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Disorders of growth Flashcards

1
Q

Outline the growth of labile, stable and permanent cells, including an example of each.

A
  • Labile cells (continuously dividing): Proliferate throughout life, replacing those that are lost. e.g. epithelia.
  • Stable cells (quiescent): Low levels of replication (G0). In response to stimuli undergo rapid division (G1) and reconstitute the tissue of origin. e.g. Mesenchymal cells
  • Permanent cells (non-dividing): Left the cell cycle, cannot undergo mitotic division in postnatal life.
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2
Q

How is destruction of permanent cells combatted in the body?

A

In case of cell destruction the space is occupied by the proliferation of supportive elements.

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3
Q

Stem cells

A

Cells that lack fully differentiated morphologic, functional and behavioral characteristics.

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4
Q

Differentiate between asymmetrical replication and self-renewal capacity of stem cells.

A

Asymmetrical replication: a stem cell divides into one father cell that is identical to the original stem cell, and another daughter cell that is differentiated.

Self-renewal capacity: the ability to go through numerous cycles of cell division while maintaining the undifferentiated state.

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5
Q

Differentiate between embryonic and adult stem cells.

A

Embryonic stem cells (totipotent): Can give rise to all tissues of the body.

Adult stem cells (pluripotent): Can give rise to a smaller variety of tissue types.

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6
Q

How can disorders of growth occur? Give examples for each.

A
  • Diminished growth: Agenesis and Aplasia, Hypoplasia, Atrophy
  • Increased growth: Hyperplasia, Hypertrophy, Neoplasia
  • Abnormal cell differentiation: Metaplasia, Dysplasia, Anaplasia (Neoplasia)
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7
Q

Explain the difference between aplasia and agenesis.

A

Agenesis: Absence of an organ or body part !! no associated primordium (first trace of a structure).

Aplasia: Failure of an organ to develop. Usually accompanied by the presence of a rudimentary organ (primordium: an organ or tissue in its earliest recognizable stage of development)

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8
Q

Hypoplasia

Definition and causes.

A

Failure of an organ to develop to the full size (less severe in degree than aplasia)

Causes: often unknown, genetic, hormone deficiency, infectious agents

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9
Q

Atrophy

Definition.

Differentiate between qualitative and quantitative,

A

Shrinkage of an organ or tissue after it has reached its normal size, caused either by a reduction of cell size or by reduction of cell number.

  • Qualitative atrophy – cells shrink: reduction in size
  • Numerical / Quantitative atrophy or involution– cell death exceed replacement: reduction in number
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10
Q

Draw a timeline of the occurence of disorders of growth during development/life.

Include agenesis, aplasia, hypoplasia, normal, hyperplasia.

A
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11
Q

Outline the causes of atrophy. (x6)

Briefly explain each

A
  • Starvation (lack of nutrients) - absorption defect
  • Lack of blood supply e.g. chronic passive hepatic congestion
  • Lack of innervation (muscle) e.g. nerve transection
  • Disuse e.g. muscle atrophy due to plaster
  • Pressure e.g. neoplasia – reduced blood supply
  • Loss of hormonal stimulation e.g. testicular atrophy
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12
Q

Hyperplasia.

Definition and causes.

When the stimulus is removed does the tissue return to normal?

A

Increase in cell numbers. - Only possible in cell types which can divide.

When the stimulus to hyperplasia is removed, the tissue revert to its normal status since the hyperplasia is reversible.

Can be caused by the physiological need need for regeneration (as in erythropoiesis) or healing, as a response to irritation, infection or endocrine imbalance.

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13
Q

Hypertrophy

Which cell type are required to increase there size using ONLY this mechanism?

Causes

A

Increase in cell size. - increase organelles

  • Mitochondria: Increased ATP requirements
  • Smooth Endoplasmic Reticulum (SER): Detoxification
  • Golgi and RER: Synthesis of extracellular proteins

Tissues made of stable cells can only increase their size using this mechanism.

Causes of hypertrophy are usually mechanical.

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14
Q

This slide shows an example of which type of atrophy? Define.

A

Qualitative - reduction in cell size

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15
Q

Give different examples for pathological and physiological hypertrophy.

A
  1. Physiological Hormonal:
    1. Mammary gland hyperplasia in pregnancy and lactation.
    2. Compensatory: Hepatectomy
  2. Pathological
    1. Hormonal: Cystic endometrial hyperplasia - high levels of estrogens
    2. Chronic irritation - parasitic infection
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16
Q

What is the physiological cause of hypertrophy?

Give two examples of the causes.

A

Causes: Demands for increased function.

