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EXAM THREE Flashcards

1
Q

Define Lymphoma

A

Malignancy of immune cells mostly in lymphoid tissues

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2
Q

Define HL Classification of Lymphoma

A
  1. Very Curable
  2. 2 Subtypes: cHL and NLPHL
  3. Similar Presentation
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3
Q

Define NHL Classification of Lymphoma

A
  1. Variable Cure Rates
  2. Many Subtypes
  3. Variable Presentation
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4
Q

Define cHL: Classical Hodgkin Lymphoma

A
  1. Bimodal Age Distribution
  2. Very Curable
  3. REED-Sternbery Cells = Owl Eyes
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5
Q

What are the typical immunophenotype on IHC in cHL?

A
  1. CD30+
  2. CD20-
  3. PDL1 and PDL2
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6
Q

What are the symptoms of Lymphoma?

A
  1. Lymphadenopathy
  2. Hepatosplenomegaly
  3. Fatigue/Malaise
  4. Whole-Body Pruritus (HL Especially)
  5. EtOH Induced Lymph Node Pain
  6. B Symptoms
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7
Q

What are the B Symptoms seen in Lymphoma Presentation?

A
  1. Fever >100.4
  2. Drenching Night Sweats
  3. Unintentional Weight Loss >10% over past 6 months
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8
Q

What things are needed the diagnosis, staging, and prognostication of Lymphoma?

A
  1. Lymph/Bone Marrow Biopsy
  2. Pathology
  3. PET/CT
  4. Labs
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9
Q

Initial cHL Treatment Considerations

A
  1. CURABLE INTENT
  2. Chemotherapy +/- Radiation
  3. Response Adapted Treatment
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10
Q

Stage I-II Favorable Initial cHL Treatment

A

ABVD x 2-4 cycles +/- Radiation

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11
Q

Stage I-II Unfavorable Initial cHL Treatment

A
  1. ABVD x 4 cycles + Radiation
  2. ABVD x 2 cycles —> AVD x 4 cycles
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12
Q

Stage III-IV Initial cHL Treatment

A

ABVD x 2 cycles —> AVD x 4 cycles
Escalated BEACOPP
A + AVD x 6 cycles

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13
Q

What is ABVD for cHL aka the Standard Care?

A
  1. Adriamycin
  2. Bleomycin
  3. Vinblastine
  4. Dacarbazine
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14
Q

When is ABVD given in a 28 day cycle treatment plan?

A

Day 1 and Day 15

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15
Q

Adriamycin aka Doxorubicin MOA and Cell Cycle

A

DNA intercalation + Topoisomerase II
Cell Cycle SPECIFIC

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16
Q

What are the dose-limiting toxicities of Adriamycin/Doxorubicin?

A
  1. Myelosupression
  2. Cardiotoxicity
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17
Q

What are the AEs of Adriamycin/Doxorubicin?

A
  1. Alopecia
  2. Urine Discoloration
  3. GI Effects
  4. Secondary AML
  5. Sterility
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18
Q

What is the vesicant for Adriamycin/Doxorubicin?

A

Cold + DMSO

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19
Q

What is the MOA and Cell Cycle of Bleomycin?

A
  1. DNA strand breakage
  2. Cell Cycle SPECIFIC G2 + M Phase
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20
Q

What is the dose limiting toxicity of Bleomycin?

A

Pulmonary Toxicity

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21
Q

What should Bleomycin NOT be used with due to increased risk of Pulmonary Toxicity?

A
  1. GCSF
  2. Brentuximab Vedotin
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22
Q

What is the MOA and Cell Cycle of Vinblastine?

A
  1. Binds to tubular and inhibits microtubule formation
  2. Cell Cycle SPECIFIC M Phase
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23
Q

What is the dose limiting toxicity and AE of Vinblastine?

A
  1. Myelosuppression
  2. Constipation
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24
Q

What is the vesicant for Vinblastine?

A

HOT + Hyaluronidase

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25
Q

What is a concern with administering Vinblastine?

A

Do NOT Administer Intrathecally

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26
Q

What is the MOA and Cell Cycle of Dacarbazine?

A
  1. Addition to Guanine, DNA break, Apoptosis
  2. Cell Cycle NONSPECIFIC
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27
Q

What is the dose limiting toxicity and emetic potential of Dacarbazine?

A
  1. Myelosuppression
  2. High Potential
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28
Q

What is Subsequent Therapy for Refractory/Relapsed (R/R) cHL?

A

Brentuximab Vedotin (mono therapy or combo)

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29
Q

What is the MOA of Brentuximab +/- Bendamustine?

A

Targeted Therapy +/- Alkylating Agent

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30
Q

What is the dose limiting toxicity of Brentuximab +/- Bendamustine?

A

Peripheral Neuropathy and Myelosuppression

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31
Q

What is the Indication for Brentuximab Vedotin?

A
  1. Advanced cHL
  2. R/R cHL
  3. Consolidation after
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32
Q

What is the MOA and dose limiting toxicities of Brentuximab Vedotin?

A
  1. Binds CD30
  2. Neutropenia and Peripheral Neuropathy
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33
Q

Can Bleomycin be used with Brentixumab Vedotin?

A

NO

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34
Q

What is the MOA and Cell Cycle for Bendamustine?

A
  1. Single and double strand cross linking
  2. Cell Cycle NONSPECIFIC
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35
Q

What is the dose limiting toxicity for Bendamustine?

A

Delayed Myelosuppression (nadir ~D21)

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36
Q

What is ICE and when is it used?

A
  1. Ifosfamide
  2. Carboplatin
  3. Etoposide
    Refractory R/R cHL
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37
Q

What is GemOx and when is it used?

A
  1. Gemcitabine
  2. Oxaliplatin
    Refractory R/R cHL
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38
Q

ICE therapy requires growth factor support due to high NF risk, but what are the other AE concerns?

A
  1. CNS Neurotoxicity (ifosfamide)
  2. Nephrotoxicity (ifosfamide)
  3. Infusion Rxn
  4. EtOH (etoposide)
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39
Q

GemOx therapy requires growth factor support due to high NF risk, but what are the other AE concerns?

A
  1. Toxicity with Infusion Rate (gemcitabine)
  2. Cold Induced Neuropathy (oxaliplatin)
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40
Q

What is the MOA of Pembrolizumab + GVD, and what is GVD?

A

Immunotherapy + Chemotherapy for TRANSPLANT Eligible patients
1. Gemcitabine
2. Vinorelbine
3. Liposomal Doxorubicin

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41
Q

What is the dose limiting toxicity of Pembrolizumab + GVD?

A

Myelosuppression

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42
Q

What are the risk factors for Non-Hodgkin Lymphoma NHL?

A
  1. Increased age, more common in white men
  2. EBV/HIV/HEP C Infections
  3. Prior exposure to radiation and alkylating agents
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43
Q

What types of NHL are consider INCIDENT and what is the presentation?

A

FL Grade 1 and 2
1. Wax and Wane Adenopathy

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44
Q

What types of NHL are consider AGRESSIVE and what is the presentation?

