Hematology & Oncology. Anatomy 56

First Aid USMLE Step 1: Hematology & Oncology.
Anatomy 56
Study online at https://quizlet.com/_ce95ee
1. Erythrocytes carry O2 to ____ and CO2 to *Tissues, Lungs*

______
2. True or false, erythrocytes are biconcave True

and anucleate
3. What is the lifespan of an erythrocyte and Glucose (90% used in glycoly-

what is its energy source? sis, 10% used in HMP shunt).
Lifespan - 120 days
4. What does the Cl/HCO3 anti porter allow Allows export of HCO3 and
RBCs to do? transport of CO2 from the pe-
riphery to the lungs for elimina-
tion
5. What is a reticulocyte? Immature RBC; reflects ery-

throid proliferation.
6. What is Erythrocytosis, anisocytosis and Erythrocytosis = polycythemia

poikilocytosis? = hematocrit.
Anisocytosis = varying sizes.
Poikilocytosis = varying shapes.
7. The small cytoplasmic fragment of a Megakaryocytic, 8-10 days

thrombocyte (platelet) is derived from
what? What is its lifespan?
8. What causes petechiae? Thrombocytopenia or “platelet

function
9. What do dense granules and alpha gran- Dense granules: ADP, Ca2z,
ules in platelets contain? Serotonin, histamine ''CASH""
Alpha granules: vWF, fibrino-
gen, fibronectin, PF4
10. Approx. 1/3rd of platelets are stored In the spleen

where?
Thrombopoietin
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First Aid USMLE Step 1: Hematology & Oncology. Anatomy 56
what stimulates megakaryocyte prolifer-
ation?
11. What is the fibrinogen receptor? GpIIb/IIIa
12. What is the vWF receptor? GpIb
13. What are my three granulocytes? Neutrophil, eosinophil, basophil
14. List the WBC differential for ranges Neutrophils (54-62%)

Lymphocytes (25-33%)
Monocytes (3-7%)
Eosinophils (1-3%)
Basophils (0-0.75%)
15. What do the specific granules in neu- Specific granules contain

trophils contain? LAP,
collagenase,
lysozyme,
lactoferrin
16. What do the azurophilic granules in neu- Azurophilic granules (lyso-

trophils contain? somes) contain
proteinases,
acid phosphatase,
myeloperoxidase,
²-glucuronidase.
17. In what deficiency do we see hyperseg- Vitamin B12/ folate deficiency.

mented neutrophils?
18. what is a left shift ? An increase in neutrophil pre-

cursor (band cells, metamyelo-
cytes) in peripheral blood
eflect states of increased

myeloid proliferation (bacterial
infections, CML).
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19. What are some neutrophil chemotactic C5a,

agents? IL-8,
LTB4,
5HETE (leukotriene precur-
sor)kallikrein,
platelet-activating factor
N-formylmethionine (bacterial
product)
20. What is a plasma cell cancer? Multiple myeloma
21. For T cells, CD8 recognizes MHC _ while I, II,

CD4 recognizes MHC _ ; also what does CD28 (costimulatory signal)
CD28 do? necessary for T-cell activation.
22. What are dendritic cells called in the Langerhans cell in the skin;
skin? What type of MHC do they bear? MHC II, and Fc receptors
23. What is a monocyte found in blood and differentiates

into Macrophages in tissues
its large nucleus looks like
kidney shape
cytoplasm
''frosted glass'' cytoplasm
24. Lipid A binds to what on macrophages to Lipid A from bacterial LPS binds
initate septic shock? CD14
25. What cytokine can activate ³-interferon

Macrophages?
26. What are the causes of eosinophilia? Parasites

Asthma
Chronic adrenal insuficiency
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Myeloproliferative disorders
Allergic processes
Neoplasia (eg, Hodgkin lym-
phoma)
Eosinophilic granulomatosis
with polyangiitis
PACMAN Eats
27. What are the products of eosinophil? Produces histaminase,

major basic protein (MBP, a
They defend against what ? helminthotoxin)
eosinophil peroxidase
describe the nucleus and the large gran- eosinophil cationic protein
ules eosinophils derived neurotoxin
function ? helminths
uniform, eosinophilic
highly phagocytic fro ag-ab

complexes
28. Basophilia is a sign of what? Myeloproliferative disease, par-

ticularly CML
29. What are the 3 main products of ba- Heparin (anticoagulant) and
sophils? Histamine (vasodilator).
Leukotrienes synthesized and
released on demand
dense basophilic granules +

mediates allergic reaction
30. Describe IgE mediated degranulation of Mast cells can bind the Fc por-
a Mast cell tion of IgE to membrane.
what is degranulation triggered by ? Activated by tissue trauma, c3a

and c5a, surface IgE cross link-
ing by antigen (IgE receptor ag-
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gregation)
causing degranulation, which

releases
histamine,
heparin,
tryptase,
eosinophil chemotactic factors.
31. What is mastocytosis? rare; proliferation of mast cells

in
skin and/or extracutaneous or-
gans.
32. What is mastocytosis associated with ? Associated with

c-KIT mutations
increase serum tryptase.
increase histamine
that results in
flushing, pruritus, hypotension,
abdominal pain, diarrhea, pep-
tic ulcer disease
33. What is used for asthma prophylaxis ? Cromolyn sodium
34. Which 3 drugs can elicit IgE independent Vancomycin, opioids, Radio-
degranulation of mast cells ? contrast dyes
35. What type of reaction (local or diffuse) do Local tissue allergic reaction
mast cells mediate ? basophils..
share a common precursor with
36. EMBRYOLOGY EMBRYOLOGY
37. Where Fetal erythropoiesis occurs in Yolk sac: 3-8wks

these ranges? Liver: 6wks-birth
3-8wks Spleen: 10-28 wks
6wks-birth Bone marrow: 18-adult
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10-28 wks
18-adult Young Liver Synthesizes blood
38. What type of antibodies are found in A IgM anti B

blood type plasma?
39. What type of antibodies are found in B IgM anti A

blood type plasma?
40. What type of antibodies are found in AB None - universal donor of

blood type plasma? PLASMA; not blood because
plasma has no antibodies but
RBCs have both A and B
antigen, universal recipient of
RBCs
41. What type of antibodies are found in O Anti A and B, predominantly

blood type plasma? IgG, IgM
-- Universal donor of RBCs, not

plasma, because O blood has
no antigen on surface, universal
recipient of plasma
42. What type of antibodies are found in Rhz No anti-D

blood type plasma? universal recipient of RBC
43. What type of antibodies are found in Rh{ IgG anti D

blood type plasma?
44. What is the treatment for Rh{ mothers? Treat Rh- mothers with Rh(D)
immunoglobulin (RÓoGAM) af-
ter each pregnancy to prevent
anti-D IgG formation. Rh(D)
wipes out fetal RBCs that have
the D Antigen before the moth-
er's immune system can react.
45. What is Rh hemolytic disease ? Rh mothers exposed to fetal

Rh+ blood (often during deliv-
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ery) may make anti-D IgG.
In subsequent pregnancies,
anti-D IgG crosses the placenta
attacks fetal and newborn RBC
= hemolysis
46. whats the presentation? Hydrops fetalis, Jaundice short-

ly after birth, kernicterus
47. During which trimester is RhoGAM ad- Prevented by administration of

ministered? RhoGAM/ anti-D IgG to Rh
pregnant women during third
trimester and early postpartum
period (if fetus is Rh+),
which prevents maternal
anti-Rh IgG production.
Rh mothers have anti-D IgG

only if previously exposed to
Rh+ blood.
48. ABO hemolytic disease of the newborn Usually occur in type O moth-
er with a type A or B fetus.
Can occur in the first pregnancy.
neonate present with jaundice
within 24hrs of birth
Tx phototherapy or transfusion
exchange
49. What are the 3 effects of bradykinin in the 1. ‘ Vasodilation

kinin cascade? 2. ‘ Permeability
3. ‘ Pain
50. What enzyme activates bradykinin? Kallikrein
51. What is HMWK? High molecular weight kinino-

gen (HMWK or HK) is a circu-
lating plasma protein initiates in
blood coagulation, and in the
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generation of the vasodilator
bradykinin via the Kallikrein-kin-
in system.
52. What are my four main types of anticoag- 1. LMWH (greatest efficacy)
ulants that target factor X? 2. heparin
3. direct Xa inhibitors (apixa-
ban, rivaroxaban)
fondaparinux
53. During gel electrophoresis, hbg Migrates from negatively

charged cathode to positive
54. who migrates fathest? - HbA: migrates the farthest

- HbF > HbS > HbC
then ?
because of the HbS and HbC:
why is that missence mutations
that replaces glutamic acid (-)
with valine (neutral) or lysine (+)
makes HbC and HbS more +

charged
A FAT SANTA ClAUS

CAN'T.....go far
55. his tests whether the patient's RBCS are DIrect

coated with an anti-RBC antibody when
adding an anti-human globulin Coombs
reagent
56. This takes pt serum and adds donor Indirect

blood with Coombs reagent to test
whether there is agglutination or not to
patients serum against donor blood:
57. What are my three main types of antico- 1. heparin (greatest efficacy)
agulants that target thrombin (IIa)? 2. LMWH (dalteparin, enoxa-
parin)
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3. direct thrombin inhibitors (ar-
gatroban, bivalirudin, dabiga-
tran)
58. What are my 4 thrombolytics which acti- THROMBOLYTICS:

vate tPA but are not part of the coagula- 1. alteplase,
tion cascade? 2. reteplase,
3. streptokinase,
4. tenecteplase
59. Plasminogen is converted to plasmin via tPA

what? Inhibits Aminocaproic acid
What does this also inhibit?
60. Prothrombin and thrombin are also Factor II and IIa

