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Pediatrics- Noelle > Hematology > Flashcards

Hematology Flashcards

1
Q

what is the most common transfusion related infection?

A

CMV

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2
Q

what proteins make up hemoglobin?

A

alpha
beta
delta
gamma

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3
Q

what proteins make up a fetus’s hemoglobin?

A

alpha

gamma

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4
Q

when does HgbA overtake HgbF?

A

HgA overtakes hemoglobin F by 3 months

by 6 months there is very little HbF

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5
Q

what is HbA

A

a2b2

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6
Q

what is HbA2

A

alpha 2 delta 2 (normally up to 3% of adult hgb)

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7
Q

what is HbH

Hb Bart

A

HbH: 4 beta

Hb Bart: 4 delta

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8
Q

are most mutations in alpha or beta??

A

beta!!

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9
Q

when do we see physiologic nadir of Hb in term babies?

A

8-10 weeks
after birth oxygen saturation increases and therefore causes decreased EPO, then EPO production is resumed with an increase in the retic count

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10
Q

when do we see physiologic nadir of Hb in preterm babies?

A

6-8 weeks

nadir is earlier and deeper (>70)

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11
Q

what is the definition of anemia

A

Hb 2 standard deviations below mean value for age, gender and race

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12
Q

how should you classify anemia?

A

decreased production

  • microcytic
  • macrocytic
  • normocytic

increased destruction

  • intrinsic- membrane, hemoglobin enzyme
  • extrinsic- immune, non-immune
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13
Q

where is your blood made?

A

bone marrow

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14
Q

where is fetus’s blood made?

A

liver

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15
Q

where is embryo’s blood made?

A

yolk sac

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16
Q

what is normal hb for men? women? newborn?

A

men: 140-180
women: 120-160
newborn: up to 200/220

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17
Q

what are markers of RBC destruction?

A 
icterus
dark urine
increased reticulocytes
increased unconjugated bilirubin
increased LDH
hemoglobin (not rbc's) in urine
urobilinogen
decreased haptoglobin
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18
Q

Ddx of microcytic anemia

A 
T- thalassemia
A- anemia of chronic disease (usually normocytic but can be microcytic)
I- iron deficiency
L- lead
S- sideroblastic
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19
Q

Ddx macrocytic anemia

A

megaloblastic:
folate
B12

marrow failure:
myelodysplasia, diamond-blackfan, falcon anemia, aplastic anemia

other: hypothyroidism, Down syndrome, chronic liver disease, drugs (AZT, alcohol)

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20
Q

Ddx of normocytic anemia

A 
chronic disease
chronic renal failure
transient erythroblastopenia of childhood
malignancy/marrow infiltration
HIV
HLH

Most common: TEC, malignancy or anemia of chronic disease

normocytic anemia with inadequate reticulocyte response should usually lead to consideration of a bone marrow exam

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21
Q

Ddx of intrinsic hemolytic disorders

A

membrane: hereditary spherocytosis, elliptocytosis
enzyme: G6PD deficiency, PK deficiency
hemoglobinopathy: HbSS, SC, S-B thal

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22
Q

Ddx of extrinsic hemolytic disorders

A

immune- autoimmune, iso-immune, drug-induced

non-immune- HUS, TTP, DIC, burns, Wilson, vit E deficiency

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23
Q

what are the 3 most important lab tests for evaluating anemia?

A

CBC: MCV, WBC, RBC, Plts
reticulocyte count
peripheral blood smear

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24
Q

what are some optional tests for iron deficiency anemia? (5)

A 
serum iron
transferrin/TIBC
ferritin
soluble transferrin receptor
bone marrow biopsy
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25
Q

when do you see pencil cell on smear?

A

iron deficiency

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26
Q

when do you see basket cell on smear?

A

pathognomonic for G6PD deficiency

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27
Q

what is the most common cause of worldwide anemia?

A

iron deficiency anemia

10% of infants and adolescent girls are iron deficient of which one third are anemic

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28
Q

what are some complications of iron deficiency anemia

A 
irritability
poor concentration
GI dysfunction
reduced immunity
pica
poor school performance
lead poisoning
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29
Q

what are 4 mechanisms causing iron deficiency anemia?

A

inadequate iron endowment at birth (prematurity)
insufficient iron in the diet
blood loss (menstruation)
malabsorption of iron (celiac disease, IBD, giardiasis)

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30
Q

why does excessive cows milk lead to iron deficiency anemia?

