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99 Cards in this Set
- Front
- Back
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What is the relationship between an injured brain the endocrine system?
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- An injured brain can set off problems with the hypothalamus and the pituitary gland
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Define hormone.
Does the distance that the hormone has to travel to its target organ affect the message? |
The endocrine's chemical messenger.
A blood-borne chemical messenger (ligand) that has an effect on target cells anatomically distant from the secreting cell. Initiates or regulates the activity of an organ or group of cells. "first messengers" -NO |
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What are the two major classifications of hormones?
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1. Water-soluble amino acid derivatives or peptide hormones (most endocrine hormones) (travel easily in plasma)
2. Lipid-soluble steroid hormones: adrenal & sex glands (require protein transport to travel in blood circulation) |
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Where are the H2O soluble hormones located?
Where are the lipid soluble hormones located? |
- Located on the cell surface (catecholamines, peptides)
- Located intracellularly (thyroid hormones, steroids) |
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Describe endocrine action.
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The hormone is distributed in blood and bind to DISTANT target cells.
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Describe paracrine action.
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The hormone acts locally (short distance) by diffusing from its source to target cells in the neighborhood; travels in ECF.
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Describe autocrine action.
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The hormone acts on the same cell that produced it (very short distance); acts on itself.
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Describe receptors for water soluble hormones.
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- Receptors for water soluble hormones are found on the surface of the target cell, on the plasma cell membrane.
- Coupled with various second messenger system which mediate the action of the hormone in the target cell These type of receptors are couple to various second messenger systems which mediate the action of the hormone in the target cell. |
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Describe the receptors for lipid soluble hormones.
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Receptors for the lipid soluble hormones reside in the nucleus (and sometimes the cytoplasm) of the target cell.
Because these hormones can diffuse through the lipid bilayer of the plasma membrane, their receptors are located on the interior of the target cell. |
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What is the job(s) of the endocrine system and how are they preformed?
What 5 mechanisms does the Metabolic process take care of? |
Job one: maintain the optimum biochemical environment (maintain homeostasis and balance)
-controls via negative feedback -regulates by excreting or inactivating hormones -Takes care of the metabolic process (1) Energy production (2) Growth (3) Fluid and electrolyte balance (4) Response to stress (5) Reproduction |
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What must occur in hormonal control to achieve homeostasis and how is it generally achieved?
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- Hormones must be inactivated or excreted to maintain internal stability (homeostasis)
- Generally achieved through the negative feedback loop |
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The three endocrine system components
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1. The CELL in which the chemical message originates in the form of a hormone.
2. The ENVIRONMENT in which the chemical (hormone) is transported. (Usually the bloodstream.) 3. The TARGET CELL which receives the chemical message (hormone). -> Goes back to original messaging cell to say, "That's enough." |
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Physiologic vs. Pharmacologic Hormones
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Physiologic hormone concentrations are extremely low in most cases, and pharmacologic levels of hormones are usually several-fold greater than would normally be secreted by endocrine tissues.
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Hormone Metabolism and Excretion
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The plasma concentration of a hormone depends not only on the rate of synthesis and release of the hormone but also on how rapidly the hormone is metabolized and excreted.
Water-soluble hormones may be excrete in the urinary filtrate. Lipid-soluble hormones, which are bound to plasma proteins and stored in adipose tissues, are less readily metabolized and remain in the circulation for a more prolonged period of time. |
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Receptor Specificity
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Refers to a molecular "fit" of a hormone within a receptor binding pocket.
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Receptor Affinity
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Affinity describes the degree of "tightness" of the hormone-receptor bond, or the inclination of the hormone to remain bound to the receptor. The higher the affinity of the receptor of the hormone, the lesser the amount of hormone needed to produce a response.
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Down-regulation
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When cells are exposed to high concentrations of hormone for a prolonged period of time, a common result is that the cell decreases the number of receptors, thus decreases the sensitivity to the hormone (i.e., insulin in obese people).
