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respiratory > Neoplasms > Flashcards

Neoplasms Flashcards

1
Q

what is the difference between a neoplasm and a tumour?

A

neoplasm = growth due to uncontrolled cell proliferation

tumour = any kind of lump/mass from any cause (i.e, haematoma, abcess etc)

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2
Q

how does hyperplasia and neoplasia differ?

A

hyperplasia = controlled cell growth

neoplasia = uncontrolled cell growth

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3
Q

what is the commonest malignant neoplasm?

A

Carcinoma

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4
Q

what makes a neoplasm benign?

A

inability to metastasise- therefore can be surgically resected and almost always cured

  • well circumscribed
  • often encapsulated
  • rarely haemorrhage
  • rarely necrosis
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5
Q

why do malignant neoplasms show a degree of haemorrhage and necrosis?

A

1) they produce blood vessels by angiogenesis which are brille and can bleed easily causing haemorrhage
2) they grow so fast they outgrow their blood suppy - leading to necrosis

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6
Q

how do pathologists tell the difference between normal cells, malignant cells, and benign neoplasma?

A

microscopic assessment of

1) nuclear features
2) architecture of the cells
3) assessment of maturation of the epithelium

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7
Q

what is the key to microscopic assessment of a neoplasm and malignancy?

A

nuclei showing varying degrees of

  • pleomorphism
  • hyperchromasia
  • mitotic activity

architectural features

  • disruption of architecture
  • loss of maturation
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8
Q

How do we classify neoplasms?

A

Benign

Borderline (very rare)

Malignant (primary or secondary)

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9
Q

What neoplasms are benign?

A

Adenomas

Papillomas

Lipoma

Neuroma

Angioma

Chondroma

*there is no such thing as a benign lymphoid neoplasm b/c lymphocytes can’t be contained in one section of hte body

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10
Q

what are the clinical features of a benign neoplasm?

A
  • lump
  • bleeding
  • mass effect
  • pain
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11
Q

how can a benign neoplasm cause death?

A

blood loss or mass effect

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12
Q

what is a ‘borderline’ neoplasm?

A

neoplasma that show nuclear features suggstive of malignancy but not enough to show that the neoplasm will behave like a malignant neoplasm

most commonly ovarian neoplasms

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13
Q

what is Carcinoma?

A

malignant tumour of the epithelium

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14
Q

what is an in situ carcinoma?

A

a carcinoma which is confined above the basement membrane - therefore does not have access to lymphatics or a blood vessels

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15
Q

can in-situ carcinomas metastisize?

A

they are not capable of mets b/c they don’t have access to blood vessels or lymphatics

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16
Q

What are the classifications of lymphoma?

A

nodal

extra nodal

or hodgkins/non-hodgkins lymphoma

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17
Q

what is leukaemia?

A

Malignancy of bone marrow cells

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18
Q

what is a sarcoma?

A

tumour of connective tissue ex)

osteosarcoma = bone

chondrosarcoma= cartilage

angiosarcoma = vessel

neurofibrosarcoma = nerve

leiomyosarcoma = smooth muscle

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19
Q

how do malignant neoplasms present clinically?

A
  • effect of primary tumour: mass, obstruction, bleeding, loss of function
  • effect of metastasis: same as primary
  • effect of hormone secretion: ACTH from small cell ca. of lung, Cushing’s syndrome, estrogen from testicular tumour
  • paraneoplastic effects: peripheral neuropathy, dermatomyositis result from cytokine production
  • general effects of malignant disease: weight loss, fatigue, anorexia, lassitude
20
Q

/what are the microscopic features of malignancy?

A
  • hyperchromasia
  • mitoses
  • high N/C ratio
  • pleomorphism/loss of maturation
21
Q

where do squamous cell carcinomas form?

A

any area lined by sqaumous epithelium (skin, mouth, oesophagus, cervix)

22
Q

how can we tell if a tumour is squamous cell?

A
  • resemblence to squamous cells
  • +keratin production
  • *
23
Q

Where do adenocarcinomas occur?

A

GIT, Breast, Thyroid, Uterus

  • all glandular areas
24
Q

how do we recognize adenocarcinomas on slides?

A
  • resemblance to glandular or columnar epithelium
  • +/- mucin production
  • +/- glandular production
  • grading
    *
25
Q
A
26
Q

where do we find transitional cell carcinoma?

A

in the transitional epithelium (urothelium)

27
Q

where do small cell carcinomas appear?

A

usually in the lung, but anywhere

= THE MOST aggressive carcinoma biologically

28
Q

What is an anaplastic carcinoma?

A

an undifferentiated carcinoma

*we know it’s a carcinoma based on tumour markers

29
Q

What is the difference between a fine needle aspirate and a trucut core needle biopsy?

