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(Other) Qbank > Hematology Oncology > Flashcards

Hematology Oncology Flashcards

1
Q

What is the appearance of an acanthocyte? What is another name?

A

“Spiny” appearance on blood smear; also called spur cell

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2
Q

What pathology is associated with a spur cell (acanthocyte)?

A

Liver disease, abetalipoproteinemia (states of cholesterol dysregulation)

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3
Q

What type of RBCs might you see in abetalipoproteinemia?

A

Acanthocytes

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4
Q

Basophilic stippling is due to aggregation of what in the RBC?

A

Residual ribosomes

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5
Q

What pathology is associated with basophilic stippling?

A

Lead poisoning, sideroblastic anemias, myelodysplastic syndromes

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6
Q

Bite cells are seen in what disease?

A

G6PD

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7
Q

What is seen on a peripheral smear in a patient with G6PD?

A

Bite cells and Heinz bodies

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8
Q

When do you see Howell-Jolly bodies on a peripheral smear?

A

Functional hypospenia, asplenia, naphthalene poisoning

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9
Q

What are Howell-Jolly bodies?

A

Basophilic nuclear remnants found in RBCs

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10
Q

What pathology is associated with echinocyte?

A

End stage renal disease, liver disease, pyruvate kinase deficiency

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11
Q

There are two categories of normocytic anemia, nonhemolytic and hemolytic. How do you differentiate between the two?

A

Nonhemolytic has a reticulocyte count that is normal or low; hemolytic has a high reticulocyte count

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12
Q

What are the symptoms for lead poisoning?

A

Lead lines on gingivae (burton lines) and on metaphyses of long bones, encephalopathy, erythrocyte basophilic stippling, abdominal colic, sideroblastic anemia, wrist/foot drop

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13
Q

What are first line treatments for lead poisoning?

A

EDTA and dimercaprol

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14
Q

A kid with lead poisoning is given what?

A

Succimer

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15
Q

What enzymes are inhibited by lead?

A

Ferrochelatase and ALA dehydratase

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16
Q

What is the rate limiting step in heme synthesis?

A

ALA synthase

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17
Q

What is the genetic mutation resulting in sideroblastic anemia?

A

X linked defect in ALA synthase gene

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18
Q

What are the lab findings in sideroblastic anemia?

A

Increased iron, increased transferrin sat %, normal/decreased TIBC, increased ferritin

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19
Q

What are increased in the serum of B12 def?

A

Homocysteine and methylmalonic acid are increased

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20
Q

Orotic aciduria without hyperammonemia is seen in what disease? What enzyne is deficient?

A

Orotic aciduria due to UMP synthase defect

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21
Q

Ornithine transcarbamoylase def is differentiated from UMP synthase def how?

A

OTC def has hyperammonemia, UMP synthase def does not

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22
Q

What drugs can cause aplastic anemia?

A

Benzene, chloramphenicol, alkylating agents, antimetabolites

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23
Q

What is the most common inheritance pattern of Hereditary spherocytosis?

A

Autosomal dominant

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24
Q

What are some examples of common defective proteins in hereditary spherocytosis?

A

Spectrin, ankyrin, band 3, protein 4.2

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25
Q

What type of hemolysis is seen in hereditary spherocytosis?

A

Extravascular - macrophages cause the hemolysis

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26
Q

What is the inheritance of pyruvate kinase def?

A

Autosomal recessive

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27
Q

What may be seen on peripheral smear in pyruvate kinase def?

A

Burr cells “echinocytes”

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28
Q

Newborn presents with persistent jaundice and reticulocytosis. Osmotic fragility test is normal. What may be the underlying disease?

A

Pyruvate kinase deficiency

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29
Q

How does pyruvate kinase def. present?

A

Neonatal hemolytic anemia - persistent jaundice with reticulocytosis

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30
Q

What is seen on peripheral smear of G6PD def?

A

Heinz bodies and bite cells

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31
Q

What drugs can cause hemolytic stress in a patient with G6PD def?

A

Isoniazid, sulfonamides, ASA, Ibuprofen, dapsone, antimalarials, nitrofurantoin

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32
Q

What type of hemolysis is seen in Pyruvate kinase def?

A

Extravascular hemolysis

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33
Q

What is the “classic triad” associated with paroxysmal nocturnal hemoglobinuria?

A

Negative direct antiglobin (Coombs) test, venous thrombosis and pancytopenia

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34
Q

RBCs in paroxysmal nocturnal hemoglobinuria are negative for what?

A

CD55 and CD59

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35
Q

What is the importance of CD55?

A

Prevents formation of C3 convertase

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36
Q

What is the importance of CD59?

A

Blocks C9 from binding to RBC and therefore MAC formation

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37
Q

What is the treatment for paroxysmal nocturnal hemoglobinuria?

A

Eculizumab - prevents C5 conversion to C5a and C5b

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38
Q

Patients with PNH are at increased risk for what cancer?

A

Acute myeloid leukemia

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39
Q

What is the cause of sickle cell anemia?

A

Single point mutation in beta chain resulting in substitution of glutamic acid with valine

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40
Q

Hemoglobin C is formed as a result of what?

A

Point mutation in the 6th codon of beta Hgb chain that leads to replacement of glutamic acid residue with a lysine residue

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41
Q

What is seen on a peripheral smear of someone with sickle cell anemia?

