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Pathophysiology > Pain and Headaches > Flashcards

Pain and Headaches Flashcards

1
Q

What is pain?

A

unpleasant sensory component that is influenced by previous experience, emotions, gender, culture, and physical, cognitive, and spiritual factors

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2
Q

Recall the two types of pain scales often used to assess the subjective nature of pain.

A

numeric scale and visual analog scale

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3
Q

What is pain threshold and pain tolerance?

A
  • pain threshold: point at which a stimulus is perceived as pain
  • pain tolerance: duration of time or the intensity of pain that a person will endure before removal from the stimulus
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4
Q

What are nociceptors?

A

pain receptors that are free nerve endings capable of responding to several different noxious stimuli including chemical, mechanical, and thermal energy

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5
Q

What are the four main phases of nociception?

A
  1. Transduction: painful stimulus is turned into action potential energy
  2. Transmission: electrical signal is transmitted to areas of the brain and CNS that will perceive it
  3. Perception: subject becomes consciously aware that they are in pain
  4. Modulation: body attempts to modulate the symptoms of pain
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6
Q

pain transduction

A

opens sodium and calcium channels and allow nociceptors to reach threshold and create an action potential.

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7
Q

Explain what Capsaicin is and how it works.

A
  • activates ligand-gated ion (Ca2+ and Na+) channels by binding to vallanoid (VR-1) receptors
  • desensitizes pain fibers and prevents substance P from being released
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8
Q

Describe the role of Substance P/ CGRP, bradykinin, ATP, H+, K+, histamine, serotonin, and prostaglandins in the transduction of pain.

A
  • Substance P/CGRP: intracellular products that can cause depolarization. inflammation and hyperalgesia
  • Bradykinin: proteases breakdown extracellular peptide kininogen into bradykinin= depolarization
  • ATP: causes depolarization and binds directly to ATP-gated K+ ion channels
  • H+: activate acid-sensing ion channels (ASICs) in nociceptors resulting in depolarization
  • K+: when released it has a depolarizing effect
  • Histamine: binds to its receptor on nociceptors=making it more painful
  • Serotonin: binds to its receptor on nociceptors=making it more painful
  • Prostaglandin: increase the cAMP levels inside nociceptors. also reduce the threshold
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9
Q

Explain peripheral sensitization and hyperalgesia

A
  • increased sensitivity to an afferent nerve stimulus

- abnormally heightened sensitivity to pain

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10
Q

Difference between allodynia and

hyperalgesia

A

Allodynia: pain due to a stimulus that does not usually provoke pain. (light touch to sunburn)
Hyperalgesia: exaggerated pain and from a stimulus that usually does provoke some pain (slap to
sunburn)
-“postherpetic neuralgia”: damage to neurons by the herpes zoster virus

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11
Q

Describe the type of sensory nerve fibers (A-alpha, A-beta, A-delta, and C). Compare their size, speed and type of sensation they carry

A
  • A-delta: lightly myelinated and transmit pain signals quite quickly (fast pain; localized)
  • C: unmyelinated fibers that transmit action potentials relatively slowly (slow wave pain; less localized)
  • A-alpha: thickly myelinated and have a rapid conduction rate
  • A-beta: myelinated (though not quite as thick) and have also have a quick conduction rate
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12
Q

Explain the primary, secondary and tertiary order neurons involved in ascending sensory information

A
  1. Substance P, norepinephrine, and glutamate released
  2. project to the thalamus and also have collateral axons that innervate the reticular activating system (RAS) of the brainstem, which helps regulate the attention and alertness we give to the pain
  3. transmit pain signals to the somatosensory cortex
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13
Q

Explain the DCML and ALS pathways and what types of sensations are conducted by both

A

-Dorsal Column Medial Lemniscus (DCML): larger, myelinated and faster variety (A-alpha and A-beta). Sensations include textures, fine touch, vibration, two point
discrimination, and proprioception
-Anterior Lateral Spinothalamic Pathway (ALS): second order neurons synapse in the thalamus where third order neurons leave the thalamus and carry the signal to the cerebral cortex. Sensations include pressure, tickle, itch, pain and temperature

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14
Q

What things contribute to the perception of pain?

A
  • limbic system for emoting
  • neurological system for modulating the amount of pain experienced for a given nociceptive stimulus
  • anxiety and depression can make pain worse
  • pain is mental
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15
Q

How does the central nervous system (PAG, nucleus raphe magnus, and spinal cord interneurons) work to modulate pain signal input

A
  • Periaqueductal gray (PAG): has a lot of opiate receptors
  • Nucleus raphe magnus: release serotonin and sends projections to the dorsal horn of the spinal cord to directly inhibit pain
  • Spinal cord interneurons: causes inhibition of the nociceptive pain transmission onto second order neurons
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16
Q

Describe where opioid receptors are found and where opioid like molecules are released in the areas mentioned just above

A
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17
Q

Describe how the enkephalin releasing neurons in the spinal cord work to modulate pain signals

A

Interneurons receive excitatory signals (serotonin) from efferent neurons of the medulla. Then release enkephalin and bind to opioid receptors and reduce intracellular calcium.

