PBL Topic 3 Case 10 Flashcards
1
Q
What is meant by states of consciousness?
A
- Levels of alertness
- Awake
- Drowsy
- Asleep
2
Q
What does EEG measure?
A
- Amount of electrical activity in the brain
- Which relate to different states of consciousness
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
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
5
Q
What two features of an EEG waveform are measured?
A
- Amplitude, measured in mV
- Frequency, measured in Hz
6
Q
What does a large amplitude on an EEG waveform indicate?
A
- Many neurons are being activated simultaneously
7
Q
What is the range of amplitudes recorded on an EEG?
A
- 0.5 to 100 mV
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
9
Q
What is the range of frequencies recorded on an EEG?
A
- 0.5 to 40 Hz
10
Q
What three diagnoses can EEG make?
A
- Epilepsy
- Comatose
- Brain death
11
Q
Describe an alpha rhythm
A
- Oscillation of 8 - 12 Hz
12
Q
Which stage of consciousness is the alpha rhythm associated with?
A
- Alert restfulness
- Individual is awake and relaxed with the eyes closed
13
Q
Where is the alpha rhythm best recorded?
A
- Parietal and occipital lobes
14
Q
Describe a beta rhythm
A
- Smaller amplitude, frequency > 12
15
Q
Which stage of consciousness is the beta rhythm associated with?
A
- Alert wakefulness
- Individual is awake and relaxed with the eyes open
16
Q
Describe the theta rhythm
A
- 4 - 8 Hz
17
Q
Which stage of consciousness is the theta rhythm associated with?
A
- N1 stage of NREM phase of sleep
18
Q
Describe the delta rhythm
A
- Less than 4 Hz
19
Q
Which stage of consciousness is the delta rhythm associated with?
A
- N3 stage of NREM phase of sleep
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
21
Q
How does sleep differ from coma?
A
- In coma the person is unconscious but cannot be aroused
22
Q
Identify the two types of sleep
A
- Non-rapid eye movement
- Rapid eye movement
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
24
Q
Describe the physiological effects of NREM sleep
A
- Decrease in blood pressure
- Decrease in respiratory rate
- Decrease in basal metabolic rate
25
Describe the physiological effects of REM sleep
- Active dreaming
- Active bodily movements
- More difficult to arouse
- Depressed muscle tone
- Irregular heart and respiratory rate
- Brain is more active, increased brain metabolism
26
What is the circadian rhythm?
- Sleep and wake cycle in a day
| - 8 hours sleep 16 hours awake
27
Where in the brain is consciousness regulated?
- Reticular activating system in the brainstem
28
What is orexin? Where is it produced? What is its role?
- 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
29
Where is the sleep centre located? What is its role?
- 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
30
What neural substrate causes cortical activity and dreaming in REM sleep?
- Increase in acetylcholine
31
Where is the suprachiasmatic nucleus located? What its role?
- Hypothalamus
- Directly above the optic chiasm
- Circadian pacemaker
- Activates orexin cells in the morning
- And melatonin at night from pineal gland
32
Identify three factors that activate orexin secreting cells
- Action potentials from suprachiasmatic nucleus
- Metabolic indicators of negative energy including decreased blood glucose
- Limbic inputs such as stress
33
What is coma?
- Extreme decrease in mental function and behavioural expression
- Incapable of arousal
- Which may be reversible or irreversible
34
Outline the criteria for brain death
- 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.
35
What score on the GCS denotes coma?
- 8 or less
36
What is epilepsy?
- Group of disorders which exhibit seizures
37
What is a seizure?
- 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
38
What symptoms may be associated with seizures in the:
[A] Cortex
[B] Hypothalamus
[C] Reticular formation
- [A] convulsions
- [B] Peripheral autonomic discharge
- [C] Coma
39
How may a seizure be detected by EEG?
- Recurrent waves of large amplitude up to 1000 mV
| - MRI and PET
40
Identify the two main categories of epilepsy
- Generalised seizure
| - Partial seizures
41
What is the difference between a simple and complex seizure?
- Simple if conscious
| - Complex if unconscious
42
Identify four types of general seizure
- Absence seizure
- Generalised tonic-clonic seizures (grand mal)
- Myoclonic seizure
- Tonic and atonic seizure
43
Identify three types of partial seizure
- Simple partial seizures (Jacksonian seizure)
- Complex partial seizures (temporal lobe seizure)
- Partial seizures with secondary generalisation
44
Identify the three main mechanisms of anticonvulsants and a drug associated with each
- Enhancement of GABA action (benzodiazepines)
- Inhibition of sodium channel function (carbamazepine, valproate)
- Inhibition of calcium channel function (lamotrigine)
45
What is a linear fracture?
- Affected area bends inwards and area around it bends outwards
- Not always associated with brain injury, spontaneous healing
46
What is a depressed skull fracture?
- 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.
