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480 Cards in this Set

  • Front
  • Back
Child has been anemic since
birth. Splenectomy would result in ↑ hematocrit in what disease?
Spherocytosis.
What is the danger of giving folate alone?
Masks signs of neural damage
with vitamin B12 deficiency.
Patient presents with anemia,
hypercalcemia, and bone pain
on palpation; bone marrow
biopsy shows a slide packed
with cells that have a large,
round, off-center nucleus.
Multiple myeloma (plasma cell
neoplasm); Bence Jones protein
(Ig light chains).
What neoplasms are associated with AIDS?
B-cell lymphoma, Kaposi’s sarcoma.
Patient with a new cancer
diagnosis and known history
of CHF is being evaluated
for chemotherapy. What chemotherapeutic agent should be avoided in this patient?
Doxorubicin (cardiotoxic).
Chromosome analysis reveals
the presence of the Philadelphia chromosome, t(9;22). What is the latest targeted therapy for this disease, and how does it work?
Imatinib (Gleevec) is used to
treat CML; inhibitor of bcr-abl
tyrosine kinase.
WBC differential from highest
to lowest:
Neutrophils Like Making
Everything Better.

Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
Erythrocytosis =
polycythemia =
↑ number of red cells.
polycythemia =
Erythrocytosis = ↑ number of red cells.
Anisocytosis =
varying sizes.
RBC varying sizes =
Anisocytosis
Poikilocytosis =
varying shapes.
RBC varying shapes =
Poikilocytosis
Reticulocyte =
immature erythrocyte.
immature erythrocyte=
Reticulocyte
Normal Erythrocyte shape and why
Anucleate, biconcave →large surface area: volume
ratio →easy gas exchange (O and CO ).
Erythrocyte energy source
glucose (90% anaerobically degraded to lactate, 10% by HMP shunt).
Erythrocyte life span
120 Days
Erythrocyte days. Membrane contains what and why is it important
the chloride-bicarbonate
antiport important in the “physiologic chloride shift,”
which allows the RBC to transport CO2 from the
periphery to the lungs for elimination.
Leukocyte types
Types: granulocytes, basophils, eosinophils, neutrophils)
and mononuclear cells (lymphocytes,
monocytes).
Leukocyte normal #'s
Normally 4000–10,000 per microliter.
Basophil #'s and where found
< 1% of all leukocytes

Found in the blood.
Basophil nuclues shape
Bilobate nucleus.
Basophil granule contnets
Densely basophilic granules
containing heparin (anticoagulant), histamine
(vasodilator) and other vasoactive amines, and
leukotrienes (LTD-4).
what cell Mediates allergic reaction
Mast cell

and

Basophil
Mast cell where found
Found in tissue.
Mast cell what cells are they like
resemble basophils structurally and functionally
but are not the same cell type.
Mast cell granule contents
histamine, heparin, and eosinophil chemotactic
factors.
Mast cell wrt Ig binding
Can bind IgE to membrane.
Mast cell which type of hypersensitivity reactions
type I
Cromolyn sodium prevents
mast cell degranulation
??????? prevents mast cell degranulation (used to treat asthma).
Cromolyn sodium
Cromolyn sodium is used to treat?
asthma).
Bilobate nucleus. Packed with large eosinophilic granules of uniform size.
Eosinophil
Eosinophil %'s
1–6% of all leukocytes.
Eosinophil structure
Bilobate nucleus. Packed with large eosinophilic granules of uniform size.
Defends against helminthic and protozoan infections (major basic protein).
Eosinophil
Eosinophil major function and mech
Defends against helminthic and protozoan infections (major basic protein). Highly phagocytic for antigen-antibody complexes.
Eosinophil produces what
major basic protein
histaminase
arylsulfatase.
Causes of eosinophilia
NAACP:
Neoplastic
Asthma
Allergic processes
Collagen vascular
diseases
Parasites
Neutrophil
what type of response cell
Acute inflammatory response cell
Neutrophil %'s
40–75% WBCs.
Hypersegmented polys are seen in
vitamin B12/folate deficiency.
Neutrophil granules and contents
Large, spherical, azurophilic 1° granules (called lysosomes) contain hydrolytic enzymes, lysozyme, myeloperoxidase,
and lactoferrin.
Monocyte %'s
2-10% of leukocytes
Monocyte structure and what they do
Large. Kidney-shaped nucleus.
Extensive “frosted glass” cytoplasm. Differentiates
into macrophages in tissues.
Differentiates into macrophages in tissues
Monocyte
Macrophage function
Phagocytoses bacteria, cell debris, and senescent red
cells and scavenges damaged cells and tissues. Macrophages Can function as APC via MHC II.
Macrophage life span
long life in tissues
Macrophage activation
Activated by gamma-interferon.
Lymphocyte appearance
Round, densely staining nucleus. Small amount of pale cytoplasm.
in general what is the role of lymphocytes
B lymphocytes produce antibodies.
T lymphocytes manifest the cellular immune response as well as regulate B lymphocytes and macrophages.
B lymphocyte cell markers
CD19
CD20
B lymphocyte is involved in which immune response
Humoral
B lymphocytes arise from what and mature where
Arises from stem cells in bone marrow.

Matures in marrow.
B lymphocyte initial migration
Migrates to peripheral lymphoid tissue (follicles of lymph nodes, white pulp of spleen, unencapsulated lymphoid tissue).
B lymphocytes when antigen is encountered
differentiate into plasma
cells and produce antibodies and Can function as (APC) via MHC II.
Off-center nucleus, clock-face chromatin
Plasma cell
Plasma cell structure
Off-center nucleus, clock-face chromatin.

abundant RER and ell-developed
Golgi apparatus.
Plasma cell function
produce large amounts of antibody
specific to a particular antigen.
Multiple myeloma is a ?????? neoplasm.
plasma cell
T lymphocyte is involed in what type of immune response
Mediates cellular immune response
T lymphocyte origins and maturation
Originates from stem cells in the bone marrow,
but matures in the thymus.
T lymphocyte differentiation and cell markers
T cells differentiate into cytotoxic T cells
(MHC I, CD8, CD3),
helper T cells (MHC II, CD4, CD3),
and suppressor T cells.
T lymphocyte CD mnemonic
MHC × CD = 8
(e.g., MHC 2 ×CD4 = 8,

and MHC 1 × CD8 = 8).
Professional APCs. Express MHC II and Fc receptor (FcR) on surface
Dendritic cells
Called Langerhans cells on skin.
Dendritic cells
Dendritic cells on the skin aka
Langerhans cells
Dendritic cells function
Professional APCs. Express MHC II and Fc receptor (FcR) on surface

