ATI RN PEDIATRICS PROCTORED EXAM STUDY GUIDE 2021/2022
For the following diagnoses, note causes, assessment findings, signs/symptoms, treatment, priority
nursing considerations, safety concerns.
Endocrinology:
chronic disorder of metabolism characterized by hyperglycemia and insulin resistance. Type 1
Diabetes-Pancreas makes no insulin. Most times in kids they have type 1. Polydipsia, polyphagia,
polyuria. Kids may also present with wt loss, nocturia, anuresis.
type 1 DM- onset usually <20 yo, abrupt onset. Affects more males than females (slightly).Type 2
beginning to increase in younger kids (due to nutrition), gradual onset, affects more females than
males.
Hyperglycemia-ketones in urine, protein in urine, glucose in urine
DKA-Life threatening. When insulin is absent and glucose is unavailable for cellular metabolism the
body chooses alternate sources of energy principally fat, which breaks down into fattyacid and
glycerol in the fat cells is converted by the liver to ketone bodies. Any excess is eliminated in the urine
(ketonuria) or lungs (acetone breath).
s/s-drowsy, dehydrating, decreased skin turgor, fruity breath (acetone), hypotension,
bradycardia hypoglycemia-low blood sugar. s/s- cold, clammy , weak, dizzy, headache,
drowsiness,
irritability, seizures, and coma are all possible. Immediate intervention should be to get BG back up. If
conscious give orange juice, glucose tab or gel. Then follow with a complex carb once alert, like bread,
crackers, and peanut butter, or milk
Hypopituitarism – diminished secretion of one or more pituitary hormones. Consequence of condition
depend on the degree of dysfunction. It often leads to gonadotropin deficiency with absenceor
regression of secondary sex characteristics, growth hormone deficiency, in which children display
stunted somatic growth; thyroid stimulating hormone deficiency, which produces hypothyroidism, and
adrenocorticotropic hormone deficiency, which results in adrenal hypofunction.
manifestations- children w/ GH deficiency generally grown normally during the first year andthen
follow a slowed growth curve below 3%. They may appear overweight, due to stunted height
how do we treat? Growth hormone injections-SQ injections daily. Growth increases the first year of
treatment then declines in subsequent years. Final height is likely to remain less than normal. Criteria to
stop GH therapy- between healthcare team and family but usually growth rates of less than 1’per year
and bone age of more than 14 yr in girls and more than 16 in boys are often used as criteria to stop GH
therapy.
Precocious Puberty-sexual development before 9 yr old in boys or 8 yr of age in girls. Normally
hypothalamic releasing factors stimulate secretion of gonadotropic hormones from the anterior pituitary
gland at the time of puberty. In boys interstitial cell stimulating hormone stimulates Leydig cells of the
testes to secrete testosterone, in girls FSH and LH stimulate the ovarian follicles to secrete estrogens.
This is known as hypothalamic pituitary gonadal axis. If the cycle is stimulated early it is precocious
puberty.
, treatment-treat the cause if known, no treatments in some cases, or monthly injections of LHinjections.
SIADH- over production of ADH, low sodium, water retention
Care management- I/O, daily weight, watch for s/s of fluid overload especially in kids getting ivfluids.
Seizure precautions. Fluid restriction
Diabetes Insipidus- Polyuria, polydipsia. principal disorder of posterior pituitary hypofunction. AKA-
neurogenic DI resulting from under secretion of antidiuretic hormone, or vasopressin producing a state
of uncontrolled diuresis. Primary cause are familial or idiopathic, secondary cause is trauma, tumors,
infections and vascular anomalies. Certain drugs such as alcohol, phenytoin, can cause a transient
polyuria. DI may be early sign of an evolving cerebral process. Dehydration is usually not a serious
problem in older children who are able to drink larger quantities of water, however any period of
unconsciousness such as after trauma or anesthesia may be life threatening because of the voluntary
demand for fluid is absent. Careful monitoring of urine volumes, blood concentration, and IV fluid
replacement is essential to prevent dehydration. Careful monitoring of VS
Cushing’s Disease-adrenal, too much steroids, excess of ACTH FROM PITUITARY, hypersecretionof
glucocorticoids from adrenal. S/S- buffalo hump, too much cortisol, ruddy cheeks
Adrenocortical insufficiency -Addison’s Disease-Muscle weakness, mental fatigue, irritability,sleeping,
listless, hyperpigmentation, sometimes vitiligo, dehydration, anorexia, wt loss, hypotension,small heart,
dizzy, syncopal, hypoglycemia, unexplained seizures, craving for salt, acute abd pain, electrolyte
imbalances.
Grave’s Disease-over production of thyroid hormone production. Peaks @ 12-14.
S/S-exophthalmos, emotional liability, physical restlessness, decrease at school performance, increase
in appetite w/weight loss, fatigue
Treatment- drugs to treat, propylthiouracil (PTU), methimazole, watch for sore throat and feverbecause
side effects- leukopenia (at risk for infection), LIVER DAMAGE. Treat leukopenia with steroids. radioactive
iodine procedure is the least invasive.
Hypothyroidism- deficient PTH. S/S- decelerated growth, dry skin, puffy eyes, sparse hair,constipation,
sleepiness, mental decline.
Treatment- thyroid replacement, Synthroid
GI/GU:
Gastroenteritis- stomach bug, inflammation
Appendicitis- Acute appendicitis is inflammation of the vermiform appendix. The cause is obstruction of
the lumen of the appendix, usually due to hardened fecal matter. Swollen lymphoid tissueoccurring after
a viral infection can also obstruct the appendix, rarely a parasite Enterobius vermicularis,or pinworms can
also obstruct the appendiceal lumen.
