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Fall 2021: Therapeutics III > Oncologic Emergencies (Weddle) > Flashcards

Oncologic Emergencies (Weddle) Flashcards

1
Q

Define tumor lysis sydrome (TLS).

A

a constellation of metabolic derangements resulting from the death of malignant cells

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2
Q

List some tumor-specific risk factors for TLS.

A
  • High tumor burden
  • High grade tumor with rapid cell turnover
  • Treatment-sensitive tumor
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3
Q

List some patient-specific risk factors for TLS.

A
  • Age
  • Preexisting renal impairment
  • Concomitant use of drugs that increase uric acid
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4
Q

List the four hallmarks of TLS pathophysiology.

A
  • HYPERkalemia
  • HYPERuricemia
  • HYPERphosphatemia
  • HYPOcalcemia
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5
Q

Give some keys to the successful management of acute TLS.

A
  • Identify and prophylax high-risk patients
  • Monitor electrolytes before and during cytoreductive regimens
  • Aggressively hydrate
  • Control hyperuricemia with uric acid-lowering drugs
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6
Q

What malignancies are associated with low risk TLS?

A
  • Most solid tumors
  • Myeloma
  • Indolent lymphomas
  • CML
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7
Q

What is the prophylaxis protocol for low-risk TLS?

A
  • Monitoring
  • Hydration
  • (maaaayyyybbeee allopurinol but probably not)
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8
Q

What malignancies are associated with intermediate-risk TLS?

A
  • DLBCL
  • SCLC
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9
Q

What is the prophylaxis protocol for intermediate-risk TLS?

A
  • Monitoring
  • Hydration
  • Allopurinol
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10
Q

What malignancies are associated with high-risk TLS?

A
  • Burkitt’s lymphoma
  • Lymphoblastic lymphomas
  • Most acute leukemias
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11
Q

What is the prophylaxis protocol for high-risk TLS?

A
  • Monitoring
  • Hydration
  • Rasburicase
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12
Q

What are the two fluid options when hydrating for TLS?

A
  • D5/0.45 NS
  • 0.9 NS
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13
Q

What is the desired urine output when hydrating for TLS?

A

80-100 mL/m2/hr

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14
Q

What should ALWAYS be considered when assessing fluid rate and volume in TLS patients?

A

cardiac function

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15
Q

What does allopurinol do?

A

blocks uric acid formation

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16
Q

How long will a TLS patient be on allopurinol?

A

until uric acid and other lab values normalize; NOT a lifelong medication

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17
Q

How does a TLS patient develop hyperuricemic AKI?

A

uric acid and xanthine crystlize within the tubular lumen

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18
Q

List some major limitations of using allopurinol for TLS.

A
  • Doesn’t reduce already-formed uric acid
  • May take several days
  • Increases concentrations of xanthine and xanthine oxidase metabolites, which can then precipitate
  • Decreased clearance of certain chemotherapies (6-MP, azathioprine, high-dose MTX)
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19
Q

What makes rasburicase different from allopurinol?

A

it can decrease already-formed uric acid also (and fast!)

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20
Q

Rasburicase catalyzes oxidation of uric acid into its soluble metabolite, __________.

A

allantoin

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21
Q

What should definitely be considered when doing a blood-draw for a high-risk TLS patient?

A

rasburicase degrades uric acid within blood samples, and could show falsely low uric acid levels

samples must be mixed with heparin, stored on ice, and evaluated within 4 hours

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22
Q

With rasburicase, risk of ____________ increases with subsequent use.

A

hypersensitivity reactions

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23
Q

In what groups is rasburicase contraindicated?

A

pregnant/breast-feeding

24
Q

Some patients of African, Mediterranea, or Southeast Asian descent are at risk of severe hemolysis reactions with rasburicase. Why?

A

G6P dehydrogenase deficiency

25
Q

What baseline levels should be taken before starting certain chemotherapy, in order to monitor TLS?

A
  • Uric acid
  • Phosphorus
  • Potassium
  • Calcium
  • LDH
  • SCr
  • Urine output
26
Q

What is the ultimate goal of TLS monitoring?

A

avoid dialysis and minimize morbidity/mortality

27
Q

Which cancers are responsible for 2/3 of all MSCC cases?

