2007 First Aid Ch 11 Hematology And Oncology

Front 1

Child has been anemic since
birth. Splenectomy would result in ↑ hematocrit in what disease?

Back 1

Spherocytosis.

Front 2

What is the danger of giving folate alone?

Back 2

Masks signs of neural damage
with vitamin B12 deficiency.

Front 3

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.

Back 3

Multiple myeloma (plasma cell
neoplasm); Bence Jones protein
(Ig light chains).

Front 4

What neoplasms are associated with AIDS?

Back 4

B-cell lymphoma, Kaposi’s sarcoma.

Front 5

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?

Back 5

Doxorubicin (cardiotoxic).

Front 6

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?

Back 6

Imatinib (Gleevec) is used to
treat CML; inhibitor of bcr-abl
tyrosine kinase.

Front 7

WBC differential from highest
to lowest:

Back 7

Neutrophils Like Making
Everything Better.

Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils

Front 8

Erythrocytosis =

Back 8

polycythemia =
↑ number of red cells.

Front 9

polycythemia =

Back 9

Erythrocytosis = ↑ number of red cells.

Front 10

Anisocytosis =

Back 10

varying sizes.

Front 11

RBC varying sizes =

Back 11

Anisocytosis

Front 12

Poikilocytosis =

Back 12

varying shapes.

Front 13

RBC varying shapes =

Back 13

Poikilocytosis

Front 14

Reticulocyte =

Back 14

immature erythrocyte.

Front 15

immature erythrocyte=

Back 15

Reticulocyte

Front 16

Normal Erythrocyte shape and why

Back 16

Anucleate, biconcave →large surface area: volume
ratio →easy gas exchange (O and CO ).

Front 17

Erythrocyte energy source

Back 17

glucose (90% anaerobically degraded to lactate, 10% by HMP shunt).

Front 18

Erythrocyte life span

Back 18

120 Days

Front 19

Erythrocyte days. Membrane contains what and why is it important

Back 19

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.

Front 20

Leukocyte types

Back 20

Types: granulocytes, basophils, eosinophils, neutrophils)
and mononuclear cells (lymphocytes,
monocytes).

Front 21

Leukocyte normal #'s

Back 21

Normally 4000–10,000 per microliter.

Front 22

Basophil #'s and where found

Back 22

< 1% of all leukocytes

Found in the blood.

Front 23

Basophil nuclues shape

Back 23

Bilobate nucleus.

Front 24

Basophil granule contnets

Back 24

Densely basophilic granules
containing heparin (anticoagulant), histamine
(vasodilator) and other vasoactive amines, and
leukotrienes (LTD-4).

Front 25

what cell Mediates allergic reaction

Back 25

Mast cell

and

Basophil

Front 26

Mast cell where found

Back 26

Found in tissue.

Front 27

Mast cell what cells are they like

Back 27

resemble basophils structurally and functionally
but are not the same cell type.

Front 28

Mast cell granule contents

Back 28

histamine, heparin, and eosinophil chemotactic
factors.

Front 29

Mast cell wrt Ig binding

Back 29

Can bind IgE to membrane.

Front 30

Mast cell which type of hypersensitivity reactions

Back 30

type I

Front 31

Cromolyn sodium prevents

Back 31

mast cell degranulation

Front 32

??????? prevents mast cell degranulation (used to treat asthma).

Back 32

Cromolyn sodium

Front 33

Cromolyn sodium is used to treat?

Back 33

asthma).

Front 34

Bilobate nucleus. Packed with large eosinophilic granules of uniform size.

Back 34

Eosinophil

Front 35

Eosinophil %'s

Back 35

1–6% of all leukocytes.

Front 36

Eosinophil structure

Back 36

Bilobate nucleus. Packed with large eosinophilic granules of uniform size.

Front 37

Defends against helminthic and protozoan infections (major basic protein).

Back 37

Eosinophil

Front 38

Eosinophil major function and mech

Back 38

Defends against helminthic and protozoan infections (major basic protein). Highly phagocytic for antigen-antibody complexes.

Front 39

Eosinophil produces what

Back 39

major basic protein
histaminase
arylsulfatase.

Front 40

Causes of eosinophilia

Back 40

NAACP:
Neoplastic
Asthma
Allergic processes
Collagen vascular
diseases
Parasites

Front 41

Neutrophil
what type of response cell

Back 41

Acute inflammatory response cell

Front 42

Neutrophil %'s

Back 42

40–75% WBCs.

Front 43

Hypersegmented polys are seen in

Back 43

vitamin B12/folate deficiency.

Front 44

Neutrophil granules and contents

Back 44

Large, spherical, azurophilic 1° granules (called lysosomes) contain hydrolytic enzymes, lysozyme, myeloperoxidase,
and lactoferrin.

Front 45

Monocyte %'s

Back 45

2-10% of leukocytes

Front 46

Monocyte structure and what they do

Back 46

Large. Kidney-shaped nucleus.
Extensive “frosted glass” cytoplasm. Differentiates
into macrophages in tissues.

Front 47

Differentiates into macrophages in tissues

Back 47

Monocyte

Front 48

Macrophage function

Back 48

Phagocytoses bacteria, cell debris, and senescent red
cells and scavenges damaged cells and tissues. Macrophages Can function as APC via MHC II.

Front 49

Macrophage life span

Back 49

long life in tissues

Front 50

Macrophage activation

Back 50

Activated by gamma-interferon.

Front 51

Lymphocyte appearance

Back 51

Round, densely staining nucleus. Small amount of pale cytoplasm.

Front 52

in general what is the role of lymphocytes

Back 52

B lymphocytes produce antibodies.
T lymphocytes manifest the cellular immune response as well as regulate B lymphocytes and macrophages.

Front 53

B lymphocyte cell markers

Back 53

CD19
CD20

Front 54

B lymphocyte is involved in which immune response

Back 54

Humoral

Front 55

B lymphocytes arise from what and mature where

Back 55

Arises from stem cells in bone marrow.

Matures in marrow.

Front 56

B lymphocyte initial migration

Back 56

Migrates to peripheral lymphoid tissue (follicles of lymph nodes, white pulp of spleen, unencapsulated lymphoid tissue).

Front 57

B lymphocytes when antigen is encountered

Back 57

differentiate into plasma
cells and produce antibodies and Can function as (APC) via MHC II.

Front 58

Off-center nucleus, clock-face chromatin

Back 58

Plasma cell

Front 59

Plasma cell structure

Back 59

Off-center nucleus, clock-face chromatin.

abundant RER and ell-developed
Golgi apparatus.

Front 60

Plasma cell function

Back 60

produce large amounts of antibody
specific to a particular antigen.

Front 61

Multiple myeloma is a ?????? neoplasm.

Back 61

plasma cell

Front 62

T lymphocyte is involed in what type of immune response

Back 62

Mediates cellular immune response

Front 63

T lymphocyte origins and maturation

Back 63

Originates from stem cells in the bone marrow,
but matures in the thymus.

