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PM Review > Oncology and PC emergencies > Flashcards

Oncology and PC emergencies Flashcards

1
Q

2 key class of checkpoint inhibitors

A

anti - CTLA 4 (cytotoxic t-lymphocyte associated antigen)
anti - PD1 (programmed death receptor) and PDL1 (programmed cell death ligand)

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2
Q

irAE - general principle
grade 1 toxicity approach

A

monitor
reduce dose of immune therapy

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3
Q

Grade 2 irAE (excluding endocrinopathy) management

A

hold immune therapy
prednisone 0.5mg/kg/d if symptoms to not resolve within a week

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4
Q

irAE grade 2 endocrinopathy management

A

hold the immune therapy
hormonal supplementation (can restart therapy after symptoms improve)

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5
Q

irAE grade 3-4 management

A

stop immune therapy (permanently in most cases)
this is life threatening
high dose steroids (pred 1-2mg/kg/d) - taper once symptoms improve to grade 1 or less

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6
Q

management of refractory irAE despite steroids

A

additional immunosuppressive (infliximab, mycophenolate etc.)

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7
Q

impact of immune suppressant on immune therapy efficacy

A

may reduce efficacy, but in very high doses
lower doses may be acceptable, and may be the only way for a patient to tolerate the immune therapy

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8
Q

how do irAE’s correlate with efficacy?

A

these patients are found to have better or equal response to those without irAE’s
(proxy for positive activation of immune system -> disease response)

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9
Q

List 3 systemic adverse events associated with immune therapy

A
  • fatigue
  • infusion related reactions - (h/a, chills, nausea -> allergy (rare))
  • cytokine release syndrome (most often seen with CAR-T therapy) - (constitutional symptoms -> SIRS)
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10
Q

3 dermatologic toxicities of immune therapy

A
  • skin reaction
  • bullous disease
  • vasculitis
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11
Q

Most frequent GI adverse effects of immune therapy

A

diarrhea
colitis

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12
Q

Most common symptoms of immune pneumonitis
AND
Proportion of patients who are asymptomatic

A

Symptoms - cough, dyspnea

1/3 of patients asymptomatic

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13
Q

Most common endocrinopathies from immune therapy

A
  • hypothyroidism
  • hyperthyroidism
  • hypophysitis
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14
Q

Outline the thyroid disorders related to immune therapy

A

1) primary hypothyroidism (high TSH, low T4) - synthroid
2) hypophysitis (low TSH and T4) - test for adrenal insufficiency first
3) thyroiditis - transient hyperthyroidism followed by hypothyroidism (monitor and only treat symptoms of hyperthyroidism with BB)
4) hyperthyroidism - prolonged for months, test for graves

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15
Q

2 most common consequences of hypophysitis and management

A
  • secondary hypothyroidism
  • secondary adrenal insufficiency
  • hormone replacement, often life long.
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16
Q

the most critical endocrinopathy

A

adrenal insufficiency

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17
Q

criteria for PCP prophylaxis in immune therapy patients also taking steroids

A
  • on glucocorticoids for > 6 weeks
  • on glucocorticoid + combined chemo/immune therapy
  • on glucocorticoid + underlying pulmonary condition
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18
Q

general criteria for PCP prophylaxis in immunosuppressed patients taking steroids

A

If using ≥20 mg of prednisone daily for one month or longer

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19
Q

List some rare neurological complications of immune therapy

A

headache
encephalitis
autonomic, cranial and peripheral neuropathies
aseptic meningitis
transverse myelitis
guillain barre syndrome
myasthenia gravis

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20
Q

Cardiac toxicities of immune therapy

A

myocarditis
pericarditis
vasculitis heart failure

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21
Q

MSK toxicities of immune therapy

A

myositis
inflammatory arthritis
vasculitis
sicca syndrome

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22
Q

Differentiate low vs. high grade spinal cord compression

A

low grade - epidural extension without cord compression (may be abutting the cord) (grade 1)
high grade - tumor displaces (grade 2) or compresses (grade 3) the cord

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23
Q

Main reasons for surgery in cord compression

A

Spinal instability
Complete compression (RT would not work expediently)

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24
Q

Pharmacological treatment for cord compression:

A

Dex 10mg IV stat, then Dex 16mg/d (8mg BID)

