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Pathophysiology > Nervous system > Flashcards

Nervous system Flashcards

1
Q

what is stroke

A
  • blood supply to brain interrupted
  • ischaemia is enough to cause irreversible damage to part of the brain
  • results in immediate loss of function
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2
Q

what is the normal metabolism and blood flow of a brain

A
  • functioning brain depends on continuous blood supply for oxygen and glucose and remove end products metabolism
  • glucose metabolism leads to conversion of ADP to ATP
  • ATP is required to
    1. maintain neuronal integrity
    2. keep major cellular Ca2+ and Na+ outside the cells and the intracellular K+ within the cell
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3
Q

define transient ischemia attack (TIA)

A

a transient episode of neurological dysfunction caused by focal CNS ischaemia, without acute infarction

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4
Q

define stroke

A
  • a neurological deficit attributed to an acute, focal injury of the CNS by a vascular cause
  • cell death attributed to ischemia, based on pathological, imaging, or other objective evidence
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5
Q

types of stroke

A

hemorrhagic stroke
- blood leaks into brain tissue
ischemic stroke
- clot stops blood supply to an area of the brain

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6
Q

blood circulation to the brain

A

circle of willis

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7
Q

signs and symptoms of stroke

A
  • hemiplegia
  • hemisensory
  • dysarthria
  • clumsy hand/ataxic
  • aphasia
  • neglect (tactile/visual)
  • gaze deviation
  • homonymous hemianopia
  • headache
  • giddiness
  • unsteady gait
  • brachiafacial weakness
  • drowsy/unconsciousness
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8
Q

what is the motor pathway

A

pyramidal tracts (efferent pathway)

  • corticospinal tract
  • corticobulbar tract
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9
Q

what is the sensory pathway

A

sensory tracts (afferent pathway)

  • spinothalamic - transmits pain and temperature related sensations to cerebrum via thalamus
  • posterior column - transmit touch, pressure and vibrations related sensations to the cerebral cortex of the brain
  • spinocerebellar - delivers kinaesthesia or proprioception related impulses to cerebellum
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10
Q

symptoms of stroke mimics

A

Face dropping
Arm weakness
Speech difficulty

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11
Q

common causes for stroke mimics

A
  • hypoglycemia
  • seizures with post ictal paralysis
  • migraine with aura
  • hypertensive encephalopathy
  • cns abscess or tumours
  • drugs
  • psychogenic
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12
Q

what is stroke mimics

A
  • presents like acute ischemic stroke but not due to vascular cause
  • account up to 21% of all stroke presentations
  • exclusion of stroke mimics is essential to avoid exposure to unnecessary risk of treatment
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13
Q

principles of stroke management

A

reperfusion (ischemic stroke)

  • tissue plasminogen activation
  • endovascular therapy

minimising complications

  • acute stroke unit
  • manage ICP
  • rehab

secondary prevention (focus on underlying etiology)

  • identify and control risk factors
  • lifestyle modification
  • surgical intervention
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14
Q

pathophysiology of a seizure

A

transient occurrence of s&s due to abnormal excessive neuronal activity in the brain

neurons may be

  • developmentally abnormal
  • damaged from prior injury
  • functioning abnormally due to change in environment

typical signs/symptoms

  • loss of awareness
  • abnormal movements
  • abnormal sensations

most seizures self-abort after several seconds to minutes

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15
Q

types of seizures

A

partial

  • simple partial seizure
  • complex partial seizure
  • partial with secondary generalisation

generalised

  • generalised tonic clonic seizure (GTCS)
  • absence
  • myoclonic
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16
Q

seizure vs epilepsy

A

seizure is a single event

epilepsy is a disease with a tendency to have recurrent unprovoked seizures

17
Q

which lobe of the brain is in charge of what function

A

frontal lobe - executive functions, thinking, planning, organising and problem solving, emotions and behavioural control, personality

motor cortex - movement

parietal lobe - perception, making sense of the world, arithmetic, spelling

sensory cortex - sensations

occipital lobe - vision

temporal lobe - memory, understanding, language

18
Q

what is the local effect of low CBF

A

decreased oxygen

  • anaerobic glycolysis -> increase lactic acid -> low pH -> impair metabolic cell function
  • increase free radical production -> perioxidation of fatty acid in cell organelles and plasma membrane -> severe cell dysfunction

neuronal ischemia
- decreased ATP, increased glutamate -> Na+ and Ca2+ enter cell, K+ exit cell -> H20 and Cl- enters cell -> cerebral edema -> increase ICP

all of the above leads to decreased CBF –> cell death

19
Q

which part of the circles of willis supply the anterior and middle part of the brain

