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Cancer > Vicki Portingale - Clinical > Flashcards

Vicki Portingale - Clinical Flashcards

1
Q

What is lpilimumab? (include mode of action) What is it used for?

A

It’s a recombinant human monoclonal antibody used in the treatment of Malignant Melanoma.
It acts by blocking CTLA-4 with its ligands (CD80 & CD86) which potentiates a T-cell immune response. The T-cells carry out anti-tumour activity.

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2
Q

What are the side effects of Ipilimumab?

A

Due to excessive immune activity:

  • Skin reactions incl. rash and pruritis
  • Fatigue
  • GI reactions incl. Diarrhoea, Abdominal Pain, and Reduced Appetite
  • N & V
  • Immune-mediated reactions - hepatitis and colitis
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3
Q

Where does Ipilimumab fall in the treatment pathway for Malignant Melanoma?

A

2nd line for NON-BRAF V600 mutations

2nd line option in those with a BRAF V600 mutation (in dual therapy with nivolumab)

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4
Q

What is the mechanism of action for Nivolumab?

A

Blocks the interaction of PD-1 (located on T-cells) with its ligands PDL1 and PDL2. This released the PD-1 pathway that is normally inhibited i.e. unmediated immune response.

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5
Q

What are the side effects of Nivolumab?

A
  • Skin (rash and pruritus)
  • Fatigue
  • GI (diarrhoea, constipation, reduced appetite)
  • Arthralgia
  • Cough
  • Immune-mediated reactions - hepatitis, colitis, pneumonitis
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6
Q

Where does Nivolumab fall in the pathway for Malignant Melanoma?

A 
1st line drug if there is NO BRAF V600 mutation (monotherapy)
2nd line (dual therapy with ipilimumab) if there is a BRAF V600 mutation - only use in patients that are healthy and monitor for immune-mediated reactions)
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7
Q

What is the mechanism of action of Pembrolizumab?

A

Blocks the interaction of PD-1 (located on T-cells) with its ligands PDL1 and PDL2. This released the PD-1 pathway that is normally inhibited i.e. unmediated immune response.

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8
Q

What are the side effects of Pembrolizumab?

A
  • Skin (rash and pruritus)
  • Fatigue
  • GI (diarrhoea, constipation, reduced appetite)
  • Arthralgia
  • Cough
  • Immune-mediated reactions - hepatitis, colitis, pneumonitis
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9
Q

Where does Pembrolizumab fall in the treatment pathway for malignant melonoma?

A

1st line option (as monotherapy) if there are no BRAF V600 mutations
Can be used following ipilimumab treatment or a BRAF inhibitor (Vemurafenib/Dabrafenib/Trametinib)

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10
Q

What is Vemurafenib’s mechanism of action?

A

Oral tyrosine kinase inhibitor which inhibits a mutated BRAF gene (specifically a change from Valine to Glutamate at AA position 600). Mutated BRAF leads to constitutive activation –> constant cell proliferation and growth.

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11
Q

What are the side effects of Vemurafenib?

A
  • Skin (pruritis, sensitivity to sun, rash, cutaneous squamous cell carcinomas, blistering)
  • Fatigue
  • Arthralgia (flu-like) - may require painkillers or heat/ice packs
  • Nausea
  • Headache
  • Alopecia
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12
Q

Where does Vemurafenib lie in the treatment pathway for malignant melanoma?

A

1st line option for patients with a BRAF V600 mutation

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13
Q

What is the mechanism of action for Dabrafenib?

A

Oral tyrosine kinase inhibitor which inhibits a mutated BRAF gene (specifically a change from Valine to Glutamate at AA position 600). Mutated BRAF leads to constitutive activation –> constant cell proliferation and growth.

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14
Q

Where does the Dabrafenib lie in the treatment pathway for Malignant Melanoma?

A

1st line option for patients with a BRAF V600 mutation

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15
Q

What are the side effects of Dabrafenib?

A
  • Skin (pruritis, sensitivity to sun, rash, cutaneous squamous cell carcinomas, blistering)
  • Fatigue
  • Arthralgia (flu-like) - may require painkillers or heat/ice packs
  • Nausea
  • Headache
  • Alopecia
  • Fever - patients should report any fever above 38C
  • Eyes (uveitis - report any irritation, blurred vision, pain etc)
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16
Q

What is the mechanism of action for Trametinib?

A

Oral tyrosine kinase inhibitor which inhibits a mutated BRAF gene (specifically a change from Valine to Glutamate at AA position 600). Mutated BRAF leads to constitutive activation –> constant cell proliferation and growth.

