Nursing: Disorders of the Endocrine System - Part 1 PDF

1 Nursing 3366 Pathologic Processes: Implications for Nursing Lecture Notes: Disorders of the Endocrine System, Part I Objectives /outcomes for this subject (some of these are in Part I and some in Part II ) DESCRIBE/DISCUSS/IDENTIFY: 1. Key...

1 Nursing 3366 Pathologic Processes: Implications for Nursing Lecture Notes: Disorders of the Endocrine System, Part I Objectives /outcomes for this subject (some of these are in Part I and some in Part II ) DESCRIBE/DISCUSS/IDENTIFY: 1. Key aspects of normal endocrine function, especially feedback systems and influences on other body systems. 2. Pathophysiology of select derangements of endocrine glands, including problems of: the pituitary gland, such as ACTH-relatedhy problems. the thyroid gland, such as hyperthyroidism & hypothyroidism. calcium movement problems caused by disorders of calcitonin and PTH hormonally-related bone disorders such as osteopenia, osteoporosis and osteoclastic aspect of menopause. the endocrine pancreas, such as diabetes mellitus and hypoglycemia. the adrenal glands, such as Cushing’s syndrome & Addison’s disease. 3. Signs and symptoms related to above pathological conditions, including the significance of diagnostic test results used to evaluate and monitor endocrine function, such as TSH, T4, T3, cortisol, blood sugar, and glycosylated hemoglobin. 4. Basic treatment modalities related to altered endocrine conditions. Outline for endocrine system disorders: I. Disorders of the Pituitary Gland A. Diabetes insipidus (DI) B. Syndrome of inappropriate ADH (SIADH) II. Disorders of Thyroid A. Overview B. Hypothyroidism C. Hyperthyroidism will be on III. Disorders of Calcium Movement test 4 A. Basics of calcium and calcium movement B. Disorders caused by calcium movement alterations C. Bringing it all together_ IV. Disorders of Adrenals will be on final exam V. Disorders of Endocrine Pancreas (25% of final) Key points about the endocrine system in general (read this brief A&P before class): explaining negative feedback simplistically: low triggers high; high triggers low. 1. the endocrine system is dependent on negative feedback systems, that is: a. a HIGH blood level of a circulating hormone (a hormone is basically a chemical messenger ) will automatically suppress the gland that secreted it and/or other glands in the feedback loop, thus decreasing secretion of that hormone. b. a LOW blood level of a circulating hormone will automatically stimulate the gland that secreted it and/or other glands in the feedback loop.. the result is that there will be MORE of the hormone in circulation. 2. most endocrine disorders are problems of either hyposecretion or hypersecretion I. Disorders of the Pituitary Gland FYI: “pituita” came from Latin for phlegm (mucus); they used to believe that the pituitary gland made phlegm; “hypohysis”—Latin for “growth attached under”—comes from fact that pituitary gland is attached under hypothalamus in brain A. Overview 1. pituitary gland is also known as hypophysis, located in brain near base of skull  2 2. known as master gland because it secretes many important hormones that govern other glands (including these that we will talk about in our 2 endocrine lectures): (see Prep 10 & pic in book, ch 31) a. antidiuretic hormone (ADH) b. thyroid-stimulating hormone (TSH) (will talk about thyroid in later section of notes) c. adrenocorticotropic hormone (ACTH)—will talk about this more in Endo II B. ADH problems (undersecretion and oversecretion) 1. diabetes insipidus (DI) [undersecretion] a. nomenclature of DI: diabetes means “to pass too much urine;” insipidus A&P review: ADH means “flavorless” (refers to the fact that the urine has no color because it is (antidiuretic very dilute) hormone) secretion is a normal process b. etiology & mechanisms of DI: that the body uses 1) renal-related etiology: —“sick” kidneys often have a decreased to compensate for response of renal tubules to ADH (“fix”) low fluid volume: when the 2) CNS-related etiologies: pituitary detects a) a lesion such as a pituitary tumor causes the gland to diminish that circulating its secretion of ADH fluid volume is low, (the body has a b) acute abnormality in the brain such as head injury or other high osmolality or causes of cerebral edema & IICP in the brain can put pressure high blood on the pituitary gland & cause it to diminish ADH secretion concentration) it secretes ADH→ 3) whatever the etiology, without the influence of ADH, you won’t “hold ADH “tells” kidneys onto” water effectively --water will indiscriminately flow