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Final FA review > 3/14 heme/onc > Flashcards

3/14 heme/onc Flashcards

1
Q

Myelodysplastic syndromes

-can progress to what cancer?

A

AML

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2
Q

Myelodysplastic syndromes

-cause?

A

-Caused by de novo mutations or environmental exposure (e.g., radiation, benzene, chemotherapy)

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3
Q

Myelodysplastic syndromes

-whats marrow look like?

A

Hypercellular bone marrow, but the cells are not
formed properly and dont get released into blood,
so pts have cytopenias.

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4
Q

Pseudo–Pelger-Huet anomaly

  • seen in what disease?
  • what is it?
A

Bilobed neutrophils seen in myelodysplastic syndromes following chemotherapy.

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5
Q

TDT

  • what is it?
  • which cells/disease is it found it?
A
  • marker for lymphoblasts, so seen in ALL.
  • TDT = DNA pol. Only present in lymphoblast nucleus, no other cells. Not in mature lymphoblasts or any other cell.
  • TDT found in the nucleus.
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6
Q

Whats the marker for myeloblasts (AML)?

A
  • myeloperoxidase => Auer rods

- AML only.

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7
Q

Age: <15

-which leukemia(s)?

A

ALL

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8
Q

Age: >60

-which leukemia(s)?

A

CLL

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9
Q

Age: 15-60

-which leukemia(s)?

A

AML

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10
Q

Age: 40-59

-which leukemia(s)?

A

CML

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11
Q

Mediastinal mass

  • which leukemia?
  • whats the mass?
  • mnemonic?
A
  • T-cell ALL
  • leukemic infiltration of the thymus
  • T cell, T-hymus
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12
Q

CD10+

-T or B cell marker?

A

pre-B cell marker.

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13
Q

Down Syndrome

-associated w/which leukemias?

A

ALL

AML

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14
Q

ALL

  • most often spreads to where?
  • is it responsive to chemo?
A
  • CNS and testes.

- Yes it is.

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15
Q

Does normal chemo help CNS & testes?

A

-Normal chemo doesn’t pass BBB or B-testicle-barrier. So give those two their own chemo.

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16
Q

Which ALL translocation has a better prognosis?

A

-t(12;21) = better prognosis

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17
Q

CLL

  • neoplasm of which cell? T or B cells?
  • markers?
A
  • B cells
  • CD20+, CD5+

*CD5 surprisingly.

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18
Q

smudge cells

-which leukemia?

A

CLL

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19
Q

Small lymphocytic lymphoma

-which leukemia?

A

CLL

-small = chronic, b/c more mitoses have gone by (compared to blast stage) so cell has gotten smaller.

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20
Q

Most pts w/CLL die how?

A
  • infection.
  • these neoplastic naive B cells do NOT become plasma cells = hypogammaglobinemia = will die of infection.
  • the ones that do make Ig are messed up and will target your own RBCs and cause autoimmune hemolytic anemia.
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21
Q

Why would you see spherocytes in CLL?

A

b/c you can get autoimmune hemolytic anemia in CLL.

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22
Q

Richter syndrome

A

CLL transforming into diffuse large B cell lymphoma = Richter syndrome.

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23
Q

Hairy cell leukemia

  • neoplasm of which cells?
  • marker?
A
  • B-Cells (its a variant of CLL)

- TRAP (+)

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24
Q

Hairy cell leukemia

-whats it do to bone marrow?

A

-marrow fibrosis => dry tap.

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25
Q

Hairy cell leukemia

  • seen in which pt pop?
  • Tx:
A
  • elderly

- cladribine an adenosine analog inhibits adenosine deaminase (like in SCID).

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26
Q

AML

-risk factors

A
  • prior exposure to alkylating chemotherapy
  • radiation
  • myeloproliferative disorders
  • down syndrome.
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27
Q

M3 AML

  • translocation?
  • Tx?
  • how does it cause DIC?
A
  • t(15;17)
  • reitnoic acid
  • DIC is a common presentation in M3 AML and can be induced by chemotherapy due to release of Auer rods.
  • since auer rods seen mostly in M3.
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28
Q

Which leukemia classically affects gums?

A
  • acute monocytic leukemia.

- obviously a sect of AML

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29
Q

CML

  • whats the main cell?
  • Tx:
A
  • myeloprolif. disorder, main cell = neutrophil.

- imatinib (gleevec): tyrosine kinase inhibitor

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30
Q

t(9;22), bcr-abl

-which leukemia?

A

CML

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31
Q

CML

-whats a “blast crisis”?

A

CML may accelerate and transform to AML or ALL (“blast crisis”).

