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BSMS202 > CSAII > Flashcards

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
Q

Timescales for acute/chronic pain?

A

Acute <3 months

chronic >3 months

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26
Q

Treatments for acute pain

A

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
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27
Q

Chronic pain epidemiology

A

20-50% of population

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28
Q

11 causes of chronic pain?

A 
chronic back pain
cancer
carpal tunnel syndrome
arthritis
fibromyalgia
diabetes
migraine
post-surgery
MS
trigeminal Neuralgia
phantom limb
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29
Q

2 types of chronic pain

A

Inflammatory
- persistent tissue inflammation eg arthritis

Neuropathic
- NS injury eg compression, traction, sever, hypoxia, demyelination, tumour

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30
Q

Neuropathic Pain Symptoms

A 
Burning pain
Stabbing pain
Aching
Electrocution pain
Radiating pain
Hypersensitivity
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31
Q

Neuropathic pain mechanisms

A

V complex
Peripheral sensitisation
spontaneous nociceptor firing
accumulation of ICs at site of injury, causes hypersensitivity

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32
Q

What is central sensitisation?

A

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)

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33
Q

What is CNS hyperalgesia?

A

Follows central sensitisation

activation of nociceptors results in amplified SC activation

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34
Q

Central Allodynia mechanism?

A

non noxious Aβ fibres also synapse onto 2nd order spinothalamic Ns

  • usually inactive as incapable of reaching threshold
  • central sensitisation causes AP firing
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35
Q

Chronic Pain treatments?

A

Difficult to treat
Tricyclic antidepressants eg Amytriptyline
anticonvulsants eg pregabalin, gabapentin
NMDA antagonists eg ketamine
CBT
SC stimulator, gate control
Placebos

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36
Q

What is the hierarchy of motor control?

A

Low level- execution, BS, SC
Middle- Tactics, motor cortex, cerebellum
High- strategy, association areas of neocortex, BG

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37
Q

Basal ganglia anatomical features?

A 
Caudate Nucleus
Putamen
Globus Pallidus (int&amp;ext)
Thalamus
Hypothalamus
Substantia Nigra
Subthalamic Nucleus

Lentiform Nucleus: putamen+pallidum
Corpus Striatum: CN+LN
Neostriatum (dorsal, motor): CN+putamen

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38
Q

What are Basal Ganglia Loops?

A

Processing pattern for motor activity

Cortical IP-Striatum-GPi-Thalamus-Cortex

39
Q

3 Key Pathways of basal ganglia?

A

Direct (exc) promote movement
Indirect (inh) withhold movement: GPe, STN
Hyperdirect pause movement: STN

Thalamus inhibition prevents movement

40
Q

What is the role of the substantia Nigra?

A

DA release
Interacts with Striatum Ns
DA/ACh balance, DA promotes movement, ACh prevents
D1 & D2 receptors

41
Q

2 categories of movement disorders and their associated conditions?

A 
Hyperkinetic movement
hemiballismus
Tics
Chorea
Myoclonus

Hypokinetic Movement
Parkinsonian conditions
Ataxia
Apraxia

42
Q

Define Hemiballismus

A

high amplitude flailing of limbs
unilateral
Impaired STN activity
Cause: stroke

43
Q

Define Tic Disorders

A

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
Q

Define Chorea

A

jerky, brief, irregular movement
Appears to flow from limb to limb

causes:
Huntington’s disease
Neuroleptics

45
Q

Define Huntington’s Disease

A

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
Q

Define Myoclonus

A

Brief movement with rapid onset & offset
+ve (muscular contractions)
-ve (muscular inhibitions)

Causes:
Juvenile myoclonic epilepsy
Hypoxia
Prion disease

Treatment: antiepileptics

47
Q

Define Dystonia

A

Abnormal twisting posture
facial, axial, truncal
Jerky tremor

Causes:
Stroke, trauma, encephalitis, PD, HD
Impaired DA activity in BG

48
Q

Define Tremor

A

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
Q

What are treatments for Hyperkinetic movement disorders?

A

Tics/Chorea/Ballismus

  • D2 antagonists: haloperidol, chlorpromazine, risperidone
  • Dopamine depleting agents: tetrapenazine
  • Atypical antipsychotics: Clozapine, olanzapine, ariprazole
50
Q

Define oculogyric crisis

A

Acute response to certain drugs
fixed upward stare
neck+trunk extension
Jaw spasms, tongue protrusion

51
Q

Define Neuroleptic Malignant Syndrome (NMS)

A 
acute medical emergency
develops over hours/days
response to D2 antagonists
rigidity, muscle breakdown
raised CPK (creatine protein kinase)
fever, confusion
autonomic instability
52
Q

Define tardive Dyskinesia

A

choreic oral-facial movements, dystonic trunk posturing
DA hypersensitivity, synaptic plasticity
treatment: gradual withdrawal from offending drug

53
Q

Define parkinsonism (akinetic rigid syndrome)

A

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
Q

Define Parkinson’s Disease

A 
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
Q

Early PD treatments?

A

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
Q

Advanced PD treatments?