A

iron is absorbed at 50% efficiency from breast milk and 10% from cows milk
excessive cow’s milk interferes with balanced nutrition and causes GI blood loss

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31
Q

what is the treatment for iron deficiency anemia?

A

limit cows milk to 16-24 ounces/day
start 4-6mg/kg/day of elemental iron (Taking vit C helps with absorption)
check CBC and retics within 1-2 weeks of treatment
therapy should continue for at least 3-6 months to replenish iron stores
if hemoglobin is not increased within 2 weeks then consider non-compliance

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32
Q 
which of the following is not a feature of iron deficiency
pica
koilonychia
cheilosis
scleral icterus
psychomotor retardation
A

scleral icterus is NOT

koilonychia- groove in nails
cheilosis- cracking at corner of mouth

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33
Q

you are seeing a child with microcytic hypo chromic anemia. You believe it is iron deficiency. What other features of the CBC would be consistent with this?

A
  1. increased RDW
  2. thrombocytosis
  3. MCV/RBC >13 (<13 is suggestive of thal trait)
  4. pencil cells
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34
Q

what is seen if a patient has 3 alpha genes (1 alpha gene missing)

A

silent carrier state
slightly reduced hemoglobin and MCV
Hb electrophoresis pattern is the same as normal

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35
Q

what is seen if a patient has 2 alpha genes missing

A

anemia (100)
microcytosis
not picked up on Hb electrophoresis

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36
Q

what are the differences between iron deficiency anemia and alpha thal trait?

A

in alpha thal, iron studies are normal
in alpha thal, RDW is normal. in IDA RDW is high.
in alpha thal, RBC is increased, usually around 5 and the MCV is very low
in IDA the platelets are often increased

Hb electrophoresis is normal in both

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37
Q

what is the Mentzer’s index?

A

MCV/RBC is >13 in IDA

<13 in thal trait

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38
Q

what is seen if a patient has 3 alpha genes missing

A 
Hb H disease
moderate anemia (70-100)
hypochromia
microcytosis
target cells
heinz bodies
splenomegaly
jaundice
HbBart may be present
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39
Q

what does Bo mean?

A

absent production (more severe thalassemia)

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40
Q

what does B+ mean?

A

reduced production

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41
Q

what does B thalassemia minor mean?

A

one defective gene

either BBo or BB+

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42
Q

how do you diagnose B thalassemia minor? what is seen on hemoglobin electrophoresis? is treatment required?

A

based on Hb electrophoresis pattern
increased HbA2 and HbF
they do not need any treatment at all other than genetic counselling
there is no increased incidence of complications

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43
Q

what is B thalassemia major?

A

either BoB+ or BoBo
severe anemia
abnormal growth
iron overload and the need for transfusion

on electrophoresis: HbF (95%)
No HbA for BoBo

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44
Q

what is the most common complication seen with B thalassemia major?

A

iron overload

mostly in the liver then the heart and endocrine glands

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45
Q

what is the treatment for thalassemia major?

A

regular transfusions and iron chelation
iron chelation: parenteral desferoxamine or oral deferasirox

bone marrow transplant can be curative

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46
Q 
what is the most likely diagnosis with the following
HbA- none
HbA2- 2%
HbF- 75%
HbS- 25%

sickle cell trait
sickle cell disease
beta thalassemia
alpha thalassemia

A

sickle cell disease

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47
Q

Ddx of normocytic anemia

A

anemia of chronic disease
malignant infiltration
diamond-blackfan anemia
transient erythroblastopenia of childhood

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48
Q

what is transient erythroblastopenia of childhood

A

normocytic anemia
usually appears in otherwise health children age 1-3
often after a viral trigger (not necessarily Parvo)
onset is gradual, anemia can be severe
recovery is spontaneous within 1-2 months
the main ddx is diamond-blackfan anemia
key is that it is transient!!
HbF normal whereas HbF increased with diamond blackfan

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49
Q

what causes an aplastic crisis

A

parvovirus B19

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50
Q

what test can help confirm the diagnosis of hereditary spherocytosis

A

osmotic fragility (although nonspecific)

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51
Q

what is the treatment for hereditary spherocytosis

A

splenectomy- corrects the anemia and normalizes the RBC survival even though the spherocytes persist

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52
Q

what is the most common presentation of spherocytosis in a newborn?

A

jaundice

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53
Q

what is the most common complication of hereditary spherocytosis?

