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33 Cards in this Set

  • Front
  • Back
Glands
• Produce chemical substances called hormones secreted into blood
• Target tissue-body tissue or organ that the hormone has its effect on
• All glands in the body belong to the endocrine system
• Two types of glands: exocrine and endocrine
• Exocrine secrete their substance into ducts that empty into a body cavity or surface
• Endocrine gland do not have ducts, secrete directly into blood
Hormones
• A chemical substance synthesized and secreted by a specific organ or tissue
• secretion in small amounts, circulation through the blood, binds to specific cellular receptors either in cell membrane, or within cell
• Classified: lipid-soluble, water-soluble
• Lipid soluble-include steroid hormones (adrenal cortex and sex glands), and thyroid hormones
• Water soluble-all others and circulate freely not dependant on proteins
• Differences in solubility are important
• Hormonal functions are for reproduction, response to stress & injury, electrolyte imbalance, energy metabolism, growth, maturation, & aging
• Also play a role in nervous system function
• Influence behavior
Hormone transport
Target and receptors
• Carried by blood to sites in body, Some bind to plasma for transport
• Water-soluble circulate freely and not dependant on proteins
• Exert their effects on target tissue
• Determined by receptors in a lock-and-key mechanism
• Only acts on cells that have a receptor specific for that hormone
• Two types of receptors: within the cell, and on the cell membrane
• Steroid hormone receptors: adrenal steroids, vit D and thyroid hormones located inside the cell, lipid soluble, pass through passive diffusion, bind to specific sites on DNA inside the cell
• Protein hormone receptors: water soluble, hypothalamic releasing hormones, ant and post pit hormones, PTH, calcitonin, insulin, glucagon. is a two step process, located in cell membrane, acts as a first messenger, stimulates second messenger, and regulates activity
Regulation of hormonal secretion
• Controlled by specific mechanisms, either Stimulate or inhibit hormone synthesis
• Simple feedback-level depend on feedback, based on blood level of particular substance
• Negative feedback-most common, responds by increasing or decreasing, similar to thermostat, cold air in room activates to release heat, hot air turns off to prevent for more hot air
• Positive feedback-increases the target organ action beyond normal
• Complex feedback-involves communication via hormones to turn off, turn on target hormone secretion
• Nervous system control-affected by activity of the nervous system, and modulate hormone secretion
• Rhythms-originate in brain structures, common is circadian rhythm which fluctuates during a 24 hour period
- the liver and kidney's are responsible for inactivation and excretion, diseases of these organs can result in increased hormone levels
Hypothalamus
• Relationship between the hypothalamus and pituitary gland one of the most important aspects of endocrine system
• Located in the most central part of diencephalons
• Two groups: hypothalamus regulates the ant and post pit by releasing to stimulate or inhibit the secretion of hormones of anterior pituitary
• Contains neurons, which receive input from the brainstem and limbic system
- by its control over the post and anter pituitary gland the hypothalamus exerts global control over the entire endocrine system
Pituitary
• Called the hypophysis, size of a pea, located in the sella turcica under hypothalamus
• Connected to the hypothalamus, and serves as a communication
• Consists of two parts: anterior and posterior
Anterior Pituitary
• Accounts for 80%, Regulated by hypothalamus through releasing and inhibiting
• Affects secretion of six hormones: growth hormone (GH, releasing hormone, GH inhibiting hormone or somatostatin), thyroid stimulating (TSH), adrenocorticotropic hormone (ACTH), gonadotropic hormone (FSH, LH), prolactin (PRL)
• GH has target tissue in all cells of the body
Posterior pituitary
• Secrete ADH (vasopressin), and oxytocin
• ADH-regulation of fluid volume by reabsorption of water, is a potent vasoconstrictor, stimulated by plasma osmolosis
• Oxytocin-ejection of milk and contraction of uterine smooth muscle and inhibited by endorphins and alcohol
