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Medicine Sem 3 > Case 10 > Flashcards

Case 10 Flashcards

1
Q

what is general anaesthesia?

A

a medically-induced coma and loss of protective reflexes resulting from the administration of one or more general anaesthetic agents

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2
Q

what are the purposes of general anaesthesia?

A
  1. analgesia - loss of response to pain
  2. amnesia - loss of memory
  3. immobility - loss of motor reflexes
  4. unconsciousness - loss of consciousness
  5. skeletal muscle relaxation
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3
Q

what is the theory of general anaesthetic action?

A
  • anaesthetics alter neuron function by interacting directly with a small number of ion channels
  • upon activation, channels change the electrical excitability of neurons by controlling the flow of depolarising (excitatory) or hyperpolarising (inhibitory) ions across the cell membrane via an ion channel that is integral with the receptor that senses the initial signal
  • general anaesthetics primarily act by either enhancing inhibitory signals or by blocking excitatory signals
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4
Q

what happens during the pre-anaesthetic evaluation?

A
  • key factors of this evaluation are the patient’s age; body mass index; medical and surgical history; current medications and fasting time
  • also, evaluation of the patient’s airway, involving inspection of the mouth opening and visualisation of the soft tissues of the pharynx, is required
  • if a tracheal tube is indicated and airway management is deemed difficult, then alternative methods of tracheal intubation may be required as part of the anaesthetic management
  • consent must be obtained
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5
Q

what is the premedication? what does it include?

A
  • this is preliminary medication which is administered on the ward - not everyone requires it
  • this is medication that is administered prior to administration of a general anaesthetic
  • anaesthetic premedication consists of a drug or combination of drugs that serve to complement or otherwise improve the quality of the anaesthetic

Premedication includes:
benzodiazepines
-diazepam, midazolam, temazepam, lorzepam
-anxiolysis, amnesia, sedation

opioids

 - morphine
      - anxiolysis, analgesia, sedation, euphoria, nausea

anticholinergics
-antivagal, antisialagogue (reduce production of saliva), antiemetic (reduce vomiting), amnesic

antibiotic
-surgical implant, endocarditis

antacids
-reflux, hiatus hernia, pregnancy

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6
Q

What has to be monitored when under general anaesthetic?

A
  • ECG - also help identify early signs of heart ischaemia
  • blood pressure - invasive or non-invasive
  • oxygen saturation - pulse oximetry - allows early detection of a fall in a patient’s haemoglobin saturation with oxygen (hypoxaemia)
  • end tidal CO2 - carbon dioxide measurement (capnography)
  • inspired oxygen - low oxygen alarm
  • inspired agent concentration
  • neuromuscular blockade
  • airway pressures and flows
  • temperature - to discern hypothermia or fever
  • depth of anaesthesia
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7
Q

what are the stages of anaesthesia?

A
  1. induction
    • there is an ‘excitement stage’ that occurs after induction and before maintenance - this is marked by excited and delirious activity - there may be an irregular heart rate and breathing rate
  2. maintenance
  3. reversal
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8
Q

Describe the induction stage

  • intravenous vs. inhalation induction
  • how they work, when they used
A

Anaesthetic agents may be administered by various routes, including inhalation, injection (intravenous, intramuscular or subcutaneous), oral, and rectal

Intravenous induction:

  • bolus of drug injected
  • travels to the brain
  • highly lipid soluble
  • rapidly enters the brain
  • onset is in one arm-brain time (less than one minute)
  • initial recovery by redistribution
  • ultimate recovery by elimination

Once in the circulatory system, they are transported to their biochemical sites of action in the central and autonomic nervous system, where they exert their pharmacologic effects

Inhalation induction:

  • vapour breathed in via lungs
  • enters the blood
  • travels to the brain
  • highly lipid soluble
  • enters the brain
  • initial recovery by exhalation
  • ultimate recovery by exhalation
  • minimal amounts are metabolised
  • onset of anaesthesia is faster with intravenous injection than with inhalation, taking about 10-20 seconds to induce total unconsciousness
  • this has the advantage of avoiding the excitatory phase of anaesthesia, and thus reduces the complications related to induction of anaesthesia
  • commonly used intravenous induction agents include propofol, sodium thiopentone, etomidate and ketamine
  • an inhalational induction may be chosen where intravenous access is difficult to obtain, where difficulty maintaining the airway is anticipated, or due to patient preference
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9
Q

Describe the maintenance phase

  • duration of action of IV induction agents
  • how is maintenance achieved
  • what else is given
  • what happens at the end of surgery
A
  • the duration of action of intravenous induction agents is in general 5-10 minutes, after which time spontaneous recovery of consciousness will occur
  • in order to prolong anaesthesia for the required duration, anaesthesia must be ‘maintained’

This is achieved by allowing the patient to breathe a carefully controlled mixture of:

- oxygen 
- nitrous oxide 
- volatile anaesthetic agent (isoflurane)  - this can also be achieved by having a carefully controlled continuous infusion propofol through an intravenous catheter
  • inhaled agents (e.g. isoflurane, sevoflurane, desflurane) are frequently supplemented by intravenous anaesthetics, such as opioids (usually fentanyl or morphine) and sedative-hypnotics (usually propofol)
  • at the end of surgery, the volatile or intravenous anaesthetic is discontinued
  • recovery of consciousness occurs when the concentration of anaesthetic in the brain drops below a certain level (usually within 1 to 30 minutes, depending upon the duration of surgery)
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10
Q

what is muscle relaxation during surgery? what does it allow?

