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Critical Care 2 > Exam 2, deck 2 > Flashcards

Exam 2, deck 2 Flashcards

1
Q

Ratio of Sickle cell trait

A

1:12 Black Americans

1:150 Hispanic Americans

300,000 babies born each yr with Sickle cell disease globally

2,000 babies with SCD born in US

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2
Q

SCD has a problem on what chromosome. What happens?

A

Chromosome 11
Point mutation for Hemoglobin S
Substitutes Glutamine for Valine

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3
Q

SCD is autosomal _____

A

Recessive
must have 2 abnormal copies to result in disease

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4
Q

Hemoglobin Genotypes for SCD

A

AA: Normal hemoglobin
AS: Sickle cell trait
SS: Sick cell disease

Other beta globin Traits
C trait (AC)
B0 trait (AB0)
B+ trait (AB+)

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5
Q

You have a mom and dad who both have Sickle Cell trait what are your genetic possibilities?

A
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6
Q

Genetic possibilities for mom with Beta Thalassemia trait (AB) and dad with Sickle cell trait (AS)

A
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7
Q

Genetic possibilities for mom with hemoglobin C trait (AC) and dad with Sickle cell trait (AS)

A
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8
Q

labs that show intravascular and extravascular hemolysis in SCD

A

Increased LDH
Increased bilirubin

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9
Q

Sickle RBC lives how long vs normal

A

8-21 days vs 120 days

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10
Q

polymerization of hemoglobin S leading to membrane rigidity

A

SCD

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11
Q

What type of anemia is seen in SCD

A

Normocytic anemia

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12
Q

what type of anemia is seen in SB and SC

A

microcytic anemia

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13
Q

target cells on smear

A

Hemoglobin SC

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14
Q

general preventative care for SS and SB0

A

Penicillin by 6 weeks of age
(spleen is impacted and not as effective to prevent infection - functional asplenia)
<3 years - 125 mg BID
>=3 years - 250 mg BID

Transcranial Doppler Ultrasound (TCD) by age 2 and at least annually until unable to obtain values - looking at cerebral blood flow to see who is at high risk for stroke

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15
Q

All types of sickle cell genotypes preventative care

A

Fever precautions: 101 is a med emergency

pneumococcal and meningococcal vaccines

annual influenza vaccine

Annual retinopathy screening starts at 10 years

annual screening for proteinuria begins at age 10 yrs

Genetic counseling for parents and adolescents

Folic acid supplementation if live outside US

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16
Q

most common cause of death in children with SCD

A

infection

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17
Q

SCD is at higher risk for what infections

A

pneumonia
Osteomyelitis which can be difficult to discern from Vaso-occlusive pain (VOP) on imaging

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18
Q

most common complication in SCD

A

Vaso-occlusive pain crisis

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19
Q

Pain in a vaso-occlusive pain crisis is what type of pain

A

Ischemic due to tissue infarction

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20
Q

Vaso-occlusive pain crisis may be precipitated by

A

dehydration
temp extremes

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21
Q

A pulmonary emboli in SCD is from

A

bone marrow breaking off

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22
Q

Defined as a new lung infiltrate, chest pain or resp sx +/- fever

A

Acute chest syndrome

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23
Q

Any fever in sickle cell disease requires

A

blood cultures
antibiotics
+/- chest x ray

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24
Q

vascular flow out of spleen blocked due to occlusion. Spleen starts blowing up like a balloon

A

splenic sequestration

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25
Q

symptoms of splenic sequestration

A

Acute and painful splenomegaly
irritability
pallor
+/- fever
Hgb below baseline +/- thrombocytopenia

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26
Q

transfusions in splenic sequestration

A

small aliquots of RBC transfusions, even though Hgb may be dramatically low. Non-sickled blood helps to release trapped native RBCs in spleen

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27
Q

After you have had splenic sequestration, do you have to worry about it happening again

A

yes

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28
Q

Unwanted, painful erection in SCD

A

Priapism

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29
Q

Early intervention may prevent what in priapism

A

irreversible penile fibrosis or impotence

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30
Q

Treatment for Priapism

A

Short episodes managed at home: increase fluids, warm bath, frequent urination, analgesics +/- pseudoephedrine

If > 2 hrs, needs medical attention
Potential Urinary catheterization
consult urology

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31
Q

hemoglobin severely below baseline with reticulocytopenia which can happen in any hemolytic anemia

A

Aplastic crisis
(in SCD lecture)

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32
Q

What illness is associated with Aplastic crisis

A

Parvovirus B19

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33
Q

Aplastic crisis recovery/treatment

A

spontaneous recovery within 7-10 days
may need transfusion support until recovery

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34
Q

Common symptoms of stroke in SCD

A

Hemiparesis
Seizures
Gait dysfunction
Speech Defects are common

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35
Q

imaging for stroke in SCD

A

initial non-contrast CT
then MRI +/- MRA

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36
Q

Treatment for stroke in SCD

A

Emergent exchange transfusion. Donor must not have Sickle cell trait!

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37
Q

Untreated stroke in SCD

A

20% mortality and 70% with permanent motor/cognitive defects

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38
Q

screening tool to determine children at increased risk of stroke

A

TCD

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39
Q

Abnormal TCD value

A

> 200 cm/s

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40
Q

when do you screen for TCD

A

begins at age 2 until at least 16 years old

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41
Q

If you have an abnormal TCD, what happens

A

start chronic transfusion therapy every 4 weeks to prevent stroke.

