Med 2 Exam #3 Endocrine/Male Reproductive

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72 Terms

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Important Thyroid hormones

TSH (Thyroid stimulating hormone)

-targets thyroid gland

-functions to stimulate synthesis and release of thyroid hormones, growth and function of thyroid gland

T4 (thyroxine)

-targets all body tissues

-precursor to T3

T3 (triiodothyronine) 

-targets all body tissues

-regulates metabolic rate of all cells and processes of cell growth and tissue differentiation

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Hyperthyroidism

hyperactivity of the thyroid gland with sustained increase in synthesis and release of thyroid hormones

  • occurs most often in women; highest frequency ages 20-40 years

-most common form is Graves disease

-Other causes: toxic nodular goiter, thyroiditis, excess iodine intake, pituitary hormones, thyroid cancer

  • may be caused by iodinated contrast media used in CT scans and other radiologic studies

-subclinical hyperthyroidism occurs when pt has serum TSH level below 0.4 mIU/L and normal T4 and T3 levels

-overt hyperthyroidism is defined by low or undetectable TSH, increased T4 and T3 levels

  • symptoma may or may not be present

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Thyrotoxicosis

physiologic effects or clinical syndrome of hypermetabolism resulting from excess circulating levels of T3, T4, or both

-usually occurs w/ hyperthyroidism

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Graves disease

autoimmune disease characterized by thyroid enlargement and excess thyroid secretion

-do not know exact cause

-women 5x more likely than men to develop disease

Risk factors:

-lack of iodine

-smoking

-infection

-stress

-may interact w/ genetic factors

Patho:

-excess thyroid hormones lead to manifestations of thyrotoxicosis

-may progress to destruction of thyroid tissue, causing hypothyroidism

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Hyperthyroidism manifestations

related to the effect of excess circulating thyroid hormones

-directly increase metabolism and tissue sensitivity to sympathetic nervous system stimulation

-palpation of thyroid may reveal a goiter (enlargement of thyroid gland in front of neck); auscultating thyroid may reveal bruits

-ophthalmopathy: abnormal eye appearance or function

  • exophthalmos = protrusion of the eyeballs from the orbit (classic finding in Graves disease)

  • corneal ulcers and loss of vision can occur

  • changes in ocular muscles result in weakness, causing diplopia

Cardiovascular:

-systolic HTN

-bounding, rapid pulse; palpitations

-↑ CO

-systolic murmurs

-dysrhythmias

-angina

Respiratory:

-dyspnea on mild exertion

-↑ RR

GI system:

-↑ appetite and thirst

-weight loss

-diarrhea

-splenomegaly

-hepatomegaly

Integumentary system:

-warm, smooth, moist skin

-thin, brittle nails

-hair loss

-clubbing of fingers; palmar erythema. Acropachy = clubbing of digits that may occur in advanced disease

-fine, silky hair; premature graying

-diaphoresis

-vitiligo

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Hyperthyroidism manifestations (2)

Musculoskeletal system:

-fatigue

-weakness

-proximal muscle wasting

-dependent edema

-osteoporosis

Nervous system:

-nervousness, fine tremors

-insomnia, exhaustion

-lability of mood, delirium

-hyperreflexia of tendon reflexes

-inability to concentrate

-stupor, coma

Reproductive system:

-menstrual irregularities

-amenorrhea

-decreased libido

-impotence

-gynecomastia in men

-decreased fertility

Other:

-intolerance to heat

-elevated basal temperature

-lid lag, stare

-eyelid retraction

-rapid speech

-pt in early stages may only have weight loss and increased nervousness

-manifestations (palpitations, tremors, weight loss) in older adults do not differ from those of younger adults

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Hyperthyroidism Younger vs. Older adults

Younger adult:

-common cause: Graves disease in over 90% of cases

-common symptoms: nervousness, irritability, weight loss, heat intolerance, warm/moist skin

-goiter: present in over 90% of cases

-ophthalmopathy: exophthalmos present in 20-40% of cases

-cardiac features: tachycardia and palpitations common but w/o HF

Older adults:

-common causes: Graves disease or toxic nodular goiter

-common symptoms: anorexia, weight loss, apathy, lassitude, depression, confusion

-goiter: present in approx. 50% of cases

-ophthalmopathy: exophthalmos less common

-cardiac features: angina, dysrhythmias (especially A-fib w/ rapid ventricular response), HF may occur

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Acute thyrotoxicosis

complication of hyperthyroidism

-acute, severe, rare condition that occurs when excess amounts of thyroid hormones are released into the circulation

-considered a life-threatening emergency

-results from stressors (infection, trauma, surgery) in a pt w/ preexisting hyperthyroidism

  • pts who have thyroidectomy at risk bc manipulation of thyroid gland results in increased release of hromones

Manifestations:

-all symptoms are prominent and severe

-severe tachycardia, HF, shock, hyperthermia (up to 10 degrees), agitation, delirium, seizures, abdominal pain, vomiting, diarrhea, and coma

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Emergency management of acute thyrotoxicosis

-Begin fluid replacement w/ isotonic saline infusions containing dextrose

-monitor airway, breathing, and circulation

-monitor vital signs at least every 30 mins

-apply continuous O2 saturation and ECG monitoring

-monitor serial serum electrolytes, serum glucose, ABGs, and serum calcium

-monitor urine output hourly'

-apply ice packs and cooling blankets to reduce fever. Acetaminophen as needed

-provide pulmonary hygiene

-assess for manifestations of HF or pulmonary edema (extra heart sounds, adventitious lung sounds)

-decrease O2 demands by decreasing anxiety and pain

-restrict visitors if needed

-give prescribed drugs and monitor effects

  • beta blockers

  • antithyroid agents

  • Iodine compounds

  • glucocorticoids

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Hyperthyroidism diagnostics

Labs:

-low or undetectable TSH levels

-increased free T4 levels

Radioactive iodine uptake (RAIU) test:

-can distinguish Graves disease from other forms of thyroiditis

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Hyperthyroidism Interprofessional care

-Goals of care are to

  • block adverse effects of thyroid hormones

  • suppress oversecretion of thyroid hormone

  • prevent complications

-treatment options include antithyroid medications, radioactive iodine therapy and surgery

-supportive therapy is aimed at managing respiratory distress, reducing fever, replacing fluid, and eliminating or managing the initiating stressors

Drug therapy:

-useful in treatment of of thyrotoxic states

-not considered curative

-include: antithyroid drugs, iodine, and beta blockers

  • first line antithyroid drugs are propylthiouracil and methimazole

Radioactive Iodine therapy:

-treatment of choice for most non-pregnant adults

-damages or destroys thyroid tissue thus limiting thyroid hormone secretion

-delayed response up to 3 months

  • treated w/ antithyroid drugs and B blockers before and during first 3 months

-80% of pts have posttreatment hypOthyroidism resulting in need for life-long thyroid hormone therapy

-usually given on outpatient basis

-pt teaching = oral care for thyroiditis/parotiditis; symptoms of hypothyroidism; limit radiation exposure to others

  • use private toileting facilities, flush 2-3 times after each use, separate laundry for towels/bed lines/clothes, do not prepare foods for other that require prolonged hand handling, avoid being close to pregnant women

Surgical therapy:

-done for those:

  • have a large goiter causing compression

  • a lack of response to antithyroid therapy

  • thyroid cancer

  • not  a candidate for RAI

-subtotal thyroidectomy is preferred procedure = removes 90% of thyroid gland

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Antithyroid drugs (hyPERthyroidism treatment)

Propylthiouracil and Methimazole (Tapazole)