A
  • ‘paralysis’ or temporary muscle relaxation with a neuromuscular blocker is an integral part of modern anaesthesia
  • muscle relaxation allows surgery within major body cavities, e.g. abdomen and thorax, without the need for very deep anaesthesia, and is also used to facilitate endotracheal intubation
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11
Q

how do muscle relaxants work? what are examples of muscle relaxants?

A
  • acetylcholine, the natural neurotransmitter substance at the neuromuscular junction, causes muscles to contract when it is released from nerve endings
  • muscle relaxants work by preventing acetylcholine from attaching to its receptor
  • e.g. atracurium, succinycholine (suxamethonium), tubocurarine (curare), rocuronium, vecuronium
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12
Q

what does paralysis of muscles of respiration, i.e. the diaphragm and intercostal muscles, and muscles of larynx require?

A
  • requires that some form of artificial respiration be implemented
  • the airways usually needs to be protected by means of an endotracheal tube due to paralysed larynx muscles
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13
Q

how are the effects of muscle relaxants reversed?

A

anticholinesterase drugs

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14
Q

what does general anaesthesia cause the loss of?

A
  • protective airway reflexes (such as coughing)
  • airway patency
  • regular pattern due to the effect of anaesthetics, opioids, or muscle relaxants
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15
Q

what is done to maintain an open airway and regulate breathing within acceptable parameters?

A
  • some form of ‘breathing tube’ is inserted in the airway after the patient is unconscious
  • to enable mechanical ventilation, an endotracheal tube is often used (intubation)
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16
Q

describe the reversal stage

A
  • this stops what is keeping the patient asleep
  • reverse any muscle relaxants (neostigmine & glycopyrrolate)
  • give the patient time to recover
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17
Q

what are the consequences of anaesthesia?

A
  • affects respiration, cardiovascular system, CNS, renal system, gastrointestinal tract and liver

respiratory:

  • spontaneous respiration
    • normal negative pressure breathing
    • supine position and V/Q matching
    • respiratory depression - increase in CO2 - hypercapnia
    • hypoxic on room air
  • positive pressure ventilation
    • inspiration is now positive pressure
    • expiration is passive
    • needs a tracheal tube
    • increased incidence of chest infection (e.g. ventilator acquired pneumonia)

Cardiovascular:

  • decreased venous return
  • decreased cardiac output
  • decreased force of contraction
  • increase in arrhythmia potential
  • vasodilation
  • change in regional flow patterns

CNS (central venous system):

  • unconsciousness
  • depression of cerebral metabolism
  • dreaming
  • awareness
  • specific EEG (electroencephalogram) changes
  • possible long-term effects
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18
Q

what might be the consequence of agents with high lipid solubility?

A

they accumulate gradually in body fat and may produce a prolonged ‘hangover’ if used for a long operation
- this is because of the low blood flow to adipose tissue, meaning it can take many hours for the drug to enter and leave the fat

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19
Q

what does postoperative recovery include?

A

taking care of the unconscious patient:
- airway management, monitoring, position, pressure points, nerve damage, lifting and handling

Monitory and assessing the following is extremely important:

  • oxygenation
  • pain control
  • fluid balance
  • postoperative nausea and vomiting (PONV)
  • cardiovascular stability
  • conscious level
  • urine output
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20
Q

what is postoperative management?

A
  • early management - ‘recovery’
  • late management:
    • wound infection
    • deep vein thrombosis (DVT)
    • chest infection
    • surgical problems
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21
Q

what is the safety of anaesthesia?

A
  • mortality and morbidity are principally related to the type of surgery
  • mortality and morbidity are also related to the type of surgery
  • risk due to anaesthesia alone < 1 in 500,000
  • anaesthesia may contribute to some deaths
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22
Q

What are the uses of anaesthetics in combination with other drugs? (summary of drugs used)

What does this combination allow?

A
  • an intravenous anaesthetic for rapid induction (propofol)
  • an inhalation anaesthetic to maintain anaesthetic during surgery (isoflurane)
  • a perioperative opioid analgesic (fentanyl)
  • a neuromuscular blocking agent to produce adequate muscle relaxation (atracurium)
  • other muscle relaxation agents (suxamethonium)
  • a muscarinic antagonist to prevent or treat bradycardia or to reduce bronchial and salivary secretions (atropine, glycopyrrolate)
  • towards the end of the procedure, an anticholinesterase agent (neostigmine) to reverse the neuromuscular blockade and an analgesic for postoperative pain relief (opioid/NSAID)

Such combinations of drugs result in much faster induction and recovery, avoiding long (hazardous) periods of semi-consciousness, and it enables surgery to be carried out with less undesirable cardiorespiratory depression

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23
Q

what are the different sites that anaesthetic agents act on?

A
  • GABA-A receptors
  • two-pore domain k+ channels
  • NMDA receptors
  • glycine, nicotinic and 5-HT receptors
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24
Q

what are GABA-A receptors?

how do anaesthetics act on them?

A

GABA-A receptors are ligand-gated ion channels (ionotropic receptors)

  • they are chlorine channels
  • they are the most abundant fast inhibitory neurotransmitter receptors in the CNS

Almost all anaesthetics potentiate the action of GABA at the GABA-A receptor

  • they have a positive modulation of the inhibitory function by causing an increased reflux of Cl- ions into the postsynaptic neurone
  • anaesthetics mainly work on extrasynaptic GABA-A receptors
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25
Q

what are two-pore domain K+ channels? what anaesthetics are they affected by? and how?

