Cancer

Question 1

Referral recommendation for skin lesion suspected of a basal cell carcinoma?

Answer 1

• consider routine referral
• only 2ww (suspected ca referral) referral if concern that delay may have impact eg. due to factors such as site or size

Question 2

When to refer pt using suspected ca pathway referral (appointment within 2w) for melanoma?

Answer 2

1) suspicious pigmented skin lesion with weighted 7 point checklist score of 3 or more

or

2) dermoscopy suggests melanoma

3) pigmented or non-pigmented lesion that suggests nodular melanoma

4) suspected SCC

5) BCC but concern that delay will have signif impact eg. due to size or site

Question 3

Pigmented lesion on the skin?

Answer 3

?melanoma

Question 4

Can get what type of melanomas rarely?

Answer 4

nodular and amelanotic

Question 5

What checklist is used to assess pigmented skin lesions?

Answer 5

7-point checklist

Question 6

Melanoma may present when?

Answer 6

after spread to regional lymph nodes or wider mets

Question 7

Main method to diagnose melanoma?

Answer 7

excision biopsy in secondary care

Question 8

Raised lesion on skin?

Answer 8

?SCC

Question 9

Diagnose SCC?

Answer 9

possible to visually but confirm by excision biopsy

Question 10

Ulcer with raised rolled edge; prominent fine blood vessels around a lesion or nodule on the skin (pearly or waxy)?

Answer 10

Basal cell carcinoma

Question 11

Diagnosis of BCC?

Answer 11

possible visually but confirm by excision biopsy

Question 12

7-point checklist for suspected melanoma?

Answer 12

Major (2 points each):
- change in size
- irregular shape
- irregular colour

Minor (1 each):
- largest diameter 7mm+
- inflam
- oozing
- change in sensation

Question 13

Most common type of ca in Western world?

Answer 13

BCC

Question 14

BCC characteristics?

Answer 14

• lesions also called Rodent ulcers
• slow growth
• local invasion
• mets v rare

Question 15

Most common type of BCC?

Answer 15

nodular

Question 16

Nodular BCC?

Answer 16

• sun exposed sites eg. head, neck
• initially= pearly, flesh coloured papule with telangiectasia
• later= ulcerate leaving central crater

Question 17

Mx options for BCC?

Answer 17

• surgical removal
• curettage
• cryotherapy
• topical cream= imiquimod, fluorouracil
• radiotherapy

Question 18

Bladder ca commonly affects who?

Answer 18

males 50-80yrs

Question 19

RFs for bladder ca?

Answer 19

• male
• current or previous (within 20yrs) smokers
• exposure to hydrocarbons eg. 2-Napthylamine
• chronic bladder inflam from Schistosomiasis infection= SCC
  -rubber manufacture
• cyclophosphamide

Question 20

Exposure to hydrocarbons eg. benzidine or 2-Naphthylamine from exposure to aniline dyes (eg. working in printing and textile industry) increases the risk of what?

Answer 20

bladder ca

Question 21

examples of benign tumours of the bladder? (uncommon)

Answer 21

• inverted urothelial papilloma
• nephrogenic adenoma

Question 22

Examples of bladder malignancies?

Answer 22

• Urothelial (transitional cell) carcinoma (>90%)
• SCC (1-7% expect is higher in regions affected by schistosomiasis- rare in UK)
• Adenocarcinoma

Question 23

Most common bladder malignancy?

Answer 23

urothelial (transitional cell) carcinoma (>90%)

Question 24

Urothelial carcinomas may arise as what?

Answer 24

solitary lesions or may be multifocal causing ‘field change’ within the urothelium

Question 25

Growth pattern of urothelial carcinomas?

Answer 25

- 70% have papillary growth pattern= superficial and better prognosis - mixed papillary and solid growth or pure solid growth= more prone to local invasion and may be higher grade, worse prognosis

Question 26

Those with T3 disease or worse in urothelial carcinoma have a 30%+ risk of what?

Answer 26

regional or distant lymph node metastasis

Question 27

TNM staging for bladder cancer= T?

Answer 27

T0= No evidence of tumour Ta= Non invasive papillary carcinoma T1= Tumour invades sub epithelial connective tissue T2a= Tumor invades superficial muscularis propria (inner half) T2b= Tumor invades deep muscularis propria (outer half) T3= Tumour extends to perivesical fat T4= Tumor invades any of the following: prostatic stroma, seminal vesicles, uterus, vagina T4a= Invasion of uterus, prostate or bowel T4b= Invasion of pelvic sidewall or abdominal wall

Question 28

TNM staging of bladder cancer: N?

Answer 28

N1= Single regional lymph node metastasis in the true pelvis (hypogastric, obturator, external iliac, or presacral lymph node) N2= Multiple regional lymph node metastasis in the true pelvis (hypogastric, obturator, external iliac, or presacral lymph node metastasis) N3= Lymph node metastasis to the common iliac lymph nodes

Question 29

Painless macroscopic haematuria?

Answer 29

?bladder ca

Question 30

CP of bladder ca?

Answer 30

- painless marcoscopic haematuria - incidential microscopic haematuria= 10% females >50yrs found to have malignancy after infection excluded

Question 31

Staging for bladder ca?

Answer 31

1) cystoscopy and biopsy or TURBT= histological diagnosis and depth of invasion 2) Pelvic MRI= locoregional spread 3) CT= distant disease 4) PET CT= nodes of uncertain significance

Question 32

Tx for bladder ca?

Answer 32

superficial lesions= TURBT in isolation recurrences or higher grade/risk on histology= intravesical chemo T2 disease= surgery (radical cystectomy and ileal conduit) or radical radiotherapy

Question 33

Prognosis of bladder ca?

Answer 33

T1 90% T2 60% T3 35% T4a 10-25% Any T, N1-N2 30%

Question 34

How is cancer classified into types?

Answer 34

based on origin and characteristics of the abnormal cells

Question 35

Carcinoma definition?

Answer 35

arises from epithelial cells that line internal organs and external surfaces

Question 36

Types of carcinoma?

Answer 36

- adenocarcinoma - SCC - BCC - transitional cel carcinoma

Question 37

Most common types of cancer?

Answer 37

carcinoma

Question 38

Types of carcinoma: adenocarcinoma definition?

Answer 38

develops in glandular tissues eg. breast, prostate, colon, pancreas

Question 39

Types of carcinoma: SCC definition?

Answer 39

found in squamous cells eg. skin or lining of organs, for example lungs, oesophagus

Question 40

Types of carcinoma: BCC definition?

Answer 40

form of skin cancer that starts in the basal cells

Question 41

Types of carcinoma: transitional cell carcinoma definition?

Answer 41

arises in lining of the bladder, ureters and renal pelvis

Question 42

Sarcoma definition?

Answer 42

develops in connective or supportive tissues such as bone, muscle, fat, cartilage and blood vessels less common than carcinomas but more aggressive

Question 43

Types of sarcoma?

Answer 43

- osteosarcoma - chondrosarcoma - liposarcoma - leiomyosarcoma

Question 44

Types of sarcoma: osteosarcoma definition?

Answer 44

originates in bone

Question 45

Types of sarcoma: chondrosarcoma definition?

Answer 45

arises in cartilage

Question 46

Types of sarcoma: liposarcoma definition?

Answer 46

develops from fat tissue

Question 47

Types of sarcoma: leiomyocarcoma definition?

Answer 47

develops in smooth muscle tissue

Question 48

Leukemia definition?

Answer 48

cancers of the blood-forming tissues, incl. bone marrow and lymphatic system

Question 49

Types of leukemia?

Answer 49

- Acute Lymphoblastic Leukemia (ALL) - Acute Myeloid Leukemia (AML) - Chronic Lymphocytic Leukemia (CLL) - Chronic Myeloid Leukemia (CML)

Question 50

Types of leukemia: Acute Lymphoblastic Leukemia (ALL) definition?

Answer 50

affects lymphoid cells, common in children

Question 51

Types of leukemia: Acute Acute Myeloid Leukemia (AML) definition?

Answer 51

affects myeloid cells, more common in adults

Question 52

Types of leukemia: Chronic Lymphocytic Leukemia (CLL) definition?

Answer 52

slow-growing form affecting lymphoid cells

Question 53

Types of leukemia: Chronic Myeloid Leukemia (CML) definition?

Answer 53

affects myeloid cells, progresses slowly

Question 54

Lymphoma definition?

Answer 54

ca of the lymphatic system, which is part of the immune system relatively common, esp non-Hodgkin

Question 55

Types of lymphoma?

Answer 55

- Hodgkin Lymphoma (Hodgkin's disease) - Non-Hodgkin Lymphoma (NHL)

Question 56

Types of lymphoma: Hodgkin Lymphoma definition?

Answer 56

characterised by presence of Reed-Sternberg cells

Question 57

Types of lymphoma: Non-Hodgkin Lymphoma definition?

Answer 57

diverse group of lymphomas that don't have Reed-Sternberg cells; including B-cell and T-cell lymphomas

Question 58

Myeloma definition?

Answer 58

ca of plasma cells, type of WBC in bone marrow rare form of ca, affects mainly older adults

Question 59

Type of myeloma?

Answer 59

multiple myeloma

Question 60

Type of myeloma: multiple myeloma definition?

Answer 60

most common form, affecting many areas of body incl. bones and kidneys (Old CRAB)

Question 61

Melanoma definition?

Answer 61

ca than originates in melanocytes, the cells that produce the pigment melanin in the skin less common than other skin ca (B/SCC) but more aggressive

Question 62

Types of melanoma?

Answer 62

- cutaneous melanoma - ocular melanoma

Question 63

Types of melanoma: cutaneous melanoma definition?

Answer 63

starts in skin

Question 64

Types of melanoma: ocular melanoma?

Answer 64

rare form that starts in the eye

Question 65

Central Nervous System (CNS) cancers definition?

Answer 65

ca that begin in brain or spinal cord can be mild or highly malignant, glioblastoma one of most severe

Question 66

Common types of CNS cancers?

Answer 66

- glioblastoma - astrocytoma - meningioma

Question 67

Types of CNS cancers: glioblastoma definition?

Answer 67

highly aggressive form of brain cancer

Question 68

Types of CNS cancers: astrocytoma definition?

Answer 68

originates in star-shaped brain cells called astrocytes

Question 69

Types of CNS cancers: meningioma definition?

Answer 69

affects meninges, the protective layers around brain and spinal cord

Question 70

Germ Cell tumours definition?

Answer 70

arises from the cells that give rise to sperm or eggs (germ cells) most common in adolescents and young adults

Question 71

Common locations of germ cell tumours?

Answer 71

usually develop in testes (testicular ca) or ovaries (ovarian germ cell tumours) but can form in other parts of body eg. brain

Question 72

Neuroendocrine tumours definition?

Answer 72

arise from cells that release hormones into the blood in response to signals from NS rare and can be slow-growing, some can be aggressive

Question 73

Types of neuroendocrine tumours?

Answer 73

- carcinoid tumours - pheochromocytoma

Question 74

Types of neuroendocrine tumours: carcinoid tumours?

Answer 74

type of neuroendocrine tumour commonly found in GI tract and lungs

Question 75

Types of neuroendocrine tumours: pheochromocytoma?

Answer 75

typically arises in adrenal glands

Question 76

Blastoma definition?

Answer 76

typically arises in embryonic tissue or immature cells, usually seen in children

Question 77

Common types of blastoma?

Answer 77

- retinoblastoma - neuroblastoma - hepatoblastoma

Question 78

Common types of blastoma: retinoblastoma definition?

Answer 78

ca of the retina, typically in young children

Question 79

Common types of blastoma: hepatoblastoma definition?

Answer 79

rare liver ca in children

Question 80

Common types of blastoma: neuroblastoma definition?

Answer 80

starts in immature nerve cells, often in adrenal glands

Question 81

Mesothelioma definition?

Answer 81

rare ca that affects lining of lungs, abdo or heart; often linked to asbestos exposure

Question 82

Thyroid ca definition?

Answer 82

ca that forms in thyroid gland, with types like papillary, follicular, medullary and anaplastic thyroid ca

Question 83

Types of cancers?

Answer 83

- carcinoma - sarcoma - leukemia - lymphoma - myeloma - melanoma - CNS ca - germ cell tumours - neuroendocrine tumours - blastoma - mesothelioma - thyroid cancer

Question 84

What is the TNM staging used for?

Answer 84

to classify and describe details about the ca size, location and degree of spread, helps in planning treatment and estimating prognosis primarily for solid tumours eg. breast, lung, colon

Question 85

TNM staging: what is T?

Answer 85

Tumour size and extent of the primary tumour

Question 86

TNM staging: what is N?

Answer 86

Nodes indicates whether the cancer has spread to nearby lymph nodes (local spread)

Question 87

TNM staging: what is M?

Answer 87

Metastasis refers to whether the ca has spread (metastasised) to distant organs or tissues (distant spread)

Question 88

What would Tx, Nx or Mx mean in TNM staging?

Answer 88

can't be assessed

Question 89

Cancer stage grouping?

Answer 89

use TNM to combine into overall stage grouping: stage I, II, III or IV some may have substage eg. IA or IIB depending on additional factors eg. tumour grade or specific molecular markers

Question 90

Cancer stages?

Answer 90

0= cancer in situ (localised and not spread) I= small tumour, localised, without spread to lymph nodes II= large tumour or has spread to nearby lymph nodes, but no distant mets III= more advanced local/regional spread to lymph nodes or nearby tissues, but no distant mets IV= metastatic ca- has spread to distant parts of the body

Question 91

TNM staging: what if the difference between N and M if in N the ca is still spreading?

Answer 91

N= local or regional involvement within the lymphatic system M= ca has spread beyond original area and reached distant organs or tissues so N is not considered metastasis

Question 92

Brain and CNS cancers typically affect who?

Answer 92

children and young people

Question 93

Symptoms of brain and CNS cancers?

Answer 93

new onset seizures, headaches, nausea, drowsiness, visual change, personality change

Question 94

Ix/Mx for brain and CNS cancers in adults?

Answer 94

urgent direct access of MRI of brain or CT if MRI contraindicated, within 2w, in adults with progressive, sub-acute loss of central neurological function

Question 95

Ix/Mx for brain and CNS cancers in children/young people?

Answer 95

very urgent referral (within 48hrs) in children with newly abnormal cerebellar or other central neurological function

Question 96

Most common intracranial tumours in adults?

Answer 96

brain metastases

Question 97

What do brain mets signify?

Answer 97

advanced disease state with significant impact on morbidity and mortality

Question 98

What primary cancers are most likely to metastasise to the brain?

Answer 98

Lung (40-50%) Breast (15-25%) Melanoma (5-20%) Renal (5-10%) Colorectal

Question 99

Pathways of spread for brain mets?

Answer 99

- hematogenous spread (most common)= via arterial circulation - lymohatic (less common)= typically involves leptomeningeal carcinomatosis - direct extension (rare)= from head and neck cancers

Question 100

CP of brain mets?

Answer 100

- headache (worse in morning) - neuro deficit (eg. hemiparesis, aphasia) - seizures - cognitive and behavioural changes - symptoms of ICP= N&V, altered consciousness

Question 101

Diagnosis of brain mets?

Answer 101

GOLD= MRI with contrast for number, size and location - Biopsy confirms in primary ca site is unknown or imaging inconclusive

Question 102

Aim of Mx of brain mets?

Answer 102

controlling symptoms, reducing tumour burden and improving QOL

Question 103

Mx for brain mets?

Answer 103

- supportive care - radiation therapy - systemic therapy - surgical resection

Question 104

Mx for brain mets- supportive care?

Answer 104

- corticosteroids eg. dexamethasone= reduce peritumoral oedema and control symptoms eg. headache - anticonvulsants= seizures - palliative care for end-of-life

Question 105

Mx for brain mets- radiation therapy, when is it used?

Answer 105

Whole Brain Radiotherapy (WBRT)= for multiple mets but associated with notable cognitive decline Stereotactic Radiosurgery (SRS)= if 1-3 mets; offers high dose radiation with minimal damage to surrounding tissues

Question 106

Mx for brain mets: systemic therapy?

Answer 106

chemotherapy, targeted therapy or immunotherapy depending on primary tumour type and molecular characteristics used to better systemic control and penetration of blood brain barrier

Question 107

Mx for brian mets: when is surgical resection indicated?

Answer 107

for accessible lesions causing signif mass effect or when histologic diagnosis required; improves neuro function and allows more effective adjuvant therapy

Question 108

Prognosis of brain mets?

Answer 108

- generally poor but improving with targeted therapies and precision medicine - median survival ranges= several months to over a yr - depends on Tx and tumour biology

Question 109

What drug class in tamoxifen?

Answer 109

selective oestrogen receptor modulator (SERM)= acts as an oestrogen receptor antagonist and partial agonist

Question 110

Drug used in the Mx of oestrogen receptor positive breast ca?

Answer 110

tamoxifen

Question 111

Adverse effects of tamoxifen (SERM)?

Answer 111

- vaginal bleeding, amenorrhoea - hot flushes (3% stop taking due to this) - VTE - endometrial ca

Question 112

What drug class are anastrozole and letrozole?

Answer 112

aromatase inhibitors= reduces peripheral oestrogen synthesis

Question 113

Drug used in the Mx of ER +ve breast ca in postmenopausal women?

Answer 113

Anastrozole

Question 114

Why is anastrozole used for ER +ve breast ca in postmenopausal women?

Answer 114

it is an aromatase inhibitor that reduces peripheral oestrogen synthesis; important as aromatisation accounts for majority of oestrogen production in postmenopausal women

Question 115

Adverse effects of anastrozole (aromatase inhibitor)?

Answer 115

- osteoporosis (DEXA scan) - hot flushes - arthralgia, myalgia - insomnia

Question 116

What should be done when initiating pt on aromatase inhibitors for breast ca?

Answer 116

DEXA scan due to risk of osteoporosis

Question 117

Malignant breast lump is usually what?

Answer 117

painless, but pain can occur

Question 118

Nipple symptoms of breast ca?

Answer 118

shape in shape, bleeding, tethering, peau d'orange

Question 119

Diagnosis of breast ca?

Answer 119

mammography and core biopsy

Question 120

Who to refer for suspected ca referral (2ww) for breast ca?

Answer 120

- 30yrs+ with unexplained breast lump with or without pain - 50yrs+ and any of: discharge, retraction, changes of concern; in one nipple

Question 121

Consider a suspected ca referral (2ww) for breast ca in who?

Answer 121

- skin changes that suggest breast ca - 30yrs+ with unexplained lump in axilla

Question 122

Non-urgent referral for breast ca in who?

Answer 122

<30yrs with unexplained breast lump with or without pain

Question 123

Symptoms suggestive of breast ca?

Answer 123

- axillary lump (unexplained) - breast lump (unexplained) - nipple changes - skin changes - DVT

Question 124

Types of referrals for ca?

Answer 124

- immediate= acute admission or referral within few hrs - urgent= within 2w - very urgent= within 48hrs - non-urgent= general referral - suspected ca pathway= within national target for ca referral eg. 2ww

Question 125

Most common type of breast ca?

Answer 125

invasive ductal carcinoma

Question 126

Pathological assessment of breast ca involves what?

Answer 126

assessment of the tumour and lymph nodes- normally using sentinel lymph node biopsy (minimises morbidity of an axillary dissection)

Question 127

Reconstruction for breast ca?

Answer 127

- option following any resectional procedure but type tailored to age and co-morbidities - common: latissimus dorsi myocutaneous flap and sub pectoral implants - want to avoid prosthesis= TRAM or DIEP flaps

Question 128

Surgical options for breast ca: when is mastectomy indicated?

Answer 128

- multifocal tumour - central tumour - large lesion in small breast - DCIS >4cm - Pt choice

Question 129

Surgical options for breast ca: when is wide local excision indicated?

Answer 129

- solitary lesion - peripheral tumour - small lesion in large breast - DCIS <4cm - pt choice

Question 130

Large breast tumour that is unsutiable for breast conserving surgery?

Answer 130

mastectomy

Question 131

How may central lesions in breast ca be managed?

Answer 131

breast conserving surgery where an acceptable cosmetic result may be obtained- rare in small breasts but more likely in large breast

Question 132

Local recurrence rate of breast ca whatever surgery option was chosen?

Answer 132

5% or less at 5yrs

Question 133

What index can be used to give indication of survival in breast ca?

Answer 133

Nottingham Prognostic Index

Question 134

Calculation of Nottingham Prognostic Index?

Answer 134

Tumour Size x 0.2 + Lymph node score +Grade score

Question 135

Nottingham Prognostic Index- lymph node and grade score score?

Answer 135

Score 1= 0 lymph nodes involved= Grade 1 Score 2= 1-3 lymph nodes= Grade 2 Score 3= >3= Grade 3

Question 136

Prognosis from Nottingham Prognostic Index for breast ca?

Answer 136

score 2-2.4= 93% 5yr survival score 2.5-3.4= 85% 3.5-5.4= 70% >5.4= 50%

Question 137

What does Nottingham Prognostic Index for breast ca not include that can affect survival?

Answer 137

vascular invasion and receptor status

Question 138

Prior to surgery for breast ca, what determines Mx?

Answer 138

presence or absence of lymphadenopathy

Question 139

Mx of breast ca: women with no palpable axillary lymphadenopathy at presentation should have what?

Answer 139

pre-op axillary USS before primary surgery if -ve then sentinel node biopsy to assess nodal burden

Question 140

Mx of breast ca: women with palpable axillary lymphadenopathy at presentation should have what?

Answer 140

axillary node clearance at primary surgery

Question 141

In the Mx of breast ca, what may happen if pt has axillary node clearance at primary surgery?

Answer 141

may lead to arm lymphedema and functional arm impairment

Question 142

Mx of breast ca: when is whole breast radiotherapy recommended?

Answer 142

- all women after wide-local excision (can reduce recurrence by 2/3rds) - if had mastectomy and have T3-T4 tumours - if had mastectomy and have 4 or more +ve axillary nodes

Question 143

When is adjuvant hormonal therapy offered for breast ca Mx?

Answer 143

if tumours are positive for hormone receptors

Question 144

What receptors are tested for breast ca at time of initial histopathological diagnosis?

Answer 144

oestrogen receptor (ER), progesterone receptor (PR) or human epidermal growth factor receptor 2 (HER2)

Question 145

Adjuvant hormonal therapy for breast ca after surgery if +ve for hormone receptors?

Answer 145

Tamoxifen= men and premenopausal women with ER +ve invasive breast ca Aromatase inhibitor eg. anastrozole= postmenopausal women with ER +ve

Question 146

Biological therapy for breast ca?

Answer 146

Trastuzumab (Herceptin) for HER2 positive breast ca 3 w intervals for 1yr in combination to surgery, chemo, endocrine therapy and radiotherapy as appropriate

Question 147

Chemotherapy for breast ca?

