Brainscape's Knowledge GenomeTM

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


See full index

AMP FPP > Cell Death > Flashcards

Cell Death Flashcards

1
Q

What is cell death

A

• The culmination of irreversible injury

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

What are the 2 types of cell death

A

• Necrosis
• Apoptosis (may be physiologic i.e. seen in non-diseased cells)

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

What is necrosis

A

results from denaturation of intracellular proteins and enzymatic digestion of the irreversibly injured cell.

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

The enzymes that digest the necrotic cells are from where

A

from the dying cell’s lysosomes as well as the lysosomes of adjacent white blood cells.

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

What causes inflammation in the dying cell

A

The dying cell loses its membrane integrity and cellular contents spill into surrounding tissues , this causes inflammation

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

changes in the necrotic cell may take hours to be morphologically visible, however, certain chemicals released from the injured cell may be detectable in body fluids . Give examples

A

M.I. & cardiac specific enzymes

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

Give 4 morphological features of a necrotic cells

A

• Increased eosinophilia (the pink colour of the cytoplasm). This is due to loss of cytoplasmic RNA which binds hematoxylin.
• Increased glassy appearance due to the loss of glycogen particles.
• Vacuolated cytoplasm due to enzyme digested cytoplasmic
organelles.
• Myelin figures: from dead cell or organellar membranes. The myelin
figures may be phagocytosed by other cells or degraded into fatty acids. These fatty acids may become calcified leading to the calcification of dead cells.

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

What are the 6 patterns of organ necrosis

A
  1. Coagulative necrosis
  2. Liquefactive necrosis e.g. C.N.S.
  3. Gangrenous necrosis e.g. Foot gangrene
  4. Caseous necrosis e.g. TB
  5. Fat necrosis e.g. pancreatitis, breast
  6. Fibrinoid necrosis e.g. blood vessels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What’s the most common type of necrosis

A

Coagulative Necrosis

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

Describe the affected organ or tissue in coagulative necrosis

A

• Affected tissue are firm because the injury denatures the enzymes
and prevents proteolysis of dead cells..
• The dead cell is eventually cleared by phagocytosis or digestion from
leukocytic enzymes

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

What is An area of localised coagulative necrosis called

A

Infarct

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

Describe the microscopic appearance of affected organs in coagulative necrosis

A

the cells retain their outlines, however the cytoplasmic and nuclear details are lost . The affected cells are swollen and more eosinophilic than usual.

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

What is is called when cells retain their outlines, however the cytoplasmic and nuclear details are lost in coagulative necrosis

A

Tombstone’/’Ghost’ appearance

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

What also causes liquefactive necrosis

A

ischaemic injury, bacterial/fungal infections. Microbes stimulate the accumulation of leukocytes and subsequent release of hydrolytic enzymes

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

What’s the shape of a coagulative infarct

A

Wedge shaped (point Of occlusion of vessels$

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

What enzymes help in the liquefactive necrosis

A

The cellular hydrolytic enzymes play a dominant role in the digestion of the affected cells creating semi-fluid material.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Examples of organs that undergo liquefactive necrosis

A

brain infarcts (CVA/”stroke”) and abscess (pus) cavities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What causes gangrenous necrosis

A

results from superimposed bacterial infection on a tissue which has lost its blood supply (coagulative necrosis). The bacterialinfection leads to more liquefactive necrosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Examples of gangrenous necrosis

A

diabetic foot gangrene, frostbite gangrene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What necrosis is Cheese-like

A

Caseous necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Where are Caseous necrosis characteristically found

A

Tuberculosis infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Describe the morphology of caseous necrosis

A

• Grossly: soft, granular, yellowish.
• Microscopically: characteristic granuloma (epithelioid cells, giant cells and peripheral cuff of lymphocytes) with central area of necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Describe the morphology of caseous necrosis

A

• Grossly: soft, granular, yellowish.
• Microscopically: characteristic granuloma (epithelioid cells, giant cells and
peripheral cuff of lymphocytes) with central area of necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Where is caseous necrosis characteristically found