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32
Q

Basophils increased in which leukemia?

A

CML

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33
Q

“-Nib” =

A

kinase inhibitor

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34
Q

Langerhans cell histiocytosis

A

-Child w/lytic bone lesions and skin rash
or
-Recurrent otitis media with a mass involving the mastoid bone.

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35
Q

Langerhans cell histiocytosis

-markers?

A

S-100, CD1a, birbeck granules

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36
Q

chronic myeloproliferative disorders

-risk of transforming into which leukemia?

A

AML

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37
Q

polycythemia vera & peptic ulcers

-connection?

A

Extra mast cells - lots of histamine.

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38
Q

Weightlifters abusing steroids can have high hct, why?

A

Androgens stimulate RBC production.

-which is also why men generally have higher hct than women.

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39
Q

Only myeloproliferative disorder w/inc in plasma volume?

-what can that lead to?

A
  • polycythemia vera

- HTN

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40
Q

Essential thrombocytosis

  • bleeding or thrombosis?
  • Tx:
A
  • either, depends on if the platelets are functional or not.

- hydroxyurea

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41
Q

Is there a big risk for hyperuricemia/gout in essential thrombocytosis?

A

No bc platelets dont have nuclei!

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42
Q

Myelofibrosis

-whats causing the fibrosis? what cells and what cytokine?

A

-Megakaryocytes produce excess PDGF (platelet derived growth factor) which results in marrow fibrosis.

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43
Q

leukoerythroblastic smear

-seen when?

A

Extra-medullary hematopoiesis

  • marrow usually prevets blasts from leaving b/c they’re too large. But spleen and liver do not do that, so you get blasts in peripheral smear.
  • can be seen in myelofibrosis.
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44
Q

CML

-JAK2 mutation?

A

NO

-other myeloprolif disorders do have JAK2 mutation.

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45
Q

antithrombin 3

-dec levels of which 2 coag factors the most?

A

-thrombin & 10a

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46
Q

Protamine sulfate

-More useful against unfractionated or LMWH?

A

unfractionated

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47
Q

LMWH

-difference vs unfractionated?

A
  • act more on factor Xa
  • have better bioavailability
  • 2–4 times longer half-life
  • not easily reversible
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48
Q

Heparin-induced thrombocytopenia

-heparin is an anti-coagulant, so why would it cause a dec. in platelets?

A

Type 2 HSR

  • development of IgG antibodies against heparin bound to platelet factor 4 (PF4).
  • Antibody-heparin-PF4 complex activates platelets Ž thrombosis and thrombocytopenia.

*IgG tagged stuff destroyed by splenic macrophages.

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49
Q

Heparin-induced thrombocytopenia

-so what do you give them instead of heparin?

A

argatroban, bivalirudin.

50
Q

Warfarin

-metabolized by which enzymes?

A

cytochrome P450

51
Q

INR

  • PT or PTT vs normal?
  • heparin or warfarin?
A
  • PT

- warfarin

52
Q

Warfarin

  • how is it administered?
  • what do you need to watch out for?
A
  • its lipid soluble, administered orally.
  • absorbed like a fat so anything causing malabsorption might affect it.
  • watch out when using w/cholestyramine, etc.
53
Q

Apixaban, rivaroxaban

A
  • anti-coagulant.

- Bind and directly inhibit the activity of factor Xa.

54
Q

Does warfarin work in vitro?

A
  • NO

- acts in vivo in the liver to prevent formation of new coag. factors.

55
Q

How soon after original insult do you want to administer thrombolytics.

A

within 3 hours

56
Q

Whats % of strokes are ischemic?

A

85% ischemic

15% hemorrhagic

57
Q

Aspirin poisoning

  • Sxs:
  • Tx:
A
  • resp. alkalosis initially, followed by metabolic acidosis.

- sodium bicarb

58
Q

Two drugs that can cause tinnitus

A

-aspirin & quinidine

59
Q

ticlopidine

-tox?

A

Neutropenia

60
Q

Cilostazol, dipyridamole

A

-Phosphodiesterase III inhibitor; inc. cAMP in platelets, thus inhibiting platelet aggregation; vasodilators.

61
Q

eptifibatide, tirofiban

-mech?

A

Same as abciximab

62
Q

Methotrexate

-tox:

A
  • Myelosuppression (leucovorin)
  • Macrovesicular fatty change in liver.
  • Mucositis
  • Teratogenic
63
Q

5-fluorouracil (5-FU)

-mech:

A

-Pyrimidine analog bioactivated to 5F-dUMP, which
covalently complexes folic acid.
-This complex then inhibits thymidilate synthase.

64
Q

5-fluorouracil (5-FU)

-Tx for OD?

