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Sandra Phase 2a > Pathology- Introduction to Clinical Sciences > Flashcards

Pathology- Introduction to Clinical Sciences Flashcards

1
Q

What is atherosclerosis?

A

A disease characterised by the formation of atherosclerotic plaques in the intima of large and medium-sized arteries, e.g. coronary arteries

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2
Q

Where does atherosclerosis occur?

A

Only occurs in high-pressure arteries

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3
Q

What is visible in atherosclerotic plaques?

A

Lipids- mainly cholesterol
Fibrous Tissue
Lymphocytes

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4
Q

Risk factors of atherosclerosis (6)

A

Cigarette smoking
High blood pressure
Diabetes
Hyperlipidaemia
Male sex
Increasing age

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5
Q

Complications of atherosclerosis
(6)

A

Cerebral infarction
Carotid atheroma, leading to TIAs
Myocardial Infarction
Aortic aneurysm (can cause sudden death)
Peripheral vascular disease
Gangrene

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6
Q

Most important risk factor in atherosclerosis

A

Hypercholesterolaemia

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7
Q

Preventative Measures for atherosclerosis (5)

A

Smoking cessation
Blood pressure control
Weight reduction
Low-dose aspirin 🡪 inhibits the aggregation of platelets
Statins 🡪 cholesterol-reducing drug

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8
Q

What is apoptosis

A

Programmed cell death

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9
Q

Define genetic disease

A

a disease that occurs primarily from a genetic abnormality

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10
Q

Define inherited disease

A

caused by an inherited genetic abnormality

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11
Q

What is a single gene disorder

A

Abnormality of a single gene causes a disease

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12
Q

How can a single gene disorder be classified

A

Dominant
Recessive

Further classified as autosomal or sex-linked.

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13
Q

What is an example of a single-gene disorder
How is it caused?

A

sickle cell anaemia

caused by a point mutation in the beta-globin chain of haemoglobin which always produces an abnormal haemoglobin which causes red blood cells to deform when oxygen saturation is low

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14
Q

What is a polygenic gene disorder

A

genetic disease which is the result of the interaction of several different genes (usually on different chromosomes)

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15
Q

Give an example of a polygenic gene disorder

A

Breast cancer

The genes BRCA1 and BRCA2 have a large individual effect on breast cancer.
Most breast cancer risk is composed of incremental rises in risks by tens to hundreds of apparently unrelated genes, even when there is a strong family history.

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16
Q

Define congenital disease

A

A disease someone is born with

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17
Q

Congenital diseases will typically be ..

A

genetic

But it can also be acquired (occurs after birth). This disease is often due to environmental factors, but it may have a strong genetic background.

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18
Q

Give an example of autosomal recessive disease

A

cystic fibrosis
sickle cell anaemia

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19
Q

Classifications of growth & development disorders

A

Congenital
Acquired
Multifactorial disease

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20
Q

How is congenital disease further subdivided?

A

Genetic: can be inherited or spontaneous
Non-genetic: e.g environmental

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21
Q

Examples of congenital spontaneous genetic disease

A

Down’s syndrome - Trisomy 21; mental retardation, flattened facial profile & short hands

Edwards’ syndrome - Trisomy 18; ear, jaw, cardiac & renal abnormalities

Patau’s syndrome - Trisomy 13; microcephaly, cleft palate & abnormal ears

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22
Q

Examples of congenital inherited genetic disease (5)

A
  • Cystic fibrosis - autosomal recessive
  • Sickle cell anaemia - autosomal recessive
  • Familial adenomatous polyposis - autosomal dominant
  • Colour blindness - X-linked, men more susceptible
  • Huntington’s - present at birth but only manifests later in life
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23
Q

Example of non-genetic congenital environmental disease

A

foetal alcohol syndrome

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24
Q

Examples of acquired disease

A
  • Tuberculosis
  • Lung cancer
  • Bone fracture
  • AIDS
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25
Q

What is the response of a cell to increase functional demand?

A

The response of an individual cell to increased functional demand is to increase tissue or organ size by; hypertrophy, hyperplasia or a combination of both

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26
Q

Define hypertrophy

A

Increase in cell size without cell division

i.e increase in the size of a tissue caused by an increase in the size of the constituent cells

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27
Q

Define hyperplasia

A

increase in the size of a tissue caused by an increase in the number of the constituent cells

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28
Q

Define atrophy

A

decrease in the size of a tissue caused by a decrease in the number of constituent cells or a decrease in their size

-often done by a mechanism called apoptosis
-occurs naturally

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29
Q

Define metaplasia

A

change in differentiation of a cell from one fully-differentiated type to a different fully-differentiated type

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30
Q

What describes an adaptive response to injurious stimuli?