A

gall stones

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54
Q

how is G6PD inherited

A

X chromosome enzyme

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55
Q

what are some oxidants that can trigger G6PD

A 
sulfa drugs
nitrofurantoin
dapsone
anti-malarial
fava beans
infection
rasburicase
56
Q

what is the treatment for G6PD

A

supportive

avoidance of triggers

57
Q

what are the 3 types of autoimmune hemolytic anemia

A

warm (IgG)
cold (IgM)
biphasic

58
Q

what is the treatment for warm autoimmune hemolytic anemia?

A

supportive care
transfusions
steroids

59
Q

What is given to moms to prevent hemolytic disease of the newborn

A

rhogam is given at 28 weeks if Rh-

also at delivery or if any invasive procedures

60
Q

the severity of Rh incompatibility at the time of birth is best predicted by what?

A

cord hemoglobin

61
Q

what is the triad for HUS

A

microwngiopathic hemolytic anemia
thrombocytopenia
renal impairment

caused by Ecoli O157:H7 toxin

62
Q

what is primary hemostasis

A

platelet plug

63
Q

what is secondary hemostasis

A

coagulation cascade

64
Q

what factors are involved in the intrinsic pathway

A

12, 11, 9 and 8

**primarily 8 and 9

65
Q

what factors are involved in the extrinsic pathway

A

factor 7

66
Q

what factors are involved in the common pathway

A

factor 10
factor 2
fibrin (factor 13)
= clot

67
Q

what does plasmin do?

A

degrades your fibrin clot

68
Q

what can activate plasminogen to plasmin

A

tPA

urokinase

69
Q

what are vit k dependent factors

A

2, 7, 9, 10

pn c and s

70
Q

what factors do protein c and s work on

A

5 and 8

71
Q

what does heparin do to antithrombin

A

binds to antithrombin and forces it to come into close proximity with thrombin

72
Q

what factors is affected by LMWH? UFH?

A

LMWH: factor 10
UFH: factor 10 and thrombin

73
Q

differences between UFH and LMWH

A 
UFH
fast onset and offset
not affected by renal function
can be given IV
cheap
monitor with PTT
LMWH
more predictable
can be given at home
less frequent monitoring
monitor with anti-Xa
74
Q

why do you need bridging when you start warfarin?

A

because protein c and s have shorter half life so they go down first and you are at increased risk of clotting for the first couple of days
therefore always need bridging with heparin

75
Q

what test should you do if you have an abnormal INR or PTT

A

mixing study

76
Q

what test should you do if you have a normal platelet count but primary hemostasis problem suspected?

A

PFA-100 to assess platelet function

77
Q

Ddx for normal INR with elevated PTT

A 
factor 8
factor 9
factor 11
vWD
heparin
78
Q

Ddx for elevated INR with normal PTT

A

factor 7
early vit k deficiency
warfarin
early liver disease

79
Q

Ddx for elevated INR and PTT

A

liver disease
late vit k deficiency
DIC

80
Q

does factor 13 affect INR or PTT

A

NO!!
therefore if bleeding disorder is strongly suspected in the face of normal coags a facto 13 level should be measured

delayed bleeding, umbilical stump separation

81
Q

what factor affects PTT but is not a bleeding disorder

A

factor 12

82
Q

what is the dose for oral vitamin k and when should it be given?

A

2mg PO

repeated at 2-4 weeks and 6-8 weeks

83
Q

what is the most common inherited bleeding disorder

A

vonwillebrands disease

84
Q

what does ristocetin test?

A

vWF function

85
Q

what is the biggest side effect from DDAVP? how does it work?

A

hyponatremia
therefore hold free water
DDAVP appears to act by causing the release of vWF from the endothelial cells

86
Q

what is the treatment for vWD

A 
DDAVP (for type 1 and 2 vWD)
factor VIII-vWF concentrate
OCP and treatment for anemia if needed for menorrhagia
supportive care: avoid NSAIDs, helmet 
TXA is useful for mucocutaneous bleeds
87
Q

what is type 3 vWD

A

absence of vWF

88
Q

what is type 1 vWD

A

quantitative deficiency of normal vWF

89
Q

what is type 2 vWD

A

qualitative problems with vWF (abnormal function)

90
Q

what is hemophilia A

A

factor 8 deficiency

91
Q

what is hemophilia B

A

factor 9 deficiency

92
Q

how is hemophilia inherited

A

x-linked

women are carriers but can have the disease with turner,s lyonizaition or homozygosity

