Facts read from oncc.org · last checked Nov 7, 2026
ONCC's outline for area III lists no conditions, only three tasks: cause and prevention, assessment and differential diagnosis, and treatment. The grouping below is ours, not ONCC's.
Practice questions
60 questions written to the AOCNP outline; each choice is explained once you pick.
Metabolic: tumor lysis syndrome, hypercalcemia of malignancy, SIADH and hyponatremia.
Structural: spinal cord compression, superior vena cava syndrome, pericardial effusion and tamponade, raised intracranial pressure, airway obstruction.
Hematologic and infectious: febrile neutropenia and sepsis, DIC, hyperviscosity, leukostasis, bleeding.
Treatment-related: infusion and hypersensitivity reactions, extravasation, cytokine release syndrome, severe immune-related events.
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Definitions that decide the answer
Febrile neutropenia (IDSA, used by ASCO/IDSA 2018): ANC below 500/µL, or expected to fall below 500 within 48 hours, with a single temperature of 38.3 °C or higher or 38.0 °C sustained over an hour. ASCO/IDSA asks for the first antibiotic dose within an hour of triage, and a MASCC score of 21 or more marks a low-risk patient who may be treated as an outpatient.
Tumor lysis (Cairo-Bishop): laboratory TLS is two or more of high uric acid, potassium or phosphate, or low calcium, from 3 days before to 7 days after therapy starts. Clinical TLS adds kidney injury, arrhythmia or seizure.
Tamponade: Beck's triad (hypotension, muffled heart sounds, raised jugular venous pressure) and pulsus paradoxus over 10 mm Hg; echocardiography confirms it and drainage treats it.
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14 emergency scenarios to work through
0 / 14 answered14 questions
Tap an option: why each one is right or wrong appears under it.
Oncologic Emergencies · 12%
A patient with squamous cell lung cancer and no bone metastases has a calcium of 13.1 mg/dL and a suppressed PTH. Which result confirms the most common mechanism of hypercalcemia of malignancy?
Bone-origin alkaline phosphatase rises with osteolytic or blastic metastases, which this patient does not have.
An M-spike points to myeloma, which raises calcium through bone destruction; it does not fit squamous lung cancer without bone disease.
About 80% of hypercalcemia of malignancy is humoral, from tumor secretion of PTH-related protein, classically by squamous cell cancers; with no bone metastases and a suppressed PTH, an elevated PTHrP confirms it.
Calcitriol-mediated hypercalcemia is mainly a lymphoma mechanism, uncommon in squamous lung cancer, and responds to steroids.
A neutropenic patient with AML has a temperature of 39.1 °C, BP 82/48 mm Hg and lactate 3.8 mmol/L. After cultures, the APRN's priority orders are:
G-CSF does not treat established sepsis, and 500 mL is far short of the volume a hypotensive patient with a high lactate needs.
Vasopressors are added if MAP stays below 65 after fluid resuscitation, not used in place of volume in a patient with a lactate of 3.8.
Oral outpatient therapy is only for low-risk, stable febrile neutropenia; this patient is in shock.
Neutropenic septic shock needs 30 mL/kg crystalloid for hypoperfusion and an antipseudomonal beta-lactam within the first hour; hemodynamic instability is one of the indications to add vancomycin.
A patient with a new mediastinal mass, facial swelling and dilated chest veins has no stridor, normal oxygen saturation and no tissue diagnosis. Chest CT confirms SVC obstruction. The APRN's next step is:
Empiric steroids and radiation can obscure lymphoma pathology and are reserved for airway compromise or other life-threatening features.
Without stridor, cerebral edema, or hypoxemia, SVC syndrome is not immediately life-threatening, and histology (small cell, lymphoma, NSCLC) decides treatment, so tissue comes first.
Chemotherapy is chosen by histology; treating presumed lymphoma could be wrong for small cell or non-small cell lung cancer.
Endovascular stenting gives the fastest relief and is used for severe symptoms such as stridor or confusion; this stable patient does not need it before diagnosis.
A 72-year-old patient with CLL, bulky nodes and creatinine clearance of 55 mL/min starts venetoclax with obinutuzumab. To prevent tumor lysis syndrome, the APRN orders:
Starting at the target dose removes the gradual debulking that the ramp-up provides and has caused fatal TLS.
