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1st Year Medicine > Pathology > Flashcards

Pathology Flashcards

0
Q

What are sequelae?

A

The range of possible outcomes of a disease.

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1
Q

What does pathogenesis mean?

A

The sequence of events between the healthy and clinical disease.

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2
Q

What mutation is associated with lung cancer?

A

Ki ras.

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3
Q

What mutation is associated with breast cancer?

A

Her2

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4
Q

What are Kochs postulates?

A

Four criteria designed to establish a causative relationship between a microbe and a disease.

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5
Q

What is apoptosis?

A

Programmed cell death.

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6
Q

What is P53?

A

A dna repair protein, when this is lost cancer can start as cells are allowed to proliferate unchecked.

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7
Q

What is a free radical?

A

An atom or molecule with unpaired valence electrons or an open electron shell making them highly chemically reactive. The molecules can spontaneously dimerise or polymerise upon contact.

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8
Q

What is a particularly important free radical to be aware of?

A

O2 - superoxide.

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9
Q

What does superoxide do? And how is it used?

A

Starts a chain reaction leading to lipid peroxidation.

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10
Q

What is a transgenic model?

A

An animal study.

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11
Q

What is superoxide normally used for in the body?

A

Biologically toxic and used by immune cells to kill invaders in an oxygen dependent mechanism.

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12
Q

What enzyme produces superoxide and on what type of cell?

A

NADPH oxidase in phagocytes.

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13
Q

What is chronic granulatomatous disease?

A

A mutation in the gene coding for NADPH oxidase. Characterised by extreme susceptibility to infection.

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14
Q

What is SOD?

A

Superoxide dismutase. A superoxide scavenging enzyme. Nearly all organisms living near oxygen contain isoforms of it.

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15
Q

Name a molecule with weak SOD activity and what does this mean?

A

Hb. Means it can easily be reduced and oxidised by superoxide.

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16
Q

What does an antioxidant do?

A

Molecule that inhibits the oxidation of other molecules.

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17
Q

Name a few free radicals?

A

Paracetamol, repercussion injury, inflammation and intracellular killing of bacteria etc.

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18
Q

What is reperfusion injury?

A

Tissue damaged that arises when blood supply returns to a tissue after a period of ischaemia. The absence of oxygen and nutrients from the blood during the ischaemic period creates a condition where the return of circulation results in inflammation and oxidative stress.

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19
Q

What factors affect the severity of a tissue injury?

A

Duration, nature, proportion of cells affected, regenerative capacity and topography.

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20
Q

What is hydropic change?

A

Also called vacuolar degeneration. Cellular swelling with microscopic small vacuoles seen within the cytoplasm which are distended and pinched of parts of the ER. It is a pattern of non lethal injury.

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21
Q

What are examples of non lethal tissue injury?

A

Hydropic change, fatty change (cells unable to metabolise fat, which are seen as vacuoles in the cytoplasm) and membrane shedding.

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22
Q

What is necrosis?

A

Pathological death of tissues. It elicits adjacent tissue response. If enough viable cells are around then regeneration may be possible.

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23
Q

What are the two types of cell death?

A

Apoptosis and necrosis.

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24
Q

What are the 6 different types of necrosis?

A

Caseous, fat, colliquative, coagulative, gangrenous and fibrinoid.

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25
Q

What is coagulative necrosis?

A

Accidental cell death from ischaemia or infarction. Cells look ghostly under microscopy as the architecture of the dead cell is maintained for a few days.

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26
Q

What is colliquative necrosis?

A

Otherwise called liquefactive necrosis. Digestion of dead cells form a liquid mass (pus). Typical of bacterial or fungal infections. Hypoxia brain injuries result in this due to high lipid and digestive enzymes in the tissues.

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27
Q

What is caseous necrosis?

A

Tissue maintains a cheese like appearance.

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28
Q

What is gangrenous necrosis?

A

Potentially life threatening condition where a large mass of tissue dies. Can be from injury, infection or chronic circulatory problems. Can be: dry, wet, gas, internal and necrotising fasciitis.

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29
Q

What is fibrinoid necrosis?

A

Form where an amorphous, basic proteinacious material accumulates in the tissue matrix. Looks like fibrin when stained. Can be caused by immune vasculitis, malignant hypertension and preeclampsia. Usually seen in immune reactions involving blood vessels.

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30
Q

What is fat necrosis?

A

Characterised by the action of enzymes in fat. Lipase releases fatty acids from triglycerides, this then joins with calcium to form soaps, giving chalky deposits. Usually associated with trauma of the pancreas. Can happen in the breast and salivary glands.

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31
Q

Describe inherited metabolic disorders?

A

Usually autosomal recessive. Cause a loss of function mutation.

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32
Q

How many people does PKU affect?

A

1 in 10000. Ireland 1 in 5000.

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33
Q

Describe PKU?

A

Autosomal recessive. Causes deficiency of phenylalanine hydroxylase leading to a build up of phenylalanine. Causes brain toxicity and retardation. Especially in growing brain. Children usually fair skin and blue eyed. Have Guthrie heel prick test at birth.

