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MD4001 > Week 7 > Flashcards

Week 7 Flashcards

1
Q

What is the definition of ADHD?

A

Developmentally inappropriate hyperactivity, impulsivity &/or inattention, leading to impairment in social, behavioural &/or academic

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2
Q

What are the 3 subtypes of ADHD?

A
  1. Hyperactive/impulsive (15%)
  2. Inattentive (20-30%)
  3. Combined (75%)
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3
Q

Describe the “Inattention” symptom group of ADHD?

A
  • Does not attend
  • Fails to finish tasks
  • Can’t organise
  • Avoids sustained effort
  • Forgetful
  • Easily distracted
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4
Q

Describe the “Hyperactivity” symptom group of ADHD?

A
  • Fidgets
  • Runs/climbs excessively
  • Cannot play/work quietly
  • Always ‘on the go’
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5
Q

Describe the “Impulsivity” symptom group of ADHD?

A
  • Talks excessively
  • Blurts out answers
  • Cannot await turn
  • Interrupts/ Intrudes others
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6
Q

What are the additional co-morbidities/co-occuring problems associated with ADHD?

A
  • Mental retardation
  • Sleep disorders
  • Epilepsy
  • Reading/writing disorder
  • Developmental coordination disorder
  • Asperger’s
  • Tic
  • Oppositional defiant disorder (ODD)
  • Sensory/Motor difficulties
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7
Q

What are the functional impairments of ADHD diagnosis?

A
  • SELF: low self-esteem, accidents, smoking, drugs, delinquency
  • SCHOOL: difficulties, employment, underachieve
  • HOME: stress, parenting difficulties
  • SOCIAL: poor, relationship difficulties
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8
Q

What is the global prevalence of ADHD?

A

~5%

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9
Q

What is the “administrative prevalence” of ADHD in Scotland?

A

0.5%

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10
Q

What is the male/female ratio of ADHD?

A
  • 3:1 in population studies

- 10:1 in clinics

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11
Q

What is increased prevalence of ADHD associated with?

A

Lower socioeconomic status

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12
Q

What studies is there evidence of core symptoms of ADHD being highly heritable?

A
  • Family pedigree studies
  • Adoption studies
  • Twin studies
  • Linkage data
  • Association analysis
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13
Q

What does linkage data for ADHD suggest?

A

It’s associated with widely distributed

markers e.g. at chromosomes 4, 5, 6, 8, 11, 16, & 17

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14
Q

What does association analysis for ADHD suggest?

A

Linkage with various dopamine receptor & transporter

genes, serotonin transport genes & others (Faraone et al 2005)

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15
Q

What are the ante/peri-natal potential factors contributing to ADHD causation?

A
  • Pre-term delivery.
  • Smoking
  • Alcohol
  • Maternal stress
  • Intrapartum asphyxia
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16
Q

What are the postnatal potential factors contributing to ADHD causation?

A
  • Brain trauma
  • Epilepsy
  • Deprivation/
    attachment
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17
Q

Where are the “Anterior attentional pathways” for ADHD?

A
  • Frontal lobes
  • Cingulate gyrus
  • Basal ganglia (corpus striatum, esp. caudate nucleus)
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18
Q

Where are the “posterior attentional pathways” for ADHD?

A
  • Locus Caeruleus

- Cerebellum

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19
Q

What does the imaging evidence base for ADHD show?

A
  • Volumetric CT & MRI studies: reduced volume of key structures
  • PET, SPECT, Functional MRI: reduced activation of key brain areas,
    esp. frontostriatal
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20
Q

What does the neuropharmacology evidence base for ADHD show?

A

Improved core symptoms in response to drugs which modify release & reuptake of key neurotransmitters (Dopamine & Noradrenaline), region specific for key brain pathways for self regulation & attention

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21
Q

What does the neuropsychology evidence base for ADHD show?

A

Identifiable alterations & deficiencies in frontal lobe functions ie. working memory, executive function, focus, distractibility

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22
Q

What is ADHD linked to?

A

Malfunctioning prefrontal cortex

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23
Q

What prefrontal regions cause the 3 classical symptoms associated with ADHD?

A
  1. Impulsivity = orbital frontal cortex
  2. Hyperactivity = prefrontal motor cortex
  3. Inattention = dorsal anterior cingulate & dorsolateral prefrontal
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24
Q

What is the role of Dopamine & Norepinephrine in information processing?

A
  • Tune prefrontal cortex to make info processing efficient

- Too much/little DA/NE input disruptive in regulating cortical info processing

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25
Q

What are the 4 different management techniques for ADHD & ASD (multimodal/
multidisciplinary)?

A
  1. Psychological/ behavioural
  2. Educational
  3. Social
  4. Pharmacological
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26
Q

What % of ADHD symptoms persist into adulthood?

A

Upto 60%

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27
Q

What is the definition of Autism Spectrum Disorders (ASD)?

A

Highly variable & heterogeneous condition, with a wide range of aetiologies & phenotypes

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28
Q

What is the “triad of impairments” (Wing & Gould) of ASD?

A
  1. Social communication
  2. Social interaction
  3. Social “imagination”
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29
Q

Describe Social communication impairments in ASD?

A
  • Difficulties in verbal & non verbal communication (eye contact, facial expression etc.)
  • Struggle in initiating & turn taking conversation
  • May struggle to understand metaphor/ sarcasm & interprets language in literal manner
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30
Q

Describe the Social interaction in ASD?

A
  • Development is different, delayed/ atypical with interaction difficulties
  • Struggle with reciprocity, lack of empathy/failure to adapt their behaviour according to others perspectives & social context
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31
Q

Describe the Social “imagination” in ASD?

