Endocrine lecture
2/5/01
Objectives and lecture mixed together
1. Know the anatomical location of the endocrine glands.
Head
- Pineal gland
- Hypothalamus
- Pituitary gland
Neck
- Thyroid gland
- Parathyroid glands (on dorsal aspect of thyroid gland)
High sternal area
- Thymus gland
LUQ/RUQ
- pancreas
- Adrenal glands
LLQ/RLQ
- Ovary (female)
External (testis-male)
Endocrine function
1. Sends messages via hormones into the blood stream
2. Differentiation of the reproductive and central nervous systems in the developing fetus.
3. Stimulation of sequential growth and development during childhood and adolescence.
4. Coordination of the male and female reproductive systems, which makes sexual reproduction possible.
5. Maintenance of an optimal internal environment throughout the life span.
6. Initiation of corrective and adaptive responses when emergency demands occur.
Hormone Characteristics
The endocrine glands respond to specific signals by synthesizing and releasing hormones into the circulation. Although a wide variety of hormones function within the body, they share certain general characteristics:
Hormones have specific rates and patterns of secretion
- Diurnal – 24 hour (i.e.. cortisol) Peaks in the AM and lowest at MN
- Cycle – every 28 days (i.e.. estrogen)
- Variable – patterns that depend on levels of circulating substrates.
Hormones operate within feedback systems, either positive or negative, to maintain an optimal internal environment. (Endocrine feedback loops involve the hypothalamus-pituitary gland and end organs (endocrine regulation))
Hormones affect only cells with appropriate receptors and then act on these cells to initiate specific cell functions or activities. (Regulates cellular activity)
Hypothalamus plays largest role in regulating endocrine function by linking CNS to endocrine via pituitary gland.
2. Characterize the functions and regulation
of the hormones secreted by the pituitary, adrenal, thyroid and parathyroid
glands.
Gland |
Functions |
Regulation |
Anterior Pituitary |
Function is regulated by
the integrated effects of hypothalamic releasing and inhibiting hormones and
feedback effects from circulating hormones.
|
GH, TSH,
adrenocorticotropic hormone (ACTH), prolactin, gonadotropic hormones (e.g.,
FSH, LH), and Beta lipotropin. Book
adds Melanocyte stimulating hormone (MSH) and prolactin (PRL) |
Posterior Pituitary |
It is seen as a storage and
releasing site for hormones synthesized in the hypothalamus. |
(Produced in the
hypothalamus as pro-hormones) ADH or vasopressin and oxytocin stored in the
posterior pituitary |
Adrenal Medulla |
The functional roles within
the adrenal glands are not know at
present. |
Secretes the catecholamines
epinephrine and dopamine |
Adrenal Cortex |
The functional roles within
the adrenal glands are not know at
present. |
Secretes 50 steroid
hormones which are classified as: -
glucocorticoids -
mineralocorticoids adrogens |
Thyroid glands (2 lobes) |
Produces hormones that control the rates of
metabolic processes throughout the body |
Thyroxine (T4)
and Triiodothyronine (T3), and calcitonin. |
Parathyroid glands (2-6 glands) |
Regulate the blood level of
calcium |
PTH * PTH is free of pituitary and hypothalamic control. The secretion of this hormone is directly
regulated by a feedback system. |
3. Specify the physical characteristics of patients with endocrine dysfunction.
Graves Disease (hyperthyroidism)
- nervousness, emotionally liability, irritability, apprehension and insomnia
- fine tremors of hands
- profuse perspiration; flushed skin heat intolerance
- Increase of appetite but weight loss/ or sign. Change in bowel habits of diarrhea, frequent stools
- Muscle fatigue and weakness, muscle wasting
- Amenorrhea
- Kids may be tall and underweight for age
- Rapid pulse at rest as well as on exertion (90 – 160 bts/min)
- Palpitations, possible A-Fib
- exophthalmos, weakness of extraocular muscles, lid edema, lid lag).