Main inducers of 1° antibody response.
Which WBC

Mediates allergic reaction. < 1% of all leukocytes. Found in the blood.
Basophil
Which WBC
granules containing heparin (anticoagulant), histamine
(vasodilator) and other asoactive amines, and
leukotrienes (LTD-4).
Basophil
Which WBC

histamine, heparin, and eosinophil chemotactic
Mast cell
Which WBC

resemble basophils structurally and functionally
but are not the same cell type. Found in tissue.
Mast cell
Which WBC

Highly phagocytic for antigen-antibody complexes.
Eosinophil
Which WBC

azurophilic 1° granules (called lysosomes) contain
hydrolytic enzymes, lysozyme, myeloperoxidase,
and lactoferrin.
Neutrophil
Which WBC

Kidney-shaped nucleus. Extensive “frosted glass” cytoplasm.
Monocyte
Which WBC

Round, densely staining nucleus. Small amount of pale cytoplasm
Lymphocyte
Which WBC

Professional APCs. Express MHC II and Fc receptor (FcR) on surface.
Dendritic cells
Which WBC

Called Langerhans cells on skin.
Dendritic cells
Protein C and protein S
function and dependance
inactivate Va and VIIIa;
vitamin K–dependent.
inactivate Va and VIIIa;
vitamin K–dependent.
Protein C and protein S
Antithrombin III
function and activation
inactivates thrombin, IXa, Xa,
and XIa;

activated by heparin.
inactivates thrombin, IXa, Xa,
and XIa;

activated by heparin.
Antithrombin III
Factor V Leiden mutation mech
resistance to activated protein C.
genetic resistance to activated protein C.
Factor V Leiden
tPA mech
generates plasmin, which cleaves fibrin.
generates plasmin, which cleaves fibrin.
tPA
Ag's and Ab's for different Blood Types

A
A antigen on RBC surface

B antibody in plasma.
Ag's and Ab's for different Blood Types

B
B antigen on RBC surface

A antibody in plasma.
Ag's and Ab's for different Blood Types

AB
A and B antigens on RBC surface,

No Ab's

"universal recipient."
Ag's and Ab's for different Blood Types

O
Neither A nor B antigen on RBC surface;
both antibodies in plasma; "universal donor.”
Incompatible blood transfusions
can cause
immunologic response, hemolysis, renal failure, shock, and death.
RBC forms when do you see

Biconcave
Normal.
RBC forms when do you see

Spherocytes
Hereditary spherocytosis, autoimmune hemolysis.
RBC forms when do you see

Elliptocyte
Hereditary elliptocytosis.
RBC forms when do you see

Macro-ovalocye
Megaloblastic anemia,
marrow failure.
RBC forms when do you see

Helmet cell, schistocyte
DIC, traumatic hemolysis.
RBC forms when do you see

Sickle cell
Sickle cell anemia.
RBC forms when do you see

Teardrop cell
Myeloid metaplasia with myelofibrosis.
RBC forms when do you see

Acanthocyte
Spiny appearance in abetalipoproteinemia.
RBC forms when do you see

Target cell
HALT.

HbC disease,
Asplenia,
Liver disease,
Thalassemia.
RBC forms when do you see

Poikilocytes
Nonuniform shapes in TTP/HUS, microvascular damage, DIC.
RBC forms when do you see

Burr cell
TTP/HUS.
What RBC forms do you see in

Normal.
Biconcave
What RBC forms do you see in

Hereditary spherocytosis
Spherocytes
What RBC forms do you see in

autoimmune hemolysis.
Spherocytes
What RBC forms do you see in

Hereditary elliptocytosis.
Elliptocyte
What RBC forms do you see in

Megaloblastic anemia
Macro-ovalocyte also hypersegmented PMNs
What RBC forms do you see in

marrow failure.
Macro-ovalocyte
What RBC forms do you see in

DIC
Helmet cell,
schistocyte,
Poikilocytes
What RBC forms do you see in

traumatic hemolysis.
Helmet cell,
schistocyte
What RBC forms do you see in

Sickle cell anemia.
Sickle cell
What RBC forms do you see in

Myeloid metaplasia with myelofibrosis.
Teardrop cell
What RBC forms do you see in

Spiny appearance in abetalipoproteinemia.
Acanthocyte
What RBC forms do you see in

HbC disease
Target cell

HALT.
What RBC forms do you see in

Asplenia
Target cell

HALT.
What RBC forms do you see in

Liver disease
Target cell

HALT.
What RBC forms do you see in

Thalassemia.
Target cell

HALT.
What RBC forms do you see in

TTP/HUS.
Poikilocytes

Burr cell
What RBC forms do you see in

microvascular damage
Poikilocytes
Psammoma bodies
when
PSaMMoma:
1. Papillary adenocarcinoma of thyroid
2. Serous papillary cystadenocarcinoma of ovary
3. Meningioma
4. Malignant mesothelioma
Laminated, concentric, calcific spherules aka
Psammoma bodies
Psammoma bodies
what
Laminated, concentric, calcific spherules
causes of Microcytic, hypochromic Anemia
Iron deficiency–
Thalassemias
Lead poisoning,
causes of macrocytic Anemia
vitamin B12/folate deficiency
Drugs that block DNA synthesis (e.g., sulfa drugs, AZT)
causes of normocytic, normochromic Anemia

with no increase in Reticulocytes
-Acute hemorrhage
-Bone marrow -aplasia/fibrosis/infiltration
-Anemia of chronic disease (ACD)
-renal insufficiency
↓ serum haptoglobin and
↑ serum LDH indicate
RBC hemolysis. Direct
???serum haptoglobin and
??? serum LDH indicate
RBC hemolysis.
↓ serum haptoglobin and
↑ serum LDH indicate
What type of Anemia do you get in

