This document discusses the endocrine system and various endocrine disorders. It describes the major glands of the endocrine system including the hypothalamus, pituitary, thyroid, parathyroid, adrenals, pancreas, ovaries/testes, kidneys, thymus and pineal gland. It then covers specific disorders such as hypothyroidism and hyperthyroidism, diabetes insipidus, SIADH, hyperparathyroidism, and their associated signs/symptoms, diagnostic tests, and treatment approaches including pharmacologic management and nursing care.
6. Adrenal Cortex
⚫ Mineralocorticoid—aldosterone.
Affects sodium absorption, loss of
potassium by kidney
⚫ Glucocorticoids—cortisol. Affects
metabolism, regulates blood sugar levels,
affects growth, anti-inflammatory action,
decreases effects of stress
⚫ Adrenal
androgens—dehydroepiandrosterone
and androstenedione. Converted to
testosterone in the periphery.
8. Thyroid
⚫ Follicular cells—excretion of
triiodothyronine (T3) and thyroxine (T4)—
Increase BMR, increase bone and calcium
turnover, increase response to
catecholamines, need for fetal G&D
⚫ Thyroid C cells—calcitonin. Lowers
blood calcium and phosphate levels
10. Pancreatic Islet cells
⚫ Insulin
⚫ Glucagon—stimulates glycogenolysis
and glyconeogenesis
⚫ Somatostatin—decreases
intestinal absorption of glucose
11. Kidney
⚫ 1, 25 dihydroxyvitamin D—
stimulates calcium absorption from
the intestine
⚫ Renin—activates the RAAS
⚫ Erythropoietin—Increases red blood
cell production
17. Assessment
⚫ Health history—energy level, hand and
foot size changes, headaches, urinary
changes, heat and cold intolerance,
changes in sexual characteristics,
personality changes, others
⚫ Physical assessment—appearance
including hair distribution, fat
distribution, quality of skin, appearance
of eyes, size of feet and hands, peripheral
edema, facial puffiness, vital signs
18. Diagnostic Evaluation
⚫ Serum levels of hormones
⚫ Detection of antibodies against
certain hormones
⚫ Urinary tests to measure by-products
(norepinephrine, metanephrines,
dopamine)
⚫ Stimulation tests—determine how an
endocrine gland responds to stimulating
hormone. If the hormone responds, then
the problem lies w/hypothalmus or
pituitary
⚫ Suppression tests—tests negative
feedback systems that control secretion
of hormones from the hypothalamus or
19. Disorders of the Pituitary
Pituitary Tumors
⚫ Eosinophilic tumors may result in
gigantism or in acromegaly. May suffer
from severe headaches, visual
disturbances, decalcification of the bone,
endocrine disturbances
⚫ Basophilic tumors may cause Cushing’s
syndrome w/features of
hyperadrenalism, truncal obesity,
amenorrhea, osteoporosis
⚫ Chromophobic tumors—90% of pituitary
tumors. Present with lowered BMR,
obesity, somnolence, scant hair, low
body temp, headaches, visual changes
20. ⚫ Growth hormone deficiency in childhood
will result in primary dwarfism.
22. Diabetes Insipidus
⚫ Deficiency of ADH
⚫ Excessive thirst, large volumes of dilute
urine
⚫ Can occur secondary to brain tumors,
head trauma, infections of the CNS, and
surgical ablation or radiation
⚫ Nephrogenic DI—relates to failure of the
renal tubules to respond to ADH. Can be
related to hypokalemia, hypercalcemia and
to medications (lithium demeocycline)
24. Assessment and Diagnostic Findings
⚫ Fluid deprivation test—withhold fluids
for 8-12 hours. Weigh patient frequently.
Inability to slow down the urinary output
and fail to concentrate urine are diagnostic.
Stop
test if patient is tachycardic or hypotensive
⚫ Trial of desmopressin and IV
hypertonic saline
⚫ Monitor serum and urine osmolality
and ADH levels
25. Pharmacologic Tx and Nursing
Management
⚫ DDAVP—intranasal bid
⚫ Can be given IM if necessary. Every 24-
96h. Can cause lipodystrophy.
