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NMSK-B II > Pathology 2.11 > Flashcards

Pathology 2.11 Flashcards

1
Q

Blood enters the brain through which arteries?

A

carotid arteries

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2
Q

How is flow controlled in vessels to the brain?

A
  • size of muscular layer

- ability of vessel to constrict and dilate

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3
Q

What is the cerebral perfusion pressure (CPP)?

A

driving force across brain capillaries

CPP = MAP - ICP

(MAP= mean arterial pressure)
(ICP = intracranial pressure)
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4
Q

How is cerebral perfusion pressure (CPP) maintained?

A
  • cerebral blood flow is regulated

- cerebral arteries can diameter to adjust flow

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5
Q

How does the brain vasculature respond to changes in mean arterial pressure?

A
  • brain arterioles constrict with increased blood pressure
  • dilate with lowered blood pressure
  • size change keeps cerebral flow constant*
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6
Q

How does the brain vasculature respond to changes in blood gases?

A
  • raised arterial CO2 causes brain arterioles to dilate and cerebral blood flow will increase
  • low CO2 leads to vasoconstriction and cerebral blood flow will decrease
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7
Q

How can CO2 increase in the blood to the brain?

A

metabolic increase; can lead to increase in H+

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8
Q

How would hyperventilation affect intracranial pressure (ICP)?

A
  • decrease CO2
  • vasoconstriction
  • decrease blood flow
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9
Q

How do small increases in CO2 affect cerebral blood flow?

A

large increase

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10
Q

How does an increase in O2 levels affect cerebral blood flow?

A

decrease

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11
Q

Are changes in CO2 or O2 are more sensitive to changes in cerebral blood flow?

A

CO2

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12
Q

Are changes in CO2 or O2 levels more important for the coronary circulation?

A

O2

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13
Q

What happens in autoregulation?

A

Flow remains constant over a range of perfusion pressures

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14
Q

What happens in active hyperemia?

A

Increase in flow in response to increased metabolic demand

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15
Q

What happens in reactive hyperemia?

A

Increase in flow following periods of occlusion (vessel blockage/hindered flow)

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16
Q

What is the myogenic hypothesis?

A
  • one of two hypotheses which explain autoregulation
  • Vascular smooth muscle around the arterioles contracts when stretched
  • wall tension = pressure X radius
17
Q

What is the metabolic hypothesis?

A
  • one of two hypotehses which explain autoregulation
  • Increase in metabolites leads to vasodilation and an increase in flow
  • Match O2 supply to demand
18
Q

How does excitotoxicity occur?

A

insufficient blood supply to cells (less oxygen and glucose gets to cells)

19
Q

How can excitotoxicity damage neurons?

A
  • oxygen-deprived cells release glutamate at nerve terminals which lead to overactivation of their receptors
  • NMDA receptors have been implicated due to their ubiquity and high Ca2+ permeability
  • active glutamate receptors leads to excessive increases in intracellular Ca2+
20
Q

How does Na+ affect neuron damage?

A

Na+ entry into cells leading to rapid cell swelling and lysis

21
Q

How does Ca2+ affect neuron damage?

A

Increased Ca2+ entry leads to damage of endoplasmic reticulum and mitochondria

22
Q

What is a Cushing reaction?

A
  • response to cerebral ischemia from increased intracranial pressure
  • compression of cerebral blood vessels leads to increased PCO2
  • compensatory increases in blood flow lead to greater cerebral blood volume which raises intracranial pressure
23
Q

What is the Cushing triad?

A
  • irregular breathing
  • increase in bp
  • bradycardia (slowing -heart rate)
24
Q

What is the relationship between glutamate receptors and ischemic damage?

A

blocking glutamate receptors protect against ischemic damage

25
Q

What is Amyotropic Lateral Sclerosis (ALS)?

A
  • initially upper motor neuron disease; loss of neurons projecting to spinal cord
  • progresses to lower motor neuron disease; loss of spinal motorneurons
  • eventually affects phrenic nerve (innervates diaphragm)
  • respiratory death
26
Q

What is the only drug for the treatment of ALS?

A

Riluzole (Rilutek); glutamate antagonist

NMSK-B II (15 decks)

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