A
  • Difficulties with thinking & behaviour
  • Poor imaginative skills leading to restricted repetitive & stereotyped patterns
  • Interests tend to be circumscribed & intense
  • Routine & Structure
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32
Q

What is an issue for ASD children & young people?

A

Anxiety

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33
Q

Describe the epidemiology of ASD?

A
  • Increased in last 20yrs, fall in other neurodevelopment disorders
  • Atleast 1% of children have ASD (maybe 2%)
  • ~50%+ children with ASD have intellectual disability
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34
Q

Describe the aetiology of ASD?

A
  • Genetic influences
  • Twin studies show high concordance for ASD in MZ versus DZ pairs
  • 4 male:1 female
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35
Q

What, in the minority of cases (~10%), does ASD occur in association with?

A

Cytogenetically detectable chromosomal abnormalities & recognised genetic conditions (Fragile X, Down’s syndrome, & Angelman’s Syndrome)

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36
Q

What can other family members of an ASD person have?

A

Relatively mild ASD-related social, communication & repetitive domain difficulties, termed as the broader autism phenotype (BAP)

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37
Q

What are the 4 clinically important other considerations in ASD?

A
  1. Childhood onset epilepsy (30% by adolescence)
  2. Sleep disorders (disrupted clock genes & dysregulatiion of melatonin)
  3. Altered Motor function (cerebellar dysfunction, neural, hypotonia, clumsy)
  4. Altered sensory function (hypo/hyper-responsiveness)
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38
Q

What is the pathophysiology of ASD?

A
  • Infancy brain volume enlarged in 90%
  • Macrocephaly in 20%
  • Reduced size & distortion of neurones & intrinsic neuronal connectivity
  • Widespread reduction in white matter volume & connectivity
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39
Q

What 3 things does suggested deficits in psychological processing & function in ASD include?

A
  1. Impairments in frontal lobe mediated “executive functioning” & working memory
  2. Deficiencies in “theory of mind”
  3. Problems achieving “central coherence”
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40
Q

What is the overall mean heritability of ADHD according to Waldman & Gizer, Thapar?

A

~75%

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41
Q

What does the DSM 5 emphasise for ASD?

A
  • Importance of early onset of signs & symptoms

- Requirement to observe impairment in social, academic, behavioural, or occupational function

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42
Q

What is the % of sibling recurrence risk for ASD?

A

10%

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43
Q

What % of ASD cases has a copy number variation (CNV) been observed at submicroscopic level?

A

10-30% (mostly found in “rare” variants)

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44
Q

Can you have both ADHD & ASD?

A

YES

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45
Q

What are the qualities of sound detected by?

A

Amplitude & Frequency

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46
Q

What is high amplitude sound?

A

Loud

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47
Q

What is low amplitude sound?

A

Soft

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48
Q

What is the range or volume & frequencies detected by the human ear?

A
  • FREQUENCIES: 20-20000Hz

- VOLUME: 0-140

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49
Q

What volume causes physical discomfort in the ears?

A

100

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50
Q

What volume is the pain threshold?

A

140

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51
Q

Describe the general anatomy of the outer ear?

A
  • Pinna

- Tympanic membrane (connective tissue)

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52
Q

Describe the general anatomy of the middle ear?

A
  • Air filled
  • Malleus, incus, stapes
  • Small muscles
  • Auditory/ Eustachian/ Pharyngotympanic tube
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53
Q

Describe the general anatomy of the inner ear?

A
  • Endolymph (scala media, semicircular canals, vestibule)

- Perilymph (scala vestibuli, scala tympani)

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54
Q

What is force transduction?

A

Conversion of sound wave into neural correlate

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55
Q

Describe the 1st & 2nd transactions of sound waves?

A
  1. (1st transduction) Strike tympanic membrane & become vibrations
  2. Energy transferred to the 3 bones of the middle ear which vibrate
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56
Q

Describe the 3rd & 4th transaction of sound waves?

A
  1. (2nd transduction) Stapes attached to membrane of oval window, vibrations create fluid waves within cochlea
  2. (3rd transduction) Fluid waves push on flexible membranes of cochlear duct, hair cells bend & release neurotransmitter
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57
Q

Describe the 5th & 6th transaction of sound waves?

A
  1. (4th transduction) Neurotransmitter release onto sensory neurons creates AP that travel through cochlear nerve to brain
  2. Energy from waves transfers across cochlear duct & dissipated back to middle ear at round window
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58
Q

What happens to the basilar fibres along the length of the cochlea during different sound frequencies?

A

Structure changes from short & stiff to long & floppy, so resonant frequencies are graded along the cochlea

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59
Q

Where is high & low frequencies located in the cochlea?

A
  • High: Base

- Low: Apex

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60
Q

What happens when resonant frequency is activated in the cochlea?

A

Absorbs all kinetic energy of wave & effectively stops it at that point, other frequencies carry on

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61
Q

Describe the process of signal detection at the organ of Corti?

A

Upward deflection of the basilar membrane moves the inner & outer hairs laterally with respect to tectorial membrane

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62
Q

Where does 95% of the cochlea nerve endings terminate?

A

Inner hair cells even though there are less of them that outer hair cells

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63
Q

What does mechanical activation & neuronal signals from brainstem do to the outer hair cells?

A

Shorten & stiffen them to tune the cochlea by amplifying select frequencies

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64
Q

How does cochlea tuning occur?

A
  • Inner hair cells depolarised & send signals to cochlea nerve then CNS
  • Outer hair cells stimulated by basilar membrane to depolarise & causes cell to contract (& AP)
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65
Q

What doesn’t mechanical displacement provide?

A

Sharpness of pitch discrimination, so there must be a system to enhance this

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66
Q

What is cochlea tuning also under?