A

Codocytes (target cells), sickle cells, Howell-Jolly bodies

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42
Q

An X ray of a patient with sickle cell anemia may reveal what?

A

Crewcut appearance

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43
Q

What drug is used for “treatment” of sickle cell anemia? What is its MOA?

A

Hydroxyurea - thought to stimulate HbF production

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44
Q

What are some causes of warm AIHA?

A

Autoimmune diseases (SLE), CLL, and various drugs (cephalosporins, penicillins, penicillin derivative, alpha-methyldopa)

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45
Q

What infectious organisms can cause cold agglutinin type immunohemolytic anemia?

A

Mycoplasma pneumoniae and EBV infectious mono

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46
Q

What are the lab values in iron def. anemia?

A

Low iron, low ferritin, low % transferrin saturation, elevated transferrin (or TIBC)

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47
Q

What are the lab values in anemia of chronic disease?

A

Low iron, elevated ferritin, low TIBC (or transferrin)

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48
Q

What are the lab values in hemochromatosis?

A

Elevated iron, elevated ferritin and % transferrin saturation, low transferrin (TIBC)

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49
Q

What are the lab values in anemia associated with prgenancy?

A

Elevated transferrin or TIBC, low % transferrin saturation

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50
Q

What are the beginning substrates for heme synthesis?

A

Glycine and succinyl CoA

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51
Q

What is the first step in heme synthesis? What enzyme is responsible for this?

A

Making delta-aminolevulinic acid; ALA synthase (rate limiting enzyme)

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52
Q

ALA synthase is responsible for what step in heme synthesis? What does it require?

A

1st step in heme synthesis - the rate limiting step; requires B6

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53
Q

What enzymes are affected by lead poisoning?

A

Ferrochelatase and ALA dehydratase

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54
Q

What accumulate in the blood in lead poisoning?

A

ALA and protoporphyrin

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55
Q

What enzyme is affected in Acute intermittent porphyria?

A

Porphobilinogen deaminase (aka uroporphyrinogen I synthase)

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56
Q

What accumulates in acute intermittent porphyria?

A

Porphobilinogen and ALA

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57
Q

What are the symptoms of acute intermittent porphyria?

A

Sxs come and go; Palpitations, port-wine urine, painful abdomen, polyneuropathy, psychological disturbances (depression), precipitated by drugs

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58
Q

What is the treatment for acute intermittent porphyria?

A

Glucose and heme (hemin) to inhibit ALA synthase

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59
Q

Defective porphobilinogen deaminase results in what condition?

A

Acute intermittent porphyria

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60
Q

What is the affective enzyme in porphyria cutanea tarda?

A

Uroporphyrinogen decarboxylase

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61
Q

What accumulates in porphyria cutanea tarda?

A

Uroporphyrin (tea-colored urine)

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62
Q

What is used to treat porphyria cutanea tarda?

A

Repeated phlebotomy

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63
Q

What exacerbates porphyria cutanea tarda?

A

Alcohol consumption

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64
Q

Defective uroporphyrinogen decarboxylase results in what disease?

A

Porphyria cutanea tarda

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65
Q

PT tests function of what?

A

Common pathway and extrinsic pathway in regards to coagulation

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66
Q

What are the hemophilias?

A

Bleeding disorders characterized by def in one of the factors involved in the intrinsic pathway of the coagulation cascade

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67
Q

Hemophilia A is a deficiency in what?

A

Factor VIII

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68
Q

What is the inheritance pattern of Hemophilia A?

A

X linked recessive

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69
Q

Hemophilia B is a defect in what?

A

Factor IX

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70
Q

What is the inheritance of Hemophilia B?

A

X linked recessive

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71
Q

What is the deficiency in Hemophilia C?

A

Factor XI

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72
Q

What is the inheritance of Hemophilia C?

A

Autosomal recessive

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73
Q

Hemophilias result in what lab findings?

A

Increased PTT and normal PT/INR

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74
Q

PTT measures what?

A

Intrinsic pathway (all factors except VII and XIII)

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75
Q

What mutation gives rise to Factor V Leiden?

A

Arg506Gln mutation - DNA point mutation in the factor V gene

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76
Q

What is the inheritance pattern of Factor V Leiden?

A

Autosomal dominant

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77
Q

What mutation results in Prothrombin gene mutation and therefore an increase in production of prothrombin>

A

Mutation in the 3’- untranslated region of the prothrombin gene

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78
Q

What disease is characterized by small than anticipated increase in PTT following administration of heparin?

A

Antithrombin deficiency

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79
Q

What disease commonly presents as skin and subcutaneous tissue necrosis following administration of warfarin?

A

Protein C or S def

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80
Q

Patients with Protein C or S def. have diminished ability to inactivate what?

A

Coagulation factors Va and VIIIa

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81
Q

What are the notable lab findings in DIC?

A

Low Plts, low fibrinogen, increased FDPs, increased PT, PTT, BT

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82
Q

What is seen on peripheral smear of DIC?

A

Schistocytes

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83
Q

What is the inheritance pattern of von Willebrand disease?

A

Autosomal dominant (vs hemophilias AR or XR)

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84
Q

What are the lab findings in von Willebrand disease?

A

Prlonged BT and PTT, normal PT

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85
Q

What is PTT prolonged in vWF disease?

A

Von Willebrand factor normally protects factor VIII

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86
Q

What is a ristocetin agglutination assay?