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34
Q

What are some of the harms of inflammation?

A

Mechanism of life threatening hypersensitivity reactions. Chronic inflammatory diseases e.g. Colitis. Fibrosis and disfiguring scars. Digestion of normal tissues, laryngeal oedema etc.

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35
Q

What is acute inflammation?

A

Initial and often transient reaction to tissue injury. Two phases: vascular phase (dilatation and increased permeability) and the exudate r and cellular phase (fluid and cells escape). Inflammatory response disrupts axial flow.

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36
Q

What is chronic inflammation?

A

Subsequent and often prolonged reaction following the initial response. Characterised by cellular reaction as opposed to time. Either develops from acute inflammation or is primary chronic inflammation.

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37
Q

What are the cardinal signs of inflammation?

A

Redness (rubor), pain (dolor), heat (calor), loss of function and swelling (tumor).

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38
Q

How do cell normally travel in a vessel?

A

Axial flow. Cells down the middle and plasma around the edges.

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39
Q

What features of vessels allow for vascular dilatation in acute inflammation?

A

Pre-capillary sphincters that are normally closed, meaning many of the capillaries lie empty, open allowing most capillaries to become full.

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40
Q

What is inflammatory fluid exudate comprised of?

A

Protein e.g. Immunoglobulin. Fibrinogen (turns to fibrin in contact with ECM. Exudate is continually being removed by the lymphatic system.

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41
Q

What are the steps in increased vascular permeability?

A

Brought about by chemical mediators including histamine and bradykinin. The leakage of fluid is confined to the post capillary venules. Endothelial cell contractile proteins contract and pull open transient pores which are largely intracellular. Endothelial cells are not damaged in the process.

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42
Q

What is the diagnostic feature of acute inflammation?

A

Neutrophils in the extra cellular space.

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43
Q

How does a neutrophil reach the site of an inflammatory stimulus?

A

Margination, adhesion and transendothelial migration.

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44
Q

Describe margination?

A

Loss of intravascular fluid makes blood more viscous allows disruption of axial flow as blood slows down and neutrophils can move into plasmatic zone (margination). Only occurs in venules.

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45
Q

Describe the steps in neutrophil adhesion?

A

In the resting state the neutrophil has surface selectin counter receptors and inactive integrins. When the neutrophil marginates the counter receptors adhere to selectin which is expressed in the surface of endothelial cells. This causes rolling adhesion. ICAM is then expressed on the endothelial cell which binds to the now activated integrins. This causes form adhesion and allows the transendothelial migration by the neutrophil inserting pseudopopia through the membrane.

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46
Q

What substances increase leukocyte surface adhesion molecule expression?

A

Complement C5a, leukotriene B4 and tumour necrosis factor (TNF).

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47
Q

What substances increase endothelial surface adhesion molecule expression?

A

IL-1, endotoxins and TNF.

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48
Q

What is chemotaxis?

A

Locomotion oriented along a chemical gradient. Is how leukocytes find antigens.

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49
Q

What compounds are chemotactic for neutrophils?

A

Bacterial products, complement proteins, cytokines and products produced by neutrophils themselves.

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50
Q

What does histamine do?

A

Vascular dilatation and transient increase in vascular permeability. Basically triggers vascular phase of inflammation.

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51
Q

What is histamine released by and what triggers it?

A

Mast cells, eosinophils, basophils and platelets. Release stimulated by: C3a, C5a and lysosomes proteins (neutrophils).

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52
Q

What are lysosomal compounds and what do they do?

A

Released from neutrophils. May increase vascular permeability and activate complement.

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53
Q

What is serotonin and what does it do?

A

5 hydroxytryptamine. Present in high concentration in platelets. Causes increased vascular permeability.

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54
Q

What are chemokines?

A

Proteins that attract various leukocytes to inflammatory site. Bind to extra cellular matrix components setting up a gradient for chemotaxis.

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55
Q

What are leukotrienes?

A

Synthesised from arachidonic acid, especially in neutrophils and have vasoactive properties. Involved in type 1 sensitivity reactions.

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56
Q

What 4 enzymatic cascade systems are in plasma?

A

Complement system, the kinins, coagulation factors and fibrinolytic system.

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57
Q

How are microorganisms recognised?

A

They become coated in opsonins. Which bind to receptors on leucocytes and enhance phagocytosis.

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58
Q

List some major opsonins.

A

Fc fragment of IgG, C3b complement protein and collectins (plasma proteins which bind to microbial cell walls.

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59
Q

What are the steps in phagocytosis?

A

Recognition, attachment, engulfment and phagolysosome formation. After this neutrophils undergo apoptosis.

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60
Q

What are the two variations of intracellular killing of microorganisms?

A

Oxygen dependent ( oxygen products do killing) and oxygen independent (lysosomes - attack bacterial coat or acidic pH inside phagocytic vacuoles).

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61
Q

What is suppuration?

