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Medicine 1 Matched to MLA Content Map > Cancer (By Condition) > Flashcards

Cancer (By Condition) Flashcards

1
Q

What breast condition is being described?

Cells lining the ducts show cytological features of malignancy but have not yet invaded the stroma

A

Ductal Carcinoma in Situ (DCIS)

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2
Q

Define Ductal Carcinoma in Situ (DCIS)?

A

Cells lining the ducts show cytological features of malignancy but have not yet invaded the stroma

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3
Q

How may DCIS be detected?

A

Focal calcification allows it to be detected by mammographic screening or it may present as a palpable mass

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4
Q

Describe LCIS in the breast?

A

• Sometimes called lobular in situ neoplasia
• Lesion is usually multifocal and bilateral
• Can progress to infiltrative carcinoma
• It is less clear with LCIS vs DCIS whether it is pre-cancer, as some women it never progresses to cancer, however it increases your risk of breast cancer overall i.e. you have more chance of getting cancer even in the opposite breast or a ductal carcinoma

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5
Q

Explain what Paget’s disease of the nipple is?

A

• Paget’s disease of the nipple is characterised by inflammatory eczema like changes of the nipple that may involve the areola
• It is caused by high grade DCIS extending along ducts to reach the epidermis of the nipple

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6
Q

What is the significance of someone having inflammatory skin changes around their nipple?

A

It could be Paget’s disease of the nipple which is a sign of underlying DCIS

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7
Q

What is the commonest form of breast cancer and how does it usually present?

A

Ductal carcinoma - usually presents as a firm hard lump

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8
Q

Describe infiltrating lobular carcinoma of the breast?

A

• Only 10% of breast cancers are this type
• There is more of a chance of the cancer being multi-focal and/or bilateral with this type
• (generally lobular things are more odd as they don’t arise as a lump like ductal things)
• Microscopically the tumour infiltrates the tissue as single files of malignant cells

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9
Q

Type of breast condition with pathology :
Microscopically the tumour infiltrates the tissue as single files of malignant cells

A

Lobular Carcinoma

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10
Q

Describe metastatic spread of breast cancer?

A

• Initially cancers spread via lymphatics to axillary nodes
• Spread via bloodstream is most common to the bone marrow and lung
• Secondaries are common to the liver, lung and bones

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11
Q

Explain some things that increase and decrease your risk of developing breast cancer?

A

• Increasing Age
• Genetics: BRCA1 and 2
• Smoking
• Lack of physical activity
• Alcohol

Risk factors to do with oestrogen (anything that prolongs cyclical exposure to sex hormones increases risk):
- Early menarche and late menopause increases risk
- Breast feeding reduces risk (because it inhibits menstruation)
- Obesity increases risk as increased adipose tissue results in increased oestrogen
- Nulliparity increases risk (when you are pregnant you aren’t being exposed to cyclical oestrogen as you are not menstruating)

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12
Q

Describe some symptoms of breast cancer?

A

• 50% of women are asymptomatic and picked up on screening
• 50% are symptomatic and of the 50% that are symptomatic 50% of them have a lump
• Symptoms of breast cancer include: dimpled or depressed skin, visible lump, nipple change, bloody discharge, texture change, colour change

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13
Q

Describe the one stop clinic for breast symptoms?

A

• Assessment for any woman with concerning breast symptoms
• Triple assessment in one clinic: clinical assessment, imaging, pathology
• Imaging depends on age group and symptoms
• Only 10% of people attending the clinic will have a cancer

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14
Q

Describe receptor status and what it means for prognosis in breast cancers?

A

• ER and/or PR+, HER2- have the best prognosis
• HER2+ but ER- and PR- have a poorer prognosis
• Triple negative cancers have the worst prognosis

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15
Q

Is breast LCIS usually treated?

A

Often no treatment is needed
if the LCIS is pleomorphic (variations in size and shape so looks worse than normal LCIS) then it may be treated - treatment would be similar to ductal treatments

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16
Q

Give an overview of management of breast cancers?

A

Surgery - WLE or mastectomy
Radiotherapy may be used as adjuvant therapy
chemotherapy mainly used in triple negative cancers
Anti oestrogen therapy or HER2 receptor blockers

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17
Q

Describe the use of anti-oestrogen therapy in breast cancer?

A

• In those with ER+ cancers this can reduce the risk of recurrence
• Pre-menopausal women should be given tamoxifen (ER receptor antagonist) for 5 years at least
• Post-menopausal women should get tamoxifen or an aromatase inhibitor e.g. letrozole for at least 5 years
• Aromatase inhibitors are thought to be better in post-menopausal women vs tamoxifen

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18
Q

Describe the use of targeted HER2 therapy in breast cancer?

A

• HER2 receptor blockers can be used in HER2+ cancers (usually given for six months to a year)
• They are a type of monoclonal antibody
• E.g. trastuzumab/ Herceptin

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19
Q

What are the leukaemias?

A

• Group of disorders characterised by the accumulation of malignant white cells in the bone marrow and blood
• These abnormal cells cause symptoms because of bone marrow failure and due to infiltration of organs

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20
Q

How can leukaemias be categorised?

A

Leukaemias can be characterised as acute or chronic, lymphoid or myeloid

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21
Q

Characteristics of acute leukaemias?

A

• Acute leukaemias are aggressive, malignant transformation causes accumulation of early bone marrow haemopoietic progenitors called blast cells
• Acute leukaemias are defined as an excess of blasts >20 %

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22
Q

Characteristics of chronic leukaemias?

A

• Chronic leukaemias have slower progression and the malignant cells are more mature - cells mature partially whereas in acute the cells don’t mature at all

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23
Q

Acute leukaemias are more fatal than chronic leukaemias but paradoxically acute leukaemias________

A

are easier to treat

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24
Q

Describe how blood cells are derived?

A

• All blood cells are derived from pluripotent stem cells
• These stem cells have 2 key properties: self renewal and proliferation and differentiation into mature blood cells through intermediate progenitor cells which have lost the ability to self renew but have high proliferative capacity
• Progenitor cells can be broadly classed as lymphoid (give rise to lymphocytes) or myeloid (give rise to all non-lymphocyte cells)
• As you move down the tree cells become smaller, DNA is condensed as genes that are not needed for the specific cell can be switched off

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25
Q

Define progenitor cells?

A

cells which have lost the ability to self renew but have high proliferative capacity (classed as lymphoid which give rise to lymphocytes or myeloid which give rise to all non-lymphocyte cells)

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26
Q

Define blast cells?

A

nucleated precursor cells e.g. lymphoblasts, erythroblasts, myeloblasts

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27
Q

Aetiology/ risk factors for leukaemias?

A

In most cases the cause is unknown, risk factors include:
• Radiation
• Chemicals e.g. chemo, benzene
• Genetics
• Viruses e.g. human T cell leukaemia virus 1

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28
Q

Describe spread of leukaemias?

A

• Leukaemic cells circulate in the blood and/ or lymph and can therefore spread anywhere in the body
• Nodular deposits are, however, uncommon
• After initially successful treatment, leukaemia infiltration may recur, especially in the CNS (meninges) and the testis

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29
Q

Which acute leukaemia is more common in children ?

A

ALL

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30
Q

Which acute leukaemia is more common in the elderly?

A

AML

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31
Q

What is the most common childhood cancer?

A

ALL

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32
Q

Clinical presentation of ALL?

A

symptoms of bone marrow failure (pancytopenia), in this form of leukaemia infiltration particularly to the CNS and testes is more common, can also cause bone pain

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33
Q

Results of investigations in ALL?

A

• The marrow is packed with blast cells and the blood shows presence of blast cells
• Immunophenotyping is required for a definitive diagnosis
• FBC may show reduced Hb, neutrophils and platelets
• WCC may be raised on FBC due to the presence of lots of blast cells (but the individual white cell counts e.g. neutrophils will be low because these blast cells are taking over)

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34
Q

Management of ALL?

A

• Treatment usually involves cycles of chemotherapy, the cycles are of varying intensity and treatment can last for 2-3 years
• Sometimes patients are given steroids along with the chemotherapy to improve effectiveness
• Targeted therapies can be used in certain subtypes

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35
Q

AML can occur ____ or ______

A

de novo (i.e. on its own) or secondary (e.g. after therapy from another cancer)

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36
Q

Presentation of AML?

