2nd hour of pain day Flashcards Preview

Behavioral Science > 2nd hour of pain day > Flashcards

Flashcards in 2nd hour of pain day Deck (22):

Several types of opioid receptors, but ____ receptors are most important for; where would these receptors be found?

Mu; pain relief;
CNS, gut, synovial lining of joints, descending pain inhibition pathway


Endorphins in CNS involved in; where does it have receptors?

inhibiting GABA and thus disinhibiting dopamine;
descending pain circuit: amygdala, mesencephalic reticular formation, PAG, rostral ventral medulla


Endorphins in PNS involved in; receptors where?

inhibition of substance P and other tachykinin release;
primary afferent neurons, peripheral sensory nerve fibers, DRG


Proposed mech of release of endorphins:

1. Peripheral: stress-mediated and ACTH co-release (corticotrophs in anterior pituitary synthesize ACTH and beta-endorphin in equimolar amounts; can be co-released)
2. Central involves innervation of the hypothalamus, midbrain, and rostral medulla (cell bodies of opioidergic neurons in the median eminence of the hypothalamus);

release mediators are 5-HETE, LTA4, LTB4 and other lipoxygenase products; Ang-II; 5HT; process involves activation of cAMP by beta-adrenoreceptor activation


NSAIDs all inhibit _____ and use what mech? What protects the stomach lining from acid and what lessens gastric irritation?

COX, which converts AA to prostaglandins and thromboxane, which provokes tissue inflamm;
normally prostaglandins would, but COX-2 specific inhibitors like celecoxib and low dose meloxicam cause less gastric irritation


What can cause fever? Aspirin does what?

Prostaglandin E2 (PGE2 signals hypothalamus to increase body's thermal set point); they can cause vasodilitation;

causes irreversible inhibition of COX, used to prevent coronary artery occlusion and colorectal cancer


NSAIDs vs opioids:

1. Neuropathic vs. inflamm pain
2. Neuropathic pain should be addressed via neural function: anticonvulsants, tricyclics
3. NSAIDs address cause of inflamm pain, like post-traumatic, post-surgical
4. Opioids make patient less concerned about pain!!


Epilepsy is a condition where; what are the drugs that treat it and how do they work?

cortical neurons kindle and then fire in synchrony causing a neuromuscular seizure to occur;
antiepileptic drugs function by lowering a neuron's ability to fire by hyperpol and disallowing depol


Besides epilepsy, what are AEDs good for?

1. Bipolar disorder
2. Anxiety disorder
3. Substance withdrawal
4. Migraines
5. Fibromyalgia
6. Diabetic neuropathy


How do you activate Abeta, Adelta, and C fibers? How are these fibers activated?

Non-noxious mech stimulus; noxious mech stimulus; noxious heat and chemical stimulus;
injury and action potentials occurring via Na and/or Ca channel activation, influx, and depol


Inflamm pain and the 3 pain bus stops...

1. Cortex conscious
2. Thalamus/Limbic semiconscious
3. Spinal reflex


Side effects and FDA approvals of carbamazepine, lamotrigine, gabapentin, pregabalin, topiramate?

1. C: aplastic anemia, needs blood levels; p450 3A4 inducer causing drug interactions; for TRIGEM NEURALGIA
2. L: Stevens-Johnson Syndrome rash; no pain approvals
3. G: weight gain, sedation; for diabetic neuropathy
4. P: mild addiction, weight gain, sedation; for diabetic neuropathy and fibromyalgia
5. T: weight loss, acidosis, oligohydrosis, glaucoma; for MIGRAINES!!


Antidepressants actually treat

1. anxiety disorders
2. fibromyalgia
3. meuropathic pain
4. vasomotor symptoms of menopause
5. premenstrual disorders
6. urinary incontinence


Antidepressants for Pain: duloxetine and milnacipran; amitryptiline

Duloxetine and milnacipran are SNRI: have serotonin SE's with headache, GI distress, insomnia, fatigue, sexual and weight gain problems; also NE SE's with dry mouth, HTN, nauesea, appetite suppression

Amitryptiline is a TCA: has 5HT and NE SE's, ACh SE's with dry mouth, constipation, blurred vision; Na channel blockade and can prolong heart QTc and cause heart attack in overdose and can dampen pain


Characteristic of taking opioids and pressure? Solution?

It will take less pressure to cause a pain reaction, aka opioid-induced hyperalgesia;
take someone off opioids to relieve pain (bring pain drivers down and augment endogenous opioid system)


If you have glutamate receptor antagonist and heroin, but former is blocked, what happens?

No opioid-induced hyperalgesia!!


Sometimes inflamm pain goes awry and becomes; what is on this slide?

neuropathic; you're at a subthreshold pain response with some small Ca influx and no pain really noted


For activity-dependent nociception in pain pathways slide:

Full pain response: significant Ca and Na influx!!


The system goes awry, gets stuck, and circuits become GLUed together, why?; how did this come about? what drugs won't work anymore?

Central sensitization and excessive/chronic pain response (neuropathic pain from Na, Ca, and now GLU release!!!);
you could have inflamm injury and could get rewiring of nerves, leading to now NEUROPATHIC pain
NSAIDs and opiates


What does lidocaine do?

Works superficially for pain management at the level of the spinal cord to stop neuronal firing at that level


The role of NE and antidepressants

1. Ascending NE projections if weak will cause depression, anxiety, ADHD
2. Descending NE projections if weak will cause PAIN!!

3. Add antidepressant with NE reuptake inhibition to strengthen ascending pathway and psychiatric symptoms could resolve!!
4. Can also add NRI to strengthen descending pathway to impinge upon a GABA interneuron system that dampens the ability of ascending pain fibers to fire and pain symptoms could resolve


Increased NE will

increase GABA and decrease pain