11 Heme/onc

Front 1

Question

Back 1

Answer

Front 2

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

Back 2

Spherocytosis.

Front 3

What is the danger of giving folate alone?

Back 3

Masks signs of neural damage with vitamin B12 deficiency.

Front 4

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 4

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

Front 5

What neoplasms are associated with AIDS?

Back 5

B-cell lymphoma, Kaposi’s sarcoma.

Front 6

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 6

Doxorubicin (cardiotoxic).

Front 7

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 7

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

Front 8

WBC differential from highest to lowest:

Back 8

Neutrophils Like Making Everything Better. Neutrophils Lymphocytes Monocytes Eosinophils Basophils

Front 9

Erythrocytosis =

Back 9

polycythemia = ↑ number of red cells.

Front 10

polycythemia =

Back 10

Erythrocytosis = ↑ number of red cells.

Front 11

Anisocytosis =

Back 11

varying sizes.

Front 12

RBC varying sizes =

Back 12

Anisocytosis

Front 13

Poikilocytosis =

Back 13

varying shapes.

Front 14

RBC varying shapes =

Back 14

Poikilocytosis

Front 15

Reticulocyte =

Back 15

immature erythrocyte.

Front 16

immature erythrocyte=

Back 16

Reticulocyte

Front 17

Normal Erythrocyte shape and why

Back 17

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

Front 18

Erythrocyte energy source

Back 18

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

Front 19

Erythrocyte life span

Back 19

120 Days

Front 20

Erythrocyte days. Membrane contains what and why is it important

Back 20

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 21

Leukocyte types

Back 21

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

Front 22

Leukocyte normal #'s

Back 22

Normally 4000–10,000 per microliter.

Front 23

Basophil #'s and where found

Back 23

< 1% of all leukocytes Found in the blood.

Front 24

Basophil nuclues shape

Back 24

Bilobate nucleus.

Front 25

Basophil granule contnets

Back 25

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

Front 26

what cell Mediates allergic reaction

Back 26

Mast cell and Basophil

Front 27

Mast cell where found

Back 27

Found in tissue.

Front 28

Mast cell what cells are they like

Back 28

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

Front 29

Mast cell granule contents

Back 29

histamine, heparin, and eosinophil chemotactic factors.

Front 30

Mast cell wrt Ig binding

Back 30

Can bind IgE to membrane.

Front 31

Mast cell which type of hypersensitivity reactions

Back 31

type I

Front 32

Cromolyn sodium prevents

Back 32

mast cell degranulation

Front 33

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

Back 33

Cromolyn sodium

Front 34

Cromolyn sodium is used to treat?

Back 34

asthma).

Front 35

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

Back 35

Eosinophil

Front 36

Eosinophil %'s

Back 36

1–6% of all leukocytes.

Front 37

Eosinophil structure

Back 37

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

Front 38

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

Back 38

Eosinophil

Front 39

Eosinophil major function and mech

Back 39

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

Front 40

Eosinophil produces what

Back 40

major basic protein histaminase arylsulfatase.

Front 41

Causes of eosinophilia

Back 41

NAACP: Neoplastic Asthma Allergic processes Collagen vascular diseases Parasites

Front 42

Neutrophil what type of response cell

Back 42

Acute inflammatory response cell

Front 43

Neutrophil %'s

Back 43

40–75% WBCs.

Front 44

Hypersegmented polys are seen in

Back 44

vitamin B12/folate deficiency.

Front 45

Neutrophil granules and contents

Back 45

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

Front 46

Monocyte %'s

Back 46

2-10% of leukocytes

Front 47

Monocyte structure and what they do

Back 47

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

Front 48

Differentiates into macrophages in tissues

Back 48

Monocyte

Front 49

Macrophage function

Back 49

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

Front 50

Macrophage life span

Back 50

long life in tissues

Front 51

Macrophage activation

Back 51

Activated by gamma-interferon.

Front 52

Lymphocyte appearance

Back 52

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

Front 53

in general what is the role of lymphocytes

Back 53

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

Front 54

B lymphocyte cell markers

Back 54

CD19 CD20

Front 55

B lymphocyte is involved in which immune response

Back 55

Humoral

Front 56

B lymphocytes arise from what and mature where

Back 56

Arises from stem cells in bone marrow. Matures in marrow.

Front 57

B lymphocyte initial migration

Back 57

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

Front 58

B lymphocytes when antigen is encountered

Back 58

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

Front 59

Off-center nucleus, clock-face chromatin

Back 59

Plasma cell

Front 60

Plasma cell structure

Back 60

Off-center nucleus, clock-face chromatin. abundant RER and ell-developed Golgi apparatus.

Front 61

Plasma cell function

Back 61

produce large amounts of antibody specific to a particular antigen.

Front 62

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

Back 62

plasma cell

Front 63

T lymphocyte is involed in what type of immune response

Back 63

Mediates cellular immune response

Front 64

T lymphocyte origins and maturation

Back 64

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

Front 65

T lymphocyte differentiation and cell markers

Back 65

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

Front 66

T lymphocyte CD mnemonic

Back 66

MHC × CD = 8 (e.g., MHC 2 ×CD4 = 8, and MHC 1 × CD8 = 8).