A

• Subgroups may have characteristic presentations
• Presentations can be similar to ALL

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37
Q

Auer rods?

A

hallmark of AML
inclusions in blast cells which are crystallised aggregates of the myeloperoxidase enzyme

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38
Q

What is required for definitive diagnosis of AML and ALL?

A

Immunophenotyping

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39
Q

What does chronic lymphocytic leukaemia have a crossover with?

A

small lymphocytic lymphoma
- if it mainly circulates - leukaemia
- if it is mainly in the lymph nodes - lymphoma

spectrum - it behaves like this so i reccommend xyz treatment

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40
Q

What group of patients tends to get CLL?

A

middle age and elderly

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41
Q

Most cases of CLL are what type?

A

B type

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42
Q

Presentation of CLL?

A

signs of anaemia, infections, lymph node enlargement and splenomegaly

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43
Q

In CLL there is monoclonal proliferation of _____

A

small lymphocytes

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44
Q

smudge cells on blood film?

A

CLL
(smudge cells which are remnants of cells that lack any identifiable cytoplasmic membrane or nuclear structure, they are associated with the abnormally fragile lymphocytes that are produced in CLL)

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45
Q

In CML there is proliferation of _______

A

myeloid cells: granulocytes and their precursors

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46
Q

Describe progression of CML?

A

There is a chronic phase with intact maturation that lasts 3-5 years followed by a ‘blast crisis’ reminiscent of acute leukaemia

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47
Q

Clinical features of CML?

A

can be asymptomatic, splenomegaly, weight loss, sweats, anorexia, gout, can get priapism

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48
Q

Blood count changes in CML?

A

normal/ decreased Hb, leucocytosis with neutrophilia and myeloid precursors (myelocytes), eosinophila, basophilia, thrombocytosis

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49
Q

Hallmark genetic change in CML?

A

Philadelphia chromosome

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50
Q

Explain the philadelphia chromosome and how it leads to CML?

A

The ABL gene on chromosome 9 translocates onto chromosome 22 and fuses with BCR gene. This results in a shorter chromosome 22 called the Philadelphia chromosome (as well as a longer chromosome 9 which has extra added from 22). The new BCR-ABL gene on the Philadelphia chromosome produces a tyrosine kinase which causes abnormal phosphorylation (signalling) leading to the haematological changes in CML

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51
Q

Treatment of CML?

A

tyrosine kinase inhibitors (imatinib)

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52
Q

Where do most uterine malignancies arise from?

A

The endometrium and so are adenocarcinoma

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53
Q

Risk factors for endometrial malignancy?

A

• High levels of oestrogen are considered to be a risk factor for endometrial malignancy
• Factors which may increase oestrogen include PCOS, late menopause, nulliparity, obesity, unopposed oestrogen HRT, tamoxifen (blocks oestrogen receptors in the breast but stimulates them in the uterus), oestrogen secreting tumours
• Lynch syndrome/ HNPCC causes microsatellite instability due to a defect in mismatch repair genes and increases the risk of colorectal and endometrial cancer (increases risk of all cancers but endometroid is most common)

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54
Q

Explain the classifications of endometrial cancers?

A

• 80% of endometrial carcinomas are type I cancers which are called endometroid tumours
• Type I cancers are related to unopposed oestrogen (i.e. oestrogen without progesterone to stop endometrium growing) and with atypical hyperplasia
• Type II tumours include serous and clear cell cancers which tend to be more aggressive than type I tumours, type II tumours are not related to unopposed oestrogen
Side note: you can get other endometrial tumours which aren’t carcinomas but these are quite rare

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55
Q

What is the principle symptom of endometrial carcinoma?

A

Abnormal uterine bleeding

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56
Q

1st line investigation for suspicions of endometrial cancer? What does result mean?

A

TVUS to measure endometrial thickness
(a smooth endometrium < 4mm makes malignancy unlikely)

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57
Q

Investigations for endometrial cancer?

A

• TV US is usually 1st line and in post-menopausal women can measure endometrial thickness (a smooth endometrium < 4mm makes malignancy unlikely)
• Endometrial biopsy
• Dilatation and curettage (scrape tissue from inside of uterus for pathology)
• Hysteroscopy can allow visualization of the uterine cavity enabling biopsy/ curettage to be done

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58
Q

Management of endometrial cancers?

A

• The mainstay of treatment is hysterectomy with bilateral salpingo-oophrectomy
• If there is spread beyond the uterus, treatment is tailored to the individual
• Radiotherapy may be used as an adjuvant to prevent recurrence
• Radiotherapy or high dose progesterones can also be used in those unsuitable for surgery
• In widespread disease, chemo may be considered

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59
Q

Prognosis of endometrial cancers?

A

Most type 1 are caught early and have good prognosis more than 90% 5 year survival
invasion of myometrium takes place slowly because there are no lymphatics in the endometrium

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60
Q

What are the four main histological types of lung cancer?

A

small cell, squamous cell, adenocarcinoma and large cell

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61
Q

Small cell lung cancer arises from __________ and it arises usually _______

A

arises from immature (small) neuroendocrine cells
usually arises centrally

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62
Q

What type of lung cancer is the most aggressive?

A

Small cell carcinoma

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63
Q

What marker does small cell lung cancer usually express?

A

NCAM-1

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64
Q

What histological type of lung cancer usually expresses N-CAM1

A

Small cell lung cancer

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65
Q

What is the most common type of lung cancer?

A

Squamous cell carcinoma

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66
Q

What type of lung cancer often produces keratin?

A

squamous cell carcinoma

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67
Q

What does squamous cell carcinoma often express?

A

p40, p63 and cytokeratin

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68
Q

What type of lung cancer often expresses p40, p63 and cytokeratin?

A

squamous cell lung carcinoma

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69
Q

What is the most common type of lung cancer in non smokers?

A

Adenocarcinoma
(although it is important to note that this is still more common in smokers overall)

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70
Q

What do most lung adenocarcinomas express?

A

TTF-1 or Napsin

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71
Q

What type of lung cancer usually expresses TTF-1 or Napsin?

A

Adenocarcinoma

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72
Q

Describe large cell carcinoma in the lung?

A

No specific cell differentiation, this is a diagnosis of exclusion, the tumour usually arises centrally

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73
Q

Describe bronchial carcinoid tumours?

A

These are low grade neuroendocrine tumours that if typical, generally do not metastasise
Atypical carcinoid tumours however can metastasise
They are not associated with smoking
Tumour is usually situated in a primary bronchus or at the lung periphery and is a smooth-surfaced yellow nodule

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74
Q

List some local effects of lung cancer? (7)

A

1) INVASION OF THE RECURRENT LARYNGEAL NERVE
2) INVASION OF THE PLEURA AND CHEST WALL
3) INVASION OF THE PERICARDIUM
4) INVASION OF THE BRACHIAL PLEXUS
5) INVASION OF THE SYMPATHETIC CHAIN
6) INVASION OF THE PHRENIC NERVE
7) INVASION OF THE SUPERIOR VENA CAVA

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75
Q

Why may a patient with lung cancer present with a persistently hoarse voice?

A

invasion of the recurrent laryngeal nerve

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76
Q

Why may a patient with lung cancer present with pleuritic chest pain and a pleural effusion?

A

invasion of the pleura

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77
Q

Why may a patient with lung cancer present with breathlessness, AF and a pericardial effusion?

A

invasion of the pericardium

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78
Q

Why may a patient with lung cancer present with arm weakness, numbness or tingling?

A

invasion of the brachial plexus

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79
Q

Why may a patient with lung cancer present with puffy eyelids, headache, distended EJV and visible anastomoses in the abdomen to the IVC?

A

Invasion of the SVC

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80
Q

Explain how Horner’s syndrome may occur in lung cancer?

A

A pancoast tumour invades the sympathetic chain causing ptosis (eyelid drooping), miosis (constricted pupil) and anhidrosis (loss of sweating) all only on ONE side of the face

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81
Q

What are pancoast tumours?

A

apical lung tumours

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82
Q

What is meant by paraneoplastic effects?

A

symptoms that are a consequence of the cancer but not due to the presence of local cancer cells, generally some sort of immune reaction

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83
Q

List some non local effects of lung cancer?