Thyroid gland
• Located in the anterior portion of the neck in front of trachea
• Regulated by TSH from anterior pituitary
- highly vascular and receives adrenergic and cholinergic innervation
- thyroid hormone is produced in response to stimuli: TSH, TRH, low serum iodine
Thyroxin and triiodothyronine
• Thyroxin (T4) most abundant thyroid hormone
• Iodine is necessary for the synthesis of thyroid hormones
• T4 and T3 affect metabolic rate, caloric requirements, oxygen consumption, carbohydrate and lipid metabolism, growth and development, brain functions
• Thyroid hormones are bound to plasma proteins
• Have target tissue in all cells of the body
Calcitonin
• Produced by the C cells of the thyroid gland in response to high circulating calcium levels
• Inhibits calcium resorption, increases renal excretion of calcium and lowering calcium levels
- serum Ca levels influence the release of calcitonin
- as serum Ca levels rise, calcitonin acts to maintain a normal level by opposing the action of PTH
Parathyroid gland
• Small, oval arranged in pairs behind each thyroid lobe, usually 4 glands
Parathyroid hormone (PTH)
• Regulate the blood level of calcium
• Acts on bone, kidneys, GI tract
• Stimulates bone resorption and inhibits bone formation resulting in the release of calcium
• Kidneys PTH increases calcium reabsorption and phosphate excretion
• Stimulates the renal conversion of vit D and enhances the intestinal absorption of calcium
• When serum calcium is low, PTH secretion increases
• When calcium level rises, PTH secretion falls
• High levels of vit D inhibits PTH and low levels of Mg stimulate PTH
Adrenal glands
• Located on the upper part of the kidneys
• Each consist of two parts the medulla and the cortex
Adrenal medulla
• Inner part of the gland and consist of sympathetic postganglionic neurons
• The medulla secretes the catecholamine epinephrine (75%) norepinephrine (25%) and dopamine
• Catecholamines usually considered neurotransmitters when they are secreted by nerve cells, hormones secreted by the adrenal medulla, because they are released into the circulation and transported to their target organs
• Exert their effects after binding to adrenergic receptors on cells and have widespread effects on all body systems
Adrenal glands cont
Adrenal cortex
• Outer part of the gland, secreting more than 50 steroid hormones
• Classified as glucocorticoids, mineralocorticoids and androgens
• Glucocorticoids (e.g. cortisol) effect on glucose metabolism (cortisol)
• Mineralocorticoids (e.g. aldosterone) essential for the maintenance of fluid and electrolyte balance
• Corticosteroid refers to any hormone synthesized by the adrenal cortex
• Cortisol is the most abundant and potent glucocorticoid, cortisol increases blood glucose through stimulation of hepatic gluconeogenesis and inhibiting protein synthesis
• Glucocorticoids have effect on anti-inflammatory action and response to stress
• Cortisol decreases inflammatory response by preventing increased capillary permeability
• Control of cortisol is by negative feedback
• Cortisol increases by stress, burns, infection, fever, acute anxiety, and hypoglycemia
• Aldosterone (mineralocorticoid) maintains extracellular fluid volume, acts at the renal tubule to promote renal reabsorption of Na and excretion of K and hydrogen
• Androgens stimulate pubic and axillary hair growth and sex drive in females
• In females androgens are converted to estrogen
Pancreas
• Located behind the stomach and anterior to the first and second lumbar vertebrae
• Has a both exocrine and endocrine function
• Hormone secreting function is called islets of langerhans, consists of four types, alpha, beta, delta, and f cells
• Alpha cells produce and secrete glucagons, insulin produced by beta cells
Glucagon
- Primary target of glucagon is the liver
• Released to low levels of blood glucose, protein ingestion, & exercise
• Increases blood glucose by gycogenolysis (breakdown of glycogen to glucose), gluconeogenesis
- When glycogenolysis fails to provide enough glucose, glucagon promotes amino acid transport from the muscle and stimulates gluconeogenesis (formation of glycogen from fatty acids and proteins rather than carbs)
• Glucagon and insulin work in a reciprocal manner