- Possible enlarged thyroid gland (goiter); bruit auscultated over gland
- P and T wave changes
- Increase in BP
Hypothyroidism (in childhood = cretinism)
Can be end result of graves disease or Hashimoto’s thyroiditis because these autoimmune diseases destroy the thyroid glands.
- lethargy, depression
- sensitivity to cold, weight gain, later enlarged thyroid
- dry skin
- normal to subnormal temperature
- normal to slow pulse
- normal respiratory rate unless affected by goiter size
- normal to slight elevation of BP
- augmentation of congested heart failure
- Myxedema – dry, waxy, non-pitting swelling due to mucin deposits in skin and tissues.
- IF SEVERE – hypotension, hypoventilation, bradycardia, hypothermia, cerebral hypoxia.
Hypoparathyroidism
* Clinical features are due to low serum calcium levels.
- s/s tetany
- tingling of the lips, finger tips, and occasionally feet
- Increased muscle tension leading to parenthesis and stiffness.
- Dysphagia, painful tonic spasms of smooth and skeletal muscles
- Chvostek’s sign (a facial muscle spasm when the face is tapped below the temple)
- Trousseau’s sign (a carpopedal spasm when arterial circulation is interrupted by applying a blood pressure cuff for 3 minutes)
- Respiratory function may be severely compromised by accessory muscle spasm and laryngeal spasm – induced airway obstruction.
- Patients are usually anxious and apprehensive
Hyperparathyroidism
* Condition involving increased secretion of (PTH). PTH helps regulate calcium and phosphate levels by stimulating bone reabsorption, renal tubular reabsorption of calcium, and activation of vitamin D.
Clinical manifestations:
- weakness, loss of appetite
- constipation, increased need for sleep
- shortened attention span
-
Major signs
- Loss of calcium from bones, broken bones
- Kidney stones
- Neuromuscular abnormalities i.e.…
- Muscle weakness, particularly in proximal muscles of the lower extremities
- Complications include renal failure, pancreatitis, collapse of vertebral bodies, cardiac changes, and long bone, and rib fractures.
Hypopituitarism
· Clinical features are due to infections, autoimmune disorders, tumors, or destruction of the gland through radiation or surgical procedures. There can be failure to secrete growth hormone (GH), deficiencies of gonadotropins, TSH, ACTH, and prolactin.
· The manifestations of hypopituitarism depend on the specific pituitary hormones that are lacking.
- Weakness, fatigue, headache, sexual dysfunction, fasting hypoglycemia, dry and sallow skin, diminished tolerance for stress, and poor resistance to infection.
- In the adult, premature, fine wrinkling around the eyes and mouth is common.
- Psychiatric symptoms include apathy, mental slowness, and delusions.
- Orthostatic hypotension may occur.
* If hypopituitarism is not detected and treated, the patient develops deficiencies of thyroid hormone and the adrenal corticosteroids. The latter deficiency causes a tendency toward shock and may result in an episode of acute adrenal insufficiency (refractory and life-threatening shock resulting from sodium and water depletion).
Hyperpituitarism: Primary Adenoma
Clinical manifestations:
- headache, neck pain, stiffness
- seizures r/t tumor
- visual changes produced by pressure on the optic chiasm
- temporary blindness
- If tumor infiltrates other areas of brain or cranial nerves, neurologic function is affected
Hypofunction of the adrenal cortex or adrenocortical insufficiency
- Primary disorder within the adrenal gland due to idiopathic atrophy or destruction of the adrenal glands, may be autoimmune; results of TB, AIDS, metastasis from lungs, breast GI, melanoma or lymphoma.
Clinical manifestations:
- progressive weakness, fatigue
- weight loss and anorexia
- Skin hyperpigmentation, a striking feature is seen primarily in sun-exposed areas of the body, at pressure points, over joints and in creases, especially palmar creases.
- Hypotension, most dangerous can cause shock especially during stress.
- Hyponatremia
- Hyperkalemia
- N/v and diarrhea
* Patients
with adrenocortical insufficiency are at risk for acute adrenal insufficiency
(Addisionian crisis) which is life-threatening
emergency.
