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MBBS - Year 2 > Vascular System & Stroke - Acute Stroke > Flashcards

Vascular System & Stroke - Acute Stroke Flashcards

1
Q

Definition of stroke

A

Clinical syndrome characterised by rapidly developing clinical symptoms and/or signs of focal neurological deficit lasting more than 24 hrs and thought to be of vascular origin

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2
Q

Why is stroke important

A

3rd leading cause of death
Incidence 150,000
Lifetime risk of 1 in 6
Number one cause of long-term disability

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3
Q

Diagnosing stroke

A

Hx
Examination
Scans
ECG, bloods, CXR, 24 hr tape

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4
Q

Hx of stroke

A 
PC - onset times (<6 hrs for thrombectomy)
PMH - risk factors 
Drug hx 
Allergies 
Social hx

Consistency of symptoms
Handedness

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5
Q

What can’t you thrombolyse with on ACE inhibitors

A

Alteplase - can cause angiodema

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6
Q

Examination for stroke

A 
HR, BP, oxygen sats, temp, BM
CVS incl for carotid bruits - listening for whooshing with stethoscope on neck 
Resp
Abdo
Cranial nerves 
Speech 
PNS
Gait if possible
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7
Q

Bloods for stroke investigations

A 
FBC 
U&E
LFTs
Bone 
Clotting 
Blood sugar 
Cholesterol 
\+/- ESR, antiphospholipid screen, haemophilia screen, vasculitis screen
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8
Q

Investigations for stroke

A 
Bloods
ECG
CT head
CXR
\+/- CT perfusion scan, MRI
Carotid dopplers/ CT angiogram
Echo + 24 hr tape +/- prolonged cardiac monitoring
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9
Q

CT perfusion scan

A

Injecting large quantities of dye and taking several CTs at once
Done when onset time is unknown and to see whether or not the pt can be thrombolysed (size of penumbra)

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10
Q

Types of stroke

A

Ischaemic

Haemorrhagic

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11
Q

Types of haemorrhagic stroke

A

Primary

Secondary

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12
Q

Primary haemorrhagic stroke causes

A

Amyloid angiopathy

Hypertensive

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13
Q

Secondary haemorrhagic stroke causes

A

AVM
Aneurysm
Coagulopathy

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14
Q

AVM

A

Arterial Venous Malformation

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15
Q

Cryptogenic

A

Idiopathic

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16
Q

Bamford (Oxford) Classification of strokes

A

Lacunar (LACS)
Partial anterior circulation (PACS)
Total anterior circulation (TACS)
Posterior circulation (POCS)

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17
Q

Signs of lacunar stroke

A

Motor or sensory impairments only
Sensorimotor
Ataxic hemiparesis

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18
Q

Signs of PACS

A

2 of following: motor or sensory; cortical; hemianopia

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19
Q

Signs of TACS

A

All of: motor or sensory; cortical; homonymous hemianopia

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20
Q

Cortical impairment

A

Aphasia, ataxias, weakness etc

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21
Q

Signs of POCS

A 
Isolated hemianopia
Brain stem signs
Cerebellar - balance (ataxia)
Dysarthria 
Hemiparesis 
Vertigo, vomiting 
Diplopia 
Facial weakness/ numbness 
Dysphagia
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22
Q

Hemianopia

A

Blindness over half the field of vision

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23
Q

Posterior circulation of brain

A 
Posterior cerebral artery 
Posterior communicating artery 
Basilar artery 
Superior cerebellar artery 
Anterior inferior cerebellar artery
Anterior spinal artery 
Vertebral artery
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24
Q

Anterior circulation of brain

A 
Anterior cerebral artery 
Anterior communicating artery 
Middle cerebral artery 
External carotid artery 
Internal carotid artery 
Common carotid artery
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25
Q

Dysphasia

A

Partial loss of language due to brain disease

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26
Q

Diplopia

A

Double vision

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27
Q

% Dead at 1 year - PACS

A

20

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28
Q

% Dead at 1 year - TACS

A

60

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29
Q

% Dead at 1 year - POCS

A

20

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30
Q

% Dependent at 1 year - LACS

A

25

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31
Q

% Dependent at 1 year - PACS

A

30

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32
Q

% Dependent at 1 year - TACS

A

35

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33
Q

% Dependent at 1 year - POCS

A

20

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34
Q

ICH score

A

Score predicting 30-day mortality after stroke
From 1 - 6. Higher the score - higher mortality
Looks at GCS, ICH volume, Infrantentorial origin of ICH and age