Front 64

T lymphocyte differentiation and cell markers

Back 64

T cells differentiate into cytotoxic T cells
(MHC I, CD8, CD3),
helper T cells (MHC II, CD4, CD3),
and suppressor T cells.

Front 65

T lymphocyte CD mnemonic

Back 65

MHC × CD = 8
(e.g., MHC 2 ×CD4 = 8,

and MHC 1 × CD8 = 8).

Front 66

Professional APCs. Express MHC II and Fc receptor (FcR) on surface

Back 66

Dendritic cells

Front 67

Called Langerhans cells on skin.

Back 67

Dendritic cells

Front 68

Dendritic cells on the skin aka

Back 68

Langerhans cells

Front 69

Dendritic cells function

Back 69

Professional APCs. Express MHC II and Fc receptor (FcR) on surface

Main inducers of 1° antibody response.

Front 70

Which WBC

Mediates allergic reaction. < 1% of all leukocytes. Found in the blood.

Back 70

Basophil

Front 71

Which WBC
granules containing heparin (anticoagulant), histamine
(vasodilator) and other asoactive amines, and
leukotrienes (LTD-4).

Back 71

Basophil

Front 72

Which WBC

histamine, heparin, and eosinophil chemotactic

Back 72

Mast cell

Front 73

Which WBC

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

Back 73

Mast cell

Front 74

Which WBC

Highly phagocytic for antigen-antibody complexes.

Back 74

Eosinophil

Front 75

Which WBC

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

Back 75

Neutrophil

Front 76

Which WBC

Kidney-shaped nucleus. Extensive “frosted glass” cytoplasm.

Back 76

Monocyte

Front 77

Which WBC

Round, densely staining nucleus. Small amount of pale cytoplasm

Back 77

Lymphocyte

Front 78

Which WBC

Professional APCs. Express MHC II and Fc receptor (FcR) on surface.

Back 78

Dendritic cells

Front 79

Which WBC

Called Langerhans cells on skin.

Back 79

Dendritic cells

Front 80

Protein C and protein S
function and dependance

Back 80

inactivate Va and VIIIa;
vitamin K–dependent.

Front 81

inactivate Va and VIIIa;
vitamin K–dependent.

Back 81

Protein C and protein S

Front 82

Antithrombin III
function and activation

Back 82

inactivates thrombin, IXa, Xa,
and XIa;

activated by heparin.

Front 83

inactivates thrombin, IXa, Xa,
and XIa;

activated by heparin.

Back 83

Antithrombin III

Front 84

Factor V Leiden mutation mech

Back 84

resistance to activated protein C.

Front 85

genetic resistance to activated protein C.

Back 85

Factor V Leiden

Front 86

tPA mech

Back 86

generates plasmin, which cleaves fibrin.

Front 87

generates plasmin, which cleaves fibrin.

Back 87

tPA

Front 88

Ag's and Ab's for different Blood Types

A

Back 88

A antigen on RBC surface

B antibody in plasma.

Front 89

Ag's and Ab's for different Blood Types

B

Back 89

B antigen on RBC surface

A antibody in plasma.

Front 90

Ag's and Ab's for different Blood Types

AB

Back 90

A and B antigens on RBC surface,

No Ab's

"universal recipient."

Front 91

Ag's and Ab's for different Blood Types

O

Back 91

Neither A nor B antigen on RBC surface;
both antibodies in plasma; "universal donor.”

Front 92

Incompatible blood transfusions
can cause

Back 92

immunologic response, hemolysis, renal failure, shock, and death.

Front 93

RBC forms when do you see

Biconcave

Back 93

Normal.

Front 94

RBC forms when do you see

Spherocytes

Back 94

Hereditary spherocytosis, autoimmune hemolysis.

Front 95

RBC forms when do you see

Elliptocyte

Back 95

Hereditary elliptocytosis.

Front 96

RBC forms when do you see

Macro-ovalocye

Back 96

Megaloblastic anemia,
marrow failure.

Front 97

RBC forms when do you see

Helmet cell, schistocyte

Back 97

DIC, traumatic hemolysis.

Front 98

RBC forms when do you see

Sickle cell

Back 98

Sickle cell anemia.

Front 99

RBC forms when do you see

Teardrop cell

Back 99

Myeloid metaplasia with myelofibrosis.

Front 100

RBC forms when do you see

Acanthocyte

Back 100

Spiny appearance in abetalipoproteinemia.

Front 101

RBC forms when do you see

Target cell

Back 101

HALT.

HbC disease,
Asplenia,
Liver disease,
Thalassemia.

Front 102

RBC forms when do you see

Poikilocytes

Back 102

Nonuniform shapes in TTP/HUS, microvascular damage, DIC.

Front 103

RBC forms when do you see

Burr cell

Back 103

TTP/HUS.

Front 104

What RBC forms do you see in

Normal.

Back 104

Biconcave

Front 105

What RBC forms do you see in

Hereditary spherocytosis

Back 105

Spherocytes

Front 106

What RBC forms do you see in

autoimmune hemolysis.

Back 106

Spherocytes

Front 107

What RBC forms do you see in

Hereditary elliptocytosis.

Back 107

Elliptocyte

Front 108

What RBC forms do you see in

Megaloblastic anemia

Back 108

Macro-ovalocyte also hypersegmented PMNs

Front 109

What RBC forms do you see in

marrow failure.

Back 109

Macro-ovalocyte

Front 110

What RBC forms do you see in

DIC

Back 110

Helmet cell,
schistocyte,
Poikilocytes

Front 111

What RBC forms do you see in

traumatic hemolysis.

Back 111

Helmet cell,
schistocyte

Front 112

What RBC forms do you see in

Sickle cell anemia.

Back 112

Sickle cell

Front 113

What RBC forms do you see in

Myeloid metaplasia with myelofibrosis.

Back 113

Teardrop cell

Front 114

What RBC forms do you see in

Spiny appearance in abetalipoproteinemia.

Back 114

Acanthocyte

Front 115

What RBC forms do you see in

HbC disease

Back 115

Target cell

HALT.

Front 116

What RBC forms do you see in

Asplenia

Back 116

Target cell

HALT.

Front 117

What RBC forms do you see in

Liver disease

Back 117

Target cell

HALT.

Front 118

What RBC forms do you see in

Thalassemia.

Back 118

Target cell

HALT.

Front 119

What RBC forms do you see in

TTP/HUS.