known as?
61. Hemophilia A is a deficiency of? Deficiency of factor VIII (XR)
62. Hemophilia B is a deficiency of? Deficiency of factor IX (XR)
63. Hemophilia C is a deficiency of? Deficiency of factor XI (AR)
64. Describe the extrinsic pathway of the co- VII leads to VIIa via TF
agulation cascade.
65. Describe the intrinsic pathway of the co- XII leads to XIIa
agulation cascade. XI leads to XIa (via XIIa)
IX leads to IXa (via XIa)
IXa aided by VIIIa to transform
X to XA -- VII becomes VIIIa (via
IIa)
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I Ia
Fibrinogen Fibrin monomers
aggregation
Ca2+
IXa
66. What ion and other macromolecule are Ca2z and phospholipid
necessary for VII to VIIa, IXa coupled VIIIa
mechanism to activate X to Xa, VIIa to
activate X to Xa, and, Xa coupled with Va
mechanism to activate II to IIa?
67. Describe the 4 pathways mediated by Ca 1. VII to VIIa,

and phospholipid. 2. VIIa to activate X to Xa
3. IXa coupled VIIIa mechanism
to activate X to Xa and,
3. Xa coupled with Va mecha-
nism to activate II to IIa
68. Describe the combined pathway. (6 X ’ Xa (via VIIa and VIIIa)

steps) V ’ Va (via IIa)
II ’ IIa (via Xa and Va)
I ’ Ia (via Thrombin)
XIII ’ XIIIa (via IIa)
XIIIa combines with Ca2z and Ia
to form fibrin mesh
69. Tue or false, Mg2 z is required for fibrin False, Ca2 z is required for fibrin
mesh to form. mesh formation
70. Factor I and Ia are also known as? Fibrinogen and Fibrin
monomers
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71. Plasmin acts on Fibrin mesh to result in? Fibrin degradation products.
72. Vit. K deficiency leads to “ synthesis of Factors, X, IX, VII, II, protein C,
what 6 proteins? protein S.
73. vWF carries what factor? VIII
74. Warfarin inhibits which enzyme? Vitamin K epoxide reductase.
75. Neonates lack enteric bacteria, which Vit. K

produce which vitamin?
76. Epoxide reductase does what to Oxi- Turns it into reduced vitamin K
dized reductase
vitamin K?
77. Antithrombin inhibits activated forms of X, IX, VII, II, XI, XII
which factors?
78. Heparin enhances the activity of? Antithrombin
79. Principal targets of antithrombin are? Thrombin and factor Xa.
80. Factor V Leiden mutation produces a fac- Activated protein C

tor V
resistant to inhibition by?
81. tPA is used clinically as a? Thrombolytic
82. Fibrinolysis is defined as (2 things) 1. cleavage of fibrin mesh

2. destruction of coagulation
factors
83. Activated protein C combines with pro- cleaves and inactivates Va, VI-
tein S to cleave and inactivate? IIa
84. Protein C is activated by what complex? Thrombin-thrombomodulin

complex
85. Primary hemostasis is also known as? Platelet plug formation

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86. What are the 5 steps of platelet plug for- 1. Injury

mation? 2. Exposure
3. Adhesion
4. Activation
5. Aggregation
87. What product causes vasoconstriction Injury ’ transient vasoconstric-

due to endothelial cell damage? tion via neural stimulation reflex
and endothelin (released from
damaged cell)
88. What binds to exposed collagen? Exposure ’ vWF binds to ex-

posed collagen
89. What 2 places are vWF found in? vWF is from Weibel-Palade
bodies of endothelial
cells and ±-
granules of platelets
90. What do platelets bind to during adhe- They bind to vWF and the
sion via the GpIb receptor? platelets undergo a conforma-
tional change
91. After undergoing conformational change They release ADP, Ca2z, and
during adhesion what three molecules TXA2. ADP helps platelets ad-
do platelets release? here to endothelium.
92. During Activation, after ADP binds to GpIIb/IIIa

P2Y12 receptor, two receptors are ex-
pressed at the platelet surface?
93. During Aggregation, what binds to GpI- Fibrinogen

Ib/IIIa receptors and links platelets?
94. What is a pro-aggregation factor re- TXA2; “ blood flow; ‘ platelet ag-
leased by platelets? What is its effect on gregation
blood flow?
95. What are anti-aggregation factors? PGI2 and NO ; ‘ blood flow; “

platelet aggregation
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96. After primary homeostasis concludes 2dary homeostasis via the co-
what happens? agulation cascade starts!
97. Clopidogrel, prasugrel, and ticlopidine ADP

inhibit ____ induced expression of Gpi-
Ib/IIIa
98. Abciximab, eptifibatide, and tirofiban in- GpIIb/IIIa

hibit ___ directly
99. Risotecetin activates ____ to bind GpIb vWF
100. Failure of agglutination with ristocetin von Willebrand disease and

assay occurs in which two conditions? Bernard-Soulier syndrome
101. Aspirin prevents TXA2 synthesis by in- Cyclooxygenase

hibiting what?
102. What is the ultimate goal of thrombogen- Formation of insoluble fibrin

esis? mesh
103. A deficiency of GpIb is known as what Bernard-Soulier syndrome

syndrome?
104. A deficiency of GpIIb/IIIa is known as? Glanzmann thrombasthenia
105. What is an acanthocyte? Spur cell:

associated with liver dis-
ease and abetalipoproteinemia
(states of cholesterol dysregu-
lation).
106. What does basophilic stippling occur Lead poisoning

due to? Sideroblastic anemias (periph-
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eral smear)
Myelodysplastic sydnrome
107. What does Dacrocyte occur due to? Teardrop cell

Bone marrow infiltration Ex.
Myelofibrosis
108. What is a bite cell? A degmacyte which results due

to G6PD deficiency.
109. What is a burr cell? AKA: Echinocyte

Associated with:
end stage renal disease
liver disease
private kinase deficiency
110. In what disease do elliptocytes occur in? Hereditary elliptocytosis.
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111. In what disease do macro-ovalocytes oc- Megaloblastic anemia (also hy-

cur in? persegmented PMNs), marrow
failure.
112. In what disease do ringed sideroblasts Sideroblastic anemia. Excess

occur in? iron in mitochondria = patholog-
ic.
see in bone marrow
113. Schistocytes/aka helmet cells occur in DIC,

which 5 conditions? TTP/HUS,
HELLP syndrome,
mechanical hemolysis (e.g.,
heart valve prosthesis).
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114. This occurs to RBCs with dehydration, Sickling. Also associated with
deoxygenation, and at high altitude. sickle cell anemia
115. What 3 conditions do we see sphero- 1. Hereditary spherocytosis

cytes in? 2. drug- and (3) infection-in-
duced hemolytic anemia.
116. What are dacrocytes? What pathology is AKA Teardrop cells. RBC
it associated with? "sheds a tear" because it's
mechanically squeezed out of
its home in the bone marrow.
Bone marrow infiltration (e.g.,
myelofibrosis).
117. In what conditions are target cells appar- HbC disease, Asplenia, Liver
ent? disease, Thalassemia. ("HALT,"
said the hunter to his target.)
118. What two pathologies are heinz bodies G6PD deficiency;

scene in? Heinz body-like inclusions seen
in ±-thalassemia.
Oxidation of Hb-SH groups
to -S—S- Hb precipitation
(Heinz bodies), with subse-
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quent phagocytic damage to
RBC membrane bite cells.
119. Seen in patients with functional hypos- Howell-Jolly bodies.

plenia or asplenia. Basophilic nuclear remnants
found in RBCs.
Howell-Jolly bodies are nor-
mally removed from RBCs by
splenic macrophages.
120. What are my microcytic anemias? TAILS

Thalassemias
ACD (Anemia of inflammation
and chronic disease)
Iron deficiency (late)
Lead poisoning
Sideroblastic anemia
121. Copper deficiency can cause which type Sideroblastic anemia

of anemia?
122. Which two types of microcytic anemias Iron deficiency and ACD
can be normocytic to begin with before
they become microcytic?
123. What is the MCV range for microcytic MCV < 80 fL

anemias?
124. What is the MCV range for normocytic MCV (80-100 fL)
anemias?
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125. What is the MCV range for macrocytic MCV > 100 fL
anemias?
126. Normocytic anemias can be classified Hemolytic and nonhemolytic

into 2 distinct categories. What are they?
127. What is the reticulocyte count in he- Non-hemolytic: (Reticulocyte

molytic vs nonhemolytic anemia? count “ or normal
Hemolytic (Reticulocyte count ‘)
128. What are 4 non-hemolytic anemias (nor- 1. Chronic kidney disease

mocytic) - two of which can be microcytic 2. Aplastic anemia
as well 3. Iron deficiency (early)
4. ACD
129. What are the two classifications of he- Extrinsic and intrinsic
molytic anemias (normocytic) ?
130. What are 5 intrinsic hemolytic anemias? 1. RBC membrane defect:

hereditary spherocytosis
2. RBC enzyme deficiency:
G6PD, pyruvate kinase
3. HbC defect
4. Paroxysmal nocturnal hemo-
globinuria
5. Sickle cell anemia
131. What are my 4 types of extrinsic hemolyt- 1. Autoimmune

ic anemais? 2. Microangiopathic
3. Macroangiopathic
4. Infections
132. What are the two classifications of Megaloblastic and non-mega-

macrocytic anemias? loblastic
133. What are my 3 megaloblastic (macrocyt- Folate & b12 deficiency, Orotic
ic) anemias? aciduria
134.
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What are my 3 non-megaloblastic Liver disease, alcoholism, retic-
(macrocytic) anemias? ulocytosis
135. What is the triad of Plummer-vinson syn- Postcricoid dysphagia, upper

drome? esophageal webs, and iron de-
ficiency anemia ; note atrophic
glossitis is also present;
136. Comment on iron, TIBC, and ferritin lev- Iron “

els for iron deficiency anemia. List 3 TIBC ‘
symptoms Ferritin “
1. Fatigue
2. conjunctival pallor
3. Koilonychia
137. What are four causes of iron deficiency 1. Hemmorhage

anemia? 2. Mennorhagia
3. Malabsorption or malnutrition
4. Pregnancy
138. How would iron deficiency appear in a Microcytosis, central pallor

blood stain? (hypochromia)
139. What happens to alpha globin in 4 al- 4 allele deletion: No ±-

globin. Ex-
lele deletion alpha thalassemia? Excess cess ³-globin forms ³4 H
( b Barts).
gamma globin forms what? Incompatible with life (causes
hydrops fetalis)
140. What happens to alpha globin in 3 allele 3 allele deletion: HbH disease.
deletion alpha thalassemia? Very little ±-
globin. Excess ²-glo-
bin forms ²4 (HbH).
141. What type of alpha globin gene deletions Cis deletion prevalent in
occur in Asian and African populations? Asian populations; trans dele-
19 / 60
tion prevalent in African popula-
tions.
142. B-thalassemia is present in what demo- Prevalent in Mediterranean

graphic? populations.
143. How is ²-thalassemia minor diagnosed; is ²-thalassemia minor (heterozy-

it hetero or homozygote? gote):
²chain is underproduced.
Usually asymptomatic.
Diagnosis confirmed by ‘ HbA2
(> 3.5%) onelectrophoresis.
144. ²-thalassemia major (homozygote) is 1. Anemia (2Ú hemochromato-

characterized by (3) conditions. What are sis)
they? 2. Marrow Expansion ("crew
cut" on skull x-ray) skeletal de-
formities. "Chipmunk" facies.
3. Extramedullary
hematopoiesis (leads to he-
patosplenomegaly)
145. What is a HbS/²-thalassemia heterozygote Mild to moderate sickle cell dis-

phenotype severity? ease depending on amount of
²-globin production.
146. What is hemochromatosis? Iron overload disease resulting

in abnormal deposition of iron
147. ²-thalassemia major can increase what Major ’ ‘ HbF ±2³2).

