Endocrinology Flashcards

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1
Q

Rickets - physical exam

A
  • Bowed legs + arms
  • Widened ankle/wrist
  • Frontal bossing
  • Delayed closure of fontanelle
  • Craniotapes
  • Pigeon chest
  • Rachitic rosary
  • Kyphosis or kyphoscoliosis
  • Poor dentition: enamel hypoplasia, delayed tooth eruption
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2
Q

When does cerebral edema and osmotic demyelination syndrome occur?

A
CE = rapid correction of hyperNa
ODS = rapid correction of hypoNa
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3
Q

4 hormones (and their mechanism) involved in sodium hemostasis

A
  1. ADH - stimulated by osmolarity receptors in hypothalamus (volume depletion or hyperNa), increased reabsorption and retainment by kidneys of H20
  2. Aldosterone - released from adrenal cortex followed by decreased renal blood flow, increased reabsorption of Na by the kidneys
  3. GC’s - some mineralocorticoid
  4. Natriuretic peptide - cardiac wall stretch, increased Na renal excretion
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4
Q

DDx for primary and secondary (most common) adrenal insufficiency

A

Primary:

  • Steroidogenesis: CAH
  • Damage: trauma, tumor, infection, autoimmune (Addison disease)
  • Adrenal hypoplasia
  • Peroxismal disorders: Adrenoleukodystrophy

Secondary:

  • Infection
  • CNS surgery or irradiation
  • Trauma
  • Exogenous steroids
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5
Q

Mid-parental height calculation

A
F = (pat ht + mat ht - 12.5cm) / 2
M = (pat ht + mat ht + 12.5cm) / 2
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6
Q

Most common cause and presentation for acquired hypothyroidism

A

Autoimmune thyroiditis - Hashimoto Disease
- Presentation: asx, goiter, dec energy/growth, poor school performance, constipation, cold intolerance, irregular menstrual periods, associated autoimmune conditions

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7
Q

Most common cause of hyperthyroidism + pathophysiology

A

Graves disease –> TSH receptor Ab binds + stimulates the thyroid

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8
Q

Congenital hypothyroidism - symptoms + signs

A

Symptoms: Lethargy, poor feeding + weight gain, constipation, cold, hoarse cry
Signs: Acrocyanosis + mottling, extended belly, coarse features, prolonged jaundice, large fontanelle, hypotonia, slow reflexes

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9
Q

Causes of congenital hypothyroidism - primary, secondary, other

A

Primary: Dysgenesis, agenesis, ectopic, dyshormonogenesis
Secondary: Hypopit, hypothalamic abnormality
Other: Maternal iodine deficiency, transient

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10
Q

Initial work-up for a goiter

A

TSH, T4, anti-thyroidal Abs, US

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11
Q

Mimics of thyroid goiter (x2)

A

Lymphoma, parathyroid enlargement

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12
Q

Name main categories for short stature ddx

A
  • Constitutional growth delay
  • Familial
  • Endocrinopathy
  • Genetic syndrome
  • Iatrogenic/medications
  • Nutritional
  • Chronic disease
  • Psychosocial
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13
Q

Definition of gonadarche

A

Sex hormone production from gonads - triggered by LH and FSH from pituitary

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14
Q

Definition of adrenarche

A

Increase in adrenal androgen production –> pubarche, acne, sweat/body odour, axillary hair

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15
Q

DDx categories for precocious puberty

A
  • Central = early onset of HPA activation
  • Peripheral = hormones not coming from the brain
  • Benign/non-progressive = pubertal variants
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16
Q

Widened wrists - what is the endo related dx?

A

Rickets

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17
Q

Bony findings of rickets

A

Delayed closure of fontanelle, craniotabes, frontal bossing, leg bowing, widened wrists, rachitic rosary

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18
Q

What SMR for breast development would you think of precocious puberty?

A

3 or higher - bilateral

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19
Q

What test would you do for adrenoleukodystrophy?