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17
Q

What are the side effects of Trametinib?

A
  • Skin (pruritis, sensitivity to sun, rash, cutaneous squamous cell carcinomas, blistering)
  • Fatigue
  • Arthralgia (flu-like) - may require painkillers or heat/ice packs
  • Nausea
  • Headache
  • Alopecia
  • Fever - patients should report any fever above 38C
  • Eyes (uveitis - report any irritation, blurred vision, pain etc)
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18
Q

Where in the treatment pathway does Trametinib lie for the treatment of Malignant Melanoma?

A

Can be used alongside Dabrafenib/Verumafenib in first line as a dual therapy.

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19
Q

What is the first line treatment for 80% of colo-rectal cancer patients?

A

Surgery

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20
Q

What is the aim of adjuvant chemotherapy in Colo-rectal cancers?

A

Eradicating micro-metastases which have been shed from tumour prior to or during the resection.

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21
Q

Why is 5-FU given with Folinic acid in adjuvant chemotherapy for the treatment of Colo-rectal cancer?

A

5-FU has a short half life, so folinic acid has to be given to prolong the inhibition of thymidylate synthetase

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22
Q

What are the side effects of 5-FU?

A
  • Diarrhoea
  • Stomatitis
  • N & V
  • Bone Marrow Suppression
  • Hand-foot syndrome
  • Excessive tear shedding
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23
Q

What are the components of the ‘Oxaliplatin de Grammont’ (FALFOX) regime and how is it given?

A
  • Oxaliplatin
  • Folinic acid
  • 5-FU
    Given via a PICC or Hickman line (central line)
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24
Q

What are the components of XELOX regimen and how is it given?

A
  • Oxaliplatin
  • Capecitabine (pro-drug for 5-FU - no need for folinic acid)
    Orally given.
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25
Q

What are the side effects of the XELOX regimen?

A
  • Diarrhoea
  • Hand-foot syndrome
  • N & V
  • Stomatitis
  • Myelosuppression
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26
Q

Define each section of the Duke’s Staging System and subsequent treatments for each.

A

Duke’s A: localised to the bowel wall - surgery only
Duke’s B: penetrating into the bowel wall - surgery (and adjuvant chemotherapy in some cases)
Duke’s C: Involvement of lymph nodes around the bowel - surgery and adjuvant chemotherapy
Duke’s D: Metastases - surgery, palliative chemotherapy +/- monoclonal antibodies to relieve symptoms and prolong survival

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27
Q

What is in Lonsurf and what is the mechanism of action for each drug?

A

Trifluridine & Tipiracil

Trifluridine - thymidine analogue - phosphorylated by tyrosine kinase which incorporates trifluridine into DNA which prevents cell proliferation.

Tipiracil - trifluridine is rapidly deteriorated by the enzyme TPase. Tipiracil is a TPase inhibitor.

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28
Q

What are the side effects of Lonsurf?

A
  • N&V
  • Constipation
  • Sore mouth
  • Taste changes
  • Hand foot syndrome
  • Alopecia
  • Tiredness
  • Myelosuppresion
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29
Q

What are the different stages of the Gleason system and what the likelihood of progression by 10 years?

A

2-4 - 25% of progression by 10 years
5-7 - 50% of progression by 10 years
8-10 - 70% of progression by 10 years

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30
Q

What symptoms may present with someone with prostate cancer?

A
  • Hesitancy
  • Post-micturition dribbling
  • Decreased void pressure
  • Frequency
  • Urgency
  • Nocturia
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31
Q

What are the risk factors involved with developing prostate cancer?

A
  • AGE - strongest risk factor
  • Race
  • Genetic - 2-3x increased risk if first degree relative is affected
  • Diet - high in fat and red meat intake
  • Protective factors - frequent ejaculation, diet high in lycopenes (tomato)
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32
Q

What tests do we use to diagnose Prostate Cancer?

A
  • Digital Rectal examination
  • PSA levels - 5-10ng/mL = 25% chance of cancer, 11-20ng/mL = 66% will have prostate cancer, >50ng/mL = associated with bony metastases
  • Transrectal Ultrasound
  • CT/MRI
  • Radio-labelled Bone Scanning
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33
Q

What are the side-effects associated with a radical prostatectomy?

A
  • Impotence

- Incontinence

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34
Q

What is the advantage of using Radical Radiotherapy vs. a radical prostatectomy?

A

There is a 50% reduction in the side effect of impotence.

35
Q

What is the rationale behind LHRH analogues and name two that are used in practice?