Answer 147

Regimen with a taxane and an anthracycline

Question 148

Side effects of chemo for breast ca (regimen that contains a taxane and an anthracycline)?

Answer 148

neuropathy, neutropenia and hypersensitivity

Question 149

When to give bisphosphonate therapy in the Mx of breast ca?

Answer 149

zoledronic acid as adjuvant therapy to post-menopausal women with node +ve invasive breast ca or node -ve but high risk recurrence

Question 150

What to offer pts who are not receiving bisphosphonates who are starting aromatase inhibitors, treatment induced menopause or starting ovarian ablation/suprression therapy in Mx of breast ca?

Answer 150

DEXA scan

Question 151

What radiotherapy is offered for pts with invasive breast ca having partial breast, whole breast or chest-wall radiotherapy without regional lymph node irradiation after breast conserving surgery or mastectomy?

Answer 151

external beam radiotherapy: 26Hy in 5 fractions over 1w

Question 152

Chemo Mx for people with ER/PR/HER2 negative (triple negative) invasive breast ca?

Answer 152

neoadjuvant chemo regimen contains a platium and an anthracycline

Question 153

Genetic testing for breast ca?

Answer 153

BRCA1 and BRCA2 mutations if under 50yrs with triple-negative breast ca and also those with no FHx of breast/ovarian ca

Question 154

Mx for Paget's disease?

Answer 154

Offer breast-conserving surgery with removal of the nipple–areolar complex as an alternative to mastectomy for people with Paget's disease of the nipple that has been assessed as localised.

Question 155

Breast reconstruction options for breast ca?

Answer 155

immediate reconstruction (during mastectomy surgery) or delayed in another operation

Question 156

Cx of local treatment of breast ca?

Answer 156

- lymphoedema= arm, breast or chest wall - arm and shoulder mobility= so carry out upper limb exercises - menopausal symptoms

Question 157

HRT and breast ca?

Answer 157

- stop HRT - don't offer HRT if Hx of breast ca - consider SSRI to relieve symptoms if not on tamoxifen

Question 158

What can you consider for premenopausal women with ER +ve invasive breast ca?

Answer 158

ovarian function suppression to reduce risk of recurrence

Question 159

How long to take tamoxifen or aromatase inhibitor for breast ca?

Answer 159

5yrs can continue taking to reduce recurrence

Question 160

Can pt get pregnant on tamoxifen?

Answer 160

not while taking it or within 2m of stopping

Question 161

Follow up imaging for pt who has been treated for breast ca?

Answer 161

annual mammography for 5yrs or longer until they enter screening programme

Question 162

Summary of Mx of breast ca?

Answer 162

- Genetic testing= BRCA1 & BRCA2 - Hormone receptor testing= ER, PR, HER2 - Pre-op= USS axilla (if abnormal then USS guided needle sampling) - Surgery= mastectomy or breast conserving surgery. Also axillary lymph node clearance or SLNB (if no evidence of LN invol on USS) - Breast reconstruction= immediate or delayed - Endocrine therapy= tamoxifen (ER) or anastrasole (PR) (and maybe extended endocrine therapy- >5yrs) - Ovarian function supression - Adjuvant chemo - Radiotherapy= after breast conserving surgery or after mastectomy who are high risk of recurrence (eg. node +ve invasive breast ca) - Biological theraoy= transtuzumab (HER2) - Bisphosphonate?

Question 163

Risk factors for breast ca?

Answer 163

- BRCA1, BRCA2 genes - 1st degree relative premenopausal relative with breast cancer (e.g. mother) - nulliparity, 1st pregnancy > 30 yrs (twice risk of women having 1st child < 25 yrs) - early menarche, late menopause - combined hormone replacement therapy, combined oral contraceptive use - past breast cancer - not breastfeeding - ionising radiation - p53 gene mutations - obesity - previous surgery for benign disease (?more follow-up, scar hides lump)

Question 164

BRCA1 and BRCA2 gene increase risk of what?

Answer 164

40% lifetime risk of breast/ovarian ca

Question 165

What is used for breast screening?

Answer 165

mammography radiography- detects small changes in breast before other S&S of breast ca develop

Question 166

How often is the breast screening programme?

Answer 166

every 3yrs

Question 167

When are women offered breast screening?

Answer 167

aged 50-70 should receive 1st invitation within 3yrs of 50th bday

Question 168

Can women >70yrs get breast screening?

Answer 168

excluded from programme but can get screening by self-referral to local breast screening service

Question 169

Who may be eligible for breast screening <50yrs?

Answer 169

if have increased risk eg. strong FHx

Question 170

What info should women be given before participating in breast screening programme

Answer 170

- benefits and harms - organisation of screening - where it is done - preparing for mammogram - what to expect during appointment

Question 171

Benefits of breast screening?

Answer 171

- early detection of breast ca - reduction in mortality

Question 172

Harms of breast screening?

Answer 172

- over-diagnosis & unnecessary Tx - false positive mammograms - false reassurance so incorrect diagnosis - pain and discomfort - psychological distress, anxiety following a false positive

Question 173

What people should be referred to breast clinic for screening from younger age?

Answer 173

- one first-degree female relative diagnosed with breast cancer at younger than age 40 years, or - one first-degree male relative diagnosed with breast cancer at any age, or - one first-degree relative with bilateral breast cancer where the first primary was diagnosed at younger than age 50 years, or - two first-degree relatives, or one first-degree and one second-degree relative, diagnosed with breast cancer at any age, or - one first-degree or second-degree relative diagnosed with breast cancer at any age and one first-degree or - second-degree relative diagnosed with ovarian cancer at any age (one of these should be a first-degree relative), or - three first-degree or second-degree relatives diagnosed with breast cancer at any age

Question 174

What if mammogram comes back suspicious for breast ca?

Answer 174

1) mammogram 2) USS 3) if imaging concerning then biopsy: core needle biopsy 4) Pathology report= type of ca, hormone receptor status and grade 5) Staging= sentinel lymph node biopsy, CT

Question 175

Types of breast cancer?

Answer 175

- invasive ductal carcinoma - invasive lobular carcinoma - ductal carcinoma-in situ (DCIS) - lobular carcinoma-in-situ (LCIS)

Question 176

Most breast cancers arise from what?

Answer 176

Duct tissue (most) or lobular tissue (so ductal or lobular carcinoma) carcinoma-in-situ= local- hasn't spread invasive= spread

Question 177

Invasive ductal carcinoma?

Answer 177

most common type breast ca (recently been named as No Special Type (NST); lobular and other rarer types classed as Special Type)

Question 178

Rarer types of breast cancer?

Answer 178

- Medullary breast cancer - Mucinous (mucoid or colloid) breast cancer - Tubular breast cancer - Adenoid cystic carcinoma of the breast - Metaplastic breast cancer - Lymphoma of the breast - Basal type breast cancer - Phyllodes or cystosarcoma phyllodes - Papillary breast cancer

Question 179

Other types of breast cancer that may be associated with underlying lesions (eg. other types of breast ca)?

Answer 179

- Paget's disease of the nipple - Inflammatory breast ca

Question 180

Paget's disease of the nipple?

Answer 180

Eczematoid change of nipple associated with underlying breast ca 1-2% will have breast ca 1/2 have associated underlying mass lesion and 90% have invasive carcinoma Some without mass lesion will have underlying carcinoma and some will have carcinoma in situ

Question 181

Inflammatory breast ca?

Answer 181

cancerous cells block lymph drainage resulting in inflamed appearance of breast rare

Question 182

Most cases of cervical ca originate from where?

Answer 182

ecto- or endocervical mucosa in the cervical transformation zone

Question 183

Cervical ca: what usually regressess?

Answer 183

low-grade dysplasia (cervical intraepithelial neoplasia 1- CIN1) but can progress to high grade dysplasia

Question 184

When does cervical ca occur?

Answer 184

when high grade dysplastic lesions extend beyond the basement membrane of the cervical epithelium

Question 185

2 most common types of cervical ca?

Answer 185

squamous cell carcinoma and adenocarcinoma

Question 186

Main cause of cervical ca?

Answer 186

persistent infection- HPV (human papillomavirus)

Question 187

How is HPV trsansmitted?

Answer 187

sexual intercourse

Question 188

What subtype of HPV account for 2/3rds of cervical ca?

Answer 188

16 and 18; 33 HPV detected in 99% cervical ca

Question 189

Only about 10% of all HPV infections become persistent, which puts women at risk of developing what?

Answer 189

precancerous cervical lesions

Question 190

Time interval between HPV infection and development of precancerous lesions?

Answer 190

1-10yrs

Question 191

RFs for development of cervical ca?

Answer 191

- increased exposure to HPV (eg. early age 1st intercourse) - impaired immune response to HPV infection eg. HIV or solid organ transplant - smoking - high parity - lower socioeconomic status - COCP

Question 192

Peak incidence rate of cervical ca?

Answer 192

30-34yrs

Question 193

Cx of cervical ca?

Answer 193

- psychosocial issues - sexual dysfunction - early menopause - loss of fertility - bladder & bowel dysfunction - pelvic or other pain - renal failure - haemeorrhage - fistuale - lymphoedema

Question 194

CP of cervical ca?

Answer 194

- abnorm vaginal bleeding or discharge (not 2 to infection or other causes) - pelvic pain +/- dyspareunia - postmenopausal bleeding not due to HRT - abnorm cervix on exam= inflamed or friable, contact bleeding, visible ulcerating or necrotic lesion - symptoms of advanced disease (rare)

Question 195

What to do if suspect cervical ca?

Answer 195

- urgent suspected ca referral (2ww) to colposcopy/gynaecology oncology - abdo, speculum and bimanual pelvic exam (may look normal) - assess for lymphadenopathy= inguinal and supraclavicular

Question 196

Prevention of cervical ca?

Answer 196

- national cervical screening programme - national HPV vaccination programme - consistent use of condoms and practicing safe sex

Question 197

Differential diagnosis for cervical ca?

Answer 197

- STI - Endometrial ca - endometriosis - ectropion or cervical polyp - hormonal contraception (in 1st 3m or 3-6m with coil or implant)

Question 198

2 ww referral for cervical ca?

Answer 198

All women with unexplained postmenopausal bleeding should be referred to gynaecology for specialist assessment. Don't delay referral because a woman has had a previously normal cervical screening result Don't delay referral until after pregnancy if a woman is pregnant.

Question 199

Cervical ca initial assessment after referral?

Answer 199

punch or excisional biopsy eg. electrosurgical excision and conization of suspicious lesions

Question 200

What when cervical ca is confirmed after biopsy?

Answer 200

staging using FIGO system - MRI: tumour size and extent - CXR and assessment for hydronephrosis (renal USS, CT or MRI) for pre-Tx - sentinel node biopsy + PET/CT for lymph node invol. and mets

Question 201

Common sites of mets from cervical ca?

Answer 201

lungs, liver, bone

Question 202

Mx for cervical ca= Stage IA1 (microinvasive)

Answer 202

- loop electrosurgical excision and conisation: aim to acheive -ve margins to both ca and dysplasia - simple hysterectomy if don't want to preseve fertility

Question 203

Mx for cervical ca: Stages IA2-IB2 (early stage disease)?

Answer 203

- radical hysterectomy and bilateral salpingectomy ( if fertility sparing appropriate in low risk) and/or bilateral oophorectomy with bilateral pelvic lymphadenectomy - radical trachelectomy (removal of cervix) and lymphadenoectomy can be considered instead for small tumours - may have adjuvant chemo or radio if intermediate/high risk recurrence

Question 204

What factors may determine risk of recurrence in cervical ca?

Answer 204

tumour size, margin invl, lymph node invl

Question 205

Mx for cervical ca: Stage IB3-IVA (locally advanced)?

Answer 205

- external beam radio, intracavity brachytherapy (radiation source placed in uterus & vagina) and chemo 1st line - surgery not recommended as unlikely to be curative

Question 206

Mx of cervical ca: Stage IVB (spread to distant organs)?

Answer 206

systemic chemo 1st line

Question 207

Mx options for recurrent or metastatic cervical ca?

Answer 207

- salvage surgery= pelvic exenteration (removal of female reproductive organs, lower urinary tract, portion of rectosigmoid bowel) if chemo failed and confined to central pelvis - chemo and/or radiotherapy if surgery not controlled disease

Question 208

What is a radical hysterectomy?

Answer 208

resection of cervix, uterus, parametria and cuff of upper vagina

Question 209

Most common type of cervical ca?

Answer 209

squamous cell cancer

Question 210

Mechanism of HPV causing cervical ca?

Answer 210

HPV 16 & 18 produce the oncogenes E6 and E7 retrospectively E6 inhibits p53 tumour supressor gene E7 inhibits RB supressor gene

Question 211

What is an oncogene?

Answer 211

mutated gene that has potential to cause cancer

Question 212

What. HPV subtypes are non-carcinogenic and associated with genital warts?

Answer 212

6 & 11

Question 213

Infected endocervical cells (infected with HPV) may undergo changes resulting in the development of what?

Answer 213

Koilocytes

Question 214

Characteristics of koilocytes?

Answer 214

- enlarged nucleous - irregular nuclear membrane contour - nucleus stains darker than normal (hyperchromasia) - perinuclear halo

Question 215

What is the Mx of cervical ca determined by?

Answer 215

FIGO staging and wishes of pt to maintain fertility

Question 216

Stages of the FIGO staging for cervical ca?

Answer 216

IA IB II III IV

Question 217

FIGO staging for cervical ca: stage IA?

Answer 217

Confined to cervix, only visible by microscopy and less than 7 mm wide: A1 = < 3 mm deep A2 = 3-5 mm deep

Question 218

FIGI staging for cervical ca: stage IB?

Answer 218

Confined to cervix, clinically visible or larger than 7 mm wide: B1 = < 4 cm diameter B2 = > 4 cm diameter

Question 219

FIGO staging for cervical ca: stage II?

Answer 219

Extension of tumour beyond cervix but not to the pelvic wall A = upper two thirds of vagina B = parametrial involvement

Question 220

FIGO staging for cervical ca: stage III?

Answer 220

Extension of tumour beyond the cervix and to the pelvic wall A = lower third of vagina B = pelvic side wall NB: Any tumour causing hydronephrosis or a non-functioning kidney is considered stage III

Question 221

FIGO staging for cervical ca: stage IV?

Answer 221

Extension of tumour beyond the pelvis or involvement of bladder or rectum A = involvement of bladder or rectum B = involvement of distant sites outside the pelvis

Question 222

What is hydronephrosis?

Answer 222

urine builds up in kidneys due to blockage in ureters so they swell eg. can be a Cx of advanced cervical ca

Question 223

Prognosis of cervical ca?

Answer 223

FIGO stage I= 99% 1yr survival; 96% 5yr II= 85%; 54% III= 74%; 38% IV= 35%; 5%

Question 224

Cx of cone biopsy or radical trachelectomy eg. in cervical ca?

Answer 224

preterm birth in future pregnancies

Question 225

Cx of radical hysterectomy?

Answer 225

ureteral fistula

Question 226

Short term Cx of radiotherapy for cervical ca?

Answer 226

diarrhoea, vaginal bleeding, radiation burns, pain on micturition, tiredness/weakness

Question 227

Long term Cx of radiotherapy for cervical ca?

Answer 227

ovarian failure, fibrosis of bowel/skin/bladder/vagina, lymphoedema

Question 228

Cervical ca screening for women aged?

Answer 228

25-64yrs (first invitation issued at 24.5yrs so ensure screening can be done by 25th bday)

Question 229

Recall intervals for cervical ca screening?

Answer 229

25-49yrs= recall every 3yrs (invitations issued 34.5m after previous test) 50-64yrs= every 5yrs (58.5m after previous)

Question 230

Can people 65yrs and older get cervical screening?

Answer 230

invited if recent cervical cytology abnormal or if not had screening since 50yrs and request one

Question 231

What does NHSCSP (cervical screening) involve?

Answer 231

- HPV screening= identify people with high-risk HPV (hrHPV) - Liquid based cytology (if hrHPV found)= detect early abnormalities of cervix, if untreated can lead to ca - Colposcopy= diagnose cervical intraepithelial neoplasia (CIN) and to differentiate high-grade lesions from low-grade abnormalities in people with abnormal cytology

Question 232

Cervical ca screening, what if hrHPV detected?

Answer 232

cytology if this is abnormal then colposcopy

Question 233

Cervical ca screening= hrHPV +ve and negative cytology?

Answer 233

repeat HPV test at 12m - if -ve then return to normal recall - if +ve then repeat HPV in 12m again - if -ve at 24m then return normal recall - if +ve at 24m then refer to colposcopy

Question 234

Cervical ca screening= hrHPV +ve with cytology abnormal at 12 or 24m?

Answer 234

refer to colposcopy

Question 235

Cervical ca screening= hrHPV test unavailable or cytology inadequate?

Answer 235

repeat sample in <3m - if inadequate at 24m repeat text, these are exception and refer to colposcopy - 2 consecutive inadequate or unavailable tests then refer to colposcopy

Question 236

Cervical ca screening= colposcopy normal and adequate?

Answer 236

follow up at 12m screening, if then HPV -ve then return to normal recall

Question 237

Cervical ca screening= colposcopy inadequate?

Answer 237

repeat screening and colposcopy in 12m; if normal and HPV -ve then return to routine recall

Question 238

Cervical ca screening: cytology negative means what?

Answer 238

no abnormality detected

Question 239

Cervical ca screening: if cytology is abnormal, the cervical samples may show what? (6)

Answer 239

- borderline changes in squamous or endocervical cells - low grade dyskaryosis - high-grade dyskaryosis (moderate) - high-grade dyskaryosis (severe) - invasive squamous cell carcinoma - glandular neoplasia

Question 240

Cervical ca screening: if cytology is inadequate, this may be because the cervical sample was...? (5)

Answer 240

- taken but the cervix was not fully visualised - taken in inappropriate manner eg. using not approved sampling device - contains insufficient cells - contains obscuring element eg. lubricant, blood, inflamm - incorrectly labelled

Question 241

What does colposcopy look at in cervical ca screening?

Answer 241

any abnormal changes in cervix which may indicate pre-cancerous changes (cervical intraepithelial neoplasia [CIN]) or the presence of cancer

Question 242

What chemicals are usually applied to cervix during colposcopy in cervical ca screening?

Answer 242

acetic acid = abnormal areas (such as CIN) tend to turn white (sometimes referred to as acetowhite). If iodine solution= normal tissue (on the outside of the cervix) stains dark brown. Pre-cancerous abnormalities may not stain with iodine. The cells on the inner part of the cervix do not stain brown.

Question 243

What may be done on colposcopy to confirm diagnosis of cervical ca?

Answer 243

biopsy

Question 244

Can pregnant women be offered cervical screening?

Answer 244

- if called while pregnant, defer until 3m post-partum + - if previous test was abnormal, do not delay colposcopy (can do in late 1st or early 2nd tri; if low grade changes can delay until after delivery; if seen in early preg may need another assessment in late 2nd tri)

Question 245

If pt has been treated for CIN, when should they be followed up for repeat cervical sample?

Answer 245

6m after Tx to test for cure

Question 246

What is cervical intraepithelial neoplasia (CIN)?

Answer 246

abnormal changes in the transformation zone of cervix

Question 247

Cervical dysplasia may indicate what?

Answer 247

HIV

Question 248

Cervical intraepithelial neoplasia (CIN) grade 1 (CIN1)?

Answer 248

sometimes referred to as low-grade squamous intraepithelial lesions) — one-third of the thickness of the surface layer of the cervix is affected.

Question 249

Cervical intraepithelial neoplasia (CIN) grade 2 (CIN2)?

Answer 249

two-thirds of the thickness of the surface layer of the cervix is affected.

Question 250

Cervical intraepithelial neoplasia (CIN) grade 3 (CIN3)?

Answer 250

(sometimes called high-grade or severe dysplasia or stage 0 cervical carcinoma in situ) — the full thickness of the surface layer is affected.

Question 251

CIN may exist at any one of the three stages, eg?

Answer 251

CIN1 lesions are morphological correlates of HPV infections. CIN2/3 lesions (collectively referred to as CIN2+) are correlates of cervical pre-cancers that, if left untreated, may progress to cervical cancer.

Question 252

How often should pt have cervical ca screening if have HIV?

Answer 252

annually and colposcopy at diagnosis

Question 253

What does dyskaryosis in cervical ca mean?

Answer 253

percancerous changes in cervical cells: can be early indication of cervical ca or HPV infection

Question 254

Cervical ca: mild dyskaryosis?

Answer 254

Indicates low-grade abnormalities in the cervical cells. Often corresponds to CIN1, which is a mild change in the cells and typically linked to an HPV infection. In many cases, mild dyskaryosis can resolve on its own without treatment, especially if caused by transient HPV infections.

Question 255

Cervical ca: moderate dyskaryosis?

Answer 255

Indicates more significant abnormality. Typically corresponds to CIN2 , which is a higher risk of progression to cervical cancer than CIN1. Treatment may be needed to prevent further progression.

Question 256

Cervical ca: severe dyskaryosis?

Answer 256

Indicates severely abnormal cells. Usually corresponds to CIN3, a precancerous stage with a significant risk of progression to cervical cancer if untreated. Requires further diagnostic testing and often surgical treatment to remove the abnormal tissue.

Question 257

What if dyskaryosis is detected on cervical smear?

Answer 257

colposcopy +/- biopsy

Question 258

Presenting features of colorectal ca may include what?

Answer 258

- change in bowel habits: C, D or alternating; increase frequency - rectal bleeding: bright red or melena - abdo pain/discomfort - unexplained weight loss: advanced -anaemia: fatigue, weakness, SOB - bowel obstruction: advanced- severe abdo pain, N&V

Question 259

Why may pt get abdo pain/discomfort/cramping with colorectal ca?

Answer 259

may be due to tumour obstructing bowel or causing inflam

Question 260

Why may pt with colorectal ca have anaemia?

Answer 260

chronic bleeding from the tumour

Question 261

Locations of ca in colorectal cancer?

Answer 261

rectal (40%) sigmoid (30%) descending colon (5%) transverse colon (10%) ascending colon and caecum (15%)

Question 262

Types of colorectal (colon) ca?

Answer 262

1) sporadic (95%) 2) hereditary non-polyposis colorectal carcinoma (HNPCC, 5%) 3) familial adenomatous polyposis (FAP, <1%)

Question 263

What may sporadic colon ca be due to?

Answer 263

genetic mutations

Question 264

Examples of genetic mutations that may cause colon (colorectal ca)?

Answer 264

- allelic loss of APC gene - activation of K-ras oncogene - deletion of p53 and DCC tumour suppressor genes

Question 265

What is HNPCC (Lynch syndrome)?

