ENDOCRINE 2 Flashcards

1
Q

Risk Factors for Endocrine Problems

A
  • age
  • heredity
  • congential factors
  • trauma
  • environmental factors
  • consequence of other health problems or surgery
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2
Q

Hypothalamus

A
  • Portion of the diencephalon of the brain, forming the floor and part of the lateral wall of the third ventricle.
  • activates, controls, and integrates the peripheral autonomic nervous system, endocrine processes, and many somatic functions, such as body temperature, sleep and appetite.
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3
Q

Hypothalamus hormones

A
  • Corticotropin-releasing hormone (CRH)
  • Gonadotropin-releasing hormone (GnRH)
  • Growth hormone-inhibiting hormone (GHIH)
  • Growth hormone-releasing hormone (GHRH)
  • Melanocyte-inhibiting hormone (MIH)
  • Prolactin-inhibiting hormone (PIH)
  • Thyrotropin-releasing hormone (TRH)
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4
Q

Testosterone/Androgen Replacement Therapy

treats hypopituitarism

A
  • treats hypopituitarism
  • used to replace deficient hormones or to treat hormone-sensitive disorders
  • can cause bleeding if the client is taking oral anticoagulants (increase the effect of anticoagulants)
  • can cause decreased serum glucose concentration, thereby reducing insulin requirements in the client with diabetes mellitus.
  • hepatotoxic medications are avoided with the use of androgens because of the risk of additive damage to the liver.
  • androgens usually are avoided in men with known prostate or breast carcinoma, because androgens often stimulate growth of these tumors.
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5
Q

Androgen side effects

A
  • masculine secondary sexual characteristics
    *
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6
Q

androgen/testosterone interventions

A
  • monitor vital signs
  • monitor for edema, weight gain, and skin changes
  • assess mental status and neurological function
  • assess for signs of liver dysfunction, including right upper quadrant abdominal pain, malaise, fever, jaundice and pruritis.
  • assess for the development of secondary sexual characteristics.
  • instruct the client to take medication with meals or a snack.
  • instruct the client to notify the PHCP if priapism develops.
  • instruct the client to notify the PHCP if fluid retention occurs.
  • instruct women to use a nonhormonal contraceptive while on therapy.
  • For women, monitor for menstrual irregularities and decreased breast size.
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7
Q

Estrogens and Progestins (women with hypopituitarism)

A
  • estrogens are steroids that stimulate femal reproductive tissue.
  • progestins are steroids that specifically stimulate the uterine lining.
  • estrogens and progestin preparations may be used to stimulate the endogenous hormones to restore hormonal balance or to treat hormone sensitive tumors (suppress tumor growth) or for contraception.
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8
Q

Estrogen contraindications

A
  • estrogens are contraindicated in clients with breast cancer, endometrial hyperplasia, endometrial cancer, history of thromboembolism, known or suspected pregnancy or lactation.
  • use estrogens with caution in clients with hypertension, gallbladder disease, or liver or kidney dysfunction.
  • estrogens increase the risk of toxicity when used with hepatotoxic medications.
  • barbiturates, phenytoin, and rifampin decrease the effectiveness of estrogen.
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9
Q

Progestins are contraindicated

A

in clients with thromboembolic disorders and should be avoided in clients with breast tumors or hepatic disease.

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10
Q

estrogen/progestin side effects and interventions

A
  • breast tenderness, menstrual changes
  • nausea, vomiting, and diarrhea
  • malaise, depression, excessive irritability
  • weight gain
  • edema and fluid retention
  • atherosclerosis
  • hypertension, stroke, myocardial infarction
  • thromboembolism (estrogen)
  • migraine headaches and vomiting (estrogen)
  • monitor vital signs
  • monitor for hypertension
  • assess for edema and weight gain
  • advise client not to smoke
  • advise the client to undergo routine breast and pelvic examinations.
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11
Q

Bromocriptine mesylate (Parlodel)

A
  • treats hyperpituitarism/acromegaly
  • dopamine agonists: stimulates dopamine receptors in the brain and inhibit the release of GH and PRL (prolactin)
  • in most cases, small tumors decrease until the pituitary gland is normal size
  • large pituitary tumors usually decrease to some extent
  • side effects of bromocriptine include orthostatic (postural) hypotension, headache, nausea, abdominal cramps, and constipation.
  • give bromocriptine with a meal or a snack to reducce GI side effects.
  • treatment starts with a low dose & is gradually increased until the desired level is reach.
  • if pregnancy occurs, the drug is stopped.
  • treac pts taking bromocriptine to seek medical care immediately if chest pain, dizziness, or water nasal discharge occurs because of the possiblity of serious side effects including cardiac dysrhythmias, coronary artery spasms, and cerebrospinal fluid leakage.
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12
Q

Octreotide (Sandostatin)

A
  • treats hyperpituitarism/acromegaly
  • inhibits GH release through negative feedback
  • assess frequenct and consistency of stools and bowel sounds throughout therapy.
  • use cautiously in gallbladder disease.
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13
Q

Desmopressin acetate (DDAVP)

A
  • treats diabetes insipidus
  • a synthetic form of vasopressin given orally, as a sublingual “melt” or intranasally in metered spray
  • the frequency of dosing varies with patient responses.
  • teach patients that each metered spray delivers 10 mcg and those with mild DI may need only one or two doses in 24 hours
  • for more severe DI, one or two metered doses two or three times daily may be needed.
  • During severe dehydration, ADH may be given IV or IM.
  • Ulceration of the mucous membranes, allergy, a sensation of chest tightness, and lung inhalation of spray may occur with the use of the intranasal preparations.
  • if side effects occur or if the patient has an upper respiratory infection, oral or subcutaneous vasopressin is used.
  • the parenteral form of desmopressin is 10 times stronger than the oral form, and the dosage must be reduced.
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14
Q

vasopressin (Vasostrict)

A
  • used in diabetes insipidus
  • allows the permeability of the renal collecting ducts, allowing reabsorption of water.
  • decreased urine output and increased urine osmolality in diabetes insipidus. Increased BP.
  • contraindicated in chronic renal railure with increased BUN
  • side effects: dizziness, pounding sensation in head, abdominal cramps, flatulence, sweating.
  • monitor BP, Hr and ECG periodically throughout therapy and continuously throughout cardiopulmonary resuscitation.
  • monitor urine osmolality and urine volume frequently.
  • monitor for S&S of water intoxication (confusion, drowsiness, headache, weight gain, difficulty urinating, seizures and coma.
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15
Q

Chlorpropamide (Diabinese)

A
  • management of neurogenic diabetes inspidus
  • lowers blood sugar by stimulating release of insulin from the pancreas and increasing the sensitivity to insulin at receptor sites. may also decrease hepatic glucose production
  • side effects: photosensitivity, hypoglycemia
  • monitor CBC periodically during therapy.. Notify health care provider promptly if decrease in blood counts occurs.
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16
Q

Tolvaptan (Samsca, Jynarque)

A
  • Used in SIADH
  • vasopressin receptor antagonists
  • Promotes water excretion without causing sodium loss.
  • Tolvaptan has a black box warning that rapid increases in serum sodium levels (those greater than a 12 meq/L increase in 24 hours) have been associated with central nervous system demyelination that can lead to serious complications and death.
  • In addition, when this drug is used at higher dosages or for longer than 30 days, there is significant risk for liver failure and death.
  • administer tolvaptan only in the hospital setting so serum sodium levels can be monitored closely for the development of hypernatremia.
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17
Q

demeclocycline (Declomycin) a tetracycline antibiotic

A
  • used for milder SIADH
  • an oral antibiotic , may help reach fluid and electrolyte balance, although the drug is not approved for this problem.
  • water excretion without sodium loss.
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18
Q

Fludrocortisone (FLorinef)

A
  • causes sodium reabsorption, hydrogen and potassium excretion, and water retention by its effects on the distal renal tubule.
  • maintenance of sodium balance and BP in patients with adrenocortical insufficiency.
  • used for hypofunction of the adrenal gland.
  • monitor the patient’s blood pressure to assess for the potential side effect of hypertension.
  • instruct the patient to report weight gain or edema because sodium intake may need to be restricted.
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19
Q

Liothyronine (Cytomel, T3, Triostat)

A
  • thyroid supplementation in hypothyroidism.
  • Treatment or suppression of euthyroid goiters.
  • Diagnostic agent for suppression tests to differentiate mild hyperthyroidism from thyroid gland autonomy.
  • Treatment of myxedema coma (IV fomulation)
  • replacement of or supplementation to endogenous thyroid hormones.
  • principle effect is increasing metabolic rate of body tissues.
  • Side effects: insomnia, irritability, headache, arrhythmias, tachycardia, weight loss, heat intolerance.
  • Assess apical pulse and BP prior to and periodically during therapy. Assess for tachyarrhythmias and chest pain.
  • toxicity manifests as hyperthyroidism.
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20
Q

Methimazole (Northyx, Tapazole)

&

Propylthiouracil (PTU)

A
  • used in hyperthyroidism
  • block thyroid hormone production by preventing iodide binding in the thyroid gland.
  • The response to these drugs is delayed because the patient may have large amounts of stored thyroid hormones that continue to be released.
  • Teach patients to check for weight gain, slow heart rate, and cold intolerance, which are indications of hypothyroidism and the need for a lower drug dose.
  • teach patients to avoid crowds and people who are ill because the drug reduces the immune response, increasing the risk for infection.
  • Teach patients taking propylthiouracil to report darkening of the urine or a yellow appearance to the skin or whites of the eyes, which indicate possible liver toxicity or failure, a serious side effect of propylthiouracil.
  • Remind women taking methimazole to notify their PHCP if they become pregnant necause the drug causes birth defects and should not be used during pregnancy.
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21
Q

Levothyroxine (T4) (Synthroid)

A
  • Purpose: management of hypothyroidism and myxedema coma
  • thyroid hormones
  • Side effects: weight loss, arrhythmias, tachycardia, insomnia, irritability, nervousness, heat intolerance, menstrual irregularities, thyroid storm, hypertension
  • PO; onset 24 hours
  • PO: take at same time daily to maintain blood level; take on empty stomach (30 before eating)
  • do not switch brands unless directed.
  • avoid OTC meds with iodine and iodized salt, soybeans, tofu, turnips, walnuts, some seafood, some bread
  • medication controls symptoms and treatment is lifelong
  • separate antacids, iron, and calcium products by 4 hours
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22
Q

Lithium (Lithmax, Lithobid)

A
  • manic episodes of bipolar i disorder (treatment, maintenance, prophylaxis)
  • alters cation transport in nerve and muscle. May also influence reuptake of neurotransmitters.
  • May cause hyper or hypothyroidism.
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23
Q

Prednisone (Deltasone)

A
  • Used in adrenal insufficiency
  • instruct the patient to report illness because the usual daily dosage may not be adequate during periods of illness or severe stress.
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24
Q

Furosemide

A
  • used in hyperparathyroidism
  • helps reduce serum calcium levels
  • a diuretic that increases kidney secretion of calcium, is used along with IV saline in large volumes to promote calcium excretion
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25
Q

H2 receptor blockers

cimetidine, famotidine, nizatidine, ranitidine

A
  • used in cushings disease where there is hypercortisolism
  • cortisol inhibits production of the thick, gel-like mucus that protects the stomach lining, decreases blood flow to the ares and triggers the release of excess hydrochloric acid
  • h2 receptor blockers inhibit the gastric proton pump and prevent the formation of hydrochloric acid.
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26
Q

Spironolactone

A
  • Used in hyperaldosteronism.
  • a potssium sparing diuretic and aldosterone antagonist
  • when surgery cannot be performed, spironolactone therapy is continued to control hypokalemia and hypertension.
  • Because spironolactone is a potassium sparing diuretic, hyperkalemia can occir in patients who have impaired kidney function or excessive potassium intake.
  • Advise the patient to avoid potassium supplements and food rich in potassium.
  • hyponatremia can occur with spironolactone therapy, and the patient may need to increase dietary sodium.
  • Instruct patients to report symptoms of hyponatremia, such as mouth dryness, thirst, lethargy or drowsiness.
  • Teach them to report any additional effects of spironolactone therapy, including gynecomastia, diarrhea, drowsiness, headache, rash, urticaria (hives), confusion, erectile dysfunction, hirutism, and amenorrhea.
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27
Q

Magnesium Sulfate

A
  • to correct hypoparathyroidism caused by hypomagnesemia
  • acute hypomanesemia is corrected with 50% magnesium sulfate in 2-mL doses (up to 4 g daily) IV.
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28
Q

Phenoxybenzamine

A
  • used before therapy for pheochromocytoma
  • the patient’s blood pressure is stabilized using adrenergic blocking agents such as phenoxybenzamine (Dibenzyline) starting 7 to 10 days before surgery because of the increased risk for severe hypertension during surgery.
  • drug dosages are adjusted until blood pressure is controlled and hypertensive attacks do not occur.
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29
Q

Calcitriol (Rocaltrol)

A
  • Hypoparathyroidism
  • treats acute vitamin D deficiency/hypocalcemia
  • promotes the absorption of calcium and decreases parathyroid hormone concentrations
  • side effects: pancreatitis, headache, weakness, abdominal pain
  • avoid concurrent use of antacids containing Mg
  • observe client for hypocalcemia.
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30
Q

Calcitonin (Miacalcin)

A
  • treatment of hyperparathyroidism
  • decreases the release of skeletal calcium and increases kidney excretion of calcium.
  • it is not effective when used alone because of its short duration of action.
  • therapeutic effects are enhanced if calcitonin is given with glucocorticoids.
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31
Q

metyraprone (Metopirone)

A
  • Treatment of hypercortisolism (Cushing’s disease)
  • decreases cortisol production
  • , is a medication which is used in the … Metyrapone test may aid in verifying the cause of Cushing’s syndrome.
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32
Q

Plicamycin (Mithracin)

A
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33
Q

Anterior pituitary hormones

A
  • Thyroid stimulating hormone (TSH), also known as thyrotropin
  • Adrenocorticotropic hormone (ACTH, corticotropin)
  • Luteinizing hormone (LH), also known as Leydig cell-stimulating hormone (LCSH)
  • Follicle-stimulating hormone (FSH)
  • Prolactin (PRL)
  • Growth Hormone (GH)
  • Melanocyte-stimulating hormone (MSH)
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34
Q

Posterior pituitary

A
  • vassopressin (antidiuretic hormome [ADH])
  • oxytocin
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35
Q

thyroid

A
  • triiodothyronine (T3)
  • thyroxine (T4)
  • calcitonin
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36
Q

Parathyroid

A
  • Parathyroid hormome (PTH)
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37
Q

Adrenal Cortex

A

Glucocorticoids (cortisol)

mineralocorticoids (aldosterone)

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38
Q

ovary

A

estrogen

progesterone

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39
Q

testes

A

testosterone

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40
Q

pancreas

A

insulin

glucagon

somatostatin

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41
Q

Thyroid-stimulating hormone or thyrotropid (TSH)

