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EOY4 > Cancer Care > Flashcards

Cancer Care Flashcards

1
Q

Which tumours most commonly metastasise to the brain?

A 
lung (most common)
breast
bowel
skin (namely melanoma)
kidney
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2
Q

What are the non-modifiable risk factors for breast cancer?

A

Female
Age 50-70
Genetics - BRCA1&2, ERBB2/HER2, TP53
Increased Oestrogen exposure - early menarche, late menopause (increased number of menstrual cycles)

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3
Q

What are the modifiable risk factors for breast cancer?

A

Oestrogen exposure - nulliparity, later age of pregnancy, HRT, COCP
Ionising radiation exposure
LIfestyle - obesity, alcohol, smoking

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4
Q

What are the 3 types of invasive breast cancer?

A

Invasive ductal carcinoma (75-85%)

Invasive lobular carcinoma (10%) (older women, more difficult to detect)

Other subtypes (5%), such as medullary carcinoma or colloid carcinoma

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5
Q

What is a carcinoma in situ? What are the two types of breast CIN?

A

Malignancies that are contained within the basement membrane tissue. Pre-Malignant and rarely symptomatic

I.e. high grade dysplasia

Ductal (most common) and Lobular

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6
Q

What is ductal carcinoma in situ?

A

malignancy of the ductal tissue of the breast that is contained within the basement membrane

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7
Q

What is lobular carcinoma in situ

A

malignancy of the secretory lobules of the breast that is contained within the basement membrane

more at risk of becoming invasive

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8
Q

What is the management of ductal and lobular carcinoma in situ?

A

Ductal = wide local excision

Lobular = Monitor if low grade

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9
Q

What is the clinical presentation of a breast carcinoma?

A

Lump! (craggy, irregular, matted, non-tender, immobile)

Nipple changes - pagets = itchy, red, crusty, retraction, abnormal discharge

Skin changes - swelling, peau d’orange

Mastalgia

Lump in axilla

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10
Q

What is the triple assessment for breast cancer?

A

Examination

Imaging - mammogram

Histology or cytology - USS biopsy

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11
Q

What are the two types of biopsy that can be taken from a breast?

A

FNAC - quick n easy but if malignant have to do a core biopsy anyway

Core = longer and more painful but gives receptor status and grading

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12
Q

Describe the vascular supply to the breast

A

External and internal mammary arteries give rise to intercostal, internal thoracic

Branch from axillary?

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13
Q

What are the localised complications of breast cancer?

A

Localised inflammation = fibrosis of suspensory ligaments and lactiferous ducts

Invasion of nearby tissue

Lymph node involvement = peau d’orange as lymph builds up but suspensory ligaments don’t allow swelling

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14
Q

Where are the 6 most common places for breast cancer to spread?

A 
Bone 
Brain
Lung 
Liver
Adrenal
Ovary
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15
Q

Describe the surgical options for breast cancer treatment

A

Mastectomy +/- reconstruction

Wide local excision - excision of the tumour ensuring a 1cm margin of macroscopically normal tissue is taken along with the malignancy.

Axillary clearance

Then give adjuvant radiotherapy

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16
Q

What are the indications for a mastectomy?

A

multifocal disease

high tumour:breast tissue ratio

disease recurrence

patient choice

risk-reducing cases

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17
Q

When would hormonal therapy be used to treat breast cancer?

A

malignant non-metastatic disease as an adjuvant therapy

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18
Q

What are the three drugs used for hormonal therapy when treating breast cancer?

A

Aromatase inhibitor (Letrozole) - prevents oestrogen production. Post menopausal women only

Tamoxifen - Oestrogen receptor antagonist. Pre and post menopausal women

Immunotherapy - Herceptin if HER2 positive, a monoclonal antibody

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19
Q

What are the positive and negatives of aromatase inhibitors?

A

+ves = lower risk of VTE

-ves = increased risk of osteoporosis

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20
Q

What are the positive and negatives of Tamoxifen?

A

+ves = Bone protection

-ves = Increased risk of VTE and endometrial cancer

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21
Q

What are the main types of lung cancer and where are they located?

A

Small Cell Lung Cancer (neuroendocrine) = Bronchial Mucosa

Non Small Cell Lung Cancer = Squamous, large cells, Adenocarcinomas

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22
Q

What are the non-modifiable risk factors for lung cancer?

