Week 8 — Part 8: Hematologic Malignancies

Difficulty: Heavy — High Yield

What it covers:

AML — 2022 WHO and ICC classification (cytogenetic and molecular subtypes); ELN 2022 risk stratification: Favorable (CBF-AML with t(8;21)/inv(16), NPM1 mutated without FLT3-ITD high allelic ratio, biallelic CEBPA), Adverse (TP53, RUNX1, ASXL1, complex karyotype, monosomy), Intermediate (all others); standard induction 7+3 (cytarabine 100–200 mg/m² CIV ×7 days + idarubicin ×3 days) for fit patients; CPX-351 (Vyxeos) for secondary AML (t-AML, MDS/MPN-related; CLLS 10301 trial); targeted additions: midostaurin for FLT3+ (any allelic ratio) in induction; gemtuzumab ozogamicin (GO) for CBF-AML in induction; venetoclax + azacitidine for older/unfit patients (VIALE-A: CR/CRi 66% vs. 28%, OS 14.7 vs. 9.6 months); alloSCT in CR1 for Intermediate and Adverse risk; APL (AML-M3) — ATRA + arsenic trioxide (ATO) ± gemtuzumab for all risk; differentiation syndrome (fever, weight gain, pulmonary infiltrates, pleural/pericardial effusions → hold ATRA/ATO, dexamethasone 10 mg BID); MRD monitoring by PCR (PML-RARA); ALL — Philadelphia chromosome (BCR-ABL; Ph+ ALL in ~25%); Ph− B-ALL induction with pediatric-inspired regimens (hyper-CVAD, CALGB 10403 for adolescents/young adults); Ph+ ALL: ponatinib + chemo or blinatumomab ± TKI; blinatumomab (CD3×CD19 bispecific) for MRD+ or relapsed B-ALL; inotuzumab ozogamicin for relapsed B-ALL; CAR-T (tisagenlecleucel for relapsed/refractory B-ALL ≤25 years; axicabtagene for adults); alloSCT for high-risk Ph+ ALL in CR1; T-ALL: nelarabine; CML — BCR-ABL fusion kinase (t(9;22) Philadelphia chromosome); TKI therapy: imatinib (first-line option), dasatinib/nilotinib (second-generation, faster deep molecular response), ponatinib (T315I "gatekeeper" mutation; third-generation; also for Ph+ ALL); treatment-free remission (TFR) goal after deep molecular response (MR4.5); TKI resistance mechanisms; chronic/accelerated/blast phase classification; CLL — Rai and Binet staging; treatment indications (not all CLL requires immediate treatment); prognostic markers (del(17p), TP53 mutation → avoid alkylating chemo; use venetoclax-based or BTK inhibitor); BTK inhibitors: ibrutinib (first-generation; ibrutinib vs. venetoclax + obinutuzumab in ILLUMINATE; CLL14), acalabrutinib, zanubrutinib (second-generation; fewer cardiac toxicities); venetoclax + obinutuzumab or venetoclax + ibrutinib; Richter transformation; Hodgkin lymphoma — Reed-Sternberg cells (CD30+, CD15+, B-cell origin but antigen loss); ABVD (doxorubicin, bleomycin, vinblastine, dacarbazine) ± radiotherapy for early-stage; escalated BEACOPP for advanced-stage high-risk; brentuximab vedotin (CD30 ADC) in frontline with AVD (ECHELON-1) or salvage; pembrolizumab/nivolumab for relapsed; second-line DHAP/ICE → autologous SCT for chemosensitive relapse; DLBCL — R-CHOP as standard; CNS prophylaxis in high-risk; polatuzumab vedotin + R-CHP in first-line (POLARIX trial); CAR-T (axi-cel, tisa-cel, liso-cel) for relapsed ≥2 lines; tafasitamab + lenalidomide for R/R DLBCL not CAR-T eligible; follicular lymphoma — watch-and-wait for asymptomatic low-burden; obinutuzumab + chemotherapy or R-CHOP; R² (rituximab + lenalidomide); mosunetuzumab or epcoritamab for relapsed; transformation to DLBCL; multiple myeloma — CRAB criteria (hyperCalcemia, Renal insufficiency, Anemia, Bone lesions); IMWG diagnostic criteria; induction regimens (VRd [bortezomib/lenalidomide/dexamethasone] for transplant-eligible standard; VRd vs. daratumumab-VRd [GRIFFIN, PERSEUS trials] → daratumumab-based preferred); autologous SCT for transplant-eligible; maintenance lenalidomide post-ASCT; daratumumab-based regimens; BCMA-targeted therapy (belantamab mafodotin, teclistamab, ciltacabtagene autoleucel); bispecifics; MDS — WHO classification (MDS-LB vs. MDS-IB1/IB2); IPSS-R risk; lower-risk MDS treatment (ESA for EPO <500; lenalidomide for del(5q); luspatercept for ring sideroblasts, MDS-RS); higher-risk MDS: azacitidine or decitabine ± venetoclax; alloSCT for fit patients; IMerge: imetelstat for lenalidomide/ESA-refractory lower-risk MDS.