A

VLCFA

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20
Q

Target for HbA1c for T1DM?

A

Less than 7.0%

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21
Q

NMS cut off for normal TSH filter paper blood spot

A

> 30

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22
Q

How to definitively confirm Addison disease?

A

ACTH stim test

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23
Q

What should you test and treat for before treating GH deficiency?

A

Hypothyroidism

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24
Q

Classic triad for pheo

A

Headache, sweating, tachycardia

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25
Q

Associated disorders with pheo (x3)

A

NF 1, MEN2, von hipple lindhau

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26
Q

Why should you monitor children with ?pheo closely during ultrasound?

A

Can increase metanephrine release

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27
Q

Phytoestrogen cannot be given to…

A

Congenital hypothyroidism

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28
Q

What test to do to distinguish rickets?

A

25-OHD

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29
Q

What thyroid diseases are TPO, TRAB, and TgAB antibodies associated with?

A

TPO - Hahimotos
TRAB - Graves’ disease
TgAB - Monitoring for thyroid cancer

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30
Q

Definition for precocious puberty (age)

A

Girls < 8 years and boys < 9 years

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31
Q

If you have an exaggerated response to glucagon what are you thinking is the dx?

A

Hyperinsulinism

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32
Q

Two best tests for ?cushing syndrome

A

Urine 24 cortisol collection

Dexamethasome suppression test

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33
Q

Canadian guidelines for target HbA1c for T1DM

A

<7.5%

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34
Q

When to check urine ketones for T1DM?

A

If glucose >14

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35
Q

If child with T1DM is having lots of lows what test would you double check?

A

Celiac

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36
Q

How many days of supraphysiogic dosing of steroids do you consider risk for AI?

A

Greater than 14 days

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37
Q

Dx criteria for PCOS

A

Two of three - hyperandrogenism, amenorrhea or oligo, and US changes

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38
Q

x2 normal growth variants

A

Constitutional delay, familial short stature

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39
Q

What syndrome is important to screen for in all females with short stature?

A

Turner Syndrome

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40
Q

What size of testicle is pre-pubertal?

A

2.5cm or 4mL

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41
Q

Age for M and F when you consider delayed puberty?

A

M >14

F >13

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42
Q

In setting of delayed puberty, what does elevated LH/FSH with low testosterone indicate?

A

Hypergonadotropic hypogonadism

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43
Q

Age and SMR stage for premature thelarche?

A
  • Birth to 2 years

- Equal to or less than SMR III

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44
Q

Age range for premature adrenarche

A

Typically 4-8 years

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45
Q

What would bone age, adrenal androgens, and LH/FSH show for premature adrenarche?

A
  • BA = mild to moderate increase
  • Androgens = normal or mild increase
  • LH/FSH = pre-pubertal
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46
Q

Age for precocious puberty for M and F?

A

M <9 years

F <8 years

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47
Q

x2 methods for correcting hyperglycemia in DM

A
  1. TDD x 10-20% as rapid insulin by subcutaneous injection or insulin pump bolus
  2. Insulin Sensitivity Factor (ISF) = 100/TDD
    1 unit of insulin will drop glucose by this much - given enough rapid insulin to drop BG to target 6-8 mmol/L
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48
Q

What factor best correlates with future cardio-metabolic risk?

A

Waist circumference

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49
Q

What x4 components need to be considered for metabolic syndrome?

A
  • Abdominal obesity (waist circumference)*
  • Dyslipidemia
  • Hypertension
  • Fasting glucose/T2DM
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50
Q

Critical sample for hypoglycemia

A
  • Glucose
  • Insulin, C-peptide
  • Ketones: BHB
  • FFA
  • Growth hormone, cortisol
  • Lactate
  • Additional: ammonia, IGF-1, LFTs, thyroid, plasma a.a.’s, total/free carnitine/acylcarnitine, urea/lytes, urine (toxicology, ketones, urine reducing substances, organic acids)
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51
Q

When should we consider a critical sample in a neonate?