( HbF is protec-
type of hemoglobin? tive in the infant and disease be-
comes symptomatic only after 6
months.
148. What RBC disorders are seen on the Anisocytosis, poikilocytosis, tar-
blood film for ²-thalassemia major? get cells, microcytosis, and
schistocytes
149. What does Lead inhibit to result in “ hemeFerrochelatase and ALA dehy-
synthesis and ‘ RBC protoporphyrin. dratase
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150. Why does basophilic stippling occur in RBCs retain aggregates of

lead poisoning? rRNA because lead inhibits
rRNA degradation.
151. What signs are apparent with lead poi- Lead Lines on gingivae (Burton
soning? lines) and on
metaphyses of long bones D on
x-ray.
Encephalopathy and Erythro-
cyte basophilic
stippling.
Abdominal colic and sideroblas-
tic Anemia.
Drops—wrist and foot drop.
152. What treatments are used for lead poi- Dimercaprol and EDTA are 1st
soning? line of treatment.
Succimer used for chelation for
kids (It "sucks" to
be a kid who eats lead).
153. What are burton lines? Lead lines on gingivae
154. What is the treatment for sideroblastic Pyridoxine (B6, cofactor for ´--
anemia? ALA
synthase).
155. Comment on iron, TIBC and ferritin levels ‘ iron, normal/“TIBC, ‘ ferritin.
for sideroblastic anemia.
156. What are the causes of sideroblastic ane- A Genetic

mia? B Acquired (myelodysplastic
syndromes),
C Reversible
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1. alcohol is most common
2. lead
3. Vitamin B6 deficiency,
4. Copper deficiency,
5, Isoniazid
157. Why does sideroblastic anemia occur at Defect in heme synthesis.

the molecular level? Hereditary: X-linked defect in ´--
ALA synthase gene.
158. What defines megaloblastic anemia ? Impaired DNA synthesis matu-

ration of nucleus of precursor
cells in bone marrow delayed
relative to maturation in cyto-
plasm.
159. What are the findings of megaloblastic 1. RBC macrocytosis

anemia? 2. Hypersegmented neu-
trophils
3. Glossitis.
160. What are the causes of folate deficiency? 1. Malnutrition and malabsorp-
tion
2. Alcoholism
3. Drugs (e.g., methotrexate,
trimethoprim, phenytoin),
4. ‘ Requirement (e.g., hemolytic
anemia, pregnancy).
161. What is the main symptom that distin- ‘ Homocysteine, normal methyl-
guishes folate deficiency from b12 defi- malonic acid.
ciency? Comment on homocysteine lev- No neurologic symptoms (vs.
els. B12 deficiency).
162. What are the causes of B12 deficiency? 1. Insuffcient intake (e.g., ve-
ganism), malabsorption (e.g.,
Crohn disease),
3. pernicious anemia,
4. Diphyllobothrium latum ( fish
22 / 60
tapeworm)
5. Gastrectomy.
163. Comment on homocysteine and methyl- ‘ homocysteine, ‘ methylmalonic

malonic acid levels for B12 deficiency. acid.
164. What are the symptoms of B12 deficien- Neurologic symptoms: suba-
cy? cute combined degeneration
(due to involvement of B12
in fatty acid pathways and
myelin synthesis): spinocere-
bellar tract, lateral corticospinal
tract, dorsal column dysfunc-
tion.
165. What is the treatment of orotic aciduria? Uridine monophosphate to by-

pass
mutated enzyme.
166. Orotic aciduria is characterized by Inabil- Inability to convert orotic acid to

ity to convert orotic acid to ___. What UMP
population does it affect? (de novo pyrimidine synthesis
pathway) because of defect in
UMP synthase. Autosomal re-
cessive. Presents in children as
failure to thrive, developmental
delay, and megaloblastic ane-
mia refractory to folate and B12.
167. No hyperammonemia is noted in orotic Orotic acid ‘ with hyperamone-

aciduria (vs. ornithine transcarbamylase mia
deficiency) Does orotic acid ‘ or “ with hy-
perammonemia).
168. What is does the blood film of nonmega- RBC macrocytosis without hy-
loblastic macrocytic anemia display? persegmented neutrophils.
169. What are the causes of nonmegaloblastic 1. Alcoholism

macrocytic anemias 2. Liver disease
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3. Hypothyroidism
4. Reticulocytosis.
170. What are the main causes of intravascu- 1. mechanical hemolysis (e.g.,
lar hemolysis? prosthetic valve),
2. paroxysmal nocturnal hemo-
globinuria
3. microangiopathic hemolytic
anemias.
171. Comment on haptoglobin, LDH, schisto- Haptoglobin “

cytes and reticulocytes levels on blood ‘ LDH
smear for intravascular hemolysis. Schistocytes present
‘ reticulocytes
172. What findings in the urine are pertinent hemoglobinuria, hemosiderin-

for intravascular hemolysis? uria, and urobilinogen
173. Describe RBCs on blood film and urine Spherocytes in peripheral

analysis for extravascular hemolysis smear, ‘ LDH
Urine: no hemoglobinuria/he-
mosiderinuria, ‘ unconjugated
bilirubin, which can cause jaun-
dice.
174. What is the treatment for anemia of Treatment: EPO (chronic kidney
chronic disease? disease only).
175. Comment on iron, TIBC, ferritin levels for “iron, “ TIBC, ‘ ferritin.
Anemia of chronic disease. Normocytic, but can become
microcytic.
176. Anemia of chronic disease is associated 1. Rheumatoid arthritis

with which other conditions? (immune 2. SLE
related) 3. neoplastic disorders
4. chronic kidney disease.
177. How is inflammation noted in anemia of Inflammation ’ ‘ hepcidin (re-

chronic disease? leased by liver, binds ferroportin
on intestinal mucosal
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cells and macrophages, thus in-
hibiting
iron transport) ’ “ release of iron
from macrophages.
178. What is the treatment for aplastic ane- 1. Withdrawal of offending

mia? agent
2. immunosuppressive regi-
mens (e.g., antithymocyte glob-
ulin, cyclosporine),
3. Bone marrow allograft,
4. RBC/platelet transfusion
5. Bone marrow stimulation
(e.g., GM-CSF).
179. What are the symptoms associated with 1. Fatigue

aplastic anemia? 2. Malaise
3. Pallor
4. Purpura
5. Mucosal bleeding
6. Petechiae
7. Infection.
180. What is aplastic anemia? Pancytopenia characterized by

*severe anemia, leukopenia,
and thrombocytopenia*. Nor-
mal cell morphology, but
hypocellular bone marrow with
fatty infiltration. (dry bone mar-
row tap).
181. Aplastic anemia is caused by failure or 1. Radiation and drugs (ben-

destruction of myeloid stem cells due to: zene, chloramphenicol, alkylat-
ing agents, antimetabolites)
2. Viral agents (parvovirus B19,
25 / 60
EBV, HIV, HCV)
3. Fanconi anemia (DNA repair
defect)
4. Idiopathic (immune mediat-
ed, 1° stem cell defect); may fol-
low acute hepatitis
182. What are all of my intrinsic hemolytic 1. Hereditary spherocytosis (E)

(normocytic) anemias and which are in- 2. G6PD deficiency (I/E)
travascular vs. extravascular? 3. Pyruvate kinase de ciency (E)
4. HbC defect (E)
5. Paroxysmal nocturnal hemo-
globinuria (I)
6. Sickle cell anemia (E)
183. What causes hereditary spherocytosis? Defect in proteins interacting

with RBC
membrane skeleton and plas-
ma membrane
(e.g., ankyrin, band 3, protein
4.2, spectrin)
184. What do labs reveal for hereditary sphe- Labs: osmotic fragility test •. Nor-
rocytosis? mal to MCV with abundance of
cells.
185. What is the treatment for hereditary Splenectomy.

spherocytosis?
186. Splenomegaly and what other 'crisis' is Aplastic crisis (parvovirus B19
noted in hereditary spherocytosis? infection).
187. Describe the RBCs qualitatively, and in Results in small, round RBCs
terms of MCHC, and RCDW, for hereditary with less surface area and no
spherocytosis. central pallor ( ‘ MCHC, ‘ red cell
distribution width) premature re-
moval by spleen.
188. What is the most common enzymatic dis- G6PD deficiency (I/E)
order of RBCs. It is X-linked recessive.
26 / 60
189. What causes G6PD deficiency? Defect in G6PD ’ “ glutathione