Physiological/Pathological:

  • Chronic exposure to drugs: Enlargement of smooth endoplasmic reticulum in hepatocytes.
  • Compensatory hypertrophy of the right ventricle due to stenosis of the pulmonary outflow
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17
Q

Metaplasia

+Example and cause

A

Metaplasia A change of one type of differentiated tissue into another

e.g. squamous metaplasia of the bronchi (normally columnar ciliated) in response to the chronic irritation caused by smoking.

It often represents an adaptative change to a new environment and reflects reprogramming of stem cells to differentiate along another pathway.

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18
Q

Dysplasia

A

Loss of uniformity of the individual cells as well as loss in their architectural orientation. A disordered growth and maturation of an epithelium (non-adaptative), which is still reversible if the factors driving it are eliminated.

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19
Q

Anaplasia

A

Anaplasia Resemblance to embryonic forms of the tissue. Lack of differentiation. The cells loose their differentiation and look “undifferentiated”. The term is used in practice almost entirely to describe changes in tumour cells (neoplasia).

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20
Q

Describe two causes of squamous metaplasia.

A

Chronic irritation: Adaptive substitution of cells sensitive to stress by other cell types better able to withstand the emergence of an adverse environment; often at the expense of normal function

Abnormal metabolism: Vit A deficiency in the urinary tract, salivary gland ducts and mucous glands of the esophageal mucosa in birds. Estrogen toxicity in the urinary tract and prostate.

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21
Q

Outline an example of mesenchymal metaplasia.

A

Transformation from fibrous tissue to cartilage or bone in response to change of microenvironment of cells, such oxygen tension

Metaplastic bone (osseous metaplasia): in injured soft tissue, tumours (mixed mammary gland tumours).

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22
Q

Neoplasm

A

“New growth”. Abnormal mass of tissue, the growth of which exceed and is uncoordinated with that of the normal tissues and persists in the same excessive manner after cessation of the stimuli which evoked the change.

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23
Q

Define tumours and cancer.

A

Oncos/Tumour: “swelling” clinical appearance Oncology: Study of neoplasia

Cancer: “crab” infiltrative behaviour (malignant neoplasia) “crab attached to the reef”

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24
Q

What is the difference between benign and malignant tumours.

A

Benign Neoplasms (Tumours): “relatively innocent, …remain localised …cannot spread …surgical removal. (Robbins)

Malignant Neoplasms (Tumours): “Invade and destroy adjacent structures …spread to distant sites ” (Robbins)

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25
Q

What are the three dogmas of tumour growth?

Which of these is considered in correct and why?

A
  1. Tumours growth is not reversible: Cutaneous histiocytomas: tumours that are probably not tumours.
  2. Change in the DNA sequence - Traditonally: Mutation, deletion, amplification, translocation Recently: Epigenetic changes (methylation, histones modification than modify gene expression)
  3. Non-transmisible disease - Vertically: Familiar cancer syndromes. Early age, generally multiple tumours due to mutations in specific genes (tumour suppressor genes and genes encoding proteins of the tumour repair mechanisms).
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26
Q

Is neoplasia a monoclonal or polyclonal proliferation? What is mean by this?

A

Neoplasms are monoclonal proliferations. all the neoplasm arise from one mutated cell (clone)

Hyperplasia is polyclonal

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27
Q

Mesenchymal tumours

Give examples using standard nomenclature.

A

Mesodermal origin

Fibrosarcoma-> Malignant tumours from fibrous tissue Lipoma -> Benign tumours from adipose tissue Osteosarcoma -> Malignant tumours from bone tissue

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28
Q

What is the standard nomenclature used for malignant and benign mesenchymal tumours?

A
  • Benign tumours Suffix -oma
  • Malignant tumours Suffix -sarcoma
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29
Q

Epithelial tumours

Outline the standard nomenclature used for these types of tumours.

A

Epithelial tumours (glandular and non glandular) Endo/meso/ectoderm origin

Benign tumours Suffix -oma

Malignant tumours Suffix -carcinoma

  • Adeno ->From glandular epithelium or tubular appearance
  • Papilloma ->Benign exophitic tumours from epithelial (nonglandular) surface
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30
Q

Round cell tumours.

What type of cells can develop into these types of tumours?

A

Cells are round to oval and discrete, although they may cluster if in large numbers.

  • Mast cells
  • Plasma cells
  • Lymphocytes
  • Histiocytes
  • Melanocytes
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31
Q

List the different types of malignant and benign round cell tumours.

