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Pediatrics > BRS #3 > Flashcards

BRS #3 Flashcards

0
Q

children who grow _______ per year between age 3 and puberty usually do not have an endocrinopathy or underlying pathologic disorder

A

2 inches (5 cm) per year

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1
Q

define short stature

A

height that is 2 SDs below the mean (below 3rd percentile)

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2
Q

all patients more than _____ SDs below the man or who have a growth velocity less than _____ per year have a pathologic growth disorder until proven otherwise

A

3 SDs

5 cm/year

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3
Q

hypoglycemia, prolonged jaundice, cryptorchidism, microphallus, short stature

A

hypopituitarism

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4
Q

male mid parental height

A

(father’s height + mother’s height + 5 inches)/2

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5
Q

female mid parental height

A

(father’s height - 5 + mother’s height)/2

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6
Q

2 classes of drugs that can cause short stature

A

steroids, stimulants

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7
Q

define upper and lower segment

what are normal U/L ratios

A

lower segment = pubic symphysis to the heel
upper segment = total height - lower segment
birth = 1.7
age 3 = 1.3
> age 7 = 1.0

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8
Q

2 types of normal variant short stature

A
  • familial short stature- 2 SDs below the mean with short MPH but with normal bone age, normal onset of puberty, normal growth of 2 inches/year
  • constitutional growth delay - 2 SDs below the mean with h/o delayed puberty in either/both parents, delayed bone age, late onset of puberty, normal growth of 2 inches/year
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9
Q

define pathologic short stature

A

height less than 3 SDs below the mean with abnormal growth velocity

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10
Q

causes of pathologic proportionate short stature

A

prenatal onset: environmental causes, chromosomal disorders, genetic syndromes, viral infection
postnatal onset: malnutrition, cyanotic heart disease, renal disease, GI disease, pulmonary disease, endocrine disease, psychosocial (ex. neglect)

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11
Q

2 causes of pathologic disproportionate short stature (very short legged with increased U/L ratio)

A

rickets

skeletal dysplasias

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12
Q

frontal bossing, bowed legs, low serum phosphorus, high serum alkaline phosphatase

A

rickets

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13
Q

short people with short limbs

A

achondroplasia

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14
Q

initial labs for short stature workup

A

CBC, ESR, T4, electrolytes including Ca and phosphorus, Cr, bicarbonate, IGF-1

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15
Q

initial imaging for short stature workup

A

bone age determination

AP and lateral skull radiographs to see if sella looks weird

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16
Q

conditions in which bone age = chronological age

A

familial short stature
IUGR
Turner syndrome
skeletal dysplasia

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17
Q

conditions in which bone age < chronological age

A 
constitutional short stature
hypothyroidism
hypercortisolism
GH deficiency
chronic diseases
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18
Q 
prolonged neonatal juandice
hypoglycemia
cherubic facies
central obesity
microphallus
cryptorchidism 
midline defects
poor growth velocity
A

GH deficiency

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19
Q

__________ must be considered in any child > 5 years of ae who is not growing 2 inches per year

A

craniopharyngioma

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20
Q

all patients with GH deficiency should have this done

A

MRI of the head

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21
Q

how to dx GH deficiency

A

low IGF-1 levels

poor response on GH stimulation testing

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22
Q

tx of GH deficiency

A

daily subcutaneous injections of GH until max growth potential (age 13-14 in girls, 15-16 in boys)

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23
Q

most common cause of hypothyroidism in kids is ________

how do you dx it?

A

Hashimoto’s thyroiditis

-increased TSH, low T4, positive antithyroid peroxidase antibodies

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24
Q

most common cause of hypercortisolism that results in short stature is ______

A

iatrogenic use of steroids

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25
Q

________ has been shown to improve ultimate height of Turner patients

A

GH treatment

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26
Q

onset of puberty is between _____ and ______ in females

A

7 and 13

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27
Q

thelarche occurs due to this hormone

adrenarche occurs due to this hormone

A

estrogen

adrenal androgens

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28
Q

in females, ______ and usually the first sign of puberty

A

breast buds

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29
Q

menarche has mean onset at age _____

A

12.5

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30
Q

_____ stimulates ovaries to produce follicles, which in turn produce estrogen

A

TSH

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31
Q

_____ is responsible for the positive feedback in the middle of the menstrual cycle resulting in the release of an egg

A

LH

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32
Q

male puberty onset is between ____ and ______ years

A

9 and 14

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33
Q

____ is usually the first sign of male puberty

A

testicular enlargement

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34
Q

_____ stimulates the seminiferous tubules in the testes to produce sperm

A

FSH

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35
Q

______ in boys stimulates the testicular Leydig cells to produce androgens, which in turn are responsible for penile enlargement and growth of axially, facial, and pubic hair

A

LH

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36
Q

precocious puberty in girls and boys

A

girls: breast or pubic hair before age 7 or menarche before age 9
boys: testicular changes, penile enlargement, or pubic or axillary hair before age 9

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37
Q

premature thelarche is a big red flag (T/F)

A

F
it is common and benign, usually present in first 2 years of life
-caused by transient activation of the HPGA
-no workup or tx is necessary

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38
Q

early onset of pubic or axillary hair w/o development of breast tissue or enlarged testes

  • this condition is more common in ____ (boys/girls)
  • can have apocrine odor
  • tx?
A

premature adrenarche
girls
no tx needed

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39
Q

_____ (girls/boys) have a higher incidence of isosexual precocious puberty

A

girls

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40
Q

isosexual precocious puberty or central precocious puberty (CPP) in boys and girls

A

boys: testicular enlargement, pubic hair, rapid growth
girls: breast development, pubic hair, rapid growth

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41
Q

causes of central precocious puberty in girls and boys

A

girls: mostly idiopathic
boys: tends to be organic –> evaluate all cases with head MRI (ex. hydrocephalus, CNS infection, CP, malignant tumors, severe head trauma)

