Pain management Flashcards

1
Q

what is pain

A

is an unpleasant sensory and emotional experience associated with actual or potential tissue damage

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2
Q

what is nociception

A

the Process by which painful stimulus is conveyed by nervous system to brain

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3
Q

what nerve fibers are associated with pain transmission (2)

A
  1. unmyelinated C fibres(small and slow)
  2. Myelinated A- delta fibres (fast)
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4
Q

unmyelinated C fibers produce what type of pain

A

dull, diffuse, aching, burning and delayed pain

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5
Q

what type of pain do A delta fibers produce

A

sharp, localized fast pain

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6
Q

what stimuli affects unmyelinated C fibers (3)

A
  1. thermal
  2. mechanical
  3. chemical
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7
Q

what stimuli affects myelinated A delta fibers

A

mechanical (pressure )

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8
Q

what are the central pain pathways (2)

A
  1. spinothalamic tract
  2. Spinoreticular tract
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9
Q
  1. the ascending pathway is responsible for what
  2. what neurons comprises the ascending pathway
  3. where is pain perceived
A
  1. Responsible for sending signals about the injury to the brain
  2. Comprises of first, second and third order neurons
  3. Pain is perceived in the the area of the brain called the Somatosensory cortex
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10
Q

what does the descending pathway do

A

Inhibits and controls the ascending pathway

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11
Q

what are excitatory neurotransmitters (2)

A
  1. Glutamate
  2. tachykinins
    - substance P
    - neurokinins A &B
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11
Q

what is acute pain (2)

A
  1. Pain of recent onset & probable limited duration
  2. Usually there is identifiable temporal & causal relationship to injury or disease
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11
Q

how do the order neurons work in the ascending pathway (3)

A
  1. 1st order neurons synapse with 2nd order neurons in dorsal horn of SC.
  2. Impulse crosses and then ascends via anterior and lateral spinothalamic tracts to thalamus where synapse with 3rd order neurons
  3. 3 rd – sensory axonal projections to sensory cortex and limbic system.
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12
Q

what are inhibitory neurotransmitters ( 2)

A
  1. GABA
  2. glycine
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12
Q

the descending pathways come from where (2)

A
  1. peri-aqueductal grey
  2. raphe nuclei
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12
Q

why treat pain (6)

A
  1. ↓ suffering
  2. ↓ complications
  3. ↓ likelihood of chronic pain development
  4. ↑ patient satisfaction
  5. ↑ speed of recovery → ↓ length of stay → ↓ cost
  6. ↑ productivity and quality of life
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13
Q

what can influence pain severity (4)

A
  1. Previous experience of pain
  2. Cultural background
  3. Coping mechanisms
  4. Fear, Anxiety, Depression
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13
Q

what is chronic pain (2)

A
  1. Persist beyond the time of healing of an injury
  2. Frequently no identifiable cause
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13
Q

which neurotransmitters are part of the descending pain regulation (3)

A
  1. Noradrenaline
  2. serotonin
  3. opioid peptides
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14
Q

why dont we manage pain better (4)

A
  1. Failure in assessment,
  2. underuse of effective analgesic techniques,
  3. poor protocol availability or application,
  4. insufficient knowledge
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14
Q

what do you do in taking a pain history (3)

A
  1. Character, intensity, location, underlying cause, associated symptoms, and current analgesic use
  2. Patient’s ideas & concerns in relation to pain, and their expectations with regard to analgesia
  3. History can be repeated after treatment to monitor progress
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15
Q

who is at risk of inadequate analgesia (5)

A
  1. Extremes of age
  2. Critically ill
  3. Communication difficulties
  4. Hx of substance misuse
  5. Chronic pain already on opioids
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15
Q

what scales can you use to assess pain (3)

A
  1. Verbal Rating Scale
  2. Numerical Rating Scale
  3. Visual Analogue Scale
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15
Q

how does the verbal scale work

A

Ask the patient: “Which of the following words best describes the pain your are experiencing at the moment?”

None 1
Mild 2
Moderate 3
Severe 4

15
Q

the numerical rating scale goes up to what

A

0-10

16
Q

for the VAS how many parameters are there

A

6

17
Q

what are effects of NSAIDs on the GI (4)

A
  1. Indigestion
  2. gastric ulceration
  3. GI bleeding
  4. perforations

*associated with chronic NSAID use

18
Q

how do NSAIDS affect the renal system (2)

A
  1. reduced renal blood flow leading to ischemia can occur in patients with prostaglandin-regulated renal blood flow who receive NSAIDs.
  2. Allergic nephritis can also occur
19
Q

how do NSAID affect the respiratory system (2)

A

Help in the treatment of :
1. atelectasis
2. pneumonia

19
Q

how do NSAIDS affect the cardiovascular system

A

NSAIDS aside from low dose-aspirin increase the risk of myocardial infraction and stroke

19
Q

what are examples of weak opioids (3)

A
  1. A/Codeine
  2. A/Dihydrocodeine
  3. Tramadol
20
Q

how do NSAID affect the hepatic system

A

elevations in serum liver enzymes can occur in chronic NSAID use.

