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pediatrics > endocrinology > Flashcards

endocrinology Flashcards

1
Q

the only organ that is not enlarged in macrosomia

A

brain

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2
Q

congenital cardiac defect associations - diabetic mother

A

trans of great vessels

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3
Q

findings in infants of diabetic mothers

A
  1. Macrosomia (2nd and 3rd trimester) –> branchial plexopathy, clavicle fracture, perinatal asphyxia
  2. Small left colon syndrome (1st trimester)
  3. Cardiac anomalies (1st trimester)
  4. renal vein thrombosis (1st trimester)
  5. metabolic findings and effects (2nd or 3rd trimester)
  6. spontaneous abortion (1st trimester)
  7. polycythemia (2nd and 3rd trimester)
  8. neural tube defects (1st)
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4
Q

macrosomia - blood

A

increased output from bone morrow –> polycythemia + hyperviscosity

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5
Q

infants of diabetic mothers - small left colon syndrome

A

congenitally smaller descending colon leads to distention from constipation
diagnosis by barium
treatment siwth smaller + more frequent feeds

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6
Q

infants of diabetic mothers - renal vein thrombosis

A
  • Flank mass + possible bruit

- hematuria + thrombocytopenia

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7
Q

infants of diabetic mothers - Metabolic findings + effects

A

hypglycemia: seizures
hypocalcemia: tetany
hypomagnesia: hypocalcemia + low PTH
hyperbilirubinemia: icterus = kernictuerus

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8
Q

infants of diabetic mothers - Cardiac anomalies

A
  1. asymmetric septal hypertrophy due to obliteration of LV lumen –> low CO (treated with b-blockers and IV fluids)
  2. trans of great vessels
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9
Q

child’s RF for vit D deficient rickets

A
  • sunless environment

- low milk intake

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10
Q

Rickets is caused by lack of

A

Vit D, Ca2+, Phosphorus

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11
Q

children of which age are highest risk for rickets

A

6-24 months because their bones are rapidly growing

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12
Q

Rickets - types

A
  1. Vit D deficinet (low D)
  2. Vit D dependent: inability to convert 25 to 1,25
  3. X-linked hypophosph: innate kidney defect –> inability to retain P
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13
Q

Rickets - presentation

A

child with ulnar/radial bowing and a waddling gait due to tibial femoral bowing

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14
Q

Rickets - diagnostic tests

A
  1. Rachitic rosary-like appearance on CXR of the costochondral joints with cupping and fraying of the epiphyesis
  2. Bowlegs is a characteristic sign
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15
Q

Rickets - types and calcium/phosphate levels

A

Vit D def: normal/low Ca2+, low P
Vit D dep: low Ca2+, normal P
X-linked hypophosph: normal Ca+, low P

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16
Q

Rickets - types and levels of vit D 25 + 1,25

A

Vit D def: both decreased
Vit D dep: normal 25, low 1,25
X-linked: both normal

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17
Q

vit D in milk

A

no

recommended to given Vit D supplements beginning at 2 months if exclusively breastfed

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18
Q

how to diagnose 21 hydroxylase def

A

elevated 17-hydroxyprogesterone

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19
Q

evaluation of precocious puberty

A

bone age (normal or advanced)
A. normal: isolated breast development (premature thelarche or isolated pubic hair delop (premature adrenache –> reassurance
B. adanced: measure basal LH
- high: central
- low: GnRH stimulation test –> If high is central, if still low is peripheral

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20
Q

premature adrenarche is caused by

A

early activation of adrenal androgens and is more common in obese children (mildy elevated dihydroepiandrosterone, normal estrogen + testosterone)
NORMAL BONE AGE

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21
Q

common pathologucal causes of gynecomastia - categories

A
  1. androgen deficiency

2. increased estrogen prodction or peripheral conversion

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22
Q

Common pathological causes of gynecomastia - androgen def

A

Primary or 2ry male hypogonadism, hyperprolactinemia, Renal failure

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23
Q

common pathological causes of gynecomastia - increased estrogen production or peripheral conversion

A
  1. HCG producing tumors
  2. cirrhosis or malnutrition
  3. thyrotoxicosis
    androgen use
  4. Drugs (spironolactone, cimetidine etx)
  5. congenital excessive aromatase activity
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24
Q