A

If hypoglycemia (BG <2.8) persisting >72 hours

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52
Q

After dx of DI is made, what is the next step to determine where the problem is?

A

Trial of ADH to differentiate between central vs nephrogenic DI

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53
Q

Dx if after fluid deprivation urine osm <300 and after desmopressin >750?

A

Central DI

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54
Q

Dx if after fluid deprivation urine osm <300 and after desmopressin <300?

A

Nephrogenic DI

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55
Q

Dx if after fluid deprivation urine osm >750 and after desmopressin >750?

A

Primary polydipsia

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56
Q

Cut off measurement for micropenis?

A

<2.5 cm

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57
Q

Cut off measurement of clitoris?

A

> 9mm

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58
Q

DDx for 46 XX DSD?

A
  • Disorders of gonadal/ovarian development: ovotesticular DSD, gonadal DSD, gonadal dysgenesis
  • Androgen excess: CAH, maternal virilizing disease, maternal androgen use
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59
Q

Basic lab work-up for 46 XX DSD

A
  • 17-OHP
  • Glucose, lytes
  • Renin
  • ACTH
  • LH/FSH
  • Testosterone
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60
Q

When do you expect Classic Salt Wasting CAH to present?

A

7-14 days of life

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61
Q

Types of CAH - what hormones are affected?

A
  • Salt wasting = GC and MC deficiency
  • Simple virilizing = GC deficiency
  • Non-classical
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62
Q

Basic lab work-up for 46 XY DSD

A
  • Testosterone
  • DHEAS
  • Androstenedoine
  • LH/FSH
  • Mullerian inhibiting substance
  • Lytes, glucose
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63
Q

Hashimoto Thyroiditis Ab’s

A
  • Anti-thyroid peroxidase

- Anti-thyroglobulin

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64
Q

1st and 2nd line treatments for Graves Disease

A
  • 1st line: methimazole

- 2nd line: PTU, radioactive iodine, thyroidectomy

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65
Q

What kind of thyroid disease would a NMS miss?

A

Central hypothyroidism

66
Q

x2 screening tests that can be considered for query cushing syndrome?

A
  • 24 hour urine cortisol collection

- low dose dexamethasone suppression test

67
Q

Once cushing syndrome is confirmed, what is the next step in investigation?

A

High dose dexamethasone suppression test - determine if ACTH-dependent (ACTH elevated) vs ACTH-independent (ACTH depressed)

68
Q

Difference between Cushing syndrome + Cushing disease?

A
  • Cushing syndrome = constellation of symptoms/signs in keeping with excess glucocorticoids
  • Cushing disease = secondary to pituitary pathology
69
Q

Most likely pathology to cause Cushing Syndrome in (a) <5 years of age and (b) >5 years of age?

A

(a) Adrenal pathology - McCune Albright Disease

(b) Pituitary disease

70
Q

Clinical signs/symptoms of Cushing Syndrome

A
  • Weight gain
  • Striae
  • Osteopenia
  • Growth retardation
  • Hypertension
  • Hyperglycemia
  • Proximal muscle weakness
  • Behavioural change
71
Q

Causes for adrenal insufficiency

A
  • Primary = adrenal: Congenital (CAH, adrenal hypoplasia) vs acquired (autoimmune - Addison, autoimmune polyglandular syndrome, infectious, hemorrhage)
  • Secondary = pituitary/hypothalamic/exogenous: Congenital (hypopituitarism) vs acquired (exogenous steroids, trauma, surgery, radiation, tumor)
72
Q

Additional features with Primary Adrenal Insufficiency

A
  • Hyperpigmentation
  • Lyte disturbance (hypoNa, hyperK)
  • Salt craving
73
Q

Screening (what is cut off that you are concerned about) + diagnostic tests to consider for Adrenal Insufficiency

A
  • Screening = AM cortisol, <100-140 = concerning

- Diagnostic = ACTH stimulation test

74
Q

If you tested renin level in primary adrenal insufficiency, would it be elevated or depressed?