A
  • also known as ‘leak channels’
  • inhalation inducing agents directly activate these channels, causing hyperpolarisation, thus reducing membrane excitability
  • this may contribute to the analgesic, hypnotic and immobilising effects of these agents
  • these channels are not affected by intravenous inducing agents
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26
Q

what are the effects of anaesthetics on the nervous system?

A
  • enhance tonic inhibition (through enhancing the actions of GABA)
  • reduce excitation (opening K+ channels - hyperpolarisation)
  • inhibit excitatory synaptic transmission (by depressing transmitter release and inhibiting ligand-gated ion channels)
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27
Q

what brain regions are most sensitive to the effects of anaesthetics? what does inhibition of these regions result in?

A
  • most sensitive appear to be the midbrain reticular formation, thalamic sensory relay nuclei and, to a lesser extent, parts of the cortex
  • inhibition of these regions results in unconsciousness and analgesia
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28
Q

where does some anaesthetics cause inhibition?

A

particularly volatile ones, cause inhibition at the spinal level, producing a loss of reflex responses to painful stimuli

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29
Q

what happens as anaesthetic concentration is increased?

A
  • all brain functions are progressively affected

- at high enough doses, all anaesthetics cause death by loss of cardiovascular reflexes and respiratory paralysis

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30
Q

what are inhalation anaesthetics?

A
  • they are all small, lipid-soluble molecules that readily cross alveolar membranes
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31
Q

what determines the overall kinetic behaviour of an inhalation anaesthetic?

A

the rates of delivery of drug to and from the lungs, via (respectively) the inspired air and bloodstream

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32
Q

how can the main factors that determined the speed of induction and recovery be summarised?

A

Properties of the anaesthetic:

  • blood:gas partition coefficient (solubility in blood) - speed of induction/recovery
  • oil:gas partition coefficient (solubility in fat) - potency

Physiological factors:

  • alveolar ventilation rate
  • cardiac output
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33
Q

how is anaesthetic potency expressed?

A

as the minimal alveolar concentration (MAC)
- it is the concentration of vapour in the lungs that is needed to prevent movement (motor response) in 50% patients in response to surgical (pain-incision) stimulus

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34
Q

the potency of drug increases with what?

A

with increasing lipid solubility (the higher the lipid solubility is the lower the MAC)

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35
Q

Propofol

  • what is it?
  • onset and distribution rates?
  • recovery rate?
  • volume of distribution?
  • mechanism of action?
  • what are the side effects?
A
  • an intravenous anaesthetic agent used for induction of general anaesthesia, after which anaesthesia may be maintained using a combination of medications
  • it has a rapid onset of action (30s) and a rapid rate of distribution
  • it is very rapidly metabolised to inactive metabolites - therefore giving rapid recovery with a small hangover effect
  • 60L/kg (healthy adults)
  • positive modulation of inhibitory function of GABA through GABA-A receptor
  • less frequent side effects than other intravenous anaesthetic agents
  • major side effects:
    • hypotension and bradycardia
    • respiratory depression
    • pain with injection
    • involuntary movement and adrenocortical suppression
      - nausea and vomiting
  • can also be given as a continuous infusion to maintain surgical anaesthesia without the need for any inhalation agent
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36
Q

isoflurane

  • what is it?
  • what is it always administered with?
  • what is its mechanism of action?
  • side effects?
A
  • the most widely used volatile anaesthetic - inhalation inducing agent - used for maintenance of general anaesthesia
  • always administered with air/pure oxygen and nitric oxide

mechanism of action:

  • remains incompletely understood
  • likely binds to GABA, glutamates (NMDA) and glycine receptors, but has different effects on each receptor
  • relatively free from side effects
  • major side effects:
    - hypotension
    - coronary vasodilator - exacerbate cardiac ischaemia in patient with coronary disease
    - respiratory suppression
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37
Q

fentanyl

  • what is it?
  • onset and duration?
  • dose?
  • mechanism of action?
A
  • a potent necrotic analgesic
  • similar actions to morphine but with a more rapid onset and shorter duration of action
  • 0.05 mg/mL intravenous

mechanism of action:

  • strong agonist at the u-opioid receptor
  • upon binding, it inhibits adenylate cyclase which causes an inhibition in the release of nociceptive substances such as substance P, GABA, dopamine etc.
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38
Q

neuromuscular-blocking drugs

  • when used?
  • how work?
  • depolarising or non-depolarising?
A
  • clinically, neuromuscular block is used only as an adjunct to anaesthesia, when artificial ventilation is available; it is not a therapeutic intervention
  • the drugs work postsynaptically, either:
    - blocking ACh receptors
    - activating ACh receptors and thus causing persistent depolarisation
  • apart from suxamethonium, all of the drugs used clinically are non-depolarising agents
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39
Q

Non-depolarising neuromuscular blocking agents

  • mechanism of action
  • pharmacokinetics - excretion
  • effects of agents
  • side effects
A

Mechanism of action:

  • act as competitive antagonists at the ACh receptors of the motor endplate
  • also block facilitatory presynaptic autoreceptors and thus inhibit the release of ACh during repetitive stimulation of the motor neurone

Pharmocokinetics:
- most are metabolised by the liver or excreted unchanged in the urine; exceptions being atracurium, which hydrolyses spontaneously in plasma

Effects:
- motor paralysis - help facilitate endotracheal intubation

Major side effects:

  • hypotension
  • bronchospasm - due to histamine release
  • ganglion block
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40
Q

