Download My Pediatric Endocrine Powerpoint

The Child with Endocrine
Dysfunction
Hockenberry Chapter 38
ATI pg. 333-373, 408-429
Dondi Kilpatrick RN, MSN
1
Learning Objectives
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List Signs and Symptoms
Verbalize treatment plan for :
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Diabetes Type I and II
Hyperglycemia
Hypoglycemia
Growth Hormone Deficiency
Growth Hormone Excess
Diabetes Insipidus
SIADH
Hypothyroidism
Hyperthyroidism
2
Disorders of
Pancreatic Hormone Function
Review
 Islets of Langerhans
3 major functioning cells

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Alpha cells
Beta cells
Delta cells

Balance out the insulin and glucagon
3
Diabetes Mellitus (DM)

Metabolic disorder

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Chronic hyperglycemia
Total /partial deficiency of hormone
INSULIN

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Impairs the body’s ability to use food for energy
Most common chronic endocrine
disorder of childhood
No cure
4
Diabetic Ketoacidosis

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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
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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

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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
7
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
9
Ketoacidosis
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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
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Insulin
Fluids
Electrolytes (particularly potassium)
Happens most frequently with
infection
From bottom of slide
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As insulin given K shifts into cells decreasing K
K given post confirmation of renal fx
Gradual reduction of BS
11
Diabetes Mellitus (DM)
Type 1

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Beta cell destruction
Leads to absolute
insulin deficiency
5-10% of all DM
cases
Type 2
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Insulin resistance
90-95% of all DM cases
Historically more
common in adults > 45
 prevalence seen in
children/adolescents
12
Causes
Type 2
Type 1

2 types
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Auto immune
Idiopathic
Not simple
inheritance
Genetic predisposition
plus trigger event
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Insulin
resistance plus
relative insulin
deficiency
13
Risk factors for Type II
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Overweight
Decreased exercise pattern
Family history of type 2 DM
Age
Non-European ancestry
14
Signs and Symptoms
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Type 1
Polyuria
Polydipsia
Polyphagia
Rapid weight loss
Dry skin
Irritability
Drowsiness/fatigue
Abdominal discomfort
Ketoacidosis
Type 2
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Polyuria
Polydipsia
↑ BP
Frequent infections
Fatigue
S/S insulin resistance
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Acanthosis nigricans
Polycystic ovary disease
15
Acanthosis nigricans
www.aocd.org/skin/dermatologic_diseases/acanthosis
Acanthosis nigricans screening program
16
Treatment
Team approach!!!
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Type 1
Insulin!
Monitor glucose
levels
Lifestyle changes
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Nutrition
Exercise
Type 2
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Lifestyle changes
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Nutrition
Exercise
Oral meds
Monitor glucose
levels
17
Insulin

Types
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Human
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Pork
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Most of what we see
Not used much at all
All types

100 units/ml
18
Types of Insulin
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Based on:
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Onset
Peak
Duration
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5 types
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Rapid
Short
Intermediate
Long
Mixed
19
Types of Insulin
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Rapid
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Intermediate
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Give within 15 minutes of a meal!!!
Is cloudy
Long acting
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Lantus can’t be mixed in a syringe
with any other insulin
20
Insulin Mixtures
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70/30; 50/50; 75/25
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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
21
Mixing Insulin
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Administer mixed insulin within 5
minutes of mixing or wait 15
minutes
Ignore this slide, she won’t test us
on it
22
Insulin Dosing
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One dose a day rarely suffices
Split mix is common
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Rapid/short acting mixed with NPH
Given prior to breakfast and supper
For better control- multiple
injections
23
Insulin Administration
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Subcutaneous administration
Rotate sites
Insulin absorption
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Abd is fastest, arm is next,
and the leg is the slowest
www.rch.org.au/diabetesmanual/manual.cfm?doc_id=2733#injection_sites
24
Insulin Administration
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Complications
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Lipoatrophy
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Where the tissue atrophies or breaks
down, little pitting areas
Lipohypertrophy
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Build up of fat, like a fatty nodule
25
Insulin Administration
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Insulin pen
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Resembles a large fountain pen
Needle is screwed onto tip
immediately prior to injection
26
Insulin Administration
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Insulin pump
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Computerized device
About the size of a pager
Worn around the waist
As close to normal insulin delivery as
possible now
Drawbacks
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Pump malfunction, can’t get air in line, have
to know how to do calculations and work
the device
27
Insulin Administration
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Absorption can be altered
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exercise
illness
Self monitoring is a must!!!
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This disease is lifelong so when the
kid gets old enough to do the shit
himself, he needs to do the shit
himself
28
Oral Medications
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Type 2 DM children only
Used if lifestyle changes are not
effective
Decreases absorption of blood
sugar from the diet, reduces the
insulin usage.
29
Monitoring
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Self- blood glucose monitoring
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At home & in hospital
Goal- blood glucose 80-120 mg/dl
Glycosylated hemoglobin (Hgb A1c)
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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
30
Monitoring
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Finger sticks / Atraumatic care
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Warm the finger
Use the ring finger and thumb
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They bleed a little bit easier
Puncture to the side of the finger pad
31
Complications
Hyperglycemia
 Caused by:
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Too little insulin
Illness/infection
Injury
Stress- physical/emotional
Decreased exercise
Diet
32
Hyperglycemia
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Symptoms
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3 P’s
Nausea
Blurred vision
Fatigue
Diabetic ketoacidosis
(DKA)
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Treatment
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Drink extra fluids
Administer additional
insulin
Monitor glucose
more closely
33
Complications- Hypoglycemia
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Caused by:
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Too much insulin
Diet
Exercise
Growth spurts
Puberty
Illness/injury
Menses
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Hypoglycemia
Symptoms
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Mild-moderate
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Shaky/sweaty
Hungry
Pale
Headache
Confusion
Disorientation
Lethargy
Change in behavior
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Severe
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Inability to swallow
Seizure/convulsion
Unconsciousness
35
Hypoglycemia
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Treatment
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Often difficult to differentiate HYPO
from HYPERglycemia
Check blood sugar if possible
When in doubt, give simple
carbohydrate
Follow with complex carbohydrate,
then protein
36
Hypoglycemia
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If unconscious, seizes or cannot
swallow
Glucagon
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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
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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
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Vascular changes
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Involve large and small vessels
Heart disease
Retinopathy
Neuropathy
Arterial obstruction
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Gangrene
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Education
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Always carry:
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Glucose tablets
Insta-glucose
Sugar cubes
Candy
**children may
fake a reaction to
get candy**
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Exercise
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With good control:
 Decreases
insulin
requirements
With poor control
 May stimulate
ketoacidosis
40
Education
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Nutrition
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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
41
Type I Diabetes
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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
42
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Estimating Portion Sizes
for eyeballing portion size:
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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 PingPong ball
1 cup of pasta equals a tennis ball
www.lillydiabetes.com
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Education
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Illness management
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Monitor glucose every 3 hours
Monitor urine ketones every 3 hours
or when glucose is > 240 mg/dl
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Urine ketones are not used for daily
management
44
Disorders of Pituitary Function
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Pituitary gland
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“Master” gland
Regulates other endocrine functions
Releases or withholds 7 other hormones
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Growth hormone (GH)
45
Hypopituitarism