A

1) FINGER CLUBBING
2) CUSHING SYNDROME
3) DILUTIONAL HYPONATRAEMIA
4) HYPERCALCAEMIA
5) HYPERTROPHIC PULMONARY OSTEOARTHROPATHY
6) THROMBOPHLEBITIS
7) EATON LAMBERT SYNDROME

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84
Q

Explain the mechanism by which lung cancer can cause cushing syndrome? in which histological subtype does this occur?

A

small cell lung cancer can secrete ACTH which results in adrenal hyperplasia and raised blood cortisol, symptoms and signs of cushing syndrome include central obesity but proximal muscle wasting, hypertension, increased blood glucose, striae (red stretch marks), round face, increased sweating, frontal balding in women

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85
Q

Explain the mechanism by which lung cancer can cause dilutional hyponatraemia? in which histological subtype does this occur?

A

small cell lung cancer can secrete ADH which results in increased water reabsorption therefore diluting the Na+ so concentration of Na+ decreases, this is called SIADH (syndrome of inappropriate ADH secretion)

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86
Q

Explain the mechanism in which lung cancer can cause hypercalcaemia? in which histological subtype does this occur?

A

squamous cell lung cancer can secrete PTHrp (parathyroid hormone related peptide) which mimics the real PTH released from the PTH. Normally PTH is released from the parathyroid when calcium levels are low so there can be more absorption of calcium from the gut and kidneys and calcium resorption from the bones, however if squamous cell lung cancer secretes PTHrp when the calcium is normal will get hypercalcaemia. Patient will have a high calcium but undetectable PTH.

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87
Q

Explain what Eaton Lambert syndrome is?

A

This syndrome has many causes but it is mainly associated with lung cancer, it is an auto-immune condition where the body attacks the nerves and get weakness in legs, arms and face. The auto-immune response causes defective Acetylcholine release at the NMJ.

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88
Q

What are the 3 groups of ovarian tumours?

A

Epithelial
Sex cord/ stromal
germinal

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89
Q

What are the 3 most common subtypes of epithelial ovarian tumours?

A

Serous (most common)
Mucinous
Endometroid

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90
Q

What is the most common malignant tumour of the ovary?

A

Serous cystadenocarcinoma

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91
Q

All subtypes of epithelial ovarian tumours can be ____

A

benign, borderline or malignant

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92
Q

Serous ovarian tumours resemble ____

A

epithelium of the fallopian tubes

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93
Q

Mucinous ovarian tumours resemble _____

A

epithelium of the endocervix

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94
Q

Endometriod ovarian tumours arise from _____

A

endometriosis directly or with a focus of endometrium in the background

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95
Q

List four types of ovarian sex cord/ stromal tumours?

A

1) Fibroma
2) Thecoma
3) Granulosa cell tumour
4) Sertoli Leydig cell tumours

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96
Q

Describe the ovarian tumours thecomas and fibromas ?

A

1) Fibroma- commonest sex cord/ stromal tumour, benign collagenous, solid tumours that resembles a thecoma but does not produce oestrogen, it is a spindle cell tumour
2) Thecoma- similar to fibroma but does secrete oestrogen

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97
Q

Describe granulosa cell tumours of the ovary?

A

potentially malignant and secrete oestogens, composed of cells resembling the granulosa cells lining the Graafian follicles

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98
Q

Where do germ cell tumours arise from? List 5 types of ovarian germ cell tumour? What is the most common?

A

Germ cell tumours arise from the cells that produce eggs (or sperm in males)

1) Mature Cystic Teratomas AKA Dermoid Cyst- 95% of germ cell tumour

2) Immature teratomas- these are predominantly solid and are malignant, they contain embryonic tissues typically of primitive nerve tissue and mesenchymal tissue

3) Yolk sac tumour

4) Choriocarcinoma

5) Dysgerminoma

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99
Q

Describe mature cystic teratomas / dermoid cysts?

A

95% of germ cell tumour are dermoid cysts, they are benign, because they have pluripotent potential can see sebum, hair, teeth, nervous tissue, respiratory tissue, intestinal epithelium and thyroid tissue.

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100
Q

Describe immature teratomas?

A

these are predominantly solid and are malignant, they contain embryonic tissues typically of primitive nerve tissue and mesenchymal tissue

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101
Q

What is the biggest risk factor for ovarian cancer, who does this mean is more at risk?

A

The biggest risk factor for ovarian cancer is number of times ovulated because every time you ovulate the follicle ruptures and there needs to be cell division to repair it, increased cell division increases risk of cancer.

Hence

increased risk with early menarche late menopause and nulliparity, and increased age
decreased risk with COCP, multiparity, breast feeding

other things that increase risk are some genetics e.g. BRCA1 and 2, lynch syndrome
endometriosis also increases risk

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102
Q

Presentation of ovarian cancer?

A

• The patient may be asymptomatic and often patients present late as symptoms are non-specific
• Bloating, early satiety, abdominal pain or swelling, constipation and menstrual changes are all potential symptoms

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103
Q

What is Ca125 a marker of? What is its use in ovarian cancer?

A

Ca125 is a marker of peritoneal and pleural inflammation, it is secreted by what is embryologically coelomic epithelium
This is raised in 80% ovarian cancers but also raised in many other conditions so lacks sensitivity and specificity when used alone It is good for monitoring progression

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104
Q

Describe the risk of malignancy index in ovarian cancer?

A

• This is used to differentiate benign from malignant = USS score x menopausal score x Ca125
• The ultrasound score is scored 1 point for each of following features: multilocular cysts, solid areas, metastases, ascites and bilateral lesions (U=0 if none, U=1 if one and U=3 if score 2-5)
• Menopausal status is scored 1 for premenopausal and 3 for postmenopausal
• Ca125 is included as the measurement in IU/ml
• If the score is > 200 the chance of cancer is 75% if the score is < 30 the chance of cancer is 3%
• Those with a score > 200 should be referred to gynaecology

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105
Q

Imaging for ovarian cancer?

A

Ultrasound
CT pelvis and abdomen

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106
Q

Management of ovarian tumours and cancer?

A

• Treatment for benign tumours is excision and drainage
• Epithelial tumours should get a combination of chemo and surgery
• May do conservative surgery if want to preserve fertility and only remove 1 ovary
• If unfit for surgery may just do chemotherapy
• Non-epithelial tumours are often sensitive to chemo and it is often more important to preserve fertility as these patients tend to be younger

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107
Q

The incidence of _____ brain tumours is much higher than primary

A

metastatic

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108
Q

The common appearance of metastatic brain tumours is ______

A

is multiple, well-delineated spherical nodules that are randomly distributed

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109
Q

What are the 2 most common sites to metastasise to the brain?

A

lung and breast
(but should note that any malignant tumour can metastasise to the brain)

110
Q

List some categories of brain tumours?

A

Gliomas
Tumours of neuronal cell types
Tumours arising from mesoderm/ supporting tissue
Tumours of the nerve sheath
pituitary tumours
germ cell tumours

111
Q

Main types of glioma?

A

Astrocytomas and oligodendrogliomas

112
Q

Describe astrocytomas?

A

• These are gliomas that arise from astrocytes
• They are histologically graded from grade I-IV
• Grade I astrocytomas grow very slowly over many years while grade IV (glioblastoma) cause death within several months

113
Q

What is a glioblastoma?

A

a grade 4 astrocytoma

114
Q

Describe oligodendrogliomas?

A

• These are gliomas that arise from oligodendrocytes
• They grow very slowly over several decades and calcification is common

115
Q

Describe tumours of neuronal cell type?

A

• Fully differentiated neurons can neither multiply nor give rise to neoplasms
• Tumours of this type are therefore derived from primitive nerve precursors (blast cells) and seen in infancy and childhood before completion of differentiation
• Depending on their site of origin they are given different names (but the tumour is mainly composed of the same cells which are blast cells- blast cells are basically a precursor to mature neurons)

Medulloblastoma
• Tumour arising from cerebellum

Retinoblastoma
• Tumour arising from the retina

Neuroblastoma and Ganglioneuroma
• These are tumours that arise from sympathetic ganglia
• In ganglioneuromas the tumour is derived from blast cells but as the tumour grows the neurons actually mature

116
Q

Describe meningiomas?

A

• These are thought to arise from arachnoid granulations and so are found most commonly adjacent to venous sinuses
• They account for 15-20% of intracranial tumours
• They are slow growing and essentially benign
• Occasionally meningiomas can arise in the spine

117
Q

What is the most common type of schwannoma? and how does it present?

