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cancer care Flashcards

1
Q

2WW appointment criteria for lung ca

A

40+ with unexplained haemoptysis

suspicious CXR findings

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2
Q

criteria for which you offer urgent CXR for ?lung ca

A

40+ with 2 of following sx / 1 sx + hx smoking

  • cough
  • fatigue
  • sob
  • chest pain
  • UEW
  • loss of appetite
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3
Q

2WW upper GI endoscopy referral criteria

A

dysphagia

55+ with UEW and upper abdo pain/reflux/dyspepsia

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4
Q

2WW gynae criteria

A

PMB; ascites; pelvic mass exc fibroid

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5
Q

2WW lower GI appt

A 
Give PR and FBC in all
Positive FOB
40+ with abdo pain + UEW
50+ with unexplained rectal bleeding
60+ with IDA or change in bowel habit
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6
Q

2WW prostate

A

suspicious PR

PSA>age-adjusted normal range + abnormal PR/normal PR but excluded infection

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7
Q

2WW urology (exc prostate)

A

40+ with visible haematuria
60+ non-visible haematuria and dysuria/raised WCC
non-painful enlargement/change in shape or texture of testicle

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8
Q

Class, MoA and S/E of cyclophosphamide?

A

Alkylating agent, crosslinks DNA, haemorrhagic cystitis, TCC, myelosuppression

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9
Q

Class, MoA and S/E of vincristine and vinblastine?

A

Vinca alkaloids - inhibits microtubule formation - VC = reversible peripheral neuropathy, paralytic ileus and myelosuppresion; VB = myelosuppression

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10
Q

Class, MoA and S/E of methotrexate?

A

Antimetabolite - dihydrofolate reductase antagonist prevents folate metabolism to prevent DNA synthesis - myelosuppression, mucositis, liver and lung fibrosis

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11
Q

Class and S/E of bleomycin?

A

cytotoxic antibiotic - lung fibrosis

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12
Q

Class and S/E of doxorubicin?

A

cytotoxic antibiotic -cardiomyopathy

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13
Q

Class, MoA and S/E of 6-mercaptopurine?

A

antimetabolite - prevents purine synthesis and thus DNA synthesis - myelosuppression

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14
Q

Class, MoA and S/E of docetaxel?

A

vinca alkaloid - prevents microtubule disassembly - neutropenia

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15
Q

Class, MoA and S/E of 5-fluorouracil?

A

antimetabolite - pyrimidine analogue causing cell cycle arrest in S phase and cell apoptosis - mucositis, dermatitis, myelosuppression

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16
Q

Class, MoA and S/E of cisplatin?

A

alkylating agent - crosslinks DNA preventing replication - peripheral neuropathy, ototoxicity, hypomagnaesaemia

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17
Q

Radiotherapy early S/E

A

occur around 2 weeks in, peak 2-4wks after rx
tiredness, N+V, diarrhoea, skin reaction (erythema, dry/moist desquamation reaction, ulceration), mucositis, dysphagia, cystitis

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18
Q

Radiotherapy late s/e

A

months years after rx
secondary ca - of greatest concern in young pt
somnolence, spinal cord myelopathy, brachial plexopathy; pneumonitis; xerostomia, benign strictures of oesophagus/bowel, fistulae, radiation proctitis; urinary frequency, vaginal stenosis, dyspareunia, ED, subfertility; hypothyroidism, panhypopituitarism

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19
Q

Monoclonal antibody tumour markers - list assoc ca

  • CA125
  • CA19-9
  • CA15-3
A

ovarian ca
pancreatic ca
breast ca

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20
Q

tumour antigens - list assoc ca

  • PSA
  • AFP
  • CEA
  • hCG
A

prostate ca
hepatocellular and testicular ca
colorectal ca
germ cell testicular ca and GTD

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21
Q

cervical ca screening programme

A

women aged 25-49 every 3yrs, women aged 50-64 every 5 years for a cervical smear test

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22
Q

breast ca screening programme

A

women aged 47-73 invited for mammogram every 3yrs

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23
Q

colorectal ca screening programme

A

open to men and women
One off Flexible sigmoidoscopy at 55
faecal immunochemical test (FIT) screening - home kit every 2yrs aged 60-74
(test for human Hb in stool (prev FOB but false positive from animal Hb in diet). Can have FIT testing 75+ but it is by request.)

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24
Q

Describe Dukes staging of colorectal cancer

A

Dukes A - invasion into but not through the bowel wall (muscular mucosa)
B - extends through bowel wall but does not involve LN
C - involvement of LNs
D - widespread metastases

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25
Q

Pre-op ix for patient having colorectal surgery

A

pregnancy test if any doubt
FBC, U+Es, clotting, glucose, LFTs (if indicated)
Group and save
ECG

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26
Q

Who should be considered for bowel prep

A

People having L sided operations, Klean-Prep macrogol night before. Not usually needed in right sided op.