A

Induces vWF to bind platelet GpIB resulting in platelet agglutination

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87
Q

What is the results of the ristocetin agglutination assay in von Willebrand disease?

A

Impaired platelet aggregation

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88
Q

What does vWF bind on the platelet?

A

GpIb

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89
Q

ADP binding to PDY12 receptor on the platelet results in what?

A

GpIIb/IIIa insertion on the platelet membrane

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90
Q

What binds GpIIb/IIIa on the platelet?

A

Fibrinogen - helps platelets bind together

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91
Q

What drugs compete for ADP at the P2Y12 receptor?

A

Clopidogrel, prasugrel, ticlopidine

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92
Q

How does thrombotic thrombocytopenic purpura present?

A

Pentad: neurologic sxs, renal failure, fever, thrombocytopenia, microangiopathic hemolytic anemia

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93
Q

What causes thrombotic thrombocytopenic purpura?

A

Deficiency of ADAMTS 13

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94
Q

What is ADAMTS13?

A

Von Willebrand factor metalloprotease - normally degrades vWF multimers

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95
Q

How does hemolytic uremic syndrome present?

A

Thrombocytopenia, microangiopathic hemolytic anemia, and acute renal failure

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96
Q

What are the lab findings in thrombotic thrombocytopenic purpura?

A

Normal PT and PTT, increased bleeding time; additionally increased LDH and megakaryocytes

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97
Q

What is the cause of immune thrombocytopenia?

A

Antibodies against GpIIb/IIIa, resulting in splenic macrophage consumption of plt-ab complex

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98
Q

What causes thrombotic thrombocytopenic purpura?

A

Def of ADAMTS13

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99
Q

What is the cause of Bernard-Soulier syndrome?

A

Low GpIb resulting in defect in plt-vWF adhesion

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100
Q

What is the result of the ristocetin assay in Bernard Soulier syndrome?

A

No aggregation

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101
Q

What is in cryoprecipitate?

A

Fibrinogen, factor VIII, factor XIII, vWF and fibronectin

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102
Q

What is given in DIC?

A

Fresh frozen plasma

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103
Q

What are the “B” symptoms? When do you classically see them?

A

Fever, night sweats, and weight loss; classically HL, but also NHL

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104
Q

What type of Hodgkins lymphoma is is seen more commonly in women over men?

A

Nodular sclerosing type

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105
Q

When do you see Reed Sternberg cells?

A

Hodgkins lymphoma

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106
Q

Reed sternberg cells are positive for what cells markers?

A

CD15 and CD30

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107
Q

What is the appearance of Reed Sternberg cells?

A

Bilobed nucleus or binucleate with prominent eosinophilic nucleoli; “owl eyes” appearance

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108
Q

What type of HL has lacunar cells? What do they look like?

A

Nodular sclerosis HL; multilobated nucleus that lies in an open, pale cytoplasm

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109
Q

HL characterized by cells with multilobated nucleus that lies in an open, pale cytoplasm

A

Nodular sclerosing type

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110
Q

What type of HL is characterized by eosinophilia?

A

Mixed cellularity type

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111
Q

What are eosinophils seen in Mixed cellularity type HL?

A

RS cells release IL-5

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112
Q

Describe the appearance of “popcorn cells.” What cancer are they seen in?

A

Polylobulated nuclei and small peripheral nucleoli without perinucleolar halos; seen in lymphocyte predominant

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113
Q

What cells are seen in nodular lymphocyte-predominant HL?

A

Popcorn cells - lymphocytic and histiocytic

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114
Q

HL that presents with negative CD15 and CD30 cells is seen in what type?

A

Nodular lymphocyte predominant HL

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115
Q

What translocation is associated with follicular NHL?

A

Translocation 14;18 - resulting in overexpression of Bcl2

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116
Q

Translocation 14;18 results in what NHL?

A

Follicular NHL

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117
Q

Ig heavy chain is on what chromosome?

A

14

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118
Q

How do you differentiate follicular hyperplasia from lymphoma?

A

Follicular lymphoma has monoclonality, Bcl2 expression, and absence of tingible body macrophage in the germinal center

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119
Q

What translocation is associated with Mantle cell lymphoma?

A

Translocation 11;14 - overexpression of Cyclin D1

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120
Q

NHL with CD5+ and CD23- B cells and translocation 11;14

A

Mantle cell lymphoma

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121
Q

What type of B cell are seen in Mantle Cell lymphoma?

A

CD5+ and CD23-

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122
Q

How do you differentiate between CLL and Mantle Cell lymphoma?

A

CLL is CD23+ and mantle cell is CD23-

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123
Q

What translocation is seen in marginal zone lymphoma?

A

Translocation 11; 18

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124
Q

Translocation 11;18 is seen in what NHL?

A

Marginal zone lymphoma

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125
Q

What disease of chronic inflammation can result in marginal zone lymphoma?

A

Sjogrens, chronic gastritis (H pylori infection) and Hashimoto thyroiditis

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126
Q

What translocation is seen in Burkitt lymphoma and what does it result it?

A

8;14 - overexpression of c-myc

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127
Q

What chromosome is c-myc on?

A

8

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128
Q

Translocation 8;14 results in what cancer?

A

Burkitt lymphoma

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129
Q

Describe the starry sky appearance seen in Burkitt lymphoma

A

Reactive histiocytes in a backdrop of blue neoplastic cells

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130
Q

Bcl-2 is on what chromosome?

