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Block 3 AR > General > Flashcards

General Flashcards

1
Q

What types of glia are there?

A

Astrocytes - star-shaped cells, bridge between neuron + blood vessels
Ependymal cell - simple ciliated cuboidal cell lining ventricular system
Microglia - small glial cells, activated by trauma
Oligodendroglia - myelin producing cells CNS, form foot processes
Schwann cells - myelin producing cells PNS, whole cell wraps around

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2
Q

What is saltatory conduction?

A

Nodes of ranvier allow action potential to travel much faster as it can jump from node to node

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3
Q

What are differences between electrical and chemical synapses?

A

Chemical - Fast transmission (slower cell-cell, but can cope with Higher
Frequency of activity), Vesicles releases from presynaptic terminal, Act on receptors in postsynaptic terminal, Major drug target
Electrical - Slower transmission (faster cell-cell, but more effective at lower freqs), Gap junctions, Small molecules and current, low-pass filter (slow down transmission), Synchrony, Up-and-coming drug target

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4
Q

What are the main neurotransmitters used by the CNS?

A

Glutamate and GABA

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5
Q

What are 3 types of Inhibition responsible for coding of activity?

A

Direct inhibition
Lateral inhibition
Disinhibition

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6
Q

Describe coding of neuronal activity

A

Excitatory neurons have regular firing in absence of inhibition
Inhibitory input sculpts this to give patterns
Coding carries the information and can be read, like morsecode
Some drugs that increase firing can lead to loss of coding and psychological side effects

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7
Q

Describe lateral inhibition

A

Activation of excitatory cells also activates associated inhibitory cells
Inhibition acts on neighbouring cells to reduce activity
Strengthens response of cell directly stimulated
Seen in sensory pathways to sharpen - Vision, Touch, Olfaction

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8
Q

What is disinhibition?

A

Two negatives make a positive
Activation of inhibitory circuit leads to excitation
Pivotal role in Basal Ganglia circuitry – shapes motor function

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9
Q

How do cells synchronise?

A

Gap junctions

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10
Q

Describe neuronal plasticity

A

Up- or down-regulation of synaptic strength
LTP long term potentiation and LTD long term depression
Synaptic morphology, Metabolic changes, Subunit changes

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11
Q

What mechanisms are involved in pathogenesis of neuronal and psychological disorders?

A 
Altered neuronal activity
Altered synchrony 
Cellular changes 
Subcellular change 
Genetic composition
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12
Q

What is speech?

A

The act of communicating ideas by the use of words

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13
Q

What is language?

A

The method of human communication, either spoken or written, consisting of the use of words in a structured and conventional way

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14
Q

What are the components of speech?

A

Motive force – expiration
Phonation – voice production
Articulation – modification of basic voice sound to create words out of a set of vowel and consonant sound units
Central processing and control

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15
Q

How is the motive force of speech generated?

A

Inspiration followed by elastic recoil of lungs and wall of thorax +/- contraction of muscles of abdominal wall
Passage of air through glottis down a pressure gradient

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16
Q

What factors may reduce the motive force of speech?

A

Chest wall deformity
Lung pathology, eg. emphysema, pulmonary fibrosis
Muscular weakness, eg. myasthenia gravis
Airway obstruction, eg. asthma; tracheal stenosis
Exhaustion

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17
Q

What is phonation?

A

The generation of a voice sound by the passage of air down a pressure gradient over appropriately positioned vocal cords

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18
Q

What determines the pitch of a voice?

A

Length and tension of the vocal cords and the pressure gradient

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19
Q

What determines the harmony of the voice?

A

smoothness or irregularity, thickness and consistency of the vocal cords

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20
Q

What determines the volume of a voice?

A

pressure gradient across the vocal cords

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21
Q

Which laryngeal muscle abducts the vocal folds?

A

Posterior cricoarytenoid

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22
Q

Which laryngeal muscles adduct the vocal folds?

A

Lateral cricoarytenoid
Transverse arytenoid
Oblique arytenoid

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23
Q

Which laryngeal muscle lengthens the vocal folds?

A

Cricothyroid

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24
Q

Which laryngeal muscle shortens the vocal folds?

A

Thyroarytenoid

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25
Q

What nerve supplies the laryngeal muscles except cricothyroid?

A

Cranial Nerve X - Recurrent Laryngeal branch

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26
Q

Which nerve supplies cricothyroid muscle of the larynx?

A

External branch of superior laryngeal nerve of vagus

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27
Q

What position are the vocal folds in during forced inspiration?

A

Vocal folds abducted and rima glottidis wide open

Vestibule open

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28
Q

What position are vocal folds in during phonation?

A

Vocal folds adducted and stridulating as air forced between them
Vestibule open

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29
Q

What problems can cause dysphonia?

A 
Laryngitis 
Vocal cord palsy 
Vocal nodules 
Vocal cord polyp
Reinke`s oedema 
Dysplasia 
Carcinoma
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30
Q

What is Functional Aphonia/Dysphonia?

A

Diagnosis by exclusion of structural or neurological abnormalities
Hypo-functional – voice breathy, vocal cords abducted, cough normal
Hyperfunctional - voice harsh with unstable vibratory patterns, false vocal cords may be involved
Psychological cause
Predominantly in young females

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31
Q

What is articulation?