A

Age >75

Male

Family history

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23
Q

What are the modifiable risk factors for lung cancer?

A

Lifestyle - Smoking!!! (adenocarcinoma)

Chronic lung disease - COPD, Pulmonary Fibrosis, TB

Radiotherapy

Toxin exposure - Asbestos (mesothelioma), Radon gas

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24
Q

What are the three types of NSCLC? How do they differ from SCLC?

A

Adenocarcinomas

Squamous Cell Carcinomas

Large cell carcinomas

Metastasise but DON’T produce hormones

SCLC met quickly, grow centrally and quickly

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25
Q

Which hormones can be produced by SCLC?

A

ACTH (Cushing’s)

ADH (SIADH)

(LEMS is also a thing but not hormones is instead antibodies)

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26
Q

Where does a mesothelioma arise from?

A

Lining of the pleura

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27
Q

What are the symptoms of a lung cancer?

A

Respiratory = cough, SOB +/- blood, recurrent chest infections, chest pain

Cancer = Weight loss, anorexia, lymphadenopathy, cachexia

NSCLC = ? hoarse voice +/- horner’s, ?hypercalcaemia

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28
Q

What are 4 signs of a lung cancer?

A

Clubbing, monophonic wheeze, consolidation, collapse

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29
Q

What are the bedside tests for a lung cancer?

A

Baseline obs

Sputum sample for cytology

PFT/peak flow

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30
Q

What are the blood tests for a lung cancer?

A

Carcinoembryonic Antigen for NSCLC

Baseline bloods otherwise (FBC, U&E, CRP, LFT, Bone profile)

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31
Q

What imaging should be done to investigate a lung cancer?

A

CXR - mass, mediastinal widening, hilar lymphadenopathy, lobar collapse

Biopsy - EBUS or bronchoscopy or CT guided

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32
Q

When should someone be referred for an urgent CXR (ie 2WW)?

A

> 40 + 2 red flags: cough, fatigue, SOB, chest pain, weight loss, anorexia OR ever smoked + 1 red flag

OR

> 40 + any of: recurrent chest infection, unexplained clubbing, thrombocytosis, chest signs, persistent supraclavicular lymphadenopathy

OR

> 40 and unexplained haemoptysis

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33
Q

What is a pancoast tumour?

A

A non-small cell lung cancer

Leads to compression of the brachiocephalic vein, sympathetic chain, recurrent laryngeal + phrenic nerves, subclavian artery

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34
Q

What are the non-modifiable risk factors for colorectal cancer?

A

Genetics - HNPCC (endometrial, ovarian, other GI), FAP (AD in APC gene), 1st degree relative <45 = familial colorectal cancer

Male

Age >70

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35
Q

What are the modifiable risk factors for colorectal cancer?

A

Lifestyle - smoking, obesity, alcohol

Diet - red meat, processed meats, low fibre

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36
Q

What is the pathophysiology behind colorectal cancer?

A

Polyp - Adenoma - Adenocarcinoma (most common)

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37
Q

Where are the most common locations for colorectal cancer?

A

Rectum

Sigmoid Colon

Rest of bowel

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38
Q

What is the clinical presentation of bowel cancer?

A

Blood in stools - fresh red = rectum, darker = partially digested so from higher +/- anaemia

Frequent change in bowel habit i.e. diarrhoea or constipation cycling v quickly

Tenesmus - feeling of incomplete emptying

Abdo/PR mass

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39
Q

How does the clinical presentation of bowel cancer change depending on the location of the tumour?

A

Left sided = pain

Right sided = bleeding +/- iron deficiency anaemia, weight loss, weakness

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40
Q

What are some trigger questions to ascertain late GI effects?

A

Woken at night?

Have to rush to toilet?

Loss of control?

Preventing from living a good life?

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41
Q

Which patients presenting with a suspcision of bowel cancer should be 2WWed?

A

> 40
PR bleeding

Change in bowel habit for >6 weeks

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42
Q

What are the blood tests to do to investigate bowel cancer?

A

FBC (anaemia)

CEA - not sensitive or specific

Tumour markers

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43
Q

What imaging should be done to investigate bowel cancer?

A

Colonoscopy + biopsy
MRI to see extent of primary tumour
CT for staging

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44
Q

What is the Duke’s Criteria?

A

A - tumour confined to bowel wall
B - tumour extends across bowel wall
C - Nodes at site of primary growth
D - Proximal nodes

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45
Q

What is the T staging of colorectal cancer?