A

vestibular schwannoma
progressive sensorineural hearing loss, tinnitus and vertigo- the tumour is often unilateral so the symptoms are too

118
Q

Describe neurofibromas?

A

• These are derived from endoneurium which is a layer of delicate connective tissue around the myelin sheath of each nerve fibre in the PNS
• They may be solitary or in neurofibromatosis they are multiple
• They can affect peripheral nerves over a wide area or occupy a single group of nerves
• Unlike schwannomas, a small but significant proportion of neurofibromas undergo transformation to malignant peripheral nerve sheath tumours

119
Q

Describe germ cell tumours in the brain?

A

• These occasionally arise in midline structures and are derived from embryologically misplaced germ cells
• Can have these misplaced cells in your brain your whole life and not find out or only find out if you get a tumour arising from these cells!
• E.g. teratoma

120
Q

Describe the symptoms and signs that could occur if someone had a tumour in their frontal lobe?

A

1) Precentral gyrus: Contralateral weakness, the part of the body that the weakness is in will depend on the position along the gyrus, it will correspond with the motor homunculus
2) Broca’s area (inferior frontal gyrus): expressive dysphasia where the patient can still comprehend words but produces faulty sentences
3) Frontal eye fields (Middle frontal gyrus): abnormalities of gaze
4) Micturation inhibition centre: incontinence
5) Personality changes, disinhibition and cognitive slowing

121
Q

Describe the symptoms and signs that could occur if someone had a tumour in their parietal lobe?

A

1) Postcentral gyrus: contralateral sensory loss, part of body will depend on location along gyrus, it will correspond with the sensory homunculus
2) Contralateral inferior quadrantopia
3) If dominant lobe affected (left in most people): dyscalculia (difficulty understanding maths), dysgraphia (difficulty writing), finger agnosia (inability to distinguish between and recognise all fingers), left-right disorientation
4) If non-dominant lobe affected (right in most people): neglect (deficit in awareness of one side of the body), dressing apraxia (inability to dress yourself automatically), constructional apraxia (inability to build, assemble or draw objects)

122
Q

Describe the symptoms and signs that could occur if someone had a brain tumour in their temporal lobe?

A

1) Auditory Cortex and Wernickes Area (superior temporal gyrus): damage to auditory cortex can lead to loss of awareness of sound, wernicke’s area is located on the superior temporal gyrus in the dominant hemisphere and damage can lead to receptive dysphasia in which an individual has impaired comprehension and produces jargon (word salad) but their speech is fluent
2) Memory deficits
3) Contralateral superior quadrantanopia

123
Q

Describe how someone with a tumour in their occipital lobe may present?

A

Visual Cortex: visual hallucinations, contralateral homonymous hemianopia

124
Q

Describe how someone with brain tumour in their cerebellum could present?

A

• Dysdiadochokinesia: impairment of rapid alternating movements e.g. quick alternating, pronation, supination of the hand
• Ataxia: broad based gait
• Nystagmus: involuntary, uncontrollable eye movements
• Intention tremor: tremor that gets worse as you approach the end point of a guided movement, finger to nose test can show this
• Scanning dysarthria: patients speaks slowly with poor articulation of speech
• Hypotonia: reduced tone

125
Q

Red flag headache symptoms for brain tumours?

A

headache that is worse in the morning (because lying down increases ICP), headache that wakes you up, headache worse with coughing or leaning forward, headache associated with vomiting (due to pressure on the medulla)

126
Q

Clinical features of brain tumours?

A

headache
direct effects
seizures

127
Q

Investigations for brain tumours?

A

• MRI is the investigation of choice
• CT may be done first though if MRI is not possible right away
• Biopsy is carried out to ascertain the histology
• Since metastases are more common than primary tumours, routine tests such as chest x-ray should be performed

128
Q

Management of Brain tumours?

A

• Low grade astrocytomas are now removed as it has been shown that these tumours if left have the potential to de-differentiate (reverse differentiation and lose specialised characteristics) into a high-grade malignancy
• The gold standard treatment for glioblastomas is surgery, radiotherapy and chemotherapy, despite these treatments these tumours unfortunately still have a poor prognosis
• Oligodendroglial tumours are given a mixture of surgery, chemotherapy and radiotherapy
• Small meningiomas can just be watched but larger ones may need surgery and potentially other treatment
• Vestibular schwannomas are often not removed (it is difficult because the tumour surface is so irregular and they grow around adjacent structures) as the surgery risks permanent hearing loss so instead they are watched and the patient is given a hearing aid

129
Q

Where on the cervix does cervical cancer and its precursor usually occur?

A

the squamo-columnar junction

130
Q

What is cervical intraepithelial neoplasia?

A

the pre invasive stage of cervical cancer where there is dysplasia, it is asymptomatic and detectable by cervical screening

131
Q

Genital warts are caused by what HPV strain?

A

6 and 11

132
Q

What are koilocytes and what do they indicate?

A

cells with a wrinkled pyknotic nucleus and perinuclear clearing
indicate HPV infection

133
Q

What are the main strains of HPV implicated in cervical cancer?

A

16 and 18

134
Q

What is the most common type of cervical cancer? What is its precursor?

A

Squamous cell carcinoma (90%)
precursor is CIN - cervical intraepithelial neoplasia

135
Q

What is another type of cervical cancer? What is its precursor? Is it easier or harder to pick up on screening?

A

Cervical adenocarcinoma
precursor is cervical glandular intraepithelial neoplasia
- harder to pick up on screening but still related to hpv

136
Q

Almost all cases of cervical cancer are caused by?

A

high risk hpv infection

137
Q

Describe how hpv is transmitted and the role in cervical cancer?

A

• HPV infection is mainly transmitted via close skin to skin contact such genital to genital contact and anal, vaginal and oral sex
• It is very common infection and the majority of sexually active women are infected sometime during their lifetime
• However, most infections are transient and are cleared by the body’s natural immunity
• Only persistent infections lead to cancer

138
Q

Define CIN 1-3?

A

CIN 1
• Basal 1/3 of epithelium occupied by abnormal cells

CIN 2
• Abnormal cells extend to middle 1/3

CIN 3 AKA Cervical carcinoma in situ
• Abnormal cells occupy the full thickness of the epithelium

139
Q

Describe spread of cervical squamous cell carcinoma?

A

• Until very late-stage disease the cancer stays in the pelvis – it initially spreads locally to the uterine body, vagina, bladder, ureters and rectum
• Lymphatic spread can occur early via the external, internal and common iliac nodes as well as aortic nodes
• Haematogenous spread to the liver, lungs and bones occurs late

140
Q

Describe the process of cervical screening?

A

• This looks for CIN before it becomes cancer
• Those with a cervix should be screened every five years from age 25-65
• Voluntary withdrawal: never had any intimate contact men or women, if won’t benefit i.e. terminally ill, unable to give adequate sample e.g. FGM, women with physical or learning disability that may make giving a sample distressing
• First the smear is tested for HPV, if negative nothing further is done, if positive the cytology is looked at
• If the smear is negative: recall in 5 years
• If HPV positive but cytology negative: recall in 12 months, only do colposcopy if 3 consecutive samples are HPV positive
• HPV positive, cytology positive, low grade: seen for colposcopy within 8 weeks
• HPV positive, positive cytology, high grade: seen for colposcopy within 4 weeks
• HPV positive, glandular abnormality or suspicion of invasion: seen within 2 weeks

141
Q

Describe the role of colposcopy in detection of cervical cancer?

A

• This allows the cervix to be examined in more detail through the use of a speculum and microscope
• The squamocolumnar junction must be visualized
• Abnormal epithelium contains more protein and less glycogen than normal epithelium meaning that when acetic acid is applied they appear white in colour and easily identifiable
• Punch biopsy can then be undertaken to identify CIN (smear doesn’t include the basement membrane only cells so can only tell if there is dyskaryosis (dysplasia) which could be due to CIN)

142
Q

Describe treatment of CIN?

A

• CIN-1: conservative management for 2 years
• CIN 2 or 3: treatment in the form of excision or ablation

143
Q

Describe presentation of cervical cancer?

A

• Often asymptomatic in early stages
• Post coital bleeding
• Foul smelling discharge which is thin, watery and sometimes blood stained
• Intermenstrual bleeding
• Pelvic pain
• Menorrhagia
• In advanced disease: backache, leg pain, haematuria, weight loss, anaemia, changes in bowel habit

144
Q

Describe management and prognosis of cervical cancer?

