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Semester 1 > Back Pain > Flashcards

Back Pain Flashcards

1
Q

What are the 4 categories that need to be met in order to be classed as a neurotransmitter?

A
  1. NT must be made in the presynaptic neurone
  2. The NT must be stored presynaptically (exception being NO)
  3. The NT must be released on demand
  4. The NT must be inactivated
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2
Q

What does monoamine oxidase do to NT?

A

break down NT’s

MAOI: Antidepressant —> prevents degradation of depleted NT

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3
Q

Name the classes of NT and an example of each

A

Amino acids:
glutamate, (excitatory in CNS)
GABA, (inhibitory via cl- channels)
glycine (inhibitory)

Biogenic amines: catecholamines (noradrenaline and dopamine) and indolamines (serotonin).

Peptides: endorphins and encephalins

Esters: acetylcholine

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4
Q

What are the excitatory and inhibitory neurotransmitters of the CNS

A

Glutamate is the primary excitatory NT
GABA is the principle inhibitory NT
Glycine is the second most common inhibitory

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5
Q

How are seizures treated?

A

Phenytoin: increases the refractory period between firings in the voltage gated sodium channels

Benzodiazepine: increases the effect of GABA

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6
Q

What are the differences between a delta and c fibres?

A 
A delta; C Fibres
myelinated; unmyelinated
sharp, localised pain; dull, throbbing, diffuse pain 
minority of nociceptor; majority
fast condution; slow
polymodal; polymodal 
not usually visceral; -
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7
Q

Transmission pathway of pain

A

Primary afferant in the tissue, the stimulus is going to activate receptors or change configuration of ion channels —> AP comes in via dorsal horn and synapses on a second order neurone —> second order neurone crosses over because spinothalamic tract crosses immediately —> ascends to thalamus —> synapses and sends third order pathway to cerebral cortex

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8
Q

What receptors do glutamate bind to?

A

AMPA
NMDA
G-protein coupled receptors

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9
Q

What are the 3 mechanisms of descending inhibition of pain?

A

GABA and glycinergic interneurones

Descending inhibition: PAG —> RVM —> DH

Endogenous opioids

higher order brain function

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10
Q

neuropathic pain
causes
examination
management

A 
Causes:
Traumatic 
Diabetic neuropathy 
Trigeminal neuralgia 
Post stroke pain

Examination:
changes in colour
changes in sensation

management: TCAs and anticonvulsants

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11
Q

Define chronic pain

A

Pain persisting beyond the usual healing time of the acute injury

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12
Q

What are promoters?

A

TATA binding proteins binds to a sequence in DNA enabling DNA helix to distort —> start breaking hydrogen bonds

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13
Q

What are enhancers and how are they different to promoters?

A

Short DNA sequences
Positive regulative element
Opposed by silencers

Different to promoters cause they:

  • bind ubiquitous and cell type specific transcription factors
  • stabilise transcription machinery assembly by protein-protein interactions
  • how they work from a distance: scanning vs looping.
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14
Q

E.g of post transcriptional modification

A
  1. Alternative promoters
  2. Alternative splicing
  3. Alternative 3 prime ends
  4. RNA editing
  5. Translational control
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15
Q

Describe the translation process

A
  1. The ribosome binds to mRNA at a specific area.
  2. The ribosome starts matching tRNA anticodon sequences to the mRNA codon sequence.
  3. Each time a new tRNA comes into the ribosome, the amino acid that it was carrying gets added to the elongating polypeptide chain.
  4. The ribosome continues until it hits a stop sequence, then it releases the polypeptide and the mRNA.
  5. The polypeptide forms into its native shape and starts acting as a functional protein in the cell.
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16
Q

What NT does pre-ganglionic neurones in parasympathetic and sympathetic system release and which receptor does it act on?

A

ACh on nicotinic receptors

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17
Q

What NT does post-ganglionic neurones in parasympathetic system release and which receptor does it act on?

A

ACh on muscarinic

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18
Q

What NT does post-ganglionic neurones in sympathetic system release?

A

Noradrenaline but some release ACh (I.e sweat glands)

19
Q

Muscarinic ACh receptor agonists

A

Pilocarpine

  • non selective
  • uses: constriction of pupils, decreased interocular pressure (glaucoma)

Bethanechol

  • non selective
  • uses: bladder and GI hypotonia
20
Q

Muscarinic ACh receptor antagonist

A

Atropine

  • non selective
  • uses: adjunct for anaesthetic, anticholinesterase poisoning, bradycardia

Glycopyrronium
- similar to atropine but does not cross blood brain barrier

21
Q

ANS Adrenergic receptors and locations

A

All are metabotropic (G-protein coupled receptors)

A1: cardiovascular (vasoconstriction), GI tract , genitourinary (smooth muscle contraction)

A2: neuronal (decrease transmitter release)

B1: kidney (decrease urine production), heart (increase HR and cardiac force)

B2: lungs (bronchodilation) smooth muscle (relaxation of visceral smooth muscle), skeletal muscle (vasodilation)

22
Q

Adrenergic receptor agonists

A

Adrenaline (non-selective)

Phenylepherine (a1 selective)
- decongestant

clonidine (a2 selective)
- hypertension

salbutamol (b2 selective)
- SABA

salmeterol (b2 selective)
- LABA

23
Q

Adrenergic receptor antagonists

A

Phenotolamine (non-selective)
- phaeochryomocytoma

Prazosin (a1 selective)
- benign prostatic hyperplasia

propranolol (b1 and b2 selective)

atenolol (b2 selective)

24
Q

what is the gate control theory of pain?