A

DLBCL FL Grade 3
1. B symptoms
2. Obstruction Adenopathy

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45
Q

What types of NHL are consider VERY AGRESSIVE and what is the presentation?

A

Double/Triple Hit, DLBCL, and Burkitt’s
1. Rapidly growing mass
2. B symptoms

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46
Q

What is the most common NHL?

A

Diffuse Large B cell Lymphoma DLBCL

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47
Q

What is the typical immunophenotype of DLBCL?

A
  1. CD20+
  2. CD19+
  3. CD79a/b+
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48
Q

What is the standard therapy for DLBCL?

A

R-CHOP

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49
Q

Define R-CHOP

A
  1. Rituximab on Day 1
  2. Cyclophosphamide on Day 1
  3. Doxorubicin on Day 1
  4. Oncovin (VINCRISTINE) on Day 1
  5. Prednisone on Day 1-5
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50
Q

Rituximab is a Anti-20 agent, what are the points to know about it’s role in R-CHOP?

A
  1. NO DLT
  2. Infusion rxns
  3. Can reactivate Hep B
  4. PRETREAT
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51
Q

What medications must you pretreat with for Rituximab?

A
  1. APAP
  2. Diphenydramine
    Given before each dose
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52
Q

Cyclophosphamide is an Alkylating agent, what are the points to know about it’s role in R-CHOP?

A
  1. Interstand DNA strand cross linking
  2. DLT = Myelosuppression
  3. AE =Alopecia, Infertility, and SIADH
  4. Emetic Potential = HIGH, acute & delayed
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53
Q

Vincristine is an Vinca Alkaloid, what are the points to know about it’s role in R-CHOP?

A
  1. DLT = Neurotoxicity (peripheral neuropathy)
  2. Hepatic Metabolism
  3. Vesicant = HOT
  4. Do not administer intrathecally
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54
Q

What is the MAX Weekly Dose for Vincristine?

A

2 mg

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55
Q

What is Double and Triple Hit (HGBL DLBCL) Lymphoma?

A

Translocations of MYC + BCL2 +/- BCL6

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56
Q

Is there a poor or good prognosis of HGBL DLBCL with R-CHOP and what is the standard of care?

A

POOR, no standard of care yet

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57
Q

For R/R DLBCL, if >12 months from the last line of chemotherapy, for 2nd line chemotherapy if responsive consider what?

A

AutoHSCT

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58
Q

For R/R DLBCL, if >12 months from the last line of chemotherapy, for 2nd line chemotherapy if unresponsive consider what?

A

CART

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59
Q

For R/R DLBCL, if <12 months from the last line of chemotherapy or primary refractory consider what?

A

CART +/- Bridging Therapy

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60
Q

What therapy regimen is Preferred for R/R DLBCL 2nd line setting?

A

RGemOx or RICE
AKA Adding Rituximab to the original GemOc or ICE

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61
Q

CART therapy cause cytotoxicity of the tumor cells, but what are the adverse reactions of this therapy used for R/R DLBCL Lymphoma?

A
  1. CRS
  2. ICANS
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62
Q

What is used in the treatment of CRS/ICANS?

A

Corticosteroids and/or Tocilizumab

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63
Q

What is used for 2nd Line Option +/- Bridging Therapy for R/R DLBCL?

A

Polatuzumab Vedotin w/ Bendamustine + Rituximab

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64
Q

Polatuzumab Vedotin targets CD79b as its MOA but what are the AEs of the agent?

A
  1. Myelosuppression
  2. Neuropathy
  3. Hepatotoxicity
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65
Q

Polatuzumab Vedotin requires what prophylaxis before starting treatment?

A
  1. PJP – bactrim
  2. HSV – acyclovir
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66
Q

What is the indication and MOA of Tafastimab + Lenalidomide?

A
  1. 2nd Line Option, potential option for patients not sutiable for intense chemotherapy (BRIDGE to autoHSCT or CART)
  2. Targeted drug therapy + iMID oral therapy
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67
Q

What is the indication and MOA of Loncastuximab Tesirine?

A
  1. 3rd Line Option, potential option for patients not suitable for intense chemotherapy
  2. Targeted drug therapy, alkylating agent
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68
Q

What are the AEs of Lenalidomide?

A

Myelosuppression and VTE

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69
Q

Use of Lenalidomide requires what?

A

ASA 81 mg QD

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70
Q

What are the AEs of Loncastuximab Tesirine?

A

Myelosuppression, Infection, and Edema

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71
Q

Use of Loncastuximab Tesirine requires what?

A

Dexamethasone to prevent edema

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72
Q

What is the 2nd most common form of NHL?

A

Follicular Lymphoma

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73
Q

What is the typical immunophenotype of Follicular Lymphoma FL?

A

CD20+

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74
Q

What is the therapy for Grade 1&2; Stage I&II FL?

A
  1. Watch and Wait
  2. Radiation +/- Rituximab
  3. Rituximab Monotherapy
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75
Q

What is therapy for Grade 1&2; Stage III&IV Grade 3a? FL?

A
  1. Rituximab or Obinutuzumab + Bendamustine
  2. RCHOP
  3. Rituximab + Lenalidomide
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76
Q

What is therapy for Grade 3b FL?

A
  1. RCHOP
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77
Q

What is maintenance therapy for FL?

A
  1. Rituximab q2-3 months x 2 years
    2.Obinutiuzumab q2months x 12 doses
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78
Q

What is the MOA of Obinutuzumab?

A

Anti-CD20

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79
Q

What is the required study prior to initiating Obinutuzumab?

A

HepB Serologies

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80
Q

What are the Non-Modifiable Risk Factors of Breast Cancer?

A
  1. Genetics
  2. Age >60
  3. Endogenous Estrogen Exposure
  4. Breast Cancer
  5. Benign Thoracic Irradiation
  6. Personal FH
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81
Q

What are the Modifiable Risk Factors of Breast Cancer?

A
  1. Obesity/BMI
  2. Physical Activity
  3. Alcohol
  4. Exogenous Estrogen Exposure
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82
Q

A decrease in weight in premenopausal women would increase their risk of breast cancer true or false?

A

True

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83
Q

What are the 2 Risk Assessment Models commonly used for Breast Cancer?

A
  1. Gail Model
  2. Modified Gail Model
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84
Q

When are annual mammograms recommended?

A

Average Risk Women >40 yrs

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85
Q

What deems a patient high risk of Breast Cancer?

A
  1. Prior History
  2. Lifetime Risk >20
  3. Prior RT
  4. 5y Gail MR
  5. BRCA1/2 Mutation
  6. FH of BRCA Mutation
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86
Q

What are forms of Primary Prevention for Breast Cancer?

A
  1. Mastectomy (90%)
  2. B/I Oophorectomy (50%)
  3. Tamoxifen
  4. Raloxifene
  5. Aromatase Inhibitors
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87
Q

When would Tamoxifen be used in Primary Prevention of Breast Cancer and what is the concern with its use?

A

Used for PRE and POST menopausal women
1. Increased Endometrial Cancer
2. Increased VTE

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88
Q

When would Raloxifene and Aromatase Inhibitors be used in Primary Prevention of Breast Cancer?

