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Semester 3: Mind and Movement > PBL Topic 3 Case 10 > Flashcards

PBL Topic 3 Case 10 Flashcards

1
Q

What is meant by states of consciousness?

A
  • Levels of alertness
  • Awake
  • Drowsy
  • Asleep
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2
Q

What does EEG measure?

A
  • Amount of electrical activity in the brain

- Which relate to different states of consciousness

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3
Q

How is EEG performed?

A
  • Electrodes are attached to head by conducting salty paste
  • Which pick up signals generated in the brain
  • And transmit them to a machine that records them
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4
Q

What type of potential does an EEG record?

A
  • Graded potentials in many hundreds of thousands of brain neurones underlying the electrodes
  • As opposed to action potentials, which are too small to be picked up on EEG
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5
Q

What two features of an EEG waveform are measured?

A
  • Amplitude, measured in mV

- Frequency, measured in Hz

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6
Q

What does a large amplitude on an EEG waveform indicate?

A
  • Many neurons are being activated simultaneously
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7
Q

What is the range of amplitudes recorded on an EEG?

A
  • 0.5 to 100 mV
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8
Q

What does a large frequency on an EEG waveform indicate?

A
  • How often it cycles from the maximal to the minimal amplitude and back
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9
Q

What is the range of frequencies recorded on an EEG?

A
  • 0.5 to 40 Hz
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10
Q

What three diagnoses can EEG make?

A
  • Epilepsy
  • Comatose
  • Brain death
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11
Q

Describe an alpha rhythm

A
  • Oscillation of 8 - 12 Hz
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12
Q

Which stage of consciousness is the alpha rhythm associated with?

A
  • Alert restfulness

- Individual is awake and relaxed with the eyes closed

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13
Q

Where is the alpha rhythm best recorded?

A
  • Parietal and occipital lobes
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14
Q

Describe a beta rhythm

A
  • Smaller amplitude, frequency > 12
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15
Q

Which stage of consciousness is the beta rhythm associated with?

A
  • Alert wakefulness

- Individual is awake and relaxed with the eyes open

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16
Q

Describe the theta rhythm

A
  • 4 - 8 Hz
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17
Q

Which stage of consciousness is the theta rhythm associated with?

A
  • N1 stage of NREM phase of sleep
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18
Q

Describe the delta rhythm

A
  • Less than 4 Hz
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19
Q

Which stage of consciousness is the delta rhythm associated with?

A
  • N3 stage of NREM phase of sleep
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20
Q

What does the N2 stage of NREM phase of sleep consist of?

A
  • Sleep spindles (high frequency bursts)
  • K complexes (large amplitudes)
  • Both of which interrupt the theta rhythm
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21
Q

How does sleep differ from coma?

A
  • In coma the person is unconscious but cannot be aroused
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22
Q

Identify the two types of sleep

A
  • Non-rapid eye movement

- Rapid eye movement

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23
Q

Outline the pattern of NREM and REM sleep

A
  • NREM makes up 75% of sleep

- REM sleep occurs every 60-90 minutes for 10 minutes

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24
Q

Describe the physiological effects of NREM sleep

A
  • Decrease in blood pressure
  • Decrease in respiratory rate
  • Decrease in basal metabolic rate
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25
Q

Describe the physiological effects of REM sleep

A
  • Active dreaming
  • Active bodily movements
  • More difficult to arouse
  • Depressed muscle tone
  • Irregular heart and respiratory rate
  • Brain is more active, increased brain metabolism
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26
Q

What is the circadian rhythm?

A
  • Sleep and wake cycle in a day

- 8 hours sleep 16 hours awake

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27
Q

Where in the brain is consciousness regulated?

A
  • Reticular activating system in the brainstem
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28
Q

What is orexin? Where is it produced? What is its role?

A
  • Neuropeptide produced in hypothalamus with widespread cortical projections
  • Innervate monoaminergic neurons in the RAS
  • Lack of orexinergic neurons explain why old people have difficulty sleeping
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29
Q

Where is the sleep centre located? What is its role?

A
  • Group of neurons in preoptic nucleus of the hypothalamus
  • They release GABA onto neurons throughout brainstem including those that secrete orexin and monoamines
  • Reducing their levels throughout the brain
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30
Q

What neural substrate causes cortical activity and dreaming in REM sleep?

A
  • Increase in acetylcholine
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31
Q

Where is the suprachiasmatic nucleus located? What its role?

A
  • Hypothalamus
  • Directly above the optic chiasm
  • Circadian pacemaker
  • Activates orexin cells in the morning
  • And melatonin at night from pineal gland
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32
Q

Identify three factors that activate orexin secreting cells

A
  • Action potentials from suprachiasmatic nucleus
  • Metabolic indicators of negative energy including decreased blood glucose
  • Limbic inputs such as stress
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33
Q

What is coma?

