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Peds-Final > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Hypoglycemia in neonates

A

very common 1st 3 days of life (metabolic needs outstrip E stores)
serum level <55 mg/dL +symptoms= abnormal

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2
Q

DDx of hypoglycemia- causative illness

A

shock
heart failure
liver dysfunction

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3
Q

DDx of hypoglycemia- intoxications

A

alcohol
drug effects
ackee fruit

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4
Q

DDx of hypoglycemia- inadequate substrate

A

SGA
ketotic hypoglycemia
maple syrup urine dz

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5
Q

DDx of hypoglycemia

A 
hyperinsulinism
including factitious (Munchausen by proxy)
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6
Q

DDx of hypoglycemia counter-regulatory hormone deficiency & metabolic d/or inhibiting normal response

A 
gluconeogenesis
glycogenolysis
fatty acid oxidation
organic acid metabolic d/o
galactosemia
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7
Q

Adrenal basics

A

hypothalamus makes CRH
CRH stimulates pituitary
pituitary makes ACTH
ACTH stimulates adrenal cortisol & androgen production

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8
Q

Adrenal aldosterone production is related to?

A

renin & angiotensin, not really ACTH

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9
Q

Congenital adrenal hyperplasia (CAH)

A

caused by absence of adequate adrenal function
adrenals may be congenitally hypertrophic from excess pituitary stimulus
may be obvious at birth d/t ambiguous genitalia at birth (excess steroid precursors converted to excess androgens)

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10
Q

salt-losing congenital adrenal hyperplasia

A

infants- manifests as mineralocorticoid deficiency, usu. w/o virilization
hyponatremia & hyperkalemia by age 5 to 7 days

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11
Q

MCC of salt losing CAH

A

21-hydroxylase deficiency

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12
Q

salt-losing CAH presentation

A

vomiting
dehydration
acidosis
often mistaken for hypertrophic pyloric stenosis
in HPS, hypochloremia & low to normal K+ is present

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13
Q

Tx of salt-losing CAH

A

oral glucocorticoids & mineralcorticoids

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14
Q

Addison dz (primary adrenal insufficiency)

A

autoimmune destruction of adrenal cortex

glucocorticoid & mineralcorticoid deficiencies

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15
Q

Addison dz presentation

A 
hyperpigmentation
salt craving
postural hypotension
fasting hypoglycemia
episodes of shock w/ severe illness
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16
Q

Tx of Addison dz

A

oral glucocorticoids & mineralcorticoids

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17
Q

What is secreted in response to low calcium

A

PTH

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18
Q

what raises serum calcium & depresses phosphate?

A

PTH

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19
Q

low PTH, low calcium, high phosphate confirms what?

A

a problem w/ PTH production= hypoparathyroidism

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20
Q

hypoparathyroidism often results from?

A

DiGeorge syndrome

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21
Q

what is necessary for PTH production?

A

magnesium

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22
Q

neonatal tetany may result from?

A

dietary hyperphosphatemia in a newborn fed cow’s milk

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23
Q

rickets results from what type of deficiency?

A

Vitamin D

not from hypoparathyroidism

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24
Q

vitamin D (after hydroxylation twice) enhances what?

A

calcium absorption & bone deposition

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25
Q

panhypopituitarism

A

typically d/t trauma or shock

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26
Q

tx of panhypopituitarism

A

growth hormone replacement (esp. in CH)
thyroxine replacement
glucocorticoid replacement
diabetes insipidus (free water loss, hypernatremia)-tx w/ desmopressin
attention to sex hormone replacement depending on age & gender

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27
Q

Diabetes Mellitus

A

defined as fasting blood sugar >126 mg/dL
-or-
2-hr postprandial blood sugar over 200

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28
Q

sporadic hyperglycemia is common in children when?

A

during illness

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29
Q

screening test for DM (diagnostic in adults)

A

glycated hemoglobin (HgbA1C)

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30
Q

Type I DM

A

insulin deficiency

autoimmune destruction of pancreatic B cells

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31
Q

What is the MC endocrine problem in CH?

A

Type I DM

1/300-500 under 18 yo

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32
Q

What is the 1st finding in Type I DM?

A

postprandial hyperglycemia

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33
Q

Type I DM has higher rates in what population?

