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Crit Care, Oncology & Hematology > Lung Cancer > Flashcards

Lung Cancer Flashcards

1
Q

What is the MOST likely cause of lung cancer? What other risk factors are there?

A

TOBACCO SMOKE
Environmental respiratory carcinogens (asbestos, arsenic, air pollution)
Radiation
Genetics

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2
Q

What are some differences between small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC)?

A

SCLC: much shorter survival (1-3 MONTHS), rapid tumor growth, rarely surgical interventions but very chemo/RT-sensitive, no target agents

NSCLC: longer survival (1 year), slower tumor growth, surgery routine but not very RT/chemo sensitive, large role for target agents

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3
Q

What are common symptoms of lung cancer?

A

Pulmonary = dyspnea, cough, chest pain
Red flag = repeat scripts for pneumonia/bronchitis
Fatigue, weight loss/anorexia, hypercalcemia
Metastasis can cause neurologic sx
Superior Vena Cava (SVC) syndrome

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4
Q

Lifetime smoke history is quantified by _____________ how do you calculate this?

A

“Pack years”
= (years smoking) x (# packs/day)

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5
Q

Who should be screened for lung cancer?

A

Adults 50-80 yo
Current or former smokers who quit ≤ 15 yrs + ≥ 20 pack-year hx

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6
Q

What is the screening test for lung cancer?

A

Low Dose CT (LDCT) annually

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7
Q

What are the two steps that need to be taken to diagnose lung cancer?

A
  1. CT scan of chest
  2. Lung tissue biopsy (confirm tumor presence and type)
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8
Q

Define Early Stage, Locally Advanced Stage and Advanced Stage lung cancer

A

Early: Stage 1 or 2 w/ negative nodes
Locally Advanced: Stage 2 or 3 w/ positive nodes
Advanced: Stage 4

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9
Q

What is the difference between limited stage and extensive stage lung cancer?

A

Limited: confined to one lung +/- lymph node involvement confined to same side

Extensive: involves both lungs +/- lymph node involvement on both sides +/- extrapulmonary metastases

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10
Q

For EARLY stage NSCLC STAGE 1 what are the steps for resectable vs unresectable cancer?

A

Resectable: just resection
Unresectable: RT alone

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11
Q

For EARLY stage NSCLC STAGE 2 what are the steps for resectable vs unresectable cancer?

A

Resectable: +/- neoadjuvant & adjuvant therapy
Unresectable: Concurrent chemo & RT

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12
Q

For EARLY stage NSCLC STAGE 3 what are the steps for resectable vs unresectable cancer?

A

Resectable: Neoadjuvant therapy, adjuvant therapy, +/- RT
Unresectable: Concurrent chemo+RT, Durvalumab maintenance

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13
Q

What are some neoadjuvant regimens for early stage NSCLC?

A

Nivolumab + platinum based chemo x 3 cycles
Pembrolizumab + cisplatin chemo x 4 cycles
Platinum based chemo x 4 cycles

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14
Q

What are some adjuvant regimens for early stage NSCLC?

A

Osimertinib daily ≤ 3 years
Atezolizumab ≤ 1 year
Pembrolizumab ≤ 1 year
Platinum based chemo x 4 cycles

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15
Q

What are the platinum-based chemotherapy regimens? Which are preferred for squamous, nonsquamous and cisplatin-intolerant patients?

A

Non-squamous:
Cisplatin/pemetrexed

Squamous:
Cisplatin/docetaxel
Cisplatin/gemcitabine

Cisplatin-intolerant:
Carboplatin/pemetrexed
Carboplatin/paclitaxel
Carboplatin/gemcitabine

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16
Q

What are some AEs that CISPLATIN has?

A

N/V
Diarrhea/constipation
Nephrotoxicity (hypokalemia, Hypomagnesemia)
Ototoxicity
Peripheral neuropathy

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17
Q

What are some AEs that CARBOPLATIN has?

A

Myelosuppression (thrombocytopenia)
Diarrhea/constipation
(Fewer AEs = better tolerated than cisplatin

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18
Q

What is the weight that should be used for dosing carboplatin?

