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Pediatrics > Endo > Flashcards

Endo Flashcards

1
Q

puberty brings on many changes

A

increase in GH released, increased production of LH and FSH in girls, development is sexual characteristics, feedback mechanism in place

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2
Q

data to collect for endocrine assessment

A

% in height/ weight, distinguishing facial features and abdominal fat, onset of puberty, routine NB screening, blood glucose levels, detection of chromosomal disorders

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3
Q

new onset DM- baseline labs

A

glucose, urea, creat, lytes, gas, urine for glucose and ketones, TSH, thyroid antibodies

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4
Q

new onset DM: diet

A

1000 kcal + 100kcal/ yr of age. ex 8 year old= 1,800kcal/ day

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5
Q

insulin therapy

A

monitored q3 months by A1c- represents amt of glucose attached to hemoglobin over period of time, roughly 120 days, good predictor of levels over 6- 8 wks

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6
Q

insulin adjustment: basic principles

A

new onset- making daily changes until stabilized
established pts- high BG same time of day for 3 consecutive days, increase 10% at a time. If unexplained lows 2x/ week same time of day, decrease 10- 20% at a time

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7
Q

factors that may affect insulin dosage in kids

A

stress, infection, illness, growth spurts (puberty), meal coverage for finicky toddlers, adolescents concerned about not wanting to gain weight/ eat in AM

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8
Q

insulin pumps

A

replace the need for periodic injections by delivering rapid- acting insulin continuously throughout the day using a catheter

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9
Q

advantages of insulin pumps in kids

A

delivers cont infusion, maintains better control of BS, decrease number of injection sites, decrease hypo/ hyper episodes, more flexible lifestyle, eat with more flexibility, improves growth in child

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10
Q

disadvantages of insulin pumps in kids

A

requires motivation and willingness to be connected to device, have to change the site every 2- 4 days, more time/ energy to monitor BS, syringe/ cath changes every 2- 3 days, infection may occur at site, weight gain common when BS is controlled

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11
Q

“sick day guidelines”

A

day the child is ill, pay close attention to glycemic control, should take BS levels more often than routine, DO NOT SKIP INSULIN, factors key to preventing DKA

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12
Q

DKA how common is it?

A

at diagnosis of diabetes- 15-67%

established pts- 1- 10% of pts/ year

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13
Q

hypoglycemia causes

A

too much exercise which you didn’t plan, not enough food and/ or delay in getting the meal/ snack

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14
Q

tx for severe hypoglycemia

A

glucagon-

5 yrs 1 mg

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15
Q

mini dose glucagon protocol

A

persistently low but alert and unable to manage orally (e.g. during illness or inadvertent insulin error)

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16
Q

risk factors for type II dm

A

ethnicity, female gender, family hx, intrauterine factors (large >4kg or small

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17
Q

common physical sign on insulin resistance

A

acanthosis nigricans- looks like dirt on skin that won’t come off

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18
Q

tx of type II dm in youth

A

education for family, set glycemic targets (A1c or equal to 9%, sx of severe hyperglycemia, ketonuria

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19
Q

maturity- onset diabetes of the young MODY

A

transmitted as autosomal dominant disorder with formation of structurally abnormal insulin with decreased biologic activity, similar to type II but not, usually before age 25, may be seen in obese teens, may be controlled by oral hypoglycemic agents and diet, more benign dx but increasingly common in peds

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20
Q

juvenile hypothyroidism (she said to read more about this in book)

A

congenital- congenital hypoplastic thyroid gland
acquired- partial or complete thyroidectomy from ca or thyrotoxicosis (following radiation from Hodgkins or other malignancy)
- rarely occurs from dietary insufficiency in US

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21
Q

clinical manifestations of juvenile hypothyroidism

A

decelerated growth, constipation, sleepiness

myxedematous skin changes (dry skin, sparse hair, periorbital edema)

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22
Q

therapeutic management of juvenile hypothyroidism

A

oral thyroid replacement therapy, prompt tx needed for brain growth in infants, may administer in increasing amounts over 4- 8 wks to reach euthyroidism
- compliance w/ meds is crucial

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23
Q

tx/ meds for juvenile hypothyroidism

A

thyroxine 75- 100mcg/ m2/ day; monitor q6 months until growth complete, and then annually.

monitor: s/s hypo/ hyper thyroid, growth, sexual maturation, TSH (want 0.25- 5mU/L), +/- FT4
- recheck TSH 4- 6 wks after dose adjustments

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24
Q

goiter

A

hypertrophy of the thyroid gland

  • congenital- usually results from maternal ingestion of antithyroid during pregnancy
  • acquired- result of neoplasm, inflammatory dx, dietary deficiency (but rarely in kids) or increased secretion of pituitary thyrotropic hormone
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25
Q

nursing considerations for goiter

A

thyroid enlargement at birth my compromise newborn airway, may become noticeable during periods of rapid growth, large goiters may be obvious but smaller ones only evident w/ palpation
-TH replacement is needed for tx of hypothyroidism

