Internal Medicine - Hematology And Oncology

Front 1

Situations in which ESR is increased?

Back 1

1. Infections
2. Inflammatory disease
3. Malignant neoplasms
4. GI disease (Ulcerative Colitis [UC])
5. Pregnancy

Front 2

Situations in which ESR is decreased?

Back 2

1. Polycythemia
2. Sickle cell anemia
3. Congestive heart failure
4. Microcytosis
5. Hypofibrinogenemia

Front 3

Main mechanism of increased ESR?

Back 3

Aggregation of RBCs; RBC aggregates have a higher density than plasma

Front 4

Acanthocytes (spur cell) are assosciated with which pathology?

Back 4

1. Liver disease
2. Abetalipoproteinemia

Front 5

Basophilic stippling is assosciated with which pathology?

Back 5

Baste the ox TAIL:
1. Thalassemias
2. Anemia of chronic disease (ACD)
3. Iron deficiency
4. Lead (Pb) poisoning

Front 6

Bite cells are assosciated with which pathology?

Back 6

G6PD deficiency

Front 7

Macro-ovalocytes are assosciated with which pathology?

Back 7

1. Megaloblastic anemia
2. Marrow failure

Front 8

Schistocytes (helmet cells) are assosciated with which pathology?

Back 8

1. DIC
2. TTP/HUS
3. Traumatic hemolysis

Front 9

Spherocytes are assosciated with which pathology?

Back 9

1. Spherocytosis
2. Autoimmune hemolysis

Front 10

Teardrop cells are assosciated with which pathology?

Back 10

1. Bone marrow infiltration (e.g., myelofibrosis)

Front 11

Target cells are assosciated with which pathology?

Back 11

HALT said the hunter to his target
1. HbC disease
2. Asplenia
3. Liver disease
4. Thalassemia

Front 12

Describe the proess of Heinz body production?

Back 12

Oxidation of iron from ferrous to ferric form leads to denatured Hb precipitation and damage to RBC membrane ––> formation of bite cells

Seen with a-thalassemia, G6PD deficiency

Front 13

What are Howell-Jolly bodies?

Back 13

Basophilic nuclear remnants found in RBCs

Seen in patients with functional hyposplenia or asplenia

Front 14

Microcytic anemias

Back 14

1. IDA
2. ACD
3. Thalassemias
4. Lead (Pb) poisoning
5. Sideroblastic anemia

Front 15

Macrocytic anemias

Back 15

May be subdivided into megaloblastic and nonmegaloblastic anemia

Megaloblastic anemias
1. Folate deficiency
2. B12 deficiency

Non-megaloblastic anemia
1. Liver disease
2. Alcoholism
3. Reticulocytosis
4. Metabolic disorders
5. Drugs

Front 16

What is the Plummer-Vinson syndrome?

Back 16

Triad of:
1. IDA
2. Esophageal web (dysphagia for solids but not liquids)
3. Atrophic glossitis

Front 17

a-thalassemias are most prevalent in which people?

Back 17

Asian and African

Front 18

Findings in lead poisoning

Back 18

Lead Lines on gingival and on epiphyses of long bones
Encephalopathy and Erythrocyte basophilic stippling
Abdminal colic ("lead colic") and siderblastic Anemia
Drops - wrist and foot

Front 19

Treatment of lead poisoning

Back 19

1. Succimer (kids)
2. Dimercaprol

Front 20

Findings in folate deficiency?

Back 20

1. Hypersegmented neutrophils
2. Glossitis
3. Decreased folate levels
4. Increased homocysteine
5. Normal methylmalonic acid

Front 21

Drugs that can cause folate deficiency?

Back 21

1. Methotrexate
2. Trimethoprim

Front 22

Findings in B12 deficiency

Back 22

1. Hypersegmented neutrophils
2. Glossitis
2. Decreased B12
4. Increased homocysteine
5. Increased methylmalonic acid
6. Neurological symptoms

Front 23

Viral agents that may cause aplastic anemia?

Back 23

1. Parvovirus B19
2. EBV
3. HIV
4. CMV
5. HCV

Front 24

Most common cause of aplastic anemia?

Back 24

Idiopathic

Front 25

Most common known cause of aplastic anemia?

Back 25

Drugs;
1. Benzene
2. Chloramphenicol
3. Antimetabolites

Front 26

Symptoms of aplastic anemia?