A 
T1 = submucosa
T2 = through submucosa and across bowel wall
T3 = into serosa
T4 = through serosa into peritoneum
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46
Q

What is the surgical management of colorectal cancer?

A

Location dependent - anterior resection or hemicolectomy (R, L, Extended R)

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47
Q

When is radiotherapy appropriate for colorectal cancer?

A

Neoadjuvant

Palliative

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48
Q

When is chemotherapy appropriate for colorectal cancer?

A

Neoadjuvant
Adjuvant
Mets

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49
Q

Which other drugs could be used as medical management for colorectal cancer?

A

VEGF inhibitors

EGFR inhibitors

SE = dry skin, acne form rash, pruritus, nail changes

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50
Q

What is a melanoma? What are the 4 different types?

A

A malignant tumour arising from melanocytes

Superficial spreading (most common)
Nodular
Lentigo Maligna
Acral Lentigous

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51
Q

What are the non-modifiable risk factors for melanoma?

A

FHx
PHx
Increasing age
Fitzpatrick skin type 1 & 2 - Red/blonde hair, lots of moles/freckles, burns easily

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52
Q

What are the modifiable risk factors for melanoma?

A

Organ transplant recipient/immunosuppression

Lifestyle - tanning beds, sunburn esp if blisters in childhood

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53
Q

Give 4 differentials for a melanoma

A

Naevus

Pigmented Basal Cell Carcinoma

Sebhorrhoeic Keratosis

Dermatofibroma

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54
Q

How does a melanoma look on examination?

A

‘Ugly duckling’

A - asymmetrical (not a mirror image in all 4 quadrants)
B - Borders = irregular e.g. notched/scalloped
C - Colour Change +/- bleeding
D - Diameter >6 mm
E - Evolution - change in size, shape and elevation

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55
Q

How does the ABCDE of a melanoma help with diagnosis and management/

A

Goes into a weighted 7 point checklist

3+ points/ strong clinical concern = 2WW
2 points = Red flags, change in size, irregular border or colour
1 point = >7mm, inflammation, oozing or crusting

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56
Q

How should a melanoma be investigated?

A

Incisional biopsy if smaller, or excisional biopsy if larger (these are the deepest biopsies so can see between lesion and normal tissue) - diagnostic and potentially curative

Shave biopsy (less invasive but can’t see if tumour has invaded)

Punch biopsy (dermis)

57
Q

What is the management of a melanoma?

A

Prevention - hat, sunscreen, protective clothing, regular skin checks

Early = complete excision, wide margin surgery, sentinel lymph node biopsy

Late = chemo or radio

58
Q

What is Bowen’s disease?

A

A squamous cell carcinoma in situ (abnormal growth of keratinocytes)

BM not invaded

Red, scaly patch that is slow growing and usually in sun exposed areas

59
Q

What is the management of Bowen’s disease?

A

Biopsy > breslow thickness

60
Q

What is actinic keratosis?

A

Thickened skin due to sunlight exposure that can be itchy

Rough and sandpapery patch that has a variable colour and diameter and can become scaly or warty

61
Q

What is the management of Bowen’s disease and actinic keratosis?

A

Chemo cream - 5-fluorouracil (gets worse before better)
Immuno cream - imiquimod

Curettage and electrocautery
Photodynamic therapy
Surgery
Cryotherapy

(can watch and wait if actinic keratosis is small)

62
Q

What are the non-modifiable risk factors for prostate cancer?

A

Age 60-80
Black and asian ethnicity
FHx (1st degree relative), BRCA2 and HNPCC

63
Q

What are the modifiable risk factors for prostate cancer?

A

Lifestyle - high red meat and low veg, smoking

High pesticide exposure

64
Q

What are 4 differentials for prostate mass?

A

Malignancy
BPH/Normal variation
Calficiation
Cyst

65
Q

Which zones of the prostate are most likely to become an adenocarcinoma?

A

1) Peripheral Zone
2) Transitional Zone surrounding prostatic urethra (more likely to be BPH)
3) Central zone surrounding ejaculatory duct

66
Q

What is the clinical presentation of prostate cancer?

A

Early = asymptomatic

Late = urinary obstruction = frequency, hesitancy, urgency, post mic dribble, incomplete emptying
Increased UTIs, haematuria, haematospermia

Mets = bone pain +/- SC compression

67
Q

Where is prostate cancer most likely to metastasise too?