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27
Q

Abx prophylaxis for urological/bowel surgery

A

IV gentamicin + metronidazole

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28
Q

Abx prophylaxis for breast/upper GI/obstetric/gynaecology surgery?

A

IV co-amoxiclav

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29
Q

Features of a colostomy

A

Typically LIF, flush to skin, thick and sludgy faeces-like output

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30
Q

Features of an ileostomy

A

typically RIF, spouted (small bowel contents are an irritant to skin), output is watery and often tinged with green.

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31
Q

What is a loop stoma and when is it used?

A

When a loop of bowel (small or large) is brought through the surgical incision in the skin and partially divided to form two adjoining stomas. This is used to definition downstream bowel by diverting faeces.

  • Loop colostomy - often temporary, can be used in severe peri-anal CD, obstructive rectal ca.
  • Loop ileostomy - in anterior resections to prevent anastomotic leak
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32
Q

Risk factors for malignant melanoma

A

Excessive UV exposure, Fitzpatrick type 1 skin, hx of multiple/atypical moles, family/personal hx melanoma

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33
Q

Features suspicious of malignant melanoma in a skin lesion?

A

ABCDE Symptoms
Asymmetrical
Border irregularity
Colours irregular, multiple colours within lesion
Diameter >6mm
Evolution of lesion (change in shape/size)
Symptoms - itching, oozing, bleeding

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34
Q

Types of malignant melanoma and how they present differently

A

Nodular - most aggressive; red/black lump which bleeds/oozes; seen mainly in middle age on sun exposed skin of trunk
Superficial spreading - most common, intermittent high intensity UV exposure, commonly lower limbs
Lentigo maligna - due to chronic UV exposure, older people face
Acral lentiginous - rare, seen in nails/palms/soles in Asian/African-Americans.

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35
Q

What is the most important prognostic factor malignant melanoma?

A

Breslow thickness measured from the top of the stratum granulosum of the epidermis to the deepest invasive cell

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36
Q

How is ?malignant melanoma investigated and managed?

A

2WW dermatology
Excision biopsy, histopathology and Breslow thickness to determine need for re-excision to clear margins .
Radiotherapy and chemotherapy may be used in metastatic

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37
Q

What is basal cell carcinoma in pathophysiological terms?

A

Slow growing, locally invasive malignant tumour of the epidermal keratinocytes. Rarely metastasises.

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38
Q

Types of BCC

A

Nodular (most common), superficial, cystic, keratotic, morphoeic

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39
Q

How does nodular BCC present?

A

Slow growing skin coloured papule or nodule with pearly rolled edge and surface telangiectasia, may have central ulceration or necrosis.

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40
Q

Risk factors for BCC?

A

UV exposure, hx freq/severe childhood sunburn, skin type I, age, male, immunosuppression, hx of skin cancer, and genetic predisposition

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41
Q

How is BCC managed?

A

Surgical excision with histopathology of tumour and margins; can use Mohs Micrographic if high-risk, recurrent or in a difficult spot e.g. face.
Metastatic - radiotherapy
Small low-risk lesions - topical imiquimod cream, cryotherapy, curettage and cautery

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42
Q

What is a squamous cell carcinoma?

A

locally invasive malignant tumour of the epidermal keratinocytes or its appendages, with potential to metastasise

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43
Q

Risk factors for SCC

A

UV exposure, immunosuppression, chronic inflammation or pre-malignant skin conditions (e.g. actinic keratosis), smoking

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44
Q

How is SCC managed?

A

2WW for surgical excision (margins 4mm if <20mm, 6mm if >20mm), Mohs micrographic surgery in high risk patients or cosmetically important sites.
Radiotherapy for large non-resectable tumour

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45
Q

How does SCC present?

A

keratotic ill defined nodule which may ulcerate

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46
Q

Risk factors for breast cancer

A

Family history (esp 1st degree relative/relatives under 40), BRCA1/2 mutation, nulliparity/late primigravida, early menarche, late menopause, combined HRT/OCP, past breast ca, not breastfeeding, ionising radiation, p53 mutations, obesity

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47
Q

Most common type of breast cancer?

A

Invasive ductal carcinoma (no special type)

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48
Q

What is DCIS and how does it usually present?

A

ductal carcinoma in-situ, where cancerous cells are contained by the basement membrane. Some will go on to become invasive malignancy. Usually picked up as incidental finding of micro calcifications on mammogram.

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49
Q

2 main classifications of breast cancer in terms of cellular origin

A

ductal and lobular

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50
Q

how does pagets disease of the nipple present?

A

eczematoid change of the nipple (spreading to areola) associated with underlying breast malignancy

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51
Q

How does breast cancer typically present?