(x6)

A

Bold = malignant

  • Mast cell
  • Plasma cell - Plasmacytoma Multiple myeloma
  • Lymphocyte - Lymphoma/lymphosarcoma
  • Histiocytes - Cutaneous histiocytoma Cutaneous histiocytosis Systemic histiocytosis Malignant histiocytic sarcoma Malignant histiocytosis
  • Melanocytes Melanocytoma Malignant melanoma
  • Transmissible Venereal Tumour
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32
Q

What is a liquid tumour also know as, how are they named?

A

Leukaemia

Naming: cell of origin + leukaemia

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33
Q

What is a teratoma?

A

Teratomas are tumours composed of cells types from at least two, and usually three, germ layers. They arise from totipotent cells and are mostly, but not exclusively, found in the gonads.

34
Q

Mixed tumour

A

“Believed to arise from a single pluripotent cell capable of differentiating into various cell types”

35
Q

Harmatoma

A

Disorganized but mature mesenchymal and epithelial tissues in their normal anatomic location.

Aberrant Differentiation rather than true neoplasms. Benign behaviour.

Normally present at birth or soon after

36
Q

Choristomas

A

Organized(normal) mature mesenchymal and epithelial tissues in ectopic anatomic location.

Normally present at birth or soon after.

Dermoids in cornea

37
Q

Lack of differentiation of tumours. More likely to occur with malignant tumours.

A

Anaplastic growth

38
Q

What morphological changes are associated with anaplastic tumours?

(x7 + brief description)

A
  1. Pleomorphism: Variation in cell size and shape.
  2. Loss of normal tissue architecture ex. Loss of polarity: orientation of cells is markedly disturbed.
  3. Increased DNA and RNA content: high nuclear/cytoplasmic ratio, large, multiple nucleoli.
  4. > Mitosis
  5. Bizarre mitotic figures (tripolar, multipolar). - loss of symmetry
  6. Loss of function
  7. Necrosis (scant vascular stroma - Invasion)
39
Q

Which pleiomorphic changes are associated with anaplastic tumour growth?

A

Pleomorphism: Variation in cell size and shape.

  • Cytoplasm: Anysocytosis
  • Nucleus: Anysokaryosis
40
Q

Describe the invasive behaviour of malignant and benign tumours.

A

Benign tumours: Cohesive, expansile masses remain localized. Grow and expand slowly & develop fibrous capsule.

Malignant tumours: Progressive infiltration, invasion and destruction of tissue. Poorly demarcated (crab-like pattern).

41
Q

Explain the process of local invasion of tissues by epithelial neoplams.

A
  1. Loss of adhesions, down-reg/mutation of E/B cadherin
  2. Changes in attachment of tumour cells to ECM proteins. Loss of polarity, > integrins (ECM binding) cover entire cell membrane
  3. Basement membrane/CT degraded by proteolytic enzymes (MMP, cathepsin-D) or ECM-sequestered (VEGF) growth factors with chemotactic, angiogenic and growth promoting effects.
  4. Ameboid migration: Squeezing through spaces in the matrix. SecreteD cytokines that impige on cytoskeleton and pseudopodes
42
Q

Squeezing through spaces in the matrix.

A

Ameboid migration

43
Q

Describe the process of metastisis of tumours.

(x7)

A
  1. Loss of cell to cell adhesion factors, i.e. E-cadherins
  2. Penetrate basement membrane (proteolytic enzymes). Locomotion through tissue spaces by secretion of enzymes.
  3. Tumour cells to vascular system - increased permeability and cellular motility.
  4. Tumour cells become attached to and invade basement membrane. Lymphatics lack basal membrane = easier
  5. Evade immune system
  6. Directed extravasation of tumour cells. Identify tumour-endothelial adhesion molecule.
  7. Extravascular tumour (metastatic tumour) create suitable environment = proliferation. Achieved by inducing neovascularisation.
44
Q

Describe the stroma of both epithelial and mesenchymal tumours.

What is stroma?

A

Supportive non-neoplastic support tissue which contains blood vessels, fibroblasts and inflammatory cells. Increases proportionally to neoplasm growth.

Epithelial - Stroma produced by non-neoplastic mesenchymal cells.

Mesenchymal - Produce their own stroma, eg fibrosarcoma produces collagen

45
Q

Which gross morphological feature is characteristic of neoplasm blood vessels?

How do their characteristics promote stroma deposition?

A

Tumour vessels are usually more dialated, tortuous and more permeable than normal vessels.

Leakage allows perivascular deposition of a fibrin network to promote stroma formation.

46
Q

A tumour would not grow over what size without a dedicated blood supply?

A

1-2mm^3

47
Q

Metastasis

Name four types of metastatic growth.

A

Transmission of microorganisms or cancerous cells from an original site to one or more sites.

