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1

Kawasaki labs

CBC: high WBC, normo anemia, elevated platelets 2 week+
blood cx, elevated liver enzymes, low albumin, elevated ESR, sterile pyuria on UA (cath may not show WBCs)

2

requirements for dx of Kawasaki

high fever for at least 5 days PLUS 4/5 of the following:
Changes in oral mucosa
Extremity changes (redness/swelling)
Unilateral cervical lymphadenopathy
Rash
Conjunctivitis
PLUS no other apparent cause for presentation

3

developmental milestones

http://www.med-u.org/the-library/developmental-milestones

4

Juvenile idiopathic arthritis (JIA) criteria

must be less than 16 years of age and have arthritis in at least one joint for more than six weeks. criteria for one category).

5

JIA subtypes

Systemic (includes constitutional symptoms such as fever and rash);
Oligoarthritis (previously called pauciarticular, this type of oligoarthritis typically affects the knee; onset of the arthritis is acute, and it is associated with an asymptomatic iridocyclitis);
Polyarthritis (rheumatoid factor positive and rheumatoid factor negative);
Psoriatic arthritis;
Enthesitis-related arthritis; and
"Other arthritis" (has overlapping features with multiple categories or does not meet full criteria for one category).

6

septic arthritis orgs in kids

Staphylococcus aureus
Streptococcus (neonate: group B; infant and older child: Group A and Streptococcus pneumoniae)
Haemophilus influenzae type b (in unimmunized children)
Neisseria gonorrhea (adolescents)
Kingella kingae (in children less than 4 years)

7

Pediatric ibuprofen dosing

Pediatric dose: 10 mg/kg every 6-8 hrs PO (maximum dose = 40mg/kg/24 hr PO)
Concentration of oral suspension: 100 mg/5 mL (20 mg/1 mL)

8

Most practice guidelines for fever evaluation would recommend routinely sending a urinalysis and culture in what age group of kids/gender?

Males less than 6 months old (less than 12 months old if uncircumcised)
Females less than 12 months old.

9

Bacterial meningitis in immunized children 2 months to 12 years of age is usually due to ?
In younger infants, ? need to be considered

S. pneumoniae or N. meningitidis, but the incidence of invasive pneumococcal disease is diminishing with routine vaccination.

gram negatives such as E. coli and organisms like GBS (Strep agalactiae)

10

Meningitis may present with classic signs including ?
Alternatively, non-specific findings may predominate, including:

increasing lethargy and irritability as well as signs of meningeal irritation (often referred to as nuchal rigidity or meningismus).

Fever (in 90-95% of cases, Anorexia and poor feeding, symptoms of a URI, Myalgias, Tachycardia

11

meningitis antibiotics

third-generation cephalosporin and vancomycin, and then tailoring antibiotics based on sensitivities, for a total of 7-14 days.

12

Complications of bacterial meningitis include:
While it is unusual for treated meningitis to be fatal, morbidity such as ? are known complications.

Stroke
Subdural effusions
Syndrome of inappropriate anti-diuretic hormone (SIADH) secretion.

developmental delays, seizures, and hearing loss

13

3 Ps of McCune-Albright syndrome

Precocious puberty
Pigmentation (cafe au lait spots)
Polyostotic fibrous dysplasia

14

craniopharyngiomas

calcified intracranial tumors in the supersellar region
may present with bitemporal hemianopsia and pit hormone deficiencies: diabetes insipid us, GH deficiency

15

Howell-Jolly bodies suggest..

functional asplenia in a SCD pt as they are nuclear remnants of RBCs typically removed by a functional spleen

16

SIDS happens in what ages?
peaks when?

1 mo to 1 yr
peaks 2-4 mos

17

1 wk hx of leg pain +low grade fever +hepatosplenomegaly +petechia on face/chest think?
next step?

ALL
CBC with platelets and differential

18

Most of the s/s of ALL result from either

replacement of normal bone marrow components with clonal proliferation of a single lymphoblast that has undergone malignant transformation, or from infiltrates of extramedullary sites by these malignant lymphoid cells.

19

ALL has a peak incidence at age ? and occurs more frequently in what gender

2 to 4 years
boys, children with certain chromosomal abnormalities, such as Down syndrome and Fanconi anemia

20

nickname of ALL

the “great imitator” because of its nonspecific symptoms, including anorexia, irritability, lethargy, pallor, bleeding, petechiae, leg and joint pain, lymphadenopathy, and fever.

21

ddx ALL

idiopathic thrombocytopenic purpura (ITP), aplastic anemia, mononucleosis, juvenile idiopathic arthritis, and leukemoid reaction

22

use ? to dx ALL from other diagnoses

bone marrow biopsy: a minimum of 25% blasts confirms the diagnosis (normal marrow contains less than 5% blasts)

23

ALL translocations with poor outcomes

t(4;11)
t(9;22) : Philadelphia chromosome in pts with pre-B ALL

24

why does ALL workup include an LP? CXR?

to examine the CNS for early leukemic involvement; a higher number of blasts in the CSF are associated with a worse prognosis.
CXR is performed to detect a mediastinal mass.

25

ALL induction therapy

prednisone, vincristine, and asparaginase, produces remission within 4 weeks in approximately 98% of children with non–high-risk ALL

26

Intrathecal therapy (± craniospinal irradiation) has decreased the incidence of ? as a primary site of relapse from 50% to approximately 3% to 6%

CNS leukemia

27

ALL Maintenance therapy

methotrexate and 6-mercaptopurine, vincristine, and prednisone is given for 2 to 3 years to prevent relapse; therapy is discontinued for children who remain in complete remission for 2 to 3 years

28

how is ALL survival rate changing?

