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Flashcards in PAIN Deck (21):

What other symptom correlates best with pain intensity during recent onset low back pain?

Poor sleep quality increases pain intensity and the duration of pain intensity after new onset low back pain.
A&R 5/14


What is the medical definition of pain?

Pain is a somatic perception with quality like those causing tissue damage, experienced as a threat, associated with unpleasantness or other negative emotions.


What is the definition of chronic pain?

Chronic pain is defined as lasting beyond the ordinary duration required for healing-three months. ACR criteria for generalized pain-bilateral, above and below the waist, involving the spine-chest, thorax, low back, cervical. DSM-IV requires 6 months.


What pathways conduct pain?

Multiple ascending pathways relay nociceptive information including spinocervical, spinomesencephalic, spinal-diencephalic, and spinotelencephalic. These combined to form the contralateral spinothalamic tract which synapse in the thalamus. The thalamus projects to multiple brain areas in the primary and secondary somatosensory cortex, cingulate cortex, prefrontal cortex, insular cortex, amygdala, and the cerebellum.


What types of neurons provide pain transmission to the anterior horn?

Nociceptors are a specialized subset of primary sensory neurons that respond only to pain stimuli. Myelinated nociceptors include A-delta fibers which respond to heat (MTR) or high-pressure mechanoreceptors (HTM) and are responsible for immediate sharp pain. Unmylinated C fibers classified as C-polymodal nociceptors (C-PMN) reduce dull pain. Response threshold may be wide-wide dynamic range (WDR) or narrow, responding only to noxious stimuli (NS).


What are some specific ion channels in nociceptive pathways?

Na(v1, 7) is the sodium channel isoform found in nociceptive and sympathetic ganglion neurons. Calcium-permeable nonselective cation channels (TRPV1, capsation receptor) may produce transient receptor potentials which are gated by heat, low pH, or chemical mediators.


What descending pathways generates central pain inhibition?

descending pathways that inhibit or facilitate nociceptive transmission include ones from the somatosensory cortex prefrontal, cingulate, hypothalamus, periaqueductal gray, and the pons. Fibers in the dorsolateral funiculus of the spinal cord synapse in the dorsal horn with nociceptive neurons.


What sort of cell membrane receptors modify nociceptive transmission.

Other systems influencing nociceptive transmission includes the opioid system, noradrenergic system, and serotonergic system.


What peripheral stimuli sensitize nociception?

Peripheral sensitization may be due to cytokines (IL-1 beta), chemokins, bradykinin, histamine, prostaglandins (leukotriene B4), growth factors, and acidic environment. These may stimulate or reduce the threshold of nociceptor stimulation.


What does the NMDA receptor work?

N-methyl-D-aspartic acid (NMDA) receptor is responsive to glutamate, more so if phosphorylated which increases its distribution. Increased responsiveness follows removal of voltage-dependent magnesium block of the NMDA channel.


What substances increase during transcription dependent sensitization?

Transcription dependent sensitization occurs due to brain derived neurotrophic factor (BDNF), substance P, neurokinin 1, dynorphin, and prostaglandin-endoperoxide synthase 2.


What causes ectopic excitability?

Ectopic excitability may affect neurons at the site of injury, in a neuroma, or in the dorsal root ganglion. This happens because of upregulated sodium channels, channel subunits, receptors in myelinated neurons, or down regulation of potassium channels. GABA or glycine mediated inhibition might also be decreased.


What changes occur in the spinal cord during chronic pain?

Chronic pain may result in sensory fibers normally activated by light touch, pressure, or vibration and ending superficially within the spinal cord moving deeper into the area where pain fivers normally connect. These fibers may also start producing BDNF, and substance P, normally produced only by C-fibers.


How are sodium channels classified?

Ion channels are classified in general as ligand-gated, light gated, voltage-gated, and stretch-activated. Sodium channels are classified as constitutively active, proton-gated, and voltage-gated. The voltage gated sodium channels are classified as Nav alpha (1.1 through 1.9) and Nav beta (1-4). These channels are expressed by SCN*A* or B* genes (sodium channel neuronal type) A or B. Various combinations account for differences in conduction in central neurons, peripheral neurons, cardiac myocytes, uninnervated skeletal muscle, smooth muscle, interstitial cells of Cajal, dorsal root ganglia, glial cells, sympathetic neurons, Schwann cells, neuroendocrine cells, astrocytes, and ganglion cells.


What sorts of conditions result from mutations affecting sodium channels

Mutations cause assorted channelopahies, resulting in epilepsy, myoclonus, hemiplegic migraine, encephalitis, hyperkinetic periodic paralysis, long QT syndrome, ventricular fibrillation, erythromelalgia, and insensitivity to pain.


What are the two main types of glutamate receptors?

ionotropic glutamate receptors are ligand gated nonselective cation channels for potassium, sodium, and calcium ions. Glutamate has a direct action on ionic channel with the receptor causing excitatory postsynaptic current.
Metabotrophic receptors activate G proteins that set off a signaling cascade that affects multiple ion channels, having a prolonged effect.


How are ligand-gated ionic channels classified?

Ligand-gated ion channels consists of three super families which lack evolutionary relationship: cys-loop receptors, ionotrophic glutamate receptors, and ATP-gated channels.
Cys-Loop receptors include anion type GABAa ( gama-amino butyric acid, C4H9NO2-11 varieties) glycine(GlyR 5 varieties) and cationic; serotonin (5-HT..x5), Nicotinic (CHRN..X17), and Zinc activated-ZAC.
Ionotropic glutamine-receptors are classified by other agonists.
NMDA (N methyl D Aspartic acid, C4H9NO4,9 genes)
Kainate (C10H15NO4, 5 genes), and
AMPA (C7H10N2O4, 4 genes).
ATP gated ion channels (PX2) are expressed by 7 genes.
Phosphatydlinisitol 4, 5-biphosphonate (PIP2) antagonizes inward rectifying potassium channels (Kir).


How many metabotrophic glutamate receptors (mGluR) are there, and what other agonists stimulate them?

mGluR are expressed by 8 genes, and other agonists include L-AP4 (L-2-amino-4-phosphanabutyric acid C4H10N05P). ACPD (1-amino-1,3-dicarboxycyclopentane C7H11NO4) and L-QA (quisqualic acid C4H7N3O5).


What is the mechanism of action for mu receptors agonists?

acute mu receptor activation of G protein receptors results in downstream activation of adenyl cyclase and phospholipase C with secondarily decrease cAMP. Chronic receptor activation produces the opposite effect on long-term use up regulates cAMP and changes in gene transcription.


How is the skin innervated?

Skin sensation is perceived through various slowly adapting (SA) and rapidly adapting (RA) low threshold mechanical receptors (LTMR). Myelinated peripheral nerves end in specialized organs (Meisner corpuscle, Pacinian corpuscle. hair shaft structure) or dedicated terminal receptor cells-Merkel cell. Merkel cells show specialized vesicles opposite the synapse and there are also present within specialized structures. Hairy skin and palmer skin (glaborous) have distinct combinations of receptors to emphasize position, light touch (Meisner corpuscle), temperature, vibration (Pacinian corpuscle). The Pacinian corpuscle is the only one not limited to the skin and is also found in the periosteum and mesentery.


what is nociceptin?

nociceptin is a 17 aa neuropeptide spliced from prepronociceptin along with nocistatin and nocil. aa sequence similar to preproenkephalin. The nociceptin receptor (NOP), a G protein-coupled receptor that causes increased nociception. Blocking NOP has an analgesic effect. Nocistatin results in analgesia via membrane effect unrelated to NOP.