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Flashcards in MOD 1 Deck (111)
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1

Define pathology

Scientific study of the structural and functional changes in cells, tissues and organs that are seen in disease.

2

What is the difference between cytopathology and histopathology?

In cytopathology the specimens consist of disaggregated cells rather than tissue. These specimens can be collected rapidly by non-invasive or relatively minimally invasive tests (fine needle aspirates, effusions, cervical smears, sputum and urine).

3

What do chemical pathologists study?

Disturbances in metabolic processes e.g. endocrinology, lipidology, diabetes, thyroid disease and other areas of clinical services

4

List 7 causes of cell injury and death

Hypoxia
Physical agents
Chemical agents and drugs
Microorganisms
Immune mechanisms
Dietary insufficiencies and dietary excess
Genetic abnormalities e.g. inborn errors of metabolism

5

What sort of physical agents can cause cell death?

direct trauma, extremes of temperature, radiation, sudden changes in atmospheric pressure, electric currents

6

Define hypoxia

A deficiency in the amount of oxygen reaching the tissues, due to any cause.

7

What are the three most biologically important free radicals?

OH. (hydroxyl, the most dangerous)
O2.- (superoxide)
H2O2

8

List some targets of cell injury

cell membranes - plasma and organelle's e.g. lysosome
nucleus
proteins - structural and functional
mitochondria

9

Explain the mechanism of reversible hypoxic injury

1. Cell deprived of oxygen
2. Decreased production of ATP by oxidative phosphorylation
3. intracellular Na+ concentration increase
(b) Water flows into cell due to high Na+ concentration (oncosis)
(c) Ca2+ enters cell -> damage of cellular components
(d) glycolysis pathway activation -> decreased cellular pH
(e) change in pH -> altered enzyme activity and chromatin clumping
(f) ribosome detach from the ER (attachment is an energy-requiring process) - protein synthesis is disrupted
(g) Intracellular accumulations of fat and denatured proteins can occur

10

Explain the mechanism of irreversible hypoxic injury

Same as reverisble, but at some point (not well understood) the damage becomes irreversible and the cell dies (most cells die in hypoxia by oncosis). Although it is unclear what actually kills the cell, the key event is the development of profound disturbances in membrane integrity -> massive influx of Ca2+.

11

What is ischaemia-reperfusion injury?

The damage that can be caused by return of blood flow to a tissue that has been subjected to ischaemia but is not yet necrotic.

12

Define ischaemia. What is the difference between hypoxia and ischaemia?

Ischemia is an insufficient supply of blood to an organ, usually due to a blocked artery, but can also be caused by reduced venous drainage. Therefore hypoxia is an insufficiency of OXYGEN, whereas ischaemia is an insufficiency in BLOOD (and therefore oxygen AND metabolic substrates) to a tissue. Ischaemia therefore causes injury more rapidly and severly than hypoxia.

13

What is the mechanism of cyanide toxicity?

Cyanide binds to mitochondrial cytochrome c oxidase, the last complex in the electron chain, and competitively inhibits it - blocks oxidative phosphorylation

14

When are free radicals produced?

Particularly in:
1. Chemical and radiation injury
2. Ischaemia-reperfusion injury
3. Cellular aging
4. At high oxygen concentrations

15

What types of cellular damage do free radicals cause?

Lipid peroxidation of membrane lipids
Protein, carbohydrate and nucleic acid damage

16

How does the body defend itself against free radicals?

The anti-oxidant system consists of:
1. Enzymes - SOD (O2.- -> H2O2, catalases and peroxidases (H2O2 -> H20 and O2)
2. Free radical scavengers - Vitamin A, C, E and glutathione
3. Storage proteins that sequester transition metals in the extracellular matrix e.g. transferrin and ceruloplasmin sequester iron and copper which catalyse the formation of free radicals

17

Describe the function of heat shock proteins

They recognise abnormal proteins and repair them by ensuring they fold correctly. If this isn't possible then they are destroyed. Therefore they play a key role in maintaining protein viability during cell injury. Ubiquitin is one form of HSP.

18

Define oncosis

Cell death with swelling. The spectrum of changes that occur prior to death in cells injured by hypoxia and some other agents.

19

Define necrosis

The MORPHOLOGIC changes that occur after a cell has been dead for some time e.g. 4-24 hours. These changes are due to to progressive degradative action of enzymes on the lethally injured cell N.B. necrosis describes the morphologic changes and is not a type of cell death i.e. it is an appearance not a process.

20

Describe the appearance of coagulative necrosis. When does it occur?

It occurs in most solid organs when the cause of death is ischameia.

21

Describe the appearance of liquefactive necrosis. When does it occur?

It occurs when cell death is associated with large numbers of neutrophils -> release of their proteolytic enzymes

22

Describe the appearance of caseous necrosis. When does it occur?

This is a special type of necrosis that only occurs under certain circumstances. It looks like soft cheese to the naked eye and is characterised by amorphous (structureless) debris. It is particularly associated with infections, especially TB. When this pattern of necrosis is seen it is often associated with a particular form of inflammation known as "granulomatous".

23

Describe the appearance of fat necrosis. When does it occur?

This occurs when there is destruction of adipose tissue. It is most typically seen in acute pancreatitis, where lipases are released which acts on the adipose tissue of the pancreas and fat elsewhere in the abdominal cavity.
Fat necrosis causes the release of free fatty acids which can react with calcium to form chalky deposits (calcium soaps) in fatty tissue. These can be seen by naked eye and on X-ray.
Fat necrosis can also occur due to direct trauma to fatty tissue, especially breast tissue. After it heals it can leave an irregular scar that can mimic breast cancer.

24

Define apoptosis

Cell death with SHRINKAGE. Cell death induced by a regulated intracellular program where a cell activates enzymes that degrades its own nuclear DNA and proteins. This is an ENERGY DEPENDENT process.

25

Describe the process of apoptosis and appearance under the light and electron microscope

Light microscope - shrunken and intensely eosinophilic cells, chromatin condensation, pyknosis and karyorrhexis are seen.
Electron microscope - cytoplasmic BUDDING (not blebbing as in oncosis) which progresses to fragmentation into apoptotic bodies containing organelles, cytoplasm and often nuclear fragments. These are eventually removed by macrophage phagocytosis.

26

How does necrosis and apoptosis differ?

Necrosis is the morphologic appearance of dead cells under the microscope and is therefore an appearance not a process. Apoptosis is a process of intracellular programmed cell death.

27

Define gangrene

A clinical term for necrosis that is visible to the naked eye.

28

What types of gangrene are there? What are their differences?

Dry - necrosis is modified by exposure of air -> drying )
Wet - infection with a mixed bacterial culuture

29

Define infarction

An area of cell death (ischaemic necrosis) caused by obstruction of a tissue's blood supply.

30

What types of infarction are there? In general why do infarcts occur?

Red and white infarcts. Most infarctions are due to thrombosis or embolism. They can occasionally be caused by external compression of a vessel (e.g. by a tumour or within a hernia) or by twisting vessels (volvolus or testicular torsion).