Endocrine Review II Revised

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_disorder


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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/Hypothyroidism


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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/Hormones


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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

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Endocrine Review II Revised

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