A
  • Extreme decrease in mental function and behavioural expression
  • Incapable of arousal
  • Which may be reversible or irreversible
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34
Q

Outline the criteria for brain death

A
  • Nature and duration of the coma must be known
  • Cerebral and brainstem function are absent e.g. pupils unresponsive, no gag or cough reflex, no spontaneous breathing, no response to painful stimuli.
  • Supplementary criteria includes a flat EEG for 30 minutes and greatly reduced cerebral circulation.
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35
Q

What score on the GCS denotes coma?

A
  • 8 or less
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36
Q

What is epilepsy?

A
  • Group of disorders which exhibit seizures
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37
Q

What is a seizure?

A
  • Episodic high-frequency discharge of impulses by a group of neurons (a focus) in the brain
  • Which may spread to other regions of the brain
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38
Q

What symptoms may be associated with seizures in the:

[A] Cortex

[B] Hypothalamus

[C] Reticular formation

A
  • [A] convulsions
  • [B] Peripheral autonomic discharge
  • [C] Coma
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39
Q

How may a seizure be detected by EEG?

A
  • Recurrent waves of large amplitude up to 1000 mV

- MRI and PET

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40
Q

Identify the two main categories of epilepsy

A
  • Generalised seizure

- Partial seizures

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41
Q

What is the difference between a simple and complex seizure?

A
  • Simple if conscious

- Complex if unconscious

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42
Q

Identify four types of general seizure

A
  • Absence seizure
  • Generalised tonic-clonic seizures (grand mal)
  • Myoclonic seizure
  • Tonic and atonic seizure
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43
Q

Identify three types of partial seizure

A
  • Simple partial seizures (Jacksonian seizure)
  • Complex partial seizures (temporal lobe seizure)
  • Partial seizures with secondary generalisation
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44
Q

Identify the three main mechanisms of anticonvulsants and a drug associated with each

A
  • Enhancement of GABA action (benzodiazepines)
  • Inhibition of sodium channel function (carbamazepine, valproate)
  • Inhibition of calcium channel function (lamotrigine)
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45
Q

What is a linear fracture?

A
  • Affected area bends inwards and area around it bends outwards
  • Not always associated with brain injury, spontaneous healing
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46
Q

What is a depressed skull fracture?

A
  • Bony fragment is depressed below the normal skull convexity
  • Leading to secondary arterial and venous damage with haematoma formation.
  • Associated with primary brain injury post-traumatic epilepsy.
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47
Q

What is a compound fracture? Identify one complication of a compound fracture

A
  • Fracture with breach of skin

- Route for infection (meningitis)

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48
Q

What is a pterion fracture? Identify one complication of a pterion fracture

A
  • Risk of injury to middle meningeal artery which runs deep to pterion
  • May produce fatal extradural haematoma
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49
Q

What is a diastatic fracture?

A
  • Fracture traverses one or more sutures causing a widening of the sututres
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50
Q

What is a basilar fracture? Identify two signs of a basilar fracture

A
  • Breakage of bones in base of skull
  • Blood in sinuses
  • CSF leaking from nose and ears
51
Q

What is cerebral oedema

A
  • Abnormal accumulation of fluid in the cerebral parenchyma

- Producing an increase in cerebral volume

52
Q

Outline three types of cerebral oedema

A
  • Vasogenic, due to increased vascular permeability (e.g. BBB dysfunction)
  • Cytotoxic, due to cellular injury involving endothelia, glia and neurons
  • Interstitial, due to damage of ventricular lining in hydrocephalus
53
Q

Identify three causes of focal brain swelling

A
  • Cerebral abscess
  • Haematoma
  • Neoplasms
54
Q

Outline the pathology of raised intracranial pressure?

A
  • Expanding intracranial lesions in a rigid cranium
  • Compensation by reduction in CSF and blood volume
  • Though pressure atrophy of the brain eventually occurs
55
Q

Outline 5 clinical features of raised intracranial pressure

A
  • Headache due to compression of pain and stretch receptors
  • Nausea and vomiting due to pressure on vomiting centres in brainstem
  • Visual disturbances due to papilloedema around optic nerve
  • Impairment of consciousness
  • Brain death
56
Q

What is neuropsychological assessment and its purpose?

A
  • Assessment of cognitive functioning and consequences of brain damage, disease, and mental illness.
  • For purpose of diagnosis, differential diagnosis, assessment of treatment response, and prediction of functional potential and functional recovery.
  • With a shift towards relationship between assessment results and performance of everyday tasks
57
Q

What is the purpose of anaesthetics?

A
  • Render patients unaware of or unresponsive to painful stimulation during surgical procedures
58
Q

Outline three effects of anaesthetics on ion channels

A
  • Potentiation of GABA at GABAA receptor
  • Reduce excitation through opening of K+ channels
  • Inhibit synaptic transmission by depressing NMDA function
59
Q

What type of anaesthetic is propofol?