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42
Q

central precocious puberty, poor growth, delayed bone age

A

hypothyroidism

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43
Q

GnRH stimulation test in CPP vs. PPP

A

give synthetic GnRH

  • CPP: dramatic increase in LH
  • PPP: flat response
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44
Q

PPP (peripheral precocious puberty) in boys and girls

A

boys: feminization (gynecomastia), premature onset of pubic hair
girls: virilization or breast development
- PPP is independent of the HPGA

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45
Q

there is usually no testicular enlargement in PPP except for the following 3 things

A

McCune-Albright syndrome
testotoxicosis
beta-HCG secreting tumors

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46
Q

bony changes (polyostotic fibrous dysplasia)
coast of Maine cafe au lait spots
PPP or hyperthyroidism

A

McCune-Albright syndrome

-enlarged gonads but secretion of sex steroids is independent of the HPGA

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47
Q

testes enlarge bilaterally independent of the HPGA

A

testotoxicosis

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48
Q

how does beta-HCG secreting tumor cause PPP?

A

beta-HCG looks like LH so it binds to LH receptor and enlarges the testes, stimulating Leydig cells and secreting androgens

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49
Q

delayed puberty definition in boys and girls

A

boys- no testicular enlargement by age 14

girls- no breast tissue by age 13, no menarche by 14 years

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50
Q

constitutional delay of puberty is much more common in _____ (boys/girls)

A

boys

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51
Q

isolated gonadotropin deficiency associated with anosmia (inability to smell)

A

kallman syndrome

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52
Q

obesity, retinitis pigmentosa, hypogonadism, polysyndactyly

A

lawrence-moon-biedl syndrome

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53
Q

causes of hypergonadotropic hypogonadism (high FSH and LH)

  • chromosomal in girls and boys
  • another cause
A

boys- klinefelter (XXY)
girls- Turner (XO)
other cause- autoimmune disorders

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54
Q

causes of hypogonadotropic hypogonadism

A 
constitutional delay of puberty
chronic dzs
pypopituitarism
primary hypothyroidism 
prolactinoma
genetic: kallman, prader-willi, lawrence-moon-biedl
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55
Q

male sexual differentiation is caused by the _____ gene on the _____

A

SRY gene on short arm of the Y chromosome

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56
Q

describe male sexual differentiation

A

SRY gene –> fetal testes

  • Sertoli cells produce anti-mullerian hormone –> regression of mullerian structures (fallopian tubes, uterus, upper 1/3 vagina)
  • Leydig cells produce testosterone
    • -> stimulates development of wolffian ducts (epididymis, vas deferens, seminal vesicles)
    • -> converted to DHT, which causes virilization of external genitalia (scrotal fusion and penile enlargement)
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57
Q

describe female sexual differentiation

A

no SRY –> ovaries form

  • no anti-mullerian hormone –> development of Fallopian tubes, uterus, upper 1/3 vagina
  • no testosterone –> wolffian ducts regress
  • no DHT –> external genitalia do not virilize (formation of labia, clitoris, and lower 2/3 vagina)
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58
Q

causes of undervirilized male (46 XY with ambiguous genitalia and 1 or more gonads palpable)

A
  • inborn errors of testosterone synthesis
  • gonadal intersex (internal structures are both male and female)
    • mixed gonadal dysgenesis
    • true hermaphroditism
  • partial androgen insensitivity (X linked)- incomplete peripheral androgen resistance results in ambiguous genitalia
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59
Q

karyotype of mixed gonadal dysgenesis (MGD)

A

45 XO/46 XY mosaic

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60
Q

presentation of mixed gonadal dysgenesis

A

ambiguous genitalia and a testis and vas deferens on one side and a “streak gonad” on the contralateral side

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61
Q

ambiguous genitalia with both ovarian and testicular gonadal tissue

A

true hermaphroditism

mostly 46XX but can be 46XY

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62
Q

complete androgen insensitivity

-normal phenotypic females (normal external genitalia) but with 46 XY karyotype

A

testicular feminization syndrome

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63
Q

differential diagnosis of virilized female

XX with no palpable gonads

A

congenital adrenal hyperplasia- esp 21-hydroxylase deficiency
virilizing drugs during pregnancy
virilizing tumor in mother during pregnancy

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64
Q

virilized female with increased blood pressure suggest ____

if decreased blood pressure

A

CAH with 11beta-OH deficiency

adrenal insufficiency

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65
Q

two parts of the adrenal gland and what they generally make

A

cortex- steroids

medulla- catecholamines

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66
Q

adrenal cortex mainly makes these 3 things

-which one is independent of the pituitary gland and ACTH

A

mineralocorticoids (aldosterone)** this one is independent and is controlled by the RAAS system
glucocorticoids (cortisol)
androgens (DHEA)

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67
Q

primary adrenal insufficiency is a problem at the level of the ____

A

adrenal gland

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68
Q

signs of cortisol insufficiency

A 
anorexia
weakness
hyponatremia
hypotension
increased pigmentation
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69
Q

signs of aldosterone deficiency

A

FTT
salt craving
hyponatremia
hyperkalemia

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70
Q

examples of primary adrenal insufficiency

A

Addision’s disease
CAH
adrenoleukodystrophy

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71
Q

in secondary adrenal insufficiency, ______ is not deficient

A

aldosterone is not deficient b/c it doesn’t depend on ACTH

there in 2ndary adrenal insufficiency, serum K is normal

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72
Q

most common cause of secondary adrenal insufficiency

A

iatrogenic- sudden stoppage of long term steroid use

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73
Q

______ is the MCC of ambiguous genitalia when no gonads are palpable

A

CAH- it is autosomal recessive

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74
Q

3 main types of CAH

A

21 hydroxylase deficiency- most common
11beta-hydroxylase deficiency
3beta-hydroxysteroid dehydrogenase deficiency

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75
Q

3 subtypes of 21-hydroxylase deficiency (most common CAH)

