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USMLE Step 1 > Hematology > Flashcards

Hematology Flashcards

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1
Q

What is a sideroblast?

A ringed sideroblast?

A

RBC with excessive iron in its mitochondria.
Normal to see these in the bone marrow.
Ringed sideroblasts = never normal. Have a ring of iron around the nucleus.

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2
Q

Clinical conditions in which you might see ringed sideroblasts (6):

A 
Lead poisoning
Heme metabolism d/o
EtOH
Drugs
Genetic disorders
Myelodysplastic syndrome
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3
Q

Four scenarios in which you might see target cells:

A 
THAL:
Thalassemias
HbC disease
Asplenia
Liver disease
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4
Q

Two pathologic RBC forms you might see in someone with liver disease:

A

Target cells

Acanthocytes

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5
Q

What is physiologic anemia of pregnancy?

A

Increase in maternal plasma volume -> dilution of iron in the serum.

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6
Q

Iron deficiency anemia is a _________ __________ anemia.

A

Microcytic

Hypochromic

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7
Q

This type of anemia may manifest as Plummer-Vinson syndrome:

The famous triad:

A

Iron deficiency
Fe-deficiency
Esophageal webs
Atrophic glossitis

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8
Q

How many copies of the gene for a-globin do you have?

A

Four.

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9
Q

Which thalassemia is more prevalant in people of Mediterranean descent?
In Asian people?
African people?

A 
b-thal = Mediterranean
a-thal = Asian, African
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10
Q

What is Hb Barts?

A

People make no a-globin.
In the fetus, so…
Gamma-globin makes a tetramer = Hb Barts

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11
Q

What is HbH disease?

A

HbH disease = 3-gene deletion of a-globin.
Make only a little a-globin
The extra b-globin makes tetramers = HbH

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12
Q

Four gamma-globin chains glued together, what am I?

A

Big trouble, you’re not making alpha-globin chains in utero.

Hb Barts -> hydrops fetalis.

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13
Q

Four beta-globin chains glued together, what am I? What disease is this associated with?

A

HbH -> HbH disease.

A type of alpha-thalassemia.

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14
Q

How many genes for b-globin do you have?

A

Two.

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15
Q

When might you see target cells?

A 
THAL
Thalassemia
HbC disease
Asplenia
Liver disease
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16
Q

How do you confirm the dx of b-thalassemia minor?

A

Will see an increase in HbA2.

HbA2 = a-globin + d-globin

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17
Q

Which thalassemia commonly puts people at risk for hemochromatosis?

A

b-thalassemia major (homozygous)

Often require blood transfusions.

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18
Q

Two skeletal abnormalities seen in b-thalassemia major:

A

Marrow expansion ->
“Crew cut” appearance on X-ray
“Chipmunk” facies

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19
Q

What is the structure of HbF?

A

a2g2

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20
Q

The macrocytic anemias can be divided into these two functional distinctions:
What is the difference between them?

A 
Megaloblastic = trouble synthesizing DNA
Non-megaloblastic = unimpaired DNA synth.
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21
Q

Three causes of megaloblastic anemia:

A

Folate def.
B12 def.
Orotic aciduria

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22
Q

Common finding on blood smear in megaloblastic anemia (other than big-ass RBC):

A

Hypersegmented neutrophils

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23
Q

Anemia in which methylmalonic acid is normal:

Anemia in which methylmalonic acid is elevated:

A

Anemia 2/2 folate deficiency

Anemia 2/2 B12 deficiency

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24
Q

Four common causes of B12 deficiency:

A 
Malabsorption
Poor intake
Pernicious anemia
PPIs
(Worms)
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25
Q

Which of the macrocytic anemias would you expect to see neurologic sx with?

A

B12 deficiency anemia

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26
Q

This macrocytic anemia is incurable by folate / B12 administration:

A

Anemia 2/2 orotic aciduria

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27
Q

What is the treatment for orotic aciduria?

A

Uridine monophosphate

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28
Q

In B12 and folate deficiency anemias, what is the homocysteine level like?

A

Increased.

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29
Q

What is the protein responsible for binding ferroportin in anemia of chronic disease?

A

Hepcidin

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30
Q

What kind of anemia is anemia of chronic disease?

