Unit 7 Flash Cards Pediatrics- Endocrine

Front 1

What do these hormones do?
Growth hormone
Thyroid Stimulating Hormone
Adrenocorticotropic hormone

Back 1

Variations
Growth hormone
-Synthesis of protein, linear growth of skeletal bones
Thyroid Stimulating Hormone
-Development of bones, teeth, and brain
Adrenocorticotropic hormone
-Stimulates gonadotropic hormone in adolescence, gonads secrete estrogen & testosterone

Front 2

Nursing diagnosis for imbalance of endocrine hormones?

Back 2

Nursing Diagnosis
-Imbalanced Nutrition
-Ineffective health maintenance
-Noncompliance
-Disturbed body image
-Low self esteem

Front 3

Pancreatic hormone function:
List the islets of langerhans cells and what they do?

Back 3

Pancreatic Hormone Function
Function of Islets of Langerhans
-Alpha cells produce glucagon
-Beta cells produce insulin
-Delta cells produce somatostatin (believed to regulate insulin and glucagon)

Front 4

Type 1 Diabetes:
Who typically gets it?
Characterized by?
How do you get it?

Back 4

Type I
-Most DM of childhood is Type 1.
-Characterized by destruction of beta cells, usually leading to absolute insulin deficiency. Typically, onset in childhood and adolescence, but can occur at any age.
-Hereditary / autoimmune component arising when a person with a genetic predisposition is exposed to a precipitating event such as viral infection

Front 5

Type 1 Diabetes:
Patho-What happens when there is too much glucose?
What is glycosuria
What is ketonuria
What BS numbers are associated with each?

Back 5

Pathophysiology
-With a deficiency of insulin, glucose is unable to enter the cell, and remains in blood, causing hyperglycemia
-When serum glucose exceeds renal threshold, glucose spills into urine (glycosuria =180)
-Cells break down protein for conversion to glucose by the liver (ketonuria =200

Front 6

Type 2 Diabetes:
What is the cause?
How is it controlled?

Back 6

Type 2 / MODY
-Similar to Type 2 DM
-Epidemic
-2007 ADA
-overweight plus (2) -Family HX
-Race -s/s insulin resistance
-maternal hx GDM/DM
May be controlled with oral hypoglycemic agents and diet modifications

Front 7

List some complications of Diabetes?
What is ketoacidosis?

Back 7

Complications
-Retinopathy
-Nephropathy
-Neuropathy
-Skin changes
-Predisposition to infection
Ketoacidosis:glucose is unavailable for cellular metabolism, the body breaks down alternate sources of energy. Ketones are released, and excess ketones are eliminated in urine (ketonuria) or by the lungs (acetone breath)…

Front 8

Type 1 DM management: 1/2

Back 8

Management of Type 1 DM
-Insulin therapy: types of insulin, duration, onset and peak action, mixing and administration of types of insulin, rotation of injection sites
-Insulin pump therapy: ?
-Glucose monitoring: goal range 80-120 mg/dl
-Labs: hemoglobin A1ⅽ 4 – 6% norm
7.5% fair
>8% poor
-Nutrition / Meal planning
-Exercise

Front 9

Type 1 DM management: 2/2

Back 9

Management of Type 1 DM
-Illness management
-Management of hypoglycemic episodes
-Management of DKA
-Urine testing: ketones
-Not routinely used EXCEPT:
to test q3h during illness and whenever glucose is ≥240 mg/dl when illness not present

Front 10

Anticipatory Guidance:
What should they be doing?

Back 10

Anticipatory Guidance
-Recognition and treatment of hypoglycemia and hyperglycemia
-Management of “minor” illnesses
-Record keeping
-Hygiene
-Family support
-Acute care
-Honeymoon phase

Front 11

Pituitary Function:
Pituitary gland also called___?
Known as the ___ _____?
Respopnsible for?

Back 11

Pituitary Function
-Pituitary gland is also called “Hypophysis”
-Pituitary gland is the “master gland”
-Responsible for regulating other glands

Front 12

Hypo-pituitarism: growth hormone deficeincy:
Does what to growth?
Inhibits:
Delays:
primary site is at the ____?
DX by:_____ & ______?

Back 12

Hypopituitarism: Growth Hormone Deficiency
-Dwarfism
-Inhibits somatic growth (normal size at birth - <3% @ 1 yr.)
-Primary site of dysfunction appears to be in the hypothalamus
-Delayed puberty
-Family history
-Growth patterns and health history
-Definitive diagnosis bases of radioimmunoassay of plasma GH -levels
-Hand x-rays to evaluate growth potential vs. ossification

Front 13

Hypo-pituitarism: growth hormone deficeincy:
MGMT:
Hormone replacements are:
Response varies by:

Back 13

Management
-Biosynthetic growth hormone (injections)
-Other hormone replacements as needed
-Thyroid extract
-Cortisone
-Testosterone or estrogens and progesterone
-GH replacement successful in 80% of affected children
-Growth rate of 3.5-4 cm/yr before treatment and increase to 8-9 cm/yr after treatment
Response varies based on age, length of treatment, frequency of doses, dosage, weight, and GH receptor amount