Back 119

Poikilocytes

Burr cell

Front 120

What RBC forms do you see in

microvascular damage

Back 120

Poikilocytes

Front 121

Psammoma bodies
when

Back 121

PSaMMoma:
1. Papillary adenocarcinoma of thyroid
2. Serous papillary cystadenocarcinoma of ovary
3. Meningioma
4. Malignant mesothelioma

Front 122

Laminated, concentric, calcific spherules aka

Back 122

Psammoma bodies

Front 123

Psammoma bodies
what

Back 123

Laminated, concentric, calcific spherules

Front 124

causes of Microcytic, hypochromic Anemia

Back 124

Iron deficiency–
Thalassemias
Lead poisoning,

Front 125

causes of macrocytic Anemia

Back 125

vitamin B12/folate deficiency
Drugs that block DNA synthesis (e.g., sulfa drugs, AZT)

Front 126

causes of normocytic, normochromic Anemia

with no increase in Reticulocytes

Back 126

-Acute hemorrhage
-Bone marrow -aplasia/fibrosis/infiltration
-Anemia of chronic disease (ACD)
-renal insufficiency

Front 127

↓ serum haptoglobin and
↑ serum LDH indicate

Back 127

RBC hemolysis. Direct

Front 128

???serum haptoglobin and
??? serum LDH indicate
RBC hemolysis.

Back 128

↓ serum haptoglobin and
↑ serum LDH indicate

Front 129

What type of Anemia do you get in

Iron deficiency

Back 129

Microcytic, hypochromic

Front 130

What type of Anemia do you get in

Thalassemias

Back 130

Microcytic, hypochromic

Front 131

What type of Anemia do you get in

Lead poisoning

Back 131

Microcytic, hypochromic

Front 132

What type of Anemia do you get in

vitamin B12/folate deficiency

Back 132

Macrocytic, Megaloblastic

Front 133

What type of Anemia do you get in

sulfa drugs

Back 133

Macrocytic

Front 134

What type of Anemia do you get in

AZT

Back 134

Macrocytic

Front 135

What type of Anemia do you get in

G6PD deficiency

Back 135

Normocytic, normochromic

Front 136

What type of Anemia do you get in

Acute Hemorrhage

Back 136

Normocytic, normochromic

Front 137

What type of Anemia do you get in

PK deficiency

Back 137

Normocytic, normochromic

Front 138

What type of Anemia do you get in

Heredotary Spherocytosis

Back 138

Normocytic, normochromic

Front 139

What type of Anemia do you get in

aplastic anemia

Back 139

Normocytic, normochromic

Front 140

What type of Anemia do you get in

leukemia

Back 140

Normocytic, normochromic

Front 141

What type of Anemia do you get in

Sickle Cell

Back 141

Normocytic, normochromic

Front 142

What type of Anemia do you get in

Autoimmune hemolytic anemia

Back 142

Normocytic, normochromic

Front 143

What type of Anemia do you get in

Anemia of chronic disease (ACD)

Back 143

Normocytic, normochromic

Front 144

Lab values in

Iron deficiency–

Back 144

↓ serum iron,
↑ transferrin/TIBC,
↓ ferritin ,
↓↓% transferrin saturation

Front 145

Lab values in

Anemia of chronic disease (ACD)

Back 145

↓ serum iron,
↓ transferrin/TIBC,
↑ ferritin ,
No change% transferrin saturation

Front 146

Lab values in

Pregnacy/OCP use
wrt Iron

Back 146

no change serum iron,
↑ transferrin/TIBC,
no change ferritin ,
↓% transferrin saturation

Front 147

Lab values in

Hereditary Hemochromatosis

Back 147

↑ serum iron,
↓ transferrin/TIBC,
↑ ferritin ,
↑↑% transferrin saturation

Front 148

Unlike folate deficiency,
vitamin B12 deficiency
is associated with

Back 148

neurologic
problems.

Front 149

used to distinguish between
immune- vs. non-immune- mediated RBC hemolysis.

Back 149

Direct Coombs

Front 150

causes of Aplastic anemia

Back 150

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.

Front 151

Aplastic anemia Symptoms

Back 151

Fatigue, malaise, pallor, purpura, mucosal bleeding, petechiae, infection.

Front 152

Aplastic anemia Pathologic features

Back 152

Pancytopenia with normal cell morphology; hypocellular bone marrow with fatty infiltration. Diagnose with bone marrow biopsy.

Front 153

Aplastic anemia Treatment

Back 153

Withdrawal of offending agent, bone marrow transplantation,
RBC and platelet transfusion, G-CSF or GM-CSF.

Front 154

Aplastic anemia Dx

Back 154

Diagnose with bone marrow biopsy.

Front 155

HbS mutation

Back 155

single amino acid replacement in β chain (substitution of normal glutamic acid with
valine).

Front 156

Sickle cell anemia

what precipitates sickling.

Back 156

Low O2 or dehydration

Front 157

Sickle cell anemia

Heterozygotes aka and features

Back 157

(sickle cell trait) are relatively
malaria resistant (balanced polymorphism).

Front 158

Sickle cell anemia

homozygotes aka

Back 158

sickle cell disease

Front 159

Sickle cell anemia

Complications in homozygotes

Back 159

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

Front 160

Sickle cell anemia

Tx

Back 160

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

Front 161

Sickle cell anemia

HbC

Back 161

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.

Front 162

Sickle cell anemia

HbS

Back 162

The Bad allele

Front 163

Sickle cell anemia

The Bad allele

Back 163

HbS

Front 164

Sickle cell anemia

The less Bad allele

Back 164

HbC

Front 165

Sickle cell anemia epidemiology wrt blacks

Back 165

8% of African-Americans carry the HbS trait; 0.2% have the disease.

Front 166

“Crew cut” on skull x-ray who and why

Back 166

thalassemias and SCD

marrow expansion/↑ erythropoiesis

Front 167

α-thalassemia
genetics and problems wrt compensation

Back 167

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.

Front 168

α-thalassemia
types

Back 168

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.

Front 169

α-thalassemia is prevalent in

Back 169

(α=A)

Asia and Africa.

Front 170

β-thalassemia is prevalent in

Back 170

Mediterranean populations.

Front 171

thalassemia is prevalent in Asia and Africa.

Back 171

(α=A)

α-thalassemia

Front 172

thalassemia is prevalent in Mediterranean populations

Back 172

β-thalassemia

Front 173

β-thalassemia different types and genes

Back 173

In β-thalassemia minor (heterozygote), the β chain is
underproduced; in -thalassemia major (homozygote), the β chain is absent.

Front 174

which type of β-thalassemia has fetal hemoglobin production compensatorily ↑ but is inadequate.

Back 174

Both major and minor

Front 175

β-thalassemia wrt Compensation

Back 175

In both case fetal hemoglobin production is compensatorily
↑ but is inadequate.

Front 176

clinical findings and complications of β-thalassemia major

Back 176

severe anemia requiring blood transfusions. Cardiac failure due to 2° hemochromatosis. Marrow expansion → skeletal deformities.

Front 177

Hemolytic anemias
lab values/what is increased

Back 177

↑ serum bilirubin (jaundice, pigment gallstones),
↑ reticulocytes

Front 178

Where is the hemolysis in Autoimmune anemia

Back 178

Mostly extravascular

Front 179

Where is the hemolysis in Hereditary spherocytosis

Back 179

extravascular

Front 180

Where is the hemolysis in Paroxysmal nocturnal hemoglobinuria

Back 180

Intravascular

Front 181

Where is the hemolysis in Microangiopathic anemia

Back 181

Intravascular

Front 182

Intravascular hemolysis seen in DIC, TTP/HUS, SLE, or malignant hypertension.

