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JMP Y2S1 > Week 38- Focal brain dysfunction: Stroke > Flashcards

Week 38- Focal brain dysfunction: Stroke Flashcards

1
Q

What is the main form of cerebral vessel control?

A

Local autoregulation play the major role

Very small role by Neural control

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2
Q

What are some autoregulation factors within cerebral vessels?

A

Metabolic:
rise in CO2, fall in pH and pO2 (similar to coronary control)
- Adenosine (ATP breakdown)
- K+ (from action potentials due to neuronal activity

Local:
vasoactive substances from astrocytes (NO)

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3
Q

How does cerebral blood flow change with Arterial pressure?

A

Is relatively steady (except for increases to about 60)

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4
Q

What allows the cerebral blood flow to remain steady?

A

Autoregulation reassures adequate CBF during fluctuations of (arterial pressure)

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5
Q

What is the mechanism of NO release by astrocytes?

A 
Increased neuronal activity
Increased glutamate release
Glutamate uptake by astrocytes
Astrocytes release NO
NO drives local vasodilation and increase in blood flow
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6
Q

What is stroke?

A

Ischaemic event leading to lack of blood supply to the brain:
Deficit of Oxygen
Deficit of glucose
Lack of waste removal

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7
Q

What is the two major types of stroke?

A

Ischaemic (80%) –> interrupted blood flow in a cerebral vessel
Haemorrhagic (20%) –> bleeding into brain tissue out of a cerebral vessel

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8
Q

What is blood supply so important to the brain?

A

No storage of crucial glucose and oxygen in the brain –> needs constant flow

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9
Q

What is a major cause of ischaemic stroke?

A

Embolism –> thrombus from other region of the body and travels to the brain

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10
Q

What side of the heart results in more thrombi and emboli from stroke?

A

Left side

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11
Q

What cardiovascular abnormalities may cause ischaemic stroke?

A 
Intracranial atherosclerosis
Penetrating artery disease
Carotid plaque with arteriogenic emboli
Flow reducing carotid stenosis
Aortic arch plaque
Cardiogenic emboli
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12
Q

How can causes of haemorrhagic stroke be described in two categories?

A

Increased pressure
OR
Decreased strength of the vessel

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13
Q

What cardiovascular abnormalities may cause haemorrhagic stroke?

A 
Hypertension
Aneurysms
Arteriovenous malfunctions
Head injury
Blood dyscrasias -->is a nonspecific term that refers to a disease or disorder, especially of theblood.
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14
Q

What happens in the brain tissue after stroke at time points: 30s, 1min, 5min, 7mins?

A

30 seconds –> metabolism alters and slows

1 minutes –> neurons stop functioning

5 minutes –> anoxia leads to the start of infarction:

- Vasodilation and blood stasis
- Oedema 
- Necrosis --> softening, liquefaction, tissue removal

7 minutes –> excitotoxic process begins to kill neurons

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15
Q

What is the cellular mechanism behind excitotoxic lesions?

A

Glucose/ O2 shortage gives two sequences of events via Loss of ATP and excess lactic acid

1. Loss of ATP --> Sodium potassium pumps stop functioning
- K+ escapes, Na+ enters and the cells depolarise
- Ca2+ released from intracellular stores AND calcium enters the cell via voltage- gated channels
- Ca2+ overload
- Calcium activates proteolytic and lipolytic enzymes, water also enters into the cells (following Ca2+) AND neurotransmitter Glutamate release
- Autolysis via activated proteins begins --> Cell swells and rupture from water excess

2. Lactic acid increase --> fall in pH
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16
Q

What is the effect of neurotransmitter release (glutamate) during excitotoxic shock?

A

Glutamate released by calcium overload feeds back to increase calcium through voltage gated and ligand gated calcium channels

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17
Q

What is the two key anatomies of a stroke region?

A

Core –> dead, infarcted brain tissue

Penumbra –> threatened, potentially salvageable tissue surrounding the infarct core soon after stroke

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18
Q

What are some signs and symptoms of stroke?

