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Medicine 1 > Anatomy - Lung cancer > Flashcards

Anatomy - Lung cancer Flashcards

1
Q

What does neoplasia mean?

What is a neoplasm?

A

Tumours

Abnormal tissue mass with exceeded and uncoordinated growth than normal and persist after cessation of stimulus

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2
Q

What is differentiation?

A

Describes how close in appearance cells of a tumour are to cell type they were derived from, predicting tumour behaviour

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3
Q

What is a well-differentiated tumour?

A

Composed of cells which closely resemble cell of origin

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4
Q

What is a poorly differentiated tumour?

A

Composed of cells which bear little resemblance to cells of origin, but enough to identify original cell

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5
Q

What is an undifferentiated tumour?

A

Composed of cells which are so undifferentiated that cell of origin is unknown

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6
Q

What are the two ways to classify a tumour?

A

Via histogenesis

Furthee classified into benign or malignant

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7
Q

What are the properties of benign tumours?

A
  • Grow by expansion
  • Compress adjacent tissue
  • Do not infiltrate
  • Stay at site of origin and don’t spread
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8
Q

What are the properties of malignant tumours?

A
  • Grow by expansion and infiltration
  • Compress and invade adjacent tissue
  • Infiltrate
  • Can spread to distant sites - metastasis
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9
Q

What are the 2 names and types of benign epithelial tumours?

A

Adenoma –> tumour of glandular epithelium

Papilloma –> tumour of squamous and transitional epithelium

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10
Q

What are the 3 types of malignant epithelial tumours?

A

(Carcinoma)

Squamous cell carcinoma

Transitional cell carcinoma

Adenocarcinoma (glandular cell origin)

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11
Q

What is the suffix for benign mesenchymal tumours and the 5 different types?

A
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12
Q

What is the suffix for malignant mesenchymal tumours and the 5 different types?

A

-OSARCOMA

Bone = osteosarcoma

Adipose tissue = liposarcoma

Cartilage = chondrosarcoma

Smooth muscle = leiomyosarcoma

Striated muscle = rhabdomyosarcoma

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13
Q

What are germ cell tumours?

A

Tumours derived from germ cells in ovary and testes

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14
Q

What are teratomas?

A

Tumours derived from germ cells, containing representatives from all 3 germ layers

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15
Q

What are embryonal tumours?

A

Tumours derived from embryonic blast tissue

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16
Q

What are gliomas?

A

Tumours derived from glial cells of the CNS

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17
Q

What are melanomas?

A

Tumours of melanocytes, usually in skin

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18
Q

What is lymphoma?

A

Tumour of lymphoid tissue

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19
Q

What is leukaemia?

A

Tumour of haemopoietic cells in bone marrow

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20
Q

What is neuroendocrine tumour?

A

Tumours derived from neuroendocrine cells, scattered in many sites

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21
Q

What are the properties of benign tumours in solid organs?

A
  • Compress adjacent tissue
  • Grow evenly
  • Spherical
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22
Q

What are the properties of benign tumours on epithelial surfaces?

A
  • Form papillary outgrowths
  • Papillomas as they have papillary shape
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23
Q

What are the properties of malignant tumours?

A
  • Expand but infiltrate and invade adjacent tissue
  • Irregular outline
  • No distinct edges
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24
Q

What is the cytology of malignant tumours?

A
  • Differentiation varies
  • Pleomorphism – cellular/nuclear
  • High nucleus to cytoplasm ratio
  • Nuclear hyperchromatism
  • High mitotic count
  • Abnormal mitoses
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25
Q

What is cellular pleomorphism?

A

Variation in size and shape of cells in tumour

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26
Q

What is nuclear pleomorphism?

A

Variation in size and shape of nuclei in tumour cells

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27
Q

What is nuclear hyperchromatism?

A
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28
Q

What is high mitotic count?

A

+ cells in mitosis, including abnormal mitosis forms

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29
Q

What does poor differentiation look like?

A
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30
Q

What does pleomorphism and abnormal mitosis look like?

A
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31
Q

What does high mitotic count, nuclear hyperchromatism and high nucleus to cytoplasmic ratio look like?

A
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32
Q

What is dysplasia and causes?

A

Abnormal cell structure

  • Loss of differentiation
  • Pleomorphism
  • Nuclear hyperchromatism
  • High nucleus/cytoplasm ratio
  • High mitotic activity
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33
Q

What is carcinoma-in-situ?

