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HemeOnc > Malignant hematology, solid tumors & cancer pharm > Flashcards

Malignant hematology, solid tumors & cancer pharm Flashcards

1
Q

Acute vs. chronic leukemia/lymphoma

A

Acute: Cx of precursor/immature cells

Chronic: Cx of mature cells

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2
Q

Diff. b/t leukemia and lymphoma

A
  • Leuk: Malignant cells circ. in blood –> find on periph smear
  • Lymphoma: dz centered in lymphoid tissues (nodes, spleen, MALT/BALT, etc)
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3
Q

Key to diagnosing the following:

  • Leukemia
  • Lymphoma
A
  • BM aspiration/biopsy & periph. smear
  • Biopsy of enlarged lymph node (or extranodal mass)
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4
Q

What are the three mainstream methods used to classify

heme malignancies by specific cell type (in addition to histopathology w/ standard stains)

A
  • Histochem (specific cell enzymes)
  • Flow cyt (surface Ag’s)
  • Xsomal analysis
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5
Q

What are the two major types of acute leukemias?

A

AML and ALL

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6
Q

Epidem. AML

A
  • Older adults (median age = 65 yo)
  • 80% adult / 15% peds
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7
Q

Epidem. ALL

A
  • Median age: 3-5 yrs
  • Most common childhood Cx
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8
Q

Major classes of R/F’s fro developing heme Cx (w/ example if appropriate) - 5

A
  1. Genetic disorder (downs)
  2. Hemetologic disorder
  3. Rads
  4. Chems
  5. Chemo-caused (alkylators)
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9
Q

What are the “top two” clinical manif’s of acute leuk?

A
  • BM failure
  • Leukocytosis (hyperprolif) –> Leukostasis (abnormal intravascular leukocyte aggregation and clumping. It is most often seen in leukemia patients. The brain and lungs are the two most commonly affected organs)
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10
Q

Why does leukostasis occur often in acute leuk’s?

What can it lead to?

A

Huge prolif. of immature WBC’s (blasts) –. very viscous blood.

Leads to: cerbral symptoms, pulm. symptoms, depending on where stasis takes place.

AML>ALL (makes sense b/c more WBC’s made in myeloid pathway)

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11
Q

What are some of the S/S of ALL outside of BM that you might see on PE?

A

Remember… ALL affects lymphoid tissues… so:

  • Lymphadenopathy, splenomeg
  • Testes (rarely)
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12
Q

Extramed. prez of AML (3)

A
  • Leuk. cutis (skin rash)
  • Gingival hypertroph.
  • Chloroma (blast tumor)
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13
Q

What is a renal complication that can take place in ALL? AML?

A
  • ALL: tumor lysis syndrome - from chemo - get hyperUric/Phosph/K. Uric acid nephropathy –> renal failure.
  • AML: HypoK from renal tubular damage (lysozyme released from blasts)
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14
Q

What is the typical morphology of ALL and AML cx cells?

A
  • ALL: Increased lymphoblasts that are TdT+
  • AML: myeloblasts + Auer rods
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15
Q

Key immunohistochemical (IHC) marker (1 each) of ALL cells? AML?

A
  • ALL: TdT+
  • AML: Myeloperoxidase crystallizes as Auer rod (and also can do IHCstaining for it), MP+
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16
Q

Auer rod

A

LInear aggreations of granules, seen only in myeloblasts (AML)

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17
Q

What is the FAB classificaton of AML that we have to know? why?

A
  • M3 (Acute Promyelocytic Leukemia, APL) promyelocytic, hypergranular
  • need to know b/c it has diff’t Rx from the rest of the AML’s
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18
Q

What is the “name” of AML:M3?

Defining morph and genetic features?

A
  • Promyelocytic leuk.
  • Morph: biolobed nuc, large gran’s, Auer rods
  • Genetic: t(15;17)
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19
Q

FAB classification in ALL is based on _____

A

morphology

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20
Q

What is the main WHO category for AML? ALL?

A
  • AML: AML w/ recurrent genetic abnorm’s
  • ALL: B cell ALL w/ genetic abnorm’s
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21
Q

What is the key histochemical + stain for ALL?

A

TdT (terminal deoxynudleotidyl transferase)

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22
Q

Key immunohistochenical + stain for AML cells?

A
  • Myeloperoxidase (in granules)
  • Lysozyme (indicates myeloid diff’tiation)
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23
Q

Immunotyping in acute leukemias. Indicate th key immune markers for the following:

  • AML
  • Precursor B cell (ALL)
  • Tc (ALL)
A
  • AML: CD 13, 33, 117
  • Precursor B cell (ALL): CD 10, 19, 20
  • Tc (ALL): CD 2,3,4,5,7,8
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24
Q

APML

  • Def
  • genetic subtype of which cancer?
  • favorable or unfavorable risk category?
  • First-line Rx?
A
  • acute promyelocyte leukemia (APML)
  • t(15:17) subtype of AML
  • favorable
  • ATRA (all-trans retinoic acide, basically vitamin A)
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25
Q

Two unfavorable cytogenetics in ALL

A
  • t(9:22): phil. xsome (seen also in CML - worse prog. w/ higher recurrence)(
  • t(v;11)
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26
Q

Favorable cytogenetics in ALL?

