Endocrine System

Nursing of Adults & Children III

ENDOCRINE SYSTEM

 

Endocrine System

One of 2 major controlling and communicating systems of the body

--Endocrine System

--Central Nervous System

The 2 systems help to coordinate and direct the activity of the body’s cells

Built for speed

Uses nerve impulses to prod the organs into immediate action so that rapid adjustment can be made in response to changes occurring both inside & outside the body

Uses chemical messengers or hormones, which are released into the blood and transported throughout the body

Regulates continuing processes that go on for a relatively long period of time

Chemical substances synthesized from amino acids & cholesterol that act on body tissues & organs and affect cellular activity

Controlled by a negative feedback system

Also called the "hypophysis"

Has 2 lobes

--anterior pituitary

--posterior pituitary

Called the "Master Gland" because it stimulates hormones that stimulate the release of other hormones from target glands including

-thyroid gland

-parathyroid glands

-adrenal glands

-gonads

Secretes 2 hormones

-antidiuretic hormone (ADH)

-oxytocin

one located atop each kidney

composed of 2 compartments

-adrenal medulla (inner section)

-adrenal cortex (section surrounding the medulla)

secretes catecholamines

-epinephrine (adrenaline)

-norepinephrine

results in "fight or flight" response

a small, usually benign tumor that typically arises within the adrenal medulla

the tumor secretes epinephrine and norepinephrine

S/S of the tumor are directly r/t the amount of these 2 hormones released

can cause death

The effects of epinephrine and norepineprhine OUT OF CONTROL!!!

Sx may occur spontaneously or may be precipitated by stress, a change in position, physical activity, the Valsalva maneuver, etc.

Episodes may last from few minutes to hours

Hypertension (primary sx)

---may be persistent or intermittent

---BP as high as 300/180

Severe headache (accompanies ^ BP)

(typically pt has attacks of ^ BP accompanied by pounding headaches)

Other s/s of sympathetic overactivity:

-sweating

-apprehension/feeling of impending doom

-palpitations/tachycardia

-N/V

-heat intolerance

-tremors

S/S of DM (b/o catecholamine release results in conversion of large amts of glycogen into glucose within the liver)

-polyuria, polydipsia, polyphagia,

fatigue, glucosuria, etc.

Dilated pupils

Cool>>>>cold extremities

Increased metabolic rate & wt loss

The severe hypertension may precipitate CVA or sudden blindness

Cardiac dysrhythmias

Without early intervention, permanent CV damage and death from cerebral hemorrhage, cardiac failure, and/or kidney failure

Because pheochromocytoma is potentially curable, early & accurate dx is essential

Complete H&P

Total Plasma Catecholamine levels

-epinephrine & norepinephrine levels

Vanillylmandelic Acid (VMA) level

-can be a single 1st a.m. voided spec (not very definitive)

-preferably a 24 hour collection is done

-preservative is needed (usually HCL acid)

-Normal = 14 mcg/100 ml or 7 mg or less

per 24 hours

Urinary tests may yield false positives b/o

Certain foods such as cheese, chocolate, citrus fruit, or bananas, beer, wine, caffeine, vitamins B & C

Certain medicines such as antibiotics and antihypertensives

Tests to localize a tumor

-E.g., CT, MRI, Ultrasound, IVP,

mataiodobenzylguanidine (MIBG) Scintigraphy

Bedrest

Surgical excision of the tumor

-scheduled only after pt normotensive for at least one week

-primary medical intervention

-adrenalectomy

-complications

Medications

Acute TX--

Intravenous alpha-adrenergic and Beta-adrenergic drugs such as

phentolamine (Regitine)

nitroprusside (Nipride)

propranolol (Inderal

Oral agents given after stabilization and for ongoing medical tx

propranolol (Inderal)

calcium channel blockers

phenoxybenzamine (Dibenzyline)

metyrosine (Demser)

Dibenzyline (an alpha-adrenergic blocker

metyrosine (a hydroxylase inbibitor that blocks the conversion of tyrosine to norepinepherine

During Acute Episode

Pre-op Management

Post-op Management

Assessment

Diagnoses (Problem List)

Goals/Outcomes

Interventions with rationales

Evaluation

Secretes

-Glucocorticoids (Cortisol, Cortisone)

-Mineralocorticoids (Aldosterone)

-Sex Hormones

androgen

estrogen, progesterone

Release is regulated by ACTH from the anterior pituitary

Affected by

-serum cortisol level

-diurnal sleep/wake cycle

-stress level

Functions:

1. Promotes gluconeogenesis (anti- insulin effect

2. Activates anti-inflammatory responses to stressors

Functions: (continued)

3. Influence cognitive & emotional fxs

4. Suppresses immune responses

5. Cause Na & H2O) retention by increased aldosterone secretion

 

 

Aldosterone

-regulates sodium and water retention

-regulates potassium secretion

Aldosterone

-regulated by renin-angiotensin system

Aldosterone

-regulated by renin-angiotensin system

-when a decr in BP or sodium is detected special kidney cells release renin

Aldosterone (continued)

-renin acts on angiotensinogen (from liver)

-angiotensinogen becomes angiotensin

-angiotensin stimulates release of aldosterone from adrenal cortex

 

Androgen (small amount secreted by adrenal cortex)

Estrogen/progesterone (very small amount secreted by adrenal cortex)

More currently called Chronic Primary Adrenal Insufficiency

Condition resulting from insufficient hormone production by the adrenal cortex

Fairly rare condition---affects approx 4 in 100,000 persons

Causes:

-idiopathic origin (probably autoimmune)

-adrenal cortex destruction associated with infections, CA, radiation, chemotherapy

-surgical removal of adrenal gland(s)

Secondary Adrenal Insufficiency

-Pituitary insufficiency (secreting too little ACTH

-Sudden cessation of exogenous

adrenocortical hormones

-Hemorrhage

Onset is slow

-sx mild early on

-usually weeks or months before sx severe enough for seeking health care

-as disorder progresses, sx increase

-symptoms usually occur after 90% of gland function is lost

Causes increased Na+ excretion resulting in

-increased water excretion

-ECF volume depletion (dehydration)

-hypotension

-decreased cardiac output

-K+ retention (dysrhythmias, cardiac arrest)

-shock, death

Deficiency causes widespread metabolic disturbances

- gluconeogenesis decreases with resulting hypoglycemia

-emotional disturbances develop

-deficiency diminishes resistance to emotional and physical stress

-failure to inhibit ACTH secretion

-deficiency diminishes resistance to

physical and emotional stress

-failure to inhibit ACTH secretion

causing Melanocyte Stimulating

Hormone (MSH) to also be

secreted

S/S of hypoglycemia

S/S of decreased Na+

S/S of decreased H2O

S/S of increased K+

Emotional disturbances

Decreased resistance to stressors

Dark skin/mucous membrane pigmentation

delayed wound healing

females---less axillary hair

---decreased pubic hair

2ndary adrenal insufficiency

-not associated with hypoaldosteronism

-cortisol & ACTH levels both low

-MSH levels also low

Serum cortisol level (decreased)

Urinary 17-Hydroxycoricoids & 17-Ketostereroids (decreased)

Serum ACTH (increased in primary adrenal insuff and may be decreased in secondary type)

ACTH Stimulation test

decreased blood glucose, decreased serum Na+ and increased serum K+ all occurring together

CT of head

EKG changes

BUN (elevated d/t dehydration)

Pharmacologic Tx

-Glucocorticoid Replacement

-Cortisone (Cortone, Cortogen)

-Hydrocortisone (Cortisol,

Hydrocortone)

-Prednisone (Orasone, Deltasone)

Hydrocortisone & Cortisone are the only 2 short-acting agents.

Compared with other glucocorticoids, they have the weakest glucocorticoid and strongest mineralocorticoid actions

RXs of choice b/o having both glucocorticoid and mineralocorticoid properties

Pharmacologic Tx

-Mineralocorticoid Replacement

-Fludrocortisone acetate (Florinef)

-Androgen Replacement

-testosterone

A serious, life-threatening response to acute adrenal insufficiency.

Can occur in any person with Addison’s disease.

BUT, it is most commonly precipitated by major stressors, especially if the disease is poorly controlled

Also occurs when glucocorticoids are abruptly stopped

May have any of the S/S of Addison’s Disease

Primary S/S are

-severe hypotension

-decr Na+, decr fld vol, incr K+

-circulatory collapse

-shock

-renal collapse, coma, death

Treatment of the crisis includes

-rapid IV fluid replacement

-rapid IV replacement of glucocorticoids

Assessment

Diagnoses (Problem List)

Goals/Outcomes

Interventions with rationales

Evaluation

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