A

classic salt wasting CAH

  • both mineralocorticoid and glucocorticoid affected
  • girls: ambiguous genitalia
  • 1-2 weeks: FTT, vomiting, electrolyte abnormalities

simple virilizing CAH

  • only glucocorticoid affected so no electrolyte abnormalities
  • girls: ambiguous genitalia at birth
  • boys: age 1-4 years with tall stature, advanced bone age, pubic hair, penile enlargement

nonclassic CAH

  • late onset with very mild cortisol deficiency, age 4-5
  • girls: premature adrenarche, clitoromegaly, acne, rapid growth, hirsutism, infertility
  • boys: premature adrenarche, rapid growth, premature acne
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76
Q

11beta-hydroxylase version of CAH- presents like the classic 21hydroxylase patients except they are _____ and _____

A

hypertensive

hypokalemic

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77
Q

3beta-hydroxysteroid dehydrogenase deficiency (rare CAH)

A

salt wasting crises
glucocorticoid deficiency
ambiguous genitalia
*b/c there is an early block in all 3 adrenal pathways

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78
Q

diagnostic workup/what to measure in 3 types of CAH

A

21 hydroxylase- increased 17-OHP
11beta hydroxylase- increased specific compound S
3beta hydroxysteroid dehydrogenase- increased DHEA and 17hydroxygrenenolone

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79
Q

how to manage CAH

A

cortisone to suppress androgen production an adequate amount

+/- fludrocortisone (mineralocorticoid) supplementation

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80
Q

septicemia caused by meningococcus in a neonate results in adrenal insufficiency

A

waterhouse-friderichsen syndrome

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81
Q

how to dx acquired adrenal insufficiency

A

ACTH stim test

  • normally, cortisol doubles in response to ACTH stim
  • in primary adrenal insufficeincy, there is a blunted cortisol response
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82
Q

how to manage adrenal crisis

A

D5 in normal saline

parenteral steroids until stabilization

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83
Q

delayed bone age, central obesity, moon facies, nuchal fat pad, easy bruisability, purplish striae, HTN, glucose intolerance

A

glucocorticoid excess

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84
Q

causes of hypercortisolism (3)

A

iatrogenic- exogenous steroids
cushing syndrome- adrenal tumor
cushing disease- excessive ACTH production

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85
Q

how to dx hypercortisolism

A

elevated 24 hour urine cortisol

absence of expected cortisol suppression on dexamethasone suppression test

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86
Q

how to differentiate excess cortisol vs. obesity

A

hypercortisolism- growth impairment, delayed bone age

obesity- normal to fast growth, advanced bone age

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87
Q

DM in children is more common in ____ (boys/girls)

A

boys

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88
Q

95% of DM1 patients have HLA ______

A

DR3 or DR4

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89
Q

genetic aspect of DM1

A

MZ 50% concordance

DZ 30% concordance

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90
Q

autoimmune factors that may be seen in DM1 patient

A

islet cell antibodies (ICA)
antibodies against insulin
antibodies against glutamic acid decarboxylase (GAD)

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91
Q

classic presentation of DM1

A

polyuria, polydipsia, nocturia

perhaps DKA

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92
Q

suspect _____ in girls with protracted cases of vaginal yeast infections

A

DM1

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93
Q

how to dx DM1

A

random glucose > 200 with polyuria, polydipsia, weight loos, nocturia

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94
Q

what’s the honeymoon period of DM1

A

months to 1-2 years

insulin requirement lessens due to transient recovery of endogenous islet cell function

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95
Q

somogyi phenomenon

A

too much insulin at bedtime –> hypoglycemic –> counter regulatory stuff –> hyperglycemic and ketones in the morning
tx by LOWERING bedtime insulin dose, not raising it

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96
Q

glucose > 300, serum bicarb < 15, serum pH <7.30

A

DKA

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97
Q

severe DKA presentation

A

severe dehydration, abdominal pain that may mimic appendicitis, rapid and deep (Kussmaul) respirations, coma

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98
Q

lab findings in DKA

A

anion gap metabolic acidosis
hyperglycemia and glucosuria
ketonemia and ketonuria
hyperkalemia due to acidosis

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99
Q

how to manage DKA

A
  • fluids!!! with isotonic saline
  • regular insulin
  • K repletion with K acetate (metabolic acidosis) or K phosphate (increase 2,3-DPG –> makes oxygen more available to tissues)
  • *don’t drop osmolality to quickly or you risk cerebral edema
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100
Q

suboptimal growth velocity and delayed bone age
goiter
myxedema (puffy skin, dry skin, occasionally orange-tinged)
amenorrhea or oligomenorrhea

A

hypothyroidism

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101
Q

most common metabolic disorder in new born

A

congenital hypothyroidism

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102
Q

causes of congenital hypothyroidism

A
  1. thyroid dysgenesis (90%)
  2. thyroid dyshormonogenesis- multiple inborn errors of thyroid hormone synthesis
    • pendred syndrome- this + sensorineural hearing loss
  3. use of PTU during pregnancy- transient
  4. maternal autoimmune thyroid disease- transient
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103
Q

thyroid screen is normally done as a newborn but some classic signs and symptoms

A
  • prolonged jaundice
  • poor feeding
  • lethargy
  • constipation
  • large anterior and posterior fontanelles, protruding tongue, umbilical hernia, myxedema, mottled skin, hypothermia, delayed neurodevelopment, poor growth
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104
Q

how to tx congenital hypothyroidism

A

L-thyroxine

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105
Q

most common cause of acquired hypothyroidism with or without a goiter in a child
what is it, what are some sxs, how to tx

A

Hashimoto’s thyroiditis

  • usually has goiter (firm and pebbly), thyroid antiperoxidase antibodies
  • short stature
  • can have transient hyperthyroidism
  • tx with levothyroxine
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106
Q

if you have hyperthyroidism + vitiligo + alopecia, you should suspect ______

A

coexistence of other autoimmune polyendocrinopathies (DM, Addison’s disease)