⚫ Can also use Diabenese and thiazide
diuretics in mild disease as they potentiate
the action of ADH
⚫ If renal in origin—thiazide diuretics,
NSAIDs (prostaglandin inhibition) and salt
depletion may help
⚫ Educate patient about actions of
medications, how to administer meds, wear
medic alert bracelet
26. SIADH
⚫ Excessive ADH secretion
⚫ Retain fluids and develop a
dilutional hyponatremia
⚫ Often non-endocrine in origin—such
as bronchogenic carcinoma
⚫ Causes: Disorders of the CNS like head
injury, brain surgery, tumors, infections or
medications like vincristine,
phenothiazines, TCAs or thiazide diuretics
⚫ Meds can either affect the pituitary or
increase sensitivity to renal tubules to
ADH
⚫ Management: eliminate cause, give
diuretics (Lasix), fluid restriction, I&O,
27. SIADH
⚫ Restoration of electrolytes must be
gradual
⚫ May use 3% NaCl in conjunction with
Lasix
28. Thyroid
⚫ T3 and T4
⚫ Need iodine for synthesis of hormones—
excess will result in adaptive decline in
utilization called the Wolf-Chaikoff
mechanism
⚫ Thyroid is controlled by TSH
⚫ Cellular metabolism, brain development,
normal growth, affect every organ in the
body
⚫ T3 is five times as potent as T4
⚫ Calcitonin—secreted in response to high
levels of serum calcium, increases
29. Thyroid
⚫ Inspect gland
⚫ Observe for goiter
⚫ Check TSH, serum T3 and T4
⚫ T3 resin uptake test useful in evaluating
thyroid hormone levels in patients who
have received diagnostic or therapeutic
dose of iodine. Estrogens, Dilantin,
Tagamet, Heparin, amiodarone,
PTU,steroids and Lithium can cloud the
accuracy
⚫ T3 more accurate indicator of
hyperthyroidism according to
text
30. Thyroid
⚫ Antibodies seen in Hashimoto’s, Grave’s
and other auto-immune problems.
⚫ Radioactive iodine uptake test measures
rate of iodine uptake. Patients with
hyperthyroidism exhibit a high uptake,
hypothyroidism will have low uptake
⚫ Thyroid scan—helps determine the
location, size, shape and size of gland.
“Hot” areas (increased function) and
“cold” areas (decreased function) can
assist in diagnosis.
31. Nursing Implications
⚫ Be aware of meds patient is taking (see list
in text) that can affect accuracy of testing
⚫ Also be aware if patient is taking
multivitamins and food
supplements
32. Hypothyroidism
⚫ Most common cause is Hashimoto’s thyroiditis
⚫ Common in those previously treated
for hyperthyroidism
⚫ Atrophy of gland with aging
⚫ Medications like lithium, iodine
compounds, antithyroid meds can cause
⚫ Radiation treatments to head and neck
⚫ Infiltrative diseases like amyloidosis,
scleroderma
⚫ Iodine deficiency and excess
⚫ Hypothalamic or pituitary abnormality
⚫ More common in women, especially over age
50
33. Manifestations
⚫ From mild symptoms to myxedema
⚫ Myxedema –accumulation of
mucopolysaccharides in sc and
interstitial tissues. Is the extreme form
of hypothyroidism. Can progress to
shock.
⚫ S/S—fatigue, hair loss, dry skin, brittle
nails, numbness and tingling of the
fingers, amenorrhea, weight gain,
decreased heart rate and temperature,
lassitude, cognitive changes, elevated
cholesterol levels, constipation,
hypotension
34. Pharmacologic Management of
hypothyroidism
⚫ Levothyroxine is preferred agent
⚫ Dosage is based on TSH
⚫ Desiccated thyroid used infrequently due
to inconsistent dosing
⚫ Angina can occur when thyroid
replacement is initiated as it enhances
effects of cardiovascular catecholamines
(in pt. w/pre- existent CAD). Start at low
dose.