Back 182

Microangiopathic anemia

Front 183

Microangiopathic anemia what is it and what are its causes

Back 183

Intravascular hemolysis seen in DIC, TTP/HUS, SLE, or malignant hypertension.

Front 184

Autoimmune anemia
wrt Warm Agglutinin

Back 184

Warm weather is GGGreat.
Warm agglutinin (IgG)––chronic anemia seen in SLE, in CLL, or with certain drugs (e.g. α-methyldopa).

Front 185

Autoimmune anemia
wrt Cold Agglutinin

Back 185

Cold ice cream . . . MMM.
Cold agglutinin (IgM)––acute anemia triggered by cold; seen during recovery from Mycoplasma
pneumoniae or infectious mononucleosis.

Front 186

Autoimmune anemia wrt babies

Back 186

Erythroblastosis fetalis––seen in newborn due to Rh or other blood antigen incompatibility → mother’s antibodies attack fetal RBCs.

Front 187

Autoimmune hemolytic anemia WRT Coombs

Back 187

Coombs positive.

Front 188

Hereditary spherocytosis anemia WRT Coombs

Back 188

Coombs negative.

Front 189

Hereditary spherocytosis confirmation

Back 189

Osmotic fragility test used to confirm.

Front 190

Hemolytic anemias where Osmotic fragility test used to confirm.

Back 190

Hereditary spherocytosis

Front 191

Hereditary spherocytosis mech and structure

Back 191

spectrin or ankyrin defect.

RBCs are small and round with no central pallor → less membrane →↑ MCHC,↑ RDW.

Front 192

Hereditary spherocytosis
after spleenectomy

Back 192

Howell-jolly bodies

Front 193

Howell-jolly bodies are present when

Back 193

Hereditary spherocytosis
after spleenectomy

Front 194

Paroxysmal nocturnal hemoglobinuria mech

Back 194

due to membrane defect →
↑ sensitivity of RBCs to the lytic activity of complement.

Front 195

due to membrane defect →
↑ sensitivity of RBCs to the lytic activity of complement.

Back 195

Paroxysmal nocturnal hemoglobinuria

Front 196

Paroxysmal nocturnal hemoglobinuria lab test

Back 196

↑ urine hemosiderin.

Front 197

DIC

What is it

Back 197

Activation of coagulation cascade leading to
microthrombi and global consumption of platelets, fibrin, and coagulation factors.

Front 198

DIC

causes

Back 198

STOP Making New Thrombi!

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

Front 199

DIC

Lab findings

Back 199

↑ PT, ↑ PTT, ↑ fibrin split products (D-dimers),
↓ platelet count.

Front 200

DIC on blood smear.

Back 200

Helmet-shaped cells and
schistocytes

Front 201

Platelet abnormalities

clinical findings

Back 201

Microhemorrhage: mucous membrane bleeding, epistaxis, petechiae, purpura, ↑ bleeding time.

Front 202

Coagulation factor defects

Clinical findings

Back 202

Macrohemorrhage: hemarthroses (bleeding into joints), easy bruising, ↑ PT and/or PTT.

Front 203

Microhemorrhage: mucous membrane bleeding, epistaxis, petechiae, purpura, ↑ bleeding time.

Back 203

Platelet abnormalities

Front 204

Macrohemorrhage: hemarthroses (bleeding into joints), easy bruising, ↑ PT and/or PTT.

Back 204

Coagulation factor defects

Front 205

Name 5 Platelet abnormality causes

Back 205

ITP
TTP
DIC
Aplastic Anemia
Immunosupressive drugs

Front 206

Clinical/Lab findings in

ITP

Back 206

antiplatelet antibodies,
↑ megakaryocytes

young and less severe that TTP

Front 207

Clinical/Lab findings in

TTP

Back 207

FAT RN

-Fever
-Anemia (microangiopathic hemolytic)
THROMBOCTOPENIA ,
RENAL ,
NERVOUS SYSTEM

Front 208

Coagulation factor defects and which factors are involved

Back 208

1. Hemophilia A (factor VIII deficiency)


2. Hemophilia B (factor IX deficiency)

Front 209

Bernard-Soulier disease =

Back 209

defect of platelet adhesion (↓ GP Ib)

Front 210

defect of platelet adhesion (↓ GP Ib)

Back 210

Bernard-Soulier disease

Front 211

Glanzmann’s thrombasthenia =

Back 211

defect of platelet aGgregation (↓ GP IIb-IIIa).

Front 212

defect of platelet aGgregation (↓ GP IIb-IIIa).

Back 212

Glanzmann’s thrombasthenia

Front 213

PT tests for

Back 213

(extrinsic)––factors II, V, VII, and X.

Front 214

test for (extrinsic)––factors II, V, VII, and X.

Back 214

PT

Front 215

dPTT Test

Back 215

(intrinsic)––all factors except VII.

Front 216

test for (intrinsic)––all factors except VII.

Back 216

PTT

Front 217

von Willebrand’s disease mech

Back 217

deficiency of von Willebrand
factor → defect of platelet adhesion and ↓
factor VIII survival)

combined platelet and coagulation problem

Front 218

most common
bleeding disorder

Back 218

von Willebrand’s disease

Front 219

Hodgkin’s cells and markers

Back 219

Presence of Reed-Sternberg cells (RS cells are CD30
and CD15+ B-cell origin)

Front 220

(CD30 and CD15) B-cell origin

Back 220

Reed-Sternberg cells

Front 221

Reed-Sternberg cells origin

Back 221

B-cell

Front 222

Reed-Sternberg cell
markers

Back 222

CD30
and CD15

Front 223

Hodgkin’s location

Back 223

Localized, single group of nodes; extranodal rare; contiguous spread

Front 224

Hodgkin’s Constitutional (“B”) signs/symptoms

Back 224

low-grade fever,
night sweats,
weight loss

Front 225

Hodgkin’s wrt lymphnode appearance

Back 225

Mediastinal lymphadenopathy

Front 226

Hodgkin’s association

Back 226

50% of cases associated with EBV

Front 227

Hodgkin’s who gets wrt age and sex

Back 227

—young and old; more common in men except for nodular sclerosing type

Front 228

Hodgkin’s prognosis markers

Back 228

Good = ↑ lymphocytes, ↓ RS

Front 229

Non-Hodgkin’s Lymphoma

who

Back 229

Peak incidence 20–40 years old

Front 230

Non-Hodgkin’s Lymphoma

associated with

Back 230

Associated with HIV and immunosuppression

Front 231

Non-Hodgkin’s Lymphoma

WRT nodes

Back 231

Multiple, peripheral nodes; extranodal involvement common; noncontiguous spread

Front 232

Non-Hodgkin’s Lymphoma

cell type

Back 232

Majority involve B cells (except those of lymphoblastic T-cell origin)

Front 233

Non-Hodgkin’s Lymphoma

WRT Ig's

Back 233

No hypergammaglobulinemia

Front 234

Non-Hodgkin’s Lymphoma

WRT B symps

Back 234

Fewer constitutional sgns/symptoms

Front 235

Which type of Lymphoma is associated with EBV

Back 235

Hodgkin’s

Front 236

Which type of Lymphoma is associated with
HIV and immunosuppression

Back 236

Non-Hodgkin’s

Front 237

Which type of Hodgkin's Lymphoma

Most common

Back 237

Nodular sclerosing

Front 238

Which type of Hodgkin's Lymphoma

collagen banding and lacunar cells

Back 238

Nodular sclerosing

Front 239

Which type of Hodgkin's Lymphoma

women > men,
primarily young adults.