Iron deficiency
Microcytic, hypochromic
What type of Anemia do you get in

Thalassemias
Microcytic, hypochromic
What type of Anemia do you get in

Lead poisoning
Microcytic, hypochromic
What type of Anemia do you get in

vitamin B12/folate deficiency
Macrocytic, Megaloblastic
What type of Anemia do you get in

sulfa drugs
Macrocytic
What type of Anemia do you get in

AZT
Macrocytic
What type of Anemia do you get in

G6PD deficiency
Normocytic, normochromic
What type of Anemia do you get in

Acute Hemorrhage
Normocytic, normochromic
What type of Anemia do you get in

PK deficiency
Normocytic, normochromic
What type of Anemia do you get in

Heredotary Spherocytosis
Normocytic, normochromic
What type of Anemia do you get in

aplastic anemia
Normocytic, normochromic
What type of Anemia do you get in

leukemia
Normocytic, normochromic
What type of Anemia do you get in

Sickle Cell
Normocytic, normochromic
What type of Anemia do you get in

Autoimmune hemolytic anemia
Normocytic, normochromic
What type of Anemia do you get in

Anemia of chronic disease (ACD)
Normocytic, normochromic
Lab values in

Iron deficiency–
↓ serum iron,
↑ transferrin/TIBC,
↓ ferritin ,
↓↓% transferrin saturation
Lab values in

Anemia of chronic disease (ACD)
↓ serum iron,
↓ transferrin/TIBC,
↑ ferritin ,
No change% transferrin saturation
Lab values in

Pregnacy/OCP use
wrt Iron
no change serum iron,
↑ transferrin/TIBC,
no change ferritin ,
↓% transferrin saturation
Lab values in

Hereditary Hemochromatosis
↑ serum iron,
↓ transferrin/TIBC,
↑ ferritin ,
↑↑% transferrin saturation
Unlike folate deficiency,
vitamin B12 deficiency
is associated with
neurologic
problems.
used to distinguish between
immune- vs. non-immune- mediated RBC hemolysis.
Direct Coombs
causes of Aplastic anemia
Radiation, benzene,
chloramphenicol, alkylating agents, antimetabolites, viral agents (parvovirus B19, EBV, HIV), Fanconi’s anemia, idiopathic (immune-mediated,
1° stem-cell defect). May follow acute hepatitis.
Aplastic anemia Symptoms
Fatigue, malaise, pallor, purpura, mucosal bleeding, petechiae, infection.
Aplastic anemia Pathologic features
Pancytopenia with normal cell morphology; hypocellular bone marrow with fatty infiltration. Diagnose with bone marrow biopsy.
Aplastic anemia Treatment
Withdrawal of offending agent, bone marrow transplantation,
RBC and platelet transfusion, G-CSF or GM-CSF.
Aplastic anemia Dx
Diagnose with bone marrow biopsy.
HbS mutation
single amino acid replacement in β chain (substitution of normal glutamic acid with
valine).
Sickle cell anemia

what precipitates sickling.
Low O2 or dehydration
Sickle cell anemia

Heterozygotes aka and features
(sickle cell trait) are relatively
malaria resistant (balanced polymorphism).
Sickle cell anemia

homozygotes aka
sickle cell disease
Sickle cell anemia

Complications in homozygotes
aplastic crisis (due to parvovirus B19 infection), autosplenectomy, ↑ risk of encapsulated organism infection, Salmonella osteomyelitis,
painful crisis (vaso-occlusive), and splenic
sequestration crisis
Sickle cell anemia

Tx
therapies for sickle cell anemia include hydroxyurea (↑ HbF) and bone marrow transplantation.
Sickle cell anemia

HbC
HbC defect is a different β-chain mutation; patients
with HbC or HbSC (1 of each mutant gene) have
milder disease than do HbSS patients.
Sickle cell anemia

HbS
The Bad allele
Sickle cell anemia

The Bad allele
HbS
Sickle cell anemia

The less Bad allele
HbC
Sickle cell anemia epidemiology wrt blacks
8% of African-Americans carry the HbS trait; 0.2% have the disease.
“Crew cut” on skull x-ray who and why
thalassemias and SCD

marrow expansion/↑ erythropoiesis
α-thalassemia
genetics and problems wrt compensation
There are 4 α-globin genes. In α-thalassemia, the α-globin chain is underproduced (as a function of number of bad genes, 1–4). There is no
compensatory increase of any other chains.
α-thalassemia
types
HbH (β4-tetramers, lacks 3 α-globin genes).

Hb Barts(gamma4-tetramers, lacks all 4 α-globin genes) results in hydrops fetalis and intrauterine fetal death.
α-thalassemia is prevalent in
(α=A)

Asia and Africa.
β-thalassemia is prevalent in
Mediterranean populations.
thalassemia is prevalent in Asia and Africa.
(α=A)

α-thalassemia
thalassemia is prevalent in Mediterranean populations
β-thalassemia
β-thalassemia different types and genes
In β-thalassemia minor (heterozygote), the β chain is
underproduced; in -thalassemia major (homozygote), the β chain is absent.
which type of β-thalassemia has fetal hemoglobin production compensatorily ↑ but is inadequate.
Both major and minor
β-thalassemia wrt Compensation
In both case fetal hemoglobin production is compensatorily
↑ but is inadequate.
clinical findings and complications of β-thalassemia major
severe anemia requiring blood transfusions. Cardiac failure due to 2° hemochromatosis. Marrow expansion → skeletal deformities.
Hemolytic anemias
lab values/what is increased
↑ serum bilirubin (jaundice, pigment gallstones),
↑ reticulocytes
Where is the hemolysis in Autoimmune anemia
Mostly extravascular
Where is the hemolysis in Hereditary spherocytosis
extravascular
Where is the hemolysis in Paroxysmal nocturnal hemoglobinuria
Intravascular
Where is the hemolysis in Microangiopathic anemia
Intravascular
Intravascular hemolysis seen in DIC, TTP/HUS, SLE, or malignant hypertension.
Microangiopathic anemia
Microangiopathic anemia what is it and what are its causes
Intravascular hemolysis seen in DIC, TTP/HUS, SLE, or malignant hypertension.
Autoimmune anemia
wrt Warm Agglutinin
Warm weather is GGGreat.
Warm agglutinin (IgG)––chronic anemia seen in SLE, in CLL, or with certain drugs (e.g. α-methyldopa).
Autoimmune anemia
wrt Cold Agglutinin
Cold ice cream . . . MMM.
Cold agglutinin (IgM)––acute anemia triggered by cold; seen during recovery from Mycoplasma
pneumoniae or infectious mononucleosis.
Autoimmune anemia wrt babies
Erythroblastosis fetalis––seen in newborn due to Rh or other blood antigen incompatibility → mother’s antibodies attack fetal RBCs.
Autoimmune hemolytic anemia WRT Coombs
Coombs positive.
Hereditary spherocytosis anemia WRT Coombs
Coombs negative.
Hereditary spherocytosis confirmation
Osmotic fragility test used to confirm.
Hemolytic anemias where Osmotic fragility test used to confirm.
Hereditary spherocytosis
Hereditary spherocytosis mech and structure
spectrin or ankyrin defect.

