Cancer Immunotherapy Nursing Guide | GCC Nursing Platform

Immunotherapy Fundamentals

What is Cancer Immunotherapy?

Cancer immunotherapy harnesses or augments the body's own immune system to recognise and destroy cancer cells. Unlike chemotherapy (directly cytotoxic) or targeted therapy (specific oncogenic driver), immunotherapy acts primarily through the immune system and can produce durable, long-lasting responses — including complete remissions — in a minority of patients.

Key principle: Immunotherapy does not kill cancer directly — it removes the brakes or turbocharges the immune system so it can do the job itself.

Types of Cancer Immunotherapy

Checkpoint Inhibitors (ICI) — most common in clinical practice; monoclonal antibodies that block inhibitory immune receptors
CAR-T Cell Therapy — engineered patient T-cells with chimeric antigen receptors; given in specialist centres
Cytokines — IL-2 (interleukin-2), IFN-alpha; earlier agents, significant toxicity
Cancer Vaccines — sipuleucel-T (prostate), neoantigen vaccines in development
Bispecific Antibodies — blinatumomab (CD19xCD3); binds tumour and T-cell simultaneously

Checkpoint Inhibitors — Drug Classes

CTLA-4 Inhibitors

Ipilimumab (ipi) — blocks CTLA-4, enhances early T-cell activation in lymph nodes

PD-1 Inhibitors

Nivolumab (nivo)
Pembrolizumab (pembro)
Cemiplimab

PD-L1 Inhibitors

Atezolizumab
Durvalumab
Avelumab

Mechanisms of Action

CTLA-4 Pathway

CTLA-4 is expressed on T-cells and acts as an early activation brake in lymph nodes. Ipilimumab blocks CTLA-4, preventing inhibition of T-cell priming — results in broader, earlier immune activation.

PD-1 / PD-L1 Pathway

PD-1 on T-cells binds PD-L1 expressed by tumour cells and stromal cells in the tumour microenvironment (TME), causing T-cell exhaustion. PD-1/PD-L1 inhibitors restore T-cell cytotoxic function within the TME.

Clinical note: Combination ipi + nivo (nivolumab) blocks both checkpoints simultaneously — greater efficacy but significantly higher irAE rates.

Biomarkers for Response Prediction

PD-L1 expression (TPS / CPS) — tumour proportion score (TPS) for NSCLC; combined positive score (CPS) for other tumours. Higher = more likely to respond to PD-1/PD-L1 inhibitors
TMB (Tumour Mutational Burden) — high TMB correlates with more neoantigens and better ICI response; pembrolizumab approved for TMB-H tumours
MSI-H / dMMR — microsatellite instability-high / mismatch repair deficient; best single predictor for pembrolizumab response across all tumour types (tumour-agnostic approval)
BRCA / HER2 — not ICI-specific biomarkers

MSI-H/dMMR testing should be performed on all advanced solid tumours — enables tumour-agnostic pembrolizumab eligibility.

Approved Indications (Selected)

NSCLC (Lung)

Pembrolizumab monotherapy first-line if PD-L1 TPS ≥50%
Pembro + chemo first-line (PD-L1 any)
Nivolumab second-line
Durvalumab — unresectable Stage III after CRT

Melanoma

Ipilimumab + nivolumab (combination) — first-line
Pembrolizumab monotherapy
Nivolumab adjuvant resected Stage III/IV

Other Tumours

TNBC — pembrolizumab + chemo (CPS ≥10)
RCC — nivo + ipi or pembro + axitinib
Bladder — atezolizumab, pembrolizumab
HNSC — pembrolizumab first-line
Hodgkin lymphoma — nivolumab, pembrolizumab
MSI-H any tumour — pembrolizumab (tumour-agnostic)

Immune-Related Adverse Events (irAE)

irAE Pathophysiology

irAEs result from T-cell activation against self-tissues — an autoimmune-like inflammatory process driven by the same immune enhancement that produces anti-tumour activity. irAEs can affect virtually any organ system. They are mechanistically similar to autoimmune conditions (e.g., inflammatory bowel disease, autoimmune hepatitis) but are drug-induced.

