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1. Rheum RC > Fibro / CRPS > Flashcards

Fibro / CRPS Flashcards

1
Q

** Fibro sx **

A

Arthralgia/myalgia/stiffness
-Muscle spasm
-Paresthesia

-Fatigue
-Sleep disturbance
-Nonrestorative sleep

-Cognitive problems (Fibrofog)
-Mood disorder

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2
Q

** Prevalence
–Fibro
– SLE w/ Fibro
–Chance of work disability**

A

3%
~30%
~30%

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3
Q

** Fibro workup **

A

CBC, ESR, CRP, TSH, 25-hydroxy vitamin D and CK
-Further testing based on clinical assessment.

-No serologies unless objective synovitis or inflamm markers elevated

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4
Q

** FM diagnostic criteria**

A

ACR 2010
-WPI ≥ 7 + SS ≥ 5 OR WPI 4-6 + SS ≥ 9
-Symptoms >3mo
-No other explanation

-2016 Revision added:
-Generalized pain = at least 4/5 must be present: left/right upper/lower, axial
-(**jaw, chest, abdo NOT included in definition)
-Dx of Fibro valid irrespective of other dx and does not exclude presence of other illness

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5
Q

Items in symptom severity score

A

Fatigue (0-3 pts)
-Waking unrefreshed (0-3 pts)
-Cognitive sx (0-3 pts)

-Somatic symptoms (H/A, abdo pain/cramps, depression) - 1 pt each

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6
Q

** Co-existing conditions with FM**

A

-Migraine/Tension H/A
-TMJ d/o
-IBS
-Urinary freq/urg
-Chronic pelvic pain
-RLS

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7
Q

Sleep disturbance assoc/d w/ FM

A

Alpha delta sleep = disruption of delta wave sleep by frequent alpha wave intrusion (reducing restorative nonREM stage 4 sleep)

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8
Q

** RF Fibro**

A

Biologic:
-Genetics
-Female
-Lack of exercise
-Sleep abnormalities
-Autonomic dysregulation: POTS

Environmental:
-Sexual/Physical abuse as child
-Job dissatisfaction
-Poor support system

Psych:
-Psych traits: perfectionists, catastrophizing, preoccupation w/ pain, poor coping mech, A&D

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9
Q

** Draw trigger points for fibro**

A

The 18 tender points for fibromyalgia include:
-Base of the skull in the back of the head
-Lower neck in front
-Back of the neck
-Back of neck/shoulders
-Edge of upper breast
-Lateral epicondyle
-Upper outer buttock
-Hip bone - posterior to greater trochanter
-Knee - medial fat pad proximal to joint line

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10
Q

** FM triggers**

A

-Early stress (life trauma)
-Acute stress (eg MVA)
-Chronic distress
-Catastrophic events (life/war)
-Sleep apnea
-Joint inflammation

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11
Q

DDx FM

A

Rheum: RA, SLE, SS, Sjogrens, PMR, AS
Endocrine: hypothyroid, hyperPTH, adrenal insuff
Myopathy (metabolic, statin)
GI: IBD, Hep C, celiac
Infxn: IE, lyme, HIV, parvo
Neuro MS, MG,
Cancer
Sleep apnea
Psych disorders

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12
Q

** Fibro /CRPS pathophys - mechanism of peripheral sensitization**

A

-Prolonged noxious stimulation (eg whiplash) causes peripheral nociceptors (previously silent polymodal C fibers) to become responsive → spontaneous signalling recognizing non-noxious stimuli as noxious due to lower threshold

-Decreased NE metabolites in CSF affects pain inhibition

-Decreased dopamine in CSF affects pain inhibition

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13
Q

** Fibro /CRPS pathophys - mech of central sensitization**

A

Wind up
–Following peripheral sensitization, persistent nerve impulses to the dorsal root of the spinal cord cause release of glutamate to act on NMDA and release inflammatory neuropeptides (eg substance P) that decrease threshold for excitability (i.e. windup)

Neuroplasticity
–More neurons transmitting pain signals expands receptive fields in the brain

Changes to brain structure
–Decreased blood flow to the thalamus and caudate nucleus (areas of brain that signal noxious stimuli)
–Increased blood flow to the insula, anterior cingulate cortex and primary/secondary somatosensory cortices (areas involved in pain perceptions, emotional modulation from any cause of chronic pain)

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14
Q

Fibro CNS pathophys evidence

A
  • Increased excitability of dorsal horn nuclei (windup) -
  • Expanded receptive fields for central pain perception
  • Increased substance P, glutamate, and aspartate in CSF
  • Decreased antinociceptive neurotransmitters eg NE, serotonin, and DA
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15
Q

