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Miscellaneous > MCB Lecture 57 Cell Death > Flashcards

MCB Lecture 57 Cell Death Flashcards

0
Q

Describe necrosis

A

This is the morphological features of cells after it has died due to a pathological injury

The cell did not control the death

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1
Q

What are the two modes of cell death?

A

Apoptosis and Necrosis

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2
Q

What is apoptosis?

A

Apoptosis is the highly controlled and regulated death of a cell

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3
Q

What causes cell death by necrosis?

What causes cell death by apoptosis?

A

Necrosis: pathological stress

Apoptosis: physiological or pathological

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4
Q

Describe the morphology of necrotic cells

A 
Increased eosinophilia staining
Nucleus: pyknosis, karyolysis, karyorrhexia
Myelin figures
Membranes are burst
Organelles have been digested
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5
Q

What are myelin figures, and when are they produced?

A

Myelin figures are whorls of phospholipid from the cell membrane that has been disrupted

They are produced in irreversible cell damage

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6
Q

Describe the different morphologies of the nucleus that are seen in necrosis

A

Karyolysis: nucleic acid has been degraded (decreased basophilia)
Pyknosis: condensation of the nucleic acid (increased basophilia)
Karyorrhexia: fragmentation of the nucleic acid

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7
Q

What does the appearance of necrotic tissue depend on?

A

Depends on which type of necrosis has occured, ie. coagulation or digestion of the protein in the tissues

Balance between coagulation and liquefactive

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8
Q

What are the six types of necrosis?

A 
Coagulative
Liquefactive
Caseous
Fat necrosis
Fibrinoid
Gangrenous
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9
Q

What causes coagulative necrosis?

A

Severe ischemia

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10
Q

What causes liquefactive necrosis?

A

Bacterial or fungal infection

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11
Q

What causes caseous necrosis?

A

Mycobacterium tuberculosis infection

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12
Q

What causes fat necrosis?

A

Acute pancreatitis

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13
Q

What causes fibrinoid necrosis?

A

Immune vasculitis

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14
Q

What causes gangrenous necrosis?

A

Blood supply to a lower extremity is cut off

Bacterial infection (wet necrosis)

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15
Q

Describe the features of coagulation necrosis

A

Denaturant ion of the enzymes within cells
Cell architecture is maintain
Cells are dead, nucleus is gone

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16
Q

Describe the features of liquefactive necrosis

A

Digestion of the proteins of cells
Cell architecture is gone
Fluid filled cysts form

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17
Q

Ischemia in the brain leads to which type of necrosis?

What is the morphology?

A

Liquefactive, a fluid filled cyst forms

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18
Q

Where does coagulative necrosis mostly occur?

A

Solid organs

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19
Q

What are the features of caseous necrosis?

A

This is when both liquefactive and coagulative are occurring
The tissue has a crumbly texture like cheese
The tissue architecture is lost

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20
Q

What is happening in fibrinoid necrosis?

A

Proteinaceious material is deposited in the tissue matrix and fibrin plugs in the blood vessels

Deposition of immune complexes in the blood vessels

21
Q

Where does fibrinoid necrosis occur?

A

In the tissue matrix and in the lumen of blood vessels

22
Q

Where does gangrenous necrosis occur?

A

Extremities, eg. Feet

23
Q

What is wet gangrene

A

This is when there is liquefactive necrosis occurring as well, in response to a bacterial infection

24
Q

What is going on in gangrene?

A

Blood supply to the extremity is lost, and the cells undergo coagulative necrosis (and sometimes liquefactive)

25
Q

Describe the morphology of cells undergoing apoptosis

A 
Cell shrinks in size
Nucleus condenses and fragments
Apoptotic bodies form
Organelles are digested 
Cytoplasmic is intensely eosinophilic
26
Q

Which physiological stimuli cause apoptosis?

A

a. Embryogenesis: eg. Developing digits
b. Involution: shrinking of an organ, eg. Uterus after pregnancy
c. Removing cells at their use by date
d. Autoreactive T lymphocytes
e. CD8+ killing

27
Q

Which pathological stimuli cause apoptosis?

A

a. Growth factor deprivation
b. DNA damage
c. Accumulation of misfolded protein
d. Infection
e. Atrophy

28
Q

What are the two apoptotic pathways?

A

Intrinsic: Mitochondrial
Extrinsic: Death receptor

29
Q

What are the stimuli for the intrinsic pathway?

A

a. DNA damage
b. Misfolded protein
c. GF withdrawal

30
Q

Describe the intrinsic apoptotic pathway

A
  1. Stimulus detected by Bcl-2 family receptor
  2. Activation of Bcl family effectors (Bax, Bak)
  3. Signalling to mitochondria to
    4a. Release cytochrome c
    4b. Release pro-apoptotic proteins
  4. Initiator caspases

Regulation:
Bcl-2 and Bcl-x

31
Q

Which stimuli activate the extrinsic pathway?

A

Cytotixic T cell killing (Fas, Fas-l)

Removal of autoreactive lymphocytes

32
Q

Describe the death receptor pathway

A 
1. Ligand - receptor interaction
Fas & Fas-L
TNF & TNF-Receptor
2. Adaptor proteins
3. Initiator caspases
33
Q

Where do the two apoptotic pathways converge?

A

At the initiator caspases

34
Q

Can the two cell death pathways coexist?

A

Yes they often do

35
Q

What is inflammation?

A

Response to eliminate the cause and consequence of injury

36
Q

What happens if we don’t have inflammation?

A

A wound or injury will never heal

37
Q

Which suffix denotes inflammation

A

-itis

38
Q

What is fat saponification, and when does it occur?

A

Fat saponification is the break down of the membranes of fat cells, releasing fatty acids

The fatty acids combine with extracellular calcium to form the patchy white lesions

39
Q

What is Bcl-2, Bax, Bak and Bcl-x?

A

Bcl-2: B-cell lymphoma receptor, receptor in the intrinsic pathway of apoptosis

Bax: Bcl-2 associated X protein
Bak: Bcl-2 homologous antagonist killer
These are effector proteins of apoptosis

Bcl-x negative inhibitor

40
Q

Describe the apoptotic pathway after the convergence of the signals

A
  1. Initiator caspases
  2. Executioner caspases
  3. Degredation of protein (nuclear, cytosolic, membrane, cytoskeleton)
  4. Formation of apoptotic bodies
  5. Phagocytosis of the apoptotic bodies
41
Q

What stimulation do phagocytes get to come and eat the apoptotic bodies?

A
  1. Dying cells release factors that attract phagocytes

2. Phosphatidyl serine flip detected

42
Q

Compare the organelles in reversible and necrosis

A

Reversible: swollen
Necrosis: digested

43
Q

Compare the cell membrane in reversible and necrosis

A

Reversible: blebs
Necrosis: discontinuous

44
Q

Compare the mitochondria in reversible and irreversible

A

Reversible: swollen
Irreversible: lost the membrane potential & cytochrome c

45
Q

Which is the most common type of necrosis?

A

Coagulative

46
Q

DNA damage is one of the stimuli for the intrinsic pathway of apoptosis.
Describe how this may occur

A
  • Radiation
  • UV damage
  • Infection
  • Hypoxia
  • ROS
47
Q

Why is cell death triggered when there is DNA damage?

A

To prevent propagation of the mutated DNA

48
Q

Misfolded proteins are one of the triggers of the intrinsic apoptosis pathway.

How does this arise?

A
  • Mutation

- Extrinsic factors

49
Q

Compare cell size in apoptosis and necrosis

A

Apoptosis: shrunken
Necrosis: swollen

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