Front 67

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

Back 67

Dendritic cells

Front 68

Called Langerhans cells on skin.

Back 68

Dendritic cells

Front 69

Dendritic cells on the skin aka

Back 69

Langerhans cells

Front 70

Dendritic cells function

Back 70

Professional APCs. Express MHC II and Fc receptor (FcR) on surface Main inducers of 1° antibody response.

Front 71

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

Back 71

Basophil

Front 72

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

Back 72

Basophil

Front 73

Which WBC histamine, heparin, and eosinophil chemotactic

Back 73

Mast cell

Front 74

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

Back 74

Mast cell

Front 75

Which WBC Highly phagocytic for antigen-antibody complexes.

Back 75

Eosinophil

Front 76

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

Back 76

Neutrophil

Front 77

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

Back 77

Monocyte

Front 78

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

Back 78

Lymphocyte

Front 79

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

Back 79

Dendritic cells

Front 80

Which WBC Called Langerhans cells on skin.

Back 80

Dendritic cells

Front 81

Protein C and protein S function and dependance

Back 81

inactivate Va and VIIIa; vitamin K–dependent.

Front 82

inactivate Va and VIIIa; vitamin K–dependent.

Back 82

Protein C and protein S

Front 83

Antithrombin III function and activation

Back 83

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

Front 84

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

Back 84

Antithrombin III

Front 85

Factor V Leiden mutation mech

Back 85

resistance to activated protein C.

Front 86

genetic resistance to activated protein C.

Back 86

Factor V Leiden

Front 87

tPA mech

Back 87

generates plasmin, which cleaves fibrin.

Front 88

generates plasmin, which cleaves fibrin.

Back 88

tPA

Front 89

Ag's and Ab's for different Blood Types A

Back 89

A antigen on RBC surface B antibody in plasma.

Front 90

Ag's and Ab's for different Blood Types B

Back 90

B antigen on RBC surface A antibody in plasma.

Front 91

Ag's and Ab's for different Blood Types AB

Back 91

A and B antigens on RBC surface, No Ab's "universal recipient."

Front 92

Ag's and Ab's for different Blood Types O

Back 92

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

Front 93

Incompatible blood transfusions can cause

Back 93

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

Front 94

RBC forms when do you see Biconcave

Back 94

Normal.

Front 95

RBC forms when do you see Spherocytes

Back 95

Hereditary spherocytosis, autoimmune hemolysis.

Front 96

RBC forms when do you see Elliptocyte

Back 96

Hereditary elliptocytosis.

Front 97

RBC forms when do you see Macro-ovalocye

Back 97

Megaloblastic anemia, marrow failure.

Front 98

RBC forms when do you see Helmet cell, schistocyte

Back 98

DIC, traumatic hemolysis.

Front 99

RBC forms when do you see Sickle cell

Back 99

Sickle cell anemia.

Front 100

RBC forms when do you see Teardrop cell

Back 100

Myeloid metaplasia with myelofibrosis.

Front 101

RBC forms when do you see Acanthocyte

Back 101

Spiny appearance in abetalipoproteinemia.

Front 102

RBC forms when do you see Target cell

Back 102

HALT. HbC disease, Asplenia, Liver disease, Thalassemia.

Front 103

RBC forms when do you see Poikilocytes

Back 103

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

Front 104

RBC forms when do you see Burr cell

Back 104

TTP/HUS.

Front 105

What RBC forms do you see in Normal.

Back 105

Biconcave

Front 106

What RBC forms do you see in Hereditary spherocytosis

Back 106

Spherocytes

Front 107

What RBC forms do you see in autoimmune hemolysis.

Back 107

Spherocytes

Front 108

What RBC forms do you see in Hereditary elliptocytosis.

Back 108

Elliptocyte

Front 109

What RBC forms do you see in Megaloblastic anemia

Back 109

Macro-ovalocyte also hypersegmented PMNs

Front 110

What RBC forms do you see in marrow failure.

Back 110

Macro-ovalocyte

Front 111

What RBC forms do you see in DIC

Back 111

Helmet cell, schistocyte, Poikilocytes

Front 112

What RBC forms do you see in traumatic hemolysis.

Back 112

Helmet cell, schistocyte

Front 113

What RBC forms do you see in Sickle cell anemia.

Back 113

Sickle cell

Front 114

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

Back 114

Teardrop cell

Front 115

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

Back 115

Acanthocyte

Front 116

What RBC forms do you see in HbC disease

Back 116

Target cell HALT.

Front 117

What RBC forms do you see in Asplenia

Back 117

Target cell HALT.

Front 118

What RBC forms do you see in Liver disease

Back 118

Target cell HALT.

Front 119

What RBC forms do you see in Thalassemia.

Back 119

Target cell HALT.

Front 120

What RBC forms do you see in TTP/HUS.