from the to “hang onto” peritubular capillaries of the kidneys into the tubules and becomes water by decreasing urine very dilute urine output→ fluids are conserved and fluid 4) S&S (in this general order): volume in the body a) you void huge amounts (polyuria) of dilute urine goes up. b) this makes you thirsty, so you drink water, but it just flows right out no matter how much you drink. c) this translates eventually to your blood compartment having less water → concentration increases→higher serum osmolality → since the blood now has a higher osmolality than the next door tissue compartment (all over the body), water will be PULLED INTO the blood compartment (and constantly “peed out”) leaving the tissue cells dehydrated & shrunken d) so you have S&S of dehydration eventually, which include poor skin turgor & dry mucous membranes. Summary of not enough ADH : A person drinks H2O, but there is less ADH to tell the kidneys to “hold on” to the 5) into domino H20→ H2O goes directly out effect urine without is Tconcentrated being to B: sincebythe plasma compartment kidneys→polyuria→ (ie, the thirst→ more blood water is all over drunk→ goes straight out into urine→ the body) thirst….etc…--ultimately, no matter how much you drink, you get dehydrated. 2. syndrome of inappropriate antidiuretic hormone (SIADH) [oversecretion] a. SIADH can be triggered by many events: 1) ectopically-produced (ectopic = “outside usual”) ADH such as from small-cell bronchogenic cancer 2) various drugs that effect the brain, especially general anesthetics (SIADH sometimes seen in post-op recovery period).  3 3) trauma to brain such as brain tumors, head injury, etc. (swelling of brain puts pressure on pituitary gland, but can be in opposite way than DI; in SIADH there is OVERsecretion of ADH.) b. mechanism of action & S&S 1) characterized by abnormally high levels of ADH: you “hold onto” water too much by abnormally decreasing urination →results in increased vascular fluid volume →essentially means that water has been added to the blood = diluted plasma compartment & lower serum osmolality→ small amounts highly concentrated urine. 2) S&S include a) decreased urine output (oliguria) because your body is holding onto water inappropriately in the vascular space b) since the plasma compartment is so dilute now, which way is water PULLED IN when the blood reaches all the tissues? B to T→ edema c) S&S are related to the above fluid overload situation, including peripheral & pulmonary edema. II. Disorders of thyroid gland A. Overview 1. regulated by the secretion of thyroid stimulating hormone (TSH) from the pituitary → TSH stimulates the thyroid as needed to produce, release, and/or store the 3 thyroid hormones: a. thyroxine (T4) and triiodothyronine (T3), which regulate many metabolic activities of body b. calcitonin, which increases calcium movement from blood into bone (calcitonin will be discussed further in the section II on calcium movement.) 2. more about T3 & T4 hormones: a. typically, these are the thyroid hormones that are most often mentioned in thyroid disorders; calcitonin is less talked about. b. their adequate production is very dependent on iodide uptake from blood -- iodide is consumed in our diet (from seafood and iodized salt) c. T3 & T4 act on receptor cells of many different organs and affect body’s: 1) metabolic rate 2) caloric requirements 3) oxygen consumption 4) carbohydrate & lipid metabolism 5) growth & development 6) brain & nervous system functions 3. regulation of thyroid function depends on negative feedback system: a. drop in levels of thyroid hormones (T3 & T4) in the bloodstream→ pituitary stimulated→ increases its secretion of TSH→ thyroid stimulated to release more T3 & T4→ normal levels of T3 & T4 are reestablished → these normal levels then suppress of TSH secretion from pituitary b. the opposite feedback loop occurs with increased levels of thyroid hormones  4 c. understanding negative feedback is important in understanding what happens as there are pathophysiological changes in the thyroid d. calcitonin is also regulated by negative feedback (more in section III) 4. main thyroid disorders discussed here will be hyperthyroidism and hypothyroidism. B. Hyperthyroidism 1. overview a. hyperthyroidism is the state of having excess T3 & T4 production and release b. the most common cause-- Graves disease: 1) an autoimmune disorder in which autoantibodies attack/stimulate TSH receptors on the thyroid 2) the autoantibodies do this by “mimicking” TSH→ results in thyroid secreting more T3 & T4 2. S&S a. lab work (this is also part of diagnosis): serum T4 will be higher than normal range and serum TSH will be lower than normal b. other features of hyperthyroidism include is one of “overactive” S&S, due to the hypermetabolic processes caused by high levels of T3, T4: 1) pysch/CNS—nervous, irritable, tremors, insomnia, emotionally labile, sometimes psychosis (hallucinations, paranoia) 2) cardiovascular—tachycardia, increased afterload, sometimes HF due to increased heart workload 3) GI—increased appetite, diarrhea 4) hair changes a) hair follicles are very sensitive to your metabolic state & get “stressed” by too much thyroid hormone—hair thins out or falls out (alopecia). 