47
What is a compound fracture? Identify one complication of a compound fracture
- Fracture with breach of skin
| - Route for infection (meningitis)
48
What is a pterion fracture? Identify one complication of a pterion fracture
- Risk of injury to middle meningeal artery which runs deep to pterion
- May produce fatal extradural haematoma
49
What is a diastatic fracture?
- Fracture traverses one or more sutures causing a widening of the sututres
50
What is a basilar fracture? Identify two signs of a basilar fracture
- Breakage of bones in base of skull
- Blood in sinuses
- CSF leaking from nose and ears
51
What is cerebral oedema
- Abnormal accumulation of fluid in the cerebral parenchyma
| - Producing an increase in cerebral volume
52
Outline three types of cerebral oedema
- 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
Identify three causes of focal brain swelling
- Cerebral abscess
- Haematoma
- Neoplasms
54
Outline the pathology of raised intracranial pressure?
- Expanding intracranial lesions in a rigid cranium
- Compensation by reduction in CSF and blood volume
- Though pressure atrophy of the brain eventually occurs
55
Outline 5 clinical features of raised intracranial pressure
- 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
What is neuropsychological assessment and its purpose?
- 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
What is the purpose of anaesthetics?
- Render patients unaware of or unresponsive to painful stimulation during surgical procedures
58
Outline three effects of anaesthetics on ion channels
- Potentiation of GABA at GABAA receptor
- Reduce excitation through opening of K+ channels
- Inhibit synaptic transmission by depressing NMDA function
59
What type of anaesthetic is propofol?
- Intravenous anaesthetic agent
60
How many minutes does it take for propofol to induce anaesthesia?
- 30 seconds
61
What is the clinical significance of the rapid metabolism of propofol?
- Produces less nausea and vomiting
| - Making it suitable for daytime surgeries
62
How does propofol differ from most IV anaesthetic agents?
- Can be used for maintenance of anaesthesia
| - When given as a continuous infusion
63
Outline three adverse effects of propofol
- Cardiovascular depression resulting in hypotension and bradycardia
- Respiratory depression
- Pain on injection
64
What is the dose of propofol?
- 1.5-2.5 mg / kg
65
What is the purpose of propofol?
- Initiation (and also maintenance) of anaesthesia
66
What type of anaesthetic is isoflurane?
- Inhalation anaesthetic
67
What does the blood gas partition coefficient of an inhalation anaesthetic agent determine?
- Rate of induction
| - Recovery of inhalation anaesthetic
68
What does the oil gas partition coefficient of an inhalation anaesthetic agent determine?
- Measure of fat solubility
| - Determines potency of anaesthetic
69
Agents with a low blood gas partition produce a [A] induction and a [B] recovery
- [A] Rapid
| - [B] Rapid
70
Agents with a high blood gas partition produce a [A] induction and a [B] recovery
- [A] Slow
| - [B] Slow (hangover effect)
71
Identify two adverse effects of isoflurane
- Hypotension
| - Vasodilation (can cause coronary steal)
72
How does isoflurane exacerbate cardiac ischaemia?
- Coronary steal
- Vessels are dilated and shunt blood away from ischaemic zone
- Producing more ischaemia
73
What is the dose of isoflurane?
- 1 - 2.5 %
74
What type of drug is atracurium?
- Non-depolarising neuromuscular blocking drug
75
When is atracurium used?
- Adjunct to anaesthesia
| - When artificial ventilation is available
76
What is the speed of onset of atracurium?
- Fast (2-3 minutes)
77
What is the duration of action of atracurium?
- Intermediate (less than 30 minutes)
78
Outline the mechanism of action of atracurium
- Competitive antagonist at postsynaptic nAChR at endplate
| - Also blocks facilitatory presynaptic ACh receptors
79
How does pH affect atracurium?
- Unstable at physiological pH
- Stable when stored at acid pH
- Duration becomes briefer in respiratory alkalosis caused by hyperventilation
80
How is atracurium metabolised? How does this differ to other similar drugs?
- Spontaneously hydrolysed in plasma
- Rather than being metabolised by liver or excreted in liver
- Significant for patients with hepatic or renal function impairment
81
What is the main side effect of atracurium? Why does this occur?
- Transient hypotension
| - Due to histamine release from mast cells
82
What is the dose of atracurium?
- 300-600 micrograms / kg by intravenous injection
| - Followed by 100-200 micrograms / kg as required
83
What percentage of ACh receptors need to be blocked by atracurium? Why?
- 70% to 80%
| - Since the amount of ACh released exceeds that required for an action potential by threefold
84
What type of drug is suxamethonium?
- Depolarising neuromuscular blocking drug?
85
Identify two uses of suxamethonium?
- Brief procedures such as tracheal intubation
| - Or ECT
86
What is speed of onset of suxamethonium?
- 2 minutes
87
What is the duration of action of suxamethonium? Why is this?