A

If not on screening, if symptomatic
Breast lump - hard, fixed, irregular
asymmetry and swelling of breast, mastalgia
nipple retraction/abnormal discharge
skin changes - e.g. peau d’orange, dimpling, tethering
palpable axillary lump

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52
Q

Ddx for a breast lump

A

Fibroadenoma (<30, breast mouse)
fibroadenosis (middle age - lumpy ± pain)
breast cyst
fat necrosis (obese, hx trauma)
mammary duct ectasia (tender lump around areola ± green nipple discharge)
breast abscess (hot, red, tender swelling commonly in lactation)

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53
Q

How would you investigate a ?breast ca

A

triple assessment - clinical history and examination, imaging (ultrasound scan/mammogram), histology and cytology (core bx or FNA if cyst)

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54
Q

How is breast cancer prognosis assessed?

A

Nottingham Prognostic Index = ( size cm x 0.2) + nodal status + bloom-richardson grade

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55
Q

What treatment modalities are available to rx breast ca?

A

Surgery - mastectomy/WLE + radiotherapy
Hormonal rx - adjuvant if ER+
Immunotherapy - if HER2+
Chemotherapy - FEC-D used mainly neoadjuvant/adjuvant in axillary node disease

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56
Q

When would you advise mastectomy vs WLE and vice versa?

A

Mastectomy - large tumour:breast ratio, multifocal disease, central tumour, DCIS>4cm.
WLE - small tumour:breast ratio, solitary lesion, peripheral tumour, DCIS<4cm

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57
Q

How would you assess whether or not LN dissection is needed in breast ca surgery?

A

Palpable axillary LN at presentation - LN clearance

No palpable axillary LN at presentation = LN USS, if positive then SLNB to assess nodal burden

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58
Q

When should you offer radiotherapy in breast ca rx?

A

After WLE - whole breast radiotherapy to reduce recurrence

After mastectomy if T3/T4 tumour or extensive nodal disease

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59
Q

What hormonal treatment is available for breast cancer and duration of rx?

A

ER positive then can give SERM tamoxifen (if premenopausal) or aromatase inhibitor (e.g. anastrozole/letrozole if post-menopausal). 5 years.

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60
Q

S/E of tamoxifen

A

Hot flushes - main reason why women stop
menstrual disturbances - abnormal PV bleeding
increased risk of endometrial cancer, VTE and osteoporosis

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61
Q

S/E of aromatase inhibitors

A

osteoporosis (baseline DEXA scan)
hot flushes
arthralgia/myalgia
insomnia

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62
Q

What specific rx is available for a HER2 positive breast ca? What are the side effects?

A

Herceptin (trastuzumab) - monoclonal antibody
Flu-like symptoms e.g. fever, chills, mild pain
Nausea and diarrhoea
Cardiomyopathy, arrhythmia, heart failure - cardiotoxicity so do not offer to pt with LVEF<55%, hx poorly controlled htn, high risk uncontrolled arrhythmia, medication requiring angina, CCF. Baseline ECHO and every 3m

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63
Q

What histological class of cancer is most common in colorectal ca?

A

adenocarcinoma

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64
Q

Risk factors for colorectal ca

A

age
polyps (adenoma-carcinoma seq)
family hx and genetics - FAP (APC mutation), HNPCC
IBD
diet - low fibre, high processed meat intake
smoking and high alcohol intake

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65
Q

Clinical features of colorectal ca

A

R sided - IDA, weightloss, FOB, abdo pain, RIF mass, presents late
L sided - change in bowel habit, rectal bleeding, tenesmus, mass in LIF/on DRE

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66
Q

Ddx in ?colorectal ca

A

diverticular disease
IBD
haemorrhoids

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67
Q

Ix in ?colorectal ca

A

FBC, U+Es, LFTs, clotting; CEA - monitoring not diagnosis
Colonoscopy and bx
CTCAP staging
rectal ca - MRI rectum and endoanal ultrasound (T1/t2)

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68
Q

What surgery would you perform for an ascending colon ca?

A

Right hemicolectomy

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69
Q

What surgery would you perform for a proximal transverse colon ca?

A

extended right hemicolectomy

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70
Q

What surgery would you perform for descending colon ca?

A

left hemicolectomy

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71
Q

What surgery would you perform for a sigmoid colon ca?

A

sigmoid colectomy

anterior resection takes superior rectum too

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72
Q

What surgery would you perform for a high rectal ca >5cm above the anal verge?

A

anterior resection with a defunctioning loop ileostomy (can be reversed)

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73
Q

What surgery would you perform for a low rectal ca <5cm above the anal verge?

A

abdominoperineal resection and permanent colostomy

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74
Q

What surgery would you perform for colorectal cancer that has perforated or obstructed?

A

Hartmanns procedure (resection of rectosigmoid colon with end colostomy and closure of the rectal stump)

75
Q

In what type of colorectal cancer is radiotherapy used as a treatment modality?