A

Metaplasia

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31
Q

Define dysplasia

A

imprecise term for the morphological changes seen in cells in the progression to becoming cancer

Also refers to a lack of development

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32
Q

In what cells does hyperplasia not occur? Why?

A

Myocardial and nerve cells
As they cannot divide

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33
Q

Where does muscle hypertrophy occur?

A

Skeletal muscle of the limbs (response to increased muscle activity)

Left ventricle (response to sustained outflow resistance)

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34
Q

When does hypertrophy of uterine smooth muscle occur

A

During puberty and pregnancy - stimulated by oestrogens

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35
Q

What happens to people living at high altitudes regarding hyperplasia?

A

Increased production of the growth factor erythropoietin stimulates hyperplasia of bone marrow cells that produce red blood cells in people living at high altitudes

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36
Q

Which hyperplasia can either be benign or cancerous

A

Hyperplasia of prostate smooth muscle

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37
Q

When does metaplasia occur?

A

response to alterations in the cellular environment

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38
Q

Examples of metaplasia?

A

Smokers: Ciliated respiratory epithelium of the trachea and bronchi 🡪 squamous epithelium

Epithelium of the ducts of the salivary glands and pancreas and bile ducts in the presence of stone 🡪 squamous epithelium

Barrett’s oesophagus: Squamous epithelium of the oesophagus due to prolonged exposure to stomach acid 🡪 columnar epithelium.

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39
Q

How does ageing occur?

A

Occurs within dividing cells: telomeres get shorter after each cell division – limiting the amount of cell division that can occur

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40
Q

Non-dividing cells:

A
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41
Q

What results in dermal elastosis

A

Accumulation of abnormal elastic in the dermis of the skin

This is the result of prolonged/ excessive sun exposure – photoaging

UV light causes protein cross-linking

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42
Q

What causes osteoporosis

A

Caused by loss of coupling in the bone remodelling process 🡪 increased bone resorption or deceased bone formation due to a lack of oestrogen (hence why so many women are affected after menopause)

Bone matrix is mineralised as normal, but the trabeculae are thinned – resulting in fractures from minor trauma

Liberates calcium – leading to hypercalciuria – the risk of renal stone formation

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43
Q

What happens when you age? Pathology of ageing (6)

A

Dermal elastosis
Osteoporosis
Cataracts
Senile dementia
Sarcopenia
Deafness

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44
Q

How do people become deaf?

A

Hair cells cannot divide/regenerate – hence once damaged cannot recover.

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45
Q

What causes sarcopenia?

A

Decreased growth hormone
Decreased testosterone
Increased catabolic cytokines.

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46
Q

What causes senile dementia?

A

Plaques and neurofibrillary tangles occur in the brain.

Due to brain atrophy since NERVE CELLS CAN NOT REPLICATE

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47
Q

What causes cataracts

A

Result of the formation of opaque proteins within the lens- results in a loss of lens elasticity

UV-B light causes protein cross-linking

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48
Q

What can osteoporosis cause?

A

Osteopenia

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49
Q

What cells have the greatest potential for division?

A

Foetal cells

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50
Q

What factors influence ageing

A

Genetic and environmental factors

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51
Q

Define Inflammation

A

the local physiological response to tissue injury

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52
Q

What are the 3 aims of inflammation?

A
  1. To bring defence cells (immune cells) to the area.
  2. Inactivate and/or destroy invaders
  3. Begin the repair
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53
Q

How is inflammation clinically denoted as

A

by the suffix -itis

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54
Q

Benefits of inflammation

A

Destruction of invading microorganisms

The walling off of an abscess cavity, thus preventing the spread of infection

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55
Q

Problems with inflammation

A

An abscess in the brain would act as a space-occupying lesion compressing vital surrounding structures.

Fibrosis resulting from chronic inflammation may distort the tissues and permanently alter their function.

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56
Q

What are the signs of acute inflammation

A

Heat
Pain
Redness
Swelling

These four signs combine to cause the fifth sign, which is the temporary loss of function.

