Cancer Complications And Emergencies Flashcards

1
Q

What are the most likely cancers to spread to the bones ?

A

Breast
Prostate
Lung
Kidney
Thyroid
Myeloma
Lymphoma

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2
Q

Which bones are usually effected in metastases ?

A

Spine
Pelvis
Proximal femurs

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3
Q

What are some complications of bone metastases ?

A

Bone pain
Hypercalcaemia
Pathological fractures
Spinal cord compression

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4
Q

Which cancer is most likely to cause osteoblastic bone metastases ?

A

Prostate

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5
Q

Which cancer is most likely to cause osteolytic bone metastases ?

A

Multiple myeloma

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6
Q

What is the pathophysiology of osteoblastic bone mets ?

A

Cancer cells activate osteoblasts, increasing deposition of new bone and increasing numbers of irregular bone
This results in dense, sclerotic / hardening of bones

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7
Q

What is the pathophysiology of osteosclerotic bone mets ?

A

Cancer cells cause excessive breakdown of bone. This results in weak, easily breakable bones

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8
Q

What cancer can result in mixed osteoblastic and osteosclerotic bone mets ?

A

Breast cancer

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9
Q

What is the clinical presentation of bone metastases ?

A

Bone pain - worse at night ( vary from dull and aching to sharp and intense )

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10
Q

Why do bone mets cause bone pain ?

A

Bone destruction
Bone instability
Subsequent fractures

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11
Q

What are some important tests to perform when suspecting bone mets ?

A

FBC
Serum calcium
Sreum alkaline phosphatase
Bone scan
CT
MRI
PET/ CT

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12
Q

What is the management of bone mets ?

A

Localised therapy - radiation
Systemic - bisphosphonates and systemic radiation

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13
Q

How do bisphosphonates manage bone pain from bone mets ?

A

It binds to hydroxyapatite on bone surfaces undergoing rapid resorption.
Internalisation of the bisphosphonate into osteoclasts which disrupts bone resorption.
Promotes osteoclast apoptosis

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14
Q

Which cancers are most likely to cause brain mets ?

A

Lung
Renal cell carcinoma
Melanoma
Breast
Colorectal

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15
Q

How do brain mets occur ?

A

Cancer cells must get into the circulation, survive in the circulation and arrest in a capillary bed. Once in the capillary bed of the brain they must extravasate into the brain parenchyma and grow.

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16
Q

What are symptoms from brain mets most likely due to ?

A

The tumour mass and oedema

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17
Q

What are the most common symptoms from brain mets ?

A

Headache
Focal weakness
Altered mental state
Seizures
Ataxia
Stroke
Nausea and vomiting

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18
Q

What can a frontal lobe tumour cause ?

A

Anosmia

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19
Q

What can a temporal or occipital lobe tumour cause ?

A

Visual field deficits - homonymous hemianopia

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20
Q

What can brainstem and cerebellar tumours cause ?

A

Ataxia and incoordination
Nystagmus
Upper motor neurone signs

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21
Q

What imaging is used when suspecting brain mets ?

A

Contrast enhanced MRI

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22
Q

What is the management of brain mets ?

A

Dexamethasone
VTE prophylaxis
Radiotherapy ( whole brain or focal )
Surgery

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23
Q

What are some factors that effect the management of brain mets ?

A

Prognosis and performance status
Quality of life
Patient preference
Extent of disease
Type of cancer
Symptoms associated with cancer

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24
Q

What is febrile neutropenia ?

A

A serious complication of chemotherapy characterised by a reduction of neutrophils below normal cell counts. Due to the blunted immune system there is an impaired ability to fight infections.

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25
Q

What is the management of febrile neutropenia ?

A

Considered a medical emergency
Empirical abx immediately- piperacillin-tazobactam

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26
Q

What happens when low levels of calcium are detected ?

A

Low serum calcium stimulate the parathyroid gland to release parathyroid hormone which increases calcium levels in 3 ways : renal tubular, vitamin D activation and mobilisation from bone.
Vitamin D increases calcium absorption from the GI tract and decreases renal excretion.

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27
Q

How does calcitonin work ?

A

Calcitonin is a hormone released by parafollicular cells in the thyroid gland that is involved in decreasing serum calcium levels by preventing renal absorption and calcium mobilisation from bone.

28
Q

What is the pathophysiology of Hypercalcaemia of malignancy ?

A

Humoral Hypercalcaemia mediated by increased parathyroid hormone related peptide
Local osteolytic Hypercalcaemia due to breakdown of bone
Excess ectopic or primary PTH secretion

29
Q

What are some signs and symptoms of Hypercalcaemia ?

A

Stones - renal (AKI, nephrolithiasis )

Bones (pain and fractures )

Moans - pyschiatric ( confusion, altered mental state, mood changes )

Groans - abdo ( constipation, pain, nausea and vomiting )

30
Q

What are some investigations when suspecting Hypercalcaemia ?

A

Serum calcium
Serum albumin
PTH
PTHrP
Vitamin D levels

31
Q

What is the management of Hypercalcaemia ?

A

IV fluids to correct dehydration
Exogenous calcitonin ( fast action )
Bisphosphonates - zolendronic acid ( longer term )
Systemic treatment of malignancy

32
Q

What are some causes of spinal cord compression due to malignancy ?

A

Primary spinal tumours
Any metastatic tumours

33
Q

What are the most common signs and symptoms of spinal cord compression ?

