1. The Endocrine System
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  13. Overview of Hypothalamic and Pituitary Hormones
  1. The pituitary gland is often portrayed as the "master gland" of the body. Such praise is justified in the sense that the anterior and posterior pituitary secrete a battery of hormones that collectively influence all cells and affect virtually all physiologic processes.

(1)The pituitary gland may be king, but the power behind the throne is clearly the hypothalamus.As alluded to in the last section, some of the neurons within the hypothalamus - neurosecretory neurons - secrete hormones that strictly control secretion of hormones from the anterior pituitary. The hypothalamic hormones are referred to asreleasing hormonesandinhibiting hormones, reflecting their influence on anterior pituitary hormones.

  1. Hypothalamic releasing and inhibiting hormones are carried directly to the anterior pituitary gland viahypothalamic-hypophyseal portal veins. Specific hypothalamic hormones bind to receptors on specific anterior pituitary cells, modulating the release of the hormone they produce.
  2. As an example, thyroid-releasing hormone from the hypothalamus binds to receptors on anterior pituitary cells called thyrotrophs, stimulating them to secrete thyroid-stimulating hormone or TSH. The anterior pituitary hormones enter the systemic circulation and bind to their receptors on other target organs. In the case of TSH, the target organ is the thyroid gland.
  3. Clearly, robust control systems must be in place to prevent over or under-secretion of hypothalamic and anterior pituitary hormones.
  4. (1) A prominent mechanism for control of the releasing and inhibiting hormones isnegative feedback. Details on the control of specific hypothalamic and anterior pituitary hormones is presented in the discussions of those hormones.
  5. The following table summarizes the major hormones synthesized and secreted by the pituitary gland, along with summary statements about their major target organs and physiologic effects. Keep in mind that summaries are just that, and ongoing research continues to delineate additional, sometimes very important effects.
  1. Hormones secreted by the hypothalamus modulate other hormones.
  2. The major hormones secreted by the hypothalamus are corticotrophin releasing hormone (CRH), thyroidstimulating hormonereleasing hormone (TRH),follicle stimulating hormonereleasing hormone (FSHRH), luteinizing hormone releasing hormone (LRH), and growth hormone releasing hormone (GHRH).
  3. CRH targets theadrenal glands. It triggers the adrenals to release adrenocorticotropic hormone (ACTH).
  4. ACTH functions to synthesize and release corticosteroids.
  5. TRH targets thethyroidwhere it functions to synthesize and release the thyroid hormones T3 andT4.
  6. FSH targets the ovaries and the testes where it enables the maturation of the ovum and of spermatozoa.
  7. LRH also targets the ovaries and the testes, and its receptors are in cells which promote ovulation and increase progesterone synthesis and release.
  8. GHRH targets the anterior pituitary to releasegrowth hormonesto most body tissues, increase protein synthesis, and increase blood glucose. Hence, the hypothalamus plays a first domino role in these cascades of events.
  9. The hypothalamus also secretes some other important hormones:
  10. prolactin inhibiting hormone (PIH),
  11. PIH targets the anterior pituitary to inhibit milk production at the mammary gland
  12. prolactin releasing hormone (PRH), and melanocyte inhibiting hormone (MIH).,
  13. PRH has the opposite effect.
  14. MIH targets skin pigment cells (melanocytes) to regulate pigmentation.

Read more:Hormones - The Hypothalamus - Targets, Releasing, Release, and Thyroid - JRank Articles

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  2. Pituitary hormones are substances that control the output of other endocrine glands and tissues. We know only some. There are myriad endocrine hormones all over the body. Hormones are the way the tissues of the body have conversations with each other and the nervous system.
  3. Pituitary:
  4. anterior lobe endocrine tissue,
  5. posterior lobe is neural tissue.
  6. It has a relationship with both systems.
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  8. Pituitary: trophic hormones
  9. These hormones, produced by the pituitary, are called trophic hormones. The name is given because they act on other endocrine glands, controlling their output. They have the same effect as the sun does on a plant leaf that follows its path across the wall. The sun causes movement or response. (trophy-loosely translates into response or movement).
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  13. Definition
  14. Acro = extremities; megaly = large
  15. Usually a benign tumor on the pituitary gland: too much growth hormone (GH)
  16. Hands, feet grow in adulthood
  17. (In childhood this is called gigantism and the supergrowth is more evenly distributed over the whole body)

Demographics

  1. Mostly young adults
  2. Men = women
  3. 11,000 have it
  4. 800 diagnoses/year in the United States

Signs and Symptoms

  1. Early: headache, vision problems from pressure
  2. Enlarged hands, feet, facial bones (mandibles and spaces between teeth)
  3. Joint pain, fatigue, hyperhidrosis, sleep apnea
  4. Can cause cranial nerve damage

