Neoplasia 2 Flashcards

1
Q

Describe the differences between benign and malignant tumours

A

Benign:

  • typically expand, compressing surrounding tissue
  • well-differentiated (similar structure to tissue of origin)
  • slow, progressive expansion
  • no anaplasia
  • little necrosis
  • no invasion
  • capsule
  • no metastasis

Malignant:

  • invade and spread (metastasise)
  • poorly differentiated
  • tissue of origin can be unclear
  • anaplasia
  • rapid growth
  • frequent mitotic figures
  • necrosis if poor blood supply
  • local invasion
  • infiltrative growth
  • capsule often absent
  • metastasis
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2
Q

What is anaplasia and atypical cells?

A
  • poorly differentiated cells
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3
Q

What is Pleomorphism?

A
  • variable appearance
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4
Q

What is Anisocytosis?

A
  • varied cell size
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5
Q

What is Anisokaryosis?

A
  • varied nuclear size
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6
Q

What is Hyperchromasia?

A
  • dark nuclei (condensation)
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7
Q

What would increased nuclear to cytoplasmic ratio mean?

A
  • increased nuclear content
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8
Q

What is Karyomegaly?

A
  • giant nucleus
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9
Q

What are tumour giant cells?

A
  • giant cells
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10
Q

Multinucleate?

A
  • more than 1 nuclei
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11
Q

What is a prominent nucleoli?

A
  • enlarged or conspicuous nucleolus
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12
Q

What is bizarre mitoses?

A
  • abnormal conformation
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13
Q

What are all of these?

A
  • cytological features of malignancy (learn together)
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14
Q

What does this show and what features can you see?

A
  • Liposarcoma
    • Anisokaryosis
    • anisocytosis
    • hyperchromasia
    • bizarre mitoses
    • tumour giant cells
    • poor differentiation - may be going anaplastic
    • multinucleate
    • haemorrhage- rbcs outside as endothelium
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15
Q

What is this?

A
  • bronchoalveolar carcinoma
    • anaplasia
    • increased nuclear to cytoplasmic ratio
    • hyperchromasia
    • bizarre mitsoses
    • arrow heads - cell death, necrosis, neutrophils (inflam)
    • multinucleation
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16
Q

What are the morphological features of malignancy?

A
  • loss of tissue organisation - effacement and disorganisation
  • invasion - destruction of adjacent tissue
  • no capsule or invasion of capsule - poorly demarcated
  • vascular invasion - blood and or lymphatic invasion
  • metastasis - spread from site of previous tumour
  • necrosis - ischaemia and inflam
  • haemorrhage - damage to vessels and angiogenesis
17
Q

What differences can you see between hyperplastic lymph node vs. lympoma (benign vs. malignant)

A
  • hyperplastic lymph- large lymph nodes
    • normal architecture but boundaries are still present
  • lymphoma - connective tissue not present so boundaries not present
    • haemorrhage due to necrosis and lack of blood supply
    • uncontrolled cell growth
18
Q

Is the showing a hyperplactic lymph node or lymphoma?

A
  • hyperplastic lymph node
19
Q

What is this?

A
  • lymphoma
20
Q

This is a squamous cell carcinoma- what features can you see?

A
  • no keratin (SS ep usually produces)
    • keratin pearls present
    • still producing keratin- just dont care where they put it
  • hyperchromasia
  • bizarre mitoses
21
Q

What is the hallmark of neoplasia?

A
  • uncontrolled proliferation
    • cell escapes all of its control mechanisms
    • escapes apoptosis
    • independent of external growth factors and regulations
22
Q

What are the genetic factors contributing to carcinogenesis?

A
  • DNA mutations
    • point mutations
    • deletion
    • insertion
    • recombination
    • amplification
    • gene conversion
  • Epigenetic changes
    • DNA methylation
    • imprinting
    • histone methylation
    • histone acetylation
  • Chromosomal alterations
    • duplication
    • deletion
    • translocation
    • inversion
23
Q

What are telomeres?

A
  • pieces of DNA at the end of chromosomes
  • pieces are cut off at each cell division
24
Q

How to tumour cells avoid ageing/ apoptosis?

A
  • add more telomeres to the end of chromosomes
  • reactiavte telomerase
  • are then immortal to aging
25
Q

How does a tumour form?

A
  • one cell undegoes damage (initiated cell)
  • transformation event - e.g. radiation
  • the initiated cell enters a proliferative event
  • the daughter cells will inherit the abnormalities
  • evolves to a preneoplastic benign tumour after promotion
  • then can progress to a malignant tumour
26
Q

What is p53?

A
  • in all cells
  • detect any damage
  • tells the cell to stop dividing
  • and undego apoptosis if DNA damage cannot be repaired
  • with no p53 - more prone to tumours
27
Q

What substances does the tumour produce to communicte with the stroma?

A
  • growth factors
  • inflammatory mediators
  • proteases
  • tumour antigens
28
Q

What is the stromal response to a tumour?

A
  1. Inflammatory cells
  2. stromal fibroblasts
  3. extracellular matrix (growth factors)
  4. vascular endothelium
29
Q

What does this show?

A
  • normal angiogenesis
    • stable
    • organised
    • limited permeability
30
Q

What does this show?

A
  • tumour angiogenesis
    • unstable
    • disorganised
    • leaky
31
Q

What are the pink cells?

A
  • pericyte