Back 26

1. Fever
2. Fatigue
3. Bleeding
4. Petechia
5. Infection

Front 27

Primary iron storage in the body?

Back 27

Ferritin

Front 28

Lead (Pb) poisoning leads to anemia by blocking which enzymes?

Back 28

1. Ferrochelatase
2. ALA dehydratase

Front 29

What are porphyrias?

Back 29

Conditions of defective heme synthesis that lead to accumulation of heme precurosors

Front 30

Symptoms of porphyria cutanea tarda?

Back 30

1. Blistering cutaneous photosensitivity
2. Most common porphyria
3. Tea-coloured urine (due to accumulation of uroporphyrin)

Front 31

Leukemia vs lymphoma?

Back 31

Leukemia – lymphoid neoplasms with widespread involvement of bone marrow. Tumor cells are found in peripheral blood

Lymphoma  – Discrete tumor masses arising from lymph nodes. Presentations often blur definitions

Front 32

What is leukemoid reaction?

Back 32

Increased WBC count with left shift (e.g., 80% bands) and increased leukocyte ALP, usually due to infection.

Often confused with leukemia

Front 33

What are Reed-Sternberg cells? And where are they seen?

Back 33

1. Distinctive tumor giant cells, seen in Hodgkin's disease
2. They are binucleate or bilobed, with the 2 halves as mirror images ("owl's eyes")
3. Necessary, but not sufficient for diagnosis of Hodgkin's disease

Front 34

Neoplasms of mature B cells (non-Hodgkin's lymphoma)

Back 34

1. Burkitt's lymphoma
2. Diffuse large B-cell lymphoma
3. Mantle cell lymphoma
4. Follicular lymphoma

Front 35

Neoplasms of mature T cells (non-Hodgkin's lymphoma)

Back 35

1. Adult T-cell lymphoma
2. Mycosis fungoides/Sézary syndrome

Front 36

Genetics of Burkitt's lymphoma?

Back 36

t(8;14), c-myc gene moves next to heavy-chain Ig gene (14); Associated with EBV

Front 37

Genetics of Mantle cell lymphoma?

Back 37

t(11;14) Deactivation of cyclin D regulatory gene; poor prognosis, CD5+

Front 38

Genetics involved in Follicular lymphoma?

Back 38

t(14;18) bcl-2 expression; difficult to cure; bcl-2 inhibits apoptosis

Front 39

Genetics of adult T-cell lymphoma?

Back 39

Caused by HTLV-1; especially affects populations in Japan, West Africa, and the Caribbean

Front 40

Findings in Burkitt's lymphoma?

Back 40

1. "Starry sky" appearance, sheets of lymphocytes with interspersed macrophages
2. Jaw lesion in endemic form in Africa; pelvis or abdomen in sporadic form

Front 41

Findings in adult T-cell lymphoma?

Back 41

1. Adults present with cutaneous lesions; very aggressive

Front 42

Findings in mycosis/Sézary syndrome?

Back 42

Adults present with cutaneous patches/nodules; indolent CD4+

Front 43

Most common primary tumor arising within bone in the elderly?

Back 43

Multiple myeloma

Front 44

What is multiple myeloma?

Back 44

Monoclonal plasma cell ("fried-egg" appearance) cancer that arises in the marrow and produces large amounts of IgG (55%) or IgA (25%). 

Most common in those >40-50 years of age

Front 45

Mnemonics for multiple myeloma?

Back 45

CRABB 
HyperCalcemia
Renal insufficiency
Anemia
Bone lytic lesions
Back pain

Multiple Myeloma: Monoclonal M protein spike

Front 46

ALL presents most commonly in?

Back 46

<15 years. May present with bone marrow involvement in childhood or mediastinal mass in adolescent males.

Front 47

Findings in ALL? (4)

Back 47

1. Bone marrow increased by massive amounts of lymphoblasts. 
2. TdT+ and CALLA+
3. t(12;21) –> better prognosis
4. May spread to CNS and testes

Front 48

SLL/CLL is most commonly seen in

Back 48

Age >60 years.

Front 49

Findings in CLL?

Back 49

1. Often asymptomatic
2. Smudge cells in peripheral blood
3. "Warm" autoimmune hemolytic anemia

Front 50

Difference between SLL and CLL?

Back 50

CLL has increased peripheral blood lymphocytosis, otherwise the same.