A

Elevated

75
Q

Stress dosing for moderate + severe illness for adrenal insufficiency?

A
  • Moderate illness = 30-50 mg/m2/day

- Severe illness = 100 mg/m2 x1 dose then same dose divided q6h

76
Q

DiGeorge Ca disorder

A

Hypoparathyroidism + HypoCa

77
Q

Criteria for osteoporosis in children

A
  • Low bone mass by DXA Z-score

- Clinically significant fracture history

78
Q

What would count as a clinically significant fracture history?

A
  • 2 or more long bone #’s by 10 years old
  • 3 or more long bone #’s by 19 years old
  • 1 or more vertebral compression #’s at any age
79
Q

3 stages of vitamin D deficiency

A
  1. Relative PTH resistance, low Ca
  2. Higher Ca levels at expense of HypoPO4
  3. HypoCa + hypoPO4 with rising PTH + ALP
80
Q

Physiology pathway in setting of hypoCa

A
  • Low Ca –> high PTH from parathyroid
  • Activates: (a) bone resorption, (b) kidney to resorb Ca + excrete PO4, (c) activate enzyme to convert vitamin D to calcitriol –> increase Ca absorption from GI
81
Q

What x2 processes regulate free ionized Ca

A
  • pH

- Protein binding

82
Q

What happens to Ca in setting of increasing pH?

A

Increase pH = less H+ to bind to proteins so increased binding to Ca = hypoCa + compensatory increase in PTH

83
Q

What is the threshold for normal growth velocity in children age 3 to puberty?

A

> 5 cm/year

84
Q

Work-up for short stature

A
  • Bone age XR

- Labs: CBC, lytes, renal function, CRP/ESR, UA, celiac screen, TSH, IGF-1, karyotype

85
Q

What is prepubertal testicular volume and size?

A

<4mL and <2.5cm

86
Q

What typically comes first axillary or pubic hair?

A

Pubic hair

87
Q

Sequence of puberty in M and F

A
M = berry, hairy, twig, big
F = boobs, pubes, grow, flow
88
Q

What diagnosis to consider in patient with delayed puberty, normal growth without a growth spurt, and anosmia?

A

Kallman Syndrome

89
Q

What two genetic syndromes would you consider for M and F with delayed puberty?

A

Klinefelter + Turner’s Syndrome

90
Q

Categories on the differential for delayed puberty?

A
  • Hypogonatropic hypogonadism - functional + permanent
  • Hypergonadotropic hypogonadism
  • Constitutional delay in growth + puberty
91
Q

DDx for precocious puberty

A
  • Central: CNS lesion/tumor, idiopathic
  • Peripheral: CAH, adrenal lesion, ovarian/testicular lesion, McCune Albright, hypothyroidism (through FSH), benign variants (benign thelarche + adrenarche)
92
Q

Work-up for Central Precocious Puberty (x2)

A
  • MRI for ALL boys and for all girls <6 years

- LH level = ensure it is prepubertal

93
Q

Premature adrenarche - age range, what investigations show

A
  • 4-8 years old
  • BA+ = chronological age
  • LH/FSH = prepubertal
  • DHEAS/testosterone normal to mildly increased
94
Q

Premature thelarche - age range

A

birth - 2 years

95
Q

What genetic condition to think of with precocious puberty?

A

McCune Albright

96
Q

When is glucagon effective for hypoglycemia?

A

Insulin-mediated hypoglycemia

97
Q

DDx for hypoglycemia

A

Non-acidemia:
(a) High FFA/low ketones = FAOD
(b) Low FFA/low ketones = hyperinsulin
Acidemia:
(a) High lactate = gluconeogenesis defects, GSD
(b) High ketones = ketotic hypoglycemia, hormone defects (GH or cortisol deficiency), GSD
Other = ingestions, illness, liver failure, malnutrition

98
Q

Why do you not make ketones in FAOD?

