Peds Sessions Flashcards

1
Q

how do you manage DKA in office vs. ER?

A

outpatient: can do glucometer, urinalysis (will show positive glucose, ketones and glucose amount)

Emergency Department:

  • Give IV fluids (Hurry up and slow down - if kid is in shock, need to make sure to act fast, but then back off otherwise could cause cerebral edema)
  • Obtain labs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are electrolyte disturbances in DKA?

A
  • potassium levels: lack of insulin decreases potassium in cells –> goes into blood –> lost in urine –> hypokalemia (problems in heart rate)
  • bicarbonate levels decrease d/t to system being overwhelmed (not recommended to replace)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Definition of anion gap acidosis

A

= ([Na+] + [K+]) − ([Cl−] + [HCO3−])

normally gap is under 10!!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Complications of DKA

A
  • Mortality: 0.15-0.5%, most often due to cerebral edema. Higher risk in younger children, initial event and severity of acidosis. Usually occurs in first 12 hrs of treatment
  • Cardiac arrhythmias
  • Venous thrombosis
  • Aspiration
  • Cognitive impairment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Sx of DKA?

A

Vomiting (coffee ground), dehydration, deep gasping breathing, confusion and occasionally coma,

** need to have high blood sugar levels to ddx **

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

how do you rehydrate pt. w/ DKA?

A
  • give IV bolus 10-20 ml/kilo to stabilize CV status
  • provide maintentance fluids (4ml/hour first 10kg, 2 ml/hour second 10 kg, 1 kilo/hour for next)
  • add K+ as Kacetate and KCl, as well as sodium (failure of sodium to improve may indicate cerebral edema)
  • add insulin 0.5-0.1 unit/kg/hr (also helps to drive K+ intracellularly)
    • also promotes metabolism of ketoacids producing HCO3, stops new ketoacid production

** fluids improve renal fn –> enhanced excretion of ketone bodies and improved tissue perfusion to decrease lactic acidosis

monitor labs!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

when do you stop fluids for DKA?

A

1) Anion gap less than 12
2) Venous pH greater than 7.3 or HCO3 greater than 15
3) Glucose less than 200
4) Tolerating oral intake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

anion gap acidosis causes?

A

MUDPILES

methanol, uremia, diabetic ketoacidosis, propylene glycol, isoniazid, lactic acidosis, ethylene glycol, salicylates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

EKG reading with DKA?

A

hypoK: flat T waves, U wave, prolonged PR interval

HyperK: peaked T waves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

why do you not give bicarb w/ DKA?

A
  • Paradoxical rise in CNS pH due to decreased resp rate
  • Slows recovery of ketosis
  • Post treatment alkalosis
  • Risk of increasing hypokalemia
  • May increase osmolality prior to decrease in glucose
  • Increased risk of cerebral edema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

presentation of thyroid cancer in adolescents

A
  • seen as a result of radiation to neck/face/brain
  • most often papillary/follicular carcinomas or mixed
  • MENII syndrome also seen
  • mets often present in anterior cervical nodes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

management of thyroid cancer in adolescents

A

-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

ddx for localized lymphadenopathy in YA’s

A

Oropharyngeal infection (viral, group A streptococcal, staphylococcal)
Scalp infection
Mycobacterial lymphadenitis (tuberculosis and nontuberculous mycobacteria)
Viral infection (EBV, CMV, HHV-6)
Cat scratch disease
Toxoplasmosis
Kawasaki disease- strawberry tongue, fever for 5+ days, swollen cervical lymph nodes, blood shot eyes, rash
Thyroid disease
Kikuchi disease- swollen gland w/ fever in young teenage women
Sinus histiocytosis
Autoimmune lymphoproliferative disease
Lymphoma, Hodgkins and nonHodgkins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

presentation/management of thyrotoxicosis in YA’s

A
  • Graves, Hashitoxicosis, pituitary tumor, TMNG, postpartum thyroiditis
  • usually see family hx of thyroid disease

sx: nervousness, disturbed sleep, w/l or w/g, tremor, sweating, heat intolerance, mm. weakness, fatigue, increased heigh, delayed sexual maturation, menstrual abnormalities
- tachycardia, palpitations

tx: antithyroid drug (firstline)
- radioactive iodine (second, proven safe for use in children)
- subtotal thyroidectomy (not often used d/t complications)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

presentation/management of prolactinoma in YA’s

A
  • Girls: present w/ delayed puberty, amenorrhea, galactorrhea
    boys: present w/ delayed puberty, gynecomastia, galactorheaa
  • decreased energy, decreased libido, impotence, growth failure

** may also be caused by pregnancy, meds, renal/hepatic disease, or marijuana!

The diagnosis of prolactinoma requires laboratory results of sustained hyperprolactinemia and imaging evidence of pituitary adenoma

Prolactin levels can be falsely elevated in the presence of macroprolactin, a complex of prolactin and an IgG antibody that has a reduced rate of clearance and reduced bioactivity. The presence of macroprolactin should be confirmed by polyethylene glycol precipitation, particularly in a patient with a moderately elevated prolactin level and less typical symptoms

tx: primary therapy is medical - dopamine receptor agonists (cabergoline)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

ddx of behavioral issues in adolescents

A
  • substance abuse
  • psychiatric disorders
  • thyroid conditions
17
Q

deformities assoc. w/ 2 vessel cord?

A
  • Typically called single umbilical artery
  • Rare condition with incidence of less than .5%
  • When there is a single umbilical artery (usually the left artery) the incidence of congenital defects is high at nearly 25%
  • In the case of a single umbilical artery the infant should have a screening ultrasound of the abdomen and kidneys
18
Q

ddx for neonate w/ persistent hypoglycemia?