RBCs are small and round with no central pallor → less membrane →↑ MCHC,↑ RDW.
Hereditary spherocytosis
after spleenectomy
Howell-jolly bodies
Howell-jolly bodies are present when
Hereditary spherocytosis
after spleenectomy
Paroxysmal nocturnal hemoglobinuria mech
due to membrane defect →
↑ sensitivity of RBCs to the lytic activity of complement.
due to membrane defect →
↑ sensitivity of RBCs to the lytic activity of complement.
Paroxysmal nocturnal hemoglobinuria
Paroxysmal nocturnal hemoglobinuria lab test
↑ urine hemosiderin.
DIC

What is it
Activation of coagulation cascade leading to
microthrombi and global consumption of platelets, fibrin, and coagulation factors.
DIC

causes
STOP Making New Thrombi!

Sepsis (gram-negative), Trauma, Obstetric complications acute Pancreatitis,
Malignancy,
Nephrotic syndrome, Transfusion
DIC

Lab findings
↑ PT, ↑ PTT, ↑ fibrin split products (D-dimers),
↓ platelet count.
DIC on blood smear.
Helmet-shaped cells and
schistocytes
Platelet abnormalities

clinical findings
Microhemorrhage: mucous membrane bleeding, epistaxis, petechiae, purpura, ↑ bleeding time.
Coagulation factor defects

Clinical findings
Macrohemorrhage: hemarthroses (bleeding into joints), easy bruising, ↑ PT and/or PTT.
Microhemorrhage: mucous membrane bleeding, epistaxis, petechiae, purpura, ↑ bleeding time.
Platelet abnormalities
Macrohemorrhage: hemarthroses (bleeding into joints), easy bruising, ↑ PT and/or PTT.
Coagulation factor defects
Name 5 Platelet abnormality causes
ITP
TTP
DIC
Aplastic Anemia
Immunosupressive drugs
Clinical/Lab findings in

ITP
antiplatelet antibodies,
↑ megakaryocytes

young and less severe that TTP
Clinical/Lab findings in

TTP
FAT RN

-Fever
-Anemia (microangiopathic hemolytic)
THROMBOCTOPENIA ,
RENAL ,
NERVOUS SYSTEM
Coagulation factor defects and which factors are involved
1. Hemophilia A (factor VIII deficiency)


2. Hemophilia B (factor IX deficiency)
Bernard-Soulier disease =
defect of platelet adhesion (↓ GP Ib)
defect of platelet adhesion (↓ GP Ib)
Bernard-Soulier disease
Glanzmann’s thrombasthenia =
defect of platelet aGgregation (↓ GP IIb-IIIa).
defect of platelet aGgregation (↓ GP IIb-IIIa).
Glanzmann’s thrombasthenia
PT tests for
(extrinsic)––factors II, V, VII, and X.
test for (extrinsic)––factors II, V, VII, and X.
PT
dPTT Test
(intrinsic)––all factors except VII.
test for (intrinsic)––all factors except VII.
PTT
von Willebrand’s disease mech
deficiency of von Willebrand
factor → defect of platelet adhesion and ↓
factor VIII survival)

combined platelet and coagulation problem
most common
bleeding disorder
von Willebrand’s disease
Hodgkin’s cells and markers
Presence of Reed-Sternberg cells (RS cells are CD30
and CD15+ B-cell origin)
(CD30 and CD15) B-cell origin
Reed-Sternberg cells
Reed-Sternberg cells origin
B-cell
Reed-Sternberg cell
markers
CD30
and CD15
Hodgkin’s location
Localized, single group of nodes; extranodal rare; contiguous spread
Hodgkin’s Constitutional (“B”) signs/symptoms
low-grade fever,
night sweats,
weight loss
Hodgkin’s wrt lymphnode appearance
Mediastinal lymphadenopathy
Hodgkin’s association
50% of cases associated with EBV
Hodgkin’s who gets wrt age and sex
—young and old; more common in men except for nodular sclerosing type
Hodgkin’s prognosis markers
Good = ↑ lymphocytes, ↓ RS
Non-Hodgkin’s Lymphoma

who
Peak incidence 20–40 years old
Non-Hodgkin’s Lymphoma

associated with
Associated with HIV and immunosuppression
Non-Hodgkin’s Lymphoma

WRT nodes
Multiple, peripheral nodes; extranodal involvement common; noncontiguous spread
Non-Hodgkin’s Lymphoma

cell type
Majority involve B cells (except those of lymphoblastic T-cell origin)
Non-Hodgkin’s Lymphoma

WRT Ig's
No hypergammaglobulinemia
Non-Hodgkin’s Lymphoma

WRT B symps
Fewer constitutional sgns/symptoms
Which type of Lymphoma is associated with EBV
Hodgkin’s
Which type of Lymphoma is associated with
HIV and immunosuppression
Non-Hodgkin’s
Which type of Hodgkin's Lymphoma

Most common
Nodular sclerosing
Which type of Hodgkin's Lymphoma

collagen banding and lacunar cells
Nodular sclerosing
Which type of Hodgkin's Lymphoma

women > men,
primarily young adults.
Nodular sclerosing
Which type of Hodgkin's Lymphoma

most RS cells.
Mixed cellularity
Which type of Hodgkin's Lymphoma

Poor prognosis
Lymphocyte depleted (rare)
Which type of Hodgkin's Lymphoma

Most rare
Lymphocyte depleted
Which type of Hodgkin's Lymphoma

Older males with disseminated
disease.
Lymphocyte depleted (rare)
Which type of Hodgkin's Lymphoma

Excellent Prognosis
Lymphocyte predominant

and

Nodullar sclerosing
Which type of Hodgkin's Lymphoma

Intermediate prognosis
Mixed cellularity
Monoclonal plasma cell (“fried-egg” appearance) cancer
Multiple myeloma
Multiple myeloma

where
arises in the marrow
Multiple myeloma

what is produced
Large amounts of IgG (55%) or IgA (25%).
Multiple myeloma

how common
Most common 1° tumor arising within bone in adults.
Multiple myeloma

clinical findings
CRAB I-
C = Calcium (elevated),
R = Renal failure,
A = Anemia,
B =Bone lesions (Destructive)
punched-out lytic bone lesions on x-ray
I =Infection (↑ susceptibility to)
Multiple myeloma