  1. Transcoelomic - seeding of body cavity and surfaces
  2. Lymphatic - sollow lymphatic drainage
  3. Skip - discontinuous metastasis
  4. Hematogenous -
48
Q

Process of metasasis.

A
  1. Intravasation due to increased permeability of vessel wall and digestion of the basement membrane.
  2. Tumour cells evade immune system forming small homotipic or heterotipic (platelets, fibrin T lymphocytes) clusters.
  3. Extravasation- Adhesion molecules (integrins, CD44), Metalloproteinases. Preferred sites: tissue specific homing, Primary tumour location, Endothelial adhesion molecules, Chemokines
  4. Extravascular tumour (metastatic) creates a suitable environment i.e. (proliferation, neovascularisation and evasion of immune response.
49
Q

What two complications can arise from metastatic growth?

A
  • Tumour emboli can induce infarction in an organ with poor or no collateral circulation i.e. kidney, brain
  • Tumour emboli can also induce oedema from a reduction in lymphatic flow (lymphatic / lymph node metastases)
50
Q

Carcinogenic

A

Cause malignant changes in cells.

Highly reactive electrophiles which form covalent bonds with DNA/RNA or neutrophiles which form covalent adducts.

Electrophiles - contain electron deficient atoms

Neutrophiles - contain electron rich atoms

51
Q

What is the difference between direct and indirect carcinogens?

A

Direct acting: require no chemical transformation (“ultimate carcinogens”). Anticancer drugs as cyclophosphamide.

Indirect acting: pro-carcinogens mostly metabolised by the liver Polycyclic hydrocarbons (Benzopyrene), natural products (Aflatoxin B1).

52
Q

What are the two stages of carcinogen action? + eg

Does a promotor work without an initiator?

A
  1. Initiation: Both direct and indirect acting carcinogens (initiators) introduce an irreversible genetic change
  2. Promotion: DNA template must be replicated so that the change becomes fixed. Promoters stimulate mutated cell division (carcinogens, viruses, parasites, dietary factors or hormones influences). Driven to proliferate, the initiated clone suffers aditional mutations, developing eventually into a malignant tumour. EG hormones and irradiation

An initiator is always required with the promotor being applied at regular intervals afterwards.

53
Q

Name some examples of indirect and direct carcinogens.

A

Indirect: Polycyclic and heterocyclic aromatic hydrocarbons (benzo-pyrene-tobacco, fossil fuels, smoked meat), Aromatic amines, amides (napathylamine, benzidine, nitrosamines (preservatives)), natural products (Aflatoxin B1, Griseofulvin)

Direct: Alkylating agents, Anticancer drugs (cyclophosphamide, clorambucil, nitrosoureas)

54
Q

Why are low doses of radiation more likely to result in neoplasms than high doses?

A

High doses: Extensive necrosis affecting more rapidly dividing cells.

Low doses: Accumulative effects. DNA damage due to production of reactive oxygen species, single base damage, single and double strands breaks and DNAprotein crosslinks.

Severe damage: Apoptosis. Mild damage: Repair/tumours (leukemias, thyroid carcinomas).

55
Q

What is meant by non-ionizing radiation? Eg (x3)

What are the three different types of UV radiation, describe the type of damage can they cause?

A

Not enough energy to displace electrons - eg UV, sound waves and microwaves.

  • UV-A: Acute damage (erithema, hiperpigmentation and reversible damage to keratinocytes).
  • UV-B: Direct action on DNA (formation of pyrimidine (thymine) dimers T-C); Portion of the spectrum most involved in cutaneous neoplasia
  • V-C: A potent mutagen, filtered out by the ozone layer
56
Q

Three outcomes of DNA virus infection:

A
  1. Virus genome is translated into viral protein. Replication is detected.
  2. Only some viral genes are expression. Replication is not detected (a few Ag are seen)
  3. No viral genese expressed & replication continues - further external factors cause expression/ tumours.
57
Q

Oncogenic viruses?

A

RNA viruses

58
Q

How do RNA viruses act when they contain viral oncogenes compared with those that don’t?

A
  • Do contain oncogenes - Insert into DNA close to transcription factor, V-Onc is transcribed
  • Don’t - Insert into DNA close to cellular proto-oncogene which is silenced and activated its transcription.
59
Q

A normal gene which becomes an oncogene due to increased activity or mutation

Examples?

A

Proto-oncogene

  1. Growth factors
  2. Growth factor receptors - increased expression increases chance of activation
  3. Signal-transducing proteins
  4. Nuclear transcription factors
60
Q

A mutated gene which promoted tumour formation and progression

A

Oncogene

61
Q

A gene that protects a cell from one step on the path to cancer.

