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growth, development, ageing, nutrition > neoplasia > Flashcards

neoplasia Flashcards

1
Q

What is a neoplasm?

A

Abnormal mass of tissue

Growth is excessive, uncoordinated w normal tissue, persists after stimulus is removed and is clonal

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2
Q

What does clonal mean?

A

Originates from a single cell

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3
Q

What does cytology mean?

A

Features of individual cells

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4
Q

What does differentiation and anaplasia mean?

A

How much do neoplasms resemble normal cells/tissue

Anaplastic (looks nothing like it)

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5
Q

What does invasion mean?

A

Unconfined growth into underlying tissues

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6
Q

What does metastasis mean?

A

Spread distant from primary lesion

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7
Q

How are neoplasms classified?

A

Clinical behaviour- benign/malignant

By histogenesis- tissue of origin
~epithelial- lining/glandular
~mesenchymal- various types

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8
Q

What is the difference between benign and malignant?

A 
BENIGN
~expansion, encapsulated, localised
~slow
~resembles histogenesis
~uniform cell/nuclear shape and size
~few mitoses
~local pressure
~excision cures 
MALIGNANT
~invasion, no capsule, metastasis
~more rapid but variable
~variable resemblance to histogenesis
~cellular/nuclear pleomorphism
~many mitoses
~infiltration and spread
~local pressure
~excision may not cure
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9
Q

What is the pathology of benign neoplasms?

A

Expansile growth pattern of neoplastic cells, supporting c. tissue (stroma) and usually encapsulated

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10
Q

What is neurofibromatosis?

A

Genetic
Massive no of small benign tumours
All over skin
Internally also

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11
Q

What are the problems w benign neoplasms?

A

Pressure on structures
Lumen may become obstructed
May have a function- excessive hormone secretion

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12
Q

What is the pathology of malignant neoplasms?

A

Irregular growth pattern of cytologically abnormal neoplastic cells of varying differentiation that invade underlying tissues
Have c. tissue (stroma) and immune response

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13
Q

What is the cytology of malignant neoplasms?

A
  • Large no of irregularly shaped dividing cells
  • Large variably shaped nucleus
  • Small cytoplasmic vol compared to nuclei
  • Variation in cell size/shape
  • Loss of normal specialised features
  • Disorganised arrangement
  • Poor defined tumour boundary
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14
Q

How do you name neoplasms?

A 
90% EPITHELIAL
Benign
~lining=papilloma
~glandular=adenoma
Malignant
~lining=carcinoma
~glandular=(adeno)carcinoma

MESENCHYMAL
Benign
~eg. Fibroma, osteoma, lipoma, myoma, chondroma
Malignant
~sarcoma eg. Osteosarcoma, leio/rhabdomyosarcoma (smooth/skeletal muscle)

ODDITIES
Melanoma- malignant melonocytes
Lymphoma- many ranging from benign—>malignant
Leukaemia- malignant bone marrow
Teratoma- germ cell tumours, most in testes, most malignant (ovaries tend to be benign)- can mimic ANY tissue

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15
Q

What is a polyp?

A

Colonic adenoma

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16
Q

Why do neoplasms arise?

A

Benign- little known, many inherited factors

Malignant- inherited/environmental factors

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17
Q

What is carcinogenesis?

A

Multi step process from a normal cell to a cancerous cell

Initiation- carcinogen causes genetic change
Promotion- cell is primed to multiply
Transformation- genetic change into malignant cell
Progression- genetic change into malignant tumour

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18
Q

What are inherited factors of cancer?

A

Genetic susceptibility

  • inherited cancer syndromes- single mutant genes, often TSGs (eg retinoblastoma, some colon cancers)
  • familial cancer- family clusters, genes and pattern of inheritance not clear (eg breast, ovary, colon)
  • defective DNA repair- increased sensitivity to carcinogens/general risk

Up to 10% breast/ovarian cancer is hereditary (mutations BRCA1 and BRCA2)

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19
Q

What are environmental factors of cancer?

A

Chemical agents
Physical agents
Viruses

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20
Q

Why are chemical carcinogens?