A

18

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131
Q

Adult T cell lymphoma is caused by infection with what?

A

Human T cell lymphotropic virus type 1

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132
Q

Infection with HTLV-1 can cause what?

A

Adult T cell lymphoma

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133
Q

What is the genome of HTLV-1?

A

+ssRNA; retroviridae family

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134
Q

What is a Pautrier microabscess? What is it associated with?

A

Intraepidermal neoplastic cell aggregates associated with mycosis fungoides

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135
Q

Describe the characteristic cells seen in Mycosis fungoides

A

Atypical CD4+ cells with cerebriform nuclei and intraepidermal neoplastic cell aggregates

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136
Q

What is mycosis fungoides?

A

CD4+ neoplasm characterized by skin patches/plaques with cells with cerebriform nuclei

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137
Q

What is Sezary syndrome?

A

Progression of Mycosis fungoides

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138
Q

What is the Pseudo-Pelger-Huet anomaly?

A

Neutrophils with bilobed nuclei. Typically seen after chemotherapy

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139
Q

How can you differentiate between Waldenstrom macroglonulinemia and Multiple myeloma?

A

WM has IgM M spike; Mult myeloma has IgG or IgA M spike

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140
Q

What is the difference between MGUS and multiple myeloma?

A

MGUS = bone marrow <10% monoclonal plasma cells; no CRAB findings

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141
Q

Tdt is a marker for what?

A

Pre-T and pre-B cells

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142
Q

CD10+ is a marker for what?

A

Marker of pre-B cells

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143
Q

Pre-T ALL expresses what cell markers on flow cytometry?

A

Tdt+, CD3+, CD7+; also is PAS positive

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144
Q

What markers are positive in both pre-T and pre-B ALL?

A

Tdt (terminal deoxynucleotidyl transferase) and PAS+

145
Q

What are unique cell markers seen on flow cytometry of pre-B ALL?

A

CD10+, CD19+, CD20+

146
Q

How does pre-T ALL usually present?

A

Male in teens/early 20s with mediastinal mass (can cause pleural effusion)

147
Q

What translocation is associated with a better prognosis in ALL?

A

12;21

148
Q

What are some risk factors for developing AML?

A

Prior treatment with alkylating agents, radiation, Down syndrome, PNH, Fanconi anemia, myeloproliferative syndromes

149
Q

What translocatin is seen in acute promyelocytic leukemia?

A

15;17 - links retinoic acid receptor alpha gene on chromosome 17 with PML gene on chromosome 15

150
Q

Translocation 15;17 is highly specific for what?

A

Promyelocytic leukemia (AML-M3)

151
Q

What cell markers can be seen on flow cytometry in CLL?

A

CD19, CD20, CD5, CD23

152
Q

What cells are characteristically seen in CLL?

A

Smudge cells

153
Q

What is Richter’s transformation?

A

CLL transformation to aggressive lymphoma, most commonly diffuse large B cell lymphoma

154
Q

How is hairy cell leukemia diagnosed?

A

Flow cytometry - CD103+ CD11c+ CD25+ CD19+ CD20+ CD22+

155
Q

Hairy cell leukemia is a tumor of what cell type?

A

Mature B cell

156
Q

How do patients with hairy cell leukemia present?

A

Massive splenomegaly and pancytopenia

157
Q

Hairy cell leukemia is positive for what stain?

A

TRAP - tartrate-resistan acid phosphatase

158
Q

What is seen on a bone marrow aspiration in hairy cell leukemia?

A

Dry tap - hairy cell leukemia causes bone marrow fibrosis

159
Q

What are the treatments for hairy cell leukemia?

A

Cladribine and pentostatin - purine analogs

160
Q

What is seen on flow cytometry in hairy cell leukemia?

A

CD103, CD11c, CD25, CD19, CD20, CD22

161
Q

Langerhans cell histiocytosis is a proliferative disorder of what cells?

A

Specialized dendritic cells - from monocyte lineage

162
Q

How does Langerhans cell histiocytosis present?

A

Commonly in a child with lytic bone lesions (primarily in skull) and eczematous rash; possibly with recurrent otitis media and a mass involving the mastoid bone

163
Q

What is the hallmark lesion seen in Langerhans cell histiocytosis?

A

Birbeck granules - tubules with dilated terminal end resembling a tennis racket

164
Q

Cells in langerhans cell histiocytosis express what cell markers?

A

CD1a and S100 (neural crest cell origin)

165
Q

Chronic myelogenous leukemia presents with a dysregulated production of what cells?

A

Neutrophils, metamyelocytes, myelocytes, basophils

166
Q

What translocation is seen in CML?

A

9;22 - BCR-ABL

167
Q

How do patients with CML present?

A

Splenomegaly on exam

168
Q

What chromosome in BCR on?

A

22

169
Q

What chromosome is ABL1 one?

A

9

170
Q

What is the philadelphia chromosome?

A

9;22 BCR-ABL1 fusion

171
Q

9;22 translocation is seen in what disease? What does it result in?

A

CML; make a constitutively active tyrosine kinase

172
Q

CML may transform to what? How is it characterized?

A

Transform to AML or ALL “blast crisis” >20% myeloblasts or lymphoblasts in peripheral blood

173
Q

How is CML differentiated from reactive neutrophilic leukocytosis?