Time course: irAEs can occur at any time — from first infusion to months or even years after treatment completion. Late-onset irAEs (post-treatment) are well-documented, particularly endocrinopathies.

CTLA-4 vs PD-1 irAEs: Ipilimumab causes higher rate of severe irAEs (especially colitis). Combination ipi+nivo has the highest rate. PD-1/PD-L1 monotherapy is generally better tolerated.

CTCAE Grading System

Grade	Description	General Action
Grade 1	Mild; asymptomatic or minimal symptoms; clinical/diagnostic findings only; no intervention indicated	Continue ICI with monitoring
Grade 2	Moderate; minimal/local intervention indicated; limiting age-appropriate instrumental ADLs	Hold ICI; initiate treatment
Grade 3	Severe; hospitalisation indicated; limiting self-care ADLs	Hold/discontinue ICI; systemic steroids
Grade 4	Life-threatening; urgent intervention indicated	Permanently discontinue ICI; high-dose IV steroids + additional immunosuppression
Grade 5	Death related to adverse event	—

Most Common Dermatological irAEs

Pruritus / maculopapular rash — most common irAE overall; typically Grade 1-2
Vitiligo — depigmentation, especially in melanoma; actually associated with better response
Psoriasiform rash
Stevens-Johnson Syndrome / TEN — rare but life-threatening (Grade 4); permanently discontinue ICI
Bullous pemphigoid

Most dermatological irAEs are Grade 1-2 and manageable with topical steroids and antihistamines without holding ICI.

Common Gastrointestinal irAEs

Colitis

Presents as diarrhoea, bloody/mucoid stool, abdominal cramping
Typical onset: 6–8 weeks (can be earlier with ipi)
More common with ipilimumab (up to 30%) vs PD-1 (~10%)
Grade 3-4: hold/discontinue ICI + IV corticosteroids; if steroid-refractory → infliximab or vedolizumab

Exclude infectious causes (C. difficile, CMV) before attributing diarrhoea to irAE colitis — stool culture, PCR, colonoscopy for Grade 2+.

Monitor Hepatitis irAE

Raised AST/ALT (± bilirubin) — usually asymptomatic
LFTs must be checked before every cycle
Grade 2: hold ICI; oral prednisolone 0.5–1 mg/kg/day
Grade 3+: hold ICI; high-dose IV methylprednisolone 1–2 mg/kg/day
Steroid-refractory: add MMF (mycophenolate mofetil)

Do NOT use infliximab in hepatitis irAE — infliximab is hepatotoxic and contraindicated.

Serious Pneumonitis irAE

Dyspnoea, dry cough, new CT infiltrates (ground-glass opacities, organising pneumonia pattern)
Higher risk: prior lung disease, thoracic radiotherapy, combination ICI
Grade 2+: hold ICI + prednisolone/methylprednisolone
Grade 3-4: hospitalise; high-dose IV steroids; consider bronchoscopy to exclude infection
Steroid-refractory: infliximab, MMF, or IVIG

Pneumonitis is a potentially fatal irAE. Any new respiratory symptoms in a patient on ICI require urgent CT chest and oncology review.

Endocrine irAEs

          Thyroid Dysfunction
          Hypothyroidism — most common endocrine irAE; fatigue, weight gain, cold intolerance
Thyroiditis then hypothyroidism — initial transient hyperthyroid phase (thyroid release), then hypothyroid
Management: levothyroxine replacement for hypothyroidism; TSH monitored every cycle
ICI does not need to be held for thyroid irAE if managed medically

        

          Hypophysitis (Pituitary)
          More common with ipilimumab; headache, visual changes, fatigue, pituitary hormone deficiency
First priority: check and replace cortisol — adrenal crisis risk is life-threatening
Hydrocortisone replacement commenced before other hormones
High-dose steroids initially (also reduces pituitary inflammation)

        