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42
Q

chronic complications of sickle cell disease and preventative measures

A

Neurocognitive abnormalities
-Neuropsychological eval for delays or declining school performance

Retinopathy
-Annual eye exams at age 10

Lung disease
-PFTs for those with pulmonary symptoms

Cholelithiasis
-Bilirubin stones in childhood or early adolescence

Leg ulcers
-more common in tropical climates

Avascular necrosis

Growth delay
-linear and puberty

Pulmonary HTN

Cardiomegaly with Left ventricular hypertrophy

Proteinuria and nephrotic syndrome
-avoid nephrotoxic drugs and contrast dye when possible

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43
Q

Treatment for SCD

A

Curative - Bone marrow transplant

-only for patients with severe disease or stroke
-Best prognosis with HLA matched sibling donors

working on gene therapy but not there yet

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44
Q

Transfusions in SCD

A

Leukoreduced
Sickle neg units
C, E, Kell matched units
Increased risk of alloimmunization, autoantibodies
Avoid overtransfusion, no need to achieve a normal Hgb
Avoid targe hgb >10 gm/dl in non-chronically transfused patients

Can have hemolytic transfusion reactions

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45
Q

transfusion calculation

A

Quick and dirty: Weight: kg x (goal hgb - current hgb) x 3.75 = mL of PRBCs

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46
Q

SCD med treatments

A

Hydroxyurea (Hydrea)

Voxelotor (Oxbryta)

Crizanlizumab ((Adakveo)) - monthly infusion

L glutamine (Endari)

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47
Q

which SCD treatment does not require lab monitoring

A

Voxelotor (Oxbryta)

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48
Q

Oldest SCD treatment

A

Hydroxyurea

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49
Q

SCD treatment that is an infusion

A

Crizanlizumab (Adakveo)

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50
Q

Medications that are FDA approved for SCD, What are the ages?

A

Hydroxyurea (Hydrea) - >=2 yrs

Voxelotor (Oxbryta) >= 12 years

Crizanlizumab ((Adakveo)) - monthly infusion - >= 16 years

L glutamine (Endari) - >= 5 years

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51
Q

Hydroxyurea (Hydrea) activates

A

Hemoglobin F

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52
Q

what type of genetic disorder is hemophilia

A

X- linked recessive bleeding disorder.

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53
Q

Hemophilia is caused by deficient or defective

A

Factor VIII (Hemophilia A) or Factor IX (Hemophilia B)

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54
Q

Hemophilia is a disorder or secondary hemostasis meaning that

A

fibrin clot formation is too unstable to adequately stop bleeding

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55
Q

what happens in hemophilia

A

Normally there is an injury to a vessel, both intrinsic and extrinsic pathways of clotting activated, leads to stabilization of platelet plug so bleeding is contained. When there is a Factor VIII or IX deficiency (these are responsible for stabilization of platelet plug by forming fibrin clot. So Secondary hemostasis is prevented (jelly like and unstable). This leads to delayed clotting and spontaneous bleeding.

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56
Q

Hemophilia B is often referred to as

A

Christmas disease

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57
Q

which type of hemophilia is most common

A

Hemophilia A

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58
Q

If a mom has a family history of hemophilia, what is important during birth

A

no use of forceps or vacuum extraction

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59
Q

Differential Dx for conditions that affect fibrin clot formation

A

Hemophilia
Von Willebrand disease
Systemic lupus erythematosus
Factor XII deficiency
Vit K deficiency
Liver disease
DIC
Heparin
Warfarin

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60
Q

In Hemophilia you would expect PTT to be
Platelet count

A

prolonged
normal platelet count
normal PT
normal fibrinogen
normal bleeding time

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61
Q

what tests look at Hemophilia

A

Assays for Factor VIII and IX

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62
Q

initial dosing for hemarthrosis in pt with factor VIII deficiency
dose for next day?

A

25-50 units/kg of Factor VIII concentrate
20 units/kg the following day
additional doses based on treatment response

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63
Q

initial dosing for hemarthrosis in pt with factor IX deficiency
dose for next day?

A

40-80 units/kg of factor IX concentrate followed by
20units/kg the following day

additional doses based on treatment response

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64
Q

total dose of factor VIII in units formula

A

= desired rise in plasma factor VIII activity x body weight in kg x correction factor of 0.5

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65
Q

formula of dose for correction of Factor IX

A

desired rise in factor IX activity times the body weight in kg

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66
Q

half life of factor VIII and factor IX

A

VIII - 8-12 hours
IX - 12-24 hrs

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67
Q

Joint aspiration generally avoided in Hemophilia except hip hemarthrosis due to associate with

A

avascular necrosis of femoral head

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68
Q

supportive care in hemophilia for joint bleeding

A

ice application
compressive dressing
resting the joint
elevating it

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69
Q

muscle hemorrhage can lead to

A

contractures
muscle atrophy
pseudotumor formation

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70
Q

In hemophilia pt, the development of _____ hemorrhage is particularly dangerous and can result in severe morbidity

A

Iliopsoas

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71
Q

life threatening bleeding in Hemophilia

A

bleeding into the CNS, into and around the airway and into the peritoneal cavity

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72
Q

The goal for treating life threatening hemorrhage in hemophilia

A

to maintain near normal levels of clotting factor for a min of 14 days and then prophylaxis doses to ensure resolution of hemorrhage.

