Vascular System & Stroke - Acute Stroke Flashcards
(198 cards)
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
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
3
Q
Diagnosing stroke
A
Hx
Examination
Scans
ECG, bloods, CXR, 24 hr tape
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
5
Q
What can’t you thrombolyse with on ACE inhibitors
A
Alteplase - can cause angiodema
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
7
Q
Bloods for stroke investigations
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FBC U&E LFTs Bone Clotting Blood sugar Cholesterol \+/- ESR, antiphospholipid screen, haemophilia screen, vasculitis screen
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
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)
10
Q
Types of stroke
A
Ischaemic
Haemorrhagic
11
Q
Types of haemorrhagic stroke
A
Primary
Secondary
12
Q
Primary haemorrhagic stroke causes
A
Amyloid angiopathy
Hypertensive
13
Q
Secondary haemorrhagic stroke causes
A
AVM
Aneurysm
Coagulopathy
14
Q
AVM
A
Arterial Venous Malformation
15
Q
Cryptogenic
A
Idiopathic
16
Q
Bamford (Oxford) Classification of strokes
A
Lacunar (LACS)
Partial anterior circulation (PACS)
Total anterior circulation (TACS)
Posterior circulation (POCS)
17
Q
Signs of lacunar stroke
A
Motor or sensory impairments only
Sensorimotor
Ataxic hemiparesis
18
Q
Signs of PACS
A
2 of following: motor or sensory; cortical; hemianopia
19
Q
Signs of TACS
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All of: motor or sensory; cortical; homonymous hemianopia
20
Q
Cortical impairment
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Aphasia, ataxias, weakness etc
21
Q
Signs of POCS
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Isolated hemianopia Brain stem signs Cerebellar - balance (ataxia) Dysarthria Hemiparesis Vertigo, vomiting Diplopia Facial weakness/ numbness Dysphagia
22
Q
Hemianopia
A
Blindness over half the field of vision
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
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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Dysphasia
Partial loss of language due to brain disease
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Diplopia
Double vision
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% Dead at 1 year - PACS
20
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% Dead at 1 year - TACS
60
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% Dead at 1 year - POCS
20
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% Dependent at 1 year - LACS
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% Dependent at 1 year - PACS
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% Dependent at 1 year - TACS
35
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% Dependent at 1 year - POCS
20
34
ICH score
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
35
TIA definition
Neurological signs that are consistent with a stroke that lasts for less than 24 hrs
Usually last << 24 hrs
No damage on CT, maybe on MRI
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Importance of TIA's
Opportunity to reduce stroke risk factors and prevent strokes
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ABCD2 score
Predicts risk of stroke 7 days after TIA
| Total out of 7
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Stroke mimcs
```
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
```
39
Least tolerant organ of ischaemia
Brain
40
Where is the highest metabolic demand in the brain
Closely packed neuronal cell bodies (metabolic centre of nerve cell)
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Brain preferred energy substrate
Glucose, transported via glucose transporters or capillary endothelial cells, neurons and astrocytes
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Key structural adaptations of brain to ensure constant blood supply
The Circle of Willis
| The Microcirculation
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Function of Circle of Willis
Helps safeguard oxygen supply from interruption by arterial blockage
Allows collateral circulation if theres an arterial blockage
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Whats included in Circle of Willis
```
Anterior cerebral artery
Anterior communicating artery
Middle cerebral artery
Posterior communicating artery
Posterior cerebral artery
Superior cerebellar artery
```
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How does blood reach brain
Through 4 source arteries (2 internal carotid arteries and two vertebral arteries)
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The microcirculation
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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How does 1-3 week(s) of chronic hypoxia exposure affect brain capillaries
Density nearly doubles
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How does HTN affects brain capillaries
Decreases no.