-inhibit thyroid hormone synthesis

-propylthiouracil is generally used for pts who are in the 1st trimester of pregnancy, had an adverse rxn to methimazole, or need a rapid reduction in symptoms

-improvement in 1-2 weeks

-good results in 4-8 weeks

-therapy for 6-15 months

-abruptly stopping drug can result in return to hyperthyroidism

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Iodine (hyperthyroidism treatment)

used w/ other antithyroid drugs to prepare client for thyroidectomy or for treatment of thyrotoxicosis

-Potassium Iodine (SSKI) and Lugol’s solution

-inhibits synthesis of T3 and T4 and blocks their release into corculation

-decreases vascularity of thyroid gland

-maximal effect in 1-2 weeks

-long-term therapy is not effective

Administartion:

-mix w/ water or juice and give after meals

-sip through straw to help decrease chance of staining teeth

Signs of Iodine toxicity:

-swelling of buccal mucosa and other mucousmembranes

-excess salivation

-N/V

-skin reactions

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Beta Blockers (Hyperthyroidism treatment)

-block the affects of SNS stimulation

  • decrease tachycardia, nervousness, irritability, and tremors

-Propranolol usually given w/ antithyroid agents

-Atenolol preferred for used in hyperthyroid pt w/ asthma or heart disease

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Nutritional therapy hyperthyroidism

-high calorie diet may be needed to satify hunger, prevent tissue breakdown, and decrease weight loss

  • 4000-5000 cal/day

-pt may need 6 full meals a day

-snack high in protein, carbohydrates, minerals, and vitamins

  • protein intake = 1-2g/kg or ideal body weight

-avoid highly seasoned and high fiber foods bc they can further stimulte hyperactive GI tract

-avoid caffeine-containing liquids s/a coffee, tea, cola

-dietitian referral

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Nursing Assessment hyperthyroidism

-Subjective Data

  • family hx, iodine intake, weight loss, increase appetite/ thirst, N/V, diarrhea, polyuria, sweating

  • dyspnea on exertion, palpitations, muscle weakness/fatigue, insomnia, chest pain, heat intolerance, pruritis

  • ↓ libido, impotence, gynecomastia, emotional lability/irritability/restlessness, personality changes, delirium

-Objective data

  • agitation, rapid speech, anxiety/restlessness, hyperthermia, enlarged or nodular thyroid gland, exophthalmos, eyelid retraction, infrequent blinking

  • warm/diaphoretic/velvety skin, thin/loose nails, fine/silky hair and hair loss, palmar erythema, clubbing, vitiligo, edema

  • tachypnea, dyspnea on exertion, tachycardia, bounding pulse, murmurs, dysrhythmias, HTN, bruit, ↑bowel sounds, ↑appetite, diarrhea, weight loss, hepatosplenomegaly

  • hyperreflexia, diplopia, fine tremors, muscle wasting, menstrual irregularities, infertility, impotence gynecomastia

  • ↑ T3, T4, and T3 resin uptake; ↓ or undetectable TSH, CXR showing enlarged heart. ECG finding of tachycardia

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Nursing management hyperthyroidism (Acute care)

-hyperthyroidism is usually treated outpatient however those who develop acute thyrotoxicosis or undergo thyroidectomy need hospitalization and acute care

Acute Care: Acute Thyrotoxicosis

-requires aggressive treatment often in ICU

-meds that block thyroid hormone production and SNS effects

-supportive therapy including monitoring for dysrhythmias and decompensation, ensuring adequate oxygenation, and giving IV fluids to replace losses

-ensure adequate rest

  • calm, cool, quiet room

  • light bed covering and change linen often if diaphoretic

-encourage and assist w/ exercise involving large muscle groups

-establish supportive, trusting relationship to promote coping

-if exophthalmos present there is risk for corneal injury related to irritation and dryness. May have orbital pain

  • apply artificial tears to soothe and moisten conjunctival membranes

  • restrict salt to reduce periorbital edema

  • pt should sit upright as much as possible

  • dark glasses to reduce glare

  • lightly tape eyelids shut for sleep

  • if severe corticosteroids, radiation or retroorbital tissues, orbital decompression, or corrective lid or muscle surgery

Pre-op:

-administer meds to achieve euthyroidism

-administer iodine to ↓ vascularity

-assess for signs of iodine toxicity

-pt teaching

  • comfort and safety measures; leg exercises, head support, neck ROM; routine post-op care

Post-op:

-monitor for complications = hypocalcemia, hemorrhage, laryngeal nerve damage, thyrotoxic crisis, infection

-maintain patent airway

  • oxygen suction equipment, tracheostomy tray in pts room

  • monitor for laryngeal stridor = harsh, vibratory sound that may occur bc of edema on laryngeal nerve or be related to tetany

  • have IV calcium readily available  to treat tetany 

-assess every 2 hours during first 24hrs for signs of hemorrhage or tracheal compression

-semi-fowler’s position, supported head w/ pillows, avoid neck flexion and tension to suture line

-monitor vital signs and calcium levels

  • signs of hypocalcemia = difficulty speaking and hoarseness, trousseau’s and chovstek’s signs, tingling in toes/fingers/around the mouth, muscular twitching, apprehension

-patient ambulates w/i hrs after surgery if recovery is uneventful

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Nursing management hyperthyroidism (ambulatory care)

provide discharge teaching

-thyroid hormone balance will be monitored periodically

-after surgery caloric intake must be greatly reduced to less than the amount that was needed to prevent weight gain

  • adequate iodine intake is needed to promote thyroid function

-encourage regular exercise to stimulate thyroid gland

-avoid high environmental temps

-see HCP biweekly for a month and then at least semiannually to assess thyroid function

-may have period of relative hypothyroidism soon after surgery due to substantial reduction in size of thyroid

  • monitor for symptoms of hypOthyroidism

-pts who had complete thyroidectomy will need lifelong hormone replacement therapy

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Hypothyroidism

deficiency of thyroid hormone that causes a general slowing of the metabolic rate

  • more common in women than men

-Subclinical hypothyroidism: occurs when TSH > 4.5 mIU/L, T4 levels normal

  • affects 10% of women over 60

-Nonthyroid illness syndrome (NTIS): low T3, T4, and TSH

  • critically ill patients

Patho:

-classified as primary or secondary

  • primary = caused by destruction of thyroid tissue or defective hormone synthesis

  • secondary = caused by pituitary disease w/ decreased TSH secretion or hypothalamic dysfunction w/ increased thyrotropin-releasing hormone (TRH) secretion

-iodine deficiency most common cause world wide; In U.S. most common cause is atrophy of thyroid gland

-can develop after treatment for hyPERthyroidism

-cab be caused by drugs s/a amiodarone and lithium

-if develops in infancy results from thyroid hormone deficiencies during fetal or early neonatal life (cretinism)

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Hypothyroidism manifestations

overall see a slowing of the body processes

  • manifestations variable depending on severity of disease

  • may develop slowly over months to years

  • in older adult we may contribute manifestations of hypothyroidism to normal aging. Those w/ confusion, lethargy, and depression should be screened for thyroid disease

General:

-tired and lethargic

-impaired memory, slowed speech, decreased initiative, somnolence

-may appear depressed

-weight gain

Cardiovascular system:

-CV problems may be significant in pts w/ pre-existing CV disease

-↓ cardiac contractility and output

-↑ serum cholesterol and triglycerides

-anemia

Respiratory system:

-low exercise tolerance

-SOB on exertion

Neurologic system:

-fatigue and lethargy

-personality and mood changes

GI system:

-decreased appetite

-N/V

-weight gain

-constipation

-distended abdomen

-enlarged, scaly tongue

-celiac disease

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Hypothyroidism manifestations (2)

