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Disease Processes > Neoplasia > Flashcards

Neoplasia Flashcards

1
Q

Definition: Tumour

A

Originally used to denote a swelling

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2
Q

Definition: Cancer

A

Malignant Tumour

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3
Q

Definition: Benign

A

Friendly, non-life threatening

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4
Q

Definition: Malignant

A

Potentially fatal

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5
Q

Definition: Apoptosis

A

Cell suicide or programmed cell death

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6
Q

Explain Metastasis

A
  • Cancer spreads to a region other than where it originated
  • Commonly develop when cancer cells break away from main tumour and enter bloodstream or lymphatic system
  • Can also develop when breaking away from main tumour (in belly, abdominal cavity) and grow in nearby areas (liver, lungs or bones)
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7
Q

What is Dysplasia?

A
  • Abnormal development of cells within tissues or organs
  • Can lead to a wide range of conditions involving enlarged tissue or pre-cancerous cells
  • Reversible
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8
Q

What is Neoplasia?

A
  • Uncontrolled, abnormal growth of cells or tissues that is not under physiologic control
    o Abnormality = neoplasm or tumour
  • Irreversible
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9
Q

What is Hyperplasia?

A
  • Cells are dividing
  • Removing initial stimulus will cause additional cells to die from apoptosis
  • Increase risk of dysplasia
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10
Q

What is Metaplasia?

A
  • Change from a well-differentiated cell type to another well-differentiated cell type
  • Generally, in response to a change in environment
  • Can be reversed by removing the initial stimulus
  • Increase risk of dysplasia
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11
Q

Definition: In Situ

A
  • Tumour confined to its site of origin and has not invaded neighbouring tissue or gone elsewhere in the body
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12
Q

Explain Carcinoma

A
  • Abnormal cells that divide without control
  • Originates in epithelial cells lining the skin or the tissue lining organs, such as the liver or kidneys
  • Epithelial cancers increase in incidence as we age
  • Cells that are dividing have the greatest chance of sustaining a mutation
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13
Q

Atrophy

A
  • Occurs at a cellular level an involves the shrinking of a tissue
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14
Q

What is Autophagy?

A
  • Self-eating so cells shrink
  • In response to reduced resources or the removal of damaged organelles
  • As we age, the cells’ ability to undergo autophagy declines
    o Defective removal of damaged mitochondria results in increased free radical generation
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15
Q

Four Classes of Normal Regulatory Genes

A

These genes are principal targets of genetic damage
o Growth promoting proto-oncogenes
o Growth inhibiting tumour suppressing genes
o Genes that regulate apoptosis
o DNA repair genes

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16
Q

8 Behavioural Changes that Occur in Cells

A
  1. Self Sufficiency in Growth Signals
  2. Insensitivity to growth-inhibitory signals
  3. Evasion of apoptosis
  4. Defects in DNA repair
  5. Limitless Replicative Potential
  6. Sustained Angiogenesis
  7. Ability to invade & metastasise
  8. Predilection for glycolysis even in the presence of oxygen (Warburg Effect)
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17
Q

Self-Sufficiency in Growth Signals

A
  • Protooncogenes regulate cell proliferation
  • Protooncogenes mutate  forming oncogenes which promote autonomous growth via the creation of oncoproteins
    o Inactivate internal regulator pathways and result in abnormal cell function and transformation
  • Many cancer cells acquire the ability to synthesise and secrete their own growth factors (creates positive feedback loop)
  • Cancer cells can tweak growth factor receptor
    o Increases number of receptors on cell surface  lower level of growth factor is required to trigger cell division
18
Q

Limitless Replicative Potential

A
  • Tumour cells can inactivate senescence signals and activate telomerase
  • Telomerase replaces telomeres with base pairs and allows unlimited replication
  • Three Cell Types that may show unlimited replication
    o Germ Cell (normal)
    o Stem Cell (normal)
    o Tumour Cells (abnormal)
19
Q

Sustained Angiogenesis

A
  • Endothelial cells release plasminogen activator and collangease, breaking down the basement membrane
  • Capillaries sprout off venules
  • Formation of new blood vessels
20
Q

Evasion of Apoptosis

A
  • P53 (guardian of the genome) is responsible for detecting DNA damage, chromosome abnormalities and arresting the cell cycle to initiate repair
    o If not possible, apoptosis is induced
  • More than half of cancers have mutated or missing gene P53
    o Therefore, it is damaged or missing
  • Cancer cells than either increase the activity of inhibitors of P53 or silence the activators of P53
21
Q

Insensitivity to Antigrowth Signals

A
  • Antigrowth signals are proteins that inhibit growth
  • At a molecular level, nearly all antigrowth signals are funnelled through the Retinoblastoma protein (Tumour Suppressor protein)
    o Can be lost through mutation of its gene
    o Cancer-promoting proteins (oncoproteins) can block the function of Retinoblastoma
  • Another antigrowth signal (TGF-Beta) blocks the advancement of cell division when present
    o Therefore, cancer cells can reduce the number of TGF-Beta receptors to be irresponsive to its presence
22
Q

Ability to Invade and Metastasise

A
  • Primary tumour masses spawn pioneer cells that invade adjacent tissue
  • Allows the tumour to colonise a new region of the body in which nutrients and spacer are not limiting
  • Successfulness is dependent on the other hallmarks of cancer
23
Q

