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Pediatrics- Noelle > Endocrinolgy > Flashcards

Endocrinolgy Flashcards

1
Q

what are the two time periods that it is normal for children to cross percentiles?

A
  1. during the first 2-3 years of life

2. during puberty

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2
Q

when should children not cross percentiles

A

during the time from 3yrs until puberty well children do not cross 2 major percentile lines

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3
Q

what is sequential loss of pituitary hormones due to mass effect?

A 
Go Look For The Adenoma Please!
G- Growth hormone
L- LH
F- FSH
T- TSH
A- ACTH
P- Prolactin
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4
Q

what are some causes of delayed bone age? (4)

A

chronic disease
hypothyroidism
constitutional delay
growth hormone deficiency

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5
Q

what are some causes of low IGF1? (4)

A

GH deficiency
renal disease
hypothyroidism
malnutrition

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6
Q

What is the normal age for males to enter puberty

A

9-14

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7
Q

what is the first sign of puberty in most males

A

Increase in testicular size

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8
Q

at what tanner stage do we see peak growth velocity for males?

A

tanner stage 4 or 5

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9
Q

what is the testicular size prepuberty? puberty?

A

prepuberty <2.5cm (4mL)

puberty >2.5cm (4mL)

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10
Q

A 4mL testis corresponds to what in cm?

A

2.5cm in length

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11
Q

What is the normal age for females to enter puberty

A

8-13 years

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12
Q

what is the first sign of puberty for most girls

A

breast development

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13
Q

at what tanner stage do we see peak growth velocity for females?

A

tanner stage 3

Females attain a peak height velocity of 8-9cm/yr at SMR 2-3

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14
Q

What Tanner stages are associated with menarche

A

Tanner stage 3-4

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15
Q

what is considered delayed puberty in girls? boys?

A

absence of secondary sexual characteristics after 13 years of age in girls and 14 years of age in boys

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16
Q

what lab results would you see with primary gonadal failure?

A

elevated LH/FSH

low testosterone/estrogen

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17
Q

what lab results would you see with permanent or functional pituitary or hypothalamic dysregulation?

A

low LH/FSH

low testosterone/estrogen

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18
Q

What are key findings with Klinefelter syndrome

A

47XXY
1 in 600 males
Puberty begins at an appropriate age, penile enlargement and pubic hair
key finding is disproportionately small, firm testes, gynecomastia, infertility
increased learning and behaviour difficulties
treatment= testosterone

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19
Q

List one important cause of primary gonadal failure in males? in females?

A 
Males= Klinefelter syndrome
Females= Turner syndrome
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20
Q

Why do we treat girls with Turner syndrome with growth hormone?

A

not because they are growth hormone deficient but to improve their final adult height

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21
Q

Any female whose height is less than the 3rd %ile what should you consider and what test should you order?

A

Turner syndrome

karyotype

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22
Q

is precocious puberty more common in girls or boys?

A

10 times more common in girls

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23
Q

what is the definition of precocious puberty

A

Pubertal signs before age 8 in girls and before age 9 in boys

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24
Q

Most precocious puberty in girls is idiopathic or pathologic? boys?

A

central and idiopathic in girls

pathologic in boys

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25
Q

what are the red flags for precocious puberty?

A

rapid progression
bone age >2 years beyond chronological age
predicted adult height <150cm or >2SD below mid parental height
CNS signs or symptoms

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26
Q

what are 2 common benign conditions in girls often confused with precocious puberty?

A
  1. premature thelarche

2. premature adrenarche

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27
Q

what is premature thelarche?

A

isolated breast development, 6-24 mo of age
breast development does not exceed tanner stage 3
no change in growth %ile

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28
Q

what is premature adrenarche?

A

pubic hair +/- axillary hair, body odor, acne but no therlarche
early secretion of adrenal androgens (DHEA)
no changes in growth %ile
bone age= height age
associated with PCOS later in life

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29
Q

what are the two broad categories of precocious puberty

A 
central= GnRH dependent (hypogonadotropic hypogonadism)
peripheral= GnRH independent (hypergonadotropic hypogonadism)
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30
Q

what is a key feature of precocious puberty

A

differs from the normal sequence (ie menarche before thelarche)
in girls estrogen dependent effects usually predominate
in boys testes are inappropriately small in size or asymmetric

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31
Q

what is the criteria for diagnosis of diabetes?

A

FBG >7
RBG ≥ 11.1
2hr OGT ≥11.1

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32
Q

if an infant less than 6 months of age develops diabetes what type is it?

A

neonatal diabetes
genetic diabetes
tx: sulfonylurea or insulin

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33
Q

what percentage of youth with Type 2DM present with DKA

A

5-20%

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34
Q

what is the treatment for monogenic diabetes

A

Tx: sulfonylurea

monogenic diabetes is autosomal dominant

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35
Q

what type of glucose is measure with continuous glucose monitoring?

A

measuring interstitial glucose

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36
Q

what is the starting dose of insulin for someone with newly diagnosed diabetes

A

~0.4-0.6 units/kg/day

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37
Q

what are 3 broad causes of DKA

A
  1. new diabetic
  2. deliberate or inadvertent insulin omission
  3. poor sick day management
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38
Q

what percentage of cases of DKA are complicated by cerebral edema?

A

0.5-1%

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39
Q

how much insulin do you give for management of hyperglycaemia for a diabetic patient

A

10-20% of total daily dose by subcutaneous injection or insulin bolus

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40
Q

what is the insulin sensitivity factor

A

the amount that blood glucose will drop for every unit of rapid insulin given
estimated as 100/TDD

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41
Q

who is considered high risk for type 2 DM and should get screening with FBG?

A

BMI >85%ile
family history of type 2 DM
high risk populations- Asian, African, indigenous

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42
Q

what is the definition of hypoglycemia

A

a plasma glucose concentration low enough to cause symptoms and/or signs of impaired brain function
most sources define it as less than 2.8mmol/L (to activate true counter-regulatory response)
consider the context within which blood glucose was measured

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43
Q

what is our body’s response to hypoglycemia

A

regular ingestion of food with storage of excess as glycogen and fat
gluconeogenesis
glycogenolysis
decreased utilization of glucose by substitution of ketones as primary energy source

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44
Q

what is the main glucose regulator and first defence against hypoglycaemia?