Down-regulation probably serves a protective function: the cells are protected against excessive activity despite pathologic processes that cause excessive hormone levels. |
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Up-regulation
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An increase in the number of receptors in response to a chronically low hormone concentrations. This would make the cell more sensitive to the hormone, and hormone-dependent cellular activity would occur at normal or nearly normal levels despite a lower than normal hormone concentration.
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Permissiveness
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An effect that hormones have may on target cells is to increase the number of receptors for other hormones, thus enhancing the effect of the second hormone.
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What are the big nine endocrine glands?
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1. Gonads: ovaries, testes
2. Pancreas 3. Thymus 4. Hypothalamus 5. Pituitary 6. Thyroid 7. Parathyroid 8. Pineal 9. Adrenals |
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Describe the anatomical location of the pituitary gland.
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Connected to the hypothalamus by the pituitary stalk and sits in a bony pocket called the sella turnica.
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Describe the pituitary gland.
What location secretes the hormones in the anterior and posterior pituitary gland? |
Also called the hypophysis.
Anterior - adenohypophysis secretes 6 hormones Posterior - neurohypophysis secretes 2 hormones |
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What are the 6 hormones secreted by the anterior pituitary gland?
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The anterior lobe has 5 endocrine cell types that secrete 6 peptide hormones:
(1) Growth hormone [GH] (2) Luteinizing hormone [LH] (3) follicle-stimulating hormone [FSH] (4) Thyroid-stimulating hormone [TSH] (5) Adrenocorticotropic hormone [ACTH] (6) Prolactin [PRL] |
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What are the 2 hormones secreted by the posterior pituitary gland?
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(1) antidiuretic hormone (vasopressin)
(2) oxytocin |
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Describe the antidiuretic hormone.
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It is secreted by the posterior pituitary gland (neurohypophysis).
It is released in response to altered serum osmolality, hypotension and when body fluid become too concentrated. It causes water retention by increasing water reabsorption by the renal collecting duct. |
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Describe the oxytocin hormone.
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It is secreted by the posterior pituitary gland (neurohypophysis).
It is released during sexual activity, childbirth, and breast-feeding and causes uterine and milk duct contractions. |
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Trophic Hormones
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A hormone released by the anterior pituitary gland that stimulates the release of other hormones, which then act on target organs.
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Anatomical Feedback Loop of Endocrine System
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CNS (+) or Input (-)
Hypothalamus Releasing or Inhibiting Hormones Anterior Pituitary Trophic Hormones Target Organs Hormones Physiologic Effect |
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What would happen to the growth hormone (GH) without the negative feedback loop?
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Too much GH; can lead to giants.
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What would happen to the gonadotropin hormone
without the negative feedback loop? |
Sexual characteristics would appear too soon, leading to precocious puberty.
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What would happen to the antidiuretic hormone (ADH) without the negative feedback loop?
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If too much ADH, would lead to Syndrome of Inappropriate Antidiuretic Hormone (SIADH).
If too little ADH, would lead to diabetes insipidus. |
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What controls the secretion of growth hormone (GH)?
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Growth hormone-releasing hormone (GHRH) and growth hormone-inhibiting hormone (somatostatin).
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What controls the secretion of the prolactin (PRL) hormone?
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The lactotropes secrete prolactin. Prolactin is best known for its trophic effects on breast tissue development and lactation and its ability to suppress reproductive function in both me and women.
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What controls the secretion of the follicle-stimulating hormone (FSH) and luteinizing hormone (LH)?
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They are both secreted by the gonadotropin-releasing hormone. FSH and LH can also be called gonadotropins.
In general, FSH and LH stimulate testosterone production in men and estrogen and progesterone production in women. |
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What controls the secretion of the thyroid stimulating hormone (TSH)?
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Thyrotropes release TSH in response to hypothalamic thyrotropin releasing hormone (TRH).
TSH regulates all aspects of thyroid function, including growth of the gland, hormone synthesis, and hormone secretion. |
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What controls the secretion of the adrenocorticotropic hormone (ACTH)?
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ACTH is produced by corticotropes in the anterior pituitary gland in response to hypothalamic corticotropin-releasing hormone (CRH).
