Neoplasia Flashcards

1
Q

What is a neoplasm? What are the different classifications?

A

Abnormal tissue mass who’s growth exceeds and is uncoordinated from normal tissue and persist after the healing and repair process (i.e. after damaging stimulus is removed)

Benign

Malignant= cancer

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3
Q

What is the difference between a driver mutation and a passenger mutation? How are these mutations involved in cancer development?

A

Driver= mutation with survival benefit for cell which promotes cancerous change

Passenger= biological inconsequential mutation

Driver and passenger mutations accumulation to produce a genetically heterogenous cancers with different subclones

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5
Q

What are the cytological features of cancer and why do they occur?

A

Increased nuclear cytoplasmic ratio i.e. large nuclei with little cytoplasm

Nuclear pleomorphism i.e. variation in nuclear size and shape

Nuclear hyperchromasia i.e. dark staining nuclei due to increase density of chromatin

Prominent nucleoli i.e. due to clusters of chromatin

Increased mitotic activity

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7
Q

How would you differentiate microscopically between benign and malignant neoplasms?

A
Benign:
Normal nuclear size 
Small nucleoli 
Absent pleomorphism 
Infrequent mitosis 
Good differentiation 
Malignant:
Enlarged nuclear size 
Prominent nucleo 
Marked pleomorphism 
Frequent mitosis 
Variable differentiation
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8
Q

How would you differentiate between benign and malignant tumours macroscopically?

A
Benign;
Well circumscribed 
Generally small 
Haemorrhage usual 
Ulceration unusual 
Necrosis unusual 
Lack of invasion into surround tissue 
No metastasis 
Malignant: 
Irregular 
Generally larger
Haemorrhage 
Ulceration 
Necrosis 
Invasion to local tissues 
Metastasis
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10
Q

Which cancer is commonly associated with seeding to the peritoneum?

A

Ovarian cancer

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11
Q

What processes are required for tumour cells to undergo invasion and metastasis? What enzymes are involved?

A

Loosening of cell junctions

  • E-cadherin mutation
  • epithelial-mesenchymal transition (EMT)

Degradation of ECM

  • MMP (matrix metalloproteinases) to enable migration through stroma
  • Cathepsin D
  • Urokinase plasminogen activator

Migration of tumour cells
-actin cytoskeleton contracts to enable movement through stroma

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12
Q

What is involved in epithelial-mesenchymal transition?

A

Expression of cytoproteins lost= loss of epithelial architecture
Actin expressed= enables increased cell motility i.e. mesenchymal characteristic

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13
Q

What are the 3 types of cancer invasion? What are the implications of these types of invasion?

A

Stromal
-degradation of tissue

Perineural

  • cancer-associated pain due to nerve irritation
  • can cause problems with surgical resection due to neoplasm associated with the nerve not being able to be removed

Venous
-dissemination + spread to distant sites

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14
Q

What organs to cancers commonly metastasis to?

A

Liver

Lungs

Bones

Brain

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15
Q

What are the 3 main routes of metastatic spread? What are the consequences of cancer spreading via these routes?

A
Lymphatic spread (tumour spread to LN ) 
-LN invasion 

Haematogenous (occurs later)
-widespread dissemination

Seeding in body cavities (local) i.e. peritoneum
-tumour cells break from mass and implant onto surface
I.e. omental cake

lymphatic spread is earliest pathway before haematogenous spread

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16
Q

Why does cancer spread to veins preferentially to arteries?

A

Veins have thinner walls

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17
Q

What is the difference in growth characteristics between benign and malignant?

A

Benign:
Slow growing
Spontaneous arrest common

Malignancy
Rapid growth
Spontaneous arrest rare

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18
Q

How would you differentiate between a malignant melanoma and a benign naevus (mole)?

A
Malignant melanoma:
Large (20mm)
Variable pigmentation 
Irregular border 
Partly flat and partly raised 
Asymmetrical 
Benign naevus:
Small (3mm)
Uniform 
Well-defined border 
Polypoid 
Symmetrical
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19
Q

Which cancers are associated with bone mets? What are the different types of bone lesions and their implications?

A
Lung 
Breast 
Thyroid (follicular carcinoma) 
Prostate 
Kidney 
I.e. organs which are bi-lobular or have 2 components 

Lytic lesions= destruction
Sclerotic= bone formation

Pain + fractures (can present before primary tumour site identified)

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20
Q
Where do the following cancers metastasis to? 
GIT cancer
Lung
Gall bladder/bile duct/salivary gland 
Renal cell carcinoma (RCC)
Malignant melanoma
A

GIT cancer= liver via portal vein
Lung= adrenal gland and brain
Gall bladder/bile duct/salivary gland = perineural invasion
Renal cell carcinoma (RCC)= renal vein + lung
Malignant melanoma= satellite deposits on skin

21
Q

What is the different staging system used for colorectal cancer? How is it used?

