nursing care of clients with disturbances of the endocrine syste1

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NURSING CARE OF CLIENTS WITH DISTURBANCES OF THE endocrine SYSTEM

PITUITARY GLAND (HYPOPHYSIS)

Located at the base of the brain

Directly affects the function of the other endocrine glands

PARTS OF THE PITUITARY GLAND

Anterior Pituitary Gland (Adenohypophysis) Posterior Pituitary Gland (Neurohypophysis)

SECRETIONS OF THE ANTERIOR PITUITARY GLAND

GROWTH HORMONE (SOMATOTROPIN)

responsible for growth of body tissues and bone

PROLACTIN (MAMMOTROPIC/LACTOTROPIC HORMONE)

responsible for tissue growth and lactation

ACTH (ADRENOCORTICOTROPIC HORMONE)

stimulates adrenal cortex to secrete CORTISOL and ALDOSTERONE

TSH (THYROID-STIMULATING HORMONE)

stimulates the thyroid gland to secrete T3 and T4

GONADOTROPINS (LH AND FSH)

influence the ovaries to secrete ESTROGENS and PROGESTERONE; testes to secrete

TESTOSTERONE

MSH (MELANOCYTE-STIMULATING HORMONE)

Stimulates melanocytes to produce pigment MELANIN

SECRETIONS OF THE POSTERIOR PITUITARY GLAND

ADH (ANTI-DIURETIC HORMONE/VASOPRESSIN)

causes RENAL RETENTION OF WATER (excluding sodium) and VASOCONSTRICTION

OXYTOCIN

hormone released during childbirth to cause UTERINE CONTRACTION and during breastfeeding

to cause “let-down reflex”

HYPERPITUITARISM

Chronic, progressive HYPERFUNCTION of the pituitary gland resulting to OVERSECRETION of the

anterior pituitary hormones

ETIOLOGY

Tumor

Hyperplasia

ASSESSMENT

ACROMEGALY – gradual, marked enlargement of the bones of the face, jaw, hands and feet. It

may be accompanied by diaphoresis, hyperglycemia, oily skin and hirsutism

GIGANTISM – proportional overgrowth of all body tissues with remarkable height

Galactorrhea

Cushing’s Disease

Hyperthyroidism

Precocious puberty

“Eternal tan”

SIADH

DIAGNOSTIC TESTS

Skull x-ray, CT Scan and MRI would reveal TUMOUR OR PITUITARY ENLARGEMENT

Serum Analysis would reveal ELEVATED GROWTH HORMONES



MEDICAL MANAGEMENT

Administration of BROMOCRIPTINE (PARLODEL) to inhibit synthesis of growth hormone

Radiation therapy

NURSING INTERVENTIONS

Provide EMOTIONAL SUPPORT if there is altered body image

Provide ROM if there is muscle weakness Apply OILY LOTION if there is dry skin

SURGICAL MANAGEMENT

TRANSPHENOIDAL HYPOPHYSECTOMY to remove the pituitary gland

PREPARING THE PATIENT FOR HYPOPHYSECTOMY

Explain the procedure to the patient

Insert INDWELLING CATHETER since DIURESIS (SIGN OF DIABETES INSIPIDUS) may be a

complication of the surgery

NURSING CARE AFTER HYPOPHYSECTOMY

Place patient on HIGH-FOWLER’S position

Place patient on BED REST on the first 24 hours and encourage ambulation on DAY 2

Remind the patient to AVOID SNEEZING, COUGHING, BENDING OVER and BLOWING THE NOSE Administer analgesics if there is pain

Monitor for signs and symptoms of DIABETES INSIPIDUS (COMMON COMPLICATION)

MANAGEMENT IF THERE IS DIABETES INSIPIDUS

Watch out for CARDINAL SIGNS (thirst, urine output of 900ml/2 hours, increased urine specific

gravity of 1.004)

Provide fluid replacement and administer VASOPRESSIN as ordered

Expect DIABETES INSIPIDUS to resolve within 72 hours

If there is rhinorrhea, check for glucose since it may be indicative of CSF LEAKAGE

