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CSAII Flashcards

1
Q

Give 6 Sensations of pain

A 
Burning
Radiating
Stabbing
Deep Ache
Freezing
Itch
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2
Q

3 Reasons for Pain

A

Warning signs:

  • avoidance of harmful stimuli
  • prevents further injury
  • Rest following injury
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3
Q

3 Classifications of Pain

A

Nociceptive
Inflammatory
Neuropathic

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4
Q

What are Nociceptors?

A 
Primary sensory (1st order) neurons
Pain detection
found in: 
-skin
-muscle
-viscera
-meninges
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5
Q

3 Types of afferent nerve fibre

A

Aβ - Myelinated, 100m/s, light touch
Aẟ- Thinly myelinated, 30-75m/s, light touch, instant sharp pain
C Fibre- unmyelinated, 1m/s, nociception

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6
Q

5 Afferent nerve endings

A 
Free nerve endings (Aẟ, C- arbourised)
Meissner's corpuscles (Aβ, light touch)
Pacinian corpuscles (Aβ, vibration)
Merkel Discs (Aβ, pressure)
Ruffini (Aβ, stretching)
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7
Q

Aẟ fibres features

A

Sharp pricking pain
Well localised
Reflex arcs
first pain, before C fibres

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8
Q

C Fibres features

A

Slow, dull ache, burning
persistent
poorly localised
second pain, after Aẟ

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9
Q

5 ways to activate nociceptors

A 
pressure
heat
cold
chemical ie H+
Tissue damage/inflammation
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10
Q

What is polymodality?

A

C fibres responding to multiple stimuli
eg pressure temperature and chemical
decoding within CNS determines which modality is being encoded

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11
Q

Pressure transduction in nociceptors?

A

Mechanically gated ICs

TRP channels

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12
Q

Temperature transduction in nociceptors?

A

TRPV1 channels (vanilloid) heat
TRPM cold
TRPA1 v cold

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13
Q

CNS pain pathway:

A 
SPINOTHALAMIC TRACT
Nociceptor -> SC via DRG
Dorsal horn
Forms tract of lissauer
1st Order Synapse in substantia gelatinosa
2nd order excited by Glu + sub P
Crossing over to anterolateral column
To thalamus
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14
Q

What is referred pain?

A

Convergence of Visceral and Cutaneous pain
synapsing onto same 2nd order neuron in SC
Brain perceives pain as cutaneous
eg angina perceived as pain in chest wall + left arm

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15
Q

Path of 3rd order neurons

A

Thalamus to somatosensory cortex
HAL homunculus
Projections to insula + cingulate cortex (emotional aspect of pain)

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16
Q

Descending regulation of pain

A
  • Stress induced analgesia: torn muscle in race and keeps running, battle victims
  • Behaviour, emotions at time, past experiences
  • Higher cortical regions activate descending modulatory pathways

PERIAQUADUCTAL GREY MATTER (PGM)
ROSTRAL VENTROMEDIAL MEDULLA (RVM)

Cortex - PAG - RVM - Dorsal Horn

Modulates Spinothalamic tract activity

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17
Q

Descending inhibition of pain factors

A
  • PAG, RVM-> ST tract
  • 5-HT projections act on inhibitory interneurons in Dorsal Horn
  • Endogenous Opiods, eg endorphins, enkephalins
  • stress induced analgesia
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18
Q

Chemicals released following tissue injury?

A

ATP, H+, Serotonin (platelets), Histamine (mast cells), Bradykinin, Prostaglandin, NGF

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19
Q

Which chemicals directly bind to nociceptors in inflammatory responses?

A

ATP binds to purinergic receptors (P2X)
H+ binds to acid-gated ion channels eg lactic acid buildup
Serotonin binds to 5-HT3 receptors

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20
Q

What is Neurogenic inflammation and what does it cause?

A

Activation of one nociceptor branch triggers release of Substance P and CGRP from another

causes:

  • vasodilation
  • increased permeability
  • mast cells release histamine
  • More inflammation
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21
Q

What benefits does inflammation hold?