          Type 1 Diabetes Mellitus
          Rare but potentially life-threatening — can present as DKA (diabetic ketoacidosis)
Rapid onset; may have no prior diabetes history
Check blood glucose routinely; urgent assessment if polyuria/polydipsia/vomiting
Insulin therapy required; usually permanent

        

          Adrenal Insufficiency
          Fatigue, hypotension, hyponatraemia, hyperkalaemia, hypoglycaemia
Check ACTH stimulation test; baseline cortisol
Life-long hydrocortisone (and fludrocortisone for primary adrenal)
Patient must carry steroid emergency card

        

Other Organ irAEs

Rheumatological

Inflammatory arthritis — joint swelling/pain
Myositis — muscle weakness/pain; check CK/troponin
NSAIDs ± corticosteroids; rheumatology referral

Neurotoxicity

Peripheral neuropathy
Guillain-Barré syndrome (ascending weakness)
Myasthenia gravis (ptosis/diplopia/bulbar symptoms)
Encephalitis (confusion/seizures)

Cardiac / Renal

Myocarditis — rare but 50% mortality; troponin/ECG/echo mandatory
Pericarditis, heart block
Nephritis — rising creatinine; usually Grade 1-2; hold ICI + steroids Grade 2+

irAE Management Protocols

General irAE Management Principles

Grade	ICI Decision	Corticosteroid	Additional
Grade 1	Continue ICI	Topical / symptomatic only	Close monitoring; re-assess next cycle
Grade 2	Hold ICI until resolves to ≤Grade 1	Oral prednisolone 0.5–1 mg/kg/day; topical for skin	Taper over 4–6 weeks; specialist referral if needed
Grade 3	Hold ICI (consider permanent discontinuation)	IV methylprednisolone 1–2 mg/kg/day → oral taper over 4–6 weeks	Hospitalisation likely; subspecialty involvement; second immunosuppressant if no improvement in 48–72h
Grade 4	Permanently discontinue ICI	IV methylprednisolone 1–2 mg/kg/day (or higher for myocarditis/neurotoxicity)	ICU/hospitalisation; add infliximab/MMF/vedolizumab depending on organ; urgent specialist input

Steroid taper rule: Taper over a minimum of 4–6 weeks. Rapid taper causes irAE flare and recurrence. Do not stop steroids abruptly.

Organ-Specific Immunosuppressants

Agent	Indication	Key Caution
Infliximab	Steroid-refractory colitis; pneumonitis	CONTRAINDICATED in hepatitis irAE (hepatotoxic)
MMF (Mycophenolate)	Steroid-refractory hepatitis; colitis; nephritis	Monitor FBC; infection risk
Vedolizumab	Gut-selective; refractory ICI colitis	Gut-specific — does not cause systemic immunosuppression
IVIG	Guillain-Barré; myasthenia gravis; encephalitis	Volume/renal monitoring
Plasmapheresis	Severe Guillain-Barré; myasthenia gravis	Specialist neurology centre

Baseline & Cycle Monitoring

The following tests should be performed before each ICI cycle:

TFTs — TSH (± free T4/T3 if TSH abnormal)
LFTs — AST, ALT, ALP, bilirubin
Renal function — creatinine, urea, eGFR
FBC — for haematological irAEs (haemolytic anaemia, thrombocytopaenia)
Glucose / HbA1c — diabetes surveillance
Cortisol / ACTH — if symptoms or at baseline
CK / troponin — if myositis/myocarditis suspected
Lipase / amylase — if pancreatitis suspected

Patient education at every visit: report any new rash, diarrhoea, cough, chest pain, confusion, or visual changes immediately — even months after last treatment.

Rechallenge After irAE

Grade 1–2 irAE

Rechallenge generally permitted after irAE resolves to Grade 0–1 and steroids tapered. Close monitoring required. Decision by oncologist.

Grade 3 irAE

Rechallenge is variable and case-by-case. Some Grade 3 irAEs may allow rechallenge (e.g., isolated rash). Oncologist decision with patient consent.