Front 51

AML is most commonly seen in

Back 51

Median onset 60 years

Front 52

Findings in AML

Back 52

1. Auer rods
2. Massively increased circulating myeloblasts
3. t(14;17) M3 AML subtype responds to all-trans retinoic acid (Vit A), inducing differentiation of myeloblasts
4. DIC is a common presentation

Front 53

CML is most commonly seen in?

Back 53

30-60 years of age

Front 54

Findings in CML

Back 54

1. Defined by the Philadelphia chromosome (t[9;22], bcd-abl)
2. Myeloid stem cell proliferation
3. Presents with increased neutrophils, metamyelocytes, basophils
4. Splenomegaly
5. May accellerate and transform to AML or ALL
6. Very low leukocyte alkaline phosphatase

Front 55

What are Auer bodies (rods)?

Back 55

Peroxidase-positive cytoplasmic inclusions in granulocytes and myeloblasts. Commonly seen in acute promyelocytic leukemia (M3). Treatment of AML M3 can release Auer rods, which leads to DIC.

Front 56

t(9;22) translocation is associated with which disorder?

Back 56

CML (bcr-abl hybrid)

Front 57

t(8;14) translocation is associated with which disorder?

Back 57

Burkitt's lymphoma (c-myc activation)

Front 58

t(14;18) translocation is associated with which disorder?

Back 58

Follicular lymphomas (bcl-2 activation)

Front 59

t(15;17) translocation is associated with which disorder?

Back 59

M3 type of AML

Front 60

t(11;22) translocation is associated with which disorder?

Back 60

Ewing's sarcoma

Front 61

t(11;14) translocation is associated with which disorder?

Back 61

Mantle cell lymphoma

Front 62

What is Langerhans cell histiocytosis (LCH)?

Back 62

1. Proliferative disorder of dendritic cells from monocyte lineage
2. Unknown etiology
3. Functionally immature and do not stimulate T-cells via APC
4. Birbeck granules ("tennis rackets" on EM) are characteristic

Front 63

Appropriate absolute polycythemia is associated with which diseases?

Back 63

1. Lung disease
2. Congenital heart disease
3. High altitude

Front 64

Inappropriate absolute polycythemia is associated with which diseases?

Back 64

1. RCC
2. Wilms' tumor
3. Cysts
4. Hepatocellular carcinoma (HCC)
5. Hydronephrosis

Due to ectopic EPO

Front 65

Antineoplastics work at three main levels, what are they?

Back 65

1. Nucleotide synthesis
2. DNA
3. Cellular division

Front 66

Antineoplastics that work at the level of nucleotide synthesis?

Back 66

1. Methotrexate and 5-FU: decreased thymidine synthesis
2. 6-MP: decreased purine synthesis

Front 67

Antineoplastics that work at the level of DNA?

Back 67

1. Alkylating agents, cisplatin: cross-link DNA
2. Dactinomycin, doxorubicin: DNA intercalators
3. Etoposide: inhibits topoisomerase II

Front 68

Antineoplastics that interfere with cell division?

Back 68

1. Vinca alkaloids: inhibit microtubule formation
2. Paclitaxel: inhibits microtubule disassembly

Front 69

Mechanism of action of methotrexate (MTX)?

Back 69

Folic acid analog that inhibits dihydrofolate reductase –> decreased dTMP –> decreased DNA and protein synthesis

Front 70

Mechanism of action of 5-FU?

Back 70

Pyridmidine analog bioactivated to 5F-dUMP, which covalently complexes folic acid. Inhibits thymidylate synthase.

Front 71

Mechanism of action of 6-mercaptopurine (6-MP)?

Back 71

Purine (thiol) analog –> decreases de novo purine synthesis

Front 72

Mechanism of action of 6-thioguanine (6-TG)?

Back 72

Purine (thiol) analog –> decreases de novo purine synthesis

Front 73

Mechanism of action of Cytarabine (ara-C)?

Back 73

Pyrimidine analog –> inhibition of DNA polymerase

Front 74

Toxicitiy of vincristine, vinblastine?

Back 74

VinBLASTine BLASTs Bone marrow (suppression)
Vincristine – neurotoxicity and paralytic ileus

Front 75

Mechanism of action of vincristine, vinblastine?

Back 75

Alkaloids that bind to tubulin in M-phase and block polymerization of microtubules so that mitotic spindle cannot form

Mnemonic: 
Microtubules are the vines of your cells

Front 76

Situations in which ESR is increased?