A

Normocytic

May progress to microcytic, hypochromic

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31
Q

Four common causes of aplastic anemia:

A 
Severe vitamin B12 and folic acid deficiency
Radiation / drugs
Viruses (parvo B19, EBV, HIV, HCV)
Fanconi's
(Idiopathic)
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32
Q

Hypocellular bone marrow with fatty infiltrate:

A

Aplastic anemia

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33
Q

Sickle cell patients are vulnerable to these viruses (4):

A

Parvovirus B19
EBV
HIV
HCV

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34
Q

Chronic kidney disease causes this kind of anemia:

A

Normocytic, normochromic

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35
Q

Triad for pancytopenia:

A

Severe anemia
Leukopenia
Thrombocytopenia

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36
Q

Protein that transports iron in blood:

A

Transferrin

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37
Q

The primary storage protein for iron in the body:

A

Ferritin

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38
Q

What effect do pregnancy and OCPs have on transferrin levels?

A

Increase

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39
Q 
What would you expect to see in hemochromatosis:
Serum Fe
Transferrin
Ferritin
% Transferrin sat.
A 
Hemochromatosis:
Serum Fe HIGH
Transferrin LOW
Ferritin HIGH
% Saturation HIIIIIGH
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40
Q

Iron studies in thalassemia:
Fe:
TIBC:
Ferritin:

A

Normal Fe, TIBC, ferritin…

Microcytic anemia with target cells.

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41
Q

This test is used to dx b-thal minor:

A

Hb electrophoresis

Look for HbA2 (>3.5%)

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42
Q

Normocytic anemia + red urine in the morning:

A

Paroxysmal nocturnal hemoglobinuria

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43
Q

Microcytic anemia reversible with B6:

A

Sideroblastic anemia

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44
Q

This megaloblastic anemia is not correctable with B12 or folate:

A

Orotic aciduria

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45
Q

Sideroblastic anemia can be congenital or acquired.
What is the defect in congenital sideroblastic anemia?
What mode of inheritance?

A

Defective d-ALA synthase = no protoporphyrin, Fe accumulates in mitochondria.
X-linked recessive.

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46
Q

Name 3 reversible etiologies of sideroblastic anemia:

A

EtOH
Lead poisoning
Isoniazid administration

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47
Q

What is the treatment for acquiredsideroblastic anemia?

Why does it work?

A

B6 = pyridoxine

This is the co-factor for ALA-synthetase.

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48
Q

What is haptoglobin?

A

A hemoglobin scavenger molecule, binds up Hb outside the cell.

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49
Q

In what case might you see a decrease in serum haptoglobin?

A

Generally, intravascular hemolysis.

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50
Q

What is the difference between intravascular and extravascular hemolysis?

A 
Intravascular = destruction in the vessels
Extravascular = destruction by the spleen
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51
Q

Three common causes of intravascular hemolysis:

A
  1. PNH = complement-mediated lysis, defect is in GPI anchor or decay accelerating factor in complement pathway
  2. Autoimmune hemolytic anemia
  3. Mechanical damage to RBC
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52
Q

Extravascular hemolysis, 5 causes:

A 
Hereditary spherocytosis
G-6-PD deficiency
Pyruvate kinase deficiency
Sickle cell disease
HbC disease
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53
Q

Expect elevated LDH in:

A

Hemolysis (both intra and extravascular)

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54
Q

Bilirubin is more an indicator of this kind of hemolysis:

A

Intravascular

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55
Q

Two defective proteins in hereditary spherocytosis:

A

Ankyrin

Spectrin

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56
Q

Small, round RBCs with no central pallor:

A

Hereditary spherocytosis

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57
Q

High RDW with high MCHC:

A

Hereditary spherocytosis

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58
Q

Heinz bodies and bite cells:

A

G6PD deficiency

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59
Q

Oxidant stress causes hemolytic anemia:

A

G6PD deficiency

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60
Q

Positive osmotic fragility test:

A

Hereditary spherocytosis

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61
Q

Aplastic crisis (2):

A

Sickle cell disease

Hereditary spherocytosis

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62
Q

Rigid RBCs:

A

Pyruvate kinase deficiency, inability to maintain RBC membrane 2/2 decreased ATP

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63
Q

Mode of inheritence for G6PD deficiency:

A

X-linked recessive

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64
Q

Triad seen in paroxysmal nocturnal hemoglobinuria:

A

Remember, it’s complement mediated:
Hemolytic anemia
Pancytopenia
Thrombosis (platelets lysed too)

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65
Q

CD55/59(-) RBCs on flow cytometry:

A

Paroxysmal nocturnal hemoglobinuria

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66
Q

Hemolytic anemia in a newborn:

A

G6PD deficiency

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67
Q

Why are newborns initially asymptomatic in SS disease?