A

t(12;21) - ++ in kids

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27
Q

Stages of chemo Rx in AML w/ def.

A
  1. Induction: initial blast of chemo
  2. Consolidation (post-remission): prevent replase by killing residual leuk. cells
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28
Q

Stagse of chemo Rx in ALL - define each one.

A
  1. Induction: killing!
  2. Intensification/consolidation: reduce total body leuk. burden
  3. Maintenance: eradicate redidual dz (lo dose)
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29
Q

What are the 4 nitrogen mustard drugs to know? What is the prototype?

A

*Cyclophosphamide
*Ifosfamide
*Chlorambucil
*Melphalan

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30
Q

What are the two phases in Gompertzian growth? Which are most effective for chemo + immunotheraphy?

A
  • Log-linear: earlier growth - ideal time for chemo and immunotherapy (the latter- specifically in first half of log-linear growth).
  • Plateau
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31
Q
  • Best time to kill tumor
A
  • Log-linear growth phase of Gompertzian growth curve
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32
Q

When is immunother. of most benefit?

A

log-linear growth phase of tumor

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33
Q

What are the 3 modalities of treating heme Cx’s (chemo)?

A
  1. Induction: KILL
  2. Consolidation: Mop up
  3. Maintenance: low dose, get rid of residual
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34
Q

Types of chemo Rx in solid tumors

A
  • Adjuvant therapy: Systemic, often post-surgery as in breast Cx - coul be chemo or hormonal.
  • Neoadjuvant ther: shrink tumor , possibly pre-surg.
  • Palliation: comfort, quality of life
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35
Q

Respnse criteria:

  • Complete response (CR)
  • Partial (PR)
  • Stable Dz (SD)
  • Progressive dz (PD)
A
  • Complete response (CR): all tumor gone
  • Partial (PR): at least 50% dec.
  • Stable Dz (SD): b/t a 50% decrease and 25% increase
  • Progressive dz (PD): incraese of more than 25% in diameter of any lesion
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36
Q

Typical chemo cycle

A

21 days, first three give drugs (single, combo) then 18 days recov.

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37
Q

What parts of the cell cycle do diff’t cX drugs work on?

A
  • Non-specific
  • Mitosis (M)
  • Synthesis (S)
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38
Q

Explain the general MOA for drugs that work at M and S in cell cycle.

A
  • M: these interrupt microtubles needed for proper mitosis.
  • S: these are anti-metabolites, and pyrimidine analogs that act as DNA chain terminators.
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39
Q

Most common chemo toxicity?

A

Nausea & vomiting.

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40
Q

What are two NT’s that can activate the emetic center?

A

5-HT and Dopamine

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41
Q

Ondansetron

  • Use
  • MOA
  • S/E
A
  • antiemetic
  • 5-HT antag. (binds serotonin in GI tract & CNS)
  • headache
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42
Q

Aprepitant

  • use
  • MOA
  • Interactions
  • Often used in combo with…
A
  • Acute & delayed vomiting - antiemetic (often used with cisplatin)
  • NK-1 antagonist
  • Many interactions inc. dexamethasone, but dexameth is not contraindicated
  • (see below)
  • Ondansetron + dexameth is a common combo Rx for chemo regimens w/ high N/V profile.
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43
Q

What are the two dopamine antagonists we shoudl know?

Discuss:

  • Use
  • MOA
  • 1st line or adjuvant?
  • Tox
A

*Prochlorperazine
*Metoclopramide

  • Antiemetics
  • Dopamine antagonists
  • Adjuvant to NK-1 / 5-HT antagonists
  • extrapyramidal SE’s, sedation
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44
Q

What kinds of drugs are Prochlorperazine and Metoclopramide

A

Dopamine-antagonist antiemetics (adjuvant to 5-HT and NK-1 antag’s)

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45
Q

Dexamethasone

  • Use
  • MOA
  • Tox
A
  • Generally a 1st- line antiemetic
  • Unknown!
  • glucose intol, insomina, agitation
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46
Q

What are the two Epo analogs to know about?

A

procrit and darbepoetin

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47
Q

Procrit , Darbepoetin

  • Use
  • Tox
  • Consideration when admistering
A
  • Rx anemia (in this context, anemia caused by chemo, rad)
  • HTN, rash
  • Must have adequate Fe stores - perhaps admminister Fe.
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48
Q

Why types of drugs are used to treat chemo-induced neutropenia? Give names

A

Myeloid GF’s: filgrastim and pegfilgrastim

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49
Q

Filgrastim, Pegfilgristim

  • Use
  • SE’s
A
  • Myeloid growth factors to increase neutrophil count (used proph and in establish neutpenia)
  • Fever, bone pain
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50
Q

Alkylating agents

  • General MOA
  • What part of cell cycle they effect
A
  • Cause abnormal covalent linkages/crosslinks which –> DNA damage
  • Not cell-cycle specific!
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51
Q

General toxicities of alkylators (6)

A
  • BM suppression (directly cytotoxic)
  • N/V (most chemo drugs do this!)
  • diarrhea, anorexia (direct dmg to GI tract cells - rapidly dividing)
  • Sterility (cytotoxic)
  • 2ndary malignancy

NB: note how most of these are caused by the killing of rapidly dividing cells!

