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7/30/2019 Endocrine Review II Revised
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Endocrine Review II
Ana Corona, MSN, FNP-C
Nursing InstructorJuly 2007
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Hypothyroidism
Can be caused by surgical removal of the thyroid gland Irradiation of the thyroid or pituitary Iodine deficiency Propylthiouracil
Prolonges excess ingestion of goitrogens Clinical Manifestations slow heart rate, decreased cardiac output, decreased
blood volume & BP decreased respiratory rate, anemia, subnormal basal
temperature, sensitivity to cold, impaired wound healing,easy bruising from capillary fragility,hypercholesterolemia, with increased risk of coronaryatherosclerosis
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Cretinism
Cretinism is a condition of severelystunted physical and mental growth due to
untreated congenital deficiency ofthyroidhormones (hypothyroidism).
The term cretin refers to a person so
affected.
http://en.wikipedia.org/wiki/Congenital_disorderhttp://en.wikipedia.org/wiki/Thyroidhttp://en.wikipedia.org/wiki/Hormonehttp://en.wikipedia.org/wiki/Hypothyroidismhttp://en.wikipedia.org/wiki/Hypothyroidismhttp://en.wikipedia.org/wiki/Hormonehttp://en.wikipedia.org/wiki/Thyroidhttp://en.wikipedia.org/wiki/Congenital_disorder7/30/2019 Endocrine Review II Revised
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Myxedema
Myxedema (British spelling: myxoedema) is askin and tissue disorder usually due to severeprolonged hypothyroidism.
Hypothyroidism can be caused by Hashimoto'sthyroiditis, surgical removal of the thyroid, andrarer conditions.
Partial forms of myxedema, especially of the
lower legs (called pretibial myxedema),occasionally occur in adults with Graves' disease,a cause of hyperthyroidism; or also Hashimoto'sthyroiditis without severe hypothyroidism.
http://en.wikipedia.org/wiki/Hypothyroidismhttp://en.wikipedia.org/wiki/Hashimoto%27s_thyroiditishttp://en.wikipedia.org/wiki/Hashimoto%27s_thyroiditishttp://en.wikipedia.org/wiki/Thyroidhttp://en.wikipedia.org/wiki/Pretibial_myxedemahttp://en.wikipedia.org/wiki/Graves%27_diseasehttp://en.wikipedia.org/wiki/Graves%27_diseasehttp://en.wikipedia.org/wiki/Pretibial_myxedemahttp://en.wikipedia.org/wiki/Thyroidhttp://en.wikipedia.org/wiki/Hashimoto%27s_thyroiditishttp://en.wikipedia.org/wiki/Hashimoto%27s_thyroiditishttp://en.wikipedia.org/wiki/Hypothyroidism7/30/2019 Endocrine Review II Revised
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Hyperthyroidism a disorder of hypermetabolism resulting from exposure
of the body tissues to excessive quantities of circulatingfree thyroxine, triiodothyronine or both
Often precipitated by severe emotional or physical stress
diagnosed most frequently at puberty or pregnancy orbetween age 30 -50 Pathophysiology Primary hyperthyroidism is also called Graves Disease Immunoglobulins (IgG) produce thyroid antibodies
similar to TSH but with stronger and longer lastingeffect.
The immunoglobulins bind at the TSH receptor sites &stimulate thyroid growth, increased vascularity &hypersecretion of thyroid hormone
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Hashimoto Thyroidism
Chronic Thyroiditis (Hashimotos Thyroiditis) Autoimmune disorder
Diagnosed by finding high titers of circulatingantithyriod antibodies Lymphocytic infiltration and fibrosis of the
thyroid tissue causes a small to moderate goiterand the patient eventually becomes hypothroidas the disease progresses
Treatment with thyroid hormone is used to treathypothyroidism when necessary
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Thyroid Cancer
Neoplasia
Can be benign or malignant
benign can secrete hormone or not
if secreting treated with radioactive iodineor surgery
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Toxic Goiter
Thyroid enlargement produces increasedsecretion of thyroid hormones
The increased hormone produces asustained hypermetabolic state
Results in increased oxygen consumption
& increased sensitivity & stimulation of thesympathetic nervous system
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Goiter
Simple Nontoxic Goiter
thyroid gland enlarges in response to the glands
inability to secrete enough thryoid hormone may develop during periods of increased
metabolic demand (adolescence or pregnancy)
iodine deficiency Neoplasia
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Exophthalmus
Exophthalmos
about 1/2 of the people with Graves disease
develop exopthalmos (an accululation of fluid inthe fat pads behind the eyeball & inflammatoryedema of the extraocular muscles)
This causes the eyeball to protrude
5% - 10% develop nonpitting edema of thepretibial area, ankles & dorsa of the feet thathas the appearance of orange peel (pretibial
myxedema)
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Hyperparathyroidism
Hyperparathyroidism Disorder of calcium metabolism caused by
excess secretion of parathyroid hormone causes increased resorption of Ca+ from the
bones, increased intestinal absorption, &increased reabsorption of calcium in the renaltubules with excess excretion of phosphorus.