A

Direct = bladder, seminal vesicles

Lymphatic = Inguinal

Haematogenous = Bone, lung, liver

68
Q

Which blood tests should be done to investigate prostate cancer?

A

PSA, calcium

FBC, U&E, LFTs

69
Q

What imaging should be done to investigate prostate cancer?

A

BONE scan
CT
MRI
BIOPSY + TRUS = DIAGNOSTIC

70
Q

Other than prostate cancer, what else can cause a raised PSA? And alternatively, what can cause a low PSA?

A 
UTI
BPH
Ejaculation
DRE
Prostatitis
Cystoscopy

Low = NSAIDs

71
Q

What is the Gleason score?

A

ranges from 1-5 and describes how much the cancer from a biopsy looks like healthy tissue (lower score) or abnormal tissue (higher score)

72
Q

What is the criteria for low risk prostate cancer?

A

PSA <10 AND
Gleason 6+ AND
Can’t feel prostate on exam

73
Q

What is the criteria for intermediate risk prostate cancer?

A

PSA 10-20 OR
Gleason 7 OR
T2b T2c

74
Q

What is the criteria for high risk prostate cancer?

A

PSA >20 OR
Gleason 8-10 OR
T3/T4

75
Q

What is the management of localised prostate cancer?

A

Active surveillance/watchful waiting
Radical prostatectomy
External beam +/- radiotherapy +/- brachytherapy +/- hormone

Have to include informed choice

76
Q

What is the different between watchful waiting and active surveillance?

A

WW = aim is symptom control, fewer tests and less close monitoring

AS = Aim is curative treatment if disease progresses. Closer monitoring and regular tests and exams

77
Q

What is brachytherapy?

A

Place a radioactive source next to the tumour to emit radiation

Kill tumour cells

Only for solid, local, small tumours that can be reached by surgery

78
Q

What is the management of intermediate risk prostate cancer?

A

Radical prostatectomy

External beal radiotherapy + brachytherapy +/- hormonal therapy

79
Q

What are the disadvantages of a radical prostatectomy?

A

Regrowth

erectile dysfunction

urinary incontinence

infertility

Bowel problems

80
Q

What are the treatment options for locally advanced prostate cancer?

A

Hormonal therapy - GnRH analogue (Goserlin, Leuprotein)

Chemo

81
Q

What is the MOA of Goserlin?

A

Same as GnRH - Increases LH and FSH

Get an initial flare of sex hormone so symptoms can worsen

Then desensitises receptors so LH and FSH are reduced

82
Q

What are the 5 oncological emergencies?

A

Metabolic = hypercalcaemia
Haematological = Neutropenic sepsis
Treatment related = Tumour lysis syndrome
Structural = Superior Vena Cava Obstruction, Spinal Cord Compression

83
Q

Define tumour lysis syndrome

A

A combination of metabolic and electrolyte abnormalities that occurs in patients with cancer, usually after beginning a cytotoxic treatment regime (chemo)

84
Q

What is the pathophysiology of tumour lysis syndrome?

A

Rapid destruction of tumour cells = rapid release of intracellular contents leading to:

Hyperuricaemia, hyperkalaemia, hyperphosphataemia

Hypocalcaemia

85
Q

What are the non-modifiable risk factors for tumour lysis syndrome?

A

Haem malignancy (NHL, ALL)

High tumour burden

Pre-existing renal compromise

86
Q

What are the modifiable risk factors for tumour lysis syndrome?

A

Recent chemo (usually within first 48hrs but have to monitor for first week)

Dehydration

87
Q

What are the symptoms of tumour lysis syndrome?

A

GI - N&V, diarrhoea, anorexia
Neuro - parasthesia and serious tetany
MSK - muscle cramps
Lethargy

88
Q

What are the signs of tumour lysis syndrome?

A

HTN
Hypotension
Arrhythmias

89
Q

What are the bedside tests to manage tumour lysis syndrome?

A

Baseline obs - need an ECG to monitor for arrhytmias

90
Q

What are the blood tests to manage tumour lysis syndrome?

A

Diagnosis = Biochemistry - serum uric acid, phosphate, potassium, calcium. LDH, FBC

91
Q

What is the conservative management of tumour lysis syndrome?