Complications

  1. Cardiovascular (CV) stress: high blood pressure, cardiomegaly, heart failure
  2. Some patients with Acromegaly or growth hormone issues have:
  3. insulin resistance,
  4. diabetes,
  5. colorectal cancer,
  6. uterine fibroids

Treatment

  1. Surgery works best when tumor is < 1 cm
  2. Balance IGF-I with medication
  3. Usually manageable condition

Massage Considerations:

  1. High blood pressure, cardiomegaly, heart failure contraindicate circulatory massage
  2. Other techniques may help with joint pain; work as part of health care team
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  2. THERE ARE SEVERAL TYPES OF DWARFISM. The most common type is ACHONDROPLASTIC DWARFISM - 70% of dwarfism cases.
  3. Dwarfism(/ˈdwɔrfɪzəm/) is short stature resulting from a medical condition. It is sometimes defined as an adult height of less than 4 feet 10inches (147cm),[2]although this definition is problematic because short stature in itself is not a disorder.
  4. Dwarfism can be caused by about 200 distinct medical conditions,[3]such that the symptoms and characteristics of individual people with dwarfism vary greatly. In theUnited States,CanadaandNew Zealand, many people with dwarfism prefer to be calledlittle people.[4]
  5. Disproportionatedwarfism is characterized by one or more body parts being relatively large or small in comparison to those of an average-sized adult, with growth variations in specific areas being apparent. In cases ofproportionatedwarfism, the body appears normally proportioned, but is unusually small. Historically, the termmidgetwas used to describe "proportionate dwarfs"; however, this term has now become offensive andpejorative(seeterminology).Hypotonia, or low muscle tone, is common in dwarfs, but intelligence and lifespan are usually normal.
  6. Achondroplasiais a bone-growth disorder responsible for 70% of dwarfism cases.[2]With achondroplasia, one's limbs are proportionately shorter than one's trunk (abdominal area), with a larger head than average and characteristic facial features. Conditions in humans characterized by disproportional body parts are typically caused by one or moregenetic disordersin bone or cartilage development. Extreme shortness in humans with proportional body parts usually has a hormonal cause, such asgrowth-hormone deficiency, once calledpituitary dwarfism.[4][5]
  7. There is no single treatment for dwarfism. Individual differences, such as bone-growth disorders, sometimes can be treated through surgery, and some hormone disorders can be treated through medication, but usually it is impossible to treat all the symptoms of dwarfism. Individual accommodations, such as specialized furniture, are often used by people with dwarfism.[6]Many support groups provide services to aid individuals with dwarfism in facing the challenges of an ableist society.[7]
  8. Dwarfism is a highly visible condition and often carries negative connotations in society. Because of their unusual height, people with dwarfism often work as spectacles in entertainment and portrayed with stereotypes. For a person with dwarfism,heightismcan lead to ridicule in childhood and discrimination in adulthood.[8][9]
  9. Short stature can be inherited without any coexisting disease. Short stature in the absence of a medical condition is not generally considered dwarfism. For example, a short man and a short woman with average health will tend to produce children who are also short and with average health. While short parents tend to produce short children, persons with dwarfism may produce children of average height, if the cause of their dwarfism is not genetically transmissible or if the individual does not pass on the genetic variation.
  10. Massage Considerations:
  11. related to access. Table access, equipment size
  12. related to deformities: various bony deformities and compression of internal organs from issues like scoliosis are of concern.
  13. Positioning and propping with bolsters and other things will help foster client comfort
  14. Respiratory issues from compression of lungs
  15. Cardiovascular issues from respiratory issues
  16. Some muscular and fascial problems from stature and hormonal differences
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  20. HYPERTHYROIDISM
  21. Definition: Thyroid produces excessive hormones that stimulate the metabolism of fuel into energy
  22. Most are autoimmune (Graves disease, diffuse toxic thyroid)