Atracurium

  • what is it?
  • duration of action?
  • optimum conditions?
  • elimination?
A
  • non-depolarising neuromuscular blocking agent - muscle relaxant
  • short duration of action
    • clinical advantage because of the decreased cardiovascular effects and decreased dependency on good kidney function
  • optimum conditions - low pH (acidosis) and high temperature
  • elimination is reduced due to respiratory acidosis
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41
Q

Suxamethonium

  • what is it?
  • duration of action?
  • mechanism of action?
  • rate of recovery?
  • side effects?
A
  • depolarising neuromuscular blocking agent - muscle relaxant
  • duration of action lasts between 3-5 minutes

mechanism of action:

  • ‘persistent’ depolarisation of neuromuscular junction
  • caused by mimicking the effect of ACh but without being rapidly hydrolysed by acetylcholinesterase
  • the constant depolarisation leads to desensitisation
  • suxamethonium is hydrolysed by plasma cholinesterase (butyrycholinesterase (BuChE))
  • rapid recovery that follows its withdrawal

Major side effects:

  • bradycardia and hyperkalaemia
  • increased intraocular pressure
  • postoperative pain
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42
Q

Cholinesterase inhibiting drugs

  • main forms of cholinesterase?
  • where do inhibitors affect?
  • clinical uses?
  • side effects?
A
  1. acetylcholinesterase (AChE)
    - mainly membrane-bound
    - relatively specific for acetylcholine
    - responsible for rapid acetylcholine hydrolysis at cholinergic synapses
  2. butyrylcholinesterase (BuChE)
    - relatively non-selective
    - occurs in plasma and many tissues
  • cholinesterase inhibitors affect peripheral as well as central cholinergic synapses

Cinical uses of anticholinesterase drugs:

  • to reverse the action of non-depolarising neuromuscular blocking drugs at the end of an operation (neostigmine)
    - atropine/glycopyrrolate must be given to limit parasympathomimetic effects
  • to treat myasthenia gravis (neostigmine)

Autonomic side effects:

  • bradycardia
  • hypotension
  • bronchoconstriction

Muscular side effects:

  • muscle fasciculation
  • twitch tension
  • depolarisation block
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43
Q

neostigmine

  • what does it do?
  • mechanism of action?
A
  • acts to reverse effects of muscle relaxants

Mechanism of action:

  • blocks acetylcholinesterase
  • increases ACh in the neuromuscular junction (both nicotinic and muscarinic receptors)
  • increases muscular contraction
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44
Q

Atropine and glycopyrrolate

  • what are they?
  • difference?
  • what used for?
A
  • these antagonise the muscarinic receptor and thus inhibit cholinergic transmission
  • atropine can cross the blood-brain-barrier, whereas glycopyrrolate cannot
  • they are used to limit parasympathomimetic effects caused by neostigmine
    - it prevents neostigmine’s muscarinic effects such as bradycardia
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45
Q

Mannitol

  • what is it?
  • what used for?
  • mechanism of action?
A
  • osmotic diuretic
  • inert in humans but it occurs naturally
  • drug used to treat raised intracranial pressure (e.g. cerebral oedema)

Mechanism of action:

  • these are pharmacologically inert substances that are filtered in the glomerulus but not reabsorbed by the nephron
  • they cause diuresis because they increase the solute content of the fluid in the proximal tubule and collecting tubules
  • this draws fluid from the body into the proximal tubule, thus decreasing the volume of fluid inside the body
  • the result of this is that less water is reabsorbed and also less sodium
  • this leads to a decrease in extracellular fluid volume
  • also, they increase the plasma osmolality
  • this increases the flow of water from tissues (brain and CSF included) into the interstitial fluid and plasma
  • this reduces the intracranial pressure
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46
Q

what is sleep?

A

a state of physiological reversible unconsciousness

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47
Q

what causes the changes between sleep and wakefulness? where are there changes?

A
  • the change from sleep to wakefulness is mediated by the reticular activating mechanism
  • the change from wakefulness to sleep is also an active process affected by an arousal inhibitory mechanism based on a partial blockade of the thalamus and upper brainstem
  • the cognitive change between sleep and wakefulness is accompanied by changes in the autonomic system, the cerebral blood flow and cerebral metabolism
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48
Q

what is wakefulness usually associated with?

A

instant awareness - defined as the ability to integrate all sensory information from the external environment and the internal environment of the body

49
Q

awareness

  • what may it be a function of?
  • what is it an essential component of?
A
  • a function of the thalamo-cortical network in the cerebral hemispheres, which forms the final path of the sleep/wake mechanism
  • an essential component of total consciousness - defined as continuous awareness of the external and internal environment, both past and present, together with the emotions arising from it
50
Q

what does full consciousness require in addition to awareness?

A

short-term and explicit memory and intact emotional responses

51
Q

Describe the circadian clock

A
  • human sleep occurs with circadian periodicity
  • the biological clock detects decreases in light levels as night approaches
  • ganglion cells containing melanopsin are depolarised by light
  • projections run via axons running the retino-hypothalamic tract, which projects to the suprachiasmatic nucleus (SCN) of the anterior hypothalamus, the site of the circadian control of homeostatic functions

Activation of SCN:

  • activation evokes responses in neurones whose axons first synapse int he paraventricular nucleus (PVN) of the hypothalamus
  • these neurones descend to the preganglionic sympathetic neurones in the intermediolateral zone (IML) in the lateral horns of the thoracic spinal cord
  • these preganglionic neurones modulate neurones in the superior cervical ganglia (SCG), whose postganglionic axons project to the pineal gland
  • this causes secretion of melatonin in the bloodstream
  • melatonin increases as the light in the environment decreases
52
Q

what happens in terms of melatonin production in the elderly?