A

Two stage process
-intitiation- permanent DNA damage
-promotion- may be reversible (promotes proliferation)
~latent period- time from initiation to clinical lesion

Important concepts

  • pro-carcinogen- often metabolised to ultimate carcinogen
  • co-carcinogen
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21
Q

What is a direct chemical carcinogen?

A

Neoplasm arises at site of carcinogen application

Eg. Smoking and lung cancer

22
Q

What is an indirect chemical carcinogen?

A

Neoplasm arises at different site form carcinogen application
Eg. Aromatic amines from industrial exposure
~inhaled in lungs
~bladder carcinoma (bladder enzymes release aminophenol)

23
Q

What are some chemic carcinogens?

A

Smoking- polycyclic, hydrocarbons

Diet- burnt hydrocarbons

Asbestos- fibrous silicates- inhaled (fibrosis, mesothelioma)

Synergy in smokers w asbestos

24
Q

What are physical carcinogens?

A

Ionising radiation- damages DNA causing mutations (X-rays, radioactive metals and gases*, atomic bombs)

Radium- bone/marrow tumours
Radon- lung cancer

UV light- damages DNA (squamous cell carcinoma, nasal cell carcinoma and melanoma)
xeroderma pigmentosum

25
Q

What is radiation sensitivity?

A

Most sensitive- labile (rapidly renewed)

Most to least-
~embryonic tissue
~haematopoietic organs (spleen, bone marrow)
~gonads
~epidermis
~intestinal mucous membranes 
~c. tissue
~muscle/nerve tissue
26
Q

What are viral carcinogens?

A

DNA viruses-
~more common
~viral DNA inserted into host DNA

RNA viruses
~reverse transcribed then inserted into host
~may contain oncogenes
~importance not certain
~act w other factors

Epstein-Barr virus- Burkitts lymphoma (change in c-myc protein)

Human papilloma virus- cervical/oropharyngeal carcinoma (sexually transmitted, viral protein binds to and inactivates tumour suppressors p53 and pRb)

Hep B/C- hepatocellular carcinoma

27
Q

What are other influences?

A

Often act as promoters
Hormones (breast cancer, prostate cancer)
Drugs, inc alcohol
Inflammation (long term, chronic- increased risk, esp. stomach [chronic gastritis], in oral cavity oral lichenplanus- higher risk)

28
Q

Why is the combination of alcohol and smoking more carcinogenic?

A

Alcohol itself- not carcinogenic, when ethanol is metabolised can grt some metabolites (acetaldehyde) which causes DNA damage

Together-

  • Ethanol acts as solvent
  • Increases permeability of oral mucosa to larger numbers of carcinogens in smoke
29
Q

What are some neoplasm names?

A

Glandular epithelium-
Adenoma, adenocarcinoma

Cartilage-
Chondroma, chrondrosarcoma

Smooth muscle
Leiomyoma, leiomyosarcoma

Surface epithelium
Papilloma, carcinoma

30
Q

What is the epidemiology of cancer?

A 
9.5M deaths (1 in 6)
2nd most common cause of death
30% population will have cancer
Caries by geography, age, race etc
90% carcinoma, 10% lymphoma/sarcoma
31
Q

How do cancers develop?

A

de novo-
salivary gland neoplasm

Benign neoplasm- adenocarcinoma of colon

Premalignant lesion- HNSCC

32
Q

What is premalignancy?

A

Changes in cells and tissue architecture before invasion

Disorganisation of tissue- dysplasia

Abnormalities- increased risk of cancer
Basis of cancer screening (cervical smears, oral cancer)

33
Q

What is oral leukoplakia?

A

White patch in mouth- increased risk of developing cancer

34
Q

How does cancer affect patients?

A 
Invasion (local spread)
~pressure/obstruction
~destruction and loss of function
Metastasis
Non-metastatic effects-
~25% will die from cancer related cachexia
35
Q

What are the modes of spread?

A

Invasion- path of least resistance, tissue destruction, perineural spread

Metastasis-
~lymphatic spread- invasion of vessels (embolism/permeation) and spread to draining lymph nodes
~haematogenous spread- invasion of veins spreading to organs (liver, lung, bone, brain)
~seeding in body cavities- spread across serous cavities eg. Abdominal cavities

36
Q

What are the mechanisms of spread?