For the following diagnoses, note causes, assessment findings, signs/symptoms, treatment, priority
nursing considerations, safety concerns.
Endocrinology:
chronic disorder of metabolism characterized by hyperglycemia and insulin resistance. Type 1
Diabetes-Pancreas makes no insulin. Most times in kids they have type 1. Polydipsia, polyphagia,
polyuria. Kids may also present with wt loss, nocturia, anuresis.
type 1 DM- onset usually <20 yo, abrupt onset. Affects more males than females (slightly).Type 2
beginning to increase in younger kids (due to nutrition), gradual onset, affects more females than
males.
Hyperglycemia-ketones in urine, protein in urine, glucose in urine
DKA-Life threatening. When insulin is absent and glucose is unavailable for cellular metabolism the
body chooses alternate sources of energy principally fat, which breaks down into fattyacid and
glycerol in the fat cells is converted by the liver to ketone bodies. Any excess is eliminated in the urine
(ketonuria) or lungs (acetone breath).
s/s-drowsy, dehydrating, decreased skin turgor, fruity breath (acetone), hypotension,
bradycardia hypoglycemia-low blood sugar. s/s- cold, clammy , weak, dizzy, headache,
drowsiness,
irritability, seizures, and coma are all possible. Immediate intervention should be to get BG back up. If
conscious give orange juice, glucose tab or gel. Then follow with a complex carb once alert, like bread,
crackers, and peanut butter, or milk
Hypopituitarism – diminished secretion of one or more pituitary hormones. Consequence of condition
depend on the degree of dysfunction. It often leads to gonadotropin deficiency with absenceor
regression of secondary sex characteristics, growth hormone deficiency, in which children display
stunted somatic growth; thyroid stimulating hormone deficiency, which produces hypothyroidism, and
adrenocorticotropic hormone deficiency, which results in adrenal hypofunction.
manifestations- children w/ GH deficiency generally grown normally during the first year andthen
follow a slowed growth curve below 3%. They may appear overweight, due to stunted height
how do we treat? Growth hormone injections-SQ injections daily. Growth increases the first year of
treatment then declines in subsequent years. Final height is likely to remain less than normal. Criteria to
stop GH therapy- between healthcare team and family but usually growth rates of less than 1’per year
and bone age of more than 14 yr in girls and more than 16 in boys are often used as criteria to stop GH
therapy.
Precocious Puberty-sexual development before 9 yr old in boys or 8 yr of age in girls. Normally
hypothalamic releasing factors stimulate secretion of gonadotropic hormones from the anterior pituitary
gland at the time of puberty. In boys interstitial cell stimulating hormone stimulates Leydig cells of the
testes to secrete testosterone, in girls FSH and LH stimulate the ovarian follicles to secrete estrogens.
This is known as hypothalamic pituitary gonadal axis. If the cycle is stimulated early it is precocious
puberty.
, treatment-treat the cause if known, no treatments in some cases, or monthly injections of LHinjections.
SIADH- over production of ADH, low sodium, water retention
Care management- I/O, daily weight, watch for s/s of fluid overload especially in kids getting ivfluids.
Seizure precautions. Fluid restriction
Diabetes Insipidus- Polyuria, polydipsia. principal disorder of posterior pituitary hypofunction. AKA-
neurogenic DI resulting from under secretion of antidiuretic hormone, or vasopressin producing a state
of uncontrolled diuresis. Primary cause are familial or idiopathic, secondary cause is trauma, tumors,
infections and vascular anomalies. Certain drugs such as alcohol, phenytoin, can cause a transient
polyuria. DI may be early sign of an evolving cerebral process. Dehydration is usually not a serious
problem in older children who are able to drink larger quantities of water, however any period of
unconsciousness such as after trauma or anesthesia may be life threatening because of the voluntary
demand for fluid is absent. Careful monitoring of urine volumes, blood concentration, and IV fluid
replacement is essential to prevent dehydration. Careful monitoring of VS
Cushing’s Disease-adrenal, too much steroids, excess of ACTH FROM PITUITARY, hypersecretionof
glucocorticoids from adrenal. S/S- buffalo hump, too much cortisol, ruddy cheeks
Adrenocortical insufficiency -Addison’s Disease-Muscle weakness, mental fatigue, irritability,sleeping,
listless, hyperpigmentation, sometimes vitiligo, dehydration, anorexia, wt loss, hypotension,small heart,
dizzy, syncopal, hypoglycemia, unexplained seizures, craving for salt, acute abd pain, electrolyte
imbalances.
Grave’s Disease-over production of thyroid hormone production. Peaks @ 12-14.
S/S-exophthalmos, emotional liability, physical restlessness, decrease at school performance, increase
in appetite w/weight loss, fatigue
Treatment- drugs to treat, propylthiouracil (PTU), methimazole, watch for sore throat and feverbecause
side effects- leukopenia (at risk for infection), LIVER DAMAGE. Treat leukopenia with steroids. radioactive
iodine procedure is the least invasive.
Hypothyroidism- deficient PTH. S/S- decelerated growth, dry skin, puffy eyes, sparse hair,constipation,
sleepiness, mental decline.
Treatment- thyroid replacement, Synthroid
GI/GU:
Gastroenteritis- stomach bug, inflammation
Appendicitis- Acute appendicitis is inflammation of the vermiform appendix. The cause is obstruction of
the lumen of the appendix, usually due to hardened fecal matter. Swollen lymphoid tissueoccurring after
a viral infection can also obstruct the appendix, rarely a parasite Enterobius vermicularis,or pinworms can
also obstruct the appendiceal lumen.