• After high-protein carbohydrate-free diet, both hormones are secreted and glucagon counteracts the inhibitory effect of insulin to maintain normal blood glucose levels
- Individuals with DM1 lose glucagon secretion early and rely on effects of adrenergic response and secretion of catecholamines
- Delta cells secrete somatostatin, which inhibits gastric motility and emptying, gallbladder contraction, intestinal absorption of fats, amino acids, glucose, glucagon secretion and insulin
- Somatastatin, inhibits glucagon and helps maintain glucose homeostasis, synthetic somatastatin analogs are used to successfully treat acromegaly
- Somatastatin analog can increase the risk of hypoglycemia
Pancreas cont
Insulin
• Principle regulator of the metabolism and storage of ingested carbohydrates, fats, and proteins
• Facilitates glucose transport across cell membrane
• Increased blood glucose levels stimulates insulin synthesis and inhibited by low blood glucose levels, glucagons, hypokalemia and catecholamines
• Effect of insulin on glucose metabolism occurs in the liver
• Another effect occurs in peripheral tissues where insulin facilitates glucose transport into cells
• Transport of amino acids across muscle membranes and synthesis into protein
• Transport of triglycerides into adipose tissue
• Insulin is a storage or anabolic hormone
• Is responsible for the storage of nutrients (anabolism)
Age changes
-search for and rule out a pathologic process before attributing hormonal alterations to aging
-the earliest hormonal sign of menopause are rising level of gonadotropins FSH and LH which are trying to stimulate the failing ovaries
-androgen production in males declines
-in response to decreased intake of Ca and Vit D intake or production via decreased exposure to sunlight, older pt my have mild elevations in PTH and a negative Ca balance, which impacts bone density and increases fracture risk
-reduced insulin sensitivity rather than reduced insulin secretion is responsible for the high prevalence of impaired glucose tolerance and DM2 in older adults
Lab evals
-basal hormone output is generally assessed by measuring serum values
-many hormones such as gonadotropins are secreted in a pulsatile fashion, such that measuring the peak (highest) versus the trough (lowest) levels may yield widely divergent values
-fasting hormone assays are generally performed after an overnight fast with blood drawn at 8am because of circadium hormonal rhythms
-dynamic testing, in suspected cases of hyperfunction, suppression of the gland is attempted
-failure to normally suppress the elevated hormone indicates a significant pathologic state
-failure to normally stimulate the gland indicates a pathologic state
Growth hormone excess (too much)
• Anabolic hormone, promotes protein synthesis, mobilizes glucose and free fatty acids
• Stimulates insulin like growth factor-1 (IGF-1) known as somatomedian, stimulates growth of bones and soft tissues, normally IGF-1 signals anterior pituitary to reduce GH production
• Overproduction caused by benign tumor (adenoma), and secretes GH despite elevated IGF-1, leading to unwanted growth of bones and soft tissue, also elevation of blood glucose through insulin antagonism, leading to glucose intolerance
• In children excess leads to gigantism, and adults leads to acromegaly which is characterized by overgrowth of bones and soft tissues
• Acromegaly manifestations begin gradually, in 20s and 30s with 7-9 yrs between initial onset of symptoms and diagnosis
• Experience enlarged hand and feet, fingertips develop clubbed like appearance
• Enlargement of bones results in mild joint pain, deforming, and arthritis
• Mandible causes jaw to jut forward, enlargement of facial features, speech difficulties
• Sleep apnea related to upper airway narrowing and obstruction, skin becomes thick, oily, coarse leathery, will experience peripheral neuropathy and proximal muscle weakness
• Likely to develop polyps in the colon and colon cancer
• Visual disturbances and headaches
• Increase in free fatty acids and predisposes to atherosclerosis, hyperglycemia, DM
• Cardiomegaly, left ventricular hypertrophy, HTN
Growth hormone excess (too much) cont
Diagnostic studies
• Acromegaly requires evaluation of plasma IGF-1, IGF binding protein-3 (IGFBP-3), and GH
• Definitive test is oral glucose challenge test, GH falls