20
Q

how do NSAID affect pregnancy

A

Use in late pregnancy (3RD Trimester) can cause premature closure of fetus ductus arteriosus.

20
Q

what makes up the WHO analgesic ladder (3)

A

Step 1- mild pain
- non opioids

Step 2- moderate pain
- weak opioids, +/- non opioids, +/- adjuvants

Step 3- severe pain
- strong opioids +/- non opioids, +/- adjuvants

20
Q

what are examples of non opioids (3)

A
  1. Aspirin
  2. Paracetamol
  3. NSAIDs
21
Q

what way is ibuprofen administered

A

orally

21
Q

what is an example of a strong opioids (3)

A
  1. morphine
  2. pethidine
  3. fentanyl
21
Q

what are the commonly used analgesics (2)

A
  1. Non-opioids
    - PCM/ acetaminophen
    - NSAIDs
  2. Opioid analgesia
    i) Weak opiates
    - Tramadol
    ii) Strong opiates
    - Morphine
    - pethidine
21
Q

in what way can diclofenac be administered (3)

A
  1. orally
  2. IM
  3. rectally
21
Q

what are methods of treating pain (3)

A
  1. Any non-invasive and causative measures
    - positioning
    - loosen bandage
    - remove unnecessary drains
    - sucking for babies
  2. Pharmacologic
    - Paracetamol
    - NSAIDs
    - Opioids
    - Ketamine
  3. Procedures
    - Regional anesthesia
    - LA infiltration at incision site
22
Q

what do you use PCM for (2)

A
  1. for mild to moderate pain
  2. fever
22
Q

what drug can substitute for glutathione and prevent hepatotoxicity

A

Acetylcysteine if given with 8hrs of ingestion

22
Q

what does PCM lack

A

significant anti inflammatory effect

23
Q

what is the major toxicity seen with overdose of PCM

A

hepatic necrosis due to depletion of antioxidant glutathione and formation of N-acetyl-p-benzoquinone

24
Q

how can you administer PCM (2)

A
  • orally
  • IV
25
Q

what are opiate receptor types (5)

A
  1. μ1
  2. μ2
  3. k
  4. δ
  5. σ
25
Q

what side effects does tramadol lack (2)

A
  1. respiratory depression
  2. decreased gastric motility
26
Q

what does opioid receptor activation do

A

inhibits the presynaptic release and postsynaptic response to excitatory neurotransmitters (glutamate, ACh, and substance P).

26
Q

the primary MOA of opiates is via what receptor

A

μ-receptor agonism.

27
Q

how do opioids affect the GIT

A
  • Opioids increase non-peristaltic smooth muscle tone in the small and large bowel via vagal and peripheral mechanisms
  • This produces an ineffective non propulsive activity that leads to an increase in bowel transit time and result in ileus
  • constipation
27
Q

what occurs with long term administration of opioids

A

opioid dependence and tolerance

27
Q

how do opioids affect the CNS (5)

A
  1. High dose opioids may cause deep sedation or hypnosis, however opioids do not produce amnesia
  2. Opioids reduce MAC of inhalation agents required during balanced GA
  3. Normeperidine, a metabolite of meperidine, can cause seizures due to its neuroexcitatory effects.
  4. Opioids cause miosis by stimulating the Edinger-Westphal nucleus of the oculomotor nerve.
  5. Opioids stimulate the chemoreceptor trigger zone in the area postrema of the brainstem which can cause nausea/vomiting.
27
Q

how do opioids affect the respiratory system (3)

A
  1. Opioids decrease minute ventilation by decreasing the respiratory rate (as opposed to decreasing the tidal volume)
  2. They have a direct effect on the respiratory centers in the medulla, producing a dose-dependent depression of the ventilatory response to CO2.
  3. Morphine and meperidine(Pethidine) can cause histamine-induced bronchospasm.
27
Q

what is tramadol

A

Synthetic opioid with weak μ-agonist activity and inhibits reuptake of serotonin and norepinephrine

27
Q

what are the effects of opioids on the cardiovascular system (3)

A
  1. At clinical doses, opioids do not cause significant myocardial depression
    - However, opioids can cause a dose-dependent bradycardia resulting in decreased CO
  2. The exception is meperidine which may cause tachycardia because of its structural similarities to atropine
    - Meperidine may also cause a decrease in myocardial contractility due to negative inotropic effects
  3. Both meperidine and methadone can prolong the QT interval
27
Q

how can tramadol be administered (3)

A
  1. orally
  2. IM
  3. IV
28
Q

how are opioid metabolites excreted

A

kidneys

29
Q

how can opioids be administered (7)

A
  1. PO
  2. IV
  3. IM
  4. subcutaneous
  5. transmucosal
  6. epidural
  7. intrathecal
30
Q

what is the distribution half life of opioids

A

short