N245: endocrine PPT notes

1. What is a hormone?
a. Chemical messenger
b. Carried by the bloodstream
c. Regulates physiologic/cellular processes
d. Under feedback control
e. Generally supports homeostasis
2. Regulation: Concept of negative feedback
a. The rate of hormone secretion may increase or decrease based on the level of
the hormones physiologic effects
b. As circulating levels of target gland hormones increase, stimulating hormone
secretion will decrease (and vice versa)
3. Overall function of hormones: classic/modernist view
a. Helps the organism respond to internal and external change
b. Adaptation theory
i. Change as stress
ii. Need to maintain homeostasis
c. Intimate connection with other messengers
i. Neuro-endocrine (mind-body axis)
4. Many diseases, medications, and treatments alter homeostasis
5. Endocrine disorders
a. Are related to either an excess or a deficiency of a specific hormone
b. Primary endocrine dysfunction is related to a deficit or excess in the gland
producing the hormone
c. Secondary endocrine dysfunction reflects an alteration in the process of
stimulating the gland
6. Homeostatic line of “hyper and hypo” to understand the effects of a
hormone/electrolyte
a. What does the hormone or electrolyte do?
b. In what form(s) does it circulate (bound, free, compound)?
c. What are the target organs/tissues?
d. What are the clinical effects of excess and deficiency states?
7. Emphasized content: thyroid hormone, anti-diuretic hormone, cortisol, aldosterone
8. Thyroid: extreme hypothyroidism (myxedema)  hypothermia coma
a. Lethargy
b. Paresthesias (numbness/tingling)
c. Hoarseness
d. Weight gain
e. Anxiety/depression
f. Cardiac problems
g. Anemia
h. Hyperlipidemia
i. Constipation
 j. Dry brittle hair/thickened skin
k. Intolerance to cold
l. Amenorrhea/menstrual changes
9. Thyroid: extreme hyperthyroidism (thyroid storm)  hyperthermia seizures
a. Fatigue
b. Anxiety/irritability
c. Proximal muscle weakness
d. Weight loss
e. Systolic hypertension
f. Arrhythmias/angina
g. Diarrhea/frequent stools
h. Heat intolerance
i. (?) eye changes
j. Oligomenorrhea/menstrual changes
k. Decreased fertility
10. Thyroid hormone axis
a. CNS  hypothalamus (thyrotropin-releasing hormone)  pituitary (thyroid
stimulating hormone)  hormone producing glad (target organ; T4 and T3) 
target tissues (physiologic effects; T4 converted to T3)
b. Hormone producing gland (target organ; adrenals for example) will send T3 and
T4 back to pituitary and hypothalamus in negative feedback mechanism
11. Actions and effects of thyroid hormone
a. Stimulates Na+ pump (increased cellular activity and metabolic rate – increased
O2 demand)
i. Increased GI motility
ii. CNS stimulation
b. Increased lipid mobilization uptake and clearance
c. Enhances B adrenergic responsiveness
i. Inotropic and chronotropic cardiac effects
d. Increases both secretion of and tissue demand for other hormones
12. Hypothyroidism
a. Metabolic processes slowed
b. Etiology
i. Primary: due to atrophy of gland or defective hormone synthesis, e.g.,
end result of Hashimoto’s thyroiditis, end stage Graves’ disease, iodine
deficiency, drug-related
ii. Secondary: inability of pituitary to secrete TSH
c. Manifestations can be insidious and on a continuum
d. Lethargy, weight gain, memory impairment, constipation, bradycardia,
decreased reflexes, menstrual irregularities
e. Complication: myxedema coma
13. Myxedema Coma
a. Life threatening hypofunction of the thyroid gland associated with thyroid
hormone deficiency
 b. Profound hypometabolism, hypothermia, hypoventilation, and depressed mental
functioning
c. Precipitated by discontinuance of an insufficient thyroid hormone replacement,
exposure to cold, trauma, infection, sedatives, anesthesia, narcotics, or
psychotropic drugs, antithyroid medications
d. Requires ventilator support, needs IV hormones (no PO because face/GI
tract/throat swells up and enteral absorption is impaired)
14. Hypothyroidism: nursing management
a. Patient/family education
i. The nature of the illness and its treatment
ii. The importance of continued self-administration of thyroid replacement,
signs of under and over dose
iii. Avoidance of foods and over-the-counter drugs high in iodide
b. Symptomatic intervention related to disease presentation, e.g., hypothermia,
