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Sem3 > Case 10 > Flashcards

Case 10 Flashcards

1
Q

What is general anaesthesia?

A

A medically induced comma 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 
Analgesia - loss of response to pain
Amnesia - loss of memory 
Immobility- loss of motor reflexes
Unconsciousness 
Skeletal muscle relaxation
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3
Q

How do anaesthetics work?

A

They will enhance inhibitory signals or block excitatory signals via interaction with ion channels

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4
Q

What is the purpose of anaesthetic premedication?

A

It improves or complements the quality of the anaesthetic

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5
Q

What are some anaesthetic premedications?

A
  • Benzodiazepines - anxiolysis (relieves anxiety)
  • Opioids
  • Anticholinergics - antisialagogue (reduces saliva production)
  • antibiotics
  • antacids - neutralises excess stomach acid to relieve heartburn, acid indigestion, stomach pain
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6
Q

What are the monitoring systems used in general anaesthesia?

A
  • ECG - identify heart ischaemia
  • Blood Pressure
  • Oxygen saturation - identify hypoxaemia
  • end tidal CO2
  • inspiration oxygen
  • neuromuscular blockade
  • airway pressures and flow
  • temperature
  • depth of anaesthesia
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7
Q

What are the stages of anaesthesia?

A

Induction

(Excitement stage - marked by excited and delirious activity with irregular heart and breathing rate)

Maintenance

Reversal

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8
Q

How can anaesthetic agents be induced?

A

Inhalation:
• vapour, Highly lipid soluble, recovery is via exhalation

Injection - Intravenous:
• bolus, highly lipid soluble, recovery via redistribution and elimination

Intravenous is quicker (takes 10-20sec for unconsciousness) hence avoids complications and excitement stage

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9
Q

What is the common intravenous induction agents?

A

Propofol, sodium thiopentone, etomidate and ketamine

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10
Q

What is the purpose of maintenance during general anaesthesia?

A

To prolong the duration (5-10mins) of intravenous induction agent and hence keep patient unconscious for duration of surgery

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11
Q

How is maintenance of induction agent achieved?

A

Patient breathes in a mixture of NO, O2 and volatile anaesthetic agent (isoflurane)

It can also be achieve by continuous infusion of propofol via catheter

Inhaled agents (Isoflurane, Sevoflurane, Desflurane) are supplemented by intravenous anaesthetics = opioids- fentanyl or morphine; sedative- hypnotics (propofol)

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12
Q

Why is a muscle relaxant used?

A

Eliminates the need for a deep anaesthesia to conduct surgery in body cavities and also facilitated endotracheal intubation

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13
Q

How do muscle relaxants works?

A

They inhibit the binding of acetylcholine to muscarinic receptors

E.G. atracurium, succinylcholine(sucamethonium), tubocurarine (carare), rocuronium, vecuronium

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14
Q

What does the endotracheal intubation do?

A

Protects the larynx while it is paralysed and allows maintenance of regular breathing via mechanical ventilation

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15
Q

How is the muscle relaxant reverted?

A

With an acetylcholinesterase drug

Neostigmine

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16
Q

What are the respiratory affects of anaesthesia?

A

Spontaneous breathing:

  • normal negative pressure breathing
  • respiratory depression - hypercapnia
  • hypoxia on room air

Positive pressure ventilation:
- Increase incidence of chest infection (ventilator acquired pneumonia)

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17
Q

What are the cardiovascular affects of anaesthesia?

A

Decreased venous return, cardiac output, and force of contraction

Increase in arrhythmia potential

Vasodilation

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18
Q

What are the CNS affects of anaesthesia?

A

Unconsciousness, depression of cerebral metabolism, dreaming and awareness

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19
Q

What is the issue caused by low blood flow to adipose tissue?

A

High lipid soluble agents accumulate in body fat and produce prolonged ‘hangover’ if used for long operation

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20
Q

What is important to monitor and assess after the operation?

A

Oxygenation, pain control, fluid balance, postoperative nausea and vomiting (PONV), cardiovascular stability, conscious l‘level and urine output

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21
Q

What is the risk of anaesthesia?

