NURS 535 Final Exam Questions Fully
Solved 2025-2026 Updated.
Growth Hormone Deficiency - Answer Absence or deficiency of growth hormone produced
by the pituitary gland to stimulate the body to grow
Etiology of GH deficiency - Answer Infections, trauma, brain tumors
Clinical manifestations of GH - Answer Short height for child's age
Increased amount of fat around waist and in face
Emotional feelings about height or weight
Younger appearance than children of same age
Decreased muscle mass
Delayed skeletal maturation Delayed onset of puberty Delayed tooth development
Hypoglycemia
GH Diagnostics - Answer Thyroid panel
Evaluate renal and liver function
Insulin like growth factors (will be low)
Growth Hormone Stimulant test
Bone density scan
Brain CT or MRI
Karotyping
GH Treatment - Answer Most children receive subcutaneous injections
Injections can be daily or three to four times per week and have increased growth velocity at
bedtime
GH must be refrigerated
Close monitoring of growth with endocrinology visits every 3 to 6 months
Treatment stops when growth plates fuse
Precocious puberty - Answer The very early onset and rapid progression of puberty
Before age 8 in girls
Before age 9 in boys
,Etiology of Precocious Puberty - Answer Hormone-secreting tumors
Brain injury caused by head trauma
Infection
Thyroid dysfunction
Ovarian dysfunction
Idiopathic (most cases)
Clinical manifestations of precocious puberty - Answer Female: Breast development, axillary
hair, pubic hair, body odor, onset of menses, acne
Male: Testicular/Penile enlargement, axillary and chest hair, deepening voice, acne
Diagnostic evaluation of precocious puberty - Answer Computed tomographic scan or
magnetic resonance imaging
Bone density scan
Pelvic and adrenal ultrasound
Gonadotropin-releasing hormone stimulation test
Blood work: Testosterone, estrogen, LH, FSH
Treatment involves the suppression of puberty
congenital hypothyroidism - Answer Condition present at birth that results in lack of thyroid
hormones; results in poor physical and mental development; formerly called cretinism
Clinical manifestations of hypothyroidism - Answer Lethargy
Weakness
Dry skin
Cold intolerance
Weight gain
Constipation
Coarse hair
Diagnostic evaluation for hypothyroidism - Answer State-required screening: TSH and T4
Low T4, elevated TSH, or both indicate hypothyroidism
Positive test results may be followed by scan for bone age
,Blood tests before 48 hours after birth may be falsely interpreted because of the rise in TSH
immediately after birth
Hyperthyroidism - Answer Excessive production of thyroid hormones
Signs and symptoms of hyperthyroidism - Answer Weakness, insomnia, tachycardia,
palpitations, dyspnea, emotional of people and extremes, "everything speeds up"
Causes of hyperthyroidism - Answer Graves Disease
Pituitary and thyroid tumors, thyroiditis, congenital due to transfer of immunoglobulins from
thyrotoxic mothers
Treatment of hyperthyroidism - Answer PTU or methimazole to control the gland
Radioactive iodine to ablate the gland
Propranolol to treat sympathetic sxs such as tremors/palpitations, etc.
Thyroidectomy
congenital adrenal hyperplasia - Answer Genetic disease in which the adrenal gland is
overdeveloped, resulting in a deficiency of certain hormones and an overproduction of others
Salt losing form CAH - Answer No cortisol = hypoglycemia
No aldosterone = salt and water loss
Increased cortisol precursors
-17-hydroxyprogesterone = salt losing tendency
Increased androgens masculinization
Excess androgen production during fetal life is associated with salt-losing and simple virilizing
CAH and masculinizes the external genitalia of female infants
Clinical manifestations of CAH - Answer Males-precocious genital development
Females-may be born with varying degrees of ambiguous genitalia
-Enlarged clitoris appears as a small phallus
-Fused labia produce sac-like structure without testes
-Internal female sex organs are intact
Diagnostic evaluation CAH - Answer Hormonal studies
, Serum electrolyte
US to visualize pelvic organs
Chromosomal typing for positive sex determination and to rule out other genetic anomalies
CAH Treatment - Answer physiological dose of exogenous corticosteroids
Phenylketonuria (PKU) - Answer An inherited disorder of protein metabolism in which the
absence of an enzyme leads to a toxic buildup of certain compounds, causing intellectual
disability
PKU Treatment - Answer Newborn screening is done by use of Guthrie blood
test at 48 hours
The infant should ingest adequate protein (24 hours of formula or breast milk) prior to test
Heel stick after 24 hours but no later than 7 days after birth
Treatment is protein restricted diet, mature breast
milk or modified protein hydrolysate formula with
phenylalanine removed
Type I DM - Answer Insulin deficiency leading to metabolic disorder characterized by
hyperglycemia due to autoimmune destruction of beta cells by T lymphocytes
Auto-antibodies against insulin can be present and seen many years before disease develops)
Type II DM - Answer End organ insulin resistance leading to a metabolic disorder
characterized by hyperglycemia
Type II DM Treatment - Answer Sulfonureas (Glyburide and Glipizide)
-These drugs help the beta cells of the pancreas increase the release insulin
Biguanides (Metformin)
-The "insulin sensitizer" reduces hepatic glucose production
Glitazones (Avandia)
-Enhances insulin action in skeletal muscle, adipose tissue, and liver; can decrease or eliminate
the need for insulin in type 2 diabetes
Alpha-glucosidase inhibitors (Acarbose)
Solved 2025-2026 Updated.