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52
Q

*Cisplatin

  • use
  • MOA
  • SE (3)
A
  • Chemo for solid tumors
  • Cross-linking via platinum
  • Nausea / vomiting, nephrotoxic, neurotoxic (axonal degen w/ stocking & glove dist.)
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53
Q

What is a major SE/complication of platinum analogues in addition to neurotoxicity & N/V?

A

Nephrotoxicity

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54
Q

Three considerations in management of nephrotoxicity of cisplatin?

A
  • avoid renally toxic drugs (NSAIDS, etc)
  • Monitor renal fxn
  • Monitor for anemia (dec. EPO)
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55
Q

How to prevent nephrotoxicity in cisplatin?

A
  • hydration
  • hypertonic saline
  • mannitol
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56
Q

Describe the neurotixicity of cisplatin

A
  • axonal degen w/ periph. neuropathy, stocking/glove dist.
  • Can also get audit. impairment
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57
Q

Carboplatin

  • Type/Use
  • MOA
  • SE (2)
  • Interaction
A
  • Platinum analogue - 2nd gen. version of cisplatin
  • Same as cisplatin - DNA dmg via crosslinks
  • Hypersens in 10%, neurotox but, **no nephrotoxicity (as in cisplatin)
  • must be administered after taxane to lower toxicity.
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58
Q

Cyclophosphamide

  • Class
  • Use/MOA
  • Cell cycle phase affected
  • Toxic metabolite created
A
  • Nitrogen mustard (alkylator)
  • Chemo - causes cross-linking
  • *non cell cycle specific!
  • Acrolein
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59
Q

Cyclophosphamide toxicity

A
  • Delayed N/V
  • Hemoragghic cystitis (acrolein)
  • Cardiotoxic
  • Immunosupression
  • Neutropenia
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60
Q

*Ifosfamide

  • Class
  • Toxicity
  • Clearance considerations
A
  • Nitrogen mustard chemo agent
  • Increased renal tox vs. cyclophosphamide (otherwise same as cyclo)
  • P450 - sensitive to inducers and inhibitors.
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61
Q

Why is mesna used in ifosfamide administration?

A

Ifosfamide produces higher levels of acrolein. Mesna binds acrolein in bladder to reduce cystic problems.

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62
Q

Main uses of glucocort’s in Cx Rx (2)?

A
  • Lympholytic (ALL, NHL)
  • Also 1st line Rx for N/V (antiemetic)
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63
Q

Main use of androgens in cx Rx?

A
  • Myelodysplastic synd
  • Other BM failure synd’s

**boosts RBC prodn

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64
Q

Danazol

  • Class
  • Use
A
  • Androgen analog
  • Boos RBC prod in myelodyspalstic, BM failure synd’s
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65
Q

flutamide, bicalutamide

  • class
  • use
  • tox
A
  • anti-androgen
  • Prostate Cx
  • hot flashes, dec. libido, gynecomastia
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66
Q

tamoxifen

  • Use, class
  • **MOA (including internal signaling molecule)
  • Tox
A
  • adjuvant, neoadjuvant, antiestrogen for breast cx
  • Competes w/ estrogen at receptor –> stimulates TGF-B –> dec. proliferation
  • menopausal sx’s
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67
Q

Raloxifene

  • Class
A

antiestrogen, akin to tamoxifen

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68
Q

What are the three aromatase INH’s to know?

A

*Anastrazole
*Letrozole
*Exemestane

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69
Q

*Anastrazole
*Letrozole
*Exemestane

  • MOA
  • Use
  • Tox
A
  • Aromatase INH’s: Reduce estrogen by INH of aromatase (testosterone–[aromatase]–>estrogen)
  • Same SE’s as tamoxifen
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70
Q

*Leuprolide
*Goserelin

  • Class
  • MOA
  • Use
  • Tox
A
  • LH-RH antagonists
  • Supress gonadotropins
  • Testicular, breast & ovarian Cx’s
  • hot flashes, gynecomastia
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71
Q

What are teh two LH-RH antagonists to know?

A

*Leuprolide
*Goserelin

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72
Q

In the scheme of heme malignancies, where does NHL fit in?

A
  • Chronic (mature cells mostly)
  • Lymphoma: dz of B,T and NKC’s (NHL can affect both B and T cells)
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73
Q

def. lymphoma

A
  • Tumor of Lc’s w. growth in nodes but may invade other organs
  • generally not a lot of circulation in blood in signficant #s
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74
Q

What is the most common hematological cx?