• MRI and CT for identifying a tumor, and ophthalmologic exam because the tumor may cause pressure on optic nerve
Surgical therapy
• Transsphenoidal resection of a pituitary adenoma to be the primary form of treatment
• Surgery is indicated if severe visual field defects are present
• Transsphenoidal procedure the surgical approach is from the nasal cavity through the sphenoid sinus or from the mouth through a gingival incision
• Complication are CSF leak and visual impairment, DI and SIADH, infection and meningitis
• After surgery, caution against coughing and the nasal packing necessitating mouth breathing
• Persistent headaches may indicate meningitis and should be reported
• Monitor for postop vision and visual fields for changes
• Hypophysectomy, treatment of choice and offers best hope for small tumors (microadenomas smaller than 10mm)
• Removal of pituitary tumors associated with acromegaly are done by transsphenoidal approach, which is removal of the tumor causing the GH secretion
• An immediate reduction in GH levels and drop in IGF-1 levels in a few weeks
• Some may require radiation therapy, some cases the entire pituitary is removed, which is going to require the essential hormones produced by target organs and continued throughout life
• Instructed to avoid vigorous coughing, sneezing, and straining at stool
• Post-op transsphenoidal, HOB elevated 30-degrees all times to avoid pressure on sella turcica and decrease headaches, monitor neuro’s and papillary response
• Nasal drainage sent to lab for testing, glucose >30mg/dl indicates cerebrospinal fluid leakage, increased risk for meningitis, CSF leaks resolve within 72hrs, antibiotics given to prevent meningitis, surgical intervention if leak persists past 72hrs
• Mouth care every 4hrs to keep surgical area clean and free of debris, tooth brushing avoided for 10 days so not to disrupt suture
Growth hormone excess (too much) cont
Radiation therapy
• Considered when surgery has failed to produce complete remission, can successfully reduce GH levels
• Can have a long delay (5-10yrs) for GH levels to normalize, and is usually offered on combination with drugs that reduce GH levels
• May experience local skin changes, oral complications, hypopituitarism results from radiation and requires hormone therapy
• Stereotactic radiosurgery may be used for small inaccessible pituitary tumors
• Consists single dose of radiation to one site from multiple angles, used to occlude blood vessels supplying the tumor and results in death
Drug therapy
• Three types for treatment of acromegaly: GH receptor antagonists, somatostatin analogs, and dopamine agonists, all reduce GH levels and used in initial treatment or as adjunct to surgery or radiation
• Most common is octreotide (sandostatin) a somatostatin analog that reduces GH levels, given by subcutaneous injection three times a week, used for acromegaly and thyroid stimulating adenomas
• Two long lasting octreotide and lanreotide SR are available as IM every 2-4 weeks
• Pegvisomant a GH receptor antagonist an alternative to somatostatin, not for primary treatment
• Dopamine agonists used for acromegaly to reduce GH, may be first, less expensive not as effective
• Bromocriptine (Parlodel), cabergoline (Dostinex) or pergolide (permax) are dopaminergic medication
• Somatotropin recombinant GH hormone available for long-term replacement therapy in adults with GH deficiency
• Gradual dosage increase 4-8 weeks intervals up to 0.008 mg/kg/week
Excess of other tropic hormones
• Tropic hormone excess, overproduction of single anterior pituitary hormone produces syndrome relate to excess from target organs
• ACTH increases results in Cushing’s disease, TSH increase results hyperthyroidism
• Prolactinomas frequently occurring tumors, manifestations by woman include galactorrhea (milk secretion not associated with childbirth or nursing) ovulation dysfunction, menstrual dysfunction, decreased libido, and hirsutism
• PRL inhibits gonadotropin releasing hormone and is necessary for lactation
• Men, impotence, decreased libido, sperm density
• Headaches, visual problems, visual due to pressure on optic nerve
• Drug therapy first line due to small size of adenoma, dopamine agonists used because of successful treatment
• Depending of size transsphenoidal approach is considered, radiation is limited and used for patients who have failed to respond to medical and surgical therapy