Back 76

1. Infections
2. Inflammatory disease
3. Malignant neoplasms
4. GI disease (Ulcerative Colitis [UC])
5. Pregnancy

Front 77

Situations in which ESR is decreased?

Back 77

1. Polycythemia
2. Sickle cell anemia
3. Congestive heart failure
4. Microcytosis
5. Hypofibrinogenemia

Front 78

Main mechanism of increased ESR?

Back 78

Aggregation of RBCs; RBC aggregates have a higher density than plasma

Front 79

Acanthocytes (spur cell) are assosciated with which pathology?

Back 79

1. Liver disease
2. Abetalipoproteinemia

Front 80

Basophilic stippling is assosciated with which pathology?

Back 80

Baste the ox TAIL:
1. Thalassemias
2. Anemia of chronic disease (ACD)
3. Iron deficiency
4. Lead (Pb) poisoning

Front 81

Bite cells are assosciated with which pathology?

Back 81

G6PD deficiency

Front 82

Macro-ovalocytes are assosciated with which pathology?

Back 82

1. Megaloblastic anemia
2. Marrow failure

Front 83

Schistocytes (helmet cells) are assosciated with which pathology?

Back 83

1. DIC
2. TTP/HUS
3. Traumatic hemolysis

Front 84

Spherocytes are assosciated with which pathology?

Back 84

1. Spherocytosis
2. Autoimmune hemolysis

Front 85

Teardrop cells are assosciated with which pathology?

Back 85

1. Bone marrow infiltration (e.g., myelofibrosis)

Front 86

Target cells are assosciated with which pathology?

Back 86

HALT said the hunter to his target
1. HbC disease
2. Asplenia
3. Liver disease
4. Thalassemia

Front 87

Describe the proess of Heinz body production?

Back 87

Oxidation of iron from ferrous to ferric form leads to denatured Hb precipitation and damage to RBC membrane ––> formation of bite cells

Seen with a-thalassemia, G6PD deficiency

Front 88

What are Howell-Jolly bodies?

Back 88

Basophilic nuclear remnants found in RBCs

Seen in patients with functional hyposplenia or asplenia

Front 89

Microcytic anemias

Back 89

1. IDA
2. ACD
3. Thalassemias
4. Lead (Pb) poisoning
5. Sideroblastic anemia

Front 90

Macrocytic anemias

Back 90

May be subdivided into megaloblastic and nonmegaloblastic anemia

Megaloblastic anemias
1. Folate deficiency
2. B12 deficiency

Non-megaloblastic anemia
1. Liver disease
2. Alcoholism
3. Reticulocytosis
4. Metabolic disorders
5. Drugs

Front 91

What is the Plummer-Vinson syndrome?

Back 91

Triad of:
1. IDA
2. Esophageal web (dysphagia for solids but not liquids)
3. Atrophic glossitis

Front 92

a-thalassemias are most prevalent in which people?

Back 92

Asian and African

Front 93

Findings in lead poisoning

Back 93

Lead Lines on gingival and on epiphyses of long bones
Encephalopathy and Erythrocyte basophilic stippling
Abdminal colic ("lead colic") and siderblastic Anemia
Drops - wrist and foot

Front 94

Treatment of lead poisoning

Back 94

1. Succimer (kids)
2. Dimercaprol

Front 95

Findings in folate deficiency?

Back 95

1. Hypersegmented neutrophils
2. Glossitis
3. Decreased folate levels
4. Increased homocysteine
5. Normal methylmalonic acid

Front 96

Drugs that can cause folate deficiency?

Back 96

1. Methotrexate
2. Trimethoprim

Front 97

Findings in B12 deficiency

Back 97

1. Hypersegmented neutrophils
2. Glossitis
2. Decreased B12
4. Increased homocysteine
5. Increased methylmalonic acid
6. Neurological symptoms

Front 98

Viral agents that may cause aplastic anemia?

Back 98

1. Parvovirus B19
2. EBV
3. HIV
4. CMV
5. HCV

Front 99

Most common cause of aplastic anemia?

Back 99

Idiopathic

Front 100

Most common known cause of aplastic anemia?

Back 100

Drugs;
1. Benzene
2. Chloramphenicol
3. Antimetabolites

Front 101

Symptoms of aplastic anemia?

