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4th Year > Oncology > Flashcards

Oncology Flashcards

1
Q

What are the main gynaecological cancers?

A

Ovarian, Uterine, Cervical and Vaginal

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2
Q

What are uterine polyps?

How do they present?

How are they diagnosed?

What is the treatment?

Why is this included in oncology of gynaecological cancers?

A

Uterine polyps are an inflammatory overgrowth of the endometrium, usually oestrogen dependent.

Usually assymptomatic but may have PMB or IMB and change to discharge. Presents in >50, post/peri-menopausal women

Dx: TVUS

Rx: watch and wait or diathermy

Some endometrial carcinoma can develop from a polyp

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3
Q

What is endometrial hyperplasia? (RF)

What are the symptoms?

What are the types?

How is it diagnosed?

A

Overgrowth of the endometrium in response to unopposed oestrogen (obesity, PCOS, HRT and peri-menopause)

DUB or PMB

Hyperplasia (simple or complex) with or without atrypical cellular changes

Dx: TVUS and biopsy for histology

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4
Q

What is the treatment of endometrial hyperplasia?

A

Rx (without atypia): Progesterone therapy (IUS or POP) with surveillance for regression. Require 2 consecutive negative biopsies spaced 6 months apart before discharge

Rx (with atypia): total hysterectomy due to risk of progression to malignancy, laparoscopic preferred as faster healing, less complications. Offer BSO to post-menopausal women.

If want to maintain fertility: counsel on risks, investigate for staging and ensure no cancer in-situ (histology, TM and imaging), propose rigarous surveillance (every 3 months) andgive LNG-IUS or POP. Refer to specialist for fertility and conception help.
NEED regression to increase chance of implantation and survival

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5
Q

Which hormone therapy can increase risk of endometrial hyperplasia and subsequent cancer?

A

Tamoxifen used in ER positive breast cancers

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6
Q

What is endometrial carcinoma? and what are the two main types?

A

Dysplastic overgrowth of endometrial tissue in response to unopposed oestrogen (PCOS, obesity, HRT and peri-menopause).

Type 1 = Endometroid, caused by endometrial hyperplasia, associated with increased oestrogen e.g. obesity with hyperlipidaemia, hyperoestrogenaemia, insulin resistance and infertility. (associated with Lynch syndrome)
Type 2 = Serous is mainly associated with TP53 mutations, tropic endometrium and more common in older or black women.

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7
Q

How are endometrial carcinomas diagnosed?

How are endometrial carcinomas graded?

A

TVUS and biopsy with CT/MRI for mets and staging

G1 = <5% non-squamous solid growth pattern (low grade)
G2 = 6-50% non-squamous solid growth pattern
G3 = >50% non-squamous solid growth pattern (high grade)
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8
Q

What tumour markers can be looked at in endometrial carcinoma?

Why is hormone status determined and used?

A

PTEN - consider Cowden’s disease
MMR - consider Lynch Syndrome, will also show signs of micro satellite instability
P53 - present in 20% of endometriod but 90% of serous (oestrogen independent cancers)
HER-2 - shows a distinct type of serous uterine cancer

Hormone status is used in the palliative treatment and for advanced disease/recurrent tumours.

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9
Q

How will endometrial cancers present?

A

DUB, pelvic mass, >50

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10
Q

What is the treatment for low grade endometrial cancers?

A

Surgery: TAH and BSO with lymphadenectomy if appropriate
+ post-op observation
+ vaginal brachytherapy if high risk of recurrence

If preserving fertility then careful monitoring and progesterone therapy. Refer to fertility specialist. TAH and BSO after pregnancy.

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11
Q

What is the treatment for intermediate grade endometrial cancers (1B and 2)?

A

Surgery: TAH + BSO with lymphadenectomy if appropriate
+ post-op observation
+ vaginal brachytherapy
+/- chemotherapy (paclitaxel and carboplatin)
+/- external beam radiotherapy (If high risk of local disease)

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12
Q

What is the treatment for high grade endometrial cancers?

A

Staging surgery + chemotherapy (paclitaxel and carboplatin)

+ external beam radiotherapy

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13
Q

What is the treatment for incurable or recurrent endometrial cancers?

A

Palliative care!
Supportive treatment for pain, N+V, lymphedema, bleeding, obstruction as well as psychosocial support
+/- radiotherapy and surgery
+/- palliative chemo with paclitaxel and carboplatin
+/- hormone therapy with progestin or aromatase inhibitor (tamoxifen)
+/- pembrolizumab if Lynch syndrome

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14
Q

What is CIN?
What causes it?
How is it prevented?

A

Cervical intra-epithelial neoplasm (dysplasia of cervical cells)

Associated with HPV 16 and 18 infection. It is associated with unprotected sex, more sexual partners, lower SE class, and earlier sex

Prevented by screening: smears every 3 years from 25-49 then every 5 years from 50-64. Vaccine given to 14yrs girls.

