Lecture 7 (Quiz 2) Flashcards Preview

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What part of the body doesn't have pain receptors?

- Brain


What is unpleasant sensory and emotional experience associated with actual or potential tissue damage? What are the three elements of pain?

- Pain
- Sensory, cognitive, emotional/affective


What is the physiological process by which information on actual/potential tissue damage is conveyed to the CNS? What are specialized ion channels on sensory nerve endings that respond to noxious stimuli? What is pain resulting from activation of nociceptors as a result of actual or potential tissue damage and processing by the CNS? What is a pathophysiological process, resulting from abnormal sensory processing, does not signal actual or potential tissue damage, does not promote healing/repair, and may be considered a disease?

- Nociception (response to harm/pain)
- Nociceptors
- Nociceptive Pain
- Neurogenic / Neuropathic Pain


What is pain associated with musculo-skeletal system and skin, and is also well defined? What is pain associated with internal organs and associated tissues, and is a dull, burning and is poorly defined? What is a selective reduction of pain perception without affecting other sensory modalities? What is absence of any sensation due to suppression of CNS function?

- Somatic Pain
- Visceral Pain
- Analgesia (Pain medications)
- Anesthesia (General and Local Anesthesia)


There are four basic processes in Nociception signal transmission. What are they starting from the initial pain signal to the brain? At what point would a Local Anesthetic or other Anesthetic be the most effective?

- Transduction (Skin pain receptor)
- Transmission (From the receptor to the spinal chord, near the ganglia)
- Modulation (Spinal chord)
- Perception (Brain)
- Transmission section


What are the specific ion channels on free nerve endings that respond to the actual or potential tissue trauma? What are the 4 types of stimuli / transducers are measured by these nociceptors? What 2 types of receptors do these transducers stimulate? _______ in an ingredient that is commonly found in peppers and is what is used in pepper spray. This acts on what polymodal nociceptor? What does this polymodal nociceptor act on to deplete the mediators of pain and cause a numbing effect?

- Transduction Nociceptors
- Mechanical, Chemical, Thermal and Polymodal (a combination of the other 3 transducers)
- TRP (Transient Receptor Potential) and P (Prostaglandin, Purino, Pyrimidine) Receptor types.
- Capsaicin
- TRPV1 (Polymodal receptors)
- Substance P (mediator for TRPV1)


Nociceptors use chemical messengers to activate more nociceptors (positive feedback). What is released during the inflammation to cause this nociceptor to be triggered and pain to be felt at the spot of inflammation? What is released by these Nociceptors to continue the inflammation until adequate healing has occurred? Where do these signals propagate before going to the spinal cord? What is this increased sensitivity and response to stimuli in and near an injured area called?

- Bradykinin
- Substance P (mediator for TRPV1)
- Dorsal Root Ganglion
- Sensitization


Sensitization is the increased sensitivity/response to a stimuli near the injured area. What is the increased perception of pain in response to painful stimuli? What is pain evoked by normally non painful stimuli? What are the two major candidates for sensitization? How do Prostaglandins stimulate the excitation of Nociceptors?

- Hyperalgesia
- Allodynia
- Substance P (SP): From nerve endings, and Prostaglandins (PGs): From damaged cells.
- PGs get stimulated which activate specific Na+ channels and make nociceptors more excitable.


What are the two main generators for Prostaglandins? What differentiates COX-1 and COX-2? (Constitutive vs Inducible, inhibited by, causes/effects)

- COX-1 and COX-2
- COX-1: Constitutive (always on/there) in many tissues. Inhibited by NSAIDS (Aspirin), Effects: GI cytoprotection, Platelet aggregation, Renal electrolyte homeostasis, Renal blood flow maintenance. (Is also the basis of some adverse effects of NSAIDS such as bleeding and stomach irritation.) and Pain, Fever and Inflammation.
- COX-2: Partially Constitutive and partially Inducible. Inhibited by NSAIDS (Aspirin) and COX-2 inhibitors (Celebrex). Effects: Constitutive: Renal electrolyte homeostasis, Renal blood flow and Cardiovascular Protection. Inducible: Pain, Fever and Inflammation.


How do NSAIDS cause an Anti-Nociceptive (Nociception Antagonist) effect?

- NSAIDS inhibit the synthesis of Prostaglandins that are involved in sensitizing the nociceptor nerve ending.


Nociception transmission to the spinal cord occurs via 2 axons (Alpha-Delta, and C Axons). What makes these axons different? (Size, myelinated, type of pain)

- Alpha-Delta Axons: Small, myelinated, fast conducting "first" or "fast" pain, associated with Mechanical and Thermal nociceptors.
- C Axons: Small, unmyelinated, slow conducting "slow" or "second" pain, associated with Polymodal nociceptors.