Back 101

1. Fever
2. Fatigue
3. Bleeding
4. Petechia
5. Infection

Front 102

Primary iron storage in the body?

Back 102

Ferritin

Front 103

Lead (Pb) poisoning leads to anemia by blocking which enzymes?

Back 103

1. Ferrochelatase
2. ALA dehydratase

Front 104

What are porphyrias?

Back 104

Conditions of defective heme synthesis that lead to accumulation of heme precurosors

Front 105

Symptoms of porphyria cutanea tarda?

Back 105

1. Blistering cutaneous photosensitivity
2. Most common porphyria
3. Tea-coloured urine (due to accumulation of uroporphyrin)

Front 106

Leukemia vs lymphoma?

Back 106

Leukemia – lymphoid neoplasms with widespread involvement of bone marrow. Tumor cells are found in peripheral blood

Lymphoma  – Discrete tumor masses arising from lymph nodes. Presentations often blur definitions

Front 107

What is leukemoid reaction?

Back 107

Increased WBC count with left shift (e.g., 80% bands) and increased leukocyte ALP, usually due to infection.

Often confused with leukemia

Front 108

What are Reed-Sternberg cells? And where are they seen?

Back 108

1. Distinctive tumor giant cells, seen in Hodgkin's disease
2. They are binucleate or bilobed, with the 2 halves as mirror images ("owl's eyes")
3. Necessary, but not sufficient for diagnosis of Hodgkin's disease

Front 109

Neoplasms of mature B cells (non-Hodgkin's lymphoma)

Back 109

1. Burkitt's lymphoma
2. Diffuse large B-cell lymphoma
3. Mantle cell lymphoma
4. Follicular lymphoma

Front 110

Neoplasms of mature T cells (non-Hodgkin's lymphoma)

Back 110

1. Adult T-cell lymphoma
2. Mycosis fungoides/Sézary syndrome

Front 111

Genetics of Burkitt's lymphoma?

Back 111

t(8;14), c-myc gene moves next to heavy-chain Ig gene (14); Associated with EBV

Front 112

Genetics of Mantle cell lymphoma?

Back 112

t(11;14) Deactivation of cyclin D regulatory gene; poor prognosis, CD5+

Front 113

Genetics involved in Follicular lymphoma?

Back 113

t(14;18) bcl-2 expression; difficult to cure; bcl-2 inhibits apoptosis

Front 114

Genetics of adult T-cell lymphoma?

Back 114

Caused by HTLV-1; especially affects populations in Japan, West Africa, and the Caribbean

Front 115

Findings in Burkitt's lymphoma?

Back 115

1. "Starry sky" appearance, sheets of lymphocytes with interspersed macrophages
2. Jaw lesion in endemic form in Africa; pelvis or abdomen in sporadic form

Front 116

Findings in adult T-cell lymphoma?

Back 116

1. Adults present with cutaneous lesions; very aggressive

Front 117

Findings in mycosis/Sézary syndrome?

Back 117

Adults present with cutaneous patches/nodules; indolent CD4+

Front 118

Most common primary tumor arising within bone in the elderly?

Back 118

Multiple myeloma

Front 119

What is multiple myeloma?

Back 119

Monoclonal plasma cell ("fried-egg" appearance) cancer that arises in the marrow and produces large amounts of IgG (55%) or IgA (25%). 

Most common in those >40-50 years of age

Front 120

Mnemonics for multiple myeloma?

Back 120

CRABB 
HyperCalcemia
Renal insufficiency
Anemia
Bone lytic lesions
Back pain

Multiple Myeloma: Monoclonal M protein spike

Front 121

ALL presents most commonly in?

Back 121

<15 years. May present with bone marrow involvement in childhood or mediastinal mass in adolescent males.

Front 122

Findings in ALL? (4)

Back 122

1. Bone marrow increased by massive amounts of lymphoblasts. 
2. TdT+ and CALLA+
3. t(12;21) –> better prognosis
4. May spread to CNS and testes

Front 123

SLL/CLL is most commonly seen in

Back 123

Age >60 years.

Front 124

Findings in CLL?

Back 124

1. Often asymptomatic
2. Smudge cells in peripheral blood
3. "Warm" autoimmune hemolytic anemia

Front 125

Difference between SLL and CLL?

Back 125

CLL has increased peripheral blood lymphocytosis, otherwise the same.

