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Pathology > Unit I: Apoptosis > Flashcards

Unit I: Apoptosis Flashcards

1
Q

Necrosis- 4 major differences from apoptosis

  1. ​
    1. 4.
A

Necrosis

  1. Cell dissolution with extrusion of contents
  2. acute inflammatory response
  3. tissue architecture is lost, cellular loss is obvious because lots of cells die at once
  4. cell swells and blebs before dying
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2
Q

Apoptosis- 4 main different features

A
  1. cell fragments, but contents do not get out
  2. no inflammation
  3. tissue changes aren’t apparent (one cell dies at a time)–architecture preserved
  4. condensation of cell, break up of cell
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3
Q

apoptotic bodies

A

cell fragments due to apoptosis. No extrusion of intracellular contents. remember cell SHRINKS before fragmenting.

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4
Q

Mechanisms of apoptosis (x5)

A
  1. loss of growth factor/stimulation
  2. Fas-Fas killing of infected cells
  3. P53 killing of damaged cells
  4. mis-folded protein accumulation
  5. maintenance of cell populations (embryogenesis, epithelial layers, immune)
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5
Q

Apoptotic cells microscopic features

A

EOSINOPHILIC

  1. cell shrinks (condensation of nucleus and cell)
  2. chromatin is at periphery of nucleus under nuclear membrane
  3. membrane blebbing
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6
Q

Why isn’t cell loss apparent in __(apoptosis or necrosis)___ ?

(x3)

A
  • Apoptosis- cell loss is not apparent due to:
    • cells die singly or in small clusters
    • space is filled in by movement of surrounding cells
    • no inflammation
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7
Q

In viral hepatitis, cells undergo

A

BOTH apoptosis and necrosis

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8
Q

What happens to cell fragments in

  1. Apoptosis
  2. Necrosis
A
  1. Apoptosis- cell fragments are phagocytosed by surrounding cells (magrophages and parynchyma)
  2. Necrosis- phagocytosed by macrophages, initiate acute inflammatory response?
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9
Q

Caspase

  1. what is it?
  2. activation?
A
  1. cysteine proteases that cleave aspartic acid= Caspase
  2. zymogens that require activation by initators or autolytic activation.
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10
Q

Caspases- function/effect (x2 major ones)

A
  • cleave nuclear and cytoskeletal scaffold (LAMINS)==> protein cross-linking and cytosolic condensation
  • triggers endonuclease activity
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11
Q

Endonucleases

  1. activation?
  2. function?
  3. mechanism?
A
  1. activated by caspases, require Mg or Ca
  2. DNA breakdown
  3. Calcium and Mg dependent endonucleases break down DNA into 50-300kB pairs==> 180-200 bp. Internucleosomal DNA cleavage.
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12
Q

How are apoptotic cells phagocytosed (mechanism)? X2 “markers”

A
  • Phosphatidyl serine on plasma membrane is flipped and faces outwards, marking a cell as an apoptotic body.
  • external expression of thrombospondin

Phagocytosed by MACROPHAGES= minimal inflammation

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13
Q

Physiological vs Pathological processes of apoptosis

A
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14
Q

Initiation of apoptosis: Major pathways

A
  1. Bcl Pathway
  2. Fas-Fas pathway
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15
Q

Bcl-2 proteins

  1. Sensors- what are they, how are they activated, what is their function?
  2. Effectors- what are they, function, regulation?
  3. Regulators - what are they, function, regulation?
A
  • Bcl-2 family of proteins in mitochondria- pro and anti-apoptotic members
    • cytoplasmic signaling influences balance of pro/anti
  1. Sensors: BH3
    • Activated by decreased survival signals, DNA damage, ER stress (protein misfolding)
    • activate Bax/Bak==>form pore
    • inhibit Bcl-xl, Bcl-2
  2. Effectors: pro-apoptotic= Bax/Bak- form pore
    • ​​activated by BH3 proteins
    • inhibited by Bcl-xl, Bcl-2
  3. Regulators: anti-apoptotic: Bcl-xl, Bcl-2- inhibit Bax/Bak and other pro-apoptotic proteins
    • increased by growth factors and other survival signals
    • inhibited by BH3 (= sensors)
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16
Q

Apoptosis Figure

(shows intrinsic and extrinsic pathways)

A
17
Q

What happens after Bax/Bak are activated?

A
  • Bax/Bak= pore formed in mitochondria==> cytochrome C leaks out of outer membrane
  • Cytochrome C binds Apaf-1 and activates caspase 9
18
Q

Follicular lymphomas- oncogene?

A

have an oncogene that activates bcl-2==> inhibition of apoptosis in neoplastic cells

19
Q

Death receptor pathway- what is it?

2 initiators

A

Extrinsic pathway of apoptosis

  1. Fas (CD95) binds FasL (virally infected t-cells)
  2. TNF/TNF-R crosslinking
20
Q

Fas-Fas ligand

  1. mechanism
  2. purpose
  3. viral adaptation
A
  1. activation of FADD (FAS associated death domain)==> pro caspase 8 activation ==> autolytic activation of other caspases
  2. killing of autoreactive t-cells
  3. FLIP (made by viruses) blocks activation of caspase 8
21
Q

How doe live cells protect themselves from phagocytosis? (how are they differentiated from apoptotic bodies?)

A

Cd31 expression

22
Q

TNF family of receptors

A
  • includes TNFR1 and Fas
  • Activate FADD or TRADD==> caspase activation
23
Q

Spinal muscle atrophy- what’s the mutaiton?

A

mutation in regulatory proteins that inhibit activation of TNF induced apoptosis.

24
Q

CTL-induced cell death- 2 ways

A
  1. CTL’s express FasL and can activate extrinsic pathway via Fas receptor ligation
  2. CTL recognizes foreign antigen==> expression of perforins create transmembrane pores==>exocytosis of granzyme B (cleave proteins at aspartate residues) ==> activated cellular caspases
    • no death receptor activation, no mitochondrial engagement– direct activation of effector phase= caspases.
25
Q

Decrease in growth factor

A

Intrinsic pathway-neurons and hormonal signaling

decreased Bcl-2, increased BH3 sensors (bim)

26
Q

ER stress- what causes it? mechanism? disease examples?

A

from accumulation of misfolded proteins

  • misfolded proteins are ubiquitinized and destroyed by proteosome, but too many overwhelm the process
  • ER stress response activates caspases==> apoptosis (intrinsic)
  • degenerative CNS disease= alzheimers, parkinsons, maybe DMII
27
Q

DNA damage apoptosis

  1. what causes DNA damage
  2. Cell response?
  3. Disease example
A
  1. heat, radiation, chemo,
  2. p53 accumulates in cell==> arrest cell cycle at G1==> [if the damge can’t be repaired] trigger apoptosis via sensors (activate Bax/Bak; inhibit Bcl-xl/2)
  3. p53 mutations allow damaged cells to divide= carcinogenesis
28
Q

Disease with inhibited apoptosis (x2)

Diseases with increased apoptosis (x3)

A
  1. Inhibited apoptosis
    • ​​p53 mutation
    • autoimmune disorder (cant remove autoreactive t-cells)
  2. Increased apoptosis
    • CNS degenerative disease
    • ischemic injury
    • virus induced lymphocyte depletion
29
Q

Autophagy

A
  • autophagic vacuole formed from ribosome free regions of ER digest cell components
  • activated by multi-protein units that sens nutrient deprivation
  • involved in clearance of misfolded proteins in neurons and hepatocytes
  • may trigger apoptosis

Pathology (7 decks)

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