These signs are produced by rapid vascular response

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57
Q

2 different types of leukocytes

A

Granulocyte
Agranulocyte

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58
Q

What cells are classified as granulocytes

A

Neutrophils
Eosinophils
Basophils
Mast cells

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59
Q

What cells are classified as agranulocytes

A

Lymphocytes
Monocytes

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60
Q

What can monocytes differentiate into?

A

Macrophage
Dendritic cells

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61
Q

Cells involved in inflammation

A

Neutrophil polymorphs
Macrophages
Lymphocytes
Endothelial cells
Fibroblasts

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62
Q

What are neutrophil polymorphs

A

First on the scene of acute inflammation

Cytoplasmic granules full of enzymes that kill bacteria

Usually die at the scene of inflammation.

Release chemicals that attract other inflammatory cells, such as macrophages

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63
Q

What properties do macrophages possess

A

Phagocytic properties

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64
Q

Are macrophages long-lived or short-lived cells

A

Long-lived cells (weeks to months)

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65
Q

What are macrophages involved in

A

Involved in inflammation

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66
Q

How are macrophages named?

A

Named according to the location:

Kupffer cell (liver)
Melanophage (skin)
Osteoclast (bone)
Microglial cell (brain)
Alveolar/ peritoneal macrophages

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67
Q

Describe macrophages

A

Ingest bacteria and debris

May carry debris away.

May present antigens to lymphocytes.

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68
Q

Are lymphocytes long-lived or short-lived

A

Long-lived cells (years)

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69
Q

What are lymphocytes involved in

A

Involved in inflammation

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70
Q

Describe lymphocytes

A

Produce chemicals which attract other inflammatory cells

Immunological memory for past infections and antigens

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71
Q

What are endothelial cells

A

Line capillary blood vessels in areas of inflammation

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72
Q

Describe endothelial cells

A

Become sticky in areas of inflammation, so inflammatory cells adhere to them

Become porous to allow inflammatory cells to pass into tissues

Grow into areas of damage to form new capillary vessels

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73
Q

4 changes in local blood vessels during inflammation

A
  1. Increased diameter
  2. Increased permeability
  3. Endothelial cells become ‘activated.’
  4. Clotting
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74
Q

Stages of inflammation

A
  1. increased vessel permeability
  2. fluid exudate
  3. cellular exudate
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75
Q

Stae the 4 outcomes of inflammation

A

resolution
supporation
organisation
progression

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76
Q

Neutrophil action involved in inflammation

A

margination
adhesion
emigration
diapedesis

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77
Q

Describe fibroblasts

A

Long-lived cells
Form collagen in areas of chronic inflammation and repair

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78
Q

Consequences of atherosclerosis

A

Vessel thickening 🡪 narrowing of lumen 🡪 poor tissue perfusion

Inelasticity of vessels 🡪 predisposition to vessel rupture and haemorrhage

Alterations in vascular endothelium 🡪 increased predisposition to thrombosis

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79
Q

Name the different autopsies

A

Hospital autopsies: 10% of all UK autopsies
Medico-legal autopsies: 90% of all autopsies in the UK

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80
Q

How can medico-legal autopsies be further subdivided

A

Coronial autopsies – standard
Forensic autopsies – deaths involving crime

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81
Q

What are hospital autopsies useful for?

A

Useful for:
Audit
Teaching
Governance
Research

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82
Q

Types of death referred to coroners

A

Presumed natural

Peri/postoperative deaths

Presumed unnatural

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83
Q

What is considered a presumed natural death

A

Cause of death not known
Not seen by a doctor with recent illness (last 14 days)
Presumed iatrogenic

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84
Q

What is considered a presumed iatrogenic death

A

Anaesthetic deaths
Abortion
Complications of therapy

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85
Q

What is considered a presumed unnatural death

A

Accidents
Industrial death
Suicide
Unlawful killing (murder)
Neglect
Custody deaths

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86
Q

Where do referrals come from?

A

doctors (GMC guidance – no statutory duty to refer),

registrar of BDM (statutory duty to refer)

relatives

police

pathological technicians

other properly interested parties.

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87
Q

Coroners Act 1988

A

Allows coroner to order an autopsy where death is likely due to natural causes to obviate the need for an inquest.

Allows coroner to order an autopsy where death is clearly unnatural, and an inquest will be needed

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88
Q

Coroners Rules 1984

A

Autopsy as soon as possible

By a pathologist with suitable qualifications and experience

Report findings promptly only to the coroner

Autopsy only on appropriate premises

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89
Q

Amendment Rules 2005

A

The pathologist must tell the coroner precisely what materials have been retained.