Front 126

AML is most commonly seen in

Back 126

Median onset 60 years

Front 127

Findings in AML

Back 127

1. Auer rods
2. Massively increased circulating myeloblasts
3. t(14;17) M3 AML subtype responds to all-trans retinoic acid (Vit A), inducing differentiation of myeloblasts
4. DIC is a common presentation

Front 128

CML is most commonly seen in?

Back 128

30-60 years of age

Front 129

Findings in CML

Back 129

1. Defined by the Philadelphia chromosome (t[9;22], bcd-abl)
2. Myeloid stem cell proliferation
3. Presents with increased neutrophils, metamyelocytes, basophils
4. Splenomegaly
5. May accellerate and transform to AML or ALL
6. Very low leukocyte alkaline phosphatase

Front 130

What are Auer bodies (rods)?

Back 130

Peroxidase-positive cytoplasmic inclusions in granulocytes and myeloblasts. Commonly seen in acute promyelocytic leukemia (M3). Treatment of AML M3 can release Auer rods, which leads to DIC.

Front 131

t(9;22) translocation is associated with which disorder?

Back 131

CML (bcr-abl hybrid)

Front 132

t(8;14) translocation is associated with which disorder?

Back 132

Burkitt's lymphoma (c-myc activation)

Front 133

t(14;18) translocation is associated with which disorder?

Back 133

Follicular lymphomas (bcl-2 activation)

Front 134

t(15;17) translocation is associated with which disorder?

Back 134

M3 type of AML

Front 135

t(11;22) translocation is associated with which disorder?

Back 135

Ewing's sarcoma

Front 136

t(11;14) translocation is associated with which disorder?

Back 136

Mantle cell lymphoma

Front 137

What is Langerhans cell histiocytosis (LCH)?

Back 137

1. Proliferative disorder of dendritic cells from monocyte lineage
2. Unknown etiology
3. Functionally immature and do not stimulate T-cells via APC
4. Birbeck granules ("tennis rackets" on EM) are characteristic

Front 138

Appropriate absolute polycythemia is associated with which diseases?

Back 138

1. Lung disease
2. Congenital heart disease
3. High altitude

Front 139

Inappropriate absolute polycythemia is associated with which diseases?

Back 139

1. RCC
2. Wilms' tumor
3. Cysts
4. Hepatocellular carcinoma (HCC)
5. Hydronephrosis

Due to ectopic EPO

Front 140

Antineoplastics work at three main levels, what are they?

Back 140

1. Nucleotide synthesis
2. DNA
3. Cellular division

Front 141

Antineoplastics that work at the level of nucleotide synthesis?

Back 141

1. Methotrexate and 5-FU: decreased thymidine synthesis
2. 6-MP: decreased purine synthesis

Front 142

Antineoplastics that work at the level of DNA?

Back 142

1. Alkylating agents, cisplatin: cross-link DNA
2. Dactinomycin, doxorubicin: DNA intercalators
3. Etoposide: inhibits topoisomerase II

Front 143

Antineoplastics that interfere with cell division?

Back 143

1. Vinca alkaloids: inhibit microtubule formation
2. Paclitaxel: inhibits microtubule disassembly

Front 144

Mechanism of action of methotrexate (MTX)?

Back 144

Folic acid analog that inhibits dihydrofolate reductase –> decreased dTMP –> decreased DNA and protein synthesis

Front 145

Mechanism of action of 5-FU?

Back 145

Pyridmidine analog bioactivated to 5F-dUMP, which covalently complexes folic acid. Inhibits thymidylate synthase.

Front 146

Mechanism of action of 6-mercaptopurine (6-MP)?

Back 146

Purine (thiol) analog –> decreases de novo purine synthesis

Front 147

Mechanism of action of 6-thioguanine (6-TG)?

Back 147

Purine (thiol) analog –> decreases de novo purine synthesis

Front 148

Mechanism of action of Cytarabine (ara-C)?

Back 148

Pyrimidine analog –> inhibition of DNA polymerase

Front 149

Toxicitiy of vincristine, vinblastine?

Back 149

VinBLASTine BLASTs Bone marrow (suppression)
Vincristine – neurotoxicity and paralytic ileus

Front 150

Mechanism of action of vincristine, vinblastine?

Back 150

Alkaloids that bind to tubulin in M-phase and block polymerization of microtubules so that mitotic spindle cannot form

Mnemonic: 
Microtubules are the vines of your cells