Endocrine Dysfunction

Question 1

At what age is precocious puberty said to occur?

Answer 1

9 years in boys and 8 years in girls

Question 2

Over production of the anterior pituitary hormones can result in _______, ________, _______(_______), and _______ ______ from excessive gondotropins.

Answer 2

giantism, hyperthyroidism, hypercortisolism (Cushing’s Syndrome) and precocious puberty.

Question 3

Hypopituitarism: What is it and what does it lead to?

Answer 3

diminished or deficient secretion of pituitary hormones.

Can lead to gonadotropin deficiency (w/ absence or regression of secondary sex characteristics), GH deficiency (retarded somatic growth), TSH deficiency (which produces hypothyroidism) and corticotropin deficiency.

Question 4

What are the clinical manifestations of hypopituitarism?

Answer 4

• Presenting Complaint- short stature
• Growth measurements below 5th percentile
• Premature aging common later in life
• Height more retarded than weight
• Appear well nourished, skeletal proportions normal
• Tend to be relatively inactive
• Primary teeth usually appear at expected age, eruption of permanent teeth delayed
• Sexual development usually delayed but normal

Question 5

Constitutional Growth Delay:

Answer 5

Usually boys w/ delayed linear growth, generally beginning as a toddler, and skeletal and sexual maturation that is behind of age-mates.

Typically these children will reach normal adult height. (1 parent often had similar growth pattern). Changes will appear normal in sequence and tx w/ GH is not usually indicated.

Question 6

The most common organic cause of pituitary under secretion is

Answer 6

Tumors in pituitary or hypothalamic areas

Question 7

Height velocity:

Answer 7

Requires at least 4 and preferably 6 months of observation.

A substantial deceleration in height velocity (crossing several percentiles) between 3 and 12 or 13 years of age indicates a pathologic condition until proven otherwise.

Question 8

Target Height Formula:

Answer 8

[father’s height (cm) + mother’s height (cm) + 13]/2 for boys.
or
[father’s height (cm) + mother’s height (cm) - 13]/2 for girls.

** most children achieve an adult stature within approximately 10 cm (4 inches of the target height.

Question 9

Bone Age:

Answer 9

a method of assessing skeletal maturity by comparing the appearance of representative epiphyseal centers (hand-wrist) obtained on x-ray examination w/ age-appropriate published standards.

** Never diagnostic or indicative of a specific diagnosis. Merely indicates that short stature is to some extend “partially reversible” since linear growth will continue until epiphyseal fusion is complete.

** Bone age that is not delayed in a short child is of much greater concern and may be of some diagnostic value.

Question 10

How is definitive diagnosis based on absent or abnormal reserves of pituitary GH made?

Answer 10

GH secretion is stimulated w/ exercise, (elevated levels can be detected after 20 min), then followed by measurements of blood levels. ** GH levels are elevated 45 to 90 minutes after the onset of sleep also.

Question 11

When is the most optimum time to administer a does of GH to a child?

Answer 11

At bedtime (physiologic release is more normally stimulated during the first 45-90 minutes after the onset of sleep).

Question 12

Acromegaly:

Answer 12

Results from over secretion of GH after epiphyseal closure, growth in the transverse direction. Typical facial features: over growth of head, lips, nose, tongue, jaw and paranasal and mastoid sinuses, separation and malocclusion of the teeth in the enlarged jaw, disproportion of the face to the cerebral division of the skull; increased facial hair, thickened, deeply creased skin, increased tendency toward hyperglycemia and DM.

Question 13

Excessive GH BEFORE epiphyseal closure results in:

Answer 13

proportional overgrowth of the long bones

Question 14

When is the mean onset of puberty for girls?

Answer 14

10.2 for caucasian girls and 9.6 years in African-American girls

Question 15

What is SIADH?

Answer 15

Syndrome of Inappropriate Antidiuretic Hormone. It is the over production from the posterior pituitary of anti-diuretic hormone.

Question 16

What conditions is SIADH observed in?

Answer 16

Infection, tumors, CNS disease/trauma.

Question 17

What are the manifestations of SIADH?

Answer 17

Fluid retention, hypotoncity, serum osmolarity is low and urine osmolarity is high. When sodium levels are below 120: anorexia, N/V, cramps, irritability, personality changes. With progressive reduction in sodium: confusion,stupor, & convulsions.

Question 18

What are the primary nursing actions for SIADH?

Answer 18

Withholding fluids per protocol (1/4-1/2 for maintenance and 2/3-3/4 with the absence of fluid abnormalities), measuring I&O, daily weight, monitoring for signs of fluid overload and instituting seizure precautions.