Back 120

Poikilocytes Burr cell

Front 121

What RBC forms do you see in microvascular damage

Back 121

Poikilocytes

Front 122

Psammoma bodies when

Back 122

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

Front 123

Laminated, concentric, calcific spherules aka

Back 123

Psammoma bodies

Front 124

Psammoma bodies what

Back 124

Laminated, concentric, calcific spherules

Front 125

causes of Microcytic, hypochromic Anemia

Back 125

Iron deficiency– Thalassemias Lead poisoning,

Front 126

causes of macrocytic Anemia

Back 126

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

Front 127

causes of normocytic, normochromic Anemia with no increase in Reticulocytes

Back 127

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

Front 128

↓ serum haptoglobin and ↑ serum LDH indicate

Back 128

RBC hemolysis. Direct

Front 129

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

Back 129

↓ serum haptoglobin and ↑ serum LDH indicate

Front 130

What type of Anemia do you get in Iron deficiency

Back 130

Microcytic, hypochromic

Front 131

What type of Anemia do you get in Thalassemias

Back 131

Microcytic, hypochromic

Front 132

What type of Anemia do you get in Lead poisoning

Back 132

Microcytic, hypochromic

Front 133

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

Back 133

Macrocytic, Megaloblastic

Front 134

What type of Anemia do you get in sulfa drugs

Back 134

Macrocytic

Front 135

What type of Anemia do you get in AZT

Back 135

Macrocytic

Front 136

What type of Anemia do you get in G6PD deficiency

Back 136

Normocytic, normochromic

Front 137

What type of Anemia do you get in Acute Hemorrhage

Back 137

Normocytic, normochromic

Front 138

What type of Anemia do you get in PK deficiency

Back 138

Normocytic, normochromic

Front 139

What type of Anemia do you get in Heredotary Spherocytosis

Back 139

Normocytic, normochromic

Front 140

What type of Anemia do you get in aplastic anemia

Back 140

Normocytic, normochromic

Front 141

What type of Anemia do you get in leukemia

Back 141

Normocytic, normochromic

Front 142

What type of Anemia do you get in Sickle Cell

Back 142

Normocytic, normochromic

Front 143

What type of Anemia do you get in Autoimmune hemolytic anemia

Back 143

Normocytic, normochromic

Front 144

What type of Anemia do you get in Anemia of chronic disease (ACD)

Back 144

Normocytic, normochromic

Front 145

Lab values in Iron deficiency–

Back 145

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

Front 146

Lab values in Anemia of chronic disease (ACD)

Back 146

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

Front 147

Lab values in Pregnacy/OCP use wrt Iron

Back 147

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

Front 148

Lab values in Hereditary Hemochromatosis

Back 148

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

Front 149

Unlike folate deficiency, vitamin B12 deficiency is associated with

Back 149

neurologic problems.

Front 150

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

Back 150

Direct Coombs

Front 151

causes of Aplastic anemia

Back 151

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 152

Aplastic anemia Symptoms

Back 152

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

Front 153

Aplastic anemia Pathologic features

Back 153

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

Front 154

Aplastic anemia Treatment

Back 154

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

Front 155

Aplastic anemia Dx

Back 155

Diagnose with bone marrow biopsy.

Front 156

HbS mutation

Back 156

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

Front 157

Sickle cell anemia what precipitates sickling.

Back 157

Low O2 or dehydration

Front 158

Sickle cell anemia Heterozygotes aka and features

Back 158

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

Front 159

Sickle cell anemia homozygotes aka

Back 159

sickle cell disease

Front 160

Sickle cell anemia Complications in homozygotes

Back 160

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

Front 161

Sickle cell anemia Tx

Back 161

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

Front 162

Sickle cell anemia HbC

Back 162

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 163

Sickle cell anemia HbS

Back 163

The Bad allele

Front 164

Sickle cell anemia The Bad allele

Back 164

HbS

Front 165

Sickle cell anemia The less Bad allele

Back 165

HbC

Front 166

Sickle cell anemia epidemiology wrt blacks

Back 166

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

Front 167

“Crew cut” on skull x-ray who and why

Back 167

thalassemias and SCD marrow expansion/↑ erythropoiesis

Front 168

α-thalassemia genetics and problems wrt compensation

Back 168

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 169

α-thalassemia types

Back 169

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 170

α-thalassemia is prevalent in

Back 170

(α=A) Asia and Africa.

Front 171

β-thalassemia is prevalent in

Back 171

Mediterranean populations.

Front 172

thalassemia is prevalent in Asia and Africa.

Back 172

(α=A) α-thalassemia

Front 173

thalassemia is prevalent in Mediterranean populations

Back 173

β-thalassemia

Front 174

β-thalassemia different types and genes

Back 174

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

Front 175

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

Back 175

Both major and minor

Front 176

β-thalassemia wrt Compensation

Back 176

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

Front 177

clinical findings and complications of β-thalassemia major

Back 177

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

Front 178

Hemolytic anemias lab values/what is increased

Back 178

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

Front 179

Where is the hemolysis in Autoimmune anemia

Back 179

Mostly extravascular

Front 180

Where is the hemolysis in Hereditary spherocytosis

Back 180

extravascular

Front 181

Where is the hemolysis in Paroxysmal nocturnal hemoglobinuria

Back 181

Intravascular

Front 182

Where is the hemolysis in Microangiopathic anemia

Back 182

Intravascular

Front 183

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

Back 183

Microangiopathic anemia

Front 184

Microangiopathic anemia what is it and what are its causes

Back 184

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

Front 185

Autoimmune anemia wrt Warm Agglutinin

Back 185

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

Front 186

Autoimmune anemia wrt Cold Agglutinin

Back 186

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

Front 187

Autoimmune anemia wrt babies

Back 187

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

Front 188

Autoimmune hemolytic anemia WRT Coombs

Back 188

Coombs positive.

