Lecture 9 (3/3) Flashcards

1
Q

what is fibromyalgia?

A

Considered a rheumatic condition
- a condition that affects the joints and/or soft tissues, causing chronic pain
- significant pain and fatigue
- generally diagnosed by a rheumatologist

But not a form of arthritis
- no inflammation or damage to joints, muscles, or tissues
- but does produce pain in soft tissues around joints and in skin and organs throughout body
- other symptoms too: cognitive (“fibro fog”), numbness and tingling

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2
Q

when and who does fibromyalgia affect?

A
  • women (6:1 or 7:1 ratio)
  • Increase with age
  • Chronic widespread pain
  • PLUS fatigue
  • No nerve damage
  • used to think it could be identified by “tender points”
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3
Q

how did doctors start believing women with fobromyalgia?

A
  • Imaging studies showed that their brain agreed with their pain description
  • Brain lighting up to much lower pressures
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4
Q

what are the 2 competing theories of fibromyalgia?

A

increased ascending transmission OR decreased descending inhibition (to explain too much pain)

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5
Q

explain Decreased Conditioned Pain Modulation in Fibromyalgia

A
  • Study showing that compared to normal women fibro women have impaired conditioned pain modulation
  • Done by cold pressure test (conditioned stimulus)
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6
Q

explain fibro and nociceptor endings

A

Take biopsies of skin and stain them
- Fibro have lower density of nociceptor endings as if they have neuropathy that is selectively affecting very small fibers like nerve ends
- Serves as example of just because we can’t see something in our scans, it doesn’t mean there isn’t a problem
- Saying things are due to psychosocial factors is giving up on treatment

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7
Q

what is idiopathic?

A

don’t know the cause of

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8
Q

why does IBS people have lower heat pain threshold?

A

Because IBS peeps also might have fibro
- why they got diagnosed with IBS and not fibro: They went to a specialist first and minimized or completely ignored other parts of the body in pain

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9
Q

what are the 4 types of headache?

A
  • sinus: pain is behind browbone and/or cheekbones
  • cluster: pain is in and around one eye
  • tension: pain is like a band squeezing the head
  • migraine: pain, nausea, and visual changes
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10
Q

how long do migraines last?

A

4-72 hours

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11
Q

difference between tension and migraines

A

Tension: activity wont make it any worse

Migraine: pulsating, more severe, unilateral, activity makes it worse, photo and phono phobia (sensitivity to light and sound)
- What makes them particularly disabling
- Nausea and vomiting

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12
Q

explain the 4 stages of migraines

A

STAGE 1: prodome - early photo and phono phobia, irritability, etc.
STAGE 2: aura - occurs right before headache starts
STAGE 3: headache itself
STAGE 4: postdrome- Headache gone, but more like a hangover

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13
Q

what are migraine triggers?

A
  • Highest for stress
  • debate over triggers – since it never happens in the lab when they try to recreate triggers, leading researcher to believe triggers to be a nocebo
  • Nitroglycerin (TNT) will 100% give a migraine within an hour of injection
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14
Q

what is the cause of migraines?

A

Vasodilation or Neuronal?
- we still don’t know

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15
Q

what is an aura caused by?

A
  • Caused by cortical spreading depression – wave of electrical excitability that starts at back of brain and waves forward
  • How do they know? The speed that aura moves is the same speed that cortical depression moves
  • Debated: whether it doesn’t or does cause pain
  • Only 20% of migraines get auras
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16
Q

what are triptans?

A
  • pretty effective, therapeutic gain at 2hrs is equivalent to the drop in pain levels at percentage terms
  • 15-45%
  • Problem; migraine has already started, it just makes it better
17
Q

what is Prophylactic?

A

what you can do to prevent migraine from happening
- Successful one would reduce the number of migraines per month
- Drugs used on the slide

18
Q

what are migraine treatments?

A
  • Big advance: CGRP drugs (all antagonists)
  • Mavs used prophylactically (state of the art), and oral CGRP are used in pill form for acute
  • Mavs used to prevent, but if they start, oral CGRPs are used