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73
Q

in hemophilia, after intracranial hemorrhage the patient should be treated with prophylaxis for at least

A

6-12 months

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74
Q

Treatment in mild to moderate hemophilia A

A

desmopressin acetate (DDAVP) either IV or intranasally.
0.3 mcg/kg for 3 doses→ if bleeding does not respond, supplemental factor VIII concentrate can be given
DO NOT give to pts with severe hemophilia.

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75
Q

treatment in severe hemophilia

A

frequently treated with prophylactic infusions of factor VIII or factor IX concentrates to prevent bleeding into joints and other tissues.

-May result in alloimmunization and the development of autoantibodies that inhibit the function of the infused factor concentrates.

Suspect pt has autoantibodies when unabated bleeding despite administration of adequate doses of factor concentrate

Bleeding in the presence of an inhibitory antibody is difficult to control and requires administration of drugs that bypass the necessity for factor VIII or IX activity→ recombinant activated factor VII or activated prothrombin complex

Ultimate goal is to get rid of autoantibodies with immune tolerance induction therapy→ administer very large doses of factor VIII in an effort to tolerize the pt against the exogenous factor. Success rate is 50-70%

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76
Q

what race is twice as likely to develop inhibitory antibodies to the factor in hemophilia

A

African Americans

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77
Q

what type of precautions are used in hemophiliac patients before surgery or an invasive procedure

A

avoid NSAIDS and products containing ASA for 1-2 weeks prior to procedure

recombinant clotting factor concentrate to achieve 100% replacement immediately preceding procedures
-Factor VIII concentrate - 50units/kg parenterally
maintenance 25 units/kg

Factor IX - 75-100units/kg parenterally
maintenance 35-50 units/kg

assess pt for presence of any inhibitors

post op administration of factor concentrate at maintenance doses for at least 3 weeks or until no further bleeding symptoms remain

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78
Q

what medications do hemophilia pt have to avoid bc it inhibits platelets or coagulation factors

A

NSAIDS
ASA
Anticoagulants
Certain abx such as
Carbenicillin
PCN G

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79
Q

Hemophilia pt should be evaluated annually for

A

annual evaluation at an HTC for
infectious diseases and other blood borne pathogens

Vaccinations recommended against Hepatitis A and B

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80
Q

contraindications (lifestyle) in hemophilia

A

no contact sports

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81
Q

ITP < 3 months from diagnosis

A

Newly diagnosed ITP (Immune Thrombocytopenia)

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82
Q

Idiopathic thrombocytopenia purpura is now called

A

Immune Thrombocytopenia (ITP)

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83
Q

ITP 3-12 months from diagnosis

A

Persistent ITP

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84
Q

ITP > 12 months from diagnosis

A

Chronic ITP

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85
Q

Thrombocytopenia that occurs due to a destruction in peripheral circulation due to inappropriate platelet0directed antibody development
(platelet production is not the problem)

A

Immune Thrombocytopenia

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86
Q

ITP ages

A

Peak ages 2-4 years but can occur at any age

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87
Q

rapid onset of petechiae, purpura, bruising, mucocutaneous bleeding

A

ITP

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88
Q

Triggers for ITP

A

usually 1-2 weeks after
viral illness
Live virus Immunization (MMR)
Allergic reaction

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89
Q

what vaccine has been related back to ITP

A

MMR

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90
Q

greatest incidence of ITP season

A

fall

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91
Q

MPV is the counterpart of ___
what does it tell you

A

MCV
tells you how big your platelets are

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92
Q

MPV in ITP

A

higher…Platelets typically bigger

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93
Q

ITP is a diagnosis of

A

exclusion

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94
Q

diagnostic criteria of ITP

A

diagnosis of exclusion

Physical exam normal except platelet type bleeding (mucous membranes, bruising)

No sig lymphadenopathy
No sig splenomegaly (tip palpable in 10%)

CBC otherwise normal unless explained by infection

50% of pt present with platelets less than 20k

In lipincott - diagnostic is <100,000; large platelets on smear

Sudden onset of bruising, mucocutaneous bleeding, petechiae

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95
Q

50% of ITP pt present with platelets less than

A

20K

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96
Q

Patho of ITP

A

Autoantibodies (IgG) against platelet antigens

Platelets are flagged with autoantibodies

Destroyed by spleen

+/- Decreased platelet production

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97
Q

Platelet transfusion in ITP

A

Contraindicated. Adding fuel to the fire.

limited role in life threatening bleeding

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98
Q

Treatment in ITP

A

IVIG 1gm/kg/day (prevents destruction of antibody coated platelets)

Steroids - first line at many centers (prednisone, Methylpred, Dexamethasone)

Anti-RhD immune globulin (WinRho SDF) (works similarly to IVIG) - only in Rh positive patients

Thrombopoietin-R agonists (TPO agonists) - tells body to make more platelets -
-Eltrombopag (Promacta) -daily, oral

Romplostim (N-Plate) - Weekly, subcutaneous

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99
Q

adverse effects of IVIG

A

n/v
headache
fever

Rare
alloimmune hemolysis infection transmission

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100
Q

IVIG is derived from

A

human plasma

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101
Q

IVIG cost

A

$1000/gm at TCH

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102
Q

Anti-RhD immune globulin (WinRho SDF) can only be used in patients who are

A

Rh +
Have a spleen

used in ITP

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103
Q

dosing for Anti-RhD immune globulin (WinRho SDF)