A

targets the thyroid

stimulates synthesis and release of thyroid hormones

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42
Q

adrenocorticotropic hormone, corticotropin (ACTH)

A

targets the adrenal cortex

stimulates synthesis and release of corticosteroids and andrenocortical growth

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43
Q

Leuteinzing Hormone (LH) (known as leydig cell-stimulating hormone in males)

A
  • targets the ovary and testes
  • stimulates ovulation and progesterone secretion
  • stimulates testosterone secretion
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44
Q

follicle-stimulating hormone (FSH) (know as interstitial cell- or Sertoli cell-stimulating hormone in males)

A
  • targets the ovary and testis
  • stimulates estrogen secretion and follicle maturation
  • stimulates spermatogenesis
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45
Q

Prolactin (PRL)

A
  • targets the mammary glands
  • stimulates breast milk production
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46
Q

Growth Hormone

A
  • Targets bones and soft tissue
  • promotes growth through lipolysis, protein anabolism, and insulin antagonism
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47
Q

Melanocyte-stimulating hormone (MSH)

A
  • targets melanocytes
  • promotes pigmentation
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48
Q

Vasopressin (antidiuretic hormone [ADH])

A
  • Targets the kidneys
  • promotes water reabsorption
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49
Q

Oxytocine

A
  • targets the uterus and mammary glands
  • stimulates uterine contractions and ejection of breast milk
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50
Q

Functions of Glucocorticoid hormones

A
  • Prevent hypoglycemia by increasing liver production (gluconeogenesis) and inhibiting peripheral glucose use.
  • maintain excitability and responsiveness of cardiac muscle
  • increase lipolysis, releasing glycerol and free fatty acids
  • increase protein catabolism
  • degrade collagen and connective tissue
  • increase the number of mature neutrophils released from bone marrow
  • exert anti-inflammatory effects that decrease the migration of inflammatory cells to sites of injury
  • maintain behavior and cognitive functions
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51
Q

Catecholamine REceptors and Effects of Adrenal Medullary Hormone Stimulation on Selected Organs and Tissues

A
  • Heart, beta 1 receptors, increased heart rate and increased contractility
  • blood vessels, alpha & beta 2, vasoconstriction and vasodilation
  • GI tract, alpoha and beta, increased sphincter tone and decreased motility
  • Kidneys, Beta2, increased renin release
  • bronchioles, beta2, relaxation; dilation
  • bladder, alpha, beta2, sphincter contractions, relaxation of detrusor muscle
  • skin, alpha, increased sweating
  • fat cells, beta, increased lipolysis
  • liver, alpha, increased gluconeogenesis and glycogenolysis
  • pancreas, alpha, decreased glucagon and insulin release, beta, increased glucagon and insulin release
  • eyes, alpha, dilation of pupils
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52
Q

Functions of Thyroid Hormones in Adults

A
  • Control metabolic rate of all cells
  • Promote sufficient pituitary secretion of growth hormone and gonadotropins
  • regulate protein, carbohydrate, and fat metabolism
  • exert effects on heart rate and contractility
  • increased red blood cell production
  • affect respiratory rate and drive
  • increase bone formation and decrease bone resorption of calcium
  • act as insulin antagonists.
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53
Q

Aging

decreased antidiuretic hormone (ADH) production

A
  • Urine is more dilute and may not concentrate when fluid intake is low
  • The patient is at greater risk for dehydration.
  • assess the older patient more frequently for dehydration.
  • if fluids are not restricted because of another health problem, teach UAP to offer fluids at least every 2 hours while awake.
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54
Q

Aging

decresed ovarian production of estrogen

A
  • Bone density decreases
  • skin is thinner, drier, and at greater risk for injury
  • perineal and vaginal tissues become drier, and the risk for cystitis increases.
  • Teach the patient to engage in regular exercise and weight bearing activity to maintain bone density.
  • Handle the patient carefully to avoid injury from pathologic fractures.
  • Avoid pulling or dragging the patient.
  • use minimal tape on the skin
  • help patients confined to bed or chairs change positions at least every 2 hours
  • Teach the patients to use skin moisturizers
  • perform or assist the patient to perform perineal care at least twice daily.
  • unless another health problem requires fluid restriction, encourage all women to drink at least 2 liters of fluids daily.
  • teach sexually active older women to urinate immediately after sexual intercourse.
  • teach sexually active women that using vaginal lubricants with sexually activity can reduce discomfort and the risk for tissue damage.
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55
Q

Aging

decreased glucose tolerance

A
  • weight becomes greater than ideal along with:
    • elevated fasting blood glucose level
    • elevated random blood glucose level
    • slow wound healing
    • frequent yeat infections
    • polydipsia
    • polyuria
  • obtain a family history of obesity and type 2 diabetes.
  • encourage the pt to engage in regular exercise and to keep body weight within 10 lb of idea.
  • teach patients the signs and symptoms of diabetes and instruct them to report any of these to the PHCP
  • suggest diabetes testing for any patient with:
    • persistent vaginal candidiasis
    • failure of a foot or leg skin wound to heal in 2 weeks or less
    • increased hunger and thirst
    • noticeable decrease in energy level
      *
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56
Q

Aging

Decreased generalized metabolism

A
  • There is less tolerance for cold
  • appetite is decreased
  • heart rate and BP are decreased
  • can be difficult to distinguish from hypothyroidism. Check for additional signs and symptoms of:
    • lethargy
    • constipation (as a change from usual bowel habits)
    • decreased cognition
    • slowed speech
    • body temperature consistently below 97 degree F.
    • Heart rate below 60 bpm
  • Teach patients to dress warmly in cool or cold weather.
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57
Q

Always palpate the thyroid gently in an adult

A

who has or is suspected to have hyperthyroidism because vigorous palpation can stimulate a sudden release of thyroid hormones and cause a thyroid storm.

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58
Q

Observe the patient’s general appearance and

A

assess height, weight, fat distribution, and muscle mass in relation to age.

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59
Q

When examining the head, focus on abnormalities of facial structure, features, and expressions, such as

A
  • Prominent forehead or jaw
  • round or puffy face
  • dull or flat expression
  • exophthalmoas (protruding eyeballs and retracted upper lid)
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60
Q

check the lower neck for

A

a visible enlargement of the thyroid gland.

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61
Q

Observe skin color and look for areas of

A

pigment loss (hypopigmentation) or excess (hyperpigmentation). Fungal iskin infections, slow wound healing, bruising, and petechiae are often seen in patients with adrena hyperfunction.

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62
Q

Vitiligo

A

(patchy areas of pigment loss) is seen with primary hypofunction of the adrenal glands and is caused by autoimmune destruction of melanocytes in the skin.

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63
Q

Inspect the fingernails for malformation, thickness, or brittleness,

A

all of which may suggest thyroid gland problems. Examine the extremities and the base of the spine for edema, which suggests impaired fluid and electrolyte imbalance.

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64
Q

Check the trunk for any abnormalities in chest size and symmetry.

A

Truncal obesity and the presence of a “buffalo hump” between the shoulders on the back may indicate adrenocortical excess.

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65
Q

Striae

A

(reddish-purple stretch marks) on the breasts or abdomen are often seen with adrenocortical excess.

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66
Q

Assess the patient’s hair distribution for signs of endocrine gland dysfunction.

A

Changes include hirsutism (excessive body hair growth, especially on the face, chest, and center abdominal line of women), excessive scalp hair loss, or changes in hair texture.

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67
Q

Distribution and quantity of pubic hair are often affected in

A

hypogonadism.

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68
Q

Thyroid gland palpation

A

Palpate the thyroid gland by standing either behind or in front of the patient. The posterior approach may be easier. Having the patient swallow sips of water during the examination helps you palpate the thyroid gland, which is not easily felt when normal.

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69
Q

Auscultate the chest to assess cardiac rate and rhythm to use later

A

as a means of assessing treatment effectiveness. Some endocrine problems include dysrhythmias.

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70
Q

If an enlarged thyroid gland is palpated, auscultate the area of enlargement for bruits

A

Hypertrophy of the thyroid gland causes an increase in vascular flow, which may result in bruits.

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71
Q

Many endocrine problems can change a patient’s behaviors, personality, and psychological responses.

A

Assess the patient;s coping skills, support systems, and health-related beliefs.

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72
Q

Salivary levels of steriod hormones (cortisol, testosterone, progesterone, and estradiol)

A

accurately reflect blood levels of these hormones. Protein hormones, such as those from the pituitary gland and thyroid gland, cannot be accurately assessed using saliva.

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73
Q

Assay

A
  • An assay measures the level of a specific hormone in blood or other body fluid.
  • The most common assays for endocrtine testing are antibody-based immunologica assays and chromatographic assays, which include mass spectrometry.
  • It is a substance, usually a peptide or steroid, rpoduced by one tissue and conveyed by the bloodstream to another to effect physiological activity.
  • It is also a synthetic compound that acts like a hormone in the body.
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74
Q

Measurement of specific hormone blood level does not always distinguish

A

between the normal and the abnormal.

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75
Q

Stimulation tests

A
  • For patients who might have an underactive endocrine gland, a stimulus may be used to determine whether the gland is capable of normal hormone production.
  • This method is called provocative testing.
  • Measured amounts of selected hormones are given to stimulate the target gland to maximum production.
  • Hormone levels are then measured and compared with expected normal values.
  • Failure of a hormone level to rise with provacation indicates hypofunction.
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76
Q

Endocrine Changes with Aging

“GET”

A

Gonads

Endocrine pancreas

Thyroid gland

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77
Q

Suppression Tests

A
  • Suppression tests are used when hormone levels are high or in the upper range of normal.
  • Example to determine Cushing’s, dexamethasone is given in pill form. The next morning a blood test is done to see if the medication decreased the hormone level.
  • Failure of suppression of hormone production during testing indicates hyper function.
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78
Q

Blood Tests endocrine testing

A
  • check your laboratory’s method of handloing the hormone test samples for tube type, timing, drugs to be administered as part of the test, etc. For example, blood samples drawn for catecholamines must be placed on ice and taken to the laboratory immediately.
  • Explain the procedure and any restrictions to the patient.
  • If your are drawing blood sampples from an IV line, clear the line throughly. Do not use a double- or triple-lumen line to obtain samples; contamination or dilution from another port is possible.
  • Emphasize the importance of taking a drug prescribed for the test on time. Tell the patient to set an alarm if the drug is to be taken during the night.
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79
Q

For Urine Tests:

A
  • Instruct the patient to being the urine collection (whether for 2, 4, 8, 12 or 24 hours) by first emptying his or her bladder.
  • Remind the patient to not save the urine specimen that begins the collection. The timing for the urine collection begins after this specimen.
  • Tell the patient to note the time of the discard specimen and to plan to collect all urine from this time until the end of the urine collection period.
  • To end the collection, instruct the patient to empty his or her bladder at the end of the timed period and add that urine to the collection.
  • Check with the laboratory to determine any special handling of the urine specimen (e.g. Is a preservative needed? Does the container need to be kept cold?
  • If needed, make sure that the preservative has been added to the collection container at the beginning of the collection.
  • Tell the patient about any preservative and the need to avoid splashing urine from the container because some preservatives make the urine caustic.
  • if the specimen must be kept cool or cold, instruct the patient to place the container in an inexpensive cooler with ice. The specimen container should not be kept with food or drinks.
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80
Q

Urine Tests

A
  • hormone levels and the metabolites of specific hormones in the urine are often measured to determine endocrine function
  • many endocrine hormones are secreted in a pulsatile fashion.
  • a 24 hour urine collection better reflects the overall function of certain glands, such as the adrena gland.
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81
Q

Imaging Assessment

A
  • Anterior, posterior, and lateral skull x-rays may be used to view the sella turcica.
  • Erosion of the sella turcica indicates invasion of the wall from an abnormal growth.
  • MRI with contrast is the most sensitive method of imaging the pituitary gland.
  • CT scan can evaluate the pituitary gland, but it is also used to evaluate the adrenal glands, ovaries, and pancreas.
  • Ultrasound evaluates the thyroid, parathyroid glands, ovaries and testes.
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82
Q

Other Diagnostic Assessment

A
  • Needle biopsy is used to indicate the composition of thyroid nodules.
  • Should check with MD if blood thinners should be stopped.
  • It is a relatively safe and quick outpatient procedure to determine if surgical intervention is needed.
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83
Q

Piuitary Glands

A
  • If one hormone is affected, it is called selective hypopituitarism.
  • If decrease in production of all the anterior pituitary hormones (rare condition) it is called panhypopituitarism.
  • It is divided into two lobes at the base of the brain
    • anterior lobe: adenohypophysis
    • posterior lobe: neurohypophysis
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84
Q

Hypopituitarism

A
  • Most life-threatening deficiencies- ACTH and TSH
  • Deficiency of gonadotropins
  • Growth hormone stimulates liver to produce somatomedins that enhance growth activity.
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85
Q

Hypopiuitarism Causes

A
  • Benign or malignant pituitary tumors can compress and destroy pituitary tissue.
  • Pituitary function can be impaired by malnutrition or rapid loss of body fat.
  • Shock or severe hypotension reduces blood flow-hypofunction and infarction.
  • Other-hed and brain trauma, brain tumors or infection, radiation or surgery of head and brain and AIDS.
  • Idiopathic hypopituitarism has an unknown cause.
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86
Q

Hypopituitarism Assessment

A
  • Look for changes in physical appearance
  • Assess changes in vision (especially peripheral vision for changes or loss)
  • Limited eye movement.
  • DECREASED Anterior Pituitary HORMONES
    • growth hormone: decreased bone density, pathological fractures, decreased muscle strength, increased serum cholesterol levels
    • Gonadotropins (Luteinizing hormone [LH}0, follicle-stimulating hormone [FSH]) : women; amenorrhea, anovulation, low estrogen levels, breast atrophy, loss of bone density, decreased axillary and pubic hair, decreased libido. Men; decreased facial hair, decreased ejaculate volume, reduced muscle mass, loss of bone density, decreased body hair, decreased libido and impotence.
    • thyroid-stimulating hormone (thyrotropin) (TSH): decreased thyroid hormone levels, weight gain, intolerance to cold, scalp alopecia, hirsutism, menstrual abnormalities, decreased libidio, slowed cognition, lethargy.
    • Adrenocorticotropic hormone (ACTH); decreased werum cortisol levels, pale, swallow complexion, malaise and lethary, anorexia, postural hypotension, headache, hypoglycemia, hyponatremia, decreased axillary and pubic hair (women)
  • Decreased Posterior Pituitary Hormones
    • Vasopressin (antidiuretic hormone [ADH]): Diabetes Insipidus: greatly increased urine output, low urine specific gravity (<1.005), hypotension, dehydration, increased plasma osmolarity, increased thirst, output does not decrease when fluid intake decreases.
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87
Q

Hypopituitarism interventions

A
  • lifelong replacement of dificient hormones
  • androgen therapy for virulization “Men”
    • most effective is parenteral & transdermal
  • Estrogens and progesterone - “Women”
    • Risk for hypertension and thrombosis.
  • Growth hormone
    • may be treated with subcutanceous injection of human GH at night to mimic normal GH release.
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88
Q