Associated with
1° amyloidosis
Multiple myeloma

WRT imaging
punched-out lytic bone lesions on x-ray
Multiple myeloma

lab findings
monoclonal
Ig spike (M protein) on serum protein electrophoresis and Ig light chains in urine (Bence Jones protein).
Multiple myeloma

WRT blood smear
Blood smear shows RBCs stacked like poker chips
(rouleau formation).
Blood smear shows RBCs stacked like poker chips
Multiple myeloma
(rouleau formation).
rouleau formation aka
Blood smear shows RBCs stacked like poker chips
Blood smear shows RBCs stacked like poker chips aka
(rouleau formation).
Waldenström’s macroglobulinemia
→M spike = IgM
(→hyperviscosity symptoms); no lytic bone lesions
→M spike = IgM
(→hyperviscosity symptoms); no lytic bone lesions
Waldenström’s macroglobulinemia
Distinctive tumor giant cell seen in Hodgkin’s disease;
Reed-Sternberg
Reed-Sternberg look
binucleate or bilobed with
the 2 halves as mirror images (“owl’s eyes”).
Reed-Sternberg variant
Variants include lacunar cells in nodular sclerosis
Variants include lacunar cells in nodular sclerosis
Reed-Sternberg variant
binucleate or bilobed with
the 2 halves as mirror images (“owl’s eyes”).
Reed-Sternberg look
which Non-Hodgkin’s lymphoma

t(14;18) bcl-2 expression
Follicular lymphoma
(small cleaved cell)
which Non-Hodgkin’s lymphoma

Like CLL with focal mass;
low grade.
Small lymphocytic lymphoma
which Non-Hodgkin’s lymphoma

Most common (adult).
Follicular lymphoma
(small cleaved cell)
which Non-Hodgkin’s lymphoma

Difficult to cure; indolent
course; bcl-2 is involved in apoptosis.
Follicular lymphoma
(small cleaved cell)
which Non-Hodgkin’s lymphoma

80% B cells
20% T cells
(mature)
Diffuse large cell
which Non-Hodgkin’s lymphoma

Usually older adults, but
20% occur in children
Diffuse large cell
which Non-Hodgkin’s lymphoma

t(11;14)
Mantle cell lymphoma
which Non-Hodgkin’s lymphoma

Poor prognosis, CD5+
Mantle cell lymphoma
which Non-Hodgkin’s lymphoma

Most common in children
Lymphoblastic lymphoma
which Non-Hodgkin’s lymphoma

T cells (immature)
Lymphoblastic lymphoma
which Non-Hodgkin’s lymphoma

commonly presents with ALL and
mediastinal mass
Lymphoblastic lymphoma
which Non-Hodgkin’s lymphoma

very aggressive T-cell
lymphoma.
Lymphoblastic lymphoma
which Non-Hodgkin’s lymphoma

t(8;14)
Burkitt’s lymphoma
which Non-Hodgkin’s lymphoma

c-myc
Burkitt’s lymphoma
which Non-Hodgkin’s lymphoma

“Starry-sky” appearance
Burkitt’s lymphoma
Burkitt’s lymphoma

Genetics
t(8;14) c-myc gene moves next to
heavy-chain Ig gene (14)
c-Myc is a very strong proto-oncogene
Burkitt’s lymphoma

associations
associated with EBV;jaw lesion in endemic form in Africa; pelvis or
abdomen in sporadic form
what exactly is the “Starry-sky” appearance of Burkitt's
(sheets of lymphocytes with interspersed macrophages);
Burkitt’s lymphoma

appearance
“Starry-sky” appearance
Mantle cell lymphoma

Genetics
t(11;14) over-express cyclin D1 (activity is required for cell cycle G1/S transition)
Follicular lymphoma

Genetics
t(14;18) overexpression of the bcl-2 gene. This overexpression causes a blockage of apoptosis,
disorder associated with

t(9;22)
CML
(Philadelphia chromosome)
(bcr-abl hybrid)
disorder associated with

t(8;14)
Burkitt’s lymphoma (c-myc activation)
disorder associated with

t(14;18)
Follicular lymphomas (bcl-2 activation)
disorder associated with

t(15;17)
M3 type of AML (responsive to all-trans retinoic acid)
disorder associated with

t(11;22)
Ewing’s sarcoma
disorder associated with

t(11;14)
Mantle cell lymphoma
Translocation associated with

CML
t(9;22)
(Philadelphia chromosome)
(bcr-abl hybrid)
Translocation associated with

Burkitt’s lymphoma
t(8;14)
(c-myc activation)
Translocation associated with

Follicular lymphomas
t(14;18)
(bcl-2 activation)
Translocation associated with

M3 type of AML
t(15;17)
(responsive to all-trans retinoic acid)
Translocation associated with

Ewing’s sarcoma
t(11;22)
Translocation associated with

Mantle cell lymphoma
t(11;14)
Leukemias General considerations
↑ number of circulating leukocytes in blood; bone marrow infiltrates of leukemic cells;
Leukemias General clinical findings
marrow failure can cause anemia (↓ RBCs), infections
(↓ mature WBCs), and hemorrhage (↓ platelets); leukemic cell infiltrates in liver, spleen, and lymph nodes are common
Leukemias
and ages
<15 = ALL
15-40 = AML
30-60 = CML
>60 = CLL
Auer rods; myeloblasts; adults.
AML
Leukemia most responsive to therapy
ALL
CLL

clinical findings
lymphadenopathy; hepatosplenomegaly; few symptoms; indolent course;
CLL

Lab findings
↑ smudge cells in peripheral blood smear; warm antibody autoimmune hemolytic
anemia; very similar to SLL (small lymphocytic lymphoma).
CML

lab findings
myeloid stem cell proliferation;
presents with ↑ neutrophils and metamyelocytes;
splenomegaly; Very low leukocyte alkaline
phosphatase (vs. leukemoid reaction).
CML vs Leukemoid Rxn
Very low leukocyte alkaline
phosphatase (vs. leukemoid reaction).
“blast crisis”
CML accelerating to AML
Very low leukocyte alkaline
phosphatase what does that tell you WRT WBC's
That it is CML and not leukemoid reaction).
final phase of CML
Blast crisis accelerating to AML
Auer rods

what are they
Auer rods are peroxidase-positive cytoplasmic inclusions in granulocytes and myeloblasts
Auer rods

when seen
Primarily in acute promyelocytic leukemia (M3).
Auer rods

why problematic
Treatment of AML M3 can
release Auer rods → DIC.
Histiocytosis X

caused by
Caused by Langerhans' cells from the monocyte lineage that infiltrate the lung.
peroxidase-positive cytoplasmic inclusions in granulocytes and myeloblasts
Auer rods
Histiocytosis X

who gets
Primarily affects young adults. Worse with smoking.
Caused by Langerhans' cells from the monocyte lineage that infiltrate the lung.
Histiocytosis X
Histiocytosis X

clinical features
range from isolated bone lesions to multisystemic disease.
Heparin

