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PBL SEM 3 > 5 - stroke pathophysiology and clinical management > Flashcards

5 - stroke pathophysiology and clinical management Flashcards

1
Q

when is someone in a hyper-acute stroke unit and when is repatriation?

A
  • <48 hrs — HASU
  • repatriation at 72 hours
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2
Q

what is the WHO definition of a stroke?

A

a clinical syndrome characterised by the rapid onset of focal or global cerebral deficit lasting more than 24 hours or leading to death with no other apparent cause than a vascular one

  • RAPID ONSET
  • FOCAL OR CEREBRAL
  • LAST MORE THAN 24 HRS (if less = TIA)
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3
Q

what are the 2 main subtypes of stroke?

A
  • ischaemic = 85%
  • haemorrhagic = 15%
    - intracerebral
    - subarachnoid
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4
Q

what are typical imaging appearances in an ischaemic stroke?

A
  • wedged-shaped hypodensity with complete loss of grey-white matter differentiation
  • localised swelling with sulcal effacement
  • in a recognisable arterial territory
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5
Q

what are some hyper acute ischaemic changes seen in scanning?

A
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6
Q

what would a stroke look like on CT angiogram?

A
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7
Q

how much tPA is given over one hour?

A

1mg/kg

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8
Q

what is the aim of intravenous thrombolysis?

A

dissolve thrombus to allow reperfusion

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9
Q

intravenous thrombolysis is only beneficial if administered when?

A

<4.5 hours after stroke

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10
Q

what % of UK patients are eligible for intravenous trhombolysis?

A

12%

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11
Q

what are 2 significant risks of intravenous thrombolysis?

A
  • haemorrhage — 1/30
  • angioedema — not usually too harmful, allergic reaction, 1/14
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12
Q

what is mechanical thrombectomy?

A

stent retriever used to pull clot out

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13
Q

what is the treatment window from onset for mechanical thrombectomy?

A

<6 hours

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14
Q

what estimated % of people are eligible for thrombectomy?

A

10-15%

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15
Q

describe secondary prevention of ischaemic stroke

A

> identify cause — athero-thrombo-embolism (50%), cardioembolic (20%), small vessel disease (25%), miscellaneous rare causes (5%)

> aspirin (1x daily for 2 weeks) then clopidogrel long term

> statin

> BP management (systolic BP <130 mmHg long-term)

> atrial fibrillation — anticoagulation if risk:benefit favourable

> carotid revascularisation

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16
Q

how does ICH lead to herniation syndromes?

A

very large haematomas — pushing structures over to the side — causes herniation syndromes

17
Q

second injury in ICH?

A

toxic products such as thrombin, Hv, heme, iron in haematoma — damage surrounding brain tissue

18
Q

what do heme and iron trigger?

A

inflammatory action — worsens damage

19
Q

what is the target systolic BP over first 24 hours in hyper acute setting?

A

130-140 mmHg

20
Q

why is there uncertainty for intensive BP lowering for larger haematomas (>30ml)?

A

raise intracranial pressure — can reduce cerebral perfusion pressure — could cause ischaemia by dropping BP dramatically

21
Q

what are risks in infratentorial ICH? what does the infratentorium region include?

A
  • brainstem compression, herniation syndromes, hydrocephalus
  • region below tentorium. includes brainstem and cerebellum (relatively small space)
22
Q

what neurosurgery procedures can be carried out for an infratentorial ICH?

A
  • EVD = external ventricular drain — to relieve hydrocephalus. goes into frontal horn of lateral ventricle to relieve pressure above when there is a blockage below in posterior fossa
  • posterior fossa decompression — remove some of posterior cranium
  • haematoma evacuation — remove mass
23
Q

neurosurgery for supratentorial ICH?

A
  • early haematoma evacuation in the stable patient
  • haematoma evacuation in the detiorating patient
  • external ventricular drainage for hydrocephalus
24
Q

are the majority of ICH infra or supratentorial?

A

supra

25
Q

what is the ABC hyper acute care bundle?

A

A : anticoagulant reversal : deliver reversal agent <90 min from arrival

B : blood pressure lowering : deliver intensive bp lowering with needle-to-target time < 60 min (time from giving 1st dose to reaching the target BP)

C : care pathway : refer patients with good pre-morbid function and any of the following to neurosurgery
- GCS < 9
- posterior fossa ICH
- obstructed 3rd/4th ventricle
- haematoma volume > 30ml

26
Q

what is the most common structural cause of ICH?

A

hypertensive microangiopathy — due to high BP on deep arteries of the brain

27
Q

what is cerebral amyloid angiopathy?

A
  • a structural cause of ICH
  • amyloid protein builds up in arteries in particular at cortico-subcortical junction, particularly posterior aspect of brain — vessels fragile and prone to rupture — causes lobar bleeds and bleeding over surface of brain — cortical superficial siderosis — bleeding in sulci

PBL SEM 3 (49 decks)

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