A

Leukocyte alkaline phosphatase stain is negative in CML, but positive in leukemoid reaction

174
Q

What is used for treatment of CML?

A

Imatinib - tyrosine kinase inhibitor

175
Q

Bone marrow aspirate in myelodysplastic syndrome reveals what?

A

Ringed sideroblasts - erythroblasts with iron-laden mitochondria

176
Q

What are some risk factors for myelodysplastic syndrome?

A

Radiation, benzene, chemotherapy

177
Q

Myelodysplastic syndromes increase risk for what?

A

AML

178
Q

What mutation is seen in polycythemia vera?

A

JAK2

179
Q

What myeloproliferative disorders have a high incidence of JAK2 mutations?

A

Polycythemia vera, myelofibrosis, essential thrombocythemia

180
Q

What is aquagenic pruritus? What is it a sign of?

A

Ithcing following exposure to warm water; sign of polycythemia vera

181
Q

How does polycythemia vera present?

A

Intense itching after hot shower, facial flushing, erythromelalgia, may have hyperuricemia (and therefore gout)

182
Q

What is first line treatment of polycythemia vera?

A

Phlebotomy; but can also use hydroxyurea and ruxolitinib

183
Q

What is ruxolitinib?

A

Jak1/2 inhibitor

184
Q

What disease is characterized by massive proliferation of megakaryocytes and platelets, and includes symptoms of bleeding and thrombosis?

A

Essential thrombocythemia

185
Q

What is seen on a peripheral smear in essential thrombocythemia?

A

Markedly increased number of platelets

186
Q

What mutation is seen in essential thrombocythemia?

A

JAK2 mutation

187
Q

During rapid hemolysis, Hgb binds what?

A

Haptoglobin - resulting in a decrease in serum haptoglobin

188
Q

What is seen on bone marrow aspiration in aplastic anemia?

A

Hypocellularity, fat cells and marrow stroma

189
Q

What is seen in bone marrow aspirate of immune thrombocytopenia?

A

Increased megakaryocytes

190
Q

What is seen in a peripheral smear in immune thrombocytopenia?

A

Few large platelets

191
Q

What is the cause of immune thrombocytopenia? How does it present?

A

Antibodies against GpIIb/IIIa; presents with petechial rash and easy bruising/bleeding

192
Q

What is the defect seen in Glanzmann thrombasthenia?

A

Defect in glycoprotein GPIIb/IIIa complex; leads to defect in platelet to platelet aggregation

193
Q

What labs do you see in von Willebrand disease?

A

Increased bleeding time, increased PTT and normal PT

194
Q

What is an important side effect of ticlopidine?

A

Neutropenia

195
Q

What is the MOA of ticlopidine?

A

Prevents ADP from binding to platelet receptors

196
Q

What is the MOA of heparin?

A

Enhances activity of ATIII - decreasing the activity of factor Xa and thrombin

197
Q

What is the antidote for heparin?

A

Protamine sulfate

198
Q

What is used for immediate anticoagulation for a PE?

A

Heparin

199
Q

What is the MOA of LMWH?

A

Enhances activity of ATIII but more selectively directed toward Xa with some activity against thrombin

200
Q

Describe the elimination of heparin.

A

Dose dependent

201
Q

Describe the elimination of LMWH

A

Dose-independent

202
Q

What is the MOA of Fondaparinux?

A

Indirect thrombin inhibitor - enhances the activity of ATIII but only acts on factor Xa

203
Q

What is the antidote for LMWH?

A

Can use protamine sulfate but has lesser effect

204
Q

What is heparin-induced thrombocytopenia?

A

IgG antibodies against heparin-bound platelet factor 4, which activates platelets and causes thrombosis and thrombocytopenia

205
Q

What is the treatment for heparin induced thrombocytopenia?

A

D/C heparin and administer direct thrombin inhibitor - bivalirudin

206
Q

What are the direct thrombin inhibitors?

A

Bivalirudin, argatroban, dabigatran

207
Q

What is the only oral agent in the direct thrombin inhibitor class?

A

Dabigatran

208
Q

What is the reversal agent for dabigatran?

A

Idarucizumab

209
Q

What is the reversal for direct thrombin inhibitors?

A

Idarucizumab for dabigatran; consider PCC and/or antifibrinolytics if no reversal agent

210
Q

What is the MOA dabigatran?

A

Oral inhibitor of thrombin

211
Q

What is the MOA of argatroban?

A

Direct inhibitor of thrombin (IIa)

212
Q

What is the MOA of bivalirudin?

A

Direct inhibitor of thrombin (IIa)

213
Q

What is the MOA of apixaban?

A

Direct inhibitor of factor Xa

214
Q

What is apixaban used for?

A

Oral agent for prophylaxis of DVT, PE, and A fib

215
Q

What is the MOA of rivaroxaban?

A

Direct inhibitor of factor Xa

216
Q

What is used for anticoagulation therapy in pregnancy?

A

Heparin - does not cross the placenta

217
Q

What is the MOA of warfarin?

A

Impairs vitamin K-dependent synthesis of clotting factors II, VII, IX, X and protein C and S by interfering with the gamma-carboxylation of the VK dependent coagulation factors

218
Q

What enzyme is inhibited by Warfarin?

A

Vit K epoxide reductase

219
Q

What are the affects of Vit K on warfarin?

A

Vit K reduces the affects of warfarin - can lead to clotting

220
Q

What are the affects of vitamin E on warfarin?