Grade 4 irAE

Permanent discontinuation in nearly all cases. Rechallenge strongly discouraged. Exceptions only in extraordinary circumstances with multidisciplinary agreement.

Endocrine irAEs are an exception — thyroid dysfunction, hypophysitis, adrenal insufficiency, and Type 1 DM rarely resolve. Life-long hormone replacement is typically required and ICI may be continued with appropriate replacement therapy in place.

CAR-T Cell Therapy Nursing

CAR-T Cell Therapy Process

1Leukapheresis (T-cell collection)

2Manufacturing (gene engineering — 3–6 weeks)

3Lymphodepletion chemotherapy (fludarabine + cyclophosphamide)

4CAR-T infusion (cryopreserved product)

5Engraftment & expansion

6Inpatient monitoring 7–14 days (CRS/ICANS)

CAR-T is patient-specific — the product is manufactured from the patient's own T-cells. Strict identity verification at every step is mandatory. Two-nurse double-check before infusion.

Current CAR-T Approvals

Product	Brand	Indication
Axicabtagene ciloleucel	Yescarta	Relapsed/refractory B-cell lymphoma; follicular lymphoma
Tisagenlecleucel	Kymriah	B-cell ALL (up to 25y); large B-cell lymphoma
Lisocabtagene maraleucel	Breyanzi	Large B-cell lymphoma
Idecabtagene vicleucel	Abecma	Relapsed/refractory multiple myeloma
Ciltacabtagene autoleucel	Carvykti	Relapsed/refractory multiple myeloma

GCC Context: CAR-T Programmes

KFSH&RC (King Faisal Specialist Hospital & Research Centre) — one of the very few CAR-T programmes in MENA; established programme for haematological malignancies
Cleveland Clinic Abu Dhabi — expanding cell therapy capabilities
HMC Qatar — checkpoint inhibitor and emerging cellular therapy programme
Requirement: FACT/JACIE-accredited CAR-T certified centre only
Specialist cell therapy nursing certification required for administration

Late-stage cancer at diagnosis is relatively common in GCC — making second-line and salvage therapies including CAR-T highly relevant in clinical practice.

Most Critical CRS — Cytokine Release Syndrome

CRS is the most important and common CAR-T complication. It results from massive cytokine release (IL-6, IFN-gamma, TNF) from activated CAR-T cells and bystander immune cells.

Onset: Typically 1–14 days post-infusion. Earlier and more severe CRS correlates with higher tumour burden and more rapid CAR-T expansion.

ASTCT Grade	Criteria	Management
Grade 1	Fever ≥38°C only	Paracetamol; IV fluids; close monitoring; consider tocilizumab if not improving
Grade 2	Fever + hypotension responsive to fluids OR O2 requirement <40% FiO2	Tocilizumab 8 mg/kg IV (max 800 mg); dexamethasone; vasopressors if needed; consider ICU
Grade 3	Hypotension requiring multiple vasopressors; O2 ≥40% FiO2	ICU; tocilizumab + high-dose dexamethasone; repeat tocilizumab in 8h if needed (max 3 doses)
Grade 4	Life-threatening; ventilation required	ICU; high-dose corticosteroids; siltuximab (IL-6 inhibitor) if tocilizumab ineffective; critical care support

Tocilizumab is an IL-6 receptor antagonist — the first-line treatment for Grade 2+ CRS. Dose: 8 mg/kg IV (max 800 mg). Can repeat in 8 hours if no response. Maximum 3 doses. Must be available at bedside in CAR-T centres.

ICANS — Immune Effector Cell-Associated Neurotoxicity Syndrome

ICANS is the second major CAR-T complication, resulting from endothelial activation, blood-brain barrier disruption, and CNS cytokine influx.