A

• Local excision can be done for IA lesions (Stage I just in cervix)
• A hysterectomy can be done for those with stage IB-IIB and may also offer radiotherapy (stage II involvement of adjacent organs)
• Stage IIB-IV is usually treated with chemoradiation and platinum-based chemotherapy (III has involvement of pelvic wall and IV has distant metastases or bladder or rectum involvement)
• Most cervical cancer recurrences are only suitable for palliative care
• Until very late stage the disease is confined to the pelvic cavity and most patients will die before distant metastases appear (most common cause of death is ureter obstruction and kidney failure)

145
Q

Describe the role in hpv vaccination to prevent cervical cancer?

A

• Being given in girls and boys (just recently) age 12-13 as 2 doses six months apart
• The current vaccine is quadrivalent for types 16, 18, 6 and 11 (two high risk types and the types that cause genital warts)
• Theoretically it offers 70% protection against cervical cancer
• There is a nanovalent one recently developed and hopefully available soon

146
Q

What is the most common subtype of bladder cancer? What are the others?

A

90% are transitional cell carcinoma, 9% squamous, 1% everything else

147
Q

Risk factors for bladder cancer?

A

• Risk increases with age
• Strong association with cigarette smoking
• Exposure to industrial carcinogens e.g. beta-naphthylamine and benzidine
• Exposure to certain drugs e.g. cyclophosphamide (used in some cancer and auto-immune disease treatment)
• Squamous cell carcinomas arise from metaplastic change due to chronic inflammation e.g. recurrent UTIs and renal stones or schistosomiasis
• In areas where schistosomiasis is endemic there is high incidence of squamous cell carcinoma of the bladder because the parasites lay eggs in the bladder causing inflammation

148
Q

Presentation of bladder cancer?

A

• Most common presentation is painless haematuria
• Pain however can occur however if clot retention
• Symptoms may be suggestive of a UTI i.e. urinary frequency, dysuria, nocturia but significant bacteruria is absent
• Presenting symptoms may be pain from local nerve involvement or metastases
• Flank pain if lesion causes ureteric obstruction

149
Q

Investigations for bladder cancer?

A

• Urine cytology for malignant cells
• Cystoscopy (camera lens into urethra)
• Urinary tumour markers
• CT or MRI of pelvis
• Excretory urography

150
Q

Management of bladder cancer?

A

Depends on staging and grading:

• In superficial disease - transurethral resection or local diathermy
• If muscle invaded – radical cystectomy or radiotherapy, may do chemo
• In metastatic disease – chemo
• If reason to preserve bladder but invaded muscle – can do systemic chemo and then resection of tumour

151
Q

Explain what multiple myeloma is?

A

• Malignant disease of bone marrow plasma cells
• The cancer isn’t circulating but in the bone marrow - all the bone marrow is becoming full of these abnormal monoclonal cells
• There is clonal expansion of abnormal, proliferating plasma cells producing a monoclonal paraprotein mainly IgG (55%) or IgA (20%)
• Note: it’s called multiple myeloma because very occasionally you can get a solitary plasma cell tumour

152
Q

What patient groups tend to present with myeloma?

A

It is a disease of the elderly
Median age at presentation is over 60, it is rare in under 40s
More common in males
More common in Black Africans but less common in Asians

153
Q

What are the direct tumour cell effects of multiple myeloma?

A
  • Bone lesions (lytic)
  • Hypercalcaemia
  • Bone pain
  • Replacement of normal marrow causing marrow failure
154
Q

What are the paraprotein mediated effects of multiple myeloma?

A
  • Renal failure
  • Immunosuppression (reduction in normal antibodies)
  • Hyperviscosity (due to increase in the amount of protein in the serum)
  • Amyloid
155
Q

Explain how lytic bone disease occurs in multiple myeloma?

A

• This involves a vicious cycle
• Malignant plasma cells produce cytokines that interact with osteoblasts and osteoclasts
• These cytokines cause an upregulation of osteoclasts but a down regulation of osteoblasts (so more bone is being destroyed but there are less osteoblasts to rebuild it)
• Activated osteoclasts in turn produce other cytokines that in turn encourage myeloma cells to divide and multiply
• Cause bone pain and commonly backache due to vertebral involvement
• Can get spinal cord compression if lesions cause compression fractures
• Skull XR may show many punched out lesions, sometimes referred to as pepper pot skull

156
Q

Pepper pot skull?

A

lytic bone lesions on skull that occur in multiple myeloma

157
Q

Why do you get hypercalcaemia in myeloma? What are the symptoms?

A

Bone destruction causes hypercalcaemia
Symptoms:
- Bones > pain, osteoporosis and pathological fractures
- Stones > renal colic from stones, polydipsia, polyuria
- Abdominal groans > abdominal pain
- Psychiatric moans > chronic hypercalcaemia can cause depression but acute hypercalcaemia can cause confusion

158
Q

Why is their kidney damage in multiple myeloma?

A

• Light chain cast nephropathy – due to low molecular weight, light chains can pass through glomerular filtrate and cause damage to the epithelial cells as the protein precipitates as casts
• Hypercalcaemia can also damage the kidneys

159
Q

hypercalcaemia, back pain and AKI

A

Multiple myeloma

160
Q

Investigations for myeloma?

A

• FBC – Hb, WBC and platelet count are normal or low
• ESR is often high
• U and E – evidence of kidney injury
• Serum calcium may be raised
• Serum electrophoresis and immunofixation
• Skeletal survey showing lytic lesions
• Check urine for Bence Jones protein (light chains)
• Rouleaux formation can be seen on blood film this is when there are stacks or aggregations of RBCs that form (although rouleaux formation can also be seen in other conditions)

161
Q

Management of myeloma? Prognosis?

A

• Myeloma is incurable and relapses are inevitable, survival is now 5-10 years for younger patients

Combination chemotherapy is the mainstay:
- Corticosteroids – dexamethasone
- Alkylating agents – cyclophosphamide, melphalan
- Novel agents – thalidomide, bortezomib and lenalidomide
- Monoclonal antibodies – daratumumab
- High dose chemo and autologous stem cell transplant can be done in fit patients where stem cells are taken out before chemo and put back in after chemo (so the patient isn’t at such high risk of infection and anaemia complications after chemo)

Symptom control:
- Treat kidney disease supportively
- Opiates for pain (avoid NSAIDs because they are not as good for the kidneys)
- Local radiotherapy – good for pain relief or spinal cord compression
- Bisphosphonates – correct hypercalcaemia and bone pain
- Vertebroplasty – inject sterile cement into fractured bone to stabalise it

162
Q

2 types of oesophageal cancer? Where in the oesophagus do they effect?

A

squamous cell carcinoma - tends to affect the upper 2/3
adenocarcinoma - tends to affect the lower 1/3

163
Q

What is squamous cell carcinoma of the oesophagus associated with?

A

smoking and alcohol

164
Q

What is adenocarcinoma of the oesophagus associated with?

A

Barretts oesophagus and GORD

165
Q

Explain what Barretts oesophagus is?

A

Barrett’s is a complication of GORD where there is intestinal metaplasia- change from the normal squamous epithelium to columnar epithelium. The oesophagus is usually lined by squamous epithelium.

166
Q

Describe presentation of oesophageal cancer?

A

• Usually these cancers are initially asymptomatic, then present with progressive dysphagia to solids first, then liquids
• Other signs are weight loss and loss of appetite, anorexia and lymphadenopathy

167
Q

Investigations for oesophageal cancer?

A

• Patients with suspected oesophageal cancer should be offered an endoscopic biopsy
• Barium swallow may be done
• PET can be useful to see metastases etc.

168
Q

Management of oesophageal cancer?

A

• Unfortunately, many patients present really late and palliative care is the only option (usually involves inserting a stent to relieve the dysphagia)
• Surgery is the best option but can only be done if there is no invasion of the oesophageal wall
• Some patients can be given preoperative chemoradiation therapy to make the surgery easier

169
Q

What is the most common cancer of the stomach?

A

gastric adenocarcinoma

170
Q

List some types of gastric cancer?

A

adenocarcinomas, lymphomas, carcinoid tumours and GISTs

171
Q

Describe the 2 types of gastric adenocarcinoma?