Back 239

Nodular sclerosing

Front 240

Which type of Hodgkin's Lymphoma

most RS cells.

Back 240

Mixed cellularity

Front 241

Which type of Hodgkin's Lymphoma

Poor prognosis

Back 241

Lymphocyte depleted (rare)

Front 242

Which type of Hodgkin's Lymphoma

Most rare

Back 242

Lymphocyte depleted

Front 243

Which type of Hodgkin's Lymphoma

Older males with disseminated
disease.

Back 243

Lymphocyte depleted (rare)

Front 244

Which type of Hodgkin's Lymphoma

Excellent Prognosis

Back 244

Lymphocyte predominant

and

Nodullar sclerosing

Front 245

Which type of Hodgkin's Lymphoma

Intermediate prognosis

Back 245

Mixed cellularity

Front 246

Monoclonal plasma cell (“fried-egg” appearance) cancer

Back 246

Multiple myeloma

Front 247

Multiple myeloma

where

Back 247

arises in the marrow

Front 248

Multiple myeloma

what is produced

Back 248

Large amounts of IgG (55%) or IgA (25%).

Front 249

Multiple myeloma

how common

Back 249

Most common 1° tumor arising within bone in adults.

Front 250

Multiple myeloma

clinical findings

Back 250

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)

Front 251

Multiple myeloma

Associated with

Back 251

1° amyloidosis

Front 252

Multiple myeloma

WRT imaging

Back 252

punched-out lytic bone lesions on x-ray

Front 253

Multiple myeloma

lab findings

Back 253

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

Front 254

Multiple myeloma

WRT blood smear

Back 254

Blood smear shows RBCs stacked like poker chips
(rouleau formation).

Front 255

Blood smear shows RBCs stacked like poker chips

Back 255

Multiple myeloma
(rouleau formation).

Front 256

rouleau formation aka

Back 256

Blood smear shows RBCs stacked like poker chips

Front 257

Blood smear shows RBCs stacked like poker chips aka

Back 257

(rouleau formation).

Front 258

Waldenström’s macroglobulinemia

Back 258

→M spike = IgM
(→hyperviscosity symptoms); no lytic bone lesions

Front 259

→M spike = IgM
(→hyperviscosity symptoms); no lytic bone lesions

Back 259

Waldenström’s macroglobulinemia

Front 260

Distinctive tumor giant cell seen in Hodgkin’s disease;

Back 260

Reed-Sternberg

Front 261

Reed-Sternberg look

Back 261

binucleate or bilobed with
the 2 halves as mirror images (“owl’s eyes”).

Front 262

Reed-Sternberg variant

Back 262

Variants include lacunar cells in nodular sclerosis

Front 263

Variants include lacunar cells in nodular sclerosis

Back 263

Reed-Sternberg variant

Front 264

binucleate or bilobed with
the 2 halves as mirror images (“owl’s eyes”).

Back 264

Reed-Sternberg look

Front 265

which Non-Hodgkin’s lymphoma

t(14;18) bcl-2 expression

Back 265

Follicular lymphoma
(small cleaved cell)

Front 266

which Non-Hodgkin’s lymphoma

Like CLL with focal mass;
low grade.

Back 266

Small lymphocytic lymphoma

Front 267

which Non-Hodgkin’s lymphoma

Most common (adult).

Back 267

Follicular lymphoma
(small cleaved cell)

Front 268

which Non-Hodgkin’s lymphoma

Difficult to cure; indolent
course; bcl-2 is involved in apoptosis.

Back 268

Follicular lymphoma
(small cleaved cell)

Front 269

which Non-Hodgkin’s lymphoma

80% B cells
20% T cells
(mature)

Back 269

Diffuse large cell

Front 270

which Non-Hodgkin’s lymphoma

Usually older adults, but
20% occur in children

Back 270

Diffuse large cell

Front 271

which Non-Hodgkin’s lymphoma

t(11;14)

Back 271

Mantle cell lymphoma

Front 272

which Non-Hodgkin’s lymphoma

Poor prognosis, CD5+

Back 272

Mantle cell lymphoma

Front 273

which Non-Hodgkin’s lymphoma

Most common in children

Back 273

Lymphoblastic lymphoma

Front 274

which Non-Hodgkin’s lymphoma

T cells (immature)

Back 274

Lymphoblastic lymphoma

Front 275

which Non-Hodgkin’s lymphoma

commonly presents with ALL and
mediastinal mass

Back 275

Lymphoblastic lymphoma

Front 276

which Non-Hodgkin’s lymphoma

very aggressive T-cell
lymphoma.

Back 276

Lymphoblastic lymphoma

Front 277

which Non-Hodgkin’s lymphoma

t(8;14)

Back 277

Burkitt’s lymphoma

Front 278

which Non-Hodgkin’s lymphoma

c-myc

Back 278

Burkitt’s lymphoma

Front 279

which Non-Hodgkin’s lymphoma

“Starry-sky” appearance

Back 279

Burkitt’s lymphoma

Front 280

Burkitt’s lymphoma

Genetics

Back 280

t(8;14) c-myc gene moves next to
heavy-chain Ig gene (14)
c-Myc is a very strong proto-oncogene

Front 281

Burkitt’s lymphoma

associations

Back 281

associated with EBV;jaw lesion in endemic form in Africa; pelvis or
abdomen in sporadic form

Front 282

what exactly is the “Starry-sky” appearance of Burkitt's

Back 282

(sheets of lymphocytes with interspersed macrophages);

Front 283

Burkitt’s lymphoma

appearance

Back 283

“Starry-sky” appearance

Front 284

Mantle cell lymphoma

Genetics

Back 284

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

Front 285

Follicular lymphoma

Genetics

Back 285

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

Front 286

disorder associated with

t(9;22)

Back 286

CML
(Philadelphia chromosome)
(bcr-abl hybrid)

Front 287

disorder associated with

t(8;14)

Back 287

Burkitt’s lymphoma (c-myc activation)

Front 288

disorder associated with

t(14;18)

Back 288

Follicular lymphomas (bcl-2 activation)

Front 289

disorder associated with

t(15;17)

Back 289

M3 type of AML (responsive to all-trans retinoic acid)

Front 290

disorder associated with

t(11;22)

Back 290

Ewing’s sarcoma

Front 291

disorder associated with

t(11;14)