A

Formation of pus. Causative stimulus almost always infective agent.

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62
Q

What is pus made of?

A

Neutrophils and bacteria/cellular debris.

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63
Q

What is an abcess?

A

Collection of pus surrounded by a membranes and sprouting capillaries, neutrophils and the occasional fibroblast. On draining the cavity collapses and is obliterated by organisation and fibrosis. Deep seated abscesses may drain along a sinus tract or fistula.

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64
Q

What are the benefits of acute inflammation?

A

Dilution of toxins and removal by lymphatics. Antibody migration, fibrin formation impeding microorganism movement, drug and nutrient transport and stimulation of the immune system.

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65
Q

What are the sequelae of acute inflammation?

A

Resolution or suppuration. Suppuration leading to discharge of pus and repair and organisation. This can then lead to fibrosis and chronic inflammation.

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66
Q

What are the cellular steps in acute inflammation?

A

Recognition, recruitment, removal and resolution.

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67
Q

What does resolution mean in relation to inflammation?

A

The complete restoration of the tissues to normal after and episode of acute inflammation.

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68
Q

What factors favour resolution?

A

Minimal cell death, regenerative capacity of organ, rapid destruction of causal agent and rapid removal of fluid and debris by vascular drainage.

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69
Q

What 3 things favour progression from acute to chronic inflammation?

A
  1. Indigestible substances (glass etc.) causing chronic suppuration (foreign body reaction)
  2. deep seated chronic suppuration with delayed drainage causes an abscess. Rigid walls can fail to come together after drainage, pus becomes organised and becomes fibrous scar.
  3. Recurrent episodes of acute inflammation and healing.
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70
Q

What is osteomyelitis?

A

Extremely difficult to eradicate chronic abscess.

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71
Q

What happens in chronic cholecystitis?

A

Replacement of wall by fibrous tissue. Lymphocytes rather than neutrophils predominate.

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72
Q

What are the predominant cells of chronic inflammation?

A

Lymphocytes, plasma cells and macrophages. Usually accompanied by granulation tissue resulting in fibrosis. May be a few eosinophils but neutrophils are scarce.

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73
Q

What are some examples of primary chronic inflammation?

A

Infective agent resistance to phagocytosis and intracellular killing e.g. tb, leprosy and viral infection.
Foreign body reaction to exogenous material e.g. Gout and UC.
Primary granulomatous disease (sarcoidosis).

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74
Q

What is the macroscopic appearance of chronic inflammation?

A

A chronic ulcer - that has breached the mucosa, has a base lined by granulation tissue and the fibrous tissue extends through the muscle layers.
A chronic abcess.
Thickening of the wall of a hollow viscous by fibrous tissue.
Granulomatous inflammation.
Fibrosis - may be the most prominent feature after cell infiltrate has subsided.

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75
Q

What are examples of chronic abcesses?

A

Osteomyelitis and empyema.

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76
Q

How does a monocyte mature?

A

In the bone marrow it goes from a stem cell to a promonocyte and then a monocyte in the blood. Then a macrophage in the tissues.

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77
Q

What is the name of a liver macrophage?

A

Kupfer cell.

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78
Q

What is the name of a lung macrophage?

A

Alveolar macrophage.

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79
Q

What is the name of a connective tissue macrophage?

A

Histiocyte.

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80
Q

What is the name of a bone macrophage?

A

Osteoclast.

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81
Q

What is a mass formed by several distinct cells, mostly macrophages?

A

Giant cell.

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82
Q

What do macrophages do and when are they apparent?

A

Appear late in the acute inflammatory response.

Responsible for clearing tissue debris and produce a range of important cytokines.

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83
Q

Which is more phagocytic a macrophage or a neutrophil?

A

Neutrophil.

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84
Q

What is a granuloma?

A

Aggregate of epithelioid histocytes.

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85
Q

What do histocytes do?

A

They have little phagocytic ability but a secretory function.

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86
Q

What is one of the main causes of granulomatous inflammation?

A

Indigestible materials.

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87
Q

What may augment granulomas?

A

Caseous necrosis or hystocytic giant cells.

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88
Q

What can cause granulomatous disease?

A

Specific infections, endogenous or exogenous foreign material, drugs or unknown e.g. Crohns or sarcoidosis.

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89
Q

Name two angiogenesis factors?

A

vEGF and PDGF.

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90
Q

What populations do cells divide into and can they be replaced?

A

Labile, stable or permanent - only the first two are replaceable.

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91
Q

What is healing?

A

Restitution with no or minimal residual effects.

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92
Q

In what type of injuries does healing by connective tissue fibrosis occur?

A

When Tissue destruction includes loss of parenchymal cells and stromal framework. the non regenerated parenchymal cells are replaced by connective tissue which in time produces fibrosis and scarring.

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93
Q

What are the four steps in repair by connective tissue fibrosis?

A
  1. Angiogenesis.
    2-3. Fibrosis
  2. Tissue remodelling/organisation.
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94
Q

Describe angiogenesis.

