Tumors Flashcards

1
Q

What are the classification of tumors?

A
  • Benign
  • Malignant
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2
Q

What is Neoplastic?

A

Uncontrolled new growth

  • wothout normal growth control mechanisms
  • can occur in any nucleated cell
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3
Q

What is hyperplasia?

A

Controlled cell growrh

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4
Q

What is:

  • Atrophy
  • Hypertrophy
  • Hyperplasia
  • Metaplasia
  • Dysplasia
A
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5
Q

What is the difference between metaplasia and dysplasia?

A

Metaplasia is reversible

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6
Q

What are the 8 hallmarks of cancer?

A
  • Sustaining proliferative signalling
  • Evading growth suppressors
  • Resisting cell death
  • Enabling replicative immortality
  • Inducing angiogenesis
  • Activating invasion and metastasis
  • Reprogramming energy metabolism (emerging)
  • Escaping immune destruction (emerging)
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7
Q

Malignant

A
  • Carcinoma = Epithelial cells
  • Sarcoma = Mesenchymal structures (bone, muscle)
  • Adnocarcinoma = Glandular
  • Osteosarcoma = Bone
    *
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8
Q

Growth rate benign/malignant

A
  • Most benign tumours grow slowly and are encapsulated, and DO NOT metastasize.
  • Most malignant tumours invade, are not encapsulated, grow quickly and metastasize (except basal cell Ca and CNS Ca).
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9
Q

Hyperchromasia

A

Refers to the dark staining nuclei which is usually due to increased DNA content

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10
Q

Pleomarphism

A

Variability in the size and shape of cells and/or their nuclei.

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11
Q

Anaplasia

A
  • Totally undifferentiated neoplastic parenchyma
  • Biochemically, anaplastic cells resemble other anaplastic cells more than they do their tissue of origin.
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12
Q

How does matastasize happen?

A

To metastasize, a cell must break free from primary tumour, enter the circulation (venous or lymphatic), survive there, enter a host tissue, anchor and form a metastasis.

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13
Q

How does different types og malignant tumors?

A
  • Carcinoma: malignant tumour arising from epithelial origin - tends to spread via lymphatics
  • Sarcoma: malignant neoplasm arising from mesenchyme - tends to spread haematogenously (especially to liver and lungs since most often invades into venous drainage and these organs are exposed to most venous drainage).
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14
Q

What is a hamartoma?

A
  • hamartoma is a benign, focal malformation that resembles a neoplasm in the tissue of its origin. This is not a malignant tumour, and it grows at the same rate as the surrounding tissues. It is composed of tissue elements normally found at that site, but which are growing in a disorganized mass.
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15
Q

What is the grading of malignant neoplasms?

A

grade

  1. Well differentiated
  2. Moderately differentiated
  3. Poorly differentiated
  4. Nearly anaplastic
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16
Q

What are the neoplasia staging?

A
  • The most common systems for staging employs the TNM classification.
  • “T” score is based upon the size and/or extent of invasion.
  • “N” score indicates the extent of lymph node involvement.
  • “M” score indicates whether distant metastases are present. Staging forms have been devised for each organ or site that a malignant neoplasm can occur.
17
Q

What are the principles of staging?

(malignant neoplasms)

A
  • Tis = In situ, non-invasive (confined to epithelium)
  • T1 = Small, minimally invasive within primary organ site
  • T2 = Larger, more invasive within the primary organ site
  • T3 = Larger and/or invasive beyond margins of primary organ site
  • T4 = Very large and/or very invasive, spread to adjacent organs
  • N0 = No lymph node involvement
  • N1 = Regional lymph node involvement
  • N2 = Extensive regional lymph node involvement
  • N3 = More distant lymph node involvement
  • M0 = No distant metastases
  • M1 = Distant metastases present
18
Q

How does neoplasia arise?

A
  • Initiator = carcinogenic agent that changes DNA irreversibly,
  • Promoter can produce a tumour in previously initiated cells only, reversible
  • Viral Oncogenesis (second only to tobacco smoke as the primary Ca risk factor):
19
Q

Congenital and Acquired neoplasia?