Integumentary system:

-dry, thick, inelastic, cold skin

-thick, brittle nails

-dry, sparse, coarse, hair

-poor turgor of mucosa

-generalized interstitial edema

-puffy face

-decreased sweating

-pallor

Musculoskeletal System:

-fatigue, weakness

-muscular aches and pains

-slow movements

-arthralgia

Reproductive system:

-prolonged menstrual periods or amenorrhea

-decreased libido, infertility

Other:

-increased susceptibility to infection

-increased sensitivity to opioids, barbiturates, anesthesia

-intolerance to cold

-decreased hearing

-sleepiness

-goiter

-pts w/ severe long-standing hypothyroidism may have myxedema

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Myxedema/ Myxedema coma

Myxedema:

results from the accumulation of mucus-like substance under the skin

-alters the appearance of the skin and sub-q tissues w/ puffiness, facial and periorbital edema, and a mask-like affect

Myxedema coma:

-medical emergency

-causes include infection, drugs (opioids, tranquilizers, barbiturates), exposure to cold, and trauma

-Manifestations

  • low temp

  • impaired consciousness

  • hypotension

  • hypoventilation

  • cardiovascular collapse can result from hypoventilation, hyponatremia, hypoglycemia, and lactic acidosis

-Treatment

  • support vital functions

  • give IV thyroid replacement therapy

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Hypothyroidism diagnostics

-history and physical exam

-TSH ↑ w/ primary hypothyroidism

-TSH ↓ w/ secondary hypothyroidism

-presence of thyroid antibodies

-high cholesterol and triglycerides, anemia (↓ RBCs), and increased CK

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Hypothyroidism interprofessional care 

treatment is to restore euthyroid as safely and as quickly as possible w/ hormone therapy

-low calorie diet can promote weight loss or prevent weight gain

-Levothyroxine drug of choice to treat hypothyroidism

  • carefully monitor pts w/ CVD who take this drug

  • monitor HR and report pulse greater than 100bpm or an irregular heartbeat

  • promptly report chest pain, weight loss, nervousness, tremors, or insomnia

  • first dosages are low to avoid increases in resting HR and BP

  • in pt w/o side effects dose is increased at 4-6 week intervals as needed based on TSH levels

  • peak action 1-3 weeks

  • must regularly take replacement medication (lifelong)

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Nursing Assessment Hypothyroidism

Health Hx:

-hyperthyroidism treatment

-Iodine-containing medications

-changes in appetite

-weight gain

-activity level

-speech, memory, or skin changes

Physical Exam:

-cold intolerance

-constipation

-signs of depression

-HR

-gland tenderness

-edema

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Nursing management hypothyroidism

Health promotion:

-routine screening of thyroid function not recommended; high-risk persons should be screened for subclinical thyroid disease

-assess for risk factors:

  • female

  • white

  • adavancing age

  • type 1 diabetes

  • down syndrome

  • family hx of thyroid disease

  • goiter

  • previous hyperthyroidism

  • external beam radiation in the head and neck area

-most people w/ hypothyroidism treated on outpatient basis but persons who develop myxedema coma needs acute care often in ICU

Acute care:

-mechanical respiratory support and cardiac monitoring

-give hormone therapy and all other meds IV

-monitor core temp for hypothermia

-prevent skin breakdown

-assess vital signs, body weight, I&Os, and edema

-cardiac assessment especially important

-note energy level and mental alertness. Should improve w/i 2-14 days

-neurologic status and TSH levels used to determine continuing treatment

Ambulatory care:

-provide patient teaching about medication management and complications

-provide written instructions, repeat info often, and assess pts comprehension level

-thyroid drugs increase the effects of anticoagulants

-CVD manifestations may persist after correcting the hormone imbalance

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Hypothyroidism patient teaching

  1. discuss importance of thyroid hormone therapy

-need for lifelong therapy

-taking thyroid hormone in the morning before food

-need for regular follow-up care and monitoring of thyroid hormone levels

  1. caution pt to not swithc drug brnads since bioavailability of thyroid hormones may differ

  2. emphasize need for comfortable, warm environement bc of cold intolerance

  3. teach ways to prevent skin breakdown. Use soap spaingly, and apply lotion to skin

  4. caution pt, especially the older adult, to avoid sedatives

-if must be used suggest lowest dose be used

-caregiver should closely monitor mental status, LOC, and respirations

  1. discuss ways to minimize constipation

-gradual increase fiber in diet

-use of stool softners

-regular bowel elimination time

-tell pt to avoid using enemas. They cause vagal stimulation, which can be hazardous if heart disease is present

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Important Adrenal/Pituitary hormones

ACTH (adrenocorticotropic hormone)

-targets adrenal cortex; produced by anterior pituitary

-fosters growth of adrenal cortex

-stimulates corticosteroid secretion

Corticosteroids (cortisol, hydrocortisone)

-targets all body tissues

-promotes metabolism

-increases response to stress

-anti-inflammatory effects

Mineralocorticoids (aldosterone)

-targets kidney

-regulates sodium and potassium and thus water balance

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Addison’s disease (adrenocortical insifficiency)

-Addisons disease is a primary cause of adrenocortical insufficiency

  • lack of glucocorticoids, mineralocorticoids, and androgens

-Secondary cause of adrenocortical insufficiency is due to lack of pituitary ACTH

  • glucocorticoids and androgens are deficient but mineralocorticoids are normal

Patho:

-80% of cases caused by autoimmune response

  • autoimmune adrenalitis

  • antibodies destroy adrenal cortex

  • loss of glucocorticoid, mineralocorticoid, and adrenal androgen hormones

-can be present along w/ other endocrine problems = autoimmune polyglandular syndrome

  • type 1 diabetes, autoimmune thyroid disease, pernicious anemia, celiac disease

Causes:

-amyloidosis

-fungal infections

-AIDS

-metastatic cancer

-Iatrogenic addison disease may be due to adrenal hemorrhage, often related to anticoagulant therapy, chemotherapy, or bilateral adrenalectomy. Ketoconazole therapy for AIDS

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Manifestations Addison’s disease

do not tned to be evident until 90% of adrenal cortex is destroyed, often advanced before diagnosed

-have slow onset

-anorexia

-nausea

-progressive weakness

-fatigue

-weight loss

-striking bronze-colored hyperpigmentation

  • mainly seen in sun-exposed areas of body, at pressure points, over joints, and in the creases especially palmar creases

-other manifestations include = abdominal pain, diarrhea, headache, orthostatic hypotension, salt craving, joint pain, irritability, depression

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Addisonian crisis

life-threatening emergency caused by insufficient adrenocortical hormones or a sudden sharp decrease in these hormones

triggers include

  • stress (infection, surgery)

  • sudden withdrawal of corticosteroid hormone therapy

  • adrenal surgery

  • sudden pituitary gland destruction

-pt will have severe manifestations of glucocorticoid and mineralocorticoid deficiencies 

  • hypotension; may lead to shock and circulatory collapse

  • tachycardia

  • dehydration

  • hyponatremia

  • hyperkalemia

  • hypoglycemia

  • fever

  • weakness

  • confusion

  • GI manifestations may include severe vomiting, diarrhea, and pain in abdomen

  • pain may occur in lower back and legs

Treatment:

-shock management

-high-dose hydrocortisone replacement

-0.9& saline solution and 5% dextrose to reverse hypotension and electrolyte imbalances

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Addison’s disease diagnostics