The coroner authorises retention and sets a disposal date.

The coroner informs the family of the retention

The family has choices;
Return material to family
Retain for research/teaching

Respectful disposal

The coroner informs the pathologist of the family’s decision.

Pathologists to keep a record

The autopsy report must declare retention and disposal

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90
Q

Coroners and Justice Act 2009

A

The coroner can now defer opening the inquest and instead launch an investigation

Enshrines a system of medical examiners

Little practical change to the pathologist

Inquests now have conclusions, not verdicts

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91
Q

Human Tissue Act 2004

A

Autopsies are only to be performed on licensed premises

License holder

Consent from relatives for any use of tissue retained at autopsy if not subject to coronial legislation or retained for criminal justice purposes

Public display requires consent from the deceased.

Penalties include up to 3 years of imprisonment and/or a fine for not following the human tissue act.

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92
Q

laws related to autopsies

A

The Coroners Act 1988
Coroners Rules 1984
Amendment Rules 2005
Coroners and Justice Act 2009
Human Tissue Act 2004

93
Q

What is the coronial autopsy

A

A systematic scientific examination that helps the coroner determine who the deceased was, when and where they died and how they came about their death

94
Q

Most deaths will prove to be from

A

natural causes

95
Q

By what are autopsies regulated by

A

legislation

96
Q

How are autopsies performed

A

on the instruction of a Medico-legal authority

97
Q

Causes of acute inflammation (5)

A
  1. Physical events e.g trauma, heat, cold, UV light, radiation
  2. Irritant and corrosive chemical substances e.g. acids and alkalis

3.Microbial infections

4.Immune-mediated hypersensitivity reactions e.g hay fever

5.Tissue necrosis e,g ischaemia resulting in myocardial infarction

98
Q

Causes of chronic inflammation (4)

A

Develops as a primary response to 🡪

microorganisms resistant to phagocytosis or intra-cellular mechanisms e.g TB

Endogenous/exogenous foreign bodies

Some autoimmune disease

Primary granulomatous disease

99
Q

When does inflammation become chronic?

A

Over a long period of time with simultaneous tissue destruction and attempted repair

May occur secondary to acute inflammation due to the persistence of the causative agent

100
Q

Comparison of acute and chronic inflammation

A
101
Q

Sequence of inflammation

A
102
Q

What is the characteristic cell recruiting cells in acute inflammation

A

Neutrophil polymorph

103
Q

Define resolution (acute inflammation)

A

complete restoration of the tissues to normal after an episode of acute inflammation

104
Q

Define suppuration

A

formation of pus: a mixture of living, dying and dead neutrophils and bacteria, cellular debris and globules of lipid

105
Q

Define organisation

A

tissue replacement by granulation tissue as part of the process of repair.

106
Q

What does acute inflammation response involve

A
  1. Changes in vessel calibre and flow
  2. Increased vascular permeability and formation of the fluid exudate
  3. Formation of the cellular exudate – emigration of the neutrophil polymorphs into the extravascular space
107
Q

Example of acute inflammation

A

acute appendicitis 🡪

Unknown precipitating factor
Neutrophils appear
Blood vessels dilate
Inflammation of the serosal surface occurs
Pain felt
The appendix is either surgically removed or inflammation resolves, or the appendix bursts with generalised peritonitis and possible death

108
Q

Example of chronic inflammation

A

tuberculosis 🡪

No initial acute inflammation
Mycobacteria ingested by macrophages
Macrophages often fail to kill the mycobacteria
Lymphocytes appear
Macrophages appear
Fibrosis occurs

109
Q

Define granulomas

A

a collection of epithelioid histiocytes (macrophages)

110
Q

What do granulomas all secrete, and what do they act as?

A

ACE act as a blood marker

111
Q

Define Granulation tissue

A

an important component of healing and comprises small blood vessels in a connective tissue matrix with myofibroblasts

112
Q

What can be used to treat inflammation, and how does it work?

A

Ibuprofen inhibits prostaglandins synthase

Prostaglandins = chemical mediators of inflammation.