Caused by:
 Organic lesions (tumors)
 Idiopathic
 Usually r/t GH deficiency
46
GH deficiency
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Manifestations
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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
47
GH deficency
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Diagnosis
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Physical exam
Family history
X rays
Endocrine studies
Growth chart
48
GH deficiency
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Treatment
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Correct underlying disease process
Replacement of GH (80-90% successful)
Biosynthetic GH drug of choice
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FDA approved for:
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GH deficiency
Chronic renal insufficiency
Prader-Willi syndrome
Turner syndrome
49
Growth Hormone Excess
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Hyperpituitarism
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Over secretion occurs prior to epiphyseal plate
closure
Grow 7-8 feet tall
Acromegaly
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Over secretion occurs after epiphyseal plate
closure
Overgrowth of head, lips, nose, tongue, jaw,
separation malocclusion of teeth, increased facial
hair
50
Growth hormone excess

Treatment

Remove tumor, pituitary gland radiation,
high dose sex steroids to close growth
plates
51
Diabetes Insipidus (DI)

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Disorder of the posterior pituitary
Results from HYPOsecretion of Antidiuretic
Hormone (ADH)
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ADH sometimes called vasopressin (Pitressin)
Produces uncontrolled diuresis
Causes

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Primary: familial or idiopathic
Secondary: trauma, tumors, CNS infection,
aneurysm
52
Diabetes Insipidus (DI)

Manifestations
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Cardinal signs: POLYURIA &
POLYDIPSIA
1st sign is often ENURESIS
Infants:
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irritability relieved with feeding of WATER
not milk
dehydration often occurs
53
Diabetes Insipidus (DI)

Management
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Instruct parents there is a difference
between DI and DM
Daily hormone replacement of
vasopressin
Drug of choice: DDAVP

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Nasal spray or IV
Treat for lifetime
54
Syndrome of Inappropriate
Antidiuretic Hormone (SIADH)
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Disorder of posterior pituitary
Produces HYPERsecretion of ADH
ADH causes reabsoption of water
back into central circulation
Causes
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Infection
Tumors
Trauma
CNS disease
55
SIADH
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Manifestations
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Fluid retention but no edema
HYPOtonicity
Anorexia
Nausea/vomiting
Irritability
Personality changes
56
SIADH

Treatment

Fluid restriction

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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

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Congenital hypoplastic thyroid
Acquired


Partial/complete thyroidectomy for CA or
thyotoxicosis
Following radiation treatment for malignancy
58
Hypothyroidism (juvenile)

Manifestations
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Decelerated growth
Myedematous skin changes
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Dry skin, periorbital edema, dry or
sparse hair
Constipation
Sleepiness
Mental decline
59
Hypothyroidism (juvenile)

Treatment
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Oral thyroid hormone replacement
Treat promptly in infants to facilitate
brain growth
Lifelong treatment
60
Hyperthyroidism
(Graves Disease)
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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
61
Hyperthyroidism
(Graves Disease)

Manifestations
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Gradually develop over 6-12 months
Excessive motion
Gradual weight loss
Muscle weakness
Vomiting/frequent stooling
Heat intolerance
Skin-warm, moist, flushed
62
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)

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
Risk for agranulocytosis, have family watch for
s/s of infection (sore throat and fever). Seek
medical attention immediately
Subtotal thyroidectomy
Ablation with radioiodine
63
References
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DM
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

www.diabetes.org
http://diabetes.niddk.nih.gov/dm/pubs/type
1and2
www.emedicine.com/ped/TOPIC581.HTM
Thyroid


www.cushings-help.com/thyroid.htm
www.healthsystem.virginia.edu/uvahealth/p
eds_diabetes/hypothd.cfm
64