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26
Q

lymphocytic thyroiditis

A

Hashimoto’s or juvenile autoimmune thyroiditis, most common cause of thyroid dx in kids and teens, accounts for largest % of juvenile hypothyroidism

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27
Q

pathophysiology of lymphocytic thyroiditis

A

genetic predisposition but specifics unclear; characterized by lymphocytic infiltration of the gland, inflammation, hyperplasia- which may be replaced with fibrous tissue
- child usually euthyroid, with some sx of hyperthyroidism

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28
Q

therapeutic management of lymphocytic thyroiditis

A

goiter may be transient, asymptomatic
may resolve spontaneously within 1- 2 yrs, oral TH often decreases the goiter significantly, surgery contraindicated for this disorder

29
Q

sx of graves disease

A

manifestations develop gradually, often 6- 12 months

  • eyes- exopthalmous
  • excessive motion, irritability, hyperactivity, short attention span, tremors, insomnia and emotional lability
  • GI hyperactivity
  • cardiac- rapid pounding pulse even during sleep, widened pulse pressure, systolic murmurs and cardiomegaly
  • dyspnea occurs during slight exertion
  • skin wamr, flushed and moist- heat intolerance may be severe and accompanied by diaphoresis
30
Q

graves dx management

A
  • diagnosis based on increased levels of t3 and t4 with suppressed TSH
  • therapy controversial
  • goal of therapy- retard rate of hormone secretion
    treatments- antithyroid drugs (PTU and methiamazole), subtotal thyroidectomy, ablation and radioiodine
31
Q

hyperthyroidism- management

A

antithyroid meds-methiamazole (MMI, TapazoleTM) or Propylthiouracil (PTU), propranolol, iodine, surgery

32
Q

s/e of antithyroids meds

A

mild- pruritis, rash, abdominal pain, neutropenia

serious- agranulocytosis, arthropathy, lupus- like syndrome, hepatits

33
Q

further management of hyperthyroidism

A

monitor- initially q 4- 6 wks until T4 stabilized on maintenance doses of MMI/ PTU, then 3- 4 months.
- generally continue tx for 2 yrs then try off tx and monitor closely for relapse

34
Q

summary of thyroid disorders

A
  • common in children and teens
  • TSH and thyroid antibodies is usually all that is required to establish dx
  • US should be limited to those w/ a palpable nodule, like you Ave!
  • normal range of TSH may be higher in peds leading to over- investigation/ dx and tx of thyroid disorders
  • mild elevations of TS should be verified on repeat testing- TSH
35
Q

cushing syndome

A

characteristic group of manifestations by excessive circulating free cortisol

  • may be caused by prolonged steroid therapy- reversible once steroids d/c’ed
  • abrupt withdrawal of steroids may precipitate acute adrenal insufficiency
36
Q

etiologies of cushings

A

pituitary- excess ACTH
adrenal- hypersecretion of glucocorticoids
ectopic- extrapituitary neoplasm
iatrogenic- administration of excessive steroids
food- dependent- inappropriate response to secretion of polypeptide

37
Q

cushingoid appearance

A 
excessive hair growth
moon face with red cheeks
weight gain
prendulous abdomen with red striae
poor wound healing
exxhymoses
38
Q

diagnostic eval for cushings

A
  • confirm excess cortisol levels
  • xrays to evaluate for osteoporosis and skull films to look for enlargement of sella turcica
  • labs- fasting blood glucose, serum electrolytes, 24 hr urine
39
Q

therapeutic management for cushings

A
  • surgery

- replacement of growth hormone, ADH, TH, gonadotropins and steroids

40
Q

precocious puberty

A

presence of secondary sexual development by age:
8 in a girl
9 in a boy
occurs more in girs

41
Q

potential causes of precocious puberty

A

disorder of the gonads, adrenal glands or hypothalmic- pituitary gonadal axis
- no causative factor in 80- 90% of girls and 50% of boys

42
Q

spectrum of precocious puberty- benign mild incomplete precocious puberty

A
  • premature thelarche (breasts)
  • premature adrenarche (pubic hair)
  • minimal impact on adult height or timing of menstruation, minimal social/ emotional impact
43
Q

spectrum of precocious puberty- pathological precocious puberty

A
  • central precocious puberty
  • peripheral precocious puberty
  • negative impact on adult height
  • early menstruation
  • social/ emotional distress
    Refer to endo for this
44
Q

therapeutic management of precocious puberty

A
  • specific to cause if known
  • may be treated with Lupron- slows prepubertal growth to normal rates, discontinued at age for normal pubertal changes to resume (i bet those asian gymnasts take this shit forever)
  • psychological support for child/ family
45
Q

Delayed puberty

A

look at growth records, bone age, LH, FSH, sex hormone levels not needed
if indicated check T4, TSH, GH, prolactin, cortisol

46
Q

Delayed puberty tx constitutional delay of growth and puberty- for boys

A

tx if psychologically distressed w/

Depot testosterone 75- 100 mg IM X3

47
Q

Delayed puberty tx constitutional delay of growth and puberty- for girls

A

usually don’t treat ( even low dose estrogen cause accelerated skeletal maturation)