Front 189

Hereditary spherocytosis anemia WRT Coombs

Back 189

Coombs negative.

Front 190

Hereditary spherocytosis confirmation

Back 190

Osmotic fragility test used to confirm.

Front 191

Hemolytic anemias where Osmotic fragility test used to confirm.

Back 191

Hereditary spherocytosis

Front 192

Hereditary spherocytosis mech and structure

Back 192

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

Front 193

Hereditary spherocytosis after spleenectomy

Back 193

Howell-jolly bodies

Front 194

Howell-jolly bodies are present when

Back 194

Hereditary spherocytosis after spleenectomy

Front 195

Paroxysmal nocturnal hemoglobinuria mech

Back 195

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

Front 196

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

Back 196

Paroxysmal nocturnal hemoglobinuria

Front 197

Paroxysmal nocturnal hemoglobinuria lab test

Back 197

↑ urine hemosiderin.

Front 198

DIC What is it

Back 198

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

Front 199

DIC causes

Back 199

STOP Making New Thrombi! Sepsis (gram-negative), Trauma, Obstetric complications acute Pancreatitis, Malignancy, Nephrotic syndrome, Transfusion

Front 200

DIC Lab findings

Back 200

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

Front 201

DIC on blood smear.

Back 201

Helmet-shaped cells and schistocytes

Front 202

Platelet abnormalities clinical findings

Back 202

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

Front 203

Coagulation factor defects Clinical findings

Back 203

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

Front 204

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

Back 204

Platelet abnormalities

Front 205

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

Back 205

Coagulation factor defects

Front 206

Name 5 Platelet abnormality causes

Back 206

ITP TTP DIC Aplastic Anemia Immunosupressive drugs

Front 207

Clinical/Lab findings in ITP

Back 207

antiplatelet antibodies, ↑ megakaryocytes young and less severe that TTP

Front 208

Clinical/Lab findings in TTP

Back 208

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

Front 209

Coagulation factor defects and which factors are involved

Back 209

1. Hemophilia A (factor VIII deficiency) 2. Hemophilia B (factor IX deficiency)

Front 210

Bernard-Soulier disease =

Back 210

defect of platelet adhesion (↓ GP Ib)

Front 211

defect of platelet adhesion (↓ GP Ib)

Back 211

Bernard-Soulier disease

Front 212

Glanzmann’s thrombasthenia =

Back 212

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

Front 213

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

Back 213

Glanzmann’s thrombasthenia

Front 214

PT tests for

Back 214

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

Front 215

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

Back 215

PT

Front 216

dPTT Test

Back 216

(intrinsic)––all factors except VII.

Front 217

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

Back 217

PTT

Front 218

von Willebrand’s disease mech

Back 218

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

Front 219

most common bleeding disorder

Back 219

von Willebrand’s disease

Front 220

Hodgkin’s cells and markers

Back 220

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

Front 221

(CD30 and CD15) B-cell origin

Back 221

Reed-Sternberg cells

Front 222

Reed-Sternberg cells origin

Back 222

B-cell

Front 223

Reed-Sternberg cell markers

Back 223

CD30 and CD15

Front 224

Hodgkin’s location

Back 224

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

Front 225

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

Back 225

low-grade fever, night sweats, weight loss

Front 226

Hodgkin’s wrt lymphnode appearance

Back 226

Mediastinal lymphadenopathy

Front 227

Hodgkin’s association

Back 227

50% of cases associated with EBV

Front 228

Hodgkin’s who gets wrt age and sex

Back 228

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

Front 229

Hodgkin’s prognosis markers

Back 229

Good = ↑ lymphocytes, ↓ RS

Front 230

Non-Hodgkin’s Lymphoma who

Back 230

Peak incidence 20–40 years old

Front 231

Non-Hodgkin’s Lymphoma associated with

Back 231

Associated with HIV and immunosuppression

Front 232

Non-Hodgkin’s Lymphoma WRT nodes

Back 232

Multiple, peripheral nodes; extranodal involvement common; noncontiguous spread

Front 233

Non-Hodgkin’s Lymphoma cell type

Back 233

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

Front 234

Non-Hodgkin’s Lymphoma WRT Ig's

Back 234

No hypergammaglobulinemia

Front 235

Non-Hodgkin’s Lymphoma WRT B symps

Back 235

Fewer constitutional sgns/symptoms

Front 236

Which type of Lymphoma is associated with EBV

Back 236

Hodgkin’s

Front 237

Which type of Lymphoma is associated with HIV and immunosuppression

Back 237

Non-Hodgkin’s

Front 238

Which type of Hodgkin's Lymphoma Most common

Back 238

Nodular sclerosing

Front 239

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

Back 239

Nodular sclerosing

Front 240

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

Back 240

Nodular sclerosing

Front 241

Which type of Hodgkin's Lymphoma most RS cells.

Back 241

Mixed cellularity

Front 242

Which type of Hodgkin's Lymphoma Poor prognosis

Back 242

Lymphocyte depleted (rare)

Front 243

Which type of Hodgkin's Lymphoma Most rare

Back 243

Lymphocyte depleted

Front 244

Which type of Hodgkin's Lymphoma Older males with disseminated disease.