A

Epithelium with cytological characteristics of malignancy but no evidence of invasion

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34
Q

What are the 3 ways malignant tumours spread?

A
  • Lymphatics
  • Blood vessel
  • Serosal surfaces
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35
Q

What happens during malignant lymphatic spread?

A
  • Invades lumen on lymphatic vessel
  • Bits break off and pass into lymph nodes
  • Bits in lymph nodes get trapped in subcapsular sinus
  • Tumour cells proliferate until whole node is tumour
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36
Q

What happens during malignant blood vessel spread?

A
  • Tumour invades wall of a small vessel
  • Breaks off and passes into circulation
  • Tunour grows where vessel becomes too small for it to pass
  • Distant metastasis produced
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37
Q

What are the 4 common sites of blood-borne metastasis?

A
  • Breast
  • Bronchus/lung
  • Kidney
  • Thyroid
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38
Q

Where do liver mets often arise from?

A
  • GI tract
  • Pancreas
  • Breast
  • Lung/bronchus
  • Kidney
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39
Q

What are the effects of benign tumours?

A
  • Bleeding e.g. gut, bladder
  • Pressure on adjacent vital structures e.g. in brain
  • Obstruction e.g. in brain, bronchus
  • Hormone secretion e.g. pituitary adenoma
  • Conversion to a malignant tumour
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40
Q

What is tumour grade?

A

Biology of the tumour

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41
Q

What is tumour stage?

A

The size of a primary tumour, the degree to which it has locally invaded, the extent to which it has spread by distant metastasis

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42
Q

What are the 5 steps for tumour diagnosis?

A
  • Symptoms: clinical history
  • Signs: physical examination
  • Imaging
  • Tumour markers - i.e. blood in urine
  • Biopsy: tissue sampling - use imaging as an aid
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43
Q

What are the 3 tumour markers?

A
  • HCG – human chorionic gonadotrophin from tumours with trophoblast elements
  • AFP - alpha fetoprotein. Liver cancer, germ cell tumours.
  • PSA – prostate-specific antigen from carcinoma of the prostate
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44
Q

What are the 3 steps of a biopsy?

A
  • Fix in formalin solution for routine histology, special stains and immunohistochemistry.
  • Fix in glutaraldehyde for electron microscopy.
  • Send fresh for cytogenetics, tumour genetics.
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45
Q

What do the dark purple areas represent?

A

Suspected tumour area

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46
Q

What are the properties of diagnostic cytology?

A
  • Examination of cells in tissue fluids or exfoliated from surfaces
  • May give a diagnosis of malignancy
  • Useful for screening – main example is cervical cytology programme
47
Q

What are the 2 assessments made of a discovered tumour?

A

Analysis of degree of differentiation and tumour growth pattern

Evaluation of how far it has spread

48
Q

What are the difference between low-grade and high-grade tumours?

A

Low = slow growing and have good prognosis

High = fast growing and poor prognosis

49
Q

What are the properties of tumour grade?

A
  • The degree of differentiation of tumour cells relative to normal tissue of origin
  • Variation in size and shape of constituent cells of the tumour (pleomorphism)
  • The proportion of cells containing mitotic figures (mitotic index)
50
Q

What are the 3 cancer assessments for a tumour?

A
  • Tubule formation
  • Nuclear pleomorphism
  • Mitotic counts
51
Q

What are the grades of breast cancer?

A
52
Q

What is the TNM breast cancer staging?

A
53
Q

What is Dukes colorectal carcinoma staging?

A
54
Q

What is the table for Dukes cancer staging?

A
55
Q

What are the tumour therapy options?

A
  • Three main modes of therapy for neoplastic disease
    • Surgery
    • Radiotherapy
    • Chemotherapy
  • Multimodal therapy is common
  • Pathology is pivotal in deciding on appropriate therapy
56
Q

What are the 4 main prognoses?

A
  • Remission
  • Disease –free survival
  • Five-year survival
  • Ten-year survival
57
Q

What type of tumours have excellent prognosis?

A

Thyroid

58
Q

What type of tumours have moderate prognosis?

A

Kidney

Breast

Prostate

Cervix

59
Q

What type of tumours have poor prognosis?

A

Pancreas

Brajn

Oesophagus

60
Q

What are the different types of neck imaging?

A
  • Bones: Plain film and CT
  • Spinal cord and nerves: MRI
  • Soft tissue (glands, lymph nodes, muscles): Ultrasound, CT and MRI
  • Vessels: Ultrasound, CT and MRI
61
Q

What are the different types of thorax imaging?