A

whites

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34
Q

People are prone to________________with more complete insulin deficiency

A

ketosis

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35
Q

Clinical presentation of Type I DM

A

polyuria (may manifest as enuresis)
polydipsia
polyphagia (often w/ paradoxical wt loss)
dehydration/ketosis- abdominal pain, vomiting, worsening mental status/fatigue, breath & sweat ketosis

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36
Q

Labs for Type I DM

A

glucose level
electrolytes & kidney function
UA- glycosuria, ketones, low pH
lab surveys for auto-antibodies & insulin-like growth factor depend on preferences of local endocrinologists

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37
Q

diabetic ketoacidosis

A

inability to maintain anabolic state

increased glucose levels

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37
Q

increased glucose levels in diabetic ketoacidosis causes what

A

renal osmotic fluid losses
loss of intravascular fluid volume
loss of total body Na+, K+: reported Na+ artefactually low w/ high glucose
ketosis by lipolysis
acidosis worsened by both ketonemia, lactic acid/ dehydration

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38
Q

What is unusual in diabetic ketoacidosis & confirmation of its source should be determined

A

fever

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39
Q

Diabetic ketoacidosis tx

A

restoration of intravascular fluids

restoration of anabolic state

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40
Q

how does restoration of intravascular fluids help in diabetic ketoacidosis

A

often helps reduce acidosis & glucose levels; excessive IV fluid repletion can cause cerebral edema & be fatal; electrolyte restoration; acid shift will alter K+ levels

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41
Q

how does restoration of anabolic state help in diabetic ketoacidosis

A

exogenous insulin restored euglycemia & halts ketone production

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42
Q

what often follows the original dx of Type I DM

A

“honeymoon” period- original DKA set off by acute illness while capacity for insulin production is low but not insufficient for well periods

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43
Q

long term tx goals of type I diabetes

A

insulin regimen
diet
exercise

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44
Q

complications to avoid in chronic mgnt of type I diabetes

A 
renal failure
visual impairment
cardiovascular dz
iatrogenic hypoglycemia
ketosis during dehydrating circumstances
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45
Q

type II DM

A

insulin resistance- hyperinsulinemia, reduced sensitivity to insulin
DKA presentation less common
gradual onset of sx’s
growing more common in younger pts (correlates w/ obesity)

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46
Q

type II DM is common in what populations?

A

Black & Latino

47
Q

risk factors for type II DM

A

FH
ethnicity
overweight
PCOS

48
Q

contributing societal factors of type II diabetes

A 
overweight
fast foods
soft drinks
school lunches
sedentary lifestyles- TV, computers, video games
falling PE requirements
49
Q

diagnosing type II DM

A

random glucose concentration >200mg/dL
fasting plasma glucose >126 mg/dL
glucose tolerance testing- 2 hr plasma glucose >200 mg/dL
glycated Hgb (HgbA1C)

50
Q

co-morbidities with type II DM

A

dyslipidemia
HTN
obesity

51
Q

tx of overweight & type II DM

A

tx focuses on glucose control & wt loss

limited data to support changes in lifestyle, diet, exercise, metformin

52
Q

metformin

A

reduces hepatic glucose production
increases sensitivity to insulin
reduces intestinal glucose absorption

53
Q

the thyroid develops from the_______&________ pharyngeal pouches starting in the_______week of gestation

A

3rd & 4th

4th week

54
Q

at which week does the thyroid migrate & the thyroglossal duct degenerates

A

7th week

55
Q

where is T4 converted to T3

A

in the tissue

56
Q

what is more physiologically active? T4 (thyroxine) or T3 (triiodothyronine)

A

T3

57
Q

most T3/T4 is bound to what?

A

thyroid binding globulin (TBG): <1% free

58
Q

physiologic activity of thyroid hormone primarily depends on….

A

free T4

59
Q

TSH surge can cause a false + in_____________when screened for hypothyroidism

A

neonates

60
Q

some things that may cause total T4 to be abnormal while FT4 is normal

A

if TBG levels are abnormal
certain drugs bind TBG (anticonvulsants)
pregnancy/estrogen can stimulate TBG

61
Q

fetal hypothyroidism may result in absence of

A

distal femoral epiphysis

62
Q

thyroid imaging can show

A

ectopic thyroid (lingual thyroid) or athyreosis

63
Q

T4

A

primarily bound to thyroxine-binding globulin, but also binds w/ lesser affinity to other proteins
free unbound T4 is active, enters cells & converted to T3

64
Q

primary hypothyroidism

A

d/t defective or absent thyroid

65
Q

secondary hypothyroidism

A

d/t defective TSH synthesis or action (hypothalamic or pituitary hypothyroidism)

