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Pediatrics Clerkship > Pediatric Endocrinology > Flashcards

Pediatric Endocrinology Flashcards

1
Q

Presentation of DKA

A
  • Tachycardia
  • Hypotension
  • Hypothermia
  • Confusion or obtundation
  • Kussmaul’s respirations
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2
Q

When do you start giving potassium to your patient with DKA?

A

When they start putting out urine again

This is how they are going to lose potassium. If you give it before this time, you are just adding to the hyperkalemia

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3
Q

Why DON’T we give bicarbonate to people in DKA?

A
  1. It may precipitate hypokalemia by proton-potassium exchange
  2. It will shift the oxygen dissociation curve to the left and worsen end-organ oxygen delivery
  3. It may overcorrect the acidosis
  4. It may result in worsening cerebral acidosis while the plasma pH is being corrected
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4
Q

Signs of cerebral edema in DKA and treatment

A
  • Headache
  • Personality change
  • Vomiting
  • Decreased reflexes
  • Treat w/ IV fluids, IV mannitol, and hyperventilation
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5
Q

You must always check for ___ in someone who presents in DKA

A

You must always check for infection in someone who presents in DKA

Infection may precipitate DKA in an otherwise compensated diabetic

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6
Q

Somogyi phenomenon

A
  • In diabetes mellitus
  • When a patient has nocturnal hypoglycemic episodes manfiesting as night terrors, headaches, or early morning sweating, then, a few hours later, experiences with hyperglycemia, ketonuria, and glucosuria.
  • Caused by counter-regulatory hormonal response to hypoglycemia, resulting in hyperglycemia.
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7
Q

Diabetes “honeymoon” phase

A
  • A few months after diagnosis, there is a progressive decrease in the daily insulin requirement
  • However, this usually lasts only a few months, and virtually all of these patients will again require insulin
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8
Q

Signs that a patient in DKA may be developing cerebral edema

A
  • Change in mental status
  • Anisochoria
  • Decorticate posturing
  • Seizures
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9
Q

Diagnosing diabetes in kids

A

HbA1c is not typially used. So, we stick to the other three:

  • Random glucose > 200
  • 2 hour challenge glucose > 200
  • Fasting glucose > 126
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10
Q

Target rate of glucose reduction in DKA

A

50-100 mg/dL/hr

Any more than this and there is a greater risk of precipitating cerebral edema. After all, glucose is an osmole, and it takes time for sodium to shift and make up for the difference in Osm.

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11
Q

When should you start buffering your insulin titrating by adding fluids with dextrose when treating a patient in DKA or HHS?

A

When the glucose hits 250-300 mg/dL

To prevent hypoglycemia

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12
Q

“Critical sample” in hypoglycemia

A

A serum sample during a time when blood glucose < 50 mg/dL. Critical for determining the etiology of the hypoglycemia. It should include:

  • Bicarbonate
  • Insulin
  • c-peptide
  • Cortisol
  • GH
  • Free fatty acids
  • Ketones (betahydroxybutyrate, acetoacetate)
  • Lactate
  • Ammonia
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13
Q

How to handle hypoglycemia in patients that cannot take PO glucose due to 1) vomiting or 2) seizure

A
  1. Vomiting: Buccal glucose gel or cake icing
  2. IV glucose OR IM glucagon (to mobilize glucose from the liver)
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14
Q

Non-fasting labs to assess hypoglycemia

A
  • Total carnatine
  • Free carnatine
  • Acyl carnatine
  • Serum amino acids
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15
Q

Normal infants become hypoglycemic after ___ hours of fasting

A

Normal infants become hypoglycemic after ~6 hours of fasting

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16
Q

Acute management of hypoglycemia

A
  • IV glucose bolus
  • Maintenance IV dextrose drip
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17
Q

Diagnosing diabetes insipidus

A

Generally, it is a clinical diagnosis made based on history and exam. However, if the diagnosis is in question, the criteria are based on dilute urine in the context of serum hypertonicity:

  • Urine specific gravity < 1.010
  • Urine Osm < 300 mOsm/kg
  • Hypernatremia
  • Plasma Osm > 295 mOsm/kg
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18
Q

Symptoms of CNS involvement in hyponatremia

A

Headache, lethargy, confusion, seizures

Begin at ~125 mEq/L Na

This is an indication for hypertonic saline to correct until symptoms resolve. These patients would NOT be managed conservatively with water restriction.

