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Pediatrics > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Normal growth rate

A

2 inches per year

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2
Q

Mid-parental height

A

Helps distinguish kids from normal variant height from pathologic short stature

Male= Father’s height + (Mother’s height + 5 inches)/2

Female= (Fathers height - 5 inches) + Mother’s height/2

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3
Q

Constitutional short stature

A

Category of normal variant short stature defined as 2 SDs below the mean with a history of delayed puberty in both parents, a delayed bone age, and the late onset of puberty in the child

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4
Q

> 3 SDs below the mean w/ an abnormal growth velocity

A

Pathologic short stature

Proportionate: normal U/L ratio
-Could be due to in utero exposure, chromosome probs, viral infxn, malnutrition, child abuse, systemic disease

Disproportionate: Increased U/L ratio
-Rickets, skeletal dysplasia

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5
Q

Lab test for growth hormone deficiency

A

IGF-1

X-ray to examine bone age

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6
Q

Disease to consider in any child older than 5 years old who is not growing 2 inches/year

A

Craniopharyngioma

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7
Q

MCC of hypothyroidism

A

Hashimoto’s thyroiditis

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8
Q

MCC of hypercortisolism

A

Iatrogenic admin. of prolonged steroid use

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9
Q

Ages of female puberty

A

Onset b/w 7-13 years

Mean onset of menarche is 12.5 years

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10
Q

Male puberty timeline

A

Onset b/w 9-14 years

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11
Q

Precocious puberty in males and females

A

Females: Breast development/pubic hair before 7; menarche before 9

Males: Testicular changes, penile enlargement, pubic hair before 9

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12
Q

Central precocious puberty

A

Early onset of gonadotropin-mediated pubery

Girls= idiopathic

Boys= Organic; (REQUIRES HEAD MRI)
-causes include hydrocephalus, CNS infxn, tumors

Labs: GnRH stimulation tests show an adult response (INCREASED LH)

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13
Q

Cause of central precocious puberty w/ poor growth and delayed bone age

A

Hypothyroidism

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14
Q

Peripheral precocious puberty

A

Precocious puberty independent of the HPGA

*FLAT response in GnRH test

Boys have no enlargement in testes due to no FSH present

Causes: Exogenous steroids, gonadal tumors, adrenal tumors
-Check FSH, LH, estradiol

-If a boy, B-hCG tumors are unique (cross-reacts w/ LH receptors)

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15
Q

McCune-Albright Syndrome

A

Polyostotic fibrous dysplasia (bony changes)

Cafe-au-lait spots

PPP or hyperthyroidism

-Pts. actually do have enlarged gonads

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16
Q

Rare disease in which the testes enlarge bilaterally independent of the HGPA

A

Testotoxicosis

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17
Q

Delayed puberty dates

A

Boys= No testicular enlargement by 14 years

Girls= No breast tissue by 13; no menarche by 14

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18
Q

Constitutional delay of puberty is more common in…

A

BOYS

-Opposite of premature adrenarche

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19
Q

Obesity, retinitis pigmentosa, hypogonadism, polysyndactyly

A

Lawrence-Moon-Biedl Syndrome

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20
Q

Week of gestation where gonads differentiate into testes

A

Week 9

  • Due to the fnxn of SRY gene
  • By 12 weeks, external genitalia differentiation is complete
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21
Q

Complete androgen insensitivity and present as normal phenotypic females BUT have a 46 XY karyotype

A

Testicular feminization syndrome

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22
Q

Mixed Gonadal Dysgenesis

A

Karyotype 45 XO/46 XY w/ mosaicism and may have ambiguous genitalia, testes and vas deferens on one side and streak gonad on other

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23
Q

Most common cause of female pseudohermaphroditism

A

21-hydroxylase deficiency (AR inherited)

  • Salt wasting
  • Simple virilizing (no electrolyte abnormalities)

Non-classic (presents at 4-5 years of age w/ mature adrenarche, acne, clitoromegaly, hirsutism)

Labs: Increased 17-hydroxyprogesterone levels

24
Q

CAH w/ increased blood pressure

A

Likely 11B-OH deficiency

-Also see hypokalemia

Labs: Increased levels of f11-deoxycortisol (specific compound S)

25
Q

Pt. w/ salt-wasting crises, glucocorticoid deficiency, and ambiguous genitalia

A

3B-hydroxysteroid dehydrogenase deficiency

  • Block in all 3 steroid pathways
  • Increased DHEA and 17-hydroxypregnenolone
26
Q

Type I polyglandular syndrome

A

Addison’s Disease + Hashimoto’s thyroiditis + Type I Diabetes

Addison’s is an autoimmune condition as well as these others with lymphocytic infiltrative destruction

27
Q

Type II polyglandular syndrome

A

Addison’s Disease + Hypoparathyroidism + Chronic mucocutaneous candidiasis

28
Q

Eval and Tx. of Addison’s Disease

A

Labs: ACTH stimulation test =» cortisol level will double after admin.

Tx: IV fluids w/ 5% dextrose and normal saline
Parenteral steroids

ADRENAL CRISIS = MEDICAL EMERGENCY

29
Q

Cushing Disease

A

Excessive ACTH prod. by a pituitary tumor

30
Q

Second most common disease of childhood

A

DM; twice as common in boys

31
Q

DM Type I

A

Causes: HLA DR3 or DR4 + environmental (rubella, coxsackie) + ICAs, anti-glutamic acid decarboxylase and anti-insulin abs

CFs:
Polydipsia
Poluria
Nocturia

Monitoring: 
   Daily blood glucose
   HbA1c 
   Hypoglycemia 
   Diet
   Education

Comps:
Microvascular = diabetic retinopathy, nephropathy, neuropathy
Macrovascular= HTN, heart disease, stroke

32
Q

Girls w/ early type I DM may have had what?