ACTH binds to the adrenal cortex and stimulates the production of cortisol and adrenal androgens. It also have trophic effects on the adrenal cortex and supports the structure and synthetic enzymes of the gland. |
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What type of steroids does the adrenal cortex produce?
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(1) Glucocorticosteroids (cortisol)
(2) Mineralocorticoids (aldosterone) (3) Sex steroids (androgen) Synthesis and secretion of these hormones are considered essential for life, regulating the body's response to normal and abnormal levels of physiologic and psychological stress. The activities can be known as the "three S's": sugar, salt, and sex. |
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What controls the secretion of triiodothyronine (T3) and thyroxine (T4)?
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The thyroid glandd secretes the thyroid hormones T3 and T4. Approximately 90% of the thyroid hormone is in the form of T4 and 10% is in the form of T3.
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What controls the secretion of epinephrine and norepinephrine?
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The adrenal glands are composed of an inner medulla and outer cortex. The adrenal medulla secrete epinephrine and norepinephrine in response to sympathetic nervous system stimulation.
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Name the three zones of the adrenal glands.
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(1) Outer zona glomerulosa
(2) Middle zona fasciculata (3) Inner zona reticularis |
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What does the zona glomerulosa of the adrenal glands produce?
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The outer zona glomerulosa produces the mineralocorticoid, aldosterone, in response to stimulation by angiotension II (AII).
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What does the zona fasciculata of the adrenal glands produce?
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The middle zona fasciculata produces the glucocorticoid, cortisol, in response to stimulation of (adrenocorticotropic hormone) ACTH from the pituitary gland.
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What does the zona reticularis of the adrenal glands produce?
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The inner zona reticularis is adjacent to the adrenal medulla and produces the androgen. It is stimulated by adrenocorticotropic hormone (ACT).
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Describe glucocorticoids.
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Glucocorticoids, principally cortisol, are named for their primary effect on glucose metabolism. Glucocorticoids oppose the effects of insulin and raise blood sugar. This is accomplished by decreasing glucose uptake by many body cells (decreased glycogenesis), increasing glucose synthesis in the liver from glycogen and amino acid and glycerol substrates in protein and fat stores (glycogenolysis, gluconeogenesis). Glucocorticoids also contribute to protein catabolism by releasing muscle stores of proteins, providing amino acids for glucose production in the liver.
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Describe mineralocorticoids.
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Mineralocorticoids, principally aldosterone, function to maintain normal salt and water balance by promoting sodium retention and potassium excretion at the distal renal tubules.
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What are the 3 ways endocrine disorders can result?
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1. Hormone deficiency (hyposecretion)
2. Hormone excess (hypersecretion) (usually caused by exogenous ingestion of hormone such as anabolic steroid abuse) 3. Hormone resistance -Hyporesponsiveness is similar to hyposecretion and is due to hormone receptor dysfunction; this phenomenon is called tissue resistance. Almost without exception, hormone deficiency causes disease. EXCEPT for calcitonin deficiency. |
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The are the 6 etiologies of endocrine disorders?
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It may be
1. congenital 2. infectious 3. autoimmune 4. neoplastic 5. idiopathic 6. iatrogenic. |
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What is the mechanism of endocrine disease?
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- The cause of hormone excess is usually exogenous ingestion of hormone.
o The most common form of exogenous hormone is steroids o for example, glucocorticoid excess or anabolic steroid abuse |
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What are the three ways that pharmacological hormones are used?
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(1) Replacement therapy (for deficiency) - insulin/DM, steroids/Addison's disease
(2) Interventional therapy (to stop disease) - steroids/inflammation (i.e., asthma) (3) Endocrine diagnostic testing - cortisol testing for levels |
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What are the signs and symptoms of growth hormone excess in children?
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Increased linear growth and tall stature
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What are the 12 signs and symptoms of growth hormone excess in adults?
