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Year 4 - Cancer Care > 1.08 - Complications of Cancer > Flashcards

1.08 - Complications of Cancer Flashcards

1
Q

Most likely cancers to spread to the bones.

A
  • breast
  • prostate
  • lung
  • kidney
  • thyroid
  • myeloma
  • lymphoma
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2
Q

Types of bone metastasis.

A
  • sclerotic
  • osteoblastic
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3
Q

Complications of bone metastasis.

A
  • bone pain
  • hypercalcaemia
  • pathological fractures
  • spinal cord compression
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4
Q

Osteoblastic bone metastasis.

a) pathophysiology

b) primary cancer site example

A

a) cancer cells activate osteoblasts, increasing deposition of new bone; this results in a sclerotic hardening of bones.

b) prostate cancer

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5
Q

Osteolytic bone metastasis.

a) pathophysiology

b) primary cancer site example

A

a) cancer cells cause excessive breakdown of bone, resulting in weak and easily breakable bones.

b) multiple myeloma

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6
Q

Mixed osteoblastic / osteolytic bone metastasis.

a) pathophysiology

b) primary cancer site example

A

a) osteolytic and osteoblastic lesions present or both types are present in the same lesion.

b) breast cancer

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7
Q

Symptoms of bony metastasis.

A
  • bone pain
  • worse at night

Cause of bone pain is due to bone destruction, bone instability and subsequent fractures.

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8
Q

Investigations of bone pain from bony metastasis.

A

Laboratory: FBC, Ca2+, ALP

Imaging: x-ray, bone scan, CT-PET, MRI

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9
Q

Management of local bony metastasis.

A

Radiation therapy is treatment of choice for localised bone pain, where there are limited lesions.

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10
Q

Management of diffuse bony metastasis.

A

Systemic radiation, bisphosphonates and pain medication can be used to treat diffuse bone pain.

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11
Q

Prevalence of brain metastasis.

A

10-30% of cancer patients.

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12
Q

Which cancers most commonly metastasize to the brain?

A
  1. Lung cancer (20%)
  2. Renal cell carcinoma (10%)
  3. Melanoma (7%)
  4. Breast cancer (5%)
  5. Colorectal cancer (2%)
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13
Q

Distribution of brain metastasis.

A
  • cerebral hemispheres (80%)
  • cerebellum (15%)
  • brainstem (5%)

The distribution of brain metastasis to each part of the brain roughly correlates with the relative amount of blood supply it receives.

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14
Q

Symptoms of brain metastasis.

A
  • headache
  • focal weakness
  • altered mental status
  • seizures
  • ataxia
  • stroke
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15
Q

Features of headaches that suggest brain metastasis.

A
  • change in headache pattern
  • nausea and vomiting
  • positional worsening (valsalva)
  • morning headache
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16
Q

Differential diagnoses to brain metastasis.

A
  • primary CNS tumour
  • paraneoplastic phenomena
  • radiation necrosis
  • stroke
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17
Q

Imaging for brain metastasis.

A

Contrast enhance MRI finding:
- multiple lesions
- localisation at junction of grey and white matter
- circumscribed margins

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18
Q

Management of brain metastasis.

A

Dexamethasone 4-8mg/day.

Higher doses can be used in patients with severe symptoms, significant mass effect, or those who do not respond in 48 hours.

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19
Q

Short-term side effects of corticosteroids.

A
  • insomnia
  • increased appetite
  • fluid retention
  • mood symptoms
  • acne
  • exacerbation of diabetes
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20
Q

Long term side effects of corticosteroids.

A
  • weight gain
  • steroid myopathy
  • immunosuppression
  • AVN of the femoral head
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21
Q

Treatment of brain metastases.

A
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22
Q

Patient factors that may impact treatment.

A
  • prognosis of performance status
  • quality of life
  • patient preference
  • extent of disease
  • type of cancer
  • symptoms associated with tumour
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23
Q

Normal physiology of calcium homeostasis.

A
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24
Q

Pathophysiology of hypercalcaemia of malignancy.

A
  • increased PTHrP
  • osteolytic bone mets
  • extrarenal activation of vitamin D
  • ectopic PTH secretion
25
Q

Symptoms of hypercalcaemia.

A

Stones, bones, abdominal moans and psychic overtones.

26
Q

Cardiovascular effects of hypercalcaemia.

A
  • shortened QT interval
  • ventricular arrythmias
27
Q

Investigations for hypercalcaemia.

A
  • serum calcium levels
  • serum albumin levels*
  • PTH
  • PTHrP
  • vitamin D levels

*if abnormal, measured calcium needs to be adjusted

28
Q

Acute management of hypercalcaemia.

A
  • IV normal saline fluid resuscitation
  • IV bisphosphonates
  • IV calcitonin
29
Q

Presentation of metastastic spinal cord compression (MSCC).

A
  • back pain
  • motor symptoms
  • sensory changes
  • bladder and bowel dysfunction
30
Q

Presentation of motor symptoms in MSCC.

A

UMN findings caudal to level of spinal cord compression:
- hyperreflexia
- extensor plantar reflexes

LMN findings at level of compression:
- hyporeflexia

30
Q

Differentials for back pain in cancer patients.