A

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
Q

Define Neurosis (5 disorders, 1 treatment)

A 
Anxiety disorders
Depression
OCD
Adjustment Disorders
Somatisation Disorders

Treatment: antidepressants

58
Q

Define Psychosis (definition, 4 disorders, treatment)

A

detachment from reality, no insight, delusions+hallucinations, psychotic episode if presented for a week

organic
schizophrenia
Bipolar disorder
Depressive psychosis

Treatment: antipsychotics

59
Q

Define Delusion

A

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
Q

Define Hallucinations

A

Perceptions without external stimulus

any sensory modality

61
Q

Schneider’s first rank symptoms? (Schizophrenia)

A

Schneider’s first rank symptoms:

  • Auditory hallucinations
  • somatic hallucinations
  • thought withdrawal, thinking out loud
  • delusional perception
62
Q

Signs of Schizophrenia

A

Appearance: unkempt, weight gain/loss
Behaviour: social withdrawal

Medication side effects:

  • Parkinsonian symptoms
  • Tardive dyskinesia
  • Skin discolouration
  • Severe weight gain- olanzapine
63
Q

What are the aspects of the Mental State Examination?

A

A Small Majority Thought Parents Created Infants

Appearance/behaviour
Mood
Thought
Perception
Cognition
Insight
64
Q

Epidemiology of Schz?

A

0.2-0.7%, 50% in monoxygotic twins
AoO: men= 21-26, women= 25-32
social drift, urban drift, household stability

65
Q

Prognosis of Schz?

A

~20% full recovery, off medication
~25% steady decline, persistent symptoms
~50% relapsing remitting, some functional impairment
Suicide in 5-10%

66
Q

Pathophysiology of Schz?

A

Ventricular enlargement
Reduced grey matter
cytoarchitectural changes
hallucinations: paracingulate sulcus morphology

67
Q

Neurophysiology of Schz?

A

Hypofrontality: decreased blood flow to PFC bilaterally
Wisconsin Card sorting: unable to detect rule changes
Auditory Cortex activation during hallucinations
Stroop test difficulties

68
Q

Psychopharmacology of Schz? (3 types)

A

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
Q

Glutamate Hypothesis in Schz?

A

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
Q

DA antagonists: psychotic or antipsychotic?

A

Antipsychotic

71
Q

DA agonists: psychotic or antipsychotic?

A

Psychotic

72
Q

DSM-V

A

Diagnostic & Statistical Manual for Mental Disorders

73
Q

ICD-10

A

International Classification of Diseases

74
Q

Major Depressive Episode Criteria/Symptoms

A 
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
Q

Mania

A 
Constantly, abnormally elevated mood
functional impairment
heightened self esteem
grandiose
racing thoughts
no need to sleep
76
Q

Mixed affective Disorders

A

meets full criteria for mania/hypomania/depression

and 3 criteria for the opposite polarity

77
Q

Major Depressive Disorder

A 
AoO: 25-35y/o
Females>males
7% prevalence
1/5 lifetime prevalence
8-19% die by suicide
78
Q

Bipolar Disorder

A

BPI: mania
BP2: hypomania and depression

AoO: 15-24
Prevalence: 0.6-2.4%
30-50% attempt suicide

symptomatic for half their lives

79
Q

Aetiology of Major Depressive Disorder (MDD)

A

HPA axis function, affected by stress, childhood trauma, genetic factors

Hypothalamus, Pituitary, Adrenal
CRH. ACTH. Cortisol

Monoamine Dysfunction

80
Q

1st Gen antidepressants

A 
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
Q

2nd Gen antidepressants

A 
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
Q

Neural systems involved in depression

A

increased activity:
- amygdala, vestibulospinal tract, PFC

Decreased activity:
- VST

83
Q

Bipolar Disorder Treatment

A

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
Q

What is an Acute Stress Reaction?

A

hours-3 days following catastrophic event

-numbness, daze, insomnia, restless, anger/anx/dep

85
Q

What is Adjustment Disorder?

A

wide range of symptoms
stressor not necessarily life threatening
out-of-proportion to stressor
lasts upto 6 months

86
Q

what is PTSD?

A

Response to exceptionally catastrophic event
witness/experienced event involving torture/death
intense fear/helplessness/horror

Flashbacks with full emotional intensity
immediate onset

87
Q

GAD

A

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
Q

Panic Disorder

A

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
Q

Agoraphobia

A

Scenarios one cannot easily escape

Avoidance, stays at home etc

90
Q

Specific Phobias

A

Inappropriate response to object/situation
eg spiders, heights
genetic role, past experience, preparedness (marks), classical conditioning, observational learning

91
Q

Social Phobia

A

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
Q

OCD

A

Obsessional thoughts/urges

compulsions reduce anxiety

contamination, order, sexual, violence

prevalence: 2-3%
67% comorbidity

5HT dysregulation, DA dysfunction

93
Q

Amygdala Fear pathway?

A

Sensory-Amygdala-hypothalamus-locus coeruleus-acute stress response

Acute stress response= hpa axis

94
Q

Chronic stress physiology

A

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

BSMS202 (1 decks)

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