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1. Soft tissue hyperplasia
2. Increased bone density 3. Large hands, feets 4. Coarse facial features 5. Thick, leathery skin 6. Weight gain 7. Glucose intolerance or hyperglycemia (GH is diabetogenic) 8. Pts usually notice increased ring or shoe size 9. enlargement of frontal sinuses cause a prominent brow 10. Growth of mandible results in progressive underbite (prognathism) 11. Organ enlargement (goiter, cardiomegaly); may cause arrythmia 12. Deepening of voice due to vocal cord thickening and enlargement of tongue, which also results in sleep apnea |
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What are the 3 signs and symptoms of growth hormone deficiency in children?
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1. Delayed growth
2. Fine features 3. Short stature, proportionate |
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What are the signs and symptoms of growth hormone deficiency in adults?
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-May be associated with hyposecretion of other pituitary hormones
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What are the clinical manifestations of growth hormone deficiency?
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- GH-deficient children fall below the third percentile of growth in comparison to their peers: dwarfism.
- Dental eruption is delayed, and the development and setting of teeth are irregular. (Overcrowded, malpositional teeth may affect nutrition.) - The hair is thin, and nail growth is poor. -This does not affect intelligence, cognition, and they are able to produce normal offspring (unlike achrondoplasia). |
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Describe achrondoplasia.
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Achrondoplasia is a common cause of dwarfism due to a mutated gene.
Children with GH deficiency are not achrondoplasic and can have produce normal offspring. |
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What are the clinical manifestations of growth hormone excess?
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-Overgrowth of long bones, viscera and muscles: acromegaly in adults or prepubertal gigantism in kids.
-Separation of teeth and malocclusion. |
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What is the therapeutic management for growth hormone deficiency?
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-Surgical intervention: removal (via nares) or irradiation (shrink or cause damage) of craniopharyngioma (tumor at junction of anterior and posterior pituitary gland).
-Endocrine: replacement of GH with recombinant DNA GH -Stop GH replacement when epiphyseal closes (or will lead to acromegaly) |
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What is the therapeutic management for growth hormone excress?
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-Surgical removal of lesion.
-Endocrine replacement of all hormones affected. (will need to replace all 8 hormones if surgically remove half of pituitary gland.) |
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What are the 5 diagnosis for precocious puberty?
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1. Gonads (sex hormones) in excess from gonadotropin
2. Very rare to see this in the U.S. 3. Hypothalamic-pituitary-gonadal Axis 4. Caucasian females < 7 y/o 5. African American females < 6 y/o |
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What are the 3 therapeutic management for precocious puberty?
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1. Family support and instructions on IM drug therapy
2. Leuprolide acetate IM q 4 weeks. Stopped at chronologically appropriate time (use Tanner scale). 3. May need GH therapy. |
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What is the nursing care management for precocious puberty?
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- Family support. Child is chronologically age appropriate
- When child reaches puberty, care must be taken with estrogen based therapy (still have mind of child by looks attractive to others). |
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What can cause growth hormone deficiency?
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GH deficiency may be idiopathic or related to tumors, radiation, or trauma.
- The Dx is confirmed by a finding of decreased GH levels in the blood or deficient GH release in response to hypoglycemia or other stimulants. |
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What can cause growth hormone excess?
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Excessive GH production is usually due to a pituitary adenoma.
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Where is the thyroid gland located and what is its shape?
What are the characteristics of the thyroid gland. What 2 products does the thyroid gland produce? |
- located in middle anterior part of neck, below larynx and in front of trachea
-butterfly-shaped 1. 2 lobes connected by isthmus 2. increase in size during puberty and pregnancy 3. has rich blood supply; able to deliver high levels of hormones in short period of time 4. Calcitonin: involved in calcium and phosphate homeostasis - produces Thyroxin (T4) & Tri-iodothyronine (T3) |
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Describe regulation and negative feedback loop of the thyroid.
What are released by the thyroid and how is it controlled? |
- Thyrotropin hormone (TRH) in the hypothalamus stimulates thyroid-stimulating hormone (TSH) in the anterior pituitary gland.
- TSH stimulates all aspects of thyroid function, including the growth of the thyroid. After some growth, TSH stimulates the thyroid to release T3 & T4. Rising plasma levels of T3 and T4 tell the anterior pituitary gland to suppress TSH. With less TSH, the thyroid shrinks and releases less T3 & T4. |
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Describe T3 and T4.