Print: 1 Mind Map, 4 Comparison Charts, 3 Cornell Notes pages

Study Tasks

☐ Read the Study Guide for Part 8 first — the ELN 2022 AML risk table and the CLL treatment indications and BTK inhibitor comparison are the two highest-yield diagnostic frameworks in this Part. Know them cold before reading the chapters.

☐ Highlight as you read:

Yellow for key terms (ELN 2022 Favorable/Intermediate/Adverse risk, MRD, differentiation syndrome, T315I gatekeeper mutation, Richter transformation, CRAB criteria, del(5q), ring sideroblasts, IPSS-R, treatment-free remission)
Blue for pathomechanisms (BCR-ABL constitutive kinase → RAS/PI3K/STAT5 activation in CML; PML-RARA fusion blocking myeloid differentiation in APL → ATRA targets PML-RARA for degradation; VHL→BCL-2 family imbalance in CLL; bortezomib → proteasome inhibition → accumulation of pro-apoptotic proteins in myeloma plasma cells)
Green for disease types and classification systems (AML WHO/ICC cytogenetic subtypes; CML phases; CLL Rai/Binet staging; HL vs. NHL; DLBCL vs. FL vs. MCL; MGUS vs. smoldering vs. active myeloma; MDS WHO subtypes)
Orange for clinical presentations (differentiation syndrome in APL: must recognize early; tumor lysis syndrome in ALL; SVC syndrome from lymphoma; bone lesions in myeloma — purely lytic, no sclerosis; cytopenias in MDS)
Red for must-know high-yield facts (APL: ATRA + ATO = standard; differentiation syndrome → dexamethasone; ELN Favorable AML may not need alloSCT in CR1 if MRD-negative; blinatumomab = bispecific CD3×CD19; AR-V7 analogy: T315I mutation = imatinib/dasatinib/nilotinib resistance → ponatinib; POLARIX: pola-R-CHP superior to R-CHOP in DLBCL; daratumumab-VRd = preferred myeloma induction)

☐ Build the AML treatment decision tree from memory: fit vs. unfit patient → fit: 7+3 ± midostaurin (FLT3+) ± GO (CBF-AML) → CR → consolidation by ELN risk (Favorable: consolidation chemo or alloSCT if MRD+; Intermediate/Adverse: alloSCT in CR1); secondary AML: CPX-351; unfit: venetoclax + azacitidine. Know the APL exception: all APL → ATRA + ATO regardless of fit/unfit, with differentiation syndrome monitoring.

☐ Drill the CML treatment framework: TKI selection (imatinib vs. dasatinib/nilotinib for newly diagnosed), monitoring milestones (complete hematologic response by 3 months, major molecular response MR3 by 12 months, deep molecular response MR4/4.5 as TFR target), switch criteria (failure to achieve milestone = switch TKI; T315I mutation = ponatinib), and phase transitions (accelerated and blast phase require more aggressive treatment including alloSCT).

☐ Work through the myeloma treatment landscape: know VRd vs. daratumumab-VRd induction, ASCT role and timing, lenalidomide maintenance data, BCMA-targeted therapies (belantamab, teclistamab, CAR-T), and the progression of the disease from MGUS → smoldering → active requiring treatment (CRAB + SLiM criteria).

☐ Complete all Part 8 Practice Questions. Immediately re-do any missed questions involving ELN risk classification, AML induction selection by patient fitness, or differentiation syndrome recognition.