A

75 mcg/kg IV x 1

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104
Q

Anti-RhD immune globulin (WinRho SDF)
contraindicated if they have what infection

A

mono
active EBV infection

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105
Q

adverse effects Anti-RhD immune globulin (WinRho SDF)

A

fever
chills
n/v
effects lessened by premedications

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106
Q

Corticosteroid therapy in ITP takes a min of how many days to work

A

3-5 days

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107
Q

Romplostim (N-Plate) - takes how long to work

A

weeks to months for effect

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108
Q

Treatment with Life threatening Bleeding in ITP

A

Platelet infusions/drip
Emergent splenectomy (sometimes does not fix)
IV Methylprednisolone
IVIG
Recombinant FVIIa

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109
Q

Antibodies that coat platelets in ITP

A

IgG, IgA, IgM

110
Q

common pediatric hematologic malignancies

A

Acute lymphocytic leukemia
Acute myeloid Leukemia

Hodgkins lymphoma
Non-Hodkins lymphoma

111
Q

Common pediatric solid tumor malignancies

A

Medulloblastoma brain tumor
Astrocytoma brain tumor
Craniopharyngioma brain tumor
Ependymoma brain tumor

Neuroblastoma

Osteosarcoma bone tumor
Ewing’s Bone tumor

Wilm’s tumor
Rhabdomyosarcoma
Retinoblastoma

112
Q

most commonly diagnosed cancer in peds 0-14 years

A
  1. Leukemia
  2. Brain tumors
  3. Lymphoma
113
Q

most commonly diagnosed cancer in peds 15-19 years

A
  1. Hodgkin
  2. Thyroid
  3. Brain tumors
114
Q

syndromes that predispose to cancer (inherited genetic mutations that predispose them)

A

Trisomy 21
Fanconi anemia
Neurofibromatosis 1
Tubular sclerosis
Beckwith-Wideman Syndrome, Isolated hemihypertrophy
Von Hippel Lindau
Li Fraumeni
Familial adenomatous polyposis

115
Q

common childhood illness symptoms that present with oncology

A

fever
infections that dont resolve
joint pain
rash
n/v/d

116
Q

physical exam findings - oncology

A

Pain
Joint or bone swelling, masses
Hepatosplenomegaly
Diplopia
nystagmus
exotropia
gait changes
ataxia
petechiae

117
Q

oncology workup

A

labs:
CBC diff
platelets
electrolytes
BUN
Creatinine
Calcium
magnesium
phosphorus
uric acid
LDH
liver enzymes
Coag panel

Urinalysis

Diagnostic imaging depends on differential
Chest x ray
CT scan
PET
MRI
US

Invasive procedures
-biopsy
-bone marrow aspiration and biopsy
-lumbar puncture (if pt has neuro symptoms, you need an MRI before the LP)

118
Q

most common site of metastasis in solid tumor cancers

A

lungs

119
Q

Neoadjuvant chemotherapy purpose

A

used in solid tumors to reduce size of tumor. Make it more sizeable for surgical resection. Also tests response to chemotherapy. When they take out the tumor. We can see what percentage of the tumor is alive and what percentage is dead. Helps guide therapy

120
Q

Staging cancer

A

Low, intermediate and high risk
local or metastatic
not same system in pediatrics as adults

121
Q

classifications of chemotherapeutic agents

A

Cell cycle specific agents
G1: RNA synthesis begins
S: DNA is replicated
G2: RNA synthesis is complete
M: Mitosis (cell division) occurs

Cell cycle nonspecific agents
-bolus dosing

122
Q

Cell cycle

A
123
Q

Immunotherapy in Oncology

A

augment, modify or restore aspects of the normal immune response to control cancer cells

Monoclonal antibodies - attach to surface markers and cause cell death

Checkpoint inhibitors- block protein receptors on cell surfaces that inhibit cell death

124
Q

Targeted therapies in oncology

A

Targets specific pathways involved in cancer growth
-Tyrosine kinase-enzyme that binds phosphates to other amino acids. functions as an on-off switch for cellular functions

Targeting specific antigens of cancer cells
Chimeric antigen receptor (CAR) T cells: patients engineered T cells to recognize, attach to and kill antigens on the tumor cells (adoptive cell transfer tharapies)

125
Q

High energy particles to break strands of DNA preventing cell replication and kill the tumor

A

radiation

126
Q

dividing the total dose into smaller fractions to allow for tumor kill and sparing of normal tissue during radiation

A

Fractionation (proton)

127
Q

what emergent oncological presentations that might warrant radiation as emergent use with chemo

A

Superior cava syndrome
airway compromise
spinal cord compression

also in
palliative care/pain control

128
Q

Radiation is not for children < ____ yrs

A

3 years age d/t underdeveloped nervous system

129
Q

types of radiation

A

Proton beam

Brachytherapy - radioactive implants (used frequently in infants)

Radiopharmaceuticals (iodine given in bloodstream to target tumor)
-MIBG therapy for neuroblastoma

130
Q

what radation used frequently in babies

A

Brachytherapy - radioactive implants (used frequently in infants)

131
Q

Radiopharmaceutical used in neuroblastoma

A

MIBG therapy

132
Q

Side effects of radiation

A

Based on target area
Fatigue
N/v
diarrhea
Xerostomia
Erythema, darkening of skin or excoriation
Pneumonitis
Pericarditis or effusion
Radiation nephritis
Radiation cystitis