A

insulin

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45
Q

With hypoglycemia what happens with insulin glucagon, epinephrine and cortisol

A 
decrease insulin
increase glucagon
increase epinephrine
increase cortisol
increase growth hormone
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46
Q

what is the main counter-regulatory factor for hypoglycemia

A

glucagon

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47
Q

what is the glycemic threshold that should prompt behavioural defence (food ingestion)

A

2.8-3.1

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48
Q

what is included in a critical sample for hypoglycemia?

A 
plasma glucose 
insulin
c-peptide (not on synthetic insulin)
BHB (serum ketones)
FFA
growth hormone
cortisol
lactate
glucagon
first urine void for ketones
extra plasma can be held for specific tests (total and free carnitine and acylcarnitine, plasma AA, ammonia, urea and lytes, liver function tests)
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49
Q

what is diabetes insipidus

A

due to loss of vasopressin production
can be central or peripheral
central= loss of ADH production
peripheral= impairment of action (nephrogenic)

low urine osmolality (<300mosmol)
increased serum osmolality (>300mosmol)
increasing serum sodium
signs of dehydration
decreased body weight
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50
Q

what is SIADH

A

inappropriate release of excess activity of vasopressin (ADH)
increased urine osmolality, increased urine Na
oliguria
hyponatremia
serum hypoosmolality
euvolemia or mild hypervolemia

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51
Q

what is the definition of micropenis?

A

stretched penile length <2.5cm in a term infant

mean penile length= 3.5cm

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52
Q

what is the definition of cliteromegaly

A

length of clitoris >9mm in a term infant

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53
Q

what is posterior labial fusion?

A

anogenital ratio >0.5

distance from anus to posterior forchette, divided by distance from anus to base of phallus

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54
Q

what is the workup for someone expected to have 46XX disorder of sexual development?

A 
17 hydroxyprogesterone
serum electrolytes
glucose
ACTH
renin
testosterone
LH
FSH
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55
Q

what is the differential for 46XX DSD (6)

A 
congenital adrenal hyperplasia
maternal androgen use
virtualizing maternal disease
ovotesticular DSD
XX testicular DSD
gonadal dysgenesis
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56
Q

what is the differential for 46XY DSD

A 
leydig cell failure
testosterone biosynthetic defect
5 alpha reductase deficiency
androgen receptor disorder
gonadal dysgenesis 
rare forms of CAH
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57
Q

what is the workup for someone expected to have 46XY disorder of sexual development?

A 
testosterone
dihydrotestosterone
LH
FSH
mullerian inhibiting substance
electrolytes
glucose
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58
Q

what is the androgen that is most important for virtualizing the external genitalia?

A

dihydrotestosterone

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59
Q

how do we screen for congenital hypothyroidism

A

heel prick TSH

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60
Q

what patients with congenital hypothyroidism are missed with newborn screening

A

those with central congenital hypothyroidism

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61
Q

what are the causes of congenital hypothyroidism?

A

permanent: thyroid dysgenesis (80%)
dyshormonogenesis (10%)
hypothaamic/pituitary (5%)
transient: intrauterine antithyroid meds
maternal blocking antibody
iodine deficiency

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62
Q

what is the most common malignancy of thyroid nodule?

A

papillary carcinoma

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63
Q

what is the most common cause of acquired hypothyroidism

A

Hashimoto thyroiditis (acquired)

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64
Q

what are the two/3 thyroid antibodies

A

thyroid peroxidase
antithyroglobulin
TSH receptor blocking antibody

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65
Q

what are the findings for Hashimoto thyroiditis

A

diffuse enlargement of thyroid gland, may be asymmetric
elevated TSH (tx if >10)
positive thyroid peroxidase
antithyroglobulin

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66
Q

what is the cause of Graves disease

A

thyrotropin receptor stimulating antibody (TRAB)

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67
Q

what is the third most common solid tumor in children and adolescents

A

thyroid cancer

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68
Q

what is the first line treatment of graves disease?what are other treatment options?

A

methimazole** (agranulocytosis- labs before starting is CBC, LFTs)
2nd line- PTU (leading cause of fulminant hepatic failure)
radioactive iodine (2nd line- fail to go into remission after 1-2 years after tx or significant side effects with the antithyroid medications)
surgery (3rd line tx- kids with significant eye disease as radioactive iodine can make that worse, bulky thyroid gland or age <5 years)

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69
Q

what is the most common preventable cause of significant cognitive impairment?

A

congenital hypothyroidism

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70
Q

what is the stress dose of hydrocortisone if age <3, age 3-12, age >12?

A

age <3: 25mg
age 3-12: 50mg
age >12: 100mg

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71
Q

what is the treatment for adrenal crisis? minor stress versus major stress

A

minor stress: 2-3x replacement dose of hydrocortisone, or 40mg/m2/day
major stress: hydrocortisone 100mg/m2 IV/IM stat and continued as divided dose q6-8 hours

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72
Q

what is the most common mutation associated with congenital adrenal hyperplasia

A

21- hydroxylase deficiency
classic- 75% classic salt wasting CAH, the rest are simple virulizing
non-classic- late onset

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73
Q

early morning cortisol <83 nmol/l is highly suggestive of what?

A

adrenal insufficiency

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74
Q

what is the expected cortisol response to ACTH stimulation test?

A

≥500 nmol/L

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75
Q

what is the triad for APS1? what is the mutation?

A

MHA
AIRE gene mutation
1. mucucutaneous candidiasis (1st sign)
2. hypoparathyroidism (usually before puberty)
3. Addisons disease (usually in adolescents)
also has hypothyroidism

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76
Q

what is the triad for APS2?

A 
TAT
polygenic
1. autoimmune thyroid disease
2. Addison disease
3. type 1 diabetes
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77
Q

what is the best screening test for Cushings?

A

24 hour urinary free cortisol- to establish if cortisol excess is present
(not a morning cortisol- use that for adrenal insufficiency)

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78
Q

what is cushing disease

A

excess pituitary ACTH production

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79
Q

what is the active form of vitamin D

A

1,25 vitamin D

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80
Q

what is the cause of cushing syndrome <5, >5?

