The Child with Endocrine Dysfunction

Hockenberry Chapter 38

ATI pg. 333-373, 408-429 Dondi Kilpatrick RN, MSN

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Learning Objectives List Signs and Symptoms Verbalize treatment plan for :

Diabetes Type I and II Hyperglycemia Hypoglycemia Growth Hormone Deficiency Growth Hormone Excess Diabetes Insipidus SIADH Hypothyroidism Hyperthyroidism

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Disorders of Pancreatic Hormone Function

Review Islets of Langerhans 3 major functioning cells

Alpha cells Beta cells Delta cells

Balance out the insulin and glucagon

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Diabetes Mellitus (DM) Metabolic disorder

Chronic hyperglycemia Total /partial deficiency of hormone INSULIN

Impairs the body’s ability to use food for energy

Most common chronic endocrine disorder of childhood

No cure

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Diabetic Ketoacidosis Insulin facilitates entry of glucose into

cells Too little insulin body burns fat for

energy Fat breaks down fatty acids Glycerol in fat ketones in the liver Excess is eliminated in urine (ketonuria)

or lungs (acetone breath) Ketones in blood are strong acids

lowering pH (ketoacidosis) 5

Stuff from bottom of slide Insulin facilitates entry of glucose/K+ into the cell. Too little insulin… * body in a state of starvation causing hunger

(polyphagia) * concentration of glucose increases in the blood stream * when glucose exceeds the renal threshold, glycosuria

occurs * this in turn causes osmotic diversion of water (to dilute the glucose) causing polyuria * increased diuresis causes excessive thirst(polydipsia) ** Body still needs energy, so it starts burning fat for energy.

Fat breaks down into fatty acids and the glycerol in fat Is converted to ketones by the liver.

Excess ketones are eliminated in the urine (ketonuria) Or by the lungs (causing acetone or fruity breath)

Ketones are strong acids in the blood (ketoacidosis)6

Ketoacidosis Ketones produce free hydrogen ions

(↓ serum pH) Bicarbonate in blood combines with

hydrogen ions to make carbonic acid (which breaks down to H2O & CO2)

Lungs try to eliminate CO2 by altering rate & depth of respirations (Kussmaul

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Stuff from bottom of slide Ketones also produce free hydrogen ions which

decreases the serum pH

To counter the decrease in pH, bicarbonate binds to the

hydrogen ions in an attempt to buffer the pH. This binding produces carbonic acid, which breaks down into H2O

and CO2

To eliminate the CO2, the lungs alter the rate and depth of respirations (Kussmaul respirations: hyperventilation associated with metabolic acidosis) 8

Ketoacidosis With cellular death:

Potassium released from cell blood stream (intra to extracellular) excreted by kidney

Total body potassium is depleted, even though serum potassium may be elevated

If not reversed dehydration, electrolyte imbalance, acidosis, coma, death

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Ketoacidosis As the acidosis worsens, cellular death occurs.

With cellular death, potassium is released from the cells to the bloodstream, and is excreted by the kidneys. The potassium loss is accelerated by the diuresis already taking

place.

Total body potassium is decreased, even though the serum potassium may be elevated (due to decreased fluid volume from the diuresis)

K → bloodstream → kidney and increase loss by osmotic diuresis

Total body potassium decreases even though serum potassium may be increased 10

Ketoacidosis Treatment

Insulin Fluids Electrolytes (particularly potassium)

Happens most frequently with infection

From bottom of slide As insulin given K shifts into cells decreasing K K given post confirmation of renal fx Gradual reduction of BS

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Diabetes Mellitus (DM)

Type 1

Beta cell destruction Leads to absolute

insulin deficiency 5-10% of all DM

cases

Type 2

Insulin resistance 90-95% of all DM cases Historically more

common in adults > 45 prevalence seen in

children/adolescents

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Causes

Type 1 2 types

Auto immune Idiopathic

Not simple inheritance

Genetic predisposition plus trigger event

Type 2 Insulin

resistance plus relative insulin deficiency

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Risk factors for Type II

Overweight Decreased exercise pattern Family history of type 2 DM Age Non-European ancestry

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Signs and Symptoms

Type 1 Polyuria Polydipsia Polyphagia Rapid weight loss Dry skin Irritability Drowsiness/fatigue Abdominal discomfort Ketoacidosis

Type 2 Polyuria Polydipsia ↑ BP Frequent infections Fatigue S/S insulin resistance

Acanthosis nigricans Polycystic ovary disease

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Acanthosis nigricans

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www.aocd.org/skin/dermatologic_diseases/acanthosis

Acanthosis nigricans screening program

Treatment

Type 1 Insulin! Monitor glucose

levels Lifestyle changes

Nutrition Exercise

Type 2 Lifestyle changes

Nutrition Exercise

Oral meds Monitor glucose

levels17

Team approach!!!

