Endocrine Disorders in Children

7/30/2019 Endocrine Disorders in Children

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NURSINGTHERAPEUTICSFORCHILDRENANDADOLESCENT

II

Prepared by: Sarah Jane L. Racal RN,MAN

Christian University of Thailand


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Love your callingwith passion; it is the

meaning of yourlife- Sir Pagsi


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THE ENDOCRINE SYSTEM

Controls orregulatesmetabolic processes,

governing energyproduction, growth, fluid

and electrolyte balance,response to stress, and

sexual reproduction.


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THE ENDOCRINESYSTEM

Hormones

Cells

Target organ

Environment ( blood, lymph,

extracellular fluids
http://localhost/var/www/apps/conversion/tmp/scratch_1/The%20Endocrine%20System.mp4


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GLANDSOFTHEENDOCRINESYSTEM


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DISORDERSOF PITUITARYFUNCTION

Hypopituitarism

Pituitary Hyperfunction

Precocious PubertyDiabetes Insipidus

Syndrome of InappropriateAntidiuretic Hormone

( SIADH)


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HYPOPITUITARISM

Is diminished or deficient secretion of pituitaryhormones.

Growth hormone (GH)Short stature

Delayed epiphyseal closure

Retarded bone age

Premature aging

Increased insulin sensitivity

Thyroid Stimulating Hormone ( TSH )Short stature with infantile proportions

Dry, coarse skin, yellow discoloration, pallorCold Intolerance

Constipation

Somnolence

Bradycardia

Dyspnea on exertionDelayed dentition, loss of teeth


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HYPOPITUITARISM : MANIFESTATIONS

Gonadotropins

Absence of sexualmaturation/loss of secondarysex characteristics

Atrophy of genitalia, prostate

gland, breastsAmenorrhea withoutmenopausal symptoms

Decreased spermatogenesis

Adrenocorticotropic Hormone( ACTH)

Severe anorexia, weight lossHypoglycemia

Hypotension

Hyponatremia, Hypokalemia

Anidiuretic Hormone( ADH )Polyuria

Polydipsia

Dehydration

Melanocyte-Stimulating Hormone

( MSH )Decreased

pigmentation


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HYPOPITUITARISM : CAUSES

Media file 1: The left photograph shows an untreated 21-month-old girl with congenital hypopituitarism. The right panel depicts thesame child aged 29 months, following 8 months of growth

hormone therapy.

Aplasia or HypoplasiaIdiopathicTraumaSurgeryAnorexia NervosaAutoimmuneHypophysisIrradiation


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HYPOPITUITARISM: MANAGEMENT

Hormone replacement and Surgical Intervention

Medications:

Somatropin

LevothyroxineHydrocortisoneVasopressinDesmopressin

Androgen


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PITUITARY HYPERFUNCTION

Gigantism ( Before epiphyseal closure)

Acromegaly ( After epiphyseal closure)

Facial features (overgrowthhead, lips, nose,tongue, jaw,increased facialhair), increasedtendency towardDM

Elevated growthhormone

Causes:Congenital Adrenal

HyperplasiaAdenoma/Carcinoma

Glucocorticoid resistance

Idiopathic

Trauma

Post- Inflammation


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TREATMENT

Treatment is directed toward the specific causeof the disorder.

Injection of a specific analog of

Luteinizing Hormone ( regulates

Pituitary secretion)

Leuprolide acetate given 0.2-0.3mg/kg

Psychological Management


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DIABETES INSIPIDUS ( POSTERIOR PITUITARY

HYPOFUNCTION )

also known as Neurogenic Diabetes Insipidus

Familial

IdiopathicTraumaInfectionAlcoholPhenytoin

DecreasedADH/Vasopressin/Pitressin

UncontrolledDiuresis

PolyuiriaPolydipsia

First sign :Enuresis


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DIABETES INSIPIDUS

Infants IrritabilityFeeding withWater and NotMilk

ALERT! For dehydration, electrolyteimbalance, elevated temperature,azotemia, potential circulatorycollapse

ALERT! Encourage patient to drink more liquids toprevent electrolyte imbalance ( special precaution tothose with trauma/under anesthesia)


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TREATMENT

Hormone replacement

Overdosage effect: SIADH symptoms

IM/SC vasopressin Tannate ( 48-72 hours

)Nasal Spray of aqueous lysinevasopressin ( every 8-12 hours)


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NURSING CARE MANAGEMENT

Assess

Body weightSerumElectrolyteBlood UreaNitrogenHematocritUrineSpecific

GravityIntake andOutput

Health Education

Wear medical alertbracelet


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SIADH ( SYNDROMEOFINAPPROPRIATE

ANTIDIURETICHORMONE )

Increased ADH Fluid retentionHypotoniciy

Low serumOsmolalityHigh urineosmolality

Anorexia,Nausea,

Stomach cramps

Irritability

Personality

changes

StuporConvulsions

Immediate Management:

RESTRICT FLUIDS ( -1/2 maintenance)


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Monitor Intake and Output

Seizure precautions

Long term ADH antagonizingmedication

Observe for signs and symptoms offluid overload

Weight

Health education


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THYROID DISORDERS

ThyroidHormone

T4 (Throxine)

T3 ( Triiodothyronine )

Calcitonin Regulates calcium levelsby decreasing itsconcentration PTH

Controls Basal MetabolicRate


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JUVENILE HYPOTHYROIDISM

CongenitalHypoplastic

Thyroid Radiotherapy

Infection

Low dietary

intake of iodine

Decreasedcirculatorythyroidhormones

Poor growthConstipationSleepiness

Mental declineMyxedematousskin ( dry skin,puffiness, sparse

hair)


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HYPOTHYROIDISM


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TREATMENT

Thyroid Hormone Replacement

Increasing amounts of Levothyroxine ( 4-8weeks )

Nursing Care Management

Early recognition of disorderHealth EducationEncourage compliance to therapy


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GOITER Enlargement or Hypertrophy of the

Thyroid gland

Can occur in deficient, excessive and normalTH secretion

DecreasecirculatingTH

Increasedsecretion ofPituitaryTSH

Enlargementof Thyroid

Low dietaryintake ofIodine

ALERT! If an infant is bornwith goiter, prepare foremergency ventilation.Hyperextension of neckcan improve ventilation.


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LYMPHOCYTIC THYROIDITIS

Hashimoto disease/ Juvenile Autoimmune

Thyroiditis

- Most common cause of thyroid disease inchildren. Accounts for the largest percentage in

juvenile hypothyroidism

- After age 6

Strong geneticpredisposition

Lymphocyticinfiltration of thegland

Symmetricallyenlarged gland


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TREATMENT

Oral Replacement of Thyroid Hormone

Surgery is NOT RECOMMENDED

Nursing Care Management

Reasure the child that the condition is

temporary

Compliance to thyroid therapyHealth education


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HYPERTHYROIDISMGraves Disease

Autoimmune response

to TSH receptors; no

specific etiologyidentified

Clinical Manifestations:

irritability, hyperactivity, short attention span,tremors, insomnia and emotional lability, warm, flushedand moist skin; hair is fine and unable to hold a wave;exophthalmos; increased blinking; absence of wrinklesin the forehead;visual disturbances.


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TREATMENT

DRUG THERAPY

(PTU: propylthiouracil and Methimazole)

THYROIDECTOMY

(subtotal thyroidectomy)

RADIATION THERAPY

(ablation with radioiodine)


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TREATMENT

Drug therapy:

Most serious side-effect:

Agranulocytosis ( severe leukopenia )

Thyroidectomy complications:

- Possible incidence of hypothyroidism

- Laryngeal nerve palsy

- Permanent hypothyroidism


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THYROTOXICOSIS

Occur from sudden release of

hormones-LIFE

THREATENING!

THYROID STORM:

Clinical Manifestations:

severe irritability,hyperthermia,hypertension,

severe tachycardia, prostration


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Early Identification

Children: Need quiet, unstimulating

environment conducive to rest.

ALERT : children taking propylthiouracil ormethimazole must be monitored for side-

effects: Sore throat + Fever ( leukopenia)=

early detection is important. See a doctor

immediately.


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SURGICAL CARE

Iodine ( given few weeks before

surgery)=unpalatable.

Mix with a strong tasting fruit juice (grape/punch

flavors) Use straw

Compliance is essential to avoid thyroid crisis.

Psychological preparation

Health education

Assess for bleeding ( damage to laryngeal

nerves: severe stridor, hoarseness )


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LARYNGOSPASM

Can occur and is life-threatening.

Characterized by stridor, hoarseness and feeling of

tightness in the throat.

Tracheostomy set

Observe for signs of hypothyroidism and

hypocalcemia especially in the immediate post

operation period.