A

Less than 1 in 500,000

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22
Q

What is the muscarinic antagonist used to prevent or treat bradycardia or reduce bronchial and salivary secretion?

A

Antropine or glycopyrrolate

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23
Q

What are the target sites of anaesthetic agents?

A

GABA-A receptors

Two-pore domain potassium channels

NMDA receptors

glycine, nicotinic and 5HT receptors

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24
Q

What type of receptors are GABA-A receptors?

A

Ligand-gated chlorine channels ionotropic receptors

Anaesthetic agents increase its influx of chlorine ions at extrasynaptic receptors

This enhances tonic inhibition

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25
Q

What are two-pore domain potassium channels?

A

Aka leak channels

These are only affected by inhalation inducing agents causing hyperpolarisation to reduce membrane excitability

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26
Q

Inhibition of which part of the CNS leads to analgesia and unconsciousness?

A

Thalamic sensory relay nuclei and midbrain reticular formation

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27
Q

What causes death innanaesthesia?

A

Loss of cardiovascular reflexes and respiratory paralysis

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28
Q

What determines the speed of induction and recovery of anaesthesia?

A

Properties of the anaesthetic:

  • blood:gas partition coefficient (solubility in blood)
  • oil:gas partition coefficient (solubility in fat)

Physiological factors:

  • Alveolar ventilation rate
  • cardiac output
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29
Q

What is anaesthetic potency?

A

Minimal alveolar concentration (MAC)

i.e. the concentration of vapour in the lungs that is needed to prevent movement (motor response) in 50% of patients in response to surgical stimulus

Higher lipid solubility = lower MAC = greater potency

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30
Q

How does propofol work and what are the side effects?

A

MOA: positive modulation of inhibitory function of GABA through GABA-A receptors

Side effects:

  • hypotension and bradycardia
  • respiratory depression
  • nausea and vomiting
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31
Q

How does Isoflurane work and what are the side effects?

A

MOA: binds to GABA, NMDA, and glycine receptors

Side Effects:

  • hypotension
  • coronary vasodilator - increases cardiac ischaemia in CVD patients
  • respiratory suppression
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32
Q

How does fentanyl work?

A

micro-opioid receptor agonist inhibiting adenylate cyclase hence inhibiting release of nociceptive substances eg Substance P, GABA, dopamine

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33
Q

How do non-depolarising Neuromuscular blocking agents work?

A

Competitive antagonists at ACh receptors of motor end plate

They block the presynaptic auto receptors, inhibiting release of ACh during repetitive stimulation of motor nerve

Effect: motor paralysis

Side effects: hypotension, bronchospasm (due to histamine release) and ganglion block

Example: Atracurium

34
Q

What is the advantage of a respiratory low pH (acidosis) for Atracurium?

A

It reduces elimination

35
Q

How do depolarising Neuromuscular blocking agents work?

A

Mimics ACh without rapid hydrolysation by AChE hence persistent depolarisation leading to desensitisation

Example: Suxomethonium (hydrolysed by BuChE - plasma cholinesterase)

Side Effects: bradycardia and Hyperkalemia, increased intraocular pressure

36
Q

What do cholinesterase inhibiting drugs do?

A

Reverse action of non-depolarising neuromuscular blocking drugs and treat myasthenia gravis

Example: neostigmine

37
Q

What are muscarinic receptor antagonists?

A

Inhibit cholinergic transmission and used to limit parasympathomimetic effects caused by neostigmine (e.g. bradycardia)

Examples: atropine (crosses BBB) and glycopyrolate

38
Q

What is a osmotic diuretic?

A

Drug used to treat intracranial pressure e.g cerebral oedema

MOA: increase solute content of fluid in proximate tubule and collecting tubule causing fluid to be drawn from the body into the proximal tubule decreasing extra cellular fluid volume

Example: Mannitol

39
Q

What is sleep?

A

State of physiological reversible unconsciousness - reduced responsiveness to and interaction with the environment

40
Q

What is wakefulness?