A

uridine (kinases will convert to UMP).

-this is the substrate that thymidilate synthase works on.

65
Q

Cytarabine (arabinofuranosyl cytidine)

  • mech
  • tox:
A
  • Pyrimidine analog => inhibition of DNA polymerase.

- panCYTopenia

66
Q

Azathioprine

  • converted into what?
  • metabolized by what?
A
  • 6-MP

- xanthine oxidase

67
Q

6-MP, 6-TG

  • activated by what enzyme?
  • mech:
A
  • Activated by HGPRT.

- inhibit PRPP amidotransferase (formation of IMP)

68
Q

HGPRT

-which anti-neoplastics does this drug activate?

A

6-MP, 6-TG

69
Q

Dactinomycin (actinomycin D)

  • mech:
  • use:
  • mnemonic:
A
  • Intercalates DNA.

- Used for childhood tumors (“children ACT out”)

70
Q

Doxorubicin (Adriamycin), daunorubicin

  • mech:
  • use:
A
  • free radicals & intercalates DNA.

- Solid tumors, leukemias, lymphomas.

71
Q

Doxorubicin (Adriamycin), daunorubicin

  • tox:
  • antidote:
A
  • Cardiotoxicity (dilated cardiomyopathy)
  • alopecia.

-Dexrazoxane (iron chelating agent), used to prevent
cardiotoxicity.

72
Q

Dexrazoxane

-use?

A

-iron chelating agent, used to prevent cardiotoxicity w/doxorubicin use.

73
Q

Bleomycin

-mech:

A

free radicals

74
Q

Bleomycin

-tox:

A

Pulmonary fibrosis, skin changes, mucositis.

75
Q

Drugs that can cause pulmonary fibrosis.

A

Bleomycin, busulfan, methotrexate & amiodarone

76
Q

Alkylating agents

  • how do they work?
  • are they cell cycle specific?
A
  • attach alkyl group to DNA = DNA damage.

- NOT cell cycle specific.

77
Q

Cyclophosphamide, ifosfamide

-mech:

A
  • alkylating agent, Covalently X-link (interstrand) DNA at guanine N-7.
  • Require bioactivation by liver.
78
Q

Nitrosoureas

  • suffix?
  • use?
  • tox?
A
  • “-ustine”
  • carmustine, lomustine, semustine, streptozocin.
  • brain tumors (crosses BBB).
  • tox: CNS toxicity
79
Q

Which alkylating agents cross the BBB?

A

Nitrosoureas

80
Q

Busulfan

  • mech:
  • use:
A

-alkylating agent
-CML. Also used to ablate patient’s bone marrow before
bone marrow transplantation.

81
Q

Nitrosoureas

-mech:

A

-alkylating agent

82
Q

Busulfan

-tox:

A
  • severe myelosuppression
  • pulmonary fibrosis
  • hyperpigmentation
83
Q

Alkylating agents

-mnemonic

A

Beat Cancer Now!

-busulfan, nitrosoureas, cyclophosphamide, ! = I = ifosfamide

84
Q

Vinca Alkaloids

  • name some
  • what do they bind?
A
  • Vincristine, vinblastine

- β-tubulin

85
Q

Vincristine: tox?
Vinblastine: tox?

A

-Vincristine—neurotoxicity (areflexia, peripheral neuritis),
paralytic ileus.

-Vinblastine blasts bone marrow (suppression).

86
Q

Taxanes

  • name some
  • tox:
A
  • paclitaxel

- Myelosuppression, alopecia, hypersensitivity.

87
Q

Cisplatin, carboplatin

  • mech:
  • tox:
  • antidote:
A
  • Cross-link DNA
  • Nephrotoxicity and acoustic nerve damage.
  • Prevent nephrotoxicity with amifostine (free radical
    scavenger) and chloride diuresis.
88
Q

Chloride diuresis

  • prevents toxicity from which drug?
  • how?
A

Cisplatin stays in a nonreactive state when in a higher chloride concentration.

89
Q

Etoposide, teniposide

  • same mechanism as what other drugs?
  • tox:
A

Fluoroquinolones

  • inhibits topoisomerase 2
  • tox: Myelosuppression, GI irritation, alopecia.
90
Q

Irinotecan, topotecan

  • mech:
  • tox:
A
  • Inhibit topoisomerase I.

- Severe myelosuppression, diarrhea.

91
Q

Hydroxyurea

-mech:

A

-Inhibits ribonucleotide reductase

-

92
Q

Most commonly used glucocorticoids in cancer chemotherapy.