A

Pain hypersensitivity

  • makes pain more painful
  • prevents contact with injury site to promote healing
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22
Q

What is allodynia?

A

A painful response from a non-noxious stimulus

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23
Q

What is hyperalgesia?

A

an exaggerated response from a noxious stimulus

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24
Q

What is peripheral sensitisation?

A

increase in the responsiveness of nociceptors
Bradykinin reduces TRPV1 threshold
PG reduces Na+ threshold
Increased pain, eg sunburn

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25
Timescales for acute/chronic pain?
Acute <3 months | chronic >3 months
26
Treatments for acute pain
Local anaethetics: - lidocaine/lignocaine (Na+ blockers) ``` Topical capsaicin (chili peppers) - repeated use reduces nociceptor firing (Ca2+ excitotoxicity?) ``` NSAIDs - inhibits PG synthesis (COX inhibition), prevents peripheral sensitisation Paracetamol - unknown mechanism Opioids - morphine, codeine, tramadol - effective but addictive + SEs - endogenous opioid system agonists - BS, SC, periphery Gate control - simultaneous activation of Aβ eg rubbing - activates inhibitory interneuron cancelling C fibre response
27
Chronic pain epidemiology
20-50% of population
28
11 causes of chronic pain?
``` chronic back pain cancer carpal tunnel syndrome arthritis fibromyalgia diabetes migraine post-surgery MS trigeminal Neuralgia phantom limb ```
29
2 types of chronic pain
Inflammatory - persistent tissue inflammation eg arthritis Neuropathic - NS injury eg compression, traction, sever, hypoxia, demyelination, tumour
30
Neuropathic Pain Symptoms
``` Burning pain Stabbing pain Aching Electrocution pain Radiating pain Hypersensitivity ```
31
Neuropathic pain mechanisms
V complex Peripheral sensitisation spontaneous nociceptor firing accumulation of ICs at site of injury, causes hypersensitivity
32
What is central sensitisation?
Increase in responsiveness of nociceptive Ns in CNS normal inputs -> abnormal OPs Reduced threshold for activation of 2nd Order Neurons - Similar process to LTP (sustained Glu, Ca2+ through NMDA, kinase cascades)
33
What is CNS hyperalgesia?
Follows central sensitisation | activation of nociceptors results in amplified SC activation
34
Central Allodynia mechanism?
non noxious Aβ fibres also synapse onto 2nd order spinothalamic Ns - usually inactive as incapable of reaching threshold - central sensitisation causes AP firing
35
Chronic Pain treatments?
Difficult to treat Tricyclic antidepressants eg Amytriptyline anticonvulsants eg pregabalin, gabapentin NMDA antagonists eg ketamine CBT SC stimulator, gate control Placebos
36
What is the hierarchy of motor control?
Low level- execution, BS, SC Middle- Tactics, motor cortex, cerebellum High- strategy, association areas of neocortex, BG
37
Basal ganglia anatomical features?
``` Caudate Nucleus Putamen Globus Pallidus (int&ext) Thalamus Hypothalamus Substantia Nigra Subthalamic Nucleus ``` Lentiform Nucleus: putamen+pallidum Corpus Striatum: CN+LN Neostriatum (dorsal, motor): CN+putamen
38
What are Basal Ganglia Loops?
Processing pattern for motor activity | Cortical IP-Striatum-GPi-Thalamus-Cortex
39
3 Key Pathways of basal ganglia?
Direct (exc) promote movement Indirect (inh) withhold movement: GPe, STN Hyperdirect pause movement: STN Thalamus inhibition prevents movement
40
What is the role of the substantia Nigra?
DA release Interacts with Striatum Ns DA/ACh balance, DA promotes movement, ACh prevents D1 & D2 receptors
41
2 categories of movement disorders and their associated conditions?
