Brainscape's Knowledge GenomeTM

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


See full index

Mechanisms of Disease > Cell Injury and Acute Inflammation (week 2) > Flashcards

Cell Injury and Acute Inflammation (week 2) Flashcards

1
Q

Increased cellular activity leads to:

A

1) hyperplasia: more cells produced

2) hypertrophy: cells increase in size

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

Decreased cell activity leads to:

A

Cell atrophy: cells decrease in size

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

Metaplasia definition:

A

Transformation of one type of differentiated cell into another fully differentiated type

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

What are the 4 different mechanisms of cell injury

A

1) Failure of membrane function e.g. ion pump damage
2) Blockage of metabolic pathwyas e.g. iterruption of protein synthesis
3) DNA damage or loss e.g. due to ionising radiation
4) Mechanical trauma e.g. due to osmotic pressure

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

How does ionising radiation cause damage to cells?

A

Generation of free radicals, direct damage to thymine dimers in DNA

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

What is the defence mechanism against ionising radiation?

A

Exonuxcleases

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

How do free radicals damage cells?

A

Remove electrons from molecules and break important bonds

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

What is apoptosis?

A

Programmed, planned cell death

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

Does apoptosis damage adjacent cells?

A

No

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

Does apoptosis cost energy?

A

Yes

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

What is necrosis?

A

Unplanned, catastrophic cell death that is always pathological

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

What causes necrosis?

A

Cell injury

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

Does necrosis cost energy?

A

No

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

What impact does necrosis have on surrounding cells?

A

Causes release of harmful substances which damage many cells at once

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

Name some physiological uses for apoptosis:

A

embryogenesis

destruction of self-reacting lymphocytes

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

How can dysfunction of apoptosisbe carcinogenic?

A

Cells can accumulate e.g. in follicular lymphoma: anti-apoptotic BCL-2 gene is over expressed –> apoptosis is inhibited

17
Q

Describe coagulative necrosis:

A

Commonest form - dead tissue becomes firm and swollen and retains microscopic structure. Typical of ischaemic injury.

18
Q

Describe colliquative necrosis:

A

Occurs in neural tissues - have little supporting structure therefore liquifies on death. Site becomes marked with a cyst.

19
Q

Describe caseous necrosis

A

Granulomatous inflammation. Dead tissue lacks any structure. Characteristic of TB.

20
Q

What is dry gangrene?

A

Form of coagulative necrosis that develops in ischaemia. Limited O2 supply limits putrefaction, bacteria cannot survive. Chronic ischaemia without infection.

21
Q

What is wet gangrene?

A

Develops rapidly due to blockage of blood. Stagnant blood allows rapid growth of bacteria, which produce toxic products which are then absorbed, causing sepsis. Requires amputation/

22
Q

What is a neutophil polymorph?

A

Characteristic cell of acute inflammation - characterised by multi-lobed nuclues

23
Q

What are the 5 physical characteristics of acute inflammation?

A 
Rubor: redness
Calor: heat
Tumor: swelling
Dolor: pain
Functio laesa: loss of function
24
Q

What are the 3 major components of acute inflammation?

A
  1. Changes in vessel calibre
  2. Increased vascular permeability and fluid exudate formation
  3. Cellular exudate formation
25
Q

What is exudate?

A

extravascular fluid with high protein concentration, contains cellular debris

26
Q

What is transudate?

A

Fluid with low protein concetration, no cellular contents

27
Q

What is oedema?

A

Excess fluid in interstitial tissue. Can be transudate or exudate

28
Q

What mediates vasodilation?

A

Histamine and NO on vascular smooth muscle

29
Q

What is suppuration?

A

Pus formation

30
Q

What is an abscess?

A

Collection of pus trapped within body

31
Q

3 types of reaction that make up an acute inflammatory response are vascular, exudative, and?

A

Cellular

32
Q

Category of death that must be reported to the coroner?

A

Unnatural

33
Q

Necrosis with putrefaction?

A

Gangrene

34
Q

The abnormal development or degeneration of a tissue

A

Dystrophy

35
Q

Cell type that is able to secrete chemical mediators of acute inflammation

A

Macrophage

Mechanisms of Disease (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions