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Integrative Phys > Types of Cell Death > Flashcards

Types of Cell Death Flashcards

1
Q

What are the types of cell death?

A
  • Autophagy
  • Apoptosis
  • Mitoptosis
  • Necroptosis
  • Necrosis
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2
Q

How can autophagy be classified?

A
  • As “self-eating”
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3
Q
  • Can components be “recycled” in autophagy?
A

YES

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4
Q

How is autophagy induced? (4)

A
  • Starvation
  • Oxidative stress
  • Misfolded proteins
  • ATP at the start of reperfusion
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5
Q

What are three types of autophagy?

A
  • Chaperone-mediated
  • Microautophagy
  • Macroautophaghy
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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
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7
Q

How can mitoptosis be classified?

A
  • as programmed elimination of the mitochondria
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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
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9
Q

What are the two possibilities from mitoptosis?

A
  • All of mitochondria is removed OR only some of the mitochondria is removed
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10
Q

How can necroptosis be classified?

A
  • As a form of programmed cell death controlled by death signals
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11
Q

What are released due to necroptosis?

A
  • DAMPs (damage associated molecular patterns)
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12
Q

What are RIPK?

A
  • Receptor Interacting Protein Kinases

- Family of serine/threonine and tyrosine kinases

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13
Q

What is MLKL?

A
  • Mixed Lineage Kinase domain-like proteins
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14
Q

What is the necroptotic pathway?

A
  • RIPK will attach to MLKL and break through the plasma membrane, releasing DAMPs and causing inflammation
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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)
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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

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17
Q

What physiological process of apoptosis aids development?

A
  • Sculpting of tissues during development
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18
Q

What physiological process of apoptosis aids in changes after childbirht?

A
  • Involution of cells in hormone-dependent tissues
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19
Q

What are two more physiological processes of apoptosis?

A
  • normal cell destruction followed by replacement

- involution of thymus

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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
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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
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22
Q

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

A
  • This serves as an “eat me” signal
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23
Q

What are the three mechanisms of apoptosis?

A
  1. initiation
  2. activation of caspases
  3. phagocytosis
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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)
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25
Q

How is the activation of caspases relevant in the mechanisms of apoptosis?

A
  • Caspases are proteolytic enzymes that act on nuclear proteins and organelles (breakdown proteins in cell)
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26
Q

How is phagocytosis relevant in the mechanisms of apoptosis?

A
  • Will respond to phosphatidylserine on the outer surface of apoptotic cells to engulf cell
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27
Q

What is necrosis by definition? What is it followed by?

A
  • Localized tissue death

- Followed by degradation via hydrolytic enzymes from dead cells

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28
Q

What is necrosis always accompanied by?

A
  • An inflammatory reaction
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29
Q

What are some causes of necrosis?

A
  • Hypoxia, chemical/physical agents, microbial agents, immunological injury
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30
Q

Is necrosis reversible?

A

NO

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31
Q

What types of irreversible nuclear damage does necrosis cause?

A
  • Pyknosis
  • Karyorrhexis
  • Karyolysis
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32
Q

What is pyknosis?

A
  • Shrinking of the nucleus
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33
Q

What is Karyorrhexis?

A
  • Nuclear fragmentation
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34
Q

What is karyolysis?

A
  • Dissolution of chromatin
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35
Q

What are the five types of necrosis?

A
  1. Coagulative
  2. Liquefactive
  3. Caseous
  4. Fat
  5. Fibrinoid
36
Q

What type of necrosis is the most common?

A

Coagulative

37
Q

Where does coagulative necrosis commonly affect?

A
  • Heart, kidney, and spleen
38
Q

What are the most common and least common causes of coagulative necrosis?

A
  • most often from ischemia

- less often from bacteria and chemicals

39
Q

What are the causes of liquefactive necrosis?

A
  • Ischemia

- Bacterial or fungal infection

40
Q

How does degradation occur in liquefactive necrosis?

A
  • Via hydrolytic enzymes
41
Q

What does liquefactive necrosis cause in the brain?

A
  • Brain infarct and abscesses
42
Q

In what disease can you see caseous necrosis occurring?

A
  • Tuberculosis infection
43
Q

TRUE/FALSE: Caseous necrosis has features of both liquefactive and coagulative necrosis.

A
  • TRUE
44
Q

What does fat necrosis cause?(Hint: in pancreas and breast)

A
  • Causes acute pancreatic necrosis and traumatic fat necrosis in the breast
45
Q

What does the pancreas secrete in fat necrosis?

A
  • The pancreas will secrete lipase which will lead to necrosis
46
Q

What is the mechanism of fat necrosis in adipose cells?

A
  • Fat will hydrolyze into glycerol and FFAs

- FFAs will complex with calcium to disintegrate membranes

47
Q

What is the complex between FFAs and calcium called?

A
  • Calcium soaps via saponification
48
Q

What is fibrinoid necrosis?

A
  • The deposition of fibrin-like material
49
Q

What type of injury causes fibrinoid necrosis?

A
  • Immunologic tissue injury (e.g. autoimmune disease)
50
Q

How can a peptic ulcer arise from fibrinoid necrosis?

A
  • Arterioles are in hypertension
51
Q

What can gangrene be the result of?

A
  • Coagulative necrosis and putrefaction
52
Q

Where does wet gangrene begin? Where could it spread to?

A
  • Naturally moist tissues and organs such as the mouth, bowel etc…
  • could spread to peritoneal cavity
53
Q

What is the mechanism of wet gangrene?

A
  • Venous obstruction
54
Q

Does wet gangrene develop slow or rapidly?

A

Rapidly

55
Q

What is the relationship between wet gangrene and bacterial growth?

A
  • Affected parts fill with blood, favouring bacterial growth
56
Q

How can wet gangrene lead to septicemia or death?

A
  • If toxic products are absorbed
57
Q

Where does dry gangrene begin?

A
  • The distal part of a limb

Furthest from blood supply

58
Q

Does dry gangrene spread rapidly or slowly? When does it stop?

A
  • Spreads slowly

- Stops when reaches a point where blood supply is adequate to keep tissue viable (line of separation)

59
Q

What is the mechanism of dry gangrene?

A
  • Arterial occlusion caused by ischemia
60
Q

What is the relationship between bacteria and dry gangrene?

A
  • There is typically little bacterial growth
61
Q

Why does dry gangrene produce a black colour?

A
  • Result of iron sulfide

- Product of hemoglobin and bacteria

62
Q

What is gas gangrene a special form of?

A
  • Wet gangrene
63
Q

What is gas gangrene?

A
  • A gas-forming clostridia (gram-positive and anaerobic bacteria)
64
Q

How does gas gangrene enter tissues?

A
  • Through wounds

- Especially in muscles

65
Q

What can cause gas gangrene?

A
  • Complications of colon operation
66
Q

What is the mechanism of gas gangrene?

A
  • Produces various toxins –> local necrosis and edema –> absorption –> systemic manifestations
67
Q

Other than gangrene, what is another after-effect of necrosis?

A
  • Calcification
68
Q

What are the two types of calcification?

A
  • Dystrophic

- Metastatic

69
Q

What is the main characteristic of dystrophic calcification?

A
  • There are normal calcium metabolism and serum calcium levels
  • it is the tissue that is the problem
70
Q

What are the two main types of dystrophic calcification?

A
  1. Deposition of calcium in dead tissue

2. Deposition of calcium in degenerated tissue

71
Q

How does the obstruction of venous flow in Gamna-Gandy bodies in dead tissue affect products in the body?

A
  • Gamna-Gandy bodies will release hemosiderin

- Hemosiderin will combine with calcium and fibrous tissue

72
Q

What is an example of dystrophic calcification in degenerated tissue?

A
  • Atheromas in the aorta and coronary

- Fatty streak eventually forms a plaque where calcification occurs

73
Q

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
A
  • Hematomas in the vicinity of bones (occurs in dead tissue)
74
Q

What is the main characteristic of metastatic calcification?

A
  • There is disturbed calcium metabolism and hypercalcemia

- Tissues are normal

75
Q

What are the two major causes of metastatic calcification?

A
  • Excessive mobilization of calcium from bone

- Ingesting too much calcium

76
Q

What are the causes of excessive mobilization of calcium from the bone?

A
  • Hyperthyroidism
  • Bony lesions
  • Prolonged immobilization
77
Q

What are the two types of hyperthyroidism?

A
  • Primary: parathyroid adenoma (cancer)

- Secondary: Parathyroid hyperplasia (chronic renal failure)

78
Q

What are bony lesions?

A
  • Multiple myeloma (can invade bone)

- Metastatic carcinoma

79
Q

What does prolonged immobilization cause?

A
  • Atrophy of bones, resulting in hypercalcemia
80
Q

What are some examples of ingesting too much calcium?

A
  • Hypervitaminosis D: causes increased calcium absorption
  • Milk-alkali Syndrome: excessive intake of calcium + calcium carbonate
  • Hypercalcemia of infancy
81
Q

What is the cause of hypercalcemia in infancy? What happens because of the root problem?

A
  • Caused by gene mutations

- Causes impaired breakdown of vitamin D and reduced phosphate levels (activates more vitamin D and thus calcium)

82
Q

What is the pathogenesis of dystrophic calcification? It is reversible?

A
  • Unclear
  • Could be due to denatured proteins binding to phosphate ions and reacting with calcium
  • This causes calcium phosphate precipitates
  • typically not reversible
83
Q

What is the pathogenesis of metastatic calcification? Is it reversible?

A
  • Excess binding of inorganic phosphate ions with elevated calcium ions to form calcium phosphate precipitate
  • typically reversible
84
Q

What are some sites that metastatic calcification occurs? (6)

A
  • Kidneys
  • Lungs (alveolar walls)
  • Stomach
  • Blood vessels
  • Cornea
  • Synovium (joints)
85
Q

Why are these common sites for metastatic calcification to occur at?

A
  • They are mostly alkaline

- Calcium fairs better in an alkaline environment

Integrative Phys (5 decks)

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