What are the plexus of nerves associated with dental nociception in the tooth called? Where does this nerve receive its sensory and sympathetic sensation from?

- Plexus of Raschkow (Sub-Odontoblastic Plexus)
- Sensory: Trigeminal nerve, Sympathetic: Superior cervical ganglion.


Modulation or the initial synapse of the nociceptive fibers into the spinal cord occurs on which part of the spinal cord? At this step, what are the important pain neurotransmitters? As the neurons ascend up the spinal cord, they cross the midline (contralaterally) in the _________ tract. What acts as the major Somatosensory relay in the brain? What nucleus inputs into the Thalamus? Once the signal enters the thalamus is sent to the somatosensory cortex and into what area?

- Synapse with Projection neurons in the Dorsal Horn.
- Glutamate and Substance P.
- Spinothalamic tract
- Thalamus
- Trigeminal Nucleus
- Limbic


Where does Nociceptive input (either facilitory or inhibitory) occur and therefor also the best places for analgesic drugs?What is it when the dorsal horn projection neurons also become sensitized and hyper-responsive to nociceptive input which contributes to hyperalgesia and allodynia (touch input)? What are thought to be involved in this?

- Dorsal Horn of the spinal chord
- Central Sensitization
- Prostaglandins


What are the major sites of Opioids, NSAIDS and Analgesic drugs?

- The Dorsal Horn of the spinal cord and Periacqueductal Gray.


Strong touch stimulation can sometimes inhibit nociception, what is this called? (Alpha-Delta and C fibers [nociception] battle with Alpha-Beta [propioception] to send the signal to the brain)

- Gate Control


What is it when visceral afferent nociceptors converge on the same pain-projection neurons as the afferents from the somatic structures in which the pain is perceived and the brain cannot distinguish the origin? (Sinusitis and dental pain)

- Referred pain


The body has a system to shut off pain in times of distress, what is this system called? The key locus is mesencephalic ________ _____ and _______ containing neurons.

- Endogenous Pain Suppressant Neural System
- Mesecephalic Periacqueductal Gray
- Enkephalin Containing Neurons (5HT and NE)


There are three types of Endogenous Opioid Peptides / Endorphins that act and inhibitors of the feedback system to cut out pain, what are they and how big are they? **(Mu and Delta drugs can have addictive properties, whereas Kappa does not)

- Enkephalin (Mu and Delta): 5 Amino Acids
- Beta-Endorphin (Mu and Delta): 91 Amino Acids
- Dynorphins (Kappa): 17 Amino Acids (Not addictive)


Drugs that enhance the action of ___ and ___ have Anti-Nociceptive effects.

- NE and 5HT (Serotonin)


What is a pain sensation that may be continuous or periodic but occur without activation of nociceptors or potential tissue damage where hyperalgesia and allodynia are common? What are some examples of this? What drugs can be somewhat effective against this?

- Neuropathic Pain
- Phantom limb, diabetes neuropathies, shingles, trigeminal neuralgia and fibromyalgia.
- Antidepressants (cymbalta), anticonculsants (lyrics and gabapentin) and corticosteroids.


What is the role of a Placebo?

- Causes an endogenous analgesia most likely due to a release of endorphins.


Hyperalgesia (increased perception of pain) and Allodynia (pain from normally non-painful stimuli) are both types of Sensitization (increased sensitivity and response to an area where an injury has occurred). What type of Transduction Nociceptor messengers cause this Sensitization?

- Chemical Messengers (Substance P and Prostaglandins)


Nociceptors that deal with visceral pain are activated by what?

- Mechanical Stimulation (This is what also may cause referred pain)


There are two types of nerve fibers related to pain (Alpha-Delta and C fibers), what makes them different? (Size, myelinated, type of pain). What are Alpha Beta receptors used for?

- Alpha-Delta Fibers: Larger in diameter, Myelinated, fast conducting associated with sharp/localized pain when Dentin is initially exposed.
- C-Fibers: Unmyelinated, slower conducting and smaller in diameter, associated with conducting a dull/diffuse pain.
- Alpha-Beta: Largest, fastest, most myelinated. Used for propioception (touch/feel)


What are the two main chemical messengers that cause the excitation of pain receptors (nociceceptors) and allow for the signal of pain to be sent? How is this done?

- Prostaglandins and Substance P
- PGs and Substance P act on receptors which causes the Na+ channels to open, and this influx of Na+ make the nociceptors more excitable.