A

Basement membrane degradation of the parent vessel.
Migration of endothelial cells towards the angiogenic stimulus.
Endothelial cells proliferate and mature. Central growth inflammation remodels the cells into tubes.
Supportive cells are recruited e.g. Vascular smooth muscle.

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95
Q

Describe fibrosis?

A

Consists of emigration and proliferation of fibroblasts and deposition of ECM by these cells.
Collagen synthesis starts after this, the amount depends on the wound size.

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96
Q

Where does fibrosis occur, during connective tissue repair?

A

Within the granulation tissue framework of new vessels and a loose ECM.

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97
Q

What happens during tissue remodelling and organisation?

A

Granulation tissue is turned into a scar.
The composition of the ECM changes.
Metalloproteinases degrade collagen and other proteins.
The connective tissue framework is remodelled.
Organised are always appears firmer, shrunken and puckered.

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98
Q

What is an ulcer?

A

Local defect or excavation that is produced by sloughing of inflammatory necrotic tissue.

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99
Q

What secretes collagen?

A

Fibroblasts and leukocytes.

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100
Q

What wounds are healed by first intention?

A

Incisional wounds with opposed edges. There is limited cell death but the basement membrane is disrupted.

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101
Q

Describe healing by first intention.

A

Incision fills with blood and a scab forms.
Neutrophils move towards the clot.
The epidermis thickens at the cut edges and epidermal cells migrate along the cut dermis edges to fuse in the midline under the scab.
The neutrophils are replaced by macrophages.
Granulation tissue invades the incision, and collagen fibres bridge it, the epidermis recovers to normal thickness.
2nd week. Proliferation of fibroblasts and collagen accumulation - inflammation virtually disappeared.
1 month - scar made of cellular connective tissue with increased strength.

102
Q

What kind of wound is healed by second intention?

A

Large defect to be filled with lots of tissue loss.

103
Q

What most differentiates first intention from second intention healing?

A

Second intention displays wound contracture.

104
Q

What does wound contracture do?

A

Decreases wound size and is attributed to myofibrils.

105
Q

What does healing by second intention involve?

A

More fibrin and necrotic tissue than first intention and therefore a larger inflammatory reaction. It also involves a much larger amount of granulation tissue.

106
Q

What wound strengths can we expect at different times of healing?

A

1 week = 10%. Third month = 70-80%. Full strength may never be recovered.

107
Q

What is the healing timeline?

A

0-3 days = inflammation.
3 hours - 10 days = granulation tissue
3-30 = days wound contracture
3-100 = collagen accumulation.

108
Q

What local factors affect wound healing?

A

Infection (most important)
Mechanical factors e.g. Early movement.
Foreign bodies.
Size, location and type of wound.

109
Q

What systemic factors affect wound healing?

A

Nutrition, metabolic status, circulatory status and hormones.

110
Q

What hormones affect wound healing?

A

Glucocorticoids are anti-inflammatory but impairs collagen synthesis.

111
Q

What are three pathological aspects of wound repair?

A 
Deficient scar formation (wound dehiscence and ulceration).
Keloid scarring (excessive formation).
Contractures (resulting in deformity).
112
Q

What are pathological wound repair process similar to?

A

Chronic inflammatory responses e.g. UC or RA.

113
Q

What causes pathological wound repair?

A

Persistence of initial inflammatory response, disordered healing, architectural damage and scarring.

114
Q

What are the benefits and drawbacks of scarring?

A

It allows parenchyma to function but may cause dysfunction depending on the size and the site e.g. MI.

115
Q

Describe the four steps of bone fracture repair.

A
  1. Blood fills and surrounds gap, forming a framework for fibroblasts, inflammatory cells and new capillaries.
  2. Organisation of haemostat a with removal of necrotic tissue.clot angiogenesis accompanied by osteoblasts which lay down bone in an irregular pattern.
  3. New bone mass - internal (medullary) and external callus (outside periosteum) splints the bone but must be resorbed. Soft tissue mecenchymal cells differentiate to chondroblasts which lay down cartilage to envelope the fracture site, this then undergoes endochondrial ossification.
  4. Woven bone replace by orderly lamellar bone according to the direction of mechanical stress. The portions not physically stressed are resorbed.
116
Q

Describe healing of neural tissue.

A

CNS cannot regenerate.
Glial cells proliferate in response to injury.
Cut nerve axons degenerate proximally.
If there is good alignment alone may regrow down the previous channel but functional recovery is very unusual.

117
Q

What is amputation neuroma?

A

Poor alignment or amputation. The cut ends still proliferate but produces a disordered tangled mass.

118
Q

What are the outcomes of an injury if the stimulus is promptly destroyed?

A

No or minimal cell necrosis therefore either:
Resolved exudate causing restitution of normal structure.

Or

Exudate organised causing scarring.

119
Q

What is the outcome of an injury to permanent cells where the initial stimulus is not destroyed?

A

Necrosis of cells causing scarring.

120
Q

What is the outcome of an injury to stable or Labile cells where the initial stimulus is not destroyed?

