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ENDOCRINE SYSTEM

STRUCTURE AND FUNCTION OF THE ENDOCRINE AND METABOLICSYSTEMBoth endocrine and exocrine glands originate from glandularepithelial tissue

During the development of the glands intracellular macromoleculesare formed and stored in vesiclesExocrine glands secrete substances that reach their target tissuesdirectly or by traveling thru a duct; they include sebaceous,salivary, mammary and sweat glandsEndocrine glands secrete hormones; neuronal stimulation, chemicalsubstances or hormones can control secretion of endocrine glands

Hormones

Types of hormones:

1. protein or peptide hormones2. amine hormones or amino acids3. steroids

Basic functions of the endocrine system:1. Exocrine glands provide a vast variety of functions

a. During lactation, milk is ejected from the mammary glandb. Salivary glands secrete saliva

1.) the mucus in the saliva protects the oral mucous membrane2.) Saliva contains 2 digestive enzymes, amylase and ptyalin

c. Sweat glands secrete sweat onto the skin to regulate bodytemperature

d. Sebaceous gland secrete sebum, composed of lipids and wax2. endocrine glands: coordinate and regulate long-term changes infunction of all body organs and tissues to maintain homeostasis

3. Regulation of secretion: the effects on the target tissue act as anegative feedback controlling mechanism to signal the initiating gland toslow or stop secretion.

Major Endocrine Glands

Pituitary Gland: located in cranial cavity in sella turcica of sphenoid bone;near optic chiasm

Posterior pituitary gland:

ADH stimulates the kidneys to reabsorb water

Oxytocin

Anterior pituitary gland

Anterior pituitary hormones are affected by releasing andinhibiting factors secreted by hypothalamus:1. PRL-inhibiting Factor (PIF)2. PRL-releasing Hormone (PRH)3. Somatostatin4. GH-releasing Hormone (GH-RH)5. Corticotropin-releasing Hormone (CRH)6. Substance P

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7. Thyrotropic-releasing Factor (TRF)8. Gonadotropic-releasing Hormone (GnRH)

a. Melanocyte-Stimulating Hormone (MSH):stimulates synthesis and dispersion of melanin in skin, causing darkening

b. Thyroid Stimulating Hormone (TSH)

c. Adrenocorticotropic Hormone (ACTH)1. stimulates growth of adrenal cortex2. stimulates the secretion of glucocorticoids; slightly stimulatesmineralocorticoid secretion

d. Follicle-Stimulating Hormone (FSH)1. stimulates primary graafian follicle to grow and develop2. stimulates follicle cells to secrete estrogen3. stimulates development seminiferous tubules and spermatogenesis

e. Luteinizing Hormone (LH)1. stimulates maturation of follicle and ovum; required for ovulation2. forms corpus luteum in ruptures follicle following ovulation; stimulatescorpus luteum to secrete progesterone3. stimulates testes to secrete testosterone

f. Prolactin1. promotes breast development during pregnancy2. initiates milk production after delivery3. stimulates progesterone secretion by corpus luteum

g. Growth Hormone/Somatotropin1. promotes protein anabolism2. promotes fat mobilization and catabolism3. slows carbohydrate metabolism

DISORDERS OF THE PITUITARY GLAND

ANTERIOR PITUITARY GLAND DYSFUNCTION (UNDERSECRETION /OVERSECRETION):

HYPOPITUITARISM

Etiology:Pituitary gland infarction associated with:

a. pituitary apoplexyb. shockc. sickle cell diseased. DMe. Sheehan syndrome

Head trauma

surgical ablation r/t tumor removalvascular malformationsinfectionsgenetic disorders or replacement with tumor tissue

Pathophysiology:extremely vascular pituitary glandvasospasm of the gland that leads to necrosisplus the portal system circulation

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edema occurs which expands the glandsfor Sheehan syndrome, increased risk for intravascular coagulation

Manifestations:Cortisol deficiency

nausea, vomiting, anorexia, fatigue and weaknesshypoglycemia

Thyroid deficiencycold intoleranceskin drynessmild myxedemalethargydecreased metabolic rate

Diabetes insipidusGonadal failure

in women, adrenal androgen productionin women of reproductive age, amenorrhea,

atropic vagina, uterus and breast

in postpubertal males, testicles atrophy andbeard growth is stunted

both men and women, decreased hair and libidoLoss of secondary sex characteristicsLow growth hormone and somatomedin levelsIn post-partum women, absence of lactation

HYPERPITUITARISM

Etiology:

secretory pituitary adenomaacute illness, CRF, cirrhosisectopic secretion

Gigantismsymmetric excessive linear growth, exceeding

3 standard deviations above mean height for agecontinues thru adolescence and into adulthoodAcromegalylinear growth is no longer possibletissues thicken and growth takes place in the acral areashypersecretion of PRL in 20 to 40% of the cases

Manifestations:progressive increase in ring, shoe, and glove sizeEnlarged tongue, interstitial edema, enlarged and overactivesebaceous and sweat glands, coarse skin and body hairperiosteal vertebral growth, and enlargement of the bones of the face, hand

and feet (protrusion of the lower jaw and forehead)ribs elongate at the bone cartilage junction leading to barrel chest

appearancearthalgias, backache, arthritisosteoporosis develops

weakness, muscular atrophy, foot drop and sensorychanges in handsCNS symptoms: headache, seizure activity, visual disturbances,

and compression hypopituitarism may occur1/3 to with acromegaly developed HPN and

left sides HF; 1/3 have impaired glucose tolerance; developed diabetes

increased reabsorption of phosphatehyperglycemia

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increased metabolic ratecoexisting hyperprolactinemia

Laboratory and Diagnostic study findings

HYPERPITUITARISM HYPOPITUITARISM1. MRI 1. Insulin-induced hypoglycemia

2. Increased GH 2. L-dopa Test

3. S/sx 3. Stimulation Test

4. S/sx

Nursing Management:Administer prescribed medications

Hyper somtatostatin analogHypo synthetic growth hormone

Prepare the client for pituitary irradiation, if ever.

Prepare the client for indicated procedure or surgeryPrepare for hypophysectomy if indicated.

TransfrontalSubcranialOronasaltransphenoidal

Monitor a postsurgical client for signs of complications:Hemorrhage

Transient diabetes insipidusRhinorrheaAdrenal insufficiency and thyroid insufficiencyInfectionVisual disturbances

POSTERIOR PITUITARY DYSFUNCTION:SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE (SIADH)

Etiology and Pathophysiology

The usual feedback mechanism does not functionto decrease posterior pituitary secretion of ADH withdecrease serum osmolality

High levels of ADH lead to renal absorption ofwater and suppression of renin-angiotensin mechanism

This leads to water intoxication, cellular edema,and dilutional hyponatremia

Causes:1. Ectopic ADH production associated with some cancers malignant tumors

a. oat cell adenocarcinoma cancer of the lung

b. carcinoma of the duodenum and pancreasc. leukemiad. lymphomae. Hodgkins diseasef. Sarcomag. Squamous cell carcinoma of the tongue

2. transient SIADH by pituitary surgery3. infectious pulmonary surgery4. response to a hypoxia-induced decreased in pulmonary perfusion

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5. psychiatric disorders6. drugs that potentiate circulating ADH or stimulate ADH releasehypoglycemic agents, barbiturates, general anesthesia, vincristine,nicotine, morphine, diuretics, synthetic hormones, SSRIs

Clinical manifestations:PATHOPHYSIOLOGY:

water retentionincrease in total body watersolute lossosmotic inactivation of cellular solutes

Clinical manifestations:serum sodium 140 mEq/L drops to 130 mEq/L

- thirst, impaired taste, anorexia, dyspnea on exertion,fatigue, and dulled sensorium

serum sodium 130 mEq/L drops to 120 meq/L

- severe gastrointestinal symptoms, including vomiting and abdominalcramps

serum sodium between 110 to 115 mEq/Lirreversible neurologic damagedecreased deep tendon reflexesweight gain without edemasmall amounts of concentrated amber colored urine

Diagnostic and laboratory test findings:high urine osmolality (> 1200 mOsm/kg H2O)specific gravity (> 1.032)low serum osmolality (

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ETIOLOGY AND PATHOPHYSIOLOGY

Neurogenic DI: renal tubules excrete excessive amount of water in theurine caused by insufficient ADH secretion by the posterior pituitary gland;results in impaired renal concentrating ability

Nephrogenic DICauses:a. disorders with lesions of the collecting tubules1. pyelonephritis2. polycystic disease3. intrinsic renal diseaseb. Certain drugs that can interfere with ADH secretion or action:1. Lithium carbonate2. demeclocycline (Declomycin)3. alcohol

4. phenytoin

Clinical Manifestations:Polyuria (5 to 25 L/24 hours)Polydipsia (primary)dry tented skindry mucous membranesevere hypotension leading to cardiovascular collapse

Diagnostic and laboratory findings:urine specific gravity (less than 1.005)urine osmolality (less than 300 mOsm/kg)(+) water deprivation tests

reduced serum ADH level in primary DIserum sodium (more than 145 mEq/L)

Nursing Diagnoses:Fluid volume deficitRisk for impaired skin integrityRisk for constipationKnowledge deficit

Nursing intervention:MIO hourly

2. Weigh daily; report weight loss3. Monitor urine specific gravity and report if it decreases; monitorserum osmolality and sodium if increases4. Encourage fluid intake greater than urine output; provide fluidswithin reach at all times5. Use skin protective barriers with incontinence

Medication therapy:lypressin (Dapid) intranasal administration, vasopressin

(Petrissin),desmopressin (DDVAP)Action: increases the permeability of renal tubular epithelium to ADPand water; the epithelium promotes reabsorption of water andproduces concentrated urine. Also increases factor VIII activity byreleasing endogenous factor VIII from plasma storage sites.

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Action: Promotes water reabsorption by the distal renal tubules andcauses vasoconstriction and increased muscle tone of the bladder, GIT,uterus, and blood vessel

Major side effects:Increased intestinal activityHyponatremia

Pallorwater intoxicationcardiac disturbancesnasal irritation

chlorpropamide (Diabenese) or carbamazepine (Tegretol

3. Pineal gland

a. Pineal hormone- may regulate diurnal fluctuations of hypothalamic-hypophyseal hormones

- inhibits numerous endocrine functions

4. Thyroid gland:

Calcitonin (thyrocalcitonin) targets bone and kidney cells to calcium ionconcentration in body fluids

T3/T4Thyroxine: stimulates metabolic rateTriiodothyronine: inhibits anterior pituitary secretion of thyroid stimulatinghormone

DISORDERS OF THE THYROIDHYPERTHYROIDISM (GRAVES DISEASE)

excess secretion of thyroid hormone from the thyroid gland, leadingto increased basal metabolic rate, CV function, GIT function,neuromuscular function, weight loss, heat intolerance, thyroid

hormone affects metabolism of fats, carbohydrate and proteins

Etiology and Pathophysiologycan be caused by excess secretion of TSH from the pituitary gland,autoimmune reaction, thyroiditis, tumor, and excessive dose of supplementalthyroid hormoneGraves diseaseEtiology is mediated by immunoglobulin G (IgG) antibody that activates TSHreceptors on the surface of the thyroid cells

Clinical manifestations:

3 components of clinical manifestations:1. Adrenergic stimulation2. Excess thyroid hormone3. Immunologic stimulation of diffuse goiter

- enlargement of the thyroida. pregnancyb. pubertyc. iodine deficiency

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d. immunologice. viralf. genetic disorder

CNS: nervousness, irritability, hyperactivity, emotional lability, anddecreased attention span, hyperreflexia, insomnia, and interrupted sleepSensory: blurred vision, photophobia, lacrimation, exophthalmos, retracted

eyelids, and staring gaze

Ocular manifestations (Categories):1. functional abnormalitiese.g. lag of the globe on upward gaze

upper lid on the downward gaze2. infiltrative changes involving the orbital contentse.g.edema of the orbital contents

globe protrusionparalysis of extraocular musclesdamage to the retina and optic nerve

to result to:exophthalmosperiorbital edemaextraorbital muscle weakness leading to diplopia

Endocrine: goiterRespiratory: dyspnea, bruits over the thyroid glandCardiovascular: hypertension, tachycardia, dysrhythmias, palpitations,elevated systolic blood pressure, widened pulse pressure, and S3 heartsoundsGIT: nausea, vomiting, diarrhea, abdominal painReproductive: amenorrhea (female), decrease fertility (female), decreaselibido (male), impotence (male)MSK: muscle, weakness, fatigueIntegumentary: fine, thin hair; flushed, moist skin; heat intolerance

Diagnostic and laboratory tests findings:- elevated serum T3 and T4- elevated serum free T4- increased protein-bound iodine (PBI)- increased long-acting thyroid stimulator

- decrease TSH levels if thyroid disorder- increased TSH levels if secondary to a pituitarydisorder

positive RAI uptake scan and thyroid scanSerum:

L-thyroxine (total T4): normal is 4.5 to 10.9 ug/dl in adultsFree T4; normal values are 0.8 to 2.7 ng/ml by actual assay or 4.6 to 11.2

by calculated methodTriiodothyronine (T3) (normal value 60 to 181 ng/dl), also called T3 RIA,

T3 resin uptake (T3RU)Additional tests: TSH (normal value 0.5 to 5.0 U/ml) and serum calcitonin

thyroid crisis or thyroid storm:

Common manifestations of thyroid storm: temp. more than 102 degreeF (39 degree C), tachycardia, systolic hypertension, abdominal pain, nausea,vomiting, diarrhea, agitation, tremors, confusion and seizure

Nursing Diagnoses- Risk for decrease cardiac output

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- Altered sensory perception- Risk for ineffective airway clearance- Altered nutrition: less than body requirements- Altered body image- Hyperthermia- Activity intolerance- Knowledge deficit

Nursing intervention

Radioactive iodine 131: the thyroid gland absorbs iodine 131,which destroys some of the thyroid cells

Not recommended to pregnant womenRadiation precautions are not required

for small doses (

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For exophthalmos,

instruct clients on methods to protect eyes and adapt to altered visual fieldsinstruct client to have regular eye examsinstruct client to call practitioner immediately for any change in vision or

appearance of eye; closure of eyelids; eye pain; eye exudates orphotophobia

protect eyes with tinted glasses or eye shields since lids do not cover eyescompletely

moistens eyes frequently with artificial tears; use caution not to contaminateeye dropper

soothe dry eye irritation with cool moist compressessleep with head of bed elevated and wear eye patches

HYPOTHYROIDISM- insufficient amount of the thyroid hormone being secreted by the

thyroid gland

Etiology and Pathophysiologya. Primary hypothyroidism (accounts for 99% of the cases)50% of cases are caused by cell-mediated andantibody-mediated destruction of \the thyroid gland

b. Other causes: thyroiditis, subacute postpartum,external irradiation of the gland, iatrogenic (30 to 40%),infections, iodine deficiency, congenital or idiopathic

c. Secondary hypothyroidism (also called central hypothyroidism):

Assessment:Clinical manifestations:

Depend on the length of time and severity of the lack of thyroidhormone

The thyroid gland gradually enlarges forming a goiterlethargy, diminished reflexes, periorbital edema, bradycardia,

dysrrythmias, hypotension, reproductive problems (menorrhagiaand infertility in females and decrease libido in males), coarse dryhair that is easily lost, coarse dry skin, signs of slowed metabolism(hypothermia, fatigue, weight gain, anorexia), anemia, elevatedserum lipids

assess myxedema coma, characterized by non-pitting edema inconnective tissues throughout the body, puffy face and tongue,severe metabolic disorders, hypothermia, cardiovascular collapse,and coma

Diagnostic and laboratory tests findings:Decrease T4 and free T4, normal T3, and increased TSH levels

Nursing DiagnosesDecrease cardiac outputConstipationRisk for activity intoleranceRisk for sexual dysfunctionDisturbed body image

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HypothermiaKnowledge deficit

Nursing interventionGive medication in the morning 1 hour before food intake or 2 hours

after food intakeAdjust environment with blankets as needed for temperature of

comfortPace activities with rest periods; instruct client report shortness of

breath, fatigue, dizziness or any discomfortEncourage intake of 1200 mL water daily and high fiber diet

Medication therapy: Thyroid replacement therapylevothyroxine sodium(Synthroid, Levothroid, Levotec, Levo-T)

Action: raises metabolic rate, promotes gluconeogenesis, increases use ofstored glycogen, stimulates protein synthesis, and affects protein andcarbohydrate metabolism and cell growth

Liothyronine sodium (Cytomel, Triostat)

Action: enhances oxygen consumption by most tissues of the body,increases the basal metabolic rate and the metabolism of

carbohydrates, lipids and proteins

Liotrix (Thyrolar)Action: stimulates metabolism of all body tissues by accelerating the rate ofcellular oxidation and provides both T3 and T4 to the tissues

Thyroid desiccated (Armour Thyroid, S-P-T)Action: stimulates metabolism of all body tissues by accelerating the rate ofcellular oxidation

Nursing considerations:

Administer in morningMonitor cardiac responseIt may decrease effects of beta blockersCholestyramine, coletipol: impairs absorption of levothyroxineWith insulin, oral antidiabetics. There will be altered glucose levels.Herbal medications: Horseraddish: Abnormal thyroid function may occur.Use with caution to patients with DMHerbal drug interaction: Lemon balm: antithyroid effects

Rapid replacement in patients with atherosclerosis may cause angina,coronary occlusion or CVA

Liothyronine may be used when a rapid-onset or a rapidly reversibledrug is desirable, or in patients with impaired peripheral conversionof levothyroxine to liothyronine.

Dont administer injection I.M. or S.C.Older than 60 years old patients should receive 25% lower than in young

adultsCompliance to medications should be emphasizedTell patient not to switch brandTell patient to report unusual bleeding and bruisingcontraindicated in patients who are sensitive to the drug, with acute MI

uncomplicated with hypothyroidism, untreated thyrotoxicosis, uncorrectedadrenal insufficiency

with oral anticoagulants: altered PT, monitor PT and INRwith sympathomimetics: increased risk of coronary insufficiency

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5. Parathyroid gland: monitor and maintain circulating concentration ofcalcium ions

2 to 12 embedded in the posterior part of the thyroidPTH stimulates osteoclasts, inhibits obsteoblastIncreases blood calcium concentration

1. Breakdown of bone with release of calcium into the blood2. Calcium absorption from the intestines into blood3. Kidney tubule reabsorption of calcium4. Decreases blood phosphate concentration byslowing its reabsorption from the kidneys

HYPERPARATHYROIDISMPrimary Hyperparathyroidism: hyperplasia of one or tumor of one of theparathyroid glands

Secondary Hyperparathyroidism: gland enlargementTertiary parathyroidism: usually associated with chronic renal failure

Etiology and Pathophysiology

increased absorption of calcium and increased secretion of phosphatekidneys increase bicarbonate excretion and decrease acid excretionbones increase rate of calcium and phosphorus releasehypercalcemia causes calcium deposits in soft tissues, renal calculi, altered

neurological function with muscle weakness and atrophy, altered GIfunction and altered CV system

ASSESSMENT:Clinical manifestations:polyuria and renal calculianorexia, constipation, nausea, vomiting, abdominal paingeneralized bone pain, pathologic fractures, muscle weakness and atrophyCNS signs

Diagnostic tests:elevated serum levels of total calciumincrease PTH

decreased phosphatepossible bone changes in skeletal x-rays and CT scan

Nursing Diagnosis:Risk for injuryPainImpaired physical mobilityRisk for altered urinary eliminationRisk for constipationKnowledge DeficitInterventions:

Promote conform and safetyStrain all urineProvide 2,000 to 3,000 ml of fluids daily as toleratedEncourage progressive activity as toleratedPromote nutrition and fluid and electrolyte balance, weigh dailyProvide pre- and postoperative carePrevent tetany caused by surgery or aggressive excretion of calcium thru

early detection of low serum calcium levelsMedications:

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AnalgesicsDiuretics and normal saline by IV infusionPhosphate and Calcitonin (Miacalcin)

i. Client education:Instruct the patient about symptoms to report

HYPOPARATHYROIDISM

Etiology and pathophysiology:Hypocalcemia raises the threshold for excitability in nerve and muscle fiberscausing the fibers to be stimulated

ASSESSMENT:Clinical manifestations:

* GI symptoms: abdominal pain, nausea,vomiting, diarrhea, and anorexia

* signs of hypocalcemia: anxiety, headache,parethesias, neuromuscular irritabilitywith tremors and muscle spasms

* possible difficulty of swallowing* possible hoarse voice* sensation of tightness of the throat* dry thin hair* patchy hair loss* ridged finger nails

Nursing diagnoses:

1. Risk for injury2. Anxiety3. Knowledge Deficit

Interventions:

Promote comfort and safetyEncourage progressive activity as tolerated, pacing activity with rest periodsPromote nutrition and fluid and electrolyte balanceMedications therapy:

Calcium supplement orally or by IV infusion

Vitamin D orally

Client education:Foods high in calcium (cheese, milk and milk product, turnip greens,

almonds, collard greens, beans, peanuts, and bologna)

7. Thymus gland: located at the root of neck and anterior thorax1. regulates immunologic processes2. just after birth produces T lymphocytes that migrate to the

lymph nodes and spleen to provide cell- mediated immunity

3. synthesis hormones that regulate the rate ofdevelopment of lymphoid cells, particularly T cells

8. Adrenal medulla:a. Secretes epinephrine (adrenaline) and

norepinephrine (noradrenaline)b. Mobilizes glycogen reservesc. Stimulates liver and skeletal muscle to break down glycogend. Increase oxygen use and carbon dioxide production

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e. Increase blood concentration of free fatty acidsf. Cause constriction of nearly all blood vessels in the bodyg. Increase heart rate and force of contractionh. Inhibit contractions of gastrointestinal and uterine smooth muscles

9. Adrenal cortex: hormone plays a vital role for thebodys survival and affect metabolism of many different tissues

a. Glucocorticoids: cortisol , corticosterone, and cortisone

accelerate liver gluconeogenesisdecrease antibody formationslow the proliferation of fibroblasts characteristic of inflammationdecreases ACTH secretionmildly accelerate sodium and water reabsorption and potassium excretion by

kidney tubules

b. Mineralocorticoids:

aldosterone stimulates the kidneys to increase reabsorption of sodium andwater, and reduces sodium and water loss by the sweat glands, salivaryglands, digestive tract

markedly accelerates potassium excretion by kidney tubulesaldosterone secretion increases as sodium ion decrease or potassium ionsincrease

c. Small amount of androgens

DISORDERS OF THE ADRENAL CORTEXCushings syndrome

- chronic hypercortisolism

Etiology and pathophysiology:

1. Hypercortisolism2. elevated cortisol causes life-threatening changes in physiological,psychological, and metabolic functioning3. Primary: caused by tumor of the adrenal cortex4. Secondary:

a. Disorder of the pituitary gland or hypothalamusb. Ectopic tissue such as ACTH-producing cancer of the lung, bronchus,

or pancreas4. Iatrogenic

ASSESSMENT:

Clinical manifestations:

generalized weakness with muscle wastingthin skin that bruises easilyemotional labilityskin infections or poor wound healingstriae, hirsutismhypertension, fluid overload, weight gainosteoporosis and renal stones

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abnormal fat depositspossible amenorrheaimpotencedecreased libidoglucose intolerance

Nursing Diagnoses:

Excess fluid volumeRisk for injuryRisk for infectionDisturbed body imageKnowledge deficit

Interventions:1. assist client to achieve fluid , electrolyte, glucose and calcium balance2. Analyze daily weight and intake and output3. Promote safety: uncluttered walking area, adequate lighting, assistivewalking devices

4. Assist patient to pace activities and rest5. Prevent infection before and after surgery6. Assist client to use effective coping strategies7. Preoperative care: ensure that client understands the planned surgicalprocedure, post-op routines, and expected outcomes8. Post-op care:

Promote effective breathing patternExplain the necessity of mouth breathing is necessaryAssist with turning and repositioning every 2 hours, and

encourage ankle dorsiflexion exercises hourlyPromote wound healing

Adrenalectomy: log roll to the side to sit up at the bedside and shoulddo the reverse to recline

Transhpenoidal incision: avoid blowing of the nose, sneezing, orcoughing if necessaryKeep HOB elevated 30 degrees, and use aseptic technique for wound careExamine pituitary surgical wound for CSF leakPrevent Addisonian crisis: give IV normal saline bolus and cortisol for the

following symptoms: dry, tenting skin, decrease blood pressure,increased pulse, decrease level of consciousness, anorexia andweakness

Medications:Medications:1. Meturapone2. Octreotide (Sandostatin)3. Mitotane

Client education:1. instruct to report symptoms2. Diet: high in protein and vitamins B and C; takesupplemental potassium and calcium3. wound care and cortisol replacement post op

ADRENAL INSUFFICIENCY/PRIMARY ADDISONS DISEASE

Etiology and Pathophysiology:decreased cortisol levels leads to hyponatremia, hyperkalemia, decreasedextracellualar fluid, decreased intravascular volume, decreasedgluconeogenesis, hypoglycemia and stress intolerancehigh ACTH levels leads to hyper pigmentation

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ASSESSMENT:Clinical manifestations:1. include hyperpigmentation2. delayed wound healing3. CV changes4. dehydration and hypovolemia5. weight loss, anorexia, nausea, vomiting, diarrhea

6. depression, lethargy, emotional lability, confusion7. muscle weakness and tremors and muscle and joint pain8. Addisonian crisis

Diagnostic tests:decreased serum cortisol, glucose and sodiumincreased serum potassium, BUN and ACTH levelsdecrease urine 17 KSno increase in cortisol in ACTH stimulation testCT scan can be positive

Nursing Diagnoses:a. Fluid volume deficitb. risk for ineffective therapeutic regimen managementc. knowledge deficitd. risk for electrolyte imbalance

Implementations:1. maintain fluid and electrolyte balance2. promote safety3. medications:

a. glucocorticoid replacementShort-acting - hydrocortisone (Solucortef)Intermediate acting - methylprednisolone (Medrol)Long-acting - dexamethasone (Decadron)

b. fludrocortisone (Florinef)4. Client education:

a. Instruct patient on Addisons disease, symptoms to report, need forlifelong medication and disease managementb. Diet: to promote immune system function and foods to increase

sodium and decrease potassium intake

6. Pancreas (islets of Langerhans):Studies of the pancreas:A.) Fasting Blood Glucose (FBG) levels or fasting plasma glucose

a. fast for at least 8 hours, water is permittedb. withhold insulin for fasting period until specimendrawnc. adult reference value: 70 to 110 mg/dl (whole blood: 60 to

100 mg/dl), elderly 70 to 120 mg/dlB.) Oral Glucose Tolerance Test (OGTT): tests for transitional gestationalglucose intolerance

a. Fast overnight, water permittedb. Start test by drawing fasting glucose specimen and obtain urine

specimenc. Give client 75 to 100 g glucose dissolved in waterd. Collect blood glucose specimen at 1, 2 and 3 hours after drinking

glucosee. Collect urine specimen(s) according to lab protocolg. Fast during entire specimen collection periodh. Reference values are measured in mg/dl for dose of 100g of glucose

3.) Capillary glucose monitoring

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a. warm extremity to encourage vasodilationb. cleanse site with soap and water or 70% alcohol, dry with gauze

spongec. avoid squeezing site to enhance blood flow since squeezingd. avoid touching skin with reagent stripe. elevate digit and apply gentle pressure with dry sterile gauze to site

4.) Glycosylated hemoglobin: prolonged hyperglycemia causes

hemoglobin (Hgb) of the RBC to be saturated with glucosea. tests determines diabetic control of blood glucose

by measuring all three subunits of Hgb Ab. value for GHB is 2 to 4% higher than the individual subunits of HgbA

c. Reference values InterpretationUp to 7.5% Good diabetic control7.6 8.9% Fair diabetic controlmore that 8.9% Poor diabetic control

d. fasting is not necessary

5.) Urine Studya. Glucose usually appears in urine once renal threshold for glucose is

exceededKetone: metabolic end product of fatty acid metabolism; body uses fattyacids for energy when there is insufficient supply of glucoseAcetone: metabolite of fatty acid metabolism

a. Retroperitoneal in abdominal cavity; both exocrine and endocrine glandb. Alpha cells produce glucagons to break down stored fat andcarbohydrate (CHO) into glucose

1. induces liver glycogenolysis2. inhibits hepatic protein synthesis3. stimulates hepatic ketogenesis and release of glycerol and

fatty acids from adipose tissuec. Beta cells produce insulin

1. promotes the cellular uptake of glucose2. stimulates intracellular macromolecular synthesis3. stimulates cellular uptake of sodium and potassium

d. Delta cells produce somatostatin

e. F Cells

DISORDERS OF THE PANCREAS:DIABETES MELLITUS:

Etiology and Pathophysiology:Classes:

Type 1results from autoimmune destruction of the beta cellshas genetic predispositioncommon in children and adolescentscharacterized by hyperglycemia and ketosis

Type IIcause: unknowncould be compromised ability of the beta cells to respond tohyperglycemia, abnormal insulin receptors on the cells

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and peripheral insulin resistancehas genetic predispositioncommon in obese clients and older adults

Clinical manifestations:Type I: polyuria, polydipsia, polyphagia, weight loss, malaise and fatigueType II: polyuria, polydipsia, blurred vision, fatigue, parethesias and skin

infections

Early manifestations:Polyuria PolyuriaPolydipsia PolydipsiaPolyphagia Blurred visionWeight lossGlycosuriaFatigue

ACUTE complications:

HyperglycemiaDKA

Hyperglycemic hyperosmolar nonketotic coma

CHRONIC complications:Neurologic:Somatic neuropathies (paresthesias, pain,loss of cutaneous sensation, loss of motor control)Visceral neuropathies (sweating dysfunction,papillary constriction, fixed heart rate, constipations,diarrhea, incomplete bladder emptying)Sensory:Diabetic retinopathy, Cataracts, glaucomaCardiovascular:Orthostatic hypotension, accelerated atherosclerosis,CVA, coronary artery disease, peripheral vascular disease,blood viscosity, and platelet disordersRenal:hypertension, albuminuria, edema, CRFMusculoskeletal:Joint contracturesIntegumentaryFoot ulcers, gangrene of the feet, atrophic changesImmune system:Impaired healing, chronic skin infections,periodontal disease, UTI, lung infections, vaginitis

Management:Manag

ement:

A. DIET:follow the recommended diet in the Food Guide Pyramid or exchange system

diet from the American Diabetes Associationcomplex CHO; avoid simple sugarsCHON 10 to 20%

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Saturated fat less than 10% of calories with cholesterol intake equal to orless than 300mg/day

Sodium intake 2,400 to 3,000 mg.dayDietary fiber 20 to 35 gm/day

B. OHAused in DM2 only

consists of sulfonylureas, alpha-glucosidase inhibitor, biguanide, and amiscellaneous agent

with sulfonylureas, avoid alcoholinstruct patient for risk of metabolic acidosisinstruct patient to discontinue medications if severe diarrhea, infection, or

dehydration occuradvise for corrective actionsC. Insulin therapy

1. use in type 1 or type 22. different preparation of insulin are available in relation to metabolic

demands

3. Source: human insulin has a faster onset of action, a shorter peak,and a shorter duration than animal derived insulin; preferred to pork or beefinsulin. Human insulin is produced thru DNA biotechnology bygenetically altering strain and closely resembles insulin produced by the betacells of the human pancreas

4. preparations:rapid acting: Insulin lispro, Humalog, regular, Humulin Rintermediate-acting: NPH, Humulin Nlong-acting: Humulin Ubuffer insulin: Humulin BR

5. combinations of insulin preparation are usually administered tomimic the pancreatic activity of the pancreas

6. only regular insulin may be given IV usually given via subcutaneousroute

continuous SC insulin infusion (CSII) insulin patch, nasal spray,inhaled aerosolized prep

Nursing Responsibility:

storage: insulin in use should be stored at room temperature,administration of insulin causes alteration in insulin absorption

extra vials of insulin not in use should be stored in the refrigeratorPreparation:

1. note date of expiration, discard vial if regularinsulin appears cloudy

2. do not shake3. roll non-regular insulin gently between the

hands4. draw regular first when mixing if with other types

of insulin; only mix insulin of the same concentration(e.g. U100 regular and U100 NPH) and from the same source

Injection: rotate injections sites with beef or pork insulin and do not injecton the area that will be involved in exercise

monitor for signs of hypoglycemia; have simple CHO availableavoid alcohol while taking insulin

Priority nursing diagnoses:ineffective individual coping

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ineffective health maintenancerisk for infectionrisk for impaired skin integrityrisk for injuryrisk for disturbed body imageknowledge deficit

Nursing interventions:Promote safety:promote lightingprotective slipperssocks and shoes that do not rub or impinge on the skinPrevent infection:appropriate foot careaseptic injectionTreat hypoglycemia with 15g CHO snack:8 oz skim milk5 Lifesaver candies

3 large marshmallows6 oz juice

Client education:instruct client about foot care:keep feet clean and dryinspect feet daily using mirror to see solesprotect feet by wearing shoesslippers at all timesavoid snug fitting socks or stockingsuse cotton socksdaily cardiovascular exercise

DIABETIC KETOACIDOSIS:

life-threatening metabolic acidosistriggered by emotional stress, uncompensated exercise, infection,

trauma, insufficient of delayed insulin administration

Clinical manifestations:1. thirst2. nausea and vomiting

3. malaise4. lethargy5. polyuria6. acetone (fruity) odor to breath7. Kussmauls respiration

Diagnostic Tests:serum glucose: more than 250 mg/dLplasma pH: less than 35plasma bicarbonate: less than 15 mEq/ Lserum ketones present

urine positive for ketones and glucosehyperkalemiaabnormal serum sodium and chloride

Therapeutic management:1. Insulina. bolus of IV regular insulin is given followed by a

continuous IV drip (0.1 unit/kg body weight) untilthe blood glucose levels drop to 250 mg/100 mL or the pH is 7.3

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b. once blood levels is reached, regular insulin isgiven on a sliding scale accdg. to blood glucose

2. Fluid therapya. Normal saline solution is usually given at a rate

of 1 to 2 L for the first hours then decreased to 500 mL/houras tolerated by cardiac and respiratory system

b. when blood glucose levels reaches 250 to 300,a 5% glucose (D5 NS) is added

c. CVP or hemodynamic monitoring is indicated

3. Potassium replacementa. initial serum potassium is usually elevatedb. with the reversal of the acidosis and the administration of insulinc. replacement is based on the serum potassium levels and urinary output

Interventions:maintain skin integrity; promote healing of impaired skin; prevent infection

HYPERGLYCEMIC HYPEROSMOLAR NONKETOTIC COMA (HHNK)

Etiology:* increased insulin resistance along with increased CHO intake lead tohyperglycemia

Clinical manifestations:symptoms gradually occur over 24 hours to 2 weeks: decreased LOC, dry

mucous membranes, polydipsia, hyperthermia, impaired sensory and motorfunction, (+) Babinski sign and seizure

Diagnostic Tests:1. elevated serum sodium2. serum osmolality: more than 340 mOsm/L3. serum glucose: more than 600 mg/dL4. abnormal seum potassium and chloride5. normal serum pH

Intervention:

promote normalized cardiac output,sensory perceptual function, fluid and electrolyte balance, normal bodytemperature

maintain intact skinprevent aspirationmedications: IV infusion of NS, regular insulin, potassium to replace fluids and shifts