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What does interruption of cerebral blood flow for a few seconds cause
Unconsciousness
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What does persistent ischaemia for a few mins cause
Irreversible cellular damage
51
How does the brain regulate mean arterial pressure
Through a feedback loop
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What does MAP play a role in
Determining CPP
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MAP
Mean arterial pressure
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CPP
Cerebral Perfusion Pressure
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What happens when MAP is increased
Detected by baroreceptors
Increase in afferent pathways
Bradycardia and vasodilation counteracts
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Physiological responses when MAP is decreased
Increased sympathetic outflow
Decreased sympathetic outflow
Vasoconstriction, tachycardia
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Definition of CPP
Amount of pressure required to maintain blood flow to the brain
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What is CPP regulated by
Two balanced opposed forces
1. MAP - driving force that pushes blood into brain
2. ICP - force keeping blood out
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ICP
Intracranial pressure
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CPP target
>60 mmgh
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CBF
Cerebral blood flow
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Major determinant of CBF
CPP
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What is ICP increased by
Intracranial bleeding
Cerebral oedema
Tumour
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What does increased ICP leads to
Collapsed veins
Decreases effective CPP
Reduced blood flow
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Calculating CPP
MAP - ICP
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Regular range of CBF
Perfusion pressures of 50 and 150 mmHg
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Ischaemic brain and CBF
Blood vessels become too dilated causing a reduction in CBF
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HTN and CBF
Remains normal
| Cerebral vascular resistance also increases
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Calculating CBF
MAP / resistance
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Cushing's Reflex
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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CBF regulation and metabolic requirements
Autoregulation ensures a basal
| CBF can change in response to brain activity
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Blood Brain Barrier
Cerebral capillaries form a tight BBB - protective mechanism
| Stops most drugs from getting in CNS
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What can freely cross BBB
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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Astrocytes regulation w/ capillaries in brain
Regulate CBF
Upregulate tight junction proteins
Contribute to ion and water homeostasis
Interface directly with neurons
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Neurovascular unit
Component of BBB
| Both astrocytes and neurons cooperate in neuromuscular coupling through glutamate signalling
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What does the neuromuscular unit produce
An increase in local blood flow that is 4x higher than their consumption of oxygen and ATP of local neurons
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What do neurons release in the neurovacsular unit
Glutamate --> increases intracellular Ca in astrocytes --> stimulates release of vasodilators.
Some release NO, PGE2, VIP - also vasodilators
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When is neuromuscular unit defective
Stroke, HTN, SCI (spinal cord injury)
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Metabolic changes causing changes in CBF
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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Myogenic changes in response to changes in perfusion pressure
Direct changes in vascular tone
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How long does a person need to be deprived of blood for to lose consciousness
10 - 12 seconds
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What happens following an arterial occlusion
A reduction in perfusion pressure leads to compensatory homeostatic changes to maintain tissue oxygenation
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What happens after homeostatic mechanisms following an arterial occlusion fail
The process of ischaemia starts
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Infarct
Region of damaged tissue caused by depriving a brain region of its blood supply for longer than a few mins
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What does an infarct consist of
Core
| Penumbra
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Infarct - core
Area of permanent damage
| Hypoxia is so profound that cells undergo necrotic cell death
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Infarct - penumbra
Area of salvageable damage
| External to core
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Cellular changes occurring after a stroke
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
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What type of molecule is glutamate
Excitatory neurotransmitter
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What do infl mediators released by microglia and astrocytes in stroke cause
Death by all cell types in area of maximum ischaemia
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How is the infarction process worsened by
Anaerobic production of lactic acid and consequent falls in pH
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Earliest event in stroke
Brain oedema