A

They still have HbF to protect them

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68
Q

Organisms you are at risk for infection from if you do not have a spleen:

A

Encapsulated

ESoHPNC

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69
Q

Glutamic acid to lysine in b-globin:

Glutamic acid to valine in b-globin:

A 
lysine = HbC
valine = HbSS
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70
Q

Treatment for paroxysmal nocturnal hemoglobinuria:

A

Eculizumab

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71
Q

Two ways of diagnosing paroxysmal nocturnal hemoblobinuria:

A 
Ham's test
Flow cytometry (CD55/59- cells)
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72
Q

Drug used in sickle cell disease:

What does it do?

A

Hydroxyurea

Increases HbF

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73
Q

Wedge-shaped splenic infarcts on CT:

A

Splenic sequestration crisis in sickle cell disease

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74
Q

Rate-limiting step in hemoglobin synthesis:

Enzyme:

A

Glycine + succinyl CoA -> d-ALA

Catalyzed by d-ALA synthetase

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75
Q

Warm agglutinin antibodies tend to be ___.

Cold agglutinin antibodies tend to be ___.

A

IgG

IgM

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76
Q

Four common sources of cold-agglutinin Ab:

A 
Viruses
SLE
Malignancies
Congenial
Immune
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77
Q

Cold-agglutinin Ab are associated with (3):

A

Mycoplasma
EBV
CLL

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78
Q

What is a direct Coomb’s test?

Indirect Coomb’s test?

A

Direct = patient’s RBC + prepped Ab.
Indirect = patient’s serum + normal RBC.
Looking for Ig bound to RBC.

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79
Q

When might you use a direct Coomb’s?

An indirect Coomb’s?

A

Direct used in hemolytic disease.

Indirect used in blood screening before transfusion.

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80
Q

Microangiopathic anemia – you would see this kind of cell on peripheral smear:

A

Schistocyte

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81
Q

Splenectomy cured this guy:

A

Hereditary spherocytosis

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82
Q

Ham’s test was positive:

A

Paroxysmal nocturnal hemoglobinuria

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83
Q

DEB test was positive:

A

Fanconi anemia

84
Q

You see Heinz bodies:

A

G6PD deficiency

85
Q

Osmotic fragility test was positive:

A

Hereditary spherocytosis

86
Q

Painful cyanosis of fingers and toes, hemolytic anemia:

A

Cold agglutinin anemia

87
Q

Red urine in the morning, fragile RBC:

A

PNH

88
Q

Basophilic nuclear remnants in RBC:

A

Howell-Jolly bodies

You got no spleen.

89
Q

Autosplenectomy

A

Sickle cell disease

90
Q

Drug used to treat sickle cell disease:

A

Hydroxyurea

91
Q

This molecule binds exposed collagen when vascular endothelium is damaged:
What binds to it in turn?

A

vWF

GpIb on platelets

92
Q

Platelets use this molecule on their surface to bind vWF, which is bound to damaged endothelium:
They then release many things. Two are integral to initiating the coagulation cascade:

A

GpIb

Calcium, ADP

93
Q

Activated platelets display this molecule on their surfaces, other platelets stick to it:
Substance that induced this activation:

A

GpIIb / IIIa

ADP

94
Q

This molecule links platelets:

A

Fibrinogen

95
Q

What do GpIIb / IIIa do?

What does GpIb do?

A

These are molecules expressed on the surface of platelets, they bind fibrin and link platelet to platelet.
GpIb initially binds vWF, which is stuck to exposed collagen; it starts the process.

96
Q

Drug that blocks GpIIb / IIIa:

A

Abciximab

97
Q

Drugs (2) that block the receptor for ADP on platelets:

These drugs are anti-platelet drugs, explain how this works:

A

Clopidogrel
Ticlopidine
ADP is necessary to induce GpIIb / IIIa expression on platelets. GpIIb / IIIa is the fibrinogen-binding molecule that links platelet-fibrinogen-platelet.

98
Q

This drug is a direct inhibitor of GpIIb / IIIa.