A

Rectal cancer as neoadjuvant rx

76
Q

Palliative surgery for colorectal ca?

A

In obstruction - Endoluminal stenting (l sided tumour), stoma formation
resection of secondaries - not commonly performed but can be done with adjuvant chemo for liver mets

77
Q

when is chemo used to treat colorectal ca?

A

adjuvant in advanced disease (Dukes C) - folfox chemo

78
Q

In what are of the prostate does prostate ca most commonly occur?

A

Peripheral zone

79
Q

What histological type of cancer are most prostate ca’s?

A

adenocarcinoma (95%) - most commonly acinar, ductal Is less common but more aggressive

80
Q

Risk factors for prostate ca

A

age, ethnicity (black African/caribbean), family hx, BRCA2. Less sig modifiable - obesity, DM, smoking, lack of exercise

81
Q

Sx of prostate ca

A

Local - LUTS inc weak stream, urgency, frequency
Locally advanced - haematuria, haematospermia, dysuria, incontinence, suprapubic/loin pain, tenesmus
Mets - bone pain, lethargy, anorexia, UEW

82
Q

Ix prostate ca

A

DRE (irregular hard nodular asymmetrical mass)
PSA
Biopsy - transrectal ultrasound guided bx (TRUS) or Transperineal bx; may have pre/post negative bx multi parametric MRI
Staging CT abdopelvis + bone scan

83
Q

How is prostate ca risk stratified?

A

Gleason score + PSA + tumour staging (from TNM)
Low risk - PSA<10, Gleason 6 or less, T1-2a
Intermediate risk - PSA10-20, Gleason 7, T2b
High risk - PSA>20, Gleason 8-10, T2c

84
Q

How is risk used to determine management of prostate ca?

A

low - active surveillance, radical rx if evidence of progression
Intermediate risk - offer radical rx, may be suitable for active surveillance
high risk - offer radical therapy
Metastatic disease - chemotherapy + anti-hormonal agents

85
Q

How is active surveillance different to watchful waiting?

A

Active surveillance is only offered to those with low risk disease or select patients with intermediate risk disease. Monitor with 3-monthly PSA, 6-12monthly DRE, and rebiopsy at 1-3yr interval. Assess for progression and intervene as appropriate.
Watchful waiting - older patients, limited life expectancy, at any stage of disease, symptom guided, definitive rx is delayed + hormonal rx often initiated at time of symptomatic disease.

86
Q

Surgical management of prostate ca?

A

Radical prostatectomy - removal of prostate gland, seminal vesicles and surrounding tissues ± pelvic LN dissection. Can be open, laparoscopic or robot assisted. S/E - ED in 60-90%, SUI, bladder neck stenosis.

87
Q

What radiotherapy is used for prostate ca and in whom?

A

External beam radiotherapy and brachytherapy can be used. Can be curative in locally advanced disease. Increased risk bladder, colon and rectal ca.

88
Q

What hormonal rx is offered in prostate ca?

A

T3/4 locally advanced disease, metastatic disease
GnRH agonist goserelin + initial anti-androgen cover to prevent tumour flare with rise in testosterone; anti-androgens; orchidectomy

89
Q

What are the main testicular ca classifications? Which is more common?

A

Germ cell tumours 95% - seminomas (35yo, good prognosis) or non-seminomatous e.g. teratoma (25Y/O), yolk sac, choriocarcinoma.
Non germ-cell

90
Q

Risk factors for testicular ca?

A 
Infertility (3x risk)
family hx
cryptorchidism
klinefelters syndrome
mumps orchiditis
91
Q

Sx of testicular ca

A

Testicular lump - irregular fixed and firm with no transillumination, minority are painful
Hydrocoele
Gynaecomastia

92
Q

Ix testicular ca

A

AFP (may be raised in NSGCT), b-hcg (raised - more likely NSGCT), LDH (raised in GCST) tumour markers
ultrasound scan testicle
CT CAP with contrast for staging

93
Q

Ddx testicular lump

A

epididymal cyst, haematoma, epididymitis, hydrocoele

94
Q

Mx of testicular ca

A

NSGCT - orchidectomy ± adjuvant chemo (may use sole rx chemo if metastatic)
seminoma - orchidectomy + surveillance, high risk relapse = + chemo. Mets = chemoradiotherapy

95
Q

Classifications of lung cancer

A

Small cell

Non-small cell lung ca inc squamous cell, adenocarcinoma, large cell

96
Q

Most common type of lung ca

A

squamous cell

97
Q

lung ca with worst prognosis

A

small cell

98
Q

of non-smokers with lung ca, this subtype is most common

A

adenocarcinoma - most of pt with it were smokers but most common type in non-smokers

99
Q

Describe the characteristics of small cell lung ca - how does it tend to present?