Pituitary Gland Problems

A
  • Anterior Pituitary
    • Hyperpituitarism
    • Hypopituitarism
  • Posterior Pituitary
    • These problems can be caused by damage to the posterios pituitary or hypothalamus:
    • Diabetes Insipidus
    • Syndrome of inappropriate antidiuretic hormone secretion (SIADH)
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89
Q

Causes of Hyperpituitarism

A
  • Hormone oversecretion occurs with pituitary tumors or hyperplasia
  • pituitary adenoma (benign tumor) : most common are prolactin secreting tumors
  • One hormone is produced in excess PRI, ACTH, or GH
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90
Q

Gigantism

A
  • Onset of growth hormone hypersecretion occurs before puberty
  • painful bones and joints
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91
Q

Acromegaly

A
  • Onset may be gradual with slow progression
  • Early detection and treatment are essential to prevent irreversible changes in soft tissues
  • Some changes are reversible but skeletal changes are permanent.
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92
Q

Hyperpitiutarism Assessment

A
  • Ask about family history
  • asku about any changes in hat, glove, ring, or shoe size and the presence of fatigue
  • ask specifically regarding headaches & changes in vision
  • Hypersecretion of PRL often reports sexual function difficulties
  • changes in appearance and target organ function occur with excessive anterior pituitary hormones
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93
Q

Hyperfunction Growth Hormone (GH) Acromegaly key features

A
  • Thickened Lips
  • coarse facial features
  • increasing head size
  • lower jaw protrusion
  • enlarged hands and feet
  • joint pain
  • barrel-shaped chest
  • hyperglycemia
  • sleep apnea
  • enlarged heart, lungs and liver
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94
Q

Hypersecretion of Prolactin

A
  • hypogonadism (loss of secondart sexual characteristics)
  • decreased gonadotropin levels
  • galactorrhea (milky nipple discharge)
  • increased body fat
  • increased serum prolactin levels
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95
Q

Hyperfunction

Adrenocorticotropic Hormone (ACTH)

Cushing’s Disease (pituitary)

Key features

A
  • elevated plasma cortisol levels
  • weight gain
  • truncal obesity
  • moon face
  • extremity muscle wasting
  • loss of bone density
  • hypertension
  • hyperglycemia
  • striae and acne
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96
Q

Thyrtropin (Thyroid-Stimulating Hormone [TSH])

Hypersecretion features

A
  • elevated plasma TSHA dn thyroid hormone levels
  • weight loss
  • tachycardia and dysrhythmias
  • heat intolerance
  • increased GI motility
  • fine tremors
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97
Q

Hypersecretion of Gonadotropins (LH and FSH) Key features

A
  • Men:
    • elevated LH and FSH levels
    • hypogonadism or hypergonadism
  • Women:
    • normal LH and FSH levels
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98
Q

hypophysectomy

A
  • surgical removal of the pituitary gland and tumor is the most common treatment for hyperpituitarism.
  • successful surgery decreases hormone levels, relieves headaches, and may reverse changes in sexual functioning,
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99
Q

hyperpituitarism interventions

A
  • nonsurgical
    • drug therapy
      • dopamine agonists: bromocriptine mesylate and cabergoline
      • other drugs: somatostatin analogs especially octreotide and lanreotide
      • octreotide inhibits GH release through negative feedback
      • Pevisomant blocks GH receptor activity and blocks production of insulin-like growth factor (IGF).
    • Radiation Therapy
      • does not have immediate effects in reduction
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100
Q

gigantism

A
  • abnormally high liner growth due to the excessice action of IGF-1 before the closure of the epiphyseal growth plates in childhood
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101
Q

acromegaly

A
  • disorder of the IGF-1 which causes excessive growth of the hands, feet, jaw and internal organs in adulthood
  • mri shows pituitary tumor in 90% of acromegalic patients
  • the best confirmatory test for acromegaly is the oral glucose suppression test.
  • in acromegaly, glucose does not suppress growth hormone
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102
Q

Hypophysectomy

A
  • selective adenomectomy leaves normal pituitary tissue undisturbed.
  • surgical removal of pituitary gland and tumor through a transphenoidal approach.
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103
Q

Hypophysectomy preoperative care

A
  • teach client that the procedure will decrease hormone levels
    • relieve headaches
    • may reverse changes in sexual function
  • Procedure will not reverse body changes, organ enlargement or visual changes.
  • client will have packing for 2-3 days
  • client will need to breathe through mouth
  • may have a mustache dressing under the nose
  • no brushing teeth, coughing, sneezing, blowing nose or bending forward is allowed.
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104
Q

hypophysectomy procedure

A
  • client is in a semi-sitting position
  • transsphenoidal incision just above the upper lip
  • if an endoscopic or tesnsphenoidal approach can not be done a craniotomy is required.
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105
Q

Hypophysectomy postoperative care

A
  • assess
    • vision, mental status, altered LOc, decreased strength in extremities
    • diabetes insipidus
    • CSF leakage
    • infection
    • increased ICP (intercranial pressure)
  • avoid bending
  • avoid constipation
  • frequent mouth care every 4-6 hours
  • no brushin teeth for 2 weeks
  • expect numbness in area of incision
  • will experience decreased sense of smell for 3-4 months
  • hormone replacement with vasopression to maintain fluid balance to prevent diabetes incipidous.
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106
Q

The patient after hypophysectomy

A
  • Monitor the patient’s neurologic status hourly for the first 24 hours and then every 4 hours.
  • monitor fluid balance, especially for output greater than intake.
  • encourage the patient to perform deep-breathing exercises.
  • instruct the patient not to cough, blow the nose, or sneeze
  • instruct the patient to use dental floss and oral mouth rinses rather than toothbrushing until the surgeon gives permission.
  • instruct the patient to avoid bending at the waist to prevent increasing intercranial pressure.
  • monitor the nasal drip pad for the type and amount of drainage.
  • Teach the patient methods to avoid constipation and subsequent straining.
  • teach the patient self-administration of prescribed hormones.
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107
Q

One cause of hyperpituitarism is multiple endocrine neoplasia, type 1, in which there is inactivation of the suppressor gene MEN1.

A

MEN1 has an autosomal-dominat inheritance pattern and may result in a benign tumor of the pituitary, parathyroid glands, or pancreas. In the pituitary, this problem causes excessive production of growth hormone and acromegaly. Ask a patient with acromegaly whether either parent also had this problem or has had a tumor of the pancreas of parathyroid glands.

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108
Q

Teach patients taking bromocriptine to seek medical care immediately if

A

chest pain, dizziness, or watery nasal drainage occurs because of the possibility of serious side effects, including cardiac dysrhythmias, coronary artery spasms, and cerebrospinal fluid leakage.

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109
Q

Assessment of the patient who has undergone nasal hypophysectomy for hyperpituitarism

A
  • Assess cardiovascular status:
    • vital signs, including apical pulse, pulse pressure, presence or absence of orthostatic hypotension, and the quality/rhythm of peripheral pulses.
  • Assess cognition and mental status.
  • Assess condition of operative site:
    • Observe nasal area for drainage:
      • if present, note color, clarity and odor
      • test clear drainage for the presence of glucose
  • Assess neuromuscular status:
    • Reactivity of patellar and biceps reflexes
    • oral temperature
    • handgrip strength
    • steadiness of gait
    • distant and near visual acuity
    • pupillary responses to light
  • Assess kidney function:
    • Observe urine specimen for color, odor, cloudiness, and amount.
    • Ask about:
      • headaches or visual disturbances
      • ease of bowel movements
      • 24-hour fluid intake and output
      • over-the-counter and prescribed drugs taken
  • Assess patient’s understanding of illness and adherence with treatment:
    • symptoms to report to health care provider
    • drug plan (correct timing and dose)
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110
Q

Posterior Pituitary Abnormalities

A
  • The posterior pituitary gland secretes:
    • Vasopressin
    • Antidiuretic hormone (ADH)
    • Two common disorders
      • Diabetes Insipidus
      • Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
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111
Q

Diabetes Insipidus (DI)

A
  • Lithium can cause DI
  • Water metabolism problem cause by an ADH deficiency
    • either decrease in ADH synthesis or
    • inability of the kidneys to respond to ADH
  • Classifications
    • nephrogenic-inhertied disorder
    • primary-defect in hypothalamus or pituitary
    • secondary
    • drug-related
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112
Q

Diabetes Insipidus Assessment

A
  • Symptoms of dehydration
  • increase in frequency of urination and excessive thirst
  • dehydration and hypertonic saline tests used for diagnosis
  • urine diluted with low specific gravity (<1.005)
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113
Q

DIABETES INSIPIDUS (DI) INTERVENTIONS

A
  • Oral chlorpropamide
  • desmopressin acetate
  • early detection of dehydration and maintenance of adequate hydration
  • lifelong vasopressin therapy with permanent condition
  • teach patients to weigh themselves daily to identify weight gain
114
Q

Ensure that no patient suspected of having DI is

A

deprived of fluids for more than 4 hours because he or she cannot reduce urine output and severe dehydration can result.

115
Q

Nephrogenic diabetes insipidus can be a genetic disorder in which the ADH receptor (vasopressin receptor) has a defect that prevents kidney tubules from interacting with ADH

A

The result is poor water reabsorption by the kidney, although the actual amount of hormone produced is not deficient. The problem is most commonly inherited as an X-linked recessive disorder in which the AVPR2 gene coding for the ADH receptor is mutated and only males are affected. There is also an autosomal form of the disorder in which the AQP2 gene is mutated and both males and females are affected. When assessing a patient with DI, always ask whether anyone else in the family has ever had this disorder.

116
Q

diabete insipidus key features.

A
  • hypotension
  • tachycardia
  • weak peripheral pulses
  • hemoconcentration
  • increased urine output
  • dilute, low specific gravity
  • poor turgor
  • dry mucous membranes
  • decreased cognition
  • ataxia
  • increased thirst
  • irritability
117
Q

The parenteral form of desmopressin is 10 times stronger

A

than the oral form, and the dosage must be reduced.

118
Q

SIADH syndrome of inappropriate antidiuretic hormone

A
  • vasopressin secreted even when plasma osmolarity is low or normal
  • fedback mechanisms does not function properly
  • water is retained, results in hyponatremia (decreased serum sodium levels)
119
Q

Conditions Causing the Syndrome of Inappropriate Antidiuretic Hormone

A
  • small cell lung cancer
  • pancreatic, duodenal, and GU carcinomas
  • thymona
  • hodgkin’s lymphoma
  • non-Hodgkin’s lymphoma
  • viral and bacterial pneumonia
  • lung abscesses
  • active tuberculosis
  • pneumonthorax
  • chronic lung diseases
  • mycoses
  • positive-pressure ventilation
  • trauma
  • infection
  • tumors (primary or metastatic)
  • strokes
  • porphyria
  • systemic lupus erythematosus
  • Exogenous ADH
  • chlorpropamide
  • Vinccristine
  • Cyclophosphasmide
  • Carbamazepine
  • Opioids
  • Tricyclic antidepressants
  • General anesthetics
  • Fluoroquinolone antibiotics
120
Q

Administer tolvaptan or conivaptan only in the hospital setting

A

so serum sodium levels can be monitored closely for the development of hypernatremia.

121
Q

SIADH

FIndings

A
  • Recent head trauma
  • cerebrovascular disease
  • TB or other pulmonary disease
  • Cancer
  • All past and current drug use
  • decrease in serum sodium levels
122
Q

SIADH INTERVENTIONS

A
  • Fluid restriction
  • drug therapy (diuretics, hypertonic saline, demeclocycline)
  • monitor for fluid overload
  • safe environment
  • neurologic assessment
123
Q

Adrenal Gland Hypofunction

A
  • Adrenocortical steriods may decrease from inadequate secretion of ACTH (adrenocorticotropic hormone)
  • dysfunction of hypothalmic-pituitary control mechanism
  • direct dysfunction of adrenal tissue
  • manifestations may develop gradually or quickly with stress.
  • adrenal crisis is a life threatening manifestation that may occur without warning (adrenocortical insufficiency)
124
Q

Acute Adrenal Insufficiency

Addisonian Crisis

A
  • Life Threatening Event; need for cortisol and aldosterone is greater than available supply.
  • Usually occurs in response to stressful advent
  • Na will fall, K will increase, and hypotension develops. Watch for hypoglycemia.
125
Q

Primary Causes of Addison’s Disease

A
  • Autoimmune disease
  • Tuberculosis
  • metastatic cancer
  • fungal lesions
  • AIDS
  • hemorrhage
  • gram-negative sepsis
  • adrenalectomy
  • abdominal radiation
  • drugs & toxins
126
Q

Secondary Causes of Addison’s Disease

A
  • Pituitary tumors
  • Sheehan’s syndrome (postpartum pituitary necrosis)
  • hypophysectomy
  • High-dose pituitary radiation
  • high-dose whole brain radiation
127
Q

Addison’s Disease

A
  • Assess s/s of:
    • hypoglycemia
    • hyperkalemia
    • lethargic, depressed, confused or psychotic
  • Diagnostic
    • Low serum cortisol
    • Low blood glucose
    • Low Na
    • Elevated K & ACTH
    • Stimulation test is most definitive test for adrenal insufficiency.
128
Q

Adrenal Gland Hyperfunction

A
  • Adrenal gland may oversecrete just one hormone or all adrenal hormones causing:
    • Cushing’s-hypercortisolism
    • Hyperaldosteronism-excessive mineralcorticoid production
    • excessive androgen production
    • Pheochromocytoma results in excessive secretion of catecholamines (epinephrine and norepinephrine).
    • Bone apin
129
Q

Hypercortisolism: Cushing’s Disease

A
  • Exaggerated secretion of cortisol from the adrenal cortex.
  • Incidence/prevalence
    • most common cause is pituitary adenoma
    • women more than men
130
Q

Hypercortisolism: Cushings Disease

A
  • Clinical manifestations
  • skin changes
  • Cardiac changes
  • musculoskeletal changes
  • glucose metabolism
  • immune changes
131
Q

Hypercortisolism: Cushing’s Disease

A
  • Cushing syndrome is caused by exogenous corticosteriods in drugs to control asthma, other respiratory problems, rheumatoid arthritis. It is more common than the disease and it effects both genders equally.
132
Q

Cushing’s Disease Signs & Symptoms

A
  • Increased boy fat-truncal obesity
  • buffalo hump & moon face
  • decreased muscle mass
  • thin skin with fragile capillaries
  • bone density loss
  • shrinks organs containing lymphocytes
  • Hirustism
133
Q

Cushing’s Disease

A
  • Psychosocial Assessment
  • Laboratory tests: blood, salivary, urine cortisol levels
  • Imaging Assessment
  • Surgical Management: hypophysectomy & adrenalectomy
134
Q

Adrenalectomy

A
  • Preoperative
  • electrolye imbalances are corrected
  • cardiac monitoring
  • control hyperglycemia
  • prevent infection
  • decrease risk of falls.
135
Q

adrenalectomy

A
  • unilateral adrenalectomy (one gland)
  • bilateral adrenalectomy (both glands)
  • abdominal cavity or lateral flank
  • laparoscopic adrenalectomy is increasing.
136
Q