Back 244

Lymphocyte depleted (rare)

Front 245

Which type of Hodgkin's Lymphoma Excellent Prognosis

Back 245

Lymphocyte predominant and Nodullar sclerosing

Front 246

Which type of Hodgkin's Lymphoma Intermediate prognosis

Back 246

Mixed cellularity

Front 247

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

Back 247

Multiple myeloma

Front 248

Multiple myeloma where

Back 248

arises in the marrow

Front 249

Multiple myeloma what is produced

Back 249

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

Front 250

Multiple myeloma how common

Back 250

Most common 1° tumor arising within bone in adults.

Front 251

Multiple myeloma clinical findings

Back 251

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 252

Multiple myeloma Associated with

Back 252

1° amyloidosis

Front 253

Multiple myeloma WRT imaging

Back 253

punched-out lytic bone lesions on x-ray

Front 254

Multiple myeloma lab findings

Back 254

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

Front 255

Multiple myeloma WRT blood smear

Back 255

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

Front 256

Blood smear shows RBCs stacked like poker chips

Back 256

Multiple myeloma (rouleau formation).

Front 257

rouleau formation aka

Back 257

Blood smear shows RBCs stacked like poker chips

Front 258

Blood smear shows RBCs stacked like poker chips aka

Back 258

(rouleau formation).

Front 259

Waldenström’s macroglobulinemia

Back 259

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

Front 260

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

Back 260

Waldenström’s macroglobulinemia

Front 261

Distinctive tumor giant cell seen in Hodgkin’s disease;

Back 261

Reed-Sternberg

Front 262

Reed-Sternberg look

Back 262

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

Front 263

Reed-Sternberg variant

Back 263

Variants include lacunar cells in nodular sclerosis

Front 264

Variants include lacunar cells in nodular sclerosis

Back 264

Reed-Sternberg variant

Front 265

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

Back 265

Reed-Sternberg look

Front 266

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

Back 266

Follicular lymphoma (small cleaved cell)

Front 267

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

Back 267

Small lymphocytic lymphoma

Front 268

which Non-Hodgkin’s lymphoma Most common (adult).

Back 268

Follicular lymphoma (small cleaved cell)

Front 269

which Non-Hodgkin’s lymphoma Difficult to cure; indolent course; bcl-2 is involved in apoptosis.

Back 269

Follicular lymphoma (small cleaved cell)

Front 270

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

Back 270

Diffuse large cell

Front 271

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

Back 271

Diffuse large cell

Front 272

which Non-Hodgkin’s lymphoma t(11;14)

Back 272

Mantle cell lymphoma

Front 273

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

Back 273

Mantle cell lymphoma

Front 274

which Non-Hodgkin’s lymphoma Most common in children

Back 274

Lymphoblastic lymphoma

Front 275

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

Back 275

Lymphoblastic lymphoma

Front 276

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

Back 276

Lymphoblastic lymphoma

Front 277

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

Back 277

Lymphoblastic lymphoma

Front 278

which Non-Hodgkin’s lymphoma t(8;14)

Back 278

Burkitt’s lymphoma

Front 279

which Non-Hodgkin’s lymphoma c-myc

Back 279

Burkitt’s lymphoma

Front 280

which Non-Hodgkin’s lymphoma “Starry-sky” appearance

Back 280

Burkitt’s lymphoma

Front 281

Burkitt’s lymphoma Genetics

Back 281

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

Front 282

Burkitt’s lymphoma associations

Back 282

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

Front 283

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

Back 283

(sheets of lymphocytes with interspersed macrophages);

Front 284

Burkitt’s lymphoma appearance

Back 284

“Starry-sky” appearance

Front 285

Mantle cell lymphoma Genetics

Back 285

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

Front 286

Follicular lymphoma Genetics

Back 286

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

Front 287

disorder associated with t(9;22)

Back 287

CML (Philadelphia chromosome) (bcr-abl hybrid)

Front 288

disorder associated with t(8;14)

Back 288

Burkitt’s lymphoma (c-myc activation)

Front 289

disorder associated with t(14;18)

Back 289

Follicular lymphomas (bcl-2 activation)

Front 290

disorder associated with t(15;17)

Back 290

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

Front 291

disorder associated with t(11;22)

Back 291

Ewing’s sarcoma

Front 292

disorder associated with t(11;14)

Back 292

Mantle cell lymphoma

Front 293

Translocation associated with CML

Back 293

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

Front 294

Translocation associated with Burkitt’s lymphoma

Back 294

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

Front 295

Translocation associated with Follicular lymphomas

Back 295

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

Front 296

Translocation associated with M3 type of AML

Back 296

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

Front 297

Translocation associated with Ewing’s sarcoma

Back 297

t(11;22)

Front 298

Translocation associated with Mantle cell lymphoma

Back 298

t(11;14)

Front 299

Leukemias General considerations

Back 299

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

Front 300

Leukemias General clinical findings

Back 300

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

Front 301

Leukemias and ages

Back 301

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

Front 302

Auer rods; myeloblasts; adults.