113
Q

Define resolution (healing and repair)

A

Initiating factor removed
Tissue undamaged or able to regenerate

114
Q

An organ that can repair and heal (lung-related)

A

Lobar pneumonia 🡪

It affects a lobe of the lung rather than the whole thing (bronchopneumonia)
Alveoli filled with neutrophil polymorphs (acute inflammation) rather than air
Pneumocytes that line the alveoli can regenerate so the lung can be regenerated – the pneumocytes divide and reline the alveoli.

115
Q

Summary of skin wound: abrasions

A

Normal skin 🡪 abrasion 🡪 scab formed over surface 🡪 epidermis growing out from adnexa, produced by scab 🡪 thin confluent epidermis 🡪 final epidermal regrowth

116
Q

Example of how skin may heal by the first intention

A

Cut

117
Q

Example of how skin may heal by second intention

A

Ulcer

118
Q

Summary of Incised skin wounds: healing by 1st intention

A

1st intention – can suture up the cut
Incision 🡪 exudation of fibrinogen 🡪 weak fibrin join 🡪 epidermal regrowth, and collagen synthesis 🡪 strong collagen join

119
Q

Summary of tissue loss: healing by 2nd intention

A

A tissue loss injury or another reason that the wound margins are not apposed requires another mechanism for repair.

You can’t bring the skin edges together. The cut is too deep.

Loss of tissue 🡪 granulation tissue 🡪 organisation 🡪 early fibrous scar 🡪 scar contraction.

Phagocytosis to remove any debris

Granulation tissue to fill in defects and repair specialised tissues lost.

Epithelial regeneration to cover the surface

120
Q

Describe repair (healing and repair)

4 components

A

Initiating factor still present
Tissue damaged and unable to regenerate
Replacement of damaged tissue by fibrous tissue
Collagen produced by fibroblasts

121
Q

Examples of wound repair

A

Heart after myocardial infarction
Brain after cerebral infarction (fibrosis in the brain -> gliosis)
Spinal cord after trauma

122
Q

Cells that regenerate

A

Hepatocytes
Pneumocytes
All blood cells
Gut epithelium
Skin epithelium
Osteocytes – help remodel bone fractures

123
Q

Cells that don’t regenerate

A

Myocardial cells
Neurones

124
Q

Define organisation (healing and repair)

A

The organisation is the process whereby specialised tissues are repaired by forming mature fibrovascular connective tissue.

It occurs through the production of granulation tissue and the removal of dead tissue by phagocytosis.

125
Q

What is granulation tissue

A

repair phenomenon

Loops of capillaries supported by myofibroblasts which actively contract to reduce wound size; this may result in a structure later.

126
Q

Why are blood clots rare

A

Laminar flow – cells travel in the centre of arterial vessels and don’t touch the sides

Endothelial cells that line vessels are not ‘sticky’ when healthy

127
Q

What prevents us from bleeding to death

A

Clot-forming cells and proteins are present in the blood to stop us bleeding to death if we cut or scratch ourselves

128
Q

Define thrombus

A

solid mass of blood constituents formed within an intact vascular system during life

129
Q

What is the Virchows triad

A

Factors that predispose any blood vessel to thrombosis:

Change in the vessel wall
Change in blood flow
Change in blood constituents

130
Q

What drug reduces the risk of thrombosis

A

Low-dose aspirin inhibits platelet aggregation.

131
Q

Define embolism

A

the process of a solid mass in the blood being carried through the circulation to a place where it gets stuck and blocks the vessel

132
Q

Define embolus

A

mass of material in the vascular system able to become lodged within a vessel and block it

133
Q

Causes of embolus

A

Usually caused by a part of a thrombus that has broken off and circulates in the blood stream (only small vessels can become blocked).

Less common causes are:
Air (pressurised systems of intravenous fluids/ bloods)
Tumour
Amniotic fluid (rare in pregnant women)
Fat (severe trauma with fractures)

134
Q

Example of thrombus

A

When a thrombus forms in an artery, such as in the heart or brain, it is called an arterial thrombosis

135
Q

What happens when embolus enters venous system

A

will travel to the vena cava and lodge in the pulmonary arteries. The lungs then act as a filter for venous emboli, because the blood vessels split down to capillary size, which is too small for the embolus to travel through

136
Q

What happens when embolus enters arterial system

A

can travel anywhere downstream of its entry point

137
Q

Reduction in blood flow can result in

A

Ischaemia
Infarction
End artery supply

138
Q

Define ischaemia

A

reduction of blood flow to a tissue without any other implications

139
Q

Define infarction

A

reduction of blood flow to a tissue that is so reduced that it cannot even support mere maintenance of the cells in that tissue so they die

140
Q

Define end artery supply

A

An organ that only receives blood supply from one artery

141
Q

Why are end arterial supplies problematic when a thrombus forms

A

because the whole blood supply to that organ is cut off leading to infarction

142
Q

What organs survive if a thrombus occurs in one arterial supply and why?