Growth hormone def
Hypothyroidism
Hypopituitarianism
Gonadotropin defi
ACTH deficiency
Neruopathies

Musculosk
-Osteochondromas
-Arrest of growth plates

133
Q

Side effects of radiation

A

Based on target area
Fatigue
N/v
diarrhea
Xerostomia
Erythema, darkening of skin or excoriation
Pneumonitis
Pericarditis or effusion
Radiation nephritis
Radiation cystitis

Growth hormone def
Hypothyroidism
Hypopituitarianism
Gonadotropin defi
ACTH deficiency
Neuropathies

Musculosk
-Osteochondromas
-Arrest of growth plates

134
Q

After your neutrophils respond, what is your next cell to respond

A

Monocytes migrate to liver, spleen and become macrophages and dendritic cells

135
Q

cell that displays Ag fragments on cell surface and present to lympocytes

A

Monocytes

136
Q

messengers between innate and adaptive immune response

A

Monocytes

137
Q

surface markers on lymphocytes (used in targeted therapies and monoclonal antibodies)

A

Stem cells: CD34
T cell markers: CD3, CD4, CD5, CD7, CD8

B cell markers: CD10, CD19, CD20, CD22

NK cell marker: CD56

CD= cluster of differentiation

138
Q

Lab testing for surface markers on lymphocytes

A

flow cytometry or immmunophenotyping

139
Q

impact of chemotherapy on hematopoiesis

A

7-10 days - neutropenia, anemia, thrombocytopenia (Count nadir)

14-21 days - counts start to recover - if recovered -> next chemo course
if not, wait

140
Q

ANC formula

Normal values

A

Absolute neutrophil Count (ANC) = WBC x % neutrophils or segs + % bands

> = 1000 - normal
<1000 - neutropenia
200-500 - moderate neutropenia
<200 severe neutropenia

141
Q

Neutropenic precautions

A

strict handwashing

social isolation

Call for temp 100.4

Immediate ER visit for blood cultures and broad spectrum antibiotics within 1 hour

No rectal temps or suppositories

assess oral mucosa, all skin, peri-rectal area

pain may be only one sign/symptom. unable to demonstrate inflammatory response ( no redness or pus)

142
Q

PJP prophylaxis for oncological

A

Bactrim
Pentamidine
Atovaquone
Dapsone

143
Q

Antibiotic Prophylaxis for onc

A

Levofloxacin

144
Q

vaccines in onc

A

NO vaccines until off chemo for 6 months

Influenza vaccine to patients, family members

no covid vaccine

145
Q

vaccines in BMT

A

none until 1 year post BMT and off immune suppression. Only attenuated vaccines

Live virus vaccines at 2 years post BMT

Siblings - no varicella vaccine. MMR okay

No influenza vaccine to patients or family early post BMT or active graft vs host disease

COVID vaccine hold while on steroids

146
Q

Fever and Neutropenia in Hemoc empiric abx

A

Outpatient low risk: Ceftriaxone/Cefepime with oral fluoroquinolone (Cipro or Levo) x 7 days

inpatient low risk - ceftriaxone

High risk such as neutropenia or with focal findings such as cellulitis, pneumonia, mucositis, tunneled line infections:
Cefepime +/- Vancomycin (concern for strep/staph; skin barrier breakdown) +/- Metronidazole (Flagyl) (concern for intraabdominal process/GI barrier breakdown)

147
Q

In bolick what infections are associated with ITP

A

measles
mumps
chicken pox
infectious mononucleosis
common cold
H. pylori
Hepatitis C

148
Q

Onc patient with no identified infectious source that have persistent fever after 4-7 days of broad spectrum abx. What should be considered

A

fungal etiology

149
Q

Granulocyte colony stimulating growth factors. What do these do. What are some agents we use

A

Enhance neutrophil recovery
-Neupogen - SQ, IV once daily
-Neulasta - pegfilgrastim
-SQ 0 once per chemo cycle, 24-72 hours after chemo

-typically used in solid malignancies
-risk of exacerbating blasts

<10kg we use Neupogen over Neulasta for tighter control

150
Q

Engraftment period for BMT

A

14-21 days

151
Q

what happens <3 months post BMT

A

Impaired neutrophil function on immunosuppressive treatment
impaired lymphocyte function

152
Q

3 mos - 1 yr post BMT

A

T4:T8 inversion
delayed production of immunoglobulins

153
Q

1-2 year post BMT

A

naïve but strengthening lymphocyte immunity

154
Q

Oncologic emergencies

A

Anaphylaxis
Septic shock (CLABSI, peri-rectal or other abscess, pneumonia, bacterial translocation in gut)

increased ICP

Spinal cord compression

Superior vena cava syndrome

Tumor lysis (Hyperkalemia, hypocalcemia, hyperuricemia)

Typhilitis

Pancreatitis

SIADH

HTN

DVT

Capillary leak syndrome (specific to T cell immunotherapy)

155
Q

peak onset of leukemia

A

2-10 years old

156
Q

uncontrolled proliferation of immature white blood cells in blood forming tissues of the body

A

leukemia

157
Q

chronic leukemia

A

Chronic myelogenous leukemia (CML)

158
Q

Acute Leukemias

A

Acute lymphoblastic leukemia (more common)