Answer 265

autosomal dominant condition, most common form of inherited colon ca 90% pts develop ca, often proximal colon, poorly differentiated and highly aggressive

Question 266

What mutation and genes are involved in HNPCC (Lynch syndrome)?

Answer 266

7 mutations, which affect genes invl in DNA mismatch repair leading to microsatelilite instability. Genes: - MSH2 (60%) - MLH1

Question 267

Pts with HNPCC are also at higher risk of what?

Answer 267

other ca eg. endometrial ca

Question 268

What is sometimes used to aid diagnosis of HNPCC?

Answer 268

Amsterdam criteria: - at least 3 family members with colon ca - the cases span at least 2 generations - at least one case diagnosed before age of 50yrs

Question 269

What is FAP?

Answer 269

rare autosomal dominant condition which leads to formation of hundreds of polyps by age 30-40yrs pts inevitably develop carcinoma (lifetime risk near 100%)

Question 270

What is FAP due to?

Answer 270

mutation in tumour supressor gene called adenomatous polyposis coli gene (APC) located on chromosome 5

Question 271

Ix and Mx for FAP?

Answer 271

Ix= genetic testing- analyse DNA from pts WBC Mx= total proctocolectomy with ileal pouch anal anastomosis (IPAA) formation in their 20s

Question 272

Pts with FAP are also at risk from what?

Answer 272

duodenal tumours

Question 273

Variant of FAP?

Answer 273

Gardner's syndrome- also feature osteomas of skull & mandible, retinal pigmentation, thyroid carcinoma and opidermoid cysts on the skin

Question 274

What does FAP stand for?

Answer 274

Familial Adenomatous Polyposis

Question 275

How to stage colorectal ca?

Answer 275

- carcinoembryonic antigen (CEA) - CT chest, abdo, pelvis - entire colon evaluated with colonoscopy or CT colonography - if tumour lies below peritoneal reflection then also need mesorectum evaulated with MRI

Question 276

Staging system for colorectal ca?

Answer 276

TNM once staging complete then MDT meeting to formulate Mx plan

Question 277

Treatment options for colorectal ca?

Answer 277

- surgery - chemo - radio - targeted therapies

Question 278

Ca of colon is nearly always treated with what?

Answer 278

surgery

Question 279

Only option for cure in pts with colon ca?

Answer 279

resectional surgery

Question 280

Confounding factors that will goven choice of procedure for surgery for colon ca?

Answer 280

eg. tumour pt from HNPCC family may be better served with panproctocolectomy rather than segmental resection

Question 281

Treatment for colon ca: surgery- what is needed for anastomosis to heal?

Answer 281

following resection, need decision regarding restoration of continuity for anastomosis to heal= adequate blood supply, mucosal apposition and no tissue tension

Question 282

What is an anastomosis?

Answer 282

surgical or natural connection between 2 structures eg. blood vessels, intestine, tubes critical in many surgeries to ensure that normal flow and function are maintained after structural changes

Question 283

Surgical options when colon ca presents with an obstructing lesion?

Answer 283

stent it or resect unusual now to defunction a colonic tumour with proximal loop stoma (this differs from situation in rectum)

Question 284

The operations for colon ca are segmental resections based on what?

Answer 284

blood supply and lymphatic drainage

Question 285

Type of resection and anastomosis for cancer of the caecal, ascending or proximal transverse colon?

Answer 285

Type of resection= right hemicolectomy Anastomosis= ileo-colic

Question 286

Type of resection and anastomosis for cancer of the distal transverse, descending colon?

Answer 286

Type of resection= left hemicolectomy Anastomosis= colo-colon

Question 287

Type of resection and anastomosis for cancer of the sigmoid colon?

Answer 287

Type of resection= high anterior resection Anastomosis= colo-rectal

Question 288

Type of resection and anastomosis for cancer of the upper rectum?

Answer 288

Type of resection= anterior resection (TME) Anastomosis= colo-rectal

Question 289

Type of resection and anastomosis for cancer of the low rectum?

Answer 289

Type of resection= anterior resection (low TME) Anastomosis= colo-rectal (+/- defunctioning stoma)

Question 290

Type of resection and anastomosis for cancer of the anal verge?

Answer 290

Type of resection= abdomino-perineal excision of rectum Anastomosis= none

Question 291

Types of stoma?

Answer 291

Colostomy: Bypass the colon, output is usually solid. Ileostomy: Bypass the small intestine, output is usually liquid. Urostomy: Bypass the bladder, output is urine. Jejunostomy and Gastrostomy: Used for feeding rather than waste diversion. (opening in jejunum or in stomach respectively)

Question 292

Temporary vs permanent stomas?

Answer 292

Temporary Stomas: Created when the bowel or bladder needs time to heal (e.g., after an injury or surgery). They are later reversed when healing is complete. Permanent Stomas: Created when the underlying condition (e.g., cancer, severe Crohn’s disease) requires permanent removal or bypass of part of the digestive or urinary tract.

Question 293

When is chemotherapy used in colorectal ca?

Answer 293

in neoadjuvant setting (particularly for rectal ca), adjuvant setting and for metastatic disease

Question 294

Common chemo regimens for colorectal ca?

Answer 294

FOLFOX and FOLFIRI

Question 295

When is radiation therapy used for colorectal ca?

Answer 295

predominantly for rectal ca in the neoadjuvant or adjuvant setting

Question 296

Targeted therapies for colorectal ca?

Answer 296

Bevacizumab (anti-VEGF) and Cetuximab (anti-EGFR), particularly for metastatic disease

Question 297

Emergency surgery in colorectal ca in a setting where the bowel has perforated so the risk of an anastomosis is much greater? (particulary when the anastomosis needed is colon-colon)

Answer 297

end colostomy is safer and can be reversed - resection of sigmoid colon and end colostomy is fashioned in operation= Hartmann's procedure - left sided resections more risky, ileo-colic anastomoses are relatively safe even in emergencies and don't need to be defunctioned

Question 298

What is used to guide referral in suspected colorectal ca?

Answer 298

Faecal Immunochemical Test (FIT) instead of doing colonoscopy 1st line

Question 299

What scenarios should pt get FIT test before colorectal ca referral?

Answer 299

- abdo mass - change in bowel habit - iron def anaemia - 40yrs+ with unexplained weight loss & abdo pain - <50yrs with rectal bleeding + abdo pain or weight loss - 50yrs+ with rectal bleeding, weight loss or abdo pain - 60yrs+ with anaemia even in absence of iron def

Question 300

What if pt needs FIT test but already had a negative result through the NHS screening programme?

Answer 300

still need another one

Question 301

What if pt with rectal mass, unexplained anal mass or unexplained anal ulceration?

Answer 301

do not need FIT test, just consider referral for ?colorectal ca

Question 302

What if FIT test comes back +ve?

Answer 302

refer on suspected ca pathway

Question 303

What if FIT test negative?

Answer 303

- safety net - refer on suspected ca pathway if ongoing signif concern (abdo mass) - still Ix for underlying diagnosis

Question 304

NHS screening programme for bowel ca offered to who?

Answer 304

every 2yrs to people 50-74yrs (England & Scotland) Wales: 51-74 NIreland: 60-74hrs

Question 305

How is FIT testing done in NHS screening programme for bowel ca?

Answer 305

Invitation letter followed by test kit: end of test tick dipped into single bowel motion, placed back in tube and returned in envelope

Question 306

How do pt get results from FIT test from the screening programme?

Answer 306

letter sent to pts home within 2 weeks of receiving the kit and GP informed electronically

Question 307

Abnormal FIT test on NHS screening programme?

Answer 307

offered colonoscopy

Question 308

Colonoscopy results if indicated after FIT test (following screening programme)?

Answer 308

No abnormal or low-risk adenoma= return to routine recall Intermediate or high risk adenoma= invited for colonoscopic surveillance/review Cancer= refer for Tx Other pathology eg. IBD or diverticulosis= referred for Tx

Question 309

Possible harms of bowel screening?

Answer 309

anxiety; Cx of colonoscopy (bleeding, bowel perforation); inappropriate reassurance from -ve screening result

Question 310

How can primary care support the bowel ca screening programme?

Answer 310

- promoting uptake - ensure that pts are aware that not all ca will be detected by screening - -ve results should not be used to guide Ix of pt presenting with symptoms of bowel ca

Question 311

What is a FIT test?

Answer 311

type of faecal occult blood (FOB) test which uses antibodies that specifically recognise human Hb used to detect and quantify amount of human blood in single stool sample abnormal result offered colonoscopy

Question 312

Most colorectal ca develop from what?

Answer 312

adenomatous polyps

Question 313

If pt gets colonoscopy following FIT test, how many will be found to have ca?

Answer 313

1/10 5/10 normal 4/10 polpys which may be removed (premalignant potential)

Question 314

Where is endometrial ca classically seen?

Answer 314

post-menopausal women 25% do occur before menopause

Question 315

Prognosis of endometrial ca?

Answer 315

good due to early detection

Question 316

RFs for endometrial ca?

Answer 316

XS oestrogen: - nulliparity - early menarche - late menopause - unopposed oestrogen metabolic syndrome: - obesity - DM - PCOS tamoxifen hereditary non-polyposis colorectal carinoma (HNPCC)

Question 317

Protective factors for endometrial ca?

Answer 317

- multiparity - COCP - smoking

Question 318

Does HRT and the COCP increase or decrease the risk of endometrial ca?

Answer 318

Reduces the risk addition of progestogen to oestrogen reduces the risk as oestrogen is no longer unopposed

Question 319

Postmenopausal bleeding classic symptom of what?

Answer 319

endometrial ca

Question 320

Features of endometrial ca?

Answer 320

- postmenopausal bleeding, usually slight and intermittent initially before becoming heavier - premenopausal= menorrhagia or intermenstrual bleeding - pain not common, signifies extensive disease - vaginal discharge unusual

Question 321

Who should be referred using suspected ca pathway for endometrial ca?

Answer 321

all women >=55yrs who present with postmenopausal bleeding consider if <55

Question 322

1st line Ix for endometrial ca once referred?

Answer 322

trans-vaginal USS: normal endometrial thickness (<4mm) has a high negative predictive value hysteroscopy with endometrial biopsy

Question 323

Mx for endometrial ca?

Answer 323

surgery - localised disease= total abdo hysterectomy with bilateral salpingo-oophorectomy high-risk disease= postop radiotherapy

Question 324

Frail elderly women with endometrial ca not suitable for surgery?

Answer 324

progestogen therapy

Question 325

How is post-menopausal bleeding defined?

Answer 325

unexplained vaginal bleeding more than 12m after menstruation has stopped because of the menopause

Question 326

Consider a direct access USS to assess for endometrial ca in women aged 55yrs and over with what?

Answer 326

Unexplained symptoms of vaginal discharge who: - Are presenting with these symptoms for the first time, or - Have thrombocytosis, or - Report haematuria, or Visible haematuria, and: - Low haemoglobin levels, or - Thrombocytosis, or - High blood glucose levels.

Question 327

Who is typically affected by gastric ca?

Answer 327

older people (1/2 are >75yrs) and male

Question 328

Most common type of gastric ca?

Answer 328

gastric adenocarcinoma

Question 329

Where does gastric adenocarcinoma arise from?

Answer 329

glandular epithelium of the stomach lining

Question 330

RFs for gastric ca?

Answer 330

- Helicobacer pylori - pernicious anaemic, atrophic gastritis - diet - ethnicity: Japan, China - smoking - blood group A

Question 331

Why is H.pylori a RF for gastric ca?

Answer 331

triggers inflam of the mucosa -> atrophy and intestinal metaplasia -> dysplasia

Question 332

What type of diet increases risk of gastric ca?

Answer 332

salt and salt-preserved foods nitrates

Question 333

Features of gastric ca?

Answer 333

abdo pain= vague, epigastric, dyspepsia weight loss & anorexia N&V dysphagia: esp if ca arises in proximal stomach overt upper GI bleeding in minority Virchow's node & Sister Mary Joseph's node

Question 334

What lymph nodes may be palpated if there is lymphatic spread in gastric ca?

Answer 334

left supraclavicular lymph node (Virchow's node) periumbilical nodule (Sister Mary Joseph's node)

Question 335

Ix and diagnosis for oesophago-gastric ca?

Answer 335

oesophago-gastro-duodenoscopy with biopsy

Question 336

Signet ring cells?

Answer 336

may be seen in gastric ca on biopsy contain large vacuole of mucin which displaces the nucleus to one side high no. of signet ring cells= worse prognosis

Question 337

How to stage gastric ca?

Answer 337

- CT chest, abdo and pelvis= ?mets - endoscopic USS: if will guide Mx - F18 FDG-PET scan: if ? metastatic disease -pre-op staging laparoscopy: if potentially curable gastric

Question 338

Mx of gastric ca?

Answer 338

surgical options depend on extent and site, include: - endoscopic mucosal resection - partial gastrectomy - total gastrectomy - chemotherapy

Question 339

Mx of T1N0 oesophageal ca?

Answer 339

endoscopic mucosal resection for staging

Question 340

Mx for T1bN0 SCC of the oeophagus?

Answer 340

- definitive chemo or - surgical resection pt choice

Question 341

Surgical Tx of oesophageal ca?

Answer 341

open or minimally invasive oesophagectomy

Question 342

Lymph node dissection in oesophageal and gastric ca?

Answer 342

When performing curative gastrectomy for gastric ca= consider D2 lymph node dissection Curative oesophectomy= consider two-field lymph node dissection

Question 343

Mx for localised oesophageal and oesophago-gastric junctional adenocarcinoma (excluding T1N0) who will have surgical rection, offer choice of what?

Answer 343

- chemo before or before & after surgery - chemoradiotherapy before surgery

Question 344

What to offer pt who is having radical surgical resection for gastric ca?

Answer 344

chemo before and after surgery or chemo/chemoradiotherapy after surgery for those with curative intent and didn't have chemo before

Question 345

Mx for SCC of oesophagus (resectable and non-metastatic)?

Answer 345

- radical chemoradio or - chemoradio before surgical resection

Question 346

Mx for non-metastaic oesophageal ca that is not suitable for surgery?

Answer 346

palliative Mx: - chemoradio for non-metastatic that can be encompassed within a radiotherapy field if can't be encompassed, consider 1 or more: - chemo - local tumour Tx (stenting or palliative radio) - best supportive care after Tx reassess response and reconsider if surgery is an option

Question 347

1st line palliative chemo for people with HER2-positive metastatic adenocarcinoma of stomach or oesophago-gastric junction?

Answer 347

trastubzumab (in combination with cisplatin and capecitabine)

Question 348

1st line palliative combination chemo to pt with advanced oesophago-gastric ca who have performance status 0 to 2 and no signif comorbidities?

Answer 348

double Tx= 5-fluorouracil or capecitabine in combination with cisplatin or oxaliplatin triple Tx= 5-fluorouracil or capecitabine in combination with cisplatin or oxaliplatin plus epirubicin.

Question 349

What can you offer pts with luminal obstruction in oesophageal and oesophageal-gastric junctional ca?

Answer 349

self-expanding stents or radiotherapy

Question 350

What can you offer pt with outflow obstruction in gastric ca?

Answer 350

uncovered self-expanding metal stents or palliative surgery

Question 351

What to offer pt immediately after having radical surgery for oesophageal and oesophago-gastric junctional ca?

Answer 351

enteral or parenteral nutrition

Question 352

Most common malignancy affecting children?

Answer 352

ALL

Question 353

What does ALL stand for?

Answer 353

Acute lymphoblastic leukaemia

Question 354

Peak incidence of ALL?

Answer 354

2-5yrs boys slightly more common

Question 355

Features of ALL may be divided into what?

Answer 355

those predictable by bone marrow failure eg. anaemia, neutropaenia, thrombocytopenia

Question 356

Features of ALL?

Answer 356

- anaemia= lethargy and pallor - neutropenia= frequent or severe infection - thrombocytopenia= easily bruising, petechiae - bone pain - splenomegaly - hepatomegaly - fever in up to 50% - testicular swelling

Question 357

Why may child get bone pain with ALL?

Answer 357

secondary to bone marrow infiltration

Question 358

Types of ALL?

Answer 358

- common ALL (75%), CD10 present, pre-B phenotype - T-cell ALL (20%) - B-cell ALL (5%)

Question 359

ALL poor prognostic factors?

Answer 359

- age <2yrs or >10yrs - WBC >20*10^9/l at diagnosis - T or B cell surface markers - non-Caucasian - male

Question 360

More common form of acute leukaemia in adults?

Answer 360

acute myeloid leukaemia

Question 361

AML may occur as what?

Answer 361

primary disease or following a secondary transformation of a myeloproliferative disorder

Question 362

What does AML stand for?

Answer 362

acute myeloid leukaemia

Question 363

Features of AML?

Answer 363

related to bone marrow failure - anaemia= pallor, lethargy, weakness - neurtopenia= WBC count may be v high, functioning neutrophil levels may be low leading to frequent infections - thrombocytopenia= bleeding - splenomegaly - bone pain

Question 364

Poor prognostic factors of AML?

Answer 364

>60yrs >20% blasts after first course of chemo cytogenetics= deletions of chromosome 5 or 7

Question 365

Classification of AML?

Answer 365

French-American-British (FAB) MO - undifferentiated M1 - without maturation M2 - with granulocytic maturation M3 - acute promyelocytic M4 - granulocytic and monocytic maturation M5 - monocytic M6 - erythroleukaemia M7 - megakaryoblastic

Question 366

Acute promyelocytic leukaemia M3 (APML, the M3 subtype of AML)?

Answer 366

associated with t(15;17) fusion of PML and RAR-alpha genes presents younger than other types of AML (average = 25 years old) Auer rods (seen with myeloperoxidase stain) DIC or thrombocytopenia often at presentation good prognosis

Question 367

Don't need to know substypes of AML except what?

Answer 367

Acute promyelocytic leukaemia (APML, the M3 subtype of AML)

Question 368

What is APML associated with?

Answer 368

the t(15;17) translocation which causes fusion of the PML and RAR-alpha genes

Question 369

Features of APML?

Answer 369

- presents younger than other types of AML (average=25yrs) - DIC or thrombocytopenia often - good prognosis

Question 370

Mx of APML?

Answer 370

all-trans retinoic acid (ATRA) to force immature granulocytes into maturation to resolve a blast crisis prior to more definitive chemo

Question 371

What type of leukaemia is treated with all-trans retinoic acid (ATRA) to force immature granulocytes into maturation to resolve a blast crisis prior to more definitive chemo?

Answer 371

APML (subtype of AML)

Question 372

Cx of CLL?

Answer 372

- anaemia - hypogammaglobulinaemia= recurrent infections - warm autoimmune haemolytic anaemia (in 10-15%) - transformation to high-grade lymphoma (Richter's transformation)

Question 373

What is Ritchter's transformation?

Answer 373

occurs when leukaemia cells enter lymph node and change into high-grade, fast-growing non-Hodgkin's lymphoma pts become unwell very suddenly

Question 374

Ritcher's transformation is indicated by one the following symptoms....

Answer 374

lymph node swelling fever without infection weight loss night sweats nausea abdominal pain

Question 375

Pt with CLL suddenly becomes very unwell?

Answer 375

Ritcher's transformation

Question 376

What does CLL stand for?

Answer 376

chronic lymphocytic leukaemia

Question 377

What causes CLL?

Answer 377

monoclonal proliferation of well-differentiated lymphocytes which are almost always B-cells (99%)

Question 378

Most common form of leukaemia seen in adults?

Answer 378

CLL

Question 379

Features of CLL?

Answer 379

- often asymptomatic= picked up incidental finding of lymphocytosis - constitutional: anorexia, weight loss - bleeding, infections - lymphadenopathy more marked than CML

Question 380

Ix for CLL?

Answer 380

- Immunophenotyping KEY - FBC - Blood film= smudge cells (smear cells)

Question 381

Immunophenotyping for CLL?

Answer 381

most cases can be identified using panel of antibodies specific for CD5, CD19, CD20, CD23

Question 382

What would FBC for CLL show?

Answer 382

anaemia (due to bone marrow replacement or autoimmune haemolyic anaemia) and thrombocytopenia (due to bone marrow replacement or immune thrombocytopenia- ITP)

Question 383

Smudge cells (smear cells on blood film)?

Answer 383

CLL

Question 384

Auer rods on myeloperoxidase stain?

Answer 384

AML (APML)

Question 385

Philadelphia chromosome is present in more than 95% of pts with what?

Answer 385

CML

Question 386

What is the philadelphia chromosome in CML due to?

Answer 386

translocation between the long arm of chromosome 9 and 22 - t(9:22)(q34; q11). This results in part of the ABL proto-oncogene from chromosome 9 being fused with the BCR gene from chromosome 22. The resulting BCR-ABL gene codes for a fusion protein that has tyrosine kinase activity in excess of normal.

Question 387

Presentation of CML?

Answer 387

60-70yrs - weight loss and sweating COMMON - marked splenomegaly= abdo discomfort - increase in granulocytes at different stages of maturation +/- thrombocytosis - decrease leukocyte alkaline phosphatase - may undergo blast transformation (AML in 80%, ALL in 20%)

Question 388

Mx of CML?

Answer 388

Imatinib 1st line - hydroxyurea - interferon-alpha - allogenic bone marrow transplant

Question 389

What is imatinib used for 1st line Mx of CML?

Answer 389

inhibitor of the tyrosine kinase associated with the BCR-ABL defect very high response rate in chronic phase CML

Question 390

What does CML stand for?

Answer 390

Chronic myeloid leukaemia

Question 391

Consider very urgent FBC (within 48hrs) to assess for leukaemia in adults with any of the following?

Answer 391

pallor persistent fatigue unexplained fever Unexplained persistent or recurrent infection. Generalized lymphadenopathy. Unexplained bruising. Unexplained bleeding. Unexplained petechiae. Hepatosplenomegaly.

Question 392

When to refer children and young people for immediate specialist assessment for leukaemia if they have what?

Answer 392

unexplained petechiae or hepatosplenomegaly

Question 393

When to do a very urgent FBC (within 48hrs) to assess for leukaemia in children and young people?

Answer 393

Pallor. Persistent fatigue. Unexplained fever. Unexplained persistent infection. Generalized lymphadenopathy. Persistent or unexplained bone pain. Unexplained bruising. Unexplained bleeding.

Question 394

Way to remember leukaemia ages?

Answer 394

ALL= <5 & >45 CeLLmates= >55, smudge cells have CoMmon= >65, philadelphia chromosome AMbitions= >75, aurer rods

Question 395

Way to remember some key info about leukaemia types?

Answer 395

ALL= ALL children have headaches because they were doing meth (methotrexate used to Tx ALL) AML= enAML (dental problems) and when you open your mouth you go ahhhh (aurer rods) CLL= geting smudged (smudge cells) in club rituximab (used to Tx) CML= CML and gout (Cx) got married in Philidelphia (chromosome)

Question 396

Refer people using suspected ca referral for lung ca if they...?

