Stroke And Vascular Flashcards

(38 cards)

1
Q

What is a stroke

A

A clinical syndrome characterised by rapidly developing clinical symptoms and/ or signs of focal neurological deficit lasting more than 24 hours and through to be of vascular origin

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2
Q

Incidence of stroke

A

150000 a year
Lifetime risk 1 in 6
1-2/ 1000 per year in the UK

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3
Q

How to diagnose stroke?

A

History: headaches, positive and negative symptoms; PMH of risk factors and migraines

Examination
HR, BP, O2 stats, temp
BMs- hypoglycaemia induces stroke like symptoms
CVS including carotid bruits
Resp- signs of pneumonia
Cardio
Abdo- risk of retention
Cranial nerves
Speech
PNS
Gait if possible

Scans
CT head scans are unreliable as they take time to show infarcts
+/- Carotid Doppler/ CT angiogram
ECG- AF
bloods- FBC; U+Es; LFTs; bone; clotting; BMs; cholesterol; maybe ESR; haemophilia screen and vasculitis screen
CXR- signs of aspiration
Echo+ 24 hour tape +/- prolonged monitoring

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4
Q

What are positive and negative symptoms of stroke?

A

Negative:
- weakness
- loss of motor control/ dexterity

Positive
- spasticity
- abnormal resting posture
- intrusive movement synergies e.g pins and needles

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5
Q

What are risk factors of stroke?

A

Giant Cell artheritis
PFOs
Diabetes
High cholesterol
hypertension
CAD
Valvular disease
AF
Smoking
Infection
Age
Sex younger men at more risk but women live longer so more chance later in life
Race and ethnicity
Family history
High stress
Bleeding disorders
Obesity and unhealthy life style

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6
Q

Classification of stroke

A

Ischaemic- interrupted blood supply to parts of the brain

Haemorrhagic- bleeding from artery into the brain’s parenchyma and the pressure leads to stroke like symptoms
(Does not include subarachnoid haemorrhage)

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7
Q

List the differences between ischaemic and haemorrhagic stroke

A
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8
Q

Bamford classification of stroke

A
  • Lacunar- motor or sensory only
  • Partial anterior circulation- 2 of: motor; sensory; cortical or hemianopia
  • Total anterior circulation: all of motor; sensory; cortical or hemianopia
  • Posterior circulation: heminaponia; brain stem; cerebellar
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9
Q

What supplies the anterior circulation of the brain

A

Carotid artery

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10
Q

What supplies the posterior circulation of the brain

A

bilateral vertebral arteries

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11
Q

TACS symptoms

A

Motor or sensory loss
Cortical e.g. dysphasia, neglect etc
Homonymous hemianopia- loss of half of the vision in the left side of both left and right eye

The signs match up in terms of L and R as it is coming from the same lesion

E.g. left sided motor loss with left sided homonymous hemianopia

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12
Q

Visual field defects in stroke

A
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13
Q

PACS

A

2 of the following
- motor or sensory loss
- cortical e.g dysphasia neglect etc
- Homonymous hemianopia

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14
Q

LACS

A

Pure motor (internal capsule, pons)
Pure sensory (thalamus)
Sensorimotor
Ataxic hemiparesis (pons)
Movement disorder

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15
Q

POCS

A

Isolated hemianopia
Brain stem signs
Cerebrallar ataxia
Hemiparesis
Hemisensory loss
Vertigo, vomiting
Diplopia
Facial weakness/ numbness
Dysphagia
Resp failure
Coma & death

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16
Q

Which type of stroke has the worst prognosis

A

TACS 60% chance of dying after a year and 35% dependent after a year

17
Q

ICH score parameters

A

GCS
ICH volume in cm2
Infratentorial origin of ICH
Age

ICH score of 3 and higher > 60% chance of death within a month

18
Q

Transient ischaemic attacks

A

Neurological signs that are consistent with a stroke that lasts for less than 24 hours
No damage on CT, may appear on MRI
Opportunity to reduce stroke risk
Fluctuating symptoms due to fluctuating swelling and blood supply around the bleed

ABCDE2 score to predict stroke 7 days post TIA

19
Q

Stroke symptoms mimics

A

Migraines
Tumours
Abscess
Epilepsy and Todd’s palsy
Subarachnoid
Subdural
Cerebral vein thrombosis
MS
MG
Bell’s palsy
Hypoglycaemia
Sepsis
Dementia
Hypothermia
Old strokes

20
Q

Where in the brain consume the most O2

A

grey matter due to a lot of the neural cell bodies being located there and they are the metabolic centre for nerve cells

