endocrine new edition

ENDOCRINESYSTEM AND MAJOR

DISORDERS

By: MISS SHENELL A. DELFIN, RN

FUNCTION:Endocrine system consist of a series of glands

“ductless” that function individually or conjointly to integrate and control innumerable metabolic activities in the body.

These glands automatically regulate various body processes by releasing chemical messengers called hormones.

OVERACTIVITY OR UNDERACTIVITY of any one of them affects the whole system.

FUNCTION:Control and coordination of the processes

which are wide spread in the body such as:Response to stress or injuryGrowth and developmentReproductionFluids and electrolytesAcid base-balanceEnergy metabolism

ENDOCRINE GLANDSENDOCRINE GLAND

HORMONES FUNCTIONS

PITUITARYANTERIOR

TSH Thyroid to release hormones

LOBE ACTH Adrenal cortex to release hormones

FSH,LH Growth, maturation & function of sex organs

GH/SOMATOTROPIN

Growth of body tissues & bones

PROLACTIN/LTH

Development of mammary glands & lactation

ENDOCRINE GLANDSENDOCRINE GLAND

HORMONE FUNCTION

PITUITARYPOSTERIOR

LOBE

ADH Regulates water metabolism

OXYTOCIN Stimulate uterine contractions release of milk

INTERME- DIATE LOBE

MSH Affects skin pigmentation

ENDOCRINE GLANDSENDOCRINE GLAND

HORMONES FUNCTION

ADRENAL CORTEX

ALDOSTERONE Fluid & electrolyte balance; Na reabsorption; K excretion

CORTISOL Glycogenolysis;GluconeogenesisNa & water reabsorptionAntiinflammatoryStress hormone

SEXHORMONES

Slightly significant

ENDOCRINEGLAND

HORMONE FUNCTION

ADRENAL MEDULLA

EPINEPHRINENOR-EPINEPHRINE

Increase heart rate & BPBronchodilation, GlycogenolysisStress hormone

ENDOCRINE GLANDSENDOCRINE GLAND

HORMONE FUNCTION

THYROID T3 & T4’ Regulate metabolic rateRegulate physical & mental

growth & development

THYRO- CALCITONIN

Decrease serum Ca by increasing bone deposition

PARA- THYROID

PTH Increase serum calcium by promoting bone decalcification

ENDOCRINE GLANDSENDOCRINEGLAND

HORMONE FUNCTION

PANCREAS BETA

CELLS

INSULIN Decrease blood glucose by: Glucose diffusion across cell

membrane;Converts glucose to

glycogen

ALPHA CELLS

GLUCAGON Increase blood glucose by:GluconeogenesisGlycogenolysis

ENDOCRINE GLANDSENDOCRINEGLAND

HORMONES FUNCTION

OVARIES ESTROGEN &PROGES- TERONE

Development of secondary sex charac in female

Maturation of sex organsSexual functioningMaintenance of pregnancy

TESTES TESTOS- TERONE

Development of secondary sex charac in male

Maturation of sex organsSexual functioning

HORMONE REGULATIONNEGATIVE FEEDBACK MECHANISM

CHANGING OF BLOOD LEVELS OF CERTAIN SUBSTANCES (e..g CALCIUM & GLUCOSE)

RHYTHMIC PATTERNS OF SECRETION (e.g. CORTISOL, FEMALE REPRODUCTIVE HORMONES)

AUTONOMIC & C.N.S. CONTROL(PITUITARY-HYPOTHALAMIC AXIS,

ADRENAL MEDULLA HORMONES)

NEGATIVE FEEDBACK MECHANISM

DECREASED HORMONE CONCENTRATION IN THE BLOOD (e.g. Thyroxine)

PITUITARY GLAND RELEASE OF STIMULATING HORMONE (e.g. TSH)

STIMULATION OF TARGET ORGANS TO PRODUCE & RELEASE HORMONE

(e.g. Thyroid gland release of Thyroxine)

RETURN OF THE NORMAL CONCENTRATION OF HORMONE

NEGATIVE FEEDBACK MECHANISM

INCREASED HORMONE CONCENTRATION IN THE BLOOD (e.g. Thyroxine)

PITUITARY GLAND IS INHIBITED TORELEASE STIMULATING HORMONE (e.g. TSH)

DECREASED PRODUCTION & SECRETION OF TARGET ORGAN OF THE HORMONE

(e.g. Thyroid gland release of Thyroxine)

RETURN OF THE NORMAL CONCENTRATION OF HORMONE

Endocrine Disorders

If you can remember what each hormone does in the body, it will be easier to remember what results from imbalances of that hormone. Most symptoms of hormone HYPERACTIVITY are the

opposite of symptoms of that hormones HYPOACTIVITY.

ANTERIOR PITUITARY DISTURBANCES

HYPOPITUITARISM

HYPERPITUITARISM

PITUITARY ANTERIOR LOBEHORMONE HYPO FXN HYPER FXN

GH Dwarfism – youngCachexia - adult

Gigantism – youngAcromegaly - adult

ACTH Atrophy of adrenal cortex

Cushing’s dse

TSH Atrophy & depressed thyroid fxn

Grave’s dse

FSH Atrophy & infertility Exaggerated fxn of sex organs

PROLACTIN Underdevelopment of mammary glands

Decreased milk production

HyperpituitarismMay be due to overactivity of gland

or the result of an adenoma

Characterized by:Excessive serum concentration

of pituitary hormones (GH, ACTH, PRL)Morphologic and functional changes

in the anterior pituitary

Growth Hormone Hypersecretion

GIGANTISM

Manifestations of acromegaly. Progressive alterations in facial appearance include enlargement of the cheekbones and jaw along with thickening of soft-tissue structures such as the nose, lips, cheeks, and the flesh above the brows. (Courtesy of Clinical Pathological Conference, American Journal of Medicine.)

Hyperpituitarism:Clinical Manifestations

ArthritisChest: barrel-shapedRough facial featuresOdd sensations: hands and

feetMuscle weakness & fatigueEnlargement of organsGrowth of coarse hairAmenorrhea; breast milk

productionLoss of vision; headachesImpotence; increased

perspiration Snoring

Hyperpituitarism:Clinical Manifestations

Hypopituitarism

Deficiency of one or moreanterior pituitary hormones

CausesInfections / Inflammatory disorders

Autoimmune diseasesCongenital absence

TumorSurgery / Radiation therapy

Hypopituitarism:Clinical Manifestations

Hypo -thermia, -glycemia, -tension

Loss of vision, strength, libido, & secondary sexual

characteristics

DWARFISM

MANAGEMENTHYPOPITUITARISM

SURGICAL REMOVAL / IRRADIATIONREPLACEMENT THERAPY

THYROID HORMONES STEROIDS SEX & GROWTH HORMONES GONADOTROPINS (restore fertility)

HYPERPITUITARISMSURGICAL REMOVAL / IRRADIATIONMONITOR FOR HYPERGLYCEMIA &

CARDIOVASCULAR PROBLEMS

Trans-sphenoidal hypophysectomy

POSTERIOR PITUITARY DISTURBANCES

DIABETES INSIPIDUS

SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE

FUNCTION:WHEN THERE IS A OF SERUM

OSMOLALITY, THE NORMAL BODY RESPONSE IS TO THE SECRETION OF ADH.

WHEN THE NORMAL FEEDBACK MECHANISM FOR ADH IS SUSTAINED, THERE IS EXCESSIVE WATER RETENTION IN THE BODY

WHEN THERE IS OR INADEQUATE AMOUNT OF ADH, THE BODY IS UNABLE TO CONCENTRATE URINE, & EXCESSIVE H2O LOSS OCCURS

DIABETES INSIPIDUSCHARACTERIZED BY A DEFICIENCY OF ADH. WHEN IT OCCURS, IT IS MOST OFTEN

ASSOCIATED WITH :NEUROLOGICAL CONDITIONS, SURGERY, TUMORS, HEAD INJURY, OR INFLAMMATORY PROBLEMS

DIABETES INSIPIDUS ABSOLUTE / PARTIAL DEFICIENCY OF VASOPRESSIN

S/SX:POLYURIA

15-29L/ DAYPOLYDIPSIASG OF URINE IS <1.010S/SX OF DHNSHOCK

DIABETES INSIPIDUS ABSOLUTE / PARTIAL DEFICIENCY OF VASOPRESSIN

MANAGEMENTHORMONAL REPLACEMENT – FOR LIFE

VASOPRESSIN (PITRESSIN TANNATE IN OIL) – IM OR NASAL SPRAY

NON-HORMONAL THERAPYCHLORPROPRAMIDE – INCREASE RESPONSE OF THE

BODY TO DECREASED VASOPRESSIN

INCREASE FLUIDSMONITOR I&O + WEIGHT (MIOW)MAINTAIN FLUID & ELECTROLYTE

BALANCE

SYNDROME OF INAPPROPRIATE ADH

(SIADH)ELEVATED ADHS/SX:DECREASED SERUM SODIUM

CX IN LOC TO UNCONSCIOUSNESSSEIZURES

WATER INTOXICATIONN/VMENTAL CONFUSIONPersistent excretion of concentrated urineSigns of fluid overloadHyponatremia

SYNDROME OF INAPPROPRIATE ADH

MANAGEMENT:WATER INTAKE RESTRICTIONADMINISTER AS ORDERED:

NaClDiureticsDemeclocycline (declamycin) – a tetracycline

analogue that interferes with the action of ADH on the collecting tubules

THYROID DISORDERS

Hypothyroidism underactive state of the thyroid gland hyposecretion of thyroid hormone most common in women, middle-age primary function is to control the level of cellular

metabolism by secreting thyroxin (T4) and triiodothyronine (T3)

DX: decreased T3, T4 Elevated TSH, cholesterol

HypothyroidismA state of low serum TH levels

or cellular resistance to TH

AutoimmuneDevelopment

alDietary

Iodine deficiencyOncologic

DrugsIatrogenicNon-

thyroidalEndocrine

Pathophysiology inadequate secretion of thyroid hormone

general slowing of all physical and mental process

metabolic rate oxidation of nutrients for energy heat production

Complications :• Cretinism – severe physical and mental

retardation resulting from severe deficiency of thyroid function in infancy or childhood (congenital hypothyroidism)

requires lifetime hormone replacement• Myxedema – occur from prolonged severe

disease accelerated devt. of coronary artery disease coma – rapid dev’t. of impaired consciousness and suppression of vital functions

MYXEDEMA COMA- a condition resulting from persistent low thyroid production.

Med. Mgt. – thyroid replacement therapy Levothyroxine (Synthyroid) , liothyronine Expected effects: diuresis, puffiness, improved reflexes and muscle tone, PR

Nsg. Interventions provide a warm environment, conducive to

rest avoid use of all sedatives assist client in choosing calorie, cholesterol

diet fluid and fiber to relieve constipation physical activity and sensory stimulation

gradually as condition improves monitor cardiovascular response to increased

hormone levels carefully provide info. about prescribed medications

(name, dosage, side effects) and importance of lifelong medical supervision

Hyperthyroidism

over-secretion of the thyroid gland also called thyrotoxicosis or graves disease, tissues are stimulated by excessive thyroid hormone a recurrent syndrome, may appear after emotional

stress or infection occurs mostly in women 20-50 yrs old

Causes : adenoma, goiter, viral inflammation, auto-immune glandular stimulation, grave’s disease - most common cause

Hyperthyroidism (cont.)

DX: > elevated T3, T4 valuesT4= 5-12mcg/dl , T3= 70-220 ng/dl , TSH= 0.2-5.4 mU/L• abnormal findings in the thyroid scan

Goiter – enlargement of the thyroid gland • due to stimulation of the thyroid gland by TSH

Simple goiter – enlarged thyroid gland• due to iodine deficiency, intake of goitrogenic

foods cabbage, turnips, soybeans• may be hereditary

Grave’s Disease disorder char. by one or more of the ff:

diffuse goiter

hyperthyroidism

infiltrative opthalmopathy exophthalmos seen in females under age 40 result from stimulation of the thyroid gland by thyroid-stimulating immunoglobulins (TSI) cause is unknown, may be hereditary, gender-

related, often occurs after severe emotional stress or infection

Complications :

cardiovascular disease (HPN, Angina, CHF) Exophthalmos – abnormal protrusion of the eyeballs

- caused by abnormal deposits of fat and fluid in the retroocular tissue

Corneal abrasion Thyroid storm or crisis life-threatening hypermetabolism and excessive adrenergic response (HR, RR, BP)

Thyroid Storm or Crisis

a medical emergency pts. develop severe manifestation of hyperthyroidism

temp., tachycardia, dysrhythmias worsening tremors, restlessness delirious or psychotic state or coma abdominal pain BP and RR

Precipitated by a major stressor: infection trauma or surgery (thyroidectomy) inadequate treatment

Do you take this woman as your wife…. In sickness and

in health…

TAKE ME! TAKE ME!!

Anxiety Flushed, smooth skin Heat intolerance Mood swings Diaphoresis Tachycardia Palpitations Dyspnea Delirium, coma Heart failure

Assessment Findings: Thyroid storm

Med. Mgt.• Medications

Propylthiouracil (PTU) – antithyroid drug - blocks thyroid hormone production- can cause agranulocytosis- monitor pt. CBC

Methimazole (Tapazole) – blocks TH prod. Iodine preparations – the size and vascularity of the thyroid gland; inhibit release of thyroid hormones 1.) Lugol’s solution

can be given with milk or fruit juice should be taken with a straw – may stain the teeth complications : brassy taste in the mouth, sore teeth and gums

2.) Saturated solution of potassium iodide (SSKI)

Med. Mgt.• Medications

Propanolal (Inderal) and other adrenergic blockers• relieve the adrenergic effects of excess thyroid

hormone (sweating, palpitations, tremors)

• Radioactive iodine – limits the secretion of the

hormone by damaging or destroying thyroid tissue

• Surgical intervention (performed only when pt. is in a

euthyroid state) subtotal thyroidectomy (large goiter) total thyroidectomy (if carcinoma is present)

Nsg. Interventions: Provide calm, restful envt.

1. physical comfort, cool envt. temp., bathe frequently w/ cool water

2. provide adequate rest, avoid muscle fatigue3. stressors in the envt.— noise and lights4. relaxation techniques

Provide adequate nutrients1. calorie, protein, balanced diet (4,000-5,000

cal/day)2. fluid intake3. Restrict stimulants (tea, coffee, alcohol)4. small, frequent feedings if hypermotility is

present5. Daily wt.

Nsg. Interventions:

Provide emotional support

Provide eye care1. eye drops, dark glasses, patch eyes if

necessary2. elevate head of bed for sleep3. restrict dietary sodium4. assess adequacy of lid closure

Be alert for complications

Post-op care after Thyroidectomy

O2 therapy, suction secretions Monitor for signs of bleeding and excessive edema elevate head of bed 30o, support head and neck –

to avoid tension on suturescheck dressing frequently, check behind the neck

for bleeding assess for signs of resp. distress, hoarseness (laryngeal edema or damage) keep tracheostomy set in patient’s room for

emergency use

Post-op Complications: be alert for the possibility of:

1. Tetany (due to hypocalcemia caused by accidental removal of parathyroid glands)

assess for numbness, tingling or muscle twitching

Chvostek’s sign and Trousseau’s sign Ca+ gluconate IV

2. HemorrhageWOF: hypotension, tachycardia, other signs of

hypovolemiaWOF: irregular breathing, swelling, choking---

possible hemorrhage and tracheal compressionWOF: early signs of hemorrhage: repeated

clearing of the throat, difficulty swallowing

Post-op Complications: be alert for the possibility of:

3. Thyroid storm - life-threatening- sudden release of thyroid hormone- fever, tachycardia, increasing restlessness

and agitation, delirium

PARATHYROID GLAND DISORDERS

Hypoparathyroidism is characterized by decrease in

the PTH level

PARATHYROID HORMONE

Mobilization of calcium and phosphorous

from bone

Promotes resorption of calcium from

bone to maintain normal serum calcium levels

Promotes absorption of calcium in the GI tract ( by stimulating kidneys to convert vit.D to its active form).

Renal: increases calcium

reabsorption and phosphate excretion

Function of calcium: maintains N muscle

and neuromuscular responses.

Necessary component for blood coagulation mechanisms

CALCIUM STAYS IN THE BONE

CALCIUM DEPOSITED

IN THE BONE

EXCRETION OF CALCIUM

HYPOCALCEMIA

• TINGLING OF FINGERS• CHVOSTEKS/

TROUSSEAU’S• FATIGUE, WEAKNESS• CARDIAC

ARRHYTHMIAS• SEIZURE• BRONCHOSPASM

TESTS USED TO ELICIT SIGNS OF CALCIUM DEFICIENCY

PARATHYROID DISORDERS

DIAGNOSTIC TESTS:HEMATOLOGICAL

SERUM CALCIUMSERUM PHOSPHORUSSERUM ALKALINE PHOSPHATASE

URINARY STUDIESURINARY CALCIUMURINARY PHOSPHATE - TUBULAR

REABSORPTION OF PHOSPHATE

HYPOPARATHYROIDISMXRAY: INCREASED BONE DENSITYMANAGEMENT:Ca SUPPLEMENTVIT D SUPPLEMENT – LIQ FORM: WITH WATER,

JUICE OR MILK, pc

SEIZURE precLISTEN FOR STRIDOR OR HOARSENESSTRACHEOSTOMY SET @ BEDSIDE

CaGLUCONATE @ BEDSIDE

T C

AKE

ARE

ETANY

RACHEOSTOMY

ALCIUM GLUCONATE

ALCIUM 8.6 – 10.6 mg / dL

Hyperparathyroidism is characterized by excesssive

secretion of PTH

PARATHYROID HORMONE

Mobilization of calcium and phosphorous

from bone

Promotes resorption of calcium from

bone to maintain normal serum calcium levels

Promotes absorption of calcium in the GI tract ( by stimulating kidneys to convert vit.D to its active form).

Renal: increases calcium

reabsorption and phosphate excretion

Function of calcium: maintains N muscle

and neuromuscular responses.

Necessary component for blood coagulation

mechanisms

CALCIUM RELEASED INTO

THE BLOOD LEADS TO BONE

DAMAGE

HYPERCALCEMIA, LACK OF RESORPTION OF CALCIUM INTO THE

BONE( BONE CYST AND PATHOLOGIC

FRACTURE)

TUBULAR CALCIUM DEPOSIT- KIDNEY

STONES, AZOTEMIA, HPN BY RF, RENAL

FAILURE

ANOREXIAN/V

CONSTIPATIONPEPTIC ULCER DSE

MUSCLE WEAKNESS

PERSONALITY CHANGESCARDIAC

ARRHYTHMIAS

HYPERPARATHYROIDISMINCREASED PTH PRODUCTIONHYPERCALCEMIAHYPOPHOSPHATEMIAPRIMARY – TUMOR OR HYPERPLASIA OF THE

PARATHYROID GLAND

SECONDARY – COMPENSATORY OVERSECRETION OF PTH IN RESPONSE TO HYPOCALCEMIA FROM:CHRONIC RENAL DSEMALABSORPTION SYNDROMEOSTEOMALACIA

HYPERPARATHYROIDISMMANAGEMENT:

TX OF CHOICE : SURGICAL REMOVAL OF HYPERPLASTIC TISSUE

IV PNSS 5L/ DAY WITH DIURETICSCRANBERRY JUICE (ACID-ASH)LOW CaSTRAIN URINE FOR STONESCARE FOR PARATHYROIDECTOMY

DISORDERS OF THE PANCREAS

DIABETES MELLITUS(TYPE I, TYPE II)

TWO TYPES OF DIABETES

Diabetes Mellitus

is a chronic disorder of carbohydrate, protein, and fat metabolism resulting from insulin deficiency or abnormality in the use of insulinPredisposing factors:

exact cause of diabetes mellitus remain unknown

genetic / hereditary predisposition viruses pancreatitis pancreatic tumor autoimmune disorder obesity (overweight people require more insulin

to metabolize the food they eat or the number of insulin receptor sites in cells is decreased)

Types1.Insulin – Dependent Diabetes Mellitus (IDDM) or

Type I destruction of beta cells of the pancreas little or no

insulin production requires daily insulin admin. may occur at any age, usually appears below age 15

2.Non Insulin–Dependent Diabetes Mellitus (NIDDM) or Type II probably caused by:

disturbance in insulin reception in the cells number of insulin receptors loss of beta cell responsiveness to glucose leading

to slow or insulin release by the pancreas

occurs over age 40 but can occur in children common in overweight or obese w/ some circulating insulin present, often do not

require insulin

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DIAGNOSTIC TEST FOR DM

1. Fasting Blood Sugar (FBS) NPO for 12 hours Normal value= 80-120 mg/dl 140 mg/dl or more – diagnostic of DM

2. Postprandial blood sugar Blood is withdrawn 2 hrs. after a meal N value = < 120mg/dl 200 mg/dl or more is diagnostic of DM

3. Oral Glucose Tolerance Test (OGTT) NPO 12 hrs, no smoking, coffee or tea,

minimize activity, minimize stress obtain FBS, administer 100 gm. Glucose by

mouth diluted in juice; obtain blood and urine specimen after 1, 2 and 3 hrs.

N value = blood glucose rise to 140 mg/dl in the 1st hour and returns to normal by 2nd and 3rd hrs.

Abnormal = blood glucose does not return to normal by 2nd and 3rd hrs.; all urine specimen positive for glucose

Diagnostic Tests for DM

4. Glycosylated hemoglobin Provides information about blood glucose

level during the previous 3 months bec. glucose in the bloodstream attaches to

some of the hemoglobin and stay attached during the 120-day lifespan of the RBC

D-I-A-B-E-T-E-SD- DIET: 50-60% CHO, 20-30% FATS,

10-20% CHONI- INSULIN– TYPE 1A- ANTIDIABETIC AGENTS– TYPE 2B- BLOOD SUGAR MONITORINGE- EXERCISET- TRANSPLANT OF PANCREASE- ENSURE ADEQUATE FOOD INTAKES- SCRUPULOUS FOOT CARE

Management of Hypoglycemia

1. Give simple sugar orally if pt. is conscious and can swallow – orange juice, candy, glucose tablets, lump of sugar

2. Give Glucagon (SQ or IM) if pt. is unconscious or cannot take sugar by mouth

3. As soon as pt. regains consciousness, he should be given carbohydrate by mouth

4. If pt. does not respond to the above measures, he is given 50 ml of 50% glucose I.V. or 1000 ml of 5%-10% glucose in water I.V.

Oral Antidiabetic AgentsClassification &

ExamplesMechanism of Action

Sulfonylureas-Tolbutamide (Orinase)- Chlorpropamide (Diabinese)- Glipizide (Glucatrol)- Glimepiride (Amaryl)- Glibenclamide

stimulate beta cells of the pancreas to secrete insulin improve binding bet. insulin and insulin receptors no. of insulin receptors

Biguanides- Metformin (Glucophage)

body tissues’ sensitivity to insulin glucose uptake inhibit glucose prod. by the liver

Alpha-Glucosidase Inhibitors- Acarbose (Precose)- Miglitol (Glyset)

delay absorption of glucose in the intestine

Thiazolidinediones- Rosiglitazone (Avandia)- Pioglitazone (Actos)

enhance insulin action at the receptor sites

Oral Antidiabetic Agents

DIABETES MILLETUSINSULIN THERAPYDISPENSED IN “U”/ml : eg 100, 80REFRIGERATEGIVEN @ ROOM TEMPGENTLY ROTATED, NOT SHAKENROUTE : SQ ; IM OR IV SYRINGE: 5/8 INCH ; SAME BRAND

INSULIN ONSET PEAK

DURATION

Ultra rapid acting Insulin analog (Humalog)

15 mins.

2-4 hrs.

6-8 hrs.

Rapid acting: Regular (Semilente)

½-1 hr 2-4 hrs.

6-8 hrs.

Intermediate: NPH (Lente)

1-2 hrs. 7-12 hrs.

24-30 hrs.

Long acting: Protamine Zinc (Ultralente)

4-6 hrs. 18 + hrs

30-36 hrs.

DIABETES MILLETUSINSULIN THERAPY:SITE OF INJECTION:

ABDOMENANTERIOR THIGHARM UPPER BACK BUTTOCKS

B. Teach pt. on correct administration of insulin and other hypoglycemic agents.

1. insulin in current use may be stored at room temp., all others in ref. or cool area

2. avoid injecting cold insulin lead to tissue reaction3. roll insulin vial to mix, do not shake, remove air

bubbles from syringe4. press (do not rub) the site after injection (rubbing

may alter the rate of absorption of insulin)5. avoid smoking for 30 mins. after injection (cigarette

smoking absorption)6. Rotate sites Failure to rotate sites may lead to Lipodystrophy Lipodystrophy – localized disturbance of fat

metabolism Ex. Lipohypertrophy – thickening of subcutaneous

tissue at injection site, feel lumpy or hard, spongy result to absorption of insulin making it

difficult to control the pt.’s blood glucose

Teach pt. to estabilish and maintain a pattern of regular exercise Benefits of exercise :

promotes use of CHO & enhances action of insulin blood glucose levels need for insulin the no. of functioning receptor sites for insulin

perform exercise after meals to ensure an adequate level of blood glucose

carry a rapid-acting source of glucose during exercise

excessive or unplanned exercise may trigger hypoglycemia

take insulin and food before active exercise

ACUTE COMPLICATIONS OF DIABETES MILLETUS

DIABETIC KETO-ACIDOSIS (DKA)

INSULIN SHOCK

HYPERGLYCEMIC, HYPEROSMOLAR, NONKETOTIC (HHONK) COMA

Diabetic Ketoacidosis (DKA) Coma

S/Sx:polyuria, thirstnausea, vomiting, abdominal pain –-- due to acidosisweakness, headache, fatigue --- due to acidosis and F/E imbalancedim visiondehydration, hypovolemic shock (PR, BP, dry skin, wt. loss)hyperpnea (Kussmaul’s breathing)acetone breath (fruity odor)lethargy COMABlood glucose level > 250-350 mg/100 ml.

Hyperglycemic, Hyperosmolar, Non-Ketotic Coma (HHNC)

can occur when the action of insulin is severely inhibitedseen in pts. w/ NIDDM, elderly persons w/ NIDDM

Precipitating factors:infection, renal failure, MI, CVA, GI hemorrhage, pancreatitis, CHF, TPN, surgery, dialysis, steroids

S/Sx: polyuria oliguria (renal insufficiency) lethargy temp, PR, BP, signs of severe fluid deficit Confusion, seizure, coma Blood glucose level > 600 mg/100 ml.

HHONKS/SX:S/SX OF DKA WITHOUT:

KAUSMAUL’S BREATHINGACETONE BREATHMETABOLIC ACIDOSISKETONURIA

Interventions for DKA and Hyperosmolar Coma

Regular insulin IV push or IV drip 0.9% NaCl IV – 1 L during the 1st hr, 2-8 L over 24 hrs. administer sodium bicarbonate IV to correct acidosis Monitor electrolyte levels, esp. serum K+ levels administer K+, monitor UO hourly (30ml/hr)

Long-term Complications of DM

1. Vascular Changesa. ) Macroangiopathy – hardening and damage of the

walls of large arteriesCoronary Artery DiseaseCVA (Stroke)Peripheral vascular disease – foot ulcers and gangrene

b. ) Microangiopathy – destruction of small blood vesselsRetinopathy – damage to retinal capillaries; hemorrhage, blindnessNephropathy – damage microcirculation of kidneys; CRF

2. Neuropathy Damage to the neurons caused by vascular insufficiency and blood glucoseSensory and motor impairmentNumbness, tingling, pain in extremities Painless neuropathy

Impotence!!

DISORDERS OF THE ADRENAL GLANDS

ADRENAL GLANDSTIMULATED BY ACTHADRENAL MEDULLA- SECRETES

CATECOLAMINE, (EPINEPHRINE, & NOREPINEPHRINE).

ADRENAL CORTEX- MAIN BODY; RESP FOR SECRETION OF GLUCO,MINERALO, SEX HORMONES (ANDRO & ESTRO)

FUNCTION IS TO CONTROL THE (-) FEEDBACK MECHANISMS REGULATING HORMONE RELEASE

ADRENAL CORTEX DISORERS

ADRENAL INSUFFICIENCY ( ADDISON’S DSE)

CUSHING’S SYNDROME

ADRENAL INSUFFICIENCY

ADDISON’S DISEASE

INCAPABILITY OF THE ADRENAL CORTEX TO PRODUCE GLUCOCORTICOIDS IN RESPONSE TO

STRESS

Addison's DiseaseReplacement of hormones

Hydrocortisone; Fludrocortisone

PNSS (0.9 NaCl)Dextrose

Diet:High-CHO & CHON

Low potassium, high sodium

Addison’s disease

Addison's DiseaseMVS [4x / day]

Infection, Addisonian crisis, dehydration

MIOW / MBP / MBGGive steroids with milk or an

antacidAvoid: Contacts & Stress

CUSHING’S SYNDROMECAUSE:SUSTAINED OVER-PRODUCTION OF

GLUCOCORTICOIDS BY ADRENAL GLAND FROM ACTH BY PITUITARY TUMOR

EXCESSIVE GLUCORTICOID ADMINISTRATION

CUSHING’S SYNDROMES/SX:TRUNCAL OBESITYBUFFALO HUMPMOON-FACEWT GAINSODIUM RETENTIONTHINNING OF EXTREMITIES – FROM LOSS OF

MUSCLE TISSUE DUE TO PROTEIN CATABOLISM

CUSHING’S SYNDROME

PURPLE STRIAE – FROM THINNING OF SKINECHYMOSIS FROM SLIGHT TRAUMAANDROGENIC EFFECTS:

OLIGOMENORRHEAHIRSUTISMGYNECOMASTIA

HYPERTENSION FROM S. Na

CUSHING’S SYNDROME

TREATMENT & NURSING CARE:

PSYCHOLOGICAL SUPPORTPREVENT INFECTION – INFLAM & IMMUNE

RESPONSE ARE SUPPRESSEDPROMOTE SAFETY SURGERY – SUB/TOTAL ADRENALECTOMYTreat HPN

ALDOSTERONISM

HYPERSECRETION OF ALDOSTERONE

CONN’S SYNDROME

CONN’S SYNDROMEPRIMARY ALDOSTERONISMCAUSE:ADRENAL ADENOMAS/SX:HYPOKALEMIAFATIGUEHYPERNATREMIA, HPNMANAGEMENT:SURGERYALDACTONE – ALDOSTERONE ANTAGONIST

ADRENAL MEDULLA

HORMONES : EPINEPHRINE NOREPINEPHRINE

EFFECTS

PHEOCHROMOCYTOMATUMOR OF ADRENAL MEDULLA SECRETES INCREASED

AMOUNT OF CATECHOLAMINES

A small tumor in the adrenal gland that secretes large amounts of epinephrine and norepinephrine.

S/SX:HPNHYPERGLYCEMIACARDIAC ARRHYTHMIA & CHF DIAGNOSTIC TEST : VMA IN 24H URINE- VANILLYMANDALIC

ACID

VMA IN 24H URINEEND PRODUCT OF CATECHOLAMINE

METABOLISMDRUGS & FOOD TO BE WITHHELD 24H B4 THE

TEST:COFFEE & TEABANANAVANILLACHOCOLATES

PHEOCHROMOCYTOMAMANAGEMENT:SURGERYMEDICAL : ADRENERGIC BLOCKING

AGENTS: PHENTOLAMINE

NURSING CARE:MONITOR BP IN SUPINE & STANDINGMONITOR URINE FOR GLUCOSE &

ACETONE

THE AGING EFFECTS OF ENDOCRINE SYSTEM

DECREASE IN TSH,TH & INSULIN

DECREASE BMR & ENERGY

DECREASE GLUCOSE TOLERANCE

DECREASE IN GHDECREASE IN MUSCLE MASS & INCREASE FAT

STORAGE

RECAP:ANTERIOR PITUITARY:GIGANTISM, ACROMEGALLY, DWARFISM

POSTERIOR PITUITARY:DIABETES INSIPIDUS, SIADHLOCATION: BASE OF THE BRAIN

RECAPADRENAL GLAND:ADDISON’S DSECUSHING SYNDROMEALADOSTERONISM

ADRENAL MEDULLA:PHEOCHROMOCYTOMA

LOCATION: ON TOP OF THE KIDNEY

RECAPPANCREAS:DMLOCATION: POSTERIOR TO LIVER

PARATHYROID:HYPORATHYROIDISMHYPERPARATHYROIDISMLOCATION: NEAR THYROID

RECAPTHYROID:HYPOTHYROIDISMCRETINISMMYXEDEMAHYPERTHYROIDISM (GRAVE’S DSE)

LOCATION: ANTERIOR PART OF NECK

QUESTION NO. 1A CLIENT IS FOUND TO BE COMATOSE &

HYPOGLYCEMIC W/ A BLOOD SUGAR OF 50 MG/DL. WHAT NURSING ACTION IS IMPLEMENTED FIRST?

A. INFUSE 1L OF D5W OVER A 12 HR PERIOD.B. ADMIN. 50% GLUCOSE IVC. CHECK THE CLIENT’S URINE FOR THE

PRESENCE OF SUGAR AND ACETONED. ENCOURAGE THE CLIENT TO DRINK ORANGE

JUICE W/ ADDED SUGAR

QUESTION NO.2WHAT IS THE PRIMARY ACTION OF INSULIN IN

THE BODY?A. ENHANCES THE TRANSPORT OF GLUCOSE

ACROSS THE CELL WALLSB. AIDS IN THE PROCESS OF

GLUCONEOGENESISC. STIMULATES THE PANCREATIC BETA CELLSD. DECREASE THE INTESTINAL ABSORPTION OF

GLUCOSE

QUESTION NO.3POSTOPERATIVE THYROIDECTOMY NURSING

CARE INCLUDES WHICH MEASURES?A. HAVE CLIENT SPEAK EVERY 5-10 MINUTES IF

HOARSENESS IS PRESENTB. PROVIDE LOW-CALCIUM DIET TO PREVENT

HYPERCALCEMIAC. CHECK THE DRESSING AT THE BACK OF THE

NECK FOR BLEEDINGD. APPLY SOFT CERVICAL COLLAR TO RESTRICT

MOVEMENT