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35
Q

TIA definition

A

Neurological signs that are consistent with a stroke that lasts for less than 24 hrs
Usually last &laquo_space;24 hrs
No damage on CT, maybe on MRI

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36
Q

Importance of TIA’s

A

Opportunity to reduce stroke risk factors and prevent strokes

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37
Q

ABCD2 score

A

Predicts risk of stroke 7 days after TIA

Total out of 7

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38
Q

Stroke mimcs

A 
Migraine 
Tumour 
Abscess
Subarachnoid/ subdural 
Cerebral vein thrombosis 
Epilepsy and Todd's palsy 
MS 
Myasthenia gravis 
Bell's palsy 
Functional neurological disorder 
Metabolic disorder e.g. hypoglycaemia 
Sepsis
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39
Q

Least tolerant organ of ischaemia

A

Brain

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40
Q

Where is the highest metabolic demand in the brain

A

Closely packed neuronal cell bodies (metabolic centre of nerve cell)

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41
Q

Brain preferred energy substrate

A

Glucose, transported via glucose transporters or capillary endothelial cells, neurons and astrocytes

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42
Q

Key structural adaptations of brain to ensure constant blood supply

A

The Circle of Willis

The Microcirculation

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43
Q

Function of Circle of Willis

A

Helps safeguard oxygen supply from interruption by arterial blockage
Allows collateral circulation if theres an arterial blockage

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44
Q

Whats included in Circle of Willis

A 
Anterior cerebral artery 
Anterior communicating artery 
Middle cerebral artery 
Posterior communicating artery 
Posterior cerebral artery 
Superior cerebellar artery
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45
Q

How does blood reach brain

A

Through 4 source arteries (2 internal carotid arteries and two vertebral arteries)

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46
Q

The microcirculation

A

A high capillary density optimises O2 transport in the brain
Red Cell Velocity is very high (1mm/sec) and heterogenous (0.3 to 3.2 mm/sec)

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47
Q

How does 1-3 week(s) of chronic hypoxia exposure affect brain capillaries

A

Density nearly doubles

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48
Q

How does HTN affects brain capillaries

A

Decreases no.

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49
Q

What does interruption of cerebral blood flow for a few seconds cause

A

Unconsciousness

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50
Q

What does persistent ischaemia for a few mins cause

A

Irreversible cellular damage

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51
Q

How does the brain regulate mean arterial pressure

A

Through a feedback loop

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52
Q

What does MAP play a role in

A

Determining CPP

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53
Q

MAP

A

Mean arterial pressure

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54
Q

CPP

A

Cerebral Perfusion Pressure

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55
Q

What happens when MAP is increased

A

Detected by baroreceptors
Increase in afferent pathways
Bradycardia and vasodilation counteracts

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56
Q

Physiological responses when MAP is decreased

A

Increased sympathetic outflow
Decreased sympathetic outflow
Vasoconstriction, tachycardia

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57
Q

Definition of CPP

A

Amount of pressure required to maintain blood flow to the brain

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58
Q

What is CPP regulated by

A

Two balanced opposed forces

  1. MAP - driving force that pushes blood into brain
  2. ICP - force keeping blood out
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59
Q

ICP

A

Intracranial pressure

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60
Q

CPP target

A

> 60 mmgh

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61
Q

CBF

A

Cerebral blood flow

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62
Q

Major determinant of CBF

A

CPP

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63
Q

What is ICP increased by

A

Intracranial bleeding
Cerebral oedema
Tumour

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64
Q

What does increased ICP leads to

A

Collapsed veins
Decreases effective CPP
Reduced blood flow

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65
Q

Calculating CPP

A

MAP - ICP

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66
Q

Regular range of CBF

A

Perfusion pressures of 50 and 150 mmHg

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67
Q

Ischaemic brain and CBF

A

Blood vessels become too dilated causing a reduction in CBF

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68
Q

HTN and CBF

A

Remains normal

Cerebral vascular resistance also increases

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69
Q

Calculating CBF

A

MAP / resistance

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70
Q

Cushing’s Reflex

A

An increase in ICP compresses blood vessel leading to brain
Increased ICP reduces CPP
Cerebral ischemia causes massive sympathetic activation –> increases systemic blood pressures