A

intestinal (well differentiated) - gastric carcinomas tend to arise as lesions on the lesser curvature
diffuse (poorly differentiated) - gastric carcinomas arise in any region of the stomach and tend to be less obvious as lesions, they can cause linitus plastica which is when there is a thick hard stomach as cancer is affecting the whole stomach, histologically see signet ring cells (cells where nucleus has been pushed right to edge in a C shape like signet rings, this is because the cell cytoplasms are full of mucin)

172
Q

Most common site of metastases for gastric cancer?

A

the liver

173
Q

What is linitus plastica?

A

hard thick stomach due to diffuse gastric adenocarcinomas

174
Q

What are signet ring cells due to?

A

occur in diffuse gastric adenocarcinoma - cells where nucleus has been pushed right to edge in a C shape like signet rings, this is because the cell cytoplasms are full of mucin

175
Q

Risk factors for gastric cancer?

A

• Smoking, alcohol and family history of gastric cancer are risk factors
• H. pylori infection is a risk factor for intestinal gastric cancer

176
Q

Presentation of gastric cancers?

A

• Gastric carcinomas tend to present late
• Epigastric pain
• Nausea and vomiting
• Haematemesis, coffee ground vomit or melaena (black coloured stool) (both dark vomit and dark stools is because the stomach has started digesting the blood)
• weight loss
• Dysphagia if the tumour is near the gastro-oesophageal junction

177
Q

Investigation for gastric cancer?

A

endoscopy and biopsy

178
Q

Management of gastric cancer?

A

• Main treatment is surgery, this may be combined with chemotherapy
• Due to late presentation may only be able to provide palliative treatment

179
Q

How do most colorectal cancers progress?

A

Most colorectal cancers develop as a result of progression from normal mucosa to adenoma to invasive cancer (adenocarcinoma)

180
Q

Explain the difference in growth in right and left sided colorectal cancer?

A

Right sided cancers tend to grow as a polyploid carcinoma, cancers on the left tend to grow as a stenosing carcinoma

181
Q

Where do colorectal cancers tend to metastasise to?

A

liver or lungs

182
Q

Explain the TNM staging for Colorectal cancer?

A

Tis Carcinoma in situ, the tumour is only in the mucosa
T1 The tumour has invaded the submucosa
T2 The tumour has invaded the muscularis propria/ externa
T3 Tumour has invaded the serosa
T4 The tumour has invaded into other organs or peritoneum
N 1,2,3 Number depends on how may lymph nodes are involved
M Either 0 or 1 metastases are present or absent

183
Q

Describe the 2 genetic conditions that predispose one to colorectal cancer?

A

1) Lynch Syndrome (AKA Hereditary Non-Polyposis Colorectal Cancer)- this is caused by mutations in genes that are responsible for repair of DNA mismatches and is autosomal dominant and predisposes to cancer as a cell only then needs to lose one copy of mismatch repair genes before cancer can develop
2) Familial Adenomatous Polyposis (FAP)- this is an autosomal dominant condition that causes numerous adenomatous polyps to develop in childhood in the colon, in untreated individuals carcinoma is inevitable by 40 yrs, gene responsible is APC gene and this condition is more easily recognised compared to lynch syndrome as if do colonoscopy hundreds of polyps will be seen lining the bowel

184
Q

Risk factors for colorectal cancer?

A

Lynch syndrome (AKA hereditary non polyposis colorectal cancer)
Familial adenomatous polyposis (FAP)
inflammatory bowel disease particularly ulcerative colitis
increasing age
male
diet high in red meat and fat
smoking
obesity
lack of physical activity

185
Q

Explain how left and right sided colorectal cancers tend to present?

A

• Left sided cancers (tend to present with symptoms of obstruction): altered bowel habit, worsening constipation, tenesmus, rectal bleeding
• Right sided cancers (vague symptoms): unexplained iron deficiency anaemia, persistent tiredness, persistent and unexplained change in bowel habit, unexplained weight loss, colicky abdominal pain, lump in the abdomen

186
Q

Investigations for colorectal cancer?

A

• Diagnosed by colonoscopy or sigmoidoscopy
• Chest, abdo and pelvis CT is done to assess spread

187
Q

Management of colorectal cancer?

A

• Treatment of cancer depends on stage, a total or partial colectomy can be done
• If cancer is advanced may do chemo or radiotherapy depending on location
• Palliation may involve stenting the colon or de-functioning the colon by leaving the cancer but bringing a stoma above to relieve symptoms of obstruction

188
Q

Describe screening for colorectal cancer?

A

• In Scotland men and women aged 50-74 are offered screening for colorectal cancer
• A testing kit is sent to house called the FIT test and this looks for blood in the stool, if it comes back positive people are usually offered a colonoscopy or sigmoidoscopy

189
Q

Most pancreatic cancers are ____ (3)

A

adenocarcinomas
in the exocrine portion
found in the head of the pancreas

190
Q

Risk factors for pancreatic cancer?

A

• Chronic pancreatitis
• Alcohol
• Smoking
• Diet high in fat and carbohydrate
• More common in males over 65

191
Q

Presentation of pancreatic cancer?

A

• Classically pancreatic cancer presents late on as painless jaundice when the tumour obstructs the common bile duct (can also be itchy with the jaundice though)
• However, may present with weight loss, anorexia and vague abdominal pain (pain often radiates to the back and may be relieved by leaning forwards)
• May also have pale stools and dark urine if bile duct obstructed

192
Q

Investigations for pancreatic cancer?

A

• Ultrasound is often done first to allow visualisation of the bile ducts and the head of the pancreas however a negative result does not exclude cancer
• CT and biopsy can then be done

193
Q

Management of pancreatic cancer?

A

• Unfortunately, pancreatic cancer has a very bad prognosis and is often picked up too late and treated palliatively
• If operable Whipple’s procedure is done for tumours of the head and neck- the head of the pancreas is removed, the duodenum, lower part of stomach, gall bladder and common bile duct (this is because of the shared blood supply everything needs removed)
• Total pancreatectomy or distal pancreatectomy can also be done depending on size and location of the tumour

194
Q

What is the most common malignancy affecting men in the UK?

A

prostate cancer

195
Q

Most prostate cancers are?

A

adenocarcinomas

196
Q

Risk factors for prostate cancer?

A

• Increasing age (by 80, 80% of men have malignant foci)
• Family history
• Hormonal factors
• Race: Common in the black population in the USA but rare in China and Japan

197
Q

Presentation of prostate cancer?

A

• Majority are asymptomatic and picked up by PSA tests or abnormal DRE findings
• The patient may have lower urinary tract symptoms similar to those of BPH e.g. nocturia, hesitancy, reduced stream, post void dribbling
• May also present with haematuria or haematospermia
• If the cancer has metastasized the patient may have bone, pain, anorexia and/ or weight loss

198
Q

Why is digital rectal exam helpful in assessing if someone may have prostate cancer?

A

• 75-80% of prostate cancers arise in the peripheral zone which is at the back of the prostate
• This is why DRE is helpful as it is the peripheral zone that will be felt when performing this exam

199
Q

What signs on DRE may indicate prostate cancer?

A

for asymmetry, nodules or a fixed craggy (uneven) mass

200
Q

PSA is produced by ____

A

the secretory epithelial cells of the prostate

201
Q

Explain the role of PSA testing in prostate cancer investigations?

A

• Serum levels increase with prostate cancer
• Sensitivity of PSA in detecting prostate cancer is very high at 90% (the test correctly identifies those with prostate cancer)
• However, specificity of the test is very low at 40% (the test picks up a lot of people who don’t have prostate cancer)
• There are other conditions that can elevate PSA: benign prostatic hyperplasia, prostatitis, UTIs, retention, catheterisation and having a DRE recently performed
• Therefore, PSA testing should only really be done in symptomatic patients
• Patients should be counselled before getting the test that cancer is identified in < 5% and if you get a raised PSA then will have to get a biopsy to further information, biopsies can be uncomfortable and carry risk of sepsis and bleeding

202
Q

What are the indications for Trans-Rectal USS Guided Prostate Biopsy?

A

men with abnormal DRE, elevated PSA, previous biopsies showing PIN (prostatic intraepithelial neoplasia) and ASAP (atypical small acinar proliferation), rising PSA trend despite previous normal biopsies

203
Q

Where are the most common sites for metastatic deposits of prostate cancer?

