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Gastrointestinal, Liver And Pain > Pain Physiology > Flashcards

Pain Physiology Flashcards

1
Q

Which of the following neurotransmitters is released by C fibers?
a. Glutamate
b. GABA
c. Substance P
d. Aspartate

A

(c) Substance P causing slow excitation of the 2nd order neurons.

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2
Q

Which other neurotransmitters are implicated in pain perception.
a. Glutamate
b. GABA
c. Substance P
d. Aspartate

A

(a) Glutamate is released by the A alpha fibres and cause fast excitation of second order neuron.

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3
Q

What is gate control theory.

A

The “Gate” is the synapse between 1st and 2nd order neurons at the substantia gelatinosa (lamina II) in the dorsal grey horn
Gate control is the idea that rubbing the surface of the injured body part can alleviate pain.

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4
Q

What neurotransmitter is implicated in prevention of 2nd neuron firing in gate control theory.
a. Glutamate
b. GABA
c. Substance P
d. Aspartate

A

(b) GABA fires from interneuron and synapses at the second order neuron inhibiting ascending limb.

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5
Q

In clinic, how can one utilise the gate control theory.

A

Pain-relieving methods that take advantage of this system include:
Massage
Acupuncture
Trans-cutaneous Electrical Nerve Stimulation (TENS)

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6
Q

What is the function of the descending limb.

A

Brain sending down signals capable of inhibiting pain.

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7
Q

Endogenous opioids are released from the raphe nucleus magnus
a. True b. False

A

(b) False serotonin is release and from the locus coeruleus norepinephrine is released on the interneuron which then release endogenous opioids onto the 2nd order neuron preventing the transmitting pain sensation.

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8
Q

Our endogenous opioids include enkephalin endorphins and dynorphins…
(a) True
b. False

A

A

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9
Q

What neurotransmitters are implicated in reducing pain perception.
a. Glutamate
b. GABA
c.Norepinephrine
d.Serotonin

A

(c) and (d)

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10
Q

Where else can our endogenous opioids be found.

A

In the descending tract where is modulates the release of serotonin and noradrenaline so the Brain: periaqueductal gray ( PAG), nucleus raphe magnus (NRM), nucleus reticularis paragigantocellularis (NRPG)

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11
Q

What are the three endogenous opioid receptors

A

Mu, Delta and Kappa all inhibiting cAMP resulting in hyper polarisation and inhibiting of calcium channels.

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12
Q

Mechanism of opioids: On-target and Off-target effect.

A

Mu (μ) receptor agonist of g-coupled protein reducing neuronal excitability and pain perception. Reduce sympathetic nervous stimulation activity relieving cardiac work and oxygen demand.

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13
Q

What are the side effects associated with opioids? And why ?

A
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14
Q

Give the names of three strong opioids. What form can they come in.

A

Diamorphine: SC injection >morphine
Fentanyl: patches (TD), IV, IM.
Oxycodone
Methadone- long-acting OD

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15
Q

Give the names of three weak opioids

A

Codeine
Dihydrocodeine
Combined with NSAIDs in OTC prep.

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16
Q

Patient comes in with pin point pupils and has been on morphine 10 mg QDS. What do you suspect? Treatment?

A

Opioid overdose—> administer naloxone.

17
Q

Prescribing good practice with Opioids

A

Switching administration route follow the guidance.
Switching between preparations (modified release to immediate to liquid) always check you are not prescribing over the original dose.
Always prescribe by brand name and type with modified preparations, patches and liquid preparation.
On prescription total quantity and figures should be written.

18
Q

Dose of morphine in acute setting, PO, SC,IM

A

Initially 10 mg every 4 hours, adjust according to pain.

19
Q

Dose of morphine in chronic setting.

A

5-10 mg every 4 hours adjust to pain.

20
Q

Dose morphine: Pain management in palliative care for opioid naive.

A

20-30 mg daily divided doses using immediate or 12 hourly preparation.

21
Q

Remedy for Opioid overdose and MAO

A

Naloxone opioid antagonist

22
Q

Monitoring: Opioids

A

Pain using numerical rating scale or visual rating scale—> move to opioid sparing agents.

23
Q

Cautions/Contraindications opioids

A

Liver impairment: can precipitate hepatic encephalopathy.
Pregnancy
Elderly more pronounced effect
Gut motility disorder

24
Q

Which enzyme synthesis the Eicosanoid (give name) that cause pain?

A

COX-2 enzyme synthesis PGE2 which causes pain.

25
Q

What are the other effects mediated by PGE2?

A

Pain, Bone formation and fever.

26
Q

What is the function of PGE1 and PGE2 in the renal vasculature?

A

Vasodilatation of the smooth muscle selectively at the afferent arterioles mediated by EP4 receptors (cAMP dependent).

27
Q

What enzyme produces Eicosanoid (give name) gastric protection and inhibits platelet aggregation?

A

COX-1 enzyme mainly catalyses the formation PGI2.

28
Q

What is the function of PGI2?

A

Prostaglandin I2 works to protect gastric mucosa and prevent platelet aggregation.

29
Q

Draw the synthesis of PGI2 and PGE2 and their pathways…

A
30
Q

Mechanism of action for traditional and selective NSAIDs.

A

Traditional NSAIDs such as ibuprofen, naproxen, indomethacin non-selectively inhibit COX-1 and COX-2 enzymes and it is the inhibition of prostaglandin E2 (E1) that reduces the potentiation of pain perception.

31
Q

NSAIDS:Counselling

A

Check if they have asthma or are on any medicines.
For short term use advise patient to take food before administering the medication and to stop use after 10 days.
For chronic users advise for to stop taking NSAIDs when they are acutely unwell or dehydrated as this may increased risk of renal injury.

32
Q

NSAIDs: Adverse effects

A

GI bleed
Nephrotoxicity in dehydrated state or while on ACE-I
Increase risk of CVD event.
Fluid retention worsening heart failure and hypertension.

33
Q

NSAIDs: Cautions/Contrindications

A

Asthmatic patient.
Aspirin: children under 16—> Reyes Syndrome
Patient on ACE-I: nephrotoxicity

34
Q

NSAIDS: Monitoring

A

Scoring patients pain to see if it decreased and step them down. GI upset or bleed based on Tx symptoms.

35
Q

Give in order of severity the NSAID that increase CVD risk.

A

Celecoxib> diclofenac > ibuprofen > naproxen.

36
Q

Give in order of severity the NSAID that increase GI bleed risk.

A

naproxen> diclofenac > ibuprofen (least risk) >COX-2 selective agents

Gastrointestinal, Liver And Pain (5 decks)

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