‘ RBC susceptibility to oxidant
stress. Hemolytic anemia fol-
lowing oxidant stress
190. What are some causes of oxidative 1. Sulfa drugs

stress in G6PD deficiency? 2. Antimalarials
3. Infections
4. Fava beans
191. What are the symptoms of G6PD defi- Back pain, hemoglobinuria a
ciency? few days after oxidant stress.
192. What do labs reveal for G6PD deficiency? Labs: blood smear shows RBCs
with Heinz bodies and bite cells.
"Stress makes me eat bites of
fava beans with Heinz ketchup."
193. What deficiency could lead to hemolytic Pyruvate kinase deficiency (E)
anemia in a newborn.
194. Is Pyruvate kinase deficiency (E) autoso- Autosomal recessive. Defect in

mal dominant or recessive? Comment on pyruvate kinase ’ “ ATP ’ rigid
ATP levels and RBC status. RBCs.
195. How does HbC DEFECT (E) MAN Patients with HbSC (1 of each
mutant gene) have milder dis-
ease than HbSS patients.
196. What amino acid mutations are seen in Glutamic acid-to-lysine muta-
HbC (E) defects? tion in ²-globin.
197. What is the triad for paroxysmal noctur- 1. Coombs • Hemolytic anemia
nal hemoglobinuria? 2. Pancytopenia
3. Venous thrombosis.
198. What do labs reveal about Paroxysmal CD55/59 • RBCs on flow cytom-
nocturnal hemoglobinuria (I)? etry.
27 / 60
199. What is the treatment for Paroxysmal Treatment: eculizumab (termi-
nocturnal hemoglobinuria (I)? nal complement
inhibitor).
200. Why does Paroxysmal nocturnal hemo- ‘complement-mediated RBC ly-

globinuria (I) occur? sis (impaired
synthesis of GPI anchor for
decay-accelerating factor that
protects RBC membrane from
complement). Acquired muta-
tion in a hematopoietic stem
cell. ‘ Incidence of acute
leukemias.
201. What are complications of sickle cell dis- 1. Aplastic crisis (due to par-
ease? vovirus B19).
2. Autosplenectomy (How-
ell-Jolly bodies) risk of infection
by encapsulated organisms.
3. Splenic infarct/sequestration
crisis.
4. Salmonella osteomyelitis.
5. Painful crises (vaso-occlu-
sive):
i) dactylics (painful swelling of
hands/feet),
ii) acute chest syndrome,
iii) avascular necrosis,
iv) stroke.
6. Renal papillary necrosis (
“Po2 in papilla) and
7. microhematuria (medullary
infarcts).
202. What is the treatment for sickle cell ane- Hydroxyurea ( HbF), hydration.
mia (e)?
203. Why are newborns initially asymptomatic because of ‘ HbF and “ HbS.
of sickle cell anemia (E)?
28 / 60
204. Heterozygotes (sickle cell trait) also have malaria
resistance to ______
205. 8% of African Americans carry an Hb_ HbS

allele. (sickle cell anemia)
206. For SS anemia we see "Crew cut" "Crew cut" on skull x-ray due to
on skull x-ray due to _______________ marrow
from erythropoiesis (also seen in tha- expansion from erythropoiesis
lassemias). (also seen in thalassemias).
207. HbS point mutation causes a single HbS point mutation causes a
amino acid replacement in __ chain (sub- single amino acid replacement
stitution of glutamic acid with ________). in ²chain (substitution of glutam-
ic acid with valine).
208. What is the pathogenesis for SS anemia? Pathogenesis: low O2, high
altitude, or acidosis precip-
itates sickling (deoxygenated
HbS polymerizes) ’ anemia and
vaso-occlusive disease.
209. What are my extrinsic hemolytic normo- 1. Autoimmune hemolytic ane-

cytic anemias? mia
2. Microangiopathic anemia
3. Macroangiopathic anemia
4. Infections
210. Describe warm agglutinin chronic ane- It is an autoimmune hemolyt-

mia. ic anemia. Warm agglutinin
(IgG)—chronic anemia seen in
SLE and CLL and with cer-
tain drugs (e.g., ±-
methyldopa)
("warm weather is Great").
211. Cold agglutinin acute anemia. What anti- It is an autoimmune hemolyt-

body type? Hemolytic or non hemolytic? ic anemia. Cold agglutinin
Seen in which diseases? (IgM)—acute anemia triggered
by cold; seen in:
1. CLL
29 / 60
2. Mycoplasma pneumonia in-
fections, and
3. infectious Mononucleosis
("cold weather is MMMiser-
able").
212. Autoimmune hemolytic anemias are usu- Autoimmune hemolytic ane-

ally Coombs ___. mias are usually Coombs •.
213. Describe the Direct Coombs test. Direct Coombs test—anti-Ig an-
tibody (Coombs reagent) added
to patient's blood. RBCs aggluti-
nate if RBCs are coated with Ig.
Indirect Coombs test—normal
RBCs added to patient's serum.
If serum has anti-RBC sur-
face Ig, RBCs agglutinate when
Coombs reagent added.
214. Describe th indirect coombs test. Indirect Coombs test—normal

RBCs added to patient's serum.
If serum has anti-RBC sur-
face Ig, RBCs agglutinate when
Coombs reagent added.
215. What is the pathogenesis of micronagio- Pathogenesis: RBCs are dam-

pathic anemia? aged when passing through ob-
structed or narrowed vessel lu-
mina.
Seen in DIC, TTP/HUS, SLE,
and malignant hypertension.
216. What type of cells are found in blood Schistocytes ("helmet cells")
smear for microangiopathic anemia? are seen on blood smear due
to mechanical destruction of
RBCs.
217. What is Macroangiopathic anemia? Prosthetic heart valves and aor-

tic stenosis may also cause he-
30 / 60
molytic anemia 2° to mechani-
cal destruction.
218. What type of cells are found in blood Schistocytes on peripheral

smear for macroangiopathic anemia? blood smear.
219. What infections can accelerate destruc- Malaria, Babesia

tion of RBCs?
220. Comment on Serum iron, Transferrin or Serum iron: “

TIBC, Ferritin, and % transferrin satura- Transferrin or TIBC: ‘
tion (serum iron/TIBC) values for Iron de- Ferritin: “
ficiency. % transferrin saturation (serum
iron/TIBC): ““
221. Comment on Serum iron, Transferrin or Serum iron: “

TIBC, Ferritin, and % transferrin satura- Transferrin or TIBC: “
tion (serum iron/TIBC) values for chronic Ferritin: ‘
disease. % transferrin saturation (serum
iron/TIBC): --
Transferrin “ because of evolu-
tionary reasoning—pathogens
use circulating iron to thrive.
The body has adapted a system
in which iron is stored
within the cells of the body and
prevents pathogens from ac-
quiring circulating iron.
222. Comment on Serum iron, Transferrin or Serum iron: ‘

TIBC, Ferritin, and % transferrin satura- Transferrin or TIBC: “
tion (serum iron/TIBC) values hemochro- Ferritin: ‘
matosis. % transferrin saturation (serum
iron/TIBC): ‘‘
223. Comment on Serum iron, Transferrin or Serum iron: --

TIBC, Ferritin, and % transferrin satura- Transferrin or TIBC: ‘
tion (serum iron/TIBC) values pregnancy Ferritin: --
(OCP). % transferrin saturation (serum
iron/TIBC): “
31 / 60
224. What is the cell count for neutropenia? < 1500 cells/mm3
225. What is the cell count for lymphopenia? < 1500 cells/mm3 (< 3000
cells/mm3 in children)
226. What are possible causes of lymphope- 1. HIV

nia? 2. DiGeorge syndrome,
4. SCID,
5. SLE,
6. corticosteroids,
7. radiation
8. sepsis
9. postoperative
227. What is neutrophilia? Increased number of neu-

trophils. i.e. leukocytosis of neu-
trophils.
228. Corticosteroids cause ________, despite Corticosteroids cause neu-

causing eosinopenia and lymphopenia. trophilia, despite causing
Corticosteroids activation of neutrophil eosinopenia and lymphopenia.
adhesion molecules, impairing migration Corticosteroids activation of
out of the vasculature to sites of in- neutrophil adhesion molecules,
flammation. In contrast, corticosteroids impairing migration out of the
sequester ______ in lymph nodes and vasculature to sites of in amma-
cause ______ of lymphocytes. tion. In contrast, corticosteroids
sequester eosinophils in lymph
nodes and cause apoptosis of
lymphocytes.
229. What are possible causes of neutrope- 1. Sepsis/post-infection

nia? 2. Drugs (including chemother-
apy)
3. Aplastic anemia
4. SLE
5. Radiation
230. What are possible causes of eosinope- 1. Cushing syndrome

nia? 2. Corticosteroid
32 / 60
231. ______________ are hereditary or ac- The porphyrias are hereditary

quired conditions of defective heme syn- or acquired conditions of defec-
thesis that lead to the accumulation of tive heme synthesis that lead to
heme precursors. _______ inhibits spe- the accumulation of heme pre-
cific enzymes needed in heme synthesis, cursors. Lead inhibits speci c
leading to a similar condition. enzymes needed in heme syn-
thesis, leading to a similar con-
dition.
232. What enzymes are affected during lead Ferrochelatase and ALA dehy-
poisoning? dratase
233. What is the accumulated substrate in Protoporphyrin, ´-ALA (blood)

lead poisoning?
234. What are the symptoms manifested due 1. Microcytic anemia (ba-
to lead poisoning ? sophilic stippling A ),
In children, adults? 2. GI and kidney disease.
Children—exposure to lead
paint *mental deterioration*.
Adults—environmental expo-
sure (e.g., batteries, ammuni-
tion) *headache, memory loss,
demyelination*.
235. What is the accumulated substrate in Porphobilinogen, ´-ALA, copor-

Acute intermittent porphyria? phobilinogen (urine)
236. What is the affected enzyme in Acute in- Porphobilinogen deaminase

termittent porphyria?
237. What are the 5 Ps of Acute intermittent 1. Painful abdomen

porphyria? 2. Port wine-colored urine
3. Polyneuropathy
4. Psychological disturbances
5. Precipitated by drugs (e.g.,
cytochrome
P-450 inducers), alcohol, star-
vation
33 / 60
238. What is the treatment for Acute intermit- Treatment: glucose and heme,
tent porphyria? which inhibit ALA synthase.
239. What is the affected enzyme in Porphyria Uroporphyrinogen decarboxy-

cutanea tarda? lase
240. What is the affected substrate in Porphyr- Uroporphyrin (tea- colored

ia cutanea tarda? urine)
241. What are the presenting symptoms of Blistering cutaneous photosen-

