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1. The Endocrine System 2. Dragon 3. No commentary 4. No commentary 5. No commentary 6. No commentary 7. No commentary 8. No commentary 9. No commentary 10. No commentary 11. No commentary 12. No commentary 13. Overview of Hypothalamic and Pituitary Hormones a. 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 as releasing hormones and inhibiting hormones, reflecting their influence on anterior pituitary hormones. b. Hypothalamic releasing and inhibiting hormones are carried directly to the anterior pituitary gland via hypothalamic-hypophyseal portal veins. Specific hypothalamic hormones bind to receptors on specific anterior pituitary cells, modulating the release of the hormone they produce. c. 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. d. Clearly, robust control systems must be in place to prevent over or under-secretion of hypothalamic and anterior pituitary hormones. a. (1) A prominent mechanism for control of the releasing and inhibiting hormones is negative feedback. Details on the control of specific hypothalamic and anterior pituitary hormones is presented in the discussions of those hormones. e. 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. 14. Hormones secreted by the hypothalamus modulate other hormones. a. The major hormones secreted by the hypothalamus are corticotrophin releasing hormone (CRH), thyroid stimulating hormone releasing hormone (TRH), follicle stimulating hormone releasing hormone (FSHRH), luteinizing hormone releasing hormone (LRH), and growth hormone releasing hormone (GHRH). i. CRH targets the adrenal glands. It triggers the adrenals to release adrenocorticotropic hormone (ACTH). ii. ACTH functions to synthesize and release corticosteroids. iii. TRH targets the thyroid where it functions to synthesize and release the thyroid hormones T3 and T4. iv. FSH targets the ovaries and the testes where it enables the maturation of the ovum and of spermatozoa. v. LRH also targets the ovaries and the testes, and its receptors are in cells which promote ovulation and increase progesterone synthesis and release. vi. GHRH targets the anterior pituitary to release growth hormones to most body tissues, increase protein synthesis, and increase blood glucose. Hence, the hypothalamus plays a first domino role in these cascades of events. 15. The hypothalamus also secretes some other important hormones: a. prolactin inhibiting hormone (PIH), i. PIH targets the anterior pituitary to inhibit milk production at the mammary gland b. prolactin releasing hormone (PRH), and melanocyte inhibiting hormone (MIH)., i. PRH has the opposite effect. ii. MIH targets skin pigment cells (melanocytes) to regulate pigmentation. Read more: Hormones - The Hypothalamus - Targets, Releasing, Release, and Thyroid - JRank Articles http://science.jrank.org/pages/3373/Hormoneshypothalamus.html#ixzz1kOnPnG6y 16. No commentary 17. 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. 18. Pituitary: a. anterior lobe endocrine tissue, b. posterior lobe is neural tissue. c. It has a relationship with both systems. 19. No commentary 20. Pituitary: trophic hormones a. 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). 21. No commentary 22. No commentary 23. No commentary 24. Definition a. Acro = extremities; megaly = large b. Usually a benign tumor on the pituitary gland: too much growth hormone (GH) c. Hands, feet grow in adulthood d. (In childhood this is called gigantism and the supergrowth is more evenly distributed over the whole body) Demographics a. Mostly young adults b. Men = women c. 11,000 have it d. 800 diagnoses/year in the United States Signs and Symptoms a. Early: headache, vision problems from pressure b. Enlarged hands, feet, facial bones (mandibles and spaces between teeth) c. Joint pain, fatigue, hyperhidrosis, sleep apnea d. Can cause cranial nerve damage Complications a. Cardiovascular (CV) stress: high blood pressure, cardiomegaly, heart failure b. Some patients with Acromegaly or growth hormone issues have: i. insulin resistance, ii. diabetes, iii. colorectal cancer, iv. uterine fibroids Treatment a. Surgery works best when tumor is < 1 cm b. Balance IGF-I with medication c. Usually manageable condition Massage Considerations: a. High blood pressure, cardiomegaly, heart failure contraindicate circulatory massage b. Other techniques may help with joint pain; work as part of health care team 25. No commentary 26. THERE ARE SEVERAL TYPES OF DWARFISM. The most common type is ACHONDROPLASTIC DWARFISM - 70% of dwarfism cases. a. Dwarfism ( /ˈdwɔrfɪzəm/) is short stature resulting from a medical condition. It is sometimes defined as an adult height of less than 4 feet 10 inches (147 cm),[2] although this definition is problematic because short stature in itself is not a disorder. b. 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 the United States, Canada and New Zealand, many people with dwarfism prefer to be called little people.[4] c. Disproportionate dwarfism 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 of proportionate dwarfism, the body appears normally proportioned, but is unusually small. Historically, the term midget was used to describe "proportionate dwarfs"; however, this term has now become offensive and pejorative (see terminology).Hypotonia, or low muscle tone, is common in dwarfs, but intelligence and lifespan are usually normal. d. Achondroplasia is 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 more genetic disorders in bone or cartilage development. Extreme shortness in humans with proportional body parts usually has a hormonal cause, such as growthhormone deficiency, once called pituitary dwarfism.[4][5] e. 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] f. 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, heightism can lead to ridicule in childhood and discrimination in adulthood.[8][9] g. 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. h. Massage Considerations: i. related to access. Table access, equipment size ii. related to deformities: various bony deformities and compression of internal organs from issues like scoliosis are of concern. 