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107
Q

most common cause of hyperthyroidism in childhood

A

Grave’s disease

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108
Q

what autoantibody in Grave’s disease

A

thyroid-stimulating immunoglobulin (TSI)

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109
Q

how to manage Grave’s disease

A
  • PTU and methimazole (antithyroid medications)- PTU inhibits conversion of T4 to T3
  • subtotal thyroidectomy
  • radioactive iodine ablation
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110
Q

_____ and _____ release Ca and phosphorus from bones

A

vitamin D and PTH

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111
Q

PTH causes ______ and ______ resabsorption and ______ excretion

A

Ca and bicarbonate

phosphorus

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112
Q

Ca source is mainly via GI tract, and this is facilitated by ______

A

vitamin D (1,25-OH vitamin D)

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113
Q

younger patients with hypocalcemia tend to present with ______ and older patients tend to present with

A

seizures or comas

neuromuscular hyperexcitability

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114
Q

early neonatal hypocalcemia ( < 4 days) is usually ______

A

transient

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115
Q

3 main causes of late neonatal hypocalcemia (> 4 days)

A
  1. hypoparathyroidism- usually 2/2 maternal hyperparathyroidism… high Ca crosses placenta and suppresses baby’s PTH
  2. DiGeorge syndrome
  3. hyperphosphatemia b/c it complexes with Ca… 2/2 too much intake or uremia
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116
Q

what is pseudohypoparathyroidism

A

rare AD disorder resulting in PTH resistance… symptoms of hypocalcemia but PTH is high!

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117
Q

how does Mg affect Ca?

A

low Mg causes low Ca b/c Mg is needed for PTH release

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118
Q

_____ causes low Ca and low phosphorus

A

vitamin D deficiency

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119
Q

hypocalcemia can cause this on EKG

A

prolonged QT

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120
Q

how to manage hypocalcemia

A

if mild, no tx needed
if Ca < 7.5 in newborns or < 8 in older children, then can give Ca
oral therapy if minor sxs
IV Ca gluconate if major sxs
give 1,25-OH vitamin D to patients with chronic hypoparathyroidism

121
Q

rickets is caused by _____ deficiency

this results in deficient _________ of growing bones with a normal bone matrix

A

vitamin D

mineralization

122
Q

causes of rickets

A

vitamin D deficiency
GI disorders- malabsorption
defective vitamin D metabolism 2/2 renal or hepatic dysfunction

123
Q

what is vitamin D-dependent rickets?

labs on presentation?

A
  • AR condition
  • deficiency of 1alpha-hydroxylase, which converts 25-OH vitamin D to 1,25-OH vitamin D in the kidney
  • increased PTH, low vitamin D/Ca/phosphorus, increased alkaline phosphatase
124
Q

what is vitamin D-resistant rickets (familial hypophosphatemia)
how is it inherited
what findings
what is the tx

A
  • most common form of rickets in the US
  • X linked dominant
  • renal tubular phosphorus leak –> normal Ca and low phosphorus –> typical bowing of the legs but no tetany
  • tx with phosphate supplements and 1,25 vitamin D
125
Q

phosphate deficient form of rickets caused by bone or soft tissue tumor

A

oncogenous rickets

*consider in pts with bone pain or a myopathy

126
Q

rickets most prominent in these 2 age ranges

A

first 2 years

adolescence

127
Q

most commonly involved areas in rickets

A

wrists, knees, ribs, weight bearing bones become bowed

128
Q

clinical presentation of rickets

A

short stature
bowed legs
rachitic rosary (prominent costochondral junction)
craniotabes- “ping pong” skull
frontal bossing
delayed suture closure
wrist xrays show widening, fraying, and cupping

129
Q

how is nephrogenic DI inherited

A

X linked recessive

130
Q

define hypoglycemia

A

serum glucose < 40

131
Q

causes of hyperinsulinism in neonate with persistent hypoglycemia

A
  • islet cell hyperplasia (nesidioblastosis)
  • beckwith-wiedemann syndrome: LGA, visceromegaly, hemihypertrophy, macroglossia, umbilical hernia, distinctive ear creases
132
Q

suspect ______ in neonate with hypoglycemia, microphallus, and midline defects like cleft palate

A

congenital hypopituitarism

133
Q

this drug can cause hypoglycemia

A

alcohol

-deplete essential cofactors needed for gluconeogenesis in the liver

134
Q

girls with hyperthyroidism are more likely to have ____ menarche

A

delayed

135
Q

you can get these electrolyte disturbances when treating DKA

A

hypoglycemia
hypocalcemia
hypokalemia

136
Q

premature adrenarche…. what they have and don’t have

A

have apocrine odor and pubic hair

do not have breast development or very advanced bone age

137
Q

in PPP boys _____ do/do not have testicular enlargement

A

do not

138
Q

breast development, cafe au lait spots, fibrous dysplasia of the long bones

A

mccune albright syndrome- girls with PPP

139
Q

thin child who develops hypoglycemia after a long fast

A

ketotic hypoglycemia

140
Q

____% of children have an innocent heart murmur at some point during childhood

A

50%

141
Q 
innocent heart murmur:
ages 2-7
mid-left sternal border
vibratory, twanging, or buzzing 
grade 1-3, systolic
loudest supine and louder with exercise
A

still’s murmur

142
Q 
innocent heart murmur:
any age
upper left sternal border
grade 1-2, peaks early in systole
blowing, high-pitched
loudest supine and louder with exercise
A

pulmonic systolic murmur (systolic ejection murmur)

143
Q 
innocent heart murmur:
any age but esp school age
neck and below the clavicles
continuous murmur heard only when sitting or standing
disappears if supine
A

venous hum

144
Q

ASD in lower portion of atrial septum
what else can it cause?
what is it associated with?

