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Mechanism of Disease > Mechanism of Cell Death > Flashcards

Mechanism of Cell Death Flashcards

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1
Q

Define

Etiology

A

Cause of a disease

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2
Q

Define

Pathogenesis

A

Biochemical and molecular mechanisms of disease development

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3
Q

Define

Morphology

A

Appearance of cells/tissues/organs

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4
Q

Define

Clinical Features

Manisfestation

A

Functional consequences of mophological changes

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5
Q

Lungs filled with fluid and bacteria.

What is the morphology? What are the clinical features? What is the disease?

A

Morphology: Fluid filled lungs
Clinical Features (functional consequence): Reduced gas exchange, shortness of breathe

Pneumonia

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6
Q

Why do cells die?

A

Lack of resources
Exposure to toxins
Removal of aging/ineffective cells
Attack by immune system

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7
Q

What are some events that can cause cell death due to lack of resources?

A

Hypoxia
Nutrient Deficiency
Growth factor withdrawal

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8
Q

Cellular Level: Signs of injury?

A

Intracellular accumulations
* Fatty deposits
* Lipofuscin
* Protein

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9
Q

Modes of Cell Death

Unregulated - Necrosis Signaling

Pathological

A

Cell breaks down/explodes and contents are released

Amount of signlaing depends on the cause
Spread/damage neighboring cells

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10
Q

Modes of Cell Death

Regulated - Apoptosis (multiple)

Physiological

A

Cell disassembles and packages contents for phagocytosis

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11
Q

Alternative Modes of Cell Death

Other modes besides regulated and unregulated

A

Necroptosis (regulated necrosis)
Anoikis (detachment-induced cell death)
Ferroptosis

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12
Q

What is the difference between stressed tissue and necrotic tissue?

A

Stressed: Blebbing, Eosinophilia, Swelling; staining variation, nuclei cluster, cells swell/rupture
Necrotic: Loss of Nuclei, Breakdown of membranes; cells have ruptured

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13
Q

What are the types of Necrosis?

A

Coagulative
Liquefactive
Caseous
Fibrinoid

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14
Q

Types of Necrosis: at tissue level

Coagulative

A

Loss of cell architecture but not tissue architecture

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15
Q

Types of Necrosis: at tissue level

Liquefactive

A

Digestion of cells results in viscous mass

Cells gone but more liquid

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16
Q

Types of Necrosis: at tissue level

Caseous

A

Fragmented cells and granular debris surrounded by inflammation

Cells gone but more solid

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17
Q

Types of Necrosis: at tissue level

Fibrinoid

A

Immune complexes and fibrin inwalls of blood vessels

Fibrin from blood gets in blood vessel wall, attaches to immune complex

Very eosinophilic staining

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17
Q

Causes of Necrosis

A

Overwhelming Damage
* Toxins
* Excessive Calcium
* Damage to ER and mitochondria
* Reactoe Oxygen Species (ROS)
* Ischemia
* Membrane damage
* Nutrient Withdrawl

Cells just fall apart

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17
Q

Specific instances of physiological cell death:

Immune Function

A

Destruction of elf-reactive lymphocytes to prevent autoimmunity
Death of cells that have served their purpose
Pyroptosis

Neutrophils die after an acute inflammatory response
Lymphocytes die at the end of an immune response
Pyroptosis - overreaction of caspases during immune function can result in cell death

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17
Q

Specific instances of physiological cell death:

Embryogenesis

origin of programmed cell death

A

Death of specific cells at specific times

During digit development

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17
Q

Apoptosis: Programmed Cell Death

Specific instances of physiological cell death:

A
  • Embryogenesis
  • Tissues that prduce new cells as part of their function
  • Loss of hormone-dependent tissues when hormone levels fall
  • Immune function
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17
Q

Specific instances of physiological cell death:

Tissues that produce new cells as part of their function

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A

Immature lymphocytes in the bone marrow and thymus that fail to express useful antigen receptors
Epitherlial cells in intestinal crypts, so as to. maintain a constant number (homeostasis)

17
Q

Specific instances of physiological cell death:

Loss of hormone-dependent tissues when hormone levels fall

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A

Endometrial cell breakdown during the menstrual cycle
Ovarian follicular atresia in menopause