A

Duke’s

T1= submucosa
T2= muscularis propria 
T3= subserosa 
T4= through peritoneal surface 
N0= none 
N1= 2+
N2= 5+
M0= none
M1= present
22
Q

Which cancers are associated with inherited cancer syndromes?

A

Retinoblastoma + osteosarcoma = RB
Epithelial tumours= Cowden syndrome (PTEN defect)
Colon cancer= FAP (APC defect) or HNCC (MMR defect)
Multiple sites= Li-Fraumeni syndrome (p53)

23
Q

Which environmental factors increase the risk of neoplasia? Which cancers are they associated with?

A
Smoking- lung 
Alcohol- UGI + liver 
Diet/obesity= CR
Infection= hepatitis B + C i.e. risk factors for liver cancer 
Reproduction= breast 
Asbestos= mesothelioma
24
Q

How is chronic inflammation linked to metaplasia?

A

Can cause epithelia metaplasia which is a risk factor for neoplastic transformation

25
Q

What types of chronic inflammation are associated with neoplasia development?

A

H pylori gastritis

IBD

Viral hepatitis

26
Q

What is the immune response to cancer? How can this be utilised in treatment?

A

Dendritic cells phagocytose tumour antigens and present to TC in lymph nodes

T-cells migrate to cancer site to attack tumour cell

PDL1 and CTLA4 inhibitors used in immunotherapies

27
Q

What is dysplasia? What is the other term used?

A

Disordered cell growth due to accumulation of non-lethal mutations

Intraepithelial neoplasia

28
Q

What differentiates malignant cells from cells undergoing dysplasia?

A

Dysplasia cells not yet invasive despite resembling malignant cells microscopically

29
Q

How is dyplasia graded? Can it be reversed?

A

Mild (CIN1)
Moderate (CIN2)
Severe/high grade (CIN3) = carcinoma-in-situ

Reversible but reversibility diminishes with grade progression

30
Q

When is dyplasia/CIN grading used?

A

Basis for screening process such as cervical smear tests

31
Q

What does differentiation refer to in terms of neoplasms? How does differentiation differ between benign and malignant neoplasms?

A

Degree which neoplasm histologically resembles its tissue of origin

Benign= well differentiated 
Malignant= variable differentiation
32
Q

What are the different cell types neoplasms can differentiate from and which types of neoplasm do they give rise to?

A

Epithelial= malignant
Mesenchymal= benign
Other i.e. haematolymphoid tumours and germ cell tumours

33
Q

What does neoplasm grading depend on? How does this relate to the character of the neoplasm?

A

Degree of differentiation
Number of mitoses
Pleomorphism of cells

Indicates the level of aggression i.e. 1 being the least and 3 the most
RELATED TO OUTCOMES

34
Q

How would you identify the origin of an undifferentiated/anaplastic tumour?

A

IHC to identify proteins which indicate cell origin

35
Q

What tissue is classified as epithelium? How would you differentiated between a benign and malignant epithelial tissue by name?

A

Squamous
Transitional
Glandular

Benign= ends in “papilloma” 
Exception= adenoma (benign glandular neoplasm) 

Malignant= ends in carcinoma

36
Q

What tissue is classified as mesenchyme? How would you differentiated between a benign and malignant mesenchymal tissue by name?

A
Fat (lipo)
Fibrous (Fibro)
SM (leio)
SKM (Rhabdomyo)
Cartilage (Chondro)
Bone (Osteo)
Benign= “oma” i.e. Leiomyoma= benign SM neoplasm 
Malignant= “sarcoma”
37
Q

What are the different histological subtypes of thyroid carcinomas? What are their different routes of spread and prognosis?

A

Papillary
Lymphatic
Very good prog

Follicular
Haematogenous (Bone mets)
Good prog

Anaplastic
Local
Poor prog

38
Q

What are teratomas and where do they usually occur? Which sites are malignant or benign?

A

Neoplasms derived from embryonic stem cells so can form cells from all 3 germ cell layers

Ovary = benign i.e. dermoid cyst
Testis = malignant
Midline structures i.e. mediastinum or retroperitoneum = variable behaviour

39
Q

What cells do embryonic tumours arise from? What is their general character? What examples are there?

A

Multi-potential embryonic blast cells i.e. “blastoma”

V malignant

Nephroblastoma (Wilm’s tumour)
Hepatoblastoma

40
Q

What is a hamartomas? How can you differentiate it from an embryonic tumour?

A

Tumour-like malformation BUT not actually a neoplasm

Not malignant and will stop growing when host stops growing

Eg Haemangioma (venous malformation)