93
Q

how is hemophilia classified into mild, moderate and severe

A

severe <1% factor activity level

moderate: 1-5%
mild: 5-30%

94
Q

what is the most common chronic sequelae of hemophilia

A

arthritis

95
Q

what is the treatment for hemophilia

A

prophylactic factor after delivery can be considered
don’t forget to give vitamin K- lots of pressure on site
acute treatment- factor should be given
DDAVP can be used for mild/moderate hemophilia A but must have a DDAVP challenge first

96
Q

list 4 clinical presentations of hemophilia in the neonatal period

A 
IVH
circumcision bleeding
IM hematoma after IM vit k
large caput or smbgaleal hemorrage
excessive bleeding with phlebotomy
97
Q

name one indication for transfusion of FFP

A

reversal of warfarin

98
Q

when would you transfuse cryoprecipitate

A

for low fibrinogen (<0.8-1.0)

for bleeding with vWD or hemophilia ONLY if factor or DDAVP is unavailable

99
Q

what does leukoreduction do?

A

reduced febrile non-hemolytic reactions
reduces Allo-immunization
reduces viral transmission

100
Q

what does irradiation do

A

reduced GVHD for immunosuppressed recipients

101
Q

what is the most common fatal reaction associated with transfusion

A

TRALI and sepsis

102
Q

what is the most common acute reaction

A

allergy

then fever

103
Q

what is the most common pathogenic infection associated with transfusions

A

parvovirus

104
Q

what should you do if there is a transfusion reaction

A

stop the transfusion
keep IV
send blood and samples to lab
provide supportive care

105
Q

what is the treatment for massive hemorrhage

A

1 unit of plts and 1 unit of FFP for every 4 units of pRBCs

106
Q

what are some complications following splenectomy

A

infection- pneumococcal/h influenza, meningococcal
thrombo-embolic complications
pulmonary hypertension

107
Q

List 3 long term effects of cyclophosphamide

A

pulmonary fibrosis
bladder cancer
Reproductive effects: Gonadal dysfunction, delayed or arrested puberty, premature menopause, germ cell dysfunction or failure, infertility

108
Q

List 4 indications for blood transfusion in sickle cell disease

A

Acute chest syndrome
Abnormal transcranial dopplers, or acute stroke
Acute splenic sequestration (but only give ½ volume BECAUSE of autotransfusion)
Aplastic crisis
Prior to surgery (for Hb around 100)

Exchange transfusion is reserved for stroke, severe ACS, and pre-op some major surgeries.
Generally, transfusion NOT indicated for vasoocclusive
crisis.

109
Q

Black kid from Kenya very sick with chest symptoms. Hgb is 48- what is underlying dx and 4 things to do (ie. symptoms of acute chest)

A
  1. Pain management
  2. supplemental O2
  3. antibiotics (ceftriaxone and azithromycin)
  4. transfusion
110
Q

Young kid with behaviour change, microcytic, hypochromic anemia with basophilic stippling. Physician has already done iron studies, which were normal. What would you test?

A

lead levels (basophilic stippling)

111
Q

Newborn with non-hemorrhagic stroke – 4 inheritable etiologies for clot

A
  1. factor V Leiden
  2. Pn C deficiency
  3. Protein S deficiency
  4. Antithrombin deficiency
  5. Prothrombin mutation
112
Q 
A full term newborn develops petechiae and bruising.  The baby is otherwise well appearing.  On bloodwork his platelets are 12, WBCs are 18 and his Hgb is 140.  He is given a platelet transfusion and a repeat platelet count is 16.  The mother’s CBC shows platelets of 80.  What is the best treatment:
PLA-1 negative platelets
IVIG
Washed maternal platelets
Steroids
A

IVIG

due to maternal ITP

113
Q

Give 4 mechanisms of anemia in a child with chronic renal disease.

A

Decreased erythropoietin production (major cause)

  • Iron deficiency
  • Anemia of chronic disease
  • Increased blood loss (dialysis, hematuria, blood tests)
  • secondary hyperparathyroidism - can suppress RBC production
114
Q

You are treating a 7-year-old girl with ALL for a
central line line-associated thrombus. Despite
regular increases in her heparin dose you can’t
achieve a therapeutic level. What is a possible
cause?
1. Antithrombin III deficiency
The way heparin works is by binding to thrombin and antithrombin and bringing them together
Antithrombin then antis-the thrombin
2. Protein C deficiency
3. Factor V Leiden
4. Factor VIII deficiency

A

Antithrombin III deficiency

115
Q

3 year old new Canadian with sickle cell disease comes to you for the first time. List 5 things that are important to do for this child right now.