A

<5: adrenal pathology (ex: McCune Albright Disease)

>5: pituitary disease most common

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81
Q

what are the main hormones that will affect your serum calcium?

A
  1. 1, 25- vit D

2. PTH

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82
Q

if checking total calcium what other investigation must you order?

A

albumin

a change in albumin by 10g/l will change your total calcium by 0.2mmol/l

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83
Q

what effect does pH have on ionized calcium?

A

alkaLOWsis

alkalosis will lower your ionized calcium

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84
Q

what is the metabolism of vitamin D

A

Vitamin D is metabolized in the LIVER to 25-OH vit D

25-OH vit D is metabolized in the KIDNEY to 1, 25(OH)2 vit D

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85
Q

what is the storage form of vitamin D?

A

25-OH vit D

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86
Q

who should you screen for vitamin D deficiency?

A 
known bone disease (rickets, osteoporosis)
chronic kidney disease
liver disease
malabsorption conditions
medications (anticonvulsants)
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87
Q

what is the appropriate response to an elevated serum calcium

A

suppression of PTH
decreased bone resorption
decrease in 1,25- vit D
increase in urinary excretion

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88
Q

what is the appropriate response to a decreased serum calcium

A

increase of PTH
increased bone resorption
increased 1, 25- vit D
decreased urinary excretion

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89
Q

list 3 clinically significant fractures *impt

A
  1. 2 or more long bone fractures by 10 years
  2. 3 or more long bone fractures by 19 years
  3. 1 or more vertebral compression fractures (loss of >20% of vertebral body height at any age)
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90
Q

what are the stages of female pubertal development?

A

breast
hair
growth
menarche

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91
Q

what are the stages of male pubertal development

A

testicular volume
penile length
hair
growth

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92
Q

what happens with calcium and phosphate as PTH increases? decreases?

A

PTH increases= Ca increases= Phosphate decreases

PTH decreases= Ca decreases= Phosphate increases

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93
Q

List some causes of hypoparathyroidism (6)

A

aplasia or hypoplasia (DiGeorge)
autoimmune parathyroiditis (isolated of with type 1 APS)
infiltrative lesions (hemosiderosis and Wilsons disease)
post surgical hypoparathyroidism
post radioactive iodine to thyroid gland
PTH receptor defects

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94
Q

List some causes of vitamin D deficiency

A

reduced intake or production (poor dietary intake/supplementation, lack of sunlight, malabsorption (fat soluble vitamin), maternal vitamin D deficiency)
severe liver disease
anti seizure medications
renal failure

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95
Q

what is the recommended daily intake of vit d for 0-12 months, 1-3 years, 4-18 years

A

0-12 months: 400IU
1-3 years: 600IU
4-18 years: 600-1000IU

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96
Q

what is the recommended daily intake of calcium for 0-12 months, 1-3 years, 4-18 years

A

0-12 months: 250mg
1-3 years: 700mg
4-18 years: 1000-1300mg

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97
Q

what is the treatment of hypocalcemia?

A

significant symptoms: IV calcium gluconate

oral: calcium carbonate (50-100mg/kg/day in divided doses)

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98
Q

what is the treatment for hypercalcemia?

A

hyperhydration *
low calcium diet
calcitonin (only works for a short time and repeated doses will lead to decreased effect)
bisphosphonates (take 48-72h to see effect)
steroids- useful for subcutaneous fat necrosis

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99
Q

list 3 key things that might suggest Williams syndrome

A

elfin facies
supravalvular aortic stenosis
hypercalcemia

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100
Q

what are the clinical features of Rickets

A 
1. widening of growth plates (epiphyses)
swelling of wrists and knees
rachitic rosary
craniotabes (softening of skull bones)
2. softening of the bones
genu valgum, varum, wind-swept deformities
fractures
3. painful bones
- delayed motor milestones
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101
Q

what are the two forms of rickets

A

calcipenic rickets

phosphopenic rickets

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102
Q

what is the laboratory marker of rickets

A

ALP

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103
Q

what is the best test for nutritional vitamin D deficiency

A

25-OH vit D

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104
Q

what screening should be done at diagnosis for Type 2 DM?

A

peripheral neuropathy- yearly
retinopathy- yearly
nephropathy- yearly (first morning or random ACR)
dyslipidemia- yearly (Fasting TC, HDL, LDL, TG
hypertension- at every clinical encounter, at least biannually)
NAFLD- yearly (ALT and/or fatty liver on ultrasound)
PCOS- yearly
OSA- yearly
depression, binge eating- biannually

105
Q

what is the target for A1C for most children with type 2 DM

A

≤ 7.0 %

106
Q

what children with type 2 DM should get insulin and metformin at diagnosis

A

A1C ≥ 9
signs of metabolic decompensation (DKA)
insulin should be weaned once glycemic targets are achieved

107
Q

screening for type 2 DM should be considered every 2 years using a combination of an A1C and a FPG or random plasma glucose in children and adolescents with any of the following conditions

A
  1. ≥3 risk factors in non pubertal children beginning at 8 years of age or ≥ 2 risk factors in pubertal children
    - obesity
    - member of high risk ethnic group (African, arab, asian, hispanic, indigenous or south asian)
    - first degree relative with type 2 DM and/or exposure to hyperglycaemia in utero
    - signs or symptoms of insulin resistance (acanthosis nigricans, hypertension, dyslipidemia, NAFLD (AST >3x upper limit of normal or fatty liver on ultrasound)
  2. PCOS
  3. IFG and/or IGT
  4. use of atypical antipsychotic medications
108
Q

Children and adolescents <18 years of age with Type 1 DM should aim for an A1C target of what?

A

A1C ≤ 7.5%
in children <6 particular care to minimize hypoglycemia because of the potential association with layer cognitive impairemnt

109
Q

when should routine screening for dyslipidemia occur in Type 1 DM

A

routine screening for dyslipidemia should begin at 12 years of age, repeat screening after 5 years (age 17)

110
Q

all children with Type 1 DM should be screened for hypertension how often?

A

biannually

111
Q

How often should children with Type 1 DM be screened for thyroid problems

A

at diagnosis and every 2 years with TSH and thyroid peroxidase antibodies
more frequent screening if antibody positive, thyroid symptoms or goiter

112
Q

when should children with Type 1 DM be screened for celiac?