A
  • Lungs: Plain film and CT
  • Heart: MRI
  • Bones: Plain film and CT
  • Spinal cord and nerves: MRI
  • Vessels: CT
62
Q

What are the different types of benign growths?

A
  • Hyperplasia- over proliferation of cells that appear otherwise normal.
  • Metaplasia – normal appearance but in wrong place, usually from an adjacent tissue layer
  • Dysplasia – cells that appear abnormal; often increased nuclear to cytoplasmic ratio and loss of features of differentiation.
  • Adenomas/polyps/warts – larger growths of dysplastic cells.
63
Q

What is a malignant tumour?

A

Invading other tissue, usually by breaking through basement membrane of epithelium.

64
Q

What are the main 5 properties of cancer?

A
  • Proliferation: grow independently of signals
  • Immortality: avoid senescence/telomere shortening
  • Avoiding cell death: apoptosis, they don’t do it
  • Angiogenesis: they must be fed
  • Metastasis: many activities needed
65
Q

What are the properties of carcinogens and mutations?

A
  • Carcinogens lead to a high rate of mutation
  • Most mutations not in genes or don’t affect gene function
  • Most that affect gene function do not affect features of cell that would lead to cancer
  • Need to identify those mutations that DO affect function of genes that regulate proliferation, apoptosis, immortality etc – these are ‘driver’ mutations
  • All other mutations that are no relevant to the promotion of cancer are ‘passenger’ mutations
66
Q

What are the 2 gene classes targeted for mutations?

A
67
Q

What are the 2 tumour growth restrictions?

A

Senescence - cells in G0 don’t proliferate

Apoptosis - programmed cell death

68
Q

What are the key points about senescence?

A
  • Metabolically active, irreversibly lost ability to re-enter cell cycle
  • Normal cells have finite proliferative capacity (Hayflick limit), stop dividing and go into replicative senescence
  • Cancers must avoid senescence if they are to keep growing
69
Q

When do cells reach crisis and what are its consequences?

A
  • If tumour suppressors, such as P53, are inactivated
  • Occurs due to shortened telomeres
  • Telomere loss = chromosome instability
70
Q

What happens during crisis?

A
  • Damage to the chromosomes will eventually make the cell unviable.
  • Cells undergo apoptosis if they can.
  • ‘genetic catastrophe’ is so severe it triggers apoptosis even in the absence of p53.
71
Q

What do tumours induce and what does this lead to?

A

Angiogenesis

O2 and nutrient supplied by blood vessels

72
Q

What is the function of VEGF?

A
  • Produced by many cancers
  • Induces new vessel growth and production of endothelial precursor cells in bone marrow
73
Q

What is the process leading to metastasis? (picture)

A
74
Q

What mutations lead to a gain-of-function?

A
  • Overexpression: amplification/ regulatory regions change
  • Point mutations/fusions
75
Q

What mutations lead to loss of function?

A
  • Point mutation
  • Deletion-frameshift
  • Loss of allele
76
Q

How do you identify key cancer genes?

A
  • Cellular and biochemical studies of normal cells and tumours
  • Find genes with damage in cancers
  • Now best approach is whole genome analyses
77
Q

What are the 3 family syndromes?

A
  • Retinoblastoma
  • Colon cancer
  • Breast cancer
78
Q

What are the properties of retinoblastoma?

A
  • Unilateral = sporadic cases
  • Bilateral = familial cases
  • Rb = retinoblastoma gene
79
Q

What is the Knudson 2-hit hypothesis?

A

Sporadic = requrie 2 random somatic events

  • Phenotype of the mutant Rb allele is dominant at the level of the whole organism
  • However - the phenotype of the mutant allele is recessive at the cellular level
  • Characteristic of tumor suppressor genes
80
Q

What is the function of the P53 gene?

A

Can trigger cell to enter apoptosis

81
Q

What is the function of TS proteins?

A

Detect errors, mediate repair, inhibit replication or mediate entry to apoptosis

82
Q

What happens when an error is spotted and repaired?

A

Proliferation

83
Q

What happens when an error is spotted and not repaired?

A

Apoptosis

84
Q

What are the properties of oncogenes?

A
  • Undergo dominant activating mutations in tumours
  • Rarely in inherited forms
  • Amplification
  • Deletion and point mutation = cell undergoes proliferation
85
Q

What are the 3 main causes of cancer?

