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Peds II Exam 1 > Hematology > Flashcards

Hematology Flashcards

1
Q

Anemia

A

2 SD below normal for age/sex

Hgb concentration <11g/dL for both male and females aged 6 mo - 5 yrs

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2
Q

Labs for anemia

A

CBC w/ diffferential
peripheral blood smear
reticulocyte count

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3
Q

Reticulocyte results

A

high- bone marrow working

low- trouble

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4
Q

normocytic, normochromic anemia

A

anemia of chronic disease

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5
Q

microcytic, hypochromic anemia

A

IDA
thalassemia
lead intoxication

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6
Q

Macrocytic anemia

A

vitamine b12

folate deficiency

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7
Q

S/sx of anemia

A

acute: lethargic, tachy, pallor; infants - irritable, poor oral intake
chronic: may present w/ few or no sx at all

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8
Q

Other findings w/ anemia

A 
jaundice
gallstone disease
petechiae
purpura
ecchmosis
bleeding
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9
Q

Types of bone marrow failure

A

fanconi anemia

acquired aplastic anemia

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10
Q

What is fanconi anemia

A

inherited bone marrow failure syndrome
auto recessive
defective DNA repair
majority develop in first 10 years of life

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11
Q

Clinical manifestation of fanconi anemia

A 
progressive panctyopenia
abnormal pigmentation
short stature
skeletal malformation
increased incidence of malignancies
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12
Q

Lab findings for fanconi

A

thrombocytopenia or leukopenia (then followed by anemia)
anemia = severe aplastic anemia
bone marrow hypoplasia or aplasia

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13
Q

Fanconi anemia may be misdiagnosed as

A

ITP

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14
Q

Tx for fanconi

A

supportive

HSCT

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15
Q

Prognosis for fanconi

A

many succumb to bleeding, infection, or malignancy in adolescence or early adult

high risk for developing Myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML)

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16
Q

Acquired aplastic anemia

A

peripheral pancytopenia w/ a hypocellular bone marrow

idiopathic (50%)
meds, toxic exposure (insecticides) and viruses (mono, hepatitis, HIV)

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17
Q

S/sx of acquired aplastic anemia

A

weakness, fatigue, pallor
frequent or severe infections
purpura, petechiae, bleeding

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18
Q

Lab findings for acquired aplastic anemia

A

anemia, usually normocytic
low WBC w/ marked neutropenia
thrombocytopenia
low reticulocyte count (bone marrow suppressed)

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19
Q

Complications of acquired aplastic anemia

A

overwhelming infection
severe hemorrhage

can lead to death

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20
Q

Tx for acquired aplastic anemia

A 
supportive
referral
stop offending agent
abx if infection
RBC transfusion for severe anemia
Platelet transfusions
immunosuppressant agents
HSCT
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21
Q

Most common nutritional deficiency in children

A

Iron deficiency

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22
Q

Prevalence of IDA

A

1-2 yo
females of chldbearing age
african american and hispanics
poverty

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23
Q

S/sx of IDA

A 
varies w/ severity
pallor
fatigue, irritability
delayed motor dev.
hx of Pica (eating ice)
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24
Q

Screening for IDA

A

12 months- determine Hb concentration and assessment of risk factors

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25
Q

Risk for IDA

A

low SE status
premature/LBW
lead exposure
exclusive breast feeding beyond 3 mo of age w/o iron supplementation
weaning to whole milk or foods w/o iron
feeding problems, poor growth, inadequate nutrition

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26
Q

Lab findings for IDA

A

microcytic, hypochromic
Hb <11 g/dL
Ferritin <12 mcg/L

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27
Q

Tx for IDA

A

Hb 10-11 mg/dL @ 12 mo screening– monitor closely or empirically treated; recheck Hb in one month