48
Q

Delayed puberty tx for hyper/ hypogonadotropic hypogonadism- for boys

A

testosterone IM injection, transdermal patch/ gel or orally, gradually increasing to adult doses

49
Q

Delayed puberty tx for hyper/ hypogonadotropic hypogonadism- for girls

A

start with low dose estrogen, increasing over 1- 2 years, then begin cycling with estrogen and progesterone

50
Q

hypopituitarism- Growth hormone (GH) deficiency

A

inhibits somatic growth, primary site of dysfuntion appears to be in the hypothalamus

51
Q

diagnostic eval of GH deficiency

A

family hx, growth patterns and health history

  • definitive dx based on radioimmunoassay of plasma GH levels
  • hand xrays to evaluate growth potential vs. ossification
  • endocrine studies to detect deficiencies
52
Q

therapeutic management of GH definiciency

A

biosynthetic growth hormon injections, other hormone replacements as needed- thyroid extract, cortisone, testosterone, estrogen, progesterone

53
Q

prognosis of GH deficiency

A

replacement therapy successful in 80% of affected children, response varies based on age, length of tx, frequency of doses, doasge weight and GH amount
- growth rate of 3.5 to 4 cm/ yr before tx and increase to 8- 9 cm/ yr after tx

54
Q

nursing considerations for GH replacement

A

fam needs support, child’s body image, preparing child for daily injections, injections given at bedtime for best results, tx very expensive ($20,000- 30,000 per year)

55
Q

pituitary hyperfunction- acromegaly

A

aka Gigantism- excess GH before closure of the epiphyseal shafts results in overgrowth of long bones

  • reach heights of 8 feet +
  • vertical growth and increased muscle
  • weight is generally proportional to height
56
Q

nursing considerations for pituitary hyperfunction

A

early identification of kids with excessive growth rates, early tx for improved outcomes, emotional support, body image concerns

57
Q

nursing measures for metabolic disorders

A

genetic counseling, dietary teaching, compliance, mixing special preparations, mainly supportive.

58
Q

inborn errors of metabolism

A

phenylketonuria, galactosemia, defects in fatty acid oxidation, maple syrup urine disease

59
Q

phenylketonuria (PKU)

A

autosomal recessive

- deficiency of liver causing phenylalanine accumulation in the blood- causing a musty or mousy body and urine odor

60
Q

phenylketonuria (PKU) s/s

A

irritability, vomiting, hyperactivity, hypertonia, hyperreflexivity, seizures and may lead to mental retardation. Screening for it required in all 50 states, needs to be done within 48 hours of birth and repeated 1- 2 weeks after birth

61
Q

phenylketonuria (PKU) tx

A

directed towards the use of a special formula (Lofenalax, Minafen, and Albumaid XP) and a diet low in phenylalanine

  • foods high in phenylalanine to avoid: high protein foods like milk, dairy products, meat, fish, chicken, eggs, beans and nuts
  • breast feeding possible if PKU levels monitored
62
Q

Galactosemia

A
  • carbohydrate metabolic dysfunction, autosomal recessive.
  • liver is deficient in GALT (one of the 3 enzumes needed to convert galactose to glucose), this leads to accumulation of galactose metabolites in the eyes, liver, kidney and brain
  • children become susceptible to gram negative sepsis- can die within a month w/o treatment, usually from sepsis
63
Q

Galactosemia s/s

A

poor sucking, failure to gain weight d/t vomiting followed by diarrhea, hypoglycemia and an enlarged liver. Later signs include mental retardation, sepsis, sz, cataracts and coma.

64
Q

diet for Galactosemia

A

all sources of galactose and lactose must be eliminated from diet- primarily means that all dairy products must be strictly avoided.
Also need to restrict other foods like legumes, some fruits because of high galactose content. Kids with this need the same kinds and amounts of nutrients as other kids to grow and develop normally- just no galactose

65
Q

defects in fatty acid oxidation

A

most common of inborn errors

66
Q

maple syrup urine disease

A

MSUD- 3 amino acids affected- leucine, isoleucine and valine. They can’t break down which causes abnormal structures such as hair, skin and muscle.
- Leucine can build up in the brain and cause cerebral edema, progressive neuro impairment and death

67
Q

MSUD s/s

A

within 3- 7 days of life, newborn exhibits poor appetite, lethargy, vomiting, variable muscle tone, seizures, high- pitched crying and sweet odor of maple syrup in the body fluids

68
Q

MSUD tx

A

initially involves the removal of the amino acids and their metabolites from the tissues and body fluids- some require dialysis

69
Q

MSUD tx cont

A

in most cases, sx of MSUD can be prevented by a diet very low in BCAA’s- but depends on type of MSUD and the gene involved.

  • This diet should begin ASAP following dx, nutritionist will recommend a special diet that includes certain vegetables, fruits, grains and a metabolic formula that provides protein w/o BCAA (branch chain amino acids)
  • some rare forms may be difficult to treat and may require thiamine
  • need regular blood tests to monitor BCAA levels

Pediatrics (17 decks)

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