Mitochondria present where ATP is made through oxidative phosphorylation > o2 and glucose

Energy deprived neurones die quickly

They also require a lot of energy due to the need to generate action potentials and create a concentration gradient and pump ions actively. They also send a lot of info and particles distally to the mitochondria

Synaptic transmission is the most energy consuming

21
Q

Where is glycogen stored in the brain

A

Astrocytes, they also transfer glucose to neurons

Glucose is also a pre cursor for neurotransmitters

If the body runs out of glucose fuel it resorts to glycogenesis and breakdown of muscle for energy sources

22
Q

Adaptive blood supply to the brain

A

Circle of Willis- helps safeguard the O2 supply from interruption by arterial blockage

Micro circulation- in chronic hypoxia (1-3 week) there is an adapted increase in capillary density in the brain to nearly double

Blood brain barrier- created by tight junctions in the endothelium of cerebral capillaries; whereby it is continuous creating the ‘barrier’

Neuromuscular component

23
Q

What causes a decrease in capillary density in the brain

24
Q

What is cerebral perfusion pressure

A

CPP is Amount of pressure needed to maintain blood flow to the brain

CPP helps cerebral blood flow (CBF) to be maintained constantly at a perfusion pressure of 50-150 mmHg
At the lower end of CBF, vessels are dilated and at the upper end they are constricted. In ischaemia that auto-regulation is lost and the arteries are super dilated to maximise flow

Regulated by opposing forces:

  • mean arterial pressure (MAP) pushes blood into the brain
  • intracranial pressure (ICP) is the force that keeps blood out 0-10 mmHg

CPP= MAP- ICP

25
What increases ICP and what are the complications?
ICP is increased by: - intracranial bleeding - cerebral oedema - tumour Increased ICP causes: - collapsed veins Decreased effective CPP - reduced blood flow
26
What is Cushing’s reflex
An increase in ICP due to intracranial haemorrhage can compress the blood vessels leading to the brain The increased ICP intracranial pressure reduces cerebral perfusion Resultant cerebral ischaemia causes massive SNS activation which leads to an increase in blood pressure in an effort to restore cerebral perfusion
27
What is the average blood flow to the brain
50ml/ min for each 100g of brain
28
How does CBF remain constant in hypertension
Due to increased cerebral vascular resistance and it falls in hypotension
29
Roles of the BBB
Protective barrier Stops most drugs getting into CNS Allows lipid soluble molecules to cross freely D glucose is carried on GLUT1 There are carriers for adenosine, metabolic acids (lactate) and amino acids
30
How do cerebral capillaries differ from the rest?
Tight junctions They are surrounded by astrocytes that interact with which they interact
31
How do astrocytes interact with the capillaries
- Regulate cerebral flow - Upregulate tight junction proteins - Contribute to ion and water homeostasis - Interface directly with neurons
32
What makes up the neurovascular unit and how does it affect the CBF
Component of the BBB Neurons Astrocytes Endothelial cells of the BBB Myocytes- smooth muscle Pericytes Extracellular matrix components Effect on CBF - neurons release glutamate > increases intracellular calcium in astrocytes then they couple > stimulate the release of vasodilators - some neurons release NO, PGE2, VIP > vasodilation
33
How do astrocytes and neurons cooperate in neurovascular coupling
Through glutamate signalling and they lead to increased blood flow It is defected in hypertension, spinal cord injury and stroke
34
How does the cerebral blood flow change in response to different metabolic demand?
Neural- PNS and SNS input Metabolic- Neural activity leads to ATP breakdown and thus adenosine Low PO2 and high PCO2 and low pH + increase in potassium> triggers vasodilation Fall in pH in extracellular fluid evokes pronounced dilation Myogenic- Independent of nerve blood supply and dependant on perfusion pressure Responsive to change in vascular tone, increase in pressure leads to vasoconstriction and vice versa
35
Types of communication disorders
Aphasia Dysarthria Apraxia of speech Symphonic
36
What is aphasia
Impairment of language Area of damage: left hemisphere- Broca’s area in the frontal lobe AND wernicke’s area- posterior section of the superior temporal gyrus in the cerebral hemisphere (usually left) Can also occur due to head injury and tumours
37
What is the arcuate fasciculus made up of?
Broca’s area and Wernicke’s area
38
What areas of communication does aphasia affect?
As it is responsible for language difficulty: Reading: acquired dyslexia Writing: acquired dysgraphia Auditory comprehension: receptive aphasia Speaking: expressive aphasia