Clinical manifestations of hyperparathyroidism Hypercalcemia & hypophosphatemia result calcium is deposited in tissues throughout the
body. Polyuria & excessive thirst may develop
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Hypoparathyroidism
Hypoparathyroidism
disorder of calcium metabolism
caused by inadequate secretion of parathyroid hormoneor failure of the target cells to respond to it
most common cause is iatrogenic
Iatrogenic Causes
accidental removal of the parathyroids during thyroidgland surgery
irradiation of the neck surgical removal of parathyroids to treat neoplasms or
hyperparathyroidism
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Addisons Disease
Adrenal Disorders
Divided into diseases of the cortex and
diseases of the medulla
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Addisons
Chronic primary adrenocortical insufficiency
Commonly results from idiopathic atrophy or
destruction of the adrenal cortex by anautoimmune process
Addisons Disease
Primary AD may happen alone or with other
autoimmune-related thyroid disease, insulin-dependent diabetes mellitus, premature gonadfailure & pernicious anemia
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Addisons
Secondary is caused by inadequate secretion ofadrenocorticotropic hormone (ACTH) either from
a pituitary or hypothalmic disorder or fromsupression of adrenal cortex function byexogenous steroid preparations
Pathologic changes usually develop aftr at least
90% of the glandualr tissue has been destroyed.
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Addisons Disease
Aldosterone deficiency of AddisonsDisease
Aldosteone deficiency results in decreasedsodium reabsorption in the kidneys andincreased potassium retention. Withsodium excretion clorides and water arealso excreted.
The result is fluid volume deficiency,hyponatremia, hyperkalemia and mild
alkalosis
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Addisons Disease
With the fluid volume deficit, renal perfusiondecreases, cardiac output decreases, BP fallsperipheral vascular collapse and hypovolemic
shock occur. This often fatal complication is called
Addisons crisis
Addisons Crisis
Crisis is usually precipitated by stress,infection, surgery, sudden withdrawl ofexogenous steroids, or fluid & salt loss duringexercise in hot weather
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Addisons Disease
Cortisol deficiency of Addisons Disease Cortisol deficiency results in inability to maintain normal
blood glucose levels between meals because ofimpaired gluconeogenesis.
Person gets weak, loses vigor, appetite and ability to
withstand stress or illness, and has impaired immuneresponse Loss of ACTH suppression decreased cortisol secretion results in loss of the
normal negative feedback suppression of ACTH
secretion. This causes increased melanin production leading to
hyper-pigmentation. May look suntaned or vitilago. Gums & mucous
membranes may become darker. Skin creases, pressure
areas, areolae & genitalia may get bronze colored
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Addisons
Androgen deficiency in Addisons Disease
Usually minimal effect on males (they
have testicular androgen)
Females get thin axillary & pubic hair,decreased libido, & amenorrhea
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Diagnosis Addisons Lab studies reveal low levels of plasma cortisol and low
24 hour urinary 17 hydroxycorticosteroids & 17ketostroids
Additionally potassium levels will be high, sodium &
clorides low and low glucose. Bun, creatinine will be highand eosinophiles and lymphocytes will be high
Treatment
Lifelong hormone replacement
Corisone acetate and hydrocortisone to replaceglucocorticoid activity
Fludrocortisone acetate (Florinef) to replacemineralocorticoid activity
Unrestricted salt intake
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Addisons Disease
With properly managed hormonereplacement therapy and patient educationto minimize the risk of Addisons crisis, aperson with Addisons Disease can expect to
live a normal, active life Possible Nursing Dx Risk for fluid volume deficit r/t loss of
extracellular sodium and water secondary to
mineralocorticoid insufficiency Risk for infection related to impaired glucose
regulating mechanisms, impaired immuneresponse & inability to tolerate stresssecondary to glucocorticoid insufficiency
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Primary Diabetes Insipidus
Primary Diabetes Insipidus is rare
Results from a tumor of the hypothalmus
or pituitary gland that destroys theportions of the hypothalmus thatmanufactures or regulates secretion of
ADH
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Secondary Diabetes Insipidus
Secondary diabetes insipidus is morecommon and results usually from head
trauma, surgical or irradiation injury orneoplastic or inflammatory processes thatexert pressure on the hypothalmus
Absence of ADH results in large amounts
of fluid & electrolytes being excreted inthe urine because the renal tubules do notreabsorb water.
