Sensory Physiology Flashcards

1
Q

What is the primary process by which sensory receptors convert external stimuli into electrical signals?

A

Sensory transduction involves stimulus-gated ion channels that open in response to mechanical, thermal, or chemical stimuli, leading to graded receptor potentials that may trigger action potentials.

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2
Q

What are the main types of sensory receptors and their functions?

A

• Mechanoreceptors – Touch, vibration, proprioception
• Thermoreceptors – Temperature changes
• Nociceptors – Pain perception
• Chemoreceptors – Taste, smell, chemical detection
• Photoreceptors – Vision (rods/cones)

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3
Q

What are the two major pathways for somatosensory information, and what do they carry?

A

• Dorsal column-medial lemniscus (DCML) – Fine touch, vibration, proprioception
• Spinothalamic tract (STT) – Pain, temperature, crude touch

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4
Q

What is the function of the thalamus in sensory perception?

A

The thalamus acts as a relay center for sensory input (except smell) before sending signals to the primary somatosensory cortex.

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5
Q

What is the difference between rapidly adapting and slowly adapting receptors?

A

• Rapidly adapting receptors (phasic) – Respond to stimulus onset and offset (e.g., Meissner corpuscles)
• Slowly adapting receptors (tonic) – Respond continuously to stimuli (e.g., Merkel cells)

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6
Q

What are the two types of thermoreceptors, and how do they function?

A

• Cold receptors (Aδ and C fibers) – Activate at lower temperatures
• Warm receptors (C fibers) – Activate at higher temperatures
• Paradoxical cold response – Extreme heat (>45°C) can activate cold receptors

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7
Q

What are the two primary types of pain fibers, and what do they transmit?

A

• Aδ fibers – Fast, sharp, localized pain (first pain)
• C fibers – Slow, dull, burning pain (second pain)

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8
Q

How do peripheral and central sensitization contribute to chronic pain?

A

• Peripheral sensitization – Increased nociceptor sensitivity due to inflammatory mediators (prostaglandins, bradykinin).
• Central sensitization – “Wind-up” phenomenon causes spinal neurons to become hyperexcitable.

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9
Q

How does the gate control theory explain pain modulation?

A

• Non-painful stimuli (Aβ fibers) activate inhibitory interneurons, which suppress pain transmission in the spinal cord, “closing the gate.”

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10
Q

What brain regions are involved in endogenous pain modulation?

A

• Periaqueductal gray (PAG) – Releases endorphins, modulates pain
• Rostral ventromedial medulla (RVM) – Regulates pain inhibition/excitation
• Dorsolateral pontine tegmentum – Inhibits spinal pain transmission

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11
Q

What is the difference between hyperalgesia and allodynia?

A

• Hyperalgesia – Increased pain perception from normally painful stimuli
• Allodynia – Pain in response to non-painful stimuli (e.g., light touch)

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12
Q

What are key inflammatory mediators that increase pain perception?

A

• Prostaglandins – Increase nociceptor sensitivity
• Bradykinin – Directly stimulates pain receptors
• Substance P – Enhances pain transmission in spinal cord
• Histamine – Released by mast cells, contributes to pain and itch

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13
Q

What causes neuropathic pain, and how is it different from nociceptive pain?

A

• Neuropathic pain results from nerve damage (e.g., diabetes, nerve injury).
• Characterized by burning, tingling, or electric shock-like pain.
• Unlike nociceptive pain, it persists without a noxious stimulus.

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14
Q

How do opioids reduce pain perception?

A

Opioids (e.g., morphine) bind to μ-opioid receptors in the brainstem, spinal cord, and peripheral nerves, inhibiting neurotransmitter release (e.g., glutamate, substance P) and reducing pain transmission.

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15
Q

What mechanisms explain phantom limb pain?

A

• Cortical reorganization – The brain remaps the missing limb’s sensory representation.
• Peripheral nerve hyperactivity – Spontaneous firing from severed nerves contributes to pain perception.

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