Genetics 2.13 Flashcards

(31 cards)

1
Q

How is the caspase family activated during apoptosis?

A

cytoplasmic calcium concentration increased

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2
Q

How are apoptotic cells removed from the environment?

A

phagocytosis

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3
Q

How does apoptosis differ from necrosis?

A
  • There is no clean-up mechanism for necrosis after cell death
  • apoptosis is non-inflammatory
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4
Q

Would regulation of apoptosis be considered the role of a proto-oncogene or a tumor suppressor gene?

A

tumor suppressor gene

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5
Q

Which cells are directly affected by ischemia?

A
  • umbra (core)

- penumbra cells still die after even though they had no hypoxic-ischemic insult

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6
Q

When does ischemia occur?

A

when blood flow drops below 25% of normal perfusion levels

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7
Q

Will treatment of a thrombo-emboli with a form of plasmin save the neurons from damage as perfusion has been restored?

A

No; most damage comes from reperfusion injury

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8
Q

What is excitotoxicity?

A

nerve cells are killed by excessive NTs (usually glutamate) stimulated by Ca2+ influx into the presynaptic neuron during nerve starvation (ischemia)

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9
Q

What is oxidative stress?

A

reactive oxygen and nitrogen species destroy cellular structures

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10
Q

What is apoptosis?

A

programmed cell death

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11
Q

How does a lack of ATP start excitotoxicity?

A
  • increases Ca2+ in axon terminals and causes release of glutamate
  • prevents astrocytes from uptaking glutamate
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12
Q

How does the influx of Ca2+ and Na+ do?

A
  • activates calpains and cathepsins
  • activates phospholipase A and C
  • activates Calsium-dependent protein kinases
  • activation of Ca2+/Mg2+-dependent endonucleases forms DNA ladders
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13
Q

What will the activation of phospholipase C probably do to the cell?

A

-induce inflammation from arachidonic acid created
-create IP3 which increases Ca2+
NOT destroy DNA through enzymatic degradation

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14
Q

What does the influx of Na+ do to the cells?

A

increase cytoplasmic volume and cause oncosis or necrosis

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15
Q

What is meant by “electrophoretic uniporter powered by the negative membrane potential”?

A

Natural electrical “drag” of cations into the cell because of free electrons in the matrix

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16
Q

What is the effect of intake of Ca2+ into the mitochondria?

A
  • impairs oxidative phosphorylation
  • mitochondria break down physically
  • mitochondria release cytochrome C into cytoplasm
17
Q

What is oncosis?

A

Neural damage from various sources can induce oncosis and lead to neuron death; necrosis of a neuron

18
Q

What is evident of oncosis?

A
  • Massive influxes of H2O and Cl- are observed (swelling opp of apoptosis)
  • cellular edema
  • no nuclear disruption (opp of apoptosis)
19
Q

Can oncosis be influenced by tumor suppressor genes?

A

No; oncosis is induced by cellular damage

tumor suppressor genes cause apoptosis

20
Q

Can neurons store oxygen?

A

No; excess amounts of oxygen can easily damage neurons because they have no capacity to store it

21
Q

What will happen when reperfusion of a damaged tissue is achieved?

A
  • calcium increase
  • shut down of mitochondria
  • osygen has nowhere to go in the cell*
22
Q

Which molecule serves as an anti-oxidant to ameliorate oxidative damage to cells?

23
Q

What is the function of endothelial nitrous oxide?

A

protects against hypoxia

24
Q

What is the function of neuronal nitrous oxide?

A

diffuse to adjacent damaged neurons and convert to a free radical and damage DNA

25
What does endothelial nitrous oxide do in the brain?
causes increase in perfusion to the tissues; protects against hypoxia
26
Why is inflammatory cytokine production probably not the best thing near neurons?
Movement of white blood cells in the tissues probably would disrupt synapses; tear through nerves to get to site of inflammation
27
Describe the metabolic consequences of hypoxia/ischemia and the features of necrotic cell death
Hypoxia-ischemia eliminated ATP production, leading to ionic imbalances that have vast metabolic consequences
28
Describe the morphological and molecular features of apoptosis
Apoptosis causes laddering of DNA, karyolysis, and blebbing of cytoplasm
29
Outline the contribution of apoptosis to ischemic brain injury
Apoptosis can be triggered by cellular signals in injured cells, particularly by mitochondrial damage
30
Differentiate between necrosis and apoptosis/programmed cell death
Oncosis leads to inflammation, apoptosis does not, but both can be triggered by hypoxia-ischemia
31
State the role of cell death in neural development and neurodegeneration
Development of the neural system requires cellular rearrangement and pruning to create the complex cellular systems and morphology in the brain