NURS 535 FINAL EXAM | COMPREHENSIVE NURSING DIAGNOSTICS
STUDY GUIDE, PRACTICE QUESTIONS & ANSWERS 2026/2027
Growth Hormone Deficiency - ANS ✔✔Absence or deficiency of growth hormone produced by the
pituitary gland to stimulate the body to grow
Etiology of GH deficiency - ANS ✔✔Infections, trauma, brain tumors
Clinical manifestations of GH - ANS ✔✔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 - ANS ✔✔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 - ANS ✔✔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 - ANS ✔✔The very early onset and rapid progression of puberty
Before age 8 in girls
Before age 9 in boys
Etiology of Precocious Puberty - ANS ✔✔Hormone-secreting tumors
Brain injury caused by head trauma
Infection
Thyroid dysfunction
Ovarian dysfunction
Idiopathic (most cases)
Clinical manifestations of precocious puberty - ANS ✔✔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 - ANS ✔✔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 - ANS ✔✔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 - ANS ✔✔Lethargy
Weakness
Dry skin
Cold intolerance
Weight gain
Constipation
Coarse hair
Diagnostic evaluation for hypothyroidism - ANS ✔✔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 - ANS ✔✔Excessive production of thyroid hormones
Signs and symptoms of hyperthyroidism - ANS ✔✔Weakness, insomnia, tachycardia, palpitations,
dyspnea, emotional of people and extremes, "everything speeds up"
Causes of hyperthyroidism - ANS ✔✔Graves Disease
Pituitary and thyroid tumors, thyroiditis, congenital due to transfer of immunoglobulins from thyrotoxic
mothers
Treatment of hyperthyroidism - ANS ✔✔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 - ANS ✔✔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 - ANS ✔✔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 - ANS ✔✔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 - ANS ✔✔Hormonal studies
Serum electrolyte
US to visualize pelvic organs
Chromosomal typing for positive sex determination and to rule out other genetic anomalies
CAH Treatment - ANS ✔✔physiological dose of exogenous corticosteroids
Phenylketonuria (PKU) - ANS ✔✔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 - ANS ✔✔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 - ANS ✔✔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 - ANS ✔✔End organ insulin resistance leading to a metabolic disorder characterized by
hyperglycemia
Type II DM Treatment - ANS ✔✔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)
-Reduces the rate of digestion of complex carbohydrates and the subsequent absorption of glucose
Type I vs Type II DM - ANS ✔✔Type I
, •Insulin deficiency
•Abrupt onset
•Ketosis prone
•Generally not obese
•Insulin dependent
•Not responsive to oral agents
•Onset usually 18 years or younger
Type II
•Insulin resistance
•Insidious onset
•Not prone to ketosis
•Usually obese
•Non-insulin dependent
•Responsive to oral hypoglycemic medications
•Onset usually adult but seen in obese children and adolescents
Type 1/11 DM Diagnosis - ANS ✔✔Clinical s/sx of hyperglycemia and acidosis if present
Ketonuria and glucosuria may also be present
Laboratory data:
-Fasting plasma glucose of >126mg/dL
-Random serum glucose >200mg/dL
-Glycosylated hemoglobin value (A1C) elevated
Illness management in Type I and II DM - ANS ✔✔Continue Insulin Treatment
-Illness often increases the amount of insulin the body needs. Instruct parents that insulin should never
be withheld.