What is the difference between T3 and T4? |
- Tri-iodothyronine (T3) and thyroxine (T4) are lipid-soluble and can cross the cell membrane by simple diffusion.
- T3 is the active form - T4 is the storage form. T4 is converted to T3 inside all of the cells in the body to become active. Need iodine to make this occur. |
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What happens to the thyroid without iodine?
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- Iodine is necessary for the body to convert T4 to T3. Without it, the thyroid will grow bigger and bigger trying to make T3 and T4. (We do not see signs of iodine insufficiency for a while. We can store up to 1 month of T4.)
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What are the 3 major types of hypothyroidism?
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(1) Congenital hypothyroidism (cretinism)
(2) Lymphocytic thyroiditis (Hashimoto thyroiditis, or autoimmune thyroiditis) is the most common cause of acquired hypothyroidism (3) Irradiation of the thyroid gland, surgical removal of thyroid tissue, and iodine deficiency |
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What is primary (1) and secondary hypothyroidism (6)?
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The majority of cases of hypothyroidism are primary, due to
1. intrinsic dysfunction of the thyroid gland (i.e., congenital cretinism, lymphocytic thyroiditis, radiation or surgery). Secondary hypothyroidism is caused by 1. defects in TSH production. This includes individuals who have been exposed to 2. severe head trauma 3. cranial neoplasms 4. brain infections 5. cranial irradiation 6. neurosurgery. |
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Describe congenital hypothyroidism.
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Also called cretinism. Thyroid dysgenesis (lack of thyroid gland development) accounts for most congenital hypothyroidism. Abnormal TSH receptors and defective synthesis of thyroid hormone are other mechanisms causing congenital hypothyroidism.
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Describe lymphocytic thyroiditis.
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Also called Hashimoto thyroiditis or auto-immune thyroiditis. Characterized by an enlarged thyroid gland caused by lymphocytic infiltration. Thyroid hormone production decreases, stimulating the release of TSH from the pituitary gland, indicating a hypoactive thyroid gland.
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Describe hypothyroidism.
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Primary hypothyroidism will manifest as elevated TSH. Low levels of T3 & T4 may not occur until later in the disease course (we store up to a month of T4 in body). In rare cases of hypothalamic-pituitary dysfunction results in low levels of TSH and T4.
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What is myxedema?
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Myxedema occurs in severe or prolonged thyroid deficiency. The term myxedema refers to the generalized, non-pitting edema that patients with long-term hypothyroidism tend to demonstrate.
These pts typically have facial puffiness and dull expressions; the edematous-looking skin is from the accumulation of glycosaminoglycans in the interstitial spaces, which then retain fluid. Without medical intervention, pts may lapse into myxemeda coma, a medical emergency with upward of 60% mortality. |
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What are the 11 clinical manifestations of hypothyroidism?
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1. Lethargy
2. Weakness 3. Dry, pale, cool, coarse skin 4. Cold intolerance 5. Weight gain 6. Constipation 7. Bradycardia 8. Dyspnea, chest pain 9. Sluggish return on reflexes 10.Facial edema 11. Heavy, prolonged menses |
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What diagnostic test can be utilized to discover if a pt has hypothyroidism?
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We can measure TSH levels. Pts with hypothyroidism will have elevated TSH levels because of the lack of feedback exerted by the T3 & T4.
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What are the 3 etiologies and pathogenesis for hyperthyroidism?
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(1) Thyroid follicular cell hyperfunction with increased synthesis and secretion of T4 and T3 (Graves disease)
(2) Thyroid follicular cell destruction with release of preformed T4 and T3 (Hashimoto thyroiditis) (3) Ingestion of excessive thyroid hormone (thyroid med/supplement) or iodide preparations (salt) |
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What is primary, secondary, and autoimmune hyperthyroidism?
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(1) Primary - autonomous (could be dysfunction of thyroid itself)
(2) Secondary - mediated through stimulus of TSH receptors by substances such as TSH (negative feedback loop not working) (3) Autoimmune - related to TSH receptor antibodies |
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What are the 12 clinical manifestations of hyperthyroidism?
