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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
Q

List key factors that influence the approach to cord compression in a patient

A

Spinal stability
Radiosensitivity of the tumor
Degree of cord compression
Stage of disease (systemic effects, treatment options)
Level of function
Patient comorbidities

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26
Q

Key prognostic factors in cord compression

A

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
Q

2 most common malignancies causing SVCO

A

SCLC
mediastinal lymphoma

28
Q

CXR findings for SVCO

A

mediastinal widening
pulm edema

29
Q

Diagnostic modality for SVCO

A

Enhanced CT (best view of surrounding structures - extrinsic comp.)
Superior venocavogram
MR venogram (patients with contrast allergy)

30
Q

What are the s/s of emergent SVCO
What is the management

A

Laryngeal edema, central airway obstruction, cerebral edema
Endovascular recanalization (thrombolysis or stent)

31
Q

What is the role of glucocorticoids in SVCO?
What is the dose?

A
  • 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
Q

What is the most important management task in the event of a catastrophic arterial bleed?

A

Stay with the patient
(arterial bleeds render patients unconscious within minutes, making sedation futile)

33
Q

3 causes of malignant hypercalcemia

A
  • PTHrp (most common)
  • lytic bone mets
  • 1,25 hydroxivitamin D
  • ectopic PTH (rare)
34
Q

Factors that aggravate hypercalcemia

A

thiazides
lithium
dehydration
calcium supplement (>1000mg/d)
high dose vit D (>800IU/d)

35
Q

2 most immediately effective treatments for hypercalcemia (severe)

A

fluids
calcitonin

36
Q

What are the limitations of calcitonin?

A

short acting
tachyphylaxis (often after 48h or so)

37
Q

List the bisphosphonates in order of efficacy (descending) for hypercalcemia

A

Zoledronic acid
Pamidronate - Ibandronate
Clodronate

38
Q

What are the indications for use of denosumab

A

Severe renal impairment
Hypercalcemia refractory to bisphosphonate

39
Q

What is the typical dosing interval for bisphosphonate?

A

q4 weeks
may be given again after 7 days in hypercalcemia

40
Q

How quickly do bisphosphonates work for hypercalcemia?

A

24-48h
nadir at 7 days

41
Q

Which patients are at risk of hypocalcemia after bisphosphonate?

A

Vit D deficient

42
Q

What 2 factors influence renal toxicity of bisphosphonates?

A
  • hydration status
  • rate of infusion (lower and slower in renal failure)
43
Q

List risk factors for catastrophic hemorrhage

A

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
Q

What are 3 steps to managing a terminal bleed?

A

1) Prepare
2) Manage
3) After the event

45
Q

Steps in preparing for a terminal bleed

A

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
Q

Key steps in managing terminal hemorrhage

A
  • 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
Q

What do you do after a bleed

A
  • Debrief with family, caregivers
48
Q

What is carotid blowout?
What are the risk factors?

A

Rupture of the extracranial carotid (or branches)
Risk factors:
- Head and neck ca.
- Prior RT
- malignant wound
- phayngocutaneous fistula
- extensive previous surgery

49
Q

What is “carotid blowout syndrome”?

A

Threatened, impending, or acute rupture of carotid artery

50
Q

What is the best diagnostic modality for CBS?

A

Angiography (stenting can be considered at the same time)

51
Q

bone scans miss metastases in what kinds of cancer?

A

lytic lesions - myeloma

highly aggressive lesions with no bone deposition - lung, melanoma

52
Q

key long term effect of WBRT

A

memory loss (after 3 months or so)

53
Q

Key late complication of stereotactic RT

A

necrosis

54
Q

Palliative RT to brain not considered for which 2 groups?

A

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
Q

median time to response for RT to bone

A

2-3 weeks

3-4 month duration of benefit

56
Q

2 therapies for widespread bone mets

A

hemi body RT

radionucleotide therapy

57
Q

what is the role of RT for pathological # and impending #’s

A

post-op - prevent further growth

tumor control for pain relief, potential for bone healing

58
Q

Liver is treated with what kind of RT, typically?

A

SBRT (oligometastatic disease)

does not handle external beam well?

59
Q

define cancer fatigue

A

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
Q

list 3 mechanisms of cancer fatigue

A
  • inflammation (cytokines)
  • HPA axis dysregulation
  • circadian rhythm desynchronization
  • skeletal muscle fatigue
61
Q

key mechanism of fatigue in survivors

A

immune activation and chronic inflammation

62
Q

2 scales to assess fatigue

A

BFI - brief fatigue inventory
MFI - multidimensional fatigue inventory

63
Q

4 classes of medications that can be used for cancer fatigue

A
  • steroid - dexamethasone
  • psychostimulant - methylphenidate
  • cholinesterase inhibitor - donepezil
  • anti-depressant - paroxetine (use if depression concurrent)
64
Q

general approach to fatigue management

A
  • educate / counsel
  • exercise
  • psychosocial interventions
  • pharmacological interventions

PM Review (19 decks)

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