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MCM test 3 > 5- Cell Death and Adaptations > Flashcards

5- Cell Death and Adaptations Flashcards

1
Q

What is the path of cell changes during apoptosis?

A

Cell shrink > Cytoskel degredation> Nuclear envelope disassemble > Chromatin condensation > DNA degradation > Apoptotic bodies > Membrane signalling

Apoptotic bodies- small vesicles occur from membrane blebbing of the cell

No inflammation

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2
Q

What is the apoptotic cell signal?

A

Phosphatidylserine moves from inner to outer leaflet to signal phagocytic cells to remove apoptotic cell.

No inflammation occurs

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3
Q

What is the big difference with necrosis and apoptosis?

A

No inflammation in apoptosis

There is inflammation in necrosis. Happens because of trauma

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4
Q

What kind of cells can apoptosis eliminate?

A

T and B lymphocytes that are self-reactive

Neurons with no connections

lymphocytes activated for infection once it is cleared

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5
Q

Caspases

Where are they cleaved?
what form are they synthesized in?

how are they activated?

A

proteases that cascade apoptotic pathway

C - cysteine (in active site)
Asp- aspartate (target on protein)

Synthesized in zymogen form– procaspase

Activated by cleavage at 1 or 2 aspartic acids,
2 caspase combine to form active. 2 small 2 large units

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6
Q

Initiator and Executioner caspases.

What is CARD?

A

Initaitor caspases: cleave and activate downstream caspases.
CARD-Caspase recruitment domain- pro domain, assemble into activation complexes, brought in close proximity to cleave each other.

Executioner caspases- target downstream capsizes AND target protiens that deal with morphological changes
- nuclear lamins, endonuclease inhibiting enzyme, cytoskeletal elements, adhesion proteins.

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7
Q

What are the death receptors characteristics?

A

three domains: extracellular, transmembrane, intra

homotrimer

Part of TNF receptor family, bind TNF and fas

EXTRINSIC PATHWAY

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8
Q

TNF family pathway for extrinsic apoptosis?

What binds to the deatch receptor?

What complex is formed?

A

Fas ligand from killer lymphocyte, juxtacrine signalling

Adaptor proteins FADD recruited > recruit initiator procaspases (8 or 10) > forms DISC (death inducing signaling complex) > initiator caspases activate executioner caspases

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9
Q

Intrinsic pathway for apoptosis.

What generally signals for this pathway?

A

Signaled by mitochondria

Cytochrome c released from mito > Apaf-1 hydrolyzes bound ATP to ADP> Apaf-1s bind cytochrome C form apoptosome (circular oligomerization) > recruited procaspase 9 (via CARD) > caspase 9 activated in apoptosome > downstream cascade

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10
Q

How does BH123 family control release of cytochrome c from mitochondria?

Two that you should definitely know.

A

Pro apoptotic proteins

Form oligomers in outer mito membrane > pores for cytochrome c to leak out.

Bak- always bound to mito membrane
Bax- translocated when activated (ER stress maybe)

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11
Q

Bcl2 family, how are they related to the proapoptotic proteins?

Which two should you remember?

A

Anti-apoptotic proteins (Bcl2 and BclX1)

Bind to Bak and Bax to inhibit apoptosis

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12
Q

What do inhibitors of anti-apoptotic proteins do?

Who are the key players?

A

Inhibit Bcl2 and BclX1 (anti-apoptotic proteins)

Enables Bak and Bax to aggregate

Activated via signal transduction which induces transcription and translation of BH3-only proteins

    • MAPK (Ras mek erk)
  • -p53- tumor suppresant
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13
Q

How are the extrinsic and intrinsic pathways linked?

A

BID also inhibit anti apoptotic proteins.

BID activated by caspase 8 (from extrinsic)

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14
Q

Which survival factors do our neurons need?

A

Neurotrophins (this is a specific example)

In general, when cell no longer has survival factor it will undergo apoptosis.

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15
Q

What markers do you look for in the blood if you suspect MI?

A

necrosis markers

Also, Cardiac troponins, creatine kinase (CK-MB)

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16
Q

Ischemia

A

Inadequate BLOOD supply.

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17
Q

How is glaucoma related to apoptosis.

Which specific factor do they think is missing that the cells need?

A

Glaucoma has elevation in intraoccqular pressure which causes damage

An example of too much apoptosis, neurodegeneration

loss of vision is due to apoptosis of Retinal Ganglion Cells

Some think its that BDNF (neurotrophin) isn’t there to support the cells.

18
Q

Autoimmune Lymphoproliferative Syndrome

Which gene is mutated?

A

ALPS- lymphoproliferative disease and susceptible to cx

Defective FAS ligand leads to accumulation of lymphocytes that are autoreactive

usually these are killed by killer lymphocytes with the FAS ligand attached to them.

Body can’t limit amount of reactive lymphocytes that are produced.

19
Q

Which proteins connected to apoptosis are usually mutated in cancer cells?