How to Use Your Templates

Mind Map: Central node = "Hematologic Malignancies." Main branches:

Leukemias → AML (ELN 2022 risk; 7+3 vs. CPX-351; ven+aza; APL: ATRA+ATO; diff syndrome); CML (BCR-ABL; TKI generations; T315I/ponatinib; TFR); ALL (Ph+ vs. Ph−; blinatumomab; inotuzumab; CAR-T); CLL (BTK inhibitors; venetoclax; del(17p) implications; Richter)
Lymphomas → HL (Reed-Sternberg, CD30; ABVD; BV-AVD; brentuximab salvage; PD-1 inhibitors); DLBCL (R-CHOP vs. pola-R-CHP; CAR-T for relapse); FL (watch-and-wait; R²; mosunetuzumab; transformation)
Multiple Myeloma → CRAB criteria; IMWG diagnostic criteria; daratumumab-VRd induction; ASCT; maintenance lenalidomide; BCMA-targeted (teclistamab, CAR-T); smoldering vs. active
MDS → WHO classification; IPSS-R; lower-risk (ESA, lenalidomide del(5q), luspatercept for RS) vs. higher-risk (aza/dec ± ven); alloSCT

Comparison Charts:

Chart 1 — AML: Fit vs. Unfit Treatment Approach: induction regimen, key targeted additions (midostaurin for FLT3, GO for CBF-AML), consolidation strategy by ELN risk, alloSCT indication, and options for older/unfit patients (venetoclax + azacitidine).
Chart 2 — CML TKI Generations: imatinib (first), dasatinib/nilotinib/bosutinib (second), ponatinib/asciminib (third) — molecular target, T315I coverage, key toxicities, monitoring milestones, and when to switch.
Chart 3 — CLL Treatment: BTK inhibitors (ibrutinib vs. acalabrutinib vs. zanubrutinib) vs. venetoclax-based regimens — mechanism, cardiac toxicity comparison, clinical trial evidence, preferred use in del(17p)/TP53-mutated disease, and fixed-duration vs. continuous therapy.
Chart 4 — Multiple Myeloma Treatment Sequence: MGUS → smoldering → active (CRAB); transplant-eligible induction (dara-VRd); ASCT; maintenance; first relapse; BCMA-targeted therapy tier (belantamab, teclistamab, ciltacabtagene autoleucel) — key trial for each step.

Cornell Notes:

Page 1 — Cue questions: "Classify the following AML patients by ELN 2022 risk and state the appropriate consolidation strategy: (a) NPM1-mutated, FLT3-ITD negative; (b) TP53 mutation; (c) inv(16)/CBF-AML MRD-negative after consolidation." "A 68-year-old patient with secondary AML (prior MDS) presents for induction. Why is CPX-351 preferred over standard 7+3 in this scenario? What is the key pharmacologic difference?"
Page 2 — Cue questions: "An APL patient on day 5 of ATRA + ATO develops fever, weight gain of 4 kg, new bilateral pulmonary infiltrates, and hypoxia. Diagnose and treat: what is happening, what is the mechanism, and what is the immediate management?" "Explain BCR-ABL constitutive kinase activity in CML: starting from the t(9;22) translocation, trace the downstream signaling pathways it activates and explain mechanistically why imatinib works. What is the T315I mutation and why does it require ponatinib?"
Page 3 — Cue questions: "A patient with DLBCL progresses 6 months after completing R-CHOP. They are in their second relapse (prior DHAP + autologous SCT). What CAR-T products are FDA-approved, and what pre-treatment criteria must be met before CAR-T infusion?" "Describe the CRAB criteria for multiple myeloma. For each criterion, explain the underlying pathophysiologic mechanism. What are the SLiM criteria and how do they change the diagnostic threshold?"

Week 9 — Part 9: Head & Neck, Skin, Bone & Soft Tissue Oncology

Difficulty: Moderate–Heavy

What it covers:

