VP1

Question 1

H&E

Answer 1

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.

Question 2

Oil Red O

Answer 2

A histology stain that turns fats red.

Question 3

PAS

Answer 3

A histology stain that turns glycogen dark pink.

Question 4

Mason’s Tricrome

Answer 4

Histological stain that colours collagen green.

Question 5

Jones stain

Answer 5

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

Question 6

Immunohistochemistry

Answer 6

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

Question 7

Hyperplasia

Answer 7

Increase in the number of cells compared to normal.

Question 8

Hypertrophy

Answer 8

Enlargement of the cells.

Question 9

Hypoplasia

Answer 9

Incomplete or underdevelopment of a tissue or organ.

Question 10

Aplasia

Answer 10

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

Question 11

Agenesis

Answer 11

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

Question 12

Metaplasia

Answer 12

Abnormal differentiation of adult cells

Question 13

Dysplasia

Answer 13

Abnormal organisation of cells. Pre-stage of neoplasia.

Question 14

Pathogenesis

Answer 14

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

Question 15

Lesion

Answer 15

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.

Question 16

Cellular swelling/hydropic change

Answer 16

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).

Question 17

Oncotic necrosis

Answer 17

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

Question 18

Morphologic diagnosis

Answer 18

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

Question 19

Aetiologic diagnosis

Answer 19

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

Question 20

Pathognomonic lesion

Answer 20

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

Question 21

Coagulative necrosis

Answer 21

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.

Question 22

Caseous necrosis

Answer 22

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.

Question 23

Liquefactive necrosis

Answer 23

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.

Question 24

Gangrenous necrosis

Answer 24

The chronic stage of a coagulative necrosis. Can either be

• moist/gas, invaded by saprophyte (something living on dead/decaying organic matter).
• dry, mummification

Question 25

Fat necrosis

Answer 25

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

Question 26

Karyorrhexis

Answer 26

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

Question 27

Karyolysis

Answer 27

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

Question 28

Pyknosis

Answer 28

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

Question 29

Lipidosis

Answer 29

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

Question 30

Fatty infiltration

Answer 30

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

Question 31

Glycogen accumulation

Answer 31

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

Question 32

Dystrophic calcification

Answer 32

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

Question 33

Metastatic calcification

Answer 33

Due to hypercalcaemia that will damage the intracellular organelles.

Question 34

Serous exudate

Answer 34

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.

Question 35

Catharral exudate

Answer 35

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.

Question 36

Fibrinous exudate

Answer 36

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).

Question 37

Fibrosis

Answer 37

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

Question 38

Suppurative or Purulent exudate

Answer 38

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…

Question 39

Abscess

Answer 39

Purulent exudate that has been walled off

Question 40

Empyema

Answer 40

A hollow in the viscera filled with purulent exudate

Question 41

Ideopathic

Answer 41

Cannot tell the pathogenesis of a lesion