``` Hyperkinetic movement hemiballismus Tics Chorea Myoclonus ``` Hypokinetic Movement Parkinsonian conditions Ataxia Apraxia
42
Define Hemiballismus
high amplitude flailing of limbs unilateral Impaired STN activity Cause: stroke
43
Define Tic Disorders
brief repetitive movements with premonitory urge blinking, coughing, limb movements Tourettes + coprolalia (swearing) severe tic expressions worse with anxiety high comorbidity (50% ADHD, 33% OCD, 50% Anxiety)
44
Define Chorea
jerky, brief, irregular movement Appears to flow from limb to limb causes: Huntington's disease Neuroleptics
45
Define Huntington's Disease
Motor/cognition deficits - cognitive: poor decision making, multitasking - behavioural: irritability, depression, apathy, anxiety, delusions - Physical: chorea, motor persistence, dystonia, eye movements Genetics: Autosomal Dominant, complete penetrance Trinucleotide repeat on C4 Longer repeat sequence= earlier onset
46
Define Myoclonus
Brief movement with rapid onset & offset +ve (muscular contractions) -ve (muscular inhibitions) Causes: Juvenile myoclonic epilepsy Hypoxia Prion disease Treatment: antiepileptics
47
Define Dystonia
Abnormal twisting posture facial, axial, truncal Jerky tremor Causes: Stroke, trauma, encephalitis, PD, HD Impaired DA activity in BG
48
Define Tremor
Involuntary, rhythmic sinosoidal alternating movements of part of the body limbs, head, chin, soft palate Pathophysiology: Postulated theory: increased activity in cerebellothalamocortical tract PD: DA dysfunction in pallidum Essential Tremor: GABAergic dysfunction in cerebellum
49
What are treatments for Hyperkinetic movement disorders?
Tics/Chorea/Ballismus - D2 antagonists: haloperidol, chlorpromazine, risperidone - Dopamine depleting agents: tetrapenazine - Atypical antipsychotics: Clozapine, olanzapine, ariprazole
50
Define oculogyric crisis
Acute response to certain drugs fixed upward stare neck+trunk extension Jaw spasms, tongue protrusion
51
Define Neuroleptic Malignant Syndrome (NMS)
``` acute medical emergency develops over hours/days response to D2 antagonists rigidity, muscle breakdown raised CPK (creatine protein kinase) fever, confusion autonomic instability ```
52
Define tardive Dyskinesia
choreic oral-facial movements, dystonic trunk posturing DA hypersensitivity, synaptic plasticity treatment: gradual withdrawal from offending drug
53
Define parkinsonism (akinetic rigid syndrome)
slowness of movement/thought stiffness shaking bradykinesia (loss of facial exp, arm swing, fine movement) Akinesia (voluntary movement dysfunction) rigidity rest tremor Depression, anxiety, autonomic involvement, sleep disturbance
54
Define Parkinson's Disease
``` Neurodegenerative DA cells in substantia Nigra 70% of cells lost when symptoms present idiopathic in 80% of cases Diffuse lewi body disease Atypical parkinsonianism - MSA (multiple system atrophy) - PSP (progressive supranuclear palsy) - CBD (corticobasal degeneration) ```
55
Early PD treatments?
Amantadine: glutamate agonist Anti-cholinergics: helps BG ACh/DA balance MAOis: prevents breakdown of 5-HT, NA, DA selegiline, rasagiline L-DOPA: crosses BBB and then promotes DA synthesis - Entacapone/Tolcapone prevents peripheral metabolism
56
Advanced PD treatments?
Duodopa Levodopa administered to duodenum via infusion pump narrow therapeutic range, unpredictable bioavailability ``` DA agonists Bypasses SN when cells are dead peroglide (ergot; no longer used due to fibromyalgia) promipexole (non ergot) apomorphine (subcutaneous infusion) ```
57
Define Neurosis (5 disorders, 1 treatment)
``` Anxiety disorders Depression OCD Adjustment Disorders Somatisation Disorders ``` Treatment: antidepressants
58