A

multiple arterial supplies

Pulmonary arteries and bronchial arteries supplying the lungs
Portal vein and hepatic artery supplying the liver
Some parts of the brain – the circle of Willis

143
Q

What is atheroma

A

Degeneration of the walls of the arteries is caused by accumulated fatty deposits and scar tissue, leading to circulation restriction and risk of thrombosis.

The fatty material forms deposits in the arteries.

144
Q

Apoptosis in disease

A

cancer: lack of apoptosis – mutated p53 gene producing faulty p53 protein

HIV: too much apoptosis – kills the antibodies in the blood so the body can’t defend itself.

145
Q

Apoptosis can be triggered by

A

DNA damage
Single-strand break
Base alteration
Cross-linkage

146
Q

Mechanism of apoptosis

A

Initiation: Intrinsic/Extrinsic/Cytotoxic
Execution
Phagocytosis

147
Q

Define Carcinogenesis

A

the transformation of normal cells to neoplastic cells through permanent genetic alterations or mutations

148
Q

What does carcinogenesis apply to

A

malignant neoplasms

149
Q

Oncogenesis refers to

A

same process only it applies to malignant or benign tumours

150
Q

Is carcinogenesis a multi-step process

A

Yes

151
Q

Define Carcinogens

A

Agents known or suspected to cause tumours

  • Act on DNA i.e. are mutagenic
152
Q

Carcinogenic vs Oncogenic

A

Carcinogenic = cancer causing
Oncogenic = tumour causing

153
Q

Problems with identification of carcinogens

A

The latent interval may last decades
Complexity of environment
Ethical constraints

154
Q

Epidemiological evidence of carcinogensis

A

Hepatocellular carcinoma
-Uncommon in UK/USA
-Common in areas with ↑ Hepatitis B/C and mycotoxins

Oesophageal carcinoma
-↑↑ incidence in Japan, China, Turkey and Iran
-? Dietary factors (Linhsien chickens)

155
Q

Occupational/ behavioural risks of carcinogensis

A
  • Lung cancer – strong association with smoking
  • Bladder cancer – increased incidence in aniline dye and rubber industries
  • Scrotal cancer – increased incidence in chimney sweeps
156
Q

Direct evidence of carcinogenesis

A

Thorotrast
Thyroid irradiation

157
Q

Experimental evidence of carcinogenesis

A

Incidence of tumours in laboratory animals
Cell/tissue cultures
Mutagenicity testing in bacterial cultures

158
Q

Issues with experimental evidence of carcinogenesis

A

Animals/cultures may metabolise agents differently from humans

The bacterial mutation may not = carcinogenicity

159
Q

Classes of carcinogens

A

Chemical
Viral
Ionising and non-ionising radiation
Hormones, parasites and mycotoxins
Miscellaneous

160
Q

Describe Chemical carcinogens

A

o No common structural features
o Some act directly
o Most require metabolic conversation from pro-carcinogens to ultimate carcinogens
o Enzyme required may be ubiquitous or confined to certain organs

161
Q

Chemical carcinogens and corresponding tumours

A
162
Q

Radiant energy carcinogens

A

Exposure to UVA or UVB
Ionising radiation
Long term effect

163
Q

Where would you find radiant energy carcinogens and related cancer

A

Skin cancer in radiographers
Lung cancer in uranium miners
Thyroid cancer in Ukrainian children

164
Q

Biological agents carcinogens

A

Hormones
Mycotoxins
Parasites

165
Q

Miscellaneous carcinogens include

A

Asbestos
Metals

166
Q

Host factors for developing cancer

A

Ethnicity:
Decreased skin cancer in black people (melanin)
Increased oral cancer in India, SE Asia (reverse smoking)

Diet / Lifestyle

Constitutional factors - age, gender etc:
Inherited disposition
Age – incidence increases with age
Gender – breast cancer F:M = 200 (more common in women)

Premalignant lesions:
Identifiable local abnormality associated with increased risk of malignancy at that site, e.g. colonic polyps, undescended testis, cervical dysplasia