A

tumour of small immature neuroendocrine cells, usually seen centrally around main bronchus. grows fast and metastasises early, commonly large tumours seen in multiple sites. sx from secretion of ectopic ACTH (cushings synd), ADH (hyponatraemia), paraneoplastic syndrome LEMS

100
Q

Signs and sx of lung ca?

A

dyspnoea, chest pain, haemoptysis, cough, UEW, anorexia, hoarseness (Pancoast), SVCO
O/E - fixed monophonic wheeze, supraclavicular/cervical lymphadenopathy, clubbing

101
Q

Paraneoplastic syndromes of squamous cell lung ca

A

PTHrP, HPOA, hyperthyroidism

102
Q

Paraneoplastic syndromes of adenocarcinoma?

A

gynaecomastia, HPOA

103
Q

What might you see on CXR in lung ca?

A

Nodule, hilar enlargement, consolidation, pneumothorax, pleural effusion, bony secondaries.

104
Q

How would you ix lung ca?

A

CXR
CT Chest with contrast for staging
If for curative rx ensure prior to this they have PET-CT, also endobronchial ultrasound guided trans bronchial biopsy/FNA

105
Q

Mx of NSCLC

A

Curative intent = radiotherapy/resection + adjuvant cisplatin-based combination chemo. Not suitable for surgery = chemotherapy ± immunotherapy

106
Q

management of small cell lung ca?

A

May consider surgery if T1/2

Cisplatin based combination chemotherapy ± radiotherapy if early.

107
Q

Side effects of immunotherapy

A

fatigue, change in mental state, headaches
GI - abdo pain, diarrhoea, ileus, perforation
skin - immune-related dermatitis, pruritis, dry skin, SJS/TEN
neuro - neuropathies, weakness, sensory changes, paraesthesia, MG, GBS
endocrine - hypophysitis, hypopituitarism, hypothyroidism, adrenal insufficiency
eye - blepharitis, conjunctivitis, uveitis, episcleritis
GCA, vasculitis, PMR, arthritis, haemolytic anaemia, hepatitis/hepatotoxicity, myocarditis

108
Q

Who is ALL most commonly seen in? briefly describe pathophysiology

A

children, rare in adults. Uncontrolled and dysregulated proliferation of immature lymphocytes can affect B or T cells. Bone marrow failure and tissue infiltration.

109
Q

Sx of ALL

A

BM failure - anaemia, thrombocytopenia (bleeding, bruising, petechiae), leukopenia (infections, pyrexia);
Bone pain from BM infiltration
hepatosplenomegaly ± testicular swelling.

110
Q

Ix ALL

A

FBC, film, clotting; BM trephine bx to confirm, LP for CNS involvement, CXR to exclude mediastinal mass

111
Q

What is AML and how does it present?

A

acute myeloid leukaemia, commonest acute leukaemia in adults. Rapidly progressive can be primary or secondary transformation of myeloproliferative disorder. Clonal proliferation of myeloid progenitor ‘blast’ cells.
Sx of BM failure, anaemia/neutropenia (may have raised WCC but functional deficiency), thrombocytopenia, splenomegaly, bone pain, DIC.

112
Q

How would you ix ?AML

A

FBC, blood film, BM bx, immunophenotyping and molecular methods. Auer rods on biopsy are diagnostic.

113
Q

Mx of AML

A

chemotherapy + hydration + allopurinol to prevent TLS
BM transplant
supportive

114
Q

What is CML?

A

Uncontrolled clonal proliferation of myeloid cells - see increased number of granulocytes of various maturation ± thrombocytosis, a MPD seen in middle age

115
Q

Sx of CML

A

Systemic - night sweats, fever, UEW, lethargy
MASSIVE HEPATOSPLENOMEGALY (abdo discomfort)
bleeding, bruising, gout, hyper viscosity

116
Q

Ix CML

A

FBC, blood film (raised WCC - polymorphic neutrophils, basophils and myelocytes; ± anaemia and low platelets), increased urate
cytogenetics of blood/BM - Philadelphia chromosome t(9;22) which results in BCR-ABL fusion gene which causes constitutive tyrosine kinase activity - good prognostic factor, present in >80%.

117
Q

Mx of CML

A

Imatinib (TK inhibitor) if Philadelphia chromosome - well tolerated, S/E nausea, cramps, headache, oedema, rash, arthralgia, myelosuppresion
hydroxyurea, interferon a

118
Q

What is CLL

A

chronic lymphocytic leukaemia - very common, usually an incidental finding on FBC in elderly men. Monoclonal proliferation of well differentiated B cells. May remain stable for years.

119
Q

Sx of CLL

A 
often none! 
constitutional - anorexia, UEW
more marked lymphadenopathy than CML
bleeding
infection
120
Q

Complications of CLL

A

anaemia, hypogammaglobulinaemia, warm AIHA, richters transformation to high grade NHL

121
Q

Ix of CLL

A

blood film (smudge cells), immunophenotyping (distinguish from NHL), positive DAT

122
Q

Rx CLL

A

mainly if symptomatic with chemotherapy, radiotherapy for LN/HSM, supportive care/
1/3 never progress, 1/3 progress with time, 1/3 actively progressing

123
Q

How does NHL present?