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25
List key factors that influence the approach to cord compression in a patient
Spinal stability Radiosensitivity of the tumor Degree of cord compression Stage of disease (systemic effects, treatment options) Level of function Patient comorbidities
26
Key prognostic factors in cord compression
Severity of the compression, and ambulatory status at time of diagnosis Rapidity of symptom onset (slower onset - better outcome) Type of tumor (RT sensitivity and systemic treatment options)
27
2 most common malignancies causing SVCO
SCLC mediastinal lymphoma
28
CXR findings for SVCO
mediastinal widening pulm edema
29
Diagnostic modality for SVCO
Enhanced CT (best view of surrounding structures - extrinsic comp.) Superior venocavogram MR venogram (patients with contrast allergy)
30
What are the s/s of emergent SVCO What is the management
Laryngeal edema, central airway obstruction, cerebral edema Endovascular recanalization (thrombolysis or stent)
31
What is the role of glucocorticoids in SVCO? What is the dose?
- Control of compression prior to and during RT (if RT will be the definitive management) - Management of a steroid responsive tumor (lymphoma) - Dex 8mg BID
32
What is the most important management task in the event of a catastrophic arterial bleed?
Stay with the patient (arterial bleeds render patients unconscious within minutes, making sedation futile)
33
3 causes of malignant hypercalcemia
- PTHrp (most common) - lytic bone mets - 1,25 hydroxivitamin D - ectopic PTH (rare)
34
Factors that aggravate hypercalcemia
thiazides lithium dehydration calcium supplement (>1000mg/d) high dose vit D (>800IU/d)
35
2 most immediately effective treatments for hypercalcemia (severe)
fluids calcitonin
36
What are the limitations of calcitonin?
short acting tachyphylaxis (often after 48h or so)
37
List the bisphosphonates in order of efficacy (descending) for hypercalcemia
Zoledronic acid Pamidronate - Ibandronate Clodronate
38
What are the indications for use of denosumab
Severe renal impairment Hypercalcemia refractory to bisphosphonate
39
What is the typical dosing interval for bisphosphonate?
q4 weeks may be given again after 7 days in hypercalcemia
40
How quickly do bisphosphonates work for hypercalcemia?
24-48h nadir at 7 days
41
Which patients are at risk of hypocalcemia after bisphosphonate?
Vit D deficient
42
What 2 factors influence renal toxicity of bisphosphonates?
- hydration status - rate of infusion (lower and slower in renal failure)
43
List risk factors for catastrophic hemorrhage
known tumor erosion into vessel "sentinel bleed" - trivial bleed occurring 24-48h prior - usually due to a pseudoaneurysm high risk cancers (head and neck, lung) thrombocytopenia
44
What are 3 steps to managing a terminal bleed?
1) Prepare 2) Manage 3) After the event
45
Steps in preparing for a terminal bleed
1) Identify high risk patients, and address modifiable risk 2) Clarify GOC and plan of action in event of bleed 3) Create a plan for the caregivers 4) Prepare "crisis pack" - pre-drawn sedative and analgesic - dark towels, face cloth - suction device (for choking) - warm blankets (cold from hypotension)
46
Key steps in managing terminal hemorrhage
- ABC's (assurance, be there, comfort and calm) - Use crisis meds when possible - Position patient (depending on the bleed) - bleeding site against gravity - recovery position (hemoptysis/hematemesis) - decubitus (bleeding lung side down in pulm. hemorrhage)
47
What do you do after a bleed
- Debrief with family, caregivers
48
What is carotid blowout? What are the risk factors?
Rupture of the extracranial carotid (or branches) Risk factors: - Head and neck ca. - Prior RT - malignant wound - phayngocutaneous fistula - extensive previous surgery
49
What is "carotid blowout syndrome"?
Threatened, impending, or acute rupture of carotid artery
50
What is the best diagnostic modality for CBS?
Angiography (stenting can be considered at the same time)
51
bone scans miss metastases in what kinds of cancer?
lytic lesions - myeloma highly aggressive lesions with no bone deposition - lung, melanoma
52
key long term effect of WBRT
memory loss (after 3 months or so)
53
Key late complication of stereotactic RT
necrosis
54
Palliative RT to brain not considered for which 2 groups?
1) poor prognosis with extensive systemic disease - supportive care alone + dex associated with 1-2 mo. progression free survival? - NSCLC study of non-inferiority 2) patient on treatment that crosses BBB (TKI, immune therapy) - RT only considered if progression
55
median time to response for RT to bone
2-3 weeks 3-4 month duration of benefit
56
2 therapies for widespread bone mets
hemi body RT radionucleotide therapy
57
what is the role of RT for pathological # and impending #'s
post-op - prevent further growth tumor control for pain relief, potential for bone healing
58
Liver is treated with what kind of RT, typically?
SBRT (oligometastatic disease) does not handle external beam well?
59
define cancer fatigue
physical, emotional, or cognitive fatigue associated with cancer or its treatment not proportional to recent activity interferes with functioning does not improve with rest or sleep
60
list 3 mechanisms of cancer fatigue
- inflammation (cytokines) - HPA axis dysregulation - circadian rhythm desynchronization - skeletal muscle fatigue
61
key mechanism of fatigue in survivors
immune activation and chronic inflammation
62
2 scales to assess fatigue
BFI - brief fatigue inventory MFI - multidimensional fatigue inventory
63
4 classes of medications that can be used for cancer fatigue
- steroid - dexamethasone - psychostimulant - methylphenidate - cholinesterase inhibitor - donepezil - anti-depressant - paroxetine (use if depression concurrent)
64
general approach to fatigue management
- educate / counsel - exercise - psychosocial interventions - pharmacological interventions

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