66
Q

congenital

A

dz developed in utero

67
Q

acquired

A

onset usually >6 mo of age

68
Q

low FT4 diagnoses

A

hypothyroidism

69
Q

high TSH diagnoses

A

primary hypothyroidism

70
Q

low FT4, low/normal TSH suggests

A

central pituitary hypothyroidism

71
Q

mildly high TSH that is incompletely glycosylated can result in

A

hypothalamic hypothyroidism d/t lack of TRH and therefore has decreased biological activity

72
Q

congenital hypothyroidism basics

A

1 in 3500/4000 newborns
girls affected twice as often as boys
most cases are sporadic- only 10-15% are inherited defects

73
Q

primary congenital hypothyroidism

A

90% d/t thyroid dysgenesis: athyreosis, ectopia, or hypoplasia
toxoplasmosis
Down syndrome
defective hormonogenesis d/t enzyme defects

74
Q

secondary congenital hypothyroidism

A

TSH or TSH-receptor defects
transplacental maternal TSH-receptor blocking antibodies (secondary to maternal autoimmune thyroiditis), causing transient fetal hypothyroidism
maternal iodine deficiency

75
Q

congenital hypothyroidism during the 1st 2 wks of life

A

large fontanelles
hypothermia
poor feeding
prolonged jaundice

76
Q

congenital hypothyroidism beyond 1 month of age

A

darkened, mottled skin
labored breathing
diminished stool frequency
lethargy

77
Q

congenital hypothyroidism after 3 months

A 
umbilical hernia
infrequent, hard stools
dry skin w/ carotenemia
macroglossia
generalized swelling (myxedema)
78
Q

acquired hypothyroidism 6 mo-3 yrs

A

deceleration of linear growth
umbilical hernia
dry skin w/ carotenemia
macroglossia, hoarse cry

79
Q

acquired hypothyroidism during CH

A

delayed eruption of teeth, shedding of primary teeth
m. weakness, pseudohypertrophy
infrequent, hard stools
precocious sexual development: breast development or enlarged testes w/o sexual hair
generalized swelling (myxedema)

80
Q

causes of acquired hypothyroidism

A 
drug-induced hypothyroidism via meds- in breastmilk, lithium, propylthiouracil (PTU), methimazole
endemic goiter (iodine deficiency)
Hashimoto's thyroiditis (autoimmune)
irradiation
excision
81
Q

Hashimoto’s thyroiditis

A

aka chronic lymphocytic, chronic autoimmune thyroiditis
insidious onset
firm, freely moveable, painless goiter (occasional sensation of tracheal compression)
hoarseness, dysphagia
T4, FT4 usually nml (may be elevated-hashitoxicosis, early- or depressed- late)
TPOAb & TGAb usually present, thought titers often low

82
Q

what is the MCC of goiter & acquired hypothyroidism

A

hashimoto’s thyroiditis

83
Q

what may decrease the size of a goiter, but is not needed in euthyroid pt’s

A

L-thyroxine

84
Q

hypothyroidism is the end result of what

A

autoimmune thyroiditis, usually in 2nd/

85
Q

acute suppurative thyroiditis

A

infection via patent thyroglossal duct

86
Q

deQuervain’s (subacute) thyroiditis

A

caused by mumps, EBV, influenza, echovirus, coxsackievirus, adenovirus

87
Q

acquired autoimmune-mediated infantile hypothyroidism

A

other rare thyroiditis

88
Q

hypothyroidism complications

A

untreated hypothyroidism results in impaired intellect- can be severe & irreversible in infants w/ congenital dz
typically reversible in CH>3 yrs who develop acquired dz

89
Q

what is the MC result of untreated acquired hypothyroidism in CH?

A

decreased linear growth

90
Q

untreated acquired hypothyroidism in CH can also be assoc. w/

A 
hypercholesterolemia
slowed school performance
slipped capital femoral epiphysis
chronic constipation
most are reversible w/ tx
91
Q

Levothyroxine (L-thyroxine)

A

must be individualized d/t individual differences in absorption & metabolism

92
Q

over tx w/ L-thyroxine can result in

A

early closure of cranial bones

93
Q

L-thyroxine should not be given at the same time as what?