A
  • Congenital (rare) – Germ line mutation e.g. Retinoblastoma, BRCA (Breast and Prostate CA)
  • Acquired (commonest type)
    • Viral infection – HPV, HepB, EBV
    • Radiation – UV, XR, Gamma – e.g. Thyroid CA in Chernobyl children or second cancers in post radiotherapy treatment
    • Chemical damage – smoking, soot (scrotal cancer in chimney sweeps)
    • Chronic inflammation – causes ^ cellular turnover, ^ risk that one of those cells may be exposed things which cause genetic mutation at a vulnerable time in their cell cycle e.g. Ulcerative colitis
20
Q

Oncovirus

A

Ca causing viruses

21
Q

What immunecell kill tumor cells?

A

NK cells

  • Are lymphocytes (non-T, non-B)
  • Need to be activated by IL-2
  • Considered the first line of defence against tumors
  • They participate in antigen dependant cell mediated cytotoxity
    • Where they can bind the Fc portion og IgG attached to cells and lyses them
22
Q

What are the two kind of staging cancer(neoplasia)?

A

TNM

  • T = size of primary tumour, 0 = in situ, 4 = big
  • N = nodal involvement, 0 = none, 3 = many
  • M = metastases

Staging be the I to IV method

  • I = one lymph node or region
  • II = lymphatic on same side of diaphragm
  • III = lymphatics on both side of diaghragm
  • IV = organ metastases
23
Q

What are different causes for acquired mutations?

A
  • Viral infection – HPV, HepB, EBV
  • Radiation – UV, XR, Gamma – e.g. Thyroid CA in Chernobyl children or second cancers in post radiotherapy treatment
  • Chemical damage – smoking, soot (scrotal cancer in chimney sweeps)
  • Chronic inflammation – causes ^ cellular turnover, ^ risk that one of those cells may be exposed things which cause genetic mutation at a vulnerable time in their cell cycle e.g. Ulcerative colitis
24
Q

Give examples og DNA and RNA viruses that causes neoplasia

A

DNA

  • Human papilloma virus (especially 16, 18 and 31) and cervical Ca
  • Ebstein Barr virus and Burkitts lymphoma or nasopharyngeal Ca
  • Hepatitis B virus and hepatocellular CA

RNA

  • Acute transforming, contain viral oncogenes (v-oncs),
  • Slow transforming, insert DNA near a proto-oncogene but do not themselves carry oncogenes,
  • HTLV - for CD4 cells
    • HTLV-1 (Human T-cell Lymphatic Virus) is the only retrovirus with a known association(casual) with a human tumor
25
Q

What is cachexia?

A

Wasting syndrome

  • In half of all cancer patiens
  • Includes
    • Bod wasting
    • Weakness
    • Anorexia
    • Anaemia
26
Q

What causes cachexia?

A

Its multofactorial

27
Q

Paraneoplastic syndromes

A

This includes many signs and symptomes that arise from local tumors effects

  • Bone erosion (secretion of osteoclast stimulating factors (including IL-1, IL-6 and TNF) which cause calcium to be leached from bones: multiple myeloma, some Ca lung)
  • DIC (disseminated intravascular coagulation) from excess tumour antigen/tumour related vascular occlusion
  • Migratory thrombophlebitis (esp. pancreatic, lung, stomach Ca) due to massive antigen release into circulation
  • Hypercalcaemia due to metastases e.g Ca breast, Ca lung
  • Ectopic hormone secretion e.g. small cell Ca of lung – which secrete ectopic antidiuretic hormone (causing over hydration) and AdrenoCorticoTropicHormone ACTH (causing Cushing’s Syndrome).
28
Q

TSA and TAA

A
  • TSA = tumor specific antigens cause an immune response
  • TAA = tumor associated antigens may be on tumor and normals cells so do not cause an immune response but can help diagnosis or therapeutics
    • e.g. PSA and prostate Ca
29
Q
A