DISCHARGE INSTRUCTIONS AFTER HYPOPHYSECTOMY

Instruct patient to REPORT PROGRESSIVE VISUAL CHANGES and DIURESIS

Advise patient NOT TO BRUSH TEETH for 2 weeks to avoid injury to suture line Advise patient AVOID USE OF COMMERCIAL MOUTHWASHES to avoid irritation of the suture

line

HYPOPITUITARISM

HYPOFUNCTION of the pituitary gland resulting to DEFICIENT SECRETION of the pituitary

hormones

Results to MARKED METABOLIC DYSFUNCTION, SEXUAL IMMATURITY AND GROWTH

RETARDATION

ETIOLOGY

Trauma

Tumour

Vascular lesion

Surgery or radiation of the pituitary gland

congenital

ASSESSMENT

Dwarfism

Absence of milk during lactation (women)

Addisonian symptoms

Symptoms of hypothyroidism



Underdeveloped genitals

No growth of body hair

Amenorrhea and infertility

Decreased libido, impotence, and aspermia

Symptoms of diabetes insipidus

DIAGNOSTIC TESTS Skull x-ray, CT scan may reveal PITUITARY TUMOUR

Serum analysis may reveal LOW LEVELS OF HORMONES

MEDICAL MANAGEMENT

Hormone replacement therapy

Radiation therapy

SURGICAL MANAGEMENT

Surgical removal of the tumour

SYNDROME OF INAPPROPRIATE ANTI-DIURETIC HORMONE (SIADH)

EXCESSIVE anti-diuretic hormone (ADH) secretion by the posterior pituitary gland

Characterized by IMPAIRED WATER EXCRETION with NORMAL SODIUM EXCRETION

ETIOLOGYCNS disorders interfering with hypothalamic-pituitary mechanisms such as:

BRAIN TUMOUR

STROKE

HEAD INJURY

GUILLAIN-BARRE SYNDROME

Pulmonary disorders such as:

PNEUMONIA,

TUBERCULOSIS,

BRONCHIECTASIS

DRUGS that increase ADH production such as: ANTIDEPRESSANTS

o

NSAIDso CHLORPROPRAMIDE (Diabinase)

o VINCRISTINE (Oncovin)

o CYCLOPHOSPHAMIDE (Cytoxan)

o CARBAMAZEPINE (Tegretol)

o METOCLOPRAMIDE (Reglan),

o MORPHINE

ASSESSMENT

USE MANIFESTATIONS

Hyponatremia THIRST, ANOREXIA, FATIGUE AND LETHARGY (FIRST SIGNS)

Vomiting and intestinal cramping

DECREASED DEEP TENDON REFLEXES

Water

retention

Weight gain

Edema

Decreased urine output



COMPLICATIONS

Cerebral edema

Brain herniation

DIAGNOSTIC TESTS

BLOOD TEST

Elevated serum ADH

Decreased serum osmolality (<280 mOsm/kg water) Decreased serum sodium (<135 mEq/L

URINALYSIS

Elevated sodium (>20 mEq/L) Increased osmolality (>150 mOsm/kg)

MEDICAL MANAGEMENT

INTERVENTION RATIONALE

Restricted Water Intake

(500 ml -1L/day)

To minimize water intoxication

200-300 ml of 3% NSS

(slow infusion)

To slowly increase the serum sodium level

Rapid infusion may cause cerebral edema

Demeclocycline

(Declomycin

To decrease or block renal response to ADH

FUROSEMIDE (LASIX)

with normal or hypertonic

saline

To maintain urine output and block ADH secretion


Monitor weight, intake and output, vital signs and serum sodium levels

Observe for restlessness, irritability, seizures, heart failure, and unresponsiveness (SIGNS OF

HYPONATREMIA AND WATER INTOXICATION)

SURGICAL MANAGEMENT

Removal of tumour causing hypersecretion of ADH

DIABETES INSIPIDUS

DEFICIENCY in VASOPRESSIN or anti-diuretic hormone (ADH) secretion by the posterior pituitary

gland

Characterized by EXCESSIVE WATER EXCRETION

ETIOLOGY

Hereditary

Tumors or injury to hypothalamus or pituitary gland

Removal of the pituitary gland (HYPOPHYSECTOMY)

