Behavioral science - Pain Flashcards

1
Q

What is transference?

A

The patient attributes beliefs and expectations of the MD-PT relationship onto the doctor. Can be positive or negative transference but always pathological

EXAMPLE: assuming that Dr. can’t or won’t help and will likely not listen, be short and possibly rude

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2
Q

What is countertransference?

A

The doctor attributes beliefs and expectations of the MD-PT relationship onto the patient. Can be positive or negative transference but always pathological

EXAMPLE: you (Dr.) likely will be stressed, irritated, short and rude as these patients don’t follow the medical rules

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3
Q

Acute pain vs chronic pain time cutoffs for Dx

A

Acute pain – 1 week or less

Chronic pain – Considered an autonomous disease by many physicians; at least 6 months

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4
Q

Pathway for endogenous opioid synthesis (what is most important endogenous opiod? What receptor does it act on?)

A

POMC > beta-lipotropin > beta-endorphin

beta endorphin

mu opioid receptors

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5
Q

What CSN structures are involved in descending pain circuit?

A

amygdala, mesencephalic reticular formation, PAG, rostral ventral medulla

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6
Q

Where are mu opioid receptors expressed?

A

Descending pain circuit

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7
Q

How do endogenous opioids work?

A

Involved at inhibiting GABA and thus disinhibiting dopamine

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8
Q

Where in the PNS are mu opioid receptors?

A

Primary Afferent Neurons, Peripheral Sensory Nerve fibers, Dorsal Root Ganglia

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9
Q

how do mu opioid receptors work in PNS?

A

Inhibition of substance P and other tachykinin release

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10
Q

What triggers endorphin release in the PNS?

A

stress and ACTH co-release

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11
Q

Where are endorphins involved in PNS release synthesized?

A

Corticotrophs in the anterior pituitary synthesize ACTH and β-endorphin in equimolar amounts

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12
Q

What triggers central endorphin release

A

activation of nociceptive circuits in the hypothalamus, midbrain, and rostral medulla

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13
Q

Where are centrally released endorphins synthesized?

A

Cell bodies of opioidergic neurons in the median eminence of the hypothalamus

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14
Q

In response to pain the peripheral nociceptive pathways trigger co-release of endorphins and ATCH from the anterior pituitary. What agents trigger release?

A

5-HETE, LTA4, LTB4, and other lipoxygenase products
Angiotensin-II
Serotonin

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15
Q

What receptors and signalling pathways are involved in release of endorphins?

A

β-adrenoreceptor activation

Gs: adenylate cyclase activated, cAMP

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16
Q

How is glutamate signaling involved in opioid pain inhibition?

A

glutamate receptor antagonists block effect of opioid suggesting glutamate signaling facilitates opioid effects

17
Q

Are high-dose opioids usually helpful for chronic non-malignant pain?

A

no

18
Q

What should cut-off be for opioid prescription be for non-malignant chronic pain?

A

longer than 1 months should be reconsidered

19
Q

MOA for NSAIDS

A

inhibit cyclooxygenase (COX), enzyme for conversion of arachidonic acid to prostaglandins and thromboxane, which provoke tissue inflammation

20
Q

Why do some NSAIDS cause GI irritation?

A

Inhibit prostaglandin production - Prostaglandins protect the stomach lining from acid

21
Q

How can GI irritation be circumvented?

A

COX-2 specific inhibitors; celecoxib and low dose meloxicam (7.5 mg/day) cause less gastric irritation

22
Q

What is the only NSAID that causes irreversible inhibition of COX

A

aspirin

23
Q

What else do NSAIDS do?

A
reversibly inhibit renal blood flow
decrease fever (PGE2 causes fever)
24
Q

Which drugs should be used to treat neuropathic pain?

A

anticonvulsants, tricyclics

25
Q

How do anticonvulsants (anti-epileptic drugs) inhibit neuropathic pain?

A

lower a neuron’s ability to fire by hyperpolarization

26
Q

What type of signalling mediates central sensitization?

A

Excessive Na+, Ca++, GLU release

27
Q

How do Carbamazepine, lamotrigine, topiramate inhibit pain?

A

Na+ channel blockers

28
Q

How do Gabapentin/Pregabalin inhibit pain?

A

Ca++ channel blockers

29
Q

Pain condition indication/Side effects of Carbamazepine?

A

trigemimal neuralgia

Aplastic anemia, requires blood levels to be monitored, p450 3A4 inducer causing drug interactions

30
Q

Pain condition indication/Side effects of lamotrigine?

A

No pain approvals

StevensJohnson Syndrome rash

31
Q

Pain condition indication/Side effects of gabapentin?

A

Weight gain, sedation

For Diabetic neuropathy

32
Q

Pain condition indication/Side effects of pregabalin?

A

Mild addiction, weight gain, sedation

For Diabetic neuropathy, fibromyalgia

33
Q

Pain condition indication/Side effects of Topiramate

A

Weight loss, acidosis, oligohydrosis, glaucoma

For migraines

34
Q

What is the connection between depression/anxiety and pain?

A

Ascending NE projections if Weak cause Depression, Anxiety ADHD… Descending NE pathways also inhibit pain; therefore if deficient NE (or NE inhibition) then leads to pain + depression/anxiety etc.

35
Q

What is the MOA for SNRI’s in neuropathic pain management?

A

descending noradrenergic and serotonergic fibers activate GABA interneurons and inactivate pain - SNRI’s increase NE/SER

36
Q

what are Duloxetine and milnacipran

A

SNRI’s - Serotonin NE reuptake inhibitors

37
Q

What are the serotonergic side effects of SNRI’s

A

Headache, GI distress, insomnia, fatigue, sexual and weight gain problems

38
Q

What are the noradrenergic side effects of SNRI’s

A

Nausea, dry mouth, hypertension, appetite suppression

39
Q

what is Amitriptyline?

A

tricyclic antidepressants - dirty side effect profile

Serotonin and norepi side effects
Anticholinergic side effects
–Dry mouth, constipation, blurred vision…
Na+ channel blockade!
– Pain dampening property like the AEDs
May prolong heart QTc and cause heart attack in overdose