Transplacental exposure

167
Q

Overview of how healthy cells are placed with cancerous cells

A

A single cell acquires mutations to become cancerous, and then this divides and divides until all of the healthy cells have been replaced with cancerous cells

168
Q

In-situ neoplasia

A
  • Only applies to epithelial neoplasms
  • May progress to invasive disease
  • Basement membrane is intact
  • Screening may allow detection and treatment before the development of carcinoma
169
Q

Describe carcinoma in-situ

A

a malignant epithelial neoplasm that has not yet invaded through the original basement membrane

170
Q

Describe what is meant by invasive carcinoma

A

a carcinoma that has breached the basement membrane – it can now spread elsewhere

171
Q

What is micro-invasive carcinoma

A

has breached the basement membrane but hasn’t invaded very far away from the original carcinoma

172
Q

What is the defining feature of malignant neoplasm

A

Invasion

173
Q

What does invasion enable neoplastic cells to do?

A

Enables the neoplastic cells to spread directly through tissue and gain access to blood vessels and lymphatic channels

174
Q

What is invasion dependent upon

A

decreased cellular adhesion
abnormal cellular motility
production of enzymes with a lytic effect on the surrounding tissues

175
Q

What is metastasis

A

Process by which a malignant tumour spreads from its primary site to produce secondary tumours at distant sites

176
Q

Name the ways that metastasis may occur.

A

via :

blood vessels
lymphatics
across body cavities
along nerves
result of the direct implantation of neoplastic cells during a surgical procedure

177
Q

What is included in the metastatic cascade

A

Detachment
Invasion
Intravasation
Evasion of host defences
Arrest
Extravasation
Vascularisation

178
Q

How do neoplastic cells invade

A

through the basement membrane

179
Q

Describe intravasation in the metastatic cascade

A

Collagenases
Cell motility

180
Q

Describe evasion of host defence in the metastatic cascade

A

Aggregation with platelets
Shedding of surface antigens
Adhesion to other tumour cells

181
Q

Describe extravasation in the metastatic cascade

A

Adhesion receptors
Collagenases
Cell motility

182
Q

Describe vascularisation in the metastatic cascade

A

Growth at the metastatic site using autocrine growth factors. Once the tumour reaches 1mm in diameter, they begin to grow its own blood vessels (angiogenesis).

183
Q

Angiogenesis promoters

A

o Vascular endothelial growth factors
o Basic fibroblast growth factor

184
Q

Angiogenesis inhibitors

A

o Angiostatin, endostatin, vasculostatin

185
Q

Routes of metastasis

A

It can invade the arterial side if it grows large enough and breaks off
* Haematogenous
* Lymphatic
* Trans-coelomic

186
Q

Haematogenous route of metastasis

A

by the bloodstream

Forms secondary tumours in organs perfused by the blood that has drained from a tumour

187
Q

Lymphatic route of metastasis

A

lymph channels

form secondary tumours in the regional lymph nodes

188
Q

Trans-coelomic route of metastasis

A

pericardial and peritoneal cavities where this invariably results in a neoplastic effusion

189
Q

Tumours which more commonly metastasise to the lung are

A

sarcomas and any common cancers

190
Q

Tumours which more commonly metastasise to the liver are

A

colon, stomach, pancreas, and carcinoid tumours of intestine

191
Q

Tumours that more commonly metastasise to bone are

A

prostate, breast, thyroid, lung and kidney

192
Q

What is a dominant single-gene disorder?

A

Dominant single-gene disorders will produce the disease where there is only one copy of the abnormal gene.

193
Q

What is a recessive single-gene disorder?

A

Recessive single-gene disorders will only be expressed if both gene copies are abnormal.

194
Q

Define acquired disease

A

Disease caused by non-genetic environmental factors

195
Q

What are neutrophil polymorphs involved in?

A

Involved in inflammation

196
Q

Are neutrophil polymorphs short-lived or long-lived?

A

Short lived

197
Q

Define neoplasm

A

Lesion resulting from the autonomous or relatively autonomous abnormal growth of cells which persists after the initiating stimulus has been removed – a new growth.