Back 291

Mantle cell lymphoma

Front 292

Translocation associated with

CML

Back 292

t(9;22)
(Philadelphia chromosome)
(bcr-abl hybrid)

Front 293

Translocation associated with

Burkitt’s lymphoma

Back 293

t(8;14)
(c-myc activation)

Front 294

Translocation associated with

Follicular lymphomas

Back 294

t(14;18)
(bcl-2 activation)

Front 295

Translocation associated with

M3 type of AML

Back 295

t(15;17)
(responsive to all-trans retinoic acid)

Front 296

Translocation associated with

Ewing’s sarcoma

Back 296

t(11;22)

Front 297

Translocation associated with

Mantle cell lymphoma

Back 297

t(11;14)

Front 298

Leukemias General considerations

Back 298

↑ number of circulating leukocytes in blood; bone marrow infiltrates of leukemic cells;

Front 299

Leukemias General clinical findings

Back 299

marrow failure can cause anemia (↓ RBCs), infections
(↓ mature WBCs), and hemorrhage (↓ platelets); leukemic cell infiltrates in liver, spleen, and lymph nodes are common

Front 300

Leukemias
and ages

Back 300

<15 = ALL
15-40 = AML
30-60 = CML
>60 = CLL

Front 301

Auer rods; myeloblasts; adults.

Back 301

AML

Front 302

Leukemia most responsive to therapy

Back 302

ALL

Front 303

CLL

clinical findings

Back 303

lymphadenopathy; hepatosplenomegaly; few symptoms; indolent course;

Front 304

CLL

Lab findings

Back 304

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

Front 305

CML

lab findings

Back 305

myeloid stem cell proliferation;
presents with ↑ neutrophils and metamyelocytes;
splenomegaly; Very low leukocyte alkaline
phosphatase (vs. leukemoid reaction).

Front 306

CML vs Leukemoid Rxn

Back 306

Very low leukocyte alkaline
phosphatase (vs. leukemoid reaction).

Front 307

“blast crisis”

Back 307

CML accelerating to AML

Front 308

Very low leukocyte alkaline
phosphatase what does that tell you WRT WBC's

Back 308

That it is CML and not leukemoid reaction).

Front 309

final phase of CML

Back 309

Blast crisis accelerating to AML

Front 310

Auer rods

what are they

Back 310

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

Front 311

Auer rods

when seen

Back 311

Primarily in acute promyelocytic leukemia (M3).

Front 312

Auer rods

why problematic

Back 312

Treatment of AML M3 can
release Auer rods → DIC.

Front 313

Histiocytosis X

caused by

Back 313

Caused by Langerhans' cells from the monocyte lineage that infiltrate the lung.

Front 314

peroxidase-positive cytoplasmic inclusions in granulocytes and myeloblasts

Back 314

Auer rods

Front 315

Histiocytosis X

who gets

Back 315

Primarily affects young adults. Worse with smoking.

Front 316

Caused by Langerhans' cells from the monocyte lineage that infiltrate the lung.

Back 316

Histiocytosis X

Front 317

Histiocytosis X

clinical features

Back 317

range from isolated bone lesions to multisystemic disease.

Front 318

Heparin

Mechanism

Back 318

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

Front 319

Heparin

Clinical use

Back 319

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

Front 320

Heparin

Toxicity

Back 320

Bleeding, thrombocytopenia, drug-drug interaction

Front 321

Heparin

how to monitor

Back 321

Follow PTT.

Front 322

Heparin

Reversal

Back 322

protamine sulfate (positively charged molecule that acts by
binding negatively charged heparin).

Front 323

low-molecular-weight heparins

names

Back 323

enoxaparin

Front 324

low-molecular-weight heparins

effects and advatages

Back 324

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.

Front 325

low-molecular-weight heparins

disadvantage

Back 325

Not easily reversible.

Front 326

Heparin

Half-life

Back 326

Short (1.5 Hours)

Front 327

Warfarin aka

Back 327

Coumadin

Front 328

Coumadin aka

Back 328

Warfarin

Front 329

Warfarin

Mechanism

Back 329

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

Front 330

Warfarin

Clinical use

Back 330

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

Front 331

Warfarin

Toxicity

Back 331

Bleeding, teratogenic, drug-drug interactions.

Front 332

Warfarin

Monitoring

Back 332

The EX-PaT went to
WAR(farin).

EXtrinsic pathway and ↑ PT.

Front 333

Warfarin

Half-life

Back 333

Long

2 days

Front 334

Heparin vs. warfarin

Structure

Back 334

Heparin-Large anionic polymer, acidic

Warfarin-Small lipid-soluble molecule

Front 335

Heparin vs. warfarin

administration

Back 335

Heparin- Parenteral (IV, SC)

Warfarin- Oral

Front 336

Heparin vs. warfarin

Site of action

Back 336

Heparin-Blood

Warfarin-Liver

Front 337

Heparin vs. warfarin

Onset of action

Back 337

Heparin-Rapid (sec)

Warfarin-Slow (days)

Front 338

Heparin vs. warfarin

Mechanism of action

Back 338

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)

Front 339

Heparin vs. warfarin

Duration of action

Back 339

Heparin- Acute (hours)

Warfarin-Chronic (weeks or months)

Front 340

Heparin vs. warfarin

Inhibits coagulation
in vitro

Back 340

Heparin-yes

Warfarin-no

Front 341

Heparin vs. warfarin

Treatment of acute
overdose

Back 341

Heparin-Protamine Sulfate

Warfarin-IV vit K and Fresh frozen plasma

Front 342

Heparin vs. warfarin

Monitoring

Back 342

Heparin-PTT (intrinsic)

Warfarin-PT (extrinsic)

Front 343

Heparin vs. warfarin

Crosses placenta

Back 343

Heparin-No

Warfarin- Yes (teratogenic)

Front 344

Thrombolytics

Names

Back 344

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

Front 345

Thrombolytics

Mechanism

Back 345

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

Front 346

Thrombolytics

Clinical use

Back 346

Early MI,
early ischemic stroke.

Front 347

Thrombolytics

Toxicity

Back 347

Bleeding.

Front 348

Thrombolytics

contraindications

Back 348

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

Front 349

Thrombolytics

Toxicity Tx

Back 349

aminocaproic acid, an inhibitor of fibrinolysis.

Front 350

aminocaproic acid

clinical use

Back 350

Tx of Thrombolytics Toxicity

Front 351

aminocaproic acid

mech

Back 351

inhibitor of Plasminogen to pasmin

Front 352

Aspirin aka

Back 352

ASA

Front 353

ASA aka

Back 353

Aspirin

Front 354

Aspirin (ASA)

Mechanism

Back 354

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

Front 355

Aspirin (ASA)

Clinical use

Back 355

Antipyretic,
analgesic,
anti-inflammatory,
antiplatelet drug.

Front 356

Aspirin (ASA)

Toxicity

Back 356

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

Front 357

Aspirin

WRT lab values (homeostasis)

Back 357

↑ bleeding time.
No effect on PT, PTT.