A

the pineal gland produces less melatonin

53
Q

what does the SCN also govern?

A

it governs other functions that are synchronised with the sleep-wake cycle, including body temperature, hormone secretion, blood pressure, and urine production

54
Q

what is the ascending arousal system? what’s its pathway?

A
  • increases arousal and mediates wakefulness

- flows from the brainstem, through the thalamus, hypothalamus, and basal forebrain to the cerebral cortex

55
Q

describe the first components of the ascending arousal system

A
  1. through the thalamus to the cerebral cortex
    - these projections activate relay neurones and reticular nuclei (in the thalamus) essential for thalamocortical transmission
    - two cholinergic structures (PPT - peduculopontine / LDT - laterodorsal tegmental) in the brainstem and basal forebrain serve as the origin of these projections
    - PPT/LDT neurones are most active during wakefulness and rapid eye movement (REM) sleep and discharge more slowly during non-REM (NREM) sleep, a period when cortical activity is reduced
    - transmission to the reticular nucleus promotes a state of excitability and wakefulness (‘reticular activating system’)
    - projections to the thalamus use acetylcholine
56
Q

describe the second component of the ascending arousal system

A
  1. through the lateral hypothalamus and basal forebrain to the cerebral cortex

It comprises a number of monoaminergic cell populations, including:

  • noradrenergic neurones of the locus coeruleus
  • serotoninergic (5-HT) dorsal and median raphe nuclei
  • dopaminergic neurones of the ventral periaqueductal grey matter
  • histaminergic neurones from TMN
  • neurones in these monoaminergic systems have broad action potentials, discharging most rapidly during wakefulness, slowing during NREM sleep, and showing little activity during REM sleep
57
Q

what is orexin?
what’s its role in wakefulness?
what happens during REM sleep?

A

a neurotransmitter that regulates arousal, wakefulness and appetite

wakefulness:

  • orexin neurones strongly excite various brain nuclei with important roles in wakefulness, including the dopamine, norepinephrine, histamine and acetylcholine systems
  • orexin system also helps stabilise wakefulness and sleep
  • during REM sleep, the activity of orexin neurons is reduced
58
Q

what is sleep? how does it differ from coma and general anaesthesia?

A

sleep is a readily reversible state of reduced responsiveness to, and interaction with, the environment

coma and general anaesthesia are not readily reversible and so do not qualify as sleep

59
Q

what are the different stages of sleep? (EEG)

A

sleep consists of non-REM stages that vary clinically with a REM stage during which the EEG (electroencephalogram) cycles between a desynchronised state and a synchronised state

60
Q

what happens during a sleep cycle?

A

one passes through non-REM sleep and then through REM sleep:

  • there are usually 4-6 sleep cycles in an 8 hr period of sleep
  • 80% of a sleep cycle is spent in non-REM sleep; the amount of time spent in non-REM sleep decreases with each cycle
  • 20% of a sleep cycle is spent in REM sleep; the amount of time spent in REM sleep increases with each cycle
61
Q

Non-REM sleep

  • what is it induced by?
  • what happens during it?
  • what characterised by?
A

induced by:

  • ‘non-REM-on’ GABA neurones in the hypothalamus
  • serotonin from the raphe nuclei
  • during non-REM sleep, brainstem noradrenergic neurones show decreased activity
  • characterised by progressively synchronised EEG
62
Q

what are the four stages of non-REM sleep?

  • description
  • EEG waveform
A

awake:

  • eyes open, alert, active mental concentration
  • eyes closed but awake
  • beta (highest frequency, lowest amplitude)
  • alpha (for eyes closed?)

NREM 1:

  • light sleep
  • this is the stage between wakefulness and sleep
  • EEG = 4-7 Hz waves
  • theta

NREM 2:

  • deeper sleep, bruxism (involuntary habitual grinding of teeth)
  • EEG = 10-15 Hz waves
  • theta + sleep spindles & K complexes

NREM 3 + 4:

  • deepest NREM sleep, sleepwalking, night terrors, bedwetting
  • ‘slow-wave sleep’
  • the sleeper is less responsive to the environment; many environmental stimuli no longer produce any reactions
  • EEG = < 3.5 Hz waves
  • delta (lowest frequency, highest amplitude)
63
Q

what are skeletal muscles like during non-REM sleep? what other changes happen in body?

A
  • skeletal muscles relax but maintain their tone
  • the parasympathetic nervous system is active and promotes gastric motility and a decrease in heart rate and blood pressure
64
Q

what is REM sleep characterised by?

A

It’s characterised by a sudden conversion from a synchronised to a desynchornised EEG, resembling that of the awake state combined with a loss of muscle tone (atonia), which results in an active nervous system in an inactive body

65
Q

describe the process of REM sleep

  • what different things happen to the body during it?
  • what causes REM sleep to go back to non-REM sleep
A
  • commences only after non-REM sleep progresses through stages 1-4 and back to stage 2, a cycle that lasts about 90 minutes
  • brainstem cholinergic neurones in the ascending arousal system act as ‘REM-on’ cells that initiate REM sleep
  • during REM sleep, inhibitory medullary reticulospinal neurones are activated, causing skeletal muscles to become flaccid and muscle stretch reflexes to be absent - only the ocular, respiration and middle ear muscles remain active
  • during REM sleep, all sensory systems are inhibited
  • there is an increase in blood pressure, metabolism, and blood flow to the brain
  • penile and clitoral erections are features
  • REM sleep is associated with rapid saccadic conjugate eye movements
  • most dreams occur during REM sleep, and the visual images perceived during dreaming are associated with PGO waves in the EEG
  • near the end of a REM sleep period, noradrenergic and serotonergic neurones act as ‘REM-off’ cells, initiating a transition from REM sleep back to non-REM sleep
66
Q

how does the amount of daily REM sleep change with age?