-ACTH stimulation test is common

  • baseline levels of cortisol and ACTH

  • IV injection of synthetic ACTH

  • levels rechecked after 30 and 60 minutes

  • ↑ blood cortisol levels is normal; little or no ↑ in cortisol levels indicative of Addison’s disease. High ACTH level in primary adrenal insufficiency

-CRH (corticotropin-releasing hormone) stimulation Test

  • done after abnormal ACTH test response

  • IV injection of synthetic CRH

  • blood drawn after 30 and 60 minutes

  • high ACTH levels w/ no cortisol indicates Addison’s disease. Absence of ACTH or delayed response common in secondary adrenal insufficiency

-hyperkalemia

-hypochloremia, hyponatremia, hypoglycemia

-anemia

-increased BUN levels

-ECG changes

-CT scan, MRI

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Addison’s disease care

Interprofessional Care:

-manage underlying cause; mainstay is ofetn lifelong hromone therapy w/ glucocorticoids and mineralocorticoids

-hydrocortisone most common form of hormone therapy

  • two-thirds on awakeneing in the morning, one-third in late afternoon

-mineralocoritocids replaced w/ fludrocortisone

  • daily in the morning

-women need androgen replacement w/ DHEA

-increased salt added to diet

Nursing management:

Acute care:

-frequent assessment necessary

-correct fluid and electrolyte imbalance

-assess vital signs and neurologic status

-daily weight, accurate I&O

-obtain complete medication hx

  • hypoglycemics, cardiac glycosides, oral contraceptives, anticoagulants, and NSAIDs can interact w/ corticosteroids

-watch for signs of Cushing syndrome

  • changes in BP, weight gain, weakness, and other manifestations

-protect against infection and help w/ daily hygiene

-protect from noise, light, and environmental temperature extremes

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Patient teaching Addison disese

-Dosing

  • glucocorticoids given in divided doses

  • mineralocorticoids once in the morning

  • reflects normal circadian rhythm

  • decrease side effects of corticosteroids

Other teaching:

  1. names, dosages, and actions of drugs

  2. symptoms of overdosage and underdosage

  3. conditions requiring increased dosage (trauma, infection, surgery, emotional crisis)

  4. actions to take related to changes in medication

-increased dose of corticosteroid

-self-administration of large dose of corticosteroid IM

  1. preventing infection and need for prompt and vigorous treatment of existing infections

  2. need for lifelong replacement therapy

  3. need for lifelong medical supervision

  4. need to carry medical identification

  5. fall prevention

  6. adverse effects of corticosteroid therapy and prevention techniques

  7. special instruction for pts w/ diabetes and management of glucose when taking corticosteroids

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Corticosteroid therapy

-effective in treating many problems; however long-term therapy at therapeutic doses often leads to serious complications and side effects

-not recommended for minor chronic conditions, should be reserved for problems that have risk for death, permanent loss of function, or for short-term therapy

-potential benefits must be weighed against risks

Expected effects:

-antiinflammatory action

-immunosuppression

-maintenance of normal BP

Side effects:

-hypokalemia and hypocalcemia

-hyperglycemia and HTN

-delayed healing

-susceptibility to infection

-supporessed immune response

-peptic ulcer disease

-muscle atrophy/weakness

-mood and behavior changes

-moon faces, truncal obesity

-protein depletion

-risk for acute adrenal crisis if therapy is stopped abruptly

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Corticosteroid therapy patient teaching

  1. follow a diet high in protein, calcium, and potassium and low in fat and concentrated simple carbs s/a sugar, syrups, and candy

  2. ensure adequate rest and sleep, s/a daily naps and avoiding ceffeine late in the day

  3. take part in an exercise program to help maintain bone integrity

  4. recognize edema and ways to restrict sodium intake to <2000mg/day if edema occurs

  5. monitor glucose levels and recognize symptoms of hyperglycemia. Report symptoms or bg > 120mg/dL

  6. notify HCP if heartburn after meals or epigastric pain that is not relieved by antacids occurs

  7. see an eye specialist yearly to assess for cataracts

  8. use safety measures, s/a getting up slowly from bed or chair and good lighting, to avoid accidental injury

  9. maintain appropriate hygiene practices

  10. avoid contact w/ persons w/ colds or other contagious illnesses to prevent infection

  11. inform all HCPs about long-term corticosteroid use

  12. recognize need for higher doses of corticosteroids in times of physical and emotional stress

  13. NEVER abruptly stop the corticosteroids bc this could lead to addisonian crisis and death

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Cushing syndrome

clinical condition that results from chronic exposure to excess corticosteroids, especially glucocorticoids

Common causes:

-iatrogenic admin of exogenous corticosteroids (prednisone)

-ACTH secreting pituitary adenoma

-adrenal tumors and ectopic ACTH production by tumors

-more common in women 20-40 years old

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Cushing syndrome manifestations

occur in most body systems and are related to excess corticosteroid levels

Glucocorticoid excess:

-pronounced changes in physical appearance, weight gain

  • centripetal obesity, “moon face”, and “buffalo hump”

-hyperglycemia related to glucose intolerance and increased gluconeogenesis

-muscle wasting → weakness

-loss of bone matrix → osteoporosis and back pain; compression fractures

-loss of collagen → thin skin, easily bruises. Florid cheeks, acne. Purple striae on abdomen

-↑ BP, hypervolemia, edema of lower extremities

-glycosuria, hypercalciuria, risk for kidney stones

-euphoria, irritability, depression, insomnia, anxiety

-delayed wound healing

Mineralocorticoid excess:

-increased BP, hypervolemia

-marked sodium and water retention, edema, marked ↓ potassium, alkalosis

Adrenal androgen excess:

-muscle wasting and weakness

-severe acne, hirsutism,

-women: menstrual irregularities, enlargement of clitoris, virilization

-men: gynecomastia, testicular atrophy, feminization

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Cushing syndrome diagnostics

-confirmation of increased plasma cortisol levels involves 3 tests

  • midnight or late night salivary cortisol

  • low-dose dexamethasone suppression test

  • 24-hour urine cortisol. Levels >100mcg/24 hrs indicates cushing syndrome

-CT scan or MRI of pituitary and adrenal glands

-Plasma ACTH levels may be low, hormal or high

  • if high or normal indicate cushing disease

  • if low indicate adrenal or medication cause

-hypokalemia and alkalosis w/ ectopic ACTH syndrome and adrenal carcinoma

Other findings present but not diagnostic:

-leukocytosis, lymphopenia, eosinopenia, hyperglycemia, glycosuria, hypercalciuria, osteoporosis

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Cushing syndrome interprofessional care

primary goal is to normalize hormone secretion

-if cause is pituitary adenoma standard treatment is surgical removal of pituitary tumor

  • radiation therapy an option for pts who are not surgical candidates

-adrenalectomy for adrenal tumors or hyperplasia are the cause

-pts w/ ectopic ACTH-secreting tumors are best managed by removing the tumor

  • usually possible when tumor is benign

  • if cancerous and has already metastasized, surgical removal may not be possible or successful

-if developed due to prolonged corticosteroid use may try several options

  • gradually discontinue therapy

  • decrease dose

  • convert to an alternate-day regimen

  • dose must be tapered gradually

Drug therapy:

-goal is to suppress the synthesis and secretion of cortisol from the adrenal gland

-Ketoconazole and mitotane

  • used cautiously bc they are often toxic at the dosages needed to reduce cortisol secretion

  • hydrocortisone or prednisone may be needed to avoid adrenal insufficiency

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Cushing syndrome nursing assessment

-Subjective data:

  • patient hx of pituitary tumor; adrenal, pancreatic, or pulmonary neoplasms; GI bleeding; frequent infections