A
  • Active Olivocochlea neuronal control
  • Fibers release Ach onto inner hair cells causing them to depolarise
  • Effectively damps down hearing in areas of pitch no interest to listener (background noise)
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67
Q

Describe the effect of displacement of steriocillia?

A

One direction opens K channels & closes in the other

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68
Q

What happens when the stereocilia are displaced towards the tallest?

A

Stimulation (depolarisation)

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69
Q

What happens when the stereocilia are displaced away from the tallest?

A

Inhibition (hyperpolarisation)

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70
Q

Describe the processes which occur due to displacement of sensory hairs (stereocilia)?

A
  • Channels constitutively open (baseline activity), can be enhanced/ diminished
  • K+ enters at steriocillia, causes receptor generator potential, opens voltage gated Ca channels –> NT release onto appropriate nerve
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71
Q

What do outer hair cells act as?

A

Amplifier for vibrations at the organ of corti

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72
Q

What does Kanamycin (antibiotic) do?

A

Kills outer hair cells in specific point along cochlea, results in specific frequency hearing loss at that point

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73
Q

What happens when you knockout Prestin?

A

Loose 40-69decibels of hearing at that frequency i.e. outer hair cell amplifier provides a 40-60decibel gain in sensitivity

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74
Q

What is Prestin?

A

Cell membrane outer hair cell motility protein

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75
Q

Describe Otoacoustic emission?

A
  • Sound comes out of ears
  • 50% spontaneous
  • Can be evoked, good tests for function up to inner hair cell
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76
Q

Describe how the signal gets to the auditory cortex in the brain?

A
  • Upper medulla contains dorsal & ventral cochleal nucleus (1st order synapse)
  • Some travelling ipsilaterally, most contralaterally upto inferior colliculus (most synapse)
  • To medial geniculate nucleus of thalamus, fibres synapse & join auditory radiation to auditory cortex
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77
Q

Where are signals from both ears transmitted to?

A

Both hemispheres of the brain

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78
Q

Where do collaterals from the pathway (auditory) project to & why?

A

Reticulum of brainstem & vermis of cerebellum causing arousal responses to noise

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79
Q

Describe the characteristics of the termination of nerves from the cochlea?

A

Topographical relationship to the cochlea

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80
Q

What does the auditory association cortex receive?

A

Secondary projections from primary & some from thalamic association areas

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81
Q

Describe the tonographical arrangement of sound in cortical areas?

A
  • Lower frequencies anterior in most maps

- 6 variations of these maps per person, each fulfilling separate function of sound cognition

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82
Q

What are the 3 principle methods of directionality?

A
  1. Volume
  2. Sound shadow
  3. Sound lag
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83
Q

Describe sound shadow?

A
  • Sound from 1 side hits the head, which
    generates sound shadow on other side in which the volume is less
  • Comparison of signal intensities from both ears determines the ear closest to sound
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84
Q

Describe sound lag?

owes for prey location

A

Sound from particular direction enters 1 ear before the other & slight delay between sound arriving ipsilaterally at the auditory cortex & contralaterally

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85
Q

What is sound lag better at determining?

A

Horizontal direction (lower frequencies) than sound shadow (high frequencies)

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86
Q

What detects front-back & above-below directionality of sound?

A

Folds in pinna which changes characteristics of sound

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87
Q

What are outer & middle ear deafness usually due to?

conduction deafness

A
  • Blockage of outer ear
  • Infection in outer/inner ear
  • Ossification of small bones in middle ear
  • Rupture of tympanic membrane
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88
Q

What is the clinical significance of the Eustachian tube in infants?

A

Angle causes predisposition to middle ear infections

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89
Q

What is sensoneural deafness usually due to?

A
  • Breakdown of cochlea & associated mechanisms

- Damage to auditory nerve &/or auditory cortex

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90
Q

What are the 2 special tests for differentiating between sensoneural & conductive deafness?

A
  1. Rinnes

2. Webbers

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91
Q

What does loss of association cortex lead to?

A

Loss of meaning of sounds such as those seen in Wernickes lesions, but not loss of differentiation of tone/frequency

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92
Q

What does loss of both primary auditory cortex areas cause?

A

Dramatically reduces sensitivity to sound

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93
Q

Describe the loss of 1 side of auditory cortex?

A

Much less effect as the auditory pathway runs bilaterally from the cochlea nucleus

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94
Q

What does Rinne negative & Ipsilateral (left) Weber suggest?

A

Left conductive deafness

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95
Q

What does Rinne (false) negative & contralateral Weber suggest?

A

Left sensory-neural deafness

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96
Q

What does (false) Rinne positive & Contralateral Weber suggest?

A

Left sensory-neural deafness

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97
Q

Where are 5 locations of the taste buds?

A
  1. Tongue
  2. Palate
  3. Tonsilar pillars
  4. Epiglottis
  5. Few on proximal oesophagus
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98
Q

What are the 3 different types of papillae on the tongue?

A
  1. Circumvallate (posterior in a V shape)
  2. Fungiform (anterior surface)
  3. Foliate (folds on lateral margins of the tongue)
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99
Q

Taste cells have been shown to be able to generate receptors that detect which 13 different chemicals?

A
  • 2 potassium
  • 2 sodium
  • 1 chloride
  • 1 adenosine
  • 1 inosine
  • 2 sweet
  • 2 bitter
  • 1 glutamate
  • 1 H+
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100
Q

What are the 5 taste categories?

A
  1. Sour- caused by H+
  2. Salty- Na ions & K
  3. Sweet- sugar, glycols, alcohols, ketones etc.
  4. Bitter- alkaloids in toxic plants
  5. Umami- L glutamate in meats & aged cheese
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101
Q

How do receptor types depolarise taste cells?