Answer 396

- have CXR that suggests lung ca or - 40yrs+ with unexplained haemoptysis

Question 397

Offer urgent CXR (within 2w) to assess for lung ca in people aged 40yrs+ if they have 2 or more of what symptoms, or if they have ever smoked and had one or more of the following unexplained symptoms?

Answer 397

- cough - fatigue - SOB - chest pain - weight loss - appetite loss

Question 398

Consider CXR (within 2w) to assess for lung ca in people aged 40yrs+ and with any of the following...

Answer 398

- persistent or recurrent chest infection - clubbing - supraclavicular lymphadenopaty or persistent cervical lymphadenopathy - chest signs consistent of lung ca - thrombocytosis

Question 399

Most mesotheliomas are what?

Answer 399

pleural peritoneal can occur

Question 400

Features of lung ca?

Answer 400

persistent cough haemoptysis dyspnoea chest pain weight loss and anorexia hoarseness laryngeal nerve superior vena cava syndrome

Question 401

When is hoarseness seen in lung ca?

Answer 401

with Pancoast tumours pressing on the recurrent laryngeal nerve

Question 402

Examination findings of lung ca?

Answer 402

- fixed monophonic wheeze - clubbing - supraclavicular lymphadenopathy or persistent cervical lymphadenopathy

Question 403

What is paraneoplastic syndrome?

Answer 403

rare disorders that occur when immune system has a reaction to ca

Question 404

Paraneoplastic features in small cell lung ca?

Answer 404

- ADH - ACTH (not typical)- HTN, hyperglucaemia, hypokalaemia, alkalosis and muscle weakness are more common than buffalo hump ect - Lamber-Eaton syndrome

Question 405

Paraneoplastic features of squamous cell lung ca?

Answer 405

- parathyroid hormone-related protein (PTH-rp) secretion causing hypercalcaemia - clubbing - hypertrophic pulmonary osteoarthropathy (HPOA) - hyperthyroidism due to ectopic TSH

Question 406

Paraneoplastic features of adenocarcinoma lung ca?

Answer 406

- gynaecomastia - HPOA

Question 407

Cx of lung ca?

Answer 407

hoarseness stridor

Question 408

What may be noted on bloods for pt with lung ca?

Answer 408

raised platelets (thrombocytosis)

Question 409

1st line Ix for lung ca?

Answer 409

CXR (10% sometimes CXR normal)

Question 410

Ix for lung ca?

Answer 410

1st line= CXR Gold= CT - Bronchoscopy with biopsy using endobrachial USS - PET scan= non-small lung ca to establish eligability for cure; 18-fluorodeoxygenase if preferentially taken up by neoplastic tissue - bloods= raised platelets

Question 411

3 subtypes of non-small cell lung ca?

Answer 411

- Squamous cell carcinoma - Adenocarcinoma - Large cell lung carcinoma

Question 412

Lung ca: squamous cell cancer?

Answer 412

typically central cavitating lesions are more common than other types HPOA

Question 413

What is squamous cell lung ca associated with?

Answer 413

Finger clubbing and PTHrP secretion -> hypercalcaemia

Question 414

Most common type of lung ca in non-smokers?

Answer 414

adenocarcinoma

Question 415

Lung ca: adenocarcinoma?

Answer 415

- typically peripheral - most common in lung ca in non-smokers, but majority are still smokers

Question 416

Lung ca: large cell lung carcinoma?

Answer 416

- typically peripheral - anaplastic, poorly differentiated tumours with poor prognosis - may secrete B-HCG

Question 417

Anaplastic?

Answer 417

term used to describe ca cells that divide rapidly and have little to no resemblance to normal cells

Question 418

Mx for non-small cell lung ca?

Answer 418

- only 20% suitable for surgery - curative or palliative radiotherapy - poor response to chemo

Question 419

What is performed prior to surgery in non-small cell lung ca if suitable for surgery?

Answer 419

mediastinoscopy as CT doesn't always show mediastinal lymph node invl.

Question 420

Non-small cell lung ma Mx: contraindications to surgery?

Answer 420

assess general health stage IIIb or IV (i.e. metastases present) FEV1 < 1.5 litres is considered a general cut-off point (for lobectomy or <2 for pneumonectomy; sometimes need further lung function tests as operations may still go ahead based on results) malignant pleural effusion tumour near hilum vocal cord paralysis SVC obstruction

Question 421

Features of small cell lung ca?

Answer 421

- usually central - arise from APUD* cells - associated with ectopic ADH, ACTH secretion - ADH → hyponatraemia - ACTH → Cushing's syndrome - ACTH secretion can cause bilateral adrenal hyperplasia, the high levels of cortisol can lead to hypokalaemic alkalosis Lambert-Eaton syndrome

Question 422

Lambert-Eaton syndrome in small cell lung ca?

Answer 422

antibodies to voltage gated calcium channels causing myasthenic like syndrome

Question 423

Small cell lung ca is usually what by the time of diagnosis?

Answer 423

metastatic disease

Question 424

Mx for small cell lung ca?

Answer 424

pts with very early stage disease (T1-2a, N0, M0) are considered for surgery. however, most pts with limited disease receive a combination of chemotherapy and radiotherapy pts with more extensive disease are offered palliative chemotherapy

Question 425

What do small cell lung ca arise from?

Answer 425

APUD cells: Amine - high amine content Precursor Uptake - high uptake of amine precursors Decarboxylase - high content of the enzyme decarboxylase

Question 426

Types of lung ca?

Answer 426

Small cell lung ca Non-small cell lung ca: - adenocarcinoma - squamous - large cell - alveolar cell carcinoma - bronchial adenoma

Question 427

How is lung ca classified?

Answer 427

histologically as SCLC or NSCLC due to different features, Mx and prognosis

Question 428

What type of lung ca has worse prognosis?

Answer 428

small cell (15%)

Question 429

Most common type of lung ca?

Answer 429

adenocarcinoma (NSCLC) often seen in non-smokers high no of cases due to increased use of low-tar cigarettes

Question 430

What type of lung ca most commonly has cavitating lesions?

Answer 430

Squamous (NSCLC)

Question 431

NSCLC: alveolar cell carcinoma?

Answer 431

not related to smoking ++ sputum

Question 432

What type of lung ca is mostly carcinoid?

Answer 432

bronchial adenoma (NSCLC)

Question 433

SCLC vs NSCLC?

Answer 433

SCLC - 10-15% - fast growing, aggressive - often widespread at diagnosis - only one major type (small cell carcinoma) - strong association with smoking - limited stage and extensive stage - more likely to present with paraneoplastic symptoms eg. SIADH, Cushings - Tx: chemo and radio; surgery rare due to early mets - poor prognosis (12-18m limited stage; 6-12m extensive) - fewer mutations, TP53, RB1 - less responsive to immunotherapy NSCLC - 85-90% - slower growing - may be localised at diagnosis - Types: adenocarcinoma, SCC, large cell carcinoma - associated with smoking and genetic mutations - Staged I to IV - CP: cough, chest pain, weight loss like SCLC but less likely to have paraneoplastic symtpoms - surgery option in early stages; chemo, radiation and immunotherapy in advanced - better prognosis - Mutations: EGFR, ALK, ROS1 and KRAS, more common in adenocarcinoma - more responsive to immunotherapy

Question 434

Burkitt's lymphoma?

Answer 434

high-grade B-cell neoplasm

Question 435

2 major forms of Birkitt's lymphoma?

Answer 435

- Endemic (African) form - Sporadic form

Question 436

Burkitt's lymphoma: endemic (African) form?

Answer 436

typically invl. maxilla or mandible

Question 437

Burkitt's lymphoma: sporadic form?

Answer 437

abdominal eg ileo-caecal tumours are the most common form; more common in pts with HIV

Question 438

What is Burkitt's lymphoma associated with? (gene)

Answer 438

c-myc gene translocation, usually t(8:14)

Question 439

What virus is implicated in the development in the development of the African form of Burkitt's lymphoma and to lesser extent the sporadic form?

Answer 439

EBV

Question 440

Microscopy findings in Burkitt's lymphoma?

Answer 440

'starry sky' appearance= lymphocyte sheets interspersed with macrophages containing dead apoptotic tumour cells

Question 441

Mx for Burkitt's lymphoma?

Answer 441

Rasburicase often given before then chemotherapy

Question 442

What does chemotherapy used for Burkitt's lymphoma tend to produce?

Answer 442

a rapid response which may cause tumour lysis syndrome

Question 443

Burkitt's lymphoma: what is usually given before chemo to reduce the risk of tumour lysis syndrome occuring?

Answer 443

Rasburicase (a recombinant version of urate oxidase, an enzyme that catalyses the conversion of uric acid to allantoin. Allantoin is 5-10x more soluble than uric acid so excretion is more effective)

Question 444

Cx of tumour lysis syndrome? (5)

Answer 444

hyperkalaemia hyperphosphataemia hypocalcaemia hyperuricaemia acute renal failure

Question 445

What is tumour lysis syndrome?

Answer 445

potentially life threatening Cx that occurs when ca cells break down rapidly, releasing intracellular contents into blood -> metabolic imbalances

Question 446

What cancers is TLS most common in?

Answer 446

ones with high cell turnover eg. leukaemia and lymphoma, occasionally highly aggressive solid tumours

Question 447

When does TLS commonly happen?

Answer 447

after initiating Tx for ca eg. chemo, radio or targeted which rapidly kill large no of tumour cells can occur spontaneous when ca cells die on own, esp in rapidly growing tumours

Question 448

Symptoms of TLS?

Answer 448

Cardiac: Arrhythmias, palpitations, or even cardiac arrest (due to hyperkalemia). Renal: Acute kidney injury, leading to decreased urine output or complete kidney failure. Neurological: Muscle cramps, seizures, and altered mental status (due to electrolyte imbalances like hypocalcemia). Gastrointestinal: Nausea, vomiting, and diarrhea. General: Fatigue, weakness, and confusion.

Question 449

Diagnosis of TLS?

Answer 449

Blood Tests: Monitoring of electrolyte levels (potassium, phosphate, calcium), uric acid, and kidney function (creatinine levels). Clinical Criteria: Based on the Cairo-Bishop classification, which includes both laboratory abnormalities and clinical manifestations like acute kidney failure or arrhythmias.

Question 450

Mx and prevention of TLS?

Answer 450

Hydration: Aggressive IV fluids to help flush out toxins and prevent kidney injury. Allopurinol: Prevents the formation of uric acid by inhibiting xanthine oxidase. Rasburicase: Converts uric acid to allantoin, a more easily excretable compound, and is used in high-risk cases. Electrolyte Management: Hyperkalemia: May require insulin, glucose, or even dialysis to reduce potassium levels. Hypocalcemia: Treated cautiously, often with calcium supplements if symptomatic. Hyperphosphatemia: May require phosphate binders. Dialysis: In severe cases of kidney failure or life-threatening electrolyte disturbances.

Question 451

Prognosis of TLS?

Answer 451

If managed quickly and appropriately, TLS can be controlled, but without timely intervention, it can lead to multi-organ failure and death.

Question 452

What is crucial in high-risk pts for TLS?

Answer 452

Prevention is crucial in high-risk patients, and prophylactic measures (hydration, medications like allopurinol or rasburicase) are often initiated before starting cancer treatment.

Question 453

RFs for TLS?

Answer 453

- ca type= rapidly proliferatng ca eg. ALL and high-grade lymphomas eg. Burkitt lymphoma - tumour burden= large tumour or extensive disease - high sensitivity to Tx= ca that respond quick to chemo - pre-existing kidney issues= exacerbate inability to handle large load of metabolic byproducts released during TLS

Question 454

Example of a high grade lymphoma?

Answer 454

Burkitt's lymphoma

Question 455

Malignant proliferation of lymphocytes characterised by the presence of Reed-Sternberg cell?

Answer 455

Hodgkin's lymphoma

Question 456

Ages most affected by Hodgkin's lymphoma?

Answer 456

bimodal age distribution: 3rd and 7th decades most common

Question 457

Histological classification of Hodgkin's lymphoma?

Answer 457

- Nodular sclerosing (70%) - Mixed cellularity (20%) - Lymphocyte predominant (5%) - Lymphocyte depleted (rare)

Question 458

What histological type of Hodgkin's lymphoma has the best prognosis?

Answer 458

Lymphocyte predominant

Question 459

What histological type of Hodgkin's lymphoma has the worst prognosis?

Answer 459

Lymphocyte depleted

Question 460

What histological types of Hodgkin's lymphoma have a good prognosis?

Answer 460

Mixed cellularity and nodular sclerosing Lymphocyte predominant= best

Question 461

What histological type of Hodgkin's lymphoma is more common in women and associated with lacunar cells?

Answer 461

Nodular sclerosing

Question 462

What histological type of Hodgkin's lymphoma is associated with a large number of Reed-Sternberg cells?

Answer 462

Mixed cellularity

Question 463

What implies a poor prognosis in Hodgkin's lymphoma?

Answer 463

- B symptoms - Lymphocyte depleted type - >45yrs - stage IV - Hb < 10.5 g/dl - lymphocyte count < 600/µl or < 8% - male - albumin < 40 g/l - white blood count > 15,000/µl

Question 464

'B' symptoms?

Answer 464

weight loss >10% in last 6m fever >38ºC night sweats

Question 465

RFs for Hodgkin's lymphoma?

Answer 465

HIV EBV

Question 466

Features of Hodgkin's lymphoma?

Answer 466

- lymphadenopathy (75%) - systemic B symptoms (25%) - possible: mediastinal mass- may be symptomatic (cough) or incidental on CXR

Question 467

Subtypes of ALL?

Answer 467

B-cell ALL (80%) T-cell ALL (20%)

Question 468

Causes of ALL?

Answer 468

1) chemoradiation 2) genetic= Down's (ALL & AML) and translocations 3) infection

Question 469

How may chemoradiation cause ALL?

Answer 469

cause mutations so increase DNA replication without lymphoblasts actually dying so not differentiating into T and B cells

Question 470

Translocations that cause ALL?

Answer 470

(12:20)t= children (9:22)t= adults, Philidelphia chromosome forming BCR-ABL gene (different Tx for diff translocation)

Question 471

What virus may cause T-cell ALL?

Answer 471

HTLV

Question 472

What is associated with good prognosis in ALL?

Answer 472

hyperdiploid blast cells

Question 473

Effects of increased lymphoblasts in bone marrow in ALL?

Answer 473

1) increased lymphoblasts -> decreased function WBC= increase risk of INFECTION & mortality eg. pneumonia, UTI, cellulitis 2) decrease RBC (less space in BM)= ANAEMIA so pallor, fatigue, SOB 3) decrease platelets (less space)= THROMBOCYTOPENIA= bruising- petechiae, purpura and bleeding (epistaxis, GI, gums) 4) increase lymphoblasts= expand bone marrow= BONE PAIN, limping

Question 474

Effects of increased lymphoblasts in blood & tissues in ALL?

Answer 474

1) Hepatosplenomegaly= N&V, abdo fullness 2) Lymphadenopathy= painless, common, eg. cervical 3) Meninges= Meningeal Leukaemia (meningitis features) and CN palsy eg. CN6 (so can't abduct eye) 4) Testes= Testicular enlargement 5) If T-cell ALL= Thymic enlargement (thymus overlies heart so if enlarged can compress...): - trachea- SOB, stridor - oesophagus- dysphagia - superior vena cave- vein enlargement eg. neck

Question 475

What types of leukaemia may result in leukostasis or TLS?

Answer 475

AML or ALL AML>>> for leukostasis

Question 476

Diagnosis of ALL?

Answer 476

1) FBC and blood smear 2) Definitive diagnosis= bone marrow biopsy 3) immunophenotyping 4) genetic studies 5) Tests of infiltration: - CNS= CT/MRI, LP - testis= USS - thymus= CXR, CT chest (enlargement of thymus/mediastinum) - Liver/spleen= USS, CT abdo

Question 477

What would FBC and blood smear show in ALL?

Answer 477

- decreased RBC and platelets - variable functional WBC (high or low) - blood smear= increased immature lymohoblasts

Question 478

What would bone marrow biopsy show in ALL?

Answer 478

Increased lymphoblasts >20% (blast cell predominance)

Question 479

Immunophenotyping for ALL?

Answer 479

Immunohistochemistry: - lymphoblasts high - Tdt +ve - mpo -ve Flow cytometry: - T-ALL= CD2-CD8 (CD3) - B-ALL= CD10,19,20

Question 480

Genetic studies in ALL?

Answer 480

(12:21)t= children, more common (9:22)t= adults, Phil. chromosome Is it BCR-ABL +ve? If so and there is (9:22)t then Tx with tyrosine kinase inhibitors

Question 481

Why is immunophenotyping and genetic studies done in ALL?

Answer 481

as different Tx for different translocations

Question 482

Treatment for ALL?

Answer 482

1) systemic chemo: induction -> consolidation -> maintenance (phase). Goal= complete remission 2) prophylactic intrathecal chemotherapy with methotrexate +/- cranial radiotherapy 3) AND TLS prophylaxsis If fail... 4) Advanced therapies: - TKIs - Bone marrow Transplant

Question 483

Systemic chemo agents for ALL?

Answer 483

C.yclophosphamide V.incristine A.sparaginase (+/-) D.oxorubicin D.examethasone (or pred)

Question 484

Why is prophylactic intrathecal chemo with methatrexate +/- cranial radiation done in ALL?

Answer 484

risk of meningeal leukaemia in ALL

Question 485

Advanced therapies for ALL if chemo fails?

Answer 485

- Tyrosine kinase inhibitors eg. imatinib - Bone marrow transplant if= fail chemo, fail TKIs and poor prognosis

Question 486

When can tyrosine kinase inhibitors be used for ALL eg. imatinib?

Answer 486

if +ve for (9:22)t and BCR-ABL

Question 487

Cx and explanation of ALL?

Answer 487

TLS Malignant cells hit with chemo, burst and release: - phosphates - uric acid - potassium so cause AKI

Question 488

Prophylaxis for TLS eg. in ALL?

Answer 488

- IV fluids - Allopurinol - Rasburicase (all 3)

Question 489

Causes of increased myeloblasts (stopping differentiation into granulocytes)? (eg. AML)

Answer 489

1) chemoradiation 2) Genetic 3) Bone marrow disorder

Question 490

Genetic causes of increased myeloblasts? (eg. AML)

Answer 490

- Down's - AML subtype APL due to (15:17)t with PML-RARA gene

Question 491

Bone marrow disorders than can cause increased myeloblasts (eg. in AML)?

Answer 491

1) Myelodysplastic syndrome -> progresses to AML 2) CML -> AML

Question 492

Effects of increased myeloblasts in the bone marrow in AML?

Answer 492

1) increased myeloblasts so decrease functional WBCs (don't kill pathogens or differentiate to N, B or E)= Increased risk of infection and mortality eg. pneumonia, UTI, cellulitis 2) decrease RBC as less space= anaemia: pallor, fatigue, SOB 3) decrease platelets as less space= thrombocytopenia: bruising (petechiae, purpura), bleeding (gums, GI, nose) 4) increase myeloblasts= expands bone marrow= bone pain, limping

Question 493

Effects of increased myeloblasts in blood and tissues in AML?

Answer 493

1) leukostasis (AML>>ALL) if >=100,000 myeloblasts 2) Tumour lysis syndrome 3) Cutaneous/mucosal= leukaemia cutis and gingival hyperplasia 4) DIC (only in APL)= increase bleeding risk

Question 494

Leukostasis in AML?

Answer 494

if >=100,000 myeloblasts clog up blood flow due to blood vessel occlusion therefore: - hypoxaemia= headache, TIA, stroke - lungs= SOB, hypoxia so acute resp failure - retina= vision changes, vision loss

Question 495

Tumour lysis syndrome in AML?

Answer 495

secondary to chemo (most common) or spontaneous secondary to high tumour burden myeloblasts burst releasing phosphate, K+ and uric acid causing AKI as uric acid forms crystals and phosphate combines with Ca to form crystals (kidney stones) causing damage to kidney SO get= low urine output, high creatinine, high BUN; high K+ can cause arrythmias

Question 496

DIC in AML (only in APL subtype)?

Answer 496

myeloblast releases: 1) tissue factor (III) -> increase clotting pathway -> decrease clotting factors (secondary to consumption) so can't clot when need to 2) TPA -> fibrinolysis -> can't clot therefore increase bleeding risk: - brain bleed= ICH - bleed into lungs= pulmonary haemorrhage - bruising, bleeding (eg. out of cannula)

Question 497

Diagnosis of AML?

Answer 497

1) FBC & blood smear 2) Definitive= bone marrow biopsy then to determine Tx and prognosis... 3) immunophenotyping 4) Genetic studies 5) Tests of Cx: - electrolyte panel if TLS - clotting screen if DIC - clinical exam if leukostasis or cutaneous/mucosal manifestations

Question 498

What would FBC and blood smear show in AML?

Answer 498

- decreased RBC - decreased platelets - variable functional WBCs (increased or decreased) blood smear= increased myeloblasts and Auer rods (esp in APL)

Question 499

Bone marrow biopsy in AML?

Answer 499

increased myeloblasts (>20%) Auer rods

Question 500

Auer rods?

Answer 500

AML

Question 501

Immunophenotyping in AML?

Answer 501

Immunohistochemistry: - mpo +ve (myloperoxodase) - Tdt -ve

Question 502

Genetic studies in AML?

Answer 502

for subtypes and Tx (15:17)t= APL AML-RARA +ve= APL if APL then different Tx needed compared to other AML subtypes

Question 503

Electrolyte panel if TLS in AML?

Answer 503

- high phosphate - high uric acid - high potassium - low Ca as combine with PO4- to form crystals - AKI so high creatinine and high BUN

Question 504

Clotting screen if DIC in AML?

Answer 504

high PTT high INR high d-dimer low fibrinogen low RBCs low platelets

Question 505

Tx for AML?

Answer 505

- systemic chemo for non-APL subtype - systemic chemo for APL subtype - Bone marrow transplant - Tx of Cx: leukostasis or TLS

Question 506

Systemic chemo for AML (non-APL subtype)?

Answer 506

agents= Cytarabine and daunorubicin induction -> consolidation -> maintenance goal= complete remission

Question 507

Systemic chemo for AML (APL subtype)?

Answer 507

agents= ATRA +/- arsenic trioxide; may give steroids to prevent differentiation syndrome good prognosis goal= promote differentiation: myeloblast -> promyelocyte -> granulocyte

Question 508

What could chemo for APL subtype of AML lead to?

Answer 508

differentiation syndrome as goal if to promote differentiation (of undifferentiated high amounts of myeloblasts to granulocytes so good prognosis) this causes cytokine storm so can give steroids too to try prevent this

Question 509

Bone marrow transplant in AML?