  • medications = corticosteroids

  • malaise, weight gain, anorexia, polyuria, prolonged wound healing, easy bruising

  • weakness/fatigue, insomnia/poor sleep quality, headache, back/joint/bone/rib pain, poor concentration and memory

  • negative feelings, amenorrhea, impotence, decreased libido, anxiety, mood disturbances, emotional lability, psychosis

-Objective data:

  • truncal obesity, supraclavicular fat pads, buffalo hump, moon faces, plethora, hirsutism of body and face

  • thinning of hair, friable skin, acne, petechiae, purpura, hyperpigmentation, striae, edema

  • HTN, muscle wasting, thin extremities, awkward gait, gynecomastia, testicular atrophy, enlarged clitoris

  • hypokalemia, hyperglycemia, dyslipidemia, polycythemia, agranulocytosis, lymphocytopenia, eosinopenia

  • ↑ serum cortisol level, abnormal ACTH levels, abnormal dexamethasone suppression test, ↑ urine free cortisol and 17-ketosteroids, glycosuria, hypercalciuria, osteoporosis

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Cushing syndrome nursing management

Health promotion:

-identify persons at risk = pts receiving long-term, exogenous corticosteroids

-teach pts about medication use and to monitor for side effects

Acute care:

-assessment focuses on s/sx of hormone and drug toxicity and complicating conditions

-monitor vital signs, daily weight, and glucose

-assess for infection; s/sx may be minimal or absent so assess for pain, loss of function, and purulent drainage

-monitor for s/sx of thromboembolic events s/a PE

-provide emotional support

  • pt may feel unattractive or unwanted

  • remain sensitive to pts feelings and be respectful

  • reassure pt that physical changes and emotional lability will resolve when hormone levels return to normal

Ambulatory care:

-discharge teaching is based on the pts lack of endogenous corticosteroids and resulting inability to react physiologically to stressors

-home health nurse referral

-always wear Medic alert bracelet and carry medical identification and instructions in a wallet or purse

-avoid exposure to extreme temps, infections, and emotional situations

-many pts need lifetime corticosteroid replacement therapy

-adjust replacement therapy by stress levels

-if cannot adjust own therapy or if weakness, fainting, fever, or N/V occur contact HCP

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Cushing syndrome surgical management

Pre-op care:

-pt should be in optimal physical condition

-control HTN and hyperglycemia

-correct hypokalemia

-high protein diet to correct protein depletion

-teaching depends on planned surgical approach

Post-op:

-increased risk of bleeding bc adrenal glands are vascular

-pt may have nasogastric tube, urinary catheter, IV therapy, and central venous pressure monitroing

-initiate VTE prophylaxis

-manipulating glandualr tissue during surgery may release large amounts of hormones into circulation

  • BP, fluid balance, and electrolyte levels may be unstable

-high doses of corticosteroids are given IV during surgery and several days after to ensure adequate response to stress of procedure

-increased risk for problems w/ glycemic control, susceptibility to infection, and delayed wound healing

-report any significant changes in vital signs

-monitor I&O

-administer corticosteroids as ordered

-obtain morning urine samples for cortisol measurement

-monitor for acute adrenal insufficiency

  • vomiting, increases weakness

  • dehydration, hypotension

  • painful joints

  • pruritis

  • peeling skin

  • severe emotional disturbances

-bed rest until BP is stabilized after surgery

-monitoring for subtle signs of infection

-meticulous care to prevent infection

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Hyperaldosteronism

characterized by excess aldosterone secretion

-main effects are

  • sodium retention

  • potassium and hydrogen ion excretion

-hallmark of this disease is HTN w/ hypokalemic alkalosis

Patho:

-primary hyperaldosteronism (PA) most often caused by a small solitary adrenocortical adenoma

-has a genetic link

-secondary hyperaldosteronism occurs in response to a nonadrenal cause of increased aldosterone levels, s/a renal artery stenosis, renin-secreting tumors, and CKD

Manifestations:

-increased aldosterone leads to hypernatremia, hypertension, and headache

  • edema does not usually occur

-potassium wasting leads to hypokalemia → generalized muscle weakness, fatigue, dysrhythmias, glucose intolerance, metabolic alkalosis that may lead to tetany

Diagnostics:

-primary aldosteronism causes

  • ↑ plasma aldosterone levels

  • ↑sodium levels

  • ↓potassium levels

  • ↓renin activity

-CT scan or MRI

-plasma 18-hydroxycortocosterone level

  • >50ng/dL indicates adenoma

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Hyperaldosteronism care

Interprofessional care:

-preferred treatment for PA is removal of adenoma

-Pre-op

  • potassium-sparing diuretics

  • antihypertensives

  • oral potassium supplements

  • sodium restrictions

-pts w/ bilateral adrenal hyperplasia

  • potassium-sparing diuretic to block aldosterone synthesis

  • calcium channel blockers to decrease BP

  • dexamethasone to decrease hyperplasia

Nursing management:

-careful assessment of fluid and electrolyte imbalance

-assessment of cardiovascular status

  • monitor BP frequently before and after surgery

-Patient teaching

  • medications and side effects = spironolactone may cause gynecomastia, impotence, menstrual disorders

  • s/sx of hypokalemia and hyperkalemia

  • frequently monitor BP

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Acromegaly

rare condition characterized by overproduction of growth hormone

-most often occurs bc of benign GH-secreting pituitary adenoma → overgrowth of soft tissues and bones in hands, feet, and face

Manifestations:

-prominent supraorbital ridge is hallmark sign

-changes occur slowly over many years

  • thickening and enlargement of bony and sift tissues of face, feet, and head

  • proximal muscle weakness and joint pain

  • carpal tunnel syndrome and peripheral neuropathy

  • tongue enlargement

  • voice deepens

  • sleep apnea

  • skin becomes thick, leathery, and oily w/ acne

  • headaches are common

  • manifestations of diabetes may occur

Diagnostics:

-evaluating plasma insulin-like growth factor (IGF-1) levels

-GH response to oral glucose tolerance test

-CT, MRI to visualize pituitary tumor

Treatment:

-surgery treatment of choice = hypophysectomy to remove pituitary tumor

-drug therapy may include Sandostatin for pts whose surgery did not result in cure

  • reduces GH levels to normal

  • given sub-q 3x/week

  • long-acting somatostatin analogs available as IM injections

-dopamine agonists may be given to reduce GH secretion from tumor

-GH antagonists may be given to block liver production of IGF-1

-provide emotional support, referral to support group may be helpful

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Care of Patient after pituitary surgery

treatment of choice for tumors in pituitary area =if entire pituitary gland is removed pt will need lifelong replacement of thyroid hormone, sex hormones, and glucocorticoids

-Monitor vital signs. Assess peripheral pulses and watch for orthostatic hypotension

-Monitor neurologic and cognitive status hourly for first 24 hrs and then every 4 hrs

-Assess extremity strength and reflexes

-Monitor field of vision, visual acuity, extraocular movements, and pupillary response. Notify HCP of any changes

-Assess dressing for type and amount of drainage. Notify HCP for excessive bleeding or CSF drainage

-Maintain strict I&O and monitor fluid balance. Assess for DI or SIADH

-Keep HOB elevated at least 30 degrees

-Encourage deep breathing exercises and incentive spirometer use

-Monitor for pain and give analgesic medications as prescribed

-Encourage high-fiber diet to decrease risk for constipation

-Perform oral care every 4hr

-Teach pt to

  • avoid vigorous coughing, sneezing, and blowing the nose

  • avoid blowing the nose for at least 48hrs after surgery

  • avoid bending over at the waist or straining at stool due to risk for increased IOP