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18
Q

Describe the DNIC modulation of pain.

A

describes how afferent pain signals coming from different areas of the body can be inhibited by one another

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19
Q

Explain the Gate-Control Theory of Pain. Explain how A-alpha and A-beta neurons can conduct signals that mitigate the pain experience

A
  • Proposes a mechanism for how pain is reduced by activating a non painful sensation.
  • primary neurons (a-delta) send signals to secondary neuron and ultimately cause a decrease in the frequency of pain signals that reach the brain.
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20
Q

Give an explanation of what causes referred pain and give examples

A

pain perceived at a location other than the site of the painful stimulus/ origin
ex. pain in the heart can be felt in the arm and chest

21
Q

Compare acute pain and chronic pain.

A

Acute: recent onset and occurs for less than 6 months
Chronic: continuous or intermittent onset and has lasted for 6 months or more

22
Q

Somatic pain

A

muscle, joint, tendon and ligament pain

23
Q

Visceral pain

A

organs, smooth muscle, body cavities, deep inside

24
Q

Superficial Pain

A

skin and mucous membranes

25
Q

Deep pain

A

tissues below skin level

26
Q

Vascular pain

A

vascular or perivascular tissue and probably accounts for the greatest percentage of migraine headache pain

27
Q

Neuropathic pain

A

results from damage to nerve fibers

28
Q

Phantom pain

A

occurs in the area of a body part that has been removed. This usually involves some type of burning, itching, tingling or stabbing

29
Q

Cancer pain

A

usually because of pressure of a tumor mass on surrounding tissues

30
Q

Central pain

A

occurs with tumors, disease or damage to central nervous tissue. Central nervous tissue itself does not have pain fibers, but the meninges, sinuses and vasculature does

31
Q

Breakthrough pain

A

pain that returns between doses of opioid drugs

32
Q

Referred pain

A

occurs when visceral nociceptors synapse and trigger ascending fibers that come from an area other than the damaged tissue area

33
Q

Recall the main categories of medication used to help relieve pain. Recall their mechanisms of action (if it is known)

A
  • Acetaminophen: affect COX enzymes in pain to reduce pain and fever
  • NSAIDS: COX-1 and COX-2 inhibitors and reduce pain and discomfort
  • Opioids: stimulate opioid receptors and inhibit pain signals
  • Local anesthetics: block voltage gated Na+ channels and prevent depolarization
  • Glucocorticoids: anti-inflammatory
  • Antidepressants: adjusting levels of neurotransmitters in the brain
  • Anticonvulsants: treat seizure disorders and could treat chronic pain
34
Q

What is the difference between primary and secondary headaches? Give examples

A
  • Primary: no structural or metabolic abnormalities (migraine, tension, cluster, and chronic daily headache)
  • Secondary: structural or metabolic abnormalities (meningitis, intracranial pressure, brain tumor, glaucoma and arteritis)
35
Q

Migraine headaches

A

more common in women and tend to run in families

36
Q

What is an aura that may precede a migraine?

A

neurological symptom that involves your vision or some other sense (zig zag lines, flashes of light that look like stars or dots, or even a blind spot)

37
Q

What are the symptoms of a migraine? Is the migraine headache bilateral or unilateral and how long do they typically last?

A
  • feeling thirsty, sleepy or craving sweets up to a few hours before
  • usually unilateral but can be bilateral and last 4-72 hours
38
Q

What are migraines accompanied with?

A

increased sensitivity to light and sound as well as nausea and vomiting

39
Q

During a migraine, which cranial nerve becomes activated?

A

trigeminal (V) cranial nerve. the nerve will release neuropeptides and neurotransmitters which will cause vasodilation and activation of nocireceptors

40
Q

How do the “triptan” drugs and “ergots” work to treat migraines?

A
  • Triptan: decrease the release of the neuropeptides from cranial nerve V, vasoconstrict
  • Ergot: same as triptan and activate alpha-1 receptors which gives an additional cerebral vessel vasoconstricting effect
41
Q

Why are they called cluster headaches?

A

headaches occur in clustered attacks that have pain free periods in between

42
Q

Describe the characteristics of cluster headaches. How long does the pain typically last and is it bilateral or unilateral?

A
  • Unilateral and lasts 15-180 minutes

- can come at regular times each day or completely random

43
Q

Do cluster headaches occur more often in men or women?

A

men

44
Q

How are cluster headaches treated?

A
  • oxygen inhalation and subcutaneous sumatriptan

- oral triptans, vasoconstrictors, corticosteroids, and anticonvulsants

45
Q

What are tension headaches?

A
  • described as dull, aching, and diffuse that occur bilaterally over the “hatband” region
  • most common and don’t interfere with daily activities
46
Q

Describe the pain distribution for these headaches

A
47
Q

What could cause tension headaches?

A
  • sustained tension in the neck and head.
  • stress, anxiety, depression
  • overuse of caffeine
48
Q

How are tension headaches treated?

A
  • relaxation

- NSAIDs, and acetaminophen

Pathophysiology (10 decks)

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