Back 302

AML

Front 303

Leukemia most responsive to therapy

Back 303

ALL

Front 304

CLL clinical findings

Back 304

lymphadenopathy; hepatosplenomegaly; few symptoms; indolent course;

Front 305

CLL Lab findings

Back 305

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

Front 306

CML lab findings

Back 306

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

Front 307

CML vs Leukemoid Rxn

Back 307

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

Front 308

“blast crisis”

Back 308

CML accelerating to AML

Front 309

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

Back 309

That it is CML and not leukemoid reaction).

Front 310

final phase of CML

Back 310

Blast crisis accelerating to AML

Front 311

Auer rods what are they

Back 311

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

Front 312

Auer rods when seen

Back 312

Primarily in acute promyelocytic leukemia (M3).

Front 313

Auer rods why problematic

Back 313

Treatment of AML M3 can release Auer rods → DIC.

Front 314

Histiocytosis X caused by

Back 314

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

Front 315

peroxidase-positive cytoplasmic inclusions in granulocytes and myeloblasts

Back 315

Auer rods

Front 316

Histiocytosis X who gets

Back 316

Primarily affects young adults. Worse with smoking.

Front 317

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

Back 317

Histiocytosis X

Front 318

Histiocytosis X clinical features

Back 318

range from isolated bone lesions to multisystemic disease.

Front 319

Heparin Mechanism

Back 319

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

Front 320

Heparin Clinical use

Back 320

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

Front 321

Heparin Toxicity

Back 321

Bleeding, thrombocytopenia, drug-drug interaction

Front 322

Heparin how to monitor

Back 322

Follow PTT.

Front 323

Heparin Reversal

Back 323

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

Front 324

low-molecular-weight heparins names

Back 324

enoxaparin

Front 325

low-molecular-weight heparins effects and advatages

Back 325

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 326

low-molecular-weight heparins disadvantage

Back 326

Not easily reversible.

Front 327

Heparin Half-life

Back 327

Short (1.5 Hours)

Front 328

Warfarin aka

Back 328

Coumadin

Front 329

Coumadin aka

Back 329

Warfarin

Front 330

Warfarin Mechanism

Back 330

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

Front 331

Warfarin Clinical use

Back 331

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

Front 332

Warfarin Toxicity

Back 332

Bleeding, teratogenic, drug-drug interactions.

Front 333

Warfarin Monitoring

Back 333

The EX-PaT went to WAR(farin). EXtrinsic pathway and ↑ PT.

Front 334

Warfarin Half-life

Back 334

Long 2 days

Front 335

Heparin vs. warfarin Structure

Back 335

Heparin-Large anionic polymer, acidic Warfarin-Small lipid-soluble molecule

Front 336

Heparin vs. warfarin administration

Back 336

Heparin- Parenteral (IV, SC) Warfarin- Oral

Front 337

Heparin vs. warfarin Site of action

Back 337

Heparin-Blood Warfarin-Liver

Front 338

Heparin vs. warfarin Onset of action

Back 338

Heparin-Rapid (sec) Warfarin-Slow (days)

Front 339

Heparin vs. warfarin Mechanism of action

Back 339

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 340

Heparin vs. warfarin Duration of action

Back 340

Heparin- Acute (hours) Warfarin-Chronic (weeks or months)

Front 341

Heparin vs. warfarin Inhibits coagulation in vitro

Back 341

Heparin-yes Warfarin-no

Front 342

Heparin vs. warfarin Treatment of acute overdose

Back 342

Heparin-Protamine Sulfate Warfarin-IV vit K and Fresh frozen plasma

Front 343

Heparin vs. warfarin Monitoring

Back 343

Heparin-PTT (intrinsic) Warfarin-PT (extrinsic)

Front 344

Heparin vs. warfarin Crosses placenta

Back 344

Heparin-No Warfarin- Yes (teratogenic)

Front 345

Thrombolytics Names

Back 345

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

Front 346

Thrombolytics Mechanism

Back 346

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

Front 347

Thrombolytics Clinical use

Back 347

Early MI, early ischemic stroke.

Front 348

Thrombolytics Toxicity

Back 348

Bleeding.

Front 349

Thrombolytics contraindications

Back 349

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

Front 350

Thrombolytics Toxicity Tx

Back 350

aminocaproic acid, an inhibitor of fibrinolysis.

Front 351

aminocaproic acid clinical use

Back 351

Tx of Thrombolytics Toxicity

Front 352

aminocaproic acid mech

Back 352

inhibitor of Plasminogen to pasmin

Front 353

Aspirin aka

Back 353

ASA

Front 354

ASA aka

Back 354

Aspirin

Front 355

Aspirin (ASA) Mechanism

Back 355

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

Front 356

Aspirin (ASA) Clinical use

Back 356

Antipyretic, analgesic, anti-inflammatory, antiplatelet drug.

Front 357

Aspirin (ASA) Toxicity

Back 357

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

Front 358

Aspirin WRT lab values (homeostasis)

Back 358

↑ bleeding time. No effect on PT, PTT.

Front 359

Drugs that Inhibit platelet aggregation by irreversibly blocking ADP receptor

Back 359

Clopidogrel, ticlopidine

Front 360

Clopidogrel has the same effects/mech as ?

Back 360

ticlopidine

Front 361

ticlopidine has the same effects/mech as ?