A

if they have symptoms of classic or atypical celiac disease

113
Q

How is hypoglycemia for type 1DM treated at home

A

mini doses of glucagon if inability or refusal to take oral carbohydrate
(10mcg per year of age)
min 20mcg max 150mcg

114
Q

an unconscious child >5 at home with hypoglycemia should be treated with what? <5?

A

1mg glucagon SC or IM

<5 0.5mg glucagon

115
Q

what screening is required for type 1 DM

A

neuropathy- children >15 with poor metabolic control should be screened yearly after 5 years of type 1 DM
nephropathy- yearly starting at age 12 in those with type 1 DM >5 years
dyslipidemia- >12 (<12 if BMI >97%ile)
retinopathy- yearly screening starting at age 15 in those with type 1 DM >5 years
hypertension- all children twice annually

116
Q

what is the average age for menarche?

A

13

117
Q

what are some features on physical exam for Turner syndrome?

A 
short stature
webbed neck
low hairline
melanocytic nevi
coarctation of the aorta/bicuspid aortic valve
cubitus valgus
peripheral lymphedema at birth
streak ovaries
118
Q

who needs an MRI for precocious puberty?

A

all boys

girls <6

119
Q

a girl with premature adrenarche is at risk for what later in life?

A

PCOS

120
Q

6 year old female with premature adrenarche. What is the mostly likely source of androgens?

A

adrenals

121
Q

what are the BMI cutoffs for normal, overweight and obese

A

normal <85th %ile
overweight 85-97th %ile
obese >97 %ile
severely obese >99.9% ile

122
Q

what are some causes of hypoglycemia with no ketone production (3)

A

hyperinsulinism (infant of diabetic both, insulin tumor, beck with wiedeman)
fatty acid oxidation disorder
GSD type I

123
Q

what is the definition of primary amenorrhea

A

no menses by age 14 in absence of secondary sexual characteristics
or
by age 16 with secondary sexual characteristics

124
Q

what is secondary amenorrhea

A

no menses for 3 months or more in a woman who was previously menstruating

125
Q

what is the normal growth velocity in prepubertal children

A

5cm/year

126
Q

What is Chvostek’s sign

A

Chvostek’s sign is the twitching of the facial muscles in response to tapping over the area of the facial nerve.

127
Q

what is Trousseau sign

A

place a blood pressure cuff on the patient’s arm and inflating to 20 mm Hg above systolic blood pressure for 3-5 minutes.
see flexion of the wrist and metacarpal phalangeal joints can be observed with extension of the interphalangeal joints and adduction of the thumb

128
Q

what are two physical exam findings of hypopituitarism

A

chvostek’s sign

trousseau sign

129
Q

what is the equation for BMI

A

weight in kg/ height in m2

130
Q

what is the treatment for central precocious puberty

A

GnRH agonist- Lupron

you take away the GnRH pulses

131
Q

what are 3 causes of dysmenorrhea and what is the treatment

A 
1. primary dysmenorrhea- absence of other diseases
 endometriosis
2. PID
3. tumor
4. polyp
5. fibroid
6. miscarriage, ectopic pregnancy
7. imperforate hymen
TX: NSAIDS, OCP
132
Q

what is McCune Albright? what is the triad?

A

a syndrome of endocrine dysfunction
Triad: precocious puberty, cafe au lait macules, polyostotic fibrous dysplasia

Endocrine manifestations:
gonads- peripheral precocious puberty
thyroid-associated with hyperthyroidism*
kidney- renal phosphate wasting
pituitary- growth hormone excess*
adrenal- rare, cushing syndrome
autonomous hyperfunction of 1 or more glands (thyroid adrenal, pituitary)

133
Q

what is the average age for girls to have breast bud, pubic hair, PHV, menarche, adult breast

A 
breast bud- 10.5
pubic hair- 11
PHV- 11.6
menarche- 13
adult breast- 14.6
134
Q

Addisons disease is associated with what lab abnormalities

A

increased ACTH

increased renin

135
Q

what is the starting dose for insulin for DKA

A

0.1 units/kg/hour of short acting insulin

after 1 hour of IV fluids

136
Q

what is the equation for correcting sodium in dka

A

measured sodium + 2x [(glucose-5.5)/ 5.5]

fall in corrected sodium is a warning sign for cerebral edema

137
Q

fall in what two things are associated with cerebral edema

A

fall in corrected sodium

fall in serum osmolality (2Na +glucose)

138
Q

what are some risk factors for cerebral edema

A

age <5
new onset diabetes
IV bolus of insulin
rapid administration of hypotonic fluids
early IV insulin infusion (within the first hour of fluids)
failure of serum sodium to rise during treatment
use of bicarbonate
high initial serum urea
low initial partial pressure or arterial carbon dioxide

139
Q

what are some symptoms of cerebral edema

A 
headache
drowsiness, irritability, confusion
voiding
decreased HR
increased BP
coma
respiratory arrest with brain herniation
140
Q

how do you treat cerebral edema?

A 
raise head of bed
decrease IV fluids
3%NS or mannitol 5mL/kg over 20 minutes
intubation with hyperventilation
once stable- imaging
141
Q

T1D insulin regime

A

TDD
2/3 TDD in AM- 2/3 intermediate acting; 1/3 rapid acting
1/3 TDD in PM- 2/3 intermediate acting; 1/3 rapid acting

142
Q

if a patient with type 1 diabetes has recurrent hypoglycemia what should you consider?

A

celiac disease

addisons

143
Q

what is the typical insulin regime for insulin pump

A

Basal insulin- 40-50% TDD
Bolus insulin- 50-60%
combination of carbohydrate ration
correction boluses: sensitivity factor (1 unit of insulin brings down the blood glucose by x mmol/L to target blood glucose)

144
Q 
what should you tell a patient with type 1 DM to do if they have an intercurrent illness and the following blood glucose values:
<6
6-14
above 14 (negative or + urine ketones)
above 14 (+++ urine ketones)
A

<6: decrease normal insulin dose at least 10-20%

6-14: give the usual dose of insulin at the normal time. Do not give extra. Recheck in 4 hours.

above 14: give more H/Rp insulin (up to 10% of TDD) NOW. Recheck in 4 hours

above 14, +++ ketones: give for H/Rp insulin (at least 10-20% of TDD) NOW. Recheck in 4 hours.