A

Tuberculosis infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Describe the fat necrosis in pancreatitis
release of lipases from pancreatic acinar cells liquefy the membranes of adipocytes in the peritoneum. The released fatty acids can combine with calcium to form areas of saponification (chalk-white visible areas)
26
Describe fat necrosis in breast
seen with loss of blood supply to breast adipose tissue resulting in the death of the adipocytes and their digestion by macrophages. May mimic a carcinoma.
27
An example of Traumatic fat necrosis
Breast necrosis
28
Where is fibrinoid necrosis found
Seen in immune reactions involving blood vessels
29
What happens in fibrinoid necrosis
Deposition of Ab-Ag complexes on the blood vessel walls leading to activation of immune reactions against the wall components. E.g. is eosinophilic granulomatosis with polyangitis.
30
What is apoptosis
programmed cell death. Literally suicide
31
Examples of physiological apoptosis
• Embryogenesis • Involution of hormone dependent tissues after hormone withdrawal e.g. shedding of endometrial lining, reduction in breast size at the end of breast feeding • Involution of the thymus at an early age • Elimination of self-reactive lymphocytes either before or after maturation to prevent damage to body tissues • Death of cells which have served their function e.g. leukocytes after inflammation. The absence of necessary stimulatory signals induces apoptosis
32
What are the morphological changes in apoptosis
1. Cell shrinkage 2. Chromatin condensation under the nuclear membrane. The nucleus may be fragmented. 3. Formation of cytoplasmic blebs and apoptotic bodies 4. Phagocytosis of apoptotic bodies
33
What are the 2 steps in apoptosis
• Initiation phase: Caspases become active • Execution phase: Caspases trigger the degradation of cellular components
34
What are the 2 pathways for the initiation phase of apoptosis
• Intrinsic (mitochondrial) pathway • Extrinsic (death receptor-mediated) pathway
35
Example of antiapoptotic proteins
BCL-2 BCL-XL MCL-1
36
What leads to production of antiapoptotic proteins in a viable cell
Growth factors
37
What’s the function of antiapoptotic proteins
Anti-apoptotic proteins maintain the integrity of the mitochondrial membrane thus preventing leakage of apoptosis inducing proteins eg cytochrome c, SMAC
38
Give examples of pro apoptotic proteins
***BAX*** ***BAK*** Cytochrome C SMAC
39
What leads to the activation of pro apoptotic proteins
when a cell is injured or deprived of survival signals,anti-apoptotic proteins are inhibited while pro-apoptotic proteins (e.g. BAX, BAK) are activated. (By BH3 only proteins)
40
How is cytochrome C and SMAC let out of the mitochondria for apoptosis
Pro-apoptotic proteins create a channel in the outer mitochondrial membrane leading to leakage of cytochrome c and SMAC from the membranous space which activates the caspases.
41
What is SMAC
It’s a pro apoptotic protein in the mitochondria as well (inhibits antiapoptotic proteins) . DIABLO is also referred to as second mitochondria-derived activator of caspases or SMAC.
42
Through which mitochondrial pore are Cytochrome C and SMAC let out of
MPTP- mitochondrial permeability transport pore
43
What’s the function of BH3 only proteins
BH3-only proteins promote apoptosis by both directly activating Bax and Bak and by suppressing the anti-apoptotic proteins at the mitochondria and the endoplasmic reticulum (They sense cellular stress levels and regulate the proteins)
44
Examples of BH3 only proteins
BAD, BID, BIM, Puma
45
What’s another name for the intrinsic pathway of apoptosis
Mitochondrial pathway
46
How is procaspace 9 activates
APAF 1 and cytochrome c bind to form an apoptosome The APAF 1 portion of the apoptosome activates procaspace 9 into Caspace 9
47
What’s the relationship between SMAC and XIAP
XIAP is an inhibitor of apoptosis (inhibits caspace 9) ***BUT*** SMAC inhibits XIAP and allows caspace 9 go on with apoptosis
48
What does the caspase 9 activate
It goes on to activate caspase 3 and caspace 6 (and 7?)
49
What’s another name for the extrinsic pathway of the initiation phase of apoptosis
• Also called the death receptor-mediated pathway
50
What activates the extrinsic pathway of apoptosis
Activated following binding of a ligand to the death receptors on the plasma membrane.
51
What is TNF-alpha1
When macrophages see a bad cell, they release ***Tumor necrosis factor alpha 1 (TNF-alpha1)*** (for signaling) This binds to ***Tumor necrosis factor receptor (TNFR-1)***
52
What are the best know death receptors
TNFR1 and FAS
53
What happens when a ligand binds to the FAS
When the FAS ligand binds to the FAS, 3 or more molecules of FAS are brought together and their cytoplasmic death domains form a binding site for an adaptor protein that also contains a death domain called FADD (FAS associated death domain). The attached FADD then binds to a pro caspase 8 /10 via the death domain and activate it Activated Caspase 8 then activated caspase 3
54
What forms the DISC for a FAS receptor
Death domain + FADD
55
What type of cells under the FAS death receptor extrinsic pathway