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Cytotoxic oedema
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
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How much of the body’s blood supply does the brain receive
15-20%
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Where does the two branches of the CoW join
Anterior communicating artery
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What part of the cerebral hemisphere is supplied by the anterior cerebral artery
Upper outer
| Medial aspect
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What part of the cerebral hemisphere is supplied by the middle cerebral artery
Lateral aspect
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What part of the cerebral hemisphere is supplied by the posterior cerebral artery
Small amount of inferior and posterior (medially) hemisphere
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How many arteries make up cerebral blood supply
4
100
How many arteries enter skull vault
3
101
What are the arteries making up the cerebral blood supply linked by
CoW - variable quality (diff sizes)
102
Watershed areas of the brain
Different parts of the brain are supplied by particular arteries
Areas where diff arteries come into close contact with each other, terminal ends
103
Is the sinus drainage in the brain venous or arterial
Venous
104
What are the lobes of the brain divided by
Sulci
105
Where is the limbic system found
Deep within the lobes
106
The lobes of the brain
Frontal
Parietal
Temporal
Occipital
107
Sulci of the brain
Central sulcus
Lateral sulcus
Parieto-occipital sulcus
108
Central sulcus
Divides frontal and parietal
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Lateral sulcus
Divides frontal and temporal lobe
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Parieto-occipital sulcus
Divides parietal and occipital lobe
111
What is found in the grey matter of the brain
Neural cell bodies - responsible for processing info and making decisions
112
What is found in the white matter of the brain
Mylineated axons - transporting signals
113
Does stroke differentiate between grey and white matter
No
114
Where is Broca's area found
Frontal cortex
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Where is Wernicke's area found
Temporal and parietal lobe
116
Where is the memory area of the brain found
Temporal lobe
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Homunculus layout
Same for somatosensory cortex and primary motor cortex
| Size corresponds with number of nerve endings and functional ability
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How is the body laid out in the cortex and internal capsule
Somato-topographically
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CVA
Cerebrovascular accident = stroke
120
Effect of stroke in cerebellum
On same side - ipsilateral
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Effects of stroke in cerebrum
On opposite side -contralateral
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Do tumours differentiate between grey and white matter
Yes
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Stroke syndromes - middle cerebral artery
```
Hemiparesis, arms worse than legs
Facial weakness
Sensory loss
Dysphasia
Dysarthria
Hemianopia
```
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Stroke syndromes - anterior cerebral artery
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Hemiparesis, legs worse than arms
Incontinence
Apathy
Disinhibition
Mutism
```
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Stroke syndromes - posterior cerebral artery
Hemianopia
Amnesia
Sensory loss (thalamus)
Thalamic pain
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Stroke syndromes - vertebrobasilar artery
```
Combinations of:
Hemiparesis
Hemisensory loss
Vertigo, vomiting
Diplopia
Facial weakness/ numbness
Dysphagia
Cerebellar ataxia
Respiratory failure
Coma & death
```
127
Cause of LACS
Occlusion of one of the penetrating arteries that provides blood to the brain's deep structures
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PICH
Primary Intracerebral Haemorrhage
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% of strokes that are ischaemic stroke
85%
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% of strokes that are haemorrhagic strokes
15%
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Recognise - management of stroke
```
Symptom recognition (FAST)
Call 999
```
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React - management of stroke
Transfer to hosp w/ Acute Stroke Unit
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Respond - management of stroke
Brain imaging and medical assessment
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Reveal - management of stroke
Confirm dx
| Assess for thrombolysis drugs
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Rx/ reperfusion - management of stroke
Thrombolysis drugs
Aspirin
Monitoring on ASU
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Rehabilitation - management of stroke
Stroke Team assessment and treatment
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Reintegration - management of stroke
Pt support groups
Family
Community
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Treating TIA to reduce risk of stroke
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
When is carotid duplex scanning required
In anterior circulation events
| Carotid endardectomy if significant (?> 50%)
140
What should people with a suspected TIA w/ symptoms >1 week ago receive
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
What GREATLY reduces risks of stroke
Lower bp and cholesterol
142
Specialist care for acute stroke
Specialist Stroke Unit Care - a/c stroke pts admitted directly
Early imaging
Pharmacological
143
When is immediate CT required - stroke
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
Early vs late CT scanning
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
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Alteplase contraindications