imbalanced nutrition, constipation, activity intolerance
c. Levothyroxine (Synthroid, Levothyroid) supplements may take 4-6 weeks to be
effective
i. Iron, calcium, and soy supplements may interfere with absorption
15. Hyperthyroidism
a. Increased thyroid hormone synthesis and secretion
b. Results in excess circulation of T4 or T3 or both
c. Occurs in approximately 2% of women and 0.2% of men
d. Graves disease – most common form, an autoimmune disorder of unknown
etiology
e. Highest in ages 30-50
16. Graves disease
a. Diffuse thyroid enlargement and excessive thyroid hormone secretion
b. Precipitation factors: temporary insufficient iodine supply, infections, stressful
life events
c. Patient develops antibodies to the TSH receptor
d. Antibodies attach to receptors and stimulate the thyroid gland to release T3 and
T4
e. Palpation may reveal a goiter
f. Exophthalmos (proptosis) is a classic finding (abnormal protrusion of the eyeball)
i. Results from enlargement of the muscles, and fat within the orbit as a
result of mucopolysaccharide infiltration
ii. Leads to dry eyes and corneal abrasions
iii. Smokers are 4x more likely to develop this pathology
g. Other symptoms are on a continuum and attributed to excess thyroid hormones
i. E.g., fatigue, heat intolerance, weight loss
17. Hyperthyroidism: Complications
a. Thyrotoxic crisis (thyroid storm) – an acute rare condition in which all
hyperthyroid manifestations are heightened
b. Cause is presumed to be stressors – infection, trauma, surgery in a patient with
pre-existing hyperthryroidism
c. If untreated, can be life threatening
d. Thyroid storm
i. Manifestations: severe tachycardia, heart failure, shock, hyperthermia,
nausea, vomiting, diarrhea, agitation, delirium, seizures, coma
e. Treatment: reduce circulating thyroid hormone levels and clinical manifestations
i. Fever reduction, fluid replacement, and elimination or management of
initiating stressors
f. Don’t use aspirin because it breaks thyroid globulin bonds, increasing the
amount of free thyroid hormone
g. Diagnostic studies
i. Decreased TSH levels and elevated free thyroxine levels (FT4)
ii. Radioactive iodine uptake (RAIU) differentiates types of thyroid
dysfunction
iii. Normal: 8-30% in 24 hours
iv. Graves: 35-95%
v. Thyroiditis: <2%
h. Hyperthyroid management
i. Goal: to block adverse effects of thyroid hormones and stop over-
secretion
1. Drug therapy
2. Radioactive iodine therapy
3. Thyroidectomy
i. Drug therapy
i. Antithyroid drugs: inhibit the synthesis of thyroid hormones, e.g.,
propylthiouracil (PTU) and methimaolze (Tapazole)
ii. Iodine: inhibits synthesis of T3 and T4 and blocks release of hormones
into circulation (pre-surgery)
iii. Beta-adrenergic blockers: used for symptomatic relief of thyrotoxicosis
(due to excess thyroid hormone) that results from beta-adrenergic
stimulation from hormones, e.g., inderol, Tenormin (esp. with asthma
and HD)
iv. Radioactive iodine
1. Treatment of choice for non-pregnant adults
2. Damages and destroys thyroid tissue thus limiting thyroid
hormone secretion
3. Maximum effects: 2-3 months
4. High incidence of post-treatment hypothyroidism, resulting in
lifelong thyroid hormone replacement
j. Thyroidectomy
i. Thyroidectomy/subtotal thyroidectomy indicated for those patients who
are unresponsive to antithyroid meds, large goiters with tracheal
compression, and possible malignancy
 ii. Post-op complication: hypothyroidism, damage to parathyroid glands 
hypocalcemia, hemorrhage, injury to laryngeal nerves, injury to lymphatic
structures, thyrotoxic crisis, and infection
iii. Nursing management
1. Nutritional management
2. Medication education
3. Eye care: with exophthalmos there is potential for corneal injury,
orbital pain
a. Exercise eyes – complete ROM
b. Elevate HOB
c. Salt restriction
4. Management of thyroid storm
a. ICU based
b. Cardiac monitoring
c. Fluid and electrolyte replacement
d. Provide quite, calm, cool room
e. Antithyroid drugs administration
5. Pre- and post-thyroid surgery care
a. Pre-op: teach how to support head while turning, ROM of
neck
b. Post-op: pain control
c. Post op: emergency equipment available
i. Oxygen, suction, trach tray, calcium gluconate
d. Assess for post-surgical complications
i. Wound infection