A 
Neoplastic cells interact w cells and molecules in the local environment 
New abilities-
~motility enhanced
~alter adhesion molecules
~make poor basement membrane
~increase protease production/reduce inhibitors
~alter ECM
Happens throughout ‘metastatic cascade’
37
Q

What are the patterns of spread?

A

Carcinomas- lymphatic then blood later
Sarcomas- blood (rarely lymphatic)

Lung cancer to local nodes in hilum, to liver, bone, brain

Tongue cancer to neck nodes then lungs and spine

Prostate cancer to bones

Melanoma to lungs

Colorectal cancer to liver

38
Q

What are the effects of neoplastic spread?

A 
Pressure and obstruction 
Destruction
Haemorrhage
Infection
Pain (esp bone)
Anaemia (colonisation of marrow)
39
Q

What are non-metastatic effects?

A

Paraneoplastic syndrome
~often caused by biochem substances released by tumour cells eg. TNF-alpha

Fever, anorexia, weight loss/cachexia
Endocrine syndromes (Cushings, metabolic effects eg. Hypocalcaemia)
Neuro problems eg. Neuropathy
Haematological syndrome eg. Erythrocytosis

40
Q

How do you grade a cancer?

A

Histological assessment

~Well differentiated- looks like tissue it arose from- not as bad
~Poorly differentiated- looks nothing like tissue it arose from- much more aggressive

Linked to prognosis

Various methods-
~numerical grades 1,2,3
~low, intermediate, high
~well, moderate, poor

41
Q

How is cancer staged?

A

Defines clinical extent of tumour

Done by radiologist first
Then done by pathologist after surgery

TNM system (WHO)
Tumour (size), nodes (regional), metastasis (distant)

T 1-4
N 0-3
M 0 or 1 (present/absent)

COLORECTAL CARCINOMA 
Early stage cancer
Stage 1- small tumour w/o metastasis 
Stage 2- larger tumour w/o metastasis 
Later stage cancer
Stage 3- tumour w regional metastasis 
Stage 4- tumour w distant metastasis
42
Q

What are the rough 5 year survival rates for patients w melanoma?

A

Stage 1- 90%
Stage 2- 65%
Stage 3- 15%

43
Q

What do cancer bio markers show?

A 
Prognostic- likely?
Diagnostic- type?
Predictive- optimal drug?
Pharmacodynamics- optimal dose?
Recurrence- return?
44
Q

How is cancer diagnosed?

A

Biopsy
Cytology (Fine Needle Aspirates)
Imaging- CT/MR/PET scanning
Molecular analysis (assess genetic changes)

45
Q

How is cancer treated?

A 
Surgery
Radiotherapy 
Chemotherapy
Biological (immune) therapy
Supportive care
46
Q

What are side effects of radiotherapy?

A 
Tiredness
Feeling sick
Difficult eating/drinking
Skin reaction
Hair loss
Haematological changes 
Possible long term side effects

Affecting rapidly dividing cells?

47
Q

What is IMRT?

A

Intensity modulated radiotherapy allows you to reduce area of dose to make sure it directly targets tumour

48
Q

What are the types of drugs used in chemo therapy?

A 
Conventional agents (cytotoxic)
~targets DNA structure or segregation of DNA as chromosomes in mitosis (targets every cell undergoing cell division)

Targeted agents
~small molecules interact w molecular target maintaining malignancy/selectively expressed by tumour

Hormonal therapies
~target biochem pathways of oestrogen and androgen function

Biological therapies
~macromolecules w particular target/ability to regulate immune response to kill

49
Q

What are side effects of chemotherapy?

A

Generally cytotoxic

Mucositis 
Nausea/vomiting 
Diarrhoea
Cystisis
Sterility
Myalgia
Neuropathy 
Alopecia
Pulmonary fibrosis 
Cardio toxicity
Local reaction
Renal failure
Myelosuppression
Phlebitis
50
Q

What are oral problems in cancer management?

A

Dry mouth
Immunocompromised
Difficulty in maintaining oral hygiene

Therefore-
~oral mucosal disease
~dental disease
~discomfort 
~social embarrassment

growth, development, ageing, nutrition (40 decks)

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