A

POSTmenopausal women

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89
Q

What are the 4 Types of Breast Cancer?

A
  1. Lobular Carcinoma in SITU (LCIS)
  2. Ductal Carcinoma in SITU (DCIS)
  3. Invasive Lobular Carcinoma (ILC)
  4. Invasive Ductal Carcinoma (IDC)
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90
Q

What two forms of “Breast Cancer” are not malignant but are considered PRE-Cancer?

A
  1. LCIS
  2. DCIS
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91
Q

What is TNM Staging in Breast Cancer?

A

T = Size of main tumor
N = Lymph node spread
M = Metastasis

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92
Q

Where are the most common sites of tumors in Stage IV Breast Cancer?

A
  1. Bones
  2. Lungs
  3. Liver
  4. Brain
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93
Q

What are the 3 markers for Breast Cancer?

A
  1. ER = estrogen receptor
  2. PR = progesterone receptor
  3. HER2 = her2 neu protein
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94
Q

Normal Cells HER2 gene number

A

2-5 copies of HER2 gene
Up to 20,000 HER2 receptors

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95
Q

Breast Cancer Cells HER2 gene number

A

20-25 copies of HER2 gene
Up to 2 million HER2 receptors

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96
Q

IHC Score for HER2 Breast Cancer

A

0-1+ = negative
2+ = equivocal
3+ = positive

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97
Q

What are the Prognostic Factors of Breast Cancer?

A
  1. Response to Systemic Chemotherapy
  2. Estrogen Receptor ER/Progesterone Receptor PR Status
  3. Grade
  4. Proliferation Rate Ki-67
  5. HER2 Amplification/Overexpression
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98
Q

For Response to Systemic Chemotherapy (prognostic factor in breast cancer), is Primary Resistance a good or poor prognosis?

A

POOR

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99
Q

For ER/PR Status (prognostic factor in breast cancer), is a Positive Status a bad prognosis true or false?

A

FALSE
Positive = GOOD prognosis

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100
Q

For a <50 yo woman with a <15 RS or >50 yo woman with <25 RS, what should be recommended?

A

Endocrine/Hormone Therapy

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101
Q

For a <50 yo woman with >15 RS or >50 yo woman with >25 RS, what should be recommended?

A

Chemoendocrine/Chemotherapy + Hormone Therapy

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102
Q

Oncotype Prognostic Tools predicts recurrence with EBC and benefit from chemotherapy, must demonstrate what to use these tools

A

ER+,, HER2-, and LN-

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103
Q

<25 RS vs >25 RS EBC means what in terms of chemotherapy?

A

> 25 = chemo + hormone
25 = NO chemo benefit

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104
Q

What role does Surgery have in treatment of BC?

A

Role in Stage I-III

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105
Q

What is BCS (Lumpectomy)?

A

Increase in loco regional recurrence >5cm

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106
Q

What role does Radiation have in treatment of BC?

A

With BCS or Mastectomy

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107
Q

What is Neoadjuvant?

A

Before Surgery

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108
Q

What is Adjuvant?

A

After surgery, prevent micrometastatic disease from progressing

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109
Q

When would you use Adjuvant Chemo?

A
  1. LN Positive
  2. HER2 Positive
  3. TNBC
  4. Oncotype Score
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110
Q

When would you use Adjuvant Hormone Therapy?

A

ER/PR+ or following cytotoxic chemo

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111
Q

What is TNBC?

A

Triple Negative

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112
Q

What 3 Categories fall under Early BC?

A
  1. HER2+ (HR+/-)
  2. TNBC
  3. HR+/HER2-
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113
Q

What are the 3 Therapy Regimens for HER2+ BC?

A
  1. TCH
  2. TCHP
  3. Weekly Paclitaxel, Trastuzumab +/- Pertuzumab
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114
Q

What is TCH Regimen?

A
  1. Docetaxel
  2. Carboplatin
  3. Tratuzumab
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115
Q

What is TCHP Regimen?

A
  1. Docetaxel
  2. Carboplatin
  3. Trastuzumab
  4. Pertuzumab
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116
Q

What drugs should be avoided with Trastuzumab?

A

AVOID Anthracycline: rubicins

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117
Q

What is AC-T?

A

A = Doxorubicin
C = Cyclophosphamide
T = Paclitaxel

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118
Q

What is recommended ACT-T or TCHP for HER2+ EBC?

A

TCHP, ACT-T has increased CHF and heart issues

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119
Q

Why add Pertuzumab to TCH or Weekly Paclitaxel+Tratsuzumab for EBC HER2+?

A

Improved invasive disease free survival

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120
Q

For HER2+ Treatment EBC, Start with TCHP or Weekly Pac+Trast (HP) then followed by surgery, what is recommended if the patient has NO residual disease?

A

Tratsuzumab +/- Pertuzumab

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121
Q

For HER2+ Treatment EBC, Start with TCHP or Weekly Pac+Trast (HP) then followed by surgery, what is recommended if the patient has residual disease?

A

Ado-Trastuzumab Emtansine or continue with Pac + Trast (HP) for 1 yr

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122
Q

What are the treatment options for HR+/HER2- EBC?

A
  1. Dose Dense AC-T
  2. Dose Dense AC + T
  3. TC
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123
Q

What is Dose Dense AC-T?

A
  1. Doxorubicin
  2. Cyclophosphamide
  3. Paclitaxel q2weeks
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124
Q

What is Dose Dense AC + T?

A
  1. Doxorubicin
  2. Cyclophosphamide
  3. Paclitaxel weekly
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125
Q

What is TC?

A
  1. Docetaxel
  2. Cyclophosphamide
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126
Q

What drugs are preferred in HR+ HER2- EBC?

A

Anthracyclines, reduce recurrence by 25%

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127
Q

What are the treatment regimen options for TNBC EBC?

A

-Neoadjuvant Pembrolizumab + [TC] Carboplatin + [TC] Paclitaxel followed by
-Pembrolizumab + [AC] Doxorubicin + [AC] Cyclophosphamide followed by
-Surgery + Pembrolizumab +/- Capcitabine

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128
Q

What is the treatment considerations for Metastatic Breast Cancer?

A
  1. Bone Disease
  2. ER/PR+, HER2-
  3. TNBC
  4. HER2+
  5. HER2 LOW +1/2/FISH Non-Amplified
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129
Q

For patients with MBC Bone Metastasis, what bone modifying agents can be added to current regimen?

A
  1. Pamidronate
  2. Zoledronic Acid
  3. Denosumab –> preferred
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130
Q

What is the treatment therapy plan for ER/PR+, HER2- NO Visceral Crisis MBC?

A
  1. Change Endocrine = Tamoxifen, Letrozole, Anastrozole, Exemesane, Fulvestrant
  2. Premenopause = Tamoxifen –> AI [aromatase inhibitor]+OAS [ovarian ablation]
  3. Fulvestrant + Alpelisib for PIK3 mutated MBC
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131
Q

What is the treatment therapy plan for ER/PR+, HER2- Visceral Crisis MBC?