Stay close to the meal plan
-If the child has an upset stomach and can not eat, give clear liquids that contain carbohydrates
Give plenty of liquids
-Encourage the child to drink-increase fluids
Choose medications wisely
-OTC may contain sugar and/or alcohol
Clinical manifestations of DM - ANS ✔✔Hypoglycemia
-Trembling, sweating, tachycardia, pallor, clammy skin
-Personality change, irritability, slurred speech, decreased LOC, seizures
Hyperglycemia
-3 P's-polyuria, polydipsia, polyphagia
-Fatigue, wt loss, blurred vision, emotional labiality, headache, hunger
Ketoacidosis
-Hyperglycemia symptoms PLUS abdominal pain, chest pain, Kussmaul respirations, N/V, acetone breath,
dehydration
STUDY GUIDE, PRACTICE QUESTIONS & ANSWERS 2026/2027
Growth Hormone Deficiency - ANS ✔✔Absence or deficiency of growth hormone produced by the
pituitary gland to stimulate the body to grow
Etiology of GH deficiency - ANS ✔✔Infections, trauma, brain tumors
Clinical manifestations of GH - ANS ✔✔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 - ANS ✔✔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 - ANS ✔✔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 - ANS ✔✔The very early onset and rapid progression of puberty
Before age 8 in girls
Before age 9 in boys
Etiology of Precocious Puberty - ANS ✔✔Hormone-secreting tumors
Brain injury caused by head trauma
Infection
Thyroid dysfunction
Ovarian dysfunction
Idiopathic (most cases)
Clinical manifestations of precocious puberty - ANS ✔✔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 - ANS ✔✔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 - ANS ✔✔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 - ANS ✔✔Lethargy
Weakness
Dry skin
Cold intolerance
Weight gain
Constipation
Coarse hair
Diagnostic evaluation for hypothyroidism - ANS ✔✔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 - ANS ✔✔Excessive production of thyroid hormones
Signs and symptoms of hyperthyroidism - ANS ✔✔Weakness, insomnia, tachycardia, palpitations,
dyspnea, emotional of people and extremes, "everything speeds up"
Causes of hyperthyroidism - ANS ✔✔Graves Disease
Pituitary and thyroid tumors, thyroiditis, congenital due to transfer of immunoglobulins from thyrotoxic
mothers
Treatment of hyperthyroidism - ANS ✔✔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 - ANS ✔✔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 - ANS ✔✔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 - ANS ✔✔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 - ANS ✔✔Hormonal studies
Serum electrolyte
US to visualize pelvic organs
Chromosomal typing for positive sex determination and to rule out other genetic anomalies
CAH Treatment - ANS ✔✔physiological dose of exogenous corticosteroids
Phenylketonuria (PKU) - ANS ✔✔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 - ANS ✔✔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 - ANS ✔✔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 - ANS ✔✔End organ insulin resistance leading to a metabolic disorder characterized by
hyperglycemia
Type II DM Treatment - ANS ✔✔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)
-Reduces the rate of digestion of complex carbohydrates and the subsequent absorption of glucose
Type I vs Type II DM - ANS ✔✔Type I
, •Insulin deficiency
•Abrupt onset
•Ketosis prone
•Generally not obese
•Insulin dependent
•Not responsive to oral agents
•Onset usually 18 years or younger
Type II
•Insulin resistance
•Insidious onset
•Not prone to ketosis
•Usually obese
•Non-insulin dependent
•Responsive to oral hypoglycemic medications
•Onset usually adult but seen in obese children and adolescents
Type 1/11 DM Diagnosis - ANS ✔✔Clinical s/sx of hyperglycemia and acidosis if present
Ketonuria and glucosuria may also be present
Laboratory data:
-Fasting plasma glucose of >126mg/dL
-Random serum glucose >200mg/dL
-Glycosylated hemoglobin value (A1C) elevated
Illness management in Type I and II DM - ANS ✔✔Continue Insulin Treatment
-Illness often increases the amount of insulin the body needs. Instruct parents that insulin should never
be withheld.
Stay close to the meal plan
-If the child has an upset stomach and can not eat, give clear liquids that contain carbohydrates
Give plenty of liquids
-Encourage the child to drink-increase fluids
Choose medications wisely
-OTC may contain sugar and/or alcohol
Clinical manifestations of DM - ANS ✔✔Hypoglycemia
-Trembling, sweating, tachycardia, pallor, clammy skin
-Personality change, irritability, slurred speech, decreased LOC, seizures
Hyperglycemia
-3 P's-polyuria, polydipsia, polyphagia
-Fatigue, wt loss, blurred vision, emotional labiality, headache, hunger
Ketoacidosis
-Hyperglycemia symptoms PLUS abdominal pain, chest pain, Kussmaul respirations, N/V, acetone breath,
dehydration