Porphyria cutanea tarda? sitivity. This is the most common
porphyria.
242. Iron poisoning leads to cell death due to Iron poisoning leads to cell
________________ of membrane lipids. death due to peroxidation of
membrane lipids.
243. What are the signs and symptoms of iron 1. Nausea

poisoning? 2. Vomiting
3. Gastric bleeding
4. Lethargy
5. Scarring leading to GI ob-
struction.
244. What is the treatment for iron poisoning? Chelation (e.g., IV deferoxam-
ine, oral deferasirox) and dialy-
sis.
245. PT—tests function of ____________ and PT—tests function of common

_____________ pathway (factors I, II, V, and extrinsic pathway (factors I,
VII, and X). Defect ’ ? PT. II, V, VII, and X). Defect ’ ‘ PT.
246. PTT—tests function of ________ and PTT—tests function of common

____________ pathway (all factors ex- and intrinsic pathway (all factors
cept ___ and ____). Defect ’ ‘ PTT. except VII and XIII). Defect ’ ‘
PTT.
247. What is the treatment for intrinsic path- Intrinsic pathway coagulation
way coagulation defects? defects = hemophaelia A, B, C
34 / 60
Treatment: desmopressin + fac-
tor VIII concentrate (A); factor IX
concentrate (B); factor XI con-
centrate (C).
248. Describe PTT Values in haemophilias A, PTT ‘ in all

B, C. Each is a deficiency of which factor? A: factor VIII ; X-linked reces-
sive.
B: factor IX; X-linked recessive.
C: factor XI; autosomal reces-
sive.
249. What is the bleeding time of Vit K de- Bleeding time normal.
ficiency? (‘ “ or -- ? ); Which factors are “ activation of factors II, VII, IX, X,
affected? (10, 9, 7, 2) protein C, protein S
250. How does Vit K deficiency affect PT and “of both PTT and PT
PTT levels?
251. How is the bleeding time affected in Defects in platelet plug forma-
platelet disorders? tion ’ ‘ bleeding time (BT); possi-
bly lower platelet count (PC)
252. Platelet abnormalities ’ microhemor- 1. Mucous membrane bleeding

rhage. Microhemorrhage consists of 2. Epistaxis
which four symptoms? 3. Petechiae,
4. Purpura
253. Bernard-soulier syndrome. Lowered “GpIb ’ defect in platelet-to-vWF

GpIb results in what? Comment on PC adhesion. No agglutination on
and BT levels. ristocetin cofactor assay.
PC: - / “
BT: ‘
254. Comment on PC and BT levels for Glanz- PC: -

mann thrombasthenia. BT: ‘
“ GpIIb/IIIa ’ What type of defect? “ GpIIb/IIIa ’ defect in
platelet-to-platelet aggregation.
255.
35 / 60
What do labs for Glanzmann thrombas- Labs: blood smear shows no
thenia reveal? platelet clumping. Agglutination
with ristocetin cofactor assay.
256. Comment on PC and BT levels for im- PC: “

mune thrombocytopenia. What type of BT: ‘
antibodies are found in immune throm- Anti-GpIIb/IIIa antibodies
bocytopenia? splenic macrophage consump-
tion of platelet-antibody com-
plex.
257. Immune thrombocytopenia is commonly Commonly due to viral illness.

due to ? What do labs reveal? What are Labs: megakaryocytes on bone
the treatments? marrow biopsy.
Treatment: steroids, intra-
venous immunoglobulin.
258. What is the pathogenesis of thrombotic Pathogenesis: ‘ large vWF mul-

thrombocytopenic purpura? timers ’ ‘ platelet adhesion ’ ‘
platelet aggregation and throm-
bosis.
259. What do labs reveal for TTP? What are the Labs: schistocytes, ‘ LDH.
treatments? Treatment: plasmapheresis,
Comment on PC and BT levels in TTP. steroids.
PC: “
BT: ’
260. What are the symptoms of TTP? Symptoms:

1. Pentad of neurologic and re-
nal symptoms
2. fever
3. thrombocytopenia
4. microangiopathic hemolytic
anemia.
261. Inhibition and deficiency of _______ re- Inhibition or deficiency of

sults in “ degradation of VwF multimers. ADAMTS 13 (vWF metallopro-
tease) ’ “ degradation of vWF
multimers.
36 / 60
262. Comment on PC, BT, PT, and PTT levels PC: --

for von Willebrand disease. BT: “
PT: --
PTT: ‘ or --
“ vWF ‘ PTT (vWF acts to car-
ry/protect factor VIII).
263. Von Willebrand disease is autosomal Autosomal dominant. Mild but

_____. Mild but most _______ inherited most common inherited bleed-
bleeding disorder. Diagnosed ing disorder. Diagnosed in most
in most cases by ristocetin cofactor as- cases by ristocetin cofactor as-
say (“ _________is diagnostic). say (“ agglutination is diagnos-
tic).
264. What is the treatment for von Willebrand Treatment: desmopressin,

disease? which releases vWF stored in
endothelium.
265. Comment on PC, BT, PT, and PTT levels PC: “

for DIC BT: ‘
PT: ‘
PTT: ‘
266. What are the causes of DIC? (STOP Making New Thrombi).
Sepsis (gram-negative),
Trauma,
Obstetric complications,
acute Pancreatitis,
Malignancy,
Nephrotic syndrome,
Transfusion
267. What do labs reveal for DIC? Labs: Schistocytes, fibrin split
products (d-dimers), fibrinogen,
factors V and VIII.
268. Widespread activation of clotting and de- DIC

ficiency in clotting factors resulting in
37 / 60
bleeding is the definition of what condi-
tion?
269. Comment on PT, PTT and thrombin time Inherited deficiency.

for antithrombin deficiency. No direct effect on the PT, PTT,
or thrombin time but diminishes
the ‘ in PTT following heparin
administration.
Can also be acquired: renal
failure/nephrotic syndrome an-
tithrombin loss in urine inhibi-
tion of factors IIa and Xa.
270. How can antithrombin deficiency be ac- Renal failure/nephrotic syn-

quired? drome ’ antithrombin loss in
urine ’ “ inhibition of factors IIa
and Xa.
271. Production of mutant factor ___ that is What is Factor V Leiden.

resistant to degradation by activated pro- Production of mutant factor V
tein ___. Most common cause of inherit- that is resistant to degradation
ed hypercoagulability in ___. by activated protein C. Most
common cause of inherited hy-
percoagulability in whites.
272. Protein C or S deficiency “ability to inactivate factors Va

“ ability to inactivate factors ___ and and VIIIa. Risk of thrombotic
___. Risk of thrombotic skin ______ with skin necrosis with hemorrhage
hemorrhage following administration of following administration of war-
______. farin. "Protein C Cancels Coag-
ulation."
273. Describe the mutation in prothrombin Mutation in 32 untranslated re-

gene mutation. Comment on prothrom- gion
bin and plasma levels. ‘ production of prothrombin ’ ‘
plasma levels and venous clots.
274. What is the clinical use of cryoprecipi- Coagulation factor deficiencies

tate? involving fibrinogen and factor
VIII.
38 / 60
275. What is the clinical use of fresh frozen DIC, cirrhosis, immediate war-
plasma? farin reversal
Result: ‘ coagulation factor lev-
els
276. What is the clinical use of platelets? Stop significant bleeding

(thrombocytopenia, qualitative
platelet defects);
Results in: ‘ platelet count ( ‘
<5000/mm3/unit)
277. What is the clinical use of packed RBCs? Acute blood loss, severe ane-
mia
Result: ‘ Hb and ‘ O2 carrying
capacity
278. What does cryoprecipitate contain? Fibrinogen, factor VIII, factor

XIII, vWF, and fibronectin
279. What are the risks of blood transfusions? 1. Infection transmission

2. Transfusion reactions
3. Iron overload
4. Hypocalcemia (citrate is a
Ca2+ chelator),
5. Hyperkalemia (RBCs may
lyse in old blood units).
280. What are lymphomas? Discrete tumor Discrete tumor mass arising
mass arising from ________. from lymph nodes.
281. What are leukemias? Lymphoid or Lymphoid or myeloid neoplasm

______ neoplasm with widespread in- with widespread involvement
volvement of ______. Tumor cells are of bone marrow. Tumor cells
usually found in _________ blood. are usually found in peripheral
blood.
282. What is a leukemoid reaction? How is it Acute inflammatory response to

different from CML? infection.
‘ WBC count with ‘ neutrophils
39 / 60
and band cells (left shift);
‘ leukocyte alkaline phos-
phatase (LAP). Contrast with
CML (also ‘ WBC count with left
shift, but “ LAP).
283. Reed-Sternberg cells characterize which Hodgkin

lymphoma?
284. Which lymphoma is strongly associated Hodgkin

with EBV?
285. Constitutional ("B") signs/symptoms: Hodgkin

low-grade fever, night sweats, weight
loss appear in which lymphoma?
286. Which has better prognosis? Hodgkin or Prognosis is much better than
non-hodgkin? with non-Hodgkin lymphoma.
287. Differentiate hodgkin vs. non-hodgkin Non hodgkin- Multiple, periph-

with regards to nodal involvement. eral, extranodal and noncon-
tiguous spread.
Hodkin - Localized, contigu-
ous, rarely extranodal and sin-
gle group of nodes
288. Which lymphoma is associated with HIV Non-Hodgkin

and autoimmune diseases?
289. Which lymphoma has the following 20-40 Non-Hodgkin

years old for peak incidence?
290. Majority involve B cells (except those of Non-Hodgkin

lymphoblastic T-cell origin). Which lym-
phoma is this?
291. Describe the demographic distribution Bimodal distribution-young

for hodgkin's lymphoma adulthood and
> 55 years; more common in
40 / 60
men except for nodular scleros-
ing type.
292. What are the biomarkers for RS cells and B cell lineage
what is the cell lineage? Biomarkers: CD15, CD30
Not sufficient to fully conclude
diagnosis for Hodgkin's Lym-
phoma
293. What chromosomes are affected in 8 and 14