A
  • Intravenous anaesthetic agent
60
Q

How many minutes does it take for propofol to induce anaesthesia?

A
  • 30 seconds
61
Q

What is the clinical significance of the rapid metabolism of propofol?

A
  • Produces less nausea and vomiting

- Making it suitable for daytime surgeries

62
Q

How does propofol differ from most IV anaesthetic agents?

A
  • Can be used for maintenance of anaesthesia

- When given as a continuous infusion

63
Q

Outline three adverse effects of propofol

A
  • Cardiovascular depression resulting in hypotension and bradycardia
  • Respiratory depression
  • Pain on injection
64
Q

What is the dose of propofol?

A
  • 1.5-2.5 mg / kg
65
Q

What is the purpose of propofol?

A
  • Initiation (and also maintenance) of anaesthesia
66
Q

What type of anaesthetic is isoflurane?

A
  • Inhalation anaesthetic
67
Q

What does the blood gas partition coefficient of an inhalation anaesthetic agent determine?

A
  • Rate of induction

- Recovery of inhalation anaesthetic

68
Q

What does the oil gas partition coefficient of an inhalation anaesthetic agent determine?

A
  • Measure of fat solubility

- Determines potency of anaesthetic

69
Q

Agents with a low blood gas partition produce a [A] induction and a [B] recovery

A
  • [A] Rapid

- [B] Rapid

70
Q

Agents with a high blood gas partition produce a [A] induction and a [B] recovery

A
  • [A] Slow

- [B] Slow (hangover effect)

71
Q

Identify two adverse effects of isoflurane

A
  • Hypotension

- Vasodilation (can cause coronary steal)

72
Q

How does isoflurane exacerbate cardiac ischaemia?

A
  • Coronary steal
  • Vessels are dilated and shunt blood away from ischaemic zone
  • Producing more ischaemia
73
Q

What is the dose of isoflurane?

A
  • 1 - 2.5 %
74
Q

What type of drug is atracurium?

A
  • Non-depolarising neuromuscular blocking drug
75
Q

When is atracurium used?

A
  • Adjunct to anaesthesia

- When artificial ventilation is available

76
Q

What is the speed of onset of atracurium?

A
  • Fast (2-3 minutes)
77
Q

What is the duration of action of atracurium?

A
  • Intermediate (less than 30 minutes)
78
Q

Outline the mechanism of action of atracurium

A
  • Competitive antagonist at postsynaptic nAChR at endplate

- Also blocks facilitatory presynaptic ACh receptors

79
Q

How does pH affect atracurium?

A
  • Unstable at physiological pH
  • Stable when stored at acid pH
  • Duration becomes briefer in respiratory alkalosis caused by hyperventilation
80
Q

How is atracurium metabolised? How does this differ to other similar drugs?

A
  • Spontaneously hydrolysed in plasma
  • Rather than being metabolised by liver or excreted in liver
  • Significant for patients with hepatic or renal function impairment
81
Q

What is the main side effect of atracurium? Why does this occur?

A
  • Transient hypotension

- Due to histamine release from mast cells

82
Q

What is the dose of atracurium?

A
  • 300-600 micrograms / kg by intravenous injection

- Followed by 100-200 micrograms / kg as required

83
Q

What percentage of ACh receptors need to be blocked by atracurium? Why?

A
  • 70% to 80%

- Since the amount of ACh released exceeds that required for an action potential by threefold

84
Q

What type of drug is suxamethonium?

A
  • Depolarising neuromuscular blocking drug?
85
Q

Identify two uses of suxamethonium?

A
  • Brief procedures such as tracheal intubation

- Or ECT

86
Q

What is speed of onset of suxamethonium?

A
  • 2 minutes
87
Q

What is the duration of action of suxamethonium? Why is this?

A
  • 10 minutes

- Hydrolysis by plasma cholinesterase

88
Q

Why may prolonged paralysis occur with suxamethonium?

A
  • In patients with plasma cholinesterase deficiency

- A rare autosomal recessive disorder

89
Q

What is the role of dibucaine?

A
  • Inhibitor of abnormal plasma cholinesterase

- For detection of plasma cholinesterase deficiency

90
Q

Outline the mechanism of action of suxamethonium

A
  • Similar structure to ACh
  • Binds to nAChRs
  • Hydrolysis is slower than that of ACh so its duration of action is longer
  • So muscle cell is not depolarised
  • ACh cannot depolarise a depolarised receptor
  • So receptor is said to be desensitised
91
Q

Why does suxamethonium cause bradycardia?

A
  • Direct muscarinic action
92
Q

Why can suxamethonium cause ventricular dysrhythmia or cardiac arrest?