```
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
```
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What should be given for a/c stroke pts, where ICH excluded
Aspirin 300mg orally for 2 weeks then clopidogrel
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When should a PPI be added for a/c stroke pts
Those aged 70+ or reporting dyspepsia
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What should be given to stroke pts allergic/ intolerant to aspirin
Alternative anti-platelet agent e.g. clopidogrel
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What should be given to stroke pts already on aspirin
Consider dual antoiplatelt (Asp + Clopi) for 2-3 weeks
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What should be given to TIA pts with AF/ PAF
NOACs
151
DVT and PE prophylaxis/ treatment post stroke
LMWH - consider contraindications
152
What should pts with ischaemic stroke and symptomatic DVT/ PE receive
Anticoagulant treatment if no contraindications
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What should pts with ICH and symptomatic DVT/PE receive
Treatment with a vena cava filter
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Treatment for MCA infarction
Consideration for Decompressive Hemicraniectomy
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Treatment for carotid/ vertebral dissection
Thrombolyse if appropriate, long-term anticoagulants or antiplatelet against
156
Treatment for venous stroke
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
What should be done for all ICH strokes
Monitoring of consciousness, if deteriorates refer immediately
Good BP control immediately (<140 mmHg)
Consider surgical intervention if hydrocephalus/ brainstem compression develops (cerebellar haemorrhage)
158
Management of 1' ICH stroke in pts on Warfarin
Combi of Prothrombin Complex Concentrate and IV vit K to reverse INR to normal
159
Management of ICH strokes 2' to DOACs
Consider spp reversal agent
160
When is surgical intervention for ICH strokes, generally NOT for
Small, deep haemorrhages
Lobar haemorrhage unless rapid neurological deterioration
Large haemorrhage and sig. prior commodities before stroke
Supratentorial haemorrhage w/ GCS < 8
161
MDT team
```
Dr
Nurses
PT
OT
SLT
Dietician
Social worker
Psychologist
Relatives
```
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Stroke pts and nutrition
Admission screening for dysphagia, malnutrition (MUST) & dehydration, repeated weekly
Bedside swallow assessment performed by staff
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Stroke pts and early mobilisation
Pts should be mobilised ASAP
Also offered active therapy - 45 mins/ 5x a week
When lying/ sitting position to minimise aspiration risk, shoulder sublaxation
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For how long can a stroke pt not drive
A month
| 3 months in multiple events
165
Modifiable thromboembolic stroke risk factors
```
HTN
Diabetes
Obesity
Oestrogen containing drugs
High cholesterol (LDL)
Alcohol
Smoking
```
166
How does HTN increases stroke risk
Increases artery damage
167
How do oestrogen containing drugs increase stroke risk
Increases clot risk e.g. contraception/ HRT
168
Calculating total risk of high cholesterol
Total cholesterol/ HDL
169
How does alcohol increase stroke risk
Can also cause AF
170
Non-modifiable thromboembolic stroke risk factors
```
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
How does AF increase risk of stroke
Irregular contraction (fibrillation - flutter) of atria can lead to blood pooling and clotting, can break off and travel to brain
172
Causes of carotid dissection
Can be caused by trauma or idiopathic
173
How does APLS increases stroke risk
Increases clot formation
174
PFO
Patent Foramen Ovale
| Hole in heart
175
How can PFO increase stroke risk
Clot can travel from heart to brain
176
Polycythemia
Increased no. RBCs
| Increased risk of clotting
177
Stroke hx taking
```
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
Visual fields examination
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
Occular motor nerve exam - Cranial nerve 3
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
Facial nerve examination
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
In AF pts, what should be given instead of clopidogrel in a TIA
Epixiban (blood thinner)
182
What are UMNs responsible for
Movement
183
What do UMN lesions cause
Hyperreflexia, increased reflexes and spasticity
184
What are LMNs responsible for
Responsible for preventing excessive movement
185
What do LMN lesions cause
Paralysis, decreased reflexes and weakness
186
Sensory aspect of facial nerve (trigeminal) exam
Touch both sides of forehead, cheek and chin and ask pt if they can feel it
187
A/c ix for stroke
CT head
ECG
Bloods
CXR
188
Imaging for TIA
Carotid Doppler ultrasound
CT or MR angiography for further evaluation of significant carotid stenosis
ECG
189
Which TIA pts will have a carotid endarterectomy
Pts fit enough to tolerate surgery, who had a symptomatic TIA with a good recovery in last 6 months, involving anterior circulation
190
Which cranial nerve is the facial nerve
7th
191
Cerebellum tests for stroke pts
Nystagmus (flickering) - follow hand with eyes
Dysdiadochokinesis - rapidly tap backs of hand
Test for sitting balance and standing balance (close eyes)
Ataxia
192
How do you assess for confusion
AMT
| Abbreviated Mental Test
193
How do you assess for consciousness
GCS
| Glasgow Coma Score under 13 is concerning
194
What can cause larger ventricles on CT scans
Old strokes - scar tissue formation after compression
195
Changes that can be seen on a stroke pts scans
```
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
What happens if the optic chiasm is damaged
Bitemporal hemianopia (can only see nasal field)
197
What does homonymous hemianopia match
Side of weakness
| If left stroke, can't see rhs and will have rhs weakness
198
Relative contraindications for thrombolysis
>75 yrs
Pregnancy
Uncontrolled HTN (180/110)
Major surgery within 3/52