Drugs that interfere with response of the kidney to ADH such as LITHIUM CARBONATE,

DEMECLOCYCLINE

PATHOPHYSIOLOGY



ASSESSMENT

CAUSE MANIFESTATIONS

Increased water excretion Large volume of dilute urinary output (POLYURIA)

Urine output of more than 4L/day (DIAGNOSTIC SIGN)

Dehydration Insatiable thirst (POLYDIPSIA)

Hypotension

Rapid but weak pulse (TACHYCARDIA)

Hypovolemia

Poor skin turgor

Dry cracked mucous membranes

DIAGNOSTIC TESTS

BLOOD BLOOD TEST Decreased serum ADH

Increased hemoglobin and hematocrit

Increased BUN

URINALYSIS Low specific gravity (less than 1.005)

decreased osmolality (50-200 mOsm/kg)

MEDICAL MANAGEMENT

INTERVENTION RATIONALE

Oral chlorpropramide(Diabinase)

To increase action of existing ADHGiven only in mild diabetes insipidus

Desmopressin acetate

(synthetic vasopressin)

Drug of choice for severe cases

Given via intranasal spray, IV, IM or SQ

Volume for volume

replacement of urine

output

To prevent dehydration

NURSING INTERVENTIONS Monitor weight, intake and output, vital signs and electrolyte levels

Monitor for signs of dehydration

Increase fluid intake by oral or intravenous route

Encourage client to drink fluids in equal amount to urine output



THYROID GLAND

Located anterior part of the neck

Controls rate of body metabolism and growth

HORMONES SECRETED BY THE THYROID GLAND

HORMONE

Triiodothyronine (T3)

Tetraiodothyronine (T4)

Thyrocalcitonin

ACTION

Regulate metabolism and growth

Catabolism and body heat production

Lowers high serum calcium levels

DIAGNOSTIC TESTS FOR THYROID FUNCTION

DIAGNOSTIC TEST

Serum T3 and T4

Protein Bound Iodine (PBI)

Radioactive Iodine Uptake

(RAIU)

CONCEPTS

HIGH levels suggest hyperthyroidism LOW levels suggest hypothyroidism

HIGH levels suggest hyperthyroidism

LOW levels suggest hypothyroidism

Iodine is withheld 7-10 days before the test

Contraceptive pills is discontinued (↑BMR) Contraindication during pregnancyI131 is given per oremPatient is exposed to cameraHIGH levels suggest hyperthyroidismLOW levels suggest hypothyroidism



Thyroid Scan Intravenous radioisotope iodine is injectedPatient is exposed to scintillation camera

Fine Needle Biopsy (FNB) Aspiration of thyroid tissue

Detects presence of malignant cells

Reflex Testing (Kinemetry) Tendon of achilles reflex (TAR) is assessedHYPERACTIVE TAR suggests hyperthyroidismHYPOACTIVE TAR suggests hypothyroidism

GOITER

enlargement of the thyroid gland

result from increased TSH may occur with HYPERTHYROIDISM, HYPOTHYROIDISM OR EUTHYROIDISM

TYPES OF GOITER

TOXIC GOITER – hyperthyroid goiter

NON-TOXIC OR SIMPLE GOITER – euthyroid goiter

HYPERTHYROIDISM

Other names include THYROTOXICOSIS, GRAVE’S DISEASE, EXOPHTHALMIC GOITER OR TOXIC

DIFFUSE GOITER

Common to females below 40 years old

ETIOLOGY

Severe emotional stress

Autoimmune disorder Thyroid inflammation

PATHOPHYSIOLOGY

ASSESSMENT

Due to increased amounts of thyroid hormone

Enlarged thyroid

Nervousness



Heat intolerance

Sweating

Weight loss

Increased appetite

Frequent bowel movements

Tremor Palpitations

Hypertension

Due to activation of cytokine-mediated activation of orbital tissue fibroblasts

Exopthalmus (may not be present in other patients)