⚫ Hypnotics and sedatives may have
profound effects on sensorium
35. Management in Myxedema
⚫ Cautious fluid replacement
⚫ Glucose to restore to normal glycemic
levels
⚫ Avoid rapid overheating due to
increased oxygen demands but keep
warm
⚫May give levothyroxine
intravenously With recovery,
⚫ Modify activity
⚫ High fiber foods
⚫ Home health for follow-up
36. Hyperthyroidism
⚫ Extreme form is Grave’s disease
⚫ Caused by thyroiditis, excessive
amount thyroid hormone, abnormal
output by immunoglobulins
⚫ Is more common in women
37. Manifestations of hyperthyroidism
⚫ Thyrotoxicosis—nervousness, irritable,
apprehensive, palpitations, heat
intolerance, skin flushing, tremors, possibly
exophthalmos
⚫ Have an increased sensitivity
to catecholamines
⚫ Can occur after irradiation or presence
of a tumor
38. Assessment and Diagnosis
⚫ Thyroid thrill and or bruit may be
present
⚫ Thyroid may be enlarged
⚫ Decreased TSH, increased free T4 and
an increased radioactive iodine
uptake
39. Management
⚫ Reduce thyroid hyperactivity—usually
use radioactive iodine, antithyroid meds
or surgery)
⚫ Beta blockers
⚫ Can be relapse with antithyroid meds
40. Pharmacologic Therapy
⚫ Irradiation with administration of
radioisotope iodine 131—initially may
cause an acute release of thyroid
hormones. Should monitor for thyroid
storm
⚫ S/S of thyroid storm—high fever.
Tachycardia, delirium, chest pain, dyspnea,
palpitations, weight loss, diarrhea,
abdominal pain
⚫ Management of thyroid storm—oxygen,
IV fluids with dextrose, hypothermic
measures, steroids to treat shock or adrenal
deficiency, iodine to decrease output of T4,
beta blockers, PTU or Tapazole impedes
41. Antithyroid Medications
⚫ PTU—propylthiouracil—blocks
synthesis of hormones
⚫ Tapazole (methimazole)—blocks synthesis
of hormones. More toxic than PTU.
⚫ Sodium Iodide-suppresses release of
thyroid hormone
⚫ SSKI (saturated solution of potassium
chloride)– suppresses release of
hormones and decreases vascularity of
thyroid. Can stain teeth
⚫ Dexamethazone—suppresses release
of thyroid hormones
42. Surgical Management
⚫ Reserved for special circumstances, e.g.
large goiters, those who cannot take
antithyroid meds, or who need rapid
normalization
⚫ Subtotal thyroidectomy
⚫ Before surgery, give PTU until s/s
of hyperthyroidism have
disappeared
⚫ Iodine may be used to decrease
vascularity
43. Nursing Management
⚫ Reassurance r/t the emotional
reactions experienced
⚫ May need eye care if has exophthalmos
⚫ Maintain normal body temperature
⚫ Adequate caloric intake
⚫ Managing potential complications such
as dysrhythmias and tachycardias
⚫ Educate about potential s/s of
hypothyroidism following any antithyroid
tx.