A

decreases

67
Q

do we need both to survive?

A

can get along without REM sleep but need non-REM sleep to survive

68
Q

what must someone be for a person to be considered fully conscious?

A

both awake and aware
- this means that they have an intact ascending reticular activating system (awake) in the brainstem, and a functioning cerebral cortex (aware)

69
Q

what is concussion?

A

a reversible state of unconsciousness that lasts for only a brief amount of time, without any structural or pathological alteration

70
Q

what is a coma? when does it generally occur?

A

a profound state of unconsciousness that is associated with depressed cerebral activity from which the individual cannot be aroused
- it generally occurs when there is dysfunction or injury involving both cerebral hemispheres or the reticular formation

71
Q

when is a person said to be comatose?

A

when they are unconscious and unable to respond to verbal command
- they might be able to show motor responses to painful stimuli

72
Q

when is a person said to be stuperose?

A

if they are unconscious but can be roused by verbal command or painful stimuli for short periods and produce verbal responses

73
Q

What is the Glasgow coma scale (GCS) used for?

A
  • its used to assess depression of consciousness
  • it’s also essential to record:
    - pupillary responses to light
    - reflex eye movements in horizontal and vertical plane
    - blood pressure, respiratory rate, pulse and temperature
74
Q

what is a vegetative state?

A

it’s a clinical condition in which the patient is unaware of self or surroundings, breathes spontaneously and has stable circulation and shows patterns of eye closure and opening that may stimulate sleep

  • however, there is no intelligent communication coming from the patient
  • a persistent vegetative state is irreversible
  • a person is said to be in a persistent vegetative state if they are still in one 12 months after a head injury
75
Q

what are seizures? what are they a sign of?

A

the most extreme form of synchronous brain activity, they are always a sign of pathology

76
Q

what is a generalised seizure?

what is a partial seizure?

A 
generalised = involves the entire cerebral cortex of both hemispheres 
partial = involves only a limited area of the cortex, but it can spread
77
Q

what happens to EEG patterns during a seizure and why?

A

the neurones within the affected areas fire with a synchrony that never occurs during normal behaviour
- therefore, seizures are usually accompanied by very large EEG patterns

78
Q

what is epilepsy?

A

when a person experiences repeated seizures

79
Q

what are very potent convulsants (seizure-promoting agents)?
what can also trigger seizures?

A

drugs that block GABA receptors

withdrawal of chronic depressant drugs, such as alcohol or barbiturates, may also trigger seizures

80
Q

how do anticonvulsants work?

A

variety of ways:

  • prolonging the inhibitory actions of GABA (e.g. barbiturates, benzodiazepines)
  • decreasing the tendency for certain neurones to fire high-frequency action potentials (e.g. phenytoin, carbamazepine)
81
Q

what happens during a generalised seizure?

A
  • virtually all cortical neurones participate, so behaviour is completely disrupted for many minutes
  • consciousness is lost, while all muscle groups may be driven by tonic (ongoing) activity or by clonic (rhythmic patterns), or by both in sequence = tonic-clonic seizures
82
Q

describe the different presentations of partial seizures depending on where in the brain they affect

A
  • partial seizures can be instructive
  • if they begin in a small area of motor cortex, they can cause clonic movement of part of a limb
  • if seizures begin in a sensory area, they can trigger an abnormal sensation, or ‘aura’, such as an odd smell or sparkling lights
  • most bizarre are the partial seizures that elicit more well-formed auras such as deja vu or hallucinations
  • sometimes involving the cortex of the temporal lobes, including the hippocampus and amygdala, they can impair memory, thought, and consciousness
  • in some cases, partial seizures may spread uncontrollably and become generalised seizures
83
Q

what are the signs of elevated intracranial pressure (ICP)?

A
  • early signs include drowsiness and a diminished level of consciousness
  • neuroimaging may reveal evidence of oedema and mass effect
  • late signs are coma and unilateral pupillary changes - they require immediate intervention
84
Q

how is emergency treatment of elevated ICP most quickly achieved?

how do you avoid provoking or worsening cerebral ischaemia?

A

by intubation and hyperventilation, which causes vasoconstriction (oxygen lack theory) and reduces cerebral blood volume

hyperventilation is best used for short periods of time until a more definitive treatment can be instituted

85
Q

what assumes greater importance as the level of consciousness declines to coma and the ability to follow the neurologic status of the patient by examination deteriorates?

A

measurement of ICP

86
Q

what is sometimes used for refractory elevations of ICP?

A

high-dose barbiturates (causes cerebral vasoconstriction and reduced metabolic demands?), decompressive hemicraniectomy, or hypothermia
- although these have significant side effects and have not been proven to improve outcomes

87
Q

what are the two main types of oedema?

A

vasogenic oedema = the influx of fluid and solutes into the brain through an incompetent blood-brain barrier (BBB)
cytotoxic oedema = cellular swelling

88
Q

what type of oedema does cranial oedema that is clinically significant usually present?

A

a combination of vasogenic and cellular components

89
Q

what is the treatment for cranial oedema?

A
  1. elevate head 30*
  2. intubate and hyperventilate - reduce cerebral blood flow due to vasoconstriction
  3. IV mannitol - osmotic diuretic
  4. ventricular drainage - removal of CSF decreases intracranial pressure
90
Q

what is a craniotomy?