Hypofunction of the pituitary gland (too little or not enough)
• Rare disorder involving decrease in one or more pituitary hormone
• Anterior pituitary secretes ACTH, TSH, FSH, LH, GH, and prolactin
• Posterior pituitary secretes ADH, and oxytocin
• Selective hypopituitarism is deficiency of one hormone, and deficiency of all hormones or total failure referred to panhypopituitarism
• Most common involve GH and gonadotropins
• Common cause is a pituitary tumor, also autoimmune disorders, infections, pituitary infarction, or destruction of gland
• Sheehan syndrome a postpartum condition of pituitary necrosis and hypopituitarism occurring after circulatory collapse form uterine hemorrhage
• Hormone deficiencies of anterior pituitary hormones lead to end organ failure, specific pituitary hormone that are lacking
• Deficiencies of TSH and ACTH are life threatening, ACTH results in acute adrenal insufficiency
Hypofunction of the pituitary gland (too little or not enough)
Treatment and management
• s/s vary are related to hyposecretion and/or growing tumor, commonly headaches, visual changes, anosmia (inability to perceive smells), and seizures
• adults with GH deficiency will have truncal obesity, decreased muscle mass, reduced strength, decreased energy, appear depressed, impaired psychologic well being common finding
• FSH and LH deficiency in woman manifested as menstrual irregularities, diminished libido, changes in secondary sex characteristics, men with FSH and LH deficiencies experience testicular atrophy, diminished spermatogenesis, loss of libido, impotence, and decreased facial hair and muscle mass
- testosterone deficiency in men can lead to osteoporosis
• ACTH and cortisol deficiency, s/s weakness, fatigue, headache, dry and pale skin, and diminished axillary and pubic hair, postural hypotension, fasting hypoglycemia
• Treatment consists of surgery or radiation for tumor removal and lifelong hormone replacement
• Somatropin used for GH replacement, side effects include swelling in feet and hands, pain in joints and headaches, given sub-q daily 1-2 times/month
• Gonadal deficiency is not life threatening, replacement improves sexual function and well being
• Replacement therapy contraindicated in breast cancer, phlebitis, and PE in women and prostate cancer in men
• Estrogen and progesterone in hypogonadal women to treat hot flashes, vaginal dryness and decreased libido
• Testosterone replacement for men
- Cortisol deficiency is to be anticipated and replacement mandatory
- Thyroid hormone replacement accelerates the metabolism of glucocorticoids such that failure to replace glucocorticoids concurrently can precipitate an acute adrenal crisis
- Glucocorticoid deficiency is replaced with hydrocortisone or one of the more potent synthetic analogs
Syndrome of inappropriate ADH (too much ADH)
• ADH is released despite normal or low plasma osmolarity
• SIADH results from abnormal production or sustained secretion of ADH, characterized by fluid retention, serum hypoosmolality (too much water), dilutional hyponatremia, hypochloremia, and normal renal function
• Occurs commonly in older adults, most common cause is malignancy, especially small cell lung cancer which are capable of producing ADH
Clinical manifestations
• leads to reabsorption of water into the circulation, extracellular fluid volume expands, plasma osmolality declines, glomerular filtration rate increases, and Na levels decline
• hyponatremia causes muscle cramps and weakness, thirst, dyspnea on exertion, fatigue
• low u/o and increased body weight, Na <120mEq/L manifestations become more severe including vomiting, abd cramps, muscle twitching and seizures
• plasma osmolality and serum Na level continue to decline, cerebral edema, lethargy, anorexia, confusion, headache, seizures, and coma occurs
- clinical symptoms depends on the absolute serum Na level and the rapidity of the fall, a rapid fall results in rapid onset cerebral edema
Collaborative care
- Water restriction is the first priority, oral salt intake is increased
• treatment is directed at the underlying cause, immediate treatment goal is to restore normal fluid volume and osmolality
