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METABOLIC > ONCOLOGY - ONCOLOGICAL EMERGENCIES > Flashcards

ONCOLOGY - ONCOLOGICAL EMERGENCIES Flashcards

1
Q

What are the oncological emergencies?

A

Hypercalcaemia
Neutropenic sepsis
Tumour lysis syndrome
Leukostasis -
Hyperviscocity syndrome -
Raised ICP -
Spinal cord compression
Cauda equine syndrome -
SVC obstruction
Syndrome of inappropriate ADH secretion -

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2
Q

How common is Hypercalcaemia in patients with malignancy?

A

10-30%
(40% of myeloma)
Most common oncological emergency

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3
Q

Which cancers is hypercalcaemia usually associated with?

A

Breast cancer
Lung cancer
Non-Hodgkin lymphoma
Multiple myeloma
Renal cancer

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4
Q

What is the 3 month mortality rate of cancer patients admitted to hospital with hypercalcaemia?

A

75% - a poor prognostic indicator in malignant disease!!

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5
Q

What are some presenting features of Hypercalcaemia?

A

Stones - kidney stones (chronic), polyuria and diabetes insipidus
Thrones - constipation, lethargy
Groans - abdo pain, nausea, vomiting, peptic ulcers and pancreatitis (last 2 chronic only)
Bones - bone pain and muscular weakness
Psychotic overtones - anxiety, depression, cognitive dysfunction, coma
Cardiac - bradycardia, hypertension and arrhythmias (at very high levels)

At low calcium levels, polyuria, depression, thirst and mild cognitive impairment are most common symptoms

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6
Q

Why are calcium levels, when measured, corrected?

A

Because calcium can exist in a free ionised form or exist bound to albumin
Total calcium levels are the sum of both
If albumin levels are low then there isn’t much albumin-bound calcium which means more of the total calcium will be ionised and active
The corrected calcium equation takes into account the albumin level and adjusts the total calcium level accordingly

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7
Q

Whats normal serum corrected calcium?

A

2.2-2.7mmol/L

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8
Q

Outline calcium control in the body?

A

High calcium levels are detected by the thyroid gland. Parafollicular cells release calcitonin which can bring the calcium levels down; it encouraged calcium deposition in the bones, reduces the reabsorption of calcium by kidneys

When calcium levels are low, parathyroid glands release parathyroid hormone. This causes calcium release from bones, increases calcium reabsorption from kidneys and increases levels of calcitriol (active vitamin D) which stimulates small intestine to absorb more calcium

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9
Q

Whats the most common pathology of Hypercalcaemia of malignant disease?

A

Tumour parathyroid-related-protein production which increases serum calcium levels as can bind same receptors as parathyroid hormone (most effects on bones and kidneys but doesn’t usually increase calcitriol)
Causes 80% of cases

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10
Q

Whats the other pathology mechanisms of hypercalcaemia of malignant disease?

A

Osteolytic metastases - bone lysis directly by tumour cells e.g. myeloma cells secrete IL-1 and TNF which increase osteoclast activity

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11
Q

How do you investigate hypercalcaemia?

A

Measure adjusted calcium
PTH - as most likely cause is primary hyperparathyroidism
Calcitriol - ?vitamin D deficiency
PTHrP - ?malignancy
Bone scan

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12
Q

How do you manage hypercalcaemia?

A

Generally no active treatment unless acute onset or severe/symptomatic hypercalcaemia (>3.5mmol/L)

Aggressive rehydration with 2-4 litres of 0.9% saline IV over 24 hours
IV Bisphosphonates e.g. zoledronic acid - inhibits osteoclast activity (take 2-4 days to see effects after introduction)
Glucocorticoids (inhibit 1,25OH vitamin D production)
Check medication list for calcium or vit D supplements

In resistance cases consider giving calcitonin or denosumab. Calcitonin has a more rapid but shorter-term effect than bisphosphonates
Long term treatment is to Manage malignancy

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13
Q

Whats the most common cause of Hypercalcaemia in hospital and in the community?