The 5-year survival rate for childhood ALL has steadily improved over the last 40 years and now is greater than 80%

29

late effects of ALL

neuropsychological deficits, seizures, and endocrine disturbances (ie, growth hormone deficiency) related to CNS prophylaxis; spermatogenesis dysfunction related to cyclophosphamide; delayed sexual maturation in boys who received irradiation of gonadal tissue due to leukemic invasion of the testes; leukoencephalopathy and neurodevelopmental problems (especially in post–CNS radiation patients); and secondary malignancies.

30

ALL vs JIA on CBC

The leukocyte and platelet counts are normal to increased in JIA,

31

causes of splenomegaly

infection (EBV, CMV, bac sepsis, endocarditis), hemolysis (SCD), malignancy (leukemia, lymphoma), storage disease (Gaucher), systemic inflammatory disease (SLE, JIA), congestion (portal HTN)

32

HSP

(also known as anaphylactoid purpura) is a self-limited, IgA-mediated, small vessel vasculitis that typically involves the skin, GI tract, joints, and kidneys.
most commonly diagnosed form of vasculitis in children (about 50% of cases)
use of steroids in treatment is controversial

33

idiopathic thrombocytopenic purpura (ITP) is caused by ?

the binding of an antiplatelet antibody to the platelet surface, leading to removal and destruction of platelets in the spleen and liver. It is the most common cause of isolated thrombocytopenia in otherwise healthy children.

34

ITP treatment

oral corticosteroids, IVIG, RhoGAM
typically until platelet count rises above 20K

35

the most common form of bowel obstruction in children between 6 months and 6 years of age

intussusception

36

diagnosis and treatment of idiopathic intussusception

air or barium enema, requires surgery if unsuccessful

37

Intussusception occurring in HSP is usually ?
diagnosis and treatment?

ileo-ileal, not ileo-colic, and will not be reduced by air or barium enema. Diagnosis requires abdominal ultrasound, and treatment is generally surgical.

38

HSP recurrence

30% recurrence rate
after initial case, follow with UAs, BP and rash evaluation for several months

39

HSP vs ITP

HSP has a normal platelet count, ITP presents with thrombocytopenia

40

VSD murmurs are typically heard later, around ?
why?

2-6 mos
pulmonary vascular pressures reach normal levels by that time (HTN before)

41

widened pulse pressure
conditions that may cause this?

An increase in the difference between systolic and diastolic pressures, resulting in a bounding arterial pulse
fever, hyperthyroidism, anemia, arteriovenous fistulas, and PDA.

42

congenital cardiac defect workup

1. presence of cyanosis via pulse ox and physical exam
2. increased/normal/decreased vascular markings on CXR
3. EKG to determine LVH/RVH or both

43

large VSDs may be accompanied by ?

dyspnea, feeding difficulties, growth failure, and profuse perspiration, and they may lead to recurrent infections and cardiac failure

44

CXR and EKG findings in large VSD

CXR: cardiomegaly with an enlarged left atrium (LA) and ventricle (LV) and increased pulmonary vascular markings. EKG shows biventricular hypertrophy
small VSDs typically normal

45

medical management of VSD

diuretics (eg, furosemide and afterload reduction agents [eg, an ACE-inhibitor]
-adequate caloric intake and may require feeding by nasogastric or gastrostomy tubes

46

Children with ASDs usually have no symptoms but large defects may cause ?

mild growth failure, frequent upper respiratory tract infections, and exercise intolerance

47

the murmur of ASD is from what? heard when/where?
also hear ?
may hear another murmur?

high-volume blood flow from the right ventricle into the normal pulmonary artery; the murmur is not blood flowing across the ASD itself (systolic murmur at the left upper and midsternal borders)
-fixed split S2
-A lower left sternal border diastolic murmur produced by increased flow across the tricuspid valve may be present

48

ASD CXR and EKG findings

CXR: enlarged right atrium, right ventricle, and pulmonary artery and increased pulmonary vascularity
ECG shows RVH and sometimes right-axis deviation

49

ASD complications

well tolerated during childhood but can lead to pulmonary HTN in adulthood or atrial arrhythmias from atrial enlargement

50

Ductus closure in term infants usually occurs within ?

10 to 15 hours of birth and almost always by 2 days of age

51

Closure of the ductus arterioles is delayed in ? infants, perhaps because of ?
Failure of the ductus to close allows shunting of blood from the systemic circulation to the pulmonary circulation, with resultant ?

premature, impaired vasoconstrictor response to increased oxygen tension
myocardial stress, pulmonary vascular congestion, and respiratory difficulty

52

A small PDA usually results in no symptoms but is still closed medically (usually with indomethacin) or surgically (if medical therapy fails or is contraindicated) due to risk of ?

infective endarteritis and paradoxical emboli

53

Closure of a large PDA is done to prevent ?

heart failure and Eisenmenger syndrome

54

treatment of ductus dependent coarctation of the aorta

infusion of prostaglandin E would be required to maintain the patent ductus until definitive repair could be done

55

test that can usually identify the site of the coarctation?
otherwise, what further interventions may be necessary?

ECHO with color doppler
CT, MRI, cardiac catheterization