Front 358

Drugs that Inhibit platelet aggregation by irreversibly blocking ADP receptor

Back 358

Clopidogrel, ticlopidine

Front 359

Clopidogrel has the same effects/mech as ?

Back 359

ticlopidine

Front 360

ticlopidine has the same effects/mech as ?

Back 360

Clopidogrel

Front 361

Clopidogrel

Mechanism

Back 361

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

Front 362

Clopidogrel

Clinical use

Back 362

Acute coronary syndrome; coronary stenting. ↓ incidence or recurrence of
thrombotic stroke.

Front 363

Clopidogrel or Ticlopidine

Neutropenia

Back 363

Ticlopidine

Front 364

Ticlopidine

Toxicity

Back 364

Neutropenia

Front 365

Acetylates and irreversibly inhibits cyclooxygenase (both COX-1 and COX-2)

Back 365

Aspirin (ASA)

Front 366

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

Back 366

Abciximab

Front 367

Abciximab

Mechanism

Back 367

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

Front 368

Abciximab

Clinical use

Back 368

Acute coronary syndromes, percutaneous transluminal coronary angioplasty.

Front 369

Abciximab

Toxicity

Back 369

Bleeding, thrombocytopenia.

Front 370

Cancer drugs

which are Cell cycle specific

Back 370

antimetabolites (MTX, 5-FU, 6-MP),
Cytarabine(ara-c),
Hydroxyurea,
etoposide,
bleomycin,
vincristine/vinblastine,
paclitaxel and other taxols.

Front 371

Cancer drugs

which are Cell cycle nonspecific

Back 371

alkylating agents, antibiotics (dactinomycin, doxorubicin, bleomycin).

Front 372

Methotrexate (MTX)

Mechanism

Back 372

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

Front 373

Methotrexate (MTX)

Clinical use

Back 373

Leukemias, lymphomas, choriocarcinoma, sarcomas. Abortion, ectopic pregnancy,
rheumatoid arthritis, psoriasis.

Front 374

Methotrexate (MTX)

Toxicity

Back 374

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

Front 375

Methotrexate (MTX)

Toxicity Tx

Back 375

Myelosuppression, which is reversible with leucovorin (folinic acid) “rescue.”

Front 376

leucovorin use

Back 376

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

Front 377

leucovorin aka

Back 377

folinic acid

Front 378

folinic acid aka

Back 378

leucovorin

Front 379

5-fluorouracil (5-FU)

Mechanism

Back 379

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.

Front 380

5-fluorouracil (5-FU)

Clinical use

Back 380

Colon cancer and other solid tumors, basal cell carcinoma (topical). Synergy with
MTX.

Front 381

5-fluorouracil (5-FU)

Toxicity

Back 381

Myelosuppression, which is NOT reversible with leucovorin; photosensitivity. Can "rescue" with thymidine.

Front 382

Synergy with MTX.

Back 382

5-fluorouracil

Front 383

Synergy with 5-fluorouracil

Back 383

MTX.

Front 384

5-fluorouracil (5-FU)

Toxicity Tx

Back 384

Myelosuppression, which is NOT reversible with leucovorin; photosensitivity.
Can "rescue" with thymidine.

Front 385

Blocks de novo purine synthesis. Activated by HGPRTase.

Back 385

6-mercaptopurine (6-MP)

Front 386

6-mercaptopurine (6-MP)

Mechanism

Back 386

S-phase specific Blocks de novo purine synthesis. Activated by HGPRTase.

Front 387

6-mercaptopurine (6-MP)

Clinical use
Toxicity

Back 387

Leukemias, lymphomas (not CLL or Hodgkin’s).

Front 388

6-mercaptopurine (6-MP)

Toxicity

Back 388

Bone marrow, GI, liver. Metabolized by xanthine oxidase; thus ↑ toxicity with allopurinol.

Front 389

Cytarabine aka

Back 389

ara-C

Front 390

ara-C aka

Back 390

Cytarabine

Front 391

Cytarabine (ara-C)

Mechanism

Back 391

Inhibits DNA polymerase.

Front 392

Cytarabine (ara-C)

Clinical use

Back 392

AML.

Front 393

Cytarabine (ara-C)

Toxicity

Back 393

Leukopenia, thrombocytopenia, megaloblastic anemia.

Front 394

Cyclophosphamide

Mechanism

Back 394

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

Front 395

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

Back 395

Cyclophosphamide, ifosfamide

Front 396

Cyclophosphamide

Clinical use

Back 396

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

Front 397

Cyclophosphamide

Toxicity

Back 397

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

Front 398

ifosfamide

mechanism

Back 398

Same as Cyclophosphamide

Front 399

Nitrosoureas

Names

Back 399

Carmustine, lomustine, semustine, streptozocin.

Front 400

Nitrosoureas

Mechanism

Back 400

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

Front 401

Nitrosoureas

Clinical use

Back 401

Brain tumors (including glioblastoma multiforme).

Front 402

Nitrosoureas

Toxicity

Back 402

CNS toxicity (dizziness, ataxia).

Front 403

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

Back 403

Nitrosoureas:
Carmustine,
lomustine,
semustine,
streptozocin.

Front 404

Cisplatin and carboplatin

Mechanism

Back 404

Act like alkylating agents.

Front 405

Cisplatin and carboplatin

Clinical use

Back 405

Testicular, bladder, ovary, and lung carcinomas.

Front 406

Cisplatin and carboplatin

Toxicity

Back 406

Nephrotoxicity and acoustic nerve damage.

Front 407

Busulfan

Mechanism

Back 407

Alkylates DNA.

Front 408

Busulfan

Clinical use

Back 408

CML.

Front 409

Busulfan

Toxicity

Back 409

Pulmonary fibrosis, hyperpigmentation.

Front 410

Doxorubicin (Adriamycin), daunorubicin

Mechanism

Back 410

Generate free radicals and noncovalently intercalate in DNA (creating breaks in DNA
strand to ↓ replication).

Front 411

Doxorubicin (Adriamycin), daunorubicin

Clinical use

Back 411

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

Front 412

Doxorubicin (Adriamycin), daunorubicin


Toxicity

Back 412

Cardiotoxicity; also myelosuppression and marked alopecia. Toxic extravasation.

Front 413

Generate free radicals and noncovalently intercalate in DNA (creating breaks in DNA
strand to ↓ replication).

Back 413

Doxorubicin (Adriamycin), daunorubicin

Front 414

Dactinomycin aka

Back 414

actinomycin D

Front 415

actinomycin D aka

Back 415

Dactinomycin

Front 416

Dactinomycin

Mechanism

Back 416

Intercalates in DNA.

Front 417

Dactinomycin

Clinical use

Back 417

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

Front 418

Dactinomycin

Toxicity

Back 418

Myelosuppression.

Front 419

Bleomycin

Mechanism

Back 419

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

Front 420

Bleomycin

Clinical use

Back 420

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

Front 421

Bleomycin

Toxicity

Back 421

Pulmonary fibrosis, skin changes, but minimal myelosuppression.