44. Parathyroid Glands
⚫ Parathormone maintains sufficient
serum calcium levels
⚫ Excess calcium can bind with phosphate
and precipitate in various organs, can
cause pancreatitis
⚫ Hyperparathyroidism will cause bone
decalcification and development of
renal calculi
⚫ More common in women
⚫ Secondary hyperparathyroidism occurs
in those with chronic renal failure and
renal rickets secondary to excess
phosphorus retention (and increased
parathormone secretion)
45. Manifestations of
Hyperparathyroidism
⚫ May be asymptomatic
⚫ Apathy, fatigue, muscle weakness,
nausea, vomiting, constipation,
hypertension and cardiac
dysrhythmias
⚫ Excess calcium in the brain can lead
to psychoses
⚫ Renal lithiasis can lead to renal damage
and even failure
⚫ Demineralization of bones with back and
joint pain, pain on weight bearing,
pathologic fractures
46. Assessment and Diagnostic Findings
⚫ Persistent elevated calcium levels
⚫ Elevated serum parathormone level
⚫ Bone studies will reveal decreased density
⚫ Double antibody parathyroid hormone
test is used to distinguish between
primary hyperparathyroidism and
malignancy
⚫ Ultrasound, MRI, thallium scan, fine
needle biopsy also can be used to
localize cysts, adenomas, or hyperplasia
47. Management
⚫ Recommended treatment for
hyperparathyroidism is surgical
removal
⚫ Hydration therapy necessary to prevent
renal calculi
⚫ Avoid thiazide diuretics as they decrease
renal excretion of calcium
⚫ Increase mobility to promote bone retention
of calcium
⚫ Avoid restricted or excess calcium in the diet
⚫ Fluids, prune juice and stool softeners to
prevent constipation
⚫ Watch for s/s of tetany postsurgically
(numbness, tingling, carpopedal spasms) as
well as cardiac dysrhythmias and hypotension
48. Hypercalcemic crisis
⚫ Seen with levels greater than 15mg/dL
⚫ Can result in life-threatening
neurologic, cardiovascular and renal
symptoms
⚫ Treatments include: hydration, loop
diuretics to promote excretion of calcium,
phosphate therapy to promote calcium
deposition in bone and reducing GI
absorption of calcium
⚫ Give calcitonin or mithramycin to
decrease serum calcium levels quickly
49. Hypoparathyroidism
⚫ Seen most often following removal of
thyroid gland, parathyroid glands or
following radical neck surgery
⚫ Deficiency of parathormone results in
increased bone phosphate and
decreased blood calcium levels
⚫ In absence of parathormone, there is
decreased intestinal absorption of dietary
calcium and decreased resorption of
calcium from bone and through kidney
tubules
50. Clinical Manifestations of
Hypoparathyroidism
⚫ Irritability of neuromuscular system
⚫ Tetany—hypertonic muscle contractions ,
numbnes, tingling, cramps in extremities,
laryngeal spasm, bronchospasm,
carpopedal spasm ( flexion of the elbows
and wrists, dorsiflexion of the feet),
seizures
51. Assessment and Diagnostic Findings
⚫ Trousseau’s sign—can check with a BP
cuff
⚫ Chvostek’s sign—tapping over facial
nerve causes spasm of the mouth, nose
and eye
⚫ Lab studies may reveal calcium levels of
5-6 mg/dL or lower
⚫ Serum phosphate levels will be
decreased
52. Management of Hypoparathyroidism
⚫ Restore calcium level to 9-10 mg/dL
⚫ May need to give IV calcium gluconate
for immediate treatment
⚫ Use of parathormone IV reserved for
extreme situations due to the probability of
allergic reactions
⚫ Monitor calcium levels
⚫ May need bronchodilators and
even ventilator assistance
⚫ Diet high in calcium and low in
phosphorus; thus, avoid milk products,
egg yolk and spinach.
53. Management of Hypoparathyroidism
⚫ Keep calcium gluconate at bedside
⚫ Ensure has IV access
⚫ Cardiac monitoring
⚫ Care of postoperative patients who have
undergone thyroid surgery,
parathyroidectomy or radical neck
surgery. Be watchful for signs of tetany,
seizures, and respiratory difficulties
54. Adrenals--Pheochromocytoma
⚫ Usually benign tumor
⚫ Originates from the chromaffin cells of
the adrenal medulla