A

The modification of basic voice sound to create words out of a set of vowel and consonant sound units

32
Q

What factors are involved in articulation?

A 
Shape and patency of resonant cavities
Closure of lips
Position of floor of mouth and tongue
Position of soft palate
Contact between tongue and palate and tongue and teeth
Motor innervation of lips (Cranial N.VII), soft palate (CranialN.X) and tongue (Cranial N.XII)
Basal ganglia function
Cerebellar function
Central control
33
Q

What can cause Dysarthria?

A 
Nasal polyps 
Antro-choanal polyp
Tonsillar hypertrophy 
Infectious mononucleosis
Cleft lip
Cleft palate 
Tongue tie
Macroglossia 
Carcinoma 
Absence of teeth 
Neurological: stroke, Cerebellar disease, Disorders of basal ganglia, Motorneurone disease, Multiple sclerosis, Myasthenia gravis, Isolated cranial nerve lesions
34
Q

What areas are involved in central speech function?

A

Auditory input (Cranial Nerve VIII)
Visual input (Cranial Nerve II)
General sensory input
Angular Gyrus involving memory and interpretation of reading and writing
Wernickes Area processing input and formulating speech output Arcuate Fasciculus transmitting information to Brocas Area
Brocas Area implementing output from Wernickes Area
Phrenic Nerve (C3, 4 & 5) output
Facial Nerve (Cranial Nerve VII) output
Vagus (Cranial Nerve X) output
Hypoglossal Nerve (Cranial Nerve XII) output
Other motor output producing associated gestures

35
Q

What is Receptive (Wernicke`s) Dysphasia?

A

Lesion of Wernicke`s area in superior temporal gyrus of dominant hemisphere
Problem with comprehension of written and spoken language
Speech fluent
Articulation, rhythm and grammar are reasonable, but speech is largely meaningless

36
Q

What is Expressive (Broca`s) Dysphasia?

A

Lesion of Brocas area in inferior frontal gyrus of dominant hemisphere Able to comprehend words and sentences, at least simple ones Speech not fluent Problems with articulation, grammar, sentence construction, word finding and word repetition “You know what you want to say but cant get it out”

37
Q

What is Global Aphasia ?

A

Combined lesion involving loss of speech production and the understanding of the spoken and written word
Both Wernickes and Brocas areas involved

38
Q

Describe the process of speech development?

A

0-3 months: Crying for food, comfort, recognition of parent`s voice
4-6 months: Babbling, laugh, eyes follows sound, notices sounds
7-12 months: Turns to sounds, listens when spoken to, understands simple words, responds to come here, maybe a few words
1-2 years: Points to named pictures, recognises body parts, understands and uses new words, answers simple questions
2- 3 years: Vocabulary increases progressively, increasing use of phrases and sentences
3-7 years:Further development of communication skills, maturation of articulation

39
Q

How can you assess speech problems?

A

Take a detailed history
Nature of defect, ie. phonation, articulation, central, developmental
Phonation: examine anatomy and function of lower respiratory tract Articulation: undertake at least a full examination of mouth, pharynx, nose and all cranial nerves; further neurological assessment may be
necessary
Central: undertake a full neurological examination
In children a full examination of the ears AND HEARING is essential

40
Q

What is sleep?

A

Period of rest for the body and mind, volition and consciousness are suspended and bodily functions are partially suspended
Behavioural state, with characteristic immobile posture and diminished but readily reversible sensitivity to external stimuli

41
Q

What is sedation?

A

An altered conscious state which allows patients to tolerate unpleasant diagnostic or surgical procedures and to relieve anxiety and discomfort Verbal contact can be maintained

42
Q

What is coma?

A

State of extreme unresponsiveness where an individual exhibits no voluntary movement or behaviour

43
Q

What is anaesthesia?

A

From Greek an – ‘without’ and aesthesia – ‘feeling’

For general anaesthesia, drug induced and predictably reversible coma

44
Q

What are the 2 classes of general anaesthetic drugs?

A

Inhalational eg Isoflurane

Intravenous eg propafol

45
Q

What are theories of mechanism of anaesthetics?

A

Not classical receptor theory
Steep concentration-response curve: potency correlates with lipid solubility
Hydrophobic protein binding: Potentiate GABAA receptors, Volatile agents – alpha & beta subunit, Intravenous agents - alpha subunit
Two-pore domain K+ channels inhaled agents only
NMDA receptor - Nitrous oxide, xenon, ketamine
Currently ‘unprovable’ - No known competitive antagonists

46
Q

What are the 3 desired effects of general anaesthetics?

A

Unconsciousness: Reticular formation, Thalamic sensory relay nucleus, Cortex
Loss of reflexes
Analgesia: Principally volatile agents, Inhibition of spinal reflexes

47
Q

What are side effects of general anaesthetics?

A

Decreased cardiac contractility
Sympathetic inhibition
Respiratory depression

48
Q

What can occur in overdose of general anaesthetics?