A

LHRH is released from the hypothalamus. LHRH acts on the pituitary gland to release LH which tells the testes to produce testosterone.

LHRH is released in a pulsatile manner, with a short half-life which is key. If LHRH is permanently occupying the pituitary - there will be desensitisation.

The analogues disrupt the pulsatility of LHRH, thereby rendering the receptors desensitised, subsequently reducing the amount of testosterone produced.

Analogues: Goserelin / Triptorelin

36
Q

Why must LHRH be given with an androgen blocker for the first few weeks of initiating therapy? Name two androgen blockers.

A

The initial increase in LH will cause tumour flare due to initial increased testosterone. Androgen blockers compete with dihydrotestosterone (DHT) at receptors and reduce its production - this reduces tumour flare.

Androgen Blockers: Bicalutamide, Cyproterone

37
Q

What are the side effects of hormonal therapy (LHRH Analogues + Androgen Blockers) for the treatment of prostate cancer?

A

Due to decreased testosterone levels:

  • Impotence
  • Loss of libido
  • Breast tenderness
  • Increased breast size
  • Hot flushes
  • Depression + mood changes
  • Fatigue
38
Q

What is Abiraterone’s mechanism of action?

A

Oral androgen inhibitor, inhibitor of CYP17A1

39
Q

What are the side effects of Abiraterone and why? How can these be combatted?

A

Due to the inhibition of CYP17A1, there is decreased cortisol production which leads to cortisol deficiency and the symptoms associated:

  • Hypertension
  • Hypokalaemia
  • Fluid retention

Other symptoms include:

  • Peripheral oedema
  • UTI
  • Elevated LFTs - monitor every 2/52 for the first 3/12
40
Q

When is Abiraterone indicated for the treatment of metastatic prostate cancer?

A

1st line in patients who are not indicated for chemotherapy

Also indicated for those who have failed Chemotherapy and/or hormonal therapy.

41
Q

What is Enzalutamide’s mechanism of action?

A

Blocks several steps in the androgen signalling pathway i.e. inhibits the binding of androgens to androgen receptors.

42
Q

What are the side effects of Enzalutamide?

A
  • Headache
  • Hot flushes
  • Memory problems
  • Visual hallucinations
  • Risk of seizures
43
Q

When is Enzalutamide indicated?

A

Treatment of metastatic prostate cancer where disease has progressed on or after docetaxel therapy.

44
Q

How does docetaxel work?

A

Interupts the microtubular network so that mitosis cannot occur ultimately leading to cell death.

45
Q

What are the side effects of docetaxol + prednisolone regime?

A
  • Bone marrow suppression
  • Severe alopecia
  • N&V low emetogenic potential
  • Myalgia/Arthralgia
  • Fluid retention - pre-med with dexameth.
  • Hypersensitivity - pre-med with dexameth.
46
Q

What do we need to monitor with Docetaxol and why?

What do we need to put the patient on to ease their course?

A

FBC - neutrophils need to be above 1.5, and platelets needs to be above 100
LFTs - decrease the docetaxol if they are hepatically impaired.

Ned to have anti-emetics e.g. domperidone or metoclopramide
Ensure patient has taken pre-med dexameth before starting chemo

47
Q

What are the risk factors in developing breast cancer?

A
  • Age
  • Geographical location
  • Age of menarche & menopause
  • Age at first full term pregnancy
  • Lactation
  • Weight
  • Diet
  • Alcohol
  • Radiation
  • Oral contraceptives
  • HRT
  • Previous benign breast disease
  • Family history/genetics (BRCA1 & BCRA2)
48
Q

Run through the TNM staging process for all cancers

A

Tumour status (T):
T0 - no palpable tumour
T1 - tumour <2cm with no fixation to underlying muscle
T2 - 2cm < tumour < 5cm with no fixation
T3 - tumour with a max diameter of 5cm
T4 - tumour with any size with fixation to the chest well of ulceration of skin

Lymph Node Status (N):
N0 - no palpable axillary nodes
N1a - palpable nodes not thought to contain tumour
N1b - papable nodes thought to contain tumour
N2 - nodes >2cm or fixed to one another & deep structures
N3 - supraclavicular or infraclavicular nodes

Distant metastases (M):
M0 - No metastases
M1 - distant metastases

49
Q

Hormonal therapies are indicated which types of tumours, and what is the rationale behind the therapy?

A

Oestrogen Receptor positive and Progesterone positive tumours.

Oestrogen is needed for oestrogen-sensitive tumours to stay alive. Therefore, decreasing/removal of oestrogen is effective in controlling or killing hormone-sensitive cells.

