Endocrinology Flashcards

(46 cards)

1
Q

Who and when to screen for T2DM

A

Prepubertal children with 3+ risk factors starting at age 8
Pubertal children with 2+ risk factors
Screen every two years with A1C and fasting glucose
Risk factors: Family hx, high risk ethnic group, obesity, signs of insulin resistance, PCOS, IDM, atypical antipsychotic use

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2
Q

Lab values to diagnose diabetes

A

Fasting glucose > 7
Random glucose 11.1+
OGTT 11.1+
A1C > 6

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3
Q

Target A1C for
1. T1DM
2. T2DM

A
  1. ≤ 7.5
  2. ≤ 7
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4
Q

When to screen for complications of T2DM

A

Yearly for everything except HTN, which is twice a year

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5
Q

Kallmann syndrome

A

Issue with migration of olfactory and GnRH expressing neurons
Hypogonadotropic hypogonadism (lack of puberty)
Anosmia
Can also get renal agenesis, abnormal hand movements, cleft lip/palate

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6
Q

How many cms per year should a child grow at ages
1. 0-12 mo
2. 12-24 mo
3. 24-36 mo
4. Childhood
5. Female puberty
6. Male puberty

A
  1. 24
  2. 10
  3. 8
  4. 6
  5. 8
  6. 10
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7
Q

How does puberty start in girls vs boys

A

Girls = thelarche
Boys = testicular enlargement

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8
Q

Delayed puberty ages in girls vs boys

A

Girls = no breast development by 13, no menarche by 16
Boys = no testicular enlargement by 14

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9
Q

Precocious puberty ages in girls vs boys

A

Girls < 8
Boys < 9

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10
Q

Zones of the adrenal gland

A

GFR, salt sugar sex
Zona glomerulosa (aldosterone)
Zona fasciculata (cortisol)
Zona reticularis (androgens)
Medulla (norepinephrine)

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11
Q

Diagnosis of adrenal insufficiency

A

Low AM cortisol
ACTH stim test

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12
Q

Addison disease

A

Primary adrenal insufficiency
Antibodies destroy the cortex
Results in low cortisol and aldosterone
Hyperpigmentation seen because of high ACTH
Hypovolemia, hyponatremia, hyperkalemia, salt craving

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13
Q

Waterhouse-Friedrichsen syndrome

A

Bilateral adrenal hemorrhage from meningococcemia
Leads to adrenal insufficiency

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14
Q

Premature adrenarche/pubarche

A

Benign condition caused by early production of adrenal androgens
Pubic or axillary hair, body odor, acne
NO gonadal involvement (breast, testicular enlargement)
Must rule out other causes, precocious puberty (testosterone, DHEAS, androstenedione, 17-OHP, bone age)

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15
Q

Familial short stature

A

Parallel to standard curves
Bone age = chronologic age
Family members are short too

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16
Q

Constitutional growth delay

A

Decreased weight and height in infancy, then follows curve in middle childhood
Accelerated growth in late adolescence and achieved expected adult height
Bone age less than chronological age

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17
Q

When and who should be screened for dyslipidemia

A

Universal fasting or nonfasting HDL-C or LDL-C between 2-10 years
Selective screening for children > 2 with positive family history of premature CVD, medical conditions, and other risk factors (obesity, HTN, smoking)

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18
Q

What to do if lipid screen is abnormal

A

2 fasting lipid profiles at least 2 weeks apart, but not more than 3 months

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19
Q

Who should get started on a statin

A

LDL ≥ 4.9
3.4-4.9 if multiple risk factors

20
Q

Familial combined hyperlipidemia vs familial hypercholesterolemia

A

Combined = elevated cholesterol and TGs
Hyperchol = just elevated cholesterol (LDL)

21
Q

When to treat congenital hypothyroidism

A

If TSH > 40 = treat immediately
If TSH 15-40 = can wait for serum results
Want to start treatment by 2 weeks

22
Q

Bone age in hypothyroidism

23
Q

Hashimoto

A

Chronic autoimmune thyroiditis
Positive TSI and TPO antibodies
Leads to hypothyroidism!