A

• Pain is multidimensional and subjective experience of perception.
• Both ascending physiological inputs and descending psychological
inputs are involved.
• ‘Gating’ mechanism in the dorsal horn of the spinal cord that ‘opens’ (permits) or ‘closes’ (inhibits) the transmission of pain impulses.

25
Q

How are neurotransmitters inactivated?

A
  • reuptake
  • enzymal inactivation
  • diffusion
26
Q

What are the dysfunctions of glutamate?

A

Synaptic plasticity
Excitotoxicity
Migraine
Epilepsy

27
Q

GABA
Features
Inactivation
Effect of Alcoholism

A

Principle inhibitory NT in the CNS
• Found predominately in CNS
• Also in striatum and globus pallidus
• Acts on ligand gated chloride channels

inactivated by presynaptic reuptake

alcoholism causes a change in GABA transmission, withdrawal results in convulsive movement and seizures.

28
Q

What are the effects of dopamine?

A

Parkinsons
Schizophrenia
Addiction

29
Q

what are the effects of serotonin?

A

depression and OCD

  • associated with serotonin dysfunction
  • fluoxetine is a SRI
30
Q

Effects of endorphins and encephalins?

A

pain

  • act on opioid receptors as endogenous ligands
  • opioids cause downregulation of opioid receptors in the CNS
  • -> leads to opioid tolerance and increased intake
31
Q

define transduction

A

conversion of a noxious stimulus into an action potential in a nociceptor

32
Q

what is visceral pain?

A
  • Visceral nociceptors respond to distension or ischaemia
  • Visceral primary afferent will activate multiple second order neurones
  • Pain more diffuse (less well localised)
  • Converge on second order neurones with somatic input
  • Referred pain (convergence)
33
Q

What are the associated features of pain

A 
sweating 
pallor
nausea
tachycardia
hypertension
34
Q

What are the non-modifiable and modifiable risk factors for chronic pain?

A 
Non modifiable: 
Gender (female)
age
genetic predisposition
lower socio-economic status
occupational factors
hx of abuse 
Modifiable:
past experience of pain 
anxiety and depression
catastrophising beliefs
surgical approach
35
Q

How does contraction of skeletal muscles occur? (molecular mechanism)

A

Contraction results from the sliding action of interdigitating actin and myosin filaments

(The Ca++ ions initiate attractive forces between the actin and myosin filaments, causing them to slide alongside each other, which is the contractile process.)

36
Q

What are the sources of energy rephosphorylation?

A
  1. phosphocreatine
  2. glycolysis
  3. oxidative metabolism
37
Q

Define force summation and describe the two types

A

increase in contraction intensity as a result of the additive effect of individual twitch contractions

  1. multiple fibre summation: results from an increase in the number of motor units contracting simultaneously
  2. frequency summation: results from an increase in the frequency of contraction of a single motor unit
38
Q

What are house keeping genes?

A

histones and actin

39
Q

ANS and the eye

A

Pupillary dilator muscle – Sympathetic innervation only •Mydriasis

Pupillary constrictor muscle – Parasympathetic innervation •Miosis

40
Q

ANS and the urinary bladder

A

Bladder filling:
Sympathetic control predominates
•Relaxation of detrusor muscle •Contraction of internal sphincter muscle

Bladder full:
Parasympathetic control predominates
•Contraction of detrusor muscle •Relaxation of internal sphincter muscle

41
Q

Predominate locations of ACh receptors in the body

A 
Nicotinic ACh receptors: 
NMJ
Sympathetic ganglia
Parasympathetic ganglia
CNS
Muscarinic ACh receptors
Parasympathetic target organs
Sweat glands (sympathetic)
Vascular smooth muscle
CNS
42
Q

Examples of drugs that presynaptically affect noradrenergic neurones

A

Drugs that affect catecholamine synthesis:
– e.g. methyldopa

Drugs that affect catecholamine release:
– Indirectly acting sympathomimetics – e.g. amphetamines
– By acting on α2 adrenoreceptors – e.g. clonidine

Inhibitors of catecholamine uptake:
– NET inhibitors – e.g. cocaine, tricylic antidepressants

Inhibitors of catecholamine metabolic degradation:
– Monoamine oxidase inhibitors used in depression

43
Q

What are the musculoskeletal red flags?

A
  • cauda equina
  • infection/sepsis
  • neoplasm
  • trauma
  • age >50
  • history of cancer
44
Q

What is the diagnostic triage of back pain?

A
  • simple mechanical backache (85-95%)
  • nerve root (5%)
  • possible serious pathology (1-2%)

Semester 1 (13 decks)

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