Introductory path

Question 0

What is Metaplasia?

Answer 0

When one adult cell type is replaced by another adult cell type.

Question 1

What Is Hyperplasia?

Answer 1

An increase in the number of Cells in a tissue/organ

Question 2

What is Dysplasia?

Answer 2

Alteration in the size/shape or organisation of a tissue.

Question 3

Describe Reversible Cell Injury

Answer 3

Reduced ATP levels - switch to anaerobic metabolism - depletion of glycogen and accumulation of lactate and inorganic phosphates - inhibition of membrane sodium/potassium pumps and water moves into the cell.

Question 4

Describe coagulative necrosis

Answer 4

Basic cell outlines are preserved due to delayed proteolysis. acute. e.g renal infarct.

Question 5

Describe Caseous Necrosis

Answer 5

Friable cheese like appearance, a chronic lesion. May develop dystrophic calcification.

Question 6

Describe Liquefactive necrosis

Answer 6

Cavity/cavities filled with liquefied debris. e.g in the CNS due to little fibrous tissue framework to support dead cells, and in abscesses: caused by pyogenic bacteria.

Question 7

Describe Gangrenous Necrosis

Answer 7

Follows on from some cases of coagulative necrosis. Can be moist, dry, gas. Eg saprophytes invade dead tissue (moist and gas), mummification (dry)

Question 8

What is Fat necrosis?

Answer 8

Specific necrosis of Fat, e.g pancreatic fat necrosis, traumatic necrosis

Question 9

Define Pyknosis

Answer 9

A small shrunken densely staining nuclei

Question 10

Define karyorrhexis

Answer 10

Nucleus has fragmented into small pieces

Question 11

Define karyolysis

Answer 11

The nucleus has lysed (fades into the background in histology)

Question 12

What is the difference between dystrophic and metastatic calcification?

Answer 12

In dystrophic calcification serum calcium levels are normal but the calcium is deposited in tissue that is already dead or dying due to cellular damage interfering with cells ability to regulate calcium. In metastatic calcification - the primary problem is Hypercalcaemia.

Question 13

Describe Suppurative Exudate

Answer 13

Has many neutrophils (dead and alive) plus dead host cells. It is often bacterial in origin.

Question 14

Describe Fibrinous Excudate

Answer 14

Histologically, a thin eosinophilic meshwork which sometimes coagulates. Increased vascular permeability - escape of plasma protein including fibrinogen. This then forms fibrin and can be seen in some inflammatory reactions as a coagulum of yellow tinged irregular soft material.

Question 15

Describe Serous Exudate

Answer 15

Occurs early in most inflammatory lesions, it is made up of fluid albumen and other plasma proteins eg serous rhinitis.

Question 16

Describe Mucous/ catarrhal Exudate

Answer 16

It is present in the respiratory and GI tract where mucous secreting cells contribute. Hypersecretion accompanying an inflammatory reaction.

Question 17

Describe the PM changes associated with barbiturates

Answer 17

1.Local reaction, 2.barbiturate crystals, 3. splenomegaly - most prominent in dogs and horses following either barbiturate euthanasia or anaesthesia. spleen can be massively enlarged making the capsule fragile.

Question 18

Describe the PM changes associated with steroids.

Answer 18

Long term steroid use can lead to steroid induced hepatopathy. Pathogenesis: glucocorticoids induce the enzyme glycogen synthetase leading to increased storage of glycogen within hepatocytes. The hepatocytes in midzonal areas are often preferentially affected and can be up to 10x normal size.

Question 19

The typical anteroventral distribution of lesions seen in association with bronchopneuomia is consistent with what?

Answer 19

Aerogenous portal of entry into the lungs as oopposed to haematogenous spread.

Question 20

Why are benign tumours often well demarcated?

Answer 20

They grow by expansion, this may or may not be the case for malignant tumours. With regard to inflammatory lesions, well demarcated inflammatory lesions are often surrounded by fibrosis whereas poorly demarcated inflammatory lesions are more acute.

Question 21

What is Algor mortis?

Answer 21

The cooling of the body after death (can aid in estimating time of death)

Question 22

What is Rigor mortis?

Answer 22

Rigidity of skeletal muscles. A burst of metabolic activity as substrates are depleted on cessation of circulation, causes a progressive decrease in muscle pH, oxygen and ATP. There is a calcium efflux from the SR of muscle cell and shortening of muscle fibres. The head and neck affected first. Disappears as putrefaction begins. (1-2 days)

Question 23

What is Autolysis?

Answer 23

The process whereby the release of intracellular lytic enzymes from lysosomes results in self digestion of tissues. The process of autolysis results in changes in the cytoplasm and nucleus of the cells which resembles those seen in necrosis. The mucosa of the stomach and intestine autolyse very rapidly as does the pancreas and renal tubules.

Question 24

What is Putrefaction?

Answer 24

Occurs when dead tissue is invaded by anaerobic organisms such as clostridia. Tissue turns green/brown due to combination of haemoglobin breakdown and formation of hydrogen sulphide.

Question 25

What is Hypostatic congestion?

Answer 25

The effect of gravity - often evident in the lungs and kidneys. Causing pooling of blood in dependant sites (resulting in asymmetric congestion)

Question 26

What is Pseudomelanosis?

Answer 26

Green/black discolouration due to conversion of iron to iron sulphide by GI bacteria.

Question 27

What is Emphysema?

Answer 27

Invasion of tissue by gas producing bacteria.

Question 28

What is Nodular Hyperplasia?

Answer 28

Nodular hyperplasia occurs when hyper plastic nodules of tissue develop in organs (most notably the liver, spleen, adrenal and pancreas of older dogs).. The lesions comprise multiple n odules of well-differentiated cells within the tissue and are important as they may be mistaken for genuine neoplasms.

Question 29

What is splenic Siderofibrosis?

Answer 29

Yellow dry encrustations on the capsule of the spleen thought to represent sites of previous local haemorrhage with subsequent deposits of Fe, Ca and fibrosis.

Question 30

Describe Anthracosis

Answer 30

In polluted areas, inhaled carbon particles phagocytosed by alveolar macrophages. Can become visible as multiple small black foci in lung tissue. In addition as the macrophages then travel to the tracheobronchial lymph nodes, the medulla of these nodes can become black.

Question 31

What is Steroid induced hepatopathy?

Answer 31

Pathogenesis: glucocorticoids induce the enzyme glycogen synthetase leading to increased storage of glycogen within hepatocytes. The hepatocytes in midzonal areas are often preferentially affected and can be up to 10x normal size.

Question 32

What would commonly cause multifocal raised lesions in sheep lungs?

Answer 32

Muellerius capillaris.