Venetoclax is escalated weekly over 5 weeks (20, 50, 100, 200, then 400 mg) with hydration, an antihyperuricemic started beforehand, and TLS labs at each step, because bulky nodes and reduced clearance raise TLS risk.
Allopurinol prevents new uric acid formation, so it starts before the first dose (typically 72 hours earlier), not after TLS risk has begun.
Urine alkalinization is no longer recommended; it adds little to uric acid clearance and promotes calcium phosphate precipitation.
A patient with pancreatic head cancer presents with fever, rigors, jaundice and right upper quadrant pain. Blood pressure is 96/60 mm Hg. After starting IV piperacillin-tazobactam, the APRN arranges:
Fever, jaundice, and right upper quadrant pain with hypotension in malignant biliary obstruction is severe acute cholangitis, which needs urgent biliary decompression, usually ERCP with stenting, alongside antibiotics.
The obstruction is in the distal common bile duct from the tumor; removing the gallbladder does not drain it.
Delaying drainage for more imaging risks septic shock; the diagnosis is already clinical and the duct needs decompression now.
Antibiotics cannot sterilize an obstructed duct, and waiting 48 hours in severe cholangitis risks septic shock.
Four hours after intrathecal methotrexate, a patient develops headache, neck stiffness, vomiting and low-grade fever. CSF Gram stain shows no organisms and glucose is normal. The APRN diagnoses:
Methotrexate leukoencephalopathy is a subacute to late cognitive and white-matter syndrome, not a meningeal reaction within hours.
Bacterial meningitis is the dangerous look-alike, but it usually appears later, with low CSF glucose and often organisms on Gram stain.
Headache, meningismus, vomiting, and low-grade fever within hours of intrathecal methotrexate, with sterile CSF and normal glucose, is acute chemical arachnoiditis, which resolves over days with supportive care.
Subarachnoid hemorrhage starts with a thunderclap headache and shows blood or xanthochromia in the CSF.
A patient on pembrolizumab develops ptosis, diplopia and proximal weakness 4 weeks after starting therapy. While holding the drug and starting steroids, which test is MOST urgent to add?
Thyroiditis is common with pembrolizumab, but it does not explain ocular and proximal weakness and would miss a cardiac overlap.
Electrodiagnostic testing can confirm a neuromuscular junction disorder later, but it does nothing about the lethal cardiac overlap that needs checking now.
Vitamin deficiency causes a slow neuropathy, not fatigable ptosis and diplopia weeks after starting a checkpoint inhibitor.
Immune-related myasthenia often overlaps with myositis and myocarditis, the most lethal checkpoint toxicity, so troponin, CK, and an ECG are checked urgently along with the neurologic workup.
A patient with glioblastoma has acute severe headache, vomiting and declining consciousness. BP is 188/96 mm Hg and heart rate 48/min with irregular respirations. The APRN recognizes:
Here the high BP is a reflex that preserves cerebral perfusion; treating it as a primary hypertensive emergency and lowering it hard can worsen ischemia.
Nonconvulsive status can depress consciousness, but it does not produce bradycardia with irregular respirations.
Steroid psychosis causes agitation or mood change with stable vital signs, not declining consciousness with a Cushing triad.
Hypertension with bradycardia and irregular breathing (Cushing triad), vomiting, and falling consciousness in a patient with glioblastoma signal critically raised intracranial pressure and impending herniation.
A patient receiving bevacizumab for colorectal cancer has a headache, cortical blindness, and a seizure. BP is 196/112 mmHg, and MRI shows bilateral parieto-occipital vasogenic edema. The APRN's priority intervention is:
Severe hypertension, seizure, and cortical blindness with symmetric parieto-occipital edema on a VEGF inhibitor is PRES; controlled BP lowering, seizure control, and stopping bevacizumab usually reverse it.
Osmotic therapy treats herniation from raised ICP; PRES edema responds to treating the blood pressure.
Venous sinus thrombosis can cause seizures and edema, but the posterior symmetric MRI pattern is PRES, and anticoagulating a bevacizumab patient adds bleeding risk.
The word edema invites steroids, but this vasogenic edema is driven by hypertension and endothelial injury, not tumor, and resolves with BP control.