ID/IDA: iron 6 mg/kg/d, 3 divided daily doses

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28
Q

Cobalamin

A

vitamin B12

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29
Q

Causes of b12 deficiency

A

malabsorption

dietary insufficiency

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30
Q

Folic acid deficiency

A

increased folate requirement (rapid growth, chronic hemolytic anemia)
malabsorptive syndromes
inadequate dietary intake (rare)
Medications

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31
Q

S/sx of megaloblastic anemia

A

pallor

glossitis

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32
Q

B12 sx

A

paresthesias, weakness, unstead gait
decreased vibratory sensation and proprioception on enuro exam
neuro sx only occur w/ B12 not folate

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33
Q

Neuro sx

A

B12 deficiency

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34
Q

Lab findings for megaloblastic anemia

A

elevated MCV/MCH
low levels of folic acid or vit B12
neutrophils large and hypersegmented nuclei
Macro-ovalocytes (large, ocal RBC)
Elevated Methylamlonic acid w/ 12
Elevated homocysteine w/ B12 and folate deficiency

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35
Q

How to tell the difference between B12 and folate?

A

Methylmalonic acid elevated in B12

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36
Q

Hypersegmented nuclei

A

megaloblastic anemia

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37
Q

Tx for megaloblastic anemia

A

Vit B12 and/or folic acid supplementation

**tx w/ folate will fix anemia picture in B12 BUT…must treat vit B12 to avoid neuro deficits

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38
Q

Congenital hemolytic anemias

A 
hereditary spherocytosis (HS)
thalassemia
sickle cell disease
G6PD
Lead poisoning
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39
Q

Hereditary Spherocytosis (HS)

A

red cell membrane defect
hemolytic anemia (jaundice, SPLENOMEGALY, gallstones)
Spherocytes*
Increased osmotic fragility*

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40
Q

Tx for HS

A

supportive +/- RBC transfusion

SPLENECTOMY

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41
Q

Test for HS

A

osmotic fragility test

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42
Q

Thalassemia

A

alpha or beta
related to # of gene deletions
microcytic, hypochromic anemia
IRON OVERLOAD

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43
Q

Dx of thalassemia

A

HgB electrophoresis

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44
Q

Tx for thalassemia

A

supportive +/- RBC transfusion
Iron monitoring + chelation
splectomy may help
HSCT (severe beta-thal)

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45
Q

Sickle Cell disease sx

A 
Sickle-shaped RBC when deoxygenated
Vaso-occlusion that leads to pain!
chronic hemolysis
splenomegaly
splenic infarcts (functional asplenia)
Increased risk of bacterial sepsis
may see growth failure and delayed puberty
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46
Q

Dx for sickle cell disease

A

HgB electrophoresis shows HbS

Howell-jolly bodies; target cells on peripheral smear

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47
Q

Tx of sickle cell

A

avoid precipitating factors
supportive
hydroxyurea*** - depress bone marrow function; used to decrease incidence of pain crises
Stem cell transplant

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48
Q

G6PD deficiency

A

red cell enzyme defect that causes hemolytic anemia
x-linked recessive
african, mediterranean, asian

episodic hemolysis at times of exposure to:

  • oxidant stress of infection
  • certain drugs/food substances
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49
Q

Clinical manifestations of G6PD deficiency

A

neonatal jaundice, hyperbilirubinemia

episodic hemolysis: pallor, jaundice, hemoglobinuria

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50
Q

Lab findings of G6PD

A

peripheral smear: rate bites; heinz bodies (denatured Hgb)

51
Q

Heinz bodies

A

G6PD

52
Q

Tx for G6PD

A

supportive

avoid certain foods/drugs known to trigger hemolysis

53
Q

Etiology of lead poisoning

A

older home w/ lead pain

54
Q

Sx of lead poisoning

A

anemia that is mild, hemolytic and normocytic

55
Q

Dx of lead poisoning

A

basophilic stippling

56
Q

Tx for lead poisoning

A

chelation

57
Q

Congenital erythrocytosis aka

A

familial polycythemia

58
Q

What is familial polycythemia?