A

Sudden onset
Combination of sensory, motor and cognitive deficits
Commonly:
- Loss of sensation and numbness in one side of the body
- Hemiplegia (same side as sensory disorder) and muscle weakness of the face (droop)
- Initial reduction of muscle tone –> replaced by muscle rigidity/spasticity and hyperreflexia on the same side

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19
Q

Why do clinical signs appear on the opposite side of the body compared to the side of the brain with the stroke?

A

There is cross-over of both sensory and motor pathways in the brain

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20
Q

What determines clinical signs in stroke?

A

Location and extent of the stroke (core and penumbra)

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21
Q

What are some signs of stroke occurring in the brainstem?

A

Altered smell, taste, hearing or vision
Decreased sensation on the face
Ptosis (drooping eyelids) and weak ocular muscles
Facial muscle weakness (cant smile)
Weakness in tongue
Decreased reflexes (swallowing, pupils to light)
Possibly altered respiration

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22
Q

What are some signs of stroke affecting the cerebellum?

A 
Altered equilibrium (not sitting/standing symmetrical)
Altered coordination of movements
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23
Q

What time points would CT and MRI show stroke?

A

CT–> no significant changes in first 24hours

MRI–> can see as early as 15mins post stroke

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24
Q

Why is CT used in ED for suspected stroke?

A

To check for haemorrhage NOT for signs of stroke

–> if no haemorrhage –> thrombolytics etc can be given to dissolve clot and return blood flow

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25
Q

What are the main treatments and managements of strokes (mainly embolic)?

A

Thrombolysis
Thrombectomy
Body cooling

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26
Q

What is CSF?

A

A filtrate from the blood

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27
Q

How often is CSF replaced?

A

Totally replaced in 5-7 hours

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28
Q

What path does CSF flow in the body?

A 
Chorioid plexus of the lateral ventricles
3rd ventricle
Cerebral aqueduct
4th ventricle 
Foramina Magendi and Luska
Subarachnoid space
Arachnoid granulations
Sagittal sinus
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29
Q

What is the primary roles of CSF?

A

Cushioning

Bringing nutrients and taking waste away

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30
Q

What produces CSF?

A

Secreted by the chorioid plexus –> a network of ependymocytes located in the lateral ventricles

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31
Q

How does the ependymocytes drive water from the blood for CSF?

A

Transport of Na+ Cl- and HCO3 from the plasma to the ventricle creating an osmotic gradient to drive H2O

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32
Q

What is normally present and not present in CSF?

A

Present –> Clear H2O, Glucose, small amount of protein

Not present –> WBC, large amounts of protein

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33
Q

What is elevated protein in CSF a sign of?

A

Damage to the blood-brain barrier

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34
Q

What is cranial volume?

A

Volume of the brain space –> inside the skull
= volume of brain + volume of blood + volume of CSF
–> its value is constant

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35
Q

What is the equation for cerebral perfusion pressure?

A

CCP = mean arterial pressure (MAP) - intracranial pressure (ICP)

36
Q

From the equation for cerebral perfusion pressure what would be the impact of a rise in ICP?

A

Reduction in cerebral perfusion

37
Q

What is the mechanism behind increase ICP during ischaemic stroke vs haemorrhagic stroke?

A

Ischaemic –> brain oedema drive increased ICP

Haemorrhagic –> extra blood within skull drives an increase in ICP

38
Q

What is atherosclerosis?

A

Progressive, degenerative arterial disease that leads to the occlusion of affected vessels reducing the blood flow through them

39
Q

What category of disease is atherosclerosis?

A

Inflammatory disease

40
Q

What is atherosclerosis characterised by?

A

Formation of lipid rich plaques in the vessel walls of medium and large sized arteries

41
Q

What are risk factors for atherosclerosis?

A

Smoking, diabetes, hypertension, hyperlipidaemia

42
Q

What is thought to be the key initiator of atherosclerosis?

A

Endothelial injury

43
Q

What is Atheroma?