A

Immunizations - encapsulated organisms
Penicillin prophylaxis
CBC + smear
Hgb electrophoresis
Educate for pain crisis/risk of infection (management of fever and spleen palp)
Transcranial doppler starting at 2yoa - if high flow may need blood transfusions to keep HbS <30% (decreases stroke risk)

116
Q

what is the main risk from partial exchange transfusion for polycythemia

A

NEC

117
Q

What is seen on peripheral smear for HUS

A

Schistocytes

118
Q

10 year old girl with Sickle Cell Disease and a history of stroke. Which treatment is most recommended given her history of stroke?
Hydroxyurea
Transfusion with PRBCs
Folic acid

A

transfusion with pRBCs

119
Q

what are 3 management strategies for tumor lysis syndrome

A
  1. IVF
  2. Rasburicase/ allopurinol
  3. Monitor electrolytes q4-6h
120
Q

A 7 year old girl comes to see you with
decreased energy and pallor for the past week.
She had a viral illness 1-2 weeks ago. You notice
that her sclerae are “a bit yellow”. Her CBC show
a Hb 70, WBC 8.6, Platelets 245, 24% retics.
1. What type of anemia is this?
2. What test would you do to confirm?
3. What treatment could you offer?

A

hemolytic anemia (autoimmune)
DAT
Steroids

121
Q

when do you see Howell-Jolly bodies on smear

A

asplenia

122
Q

what are two causes of osteomyelitis in sickle cell disease

A

salmonella and staph aureus

123
Q

what is the treatment for stroke in SCD? How can you prevent a second stroke?

A

exchange transfusion

After a stroke, chronic transfusion to maintain Hb S below 30% can prevent a second stroke by 80%.

124
Q

when should transcranial dopplers be performed on patients with sickle cell disease

A

starting at age 2, annually

if abnormal then indefinite transfusion

125
Q

what are some risk factors for stroke in sickle cell patients

A
  1. rate of and recent episode of acute chest crisis
  2. low baseline hemoglobin
  3. previous TIA
  4. high blood pressure
  5. SS genotype
126
Q

what is required for a diagnosis of acute chest crisis

A

fever and new infiltrate

hypoxia is not necessary for the diagnosis

127
Q

what is the treatment for an acute chest crisis

A

Tx: Antibiotics (including cephalosporin and macrolide), oxygen, hydration, incentive
spirometry, bronchodilators.
Simple transfusion for hypoxia needing oxygen or a Hct<18%.
Exchange transfusion for progressive multilobe infarcts and hypoxia.
Recurrent ACS should have referral to respirology for PFTs.

128
Q

how does hydroxyurea work

A

Hydroxyurea: raises fetal Hb levels

129
Q

Question. A 14 yo girl with sickle cell disease presents
with a red, swollen, painful hand. (No vitals
mentioned).
What are three things you would do for management?
After leaving the hospital, what is one medication that can
be taken for prevention of these episodes?

A
  1. Admit
  2. Pain management
  3. IVF
  4. antibiotics
  5. imaging
  6. physio
  7. hydroxyurea
130
Q

what are 3 inherited bone marrow failure syndrome

A
  1. dyskeratosis congenita
  2. fanconi anemia
  3. shwachman-diamond
131
Q

List 5 causes of neonatal thrombocytopenia

A
  1. TAR
  2. sepsis
  3. TORCH
  4. Maternal ITP
  5. NAIT
  6. NEC
  7. RDS
132
Q

what is a treatment option for a baby with low platelets secondary to maternal ITP

A

IVIG

133
Q

what is the treatment for a baby with NAIT

A

PLA-1 negative platelets

134
Q 
Question. What would you advise a child with
hemophilia regarding immunization?
A. Delay Immunization
B. Give factor VIII before immunization
C. Apply pressure for 10 minutes after
immunization
D. Have factor VIII readily available in office to
use if bleed occurs
A

Apply pressure for 10 minutes after immunization

135
Q

What is the probable diagnosis of a 6-year-old child with pancytopenia, short
stature, abnormal thumbs, and areas of hyperpigmentation?

A

Fanconi anemia

Diagnosed with chromosomal breakage analysis

Pediatrics- Noelle (28 decks)

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