A

Either by inotropic or metabotropic pathways

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102
Q

Why is sensitivity to bitter tastes high?

A

Because they are generally indicative of a more dangerous substance

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103
Q

Describe the taste pathway to the cortex?

A

Via CN VII, IX, X principally to solitary nucleus, then thalamus, then insula & anterior operculum

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104
Q

What does the limbic component gustation activate?

A

Brainstem nuclei for salvation or vomiting

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105
Q

How is taste pain (from chilli or ethanol) carried?

A

From posterior parts of tongue in cranial nerve V (trigeminal)

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106
Q

What is the other main sensory input to recognition of foodstuff?

A

Olfaction

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107
Q

What is the olfaction system composed of?

A
  • Olfactory epithelium
  • Receptor cells (bipolar neurons)
  • Axons that project through base of skull to olfactory bulb
  • Neuronal tract to multiple olfactory destinations in the brain
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108
Q

What are the 3 steps to activation of the odorant receptor (7 transmembrane protein)?

A
  1. Odorant molecule binds to receptor of primary olfaction neuron
  2. Activates G protein which stimulates adenylyl cyclase to convert ATP to cAMP
  3. cAMP activates cation channel, making it permeable for Na+ & Ca2+
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109
Q

What does activation of the odorant receptor cause?

A
  • Cells to depolarise as generator potentials

- Sufficient depolarisation leads to action potentials

110
Q

What is the frequency of action potential generation in the odorant receptor proportional to?

A

Log concentration of the odorant

111
Q

Describe the location of the lower end of the bipolar neurons?

A

Extends into layer of mucus secreted from Bowman gland in the olfactory epithelium, forming olfactory knob

112
Q

What does the olfactory knob develop?

A

Olfactory cilia which detects odourants in nasal cavity

113
Q

What is a special feature of the bipolar neurons in odour detection?

A

Continually develop & replace each other over time

114
Q

Where is the olfactory bulb located?

A
  • High in nasal cavity

- 2.5cm squared area of olfactory epithelium

115
Q

What are the 4 steps for information to be passed from the olfactory bulb to the cortex?

A
  1. Info from bipolar cells to dendrites of mitral cells in neuropil of glomeruli in the bulb
  2. Massive convergence, which helps ensure sensitivity
  3. Also synapsing in glomeruli are Tufted cells which provide ‘lateral inhibition’ for signal enhancement
  4. 2nd layer of lateral inhibition- Granule cells in bulb make dendritic connections between mitral cells
116
Q

What is thought to be the case for glomeruli within the olfactory bulb?

A

Specific glomeruli respond to particular odorants in a dose dependent manner

117
Q

How many genes are there in humans for different odorant receptors?

A

Over 300 (each bipolar neuronal expressed just 1 of these genes per neuron)

118
Q

What are the 7 groups of odours?

A
  1. Camphoraceous
  2. Musky
  3. Floral
  4. Pepperminty
  5. Ethereal
  6. Pungent
  7. Putrid
119
Q

Describe the medial olfactory pathway?

A
  • Ancient part of brain

- Feeds into limbic system & encodes emotional aspects of olfaction & memory

120
Q

Describe the lateral olfactory pathway?

A
  • Feeds to ancient parts of brain (pyriform & pre-pyriform cortex in temporal lobe)
  • Likes & dislikes for taste
  • Visceral reactions via brainstem
121
Q

Where does the lateral olfactory pathway NOT go via?

A

Thalamus

122
Q

Describe the more recent olfactory pathway?

A
  • Pass through thalamus & onto orbitofrontal cortex
  • Involved with conscious discernment of odour & can be under conscious control for salience
  • Works with limbic aspects of memory
123
Q

What 3 things can cause nasal/sinus disease (25%)?

A
  1. Colds
  2. Polyps
  3. Other blockages
124
Q

Describe Parosmia (20%)?

A

Distorted often unpleasant sense of smell caused by damage to the lining at top of the nose (upper respiratory viral infections)

125
Q

How common is congenital anosmia?

A

1%

126
Q

How common is Alzheimer’s preceding anosmia?

A

2-5%

127
Q

How common is idiopathic anosmia’s?

A

25%

128
Q

What 3 things can head trauma anosmia (15%) lead to?

A
  1. Damage to frontal lobe processing
  2. Damage to ascending nerves at cribriform plate
  3. Permanent compression of nasal passages
129
Q

What is the definition of pain?

A

Unpleasant sensory & emotional experience associated with either actual/potential tissue damage, its subjective

130
Q

What are the nociceptors 4 peripheral aspects of pain?

A
  1. Nociceptive receptors
  2. Nociceptive activation
  3. Sensitization of receptors
  4. Nociceptive fibres
131
Q

Describe Nociceptive receptors?

A
  • Free unspecialised nerve endings with ‘pain’ channels inserted in membrane
  • Sensitive to O2, pH osmolarity, valinoids (capsicum) & heat
  • Allows Ca2+ into cell
132
Q

What is the most common “pain” channels for nociceptive nerves?

A

Transient Receptor Potential family of channels (TRP)

133
Q

What can nociceptive receptors be sensitised by?

A
  • Substance P
  • Bradykinins
  • Serotonin
  • pH
  • ATP
  • NO
134
Q

Describe the structure of a nociceptive receptor?

A

6 unit trans-membrane portion & ‘basket’ of regulatory complex in the cytoplasm

135
Q

Describe the Nociceptive receptor activation due to temperature?

A
  • Extreme heat & cold open ‘Transient receptor potential vanilloid’ (TRPV) channels in membrane
  • Na2+ & Ca2+ entry & depolarises cell to give action potential
136
Q

Describe the Nociceptive receptor mechanical activation?