- 10 minutes
| - Hydrolysis by plasma cholinesterase
88
Why may prolonged paralysis occur with suxamethonium?
- In patients with plasma cholinesterase deficiency
| - A rare autosomal recessive disorder
89
What is the role of dibucaine?
- Inhibitor of abnormal plasma cholinesterase
| - For detection of plasma cholinesterase deficiency
90
Outline the mechanism of action of suxamethonium
- 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
Why does suxamethonium cause bradycardia?
- Direct muscarinic action
92
Why can suxamethonium cause ventricular dysrhythmia or cardiac arrest?
- Increase in cation permeability
- Efflux of K+
- Rise in plasma [K+]
- Hyperkaleamia
93
Aside from plasma cholinesterase deficiency, outline two other causes of prolonged paralysis with suxamethonium
- Liver disease
| - Anti-cholinesterase drugs
94
What is malignant hyperthermia?
- Rare side effect of suxamethonium
- Mutation of ryanodine receptor
- Resulting in muscle spasm and a dramatic rise in temperature
95
Postoperative muscle pain following suxamethonium is correlated with what?
- Amount of fasciculation prior to muscle relaxation
96
What is the dose of suxamethonium?
- 1- 1.5 mg / kg
97
What type of drug is neostigmine?
- Anticholinesterase
98
What is the role of neostigmine?
- Reverse competitive neuromuscular drug block by non-depolarising neuromuscular blocking agents e.g. atracurium
99
Outline the mechanism of action of neostigmine
- Inhibition of acetylcholinesterase
- Which gives ACh a greater chance of binding with a vacant receptor
- Thus increasing EPP so that it reaches threshold
100
What is myasthenia gravis? Why can neostigmine be used to teat t?
- Condition in which there are too few ACh receptors
| - Gives ACh a greater chance of binding with a vacant receptor
101
What is the dose of neostigmine?
- 2.5 mg
102
What is the cause of the side effects of neostigmine?
- Stimulation of autonomic ganglia
| - Producing complex autonomic effects
103
Identify five side effects of neostigmine
- Mydriasis
- Bronchoconstriction
- Bradycardia
- Salivary secretions
104
What class of drug is used to prevent side effects of neostigmine?
- Muscarinic antagonists
105
Name two muscarinic antagonists
- Atropine
| - Glycopyrrolate
106
Which side effects of neostigmine does atropine limit?
- Mydriasis
- Bronchoconstriction
- Bradycardia
107
Which side effects of neostigmine does glycopyrrolate limit?
- Salivary secretions
108
What are the different responses in eye opening and what scores are attributed to them?
- Spontaneous: 4
- To speech: 3
- To pain: 2
- Nil: 1
109
What are the different motor responses and what scores are attributed to them?
- Obeys: 6
- Localises: 5
- Withdraws: 4
- Abnormal flexion: 3
- Extensor response: 2
- Nil: 1
110
What are the different verbal responses and what scores are attributed to them?
- Orientated: 5
- Confused conversation: 4
- Inappropriate words: 3
- Incomprehensible sounds: 2
- Nil: 1
111
What are the roles of ghrelin and leptin and how do they affect orexin secreting cells?
- Ghrelin stimulates appetite, increased [plasma] stimulates orexin secreting cells
- Leptin depresses appetite, decreased [plasma] stimulates orexin secreting cells
112
When does the concentration of adenosine increase? What is the effect of this on orexinergic cells? Name an antagonist of adenosine receptors
- Increased content following prolonged waking period
- Reduces firing by orexinergic neurons
- Caffeine
113
What is the role of IL-1 in consciousness?
- Sleep inducing effect
114
What class of drug is mannitol and what is it used to treat?
- Osmotic diuretic
| - Cerebral oedema
115
Outline the mechanism of action of mannitol
- Causes increase in plasma osmolarity by solutes that do not enter the brain or eye
- Resulting in efflux of water from these compartments
116
What is the dose of mannitol?
- 0.25-2 g/Kg
117
Outline the social capital concept
- Affluent areas relate to stronger sense of cohesion
- Which results in fewer neighbourhood problems and higher levels of mental wellbeing
-
118
Identify four types of social support
- Advice
- Esteem support
- Companionship
- Instrumental / tangible support
119
What is network support
- Network support refers to type, density and frequency of contact with social support network
120
How does available functional support differ to enacted social support?
- Available is the perceived benefit of potential access to a support network
- Enacted is the perceived benefit of actual access to support network
121
What is stress buffering hypothesis?
- Social support helps people to cope with stress
122
What is social comparison theory?
- Social support helps individual to choose a coping strategy
123
What is social support reactivity hypothesis?
- Social support reduces physiological responses to stress
124
Identify a non-depolarising neuromuscular blocking drug other than atracurium and how it is broken down
- Mivacurium
| - Plasma cholinesterase (like suxamethonium)