A

Need fatty acids to enter metabolism cycle at level of Acetyl CoA to then make ketones

99
Q

In acute management, what should you glucose infusion rate be?

A

6-8 mg/kg/min

100
Q

How to calculate water deficit in setting of hyperNa?

A

Water deficit = (0.6 x wt) x (current Na - ideal Na/ideal Na)

101
Q

How fast to correct hyperNa or hypoNa?

A

No faster than 10-12 mEq/L in 24 hours (no more than 1 mEq/L per hour)

  • Replace over 48 hours in moderate
  • Replace over 72 hours in severe
102
Q

DDx for hyperNa

A
  • Water deficit: Renal losses (DI), GI losses, insensible losses, decreased intake (including midline defect to cause impaired thirst)
  • Excessive Na: Increased intake, hyperaldosteronism
103
Q

Most important investigation in hyperNa

A

Urine osm

104
Q

DDx for low serum osmolality hypoNa

A
  • Hypovolemic: High urine Na (renal losses = diuretics, renal dysfunction, RTA, AI), low urine Na (extra renal losses = GI, insensible)
  • Euvolemic: SIADH, DI, hypothyroidism, AI
  • Hypervolemic: High urine Na (renal failure), low urine Na (CHF, cirrhosis)
105
Q

x4 most important points in assessment in disorders of sexual development

A
  1. Gonads - palpable?
  2. Phallic length - clitoris (<9mm) + penis (>2.5cm)
    - Posterior labial fusion
  3. # and location of urogenital openings
  4. Other dysmorphic features or malformations
106
Q

x2 initial investigations for DSD

A
  • US to visualize gonads

- Karyotype

107
Q

Most likely group of diagnoses if (a) gonads are palpable and (b) if gonads are NOT palpable

A

(a) XY DSD

(b) XX DSD

108
Q

Work-up if you are thinking XY DSD

A
  • Testosterone, androstendione, DHEAS, LH/FSH, MIS
  • US
  • Karyotype
109
Q

Work-up if you are thinking XX DSD

A
  • 17-OH progesterone, cortisol, lytes
  • Testosterone
  • Karyotype
  • US
110
Q

Main categories of DDx for XY DSD

A
  • Disorders of gonadal/testicular development

- Disorders of androgen synthesis or action

111
Q

Main categories of DDx for XX DSD

A
  • Disorders of gonadal/ovarian development

- Disorders of androgen excess

112
Q

CAIS vs PAIS

A
CAIS = complete, feminized
PAIS = partial, variably virilized
113
Q

Chronic AI therapy - CC dose + other addition

A
  • HCT 6-8 mg/kg2/day divided TID

- For primary AI = mineralocorticoid with fludracortisone

114
Q

HypoCa ddx

A
  • Low PTH/hypoparathyroidism = impaired synthesis or secretion of PTH (DiGeorge, autoimmune, infiltration of gland)
  • High PTH = deficient Ca intake/intestinal absorption, vitamin D deficiency, defects in vitamin D metabolism (renal dysfunction, hepatic dysfunction), defects in vitamin D action, end organ resistance to PTH (pseudohypoparathyroidism)
115
Q

Acute manifestations of hypoCa

A
  • Neuromuscular excitability = muscle contractions, tetany, seizures, broncho/larygnospasm, Trousseau’s (BP), Chvostek (facial nerve)
  • CVS = prolong QT, hypotension, arrhythmia
  • Papilledema
116
Q

What electrolyte should you also correct in hypoCa?

A

Mg

117
Q

Management strategies for hyperCa

A
  • Stop Ca + vit D
  • Increase excretion = IV fluids, avoid diuretics, dialysis
  • Stop bone resorption = calcitonin, bisphosphonates, GC’s
118
Q

DDx for hyperCa

A
  • Increased intestinal absorption = increased intake, vitamin D mediated/intoxication (increased intake, granulomatous disease, chronic inflammatory d/o)
  • Increased bone resorption = malignancy, hyperparathyroidism (adenoma, secondary/tertiary from chronic renal disease)
  • Diminished excretion = diuretics
  • Familial hypoCa-uria hyperCa
  • Hyperthyroidism, thyrotoxicosis
  • HypoPO4
  • Other: subcutaneous fat necrosis, AI, pheo, William’s syndrome, RTA, IEM
119
Q

Where is vitamin D activated?

A

Liver

120
Q

Extra-skeletal effects of vitamin D

A
  • Skin (tx for psoriasis)
  • Immune effects (for B+T cell function)
  • Cancer
  • Psychiatric conditions
121
Q

x2 most important minerals for bone mineralization

A
  • Ca

- PO4

122
Q

What does CPS recommend for GC taper?

A
  • <1 month = no taper
  • 1-3 months = 1-2 week taper
  • 3-6 months = 2-3 week taper
  • > 6 months = 3-4 week taper
123
Q

What range for AM cortisol would be suspicious for (a) AI vs (b) AS?

A

(a) <100

(b) 100-275

124
Q

What children are considered higher risk for AS and should be considered for screening?

A
  • High dose ICS (flut >500mcg/d) for >3 months
  • Systemic CC’s for >2 weeks
  • Swallowed ICS for >1 month
  • Concomitant use of nasal steroids
  • ICS for >3 months in conjunction with CYP3A4 inhibitors
125
Q

What medications can prolong GC half-life?

A

CYP3A4 = antiretrovirals, antifungal agents, some Abx

126
Q

What time of day is it better to dose GC’s?

A

Morning - to not interfere with HPA axis

127
Q

Symptoms/signs of possible AS

A
  • Poor linear growth + weight gain
  • Anorexia
  • Fatigue + weakness
  • Abdo pain, N/V
  • Headaches
  • Myalgia/arthralgia
  • Psychiatric symptoms
128
Q

x2 types of rickets

A

Hypophosphatemic and hypocalcemic

129
Q

In hypophosphatemic rickets, what would PTH, PO4, and Ca look like?

A
  • PTH normal/mildly high
  • PO4 low
  • Ca normal
130
Q

In hypocalcemic rickets, what would PTH, PO4, and Ca look like?

A
  • PTH high
  • PO4 normal/low
  • Ca normal/low
131
Q

Best test for Cushing Syndrome

A

Dexamethasone supression test

132
Q

If the dexamethasone suppression test is positive, what does this mean for Cushing Syndrome?

A
  • Means that the AM cortisol following dose of dexamethasone remains elevated
  • Must be another source for steroid
133
Q

What to think about for a teenage girl with advanced breast development but no adrenarche?

A

Androgen sensitivity syndrome

134
Q

6 year old boy with pubic hair but testes <2mL - what is the most likely cause?

A

Benign premature adrenarche

135
Q

Initial screening investigations for patient who is 3rd%tile for height while MPH is 75th%tile

A
  • CBC
  • ESR
  • Bone age
  • Cr, electrolytes, extended lytes
  • Karyotype (for all girls)
  • TSH
  • Celiac screen
  • IGF-1 (if GV off)
136
Q

What do you see in the serum at the end of a water-deprivation test if central DI?

A

Increased serum osmolarity

137
Q

When do you screen for T2DM?

A

At least 2 or more risk factors once child is 10 years old or has reached puberty:

  • Family history or of high ethnic group
  • Obesity
  • Evidence of impaired glucose tolerance
  • Impaired glucose tolerance
  • Use of psychotropic medications
138
Q

Triad for McCune Albright

A
  • Peripheral precocious puberty
  • CALM
  • Polyostotic fibrous dysplasia
139
Q

What endocrinopathy can present similarly to PCOS?

A

Non-classical CAH = especially in certain ethnic groups (Mediterranean, Hispanics, and Eastern European Jews)

140
Q

How to differentiate PCOS from non-classical CAH? (By labs)

A
  • 17 OHP level

- ACTH stimulation test

141
Q

What is androgen insensitivity syndrome?

A
  • One of the most common XY DSD
  • X-linked recessive
  • Wide variation on presentation: phenotypic female (complete) to various forms of ambiguous genitalia to phenotypic male with infertility
142
Q

What classification of disease is 5-alpha reductase deficiency? What does this enzyme typically do?

A

Abnormal androgen synthesis
-Impaired virilization secondary to inability to convert testosterone to DHT (typically converts 8% of testosterone to a stronger form = DHT)

143
Q

What other XY DSD is difficult to differentiate with androgen insensitivity syndrome?

A

5-alpha reductase deficiency

144
Q

At what age is it considered safe to start a statin?

A

> 10 years old

145
Q

What maternal anti-arrhythmia medication causes a thyroid goiter in the child?

A

Amiodarone

146
Q

Karyotype = 46, XY

(a) gonads/ducts
(b) gonadal cells
(c) gonadal hormones
(d) effect on ipsilateral ducts
(e) internal genitalia

A

(a) testis + mullerian
(b) leydig + sertoli
(c) testosterone + AMH
(d) +wolfian / -mullerian
(e) vas, epididymis, seminal vesicles

147
Q

What is the M + F structure that is:

(a) genital tubercle
(b) urogenital folds
(c) labioscrotal swelling

A

(a) Penis / Clitoris
(b) Penile urethra / labia minora
(c) Scrotum / labia majora

148
Q

What are the two most common types of DSD or ambiguous genitalia?

A
  • 46, XX CAH

- 45X/46XY mixed gonadal dysgenesis

149
Q

3 forms of 46 XX CAH

A
  • Salt wasting (75%)
  • Simple virilizing
  • Late onset, non-classical
150
Q

What are the x2 main functions of hydrocortisone in CAH?

A
  1. To restore cortisol

2. Suppress further virilization by providing a negative feedback to the hypothalamus + pituitary gland

151
Q

Newborn exam: penis with incomplete foreskin + urethral meatus on underside of penis, testicles descended bilaterally
- what is this?

A

Isolated hypospadias

152
Q

What would make you worry about DSD if there is hypospadias?

A

Undescended testes

153
Q

What other x2 associations (specific to penis) can be found with hypospadias?

A
  • Foreskin incomplete ventrally

- Erections curve downward (chordee)

154
Q

Risk factors to consider screening for T2DM (+how many RF’s do you need to go ahead with screening)

A
  • Obesity
  • Family history
  • Ethnicity
  • Evidence of insulin resistance
  • PCOS
  • Impaired glucose tolerance
  • Exposure to DM in-utero
  • NAFLD
  • HTN/dyslipidemia
  • Need x3 if pre-pubertal
  • Need x2 if post-pubertal
155
Q

Most important investigation when query PCOS

A

testosterone

156
Q

What is important to r/o for a query PCOS?

A

Other causes of hyperandrogenism - Cushing, exogenous, sex differentiation disorder (e.g., late onset CAH)

157
Q

Once you have the mid-parental height = then how do you decide the expected adult height for this child?

A

+/- 8.5

158
Q

When do you start screening for (a) retinopathy and (b) nephropathy (including test) and (c) dyslipidemia for patient with T1DM?

A

(a) 15 years old or >5 years since dx
(b) 12 years old or >5 years since dx
- Urine PCR
(c) 12 and 17 years old

159
Q

Dx for 14 years old M with 3-6 month history of gynecomastia (SMR 3) - counselling?

A
  • Physiological/pubertal gynecomastia

- Should not be greater than SMR 3 and should resolve after 2 years

160
Q

What should you look out for in a boy with Physiological/pubertal gynecomastia?

A

?Klinefelter’s

?Prolactin level if galactorrhea or anti-psychotic

161
Q

What is stage 4 neuroblastoma?

A

Good prognosis - involvement of skin

162
Q

Once confirm dx of neuroblastoma - what are investigations to consider for staging?

A
  • MRI: chest, pelvis, abdo

- BMA