A

In hospital its metastatic cancer
In the community its primary hyperparathyroidism

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14
Q

What are the side efefcts of zoledronic acid?

A

Renal impairment
Flu-like symptoms
Hypocalcaemia
Chronic use can cause osteonecrosis of the jaw and external auditory canal

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15
Q

What are the causes of hypercalcaemia?

A

CHIMPANZEES

Calcium supplements
*Hyperparathyroidism
Iatrogenic e.g. thiazides and lithium
Milk alkali syndrome
Pager disease of the bone
Acromegaly and Addison’s disease
*Neoplasia
Zolinger-Ellison syndrome (MEN type 1)
*Excessive vitamin D
Excessive vitamin A
*Sarcoidosis

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16
Q

When would you do an ECG in patients with hypercalcaemia?
What would you expect?

A

> 3.5mmol/L
Decreased QT interval

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17
Q

What PTH, PTHrP and calcitriol levels would you expect in tumour PTHrP production?

A

Low PTH

High PTHrP

Normal-low calcitriol

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18
Q

What PTH, PTHrP and calcitriol levels would you expect in osteolytic metastases?

A

Low PTH
Low or normal calcitriol levels
Low or normal PTHrP

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19
Q

What are the most common organs for cancers to metastasize to?

A

Lung
Liver
Bones

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20
Q

Which primary tumours are most likely to metastasises to bones?

A

Prostate
Breast
Lung
Kidney
Myeloma

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21
Q

How does metastatic bone cancer usually present?

A

Pain
Pathological fractures
Spinal cord compression
Hypercalcaemia
Symptoms of nerve root compression
Swelling/deformity and loss of mobility

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22
Q

What are the most common sites for bone metastases?

A

Spine, pelvis, femur, ribs and humerus

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23
Q

What is appendicular bone mets? Which primary tumours typically cause it?

A

bone metastases. located distal to the elbow and knee
Renal and lung tumours

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24
Q

What characteristics of bone pain would make you worry about bone metastases?

A

Progressive pain over time
Pain that doesnt respond to simple analgesia
Pain that disturbs sleep
Pain associated with bone tenderness
Pain associated with weight loss

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25
Q

What is the mechanism by which bony metastases occur?

A

bone metastases disturb the dynamic balance between osteoclasts and osteoblasts
If there is greater osteoclast activity then lytic metastases is likely
If there is greater osteoblast activity then disordanised ossification is more likely

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26
Q

Does sclerotic or lytic bony metastases have. A higher risk of fracture?

A

Lytic

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27
Q

How do we investigate bone metastases?

A

FBC
Bone related ALP
Kidney function and liver function tests
PSA to rule out prostate cancer
Paraproteins and bence jones proteins in urine to rule out multiple myeloma
Plain x-ray
Bone scans

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28
Q

Why do we test for ALP in suspected bone metastases?

A

Your bones make an isoenzyme called ALP-2. Levels of this enzyme increase when your bones are growing or bone cells are active

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29
Q

Why are x-rays not as sensitive as bone scans for bone metastases?

A

The lesion has to be at least 1-2cm to be seen

In contrast, bone scans use a radioactive tracer to detect areas of abnormal bone turnover, which can help detect bone metastases earlier and more accurately than x-rays

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30
Q

How can you manage bone pain?

A

Pain meds using the analgesia ladder
Palliative radiotherapy
Zoledronic acid IV every 3-4 weeks
Surgical fixation if fractures

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31
Q

Whats a serious side effects of bisphosphonates?

A

Osteonecrosis of the jaw

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32
Q

Moa of denosumab?

A

A human monoclonal antibody specific for RANKL that inhibits the formation, activation and survival of osteoclasts which decreases bone resorption

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33
Q

What is a vertebroplasty?

A

an outpatient procedure for stabilizing compression fractures in the spine. Bone cement is injected into back bones (vertebrae) that have cracked or broken. The cement hardens, stabilizing the fractures and supporting your spine.

