stroke

Question 1

describe the types of stroke

Answer 1

ischemic - blockage of blood vessels

hemorrhagic - rapture of blood vessels

strokes are mostly focal (loss of blood supply to a certain area of the brain) but can also be global (caused by cardiac arrest)

Question 2

describe the risk factors for stroke

Answer 2

diabetes
hypertension
atherosclerosis
genetic polymorphisms

Question 3

describe penumbra

Answer 3

around the infarct/ core zone of necrotic tissue is called the penumbra. these nerve cells die slower (24-72hrs) via apoptosis

Question 4

causes of necrosis

Answer 4

cell lysis

Question 5

causes of delayed cell death

Answer 5

• massive release of glutamate (saturation)
• influx of intra-cellular calcium
• free-radical production
• activation of brain macrophages (microglia) releasing NO, superoxide, cytokines
• activation of intrinsic apoptotic mechanisms
  etc

Question 6

excitatory theory

Answer 6

explains how neurons die during stroke. Excessive activation of glutamate in the brain causes nerve cell death, transporters become saturated.

Question 7

glutamate receptors

Answer 7

1. Ionotropic (ion channels): AMPA/kainate; NMDA

2. metabotropic - G-protein linked

Question 8

AMPA receptors

Answer 8

ligand-gated ion channel

• glutamate binds causing an influx of Na+ and nueronal depolarization
• GluR1-4

Question 9

kainate receptors

Answer 9

ligand-gated ion channel

• glutamate binds causing an influx of Na+ and nueronal depolarization
• GluR5-7

Question 10

NMDA receptors

Answer 10

both ligand-gated & voltage-gated

• glutamate binds causing the channel to open and an influx of Ca2+ which depolarizes the neuron
• When polarized, Mg2+ occupy and block the channel
• Depolarization leads to Mg2+ efflux (hence voltage-dependent)

PCP (phencyclidine, ‘angel dust’) binds inside the channel and blocks ion flow (non-competitive antagonists)

Question 11

metabotropic - G-protein linked

Answer 11

mGluR 1&5
-activate phospholipase C and depolarize neurons

mGluR 2&3
-inhibit adenylate cyclase and cause inhibition of NT release