145
Q

what is the criteria for DKA

A
  • Hyperglycemia (blood glucose >11 mmol/L
  • Venous pH <7.3 or serum bicarbonate <15 mmol/L
  • Ketonemia (blood ß-hydroxybuyrate ≥3 mmol/L) or moderate or large ketonuria.
146
Q

what 3 things do the adrenal glands produce

A

corticosteroids
mineralocorticoids
androgens

147
Q

what is the typical daily treatment for adrenal insufficiency

A

Hydrocortisone 6-8 mg/m2/day DIV TID

148
Q

what would you see with morning cortisol, corticotropin stimulating test for adrenal insufficiency

A

morning cortisol <140

ACTH stimulation: peak >500 at 60 minutes excludes adrenal insufficiency

149
Q

How do you assess mineralocorticoid deficiency for AI

A

renin and aldosterone

High renin and low aldosterone

150
Q

what is the treatment for mineralocorticoid deficiency with AI

A

fludrocortisone (florinef)

151
Q

what is Cholecalciferol? Calcitriol?

A

Cholecalciferol = 25(OH)D

Calcitriol / Alfacalcidol = 1, 25(OH)D

152
Q

what two genetic conditions are predisposed to the development of autoimmune thyroiditis?

A

Trisomy 21 and Turner syndrome are predisposed to the development of autoimmune thyroiditis.

153
Q

List some physical exam findings for congenital hypothyroidism

A 
hypothermia
acrocyanosis
respiratory distress
large fontanels
abdominal distention
lethargy and poor feeding
prolonged jaundice
edema
umbilical hernia
constipation
large tongue
dry skin
hoarse cry
sinus bradycardia
154
Q

what is the treatment for hypothyroidism

A

levothyroxine

155
Q

what are the electrolyte findings with CAH

A

hyponatremia
hyperkalemia
acidosis

156
Q

what are the clinical manifestations of Cushing syndrome

A 
progressive central or generalized obesity
marked failure of longitudinal growth
hirsutism
weakness 
a nuchal fat pad
acne
striae
hypertension
and often hyperpigmentation when ACTH is elevated.
157
Q

what is the inheritance pattern of nephrogenic diabetes inspidius

A

x-linked recessive

predominantly in males

158
Q

how do you screen for primary hypothyroidism?

A

TSH

159
Q

what is the optimal time frame for treatment of congenital hypothyroidism?

A

within the first 7-14 days of life

160
Q

What is considered an elevated screen for congenital hypothyroidism and what do you do?

A

elevated: TSH >=15
TSH 15-(30)40- repeat TSH with free T4
TSH >40, repeat labs first to confirm diagnosis, start thyroxine immediately and imaging(nuclear scan/ultrasound) for diagnosis

161
Q

what causes neonatal hyperthyroidism

A

Transplacental passage of thyroid stimulating antibodies

identify at risk mother by TRAb titre (fetus should be monitored carefully)

162
Q

what are some symptoms of hypothyroidism

A 
growth failure
weight gain
dry skin and hair
constipation
slow heart rate
normal brain development if hypothyroidism starts after first 3 years of life
163
Q

what are some symptoms of hyperthyroidism

A 
fidgety
hyperactive
weight loss despite large appetite
tremor
sweaty
hot
poor concentration
anxiety
increased frequency of bowel movements
palpitations
fatigue
164
Q

what is the normal growth velocity from 0-12 months

A

24cm/year

165
Q

what is the normal growth velocity from 12-24 months

A

12-18cm/year

166
Q

what is the normal growth velocity from 24-36 months

A

8-12cm/year

167
Q

what is the normal growth velocity in adolescence

A

8-12cm/year

168
Q

what is the differential for peripheral precocious puberty in girls? boys? both?

A

girls: ovarian tumor, ovarian cyst
boys: leydig cell tumor, hCG secreting tumor
both:
exogenous sex steroids
untreated CAH
adrenal tumor
McCune Albright
primary hypothyroidism

169
Q

what are causes of central precocious puberty?

A

hypothalamic hamartomas (galactic seizures)
other tumprs
cerebral malformations
idiopathic (majority of girls)

170
Q

what is the most common cause of delayed puberty in both boys and girls?

A

constitutional delayed puberty

171
Q

what are the goals of treatment for precocious puberty?

A

to preserve adult height

psychosocial concerns associated with precocious pubertal onset

172
Q

What is the equation for mid parental height

A

moms height + dads height +/- 13/ 2

173
Q

what are features of ketotic hypoglycemia

A 
Common form of childhood hypoglycemia
18M-5Y 
Typically during periods of intercurrent illness, limited food intake 
Associated with ketonuria and ketonemia
diagnosis of exclusion
174
Q

what are the stages of female pubertal development?

A

thelarche, adrenarche, growth, menarche

175
Q

what are the stages of male pubertal development

A

testicular size, penile length, hair, growth

176
Q

what is a clue to peripheral precocious puberty in girls

A

estrogen depends effects predominate

177
Q

what is a clue to peripheral precocious puberty in boys

A

testes are inappropriately small

178
Q

what is most likely for a child with ambiguous genitalia with bilateral masses in the folds

A

almost always testes, therefore a undervirilized male

179
Q

what percentage of thyroid nodules are malignant?

A

20%

much greater than in adults (most thyroid nodules in adults are benign)

180
Q

what is the pathogenesis of type 1 DM

A

destruction of the beta cells of the pancreas

80% must be destroyed to affect glycemic control

181
Q

what is the initial ketone formed in DKA

A

Acetoacetic acid

182
Q

what are possible complications of DKA

A

cerebral edema
DVT
aspiration
cardiac arrhythmias (from electrolyte derangement)
increased amylase and lipase (mild elevation in approx 40%)
acute kidney injury
cognitive impairment

183
Q

what is required for differentiation of sex organs?

A

sex determining region on Y chromosome

gonads are biopotential until 6-8 weeks

184
Q

what are adverse effects of steroids

A 
growth suppression
myopathy
AVN
osetopenia
immunosuppression
peptic ulceration
HTN
hyperlipidemia
cataracts
pseudotumor cerebri
185
Q

what are the causes of hypercalcemia?

