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MCQ Questions > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What type of medical screening do you do for children who are obese?

A
  1. 85th -94th %:
    - BP + exam
    - Fasting lipid profile
    - Conditional testing for glucose + liver
  2. >95th %
    - BP + exam
    - Fasting lipid profile
    - HbA1c or FPG Q2y
    - ALT, AST Q2y
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2
Q

What are the ways to test for T2DM and their cut-offs?

A
  1. FPG (typical screen): ≥ 7 mmol/L (≥ 11.1 if random plasma glucose sent)
  2. HbA1C: ≥ 6.5% (convenient alternative or additional test)
  3. OGTT 2h PG: ≥ 11.1 mmol/L (gold standard, but more inconvenient - consider if 3+ RFs or discrepancy in FPG and AIC testing)
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3
Q

What are the indications to screen for T2DM?

A

Screen kids Q2years at risk:

  • PCOS
  • Use of antipsychotics
  • ≥3 RFs in pre-pubertal children ≥8yo
  • ≥2 RFs in pubertal children

RFs:
Obesity, high risk ethnic group, 1st degree relative T2DM, maternal hx of GDM, symptoms insulin resistance (e.g. dyslipidemia, NAFLD, HTN, acanthosis)

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4
Q

What are the complications and co-morbidities of T2DM that need to be monitored?

A
  1. Neuropathy (annually starting at diagnosis)
  2. Retinopathy (annually starting at diagnosis)
  3. Nephropathy (annually starting at diagnosis)
  4. Dyslipidemia (annually starting at diagnosis)
  5. HTN (annually starting at diagnosis)
  6. NAFLD (annually starting at diagnosis)
  7. PCOS (annually clinical screening in post-pubertal girls)
  8. OSA (annually starting at diagnosis)
  9. Depression (annually starting at diagnosis)
  10. Binge eating (annually starting at diagnosis)
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5
Q

What are the management / screening guidelines for girls diagnosed with Turner syndrome?

A
  • Weight, BMI annually
  • Cardiac: refer to cardiology - initial evaluation and then yearly ECHO
    • 4 limb BP at all visits
  • Endocrine
    • Short stature: GH to increase stature
    • Delayed Puberty: Monitor LH and FSH after age 10yo
      • Estrogen replacement therapy
    • Metabolic syndrome
      • Lipid screening annually if 1+ RF
      • ALT, GGT, ALKP annually > 10y
      • HbA1c +/- FPG annually >10y
    • Annual thyroid function tests
    • Celiac screen at 2yo, Q2y or symptoms
  • Renal: screening ultrasound
  • MSK: Early treatment of scoliosis (check at 5-6y, 12-14yo)
  • Skin: Annual skin exams
  • Hearing: Q3y hearing screen
  • Development: School accomodations
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6
Q

At what age would you consider investigating premature thelarche? What investigations?

A

After the age of 2-years old

FSH, LH, estradiol

Bone age

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7
Q

What are the clinical signs of cushing’s syndrome (8 systems)?

A

HEENT - rounded face, flushed cheeks

CVS - HTN, CHF

GI - generalized obesity, central adipose tissue

Endo - hyperglycemia, hirsutism, pubic hair, acne, deepening voice, enlargement of clitoris

Gyne - delayed puberty, amenorrhea

ID - increased susceptibility to infection

Bone - osteoporosis

Skin - striae

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8
Q

What are the two different types of Cushing’s?

A
  1. ACTH-independent - exogenous
  2. ACTH-independent - endogenous (adrenocortical tumour, McCune Albright, MEN1)
  3. ACTH-dependent - excessive ACTH secretion from pituitary gland
  4. ACTH-dependent - from tumors (e.g. islet cell carcinoma of pancreas, NB, Wilm’s, thymic)
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9
Q
  1. What is the diagnostic test for Cushing’s syndrome?
  2. If confirmed, what type of imaging should be done?
A
  1. Dexamethasone suppression test
  2. CT for adrenal tumours, MRI + contrast of pituitary
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10
Q

What is the diagnostic criteria for PCOS?