1. Positioning and propping with bolsters and other things will help foster client comfort iii. Respiratory issues from compression of lungs iv. Cardiovascular issues from respiratory issues v. Some muscular and fascial problems from stature and hormonal differences 27. No commentary 28. No commentary 29. No commentary 30. HYPERTHYROIDISM a. Definition: Thyroid produces excessive hormones that stimulate the metabolism of fuel into energy b. Most are autoimmune (Graves disease, diffuse toxic thyroid) Etiology a. Usually one of three possibilities a. Autoimmune attack on thyroid b. Nodule or group of nodules that become hyperactive c. Inflammation of thyroid b. Issues in thyroid diseases a. Graves disease is most common: 70–80% b. Thyroid-stimulating immunoglobulins attack; thyroid grows (goiter) c. Excessive thyroxine produced d. Conversion of fuel to energy increases 60–100% e. Triggered by stressful event f. Toxic multinodular goiter: idiopathic g. Toxic adenoma: iodine deficiency h. Thyroid inflammation: infection or childbirth c. 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 d. Complications i. Graves disease also effects bones, eyes, skin 1. Bones: osteoporosis from calcitonin/parathyroid hormone imbalance 2. Eyes: exophthalmus, Graves ophthalmopathy (tissues behind the eye swell) 3. Skin: red patches on shins, feet: pretibial myxedema; thyroid acropachy ii. Thyroid storms: sudden onset of sympathetic reaction, rapid heartbeat, fever, confusion, agitation, shock: medical emergency 31. Graves disease is most common: 70–80% a. Thyroid-stimulating immunoglobulins attack; thyroid grows (goiter) b. Excessive thyroxine produced c. Conversion of fuel to energy increases 60–100% d. Triggered by stressful event e. 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 f. 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 32. No commentary 33. HYPOTHYROIDISM a. Definition: 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 iv. In early hypothyroidism 1. TSH is high 2. T4 is low 3. T3 is normal c. Contributing factors: i. Hashimoto thyroiditis ii. Complication of treatment for hyperthyroidism iii. Congenital birth defect iv. Postpartum v. Medications vi. Exposure to radiation vii. Iodine deficiency viii. Idiopathic d. Signs and Symptoms (Fig 9.5) 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 34. Cretinism: No commentary, see slide 35. No commentary 36. 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 37. No commentary 38. 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 39. 40. 41. 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 i. 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 iv. Symptoms usually show before age 30 v. LADA may show later vi. 500,000–1 million in the United States have it: 5–10% of cases vii. High risk for big fluctuations in BG, diabetic emergencies Type 2 i. 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 i. Gestational diabetes (discussed with pregnancy) ii. Complication of trauma, other endocrine disorder or treatment 42. Diabetes mellitus is a chronic disease characterized by relative or absolute deficiency of insulin, resulting in glucose intolerance. a. It occurs in 4-5 million persons in the United States (approximately 2% of the population). b. The classic symptoms of diabetes mellitus result from abnormal glucose metabolism. i. The lack of insulin activity results in failure of transfer of glucose from the plasma into the cells. ii. 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). iii. 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. c. 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. 43. Causes of Diabetes Diabetes mellitus occurs when the pancreas doesn't make enough or any of the hormone insulin, or when the insulin produced doesn't work effectively. In diabetes, this causes the level of glucose in the blood to be too high. In Type 1 diabetes the cells in the pancreas that make insulin are destroyed, causing a severe lack of insulin. This is thought to be the result of the body attacking and destroying its own cells in the pancreas - known as an autoimmune reaction. It's not clear why this happens, but a number of explanations and possible triggers of this reaction have been proposed. These include: infection with a specific virus or bacteria; exposure to food-borne chemical toxins; and exposure as a very young infant to cow's milk, where an as yet unidentified component of this triggers the autoimmune reaction in the body. However, these are only hypotheses and are by no means proven causes. Type 2 diabetes is believed to develop when: the receptors on cells in the body that normally respond to the action of insulin fail to be stimulated by it - this is known as insulin resistance. In response to this more insulin may be produced, and this over-production exhausts the insulinmanufacturing cells in the pancreas; there is simply insufficient insulin available; and the insulin that is available may be abnormal and therefore doesn't work properly. The following risk factors increase the chances of someone developing Type 2 diabetes: Increasing age; obesity; and physical inactivity. Rarer causes of diabetes include: Certain medicines; ~ pregnancy (gestational diabetes); ~ any illness or disease that damages the pancreas and affects its ability to produce insulin e.g. pancreatitis 44. No commentary 45. End results of badly managed diabetes: Neuropathy, cardiopathy, myopathy, kidney failure, decubitus ulcers on extremities, necrosis, gangrene 46. S/S = signs and symptoms With a hypoglycemic attack -- Offering water to someone with hyperglycemia will dilute the blood sugar. It is not a fix, but it can by a little time until other aid/assistance is possible. 47. No commentary 48. Massage and Diabetes: a. Can be appropriate: weigh risks and benefits b. Cardiovascular and kidney problems contraindicate rigorous circulatory massage c. Work when insulin is not at peak (to avoid double whammy) d. Be cautious about numbness, reduced sensation, skin lesions 49. No commentary 50. No commentary 51. No commentary 52. Last slide