A

IBW - standard
Adjusted BW - if actual body weight is 1.2 x IBW
Actual BW - if IBW is less than ABW

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19
Q

What is the equation for IBW?

A

Male = 50 + (2.3 x inches over 5 foot)
Female 45.5 + (2.3 x inches over 5 foot)

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20
Q

What is the adjusted body weight equation?

A

IBW + 0.4 x (ABW - IBW)

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21
Q

What is the Cockcroft-Gault equation

A

(140 - age) x weight kg
——————————- x 0.85 if female
72 x SCr

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22
Q

What is the equation for carboplatin dosing? What is the max CrCl used?

A

Target AUC x (CrCl + 25)
CrCl ≤ 125 mL/min

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23
Q

What are some major AEs of the taxanes (paclitaxel/docetaxel)?

A

Alopecia
Peripheral neuropathy
Hypersensitivity reaction (premeditate, from the solvent)
Peripheral edema (docetaxel only)

24
Q

How is Pemetrexed eliminated? What level should it be avoided in?

A

Renal elimination
Avoid use if CrCl < 45

25
Q

What are some AEs of Pemetrexed? What should it be supplemented with??

A

Red/pruritic skin rash
Diarrhea
Fatigue
Supplement with: Folic acid + Vitamin B12
- use dexamethasone BID the days around chemo to decrease rash incidence

26
Q

For advanced NSCLC, we primarily use targetable genetic mutation therapy. Which mutations do we target?

A

EGFR (epidermal growth factor receptor)
ALK
KRAS
(ROS-I, BRAF, NTRK, MET, RET, HER-2)

27
Q

EGFR mutations are most prevalent in _______ and ________ in lung cancer. They target exon ____ deletions and exon ____ mutations

A

Most prevalent in adenocarcinomas and non-smokers
Target exon 19 deletion and exon 21 point mutations

28
Q

What are some EGFR drugs used in advanced NSCLC? Which is first line?

A

1st gen: erlotinib, gefitinib, afatinib
2nd gen: dacomitinib
3rd gen: Osimertinib (1st line)
-improved CNS activity and tolerability

29
Q

What are some AEs of of EGFR inhibitor Osimertinib?

A

Skin rash
Dry skin
Conjunctivitis
Diarrhea
Fatigue
Nail Toxicity
Stomatitis
Myelosuppression
QTc prolongation

30
Q

What are some nonpharmacologic PREVENTION strategies for EGFR inhibitor-related rash? What are some TREATMENTS?

A

Prevention = sun screen, gentle skin care (loose clothes, avoid hot showers, avoid OTC acne products, use hydrophilic creams)

Rx = topical or systemic corticosteroids/antibiotics

31
Q

ALK inhibitor drugs for advanced NSCLC are all _____ drugs

A

Oral

32
Q

Of the ALK inhibitor drugs for advanced NSCLC, why are Alectinib and Lorlatinib preferred?

A

Alectinib = only ALK inhibitor with significant improvement in survival
Lorlatinib = 3rd gen, improved potency and BBB penetration

33
Q

Only 2nd and 3rd gen ALK inhibitors are used in practice for NSCLC. Name these drugs!

A

2nd gen = Alectinib, brigatinib
3rd gen = Lorlatinib

34
Q

What are some AEs of ALK inhibitor brigatinib?

A

Interstitial lung disease
HTN
Diarrhea
Myalgia

35
Q

What are some AEs of ALK inhibitor Alectinib?

A

LFT abnormalities
Anemia
Constipation
Myalgia

36
Q

What are some AEs of ALK inhibitor Lorlatinib?

A

Higher BBB penetration = more CNS AEs
**Mood disorders
Neuropathy
Cognitive effects

Dyslipidemia & weight increase**

37
Q

KRAS inhibitors used for advanced NSCLC is most common in ________ patients and confer a _____ prognosis

A

Common in SMOKERS
Has POOR prognosis

38
Q

Name the two KRAS inhibitors used in NSCLC.

A

Sotorasib
Adagrasib
“-rasib”

39
Q

What is a special consideration with KRAS inhibitor sotorasib?