⚫ Any age but usu. Between 40-50 years old
⚫ Can be familial
⚫ 10% are malignant
⚫ May be associated with thyroid carcinoma
or parathyroid hyperplasia or tumor
55. Clinical Manifestations
⚫ Headache, diaphoresis,
palpitations, hypertension
⚫ May have hyperglycemia related to
excess epinephrine secretion
⚫ Tremors, flushing and anxiety as well
⚫ Blurring of vision
⚫ Feeling of impending doom
⚫ BPs exceeding 250/150 have occurred
56. Assessment and Diagnostic Findings
⚫ Associated with the 5 H’s—hypertension,
headache, hyperhidrosis, hypermetabolism
and hyperglycemia
⚫ Urinary catecholamines and metanephrine
are direct and conclusive tests
⚫ Serum epinephrine and norepinephrine
levels will be elevated
⚫ Urinary vanillymandelic acid also diagnostic
⚫ Must avoid coffee, tea, bananas,
chocolate, vanilla and ASA, nicotine,
amphetamines, decongestants before
24h urine testing
⚫ Clonidine suppression test—in normal
individual, would block catecholamine release
⚫ Imaging studies
57. Management
⚫ Bedrest
⚫ Elevated HOB
⚫ ICU
⚫ Nipride
⚫ Calcium channel blockers and Beta
blockers
⚫ Surgical management (manipulation of
the tumor can cause excessive release of
catecholamines)
⚫ Steroid therapy if adrenalectomy
performed
⚫ Hypotension and hypoglycemia can
58. Addison’s Disease
⚫ Adrenocortical insufficiency
⚫ Autoimmune or idiopathic atrophy
⚫ Can be caused by inadequate ACTH
from pituitary
⚫ Therapeutic use of steroids
59. Manifestations
⚫ Muscle weakness
⚫ Anorexia
⚫ Dark pigmentation
⚫ Hypotension
⚫ Hypoglycemia
⚫ Low sodium levels
⚫ High potassium levels
⚫ Can result in Addisonian
crisis
60. Addisonian crisis
⚫ Circulatory shock
⚫ Pallor, apprehension, weak&rapid
pulse, rapid respirations and low blood
pressure
⚫ Headache, nausea, abdominal pain
and diarrhea
⚫ Can be brought on by overexertion,
exposure to cold, acute infection, decrease
in salt intake
61. Assessment and Diagnostic Findings
⚫ Early morning serum cortisol and plasma
ACTH are performed. Will distinguish
between primary and secondary adrenal
insufficiency. In primary, will have elevated
ACTH levels and below normal cortisol
levels.
⚫ If the adrenal cortex is not stimulated by
the pituitary, a normal response to doses
of exogenous ACTH (see text)
⚫ Blood sugar levels and electrolyte values
62. Management
⚫ Restore circulatory status—fluids, steroids
⚫ May need antibiotics if infection
precipitated crisis
⚫ May need lifelong steroid therapy
and mineralocorticoid therapy
⚫ May need additional salt intake
⚫ Check orthostatics
⚫ Daily weights
⚫ Aware that stressors can precipitate crises
⚫ Medic alert bracelet or similar
identification of history
63. Cushing’s Syndrome
⚫ Results from excessive adrenocortical
activity
⚫ May be related to excessive use of
corticosteroid medications or due
to hyperplasia of the adrenal
cortex
⚫ Oversecretion of corticosteroids can also
be caused by pituitary tumor
⚫ Can be caused by bronchogenic
carcinoma or other malignancy
65. Assessment and Diagnostic Findings
⚫ Overnight dexamethasone suppression
test frequently used for diagnosis
⚫ Administered at 11pm and cortisol
level checked at 8am
⚫ Suppression of cortisol to less than
5mg/dL indicates normal functioning
⚫ Measurement of plasma ACTH
(radioimmunoassay) in conjunction with
dexamethasone suppression test helps
distinguish pituitary vs. ectopic sites of
ACTH.
⚫ MRI, CT and CT also help detect tumors
of adrenal or pituitary
66. Medical Management
⚫ If pituitary source, may warrant
transphenoidal hypophysectomy
⚫ Radiation of pituitary also appropriate
⚫ Adrenalectomy may be needed in case of
adrenal hypertrophy
⚫ Temporary replacement therapy
with hydrocortisone or Florinef
⚫ Adrenal enzyme reducers may be indicated if
source if ectopic and inoperable. Examples
include: ketoconazole, mitotane and
metyrapone.
⚫ If cause is r/t excessive steroid therapy,
tapering slowly to a minimum dosage may be
appropriate.