A

NHL (85% are of B cell origin)

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75
Q

NHL: clinical pres

A
  • Swollen nodes
  • Pain
  • Fevers, night sweats, fatigue
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76
Q

Two main categories of NHL (w/ most common dz)

A
  • Indolent (follicular lymphoma - FL)
  • Aggressive (diffuse large B cell - DLBC)
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77
Q

Dx of NHL

A
  • Core needle biopsy (not fine needle asp) of node/extramed/marrow.
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78
Q

Staging schematic for NHL

A
  • I: single node
  • II: 2+ nodes, same side diaph.
  • III: 2+ node groups, both sides diaph.
  • IV: extranodal dz
  • plus A = asympt, B = symptomatic
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79
Q

What is the IPI in context of NHL?

A

Just a more systemic way to index prognosis - don’t have to know specifics.

80
Q

What are ther. goals in Rxing indolent vs. aggressive NHL?

A
  • Indolent: sympt. control (not goin for cure)
  • Aggressive: cure
81
Q

Rx modalities, NHL

A
  • Rad
  • Chemo
  • Possible stem cell xplant (aggressive)
  • (not surg.)
82
Q

What is an adjuvant drug that has increased overall survival in NHL and CLL?

A

Rituximab (causes cell death) - used w/ success in lymphomas b/c it is a direct CD 20 antibody (Mab). CD 20 is present on Bc’s in both NHL and CLL.

83
Q

Epidemiology of Hodgkin’s lymphoma

A

Bimodal dist - peark in early 20’s, early 60’s

84
Q

Relationship b/t Epstein-Barr Virus (EBV) and Hodgkin’s lymphoma?

A

50% of cases have EBV DNA in the Reed-Sternberg cells.

85
Q

What is the diagnostic cell of HL? Describe.

A

Reed-Sternberg cell :binucleated large cell, represents a malignant B Lc.

86
Q

R/S cell in HL - immuno+ for what CD’s?

A

CD 15 and 30

87
Q

What is the most common classical HL? Non-classical?

A

Classical: Nodular sclerosis (NS)

Non-classical: Nodular lymphocyte predominance (NLP)

88
Q

Explain Ann Arbor staging for HL (Stages (I-IV)

A

I: Single lesion (remember that HL will generally make a chain of involved LN’s whereas NHL is more spurious)

II: 2 lesion same side

III: Dz above AND below diaph.

IV: Diffuse non-lymphoid spread, extranodal dz

plus

A: Absence of sx’s

B: “B symptoms” - fever, night sweats

M: Bulky mediastinal mass

E: Extranodal

89
Q

What is the general Rx approach to HL?

A

Rx as aggressive dz –> aim for CURE.

90
Q

What is the CD difference b/t nodular sclerosis HL and nodular lymphocyte predominance HL?

A

NS: CD 15,30+

NLP: CD 20+

91
Q

What is the advantage of ABVD therapy vs MOPP?

A

Lowers r/o secondary leukemia or loss of fertility.

92
Q

What are the three antimetabolite drugs we should know? Where do they work in the cell cycle?

A

*Methotrexate
*5-Fluorouracil
*Hydroxyurea

These work in the S phase of cycle - make problems during DNA synth.

93
Q

MTX

  • MOA
  • Kinetics consideration (1)
  • Elimination
A
  • Inhibits creation of purines
  • Tends to accumulate in third spaces due to hi water solubility (ascites, effusions)
  • Renal
94
Q

Leucovorin

  • Use
  • Dosing consideration
A
  • A MTX rescue drug - increased mTHF to nl cells > cx cells.
  • Dosing: timing very important
95
Q

R/F’s for developing MTX toxicity (renal)

A
  • Poor hydration
  • acidic urine
  • low Cr-Cl
  • Third spacing
96
Q

In addition to renal tox, what are the other tox’s of MTX (3)?

A
  • GI - use anti emetics
  • Hepato: monitor liver enzymes
  • mucositis: due to increased sloughing, cell death
97
Q

What are two important interactions to consider (with an example) w/ MTX?

A
  • Drugs that affects plasma protein binding (Salicylates)
  • Drugs that affect Cr-Cl (NSAIDS)
98
Q

Ara-C (cytaribine)

  • Type/MOA
  • Clearance
  • Tox nl dose (3)
  • Tox hi dose (3)
A
  • Type/MOA: antimetabolite, S-phase chemotherapy, falsely incorporates into DNA (a pyrimidine analog)
  • Clearance: renal
  • Tox nl dose (3): myelosuppression, flu-like synd, mucositis
  • Tox hi dose (3): cerebellar tox, ocular tox, noncardiogen. pulm. edema
99
Q

5-FU (5-Fluorouracil)

  • Use/MOA
  • Specific to what phase of cycle?
  • Syergistic w/ ??
  • Advantage WRT clerance/metab.
  • Main toxicities to remember (2)
A
  • Use/MOA: antimetabolite chemo drug
  • Specific to what phase of cycle?: S phase
  • Syergistic w/ ??: leucovorin
  • Advantage WRT clerance/metab.: can be used in pts w/ mild to moderate renal & hepatic failure
  • Main toxicities to remember (2): mucositis/diarrh & myelosupression
100
Q

What are the two pyrimidine analog drugs used in chemo?