A

Anterior cerebral artery (ACA)
Internal carotid arter (ICA)
Middle cerebral artery (MCA)

20
Q

which part of the circles of willis supply the posterior part of the brain

A 
Vertebral artery (VA)
Basilar artery (BA)
21
Q

what is involved in the language pathway

A

brocca’s area (frontal lobe) - for expressing
wernickie’s area (temporal lobe) - for receptive and understanding
auditory cortex (temporal lobe) - for hearing
mouth and throat area of motor cortex (frontal lobe) - for talking

22
Q

top of basilar syndrome - basilar artery occlusion

A
  • tetraparesis/ quadriparesis with upgoing toes
  • bulbar involvement
  • nystagmus
  • abnormal eye movement
  • doll’s negative
  • small and pinpoint pupils
  • coma/unconscious
  • apnea/ cardiorespiratory collapse
23
Q

what is penumbra

A
  • zone of destruction not structurally dead yet

- area at risk of infarction but still salvageable

24
Q

how are the neurons affected if stroke is left untreated

A

in 1 min, 1.9million neurons die

each hour in which treatment fails to occur, brain loses 3.6 years of normal aging worth of neurons

25
Q

door to needle recommendation

A 
0min - suspected stroke patient arrives
10mins - physician's initial assessment
15mins - stroke team notified
25mins - CT scan initiated
45mins - CT scan and labs interpreted
60mins - tPA given if patient is eligible
26
Q

within how long should tPA and endovascular therapy be given

A

tPA - 4.5h

endovascular therapy - 6h

27
Q

when is endovascular therapy needed

A

large vessel occlusion

28
Q

possible complications of stroke

A
  • neurological
  • cardiovascular
  • pulmonary
  • gastrointestinal
  • genitourinary
  • depression, pain etc
29
Q

how to minimise complications in ASU

A 
manage ICP:
non-pharmacological:
- head of bed 30deg
- manage BP
- monitor conscious level and change in functional
pharmacological:
- IV hydration
surgical:
- decompressive hemicraniectomy

bladder scan
DVT prophylaxis
dysphagia screen
rehab

30
Q

ASU management of stroke

A
  • identify etiology
  • secondary prevention
  • rehab
31
Q

investigations of stroke

A
  • radiology imaging
  • blood investigations
  • 12 lead ECG
  • KIV
32
Q

what are some medical secondary prevention methods

A

anti-thrombotic

  • anti-platelet
  • anti-coagulation

risk factor screening and management

  • blood test
  • start statin
  • OHGA
  • smoking cessation prog
  • lifestyle modification prog
33
Q

what is the difference between anti platelet and anti coagulation

A

anti-platelet

  • target platelet
  • prevents clot by prevention of platelet aggregation
  • used for patients with non-cardioembolic stroke

anti-coagulation

  • target blood clotting factors to prevent formation of clot
  • used for patients with existing clots or cardioembolic stroke
34
Q

risk factor of stroke

A
  • hypertension
  • diabetes
  • lipids
  • obesity
  • physical inactivity
35
Q

management of epilepsy

A

prevent seizure recurrence

  • anti-epileptic drugs
  • lifestyle modification

counselling

  • lifestyle modifcation
  • seizure first aid
  • medication side effect
36
Q

what are some anti epileptic drugs and what they work on

A

work on:

  • Na channels (carbamazepine, lamotrigine, phenytoin)
  • GABA (benzodiazepines)
  • receptors (levetiracetam)
37
Q

common side effect of AED

A
  • fatigue, sleepiness
  • drug toxicity
  • liver toxicity (carbamazepine, phenytoin, valproate, phenobarbitone)
  • rash (carbamazepine, lamotrigine, phenytoin)
  • weight gain, hair fall, low platelet (valproate)

Pathophysiology (12 decks)

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