A
  1. IV Chemo
  2. Combination? –> increased toxicity and no OS benefit
  3. Treat with previous agents is okay for TAXANES!!
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132
Q

What is the treatment agent options for HER2- MBC?

A
  1. Liposomal Doxorubicin
  2. Weekly Paclitaxel
  3. Oral Capecitabine
  4. Gemcitabine
  5. Vinorelbine
  6. Eribulin
  7. Ixabepilone
  8. Albumin-Bound Paclitaxel
  9. Carboplain + Gemcitabine
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133
Q

Sacituzumab is approved ONLY for what type of MBC?

A

TNBC

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134
Q

What is first line therapy for HER2+ MBC?

A
  1. Trastuzumab + Pertuzumab + Docetaxel or Paclitaxel
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135
Q

What is second line therapy for HER2+ MBC?

A
  1. Ado-Tratuzumab Emtansine
  2. Fam-Tratuzumab Emtansine
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136
Q

What is the BBW and Max Lifetime Dose of Doxorubicin which inhibits Topoisomerase II?

A

Cardiomyopathy
MAX = 550 mg/m2

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137
Q

What is the Monitoring and AEs of Doxorubicin?

A
  1. ECHO/MUGA at baseline
  2. Cardiotoxcitiy, Discoloration of Bodily Fluids
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138
Q

If CHF develops from Doxorubicin there is a 50% mortality rate, what is used for the prevention of cardiomyopathy and treatment of extravasation of Doxorubicin?

A

Dexrazoxane

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139
Q

What is Doxorubicin and Cyclophosphamide used for?

A

AC and AC-T therapy regimens in HR+/HER2- EBC

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140
Q

What is the AE of Cyclophosphamide that is an alkylating agent preventing cell division by cross linking DNA strands?

A

Hemorrhagic Cystitis

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141
Q

Are Doxorubicin and Cyclophosphamide highly emetic agents true or false?

A

True

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142
Q

Paclitaxel is used in AC-T for HR+/HER2- EBC, what is its AEs?

A
  1. Infusion Reactions –premedicate (famotidine/dex/diphen)
  2. Peripheral Neuropathy – EXAM
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143
Q

Docetaxel is used in TC [HR+/HER2-] and TCHP [HER2+], what is its AEs?

A
  1. Neurotoxicity
  2. Edema
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144
Q

What must you premeditate with for Docetaxel to prevent Fluid Retention?

A

Dexamethasone 8 mg PO BID x 3 days

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145
Q

Carboplatin is used in TC+Pem [TNBC] and TCHP [HER2+], what is its AEs?

A
  1. N/V
  2. Neuropathy
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146
Q

What is the CrCl cutoff for Carboplatin?

A

CrCl <50 = dose reductions

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147
Q

Gemcitabine is only used in MBC and inhibits ribonucleotide reductase, when do you dose reduce with Gemcitabine?

A

Bilirubin >1.6 mg/dL

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148
Q

Vinorelbine is a single agent that inhibits microtubule formation for HER2- MBC what do you have to monitor for?

A
  1. Neuropathy/Pulmonary sis
    Neurotoxicity = AE
149
Q

Eribulin inhibits formation of mitotic spindles and used as a single agent for HER2- MBC, what is its AEs?

A

Peripheral Neuropathy

150
Q

Ixabepilone inhibits formation of mitotic spindles and used as a single agent for HER2- MBC, what is its AEs?

A
  1. Neuropathy
  2. Arthralgia/Myalgia
  3. Infusion Reactions
151
Q

Albumin Bound Paclitaxel is used as a single agent for HER2- MBC, what is its AEs?

A

Neuropathy

152
Q

What is the MOA of Sacituzumab Govitecan-hziy?

A

Antibody Drug Conjugate: humanized anti-trophoblast cell surface antigen (Trop-2) + Topoisomerase 1 Inhibitor SN-38

(used for TNBC following 2 prior therapies)

153
Q

What is the main AE of Sacituzumab Govitecan-hziy?

154
Q

Tratuzumab is used in TCHP HER2+ EBC, what is its BBWs and AEs?

A

BBW = Cardiomyopathy, Infusion Rxn, Pulmonary Toxicity
AE DECREASED LVEF

155
Q

What are 3 forms of resistance to Trastuzumab?

A
  1. Steric Effects
  2. Alternate Elevations
  3. Intracellular Alteration Signaling
156
Q

What is the MOA of Pertuzumab used in TCHP HER2+ EBC?

A

Binds to dimerization domain of HER2 protein, inhibits dimerization = apoptosis

157
Q

What are the AEs of Pertuzumab?

A
  1. Diarrhea
  2. DECREASED LVEF
158
Q

Pertuzumab can ONLY be given with Trastuzumab, not as monotherapy or with any other agent true or false?

159
Q

What is the MOA of Ado-Tratuzumab Emtansine?

A
  1. Tratuzumab MOA: binds HER2 and inhibits proliferation
  2. Microtubule Inhibitor DM1 = apoptosis
160
Q

What is the BBW/AEs of Ado-Trastuzumab Emtansine?

A

BBW = cardiomyopathy, hepatotoxicity
AE = DECREASED LVEF

161
Q

What is the MOA and USE of Fam-Trastuzumab Deruxtecan?

A
  1. Tratuzumab MOA: binds HER2 and inhibits proliferation
  2. Topoisomerase I Inhibitor = apoptosis
    USED in HER+ MBC after failure of 2 previous lines of treatment
162
Q

What is the AEs of Fam-Trastuzumab Deruxtecan?

A
  1. Cardiotoxicity
  2. Pulmonary Toxicity
163
Q

What is the indication of Margetuximab?

A

HER2+ MBC, in combination with chemotherapy = 3rd Line

164
Q

What is the Adjuvant Endocrine Therapy options for Normal Risk/HER2+ patients?

A
  1. Endocrine Therapy: AIs
  2. SERM: Tamoxifen
165
Q

What is the Adjuvant Endocrine Therapy options for High Risk of Recurrence patients?

A

Abemaciclib + Endocrine Therapy

166
Q

Low Levels of ER, ER/PR, and BC = better outcomes true or false?

A

False, you want HIGH levels

167
Q

Do Aromatase Inhibitors AIs work well in younger patients?

A

NO, they target fat tissues and convert androgen to estrogen

168
Q

What is the Indication and MOA of Tamoxifen?

A
  1. Hormone Receptor HR + BC; use independent of menopausal status
  2. Selective Estrogen Receptor Modulator SERM, that competitively binds to estrogen receptors
169
Q

What is the dosing for Tamoxifen?

A

20 mg po d, x 5-10 yrs

170
Q

Tamoxifen acts as an ER Agonist where and what are the effects?

A
  1. Bone = strengthens bone aka GOOD
  2. Uterine ER = increased risk of uterine cancer aka BAD
171
Q

Tamoxifen acts as an ER Antagonist where and what are the effects?

A

Breast = reduces breast cancer recurrence aka GOOD

172
Q

What is the trial and dose for Anastrozole that determined initial therapy?

A

ATAC Trial
1 mg po qd x 5 years

173
Q

What is the trial and dose for Letrozole that determined initial therapy?