Answer 509

if: - AML with poor prognostic findings (likely to fail chemo) or - AML that failed chemo (didn't undergo complete remission)

Question 510

Tx of leukostasis in AML?

Answer 510

1) cytoreduction= leukapheresis (take away myeloblasts blocking vessels) and hydroxyurea (reduce no. of myeloblasts) 2) then chemo

Question 511

Prevention/Tx of TLS in AML?

Answer 511

- allopurinol + - rasburicase + - IV fluids

Question 512

Why is allopurinol and rasburicase used in TLS?

Answer 512

Myeloblasts burst and release purines which convert to uric acid which then go to kidney to damage and cause AKI. Allopurinol prevents purines converting to uric acid. Rasburicase converts the uric acid into allantoin which is not toxic to kidney

Question 513

Haemoptysis pathway?

Answer 513

Haemocytoblast (stem cell in bone marrow which differentiates...) into 1)Myeloid stem cells into 2) RBCs (using erythropoeitin), platelets (using TPO) or myeloblasts (CSF) 3) myeloblasts -> promylocyte 4) promylocyte -> neutrophil, basophil or eosinophil (all granulocytes) or 1) Lymphoid stem cells into 2) lymphoblast into 3) B lymphoblasts -> T-cells -> go to thymus and lymph nodes or 3) T lymohoblasts -> B-cells -> go to lymph nodes

Question 514

Subtype of AML?

Answer 514

APL (Acute promyelocytic leukemia)

Question 516

alcohol-induced lymph node pain?

Answer 516

Hodgkin's lymphoma

Question 517

Lymphadenopathy in Hodgkin's lymphoma?

Answer 517

- common in neck (cericval/supraclavicular) > axillary > inguinal - usually painless, non-tender, asymmetrical - alcohol induced LN pain (<10% pts)

Question 518

B symptoms in Hodgkin's lymphoma?

Answer 518

weight loss pruritus night sweats fever (Pel-Ebstein)

Question 519

Ix for Hodgkin's lymphoma?

Answer 519

- normocytic anaemia - esosinophilia - LDH raised - Lymph node biopsy= Reed-Sternberg cells diagnostic

Question 520

Normocytic anaemia in Hodgkin's lymphoma?

Answer 520

may be multifactorial eg. hypersplenism, bone marrow replacement by HL, Coombs-positive haemolytic anaemia

Question 521

What causes eosinophilia in Hodgkin's lymphoma?

Answer 521

production of cytokines eg. IL-5

Question 522

What is diagnostic for Hodgkin's lymphoma?

Answer 522

Lymph node biopsy= Reed-Sternberg cells large cells; multinucleated or bilobed nucleus with eosinophilic inclusion-like nuclei (giving owl's eye appearance)

Question 523

Reed-Sternberg cells seen in what?

Answer 523

Hodgkin's lymphoma

Question 524

Old classification for Hodgkin's lymphoma?

Answer 524

Ann-Arbor staging Stage I: single lymph node II: 2 or more lymph nodes/regions on the same side of the diaphragm III: nodes on both sides of the diaphragm IV: spread beyond lymph nodes Each stage may be subdivided into A or B A = no systemic symptoms other than pruritus B = weight loss > 10% in last 6 months, fever > 38c, night sweats (poor prognosis)

Question 525

Classification used to stage Hodgkin's lymphoma (and other lymphomas)?

Answer 525

Lugano classification (updated version of Ann-Arbor) Stages I-IV; A/B, E, S and X

Question 526

Stages in the Lugano classification for Hodgkin's lymphoma?

Answer 526

Stage I: invl. of a single lymph node region (I) or a single extralymphatic organ or site (IE). Stage II: invl. of 2 or more LN regions on the same side of the diaphragm (II) or localized involvement of an extralymphatic organ or site and one or more LN regions on the same side of the diaphragm (IIE). Stage III: invl. of LN regions on both sides of the diaphragm (III), which may also be accompanied by localized involvement of an extralymphatic organ or site (IIIE), involvement of the spleen (IIIS), or both (IIIE+S). Stage IV: Diffuse or disseminated involvement of one or more extralymphatic organs, with or without associated lymph node involvement.

Question 527

What else does the Lugano classification for Hodgkin's lymphoma in addition to the stages? (4)

Answer 527

A/B symptoms= no B symptoms then classed as A, if B symptoms then B E= presence of extranodal disease S= involvement of the spleen X= bulky disease (large tumour mass)

Question 528

What does the Lugano classification system for Hodgkin's lymphoma emphasise the role of?

Answer 528

PET scans to determine staging- assess whether lymphoma is metabolically active in diff parts of body

Question 529

Mx for Hodgkin's lymphoma?

Answer 529

- chemo -radiotherapy - combined modality therapy (CMT)= chemo followed by radio - hematopoeitic cell transplant= for relapsed or refractory classic Hodgkin lymphoma

Question 530

What is combined modality therapy (CMT)?

Answer 530

chemotherapy followed by radiotherapy

Question 531

2 combinations of chemotherapy that can be used for Hodgkin's lymphoma?

Answer 531

ABVD= standard BEACOPP= alternative with better remission rates but higher toxicity

Question 532

ABVD chemo regimen for Hodgkin's lymphoma?

Answer 532

doxorubicin bleomycin vinblastine decarbazine

Question 533

BEACOPP chemo regimen for Hodgkin's lymphoma?

Answer 533

bleomycin etoposide doxorubicin cyclophosphamide vincristine procarbazine prednisone

Question 534

Cx of treatment for Hodgkin's lymphoma?

Answer 534

most pts achieve long-term survival free of HL secondary malignancies are a risk eg. solid tumours- breast, lung

Question 535

Differences between Hodgkin's lymphoma vs Non-hodgkin's lymphoma?

Answer 535

- higher prevalence of NHL - older mean age of diagnosis of NHL - in NHL there is non-contigous, multicentric spread - in NHL extranodal invl. is common - HL= Reed-Sternberg cells; NHL= NO R-S cells

Question 536

Lymphoma definition?

Answer 536

malignant proliferation of lymphocytes which accumulate in lymph nodes or other organs

Question 537

How is lymphoma classified?

Answer 537

Hodgkin's lymphoma= presence of Reed-Sternberg cells Non-Hodgkins= every other type of lymphoma that is not Hodgkin's; NO Reed-Sternberg cells

Question 538

Non-hodgkin's lymphoma may affect what cells?

Answer 538

B or T cells further classified as high or low grade

Question 539

What is more common: NHL or HL?

Answer 539

NHL

Question 540

What age is usually affected by non-hodgkin's lymphoma?

Answer 540

typically elderly, >75yrs

Question 541

RFs for Non-Hodgkin's lymphoma?

Answer 541

- elderly - caucasian - Hx of viral infection esp EBV - FHx - chemical agents (pesticides, solvents) - Hx of chemo or radio - Immunodeficiency (transplant, HIV, DM) - Autoimmune (SLE, Sjogren's, coeliac)

Question 542

Symptoms of Non-Hodgkin's lymphoma?

Answer 542

- painless lymohadenopathy (non-tender, rubbery, asymmetrical) - constitutional/B symptoms - extranodal disease: gastric (dyspepsia, dysphagia, weight loss, abdo pain); bone marrow (pancytopenia, bone pain); lungs; skin; CNS (nerve palsies)

Question 543

How to differentiate between HL and NHL?

Answer 543

biopsy and CP HL= can have alcohol induced LN pain B symptoms typically earlier in HL and later in NHL extra-nodal disease much MORE common in NHL

Question 544

Signs of Non-Hodgkin's lymphoma?

Answer 544

- weight loss - lymohadenopathy (cervical, axillary, inguinal) - palpable abdo mass: hepatomegaly, splenomegaly, lymph nodes - testicular mass - fever

Question 545

Ix for Non-Hodgkin's lymphoma?

Answer 545

Diagnostic= excisional node biopsy - CT chest, abdo, pelvis (staging) - HIV test (RF for NHL) - FBC and blood film - ESR (prognostic indicator) - LDH (prognostic indicator) - other if clinically indicated eg. LFTs if ?liver mets, PET CT, bone marrow biopsy (BM invl?), LP if neuro CP

Question 546

Why may FBC and blood film be done for NHL? ESR? LDH?

Answer 546

FBC & blood film= may have normocytic anaemia; helpful to rule out other haem malignancy eg. leukaemia ESR= good prognostic indicator LDH= marker of cell turnover, useful prognostic indicator

Question 547

Classification to stage NHL?

Answer 547

Lugano staging

Question 548

Mx of NHL depends on what?

Answer 548

the sub-type

Question 549

Mx for NHL?

Answer 549

typically watchful waiting, chemo or radio Rituximab is used in combination with conventional chemo regimens (eg. CHOP) for variety of NHL types - all pts= flu/pneumococcal vaccines - neutropenia= may need Abx prophylaxis

Question 550

Example chemo regimen for NHL?

Answer 550

CHOP: cyclophosphamide doxorubicin (hydroxydaunorubicin) vincristine (Oncovin®) prednisolone

Question 551

Cx of NHL?

Answer 551

Bone marrow infiltration causing anaemia, neutropenia or thrombocytopenia Superior vena cava obstruction Metastasis Spinal cord compression Complications related to treatment e.g. Side effects of chemotherapy

Question 552

Prognosis of NHL?

Answer 552

Low-grade non-Hodgkin's lymphoma has a better prognosis High-grade non-Hodgkin's lymphoma has a worse prognosis but a higher cure rate

Question 553

When to consider a suspected ca pathway referral for NHL in adults?

Answer 553

present with unexplained lymphadenopathy or splenomegaly take into account associated features eg. fever, night sweats, SOB, pruritus, weight loss

Question 554

When to consider a very urgent referral (appointment within 48hrs) for specialist assessment of NHL in children and young adults?

Answer 554

present with unexplained lymphadenopathy or splenomegaly take into account associated features eg. fever, night sweats, SOB, pruritus, weight loss

Question 555

What referral do you use for NHL or HL if pt is 16-24yrs, adult or children/young adult?

Answer 555

either depending on age and local arrangements

Question 556

Type of referrals for NHL or HL?

Answer 556

- adult= suspected ca pathway referral (within 2w) - children/young adult= very urgent (within 48hrs)

Question 557

When to consider a suspected ca pathway referral for HL in adults?

Answer 557

presenting with unexplained lymphadenopathy take into account: fever, night sweats, SOB, pruritus, weight loss or alcohol-induced lymph node pain

Question 558

When to consider a very urgent referral (appointment within 48hrs) for specialist assessment of HL in children and young adults?

Answer 558

presenting with unexplained lymphadenopathy. When considering referral, take into account any associated symptoms, particularly fever, night sweats, shortness of breath, pruritus, or weight loss.

Question 559

Most aggressive form of malignant melanoma?

Answer 559

nodular other forms spread more slowly

Question 560

Subtypes of melanoma?

Answer 560

1) Nodular 2) Superficial spreading 3) Lentigo maligna 4) Acral lentiginous

Question 561

Melanoma: superfical spreading type?

Answer 561

70% of cases Typically= arms, legs, back & chest, young people Appearance= growing mole with diagnostic features

Question 562

Melanoma: nodular type?

Answer 562

second commonest Sun-exposed skin, middle aged Red or black lump or lump which bleeds or oozes

Question 563

Melanoma: lentigo maligna type?

Answer 563

less common chronically sun exposed skin, older people a growing mole with diagnostic features

Question 564

Melanoma: acral lentiginous form?

Answer 564

rare form nails, palms or soles; people with darker skin pigmentation subungal pigmentation (Hutchinson's sign) or on palms or feet

Question 565

Rare forms of melanoma?

Answer 565

desmoplastic melanoma, amelanotic melanoma, or melanoma arising in other parts of the body such as ocular melanoma.

Question 566

Main diagnostic features and secondary features of melanoma?

Answer 566

The main diagnostic features (major criteria): - Change in size - Change in shape - Change in colour Secondary features (minor criteria) - Diameter >= 7mm - Inflammation - Oozing or bleeding - Altered sensation

Question 567

Mx for melanoma?

Answer 567

- suspicious lesions= excision biopsy: do not biopsy in primary care if suspected or uncertain- refer! - once confirmed= determine whether re-excision of margins is required (Breslow thickness) - sentinel lymph node mapping, isolated limb perfusion and block dissection of regional lymoh node groups should be selectively applied

Question 568

Margins of excision related to Breslow thickness for melanoma?

Answer 568

Lesions 0-1mm thick= 1cm Lesions 1-2mm thick= 1- 2cm (Depending upon site and pathological features) Lesions 2-4mm thick= 2-3 cm (Depending upon site and pathological features) Lesions >4 mm thick= 3cm

Question 569

Most important factor in determining prognosis of pts with malignant melanoma?

Answer 569

the invasion depth of a tumour (Breslow depth)

Question 570

Breslow depth and approximate 5yr survival for melanoma?

Answer 570

< 0.75 mm= 95-100% 0.76 - 1.50 mm= 80-96% 1.51 - 4 mm= 60-75% > 4 mm= 50%

Question 571

Urgent suspected ca pathway referral for pigmented lesion ?melanoma?

Answer 571

The lesion has a weighted 7-point checklist score of 3 or more. Dermoscopy suggests melanoma. There are nail changes, such as a new pigmented line in the nail (especially if there is associated damage to the nail), or a lesion growing under the nail. They have a new persistent skin condition, especially if growing, pigmented, or vascular in appearance and the diagnosis is unclear. There is any doubt about the lesion. A biopsy has confirmed the diagnosis of malignant melanoma. Note: if a lesion is suspected to be melanoma, an excision in primary care should be avoided.

Question 572

Most common tumour causing bone mets? (in descending order)

Answer 572

prostate breast lung

Question 573

Most common sites for bone mets (in descending order)?

Answer 573

spine pelvis ribs skull long bones

Question 574

Features of bone mets?

Answer 574

bone pain pathological fractures hypercalcaemia raised ALP

Question 575

Lung mets are seen with what cancers?

Answer 575

breast colorectal renal cell bladder prostate

Question 576

Cannonball mets?

Answer 576

multiple round well-defined lung secondaries most commonly seen with renal cell ca, may also occur 2 to choriocarcinoma and prostate ca

Question 577

Clacification in lung mets?

Answer 577

uncommon except in chondrosarcoma or osteosarcoma

Question 578

Metastatic disease of unknown primary: Ix for initial diagnostic phase?

Answer 578

All pts: - FBC, U&E, LFT, calcium, urinalysis, LDH - CXR - CT chest, abdomen and pelvis - AFP and hCG Specific pts: - myeloma screen (if lytic bone lesions) - endoscopy (?symptoms) - PSA (men) - CA125 (women with peritoneal malignancy or ascites) - Testicular US (men with germ cell tumours) - Mammography (features of breast ca)

Question 579

For pts presenting with MUO (mets of unknown origin), diagnosis can be divided into 2 phases. Aim of inital phase is to perform most appropritate Ix efficiently to identify what?

Answer 579

1) primary site which will guide Tx or 2) non-epithelial malignancy, which can be Tx regardless of primary site or metastatic epithelial or neuro-endrocrien malignancy without an identifiable primary site (diagnosis of provisional CUP- carcinoma of unknown primary)

Question 580

Example of non-epthelial malignancies? (can be treated regardless of primary site)

Answer 580

lymphoma other haem malignancies melanoma sarcoma germ-cell tumours

Question 581

Metastatic disease of unknown primary: secondary diagnostic phase Ix (special Ix)?

Answer 581

- tumour markers (but always do AFP and hCG, PSA, CA125 in all pts if relevant) - upper and lower GI endoscopy - mammogram - MRI breast - PET CT eg. if present with cervical lymphadenopathy - Antibodies= CK7, CK20, TTF-1, PLAP, ER, PSA with adenocarcinoma of MUO - Flexible bronchoscopy with biopsy, brushings and washing= present with intrapulmonary nodules and unsuitbale for peercutaneous biopsy - Tissue sample for histology if MUO with ascites

Question 582

Mx for MUO: what presentations may benefit from radical Tx?

Answer 582

- SCC invl. upper or mid neck nodes - adenocarcinoma invl. axillary nodes - SCC invl. inguinal nodes - solitary mets

Question 583

Presentations of MUO with poor prognosis?

Answer 583

multiple mets incl. brain involvement- do not offer chemo unless clinical trial

Question 584

When to offer pts chemo if they have confirmed carcinoma with unknown primary (CUP)?

Answer 584

confirmed CUP with clinical and/or laboratory features of a specific treatable syndrome and adequate performance status.

Question 585

How are metastatic bone tumours described?

Answer 585

blastic lytic or mixed

Question 586

What metastatic bone tumours have the lowest risk of spontaneous fractures?

Answer 586

osteoblastic metastatic disease lower risk compared to oestolytic lesions of similar size

Question 587

What metastatic bone lesions are most prone to spontaneous fracture?

Answer 587

lesions affecting peritrochanteric region because of the loading forces at that site

Question 588

Scoring system to stratify the risk of spontaneous fracture for bone mets of varying types?

Answer 588

Mirel Scoring system

Question 589

Mirel scoring system: work out score points for each type?

Answer 589

1 point= upper extremity; blastic radiographic appearance; <1/3 width of bone invloved; mild pain 2 points= lower extremity; mixed; 1/3-2/3; moderate pain 3 points= peritrochanteric; lytic; >2/3; pain aggravated by function

Question 590

Tx for metastatic bone lesions depending on the Mirel scoring system?

Answer 590

Score 9+= risk of fracture is impending (33%); Tx is prophylactic fixation Score 8= borderline risk; consider fixation Score 7 or less= not impending risk (4%); non-operative Mx

Question 591

What to do if spinal mets are thought to be the cause of spinal cord compression pain?

Answer 591

urgent specialist advice within 24hrs; immediate advice if neuro features unless contraindicated (signif suspicion of lymphoma) offer all pt with met spinal cord compression a loading dose of 16mg of dexamethasone asap

Question 592

Pts may present with spinal mets before developing metastaic spinal cord compression, so it is important to do what?

Answer 592

identify these pts early before any neuro symptoms develop

Question 593

Symptoms and findings of spinal mets?

Answer 593

- unrelenting lumbar back pain - any thoracic or cervical back pain - worse sneezing, coughing or straining - nocturnal - associated with tenderness - wakes pt up at night

Question 594

Spinal mets: what if any neuro features are present?

Answer 594

suspect spinal cord compression and act promptly without neuro features= whole spine MRI within 1w (whole spine imaged as pts commonly present with multi-level disease)

Question 595

Another name for myeloma?

Answer 595

multiple myeloma (same thing)

Question 596

Multiple myeloma?

Answer 596

progressive malignant disease characterised by proliferation of abnormal plasma cells in bone marrow and abnormal monoclonal immunoglobulins in the blood

Question 597

What organs/systems does multiple myeloma afffect?

Answer 597

bones kidneys blood immune system

Question 598

Multiple myeloma more common in what gender/age?

Answer 598

men increases with age

Question 599

Prognosis of multiple myeloma?

Answer 599

usually incurable but can disease control can be achieved for several yrs

Question 600

What is associated with a worse prognosis in multiple myeloma?

Answer 600

pt has high levels of serum beta-2 microglobin; high plasma cell count; diffuse multiple bone lesions; hypercalcaemia; very high levels of M protein in blood and urine; renal impairment

Question 601

Cx of multiple myeloma?

Answer 601

- Pathological bone fractures. - Spinal cord compression. - Renal damage. - Hypercalcaemia. - Impaired resistance to infection. - Anaemia. - Bleeding disorders. - Hyperviscosity of the blood.

Question 602

CP of multiple myeloma?

Answer 602

- bone pain, often lower back - fatigue - confusion, muscle weakness, constipation, thirst and polyuria (due to hypercalcaemia) - weight loss - recurrent infection - headache, visual disturbance, cognitive impairment, mucosal bleeding, SOB (due to hyperviscosity of blood) - sensory loss, paraesthesia, limb weakness, walking difficulty, sphincter disturbance (due to spinal cord compression) - occasionally asymptomatic

Question 603

Occasionally multiple myeloma is asymptomatic, so how would it present?

Answer 603

with abnormalities on blood tests eg: - normochromic, normocytic anaemia - renal impairment - hypercalcaemia - raised ESR, plasma viscosity, serum protein or globulin

Question 604

What to do if suspect multiple myeloma in pt over 60yrs with persistent bone pain, esp back, or unexplained fracture?

Answer 604

arrange FBC, serum Ca and plasma viscosity or ESR

Question 605

What to do if suspect multiple myeloma in pt over 60yrs with hypercalcaemia or leukopenia and presentation consistent with possible myeloma?

Answer 605

arrange very urgent serum electrophoresis, serum-free light chain assay and Bence-Jones protein urine assessment (within 48hrs)

Question 606

What to do if pt has plasma viscosity, ESR or incidental finding on bloods and presentation are consistent with possible myeloma?

Answer 606

Consider very urgent serum electrophoresis, serum-free light chain assay, and Bence-Jones protein urine assessment (within 48 hours)

Question 607

What else should be done in pts who u suspect multiple myeloma?

Answer 607

consider additional Ix: peripheral blood film, serum urea, creatinine and electrolytes, liver function tests, and for people with bone pain, X-rays of symptomatic areas (to rule out pathological fractures).

Question 608

Multiple myeloma: when to arrange urgent hospital admission?

Answer 608

- for people with symptoms of spinal cord compression - if Ix reveal moderate to severe hypercalcaemia (corrected Ca 3.01mmol/L or higher) or AKI

Question 609

What to do if serum and/or urine protein electrophoresis suggest myeloma?

Answer 609

urgent referral to haematologist within 2w for further Ix to confirm

Question 610

Tx for multiple myeloma depends on what?

Answer 610

age disease stage prognosis cormorbidities

Question 611

What might the Tx of mutiple myeloma inclue?

Answer 611

Bisphosphonates to reduce bone disease and pain. eg. zolendronic acid Treatments for anaemia. eg. erythropoietin analogues or blood transfusion Chemotherapeutic drugs. High-dose drug therapy and stem cell transplantation. Immunomodulatroy drugs eg. thalidominde, lenalidomine and pomalidomide + DVT prophylaxis (aspirin or LMWH) Steroids eg. prednisolone or dexamthasone

Question 612

Symptoms of hypercalcaemia eg. in myeloma?

Answer 612

bone pain, abdominal pain, depression, confusion, muscle weakness, constipation, thirst, and polyuria

Question 613

Multiple myeloma may present with what?

Answer 613

pathological fractures and recurrent infection

Question 614

Examination in myeloma?

Answer 614

may be normal Hepatomegaly — present in about 4% of people. Splenomegaly — present in about 1% of people. Lymphadenopathy — present in about 1% of people.

Question 615

Differential diagnosis of multiple myeloma?