A

Back pain - radiating
Reduced power, difficulty walking
Hyperreflexia - UMN lesion
Bladder and bowel dysfunction

34
Q

What are some differentials for back pain in cancer patients ?

A

MSK disease - muscle spasm, spinal stenosis
Spinal epidural abscess
Metastatic disease
Radiation myelopathy

35
Q

What imaging is used when back pain is present in cancer patients ?

A

MRI
CT

36
Q

What is the management of spinal cord compression in cancer patients ?

A

Dexamethasone 16mg + PPI
Analgesia
Surgery
Radiation therapy

37
Q

What is superior vena cava syndrome ?

A

The impediment of blood flow through the SVC caused by thrombosis, invasion or compression by pathology involving nearby anatomical structures.
It is a medical emergency

38
Q

Wht are the causes of impediment of blood flow in the superior vena cava ?

A

Thrombosis in the SVC
Invasion
Extrinsic pressure exerted by pathology involving nearby anatomical structures

39
Q

When do clinical features of SVC syndrome present ?

A

The degree of obstruction is no longer adequately compensated for by the formation of venous collaterals

40
Q

What are some benign causes of SVC obstruction ?

A

Thrombosis
Aortic aneurysm
Retrosternal thyroid

41
Q

What are some malignant causes of superior vena cava obstruction ?

A

Non-small cell lung cancer
Small cell lung cancer
Non-Hodgkin’s lymphoma

42
Q

What are the major features of SVC obstruction ?

A

Dyspnoea
Distension ( oedema of face with erythema )
Dilated chest wall veins

43
Q

What is the management for SVC obstruction ?

A

Dexamethasone 16mg + PPI
Stent
Radiotherapy
Chemotherapy ( SCLC, lymphoma and teratoma \
Anti coagulation if thrombus

44
Q

How does malignancy increase the risk of developing VTE ?

A

Venous stasis secondary to prolonged periods of immobility
Tumours can compress the vasculature impairing venous return
Hypercoagulability is increased by cancer cells

45
Q

What is virchow’s triad ?

A

Venous stasis
Endothelial dysfunction
Hypercoagulable state

46
Q

What are some patient related risk factors for a VTE ?

A

History of previous VTE
Thrombophilia
Obesity
Age over 50
Comorbidity

47
Q

What are some treatment related risk factors for a VTE ?

A

Surgery
Having chemotherapy
Having hormonal therapy
EPO stimulating agents
Hospitalisation

48
Q

What investigation should be performed when you are suspecting a DVT ?

A

Doppler USS

49
Q

What should be performed when suspecting a PE ?

A

D dimer
CTPA
VQ scan

50
Q

What is the management of VTE ?

A

Prophylaxis - aspirin, Dalteparin

Mainstay treatment - low molecular weight heparin

51
Q

What are oncological emergencies ?

A

Group of conditions that occur as a direct or indirect result of cancer or its treatment that are potentially life threatening

52
Q

What are some signs and symptoms of neutropenic sepsis ?

A

Fever
Tachycardia
HYPOTENSION
Raised RR
Drowsy
Confusion

53
Q

What increases the risk of infection in cancer patients ?

A

Prolonged neutropenia
Severe neutropenia
Significant co-morbidities
Aggressive cancer
Central lines
Mucosal disruption
Hospitalisation

54
Q

If suspecting neutropenic sepsis what investigations should be performed ?

A

FBC
U&E’s
LFTs
Lactate / ABG
CRP
Cultures / swabs - blood, urine, sputum, wound
CXR

55
Q

What is the management of neutropenic sepsis ?

A

Don’t wait for FBC
Empirical IV broad spectrum abx within an hour
Fluid resus
O2
Consider catheter
Consider G-CSF

56
Q

What is the smog common site for a spinal cord compression due to mets ?

A

Thoracic

57
Q

If there are signs of spinal cord compression due to malignancy what should be ordered and how quickly ?

A

MRI of the spine within 24 hours

58
Q

Why is surgery used in the management of spinal cord compression due to malignancy ?

A

Relieves compression
Removes tumour
Stabilises spine
Preserves greater degree of mobility

59
Q

Why is radiotherapy given in spinal cord compression due to malignancy ?

A

Relieves compression of the spine and nerve roots by causing cell death in rapidly dividing tissue
Relieves pain
Stabilises neurological deficit

60
Q

What is the normal range of corrected calcium ?

A

2.2-2.51 mmol/L

61
Q

What cancers is Hypercalcaemia common in ?

A

Breast
SCC
Renal
Myeloma
Lymphoma

62
Q

How quickly do bisphosphonates take to work ?

A

Up to 4 days

63
Q

What is tumour lysis syndrome ?

A

A metabolism emergency that presents as severe electrolyte abnormalities.
Massive tumour cell lysis —- release of large amounts of K+, phosphate and uric acid into circulation

64
Q

What electrolyte imbalances can occur from tumour lysis syndrome ?

A

Hyperuricaemia
Hyperkalaemia
Hyperphosphataemia
Hypocalcaemia

65
Q

What is the most common cancers to cause tumour lysis syndrome ?

A

Haematological cancers - lymphomas and leukaemia
Myeloma

66
Q

How does tumour lysis syndrome present ?

A

3-7 days after chemo
N + V
Diarrhoea
Anorexia
Lethargy
Haematuria
Fluid overload
Cardiac arrhythmias
Muscle cramps, tetany and seizures

67
Q

How can tumour lysis syndrome be prevented ?

A

Focus on hydration
Allopurinol
Rasburicase
Dialysis