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34
Q

What are the most commonly used isotopes in treatment of painful bone metastases?

A

Strontium 89 and samarium 153

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35
Q

How does spinal cord compression present?

A

Pain in back that’s worse on lying down/worse on movement/increases with vasalva manoeuvre
May cause radicular pain
Tenderness
Autonomic dysfunction
Sensory deficits
Motor weakness
Hypereflexia and increased tone
Bowel and bladder dysfunction

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36
Q

Whats the prevalence of MSCC?

A

3-5% of all cancer patients

37
Q

What are the most common causes of Spinal cord Compression?

A

Tumours
Trauma
Osteoarthritis
Herniated disc
RA
Spinal injury
Infection
Etc…

38
Q

How do we grade spinal cord compression?

A

Epidural spinal cord compression scale

grade 0: bone-only disease
grade 1: epidural extension without cord compression
1a: epidural extension only
1b: deformation of thecal sac
1c: deformation of the thecal sac with spinal cord abutment
grade 2: spinal cord compression, with CSF visible around the cord
grade 3: spinal cord compression, no CSF visible around the cord

39
Q

Why is there often a delay in diagnosis of spinal cord compression?

A

Slow onset progressive pain that precedes other symptoms by 7 weeks

40
Q

At what vertebral level does the spinal cord end?

A

L1-L2 junction (conus medularis)

41
Q

What region of the spinal cord is spinal cord compression most likely and why?

A

60% thoracic
30% lumbar and sacral
10% cervical
This is roughly equivalent to the relative bone mass in each segment

42
Q

How does Cauda equina present?

A

Pain
Flaccid paralyses
Sensory deficits
Bladder retention and bowel dysfunction
Sexual dysfunction
Areflexia and decreased muscle tone

43
Q

At what level can spinal cord injury cause neurogenic shock?

A

Above T6

44
Q

What is neurogenic shock?

A

a distributive type of shock resulting in hypotension often with bradycardia caused by disruption of autonomic nervous system pathways (loss of SNS so PNS is unopposed)

45
Q

Why can neurogenic shock only happen with spinal cord compression above T6?

A

loss of thoracic sympathetic outflow which results in decreased venous tone, causing pooling of the blood volume in the extremities and hypotension.

46
Q

How can you prevent neurogenic shock?

A

Compression stockings

47
Q

How do you manage spinal cord compression/Cauda equina syndrome?

A

Immobilisation (consider compression socks and thromboprophylaxis)
Dexamethasone with a PPI
Whole spine MRI urgently
If MRI confirms then urgent neurosurgical referral or radiotherapy if not indicated
Analgesia

48
Q

Who should get surgery for spinal cord compression/Cauda equina syndrome?

A

Those who can still walk or have residual distal sensory and motor function and a good prognosis
If completely paraplegic for >24 hours then only offer spinal re-alignment for pain relief

49
Q

What makes MSCC and Cauda equina syndrome have a good prognosis?

A

A single lesion
Responsive to steroids
Limited neurological deficits
Radiation sensitive e.g. multiple myeloma and small cell lung cancer
Moderately sensitive e.g. breast and prostate cancers
Early surgery and radiotherapy within 24 hours of developing neurological signs

50
Q

What is superior vena cava syndrome?

A

SVC becomes blocked, commonly due to tumours. They either compress the vessel or invade the vessel itself. This causes reduced venous return from head, neck and upper limbs

51
Q

Which cancers is SVC most associated with?

A

Lung cancers (50% cases by non-small cell cancers but this may just be because they’re more common)
Lymphomas
Metastatic

Note 90% of cases are caused by maliganncy

52
Q

What are non-cancer causes of SVC syndrome?

A

Aortic aneurysms
Blood clots near a pacemaker or intravascular catheter
TB (very rare)

53
Q

What are the signs and symptoms of SVC syndrome?