Back 361

Clopidogrel

Front 362

Clopidogrel Mechanism

Back 362

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

Front 363

Clopidogrel Clinical use

Back 363

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

Front 364

Clopidogrel or Ticlopidine Neutropenia

Back 364

Ticlopidine

Front 365

Ticlopidine Toxicity

Back 365

Neutropenia

Front 366

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

Back 366

Aspirin (ASA)

Front 367

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

Back 367

Abciximab

Front 368

Abciximab Mechanism

Back 368

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

Front 369

Abciximab Clinical use

Back 369

Acute coronary syndromes, percutaneous transluminal coronary angioplasty.

Front 370

Abciximab Toxicity

Back 370

Bleeding, thrombocytopenia.

Front 371

Cancer drugs which are Cell cycle specific

Back 371

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

Front 372

Cancer drugs which are Cell cycle nonspecific

Back 372

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

Front 373

Methotrexate (MTX) Mechanism

Back 373

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

Front 374

Methotrexate (MTX) Clinical use

Back 374

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

Front 375

Methotrexate (MTX) Toxicity

Back 375

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

Front 376

Methotrexate (MTX) Toxicity Tx

Back 376

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

Front 377

leucovorin use

Back 377

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

Front 378

leucovorin aka

Back 378

folinic acid

Front 379

folinic acid aka

Back 379

leucovorin

Front 380

5-fluorouracil (5-FU) Mechanism

Back 380

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 381

5-fluorouracil (5-FU) Clinical use

Back 381

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

Front 382

5-fluorouracil (5-FU) Toxicity

Back 382

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

Front 383

Synergy with MTX.

Back 383

5-fluorouracil

Front 384

Synergy with 5-fluorouracil

Back 384

MTX.

Front 385

5-fluorouracil (5-FU) Toxicity Tx

Back 385

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

Front 386

Blocks de novo purine synthesis. Activated by HGPRTase.

Back 386

6-mercaptopurine (6-MP)

Front 387

6-mercaptopurine (6-MP) Mechanism

Back 387

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

Front 388

6-mercaptopurine (6-MP) Clinical use Toxicity

Back 388

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

Front 389

6-mercaptopurine (6-MP) Toxicity

Back 389

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

Front 390

Cytarabine aka

Back 390

ara-C

Front 391

ara-C aka

Back 391

Cytarabine

Front 392

Cytarabine (ara-C) Mechanism

Back 392

Inhibits DNA polymerase.

Front 393

Cytarabine (ara-C) Clinical use

Back 393

AML.

Front 394

Cytarabine (ara-C) Toxicity

Back 394

Leukopenia, thrombocytopenia, megaloblastic anemia.

Front 395

Cyclophosphamide Mechanism

Back 395

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

Front 396

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

Back 396

Cyclophosphamide, ifosfamide

Front 397

Cyclophosphamide Clinical use

Back 397

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

Front 398

Cyclophosphamide Toxicity

Back 398

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

Front 399

ifosfamide mechanism

Back 399

Same as Cyclophosphamide

Front 400

Nitrosoureas Names

Back 400

Carmustine, lomustine, semustine, streptozocin.

Front 401

Nitrosoureas Mechanism

Back 401

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

Front 402

Nitrosoureas Clinical use

Back 402

Brain tumors (including glioblastoma multiforme).

Front 403

Nitrosoureas Toxicity

Back 403

CNS toxicity (dizziness, ataxia).

Front 404

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

Back 404

Nitrosoureas: Carmustine, lomustine, semustine, streptozocin.

Front 405

Cisplatin and carboplatin Mechanism

Back 405

Act like alkylating agents.

Front 406

Cisplatin and carboplatin Clinical use

Back 406

Testicular, bladder, ovary, and lung carcinomas.

Front 407

Cisplatin and carboplatin Toxicity

Back 407

Nephrotoxicity and acoustic nerve damage.

Front 408

Busulfan Mechanism

Back 408

Alkylates DNA.

Front 409

Busulfan Clinical use

Back 409

CML.

Front 410

Busulfan Toxicity

Back 410

Pulmonary fibrosis, hyperpigmentation.

Front 411

Doxorubicin (Adriamycin), daunorubicin Mechanism

Back 411

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

Front 412

Doxorubicin (Adriamycin), daunorubicin Clinical use

Back 412

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

Front 413

Doxorubicin (Adriamycin), daunorubicin Toxicity

Back 413

Cardiotoxicity; also myelosuppression and marked alopecia. Toxic extravasation.

Front 414

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

Back 414

Doxorubicin (Adriamycin), daunorubicin

Front 415

Dactinomycin aka

Back 415

actinomycin D

Front 416

actinomycin D aka

Back 416

Dactinomycin

Front 417

Dactinomycin Mechanism

Back 417

Intercalates in DNA.

Front 418

Dactinomycin Clinical use

Back 418

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

Front 419

Dactinomycin Toxicity

Back 419

Myelosuppression.

Front 420

Bleomycin Mechanism

Back 420

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

Front 421

Bleomycin Clinical use

Back 421

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

Front 422

Bleomycin Toxicity

Back 422

Pulmonary fibrosis, skin changes, but minimal myelosuppression.