Acute myelogenous leukemia

159
Q

ages associated with poor outcomes in leukemia

A

<12 mos
>12 yrs

160
Q

most common leukemia

A

Acute lymphoblastic leukemia (ALL)

161
Q

s/s leukemia

A

fatigue
bone pain
fever
recurrent infections
anorexia
weight loss
pallor
gingival bleeding
bruising
hepatosplenomegaly

162
Q

what lab findings are we looking for in leukemia

A

anemia
thrombocytopenia
elevated WBC with blasts and low neutrophils

Elevated LDH

tumor lysis (hyperkalemia, hypocalcemia, hyperphosphatemia, hyperuricemia)

163
Q

treatment in leukemia

A

Chemotherapy +/- radiation

Relapse - chemo, radiation, BMT

164
Q

length of treatment for leukemia

A

2 1/2 years

165
Q

race higher risk for ALL

A

Hispanic followed by
white

166
Q

CML develops due to

A

translocation of chromosomes 9 and 22 that produce the Philadelphia chromosome→ results in BCR-ABL1 chimera mRNA that allows for growth of leukemia cells

167
Q

Testes and CNS are important sites to check for leukemia …..why?

A

very hard to treat

168
Q

localized masses of leukemic cells

A

Chloromas

169
Q

small, colorless to blue/purple nodules under the skin which are signs of leukemic infiltrates (most common in infants with congenital leukemia)

A

Leukemia cutis

170
Q

Hgb requirement to go for radiation

A

at least 10

171
Q

new dx of ALL/AML, when would you start allopurinol, rasburicase and aggressive IV fluid management

A

WBC>100,000 or in acute tumor lysis syndrome

172
Q

Which is higher risk for leukocytosis

A

AML (more cell lines affected)

173
Q

induction therapy for ALL lasts approx

A

4-6 weeks with goal of eliminating leukemia

174
Q

chemo and meds for induction therapy for ALL

A

Vincristine
Corticosteroids
Asparaginase (PEG)

If high risk they will add in
anthracycline

175
Q

What is done at end of induction therapy for ALL to help guide treatment plan

A

BMA + LP using flow cytometry

176
Q

phases in ALL treatment

A

Induction phase
consolidation phase
maintenance phase

177
Q

Goal of consolidation phase

A

eliminate submicroscopic levels of leukemia

178
Q

meds used in consolidation phase

A

High dose methotrexate
Oral mercaptopurine
Asparaginase (PEG)
Vincristine
Decadron

high risk add
Anthracycline
Cytarabine
Cyclophosphamide

179
Q

why do males get longer maintenance therapy

A

testes being a sanctuary site for leukemia to hide

180
Q

ALL with CNS involvement, do you need to add radation

A

yes

181
Q

CD 19 CAR T cells serious AE

A

tumor lysis syndrome
Cytokine release syndrome
encephalopathy
(all reversible but dangerous and can occur in the weeks following)

182
Q

Cancer of the blood and blood-forming organs, such as the bone marrow, lymph nodes, and spleen.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 834). Wolters Kluwer Health. Kindle Edition.

A

leukemia

183
Q

leukemia is classified by

A

the cell line affected and level where differentiation has been interrupted

184
Q

inherited conditions that predispose patients to ALL

A

Fanconi anemia, trisomy 21, ataxia telangiectasis, Klinefelter syndrome, and Shwachman–Diamond syndrome.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 834). Wolters Kluwer Health. Kindle Edition.

185
Q

increased incidence to AML with previous exposure to ______ and what inherited conditions

A

exposure to chemotherapy and inherited conditions, including trisomy 21, Diamond–Blackfan anemia, Fanconi anemia, Li–Fraumeni syndrome, paroxysmal nocturnal hemoglobinuria, and neurofibromatosis.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 834). Wolters Kluwer Health. Kindle Edition.

186
Q

which leukemia is associated with chromosomal translocation known as philadelphia chromosome

A

CML

187
Q

CML may progress after a variable amount of time to the accelerated phase and blast crisis which resembles

A

acute leukemia

188
Q

In ALL very high WBC may cause

A

Leukostasis

189
Q

what leukemia tend to appear more ill and why

A

AML,
cytopenias are more significant, ecchymoses, petechiae, epistaxis and other bleeding

190
Q

Chloromas seen in

A

AML

191
Q

what leukemia is often symptomatic and is often diagnosed incidentally

A

CML

192
Q

In leukemia what is diagnostic

A

Bone marrow aspirate is diagnostic when blasts comprise >25% of the marrow space

LP is done to determine if CNS is involved

193
Q

Hyperleukocytosis Is a WBC >

A

100,000

194
Q

Hyperleukocytosis results in

A

increased blood viscosity (may result in neurologic, pulmonary, or cardiac sequelae) and is a medical emergency.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 836). Wolters Kluwer Health. Kindle Edition.

195
Q

Therapy for Hyperleukocytosis

A

aggressive hydration, correction of metabolic disturbances, and prevention of tumor lysis syndrome. May require leukopheresis or exchange transfusion.

Transfusion may be indicated

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 836). Wolters Kluwer Health. Kindle Edition.

196
Q

Treatment for CML

A

Current therapy is tyrosine kinase inhibitor (imatinib mesylate) while in chronic phase. The only curative therapy for CML is HSCT from an allogeneic donor; indicated if the patient does not tolerate or fails to achieve or maintain a remission with imatinib mesylate.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 837). Wolters Kluwer Health. Kindle Edition.