These two drugs are indirect:

A

Abciximab = direct

Clopidogrel, ticlodipine = indirect

99
Q

Two main functions of vWF:

A

Stabilize factor VIII

Platelet adhesion to collagen via GpIb

100
Q

Defects in vWF cause two main abnormalities in bleeding studies:

A

Increased bleeding time

Increase in PTT (factor VIII is unstable w/o vWF, coag cascade affected)

101
Q

Deficiency in GpIIb / IIIa =

A

Glanzmann’s thrombasthenia

102
Q

Deficiency in GpIb =

A

Bernard-Soulier syndrome

103
Q

Bite cells

A

G6PD deficeincy

The Heinz body got bitten out

104
Q

Acanthocytes (2 pathologic causes):

A

Liver disease

Abetalipoproteinemia

105
Q

Hemophilia A = deficiency in what factor?

A

Factor 8 = factor AIGHT

106
Q

Vitamin K deficiency results in decreased synthesis of:

A

Factors II, VII, IX, X

Proteins C & S

107
Q

Hemophilia A and B both increase…

A

PTT

108
Q

Platelet abnormalities are associated with this kind of hemorrhage:

A

Microhemorrhage

109
Q

Bernard-Soulier syndrome is a defect in:

A

Defect in platelet plug formation

GpIb, can’t stick to vWF

110
Q

Platelet disorder with a roughly normal platelet count and increased bleeding time:

A

Bernard-Soulier syndrome

111
Q

Platelet adhesion defect in Glanzmann’s thrombasthenia:

A

GpIIb / IIIa - defect in platelet - platelet adhesion

Remember platelet 2 platelet 3 platelet…

112
Q

Pt has increased bleeding time. On blood smear, you see no platelet to platelet clumping:

A

Glanzmann’s thrombasthenia

113
Q

Pathophys. behind ITP:

A

IMMUNE
Anti-GpIIb / IIIa Ab
Spleen eats the platelets

114
Q

Treatment for ITP (2):

A

IVIG

Splenectomy

115
Q

Normal platelet count, increased bleeding time (1).

Low platelet count, increased bleeding time (3).

A

Normal platelets = Glanzmann’s thrombasthenia.

Low platelets = Bernard-Soulier, ITP, TTP

116
Q

Schistocytes, high LDH, setting of thrombocytopenia:

A

TTP.
Defect in vWF metalloprotease.
Platelet consumption 2/2 vWF multimers.
Causes microangiopathic hemolytic anemia -> shearing RBCs.

117
Q

TTP: What is the defect that causes this disorder?

A

Defect in ADAMTS13 = vWF metalloprotease

118
Q

Sx of TTP are a pentad:

A 
Nasty Fever Torched His Kidneys:
Neurologic
Fever
Thrombocytopenia
Hemolysis
Kidneys (uremia)
119
Q

Hemolytic uremic syndrome in a kid may be caused by this pathogen:

A

E. coli 0157H7

120
Q

Difference in presentation between HUS and TTP:

A 
TTP = pentad of neurologic, fever, thrombocytopenia, hemolysis, renal involvement.
HUS = no neuro and no fever.
121
Q

Treatment for vW disease:

Why does this work?

A

Desmopressin (releases stored vWF for whatever reason)

122
Q

Mode of inheritence for vW disease:

A

Autosomal dominant

123
Q

Causes of DIC:

A 
STOP Making Thrombi:
Sepsis
Trauma
OB
Pancreatitis
Malignancy
Transfusion
124
Q

Your friend has vWF disease. What do her bleeding time / coag studies look like?

A 
vWF = increased bleeding time (platelet dysfunction)
Increased PTT (factor VIII instability)
125
Q

T/F: Aspirin increases PTT.

A

F. Aspirin affects platelet function, not the coag cascade.
It increases BLEEDING TIME.

126
Q

Tinnitus on OD:

A

Aspirin

127
Q

These drugs are ADP receptor inhibitors (4):

How do they work?

A 
Clopidogrel
Ticlopidine
Prasugrel
Ticagrelor
Block ADP receptor, activation necessary for GpIIb / IIIa induction and platelet + platelet + platelet action
128
Q

Direct GpIIb / IIIa inhibitors (3):

A

Abciximab
Eptifibatide
Tirofiban

129
Q

Where does this drug act in the platelet activation pathway – Clopidogrel:

A

ADP receptor inhibitor

Blocks GpIIb / IIIa induction

130
Q

Where does this drug act in the platelet activation pathway – Abciximab:

A

GpIIb / IIIa inhibitor

131
Q

Where does this drug act in the platelet activation pathway – Ticlopidine:

A

ADP receptor blocker

Blocks GpIIb / IIIa induction

132
Q

This drug acts like clopidogrel:

A

CLOpidogrel
TiCLOdipine
anti-“CLOT”

133
Q

What is the cause of ITP?

