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Biochemistry > Lecture 37 - Ischemia and Reperfusion > Flashcards

Lecture 37 - Ischemia and Reperfusion Flashcards

1
Q

Metabolic rates are higher in the (white/gray) matter.

A

gray - these are neurons that require energy for signal transduction/resetting of membrane potential

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2
Q

The Blood Brain Barrier (BBB) has transporters specifically for what molecules that are used by the brain?

A

glucose

monocarboxylic acids

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3
Q

This is a measurement of the carbohydrate metabolism in the brain.

A

Respiratory quotient

CO2 produced/O2 consume

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4
Q

[Oxygen] is lower in the cerebral (venous blood/arterial blood).

A

venous blood

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5
Q

The brain contains small stores of _____, which may be utilized instances of anoxia when the brain cannot undergo anaerobic metabolism.

A. glycogen
B. G-6-P
C. ATP
D. lactate

A

A. glycogen

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6
Q

Cerebral neurons are known to be ____ and use ____ for their neurotransmitter.

A. inhibitory; glutamate
B. excitatory; glutamate
C. Inhibitory; GABA
D. excitatory; GABA

A

B. Excitatory; glutamate

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7
Q

Cortical neurons are known to be _____ and use ____ as their neurotransmitter.

A. inhibitory; glutamate
B. excitatory; glutamate
C. Inhibitory; GABA
D. excitatory; GABA

A

C. Inhibitory; GABA

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8
Q

Brain imaging is capable of detecting gross changes to the brain’s anatomical structure, true or false?

A

True

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9
Q

A patient is brought in for evaluation of a potential stroke. He is given a glucose analog, which allows for monitoring of the activity of hexokinase. Decreased hexokinase activity is an indicator of damage to the brain parenchyma. What imaging study was performed?

A. PET scan
B. MRI
C. MRS
D. CT scan

A

A. PET scan

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10
Q

A patient is suspected of having had a stroke. They are given a radioactive form of glucose, and is the resulting image is used to determine the metabolic activity of the neurons and glial cells in the brain. Wha imaging study was performed?

A. PET scan
B. MRI
C. MRS
D. CT scan

A

C. MRS (Magnetic Resonance Spectroscopy)

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11
Q

Disruption of blood flow to a small region of the brain is known as ______.

A

Focal cerebral ischemia; usually results from blockage to a small blood vessel

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12
Q

In focal ischemia, the total area of infarction is often less than the area of tissue supplied by the occluded vessel. Why is that so?

A

Collateral circulation

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13
Q

The ischemic core, or _________, is the a region caused by the ischemia that results in electrophysiology changes, metabolic and perfusion disturbances.

A

umbra

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14
Q

Impaired protein synthesis is characteristic of the _____ of focal ischemia.

A. ischemic core
B. umbra
C. periumbra
D. thrombolytic zone

A

C. periumbra

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15
Q

If reperfusion is not successful in _____ hours, necrosis extends to the penumbra.

A

3

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16
Q

These cells are responsible for many signalling actions in the CNS. As a result, they require many pumps and gradients, and are therefore more sensitive to ischemia. What are they?

A

neurons

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17
Q

Absence of oxygen due to ischemia causes reduced levels of _____. This produces disf(x) in ____.

A

ATP;

ATPases necessary for maintaining ion gradients

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18
Q

When ion pumps are disrupted due to ischemia, the membrane becomes depolarized. This results in _____.

A

voltage gated Na pump opening

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19
Q

Describe the “Pasteur effect.”

A. A decrease in PO2 causes lactate production
B. Changes to ion channels from decreased pH causes depolarization
C. Necrosis of brain tissue occurs from low arterial [oxygen]
D. K+ efflux from opening of K+ channels

A

A. A decrease in PO2 causes lactate production

20
Q

Anaerobic metabolism from ischemia produces lactate, reducing the brain pH to _____ from 7.3.

A

6.2-6.8

21
Q

Membrane proteins change shape through denaturation after acidosis secondary to ischemia. What major ion begins to efflux when this occurs?