If lost the cell can have reduced or lost function and progression to cancer

A

Tumour suppressor gene

62
Q

Epigenetic changes.

A

No change in the DNA but in the expression of the existing DNA

63
Q

Rate of growth of tumours depends on what three factors?

A
  1. Rate of cell division - doubling time
  2. Proportion of replicating cells - growth fraction
  3. Rate of cell death and differentiation - post mitotic phase
64
Q

A normal cells acquires the phenotype of a malignant cell

A

Malignant transformation

65
Q

Stochastic theory

A

Different cancer cells, derived by division and differentiation of the original clone acquire different characteristics which contributed to the progression of the tumour.

Env/ natural selection

66
Q

Stem cell theory

A

Only small percentages of neoplasms can initiate, maintain and possibly lead to effective metastasis. These are the tumour stem cells.

67
Q

Cells with the malignant phenotype acquire more characteristics that are deleterious to the host.

A

Tumour progression

68
Q

Tumour heterogenicity

A

Initially all tumour cells are identical but due to lack of regulation of genetic integrity genetic changes lead to tumour heterogenicity.

69
Q

Cell cycle

(x5 stages)

A

G0 - Quiescent (stable) cell

G1 - Pre-synthetic stage

S - Synthetic

G2 - Premitotic

M - mitotic

70
Q

Which stage of the cell cycle do most benign and malignant tumours reside in?

A

Benign - G0

Malignant - More rapid the tumours growth the more cells are found in growth phases rather than the quiescent phase

71
Q

How can mutations in the somatic cell genome cause malignant tumours?

A
  1. Activation of growth-promoting oncogenes
  2. Alteration of genes that regulate apoptosis
  3. Inactivation of tumour supressor genes

These lead to expression of gene products and loss of regulatory gene products = clonal expansion, more mutation, heterogenicity = malignant neoplasms

72
Q

What aspect of a tumour causes an immunological response?

A

Tumour-specific antigens

73
Q

How do tumours resist the immunological response of the host?

A
  • Contain no TSAs
  • Host recognises secondary tumours but leaves primary
  • May be part of a host cell? Viral tumours
  • Expressing embryonic antigens
74
Q

Tumour surveillence theory.

Evidence

A

Tumour cells arise frequently but are often killed by the immune system. Clinically relevant tumours are rare.

Tumours are more common in those with immunosupression, deficiency.

75
Q

What immune responses are possible against tumours?

A
  1. Tc cells
  2. Lymphokines activate macrophages
  3. ADCC
  4. NK cells
76
Q

How can tumours avoid immune mechanisms?

A
  1. Lack of antigenicity
  2. Genetic - Some MHC-antigen complexes are low responders of the immune response
  3. Tumour gets to large for the immune response
  4. Blocking lymphocyte receptors or complexing with antigens
77
Q

Immunotherapy (x2 methods)

A
  • In combi with chemotherapy aims to immunise animals against their cancer
  • Some aduvants have immunopotentiating effect against tumours
78
Q

What direct effects can tumours have on their host?

A
  1. Obstruction - direct or emboli formation
  2. Pressure - Space-occupying & lead to pressure increases
  3. Replace normal tissue - invasive or pressure
  4. Haemorrhage - Vascular endothelium or fast growth
  5. Dyshaemopoiesis - Invasion of myeloid tissue
  6. Bone fracture - primary or invasive secondary
  7. Malabsorption - of gut wall
  8. Infection - immunosupression and ulceration
79
Q

What indirect effects can tumours have on their host?

A
  • Hormone effects - insulinoma, adrenal or pituitary hormones (hyperadrenocorticism),
  • Hypertrophic-pumonary osteoarthropathy - bone to lungs
  • Cachexia - chronic wasting due to anorexia. Changes in metabolism
  • Blood coagulability - Hyperviscocity or increased bleeding tendancies (due to histamine release in mast cell tumours)
80
Q

What methods can be used to diagnose tumours?

A
  1. Histopathology
  2. Cytology
  3. Immunohistochemistry
  4. PCR
81
Q

How do tumours evade the immune system?

A
  1. Reduce MHC1 expression
  2. Antigen masking - overexpression of glycocalyx molecules
  3. Immunosupression - tumoural immunosupressive products TGF-beta
  4. Tolerence - express self antigens or lack of costimulatory molecules
82
Q

Describe RAS as a system of tumour expression.

A

RAS > GDP-GTP > triggers MAPK (activates transcription, cell cycles and division)

GTPase in the cell rapidly inactives RAS

With mutated RAS GTPase fails to act and therefore cell division is unregulated.

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