A

Degeneration of the walls of the arteries caused by accumulated fatty deposits and scar tissue, and leading to restriction of the circulation and a risk of thrombosis also known as the fatty material which forms deposits in the arteries.

44
Q

What are the constitution and modifiable risk factors of atherosclerosis?

A

Constitutional –> genetics, age, gender

Modifiable risk factors –> hyperlipidaemia, hypertension, smoking, diabetes

45
Q

What is the mechanism of pathogenesis of atherosclerosis?

A
  1. Endothelial injury and dysfunction –> increased vascular permeability, leukocyte adhesion and thrombosis
    1. Accumulation of lipoproteins –> mostly LDLs in vessel walls
    2. Monocyte adhesion to endothelium –> migrate into the intima and transformation into macrophages and foam cells
    3. Platelet adhesion
    4. Factors released from platelets, macrophages and vascular cell walls inducing smooth muscle cell recruitment
    5. Smooth muscle cell proliferation, extracellular matrix production and recruitment of T cells
    6. Lipid accumulation both inside and outside cells
46
Q

What is the impact of haemodynamic changes in atherosclerosis?

A

Turbulent blood flow –> important in atherogenesis and plaque formation
Non-turbulent flow is actually protective against atherosclerosis through gene induction in endothelial cells

47
Q

How are lipids transported in the blood stream?

A

Bound to apoproteins

48
Q

What are fatty streaks composed of?

A

Lipid filled foamy macrophages

49
Q

What is the impact of atherosclerotic disease involving the heart?

A

MI, angina

50
Q

What is the impact of atherosclerotic disease in/ involving the Brain?

A

Cerebral infarction (stroke)

51
Q

What is the impact of atherosclerotic disease in/ involving the aorta?

A

Aneurism

52
Q

What is the impact of atherosclerotic disease in/ involving the peripheries?

A

Gangrene of the legs etc

53
Q

What is the impact of atherosclerotic disease in/ involving the Kidneys?

A

Atherosclerotic renovascular disease (ARVD)

54
Q

How many people will have a stroke in their lifetime in Australia?

A

1 in 4

55
Q

How many strokes occur each year in Australia?

A

50000ish and the number is expected to rise to 100,000 by 2050

56
Q

What are the risk factors for ischaemic stroke?

A 
Hypertension
Diabetes mellitus
Cardiac disease
Hypercholesterolemia 
Past TIAs
Carotid stenosis
Obesity 
Sickle cell disease
Use of oral contraceptives
57
Q

What are the risk factors for haemorrhagic stroke?

A 
Advanced age
Hypertension (up to 60% of cases)
Previous history of stroke
Alcohol abuse
Use of illicit drugs (eg, cocaine, other sympathomimetic drugs)
58
Q

What are Focal neurological signs?

A

CNS signs are impairments ofnerve, spinal cord, or brain function that affects a specific region of the body,
e.g. weakness in the left arm, the right leg, paresis, or plegia.

59
Q

What is the significance of focal neurological signs during examination?

A

They can be used to identify a particular area which has potentially been damaged

60
Q

Symptoms of ischaemic stroke?

A

The symptoms of an ischemic stroke depend on which parts of your brain are affected.
They can include things like:
Sudden numbness or weakness of your face, arm, or leg, often on one side of the body
Confusion
Problems speaking or understanding others
Dizziness, loss of balance or coordination, or trouble walking
Vision loss or double vision

61
Q

Symptoms of haemorrhagic stroke?

A 
Haemorrhagic stroke symptoms usually increase gradually over minutes or a few hours, although a subarachnoid haemorrhage may come on suddenly. Some things that can happen:
Intense headache that some people describe as "the worst headache they've ever had"
Confusion
Nausea or throwing up
Sensitivity to light
Problems with vision
Passing out
Neck stiffness
62
Q

What is a cortical stroke?

A

A stroke affecting the cerebral cortex

63
Q

What is a subcortical stroke?