Insulin

Types Human

Most of what we see Pork

Not used much at all

All types 100 units/ml

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Types of Insulin

Based on: Onset Peak Duration

5 types Rapid Short Intermediate Long Mixed

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Types of Insulin Rapid

Give within 15 minutes of a meal!!! Intermediate

Is cloudy Long acting

Lantus can’t be mixed in a syringe with any other insulin

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Insulin Mixtures

70/30; 50/50; 75/25 1st # - % of intermediate insulin 2nd # - % of short or rapid acting insulin

Pay attention to the name of the mix!!!!

70/30 is 70% NPH and 30% short acting

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Mixing Insulin

Administer mixed insulin within 5 minutes of mixing or wait 15 minutes

Ignore this slide, she won’t test us on it

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Insulin Dosing

One dose a day rarely suffices Split mix is common

Rapid/short acting mixed with NPH Given prior to breakfast and supper

For better control- multiple injections

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Insulin Administration

Subcutaneous administration Rotate sites Insulin absorption

Abd is fastest, arm is next, and the leg is the slowest

24www.rch.org.au/diabetesmanual/manual.cfm?doc_id=2733#injection_sites

Insulin Administration

Complications Lipoatrophy

Where the tissue atrophies or breaks down, little pitting areas

Lipohypertrophy Build up of fat, like a fatty nodule

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Insulin Administration

Insulin pen Resembles a large fountain pen Needle is screwed onto tip

immediately prior to injection

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Insulin Administration Insulin pump

Computerized device About the size of a pager Worn around the waist As close to normal insulin delivery as

possible now Drawbacks

Pump malfunction, can’t get air in line, have to know how to do calculations and work the device

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Insulin Administration

Absorption can be altered exercise illness

Self monitoring is a must!!! This disease is lifelong so when the kid

gets old enough to do the shit himself, he needs to do the shit himself

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Oral Medications

Type 2 DM children only Used if lifestyle changes are not

effective Decreases absorption of blood

sugar from the diet, reduces the insulin usage.

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Monitoring Self- blood glucose monitoring

At home & in hospital Goal- blood glucose 80-120 mg/dl

Glycosylated hemoglobin (Hgb A1c) Typically levels of 6.5%-8% are acceptable Blood sugar attaches to the hemoglobin for the

life of the hemoglobin, the hemo lives about 120 days

A level of 6% means your avg blood sugar is about 120

Every number increase is about an increase of 30. So 7% is about 150

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Monitoring

Finger sticks / Atraumatic care Warm the finger Use the ring finger and thumb

They bleed a little bit easier Puncture to the side of the finger pad

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Complications

Hyperglycemia Caused by:

Too little insulin Illness/infection Injury Stress- physical/emotional Decreased exercise Diet

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Hyperglycemia

Symptoms 3 P’s Nausea Blurred vision Fatigue Diabetic

ketoacidosis (DKA)

Treatment Drink extra fluids Administer additional

insulin Monitor glucose

more closely

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Complications- HypoglycemiaHypoglycemia

Caused by: Too much insulin Diet Exercise Growth spurts Puberty Illness/injury Menses

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HypoglycemiaHypoglycemia

Mild-moderate Shaky/sweaty Hungry Pale Headache Confusion Disorientation Lethargy Change in behavior

Severe Inability to swallow Seizure/convulsion Unconsciousness

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Symptoms

HypoglycemiaHypoglycemia Treatment

Often difficult to differentiate HYPO from HYPERglycemia

Check blood sugar if possible When in doubt, give simple

carbohydrate Follow with complex carbohydrate,

then protein

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HypoglycemiaHypoglycemia

If unconscious, seizes or cannot swallow

Glucagon Mixed and given IM/SQ Releases stored glycogen from liver Should increase blood glucose in 15 minutes

Can cause nausea/vomiting Protect from aspiration

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Somogyi Effect Hypoglycemia followed by rebound

hyperglycemia More common for type I, especially

in children

Signs and symptoms Treatment – reduce bedtime insulin

to prevent early a.m. hypoglycemia

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Long Term Complications

Vascular changes Involve large and small vessels Heart disease Retinopathy Neuropathy Arterial obstruction

Gangrene

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Education Always carry:

Glucose tablets Insta-glucose Sugar cubes Candy

**children may fake a reaction to get candy**

Exercise With good control:

Decreases insulin requirements

With poor control May stimulate

ketoacidosis

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Education Nutrition

Sufficient calories to balance daily expenditure for energy and growth

Constant carbohydrate diet-exchange system Consistent intake/timing of food Timing of food coincides with time/action of

insulin Total # of calories/proportions of basic nutrients

needs to be consistent day to day

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Type I Diabetes

Allow toddler and preschooler to make food choices - monitor Carbohydrates

Monitor temper tantrums as possible signs of hypoglycemia

Snacks should be available during increased activity such as sports activities

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Estimating Portion Sizes for eyeballing portion size:

1 ounce of cheese is as big as 4 dice ½ cup of rice is as big as half a baseball A 4-ounce bagel is the size of a hockey puck 3 ounces of meat is as big as a deck of cards 2 tablespoons of peanut butter is about a

Ping-Pong ball 1 cup of pasta equals a tennis ball

43www.lillydiabetes.com

Education

Illness management Monitor glucose every 3 hours

Monitor urine ketones every 3 hours or when glucose is > 240 mg/dl

Urine ketones are not used for daily management

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Disorders of Pituitary Function

Pituitary gland “Master” gland Regulates other endocrine functions Releases or withholds 7 other hormones

Growth hormone (GH)

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Hypopituitarism

Caused by: Organic lesions (tumors) Idiopathic

Usually r/t GH deficiency

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GH deficiency Manifestations

Short stature – usually below 5th percentile Usually grow normally 1st year During the 2nd year growth drops off established

percentile Height may be more retarded than weight Normal skeletal proportions Sexual development usually delayed, but normal Most have normal intelligence

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GH deficency

Diagnosis Physical exam Family history X rays Endocrine studies Growth chart

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GH deficiency Treatment

Correct underlying disease process Replacement of GH (80-90% successful) Biosynthetic GH drug of choice

FDA approved for: GH deficiency Chronic renal insufficiency Prader-Willi syndrome Turner syndrome

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Growth Hormone Excess Hyperpituitarism

Over secretion occurs prior to epiphyseal plate closure

Grow 7-8 feet tall Acromegaly

Over secretion occurs after epiphyseal plate closure

Overgrowth of head, lips, nose, tongue, jaw, separation malocclusion of teeth, increased facial hair

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Growth hormone excess

Treatment Remove tumor, pituitary gland

radiation, high dose sex steroids to close growth plates

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Diabetes Insipidus (DI)

Disorder of the posterior pituitary Results from HYPOsecretion of Antidiuretic

Hormone (ADH) ADH sometimes called vasopressin (Pitressin)

Produces uncontrolled diuresis Causes

Primary: familial or idiopathic Secondary: trauma, tumors, CNS infection,

aneurysm

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Diabetes Insipidus (DI)

Manifestations Cardinal signs: POLYURIA &

POLYDIPSIA 1st sign is often ENURESIS Infants:

irritability relieved with feeding of WATER not milk

dehydration often occurs

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Diabetes Insipidus (DI)

Management Instruct parents there is a difference

between DI and DM Daily hormone replacement of

vasopressin Drug of choice: DDAVP

Nasal spray or IV Treat for lifetime

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Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

Disorder of posterior pituitary Produces HYPERsecretion of ADH ADH causes reabsoption of water

back into central circulation Causes

Infection Tumors Trauma CNS disease

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SIADH Manifestations

Fluid retention but no edema HYPOtonicity Anorexia Nausea/vomiting Irritability Personality changes

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SIADH

Treatment Fluid restriction

¼-½ of maintenance We don’t want further dilution in their body

Correction of underlying disorder (infection, tumor resection, etc.)

They may receive some diuretics, make sure to tell the families to get rid of other sources of water (toilet, plants, dog bowls) 57

Disorders of Thyroid function

Hypothyroidism (juvenile) One of the most common endocrine

disorders of childhood Congenital

Congenital hypoplastic thyroid Acquired

Partial/complete thyroidectomy for CA or thyotoxicosis

Following radiation treatment for malignancy58

Hypothyroidism (juvenile)

Manifestations Decelerated growth Myedematous skin changes

Dry skin, periorbital edema, dry or sparse hair

Constipation Sleepiness Mental decline

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Hypothyroidism (juvenile)

Treatment Oral thyroid hormone replacement Treat promptly in infants to facilitate

brain growth Lifelong treatment

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Hyperthyroidism (Graves Disease)

Most common cause of HYPERthyroidism in children

?? Caused by serum thyroid stimulating immunoglobulin, but no specific etiology

Peak incidence: 12-14 years, but can present at birth

Familial association Diagnosis: ↑ T4 and T3, suppressed TSH

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Hyperthyroidism (Graves Disease)

Manifestations Gradually develop over 6-12 months Excessive motion Gradual weight loss Muscle weakness Vomiting/frequent stooling Heat intolerance Skin-warm, moist, flushed

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Hyperthyroidism (Graves Disease)

Treatment Goal to retard rate of hormone secretion When S/S noted activity should be limited to

classwork only Some controversy as to which treatment is

best Antithyroid drugs (PTU and methimazole)

Risk for agranulocytosis, have family watch for s/s of infection (sore throat and fever). Seek medical attention immediately

Subtotal thyroidectomy Ablation with radioiodine

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References DM

www.diabetes.org http://diabetes.niddk.nih.gov/dm/pubs/type1

and2 www.emedicine.com/ped/TOPIC581.HTM

Thyroid www.cushings-help.com/thyroid.htm www.healthsystem.virginia.edu/uvahealth/p

eds_diabetes/hypothd.cfm

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