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PBL SEM 3 > 5 - blood supply to the brain and cerebral ischaemia lecture > Flashcards

5 - blood supply to the brain and cerebral ischaemia lecture Flashcards

1
Q

what is the major vessel type in the brain?

A

capillaries

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2
Q

blood supply to the brain is supplied by what 2 pairs of arteries?

A
  • internal carotid arteries
  • vertebral arteries
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3
Q

what arteries are included in the anterior and posterior circulation?

A

anterior = common carotid artery + internal carotid artery

posterior = subclavian artery + vertebral arteries

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4
Q

what artery runs along the pons and medulla?

A

basilar artery

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5
Q

describe the anterior cerebral artery

A
  • smaller branch of ICA
  • has important branches — anterior communicating, mediate striate artery
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6
Q

what does occlusion of the ACA cause?

A

paralysis and sensory loss in contralateral leg and perineum

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7
Q

what is the major artery affected in stroke?

A

middle cerebral artery

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8
Q

describe the MCA

A
  • larger branch of ICA
  • has numerous branches
  • passes through the lateral sulcus and travels along lateral surface of frontal and parietal lobes
  • most common site of stroke
  • divided into M1, M2 and M3
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9
Q

what are the lateral lenticulostriate arteries?

A

branches of the MCA that provide supply to basal ganglia

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10
Q

M1 vs M2 vs M3 of middle cerebral artery

A
  • M1 = horizontal segment (gives rise to lateral lenticlostriate arteries which supply basal ganglia)
  • M2 = sylvian segment
  • M3 = cortical segment
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11
Q

what does occlusion of the MCA cause?

A
  • contralateral paralysis (mostly in lower face and in the ar)
  • general somatosensory deficits
  • speech deficits (aphasia) if dominant hemisphere affected
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12
Q

describe the basilar artery

A
  • runs forward in midline on ventral surface of pons
  • numerous branches — anterior inferior cerebellar, pontine, superior cerebellar
  • divides at rostral end of midbrain - posterior cerebral arteries
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13
Q

what does occlusion of the basilar artery cause?

A

coma — followed by death due to respiratory failure (as it supplies brainstem = where CV and resp centres are)

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14
Q

describe the posterior cerebral artery

A
  • curve around midbrain and reach medial surface of cerebral hemisphere
  • important branches — cortical branches supply visual cortex, posterior choroidal, posterior communicating
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15
Q

what does occlusion of posterior cerebral artery cause?

A

blindness

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16
Q

what is the circle of willis? function? limitations?

A
  • ring of arteries at base of brain — forms an anastomoses
  • provides a safety mechanism — if one artery gets blocked the circle will still provide the brain with blood
  • however actual significance of this is dependent on size of communicating arteries = highly variable between individuals in elderly population, anastomoses are not sufficient dye to narrowing of large vessels and communicating arteries because of vascular disease
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17
Q

laterally, what are the arterial territories (ACA, MCA, PCA)?

A
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18
Q

medially, what are the arterial territories (ACA, MCA, PCA)?

A
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19
Q

fill in the gaps with what would be affected by a stroke in each location

A
20
Q

what does FAST stand for in ACT FAST?

A

face, arm, speech, time

21
Q

describe the acute pathophysiology in an ischaemic stroke

A
  1. energy failure (due to drop in blood supply — drop in O2 and ATP)
  2. anoxic depolarisation of cell membranes, excitotoxicity, oxidative stress, necrosis
  3. peri-infarct depolarisation, calcium overload, mitochondrial damage (release reactive O2 species)
  4. inflammation, programmed cell death
  5. infarcted tissue
22
Q

what is haemorrhage?

A

rupture of a blood vessel

23
Q

describe the intracerebral haemorrhage pathophysiology

A
24
Q

what is the penumbra?

A

vulnerable tissue ‘under threat’ — will turn into core dead tissue if not treated early

25
Q

describe the core vs penumbra after a stroke

A

core
- cells in immediate area
- die within minutes-hours
- beyond rescue

penumbra
- surrounding regions
- blood supply compromised but not cut off
- cells under ‘threat’ but not dead
- potential for rescue
- must start treatment early

26
Q

what provides close coupling between vessel and neurone and allow blood supply to change very quickly to allow supply to active neurones?

A

astrocytes

27
Q

what is the major excitatory neurotransmitter in the brain?