A

SOB
Facial swelling, particularly worse lying down
Arm swelling
Cough and chest pain

Distended veins in neck and chest
Distended collateral veins
Pembertons test - elevation of arms to side of head causes facial cyanosis

54
Q

Why is SVC syndrome a oncological emergency?

A

Itself is not life-threatening but if left untreated, tumours can go on to invade the trachea and block the airway leading to cardio-respiratory arrest
There is also a risk of cerebral oedema due to excess fluid which potentially could cause ischaemia and increased ICP

55
Q

What are symptoms of cerebral oedema?

A

Headaches
Confusion
Loss of consciousness

56
Q

How is SVC syndrome diagnosed?

A

Clinical signs
Abnormal chest X-ray (in 85% of cases) - most commonly mediastinal widening and pleural effusion
Contrast CT to identify level of obstruction and presence of collateral veins
Sputum cytology, pleural fluid cytology or biopsy of supraclavicular lymph nodes (if not possible then bronchoscope or mediastinoscopy)

57
Q

How do you treat superior vena cava syndrome?

A

Sit patient up and assess for hypoxia. give oxygen if required.
endovascular stenting is often the treatment of choice to provide symptom relief
certain malignancies such as lymphoma, small cell lung cancer may benefit from radical chemotherapy or chemo-radiotherapy rather than stenting
the evidence base supporting the use of glucocorticoids is weak but they are often given

58
Q

Which cancers is spinal cord compression and Cauda equina syndrome most commonly associated with?

A

Lung
Prostate
Breast
Myeloma
Melanoma

59
Q

How soon should you treat spinal cord compression and Cauda equina syndrome?

A

Within 24 hours wherever possible

60
Q

What is neutropenic sepsis?

A

It may be defined as a neutrophil count <0.5 x 10 power 9/L in a patient who is having anti cancer treatment

Temperature over 38 degrees or other signs/symptoms consistent with clinically significant sepsis

61
Q

What is febrile neutropenia?

A

The presence of fever in a person with neutropenia

62
Q

Who should you suspect neutropenic sepsis in?

A

Any patients who are unwell within 6 weeks of recieving chemotherapy

63
Q

What are the main causes of neutropenic sepsis?

A

Indwelling catheters e.g. PICC or hickman lines
Commonly caused by coagulase-negative, Gram-positive bacteria - particularly Staphylococcus epidermidis

64
Q

How do you manage neutropenic sepsis?

A

Sepsis 6 bundle of care within the first hour following recognition of sepsis
This includes empirical broad spectrum antibiotic therapy with piperacillin and tazobactam within 1 hour of arriving at hospital
the addition of antifungal coverage considered in high risk patients who remain febrile 3-7 days after antibiotics given
Chest X-ray

65
Q

How long after chemo is the lowest neutrophil count?

A

5 to 10 days after the last dose of chemotherapy

66
Q

How can we prevent neutropenic sepsis?

A

For adult patients with acute leukaemias, stem cell transplants or solid tumours in whom significant neutropenia is an anticipated consequence of chemotherapy, fluoroquinolone is offered prophylactically

67
Q

What is tumour lysis syndrome

A

An oncological emergency with a severe metabolic disturbance caused by the abrupt release of large quantities of cellular components into the blood following the rapid lysis of malignant cells.

It leads to a high potassium, high urate and high phosphate level in the presence of a low calcium.

68
Q

Who should tumour lysis syndrome be suspected in?

A

any patient presenting with an acute kidney injury in the presence of a high phosphate and high uric acid level

69
Q

How is laboratory tumour lysis syndrome diagnosed? (Cairo-bishop classification)

A

Abnormality in 2 or more of the following, occurring within 3 days before or 7 days after chemotherapy:
- uric acid >8mg/dL
- potassium >6mmol/L
- phosphate >2.1mmol/L
- Calcium <1.75mmol/L
(Or 25% change in these)

70
Q

How is clinical tumour lysis syndrome diagnosed?