Von Gierke disease (type 1) pathophysiology

A

Glucose-6-phosphatase deficiency –> impaired gluconeogenesis and glycogenolysis

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25
Von Gierke disease (type 1) findings
1. Severe fasting hypoglycemia 2. Increased glycogen in liver 3. Increased blood lactate 4. Hepatomegaly 5. incdreased TG 6. increased Uric acid (Gout) DOLL LIKE FACE, SHORT STATURE
26
Pompe disease (type 2) pathophysiology
lysosomal a-1,4-glucosidase with α-1,4-glycosidase activity (Acid maltase) deficiency
27
Pompe disease (type 2) findings
1. Cardiomyopathy 2. hypertrophic cardiomyopathy 3. exercise intolerance 4. Systemic findings leading to early death
28
Cori disease (type 3) pathophysiology
a-1,6-glucosidase deficiency
29
Cori disease (type 3) findings
- Milder form of type 1 with normal blood lactate (and gluconeogenesis is intact) - Accumulation of limit dextrin-like structures in cytosol
30
McArdle disease (type 4) pathophysiology
Skeletal muscle phosphorylase (myophosphorylase deficiency)
31
McArdle disease (type 4) findings / mechanism
1. Increased glycogen in muscle, but cannot break it down leading to painful muscle cramps 2. Myoglobinuria (red urine) with strenuous exercise 3. Arrythmia from electrolyte abnormalities 4. 2nd wind phenomenon noted during exercise due to increased muscular blood flow
32
MCC of congenital hypothyroidism worldwide
thyroid dysgenesis
33
Refeeding syndrome
nutritional rehabilitation in anorexia nervosa --> carbohydrate intake -->insulin secretion --> cellular uptake of P, K+ Mg+ --> arrhythmia and cardiopulmonary failure
34
precocious uberty?
onset of 2ry sexual characteristics in girls younger than 8 and boys younger than 9
35
McCune-Albright syndrome
Gonadotropin-independet precocious puberty that presents with irregular cafe-au-lait macules and fibrous dyspasia of bone
36
MCC of central precocious puberty
idiopathic (negative MRI)
37
congenital adrenal hyperplasia - enzyme deficiency
1. 17α-hydroxylase 2. 21-hydroxylase 3. 11β-hydroxylase
38
17a hydroxylase deficiency - presentation
XY: psuedohermaphroditism (ambiguous genitalia, undescended testes XX: lack secondary sexual development - low cortisol, low sex hormones, high aldosterone
39
21 hydroxylase deficiency - presentation
1. present in infancy (salt wasting) or 2. childhood (precosious puberty) 3. XX: virilization - low cortisol, high sex hormones, low mineralcorticoids
40
21 hydroxylase deficiency - labs
1. increased renin activity | 2. increased 17-hydroxyprogesterone
41
11β-hydroxylase deficiency - presentation
XX virilization - low aldosterone but hugh deoxycorticosteone) - low cortisone
42
congenital hypothyroidism presebts with
1. constipation 2. prolonged jaundice 3. failure to thrive 4. open fontanels MC asymptomatic
43
1. ..... is frequtnely the 1st sign of cretinism | 2. radiology of cretinism
1. prolonged jaundice 2. radiology: X-rays shows poor bone development, thyroid scan shows decreased uptake with malformed thyroids and increased with iodide def
44
short stature - ddx
A. bone age smaller than chronological age: 1. normal growth velocity: constitutional delay 2. abnormal GV: chronic illness, nutritional, endocrine B. Bone age = chronological age 1. normal GV: familiar short stature 2. abnormal GV: genetic,
45
tall stature - ddx
Bone age bigger than chronological age - normal GV: familial tall stature, obesity - abnormal GV: genetic, endocrine, CNS lesions
46
constitutional delay - manifestation
short stature, delay puberty, delayed bone age | schedule follow up
47
RF for infant butilism
honey or canned food
48
CAH with increased androgen - bone age?
increased
49
granulosa cell tumors secrete ...
estrogen/progesterone
50
Obese children are at high risk for precocious development as
adiposity can trigger excess insulin production, which then stimulates the adrenal glands to produce hormones
51
precosious puberty - CAH?
peripheral
52
inadequate total body glycogen stores?
newborns as a results of prematurity or intrauterine growth restriction --> low glucose at first 24 hours
53
macrosomic infant weight?
more than 4
54
ketoacidosis in children - glucose?/ management
more than 200 | - 10ml/kg isotonic fluid / h AND insulin infusion + K+
55
clinical manifestation of refeeding sydnrome - clinical manifestation
1. arrhythmia 2. CHF 3. pulm edema 4. seizures 5. wernicke enc
56
hypothyroidism - precocious puberty
severe untreated hyothyroidism can cause gonadotropin DEPENDED precocious puberty
57
constitutional age - at born?
normal delay between 6 months - 3 years
58
isolated pubarche is more common in
obese (early activation of adrenal androgen)
59
increased risk for male breast cancer
Klinefelter
60
normal gynecomastia of puberty - uni or blateral ?
both

pediatrics (16 decks)

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