A

Monilial vulvovaginitis

33
Q

Honeymoon period

A

Period after Type I DM diagnosis where there is a temporary regression in daily insulin requirements due to transient recovery of remaining islet cells

34
Q

Smogyi phenomenon

A

Evening dose of insulin is too high causing hypoglycemia in the early morning hours

=»Release of epinephrine and glucagon

=» High blood glucose and ketones in the morning

Tx: LOWER bedtime insulin dose

35
Q

DKA

A

Hypoglycemia >300mg/dL with ketonuria and a serum HCO3 <15mmol/L or pH <7.30

Insulin deficiency =» hyperglycemia =» osmotic diuresis

Counter regulator hormones (glucagon, epinephrine) cause formation of ketone bodies

CFs:   
   Vomiting, dehydration, polyuria 
   Kussmaul respirations 
   Generalized abdominal pain (mimics appendicitis) 
   Fruity breath 
Labs: 
   Anion gap metabolic acidosis 
   Hyperglycemia 
   Glucosuria
   Ketonemia/Ketonuria 
   Hyperkalemia

Tx: Fluids, insulin, Potassium phosphate (increases 2,3-DPG shifting O2 curve to right)

Comps: CEREBRAL EDEMA (rapid correction of fluids or glucose at greater than 100mg/dL an hour)

36
Q

Two thyroid binding proteins

A

Thyroid binding globulin

Thyroid binding pre albumin

37
Q

Most common metabolic disorder

A

Congenital hypothyroidism; may have aplasia or hypoplasia, maternal PTU history, maternal autoimmune thyroid disease, or thyroid hormone dyshormonogenesis

CFs: 
   LETHARGY, CONSTIPATION 
   Large anterior and posterior fontanelles 
   Protruding tongue 
   Umbilical hernia 
   Hypothermia

Tx: Thyroid hormone before symptoms appear to prevent neurologic sequelae

38
Q

Most common cause of acquired hypothyroidism with or without a goiter

A

Hashimoto’s thyroiditis

  • More common in girls
  • Develops thyroid autoantibodies (anti-TPO)

CFs: Short stature, goiter, possible transient hyperthyroidism (hashitoxicosis)

39
Q

Sensorineural hearing loss + thyroid hormone organification defect

A

Pendred Syndrome

40
Q

Most common cause of hyperthyroidism in childhood

A

Grave’s Disease

CFs: Tachycardia, flushed skin, proptosis, exopthalmos, delayed menarche, gynecomastia

Labs: Increased T4 and T3, decreased TSH, TSI

Tx: PTU (also impairs peripheral conversion of T4 to T3)

=»Thyroidectomy if tx. fails

41
Q

Pseudohypocalcemia

A

Factitious decrease in calcium actually due to low serum albumin levels

-Seen in nephrotic syndrome

42
Q

Tetany

A

Presents w/ carpopedal spasm (hyperexcitability of wrists and ankles)

Laryngospasm

Paresthesias

-Hypocalcemia also causes seizure

43
Q

Pseudohyperparathyroidism

A

AD disorder of PTH resistance

CFs: 
   Short stature
   Short metacarpals
   Developmental delay 
   Elevated PTH
44
Q

EKG finding w/ hypocalcemia

A

Prolonged QT interval

-Also possible w/ hypomagnesemia (impairs PTH release) or hyperphosphatemia (binds calcium)

45
Q

Tx for symptomatic hypocalcemic pts.

A

Calcium gluconate

46
Q

Most common form of Ricket’s in the US

A

Familial hypophosphatemia or Vitamin-D resistant Ricket’s

XLD disorder !!!!!

-Caused by a renal tubular phosphorus leak

  • *Pts. have rickets w/ normal calcium levels but low phosphorus
    • also will not develop tetany

Tx: Phosphate supplements

47
Q

Patient w/ bone pain or myopathy alongside Ricket’s signs

A

Oncogenous Rickets

-Phosphate deficient form of Ricket’s caused by a bone or soft tissue tumor

48
Q

Vitamin-D dependent Ricket’s

A

AR deficiency of 1a-hydroxylase

=» Decreased 1,25 (OH)-D

Lab: Increased PTH, low vitamin D, low phosphorus, increased ALP

-Rare in the U.S.

CFs:   
   Rachitic rosary 
   Short stature 
   Leg bowing 
   Wrist radiographs show widened, and cupperd appearance
49
Q

Nephrogenic DI inheritance

A

XLR

50
Q

Causes of central DI

A

AI

Trauma

Tumors

Langerhan’s cell histiocytosis

Granulomatous disease

Aneurysm

AD inheritance

51
Q

DI eval and tx.

A

Dilute urine w/ increased serum osmolality

***Early morning urine w/ SG >1.018 will RULE OUT

Water deprivation test; patient is administered ADH and seen what happens

MRI of head

Bone scan for Langerhan’s

Tx: DDAVP

52
Q

Islet Cell Hyperplasia

A

“Nesidioblastosis”

-Case of persistent neonatal hypoglycemia

53
Q

Neonate LGA w/ visceromegaly, hemihypertrophy, macroglossia, umbilical hernia, and distinctive ear creases

A

Beckwith-Wiedemann Syndrome

Big tongue

Macroglossia

Weird arms

54
Q

Condition to suspect in neonate w/ hypoglycemia, microphallus, and cleft palate

A

Congenital hypopituitarism

55
Q

Most common cause of hypoglycemia in children 1-6 years of age

A

Ketotic hypoglycemia

Pediatrics (9 decks)

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