Adrenalectomy

A
  • critical care after surgery
  • bilateral adrenalectomy-client on life-long glucocorticoid and mineralocorticoid replacement, starting immediately after surgery.
137
Q

Hyperaldosteronsim

Conn’s Syndrome

A
  • Primary hyperaldosteronism- caused by benign adrenal tumor : hypersectrion of aldosterone
  • results in Na and K excretion
  • Secondary hyperaldosteronism- causes high levels of angiotensin II- high serum renin levels
  • complications: hypertension, brain attach (stroke), kidney disease.
138
Q

Pheochromocytoma

A
  • Is a catecholamine producing tumor which causes release of epinephrine & norepinephrine
  • tumor is usually benign
  • do not maniuplate the tumor as it can cause release of epinephrine & norepinephrine
  • Once surgery is performed it can result in a sudden drop in cortisol levels.
139
Q

Thyroid Gland

A
  • Has a rich blood supply
  • approximately 5 times the blood flow to the liver
  • 5 ml/min per gram of thyroid tissue
  • iodine is essential for thyroid to synthesize it hormones
140
Q

Hyperthyroidism Graves Disease

A
  • Thyrotoxicosis - is hyperthyroidism regardless of origin
  • hyperthyroidism causes hypermetabolsim and increased sympathetic nervous system activity.
141
Q

Hyperthyroidism

A
  • May be due to overproduction originating outside the thyroid
  • loss of storage function and leakage from the glands
142
Q

Hyperthyroidism Symptoms

A
  • goiter
  • exophthalmos (bug eyes)
  • pretibial myxedema
143
Q

Hyperthyroidism nonsurgical management

A
  • monitoring
  • reducing stimulation
  • promoting comfort
  • drug therapy (antithyroid drugs, iodine preparations, lithium, betaadrenergic blocking drugs)
144
Q

Hyperthyroidism Surgical Management

A
  • Total or subtotal thyroidectomy
  • monitor client for hoarseness or stridor, hypocalcemia & tetany, and thyroid storm
  • postoperative complications:
    • hemorrhage
    • respiratory distress
    • hypocalcemia and tetany (chvoteks & Trousseaus)
    • laryngeal nerve damage
    • thyroid storm or thyroid crisis
    • eye and vision problems of Graves disease
145
Q

Hypothyroidism causes

A
  • Differentiating: Aging vs. hypothyroidism
  • decreased metabolism from low thyroid hormone levels
146
Q

Risk of Myxedema Coma

A
  • Factors leading to myxedema coma include:
    • acute illness
    • surgery
    • chemotherapy
    • use of sedative or opioids
147
Q

Problems that can occur with Myxedema Coma

A
  • Coma
  • Respiratory failure
  • hypotension
  • hyponatremia
  • hypothermia
  • hypoglycemia
148
Q

Myxedema Coma

A
  • Is Rare
  • The heart muscle becomes flabby and the chamber size increases.
  • decreased cardiac output and perfusion
  • slowed perfusion
  • mucus and water under the skin
  • makes cellular metabolism worse
  • mortality rate is high and is a life-threatening emergency.
  • it can be caused by a variety of events, drugs, or conditions.
149
Q

Thyroid Storm

A
  • Caused by excessive thyroid hormone release: which dramatically increases the metabolic rate.
  • even with treatment, thyroid storm may lead to death.
150
Q

Thyroiditis

A
  • Inflammation of thyroid gland
  • Three Types:
    • acute
    • subacute (granulomatous)
    • chronic (Hashimoto’s disease-most common type)
  • Thyroiditis vs: hyperthyroidism or hypothyroidism
  • nonsurgical management: drug therapy
  • surgical management
151
Q

Hyperparathyroidism

A
  • Parathyroid glands-calcium and phosphate balance
  • Hypercalcemia and hypophosphatemia
  • nonsurgical vs. surgical management
152
Q

hypoparathyroidism

A
  • decreased function of parathyroid gland
    • latrogenic
    • idiopathic
    • hypomagnesemia
  • Intervention
    • correcting hypocalcemia
    • vitamin D deficiency
    • hypomagnesemia
153
Q

Functions of the Endocrine Glands

A
  • Maintenance and regulation of vital functions
  • response to stress and injury
  • growth and development
  • energy metabolism
  • reproduction
  • fluid, electrolyte and acid-base balance
154
Q

endocrine glands

A
  • adrenal
  • hypothalamus
  • ovaries
  • pancreas
  • parathyroid
  • pituitary
  • testes
  • thyroid
155
Q

Hypothalamus Hormones

A
  • Corticotropin-releasing hormone (CRH)
  • Gonadotropin-releasing hormone (GnRH)
  • Growth hormone-inhibiting hormone (GHIH)
  • Growth hormone-releasing hormone (GHRH)
  • Melanocyte-inhibiting hormone (MIH)
  • Prolactin-inhibiting hormone (PIH)
  • Thyrotropin-releasing hormone (TRH)
156
Q

Hypothalamus

A
  • Portion of the diencephalon of the brain, forming the floor and part of the lateral wall of the third ventricle.
  • activates, controls, and integrates the peripheral autonomic nervous system, endocrine processes, and many somatic functions, such as body temperature, sleep and appetite.
157
Q

Anterior Pituitary Lobe Hormones

A
  • adrenocorticostropic hormone (ACTH)
  • follicle-stimulating hormone (FSH)
  • Growth Hormone (GH)
  • Luteinizing Hormone (LH)
  • Melanocyte-stimulating hormone (MSH)
  • Prolactin (PRL)
  • Somatotropic growth-stimulating hormone
  • Thyroid-stimulating hormone (TSH)
158
Q

Posterior Pituitary Lobe Hormones

A
  • These hormones are produced by the hypothalamus, stored in the posterior lobe, and secreted into the blood when needed.
  • oxytocin
  • vasopressin, antidiuretic hormone (ADH)
159
Q

Pituitary Gland

A
  • The master gland; located at the base of the brain.
  • Influenced by the hypothalamus; directly affects the function of the other endocrine glands.
  • Promotes growth of body tissue, influences water absorption by the kidney, and controls sexual development and function.
160
Q

Adrenal Cortex Hormones

A
  • Glucocorticoids: Cortisol, Cortisone, Corticosterone
    • Responsible for glucose metabolism, protein metabolism, fluid and electrolyte balance, suppression of the inflammatory response to injury, protective immune response to invasion by infectious agents, and resistance to stress
  • Mineralocorticoids: Aldosterone
    • Regulation of electrolyte balance by promoting sodium retention and potassium excretion.
161
Q

Adrenal Gland

A
  • one adrenal gland is on top of each kidney
  • regulates sodium and electrolyte balance; affects carbohydrate, fat, and protein metabolism; influences the development of sexual characteristics; and sustains the fight or flight response.
  • adrenal cortex:
    • the cortex is the outer shell of the adrenal gland
    • the cortex synthesizes glucocorticoids and mineralocorticoids and secretes small amounts of sex hormones.
  • adrenal medulla
    • the medulla is the inner core of the adrenal gland
    • the medulla works as part of the sympathetic nervous system and produces epinephrine and norepinephrine.
162
Q

Thyroid gland

A
  • Located in the anterior part of the neck
  • controls the rate of body metabolism and growth and produces thyroxine (T4), triiodothyronine (T3), and thyrocalcitonin.
163
Q

Parathyroid glands

A
  • located on the thyroid gland
  • controls calcium and phsophorus metabolism; produces parathyroid hormone
164
Q

pancreas

A
  • located posteriorly to the stomach
  • influences carbohydrate metabolismm indirectly influences fat and protein metabolism, and produces insulin and glucagon.
165
Q

ovaries and testes

A
  • the ovaries are located in the pelvic cavity and produce estrogen and progesterone
  • the testes are located in the scotum, control the development of the secondary sex characteristics, and produce testosterone.
166
Q

Negative Feedback Loop

A
  • Regulates hormone secretion by the hypothalamus and pituitary gland
  • increased amounts of target gland hormones in the bloodstream decrease secretion of the same hormone and other hormones that stimulate its release.
167
Q

Stimulation Tests

A
  • In the client with suspected underactivity of an endocrine gland, a stimulus may be provided to determine whether the gland is capable of normal hormone production.
  • Measured amounts of selected hormones or substances are administered to stimulate the target gland to produce its hormone.
  • Hormone levels produced by the target gland are measured.
  • failure of the hormone level to increase with stimulation indicates hypofunction.
168
Q

Suppression Tests

A
  • Suppression tests are used when hormone levels are high or in the upper range of normal
  • agents that normally induce a suppressed response are administered to determine whether normal negative feedback is intact.
  • failure of hormone production to be suppressed during standardized testing indicates hyperfunction.
    *
169
Q

Overnight dexamethasone suppression test

A
  • used to distinguish between Cushing’s syndrome and Cushing’s disease
  • In Cushing’s disease the source of excess cortisol is the pituitary gland rather than the adrenal cortex or exogenous corticosteroid administration.
  • Dexamethasone, a potent long-acting corticosteriod given at bedtime, should suppress the morning cortisol in clients without Cushing’s disease by suppressing adrenocroticotropic hormone (ACTH) production; in the client with Cushing’s disease, this suppression will not occur.
170
Q

Radioactive Iodine Uptake

A
  • This thyroid function test measures the absorption of an iodine isotope to determine how the thyroid gland is functioning.
  • a small dose of radioactive iodine is given by mouth or IV; the amount of radioactivity is measured in 2 to 4 hours and again at 24 hours.
  • Normal values are approximately 3% to 10% at 2 to 4 hours. and 5 % to 30% in 24 hours.
  • Elevated values indicate hyperthyroidism, decreased iodine intake, or increased iodine excretion.
  • Decreased values indicate a low T4 level, the use of antithyroid medications, thyroiditis, myxedema, or hypothyroidism.
  • The test is contraindicated in pregnancy.
171
Q

T3 abd T4 resin uptake test

A
  1. Blood tests are used to diagnose thyroid disorders.
  2. T3 and T4 regulate thyroid-stimulating hormone.
  3. Normal values (normal findings vary between laboratory settings)
    1. Triiodothyronine, Total T3: 110.4 to 447.7 ng/dl
    2. Thyroxine, total T4: 5 to 12 mcg/dl
    3. Thyroxine, free (FT4): 0.8 to 2.8 ng/dL
  4. The T4 level is elevated in hyperthyroidism and decreased in hypothyroidism.
172
Q

Thyroid-stimulating hormone

A
  1. Blood test is used to differentiate the diagnosis of primary hypothyroidism.
  2. Normal value is 2 to 10 mclU/mL.
  3. Elevated values indicate primary hypothyroidism.
  4. Decreased values indicate hyperthyroidism or secondary hypothyroidism.
173
Q

Thyroid Scan

A
  1. A thyroid scan is performed to identify nodules or growths in the thyroid gland.
  2. A radioisotope of iodine or technetium is administered before scanning the thyroid gland.
  3. Reaasure the client that the level of radioactive medication is not dangerous to self or others.
  4. Determine whether the client has received radiographic contrast agents within the past 3 months, because these may invalidate the scan.
  5. Check with the primary health care provider regarding discontinuing medications containing iodine for 14 days before the test and the need to discontinue thyroid medication before the test.
  6. instruct the client to maintain NPO status after midnight on the day before the test; if iodine is used, the client will fast for an additional 45 minutes after ingestion of the oral isotope and the scan will be performed in 24 hours.
  7. If technetium is used, it is administered by IV route 30 minutes before the scan.
  8. The test is contraindicated in pregnancy.
174
Q

Needle Aspiration of thyroid tissue

A
  1. Needle aspiration of thyroid tissue is done for cytological examination.
  2. No client preparation is necessary; NPO status may or may not be prescribed.
  3. Light pressure is applied to the aspiration site after the procedure.
175
Q

24-hour urine collection of vanillylmandelic acid (VMA)

A
  1. Diagnostic tests for pheochromocytoma include a 24 hour urine collection for VMA, a product of catecholamine metabolism, metanephrine, and catecholamines, all of which are elevated
  2. The normal range of urinary catecholamines:
    1. Epinephrine: less than 20mcg/day
    2. Norepinephrine: less than 100mcg/day
176
Q

Pituitary Gland Problems

A
  • anterior pituitary
    • hyperpituitarism
    • hypopituitarism
  • posterior pituitary
    • these problems can be caused by damage to the posterior pituitary or hypothalamus:
      • Diabetes insipidus
      • syndrome of inappropriate antidiuretic hormone secretion (SIADH)
177
Q

Hypopituitarism

A
  1. Hyposecretion of 1 or more of the pituitary hormones caused by tumors, trauma, encephalitis, autoimmunity, or stroke.
  2. Hormones most often affected are growth hormone (GH) and gonadotropic hormones (luteinizing hormone, follicle-stimulating hormone), but thyroid stumulating hormone (TSH), adrenocorticotropic hormone (ACTH), or antidiuretic hormone (ADH) may be involved.
  3. assessment:
    1. mild to moderate obesity( GH, TSH)
    2. reduced cardiac output (GH, ADH)
    3. Infertility, sexual dysfunction (gonadotropins, ACTH)
    4. Fatigue, low blood pressure (TSH, ADH, ACTH, GH)
    5. Tumors of the pituitary also may cause headaches and visual defects ( the pituitary is located near the optic nerve)
  4. Interventions:
    1. client may need hormone replacement for the specific deficient hormones.
    2. Provide emotional support to the client and family.
    3. Encourage the client and family to express feelings related to disturbed body image or sexual dysfunction.
    4. Cleint education is needed regarding the signs and symptoms of hypofunction and hyperfunction related to insufficient or excess hormone replacement,
178
Q

Hypopituitarism

A
  • hormones= ACTH, TSH, Gonadotropins, GH
  • Assessment/Labs
    • changes in physical appearance
    • temporal headache
    • diplopia, occular muscle paralysis
    • stimulating test
  • Interventions/Drugs
    • CT or MRI with contrast
    • testosterone/androgen replacement
    • surgical procedure: hypophysectomy
179
Q

Hyperpituitarism

A
  • Hormones: excessive PRL, ACTH, GH
  • Assessment/Labs: gigantism, acromegaly
  • intervention/drugs:
    • Bromocriptine (parlodel)
    • octreotide (Sandostatin)
    • hypophysectomy
180
Q

Diabetes Insipidus

A
  • hormones: ADH deficiency
  • Assessment/labs:
    • lithium use
    • head trauma
    • polyuria
    • dilute urine (decreased specific gravity)
  • 24 hour urine collection
  • interventions/drugs:
    • strict I&O
    • daily weight : call MD >2.2 lb gain
    • call if persistant headache or acute confusion
    • desmopressinacetate DDAVP
    • Vasopressin (Pitressin
    • chlopropamide (diabinese)
181
Q