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PARATHYROID DISORDERS

Function: Homeostasis inserum calcium

Parathyroid gland ParathyroidHormone +

Vitamin D +Calcium

PTH

Increases serumcalciumBone

demineralization

CalcitoninDecreases serumcalciumBone formation


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HYPOPARATHYROIDISM: DEFICIENT PTH

Deficient in the

synthesis or cellular

processing of PTH

Aplasia/Hypoplasia of

the gland

CongenitalHypothyroidism

Postthyroidectomy Hypoparathyroidism

Decreased Calcium

Clinical Manifestations: Numbness, tingling inhands and feet, + Chvostekssign,+trousseaus sign, larygospasm.Convulsion may occur.


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HYPOPARATHYROIDISM

Treatment goal:

Maintain normal serum calcium and phosphoruslevels with minimal complications.

Acute/sever tetany: IV/PO Calcium gluconate

Vitamin D- prolonged onset; long half life

Long term management- massive doses ofvitamin D; Oral calcium supplementation


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NURSINGCAREMANAGEMENT

Recognition of Hypocalcemia

convulsions, irritability, GI symptoms,

seizures

Establish seizure and safety

precautions and reduce environmental

stimuli.

Observe for signs of larygospasm

Always prepare calcium gluconate for

emergency.


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HYPERPARATHYROIDISM

A rare condition in children

Primary:

Glandadenoma

Hyperparathyroidism

Nausea, vomiting,abdominal

discomfort, vaguebone pain, polyuria,polydipsia

Secondary:Chronic renal disease; Renal osteodystrophy;

congenital anomalies of urinary tract;

hypercalcemia


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TREATMENT: DEPENDINGONTHECAUSE

Primary :

Surgical removal of tumors or

hyperplasic tissue

Secondary:Calcium and Vitamin D


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1. Early recognition of the disorder

2. Assess complications : Bone pain/fracture

3. Assess for unexplained GI symptoms and

cardiac irregularities4. Hydration to minimize renal calculi

formation

5. Take fruit juices to decrease urinary PH (cranberry or apple juice


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6. Strain urine

7. Keep side rails in place and assist inambulation.

8. Take vital signs and pulse for one full minute

( report bradycardia and cardiac arrest ) 9. Health education re diet ( Calcium and

Vitamin D )

10. Surgery may lead to hypocalcemia ( observe

for signs of tetany, instituting seizureprecautions.

Have calcium gluconate ready for emergency


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ADRENAL GLAND

Adrenal Medulla :

catecholamines ( Epinephrine and

Norepinephrine

Adrenal Cortex :Steroids

Glucocorticoid ( cortisol, corrtisone)

Mineralocorticoid ( aldosterone )Sex steroids ( androgen, estorgen,and progestine )


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MINERALOCORTICOID

Aldos

teron

e Sodium and water retention

and Potassium excretion

Renin-angiotensionAldosterone system


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RENIN-ANGIOTENSIN-ALDOSTERONE

SYSTEM

C


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ADRENALMEDULLA

Catecholam

ines

ActivityVasoconstriction

RespirationBronchialdilation

Heightened

sensory awarenessPupillary dilation

Metabolic rate


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ACUTEADRENOCORTICALINSUFFICIENCY

AD

RENALC

RISIS

Hemorrhage intothe gland fromtrauma( prolonged difficult

labor, fulminatinginfectionsmeningococcemia

,abrupt

withdrawal of

cortisone)

AAIIncreasedIrritabilityHeadache

Diffuseabdominalweakness,nausea,

vomiting,diarrhea


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TREATMENT

Cortical Replacement

Replace body fluids

Administer glucose solution

Antibiotic if with infection


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Prompt recognition is essential

VS and BP every 15 minutes ( hyperpyrexia;shocklike state)

MIOMonitor response to treatment

Rapid administration of fluids : heart failure

High dosage of cortisol: sudden fall in blood

pressure and temperature.

Increased sodium and cortisol tx: decreasedpotassium---flaccif paralysis


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ALERT!

Monitor electrolyte level especially a

decrease or increase in potassium (

weakness, poor muscle control,

paralysis,cardiac dysrhythmias, apnea

Intravenous or oral Potassium- mixed with fruit

juice


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CHRONIC ADRENOCORTICAL

INSUFFICIENCY ADDISONS DISEASE

Rare in children

Generalized TB

Destructivelesion inAdrenal glandNeoplasm

Idiopathic

Adrenal Gland

Destruction


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TREATMENT

Glucocorticoid replacement

1. mineralocorticoid=== liberal salt intake

BUT:

Fever, infection, emotional upset, surgery= triple

dose ( if not, may lead to ACUTE CRISIS

Monthly injections of desoxycorticosterone

Implantation of desoxycorticosterone acetatepellets SC every 12 months.


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Health education- continued need for

cortisol replacement

Drug side-effect:

Gastric Irritation ( ingest food or use

antacid )

Increased excitability and sleeplessness

May require dietary management toprevent obesity.


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ALERT!

Taste different preparations of

cortisone. Smaller volume of liquid to

ingest is also the most bitter.

Side Effects of Mineralocorticoidgeneralized edema ( eyes, headache.

Cardiac arrhythmias, signs andsymptoms of decreased potassium)


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CUSHING SYNDROME

Excessivec

irculatingfreecortiso

l

AdrenalHyperplasiaAdrenocorticalneoplasmExtra pituitaryneoplasmsAdministration oflarge amounts ofexogenouscorticosterone

Glucocorticoid/cortisol

Poor wound healingExcessive hair growthMoon faceBuffalo hump

Pundulum abdomenEcchymosisRed abdominal StriaeBruisesWeight gain


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CUSHING SYNDROME


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TREATMENT

Depending on the case

Surgery:

Bilateral Adrenalectomy (post-op replacement of cortical

hormones)


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Depending on the cause

To decrease cushingoid features = give

during early am to maintain normal

diurnal pattern of cortisol secretion.

= at night: decrease level of cortisol (

more pronounced effect if withincreased supply of medication)


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ALERT!

Post operation complications ofadrenalectomy

( sudden withdrawal of cortisol)

Observe for shock-like

symptoms ( hypotension,

hyperglycemia )


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CONGENITALADRENALHYPERPLASIA

Family of disorders caused by a decreased

enzyme activity required for cortisol

production in the adrenal cortex.

21-hydroxylase deficiency :most common defect ( 90% of all

cases of CAH)

1/12000-15000 births

Causes over production of the adrenal

androgen = virilization of female fetus


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CONGENITAL ADRENAL HYPERPLASIA

Interference in thebiosynthesis of cortisolduring fetal life

Increased production of ACTH

Hyperplasia of

adrenal gland


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SIGNSANDSYMPTOMS

Girls will usually have normal female reproductiveorgans (ovaries, uterus, and fallopian tubes).They may also have the following changes:

Abnormal menstrual periods

Deep voiceEarly appearance of pubic and armpit hair

Excessive hair growth and facial hair

Failure to menstruate

Genitals that look both male and female(ambiguous genitalia), often appearing moremale than femal
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SIGNSAND SYMPTOMS

Boys won't have any obvious problems at birth.However, they may appear to enter puberty as early

as 2 - 3 years of age. Changes may include:

Deep voice

Early appearance of pubic and armpit hair

Early development of male characteristics

Enlarged penis

Small testes Well-developed muscles
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SIGNS AND SYMPTOMS

Both boys and girls will be tall as children but much

shorter than normal as adults.

Some forms of congenital adrenal hyperplasia are

more severe and cause adrenal crisis in thenewborn due to a loss of salt. Newborns with these

forms develop severe symptoms shortly after birth,

including:

Cardiac arrhythmias

Dehydration

Electrolyte changes

Vomiting
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TREATMENT

Protecting normal growth

Androgen blockade (sprinolactone)

Inhibition of estrogen synthesis ( testosterone )

GH therapy Lupon therapy

Cortisol replacement choices

Dexamethasone day at low dosage

Laboratory assessments of control

Androstenedione emphasis in adolescent females


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PHEOCHROMOCYTOMA

Pheochromocytomas are a type oftumorof the adrenal glands that

can release high levels of

epinephrine and norepinephrine

W
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WHATARESYMPTOMSOF

PHEOCHROMOCYTOMA?

Classic symptoms

SweatingPalpitations

Headache

O


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OTHERCONDITIONSTHATMAYACCOMPANY

THECLASSICSYMPTOMSARE:

Anxiety

Nausea

TremorsWeakness

Abdominal

painWeight loss


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TREATMENT

Surgery is the definitive treatment until

the tumor is removed.

Top Priority!!!! Control BloodPressure

In rare cases, rediationtherapy or

chemotherapy may berequired after surgery


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DIABETES MELLITUS

Diabetes is an autoimmune disorder that occursin children that have a certain geneticpredisposition. It is not yet known what triggersor causes the autoimmune reaction to occur in

these kids

At about 6-7 years old:Type I Insulin Dependent DiabetesMellitus ( more common in children )


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MAIN SYMPTOMS

Polyuria

Polydipsia

Polyphagia

Weight loss


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TYPE IAND TYPE II DIABETES MELLITUS

Completely unable to

produce insulin

Autoimmune disease ofinsulin-producing beta

cells of the pancreas.

Almost 10% of diabeticchildren

More common in adults Usually overweight

May have acanthosisnigricans

Produce insulin butcells dont respond toit.

Type I IDDM Type II NIDDM

POPULATION AT RISK OF DEVELOPING TYPE II


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POPULATIONATRISKOFDEVELOPING TYPE II

DIABETES MELLITUS

people who are overweight or obese (more than 20 percentabove their ideal body weight)

people who have a parent or sibling with type 2 diabetes thosewho belong to a high-risk ethnic population (African-American,Native American, Asian-American, Hispanic, or PacificIslander)

people who live a sedentary lifestyle (i.e., exercise less thanthree times a week) women who have been diagnosed withgestational diabetes or have delivered a baby weighing morethan 9 lbs (4 kg)

people with high blood pressure (140/90 mmHg or above)

people with high density lipoprotein cholesterol (HDL, or "good"cholesterol) level less than or equal to 35 mg/dl and/or atriglyceride level greater than or equal to 250 mg/dl


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MANAGEMENT

When to call a doctor?

Any child displaying

symptoms of diabetesshould be taken to a doctoror emergency care facilityfor evaluation immediately.


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MANAGEMENT

Diagnosis

Suspected based on symptoms

and confirmed by blood tests

that measure the level of

glucose in blood plasma


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BLOOD TESTS

Fasting Plasma Glucose Test

Random Plasma Glucose Test

Oral Glucose Tolerance Test


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FASTINGPLASMAGLUCOSETEST

Blood is drawn from a vein in the child's armfollowing an eight-hour fast (i.e., no food ordrink), usually in the morning beforebreakfast. The red blood cells are separated

from the sample and the amount of glucoseis measured in the remaining plasma. Afasting plasma glucose level of 126 mg/dl(7.0 mmol/l) or higher indicates diabetes

(with a confirming retest on a subsequentday).


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RANDOMPLASMAGLUCOSETEST

Blood is drawn at any time ofday, regardless of whether thepatient has eaten. A random

plasma glucose concentrationof 200 mg/dl (11.1 mmol/l) orhigher in the presence of

symptoms indicates diabetes.


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ORALGLUCOSETOLERANCETEST

Blood samples are taken both beforeand several times after a patient drinks75 grams of a glucose-based

beverage. If plasma glucose levelstaken two hours after the glucosedrink is consumed are 200 mg/dl (11.1

mmol/L) or higher, the test isdiagnostic of diabetes (and should beconfirmed on a subsequent day ifpossible).


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MANAGEMENTOFDIABETESMELLITUS

Medication

D

iet

Exercise


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TREATMENT

Type I Diabetes insulin injections orinfusions

operate a home blood

glucose monitor

Insulin height, weight, age, food intake, and activitylevel

given subcutaneously

upper arm, abdomen, or upperthigh.


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INSULIN

Insulin Onset ofaction

Peak ofaction/Duration

Regular Insulin 15 to 30minutes

Two hours ( 4-6hrs)

Intermediate Acting Insulin( NPH and Lente)

1 to 3 hours 18 to 26 hours

Ultra-lente 4 to 8 hours 28 to 36 hours

Basal action insulin (peakless insulin)glargine orLantus

15 minutes Duration : 18-26hours


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INSULININJECTIONSITE


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ADMINISTRATIONOFINSULIN


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INSULINANDINSULINSYRINGE


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NUTRITIONAL CONCERNS

10 to 20 % ofcalories from

protein

50 to 60 % ofcalories fromcarbohydrates

Less than 30% ofcalories from fats


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ORAL MEDICATIONS

Metformin (Glucophage)

Only medication approved by

the U.S. FDA for use inchildren over age ten

Works by reducing the amount ofglucose the liver produces and theamount of circulating insulin in thebody.


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METFORMIN


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"WHATEVERTHEMINDOFMANCANCONCEIVEANDBELIEVE, ITCANACHIEVE."NAPOLEON

HILL

Have a healthy dayahead of all of you!
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Documents

Endocrine Disorders in Children