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19
Q

SIADH is a diagnosis of exclusion. What five things need to be ruled-out to presume a diagnosis of SIADH?

A
  1. Hyperglycemia
  2. Hyperlipidemia
  3. Hyperproteinemia
  4. Hypothyroidism
  5. Adrenal insufficiency
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20
Q

Demeclocycline

A
  • Semisynthetic tetracycline antibiotic, but has even better activity as an ADH antagonist
  • Used to treat chronic SIADH
21
Q

Key numbers for rate of correction of hyponatremia

A

Correct at 0.5 mEq/L/hr

Maximum of 12 mEq/L correction over 24 hours

Check the sodium q3-4 hours

22
Q

Age cut-offs for precocious puberty

A
  • Appearance of secondary sex characteristics before age. . .
    • 7 for females (6 for African American specifically, higher baseline estrogen)
    • 9 for males
23
Q

Risk factors for ricketts from vitamin D deficiency

A
  • Prolonged breastfeeding
  • Lack of nutritional vitamin D supplementation
24
Q

Stigmata of ricketts

A
  • Bead-like costochondral junctions (“rachitic rosary”)
  • Erosion of tooth enamel
  • Bone pain
  • Bone weakening (frontal bossing)
  • Abnormal bowing (genu varum)
  • and distention of the bone (widened joints)
25
Q

Achondroplasia

A
  • Deficiency in FGFR3
26
Q

Phenylketonuria syndrome and treatment

A
  • Autosomal recessive loss of phenylalanine hydroxylase (PAH) gene, accumulation of phenylalanine
  • Syndromic features:
    • Developmental delay starting at 4-6 months
    • Blue eyes, pale hair and skin (tyrosine is a precursor to melanin, ergo no melanin)
    • Musty odor (from elevated aromatic amino acids)
    • Eczema
    • Seizures
  • Dx: Measurement of phenylalanine levels, usually done as newborn screen
  • Tx: Dietary restriction of phenylalanine, high tyrosine diet. AVOID ASPARTAME (artificial sweetener)
27
Q

Marfan syndrome vs homocystinuria

A

Also, homocystinuria may be associated with intellectual disability while Marfan is not.

28
Q

Signs of salt wasting CAH and treatment

A

Clitoromegaly in a female

Mild hyponatremia (<135 mEq/L) and hyperkalemia (>5.0 mEq/L) in a baby a few days old

Treat with hydrocortisone and fludricortisone

29
Q

Non-classical CAH

A

Caused by 21b-hydroxylase deficiency, like most CAH, but with less severe presentation often missed at birth.

Presents with signs of elevated adrenal androgen activity starting around teenage years

30
Q

Classical CAH

A

95% of cases 21b-hydroxylase deficiency, 5% of cases 11b-hydroxylase deficiency

Presents with signs of congenital virilization (21b and 11b) and salt wasting (with 21b) OR abnormal salt retention and hypertension (11b and 17a) within the first few days of life

31
Q

“1 DOC, AND 1”

A

1 DOC: If the enzyme missing in CAH starts with a 1, there is overproduction of DOC (11-deoxycorticosterone) and underproduction of aldosterone.

AND 1: If the enzyme missing in CAH ends with a 1, there is increased production of androgens.

21b-hydroxylase: elevated androgens, low DOC

11b-hydroxylase: elevated androgens, elevated DOC

17a-hydroxylase: low androgens, elevated DOC

32
Q

Treating neonatal Graves thyrotoxicosis

A
  • Symptoms may appear up to 10 days following delivery and are transient (due to gradual loss of antibody), lasting up to 12 weeks
  • Treat with methimazole and propranolol in the interim, until the antibody clears
33
Q

Advising type 1 diabetics about exercise

A
  • Patients with T1DM have a larger drop in blood glucose during exercise than healthy controls, putting them at risk for hypoglycemia during exercise
  • They should be advised to reduce insulin by 1–2 units per 20–30 minutes of physical activity on days of exercise
  • Closely monitor their blood glucose before, during, and after exercise, to watch out for symptoms of hypoglycemia
  • Eat complex, slowly-absorbed carbohydrates after exercising
34
Q

Stigmata of congenital hypothyroidism

A
  • Hypotonia
  • Umbilical hernia (secondary to rectus abdominus hyptonia)
  • Delayed bone age
  • Delayed closure of posterior fontanelle (past 1 wk, secondary to delayed bone age)
  • Scleral icterus and/or jaundice (due to unconjugated hyperbilirubinemia)
  • Enlarged thyroid gland
35
Q