Front 422

Hydroxyurea

Mechanism

Back 422

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

Front 423

Hydroxyurea

Clinical use

Back 423

Melanoma, CML, and Sickle Cell disease

Front 424

Hydroxyurea

Toxicity

Back 424

Bone marrow supression and GI upset

Front 425

Prednisone

Mechanism

Back 425

May trigger apoptosis. May even work on nondividing cells.

Front 426

Prednisone

Clinical use

Back 426

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.

Front 427

Prednisone

Toxicity

Back 427

Cushing-like symptoms; immunosuppression, cataracts, acne, osteoporosis, hypertension,
peptic ulcers, hyperglycemia, psychosis.

Front 428

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

Back 428

Tamoxifen, raloxifene

Front 429

Tamoxifen, raloxifene

Mechanism

Back 429

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

Front 430

Tamoxifen, raloxifene

Clinical use

Back 430

Breast cancer. Also useful to prevent osteoporosis.

Front 431

Tamoxifen, raloxifene

Toxicity

Back 431

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.

Front 432

Trastuzumab aka

Back 432

Herceptin

Front 433

Herceptin aka

Back 433

Trastuzumab

Front 434

Trastuzumab

Mechanism

Back 434

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

Front 435

Trastuzumab

Clinical use

Back 435

Metastatic breast cancer.

Front 436

Trastuzumab

Toxicity

Back 436

Cardiotoxicity.

Front 437

Monoclonal antibody against HER-2 (erb-B2).

Back 437

Trastuzumab (Herceptin)

Front 438

Philadelphia chromosome brc-abl tyrosine kinase inhibitor.

Back 438

Imatinib (Gleevec)

Front 439

Gleevec aka

Back 439

Imatinib

Front 440

Imatinib aka

Back 440

Gleevec

Front 441

Imatinib

Mechanism

Back 441

Philadelphia chromosome brc-abl tyrosine kinase inhibitor.

Front 442

Imatinib

Clinical use

Back 442

CML, GI stromal tumors.

Front 443

Imatinib

Toxicity

Back 443

Fluid retention.

Front 444

Vincristine, vinblastine

Mechanism

Back 444

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

Front 445

Vincristine, vinblastine

Clinical use

Back 445

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

Front 446

Vincristine, vinblastine

Toxicity

Back 446

Vincristine––neurotoxicity (areflexia, peripheral neuritis), paralytic ileus.
VinBLASTine BLASTs Bone marrow (suppression).

Front 447

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

Back 447

Vincristine, vinblastine

Front 448

Paclitaxel, other taxols

Mechanism

Back 448

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

Front 449

Paclitaxel, other taxols

Clinical use

Back 449

Ovarian and breast carcinomas.

Front 450

Paclitaxel, other taxols

Toxicity

Back 450

Myelosuppression and hypersensitivity.

Front 451

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

Back 451

Paclitaxel, other taxols

Front 452

Which Cancer Drug

Myelosuppression, which is reversible with leucovorin (folinic acid) “rescue.”

Back 452

Methotrexate (MTX)

Front 453

Which Cancer Drug

Myelosuppression, which is NOT reversible with leucovorin; photosensitivity.
Can "rescue" with thymidine.

Back 453

5-fluorouracil (5-FU)

Front 454

Which Cancer Drug

Bone marrow, GI, liver. Metabolized by xanthine oxidase; thus ↑ toxicity with allopurinol.

Back 454

6-mercaptopurine (6-MP)

Front 455

Which Cancer Drug

Leukopenia, thrombocytopenia, megaloblastic anemia.

Back 455

Cytarabine (ara-C)

Front 456

Which Cancer Drug

used for AML only

Back 456

Cytarabine (ara-C)

Front 457

Which Cancer Drug

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

Back 457

Cyclophosphamide, ifosfamide

Front 458

Which Cancer Drug

Also immunosuppressants.

Back 458

Cyclophosphamide, ifosfamide

and

Prednisone

Front 459

Which Cancer Drug

CNS toxicity (dizziness, ataxia).

Back 459

Nitrosoureas

Front 460

Which Cancer Drug

Nephrotoxicity and acoustic nerve damage.

Back 460

Cisplatin, carboplatin

Front 461

Which Cancer Drug

used for Brain tumors (including glioblastoma multiforme).

Back 461

Nitrosoureas

Front 462

Which Cancer Drug

Pulmonary fibrosis, skin changes

Back 462

Busulfan
and
Bleomycin

Front 463

Which Cancer Drug

used for CML not Gleevac.

Back 463

Busulfan

Front 464

Which Cancer Drug

Cardiotoxicity; also myelosuppression and marked alopecia. Toxic extravasation.

Back 464

Doxorubicin (Adriamycin), daunorubicin

Front 465

Which Cancer Drug

used for Wilms’ tumor, Ewing’s sarcoma, rhabdomyosarcoma.

Back 465

Dactinomycin (actinomycin D)

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

Front 466

Which Cancer Drug

Pulmonary fibrosis, skin changes, but minimal myelosuppression.

Back 466

Bleomycin

Front 467

Which Cancer Drug

Myelosuppression, GI irritation, alopecia.

Back 467

Etoposide (VP-16)

Front 468

Which Cancer Drug

does not cause endometrial carcinoma because it is an
endometrial antagonist.

Back 468

Raloxifene

Front 469

Which Cancer Drug

used for Metastatic breast cancer.

Back 469

Trastuzumab (Herceptin)

Front 470

Which Cancer Drug

Fluid retention.

Back 470

Imatinib (Gleevec)

Front 471

Which Cancer Drug

neurotoxicity (areflexia, peripheral neuritis), paralytic ileus.

Back 471

Vincristine

Front 472

Which Cancer Drug

Myelosuppression and hypersensitivity.

Back 472

Paclitaxel, other taxols

Front 473

causes of normocytic, normochromic Anemia

with increase in Reticulocytes
and inherited

Back 473

Hereditary spherocytosis
G6PD dificiency
PK deficiency
Sickle cell

Front 474

causes of normocytic, normochromic Anemia

with increase in Reticulocytes
and aquired

Back 474

Autoimune (cold and warm)
Alloimune
Trauma(HUS/TTP/DIC/HELLP/mechanical valves)
Hypersplenism
PNH
Infection
Toxin
Osmotic damage
blood loss (non acute)

Front 475

Etoposide (VP-16)

Mechanism

Back 475

G2-phase-specific agent that inhibits topoisomerase II and ↑ DNA degradation.

Front 476

Etoposide (VP-16)

Clinical use

Back 476

Small cell carcinoma of the lung and prostate, testicular carcinoma.

Front 477

Etoposide (VP-16)

Toxicity

Back 477

Myelosuppression, GI irritation, alopecia.

Front 478

Etoposide aka

Back 478

VP-16

Front 479

VP-16 aka

Back 479

Etoposide

Front 480

PNH

1. Screen

2. Confirm

Back 480

1. sucrose lysis test

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