Neoplasia Flashcards

1
Q

Neoplasia

A
  • an excessive, irreversible and uncontrolled growth which persists even after withdrawal of the stimuli which caused it
  • tumour: swelling/lump
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2
Q

Normal tissue adapting

A
  • when normal cells are under stress, they undergo changes to help respond to this stress
  • hyperplasia: increase in cell number
  • hypertrophy: increase in cell size
    -atrophy: decrease in cell size and number
    -metaplasia: cell changes to another type of
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3
Q

Hyperplasia

A
  • can be physiological/pathological
  • production of new cells from stem cells
  • can only occur in tissues which are not permanent (not in heart)
  • pathological hyperplasia: another method of leading to malignancy in select tissue
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4
Q

Hypertrophy

A
  • can be physiological or pathological
  • gene activation -> protein synthesis-> production of cellular organelles
  • PI3K/AKT pathway import net in physiological hypertrophy
  • multiple G protein linked signalling pathways are importantly in pathologic hypertrophy
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5
Q

Atrophy

A
  • decrease in stress-> decrease in cell number and size
  • decrease cell number-> apoptosis
  • ubiquitin- protea some degradation of cytoskeleton by tagging intermediate filaments with ubiquitin and degradation by proteasomes
  • autophagy of cellular components by autophagosomes fused to lysosomes-> hydro lyric enzyme breakdown
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6
Q

Metaplasia

A
  • reprogrammed of stem cells
  • can occur across any of the cell categories but most frequently epithelium
  • can be a step on the malignancy pathway
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7
Q

Aplasia and hypoplasia

A
  • aplasia: failure of cell production in embryogenesis, on a spectrum between complete agenesis and hypoplasia eg. Pulmonary agenesis
  • hypoplasia: decrease in cell production during embryogenesis which leads to a smaller overall organ seize
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8
Q

Severe changes if stress lasts a long time

A
  • causes more severe changes
    • apoptosis: programmed cell death
    •necrosis: uncontrolled cell death
    •inflammation: a reaction to cell death, inflammatory cell “clean-up”
    •neoplasia: long term
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9
Q

Benign disease

A
  • localised, well encapsulated, slow growing, resemble the tissue of origin, regular nuclei, few mitosis, damage at the local level
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10
Q

Dysplasia

A
  • abnormal/atypical cells due to a failure of differentiation
  • in some areas of the body, it is called intraepithelial neoplasia
  • ## the degree of dysplasia helps the pathologist identify those tissues which are high risk of malignancy in the future
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11
Q

Malignancy

A
  • invasive, can metastasise, grows fast, may not resemble tissue of origin, shows features of dysplasia, damage at local or distant sites
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12
Q

Metastasis

A
  • where the invasive neoplasm spreads to other areas of the body through:
    -lymphatics , blood or transcoelomic
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13
Q

Cancer of unknown primary

A
  • sometime have metastasis but cannot easily identify the site the cancer originated in
  • this requires a pathologist to try and identify, where possible, the origin of the cancer to help direct treatment
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14
Q

Naming epithelial neoplasms

A
  • tissue
    • covering epithelia
  • example of benign (-oma)
    • papilloma
  • example of malignant (-carcinoma)
    • carcinoma
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15
Q

Signalling in neoplasia

A
  • in various neoplasms, alternation in cell signalling pathways can change the available treatment and prognosis of the patient
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16
Q

HER2 and breast cancer

A
  • HER2 works via a receptor tyrosine kinase pathway
  • if there is an overexpression of HER2 in breast cancer, this suggest a more aggressive cancer
  • there are also good treatment specifically targeting HER2 positive breast cancer
  • knowing the signalling pathway allows us to both identify prognosis and use targeted treatment for patient
17
Q

Immunohistochemistry

A
  • shows us where certain proteins are expressed within the cel and in roughly what quantities they are expressed
  • HERS2 can be measured on the membrane of cells, using this technique
18
Q

Cell cycle in neoplasia

A
  • look for specific changes in the cell cycle in neoplasms, as part of diagnosis and to help with creating management plans
  • presence/absences of mutations in the cycle can help determine prognosis and treatment
    -eg. Looking for micro satellite instability MSI in various cancers
19
Q

MSI

A
  • occurs when there is failure of the mechanisms to repair damaged DNA in the cell cycle
  • repair system is known as as the mismatch repair system MMR
  • if there is damage to MMR system, damaged DNA can be passed down to new cells, making them prone to the mutations causing cancer
  • higher chance of mutation caused by failure of MMR system is MSI
20
Q

Multidisciplinary team and neoplasm

A
  • neoplasms are often discussed at MDT to decided on best management for patient
  • management depends on the grade and stage of neoplasm
21
Q

What is grading

A
  • grading: how closely (or not) does the neoplasm correspond with normal cells for that tissue
  • the more dysplastic the cells are the higher the grade
  • grade can be correlated with likelihood to respond to treatment and with prognosis
22
Q

What is staging

A
  • staging: how far the neoplasm spread through the body
  • classical staging tool is TNM classification:
    • tumour: measures local invasion
    • node: measures spread to lymph nodes
    • metastasis: measures spread to distant tissue
  • however, several neoplasms have their own special classification
23
Q

Effects of neoplasms: local

A
  • generalised sunrooms (pain, lump)
  • compression of surround structures
  • ulceration
  • bleeding/anaemia
  • obstruction
24
Q

Different effect of neoplasms: metastatic

A
  • depends on the site of metastasis
25
Different effect of neoplasm: systemic
-weight loss, loss of appetite, cachexia - fever or feeling non-specifically unwell - infection
26
Different effect of neoplasm: para- neoplastic
- secretion if excess substances - raised calcium ( leads to confusion)
27
Different effects of neoplasms: mental health
- depression, anxiety, frustration- worsening quality of life