Question 19

What is the management for chronic SIADH?

Answer 19

ADH-antagonizing medications.

Question 20

What action does the excessive ADH in SIADH have on the body?

Answer 20

Causes most of the filtered water to be reabsorbed from the kidneys back into central circulation, leading to fluid retention and hypotonicity.

Question 21

What causes Ambiguous Genitalia?

Answer 21

Decreased enzyme activity for cortisol of the adrenal cortez, especially 21-hydroxylase deficiency. This leads to over production of androgens which causes masculinity of the clitoris with fused labia. There is no change in the internal genitalia.

Question 22

How is Ambiguous Genitalia diagnosed?

Answer 22

Increased 17-ketosteriod levels
low 21-hydroxylase
Loss of Na & Chl w/ elevated K
Ultrasound is used to ID female reproductive organs.

Question 23

What is the treatment for Ambiguous Genitalia?

Answer 23

Cortisone is given to suppress ACTH. This may cause masculization of female genitalia to disappear. You MUST increase the dose during stress, infection or fever

Question 24

Children with salt-losing Ambiguous Genitalia require _______, so parents must know the signs of dehydration and have IM needle with hydrocortisone ready.

Answer 24

Aldosterone

Question 25

At what age is puberty considered Precocious?

Answer 25

9 in boys and 8 in girls.

Question 26

What is Central Precocious Puberty?

Answer 26

Pubertal development is activated by the hypothalamic gonadotropin-releasing hormone (GnRH). This produces early maturation and development of the gonads with secretion of sex hormones, development of secondary sex characteristics and sometimes production of mature sperm and ova.

Question 27

What can cause Central Precious Puberty?

Answer 27

Congenital anomalies, infectious, neoplastic or traumatic insults to the CNS or treatment of longstanding sex hormone exposure. Encephalitis, meningitis, abscess, granlomatous disease. Radiotherapy.
More common in girls
A CNS insult or structural abnormality found in more than 90% of boys with Central PP.

Question 28

What is Peripheral Precocious Puberty?

Answer 28

Early Puberty resulting from hormone stimulation other than GnRH (gonadotropin-releasing hormone). Usually caused by unusual end-organ sensitivity to prepubertal levels of estrogen or androgen.

Can also be caused by familial male-limited precocious puberty, Albright’s Syndrome, gonadal or extragonadal tumors, Adrenal (congential adrenal hyperplasia, adenoma, carcinoma, glucocorticoid resistance), exogenous sex hormones, primary hypothyroidism.

Question 29

What are the manifestations of Peripheral Precocious Puberty?

Answer 29

Premature thelarche (development of breasts in prepubertal girls), premature pubarhe (early development of sexual hair), and premature menarche (isolated menses without other evidence of sexual development).

Question 30

What is the treatment for Precious Puberty?

Answer 30

0.2-0.3mg/kg of leuprolide acetate (Luprom Depot) IM once every 4 weeks. Breast development regresses or does not advance and growth returns to normal. Stopped when puberty should naturally be present. Not all pt attain adult target heights and GH therapy may be warranted.

Question 31

Why isn’t Estrogen or birth-control pills not used to treat Precocious Puberty?

Answer 31

Growth plates will close, stopping growth.

Question 32

What is hypoparathyroidism?

Answer 32

A spectrum of disorders that results in deficient PTH (which is responsible for homeostasis of serum calcium concentration.

Question 33

What can cause hypoparathyroidism?

Answer 33

• Congenital causes (specific defect in synthesis or production of PTH or aplasia or hypoplasia of the gland.
• Thyroidectomy
• Transient Hypoparathyroidism forms (A: Maternal hyperparathyroidism or maternal DM. B: Infants fed a milk formula with a high phosphate-to-calcium ratio (more common).

Question 34

What are the symptoms of Hypoparathyroidism?

Answer 34

• Muscle cramps, anxiety, mental depression (early signs), numbness, stiffness, tingling in hands and feet.
• Positive Chvostek’s (facial spasm when tapping facial nerve), positive
• Trousseau’s sign: Carpal spasm elicited by pressure applied to nerves of upper arm.
• Tetany: carpopedal spasm (sharp flexion of wrist and ankle joints)
• Cyanosis, laryngospasm, stridor, abdominal pain, dry skin, brittle nails & hair, retarded growth.

Question 35

How is hypoparathyroidism diagnosed?