A

BIG 1-98
2.5 mg po qd x 5 yrs

174
Q

What is the trial for Exemestane that determined initial therapy?

175
Q

What is the max amount of years for AI use?

176
Q

What is the MOA of AIs: Letrozole, Anastrozole, and Exemestane?

A

Selective aromatase inhibitor; inhibits peripheral conversion of androgens to estrogen

177
Q

What are the AEs of AI agents?

A
  1. Bone Loss
    –Recommend Calcium + Vitamin D +/- Denosumab
178
Q

Endocrine Therapy can caused related Hot Flashes, what is the preferred treatment of choice to treat this symptom?

A

Antidepressants = VENLAFAXINE

179
Q

What Endocrine Therapy is used in postmenopausal metastatic women ONLY?

A

Fluvestrant

180
Q

What is the MOA and Route of Fluvestrant?

A

Estrogen receptor antagonist, causes down regulation of estrogen receptors
IV ONLY

181
Q

What agents are CDK4/6 Inhibitors used in HR+, HER2- BC?

A
  1. Palbociclib
  2. Ribociclib
  3. Abemaciclib
182
Q

CDK4/6 Inhibitors are indicated for what type of BC?

A

HR+, HER2-

183
Q

What is the AE of Palbociclib and Ribociclib?

A

Neutropenia

184
Q

What is the AE of Abemaciclib?

A
  1. Diarrhea
  2. Neutropenia
  3. Nausea
  4. Fatigue
  5. VTE
185
Q

What is the monitoring for CDK4/6 Inhibitors?

A
  1. CBC
  2. CMP
    Neutropenia concerns
186
Q

What is the special monitoring parameters for Ribociclib and Abemaciclib?

A
  1. Ribociclib = ECG Baseline = QT Prolongation
  2. Abemaciclib = VTE
187
Q

What is the MOA of mTOR Inhibitors?

A

Macrolide immunosuppressant and a mechanistic target of rapamycin inhibitor aka anti proliferative and antiangiogenic (inhibit VEGF)

188
Q

Everolimus is an mTOR Inhibitor used in HR+, HER2- BC, what are its AEs?

A
  1. Stomatitis
  2. Diarrhea
189
Q

What is the MOA and Indication of PI3K Inhibitors?

A

PI3K inhibitor inhibits Act-signaling, cellular transformation, and tumor generation
Indicated for:
1. PI3KCA mutated HR+ MBC in combo with Fulvestrant

190
Q

Aleplisib is the PI3K inhibitor used in HR+ MBC, what is its AEs?

A

Hyperglycemia

191
Q

Capecitabine is used as a single agent 5-FU for BC, what are its AEs?

A
  1. Palmar Plantar Erythrodysethesia
  2. Diarrhea
  3. Stomatitis
192
Q

What drugs are PARP Inhibitors used for BRCA Mutation MBC HER2-?

A
  1. Olaparib
  2. Talazoparib
193
Q

What is the MOA and Indication of Lapatinib?

A

Tyrosine kinase inhibitor inhibits EGFR and HER2 blocking cell proliferation
Used after Trastuzumab FAILURE

194
Q

Is Lapatinib an Oral or IV medication?

195
Q

What is the MOA and Indication of Tucatinib?

A

Tyrosine Kinase Inhibitor, inhibits cell proliferation
Used with and without BRAIN Metastases

196
Q

What is the AE of Tucatinib?

A

Hepatotoxicity

197
Q

What drug is given if BC reaches Bone Metastases?

A

Zolendronic Acid

198
Q

Define Leukemia

A

Immature proliferating leukemia cells (BLASTS) inhibit normal cellular maturation in bone marrow = crowding out

199
Q

Leukemia can result in what 3 diseases?

A
  1. Anemia
  2. Neutropenia
  3. Thrombocytopenia
200
Q

What are the types of Leukemia?

A
  1. Acute Myeloid Leukemia AML
  2. Acute Lymphoblastic Leukemia ALL
  3. Chronic Myeloid Leukemia CML
  4. Chronic Lymphocytic Leukemia CLL
201
Q

What is the Etiology of Leukemia?

A

No balance between proliferation and differentiation leads to cells not differentiating past particular stage of hematopoiesis

202
Q

What are common Lab Findings for the types of Leukemia?

A
  1. Thrombocytopenia = all leukemias
  2. Leukocytes = AML/ALL/CML
  3. Lymphocytosis = CLL/ALL
  4. Disseminated Intravascular Coagulation =APL
203
Q

What are 3 Risk Factors of Acute Myeloid Leukemia AML?

A
  1. Prior exposure to Topo II Inhibitors
  2. Prior exposure to Cytotoxic/Alkylating Agents
  3. Prior Radiation
204
Q

What are the 4 Categories of AML?

A
  1. AML with recurrent cytogenetic abnormalities
  2. AML with myelodysplasia related changes
  3. Therapy related myeloid neoplasms
  4. AML not otherwise specified [NOS]
205
Q

What is the short term goal for AML treatment?

A

Complete Response CR

206
Q

What is the long term goal for AML treatment?

A

5 years considered cured

207
Q

What is the treatment algorithm for AML?

A
  1. Induction
  2. Achieve CR
  3. Determine Risk
  4. Favorable = Consolidation
  5. Unfavorable = Stem Cell Transplant
208
Q

What is Induction Therapy for AML?

A

7+3 Regimen
7 days Cytarabine
3 Days Anthracycline (idarubicin or daunorubicin)

209
Q

What should be the dose for Daunorubicin in induction therapy for AML in patients <65 yrs?

A

INTENSE = 90

210
Q

What is Consolidation Therapy for AML?

A

HIGH DOSE Cytarabine = 3 grams

211
Q

Is Maintenance Therapy, low dose chemo for 1-3 years used in AML?

A

NO, used in APL

212
Q

What is the MOA/Class of Cytarabine?

A
  1. Antimetabolite S Phase Specific
  2. Inhibits DNA polymerase halting chain synthesis
213
Q

What is the dose limiting toxicity of Cytarabine?

A
  1. Leukopenia
  2. Thrombocytopenia
214
Q

What should be given with Cytarabine to prevent Conjunctivitis?

A

Dexamethasone Eye Drops 0.1% q6hrs and continues 24hrs after last dose

215
Q

What is Vyxeos?

A

Liposomal Daunorubicin and Cytarabine

216
Q

What is the indication of Vyxeos?

A

Treatment of patients with newly diagnosed therapy related AML or AML with myelodysplasia related changes

217
Q

Vyxeos does not work for the general public due to risks that are what?

A

It accumulates in bone marrow with preferential uptake by leukemia cells = PROLONGED CYTOPENIAS

218
Q

What is Mylotarg?

A

Gemtuzumab = CD33
Ozogamicin = dna strand breaks

219
Q

What is the toxicity associated with Mylotarg that would cause patients to immediately seek care?

A

Liver Toxicity

220
Q

The goal of treatment in Acute Lymphoblastic Leukemia ALL is what?

221
Q

What agents are used in Induction of Adult ALL?