Front 423

Hydroxyurea Mechanism

Back 423

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

Front 424

Hydroxyurea Clinical use

Back 424

Melanoma, CML, and Sickle Cell disease

Front 425

Hydroxyurea Toxicity

Back 425

Bone marrow supression and GI upset

Front 426

Prednisone Mechanism

Back 426

May trigger apoptosis. May even work on nondividing cells.

Front 427

Prednisone Clinical use

Back 427

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 428

Prednisone Toxicity

Back 428

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

Front 429

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

Back 429

Tamoxifen, raloxifene

Front 430

Tamoxifen, raloxifene Mechanism

Back 430

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

Front 431

Tamoxifen, raloxifene Clinical use

Back 431

Breast cancer. Also useful to prevent osteoporosis.

Front 432

Tamoxifen, raloxifene Toxicity

Back 432

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 433

Trastuzumab aka

Back 433

Herceptin

Front 434

Herceptin aka

Back 434

Trastuzumab

Front 435

Trastuzumab Mechanism

Back 435

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

Front 436

Trastuzumab Clinical use

Back 436

Metastatic breast cancer.

Front 437

Trastuzumab Toxicity

Back 437

Cardiotoxicity.

Front 438

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

Back 438

Trastuzumab (Herceptin)

Front 439

Philadelphia chromosome brc-abl tyrosine kinase inhibitor.

Back 439

Imatinib (Gleevec)

Front 440

Gleevec aka

Back 440

Imatinib

Front 441

Imatinib aka

Back 441

Gleevec

Front 442

Imatinib Mechanism

Back 442

Philadelphia chromosome brc-abl tyrosine kinase inhibitor.

Front 443

Imatinib Clinical use

Back 443

CML, GI stromal tumors.

Front 444

Imatinib Toxicity

Back 444

Fluid retention.

Front 445

Vincristine, vinblastine Mechanism

Back 445

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

Front 446

Vincristine, vinblastine Clinical use

Back 446

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

Front 447

Vincristine, vinblastine Toxicity

Back 447

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

Front 448

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

Back 448

Vincristine, vinblastine

Front 449

Paclitaxel, other taxols Mechanism

Back 449

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

Front 450

Paclitaxel, other taxols Clinical use

Back 450

Ovarian and breast carcinomas.

Front 451

Paclitaxel, other taxols Toxicity

Back 451

Myelosuppression and hypersensitivity.

Front 452

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

Back 452

Paclitaxel, other taxols

Front 453

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

Back 453

Methotrexate (MTX)

Front 454

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

Back 454

5-fluorouracil (5-FU)

Front 455

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

Back 455

6-mercaptopurine (6-MP)

Front 456

Which Cancer Drug Leukopenia, thrombocytopenia, megaloblastic anemia.

Back 456

Cytarabine (ara-C)

Front 457

Which Cancer Drug used for AML only

Back 457

Cytarabine (ara-C)

Front 458

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

Back 458

Cyclophosphamide, ifosfamide

Front 459

Which Cancer Drug Also immunosuppressants.

Back 459

Cyclophosphamide, ifosfamide and Prednisone

Front 460

Which Cancer Drug CNS toxicity (dizziness, ataxia).

Back 460

Nitrosoureas

Front 461

Which Cancer Drug Nephrotoxicity and acoustic nerve damage.

Back 461

Cisplatin, carboplatin

Front 462

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

Back 462

Nitrosoureas

Front 463

Which Cancer Drug Pulmonary fibrosis, skin changes

Back 463

Busulfan and Bleomycin

Front 464

Which Cancer Drug used for CML not Gleevac.

Back 464

Busulfan

Front 465

Which Cancer Drug Cardiotoxicity; also myelosuppression and marked alopecia. Toxic extravasation.

Back 465

Doxorubicin (Adriamycin), daunorubicin

Front 466

Which Cancer Drug used for Wilms’ tumor, Ewing’s sarcoma, rhabdomyosarcoma.

Back 466

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

Front 467

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

Back 467

Bleomycin

Front 468

Which Cancer Drug Myelosuppression, GI irritation, alopecia.

Back 468

Etoposide (VP-16)

Front 469

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

Back 469

Raloxifene

Front 470

Which Cancer Drug used for Metastatic breast cancer.

Back 470

Trastuzumab (Herceptin)

Front 471

Which Cancer Drug Fluid retention.

Back 471

Imatinib (Gleevec)

Front 472

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

Back 472

Vincristine

Front 473

Which Cancer Drug Myelosuppression and hypersensitivity.

Back 473

Paclitaxel, other taxols

Front 474

causes of normocytic, normochromic Anemia with increase in Reticulocytes and inherited

Back 474

Hereditary spherocytosis G6PD dificiency PK deficiency Sickle cell

Front 475

causes of normocytic, normochromic Anemia with increase in Reticulocytes and aquired

Back 475

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

Front 476

Etoposide (VP-16) Mechanism

Back 476

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

Front 477

Etoposide (VP-16) Clinical use

Back 477

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

Front 478

Etoposide (VP-16) Toxicity

Back 478

Myelosuppression, GI irritation, alopecia.

Front 479

Etoposide aka

Back 479

VP-16

Front 480

VP-16 aka

Back 480

Etoposide

Front 481

PNH 1. Screen 2. Confirm

Back 481

1. sucrose lysis test 2. HAM's test (Ham's acid hemolysis)