This mechanism is seen in cytotoxic T-cell activity (kills virus infected and tumour cells) as well as on T-cells that recognise self-antigens (eliminate self-reactive lymphocytes)
56
What type of cells undergo the TNFR extrinsic pathway
Macrophages
57
What inhibits the FAS extrinsic pathway
A protein called FLIP which binds to pro caspase 8 Some viruses and normal cells produce FLIP and use it to protect themselves from FAS mediated apoptosis eg Herpes virus
58
What happens when the TNF-alpha (ligand) binds to the TNFR on the cell membrane
59
What happens in the execution phase of apoptosis
• Both the intrinsic and extrinsic initiator pathways converge on the same execution phase. • Activated caspase-8 (extrinsic pathway) and caspase 9 (intrinsic pathway) now activate caspases 3 & 6.
60
What does the activated caspase 3 and 6 do
• Activate DNAase which cleaves DNA • Degrade structural components of the nuclear matrix leading to nuclear fragmentation
61
What are the biochemical features of apoptosis
1. Activation of caspases: Caspases exist as inactive proenzymes. Functionally divided into 2: initiator (8 , 9) and executioner (3 , 6). 2. DNA & protein breakdown – this involves the action of Ca and Mg endonucleases which cleave DNA. Endonuclease activity is the basis for detection of cell death by cytochemical techniqies 3. Membrane alteration and recognition by phagocytes – the plasma membrane phospholipid orientation changes so that it is easily recognised by phagocytes. These phospholipids are easily recognised by Annexin V staining (immunohistochemistry).
62
What is the basis for detection of cell death by cytochemical techniqies
Endonuclease activity
63
How does the membrane alteration help recognition by phagocytes
Phosphatidyl serine is very prone to phagocytosis but is found on the inside of the membrane. during alteration, the membrane is flipped inside out so that the phosphatidyl serine is recognized easily by phagocytes and the cell undergoes phagocytosis
64
Give 5 examples of apoptosis
1. Deprivation of growth factors: e.g. hormones, antigens (lymphocytes), nerve growth factor (nerves). Occurs via the intrinsic pathway 2. DNA damage: this causes accumulation of p53 protein which in cases of excessive damage activates the intrinsic pathway of apoptosis. In the absence of p53 (Li Fraumeni syndrome), accumulation of damaged DNA may lead to cancer 3. Protein misfolding: Seen in neurodegenerative diseases e.g. Alzheimer’s, cystic fibrosis, Alpha1 antitrypsin disease. Misfolded proteins accumulate in the cytosol and lead to apoptosis. • 4. Extrinsic pathway (Fas/FasL): FasL on T cells bind Fas on neighbouring lymphocytes leading to destruction of T lymphocytes that recognise self-antigen. • 5. Cytotoxic T-lymphocytes: recognise foreign Ag on the surface of infected cells. The T-cells secrete perforin which forms pores in the membrane of the infected cells. The T-cell now secretes granzymes through the pores into the affected cell. Granzymes activate caspases.
65
What initiates intrinsic pathways
Radiation (DNA damage) Oxidative stress Mitochondria Deprivation of growth factors
66
What does the deficiency of p53 cause
Li Fraumeni syndrome
67
What disease can protein misfolding be seen
Alzheimer’s, cystic fibrosis, Alpha1 antitrypsin disease.
68
How does cytotoxic T cell perform apoptosis on foreign antigen in the body
Cytotoxic T-lymphocytes: recognise foreign Ag on the surface of infected cells. The T-cells secrete ***perforin*** which forms pores in the membrane of the infected cells. The T-cell now secretes ***granzymes*** through the pores into the affected cell. ***Granzymes activate caspases***.
69
Give 6 differences between apoptosis and necrosis
***Cell size*** NECROSIS: Enlarged (swelling) APOPTOSIS: Reduced (shrinkage) ***Nucleus*** NECROSIS: Pyknosis ➙ karyorrhexis ➙ karyolysis APOPTOSIS: Fragmentation into nucleosome-size fragments ***Plasma membrane*** NECROSIS: Disrupted APOPTOSIS: Intact; altered structure, especially orientation of lipids ***Cellular content*** NECROSIS: Enzymatic digestion; may leak out of cell APOPTOSIS: Intact; may be released in apoptotic bodies ***Adjacent inflammation*** NECROSIS: Frequent APOPTOSIS: No *** Physiologic or pathologic role*** NECROSIS: Invariably pathologic (culmination of irreversible cell injury) APOPTOSIS: Often physiologic, means of eliminating unwanted cells; may be pathologic after some forms of cell injury, especially DNA damage
70
What is necroptosis
• Resembles both necrosis and apoptosis • Sometimes called programmed necrosis
71
What’s the difference between necroptosis and apoptosis
I’m necroptosis, there’s no activation of caspases
72
Examples of necroptosis
Steatohepatitis, acute pancreatitis, back-up defense for apoptosis evading microbes e.g. CMV
73
What is autophagy
Cell eats its own contents.
74
Examples of autophagy
• Cancer • Neurodegenerative diseases e.g. Alzheimers • Infections e.g. Mycobacteria, HSV-1 • IBD • Intermittent fasting
75
Types of autophagy
Micro autophagy Macro autophagy Chaperone mediated autophagy

AMP FPP (6 decks)

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