  • avoid use of toothbrushes until incision heals. Avoid brushing teeth for at least 10 days to protect suture line. May perform gentle mouth care every 4hrs

  • follow replacement hormone therapy plan

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Syndrome of Inappropriate Antidiuretic hormone (SIADH)

results from the overproduction of ADH or the release of ADH despite normal or low plasma osmolarity

-”soaked inside”

-most common cause is cancer

Manifestations:

-low urine output and increased body weight

-fluid retention, ↑BP

-concentrated urine, hypochloremia

-at first has thirst, dyspnea on exertion, and fatigue

-dilutional hyponatremia causes muscle cramping, irritability, and headache, vomiting, abdominal cramps, and muscle twitching

-cerebral edema may occur → lethargy, confusion, seizures, coma

Diagnostics:

-low serum osmolality

-high urine osmolality

-high urine specific gravity

Treatment:

-monitor vitals, I&O, daily weights, and observe for signs of hyponatremia

-loop diuretics may be used to promote diuresis

-demeclocycline may be given = blocks the effect of ADH on the renal tubules, resulting in more dilute urine

-initiate seizure and fall precautions, keep HOB flat 

-in severe hyponatremia small amounts of IV hypertonic saline solution (3% sodium chloride) may be given

-fluid restrictions

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Diabetes Insipidus

caused by deficient production or secretion of ADH or a decreased renal response to ADH

-may be transient, or a chronic, lifelong condition

-”dry inside”

Manifestations:

-increased urine output = polyuria

-polydipsia

-dehydration

-hypernatremia

-general weakness

-hypotension, tachycardia, hypovolemic shock

-irritability, mental dullness, coma

Diagnostics:

-water deprivation test

-low urine osmolality (dilute urine that contains fewer solutes and more water)

Treatment:

-replace fluids orally or IV = IV hypotonic saline or dextrose 5% in water

-DDAVP (desmopressin) = hormone replacement therapy of choice

-carbamazepine can help decrease thirst

-monitor pulse, BP, LOC, I&O, and specific gravity

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Hyperparathyroidism

increased parathyroid hormone (PTH) secretion

-PTH plays important role in stimulating bone resorption of calcium, renal tubular reabsorption of calcium, and activation of vitamin D

-can be caused by tumor, vitamin D deficiency

Manifestations:

-hypercalcemia and hypophosphatemia

  • too much calcium and too little phosphate

-osteoporosis

-kidney stones

-constipation

-cardiac changes, HTN

-pancreatitis

-long bone, rib, and vertebral fractures

-polyuria

-N/V, anorexia

-fatigue, muscle weakness

Diagnostics:

-increased PTH levels

-increased serum calcium levels

-DEXA scan, MRI, CT, US

Treatment:

-complete or partial removal of parathyroid gland

-conservative therapy including regular measurements of serum PTH, calcium, and phosphorus  and DEXA scans

-IV sodium chloride and loop diuretics to increase urinary calcium excretion

-Bisphosphonates = inhibit osteoclastic bone resorption

  • take w/ full glass of water on empty stomach

  • sit upright 30 mins after taking

-Phosphates

-Calcimimetic agents = reduce PTH secretion

-Estrogen, phosphate binders

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Hypoparathyroidism

uncommon condition associated w/ inadequate circulating PTH

-most common cause is iatrogenic = accidental removal of parathyroid glands or damage to glands during neck surgery

-severe hypomagnesemia can suppress PTH secretion

  • malnutrition, renal failure, alcohol use

-other causes include tumors and heavy metal poisoning

Manifestations:

-hypocalcemia

-positive Chvostek and Trousseaus sign

-tetany = tingling of the lips and stiffening in the extremities

-osteosclerosis

-hypotension

-urinary frequency

-dysphagia, laryngospasms = compromise breathing

-muscle cramps

Diagnostics:

-decreased serum calcium and PTH

-increased phosphate levels

Treatment:

-emergency treatment for treatment of tetany = IV calcium

  • give slowly, use ECG monitoring to monitor hypotension, dysrhythmias, and cardiac arrest

-oral calcium, magnesium, and vitamin D supplements for maintenance therapy

-high calcium diet = dark leafy green vegetable, soybeans, and tofu

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Pheochromocytoma

rare condition characterized by a tumor in the adrenal medulla

-results in excess production of catecholamines (epinephrine, norepinephrine)

-may be inherited in persons w/ MEN (multiple endocrine neoplasia)

Manifestations:

-severe, episodic HTN

-severe pounding headache

-tachycardia w/ palpitations

-unexplained abdominal or chest pain

-can be induced by direct trauma, mechanical pressure to tumor, stress, and drugs

Diagnostics:

-24hr urine for catecholamines

-CT and MRI to detect tumors

Treatment:

-primary treatment is surgical removal of tumor = adrenalectomy

  • treat w/ alpha and beta blockers before surgery

  • alpha blockers (doxazosin, prazosin, phenoxybenzamine) started 10-14 days before surgery to reduce BP and prevent hypertensive crisis

  • once adequate alpha blocker level reached, beta blockers used to decrease tachycardia and dysrhythmias

-if surgery not an option metyrosine can decrease catecholamine production by the tumor

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Benign prostatic hyperplasia (BPH)

prostatev gland increases in size, disrupting the outflow of urine from th bladder through the urethra

-hormonal changes associated w/ aging a contributing factor

  • DHT stimulates prostate cell growth; excess DHT causes overgrowth of prostate tissue leading to BPH

  • as men age the amount of testosterone they make ↓ leading to higher proportion of estrogen; ↑ estrogen increases activity of BPH

-usually develops in inner part of prostate known as transition zone

  • gradually compresses urethra leading to partial or complete obstruction

Risk factors:

-aging

-obesity

-lack of physical activity

-high intake of red meat and animal fat

-alcohol use

-ED

-smoking

-diabetes

-family hx of 1st degree relative 

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BPH manifestations

occur gradually

Early symptoms:

-bladder may initially compensate for small amounts of resistance to urine flow

-symptoms worsen as obstruction increases

-LUTS (lower urinary tract symptoms): can be irritatve or obstructive

Irritative symptoms: related to inflammation or infection

-nocturia

-urinary frequency

-urgency

-dysuria

-bladder pain

-incontinence

Obstructive symptoms: caused by prostate enlargement

-decrease in caliber and force of urinary stream

-difficulty in starting a stream

-intermittency (stopping and starting several times while voiding)

-dribbling at end of urination

Symptom Index:

-AUA uses this tool to assess voiding symptoms

-not diagnostic but provides guidelines for treatment

-high score = increased symptom severity

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BPH complications

relatively rare

Acute Urinary Retention:

-sudden painful inability to urinate

-treatment involves inserting catheter to drain bladder

-surgery may be needed in severe situations

-bladder damage if treatment delayed

UTI:

-incomplete bladder emptying/residual urine allows for bacterial growth

-in severe cases infections can progress to kidney and cause pyelonephritis or spread into blood stream and cause sepsis

Bladder caliculi:

-dues to alkinization of residual urine

-bladder stones often indicate BPH

Renal failure:

-due to hydronephrosis

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BPH diagnostics

-history and physical assessment

-digital rectal exam (DRE) to evaluate size, symmetry, and consistency of prostate

-urinalysis, urine culture and sensitivities

-prostate specific antigen (PSA) level = may be slightly increased

-serum creatine, renal US

-neurologic exam

-postvoid residual (bladder scan)

