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1. The Endocrine System
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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
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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.
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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).
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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
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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
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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
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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
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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
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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
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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
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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.
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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
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