A

All brain function depressed
Respiratory Failure
Death

49
Q

How are volatile anaesthetics metabolised?

A

Almost none

Blown off by respiration

50
Q

How are intravenous anaesthetics metabolised?

A

By the liver

51
Q

What are risks associated with volatile anaesthetics?

A 
Malignant Hyperpyrexia (ethers)
Bone marrow suppression (N2O)
52
Q

What is a risk associated with intravenous anaesthetics?

A

Anaphylaxis

53
Q

Describe the chemical structure of local anaesthetic agents

A

Aromatic region
Amide or ester linkage
Basic amine side chain

54
Q

What is the site of action of local anaesthetics?

A

Non ionised form crosses lipid membrane
Becomes ionised
Blocks Na channel intracellularly

55
Q

What factors do the effects of local anaesthetics depend on?

A

Diffusion gradient
Fibre size
Myelination

56
Q

Why are local anaesthetics less effective in acid tissues?

A

Weak bases due to amide side chain

57
Q

What tissues can local anaesthetics affect?

A

The brain: Intravenous overdose or inadvertent injection, Spinal anaesthesia (gravity effect), Ophthalmic anaesthesia, Initially excitatory, Epileptic fit, Then CNS depressant, Loss of consciousness, Respiratory Arrest
The heart: Myocardial depressant - Cardiac Arrest

58
Q

Describe the release of ACh at the neuromuscular junction

A

Acetyl coA combines with choline to form ACh
This is packaged into synaptic vesicles which are exocytosed out of the cell into the synaptic cleft when AP arrives and calcium influxes
ACh binds to nicotinic receptor postsynaptically and causes a contraction
Acetylcholinesterase breaks down ACh to be recycled

59
Q

What is Suxamethonium?

A

Nicotinic ACh receptor agonist non competitive
Depolarising - maintains membrane potential above threshold so muscle cannot repolarise
Short term muscle relaxer

60
Q

What is atracurium?

A

Non depolarising neuromuscular blocker
Muscle relaxant of intermediate duration IV
Competitive antagonist of ACh nicotinic receptor

61
Q

What is neostigmine?

A

Acetylcholinesterase inhibitor reversible

62
Q

At what 4 locations are nicotinic ACh found?

A 
Neuromuscular junction
Pre gang symp to blood vessels
Pre gang symp to sweat glands
Adrenal medulla
Pre gang parasymp to salivary glands
63
Q

What effects does ACh have on the parasymp nervous system?

A 
Bradycardia 
Increased secretions
Saliva 
Bronchial 
GI – peristalsis
64
Q

What would atropine be used for?

A

Competitive antagonist of muscarinic ACh receptors

Dilates pupils, Increases heart rate, reduces salivation

65
Q

What is Suxamethonium apnoea?

A

Rare condition where patient is incapable of metabolising the drug rapidly enough so they remain paralysed and unable to breathe after surgery

66
Q

What is Myasthenia Gravis?

A

Autoimmune destruction of nicotinic ACh receptors

67
Q

How does Botulism toxin exert its effects?

A

Prevents release of acetylcholine vesicles from nerve endings so paralyses muscles

68
Q

What is organophosphate poisoning?

A

Irreversible Inhibition of ACh esterase leading to accumulation of ACh in neuromuscular junction

69
Q

What 3 things are required for balanced anaesthesia?

A

Analgesia
Muscle relaxation
Hypnosis (anaesthesia)

70
Q

What are options for anaesthesia?

A 
General anaesthetic
Regional 
Spinal 
Epidural 
Plexus block 
Nerve block(s) 
Infiltration
IV regional anaesthesia
71
Q

How does the American Society of Anesthesiologists define anaesthesia and sedation?

A

Minimal Sedation: Normal response to verbal stimuli
Moderate Sedation: Purposeful response to verbal/tactile stimulation
Deep Sedation: Purposeful response to repeated or painful stimulation
General Anesthesia: Unrousable even with painful stimulus

72
Q

What is the Ramsay scale?

A
  1. anxious, agitated, restless
  2. co-operative, oriented, and calm (sedation)
  3. responsive to commands only
  4. exhibit brisk response to light glabellar tap or loud auditory stimulus
  5. exhibit sluggish response to light glabellar tap or loud auditory stimulus
  6. unresponsive
73
Q

What is the Richmond Agitation Sedation Scale?

A

From +4 combative to -5 Unrousable where 0 is alert and calm

74
Q

How can you Monitor the depth of anaesthesia?

A 
Clinical signs - sedation scales
Isolated forearm technique  
Lower oesophageal contractility 
Heart rate variability (HRV)  
Frontalis (scalp) electromyogram (EMG) 
Evoked potentials: Visual evoked potentials, Auditory evoked potentials   EEG 
Cerebral function analysis monitor (CFAM) 
Cerebral function monitor (CFM) 
Frequency domain analysis 
Compressed spectral array  
Bispectral analysis (BiS)
75
Q

What can cause dysfunction of the nervous system?

A

Damage by trauma or disease
Neurons lose ability to produce transmitters
Neurons over- or under-produce transmitters
Neurons fail to recognise transmitters
Effector organs fails to respond

Block 3 AR (8 decks)

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