A

Presumed form of insensitive mechanoreceptor which allows Na entry when activated

137
Q

Describe the Nociceptive receptor chemical activation?

A

Apart from TRPV receptors, largely unknown but chemical transmission can cause sensitisation of pain receptors

138
Q

What does Calcitonin gene related peptide (CGRP) & SP both do during sensitisation of receptors?

A

Recruit silent receptors which increase summation in the dorsal horn

139
Q

What does Histamine do during sensitisation of receptors?

A

Causes hyperalgesia through its effects on blood vessels

140
Q

What does Bradykinin do during sensitisation of receptors?

A

Activates pain fibres directly & causes increase in prostaglandins

141
Q

What does tissue damage cause?

A

Produces H ions which give muscle ache (weight lifting)

142
Q

What makes prostaglandin E2 & what drugs inhibit it?

A
  • Made by cyclooxygenase

- Aspirin & other NSAIDs inhibit enzyme

143
Q

What do neurotransmitters for nociceptive fibres release on stimulation?

A
  • Glutamate
  • Substance P
  • Calcitonin gene-related peptide (CGRP)
    (both central & peripheral synapses)
144
Q

What does peripheral release of nociceptive neurotransmitters give?

A

Red flare & tenderness associated with pain

145
Q

Substance P & CGRP release is responsible for what 3 local physiological signs of pain?

A
  1. Calor (heat)
  2. Rubor (redness)
  3. Tumor (swelling)
146
Q

What is color (heat) & rubor (redness) caused by?

A

Hyperaemia

147
Q

What is tumour (swelling) caused by?

A

Plasma extravasation

148
Q

Where does pain signal processing begin in?

A

Dorsal horn (synaptic targets & wind up)

149
Q

What are the 2 types of nociceptive ascending axons from the dorsal horn?

A
  1. Nociceptive specific (NS)- C & Aδ
  2. Wide dynamic range neurons (WDR)- any sensory input incl. pain, fire in graded fashion based on C fibre frequency of input (higher pain, higher input)
150
Q

What are the Nociceptive specific (NS) & Wide dynamic range neurons (WDR)?

A

Points of descending pain modulation from PAG in the brainstem

151
Q

What is “Wind up”?

A

Long term sensitisation of post synaptic neurons in dorsal horn

152
Q

What is the central sensitisation “wind up” mediated by?

A

Wide dynamic range neurons (WDR) which, when firing at high frequency, open NMDA channels

153
Q

What does the inrush of Calcium do during central sensitisation “Wind up”?

A
  • Nuclear expression resulting in increased Na channels & blockade of K channels
  • Net result is resting potential closer to threshold & more sensitive cell
  • Amplifies pain signal
154
Q

What controls the dorsal horn sensitisation “wind up” system?

A

Intensity of signal from C fibres translated through the WDR neurons into variation in sensitivity

155
Q

Wind up can occur in seconds & last for hrs, this conveys what 3 things?

A
  1. Priority salience in cortex
  2. Protection from further injury
  3. Memory- increased duration of stimulation increases chance of consolidation
156
Q

What are the 3 parts to pain modulation?

A
  1. Gate theory
  2. Sensitisation (wind up)
  3. Descending analgesia & Endogenous opioids
157
Q

Describe how the gate theory of pain modulation at the dorsal horn can be damped down?

A
  • By rubbing area around source of pain activates inhibitory input (Aß fibres) to anterolateral system
  • Similar theory behind transcutaneous nerve stimulation TENS & capsaicin treatment
158
Q

Describe descending analgesia in pain modulation?

A

Shows (1) inhibition of incoming pain signals at cord level, (2) encephalin-secreting neurons that suppress pain signals in cord

159
Q

What is the descending analgesia in pain modulation system exploited by?

A

CNS centers to increase salience of selected signals as well as decrease certain prolonged unimportant signals

160
Q

Give 3 examples of Endogenous opioids? (group of neurotransmitters)

A
  1. Endorphinins
  2. Encephalins
  3. Dynorphins
161
Q

Describe the endogenous opioid system neurotransmitters?

A

Sensitive to opiates & present at all levels of pain pathways,
therefore doses of opiates can act simultaneously at all levels, hence their high efficacy

162
Q

Describe the 3 parts of the cortical pain matrix?

A
  1. Somatosensory topographic discrimination
  2. Limbic system including the cingulate gyrus & insula- emotional, motivational, modulatory
  3. Saliency- relative potentiation of a specific nociceptive input
163
Q

Describe the brainstems purpose in the cortical pain matrix?

A
  • Can up/down modulate nociception to provide saliency (gate system)
  • Based on info from other brain centres
164
Q

What does electrical stimulation of the PAG induce?

A

Strong analgesia (blocked by Nalaxone)

165
Q

List the different types of pain?

A
  • Chronic/Acute
  • Nociceptive/ Neuropathic/ Phantom limb
  • Maladaptive
    Visceral (hollow structures)
  • Referred
  • Sharp/Ache
  • Headache
  • Complex regional pain syndrome
166
Q

What usually results in nociceptive pain?

A

Conditions such as sprains, bone fractures, burns, bumps bruises, inflammation (from infection/arthritic disorder)

167
Q

When does nociceptive pain usually stop?

A
  • When problem is healed

- Normally responds well to painkillers such as opioids

168
Q

What are the 3 types of chronic pain?

A
  1. Nociceptive pain
  2. Neuropathic pain
  3. Central maladaption
169
Q

Give 5 examples of persistent neuropathic pain?

A
  1. Causalgia (peripheral nerve trauma)
  2. Phantom limb pain
  3. Entrapment neuropathy (carpel tunnel syndrome)
  4. Peripheral neuropathy (widespread nerve damage
  5. Nociceptive pathway damage
170
Q

Give 4 examples of when pain persists beyond the healing process of damaged tissues?