Burkitt's Lymphoma? t(8;14)—translocation of c-myc
(8) and heavy-chain Ig (14)
294. What types of lesions occur in the en- Jaw lesion in endemic form in
demic vs sporadic form of burkitt's lym- Africa; pelvis
phoma? What does the histopathology or abdomen in sporadic form.
show? Histo: "Starry sky" appearance
A, sheets of lymphocytes with
interspersed macrophages (ar-
rows).
295. What virus is Burkitt's lymphoma associ- EBV

ated with?
296. What is the most common type of Diffuse large B-cell lymphoma
non-hodkin's lymphoma in adults?
297.
41 / 60
What chromosomes are implicated in t(14;18)—translocation of
Follicular lymphoma? heavy-chain Ig (14) and BCL-2
What is its main target population? (18)
Target pop: Adults
298. Re: Follicular lymphoma: Indolent Indolent course; Bcl-2 inhibits

course; Bcl-2 inhibits _____. Presents apoptosis. Presents with pain-
with painless "waxing and waning" less "waxing and waning" lym-
_____________. Nodular, small cells; phadenopathy. Nodular, small
cleaved _______. cells; cleaved nuclei.
299. What chromosomes are affected in Man- t(11;14)—translocation of cyclin

tle cell lymphoma? D1 (11) and heavy-chain Ig
(14);
300. What is the target population of mantle Pop: Older males

cell lymphoma and what is its biomark- Biomarker: CD5+
er?
301. What are all the Non Hodgkin's lym- 1. Burkitt's lymphoma
phomas? 2. Diffuse large B-cell lym-
phoma
3. Follicular lymphoma
4. Mantle cell lymphoma
5. Adult T-cell Lymphoma
6. Mycosis fungoides/ Sezary
syndrome
302. What causes adult T cell lymphoma? HTLV

What are the signs and what are the tar- Target populations: Populations
get populations? in Japan, West Africa, and the
Caribbean.
Symptoms: Lytic bone lesions,
hypercalcemia.
303. Mycosis fungoides presents with skin Mycosis fungoides presents

patches and plaques (cutaneous T-cell with skin patches C / plaques
lymphoma), characterized by atypical (cutaneous T-cell lymphoma),
CD4+ cells with ____________ nuclei. characterized by atypical CD4+
cells with "cerebriform" nuclei.
42 / 60
304. What are the red flag symptoms for mul- CRAB:
tiple myeloma? HyperCalcemia
Renal involvement
Anemia
Bone lytic lesions/Back pain
305. What other findings are associated with 1. Susceptibility to infection

multiple myeloma (not CRAB)? 2. Primary amyloidosis (AL)
3. M spike on serum protein
electrophoresis
4. Ig light chains in urine (Bence
Jones
protein)
Rouleaux formation B (RBCs
stacked like
poker chips in blood smear)
306. What syndrome also has an M spike but Waldenstrom macroglobuline-

is not multiple myeloma. mia ’ M spike = IgM ’ hypervis-
cosity syndrome (e.g., blurred
vision, Raynaud phenomenon);
no "CRAB" findings.
307. What antibodies do monoclonal plasma Large amounts of IgG (55%) or

cells produce in Multiple myeloma? IgA (25%). Most common 1° tu-
mor arising within bone in peo-
ple > 40-50 years old.
308. What is Monoclonal gammopathy of un- Monoclonal expansion of plas-

determined significance (MGUS)? ma cells, asymptomatic, may
lead to multiple myeloma. No
"CRAB" findings. Patients with
43 / 60
MGUS develop multiple myelo-
ma at a rate of 1-2% per year.
309. What are myelodysplastic syndromes? Stem-cell disorders involving in-

What is there a isk of transformation to? effective hematopoiesis defects
in cell maturation of all non-
lymphoid lineages. Caused by
de novo mutations or environ-
mental exposure (e.g., radia-
tion, benzene, chemotherapy).
Risk of transformation to AML.
310. Neutrophils with bilobed nuclei are typ- Pseudo-Pelger-Huet anomaly

ically seen after chemotherapy. What is
this called?
311. Why do infections, haemorrhage, and Infections ’ “ WBC

anemia occur in leukemia? Haemorrhage ’ “ platelets
Anemia ’ “ RBCs
Uncontrolled differentiation and
production of WBCs cause BM
to fail, thus affecting other cell
lines.
312. List all lymphoid lineage leukemias. 1. Acute lymphoblastic

leukemia/lymphoma (ALL)
2. Small lymphocytic lymphoma
(SLL) / Chronic lymphocytic
leukemia (CLL)
4. Hairy cell leukemia
313. What is the difference between SLL and SLL same as CLL except CLL
CLL? has peripheral blood lymphocy-
tosis or bone marrow involve-
ment.
314. What is the most common adult SLL/ CLL

leukemia, what are its biomarkers and Age: > 60 years.
what is seen on the blood smear? Biomarkers: CD20+, CD5+
B-cell neoplasm. Often asymp-
44 / 60
tomatic, progresses slowly;
Blood smear: smudge cells B in
peripheral blood ; autoimmune
hemolytic anemia.
315. ALL is associated with which syndrome T-cell ALL can present as me-
and appears to be like which syndrome diastinal mass (presenting as
(disguised) SVC-like syndrome). Associat-
ed with Down syndrome.
316. What are the biomarkers of ALL? What's TdT+ (marker of pre-T and
revealed in the blood smear of ALL? pre-B cells), CD10+ (pre-B cells
only). Peripheral blood and
bone marrow have ‘ ‘ ‘ lym-
phoblasts
317. What chromosomal abnormalities have a May spread to CNS and testes.
better prognosis for ALL and what are the t(12;21) = better prognosis.
2 main sites of metastases?
318. Which leukemia is associated with cells Hairy Cell leukemia - Mature B
that have lamentous, hair like pro- cell tumor in the elderly
jections, marrow fibrosis and a posi-
tive TRAP (tartrate-resistant acid phos-
phatase ) result?
319. What is the treatment for hairy cell Cladribine and Pentostatin.
leukemia?
320. Auer rods; peroxidase • cytoplasmic in- AML !

clusions; ‘ ‘ ‘ circulating myeloblasts on
peripheral smear ; median age of onset
> 65
321. What type of cells overproliferate in Peak incidence 45-85 years,

CML? What's the peak age of incidence? median age at diagnosis 64
years. Myeloid stem cell prolifer-
ation
45 / 60
‘ neutrophils, metamyelocytes,
basophils
322. What is the small-molecule inhibitor of 1. Very low LAP as a result of

the bcr-abl tyrosine kinase used for CML, low activity in mature granulo-
and what are the LAP levels? cytes (vs. leukemoid reaction, in
which LAP is ).
2. Responds to imatinib (a
small-molecule inhibitor of the
bcr-abl tyrosine kinase).
323. What is Langerhans cell histiocytosis? Collective group of proliferative

disorders of dendritic (Langer-
hans) cells. Presents in a child
as lytic bone lesions A and skin
rash or as recurrent otitis media
with a mass involving the mas-
toid bone. Cells are functionally
immature and do not effective-
ly stimulate primary T cells via
antigen presentation.
Cells express S-100 (mesoder-
mal origin) and CD1a. Birbeck
granules ("tennis rackets" or rod
shaped on EM) are characteris-
tic
324. What are the symptoms of Langerhans Presents in a child as lytic bone
cell histiocytosis?. lesions and skin rash or as re-
current otitis media with a mass
involving the mastoid bone.
325. What's wrong with the Dendritic cells in Cells are functionally immature
Langerhans cell histiocytosis? What are and do not effectively stimulate
the biomarkers? primary T cells via antigen pre-
sentation.
Biomarkers: S-100 (mesoder-
mal origin) and CD1a. Birbeck
granules ("tennis rackets" or rod
46 / 60
shaped on EM) are characteris-
tic.
326. What mutation is most often found JAK2 is involved in hematopoi-

in myeloproliferative disorders except etic growth factor signaling.
CML? JAK2 gene mutation is often
found in chronic myeloprolif-
erative disorders except CML
(which has BCR-ABL transloca-
tion).
327. What are all the chronic myeloprolifera- 1. Polycythemia vera

tive disorders? 2. Essential thrombocytosis
3. Myelofibrosis
328. Disorder of ‘ hematocrit, often associ- Polycythemia Vera

ated with JAK2 mutation. May present
as intense itching after hot shower (due
to basophils). Rare but classic symptom
is erythromelalgia (severe, burning pain
and red-blue coloration) due to episodic
blood clots in vessels of the extremities.
What disease is it?
329. Similar to polycythemia vera, but specific Essential thrombocytosis

for overproduction of abnormal platelets ’
bleeding, thrombosis. Bone marrow con-
tains enlarged megakaryocytes.
330. An artificial or natural ‘ in EPO levels 2° polycythemia

could result in what disease?
47 / 60
331. Obliteration of bone marrow due to ‘ fi- What is myelofibrosis.

broblast activity in response to prolifera-
tion of monoclonal cell lines. "Teardrop"
RBCs and immature forms of the myeloid
line. "Bone marrow is crying because it's
brosed and is a dry tap." Often associat-
ed with massive splenomegaly.
332. Associated with "Teardrop" RBCs and What is myelofibrosis.

immature forms of the myeloid line.
"Bone marrow is crying because it's fi-
brosed and is a dry tap." Often associat-
ed with massive splenomegaly.
333. Comment on RBCs, WBCs, and platelets RBCs - ‘

for polycythemia vera. WBCs - ‘
platelets: ‘
334. Comment on RBCs, WBCs, and platelets RBCs: -

for Essential thrombocytosis WBCs: -
platelets: ‘
335. Comment on RBCs, WBCs, and platelets RBCs - “

for Myelofibrosis WBCs - Variable
platelets - Variable
336. Comment on RBCs, WBCs, and platelets RBCs - “

for CML? WBCs - ‘
platelets - ‘
337. What does heparin activate? What (2) Activator of antithrombin; “

things does this decrease? Short or long thrombin and “ factor Xa. Short
half life? half-life.
338. What is the clinical use for heparin? Immediate anticoagulation for
pulmonary embolism (PE),
acute coronary syndrome, MI,
deep venous thrombosis (DVT).
48 / 60
Used during pregnancy (does
not cross placenta). Follow PTT.
339. What are the toxicities for heparin? 1. Bleeding