Define Psychosis (definition, 4 disorders, treatment)
detachment from reality, no insight, delusions+hallucinations, psychotic episode if presented for a week organic schizophrenia Bipolar disorder Depressive psychosis Treatment: antipsychotics
59
Define Delusion
Firmly held belief inadequate grounds doesn't change mind following contradictory evidence ``` Primary: delusional perception Secondary: incorrect perception but based off understandable grounds Persecutory Grandiose Responsibility for world tragedy ```
60
Define Hallucinations
Perceptions without external stimulus | any sensory modality
61
Schneider's first rank symptoms? (Schizophrenia)
Schneider's first rank symptoms: - Auditory hallucinations - somatic hallucinations - thought withdrawal, thinking out loud - delusional perception
62
Signs of Schizophrenia
Appearance: unkempt, weight gain/loss Behaviour: social withdrawal Medication side effects: - Parkinsonian symptoms - Tardive dyskinesia - Skin discolouration - Severe weight gain- olanzapine
63
What are the aspects of the Mental State Examination?
A Small Majority Thought Parents Created Infants ``` Appearance/behaviour Mood Thought Perception Cognition Insight ```
64
Epidemiology of Schz?
0.2-0.7%, 50% in monoxygotic twins AoO: men= 21-26, women= 25-32 social drift, urban drift, household stability
65
Prognosis of Schz?
~20% full recovery, off medication ~25% steady decline, persistent symptoms ~50% relapsing remitting, some functional impairment Suicide in 5-10%
66
Pathophysiology of Schz?
Ventricular enlargement Reduced grey matter cytoarchitectural changes hallucinations: paracingulate sulcus morphology
67
Neurophysiology of Schz?
Hypofrontality: decreased blood flow to PFC bilaterally Wisconsin Card sorting: unable to detect rule changes Auditory Cortex activation during hallucinations Stroop test difficulties
68
Psychopharmacology of Schz? (3 types)
1) Typical Antipsychotics - Haloperidol, Chlorpromazine - D2 antagonists, prevent acute (+ve) symptoms - Parkinsonian Symptoms, TD 2) Atypical Antipsychotics - Clozapine, Olanzapine - Lowered D2 activity, fewer extrapyramidal SEs - Mainly D4, but affects all Ds + 5HT - improves +ve & -ve symptoms - SEs: severe weight gain, sedation, salivation - Increased PFC DA activity, Decreased DA in NAcc 3) DA agonists - cocaine, amphetamine, OD of L-DOPA - Drug-induced psychosis - treated by drugs in (1)
69
Glutamate Hypothesis in Schz?
1)PCP causes +ve, -ve, cog symptoms NMDAR antagonists 2) lower NMDAR count in mice model - schz symptoms, social withdrawal 3) NMDA antagonists model Schz - PFC: less Glu firing to VTA GABAergic Ns - Less GABAergic inhib. of VTA-NAcc DA Ns - Greater DA release in NAcc - Less activation of VTA-NAcc DA Ns: less Glu - hypofrontality
70
DA antagonists: psychotic or antipsychotic?
Antipsychotic
71
DA agonists: psychotic or antipsychotic?
Psychotic
72
DSM-V
Diagnostic & Statistical Manual for Mental Disorders
73
ICD-10
International Classification of Diseases
74
Major Depressive Episode Criteria/Symptoms
``` 5 or more symptoms for 2w constant depressed mood diminished interest weight loss/gain insomnia/hypersomnia psychomotor agitation/retardation fatigue/loss of energy feeling of worthlessness/guilt impaired concentration/decision making recurrent suicidal thoughts, plans, attempts ```
75
Mania
``` Constantly, abnormally elevated mood functional impairment heightened self esteem grandiose racing thoughts no need to sleep ```
76
Mixed affective Disorders
meets full criteria for mania/hypomania/depression | and 3 criteria for the opposite polarity
77
Major Depressive Disorder
``` AoO: 25-35y/o Females>males 7% prevalence 1/5 lifetime prevalence 8-19% die by suicide ```