A

this is the surgical removal of part of the cranium, performed to expose brain and meninges for inspection or biopsy or to relieve excessive intracranial pressure

91
Q

what is the procedure of a craniotomy?

A
  • the hair is shaved, the scalp is cleaned with iodine solution, and an incision is then made to expose the skull
  • burr holes are drilled through the skull at several locations
  • the burr holes are then joined together
  • the bone flap is removed, exposing the dura
  • the dura is hen carefully opened and folded back
92
Q

what is the blood supply of the scalp?

A

the blood supply of the scalp is via five pairs of arteries, two from the internal carotid and three from the external carotid

internal carotid:

  • supratrochlear artery to the midline forehead - branch of the ophthalmic branch of the ICA
  • supraorbital artery to the lateral forehead and scalp as far as the vertex - branch of ophthalmic branch of ICA

external carotid:

  • superficial temporal artery gives off frontal and parietal branches to supply much of scalp
  • occipital artery runs posteriorly to supply much of posterior aspect of scalp
  • posterior auricular artery ascends behind the auricle to supply the scalp above and behind the auricle
93
Q

what are the walls of the blood vessels attached to? and what does this mean?

A

they are firmly attached to the fibrous tissue of the superficial fascial layer, hence cut ends of vessels here do not readily retract; even a small scalp wound may bleed profusely

94
Q

what is a skull fractures?

A

a break in one or more of bones of the skull caused by a head injury

95
Q

are isolate skull fractures serious? what do they mean?

A

they are not very serious injuries but the presence of a skull fracture can indicate that a significant enough force was applied to cause brain trauma

  • the broken fragments of a skull can lacerate or bruise the brain or damage blood vessels
  • bone fragments can cause a penetrating head injury (i.e. breaching the dura mater)
96
Q

what is a compound fracture?

A

compound (open) fracture = fracture in which the skin is also broken

97
Q

what are the different types of fracture?

A

linear:

  • most common
  • caused by widely distributed force
  • they occur when the area that is impacted bends inwards causing the area around it to bend outwards

diastatic:
- the fracture line transverses one or more sutures of the skull, causing a widening of the suture

depressed:

  • the broken bones are displaced inwards
  • carries a high risk of increasing intracranial pressure, crushing delicate tissue
  • require surgery to life the pieces of bone off the brain if they are causing pressure on it

basilar:

  • breaks in bones at the base of skull
  • more force is required to cause these than with cranial vault fractures
  • has some characteristic signs; blood in the sinuses, CSF leaking from the nose or ears
98
Q

neuropsychological assessment

  • simple procedure
  • complex neurological examination
A

simple:
- ask whether patient is able to move and react to physical stimuli
- if so, see whether patient can respond in a meaningful way to questions and commands
- if so, patient is asked name, current location, and current day and time
- a patient who can answer all of these questions is said to be ‘oriented three times’ (sometimes denoted Ox3 on a medical chart), and is usually considered fully conscious

Complex:
- a formal neurological examination runs through a precisely delineated series of tests, beginning with tests for basic sensorimotor reflexes, and culminating with tests for sophisticated use of language

99
Q

cognition is associated with what?

A
  • intellectual functioning - problem solving, abstract/verbal reasoning, speed of processing, concentration, spatial awareness
  • perception - the processes by which information about the external environment is analysed and made meaningful - first stage of memory
    memory - mental process of recalling and reproducing that which has been learned and retained - 3 stages - 1 = perception, 2 = storage, 3 = retrieval
  • mood
  • speech & language
100
Q

what are the two types of assessment?

A
  1. descriptive - type and severity of problem

2. predictive - to explain causes and consequences of deficit

101
Q

Describe what an assessment includes

A

intellectual functioning:

  • higher executive functioning (WAIS-R)
  • reduced accuracy / or speed in time pressure processing
  • reduced concentration span
  • executive functioning (planning, organisation, decision making) - initiate and maintain and also disengage from goal-directed behaviour

perception:

  • visuo-perceptual (object recognition)
  • audition (sound recognition, localisation)
  • hallucinations
  • altered olfactory, kinaesthetic or gustatory experiences

memory:

  • impaired recent memory
  • frequency estimation
  • sequencing
  • delayed response task
  • verbal memory
  • working memory

mood:

  • lability (swings)
  • aggression
  • depression
  • anxiety

behaviour:

  • sexual disinhibition
  • aggression
  • uncharacteristic responses

language:
- receptive and expressive language functions
- verbal knowledge
- reading skills

102
Q

what are the different levels of assessment?

A

1st level: basic neurological examination
2nd level: interview, observation, assessment
3rd level: full measurement using standardised measures
-> rehabilitation plan

103
Q

what are the possible problems caused by the following?

  1. right temporal lobe damage & part removal
  2. preoperative oedema
  3. dense hemiparesis
  4. seizures
A
  1. memory, hearing, language understanding, info processing
  2. additional damage to residual tissue
  3. on-going disability, consequences
  4. stigma, additional demand on coping, dependent
104
Q

what does a rehabilitation programme include?

A
  • pharmacology
  • behavioural therapy
  • social retaining
  • physical retaining
  • family therapy
  • cognition therapy
105
Q

what are the different types of social support?

A
  • esteem support = other people increase one’s own self-esteem
  • informational support = other people available to offer advice
  • companionship = involves support through activities
  • instrumental support = involves physical help
106
Q

what does the reticular activating system include?