2. Thrombocytopenia (HIT),
3. Osteoporosis
4. drug-drug interactions.
For rapid reversal (antidote),
use protamine sulfate (positive-
ly charged molecule that binds
negatively charged heparin).
340. What is Heparin-induced thrombocy- Development of IgG antibodies

topenia (HIT) ? against heparin- bound platelet
factor 4 (PF4). Antibody-he-
parin-PF4 complex activates
platelets thrombosis and throm-
bocytopenia.
341. Why are low molecular weight heparins Low-molecular-weight heparins

"better"? (e.g., enoxaparin, dalteparin)
and fondaparinux act *more
on factor Xa*, have *better
bioavailability*, and *2-4 times
longer half-life*; can be admin-
istered *subcutaneously* and
without laboratory monitoring.
Not easily reversible.
342. Bivalirudin is related to hirudin, the Bivalirudin is related to hirudin,

________ used by leeches; inhibit the anticoagulant used by
________ directly. Alternatives to heparin leeches; inhibit thrombin direct-
for anticoagulating patients with HIT. ly. Alternatives to heparin for an-
ticoagulating patients with HIT.
343. What does warfarin interfere with? ³-carboxylation of vitamin K- de-

pendent clotting factors II, VII,
IX, and X, and proteins C and
S.
49 / 60
344. What is seen in the laboratory assay for In laboratory assay, has effect
warfarin? on Extrinsic pathway and ‘ PT.
Long half-life.
345. What is warfarin used for clinically? Chronic anticoagulation (e.g.,

venous thromboembolism pro-
phylaxis, and prevention of
stroke in atrial fibrillation). Fol-
low PT/INR.
346. Does warfarin cross the placenta? Yes. Therefore not used in preg-
nant women (because warfarin,
unlike heparin, crosses placen-
ta).
347. Proteins C and S have ________ Proteins C and S have shorter

half-lives than clotting factors half-lives than clotting factors
II, VI, IX, and X, resulting in early transient II, VI, IX, and X, resulting in
hypercoagulability with warfarin use. early transient hypercoagulabil-
ity with warfarin use.
348. What is the antidote for warfarin? For reversal of warfarin, give vi-
tamin K.
For rapid reversal, give fresh
frozen plasma.
349. What is heparin bridging? Heparin "bridging": heparin fre-

quently used
when starting warfarin. He-
parin's activation of antithrom-
bin enables anticoagulation
during initial, transient hyperco-
agulable state caused by war-
farin. Initial heparin therapy re-
duces risk of recurrent venous
thromboembolism and skin/tis-
sue necrosis.
350. True or false, Heparin and Warfarin's site True for Heparin. False for War-
of action is in the blood. farin. Warfarin acts on the liver.
50 / 60
351. True or false, Warfarin's onset of action is False. Heparin is rapid (hours)
faster than that of heparin. while warfarin is slow (days)
352. What is the route of administration for Heparin: Parenteral

warfarin vs heparin? Warfarin: Oral
353. Compare the molecular structure of war- Warfarin: Small, amphipathic

farin and heparin. molecule
Heparin: Large, anionic, acidic
polymer
354. What diseases are Direct factor Xa in- DVT and PE (rivaroxaban);
hibitors used for (prophylaxis and treat- Stroke prophylaxis in patients
ment) (Apixaban, rivaroxaban) ? with atrial fibrillation.
Oral agents do not usually re-
quire coagulation monitoring.
355. How is heparin and warfarin monitored Heparin : PTT (intrinsic path-
(what measure)? way)
Warfarin : PT/INR (extrinsic
pathway)
356. What is a toxicity for direct factor Xa in- Bleeding

hibitors?
357. List all the thrombolytics 1. Alteplase (tPA)

2. Reteplase (rPA)
3. Streptokinase
4. Tenecteplase (TNK-tPA).
358. What are the clinical uses for thrombolyt- 1. Early MI

ics? 2. Early ischemic stroke
3. Direct thrombolysis of severe
PE.
359. What is the MoA for thrombolytics? Com- Directly or indirectly aids con-
ment on PT, PTT and platelet levels. version of plasminogen to plas-
min, which cleaves thrombin
and fibrin
51 / 60
clots.
‘PT, ‘ PTT, no change in platelet
count.
360. What are the contraindications for throm- 1. Active bleeding

bolytics? What can be used to treat the 2. history of intracranial bleed-
toxicity? ing
3. Recent surgery
4. Known bleeding diatheses, or
severe hypertension.
Treat toxicity: aminocaproic
acid, an inhibitor of fibrinolysis.
Fresh frozen plasma and cryo-
precipitate can also be used to
correct factor deficiencies.
361. Aspirin irreversibly inhibits Irreversibly inhibits cyclooxyge-

________________ (both COX-1 and nase (both COX-1 and COX-2)
COX-2) enzyme by covalent enzyme by covalent acetyla-
___________. Platelets cannot synthe- tion. Platelets cannot synthe-
size new enzyme, so effect lasts until size new enzyme, so effect
new platelets are produced: ___ bleeding lasts until new platelets are pro-
time, __ TXA2 and prostaglandins. No ef- duced: ‘ bleeding time, “ TXA2
fect on ___ or PTT. and prostaglandins. No effect
on PT or PTT.
362. What are the clinical uses of aspirin? 1. Antipyretic

2. Analgesic
3. Anti-inflammatory
4. Antiplatelet (“ aggregation).
363. What are the toxicities of aspirin? 1. Gastric ulceration

Overdose initially causes hyperven- 2. Tinnitus (CN VIII)
tilation and respiratory _________, 3. Chronic use can lead to acute
but transitions to mixed metabolic renal failure, interstitial nephri-
_________-respiratory alkalosis. tis, and upper GI bleeding.
4. Reye syndrome in children
with viral infection.
5. Overdose initially causes
hyperventilation and respirato-
52 / 60
ry alkalosis, but transitions to
mixed metabolic acidosis-respi-
ratory alkalosis.
364. List all ADP receptor inhibitors 1. Clopidogrel

2. Prasugrel
3. Ticagrelor (reversible),
4. Ticlopidine.
365. ADP receptor inhibitors inhibit ______ ADP receptor inhibitors inhib-
aggregation by irreversibly blocking it platelet aggregation by irre-
____ receptors. Prevent expression of versibly blocking ADP recep-
glycoproteins ____ on platelet surface. tors. Prevent expression of gly-
coproteins IIb/IIIa on platelet
surface.
366. What are the clinical uses of ADP Recep- 1. Acute coronary syndrome
tor inhibitors ? 2. Coronary stenting
3. “ incidence or recurrence of
thrombotic stroke.
367. What are the toxicities associated with 1. Neutropenia (ticlopidine).

ADP receptor inhibitors? 2. TTP may be seen.
368. Cilostazol, dipyridamole are Phosphodiesterase III inhibitor;

_________________ inhibitors; They __ ‘ cAMP in platelets, resulting in
cAMP in platelets, resulting in ________ inhibition of platelet aggrega-
of platelet aggregation. Are they vation; vasodilators.
sodilators or vasoconstrictors?
369. What are the clinical uses of cilostazol 1. Intermittent claudication

and dipyridamole? 2. Coronary vasodilation
3. Prevention of stroke or TIAs
(combined with aspirin), angina
prophylaxis.
370. What are the toxicities of cilostazol and 1. Nausea

dipyridamole? 2. Headache
3. Facial flushing
53 / 60
4. Hypotension
5. Abdominal pain.
371. What are GP IIb/IIIa inhibitors? 1. Abciximab

2. Eptifibatide
3. Tirofiban
372. GP IIb/IIIa inhibitors bind to the gly- Bind to the glycoprotein recep-
coprotein receptor IIb/IIIa on activated tor IIb/IIIa on activated platelets,
________, preventing aggregation. preventing aggregation.
373. What are the clinical uses of GP IIb/IIIa 1. Unstable angina

inhibitors? 2. Percutaneous transluminal
coronary angioplasty
374. What are the toxicities of GP IIb/IIIa in- Bleeding, thrombocytopenia.

hibitors?
375. List some antimetabolites used against 1. Azathioprine

cancer. 2. Cladribine
What cell cycle phase do they all target? 3. Cytarabine
4. 5-fluorouracil
5. Hydroxyurea
6. Methotrexate
7. 6-mercaptopurine
8. 6-thioguanine
S-Phase
376. Vinca alkaloids and microtubule in- Vinca alkaloids (Vinblastine,

hibitors are similar in what way? Vincristine): Inhibit microtubule
formation
Microtubule inhibitors (Paclitax-
el): inhibits microtubule disas-
sembly
377. Which antimetabolite “ thymidine synthe-MTX, 5-FU

sis?
378. 6 MP
54 / 60
Which antimetabolite “ de novo purine
synthesis?
379. Hydroxyurea inhibits ___________ re- Hydroxyurea:

ductase inhibits ribonucleotide reduc-
tase
380. Etoposide inhibits ? Etoposide inhibits topoiso-

merase II
381. Irinotecan inhibits ? Irinotecan:

inhibits topoisomerase I
382. Dactinomycin, doxorubicin are DNA Dactinomycin, doxorubicin are

________________ DNA intercalators
383. Cisplatin is an alkylating agent. It Cisplatin is an alkylating agent.

__________ DNA It cross-links DNA
384. Azathioprine, 6-MP, 6-TG are all _____ Azathioprine, 6-MP, 6-TG are all
analogs, “______synthesis and are acti- purine analogs, “ purine synthe-
vated by ________. sis and are activated by HG-
PRT.
385. What are the clinical uses of Azathio- 1. Preventing organ rejection
prine, 6-MP, 6-TG? 2. Rheumatoid arthritis
3. IBD
4. SLE
5. used to wean patients off
steroids in chronic disease and
to treat steroid-refractory chron-
ic disease.
386. What are the toxicites associated with Myelosuppression, nephrotoxi-