17
Q

Apoptotic Initiators

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A
  • Viral infections
  • Ionizing radiation
  • Chemical damage to cells
    *** Cytokines (TNF, Fas, ligand)
  • Mitochondrial damage**
  • UPR
  • Calcium influx
  • Unresolved stress
17
Major morphological features of apoptosis
* Cell rounding/condensation * Nuclear condensation/fragmentation * Membrane Blebbing * Formation of apoptotic bodies ## Footnote * Nuclear condensation/fragmentation - visible with DAPI * Membrane Blebbing - Visible with light microscopy * Formation of apoptotic bodies - Packaging of cell contents into vesicles
17
# Apoptosis Signaling Extrinsic starting point of Apoptosis
Death receptors on the plasma membrane are actvivated and transduce a signal through intracellular signaling pathways to activate caspases | Initiated by things outside of the cell
17
# Define Apoptosis
programmed cell death Damage but sufficent resources to manage process instead of just falling apart
18
# Apoptosis Signaling Intrinsic starting point of Apoptosis
Mitochondrial signals induce release of pro-apoptotic proteins that activate caspases | Initiated by things inside the cell ## Footnote Damage to mitochondria can initiate
19
What are Caspases? | **Cy**steine **Asp**art**ases**
Specific proteases that disasseble the cell Biochemical markers of apoptosis Consensus sequences: cleave after aspartic acid residue Inflammatory: Involved with NFkB signaling
20
Initiator Caspases
2 8 - extrinsic 9 - intrinsic 10 - extrinsic
21
Executioner caspases
3 6 7
22
Extrinsic Apoptotic Signaling
23
TNF/TNFR vs. FasL/Fas
24
# Death Domain Superfamily Four subfamilies involved in protein complex assembly:
1. **D**eath **D**omain (DD) subfamily 2. **D**eath **E**ffector **D**omain (DED) subfamily 3. **Ca**spase **R**ecruitment **D**omain (CARD) subfamily 4. **Py**rin **D**omain (PYD) subfamily | Homotypic binding ## Footnote Proteins MUST have the same domain to bind - through homotypic binding
25
Process to caspase activation
Initiators (autocatalytic) Executioners (cleavage) DED (extrinsic) CARD (intrinsic) Inflammation
26
Intrinsic Apoptotic Signaling
27
What are the 2 groups of the conserved domains (BH1-4) of the Bcl-2 Protein Family? | B cell lymphoma 2 Bc2 homology domains
**Antiapoptotic BCL-2 Proteins** BH4-BH3-BH1-BH2-TM **Pro-apoptotic BCL-2 proteins** Effectors: BH3-BH1-BH2-TM BH3 Only
28
Mitochondrial Pro-Apoptotic Factors
Activaed by caspases through tBID
29
How does tBid function as a mitochondrial pro-apoptotic factor?
Bid is truncated by multiple different proteases including calapins and caspases Bid will sequester antiapoptotic BCL-2 family members or activate pro-apoptotic members (Bax and Bak)
30
Apoptosome formation
31
Types of Failed stress response
p53-induced cell death (DNA damage, genotoxic stress) ER stress/UPR - halts protein translation and upregulated chaperone expression Calcium signaling
32
What is the function of p53? | anti-oncogene
Critical in DNA damage repair Transcription Factor Negative regulators of cell cycle progression promotes apoptosis
33
What happens if p53 is unbalanced?
Underexpression - increases cancer susceptibility Overexpression - promotes aging
34
PIDDosome | p53-induced death domain
35
# Define ER Stress
accumulation of misfolded proteins
36
# Define Unfolded Protein Response
Stress response that promotes degredation of proteins and increased chaperone production to improve folding
37
How does the ER participate in death signaling?
Release of ER calcium can prime mitochondria (intrinsic pathway) ER propagates death-inducing stress signals through Bcl-2 family members
38
ER stress-induced cell death contributes to:
Fas-induced cell death (BAP31 cleavage by Caspase 8) p53-induced cell death
39
What are the effects of cellular calcium?
Overload of cellular calcium is a known factor of necrosis homeostasis is effected by Bcl-2 family
40
# Calcium Toxicity ER calcium depletion...
induces UPR
41
# Calcium Toxicity ER calcium release...
may activate specific enzymes ## Footnote Calpain (protease) - Bid/Bax/Bcl-2 cleavege; Cadpase 12 activation Calcineurin (phosphatase) - bad dephosphorylation
42
# Calcium Toxicity Excessive mitochondrial calcium...
Impairs mitochondrial function (depolarization) Increased ROS generation Induces release of proapoptic factors
43

Mechanism of Disease (11 decks)

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