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CKPeds > ENDO > Flashcards

ENDO Flashcards

1
Q

Deficiency of growth hormone ± other hormones; also delay in pubertal development is common; results in postnatal growth impairment corrected by growth hormone

A

Hypopituitarism

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2
Q

Congenital Hypopituitarism SSx

A

° Normal size and weight at birth; then severe growth failure in first year

° Infants—present with neonatal emergencies,

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3
Q

Examples of Neonatal emergencies in pts with congential hypopit

A

e.g., apnea, hypoglycemic seizures, hypothyroidism, hypoadrenalism in first weeks or boys with microphallus and
small testes ± cryptorchidism

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4
Q

SSx of Acquired hypopituitarism:

A

Findings appear gradually and progress: growth failure; pubertal failure, amenorrhea;
symptoms of both decreased thyroid and adrenal function; possible DI

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5
Q

Screening for hypopituitarism

A

Screen for low serum insulin-like growth factor (IGF)-1 and IGF-binding
protein-3 (IGF-BP3

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6
Q

Definitive test for hypopituitarism—

A

growth-hormone stimulation test

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7
Q

If there is a normal response to hypothalamic-releasing hormones, the pathology
is located within the ________

A

hypothalamus.

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8
Q

Bone age of pts with hypopituitarism—

A

skeletal maturation markedly delayed (BA 75% of CA)

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9
Q

Treatmenthypopituitarism—

− Classic growth-hormone deficiency—_______

A

recombinant growth hormone

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10
Q

Indications—growth hormone currently approved in United States for

A

− Documented growth-hormone deficiency
− Turner syndrome
− End-stage renal disease before transplant
− Prader-Willi syndrome
− Intrauterine growth retardation (IUGR) without catch-up growth by 2 years of age
– Idiopathic pathologic short stature

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11
Q

Hyperpituitarism

• Primary—rare; most are ______

A

hormone-secreting adenomas

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12
Q

Screening for hyperpituitarism

A

Screen—IGF-1 and IGF-BP3 for growth hormone excess; confirm with a glucose
suppression test

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13
Q

When to Tx hyperpituitarism

A

Treatment only if prediction of adult height (based on BA) >3 SD above the mean
or if there is evidence of severe psychosocial impairment

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14
Q

Breast tissue in the male: common (estrogen: androgen imbalance)

A

Physiologic Gynecomastia

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15
Q

Physiologic Gynecomastia Tx

A

• If significant with psychological impairment, consider danzol (anti-estrogen) or surgery
(rare)

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16
Q

− Girls—sexual development age <8 years

− Boys—sexual development age <9 years

A

Precocious Puberty

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17
Q

Precocious Puberty MC etiology

A

− Sporadic and familial in girls

− Hamartomas in boys

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18
Q

SSX of Precocious Puberty

A

advanced height, weight, and bone age; early epiphyseal closure and early/fast advancement of Tanner stages

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19
Q

Definitive test for Precocious Puberty

A

GnRH stimulation test; give intravenous GnRH analog for a brisk, leuteinizing
hormone response

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20
Q

Tx for Precocious Puberty

A

Treatment—stop sexual advancement and maintain open epiphyses (stops BA advancement) with leuprolide

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21
Q

•____________
− Usually isolated, transient (from birth due to maternal estrogens)
− May be first sign of true precocious puberty

A

Premature thelarche

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22
Q

Congenital hypothyroidism—most are ________(i.e., from thyroid gland)

A

primary

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23
Q

Causes of Sporadic or familial; with or without a goiter

A

° Most common is thyroid dysgenesis (hypoplasia, aplasia, ectopia); no goiter
° Defect in thyroid hormone synthesis—goitrous; autosomal recessive
° Transplacental passage of maternal thyrotropin (transient)
° Exposure to maternal antithyroid drugs

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24
Q

MC etiologies of Acquired hypothyroidism

A

Hashimoto; thryroiditis is most common cause; may be part of autoimmune polyglandular syndrome

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25
Q

WHen does Hashimoto usually present?

A

adolescence

26
Q

First sign of Hashimoto?

A

First sign usually deceleration of growth

27
Q

What type of Autoimmune Polyglandular
Disease

  • Hypoparathyroidism
  • Addison disease
  • Mucocutaneous candidiasis
  • Small number with autoimmune thyroiditis
A

Type I

28
Q

What type of Autoimmune Polyglandular
Disease

  • Addison disease, plus:
  • Insulin-dependent DM
  • With or without thyroiditis
A

Type II (Schmidt syndrome)

29
Q

MCC og HYperthy

A

• Almost all cases are Graves disease

30
Q

Common associations of pts with Graves

A

In whites, association with HLA-B8 and DR3 is also seen with other DR3-related disorders
(Addison disease, diabetes mellitus, myasthenia gravis, celiac disease).