A

lymphadenopathy - classically painless, rubbery, at multiple sites
B sx - UEW, fever, night sweats
Splenomegaly
extranodal disease - gastric (dyspepsia, dysphagia, abdo pain), BM, CNS (nerve palsy), lung, skin

124
Q

Ix NHL

A

FBC (normocytic anaemia), LDH, ESR, blood film (r/o leukaemia), HIV test (risk factor)
LN excisions bx and Ann Arbor staging
Staging CT CAP
Other ix as clinical picture suggests - LP ?CNS involvement, BM bx for ?BM infiltration

125
Q

Mx of NHL

A

high grade - R-CHOP chemotherapy, flu and pneumococcal vaccines, BMT for relapse
low grade - watchful waiting

126
Q

How does Hodgkins lymphoma present?

A

bimodal age distribution peak in 3rd and 7th decades
Lymphadenopathy - painless, non tender, asymmetrical w/contiguous spread, alcohol-induced pain, mediastinal LN involvement can cause SVCO/bronchial obstruction
B sx - UEW, fever, night sweats
Itch, Pel-Ebstein fever (cyclical), hepato/splenomegaly

127
Q

Ix Hodgkins lymphoma

A

FBC, U+Es, LFTs, LDH, Ca, blood film
LN excision biopsy - reed Sternberg cells with owl eye nucleus
staging CT CAP
BM bx if B sx or stage 3/4

128
Q

Mx for Hodgkins lymphoma

A

chemo/radio/both - ABVD chemo

BMT for relapse

129
Q

What is multiple myeloma?

A

haematological malignancy characterised by clonal proliferation of plasma cells due to genetic mutations which occur as B cells differentiate into mature plasma cells. May see raised monoclonal IgG (less commonly IgA), free light chain (deposit in renal tubules, causing renal impairment; seen in urine Bence-Jones protein), clones produce IL6 which inhibit osteoblasts and activate osteoclasts (hypercalcaemia and lytic lesions)

130
Q

Sx of myeloma

A

CRABBI
hyperCalcaemia - constipation, nausea, anorexia, confusion
renal impairment - polydipsia, polyuria
anaemia - fatigue and pallor, due to BM crowding
bleeding (BM crowding -> thrombocytopenia)
bone lytic lesions (BM infiltration and IL6 mediated osteoclast activity - back pain, fragility #)
Infections - reduced normal Ig increasing susceptibility to infection

131
Q

How would you ix myeloma?

A

FBC, U+Es, Ca, serum electrophoresis (raised monoclonal IgA/IgG proteins), blood film (rouleaux ± cytopenia)
urine dipstick - increased specific gravity
urine electrophoresis- bence jones protein
BM aspiration and trephine bx - plasma cells 10%+
MRI/CT skeletal survey - punched out lytic lesions, vertebral collapse, fracture

132
Q

Mx of myeloma

A

relapsing and remitting malignancy not cured
induction therapy - chemotherapy + autologous bone marrow transplant if fit; 3-monthly blood tests and electrophoresis to assess for relapse. If relapse mono therapy chemo ± repeat BMT.
Sx relief - analgesia (avoid NSAIDs), anaemia (transfusions and EPO), zolendronic acid, annual flu vaccines, VTE prophylaxis

133
Q

When would you expect neutropenic sepsis to occur in a cancer patient?

A

usually 7-14d after chemo, but suspect in anyone who is unwell and has had chemo in the last 6wks

134
Q

Sx of neutropenic sepsis, and what WCC is neutropenic?

A

WCC<0.5*10^9
T>38, or T>37.5 taken on two occasions 30 mins apart; or less commonly T<36. Other clinically sig sepsis sx - EWS3+, tachypnoea, tachycardia, hypotension, low sats, oliguria/anuria, delirium/unresponsive.

135
Q

prophylaxis for neutropenic sepsis?

A

prophylactic fluoroquinolone - levofloxacin, if neutropenic sepsis is anticipated/high risk
GCSF is not routinely given for prophylaxis, maybe in select patients

136
Q

How would you manage neutropenic sepsis?

A

Low threshold - sx infection + chemo in last 6/52 = neutropenic sepsis until proven otherwise
Initiate sepsis 6 bundle (chemo red flag) - IV tazocin 4.5g QDS before blood results, ± vancomycin if ?indwelling venous catheter infection/sig mucositis. Mero if pen allergic. Still unwell and febrile after 48h ?change abx, after 4-6d ?fungal infection
Escalate to senior r/v and haem-onc r/v
May be a role for GCSF in select patients.