A
Prematurity
Intrauterine growth retardation (IUGR)
Infant of diabetic mother
Hypothermia
Perinatal Asphyxia
Sepsis
Disorders of gluconeogenesis/glycogenolysis
Hyperinsulinism
Primary and secondary adrenal insufficiency
Congenital hypopituitarism
19
Q

Smith-Lemli-Opitz syndrome

A
  • Microcephaly, low set ears, micrognathia
  • Genital abnormalities occur 70% of the time and include, cryptoorchism, micropenis, hypoplastic scrotum
  • Cardiac defects 50% of the time most commonly endocardial defects
20
Q

Kallmann syndrome

A
  • a form of hypogonadotropic hypogonadism (HH), which is a condition affecting the production of hormones that direct sexual development
  • born with an unusually small penis (micropenis) and undescended testes (cryptorchidism)
  • . At puberty do not develop secondary sex characteristics, such as the growth of facial hair and deepening of the voice in males
  • females have amenhorrhea with little or no breast development
  • patients also have loss of sense of smell!!!! this is due to GnRH cells staying in the nose
  • unilateral renal agenesis
  • cleft lip/ clef palate
  • abnormal eye mvmts, abnormal tooth development
  • bimanual synkinesis - mvmt of one hand is mirrored by the other hand
21
Q

Prader-Willi syndrome

A
  • abnormal seratonin receptor
  • Most common form of syndromic obesity (1 in 15,000 live births)
  • Characterized at birth by hypotonia, failure to thrive, feeding difficulties, hypogonadism and developmental delays
  • At approximately 2 years of age hyperphagia and obesity are noted with growth hormone deficiency, short stature, small hands and feet, behavioral problems and characteristic facial features
22
Q

common endocrine Causes of Micropenis in the Newborn?

A
  • Hypogonadotrophic - hypogonadism secondary to pituitary and hypothalamic lesions
  • Primary testicular failure
  • Apparent micropenis secondary to virilization of external genitalia secondary to 21α-hydroxylase and 11β-hydroxylase deficiency
23
Q

what do you think when se ehypogonadism (micropenis) and hypoglycemia

A

suggests a hypopituitary state - lack of GnRH and ACTH and GH
= congenital panhypopituitarism

24
Q

congenital hypopituitarism

A

Growth hormone deficiency:

  • Severe prenatal GH deficiency occurs but has little effect on fetal growth that is dependent on insulin, insulin growth factor 1 and 2 but can present as micropenis, especially if gonadotropins are decreased as well. (this is why fetal growth was normal)
  • GH deficient in the newborn may include hypoglycemia and exaggerated jaundice with both direct and indirect bilirubin

LH and FSH deficient:
- micropenis, testicular hypoplasia and undescended testes

ACTH deficiency:
- hypoglycemia
(not assoc. w/ salt wasting or hyperkalemia)

TSH deficiency:
- large fontanelle, lethargy, constipation, hoarse cry, hypotonia, hypothermia, jaundice

25
Q

Lab support for ddx of congenital hypopituitarism?

A

Diagnosis based on the sum of the clinical findings (micropenis, undescended testes, hypoglycemia and jaundice) and laboratory findings that evaluated each of the pituitary hormonal axis

ACTH-cortisol (hypoglycemia)

TSH-free T4 (very low level of free T4)

GH-IGF-1 (hypoglycemia, jaundice and micropenis)

LH-FSH-testosterone (undescended testes)

MRI of pituitary

26
Q

bright spot on MRI?

A

Posterior pituitary seems to be functioning as evidenced by normal sodium levels and bright spot on MRI indicating presence of araginine-vassopressin containing cells

27
Q

midparental height calculation? predicted height

A

Girls: 13 cm (or 5 inches) is subtracted from the father’s height and averaged with the mother’s height.

(Father’s ht – 13 cm) + Mother’s ht / 2

Boys: 13 cm (or 5 inches) is added to the mother’s height and averaged with the father’s height.

Father’s ht + (Mother’s ht + 13 cm) / 2

The child should be on track towards an adult height within 8.5 cm (= 2 SD) of predicted (the calculated midparental) height.

28
Q

how much do kids grow per year?

A

about 2 inches per year (5 cm /year)

29
Q

most imp. factor in evaluating child growth?

A

Abnormal growth velocity is the single most important factor in evaluating growth of a child between age 2 and onset of puberty!

height velocity is abnormal if: the height-for-age curve has deviated downwards across two major height percentile curves (eg, from above the 25th percentile to below the 10th percentile).

30
Q

constitutional delay of growth and puberty?

A
  • Normal height for bone age, but not for chronological age
  • Family hx positive for delayed growth and/or puberty
  • H&P, bone age (delayed); labs if height velocity slowed
  • Reassure and monitor growth q 6 months
  • Consider treatment with steroids during puberty
  • Slow height velocity early, then normal; pubertal growth spurt is delayed but prolonged –> normal adult height
  • end up normal, but start out really small for their age
31
Q

Turner syndrome:

A

cause for short stature

  • short stature may be only presenting sign!
  • make sure in delayed puberty in female
  • patient is XO: might look normal and havn’t had period yet
  • have short neck
  • have wide spaced nipples
  • hyperpigmented nevi, a increased carrying angle (angle at elbow)
  • karyotype to ddx this!
32
Q

go over growth charts

A

at end of dow’s slideshow