A 
High 5-Is
hyperparathyroidism
Idiopathic: williams
Infantile: subQ fat necrosis
Infection: TB
Infiltration: Malignancy, sarcoid
Ingestion
skeletal disorders
186
Q

what are the main causes of hypocalcemia

A 
vit D deficiency
renal insufficiency
nephrotic syndrome
hypoparathyroidism
pseudohypoparathyroidism
187
Q

what are the possible side effects of growth hormone (4)

A

SCFE**
pseudotumor cerebri**
worsening scoliosis
hyperglycaemia

188
Q

who can be treated with GH even if they are not GH defieicnt

A 
Turner syndrome
noonan symdrome
ISS
chronic renal failure
PWS
SGA
189
Q

what hormones are secreted by the anterior pituitary gland?

A 
FATPIG
F- FSH/LH
A- ACTH
T- TSH
PI-Prolactin
G- GH
190
Q

What are the two hormones secreted by the posterior pituitary gland?

A

oxytocin

ADH

191
Q

how do you distinguish between primary and secondary adrenal insufficiency on clinical features and lab work?

A

Primary adrenal insufficiency: adrenal gland dysfunction

  • elevated ACTH
  • low cortisol or low mineralcorticoid (hyponatremia/hyperkalemia)
  • will see hyperpigmentation (due to pituitary gland trying to stimulate the adrenals and also secreting MSH)

Secondary adrenal insufficiency:
hypothalamic or pituitary dysfunction
-low ACTH
-low cortisol, normal mineralocorticoid (controlled by RAAS system, not hypothalamus or pituitary; thus no hyponatremia/hyperkalemia)

192
Q

what are the clinical features of hypoparathyroidism? (5)

A 
hypocalcemia
delayed teeth eruption/strength
scaly skin
mucucuntaneous candidiasis
cataracts
***all from hypocalcemia
193
Q

what are the exam findings of hypocalcemia? (6)

A

muscle spasms
chovtek’s sign: facial nerve spasm on tapping
trousseaus: hand spasm with blood pressure cuff inflated
seizures
tetany
hyperreflexia

194
Q

which is the only pituitary hormone that is suppressed by a hypothalamic factor?

A

prolactin- inhibited by hypothalamic release of dopamine
thus in hypothalamic deficiency, you get a decrease in most pituitary hormone secretions but can have increase in prolactin secretion

195
Q

what is the screening test for growth hormone deficiency?

A

IGF-1

if this is abnormal then do GH stimulations test

196
Q

what is a complication of Lupron

A

sterile abscesses at site of injection

197
Q

what tests should be included in a critical sample for hypocalcemia? (10)

A 
***MOST IMPORTANT
PO4 ***
PTH ***
Calcium ***
25-OH vIt V
1,24 OH vit D
ALP
Mg ***
consider liver function/enzymes
consider renal function
urine calcium: creatinine ration ***
**2 lavender + 2 green tubes
198
Q

how do you calculate glucose infusion rate

A

(%glucose in solution)(TFI)/144

199
Q

what are the diagnostic criteria for hyperglycemic hyperosmolar syndrome?

A

severe hyperglycaemia (BG >33)
serum osmolality >330 mol/L
absence of significant ketosis: HCO3>15, urine ketones negative or trace

200
Q

what is the management of hyperglycemic hyperosmolary syndrome

A

Bolus NS 20mL/kg
- assume 12-15% fluid deficit
calculate this and correct deficit over 24-48 hours
don’t be afraid to bolus
begin insulin when glucose concentration no longer declining with fluid alone
- 0.025-0.05 units/kg/h
aim to decrease BG by 3-4 mmol/L/h
tend to have higher fluid requirements than DKA
consider lower dose and later initiation of insulin infusion

201
Q

what are possible causes of central diabetes insipidus?

A 
post head trauma (ie basal skull fracture)
post neurosurgery
post radiation
CNS tumor of the pituitary gland
septo-optic dysplasia
202
Q

You have diagnosed a child with diabetes insipidus and would like to figure out if it’s central vs. nephrogenic (ie. is the posterior pituitary gland not making any ADH or is the kidney unable to respond to ADH?). What is your next best test?

A

Trial dose of DDAVP (desmopressin), then measure lytes, serum osmolality, urine lytes and urine osmolality.

  • if there is a response to the DDAVP and the kidneys are able to concentrate the urine, then this means the post pit is not making ADH! Next step would then be MRI head to r/o tumor
  • if there is NO response to the DDAVP, then you’ve made the diagnosis of nephrogenic DI
203
Q

What is the classic triad of pheochromocytoma?

A
  1. Headache - ? from htn
  2. Palpitations/tachycardia
  3. Diaphoresis
    * ***will have sustained hypertension so if you see palpitations/diaphoresis but you don’t see hypertension, it’s most likely not a pheo
  • **spot urinary catecholamines are highly sensitive but NOT specific! Ie. lots of false positives
  • best test: 24 hr urinary catecholamines
204
Q

What is the differential diagnosis for hyperthyroidism? (4)

A
  1. Graves disease = most common = thyroid gland stimulated by anti thyroid receptor antibodies
  2. Subacute thyroiditis
  3. Suppurative thyroiditis
  4. Toxic uninodular goitre
205
Q

During what age group is the following most likely to present:

  • complete androgen insensitivity
  • partial androgen insensitivity
A
  • complete androgen insensitivity: presents in adolescence since the patient is phenotypically female so no one will suspect the diagnosis until she presents with primary amenorrhea
  • partial androgen insensitivity: presents at birth since the patient will have some virilization of external genitalia but not enough
206
Q

Why do you see hypocalcemia in patients with DiGeorge syndrome?

A

Hypoplasia or agenesis of parathyroid glands = thus no PTH to regulate serum calcium levels

207
Q

What is an ACTH stim test used to diagnose?

-how is it done?

A

Adrenal insufficiency = used to determine whether glucocorticoid insufficiency is due to primary or secondary cause

  • steps:
    1. measure cortisol level
    2. give ACTH
    3. re-measure cortisol level to see if it has risen! If it has, then this means that the adrenal gland is working fine and there is a central cause of adrenal insufficiency (hypothalamic or pituitary gland dysfunction). If there is no change, then it is a primary adrenal gland problem (most likely autoimmune)
208
Q

What are the types of adrenal androgens?