A

Ab generated against the GpIIb / IIIa receptor

134
Q

Life span of a platelet in circulation:

A

8-10d

135
Q

DIC, labs (4):

A

D-dimer increase
Low platelets
High PT/PTT
Increased bleeding time

136
Q

What is the mechanism of action of clopidogrel?

A

ADP receptor blocker

137
Q

What is the mechanism of action of abciximab?

A

Blocks GpIIb / IIIa

138
Q

What is the mechanism of action of tirofiban?

A

Blocks GpIIb / IIIa

139
Q

What is the mechanism of action of ticlodipine?

A

ADP receptor blocker

140
Q

What is the mechanism of action of enoxaparin?

A

LMW heparin

141
Q

What is the mechanism of action of eptifibatide?

A

Blocks GpIIb / IIIa

142
Q

What is a leukemoid reaction?

Leukemoid reaction is distinguishable from CML on the basis of one lab finding, what is it?

A

Leukemoid reaction is an increased WBC with high neutrophils (L shift).
CML appears the same way. Difference is that leukocyte alk. phos is high in leukemoid reaction, low in CML. CML = not mature, doesn’t get around to making alk. phos.

143
Q

These two lymphomas are associated with EBV:

A

Burkitt’s

Non-Hodgkin

144
Q

Two antigens that are (+) on Reed Sternberg cells:

A

CD30, CD15

145
Q

Features of Hodgkin’s lymphoma nodal involvement (3):

A

Localized
Rare extra-nodal involvement
Contiguous spread

146
Q

Age distribution in Hodgkin’s lymphoma:

A

Bimodal: 20 / 50 years of age.

147
Q

Four subtypes of Hodgkin’s lymphoma, order of best to worst prognosis:

A

Lymphocyte-predominant
Nodular sclerosing
Mixed
Lymphocyte-depleted

148
Q

Features of nodal involvement in non-Hodgkin’s lymphoma:

A

Multiple, peripheral nodes
Extranodal involvement common
Non-contiguous spread

149
Q

“Owl’s eye” cell:

A

Reed Sternberg cell

Hodgkin’s lymphoma

150
Q

Burkitt’s lymphoma on histology:

A 
Starry sky 
(sky = sheets of lymphocytes
stars = macrophages that eat them)
151
Q

Three types of Burkitt’s lymphoma:
What type is EBV associated?
Which type affects the pelvis / abdomen?

A

Endemic (EBV, huge jaw lesions)
Sporadic (pelvis / abdomen)
Immune-deficient

152
Q

Most common non-Hodgkin lymphoma in adults:

A

Diffuse large B cell lymphoma

153
Q

Translocation in diffuse large B cell lymphoma:

A

14;18

154
Q

Genetic defect in Burkitt’s lymphoma

A

c-myc translocated with Ig heavy chain

155
Q

Genetic defect in follicular lymphoma:

A

bcl-2 translocated with Ig heavy chain

156
Q

This CD5+ lymphoma has a poor prognosis:

A

Mantle cell lymphoma

157
Q

Which lymphoma am I?
c-myc translocated with Ig heavy chain:
bcl-2 translocated with Ig heavy chain:
cyclin D translocated with Ig heavy chain:

A

c-myc = burkitts
bcl-2 = follicular
cyclin D = mantle cell

158
Q

Cutaneous lesions, HTLV-1 associated lymphoma:

A

Adult T-cell lymphoma

159
Q

Three disorders associated with marginal cell MALToma:

A

Sjogrens
Hashimoto
H. pylori

160
Q

Intestinal T cell lymphoma is associated with this disease:

A

Celiac

161
Q

“Starry sky” appearance on histology:

A

Burkitt’s lymphoma

162
Q

Monoclonal plasma cell proliferation, punched out lytic bone lesions, tumor usually produces these Ab (2):

A

This is multiple myeloma
Mostly IgG
Sometimes IgA

163
Q

Bence Jones protein: What is it, what is it associated with?

A

Ig light chains in urine

Associated with multiple myeloma

164
Q

T/F: You can measure Bence-Jones protein on a urine protein dip.

A

F. Need urine protein electrophoresis.

165
Q

Rouleaux formation, what is it and what disease do you see it in?

A

Stacked up RBCs, see this in multiple myeloma

166
Q

On electrophoresis, what do you observe with multiple myeloma?