A

only RBC affected

increased HgB as high as 27 g/dL

59
Q

Sx of polycythemia

A

plethora and splenomegaly

h/a, lethargy

60
Q

Tx for familial polycythemia

A

phlebotomy

61
Q

Secondary polycythemia cause

A

occurs in response to hypoexmia

  • cyanotic congenital heart disease
  • chronic pulmonary disease (CF)
62
Q

Tx of secondary polycythemia

A

correct underlying disorder

phlebotomy when indicated

63
Q

Tests for bleeding disorders

A 
CBC
peripheral smear
PT/INT, aPTT
\+/- bleeding time
Platelet count (N: 150k-400k)
64
Q

Risk of spontaneous bleeding platelet level

A

<20k

65
Q

PT (prothrombin time)

A

extrinsic and common pathway

I, II, V, VII*, X + TF

66
Q

PTT/aPTT (activated partial thromboplastin time)

A

intrinsic and common

I, II, V, VIII, IX, X, XI*, XII

67
Q

Common pathway factors

A

I, II, V, X

68
Q

intrinsic factors

A

VIII, IX, XI, XII

69
Q

Extrinsic factors

A

VII and TF

70
Q

Prothrombin

A

II

71
Q

Thrombin

A

IIa

72
Q

Fibrinogen

A

I

73
Q

INR

A

more accurate reflection of PT

used to monitor warfarin

74
Q

Bleeding time

A

measure of time for hemostasis
screen test for platelet dysfunction
prolonged in platelet disorder (von Willebrand disease) and severe thrombocytopenia

75
Q

most common bleeding disorder of childhood

A

idiopathic thrombocytopenic purpura (ITP)

76
Q

ITP epidemiology

A 
2-5 yo
often follows infection w/viruses
immune-mediated
90% have spontaneou remission
10-20% chronic
77
Q

Pathophys behind ITP

A

immune-mediated attac against its own platelets (autoantibody bind platelet–> platelets phagocytized primarily by splenic macrophages –> decreased platelet life span)

78
Q

Clinical manifestations of ITP

A

petechiae
ecchymosis
epistaxis

79
Q

Lab findings for ITP

A

thrombocytopenia
normal WBC
normal Hgb (unless hemorrhage)
PT and aPTT are normal

80
Q

Dx of ITP

A

exclusion of others

81
Q

Tx for ITP

A 
observation in asymptomatiic children
avoid medications that compromise platelet function
bleeding precautions
PREDNISONE
IVIG
Splenectomy
82
Q

Inherited bleeding disorders

A

Von Willebrand disease

Hemophilia

83
Q

Most common inherited bleeding disorder

A

Von Willebrand Disease

84
Q

von willebrand disease

A

auto dominant
M=F
decrease in the level or impairment in the action of vWF

85
Q

Most common type of von willebrand disease

A

Type 1

86
Q

vWF

A

bind to factor VIII and is a cofactor for platelet adhesion to the endothelium

87
Q

Clinical presentation of VWD

A

prolonged bleeding from mucosal surfaces (epistaxis, menorrhagia, GI)
easy bruising

88
Q

Lab findings for VWD

A

normal PT
prolonged or normal aPTT
normal or decreased vWF
PROLONGED BLEEDING TIME (helps differentiate from hemophilia)

89
Q

Difference between VWD and hemophilia

A

VWD has prolonged bleeding time

90
Q

Tx for VWD

A

desmopressin (DDAVP)

vWF replacement therapy

91
Q

DDAVP

A

causes release of vWF and factor VIII from endothelial stores

92
Q

Hemophilia A

A

factor VIII deficiency (most common)

93
Q

Hemophilia B

A

factor IX deficiency (Christmas disease)

94
Q

Clinical presentation of hemophilia

A

bleeding from impaired hemostasis
mild: bleed in response to injury/trauma or surgery; may not be clinically apparent til later in life

severe: spontaneous bleeding, earlier age

bleeding can occur anywhere -- into joints and mm. is common
spontaneous hemarthrosis (severe disease) - can lead to joint destruciton if recurrent
95
Q