A

Vitamin E can enhance the affects of warfarin

221
Q

What vitamins can affect warfarin?

A

Vitamin K and Vitamin E

222
Q

How does Vit E affect warfarin?

A

Vit E enchances warfarin by slowing the synthesis of VK dependent coagulation factors

223
Q

What antibiotics notably affect warfarin?

A

3rd gen cephalosporins and macrolides

224
Q

What affect does cefidinir (3rd gen) have on warfarin?

A

3rd gens kills VK synthesizing bacteria in gut and inhibit Vit K epoxide reductase, enhancing the affects of warfarin

225
Q

What affect do macrolides have on warfarin?

A

Macrolides (exception azithromycin) inhibit Cyp450 - enhancing warfarin affects

226
Q

How is warfarin monitored?

A

PT/INR

227
Q

How is warfarin reversed?

A

Rapid: FFP or 4-factor prothrombin complex concentrate (PCC); non-rapid: Vit K1 (phytonadione)

228
Q

What is the site of action for warfarin?

A

Liver

229
Q

What is the site of action for heparin?

A

Blood

230
Q

How is heparin monitored?

A

PTT

231
Q

What are the thrombolytic drugs?

A

Alteplase, streptokinase, reteplase, tenecteplase

232
Q

What fibrinolytic drug can cause anaphylaxis?

A

Streptokinase

233
Q

What are the contraindications for fibrinolytics?

A

Recent surgery, active bleeding, H/O diatheses, h/o intracranial bleeding, or severe hypertension

234
Q

What are the uses for thrombolytics?

A

Early MI, early ischemic stroke, direct thrombolysis of severe PE

235
Q

Fibrinolytics have what effects on lab values?

A

Increased PT and PTT, no effect on bleeding time

236
Q

What are the reversal agents for fibrinolytics?

A

Aminocaproic acid and tranexamic acid, or platelet transfusions and factor corrections

237
Q

What is the MOA of aminocaproic acid in reversal of fibrinolytics?

A

Opposes action by competing for lysing binding sites on plasminogen and plasmin, ultimately blocking interaction with fibrin

238
Q

What is the MOA of tranexamic acid?

A

Forms reversible complex that displaces plasminogen from fibrin and inhibits proteolytic activity of plasmin

239
Q

In order to block the interaction between plasminogen or plasmin with fibrin, what reversal agent would you use?

A

Aminocaproic acid

240
Q

Low dose aspirin has what effect?

A

Inhibits platelet aggregation

241
Q

At an intermediate dose, what are the affects of aspirin?

A

Antipyretic and analgesic

242
Q

At high doses, what are the affects of aspirin?

A

Anti-inflammatory

243
Q

What are the ADP inhibitors?

A

Clopidogrel, prasugrel, ticlopidine, and ticagrelor (reversible)

244
Q

What is the MOA of ADP receptor inhibitors?

A

Prevent ADP from binding P2Y12 receptor, preventing the ADP-induced expression of gp IIb/IIIa on the surface of platelets

245
Q

Patient presents a few weeks after an acute MI with fever and mouth ulcers, what drug might be causing the issue?

A

Ticlopidine

246
Q

What is an adverse effect of ticlopidine?

A

Neutropenia

247
Q

What is a common adverse effect of the ADP receptor inhibitors?

A

Thrombotic thrombocytopenic purpura

248
Q

What is the MOA of ticagrelor?

A

Reversibly inhibits ADP binding to P2Y12 receptor, preventing expression of gp IIb/IIIa on platelet membrane

249
Q

What is the MOA of abciximab?

A

Binds to gp IIb/IIIa receptor on platelets, preventing platelet interaction with fibrinogen and therefore aggregation

250
Q

What are the gp IIb/IIIa inhibitors?

A

Abciximab, eptifibatide and tirofiban

251
Q

What is the MOA of eptifibatide?

A

Bind to gp IIb/IIIa and therefore inhibit platelet aggregation

252
Q

What are the phosphodiesterase inhibitors used to inhibit platelet aggregation?

A

Cilostazol and diphyridamole

253
Q

What is the MOA of dipyridamole?

A

PDE inhibitor, increasing cAMP in platelets inhibiting the platelet aggregation and inducing vasodilation

254
Q

What is the MOA of cilostazol?

A

PDE inhibitor in platelets, causing increase in cAMP and therefore reducing platelet aggregation and causing vasodilation

255
Q

What is used for the treatment of intermittent claudication?

A

PDE inhibitors - dipyridamole and cilostazol

256
Q

What are the toxicities of the PDE inhibitors?

A

Facial flushing, headache, abdominal pain, hypotension, nausea

257
Q

What is the MOA of methotrexate?

A

Folate analog - inhibits dihyrdofolate reductase

258
Q

What are the AEs of methotrexate?

A

Myelosuppression, mucositis, hepatotoxicity, and pulmonary fibrosis

259
Q

What is given in conjunction with methotrexate? Why?

A

Leucovorin - folinic rescue

260
Q

What cancers is methotrexate used for?

A

Leukemias (ALL), lymphomas, choriocarcinoma, sarcomas

261
Q

What non-cancer treatments is methotrexate used for?

A

Ectopic pregnancy, abortion (with misoprostol), rheumatoid arthritis, psoriasis, IBD, polymyositis/dermatomyositis

262
Q

What is the MOA of 5-fluorouracil?