Answer 615

- depression - osteoarthritis - DM - polymyalgia rheymatica - MGUS - Waldenstrom's macroglobulinaemia - Osteosclerotic myeloma - AL amyloidosis - heavy chain disease - NHL - plasma cell leukaemia

Question 616

Waldenstrom's macroglobulinaemia

Answer 616

Clinical features include hyperviscosity syndrome, organomegaly, and lymphadenopathy presenting in a person with an average age of 65 years. (differential for myeloma)

Question 617

Amyloid light chain (AL) amyloidosis (differential for myeloma)?

Answer 617

Clinical features include fatigue, weight loss, hepatomegaly, macroglossia, chronic kidney disease, heart failure, postural hypotension, carpal tunnel syndrome, and peripheral neuropathy.

Question 618

Heavy chain disease (differential for myeloma)?

Answer 618

Clinical features include weakness, fatigue, fever, lymphadenopathy and hepatosplenomegaly, with a portion of the immunoglobulin heavy chain in the serum and/or urine.

Question 619

Plasma cell leukaemia (differential for myeloma)?

Answer 619

Clinical features include bone pain, fatigue, recurrent infection, mucosal bleeding, hypercalcaemia, renal impairment, hepatomegaly, and splenomegaly.

Question 620

Osteosclerotic myeloma?

Answer 620

(polyneuropathy, organomegaly, endocrine disease, M protein in the blood, and skin lesions [POEMS] syndrome) Clinical features include marked polyneuropathy with widespread neurological involvement, hepatomegaly, splenomegaly, sclerotic bone lesions, endocrine disease which might manifest as gynaecomastia, M protein in the blood, and skin lesions.

Question 621

Can serum/urine electrophoresis be negative in multiple myeloma?

Answer 621

in 1-5% who have a 'non-secretory' form of the disease that produces no serum M protein or urinary Bence-Jones protein.

Question 622

Ix for myeloma?

Answer 622

Back pain/unexplained fracture= FBC, serum Ca, plasma viscosity or ESR Hypercalcaemia/leukopenia + CP consistent= Very urgent (within 48 hours) serum electrophoresis, serum-free light-chain assay, and Bence-Jones protein urine assessment. Additional to confirm: - peripheral blood film - serum urea, creatinine, electrolytes and LFTs - X-rays if bone pain

Question 623

What may peripheral blood film show in multiple myeloma?

Answer 623

rouleaux (aggregations of red blood cells), which might suggest underlying paraproteinaemia.

Question 624

Why may urea, creatinine, electrolytes and LFTs be done if suspect myeloma?

Answer 624

detect renal impairment, raised uric acid from increased tumour cell turnover, and to determine total protein concentration, which is usually raised in multiple myeloma.

Question 625

Secondary care Ix to confirm multiple myeloma?

Answer 625

- immunofixation of serum & urine= confirm presence of paraprotein - bone marrow aspirate and trephine biopsy, with plasma cell phenotyping= confirm the presence of monoclonal plasma cells in the bone marrow. - MRI GOLD to confirm extent of myeloma bone disease; CT if contraindicaated -- Estimate tumour burden and prognosis= FISH analysis of bone marrow aspirate; Serum beta-2 microglobulin concentration; next-generation DNA sequencing.

Question 626

How often should pt with multiple myeloma be reviewed by a haematologist?

Answer 626

Symptomatic (active)= at least every 3m Asymptomatic (smouldering)= every 3m for 1st 5yrs then depends on long-term stability of the disease

Question 627

What should be avoided in pts with myeloma?

Answer 627

aminoglycosides due to risk of renal toxicity

Question 628

Chemotherapeutic drugs for myeloma?

Answer 628

cyclosphoshamide, doxirubicin, carfilozmib, bortezombin or melphalan

Question 629

When to suspect end-stage myeloma?

Answer 629

when symptoms become refractory to Tx Bone pain. Renal failure. Bone marrow failure. Infection — infection is a common cause of death in people with multiple myeloma. Increasing fatigue. Anorexia and weight loss. Changes in communication, deteriorating mobility or performance status, or social withdrawal.

Question 630

Myeloma disease course?

Answer 630

difficult to predict, may go through multiple lines of Tx and experience periods of relapse and remission. after each line of Tx, chance of remission decreases movement from stable to late stage disease can be rapid

Question 631

Myeloma arises due to what?

Answer 631

genetic mutations that occur as B-lymphocytes differentiate into mature plasma cells

Question 632

Median age at presentation of myeloma?

Answer 632

70yrs

Question 633

Mnemonic to remember multiple myeloma?

Answer 633

Old CRABBI Old= age at presentation C.alcium= hypercalcaemia R.enal impairment A.naemia B.leeding= thrombocytopenia B.one lytic lesions I.nfection= more susceptible other= amyloidosis (eg. macroglossia), carpal tunnel, neuropathy, hyperviscosity

Question 634

Why do you get hypercalcaemia in myeloma?

Answer 634

increased osteoclastic bone resorption caused by local cytokines (eg. IL-1, tumour necrosis factor) released by myeloma cells also less commonly: impaired renal function, increased renal tubular calcium resabsorption and elevated PTH-rP levels

Question 635

What can constipation, nausea, anorexia and confusion in myeloma be caused by?

Answer 635

hypercalcaemia

Question 636

Why do you get renal damage/impairment in myeloma?

Answer 636

monoclonal production of immunoglobulins results in light chain deposition within the renal tubules causes renal damage which presents as dehydration and increasing thirst other causes in myeloma: amyloidosis, nephrocalcinosis, nephrolithiasis

Question 637

Why do you get anaemia in myeloma?

Answer 637

bone marrow crowding suppresses erythropoiesis leading to anaemia fatigue and pallor

Question 638

Why do pts with myeloma have increased risk of bleeding?

Answer 638

bone barrow crowding results in thrombocytopenia which puts pts at risk of bleeding and bruising

Question 639

Why may pt get bone lytic lesions in myeloma?

Answer 639

bone marrow infiltration by plasma cells and cytokine-mediated osteoclast overactivity creates bone lytic lesions may present as pain (esp in back) and increases risk of pathological fractures

Question 640

Why may pts with myeloma have increased susceptibility to infection?

Answer 640

a reduction in normal production of immunoglobulins

Question 641

Summary of Ix for myeloma?

Answer 641

- bloods= FBC (anaemia), peripheral blood film (rouleaux formation), U&E (renal failure), bone profile (hypercalcaemia) - protein electrophoresis= raised conc of monoclonal IgA/IgG in serum; in urine they are known as Bence Jones proteins - bone marrow aspiration= plasma cells signif raised- confirms diagnosis - whole body MRI and X-rays. X-rays= 'rain drop skull' (random pattern of dark spots; very similar to pepperpot skull in hyperparathyroidism)

Question 642

Diagnostic criteria for myeloma?

Answer 642

one major and one minor criteria or three minor criteria in an individual who has signs or symptoms of multiple myeloma. Major criteria: - Plasmacytoma (as demonstrated on evaluation of biopsy specimen) - 30% plasma cells in a bone marrow sample - Elevated levels of M protein in the blood or urine Minor criteria - 10% to 30% plasma cells in a bone marrow sample. - Minor elevations in the level of M protein in the blood or urine. - Osteolytic lesions (as demonstrated on imaging studies). - Low levels of antibodies (not produced by the cancer cells) in the blood.

Question 643

What type of malignancy is a chronic relapsing and remitting and deemed incurable?

Answer 643

myeloma

Question 644

Aims of Mx for myeloma?

Answer 644

control symptoms, reduce Cx and prolong survival

Question 645

The combination of drugs used to treat myeloma (induction therapy) depends on what?

Answer 645

whether a patient may be suitable for autologous hematopoietic cell transplantation or not.

Question 646

Autologous hematopoiectic cell transplantation for myeloma?

Answer 646

involves the removal of a patient's own stem cells prior to chemotherapy, which are then replaced after chemotherapy prolong both event-free and overall survival when compared with non-transplant strategies typically it is younger, healthier patients who are suitable for stem cell transplantation and rigorous chemotherapy regimes.

Question 647

Is allogenic hematopoiectic cell transplant used in myeloma?

Answer 647

not commonly due to high rates of overall mortality and symptoms of graft-versus-host disease. It is currently only used as part of clinical trials when treating multiple myeloma.

Question 648

Autologous vs allogeneic hematopoiectic cell transplant?

Answer 648

autologous= transplant from same person who will get the transplant allogenic= from someone else eg. matched relative or unrelated donor

Question 649

Cx of myeloma and their Mx?

Answer 649

pain: treat with analgesia (using the WHO analgesic ladder) pathological fracture: zoledronic acid is given to prevent and manage osteoporosis and fragility fractures as these are a large cause of morbidity and mortality, particularly in the elderly. infection= receive annual influenza vaccinations they may also receive Immunoglobulin replacement therapy. VTE prophylaxis fatigue= treat all possible underlying causes, if symptoms persist consider an erythropoietin analogue.

Question 650

How many ca pts are affected by spinal cord compression?

Answer 650

up to 5%

Question 651

Neoplastic spinal cord compression- most common type?

Answer 651

extradural compression- usually due to vertebral body mets

Question 652

Neoplastic spinal cord compression is more common in pts with what ca?

Answer 652

lung, breast and prostate

Question 653

Earliest and most common symptom of neoplastic spinal cord compression?

Answer 653

back pain may be worse lying down and coughing

Question 654

Features of neoplastic spinal cord compression?

Answer 654

- back pain - lower limb weakness - sensory loss and numbness - neuro signs depend on level of lesion

Question 655

Neoplastic spinal cord compression: lesions above L1 usually result in what?

Answer 655

UMN signs in legs and a sensory level

Question 656

Neoplastic spinal cord compression: lesions below L1 usually result in what?

Answer 656

LMN signs in legs and perianal numbness

Question 657

Neoplastic spinal cord compression: what happens to tendon reflexes?

Answer 657

tend to be increased below the level of the lesion and absent at the level of lesion

Question 658

Ix for neoplastic spinal cord compression?

Answer 658

urgent (within 24hrs of presentation) whole MRI spine

Question 659

Mx for neoplastic spinal cord compression?

Answer 659

high dose oral dexamethasone urgent oncology assessment to consider radiotherapy or surgery

Question 660

Most common type of oesophageal ca?

Answer 660

adenocarcinoma

Question 661

What pts are more likely to develop adenocarcinoma of the oesophagus?

Answer 661

those with Hx of GORD or Barrett's

Question 662

Oesophageal ca: adenocarinoma vs squamous cell cancer epidemiology?

Answer 662

A= most common type in UK/US SCC= most common type in developing world

Question 663

Oesophageal ca: adenocarinoma vs squamous cell cancer location?

Answer 663

A= lower third, near the gastroesophageal junction SCC= upper 2/3rds of oesophagus

Question 664

Oesophageal ca: adenocarinoma vs squamous cell cancer RFs?

Answer 664

A= GORD; Barrett's; smoking; obesity SCC= smoking, alcohol, achalasia; Plummer-Vinson syndrome; diets rich in nitrosamines

Question 665

Features of oesophageal ca?

Answer 665

- dysphagia (most common): progressive - anorexia and weight loss - vomiting - odynophagia, hoarseness, malaena, cough

Question 666

Diagnosis of oesophageal ca?

Answer 666

- Upper GI endoscopy with biopsy - Endoscopic USS for locoregional staging - CT chest, abdo and pelvis for initial staging: laparoscopy can be used to detect occult peritoneal disease; FDG-PET CT may be used for occult mets if mets not seen on initial CT

Question 667

Mx for operable disease (T1N0M0) in oesophageal ca?

Answer 667

surgical resection- most common procedure is Ivor-Lewis type oesophagectomy

Question 668

Mx for oesophageal ca?

Answer 668

surgical resection if possible may need adjuvant chemo

Question 669

Biggest challenge in surgical resection for oesophageal ca?

Answer 669

anastomotic leak, with an intrathoracic anastomosis resulting in mediastinitis

Question 670

Types of ovarian ca?

Answer 670

Epithelial ca (90%)= serous, mucinous, endometroid, clear cell, transitional cell and squamous Non-epithelial (10%)= germ cell tumours, sex cord/stromal cell

Question 671

Most common ovarian ca?

Answer 671

Serous epithelial ca

Question 672

Secondary mets can occur in ovary, most commonly from where?

Answer 672

ca of endometrium, breast and GI tract

Question 673

Where may ovarian ca spread?

Answer 673

intraperitoneal structures and organs (causing intestinal obstruction and cachexia), liver, para-aortic lymph nodes and the lungs (causing pleural effusions)

Question 674

Lifetime risk of women being diagnosed with ovarian ca?

Answer 674

1 in 50

Question 675

What reduces risk of ovarian ca?

Answer 675

- high no. of pregnancies - breastfeeding - COCP

Question 676

When should you suspect ovarian ca in women (particularly if >50yrs)? (CP)

Answer 676

any persistent or frequent (>12x per month): - abdo distension (bloating) - feeling full (early satiety) and/or loss of appetite - pelvic or abdo pain - increased urinary urgency and/or frequency - symptoms suggestive of IBS within last 12m if >50yrs - unexplained symptoms: - weight loss - malaise or fatigue - change in bowel habit - abnormal or postmenopausal bleeding - GI symptoms= dyspepsia, nausea and bowel obstruction - SOB (due to pleural effusion)

Question 677

What to do if suspect ovarian ca?

Answer 677

- exam abdo and pelvis - if normal then CA125

Question 678

Suspect ovarian ca and exam of abdo and pelvis= ascites or pelvic/abdo mass that is not caused by uterine fibroids?

Answer 678

urgent referral

Question 679

Suspect ovarian ca, exam normal so do CA125: what if serum CA125 conc is raised?

Answer 679

urgent USS of abdo and pelvis arranged and urgent referral if this is suggestive of ovarian ca if USS and CA125 suggest ovarian ca then perform CT pelvis and abdo to establish extent of disease; + thorax if indicated

Question 680

Suspect ovarian ca, exam normal so do CA125: what if serum CA125 conc is normal, or raised with normal USS?

Answer 680

consider other causes of symptoms

Question 681

Peak age for ovarian ca?

Answer 681

60yrs

Question 682

Why does ovarian ca have poor prognosis?

Answer 682

due to late diagnosis

Question 683

Where is often the site of origin of many 'ovarain ca'?

Answer 683

distal end of fallopian tube

Question 684

RFs for ovarian ca?

Answer 684

- FHx= mutations of BRCA1 or BRCA2 gene - many ovulations= early menarche, late menopause, nulliparity eg. when have 'more' ovulations

Question 685

What cancers have notoriously vague symptoms/non specific presentation so often diagnosed late?

Answer 685

ovarian

Question 686

Abdo distension and bloating, abdo and pelvic pain, urinary symptoms eg. urgency, early satiety and diarrhoea?

Answer 686

?ovarian ca

Question 687

What is classed as a raised CA125?

Answer 687

35 IU/mL or greater

Question 688

What may increase CA125?

Answer 688

ovarian ca endometriosis menstruation benign ovarian cysts other conditions

Question 689

Can CA125 be used for screening for ovarian ca in asymptomatic women?

Answer 689

NO not very specific

Question 690

Diagnosis for ovarian ca?

Answer 690

difficult, usually involves diagnostic laparotomy

Question 691

Mx for ovarian ca?

Answer 691

usually combination of surgery and platinum-based chemo

Question 692

Prognosis of ovarian ca?

Answer 692

- 80% have advanced disease at presentation - 5yr survival is <35%

Question 693

In women under 40yrs with suspected ovarian ca, measure what on top of CA125 to identify women who may not have epithelial ovarian ca?

Answer 693

AFP and beta-hCG

Question 694

Confirmed ovarian ca after exam, raised CA125 and USS (then CT for extent); what to do next?

Answer 694

Confirm tissue diagnosis by histology by laparotomy or if surgery not been performed can use percutaneous image guided biopsy if feasible

Question 695

Mx for early (stage I) ovarian ca?

Answer 695

1) retroperitoneal lymph node assessment + optical surgical staging (surgery- resection) 2) Adjuvant if high risk stage I disease (grade 3 or stage Ic)= 6 cycles of carboplatin

Question 696

What does optical surgical staging in ovarian ca involve?

Answer 696

optical surgical staging involves= midline laparotomy; total abdo hysterectomy; bilateral salpingo-oophorectomy or infracolic omentectomy; biopsies of any peritoneal deposits, random biopsies of plevis and abdo peritoneal

Question 697

Mx of advanced (stage II to IV) ovarian ca?

Answer 697

1) primary surgery= complete resection of all macroscopic disease 2) chemo after surgery (debulking surgery with adjuvant chemo) or chemo before and after (neoadjuvant chemo and interval debulking surgery)

Question 698

Over 80% of pancreatic tumours are what?

Answer 698

adenocarcinoma

Question 699

Where do adenocarcinomas of the pancreas typically occur?

Answer 699

head of the pancreas

Question 700

Is pancreatic ca often diagnosed early or late?

Answer 700

late as non-specific

Question 701

Pancreatic ca associations?

Answer 701

- age - smoking - DM - chronic pancreatitis (but alcohol is not independent RF) - hereditary non-polyposis colorectal carcinoma - multiple endocrine neoplasia - BRCA2 gene - KRAS gene mutation

Question 702

Painless jaundice

Answer 702

pancreatic ca

Question 703

Features of pancreatic ca?

Answer 703

- painless jaundice= pale stools, dark urine, pruritus, cholestatic LFTs - abdo masses: hepatomegaly, gallbladderm epigastric mass - non-specific: anorexia, weight loss, epigastric pain - loss of exocrine function eg. steatorrhoea - loss of endocrine function eg. DM - atypical back pain - migratory thrombophlebitis (Trousseaus sign)

Question 704

What picture do LFTs show in pancreatic ca?

Answer 704

cholestatic LFTs

Question 705

What abdo masses may be found in pancreatic ca (in descending order of frequency)?

Answer 705

- hepatomegaly= due to mets - gallbladder= Courvoisier's law - epigastric mass= from primary tumour

Question 706

What is Courvoisier's law in pancreatic ca?

Answer 706

Courvoisier's law states that in the presence of painless obstructive jaundice, a palpable gallbladder is unlikely to be due to gallstones

Question 707

What is Trousseau's sign/syndrome in pancreatic ca?

Answer 707

paraneoplastic syndrome that can be associated with pancreatic cancer Recurrent episodes of thrombophlebitis in the upper and lower limbs, thoracic and abdominal wall, and major blood vessels of the abdomen. Due to coagulopathy associated with underlying malignancy.

Question 708

Ix for pancreatic ca?

Answer 708

- high-resolution CT scanning Ix of choice - can do USS 'double duct' sign on imaging

Question 709

'Double duct' sign on imaging?

Answer 709

pancreatic ca presence of simultaneous dilation of the common bile and pancreatic ducts

Question 710

Mx for pancreatic ca?

Answer 710

<20% suitable for surgery at time of diagnosis - Whipple's resection (pancreaticoduodenectomy)= for resectable lesions in head of pancreas - Adjuvant chemo following surgery - ERCP with stenting used for palliation

Question 711

Side-effects of a Whipple's resection for pancreatic ca?

Answer 711

dumping syndrome and peptic ulcer disease

Question 712

Dumping syndrome?

Answer 712

diarrhea, nausea, and feeling light-headed or tired after a meal, that are caused by rapid gastric emptying. Rapid gastric emptying is a condition in which food moves too quickly from your stomach to your duodenum. Cx of Whipple's

Question 713

Common chemo drugs for pancreatic ca?

Answer 713

1 or more than 1 of: gemcitabine capecitabine fluorouracil (5FU) irinotecan oxaliplatin nab-paclitaxel (Abraxane) cisplatin

Question 714

A pathological fracture occurs in...

Answer 714

abnormal bone due to insignificant injury

Question 715

Causes of pathological fractures?

Answer 715

- metastatic tumours - bone disease= osteogenesis imperfecta; osteoporosis; metabolic bone disease; Paget's disease - local benign conditions= chronic osteomyelitis; solitary bone cyst - primary malignant tumours

Question 716

Metastatic tumours that may cause pathological fractures?

Answer 716

breast lung thyroid renal prostate

Question 717

Primary malignant tumours that may cause pathological fractures?

Answer 717

chondrosarcoma osteosarcoma Ewing's tumour

Question 718

Red flags for breast ca?

Answer 718

lump, changes to skin or nipple, change in shape, discharge

Question 719

Red flags for lung ca?

Answer 719

persitent cough, haemoptysis, chest pain, SOB, non-resolving LRTI

Question 720

Red flags fro prostate ca?

Answer 720

nocturia, hesitancy, incomplete bladder emptying

Question 721

Red flags for bowel ca?

Answer 721

PR bleeding, change in bowel habit, abdo pain, tenesmus

Question 722

Red flags for ca (systemic symptoms)?

Answer 722

unexplained weight loss, fall in appetite, decreased energy levels, back pain, night sweats, unexplained anaemia, change in bowel habit (esp in elderly)

Question 723

What is discussed at MDT for ca?

Answer 723

Presentation and age Comorbidities WHO Performance status – indicator of patient’s fitness Biopsy findings – endoscopy, histological type Radiological findings – CT, MRI, PET TNM staging for each tumour type : Tumour Nodes Metastases Radical or Palliative Intent? Surgical or Non Surgical Management? Treatment plan based on patient’s wishes Referral to appropriate team

Question 724

Performance Status: ECOG/WHO?

Answer 724

0 Fully active, able to carry on all pre-disease performance without restriction 1 Restricted in physically strenuous activity but ambulatory and able to carry out work of a light or sedentary nature, e.g., light housework, office work 2 Ambulatory and capable of all selfcare but unable to carry out any work activities. Up and about more than 50% of waking hours 3 Capable of only limited selfcare, confined to bed or chair more than 50% of waking hours 4 Completely disabled. Cannot carry on any selfcare. Totally confined to bed or chair

Question 725

Non surgical oncology: what does curative/radical mean?

Answer 725

aim to cure

Question 726

Non surgical oncology: what does neoadjuvant mean?

Answer 726

therapy given before surgery/radiotherapy to shrink cancer down, improve outcome of resection and reduce risk of recurrence

Question 727

Non surgical oncology: what does adjuvant mean?

Answer 727

aimed at reducing risk of local recurrence or distant recurrence by treating micrometastatic disease can be chemo, radio, immuno ect.

Question 728

Non surgical oncology: what goes palliative/disease control mean?

Answer 728

not curative, but aimed at improving quality of life and survival

Question 729

Examples of systemic anti-cancer therapy?

Answer 729

- cytotoxic therapy - targeted therapy - endocrine therapy - immunotherapy - bisphosphonates

Question 730

What does chemotherapy do?

Answer 730

multiple classes of agents all affect cell cycle in some way cytotoxic agents- cause cell death

Question 731

Examples of endocrine Tx?

