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NMSK-B II > Genetics 2.13 > Flashcards

Genetics 2.13 Flashcards

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?

A

glutathione

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
Q

What does endothelial nitrous oxide do in the brain?

A

causes increase in perfusion to the tissues; protects against hypoxia

26
Q

Why is inflammatory cytokine production probably not the best thing near neurons?

A

Movement of white blood cells in the tissues probably would disrupt synapses; tear through nerves to get to site of inflammation

27
Q

Describe the metabolic consequences of hypoxia/ischemia and the features of necrotic cell death

A

Hypoxia-ischemia eliminated ATP production, leading to ionic imbalances that have vast metabolic consequences

28
Q

Describe the morphological and molecular features of apoptosis

A

Apoptosis causes laddering of DNA, karyolysis, and blebbing of cytoplasm

29
Q

Outline the contribution of apoptosis to ischemic brain injury

A

Apoptosis can be triggered by cellular signals in injured cells, particularly by mitochondrial damage

30
Q

Differentiate between necrosis and apoptosis/programmed cell death

A

Oncosis leads to inflammation, apoptosis does not, but both can be triggered by hypoxia-ischemia

31
Q

State the role of cell death in neural development and neurodegeneration

A

Development of the neural system requires cellular rearrangement and pruning to create the complex cellular systems and morphology in the brain

NMSK-B II (15 decks)

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