5) exophthalmus (bulging eyes from deposits of excess tissue behind eyes) 6) goiter– an enlargement of the thyroid gland that can sometimes be easily visualized; causes: a) in hyperthyroidism, hypertrophic changes occur because the cells are being pathologically stimulated by autoantibodies to increase their thyroid hormone output (“overdrive” = increased size of cells) 7) other body changes: a) fatigue & weight loss (due to “overdrive” state using up energy) b) increased body temp & overall heat-intolerance c) skin is usually flushed, warm, and damp from excessive sweating. ***Do memorize and remember, “now and forever,” normal temperature =98.6 ° F 3. as with most endocrine disorders, hyperthyroidism has an extreme state; it is called thyrotoxic crisis (AKA thyroid storm) a. this is a hyperthyroid emergency triggered by some stressor such as infection, trauma, surgery, etc b. S & S's: 1) neuro: extreme restlessness & agitation; delirium; seizures; coma. 2) circulatory: severe tachycardia, heart failure, shock  5 3) other: diaphoresis, hyperthermia (103-105 F) 4. treatment: a. antithyroid meds that inhibit synthesis of thyroid hormones b. surgery-- thyroidectomy (usually ~ 90 % removed) CTQ (critical thinking question); If the dose of antithyroid medication was too low, what S&S would the nurse see? S&S or HYPERthyroidism If the antithyroid medication dose was too high, what S&S would the nurse see? S&S of HYPOthyroidism C. Hypothyroidism 1. overview a. hypothyroidism is the state of deficient T3 & T4 production and release b. is one of most common medical disorders in US -- affects 8% of women & 2% of men over 50. c. caused by loss of functional thyroid tissue from one or more of the following: 1) congenital defects 2) direct removal of tissue (tumor) or direct destruction of tissue (ex-- radiation) 3) autoimmune thyroiditis, (AKA Hashimotos’s thyroiditis) a) autoantibodies actually destroy tissue b) has insidious onset with thyroid tissue slowly replaced by lymphocytes & scar tissue 4) endemic iodide deficiency (endemic—prevalent in certain populations and/or geographical areas) a) because of lack of iodide in diet, thyroid hormone synthesis drops b) can be especially significant in children: because of pregnant mom not getting enough iodide in diet, baby can have congenital hypothyroidism with stunted mental & physical growth--cretinism d) this cause of hypothyroidism rarely seen now in either children or adults in U.S. because of diet education and adding iodide to salt, but still seen in other areas of the world 5) overactivity of antithyroid drugs—patient starts out being treated for hyperthyroidism, but goes too far 2. S&S a. lab work (this is also part of diagnosis): serum T4 will be lower than normal range and serum TSH will be higher than normal b. everything HYPOmetabolic: 1) psych/CNS—confusion, slow speech & thinking, sluggish, memory loss, depression. 2) circulatory—anemia, bradycardia, decreased CO 3) pulmonary—dyspnea, hypoventilation, CO2 retention 4) GI—decreased appetite, constipation 5) hair is dry and brittle, and may fall out (alopecia); this is secondary to not having enough thyroid hormone to support metabolic needs of follicles  6 6) skin a) often patient has myxedema, which is due to changes in the dermis that cause water to get trapped under the skin over a period of time, till patient takes on overall puffy appearance. b) also skin is very coarse and dry. 7) goiter—in hypothyroidism, the enlargement is caused by two factors: a) hyperplasia & hypertrophy of the tissue as a compensatory response trying to “desperately” increase thyroid hormone secretion b) inflammation and eventual scar tissue from autoimmune attack 8) other body changes: a) weight gain despite decreased appetite. b) decreased body temp and cold-intolerance. 