A

Cytaribine & gemcitibine (notice that these are analogs to pyrimidINEs)

101
Q

Gemcitabine

  • Type/MOA
  • Major toxicity to remember (1)
  • Interactions
A
  • Pyrimidine analog chemo drag (S phase specific)
  • Myelosupression
  • Potent radiosensitizer (‘preps’ cells for rad Rx); enhances cytotoxicity of cisplatin.
102
Q

What part of the cell cycle do anthracyclines affect?

A

Non-cell-cycle specific

103
Q

Anthracyclines

  • Ones we need to know
  • Class
  • Cell-cycle specific?
  • MOA
A
  • *Doxorubicin
    *Daunorubicin
  • Chemo Ab’s
  • Mess up DNA Topo2 INH
  • Not cell-cycle specific
  • Intercalates into DNA –> breaks in DNA –> poor replication.
104
Q

Anthracyclines

  • Elimination
  • Tox/ SE’s (4)
  • Key complications (1)
A
  • Hepatic
  • Myelosuppression, alopecia, N/V, cardiotoxic
  • Extravasation –> skin necrosis
105
Q

Discuss acute & chronic cardiotoxicity assoc. w/ anthracyclines

A
  • Acute: acute changes EKG sim. to MI
  • Chronic (more common): dec in LVEF akin to LHF/CHF.
106
Q

What is presumed mechanism of cardiotox in anthracyclines?

A

Production of reactive O2 species to which cardiomyocytes are esp. sensitive.

107
Q

What drug is cardioprotective in anthracycline cardiotoxicity? S/E’s?

A
  • dexrazoxane: an Fe chelator - decreases free rad. formation
  • SEs: Very similar to the anthracyclines but no cardiotox. (myelosuppression, alopecia, N/V, mucositis)
108
Q

What mediates anthracycline resistance?

A
  • MDR transporter
109
Q

What are the two antracyclines to know?

Primary uses of each (types of cx)?

A
  • *Doxorubicin: breast, lymphomas (solid)
    *Daunorubicin: leukemias (liquid)
110
Q

Bleomycin

  • Drug class
  • Cancer use
A
  • Antitumor antibiotic
  • HL
111
Q

camptothecin drugs

  • representative
  • MOA
  • Cell cycle specific?
  • SEs (only rep. drug)
A
  • Irinotecan
  • Topo I INH
  • S phase
  • SE’s: neutropenia, early & late onset diarrh
112
Q

Irinotecan

  • Class
  • MOA
  • Use
A
  • Camptothecin (plant alkaloid)
  • TopoI INH
  • Colon & lung xc
113
Q

Why do TopoI INH’s work in fighting cx? Example drug?

A

B/c evidently Cx cells have more TopoI than nl cells. Irinotecan.

114
Q

How to Rx the early onset diarrh from irinotecan?

A

Atropine (the GI probs though to be due to hypercholinergic syndrome)

115
Q

Vinca alkaloids

  • Three representative drugs to know
  • Cell cycle specificity?
  • MOA
A
  • Three representative drugs to know:

*Vincristine
*Vinblastine
*Vinorelbine

  • Cell cycle specificity?: M1
  • MOA: distrub MT formation
116
Q

Primary toxicities of:

  • *Vincristine
    *Vinblastine
    *Vinorelbine
A
  • *Vincristine: perhiph neuropahty
  • *Vinblastine: myelosuppression
  • *Vinorelbine: both of above
117
Q

Chronic leukocytic leukemia (CLL)

  • Def
A
  • Type of chronic leukemia w/ accum of mature cells, high WBC count.
118
Q

CLL

  • Prolif ot what type of cell
  • Cell surface marker
  • Smear shows?
  • Clinical sign
A
  • Prolif of mature but naive Bc’s
  • CD 20+
  • Smear: Increased leukocytes, smudge cells
  • LAD
119
Q

Complication of CLL (2)

A
  1. Autoimmune hemolytic anemia: can produce Ab against RBC’s
  2. Can transform to Diffuse Large B-Cell Lymphoma (DLBC) - this will be seen via an increasing size of LN’s and spleen.
120
Q

CLL

  • Epi
  • Diagnosis
A
  • Most common leukemia in western world
  • Lymphocytosis (increase in # of small, mature Lc’s), BM involvement, clonal expansion of Bc’s.
121
Q

How does Rai staging (simplified) work in CLL?

A

Stage 0 = low

I-II: Intermed.

III-IV: Hi

122
Q

What surface proteins, assay proteins and cytogenetics assoc. w/ worse prognosis in CLL (1 assay protein, 2 genetic, 1 surface marker)?

A

ZAP-70

del(17p)

del(11q)

CD 38

123
Q

Unfavorable cell surface marker in CLL?

A

CD 38 = poor prognosis

124
Q

CLL Rx goals

A

An indolent dz. Goal: sx control not cure.

125
Q

What is a targeted therapy being used in CLL Rx?