A

Necrosis of cells causing:
If intact framework- regeneration or restitution of normal function.

Or

Framework destroyed - scarring.

121
Q

What 4 types of mechanisms of growth disorders can be reversed?

A

Hyperplasia, hypertrophy , accretionary and atrophy.

122
Q

What is a multiplicative growth disorder?

A

Hyperplasia, which is an increased number of cells, can be physiological or pathological.

123
Q

What is an auxetic growth disorder?

A

Hypertrophy, which is an increase in cell size which can be physiological or pathological.

124
Q

What is an accretionary growth disorder?

A

Increase connective tissue.

125
Q

What is atrophy?

A

Cell size reduction.

126
Q

What is hypoplasia?

A

Reduced size of an organ that never fully developed. Can be a developmental defect e.g. Pulmonary hypoplasia.

127
Q

What is differentation?

A

Acquisition of overt specialised morphology or function.

128
Q

What is metaplasia?

A

Acquired form of altered differentiation. One fully mature cell type changes to another. Can be in response to stress e.g. Barretts. Isn’t neoplastic in itself but can progress to dysplasia or malignancy.

129
Q

How do we maintain tissue homeostasis?

A

Cell division must equal cell loss e.g. Senescence vs proliferation and cell death.

130
Q

What is a Labile cell?

A

Continuously dividing cell.

131
Q

What is a stable cell?

A

Low replicative activity but can divide rapidly when stimulated.

132
Q

What two ways can we increase growth?

A

Shortening of cell cycle times or recruitment of cells from resting or quiescent populations.

133
Q

What is the principal task of the cell cycle?

A

To replicate DNA and segregate it into chromosomally equal daughter cells.

134
Q

What is apoptosis?

A

Programmed cell death.

135
Q

What can inhibit apoptosis?

A

Growth factors, cell matrix component and viral proteins.

136
Q

What can induce apoptosis?

A

Growth factor withdrawal, loss of matrix attachment, viruses, free radicals, radiation and DNA damage.

137
Q

What conditions cause increased apoptosis?

A

AIDS, neurodegenerative diseases and reperfusion injury.

138
Q

What conditions can cause decreased apoptosis?

A

Neoplasia and autoimmune diseases.

139
Q

What is senescence?

A

Growth arrest mediated by telomere length. When length decreases to a certain point, growth increases. Cancer cells bypass this.

140
Q

What is differentiation?

A

Selective expression or repression of genes leading to an altered phenotype.

141
Q

What is neoplasia?

A

Abnormal mass of tissue whose growth exceeds and is uncoordinated with that of normal tissues and persists in an excessive manner after the cessation of the stimulus. It is monoclonal, the mass derives from a single common ancestor.

142
Q

What are the classifications of neoplasia?

A

Benign, malignant and histogenetic.

143
Q

What are the features of benign neoplasia?

A

Resemble normal tissues, are well differentiated, show expansive growth but no invasion (encapsulated). No necrosis. Normal nucleus to cytoplasm ratio. Minimal pleomorphism. Few mitosis figures. Nuclei not hyperchromatic. Diploid and don’t metastasis.

144
Q

What is pleomorphism?

A

Variability in cell size, shape and staining.

145
Q

What are mitotic figures?

A

Cells undergoing mitosis.

146
Q

What is a hyperchromatic nuclei?

A

Highly coloured or excessively stained one.

147
Q

What are the features of malignant neoplasms?

A

Invasive growth, not encapsulated, degree of differentiation is variable, necrosis common, increased N:C. Pleomorphic. Frequent and abnormal mitotic figures. Hyperchromatic nuclei, aneuploid, may metastasise.

148
Q

What are the two types of epithelial tumours and their names?

A

Squamous - squamous papilloma or carcinoma.

Glandular - adenoma or adenocarcinoma.

149
Q

What are the six types of mesenchymal tissues and their names?

A

Fat - lipoma or liposarcoma.
Endothelial - angioma or angiosarcoma.
Chondrocyte - chondroma or chondrosarcoma.
Osteoblast - osteoma or osteosarcoma.
Smooth muscle - leiomyoma or leiomyosarcoma.
Skeletal muscle - rhabdomyoma or rhabdomyosarcoma.

150
Q

What is a malignant tumour of the male germ cells?

A

Seminoma.

151
Q

What is a teratoma?

A

A benign or malignant mass with components resembling derivatives of more than one germ layer. May be quite different from the surrounding tissue e.g. Hair or teeth.

152
Q

What is a hamartoma?

A

Benign focal malformation resembling a neoplasm in its tissue of origin. It grows at the same rate and contains the same cells as surrounding tissues, but grows in a disorganised mass. Often Asymptomatic and undetected.

153
Q

What are key elements in the growth of a tumour?

A

Replication, escape from senescence, evasion of apoptosis, limitless replicative potential, angiogenesis, invasion and metastasis.

154
Q

What is dysplasia?

A

A premalignant process which can be identified in many cells e.g. Big dark nuclei. This results in distorted maturation of cells. They show differences but haven’t yet invaded.