• if symptoms are mild and Na >125mEq/L treatment includes fluids restriction to 800-1000ml/day, should result weight reductions, rise in Na and osmolality
• in severe hyponatremia <125mEq/L with neuro symptoms IV hypertonic saline (3%NS) and lasix are administered, which requires very slow infusion on pump to avoid too rapid Na rise
• lasix used to promote diuresis only if Na is at least 125mEq/L, supplements my be needed because of K, Ca, and Mg losses
• fluid restriction of 500ml/day indicated for severe hyponatremia
• chronic SIADH water restriction of 800-1000ml/day is recommended, demeclocycline and lithium administered too block effects of ADH on renal tubule
- Too rapid an increase in the plasma Na level can produce a hypertonic plasma solution and a fluid shift from the intracellular to the extracellular compartment
• alerted for low u/o with a high specific gravity, sudden weight gain without edema, or Na decline
• chronic SIADH learn to self manage treatment
• fluid restrictions to 800-1000ml/day
• ice chips or sugarless gum can help decrease thirst
• diuretics to remove excess fluid volume, diet supplement with K and Na and should be diluted to prevent GI irritation or damage, best taken at mealtime
• teach for symptoms of fluid and electrolyte imbalances
Diabetes insipidus
• a deficiency of production or secretion of ADH, or decreased renal response to ADH
• results in electrolyte imbalances caused by urinary output and increased plasma osmolality (too much plasma not enough water)
• central neurogenic DI occurs when any organic lesion of the hypothalamus, infundibular stem, posterior pituitary interferes with ADH synthesis, transport or release
• nephrogenic DI condition in which there is adequate ADH, but there is decreased response to ADH in the kidney, lithium most common cause of drug induced nephrogenic DI, hypokalemia and hypocalcemia may also lead too
• psychogenic DI, less common, associated with excessive water intake, caused by structural lesion in thirst center or by psychiatric problems
Clinical manifestations
• characterized by increased thirst (polydipsia), and increased urination (polyuria)
• characteristic of large quantities of urine, 5-20 L/day, with low specific gravity (<1.003-1.030 is normal) indicating urine is very dilute and urine osmolality of <100 mOsm/kg
• serum osmolality is elevated usually greater than >295 mOsm/kg as a result of hypernatremia due to pure water loss in the kidney
• may experience fatigue and generalized weakness
• central DI occurs suddenly with excessive fluid loss, after intracranial surgery DI has triphasic pattern: acute phase with abrupt onset of polyuria, interphase which urine volume apparently normalizes, third phase which central DI is permanent and apparent in 10-14 days post-op
• central DI from head injury self limiting improves with treatment of underlying problem
• weight loss, constipation, poor tissue turgor, hypotension, tachycardia, shock, CNS manifestations, irritability, which are related to increasing serum osmolality and hyponatremia
Collaborative care
• Determining primary cause is key to collaborative management of DI, therapeutic goal is maintenance of fluid and electrolyte balance
• Central DI, fluid and hormonal replacement is treatment, acute DI hypotonic saline or D5W IV titrated to u/o, hormonal replacement necessary for the lack of ADH (desmopressin for central DI), partial central DI include chlorpropamide and carbamazepine
• Nephrogenic DI involves dietary measures (low Na), low protein diet and thiazide diuretics, Na decrease of <3g/day helps reduce u/o
• When low sodium intake and diuretics are not effective use indomethacin which helps increase renal responsiveness to ADH
- Desmopressin is given by nasal spray or SQ injection
- If nasal congestion occurs drug effectiveness may decrease and polyuria and thirst will result
Hyperthyroidism
• Hyperactivity of the thyroid gland with increase in synthesis and release of thyroid hormones
• Thyrotoxicosis refers to the physiologic effects or clinical syndrome of hypermetabolism, results from excess of circulation levels of T4, T3, or both
• Both usually occur together as Graves disease
• Hyperthyroidism occurs more in woman, high frequency in 20-40yrs, most common in graves disease
Graves disease
• Autoimmune disorder of unknown etiology, marked by diffuse thyroid enlargement and excessive thyroid hormone secretion