ii. Laryngeal nerve damage – change in voice quality,
swallowing reflex and respiratory status
iii. Chyle leak due to dissection of lymph nodes and
damage to lymphatic ducts – monitor color,
consistency, and amount of wound drainage
iv. Hypocalcemia due to parathyroid damage
e. Replacement hormone teaching
18. Endocrine control of water balance
a. Antidiuretic hormone (or AVP – arginine vasopressin)
i. Produced in the hypothalamus and stored and released from the
posterior pituitary
ii. Promotes free water resorption mostly by regulating permeability of
distal tubules and collecting ducts
19. Osmolality: Solvent and solutes
a. Number of particles of solute per liter of solvent
b. Serum osmolality = 2x sodium + glucose/18 + BUN/3
c. 280-295 mOsmols is normal
20. Hypophysectomy is removal of the pituitary gland (reduced arginine vasopressin/anti-
diuretic hormone)
21. Causes of diabetes insipidus
a. Central (affecting hypothalamus or posterior pituitary)
i. Heredity, idiopathic, traumatic/post-surgical, neoplasms, ischemia,
granulomatous disease, infections, autoimmune disorders
b. Nephrogenic (disruption of countercurrent mechanism – kidney doesn’t respond
to ADH)
i. Heredity, hypokalemia, hypercalcemia, post renal obstruction, drugs,
sickle cell, amyloidosis, pregnancy
c. Primary DI is associated with excessive water intake
i. Structural lesion in thirst center
ii. Psychological disorder, e.g., schizophrenia
d. Clinical manifestations
i. Characterized by increased thirst (polydipsia) and increased urination
(polyuria)
ii. Excretion of large quantities of urine (5-20 L/day) with a low specific
gravity and urine osmolality (<100 mOsm/kg). Increased serum osmolality
(>292 mOsm/kg, hypernatremia >145 mEq/liter).
iii. Cardiac/vascular – tachycardia, orthostatic hypotension
iv. Skin – poor turgor, dry mucus membranes, decreased tears, sweat, and
saliva, weight loss
v. CNS – confusion, lethargy, seizures, coma
e. Head trauma – biphasic: DI presents in 3-6 days, persists for 7-10 days with
resolution
f. Post intracranial surgery – triphasic pattern
i. Acute phase – abrupt onset of polyuria
ii. Interphase – urine volume normalizes
iii. Third phase – 10 to 14 days post-op where central DI is permanent
g. Plasma and urine tests
h. Water deprivation test – helps differentiate primary polydipsia (compulsive
water drinking) from DI
i. Vasopression test – often done in conjunction with water deprivation test, helps
differentiate nephrogenic from central DI
22. Management: DI
a. Restore/maintain fluid and electrolyte balance
b. Fluid and hormone replacement – may be a lifelong need in central DI – replace
judiciously to avoid compartment shifts that are too rapid
c. Desmopresser (DDAVP) AVP analog – administer orally, IV, nasal spray
d. Nephrogenic DI – kidney unable to respond to ADH. Tx: dietary measures and
thiazide diuretics; Indocen – increases renal response to ADH
e. Daily weights – accurate I&Os
23. SIADH: syndrome of inappropriate anti-diuretic hormone
a. Will present with hyponatremia, decreased serum osmolality (normal range:
280-295 mOsms), and concentrated urine or elevated specific gravity (since
water not being excreted to dilute urine)
 b. Excess antidiuretic hormone (arginine vasopressin)
c. Characterized by fluid retention, serum hypoosmolality (<280 mOsm/kg),
dilutional hyponatremia (<130 mEq/L)
d. Most common cause of hyponatremia in adults
e. Most common cause of SIADH is small cell lung cancer
f. Other causes: trauma, tumor, infection, drugs
g. Clinical manifestations of syndrome of inappropriate anti-diuretic hormone
(SIADH)
i. CNS changes result from brain cell volume increase and swelling. S/Sx
include confusion. Headache, agitation, lethargy, dysarthrosis (a
condition of reduced joint motion due to deformity, dislocation, or
disease), impaired memory, weakness, hyporeflexia, seizures, coma
ii. General malaise, anorexia, nausea, and vomiting
iii. In severe cases, the ECF compartment will demonstrate fluid excess:
weight gain and mild edema
h. Diagnostic tests
i. Urine Na+ levels exceed 30 mEq/L
ii. Urine is hyperosmolar in relation to plasma hypoosmolality
iii. Urine specific gravity is elevated (>1.030)
iv. Normal renal, adrenal, and thyroid function tests
v. Inappropriate plasma ADH levels