A
  • Increase in cation permeability
  • Efflux of K+
  • Rise in plasma [K+]
  • Hyperkaleamia
93
Q

Aside from plasma cholinesterase deficiency, outline two other causes of prolonged paralysis with suxamethonium

A
  • Liver disease

- Anti-cholinesterase drugs

94
Q

What is malignant hyperthermia?

A
  • Rare side effect of suxamethonium
  • Mutation of ryanodine receptor
  • Resulting in muscle spasm and a dramatic rise in temperature
95
Q

Postoperative muscle pain following suxamethonium is correlated with what?

A
  • Amount of fasciculation prior to muscle relaxation
96
Q

What is the dose of suxamethonium?

A
  • 1- 1.5 mg / kg
97
Q

What type of drug is neostigmine?

A
  • Anticholinesterase
98
Q

What is the role of neostigmine?

A
  • Reverse competitive neuromuscular drug block by non-depolarising neuromuscular blocking agents e.g. atracurium
99
Q

Outline the mechanism of action of neostigmine

A
  • Inhibition of acetylcholinesterase
  • Which gives ACh a greater chance of binding with a vacant receptor
  • Thus increasing EPP so that it reaches threshold
100
Q

What is myasthenia gravis? Why can neostigmine be used to teat t?

A
  • Condition in which there are too few ACh receptors

- Gives ACh a greater chance of binding with a vacant receptor

101
Q

What is the dose of neostigmine?

A
  • 2.5 mg
102
Q

What is the cause of the side effects of neostigmine?

A
  • Stimulation of autonomic ganglia

- Producing complex autonomic effects

103
Q

Identify five side effects of neostigmine

A
  • Mydriasis
  • Bronchoconstriction
  • Bradycardia
  • Salivary secretions
104
Q

What class of drug is used to prevent side effects of neostigmine?

A
  • Muscarinic antagonists
105
Q

Name two muscarinic antagonists

A
  • Atropine

- Glycopyrrolate

106
Q

Which side effects of neostigmine does atropine limit?

A
  • Mydriasis
  • Bronchoconstriction
  • Bradycardia
107
Q

Which side effects of neostigmine does glycopyrrolate limit?

A
  • Salivary secretions
108
Q

What are the different responses in eye opening and what scores are attributed to them?

A
  • Spontaneous: 4
  • To speech: 3
  • To pain: 2
  • Nil: 1
109
Q

What are the different motor responses and what scores are attributed to them?

A
  • Obeys: 6
  • Localises: 5
  • Withdraws: 4
  • Abnormal flexion: 3
  • Extensor response: 2
  • Nil: 1
110
Q

What are the different verbal responses and what scores are attributed to them?

A
  • Orientated: 5
  • Confused conversation: 4
  • Inappropriate words: 3
  • Incomprehensible sounds: 2
  • Nil: 1
111
Q

What are the roles of ghrelin and leptin and how do they affect orexin secreting cells?

A
  • Ghrelin stimulates appetite, increased [plasma] stimulates orexin secreting cells
  • Leptin depresses appetite, decreased [plasma] stimulates orexin secreting cells
112
Q

When does the concentration of adenosine increase? What is the effect of this on orexinergic cells? Name an antagonist of adenosine receptors

A
  • Increased content following prolonged waking period
  • Reduces firing by orexinergic neurons
  • Caffeine
113
Q

What is the role of IL-1 in consciousness?

A
  • Sleep inducing effect
114
Q

What class of drug is mannitol and what is it used to treat?

A
  • Osmotic diuretic

- Cerebral oedema

115
Q

Outline the mechanism of action of mannitol

A
  • Causes increase in plasma osmolarity by solutes that do not enter the brain or eye
  • Resulting in efflux of water from these compartments
116
Q

What is the dose of mannitol?

A
  • 0.25-2 g/Kg
117
Q

Outline the social capital concept

A
  • Affluent areas relate to stronger sense of cohesion
  • Which results in fewer neighbourhood problems and higher levels of mental wellbeing

-

118
Q

Identify four types of social support

A
  • Advice
  • Esteem support
  • Companionship
  • Instrumental / tangible support
119
Q

What is network support

A
  • Network support refers to type, density and frequency of contact with social support network
120
Q

How does available functional support differ to enacted social support?

A
  • Available is the perceived benefit of potential access to a support network
  • Enacted is the perceived benefit of actual access to support network
121
Q

What is stress buffering hypothesis?

A
  • Social support helps people to cope with stress
122
Q

What is social comparison theory?

A
  • Social support helps individual to choose a coping strategy
123
Q

What is social support reactivity hypothesis?

A
  • Social support reduces physiological responses to stress
124
Q

Identify a non-depolarising neuromuscular blocking drug other than atracurium and how it is broken down

A
  • Mivacurium

- Plasma cholinesterase (like suxamethonium)

Semester 3: Mind and Movement (21 decks)

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