A

ostium primum
can also cause mitral regurg
associated with Down syndrome

145
Q

ASD in middle portion of the atrial septum

most common type of ASD

A

ostium secundum

146
Q

ASD high in the septum… right pulmonary veins drain anomalously into the right atrium or SVC instead of into the left atrium

A

sinus venosus

147
Q

ASDs cause a ____ to _____ shunt

what does this lead to?

A
  • left to right

- leads to increase in size of RA and RV and to increased pulmonary blood flow

148
Q

sxs of ASD

A

usually minimal

149
Q

3 physical exam findings in ASD

A
  1. increased RV impulse
  2. systolic ejection murmur in the mid and upper left sternal border
    - can also hear mid-diastolic filling rumble due to turbulence at tricuspid valve
  3. fixed split S2
150
Q

how to tx ASD

A

close the defect

151
Q

after birth, what direction is the blood flow in VSD?

what can this lead to?

A

LV to RV due to lower pulmonary vascular resistance

increased pulmonary circulation –> pulmonary vessel hypertrophy –> pulmonary HTN

152
Q

amount of blood shunted from one side to the other of VSD depends on _______ and ______

A

size of VSD

degree of pulmonary vascular resistance (PVR)

153
Q

small VSDs presentation and prognosis

A

grade 4 high-pitched holosystolic murmur (smaller VSD = louder murmur)
it usually closes spontaneously

154
Q

in moderate-severe VSDS, you may hear a ______ murmur and a ______ murmur

A

holosystolic
diastolic mitral filling murmur if there’s a lot of blood flow to the lungs that now needs to pass through the mitral valve

155
Q

signs of elevated PVR in VSD

A
  • RV heave
  • S2 may be single and loud
  • mitral filling rumble disappears b/c there is decreased left to right shunt
  • symptoms of CHF also decreases 2/2 decrease in pulmonary blood flow
156
Q

what happens if PVR remains irreversibly elevated?

A

shunting from right to left

Eisenmenger syndrome

157
Q

how to tx VSD

A
  • medical management of CHF
  • surgical closure for heart failure refractory to medical management, large VSDs with pulmonary HTN (3-6 months), small-moderate VSDs (2-6 years)
158
Q

what is the blood flow in PDA?

A

from aorta to ductus to pulmonary artery (left to right shunt) –> increased pulmonary blood flow

159
Q

physical exam findings of PDA

A

machinery-like continuous murmur at LUSB

if large left-to-right shunt, you may hear diastolic mitral rumble, widened pulse pressure (>30mmHg) and brisk pulses

160
Q

how to manage PDA

A

indomethacin in premature infants to close PDA medically

various surgical techniques

161
Q

define coarctation of the aorta

A

narrowing in the aorta usually between left subclavian artery and ductus arteriosus

162
Q

infants with severe coarcation may depend on right to left shunt through the _____ for perfusion of the LE

A

PDA

as the PDA closes, they may develop sxs of CHF

163
Q

hypertension in the right arm, reduced BP in the LE

radio-femoral delay (femoral is after radial, which is abnormal)

A

coarctation of the aorta

164
Q

______ is found in 50% of patients with coarctation of the aorta

A

bicuspid aortic valve or aortic stenosis

165
Q

where to listen to the bruit of coarctation of the aorta

A

left upper back near the scapula

166
Q

initial management of coarctation of the aorta in the symptomatic neonate

A
  • IV prostaglandin (PGE) to keep the ductus arteriosus open

- inotropic meds and low dose dopamine to maximize end organ (specifically renal) perfusion

167
Q

how to definitively tx coarctation of the aorta

A

surgery
balloon angioplasty- good for recurrent coarctation
prognosis is excellent!

168
Q

in aortic stenosis, there is an imbalance between ______ and ______
this can lead to ______
if severe AS occurs during development, you might have _

A
  • myocardial supply (outflow obstruction) and demand (increased work 2/2 outflow obstruction)
  • myocardial ischemia
  • hypoplasia of the LV 2/2 impaired fetal LV development
169
Q

neonate who is normal at birth but then develops signs and sxs of CHF at 12-24 hours of age

A

neonates with severe stenosis (critical aortic stenosis)

170
Q

presentation of aortic stenosis in older children

A

exercise intolerance, chest pain, syncope, sudden death

171
Q

how to manage aortic stenosis

A

balloon valvuloplasty

surgery with replacement of the valve

172
Q

clinical presentation of pulmonary stenosis

  • neonate with severe pulmonary stenosis
  • older children/most children
A
  • neonate with severe PS: can cause cyanosis 2/2 right to left shunting through a PFO
  • most children: no sxs
173
Q

how to manage pulmonary stenosis if it’s symptomatic or gradient or RV pressure is high

A

balloon valvuloplasty

174
Q

peripheral vs. central cyanosis

A
  • peripheral- vasomotor instability or vasoconstriction as a result of cold temperature
  • central- tongue and inner mucous membranes
    • noncardiac: sepsis, hypoglycemia, polycythemia, pulmonary dz
    • cardiac: 5 Ts
175
Q

what are the 5Ts of cyanotic heart disease?

A 
tetralogy of fallot
TGA
tricuspid atresia
truncus arteriosus 
total anomalous pulmonary venous connection
176
Q

results of the 100% oxygen test in cyanotic CHD

A

PaO2 fails to rise despite administration of 100% O2

177
Q

most common cause of central cyanosis beyond the newborn period

A

tetralogy of fallot

178
Q

define tetralogy of fallot

A
  1. VSD
  2. overriding aorta
  3. pulmonary stenosis
  4. RV hypertrophy
179
Q

pathophys of TOF

A

RV outflow tract obstruction… blood flows from RV to pulmonary artery but also to the overriding aorta –> right to left shunt
-less pulmonary blood flow results in cyanosis

180
Q

physical exam findings in TOF

A

increased RV impulse 2/2 RVH
systolic ejection murmur 2/2 pulmonary stenosis
cyanosis

181
Q

actions that increase cyanosis in TOF

ex. things that increase right to left shunting

A
  • decrease SVR- exercise, vasodilation, volume depletion

- increase resistance through the RVOT- crying, tachycardia

182
Q

actions that decrease cyanosis in TOF

-reduces the right to left shunt

A
  • increase SVR or reduce resistance through RVOT

- volume infusion, systemic hypertension, valsalva, bradycardia

183
Q

neonates with severe pulmonary stenosis in TOF may present with cyanosis immediately after birth due to _____

A

closure of the PDA

184
Q

a tet spell in TOF is characterized by sudden cyanosis and decreased murmur intensity

A

yep

185
Q

pathophys of test spells and what do kids normally do during it?