Warburg Effect

A
  • Form of modified cellular metabolism found in cancer cell
    o Tend to favour a specialised fermentation over the aerobic respiration pathway
  • Cancer cells predominantly produce energy by a high rate of glycolysis followed by lactic acid fermentation in the cytosol
    o Rather than glycolysis, followed by the oxidation of pyruvate
  • Aerobic glycolysis produces ATP synthesis  promotes cell proliferation by reprogramming metabolism to increase glucose uptake and stimulate lactate production
    o High proliferating cancer cells use increased fatty acid synthesis to support the rate of cell division
24
Q

Defects in DNA Repair

A
  • Enable cancer cells to accumulate genomic alterations that contribute to their aggressive phenotype
  • When erroneous DNA repair leads to mutations/chromosomal aberrations affecting oncogenes and tumour suppressor genes
    o Cells undergo malignant transformation resulting in cancerous growth
25
Q

Benign vs Malignant

A

Benign

  • Never metastasises
  • Well differentiated
  • Homogenous
  • Encapsulated

Malignant

  • Can potentially metastasise
  • Well differentiated or undifferentiated
  • Heterogeneous
  • Infiltrative growth
26
Q

Benign Tumors of Connective Tissue

A
  • Fibrous Tissue / Fibrocyte / Fibroma
  • Muscle / Myocyte / Leiomyoma
  • Cartilage / Chondrocytes / Chondroma
  • Bone / Osteocyte / Osteoma
  • Others include:
    o Lipoma
    o Haemangioma
27
Q

Malignant Tumors of Connective Tissue

A

Sarcomas
o Name (Sarc = Malignant + CT cells of origin)
 Fibrosarcoma
 Leiomyosarcoma

28
Q

Epithelial Benign Tumours

A
  • Papil- (finger like projection)
  • Adeno- (relating to glands)
  • Cystadena- (cyst like)
  • -oma- (denoting tumour and other abnormal growths)
29
Q

Malignant Epithelial Tumors

A

Carcinomas
- >90% of cancers
o Proliferation, stress

Example
o	Squamous Cell Carcinoma 
o	Renal Cell Carcinoma 
o	Adenocarcinoma 
o	Basal Cell Carcinoma 
o	Cystadenocarcinoma
o	Papillocarcinoma
30
Q

Benign Tumors (Other than Epithelial and CT)

A
  • Meningioma (occur in the meninges of the brain or spine)

- Mature Ovarian Teratoma ‘dermoid cyst’ (germ cell mutates)

31
Q

Testicular Tumors (Malignant)

A
  • Immature Teratoma

- Seminoma

32
Q

Malignant Tumor Types

A
  • Carcinomas
  • Sarcomas
  • Testicular Tumours (Germ Cells)
  • Mesothelioma (Mesothelial Cells)
  • Melanoma (Melanocytes)
  • Gliomas
  • Lymphomas (Lymphoid Tissue)
  • Leukaemias (Hematopoietic Stem Cells)
  • Blastomas = Never a normal well-differentiated cell (generally, a childhood cancer)
33
Q

3 Main Routes for Metastasis

A
  • Blood (haematogenous)
    o Bone and Soft Tissue Tumours
  • Lymphatics (vessels and nodes)
    o Melanoma, Breast, Lung and Gastrointestinal Tumours
  • Direct Seeding (through/within body cavities)
    o Certain tumour cells can only successfully colonise selective organs that have suitable growth environments
34
Q

Importance of Early Detection

A
  • If it is found early, it may be easier to treat
  • If cancer has begun to spread, alternative treatment must be utilised
  • If cancer has not spread, tumour may have the ability to be removed without further treatment required
35
Q

Signs and Symptoms of Cancer

A 
•	Location important 
•	Hormones, blood and mucous
•	Cancer Cachexia – Fat and Muscle Loss 
•	Paraneoplastic syndromes (associated with a hormone imbalance e.g., too much calcium) 
o	10-15%
36
Q

Cancer Cachexia

A
  • Reduced muscle strength and mass (e.g., sarcopenia)
  • Fat loss
  • Loss of functional tissue
  • Severe fatigue
  • Anorexia
  • Anaemia and other biochemical changes
37
Q

Treatments

A
  • Surgery – Exercise as much as possible
  • Radiotherapy – X Rays
  • Chemotherapy – Drugs
  • Hormone Therapy – Use hormones or their blockers

Immunotherapy
o Monoclonal antibodies
o Stimulate the immune system to kill the cancer cells

38
Q

Pathogenesis

A
  1. Normal - Multiple Mutation - Cancer
  2. Normal - Multiple Mutation - Benign
  3. Normal - Multiple Mutation - Benign - Further Mutation - Cancer
  4. Normal - Sustained Stress -Metaplasia - Multiple Mutation - Dysplasia - Further Mutation - Cancer
39
Q

Cancer Grading

A

I-IV

  • Estimates how aggressive the cancer is
  • Varies depending on the cancer type
  • Cytological/Histological examination from biopsy
40
Q

Cancer Staging

A

TNM

T1-T4 (dependent on size of primary tumour)

N0-N3 (dependent on no. of lymph nodes that have cancerous cells within them)

M0 or M1 (dependent on whether the cancer has metastasised)

Disease Processes (13 decks)

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