197
Q

side effects of chemotherapy and radiation

A

n/v
alopecia
mucositis
anorexia
pancytopenia

198
Q

s/s lymphoma

A

fixed and non tender lymphadenopathy

B-symptoms
-fever
-drenching sweats
-Unintentional weight loss

199
Q

Lymphoma typically occurs in what age

A

15-35

200
Q

what virus is believed to have an association with lymphoma

A

EBV

201
Q

Children with immunodeficiencies are at greatest risk for what type of lymphoma

A

Hodgkin lymphoma

202
Q

which lymphoma spreads faster

A

Non Hodgkin lymphoma

203
Q

is the result of proliferation of T, B, or indeterminant-cell origin lymphocytes,

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 838). Wolters Kluwer Health. Kindle Edition.

A

Non Hodgkin lymphoma

204
Q

spreads more slowly and orderly, typically to adjacent lymph nodes and possibly involving the liver, spleen, bone, bone marrow, lungs, or brain.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 838). Wolters Kluwer Health. Kindle Edition.

A

Hodgkin lymphoma

205
Q

Non Hodgkin lymphoma symptoms

A

Lymphadenopathy may be present. If abdomen is involved, palpable mass may be present and associated with pain, nausea, vomiting, abdominal distension, hepatosplenomegaly, changes in bowel habits, or hematochezia. Mediastinal involvement may present as superior vena cava syndrome, facial/neck swelling, snoring, dysphagia, or chest pain. Systemic symptoms may include fatigue, fever, malaise, weight loss, anorexia, and night sweats. Pancytopenia and related complications may be present if the bone marrow is involved.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 838-839). Wolters Kluwer Health. Kindle Edition.

206
Q

What differentiates NHL from HL

A

Reed sternberg cells
presence ->HL
absent -> NHL

207
Q

Tumor of lymphocytes

A

Lymphoma

208
Q

what “better” to have
HL
NHL

A

HL

209
Q

Reed-Sternberg cells have the appearance of

A

an owls eye

210
Q

3 types of NHL

A

Lymphoblastic lymphoma
Anaplastic large cell lymphoma
Mature B cell lymphoma (Burkitt, primary mediastinal B cell lymphoma, and diffuse large B cell lymphoma)

211
Q

risk for developing NHL

A

-Congenital and acquired immunodeficiencies
-Solid organ transplants are 200-300xs more likely
-EBV

212
Q

oncological process
Contains 2 cell types: Neuroblasts and Schwann cells

A

Neuroblastoma

213
Q

most frequently diagnosed malignancy in infancy

A

Neuroblastoma

214
Q

Med diagnosis age for Neuroblastoma

A

19 mos

215
Q

Most common race for neuroblastoma

A

white

216
Q

neuroblastoma can develop anywhere within

A

the sympathetic nervous system
-most found chest, abd, pelvis

217
Q

50% of neuroblastoma arise from

A

adrenal medulla

218
Q

s/s neuroblastoma

A

asymptomatic
Edema - large masses can alter venous return from lower extremities

abd involvement: tenderness, distention, hepatosplenomegaly

Lesion in upper thoracic spine or posterior mediastinum -> superior vena cava syndrome due to vascular compression

Spinal cord compression: motor weakness, sensory loss, difficulty urinating/pooping
Oncological emergency: steroids, chemo, with possible radiation or surgery
Cervical mass: Horner syndrome = unilateral ptosis, myosis, and anhidrosis
Most common sites for metastatic disease: lymph node, liver, bone, bone marrow, skin (rarely metastasize to lung or brain)

219
Q

spinal cord compression symptoms

A

motor weakness, sensory loss, difficulty urinating/pooping

emergency!

220
Q

spinal cord compression syndrome treatment

A

steroids
chemo
possible radiation or surgery

221
Q

Cervical mass symptoms

A

horner syndrome: Unilateral ptosis, myosis, anhidrosis

222
Q

Most common sites for metastatic disease of Neuroblastoma

A

lymph node
liver
bone
bone marrow
skin

(rare for it to metastasize to lung or brain)

223
Q

Opsoclonus-myoclonus ataxia syndrome (OMA) in Neuroblastoma

A

Myoclonic jerking, nystagmus, cerebellar ataxia
Tx: surgical resection, glucocorticoids, IVIG

224
Q

Elevated LDH and ferritin in Neuroblastoma may suggest

A

more aggressive disease

225
Q

Urine vanillylmandelic acid and homovanillic acid are elevated
in

A

Neuroblastoma

226
Q

what is preferred test to check for metastatic disease in neuroblastoma

A

metaiodobenzylguanidine (MIBG)

227
Q

what test is needed to confirm neuroblastoma

A

Biopsy

228
Q

chemo treatment phase in neuroblastoma

A

Induction – multi agent chemo
Local control – surgical resection of tumor and radiation to tumor bed
Consolidation – high dose, myeloablative chemo followed by autologous stem cell rescue
Maintenance – eradicate any residual, circulating tumor cells

229
Q

2nd most common abd malignancy

A

Wilms Tumor (Nephroblastoma)

230
Q

3 most common gene involvement: WT 1 loss, WNT signaling pathway activation, and IGF2 overexpression

A

Wilms Tumor (Nephroblastoma)

231
Q

Well-demarcated from renal tissue and surrounded by a fragile, gelatinous capsule

A

Wilms Tumor (Nephroblastoma)

232
Q

median age of dx for Wilms Tumor (Nephroblastoma)

A

3.5 years

233
Q

Smooth painless abd mass that does not cross midline most often found during bath or well child ecam

A

Wilms Tumor (Nephroblastoma)

234
Q

what should you be careful with during exam when you suspect Wilms tumor?