A

any trigger decreases O2 sat –> kid becomes irritable and cries –> crying increases resistance through the RVOT –> increases right to left shunt –> cyanosis worsens –> terrible cycle
-to compensate, kids learn to squat (increase venous return, increase SVR which decreases the right to left shunt)

186
Q

how to fix TOF

A

definitive surgical repair at 4-8 months

187
Q

in TGA, when is cyanosis present

A

at or shortly after birth

188
Q

central cyanosis, single S2, no murmur

A

TGA

189
Q

how to tx TGA

A

initial management: PGE to keep PDA open +/- emergent balloon atrial septostomy (make ASD or PFO) bigger
definitive management: arterial switch operation

190
Q

anatomy of tricuspid atresia

A

essentially, the tricuspid valve does not exist and that area is closed
-an ASD or PFO must be present

191
Q

in tricuspid atresia… describe what it’s like if VSD is present vs. absent

A
  • VSD absent- pulmonary atresia is also present… blood can only get to the lungs via PDA
  • VSD present- LV –> VSD –> pulmonary artery (left to right shunt)
192
Q

physical signs of tricuspid atresia

  • no VSD
  • VSD
A
  • no VSD: no murmurs, single S2

- VSD: VSD murmur

193
Q

tricuspid atresia is the only cause of cyanosis in the newborn period that results in ______ and ______
______is also present

A

left axis deviation and LV hypertrophy

right atrial enlargement is also present

194
Q

how to tx tricuspid atresia

A

Fontan procedure

systemic venous return drains into pulmonary artery

195
Q

truncus arteriosus anatomy

A

aorta and pulmonary artery originate from a common artery, the truncus
-VSD is almost always present

196
Q

pathophys of truncus arteriosus

A

excessive blood flow to lungs –> CHF develops
mixing occurs in the truncus
pts are commonly only mildly desaturated and sometimes cyanotic

197
Q

clinical features of truncus arteriosus

A
  • CHF
  • systolic ejection murmur from increased flow across truncal valve
  • single S2
  • diastolic murmur 2/2 increased flow across mitral
  • high pitched systolic murmur at the base 2/2 insufficiency of the truncal valve
198
Q

how to treat truncus arteriosus

A

medications for CHF

surgical repair in infancy

199
Q

anatomy of total anomalous pulmonary venous connection (TAPVC)

A

pulmonary veins drain into the systemic venous side rather than into the left atrium
-supracardiac, cardiac, infracardiac

200
Q

pathophys of TAPVC

physical exam features

A

systemic and pulmonary venous blood mixes in the right atrium –> desaturated blood –> cyanosis on exam
-exam features: cyanosis, pulmonary flow murmur

201
Q

how to tx TAPVC

A

surgical repair shortly after dx

202
Q

MCC acquired heart disease in children in the US

A

Kawasaki disease

203
Q

MCC acquired heart disease worldwide

A

acute rheumatic fever

204
Q

most commonly seen organisms in endocarditis

A

gram positive cocci

  • alpha-hemolytic streptococci (strep viridans)
  • staph
205
Q

how to dx endocarditis

A

blood cultures!!!
ESR
TEE > TTE in terms of sensitivity

206
Q

how to tx endocarditis

what about ppx?

A

anti-microbial therapy for 4-6 weeks
ppx before procedures for the following pts:
-all pts with structural heart disease except secundum ASD
-all post op cardiac surgery pts for at least 6 months

207
Q

causes of pericarditis

A

infection
collagen vascular disease
uremia
postpericardiotomy syndrome

208
Q

most common organisms in bacterial pericarditis

A

staph aureus and strep pneumo

*pts with purulent pericarditis have a high incidence of constrictive pericarditis

209
Q

if severe enough, pericarditis can lead to ______

A

cardiac tamponade

210
Q

characteristic chest pain in pericarditis

A

intense while supine and relieved when sitting upright

211
Q

physical exam of pericarditis

A

pericardial friction rub
distant heart sounds
pulsus paradoxus
hepatomegaly

212
Q

how to dx pericarditis

A 
pericardiocentesis
ESR
EKG- ST changes and low voltage QRS
CXR- enlarged heart shadow
echo- definitive
213
Q

how to tx pericarditis

  • bacterial
  • viral or postpericardiotomy
A

bacterial: abx
viral or postpericardiotomy: ASA, NSAIDs, steroids
+/- drainage via pericardial catheter or surgical window

214
Q

common causes of myocarditis

A

viruses- enteroviruses esp coxsackievirus
bacteria- corynebacterium diphtheriae, strep pyogenes, staph aureus, mycobacterium tuberculosis
fungi- candida, cryptococcus
protoza- T cruzi (chaga’s disease)
autoimmune- SLE, rheumatic fever, sarcoidosis
kawasaki disease

215
Q

some lab and imaging findings with myocarditis

A

elevated ESR, CKMB fraction and CRP
viral serology or PCR of endomyocardial bx specimen
echo shows anatomically normal heart with global ventricular dysfnc

