Types of Cell Death Flashcards

(85 cards)

1
Q

What are the types of cell death?

A
  • Autophagy
  • Apoptosis
  • Mitoptosis
  • Necroptosis
  • Necrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How can autophagy be classified?

A
  • As “self-eating”
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q
  • Can components be “recycled” in autophagy?
A

YES

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

How is autophagy induced? (4)

A
  • Starvation
  • Oxidative stress
  • Misfolded proteins
  • ATP at the start of reperfusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are three types of autophagy?

A
  • Chaperone-mediated
  • Microautophagy
  • Macroautophaghy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How to AMPK and mTOR affect autophagy? When is either of them activated/inhibited?

A
  • AMPK will increase when nutrients and energy are low in order to regulate energy homeostasis
  • mTOR is inhibited when nutrients and energy are low to regulate growth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How can mitoptosis be classified?

A
  • as programmed elimination of the mitochondria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What leads to mitoptosis? (4)

A
  • Mitochondrial dysfunction (and therefore ROS)
  • Loss of membrane potential
  • Apoptotic signals or loss of components (via MPTP)
  • Disruption of the ETC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the two possibilities from mitoptosis?

A
  • All of mitochondria is removed OR only some of the mitochondria is removed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How can necroptosis be classified?

A
  • As a form of programmed cell death controlled by death signals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are released due to necroptosis?

A
  • DAMPs (damage associated molecular patterns)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are RIPK?

A
  • Receptor Interacting Protein Kinases

- Family of serine/threonine and tyrosine kinases

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

What is MLKL?

A
  • Mixed Lineage Kinase domain-like proteins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the necroptotic pathway?

A
  • RIPK will attach to MLKL and break through the plasma membrane, releasing DAMPs and causing inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the extrinsic apoptotic pathway called? How does it work?

A
  • The death receptor pathway (contains death ligands and receptors)
  • Activates caspases leading to proteolysis (breakdown of proteins)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the intrinsic apoptotic pathway called? How does it work?

A
  • The mitochondrial pathway

- Activates pro-apoptotic family BCI-2 when activated

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

What physiological process of apoptosis aids development?

A
  • Sculpting of tissues during development
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What physiological process of apoptosis aids in changes after childbirht?

A
  • Involution of cells in hormone-dependent tissues
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are two more physiological processes of apoptosis?

A
  • normal cell destruction followed by replacement

- involution of thymus

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

What are some pathological process of apoptosis?

A
  • Cell death in tumors via chemotherapeutics
  • Degenerative diseases in the CNS such as Alzheimer’s
  • Heart diseases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How can you identify an apoptotic cell? (4)

A
  • Stain chromatin to view condensation
  • Flow cytometry to visualize rapid cell shrinkage
  • DNA changes detected by gel electrophoresis
  • Using a marker for cell membranes with phosphatidylserine on the exterior
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the significance of phosphatidylserine on the outer leaflet of the cell membrane?

A
  • This serves as an “eat me” signal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the three mechanisms of apoptosis?

A
  1. initiation
  2. activation of caspases
  3. phagocytosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are three ways in which initiation can occur for apoptosis?