A

Rituximab - anti-CD20

126
Q

What is a key lab finding (gel) for plasma cell malignancies?

A

M-spike (Mab)

127
Q

What are the parts of an Ig and which xsomes code for them?

A
  • 2 heavy chains (c14)
  • 2 light chains - either Kappa (c2) or Lambda (c22)
128
Q

Monoclonal gammopathy of uknown significance (MGUS)

  • Def
  • Type of what disorder?
  • Diagnosis
  • Clinical course
A
  • Def: plasma cell disorder w/ abnormally hi levels of serum Ig
  • Type of what disorder? as above
  • Diagnosis: serum Ig >- 3g/dL
  • Clinical course: progresssion 1%/yr.
129
Q

Multiple Myeloma

  • Type of dz
  • Epi
  • Dx
  • S/S
A
  • Plasma cell neoplasm
  • Epi: rare, adult (65 median age)
  • Dx: higher M-spike + can do BM aspirate and skeletal survey also.
  • CRAB (hyperCa, Renal dysfx, Anemia, Bone lesions)
130
Q

What is the cause of the lytic bone lesions in multiple myeloma?

A

The cancer cells (plasma cells) are closely assoc. w/ osteoclasts and boost their activity –> lesions.

131
Q

What are the 2 components of the ISS prognostic scoring system for Mult. myeloma?

A

albumin and beta-2
microglobulin

132
Q

In addition to Multiple Myeloma, what are three other plasma cell disorders to recognize?

A
  • heavy chain disease
  • Waldenstrom’s
  • cryoglobulinemia
133
Q

Myelodysplastic syndrome DEF

A

Cytopenia with hypercellular marrow and dysplastic cells.

134
Q

What is the cause of cytopenias in myelodysplastic synd?

A

Innefective hematopoeisis of 1+ myeloid lineage caused by defects in the HSC.

135
Q

Myelodysplastic syndrome: greater risk for / can progress to ____

A

AML

136
Q

Myelodysplastic synd’s

  • Etiology
  • Clinical
  • Smear
  • BM morphology
  • Cytogenetics
A
  • Post-chemo (esp. alkylators, topo INH), post-XRT, benzene, tobacco, Fanconi anemia
  • Cytopenias, B symptoms, risk AML progression
  • Anemia w/ megalobastic RBC’s (large, nucleated), basophilic stippling
  • Hypercellular marrow w/ ringed sideroblasts
  • Del(5q): good, Monosomy 7/Del(7q): poor, 11q23, poor.
137
Q

Rx of myelodysplastic syndromes

A
  • Support for cytopenias (xfusion, chelation)
  • Hypomethylating agents (eg decitabine)
  • Allogeneic HSC xplant (curative)
138
Q

What are the distinctive smear cells in myelodys. synd’s?

A

pseudo pelger-huet neutrophil w/ bilobed nucleus

139
Q

How does IPSS scoring work in myelodysp. syndromes?

A

Based on

  • % blasts (BM)
  • Marrow karyotype
  • # and degree of cytopenias
  • age
140
Q

Describe 5q- syndrome (a myelodysplastic synd.)

  • Epi
  • Smear
  • Clinical
  • Pt count?
  • Clinical course
A
  • F>M
  • Mk’s w/ hypolobated nuclei
  • refractory macrocytic anemia
  • nl or increased Pt’s
  • favorable
141
Q

BM xplant DEF

A

Transplant of HSCs (CD34+)

142
Q

Sources of BM for xplant (3)

A
  • BM aspirate
  • Periph blood
  • Cord blood
143
Q

Autologous BM xplant

A

refers to source being pt’s own marrow or cord blood; allows for pre-xplant myeloabaltive chemo

144
Q

Myeloablative chemo

A

Agressive chemo performed before an autologous BMT - used to basically kill all cells in BM including cx cells.

145
Q

Syngeneic BMT

A

From an ident. twin

146
Q

allogeneic BMT

A

could be from twin, HLA-matching siblign, or unrelated donor

147
Q

Primary indications of the following:

  • Autologous BMT
  • Allogeneic BMT
A
  • Autologous BMT: used primarily in lymphoprolif. disorders (mult. myeloma, NHL, HL)
  • Allogeneic BMT: used primarily in myelogenous disorders (AML, CML plus ALL, MDS/MPD, aplastic anemia)
148
Q

Graft-vs-tumor effect in BMT

A

An effect taken advantage of in allogeneic BMT where the graft cells kill the tumor cells. Part of the curative process of the BMT.

149
Q

Haplotype DEF

A

A set of closely linked DNA sequence variants on a single chromosome - in BMT, used for matching.

150
Q

GvHD

  • Def
  • Acute vs. chronic
A
  • Def: Graft (BMT) immune system attacks host (takes place in 50%)
  • Acute vs. chronic:
  • Acute: Mucosal disruption in gut lining –> Tc and cytokine-mediated reaction –> severe rash, GI sx’s, hepatic.

