Cell Injury

Question 1

Types of necrosis

Answer 1

Coagulative
Colliquative
Caseous
Grangrenous
Fat

Question 2

Coagulative necrosis

Answer 2

Tissue with connective tissue —> basic arrangement preserved

Question 3

Colliquative necrosis

Answer 3

Tissue with minimal connective tissue —> ‘liquifies’

Question 4

Caseous necrosis

Answer 4

‘Cheese’-like necrotic debris contained within

Question 5

Grangrenous necrosis

Answer 5

DRY – sterile coagulative necrosis e.g. distal limb
WET - coagulative necrosis with superimposed infection

Question 6

Fat necrosis

Answer 6

Focal necrosis in fat due to action of lipases (also trauma)

Question 7

Causes of cell injury

Answer 7

O2 deprivation
Trauma
Microbial
Immunological
Chemical

Question 8

Hypoxia

Answer 8

Low O2 to tissues

Question 9

Ischaemia

Answer 9

Decreased O2 to part of the body

Question 10

Free radical

Answer 10

An atom, molecule or ion with one or more unpaired valence electron

Question 11

Atrophy

Answer 11

Shrinkage in the size of a cell by the loss of cell substance

Question 12

Hypertrophy

Answer 12

Increase in size of cells and organ

Question 13

Hyperplasia

Answer 13

Increase in number of cells in an organ/tissue

Question 14

Metaplasia

Answer 14

Reversible change in which one adult cell type is replaced by another adult cell type

Question 15

Forms of cell death

Answer 15

APOPTOSIS - cell contents contained, no surrounding damage
NECROSIS - cell contents spill out, tissue damage

Question 16

Example of Coagulative necrosis

Answer 16

MI

Question 17

Example of caseous necrosis

Answer 17

Tuberculosis (TB)

Question 18

Example of colliquative necrosis

Answer 18

Focal bacterial infections —> accumulation of pus, liquefies tissue

Often in brain

Question 19

Example of Grangrenous necrosis

Answer 19

WET - GI tract, bacterial
DRY - Limbs (diabetic)

Question 20

Autolysis

Answer 20

Lysis of tissues by their own enzymes —> death

“Rotting of the tissue”

Question 21

Primary and secondary healing/repair intention

Answer 21

Primary - restitution with no/minimal residual defect (eg. Suturing leaving a fine scar)

Secondary - organisation and repair where there’s tissue loss, granulation tissue

Question 22

Regeneration of labile cells

Answer 22

Good capacity to regenerate

eg. Surface epithelial cells

Question 23

Regeneration of stable cells

Answer 23

Divide at slow rate, but can regenerate if needed

eg. Hepatocytes in liver

Question 24

Regeneration of permanent cells

Answer 24

Unable

eg. Nerve cells, striated muscle cells

Question 25

Bacterial exotoxins

Answer 25

Chemicals released by bacteria which stimulate inflammation

Question 26

Bacterial endotoxins

Answer 26

Associated with bacterial cells walls, also stimulate inflammation

Question 27

Tissue necrosis

Answer 27

Dead tissue releases peptides Triggers acute inflammation

Question 28

Cardinal signs of acute inflammation

Answer 28

Redness - vasodilation Heat - increased blood flow Swelling - accumulation of fluid Pain - physical distortion of tissue Loss of function

Question 29

Stages of inflammation

Answer 29

1. Release of chemical mediators 2. Vasodilation 3. Increased vascular permeability 4. Fluid accumulation 5. Cellular recruitment 6. Phagocytosis

Question 30

Cellular exudation

Answer 30

Increased vascular permeability Increased net flow of fluid out of vessels = exudation

Question 31

What can neutrophils do

Answer 31

Move/migrate Bind to opsonised microorganisms Phagocytosis

Question 32

Emigration

Answer 32

Cells (neutrophils) pass between endothelial cells, through basal lamina and into adventitia

Question 33

What are the early chemical events of inflammatory response

Answer 33

Histamine and thrombin released Up regulation of platelet activating factor (PAF) on endothelial cells Neutrophil adhesion to endothelial surface

Question 34

Histamine

Answer 34

Causes vascular dilation and permeability Released by mast cells

Question 35

Chemokines

Answer 35

Chemicals (types of cytokines) which attract more WBC to site of inflammation eg. IL-8 attracts neutrophils

Question 36

Coagulation system in plasma

Answer 36

Converts soluble fibrinogen into fibrin

Question 37

Benefits of inflammation

Answer 37

Dilution of toxins Entry of antibodies Transport of drugs Fibrin formation Delivery of nutrients and O2 Stimulation of immune response

Question 38

Harmful effects of inflammation

Answer 38

Digestion of normal tissue Swelling Inappropriate inflammatory response (eg. anaphylaxis)

Question 39

What is resolution

Answer 39

Everything is back to normal

Question 40

Outcomes of inflammation

Answer 40

Resolution Suppuration Scarring or fibrosis Chronic inflammation

Question 41

Suppuration

Answer 41

Formation of pus - mix of neutrophils, debris, bacteria If walled off = abscess

Question 42

How does granulation tissue form

Answer 42

New capillaries —> more macrophages —> proliferation of fibroblasts —> fibrosis or scarring

Question 43

What are neutrophils replaced by in the progression from acute to chronic inflammation

Answer 43

Lymphocytes

Question 44

Cells of chronic inflammation

Answer 44

Lymphocytes - small purple dots Plasma cells - fried eggs Macrophages - bigger blobby ones (Sometimes eosinophils) - tomatoes with sunglasses

Question 45

B lymphocytes

Answer 45

Meet antigens, turn into plasma cells Plasma cells then produce antibodies

Question 46

T lymphocytes

Answer 46

Killer T cells (CD8+) Helper T cells (CD4+)

Question 47

Killer T cells (CD8+)

Answer 47

Cytotoxic function, and recruiting other immune cells

Question 48

Helper T cells (CD4+)

Answer 48

Activate killer T and plasma cells

Question 49

What are cytokines

Answer 49

Small proteins which: Enhance cell mediated immunity Enhance antibody response

Question 50

Granuloma

Answer 50

A collection of histiocytes