A

Prednisone (prednisolone)

93
Q

Tamoxifen, raloxifene

A 
Both = antagonists at breast
Both = agonist at bone
Tamoxifen = partial agonist at endometrium (hot flashes)
Raloxifene = antagonist at endometrium
94
Q

HER-2 (c-erbB2)

  • codes for what?
  • involved in what types of cancers?
  • which drug helps w/this type of cancer?
A
  • tyrosine kinase receptor
  • breast & gastric
  • Trastuzumab (Herceptin)
95
Q

Trastuzumab (Herceptin)

  • toxicity?
  • mnemonic:
A

-Cardiotoxicity.

“HEARTceptin” damages the HEART.

96
Q

Imatinib (Gleevec)

-tox?

A

fluid retention

97
Q

Rituximab

  • mech:
  • tox:
A
  • Mab against CD20 (found on most B-cell neoplasms).
  • risk of progressive multifocal leukoencephalopathy.

*PML also associated w/JC virus = polyomavirus

98
Q

Vemurafenib

  • mech:
  • use:
A
  • inhibitor B-Raf kinase with the V600E mutation.

- Metastatic melanoma.

99
Q

Bevacizumab

  • mech:
  • tox:
A
  • Mab against VEGF. Inhibits angiogenesis.

- tox: Hemorrhage and impaired wound healing.

100
Q

Drugs that cause alopecia

-mnemonic?

A

Propecia Every Day = PED
P = paclitaxel
E = Etoposide (& teniposide)
D = Doxorubicin (& daunorubicin)

101
Q

Michaelis menton constant

A

Km

102
Q

Lineweaver-Burk plot

  • is this the inverse one? or is that michaelis menton?
  • slope =?
  • y-intercept =
  • x-intercept =
A
  • this = inverse/reciprocal one.
  • slope = Km/Vmax
  • y-int = 1/Vmax
  • x-int = 1/-Km
103
Q

Effects of comp/noncomp inhibitors on Lineweaver-Burk plot.

A
  • competetive inhib: inc. Km (closer to 0)

- noncomp inhib: dec. Vmax = higher y-int.

104
Q

Irreversible competetive inhibitors

  • what do they do to lineweaver burke plot?
  • do they resemble a comp or noncomp inhibitor?
A
  • just like a non-comp inhibitor

- Km same, Vmax dec. (higher y-int).

105
Q

The effects of the body on the drug.

-pharmacokinetics or dynamics?

A

Pharmacokinetics

ADME: 
 ƒ Absorption
 ƒ Distribution 
 ƒ Metabolism 
 ƒ Excretion
106
Q

The effects of the drug on the body.

-pharmacokinetics or dynamics?

A

Pharmacodynamics

-Includes concepts of receptor binding, drug efficacy, drug potency, toxicity.

107
Q

Link btwn wide-spectrum antibiotics and bleeding disorders?

A

May kill off bugs that are making vitamin K.

108
Q

Diamond-Blackfan anemia

A

Pure RBC aplasia

  • anemia, not pancytopenia.
  • radial abnormalities
  • cleft lip
  • shield chest
  • web neck
  • short stature
109
Q

Pancytopenia w/thumb anomalies

A

Fanconis anemia

-auto recessive aplastic anemia

110
Q

Which leukemia was most associated w/radiation exposure?

A

AML

111
Q

greater than 10% band neutros, tachy.

-think what?

A

sepsis

-bands are present during a systemic inflammatory response.

112
Q

ribavirin

  • use:
  • tox:
A
  • RSV, chronic hepatitis C

- hemolytic anemia, teratogen

113
Q

Volume of distribution (Vd)

  • equation?
  • will they give you the Vd of the particular drug?
A
  • Vd = total dose/plasma conc.

- yes, for instance they’ll say 1L/kg. So if you weigh 70kg, the Vd will be 1*70 = 70L

114
Q

How many half-lives to reach 90% of the steady-state level.

A

3.3 half lives.

115
Q

Half life

-equation:

A

t1/2 = (.693*Vd)/Cl

116
Q

How to Dx B12 deficiency definitively?

A

blood methylmalonic acid levels.
-cant do serum B12 b/c there can be B12 bound to protein in blood but its not free B12 so they can still have B12 deficiency.

117
Q

Why do you see target cells in hemoglobinopathies?

ie. beta-thal

A

Not enough Hb = RBC less full = membrane blebs in the middle.

118
Q

Sideroblastic anemia

-iron status?

A

Iron overloaded state.

-high ferritin

119
Q

hydrops fetalis

-which thalassemia?

A

alpha-thal

-4 allele deletion.

120
Q

anaphylaxis: complement components that cause degranulation?

A

C3a, C4a, C5a

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