** FM Nonpharm Tx**

A

Education
-Analgesia
-PT/Aerobic/Strength Training Exercise (endorphins, less microtrauma)
-Treat assoc’d: mood, sleep hyiene, IBS, migraine
-CBT
-Heated pool

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16
Q

** FM Pharm Tx and doses **

A

SNRI
– Duloxetine (20-60mg/d),
– Milnacipran (12.5mg daily → 50mg BID) for fibrofog/fatigue
– Venlafaxine (37.5mg daily → 75-150mg BID)
– **Tramadol **

– SSRI: fluoxetine, duloxetine

-Anticonvulsant
–Pregabalin (50qhs→ BID→ 75-150BID)
–Gabapentin (300-600TID)

-TCAs:
– Amitriptyline 10-25mg qhs
– Nortryptyline
– Cyclobenzaprine

-Others:
– Modafinil - for fatigue
– Trazodone - for sleep
– Naltrexone - for pain/mood
– Pramipexole

-Trigger point injxn w/ lidocaine +/- GC

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17
Q

TCA side fx

A

Anticholinergic/ antihistamine:
–drowsy, dry mouth, constipation

18
Q

SNRI side fx

A

Suicidal ideation,
-Serotonin syndrome

19
Q

Anticonvulsant side fx

A

fatigue, dizziness

20
Q

** List 3-4 mechanisms by which tricyclic antidepressants may improve fibromyalgia? Ie TCA eg duloxetine MOA **

A

Inhib uptake of serotonin (5HT) and norepinephrine at synapse:
-Improves stage 4 sleep
-Treats comorbid depression/anxiety

-Activating descending pathways to decrease pain
-Inhib NMDA R and block Na/Ca channels for peripheral analgesia
-Potentiate endogenous opioids

21
Q

** Anticonvulsants (Gabapentin,pregabalin) MoA **

A

Bind to the voltage-gated Ca channels (preventing Ca influx) to decrease release of excitatory neurotransmitters (glutamate, substance P)

22
Q

** List 5 drugs with evidence used in the treatment of fibromyalgia?**

A

SSRI
-SNRI
-TCAs
-Gabapentin
-Tramadol

23
Q

** SNRI MoA**

A

Same as TCA
-Inhib uptake of serotonin (5HT) and norepinephrine at synapse, activating descending pathways to decrease pain

24
Q

** Tramadol MoA**

A

Analgesia most likely from SNRI fx and NOT weak binding to mu opioid receptor

25
Q

** Cannabinoid MoA**

A

CB1 receptor in PNS and CNS; CB2 R on inflammatory cells

– Activation DECREASES dorsal horn excitability and proinflammatory peptide release
– Activates descending inhibitory pain pathways

26
Q

** Opioid MoA**

A

Opiod R close Ca channel and stimulate K efflux to cause hyperpolarization to decrease neuronal excitability and blocking pain signals and NT release (eg glutamate, substance P)

27
Q

** Evidence of narcotics in chronic pain **

A

-Cochrane = No evidence to support oxycodone use in FM
-2017 Canadian guidelines showed no difference in pain control or function
- Only if nonopioids maximized w/ ongoing pain
- NOT IF substance use d/o

-Tramadol analgesia via SNRI fx not weak binding to mu opioid R
-Mu opioid R are downregulated in brains of people w/ FM

-Start w/ no more than 90mg morphine daily

28
Q

** CRPS types and difference **

A

MC = Type 1 (reflex sympathetic dystrophy) = NO peripheral nerve injury

-Type 2 (causalgia) = WITH peripheral nerve injury

29
Q

** Manifestations of CRPS **

A

Eg Hand pain, swelling, cool hand, hyperhidrotic

-Ipsilateral limb involvement (eg shoulder hand)
-Extremity pain/swelling/limited ROM
-Skin atrophy/texture/pigment/hair change
-Nail change

-Vasomotor instability (unusual sweating, blue/cool, or red/warm)

-Motor findings: weakness/neglect, pseudoparalysis, dystonia, spasms/Myoclonus, contracture, tremor

30
Q

Allodynia vs Hyperpathia

A

Allodynia - pain from nonnoxious stim
-Hyperpathia - prolonged pain on stimulation

31
Q

** Diagnostic criteria for CRPS **

A

Budapest criteria (all must be met)
– Continuing pain disproportionate to cause
– NO other cause that could explain
– 1 symptom in 3 of 4; and 1 sign in 2 of 4:

1) Sensory: hyperesthesia (pinprick) or allodynia (light touch)
2) Vasomotor: asymmetry temperature (>1C)/skin color change
3)Sudomotor/edema: edema, sweating changes
4) Motor/trophic: decreased ROM, motor dysfcn (tremor, weakness, dystonia), or trophic changes (hair, skin, nail)

32
Q

CRPS precipitating factors

A

-Fractures, immobilization
-Peripheral/central nerve injury
-Trauma: contusion, crush, laceration, burns
-Strokes/MI
-Drugs
-Pregnancy
-Cancer

33
Q

CRPS RF

A

-Endocrine: DM, DLPD, HyperPTH, Hypothyroid
-Neuro: MS
-Drugs: ACEi, ETOH, smoking,
-LBP

34
Q

** CRPS stages, duration and manifestations**

A

1 (acute) - 6-12mo: pain/swelling, color change, early OP

-2 (dystrophic)1-2y: pain, skin hardens (brawny edema), muscle atrophy, bone osteopenia

-3 (atrophic): stiffness → limited ROM, periarticular thickening, smooth/glossy skin, brittle nails, muscle spasms, dystonia, tremor, OP → #, ankylosis

35
Q

DDx CRPS (tender/swollen limb)

A

Arthritis, SSc
-Cellulitis, OM
-DVT, #,
-Compartment syndrome
-Cancer, pancoast
-Osteonecrosis
-Angioedema

36
Q

** XR findings CRPS**

A

Soft tissue swelling & regional patchy/mottled osteopenia
-(aka sudeck’s atrophy)

37
Q

** Diagnostic test CRPS - Three phase bone scan (TPBS) results by stage**

A

1: increased blood velocity/pooling.
– Early & delayed hyperfixation w/ increased radiotracer uptake
–AbN scan in 80%

-2: normal blood velocity/pooling.
–Persistent early & delayed hyperfixation
–AbN scan in 50%

-3: reduced blood velocity/pooling. Often normal scan.

38
Q

Other tests supporting CRPS dx

A

Autonomic testing (sweat output, skin temp, axon reflexes)
-Stress thermography w cold exposure
-Sympathetic nerve block (confirms pain is sympathetic nervous system driven)

39
Q

How does ACEi cause CRPS

A

ACEi block normal metab of neuropeptides (substance P)

40
Q

** CRPS Tx**

A

Bold = stronger evidence

Spinal Cord stimulation (stim inhibitory neurons)

PT, massage, US, electroacupuncture, transcutaneous nerve stimulator

Antiinflam: NSAID, Ketorolac, Steroids

Sympathetic block: lidocaine/bupivcaine into sympathetic ganglion, Bier block, alpha1 adrenergic blocker (eg prazocin, terazosin, phentolamine), sympathectomy

Anticonvulsants: phenytoin, carbamazepine, gabapentin/pregab, valproate

AntiOP: calcitonin, bisphosphonates

Dystonia: Intrathecal GABA Ag (baclofen) or local botux injxn

Other:
IV lidocaine or IV ketamine (blocks NMDA R)

Psych: CBT, thermal biofeedback, relaxation training, smoking/EtOH cessation

41
Q

**CRPS approach **

A

Multidisciplinary approach
-Education regarding their disease
-PT, OT and psychological support

Early CRPS (<3 to 6 months) with pain, swelling and a positive bone scan should be treated with Prednisone (60 to 80mg daily) for 2 weeks with subsequent taper over 4 weeks.

Analgesics (choice depends on severity and quality of pain: Opioids, NSAIDs, TCAs, gabapentin, carbamazepine

If severe (pain w/ rest/movement), more aggressive therapy: eg sympathetic blocks

Treatment resistant or prolonged:
– Epidural spinal cord stimulator can be used and will reduce pain by 50% in 50% of patients
– IV Ketamin
–IVIg

42
Q

** 2 types of pain, describe differences, and 1 tx for each**

A

Nociceptive
–Precipitated by actual tissue damage (nociceptors)
– Acute or chronic
– Pain: throbbing, aching, pressure (eg visceral / inflammatory / mechanical/ compressive pain),
– No allodynia or hyperalgesia
– Uncommon autonomic signs
– Tx: NSAID, Tylenol, Opioid > TCA

-Neuropathic:
– CHRONIC pain from nervous system lesion/dysfunction
– Pain: burning, shooting pain,
– Allodynia, hyperalgesia
– Autonomic: color/temp change, sweating
– Tx: gabapentin, pregabalin, TCA useful > NSAIDs or opioids
–Sympathetic blocks, TENS, acupuncture

1. Rheum RC (23 decks)

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