vi. No evidence of volume depletion (e.g., dehydration) that may have
triggered an increase in ADH release
i. Treatment
i. Correct underlying problem
1. Stop chorpropamide (diabenese)
ii. Correct free water excess judiciously
1. Avoid rapid shifts between compartments
2. Fluid restriction (800-1000 mL/day) to decrease weight, permit
rise in serum Na concentration nd symptom improvement
3. Severe hyponatremia (Na < 120 mEq/L IV hypertonic saline (3-
5%). Use infusion pump
4. IV diuretic to promote diuresis if Na > 125 mEq/L
5. Chronic SIADH – fluid restriction and meds: declomycin, lithium –
block effects of ADH on renal tubules; daily weights
6. AVP receptor antagonists, e.g., conivaptan (IV), Tolvaptan (PO)
j. Address associated problems
i. Fatigue – energy conservation
ii. Safety issues – falls, memory issues
k. Monitor response to therapy
i. Mental status and neuro exam
ii. GI exam
iii. Functional exam
24. Glucocorticoid homeostatic line (polar ends are Addisonian and Cushingoid)
 a. Addisonian
i. Primary adrenal insufficiency
1. Glucocorticoid/mineralocorticoid
a. Volume depletion/dehydration
b. Hypotension
c. Hyponatremia/hyperkalemia
ii. Secondary adrenal insufficiency
1. Glucocorticoid deficiency
a. Hypotension
b. Dampened adrenergic response
c. Hypoglycemia
d. Impaired wound healing
e. Impaired stress/immune response
b. Cushingoid
i. Fluid retention
ii. Weight gain
iii. Protein wasting
1. Bone
2. Skin
3. Muscle
4. Blood vessel supports
iv. Hyperglycemia
v. Impaired wound healing
25. Cushing syndrome: Causes
a. Prolonged use of high-dose corticosteroids
b. ACTH secreting pituitary tumor (Cushing’s disease)
c. Cortisol-secreting neoplasm within adrenal cortex
d. Excess secretion of ACTH from lung carcinoma or other malignant growth
e. Hyperplasia
26. Cushing syndrome: Manifestations
a. Weight gain – from accumulation of adipose tissue in trunk, face, and cervical
area
b. Water retention, HTN, hyperglycemia
c. Protein wasting in extremities, weakness
d. Osteoporosis, fractures due to loss of bone matrix
e. Skin thinning, bruising, delayed wound healing
f. Mood disturbances – irritability, anxiety, psychosis
g. Acne and virilization in women, feminization in men
h. Gonadal dysfunction – in men, decreased libido and erectile dysfunction; in
women, menstrual irregularity
27. Cushing syndrome: Management
a. Surgical: removal of pituitary adenoma with transsphenoidal approach
b. Adrenalectomy for adrenal tumors or hyperplasia
 c. Drug tx: to inhibit adrenal. Adrenal blocking, e.g., Mitotane – used to produce a
“medical adrenalectomy”; neuromodulatory types under investigation
d. Alter corticosteroid tx protocol
28. Cushing syndrome: nursing care
a. Emotional support – changes in physical appearance can be devastating
b. Pre/post-op: control HTN, hyperglycemia, normalize electrolytes
c. Monitor VS, corticosteroid replacement
d. Risk of infections
e. Lifelong hormone replacement teaching
29. Adrenocortical insufficiency
a. Primary
i. Due to hypofunction of adrenal cortex as in Addison’s disease
b. Secondary
i. Due to lack of pituitary ACTH
30. Addison’s disease
a. All three classes of adrenal corticosteroids are reduced (glucocorticoids,
mineralocorticoids, androgens)
b. Most common cause – autoimmune response
c. Other causes: infarction, fungal infections, metastatic cancer, hemorrhage,
adrenal surgery
d. Manifestations
i. 90% of cortex is destroyed before symptoms are evident
ii. Slow insidious manifestation
1. Progressive weakness, fatigue, weight loss, anorexia
2. Skin hyperpigmentation
3. Hypotension, hyponatremia, hyperkalemia
4. Nausea, vomiting, diarrhea
e. Addisonian crisis
i. Triggered by stress – infection, surgery, trauma, psychologic distress
ii. Profound manifestations of glucocorticoid and mineralocorticoid
deficiencies – hypotension, tachycardia, dehydration – may lead to shock
iii. May also see acute abdominal pain, vomiting, hypoglycemia
iv. This type of shock responds poorly to usual treatment (vasopressors and
fluid replacement)
f. Management of Addison’s disease
i. Replacement therapy with hydrocortisone
ii. Patient teaching – to adjust dose during illness, physical, or psychological
stress to prevent crisis
iii. Need to check BP with mineralocorticoid replacement, e.g., Florinef
iv. Need for emergency kit