A
  • Withdrawal of signals that are required for cell survival
  • Extracellular signals (activation of FAS receptor)
  • Intracellular signals (heat, radiation, hypoxia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
How is the activation of caspases relevant in the mechanisms of apoptosis?
- Caspases are proteolytic enzymes that act on nuclear proteins and organelles (breakdown proteins in cell)
26
How is phagocytosis relevant in the mechanisms of apoptosis?
- Will respond to phosphatidylserine on the outer surface of apoptotic cells to engulf cell
27
What is necrosis by definition? What is it followed by?
- Localized tissue death | - Followed by degradation via hydrolytic enzymes from dead cells
28
What is necrosis always accompanied by?
- An inflammatory reaction
29
What are some causes of necrosis?
- Hypoxia, chemical/physical agents, microbial agents, immunological injury
30
Is necrosis reversible?
NO
31
What types of irreversible nuclear damage does necrosis cause?
- Pyknosis - Karyorrhexis - Karyolysis
32
What is pyknosis?
- Shrinking of the nucleus
33
What is Karyorrhexis?
- Nuclear fragmentation
34
What is karyolysis?
- Dissolution of chromatin
35
What are the five types of necrosis?
1. Coagulative 2. Liquefactive 3. Caseous 4. Fat 5. Fibrinoid
36
What type of necrosis is the most common?
Coagulative
37
Where does coagulative necrosis commonly affect?
- Heart, kidney, and spleen
38
What are the most common and least common causes of coagulative necrosis?
- most often from ischemia | - less often from bacteria and chemicals
39
What are the causes of liquefactive necrosis?
- Ischemia | - Bacterial or fungal infection
40
How does degradation occur in liquefactive necrosis?
- Via hydrolytic enzymes
41
What does liquefactive necrosis cause in the brain?
- Brain infarct and abscesses
42
In what disease can you see caseous necrosis occurring?
- Tuberculosis infection
43
TRUE/FALSE: Caseous necrosis has features of both liquefactive and coagulative necrosis.
- TRUE
44
What does fat necrosis cause?(Hint: in pancreas and breast)
- Causes acute pancreatic necrosis and traumatic fat necrosis in the breast
45
What does the pancreas secrete in fat necrosis?
- The pancreas will secrete lipase which will lead to necrosis
46
What is the mechanism of fat necrosis in adipose cells?
- Fat will hydrolyze into glycerol and FFAs | - FFAs will complex with calcium to disintegrate membranes
47
What is the complex between FFAs and calcium called?
- Calcium soaps via saponification
48
What is fibrinoid necrosis?
- The deposition of fibrin-like material
49
What type of injury causes fibrinoid necrosis?
- Immunologic tissue injury (e.g. autoimmune disease)
50
How can a peptic ulcer arise from fibrinoid necrosis?
- Arterioles are in hypertension
51
What can gangrene be the result of?
- Coagulative necrosis and putrefaction
52
Where does wet gangrene begin? Where could it spread to?
- Naturally moist tissues and organs such as the mouth, bowel etc... - could spread to peritoneal cavity
53
What is the mechanism of wet gangrene?
- Venous obstruction
54
Does wet gangrene develop slow or rapidly?
Rapidly
55
What is the relationship between wet gangrene and bacterial growth?
- Affected parts fill with blood, favouring bacterial growth
56
How can wet gangrene lead to septicemia or death?
- If toxic products are absorbed
57
Where does dry gangrene begin?
- The distal part of a limb | Furthest from blood supply
58
Does dry gangrene spread rapidly or slowly? When does it stop?
- Spreads slowly | - Stops when reaches a point where blood supply is adequate to keep tissue viable (line of separation)
59
What is the mechanism of dry gangrene?
- Arterial occlusion caused by ischemia
60
What is the relationship between bacteria and dry gangrene?
- There is typically little bacterial growth
61
Why does dry gangrene produce a black colour?
- Result of iron sulfide | - Product of hemoglobin and bacteria
62
What is gas gangrene a special form of?
- Wet gangrene
63
What is gas gangrene?
- A gas-forming clostridia (gram-positive and anaerobic bacteria)
64
How does gas gangrene enter tissues?
- Through wounds | - Especially in muscles
65
What can cause gas gangrene?
- Complications of colon operation
66
What is the mechanism of gas gangrene?
- Produces various toxins --> local necrosis and edema --> absorption --> systemic manifestations
67
Other than gangrene, what is another after-effect of necrosis?
- Calcification
68
What are the two types of calcification?
- Dystrophic | - Metastatic
69
What is the main characteristic of dystrophic calcification?
- There are normal calcium metabolism and serum calcium levels - it is the tissue that is the problem
70
What are the two main types of dystrophic calcification?
1. Deposition of calcium in dead tissue | 2. Deposition of calcium in degenerated tissue
71
How does the obstruction of venous flow in Gamna-Gandy bodies in dead tissue affect products in the body?
- Gamna-Gandy bodies will release hemosiderin | - Hemosiderin will combine with calcium and fibrous tissue
72
What is an example of dystrophic calcification in degenerated tissue?
- Atheromas in the aorta and coronary | - Fatty streak eventually forms a plaque where calcification occurs
73
Which is the following is NOT a part of calcification in degenerated tissue? - Stroma of tumours - long-term cysts - hematomas in the vicinity of bones
- Hematomas in the vicinity of bones (occurs in dead tissue)
74
What is the main characteristic of metastatic calcification?
- There is disturbed calcium metabolism and hypercalcemia | - Tissues are normal
75
What are the two major causes of metastatic calcification?
- Excessive mobilization of calcium from bone | - Ingesting too much calcium
76
What are the causes of excessive mobilization of calcium from the bone?
- Hyperthyroidism - Bony lesions - Prolonged immobilization
77
What are the two types of hyperthyroidism?
- Primary: parathyroid adenoma (cancer) | - Secondary: Parathyroid hyperplasia (chronic renal failure)
78
What are bony lesions?
- Multiple myeloma (can invade bone) | - Metastatic carcinoma
79
What does prolonged immobilization cause?
- Atrophy of bones, resulting in hypercalcemia
80
What are some examples of ingesting too much calcium?
- Hypervitaminosis D: causes increased calcium absorption - Milk-alkali Syndrome: excessive intake of calcium + calcium carbonate - Hypercalcemia of infancy
81
What is the cause of hypercalcemia in infancy? What happens because of the root problem?
- Caused by gene mutations | - Causes impaired breakdown of vitamin D and reduced phosphate levels (activates more vitamin D and thus calcium)
82
What is the pathogenesis of dystrophic calcification? It is reversible?
- Unclear - Could be due to denatured proteins binding to phosphate ions and reacting with calcium - This causes calcium phosphate precipitates - typically not reversible
83
What is the pathogenesis of metastatic calcification? Is it reversible?
- Excess binding of inorganic phosphate ions with elevated calcium ions to form calcium phosphate precipitate - typically reversible
84
What are some sites that metastatic calcification occurs? (6)
- Kidneys - Lungs (alveolar walls) - Stomach - Blood vessels - Cornea - Synovium (joints)
85
Why are these common sites for metastatic calcification to occur at?
- They are mostly alkaline | - Calcium fairs better in an alkaline environment