A

Low risk = monitor

Med - high risk = IV fluids prior to chemo/intensive fluid resus if acute syndrome

92
Q

What is the medical management of tumour lysis syndrome?

A

Acute = Rasbiscurase or Allopurinol

Phosphate binder

Correct electrolyte imbalance

93
Q

What is the MOA of Rasbiscurase?

A

Converts uric acid to allantoin which is easier to excrete than uric acid

Only acts on current UA so not prophylactic

94
Q

What is the MOA of Allopurinol?

A

Xanthine Oxidase inhibitor

Prevents uric acid formation so can be used prophylactically

95
Q

What is a fibroadenoma?

A

Common in women under the age of 30 years

Often described as ‘breast mice’ due as they are discrete, non-tender, highly mobile lumps

96
Q

What is Fibroadenosis?

A

fibrocystic disease, benign mammary dysplasia

Most common in middle-aged women
‘Lumpy’ breasts which may be painful. Symptoms may worsen prior to menstruation

97
Q

What is Paget’s disease of the breast?

A

intraductal carcinoma associated with a reddening and thickening (may resemble eczematous changes) of the nipple/areola

98
Q

What is mammary duct ectasia?

A

Dilatation of the large breast ducts

Most common around the menopause

May present with a tender lump around the areola +/- a green nipple discharge

If ruptures may cause local inflammation, sometimes referred to as ‘plasma cell mastitis’

99
Q

What is a duct papilloma?

A

Local areas of epithelial proliferation in large mammary ducts

Hyperplastic lesions rather than malignant or premalignant

May present with blood stained discharge

100
Q

What is fat necrosis relating to the breast?

A

More common in obese women with large breasts

May follow trivial or unnoticed trauma

Initial inflammatory response, the lesion is typical firm and round but may develop into a hard, irregular breast lump

Rare and may mimic breast cancer so further investigation is always warranted

101
Q

What is the purpose of cancer screening?

A

Detection of cancers in otherwise healthy people as early as possible when the chance of curing is the highest

102
Q

Describe the cervical cancer screening programme

A

Women aged 25-49 are invited every 3 years
Women aged 50-64 are invited every 5 years
If they are registered with a GP

Tests for HPV and if they are high risk then they are tested for dyskaryosis and if they are low risk they return to the screening programme

Can’t do it if you’re on your period

103
Q

Describe the breast cancer screening programme (in England)

A

Women (who are registered with a GP) aged 50-70 are invited for a mammogram + UUS +/- biopsy (triple assessment) every 4 years

104
Q

Describe the screening for colon cancer in England

A

Everyone aged 60-74 is sent a home testing kit every 2 years

Send off a poo sample for faecal immunochemical testing

+/- bowel scope screening at 55 (only available in some areas)

105
Q

What counts as a ‘higher risk woman’ who are invited for breast screening earlier?

A

Strong FHx =

2+ close relatives on the same side have had cancer
Cancer developed before 50
1 Relative has a known gene fault (BRCA or TP53)

106
Q

Give 2 positives of screening for cancer

A

Reduces incidence of cancer and advanced disease

Reduces mortality as more likely to be treated

107
Q

Give 5 negatives of screening for cancer

A

Lead time bias - early diagnosis gives false impression that people are living longer (but there’s actually no difference)

Length time bias - overestimation of survival due to relative excess of cases that are slowly progressing asymptomatically

Detection not prevention

Over diagnosis = over treatment?
False positives

108
Q

Define sensitivity

A

% of true positives

Good at recognising disease/people who have the disease and does not miss those who are ill

109
Q

Define specificity

A

% of true negatives

Good at recognising when the disease is not present

110
Q

Give 4 examples of hereditary/genetically linked cancers

A

BRCA1 and BRCA2 - breast, ovarian and prostate cancer

HNPCC - Autosomal dominant for colorectal and endometrial (and ovarian, stomach etc)

FAP - colorectal

MEN1 - Thyroid, parathyroid, pituitary, bowel

111
Q

What are the 6 hallmarks of cancer?

A
  • Self sufficiency/growth factor independence
  • Insensitive to anti-growth signals
  • Avoidance of apoptosis
  • Angiogenesis
  • No limit to cell division
  • Invasion and metastases
112
Q

What is tumour burden?

A

The ability of malignant cells to spread to distant sites

113
Q

What are the 4 most common sites of mets?