Cladribine (2-CDA)? city, and neurotoxicity.
387. What is the clinical use for Cladribine? Hairy cell leukemia.
388. Cladribine is a purine analog

multiple mechanisms (e.g., inhi-
55 / 60
Cladribine is a _______ analog multi- bition of DNA polymerase, DNA
ple mechanisms (e.g., inhibition of DNA strand breaks).
__________, DNA strand breaks).
389. What are the toxicities associated with 1. Leukopenia

cytarabine? 2. Thrombocytopenia
3. Megaloblastic anemia
4. CYTarabine causes panCY-
Topenia.
390. What is the clinical use for Cytarabine? Leukemias (AML), lymphomas.
391. Cytarabine is a ________ analog that in- Cytarabine is a Pyrimidine ana-

hibits DNA polymerase. log that inhibits DNA poly-
merase.
392. What is the clinical use for 5-FU? 1. Colon cancer

2. Pancreatic cancer,
3. Basal cell carcinoma (topi-
cal).
393. 5-FU is a pyrimidine analog bioactivat- 5-FU is a pyrimidine analog

ed to 5F-dUMP, which covalently com- bioactivated to 5F-dUMP, which
plexes folic acid. This complex inhibits covalently complexes folic acid.
__________ synthase ’ “ dTMP ’ “ DNA syn-This complex inhibits thymidy-
thesis. late synthase ’ “ dTMP ’ “ DNA
synthesis.
394. What is the clinical use of MTX? 1. Leukemias (ALL)

2. Lymphomas,
3. Choriocarcinoma,
4. Sarcomas.
Non-neoplastic:
1. Ectopic pregnancy
2. Medical abortion (with miso-
prostol)
3. Rheumatoid arthritis
4. Psoriasis
5. IBD
6. Vasculitis.
56 / 60
395. Folic acid analog that competitively in- What is methotrexate!

hibits dihydrofolate reductase ’ “ dTMP ’ “
DNA synthesis.
396. Methotraxate is a folic acid analog that Folic acid analog that compet-
competitively inhibits __________. itively inhibits dihydrofolate re-
ductase.
397. What are the toxicities of methotrexate? 1. Myelosuppression,

2. Hepatotoxicity.
3. Mucositis (e.g., mouth ul-
cers).
4. Pulmonary fibrosis.
398. Clinical use of Bleomycin 1. Testicular cancer

2. Hodgkin lymphoma.
399. Clinical use of Dactinomycin (*act*ino- 1. Wilms tumor

mycin D) 2. Ewing sarcoma
3. rhabdomyosarcoma.
Used for childhood tumors
("children *act* out").
400. Clinical use of Doxorubicin, daunoru- Solid tumors, leukemias, lym-

bicin phomas.
401. Clinical use of the alkylating agent busul- CML. Also used to ablate
fan? patient's bone marrow before
bone marrow transplantation.
402. Clinical use of the alkylating agent Cy- 1. Solid tumors

clophosphamide, ifosfamide? 2. leukemia
3. lymphomas.
403. Clinical use of the alkylating agent Ni- 1. Brain tumors (including
trosoureas (carmustine, lomustine, se- glioblastoma multiforme).
mustine, streptozocin)?
404. Clinical use of taxols or paclitaxel?

57 / 60
1. Ovarian
2. Breast carcinomas.
405. Clinical use of vincistrine and vinblas- 1. Solid tumors

tine? 2. leukemias
3. Hodgkin (vinblastine)
4. Non-Hodgkin (vincristine)
lymphomas.
406. Clinical use of cisplatin and carboplatin? 1. Testicular

2. Bladder
3. Ovary,
4. Lung carcinomas.
407. Clinical use of etoposide and tenipo- 1. Solid tumors (particularly tes-
side? ticular and small cell lung can-
cer),
2. leukemias
3. lymphomas.
408. Clinical use of ironotecan and topote- 1. Colon cancer (irinotecan);

can? 2. Ovarian
3. Small cell lung cancers
(topotecan).
409. Clinical use of hydroxurea? 1. Melanoma

2. CML
3. Sickle cell disease ( HbF).
410. Clinical use of Prednisone, prednisolone Most commonly used glucocor-

ticoids in cancer chemotherapy.
Used in:
1. CLL
2. non-Hodgkin lymphoma
3. immunosuppressants (e.g.,
in autoimmune diseases).
411. Clinical use of Bevacizumab (Monoclon- Solid tumors (colorectal cancer,

al antibody against VEGF. Inhibits angio- renal cell carcinoma).
genesis.)
58 / 60
412. Clinical use of Erlotinib (EGFR tyrosine Non-small cell lung carcinoma.
kinase inhibitor.)
413. Clinical use of Imatinib (Tyrosine kinase CML, GI stromal tumors.

inhibitor of BCR-ABL)
414. Clinical use of Rituximab (Monoclonal Non-Hodgkin lymphoma, CLL,

antibody against CD20) IBD, rheumatoid arthritis.
415. Clinical use of Tamoxifen, raloxifene. Breast cancer treatment (ta-

(Block the binding of estrogen to ER • moxifen only) and prevention.
cells.) Raloxifene also useful to pre-
vent osteoporosis.
416. List the toxicities of: Cisplatin/Carboplatin : acoustic

Cisplatin/Carboplatin nerve damage and nephrotoxi-
Vincristine peripheral city
Bleomycin, Busulfan Vincristine: peripheral neuropa-
Doxorubicin thy
Trastuzumab Bleomycin, Busulfan: pul-
Cisplatin/Carboplatin monary fibrosis
CYclophosphamide Doxorubicin: cardiotoxicity
5-FU Trastuzumab: cardiotoxicity
6-MP Cisplatin/Carboplatin: nephro-
Methotrexate toxic (and acoustic nerve dam-
age)
CYclophosphamide: hemor-
rhagic CYstitis
5-FU: myelosuppression
6-MP: myelosuppression
Methotrexate: myelosuppres-
sion
417. Clinical use of Trastuzamab (Monoclon- HER-2 • breast cancer and gas-
al antibody against HER-2, a tyrosine ki- tric cancer (tras2zumab).
nase receptor)
418. Metastatic melanoma.
59 / 60
Clinical use of Vermurafenib (Small mole-
cule inhibitor of BRAF oncogene • ______
)
60 / 60

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Hematology &amp; Oncology. Anatomy 56

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First Aid USMLE Step 1: Hematology & Oncology.

1. Erythrocytes carry O2 to ____ and CO2 to *Tissues, Lungs*

2. True or false, erythrocytes are biconcave True

3. What is the lifespan of an erythrocyte and Glucose (90% used in glycoly-

Lifespan - 120 days

5. What is a reticulocyte? Immature RBC; reflects ery-

6. What is Erythrocytosis, anisocytosis and Erythrocytosis = polycythemia

7. The small cytoplasmic fragment of a Megakaryocytic, 8-10 days

8. What causes petechiae? Thrombocytopenia or “platelet

10. Approx. 1/3rd of platelets are stored In the spleen

11. What is the fibrinogen receptor? GpIIb/IIIa

12. What is the vWF receptor? GpIb

13. What are my three granulocytes? Neutrophil, eosinophil, basophil

14. List the WBC differential for ranges Neutrophils (54-62%)

15. What do the specific granules in neu- Specific granules contain

16. What do the azurophilic granules in neu- Azurophilic granules (lyso-

17. In what deficiency do we see hyperseg- Vitamin B12/ folate deficiency.

18. what is a left shift ? An increase in neutrophil pre-

eflect states of increased

19. What are some neutrophil chemotactic C5a,

20. What is a plasma cell cancer? Multiple myeloma

21. For T cells, CD8 recognizes MHC _ while I, II,

23. What is a monocyte found in blood and differentiates

25. What cytokine can activate ³-interferon

26. What are the causes of eosinophilia? Parasites

27. What are the products of eosinophil? Produces histaminase,

highly phagocytic fro ag-ab

28. Basophilia is a sign of what? Myeloproliferative disease, par-

dense basophilic granules +

what is degranulation triggered by ? Activated by tissue trauma, c3a

causing degranulation, which

31. What is mastocytosis? rare; proliferation of mast cells

32. What is mastocytosis associated with ? Associated with

33. What is used for asthma prophylaxis ? Cromolyn sodium

36. EMBRYOLOGY EMBRYOLOGY

37. Where Fetal erythropoiesis occurs in Yolk sac: 3-8wks

38. What type of antibodies are found in A IgM anti B

39. What type of antibodies are found in B IgM anti A

40. What type of antibodies are found in AB None - universal donor of

41. What type of antibodies are found in O Anti A and B, predominantly

-- Universal donor of RBCs, not

42. What type of antibodies are found in Rhz No anti-D

43. What type of antibodies are found in Rh{ IgG anti D

45. What is Rh hemolytic disease ? Rh mothers exposed to fetal

46. whats the presentation? Hydrops fetalis, Jaundice short-

47. During which trimester is RhoGAM ad- Prevented by administration of

Rh mothers have anti-D IgG

49. What are the 3 effects of bradykinin in the 1. ‘ Vasodilation

50. What enzyme activates bradykinin? Kallikrein

51. What is HMWK? High molecular weight kinino-

53. During gel electrophoresis, hbg Migrates from negatively

54. who migrates fathest? - HbA: migrates the farthest

makes HbC and HbS more +

A FAT SANTA ClAUS

55. his tests whether the patient's RBCS are DIrect

56. This takes pt serum and adds donor Indirect

58. What are my 4 thrombolytics which acti- THROMBOLYTICS:

59. Plasminogen is converted to plasmin via tPA

60. Prothrombin and thrombin are also Factor II and IIa

61. Hemophilia A is a deficiency of? Deficiency of factor VIII (XR)

62. Hemophilia B is a deficiency of? Deficiency of factor IX (XR)

63. Hemophilia C is a deficiency of? Deficiency of factor XI (AR)

67. Describe the 4 pathways mediated by Ca 1. VII to VIIa,

Hematology & Oncology. Anatomy 56

Hematology & Oncology. Anatomy 56

1. Erythrocytes carry O2 to ____ and CO2 to Tissues, Lungs