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15
Q

How does CIN present?
How is CIN diagnosis achieved?
What are the stages of CIN?
What is the treatment?

A

Normally asymptomatic and discovered at smear.

Smear shows evidence of koilocytosis which is vacuolation as a result of persistent HPV infection. If dyskaryosis (abnormal cells) are identified then can invite back in 3 months to observe any change or if actually normal. Refer for colposcopy to investigate further.

CIN1 = 1/3 closest to BM; CIN2 = 2/3 closest to BM; CIN3 3/3 without invasion of the BM.

Treat CIN2 and 3 with large loop excision of TZ (LLETZ)

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16
Q

What is CGIN?

What are the RF for this?

A

Cervical glandular intra-epithelial neoplasia

RF: higher SE class, later sex, fewer partners, HPV18

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17
Q

How long is the progression from CIN to cancer?

What are the stages of cervical cancer?

A

5-20 years

1 = confined to cervix
2 = invasion of local structures
3 = invasion of pelvic wall
4 = metastasis to other structures
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18
Q

What are the symptoms of cervical cancer?

A

Usually asymptomatic and picked up at smear
May present with DUB (IMB, PCB and PMB), pain, change to vaginal discharge, dysparenuria, haematuria or renal/bladder dysfunction

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19
Q

How is cervical cancer diagnosed?

A

Smear + colposcopy + biopsy + CT/MRI (for mets and invasion)

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20
Q

How is cervical cancer treated?

A

<2cm or desire fertility = trachelectomy + lymphadenectomy
>2cm or fertility not required = TAH + lymphadenectomy
(can also give adjuvant radiotherapy)

if locally/widespread advanced disease then chemotherapy with paclitaxel and carboplatin
(can also use surgery for debulking and radiotherapy)

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21
Q

What are the survival rates for cervical cancer?

A 
100% for stage 1A
70-90% for stage 1B
45-80% for stage 2
30-65% for stage 3
5-20% for stage 4
22
Q

What is ovarian cancer?

A

90% are epithelial ovarian cancers (serous, endometroid, clear cell etc)
10% are germ cell, granulosa cancers (teratoma or thecal/granulosa cell)

23
Q

Thecal and granulosa ovarian cancers produce which hormone?

A 
Thecal = adrogens
Granulosa = oestrogens
24
Q

What are the symptoms of ovarian cancer?

A

non-distinct!
Bloating, pelvic mass, weight loss, early satiety, heart burn, bladder dysfunction, ascites, pleural effusion or SOB

Usually presents late with mets

25
Q

How is ovarian cancer diagnosed?

A

CA-125 = sensitive but not specific (raised in other conditions like pancreatitis)
CEA
USS - TV or abdominal
Cytology of pleural fluid or ascites aspirate
Pathology

26
Q

What are you looking for on a TVUSS of ovarian cancer?

A

Multiloculated mass with cystic and solid qualities and thickened separations.

27
Q

What are the FIGO stages for ovarian cancer?

A 
1 = confined to one or both ovaries
2 = spread to other pelvic organs e.g. Fallopian tubes, uterus
3 = spread beyond pelvis but within abdomen e.g. omentum
4 = spread to other organs e.g. liver and lung
28
Q

What is the treatment for ovarian cancer?

A

TAH + BSO + lymphadenectomy and removal of omenta
Investigate the peritoneum further (may require debulking)
Chemotherapy with carboplatin and paclitaxel 9around 70% respond but there is a high relapse rate)

There is palliative chemotherapy for those with recurring disease - a cure is unlikely but may extend life expectancy

29
Q

What is a new mode of administration for chemotherapy in ovarian cancer and why?

A

Intraperitoneal chemotherapy - this is given as a direct injection to the peritoneum to allow a greater concentration of the drug to the affected site. Trials have demonstrated that administration of drug this way gives superior results than IV

30
Q

What biological therapy can be used in ovarian cancers?

A

Bevacuzimab - VEGF inhibitor. Goof for paclitaxel resistent cancers

31
Q

What are red flags for lung cancer?

A 
Coughing up blood
Persistent cough >3 weeks - 6
Weight loss (unexpected)
Progressive SOB
Hoarseness
Chest pain or shoulder pain (persistent)
Finger clubbing
Persistent lymphadenopathy (cervical and supraclavicular)
32
Q

What is a pancoast tumour?

A

Tumour primarily defined by its location in the apex of the lung. It is usually a non-small cell cancer. Can present with ipsilateral horners syndrome (due to invasion of the cervical sympathetic plexus) and shoulder/arm pain due to invasion of brachial plexus.

33
Q

What is Horner’s Syndrome?

A

Condition caused by damage to the sympathetic nerves to the face resulting in pupillary constriction (miosis), eyelid drooping (ptosis) and absence of sweating (anhydrosis)

34
Q

What are features suggestive of mets? (lung)

A

Confusion, weight loss, bone pain, headache, unsteady gait

35
Q

What are the investigations required in Lung cancer (suspected)?

A

CXR
CT
Cytology and typing of tumour (CT-guided biopsy for peripheral or bronchoscopy for more central)
Staging disease: MRI, ultrasound and PET-CT

36
Q

What are the risks of CT-guided lung biopsy?

A

Risk of pneumothorax

37
Q

What are the types of non-small cell lung cancer?

What proportion of lung cancers are small cell?

A

Squamous (30%) - keratinising
Adenocarcinoma (30%) - gland forming
Large cell carcinoma (15%)
Alveolar cell (<1%)

Small cell equates for 25% of all lung cancers

38
Q

How are lung cancers staged and why?

A

Non-small cell cancers are staged by the TNM system

Small cell cancer are staged by either ‘limited disease’ or extensive disease’. Staged this way as SC cancers spread early, are rapidly growing and highly malignant.

39
Q

What are indicators of a poor prognosis in lung cancer?

A 
Pancoast tumour with cervical plexus involvement or brachial
Involvement of recurrent laryngeal nerve
SVC obstruction
Bone mets and pathological fractures
Brain mets
Adrenal gland mets
Spinal cord compression
Paraneoplastic syndromes (SIADH)
40
Q

Where are common mets from lung cancers found and how?

A

Bones - bone scan
Brain
Adrenal gland
Liver

Bone scan involved injection of radionucleotides and monitoring areas of increased uptake

41
Q

What is the relationship between smoking and lung cancer?

A

90-95% of lung cancer patients have a history or are current smokers
Continued smoking in lung cancer reduces life expectancy, increases risk of recurrence and mets, reduces the efficacy of treatment, and exacerbates treatment SE.

Adenocarcinoma is the most common cancer in non-smokers

42
Q

What is the WHO performance status?

A

0 - Fully active, able to do all activities
1 - Restricted in physically strenuous work but can do light activities
2 - can do activities of daily living for up to 50% of waking hours
3 - capable of limited self-care, bed or chair for >50% of day
4 - completely disabled, unable to selfcare and confined to bed/chair

43
Q

Which lung cancer patients are considered operable?

A

Stage 1 or 2 NSCLC

Stage 1 SCLC

44
Q

What makes a LC patient inoperable?

A

Stage 3 or 4 cancer
Poor FEV1
Multiple co-morbidities
WHO performance status of 3 or 4

45
Q

When is chemotherapy recommended for LC patients?

A

Type 3 and 4 NSCLC (maximum 4 cycles)

Chemo is recommended for most SCLC partly due to fast growth of the cancer and ability to met quickly. Give a platinum agent (carboplatin) and etoposide for 3-6 cycles.

46
Q

What are side effects to chemotherapy?

A

GI - nausea, vomiting, diarrhoea, mucositis
Lassitude - lack of energy
Infertility
Alopecia (temp)
Bone marrow suppression (anaemia, neutropenia, thrombocytopenia)
Organ toxicity: kidneys (carboplatin) and nerves (vincristine)
NEUTROPENIC SEPSIS

47
Q

What is neutropenic sepsis?

A

Ocological emergency
Fever (>38°C) for ≥2h when neutrophil count < 1.0 x 109/L
(Fever in an individual with neutropenia)
Most common 10-14 days after chemo, although could be after 7 days with taxane therapy.
Presentation may be minimal but also may have symptoms of sepsis (fever, riggers etc)

48
Q

How is neutropenic sepsis treated?

A

Tazocin 4.5g TDS IV and gentamicin

Sepsis screen initiated (blood, urine, stool and sputum culture)

49
Q

What are some side effects of radiotherapy?

A 
Local to the area of radiation
Skin erythema and burning
Telanectasia/vasculitis
Tiredness
N+V+D and mucositis
dysphagia
50
Q

What is SABR?

A

Stereotactic ablative radiotherapy - different type of radiotherapy that delivers a higher dose over a shorter period of time e.g. 18Gy x 3 (with 2-4 days between doses). It also delivers to a smaller area (good for small cancers) to reduce the impact of higher radiation on organs (reduces toxicity).

51
Q

How does superior vena cava obstruction present?

A 
Facial swelling (with a dark red complexion)
Headaches
Breathlessness
Swollen neck arms and hands
Visible swollen veins on chest
Raised JVP
52
Q

Which (SCLC or NSCLC) is more receptive and responsive to radiotherapy?

A

SCLC

4th Year (2 decks)

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