50
Q

What is tamoxifen and what’s its mechanism of action?

A

Tamoxifen is a oestrogen receptor antagonist. It doesn’t allow oestrogen to bind to its respective receptor and facilitate growth/proliferation of the cell.

51
Q

What are the side effects of Tamoxifen?

A
  • Hot flushes
  • Weight gain
  • Sweats
  • Increased risk of developing endometrial cancer (mucus that lines the womb)
52
Q

What is the mechanism of action of Aromatase inhibitors? (Give three examples) When are they indicated and why?

A

Blocks the conversion of androgens to oestrogens which means cell growth and/or proliferation.

  • Anastrazole
  • Letrozole
  • Exemestane

They are indicated in post-menopausal ER/PR+ve women only, as the aromatase inhibitors do not inhibit the production of oestrogen from the ovaries in pre-menopausal women.

53
Q

What is the main side effect of aromatase inhibitors? What monitoring is done?

A

Decreased bone density, monitored with a DEXA scan before initiation of treatment.

54
Q

What are the drugs used in the FEC-T treatment?

A

(5-)Fluorouracil
Epirubicin
Cyclophosphamide
Docetaxol

55
Q

What are the side effects of the FEC-T regimen?

A
  • Infection risk
  • Bruising & Bleeding
  • Anaemia
  • Feeling tired
  • Tiredness
  • Sore mouth
  • Loss of appetite
  • Skin changes
  • Taste changes

Epirubicin - red urine
Docetaxol - nail changes, myalgia/arthralgia

56
Q

What monitoring do you need to do for FEC-T?

A
  • Renal function
  • LFTs
  • FBCs - platelets and neutrophils
57
Q

How does Herceptin (Trastuzumab) work?

A

Binds over-expression of the HER2 protein which prevents the binding of EGF to the receptor - therefore preventing downstream signalling to drive cell growth and/or proliferation.

58
Q

What are the side effects of Herceptin?

A
  • Cardiotoxicity
  • N&V
  • Diarrhoea
  • Myalgia/arthralgia
  • Rash
59
Q

What is Palbociclib’s mechanism of action?

A

Inhibitor of cyclin dependent kinases 4 & 6. CDK4/6 are involved in downstream signalling, so blocks the cell proliferation/growth

60
Q

What are the side effects of Pablociclib?

A
  • Neutropenia
  • Infections
  • Fatigue
  • Nausea
  • Stomatitis
61
Q

What are the differences between small cell and non-small cell lung cancer?

A

Small-cell lung cancer:

  • 15% of cases
  • cells are small and uniform
  • aggressive tumour
  • usually metastatic at diagnosis
  • surgery - limited role
  • responds well to chemo
  • overall survival 5-10%

Non-small cell lung cancer:

  • 85% of cases
  • Several different types (squamous cell, adenocarcinoma, large cell)
  • surgery used more often
  • less responsive to chemo
  • metastasises to brain, liver and bones
62
Q

What symptoms do patients typically present with, with lung cancer?

A
  • Persistent chronic cough
  • SOB/Wheezing
  • Haemoptysis
  • Chest/Shoulder/Back Pain
  • Weight loss
  • Fatigue
  • > 50% patients have a metastatic disease at presentation
  • Early disease can be confused with COPD
  • Early disease often diagnosed on routine chest X-RAY
63
Q

How do we stage Non-Small Cell Lung Cancer?

A

Stage I & II - primary tumour in 1 lung lobe with lymph node involvement confined to hilar nodes
Stage IIIa - locally advanced with involvement of mediastinal lymph nodes
Stage IIIb - locally advanced with pleural effusion and involvement of contrlateral mediastinal lymph nodes
Stage IV - metastases to other organs

64
Q

When is surgery indicated in NSCLC?

A

Stages I & II

65
Q

What is Crizotinib’s mechanism of action?

A

An ALK protein inhibitor who’s genes have been chromosomally translated and fused with another gene resulting in constitutive activation which drives cell growth and/or proliferation.

66
Q

What are Crizotinib’s side effects?

A
  • Visual problems e.g. blurred vision, diplopia, photophobia
  • Diarrhoea
  • N&V
  • Oedema (face and general)
  • Neuropathy
  • Neutropenia
  • Interstitial lung disease
67
Q

What is Alectinib’s mechanism of action?

A

An ALK protein inhibitor who’s genes have been chromosomally translated and fused with another gene resulting in constitutive activation which drives cell growth and/or proliferation (same as crizotinib) BUT ALSO anti-RET activity (another gene contributing to cell proliferation and/or growth)

68
Q

What chemotherapeutic agents are used in the treatment of someone with a NSCLC adenocarcinoma with no EGFR/ALK mutations?

A

Cisplatin / Pemetrexed

69
Q

What are the side effects of the cisplatin / pemetrexed chemo combination used in NSCLC treatment?

A
  • N&V
  • Myelosuppresion
  • Peripheral neuropathy
  • Ototoxicity
  • Nephrotoxicity
  • Stomatitis
  • Diarrhoea
  • Alopecia
70
Q

What pharmaceutical care issues arise from the cisplatin / pemetrexed combination?

A
  • FBC
  • Renal function check - GFR must be >55ml/min (MUST DO THIS FORMALLY)
  • Antiemetics
  • Pre- and post-hydration prescribed (3L IV Fluids before and after cisplatin)
  • Ensure an output of >100ml/min during and for 6-8 hours post cisplatin administration
  • Patients may need additional levels of diuresis if the urine output is inadequate or there is oedema
  • Monitor patient for cisplatin-induced wasting of metabolites e.g. Mg, Ca, K - supplements may be needed.
  • Pemetrexed = anti-folate agent - give pre-med Vit B12 and Folic acid
  • Give dexamethasone 4mg PO 3/7 before chemo (to avoid pemetrexed-related skin reactions)
71
Q

What is the mechanism of action of Afatinib/Gefitinib/Erlotinib?

A

Targets the tyrosine kinase of EGFR. Blocks the EGFR promoting downstream signalling and therefore cell proliferation/growth.

72
Q

What are common oncological emergencies (cancer-related and treatment-related)?

A

Cancer-related:

  • Hypercalcaemia
  • Spinal cord compression
  • Superior Vena Cava Obstruction
  • Large airway obstruction
  • Pleural effusion
  • Haemoptysis
  • Ureteric obstruction
  • GI obstruction
  • Gut perforation
  • Hyper-viscosity syndrome

Treatment-related:

  • Neutropenic sepsis
  • Extravasation
  • Tumour lysis syndrom e
  • Thrombocytopenia
73
Q

How does hypercalcaemia arise in cancer?

A

Tumour cells secrete cytokines that activate osteoclasts that start deforming bone (causing bone lesions) and causing an excess of calcium in the skin.

74
Q

How does hypercalcaemia present itself?

A
  • Polyuria & Polydipsia
  • Abdominal pain
  • Drowsiness and confusion
  • Impaired consciousness
  • Cardiac arrhythmias
75
Q

How do we treat hypercalcaemia?

A

Rehydration and bisphosphonates:

Rehydration: 3L IV Fluids over 24 hours

Bisphosphonates: IV bisphosphonates for 3 weeks (dose dependent on calcium levels)

76
Q

What is classified as neutropenia?

A

< 1.5 x 10^9/L neutrophils

77
Q

What may have caused neutropenia?

A

Chemotherapy
Radiotherapy
Disease with bone marrow involvement

78
Q

What are the most common organisms causing neutropenic sepsis?

A 
NORMALLY HOST'S OWN FLORA: 
Bacteria: 
- Staph Aureus 
- Strep 
- Kleb Pneu 
- E. Coli

Fungal:

  • Candida
  • Aspergillus

Viral:

  • Herpes simplex
  • Varicella zoster
79
Q

What are the risk factors for neutropenic sepsis?

A
  • Neutrophil count < 0.5 x 10^9/L
  • Neutropenia for more than 7/7
  • Patients with mucositis
80
Q

How does neutropenic sepsis present?

A
  • Pyrexia

Treat as neutropenic sepsis if:
- 1 x reading above 39C
OR
- 2 x readings above 38C

81
Q

How do we treat neutropenic sepsis?

A

1st line antibiotic IV: Tazocin (and Gentamicin if haemodynamically unstable)
Metronidazole if colonic symptoms (diarrhoea)

if still pyrexic after 48hrs, change antibiotics to Ceftazidime and Vancomycin

If still pyrexial after 96hrs, add an antifungal such as amphotericin B

82
Q

What prophylaxis can we use for neutropenic patients?

A

Antibiotic: Broad spectrum (amox) with good G-ve cover
Antifungal: nystatin, fluconazole, itraconazole
Mouthcare: chlorhexidine mouthwash

83
Q

When is lenograstim (G-CSF) implicated in neutropenic sepsis?

A

Due to £40 per dose, this is only used when we can use it to delay treatment.

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