Head and neck squamous cell carcinoma (HNSCC) — anatomic subsites (oral cavity, oropharynx, hypopharynx, larynx, nasopharynx treated separately) and their distinct biology; HPV-positive oropharyngeal SCC (HPV-16 dominant; p16 IHC surrogate at ≥70%; E6 degrades p53, E7 inactivates Rb; younger non-smokers; 3-year OS ~80–85%; AJCC 8th edition p-staging separates from HPV-negative OPC) vs. HPV-negative HNSCC (tobacco/alcohol; TP53 mutations; field cancerization; 3-year OS ~45–60%); de-escalation trials for HPV+ OPC; treatment of locally advanced HNSCC — concurrent CRT (cisplatin 100 mg/m² q3w ×3 or 40 mg/m² weekly + RT); organ preservation for larynx/hypopharynx; recurrent/metastatic HNSCC first-line: PD-L1 CPS ≥20 → pembrolizumab monotherapy (KEYNOTE-048); CPS 1–19 → pembrolizumab + cisplatin/5-FU; CPS <1 → platinum + 5-FU + cetuximab (EXTREME); platinum-refractory: nivolumab (CheckMate 141) or pembrolizumab; nasopharyngeal carcinoma (NPC) — EBV-driven (latency-associated oncoproteins LMP1/LMP2; geographic distribution: Southern China, Southeast Asia, North Africa; EBV DNA as tumor marker); gemcitabine + cisplatin (NAXOS trial); concurrent CRT + adjuvant chemotherapy; melanoma — BRAF V600E in ~50% of cutaneous melanomas; NRAS ~20%; UV-induced mutation signature (high TMB, ~150–200 mutations/Mb); BRAF inhibitor + MEK inhibitor combinations (dabrafenib + trametinib; vemurafenib + cobimetinib; encorafenib + binimetinib) for BRAF V600E/V600K; paradoxical MAPK reactivation with single-agent BRAF inhibition; immunotherapy for melanoma: nivolumab + ipilimumab (CheckMate 067); pembrolizumab (KEYNOTE-006); nivolumab adjuvant (CheckMate 238); pembrolizumab adjuvant (KEYNOTE-716 for resected Stage IIB/C/III); relatlimab + nivolumab (LAG-3 + PD-1; RELATIVITY-301); uveal melanoma (GNAQ/GNA11 mutations; tebentafusp for HLA-A*02:01+; distinct biology and poor response to standard immunotherapy); acral/mucosal melanoma (low TMB, fewer BRAF mutations); thyroid cancer — papillary (BRAF V600E ~60%; RET/PTC fusions; excellent prognosis; RAI-avid; BRAF+MEK inhibitor combination therapy for RAI-refractory), follicular (RAS mutations; PAX8-PPARγ fusion; hematogenous spread; thyroglobulin tumor marker; RAI-avid), medullary (RET point mutations in MEN2A/MEN2B and sporadic; calcitonin tumor marker; selpercatinib or pralsetinib for RET-mutant advanced disease), anaplastic (near-universal TERT promoter mutations + BRAF V600E; dismal prognosis; BRAF V600E → dabrafenib + trametinib ± pembrolizumab; urgent multidisciplinary evaluation); sarcomas — translocation-driven: Ewing sarcoma (EWSR1-FLI1 t(11;22); neuroendocrine features; VAC/IE; mifamurtide in some guidelines), synovial sarcoma (SS18-SSX fusion; adolescents/young adults; NY-ESO-1 expression → afami-cel T-cell therapy), myxoid liposarcoma (FUS-DDIT3 fusion; trabectedin sensitivity); MDM2-amplified tumors: dedifferentiated liposarcoma (MDM2 amplification; MDM2 FISH diagnostic); DFSP (COL1A1-PDGFB fusion → PDGFR activation → imatinib); rhabdomyosarcoma (pediatric; PAX3-FOXO1 in alveolar subtype); osteosarcoma (TP53/RB1 loss; methotrexate + cisplatin + doxorubicin [MAP regimen]); chondrosarcoma (IDH1/2 mutations in central; ivosidenib in IDH1-mutant); GIST (covered in Part 6 but molecular principles relevant here); general sarcoma management — histology-specific chemotherapy, ifosfamide/doxorubicin-based regimens, and emerging targets (TRK inhibitors for NTRK fusions, crizotinib for ALK+ inflammatory myofibroblastic tumor).

Print: 1 Mind Map, 3 Comparison Charts, 3 Cornell Notes pages

Study Tasks

☐ Read the Study Guide for Part 9 first — the Side-by-Side Breakdowns of HPV-positive vs. HPV-negative HNSCC and the BRAF-mutant melanoma treatment section are the two highest-yield areas in this Part.

☐ Highlight as you read:

Yellow for key terms (CPS scoring, p16 IHC, field cancerization, LMP1/LMP2, EBV DNA, thyroglobulin, calcitonin, EWSR1-FLI1, MDM2 amplification, PDGFRA D842V analogy to PDGFB in DFSP)
Blue for molecular mechanisms (HPV E6 → p53 proteasomal degradation via E6AP ubiquitin ligase; HPV E7 → Rb hyperphosphorylation → E2F release → uncontrolled S-phase entry; paradoxical MAPK reactivation with single-agent BRAF inhibition; EWSR1-FLI1 fusion → aberrant transcription factor driving neuroectodermal differentiation)
Green for cancer types and subclassifications (HPV+ vs. HPV− OPC; NPC as distinct from HNSCC; four thyroid cancer subtypes; sarcoma histologic types and their defining molecular events)
Orange for clinical presentations (stridor/hoarseness in laryngeal cancer; dysphagia in hypopharyngeal cancer; painless neck node as first sign of OPC; elevated calcitonin in MEN2 screening; pathologic fracture in osteosarcoma)
Red for must-know facts (KEYNOTE-048: CPS ≥20 → pembrolizumab monotherapy first-line R/M HNSCC; BRAF V600E in ~50% of cutaneous melanoma; ~60% of papillary thyroid cancer; selpercatinib for RET-mutant medullary thyroid; DFSP → COL1A1-PDGFB → imatinib sensitive; EWSR1-FLI1 t(11;22) defines Ewing sarcoma)