SIADH

A
  • hormones: vasopressin in response to low osmolarity
  • Assess/labs:
    • assess pulmonary edema
    • decreased tendon reflexes
    • bounding pulse
    • hyponatremia
    • water intoxication
  • Interventions/drugs
    • fluid restriction 500-1000 ml in 24 hours
    • strict I&O
    • daily weights
    • hypertonic IV
    • monitor Na and change to 0.9 NS
    • tolvaptan (Jynarque)
    • demeclocycline
182
Q

addison’s

A
  • hormones: aldosterone & cortisol
  • assessment/labs:
    • Na & water excretion causing hyponatremia & hypovolemia
    • k retention
    • lactic acidosis
    • check for hypoglycemia
    • hyperkalemia
    • increase potassium and ACTH
    • decreased serum cortical
    • stimulation test
  • Interventions/drugs
    • fludrocortisone
    • deltasone
    • check for addisonian crisis
    • correct hypogycemia
    • utilize lift sheet to prevent fractures
183
Q

Cushings

A
  • hormones: cortisol
  • assess/labs:
    • increased blood glucose
    • increased appetite
    • blood, saliva and urine tests
    • cortisol levels are high
    • hursutism (masculine characteristics in females)
    • buffalo hump
    • fat pads
    • weight gain
  • Interventions/drugs
    • weight
    • lifelong (bilateral adrenalectomy) glucocorticoid replacement/in unilateral hormone replacement continues until the remaining adrenal gland increases hormone production, may be needed for up to 2 years after surgery.
    • H2 receptor blockers: GI bleeding is common with hypercortisolism.
      • cimetidine
      • famotidine
      • ranitidine
      • nizotydine
    • Metyrapone
184
Q

Conns

A
  • hormones: aldosterone & increased angiotensin II
  • Assess/labs:
    • Na Retention
    • Potassium exretion
    • metabolic acidosis
    • increased BP
    • Headache
  • Interventions:
    • Prep Adrenalectomy
    • Glucocorticoid replacement
    • Spironalactone (Aldactone)
185
Q

Pheochromocytoma

A
  • Hormones: Catecolamine (tumor-adrenal medulla)
  • Assess/Labs
    • intermittent hypertension
    • severe headache
    • profuse diaphoresis
    • flushing
  • Intervention/drugs
    • do not palpate abdomen
    • 24 hr urine
    • Phenoxybenzamine
186
Q

hyperpituitarism (acromegaly & gigantism)

A
  1. hypersecretion of growth hormone by the anterior pituitary gland in an adult; caused primarily by pituitary tumors.
  2. Assessment:
    1. large hands and feet
    2. thickening and protrusion of the jaw
    3. arthritic changes and joint pain, inpingement syndromes
    4. visual disturbances
    5. diaphoresis
    6. oily, rough skin
    7. organomegaly
    8. hypertension, atheroscelerosis, cardiomegaly, heart failure
    9. dysphagia
    10. deepening of the voice
    11. thickening of the tongue, narrowing of the airway, sleep apnea
    12. hyperglycemia
    13. colon polyps, increased colon cancer risk.
  3. inteventions:
    1. provide pharmacological interventions to suppress GH or block the action of GH
    2. prepare the client for radiation of the pituitary gland or or stereotactic radiosurgery if prescribed.
    3. prepare the client for hypophysectomy if planned.
    4. provide pharmacological and nonpharmacological interventions for joint pain.
    5. provide emotional support to the client and family, and encourage the client and family to express feelings related to disturbed body image.
187
Q

Hypophysectomy (pituitary adenectomy, sublabial transsphenoidal pituitary surgery)

A
  1. removal of a pituitary tumor via craniotomy or a sublabial transsphenoidal (endscopic transnasal) approach (the latter approach is preferred because it is associated with fewer complications).
  2. Complications for craniotomy include increased intracranial pressure, bleeding, meningitis, and hypopituitarism.
  3. complications for the sublabial transsphenoidak surgery include cerebrospinal fluid leak, infection, diabetes insipidus, and hypopituitarism.
  4. if the sublabial approach is used, an incision is made along the gum line of the inner upper lip.
  5. Postoperative interventions
    1. monitor vital signs, neurological status, and level of consciousness.
    2. Elevate the head of the bed.
    3. monitor for increased intracranial pressure.
    4. Instruct the client to avoid sneezing, coughing and blowing the nose.
    5. Monitor for bleeding.
    6. Monitor for and report signs of temporary diabetes insipidus; monitor intake and output, and report excessive urinary output.
    7. If the entire pituitary is removed, clients will require lifelong replacement of ADH, cortisol, and thyroid hormone.
    8. monitor for and report signs of infection and meningitis.
    9. administer antibiotics, analgesics, and antipyretics as prescribed.
    10. Administer oral mouth rinses as prescribed. Clients may be instructed to avoid using a toothbrush or to brush teeth gently with an ultrasoft toothbrush fo 10 days to 2 weeks after surgery.
    11. Instruct the client in the administration of prescribed medications.
188
Q

Following transsphenoidal hypophysectomy, monitor for and report postnasal drip or clear nasal drainage, which might indicate a cerebrospinal fluid leak.

A

Clear drainage should be checked for glucose.

189
Q

Diabetes Insipidus

A
  1. hyposecretion of ADH by the posterior pituitary gland caused by stroke, trauma, or surgery, or it may be idiopathic.
  2. Kidney tubules fail to reabsorb water
  3. in central diabetes insipidus there is decreased ADH production.
  4. In nephrogenic diabetes insipidus, ADH production is adequate, but the kidneys do not respond appropriately to the ADH.
  5. Assessment
    1. excretion of large amounts of dilute urine
    2. polydipsia
    3. dehydration (decreased skin turgor and dry mucous membranes)
    4. inability to concentrate urine
    5. low urinary specific gravity; normal is 1.005 to 1.030
    6. fatigue
    7. muscle pain and weakness
    8. headache
    9. postural hypotension that may progress to vascular collapse without rehydration
    10. tachycardia
  6. Interventions
    1. Monitor vital signs and neurological and cardiovascular status.
    2. Provide a safe environment, particularly for the client with postural hypotension.
    3. monitor electrolyte values and for signs of dehydration.
    4. maintain client intake of adequate fluids; IV hypotonic saline may be prescribed to replace urinary losses.
    5. monitor intake and output, weight, serum osmolality, and specific gravity of urine for excessive urinary output, weight loss, and low urinary specific gravity.
    6. instruct the client to avoid foods or liquids that produce diuresis.
    7. vasopressin or desmopressin acetate may be prescribed; these are used when the ADH deficiency is severe or chronic.
    8. Instruct the client in the administration of medications as prescribed; desmopressin acetate may be administered by subcutaneous injection, intravenously, intranasally, or orally; watch for sings of water intoxication indicating overtreatment.
    9. Instruct the client to wear a medicalert bracelet.
190
Q

Syndrome of inappropriate antidiuretic hormone secretion (SIADH)

A
  1. Condition of hyperfunctioning of the posterior pituitary gland in which excess ADH is released, but not in response to the body’s need for it.
  2. causes include trauma, stroke, malignancies (often in lungs or pancreas), medications, and stress.
  3. The syndrome results in increased intravascular volume, water intoxication, and dilutional hyponatremia.
  4. May cause cerebral edema, and the client is at risk for seizures.
  5. Assessment:
    1. signs of fluid volume overload
    2. changes in level of consciousness and mental status changes
    3. weight gain without edema
    4. hypertension
    5. tachycardia
    6. anorexia, nausea and vomiting
    7. hyponatremia
    8. low urinary output and concentrated urine.
  6. Interventions
    1. Monitor vital signs and cardiac and neurological status.
    2. provide a safe environment, particularly for the client with changes in level of consciousness or mental status.
    3. Monitor for signs of increased intracranial pressure.
    4. Implement seizure precautions
    5. Elevate the head of the bed a maximum of 10 degrees to promote venous return and decrease baroreceptor-induced ADH release.
    6. Monitor intake and output and obtain weight daily.
    7. Monitor fluid and electrolyte balance.
    8. Monitor serum and urine osmolality.
    9. Restrict fluid intake as prescribed.
    10. Administer IV fluids (usually normal saline [NS] or hypertonic saline) as prescribed; monitor IV fluids carefully because of the risk for fluid volume overload.
    11. Loop diuretics may be prescribed to promote diuresis, but only if serum sodium is at least 125 mEq/L; potassium replacement may be necessar if loop diuretics are prescribed.
    12. Vasopressin antagonists may be prescribed to decrease the renal response to ADH
191
Q

Adrenal Gland Problems

A
  • adrenal cortex
    • addison’s disease
    • primary hyperaldosteronism (Conn’s syndrome)
    • Cushing’s disease
  • Adrenal Medulla
    • Pheochromocytoma
192
Q

Addison’s Disease Assessment

A
  • lethargy, fatigue, and muscle weakness
  • gastrointestinal disturbances
  • weight loss
  • menstrual changes in women; impotence in men
  • hypoglycemia, hyponatremia
  • hypotension
  • hyperpigmentation of skin (bronze) with primary disease
193
Q

Cushing’s Disease and Cushing’s Syndrome Assessment

A
  1. general muscle wasting and weakness
  2. moon face, buffalo hump
  3. truncal obesisty with thin extemities, supraclavicular fat pads; weight gain
  4. hirutism (masculine characteristics in females)
  5. hyperglycemia, hypernatremia
  6. hypokalemia, hypocalcemia
  7. hypertension
  8. fragile skin that bruises easily, reddish-purple striae on the abdomen and upper thighs
194
Q

Adrenal Cortex insufficiency (Addison’s Disease)

A
  1. Primary adrenal insufficiency
    1. also known as Addison’s disease, refers to hyposecretion of adrenal cortex hormones (glucocorticoids, mineralcorticoids, and androgen); autoimmune destruction is a common cause.
    2. requires lifelong replacement of glucocorticoids and possibly of mineralcorticoids if significant hyposecretion occurs; the condition is fatal if left untreated.
  2. Secondary adrenal insufficiency is caused by hyposecretion if ACTH from the anterior pituitary gland; mineralocorticoid release is spoared.
  3. Loss of glucocorticoids in Addison’s disease leads to decreased vascular tone, decreased vascular response to the catecholamines epinephrine and norepinephrine, and decreased gluconeogenesis.
  4. In addison’s disease, loss of the mineralocorticoid aldosterone leads to dehydration, hypotension, hyponatremia, and hyperkalemia.
  5. Interventions:
    1. monitor vital signs (particularly for hypotension), for weight loss, and intke and output.
    2. Monitor WBC count, blood glucose; and potassium, sodium, and calcium levels.
    3. administer glucocorticoid and/or mineralocorticoid medications as prescribed.
    4. Observe for addisonian crisis caused by stress, infection, trauma, or surgery.
195
Q

Addison’s disease client education

A
  • need for lifelong glucocorticoid replacement and possibly lifelong mineralcorticoid replacement.
  • corticosteroid replacement will need to be increased during times of stress.
  • avoid individuals with an infection
  • avoid strenous exercise and stressful situations
  • avoid over the counter medications
  • diet should be high in protein and carbohydrates; clients taking glucocorticoids should be prescribed calcium and vitamin D supplements to maintain normal levels and to protect against corticosteroid-induced osteoporosis; some clients taking mineralocorticoids may be prescribed a diet high in sodium.
  • wear a medicalert braclet
  • report signs and symptoms of complications, such as underreplacment and overreplacement of corticosteroid hormones.
196
Q

Addisonian Crisis

A
  1. a life threatening disorder causes by acute adrena insufficiency
  2. precipitated by stress, infection, trauma, surgery, or abrupt withdrawal of exogenous corticosterioid use.
  3. Can cause hyponatremia, hyperkalemia, hypoglycemia, and shock.
  4. Assessment:
    1. severe headache
    2. severe abdominal, leg, and lower back pain
    3. generalized weakness
    4. irritability and confusion
    5. severe hypotension
    6. shock
  5. Interventions:
    1. prepare to administer glucocorticoids intravenously as prescribed.
    2. administer IV fluids as prescribed to replace fluids and restore electrolyte balance.
    3. Following resolution of crisis, administer glucocorticoid and mineralcorticoid orally as prescribed.
    4. monitor vital signs, particularly blood pressure.
    5. monitor neurological status, noting irritability and confusion.
    6. monitor intake and output.
    7. monitor laboratory values, particularly sodium, potassium, and blood glucose levels.
    8. Protect the client from infection.
    9. Maintain bed rest and provide a quiet environment.
197
Q

Clients taking exogenous corticosteroids must

A

establish a plan with their PHCPs or endocrinologist for increasing their corticosteroids during times of stress.

198
Q

Cushing’s Syndrome (hypercortisolism)

A
  1. A metabolic disorder resulting rom the chronic and excessive production of cortisol by the adrenal cortex or from the administration of glucocorticoids in large doses for several weeks or longer (exogenous or iatrogenic (meds).
  2. ACTH secreting tumors (most often of the lung, pancreas, or gastrointestinal [GI] tact) can cuase Cushing’s syndrome.
199
Q

Cushing’s Disease

A
  1. Is a metabolic disorder characterized by abnormally increased secretion (endogenous) of cortisol, caused by increased amounts of ACTH secreted by the pituitary gland.
200
Q

Cushing’s Syndrome and Cushing’s disease interventions

A
  1. Monitor vital signs, particularly blood pressure
  2. Monitor intake and output and weight.
  3. Monitor laboratory values, particularly WBC count and serum glucose, sodium, potassium, and calcium levels.
  4. Prepare the client for radiation as prescribed if the condition results from a pituitary adenoma.
  5. Administer chemotherapeutic agents as prescribed for inoperable adrenal tumors.
  6. Prepare the client for removal of the pituitary tumor (hypophysectomy, sublabial transsphenoidal adenectomy) if the condition results from increased pituitary secretion of ACTH.
  7. Prepare the client for adrenalectomy if the condition results fro an adrenal adenoma; glucocorticoid replacement may be required following adrenalectomy.
  8. Clients requiring lifelong glucocorticoid replacement following adrenalectomy should obtain instructions from their PHCPs about increasing their glucocorticoid during times of stress.
  9. Assess for and protect against postoperative thrombus formation; Cushing’s syndrome predisposes to thromboemboli.
  10. Allow the client to discuss feelings related to body appearance.
  11. instruct the client about the need to wear a MedicAlert bracelet.
201
Q

Addison’s disease is characterized by the hyposecretion of the adrenal cortex hormones, whereas Cushing’s syndrome and Cushing’s disease

A

are characterized by a hypersecretion of glucocorticoids.