3. as with most endocrine disorders, hypothyroidism has an extreme state; it is called myxedema coma or crisis. a. precipitated by stressor such as infection, drug, exposure to cold, trauma b. manifested by progression of hypothyroid sluggishness & drowsiness into gradual or sudden impaired consciousness and often hypotension and hypoventilation. 4. tx of hypothyroidism most often is synthetic thyroid hormone -- levothyroxine (Synthroid) Note: GOITER can occur in both hyper and hypothyroidism: 1) in hyperthyroidism the enlargement is a result of overactive cells. 2) in hypothyroidism the enlargement is a result of compensatory change + scar tissue formation from inflammatory process. ALOPECIA can occur in both hyper and hypothyroidism: 1) in hyperthyroidism the hair follicles become stressed by too much thyroid hormone— hair thins out or falls out (alopecia). 2) in hypothyroidism hair becomes dry and brittle, because of the lack of thyroid hormone to support metabolic needs of follicles. III. Disorders of Calcium Movement A. Overview of calcium, calcitonin, & PTH 1. basics of calcium & calcium movement a. calcium needed for many important functions in the body, including building & maintenance of appropriate bone density, cell electrical activity, clotting, and others. b. bone is the biggest storage area for calcium, but it is often needed elsewhere in the body (as noted above), so there is always movement from bone to blood and back again.  7 c at any given time there is a certain, normal amount of calcium in circulation; when the serum calcium is lower than normal, called hypocalcemia; when higher than normal, hypercalcemia. 2. regulation a. the hormones calcitonin & PTH (parathyroid hormone) are chief regulators of calcium movement. calcitonin rhymes with “BONE IN”— 1) calcitonin is secreted by the thyroid gland and enhances movement of it causes calcium calcium from blood into bone. Calcitonin inhibits bone resorption by to go INTO bone decreasing osteoclastic activity. 2) PTH is secreted by parathyroid gland & stimulates resorption a) this word means movement of a substance back into the circulation note: sometimes the from somewhere else; in this case refers to movement of calcium from term “bone resorption” is used bone to circulation & is sometimes referred to as “bone resorption” interchangeably with b) PTH enhances movement of calcium from bone into bloodstream by the term “calcium resorption” -- they increasing osteoclastic activity (calcium goes from BONE TO BLOOD) BOTH refer to (1) osteoclasts are cells that migrate along the walls of capillaries calcium moving from bone to blood. found in bones (2) their job is to break down bone cells to free up calcium, which then can move into bloodstream b. calcitonin & PTH work by negative feedback & balance each other. 1) if there is a state of hypocalcemia, or if calcium is needed in other parts of body, PTH secretion is increased and calcitonin secretion by thyroid is suppressed, resulting in increased osteoclastic activity and bringing up serum calcium levels. 2) if there is a state of hypercalcemia, or if more calcium is needed in the bone (e.g., for building more bone matrix), calcitonin secretion by thyroid is increased, and PTH secretion is suppressed, resulting in decreased osteoclastic activity and bringing down serum calcium levels. B. Disorders caused by calcium movement alterations 1. osteoporosis--general term meaning pathologically “porous bone.” a. normally there is a perfect balance between calcium going into the bone and being used for bone-building by osteocytes, and osteoclastic activity—bone being broken down to release calcium to the blood (resorption). b. unfortunately, as a part of the aging process & genetics, resorption will slowly increase due to increased osteoclastic activity—ie, osteoclastic break down of bone & movement of calcium into the blood exceeds the bone formation that is maintained by the osteocytes c. this causes bone density to decrease, and bone becomes more porous 1) happens in both genders as they age, but women are much more likely to have problems, due to two factors: a) women’s bones are significantly less dense than men’s to begin with b) menopausal loss of estrogen  8 (1) bones have estrogen receptors; when stimulated by estrogen, bone-building & maintenance of density results (2) during and after menopause there is atrophy of ovaries & therefore less estrogen (3) less estrogen = less bone building →balance is tipped toward osteoclastic activity→more resorption than bone-building→less density 2) a drop in bone density is often categorized according to severity on a spectrum that includes osteopenia & osteoporosis (bone density is calculated by undergoing a bone density scan) Spectrum of