137
Q

what symptom/sign differentiates spinal cord mets from spinal cord compression?

A

neurological compromise seen in spinal cord compression

138
Q

Sx of spinal cord METS and how would you investigate this?

A

back pain - thoracic/cervical/unrelenting lumbar, may be worse on coughing, sneezing or straining, may be nocturnal, associated with tenderness on examination
Whole spine MRI within 1wk (urgent if ?compression)

139
Q

What is the usual mechanism of malignant spinal cord compression?

A

extradural compression as a result of vertebral body mets (usually thoracic)- most common in myeloma, lung, breast and prostate ca.

140
Q

clinical features of malignant spinal cord compression

A

Back pain - earliest and most common sx
sensory loss and numbness
motor weakness - usually in legs.
- Lesion above L1 = UMN sx in legs below level of lesion - spastic paresis, hypertonia, clonus, brisk reflexes and upgoing plantars
- Lesions below L1 = LMN sx, caudal equina sx - flaccid paraperesis and saddle anaesthesia.
bladder and anal sphincter involvement is a late sx

141
Q

What is your immediate management of malignant spinal cord compression?

A

Immobilise - complete bed rest and lie flat
PO dexamethasone 16mg STAT and 24h then on, + PPI for gastroprotection, + prophylactic LMWH and TEDs
contact MSCC co-ordinator, alert senior + clinical oncology r/v

142
Q

How would you investigate malignant spinal cord compression?

A

Urgent MRI whole spine - within 24h

if for surgery - bloods - FBC, U+Es, LFTs, bone profile inc calcium, clotting and G+S

143
Q

How is malignant spinal cord compression treated?

A

PO dexamethasone until surgery/radiotherapy started
Surgical decompression and stabilisation + adj radio
Radiotherapy within 24h

144
Q

What factors in patient history and examination would make them unlikely candidates for surgical mx MSCC?

A

clearly not fit for surgery - PS 3 or worse
life expectancy <3months
no motor function for >24h
multiple levels compression
radiosensitive malignancy without spinal instability - lymphoma, myeloma, SCLC, seminoma

145
Q

by what timepoint should radiotherapy be started in MSCC unless patient is for surgery?

A

within 24h presentation unless they have had complete paraplegia with loss of sphincter control for >48h at which point radiotherapy is for palliation of pain, and is not urgent.

146
Q

For how long should PO high dose steroids be taken in MSCC?

A

Start tapering dose as soon as the radiotherapy/surgery has taken place

147
Q

What is superior vena cava obstruction?

A

external pressure by tumour (most common), thrombus or direct invasion by tumour causes reduced venous return from the head, neck and upper limbs by obstructing the superior vena cava.

148
Q

What cancers is malignant SVCO most commonly associated with?

A

lung cancer (both NSCLC and SCLC) and NHL thought to account for 95% SVCO. Others = thymoma, germ cell neoplasm, mesothelioma, mediastinal LN mets from solid tumour e.g. breast

149
Q

How would SVCO typically present

A

Dyspnoea
swelling of face, neck and arms - Pembertons sx +
dilatation of chest wall veins + raised non-pulsatile JVP
signs of severe SVCO - headache, confusion, altered consciousness (cerebral oedema), stridor (laryngeal oedema)

150
Q

How would you manage SVCO?

A

Prop up, A to E assessment to stabilise - checking for hypoxia and O2 needs, alert senior and oncology r/v to guide mx
Life threatening sx - PO dexamethasone 16mg, balloon venoplasty and stenting
Non-life threatening sx - SCLC = chemo + radio, NSCLC = radiotherapy.

151
Q

which malignancies most commonly cause hypercalcaemia?

A

bony mets, myeloma, PTHrP in squamous cell lung ca

152
Q

How does hypercalcaemia of malignancy present?

A

Bones, groans, thrones and stones
abdo pain, N+V, constipation; polyuria, polydipsia; renal stones; depression, confusion; fragility fracture
anorexia + UEW, weakness, severe - htn, seizures, coma, arrhythmia, cardiomyopathy

153
Q

Ix ?hypercalcaemia of malignancy

A

bloods - corrected ca, U+Es, PTH, vitamin D, phosphate

ECG - shortened QTc

154
Q

Mx hypercalcaemia of malignancy

A

stop any thiazides and vit D/Ca supplements, ?stop nephrotoxins such as NSAIDs/ACEis/diuretics
aggressive rehydration with IV NaCl 0.9% 2-4L
severe/12-24h no improvement = add IV bisphosphonates (e.g. zoledronic acid)
definitive rx is rx ca

155
Q

What is the context in which tumour lysis syndrome is usually seen?

A

combination chemo treatment of rapidly proliferating tumours e.g. high grade lymphoma and leukaemia

156
Q

what electrolyte changes are associated with tumour lysis syndrome?

A

increased - urate, potassium, phosphate

decreased - calcium

157
Q

what are some of the consequences of TLS?

