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PoP Unit 4 Mechanisms and selectivity of drug action > Anaesthesia and analgesics drugs > Flashcards

Anaesthesia and analgesics drugs Flashcards

(48 cards)

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1
Q

What is the definition of Pain?

A

An unpleasant sensory and emotional experience associated with or resembling the associated with actual or potential tissue damage

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2
Q

Give some key points about pain?

A

Pain is subjective
Pain and nociception are different
Pain may be adaptive or maladaptive
Inability to communicate does not mean that pain is not being experienced
Life experiences may shape ones perception of pain

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3
Q

What are the consequences of untreated pain?

A

Causes sympathetic stimulation and a stress response
Increases morbidity or mortality
Leads to poorer recovery and slower return to function
Early experiences have negative impacts on late life
Risk developing chronic pain

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4
Q

What is the general overview of HPA Hypothalamic pituitary axis?

A

HPA activated by trauma, stress, and pain
Pain—>CRH—>pit gland—>ACTH–>adrenal glands—>Glucocorticoids-ve

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5
Q

What is the general overview of the Sympatho-adreno-medullary axis (SAM) (sec-mins)?

A

Pain—>CRH—>pit gland—>ACTH—>adrenal glands—>GCs or Catecholamines

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6
Q

Give examples of Catecholamines?

A

Nor/adrenaline
Cortisol, corticosterone
Alterations in levels of:
Oxytocin
Dopamine
Endogenous opiates

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7
Q

What does The DOdo (is) Not Alive mean?

A

Tryosine
DOPA
Dopamine
Noradrenaline
Adrenaline

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8
Q

What are the adverse consequences of the stress response on the body system? there are 9.

A

Immune system supression

Hyperglycaemia- Catecholamine induces glycogenolysis/gluconeogenesis

GI disease (alterations to GI microflora and motility, bacterial translocation)

Reduced dermatologic health- increased susceptibility to infection/reduced wound healing

Pain perception alterations: stress induced hypera;gesia and analgesia

Cardivascular events

Delirium/post car syndrome

Stress induced seizures and fits

Decline of neuronal viability

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9
Q

Give the steps of nociception?

A

Nociception—>transduction—>transmission into the spinal cord—->modulation—>perception (sensory cortex of the brain)

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10
Q

What are the 3 different nociceptors?

A

Mechano-nociceptors
Chemo-Nociceptors
Thermo-nociceptors

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11
Q

Which fibres are responsible for Transmission

A

A-delta and C fibres

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12
Q

A-delta fibres are responsible for ….
C fibres are responsible for …

A

A delta: sharp pain
C fibres: Dull pain

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13
Q

What is the only way to manage nociceptive pain?

A

Local anaesthetic

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14
Q

What is inflammatory pain, how is it managed?

A

Sufficent stimulation of nociceptors to release inflamm mediators including PGs histamines and badykinin
Medators may cause sensitization or activation of surrounding cells
Can be managed by NSAIDs, opoids, steroids

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15
Q

What is neuropathic pain?

A

Pain from dmg to the peripheral nerves or spinal cord

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16
Q

What is Nociplastic pain?

A

Pain resulting from altered nociception despite there no longer being reason for nociceptors to be activated

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17
Q

What is hyperalgesia?

A

Increased pain from a stimulus normally regarded as painful

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18
Q

What is Primary and seconday hyperalgesia?

A

Primary: In damaged tissues, causing sensitization of the nociceptors
Secondary: In the surrounding tissues causing sensitization of second order

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19
Q

What is Allodynia?

A

Pain from a stimulus that is not normally regarded as painful (maladaptive)
may be part of the neuropathic pain
Mechanism causing allodynia is unclear

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20
Q

What is peripheral sensitisation?

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A

A sensitizing soup of inflammatory mediators impacts nociceptors
Increase sensitivity of nociceptors

21
Q

What is central sensitisation?

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A

Altered gene expression and synaptic activity
Increased CNS responsiveness
Hypersensitivity to pain
Reduction in neuronal activation threshold
Increased pain intesity

22
Q

What are the 3 types of pain assessments?

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A

Sunjective(qualitative)
Biochemical parameter
Semi-quantative measures (visual analog, simple descriptive etc.)

23
Q

What are some physiological markers for pain?

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A

Increase in heart rate, resp rate, temperature, BP
Pupil size changes/diameter, sewating, body condition
All may change with pain but are fallible

24
Q

What are some biochemical markers for pain?