A
  • Carcinogens - react with free radicals, mechanism of mutation (adducts, cross links, breaks), increase rate of mutation, leads to errors
  • Infectious agents - inflammation, inflammation and genes HBV), oncogenes E6 and E7 (HPV), oncogene (EBV), immune suppression (HIV)
  • Inherited predisposition - inherited mutation in a gene, causing defects leading to genome damage (BRCA1)
86
Q

What are the 4 cancer screening programmes?

A
  • Breast –47-73yrs
  • Colon – 60-74yrs –> fecal blood test, colonoscopy (+ effective)
  • Prostate – 50 plus
  • Cervical 25-65yrs
87
Q

What are the properties of radiotherapy?

A
  • X-rays or radioisotopes
  • Equivalent to placing cancer cells less than 2km from the epicentre of the nuclear bombs dropped on Hiroshima or Nagasaki
  • To damage cells to such an extent that they cannot survive. If this radiation was experienced body-wide this would kill us, but therapy targets the tumour
  • Often ‘fractionated’ or ‘brachytherapy’ used
88
Q

What is mitotic catastrophe?

A
  • Dividing cells, most initially survive, but continue to progress through the cell cycle despite the breaks in their DNA.
  • Genome becomes progressively more damaged until it is insufficiently intact to continue, and they die from ‘mitotic catastrophe
89
Q

What are targeted cancer therapies examples?

A
  • Antibodies to specific antigens eg. Herceptin, EGFR, breast cancer
  • Small molecule inhibitors eg …, Abl, leukaemias; …, BRAF, melanoma.
  • Angiogenesis inhibitors eg. Avastin, VEGF, colon cancer
  • Immune system booster, vaccines etc.
90
Q

What are the cancer prevention methods?

A
  • Lifestyle – smoking, UV, processed meat
  • Immunization – HPV, Hepatitis
  • Prenatal genetic Diagnosis
91
Q

What are the clinical features of oesophageal carcinoma?

A
  • Dysphagia
  • Mild food regurgitation
  • Weight loss
92
Q

What are the most common type of oesophageal carcinomas?

A

Squamous carcinoma - as oesophagus has squamous epithelium

93
Q

Where does adenocarcinoma (oesophageal carcinoma) arise?

A

In metaplastic epithelium

94
Q

How does oesophageal carcinoma spread?

A
  • Local extension
  • Nodal spread
  • Vascular spread
95
Q

What are the symptoms of stomach carcinoma?

A
  • Indigestion
  • Weight loss
  • Loss of appetite
  • Repeated vomiting
96
Q

What type of carcinoma is stomach carcinoma?

A

Adenocarcinoma

97
Q

What are the histological features of poorly differentiated adenocarcinoma?

A

Singet ring cell pattern

98
Q

What is a common complication of stomach cancer?

A

Metastasis to the liver

99
Q

What type of carcinoma is colon cancer?

A

Adenocarcinoma

100
Q

Where do colon carcinomas commonly present and why?

A

Right side (caecum)

Due to bleeding with anaemia

101
Q

Where does colon carcinoma spread to?

A

Lymph nodes and liver (by blood)

102
Q

What type of carcinoma is rectal cance4r?

A

Adenocarcinoma

103
Q

What are the clinical features of rectal cancer?

A
  • Bleeding
  • Obstruction
104
Q

What is the prognosis for rectal cancer?

A

Curative if resected at its early stages

105
Q

What type of carcinoma is lung cancer related to smoking and where does it arise?

A

Squamous cell carcinoma

Arises in metaplastic epithelium

106
Q

What are the clinical features of lung cancer?

A
  • Cough
  • Haemoptysis
  • Ulceration
107
Q

How do you diagnose lung cancer?

A

Sputum cytology

Biopsy

108
Q

What type of carcinoma is lung cancer not related to smoking?

A

Adenocarcinoma

109
Q

What are the clinical features of lung cancer not related to smoking?

A

Pleural effusion

110
Q

How do you diagnose lung cancer not related to smoking?

A

Image-guided biopsy

111
Q

What treatment is appropriate for localised, non-smoking related lung cancer?

A

Surgery

112
Q

What is the worse type of smoking related carcinoma and its derivative?

A

Small cell carcinoma

Derived from pulmonary neuroendocrine cells

113
Q

How do you diagnose small cell carcinoma of lung?

A

Cytology and biopsy

114
Q

What is the prognosis for small cell carcinoma of the lung?

A

Terrible - would have spread at time of diagnosis

Medicine 1 (28 decks)

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