A

Bcl2- leads to B cell lymphoma

p53- p53 mutation in about 50% of cancers.
– usually mutation makes it unable to bind DNA, inhibiting ability to induce p21

20
Q

Causes of cell Injury

Just read them. Don’t memorize

A
  1. Oxygen deprivation
  2. Physical Insult
  3. Chemical Agents
  4. Infectious agents
  5. Immune reaction
  6. Genetic Abnormality
  7. Nutritional imbalance
21
Q

Reactive oxygen Species (ROS)

A

Oxygen derived free radical made in peroxisomes or lysosomes.

Released during inflammation with intent to destroy microbes

examples
superoxide O2
hydrogen peroxide H2O2
Hydroxyl radical OH

22
Q

What are the two main targets of Oxidative stress?

A

Protein modification: Oxidation of aa R groups and peptide backbone. Destroy 3D confirmation, enhance degradation

DNA lesions: ss or ds breaks, adducts and cross linking

23
Q

3 Antioxidants to remember

What ratio do we need to know?

A
  1. Catalas- H2O2 > O2 and H2O
  2. Superoxide Dismutase (SOD): superoxide > H2O2
    cytosolic and mitochondrial
  3. Glutathione peroxidase:
    Breaks H2O2/OH by oxidizing itself to homodimer
    oxidized form: GssG Reduced form: GSH
    – ratio of reduced to oxidized is important indicator or redox status**

reduced ratio in neurodegenerative diseases because you have more inflammation occurring in those processes

24
Q

Why does the cell swell in result of hypoxia?

A

Loss of os/phos > decrease ATP > sodium pump failure > Na+ and H20 build up > swelling

Other ATP requiring processes will be in trouble too.

25
Q

Response to chronic vs acute injury?

A

chronic = apoptosis

acute = necrosis

26
Q

what are the sources of influx of Ca2+ into the cytoplasm?

A

Mitochondria and ER and extracelluar (loss of membrane potential– K+ gone)

mitochondrial increase permeability, depolarize membrane, swell, increase Ca2+ and oxygen species, worse ATP production, Ca2+ cannot be pumped out of cell (Ca2+/Na+ exchanger)

27
Q

Which enzymes are activated by influx in Ca2+

A

ATPase

Phospholipase- phospholipids, damage membrane form blebs

Endonuclease- break down chromosomal DNA

Protease-

28
Q

Mechanism for injury by ischemia?

A

Like hypoxia but there is also no nutrients:

No substrates for glycolysis

    • No glycolytic metabolism
    • intracellular glycogen stores used up
    • accumulate metabolites, can’t be taken away because of disrupted blood flow.
29
Q

Necrosis often has a leaky membrane, what is the significance of that?

A

Leaks out enzymes- can be used clinically as an indicator.
can damage nearby cells

Can leave behind plasma skeleton
Degraded, or eaten, sometimes seen in microscope.

30
Q

Hypoxia-inducible factor 1

A

Induced by hypoxia

activity promotes angiogenesis, production of new blood vessels.

31
Q

Agenesis

A

Failure to form an embryonic cell mass

32
Q

Aplasia

A

Failure to differentiate into organ-specific tissues

33
Q

Dysgenesis

A

Failure of structural organization

tissues into an organ

34
Q

Hypoplasia

A

Failure to grow to full size

35
Q

Pathological reasons for atrophy.

Mechanism

A

Decreased stimulus: workload, innervation, blood supply, nutrition, endocrine,

Compression: probably result of ischemia

Cells diminish in size and function

    • decreased protein synthesis
    • increased protein degradation
  • ——- both through proteolysis and autophagy
36
Q

Involution

A

Decrease in the number of cells compared to the normal number. drop in cell types

Happens in mammary glands once lactation has ceased

Happens in uterus after pregnancy

37
Q

Metaplasia

A

Substitution of one cell for another

Ex. GERD esophageal changes to stomach like tissue
– reprogramming of stem cells based on the environmental stimulus. related to esophageal cancer

38
Q

Steatosis

A

Triglyceride accumulation within the cell.

Imbalance of uptake, utilization or secretion

39
Q

atherosclerosis and xanthomas

A

Cholesterol accumulation within the cell.

40
Q

What causes protein deposits

A

Will appear extracellular or cytoplasmic.

Caused by: protein produced in excess,
endocytosis of extracell protein in excess,
defects in protein trafficking and secretion
accumulation of cytoskeletal proteins
Aggregation of mutated/misfolded protein

41
Q

Calcification

A

Deposition of crystalline calcium phosphate with other mineral salts

Dystrophic calcification- occurs in dying tissues

    • caused by necrosis:
  • ——excess Ca interacts with phospholipids and acquires phosphate
    • —-exported via membrane bound vesicles
42
Q

Starvation

A

Cell deprived of nutrients
Autophagy- digests own components to gain nutrients

Autophagic vacuoles- membrane bound vesicles containing sub cellular components. Undergoes lysosomal maturation: autophagolysosome

Residual bodies- debris resist digestion and remain in membrane bound vesicle.

    • lipofuscin: indicator of tissue degeneration
  • —– presence is a sign of free radical injury
  • —– liquid peroxidation of membrane components

MCM test 3 (12 decks)

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