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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
What nerve supplies the laryngeal muscles except cricothyroid?
Cranial Nerve X - Recurrent Laryngeal branch
26
Which nerve supplies cricothyroid muscle of the larynx?
External branch of superior laryngeal nerve of vagus
27
What position are the vocal folds in during forced inspiration?
Vocal folds abducted and rima glottidis wide open | Vestibule open
28
What position are vocal folds in during phonation?
Vocal folds adducted and stridulating as air forced between them Vestibule open
29
What problems can cause dysphonia?
``` Laryngitis Vocal cord palsy Vocal nodules Vocal cord polyp Reinke`s oedema Dysplasia Carcinoma ```
30
What is Functional Aphonia/Dysphonia?
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
31
What is articulation?
The modification of basic voice sound to create words out of a set of vowel and consonant sound units
32
What factors are involved in articulation?
``` 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
What can cause Dysarthria?
``` 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
What areas are involved in central speech function?
Auditory input (Cranial Nerve VIII) Visual input (Cranial Nerve II) General sensory input Angular Gyrus involving memory and interpretation of reading and writing Wernicke`s Area processing input and formulating speech output Arcuate Fasciculus transmitting information to Broca`s Area Broca`s Area implementing output from Wernicke`s 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
What is Receptive (Wernicke`s) Dysphasia?
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
What is Expressive (Broca`s) Dysphasia?
Lesion of Broca`s 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 can`t get it out”
37
What is Global Aphasia ?
Combined lesion involving loss of speech production and the understanding of the spoken and written word Both Wernicke`s and Broca`s areas involved
38
Describe the process of speech development?
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
How can you assess speech problems?
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
What is sleep?
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
What is sedation?
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
What is coma?
State of extreme unresponsiveness where an individual exhibits no voluntary movement or behaviour
43
What is anaesthesia?
From Greek an – ‘without’ and aesthesia – ‘feeling’ | For general anaesthesia, drug induced and predictably reversible coma
44
What are the 2 classes of general anaesthetic drugs?
Inhalational eg Isoflurane | Intravenous eg propafol
45
What are theories of mechanism of anaesthetics?
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
What are the 3 desired effects of general anaesthetics?
Unconsciousness: Reticular formation, Thalamic sensory relay nucleus, Cortex Loss of reflexes Analgesia: Principally volatile agents, Inhibition of spinal reflexes
47
What are side effects of general anaesthetics?
Decreased cardiac contractility Sympathetic inhibition Respiratory depression
48
What can occur in overdose of general anaesthetics?
All brain function depressed Respiratory Failure Death
49
How are volatile anaesthetics metabolised?
Almost none | Blown off by respiration
50
How are intravenous anaesthetics metabolised?
By the liver
51
What are risks associated with volatile anaesthetics?
``` Malignant Hyperpyrexia (ethers) Bone marrow suppression (N2O) ```
52
What is a risk associated with intravenous anaesthetics?
Anaphylaxis
53
Describe the chemical structure of local anaesthetic agents
Aromatic region Amide or ester linkage Basic amine side chain
54
What is the site of action of local anaesthetics?
Non ionised form crosses lipid membrane Becomes ionised Blocks Na channel intracellularly
55
What factors do the effects of local anaesthetics depend on?
Diffusion gradient Fibre size Myelination
56
Why are local anaesthetics less effective in acid tissues?
Weak bases due to amide side chain
57
What tissues can local anaesthetics affect?
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
Describe the release of ACh at the neuromuscular junction
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
What is Suxamethonium?
Nicotinic ACh receptor agonist non competitive Depolarising - maintains membrane potential above threshold so muscle cannot repolarise Short term muscle relaxer
60
What is atracurium?
Non depolarising neuromuscular blocker Muscle relaxant of intermediate duration IV Competitive antagonist of ACh nicotinic receptor
61
What is neostigmine?
Acetylcholinesterase inhibitor reversible
62
At what 4 locations are nicotinic ACh found?
``` Neuromuscular junction Pre gang symp to blood vessels Pre gang symp to sweat glands Adrenal medulla Pre gang parasymp to salivary glands ```
63
What effects does ACh have on the parasymp nervous system?
``` Bradycardia Increased secretions Saliva Bronchial GI – peristalsis ```
64
What would atropine be used for?
Competitive antagonist of muscarinic ACh receptors | Dilates pupils, Increases heart rate, reduces salivation
65
What is Suxamethonium apnoea?
Rare condition where patient is incapable of metabolising the drug rapidly enough so they remain paralysed and unable to breathe after surgery
66
What is Myasthenia Gravis?
Autoimmune destruction of nicotinic ACh receptors
67
How does Botulism toxin exert its effects?
Prevents release of acetylcholine vesicles from nerve endings so paralyses muscles
68
What is organophosphate poisoning?
Irreversible Inhibition of ACh esterase leading to accumulation of ACh in neuromuscular junction
69
What 3 things are required for balanced anaesthesia?
Analgesia Muscle relaxation Hypnosis (anaesthesia)
70
What are options for anaesthesia?
``` General anaesthetic Regional Spinal Epidural Plexus block Nerve block(s) Infiltration IV regional anaesthesia ```
71
How does the American Society of Anesthesiologists define anaesthesia and sedation?
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
What is the Ramsay scale?
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
What is the Richmond Agitation Sedation Scale?
From +4 combative to -5 Unrousable where 0 is alert and calm
74
How can you Monitor the depth of anaesthesia?
``` 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
What can cause dysfunction of the nervous system?
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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