Answer 731

Tamoxifen and aromatase inhibitors for breast ca Prostate= GNRH analogues eg. zoladex

Question 732

What are targeted therapies?

Answer 732

Act on different parts of the pathway/cascade which lead to cell proliferation, growth, transformation, angiogenesis and invasion Aim is to inhibit the pathway at various points to stop the stimulus to the cancer and cause apoptosis

Question 733

What is immunotherapy?

Answer 733

using pts own immune system to kill ca caused activation of T cells that recognise and kill ca cells eg. ipilimumab for metastatic melanoma as lung ca autoimmune toxicities (colitis most common) which can be multisystem (as uses immune system)

Question 734

What is radiotherapy?

Answer 734

Ionising radiation= xrays (or gamma rays); xrays can directly break DNA bonds used to damage ca cells, whose repair mechanisms are inadequate end result is cell death different dose depths dependent on energy

Question 735

Principle of radiotherapy?

Answer 735

Use maximum dose for tumour control Whilst minimising dose to normal surrounding tissue

Question 736

Radiotherapy techniques?

Answer 736

- IMRT - SABR

Question 737

SABR (radiotherapy technique)?

Answer 737

Stereotactic ablative body radiotherapy: - Liver - Lung - Prostate - Oligometastases: lymph nodes, spine, adrenals, bone Precise irradiation with a higher radiation dose per fraction Highly conformal dose delivery with steep dose gradients Immobilisation - Passive - 4DCT, breathing control - Active - motion tracking, compression OARs

Question 738

IMRT (radiotherapy technique)?

Answer 738

produce tightly conformal plans with concave structures; needs excellent immobolisation and image guidance to allow reduced margins and reduced dose to organs at risk, while maintaining or increasing doses to the tumour

Question 739

General side effects of chemo?

Answer 739

fatigue, nausea and vomiting, mucositis, myelosuppression, sepsis, impact on renal and liver function, alopecia, taste change, unstable BMs, blood clots, infertility, allergic reactions Some chemo agents will have a greater risk of nephrotoxicity and cardiotoxicity

Question 740

General side effects of immunotherapy?

Answer 740

can be multisystem inflammation, including endocrine disturbance. Usually treated with high dose steroids – SPEAK TO AOS team early

Question 741

General side effects of radiotherapy?

Answer 741

LOCALISED treatment and side effects are dependent on the anatomical site being treated. Subdivided into acute and late side effects. (depends on structures around area trying to treat)

Question 742

Mx for chemo side effects: N&V? (preventative/Mx)

Answer 742

Dexamethasone with chemo Granisetron iv (5-HT3 antagonist), PRN Ondansetron, metoclopramide Haloperidol and Levomepromazine if above fail IV fluids as needed

Question 743

Mx for chemo side effects: diarrhoea? (preventative/Mx)

Answer 743

Really important to check it is not immunotherapy treatment first Loperamide, codeine – don’t always wait for MC&S stool Significant risk with 5FU/Capecitabine

Question 744

Mx for chemo side effects: constipation? (preventative/Mx)

Answer 744

Esp. if on 5HT3 antagonists (ondansetron) Laxatives, enema Consider bowel obstruction

Question 745

Mx for chemo side effects: stomatitis/mucositis? (preventative/Mx)

Answer 745

Difflam, Bioxtra gel, analgesia Mucositis

Question 746

Mx for chemo side effects: other? (preventative/Mx)

Answer 746

5FU/Capecitabine can causes coronary spasm-chest pain/ bradycardias See UKONS for Ix and management.

Question 747

Targeted agents exampoles and side effects?

Answer 747

nibs” Sunitinib Pazopanib Tivozanib SIDE EFFECTS ARE VARIED …all of them cause fatigue and GI toxicity Tyrosine Kinase Inhibitors – diarrhoea, HTN (some), hepatitis, hypothyroidism (some), QT prolongation, less likely bone marrow suppression(but may be if used in combination i.e. dabrafanib and trametinib)

Question 748

Immunotherapy toxicity?

Answer 748

Hepatitis Nephritis Colitis Pneumonitis MYOCARDITIS Skin, joints Hypophysitis…. But can affect any organ

Question 749

Mx of immunotherapy toxicity?

Answer 749

Grade 1 – observe/monitor Grade 2 – oral Pred 1mg/kg Grade 3- 4 – IV Methyl pred If already on steroids, go back up to previous dose; if not weaning d/w specialty of organ and start additional immunosuppression – MMF, Infliximab

Question 750

Examples of oncology emergencies?

Answer 750

- Metastatic Spinal Cord Compression (MSCC) - Hypercalcaemia - SVC Obstruction - Seizure - Venous or Arterial - Thromboembolism - Pleural Effusion - Bowel Obstruction

Question 751

What is neutropenic sepsis?

Answer 751

Sepsis with neutrophils <1.0 may present with fever alone, with no obvious source chemo hotline in all ca centres door to needle time <1hr ie to delivery of Abx early discussion with on call oncology team esp if organ failure high risk regimens- prophylactic GCSF

Question 752

Pathogens in neutropenic sepsis?

Answer 752

Gram positive bacteraemia 70%: Staphylococcus aureus Coagulase-negative staphylococcus alpha and beta haemolytic streptococcus Gram negative bacteraemia 30%: Escherichia coli Klebsiella pneumoniae Pseudomonas aeruginosa Fungi: Candida , Aspergillus

Question 753

Mx of neutropenic sepsis?

Answer 753

ABCDE Must be given the first dose of IV Abx within one hour of presentation  Do not wait for FBC or culture results before giving first dose. Piperacillin/Tazobactam (Tazocin) 4.5g QDS + Gentamicin (dose according to STHFT gentamicin chart) +/-  Vancomycin  -  if line infection suspected (as per vancomycin dosing guidelines) See local guidelines for penicillin allergy, renal impairment Need to know local Trust policy – not always the same AB

Question 754

Assessment for neutropenic sepsis?

Answer 754

1) Temperature + observations + calculate Early Warning Score (NEWS)  2) Urgent bloods: FBC, Clotting, blood cultures (peripheral +/- CVAD), U&E, LFT, CRP and serum lactate. 3) Urgent medical review and clinical examination. Assess for symptoms and signs of infection. Assess any lines (e.g., Portacath, Hickman line) History: chemo and timings, allergies, previous episodes 4) Micro/virology specimens as clinically indicated (e.g. CVAD exit site, sputum, urine, throat swab). 5) CXR if respiratory symptoms, signs or hypoxia. 6) Consider septic shock and need for fluid challenge. (EARLY) 7) Monitor fluid balance but do not catheterise routinely due to risk of infection.  Do not routinely PR/PV – risk of bacteraemia 8) If Oxygen saturations less than 95% consider appropriate oxygen administration.

Question 755

Neutropenic sepsis monitoring?

Answer 755

1)Monitor (NEWS) (4 hourly minimum, increase if indicated) 2) Record fluid intake and output  3) Arrange repeat blood tests including FBC, U&E’s, CRP + Gentamicin/Vancomycin levels if required. 4) Minimum once daily clinical team review Seek advice: 1) Discuss with senior member of the oncology on-call team (SpR or Consultant) via switch board or AOS team 2) Discuss and document appropriate level of escalation of care (e.g. HDU, active treatment on ward) 3) Discuss need for other treatments e.g. G-CSF. 

Question 756

Malignant spinal cord compression summary?

Answer 756

Spinal cord ends at around L1 in adults Above this level – spinal cord compression Below this – cauda equina Can be caused by: Vertebral metastases Soft tissue mass Retropulsed bony fragment due to fracture WORSENING BACK PAIN is a LATE SIGN. Do NOT wait for the neurological deficit, especially in a patient known to have cancer

Question 757

Typical history for spinal cord compression?

Answer 757

Back pain, radicular pain Common in prostate/breast/lung cancers Limb weakness – progressive, can be sudden Sensory level Bladder/bowel dysfunction Anal tone ↓

Question 758

Diagnosis for spinal cord compression?

Answer 758

MRI WHOLE SPINE

Question 759

Mx for spinal cord compression?

Answer 759

Once established neurology- 24h to surgery or radiotherapy - Steroids (dexamethasone 8mg BD with PPI and monitor BMs) - Same day MRI scan (including out of hours) - Urgent discussion with oncology and spinal surgeons - Surgical decompression/stabilisation vs radiotherapy

Question 760

What electrolyte abnormality is common in advanced ca?

Answer 760

hypercalcaemia

Question 761

Example of why you get hypercalcaemia in advanced ca?

Answer 761

bone mets production of ectopic PTHrp (parathyroid hormone related peptide) by ca- esp SCC

Question 761

Mx of hypercalcaemia in ca?

Answer 761

rehydrate- manage AKI IV bisphosphonates (zolendronate, pamidronate) manage the cause if possible- treat the ca

Question 762

Symptoms of hypercalcaemia in ca?

Answer 762

bones, moans, stones, abdo groans

Question 763

Hypercalcaemia in ca is often associated with what?

Answer 763

AKI

Question 763

What does the SVC provide?

Answer 763

the venous drainage for the head, neck, upper limbs and the upper thorax

Question 764

What happens when SVC is obstructed?

Answer 764

collateral pathways form to provide an alternative route for blood to return to the right atrium

Question 765

Causes of SVC obstruction?

Answer 765

- inside the vessel= thrombus or intravascular device - inside the vessel wall= direct tumour invasion - outside the vessel= tumour, lung ca, lymphoma

Question 766

Symptoms of SVCO?

Answer 766

- dyspnoea - chest pain, often at rest - cough - neck and face swelling - arm swelling - others= dizziness, headache, visual disturbance, nasal stuffiness, syncope

Question 767

Signs of SVCO?

Answer 767

- dilated veins over arms, neck and anteroir chest wall - oedema of upper torso, arms, neck and face - severe resp distress - cyanosis - engorged conjunctiva - convulsions and coma

Question 768

Ix for SVCO?

Answer 768

- may be clinical diagnosis - CXR (widened mediastinum or mass on right side of heart) - May be incidental finding on CT - CTPA to define tumour extent, site of occlusion or stenosis and extent of any thrombus

Question 769

Mx for SVCO?

Answer 769

- elevation of the head and oxygen therapy- symptomatic relief - high dose steroids if acute - endovascular stenting - consider: radio; chemo (esp in chemo-sensitive tumours eg small cell lung ca; anticoag if central vein thrombosis is present

Question 770

Why are lots of pts with ca on dexamethasone or prednisolone?

Answer 770

- anti-inflamm/tumour effects: spinal cord compression, SVCO, brain mets (reduces oedema) ect - symptom control eg. appetite/sickness - immunotherapy related effects

Question 771

What to do for all ca pts on steroids?

Answer 771

- always check if they were taking at admission - blood glucose monitoring QDS as inpatient for all - any pts discharged on steroids needs a BM monitoring kit - all pts need gastro-protection - refer to hyperglycaemia guidlines and do diabetic nurse referral on ICE if any issues with control/starting diabetes meds

Question 772

Pt with ca complains of N/V, what to consider and Mx?

Answer 772

consider CAUSE chemo related= metoclopramide/ondansetron obstruction= avoid prokinetics, consider cyclizine/steroids instead, NBM, fluids, ryles tube brain mets= steroids, remeber metoclopramide CI in epilepsy, give alternative

Question 773

In ca pts with N/V what antiemetics should you not prescribe together?

Answer 773

metoclopramide and cylixine DO NOT prescribe together

Question 774

What antiemetics can be used in ca pts with N/V in difficult cases?

Answer 774

haloperidol, olanzapine, levomepromazine

Question 775

What antiemetic is contraindicated in epilepsy?

Answer 775

metoclopramide

Question 776

What might cause seizures in ca pts?

Answer 776

brain mets primary CNS ca

Question 777

Mx for seizures in ca pts?

Answer 777

treat like any other- lorazepam if not self-terminating, commence keppra CT initially then MRI start steroids if known brain tumour, pending scan (8mg BD, reducing over next few days to 2-4mg per day depending on neuro symptoms) consider referral to neurosurgeons (refer a pt) and add to neuro oncology MDT

Question 778

Electrolyte disturbances in ca pts may be secondary to what?

Answer 778

ca or Tx

Question 779

Causes of hyponatraemic in ca pts?

Answer 779

tumour, recent steroids

Question 780

Causes of hypercalcaemia in ca pts?

Answer 780

bone mets, SCC lung

Question 781

Causes of hypocalcaemia in ca pts?

Answer 781

chemo, bisphosphonates, refeeding

Question 782

Causes of hyperkalaemia in ca pts?

Answer 782

renal failure, tumour lysis syndrome

Question 783

Causes of hypokalaemia in ca pts?

Answer 783

chemo, refeeding, diarrhoea

Question 784

Causes of hypomagnasaemia in ca pts?

Answer 784

chemo, refeeding, EGFR inhibitor

Question 785

Mx for replacement strategies for electrolyte disturbances in ca pts?

Answer 785

clinical guidelines

Question 786

Suspected DVTs/PEs in ca pts?

Answer 786

- LOW THRESHOLD to consider doppler, CTPA - check clotting/platelets before LMWH - VTE referral - start LMWH in acute setting before switching to DOAC later (as some ca pts can't have DOACs

Question 787

Some ca pts can't have what medication?

Answer 787

DOACs= GI infiltration, rectal tumours that are bleeding, varices

Question 788

Ca pt with ascites?

Answer 788

if urgent, admit, US guided drain, check clotting (?does pt need restaging CT) if non urgent, can request as elective for future date malignant ascites can keep drain in for up to 30d, HAS not required

Question 789

Any oncology emergency?

Answer 789

ask acute oncology team for advice

Question 790

Prostate ca?

Answer 790

malignant tumour of prostate

Question 791

Most cancers of the prostate (95%) are what?

Answer 791

adenocarcinomas

Question 792

Prostate ca is multifocal, what does this mean?

Answer 792

the different foci may be caused by different genetic mutations, which can differ greatly in growth rate and ability to metastasize

Question 793

Most prostate ca are slow or fast growing?

Answer 793

indolest and grow slowly- minority are aggressive and invade local structures or metastasise to remote tissues

Question 794

Localised prostate ca usually develops where?

Answer 794

in outer zone of prostate where it rarely causes symptoms

Question 795

Locally advanced prostate ca?

Answer 795

extends beyond the capsule of prostate and is often asymptomatic when diagnosed

Question 796

Metastatic prostate ca mostly affects where?

Answer 796

bones- causes pain and fragility fractures

Question 797

RFs for prostate ca?

Answer 797

age black ethnicity FHx

Question 798

Symptoms of prostate ca?

Answer 798

unexplained... - lower back or bone pain - lethargy - erectile dysfunction - haematuria - anorexia/weight loss

Question 799

Assessment of pt with suspected prostate ca?

Answer 799

- digital rectal exam (DRE) - prostate-specific antigen (PSA) test

Question 800

Referral for suspected prostate ca?

Answer 800

suspected ca pathway= if prostate hard and nodular on DRE or benign enlargement consider suspected ca pathway if= PSA level above threshold for age (eg. >4.5 in pt 60-69yrs)

Question 801

Mx for prostate ca?

Answer 801

- watchful waiting= older men, slowly progressing tumour, multiple co-morbidities, low Gleason score - Active surveillance= early prostate ca to avoid over treatment (as ca unlikely to cause harm). Involves prostate biopsy at intervals and PSA. Particularly suitable for men with clinical stage T1c, Gleason score 3+3 and PSA density < 0.15 ng/ml/ml who have cancer in less than 50% of their biopsy cores, with < 10 mm of any core involved. - Radical treatements= radical prostatectomy; external beam radiotherapy; or brachytheraoy - Adjunctive and palliative= hormone therapy; chemo (for hormone relapsed metastatic disease); bisphosphonates if taking androgen deprivation therapy and have osteoporosis

Question 802

Examples of hormone treatments that can be used in prostate ca (removes and/or blocks effects of hormones which stimulate growth of prostate ca cells)?

Answer 802

- androgen deprivation (lowers testosterone)= bilateral orchidectomy or LHRH agonists eg. goserelin or antagonists eg. degarelix - androgen blockage= eg. cyproterone acetate, bind and block to hormone receptors of ca cells so preventing androgens stimualting growth

Question 803

What does LHRH agonists stand for eg. goserelin?

Answer 803

luteninizing horomone releasing hormone agonists

Question 804

Examples of chemo regimens for prostate ca?

Answer 804

- docetaxel + prednisolone - cabazitaxel + pred (2nd line) - 3rd line: dexamethasone

Question 805

Mx of adverse effects of hormonal Tx in pt with prostate ca?

Answer 805

Hot flushes= medroxyprogesterone acetate 20mg od 10w Fatigue= supervised resistance and aerobic exercise twice a w for 12w Osteoporosis= bisphosphonates Gynaecomastia= if long-term bicalutamide monotherapy (>6m) refer for prophylactic radio to both breast buds within 1st month of Tx

Question 806

Mx for sexual dysfunction in pt with prostate ca?

Answer 806

phosphodiesterase-5 (PDE-5) inhibitor eg. sildenafil

Question 807

Ix for prostate ca?

Answer 807

- PSA - Digital rectal exam - multiparametric MIR (1st line) or trans rectal USS (+/-) biopsy (2nds line) - MRI/CT and bone scan for staging

Question 808

How is prostate ca graded?

Answer 808

Gleason grading system, two grades awarded 1 for most dominant grade (on scale of 1-5) and 2 for second most dominant grade (scale 1-5). The two added together give the Gleason score. Where 2 is best prognosis and 10 the worst.

Question 809

Lymphatic spread in prostate ca?

Answer 809

occurs first to the obturator nodes and local extra prostatic spread to the seminal vesicles is associated with distant disease.

Question 810

Candidates for active surveillance in prostate ca Mx should...

Answer 810

have had at least 10 biopsy cores taken have at least one re-biopsy.

Question 811

Features of prostate ca?

Answer 811

localised often asymptomatic - bladder outlet obstruction: hesitancy, urinary retention haematuria, haematospermia pain: back, perineal or testicular digital rectal examination: asymmetrical, hard, nodular enlargement with loss of median sulcus

Question 812

Cx of TRUS biopsy eg. in suspected prostate ca?

Answer 812

sepsis: 1% of cases pain: lasting >= 2 weeks in 15% and severe in 7% fever: 5% haematuria and rectal bleeding

Question 813

1st line Ix for suspected clinically localised prostate ca?

Answer 813

multiparametric MRI: results reported using a 5-point Likert scale

Question 814

Likert scale in suspected prostate ca?

Answer 814

results from multiparametic MRI are reported using a 5-point Likert scale If the Likert scale is >=3 a multiparametric MRI-influenced prostate biopsy is offered If the Likert scale is 1-2 then NICE recommend discussing with the patient the pros and cons of having a biopsy.

Question 815

Cx of radical prostatectomy?

Answer 815

erectile dysfunction

Question 816

Adverse effects of radiotherapy for prostate ca?

Answer 816

develop proctitis and are also at increased risk of bladder, colon, and rectal cancer following radiotherapy for prostate cancer

Question 817

How do GnRH agonists work for prostate ca Mx?

Answer 817

e.g. Goserelin (Zoladex) paradoxically result in lower LH levels longer term by causing overstimulation, resulting in disruption of endogenous hormonal feedback systems. The testosterone level will therefore rise initially for around 2-3 weeks before falling to castration leves initially therapy is often covered with an anti-androgen to prevent a rise in testosterone - 'tumour flare'. The resultant stimulation of prostate cancer growth may result in bone pain, bladder obstruction and other symptoms

Question 818

Bicalutamide for prostate ca Mx?

Answer 818

non-steroidal anti-androgen blocks the androgen receptor

Question 819

Cyproterone acetate for prostate ca Mx?

Answer 819

steroidal anti-androgen prevents DHT binding from intracytoplasmic protein complexes used less commonly since introduction of non-steroidal anti-androgens

Question 820

Abiraterone for prostate ca?

Answer 820

androgen synthesis inhibitor option for the treatment of hormone-relapsed metastatic prostate cancer in patients who have no or mild symptoms after androgen deprivation therapy has failed, and before chemotherapy is indicated

Question 821

Bilateral orchidectomy for prostate ca?

Answer 821

used to rapidly reduce testosterone levels

Question 822

What is PSA?

Answer 822

serine protease enzyme produced by normal and malignant prostate epithelial cells

Question 823

Age-specific PSA thresholds for people with possible symptoms of prostate ca?

Answer 823

40 Use clinical judgement 40–49 > 2.5 50–59 > 3.5 60–69 > 4.5 70–79 > 6.5 > 79 Use clinical judgement

Question 824

What may also raise PSA levels?

Answer 824

- BPH - prostatitis and UTI (NICE recommend to postpone the PSA test for at least 6 weeks after treatment) - ejaculation (ideally not in the previous 48 hours) - vigorous exercise (ideally not in the previous 48 hours) - urinary retention - instrumentation of the urinary tract

Question 825

What % of prostate ca will have normal PSA?

Answer 825

15%

Question 826

Suspected testicular ca on clinical exam (or incidentially following USS of scrotum)?

Answer 826

urgent urology referral (using suspected ca pathway)

Question 827

Consider arranging bloods for what at the time of referral for suspected testicular ca?

Answer 827

tumour markers= AFP, hCG, LDH

Question 828

Most common malignancy in men 20-30yrs?

Answer 828

testicular

Question 829

95% of testicular ca are what type of tumour?

Answer 829

germ-cell tumours

Question 830

Types of germ cell tumours?

Answer 830

seminomas non-seminomas: including embryonal, yolk sac, teratoma and choriocarcinoma

Question 831

Types of non-germ cell tumours?

Answer 831

Leydig cell tumours Sarcomas

Question 832

Peak incidence for teratoma and seminomas?

Answer 832

T= 25yrs S= 35yrs

Question 833

RFs for testicular ca?

Answer 833

- infertility (x3 increase risk) - cryptorchidism - FHx - Klinefelter's syndrome - mumps orchitis

Question 834

Features of testicular ca?

Answer 834

- painless lump (most common) - pain (minority) - hydrocele - gynaecomastia

Question 835

Why may pts get gynaecomastia?

Answer 835

due to increased oestrogen:androgen ratio germ-cell tumours → hCG → Leydig cell dysfunction → increases in both oestradiol and testosterone production, but rise in oestradiol is relatively greater than testosterone leydig cell tumours → directly secrete more oestradiol and convert additional androgen precursors to oestrogens

Question 836

Tumour markers for germ cell tumours (testicular ca)?

Answer 836

seminomas= hCG may be elevated in 20% non-seminomas= AFP and/or beta-hCG elevated in 80-85% LDH elevated in 40% germ cell tumours

Question 837

Diagnosis of testicular ca?

Answer 837

USS

Question 838

Mx of testicular ca?

Answer 838

depends if tumour is seminoma or non-seminoma orchidectomy chemo and radio may be given depending on staging and tumour type

Question 839

Prognosis of testicular ca?

Answer 839

generally excellent Seminomas= 5yrs survival 95% if stage I Teratomas= 85% if stage I

Question 840

What are germ cell tumours?

Answer 840

group of tumours that originate from germ cells- cells responsible for developing into sperm or eggs germ cells normally migrate to gonads (testes/ovaries) during fetal development but can sometimes remain in other parts of body= potential for tumour development (reproductive organs and other areas)

Question 841

Seminomas vs non-seminomas?

Answer 841

Seminomas and early-stage germ cell tumors= tend to have a high cure rate with appropriate treatment, often exceeding 90%. Non-seminomas, particularly those that are advanced or spread (metastatic), can be more challenging to treat but still have good outcomes with modern chemotherapy regimens.

Question 842

Differential diagnosis for abdo swelling?

Answer 842

preg= young, female, amenorrhoea obstruction= Hx malignany/prev surgery; vomiting; not opened bowel recently; tinkling bowel sounds ascites= Hx of alcohol excess, cardiac failure urinary retention= Hx of prostate problems; dullness to percussion around suprapubic area ovarian ca= older female, pelvic pain, urinary symptoms (urgency), raised CA125, early satiety, bloating

Question 843

Summary of breast fibroadenoma?

Answer 843

Develop from a whole lobule Mobile, firm, smooth breast lump - a 'breast mouse' 12% of all breast masses Over a 2 year period up to 30% will get smaller No increase in risk of malignancy If >3cm surgical excision is usual

Question 844

Head and neck ca?

Answer 844

umbrella term, typically includes: - oral cavity ca - ca of the pharynx (incl oropharynx, hypopharynx, nasopharynx) - ca of the larynx

Question 845

Features of head and neck ca?

Answer 845

neck lump hoarseness persistent sore throat persistent mouth ulcer

Question 846

Consider suspected ca pathway referral for laryngeal ca in people...

Answer 846

aged 45yrs+ with: - persistent unexplained hoarseness or - unexplained lump in neck

Question 847

Consider suspected ca pathway referral for oral ca in people with...

Answer 847

- unexplained ulceration in oral cavity lasting more than 3w or - persistent and unexplained lump in the neck

Question 848

Consider urgent referral (within 2w) for assessment for possible oral ca by dentist in people who have...

Answer 848

- lump on the lip or in the oral cavity or - red or red and white patch in oral cavity consistent with erythroplakia or erythroleukoplakia

Question 849

Consider suspected ca referral for thryoid ca in people with...

Answer 849

unexplained thyroid lump

Question 850

Differential diagnosis for acute scrotal presentations in children?

Answer 850

testicular torsion= most common around puberty irreducible inguinal hernia= most common in children <2yrs epididymitis= rare in prepubescent children

Question 851

Pathology of non seminomatous germ cell tumours?

Answer 851

heterogenous texture with occasional ectopic tissue such as hair

Question 852

Pathology of seminomas?

Answer 852

Sheet like lobular patterns of cells with substantial fibrous component. Fibrous septa contain lymphocytic inclusions and granulomas may be seen.

Question 853

Types of non seminomatous germ cell tumours?

Answer 853

Teratoma Yolk sac tumour Choriocarcinoma Mixed germ cell tumours (10%)

Question 854

Key features of seminoma (type of germ cell tumour)?

Answer 854

Commonest subtype Average age at diagnosis = 40 Even advanced disease associated with 5 year survival of 73%

Question 855

Key features of non seminomatous germ cell tumours?

Answer 855

Younger age at presentation =20-30 years Advanced disease carries worse prognosis (48% at 5 years) Retroperitoneal lymph node dissection may be needed for residual disease after chemotherapy

Question 856

Tumour markers for seminoma?

Answer 856

AFP usually normal HCG elevated in 10% seminomas Lactate dehydrogenase; elevated in 10-20% seminomas (but also in many other conditions)

Question 857

Tumour markers in non seminomas?

Answer 857

AFP elevated in up to 70% of cases HCG elevated in up to 40% of cases Other markers rarely helpful

Question 858

Cell type in seminomas vs non-seminomas (NSGCTs)?

Answer 858

S= germ cells that are undifferentiated N-S= germ cells that are differentiated into various tissues

Question 859

Seminomas vs non seminomas?

Answer 859

S= slow growing; may elevate b-hCG but normal AFP; highly sensitive to radio and chemo; excellent prognosis; subtypes= classic and spermatocytic seminoma N-S= faster growing & more aggressive; often elevated AFP and b-hCG; less sensitive to radio; treated with chemo; prognosis good but worse than S and varies with stage and subtype; sybtypes= embryonal carcinoma, yolk sac tumour, choriocarcinoma, teratoma

Question 860

Examples of carcinogens and the cancer they may cause?

Answer 860

Aflatoxin (produced by Aspergillus)= Liver (hepatocellular carcinoma) Aniline dyes= Bladder (transitional cell carcinoma) Asbestos= Mesothelioma and bronchial carcinoma Nitrosamines= Oesophageal and gastric cancer Vinyl chloride= Hepatic angiosarcoma

Question 861

RFs for developing N&V side effects of chemo?

Answer 861

- anxiety - <50yrs - concurrent use of opioids - type of chemo used

Question 862

Drugs used for N&V in chemo pts?

Answer 862

low risk of N&V= metoclopramide high risk of symptoms= 5HT3 receptor antagonists such as ondansetron are often effective, especially if combined with dexamethasone

Question 863

Cyclophosphamide?

Answer 863

alkylating agent used in the management of cancer and autoimmune conditions. It works by causing cross-linking of DNA

Question 864

Adverse effects of cyclophosphamide?

Answer 864

haemorrhagic cystitis: incidence reduced by the use of hydration and mesna myelosuppression transitional cell carcinoma

Question 865

Mesna?

Answer 865

2-mercaptoethane sulfonate Na a metabolite of cyclophosphamide called acrolein is toxic to urothelium mesna binds to and inactivates acrolein helping to prevent haemorrhagic cystitis

Question 866

Examples of cytotoxic agents?

Answer 866

Alkylating agents= cyclophosphamide Cytotoxic antibodies= bleomycin, anthracyclines (eg. doxorubicin) Antimetabolites= methotrexate, fluorouracil (5-FU), 6-mercaptopurine, cytarabine Acts on microtubules= vincritine, vinblastine, docetaxel Topoisomerase inhibitors= irinotecan Other= cisplatin, hydroxyurea (hydroxycarbamide)

Question 867

Cytotoxic agents: alkylating agents= cyclophosphamide MOA and adverse effects?

Answer 867

Alkylating agent - causes cross-linking in DNA Haemorrhagic cystitis, myelosuppression, transitional cell carcinoma

Question 868

Cytotoxic agents: cytotoxic antibodies= bleomycin MOA and adverse effects?

Answer 868

Degrades preformed DNA Lung fibrosis

Question 869

Cytotoxic agents: cytotoxic antibodies= anthracyclines (eg. doxorubicin) MOA and adverse effects?

Answer 869

Stabilizes DNA-topoisomerase II complex inhibits DNA & RNA synthesis Cardiomyopathy

Question 870

Cytotoxic agents: antimetabolites= methotrexate MOA and adverse effects?

Answer 870

Inhibits dihydrofolate reductase and thymidylate synthesis Myelosuppression, mucositis, liver fibrosis, lung fibrosis

Question 871

Cytotoxic agents: antimetabolites= fluorouracil (5-FU) MOA and adverse effects?

Answer 871

Pyrimidine analogue inducing cell cycle arrest and apoptosis by blocking thymidylate synthase (works during S phase) Myelosuppression, mucositis, dermatitis

Question 872

Cytotoxic agents: antimetabolites= 6-mercaptopurine MOA and adverse effects?

Answer 872

Purine analogue that is activated by HGPRTase, decreasing purine synthesis Myelosuppression

Question 873

Cytotoxic agents: antimetabolites= cytarabine MOA and adverse effects?

Answer 873

Pyrimidine antagonist. Interferes with DNA synthesis specifically at the S-phase of the cell cycle and inhibits DNA polymerase Myelosuppression, ataxia

Question 874

Cytotoxic agents: acts on microtubules= vincristine, vinblastine MOA and adverse effects?

Answer 874

Inhibits formation of microtubules Vincristine: Peripheral neuropathy (reversible) , paralytic ileus Vinblastine: myelosuppression

Question 875

Cytotoxic agents: acts on microtubules= docetaxel MOA and adverse effects?

Answer 875

Prevents microtubule depolymerisation & disassembly, decreasing free tubulin Neutropaenia

Question 876

Cytotoxic agents: topoisomerase inhibitors= irinotecan MOA and adverse effects?

Answer 876

Inhibits topoisomerase I which prevents relaxation of supercoiled DNA Myelosuppression

Question 877

Cytotoxic agents: other= cisplatin MOA and adverse effects?

Answer 877

Causes cross-linking in DNA Ototoxicity, peripheral neuropathy, hypomagnesaemia

Question 878

Cytotoxic agents: other= hydroxyurea (hydroxycarbamide) MOA and adverse effects?

Answer 878

Inhibits ribonucleotide reductase, decreasing DNA synthesis Myelosuppression

Question 879

Li-Fraumeni Syndrome?

Answer 879

- Autosomal dominant - Consists of germline mutations to p53 tumour suppressor gene - High incidence of malignancies particularly sarcomas and leukaemias - Diagnosed when: *Individual develops sarcoma under 45 years *First degree relative diagnosed with any cancer below age 45 years and another family member develops malignancy under 45 years or sarcoma at any age

Question 880

BRCA 1 and 2?

Answer 880

- Carried on chromosome 17 (BRCA 1) and Chromosome 13 (BRCA 2) - Linked to developing breast cancer (60%) risk. - Associated risk of developing ovarian cancer (55% with BRCA 1 and 25% with BRCA 2). - BRCA2 mutation is associated with prostate cancer in men

Question 881

Lynch Syndrome?

Answer 881

Autosomal dominant Develop colonic cancer and endometrial cancer at young age 80% of affected individuals will get colonic and/ or endometrial cancer High risk individuals may be identified using the Amsterdam criteria

Question 882

Amsterdam criteria?

Answer 882

Three or more family members with a confirmed diagnosis of colorectal cancer, one of whom is a first degree (parent, child, sibling) relative of the other two. Two successive affected generations. One or more colon cancers diagnosed under age 50 years. Familial adenomatous polyposis (FAP) has been excluded.

Question 883

Gardners syndrome?

Answer 883

Autosomal dominant familial colorectal polyposis Multiple colonic polyps Extra colonic diseases include: skull osteoma, thyroid cancer and epidermoid cysts Desmoid tumours are seen in 15% Mutation of APC gene located on chromosome 5 Due to colonic polyps most patients will undergo colectomy to reduce risk of colorectal cancer Now considered a variant of familial adenomatous polyposis coli

Question 884

What is PET?

Answer 884

Positron Emission Tomography (PET) is a form of nuclear imaging which uses fluorodeoxyglucose (FDG) as the radiotracer. This allows a 3D image of metabolic activity to be generated using glucose uptake as a proxy marker. The images obtained are then combined with a conventional imaging technique such as CT to decide whether lesions are metabolically active. Uses - evaluating primary and possible metastatic disease

Question 885

Tumour markers may be divided into what?

Answer 885

- monoclonal antibodies against carbohydrate or glycoprotein tumour antigens - tumour antigens - enzymes (alkaline phosphatase, neurone specific enolase) - hormones (e.g. calcitonin, ADH)

Question 886

What tumour markers are monoclonal antibodies?

Answer 886

CA 125 CA 19-9 CA 15-3

Question 887

What tumour markers are tumour antigens?

Answer 887

PSA AFP CEA S-100 Bombesin

Question 888

Tumour markers: CA 125 association?

Answer 888

ovarain ca endometriosis, PID, menstruation, pregnancy

Question 889

Tumour markers: CA 19-9 association?

Answer 889

pancreatic ca, gallbladder ca gallstones, pancreatitis, liver disease

Question 890

Tumour markers: CA 15-3 association?

Answer 890

breast ca benign breast conditions, liver disease

Question 891

Tumour markers: prostate specific antigen (PSA) association?

Answer 891

prostate ca BPH, prostatitis

Question 892

Tumour markers: Alpha-feto protein (AFP) association?

Answer 892

hepatocellular carcinoma, testicular ca, teratoma pregnancy, liver cirrhosis, hepatitis

Question 893

Tumour markers: Carcinoembryonic antigen (CEA) association?

Answer 893

colorectal ca also breast, lung, pancreatic ca smoking, IBD, liver disease

Question 894

Tumour markers: S-100 association?

Answer 894

melanoma schwannomas

Question 895

Tumour markers: bombesin association?

Answer 895

small cell lung carcinoma gastric ca neuroblastoma

Question 896

Tumour markers: hCG?

Answer 896

testicular ca, choriocarcinoma pregnancy

Question 897

Tumour markers: lactate dehydrogenase (LDH)?

Answer 897

lymphoma, leukaemia, testical ca general tissue damage, HF, anaemia, infections

Question 898

Tumour markers: thyroglobulin?

Answer 898

thyroid ca thyroiditis, goiter

Question 899

What are tumour markers?

Answer 899

often proteins produced by body in response to ca or by ca itself found in blood, urine or tissue can help diagnosis, monitor, prognosis of ca most aren't exclusive to ca not specific or sensitive enough so used in conjunction with other diagnostic tools eg. imaging and biopsy

Question 900

Most common cause for hepatocellular carcinoma (HCC)

Answer 900

chronic hep B worldwide chronic hep c in europe

Question 901

Main RF for developing HCC?

Answer 901

liver cirrhosis, eg. secondary to hep B & C, alcohol, haemochromatosis and primary biliary cirrhosis Wilson's is the exception

Question 902

RFs for HCC?

Answer 902

liver cirrhosis chronic hep B & C alcohol haemochromatosis primary biliary cirrhosis alpha-1 antitrypsin deficiency hereditary tyrosinosis glycogen storage disease aflatoxin drugs: oral contraceptive pill, anabolic steroids porphyria cutanea tarda male sex diabetes mellitus, metabolic syndrome

Question 903

Features of HCC?

Answer 903

- tends to present late - features of liver cirrhosis/failure= jaundice, ascites, RUQ pain, hepatomegaly, pruritus, splenomegaly - possible presentation is decompensation in pt with chronic liver disease - raised AFP

Question 904

What should be considered for high risk groups for HCC?

Answer 904

screening with USS (+/- alpha-fetoprotein)

Question 905

Examples of pts who are high risk for HCC and may have screening with ultrasound (+/- alpha-fetoprotein)?

Answer 905

- pts with liver cirrhosis secondary to hep B&C or haemochromatosis - men with liver cirrhosis secondary to alcohol

Question 906

Mx options for HCC?

Answer 906

early disease: surgical resection liver transplantation radiofrequency ablation transarterial chemoembolisation sorafenib: a multikinase inhibitor

Question 907

Do pts with thyroid ca get features of hyper or hypothyroidism?

Answer 907

not commonly as they rarely secrete thyroid hormones

Question 908

Type of thyroid ca?

Answer 908

- papillary (70%) - follicular (20%) - medullary (5%) - anaplastic (1%) - lymohoma (rare)

Question 909

What type of thyroid ca has an excellent prognosis and is often in young females?

Answer 909

papillary

Question 910

What is medullary thyroid ca?

Answer 910

ca of parafollicular (C) cells, secrete calcitonin, part of MEN-2

Question 911

What type of thyroid ca is not responsive to treatment and can cause pressure symptoms?

Answer 911

anaplastic

Question 912

What type of thyroid ca is associated with Hasimoto's thyroiditis?

Answer 912

lymphoma thyroid ca

Question 913

Mx of papillary and follicular ca?

Answer 913

- total thyroidectomy - followed by radioiodine (I-131) to kill residual cells - yearly thyroglobulin levels to detect early recurrent disease

Question 914

Thyroid ca: papillary carcinoma?

Answer 914

Usually contain a mixture of papillary and colloidal filled follicles Histologically tumour has papillary projections and pale empty nuclei Seldom encapsulated Lymph node metastasis predominate Haematogenous metastasis rare

Question 915

Thyroid ca: follicular adenoma?

Answer 915

Usually present as a solitary thyroid nodule Malignancy can only be excluded on formal histological assessment

Question 916

Thyroid ca: follicular carcinoma?

Answer 916

May appear macroscopically encapsulated, microscopically capsular invasion is seen. Without this finding the lesion is a follicular adenoma. Vascular invasion predominates Multifocal disease raree

Question 917

Thyroid ca: medullary carcinoma?

Answer 917

C cells derived from neural crest and not thyroid tissue Serum calcitonin levels often raised Familial genetic disease accounts for up to 20% cases Both lymphatic and haematogenous metastasis are recognised, nodal disease is associated with a very poor prognosis.

Question 918

Thyroid ca: anaplastic carcinoma?

Answer 918

Most common in elderly females Local invasion is a common feature Treatment is by resection where possible, palliation may be achieved through isthmusectomy and radiotherapy. Chemotherapy is ineffective.

Question 919

Penile ca?

Answer 919

rare malignancy that affects the penis

Question 920

How does penile ca typically present?

Answer 920

painless lesion or ulcer on glans or foreskin may get discharge or bleeding

Question 921

RFs for penile ca?

Answer 921

phimosis poor hygiene smoking HPV infection

Question 922

Diagnosis of penile ca?

Answer 922

biopsy and histopathological exam of lesion

Question 923

Mx of penile ca?

Answer 923

depends on stage surgery, radio, chemo or combination

Question 924

CP of penile ca?

Answer 924

painless penile lesion or ulceration, which may be accompanied by bleeding or discharge. - Changes in the colour or texture of the skin on the penis - Thickening or nodularity of the penile skin - Enlargement of regional lymph nodes - Erectile dysfunction or difficulty urinating - The location and size of the lesion may vary, with the glans and foreskin being the most commonly affected sites.

Question 925

Consider suspected ca referral for penile ca in men if they have what?

Answer 925

either - a penile mass or ulcerated lesion, where a sexually transmitted infection has been excluded as a cause, or -a persistent penile lesion after treatment for a sexually transmitted infection has been completed, or - unexplained or persistent symptoms affecting the foreskin or glans

Question 926

Follow up for pt with prostate ca being managed with watchful waiting?

Answer 926

- PSA at least once per yr -DRE not recommended on routine basis

Question 927

Follow up for pt with prostate ca who are being managed with active surveillance

Answer 927

In year 1 of active surveillance: - Every 3–4 months: measure prostate-specific antigen. - Throughout active surveillance: monitor PSA kinetics (could include PSA density and velocity). - At 12 months: perform a DRE. - At 12–18 months: multiparametric MRI. In year 2 and every year thereafter until active surveillance ends: - Every 6 months: measure PSA. - Throughout active surveillance: monitor PSA kinetics (could include PSA density and velocity). - Every 12 months: perform a DRE. If there is concern about clinical or PSA changes at any time during active surveillance, the person should be reassessed with multiparametric MRI and/or re-biopsy.

Question 928

People with localized prostate cancer who have chosen watchful waiting and who have evidence of significant disease progression (that is, rapidly rising PSA level or bone pain) should what?

Answer 928

have their situation reviewed by uro ca specialist

Question 929

Follow up for pt with prostate ca who are being managed with radical treatment?

Answer 929

PSA levels should be measured no earlier than 6 weeks after treatment, then at least every 6 months for 2 years, and once a year thereafter. After at least 6 months' initial follow up, consider a remote follow-up strategy for people with a stable PSA who have had no significant treatment complications, unless they are taking part in a clinical trial that needs formal clinic-based follow up. Do not routinely offer DRE to people with localized prostate cancer who are not on active surveillance while their PSA remains at baseline levels.

Question 930

Tumour lysis syndrome?

Answer 930

potentially deadly condition related to the treatment of high-grade lymphomas and leukaemias. It can occur in the absence of chemotherapy but is usually triggered by the introduction of combination chemotherapy. On occasion, it can occur with steroid treatment alone. Awareness of the condition is critical as prophylactic medication can be given to prevent the potentially deadly effects of tumour cell lysis.

Question 931

Why does tumour lysis syndrome (TLS) occur?

Answer 931

occurs from the breakdown of the tumour cells and the subsequent release of chemicals from the cell. It leads to a high potassium and high phosphate level in the presence of a low calcium. It should be suspected in any patient presenting with an acute kidney injury in the presence of a high phosphate and high uric acid level.

Question 932

Prevention for tumour lysis syndrome?

Answer 932

IV fluids patients are higher risk should receive either allopurinol or rasburicase rasburicase= a recombinant version of urate oxidase, an enzyme that metabolizes uric acid to allantoin. Allantoin is much more water-soluble than uric acid and is, therefore, more easily excreted by the kidneys generally preferred now for patients at a higher risk of developing TLS allopurinol= generally used for patients in lower-risk groups rasburicase and allopurinol should not be given together in the management of tumour lysis syndrome as this reduces the effect of rasburicase

Question 933

How is tumour lysis syndrome graded?

Answer 933

LS has been graded using the Cairo-Bishop scoring system: Laboratory tumor lysis syndrome: abnormality in two or more of the following, occurring within three days before or seven days after chemotherapy: uric acid > 475umol/l or 25% increase potassium > 6 mmol/l or 25% increase phosphate > 1.125mmol/l or 25% increase calcium < 1.75mmol/l or 25% decrease

Question 934

Clinical tumour lysis syndrome?

Answer 934

laboratory tumour lysis syndrome plus one or more of the following: increased serum creatinine (1.5 times upper limit of normal) cardiac arrhythmia or sudden death seizure

Question 935

Bone sarcomas?

Answer 935

osteosarcoma chondrosarcoma Ewing's sarcoma

Question 936

Soft tissue sarcomas?

Answer 936

Liposarcoma Rhabdomyosarcoma (striated muscle origin) Synovial sarcoma Fibrosarcoma Angiosarcoma Leiomyosarcoma (smooth muscle origin))

Question 937

Presentations of sarcoma?

Answer 937

- pain - swelling or palpable mass (soft tissue>bone) - impaired function - pathologic fractures (bone) - systemic symptoms

Question 938

Ix for sarcoma?

Answer 938

X-ray, CT, MRI, PET biopsy= fine needle aspiration, core needle biopsy or incisional biopsy for histopath

Question 939

Mx for sarcomas?

Answer 939

- surgery= limb-sparing or amputation - radio= neoadjuvant or adjuvant or intraoperative radiation therapy (IORT) - chemo - Targeted therapy: For specific sarcoma subtypes, such as GIST, targeted therapy with tyrosine kinase inhibitors (e.g., imatinib)