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Clinical Manifestations
Patients can lose as much as 20 liters ofurine/day
Water loss causes polydipsia Urine is pale and the specific gravity is less than
1.006
anorexia and weight loss occur
People who cannot drink quickly becomedehydrated & sodium depletion & vascularcollapse develop rapidly
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Diagnosis
Water deprivation test - deprives thepatient of water to see if the plasma and
serum osmolality patient continues toexcrete urine in large volume with lowspecific gravity despite not taking in fluids
Vasopressin stimulation test - tests
whether the renal tubules fail toconcentrate urine (checks to see if it is akidney problem or head problem)
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Treatment Diabetes Insipidus
Vasopressin (the pharmacologic form ofADH) used if the problem is cerebral
edema Pitressin is Aqueous vasopressin has short
duration & is given q 6 -8 hrs Vasopressin
tannate is longer half life given q 36-72hrs
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Treatment
Desmopressin acetate (DDAVP) is given for longterm therapy (given intranasally - probably
through a straw) daily or bid Diapid is a synthetic vasopressin given as a
nasal spray tid or qid
Teach the patient to weigh daily and report 3%
weight loss
Teach how to take medication properly
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Hyperpituitarism
Hyperpituitarism is the result of excesssecretion of adenohypophyseal trophic
hormones most commonly by a functionalpituitary adenoma.
Other causes are hyperplasias and
carcinomas of the adenohypophysis,secretion by non-pituitary tumours andcertain hypothalamic disorders.
http://en.wikipedia.org/wiki/Hormoneshttp://en.wikipedia.org/wiki/Pituitary_adenomahttp://en.wikipedia.org/wiki/Pituitary_adenomahttp://en.wikipedia.org/wiki/Hormones7/30/2019 Endocrine Review II Revised
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Hypopituitarism
In hypopituitarism, there is an absence ofone or more pituitary hormones.
Lack of the hormone leads to loss offunction in the gland or organ that itcontrols.
For example, loss of thyroid stimulatinghormone leads to loss of function in thethyroid gland
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Acromegaly
Cardiomegaly develops r/t increasedworkload on heart
blood glucose, lipids and electrolyte levelscontribute to hypertension, coronaryatherosclerosis and CHF
The heart fails and premature deathensues
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Acromegaly
Hypersecretion of Somatotropin
Excess secretion of growth hormone
Occurs most commonly between the ages of 10& 40
If it happens before the epiphyses close,gigantism develops with excess of growth of theskeleton and soft tissues
If it happens after the epiphyses close thenacromegaly develops
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Clinical Manifestations Acromegaly
slow growth of may go undetected but personmay remember progressive increase in ring, hat,
shoe enlargement of ears & nose, circumference of
the chest, arthritic changes in joints & spine
Overgrowth of maxilla, projection of the
mandible - spaces between the teeth
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Gigantism
Growth is symetrical and proportional
May reach 8 -9 feet and 350 #
Have same internal manifestations asacromegaly
Muscle weakness, osteoporosis and arthritis arecommon
Cardiac hypertrophy develops at an early agewhich leads to CHF and premature death
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Diagnosis Gigantism continue
History, clinical manifestations and oldphotographs
elevated serum growth hormone levels -measured by radioimmunoassay (patient mustfast for 8 - 10 hours by free of stress & atcomplete rest for 30 minutes before the test
Normal levels of growth hormone is 10 ng/ml inaffected patients the level may reach 400 ng/ml
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Treatment Gigantism
Transsphenoidal microsurgery or a transfrontalcraniotomy if the tumor has extended to
surrounding structures Early diagnosis and treatment reduces the
severity of permanent alterations
Features may normalize somewhat (decrease in
soft tissue bulk) but bone growth that hasalready occurred does not reverse
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Syndrome of Inappropriate
Antidiuretic Hormone (SIADH) SIADH
Lack of control of ADH by hypothalmic
osmoreceptors results in excessive reabsorption of water in the
distal renal tubules, leading to expansionof extracellular fluid volume withhemodilution and dilutional hyponatremia
Treated by fluid restriction and diuretics
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Pheochromocytoma Usually benign
arise from the adrenal medulla (but sometimes outside theadrenal gland)
secrete catecholamines that results in heightenedphysiologic response
Pheocromocytoma symptoms
increased vasoconstriction, increased heart rate, increasedmyocardial contractility, irritability, increased metabolism,
oxygen utilization, increased respiratory rate, increasedglucogenolysis, decreased peristalsis, stimulation of sweatglands and pupilary dilation