Mechanism
Catalyzes the activation of antithrombin III, ↓ thrombin and Xa.
Heparin

Clinical use
Immediate anticoagulation for pulmonary embolism, stroke, angina, MI, DVT. Used
during pregnancy (does not cross placenta).
Heparin

Toxicity
Bleeding, thrombocytopenia, drug-drug interaction
Heparin

how to monitor
Follow PTT.
Heparin

Reversal
protamine sulfate (positively charged molecule that acts by
binding negatively charged heparin).
low-molecular-weight heparins

names
enoxaparin
low-molecular-weight heparins

effects and advatages
Newer low-molecular-weight heparins (enoxaparin) act more on Xa, have better
bioavailability and 2–4 times longer half-life. Can be administered subcutaneously
and without laboratory monitoring.
low-molecular-weight heparins

disadvantage
Not easily reversible.
Heparin

Half-life
Short (1.5 Hours)
Warfarin aka
Coumadin
Coumadin aka
Warfarin
Warfarin

Mechanism
Interferes with synthesis and gamma-carboxylation
of vitamin K–dependent clotting factors II, VII, IX,
and X and protein C and S.
Warfarin

Clinical use
Chronic anticoagulation. Not used in pregnant women (because warfarin, unlike heparin, can
cross the placenta).
Warfarin

Toxicity
Bleeding, teratogenic, drug-drug interactions.
Warfarin

Monitoring
The EX-PaT went to
WAR(farin).

EXtrinsic pathway and ↑ PT.
Warfarin

Half-life
Long

2 days
Heparin vs. warfarin

Structure
Heparin-Large anionic polymer, acidic

Warfarin-Small lipid-soluble molecule
Heparin vs. warfarin

administration
Heparin- Parenteral (IV, SC)

Warfarin- Oral
Heparin vs. warfarin

Site of action
Heparin-Blood

Warfarin-Liver
Heparin vs. warfarin

Onset of action
Heparin-Rapid (sec)

Warfarin-Slow (days)
Heparin vs. warfarin

Mechanism of action
Heparin- Activates ATIII, which ↓ the action of IIa (thrombin) and Xa

Warfarin-Impairs the synthesis of vitamin K–dependent clotting factors II, VII, IX, and X (vitamin K antagonist)
Heparin vs. warfarin

Duration of action
Heparin- Acute (hours)

Warfarin-Chronic (weeks or months)
Heparin vs. warfarin

Inhibits coagulation
in vitro
Heparin-yes

Warfarin-no
Heparin vs. warfarin

Treatment of acute
overdose
Heparin-Protamine Sulfate

Warfarin-IV vit K and Fresh frozen plasma
Heparin vs. warfarin

Monitoring
Heparin-PTT (intrinsic)

Warfarin-PT (extrinsic)
Heparin vs. warfarin

Crosses placenta
Heparin-No

Warfarin- Yes (teratogenic)
Thrombolytics

Names
Streptokinase,
urokinase,
tPA (alteplase),
APSAC (anistreplase).
Thrombolytics

Mechanism
Directly or indirectly aid conversion of plasminogen to plasmin, the major fibrinolytic
enzyme, which cleaves thrombin and fibrin clots.
Thrombolytics

Clinical use
Early MI,
early ischemic stroke.
Thrombolytics

Toxicity
Bleeding.
Thrombolytics

contraindications
patients with active bleeding, history of intracranial
bleeding, recent surgery, known bleeding diathesis, or severe hypertension.
Thrombolytics

Toxicity Tx
aminocaproic acid, an inhibitor of fibrinolysis.
aminocaproic acid

clinical use
Tx of Thrombolytics Toxicity
aminocaproic acid

mech
inhibitor of Plasminogen to pasmin
Aspirin aka
ASA
ASA aka
Aspirin
Aspirin (ASA)

Mechanism
Acetylates and irreversibly inhibits cyclooxygenase (both COX-1 and COX-2) to prevent
conversion of arachidonic acid to prostaglandins.
Aspirin (ASA)

Clinical use
Antipyretic,
analgesic,
anti-inflammatory,
antiplatelet drug.
Aspirin (ASA)

Toxicity
Gastric ulceration,
bleeding,
hyperventilation,
Reye’s syndrome,
tinnitus (CN VIII).
Aspirin

WRT lab values (homeostasis)
↑ bleeding time.
No effect on PT, PTT.
Drugs that Inhibit platelet aggregation by irreversibly blocking ADP receptor
Clopidogrel, ticlopidine
Clopidogrel has the same effects/mech as ?
ticlopidine
ticlopidine has the same effects/mech as ?
Clopidogrel
Clopidogrel

Mechanism
Inhibit platelet aggregation by irreversibly blocking ADP receptors. Inhibit fibrinogen
binding by preventing glycoprotein IIb/IIIa expression.
Clopidogrel

Clinical use
Acute coronary syndrome; coronary stenting. ↓ incidence or recurrence of
thrombotic stroke.
Clopidogrel or Ticlopidine

Neutropenia
Ticlopidine
Ticlopidine

Toxicity
Neutropenia
Acetylates and irreversibly inhibits cyclooxygenase (both COX-1 and COX-2)
Aspirin (ASA)
Monoclonal antibody that binds to the glycoprotein receptor IIb/IIIa on activated platelets, preventing aggregation.
Abciximab
Abciximab

Mechanism
Monoclonal antibody that binds to the glycoprotein receptor IIb/IIIa on activated platelets, preventing aggregation.
Abciximab

Clinical use
Acute coronary syndromes, percutaneous transluminal coronary angioplasty.
Abciximab

Toxicity
Bleeding, thrombocytopenia.
Cancer drugs

which are Cell cycle specific
antimetabolites (MTX, 5-FU, 6-MP),
Cytarabine(ara-c),
Hydroxyurea,
etoposide,
bleomycin,
vincristine/vinblastine,
paclitaxel and other taxols.
Cancer drugs

which are Cell cycle nonspecific
alkylating agents, antibiotics (dactinomycin, doxorubicin, bleomycin).
Methotrexate (MTX)

