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May 2015: Post summaries and take home points

Deconditioning, orthostatic intolerance, exercise and chronic illness: Part 1

  • Deconditioning is when the body becomes acclimated to less physical stress and becomes less able to function properly under normal conditions.
  • Bed rest can cause deconditioning.
  • The cardiovascular system changes within 24 hours of bed rest.
  • In less than a week, 10% of blood volume is lost.
  • When deconditioned, your body does not make appropriate changes when changing position.
  • This is called orthostatic intolerance (OI).
  • Chronic illness can cause deconditioning.

Deconditioning, orthostatic intolerance, exercise and chronic illness: Part 2

  • Orthostatic intolerance(OI) is symptoms that interfere with or prevent standing up.
  • OI affects heart rate, blood pressure and distribution of blood to the brain.
  • In OI, the body incorrectly initiates a fight or flight response.
  • Orthostatic hypotension is a reduction of systolic blood pressure of more than 20 mm Hg or diastolic blood pressure of more than 10 mm Hg within three minutes of standing.
  • POTS patients have daily OI symptoms with excessive tachycardia when standing (increase of 30 bpm when standing or over 120 bpm in adults).
  • Postural syncope (fainting) can be caused by orthostatic intolerance or vasovagal syncope (VVS).
  • Fainting is caused by lack of blood flow to the brain.
  • Mast cell disease is known to cause orthostatic intolerance.

Deconditioning, orthostatic intolerance, exercise and chronic illness: Part 3

  • POTS (postural orthostatic tachycardia syndrome) is one type of orthostatic intolerance (OI).
  • POTS is characterized by an increase of heart rate of 30 bpm or more when standing in the absence of orthostatic hypotension.
  • Neuropathic POTS is caused by the veins in the legs not constricting enough to maintain blood pressure when standing.
  • Hyperadrenergic POTS is caused by the nervous system telling the heart to beat faster and harder.
  • HyperPOTS patients have fluctuating or elevated blood pressure, tachycardia, hypertension and excessive sweating.
  • One study found that 38% of mast cell patients had hyperPOTS.
  • One study found that 28.9% of POTS patients had less blood volume than normal.
  • POTS patients have persistent tachycardia, push less blood out of the heart per beat than normal, have a smaller than normal part of the heart, and do not use oxygen effectively during exercise.
  • POTS is often associated with conditions that provoke exercise intolerance, like fibromyalgia, chronic fatigue syndrome and deconditioning.

Deconditioning, orthostatic intolerance, exercise and chronic illness: Part 4

  • Syncope (fainting) is loss of consciousness due to temporary loss of blood supply to the brain.
  • About 40% of people will faint in their lifetime.
  • Vasovagal syncope(VVS) is a form of orthostatic intolerance (OI).
  • VVS is often preceded by lightheadedness, sweating, weakness, nausea and visual disturbances.
  • VVS patients can go long periods without OI symptoms.
  • Ingestion of 16 oz of water in five minutes effectively treats OI episodes of all types.
  • OI symptoms can be triggered by large meals, sudden change in position, extended time laying down, heat and alcohol.
  • Physical maneuvers and compression garments can decrease OI symptoms in some patients.
  • Increasing salt and water intake is recommended for adults with orthostatic hypotension or POTS.

Deconditioning, orthostatic intolerance, exercise and chronic illness: Part 5

  • Deconditioning and physical inactivity increase risk for cardiovascular disease.
  • A person can lose 10-20% of muscle strength in one week of bed rest.
  • Muscle loss is greatest in lower back and legs.
  • After three days of bed rest, connective tissue and muscles begin to contract.
  • Osteoporosis is more likely in deconditioned patients.
  • After twelve weeks of bed rest, almost 50% of bone density can be lost.
  • Frequent bed rest increases risk of blood clots.
  • Bed rest can reduce strength of muscles supporting the respiratory system, leading to cough and pneumonia.
  • 15-30% of bedrest patients develop kidney stones.
  • Frequent bed rest can cause neurologic, cognitive and psychiatric disturbances.
  • Thyroid, adrenal and pituitary hormones become dysregulated with bed rest.

Exercise and mast cell activity

  • Exercise induces mast cell degranulation and release of newly made mediators.
  • Histamine, tryptase and leukotrienes increase following exercise in patients who have exercise induced bronchoconstriction.
  • Treating with montelukast and loratadine suppressed release of histamine and leukotrienes.
  • Leptin is elevated in obese patients.
  • Leptin makes airways more reactive and more inflamed.
  • Leptin increases the allergic response including leukotriene production.
  • Asthmatics who are obese are less likely to respond to inhaled corticosteroids but respond to anti-leukotriene medications.
  • Leukotriene E4 was elevated in both obese and lean asthmatics after exercise.
  • 9a,11b-PGF2 (metabolite of PGD2) was elevated in obese and lean asthmatics after exercise.

Histamine depletion in exercise

  • Regular exercise can be protective against asthma.
  • Histamine is released in lungs due to exercise.
  • Histamine becomes depleted during exercise.
  • Plasma epinephrine does not rise in asthmatics following exercise.
  • Inhalation of cromolyn before exercise can prevent or mitigate induced asthma in many patients.
  • Treating with H1 and H2 antihistamines decreased endurance during exercise.
  • Histamine is important in inducing exercise tolerance.

Chronic urticaria and angioedema: Part 3

  • There are several pathways that can cause urticaria and angioedema:
  • IgE activation of mast cells
  • C3a and C5a activation of mast cells
  • Production of bradykinin
  • IgG activation of mast cells
  • NSAIDs
  • Non-immunologic methods such as radiocontrast dyes, pressure on the skin, heat, etc.

Chronic urticaria and angioedema: Part 4

  • There are several conditions that present similarly to chronic urticaria and angioedema.
  • Development of urticaria during pregnancy is not unusual.
  • Cutaneous mast cell patients often have urticaria like lesions.
  • MCAS can also cause angioedema and urticaria.
  • Angioedema in the absence of urticaria is rare.
  • Hereditary angioedema (HAE) is caused by deficiency or dysfunction of C1 esterase inhibitor in most patients.
  • HAE patients do not have coincident urticaria.
  • Acquired angioedema is caused by antibodies to the C1 esterase inhibitor, which can be from cancer.
  • Angioedema can affect any part of the body.

Chronic urticaria and angioedema: Part 5

  • Treatment scheme:
  • Second generation H1 antihistamine
  • Increase dose of second generation H1 antihistamine
  • Add another second generation H1 antihistamine
  • Add an H2 antihistamine
  • Add a leukotriene receptor antagonist.
  • Add a first generation H1 at bedtime.
  • Add a strong antihistamine like hydroxyzine.
  • Consider Xolair or immunosuppressants.

Premedication and surgical concerns in mast cell patients

  • Exact incidence of immediate anaphylaxis from surgery or anesthesia is unknown in mast cell patients
  • Mast cell patients should premedicate for surgery.
  • Anxiety, temperature changes, irritation of skin, physical trauma and pain can all cause mast cell activation.