A 
DHEAS = weak androgen
Androstenedione = weak androgen 
Testosterone = strong androgen 
DHT = strong androgen
  • **In adult males: adrenals produce 5% of androgens
  • **In adult females: adrenals produce 50% of androgens
209
Q

What is secreted by medullary carcinoma of the thyroid?

A

Calcitonin!

-but usually see normal calcium and phosphorus levels

210
Q

What hormones influence growth? (6)

A
  1. Growth hormone
  2. Insulin
  3. Insulin Growth Factor -1
  4. Cortisol
  5. TSH
  6. Androgens/estrogen
211
Q

What is the most accurate way of predicting adult height? What is the least accurate way?

A

Most accurate - bone age

Least accurate - mid parental height

212
Q

At what Tanner/SMR stage does axillary hair production occur for:

  • boys
  • girls
A

Boys: stage 4
Girls: stage 3

**Remember that girls mature more quickly than boys!

213
Q

What does the adrenal medulla secrete?

What does the adrenal cortex secrete?

  • glomerulosa
  • fasciculata
  • reticularis
A

Adrenal medulla:
-catecholamines

Adrenal cortex:

  • zona glomerulosa: mineralocorticoids aka aldosterone (think glomerulus in kidney)
  • zona fasciculata: glucocorticoids
  • zona reticularis: sex hormones + small amt glucocorticoids (“I had sex with reticularis”)
214
Q

What are the 3 urine catecholamines you test for in cases of possible adrenal medulla tumors?

A
  1. VMA
  2. Metanephrine
  3. Normetanephrine
215
Q

What are the steps of sex differentiation in utero?

A
  1. If there is a Y chromosome, then the bipotential gonads can differentiate into testes between 6-8 wks.
  2. The testes produce testosterone (Leydig cells) and anti-Mullerian hormone (Sertoli cells) –> testerone directs formation of the internal male reproductive organs from Wolffian ducts and AMH suppresses development of the Mullerian ducts (ie. preventing female internal reproductive organ formation)
  3. At 8-12 wks, the testosterone made by testes is changed to DHT (by 5 alpha reductase). DHT causes formation of male external genitalia. If there is no DHT, then female external genitalia develops.

**In infants with CAH, there is an excess of DHT due to build up of intermediate metabolites and thus female babies can have virilization (formation of male external genitalia) while still having normal female internal reproductive organs

216
Q

What is the classic triad of septo-optic dysplasia?

-diagnostic criteria?

A

Triad:

  1. Optic nerve hypoplasia (manifests as nystagmus)
  2. Pituitary hormone abnormalities: growth failure, hypothyroidism, adrenal insufficiency, diabetes insipidus (varying degrees)
  3. Midline brain defects: agenesis of septum pellucidum and/or corpus callosum
    - need 2/3 of features for diagnosis (this is up for debate)
217
Q

what is MEN2

A

MPP
medullary thyroid cancer, pheochromocytoma, parathyroid adenoma

Medullary thyroid cancer: 98% to 100% with MEN2A are affected

Pheochromocytoma, a typically benign (noncancerous) tumor of the adrenal glands: 50% with MEN2A affected

Parathyroid adenoma (a benign tumor) or hyperplasia, meaning increased size of the parathyroid gland: 5% to 10% with MEN2A affected

218
Q

Diff Dx of secondary amenorrhea:

A 
Central
·      Systemic illness
·      Malnutrition
·      Excessive exercise
·      Stress
·      Hypo/hyperthyroidism
·      Cushing’s syndrome
·      Prolactinoma
·      Tumor
·      Surgery
·      Radiation
Gonadal
·      PCOS
·      Knocked up
·      Ovarian failure
219
Q

What are 2 tests that can help in the investigation of secondary amenorrhea?

A 
beta-hCG
FSH / LH (elevated in ovarian failure, low if central cause)
TSH/Free T4
Protactin
CBC, ESR, RFT, LFT, lytes
Cortisol
220
Q

Ddx of pubertal gynecomastia

A 
Physiologic gynecomastia
Decreased androgen production
Congenital abnormalities of testosterone production
Drugs that decrease androgen production 
Estrogen-producing tumors
Adrenal disease
Liver disease/cirrhosis
Starvation
221
Q

Parents fearful of Listeria and thus have become vegan (no meats, eggs, milk). What dietary deficiency are they at risk for?

A 
Iron **
Vit B12 **
Vit D
Calcium
Zinc
EPA/DHA
222
Q

what is the most common fatty acid oxidation disorder

A

MCAD

223
Q

what is the treatment for hyperinsulinism

A

IV glucose
diazoxide
somatostatin analogs (octreotide)

224
Q

what is physiologic gynecomastia? how many boys get this? is it tender? when does it usually resolve?

A

presence of true breast tissue (not adipose tissue) in males
Up to two thirds of boys develop physiologic gynecomastia during puberty
Boys who have physiologic gynecomastia exhibit palpable, sometimes tender, subareolar breast tissue. Breast enlargement is often asymmetric; tissue may appear only unilaterally or may appear bilaterally, but at different times.
Breast enlargement typically regresses spontaneously after several months, but it may persist for as long as 2 years. Gynecomastia that persists beyond 2 years is unlikely to resolve on its own.

225
Q

what are the counter regulatory hormones

A 
Insulin
Glucagon- opposite of insulin
Growth hormone- helps with gluconeogenesis and glycogenolysis
Cortisol- helps with gluconeogenesis
Epinephrine- helps with gluconeogenesis
226
Q

what is the best test for precocious puberty?

A

GnRH stimulation test

if LH increased >5 after stimulation= central

227
Q

what is the classic tumor associated with central precocious puberty?

