Brainscape's Knowledge GenomeTM

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


See full index

Microbiology of Disease > Mechanisms of the disease two: cell death and cell damage > Flashcards

Mechanisms of the disease two: cell death and cell damage Flashcards

You may prefer our related Brainscape-certified flashcards:
Biology 101 flashcards
1
Q

What are the function of necrosis?

A

-removes damaged cells from an organism

-otherwise it can lead to chronic inflammation
necrosis causes acute inflammation to clear cell debris via phagocytosis.

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

What are the causes of necrosis?

A
  • usually due to a lack of blood
    example:
    injury
    infection
    cancer
    infarction
    inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What would be the mechanism of necrosis?

A
  1. An injurious agent or event - whole group of cells are affected
  2. The initial events are reversible unlike the later ones
  3. Lack of oxygen will prevent the ATP production
  4. Cell will swell because of the influx of water
    Because ATP is required for ion pumps to work.
  5. Lysosomes rupture: enzymes degrade other organelles and nuclear material hapzardly.
  6. Cellular debris released and this triggers inflammation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Necrosis step by step process brief

A
  1. Normal
  2. Reversible swelling
  3. Irreversible swelling: mitochondrial changes,changes in the pattern conserved
  4. Swelling- disintegration and membrane breakdown
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Microscopic appearance of necrosis:

What are the nuclear changes?

A
  1. Chromatin condensation/shrinkage
  2. Fragmentation of nucleus
  3. Dissolution of the chromatin by DNAs.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Microscopic appearance of necrosis:

What are the cytoplasmic changes?

A
  1. Opacification: protein denaturation and aggregation

2. complete digestion of cells by enzymes causing cell to liquify (liquefactive necrosis)

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

Microscopic appearance of necrosis:

What are the biochemical changes?

A
  1. release of enzymes such as creatine kinase or lactate dehydrogenase
  2. release of other protein such as myoglobin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the function of apoptosis?- what is it involved in

A

selective process for the deletion of superfluous infected and transformed cells

involved in: embryogenesis, metamorphosis, normal tissue turnover, endocrine dependent tissue atrophy, a a variety of pathological condition

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

What is the mechanism of apoptosis?

A
  1. programmed cell death of one or a few cells
  2. events are irreversible and energy (ATP) dependent
  3. Cells shrink as the cytoplasm is disassembled
  4. Orderly packaging of organelles and nuclear fragments into membrane bound vesicles.
  5. New molecules are expressed on the vesicle membranes that stimulate phagocytosis without an inflammatory response.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Microscopic appearance of apoptosis:

What are the cytoplasmic changes?

A
  1. shrinkage of the cell. organelles packed into membrane vesicles
  2. cell fragmentation. membrane bound vesicles bud off
  3. Phagocytosis of cell fragments by macrophages and adjacent cell.
  4. No leakage of cytosolic compartments
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Microscopic appearance of apoptosis:

What are the nuclear changes?

A
  1. nuclear chromatin condenses on nuclear membrane

2. DNA cleavage

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

Microscopic appearance of apoptosis:

What are the biochemical changes?

A
  1. expression of charged sugar molecules on outer surface of cell membranes (recognised by macrophages to enhance phagocytosis)
  2. Protein cleavage by proteases, caspases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the factors which causes?

A

SURVIVAL: cell-cell and/or cell matrix contacts, growth factors and cytokines
APOPTOSIS: disruption of cell to cell contacts, lack of growth factors, DNA damaging agents and death domain ligands

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

What are the two types of apoptosis?- what are the key features of them ?

A

INTRINSIC:

  • DNA damage - p53 dependent pathway
  • interruption of the cell cycle
  • inhibition of protein synthesis
  • virus infection
  • change in redox state

EXTRINSIC:

  • withdrawal of survival factors -e.g mitogens
  • extracellular signals (e.g TNF)
  • T cell or NK (natural killer)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are caspases and what do they do?

A

capases are cysteine pro teases.

  • They are the point of convergence for the causes of apoptosis.
    Intrinsic and extrinsic causes will cause the activation of the caspases and this will reuslt in apoptosis.

-caspases they will form an activation cascade where one will cleave and activate the next.

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

Caspases and their substrates

A
  • hundreds of substrates for activated caspases

- substrates fall into most classes of important genes

17
Q

What is the effect of caspase activation?

A

caspase activation leads to characteristic morphological changes such as shrinkage and chromatin condensation, DNA fragmentation and plasma membrane blebbing

18
Q

How do we activate the initiator caspases?

A
  • initiator capases activate themselves when in close proximity
  • activation means bringing the caspases together.
19
Q

Describe the process of extrinsic apoptosis?

A

-induced by ligand binding to receptors, causing receptor dimerisation

20
Q

Extrinsic apoptosis:
Ligand induced multimerisation: The players

Explain the pathway of extrinsic apoptosis?

A 
Receptor is made from:
- ligand binding 
-death domain 
Death adaptor is made from:
-death domain 
-death effector domain 
Procaspase-8 contains the death effector domain.
  1. The ligand binds onto the receptor at the ligand binding site.
  2. The receptor contain a death domain
  3. You have a death adaptor molecule which will be able to bind to the receptor as they both will contain a death domain.
  4. The death adaptor molecule as well as the death domain contains a death effector domain which will bind to the death effector domain of pro caspase 8.
  5. The binding of these components will induce the release of a death inducing signalling complex (DISC).
  6. The death inducing signalling complex will covert the procaspase 8 to caspase 8.
21
Q

Explain the extrinsic pathway of TNF ?

A
  1. You start with the tumour necrosis factor.
  2. This will bind onto the tumour necrosis factor receptor which contains the death domain.
  3. The receptor will then bind to a FADD (FAS associated protein with the death domain).
  4. The FADD contain a death effector domain which will bind to the death effector domain of Pro caspase 8.
  5. The binding of these components will result in the production of death inducing signalling complex.
  6. Through autoproteoloysis (?) you will have the change from pro caspase 8 to caspase 8.
22
Q

What is intrinsic apoptosis induced by?

A
  • Induced by cytochrome C released from the mitochondria

Microbiology of Disease (5 decks)

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