Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

NMSK B Test 1 > LG 2.13 Neuronal Cell Death > Flashcards

LG 2.13 Neuronal Cell Death Flashcards

1
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the morphological and molecular features of apoptosis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How does apoptosis affect embryonic development?

A
  • During embryonic development, the nervous system is “Sculpted” by neuronal cell death
  • Excess neurons are removed to ensure proper and precise synaptic connections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

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

A

Tumor suppressor gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

When does ischemia occur?

A

Ischemia of the brain usually occurs when blood flow drops below 25% of normal perfusion levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is another word for the core?

A

Umbra

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the penumbra?

A

Outside the umbra

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Treatment of a thrombo-emboli with a form of plasmin will save the neurons from damage as perfusion has been restored.

A

No. Most damage comes from reperfusion injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is excitotoxicity?

A

– nerve cells are killed by excessive neurotransmitters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is oxidative stress?

A

reactive oxygen and nitrogen species destroy cellular structures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is apoptosis?

A

programmed cell death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How do NMDA affect excitotociciy?

A
  • NMDA receptors create fast excitotoxicity (>3 min) by increasing [Ca2+]i and interfering with calcium proteins in the cytoplasm
  • Activation of calpains and cathepsins
  • Activation of phospholipase A and C
  • Activation of Calcium dependent protein kinases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What will the activation of Phospholipase C probably not directly do to the cell?

A

Destroy the DNA through enzymatic degradation

17
Q

“Electrophoretic uniporter powered by the negative membrane potential?” Seriously? What the frick is that?

A

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

18
Q

How does Mitochondria and Ca2+ affect each other?

A
  • Intake of excessive Ca2+ impairs oxidative phosphylation
  • Lack of ATP prevents ATP-dependent Ca2+ pumps
  • Mitochondrial permeability increase releases cytochrome C, etc., into cytoplasm
19
Q

What is the main differences between Oncosis and Necrosis?

A
  • No nuclear disruption is evident (opposite of apoptosis)

- No inflammation

20
Q

Oncosis can probably be influenced by tumor suppressor genes.

A

No, because tumor suppressor genes probably cause apoptosis, and oncosis is induced by cellular damage.

21
Q

What do you think will happen when reperfusion of the tissue is achieved?

A
  • Hypoxic-ischemic damage has caused [Ca2+]i increase
  • Hypoxic-ischemic damage has shut down the mitochondria
  • Oxygen will have nowhere to go inside of the cell
22
Q

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

A

Glutathione

23
Q

What generates ROS?

A

Lack of ATP, uncoupled electron transport, and re-perfusing oxygen generate ROS

24
Q

What also causes ROS?

A

Ferrous ions also increase ROS

Note: cyclooxygenase activity increases after reperfusion

25
Q

What type of NO protects against hypoxia?

A

eNO

26
Q

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

A

nNO

27
Q

What does endothelial NO do in the brain?

A

It causes an increase in perfusion to the tissues

28
Q

What will create inflammatory chemicals in Oncosis?

A

Cyclooxygenase will create inflammatory chemicals

29
Q

What does p53 activate?

A

Apoptosis

30
Q

What are two methods of activating apoptosis?

A

-Caspase cascade and cytochrome C

31
Q

What does caspases require for activation?

A

Calcium

32
Q

Does apoptosis cause inflammation?

A

No inflammation involved

33
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

34
Q

What is ROS?

A

Reactive oxygen species

NMSK B Test 1 (27 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions