Neoplasia - Lecture 12 Flashcards
Neoplasia pathologies
Soft-tissue Sarcoma: (Sarcoma developing from connective tissue/soft-tissue)
Ewing’s Sarcoma: (Bone cancer affecting children and adolescents)
Osteosarcoma: (Aggressive, malignant form of bone cancer)
Chondrosarcoma: (Malignant cartilaginous tumours)
Pancoast Tumour: (Apical lung tumour that can mimic symptoms of Thoracic Outlet Syndrome)
Most common cancers
- Prostate & Colorectal 14%
- Breast cancer & Melanoma 2nd
- Lung cancer accounted for most deaths
Common Cancer and deaths by age
0-24: Common: Leukaemia M+F.
Died: Leukaemia or brain cancer M, Leuk. F.
25-44: Common: Melanoma M, Breast cancer F.
Died: M stomach C, F Breast C.
45-64: Common: Prostate M, Breast C. F,
Died: Lung C. M, Breast C. F.
65-74: Common: Prostate C. M, Breast C. F.
Died: Lung C. M + F
75+: Common: Prostate C. M, Colorectal C. W.
Died: Prostate M, Colorectal F.
Discuss Neoplasia
New growth- uncontrollable or abnormal, no coordination or useful fxn
Benign (slow) or Malignant (fast)
Neoplasia’s are autonomous of other surrounding tissues & grow independently
Some Neoplasias require endocrine support from primary tissue(glands)- therefore is hormone secretion stops= cancer growth can stop but normally temporary
Neoplasia vs Hyperplasia
Neo: spontaneous. Hyper: excess or abnorm stimuli
Neo: abnorm stimuli e.g. chems. Hyper: degree stim dictates growth
Neo:continuos growth. Hyper: remove stimulus to stop growth
Neo: base cells change. Hyper: cells remain normal
Development of Neoplasia due to Genetic Mutation
- Oncogenes
- Tumour Suppressor genes
Oncogen: abnorm genes arising from norm. genes that regulate cell growth & division.
Arise point mutation (due to chem damage), gene amplification or translocations between genes.
Tumour Suppressor Genes: particular genes responsible for detecting DNA damage or inaprop. growth in cell division, can help repair DNA.
Damage or dysfxn = rapid development of oncogenes
Internal development Neoplasia
-most common tissues
Common Neoplasia from Cells that turn over quickly: Skin, GI, Resp.
Liver is slower & decrease neoplastic development
MM & NN least likely
Name environmental factors for the External Development of Neoplasia
Environmental factors increase risk:
- Infections
- Radiation
- Drugs/ chemical (asbestos, smoking)
- Dietary substances (high fat diet, alcohol)
- Co-existing Disease (chron. inflam)
Clinical Classifications of Neoplasia
Benign (never metastasises)
Malignant (almost always invades & met.)
Inteermediate (no set pattern, may not spread)
Characteristics of Benign Neoplasia
- Non invasive
- Localised (one tissue/area as capsulised containing the neoplasia)
- Good prognosis (unless space occupying lesion)
- Slow growing
Characteristics of Malignant Neoplasia
- Poor prognosis
- Invasive
- Non capsulised
- Highly metastatic
- large cellular variance in growth and poorly differentiated = little resemblance to original tissue
- behaviour correlates with cellular differentiation e.g. anaplastic malig. neo grows rapidly
Discuss Anaplasia
Refers to a lack of differentiation in neoplastic cells
- appears primitive & lacks specialisation of a cell line
- Pleomophism (vary size & shape)
- Abnorm. nuclear morphology (dark nuclei, multi nulei)
- Mitoses (Large #s & abnormal cells)
- Loss of polarity
Discuss why malignant neoplasia’s metastasise
- Cancer cell poorly held together, poor stromal support & fragile blood vessels, allowing for increased collapse of vasc. system + increased necrosis.
- undefined borders between malig. and surrounding cells, continued necrosis causes cancer cells continue to proliferate + fills vacant spaces.
- Cancer cells infiltrate between lines of weakness, generally between lymph and small blood Vessels.
- Cancer results in erosion + expansion. Bone can result in Lytic lesions (bone destruction) or Blastic lesions (filling empty spaces with cancer cells)
- If metastasises invade lymph/blood vessels, small pieces tumour can break off and spread around the body.
Benign vs Malignant
- general features
- growth
- rate
- end of growth
- matast.
B: well defined & typical of orig. tissue
M: imperfectly differentiated & not typical or original tissue B:Well formed stroma, can haemorrhage & necroses.
M: Stroma poorly formed, haemmorahge + necroses often
B:Encapsulated, not well expanded
M: invasiv, expands & infiltrates, can have pseudo capsule
B: Slo growth rate M:Extremely rapid
B:may stop growing spontaneously M: rare remission
B:absent metast. B: Frequent met. & Dx tool
Clinical effects of Benign & Malignant cancer
B: complication 1. situational 2. Accidental complication
3. production active hormones
M: same as benign plus 1. Infiltrate & invasion 2. Metastasis of secondary tumours 3. Infection, haemorrhage