☐ Work through the KEYNOTE-048 treatment algorithm for recurrent/metastatic HNSCC: test PD-L1 CPS first. CPS ≥20 → pembrolizumab monotherapy (superior OS vs. EXTREME, better toxicity profile). CPS 1–19 → pembrolizumab + platinum/5-FU (combination superior to EXTREME). CPS <1 → EXTREME regimen (cetuximab + cisplatin/carboplatin + 5-FU). After platinum, second-line: nivolumab (CheckMate 141) or pembrolizumab. Know the CPS thresholds and their clinical implications cold.

☐ Master the BRAF-mutant melanoma signaling cascade and paradoxical reactivation: BRAF V600E constitutively activates MEK → ERK → proliferation. Single-agent BRAF inhibitor suppresses mutant BRAF → paradoxical transactivation of wild-type BRAF dimers through RAS → downstream MEK/ERK reactivation. Adding MEK inhibitor downstream prevents this reactivation — this is why combination is mandatory, not optional.

☐ For translocation-driven sarcomas, build a table: sarcoma → translocation → fusion gene → functional consequence → first-line chemotherapy → whether a targeted agent exists (Ewing: no approved targeted therapy yet; synovial sarcoma: afami-cel for NY-ESO-1+; DFSP: imatinib; myxoid liposarcoma: trabectedin).

☐ Complete all Part 9 Practice Questions. Immediately re-do any missed questions on thyroid cancer subtype management or melanoma treatment selection (targeted vs. immunotherapy).

How to Use Your Templates

Mind Map: Central node = "Head & Neck, Skin, Bone & Soft Tissue Oncology." Main branches:

HNSCC → HPV+ OPC (p16, E6/E7, better prognosis, de-escalation trials) vs. HPV− (tobacco/alcohol, worse prognosis); CRT backbone; R/M: KEYNOTE-048 CPS algorithm; NPC (EBV, gem/cis + CRT)
Melanoma → BRAF V600E (~50%); BRAF+MEK inhibitor combinations; paradoxical reactivation; nivolumab + ipilimumab; relatlimab + nivolumab; adjuvant immunotherapy; uveal (GNAQ/GNA11; tebentafusp)
Thyroid Cancer → Papillary (BRAF/RET, RAI-avid, excellent prognosis); Follicular (RAS/PAX8-PPARγ, hematogenous); Medullary (RET, calcitonin, selpercatinib); Anaplastic (TERT+BRAF, dismal, BRAF → dab+tram)
Translocation Sarcomas → Ewing (EWSR1-FLI1, VAC/IE); Synovial (SS18-SSX, afami-cel); Myxoid liposarcoma (FUS-DDIT3, trabectedin); DFSP (COL1A1-PDGFB, imatinib)
Other Bone/Soft Tissue → Osteosarcoma (MAP regimen); Dedifferentiated liposarcoma (MDM2 amplification); RMS (PAX3-FOXO1); Chondrosarcoma (IDH1/2)

Comparison Charts:

Chart 1 — HPV-Positive vs. HPV-Negative HNSCC: anatomic predilection, demographics, p16 status, molecular oncogenesis mechanism, AJCC 8th edition staging impact, prognosis difference, and whether de-escalation is appropriate.
Chart 2 — BRAF-Mutant Melanoma: Single-Agent BRAF Inhibitor vs. BRAF+MEK Inhibitor Combination vs. Immune Checkpoint Blockade — mechanism of action, why single-agent BRAF is insufficient (paradoxical reactivation), response rate/durability comparison, toxicity profile, and which to choose based on tumor burden and pace of disease.
Chart 3 — Four Thyroid Cancer Subtypes: cell of origin, key molecular alteration(s), lymphatic vs. hematogenous spread, tumor marker, RAI avidity, prognosis, and targeted therapy option for advanced disease.