A

Lung

Bone

Liver

Brain

114
Q

Which cancers most commonly metastasise to the bone?

A 
Breast
Bronchus
Kidney
Thyroid 
prostate
115
Q

What is adjuvant and neoadjuvant in terms of treatment?

A

Adjuvant = eliminates micrometastases and is given in addition to the primary treatment

Neoadjuvant = given before metastasis and in advance to the primary treatment

116
Q

Define neutropenic sepsis

A

Neutrophil levels <0.5, temperature >38, +/- other signs of sepsis

Recent chemo (in past 7-10 days)

117
Q

Why does neutropenic sepsis occur?

A

Patient is neutropenic due to recent chemo (kills rapidly dividing cells), have a haem cancer or radiotherapy

then get an infection/more likely to get an infection anyway

118
Q

How does neutropenic sepsis present?

A

Really unwell = get sepsis signs, high NEWS score

Post chemo

?have an infection site e.g. picc/hickmann line, skin wounds, mouth ulcer

119
Q

What is the management of neutropenic sepsis?

A

Activate sepsis 6
Give empirical abx (tazocin) within the hour

Supportive care - A-E, escalation, GCSF if very profound

120
Q

What is superior vena cava obstruction?

A

Compression of the superior vena cava due to malignancy. Usually lung (NSCLC), NH Lymphoma or IVC thrombosis

Quite rare

121
Q

What are the early and late signs of SVCO?

A

Early = puffy neck and face, non-collapsible veins

Late = distended neck and chest wall veins, swollen neck, face and arms, drowsy

122
Q

How is SVCO managed?

A

Conservative - sit up and give high flow o2

Medical - steroids, ?chemo ?radio

Surgical - SVC stent (rapid symptom relief but doesn’t treat cause)

123
Q

Define malignant spinal cord compression

A

Spinal cord/cauda equina compression by direct pressure (cauda equine if below L2)

+/- induction of vertebral collapse/instability by metastatic spread or direct extension of malignancy that may lead to neurodisability

Most common in breast, lung, prostate cancer, myeloma

124
Q

What is the clinical presentation of malignant spinal cord compression?

A

Initial = oedema, venous compression, demyelination (reversible)

Later = vascular and cord injury = damage = saddle anaesthesia, loss of urinary and bowel continence OR retention and constipation, motor weakness

BACK PAIN - worse when lying, radicular pain

125
Q

What investigations should you do for hypercalcaemia of malignancy?

A

Bed = urinalysis

Bloods - serum calcium and bone profile (and baseline bloods)

Imaging - Bone profile/scan, XR to areas of pain for pathological fractures, CT for staging

126
Q

What is the management of hypercalcaemia of malignancy?

A

Hyperhydration - 3l/hr ish

Bisphosphonates (zolendronic acid/pamidronate)

Manage nausea - haloperidol

127
Q

What are the most likely causative organisms of neutropenic sepsis?

A

Gram +ve = staph aureus/epidermidis, MRSA, enterococcus

Gram -ve = pseudomonas

128
Q

What medication can be given as neutropenic sepsis prophylaxis?

A

Fluoroquinolone

129
Q

Define paraneoplastic syndrome

A

A collection of symptoms that are a consequence of a signalling or immune response and not a direct effect of the cancer itself

Cushings, SIADH, LEMS,

130
Q

What is the management of malignant spinal cord compression?

A

Analgesia

Steroids - PO Dexamethasone

Anticoagulation

Surgery/radiotherapy to remove/shrink

131
Q

Which tumours may secrete ACTH?

A

Pituitary adenoma

Ectopic = Small Cell lung cancer, thyroid cancer

132
Q

Which tumours may secrete ADH?

A

Small cell lung cancer

Pancreatic cancer

Head and neck SCC

Lymphoma

133
Q

Which tumours may secrete PTHrP?

A

SCC, Breast, Renal, Melanoma, Prostate

134
Q

Which tumours may secrete calcitriol?

A

Lymphoma

135
Q

What is a side effect of bleomycin?

A

Pulmonary Fibrosis

136
Q

What is a side effect of Doxorubicin?

A

Cardiotoxicity/myopathy

137
Q

What are 3 side effects of Methotrexate?

A

Myelosuppression
Mucositis
Liver and Lung fibrosis

138
Q

What is a side effect of vincristine?

A

Peripheral neuropathy

EOY4 (22 decks)

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