A

2 of 3:

  • Oligo (>35 day cycle) or amenorrhea (no cycles, no menses, no ovulation)
  • Lab or clinical evidence of elevated androgens
    • Hirsutism, male pattern hair loss, acne
    • Free testosterone or increased androstenedione
  • Polycystic ovaries on ultrasound
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11
Q

What is the differential diagnosis for PCOS?

A
  • CAH - do 17-OHP to assess
  • Cushing’s - should see signs of cortisol excess (striae, thin skin, HTN, abnormal fat distribution); do AM cortisol
  • Hyperprolactinemia - usually has galactorrhea, test PRL levels
  • Hypothyroidism - do TSH
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12
Q

What are the treatments for PCOS?

A
  1. Infertility - weight loss, clomiphene citrate (estrogen receptor blocker → produce more LH/FSH → stimulate follicle development), metformin, FSH injections, IVF
  2. Hirsutism / acne / male pattern hair loss - combined OCP, anti-androgens (often spironolactone)
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13
Q

What are four suspicious indications for familial hypercholesterolemia?

A
  1. Family member with known FH or elevated cholesterol
  2. Tendon xanthomas in child or family members
  3. Premature CVD in child or family members
  4. Sudden premature cardiac death in family member
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14
Q

What is the cut-off for suspecting micropenis? What are associated genetic conditions? What investigations can help determine the underlying etiology?

A
  1. Cut-off: < 1.9cm (avg 3.5cm +/- 0.7cm)
  2. Conditions: Hypogonadotropic hypogonadism (Kallmann syndrome, PWS, Lawrence-Mood-Biedl syndrome); Hypergonadotropic hypogonadism (AKA primary testicular failure - Robinow syndrome)
  3. Investigations: Endo & uro referrals, karyotype, anterior pituitary function and testicular function, MRI to look at HT & pituitary
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15
Q

What are is the screening timeline for complications for children with T1 DM?

A
  1. Nephropathy (1st AM random urine ACR) - annual screening starting at 12yo or >5y with T1DM
  2. Retinopathy (ophtho) - annual screening starting at 15yo or >5y with T1DM
  3. Neuropathy (light touch, vibration) - kids >15y+ with poor metabolic control after 5y with T1DM
  4. Dyslipidemia (fasting TC, HDL-C, TG, calculated LDL-C) - screen b/w 12-17yo, <12yo if BMI >97th %
  5. HTN - screen all children with T1DM at least twice per year
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16
Q

What are the screening guidelines for co-morbidities in T1DM?

A
  1. Autoimmune thyroid disease - serum TSH + peroxidase antibodies → at diagnosis and Q2y thereafter (do not repeat antibodies if initially neg)
  2. Primary adrenal insufficiency - only do in kids with recurrent hypoglycemia or decreasing insulin requirements → 8am cortisol and serum K/Na
  3. Celiac disease - GI symptoms, FTT, poor metabolic control → TTG, IgA
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17
Q

What is the most common cause of congenital hypothyroidism?

A

Thyroid dysgenesis (80-85%)

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18
Q

Name 10 early clinical features of congenital hypothyroidism.

A
  • General: hypothermia, lethargy, cold & mottled skin
  • HEENT: large anterior fontanelle
  • Feeding: choking, sluggish feeds
  • Resp: large tongue, apneic episodes
  • GI: constipation
  • CVS: bradycardia, cardiomegaly, asymptomatic pericardial effusions, edema
  • Heme: prolonged jaundice, macrocytic anemia
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19
Q

Name 8 clinical features of growth hormone deficiency.

A
  • Growth delay
  • Delayed bone age
  • Delayed puberty
  • Micropenis
  • Frontal bossing, small facies, hypoplastic nasal bridge, blue sclera
  • Hypoglycemia
  • Delay in dentition
  • Hip dysplasia, AVN of femoral head, osteopenia
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20
Q

What are the management steps for growth hormone deficiency?