A

Pyrimidine analog - Inhibits thymidylate synthase

263
Q

What cancers is 5-FU used in?

A

Colon, pancreatic, basal cell

264
Q

What can be used to enhance the efects of 5-FU?

A

Leucovorin

265
Q

What is the MOA of cytarabine?

A

Pyrimidine analog that inhibits DNA polymerase

266
Q

What cancers is cytarabine used in?

A

Leukemia (AML), and lymphoma

267
Q

What are the two pyrimidine analog anti-metabolites?

A

Cytarabine (inhibits DNA polymerase) and 5-FU (inhibits thymidylate synthase)

268
Q

What are the AEs of 5-FU?

A

Myelosuppression, hand-foot syndrome

269
Q

What are the AEs of cytarabine?

A

Myelosuppression and pancytopenia

270
Q

What is the MOA of cladribine?

A

Purine analog that can lead to inhibition of DNA polymerase and DNA strand breaks

271
Q

What is cladribine used in?

A

Hairy cell leukemia

272
Q

What is the AEs of cladribine?

A

Myelosuppression, nephrotoxicity, and neurotoxicity

273
Q

What is the MOA of gemcitabine?

A

Cytosine analog that inhibits DNA polyermase and ribonucleotide reductase resulting in chain termination

274
Q

What is the MOA of azathioprine?

A

Purine analog that inhibits de novo purine synthesis

275
Q

What is azathioprine and 6-mercaptopurine metabolized by?

A

Xanthine oxidase

276
Q

What drug inhibits azathioprine metabolism?

A

Allopurinol or febuxostat (both inhibit xanthine oxidase)

277
Q

What is the MOA of bleomycin?

A

Induces free radical formation into DNA that induces DNA strand breaks

278
Q

What is the MOA of dactinomycin?

A

Intercalates into DNA between guanine and cytosine basepairs resulting in single stranded breaks and inhibits DNA dependent RNA polymerase

279
Q

What is bleomycin used for?

A

Testicular cancer and HL

280
Q

What is dactinomycin used for?

A

Childhood cancers: Wilms tumor, Ewing sarcoma, Rhabdomyosarcoma

281
Q

What are the AEs of bleomycin?

A

Pulmonary fibrosis, skin hyperpigmentation, myelosuppression is RARE and minimal

282
Q

What are the AEs of dactinomycin?

A

Myelosuppression

283
Q

What is the MOA of doxorubicin?

A

Intercalates into DNA and produces free radicals via forming iron complexes

284
Q

What are the AEs of doxorubicin?

A

Dilated cardiomyopathy, alopecia, myelosuppression

285
Q

How can cardiotoxicity be avoided in doxorubicin use?

A

Dexarazoxane - iron chelator

286
Q

What is dexrazoxane?

A

Iron chelator used to prevent cardio toxicity with doxorubicin use

287
Q

What antitumor drugs generate free radicals and intercalate into the DNA?

A

Doxorubicin and daunorubicin

288
Q

What class of drugs is cyclophosphamide in?

A

Alkylating agent - nitrogen mustards

289
Q

What is the MOA of cyclophosphamide?

A

Alkylates N7 on guanine and cross likes DNA

290
Q

Cyclophosphamide requires what?

A

Bioactivation by the liver.

291
Q

What is the MOA of ifosfamide?

A

Cross links DNA at N7 on guanine; also a nitrogen mustard

292
Q

What are the AEs of cyclophosphamide and ifosfamide?

A

Hemorrhagic cystitis, transitional cell carcinoma, myelosuppression, SIADH

293
Q

How is hemorrhagic cystitis from cyclophosphamide prevented?

A

Mensa - binds toxic metabolite acrolein; or can use n-acetylcysteine

294
Q

What is acrolein?

A

Toxic metabolite that causes hemorrhagic cystitis

295
Q

What is mensa?

A

Used for preventing hemorrhagic cystitis in cyclophosphamide

296
Q

What are nitrosureas primarily used to treat?

A

Brain tumors such as GBM

297
Q

What is the MOA of nitrosureas?

A

Cross link DNA by alkylating O6 on guanine

298
Q

What are the AEs of nitrosoureas?

A

CNS toxicity - dizziness, convulsions, ataxia

299
Q

What is the MOA of platinums?

A

Cross link DNA

300
Q

What are the platinum agents used in oncology?

A

Cisplatin, carboplatin, oxaliplatin

301
Q

What are the AEs of cisplatin and carboplatin?

A

Nephrotoxicity, ototoxicity, peripheral neuropathy, and emesis

302
Q

What agents should be give prior/with cisplatin/carboplatin?

A

Chloride diuresis prior and amifostine to prevent nephrotoxicity; use 5HT3 antagonists to prevent emesis

303
Q

What is amifostine? What is it used for?

A

Free radical scavenger; used to prevent nephrotoxicity from platinums

304
Q

What are the AEs of oxaliplatin?

A

Neurotoxic

305
Q

What is oxaliplatin used for?

A

Cancers resistant to other platinums

306
Q

What is cisplatin/carboplatin used to treat?

A

Testicular, bladder, ovarian and lung cancers

307
Q

What is the MOA of busulfan?

A

Cross links DNA

308
Q

What is Busulfan used for?

A

Ablate bone marrow prior to bone marrow transplant

309
Q

What are the AEs of busulfan?