198
Q

Define tumour

A

any abnormal swelling, e.g. neoplasm, inflammation, hypertrophy, hyperplasia

All neoplasms are tumours, but not all tumours are neoplasms

199
Q

Are neoplasms:
Normal/abnormal
Harmful/Unharmful

A

Abnormal
Can be harmful or unharmful

200
Q

What is neoplasia

A

autonomous, abnormal, persistent new growth

201
Q

Tumour classification based on behaviour

A

Benign
Borderline
Malignant

Borderline tumours (e.g. some ovarian lesions) defy precise classification

202
Q

What do solid neoplasms always have?
What is the one exception to this

A

Exception is leukaemia

203
Q

What are neoplastic cells derived from?

A

Nucleated cells

204
Q

What is essential for neoplasm growth

A

Angiogenesis essential for growth

205
Q

Methods of classification of neoplasms

A

Behavioural: benign/malignant

Histogenetic: cell of origin

206
Q

Benign neoplasms

A

Localised, non-invasive
Close resemblance to normal tissue
Circumscribed or encapsulated
Nuclear morphometry is often normal
Necrosis/Ulceration rare
Growth on mucosal surfaces is often exophytic

207
Q

Do benign neoplasms fast or slow growth rate

A

Slow growth rate?

208
Q

Mitotic activity of benign neoplasms

A

Low-mitotic activity

209
Q

Why worry about “benign” neoplasms

A

They cause morbidity and mortality:
Pressure on adjacent structures
Obstruct flow
Production of hormones
Transformation to malignant neoplasm
Anxiety

210
Q

Malignant neoplasms growth rate?

A

Rapid growth rate

211
Q

Malignant Neoplasms

A

Invasive
Metastases
Variable resemblance to normal tissue
Poorly defined or irregular border
Hyperchromatic nuclei
Pleomorphic nuclei
Necrosis/Ulceration common
Growth on mucosal surfaces and skin is often endophytic
Encroach upon and destroy surrounding tissue
Are poorly circumscribed

212
Q

Describe mitotic activity in malignant neoplasms

A

Increased mitotic activity

213
Q

Describe the surface of malignant neoplasms

A

Have a ‘crab-like’ cut surface (Latin: cancer)

214
Q

Why worry about “malignant” neoplasms?

A

They cause morbidity and mortality:

Destruction of adjacent tissue
Metastases
Blood loss from ulcers
Obstruction of flow
Hormone production
Paraneoplastic effects
Anxiety and pain

215
Q

Histogenetic Classification

A

Histogenesis: the specific cell of origin of a tumour
Histopathological examination
Specifies tumour type

216
Q

Nomenclature of Neoplasia: Neoplasms may arise from

A

Epithelial cells
Connective tissues
Lymphoid/haematopoietic organs

217
Q

Suffix of neoplasms

A

-oma

218
Q

Prefix of neoplasms

A

Prefix depending on behavioural classification and cell type

219
Q

Define carcinoma

A

Malignant epithelial neoplasm

220
Q

Benign epithelial neoplasms: papilloma

A

Benign tumour of non-glandular, non-secretory epithelium

Prefix with a cell type of origin e.g. squamous cell papilloma

221
Q

Benign epithelial neoplasms: adenoma

A

Adenoma - benign tumour of the glandular or secretory epithelium
Prefix with cell type of origin e.g. colonic adenoma, thyroid adenoma.

222
Q

Malignant epithelial neoplasms: Carcinoma

A

malignant tumour of epithelial cells
Prefixed by name of epithelial cell type e.g. urothelial Ca.
Carcinomas of glandular epithelium = Adenocarcinomas

223
Q

Benign connective tissue neoplasms

A

Named according to cell of origin, suffixed by ‘-oma’
Lipoma: adipocytes
Chondroma: cartilage
Osteoma: bone
Angioma: vascular
Rhabdomyoma: striated muscle
Leiomyoma: smooth muscle
Neuroma: nerves

224
Q

Liposarcoma =

A

Sarcoma of adipose tissue

225
Q

Rhabdomyosarcoma =

A

Sarcoma of striated muscle

226
Q

How are Carcinomas and Sarcomas further classified

A

according to degree of differentiation

227
Q

Where the cell type of origin is unknown, the tumour is said to be

A

anaplastic

228
Q

Which “omas” are not neoplasms

A

granuloma, mycetoma, tuberculoma

229
Q

Not all malignant tumours are carcinoma or sarcoma e.g

A

melanoma: malignant neoplasm of melanocytes
Mesothelioma: malignant neoplasm of mesothelial cells
lymphoma: malignant neoplasm of lymphoid cells

Sandra Phase 2a (17 decks)

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