A
  1. Refer to endocrinology
  2. Labs: GH, IGF-1, IGF-BP3, GH stim test
  3. Bone age
  4. MRI or CT of head (examine HPA)
  5. Consider genetic testing
21
Q

What are the 5 S’s in managing adrenal insufficiency?

A
  1. Salt = restore volume and Na appropriately
  2. Sugar = support hypoglycemia as needed
  3. Steroids = IV HC +/- fludrocortisone if electrolyte disturbance
  4. Support = BP, BW, Endo, PICU
  5. Search = for etiology of crises
22
Q

What investigations should you do for short stature?

A
  1. Determine mid-parental height
  2. Bone age
  3. Endocrine: TSH, FT4, GH stim test
  4. Chronic illness: lytes, Cr, BUN, LFT, IgG/M/A, ESR, UA
  5. Malabsorption: fecal fat, albumin, ferritin, celiac screen, sweat chloride
  6. Consider karyotype to R/O Turner syndrome or dysmorphic features are present
23
Q

What are the components of a critical sample?

A
  • Glucose
  • Insulin
  • Growth hormone
  • Cortisol
  • Lactic acid
  • Gas
  • Ammonia
  • Carnitine - Total, free
  • Acyl carnitine profile
  • Amino acids
  • Free fatty acids
  • Beta-Hydroxybutyrate
  • Also urine ketones and organic acids
24
Q

What are four clues to indicate T1DM instead of T2DM?

A
  1. Elevation of multiple autoantibodies (e.g. glutamic acid decarboxylase antibody, insulinoma-associated protein 2 antibody) 2. Low insulin C-peptide level 3. FHx of autoimmune disease 4. Normal BMI
25
Q

What investigations should you do in the case of a patient with a micropenis?

A
  • Refer to endo, uro
  • Karyotype
  • Anterior pituitary function and testicular function
  • MRI to look at HT and pituitary
26
Q

What are the characteristic features of Familial Hypercholesterolemia?

A
  • Elevated LDL-C levels since birth
  • Xanthomata in untreated adults and homozygous patients
  • Early onset coronary heart disease -TG NOT elevated -> if elevated, consider familial combined dyslipidemia
27
Q

What are the risk factors for cerebral edema in DKA?

A
  • Younger age
  • New presentation / diagnosis
  • High BUN at presentation
  • Profound acidosis
  • Administration of insulin in 1st hour of fluid treatment
  • Attenuated rise in measured serum Na with treatment
  • Administration of bicarbonate
28
Q

What are the physiologic effects of T3, T4?

A
  • Growth
  • Brain development
  • Metabolism increase
  • Increases insulin sensitivity
  • Stimulates bone turnover
  • Improves cardiac contractility
  • Promotes GI motility
  • Increases EPO
29
Q

What are the different types of rickets?

A
30
Q

What is a red flag for growth velocity between 6yo to the age of puberty?

A

Girls: if growth < 4.5 cm/year

Boys: if growth < 6 cm/year

31
Q

What is the role of FSH, LH, and adrenal androgens in puberty?

A
  • Start of puberty: unclear mechanism -> GnRH gets stimulated -> release of FSH + LH
  • FSH
    • Girls: Increases estrogen production -> causes breast development
    • Boys: testicular growth + maturing spermatozoa
  • LH
    • Girls: initiates ovulation + creates corpus luteum
    • Boys: act on Leydig cells to increase testosterone production
  • Adrenal androgens (testosterone, estradiol, DHEA-S)
    • Leads to acne, axillary & pubic hair, body odor
    • Separate process -> does NOT always indicate true pubertal onset
32
Q

What is the differential diagnosis of precocious puberty (peripheral and central)?

A

Central (↑LH/FSH + ↑ testosterone/estradiol):

  • Idiopathic (premature activation of HCG axis *most common in girls)
  • Obesity
  • CNS: cysts, tumors, head trauma, encephalitis, meningitis , HC, increased ICP, irradiation
  • Primary hypothyroidism (Van Wyk-Grumbach syndrome)
  • NF

Peripheral (↓ LH/FSH + ↑ testosterone/estradiol):

  • Adrenal disorders: CAH, adrenal neoplasm (contrasexual precocity)
  • Ovarian cysts, granulosa cell tumors (estrogen-secreting)
  • Theca cell and Leydig cells tumors (testosterone-secreting)
  • Germ cell tumors such as hepatoblastoma, teratoma, germinoma (GnRH/BHCG secreting)
  • Endogenous steroids
  • McCune Albright syndrome
33
Q

What are the investigations to consider in precocious puberty?