Growth Hormone Deficiency - Answer Absence or deficiency of growth hormone produced
by the pituitary gland to stimulate the body to grow
Etiology of GH deficiency - Answer Infections, trauma, brain tumors
Clinical manifestations of GH - Answer Short height for child's age
Increased amount of fat around waist and in face
Emotional feelings about height or weight
Younger appearance than children of same age
Decreased muscle mass
Delayed skeletal maturation Delayed onset of puberty Delayed tooth development
Hypoglycemia
GH Diagnostics - Answer Thyroid panel
Evaluate renal and liver function
Insulin like growth factors (will be low)
Growth Hormone Stimulant test
Bone density scan
Brain CT or MRI
Karotyping
GH Treatment - Answer Most children receive subcutaneous injections
Injections can be daily or three to four times per week and have increased growth velocity at
bedtime
GH must be refrigerated
Close monitoring of growth with endocrinology visits every 3 to 6 months
Treatment stops when growth plates fuse
Precocious puberty - Answer The very early onset and rapid progression of puberty
Before age 8 in girls
Before age 9 in boys
,Etiology of Precocious Puberty - Answer Hormone-secreting tumors
Brain injury caused by head trauma
Infection
Thyroid dysfunction
Ovarian dysfunction
Idiopathic (most cases)
Clinical manifestations of precocious puberty - Answer Female: Breast development, axillary
hair, pubic hair, body odor, onset of menses, acne
Male: Testicular/Penile enlargement, axillary and chest hair, deepening voice, acne
Diagnostic evaluation of precocious puberty - Answer Computed tomographic scan or
magnetic resonance imaging
Bone density scan
Pelvic and adrenal ultrasound
Gonadotropin-releasing hormone stimulation test
Blood work: Testosterone, estrogen, LH, FSH
Treatment involves the suppression of puberty
congenital hypothyroidism - Answer Condition present at birth that results in lack of thyroid
hormones; results in poor physical and mental development; formerly called cretinism
Clinical manifestations of hypothyroidism - Answer Lethargy
Weakness
Dry skin
Cold intolerance
Weight gain
Constipation
Coarse hair
Diagnostic evaluation for hypothyroidism - Answer State-required screening: TSH and T4
Low T4, elevated TSH, or both indicate hypothyroidism
Positive test results may be followed by scan for bone age
,Blood tests before 48 hours after birth may be falsely interpreted because of the rise in TSH
immediately after birth
Hyperthyroidism - Answer Excessive production of thyroid hormones
Signs and symptoms of hyperthyroidism - Answer Weakness, insomnia, tachycardia,
palpitations, dyspnea, emotional of people and extremes, "everything speeds up"
Causes of hyperthyroidism - Answer Graves Disease
Pituitary and thyroid tumors, thyroiditis, congenital due to transfer of immunoglobulins from
thyrotoxic mothers
Treatment of hyperthyroidism - Answer PTU or methimazole to control the gland
Radioactive iodine to ablate the gland
Propranolol to treat sympathetic sxs such as tremors/palpitations, etc.
Thyroidectomy
congenital adrenal hyperplasia - Answer Genetic disease in which the adrenal gland is
overdeveloped, resulting in a deficiency of certain hormones and an overproduction of others
Salt losing form CAH - Answer No cortisol = hypoglycemia
No aldosterone = salt and water loss
Increased cortisol precursors
-17-hydroxyprogesterone = salt losing tendency
Increased androgens masculinization
Excess androgen production during fetal life is associated with salt-losing and simple virilizing
CAH and masculinizes the external genitalia of female infants
Clinical manifestations of CAH - Answer Males-precocious genital development
Females-may be born with varying degrees of ambiguous genitalia
-Enlarged clitoris appears as a small phallus
-Fused labia produce sac-like structure without testes
-Internal female sex organs are intact
Diagnostic evaluation CAH - Answer Hormonal studies
, Serum electrolyte
US to visualize pelvic organs
Chromosomal typing for positive sex determination and to rule out other genetic anomalies
CAH Treatment - Answer physiological dose of exogenous corticosteroids
Phenylketonuria (PKU) - Answer An inherited disorder of protein metabolism in which the
absence of an enzyme leads to a toxic buildup of certain compounds, causing intellectual
disability
PKU Treatment - Answer Newborn screening is done by use of Guthrie blood
test at 48 hours
The infant should ingest adequate protein (24 hours of formula or breast milk) prior to test
Heel stick after 24 hours but no later than 7 days after birth
Treatment is protein restricted diet, mature breast
milk or modified protein hydrolysate formula with
phenylalanine removed
Type I DM - Answer Insulin deficiency leading to metabolic disorder characterized by
hyperglycemia due to autoimmune destruction of beta cells by T lymphocytes
Auto-antibodies against insulin can be present and seen many years before disease develops)
Type II DM - Answer End organ insulin resistance leading to a metabolic disorder
characterized by hyperglycemia
Type II DM Treatment - Answer Sulfonureas (Glyburide and Glipizide)
-These drugs help the beta cells of the pancreas increase the release insulin
Biguanides (Metformin)
-The "insulin sensitizer" reduces hepatic glucose production
Glitazones (Avandia)
-Enhances insulin action in skeletal muscle, adipose tissue, and liver; can decrease or eliminate
the need for insulin in type 2 diabetes
Alpha-glucosidase inhibitors (Acarbose)