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A

Chnges in stress hormones, e.g. cortisol, glucose, insulin, adrenaline, endorphins
Can be altered not only by pain but stress disease, anxiety, anaesthesia etc.
Pain inflamm mediators e.g. PGs

25
What features make a pain scale good?
Reliable: consistency of a measure Valid: measure what you intend to measure Sensitive Specific Repeatable Responsineness
26
What are pre-emptive analgesia?
Analegsia administered prior to surgical trauma tissue injury Likely to have better analgesic effects, especially in reducing central sensitisation Reduces overall post operative analgesic requirement
27
What is multimodal analgesia?
Multimodal analgesia means using different types of pain relief together that work in different ways — to get better pain control with fewer side effects.
28
What we use on nociception?
Local anaesthetics
29
What we use in transduction?
Local anaesthetics, opoids, NSAIDs, corticosteroids
30
What we use in transmission?
Local anaesthetics, alpha 2 agonists
31
What we use in modulation?
Local anaesthetics, opoids, Alpha 2 agonists, TCA, NMDA antagonists, NSAIDs
32
What we use in perception?
Opoids, Alpha-2 agonists, Benzodiazepines, Phenothiazines, Anaesthetics
33
What is the classification by efficacy activity at receptors?
Full agonist e.g. morphine... Partial agonist e.g. buprenorphine Agonist-antagonist e.g.Butorphanol
34
Where are opioid receptors located?
In the brain, spinal cord, chemoreceptors trigger zone, GI tract, Synovium, Urinary tract, Leukocytes etc. Exert diff effects based on the subtypes Distinction between efficacy and potency
35
What does inverse do that diffs from full agonist?
Inverse agonist: will cause pain for research Full agonist will cause analgesia
36
What effects are dose dependent?
Sedation Resp depression Bradycardia but depends on specific opioid Nausea and vomiting mainly with morphine
37
What is Buprenorphine?
Partial agonist of the mu-poioid receptor, analgesia tends to be less profound than a full agonist High affinty but low efficacy
38
What is butorphanol?
Agonist-antagonist at the kappa mu receptor
39
What is kappa receptor
Activated by some opioids, including certain mixed agonists Effects: 🔥 Pain relief (mainly spinal level) 😐 Dysphoria (uneasy or unpleasant mood) 🧠 Less addictive potential 🌬️ Less respiratory depression than mu 😵 Can cause hallucinations/dream-like states at high doses
40
What is mu receptor?
Main target for strong opioids like morphine, fentanyl Effects: 🔥 Pain relief (analgesia) 😌 Euphoria (feel-good effect) 😴 Sedation 😰 Respiratory depression (dangerous in overdose) 💩 Constipation 🧠 High risk of addiction/dependence
41
What is the order of local anaesthetic blockade in nerves?
B>C=A-delta>A-gamma>A-beta>A-alpha BeCause (one should) Drink Good Beer Always
42
What are the benefits of locoregional anaesthesia?
Only affects the local area Improved perioperative control of pain Reduced morbidity, hospital time Potential economic benefits Local anaesthetics freely available Uses in management of chronic pain
43
What is lidocaine?
The only local anaesthetic with toxicity low enough to be used intravernously Prokinetic and antioxidant effect, antiarrhythmic Class Ib antiarrhythmic acting on fast sodium channels to inhibit depolarisation Effects could be due to: Na/Ca pump inhibition ROS scavenger inflammatory modulation
44
What is the role of NSAIDs in the context of Analgesia?
Analgesia via blocking PGs synthesis COX-1 & 2 enzye inhibition Block peripheral sensitization can be classed based on selectivity Car with GIT side effects
45
What is paracetamol and how does it act?
Acts by inhibition of COX enzymes, although mechanism not fully understood Thought to act on COX-2 iso enzymes within the CNS analgesic antipyretic but not anti inflammatory Not suitable for cats due to deficent liver glucuronidation pathways
46
What is the function of alpha-2 agonists in terms on analgesia?
A-2 receptors found centrally and peripherally Action on the locus coeruleus in the brainstem, reducing sympathetic outflow Can have profound sedative effects: Vasoconstrcition Reflex bradycardia Different seelctivity for the alpha 2 alpha 1 receptor The more specific the drug the lower the dose needed.
47
If an animal has cardio problems why is an alpha 2 agonist not a suitable analgesia?
If animal has cardiovascular problems this is not suitable for them as they cannot deal with the bradycardia
48

PoP Unit 4 Mechanisms and selectivity of drug action (9 decks)

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