67. Primary Aldosteronism or Conn’s
Syndrome
⚫ Excessive aldosterone secondary to
adrenal tumor
⚫ retain sodium and excrete potassium
⚫ Results in alkalosis
⚫ Hypertension—universal sign
of hyperaldosteronism
⚫ Inability of kidneys to concentrate the
urine
⚫ Serum becomes concentrated
⚫ Excessive thirst
⚫ Hypokalemia interferes with insulin
secretion thus will have glucose
68. Assessment and Diagnostic Findings
⚫ High sodium
⚫ Low potassium level
⚫ High serum aldosterone level
⚫ Low renin level
⚫ Aldosterone excretion rate after salt
loading is diagnostic for primary
aldosteronism
⚫ Renin-aldosterone stimulation test
69. Management
⚫ Surgical removal of tumor
⚫ Correct hypokalemia
⚫ Usual postoperative care with
abdominal surgery
⚫ Administer steroids
⚫ Fluids
⚫ Monitoring of blood sugar
⚫ Control of hypertension with
spironolactone
71. Indications
⚫ RA
⚫ Asthma
⚫ MS
⚫ COPD exacerbations
⚫ Lupus
⚫ Other autoimmune
disorders
⚫ Dermatologic disorders
72. Dosing
⚫ Lowest dose
⚫ Limited duration
⚫ Best time to give dose is in early
morning between 7-8 am
⚫ Need to taper off med to allow normal
return of renal function
73. Side Effects of Steroids
⚫ Hypertension, thrombophlebitis,
accelerated atherosclerosis
⚫ Increased risk of infection
⚫ Glaucoma and corneal lesions
⚫ Muscle wasting, poor wound
healing, osteoporosis, pathologic
fractures
⚫ Hyperglycemia, steroid withdrawal
syndrome
⚫ Moon face, weight gain, acne
74. Case Study 1
⚫ 35 year old male presents with BP of
188/112 at a yearly physical exam.
Previous exams noted blood pressures of
160/94 and 158/92. On questioning, patient
admits to twice a month episodes of
apprehension, severe headache,
perspiration, rapid heartbeat, and facial
pallor. These episodes had an abrupt
onset and lasted 10-15 minutes.
⚫ Routine hematology and chemistry
studies are wnl and chest xray and ECG
are normal.
⚫ What is your impression?
⚫ What labs would you draw?
75. Case Study 2
⚫ 50 year old woman presents with
enlargement of left anterior neck. She has
noted increased appetite over the past
month with no weight gain, and more
frequent bowel movements over the same
period. Patient feels jittery at times,
experiences palpitations and feels “hot” a
lot recently.
⚫ She is 5’8” tall and weighs 150#. Heart rate
is 110 and blood pressure is 110/76.
⚫ What might be this patient’s problem?
⚫ What lab tests might you draw?
76. Case study 3
⚫ 48 year old woman with a past history of
mental illness presents with a new onset
of bizarre psychotic behavior. She had
been well over the past two years.
⚫ She is 5’5” tall and weighs 138#. Her
heart rate is 65, irreg and BP is 130/75.
Exam is normal except that she is confused
to place, time and year. Patient c/o joints
aching and of feeling fatigued.
⚫ Lab tests reveal serum calcium level of
13.8mg/dL (reference range is 8.4-10.1)
⚫ Phosphorus is 2.4 (reference range is 2.5-
4.5)
⚫ What is your diagnosis?
77. Case Study 4
⚫ 40 year old deeply tanned woman presents
with a 6 month history of increasing
fatigue. For the past three months she has
suffered from recurrent URIs, poor
appetite, abdominal cramps, fatigue and
diarrhea. She has lost 25#. She has noted
joint pains, muscle weakness, and has not
menstruated for the past 3 months.
⚫ Labs reveal blood glucose of 59, Na+ 130,
K+ 6.0.
⚫ What disorder do you expect?
78. Case Study #5
⚫ 27 year old woman presents with depression,
insomnia, increased facial fullness and recent
increase in acne. She had an episode of
depression and acute psychosis following
uncomplicated delivery of normal baby boy 9
months previously. Her menses have been
irregular since their resumption after the birth
(she is not breast feeding). Patient relates has
had several vaginal yeast infections recently.
⚫ Heart rate is 90bpm, BP is 146/100. Her face is
puffy and has acne vulgaris. Thin extremities
and with truncal obesity.
⚫ What are your suspicions?
⚫ What labs will you draw?