Clinical Presentation

Confusion, disorientation, word-finding difficulty
Aphasia (expressive more than receptive)
Encephalopathy, agitation
Tremor, ataxia
Seizures (generalized or focal)
Cerebral oedema (Grade 4 — life-threatening)

ICE Score Assessment (Nursing Tool)

Orientation — year/month/city/hospital (0–4 pts)
Naming — name 3 objects (0–3 pts)
Commands — follow simple commands (0–1 pt)
Writing — write standard sentence (0–1 pt)
Attention — count backward from 100 by 10 (0–1 pt)
Total: 10 points; lower = more severe ICANS

Daily ICE score assessment is mandatory during inpatient CAR-T monitoring period. Any acute deterioration → urgent neurology/oncology review + CT/MRI head.

ICANS Management

Grade 1–2: Dexamethasone 10 mg IV q6h; seizure prophylaxis with levetiracetam
Grade 3–4: High-dose dexamethasone or methylprednisolone; neurocritical care; MRI brain; EEG; consider intubation for cerebral oedema
CRS and ICANS may co-exist but have distinct management — treating CRS with tocilizumab does not fully prevent ICANS

Infusion Reactions & Nursing Care

Infusion-Related Reactions (IRR)

IRRs are acute reactions occurring during or shortly after infusion. It is critical to distinguish between:

Infusion-related reaction — non-IgE-mediated; cytokine release; first infusion most common
Anaphylaxis — IgE-mediated allergic reaction; urticaria, angioedema, bronchospasm, cardiovascular collapse
CRS (CAR-T) — immune activation; delayed onset (days); distinct from infusion reaction

Key distinction: Anaphylaxis features urticaria and skin involvement alongside hypotension/bronchospasm. CRS features fever and systemic inflammation without urticaria.

IRR & Anaphylaxis Management

Immediately slow/stop infusion
Maintain IV access; administer 0.9% NaCl fluid challenge
Oxygen (target SpO2 ≥95%)
Antihistamine: chlorphenamine 10–20 mg IV
Paracetamol 1 g IV/PO for fever
Dexamethasone 8 mg IV if moderate reaction
Anaphylaxis → adrenaline 0.5 mg IM (0.5 mL 1:1000) — anterolateral thigh; repeat every 5 min if needed
Call for emergency assistance; crash team if cardiovascular collapse
Document reaction grade and report to oncologist

Resuscitation equipment, adrenaline, antihistamine, and corticosteroids must be at the bedside before each ICI infusion.

Premedication Protocol

Standard premedication given 30–60 minutes before ICI infusion to reduce IRR risk:

Paracetamol

1 g IV or oral
30–60 min pre-infusion
Reduces fever/chills

Antihistamine

Chlorphenamine 10 mg IV (or diphenhydramine 25–50 mg)
Reduces urticaria/flushing

Corticosteroid

Dexamethasone 8 mg IV
For high-risk agents or prior reaction history

For patients who had a previous Grade 1 IRR: can re-challenge with premedication and slower infusion rate. Grade 2 reaction: decision by oncologist with intensified premedication. Grade 3+: discuss risk/benefit; likely discontinue that agent.

Checkpoint Inhibitor Infusion Times

Drug	Standard Infusion Duration	Filter Required	Notes
Pembrolizumab	30 minutes	0.2–5 micron in-line filter	Dilute in 0.9% NaCl or 5% dextrose; do not shake
Nivolumab	30–60 minutes	0.2–1.2 micron in-line filter	Can extend to 60 min if prior IRR
Ipilimumab	90 minutes	0.2–1.2 micron in-line filter	Longer infusion time; higher IRR risk; given with nivo = separate infusions
Atezolizumab	First infusion 60 min; subsequent 30 min if tolerated	0.2–0.22 micron in-line filter	Do not freeze; protect from light
Durvalumab	60 minutes	0.2–0.22 micron in-line filter	—
Avelumab	60 minutes	0.2 micron in-line filter	Premedication mandatory before first 4 doses

Vital Signs Monitoring Protocol

Baseline — before starting infusion (BP, HR, RR, SpO2, temperature)
Every 15 minutes — during first hour of infusion
Every 30 minutes — remainder of infusion
At completion — post-infusion assessment
30–60 minutes post-completion — observation period before discharge

Patient positioning: recumbent or semi-recumbent. Ambulation permitted but nurse must stay accessible. Ensure IV access is patent throughout.