155
Q

What are the different degrees of dysplasia?

A

Mild, moderate and severe/carcinoma in situ.

156
Q

What can sever dysplasia progress to?

A

Carcinoma in situ can progress to invasive malignancy.

157
Q

What is invasive growth and how can this happen?

A

Cells that have detached from the primary tumour. The mass can move by utilising defects or using ameboid movement.

158
Q

How does cancer develop?

A

Invasive growth
Desmoplasia
Angiogenesis
Metastasis.

159
Q

How do groups of cells move?

A

Requires cell to cell adhesion and accumulation. Well differentiated carcinomas do this, they hide the centre cells from the immune system and the outer cells have proteolytic enzymes to allow movement through tissues. heterogeneous cells move together.

160
Q

What is desmoplasia?

A

Creation of tissue stroma through growth of fibrous or connective tissue, it varies between tumours.

161
Q

What kind of desmoplasia tissue is associated with malignant tumours?

A

Fibro-connective tissue, gives cancer its firm craggy feel.

162
Q

Where will a primary CNS tumour most likely spread?

A

Nowhere outwith the CNS.

163
Q

What is the angiogenic switch?

A

Tight physiological control of angiogenesis which is lost in tumours.

164
Q

Describe tumour angiogenesis features?

A

It sustains the mass of tumour cells. The new vessels are abnormal.

165
Q

What are the metabolic features of tumours?

A

They require less O2 and metabolites than normal tissues.

166
Q

What are some key modulators of angiogenesis?

A

Hypoxia, VEGF, FGF, and TNF alpha. Thrombospondin 1 is an endogenous inhibitor.

167
Q

What are the different types of metastasis and what tumours utilise them?

A

Local invasion
Direct implantation e.g. Mesothelioma and chondrosarcoma.
Lymphatic spread - carcinomas.
Blood spread - sarcoma.

168
Q

What are common sites of metastasis?

A

Lymph nodes, lung, liver, bone, brain, adrenal glands and skin.

169
Q

If there is an unusual site of metastasis, what cancers should we consider?

A

Renal, thyroid, and melanoma.

170
Q

What is the hypothesis of cancer spread?

A

The seed and soil hypothesis. Seed is the cancer cell and soil is the metastatic site. Spread is purely mechanical e.g. Through blood, but some tissues are particularly good at arresting cells e.g. Lung and liver.

171
Q

What are MHC class 1 molecules?

A

Found on nearly every uncleared cell. They display fragments of proteins from within cells to Tcells.

172
Q

What are the steps in tumour growth?

A

Normal cell
Transformed cell
Clinal expansion
Tumour progression - collagen, altered MHC cell and hypoxia resistant cell types.
Further tumour progression - new types of cells included e.g. Metastatic and drug resistant.

173
Q

How can we describe tumour progression?

A

The permanent irreversible, qualitative change in one or more characteristic of a neoplasm.

174
Q

What size is the earliest clinically detectable lesion?

A

10^9 cells, 1g - is 30 doublings.

175
Q

What size is an advanced cancer that is incompatible with life?

A

10^12 cells - 1kg - 40 doublings.

176
Q

What are the key elements in the development in cancer?

A 
Self sufficiency from growth signals.
Escape from senescence.
Apoptosis evasion.
Genomic instability.
Epibenthic changes e.g. Histone modification.
Autophagy.
177
Q

What is autophagy?

A

Catabolic mechanism involving degradation of uses essay or dysfunctional cellular components through lysosomes.

178
Q

What is the Warburg effect?

A

Observation that most cancer cells produce energy from a high rate of glycolysis followed by lactic acid formation in cytosol which differs from normal cells. Means they don’t need as much O2. Malignant glycolysis rates are up to 200x normal cells.

179
Q

What are some causes of cancer? And what types of cancer can they cause?

A 
Hydrocarbons - scrotal.
aniline dyes - bladder.
wood dust -nasal sinus cancer,
sunlight - melanoma.
EBV - nasopharyngeal and hodgkins.
HPV - cervical and head and neck cancers.
180
Q

What are some risk factors for oral cancers?

A

Smoking, alcohol, HPV, immunosuppression, previous max fax cancer, oral lesions and sun exposure.

181
Q

How does radiation cause cancer?

A

Cause oxidative stress and free radical production.

Increased mutational load and nuclear changes in exposed cells.

182
Q

What are the steps of chemical carcinogenesis?

A

Procarcinogen changed to a carcinogen by metabolic activation.
Carcinogen binds to DNA.
When initiated it causes DNA damage.
This results in either:
No repair in a viable cell which results in a transformed cell.
A non viable cell which then undergoes apoptosis.
DNA repair which returns the cell to normal.

183
Q

What does chemical carcinogenesis require?

A

Initiation and promotion which stimulates proliferation.

184
Q

Name two cancer types that ‘cancer families’ cause?

A

Retinoblastoma and familial adenomatous polyposis coli.