A

Requires an acidic environment for proper oral bioavailability
Avoid PPIs or H2RAs

40
Q

Classifying treatments for advanced NSCLC is dependent on PD-LI positive (PD-LI 1-49%, >50%) or negative (PD-LI <1%) status. What is the regimen for pts w PD-LI 1-49%? >50%? What is the regimen for negative pts?

A

POSITIVE:
PD-LI > 50% = PD-I/PD-LI inhibitor only

PD-LI 1-49% = PD-I/PD-LI inhibitor + chemo

NEGATIVE:
PD-I/PD-LI inhibitor + chemo

41
Q

What are some immunotherapy agents that can be used to treat PD-LI in advanced NSCLC?

A

Pembrolizumab, Cemiplimab (can be be used with chemo)
Atezolizumab

42
Q

If a lung cancer patient has disease progression even with therapy (NON-CHECKPOINT) what should they try?

A

Pembrolizumab
Nivolumab
Atezolizumab

43
Q

If a lung cancer patient has disease progression even with therapy (PRIOR CHECKPOINT) what should they try?

A

Docetaxel + Ramucirumab (preferred over single agent)
Docetaxel
Gemcitabine
Albumin-Bound Paclitaxel
Pemetrexed (if nonsquamous)

44
Q

What is the MOA of PD-L1? Aka why are PD-L1 inhibitors effective?

A

PD-L1 makes T-cells recognize the cancer cells as normal/prevents it from attacking. PD-L1 inhibitors cover the site from recognition and allow the T cell to attack and recruit the immune system.

45
Q

What are the grades of immunotherapy-related AEs? (Similar to exam 1) describe what actions should be taken for each grade

A

Caution in autoimmune disorder pts!
Grade 1 = continue immunotherapy
Grade 2 = hold therapy and consider corticosteroid
Grade 3+ = 0.5-2 mg/kg/day x 1 month prednisone until grade 1

46
Q

What is VEGF MOA and why is it crucial to inhibit?

A

VEGF is an angiogenic factor that is secreted by cancer cells to create new vessels. By inhibiting VEGF, we cut off nutrition to the cancer

47
Q

What are the two VEGF inhibitors used in NSCLC?

A

Bevacizumab
Ramucirumab

48
Q

What are acute AEs of VEGF inhibitors? What are some delayed AEs?

A

Acute: HTN
Delayed: [deals w bleeding] thrombosis, epistaxis, major bleeding, GI tears, proteinuria, diarrhea (ramcirumab)

49
Q

In what type of pts should we avoid use of VEGF inhibitors?

A

Squamous histology (bevacizumab)
Recent hemoptysis [blood from mouth]
On anticoag therapy for VTE
Recent surgery
(Aka any recent risk for bleeding)

50
Q

In SCLC, how quick is relapse after complete drug response? What kind of radiation is offered after partial/complete drug response?

A

Relapse usually 6-8 months after complete response
Prophylactic cranial radiation 🧠 is offered post-response

51
Q

What chemo/RT is offered FIRST LINE in limited stage SCLC?

A

Cisplatin + Etoposide + RT
Carboplatin + Etoposide + RT

52
Q

What chemo/RT is offered FIRST LINE in extensive stage SCLC?

A

Carboplatin + Etoposide + Atezolizumab (immunotherapy)
Carboplatin + Etoposide + Durvalumab
Cisplatin + Etoposide + Durvalumab

53
Q

What chemo/RT is offered SECOND LINE in SCLC?

A

Topotecan
Lurbinectedin

54
Q

What is the MOA of Etoposide (SCLC)? What is a notable AE?

A

MOA - topoisomerase II inhibitor, DNA double strand breaks
AE - myelosuppression

55
Q

What is the MOA of topotecan (SCLC)? What are some notable AEs?

A

Topoisomerase I inhibitor, leads to DNA single strand breaks
AEs - Myelosuppression, neutropenia

56
Q

What is the MOA of Lurbinectedin (SCLC)? What are some notable AEs? What should be used for pretreatment?

A

MOA - alkylates DNA residues and results in DNA damage
AEs - Fatigue, hepatic enzyme elevation, nausea, extravasation (leakage of blood)
Pretreat w dexamethasone (decrease hepatic elevations) and 5-HT3 antagonists for antiemetic

Crit Care, Oncology & Hematology (18 decks)

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