic fragmentation, and pyknosis (condensation of chromatin) or karyorrhexis (nucleus fragmentation).

105
Q

identify

A

Fragmentation of the myocardium (fatal)

Cardiomyocytes that appeared clearly necrotic, as indicated by loss of cross-striations, cytoplasmic fragmentation, and pyknosis (condensation of chromatin) or karyorrhexis (nucleus fragmentation).

106
Q

identify

A

Gastric ulcer

-Mucosal defect, where epithelial thickness has been lost
-Acute stress ulcers shallow, soft hyperemic margins
-Chronic ulcers lack hyperemic ring but are deeper and have fibrotic margins
- infiltration of neutrophils and eosinophils
-Surrounding area: acanthotic and parakeratotic
-Often have exudate or pseudomembrane

107
Q

identify

A

peptic (gastric ulcer)

108
Q

identify

A

actinomycosis

109
Q

identify

A

Hemorrhagic nephritis

-Interstitial edema
-Tubular epithelium: hyaline droplets, casts of protein, erythrocytes and leukocytes from urine

110
Q

identify

A

renal necrosis with interstitial hemorrhage / hemorrhagic nephritis

111
Q

identify

A

Subacute glomerulonephritis

-Glomeruli -> ischemic, neutrophils marginate in capillaries
-Fibrous scarring

112
Q

identify

A

Chronic glomerulonephritis

-cellular proliferation and adhesion of tuft and capsule.

 

113
Q

identify

A

Chronic glomerulonephritis

Atrophic renal tubules with chronic inflammatory infiltrate and hemorrhage in fibrous stroma.

114
Q

identify

A

Chronic glomerulonephritis

-Increased number of cells (endothelial, mesangial,
epithelial), disorganisation of glomerular capillaries
-Epithelial crescents
-Lumens of capillaries occluded
-Advanced cases: glomerulus replaced by hyaline
connective tissue

115
Q

identify

A

Hemorrhagic nephritis

  • Glomeruli: infiltration, inflammation,
    erythrocytes
  • Tubules with degeneration
  • Hyperemia
116
Q

identify

A

renal cysts

-Spherical, thin-walled, variably sized, on cortical or medullary tubules, filled with clear, watery fluid

-Commonly from renal tubules, sometimes from collecting ducts and Bowman’s space

-Kidneys can have single or multiple cysts

-Some cysts do not cause alteration in renal function -> incidental findings/cysts

117
Q

identify

A

chronic glomerulonephritis

more fibrotic than acute. the fibrosis infiltrates the glomeruli too.
the homogenously pink areas are cysts.
the abundant cellularity indicates inflammatory infiltration.
tubular lumens begin to be lost.

118
Q

identify

A

Hepatic fascioliasis

  • Hemorrhage, necrosis, fibrosis, active granulomas in the liver.
    -Parasitic disease (worms, eggs)
    -Presence of lymphocytes and macrophages
    -Track -like lesions either necro-hemorrhagic or
    chronic fibrous, cellular debris possible
    -Mostly around portal spaces
    -Inflammatory infiltrates (neutrophils, eosinophils)
119
Q

identify

A

Hepatic fascioliasis

  • Hemorrhage, necrosis, fibrosis, active granulomas in the liver.
    -Parasitic disease (worms, eggs)
    -Presence of lymphocytes and macrophages
    -Track -like lesions either necro-hemorrhagic or
    chronic fibrous, cellular debris possible
    -Mostly around portal spaces
    -Inflammatory infiltrates (neutrophils, eosinophils)
120
Q

identify

A

renal cysts

-Spherical, thin-walled, variably sized, on
cortical or medullary tubules, filled with
clear, watery fluid

-Commonly from renal tubules,
sometimes from collecting ducts and
Bowman’s space

-Kidneys can have single or multiple cysts

-Some cysts do not cause alteration in
renal function -> incidental findings/cysts

121
Q

identify

A

Hepatic coccidiosis

-Highly dilated bileducts, flattened epithelium, possibly hyperplastic walls

-Dilation and congestion of central veins, vacuolar degeneration, necrosis of
hepatocytes

-Portal areas, liver parenchyma: Mononuclear cells, severe hemorrhages in necrotic area

122
Q

identify

A

hepatic coccidiosis

123
Q

identify

A

Hepatic cysticercosis
Parasitic tissue infection caused by larval cysts of the tapeworm Taenia Solium.

-Degenerating cysts, by parasite

-Inflammatory cells infiltrate, thickened
capsule, colloid fluid inside cyst

-Cysts cavity filled with caseous material, may calcify

-Calcareous corpuscles

124
Q

identify

A

hepatic coccidiosis

-1mm to 2cm size yellowish nodules on liver and bileducts (postmortem finding)

-Protozoal stages: microgametocytes, macrogameteocytes, oocysts

-Highly dilated bile ducts, flattened epithelium, possibly hyperplastic walls

-Dilation and congestion of central veins, vacuolar degeneration, necrosis of hepatocytes

-Portal areas, liver parenchyma: Mononuclear cells, severe hemorrhages in necrotic area

125
Q

identify

A

hepatic cysticerosis

Parasitic tissue infection caused by larval cysts of the tapeworm Taenia Solium.

126
Q

identify

A

Myocardial sarcocystosis

-Sarcocystis spp. commonly found within skeletal and cardiac muscle fibers

-Eosinophilic myositis rare in sheep

127
Q

identify

A

Muscular trichinellosis (trichinosis)

-Nematode parasite infection (pigs show no clinical symptoms -> zoonosis)

-Adult nematodes -> mucosa of small intestine

-Larvae go to blood flow and encyst within myocytes

-Focal inflammation (eosinophils, neutrophils, lymphocytes)

-After cyst formation, larvae are protected from host’s immune reaction -> inflammation minimal or absent

-Larvae can die and calcify in tissues -> white no

128
Q

identify

A

Myocardial sarcocystosis

-Sarcocystis spp. commonly found within skeletal and cardiac muscle fibers

-Eosinophilic myositis rare in sheep

129
Q

identify

A

Muscular trichinellosis

-Nematode parasite infection (pigs show no clinical symptoms -> zoonosis)

-Adult nematodes -> mucosa of small intestine

-Larvae go to blood flow and encyst within myocytes

-Focal inflammation (eosinophils, neutrophils, lymphocytes)

-After cyst formation, larvae are protected from host’s immune reaction -> inflammation minimal or absent

-Larvae can die and calcify in tissues -> white no

130
Q

identify

A

Myocardial sarcocystosis

131
Q

identify

A
132
Q

identify

A

Muscular trichinellosis (trichinosis)

133
Q

identify

A

Muscular trichinellosis (trichinosis)