A
  1. Hyperalgesia (strong reaction to low intensity stimuli)
  2. Allodynia (painful reaction to non-noxious stimuli like light touch)
  3. Summation (repeated low innocuous stimuli increasing intensity of response)
  4. Paresthesias (tingling without stim) or Dysesthesias (burning or shooting pain without stim)
171
Q

What causes persistent neuropathic pain?

A

Maladaptation of the dorsal horn wind up & sensitisation systems

172
Q

What can central maladaption sensitisation lead to?

A

Long term changes in structure of the synapses in dorsal horn or spinal cord

173
Q

What can increases in inotropic glutamate receptors (NMDA) cause?

A

Sensitivity in 2nd order neurons which then more readily send pain signals to the thalamus

174
Q

What is a second component of central maladaption?

A
  • Descending modulation of inhibitory interneurons becomes maladapted
  • Can lead to reduction in inhibition of WDR neurons & disinhibition of 2nd order neurons
175
Q

What are headaches due to?

A

Irritation/destruction of sensitive areas around the venous sinuses, dura at the base of the skull or meninges & associated blood capillaries

176
Q

What results in the worst headaches?

A

Meningitis

177
Q

What does hangovers do?

A

Caused by excessive drinking, in extreme cases due to alcohol irritating meninges, most cases due to dehydration

178
Q

What does Low CSF cause?

A

Brain to settle onto base of the skull causing deformation of dura & meninges & so this causes headaches

179
Q

What causes a Migraine?

A

Possible due to vasoconstriction followed by massive vasodilation, but unproven

180
Q

Describe the mechanism of referred pain?

A
  • Signals of noxious stimuli & normal cutaneous stimuli enter spinal cord at same point
  • Cross talk in dorsal horn
  • Signals from viscera picked up by ascending nerve fibres that are mapped cortically to dermis
181
Q

Can pain be re-experienced from memory?

A
  • No, it is only an intellectualisation of the experience

- Fear of pain is very real & important

182
Q

What are the 4 steps to the WHO analgesic ladder?

A

STEP 1: nonopioid analgesics NSAIDS
STEP 2: weak opioids
STEP 3: strong opioids, methadone, oral administration, transdermal patch
STEP 4: nerve block, epidurals, PCA pump, neurolytic block therapy, spinal stimulators

183
Q

What is the definition of an opium?

A
  • Natural extract of the poppy Papaver somniferum

- Contains morphine & other related compounds

184
Q

What is the definition of an opioid?

A

Any substance (natural/synthetic) that produces morphine like effects which are blocked by morphine antagonist

185
Q

What are the 7 different structures/questions for thinking about any drug?

A
  1. What is it? (class of drug)
  2. How’s it given?
  3. It’s mechanism of action? (Pharmacodynamics)
  4. Main clinical uses?
  5. How’s it metabolised?
    (Pharmacokinetics)
  6. Consider effect on each system in turn
  7. Should I know anything else about the drug?
186
Q

List 7 strong opioids?

A
  1. Morphine
  2. Oxycodone
  3. Diamorphine
  4. Fentanyl Pethidine
  5. Remifentanil
  6. Methadone
187
Q

List 4 weak opioids?

A
  1. Codeine
  2. Dihydrocodeine
  3. Tramadol
  4. Loperamide
188
Q

What are 2 antagonists of strong opioids?

A
  1. Naloxone

2. Naltrexone

189
Q

What is the oral bioavailability of morphine?

A

30%

190
Q

What is the oral bioavailability of Oxycodone?

A

70%

191
Q

What is the oral bioavailability of Fentanyl?

A

50% (lozenge)

- very lipophilic so given transdermal

192
Q

What is the oral bioavailability of Codeine?

A

60%

193
Q

What is the oral bioavailability of Tramadol?

A

70%

194
Q

What are the 4 different sites of action for opioids? (opioid receptors)

A
  1. mu opioid peptide receptor (MOP)
  2. Kappa (KOP)
  3. Delta (DOP)
  4. Nociception (NOP)
195
Q

What does morphine do at a cellular level?

A
  • Binds to morphine receptors
  • Closes Ca2+ channel but enhances the K+
    channel which floods out of cell
  • Hyperpolarises cell making it less likely to discharge
  • Decreases cAMP release preventing neurotransmitter release!
196
Q

What are the systemic actions of opioids?

A
  • Meiosis
  • Euphoria
  • Depress CVS & RS
  • Sedation
  • Urticaria, itch
  • Stops coughing
  • Analgesia
  • Constipation & nausea
  • Histamine release = bronchospasm
  • Urinary retention
  • Decrease immunity
197
Q

How are opioids metabolised?

A
  • Prodrugs
  • Exceptions
  • Active metabolites
  • Pharmacogenetics
198
Q

What is the definition of an antagonist?

A
  • Drug with a high affinity for the receptor but no intrinsic activity (Naloxone)
  • Naltrexone given to wean addicts off opioids
199
Q

Whats the parenteral & oral doses of Morphine?

A
  1. Parental- 10mg (0.1mg /kg)

2. Oral- 30mg (0.3mg/kg)

200
Q

What is the parenteral dose of Fentanyl?

A

100 micrograms

201
Q

What are the 3 guidelines for prescribing opioids?

A
  1. Controlled Drugs
  2. Misuse of Drugs Act, 1971 classified according to the “harmfulness attributable to a drug when it is misused”
  3. Misuse of Drugs Regulations 2001
202
Q

What happens when you increase the dose of a weak opioid?

A

Have a “ceiling effect” where escalation of dose causes side effects without improving analgesia

203
Q

What is the functions of pain?