-transrectal US if abnormal DRE and high PSA; biopsy

-MRI of pelvis; targeted biopsy

-Uroflowmetry = measures voulme of urine expelled from bladder

-cystoscopy

-urodynamic/pressure flow studies

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BPH interprofessional care

-treatment based on how bothersome symptoms are and presence of complications

-options = surveillance, drug therapy, or minimally invasive procedures

Conservative therapy:

-”watchful waiting” when pt has mild symptoms

-teaching about lifestyle changes

-diet changes = decreasing intake of bladder irritants, avoiding decongestants and anticholinergics, restricting evening fluid intake, and creating a timed voiding schedule

Drug therapy:

-5a reductase inhibitors and alpha adrenergic receptor blockers

-more effective when used in combo

-treatment guided by AUA symptom index

-tadalifil effectively reduces symptoms of both BPH and ED

-saw palmetto does not have supportive research evidence

Minimally invasive therapy:

-fewer adverse effects

-outcomes comparable to invasive techniques

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5a reductase inhibitors

finasteride, dutasteride, Jalyn (finasteride + tamsulosin)

-work by reducing size of prostate gland

-block enzyme necessary to make DHT

-more effective for men w/ larger prostates who have bothersome symptoms

-may lower risk of prostate cancer

-not recommended in prevention of prostate cancer

-discuss prostate screening w/ HCP

*women who may be or are pregnant should not touch tablets due to potential risk to male fetus (anomaly)

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alpha adrenergic receptor blockers

alfuzosin, doxazosin, prazosin, tamsulosin, silodosin

-offer symptom relief by relaxing smooth muscle of prostate that surrounds urethra, thus facilitating urinary flow through urethra

-DO NOT decrease size of prostate

-common side effect is retrograde ejaculation

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BPH minimally invasive surgeries

-Photo selective vaporization of prostate (PVP)

  • laser light, w/ visual or US guidance, used to vaporize prostate tissue

  • works well for larger prostate glands

  • increased urine flow and decreased symptoms immediate

  • irritative voiding symptoms persist for several weeks

-Laser enucleation of prostate

  • transurethral beam used for rapid coagulation and vaporization of prostatic tissue

  • HoLEP, ThuLEP; neither penetrate deep tissue

-Prostatic urethral lift (PUL)

  • permanent transprostatic implants or tension sutures delivered through the urethra via cystoscope

  • compress prostate tissue to mechanically open the prostatic urethra; no ablation

  • alters prostate tissue w/o ablating any tissue

-Transurethral microwave therapy (TMUT)

  • outpatient procedure; hold anticoagulants 10 days before procedure. Takes apporx. 90 min

  • -delivers heat via microwaves directly to prostate through transurethral probe

  • -heat (113 degrees F) causes death of tissue, relief of obstruction. Rectal probe monitors temp. to prevent rectal tissue damage

  • common complication = postprocedure urinary retention = urinary catheter for 2-7 days

  • antibiotics, pain medication, and bladder antispasmodic meds used to treat symptoms and prevent problems

-Transurethral needle ablation (TUNA)

  • heat delivered from low-wave frequency via needle to prostatic tissue leads to localized necrosis

  • only tissue in direct contact w/ needle affected

  • outpatient; approx. 30 min

-Transurethral vaporization of prostate (TUVP)

  • electrosurgical modification of TURP

  • vaporization and dessication destroy obstructive prostatic tissue

  • results, side effects, and long-term outcomes are the same as TURP

  • uses bipolar energy delivery surface

  • saline used for irrigation results in decreased risk for TUR syndrome

-Water vapor thermal therapy:

  • water vapor/steam destroys obstructive prostate tissue

  • transurethral delivery of steam by handheld device w/ retractable needle; 9 second doses

  • minimizes risk of post-procedure ED

  • newer procedure; long-term durability data pending

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BPH Invasive surgery

approach used depends on size and location of prostatic enlargement and pt factors s/a age and surgical risk

Indications:

-decreased urine flow causes discomfort

-persistent residual urine

-acute urinary retention

-hydronephrosis

Transurethral incision of prostate (TUIP):

-done under local anesthesia for men w/ moderate to severe symptoms

-several small incisions are made into prostate gland to expand the urethra

-relives pressure on urethra and improves urine flow

Transurethral resection of the prostate (TURP)

-removal of prostate tissue using a resectoscope inserted through the urethra

-gold standard for surgical treatment of obstructing BPH

-large 3-way indwelling catheter inserted after procedure to provide hemostasis and to facilitate urinary drainage

-assess for TUR or TURP syndrome

  • N/V, confusion, bradycardia, HTN

-other complications = bleeding and clot retention

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BPH nursing assessment

Subjective data:

-medications: testosterone supplementation

-surgery or other treatments: previous treatment for BPH

-Functional health patterns

  • health-perception-health management knowledge of condition

  • nutritional-metabolic: voluntary restriction

  • elimination: urinary urgency, diminution in caliber and force of urinary stream, hesitancy in initiating voiding, postvoid dribble, urinary retention, urinary incontinence

  • sleep-rest: nocturia

  • cognitive perceptual: dysuria, sensation of incomplete voiding, bladder discomfort

  • sexuality-reproductive: anxiety about sexual dysfunction

Objective data:

-general: older adult male

-urinary: distended bladder on palpation; smooth, firm, elastic enlargement of prostate on rectal examination

-possible diagnostic findings: enlargement on US, obstruction on cystoscopy, residual urine, urinalysis findings, increased creatinine levels

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Nursing management BPH

Health promotion:

-focuses on early detection and treatment of BPH

-some men find that consuming alcohol, caffeine, or other bladder irritants tends to increase prostatic voiding symptoms

-compounds found in common cough and cold remedies s/a pseudophedrine and pheylephrine often worsen symptoms of BPH

-teach pts w/ obstructive symptoms

  • urinate every 2-3 hrs and when first feel urge

  • maintain normal fluid level; restricting fluid actually increases risk of infection while concentrating urine

Acute care:

Pre-op care:

-antibiotics usually given before any invasive GU procedure

-UTI must be treated b4 surgery

-urinary drainage but be restored b4 surgery; urethral foley catheter may be needed

-provide opportunity for pt and partner to express concerns about sexual function

  • ejaculate volume may be ↓ or absent after procedure

  • retrograde ejaculation = some semen travels back into bladder instead of traveling out of penis; is NOT harmful

Post-op care:

-main complications are bleeding, bladdr spasms, urinary incontinence, and infection

-pt will have standard 2-way or 3-way catheter

  • bladder is irrigated either manually on intermittenent basis or more often as continuous bladder irrigation (CBI)

-urine drainage should be light pink w/o clots

-pt should avoid activities that increase abdominal pressure

  • sitting or walking for prolonged periods and straining during bowel movement

-bladder spams occur due to irrtation of bladder mucosa

  • chech catheter for clots, do not urinate around catheter, belladonna and opium suppositories for spasm and pain, antispasmodics, relaxation techniques

-remove catheter 2-3 days after surgery

sphinter tone may be poor right after catheter removal, resulting in urinary continence or dribbling

-can take several weeks to achieve urinary continence

-observe pt for signs of infection; avoid rectal procedures

-prevent straining = diet and stool softeners

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BPH ambulatory care

-teaching includes

  • caring for indwelling catheter

  • managing urinary incontinence

  • maintaining fluid intake

  • observing for s/sx of UTI and wound infection

  • preventing constipation

  • avoiding heavy lifting

  • refraining from driving or intercourse after surgery as directed by HCP

-sexual counseling and treatment options may be needed if ED becomes a chronic issue

