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
2
Q
What is anaplasia and atypical cells?
A
- poorly differentiated cells
3
Q
What is Pleomorphism?
A
- variable appearance
4
Q
What is Anisocytosis?
A
- varied cell size
5
Q
What is Anisokaryosis?
A
- varied nuclear size
6
Q
What is Hyperchromasia?
A
- dark nuclei (condensation)
7
Q
What would increased nuclear to cytoplasmic ratio mean?
A
- increased nuclear content
8
Q
What is Karyomegaly?
A
- giant nucleus
9
Q
What are tumour giant cells?
A
- giant cells
10
Q
Multinucleate?
A
- more than 1 nuclei
11
Q
What is a prominent nucleoli?
A
- enlarged or conspicuous nucleolus
12
Q
What is bizarre mitoses?
A
- abnormal conformation
13
Q
What are all of these?
A
- cytological features of malignancy (learn together)
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
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
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
How does a tumour form?
* 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
What is p53?
* 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
What substances does the tumour produce to communicte with the stroma?
* growth factors
* inflammatory mediators
* proteases
* tumour antigens
28
What is the stromal response to a tumour?
1. Inflammatory cells
2. stromal fibroblasts
3. extracellular matrix (growth factors)
4. vascular endothelium
29
What does this show?
* normal angiogenesis
* stable
* organised
* limited permeability
30
What does this show?
* tumour angiogenesis
* unstable
* disorganised
* leaky
31
What are the pink cells?
* pericyte