185
Q

What kind of genetic predispositions to cancer are there?

A

Chromosome breakage syndromes.
Bloom syndrome.
Ataxia telangiectasia.
Defective DNA repair.

186
Q

Give an example of a chromosome breakage syndrome?

A

Fanconis anaemia - inherited bone marrow failure.

187
Q

What is Bloom’s syndrome?

A

Sufferers are short, sun sensitive and predisposed to cancer.

188
Q

What is ataxia telangiectasia?

A

Rare neurodegenerative disease causing severe disability.

189
Q

Give two examples of genetic problems with DNA repair?

A

Xeroderma pigmentosa- can’t repair uv light damage.

Hereditary nonpolyposis colorectal cancer (HNPCC).

190
Q

Give an example of an RnA viral carcinogen?

A

Rous sarcoma.

191
Q

How to RNA viral carcinogens work?

A

They create Proto-oncogenes and the resultant protein may be termed an oncogene.

192
Q

What are proto-oncogenes?

A

Normal gene that becomes an oncogene due to mutations or increased expression.

193
Q

Give examples of DNA viral carcinogens.

A

SV40, HPV and HBV etc.

194
Q

How do DNA viral carcinogens work.

A

Contain proteins that bind to and inactivate host proteins.

195
Q

What are 3 classical oncogenes?

A

PDGF, EGFR and Ras.

196
Q

What is PDGF?

A

Platelet derived growth factor. Has a significant role in angiogenesis.

197
Q

What is EGFR?

A

Epidermal growth factor receptor.

198
Q

What is Ras?

A

Family of proteins involved in intracellular signalling that is present in all cell lineages. When switched on it switches on other cells involved in growth, differentiation and survival. So can cause overactive signalling even without external stimuli.

199
Q

What ways can tumour suppressors be inactivated?

A

Both alleles lost through deletion or point mutation. Or the protein could be degraded by a virus etc.

200
Q

What is P53?

A

It is the guardian of the genome, it is activated by cell stress. Is a transcription factor that regulates gene expression. It regulates transcription of down stream target genes causing: cell cycle arrest or apoptosis.

201
Q

Give some examples of tumour suppressor genes?

A

P53, pRB, APC, BRCA-1 etc.

202
Q

What do classical oncogenes do?

A

Stimulate proliferation, inhibit apoptosis and are dominant.

203
Q

What do tumour suppressors do?

A

Inhibit proliferation, stimulate apoptosis and are recessive.

204
Q

What is genomic instability?

A

Defective DNA repair mechanisms.

205
Q

What are epigenetic changes?

A

Reversible, heritable altered gene expression without mutation.

206
Q

What is involved in molecular carcinogenesis?

A

Involves multiple genetic abnormalities and both classical oncogenes and tumour suppressors. The order of the accumulation is less important than the number of abnormalities.

207
Q

What is the proposed path of colorectal carcinogenesis?

A 
Normal mucosa
Hyper plastic mucosa
Early adenoma
Adenocarcinoma
Metastatic disease.
208
Q

What are some screening tests for cancers?

A

FOB - fecal occult blood testing.
Serum PSA - prostate serum antigen.
Cyto- and histopathology tests.

209
Q

What are the three levels of risk for breast cancer and what gives them that level of risk?

A 
Low risk - person whose mother had great cancer at 70.
Medium risk (10 year risk is 3%) - mother and sister had cancer by the age of 45.
High risk (10 year risk is 8%) - with BRCA 1 mutation.
210
Q

What is a paraneoplastic syndrome?

A

Is a disease or symptom that is a consequence of cancer but not due to the direct present of a tumour e.g. Hypercalcaemia. Occurs in 10% of patients, and may be the the first sign of underlying cancer. They can be clinically significant and lethal in themselves and may mimic Mets and mess up staging.

211
Q

What kind of presentation when we get when cancer have infiltrated or destroyed tissues?

A 
Ulceration - bleeding.
Narrowed lumen - strider dysphasia or jaundice etc.
Raised ICP, epilepsy or CVA.
Effusions ascites etc.
Bone destruction.
212
Q

What does Cushings cause and what types of cancer is it associated with?

A

Secretes ATCH/ACTH like substance. Associated with small cell lung cancer.

213
Q

What kind of cancer is inappropriate ADH secretion associated with?

A

Small cell lung cancer.

214
Q

What kind of cancer is hypercalcaemia associated with?

A

Squamous lung cancer or T-cell leukaemia/lymphoma.

215
Q

What does myasthenia cause and what types of cancer is it associated with?

A

Bronchogenic carcinoma. Is is an immunologic response e.g. Eaton lambert syndrome.

216
Q

What does acanthosis nigricans cause and what types of cancer is it associated with?

A

Immunologic problem that secretes EGF and is associated with gastric carcinoma.

217
Q

What type of cancer isHypertrophic osteoarthropathy associated with?

A

Bronchogenic carcinoma.

218
Q

What does nephrotic system cause and what types of cancer is it associated with?