202
Q

Conn’s Syndrome (primary hyperaldosteronism)

A
  1. Hypersecretion of mineralcorticoids (aldosterone) from the adrenal cortex of the adrenal gland.
  2. Most commonly caused by an adenoma.
  3. Excess secretion of aldosterone causes sodium and water retention and potassium secretion, leading to hypertension and hypokalemic alkalosis.
203
Q

Conn’s syndrome Assessment

A
  • symptoms related to hypokalemia, hypernatremia, and hypertension.
  • headache, fatigue, muscle weakness
  • cardiac dysrhythmias
  • paresthesia, tetany
  • visual changes
  • glucose intolerance
  • elevated serum aldosterone levels
204
Q

Conn’s Syndrome Interventions

A
  1. Monitor vital signs, particularly blood pressure.
  2. monitor potassium and sodium levels.
  3. monitor intake and output and urine specific gravity.
  4. Monitor for hyperkalemia, particularly for clients with impaired renal function or excessive potassium intake, because potassium retaining diuretics and aldosterone antagonists may be prescribed to promote fluid balance and control hypertension.
  5. Administer potassium supplements as prescribed to treat hypokalemia; clients taking potassium-retaining diuretics and potassium supplementation are at risk for hyperkalemia.
  6. Prepare the client or adrenalectomy.
  7. Maintain sodium restriction, if prescribed, preoperatively.
  8. Administer glucocorticoids preoperatively, as prescribed, to prevent adrenal hypofunction and prepare for sgtress of surgery.
  9. Monitor the client for adrenal insufficiency postoperatively.
  10. Instruct the client regarding the need for glucocorticoid therapy following adrenalectomy.
  11. Instruct the client about the need to wear a MedicAlert bracelet.
205
Q

Pheochromocytoma

A
  1. catecholamine-producing tumor usually foundin the adrenal medulla, but extraadrenal locations include the chest, bladder, abdomen, and brain; typically is a benign tumor but can be malignant.
  2. Excessive amounts of epinephrine and norepinephrine are secreted.
  3. Diagnostic test includes a 24-hr urine collection for VMA.
  4. Surgical removal of the adrenal gland is the primary treatment.
  5. Symptomatic treatment is initiated if surgical removal is not possible.
  6. The complications associated with pheichromocytoma include hypertensive crisis; hypertensive retinopathy and nephropathy, cardiac enlargement, and dysrhythmias; heart failure; myocardial infarction; increased platelet aggregation; and stroke.
  7. death can occur from shock, stroke, renal failure, dysrhythmias, or dissecting arotic aneurysm.
206
Q

Pheochromocytoma Assessment

A
  1. Paroxysmal or sustained hypertension
  2. palpitations
  3. severe headache
  4. flushing and profuse diaphoresis
  5. pain in the chest or abdomen with nausea and vomiting.
  6. heat intolerance
  7. weight loss
  8. tremors
  9. hyperglycemia.
207
Q

Pheochromocytoma Interventions

A
  1. Monitor vital signs, particularly blood pressure and heart rate.
  2. Monitor for hypertensive crisis; monitor for compliactions that can occur with hypertensive crisis, such as stroke, cardiac dysrhythmias, and myocardial infarction.
  3. Instruct the client not to smoke, drink caffeine-containing beverages, or change position suddenly.
  4. Prepare to administer alpha adrenergic blocking agents and Beta adrenergic blocking agents as prescribed to control hypertension. Alpha adrenergic blocking agents are started 7 to 10 days before beta adrenergic blocking agents.
  5. Monitor serum glucose level.
  6. Promote rest and a nonstressful environment.
  7. Provide a diet high in calories, vitamins, and minerals.
  8. Prepare the client for adrenalectomy.
208
Q

For the client with pheochromocytoma, avoid stimuli that can precipitate a hypertensive crisis,

A

such as increased abdominal pressure and vigorous abdominal palpation.

209
Q

Adrenalectomy

A
  1. surgical removal of an adrenal gland.
  2. Lifelong glucocorticoid and mineralcorticoid replacement is necessary with bilateral adrenalectomy.
  3. Temporary glucocorticoid replacement, ususally up to 2 years, is necessary after a unilateral adrenalectomy.
  4. Catecholamine levels drop as a result of surgery, which can result in cardiovascular collapse, hypotension, and shock, and the needs to be monitored closely.
  5. Hemorrhage also can occur because of the high vascularity of the adrenal glands.
210
Q

Adrenalectomy Interventions

A

Preoperative

  1. Monitor electrolyte levels and correct electrolyte imbalances.
  2. Assess for dysrhythmias
  3. Monitor for hyperglycemia
  4. Protect the client from infections.
  5. Administer glucocorticoids as prescribed.

Postoperative

  1. monitor vital signs.
  2. Monitor intake and output; if the urinary output is lower than 30ml/hr, notify the PHCP or nephrologist, because this may result in acute kidney injury and indicate impending shock.
  3. Monitor weight daily.
  4. Monitor electrolyte and serum glucose levels.
  5. Monitor for signs of hemorrhage and shock, particularly during the first 24 to 48 hours.
  6. Monitor for manifestations of adrenal insufficiency.
  7. Assess the dressing for drainage.
  8. monitor for paralytic ileus.
  9. Administer IV fluids as prescribed to maintain blood volume.
  10. Administer IV fluids as prescribed to maintain blood volume.
  11. Administer glucocorticoids and mineralocorticoids as prescribed.
  12. Administer pain medication as prescribed.
  13. Provide pulmonary interventions to prevent atelectasis (coughing and deep breathing, incentive spirometry, splinting of incision).
  14. Instruct the client in the importance of hormone replacement following surgery.
  15. Instruct the client regarding signs and symptoms of complications such as underreplacement and overreplacement of hormones.
  16. Instruct the client regarding the need to wear a medicalert bracelet.
211
Q

Hypothyroidism Assessment

A
  1. lethargy and fatigue
  2. weakness, muscle aches, paresthesia
  3. intolerance to cold
  4. weight gain
  5. dry skin and hair l oss of body hair.
  6. bradycardia
  7. constipation
  8. general puffiness and edema around the eyes and face (myxedema)
  9. forgetfulness and loss of memory
  10. menstrual disturbances
  11. goiter may or may not be present
  12. cardiac enlargement, tendency to develop heart failure.
212
Q

Hyperthyroidism assessment

A
  1. Personality changes such as irritability, agitation, and mood swings.
  2. Nervousness and fine tremors of the hands.
  3. weakness, muscle aches, paresthesias.
  4. Heat tolerance.
  5. Weight loss
  6. Smooth, soft skin and hair.
  7. Palpitations, cardiac dysrhythmias, such as tachycardia or atrial fibrillation
  8. diarrhea
  9. protruding eyeballs (exophtalmos) may be present
  10. Diaphoresis
  11. hypertension
  12. enlarged thyroid gland (goiter)
213
Q

Hypothyroidism

A
  1. Hypothyroid state resulting from hyposecretion of thyroid hormones and characterized by a decreased rate of body metabolism.
  2. The T4 is low and the TSH is elevated.
  3. In primary hypothyroidism the source of dysfunction is the thyroid gland, and the thyroid can not produce the necessary amount of hormones. In secondary hypothyroidism, the thyroid is not being stimulated by the pituitary to produce hormones.
214
Q

Hypothyroidism interventions

A
  1. Monitor vital signs, including heart rate, and rhythm.
  2. Administer thyroid replacement; levothyroxine sodium is most commonly prescribed.
  3. Instruct the client about thyroid replacement therapy and about the clinical manifestations of both hypothyroidism and hyperthyroidism related to underreplacement or overreplacement of the hormone.
  4. Instruct the client in a low-calorie, low choleterol, low-saturated fat diet; discuss a daily exercise program such as walking.
  5. Assess the client for constipation; provide roughage and fluids to prevent constipation.
  6. Provide a warm environment for the client.
  7. Avoid sedatives and opioid analgesics because of increased sensitivity to these medications; may precipitate myxedema coma.
  8. Monitor for overdose of thyroid medications, characterized by tachycardia, chest pain, restlessness, nervousness, and insomnia.
  9. Instruct the client to report episodes of chest pain or other signs of overdose immediately.
215
Q

Myxedema Coma

A
  1. This rare but serious disorder results from persistently low thyroid production.
  2. Coma can be precipitated by acute illness, rapid withdrawal of thyroid medication, anesthesia and surgery, hypothermia, or the use of sedatives and opioid analgesics.
216
Q

Myxedema coma Assessment

A
  1. Hypotension
  2. bradycardia
  3. hypothermia
  4. hyponatremia
  5. hypoglycemia
  6. generalized edema
  7. respiratory failure
  8. coma
217
Q

Myxedema Coma Interventions

A
  1. Maintain a patent airway.
  2. Institute aspiration precautions.
  3. Administer IV fluids (normal or hypertonic saline) as prescribed.
  4. Administer levothyroxine sodium intravenouslhy as prescribed.
  5. administer glucose intravenously as prescribed.
  6. administer corticosteroids as prescribed.
  7. assess the client’s temperature hourly.
  8. monitor blood pressure frequently.
  9. keep the client warm.
  10. monitor for changes in mental status.
  11. monitor electrolyte and glucose levels.
218
Q

Hyperthyroidism

A
  1. Hyperthyroid state resultig from hypersection of thyroid hormones (T3 and T4)
  2. Characterized by an increased rate of body metabolism.
  3. A common cause is Grave’s Disease, also known as toxic diffuse goiter.
  4. Clinical manifestations are referred to as thyrotoxicosis.
  5. The T3 and T4 are usually elevated and the TSH level is low.
219
Q

Hyperthyroidism interventions

A
  1. Provide adeqaute rest.
  2. administer sedatives as prescribed.
  3. Provide a cool and quiet environment.
  4. Obtain weight daily.
  5. Provide a high-calorie diet.
  6. Avoid the administration of stimulants.
  7. Administer antithyroid medications, such as methimazole or propylthiouracil, that block thyroid synthesis as prescribed.
  8. Administer iodine preparations that inhibit the release of thyroid hormone as prescribed.
  9. Administer propranolol for tachycardia as prescribed.
  10. Prepare the client for radioactive iodine therapy, as prescribed, to destroy thyroid cells.
  11. Prepare the cliet for subtotal thyroidectomy if prescribed.
  12. Elevate the head of the bed of a client experiencing exophthalmos; in addition, instruct on low-salt diet, administer artificial tears, encourage the use of dark glasses, and tape eyelids closed at night if necessary.
  13. Allow the client to express concerns about body image changes.
220
Q

Thyroid storm

A
  • This acute and life threatening condition occurs in a client with uncontrollable hyperthyroidism.
  • It can be caused by manipulation of the thyroid gland during surgery and the release of thyroid hormone into the bloodstream; it also can occur from severe infection and stress.
  • Antithyroid medications, beta blockers, glucocorticoids, and iodides may be administered to the client before thyroid surgery to prevent its occurrence.
221
Q

Thyroid Storm Assessment

A
  1. Elevated temperature (fever)
  2. tachycardia
  3. systolic hypertension
  4. Nausea, vomiting, and diarrhea
  5. agitation, anxiety, tremors.
  6. Irritability, agitation, restlessness, confusion, and seizures as the condition progresses
  7. Delirium and coma
222
Q

Thyroid Storm Interventions

A
  1. Maintain a patent airway and adequate ventilation.
  2. Administer antithyroid medications, iodides, propranolol, and glucococorticoids as prescribed.
  3. Monitor vital signs.
  4. Monitor continually for cardiac dysrhythmias.
  5. Administer nonsalicylate antipyretics as prescribed (salicylates increase free thyroid hormone levels).
  6. Use a cooling blanket to decrease temperature as prescribed.
223
Q

Signs of Tetany

A
  1. Cardiac dysrhythmias
  2. carpopedal spasm
  3. dysphagia
  4. muscle and abdominal cramps
  5. numbness and tingling of the face and extremities
  6. Positive Chvostek’s sign
  7. Positive Trousseau’s sign
  8. Visual disturbances (photophobia)
  9. Wheezing and dyspnea (bronchospasm, laryngospasm)
  10. Seizures
224
Q

Thyroidectomy

A
  • Removal of the thyroid gland
  • Performed when persistent hyperthyroidism exists
  • Subtotal thyroidectomy, removal of a portion of the thyroid gland, is the preferred surgical intervention.
  • PreOp:
    • Obtain VS and weight
    • assess electrolyte levels
    • assess for hyperglycemia
    • instruct the client in how to perform coughing and deep-breathing exercises and how to support the neck in the posoperative period when coughing and moving.
    • administer antithyroid medications, iodides, propranolol, and glucocorticoids as prescribed to prevent the occurrence of thyroid storm.
  • Postoperative interventions
    • Monitor for respiratory distress
    • have a tracheotomy set, oxygen, and suction at the bedside.
    • limit client talking and assess level of hoarseness.
    • Avoid neck flexion and stress on the suture line.
    • Monitor for laryngeal nerve damage, as evidenced by airway obstruction, dysphonia, high-pitched voice, stridor, dysphagia, and restlessness.
    • Monitor for signs of hypocalecemia and tetany, which can be caused by trauma to the parathyroid gland.
    • Prepare to administer calcium gluconate as precribed for tetany.
    • Monitor for thyroid storm
225
Q

Following thyroidectomy, maintain the client in a semi-fowler’s position. Monitor the surgical site for edema and for signs of bleeding and check the dressing anteriorly and at the back of the neck.

A

Monitor for inflammation, which may block the airway. An emergency tracheostomy kit should be at the bedside.