A

Strokes affecting the inner structures of the brain

64
Q

How does a cortical stroke typically present?

A

Strokesaffecting the cerebralcortex(i.e.cortical strokes) classically present with deficits such as neglect, aphasia, and hemianopia.

65
Q

How does a subcortical stroke typically present?

A

Subcorticalstrokesaffect the small vessels deep in the brain, and typically present with purely motor hemiparesis affecting the face, arm, and leg.

66
Q

What is speech?

A

The actual process of producing sound

67
Q

What is language?

A

Deals with meaning/understanding behind the spoken words.

68
Q

What are neurological pathways involved in speech production?

A
  1. Broca’s area –> speech production

2. Motor cortex –> muscle movements required for speech

69
Q

What is the neurological pathway of understanding language?

A
  1. Auditory cortex (for auditory information), Visual cortex (reading, sign language)
    1. Wernicke’s area (language comprehension)
    2. Information travels via Arcuate fasciculus (nerve fibres) to the Broca’s area
70
Q

Where is Wernicke’s are located in the brain?

A

posterior section of the superiortemporalgyrus (STG)

71
Q

Where is Broca’s area located in the brain?

A

Frontal lobe

72
Q

What kind of aphasia may be produced by damage to Wernicke’s area?

A

Produces problems with comprehension:

Sensory aphasia/Receptive aphasia (these 2 are the same thing)

73
Q

What kind of aphasia may be produced by damage to Broca’s area?

A

Speech production problems:

Expressive/motor/non-fluent aphasia (all these 3 are the same thing)

74
Q

Where is the swallowing centre in the brain?

A

Medulla (in the brain stem)

75
Q

What is the neurological pathway of swallowing?

A

Precentral gyrus, frontal gyrus and posterior-inferior gyrus initiate (in voluntary)
Information travels to the brainstem (medulla)
Medulla relays signal to swallow via cranial verves:
Trigeminal (5)
Facial (7)
Glossopharyngeal (9)
Vagus (X)
Hypoglossal (12)

76
Q

What are the stages of swallowing?

A

Oral phase
Pharyngeal phase
Oesophageal phase

77
Q

What are the two areas that are subject to thrombosis?

A

Venous

Arterial

78
Q

What are the risk factors of venous thrombosis?

A 
History of DVT (family or patient)
Hormone therapy/ contraceptive pill
Pregnancy
Vein injury (surgery/trauma etc)
Immobility 
Inherited blood clotting disorder
Older age
Smoking
Overweight/obesity 
Health conditions (cancer, heart disease, lung disease etc)
79
Q

What are the risk factors of arterial thrombosis?

A 
Smoking
Diabetes
High blood pressure
High cholesterol
Lack of activity (immobility)
Obesity
Family history of arterial thrombosis
Older age
80
Q

What are some neurological signs of clotting?

A 
Symptoms on the opposite side of the body to where the clot has impacted the brain
Facial droop
Weakness
Headaches
Confusion
Slurred speech
Vision changes
Loss of consciousness 
Dizziness
81
Q

What are some signs of clotting in the venous system?

A 
Venous blood clots occur most commonly in the arms and legs
swelling of the affected area
Warmth
Redness
pain
82
Q

What are some signs of clotting in the arterial system?

A 
Pain 
Peripheral clots can give pallor
Weakness
Loss of sensation
paralysis
83
Q

What is a stroke unit?

A

Astroke unitis an organized in-hospital facility that entirely (or next to entirely) is devoted to care for patients withstroke. It is staffed by a multidisciplinary team with special knowledge instrokecare.

84
Q

What is the role of stroke rehabilitation?

A

Helping patients relearn lost skills due to stroke damage

85
Q

What are stroke scores?

A

A scoring system based on presenting stroke symptoms

86
Q

How is a stroke scoring system valuable in evaluating stroke?

A

Can help guide where the stroke may be occurring and the extent of damage/severity

87
Q

What type of stroke typically only impacted motor functions in stroke?

A

Lacunae

JMP Y2S1 (24 decks)

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