bone density normal low Bone formation & bone Osteopenia Osteoporosis—bone resorption resorption are balanced. greatly exceeds bone formation. a. osteopenia –the condition of having somewhat less than normal bone density b. osteoporosis—bone density that is markedly lower than normal d. sequelae in either osteopenia or osteoporosis 1) bones more easily fractured, especially in the hip & vertebra. A recent news 2) By age 80, one in 5 women will fracture a hip. series about hip 3) If admitted to the hospital with a hip fracture, ~30% will die within the first fractures: year after surgery. http://keranews.org /post/broken-hips- 4) Deaths from hip fracture are related to of medical preventing-fall-can- complications caused by the fracture or the resulting save-your-life immobility. 5) Complications of a hip fracture include: immobility, infection, DVT, PE, fat embolism, pneumonia, hemorrhage, and shock. FYI: Fat emboli occur when a long bone (ribs, tibia, femur,pelvis) is injured and fat is released from the marrow of the injured bone to systemic circulation. These fat globules can lodge in the smaller circulation of the lungs, brain, or kidney causing inflammation and ischemia. e. treatment 1) once osteopenia is identified by a bone density study, medications may be prescribed to decrease osteoclastic activity, such as nasal calcitonin and biphosphonates(Fosamax). 2) hip fracture: surgery (best if done within 24 hours of fracture) and subsequent rehabilitation / physical therapy. 2. other calcium-movement-related problems: a. electrical issues: as discussed in previous lectures, hypo or hypercalcemia can affect Na+ movement in and out of cells, thus affecting RMP & causing certain S&S (see chart below and/or go back and study hyper/hypopolarization)  9 b. clotting issues: low calcium = low clotting ability, so if a disorder results in hypocalcemia, a patient might have easy bleeding, manifested by S&S such as petechiae and purpura. c. urologic issues: hypercalcemia can cause kidney stones. C. Bringing it all together—fill in the blanks using the choices at the bottom (ANSWERS ARE POSTED WITH CS ANSWERS) Hormone characteristics The states/situations in each column “go together” PTH release HYPOCALCEMIA HYPERCALCEMIA is triggered by ________ calcemia Causes & patho: Causes & patho: __________________ Hyperparathyroidism osteoclastic activity Hypoparathyroidism excess PTH→ excess resorption of results in decreased PTH→ decreased calcium→ _________________calcemia _________________ resorption of calcium→ resorption (calcium _____________ calcemia →__________________polarized RMP moving from bone to → __________ polarized RMP Calcitonin hyposecretion blood) decreased calcitonin→ increased bone is suppressed by Calcitonin hypersecretion resorption of calcium→ ________ calcemia increased calcitonin→ decreased ______________________calcemia→ resorption of calcium→ ___________________polarized RMP Calcitonin release ________ calcemia is triggered by → __________ polarized RMP ******** ________ calcemia Menopause /aging—less bone-building, _______________ more osteoclastic activity, thus osteoclastic activity S&S and/or associated with commonly causes ________________, results in (see choices below): (though not always hypercalcemia.) __________________ resorption so that S&S and/or associated with (see calcium moves from choices below): blood to bone instead of bone to blood is suppressed by ________ calcemia Choices: hypo tetany osteoporosis petechiae hyper muscle spasms renal calculi purpura increases lethargy decreases weakness positive Chvostek’s sign  10 Case Study for Endocrine Part I, Test 4-related material A 68-year-old female patient’s bone density scan shows osteoporosis. Her healthcare provider is trying to figure out the primary etiology. The possibilities are these: 1) age-related and gender-related changes; 2) a problem with the parathyroid gland; 4) a sequela of chronic kidney disease (CKD). Take each of the 3 possible etiologies and explain how each can cause osteoporosis. (I know some of this pertains to the renal lecture; answer this after reviewing the renal content as this is a good exercise in “bringing everything together”). 1. patho of age- and gender-related changes in calcium movement: 2. problem with the parathyroid: hypo or hyper—which would cause osteoporosis and how? 3. CKD— explain how CKD (go back to renal notes if you need to) can cause there to be less calcium for the bone What kind of medications should this patient be on (ie, what would be the mechanism of action of the medicines—what would you want them to do?)