A

K+

22
Q

K+ efflux from acidosis results in a collapse of Na+ and Ca2+ gradients. What is the ultimate result?

A

Release of neurotransmitters

23
Q

Ion gradient loss results in an increase of extracellular _______. This elevates intracellular Ca2+, which causes NT release.

A

glutamate

24
Q

Glutamic activated Ca2+ and Zn2+ influx activates ______.

A. caspase
B. complement
C. cytotoxic intracellular pathways

A

C. cytotoxic intracellular pathways

25
Q

The activation of NMDA-R is prevented by what molecule?

A. DAPK1
B. CT
C. ROS-reductase
D. NRTBCT

A

B. CT

26
Q

The neuron contains large amounts of ____, that can be damaged with reactive oxygen species.

A. poly-unsaturated fatty acids
B. trans unsaturated fatty acids
C. glycosylated proteins

A

A. poly-unsaturated fatty acids

27
Q

In ischemia, mitochondria will donate electrons to oxygen. However, instead of producing water, the ischemia results in reactive oxygen species. These go on to produce damage to ____, _____, and ______.

A

proteins;
lipids;
DNA

28
Q

Endothelial damage in the BBB secondary to reperfusion will result in _____.

A. production of ROS
B. leaky capillaries secondary to damage
C. extravasation of leukocytes

A

B. leaky capillaries secondary to damage

29
Q

What are the two types of ischemic apoptosis?

A

Extrinsic and intrinsic

30
Q

What are the signalling factors that cause extrinsic apoptosis?

A

FAS

Tumor Necrosis Factor alpha

31
Q

What are the signalling factors that cause intrinsic ischemic apoptosis?

A

Release of cytochrome C from mitochondria

Disfunction of the ER

32
Q

The extrinsic ischemic pathway produces ______, causing activation of procaspase-8.

A. DISC
B. FAS
C. Caspase-3
D. tBID

A

A DISC

33
Q

DISC activates procaspase-8 by promoting ______.

A

oligomerization of procaspase-8.

34
Q

BID is cleaved by caspase-3 to form ______, which causes apoptosis after translocation from the mitochondria.

A. tBID
B. Caspase-8
C. TNF-alpha
D. proteosome promoting factor

A

A. tBID

35
Q

The primary effector of intrinsic ischemic activation is ______.

A. Na+
B. K+
C. Ca2+
D. Cl-

A

C. Ca2+

36
Q

Calcium influx in the intrinsic apoptotic pathway causes the release of ______.

A

cytochrome C from the mitochondria.

37
Q

The proapoptotic proteins Bcl-2 are localized to the _____?

A

mitochondria and ER

38
Q

Caspases are primarily responsible for the cleavage of ______.

A

nucleus

cytoskeleton

39
Q

Antagonists to ______ prevent the excitation of damaged neurons.

A

NMDA-receptors

40
Q

____ agonists activate chloride channels to hyperpolarize neurons that have been damaged.

A

GABA

41
Q

____ may result in fatal edema or intracranial hemorrhage when used to break up cerebral emboli

A

tPA

42
Q

This molecule is used to protect the penumbra. It is anti-inflammatory and protects against apoptosis, ischemia, reperfusion mediated leukocyte infiltration, and other post-reperfusion damage.

A

DHA

43
Q

DHA is a precursor to _____, a known penumbra protectant.

A

NPD1

44
Q

The brain is known to account for only 2% of body weight. However, it is a very inefficient organ, requiring much more blood than other organs. Approximately what percentage of energy is consumed by the brain?

A. 10%
B. 20%
C. 30%
D. 40%

A

B. 20%

45
Q

Approximately ____% of the energy utilized by the brain is dedicated for signalling.

A

75

46
Q

These are immortal cell lines that are used in experimentation.

A

Cell lines

47
Q

When studying brain tissue, either brain slices or _______ can be utilized.

A. isolated organelles
B. synaptosomes
C. mitochondria
D. excitatory neurones

A

A. isolated organelles (B and C are incorrect because they are organelles; D is part of the primary neuronal culture model of brain studying)

Biochemistry (43 decks)

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