Due to increased activity in spinal cord area that controls muscle tone

Fine tremor

Shaky handwriting

Clumsiness

signs and symptoms of THYROID STORM due to hyperthyroid state

Tachycardia

Vomiting High fever

Vomiting

Shock

Coma

COMPLICATIONS

Muscle wasting, atrophy, and paralysis

Heart failure

Hypoparathyroidism (after thyroidectomy)

Hypothyroidism (after radioactive iodine treatment)

DIAGNOSTIC TESTS

Radioimmunoassay: increased serum T3 and T4 levels Blood testing: decreased TSH level

Thyroid Scan: increased uptake

MEDICAL MANAGEMENT

THALIDOMIDES

Propylthiouracil (PTU) and Methimazole (Tapazole)

Blocks synthesis of thyroid hormones

Should be taken with meals

Side Effects: unexplained fever, sore throat, skin rashes

RADIOACTIVE IODINE (I131) TREATMENT

Treatment of choice for patients not planning to have children

Produces effects after 6-8 weeks May cause hypothyroidism

LUGOL’S SOLUTION (SATURATED SOLUTION OF POTASSIUM IODIDE)

Inhibits release of thyroid hormone

Mix with fruit juice or glass of water to improve the taste

Provide drinking straw to prevent staining

Side effects: allergic reaction, increased salivation, colds



DEXAMETHASONE

Inhibit action of thyroid hormones

Prevents conversion of T3 and T4

BETA-BLOCKERS: PROPANOLOL (INDERAL)

Controls hypertension and tachycardia

Blocks conversion of T4 to active T3 May cause hypotension

EMERGENCY TREATMENT OF THYROID STORM

Thalidomide

Dexamethasone

Supportive Measures: nutrients, vitamins, oxygen, hypothermia blankets and sedatives


Provide NON-STIMULATING ENVIRONMENT cool environment

Provide diet that is HIGH-CALORIE, HIGH-PROTEIN, VITAMINS AND MINERALS

Increase fluid intake (if with diarrhea)

Avoid stimulants like coffee, tea and nicotine

Administer artificial tears at regular intervals Instruct client to wear artificial tears when going out under the sun

AVOID EXCESSIVE PALPATION OF THE THYROID to prevent thyroid storm

SURGICAL MANAGEMENT

Subtotal Thyroidectomy – removal of about 5/6 of the gland

NURSING CARE AFTER THYROIDECTOMY

Monitor for respiratory distress; keep tracheostomy tray at the bedside

Monitor for signs of hemorrhage

Monitor for signs of hypocalcemia (tetany and numbness) indicative of accidental removal of the

parathyroid gland

Monitor for dysphagia or hoarseness (indicative of laryngeal nerve injury)

Change dressing as ordered Place patient on SEMI-FOWLER’S position and support neck with sandbags to ease tension on

the incision

Inform client that HYPOTHYROIDISM may develop 2-4 weeks after the surgery

NURSING CARE AFTER RADIOACTIVE IODINE (I131) TREATMENT

Instruct patient to AVOID EXPECTORATING since saliva will be radioactive for 24 hours after

treatment

Instruct to avoid taking OTC COUGH medications because it contains iodine

Instruct that iodine may remain the body for 1 week

Instruct to avoid breastfeeding

HYPOTHYROIDISM

Also called MYXEDEMA in adults or CRETINISM in children Results from DEFICIENCY of thyroid hormones

ETIOLOGY

Thyroidectomy

Autoimmune disorder e.g. Hashimoto’s Disease

Radiation therapy

Thalidomides



TYPES OF HYPOTHYROIDISM

1) PRIMARY – due to THYROID hypofunction

2) SECONDARY – due to PITUITARY hyposecretion of TSH

3) TERTIARY – due to HYPOTHALAMIC hyposecretion of TRH ( Thyrotropin Releasing Hormone )

PATHOPHYSIOLOGY

ASSESSMENT

Due to DECREASED BASAL METABOLIC RATE

Weakness

Fatigue

Forgetfulness

SENSITIVITY TO COLD

UNEXPLAINED WEIGHT GAIN

CONSTIPATION

Due to FLUID ACCUMULATION

Decreasing mental state (sign of myxedema coma)

Hoarseness

PUFFY FACE, HANDS, AND FEET

PERIORBITAL EDEMA

UPPER EYELID DROOP

Dry, sparse hair

Coarse, dry, flaky, inelastic skin

Thick, brittle nails

Late signs indicating disease progression

Progressive stupor

Hypoventilation

Hypoglycemia

Hyponatremia Hypotension

Hypothermia

Signs of MYXEDEMA COMA (severe form of hypothyroidism)

Hypothermia

Unconsciousness

COMPLICATIONS

Heart failure

Myxedema coma

Infection

Megacolon

Organic psychosis Infertility

Hyperlipidemia

DIAGNOSTIC TESTS

T3 and T4 – decreased

TSH – increased (primary hypothyroidism)

ABG analysis – RESPIRATORY ACIDOSIS



MEDICAL MANAGEMENT

Synthetic thyroid hormones

Proloid (Thyroglobulin)

SYNTHROID (LEVOTHYROXINE)

Cytomel

Remove tumour (if it is the cause) Surgical excision

Chemotherapy

Radiation


1) To manage constipation

HIGH-FIBER, LOW-CALORIE DIET

Increased physical activity

laxatives

2) Monitor for signs and symptoms of HYPERTHYROIDISM (common complication of thyroid

replacement)

Restlessness Sweating

excessive weight loss

3) Provide WARM ENVIRONMENT

The nurse implements which interventions in the plan of care of clients with hypothyroidism.

Providing a warm environment.

Providing cool temperature in the room

scheduling period of Rest.

Administering p.r.n. medications for diarrhea

PARATHYROID GLANDS

Gland located near the thyroid gland

Produces PARATHORMONE which regulates CALCIUM and PHOSPHOROUS levelsHYPERPARATHYROIDISM

Due to EXCESSIVE PARATHORMONE secretion

CLASSIFICATION

1) PRIMARY – due to presence of TUMOUR

2) SECONDARY – due to OVERCOMPENSATION to decreased calcium levels

ETIOLOGY

Congenital

Tumour

Vitamin D deficiency

Chronic renal failure PHENYTOIN AND LAXATIVE

PATHOPHYSIOLOGY



ASSESSMENT

1) Effects of HYPERCALCEMIA

Nephrolithiasis

Dehydration

Psychomotor and personality disturbances

2) Effects of BONE DEGENERATION Chronic low back pain

Bone tenderness

Fractures

DIAGNOSTIC TESTS

PTH – INCREASED (CONFIRMATIVE)

Increased serum calcium

Decreased serum phosphate

X-ray – demineralization of bones

MEDICAL MANAGEMENT

1) Promote EXCRETION OF CALCIUM

INCREASE FLUID INTAKE Diuretic e.g. FUROSEMIDE (LASIX)

Oral SODIUM PHOSPHATE

CALCITONIN

VITAMIN D to promote bone absorption of calcium

2) Correct Hyperphosphatemia

Administer ALUMINUM HYDROXIDE

Dialysis


STRAIN URINE to check for calculi

Provide at least 3L OF FLUID PER DAY

Give CRANBERRY OR PRUNE JUICE to increase urine acidity and prevent stones formation LIMIT CALCIUM INTAKE

AVOID DRUGS WITH CALCIUM e.g. ANTACIDS and THIAZIDE DIURETICS

SURGICAL MANAGEMENT

PARATHYROIDECTOMY – removal of the parathyroid gland

PREPARING PATIENT FOR SURGERY

ADMINISTER MAGNESIUM AND PHOSPHATE to prevent postoperative complications

ADMINISTER CALCIUM, VITAMIN D to prevent hypocalcemia 4-5 days after the surgery

HYPOPARATHYROIDISM

Disorder characterized by DEFICIENCY OF PTH

ETIOLOGY

Congenital Autoimmune disease

Parathyroidectomy

Massive radiation therapy

PATHOPHYSIOLOGY



SIGNS OF HYPOCALCEMIA

POSITIVE CHVOSTEK’S SIGN

POSITIVE TROSSEAU’S SIGN

Seizures

Paresthesia

Arrhythmias Weakened tooth enamel

DIAGNOSTIC TEST

DECREASED SERUM PTH

DECREASED CALCIUM

ELEVATED PHOSPHATE

X-ray – increased bone density

ECG changes

MEDICAL MANAGEMENT

VITAMIN D AND CALCIUM supplements

CALCIUM GLUCONATE in emergency conditions

SEDATIVES AND ANTI-CONVULSANTS to prevent seizuresNURSING INTERVENTIONS

Institute SEIZURE PRECAUTIONS

WATCH OUT FOR CARDIAC ARRHYTHMIAS

Offer HIGH CALCIUM AND LOW PHOSPHATE DIET

ADRENAL GLANDS

Small structures which cap the kidney

PARTS OF THE ADRENAL GLAND

1) MEDULLA – secretes EPINEPHRINE and NOREPINEPHRINE

2) CORTEX – secretes ALDOSTERONE (mineralocorticoid), CORTISOL (glucocorticoid) and ANDROGEN

(adrenocorticoid)

FUNCTION OF ADRENAL GLAND HORMONESCUSHING’S DISEASE

Hypersecretion of adrenal cortex leading to INCREASED CORTISOL (MAIN REASON),

ALDOSTERONE, ANDROGEN and ESTROGEN

ETIOLOGY

Tumour of the adrenal gland or the pituitary gland

Prolonged steroid therapy

PATHOPHYSIOLOGY

ASSESSMENT


Increased glucose Diabetes mellitusGlycosuria

Hypokalemia Muscle weakness

Increased protein catabolism Loss of muscle massHeart failure



Decreased collagen PURPLE STRIAE BUFFALO HUMP (fat pads over the back)MOON FACE (fat pads over face)TRUNCAL OBESITY (fat pads on trunk)Poor wound healing

COMPLICATIONS

Osteoporosis

Infections

Ureteral calculi

Metastasis of malignant tumors

DIAGNOSTIC TESTS

INCREASED – cortisol, glucose and sodium

DECREASED – potassium and calcium

MEDICAL MANAGEMENT

LOWER CORTISOL LEVELS

KETOCONAZOLE (NIZORAL) – Inhibit cortisol synthesis AMINOGLUTETHIMIDE (CYTADREN) – inhibit cortisol synthesis

MITOTANE (LYSODREN) – destroy adrenocortical cells

BROMOCRIPTINE (PARLODEL) – inhibit prolactin secretion

Radiation therapy for tumour


Provide diet HIGH-PROTEIN, LOW-CARBOHYDRATE DIET

Give POTASSIUM AND SODIUM SUPPLEMENTS

Watch out for side effects of mitotane, aminoglutethimide

slowed mentation

Weakness

SURGICAL MANAGEMENTBILATERAL ADRENALECTOMY

NURSING CARE AFTER SURGERY

Watch for signs of shock

Give VASOPRESSORS

INCREASE RATE OF IV FLUIDS as needed

Administer STEROIDS as needed

NURSING CARE FOR PATIENTS IN STEROID REPLACEMENT THERAPY

CHECK FOR SIGNS OF ADRENAL HYPOFUNCTION

Orthostatic hypotension

Apathy

Weakness Fatigue

Give STEROIDS WITH ANTACIDS OR MEALS to minimize gastric irritation

DISCOURAGE ABRUPT DISCONTINUATION OF STEROIDS to prevent adrenal crisis

ADDISON’S DISEASE



Hyposecretion of adrenal cortex leading to DECREASED CORTISOL, ALDOSTERONE AND

ANDROGEN

ETIOLOGY

Autoimmune disorder

Abrupt withdrawal of steroid therapy

TumourPATHOPHYSIOLOGY

ASSESSMENT


↓ glucose WEAKNESSWEIGHT LOSS

↑ melanin BRONZE SKIN COLORdarkening of scarsareas of vitiligo

↓ sodium↑ water excretion

Dehydration, HypotensionCraving for salty food

↓ androgen Decreased axillary and pubic hairHair loss

COMPLICATIONS

Profound hypoglycemia

Ultimate vascular collapse Renal shutdown

Coma

Death

DIAGNOSTIC TESTS

DECREASED PLASMA CORTISOL LEVEL

INCREASED – potassium

DECREASED – glucose, sodium

MEDICAL MANAGEMENT

lifelong corticosteroid replacement with CORTISONE OR HYDROCORTISONE to replace cortisol