A

Associated with awareness - The ability to integrate all sensory information from the external environnement and the internal environment of the body

41
Q

What is total consciousness?

A

Continuous awareness of the external and internal environment, both past and present, together with the emotions arising from it

Requires short-term and explicit memory and intact emotional response

42
Q

What is the Circadian Rhythm?

A

It is the control of human sleep through detection of decreased light levels over 24H

43
Q

How is the circadian rhythm controlled?

A

Ganglion cells contain melanopsin which is depolarised by light provides input to suprachiasmatic nucleus (SCN) via retinohypothalamic tract

From SCN output is set to the paraventricular nucleus (PVN) to intermediolateral zone (IML) on lateral horn of thoracic spinal cord, to superior cervical ganglia (SCG) to the pineal gland

Pineal gland is stimulated to secret melatonin into the blood by decreased light

44
Q

What other functions other than light synchronise the sleep-wake cycle?

A

Body temperatures hormone secretion, blood pressure and urine production

All governed by SCN

45
Q

How is wakefulness mediated?

A

By the ascending arousal system flowing from brainstem to the cerebral cortex through thalamus, hypothalamus and basal forebrain

46
Q

What are the two components of the ascending arousal system?

A
  1. Thalamus to the cerebral cortex

2. Lateral hypothalamus and basal forebrain to the cerebral cortex

47
Q

What is the ascending arousal system through the thalamus to the cerebral cortex?

A

Cholinergic structures (PPT/LDT) in brainstem send acetylcholine to thalamus reticular nuclei > transmission promotes a state of excitability and wakefulness (reticular activating system)

PPT/LDT more active during wakefulness and REM sleep and less active during NREM sleep

48
Q

What is the ascending arousal system through the lateral hypothalamus and basal forebrain to the cerebral cortex?

A

LH and BF are comprised of monoaminergic cells:

  • noradtenergic neurons of locus coeruleus
  • serotonergic dorsal and median raphe nuclei
  • dopaminergic neurons of ventral periaqueductal grey matter
  • histaminergic neurons from TMN (tuberomammillary nucleus)

Active during wakefulness, slow during NREM sleep and no activity during REM sleep

49
Q

What is Orexin?

A

Neurotransmitter that regulates arousal, wakefulness and appetite

(Helps stabilise wakefulness and sleep)

50
Q

How does orexin regulate wakefulness?

A

It strongly excites dopamine, noradrenaline, histamine and acetylcholine brain nuclei

Activation for orexin neurons reduces during REM sleep

51
Q

What is the sleep cycle?

A

Moving through NREM sleep (80%) and then REM sleep (20%)

  • In 8H sleep there is about 4-6 cycles (durations in NREM sleep decreases after each cycle and amount in REM sleep increases)

NREM sleep is required to survive

52
Q

What induces NREM sleep?

A

NREM-on GABA neurones in the hypothalamus And Serotonin from Raphe Nuclei

53
Q

What happens during NREM sleep?

A

Decreased activity of noradrenergic neurones in brainstem

Skeletal muscles relax but maintain tone

active parasympathetic nervous system w/ gastric motility and decreased HR and BP

54
Q

What are the four stages of NREM sleep?

A

Awake:
• active mental concentration [EEG Beta, 14-30Hz]
• closed eyes [EEG Alpha, 8-13Hz]

NREM 1: light sleep [EEG Theta, 4-7Hz]

NREM 2:
• deeper sleep, bruxism [EEG Theta]
• sleep spindle (10-15Hz) and K-complex

NREM 3 + NREM 4:
• deepest sleep, sleepwalking, night terrors, bedwetting, ‘slow-wave sleep’ [EEG Delta, <3.5Hz]

55
Q

What is Bruxism?

A

Involuntary habitual grinding of teeth

Occurs during NREM 2

56
Q

What is atonia?

A

Loss of muscle tone

57
Q

When does REM sleep start?

A

Once NREM sleep has completed cycle from 1-4 and back to 2 (lasts 90mins)

It is induced by cholinergic neurones in ascending arousal system

58
Q

What happens during REM sleep?