Cornell Notes:

Page 1 — Cue questions: "A 48-year-old non-smoker presents with a cystic neck node and biopsy shows SCC. p16 IHC is strongly positive. How does the AJCC 8th edition stage this differently from a HPV-negative SCC with the same node? What is the treatment approach and why is de-escalation being investigated?" "Explain how HPV E6 inactivates p53 and E7 inactivates Rb. Why does this make HPV+ OPC biologically distinct from tobacco-related HNSCC at the molecular level?"
Page 2 — Cue questions: "A patient with metastatic BRAF V600E melanoma asks whether to start targeted therapy or immunotherapy. Walk through the considerations: pace of disease, tumor burden, expected response rate, durability of response, and the key tradeoffs between each approach." "What is the relatlimab + nivolumab combination? What is LAG-3, and what was the rationale for combining LAG-3 blockade with PD-1 blockade in melanoma?"
Page 3 — Cue questions: "A patient is found to have a 3 cm thyroid nodule. FNA shows medullary thyroid carcinoma. What are your next steps, and why? What genetic testing is mandatory, what does it look for, and what are the implications for the patient's family?" "Explain why DFSP is treated with imatinib. What is the COL1A1-PDGFB fusion, how does it drive oncogenesis, and what response rates does imatinib achieve in locally advanced or metastatic DFSP?"

Week 10 — Part 10: Supportive Care, Emergencies & Survivorship

Difficulty: Moderate

What it covers:

Cancer pain management — WHO analgesic ladder (Step 1: non-opioids [NSAIDs, acetaminophen]; Step 2: weak opioids [codeine, tramadol]; Step 3: strong opioids [morphine, oxycodone, fentanyl, hydromorphone]); opioid titration principles (10–15% of total daily dose for breakthrough; increase scheduled dose by 25–50% per day based on rescue use); equianalgesic dosing conversions (morphine oral:IV ratio 3:1; morphine-to-oxycodone 1.5:1 oral; PO morphine to transdermal fentanyl [mcg/hr] = PO morphine mg/day ÷ 2.4); opioid rotation (reduce new opioid by 25–50% for incomplete cross-tolerance); nociceptive vs. neuropathic pain distinction (nociceptive: opioid-responsive; neuropathic: partial opioid response, adjuvant essential [gabapentin, pregabalin, duloxetine, TCAs, SNRIs, ketamine for refractory]); bone pain (NSAIDs, steroids, bisphosphonates, denosumab/RANKL inhibitors, palliative RT; 8 Gy ×1 equivalent to multi-fraction for pain relief); opioid-induced constipation (methylnaltrexone, naloxegol; scheduled laxatives); opioid-induced respiratory depression (naloxone 0.04 mg IV q2–3 min; goal adequate respiration without full reversal); palliative vs. curative intent — symptom burden, goals of care, hospice criteria (prognosis ≤6 months); oncologic emergencies — tumor lysis syndrome (uric acid, potassium, phosphate elevated; calcium low; AKI; prevention: allopurinol or rasburicase for high-risk; aggressive hydration; rasburicase for established TLS in high-risk); febrile neutropenia (ANC <500 or expected <500 with fever ≥38.3°C; immediate blood cultures × 2; Pseudomonas coverage: piperacillin-tazobactam or cefepime IV; risk stratification by MASCC score; low-risk: oral fluoroquinolone; high-risk: IV broad-spectrum; G-CSF role); SVC syndrome (thoracic malignancy compression; facial swelling/venous distension/cyanosis/arm edema; management by histology: SCLC/NHL → chemotherapy first; NSCLC or solid tumor → stent vs. RT); spinal cord compression (epidural metastasis; back pain → neurologic deficits if untreated; MRI spine urgent; dexamethasone 10 mg IV immediately → definitive: surgical decompression vs. conventional RT vs. stereotactic RT based on stability and prognosis); hypercalcemia of malignancy (PTHrP in ~80% solid tumors; osteolytic metastases; lymphoma/1,25-OH₂D₃; management: IV fluids, bisphosphonates or denosumab, calcitonin for rapid effect, dialysis for severe); DIC in APL (ATRA + ATO reverse it; fresh frozen plasma, cryoprecipitate, platelet transfusion bridges); CIPN (chemotherapy-induced peripheral neuropathy — taxanes, platinums, bortezomib; prevention limited; duloxetine modest benefit; dose reduction); cardiotoxicity monitoring (anthracycline cumulative dose limits; trastuzumab → reversible LV dysfunction; echocardiogram surveillance; cardio-oncology collaboration); survivorship — late effects of treatment (secondary malignancies after alkylating agents and RT; cardiac effects post-anthracyclines/RT; cognitive effects; premature menopause; fertility preservation counseling before gonadotoxic therapy; osteoporosis screening; psychosocial support and depression screening); care coordination — primary care reintegration, survivorship care plans, NCCN survivorship guidelines.