A
  • MSCC
  • musculoskeletal disease (ie. disk degeneration, spinal stenosis)
  • spinal epidural abscess
  • metastatic disease without compression
  • radiation myelopathy
31
Q

Management of MSCC.

A
  • immobilisation
  • glucocorticoids
  • surgery
  • radiation
32
Q

Good prognostic factors for MSCC.

A
  • responsive to radiotherapy
  • stable vertebral column
  • able to ambulate
  • normal bladder function

Acute onset and rapid progression of symptoms is a POOR prognostic factor for MSCC.

33
Q

Impediment of blood flow in the SVC can be caused by:

A
  • thrombosis in SVC
  • invasion
  • extrinsic pressure exerted by nearby anatomical structures
34
Q

Most common cancers associated with SVCO.

A
  • NSCLC
  • SCLC
  • non-hodgkin lymphoma
35
Q

Clinical features of SVCO.

A

The 3 D’s:
- dyspnoea
- distension (oedema of face, arms)
- dilated chest wall veins

36
Q

Management of SVCO.

A
  • high-dose corticosteroid therapy
  • radiotherapy
37
Q

Prognosis of SVCO.

A

Poor prognosis ~6 months.

38
Q

Normal haemostasis physiology.

A
  1. Vessel wall damage
  2. Damaged vessel contracts to reduce the blood pressure and slow bleeding (seconds)
  3. Primary haemostatic plug of activated platelets forms at the site of injury (minutes)
  4. Secondary haemostatic plug of fibrin-stabilised platelets (hours)
39
Q

Platelet activation.

A
  1. Contact with collagen surface (ie. vessel wall damage) activates platelets
  2. Activated platelets release ADP and thromboxane A2 to activate more platelets…
  3. Activated platelets adhere to von Willebrand factor (vWF) and form a primary haemostatic plug
40
Q

Abnormal thrombus formation (Virchow’s triad).

A
  • venous stasis
  • hypercoagulability
  • vessel wall injury
41
Q

Risk factors for VTE.

A
  • smoking
  • malignancy
  • advancing age
  • immobility
  • previous VTE
  • diabetes, HTN
42
Q

Provoked VTE causes.

A
  • chemotherapy
  • recent hospitalisation
  • recent trauma
  • prolonged travel
  • pregnancy / postpartum
43
Q

Types of cancer associated thrombosis (CAT).

A
  • VTE
  • arterial thrombosis
  • DIC
44
Q

Patient risk factors for CAT.

A
  • advancing age
  • female sex
  • black race
  • obesity
  • CVD
  • poor performance status
45
Q

Cancer associated risk factors for CAT.

A
  • type of cancer (ie. lung, pancreatic etc.)
  • cancer stage
  • time since diagnosis*

*immediate period after diagnosis is highest risk

46
Q

Cancer treatment risk factors for CAT.

A
  • chemotherapy
  • surgery and hospitalisation
  • central venous catheters
  • EPO stimulating agents
47
Q

Mechanism of cancer-associated hypercoagulability.

A

Direct mechanism: cancer cells release tissue factor that activates clotting cascade (ie. external pathway).

Indirect mechanism: inflammatory cytokine secretion results in platelet aggregation; NETs released by neutrophils trap platelets.

48
Q

Which cancers are at highest risk of venous thrombosis?

A
  • haematological malignancies
  • lung cancer
  • GI cancer
49
Q

Which cancers are at highest risk of arterial thromboembolism?

A
  • lung cancer
  • gastric cancer
  • pancreatic cancer
50
Q

Investigations for DVT (likely).

A
  1. proximal leg ultrasound scan
  2. (if -ve) D-dimer
51
Q

Investigations for DVT (unlikely).

A
  1. D-dimer
  2. (if +ve) proximal leg ultrasound scan
52
Q

Investigations for PE (likely).

A
  1. CTPA
  2. (if -ve) ?proximal leg ultrasound scan
53
Q

Investigations for PE (unlikely).

A
  1. D-dimer
  2. (if +ve) CTPA

If -ve stop interim therapeutic anticoagulation.

54
Q

Clinical presentation of PE.

A
  • tachycarcia
  • dyspnoea
  • tachypnoea
  • haemoptysis
  • pleuritic chest pain
55
Q

Clinical presentation of DVT.

A
  • unilateral leg pain
  • erythema
  • swelling
  • dilated superficial veins
  • calf tenderness
56
Q

Prevention of VTE in cancer patients.

A

● Haemostasis: prevented by encouraging movement, compression stockings, intermittent pneumatic compression.

● Hypercoagulability: give medications such as LMWH, aspirin, warfarin to patients deemed to be high risk

● Endothelial damage: minimise invasive procedures (ie. PICC line insertion, trained nurses to take blood from PICC line)

Encourage patient to optimise lifestyle factors (ie. smoking cessation, exercise, good control of diabetes) to help reduce the likelihood of VTE.

57
Q

Pharmacological Options for Treatment of VTE in a cancer patient.

A

(1) DOAC for people with active cancer and confirmed proximal DVT or PE.

(2) If DOAC is unsuitable, consider LMWH (shorter-acting so preferred if there is a big risk of bleeding).

Treatment duration is 3 to 6 months.

Measure heparin levels to assess response to treatment.

Year 4 - Cancer Care (13 decks)

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