A

Is an immune complex with tumour antigens. Associated with colorectal cancer and Hodgkin’s disease.

219
Q

What causes polycythaemia and what kind of cancer is it associated with?

A

Erythropoetin. Associated with renal carcinoma.

220
Q

What kind of cancer is venous thrombosis associated with?

A

Pancreatic carcinoma.

221
Q

What kind of cancer is nonbacterial thrombotic endocarditis associated with and why?

A

Advanced cancers due to hypercoagulability.

222
Q

What factors do we look at to arrive at a cancer prognosis?

A

Type, grade, stage and comorbidities.

223
Q

What is a tumour grading?

A

Histological assessment of how well differentiated cells are. Poorly differentiated tumours have a worse prognosis.

224
Q

What is a tumour stage?

A

Clinical and histological assessment of advancement and infiltration.

225
Q

What kind of staging do we use in colorectal cancer and what are the stages?

A 
Dukes staging.
A - confined to wall with no LNM.
B - penetrates wall with no LNM.
C - LNM.
D - metastatic disease.
226
Q

What is TNM staging?

A

Tumour, nodes and metastasis.

227
Q

What are the T stages of colorectal cancer?

A

T1 - invasion of the sub mucosa.
T2 - invasion of the muscularis propria.
T3 - invasion of subserosa and non-peritoneal pericolic and pararectal tissues.
T4 - invasion of adjacent organs or perforation of visceral peritoneum.

228
Q

What is the N staging in colorectal cancer?

A

N0 - no LNM.
N1 - 1-3 LNM.
N2 - 4 or more LN.

229
Q

What is M staging?

A

M0 - no metastatic disease.

M1 - distant metastasis.

230
Q

What are the clinical stages of colorectal cancer?

A

I = T1/T2, N0 and M0.
IIA - T3, N0 and M0. IIB - T4, N0 and M0.
IIIA - T1/T2, N1 and M0. IIIB - T3/T4, N1 and M0.
IIIC - any T, N2 and M0.
IV- any T, any N and M1.

231
Q

What tool do we use for prognosis of breast cancer?

A

Nottingham prognostic index.

232
Q

How do we calculate the Nottingham prognostic index?

A

0.2 x size (in cm) + N score + G score.
N score = nodes involved. None = 1, 1-3 get a score of 2 and more than 3 get a score of 2.
G score = grade either 1,2 or 3.

233
Q

What is an indolent tumour?

A

A slow growing one.

234
Q

What is a metabolic disorder?

A

Biochemical abnormality, may be deleterious. Also causes target organ damage, usually by accumulation of injurious agent.

235
Q

What are the features of type 1 diabetes?

A

Young onset, may be of normal weight, reduced insulin levels. Anti islet antibodies attach to islet B cells on the pancreas and T cells attach to them and destroy them. Linked to Hla.

236
Q

What does Hla stand for?

A

Human leukocyte antigen.

237
Q

What is type 2 diabetes?

A

Onset over 30 usually. Overweight people with normal or decreased insulin. No islet antibodies, no DKA, no HLA linkage. Target cells are unresponsive to insulin.

238
Q

What are some complications of DM?

A

DKA, hypos and lactic acidosis. Macroangiography (version of atheroma). Diabetic neuropathy, retinopathy and cataracts.

239
Q

What is an embolism?

A

Blockage of a vessel by an embolis, which has moved from its site of origin to lodge In a distant vessel.

240
Q

What is a thrombus?

A

Solid mass of blood constituents formed within a vessel.

241
Q

What is virchows triad?

A

Vessel wall.
Flow.
Constituents.

242
Q

How are thrombus formed?

A

Platelets the coagulation cascade and fibrinolytic cascade.

243
Q

What are platelets?

A

Anucleated cell fragments with adherence properties. Have pro coagulant contents and growth factors.

244
Q

What is infarction?

A

Zonal necrosis due to sudden occlusion of blood supply. Necrosis due to lack of nutrients and O2.

245
Q

What is ischaemia?

A

Restriction of blood flow to a tissue causing hypoxia and possibly cellular damage. Nutrient impairment causes impairment of function. Tissue responds to ischaemia by first reducing function.

246
Q

What is a fatty streak?

A

Grossly visible irregular yellow white discolouration on the luminal surface of an artery.

247
Q

What is cell differentation?

A

How closely it resembles the tissue of origin e.g. Lipoma looks like a mature fatty tissue cell.

248
Q

Why do cancer cells N:C ratio change?

A

Nuclei become large and dark due to having more chromosome copies.

249
Q

What is apoptotic debris and where do we see it?

A

In cancer masses as proper cells are trying to kill of the cancer cells.

250
Q

How do normal cells grow differently from cancer cells in culture?

A

Normal cells grow in a mono layer whereas cancer cells pile up.

251
Q

What is parenchyma?

A

The functional part of tissues as opposed to its underlying groundwork e.g. Stroma.

252
Q

What does aetiology mean?

A

The causative element of a disease e.g. Smoking in COPD.

1st Year Medicine (64 decks)

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