Download Endocrine Dysfunction

Endocrine Dysfunction
Nursing 355
Maria Rubolino-Gallego
Endocrine System
Hormones – make up the endocrine system, stimulate and regulate the action of other
tissues, exert a physiological effect on other cells
Endocrine system and the autonomic nervous system function together to regulate 3
items: growth, metabolism and reproduction
Sympathetic and parasympathetic release:
Hypothalamus secretes hormones
Negative feedback effect
At birth the endocrine system is the least developed
Hormonal control minimal until
months of age
Glands and Hormones
Hypothalamus and pituitary
-Ant. Pit. – secretes hormones, ACTH, TSH,
Pit. – stores and secretes
antidiuretic hormone and oxytocin
Thyroid Gland
-Thyroxine, Triiodothyronine, and calcitonin
-Post
Adrenal Gland
-Cortisol, Aldosterone, Androgen,
Norepinephrine
Ovary
-secretes hormones: Estrogen and progesterone
Islet of Langerhans
-secretes hormones: Insulin
Epinephrine,
Testes
-Testosterone
Diagnosis and Treatment
Dx of Endocrine Dysfunction
-Lab tests
-Normal hormone levels are related to patients age and stage of puberty
-May need to do peak and trough levels to determine accurate interpretation
-X-ray for bone growth
-MRI or CT scan for tumors or cysts
Accurate height and weight measurements
Tanner staging
Milestones
School performance
Treatment
Long-term and ongoing
Usually through pharmacotherapy
Congenital Hypothyroidism
Thyroid gland does not produce sufficient thyroid hormone
Present at birth
1 in 4,000 live births
Usually unknown cause
Mother taking PTU during pregnancy can cause transient hypothyroidism
Sxs: prolonged jaundice, skin mottling, large fontanel, large tongue, hypotonia,
distended abdomen
Dx: mandatory newborn testing,
Goal for newborn screening: no sooner than 48 hours after delivery
Tx: lifelong hormone replacement therapy, monitor growth and development
Hashimoto’s Thyroiditis
acquired hypothyroidism
Thyroid gland produces an inadequate amount of thyroid hormone
Autoimmune hypothyroidism
Usually in families with a hx of thyroid disease
Sxs: goiter, dry, thick skin, coarse, dull hair, fatigue
Dx:labs, TSH, T4
Tx: thyroxine
Hyperthyroidism (Grave’s Disease)
Excessive thyroid hormones are produced by an enlarged thyroid gland
Most common cause of hyperthyroidism in children
Grave’s accounts for 5-10% of thyroid disorders in children
Female to male (4:1), with a familial tendency
Sxs: nervousness, diarrhea, increased perspiration, heart rate changes, exophthalmos,
poor attention span, school problems
Dx: TSH
Tx: PTU or methimazole, radioactive iodine, or surgery
Comparing Hypo vs. Hyperthyroidism
Energy
Bowels
Intolerance to heat vs. cold
Weight
Skin
muscles
Energy
Bowels
Intolerance to heat vs. cold
Weight
Skin
Heart rate
Blood pressure
muscles
Phenylketonuria (PKU)
Genetic metabolic disorder resulting in CNS damage from toxic levels of phenylalanine
Autosomal recessive disorder
1 in 10,000 to 25,000 live births in the US
Signs may not be present until 3 months old
Sxs:vomiting, musty odor to urine, eczema, hypertonia, hyperactive behavior
Mental retardation is long term consequence
PKU
DX: routine neonatal screening
Goal:
Tx: special diets that restricts phenylalanine intake
Precocious Puberty
Early onset puberty
Prior to 8 y.o. in girls and 9 y.o. in boys
Premature appearance of secondary sexual characteristics, accelerated growth rate,
advanced bone maturation
Rapid bone growth leads to early growth-plate fusions leads to short stature
Precocious Puberty
Idiopathic or by CNS tumors
More in girls than boys
Dx: Hx, labs
Tx: administration of GnRH agonist
Once therapy is discontinued, puberty resumes