216
Q

how to manage myocarditis

A

supportive: inotropes, diuretics, after load reducers

may need cardiac transplant

217
Q

cardiomyopathy with ventricular dilation and reduced cardiac function

A

dilated cardiomyopathy

218
Q

causes of dilated cardiomyopathy

A 
viral myocarditis
mitochondrial abnormalities 
carnitine deficiency
nutritional deficiency- selenium and thiamine 
hypocalcemia
chronic tachydysrhythmias
anomalous origin of left coronary artery from pulmonary artery (ALCAPA)
meds- doxorubicin
219
Q

evaluation of dilated cardiomyopathy should include ______ and _____

A

viral serologies

carnitine level

220
Q

hypertrophic cardiomyopathy is inherited as ______

most typical anatomic finding is _______

A

autosomal dominant

asymmetric septal hypertrophy

221
Q

these are impaired in HOCM

A

poor LV filling

dynamic LVOT obstruction

222
Q

MCC sudden death in young athletes

A

hypertrophci cardiomyopathy

223
Q

harsh, systolic ejection murmur at the apex

-accentuated with maneuvers that reduce LV volume (Valsalva and standing)

A

hypertrophic cardiomyopathy

224
Q

management of HOCM

A

beta adrenergic blockers or CCBs
surgical myomectomy
antiarrhythmic medication
dual chamber pacing

225
Q

causes of restrictve cardiomyopathy

A

amyloidosis

inherited infiltrative disorders

226
Q

how to tx restrictive cardiomyopathy

A
  • diuretics to improve diastolic compliance

- beta blockers and CCBs

227
Q

most common dysrhythmia in childhood

which is associated with sudden cardiac death

A

SVT (AVRT/WPW or AVNRT)

WPW is associated with sudden cardiac death

228
Q

delta wave suggests ______

A

WPW

229
Q

acute management of SVT

A
  • vagal maneuvers- valsalva, ice pack on face, unilateral carotid massage, placing child upside down, orbital pressure
  • IV adenosine (also propranolol, digoxin, procainamide, amiodarone)
  • cardioversion for hemodynamic instability
230
Q

chronic management of SVT

A
  • meds like propranolol

- catheter ablation of the accessory pathway

231
Q

on CXR for congenital heart disease

  • boot shaped
  • egg on a string
  • snowman appearance
A
  • TOF
  • TGA
  • TAPVC
232
Q

congenital 3rd degree AV block is associated with children born to moms with ______
-other causes of heart block?

A

SLE

  • post cardiac surgery
  • bacterial endocarditis
233
Q

how to tx symptomatic AV block

A

cardiac pacing

234
Q

2 inherited causes of long QT

A
  • jervell-lange-nielsen syndrome- AR, associated with congenital deafness
  • romano-ward syndrome- AD, not associated with congenital deafness
235
Q

what defines a long QT

A

QTc > 440 msec

236
Q

how to tx long QT

A

beta-blocker for symptoms

cardiac pacing, AICD, etc. for asymptomatic people

237
Q

inspiratory stridor suggests _______ such as _______

A

extrathoracic obstruction

croup and laryngomalacia

238
Q

expiratory wheezing suggests _________ such as _______

A

intrathoracic obstruction
asthma
bronchiolitis

239
Q

most common age range for epiglottitis

A

age 2-7 years

240
Q

MCC of epiglottitis prior to immunization

A

HIB

-also GABHS, strep pneumo, and staph

241
Q

abrupt onset of rapidly progressive upper airway obstruction w/o prodrome

  • high fever, toxic looking
  • muffled speech
  • dysphagia and drooling
  • sitting forward/tripoding
A

epiglottitis

242
Q

xray finding in epiglottitis

A

thumbprinting on lateral neck xray

243
Q

how to manage epiglottitis

A
  • emergency* avoid causing distress as airway may close
  • nasotracheal intubation
  • abx: 2nd or 3rd gen IV cephalosporin
244
Q

if epiglottitis is due to HIB, then give _________ as ppx for unvaccinated household contacts < 6 years

A

rifampin

245
Q

inflammation of the subglottic larynx, trachea, and bronchi

A

croup

246
Q

2 types of croup and ages affected

A

viral croup- MCC stridor, ages 3month-3years, late fall-winter
spasmodic croup- year round in preschool children

247
Q

MCC viral croup

A

parainfluenza viruses

248
Q

URI for 2-3 days –> inspiratory stridor, fever, barky cough

A

viral croup

249
Q

steeple sign on CXR indicates

A

croup

250
Q

characteristic acute onset of stridor usually at night

A

spasmodic croup

-recurs and resolves w/o treatment

251
Q

tx for croup

A

cool mist and fluids
if stridor at rest –> systemic corticosteroids
if respiratory distress –> racemic epinephrine aerosol
if wheezing –> albuterol

252
Q

a non-croup cause of stridor
toxicity, high fever, mucous and pus in the airway
what are some organisms involved?

A

bacterial tracheitis
staph aureus (60%), strep, nontypeable H flu
tx with abx

253
Q

viral infection that causes inflammatory bronchiolar obstruction

A

bronchiolitis

254
Q

__________ is the most common lower respiratory tract infection in the first 2 years
it is also predominantly in kids < 2 years

A

bronchiolitis

255
Q

when is bronchiolitis most active?

A

winter

256
Q

MCC of bronchiolitis

A

RSV

257
Q

clinical progression of bronchiolitis

A

URI –> tachypnea, rales, wheezing

+/- apnea, hypoxemia

258
Q

CXR of bronchiolitis

A

hyperinflation with air trapping, patchy infiltrates, atelectasis

259
Q

more than _____ of kids with bronchiolitis have recurrent wheezing

A

50%

260
Q

how to manage bronchiolitis

A

mostly supportive: nasal bulb suctioning, hydration, etc
bronchodilators and steroids are controversial
nebulized racemic epinephrine can reduce airway constriction
aerosolized ribavirin for very ill infants
monthly ppx with RSV antibody injections for high risk kids

261
Q

______ are the MCC pneumonia in all age groups

A

viruses

262
Q

______ is the MCC afebrile pneumonia at 1-3 months of age

A

chlamydia trachomatis

  • staccato-type cough, h/o conjunctivitis at birth
  • eosinophilia and CXR with interstitial infiltrates
263
Q