A

AKI, cardiac arrhythmia, seizure, sudden death

158
Q

How can you prevent tumour lysis syndrome?

A

Hydration and prophylactic IV rasburicase before chemo (up to 7d after); lower risk may give PO allopurinol.

159
Q

How does allopurinol prevent TLS?

A

xanthine oxidase inhibitor, reduces conversion of hypoxanthine to xanthine to uric acid; hypoxanthine and xanthine more water soluble so less likely to crystallise in tubules and precipitate AKI

160
Q

How does rasburicase prevent TLS?

A

rasburicase is a recombinant version of urate oxidase, it converts uric acid to water-soluble allantoin. Used for acute rx of TLS because it metabolises already formed urate, rather than preventing further build up as allopurinol does.

161
Q

In high risk patients you may give both allopurinol and rasburicase true or false?

A

false - allopurinol would reduce the efficacy of rasburicase

162
Q

How would you mx TLS?

A

Aggressive IV fluid hydration + IV rasburicase, rx electrolyte abnormalities
(high K - insulin/dextrose infusion, calcium gluconate to stabilise cardiac membrane if ECG changes; low ca = calcium gluconate)

163
Q

How would you start opioids in an opioid-naive patient in palliative care?

A

Start low and go slow, increase dose 30-50% every 24h - could start MR zomorph 15mg BD + oramorph 5mg PRN
prescribe laxative, anti-emetics if nausea persists
can use non-opioids as sparing agents

164
Q

S/E of opioids?

A

drowsy, N+V (usually improve in ~5d), constipation and dry mouth

165
Q

sx opioid toxicity?

A

sedation
respiratory depression
visual hallucinations and delirium
myoclonic jerks

166
Q

what opioids should be used in impaired renal function?

A

mild impairment could use oxycodone

severe impairment - fentanyl, alfentanil, buprenorphine (hepatic metabolism)

167
Q

What fraction of daily dose do you give PRN?

A

1/6

168
Q

conversion rate from oral codeine or tramadol to oral morphine?

A

dose/10

169
Q

conversion rate from oral morphine to oral oxycodone?

A

dose/1.5

170
Q

conversion rate from PO morphine to SC morphine?

A

dose/2

171
Q

conversion rate from PO morphine to SC diamorphine?

A

dose/3

172
Q

Causes of N+V in cancer patient?

A 
chemo/drugs
constipation
GI obstruction
hypercalcaemia
oral candidiasis
severe pain
infection
renal failure
173
Q

How would reduced gastric motility N+V present? How would you rx this?

A

feeling of fullness and distension, regurgitation, vomiting large volumes which relieves nausea, epigastric discomfort, reduced appetite, hiccups
Metoclopramide - blocks CTZ, peripheral pro kinetic (also domperidone)

174
Q

How would chemical N+V present? How would you rx this?

A

persistent and often severe nausea unrelieved by vomiting, aggravated by sight/smell of food, drowsiness, confusion
haloperidol

175
Q

How would you rx bowel obstruction or raised ICP related N+V?

A

cyclizine - centrally acting, antihistaminergic and anticholinergic

176
Q

Rx anticipatory N+V

A

short-acting benzodiazepine e.g. lorazepam

177
Q

post-op/radiotherapy related N+V

A

ondansetron - 5ht3 antagonist acts in CTZ

178
Q

What laxative would you prescribe with strong opioids?

A

stimulant laxative - senna

179
Q

how would you treat constipation with faecal loading

A

stimulant laxative (Senna) + osmotic agent (macrogol/lactulose) or stool softener docusate

180
Q

How would you rx breathlessness in palliative care?

A

simple measures - improve air circulation in room, pursed lip breathing, positioning - sat up, leaning forward, relax shoulders; reassure; exercise within limits
medication - IR oramorph to reduce respirator drive
if sig anxiety component could consider lorazepam second line

181
Q

how would you rx intractable hiccups?

A

1st line chlorpromazine (low potency typical antipsychotic)

2nd - haloperidol/gabapentin

182
Q

rx agitation and confusion in palliative care?

A

correct any underlying cause e.g. hypercalcaemia, infection, urinary retention, medications
1st line - haloperidol
terminal agitation - midazolam

183
Q

rx secretions in palliative care?

A

reassure loved ones it is not uncomfortable to patients, more distressing for them due to noise
avoid fluid overload
glycopyrronium bromide/ hyoscine hydrobromide

184
Q

give examples of a typical set of anticipatory medications prescribed in palliative care

A

assuming none of these medications are already in place (otherwise would stick with the dose and class of drug they’ve found works)
SC morphine 2.5-5mg - pain
SC midazolam 2.5-5mg - agitation and confusion
SC levomepromazine 2.5-5mg - N+V
SC glycopyrronium bromide 200-400mcg - resp secretions

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