A

pelvic lymph nodes and skeleton (sclerotic lesions)

204
Q

Explain what grading system is used for prostate cancer?

A

Gleason system is used and has grades 2-10 and indicates degree of differentiation from grade 2 which is well differentiation to grade 10 which is an aggressive cancer with poor prognosis

205
Q

In prostate cancer what are the management options for organ confined disease?

A
  • Watchful waiting – conservative approach, when tumour progresses can do palliative care
  • Active surveillance – close surveillance until at thresholds, designed to be curative
  • Radical surgery – radical prostatectomy, this would hopefully be curative however there is the risk of complications such as erectile dysfunction, incontinence and bladder neck stenosis
  • Radical radiotherapy – this can also be curative but come with the side effects of radiotherapy
206
Q

In prostate cancer what are the management options for locally advanced disease?

A
  • Radiotherapy with neo adjuvant hormonal therapy
  • Watchful waiting – done in those with well differentiated tumours and life expectancy < 10 years or patients who do not accept the treatment related complications
  • Hormonal therapy – done in symptomatic patients who need palliation of symptoms but are unfit for curative surgery
207
Q

In prostate cancer what are the management options for metastatic disease?

A

Androgen deprivation therapy: growth of prostate cancer cells is under influence of testosterone, if prostate cells are deprived of androgenic stimulation they undergo apoptosis
- Hormonal therapy with LHRH analogues or anti-androgens
- Bilateral subcapsular orchidectomy (removing the testis removes testosterone)
- Maximal androgen blockade

Hormonal therapy will come with expected side effects e.g. loss of libido, hot flushes and sweats, weight gain, gynaecomastia, osteoporosis, anaemia, cognitive changes

• Diethylstibesterol which blocks testosterone synthesis is another treatment option (this is a synthetic oestrogen so will also cause hormonal side effects)
• Cytotoxic chemotherapy can also be used

208
Q

What is the most common type of testicular cancer?

A

Germ cell tumours
seminomas or teratomas

209
Q

Where do seminomas and teratomas arise from?

A

• Seminomas arise from the germinal epithelium of the seminiferous tubules
• Teratomas arise from totipotent germ cells capable of differentiating into derivatives of ectoderm, endoderm and mesoderm

210
Q

What age does testicular cancer tend to affect?

A

• Largely a disease of young and middle aged men (most common malignancy in young men)

211
Q

Risk factors for testicular cancer?

A

• Previous testicular malignancy
- cryptoorchidism
• Family history
• Congenital abnormalities e.g. hypospadias, inguinal hernias
• Infections e.g. mumps causing orchitis

212
Q

classic presentation of testicular cancers?

A

Testicular cancers usually present as a painless, insensitive testicular swelling – a hardy stony mass

213
Q

Investigations for testicular cancer?

A

• 95% sensitivity and specificity on ultrasound
• If a patient has a hard testicular lump they should receive an ultrasound that day
• Tumour markers: AFP, HCG and LDH

214
Q

Management of testicular cancers?

A

• Radical orchidectomy is usually performed for treatment
• Orchidectomy is usually done as first step in all testicular cancers, may then do radiotherapy, chemotherapy etc.

215
Q

List some common symptoms of lung cancer

A

A persistent cough > 3 weeks
a long-standing cough that gets worse
chest infections that keep coming back
Haemoptysis
an ache or pain when breathing or coughing
persistent breathlessness
persistent tiredness or lack of energy
loss of appetite or unexplained weight loss
Persistently hoarse voice
Lymphadenopathy

216
Q

Define radical?

A

Treatment given with curative intent

217
Q

Define concurrent?

A

giving two modes of treatment at the same time e.g. chemotherapy with radiotherapy. Usually this is with radical (curative) intent.

218
Q

Define adjuvant and neo-adjuvant?

A

treatment given following radical therapy, with the intention of reducing the risk of disease recurrence. This may be given “Neo” adjuvantly i.e. prior to the radical treatment, rather than afterwards.

219
Q

What is XRT?

A

radiotherapy, usually external beams of ionising radiation directed to the tumour site, prescribed in Gray ( 1 Gy – 1 Joule /kg).

220
Q

Define Brachytherapy?

A

the source of radiation is implanted or inserted in the patient to deliver a dose of radiotherapy to local tumour.

221
Q

What are the 8 hallmarks of cancer?

A

1) Sustained growth signalling
2) Loss of growth inhibition
3) Unlimited replicative potential
4) Avoiding apoptosis
5) Inducing angiogenesis
6) Evasion of the immune system
7) Disordered repair mechanisms
8) Activating invasion and metastases

222
Q

Explain what is meant by performance status in oncology?

A

scoring system to express patient’s level of fitness, more important than age in deterring prognosis and toxicity in thinking about treatment. there are different scales.

223
Q

Common chemotherapy side effects?

A

It helps to remember that chemotherapy targets rapidly dividing cells NOT cancer cells. Hence most of the side effects are due to this. For example hair is rapidly growing part of the body- hence one of the most infamous side effects is alopecia.

Others include malaise, fatigue, lethargy, diarrhoea, mucositis, altered tase, neutropenia, thrombocytopenia, renal and liver impairment.

224
Q

How does chemotherapy work?

A

It targets rapidly dividing cells and as cancer cells are often rapidly dividing these will be killed off.

225
Q

How does radiotherapy work?

A

It ionises cell DNA and breaks the double strand

226
Q

Common radiotherapy side effects? Name 8 chronic and 3 acute?

A

acute - fatigue, skin peeling (erythema desquamation) and head and neck pain
chronic - skin fibrosis, dysphagia, bowel dysfunction, incontinence and bladder instability, pneumonitis, menopause, infertility and secondary cancer

227
Q

Explain simply what lymphoma is?

A

• Malignant tumours derived from lymphoid cells which usually accumulate in the lymph nodes but they can also be extranodal and can aslso spill over into the blood
• (so basically lymphomas are more lump cancers whereas leukaemias are like circulating cancers but there’s some overlap)

228
Q

What 2 groups are lymphomas divided into and what are the percentages for each?

A

Hodgkin Lymphoma (20-25% of lymphomas) and Non-Hodgkin Lymphoma (75-80% of lymphomas)

229
Q

Explain Ann Arbor staging?

A

Ann Arbor staging is used for Hodgkins and NHL

Part of the staging involves using A for absence or B for presence of specific systemic symptoms:

A= a lump/ the lymphadenopathy
B symptoms= fever or night sweats or weight loss (10% over a 6 month period)

230
Q

Symptoms of lymphoma?

A

A= a lump/ the lymphadenopathy
B symptoms= fever or night sweats or weight loss (10% over a 6 month period)

Other potential symptoms of lymphoma not listed as B symptoms include:
- Itch without rash
- Alcohol induced pain of the lymph nodes
- Symptoms relevant to compression e.g. renal failure, SVC obstruction, effusions, marrow failure
- Haematological features: anaemia, thrombocytopenia, neutropenia, leucoerythoblastic features, inflammatory features e.g. raised ESR and CRP, LDH may also be raised

231
Q

Investigations for lymphoma?

A

• Blood counts and blood films
• In most FNA and core biopsy of the lymph nodes will be insufficient and excision biopsy is the best
• May do imaging and CT to check the extent of spread
• There are specific genes that can be tested for in some lymphomas and immunophenotyping can be done
• With the biopsy pathology tend to do lots of immune/ genetic tests to categorise the lymphoma and the immunophenotyping can be done on the biopsy or using flow cytometry

232
Q

Are B symptoms more common in Hodgkins or NHL?

A

b symptoms more common in hodgkins

233
Q

List some features of hodgkins lymphoma?

A

• Almost always lymph node origin
• Characterised by the presence of Reed-Sternberg cells
• Owl eye appearance of cells
• Spread to lymph node groups is orderly
• Generally ,has better prognosis than NHL

234
Q

List some features of non-hodgkins lymphoma?

A

• ¾ of these arise in the lymph nodes
• Extranodal involvement is more common than in Hodgkins and these cancers have a less regular pattern of spread, some patients may have leukaemic manifestations
• Extranodal lymphomas are still arising from lymphoid tissue just not the lymph nodes this e.g. lymphoid tissue in the testes or gastrointestinal tract
• 90% are B cell and B cell cancers are usually lower grade, T cells cancers are high grade

235
Q

Reed sternberg cells?