________ is a very common cause of pneumonia in older children and adolescents
CXR and how to tx?

A

mycoplasma pneumoniae
CXR: interstitial infiltrates
tx: oral erythromycin or azithromycin

264
Q

whooping cough is caused by ________

A

bordetella pertussis

265
Q

infants younger than _____ are most at risk for pertussis complications

A

6 months

266
Q

3 stages of pertussis

A
  1. catarrhal (1-2 weeks)- URI
  2. paroxysmal (2-4 weeks)- coughing fits followed by inspiratory whoop… cyanosis, apnea, choking can happen in young infants
  3. convalescent phase (weeks to months)- getting better
267
Q

how to dx pertussis

A

tests on nasal secretion

268
Q

how to manage pertussis

A
  • if super young, probably hospitalize
  • abx for all pts to prevent spread (azithromycin or erythromycin)
  • respiratory isolation until abx are given for 5 days
269
Q

_____ is the most common chronic pediatric disease

A

asthma

270
Q

pathophys of asthma

A

smooth muscle bronchoconstriction
airway mucosal edema
increased secretions with mucous plugging
eventual airway wall remodeling
production of inflammatory mediators (ex. IgE)

271
Q

some asthmatics don’t wheeze, they _____

A

cough

272
Q

CXR of asthmatic

A

hyperinflation
peribronchial thickening
patchy atelectasis

273
Q

PFTs of asthma

A

increased lung volumes

decreased expiratory flow rate

274
Q

asthma management

what is cromolyn?

A

anti-inflammatory ppx

no effect on acute sxs

275
Q

asthma management

role of steroids

A

systemic steroid course for severe exacerbations

inhaled steroids for preventing exacerbations

276
Q

asthma management

role of anticholinergic agents (atropine, ipratropium)

A

second line bronchodilators b/c they decrease airway vagal tone and block reflex bronchoconstriction
-may be useful in sever exacerbations

277
Q 
asthma management 
leukotriene modifier (montelukast, zafirlukast)
A

oral anti-inflammatory agents for long term control of mild, persistent asthma

278
Q

asthma classification: intermittent

A

daytime < 2/week
nighttime <2/month
-albuterol for sx relief

279
Q

asthma classification: mild persistent

A 
daytime > 2/week but not daily
nighttime > 2/month
FEV > 80% predicted (normal)
-albuterol for sx relief
-low dose inhaled steroid (preferred) or cromolyn or leukotriene modifier for daily use
280
Q

asthma classification: moderate persistent

A 
daily sxs
nighttime > 1/week
FEV1 60-80% predicted
daily use of albuterol
-albuterol for sx relief
-medium dose inhaled steroid OR low dose inhaled steroid + LABA (like advair)
281
Q

asthma classification: severe persistent

A 
continuous sxs
frequent nighttime sxs
limited physical activity
FEV1 < 60%
-albuterol for sx relief
-high dose inhaled corticosteroid and LABA
-long term systemic steroids, if needed
282
Q

CF is inherited as ______ and gene is on chromosome ______

A

AR

7

283
Q

chronic progressive pulmonary insufficiency, pancreatic insufficiency (steatorrhea, FTT), high sweat electrolytes

A

CF

284
Q

meconium ileus at birth

A

CF

285
Q

PFTs of CF

A

decreased respiratory flow rates (obstruction) and then eventually decreased lung volumes (restriction)

286
Q

common organisms in CF pneumonia

A

staph aureus and then **pseudomonas aeruginosa

287
Q

aside from recurrent pneumonia, bronchiectasis, pulmonary fribrosis, cor pulmonale, this feature can be seen in CF

A

nasal polyps

288
Q

in CF sweat chloride is _____

what are the serum electrolytes like?

A

> 60 mmol/L

hyponatremic, hypochloremic, hypokalemic metabolic alkalosis

289
Q

tx for CF

A 
abx
pulmonary toilet
bronchodilators for wheezing
good nutrition, pancreatic enzyme replacement, fat soluble vitamins 
oxygen
lung transplant
psych support
290
Q

define chronic lung disease

A

oxygen dependency beyond 28 days

291
Q

MCC cause of chronic lung disease

A

premature children with respiratory distress syndrome (hyaline membrane disease or surfactant deficiency)

292
Q

pathophys of chronic lung disease

A

acute and secondary lung injury
healing of lung tissue is typically abnormal
results in restrictive and obstructive lung disease –> diminished PaO2 and increased PaCO2

293
Q

CXR of chronic lung disease (aka bronchopulmonary dysplasia)

A

hyperinflation
atelectasis
linear or cystic radiodensities

294
Q

how to manage chronic lung disease (aka. BPD)

prognosis?

A 
supplemental O2 or vent support
optimize pulmonary function
optimize caloric intake and growth
prevent complication infections
early identification of complications 
-prog: pulm sxs and disease often diminish with time and growth but various complications may still occur
295
Q

foreign body aspiration usually occurs in ages ________

what are some clinical features?

A

3 months - 5 years

  • laryngotracheal foreign bodies (extrathoracic): inspiratory stridor, cough, hoarseness
  • bronchial foreign bodies (intrathoracic): asymmetric exam findings, can be complete to partial to no obstruction, localized wheezing/persistent pneumonia
  • esophageal obstruction can press on the trachea
296
Q

how to dx foreign body aspiration

A

CXR

consider inspiratory and expiratory films, bilateral decubitus films in those who can’t inspire and expire on command

297
Q

how to tx foreign body aspiration

A

cough it up

if not, bronchoscopy to remove it

298
Q

unexplained cessation of breathing for > 20 seconds

A

apnea of infancy or prematurity

299
Q

three or more respiratory pauses lasting at least 3 seconds each, with less than 20 secs of normal respiration in between

A

periodic breathing

300
Q

peak ages of SIDS

A

2-4 months

301
Q

cause of apnea of prematurity

A

immature central respiratory center control

Pediatrics (14 decks)

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