CAR-T Product Handling

Product is cryopreserved in liquid nitrogen; patient-specific autologous product
Thawing performed by pharmacy/cell therapy team using validated protocol (usually 37°C water bath)
Infuse within 30 minutes of thaw — product viability declines rapidly
Two-nurse independent identity verification before infusion
Match: patient name, DOB, MRN, product lot number, expiry date
Do not irradiate or filter CAR-T products
Blood bank-type handling — treat as cellular product, not a drug

A CAR-T product mix-up is a never event. The product is only effective (and possibly harmful) in the correct patient. Triple identity checks are non-negotiable.

GCC Context & Exam Preparation

Immunotherapy in the GCC

KFSH&RC — one of the few CAR-T programmes in MENA; reference centre for haematological malignancies
Cleveland Clinic Abu Dhabi (CCAD) — comprehensive cancer centre; expanding ICI and cell therapy programme; DHA regulated
HMC Qatar (National Center for Cancer Care & Research) — major checkpoint inhibitor programmes; JCI accredited
SKMC / SEHA (Abu Dhabi) — active ICI programmes
Oncology at KSA MOH hospitals — pembrolizumab/nivolumab commonly used

Late-stage cancer at diagnosis is more prevalent in GCC compared to Western countries (later healthcare-seeking behaviour, lack of screening uptake historically) — making second-line immunotherapy a particularly high-value intervention in this population.

Regulatory & Exam Context

DHA (Dubai Health Authority) — nursing licensing exam includes oncology competencies; irAE recognition and management increasingly tested
DOH (Department of Health Abu Dhabi) — Haad/DOH exams; oncology nursing competency framework
SCFHS (Saudi Commission for Health Specialties) — oncology nursing SFE; immunotherapy is emerging exam topic
OMSB Oman / NHRA Bahrain / SMLE — cancer nursing topics included
Expect questions on: irAE grading and management, CRS vs ICANS, ICI mechanisms, first-line indications

Interactive irAE Severity Grader & Action Guide

irAE Severity Grader

Select the affected organ system and CTCAE grade to receive the specific management protocol, ICI decision, and nursing actions.

Organ System Affected

CTCAE Severity Grade

MCQ Practice — Cancer Immunotherapy Nursing

Click "Show Answer" to reveal the correct answer and explanation.

1. A patient on pembrolizumab develops grade 3 diarrhoea (7+ stools above baseline per day, incontinence). What is the FIRST priority nursing/medical action?

A. Continue pembrolizumab and start loperamide
B. Hold pembrolizumab and initiate IV methylprednisolone 1–2 mg/kg/day
C. Permanently discontinue pembrolizumab
D. Start infliximab immediately

Answer: B — Grade 3 irAE colitis requires holding ICI and starting systemic corticosteroids (IV methylprednisolone 1–2 mg/kg/day). Permanent discontinuation is reserved for Grade 4. Infliximab is second-line if steroids fail after 48–72h. Loperamide alone is insufficient for irAE colitis.

2. Which biomarker is the BEST single predictor of response to pembrolizumab across all solid tumour types?

A. PD-L1 TPS score
B. BRCA1/2 mutation
C. MSI-H / dMMR status
D. HER2 amplification

Answer: C — MSI-H/dMMR (microsatellite instability-high / mismatch repair deficient) is the basis for the tumour-agnostic pembrolizumab approval — it works across all solid tumour histologies. PD-L1 is organ-specific. BRCA and HER2 are not ICI biomarkers.

3. A CAR-T patient on Day 5 post-infusion develops fever 38.9°C, BP 88/52 mmHg (responsive to 1L IV fluids), and requires 2L O2 via nasal cannula. What is the MOST appropriate immediate management?