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71
Q

CBF regulation and metabolic requirements

A

Autoregulation ensures a basal

CBF can change in response to brain activity

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72
Q

Blood Brain Barrier

A

Cerebral capillaries form a tight BBB - protective mechanism

Stops most drugs from getting in CNS

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73
Q

What can freely cross BBB

A

Lipid soluble molecules e.g. O2, CO2 and general anaesthetic
D-glucose carried on GLUT1
Carriers for adenosine, metabolic acids (lactate), amino acids

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74
Q

Astrocytes regulation w/ capillaries in brain

A

Regulate CBF
Upregulate tight junction proteins
Contribute to ion and water homeostasis
Interface directly with neurons

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75
Q

Neurovascular unit

A

Component of BBB

Both astrocytes and neurons cooperate in neuromuscular coupling through glutamate signalling

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76
Q

What does the neuromuscular unit produce

A

An increase in local blood flow that is 4x higher than their consumption of oxygen and ATP of local neurons

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77
Q

What do neurons release in the neurovacsular unit

A

Glutamate –> increases intracellular Ca in astrocytes –> stimulates release of vasodilators.
Some release NO, PGE2, VIP - also vasodilators

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78
Q

When is neuromuscular unit defective

A

Stroke, HTN, SCI (spinal cord injury)

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79
Q

Metabolic changes causing changes in CBF

A

Neural activity leads to ATP breakdown - adenosine, lactate
Lowering of pO2, rising pCO2 trigger vasodilation
Fall in pH in blood extracellular fluid evokes pronounced dilation

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80
Q

Myogenic changes in response to changes in perfusion pressure

A

Direct changes in vascular tone

81
Q

How long does a person need to be deprived of blood for to lose consciousness

A

10 - 12 seconds

82
Q

What happens following an arterial occlusion

A

A reduction in perfusion pressure leads to compensatory homeostatic changes to maintain tissue oxygenation

83
Q

What happens after homeostatic mechanisms following an arterial occlusion fail

A

The process of ischaemia starts

84
Q

Infarct

A

Region of damaged tissue caused by depriving a brain region of its blood supply for longer than a few mins

85
Q

What does an infarct consist of

A

Core

Penumbra

86
Q

Infarct - core

A

Area of permanent damage

Hypoxia is so profound that cells undergo necrotic cell death

87
Q

Infarct - penumbra

A

Area of salvageable damage

External to core

88
Q

Cellular changes occurring after a stroke

A
  1. Hypoxia leads to inadequate supply of ATP
  2. Leading to failure of membrane pump
    allowing influx of Na and water into cells (cytotoxic oedema)
  3. Release of glutamate into extracellular fluid opens membrane channels
  4. Allowing influx of Ca and more Na into neurones
  5. Ca activates intracellular enzymes completing the destructive process
89
Q

What type of molecule is glutamate

A

Excitatory neurotransmitter

90
Q

What do infl mediators released by microglia and astrocytes in stroke cause

A

Death by all cell types in area of maximum ischaemia

91
Q

How is the infarction process worsened by

A

Anaerobic production of lactic acid and consequent falls in pH

92
Q

Earliest event in stroke

A

Brain oedema

93
Q

Cytotoxic oedema

A

Swelling of neurone increases ICP
Causes compression of ventricles and cerebral blood vessel –> reduces blood flow and oxygen supply
Vicious circle leading to rapid decline in cerebral perfusion

94
Q

How much of the body’s blood supply does the brain receive

95
Q

Where does the two branches of the CoW join

A

Anterior communicating artery

96
Q

What part of the cerebral hemisphere is supplied by the anterior cerebral artery

A

Upper outer

Medial aspect

97
Q

What part of the cerebral hemisphere is supplied by the middle cerebral artery

A

Lateral aspect

98
Q

What part of the cerebral hemisphere is supplied by the posterior cerebral artery

A

Small amount of inferior and posterior (medially) hemisphere

99
Q

How many arteries make up cerebral blood supply

100
Q

How many arteries enter skull vault

101
Q

What are the arteries making up the cerebral blood supply linked by

A

CoW - variable quality (diff sizes)

102
Q

Watershed areas of the brain

A

Different parts of the brain are supplied by particular arteries
Areas where diff arteries come into close contact with each other, terminal ends

