VP1 Flashcards Preview

Veterinary Pathology > VP1 > Flashcards

Flashcards in VP1 Deck (41)
Loading flashcards...
1

H&E

Histological stain in pink and purple where acidic parts turn pink, such as proteins, and basic parts turn purple, such as nuclei. Fat, glycogen and water cannot be distinguished.

2

Oil Red O

A histology stain that turns fats red.

3

PAS

A histology stain that turns glycogen dark pink.

4

Mason’s Tricrome

Histological stain that colours collagen green.

5

Jones stain

Histological stain that turns basement membranes dark brown. Great to the the organisation of the stoma in the tissue or protection (eg tumorous growths)

6

Immunohistochemistry

Histological stain with antibodies for specific sequences, like viral genetic material.

7

Hyperplasia

Increase in the number of cells compared to normal.

8

Hypertrophy

Enlargement of the cells.

9

Hypoplasia

Incomplete or underdevelopment of a tissue or organ.

10

Aplasia

An organ not developing past the embryonic state. A rudiment will be present.

11

Agenesis

An organ that has not developed at all in an animal.

12

Metaplasia

Abnormal differentiation of adult cells

13

Dysplasia

Abnormal organisation of cells. Pre-stage of neoplasia.

14

Pathogenesis

The sequence of events occurring after exposure to the inciting agent or event - disease development.

15

Lesion

A pathological or traumatic discontinuation of a tissue or a partial loss of its function. Includes wounds, sores, ulcers, tumours, cataracts, eczema, scars, abscesses and bacterial or viral changes.

16

Cellular swelling/hydropic change

Cellular swelling is due to two things:
1) Dysfunction of membrane proteins eg the Na/K-ATPase-pumps. This will cause sodium to travel into the cells and water will follow, causing the cell to swell.
2) Hypoxia —> less aerobic output(ie ATP) —> switch (if possible)to anaerobic metabolism —> deplete glycogen and accumulate lactate and phosphate

Cellular swelling appears as clear vacuoles no matter the stain (no stain for water).

17

Oncotic necrosis

Cell death due to cell swelling (onco meaning swelling). Cell swelling is reversible but if stimuli is not removed then it will lead to cell death. Oncotic necrosis is divided into:
Coagulative
Caseous
Liquefactive
Gangrenous
Fat

18

Morphologic diagnosis

Diagnosis based on the predominant lesions - referring to the structural changes rather than the causative agent.

19

Aetiologic diagnosis

A diagnosis that specifies the aetiology, ie the causative agent. This could be done by eg immunohistochemistry stains.

20

Pathognomonic lesion

A lesion that is so typical for a disease that you can diagnose based on it

21

Coagulative necrosis

Acute lesion caused by ischemia (inadequate blood supply) or infarction (obstruction of blood supply) —> think blood clot. Basic cell outlines are preserved.

Typically occurs in tissues with a high blood demand, eg the kidneys, adrenals and heart.

22

Caseous necrosis

Caused by a chronic lesion. Tissue becomes friable (non-resistant to pressure) and cheese-like (Tip, caseous sounds like casein... cheese-ish). Can develop into dystrophic calcification.

23

Liquefactive necrosis

Dead cells turn into a liquefied debris since there’s not enough tissue framework to support the dead cells, eg in the CNS, or by pyogenic (pus-generating) bacteria, eg in abscesses.

24

Gangrenous necrosis

The chronic stage of a coagulative necrosis. Can either be
- moist/gas, invaded by saprophyte (something living on dead/decaying organic matter).
- dry, mummification

25

Fat necrosis

Specific for when there is extracellular fat accumulations (rather than oncotic necrosis).

26

Karyorrhexis

During necrosis (cell death), the nucleus is divided into several small fragments.

27

Karyolysis

During necrosis (cell death), the nucleus fades as it is destroyed. Common at coagulative necrosis.

28

Pyknosis

During cell death, the cell and nucleus shrinks, flattens and the nucleus becomes densely stained- more asociated with apoptosis than necrosis.

29

Lipidosis

Intracellular accumulation of fat. Hepatocytes (liver cells) are especially susceptible of their role in lipid metabolism. Heart muscle, skeletal muscle and kidney cells are all also at higher risk.

Tissue will have a greasy texture. Histologically you will need an Oil Red O stain to differentiate from glycogen and water.

Lipidosis happens of two reasons
1) Excessive free fatty acids into the liver
- Too much in the diet
- Adipose tissue breakdown due to starvation, eg during late multiple-offspring pregnancy
2) Toxic damage to cells so that they cannot handle (even normal) levels of fatty acids, eg alcoholism

30

Fatty infiltration

Adipocytes replacing tissue-specific cells due to old age or obesity.

31

Glycogen accumulation

Abnormal amounts of glycogen in the cells, eg hepatocytes.

Glycogen accumulation can be due to three things:
1) Corticosteroid therapy why
2) Diabetes mellitus,
3) Glycogen storage disease

32

Dystrophic calcification

Calcium is deposited in tissues that are already dead/dying. A crippling noice can be hear in macro. Serum calcium levels will be normal.

33

Metastatic calcification

Due to hypercalcaemia that will damage the intracellular organelles.

34

Serous exudate

Occurs early in inflammatory lesions, eg burns, blisters and allergic reactions.

The exudate is clear to yellow and watery. It has non to few cells and acts to separate connective tissue fibres.

35

Catharral exudate

Arise in areas with mucus producing cells like the respiratory and GI tract.

Thick and gelatinous consistency. Some connective tissue and hyperplastic (swollen) epithelial cells.

36

Fibrinous exudate

Due to acute bacterial or viral infection, ie more severe damage.

White to yellow, soft and viscous, easy to remove and expose hyperaemic organs/tissues (active increase of blood supply). Fluid has high concentration of plasma proteins and a fibrin network (escapes from the blood vessels at high vascular permeability (hyperaemia)) but no/few cells (eosinophils).

37

Fibrosis

Chronic reaction. Scar formation, fibroblasts laying down collagen to replace specialised cells.

38

Suppurative or Purulent exudate

Bacterial origin, especially staphylococcus, streptococcus and e. coli.

Thick white to yellow, liquid or dried out (lamination). High in plasma proteins and neutrophils, dead/dying cells, debris, fibrin, bacteria...

39

Abscess

Purulent exudate that has been walled off

40

Empyema

A hollow in the viscera filled with purulent exudate

41

Ideopathic

Cannot tell the pathogenesis of a lesion