Print: 1 Mind Map, 3 Comparison Charts, 2 Cornell Notes pages

Study Tasks

☐ Read the Study Guide for Part 10 first — the Stepwise Processes for opioid rotation and for febrile neutropenia management are the most procedure-like sections in the book and repay careful sequential reading before the chapter content.

☐ Highlight as you read:

Yellow for key terms (equianalgesic dosing, opioid rotation, MASCC score, TLS, SVC syndrome, spinal cord compression, DIC, CIPN, cardiotoxicity, survivorship care plan, hospice criteria)
Blue for mechanisms (why neuropathic pain requires adjuvants — VGCC/SNRI/TCA mechanisms; how rasburicase works to eliminate uric acid; how methylnaltrexone reverses OIC without CNS effects; how bisphosphonates inhibit osteoclasts)
Purple for tumor progression context (spinal cord compression as epidural extension of vertebral metastasis; SVC syndrome as direct tumor invasion or extrinsic compression)
Orange for clinical presentations (TLS lab pattern: ↑uric acid, ↑K, ↑phosphate, ↓Ca, ↑creatinine; febrile neutropenia diagnostic criteria; classic triad of SVC syndrome; early back pain as warning sign preceding paraplegia in cord compression)
Red for must-know high-yield facts (naloxone: dilute to 0.04 mg/mL; give slowly to preserve analgesia; rasburicase contraindicated in G6PD deficiency; MASCC ≥21 = low-risk febrile neutropenia → oral ciprofloxacin acceptable; spinal cord compression → dexamethasone immediately, then MRI; hypercalcemia of malignancy: IV fluids first, then bisphosphonate/denosumab; single-fraction 8 Gy = multi-fraction for palliative bone pain)

☐ Master opioid equianalgesic conversions with clinical scenarios: practice converting a patient on morphine 90 mg/day oral to transdermal fentanyl, accounting for incomplete cross-tolerance (reduce by 25–50%). Then practice converting to IV hydromorphone during a hospitalization. These calculations appear directly on ABIM boards.

☐ Build the oncologic emergency management algorithm for the four most tested emergencies: TLS, febrile neutropenia, SVC syndrome, and spinal cord compression. For each: diagnostic criteria, immediate first intervention, definitive treatment, and what makes the case high-risk enough to escalate.

☐ Work through the survivorship late effects table: for each major treatment modality (anthracyclines, alkylating agents, radiation, platinum, taxanes, aromatase inhibitors, ADT), list the organ system affected, the late effect, the monitoring approach, and the prevention/treatment strategy.

☐ Complete all Part 10 Practice Questions. Re-do immediately any missed questions about febrile neutropenia management or opioid rotation calculations.

How to Use Your Templates

Mind Map: Central node = "Supportive Care, Emergencies & Survivorship." Main branches:

Pain Management → WHO ladder (Step 1–3); opioid titration; equianalgesic conversions; rotation (−25–50%); nociceptive vs. neuropathic (adjuvants); OIC (methylnaltrexone); respiratory depression (naloxone); bone pain (palliative RT, bisphosphonates)
Oncologic Emergencies → TLS (prevention: allopurinol/rasburicase; treatment: rasburicase + IVF; G6PD caveat); Febrile Neutropenia (MASCC score; pip/tazo or cefepime IV; low-risk → oral FQ); SVC syndrome (histology-driven: chemo vs. stent vs. RT); Spinal Cord Compression (MRI urgent; dexamethasone immediately; decompression/RT)
Metabolic Emergencies → Hypercalcemia (PTHrP ~80%; IVF → bisphosphonate/denosumab → calcitonin); DIC in APL (ATRA + ATO reverses; support with FFP/cryo/platelets)
Toxicity Management → CIPN (duloxetine modest benefit); Cardiotoxicity (anthracycline limits; trastuzumab monitoring; echo surveillance); Palliative vs. Curative Intent
Survivorship → secondary malignancy risk (alkylating agents, RT); fertility preservation counseling; cardiac/cognitive/reproductive late effects; survivorship care plans; depression screening; primary care reintegration

Comparison Charts:

Chart 1 — Four Major Oncologic Emergencies: TLS, febrile neutropenia, SVC syndrome, spinal cord compression — defining criteria, first immediate intervention, definitive treatment, and the common error to avoid in each.
Chart 2 — Nociceptive vs. Neuropathic Cancer Pain: character of pain, opioid responsiveness, first-line adjuvants, mechanism of each adjuvant class, and special considerations (ketamine for opioid-refractory neuropathic pain; methadone's NMDA antagonism).
Chart 3 — Treatment Late Effects by Modality: anthracyclines, alkylating agents, platinum, taxanes, RT to chest/pelvis, aromatase inhibitors, ADT — affected organ system, specific late effect, monitoring test, timeline, and management.