A
  1. Anthracycline
  2. Vincristine
  3. Corticosteroid
  4. Asparginase
222
Q

Is Maintenance chemotherapy recommended in ALL? Such as Methotrexate + Vincristine once a month

223
Q

What corticosteroids are used in ALL?

A
  1. Prednisone
  2. Dexamethasone
224
Q

What toxicities are of concern with corticosteroid treatment?

A

Infection, should be on PJP prophylaxis with bactrim

225
Q

Patients with Heterozygous TPMT genotype tend to experience moderate to severe what when using 6-Mercaptopurine for ALL?

A

Myelosuppression

226
Q

What is the Pearl/DDI for 6-MP used for ALL?

A
  1. Take on an empty stomach
  2. Allopurinol reduced 6-MP by 75%
227
Q

Asparaginase is used for ALL, what is the MOA/Toxicity?

A
  1. Depletion of asparaginase in leukemia cells
  2. Allegic Rxns
228
Q

What is the MOA of Blinatumomab?

A
  1. Monoclonal antibody designed to direct cytotoxic T Cells
  2. Targets CD19
229
Q

What is the indication for Blinatumomab?

A
  1. R/R ALL
  2. Consolidation for <65 yrs without substantial comorbidity MRD+
230
Q

What are the pearls for Blinatumomab?

A

Do NOT flush infusion line

231
Q

What are the AEs of Blinatumomab?

A
  1. Cytokine Release Syndrome CRS
  2. Neurological Toxicities
  3. Infections
232
Q

What is the MOA of Inotuzumab Ozogamicin?

A

Binds CD22, induced dna strand breaks/apoptosis

233
Q

What drugs are considered CART?

A
  1. Tisagenlecleucel-T
  2. Brexucabtagene Autoleucel
234
Q

What is an Actionable Mutation?

A

Isocitrate Dehydrogenase (IDH) mutations occur in 15-20% of AML

235
Q

FLT3 Mutations occur in 30-35% of AML, what is FLT3?

A

FMS-Like Tyrosine Kinase 3
-Transmembrane protein leads to uncontrolled proliferation in bone marrow

236
Q

What is FLTL3-ITD?

A

Internal Tandem Duplication, prevents ASSOCIATION

237
Q

What is FLT3-TKD?

A

Tyrosine Kinase Doman, occurs in ACTIVATING LOOP

238
Q

What agents are FLT3 Inhibitors?

A
  1. Midostaurin = 1st gen
  2. Fliterinib = 2nd gen
239
Q

What is the indication and dose of Midostaurin?

A
  1. AML with FLT3 mutation in combination with chemotherapy
  2. Take with food
240
Q

What are the common AEs of Midostaurin?

A
  1. Neutropenia
  2. N/V/D
241
Q

What are the DDIs of Midostaurin?

A
  1. Strong 3A4 Inhibitros = fluconazole
  2. QTc prolonging drugs
242
Q

What is the MOA of Gilteritinib?

A

FLT3 TKI that is highly selective

243
Q

What is the dose/indication of Gilteritinib?

A
  1. R/R AML with FLT3 Mutation
  2. 120 mg once daily for 6 months minimum
244
Q

What are the AEs of Gilteritinib?

A
  1. Prolonged QTc
  2. Differentiation Syndrome (cytokine)
245
Q

What is the Treatment for Differentiation Syndrome?

A
  1. Stop therapy causing differentiation
  2. > 48 hrs later if symptoms persist start steroid therapy
  3. Start dexamethasone 10 mg BID x 3 days
246
Q

What are IDH Mutations?

A

IDH = Isocitrate Dehydrogenase = leads to imapired differentiation
IDH1, IDH2, IDH3

247
Q

What is the MOA/Indication of Enasidenib?

A
  1. Used for R/R AML
  2. Selective IDH2 Inhibitor
248
Q

What is the dose/BBW of Enasidenib?

A
  1. Treat for 6 months minimum
  2. Differentiation Syndrome
249
Q

What are the AEs of Enasidenib?

A

Indirect Hyperbilirubinemia -> off target UGT1A1 inhibition

250
Q

What is the MOA/Indication of Ivosidenib?

A
  1. Used for R/R AML
  2. Selective IDH1 Inhibitor
251
Q

What is the dose/warning of Ivosidenib?

A
  1. treat 6 months minimum
  2. QTc Prolongation
  3. Differentiation Syndrome
252
Q

What drugs are Hypomethylating Agents that directly incorporate into DNA?

A
  1. Azacitidine
  2. Decitabine
253
Q

What is the MOA of Venetoclax for AML?

A
  1. Selective BCL-2 Inhibitor
  2. Anti-Apoptic B Cell Lymphoma Protein
254
Q

What is the Indication for Ventoclax in AML?

A

Combinatoin with Azactidine of Decitabine for treatment of NEW diagnosed AML patients >75 yrs OR >65 yrs patients with comorbidites that preclude use of intensive induction chemo

255
Q

For Dose Escalation of Venetoclax, what should be administered with it?

A
  1. Hydration
  2. Allopurinol
256
Q

Reduce Ventoclax by 50% or 75% with what?

A

50% with fluconazole/isavuconazole
75% with voriconazole/posaconazole

257
Q

What is the most curable AMLsubtype and is associated with high incidence of disseminated intravascular coagulation DIC?

A

Acute Promyelocytic Leukemia APL

258
Q

APL has what genetic problems?

A
  1. t(15;17) results in promyeloctic gene with retinoic acid receptor alpha
  2. PML-RARa causes failure to differentiate and blocks apoptosis
259
Q

What is used in HIGH Risk WBC >10k APL Induction Therapy?

A
  1. ATRA (Tretinoin)
  2. Anthracycline (danuo or idarub)
  3. Arsenic – ONLY for those that cannot receive anthracyclines
260
Q

What is used in LOW Risk WBC <10k APL Induction Therapy?

A
  1. ATRA Tretinoin
  2. Arsenic ATO
261
Q

What is the treatment regimen for APL Consolidation?

A
  1. ATRA
  2. Anthra = high risk
  3. Or Arsenic = low risk
262
Q

What is the treatment regimen for APL Maintenance?

A
  1. ATRA
  2. 6-MP
  3. Methotrexate
    1-2 years
263
Q

What is the MOA of ATRA, Tretinoin?

A

Allows for differentiation of leukemic cells

264
Q

What is the MOA of Arsenic Trioxide?

A
  1. Damages or Degrades the fusion protein PML-RAR Alpha
  2. Allows differentiation of promyelocytic cells
265
Q

Arsenic Trioxide can cause QTc Prolongation, when should you DC or Reinitiate therapy?

A

> 500 msec or irregular heartbeat = DC
<460 msec = Reinitate

266
Q

What is the Etiology of Chronic Myeloid Leukemia?

A

Philadelphia Chromosome

267
Q

What are the 3 Classifications for CML?

A
  1. Chronic Phase CP = Benign
  2. Accelerated Phase AP = Aggressive
  3. Blast Crisis BC = Very Aggressive
268
Q

What is the MOA/Indication of Imatinib?

A
  1. Initial or Salvage Therapy for CP/BC CML
  2. Binds to ATP binding site on BCR-ABL inhibits phosphorylation
269
Q

What is the toxicities of Imatinib?

