Fibromyalgia

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Fibromyalgia

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Cortisol
Hypercalcemia
Hypocalcemia
Hypoglycemics: Insulin secretagogues
Miscellaneous hypoglycemics
Skeletal muscle histology
Bone remodeling and repair
Fibrous, cartilage, and synovial joints
Cartilage structure and growth
Skeletal system anatomy and physiology
Neuromuscular junction and motor unit
Muscle spindles and golgi tendon organs
Sciatica
Rheumatoid arthritis
Psoriatic arthritis
Reactive arthritis
Ankylosing spondylitis
Dermatomyositis
Polymyalgia rheumatica
Fibromyalgia
Muscular dystrophy
Limited systemic sclerosis (CREST syndrome)
Systemic lupus erythematosus
Antiphospholipid syndrome
Scleroderma
Seronegative and septic arthritis: Pathology review
Systemic lupus erythematosus (SLE): Pathology review
Rheumatoid arthritis and osteoarthritis: Pathology review
Scleroderma: Pathology review
Myalgias and myositis: Pathology review
Glucocorticoids
Non-biologic disease modifying anti-rheumatic drugs (DMARDs)
Osteoporosis medications
Papulosquamous and inflammatory skin disorders: Pathology review
Blood groups and transfusions
Platelet plug formation (primary hemostasis)
Coagulation (secondary hemostasis)
Clot retraction and fibrinolysis
Autoimmune hemolytic anemia
Sickle cell disease (NORD)
Glucose-6-phosphate dehydrogenase (G6PD) deficiency
Hemophilia
Hemolytic-uremic syndrome
Thrombotic thrombocytopenic purpura
Heparin-induced thrombocytopenia
Von Willebrand disease
Disseminated intravascular coagulation
Factor V Leiden
Hodgkin lymphoma
Non-Hodgkin lymphoma
Chronic leukemia
Acute leukemia
Myelodysplastic syndromes
Myelofibrosis (NORD)
Polycythemia vera (NORD)
Essential thrombocythemia (NORD)
Coagulation disorders: Pathology review
Mixed platelet and coagulation disorders: Pathology review
Plasma cell disorders: Pathology review
Platelet disorders: Pathology review
Thrombosis syndromes (hypercoagulability): Pathology review
Leukemias: Pathology review
Myeloproliferative disorders: Pathology review
Anticoagulants: Heparin
Antiplatelet medications
Thrombolytics
Anatomy clinical correlates: Cerebellum and brainstem
Basal ganglia: Direct and indirect pathway of movement
Guillain-Barre syndrome
Charcot-Marie-Tooth disease
Migraine medications

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The term fibromyalgia can be broken down. Fibro- refers to fibrous tissue, -my- refers to muscle and -algia refers to pain.

Fibromyalgia is a chronic condition, which occurs more often in women, that causes widespread muscle pain, extreme tenderness in various parts of the body, and sleep disturbances.

Normally, if a person cuts their finger, a specific type of sensory neuron called a nociceptor or pain receptor, converts that stimulus into an electrical signal.

These are the first neurons and they’re primarily found in the skin, joints, or the walls of organs.

The electrical signal goes from the dendrite of the nociceptor into its peripheral axon branch and heads up the hand and arm towards its cell body.

The cell body is located in the dorsal root ganglion which is a cluster of nerve cell bodies located in a dorsal root of the spinal nerve.

The dorsal root ganglia contains the cell bodies of many sensory neurons that receive information.

So in this case, the cell body would receive the electrical signal, and if it’s strong enough, it would start to release substance P, which is a small chemical involved in pain perception.

Substance P would go down the other axon branch of the nociceptor and would get released from the neuron’s terminal button.

Substance P then binds to receptors on a second neuron which has its cell body located in the dorsal horn of the spinal cord, which makes up the back portion of the spinal cord that receives sensory information.

There is also a separate group of neurons called inhibitory neurons in the spinal cord that dampen or reduce the pain response, counteracting the effect of nociceptors.

These inhibitory neurons release neurotransmitters such as serotonin and norepinephrine and they also act on the second neuron in the spinal cord to inhibit the pain signal.

If the signal from the nociceptors is greater than the signal from the inhibitory neurons, then it triggers the second neuron in the spinal cord to fire an action potential.

This electrical signal goes all the way up the spinal cord to the brain where the pain is perceived.

So while, the pain signal races towards the brain, important events are happening in the damaged finger as well.

Epithelial cells near the damaged area start to release nerve growth factor.

That nerve growth attracts nearby mast cells which start to release even more nerve growth factor - amplifying the effect.

The high levels of nerve growth factor do a few important things to nociceptors.

It boosts the growth, makes them more sensitive to pain, and makes them produce even more substance P.

In fibromyalgia, the underlying mechanism isn’t well understood, but there seems to be a problem with how the brain receives pain signals.

Generally speaking, individuals have low levels of serotonin, which is involved in inhibiting pain signals, and elevated levels of substance P, and nerve growth factor, which are involved in propagating pain signals.

Together, these are thought to play a role in the hypersensitivity to pain, which hints that fibromyalgia might be a condition of central sensitization.

Sources

  1. "Robbins Basic Pathology" Elsevier (2017)
  2. "Role of Nerve Growth Factor in Pain" Pain Control (2015)
  3. "Spinal Cord Mechanisms of Chronic Pain and Clinical Implications" Current Pain and Headache Reports (2010)
  4. "Fibromyalgia Syndrome: Etiology, Pathogenesis, Diagnosis, and Treatment" Pain Research and Treatment (2012)