Etiology

  1. Usually one of three possibilities
  2. Autoimmune attack on thyroid
  3. Nodule or group of nodules that become hyperactive
  4. Inflammation of thyroid
  5. Issues in thyroid diseases
  6. Graves disease is most common: 70–80%
  7. Thyroid-stimulating immunoglobulins attack; thyroid grows (goiter)
  8. Excessive thyroxine produced
  9. Conversion of fuel to energy increases 60–100%
  10. Triggered by stressful event
  11. Toxic multinodular goiter: idiopathic
  12. Toxic adenoma: iodine deficiency
  13. Thyroid inflammation: infection or childbirth
  14. Signs and Symptoms
  15. Related to too much thyroxine
  16. Anxiety, irritability, insomnia, rapid heartbeat, tremor, increased perspiration, sensitivity to heat, frequent bowel movements, and unintentional weight loss
  17. Skeletal muscles become weak, lighter menstrual flow, dry skin, brittle nails, problems with skin and eyes, goiter
  18. Complications
  19. Graves disease also effects bones, eyes, skin
  20. Bones: osteoporosis from calcitonin/parathyroid hormone imbalance
  21. Eyes: exophthalmus, Graves ophthalmopathy (tissues behind the eye swell)
  22. Skin: red patches on shins, feet: pretibial myxedema; thyroid acropachy
  23. Thyroid storms: sudden onset of sympathetic reaction, rapid heartbeat, fever, confusion, agitation, shock: medical emergency
  1. Graves disease is most common: 70–80%
  2. Thyroid-stimulating immunoglobulins attack; thyroid grows (goiter)
  3. Excessive thyroxine produced
  4. Conversion of fuel to energy increases 60–100%
  5. Triggered by stressful event
  6. Signs and Symptoms
  7. Related to too much thyroxine
  8. Anxiety, irritability, insomnia, rapid heartbeat, tremor, increased perspiration, sensitivity to heat, frequent bowel movements, and unintentional weight loss
  9. Skeletal muscles become weak, lighter menstrual flow, dry skin, brittle nails, problems with skin and eyes, goiter
  10. Treatment
  11. Radioactive iodine: can kill off part of thyroid
  12. Beta blockers: reduce heart rate, feeling of palpitations
  13. Antithyroid medications: can prevent thyroid from producing too much thyroid hormone
  14. Surgery: thyroidectomy; has risks of complications
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  16. HYPOTHYROIDISM
  17. Definition: Thyroid hormones are abnormally low; body can’t generate energy from fuel
  18. Demographics
  19. Most common pathological hormone deficiency
  20. Numbers difficult to track: numbers don’t always match symptoms
  21. Women > men 2–8:1
  22. In early hypothyroidism
  23. TSH is high
  24. T4 is low
  25. T3 is normal
  26. Contributing factors:
  27. Hashimoto thyroiditis
  28. Complication of treatment for hyperthyroidism
  29. Congenital birth defect
  30. Postpartum
  31. Medications
  32. Exposure to radiation
  33. Iodine deficiency
  34. Idiopathic
  35. Signs and Symptoms (Fig 9.5)
  36. Weight gain, fatigue, depression, sluggish digestion, intolerance to cold, puffy skin
  37. Edema may → carpal tunnel syndrome, nerve entrapments
  38. Hair may become brittle, fall out (especially at lateral eyebrows)
  39. Heavy menstrual periods
  40. Goiter
  41. High risk of heart disease
  42. Severe, untreated cases can →myxedema coma
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  45. Diagnosis

Three of five risk factors

High fasting blood glucose (>100 mg/dL after 9 hours of fasting)

Abdominal obesity (waist > 35 inches for women, > 40 inches for men); somewhat flexible

Elevated triglyceride levels (over 150 mg/dL)

Low high-density lipoproteins (<40 mg/dL for men; <50 mg/dL for women)

Hypertension (systolic >130; diastolic >85)

Treatment

Short-term and long-term goals:

Short term: low BG, correct cholesterol with medication

Long term: increase physical activity, lose weight

Reducing weight by 5–7% reduces risk of complications

Limit alcohol use, quit smoking if necessary

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  2. Diagnosis

Three of five risk factors

High fasting blood glucose (>100 mg/dL after 9 hours of fasting)

Abdominal obesity (waist > 35 inches for women, > 40 inches for men); somewhat flexible

Elevated triglyceride levels (over 150 mg/dL)

Low high-density lipoproteins (<40 mg/dL for men; <50 mg/dL for women)

Hypertension (systolic >130; diastolic >85)

Treatment

Short-term and long-term goals:

Short term: low BG, correct cholesterol with medication

Long term: increase physical activity, lose weight

Reducing weight by 5–7% reduces risk of complications

Limit alcohol use, quit smoking if necessary

  1. Demographics

Number 6 cause of death in the United States: 224,000 deaths/year (probably underreported)

a. 18 million to 21 million probably have it; 5 million to 6 million don’t know yet

b. 1.5 million diagnoses/year:

c. Aging population + more obese young people + sedentary lifestyle

d. $132 billion in direct and indirect costs: 11% of health care costs

e. Most common among Native Americans, Aleuts, African Americans, Pacific Islanders, Hispanics

f. Type 2 used to be adults only; now it is frequently diagnosed in people < 25

B. Etiology

a. Insulin is in short supply or

b. Insulin resistance

c. Either way: glucose accumulates in blood while cells have to burn fat, protein for fuel