Diabetes Insipidus
Inability to concentrate urine because of a deficiency of vasopressin (AKA
antidiurectic hormone)
Causes: commonly from head trauma, tumors, infection in the area of the hypothalamus
Sxs: polyuria, polydipsia, nocturia, dehydration
Dx: hypernatremia, low urine specific gravity, water deprivation test
Tx: Maintain fluid balance and (synthetic vasopressin) DDAVP
Growth Hormone Deficiency
Inadequate production or secretion of GH
Sxs: immature face, decreased muscle mass, micropenis, hypoglycemia, short stature
Causes: hypopituitarism, brain tumors, cranial radiation
Dx: careful measurements over time (Ht), TSH, BUN/Creatnine, CBC, electrolytes
Tx: Synthetic GH, sq inj. 6-7 times/wk at HS or a time release sq inj., until growth
plates close
Galactosemia
Deficiency of galactose-1-phosphate
Prevents the conversion of galactose to glucose
Cannot properly digest milk or sugar
1 in 60,000 to 80,000 live births
Infants can exhibit: hypoglycemia, liver damage, cataracts, infections
Tx: lifelong lactose-restricted diet
Maple Syrup Urine Disease
1 in 250,000 to 300,000 live births
Affects metabolism of certain amino acids
Build up of acids causes ketoacidosis
Sxs: lethargy, poor feeding, vomiting, weight loss, seizures, loss of reflexes
Urine smells like maple syrup
Tx: lifelong low protein, limited amino acid diet
Tay-Sachs Disease
Affects primarily infants in the Ashkenazi Jewish population
Abnormal build-up of gangliosides in the neurons
After a 6 month normal development, the infant has developmental delays and
neurologic deterioration
Sxs: macrocephaly, seizures, blindness, deafness, death
Tx: symptomatic and supportive care
Neonatal Hypoglycemia
Low level of glucose in the serum
Less than
Risk Factors:
Respiratory Distress
Asphyxia
Prematurity
SGA (less than 2500 grams)
Maternal Toxemia
Infant with Rh incompatability
Infant of diabetic mother
Neonatal Hypoglycemia
2-10 in 1000 live births
Many infants are asymptomatic
If symptoms occur:
Jitteriness
Poor feeding
Lethargy
Seizures
Apnea
Hypotonia
High-pitched cry
Bradycardia
cyanosis
Neonatal Hypoglycemia
Glucose concentrations reach their lowest level at
hours posnatal age
Treatment: D5W, formula via nipple or gavage
Type 1 DM
Pancreas is unable to produce or secrete insulin
Causes: genetic, autoimmune process
Tx: insulin therapy, may experience a honeymoon phase characterized by
hypoglycemia
Type 2 DM
Production of excess insulin, but the cells are not able to utilize it properly
Youth tend to be obese
Peak incidence occurs with onset of puberty
Incidence is on the rise (5 y.o. have been diagnosed)
Higher in certain ethnicities
DM
Sxs:
3 P’s
Wt. loss
Fatigue
Blurred vision
Recurrent vaginal infections
Typically overweight
Acanthosis nigricans
If untreated can lead to ketoacidosis
Tx with insulin and IV NS, lower blood sugars. Swith to oral agents
Blood glucose monitoring
If not managed well: retinopathy, nephropathy, neuropathy
Dx: random glucose elevated, FBS elevated, elevated HbA1c
Tx: check blood sugars, exercise, insulin injections, meal planning
Goals: Normal growth and development, absence of complications, normal HbA1c
Diabetic Ketoacidosis
DKA
Absolute insulin defecit
Sxs:
Abdominal and chest pain
N/V
Fruity breath
Decreased LOC
Kussmau respirations
DKA
Dx:
Blood glucose
Arterial pH
Urine ketones
Serum ketones
Serum potassium
Serum phosphorus
WBCs
Hypocalcemia
Inadequate stores of calcium
Neonatal hypocalcemia serum level of less than 7/0mg/dl
Occurs typically in infant of diabetic mothers
Sxs: twitching, tremors, irritability, jitteriness, ECG changes
Tx: formula feedings or IV supplement