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B33CAN - Professionalism & Leadership; Clinical & Pharmacy Practice > Complications of Cancer and Chemotherapy > Flashcards

Complications of Cancer and Chemotherapy Flashcards

1
Q

What is SVCO, and how can it come about due to cancer?

A
  • Superior Vena Cava Obstruction (SVCO)
  • Narrowing or occlusion (blockage) of the SVC
  • Obstructs venous return to the right side of the heart

Reasons:
> External compression; tumour (in close proximity)
> Thrombus; more likely in cancer (inflammatory cascade activation, predisposed to clots)

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2
Q

Which cancers are often responsible for SVCO?

A
  • Carcinoma of the bronchus (80% of cases; SCLC > NSCLC)
  • Lymphoma, germ cell tumours, mesothelioma (asbestos-induced) and thymoma (chest & thymus gland) may also be responsible
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3
Q

What are the signs and symptoms for SVCO?

A

SVCO blocks drainage of upper body (H&N):

  • Oedema: face, neck, arms
  • Fixed engorged jugular veins (increased JVP); veins stand out on neck
  • Dilation of superficial skin veins; head, neck, chest
  • SOB or stridor (noisy breathing)
  • Cyanosis (venous congestion; looks blue)
  • Cough, hoarse voice
  • Headache, confusion (intracranial venous congestion = increased intracranial pressure)
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4
Q

What investigations are undertaken as a result of SVCO?

A
  • Chest X-ray (looking for mediastinal mass)
  • CT scan/MRI of chest; defining extent of disease, assisting RT planning.
  • Venography; dye injected to see how occluded SVC is
  • Biopsy; establish diagnosis if initial presentation, assists treatment decisions
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5
Q

What is the acute treatment for SVCO?

A

Corticosteroids

  • High dose dexamethasone (8mg BD)
  • Reduces swelling and pressure around vessel, as well as oedema
Vascular stenting (within 2-3 days)
- Particularly if urgent symptom relief required
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6
Q

What is the definitive treatment for SVCO?

A
  • Radiotherapy (2-3 weeks before effect seen)
  • Chemotherapy (if chemo-sensitive tumour; biopsy)
  • LMWH; treatment for thrombus if indicated (1.5 mg/kg OD)
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7
Q

What is the Pharmacist’s role in SVCO treatment? (Corticosteroids? LMWH?)

A

Corticosteroids:

  • Given promptly
  • Timing of dose (steroids compromise sleep so no systemic dosing; morning and 2PM instead)
  • PPI cover if appropriate for duration of steroids ONLY
  • Dose review/reduction
  • Blood glucose monitoring

LMWH:

  • Dose recommendation
  • Conversion to warfarin if appropriate; but a lot of patients stay on enoxaparin instead (INR difficult to keep in range w/warfarin w/chemotherapy patients; inflammatory cascade etc.)
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8
Q

WHat is SCC, and what is the source?

A
  • Spinal cord compression
  • Mainly occurs where bone metastases are common; prostate, breast cancer etc.
  • Results from pressure on spinal cord:
    > Tumour/bone metastases growing directly between vertebral bodies
    > Crush fracture/collapse from vertebral metastasis
    > Intramedullary metastases causing acute compression from within (rare)
  • Can be first presentation of cancer
  • Most common in thorax (high up)
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9
Q

What are the signs and symptoms of SCC?

A
  • Onset can be gradual or acute; e.g. not managing stairs well, difficulty passing urine, numb areas leg/feet
  • Depend on site of compression; low down = bladder/leg, thorax = coughing, deep breaths
  • Pain at level of compression and movement
  • Motor weakness; can’t walk as far, stairs hard, numb
  • Sensory loss (numb)
  • Bladder/bowel dysfunction
  • Cauda equina; pressure on bottom of spinal cord = sacral anaesthesia, urinary retention, erectile dysfunction
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10
Q

What investigations are undertaken for suspected SSC?

A

Urgent whole spine MRI scan:

  • Detects level of compression
  • Definitive; know exact cause
  • Allows planning of RT/surgery

Plain X-ray:
- May show evidence of bone metastases, mass or crush fracture at site

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11
Q

How is SCC treated acutely?

A

Corticosteroids (within 24 hours):

- Dexamethasone 8mg BD (similar to SVCO)

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12
Q

What is the definitive treatment for SCC?

A

Radiotherapy; symptomatic; as dead nerves in spinal cord do not regenerate.
- Days-weeks for effect; titrate steroids down upon improvement

Bedrest (flat)

  • Until possibility of spinal instability discontinued
  • Eat, drink etc. all FLAT; “long-rolling” of patient like spinal may be required.

Symptom management:

  • Catheterisation
  • Analgesia
  • Bowel mangement
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13
Q

When is surgery an option for SCC?

A
  • If spine unstable (tumour eaten away vertebrae); risk of severing cord, put wires/rods in to protect nerves
  • If insensitive to RT (e.g. melanomas)
  • Unknown tissue diagnosis; biopsy
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14
Q

What are the prognostic signs for SCC?

A
  • Linked to onset and duration of symptoms
  • Prompt diagnosis and treatment vital
    > Ability to walk at diagnosis indicative to overall survival
    > Loss of sphincter function at diagnosis; indicative of delayed presentation, bad prognostic sign.
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15
Q

What is the pharmacist’s role w/SCC treatment?

A

Corticosteroids:

  • Given promptly
  • Timing of dose (steroids compromise sleep so no systemic dosing; morning and 2PM instead)
  • PPI cover if appropriate for duration of steroids ONLY
  • Dose review/reduction
  • Blood glucose monitoring

DVT/PE (pulmonary embolism) prophylaxis:
- Pressure stockings, enoxaparin 40mg OD

Analgesia

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16
Q

What is TLS, and how can it manifest?

A

Tumour lysis syndrome

  • Group of metabolic disturbances
  • May occur before or after start of chemo; large tumour burden, high proliferative rate and high chemosensitivity
  • Rapid destruction of malignant cells = release of intracellular contents = acute metabolic disturbance
Manifests as:
> Hyperuricemia 
> Hyperphosphataemia
> Hyperkaleamia
> Hypocalcaemia
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17
Q

How does TLS present (signs/symptoms)?

A

Biochemical disturbances can cause:

  • Nausea
  • Diarrhoea
  • Muscle weakness (hypocalcaemia)
  • Tetany; intermittent muscle spasms (hypocalcaemia)
  • Seizures (electrolyte imbalances)
  • Arrhythmias (hyperkalemia)
  • Renal failure
  • Sudden death
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18
Q

What is the pathophysiology of TLS?

A

48-72 hours following chemotherapy (can be spontaneous):

Uric acid; from breakdown of purines
- Up to 10g/day (kidney normally excretes 500mg/day) due to rapid breakdown of malignant cells; formation of uric acid crystals, obstruction of renal tubules = AKI/hyperuricemia
> AKI = oliguria/anuria (little to no urine)
> Fluid overload = pulmonary oedema

Phosphate

  • Large amount in malignant cells
  • Renal excretion overloaded (impaired if urate nephrology has caused AKI already) = hyperphosphataemia

Calcium

  • Hyperphosphataemia results in hypocalcaemia (forms calcium phosphate crystals)
  • Renal excretion overloaded

Potassium
- Lysed cells release large amounts of potassium = hyperkalemia
- Renal excretion overloaded
> Can lead to heart failure

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19
Q

What is the prognosis for TLS?

A
  • Prevention/early intervention important
  • Prompt treatment usually successful w/metabolic disturbances
  • Resolves within 5-7 days of chemotherapy
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20
Q

What is the prophylactic treatment for high-risk TLS?

A
  • IV fluids; 3L/m^2/day
  • Maintain urine output > 100ml/hour
  • Rasburicase
  • TLS screen; checking U&Es
  • Consider delaying chemotherapy for 24-48 hours
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21
Q

What is the prophylactic treatment for moderate risk TLS?

A
  • IV fluids
  • Maintain urine output > 100ml/hour
  • Allopurinol (NOT Rasburicase)
  • TLS screen
22
Q

What is the prophylactic treatment for low risk TLS?

A
  • Allopurinol (on its own)
23
Q

What cancers are high, moderate or low risk for TLS?

A

High:

  • Burkitt lymphoma, Burkitt lymphoma type ALL
  • ALL (Acute lymphoblastic leukemia), AML (Acute myeloid leukemia)
  • WCC > 100 x 10^9/L

Moderate:

  • AML w/WCC > 50 x 10^9/L
  • Other ALL
  • High grade NHL (Non-Hodgkin’s lymphoma) w/bulky disease

Low:

  • Other AML
  • Myeloma
  • CLL (Chronic lymphocytic leukemia)
  • Hodgkin Lymphoma
  • MDS (Myelodysplastic Syndromes)
24
Q

What is the treatment strategy for established TLS?

A
  • Vigorous hydration to maintain urine output > 100ml/hour
  • Correct hyperkalemia
  • Rasburicase
  • Seek ICU/renal specialist help; patients may need haemofiltration/haemodialysis (remove electrolytes)
  • Only symptomatic hypocalcaemia should be treated
25
Q

Why is hypocalcaemia only treated in TLS if symptomatic?

A
  • Supplementing calcium could result in calcium phosphate crystal formation (hyperphosphataemia already)
  • Insoluble crystals in renal tubules/urine
  • More renal damage
26
Q

What is rasburicase’s mechanism of action?

A
  • Recombinant form of urate oxidase (not found in humans)
  • Catalyses the oxidation of uric acid to allantoin
  • Allantoin 5 times more soluble; readily excreted
27
Q

What is the mechanism of action of allopurinol, and why is it not used in conjunction w/rasburicase?

A
  • Blocks conversion of xanthines to uric acid (inhibits xanthine oxidase)
  • Reducing effect of rasburicase as a result; conversion of Xanthine to Uric Acid desired so that Rasburicase can convert UA to Allantoin to be readily excreted
  • Allantoin more soluble than Xanthine
28
Q

How is rasburicase given for TLS, and when is it given?

A
  • Give in 50ml 0.9% NaCl over 30 mins (max dose 20 mg)

- First dose PRIOR to starting chemotherapy

29
Q

What is the pharmacist’s role in TLS treatment?

A
  • Identification of high risk patients
  • Ensure allopurinol is stopped in patients due to receive rasburicase
  • But also ensure allopurinol is commenced in medium/low risk patients
  • Dosing of rasburicase
  • Ensure TLS screen completed
  • Advice re-electrolyte replacement (e.g. treating hyperkalaemia)
  • Restarting allopurinol when rasburicase stopped (the next day)
30
Q

What is CINV, and why is it an important issue?

A
  • Chemotherapy induced N&V

- CINV is one of the most distressing symptoms; significant impact on QoL

31
Q

What are the risk factors of CINV?

A
  • < 50 years old
  • Female
  • Vomiting during previou chemotherapy
  • Pregnancy induced N&V (morning sickness etc.)
  • History of morning sickness
  • LOW ALCOHOL INTAKE (high intake = less susceptible)
32
Q

What are other causes of N&V as opposed to CINV?

A
  • Radiotherapy (particularly abdomen/brain)
  • Brain metastases (increased intracranial pressure)
  • Migraine
  • UTIs
  • Bowel obstruction
  • Hypercalcaemia
  • Other medications e.g. opioids, antibiotics (erythromycins, macrolides)
33
Q

What are the types of N&V associated w/chemotherapy?

A
  • Acute vomiting (first 24hrs)
  • Delayed N&V (24hrs - 5 days; hard to treat)
  • Breakthrough N&V; where normally well controlled but certain things trigger it e.g. warm food, car journey
  • Refractory vomiting (when antiemetic ineffective)
  • Anticipatory N&V; the thought of chemotherapy, especially if bad experience before
34
Q

What are the potential consequences of CINV?

A
  • Delayed therapy, omitted doses (PO)
  • Dose reductions (want MTD though)
  • Dehydration
  • Physical damage; oesophageal tears w/violent vomiting
  • Electrolyte imbalance
  • Increased hospitalization
  • Increased institutional costs
  • Patient stops treatment completely
35
Q

What is the treatment of CINV dependent on?

A

The emetogenicity of the chemotherapy and the type of CINV experienced.

36
Q

For minimal emetogenicity of chemo regimen, what treatment is given for CINV?

A

Post chemotherapy:

- Metoclopramide (10mg QDS, PRN orally)

37
Q

For low emetogenicity of chemo regimen, what treatment is given for CINV?

A

Pre chemo:
- Metoclopramide 20mg PO (acts on 5-HT3 at higher doses as antagonist as well as DA)

Post chemo:
- Metoclopramide (10mg QDS, PRN orally; as minimal emetogenicity)

38
Q

For moderate emetogenicity of chemo regimen, what treatment is given for CINV?

A

Pre chemo:

  • Ondansetron 8mg IV/O
  • Dexamethasone 8mg IV/O

Post chemo:

  • Metoclopramide (10mg QDS for 2 days, then QDS PRN)
  • Dexamethasone (2mg BD for 2 days)
39
Q

For high emetogenicity of chemo regimen, what treatment is given for CINV?

A

Pre chemo:

  • Ondansetron 8mg IV/O
  • Dexamethasone 8mg IV/O (as moderate)

Post chemo:

  • Metoclopramide (10mg QDS for FOUR (4; instead of 2 in moderate) days, then QDS PRN)
  • Dexamethasone (4mg BD for 2 days, then 2mg BD 2 days; taper dose, unlike moderate)
40
Q

Why is Dexamethasone given for CINV?

A
  • Mode of action not known; thought to act on PGs in the brain
  • Has anti-emetic properties for acute and delayed N&V
41
Q

Which anti-emetics are more effective for acute and delayed N&V respectively?

A

Acute: metoclopramide
Delayed: ondansetron

42
Q

What is Aprepitant, and when is it used?

A
  • Neurokinin 1 (NK1) receptor antagonist
  • Mediates action of Substance P (emetogenic)
  • For use w/platinum based compounds and moderately emetogenic regimens
    »> Add-on therapy
  • Interaction w/dexamethasone (enhances effects, but no dose reduction in practice)
  • Dose; 125mg one hour prior to chemotherapy
  • 80mg OD on days 2 and 3 (for one day course of chemotherapy)
43
Q

What does Anticipatory N&V entail, and what is the treatment?

A
  • N&V that can occur prior to a new cycle of chemo
  • Usually a result of poor controlled acute and delayed N&V in previous cycles, or in chemotherapy naive patients
    »> Sublingual lorazepam 0.5-1mg prior to treatment can help; SL instead of PO as N&V
    > Hypnosis, CBT can be helpful
44
Q

What is the pharmacist’s role in CINV?

A
  • Identification of high risk patients
  • Ensuring the appropriate antiemetic regimen regimen has been prescribed
  • Counselling patient; Metoclopramide 30 mins - 1 hour before meals
  • W/aprepitant; prescribed for next cycle of chemotherapy (patient can take loading dose at home; less waiting around)
  • Ensuring antiemetics are stepped up if patient is admitted w/N&V
45
Q

What is neutropenic sepsis, and how is it defined?

A
  • Whole body reaction triggered by infection (low neutrophil count)
  • Patient has recently received cytotoxic chemotherapy AND has had a temperature of 38.5 Degrees on a single occasion, or 38.0 Degrees on two occasions
  • Neutropenia; neutrophil count < 1 x 10^9/L
  • Treat before FBC results back; can always stop antibiotics if needed (prevent death)
46
Q

What investigations are undertaken for suspected Neutropenic sepsis?

A
  • FBC (full blood count)
  • Blood cultures
  • CRP; C-reactive protein, marker for inflammation produced by liver following IL-6 secretion by macrophages/T-cells
  • U&Es
  • Lactate; how sick is the patient?
47
Q

What is the treatment for neutropenic sepsis?

A

Treat the cause of infection:

  • Piperacillin/tazobactam (4.5g TDS)
  • Add in vancomycin/teicoplanin if patient is known/previously MRSA +ve (or if patient has in-dwelling line, Hickman/Brotac etc anything under skin)
  • Gentamicin single dose (5mg/kg)
48
Q

What is the treatment for neutropenic sepsis in moderate penicillin allergy?

A
  • Meropenem (switch to)

- Add in vancomycin/teicoplanin if patient is known/previously MRSA +ve etc. as before

49
Q

What is the treatment for neutropenic sepsis in severe penicillin allergy?

A
  • Ciprofloxacin oral/IV (similar bioavailability); but cross-reactivity w/carbapenems + penicillins
  • Add in vancomycin/teicoplanin if patient is known/previously MRSA +ve etc. as before
  • Gentamicin single dose
50
Q

What is the pharmacist’s role in neutropenic sepsis treatment?

A
  • Establish nature of any penicillin allergy (what patient classes as an ‘allergy’ may just be mild reaction), advise accordingly
  • Ensure door to needle time is < 1 hour (after patient turns up on ward/day care, antibiotics to be given within 1 hour; increased survival)
  • Check antibiotic therapy is reviewed regularly; change if necessary, switch to PO where possible.
  • Monitor U&Es, FBC, CRP, lactate and vancomycin levels

B33CAN - Professionalism & Leadership; Clinical & Pharmacy Practice (8 decks)

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