Front 14

Hypo-pituitarism: growth hormone deficeincy:
Anticipatory guidance:

Back 14

Anticipatory Guidance
-Family support needs
-Child’s body image
-Preparing child for daily injections
-Treatment very expensive ($20,000 - $30,000/year)

Front 15

Pituitary Hyperfunction:
What is it?
Acromegaly is?
Excess ____ after epiphyseal.
Facial features are:
DX:

Back 15

Pituitary Hyperfunction
-Gigantism
-Excess GH before closure of epiphyseal shafts results in overgrowth of long bones
-Reach heights of 8 feet or more
-Weight generally in proportion to height
-Acromegaly
-Excess GH after epiphyseal
-Typical facial features
-Transverse growth of bones, increased facial hair, thick skin
-DX: XRay, endocrine

Front 16

Pituitary Hyperfunction:
Management:
What can be done?

Back 16

Management
-Surgical treatment to remove tumor
-Radiation and radioactive implants
-Hormone replacement therapy after surgery in some cases
-Early treatment for improved outcomes
-Early identification of children with excessive growth rates

Front 17

Precocious Puberty:
What is it?
Causes:

Back 17

Precocious Puberty
-Defined as sexual development before age 9 in boys or before age 8 in girls
-Occurs more frequently in girls
-True or complete precocious puberty/pseudopuberty
-Potential causes
-Disorder of gonads, adrenal glands, or hypothalamic-pituitary gonadal axis
-No causative factor in 80%-90% of girls and 50% boys

Front 18

Precocious Puberty:
Management:
TMT: (2)

Back 18

Management
-Treatment of specific cause if known
-May be treated with Lupron
-Slows prepubertal growth to normal rates
-Treatment is discontinued at age for normal pubertal changes to resume
-Psychologic support for child and family

Front 19

Congenital Hypothyroidism:
When what is low?
Hypotonia is?
can cause?
treat with?

Back 19

Congenital Hypothyroidism
-Cretinism: Low T3 & T4
-Hypotonia, short stature with shorter legs, enlarged tongue, short thick neck, hypothermia, cool extremities
-Newborn screening (maternal hormones for three months)
-Mental retardation
-Thyroxine, Vitamin D

Front 20

Juvenile Hypothyroidism:
What is it?
S/S?
TMT:
Why is prompt treatment needed?
What is crucial?

Back 20

Juvenile Hypothyroidism
-Decelerated growth
-Constipation
-Sleepiness
-Myxedematous skin changes
Dry skin
Sparse hair
Periorbital edema
-Oral thyroid hormone replacement
-Prompt treatment needed for brain growth in infant
-May administer in increasing amounts over 4-8 weeks to reach euthyroidism
-Compliance with medication regimen is crucial

Front 21

Goiter:
What is it?
Is it obvious?
TMT:
Largest percent of what?
What is contraindicated?

Back 21

Goiter
-Hypertrophy of the thyroid gland
-Thyroid enlargement at birth may compromise newborn’s -airway
-May become noticeable during periods of rapid growth
-Large goiters may be obvious, smaller nodules evident only on palpation
-TH replacement necessary for treatment of hypothyroidism
-Hashimoto disease or juvenile autoimmune thyroiditis
-Accounts for largest percent of juvenile hypothyroidism
-Goiter may be transient, asymptomatic
-May resolve spontaneously within 1-2 yrs
-Oral TH often decreases the goiter significantly
-Surgery contraindicated for this disorder

Front 22

Hyperthyroidism:
AKA_____ ______:
most common cause of _____?
caused by?
peak incidence is___ yrs old?
develops over __ to ___ months?
DX by:
TMT:

Back 22

-Graves Disease
-Most common cause of hyperthyroidism in childhood
-Believe caused by serum thyroid-stimulating immunoglobulin, but no specific etiology, familial
-Enlarged thyroid gland and exophthalmos
-Peak incidence 12-14 yrs
-Manifestations develop gradually, often over 6-12 months
-Diagnosis based on increased levels of T4 and T3 with suppressed TSH
-Treatments
Antithyroid drugs (PTU and methimazole)
Subtotal thyroidectomy
Ablation with radioiodine

Front 23

Thyrotoxicosis:
This is a thyroid ____?
may occur from ............?
Unusual in _____?
cause may be:
TMT:

Back 23

Thyroid “crisis” or “storm”
-May occur from sudden release of hormone
-Unusual in children, but can be life threatening
-May be precipitated by infection, surgery, or discontinuation of antithyroid therapy
-Treatment of thyroid storm
-Antithyroid drugs
-Propranolol

Front 24

Impact of Chronic Illness:
need to:
parents response can be:

Back 24

Coping mechanisms
-Approach behaviors adjust/ resolve
-Avoidance behavior no resolution
-Parental responses
-Shock, denial, guilt, self blame
-Bitterness, anger, overprotection, rejection, denial
-Acceptance
-Chronic sorrow

Front 25

Anticipatory Guidance: of chronic illness:

Back 25

Anticipatory Guidance
-Provide support at time of diagnosis
-Accept family’s emotional reactions
-Support family’s coping methods
-Advocate for empowerment
-Educate about the disorder and general health care