Mechanism
S-phase-specific antimetabolite. Folic acid analog that inhibits dihydrofolate reductase, resulting in ↓ dTMP and therefore ↓ DNA and protein synthesis.
Methotrexate (MTX)

Clinical use
Leukemias, lymphomas, choriocarcinoma, sarcomas. Abortion, ectopic pregnancy,
rheumatoid arthritis, psoriasis.
Methotrexate (MTX)

Toxicity
Myelosuppression, which is reversible with leucovorin (folinic acid) “rescue.”
Macrovesicular fatty change in liver.
Methotrexate (MTX)

Toxicity Tx
Myelosuppression, which is reversible with leucovorin (folinic acid) “rescue.”
leucovorin use
Methotrexate (MTX) induced Myelosuppression, which is reversible with leucovorin (folinic acid) “rescue.”
leucovorin aka
folinic acid
folinic acid aka
leucovorin
5-fluorouracil (5-FU)

Mechanism
S-phase-specific antimetabolite. Pyrimidine analog bioactivated to 5F-dUMP, which covalently complexes folic acid. This complex inhibits thymidylate synthase, resulting in ↓ dTMP and same effects as MTX.
5-fluorouracil (5-FU)

Clinical use
Colon cancer and other solid tumors, basal cell carcinoma (topical). Synergy with
MTX.
5-fluorouracil (5-FU)

Toxicity
Myelosuppression, which is NOT reversible with leucovorin; photosensitivity. Can "rescue" with thymidine.
Synergy with MTX.
5-fluorouracil
Synergy with 5-fluorouracil
MTX.
5-fluorouracil (5-FU)

Toxicity Tx
Myelosuppression, which is NOT reversible with leucovorin; photosensitivity.
Can "rescue" with thymidine.
Blocks de novo purine synthesis. Activated by HGPRTase.
6-mercaptopurine (6-MP)
6-mercaptopurine (6-MP)

Mechanism
S-phase specific Blocks de novo purine synthesis. Activated by HGPRTase.
6-mercaptopurine (6-MP)

Clinical use
Toxicity
Leukemias, lymphomas (not CLL or Hodgkin’s).
6-mercaptopurine (6-MP)

Toxicity
Bone marrow, GI, liver. Metabolized by xanthine oxidase; thus ↑ toxicity with allopurinol.
Cytarabine aka
ara-C
ara-C aka
Cytarabine
Cytarabine (ara-C)

Mechanism
Inhibits DNA polymerase.
Cytarabine (ara-C)

Clinical use
AML.
Cytarabine (ara-C)

Toxicity
Leukopenia, thrombocytopenia, megaloblastic anemia.
Cyclophosphamide

Mechanism
Alkylating agents; covalently x-link (interstrand) DNA at guanine N-7. Require
bioactivation by liver.
Alkylating agents; covalently x-link (interstrand) DNA at guanine N-7. Require
bioactivation by liver.
Cyclophosphamide, ifosfamide
Cyclophosphamide

Clinical use
Non-Hodgkin’s lymphoma, breast and ovarian carcinomas. Also immunosuppressants.
Cyclophosphamide

Toxicity
Myelosuppression; hemorrhagic cystitis, which can be partially prevented with mesna.
ifosfamide

mechanism
Same as Cyclophosphamide
Nitrosoureas

Names
Carmustine, lomustine, semustine, streptozocin.
Nitrosoureas

Mechanism
Alkylate DNA. Require bioactivation. Cross blood-brain barrier → CNS.
Nitrosoureas

Clinical use
Brain tumors (including glioblastoma multiforme).
Nitrosoureas

Toxicity
CNS toxicity (dizziness, ataxia).
Alkylate DNA. Require bioactivation. Cross blood-brain barrier → CNS.
Nitrosoureas:
Carmustine,
lomustine,
semustine,
streptozocin.
Cisplatin and carboplatin

Mechanism
Act like alkylating agents.
Cisplatin and carboplatin

Clinical use
Testicular, bladder, ovary, and lung carcinomas.
Cisplatin and carboplatin

Toxicity
Nephrotoxicity and acoustic nerve damage.
Busulfan

Mechanism
Alkylates DNA.
Busulfan

Clinical use
CML.
Busulfan

Toxicity
Pulmonary fibrosis, hyperpigmentation.
Doxorubicin (Adriamycin), daunorubicin

Mechanism
Generate free radicals and noncovalently intercalate in DNA (creating breaks in DNA
strand to ↓ replication).
Doxorubicin (Adriamycin), daunorubicin

Clinical use
Part of the ABVD combination regimen for Hodgkin’s and for myelomas, sarcomas, and
solid tumors (breast, ovary, lung).
Doxorubicin (Adriamycin), daunorubicin


Toxicity
Cardiotoxicity; also myelosuppression and marked alopecia. Toxic extravasation.
Generate free radicals and noncovalently intercalate in DNA (creating breaks in DNA
strand to ↓ replication).
Doxorubicin (Adriamycin), daunorubicin
Dactinomycin aka
actinomycin D
actinomycin D aka
Dactinomycin
Dactinomycin

Mechanism
Intercalates in DNA.
Dactinomycin

Clinical use
ACTinomycin D is used for childhood tumors (children
ACT out).
Wilms’ tumor, Ewing’s sarcoma,
rhabdomyosarcoma.
Dactinomycin

Toxicity
Myelosuppression.
Bleomycin

Mechanism
G2 specific
Induces formation of free radicals, which cause breaks in DNA strands.
Bleomycin

Clinical use
Testicular cancer, lymphomas (part of the ABVD regimen for Hodgkin’s).
Bleomycin

Toxicity
Pulmonary fibrosis, skin changes, but minimal myelosuppression.
Hydroxyurea

Mechanism
s-cycle specific Inhibits Ribonucleutide Reductase leading to decreased DNS synthesis
Hydroxyurea

Clinical use
Melanoma, CML, and Sickle Cell disease
Hydroxyurea

Toxicity
Bone marrow supression and GI upset
Prednisone

Mechanism
May trigger apoptosis. May even work on nondividing cells.
Prednisone

Clinical use
Most commonly used glucocorticoid in cancer chemotherapy. Used in CLL, Hodgkin’s lymphomas (part of the MOPP regimen). Also an immunosuppressant used in
autoimmune diseases.
Prednisone