- Chronic: Months after BMT w/ autoimmune-like sx’s (lots of skin abnl’s, GI strictures esp. esophageal)

151
Q
  • Short-term risks/complications of autologous & allogeneic BMT (4)
  • Which complication has a higher chance of happening in allogeneic?
A
  • Neutropenia (give antibios)
  • Anorexia (give TPN)
  • Hepatic failure
  • GvHD (higher chance in allogeneic)
152
Q

Rituximab

  • Use & target
  • Type
  • Tox (1)
  • Syndrome that can result from Rx?
  • What dz can reactivate?
A
  • Use: NHL, CLL (anti-CD20)
  • Type: Mab
  • Toxicities: Immunosuppresive (can reactivate Hepatitis), tumor lysis syndrome (HI YIELD: this is from killing of the CD20+ cells, resulting in release of purines which can lead to uric acid nephropathy)
153
Q

Cetuximab

  • Target
  • Uses
  • Tox (2)
A
  • Target: EGFR
  • Uses: solid tumors
  • Tox: Acneiform rash (tox-man!)
154
Q

Trastuzumab

  • Target
  • Use
  • Tox (1)
A
  • Target: HER2/neu (an oncoprotein that binds a Tyr kinase)
  • Use: breast cx
  • Tox: Cardiotoxic
155
Q

Bevacizumab

  • Target
  • Use
  • Tox
A
  • Target: VEGF
  • Use: solid tumors
  • Tox: impaired would healing (black box), HTN, thrombosis, bleeding
156
Q

Action of the “-nib” drugs, in general

A

Tyr Kinase INH’s

157
Q

Erlotonib

  • Target
  • Use
  • Tox (2)
A
  • Target: EGFR Tyr kinase
  • Use:NSCLC
  • Tox: Acneiform rash, diarrhea
158
Q

Imatinib

  • Target
  • Use
  • Tox (3)
A
  • Target: **INH’s Bcr-Abl Tyr Kinase **
  • Use: CML
  • Tox: Edema, cytponeias, cardiotox
159
Q

Thalidomide

  • Use
  • MOA
  • Adverse rxns (4)
A
  • Multiple myeloma
  • MOA: unknown
  • Adverse rxns: Teratogenic, neorotoxic, sensory sx’s, sedative.
160
Q

Lenalidomide

  • Advantages over thalidomide?
A
  • less neurotoxicity than thalidomide
161
Q

Azacytidine

  • Use
  • MOA
  • Tox (3)
A
  • Use: Myelodysplastic synd.
  • MOA: hypomethylation
  • Tox: Myelosuppression, N/V, Diarrh
162
Q

Decitabine

A

see azacytidne

163
Q

Bortezomib

  • Use:
  • MOA:
  • Tox (2)
A
  • Use: Mult. myeloma, NHL
  • MOA: proteosome INH
  • Tox: myelosupression, sensory neuropathy
164
Q

Major tox of interferons?

A

flu-like syndrome

165
Q

What are the specific immunohistochemical stains for the following cx types?

Carcinomas (2)
Lymphomas
Melanoma
Neuroendocrine tumors (3)
Germ cell tumors (2)
Soft tissue tumors

A
  • Carcinomas – CK, EMA
  • Lymphomas – LCA
  • Melanoma – S100
  • Neuroendocrine tumors – chromogranin, synaptophysin, NSE
  • Germ cell tumors – beta-HCG, AFP
  • Soft tissue tumors – vimentin
166
Q

5 most common cancers, males:

A
  • Prostate
  • Lung
  • Colon
  • Bladder
  • Melanoma (skin)
167
Q

5 most common cx’s, females

A
  • breast
  • lung
  • colon
  • uterine
  • thyroid
168
Q

What is the avg age dx of breast cx?

A

60

169
Q

What cx dominates the younger age groups (0-9)?

A

leukemia

170
Q

Myeloprolif disorder

  • DEF
  • Major features
A
  • Abnormal (neoplastic) accum. of mature myeloid cell types.
  • High WBC, hypercellular BM
171
Q

Complications of myeloprolif disorders (3)

A
  • Hyperuricemia/gout (too much cell tunrover –> cell death –> more purines)
  • Marrow fibrosis
  • can xform to acute leukemia (if mutation progresses back to HSC’s)
172
Q

CML

  • Class of dz and Def
  • Smear
  • Abnormal cytogenetics
A

CML

  • Chronic myelogenous leukemia: a type of myeloprolif. disorder
  • Smear: prolife of myeloid cells but basophils in particular
  • Abnormal cytogenetics: Philadephia xsome, t(9;22) - Bcr-Abl.
173
Q

What is the abnormal cytogenetics in CML?

What is a targeted therapy?

A
  • t(9;22) - bcr/abl (an abnormal Tyr kinase)
  • Imatinib blocks Tyrk kinase activity.
174
Q

CML

  • Risks for transformation (to what dz’s?)
  • Sign of transformation
A
  • 2/3 –> AML, 1/3 –> ALL
  • Splenomegaly incidates increase in pace of dz w/ higher chance of preogression to acute leukemia.
175
Q

How is it possible for CML ( a dz of myeloid lineage) to progress to ALL?

