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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