Answer 35

On the basis of clinical manifestations associated with decreased serum calcium levels and increased serum phosphorus.

Question 36

Levels of PTH are _______ in idiopathic hypoparathyroidism but _________ in psuedohypoparathroidism.

Answer 36

Idiopathic hypoparathyroidism- low PTH

Pueudohypoparathroidism- high PTH

Question 37

What is the treatment for hypoparathyroidism?

Answer 37

Calcium Gluconate for tentany, vitamin D therapy, oral calcium supplements. Renal, BP Vit D levels are drawn ever 6 months. Tracheotomy and Ca Gluconate should be present for emergency.

Question 38

What is the s/s of vitamin D toxicity (in regard of vitamin D therapy for hypoparathyroidism)?

Answer 38

Weakness, fatigue, lassitude, headache, N/V and diarrhea.

Question 39

What are the main nursing actions for hypoparathyroidism?

Answer 39

Recognition of hypocalcemia (unexplained convulsions, irritability, diarrhea, N/V, tetany), institution of seizure precautions, reduction of environmental stimuli, observing for s/s of laryngospasm (stridor, hoarseness, tightness in throat).

Question 40

Rapid Insulin:

Answer 40

Trade Name: Novalog, Humalog. Onset: 15 min, peak: 30 min - 1hr, Duration: 3-4 hr

Question 41

Short Acting Insulin:

Answer 41

Trade Name: Regular Insulin (Humulin N) Onset: 30 min-1hr Peak: 2-3 hr Duration: 5-7 hr

Question 42

Intermediate acting Insulin:

Answer 42

Trade name: NPH Insulin Onset: 1-2 hr Peak:4-12 hr Duration: 18-24 hr

Question 43

Long Acting Insuling:

Answer 43

Trade name: Insulin glargine (Lantus) Onset: 1 hr Peak: None Duration: 10.4- 24 hr

Question 44

Glucagon:

Answer 44

for hypoglycemia, admin IM or SubQ. Takes 15-20min,may cause vomiting so put on side.

Question 45

Symptoms of Type 1 Diabetes Mellitus:

Answer 45

Polyphagia (excessive hunger), polyuria, polydipsia, weight loss, enuresis or nocturia, irritability, shortened attention span, lowered frustration tolerance, dry skin, blurred vision, poor wound healing, fatigue, flushed skin, headache, frequent infection, elevated blood glucose levels and glucosuria, Diabetic ketosis: ketones and glucose in urine, dehydration in some cases Diabetic Ketoacidosis: dehydration, electrolyte imbalance, acidosis, deep rapid breathing (Kussmaul’s).

Question 46

Symptoms of Type 2 Diabetes Mellitus:

Answer 46

increased thirst, increased hunger (especially after eating), dry mouth, frequent urination, unexplained weight loss, fatigue, blurred vision, headaches and loss of consciousness

Question 47

Symptoms of Hypoglycemia:

Answer 47

Rapid onset, mood: labile, irritable, nervous, weepy. Confusion. Pallor, sweating. Normal mucous membranes. Shallow to normal resporations. Tachycardia, palpitations. No breath odor. Tremors. blood glucose below 60mg/dl. No ketones. Urine and blood values normal. Diplopia. Ominous Signs: Late- hyperreflexia, dilated pupils, seizure, shock, coma.

Question 48

Symptoms of Hyperglycemia:

Answer 48

Gradual onset. Mood: lethargic. Dulled senses, confusion. Thirst. N&V, abdominal pain. Flushed skin. Signs of dehydration. Dry crusty membranes. Deep, rapid respirations (Kussmaul’s). Less rapid, weak pulse. Fruity acetone breath. Diminished reflexes, paresthesia. Blood glucose above 250mg/dl. Lots of ketones in urine & blood, low blood pH (< or equal to 7.25), bicarbonate <20mEq/L. Polyuria (early) to oliguria (late). Blurred vision. Ominous signs: acidosis, coma.

Question 49

What is the normal glucose range?

Answer 49

80-120 mg/dl

Question 50

Glycosylated Hemoglobin: What is it and what is the acceptable range?

Answer 50

The measurement of hemoglobin levels is a satisfactory method for assessing control of diabetes. Diabetes control depends on age, with hemoglobin levels of 6.5% to * % indicating a slightly elevated but acceptable range.

Question 51

Urine Testing for Glucose:

Answer 51

urine testing for glucose is no longer used for diabetes management, there is poor correlation between simultaneous glycosuria and blood glucose concentrations. ((Urine testing can be used to detect ketonuria)).