A

Indicates that mutation started (or got into) the HSC CD34+ cell line and then went into lymphoid lineage.

176
Q
  • DEF leukemoid rxn
  • How to distinguish b/t that, and CML (3)?
A
  • DEF leukemoid rxn: elevated WBC counts, genearally due to acute medical condition.
  • How to distinguish b/t that, and CML?:
  1. CML cells are LAP- (a normal granuclocyte protein)
  2. CML: increased basophils
  3. cytogenetics - t(9;22)
177
Q

Polycythemia vera

  • DEF
  • Mutation
  • Clinical picture
  • Rx
  • How to distinguish from reactive polycythemia?
A
  • DEF: myelodysplastic disorder w/ prolif esp of RBC’s
  • Mutation: JAK-2 Tyr kinase
  • Clinical picture: hypervisious blood –> blurry vision, headache, inc. risk thrombosis.
  • Rx: Phlebotomy, hydroxyurea (antimetabolite, S phase)
  • How to distinguish from r_eactive polycythemia (RP)_?: In RP, Sat will be low and EPO will be HI.
178
Q

Essential Thrombocythemia

  • Def
  • Smear
  • S/S
  • Major diff b/t this and polycythemia v., CML?
A
  • Myeloprolif. disorder of mature cells, with especially increased pt’s
  • Lots of platelets!
  • S/S: increase r/o bleeding or thormobsis
  • Major diff b/t this and polycythemia v., CML? No increase in gout, lower chance of progressing to marrow fibrosis or acute leuk.
179
Q

Chronic Eosinophilic Leukemia

  • Def
  • Smear
  • Mutation
  • Complications
A
  • Def: myeloprolif. disorder w/ hypereosinophilia
  • Smear: as above - lots of eosins!
  • Complications: thrombosis or pulmonary/ cardiac fibrosis due to eosinophilic degranulation.
180
Q

Rx of CML

A
  • Imatinib (anti bcr/abl Tyr kinase)
  • BM xplant
181
Q

Myelofibrosis

  • DEF
  • Clinical (1)
  • Smear (2)
  • Complications/risks
A
  • Myekloproliferative disorder (neoplasm) w/ elevated Mk’s
  • Clincal: (1) splenomeg (increased splenic hematopoeisis)
  • Smear: lots of immature cells inc. nucleated RBC’s due to extramed. h’poeisis, teardrop RB cells (fibrosed BM –> defomration)
  • Complications/risks: infection, thromosis, bleeding
182
Q

What is meant by neoadjuvant therapy? Give example of one for breast cx.

A
  • Refers to a Rx to use before the “main treatment”
  • Best example is use of tamoxifen to reduce size of tumor before surgery.
183
Q

When are benzos used for in chemotherapy?

A

To treat anticipatory N/V

184
Q

Use of Deferoxamine, Deferasirox

A

Fe chelators, used w/ xfusion therapy.

185
Q

Tumor lysis syndrome tends to take place in what dz?

What is a drug that can be used to Rx its main complication?

A

Tumor lysis synd: lots of cells are destroyed via chemo (in acute leukemias). This frees up lots of purines which can build up and cause uric acid nephropathy, a complication of chemo.

Allopurinol: blocks creation of uric acid from purine metabolites.

186
Q

Allopurinol

  • Use
  • MOA
A

Allopurinol

  • Use: To reduce uric acid production during chemo.
  • MOA: prevents purine metabolites from producing uric acid.
187
Q

What are the three Pt analogs to know?

A

Cisplatin

Oxaliplatin

Carboplatin

188
Q

Primary use of cyclophosphamide?

A

For lymphomas (targets B and T cells)

189
Q

Common combination therapy for HL? Indicate the class of each drug.

A
  • Anthracycline
  • Dacarbazine (also an alkylator)
190
Q

what glucocorticoids commonly used as chemo agents?

for what dz’s, based on their MOA?

A

Prednisone, dexamethasone.

These are lympholytic - so used for lymphocytic leukemias and lymphomas

191
Q

What 2 drugs are mainstay Rx for ALL? Give class/MOA.

A
  • MTX (antimetabolite)
  • Cytaribine (pyr. analog/chain terminator)
192
Q

What enzyme helps to metabolize F-fluorouracil? What is the implicationf for usage/dosing?

A

DpD (dihydropyrimidine dehydrogenase)

  • Pt’s with deficient DpD may have increased 5-FU toxicity.
193
Q

Other than risk of hemorrhagic cystitis & nephrotoxicity, what is another SE of ifosfamide? What is given to treat the SE?

A
  • Encephalopathy
  • Methylene blue
194
Q

Major SE of irinotecan?

A

Early and late onset diarrhea.

195
Q

WHat drug is used particularly w/ cisplatin for acute adn delayed n/v?

A

aprepitant (NK-1 inh)

196
Q

What are two chemo agents (there are more) that can be given intrathecally?

A

MTX, cytaribine

HemeOnc (2 decks)

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