226
Q

Hypoparathyroidism

A
  • Condition caused by hyposecretion of parathyroid hormone by the parathyroid gland.
  • Can occur following thyroidectomy because of removal of parathyroid tissue.
227
Q

Hypoparathyroidism assessment

A
  1. hypocalcemia and hyperphosphatemia
  2. numbness and tingling in face
  3. muscle cramos and cramps in the abdomen or in the extremities.
  4. Positive Trousseau’s sign or Chvostek’s sign.
  5. Signs of overt tetany, such as bronchospasm, laryngospasm, carpopedal spasm, dysphagia, photophobia, cardiac dysrhythmias, seizures
  6. hypotension
  7. anxiety, irritability, depression
228
Q

Hypoparathyroidism interventions

A
  • Monitor vital signs
  • monitor for signs of hypocalcemia and tetany.
  • Initiate seizure precautions.
  • Placed a tracheotomy set, oxygen, and suctioning equipment at the bedside.
  • Prepare to administer calcium gluconate intravenously for hypocalcemia.
  • Provide a high-calcium diet, low phorphorus diet.
  • Instruct the client in the administration of vitamin D supplements as prescribed; vitamin D enhances the absorption of calcium from the GI tract.
  • Instruct the client in the use of thiazide diuretics if prescribed, to protect the kidney if vitamin D is also taken.
  • Instruct the client in the administration of phosphate binders as prescribed, to promote excretion of phosphate through the GI tract.
  • Instruct the client to wear a MedicAlert bracelet.
229
Q

Hyperparathyroidism

A

Condition caused by hypersectrion of parathyroid hormone (PTH) by the parathyroid gland

230
Q

Hyperparathyroidism assessment

A
  1. hypercalcemia and hypophosphatemia
  2. fatigue and muscle weakness
  3. skeletal pain and tenderness
  4. bone deformities that result in pathological fractures.
  5. Anorexia, nausea, vomiting, epigastric pain.
  6. weight loss
  7. constipation
  8. hypertension
  9. cardiac dysrhythmias
  10. renal stones
231
Q

Parathyroidism Interventions

A
  1. Monitor vital signs, particularly blood pressure.
  2. Monitor for cardiac dysrhythmias.
  3. monitor intake and output and for signs of renal stones.
  4. Monitor for skeletal pain; move the client slowly and carefully.
  5. Encourage fluid intake.
  6. Administer furosemide as prescribed to lower calcium levels.
  7. Administer NS intravenously as prescribed to maintain hydration.
  8. Adminster phosphates, which interfere with calcium reabsorption, as prescribed.
  9. Administer calcitonin as prescribed to decrease skeletal calcium release and increase renal excretion of calcium.
  10. Administer IV or oral biphosphonates to inhibit bone resorption.
  11. Monitor calcium and phosphorus levels.
  12. Prepare the client for parathyroidectomy as prescribed.
  13. Encourage a high-fiber, moderate calcium diet.
  14. Emphasize the importance of an exercise program and avoiding prolonged inactivity.
232
Q

Parathyroidectomy

A
  1. Removal of 1 or more of the parathyroid glands.
    1. endoscopic radioguided parathyroidectomy with autotransplantation is a common procedure.
    2. Parathyroid tissue is transplanted in the forearm or near the sternocleidomastoid muscle, allowing PTH secretion to continue.
  2. Preoperative Interventions
    1. monitor electrolytes, clacium, phosphate, and magnesium levels.
    2. endure that calcium levels are decreased to near-normal values.
    3. Inform the client that talking may be painful for the first day or two after surgery.
  3. Postoperative Interventions:
    1. Monitor for respiratory distress.
    2. Place a tracheotomy set, oxygen, and suctioning equipment at the bedside.
    3. Monitor vital signs.
    4. Position the client in semi-fowler’s position.
    5. Assess neck dressing for bleeding.
    6. Monitor for hypocalcemic crisis, as evidenced by tingling and twitching in the extremities and face.
    7. Assess for positive Trousseau’s sign or Chvostek’s sign, which indicates tetany.
    8. Monitor for changes in voice pattern and hoarseness.
    9. Monitor for laryngeal nerve damage.
    10. Instruct the client in the administration of calcium and vitamin D supplements as prescribed.
233
Q

Propylthiouracil (PTU)

A
  1. Treats Hyperthyroidism
  2. antithyroid medicine
  3. used less often because of liver toxicity
  4. teach patient to avoid crowds and people who are ill because the drug reduces the immune response, increasing the risk for infection.
234
Q

Cinacalcet (Sensipar)

A
  1. A calcimimetic
  2. when taken orally, the drug bonds to calcium-sensitive receptors
235
Q

Functions of Glucocorticoid hormones

A
  1. prevent hypoglycemia by increasing liver glucose production (gluconeogenesis) and inhibiting peripheral glucose use.
  2. Maintain excitability and responsiveness of cardiac muscle.
  3. Increase lipolysis, releasing glycerol and free fatty acids.
  4. Increase protein catabolism
  5. Degrade collagen and connective tissue
  6. Increase the number of mature neutrophils released from bone marrow.
  7. Exert anti-inflammatory effects that decrease the migration of inflammatory cels to site of injury.
  8. Maintain behavior and cognitive functions.
236
Q

Functions of Thyroid Hormones in Adults

A
  1. Control metabolic rate of all cells
  2. promote sufficient pituitary secretion of growth hormone and gonadotropins
  3. Regulate protein, carbohydrate, and fat metabolism.
  4. Exert effects on heart rate and contractility.
  5. increase red blood cell production
  6. affect respiratory rate and drive
  7. increase bone formation and decrease bone resorption of calcium
  8. act as insulin antagonists.
237
Q

Endocrine Testing:

Blood tests

A
  1. Check you laboratory’s method of handling hormone test samples for tube type, timing, drugs to be administered as part of the test, etc. For example, blood samples drawn for catecholamines must be placed on ice and taken to the laboratory immediately.
  2. Explain the procedure and any restrictions to the patient.
  3. If you are drawing blood samples from an IV line, clear the line thoroughly. Do not use a double- or triple- lumen line to obtain samples; contaimination or dilution from another port is possible.
  4. Emphasize the importance of taking a drug prescribed for the test on time. Tell the patient to set an alarm if the drug is to be taken during the night.
238
Q

Endocrine Testing:

Urine Tests

A
  1. Instruct the patient to begin the urine collection (whether for 2,4,8,12 or 24 hours) by first emptying his or her bladder.
  2. Remind the patient to not save the urine specimen that begins the collection. The timing for the urine collection begins after this specimen.
  3. Tell the patient to note the time of the discarded specimen and to plan to collect all urine from this time until the end of the urine collection period.
  4. To end the collection, instruct the patient to empty his or her bladder at the end of the timed period and add that urine to the collection period.
  5. Check with the laboratory to determine any special handling of the urine specimen (e.g. Is a preservative needed? Does the container need to be kept cold?)
  6. If needed, make sure that the preservative has been added to the collection container at the beginning of the collection.
  7. Tell the patient about any preservative and the need to avoid splashing urine from the container because some preservatives make the urine caustic.
  8. If the specimen must be kept cool or cold, instruct the patient to place the container in an inexpensve cooler with ice. The specimen container should not be kept with food or drinks.
239
Q

Deficient Growth Hormone S&S

A
  1. decreased bone density
  2. pathologic fractures
  3. decreased muscle strength
  4. increased serum cholesterol levels
240
Q

Deficient Gonadotropins (LH, FSH) S&S

A
  1. women:
    1. amenorrhea
    2. anovulation
    3. low estrogen levels
    4. breast atrophy
    5. loss of bone density
    6. decreased axillary and pubic hair
    7. decreased libido
  2. Men:
    1. decreased facial hair
    2. decreased ejaculate volume
    3. reduced muscle mass
    4. loss of bone density
    5. decreased body hair
    6. decreased libido impotence
241
Q

Deficient TSH (thyrotropin/thyroid stimulating hormone)

A
  1. decrease thyroid hormone levels
  2. weight gain
  3. intolerance to cold
  4. scalp alopecia
  5. Hirsutism
  6. menstrual abnormalities
  7. decreased libido
  8. slowed cognition
  9. lethargy
242
Q

deficient Adrenocorticotropic hormone (ACTH)

A
  1. decreased serum cortisol levels
  2. pale, sallow complexion
  3. malaise and lethargy
  4. anorexia
  5. postural hypotension
  6. headache
  7. hypoglycemia
  8. hyponatremia
  9. decreased axillary and pubic hair (women)
243
Q

Deficient Vasopressin (antidiuretic hormone [ADH])

S&S

A
  1. Diabetes Insipidus:
    1. Greatly increased urine output
    2. low urine specific gravity (<1.005)
    3. hypotension
    4. dehydration
    5. increased plasma osmolarity
    6. increased thirst
    7. output does not decrease when ffluid intake decreases
244
Q

Anterior Pituitary Hyperfunction Key features

A
  1. Prolaction PRL:
    1. hypogonadism (loss of secondary sexual characteristics)
    2. decreased gonadotropin levels
    3. galactorrhea
    4. increased body fat
    5. increased serum prolactin levels
  2. Growth hormone GH:
    1. Acromegaly
      1. thickened lips
      2. coarse facial features
      3. increasing head size
      4. lower jaw protrusion
      5. enlarged hands and feet
      6. joint pain
      7. barrel-shaped chest
      8. hyperglycemia
      9. sleep apnea
      10. enlarged heart, lungs and liver
  3. Adrenocorticotropic Hormone (ACTH)
    1. Cushing’s Disease (Pituitary)
      1. Elevated plasma cortisol levels
      2. weight gain
      3. truncal obesity
      4. “moon face”
      5. extemity muscle wasting
      6. loss of bone density
      7. hypertension
      8. hyperglycemia
      9. striae and acne
  4. Thyrotropin (Thyroid-Stimulating Hormone [TSH])
    1. Elevated plasma TSH and thyroid hormone levels
    2. weight loss
    3. tachycardia and dysrhythmias
    4. heat intolerance
    5. increased GI motility
    6. fine tremors
  5. Gonadotropins (LH and FSH)
    1. Men:
      1. Elevated LH and FSH levels
      2. hypogonadism or hypergonadism
    2. Women:
      1. Normal LH and FSH levels
245
Q

Teach the patient taking bromocriptine to seek medical care immediately if chest pain, dizziness, or watery

A

nasal discharge occurs because of the possiblity of serious side effects, including cardiac dysrhythmias, coronary artery spasms, and cerebrospinal fluid leakage.

246
Q

The patient after hypophysectomy

A
  1. Monitor the patient’s neurological status hourly for the first 24 hours and then every 4 hours.
  2. Monitor fluid balance, especially for output greater than intake.
  3. encourage the patient to perform deep-breathing exercises.
  4. Instruct the patient not to cough, blow the nose, or sneeze.
  5. instruct the patient to use dental floss and oral mouth rinses rather than toothbrushing until the surgeon give permission.
  6. instruct the patient to avoid bending at the waist to prevent increasing intracranial pressure.
  7. Monitor the nasal drip pad for the type and amount of drainage.
  8. Teach the patient methods to avoid constipation and subsequent “straining”.
  9. Teach the patient self-administration of the prescribed hormones.
247
Q

Focused Assessment

The Patient who has undergone Nasal Hypophysectomy for Hyperpituitarism

A
  1. Assess Cardiovascular status:
    1. Vital signs, including apical pulse, pulse pressure, presence or absence of orthostatic hypotension, and the quality/rhythm of peripheral pulses.
  2. Assess cognition and mental status.
  3. Assess condition of operative site:
    1. Observe nasal area for drainage:
      1. If present, note color, clarity, and odor.
      2. Test clear drainage for the presence of gluchose
  4. Assess neuromuscular status:
    1. reactivity of patellar and biceps reflexes
    2. oral temperature
    3. handgrip strength
    4. steadiness of gait
    5. distant and near visual acuity
    6. pupillary responses to light
  5. Assess kidney function:
    1. Observe urine specimen for color, odor, cloudiness, and amount.
    2. Ask about:
      1. headaches or visual disturbances
      2. ease of bowel movements
      3. 24-hour fluid intake and output
      4. over-the-counter and prescribed drugs taken.
  6. Assess patient’s understanding of illness and adherence with treatment:
    1. Symptoms to report to health care provider.
    2. Drug plan (correct timing and dose)
248
Q

Nephrogenic diabetes insipidus can be a genetic disorder in which the ADH receptor (vasopressin receptor) has a defect that prevents kidney tubules from interacting with ADH. The result is poor water reasborption by the kidney, although the actual amount of hormone produced is not deficient.

A

The problem is most commonly inherited as an X-linked recessive disorder in which the AVPR2 gene coding for the ADH receptor is mutated and only males are affected. There is also an autosomal form of the disorder in whihc the AQP2 gene is mutated and both males and females are affected. When assessing a patient with DI, always ask whether anyone else in the family has ever had this dosorder.

249
Q

Key Features of Diabetes Insipidus

A
  1. Hypotension
  2. tachycardia
  3. weak peripheral pulses
  4. hemoconcentration
  5. increased urine output
  6. dilute, low specific gravity
  7. poor skin turgor
  8. dry mucous membranes
  9. decreased cognition
  10. ataxia (slurred speech, stumbling, uncooridnated)
  11. increased thirst
  12. irritability
250
Q

Ther parental form of desmospressin

A

is 10 times stronger than the oral form, and the dosage must be reduced.

251
Q

Conditions Causing the Syndrome of Inappropriate antidiuretic hormone

A
  1. malignancies:
    1. small cell lung cancer
    2. pancreatic, duodenal, and GU carcinomas
    3. Thymoma
    4. Hodgkin’s lymphoma
    5. non-Hodgkin’s lymphoma
  2. Pulmonary Disorders
    1. viral and bacterial pneumonia
    2. lung abscesses
    3. active tuberculosis
    4. pneumothorax
    5. chronic lung disease
    6. mycoses
    7. positive-pressure ventilation
  3. CNS disorders
    1. tauma
    2. infection
    3. tumors (primary or metastatic)
    4. Strokes
    5. Porphyria
    6. systemic lupus erthematosus
  4. Drugs
    1. exogenous ADH
    2. chlorpropamide
    3. vincristine
    4. cyclophosphamide
    5. carbamazepine
    6. opioids
    7. tricyclic antidepressants
    8. general anesthetics
    9. fluoroquinolone antibiotics
252
Q

administer tolvaptan or conivaptan only

A

in the hospital setting so serum sodium levels can be monitored closely for the development of hypernatremia.

253
Q

Emergency Care of the patient with Acute Adrenal Insufficiency

A

Hormone Replacement

  • start rapid infusion of NS or dextrose 5% normal saline.
  • Initial dose of hydrocortisone sodium (SOlu-Cortef) is 100 to 300 mg or dexamethasone 4 to 12 mg as an IV bolus.
  • Admini inster additional 100 mg of hydrocortisone sodium by continuous IV infusion over the next 8 hours.
  • Give hydrocortisone 50 mg IM concomitantly with hydration every 12 hours.
  • Initiate an H2 histamine blocker (eg. ranitidine) IV for ulcer prevention.

Hyperkalemia Management

  • administer insulin (20 TO 50 UNITS) WITH DEXTROSE (20 TO 50 MG) in normal saline to shift potassium into cells.
  • Administer potassium binding and excreting resin (e.g., kayexalate)
  • Give loop or thiazide diuretics, as prescribed.
  • Initiate potassium restriction.
  • Monitor intake and output.
  • Monitor heart rate, rhythm, and ECG for signs and symptoms of hyperkalemia (slow heart rate; heart block; tall, peaked T waves; fibrillation; asystole).

Hypoglycemia Management

  • Administer IV glucose as prescribed.
  • Administer glucagon as needed and prescribed.
  • Maintain IV access.
  • Monitor blood glucose level hourly.
    *
254
Q

Addison’s Disease/Adrenal Insufficiency Key Features

A
  1. Muscle weakness
  2. Fatigue
  3. Joint/Muscle pain
  4. anorexia
  5. nausea/vomiting
  6. abdominal pain
  7. constipation or diarrhea
  8. weight loss
  9. Salt craving
  10. Vitiligo
  11. hyperpigmentation
  12. anemia
  13. hypotension
  14. hyponatremia
  15. hyperkalemia
  16. hypercalcemia
255
Q

Labs in Hypofunction of adrenal gland/ addisons disease

A
  • sodium is decreased
  • potassium increased
  • glucose normal to decreased
  • calcium increased
  • bicarb increased
  • BUN increased
  • cortisol (serum) decreased
  • cortisol (salivary) decreased
256
Q

TESTS IN HYPERFUNCTION OF THE ADRENAL GLAND

A
  • sodium is increased
  • potassium is decreased
  • glucose is normal to increased
  • calcium is decreased
  • bicarb is decreased
  • BUN normal
  • cortisol (serum) increased
  • cortisol (salivary) increased.
257
Q

Prednisone and prednisolone are sound-alike drugs, and care is needed not to confuse them.

