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Physio: 1# Pain Sensation
Q1. Which characteristic best distinguishes fast pain from slow pain?
Transmission via unmyelinated C fibers
Localization and conduction through neospinothalamic tract
Association with emotional unpleasantness
Activation mainly by chemical mediators
Explanation:
Fast pain is well localized, conducted by Aδ fibers, and transmitted through the neospinothalamic tract, conveying precise information about pain quality and location.
Q2. Which neurotransmitter is primarily responsible for fast pain transmission in the dorsal horn?
Glutamate
Substance P
GABA
Serotonin
Explanation:
Fast pain fibers (Aδ) release glutamate, which acts on NMDA receptors to rapidly excite second-order neurons.
Q3. Which lamina of the dorsal horn is most associated with slow chronic pain transmission?
Lamina I
Lamina V
Lamina II (substantia gelatinosa)
Lamina III
Explanation:
Slow pain (C fibers) synapses mainly in lamina II, which plays a major role in pain modulation and gating.
Q4. Bradykinin contributes to pain primarily by:
Direct inhibition of pain fibers
Blocking NMDA receptors
Enhancing opioid receptor sensitivity
Direct excitation of nociceptors during tissue injury
Explanation:
Bradykinin is the most important chemical mediator directly exciting pain endings during tissue damage.
Q5. Which statement about pain receptors is TRUE?
They adapt very little or not at all
They are encapsulated receptors
They respond only to mechanical stimuli
They adapt rapidly to persistent injury
Explanation:
Pain receptors are free nerve endings that show minimal adaptation, ensuring continuous awareness of injury.
Q6. Pain perception begins when skin temperature exceeds:
40°C
45°C
50°C
55°C
Explanation:
Pain is perceived when tissue damage begins, which occurs when temperature exceeds approximately 45°C.
Q7. Which neuron type responds to both noxious and non-noxious stimuli?
Nociceptive specific neurons
C-fiber neurons
Wide dynamic range neurons
Spinothalamic projection neurons
Explanation:
WDR neurons receive input from Aβ, Aδ, and C fibers and respond to both painful and non-painful stimuli.
Q8. Which condition represents pain from a normally non-painful stimulus?
Allodynia
Hyperalgesia
Referred pain
Neuropathic pain
Explanation:
Allodynia is pain elicited by stimuli that do not normally provoke pain, such as light touch.
Q9. Secondary hyperalgesia is characterized by:
Thermal hyperalgesia at injury site
Inflammation-mediated pain only
Increased chemical sensitivity
Mechanical hyperalgesia outside the injury
Explanation:
Secondary hyperalgesia occurs in non-injured tissue and is mechanical in nature.
Q10. Visceral pain is poorly localized because:
Viscera lack nociceptors
Visceral afferents converge with somatic afferents
Pain fibers bypass the spinal cord
It travels only via C fibers
Explanation:
Visceral and somatic afferents synapse on the same second-order neurons, leading to poor localization.
Q11. Which stimulus most reliably produces visceral pain?
Cutting the gut
Localized mucosal injury
Overdistension of hollow organs
Superficial inflammation
Explanation:
Diffuse stimuli like ischemia and overdistension strongly activate visceral pain receptors.
Q12. Which fibers close the pain gate in gate-control theory?
Large diameter Aβ fibers
Aδ fibers
C fibers
Spinothalamic fibers
Explanation:
Activation of large Aβ fibers stimulates inhibitory interneurons in substantia gelatinosa, closing the gate.
Q13. The periaqueductal gray (PAG) produces analgesia by:
Blocking thalamic relay
Inhibiting Aβ fibers
Destroying dorsal horn neurons
Activating descending inhibitory pathways via NRM
Explanation:
PAG excites nucleus raphe magnus neurons, which descend to inhibit pain transmission in the dorsal horn.
Q14. Which opioid receptor is primarily associated with endorphins?
δ
μ
κ
σ
Explanation:
Endorphins exert their analgesic effect mainly through μ-opioid receptors.
Q15. Capsaicin relieves pain primarily by:
Blocking sodium channels
Enhancing serotonin release
Depleting substance P from nerve endings
Inhibiting prostaglandin synthesis
Explanation:
Capsaicin depletes substance P, reducing peripheral pain signaling.
Q16. Removal of somatosensory cortex causes:
Loss of pain quality discrimination
Complete analgesia
Loss of pain perception
Loss of affective pain
Explanation:
Pain is still perceived, but cortex is needed for accurate localization and quality assessment.
Q17. Neuropathic pain commonly involves:
Only inflammatory mediators
Pure Aβ fiber dysfunction
Loss of nociceptors
Dysesthesia and allodynia
Explanation:
Neuropathic pain results from damage to the somatosensory system and features abnormal sensations.
Q18. Which neurotransmitter in descending pathways is most potent in activating inhibitory interneurons?
Noradrenaline
Serotonin
Dopamine
Glycine
Explanation:
Serotonin from NRM activates inhibitory interneurons more powerfully than noradrenaline.
Q19. Visceral pain differs from somatic pain by being:
Sharp and well localized
Unaffected by ischemia
Associated with autonomic symptoms
Transmitted only by Aδ fibers
Explanation:
Visceral pain is colicky, poorly localized, and often accompanied by nausea and autonomic disturbances.
Q20. The IASP definition of pain emphasizes:
Both sensory and emotional components
Only tissue damage
Purely subjective experience
Only nociceptor activation
Explanation:
Pain is defined as an unpleasant sensory and emotional experience related to actual or potential tissue damage.