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1. Changes in behavior
2. Insomnia 3. Restlessness 4. Tremor 5. Irritability 6. Palpitations 7. Heat Intolerance (can tolerate heat or not) 8. Diaphoresis 9. Inability to concentrate that interferes with work performance 10. Increased basal metabolic rate leads to weight loss, although appetite and dietary intake increases 11. Amenorrhea/scant menses 12. Thyroid storm |
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What is a thyroid storm?
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It is a form of life-threatening thyrotoxicosis that occurs when excessive amounts of thyroid hormones are acutely released into the circulation. This may occur under conditions of psychological pr physiological stress or wih physical manipulation o the gland during diagnostic or surgical procedures.
It presents with the clinical features of elevated temperatures, significant tachycardia, cardiac arrythmias, and congestive heart failure. Extreme restlessness, agitation, and psychosis may occur. The pt may also experience vomiting, nausea and diarrhea; jaundice may develop due to hepatic dysfunction. Prompt Tx is required. |
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What are the 3 treatments for hyperthyroidism/ Graves Disease?
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1. Propylthiouracil (PTU)
2. radioactive iodione 3. surgery |
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What is Graves disease?
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The most common etiology of hyperthyroidism is from autoantibodies that bind and stimulate TSH receptors on the thyroid gland. This stimulation leads to a diffuse toxic goiter and a type of primary hyperthyroidism called Graves disease.
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What are the 3 clinical manifestations of Graves disease?
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1. thyromegaly (diffused enlarged thyroid, goiter)
2. thyrotoxicosis 3. exophthalmos (enlargement of retro-orbital muscles causing protrusion of the eyes) - Spasm and retraction of the eyelids leads to widening of the palpebral fissure, resulting in exposed sclera. Lid lag develops, and severe, progressive exophthalmos may occur. Eye complaints may include vision changes and photophobia. |
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What are the 3 things that the Adrenal Cortex synthesizes?
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1. Glucocorticoids
a. Cortisol is the primary glucocorticoid and negative feedback suppresses ACTH release 2. Mineralocorticoids 3. Androgens |
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What is the Primary, secondary, and tertiary etiologies of Adrenocortical insufficiency?
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- Primary: hyposecretion due to disease of adrenal cortex (Addison disease) --> gland
- Secondary: inadequate secretion of ACTH from the anterior pituitary --> Brain - Tertiary: lack of CRH (cortisol releasing hormone) secretion from the hypothalamus due to hypothalamic malfunction or injury •Injury: car crash, coup, counter coup |
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What are the characteristics of secondary Adrenocortical Insufficiency?
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- Hypothalamic-pituitary dysfunction related to corticosteroid therapy (asthmatics), which supress ACTH, CRH
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What are the 5 ways Adrenalcortical Insufficiency diagnosed?
What are the signs/symptoms of a person with adrenal cortical insufficiency? |
1. Patient history
2. Physical exam 3. Decreased plasma cortisol levels 4. ACTH provocation test 5. Abdominal CT/MRI to evaluate the size of the adrenal gland 1. Person will look very stressed 2. Rapid speech (at first) 3. Patient history about how the person has changed and what normal behavior is |
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What are treatments for an Adrenalcortical Insufficiency?
What are the 2 treatments of an adrenal crisis (a life threatening event)? |
1. Replacing the absent or deficient hormones in a manner that mimics natural production/ pattern
2. 2/3 OF THE DAILY DOSAGE IS GIVEN IN THE MORNING AND 1/3 IN THE EVENING- to follow the natural rhythm 1. Intravenous glucocorticids (insufficiency -> administer cortisol) 2. Volume replacement using a large bore canula |
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What are some stressful situations that affect cortisol needs?
How do stressful situations affect cortisol needs? How is cortisol brought back to normal levels? How do we know when its time to back off with supplementation? |
- Double or triple the daily cortisol needs
- Acute illness - Injury (trauma, burns, surgery) - Psychological episodes - ALL SITUATIONS ABOVE REQUIRE SUPPLEMENTATION - Monitor VS, they should come back to normal |
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What are that characteristics of hyperaldosteronism?