ALDOSTERONE REPLACEMENT WITH FLUDROCORTISONE (FLORINEF) to prevent dehydration,

hypotension, hyponatremia, and hyperkalemiaNURSING INTERVENTIONS

Monitor the following

Signs of shock

Hyperkalemia

INCREASE FLUID INTAKE with oral fluids and intravenous fluids

If patient has diabetes, CHECK BLOOD GLUCOSE regularly

NURSING CARE IF THE PATIENT IS RECEIVING STEROIDS



If patient is anorexic, suggest 6 SMALL FREQUENT FEEDINGS

Watch for complications

FLUID AND ELECTROLYTE IMBALANCE – if patient is taking aldosterone

ORTHOSTATIC HYPOTENSION – patient is receiving cortisol

OFFER ANTACID while on steroid to prevent GI irritation

ADDISONIAN CRISIS Critical LACK OF MINERALOCORTICOIDS AND GLUCOCORTICOIDS

TRIGGERS OF ADDISONIAN CRISIS

acute stress

Surgery

omission of steroid therapy

MANAGEMENT FOR ADDISONIAN CRISIS

IV bolus of HYDROCORTISONE

3-5 L of IV NORMAL SALINE AND GLUCOSE SOLUTION

DIABETES MELLITUS

Metabolic disorder characterized by HYPERGLYCEMIA (elevated serum glucose) from LACK OF

INSULIN (TYPE I) or INCREASED RESISTANCE TO INSULIN (TYPE II) or bothCLASSIFICATIONS

1) TYPE 1 – Insulin Dependent Diabetes Mellitus (IDDM)

2) TYPE 2 – Non-Insulin Dependent Diabetes Mellitus (NIDDM)

3) Gestational Diabetes Mellitus

PREDISPOSING FACTORS

Stress

Heredity

Obesity

Viral infection

Autoimmune disorders

Women

PARAMETER TYPE 1 TYPE 2 Gestational

Other Name IDDM NIDDM GDM

Cause Lack of insulin Increased insulin resistance Increased human placental lactogen (HPL)

Onset Juvenile-onset Non-obese

Maturity-onset Obese adults

Pregnancy

Management Insulin

Diet Exercise

OHA, Insulin

Diet

Exercise

Insulin

Complication Diabetic

Ketoacidosis (DKA)

Hyperglycemic,

Hyperosmolar, Non-Ketotic

Syndrome (HHNS)

Dystocia



PATHOPHYSIOLOGY

ASSESSMENT


Hyperglycemia Glycosuria,POLYURIAPOLYDIPSIA

Cellular Starvation POLYPHAGIAFatigueLethargyPoor wound healing

Increased Fat and Protein Catabolism WEIGHT LOSSAcidosisAcetone breathIncreased BUN and creatinine

Small vessel injuries NeuropathyNephropathyRetinopathy

CARDINAL SIGNS OF DIABETES MELLITUS (3PsWF)

P – olyuria

P – olydipsia

P – olyphagia

W- eight loss

F- atique

COMPLICATIONS

MICROVASCULAR – retinopathy, neuropathy, nephropathY

MACROVASCULAR – coronary artery disease, stroke

Diabetic Ketoacidosis (if type 1)

Hyperosmolar Hyperglycemic Non-Ketotic Coma (if type 2)

DIAGNOSTIC TESTS

Fasting plasma glucose level 126 mg/dl or more on at least 2 occasions

Random blood glucose level 200 mg/dl or more

2-hour blood glucose test 200 mg/dl or moreDone after ingesting 75 g of oral dextrose

Glycosylated hemoglobin (HbA1c

) IncreasedReflects glycemic control in last 2-3 months



Urinalysis Elevated acetone and glucose

MEDICAL MANAGEMENT Insulin administration

Use of Oral hypoglycemic agents (OHAs)