103
Q

Is the sinus drainage in the brain venous or arterial

104
Q

What are the lobes of the brain divided by

105
Q

Where is the limbic system found

A

Deep within the lobes

106
Q

The lobes of the brain

A

Frontal
Parietal
Temporal
Occipital

107
Q

Sulci of the brain

A

Central sulcus
Lateral sulcus
Parieto-occipital sulcus

108
Q

Central sulcus

A

Divides frontal and parietal

109
Q

Lateral sulcus

A

Divides frontal and temporal lobe

110
Q

Parieto-occipital sulcus

A

Divides parietal and occipital lobe

111
Q

What is found in the grey matter of the brain

A

Neural cell bodies - responsible for processing info and making decisions

112
Q

What is found in the white matter of the brain

A

Mylineated axons - transporting signals

113
Q

Does stroke differentiate between grey and white matter

114
Q

Where is Broca’s area found

A

Frontal cortex

115
Q

Where is Wernicke’s area found

A

Temporal and parietal lobe

116
Q

Where is the memory area of the brain found

A

Temporal lobe

117
Q

Homunculus layout

A

Same for somatosensory cortex and primary motor cortex

Size corresponds with number of nerve endings and functional ability

118
Q

How is the body laid out in the cortex and internal capsule

A

Somato-topographically

119
Q

CVA

A

Cerebrovascular accident = stroke

120
Q

Effect of stroke in cerebellum

A

On same side - ipsilateral

121
Q

Effects of stroke in cerebrum

A

On opposite side -contralateral

122
Q

Do tumours differentiate between grey and white matter

123
Q

Stroke syndromes - middle cerebral artery

A 
Hemiparesis, arms worse than legs 
Facial weakness
Sensory loss 
Dysphasia 
Dysarthria 
Hemianopia
124
Q

Stroke syndromes - anterior cerebral artery

A 
Hemiparesis, legs worse than arms 
Incontinence 
Apathy
Disinhibition 
Mutism
125
Q

Stroke syndromes - posterior cerebral artery

A

Hemianopia
Amnesia
Sensory loss (thalamus)
Thalamic pain

126
Q

Stroke syndromes - vertebrobasilar artery

A 
Combinations of:
Hemiparesis 
Hemisensory loss 
Vertigo, vomiting 
Diplopia 
Facial weakness/ numbness 
Dysphagia 
Cerebellar ataxia 
Respiratory failure 
Coma & death
127
Q

Cause of LACS

A

Occlusion of one of the penetrating arteries that provides blood to the brain’s deep structures

128
Q

PICH

A

Primary Intracerebral Haemorrhage

129
Q

% of strokes that are ischaemic stroke

130
Q

% of strokes that are haemorrhagic strokes

131
Q

Recognise - management of stroke

A 
Symptom recognition (FAST) 
Call 999
132
Q

React - management of stroke

A

Transfer to hosp w/ Acute Stroke Unit

133
Q

Respond - management of stroke

A

Brain imaging and medical assessment

134
Q

Reveal - management of stroke

A

Confirm dx

Assess for thrombolysis drugs

135
Q

Rx/ reperfusion - management of stroke

A

Thrombolysis drugs
Aspirin
Monitoring on ASU

136
Q

Rehabilitation - management of stroke

A

Stroke Team assessment and treatment

137
Q

Reintegration - management of stroke

A

Pt support groups
Family
Community

138
Q

Treating TIA to reduce risk of stroke

A
  1. Immediate aspirin 300mg or Clopidogrel 300mg, then 75 mg daily
  2. Specialist assessment within 24 hrs of symptom onset
  3. 2’ prevention as soon as dx is confirmed e.g. statin
139
Q

When is carotid duplex scanning required

A

In anterior circulation events

Carotid endardectomy if significant (?> 50%)

140
Q

What should people with a suspected TIA w/ symptoms >1 week ago receive

A

Specialist assessment ASAP
MRI imaging (T2) mode of choice to excl haemorrhage
Immediate initiation of clopidogrel
2’ prevention as soon as dx confirmed - duplex scanning, lifestyle modification, BP, lipids
Anti-coagulation for those w/ AF

141
Q

What GREATLY reduces risks of stroke

A

Lower bp and cholesterol

142
Q

Specialist care for acute stroke

A

Specialist Stroke Unit Care - a/c stroke pts admitted directly
Early imaging
Pharmacological