A
  • Unpleasant therefore alerts us to potential damage of body

- Signal onset of disease –> help-seeking behaviour

204
Q

What happens to people with congenital universal insensitivity to pain (CUIP)?

A

Usually die at young age because failing to respond to illnesses of which the main symptom is pain (appendicitis) or avoid situations that risk their health

205
Q

What happens if pain continues?

A

Becomes destructive & problematic

206
Q

What are the 3 different types of chronic pain?

A
  1. Chronic recurrent pain
  2. Chronic benign pain
  3. Chronic progressive pain
207
Q

Describe acute pain?

A
  • Often result of some specific & readily identifiable tissue damage (a broken leg, surgical lesion, toothache)
  • Less than 3-6 months
  • Pain disappears once damaged tissue healed
208
Q

When can we classify pain as being Chronic?

A
  • More than 3-6 months
  • Starts with episode of acute pain but doesn’t improve
  • Can have identifiable cause (rheumatoid arthritis) or unidentifiable (most back pains)
209
Q

Describe Chronic recurrent pain?

A

Repeated, intense episodes of pain separated by periods without pain (migraine, myofascial pain)

210
Q

Describe Chronic benign pain?

A

Long-term pain that is typically present all of the time, with varying levels of intensity (chronic low back pain)

211
Q

Describe Chronic progressive pain?

A

Pain becomes progressively worse as the underlying condition worsens (rheumatoid arthritis)

212
Q

What is the Specificity theory of biological models of pain?

A
  • Pain receptors in skin when activated transmit info to centre in brain that processes pain-related info
  • Sensation of pain is a direct representation of degree of physical damage experienced by the individual
213
Q

When/Who proposed the Specificity theory?

A

1st proposed in 3BC by

Epicurus & taken up by Descartes in 17th C

214
Q

Give an example of when we experience pain in the absence of pain receptors?

A

Phantom limb pain

215
Q

Give an example of “pain receptors” that do not transmit pain?

A

Congenital universal insensitivity to pain (CUIP)

216
Q

Give an example of psychological influences on pain?

A
  • Mood, attention, cognitive factors (e.g, expectations)

- Depressed/anxious people report the equivalent pain stimulus as more painful than people who are not

217
Q

Who developed the Gate control theory for pain?

A

Melzack & Wall (1965)

218
Q

Describe the Gate control theory for pain?

A
  • ‘Gate’ used as metaphor for the chemicals, including endorphins, that mitigate the experience of pain
  • Account both the sensory info & the psychological processes
  • Pain as a perception rather than sensation
219
Q

Describe the relationship of attention and pain?

A

Focusing on pain increases its impact & focusing on other things seems to reduce it (bed rest is no longer treatment for back pain)

220
Q

What did James & Hardardottir (2002) do to research attention & pain?

A
  • Participants put their lower arm in cold water (0-3C, cold pressor test) & to concentrate on computer-based task or the pain sensations
  • Those focused on pain were least able to tolerate the pain
221
Q

What can attentional bias explain?

A

Why some people with acute pain develop chronic pain in the absence of physical injury/inflammation

222
Q

What are 3 types of cognition & pain?

A
  1. Meaning of pain ie. childbirth
  2. Catastrophizing
  3. Expectations of pain relief (placebo)
223
Q

What are the 3 components of catastrophizing & experiencing pain?

A
  1. Rumination- focus on internal & external info
  2. Magnification- overestimating extent of threat
  3. Helplessness- underestimating resources.
224
Q

Describe the effects of living with chronic pain?

A
  • Organise day around pain
  • Social, financial & physical
  • Anger, fear, sadness
  • Depression levels high
225
Q

What is the prevalence rates for major depression in 1. pain clinics/inpatient pain programmes, 2. orthopaedic/ rheumatology clinics?

A
  1. 52%

2. 56%

226
Q

Why is depression levels higher in chronic pain patients?

A
  • Focusing on bodily symptoms more & reporting pain symptoms
  • Pain –> strain of living with pain & restrictions on life  depression
  • Reciprocal relationship between depression & pain
227
Q

What are 4 different pain behaviours?

A
  1. Facial/audible expression (clenched teeth & moaning)
  2. Distorted posture/ movement (limping, protecting the pain area)
  3. Negative emotions (irritability, depression)
  4. Avoidance of activity (not going to work, lying
    down)
228
Q

Describe the 3 “gains” associated with pain?

A
  1. Primary (intrapersonal)- expression results in reduction/cessation of aversive consequence (someone taking over a household chore)
  2. Secondary (interpersonal)- pain behaviour gives positive outcome (sympathy/ care)
  3. Tertiary- pleasure/ satisfaction of person who is helping the pain sufferer
229
Q

What are the 5 D’s?

A
  1. Dramatization of complaints
  2. Disuse through inactivity
  3. Drug misuse as result of over-medication
  4. Dependency on others due to learned helplessness & impaired use of coping skills
  5. Disability due to inactivity
230
Q

Describe what good social support is for pain sufferers?

A

Discouraging avoidance of physical & social activities, offering assistance by multiple solutions to problems & providing emotional support

231
Q

What is the management for acute pain?

A

Usually pharmacological interventions

232
Q

What is the management for chronic pain?

A

Psychological approaches to minimise amount of painkiller & maintain/improve quality of life

233
Q

What are the 2 different easy to administer techniques for measuring pain?

A
  1. Numerical rating scales- 0 (no pain) to 100
    (most pain you could imagine)
  2. Descriptive adjectives- mild, distressing, excruciating
234
Q

Describe the 4 parts to the McGill pain questionnaire?

more difficult to administer but captures the multidimensional nature

A
  1. Type of pain- throbbing, shooting, hot, tender, etc
    using a 4-point scale
  2. Emotional responses- tiring, fearful, punishing
  3. Intensity of pain- ‘no pain’ to ‘worst possible pain’
  4. Timing of pain- brief, continuous or intermittent
235
Q

What are 4 other things to remember when assessing other aspects of pain (Turk & Okifuji)?