Lab findings for hemophilia

A

normal platelet count, PT and bleeding time
prolonged aPTT (normal in mild disease)
normal vWF

96
Q

Tx for hemophilia

A 
DDAVP (hemo A)
factor replacement (VIII and IX)
97
Q

Inherited bleeding disorders

A

VWD

Hemophilia

98
Q

Acquired bleeding disorders

A

Disseminated Intravascular Coagulation (DIC)
Liver Disease
Kidney Disease

99
Q

DIC cause

A

triggered by event: sepsis, trauma or tissue injury, malignancies

100
Q

What is DIC

A

hemorrhage and microvascular thrombosis

101
Q

Pathophys behind DIC

A

triger –> widespread activation of coagulation cascade leading to microthrombi –> massive consumption of platelets, fibrin and coagulation factors –> severe bleeding

102
Q

s/sx of DIC

A

shock- end organ dysfunction
diffuse bleeding tendency (hematuria, melena, purpura, petechiae; persistent oozing from punctures)
evidence of thrombotic lesion (major vessel thrombosis, purpura fulminans)

103
Q

lab findings for DIC

A

decreased platelet count
prolonged aPTT and PT
decreased fibrinogen level (may be normal until late in course)
Elevated D-Dimer and fibrin degradation products (FDPs)

104
Q

Tx for DIC

A

identify and treat triggering event
replacement therapy for consumptive coagulopathy
anticoagulant therapy when indicated

105
Q

Liver synthesizes

A

prothrombin, fibrinogen

Factors V, VII, IX, X, XII, XIII

106
Q

Vitamin K dependent factors

A

II, VII, IX, X

107
Q

Lab findings for liver disease/vit K def.

A

platelet count: normal in vitamin K deficiency; normal/low in liver disease
Prolonged PT, aPTT

108
Q

Tx for liver disease and vit K

A

treat underlying condition

vitamin K at birth

109
Q

Inherited thrombotic disorders

A

Protein C def
Protein S def
antithrombin def
factor V Leiden Mutation

110
Q

Protein C def

A

homo and hetero forms

activated protein C inactivated activated factors V and VIII

111
Q

Warfarin induced skin necrosis

A

associated w/ protein C def

112
Q

Protein S def

A

homo and hetero forms

Protein S is a cofactor for protein C

113
Q

Factor V Leiden Mutation

A

point mutation in factor V that leads to resistance to inactivation by activated protein C

hetero and homo forms

114
Q

Risk with factor V Leiden mutation

A

increased risk of VTE 2-7x

35 fold with hetero taking oral contraceptives
80 fold in homo

115
Q

Antithrombin

A

inhibits thrombin

116
Q

Clinical presentation of antithrombin def

A

VTE (efficiency of heparin may be diminished)

117
Q

Tx of thrombotic disorders

A

anticoagulant prophylaxis
(UFH, LMWH, warfarin)

1st episode VTE - anticoag for at least 3 mo; may need longer

118
Q

Type of vasculitis

A

Henoch-Schonlein Purpura (HSP)

119
Q

most common type of small vessel vasculitis

A

HSP

120
Q

Epidemiology of HSP

A

boys, ages 2-7
spring and fall
URI often precedes diagnosis

121
Q

Cause of HSP

A

deposition of IgA immune complexes in small vessels of the skin, GI tract and kidneys

122
Q

Clinical presentation of HSP

A

PALPABLE PURPURA
arthritis/arthralgias
abdominal pain
renal disease

123
Q

Labs for HSP

A 
normal/elevated platelet count
antistreptolysin O (ASO) titer elevated
serum IgA may be elevated
hemoccult +
urinalysis: hematuria, sometimes proteinuria
124
Q

Tx for HSP

A

supportive

prognosis generally good

Peds II Exam 1 (4 decks)

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