A

breast, lung, and prostate

28
Q

List some common symptoms of MSCC.

A
  • Pain/tenderness
  • Bladder/bowel dysfunction
  • Paresthesia/decreased sensation/numbness of fingers or toes
  • Hyperreflexia
  • Limb weakness/motor deficits
29
Q

In MSCC, _________________ as a result of spinal cord compression ischemia leads to white matter necrosis and gliosis.

A

vasogenic edema

30
Q

What is the method of choice for diagnosing MSCC?

A

MRI of the whole spine

31
Q

The strongest predictor of neurologic outcome with MSCC treatment is _________________________.

A

the neurologic status when treatment is initiated

32
Q

What medication should be started immediately if MSCC is strongly suspected?

A

dexamethasone IVP

33
Q

What are the only treatments that lead to immediate relief of MSCC?

A

surgery and radiotherapy

34
Q

Define laminectomy.

A

surgical removal of some or all of the pathological vertebral body and tumor mass

35
Q

Define vertebroplasty.

A

bone cement injected into fractured bone

36
Q

Define kyphoplasty.

A

a balloon inserted and inflated to expand the compressed vertebra, before filling the space with bone cement

37
Q

What drug should be offered to MSCC patients after surgery if they have vertebral involvement?

A

bisphosphonates; reduce the risk of vertebral fracture/collapse

38
Q

What is SVC syndrome?

A

when the superior vena cava is compressed by tumors outside

39
Q

What are some common signs/symptoms of SVC syndrome?

A
  • Distention of the neck and chest wall veins
  • Facial/arm edema
  • Hypotension
  • Dyspnea at rest
  • Cough
  • Stridor
  • Dysphagia
  • Headaches
  • Syncope
  • Dizziness
40
Q

What can happen if SVC syndrome is left untreated?

A
  • Hemodynamic compromise
  • Airway compromise
  • Increased intracranial pressure = cerebral edema, intracerebral bleeding
41
Q

True or false: most SVC syndrome cases are true oncologic emergencies.

A

false

42
Q

Based on the severity of SVC symptoms, what interventions may be considered?

A
  • Resection
  • Stenting
  • Radiation
  • Chemotherapy
  • Anticoagulation
43
Q

What are some adjunctive therapies that can be used to alleviate SVC syndrome symptoms?

A
  • Head elevation (decrease hydrostatic pressure/edema)
  • Steroids (only in patients with steroid-sensitive tumors/undergoing radiation)
  • Diuretics (decrease arterial pressure to affect venous pressure distal to the obstruction)
44
Q

What is malignant pleural effusion (MPE)?

A

uniformly fatal fluid accumulationin the pleural space

45
Q

What is the most common presenting symptom of MPE?

A

dyspnea

46
Q

What is the first radiodiagnostic to be used for MPE?

A

chest x-ray

47
Q

When would an ultrasound be used in MPE?

A

pre-procedure, to identify appropriate drainage sites

48
Q

What procedure is frequently perfomed for MPE diagnosis and therapeutics?

A

thoracentesis

49
Q

What is thoracentesis?

A

needle aspiration of fluid from a pleural effusion

50
Q

What MPE patient population(s) would you recommend thoracentesis for?

A
  • Those seeking temporary relief of acute symptoms
  • Patients with life expectancy < 1-3 months
51
Q

What can happen if more than 1.5 L are taken out during thoracentesis?

A

re-expansion pulmonary edema

52
Q

What is the recommended course of treatment for MPE patients with a life expectancy > 1-3 months?

A

pleurodesis

53
Q

What is pleurodesis?

A

drainage of the pleural space with subsequent injection of either talc, doxycycline, or bleomycin

54
Q

What is the mechanism of action of pleurodesis?

A

activates the inflammatory cascade, leading to adhesion of pleural layers

55
Q

How often is a pleural catheter for MPE drained?

A

frequently, to comfort

56
Q

What are some pros of using an indwelling pleural catheter for MPE?

A
  • Decreased hospital stay
  • Less frequent need for thoracentesis/pleurodesis
57
Q

Provide two risks of an indwelling pleural catheter for MPE.

A
  • Infection
  • Tumor seeding of catheter

Fall 2021: Therapeutics III (25 decks)

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