Radiation and risk of thyroid neoplasia

A

Radiation to the thyroid increases risk of thyroid neoplasia and requires screening ultrasounds starting 10 yrs after exposure

36
Q

Classical vs Non-Classical CAH

A
37
Q

Steroid pathway

A
38
Q

Chronic therapies for the three major CAH variants

A
  • 21b: Lifelong glucocorticoids, lifelong fludricortisone, salt supplements during infancy.
  • 11b: Lifelong glucocorticoids, lifelong spironolactone, reduced dietary sodium.
  • 17a: Lifelong glucocorticoids, lifelong spironolactone, reduced dietary sodium, AND estrogen for females started at puberty
    • Note: In neonates and children, hydrocortisone is the glucocorticoid of choice. In adolescents and adults, dexamethasone is the glucocorticoid of choice.
    • Note: Just like Addison’s patients, these patients must stress dose their glucocorticoids as appropriate.
39
Q

Methods of prenatal diagnosis of CAH

A
  • If parents are both known carries for CAH:
    • Non-invasive cfDNA to determine maternal and paternal inheritance – if male, do not start dex. If female, start dex.
    • Chornionic villus sampling (10-13 wks) OR,
    • Amniocentesis measurement of 17OHP (>16 wks)
  • If mom previously gave birth to a child with CAH:
    • Chorionic villus sampling (10-13 wks) OR,
    • Amniocentesis measurement of 17OHP (>16 wks)
  • If diagnosed prenatally, mom is treated with continuous dexamethasone if prior to 9 weeks and genetic sex is determined. If male, stop dex, if female, continue dex.
40
Q

Low-dose ACTH stim vs high-dose ACTH stim

A
  • Low dose: Do the adrenals respond to physiologic levels of ACTH? (A test for secondary adrenal insufficiency)
  • High dose: Do the adrenals respond to supraphysiologic levels of ACTH? (A test for primary adrenal insufficiency)
41
Q

Laryngospasm in the setting of hypocalcemia

A

Think of this as the effects of hypocalcemic tetany on the larynx

May produce dyspnea and stridor

42
Q

“Early” vs “Late” neonatal hypocalcemia

A
  • Early: First 24-72 hours of life. Ca naturally decreases during this timeperiod, but may be exaggerated by GDM, asphyxia, sepsis, or hypomagnesemia.
  • Late: After post-natal day 5. May be transient. Often due to immaturity of parathyroids, resulting in intolerance of a large phosphate load in cow’s milk or cow’s milk-based formula. A low phosphate formula can resolve this. If that fails or if baby is not drinking cow’s milk, genetic hypoparathyroidism, FHH (CaSR GoF), defective PTH production, or DiGeorge syndrome should be considered.
43
Q

Type I Familial Hyperaldosteronism

A

Aldosterone-producing CYP enzymes are under an ACTH-controlled promoter

Also called “glucocorticoid remediable hyperaldosteronism”

Autosomal dominant

44
Q

Elevated metabolites in 21bOHD vs 11bOHD

A

21bOHD: 17-OH-P is greatly elevated

11bOHD: 17-OH-P is mildly elevated, 11-DOC is greatly elevated

45
Q

Hypercalcemia mnemonic

A

“Stones, Bones, Groans, and Psychiatric Overtones”

46
Q

Biologic activity of 25-hydroxy-vitamin D

A

At high enough levels, 25-hydroxy-vitamin D can induce transciption at vitamin D binding domains independent of 1-25-dihydroxy-vitamin D

This is seen in severe vitamin D toxicity.

47
Q

24-hydroxylase deficiency

A

Without 24 hydroxylase, vitamin D just builds up!

These individuals will eventually develop hypervitaminosis D

48
Q

Treating hypervitaminosis D

A
  • Furosemide to encourage Ca diuresis
  • Dietary Ca and vitamin D restriction
  • Bisphosphonates, calcitonin
49
Q

Sick euthyroid syndrome from 10,000 feet

A
  • When the body is stressed, lots of tissues are converting T4 to T3, since they need to become more metabolically active
  • Sick euthyroid occurs when the body’s demand for T3 outpaces the thyroid’s supply of T4 (maybe, questioning this mechanism)
  • TSH may be low, normal, or elevated in euthyroid sick syndrome, but is never as high as it would be in true hypothyroidism.

Pediatrics Clerkship (23 decks)

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