Toxicity
Cushing-like symptoms; immunosuppression, cataracts, acne, osteoporosis, hypertension,
peptic ulcers, hyperglycemia, psychosis.
Receptor antagonists in breast, agonists in bone; block the binding of estrogen
to estrogen receptor–positive cells.
Tamoxifen, raloxifene
Tamoxifen, raloxifene

Mechanism
Receptor antagonists in breast, agonists in bone; block the binding of estrogen
to estrogen receptor–positive cells.
Tamoxifen, raloxifene

Clinical use
Breast cancer. Also useful to prevent osteoporosis.
Tamoxifen, raloxifene

Toxicity
Tamoxifen may ↑ the risk of endometrial carcinoma via partial agonist effects; “hot
flashes.” Raloxifene does not cause endometrial carcinoma because it is an
endometrial antagonist.
Trastuzumab aka
Herceptin
Herceptin aka
Trastuzumab
Trastuzumab

Mechanism
Monoclonal antibody against HER-2 (erb-B2). Helps kill breast cancer cells that
overexpress HER-2, possibly through antibody-dependent cytotoxicity.
Trastuzumab

Clinical use
Metastatic breast cancer.
Trastuzumab

Toxicity
Cardiotoxicity.
Monoclonal antibody against HER-2 (erb-B2).
Trastuzumab (Herceptin)
Philadelphia chromosome brc-abl tyrosine kinase inhibitor.
Imatinib (Gleevec)
Gleevec aka
Imatinib
Imatinib aka
Gleevec
Imatinib

Mechanism
Philadelphia chromosome brc-abl tyrosine kinase inhibitor.
Imatinib

Clinical use
CML, GI stromal tumors.
Imatinib

Toxicity
Fluid retention.
Vincristine, vinblastine

Mechanism
M-phase-specific alkaloids that bind to tubulin and block polymerization of microtubules
so that mitotic spindle cannot form.
Vincristine, vinblastine

Clinical use
Part of the MOPP (Oncovin [vincristine]) regimen for lymphoma, Wilms’ tumor,
choriocarcinoma.
Vincristine, vinblastine

Toxicity
Vincristine––neurotoxicity (areflexia, peripheral neuritis), paralytic ileus.
VinBLASTine BLASTs Bone marrow (suppression).
M-phase-specific alkaloids that bind to tubulin and block polymerization of microtubules
so that mitotic spindle cannot form.
Vincristine, vinblastine
Paclitaxel, other taxols

Mechanism
M-phase-specific agents that bind to tubulin and hyperstabilize polymerized
microtubules so that mitotic spindle cannot break down (anaphase cannot occur).
Paclitaxel, other taxols

Clinical use
Ovarian and breast carcinomas.
Paclitaxel, other taxols

Toxicity
Myelosuppression and hypersensitivity.
M-phase-specific agents that bind to tubulin and hyperstabilize polymerized
microtubules so that mitotic spindle cannot break down (anaphase cannot occur).
Paclitaxel, other taxols
Which Cancer Drug

Myelosuppression, which is reversible with leucovorin (folinic acid) “rescue.”
Methotrexate (MTX)
Which Cancer Drug

Myelosuppression, which is NOT reversible with leucovorin; photosensitivity.
Can "rescue" with thymidine.
5-fluorouracil (5-FU)
Which Cancer Drug

Bone marrow, GI, liver. Metabolized by xanthine oxidase; thus ↑ toxicity with allopurinol.
6-mercaptopurine (6-MP)
Which Cancer Drug

Leukopenia, thrombocytopenia, megaloblastic anemia.
Cytarabine (ara-C)
Which Cancer Drug

used for AML only
Cytarabine (ara-C)
Which Cancer Drug

Myelosuppression; hemorrhagic cystitis, which can be partially prevented with mesna.
Cyclophosphamide, ifosfamide
Which Cancer Drug

Also immunosuppressants.
Cyclophosphamide, ifosfamide

and

Prednisone
Which Cancer Drug

CNS toxicity (dizziness, ataxia).
Nitrosoureas
Which Cancer Drug

Nephrotoxicity and acoustic nerve damage.
Cisplatin, carboplatin
Which Cancer Drug

used for Brain tumors (including glioblastoma multiforme).
Nitrosoureas
Which Cancer Drug

Pulmonary fibrosis, skin changes
Busulfan
and
Bleomycin
Which Cancer Drug

used for CML not Gleevac.
Busulfan
Which Cancer Drug

Cardiotoxicity; also myelosuppression and marked alopecia. Toxic extravasation.
Doxorubicin (Adriamycin), daunorubicin
Which Cancer Drug

used for Wilms’ tumor, Ewing’s sarcoma, rhabdomyosarcoma.
Dactinomycin (actinomycin D)

ACTinomycin D is used for
childhood tumors (children
ACT out).
Which Cancer Drug

Pulmonary fibrosis, skin changes, but minimal myelosuppression.
Bleomycin
Which Cancer Drug

Myelosuppression, GI irritation, alopecia.
Etoposide (VP-16)
Which Cancer Drug

does not cause endometrial carcinoma because it is an
endometrial antagonist.
Raloxifene
Which Cancer Drug

used for Metastatic breast cancer.
Trastuzumab (Herceptin)
Which Cancer Drug

Fluid retention.
Imatinib (Gleevec)
Which Cancer Drug

neurotoxicity (areflexia, peripheral neuritis), paralytic ileus.
Vincristine
Which Cancer Drug

Myelosuppression and hypersensitivity.
Paclitaxel, other taxols
causes of normocytic, normochromic Anemia

with increase in Reticulocytes
and inherited
Hereditary spherocytosis
G6PD dificiency
PK deficiency
Sickle cell
causes of normocytic, normochromic Anemia

with increase in Reticulocytes
and aquired
Autoimune (cold and warm)
Alloimune
Trauma(HUS/TTP/DIC/HELLP/mechanical valves)
Hypersplenism
PNH
Infection
Toxin
Osmotic damage
blood loss (non acute)
Etoposide (VP-16)

Mechanism
G2-phase-specific agent that inhibits topoisomerase II and ↑ DNA degradation.
Etoposide (VP-16)

Clinical use
Small cell carcinoma of the lung and prostate, testicular carcinoma.
Etoposide (VP-16)

Toxicity
Myelosuppression, GI irritation, alopecia.
Etoposide aka
VP-16
VP-16 aka
Etoposide
PNH

1. Screen

2. Confirm
1. sucrose lysis test

2. HAM's test (Ham's acid hemolysis)