A
  1. Myelosuppression
  2. N/V
  3. Myalgias
270
Q

What are the Pearls of Imatinib?

A
  1. Take with food
  2. Limit APAP to 1300 mg/day due to liver toxicity
271
Q

What is the MOA/Indication of Dasatinib?

A
  1. Inhibits BCR-ABL
  2. Initial chronic phase or resistant CML
272
Q

What are the DDIs/dose limiting toxicities of Dasatinib?

A
  1. AVOID PPI/H2RA
  2. DLT = Pleural Effusions
273
Q

What is the MOA/Indication for Nilotinib?

A
  1. CP/AP CML
  2. Inhibits BCR-ABL
274
Q

What is the DDI/DLT of Nilotinib?

A
  1. AVOID PPIs
  2. DLT= QTc prolongation
275
Q

How do you take Nilotinib?

A

With an EMPTY stomach

276
Q

What is the MOA/Indication for Bosutinib?

A
  1. CP or R/R CML, not 1st or 2nd line
  2. Inhibit BCR-ABL
277
Q

What are the DDIs/Toxicities of Bosutinib?

A
  1. AVOID PPI
  2. Diarrhea
278
Q

How do you take Bosutinib?

279
Q

What is the MOA/Indication of Ponatinib?

A
  1. Last line R/R CML
  2. Inhibits BCR/ABL
280
Q

What are the toxicities associated with Ponatinib?

A
  1. Peripheral/Arterial Thrombosis
  2. HF
  3. VTE
  4. Hepatic
281
Q

What is used first line in CML?

A

Imatinib
or Dasatinib, Nilotinib, Bosutinib

282
Q

Therapy for CLL Upfront without Deletion of 17p for Frail or >65 yrs or with Comorbidity CrCl <70 or <65 yrs without comorbidity is what?

A
  1. Acalabrutinib +/- Obinutuzumab
  2. Venetoclax +
  3. Obinutuzumab +
  4. Zanabrutunub
283
Q

Therapy for CLL R/R without Deletion of 17p for Frail or >65 yrs or with Comorbidity CrCl <70 or <65 yrs without comorbidity is what?

A
  1. Acalabrutinib +
  2. Zanabrutinib
  3. Venetoclax +
  4. Rituximab
284
Q

Therapy for CLL Upfront WITH Deletion of 17p is what?

A
  1. Acalabrutinib +/- Obinutuzumab
  2. Venetoclax +
  3. Obinutuzumab +
  4. Zanabrutunub
285
Q

Therapy for CLL R/R WITH Deletion of 17p is what?

A
  1. Acalabrutinib +
  2. Venetoclax +
  3. Rituximab
  4. Zanabrutinib
286
Q

What is the MOA of Obinutuzumab used in CLL without deletion?

A
  1. Anti CD20
  2. Type II Antibodies induce apoptosis without cross-linking antibody
287
Q

What drugs are BCR inhibitors?

A
  1. Ibrutinib
  2. Acalabrutinib
  3. Zanabrutinib
288
Q

What is the preferred frontline treatment of CLL with 17p deletion?

289
Q

What are AEs of Ibrutinib?

A

Lymphocytosis

290
Q

What is the target of Idelalisib?

A

Used in CLL
Inhibits PI3K

291
Q

Acalabrutinib is highly potent, has a DDI with CYP3A4 substrates, and is used in CLL, what is the most common AE associated with this agent?

292
Q

Zanabrutinib is better tolerated but has what AEs?

A

Lymphocytosis

293
Q

Fludarabine is an Antimetabolite, what toxicities does it have?

A
  1. Myelosuppression
  2. Tumor Lysis Sundrome
  3. CNS Toxicity
294
Q

Fludrarabine requires prophylaxis for myelosuppresion AE, what are the premedications?

A
  1. Acyclovir
  2. Bactrim
295
Q

Deleted 17p in CLL leaned what?

A

Loss of TP53 gene, decreased survival and chemotherapy resistance

296
Q

What are the Risk Factors associated with Lung Cancer?

A
  1. Cigarette Smoking
  2. Older Age
  3. Radium 226 Decay
  4. Occupational exposure to carcinogens
  5. Radiation Therapy
297
Q

When is Low Dose Chest CT [LDCT] Recommended for Screeningn of Lung Cancer?

A

High Risk Individuals: adults age 50-80 yrs who have a 20 pack year smoking history and currently smoke or have quit within the past 15 years

298
Q

Define Small Cell Lung Cancer SCLC

A
  1. Strong correlation with smoking
  2. More agresive
  3. Highly sensitive to chemo/RT
  4. Poor prognosis, long term survival rare
299
Q

Define Non Small Cell Lung Cancer NSCLC

A
  1. Genetic
  2. 3 Subtypes: adenocarcinoma, squamous cell, large cell
  3. Squamous Cell NSCLC CORRELATED WITH SMOKING
  4. Less aggressive
300
Q

What are 2 symptoms associated with Lung Cancer?

A
  1. Superior Vena Cava SVC Syndrome
  2. Paraneoplastic Syndrome = SCLC
301
Q

What is the treatment standard for Limited Staged SCLC?

A

Systemic Chemo [Platinum Doublet] + RT

302
Q

What is the Platinum Doublet used in SCLC Limited Stage?

A

CISPLATIN + Etoposide
Use Carboplatin if Cisplatin not tolerated

303
Q

What is the treatment standard for Extensive Staged SCLC?

A

Systemic Chemo [Platinum Doublet] + Immunotherapy

304
Q

What is the Platinum Doublet used in SCLC Extensive Stage?

A

Carboplatin + Etoposide

305
Q

What is the immunotherapy in Extensive Stage SCLC?

A

Atzeolizumab

306
Q

Whole Brain Radiation WBRT, is given in what type of SCLC?

A

Extensive Stage

307
Q

Define Localized SCLC

A

There is no sign that the cancer has spread outside the lung

308
Q

Define Regional SCLC

A

The cancer has spread outside the lung to nearby structures or lymph nodes

309
Q

What is the Preferred Regimen for Relapse SCLC <6 Months? Platinum Resistance

A
  1. Topotecan
  2. Lubrinectedin
310
Q

What is Preferred Regimen for Relapse SCLC >6 Months? Platinum Sensitive

A

Use same platinum doublet regimen

311
Q

What are 3 reasons to not be a candidate for Cisplatin therapy?

A
  1. Renal Failure
  2. Ototoxicity
  3. Neuropathy
312
Q

What type of mutations are categorized as NSCLC?

A
  1. KRAS Mutations
  2. EGFR Mutations
  3. ALK Rearrangements
313
Q

What Exon mutations are EGFR Mutations?

A

Exon 19 deletions
Exon 21 Point mutation

314
Q

What is the MOA/Indication of Pemetrexed?

A
  1. Inhibits multiple enzymes
  2. Preferred in Non-Squamous and AVOID in Squamous NSCLC
315
Q

Pemetrexed has toxicities that are myelosuppression (DLT) and N/V/D, what should be given to decrease these?