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1. Huge retention of Na+ and H2O
2. Aldosterone facilitates Na+ and H2O rentention by the kidney with resultant K+ excretion 3. Hypernatremia would cause hypocalemia 4. Typically low K+ levels |
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What are the 2 treatments for hyperaldosteroneism?
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1. SPIRONOLACTONE to increase sodium excretion and potassium retention
a. used if you want to get ride of H2O but retain K+ 2. Dietary sodium restriction and potassium replacement may also be necessary |
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What are the 5 hormones from the adrenal and where are they synthesized?
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Cortex:
1. Mineralocorticoid (Aldosterone) 2. Glucocorticoid (Cortisol) 3. Androgens Medulla: 4. Epinephrine (Adrenaline) 5. Norepinephrine (Noradrenaline) |
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What are the 2 effects of mineralocoticoids?
What are the 3 effects of glucocorticoids and Androgens? What are the effects of epinephrine and norepinephrine? |
1. Increases renal reabsorption of Na+ ions & H2O
2. Increases renal K+ ion loss 1. Releases amino acids from skeletal muscle & lipids from adipose 2. Promotes liver glycogen & glucose formation 3. Anti-inflammatory effect 1. Increases cardiac activity 2. Increases blood pressure 3. Increases glycogen breakdown 4. Increases blood glucose |
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1. What is the role of the parathyroid gland?
2. How do Parathyroid gland disorders manifest? |
1. Regulation and action of parathyroid hormone
a. Detect serum Ca+ concentration and maintain constant levels through the regulation of Ca+ absorption and reabsorption 2. Disorder may occur when absorption of Ca+ from the intestine and renal tubules is Vit D dependent and may be impaired in conditions where Vit D is deficient a. W/O Vit D, there will be a problem mobilizing Ca+ b. Vit D is dependent on the exposure of the sun |
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1. How does Antidiuetic Hormone (ADH) function normally?
2. What is the difference between osmolarity and osmolality? |
1. • ADH acts directly on the renal collecting ducts and distal tubules, increasing membrane permeability to and reabsorption of water
a. Action happens In the kidneys b. Secreted by the pos. pituitary in response to changes in blood osmolality 2. |
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What are the 8 clinical manifestations of Diabetes Insipidus?
What cause the 3 causes of these manifestations? |
1. Polyuria
2. Polydipsia 3. Dehydration 4. Imbalance 5. Hyperthermia (fever) 6. Azotemia (high levels of urea and other waste products) 7. Poss. urine dilute 8. Circulatory collapse 1. Closed head trauma 2. Brain tumors 3. Tumors of the hypothalamus |
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How is Diabetes Insipidus diagnosed?
What are the 3 therapeutic managements for Diabetes insipidus? |
1. Restricted oral intake and output
2. CT of the brain 3. Kidney function tests- renal failure 1. Vessopressin SQ or IM 2. DDAVP (Life long therapy) 3. Nasal spray q 8-12 hrs. |
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What are the 5 symptoms of diabetes insipidus?
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1. Polyuria and polydipsia
2. Neurologic (problem interpreting ADH) 3. Nephrogenic (Kidney has a problem reading ADH) 4. Inability to concentrate urine 5. Rapid development of dehydration |
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What are the etiologies of diabetes insipidus?
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1. Disorder of insufficient ADH activity resulting in excessive loss of H2O in urine
2. Damage to ADH producing cells in the hypothalamus can result from: a. Traumatic brain injury b. Intracranial tumors c. Neurosurgical procedures. 3. Some pharmacologic agents can lead to abnormalities in ADH secretion |
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How is SIADH diagnosed and who is susceptible?
What are the 3 therapeutic managements of SIADH? |
1. Pre-disposing conditions to SIADH: Infections, tumors, or CNS disease or Trauma
2. Osmolality: Blood serum low and high urine, Low Na+ - Fluid retention 1. Restrict fluids to 1/4-1/2 managment a. at 1st notice retention of fluid is the loss of LOC, evaluate mentation 2. Monitor electrolytes 3. Observe for neurologic deterioration |