A. Paracetamol and observation only — likely Grade 1 CRS
B. Start broad-spectrum antibiotics for sepsis
C. Administer tocilizumab 8 mg/kg IV and escalate to HDU/ICU — Grade 2 CRS
D. Give infliximab — first-line for CRS

Answer: C — This is Grade 2 CRS (fever + hypotension responding to fluids + O2 requirement). Tocilizumab (IL-6 receptor antagonist) 8 mg/kg IV is first-line for Grade 2 CRS. Infliximab is NOT used for CRS. Antibiotics are considered concurrently to exclude sepsis, but tocilizumab should not be delayed.

4. Which immunosuppressant is CONTRAINDICATED in Grade 3 hepatitis irAE?

A. Methylprednisolone
B. Mycophenolate mofetil (MMF)
C. Infliximab
D. Prednisolone

Answer: C — Infliximab is hepatotoxic and must NOT be used in irAE hepatitis. For steroid-refractory hepatitis, MMF (mycophenolate mofetil) is the preferred second-line agent. Infliximab is appropriate for colitis and pneumonitis but is contraindicated in liver irAE.

5. A patient on nivolumab presents 8 months after treatment completion with fatigue, hypotension (BP 88/58), hyponatraemia (Na 128), and fasting hypoglycaemia. What is the MOST likely irAE?

A. Hypothyroidism
B. Hypophysitis with central hypothyroidism
C. Adrenal insufficiency
D. ICI-induced nephritis

Answer: C — The triad of hypotension, hyponatraemia, and hypoglycaemia is classic for adrenal insufficiency. This can occur months after ICI completion. Urgent cortisol/ACTH assessment and hydrocortisone replacement are required. Adrenal crisis requires IV hydrocortisone 100 mg immediately.

6. Which checkpoint inhibitor has the LONGEST standard infusion duration?

A. Pembrolizumab (30 min)
B. Nivolumab (30–60 min)
C. Ipilimumab (90 min)
D. Atezolizumab (60 min)

Answer: C — Ipilimumab (CTLA-4 inhibitor) has the longest standard infusion time at 90 minutes. Pembrolizumab is the shortest at 30 minutes. Knowing infusion times is important for scheduling and monitoring.

7. In CAR-T therapy, what is the maximum time from thawing the cryopreserved product to infusion?

A. 2 hours
B. 30 minutes
C. 4 hours
D. 1 hour

Answer: B — CAR-T products must be infused within 30 minutes of thawing to maintain cell viability. Once thawed, cell viability declines rapidly. This requires careful coordination between the cell therapy team, pharmacy, and infusion nurse.

8. A patient on ipilimumab develops a new severe headache and visual disturbance. MRI shows pituitary enlargement. Which hormone should be checked and replaced FIRST?

A. TSH / thyroxine
B. FSH / LH
C. Cortisol (adrenal axis)
D. Growth hormone

Answer: C — In hypophysitis, cortisol/adrenal insufficiency must be assessed and treated FIRST before replacing other hormones (thyroid, gonadal). Undetected adrenal insufficiency can cause adrenal crisis if thyroid hormone is replaced without cortisol (thyroxine increases cortisol clearance).

9. ICANS (Immune Effector Cell-Associated Neurotoxicity Syndrome) is assessed using which scoring tool?

A. GCS (Glasgow Coma Scale)
B. MMSE (Mini-Mental State Examination)
C. ICE (Immune Effector Cell Encephalopathy) Score
D. NIHSS (National Institutes of Health Stroke Scale)

Answer: C — The ICE score (Immune Effector Cell Encephalopathy Score) is the validated 10-point tool for ICANS assessment. It tests orientation, naming, following commands, writing, and attention. Lower scores = more severe ICANS. GCS can supplement but ICE is the ICANS-specific tool.

10. Which irAE is associated with the highest mortality risk and requires urgent troponin, ECG, and echocardiogram?

A. Grade 3 colitis
B. Grade 2 pneumonitis
C. Hypothyroidism
D. Myocarditis

Answer: D — ICI-associated myocarditis has a mortality rate of approximately 25–50%, the highest of any irAE. Early recognition with troponin, ECG, and echocardiography is critical. ICI must be permanently discontinued and high-dose IV corticosteroids started immediately. Cardiology involvement is mandatory.