Proper diet

Regular Exercise

INSULIN THERAPY FOR A DIABETIC PATIENT

PARAMETER REGULAR INTERMEDIATE LONG-ACT

Indication KetoacidosisSurgeryInfection

Maintenance Maintenanc

Description Short-actingHumulin RSemilente

Intermediate-actingNPH, Humulin NLente

Long-actingPZIUltralente

Color Clear Cloudy Cloudy

Onset 30 mins – 1 hour 1-2 hours 3-4 hours

Peak 2-4 hours 6-8 hours 16-20 hours

Duration 6-8 hours 18-24 hours 30-36 hours

NURSING INTERVENTIONS DURING INSULIN THERAPY

USE SUBCUTANEOUS ROUTE

Use INTRAVENOUS route only during emergency such as DKA

AVOID COLD ADMINISTRATION to prevent LIPODYSTROPHY

ROTATE INJECTION SITE to prevent lipodystrophy

GENTLY ROLL VIAL IN BETWEEN THE PALMS to redistribute insulin particles

SIDE EFFECTS OF INSULIN

LOCAL SIDE EFFECTS Induration or rednessSwellingLesion at the siteLIPODYSTROPHY

GENERAL SIDE EFFECTS HYPOGLYCEMIA SOMOGYI PHENOMENON (rebound hyperglycemia)Dawn’s phenomenon



ORAL HYPOGLYCEMIC AGENTS

DRUG NAMES (1) SULFONYLUREAS – DIABINASE, DIAMIC

(2) BIGUANIDE – Glucophage (Metformin)(3) ACARBOSE – Glucobay

INDICATION Type II DM

ACTION (1) Stimulate endogenous INSULIN PRODUCTION(2) INCREASE CELL SENSITIVITY TO INSULIN (3) SUPRESS GLUCONEOGENESIS(4) DELAY GI ABSORPTION of carbohydrates

SIDE EFFECTS GI upset

Hypoglycemia

NURSING CONSIDERATIONS Stress importance of TAKING IT RELIGIOUSLYAVOID ALCOHOL while on therapy to prevent vomiting

PROVIDING DIABETIC FOOT CARE

INSPECT FEET DAILY, use mirror to inspect bottom of the feet

Wash feet with WARM WATER AND MILD SOAP

PAT DRY the feet – do not rub

Wear COMFORTABLE PROPERLY-FITTED PAIR OF SHOES (LEATHER OR CANVASS)

USE COTTON SOCKS and avoid synthetic fibers

Do not go barefooted

Trim the toenails STRAIGHT ACROSS; use nail file instead



MANAGING COMPLICATIONS OF DIABETES

PARAMETER HYPOGLYCEMIA

HYPERGLYCEMIA

DKA

SIGNS ANDSYMPTOMS

WeaknessTremorsPallorDiaphoresisCold clammy skinFaintnessCBG < 50 MG/DL

Symptoms of DM+

Extreme hyperglycemiaKUSSMAUL’S BREATHING

Acetone breathMetabolic acidosis

Hypokalemia

TREATMENT SIMPLE SUGARS D50/50 50 ML 1 MG IV GLUCAGON

Administer 0.9% NACL THEN 0.45ADD 5% DEXTROSE if CBG is 25Add POTASSIUM CHLORIDE IV dREGULAR INSULIN IV or SQ

LIST OF SIMPLE SUGARS

3-4 oz regular softdrink

8 0z fruit juice

5-7 pcs. lifesaver’s candies

1 tbsp sugar

5 ml pure honey or karo soup

10-15 mg carbohydrate

LOW BLOOD SUGAR – HYPOGLYCEMIA 15/15 RuleCONSUME 15 GRAMS OF CARBOHYDRATE

- 3 squares of glucose tablets

- 8 ounces of milk

- ½ c fruit juice

- 1 tablespoon of sugar/honey/syrup

- 8 lifesavers

- 1 roll of Smartee Candy

- 1 small tube of cake decorator frosting

Wait 15 minutes. If the symptoms have not gone away: eat or drink another serving from this

list. If your meal is more than 30 minutes away, eat ½ sandwich or crackers with cheese or

peanut butter

nursing care of clients with disturbances of the endocrine syste1

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