A

glutamate

28
Q

describe excitotoxicity

A
  • drop in ATP — failure of membrane pumps
  • glutamate remains in synaptic clefts
  • cell remains polarised
  • failure if AMPA and NMDA receptors
  • excessive levels of calcium in cell
  • free radical formation
  • cell death
29
Q

describe oxidative stress

A

= overproduction of reactive O2 species
> drives inflammation

  • reduction in ATP
  • mitochondria membranes collapse
  • reactive oxygen species (H2O2) released
  • acted upon by free radials such as superoxide, causing them to release hydroxide radicals
  • these are extremely toxic
  • leads to changes within the cell —> leads to oxidation of proteins and lipids —> eventually CELL DEATH
30
Q

describe post-ischaemic inflammation

A
31
Q

reperfusion is changes in vasculature which allow what to happen?

A

allow the activation of inflammatory cells and migration of immune cells into brain tissue

32
Q

what 2 things does reperfusion cause?

A
  • inflammatory cell activation — releases cytokines which activate different membrane proteases
  • free radical formation — cell membrane injury and changes in intracellular processes — cell death
33
Q

what happens when there is a clot/damage to a vessel?

A
  • tight junctions broken down
  • exposure of underlying basement membrane
  • vWF released
  • binds platelets — bind fibrin, RBCs, neutrophils etc
34
Q

what is the result of migration of neutrophils and other immune cells into brain tissue?

A

they release contents (cytokines, proteases, reactive O2 species) which damage neurones

35
Q

what is the result of thrombo-inflammation?

A

neuronal death

36
Q

name some post-stroke complications

A
  • motor impairment
  • aphasia
  • visual problems
  • cognitive problems
  • new onset dementia
  • anxiety
  • language comprehension
  • depression
37
Q

what do damaged neurones release?

A

DAMPs = damaged associated molecular patterns

38
Q

what do DAMPs do?

A
  • they are recognised by brain resident microglia and infiltrating monocytes via pathogen recognition receptors (activate microglia and infiltrating cells)
  • upregulation of receptors on cell surface and release of cytokines/chemokines, ROS, MMPs etc
39
Q

what is sterile inflammation?

A

= inflammation in the absence of a pathogen
- no pathogen therefore the released substances cause damage instead of activating neurtophils

40
Q

what does infiltration of cells and activation of resident cells happen in response to?

A

damage to basement membrane and BBB

41
Q

what is Il-1?

A
  • pro-inflammatory cytokine
  • acts on hypothalamus to cause fever
  • also released by brain in response to injury
42
Q

Il-1 in stroke treatment?

A
  • il-1 receptor antagonist (IL-1Ra) = anakinra
  • time of first dose within 6 hours
  • in phase 3 of clinical trials
  • safe and effective for ischaemic stroke
  • being trialled in subarachnoid haemorrhage
43
Q

what happens in the brain in repair and recovery after a stroke?

A

> the brain can produce new cells — neurogenesis and angiogenesis

> brain areas can take over functions from damaged area — plasticity

> inflammation may be important — stem cells release inflammatory substances and glial cells secrete growth factors

44
Q

what is tPA?

A
  • tissue plasminogen activator
  • catalyses the conversion of plasminogen to plasmin
  • given in a hyper-acute setting
  • open up vessels and allow recovery
45
Q

what are problems with tPA?

A

> currently only a small proportion (12%) of patients treatment
- needs to be given early and in a controlled setting
- stroke services need to be optimal for this to happen

> increased risk of haemorrhage

> incomplete re-canalisation and high (27%) re-occlusion rate

> reperfusion itself can be detrimental (results in inflammation and oxidative stress)

> new treatments still required (not thrombectomy as this needs specialist centres and highly trained specialists)

46
Q

what are some possible treatment targets in the pathophysiology of stroke?

A
  • free radical scavengers/antioxidants
  • nootropic/stimulator — stimulate GFs
  • growth factors to stimulate neurogenesis, synaptogenesis, axogenesis
  • antiapoptotic agents
  • anti inflammatory agents (prevent cytokine release, microglia and leukocyte activation)
  • calcium antagonists (prevent calcium overload from failure of NMDA receptors)
47
Q

stroke is a dynamic phenomenon :

initiates with an ____ insult resulting in a ____ ____ infarct, followed by ______ and _____ events leading to delayed, penumbra cell death

A
  • excitotoxic insult
  • necrotic core infarct
  • inflammatory and oxidative events

PBL SEM 3 (49 decks)

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