78
Bipolar Disorder
BPI: mania BP2: hypomania and depression AoO: 15-24 Prevalence: 0.6-2.4% 30-50% attempt suicide symptomatic for half their lives
79
Aetiology of Major Depressive Disorder (MDD)
HPA axis function, affected by stress, childhood trauma, genetic factors Hypothalamus, Pituitary, Adrenal CRH. ACTH. Cortisol Monoamine Dysfunction
80
1st Gen antidepressants
``` 1) MAOi phenelzine, tranylcypromine nonselective inhibition of MAOs -retention of 5HT, DA, NA SEs: dry mouth, GI disturbances, headache, drowsiness, food interactions ``` ``` 2) Tricyclic Antidepressants amitriptyline, clomipraline Nonselective inhibition of MA reuptake - retention of 5HT, NA, DA SEs: constipation, dry mouth, orthostatic hypotension, cardiac/pulmonary fibrosis, drowsiness ```
81
2nd Gen antidepressants
``` 1) SSRIs sertraline, citalopram, fluoxetine Equal efficacy to tricyclics broad spectrum: OCD, PTSD, Panic, GAD, Social Anxiety low toxicity ``` 2) SNRIs serotonin-NE reuptake inhibitors venlafaxine, duloxetine
82
Neural systems involved in depression
increased activity: - amygdala, vestibulospinal tract, PFC Decreased activity: - VST
83
Bipolar Disorder Treatment
Antipsychotics - D2/D3 antagonists: haloperidol, olanzapine, risperidone - DA partial agonists: ariprazole - Rapid antimanic effect Lithium - multiple mechanisms, antisuicide - prevention of relapse Anticonvulsants - Valproate, lamotrigine, carbamezapine - GABA activity
84
What is an Acute Stress Reaction?
hours-3 days following catastrophic event | -numbness, daze, insomnia, restless, anger/anx/dep
85
What is Adjustment Disorder?
wide range of symptoms stressor not necessarily life threatening out-of-proportion to stressor lasts upto 6 months
86
what is PTSD?
Response to exceptionally catastrophic event witness/experienced event involving torture/death intense fear/helplessness/horror Flashbacks with full emotional intensity immediate onset
87
GAD
persistent symptoms, no particular stimulus worry, apprehension, autonomic hyperactivity fearful anticipation, sleep disturbances, sadness prevalence 9% women>men 70% comorbidity Genetic & environmental roles HPA axis Treatment: SSRIs, BZD
88
Panic Disorder
Fear of losing control, going mad, fainting, dying etc Palpitations, tachycardia, chest pain, sweating, trembling, dyspnoea, faintness, nausea, paraesthesia, chills prevalence: 7-9% AoO: 15-24, 45-54 Genetic and environmental roles locus coeruleus SSRIs, BZD, CBT
89
Agoraphobia
Scenarios one cannot easily escape | Avoidance, stays at home etc
90
Specific Phobias
Inappropriate response to object/situation eg spiders, heights genetic role, past experience, preparedness (marks), classical conditioning, observational learning
91
Social Phobia
Fear of being judged, observed avoidance of trigger situations lifetime risk: 2.4-13.3% 81% of sufferers will at some point meet be comorbid AoO: <5yo, 11-15yo Treatment: Beta Blockers, MAOi
92
OCD
Obsessional thoughts/urges compulsions reduce anxiety contamination, order, sexual, violence prevalence: 2-3% 67% comorbidity 5HT dysregulation, DA dysfunction
93
Amygdala Fear pathway?
Sensory-Amygdala-hypothalamus-locus coeruleus-acute stress response Acute stress response= hpa axis
94
Chronic stress physiology
Chronic activation of glucocorticoid Rs in hippocampus -increased Ca2+ influxes, excitotoxicity Therefore some anxiety disorders can result from diminished hippocampal activity Amygdala+HC receive highly processed info from cortex -diffuse modulatory systems: NE (FoF), 5HT (mood/emotion) GABAergic dysfunction: fewer BZD binding sites: inability to suppress inappropriate fear responses

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