A

Laboratory tumour lysis syndrome plus one or more of the following:
- increased serum creatinine (1.5 times upper limit of normal) - i,.e. AKI
- cardiac arrhythmia or sudden death
-seizure

71
Q

Outline the pathology of tumour lysis syndrome?

A

When cancer cells lyse, they release potassium, phosphorus, and nucleic acids, which are metabolized into hypoxanthine, then xanthine, and finally uric acid, an end product in humans
Uric acid precipitates out in the DCT and collecting tubules of kidney and damage the kidneys, causing AKI
Malignant cells often have 4x the phosphorous. It meets with calcium in blood stream and forms calcium phosphate. This can deposit in the kidneys causing AKI and can deposit in the heart. this causes secondary hypocalcaemia which causes prolonged QT interval and has effects on CNS causing seizures
Release of high levels of K+ cause unstable myocardial cells which can cause arrhythmias and cardiac arrest

72
Q

What are the risk factors for tumour lysis syndrome?

A

High proliferation rate of tumour
Those recieving chemo/radiotherapy
Those with haematological cancers
Those with bulky disease
Pre-existing hyperuricaemia
Pre-existing renal disease
Dehydration

73
Q

What symptoms can tumour lysis syndrome cause?

A

Nausea, vomiting diarrhoea, anorexia, lethargy, muscle cramps, syncope, tetany, dark urine or reduced urine output, heart palpitations

74
Q

How is tumour lysis syndrome treated prophylactically?

A

Rasburicase and IV hydration for high risk cases (uric oxidase)
Allopurinol and IV hydration for intermediate risk

Give these immediately prior to and during the first days of chemotherapy

75
Q

How do we manage tumour lysis syndrome?

A

Monitor K+, Calcium and phosphate levels
Treat any electrolyte abnormalities that occur e.g. phosphate binders, calcium replacement,
Haemofiltration if AKI, fluid overload or refractory hyperkalaemia

76
Q

What are the side effects of rasburicase

A

Methaemoglobinaemia
Anaphylaxis
Vomiting and nausea
Headache
Fever
Diarrhoea

77
Q

How does rasburicase work?

A

a recombinant version of urate oxidase, an enzyme that metabolizes uric acid to allantoin. Allantoin is much more water-soluble than uric acid and is, therefore, more easily excreted by the kidneys

78
Q

Who is rasburicase contraindicated in

A

G6PD deficiency - causes haemolysis

79
Q

What is leukostasis?

A

a pathologic diagnosis in which white cell plugs are seen in the microvasculature
It’s associated with a very high WCC, resp failure, intercranial haemorrhage and early death

80
Q

Which cancer is leukostasis mostly associated with?

A

Acute leukaemias

81
Q

What is syndrome of inappropriate ADH secretion?

A

the unsuppressed release of ADH from the pituitary gland or nonpituitary sources or its continued action on vasopressin receptors.
It should be considered whenever a patient with malignancy presents with hyponatraemia

82
Q

Which cancer is most commonly associated to SIADH?

A

70% of cases are associated with small cell carcinoma of the lung

83
Q

What score tool can be used to identify patients at low risk for poor outcome with febrile neutropenia?

A

MASCC risk index

84
Q

What does the MASCC risk index use to calculate risk for poor outcome with febrile neutropenia?

A

Symptom severity
Hypotension sBP<90
Active COPD
Type of cancer
Dehydration requiring IV fluids
Inpatient or outpatient at onset of fever
<60 or >60

85
Q

What are symptoms of brain metastases?

A

Headache that is often worse in the morning or when coughing or bending
Focal neurological signs
Ataxia
Fits\
Nausea vomiting
Papilloedema

86
Q

Whats the first sign of spinal cord compression?

A

Loss of reflexes

87
Q

When does hypercalcaemia typically become symptomatic?

A

> 3mmol/L

88
Q

What could a raised ALP with normal liver function tests mean??

A

Malignancy - particularly bone metastasis

89
Q

whats the most common cause of SVC syndrome in cancer patients

A

Non-small cell lung cancer

METABOLIC (43 decks)

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