A patient who completed chemoradiation for oropharyngeal cancer has a brief bleed of bright red blood from a neck wound that stops on its own. Vital signs are stable. The APRN's most appropriate action is:
Waiting for the next visit ignores the warning; carotid blowout after a sentinel bleed can follow within hours to days.
A self-limited bleed from an irradiated neck is a sentinel bleed that often precedes carotid blowout, so the patient is admitted for CT angiography and endovascular evaluation while stable.
Because the bleeding stopped, treating it as minor wound oozing is tempting, but discharge risks a catastrophic rebleed outside the hospital.
Infection may contribute to wound breakdown, but antibiotics do nothing about an exposed, weakened carotid artery.
During a first rituximab infusion, a patient develops chills, fever, and BP 88/50 mmHg. The infusion is stopped, and symptoms fully resolve with fluids, acetaminophen, and diphenhydramine. The APRN orders:
Rituximab infusion reactions are mostly cytokine-mediated; once symptoms fully resolve, the label restarts the infusion at 50% of the rate at which the reaction occurred.
Discontinuation is for grade 4 or anaphylactic reactions; a reaction that resolves fully with fluids and supportive drugs allows rechallenge.
Restarting at the same rate invites the same cytokine surge that caused the reaction.
Subcutaneous rituximab is given only after the patient has received at least one full IV dose.
A patient with renal cell carcinoma has MRI-confirmed high-grade epidural compression at one thoracic level, is still ambulatory, is ECOG 1, and has a life expectancy over 6 months. After dexamethasone, the APRN recommends:
Conventional external beam radiation suits radiosensitive tumors such as myeloma or lymphoma, multilevel disease, or poor surgical candidates; renal cell carcinoma responds poorly to it.
Dexamethasone reduces edema for a time but leaves the tumor compressing the cord.
For single-level high-grade compression from a radioresistant tumor in a fit patient, decompressive surgery followed by radiation preserves ambulation better than radiation alone (Patchell), and renal cell carcinoma responds poorly to conventional radiation.
A tyrosine kinase inhibitor has a later role in metastatic RCC, but it acts too slowly to decompress the cord and protect function.
A 71-year-old with Waldenström macroglobulinemia (serum IgM 6,800 mg/dL) has headache, blurred vision, epistaxis, and dilated, segmented retinal veins. The APRN's priority treatment is:
Transfusing red cells before the IgM is lowered raises whole-blood viscosity further; the anemia is partly dilutional and transfusion waits for plasma exchange.
Symptomatic hyperviscosity from an IgM paraprotein is an emergency, and plasma exchange removes intravascular IgM quickly, relieving visual, neurologic, and bleeding symptoms before disease-directed therapy starts.
Steroids treat tumor-related cerebral edema, but they do not lower serum viscosity fast enough to protect vision or stop bleeding.
Rituximab is part of definitive Waldenström therapy, but given alone with a high IgM it can cause an IgM flare that worsens hyperviscosity, so plasma exchange comes first.
A running total sits here; it fills in after your last pick.
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First-step errors in area III
Rasburicase and G6PD. It is contraindicated in G6PD deficiency because it can cause hemolysis and methemoglobinemia; test first when the risk is plausible.
Hypercalcemia in order. IV fluids come first, calcitonin works fast but briefly, and zoledronic acid or denosumab gives the lasting effect. The Endocrine Society's 2023 guideline suggests denosumab over an IV bisphosphonate, a conditional recommendation on low-certainty evidence.
Correcting sodium too fast. In chronic hyponatremia, overcorrection within 24 hours risks osmotic demyelination; the limit is set per day, not per hour.
APL and DIC. When acute promyelocytic leukemia is suspected, all-trans retinoic acid starts before genetic confirmation, because the coagulopathy kills early.
Reaction timing. Taxane hypersensitivity usually appears in the first or second infusion; carboplatin reactions appear after repeated exposure, often many cycles in.
None by name: ONCC's 2025 outline gives area III three tasks without a condition list. Expect the common metabolic, structural and hematologic emergencies plus reactions to treatment.
How many AOCNP questions cover emergencies?
Area III is 12% of the 125 scored questions, about 15 on a form.