A

Pulmonary fibrosis, myelosuppression, hyperpigmentation

310
Q

Chemotherapeutic Topoisoerase inhibitors are specific for what stages of the cell cycle?

A

S phase and G2

311
Q

What is the MOA of irinotecan?

A

Inhibit topoisomerase I and prevent DNA unwinding and replication

312
Q

What is the MOA of etoposide?

A

Inhibit topoisomerase II and therefore increase DNA degradation

313
Q

What is the MOA of topotecan?

A

Inhibit topoisomerase II and prevent DNA unwinding and replication

314
Q

What is irinotecan used for?

A

Colon cancer

315
Q

What is topotecan used for?

A

Ovarian cancer and small cell lung cancer

316
Q

What is the MOA of teniposide?

A

Inhibits topoisomerase I

317
Q

What are the AEs of irinotecan?

A

Myelosuppression and diarrhea

318
Q

What are the AEs of etoposide and teniposide?

A

Myelosuppression and alopecia

319
Q

What is etoposide and teniposide used to treat?

A

Testicular cancer and small cell lung cancer and leukemias/lymphomas

320
Q

What is the MOA of paclitaxel?

A

Binds B-tubulin and enhances assembly of tubulin dimers into microtubules; stabilizes existing tubules. Microtubules are unable to depolymerize - mitotic arrest

321
Q

Taxanes are used in the treatment of what?

A

Breast and ovarian cancer

322
Q

What are the toxicities of taxanes?

A

Peripheral neuropathy, myelosuppression, hypersensitivity (infusion reaction) and alopecia

323
Q

What lymphoma is vinblastine used to treat?

A

Hodgkin lymphoma

324
Q

What lymphoma is vincristine used to treat?

A

NHL

325
Q

What are the toxicities associated with vincristine?

A

Paralytic ileus (constipation), areflexia, peripheral neuropathy

326
Q

What toxicities are associated with vinblastine?

A

Myelosuppression

327
Q

What is the MOA of vinca alkaloids?

A

Bind to beta-tubulin and prevent microtubule polymerization

328
Q

What is the MOA of hydroxyurea?

A

Inhibits ribonucleotide reductase, decreasing DNA synthesis

329
Q

What are the SERMs?

A

Tamoxifen and raloxifene

330
Q

What is the MOA of tamoxifen?

A

Competitive inhibitor of estradiol binding to ER; Acts as a partial estrogen agonist in endometrium (increased risk of endometrial cancer)

331
Q

What is the most common SE of tamoxifen therapy?

A

Hot flashes

332
Q

Tamoxifen and raloxifene both increase the risk for what?

A

Thromboembolic disease

333
Q

What is trastuzumab?

A

MAB against Her2

334
Q

Binding of trastuzumab to HER2 has what effects?

A

Inhibits HER2 signaling pathway and activates antibody-dependent cytotoxicity

335
Q

What is the MOA of anastrozole?

A

Aromatase inhibitor

336
Q

What are aromatase inhibitors used?

A

Postmenopausal women with ER + breast cancer

337
Q

Imatinib inhibits the activity of what?

A

Tyrosine kinases - BCR-ABL (in CML), and c-KIT and PDGF (in GI stromal tumors)

338
Q

What is the MOA of bevacizumab?

A

Mab against VEGF. Inhibits angiogenesis

339
Q

What are the AEs of bevacizumab?

A

Hemorrhage, blood clots, impaired wound healing

340
Q

What is the MOA of erlotinib?

A

EGFR tyrosine kinase inhibitor

341
Q

What is the MOA of Cetuximab?

A

Mab to EGFR

342
Q

What is the AE of erlotinib?

A

Rash

343
Q

What is erlotinib used for?

A

Non-small cell lung cancer

344
Q

What is cetuximab used for?

A

Stage IV CRC (wild type KRAS), and head and neck cancer

345
Q

In order to use cetuximab, what needs to be true of the cancer type?

A

KRAS wild type

346
Q

What is the MOA of rituximab?

A

Mab against CD20

347
Q

What is an AE of rituximab?

A

Increased risk of PML

348
Q

What is the MOA of bortezomib?

A

Proteasome inhibitor - induce arrest at G2-M phase and apoptosis

349
Q

What is the MOA of carfilzomib?

A

Proteasome inhibitor - induces arrest at G2-M phase and apoptosis

350
Q

What are two proteasome inhibitors used in the treatment of multiple myeloma?

A

Bortezomib and carfilzomib

351
Q

What is borezomib/carfilzomib used in the treatment of?

A

Multiple myeloma, mantle cell lymphoma

352
Q

What are the AEs of bortezomib/carfilzomib?

A

Peripheral neuropathy, herpes zoster reactivation

353
Q

What is the MOA of vemurafenib?

A

Inhibitor of BRAF oncogene in melanoma

354
Q

What drug is used to treat metastatic melanoma + for the BRAF oncogene?

A

Vemurafenib

355
Q

What BRAF mutation is Vemurafenib active against?

A

V600E

356
Q

What is the MOA of Rasburicase?

A

Recombinant uricase that catalyzes the metabolism of uric acid to allantoin

357
Q

What labs are associated with tumor lysis syndrome?

A

Hyperkalemia, hyperphosphatemia, hypocalcemia, and hyperuricemia

358
Q

What is used to treat tumor lysis syndrome?

A

Rasburicase, allopurinol and hydration

(Other) Qbank (33 decks)

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