A
  • midbrain reticular formation
  • mesencephalic nucleus (midbrain)
  • thalamic intralaminar nucleus
  • dorsal hypothalamus
  • tegmentum
107
Q

what are the ways of optimising elective surgery?

A
  • Physiology: stop smoking, loosing weight, improve exercise tolerance
  • Pharmacology: diabetes, heart failure, COPD, asthma, angina
  • Psychological: awareness, information, anticipation, mindset
108
Q

when is regional anaesthesia possible?

A
  • Peripheral limbs – can just block the nerves that are going in e.g. block the left brachial plexus
  • Lower abdomen
  • Supplied by a distinct set of nerves
109
Q

what are the different components of anaesthesia?

A
  • Hypnosis (posh word for sleep)
  • intravenous agents: propofol, barbiturates (thiopenton), benzodiazepines
  • Analgesia (inability to feel pain)
  • opiates: synthetic or natural
  • non-opiates
  • Muscle relaxation
  • depolarising e.g. suxamethonium
  • non-depolarising
110
Q

how does solubility of inhalation anaesthetics affect the time taken for them to have their effect?

A
  • For different agents, depending on their physical characteristics, the rate at which the blood concentration increases (alveolar concentration increases), depends on how soluble these agents are
  • If you take an agent that is very soluble, e.g. halothane, you can give a lot, but it all becomes solution and that is not effective – you need the agents in the gaseous phase for them to have a physiological effect on the brain
  • Therefore, with less soluble agents, e.g. N2O, desflurane, sevoflurane, isoflurane, the effect tends to come on much faster than with agents that are highly soluble, e.g. halothane
  • How quickly an inhalational anaesthetic agent’s effect comes on, is determined by blood-gas solubility coefficient or Ostwald coefficient ‘
  • Cb/Cg – when the partial pressure in both compartments are equal
  • More soluble agents have a higher coefficient -> agents with a lower coefficient have a faster onset and faster emergence
111
Q

what is potency of anaesthetic agents related to?

A
  • Related to lipid solubility – if highly soluble in lipid, then it can reach the brain in high concentrations, and therefore tends to be a lot more potent
  • Measured by oil-gas partition coefficient
  • Not related to blood-gas solubility coefficient – that’s to do with how quickly the effect comes on, not to do with potency
  • An inherent property of the agent itself
  • N2O has low potency
  • MAC (minimum alveolar concentration) – an inverse indicator of potency
  • Halothane > isoflurane > sevoflurane > desflurane > N2O
112
Q

what are the adverse effects of anaesthetics?

A
  • PONV – post-operative nausea and vomiting
  • Cardiovascular depression
  • negatively inotropic – these agents weaken the force of muscular contractions
  • variable action on heart rate
  • Arrhythmogenesis
  • Hypotension: vasodilatation
  • Loss of airway tone: airway obstruction
  • Malignant hyperthermia
  • Bronchial muscle relaxation & impaired cough reflex
  • Agitation and confusion – particularly in elderly – takes much longer to get back to original state
  • Nephrotoxicity: RBF, GFR, UOP…vs. fluoride-induced nephrotoxicity
  • Nephrotoxicity: halothane hepatitis
113
Q

what are examples of different opiates?

A
  • Natural
  • morphine
  • dihydro-morphine
  • codeine
  • Opiate analogues (opiate-like substances)
  • tramadol
  • Synthetic or semisynthetic
  • pethidine
  • fentanyl
  • alfentanyl
  • remifentanyl
114
Q

why do you have to monitor respiration with analgesia?

A

Analgesia and respiratory depression are mediated via the u receptors

  • u1: analgesia
  • u2: respiratory depression
  • u3: vasodilatation
115
Q

what is naloxone? what’s it used for?

A

structurally similar to opiates but binds to opiate receptors much more rapidly but it’s not as potent, therefore patients will wake up – the naloxone displaces the morphine

116
Q

what is neuropsychology?

A

the study of the relationship between the brain and the mind

117
Q

what do different lobes/part of brain do control?

A

Frontal lobe:
Emotional control, self-awareness, motivation, judgement, problem-solving, talking, movement and initiation

Parietal lobe: sense of touch, awareness of spatial relationships and academic functions such as reading

Temporal lobe: memory, hearing, understanding, language, and processing information

Occipital lobe: vision

Cerebellum: balance, coordination, skilled motor activity

Brainstem: breathing, hear rate, arousal and consciousness, sleep and wake cycles

118
Q

what do assessment techniques include?

A

Perception:

  • Object recognition (visuo-perceptual skills)
  • Sound recognition/localisation (auditory processing)
  • Block design test, picture completion task (visual-spatial and constructional skills)

Memory:

  • Visual reproductions (impaired recent memory, visual learning)
  • Delayed recall tasks (auditory & visual declarative memory)
  • Digit span tests (repeat string of digits of increasing length), vigilance and continuous performance tests (working memory)
  • Spatial working memory tests

Language:

  • Vocabulary knowledge tests (‘crystallised’ verbal knowledge)
  • Reading comprehension tasks and aurally presented instruction (receptive language))
  • Naming tests and letter fluency tasks (expressive language)

Intellectual ability:

  • Card sorting task (attention, executive functioning)
  • Digit symbol task, trail making task (mental processing and psychomotor speed)
  • WAIS-IV (IQ test), Stroop task (executive functioning)

OTHER COMPONENTS OF ASSESSMENT

  • Alongside standardised tests of cognitive function
  • Also assessing other factors: e.g. assessment of personal, interpersonal and contextual factors
  • Assessment may include history taking, interviewing, tests of motor functioning

Medicine Sem 3 (23 decks)

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