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Flashcards in Oncological emergencies Deck (34)
1

What are the 3 most common malignancies associated with hypercalcaemia?

Breast, lung and multiple myeloma

2

What are some different mechanisms by which cancers cause hypercalcaemia?

Osteolytic bone metastasis
PTHrP release
Ectopic (extra-renal) activation of Vitamin D
Ectopic PTH production (rare)

3

How do osteolytic bone metastases cause hypercalcaemia?

Small amount due to the immediate destructive effect on bone but most due to the release of local mediators of osteolysis. Breast cancer secretes PTHrP and other cytokines which increases RANK-ligand which binds to RANK and stimulates osteolytic activity

4

What is the most common mechanism of hypercalcaemia or malignancy?

PTHrP release - most common cause of hypercalcaemia in solid non metastatic tumours

5

What cancers cause PTHrP release?

Squamous (head/neck/lung)
Renal
Bladder
Breast
Ovarian
Occasionally NHL

6

What effect of PTH does PTHrP not mimic?

Does not stimulate activation of vitamin D, therefore does not increase calcium absorption at the gut

7

What are the main cancers to cause hypercalcaemia by ectopic activation of Vit D?

Hodgkins lymphoma
1/3 of NHL
Extra-renal activation by malignant lymphocytes and macrophages

8

Clinical features of hypercalcaemia?

Weakness, vomitting, constipation, confusion, seizures, arrythmias, polyuria, polydipsia, renal impairment, anorexia, pancreatitis, PUD, bone pain, shortened QT, bradycardia, hypertension

9

Treatment options for hypercalcaemia?

Initally IVF hydration
Bisphosphonates (Zoledronic acid has been shown to be better then pamidronate at effect and duration of effect)
Denosumab - in bisphosphonate refractory hypercalcaemia
Renal replacement therapy
Steroids can be used if ectopic activation of Vit D

10

Pathogenesis of tumour lysis syndrome?

Massive cell breakdown of tumour cells leads to release of large amounts of phosphate, pottassium and nucleic acids. Nucleic acids get catabolised to uric acid which causes crystalisation and vasconstriction of renal blood flow leading to renal impairment

11

Lab findings in TLS?

High potassium, high phosphate, high uric acid, low calcium (due to being taken up and made into calcium phosphate crystals in the kidneys)

12

Risk factors for TLS?

High tumour cell proliferation rate
Chemosensitive malignancy
Bulky disease - greater then 10cm, WCC greater then 50,000, LDH greater then 2x ULN
Pre-treatment hyperuricaemia
Pre-existing renal impairment or exposure to nephrotoxins
Dehydration
Oliguria/acidic urine (crystals precipitate in acidic environments)

13

Common causes of TLS?

Burkitts lymphoma
ALL
Small cell lung cancer
Breast cancer
Germ cell cancer

14

Prevention of TLS?

In high risk disease - rasburicase prophylaxis (one dose) and aggressive hydration
In medium risk disease - Allopurinol and IVF
Low risk - watch and wait

15

How does allopurinol prevent tumour lysis?

Xanthene oxidase inhibitor prevents formation of uric acid from hypoxanthene and xanthene

16

What are some problems with allopurinol in TLS?

Does not get rid of pre-formed uric acid, only stops further being formed.
Hypoxanthene and xanthene can accumulate and cause xanthene crystals in renal tubules

17

What is rasburicase?

Re-combinant urate oxidase (enzyme not usually found in humans) which metabolises uric acid to allantoin (a less nephrotoxic, more water soluble substance)

18

Who should rasburicase not be given to?

Patients with G6PD

19

Treatment of establised TLS?

Regular bloods 4-6 hourly
IVF
Cardiac monitoring
Repeated dosing of rasburicase
Renal replacement therapy if indicated - high K, low ca, anuria

20

What are some causes of SVCO?

Malignancy - most common 90%
Infection - histoplasma (fibrosing mediastinitis)
Device associated thrombus (becoming more common)

21

What are cancers that commonly cause SVCO?

Non small cell lung cancer (50%)
Small cell lung cancer (25%)
NHL (10%)
rare: thymoma, germ cell, mesothelioma
*10% of patients with SCLC get SVCO compared with only 2% of NSCLC

22

Pathogenesis of SVCO

invasion or external compression of SVC leads to development of collaterals over several weeks
Due to mass in right lung, mediastinum or lymph nodes

23

Symptoms of SVCO?

Swollen head
SOB, wheeze, stridor
Distended neck veins
Cough
Headache, reduced level of consiousness

24

Treatment of SVCO

Previously thought to be an emergency but now getting a histological diagnosis is most important to direct treatment (unless upper airway compromise or coma due to raised ICP = urgent stent placement and RT needed)
Nurse with head of bed elevated
Anticoagulate if clot present
Chemotherapy if chemosensitive
Endovascular stent insertion gives immediate relief followed by radiotherapy

25

Pathogenesis of spinal cord compression?

Cauda equina starts at L1
Tumour usually originates at bony metastasis in vertebral body then extends around thecal sac taking the path of least resistance

26

What is the most common site of spinal cord compression?

Thoracic spine (60%)
Lumbosacral (30%)
Cervical (10%)

27

Clinical features of spinal cord compression?

Pain - predominant symptom
Weakness - typically pyramidal (upper limb extensor weakness and lower limb flexor weakness)
Hyper-reflexic (depending on level of compression, in cauda equina hypotonic reflexes)
Ascending numbness and parasthesia
Bowel and bladder disturbance - late sign
Gait disturbance

28

Best imaging study for spinal cord compression?

Gadolinium enhanced MRI scan

29

Treatment of spinal cord compression?

Analgesia
Steroids - for analgesia and reduce vasoactive odema
Surgical decompression and stabilisation is recommended first line for unstable fractures or radio-resistant tumours
External beam RT for those who are not surgery canidates

30

What are some poor prognostic factors for spinal cord compression?

Short time to development of motor deficits
Level of impairment of motor function pre-treatment (ie walking vs paralysis)
Short interval from cancer diagnosis to spinal cord compression

31

What are some common causes of brain mets causing raised ICP?

Lung
Melanoma
Breast
Renal cell
Colorectal

32

Where do metastases usually form in the brain?

The junction of white and grey matter where vessels get smaller and tumour emboli lodge
Most occur in cerebral hemispheres

33

Treatment of elevated ICP due to brain mets?

Steroids
Drainage if hydrocephalus
Resection of a single metastasis
Radiotherapy

34

Symptoms of raised ICP?

Focal neurology
Headache
Vomitting and nausea
Cognitive dysfunction
Seizures