A

Although both are corticosteroids, they are not interchangeable because prednisolone is several times more potent than prednisone and dosages are not the same.

258
Q

Drug Therapy for Hypofunction of the Adrenal Gland (Addison’s disease)

A
  1. Cortisone : instruct the patient to take the drug with meals or a snack to avoid gastric irritation.
  2. hydrocortisone (cortef, Hycort): Instruct the patient to report the following symptoms of excessive drug therapy, which indicate Cushing’s syndrome and a possible need for a dosage adjustment: rapid weight gain, round face and fluid retention
  3. Prednisone (Winpred): Instruct the patient to report illness because the usual daily dosage may not be adequate during periods of illness or severe stress.
  4. Fludrocortisone (Florinef): Monitor the patient’s blood pressure to assess for the potential side effect of hypertension. Instruct the patient to report weight gain or edema because sodiumintake may need to be restricted.
259
Q

Conditions Causing Increased Cortisol SEcretion (Cushing’s disease/syndrome)

A

Endogenous Secretion (Cushing’s Disease)

  • Bilateral adrenal hyperplasia
  • Pituitary adenoma increasing the production of ACTH (pituitary Cushing’s disease)
  • Malignancies: carcinomas of the lung, GI tract, pancreas
  • Adrenal adenomas or carcinomas

Exogenous Adminisration (Cushing’s Syndrome)

  • Therapeutic use of ACTH or glucocorticoids-most commonly for treatment of:
    • asthma
    • autoimmune disorders
    • organ transplantation
    • cancer chemotherapy
    • allergic responses
    • chronic fibrosis
260
Q

Key Features of Cushing’s Disease/Syndrome (Hypercortisolism)

A
  • Moon face
  • buffalo hump
  • truncal obesity
  • weight gain
  • hypertension
  • frequent dependent edema
  • bruising
  • petechiae
  • muscle atrophy (most apparent in extremities)
  • osteoporosis (bone density loss)
    • pathologic fractures
    • decreased height with vertebral collapse
    • aseptic necrosis of the femur head
    • slow or poor healing of bone fractures
    • thinning skin
    • striae and increased pigmentation
    • increased risk for infection
    • reduced immunity
    • decreased inflammatory responses
    • signs and symptoms of infection/inflammation possible masked.
261
Q

Mifepristone (Korlym) cannot be used

A

during pregnancy because it also blocjs progesterone receptors and would cause termination of the pregnancy.

262
Q

Teach patients who are taking a corticosteriod for more than one week not the stop the drug suddenly.

A

The drug should be tapered gradually under the care of the PHCP>

263
Q

Cortisol Replacement Therapy

A
  1. Take your medication in divided doses, as prescribed (e.g. the first dose in the mornin and the second dose between 4pm and 6pm)
  2. take your medication with snacks or meals.
  3. Weigh yourself daily and keep a record to show your primary health care provider.
  4. Increase your dosage as directed by your PHCP for increased physical stress or severe emotional stress.
  5. Never skip a dose of medication. If you have persistent vomiting or severe diarrhea and can not take your medication by mouth for 24 hour to 36 hours, call your physician. If you can not reach your PHCP, go to the nearest emergency department. You may need an injection to take the place of your oral medication.
  6. Always wear your medical alert bracelet or necklace.
  7. Make regular visits for health care follow-up.
  8. Learn how to give yourself an intramuscular injection of hydrocortisone.
264
Q

DO not palpate the abdomen of a patient with a pheochromocytoma,

A

because this action could stimulate a sudden release of catecholamines and trigger severe hypertension.

265
Q

Hyperthyroidism (Grave’s disease)

key features

A
  • diaphroesis (excessive sweating)
  • fine, soft, silky body hair
  • smooth, warm, moist skin
  • thinning of scalp hair
  • palpitations
  • chest pain
  • increased systolic blood pressure
  • tachycardia
  • dysrhythmias
  • rapid, shallow respirations
  • weight loss
  • increased appetite
  • increased stools
  • blurred or double vsion
  • eye fatigue
  • increased tears
  • injected (red) conjunctiva
  • photophobia
  • exophtalmis
  • eyelid retraction, eyelid lag
  • globe lag
  • hyperactive deep tendon reflexes
  • tremors
  • insomnia
  • increased basal metabolic rate
  • heat intolerance
  • low-grade fever
  • fatigue
  • decreased attention span
  • restlessness and irritability
  • emotional instability
  • manic behavior
  • amenoohea
  • increased libido
  • goiter
  • wide-eyed or startled appearance (exophthalmos)
  • enlarged spleen
  • muscle weakness and wasting
266
Q

Susceptibility to Grave’s disease is associated with several gene mutations. The pattern of inheritance is autosomal-recessive with link limitation to females.

A

Grave’s disease is associated with other autoimmune disorders, such as diabetes mellitus, vitiligo, and rheumatoid arthritis and often occurs in both members of identical twins. Ask the patient with Grave’s disease whether any other family members also have the problem.

267
Q

Goiter classification

A
  • 0 There is o palpable or visivle goiter
  • 1 Mass is not visible with neck in the normal position. Goiter can be palpated and moves up when the patient swallows.
  • 2 Mass is visible as swelling when the neck is in the normal position. Goiter is easily palpated and is usually asymmetric.
268
Q

Thyroid function tests

A
  • Serum T3 (70-205) hyperthyroidism increased, hypothyroidism decreased
  • serum T4 (4-12) Hyperthyroidism increased, hypothyroidism decreased
  • Free T4 index (0.8-2.28) hyperthyroidism increased, hypothyroidism decreased
  • TSH stimulation test (>10) test differentiates between primary hypo and secondary hypo, no response in primary.
  • Thyroid-stimulating immunoglobulins (TSI) (<130% of basal activity) hyperthyroidism: elevated in Grave’s disease, normal in other types of hyperthyroidism,; hypothyroidism: no change
  • Thyrotropin receptor antibodies (TRAb), Titer (0%), hyperthyroidism: 80-95% indicates Graves’ Disease; hypothyroidism: no response
  • TSH (2-10mU/mL) Hyperthyroidism: low in Grave’s disease, high in secondary or tertiary hyperthyroidism; Hypothyroidism: high in primary disease and low in secondary or tertiary disease
269
Q

Drug Therapy for Hyperthyroidism

A
  • Propylthiouracil (PTU, PropylThyracil), Methimazole (Northyx, Tapazole) :
    • Teach the pagtient to avoid crowds and people who are ill becaue the drug reduces the immune responsed, increasing the risk for infection.
    • Teach patients to check for weight gain, slow heart rate, and cold intolerance, which are indications of hypothyroidism and the need for a lower drug dose.
    • Teach patients taking propylthiouracil to report darkening of the urine or a yellow appearance to the skin or whites of the eyes, which indicate possible liver toxicity or failure, a serious side effect of propylthiouracil.
    • Remind women taking methimazole to notify their primary health care providers if they become pregnant because the drug causes birth defects and should not be used during pregnancy.
  • , Lugol’s solution, saturated solution of potassium iodide (SSKI):
    • Administer these drugs orally 1 hour after a thionamide has been given because initially the iodine agents can cause an increase in the production of thyroid hormones. Giving a thionamide first prevents this inital increase in thyroid hormone production.
    • Check patient for a fever or rash and ask about a metallic tast, mouth sores, sore throat, or GI distress as these are indications of iodism, a toxic effect of the drugs, and may require that the drug be discontinued.
270
Q

Althrough similar in action, methimazole and propulthiouracil are not interchangeable.

A

The dosages for propylthiouracil are much higher than those for methimazole.

271
Q

Methimazole can cause birth defects and should not be used during pregnancy,

A

especially during the first trimester. Instruct women to notify their primary health care provider if pregnancy occurs.

272
Q

Safety Precautions for the Patient Receiving an Unsealed Radioactive Isotope

A
  • Use a toilet that is not used by others for at least 2 weeks after receiving the radioactive iodine.
  • Sit to urinate (males and females) to avoid splashinh the seat, walls, and floor.
  • Flush the toilet three times after each use.
  • If urine is spilled on the toilet seat or floor, use paper tissues or towels to clean it up, bag them in sealable plastic bags, and take them to the hospital’s radiation therapy department.
  • Men with urinary incontinence should use condom catheters and a drainage bag rather than absorbant gel-filled briefs or pads.
  • Women with urinary incontinence should use facial tissue layers in their clothing to catch the urine rather than absorbent gel-filled briefs or pads. These tissues should be flushed down the toilet exclusively used by the patient.
  • Using a laxative on the second and third days after receiving the radioactive drug helps you excrete the contaminated stool faster (this also decreases the exposure of your abdominal organs to radiation).
  • Wear only machine-washable clothing and wash these items separately form others in your household.
  • After washing your clothing, run the washing machine for a full cycle on empty before it is used to wash the clothing of others.
  • Avoid close contact with pregnant women, infants, and young children for the first week after therapy. Remain at least 3 feet (about 1 meter) away from these people and limit your exposure to them to no more than 1 hour daily.
  • Some radioactivity will be in your saliva during the first week after therapy. Precautions to avoid exposing others to this contamination (both household members and trash collectors) include:
    • not sharing toothbrushes or toothpaste tubes.
    • using disposable tissues rather than cloth hankerchiefs and either flushing used ones down the toilet or keeping them in a plastic bag and turning them in to the radiation department of the hospital for disposal.
    • Using disposable utensils, paltes and cups.
    • Selecting foods that can be eaten completely and that do not result in saliva-coated remnant (Foods to avoid are fruit with a core that can be contaminated, meat with a bone [e.g. chicken wings, or legs, ribs]). Consider preparing these foods by cutting out the core and removing the bone before eating.
273
Q

A potentially life-threatening complication of thyrotoxicosis is periodic paralysis (thyrotoxic periodic paralysis, TPP), which results from low blood potassium levels caused by increased skeletal muscle uptake of potassium. The potassium movement is throught to result from direct thyroid hormone action or the increased adrenergic response of hyperthyroidism. The change in both intracellular and extracellular potassium levels reduces skeletal muscle membrane and excitiability and leads to temporary paralysis, including paralysis of the respiratory muscles.

A

TPP is most common in men of Chinese and Japanese descent.

Emergency management involves treating the thyrotoxicosis and the hypokalemia. In addition to antithyroid drug therapy, potassium is replaced IV. This condition is increasing in frequency in North America and is not always recognized. Be alert to any adult male of Asian descent who has lower limb paralysis or weakness along with signs and symptoms of hyperthyroidism.

274
Q

Monitor the patient to identify symptoms of obstruction and poor gas exchange (stridor, dyspnea, falling oxygen saturation, inability to swallow, drooling) after thyroid surgery.

A

If any indications of obstruction are present, respond by immediately notifying the Rapid Response Team.

275
Q

When caring for a patient with hyperthyroidism, even after a thyroidectomy, assess temperature often because an increase of even 1 degree F

A

may indicate an impending thyroid crisis. If an increase occurs, respond by reporting it immediately to the PHCP>

276
Q

Thyroid Storm or thyroid crisis

A
  • is a life threatening event that occurs in patients with uncontrolled hyperthyroidism, most often with Grave’s disease.
  • Symptoms develop quickly and the problem is fatal if left untreated.
  • It is often triggered by stressors such as trauma, infection, diabetic ketoacidosis, and pregnancy.
  • Symptoms of thyroid storm are caused by excessive thyroid hormone release, which dramatically increases metabolic rate.
  • Key symptoms include fever, tachycardia and systolic hypertension.
  • Even with treatment thyroid storm can lead to death.
277
Q

Emergency Care of the Patient during Thyroid Storm

A
  • Maintain a patent airway and adequate ventilation.
  • Give oral antithyroid drugs as prescribed: methimazole (Tapazole), up to 60 mg daily; propylthiouracil (PTU, Propyl-Thyracil), 300 to 900 mg daily.
  • Administer sodium iodide solution, 2g IV daily as prescribed.
  • Give propranolol (Inderal, Detensol), 1 to 3 mg IV as prescribed. Give slowly over 3 minutes. The patient should be connected to a cardiac monitor and a central venous pressure catheter should be in place.
  • Give glucocorticoids as prescribed: hydrocortisone, 100 to 500 mg IV daily; prednisone, 4 to 60 mg oral daily; or dexamethasone, 2 mg IM every 6 hours.
  • Monitor continually for cardiac dysrhythmias.
  • Monitor vital signs every 30 minutes.
  • Provide comfort measures, including a cooling blanket.
  • Give nonsalicylate antipyretics as prescribed.
  • Correct dehydration with normal saline infusions.
  • Apply cooling blanket or ice packs to reduce fever.
278
Q

Key Features of Hypothyroidism

A
  • cool, pale or yellowisj, dry coarse, scaly skin
  • thick, brittle nails
  • dry, coarse, brittle hair
  • decreased hair growth, with loss of eyebrow hair
  • poor wound healing
  • hypoventilation
  • pleural effusion
  • dyspnea
  • bradycardia
  • dysrhythmias
  • enlarged heart
  • decreased acitivity tolerance
  • hypotension
  • decreased basal metabolic rate
  • decreased body temperature
  • cold intolerance
  • apathy
  • depression
  • paranoia
  • anorexia
  • weight gain
  • constipation
  • abdominal distention
  • slowing of intellectual functions:
    • slowness or slurring of speech
    • impaired memory
    • inattentiveness
  • Lethargy or somnolence
  • confusion
  • hearing loss
  • paresthesia (numbness and tingling) of the extremities
  • decreased tendon reflexes
  • muscle aches and pain
  • Women:
    • changes in menses (amenorrhea or prolonged menstrual periods)
    • anovulation
    • decreased libido
  • Men:
    • decreased libido
    • impotence
  • Periorbital edema
  • facial puffiness
  • nonpitting edema of the hands and feet
  • hoarseness
  • gotier (enlarge thyroid gland)
  • thick tongue
  • increased sensitivity to opioids and tranquilizers
  • weakness, fatigue
  • decreased urine output
  • easy bruising
  • iron dificency anemia
  • vitamin deficiencies
279
Q

Myxedema coma

A
  • cellular energy is decreased and metabolites that care compounds of proteins and sugars called glycoaminoglycans (GAGs) build up inside cells.
  • This GAG build up increases the mucus and water, forms edema, and changes organ texture.
  • The edema is mucinous and called myxedema, rather than edema caused by water alone.
  • This edema changes the patient’s appearance. Non pitting edema forms everywhere, especially around the eyes, in the hands and feet, and between the shoulder blades. The tongue thickens; and edema forms in the larynx,making the voice husky. General physiologic function if decreased.
  • Sometime called hypothyroid crisis is a rate serious complication of untreated or poorly treated hypothyroidism and has a mortality rate of 60%.
  • The decreased metabolism cause the heart muscle to become flabby and the chamber size to increase.
  • the result is decreased cardiac output with decreased perfusion and GAS exchange in the brain and other vital organs, which makes the already slowed cellular metabolism worse, resulting in tissue and organ failure.
  • The mortality rate for myxedema coma is extremely high and this condition is a life-threatening emergency.
280
Q

Causes of Hypothyroidism

A