A

fine needle aspirate = contains cells only, no stroma tissue so architecture cannot be assessed

trucut core needle biopsy = shows cells AND stroma, so you can assess architecture

30
Q

how do we determine the prognosis of a neoplasm?

A
  • grade
  • stage (MOST IMPORTANT) S= spread
  • size
  • site
  • type
  • host response
  • adequacy of therapy
31
Q

what is the prognostic associated with well differentiated tumours, moderately differentiated tumours, or poorly differentiated turmous?

A

well differentiated = low grade = good prognosis

moderately differentiated = intermediate grade

poorly differentiated = high grad = poor prognosis

*differentiation is the degree to which the tumour resembles mature tissue and the degree of nuclear abnormality

32
Q

how do we assess the grade of a tumour?

A
  1. cytological features: hyperchomasia, pleomorphism, nuclear/cytoplasmic ratio, and mitotic activity
  2. architectural features: degree of gland formation, degree of maturation
  3. functional features: degree of keratin or mucin production
33
Q

how do we determine the stage of a tumour?

A

remember the TMN criteria?

T= size of tumour/level of involvement

M = number of mets

N = number of lymph involvement

34
Q

what is the ‘sentinel node’?

A

it is the lymph node which the tumour first spreads

  • identified using blu dye injected into the site of the tumour and observed in the lymph node shortly there after- note this is associated with false negatives b/c if a tumour is present in the lymph, it may not absorb any dye
35
Q

lymphocytic infiltrate in a tumour is a good or bad prognostic sign?

A

it is a good prognostic sign - it reflects the ability of the body to generate an immune response against the tumour

36
Q

Why do we ink the tumour after it has been cut out?

A

to identify lateral, proximal, distal etc. margins - otherwise, if the tumour hasn’t been completely resected on one side, the pathologist can phone in and say “take more of the lateral end of the tumour margin”

37
Q

how do metastatic tumours spread?

A
  1. direct to adjacent tissues
  2. lymphatics
  3. blood vessels
  4. transcoelomic = across the peritoneum
  5. perineural
  6. along natural passages
38
Q

what are the most common sites of metastasis from blood spread?

A
  • lung
  • liver
  • bone
39
Q

What facilitates a neoplasm spread?

A
  1. enzyme degradation of basement membrane and connective tissue by collagenases (breaks down the barriers to spread)
  2. reduced cell to cell adhesion between tumour cells ( allows cells to separate)
  3. increased cell-cell adhesion between tumour and endothelial cells (attaches to vessel walls)
  4. tumour embolisation
  5. increased vessel formation - VEGF
40
Q

what are the most common clinical signs of metastasis?

A
  • lymphadenopathy
  • Jaudice
  • Bone pain/fracture
  • cerebral stroke
  • cachexia, anorexia, lassitude
41
Q

How does Tamoxifen work?

A

it is a growth receptor blocker

  • estrogen is a growth stimulant
  • breast tumour cells have an increased number of estrogen receptors
  • tamoxifen vinds to these growth receptors and prevents estrogen binding and thereby blocks its activity
  • the histopath. determines which neoplasms will respond to tamoxifin performing immunohistochemistry
42
Q

What is Herceptin? How does it work?

A

Her2 is a member of the estrogen growth factor tyrosine kinas efamily

it is amplified in 20-30% of breast cancers

Herceptin is a monoclonal antibody which binds to and blocks the EGF receptor on the membrane of hte breast cancer cells

43
Q

how do Small molecule inhibitors work?

A

these inhibit intracellular tyrosine kinase components of the transmembrane receptor

the kinases cause phosphorylation which activates the signalling pathway in cells

They inactivate the “switching on” of cell signalling pathways by inhibiting tyrosine kinase activity and therefore the activating step of phosphorylation

44
Q

what is a carcinoma in situ?

A

it is a carcinoma which has not invaded beyond the epithelium

  • no metastatic potential at this stage
45
Q

what is dysplasia?

A

a neoplastic change in the epithelium which shows some of the microscopic features of malignancy but does not involve the full thickness of the epithelium = early manifestation of malignancy

46
Q

what are the haematological effects of malignancy on a host?

A
  • iron deficiency anaemia (commonest)
    • blood loss
  • megaloblastic anaemia
  • hypoplastic anaemia
    • marrow infiltration by tumour
    • chemotherapy destruction of haemopoietic cells
    • radiotherapy destruction of haemopoietic cells
  • haemolytic anaemia
    • immune mediated destruction of RBCs
  • INCREASED CLOTTING - tumour activates clotting factors, platelets, endothelial cells, and inhibits fibrinolysis
47
Q

how does malignancy cause hypercalcaemia?

A

bone destruction by the tumour causes the release of calcium into the blood

respiratory (12 decks)

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