Hyperfunction of the adrenal cortex (Cushing Disease, Cushing Syndrome)
Hyperfunction of the adrenal cortex causes increased levels of circulating cortisol leads to Cushing disease. Hyperfunction that causes increased secretion of adrenal androgens and estrogens leads to virilization or feminization; and hyperfunction that causes increased levels of aldosterone leads to hyperaldosteronism, which may be primary or secondary.
Clinical manifestations:
- weight gain
- especially accumulation of adipose tissue in the trunk, facial and cervical areas (moon face, buffalo hump and truncal obesity)
- transient weight gain from sodium and water retention may be present because of the mineralocorticoid effects of cortisol, exhibited when cortisol is present in high levels
- glucose intolerance because of cortisol-induced insulin resistance and increased Gluconeogenesis and glycogen storage by the liver
- Overt diabetes mellitus develops in approximately 20% of individuals with hypercortisolism.
- Polyuria, glycosuria
- Protein wasting
- Muscle wasting especially of the muscles of the extremities.
- Osteoporosis with pathologic fractures
- Vertebral compression fractures
- Bone and neck pain
- Kyphosis and reduced height
- Hypercalciuria and resulting renal stones
- Loss of collagen
- Purple striae in trunk area
- Loss of collagenous supports around small vessels makes them susceptible to rupture causing easy bruising even with minor trauma.
4. Discuss the effects of aging on the endocrine system.
*** ALL TAKEN WORD FOR WORD OUT OF PATHOPHYS BOOK ***
* these are theories, it has been difficult to identify who affects who*
Thyroid
- glandular atrophy and fibrosis occur with nodularity and increasing inflammatory infiltrates
- these infiltrative changes may reflect age related autoimmune damage
- T4 secretion and turnover are decreased.
- Plasma levels of T3 decline, especially in men
- Hypothyroidism is seen with increasing frequency as age advances
- Overall TSH secretion is diminished
- Responsiveness of plasma TSH concentration to TRH administration is reduced especially in men.
* The overall dose for TH replacement appears to be lower in elderly persons because the peripheral metabolism of TH decreases with age. TH must be replaced slowly in elderly individuals with CAD to prevent angina and MI. Clinical signs of thyroid disease are more difficult to detect in elderly persons.
Parathyroid gland
- Calcium intake especially in women, tends to decrease with age.
- Older adults show decreased intestinal adaptation to variations in calcium intake.
- Many older adults also have a mild, persistent Hypercalciuria, which indicates a defective renal mechanism for responding to decreased calcium intake.
- Decreased circulating levels of vitamin D also have been documented.
* The decrease in calcium intake, an age-related decrease in circulating vitamin D, and a blunted response of older persons to PTH may explain these changes seen in aging.
Adrenal Glands
- The adrenal cortex loses some weight and has more fibrous tissue after the age of 50years old.
- Age does not appear to affect the feedback mechanism involved in maintaining glucocorticoid levels, but the decrease in the metabolic clearance rate of the glucocorticoids is age related.
- The metabolic clearance of cortisol decreases with an age-related decline in liver and kidney function.
- Less cortisol appears to be used by the body when aging is accompanied by a loss of lean body mass
- Plasma levels of the adrenal androgens, as well as urinary excretion of the metabolic end products, decrease gradually but dramatically with age to as much as 50% - 70% of the young adult.
- Changes in both the testis and hypothalamic-pituitary axis may be responsible for decreased testosterone levels.
Posterior pituitary
- Hyponatremia appears related to changes in renal function rather than ADH-related mechanisms.
Anterior pituitary
- a number of morphologic changes occur
- increases in fibrosis
- focal necrosis
- iron deposits
- microadenoma formation
- moderate decrease in size
5. Differentiate between the SCR and HDSCR as they pertain to endocrine disorders.
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6. Articulate the kinds of tests used to diagnose endocrine disorders and related nursing responsibilities.