• Insufficient iodine supply, infection, and stressful life may interact with genetic factors
• Accounts for 75% of hyperthyroidism cases, develops antibodies to TSH receptor, they attach to receptors and stimulate thyroid glands to release T3, T4, or both
• Excessive release leads to clinical manifestations with thyrotoxicosis, characterized by remission and exacerbations, my progress to destruction of thyroid tissues causing hypothyroidism
Toxic Nodular Goiters
• Are thyroid hormone secreting nodules that function independent of TSH stimulation, If associated with hyperthyroidism, are termed toxic
• Usually benign follicular adenomas, occur equally in men and woman at any age, greatest over 40yrs
• Larger nodules greater than 3cm may result in clinical disease
Hyperthyroidism cont
Clinical Manifestations
• Related to the effect of thyroid hormone excess, which increases metabolism, and tissue sensitivity to stimulation by the SNS
• Palpation may reveal a goiter, noted on inspection, auscultation reveals a bruit a reflection of increased blood supply
• Ophthalmopathy is abnormal eye appearance or function, exophthalmos is a protrusion of the eye balls from the orbits, due to impairment of venous drainage from the orbit, causes increased fat deposits and fluid in the retroorbital tissues
• Seen in 20-40% of Graves disease pts, usually bilateral
• Corneal ulcers and loss of vision can occur
• Advanced disease may exhibit acropachy, early may exhibit weight loss and increased nervousness
Complications
• Thyrotoxic crisis (thyroid storm), acute, rare, life-threatening,
• Thought to be caused by stressors (infection, trauma, surgery) in a pt with preexisting hyperthyroidism
• Heart and nerve tissues become more sensitive to catecholamines
• Tachycardia, heart failure, shock, hyperthermia, restlessness, agitation, seizures, abd pain, n/v, diarrhea, delirium, and coma
Hyperthyroidism cont
Collaborative management
Diagnostic studies
• Hyperthyroidism diagnosis confirmation; decreased TSH levels and elevated free thyroxine (free T4) levels
• T3 and T4 may also be used, they measure free and bound (to protein) hormone levels, and only form that is biologically active
• RAIU (radioactive iodine uptake) used to differentiate Graves disease from thyroiditis
• Graves disease will show uptake of 35-95%
Collaborative care
• Goal is to block the adverse the effects of thyroid hormones and stop over secretion
• Antithyroid meds, radioactive iodine therapy, and subtotal thyroidectomy
• Treatment of choice in nonpregnant pts is radioactive therapy
• Influenced by age, preferences, severity, and complications
• If surgery, antithyroid meds given and iodine, also B-blockers to relieve symptoms preop
Drug Therapy
Antithyroid Drugs
• First line; propylthiouracil PTU and methimazole, which inhibit the synthesis of thyroid hormones
• PTU blocks conversion of T4 to T3
• Good results seen 4-8 weeks, continued for 6-15mths to allow for spontaneous remission which occurs in 20-40% of individuals with hyperthyroidism
• Disadvantage is noncompliance and recurrence of hyperthyroidism when discontinued
• PTU lowers levels faster but taken X3 per day, methimazole X1 daily
• Indications is Graves disease in young pts, hyperthyroidism during pregnancy, and need to achieve euthyroid state preop or before radiation therapy
Iodine
• Used with other antithyroid drugs to prepare for thyroidectomy or for TX of thyrotoxic crisis
• Large doses inhibits synthesis of T3 and T4 & blocks release into circulation
• Also decreases the vascularity of thyroid gland, making surgery safer and easier
• Effects seen in 1-2 weeks, long term not effective in controlling hyperthyroidism
• Available as saturated solution of potassium iodine SSKI and lugols solution
B-blockers
• Used for symptom relief of thyrotoxicosis that results from increased Beta stimulation caused by thyroid hormone excess
• Propranolol used with antithyroid meds to provide symptom relief
• Atenolol is preferred B-blocker for hyperthyroid pt with asthma or heart disease
Collaborative management
Radioactive Iodine Therapy
• Treatment of choice for nonpregnant adults, which destroys thyroid tissue, limiting thyroid hormone secretion
• Delayed response, effects not seen for 2-3mths, pts usually treated with antithyroid drugs and propranolol before and during the first 3mths after initiation of RAI, until effects of radiation become apparent
• High incidence of posttreatment hypothyroidism, resulting in lifelong thyroid hormone replacement
• Iodine for relief of hyperthyroid symptoms should be mixed with water or juice, use a straw, and given with meals, assess for iodine tox; swelling of buccal mucosa and other membranes, excessive salivation, n/v, and skin reactions
Surgical Therapy
• Indicated for those unresponsive to antithyroid therapy, large goiters causing tracheal compression, and with possible malignancy
• When an individual is not a candidate for RAI
• A more rapid reduction in T3 & T4 levels
• Subtotal thyroidectomy is preferred procedure, involves removal of a significant portion of the thyroid gland, 90% must be removed to be effective, hypothyroidism may occur
• Endoscopic thyroidectomy is minimally invasive
• Appropriate procedure for pts with small nodules (<3cm), with no evidence of malignancy
• Advantages of endoscopic over open include less scarring, less pain, faster return to normal
• Antithyroid drugs, iodine, B-blockers administered to achieve a euthyroid state and control symptoms
• Iodine reduces vascularization of the gland reducing the risk of hemorrhage
• Postop complications include hypothyroidism, damage or inadvertent removal of parathyroid gland causing hypocalcemia, hemorrhage, injury to laryngeal nerve, thyrotoxic crisis and infection
• Assess q2hrs/24hrs for signs of hemorrhage, tracheal compression such as irregular breathing, neck swelling, frequent swallowing, choking, blood in anterior and posterior dressings
• Semi-fowler pos, support head, avoid neck flexion and tension on the suture line
• Vitals, assessment of tetany secondary to hypoparathyroidism, evaluation speaking and hoarsenss, trousseaus and chvosteks sign
• Hoarseness expected 3-4days postop due to edema
Myxedema Coma
(hyperthyroidism)
-brought on by extreme hypothyroidism
-deficient production of thyroid hormone
-primary causes include congenital defects, loss of thyroid tissue after treatment for hyperthyroidism, defective hormone synthesis due to an autoimmune process, and antithyroid drug admin of iodine deficiency
-secondary causes, peripheral resistance to TH, pituitary infarction, hypothalamic disorders
-a low basal metabolic rate and decreased energy metabolism and heat production are characteristic
-will have nonpitting boggy edema, especially around the eyes, hands, and feet
-thickening of the tongue and the laryngeal and pharyngeal mucous membranes, resulting in slurred speech and hoarsness
-s/s, fatigue, weakness, dec bowel sounds, dec appetite, weight gain, ECG changes
Myxedema Coma cont
(hyperthyroidism)
-myxedema coma, characterized by severe depression of the sensorium, hypothermia, hypoventilation, hypoxemia, hyponatremia, hypoglycemia, hyperreflexia, hypotension, and bradycardia
-a dec in T4 is common, Na is dec and K is inc, Thyroid Stimulating Hormone is elevated in severe hypothyroidism
Management:
-thyroid hormone and corticosteroid admin
-T4 admin initialy to establish a normal T4 level
-
Adrenal Crisis
(Addisons Disease)
-primary adrenal insufficiency, it is an autoimmune disease
-the most common cause is abrupt withdrawal of exogenous ACTH or as a complication of cortisol therapy or steroid therapy
-suppressed ACTH secretion as a result of exogenous cortisol or steroid therapy disrupts the body's natural feedback loop that controls cortisol secretion
-pt is unable to meet the requirements for normal metabolic function or increased metabolic demands as necessary for stress or illness
-adrenal insufficiency affects both glucocorticoids and mineralocorticoids, resulting in alterations in glucose metabolism and fluid and electrolyte imbalance
-weakness, fatigue, anorexia, n/v, diarrhea, dec BP that does not respond to pressors
-dehydration occurs secondary to the nephrons insufficient ability to reabsorb Na and water due to aldosterone deficiency
Adrenal Crisis cont
(Addisons Disease)
-glucocorticoid and mineralocorticoid deficiency show hyponatremia, hyperkalemia, dec bicarb, and elevated BUN (dehydration), dec BP
-hypoglycemia is present
-failure to respond to exogenous pressor agents
Management
-hydrocortisone, 100mg IV q 6-8 hours
-fluids with D5W