A
  • BW - LH, FSH, testosterone, estradiol, DHEA-S, 17-hydroxyprogesterone, TSH/FT4
  • Imaging - Bone age
  • Consider: pelvic US, MRI head, B-HCG, GnRH stim test, ACTH stim test
34
Q

What is the most common cause of congenital hypothyroidism?

A

Thyroid dysgenesis

35
Q

What is the evidence for GCs (forms other than PO, IV and inhaled) for causing adrenal suppression?

A
  • Intranasal: Unclear if use of intranasal glucocorticoids ONLY can cause AS
  • Liquid GCs: AS has been seen in oral budesonide or swallowed fluticasone for EOE / IBD
  • Ocular GCs: Rare reports of AS
  • Topical GCs: rare reports with potent topical GCs
  • Intra-articular GCs: AS has been reported in adults
36
Q

What class of medication can prolong the biological half-life of glucocorticoids?

A

CYP3A4 inhibitors (e.g. antiretrovirals (e.g. ritonavir), antifungal (e.g. ketoconazole), some antibiotics (e.g. clarithomycin) prolong biologic half-life of GCs → have been implicated in symptomatic AS with relatively low doses of ICS → prolong duration of systemic GC exposure

37
Q

Describe the tests available to screen and diagnose adrenal insufficiency

A
  • AM Cortisol (7-9am)
    • Diagnosis of AI: ≤ 100 nmol/L (normal sleep-wake cycle, GC held 24-48h)
    • Possible AI: 100-275 nmol/L → needs empiric-treatment (GC replacement) and provocative testing
    • Normal HPA axis: predicted if 350-500 nmol/L
      • ≥ 275 nmol/L has been used as screening threshold in asymptomatic patients
  • ACTH stim test
    • Indicated if: abnormal sleep wake cycle (e.g. infants) + low AM cortisol OR possible AI on AM cortisol
    • Low dose: 1mcg + Standard dose: 250 mcg → debate on which is superior → either is reasonable
    • *Hold GCs 24-48h (24h for short acting, 48h for long acting) before test
38
Q

What are investigations that can be considered to investigate short stature?

A
  • Determine Mid-Parental Height
  • Bone Age (AP x-ray of L hand and wrist)
    • Delayed differential:
      • Constitutional delay
      • GH deficiency, chronic illness, malnutrition, thyroid hormone deficiency
  • Endocrine: TSH, Free T4, GH stimulation test
  • Chronic illness: Lytes, Cr, BUN, LFT, Ca, IgG/IgM/IgA, ESR, urinalysis
  • Malabsorption: fecal fat, albumin, ferritin, celiac screen, sweat chloride
  • Consider karyotype to rule-out Turner in females or if dysmorphic features are present
39
Q

What is the differential diagnosis for hypoglycemia?

A
  • Ketotic process:
    • Fasting
    • Malabsorption, gastroenteritis
    • Galactosemia
    • Hereditary fructose intolerance
    • Glycogen storage disease type 1
    • Idiopathic ketotic hypoglycemia
  • Non-ketotic process:
    • Hyperinsulinism
    • Infants of diabetic mothers
    • Congenital panhypopituitarism
    • Adrenal insufficiency
    • Fatty acid oxidation defects
    • Beckwith-Wiedman syndrome
  • Other diagnoses
    • Sepsis
    • Ingestion, poisoning
    • Liver failure
40
Q

What are the indications for pharmacotherapy in dyslipidemia in children?