A

hodgkins lymphoma
(cells are abnormal and have more than one nucleus)

236
Q

Owl eye appearance of cells?

A

hodgkins lymphoma

237
Q

Describe categorisation of hodgkins lymphoma?

A

There are two main types of Hodgkin lymphoma – classical Hodgkin lymphoma and lymphocyte- predominant

  1. Classical Hodgkin Lymphoma Subtypes:
    - Nodular sclerosing (most common 70%) – lacunar cells are often numerous
    - Mixed cellularity (20%) – plasma cells and eosinophils present in addition to RS cells and lymphocytes
    - Lymphocyte depleted (<2%)
    - Lymphocyte rich (<2 %)
  2. Lymphocyte Predominant:
    - Nodular lymphocyte predominant (5%) – popcorn cells, tends to affect young males and has a good prognosis
238
Q

What age groups tend to be affected by Hodgkins lymphoma?

A

• There are two peaks of incidence: around adolescence and late middle age

239
Q

Presentation of hodgkins lymphoma?

A

• Most patients present with painless enlargement of one or more lymph node groups e.g. cervical, axillary or mediastinal
• One quarter will complain of B symptoms

240
Q

Management and prognosis of hodgkins lymphoma?

A

• Generally treated with chemotherapy and radiotherapy
• It has a good cure rate in younger individuals
• There can however be long term toxicity from the treatment including secondary cancers, CVS disease and infertility (mainly with intensive treatments)

241
Q

What age groups does NHL tend to affect?

A

elderly

242
Q

What is the commonest subtype of NHL?

A

Diffuse large B cell

243
Q

What is the fastest growing human tumour?

A

Burkitt lymphoma

244
Q

How does burkitt lymphoma classically present?

A

• Presents with massive lymphadenopathy of the jaw (often in children)
• Get a characteristic facial swelling due to extensive tumour involvement of the mandible and surrounding soft tissues

245
Q

What does burkitt lymphoma have a relationship with?

A

EBV

246
Q

Where is burkitt lymphoma seen a lot?

A

Equatorial Africa, New Guinea and other malaria endemic areas

247
Q

Starry sky appearance on histology?

A

burkitt lymphoma

248
Q

What is Mycosis Fungoides?

A

• This is a primary T cell lymphoma of the skin that usually occurs in middle age
• It presents as a scaly red macule progressing to skin plaques and then nodules

249
Q

Management and prognosis of NHL?

A

• Treatment is generally with chemotherapy or radiotherapy
• High grade NHL is potentially curable
• Low grade NHL is incurable but many patients may not need any treatment and a “wait and see” approach can be undertaken

250
Q

In lymphoma how would lymphadenopathy appear?

A

painless, rubbery and soft, smooth surface, not tethered and no skin inflammation

251
Q

Causes of hypercalcaemia of malignancy?

A

• Tumour secretion of PTHrp
• Local osteolytic hypercalcaemia by bony metastases
• Calcitriol mediated in Lymphoma
• Rarely ectopic PTH production

252
Q

Treatment of hypercalcaemia of malignancy?

A

• Fluids- rehydrate with 0.9% saline 4-6L in 24hours
• Consider loop diuretics once rehydrated- avoid thiazides
• Bisphosphonates- single dose will lower Ca over 2-3d, maximum effect at 1 week
• Hopefully the issue resolves with anti-cancer treatment

253
Q

What cancer treatment is a erythematous vesicular rash a side effect of?

A

immunotherapy

254
Q

Why is chemotherapy given in cycles?

A

To try and maximise tumour cell death whilst
minimising normal cell death, chemotherapy is typically given in
cycles. Normal cells have greater propensity for recovery than
malignant cells, therefore rest between cycles allows normal cell
recovery.

255
Q

Chemotherapy induced nausea and vomiting is most commonly treated with what?

A

ondansetron prior to administering the therapy in combination with dexamethasone

256
Q

Why is radiation given in fractionation?

A

to distribute damage to the cancer cells, increasing chance of radiation catching cancer cells in M phase to cause adequate DNA damage
fractionation also gives normal cells a chance to recover as normal cells heal defects better than cancer cells

257
Q

Explain the 4rs of radiotherapy?

A

Repair - normal cells repair better than cancer cells, fractionation gives normal cells time to repair

repopulation - tumour cells repopulate if incompletely damage, each fraction must cause more damage than a tumour cells ability to repopulate

reassortment - each fraction allows re-assortment of tumour cells to be in m phase and allow considerable DNA damage

reoxygenation - tumour cells further from blood supply are more hypoxic, oxygen is key in produce toxic super radicals, fractionation allows hypoxic cells to reoxygenate so more susceptible in next fraction

258
Q

What stage of the cell cycle is radiotherapy most effective at?

A

M (mitosis phase)

259
Q

List some common causes of oncological spinal cord compression?

A

• Most common – tumour invasion from vertebral body into epidural space
• Tumour invasion through intervertebral canal (mainly occurs in lymphomas)
• Direct metastases into the spin canal (rare)
• Tumour induced vascular damage
• Paraneoplastic syndromes

260
Q

List some common cancers that can cause spinal cord compression?

A

• Lung
• Breast
• Prostate
• Melanoma
• Lymphoma
• Multiple myeloma

261
Q

Presentation of spinal cord compression?

A

• Most commonly pain – worse on coughing, straining and sneezing, worse on lying down and relieved by sitting
• Bowel changes
• Urinary changes
• Sensory changes – one or more of proprioception, light touch and pin prick affected

Note: often spinal cord compression is protracted over a long period of time, with symptoms getting worse gradually but neurological deficits can occur in a few hours in some cases

262
Q

Management of spinal cord compression?

A

• Urgent MRI
• Immediate dexamethasone to reduce oedema
• Surgery may be done if only single vertebra involved and no metastases
• Radio or chemo are other options
• May only be suitable for best supportive care if disease advanced

263
Q

Causes of oncological superior vena cava obstruction?

A

• This is most common in lung cancer (esp small cell) or Hodgkins
• Can either be due to intrinsic causes e.g. tumour induced thrombosis, or extrinsic causes e.g. the tumour compressing the SVC from the outside

264
Q

Presentation of superior vena cava obstruction?

A

• Usually rapid onset within 6 weeks
• Swelling of face, neck, 1 or both arms
• Distended veins
• Shortness of breath
• Headache
• CNS symptoms
• Lethargy
• Puffy neck
• Veins that don’t collapse
• Distended neck and chest veins

265
Q

Management of superior vena cava obstruction?

A

• Depends on cause
• Blood clots – thrombolysis and anticoagulants
• Extrinsic causes e.g. outside compression – steroids are often given but there is no evidence, chemotherapy, radiotherapy or stent for symptoms may be done

266
Q

Explain what causes neutropenic sepsis?

A

In cancer patients receiving chemotherapy
Due to combination of:
- Suppression of bone marrow
- Patient’s gut mucosa is unable to divide fast enough to maintain the protective structure, bacteria that usually can’t cross the mucosa do and get into the bloodstream

267
Q

What is often the only sign of neutropenic sepsis?

A

fever
patients on chemo don’t mount immune responses in the way you would expect

268
Q

Definition of neutropenic sepsis?

A

Patient on chemotherapy with:
- Neutrophil count < 0.5 x 109 /L PLUS either temp > 38 degrees or signs/ symptoms of sepsis

269
Q

Definition of sepsis?

A

NEWS more than 5 and signs of infection

270
Q

Management of neutropenic sepsis?

A

Initiate Sepsis 6 protocol:
Take – blood cultures, lactate, urine output
Give – IV fluids, broad spectrum antibiotics (AFTER taking blood cultures) and oxygen
BUFALO

Antibiotics recommended are pipercillin and tazobactam
Get senior help, confirm results and tailor antibiotics accordingly

271
Q

Presentation of tumour lysis syndrome?

A

Oliguria/ AKI, cardiac arrhythmia, seizure, typical lab findings high K, high phosphate, high urate, low calcium

272
Q

Management of tumour lysis syndrome?

A

• Calcium gluconate, urgent treatment of cardiac arrhythmia and hyperkalaemia, fluid resus, close monitoring input and output, electrolyte abnormalities resistant to medical management – consider dialysis
• Generally, only seen in haem or oncology specialities and generally prevention is thought to be best
• Patients starting chemo are risk assessed
• Prophylaxis involves allopurinol and hydration

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