24
Q

Features of hyperinsulinism on labs

A

Detectable insulin
Suppressed ketones/FFAs
Response to glucagon (>1.7)
Positive C-peptide (endogenous insulin)

25
Idiopathic short stature
Otherwise normal children who are short Normal GH response to stim testing May have normal or low IGF-1 Increased rates of growth when treated with GH
26
21 hydroxylase deficiency
Most common cause of CAH Most have salt wasting and virilizing form, can just have virilizing form Males asymptomatic until 2-3 weeks, females are virilized Elevated 17OHP, progesterone, testosterone Can have hyperpirgmentation
27
11B hydroxylase deficiency
Second most common CAH NO salt wasting! 11-DOC builds up and has enough mineralocorticoid effect to make aldosterone Often presents with hypertesion Virilization is common
28
3B hydroxysteroid dehydrogenase deficiency
Third type of CAH Results in low aldosterone, cortisol, and androstenedione Elevated DHA +/- salt wasting Girls are mildly virilized, boys have hypospadias
29
When to screen children with T1DM for 1. Autoimmune thyroid disease 2. Primary adrenal insufficiency 3. Celiac disease
1. At diagnoses, then q2 years 2. If symptomatic 3. If symptomatic
30
When to screen children with T1DM for 1. Nephropathy 2. Retinopathy 3. Neuropathy 4. Dyslipidemia 5. HTN
1. Yearly starting at 12 if DM > 5 years 2. Yearly at 15 if DM > 5 years 3. Yearly at 15 if > 5 years and poor control 4. Once metabolic control has stabilized, 12 and 17 5. Twice a year
31
When is the girls vs boys growth spurt in SMR
Boys: 3-4 Girls: 2-3
32
Risk factors for developing adrenal insufficiency on exogenous steroids
High dose ICD ≥ 3 mo Systemic steroids > 2 weeks Swallowed ICS > 1 week Any ICS and CYP3A4 inhibitor for ≥ 3 mo
33
Microphallus length
Stretched length in term infant < 1.9 cm
34
Clue for central vs peripheral precocious puberty
Peripheral will NOT have increased testicle size in boys Testicles grow in response to FSH from pituitary Bone age and growth velocity will be increased in both
35
How to tell if calcium is a PTH or vitamin D problem
If calcium and phos are both low/high = GI = vitamin D If calcium and phos are in opposite directions (one low, one high) = renal = PTH
36
Premature thelarche
Isolated breast development in first 2 years (if after 3, different diagnosis!!) NO involvement of adrenal glands Labs should be normal, bone age might be slightly advanced Should regress without treatment Monitor in 3-6 months to ensure not start of true precocious puberty
37
Labs in vitamin D deficiency rickets
Low 25 OHD and 1,25 OHD Elevated ALP Hypocalcemia Hypophosphatemia Elevated PTH
38
Autoimmune polyglandular syndromes Type 1 vs type 2
Type 1: candidiasis + hypoparathyroidism + primary adrenal failure Type 2: thyroiditis + primary adrenal insufficiency +/- diabetes
39
Cushing disease
ACTH dependent Pituitary hypersecretion of ACTH Most commonly a pituitary ademona Causes Cushing syndrome
40
Complete androgen insensitivity syndrome
Cellular resistance to testosterone Phenotypical female - vagina ends in blind pouch, no uterus or fallopian tubes, testes are intraabdominal Breasts will develop at puberty (testosterone converts to estrogen) but no menses or pubic hair Must remove testicles
41
Multiple endocrine neoplasia 1. Type 1 2. Type 2A 3. Type 2B
1. Pancreas, pituitary, parathyroid 2. Pheochromocytoma, medullary thyroid carcinoma, hyperparathyroidism 3. Pheochromocytoma, medullary thyroid carcinoma, mucosal neuromas - also Marfanoid body habitus
42
Monitoring for neonates born to mothers with Graves
T4/3, TSH stimulating immunoglobulins from cord blood or soon after birth If abs negative = discharge If abs positive = repeat function at 3-5 days and 10-14 days
43
Bartter and Gitelman syndromes
Both cause HYPOkalemia! Bartter looks like they are on a loop diruetic Gitelman looks like they are on a thiazide diuretic + severe Mg wasting Bartter = hypercalciuria Gitelman = hypomagnesemia
44
Pseudohypoparathyroidism
PTH resistance! Will have low Ca but high PTH
45
Benign pubertal gynecomastia
Occurs during SMR 2-4 If during stage 1 or 5 = red flag Usually < 4 cm Should resolve on its own in 6-24 months May need surgical removal
46
Dose of hydrocortisone replacement for 1. Adrenal crisis, severe illness/injury 2. Major surgery 3. Minor/moderate surgery needing GA 4. Moderate illness
1. 100 mg/m2 2. 50-100 mg/m2 3. 30 mg/m2 4. 30-50 mg/m2