A

soy or iron-enriched formula
supplemental iron or Ca2+
fiber supplements
these impair absorption

94
Q

Monitoring L-thyroxine

A

careful monitoring of TSH/FT4 until values normalize

after 3 yrs of age, annual monitoring of TSH (primary hypo) & FT4 (secondary or central) is adequate

95
Q

hypothyroidism screening

A

if TSH is elevated a confirmatory serum test is required

start tx ASAP while waiting on confirmatory tests

96
Q

prior to neonatal screening pts w/ hypothyroidism presented w/

A 
neurologic impairment
protrusion of tongue
thick dark hair
mottling
umbilical hernia
widened fontanelles consistent w/ delayed bone maturation
97
Q

screening for hypothyroidism in healthy children

A

monitor ht & growth velocity annually

should be at least 5 cm/yr for CH ages 4 to onset of puberty

98
Q

hyperthyroidism

A

overactive thyroid
95% of CH cases are d/t Graves dz
-autoimmune, Ab-mediated stimulation of thyroid
-thyroid stimulating immunoglobulins (TSI) directed against TSH receptors
can manifest as thyrotoxicosis

99
Q

graves dz

A 
autoimmune d/o
occurs in 1/5000 CH
-most commonly seen in adolescents
-only 2% present before age 10
5x's more common in females than males
FH is common
can occur in conjunction w/ other endocrine d/o
can be cyclic w/ spontaneous remissions & exacerbations
100
Q

Clinical presentation of Graves dz

A
  • difficulty concentrating & sleeping, nervousness, fatigue
  • facial flushing, sweating, heat intolerance
  • tremors, palpitations
  • wt loss despite increase in appetite
  • diarrhea
  • proximal m. weakness
  • palpitations, tachycardia, systolic HTN w/ wide pulse pressure, overactive precordium
  • goiter (diffusely enlarged, soft), proptosis
  • menstrual irregularities
101
Q

Graves dz lab findings

A

elevated T4 & FT4, TSH low
I-123 uptake elevated, not suppressed w/ T3
TGAb & TSI often found in 95%

102
Q

bone findings in Graves dz

A

advanced skeletal maturation
premature closure of cranial sutures
osteoporosis w/ longstanding hyperthyroidism

103
Q

tx of hyperthyroidism

A

B-blockers- large doses of propranolol can decrease conversion of T4 to T3
Iodide for acute mngt- blocks the effect of TSH on thyroid, reduces iodine trapping, reduces vascularity, inhibits release of hormone

104
Q

Thioamides for treating hyperthyroidism

A

reduce hormone production, may take 2-3 wks for a response
-propylthiouracil (PTU)
-methimazole (MMI)
both cross placenta, but PTU preferred during pregnancy
both present in breastmilk, but concentrations so low that they are not a CI

105
Q

PTU

A

blocks peripheral conversion of T4 to T3

106
Q

MMI

A

longer half life

carbimazole converts to MMI

107
Q

Side effects of PTU & MMI

A 
pruritic papular/urticarial rash
hair loss
joint pain/stiffness
nausea, HA
transient granulocytopenia
rarely, agranulocytosis occurs requiring discontinuation of drug
108
Q

radioiodine ablation

A

oral I-131 concentrates in thyroid
cure rate 90%
for people who have sig SE from meds or who do not achieve remission w/ drug therapy
perm. hypothyroidism occurs in 40-80%
avoided in young CH since risk of thyroid CA after radiation greates in children <5 yrs

109
Q

surgical thyroidectomy (subtotal or total)

A

for those who fail medical therapy, have significant SE, have large (>80g) goiters, or severe opthalmopathy
cure rate 90%

110
Q

Potential complications of surgical thyroidectomy

A

hypoparathyroidism
recurrent laryngeal n. damage
permanent hypothyroidism

111
Q

neonatal hyperthyroidism

A

newborns of affected mothers are at risk for thyrotoxicosis b/c TSIs cross the placenta
-duration after birth depends on 1/2 life of maternal Abs, ranging from wks to months

112
Q

neonatal hyperthyroidism can present w/

A

arrhythmias
heart failure
exopthalmos

113
Q

long term sequelae of neonatal hyperthyroidism

A

craniosynostosis
cognitive defects
rebound hypothyroidism

114
Q

tx of neonatal hyperthyroidism includes

A

iodide followed by PTU or MMI

  • reserpine/propranolol may be needed for arrhythmias
  • transection of thyroid isthmus may be considered if there is RDS d/t tracheal compression
116
Q

Diabetic ketoacidosis is defined as

A

Arterial pH less than 7.5
Bicarbonate less than 15
Ketonemia/ketonuria

Peds-Final (10 decks)

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