A
  • Kids < 10yo
    • High risk CVD conditions
    • LDL-C levels > 10.4 mmol/L (suggests FH)
    • Very elevated TG (> 11.3 mmol/L)
    • Very strong FHx premature atherosclerotic CVD events
  • Kids >10yo
    • If high-risk + LDL > 3.4 mmol/L: start lifestyle changes and statin therapy
    • If moderate risk (e.g. severe obesity, confirmed HTN, 3+ at risk RFs): start with lifestyle changes. If LDL-C remains > 4.1 after 3mo, start statin
41
Q

What are the high risk conditions for dyslipidemia?

A
  • Homozygous FH
  • Diabetes mellitus (type 1 or 2)
  • End-stage kidney disease
  • Kawasaki disease with persistent coronary aneurysms
  • Solid-organ transplant vasculopathy
  • Childhood cancer survivor following stem cell transplantation
  • Multiple comorbidities – Any moderate-risk condition plus ≥2 additional moderate- or at-risk factors
42
Q

What is the differential diagnosis for a child with short stature and delayed bone age?

A
  • Constitutional delay
  • GH deficiency, chronic illness, malnutrition, thyroid hormone deficiency
43
Q

What is the differential diagnosis for gynecomastia?

A
  • Physiologic
    • Neonatal: may be associated with galactorrhea, resolves in 1st year of life
    • Pubertal: occurs mid-puberty
  • Pathological
    • Drugs - exogenous (e.g. OCP), other
    • Hypogonadism
      • Primary - Klinefelter, cryptorchidism, defect in testosterone synthesis
      • Secondary - hyperprolactinemia, surgery, radiation, trauma
    • Tumors - testicular cancer (Leydig or Sertoli), adrenal tumor, prolactinoma, HCG-producing tumors
    • Other - CKD, liver disease, malnutrition, hyperthyroidism, androgen resistance, CAH
44
Q

What are the six most common causes of ambiguous genitalia?

A
  • Congenital adrenal hyperplasia (14%) - no gonads, uterus present, +/- sick baby
    • Labs: elevated 17-OHP, possibly abnormal electrolytes, 46,XX
  • Androgen insensitivity syndrome (10%) - palpable gonads, no uterus, baby well
    • Labs: normal 17-OHP, normal lytes, 46,XY
  • Mixed gonadal dysgenesis (8%) - +/- palpable gonads, uterus present, baby well, may be dysmorphic
    • Labs: normal 17-OHP, normal lytes, 46,XX
  • Clitoral/labial anomalies (7%)
  • Hypogonadotropic hypogonadism (6%)
  • 46,XY small-for-gestational-age males with hypospadias (6%)
45
Q

What are the approved indications for GH in short stature? (SPRING ST)

A
  • SGA short stature
  • Prader-Willi syndrome
  • Renal failure (chronic not acute) before transplantation
  • Idiopathic short stature
  • Noonan syndrome
  • GH deficiency
  • SHOX gene abnormality
  • Turner syndrome
46
Q

What are the lab findings in CAH?

A
  • Glucocorticoid deficiency: ↓ cortisol, ↑ ACTH, ↑ 17-OH progesterone
  • Mineralocorticoid deficiency (salt wasting crisis): hyponatremia, hyperkalemia, ↑ plasma renin
  • Ambiguous genitalia: ↑ serum androgens
    • Females: elevated androstenedione, elevated testosterone
    • Males: testosterone not elevated
  • Postnatal virilization in males & females: ↑ serum androgens
47
Q

If a patient started on L-thyroxine for hypothyroidism develops headaches, what is the diagnosis to rule out?

A

Pseudotumour cerebri

48
Q

In schools with 1+ children with T1 DM, how many trained personnel should be present?

A

Two - Staff members may be unlicensed (ie, not regulated by a health-professional college), and will be provided with diabetes education resources and enabled to attend annual diabetes updates

49
Q

In what scenarios should clinicians be aware of the risk factors for developing AS and consider screening asymptomatic children at greater risk?

A
  • High-dose ICS therapy for ≥3 months
  • Systemic therapy for >2 weeks
  • Swallowed ICS therapy for > 1 month
  • ICS of any dose for ≥3 months in conjunction with CYP3A4 inhibitors

MCQ Questions (23 decks)

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