Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Foundations Of Medicine 1 > Cell Injury > Flashcards

Cell Injury Flashcards

1
Q

Types of necrosis

A

Coagulative
Colliquative
Caseous
Grangrenous
Fat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Coagulative necrosis

A

Tissue with connective tissue —> basic arrangement preserved

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Colliquative necrosis

A

Tissue with minimal connective tissue —> ‘liquifies’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Caseous necrosis

A

‘Cheese’-like necrotic debris contained within

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Grangrenous necrosis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Fat necrosis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Causes of cell injury

A

O2 deprivation
Trauma
Microbial
Immunological
Chemical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Hypoxia

A

Low O2 to tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Ischaemia

A

Decreased O2 to part of the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Free radical

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Atrophy

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Hypertrophy

A

Increase in size of cells and organ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Hyperplasia

A

Increase in number of cells in an organ/tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Metaplasia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Forms of cell death

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Example of Coagulative necrosis

A

MI

17
Q

Example of caseous necrosis

A

Tuberculosis (TB)

18
Q

Example of colliquative necrosis

A

Focal bacterial infections —> accumulation of pus, liquefies tissue

Often in brain

19
Q

Example of Grangrenous necrosis

A

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

20
Q

Autolysis

A

Lysis of tissues by their own enzymes —> death

“Rotting of the tissue”

21
Q

Primary and secondary healing/repair intention

A

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

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

22
Q

Regeneration of labile cells

A

Good capacity to regenerate

eg. Surface epithelial cells

23
Q

Regeneration of stable cells

A

Divide at slow rate, but can regenerate if needed

eg. Hepatocytes in liver

24
Q

Regeneration of permanent cells

A

Unable

eg. Nerve cells, striated muscle cells

25
Q

Bacterial exotoxins

A

Chemicals released by bacteria which stimulate inflammation

26
Q

Bacterial endotoxins

A

Associated with bacterial cells walls, also stimulate inflammation

27
Q

Tissue necrosis

A

Dead tissue releases peptides

Triggers acute inflammation

28
Q

Cardinal signs of acute inflammation

A

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

29
Q

Stages of inflammation

A
  1. Release of chemical mediators
  2. Vasodilation
  3. Increased vascular permeability
  4. Fluid accumulation
  5. Cellular recruitment
  6. Phagocytosis
30
Q

Cellular exudation

A

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

31
Q

What can neutrophils do

A

Move/migrate
Bind to opsonised microorganisms
Phagocytosis

32
Q

Emigration

A

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

33
Q

What are the early chemical events of inflammatory response

A

Histamine and thrombin released

Up regulation of platelet activating factor (PAF) on endothelial cells

Neutrophil adhesion to endothelial surface

34
Q

Histamine

A

Causes vascular dilation and permeability

Released by mast cells

35
Q

Chemokines

A

Chemicals (types of cytokines) which attract more WBC to site of inflammation

eg. IL-8 attracts neutrophils

36
Q

Coagulation system in plasma

A

Converts soluble fibrinogen into fibrin

37
Q

Benefits of inflammation

A

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

38
Q

Harmful effects of inflammation

A

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

Foundations Of Medicine 1 (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions