Chapter 9
Endocrine System Conditions
Introduction
1. A collection of glands that secrete hormones
a. Hypothalamus is control center for endocrine (chemical) reactions and autonomic
(electrical) reactions
i. Hypothalamus connects to pituitary (master gland) via motor neurons and
hormones
ii. Hormones from hypothalamus and pituitary travel through bloodstream to
target organs and tissues
iii. Many targets are other endocrine glands
b. When hypothalamus (or other gland) senses that secretions are normal, the signals
stop: negative feedback loop
c. Most hormone cycles work best in gentle, rhythmic fluctuations
i. Cycle can last hours, days, weeks
2. Three classes of hormones:
a. Peptides: growth hormone, erythropoietin, parathyroid hormone
b. Amines: from tyrosine, stored in cellular deposits; adrenaline, thyroxine
c. Steroids: cortisol, testosterone
3. Key hormones for massage therapists to know:
a. Growth hormone
i. Converts fuel into new cells for growth (in children) and repair (in adults)
ii. Secreted mostly in stage IV sleep
b. Adrenaline
i. Also called epinephrine
ii. From adrenal medulla, associated with short-term, high-grade stress;
reinforces and prolongs sympathetic response
c. Cortisol
i. A steroid glucocorticoid from adrenal cortex
ii. Secreted during long-term, low-grade stress, measurable in saliva
iii. Powerful anti-inflammatory; dissolves connective tissue, suppresses
immune system
d. Mineralocorticoids
i. From adrenal cortex for regulation of water, electrolytes; aldosterone is
primary mineralocorticoid
e. Insulin/glucagon
i. Antagonistic hormones from pancreas: insulin decreases blood glucose,
glucagon raises it
f. Thyroxine
i. From thyroid, in two forms: T3 and T4
ii. Stimulates metabolism of fuel into energy (rather than storage or growth)
g. Calcitonin
i. Also from thyroid, stimulates osteoblasts, increases bone density and
decreases blood calcium
h. Parathyroid hormone
1
i. From parathyroid glands, antagonist of calcitonin: stimulates osteoclasts,
decreases bone density, increases blood calcium
i. Testosterone, estrogens, progesterone
i. From gonads and other cells for secondary sexual characteristics
ii. Environmental exposures (estrogen dominance) can upset balance
j. Other hormones
i. Erythropoietin from kidneys increases red blood cell (RBC) production
ii. Thymosin from thymus helps mature T cells
iii. Melatonin from pineal gland helps determine sleep-wake cycle
iv. Prostaglandins are all over: promote inflammation, pain sensation, smooth
muscle contraction
v. Ability to measure and compare “normal” endocrine secretions is limited;
this is a young science!
4. Endocrine system disorders
a. Acromegaly
b. Addison disease
c. Cushing syndrome
d. Diabetes mellitus
e. Hyperthyroidism
f. Hypothyroidism
g. Metabolic syndrome
h. Thyroid cancer
5. Acromegaly
a. Definition
i. Acro = extremities; megaly = large
ii. Usually a benign tumor on the pituitary gland: too much growth hormone
(GH)
iii. Hands, feet grow in adulthood
iv. (In childhood called gigantism)
b. Demographics
i. Mostly young adults
ii. Men = women
iii. 11,000 have it
iv. 800 diagnoses/year in the United States
c. Etiology
i. GH from pituitary → somatomedin C (IGF-I)
ii. Too much GH → too much IGF-I
iii. Bone enlargement, joint distortion and pain, enlarged weak heart
iv. Tumor can press on central nervous system (CNS) structures
d. Signs and Symptoms
i. Early: headache, vision problems from pressure
ii. Enlarged hands, feet, facial bones (mandibles and spaces between teeth)
iii. Joint pain, fatigue, hyperhidrosis, sleep apnea
iv. Can cause cranial nerve damage
e. Complications
i. Cardiovascular stress: high blood pressure, cardiomegaly, heart failure
2
ii. Some have insulin resistance, diabetes, colorectal cancer, uterine fibroids
f. Diagnosis
i. Abnormal growth and elevated IGF-I
ii. Computed tomography (CT), magnetic resonance imaging (MRI) to find
tumor
iii. Delay in diagnosis can allow tumor to grow; removal becomes difficult
g. Treatment
i. Surgery works best when tumor is < 1 cm
ii. Balance IGF-I with medication
iii. Usually manageable condition
h. Massage
i. High blood pressure, cardiomegaly, heart failure contraindicate circulatory
massage
ii. Other techniques may help with joint pain; work as part of health care
team
6. Addison disease
a. Definition
i. Adrenal cortex insufficiency: low cortisol, aldosterone, androgenic
hormones
b. Demographics
i. Affects about 13,000 in the United States
ii. Men = women
iii. Mostly 30–50 years old
c. Etiology
i. Adrenal cortex produces glucocorticoids, mineralocorticoids, androgens
ii. Primary Addison disease: not enough key hormones are manufactured
iii. 70% cases = autoimmune attack on adrenal medulla
iv. Adrenal glands alone = idiopathic adrenal insufficiency
v. Adrenals with other glands = polyendocrine deficiency syndrome
vi. Tuberculosis infections of the adrenal glands can cause it (rare in the
United States, common in developing countries)
vii. Secondary Addison disease: low pituitary secretions of
adrenocorticotropic hormone (ACTH)
viii. Suddenly stopping steroid medication
ix. Pituitary tumor or surgery
d. Signs and Symptoms
i. Cortisol depletion, along with low aldosterone, androgens
ii. Muscle weakness, fatigue, low blood pressure, hypoglycemia, irritability,
depression, loss of pubic hair in women, hyperpigmentation
e. Complications
i. Addisonian crisis: sudden onset of extreme symptoms:
ii. Sharp abdominal pain, nausea, vomiting, diarrhea
iii. Low back pain, pain in extremities, low blood pressure, loss of
consciousness
f. Diagnosis
3
i. Tests to measure cortisol, reactivity to hormones, CT, MRI of adrenals,
pituitary
ii. Test for adrenal cortex antibodies (indicates autoimmune potential)
g. Treatment
i. Treatable with steroids; establish dosage can be challenging
h. Massage
i. Guided by client’s health, resilience
ii. Be careful about blood pressure (hypotension can be worse with massage)
7. Cushing Syndrome
a. Definition
i. Hypercortisolism leading to tissue changes and possible death
b. Demographics
i. 3,000–4,500 people have it in United States
ii. Different types are more prevalent in different genders
c. Etiology
i. Can be exogenous or endogenous
1. Exogenous:
a. Autoimmune disease, cortisol-based steroid medication
(most common form)
2. Endogenous:
a. Too much ACTH from pituitary or too much cortisol from
adrenals:
ii. Pituitary adenoma: benign tumor grows on pituitary
1. Also called Cushing disease; women > men 5:1
iii. Ectopic ACTH syndrome:
1. ACTH secreted by tissues outside pituitary: cancer cells in
pancreas, thymus, thyroid
2. Men > women 3:1
iv. Adrenal tumors:
1. Rare: tumors on adrenal glands secrete cortisol
2. Can be benign or malignant
d. Signs and Symptoms
i. Fatty deposits around neck and face, abdomen, upper back
ii. Arms, legs become thin and weak (Fig. 9.1)
iii. Collagen degenerates:
iv. Bone thinning, purple stretch marks
v. High blood pressure, blood glucose (with risk of diabetes), mood changes,
acne, slowed healing, hirsutism, disrupted menstrual cycle, erectile
dysfunction
e. Diagnosis
i. Test cortisol through blood, urine, saliva
ii. Hormone challenge tests, CT, MRI of adrenals, pituitary
f. Treatment
4
i. Depends on cause: adjust medication, remove pituitary tumors, deal with
cancer if necessary
g. Massage
i. Risks = high blood pressure, delicate skin, bones, compromised immunity
ii. Many modalities can be adjusted to account for these risks
8. Diabetes Mellitus
9. Definition
a. Group of related disorders that all result in hyperglycemia
b. 98% are type 1 or type 2
10. Demographics
a. Number 6 cause of death in the United States: 224,000 deaths/year (probably
underreported)
b. 18 million to 21 million probably have it; 5 million to 6 million don’t know yet
c. 1.5 million diagnoses/year:
d. Aging population + more obese young people + sedentary lifestyle
e. $132 billion in direct and indirect costs: 11% of health care costs
f. Most common among Native Americans, Aleuts, African Americans, Pacific
Islanders, Hispanics
g. Type 2 used to be adults only; now it is frequently diagnosed in people <25
11. Etiology
a. Insulin in short supply or insulin resistance
b. Either way: glucose accumulates in blood while cells have to burn fat, protein for
fuel
i. Type 1
1. Used to be called IDDM (insulin-dependent diabetes mellitus) or
juvenile onset (now neither is exclusive to type 1)
2. Exposure to drugs or chemicals, complication of infections
3. Autoimmune attack on beta cells → lifelong deficiency in insulin
4. Symptoms usually show before age 30
5. LADA may show later
6. 500,000–1 million in the United States have it: 5–10% of cases
7. High risk for big fluctuations in blood glucose, diabetic
emergencies
ii. Type 2
1. Used to be called NIDDM (non–insulin-dependent diabetes
mellitus), adult onset (now neither is consistently true)
2. Women > men
3. 90% obese at diagnosis
4. Usually controllable with diet, exercise, some medication, but
many patients end up supplementing insulin
5. Can be wear-and-tear on pancreas → reduce insulin production
6. Can be insulin resistance
iii. Other types:
1. Gestational diabetes (discussed with pregnancy)
2. Complication of trauma, other endocrine disorder or treatment
5
c. Signs and Symptoms
i. Three poly- traits:
ii. Polyuria
iii. Polydipsia
iv. Polyphagia
v. Also: fatigue, weight loss, nausea, vomiting
vi. Early signs are often missed; complications develop
d. Diabetic emergencies
i. Ketoacidosis
1. Type 1 diabetes only
2. Shortage of insulin and glucose in cells
3. Metabolism of fat and protein → ketones, acidosis
4. Triggered by stress, infection, trauma
5. Can lead to shock, coma, death
ii. Hyperosmolality
1. Similar to ketoacidosis with type 1; seen in type 2
iii. Insulin shock
1. Too much insulin; blood glucose dangerously low
2. Dizziness, confusion, weakness, tremors
3. Treated with milk, juice, candy, sugared (not diet) soda to replace
blood glucose
e. Complications
i. Cardiovascular disease
1. Endothelium becomes vulnerable to damage, atherosclerosis
2. Plaque accumulates everywhere
3. Increased risk of stroke, hypertension, aneurysm
4. Most die of cardiovascular problems
ii. Edema
1. Sluggish blood return, stasis dermatitis
iii. Ulcers, gangrene, amputations
1. Poor circulation → risk of skin, tissue damage especially at feet
(fig. 9.2)
2. 82,000 amputations/year
iv. Kidney disease
1. Renal arteries have plaque; glucose is hard on nephrons
2. Number 1 cause of end-stage renal failure
v. Impaired vision
1. Thickened capillaries in eye; microaneurysms, glucose in lens
2. Number 1 cause of new blindness in people 20–70
vi. Neuropathy
1. Lack of circulation and excess sugar contribute to peripheral nerve
damage
2. Tingling, pain, numbness
3. At cranial nerves → poor gastrointestinal (GI) motility, low blood
pressure
vii. Others
6
1. Every system affected
2. Urinary tract infections, candidiasis, birth defects, aggressive
infections, gingivitis, tooth loss
f. Diagnosis
i. Fasting blood sugar:
ii. Normal is 110 mg/dL of blood
iii. 125+ mg/dL means diabetes
g. Treatment
i. Insulin developed in 1921: diabetes become manageable
ii. Four goals: improve insulin production if possible; inhibit release of
glucose from liver; increase sensitivity to insulin; decrease absorption of
carbohydrates in small intestine
iii. Also: maintain eyes, feet, skin carefully
1. Type 1: insulin supplementation (through pump, not huge
injections)
2. Type 2: diet and exercise, then medication and insulin
iv. Renal insufficiency happens for many; hemodialysis can help while
hoping for transplant
h. Massage
i. Can be appropriate: weigh risks and benefits
ii. Cardiovascular and kidney problems contraindicate rigorous circulatory
massage
iii. Work when insulin is not at peak (to avoid double whammy)
iv. Be cautious about numbness, reduced sensation, skin lesions
12. Hyperthyroidism
a. Definition
i. Thyroid produces excessive hormones that stimulate the metabolism of
fuel into energy
ii. Most are autoimmune (Graves disease, diffuse toxic thyroid)
b. Demographics
i. 1–2% adults in the United States
ii. 350,000 diagnosed/year
iii. Women > men 8:1
iv. Mostly aged 20–40 years
v. Genetic predisposition: if one person has Graves disease, a first-degree
relative probably has some thyroid dysfunction
vi. Can appear with other autoimmune diseases:
vii. Autoimmune polyglandular syndrome:
viii. Graves, type 1 diabetes, lupus, others
c. Etiology
i. Usually one of three possibilities:
ii. Autoimmune attack on thyroid
iii. Nodule or group of nodules that become hyperactive
iv. Inflammation of thyroid
v. Graves disease is most common: 70–80%
7
d.
e.
f.
g.
h.
vi. Thyroid-stimulating immunoglobulins attack; thyroid grows (goiter)
vii. Excess thyroxine produced
viii. Conversion of fuel to energy increases 60–100%
ix. Triggered by stressful event
x. Toxic multinodular goiter: idiopathic
xi. Toxic adenoma: iodine deficiency
xii. Thyroid inflammation: infection or childbirth
Signs and Symptoms
i. Related to too much thyroxine:
ii. Anxiety, irritability, insomnia, rapid heartbeat, tremor, increased
perspiration, sensitivity to heat, frequent bowel movements, and
unintentional weight loss
iii. Skeletal muscles become weak, lighter menstrual flow, dry skin, brittle
nails, problems with skin and eyes, goiter (Fig. 9.3)
Complications
i. Graves disease also affects bones, eyes, skin
ii. Bones: osteoporosis from calcitonin/parathyroid hormone imbalance
iii. Eyes: exophthalmus, Graves ophthalmopathy (tissues behind the eye
swell) (Fig. 9.4)
iv. Skin: red patches on shins, feet: pretibial myxedema; thyroid acropachy
v. Thyroid storms: sudden onset of sympathetic reaction, rapid heartbeat,
fever, confusion, agitation, shock: medical emergency
Diagnosis
i. Physical examination, blood test, iodine test
Treatment
i. Radioactive iodine: can kill off part of thyroid
ii. Beta blockers: reduce heart rate, feeling of palpitations
iii. Antithyroid medications: can prevent thyroid from producing too much
thyroid hormone
iv. Surgery: Thyroidectomy; has risks of complications
Massage
i. If skin is healthy massage can be beneficial
ii. Can help ameliorate sympathetic symptoms
13. Hypothyroidism
a. Definition
i. Thyroid hormones are abnormally low: body can’t generate energy from
fuel
b. Demographics
i. Most common pathological hormone deficiency
ii. Numbers difficult to track: numbers don’t always match symptoms
iii. Women > men 2–8:1
c. Etiology
i. Pituitary (under control of hypothalamus) secretes thyroid-stimulating
hormone (TSH)
ii. Thyroid secretes
8
d.
e.
f.
g.
1. T3 = triiodothyronine
2. T4 = thyroxine
iii. When T3, T4 levels are high, TSH is suppressed: negative feedback loop
1. T3, T4 stimulate conversion of fuel into energy
2. T4 → T3
iv. In early hypothyroidism:
1. TSH high
2. T4 low
3. T3 normal
v. Contributing factors:
1. Hashimoto thyroiditis: autoimmune attack
2. Complication of treatment for hyperthyroidism: result of taking
radioactive iodine or thyroid surgery
3. Congenital birth defect: some born with no thyroid gland
4. Postpartum: especially for mothers with type 1 diabetes
5. Medications: Lithium, some iodides suppress thyroid function
6. Exposure to radiation: for cancers in the neck or from other
sources
7. Iodine deficiency: worldwide, most common cause
8. Idiopathic: Unrelated to underlying disorder; signs and symptoms
may be present without confirming blood tests
Signs and Symptoms
i. Weight gain, fatigue, depression, sluggish digestion, intolerance to cold,
puffy skin
ii. Edema may → carpal tunnel syndrome, nerve entrapments
iii. Hair may become brittle, fall out (especially at lateral eyebrows)
iv. Heavy menstrual periods
v. Goiter
vi. High risk of heart disease
vii. Severe, untreated cases can → myxedema coma
Diagnosis
i. Blood test: high TSH
ii. Goiter, slow heart rate, slowed reflexes
iii. Pregnancy can hide some symptoms: complications for baby
iv. Can look like depression, fibromyalgia, chronic fatigue syndrome, etc.:
diagnosis can be controversial
Treatment
i. Supplement thyroid hormone
ii. Synthetic T4 (most can metabolize to T3)
iii. T3 can be supplemented with desiccated pig glands or a synthetic form
Massage
i. Respect risk of atherosclerosis
ii. Otherwise massage is safe and appropriate, may help alleviate fatigue and
lethargy
9
14. Metabolic Syndrome
a. Definition
i. Also called syndrome X, dysmetabolic syndrome, insulin resistance
syndrome, prediabetes, the deadly quartet
ii. A collection of physical signs and symptoms that increase the risk of heart
disease and type 2 diabetes
b. Demographics
i. An estimated 47 million people in the United States
ii. Women > men
iii. Latinos > other groups
c. Etiology
i. Five main features (see diagnosis)
ii. Other possibilities: risk of blood clotting, high C-reactive protein,
polycystic ovary disease
iii. Any one of these is not alarming; in combination → risk of cardiovascular
disease (increased 2x) and/or type 2 diabetes (increased 5x)
iv. Major risk factors: obesity, insulin resistance (this can form a vicious
circle)
d. Signs and Symptoms
i. Central obesity (apple versus pear shape)
ii. Other signs listed below
e. Diagnosis
i. Three of five risk factors are present:
ii. High fasting blood glucose (over 100 mg/dL after 9 hours of fasting)
iii. Abdominal obesity (a waist measurement of over 35 inches for women,
over 40 inches for men); somewhat flexible to allow for individual
variations
iv. Elevated triglyceride levels (over 150 mg/dL)
v. Low levels of high-density lipoproteins (under 40 mg/dL for men; under
50 mg/dL for women)
vi. Hypertension (systolic over 130; diastolic over 85)
f. Treatment
i. Short-term and long-term goals
1. Short-term: low blood glucose, correct cholesterol with medication
2. Long-term: increase physical activity, lose weight
ii. Reducing weight by 5–7% reduces risk of complications
iii. Limit alcohol use, quit smoking if necessary
g. Massage
i. Depends on general health, resilience of client
ii. Match to activities of daily living
15. Thyroid Cancer
a. Definition
i. Any type of cancer that begins in thyroid gland
ii. Three types:
iii. Follicular cell
10
iv. C cell
v. Lymphocyte
b. Demographics
i. 31,000 diagnoses/year (rising)
ii. Women > men 2–3:1
iii. 1,500 deaths/year in the United States
iv. High treatment success: 350,000 survivors alive today
c. Etiology
i. DNA in thyroid cells is damaged; cell growth is uncontrolled,
disorganized
ii. Often be related to radiation exposure
iii. Can have genetic predisposition
d. Types of thyroid cancer
i. Papillary thyroid cancer:
1. 70–80% of diagnoses
2. Usually stays local to thyroid and nearby nodes
3. Mostly diagnosed in women 30-50 years old
ii. Follicular thyroid cancer:
1. 10% of diagnoses
2. More likely to metastasize, especially in people > 50 years old
iii. Hürthle cell carcinoma: A subtype of follicular thyroid cancer, poor
prognosis
iv. Medullary thyroid cancer:
1. 3–5% of diagnoses
2. Arises from C cells; rare, aggressive
3. Two subtypes:
4. Multiple endocrine neoplasia (MEN) type II (MEN-IIA)
5. MEN-IIB
6. Both of these involve tumors on other glands too
v. Familial thyroid cancer:
1. Inherited, affects only thyroid
2. Slow-growing, mostly in people 40–60 years old
vi. Anaplastic thyroid cancer:
1. 7% of diagnoses
2. Also called undifferentiated thyroid cancer
3. Highly aggressive, metastasizes
vii. Thyroid lymphoma:
1. 4% of diagnoses
2. Lymphocytes have DNA damage
3. Happens mostly with Hashimoto thyroiditis
11
e. Signs and Symptoms
i. Unaggressive forms may be silent
ii. Later: painless enlargement in the throat, pressure on esophagus or
trachea; tumors in lungs, bones
f. Diagnosis
i. Hard to diagnose accurately: lots of thyroids grow tumors, only 5% are
malignant
ii. Radioactive iodine can find extra activity
iii. Genetic testing
g. Treatment
i. Most are treated successfully with surgery to remove thyroid gland
ii. Then supplement thyroid hormone
iii. Lymph nodes in neck examined for signs of metastasis
iv. Radiation decrease risk of recurrence
h. Massage
i. Depends on treatment options, general resilience of patient
ii. Get clearance for radioactivity risks
12