Pain and Analgaesics Flashcards
What are the 2 types of pain?
Nociceptive
Neuropathic
What is hyperalgesia?
Condition were moderately painful stimuli results in excruciating pain
Describe nociceptive pain
Physical damage or response to inflammatory soup
Activation of free-nerve endings
Respond to mechanical, chemical, pressure, and temperature changes
Responds to analgaesics
Describe neuropathic pain
Resulting from damage/changes in the pain neurons themselves
Chronic and difficult to treat
What are the classic symptoms of neuropathic pain?
Shooting/burning pain
Paraesthesias: Tingling Numbness Burning Throbbing
Give some examples of nociceptive pain
Low-back pain
Myofascial pain
Arthritis
Visceral pain e.g. pancreatitis, surgery
Give some examples of neuropathic pain
Phantom limb
Malignant pain
Trigeminal neuralgia
Post-stroke pain
Post-herpetic pain
Complex regional pain syndrome
Describe referred pain
Sensory information is detected in a part of the body and the information is carried along the sympathetic fibres.
These fibres cross-communicate with other fibres along the dermatome causing pain in a different part of the body that is innervated by the same spinal nerve.
E.g. cardiac pain, sensory T1-5, MI causes pain along the T1-5 dermatome, causing pain in the front of the chest and down the arm
Name the 5 types of headache
Tension
Sinus
Migraine
Cluster
Medication overuse headache
How would a subarachnoid haemorrhage present?
Worst ever headache
Thunderclap headache
Spontaneous, acute headache
At what 3 levels can the pain pathway be modified?
Periphery level
Spinal level
Central level
Which ascending tract carries pain information?
Spinothalamic tract (lateral)
Where does the spinothalamic tract decussate?
2 vertebral levels above the point of entry into the spinal cord.
What does damage to tissues produce that can cause pain?
Inflammatory response
Which fibres sense pain?
A delta fibres
C fibres
Describe the difference between A delta fibres and C fibres
A delta - lightly myelinated, ‘ouch’ response, quick onset of pain, quick to die down
C fibres - unmyelinated, longer term activation, slow response
Describe the gate control theory of pain
When a pain signal from C/Adelta is sensed, it turns off local inhibitory neurons, strengthens original pain stimulus
Pain signal travels onwards to thalamus and cortex
Mechanical stimulation (rubbing) of Abeta neurons activates inhibitory interneurons
Reduces pain transmission by inhibiting 2nd order cells
What is descending inhibition?
Higher centres modify response to painful stimuli
Descending signals increase the activity of 2nd order inhibitory neuron to decrease original pain stimulus.
Carried to spinal level in dorsolateral funiculus (alongside motor neurons)
5HT and NA dominant (dampens things down)
Describe higher pain centre involvement in a pain response
Amygdala - negative emotional region
Prefrontal cortex - reward/positivity region
Hypothalamus - controls autonomic i.e. fight or flight in response to painful stimuli
Periaqueductal gray (PAG) - defence region
Brainstem nuclei - respiratory centres
Why do patients with chronic pain have an increased risk of CVD?
Continued pain input = dorsal horn continually sensitised = brain stem activation = CVS/RS activated, always in state of activation, raised HR and BP.
Describe the biopsychosocial model o pain perception
Incorporates all aspects of an individuals personality.
Not just the biological process of pain, but how it affects their mood, behaviour, and social activities e.g. work, socialising.
Give 4 non-pharmacological options used to treat chronic pain
Exercise
Physiotherapy
Acupuncture
TENS (transcutaneous electrical nerve stimulation)
Give 3 invasive procedures used to treat chronic pain
Nerve blocks/injections
Ablation (cut out neurons)
Implants
- pumps (SD)
- neuromodulators (zaps the spinal cord)
What pharmacological options are there for nociceptive pain?
NSAIDS
- ibuprofen
Opioids
- morphine
What pharmacological options are there for neuropathic pain?
Tricyclic antidepressants
- nortriptyline/ amitriptyline
Antiepileptics
- gabapentin
- carbamazepine
Describe the 4 steps on the WHO pain ladder
Pain free
Non-opiod +/- adjuvant (paracetamol, NSAIDs)
Weak opiod +/- non-opiod +/- adjuvant
(codeine, paracetamol)
Strong opiod +/- non-opioid +/- adjuvant
(morphine, fentanyl)
Describe 3 OTC forms of NSAIDs
Aspirin
Ibuprofen
Diclofenac
Describe the mechanism of action of NSAIDs.
Cyclooxygenases break down arachidonic acid to give PGs
NSAIDs block production of PGs by inhibiting cyclooxygenase (COX) enzymes
Name some COX-2 inhibitors
Celecoxib
Etoricoxib
Parecoxib
What is paracetamol’s mechanism of action?
Not entirely sure, may work on COX-3, but it doesn’t provide any anti-inflammatory response
Name 4 side-effects of NSAID use
GI problems - heartburn, ulceration
CV incidents - thrombosis
Headache
Tinnitus (indicator of overuse)
Give some symptoms of NSAID intoxication
Auditory - tinnitus
Pulmonary - oedema, respiratory arrest
Cardiovascular - tachycardia, hypotension
CNS - depression
GI - pancreatitis, hepatitis
Renal failure
Coma
What can help reverse NSAID toxicity?
Activated charcoal
Name 2 types of opioids
Morphine
Diamorphine
Name the 4 opioid receptors.
Which receptor do most of our drugs work on?
μ (MOP/OP3) (mui) most drugs work on this one
κ (KOP/OP2) (kapa)
δ (DOP/OP1) (delta)
ORL1 (OP4)
Name the 3 groups of opioids
Agonist
Mixed agonist/antagonist
Antagonist
Give an example of an opioid agonist
Morphine
Diamorphine
Codeine
Dihydrocodeine
Give an example of an opioid mixed agonist-antagonist
Buprenorphine
Give an example of an opioid antagonist
Naloxone
Naltrexone
(used in morphine overdose)
Describe the neuronal MoA of opioids
Decreasing opening of voltage-dependent Ca2+ channels
Increasing K+ outflow via KATP and KIR channels*
Decreasing Ca2+ release from intracellular stores (via reduction of cAMP)
Decreasing exocytosis of transmitter vesicles
GENERAL OVERVIEW:
Reduction of neural transmission via hyperpolarisation, reduction in activity of voltage-dependent sodium channels and reduction of transmitter release
What are the 3 cardinal signs of opioid toxicity?
Respiratory depression
Conscious depression
Miosis
Give some general side effects of opioids
Reduced gastric motility
N&V
Smooth muscle spasm
Anaphylaxis
Psychiatric changes
Tolerance and dependency
What 5 things would you give to manage opioid toxicity?
Naloxone - 0.8-2mg every 2-3 min
O2
Glucose
Thiamine
Flumazenil (PAMs group - but can trigger epilepsy