Cornell Notes:

Page 1 — Cue questions: "A patient on morphine SR 60 mg q12h with 10 mg IR q4h as needed (used 3 times yesterday) needs a dose adjustment. Calculate the new scheduled dose. Then convert to equianalgesic transdermal fentanyl, accounting for cross-tolerance reduction." "A febrile neutropenic patient has ANC of 80, temperature 38.9°C, and no obvious source. Their MASCC score is 24. What is the appropriate management, and at what point can you de-escalate or discharge?"
Page 2 — Cue questions: "A patient with known L3 vertebral metastasis from prostate cancer presents with new-onset mid-back pain and bilateral leg weakness developing over 24 hours. What is the diagnosis, what is the very first intervention, what imaging do you order and why urgently, and what are the definitive treatment options?" "Describe the pathophysiology and treatment of tumor lysis syndrome. Why is rasburicase contraindicated in G6PD deficiency, and what do you use instead?"

Week 11 — Final Review & Exam Simulation

Your final week is about consolidation and exam-style execution, not new content. Every hour should be tied directly to your identified weak spots.

Final Review Tasks

☐ Re-draw one Mind Map from memory for each of your three to four weakest Parts — determined by your quiz bank performance across Weeks 1–10. After drawing each, open your original Mind Map, compare them side by side, and fill every missing branch or connection in a different color. This reveals exactly which conceptual links are still fragile.

☐ Work through the cue column of all your Cornell Notes pages across all ten Parts: cover the right-hand notes, answer aloud from each cue question, then uncover and fill gaps. Prioritize any cue questions that require mechanism sequences, treatment algorithms, or comparative distinctions — these are exactly the format ABIM uses.

☐ Re-do every quiz bank question you missed on earlier attempts. For each missed question, write one sentence: "I missed this because ___. Next time I will look for ___." This forces diagnostic specificity and prevents pattern-blind re-reading.

☐ Re-read the "Must-Know Facts & Values," "Common Mistakes & How to Avoid Them," and "2-Minute Rapid Review" sections from your three weakest Parts. Convert any worst-offender topics into mini comparison tables if you haven't already — the act of building the table embeds the distinctions.

☐ Build cross-Part integration sheets for the highest-yield themes that span multiple Parts:

PARP inhibitor eligibility across cancer types: BRCA-mutant breast (Part 5), HGSOC ovarian (Part 7), metastatic CRPC (Part 7), BRCA-mutant pancreatic (Part 6), AML HRD (emerging) — confirm the shared mechanism (HRD) and the distinct clinical context for each.
MSI-H / dMMR pan-tumor immunotherapy: pembrolizumab approved regardless of histology; know which Parts contain MSI-H–relevant cancers (Parts 6, 7, 8) and the screening/testing trigger for each.
ADCs in clinical practice: review T-DM1, T-DXd, sacituzumab, enfortumab vedotin, brentuximab vedotin, polatuzumab vedotin across Parts 5, 6, 7, 8 — antibody target, payload, approved indication, unique toxicity.
BRCA1/2 germline testing implications: which cancer diagnoses trigger mandatory germline testing (breast, ovarian, pancreatic, prostate, colorectal via Lynch overlap) and what cascade testing means for family members.

Exam Simulation

☐ Take the included full-length ABIM Medical Oncology simulated exam using the QR code in the front or back of your book. Complete it timed, in a single sitting, under conditions that match real test day as closely as possible — no notes, no textbook, no highlights.

☐ After completing the exam, map your missed questions back to their source Part. Build a targeted list: treatment sequencing question → Parts 5, 6, 7, or 8; molecular mechanism → Parts 1 or 4; supportive care scenario → Part 10; screening/prevention → Part 2; diagnostic/staging question → Part 3; hematologic malignancy → Part 8; head and neck or melanoma → Part 9.

Spend remaining study time on:

Mind Map redraws for those Parts
Cornell cue-column drills on the specific topics you missed
Targeted quiz bank sets restricted to those weak areas only

NASM-CPT Exam Prep