A
  1. Folic Acid qd
  2. Vitamin B12 IM
316
Q

Pemetrexed can cause cutaneous reactions, what should be used for premedications to avoid this toxicity?

A

Dexamethasone x3 days

317
Q

Pemtrexed is cleared by the kidneys, and should be AVOIDED when?

A
  1. USE with NSAIDS (avoid NSAIDs)
  2. CrCl 45-79
318
Q

What two drugs are Anti-Angiogenic Inhibitors used in NSCLC?

A
  1. Bevacizumab
  2. Ramucirumab
319
Q

What is the MOA of Ramucirumab?

A

Inhibits VEGF2 by binding to it and blocks ligand binding

320
Q

What drugs are PDL1 Inhibitors and are recommended for first line NSCLC?

A
  1. Atezolizumab
  2. Avelumab
  3. Durvalumab
321
Q

What drugs are PD-1 Inhibitors for NSCLC?

A
  1. Cemiplimab
  2. Desterlimab
322
Q

What is the Management of irAE Colitis: diarrhea, abdominal pain, blood in stool?

A
  1. Supportive Care
  2. Antidiarrheals
  3. Corticosteroids
  4. Infliximab if refractory
323
Q

What is the Management of irAE Pneumonitis: dyspneaa, dry cough, SOB?

A
  1. Corticosteroids
  2. Infliximab
  3. IVIG
  4. Mycophenolate Mofetil if refractory
324
Q

What is the Management of irAE Hepatitis: ALT/AST, Bilirubin elevation?

A
  1. Corticosteroids
  2. Mycophenolate Mofetil if refractory
    AVOID Infliximab
325
Q

What is the Management of irAE Dermatitis: rash, SJS, TEN?

A
  1. Topical bethamethasone/antihistamine
  2. Corticosteroids
326
Q

What is the Management of irAE Neuropathy: myasthenia graves?

A

Corticosteroids

327
Q

What is the Management of irAE Endocrinpathy: hypo/hyper-thryoidism, gonadism, cushing’s?

A

Hormone Replacement

328
Q

If irAEs present do you dose adjust immunotherapy?

A

NO, stop and go approach

329
Q

Grade 1 irAE Steroid Dosing

A

NO, supportive care

330
Q

Grade 2 irAE Steroid Dosing

A

0.5-1 ng/kg prednisone

331
Q

Grade 3 irAE Steroid Dosing

A

1-2 mg/kg prednisone

332
Q

Grade 4 irAE Steroid Dosing

A

1-2 mg/kg methylprednisolone

333
Q

What mutations indicates RESPONSIVENESS to EGFR Tyrosine Kinase Inhibitors TKIs?

A
  1. Exon 19 Deletion
  2. Exon 21 L858R
334
Q

What mutation indicates RESISTANCE to EGFR TKIs?

335
Q

What mutation is acquired while on 1st-2nd gen EGFR TKIs, but is susceptible to Osimertinib?

336
Q

What drugs are EGFR TKI 1st gen?

A
  1. Getitinib
  2. Erlotinib
    Reversible binding
337
Q

What drugs are EGFR TKI 2nd gen?

A
  1. Afatinib
  2. Dacomitinib
    Irreversible binding
338
Q

What drugs are EGFR TKI 3rd gen?

A

Osimertinib

339
Q

What is the most common AE of EGFR Inhibitors?

A

Cuatneous Acneiform Rash

340
Q

What EGFR TKIs need to be taken on an Empty Stomach?

A
  1. Afatinib
  2. Erlotinib
341
Q

What EGFR TKI has an AE of cardiotoxicity?

A
  1. Afatinib
  2. Osimertinib
342
Q

What EGFR TKI has an AE of hyperglycemia?

A

Dacomitinib

343
Q

What EGFR TKI has an DDI of AVOIDING: PPI/H2 antagonist/Antacids?

A
  1. Erlatinib
  2. Gefitinib
344
Q

What protein leads to constitutive activation of downstream pathways leading to inhibition of apoptosis?

A

EML-4-ALK
Anaplastic Lymphoma Kinase ALK

345
Q

List the ALK Inhibitors

A
  1. Alectinib
  2. Brigatinib
  3. Ceritinib
  4. Crizotinib
  5. Lorlatinib
346
Q

List the AEs of Alectinib

A
  1. Myalgia/CPK elevation
  2. Photosensitivity
347
Q

List the AEs of Brigatinib

A
  1. HTN
  2. CPK up
  3. Elevated pancreatic enzyme
  4. Hyperglycemia
  5. Pulmonary toxicity
  6. Photosensitivity
348
Q

List the AEs of Certinib

A
  1. Diarrhea
  2. Hyperglycemia
  3. Pancreatitis
  4. QTc prolongation
349
Q

List the Aes of Crizotinib

A
  1. Ocular toxicity
  2. QTc prolongation
350
Q

List the AEs of Lorlatinib

A
  1. CNS effects
  2. Hyperlipidemia
  3. PR interval prolongation
  4. AV Block
351
Q

What is the preferred ALK Inhibitor?

A

Alectinib, take with food, and monitor CPK

352
Q

What is the indication for Sotorasib?

A

Treatment of KRAS G12C mutated locally advanced or metastatic NSCLC in patients ho have received at least 1 prior systemic therapy

353
Q

What is the dose for Sotorasib?

354
Q

What are the DDIs of Sotorasib?

A

AVOID PPIs, H2RAs, Apixaban, and Rivaroxaban

355
Q

What is the recommended therapy for Stage IA of NSCLC?

A

Surgery alone

356
Q

What ist he recommended therapy for Stage IB, II, IIIA of NSCLC?

A

Sugery + Chemo [platinum doublet]

357
Q

What is the timeline for Osimertinib for adjuvant therapy?

358
Q

What agent is used as adjuvant therapy for patietns with completely resected stage IIB-IIIA or high risk stage IIA PDL1 >1% for up to 1 year?

A

Atezolizimab

359
Q

What are the 3 histogolic classifications of NSCLC?

A
  1. Squamous Cell Carcinoma SCC
  2. Adenocarcinoma
  3. Large Cell
360
Q

When do you AVOID Bevacizumab and Pemetrexed?

361
Q

When is Pemetrexed Preferred treatment?

A
  1. Adenocarcinoma
  2. Large Cell
362
Q

SCC NSCLC patients have improved survival with what therapy?

A

Cisplatin/Gemcitabine

363
Q

What is preferred therapy for Unresectable Stage III NSCLC?

A

Paclitaxel + Carboplatin + RT + followed by Durvalumab

364
Q

What 2 mutations have targetable drugs but only in the 2nd Line setting?

A
  1. Exon 20
  2. KRAS G12C
365
Q

If patients received immunotherapy monotherapy then can go on to receive what for NSCLC?

A

Histology based on platinum doublet

366
Q

If patients progressed on immunotherapy + chemotherapy, upon progession they can receive what in NSCLC?

A

Docetaxel +/- Ramucirumab

367
Q

MOA of Platinum Agents

A

DNA crosslinks to cause damage

368
Q

MOA of Lurbinectedin

A

Alkylating agent and binds to guanine resides in DNA

Hem/Onc Module (5 decks)

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