A

hypothalamic hamartoma (gelastic seizures)- secretes GnRH

228
Q

tanner staging penis

A 
tanner 1 preadolescent
tanner 2 minimal change/enlargement
tanner 3 lengthens
tanner 4 larger; gland and breadth increase in size
tanner 5 adult size
229
Q

tanner staging scrotum

A 
tanner 1 preadolescent
tanner 2 enlarged scrotum, pink, altered texture
tanner 3 larger
tanner 4 larger, SCROTUM DARK
tanner 5 adult size
230
Q

tanner staging breast development

A

tanner 1 preadolescent
tanner 2 breast budding
tanner 3 breast and areola enlarged, no contour separation
tanner 4 areola and papilla form SECONDARY MOUND
tanner 5 mature, nipple projects, areola part of general breast contour

231
Q

tanner staging public hair

A

tanner 1 none
tanner 2 sparse, long downy hairs, lightly pigmented
tanner 3 darker, beginning to CURL, increase amount
tanner 4 coarse, curly, abundant but less than adult
tanner 5 adult distribution, spread to MEDIAL SURFACE OF THE THIGHS

232
Q

what is the pattern on growth charts for systemic illness versus endocrinopathies

A

Chronic illnesses cause poor weight gain/weight loss, followed by poor growth. Therefore, if both weight AND height are low it’s likely due to a systemic illness -> “thin and short”

Endocrinopathies tend to cause increased weight and short stature -> “short and fat”

233
Q

what is the first test to order if you suspect precocious puberty?

A

The first step in work-up up precocious puberty is to determine whether it is central or peripheral.
LH/FSH

234
Q

most common germ cell tumor in prepubertal children

A

yolk sac tumor

high AFP

235
Q

Give the most common reason for false positive newborn screen for congenital hypothyroidism

A

Screening too early (before 48hrs)

236
Q

What is best test to determine initial dose of thyroid replacement in Hashimoto’s

A

TSH

237
Q

how do you determine anticipated adult height

A

MPH +/- 8.5cm

238
Q

what are two recommendations to ensure maximal absorption of levothyroxine?

A

take on an empty stomach

do not take it with soy/milk

239
Q

after being diagnosed with congenital hypothyroidism and starting treatment when should you repeat TSH?

A

in 2 weeks and every 4-6 weeks after a dose change, every 3 months once stable

240
Q

At what age are most children sure of their gender identity?

A

4

241
Q

Most common sign on exam for hypocalcelmia

A

Most common sign on exam: hyperreflexia!
Chvostek sign – tapping on the facial nerve makes the side of their mouth twitch
Trousseau sign – sustained BP cuff ~20mmHg above systolic BP for 3 minutes produces a carpopedal spasm (more specific)

242
Q

what is one cause of congenital growth hormone deficiency? acquired growth hormone deficiency?

A

congenital- septo-optic dysplasia

acquired- craniopharyngioma

243
Q

what is the main difference between SIADH and CSW

A

SIADH- low urine output
CSW- high urine out and hypovolemia

SIADH
hydration status: euvolemia
urine output: low
Serum Na: low
serum osmolality: low
urine Na: high
urine osmolality: high
CSW:
hydration status: HYPOVOLEMIA
urine output: HIGH
Serum Na: low
serum osmolality: low
urine Na: high ++
urine osmolality: high
244
Q

DI versus SIADH

A 
SIADH
hydration status: euvolemia
urine output: low
Serum Na: low
serum osmolality: low
urine Na: high
urine osmolality: high
DI:
hydration status: hypovolemia
urine output: high
Serum Na: high
serum osmolality: high
urine Na: low
urine osmolality: low
245
Q

TSH <40 on newborn screen for congenital hypothyroidism what would you do?

A

repeat TSH and free T4 and followup in 1-2 weeks

246
Q

what are the two main causes of primary adrenal insufficiency? secondary?

A

Addisons
CAH

secondary or central: withdrawal of glucocorticoid administation

247
Q

how might a patient with Addisons disease present?

A 
non-specific symptoms
weight loss
fatigue
hypotension
hyperpigmentation
hyponatremia *
hyperkalemia *
hypoglycemia *
248
Q

what is the screening test for adrenal insufficiency

A

early morning cortisol

249
Q

stress doses for illness or surgery for someone who has been on chronic glucocorticoids should continue for how long?

A

continue stress dosing for 6-12 months after discontinuation of glucocorticoids

250
Q

how much vitamin D should be given to pregnant and lactating mothers especially during the winter months?

A

consider 2000IU

251
Q

how much vitamin D during the first year of life for someone living north of the 55th parallel (Edmonton)

A

800IU vit D

252
Q

what is osteoporosis

A

skeletal disorder characterized by decreased bone strength
usually caused by an underlying medical disorder or medication
look for clinically significant fractures
1. 2 or more long bone fractures by 10 years
2. 3 or more long bone fractures by 19 years
3. 1 or more vertebral compression fractures (loss of >20% of vertebral body height at any age)

253
Q

what are 2 causes of primary osteoporosis? 5 causes of secondary osteoporosis?

A
  1. osteogenesis imperfecta
  2. Ehlers Danlos
    other connective tissue problems

secondary:
1. GH
2. Hyperthyroidism
3. vit D deficiency
4. chronic illness
5. physical inactivity

254
Q

what test should be done if you have an infant <6 mo of age with diabetes

A

GENETIC TESTING
infants less than 6 months of age do not get type 1 DM
would be neonatal diabetes

255
Q

what is the diagnostic criteria for PCOS

A
  1. evidence of hyperandrogenism

2. abnormal uterine bleeding pattern

256
Q

who should have lipid screening

A

Positive family history of dyslipidemia or premature cardiovascular disease (1st or 2nd degree relative)
< 55 years of age for males
< 65 years of age for females
If family history unknown or in presence of other cardiovascular disease factors
Overweight (BMI > 85th%) or Obese (BMI > 95th%)
Hypertension (BP > 95th %)
Cigarette smoking
Diabetes Mellitus

Start between the ages of 2-10 years
Retest q 3-5 years- if initial screen normal
screen with a fasting lipid profile

257
Q

Pharmacotherapy (statin) should be considered in children > 8 years if:
LDL-C >???

A

Pharmacotherapy (statin) should be considered in children > 8 years if:
LDL-C > 4.9 mmol/L
LDL-C > 4.1 mmol/L + family history of early heart disease or > 2 risk factors present
LDL-C > 3.4 mmol/L + Diabetes Mellitus

258
Q

what is the target for LDL while on statin?

A

LDL-C < 3.0 mmol/L

Pediatrics- Noelle (28 decks)

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