A

when there is concern the patient has wilm’s tumor, care should be taken to avoid deep or repetitive and palpation because there is risk for capsular rupture (impacts staging and therapy)

235
Q

why is biopsy contraindicated in Wilms tumor

A

capsular spillage ->advances pt stages and would require chemo and radiation as a part of plan

236
Q

treatment for Wilms tumor

A

Goal: complete ureteronephrectomy with lymph node sampling before chemo (unless you have bilateral disease)
Bilateral: chemo and nephron-sparing surgery
Radiation if patient has stage III or IV, anaplastic histology, or to the lungs if metastases
85-95% survival rates

237
Q

in this onc, lab findings may include acquired vWD or polycythemia

A

Wilms tumor

238
Q

in wilms tumor, always assess for

A

Global Devlopmental Delay, aniridia, macroglossia, hemihypertrophy, overgrowth, history of omphalocele, or genitourinary abnormalities

239
Q

Neoplasm from the sympathetic nervous system, most common extracranial solid tumor of childhood, typically disease of infants and young children.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 840). Wolters Kluwer Health. Kindle Edition.

A

Neuroblastoma

240
Q

Benign counterpart of neuroblastoma

A

Ganglioneuroma

241
Q

In Neuroblastoma, MYCN gene amplification is associated with

A

poorer prognosis

242
Q

Neuroblastoma, DNA index of ___ is associated with poorer prognosis

A

1

243
Q

In neuroblastoma ages >= ______ is associated with poorer prognosis

A

12-18 mos

244
Q

abdominal mass who presents with palpable mass, constipation and refusal to walk

A

Neuroblastoma

245
Q

Neuroblastoma with metastatic disease may also present with

A

bone pain
malaise
fever
raccoon eyes (periorbital ecchymosis)
Blueberry muffin spots (metastasis to subcutaneous tissue)

246
Q

Fastest growing tumor in pediatric oncology

A

Burkitt’s (Non-Hodgkin Lymphoma)

247
Q

Fast growing tumor often presents with bowel perf

A

Burkitt’s (Non-Hodgkin Lymphoma)

248
Q

which type of lymphoma that effects deeper lymph nodes

A

NHL

249
Q

type of lymphoma that effects superficial lymph nodes

A

HL

250
Q

lymphoma that more commonly affects children 15-19

A

HL

251
Q

lymphoma that more commonly affects children <14

A

NHL

252
Q

Treatment time for HL and NHL

A

HL 6 months
NHL - 3+mos but can be long 2.5 years like leukemia

253
Q

most common solid tumors in children

A

brain tumors

254
Q

60% of Brain tumors are located

A

Infratentorial (cerebellum)
40% are in the anterior 2/3 or brain mainly in the cerebrum (Supratentorial)

255
Q

s/s brain tumors

A

depends on location and size
Headaches (usually in the AM)
lethargy
n/v
visual changes
polydipsia
personality or academic changes

Physical exam
Nystagmus
diplopia
ataxia
cranial nerve defects

256
Q

Cranial nerves

A

I olfactory
II optic
III oculomotor
IV Trochlear
V trigeminal
VI Abducens
VII facial
VIII vestibulocochlear
IX Glossopharyngeal
X vagus
XI Accessory

257
Q

which cranial nerves are for eye movement

A

III, IV, VI

258
Q

which cranial nerves
sensation of face, biting, chewing

A

V

259
Q

Which cranial nerves
facial muscles of face

A

VII

260
Q

Which cranial nerves
Hearing and balance

A

VIII

261
Q

Which cranial nerves?
oral, taste

A

IX

262
Q

Which cranial nerves? brainstem, parasympathetic control of heart, lungs, GI tract

A

X

263
Q

Which cranial nerve?
Shoulder elevation

A

XI

264
Q

Which cranial nerve tongue movement

A

XII

265
Q

Cerebellar tumors you will see changes in

A

gait
coordination issues
may present with increased ICP symptoms

266
Q

Treatment for brain tumor

A

Surgical resection
Radiation
Chemo
Length ranges from 6mos to 1 year

267
Q

IN tumor lysis syndrome, hyperurecemia is due to the breakdown of

A

nucleic acids

268
Q

symptoms of tumor lysis syndrome

A

n/v/d
muscle weakness
if hypercalemic -> Trousseau’s sign and Chvostek’s sign

269
Q

tumor lysis syndrome can cause

A

AKI
cardiac arrhythmias
seizures
lactic acidosis

270
Q

what elevated labs coorelate with increased risk of tumor lysis syndrome

A

WBC
LDH

271
Q

Treatment in tumor lysis syndrome

A

for Hyperkalemia -> calcium gluconate, insulin + dextrose, polystyrene sulfonate

for hyperphosphatemia -> phosphate binders

Hyperuricemia -> Allopurinol - inihibits
Rasburicase breaks it down

Renal dialysis
Serial cardiac monitoring

Critical Care 2 (14 decks)

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