31
Q

What other labs can be done for Graves

A

− Increased T4, T3, free T4
− Decreased TSH
− Measurable TRS-AB (and may have thyroid peroxidase antibodies

32
Q

Etiologies of PTH deficiency

A

− Aplasia/hypoplasia—most with DiGeorge or velocardiofacial syndrome
− X-linked recessive—defect in embryogenesis
− Autosomal dominant—mutation in calcium-sensing receptor
− Postsurgical (thyroid)
− Autoimmune—polyglandular disease
− Idiopathic (cannot find other cause)

33
Q

MC SSx of PTH def

A

− Laryngeal and carpopedal spasm

− Seizures (hypocalcemic seizures in newborn; think DiGeorge)

34
Q

Lab evaluation of PTH deficiency

A

− Decreased serum calcium (5–7 mg/dL)
− Increased serum phosphorus (7–12 mg/dL)
− Low 1,25 [OH]2D3 (calcitriol)
− Low parathyroid hormone (immunometric assay)

35
Q

What are normal values in PTH def

A

Normal magnesium

Normal or low alkaline phosphatase

36
Q

Acute Tx of neonatal tetany

A

Emergency for neonatal tetany → intravenous 10% calcium gluconate and then
1,25[OH]2D3 (calcitriol); this normalizes the calcium

37
Q

Chronic Tx for hypoparathy

A

Chronic treatment with calcitriol or vitamin D2 (less expensive) plus adequate calcium
intake (daily elemental calcium)

38
Q
  • Most common cause of rickets

* Poor intake, inadequate cutaneous synthesis

A

Vitamin D Deficiency

39
Q

Labs of Vitamin D Deficiency

A

• Low serum phosphate, normal to low serum calcium lead to increased PTH and
increased alkaline phosphatase

40
Q

Primary Hypo

PTH

Calcium

Phosphate

Alkaline Phosphatase

A

Decreased

Low

High

Normal

41
Q

Primary Hypo

PTH

Calcium

Phosphate

Alkaline Phosphatase

A

Decreased

Low

High

NL or SL increased

42
Q

Primary Hyper

PTH

Calcium

Phosphate

Alkaline Phosphatase

A

Increased

High

Low

Increased

43
Q

Secondary Hyper

PTH

Calcium

Phosphate

Alkaline Phosphatase

A

Increased NL to SL

decreased

Low Huge

increase

44
Q

MCC of CAH

A

• 21-Hydroxylase deficiency (most common)

45
Q

Pathophysio of CAH

A

− Decreased production of cortisol → increased ACTH → adrenal hyperplasia

46
Q

Problem with CAH

A

− Salt losing (not in all cases; some may have normal mineralocorticoid synthesis)

47
Q

What increasis in CAH

A

Precursor steroids (17-OH progesterone) accumulate

48
Q

CAH

Shunting to androgen synthesis → ____________

A

masculinizes external genitalia in females

49
Q

Labs for CAH

A

− Increased 17-OH progesterone
− Low serum sodium and glucose, high potassium, acidosis
− Low cortisol, increased androstenedione and testosterone
− Increased plasma renin and decreased aldosterone

50
Q

Definitive Dx for CAH

A

measure 17-OH progesterone before and after an intravenous bolus of ACTH

51
Q

Tx of CAH

A

− Hydrocortisone
− Fludrocortisone if salt losing
− Increased doses of both hydrocortisone and fludrocortisone in times of stress

52
Q

MCC of Cushing Syndrome

A

Exogenesis—most common reason is prolonged exogenous glucocorticoid administration.

53
Q

Most important labs for Cushing

A

− Dexamethasone-suppression test (single best test)
− Determine cause—CT scan (gets most adrenal tumors) and MRI (may not see if
microadenoma)

54
Q

Etiology of Type 1 DM

A

T-cell−mediated autoimmune destruction of islet cell cytoplasm, insulin
autoantibodies (IAA

55
Q

Reason for MAC in Type 1 DM

A

Accelerated lipolysis and impaired lipid synthesis → increased free fatty acids → ketone
bodies → metabolic acidosis and Kussmaul respiration → decreased

56
Q

Dx of IFG

A

° Fasting blood sugar 110–126 mg/dL or 2-hour glucose during OGTT<200 mg/dL
but ≥125 mg/dL

57
Q

Dx of DM

A

° Symptoms + random glucose ≥200 mg/dL or
° Fasting blood sugar ≥126 mg/dL or
° 2 hour OGTT glucose ≥200 mg/dL

58
Q

Labs of DKA

A

Diabetic ketoacidosis—hyperglycemia, ketonuria, increased anion gap, decreased
HCO3 (or total CO2), decreased pH, increased serum osmolality

59
Q

Who should be screened for Type II DM

A

All who meet the BMI criteria + 2 risk factors

60
Q

How to screen pts with Type II DM

A

fasting blood glucose every 2 years beginning at age 10 years or onset
of puberty if above criteria are met

CKPeds (20 decks)

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