143
Q

When is immediate CT required - stroke

A

Indications from thrombolysis (or early anticoagulation)
Been taking anticoagulant therapy
Depressed levels of consciousness (GCS < 13)
Unexplained progressive or fluctuating symptoms
Papilledema, neck stiffness or fever
Severe headache at onset of stroke

144
Q

Early vs late CT scanning

A

Early acute ischaemic stroke (first few hrs) CT scans can be normal or show only subtly
Early after a/c haemorrhage almost all changes will be seen

145
Q

Alteplase contraindications

A 
Time of symptom onset > 4.5 - 6 hrs
Bacterial endocarditis/ pericarditis
Treated w/ LMWH within 48 hrs
Hx/ evidence of ICH 
INR > 1.7
Low platelets
146
Q

What should be given for a/c stroke pts, where ICH excluded

A

Aspirin 300mg orally for 2 weeks then clopidogrel

147
Q

When should a PPI be added for a/c stroke pts

A

Those aged 70+ or reporting dyspepsia

148
Q

What should be given to stroke pts allergic/ intolerant to aspirin

A

Alternative anti-platelet agent e.g. clopidogrel

149
Q

What should be given to stroke pts already on aspirin

A

Consider dual antoiplatelt (Asp + Clopi) for 2-3 weeks

150
Q

What should be given to TIA pts with AF/ PAF

151
Q

DVT and PE prophylaxis/ treatment post stroke

A

LMWH - consider contraindications

152
Q

What should pts with ischaemic stroke and symptomatic DVT/ PE receive

A

Anticoagulant treatment if no contraindications

153
Q

What should pts with ICH and symptomatic DVT/PE receive

A

Treatment with a vena cava filter

154
Q

Treatment for MCA infarction

A

Consideration for Decompressive Hemicraniectomy

155
Q

Treatment for carotid/ vertebral dissection

A

Thrombolyse if appropriate, long-term anticoagulants or antiplatelet against

156
Q

Treatment for venous stroke

A

Cerebral venous sinus thrombosis (incl those with 2’ ICH) should be given full dose anticoagulation treatment (initially full-dose heparin and then warfarin [INR 2-3])

157
Q

What should be done for all ICH strokes

A

Monitoring of consciousness, if deteriorates refer immediately
Good BP control immediately (<140 mmHg)
Consider surgical intervention if hydrocephalus/ brainstem compression develops (cerebellar haemorrhage)

158
Q

Management of 1’ ICH stroke in pts on Warfarin

A

Combi of Prothrombin Complex Concentrate and IV vit K to reverse INR to normal

159
Q

Management of ICH strokes 2’ to DOACs

A

Consider spp reversal agent

160
Q

When is surgical intervention for ICH strokes, generally NOT for

A

Small, deep haemorrhages
Lobar haemorrhage unless rapid neurological deterioration
Large haemorrhage and sig. prior commodities before stroke
Supratentorial haemorrhage w/ GCS < 8

161
Q

MDT team

A 
Dr
Nurses 
PT 
OT 
SLT 
Dietician 
Social worker 
Psychologist 
Relatives
162
Q

Stroke pts and nutrition

A

Admission screening for dysphagia, malnutrition (MUST) & dehydration, repeated weekly
Bedside swallow assessment performed by staff

163
Q

Stroke pts and early mobilisation

A

Pts should be mobilised ASAP
Also offered active therapy - 45 mins/ 5x a week
When lying/ sitting position to minimise aspiration risk, shoulder sublaxation

164
Q

For how long can a stroke pt not drive

A

A month

3 months in multiple events

165
Q

Modifiable thromboembolic stroke risk factors

A 
HTN 
Diabetes 
Obesity 
Oestrogen containing drugs 
High cholesterol (LDL)
Alcohol 
Smoking
166
Q

How does HTN increases stroke risk

A

Increases artery damage

167
Q

How do oestrogen containing drugs increase stroke risk

A

Increases clot risk e.g. contraception/ HRT

168
Q

Calculating total risk of high cholesterol

A

Total cholesterol/ HDL

169
Q

How does alcohol increase stroke risk

A

Can also cause AF

170
Q

Non-modifiable thromboembolic stroke risk factors

A 
Previous stroke or TIA - any vascular event e.g. MI 
AF 
Carotid artery dissection 
FHx of any vascular incident 
APLS
Increasing age 
Male 
Ethicity - Afro-carribbeans > Asians > Caucasians
PFO 
Vasculitis 
PVD 
Polycythemia
171
Q