-bladder may take 2 months to return to normal capacity

  • continue to drink 2-3 L/day and void every 2-3 hrs

-yearly DRE

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Prostate cancer

tumor of the prostate gland

-most common cancer among men excluding skin cancer

-most likely to develop in outer part of prostate called peripheral zone

-can spread via direct extension, through lymph system, or through the bloodstream

Risk factors:

-age, ethnicity, family hx

-incidence rises markedly after age 50

-diet high in red and processed meat and high-fat dairy products

-low intake of vegetables and fruits

-increased risk in farmers and commercial pesticide applicators

-not clear if smoking is risk factor

-having a family hx does not mean that a man will develop prostate cancer. It means that he has an increased risk

Manifestations:

-typically no symptoms in early stages

-eventually has LUTS similar to BPH

  • pain in lumbosacral area that radiates to hips or legs, when combined w/ LUTS may indicate metastasis

Complications:

-can spread to pelvic lymph nodes, bones, bladder, lungs, and liver

-once spread to distant sites, major problem becomes pain

-spread to bones = pain can become severe especially in back and legs

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Prostate cancer diagnostics

-PSA screening

  • many men live and die w/ prostate cancer, but most will not die from it

  • potential risks = subsequent evaluation and tretament that may not be needed

  • potential benefits = early detection of prostate cancer

  • men who want to be screened may have annual PSA test and DRE. On DRE abnormal prostate may feel hard, nodular, and asymmetric

-AUA states men ages 55-69 have greatest potential benefit for PSA screening and should be screened every 2yrs

-ACS recommends men decide about screening after they discuss info about risks and benefits w/ HCP. Should be discussed

  • age 50 if at average risk and expected to live at least 10 more years

  • age 45 if at high risk; blacks and medn who had 1st degree relative w/ prostate cancer at age less than 65 years

  • age 40 if even higher risk = more than one 1st degree relative w/ prostate cancer at an early age

-high PSA levels do NOT always indicate prostate cancer

  • aging, BPH, recent ejaculation, constipation, prostatitis, long bike rides, cystoscopy, indwelling urinary catheters, and prostate biopsies can cause increase

-neither PSA or DRE definitve diagnostic test for prostate cancer

-biopsy can confirm diagnosis of prostate cancer

-PSA uses to monitor treatment success; should decrease to undetectable levels

-indicators of advanced prostate cancer w/ bone metastasis

  • serum alkaline phosphate

-other tests used to determine location and extent of metastasis

  • whole body bone scan

  • CT scan of abdomen and pelvis

  • MRI of pelvis

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Prostate cancer interprofessional care

-finasteride and dutasteride, used to treat BPH, may reduce chance for getting prostate cancer

-early recognition and treatment are important to control tumor growth, prevent metastasis, and preserve qulaity of life

-most common classification system for determining extent of cancer is tumor, node and metastasis (TNM) system

-histologic grading systems = gleason scale, grade group

Gleason scale:

-tumors graded from 3-5

  • grade 3 = most well differentiated or lowest grade

  • grade 5 = most poorly differentiated or highest grade

-2 most commonly occurring patterns of cells are graded and then 2 scores are added together

  • score ranges from 6-10, lowest risk score is 6

Grade group system:

-grades cells bases on differentiation. Range 1-5. 1 lowest risk, 5 highest

-currently gleason and grade group used together, but trend id moving to grade group scoring only

-PSA level at diagnosis + gleason + grade group are used w/TNM system to stage tumor and determine treatment options

Active surveillance:

-strategy appropriate when

  • life expectancy less than 10 years

  • low grade, low-stage tumor and

  • serious coexsting medical condition

-pts followed w/ frequent PSA measurements and DRE to monitor progress of disease

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Prostate cancer surgical therapy

Radical prostatectomy:

-entire prostate gland, seminal vesicles, and part of bladder neck is removed

-pelvic lymph node dissection typically done at asme time to assess for nodal metastases in local pelvic area

-usually not an option for advanced disease except to releive symptoms from obstruction

-approaches = retropubic and perineal

  • robotic assisted prostateectomy = less bleeding, less pain, and faster recovery

-after surgery pt has indwelling urinary catheter. Drain is left in surgical site

-careful dressing changes and perineal care important after each bowel movement for comfort and infection prevention

-adverse outcomes are ED and urinary incontinence

  • overtime bladder adjusts, and most men regain urinary continence

  • kegel exercises may help

-other complications = bleeding, lymphocele, urinary retention, infection, wound dehisence, and VTE

Nerve sparing procedure:

-preserves nerves responsible for erection

-only for pts w/ cancer confined to prostate

-no guarantee that potency will be maintained

Cryotherapy:

-surgical technique that destroys cancer cells by freezing he tissue

-initial and second-line treatment after radiation therapy has failed

-liquid nitrogen = freezing agent delivered via TRUS probe

-complications

  • damage to urethra

  • urethrorectal fistula

  • urethrocutaneous fistula

  • tissue sloughing, ED, urinary incontinence, prostatitis, and bleeding

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Prostate cancer radiation therapy

may be used alone or in combo w/ surgery or hormone therapy

External beam radioation:

-most widely used method of delivering radiation treatments

-can be used to treated cancer confined to prostate and/or surrounding tissue

-outpatient basis 5 days a week for 4-8 weeks

-side effects may be acute or delayed

  • changes to skin, GI tract, urinary tract, and sexual function, fatigue

Brachytherapy:

-involves placing radioactive seed implants into prostate gland

-delivers high doses of radiation directly to tissue while sparing surrounding tissue

-1 time outpatient procedure; best suited for pts w/ early-stage disease

-most common side effect is development of irritative or obstructive urinary problems

-may have ED

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Prostate cancer drug therapy

-for treatment of advanced or metastatic prostate cancer

Androgen deprivation therapy:

-reduces levels of circulating androgens to reduce tumor growth

-deprivation can be produced by inhibiting androgen production or blocking androgen receptors

-hormone refractory tumors become resistant to therapy w/i a few years. High PSA often 1st sign therapy no longer effective

-increases serum cholesterol and triglycerides

-increases risk of osteoporosis and fractures

-may cause osteonecrosis of jaw

-includes drugs classes:

  • Androgen synthesis inhibitors = Lutenizing hormone releasing hormone agonists, LHRH antagonist, CYP17 enzyme

  • androgen receptor blockers

Chemotherapy:

-limited to treatment for those w/ hormone-resistant prostate cancer (HRPC) in late stage disease

-goal is mainly palliative

-sipuleucel T (provenge) prepared vaccine

  • combines pts WBCs w/ granulocyte macrophage colony- stimulating factors to attack prostate tumor cells

Radiotherapy:

-radium 223 dicholride

-for treatment of pts w/

  • castration-resistant prostate cancer

  • symptomatic bone metastasis

  • no known visceral metastatic disease

Orchiectomy:

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Androgen synthesis inhibitors

LHRH agonists:

-Goserelin, leuprolide, triptorelin

-super stimulate pituitary, downregulating LHRH receptors

-results in anterior pituitary unresponsive to LHRH; transient ↑ in LH and FSH

-leads to initial increase in testosterone production (flare), then LH and testosterone ↓

-aviailable in sub-q or IM injection

LHRH antagonists:

-degarelix = sub-q injection

-blocks LH and FSH receptos to lower testosterone

CYP17 enzyme inhibitor:

-abiraterone = given orally

-CYP17 needed to produce testosterone

-given w/ prednisone for castration-resisitant prostate cancer

-improves survival by 4-5 months

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Androgen receptor blockers

bicalutamide, enzalutamide, apalutamide, darolutamide, nilutamide

-compete w/ circulating androgens at receptor sites; blocks action of testosterone

-available in oral form

-can be combined w/ LHRH agonists for combined androgen blockade