Type 1

  1. Used to be called IDDM or juvenile onset (now neither is exclusive to type 1)

ii. Exposure to drugs or chemicals, complication of infections

iii. Autoimmune attack on beta cells → lifelong deficiency in insulin

  1. Symptoms usually show before age 30
  2. LADA may show later
  3. 500,000–1 million in the United States have it: 5–10% of cases
  4. High risk for big fluctuations in BG, diabetic emergencies

Type 2

  1. Used to be called NIDDM, adult onset (now neither is consistently true)

ii. Women > men

iii. 90% are obese at diagnosis

vi. Usually controllable with diet, exercise, some medication but many patients end up supplementing insulin

v. Can be wear and tear on pancreas → reduce insulin production

vi. Can be insulin resistance

Other types

  1. Gestational diabetes (discussed with pregnancy)

ii. Complication of trauma, other endocrine disorder or treatment

  1. Diabetes mellitus is a chronic disease characterized by relative or absolute deficiency of insulin, resulting in glucose intolerance.
  2. It occurs in 4-5 million persons in the United States (approximately 2% of the population).
  3. The classic symptoms of diabetes mellitus result from abnormal glucose metabolism.
  4. The lack of insulin activity results in failure of transfer of glucose from the plasma into the cells.
  5. This situation so called “starvation in the midst of plenty”. The body responds as if it were in the fasting state, with stimulation of glucogenolysis, gluconeogenesis and lipolysis producing ketone bodies.
    1. The glucose absorbed during a meal is not metabolized at the normal rate and therefore accumulates in the blood (hyperglycemia) to be excreted in the urine (glycosuria).
  6. Glucose in the urine causes osmotic diuresis, leading to increase urine production (polyuria). Stimulation of protein breakdown to provide amino acids for gluconeogenesis results in muscle wasting and weight loss.
  7. These classic symptoms occur only in patients with severe insulin deficiency, most commonly in type I diabetes. Many patients with type II diabetes do not have these symptoms and present with one of the complications of diabetes.

d. Generally, there are two types of diabetes: Type I Diabetes Mellitus (insulin- dependent diabetes mellitus, IDDM) and Type II Diabetes Mellitus (non-insulin- dependent diabetes mellitus, NIDDM).

GENERAL INFORMATION:
Type I Diabetes Mellitus (insulin- dependent diabetes mellitus, IDDM) is due to destruction of pancreatic B cells. The cause of B cell destruction in type I diabetes is unknown. A few cases have followed viral infections, most commonly with coxsakievirus B or mumps virus. Autoimmunity is believed to be the major mechanism involved. Islet cell autoantibodies are present in the serum of 90% of newly diagnosed cases. Such antibodies are directed against several cell components, including cytoplasmic and membrane antigens or against insulin itself (IgG and IgE antibodies). Sensitized T lymphocytes with activity against B cells have also been demonstrated in some patients.
Plasma insulin levels are very low or even absent in type I diabetes, and ketoacidosis develops if the patients do not receive exogenous insulin. Type I diabetes occurs most commonly in juveniles, with the highest incidence worldwide among the 10- to 14-year-old group, but occasionally occurs in adults, especially the nonobese and those who are elderly when hyperglycemia first appears.
The etiology of type II diabetes mellitus (non-insulin- dependent diabetes mellitus, NIDDM) is even less clearly understood. Two factors have been identified:
a) Impaired insulin release-basal secretion of insulin is often normal, but the rapid release of insulin follows a meal is greatly impaired, resulting in failure of normal handling of a carbohydrate load. In most patients, some level of insulin secretion is maintained, so that the abnormality of glucose metabolism is limited and ketoacidosis is uncommon. In these patients, insulin secretion can be stimulated by drugs such as sulfonylureas. Exogenous insulin is therefore not essential in treatment. It also have been suggested that inheritance of a defective pattern of insulin secretion is responsible for the familial tendency of diabetes. The genetic factor is very strong in type II diabetes, with a history of diabetes present in about 50% of first degree relatives.
b) Insulin resistance-a defect in the tissue response to insulin is believed to play a major role. This phenomenon is called insulin resistance and is caused by defective insulin receptors on the target cells.Insulin resistance occurs in association with obesity and pregnancy. In normal individuals who become obese or pregnant, the B cells secrete increased amounts of insulin to compensate. Patients who have genetic susceptibility to diabetes cannot compensate because of their inherent defect in insulin secretion. Thus, type II diabetes is frequently precipitated by obesity and pregnancy. In a few patients with extreme insulin resistance, antibodies against the receptors have been demonstrated in plasma. These antibodies are mostly of the IgG class and act against the insulin receptors, causing the decreased numbers of insulin receptors and defective binding of insulin to receptors.