How does AF increase risk of stroke

A

Irregular contraction (fibrillation - flutter) of atria can lead to blood pooling and clotting, can break off and travel to brain

172
Q

Causes of carotid dissection

A

Can be caused by trauma or idiopathic

173
Q

How does APLS increases stroke risk

A

Increases clot formation

174
Q

PFO

A

Patent Foramen Ovale

Hole in heart

175
Q

How can PFO increase stroke risk

A

Clot can travel from heart to brain

176
Q

Polycythemia

A

Increased no. RBCs

Increased risk of clotting

177
Q

Stroke hx taking

A 
PC - symptoms (work out type of stroke; incl -ves as well)
HPC 
ICE 
PMH - risk factors 
Past surgical hx 
DH 
Allergies 
SH - incl normal functional status 
Fhx - MI, stroke
Long-term effects 
Current meds
178
Q

Visual fields examination

A
  1. Intro - start v close
  2. Ask pt to cover one eye and you cover the opposite and wiggle fingers above head - ask if they can see which side is moving
  3. Wiggle fingers at waist level
  4. Repeat with same eye covered with opposite hand to test nasotemporal field
  5. Repeat whole thing with other eye covered for myself and pt
179
Q

Occular motor nerve exam - Cranial nerve 3

A
  1. Ask pt to focus on finger and follow finger with hand, not moving head
  2. Move finger in H formation (medial rectus, lateral rectus, superior rectus, inferior rectus, superior oblique - CN6, lateral oblique rectus - CN4
  3. Watch eye movement
180
Q

Facial nerve examination

A
  1. Ask pt to wrinkle forehead
  2. Ask pt to close eyes and try to open it
  3. Ask pt to clench jaw and feel jaw muscles
  4. Ask pt to show teeth
181
Q

In AF pts, what should be given instead of clopidogrel in a TIA

A

Epixiban (blood thinner)

182
Q

What are UMNs responsible for

183
Q

What do UMN lesions cause

A

Hyperreflexia, increased reflexes and spasticity

184
Q

What are LMNs responsible for

A

Responsible for preventing excessive movement

185
Q

What do LMN lesions cause

A

Paralysis, decreased reflexes and weakness

186
Q

Sensory aspect of facial nerve (trigeminal) exam

A

Touch both sides of forehead, cheek and chin and ask pt if they can feel it

187
Q

A/c ix for stroke

A

CT head
ECG
Bloods
CXR

188
Q

Imaging for TIA

A

Carotid Doppler ultrasound
CT or MR angiography for further evaluation of significant carotid stenosis
ECG

189
Q

Which TIA pts will have a carotid endarterectomy

A

Pts fit enough to tolerate surgery, who had a symptomatic TIA with a good recovery in last 6 months, involving anterior circulation

190
Q

Which cranial nerve is the facial nerve

191
Q

Cerebellum tests for stroke pts

A

Nystagmus (flickering) - follow hand with eyes
Dysdiadochokinesis - rapidly tap backs of hand
Test for sitting balance and standing balance (close eyes)
Ataxia

192
Q

How do you assess for confusion

A

AMT

Abbreviated Mental Test

193
Q

How do you assess for consciousness

A

GCS

Glasgow Coma Score under 13 is concerning

194
Q

What can cause larger ventricles on CT scans

A

Old strokes - scar tissue formation after compression

195
Q

Changes that can be seen on a stroke pts scans

A 
Areas of hypo-attenuation (dark) or hyper-attenuation (white)
Larger ventricles 
Loss of sulci
Loss of grey-white differentiation 
Midline shift caused by oedema
196
Q

What happens if the optic chiasm is damaged

A

Bitemporal hemianopia (can only see nasal field)

197
Q

What does homonymous hemianopia match

A

Side of weakness

If left stroke, can’t see rhs and will have rhs weakness

198
Q

Relative contraindications for thrombolysis

A

> 75 yrs
Pregnancy
Uncontrolled HTN (180/110)
Major surgery within 3/52

MBBS - Year 2 (20 decks)

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