A
  1. Verbal/vocalisations (sighs, moans)
  2. Motor behaviour (limping, facial grimacing)
  3. Taking medication (use of cane)
  4. Functional limitations (resting, reduced activity)
236
Q

What is behavioural interventions (Fordyce 1976) based on?

A

Operant conditioning processes

237
Q

What are the 3 methods for behavioural interventions?

A
  1. Reinforcement of adaptive behaviours
  2. Withdrawal of attention/ other rewards that were previous responses to pain behaviour
  3. Providing analgesic medication at set times rather than in response to behaviour
238
Q

What are the 3 goals of cognitive-behavioural interventions?

A
  1. Alter beliefs that their problems are manageable
  2. Identify how catastrophic/ other negative thoughts can lead to increased pain, distress & psychosocial difficulties
  3. Strategies to manage pain, emotional distress & psychosocial difficulties
239
Q

Describe the use of relaxation for pain management?

A
  • Relax whole body/specific muscle groups
  • Systematic & methodical approach to learning deep muscle relaxation
  • Controlled breathing, from short/shallow breathing to deeper/longer breaths
240
Q

What is biofeedback?

A
  • Control of bodily processes
  • EMG, galvanic skin response
  • Guided by auditory/visual feedback on physiological changes
  • Relax muscle tension
  • Used successfully with chronic headaches
241
Q

What 2 things detect static tilt & translation?

A
  1. Saccule (vertical movement)

2. Utricle (horizontal movement)

242
Q

What detects rotational acceleration (pitch roll & yaw)?

A

Semi-circular canals

243
Q

What are the 2 otolith containing organs in the vestibule?

A
  1. Saccule macula (continuous with cochlea)

2. Utricle macula (continuous with semi-circular canals)

244
Q

Where do hair cells project hairs into?

A

Otolithic (ear stone) containing gelatinous structure

245
Q

What does cilia + kinocilium provide?

A

Directional information

246
Q

What does movement of otolithic membrane (tilting/translational movement) do?

A

Bends cilia/kinocilium in a very direction specific way

247
Q

What opens/closes hair cell cation channels?

A

0.5micron movement of kinocillium

248
Q

What are the 2 orientations of the hair cells in the ventricle?

A

Vertical & horizontal (when head is normally held upright)

249
Q

What is the base of hair cells supported by?

A

Area of supporting cells called the macula

250
Q

What are fat ends & thin ends?

A
  • FAT: kinocillia

- THIN: steriocillia

251
Q

What happens when hairs are bent away from kinocillium?

A
  • Hyperpolarisation
  • Decreased impulse frequency
  • Inhibition
252
Q

What happens when hairs are bent towards the kinocillium?

A
  • Depolarisation
  • Increased impulse frequency
  • Excitation
253
Q

What do we also monitor for a better triangulation of movement?

A

Rotational movement

254
Q

Describe how semi-circular canals monitor rotational acceleration & deceleration?

A
  • 3 planes of orientation (yaw, roll, pitch)
  • Within each canal is semi-circular duct
  • Within duct, ampulla
255
Q

What does the ampulla have within?

A

Supporting cells, hair cells, cilia & kinocilium

256
Q

What causes movement of cupola?

A

Endolymph in semi-circular canal

257
Q

What does dynamic equilibrium measure?

A

Changes in rotation

258
Q

Describe how dynamic equilibrium measures changes in rotation?

A
  • Signal transduction
  • Resting rate of transmitter release
  • Bending towards the kinocilium ↑AP rate
  • Bending in other direction ↓AP rate
259
Q

What is the vestibular apparatus bathed in?

A

Endolymph

260
Q

How is the vestibular apparatus endolymph usually drained?

A

To venous sinus

261
Q

What causes Ménière’s disease?

A

Build-up of endolymph (blockage of venous sinus) causing vertigo, nausea, tinnitus & hearing loss

262
Q

Where does information from the vestibular apparatus go?

A

To cerebellum & brainstem (integrated with other info)

263
Q

What is the 3 vestibular apparatus functions?

A
  1. Control eye muscles (oculomotor nerve)
  2. Maintain an upright position (spinal motor nuclei)
  3. Aware of body position & acceleration
264
Q

What does the caloric test in comatose patients test for?

A

Condition of brainstem

265
Q

Describe the caloric test?

A
  • Putting warm water in external meatus mimics moving head towards the irrigated ear
  • Cold water does the opposite
266
Q

What Particular plane is the caloric test done in?

A

Supine patient with head at 30 degrees from horizontal mimics left/right movement of head

267
Q

What is the nystagmus pattern for a movement?

A

Towards irrigated ear is slow away from direction of rotation & fast return in same direction

268
Q

What does the caloric test show in comatose patients?

A

No fast saccade, only slow component

269
Q

What would be shown in the caloric test if the vestibular nucleus is undamaged?

A

Cold irrigation (mimics head being turned away from irrigation) will cause slow movement towards the irrigated ear

270
Q

When does spontaneous nystagmus occur?

A

When 1 side of the patients system has damage to 1 of the semi-circular canals, there is a difference between 2 signals when the head is stationary

271
Q

What are the 2 steps when putting warm water in the external acoustic meatus?

A
  1. Endolymph rises

2. Increased firing

272
Q

What are the 2 steps when putting cold water in the external acoustic meatus?

A
  1. Endolymph falls

2. Decreased firing

MD4001 (11 decks)

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