A

EEG = synchronised to desynchronised waves (resembles awake state w/ atonia)

skeletal muscles are flaccid and muscle stretch reflexes to be absent

Sensory systems are inhibited

Increased BP, metabolism and blood flow to brain

Penile and Clitoral erection

Dreams

59
Q

What are REM- off cells?

A

Noradrenergic and serotonergic neurones

Causes transition back to NREM sleep

60
Q

What is consciousness?

A

Alert cognitive state in which you are aware continually of the external and internal environment, both past and present, together with the emotions arising from it

To be considered full conscious you need:
1. Intact ascending reticular activating system (awake)

  1. Functioning cerebral cortex (aware)
61
Q

What is a concussion?

A

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

62
Q

What is a coma?

A

Profound state of unconsciousness that is associated with depressed cerebral activity from which individual cannot be aroused

Dysfunction or injury involving both cerebral hemispheres or the reticular formation leads to coma

63
Q

What is comatose?

A

Unconsciousness and inability to respond to verbal commands (might show motor responses to painful stimuli)

64
Q

What is stuporose?

A

Unconsciousness but can be roused by verbal command or painful stimuli for short periods and produce verbal responses

65
Q

What does the Glasgow Coma Scale look at?

A

Assess depression of consciousness

Records:
Pupillary responses to light

Reflex eye movement in horizontal and vertical plane

BP, respiratory rate, pulse and temperature

66
Q

What is a seizure?

A

Extreme form of synchronous brain activity accompanied by very large EEG patterns

  • Generalised - entire cerebral cortex of both hemispheres
  • Partial - limited area of the cortex but can spread
67
Q

What is epilepsy?

A

Repeated seizures

68
Q

What is a convulsant?

A

Drugs that block GABA receptors = seizure promoting agents

69
Q

Seizures can be caused by…

A

CNS Depressant drugs (Alcohol or barbiturate)

70
Q

How do anticonvulsants work?

A

Prolong inhibitory action of GABA (e.g. barbiturates and benzodiazepines)

Decrease the tendency for certain neurones to fire high frequency action potentials (e.g. phenytoin, carbamazepine)

71
Q

What are signs of Elevated Intracranial Pressure?

A

Early = drowsiness and diminished level of consciousness

Late = coma and unilateral pupillary changes

72
Q

How is ICP treated?

A

• Emergency = intubation and hyperventilation - causing vasoconstriction and reduces cerebral blood volume
(hyperventilation must be used for short time to avoid worsening or causing cerebral ischaemia)

• high-dose barbiturates, decompressive hemicraniectomy or hyperthermia

73
Q

What are the types of cranial oedema?

A
  • Vasogenic - influx of fluid and solutes into brain through BBB
  • Cytotoxic - cellular swelling

Cranial oedema represents a combination of both

74
Q

How is cranial oedema treated?

A

Elevate head 30 degrees

Intimate and hyperventilate - to 25-30 mmHg PCO2

IV mannitol (osmotic diuretic)

Ventricular damage

75
Q

What is a craniotomy?

A

Surgical removal of part of the cranium to help relieve excess intracranial pressure

76
Q

What is the blood supply of the scalp?

A

Internal Carotid:
• supratrochlear- to midline forehead
• supraorbital - to lateral forehead and scalp

External Carotid:
• superficial temporal
• occipital - posterior aspect of scalp
• posterior auricular - scalp above and behind the auricle

77
Q

What is a compound fracture?

A

Skin is also broken with the fracture

78
Q

What is a linear fracture?

A

Impacted area bends inwards causing area around it to bend outwards

Most common cranial fracture

79
Q

What is a diastatic fracture?

A

Fracture line transverse one or more suture lines causing a widening of sutures

80
Q

What is a depressed fracture?

A

Inward displacement of broken bone

High risk of intracranial pressure

Surgery required

81
Q

What is basilar fracture?

A

Breaks in bones at the base of the skull

Characteristics: blood in sinuses, CSF leaking from the nose or ears

Sem3 (10 decks)

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