A

A Monoclonal M protein spike

167
Q

Four signs / sx of multiple myeloma:

A 
CRAB:
hyper-Calcemia
Renal insufficiency
Anemia
Bone lytic lesions / Back pain
168
Q

Where would you see a monoclonal M protein spike made of IgM?

A

Waldenstrom’s macroglobulinemia

169
Q

This disorder is a precursor to multiple myeloma:

A

MGUS = monoclonal gammopathy of undetermined significance

170
Q

What is a plasmacytoma?

A

A solid tumor of plasma cells.

171
Q

T/F: Lytic bone lesions in a plasmacytoma.

T/F: Lytic bone lesions in Waldenstrom’s.

A

F on both counts. Only see these in multiple myeloma.

172
Q

This plasmacytoma is seen in the head / neck region:

A

Extramedullary plasmacytoma

173
Q

These two leukemias are associated with Down syndrome:

A

ALL

AML

174
Q

This leukemia is sometimes Philadelphia chromosome (+):

A

ALL

175
Q

This leukemia is always Philadelphia chrom. (+):

A

Philadelphia CreaML cheese

CML

176
Q

Pancytopenia: acute or chronic leukemia?

A

Acute.

177
Q

Smudge cells in a much much older adult:

A

CLL.

Usually in people >60yo.

178
Q

TRAP-staining B cell tumor:

A

Hairy cell leukemia.

179
Q

Associated with autoimmune hemolytic anemia, warm or cold agglutinins:

A

CLL

180
Q

Auer rods:

A

AML

181
Q

Treatment for AML:

A

all-trans-retinoic acid

182
Q

Treatment for CML:

A

Imatinib

183
Q

Treatment for hairy cell leukemia:

A

Cladribine

184
Q

Philadelphia chromosome translocation:

A

t(9;22)

185
Q

Disorder associated with this translocation, protein involved:
t(8;14)

A

Burkitt’s, c-myc

186
Q

Disorder associated with this translocation, protein involved:
t(11;14)

A

Mantle cell lymphoma, cyclin D1

187
Q

Disorder associated with this translocation:

t(15;17)

A

M3 type of AML

188
Q

Disorder associated with this translocation, protein involved:
t(14;18)

A

Follicular lymphoma, bcl-2

189
Q

Disorder associated with this translocation, protein involved:
t(18;21)

A

AML

190
Q

Disorder associated with this translocation, protein involved:
t(9;22)

A

This is the Philadelphia chromosome.
CreaML = CML
(Sometimes ALL)

191
Q

What is an Auer body?
What leukemia do you see them in?
What happens if you treat this leukemia?

A

Peroxidase-positive cytoplasmic inclusion in myeloblasts.
AML M3 subtype.
Treatment -> lysis and DIC.

192
Q

Lytic bone lesions and skin rash in a child, S-100(+) cells:

A

Langerhans cell histiocytosis.

S-100 is a neural crest marker.

193
Q

These three chronic myeloproliferative disorders are JAK2 positive:

A

Polycythemia vera
Essential thrombocytosis
Myelofibrosis

194
Q

Cells proliferate without epo stimulation and cause this myeloproliferative disease:

A

Polycythemia vera

195
Q

Cells proliferate without thrombopoieitin stimulation and cause this myeloproliferative disease:

A

Essential thrombocytosis

196
Q

Fibrotic obliteration of bone marrow with teardrop cells:

A

Myelofibrosis

197
Q

Polycythemia: 4 causes:

A

Polycythemia vera
Too much epo (from renal cell ca, pheo, HCC, or hemangioma)
Chronic hypoxia
Trisomy 21

198
Q

This myeloproliferative disorder may present as intense itching after a hot shower:

A

Polycythemia vera

199
Q

Symptoms / signs of polycythemia vera (4):

A

Plethora
HA
Splenomegaly
Itching

200
Q

Most common type of non-Hodgkin lymphoma in adults?

In children?

A

Diffuse large B cell in adults

Lymphoblastic leukemia in kids

201
Q

Most common leukemia in children:

A

ALL

202
Q

Most common leukemia in adults in the US:

A

CLL

203
Q

Leukemia associated with Auer rods:

A

AML

204
Q

PAS (+) acute leukemia:

PAS (-) acute leukemia:

A

ALL

AML

205
Q

This leukemia commonly presents with bone pain:

A

ALL

206
Q

This leukemia is positive for peroxidase:

A

AML

207
Q

BCR-ABL gene associated leukemia:

A

CML

This is none other than the Philadelphia chromosome

USMLE Step 1 (18 decks)

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