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phase 2a > Pathology > Flashcards

Pathology Flashcards

1
Q

Define inflammation.

A

The body’s response to injury or infection using different cells.

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2
Q

Define acute inflammation.

A

Neutrophil-mediated inflammation.

Sudden onset, short duration, usually resolves.

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3
Q

Give 6 causes of acute inflammation.

A
  • Microbial infections (most common)
  • Chemicals
  • Physical agents
  • Hypersensitivity reactions
  • Bacterial toxins
  • Tissue necrosis
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4
Q

Describe how microbial infections cause acute inflammation.

A

Viruses: cell death due to intracellular multiplication.

Bacteria: The release of exotoxins (involved in the initiation of inflammation) or endotoxins.

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5
Q

Describe how chemicals cause acute inflammation.

A

Corrosive chemicals (acids, alkalis, oxidising agents) cause inflammation through gross tissue damage.

Infecting agents may release specific chemical irritants that lead to inflammation.

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6
Q

Describe how physical agents cause acute inflammation.

A

Tissue damage as a result of physical trauma, UV, ionising radiation, burns or excessive cooling (frostbite).

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7
Q

Describe how hypersensitivity reactions cause acute inflammation.

A

An altered state of immunological responsiveness causes an inappropriate or excessive immune reaction, damaging tissues.

The types of reactions all have cellular or chemical mediators similar to those involved in inflammation.

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8
Q

Describe how tissue necrosis causes acute inflammation.

A

Death of tissues from lack of oxygen or nutrients resulting from inadequate blood flow (infarct) is a potent inflammatory stimulus.

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9
Q

Describe chronic inflammation.

A

Macrophage/lymphocyte-mediated inflammation.

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10
Q

What are neutrophil polymorphs?

A

White blood cells produced in the bone marrow, they have a very short lifespan (2 or 3 days).

They have a polylobed nucleus, hence the name ‘polymorph’.

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11
Q

What is the function of neutrophil polymorphs?

A

Phagocytosis of debris and bacteria.

Release of lysosomes which digest phagocytosed bacteria.

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12
Q

What are macrophages?

A

White blood cells with longer lifespans than neutrophils (months to years).

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13
Q

What is the function of macrophages?

A

Phagocytosis of debris and bacteria.

Transportation of material to lymph nodes and lymphocytes to induce a secondary immune reaction.

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14
Q

What are macrophages called in the liver, bone and brain respectively?

A

Kupffer cells (liver)

Osteoclasts (bone)

Microglial cells (brain)

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15
Q

What are lymphocytes?

A

Long-lived white blood cells (years).

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16
Q

What is the function of lymphocytes?

A

Producing chemicals involved in controlling inflammation.

Production of antibodies from B lymphocyte plasma cells (immunological memory).

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17
Q

What are fibroblasts?

A

Cells which produce collagenous connective tissue in scarring following certain types of inflammation.

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18
Q

Describe the sequence of acute inflammation.

A
  1. Injury or infection
  2. Neutrophils arrive and phagocytose and release enzymes
  3. Macrophages arrive and phagocytose
  4. Either resolution (with clearance of inflammation) or progression (chronic inflammation)
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19
Q

Give 3 examples of acute inflammation.

A

Acute appendicitis, physical trauma, streptococcal sore throat.

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20
Q

Describe the sequence of chronic inflammation.

A
  1. Either progression from acute inflammation or starts as ‘chronic’ inflammation (eg. infectious mononucleosis)
  2. No or very few neutrophils
  3. Macrophages and lymphocytes arrive, then fibroblasts
  4. Can resolve if no tissue damage (eg. glandular fever) but often results in repair and formation of scar tissue
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21
Q

Give 3 examples of chronic inflammation.

A

Tuberculosis, Crohn’s disease, rheumatoid arthritis.

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22
Q

What are granulomas?

A

An aggregate of epithelioid histiocytes (derivatives of activated macrophages resembling epithelial cells).

These cells secrete ACE (a blood marker of someone who has granulomatosis disease eg. TB, leprosy and Crohn’s)

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23
Q

Describe the systemic effects of inflammation.

A
  • Pyrexia
  • Weight loss
  • Reactive hyperplasia of the reticuloendothelial system
  • Haematological changes
  • Amyloidosis
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24
Q

What is reactive hyperplasia of the reticuloendothelial system?

A

Hyperplasia of the reticuloendothelial system (RES), which removes immune complexes from the circulation in healthy persons.

The RES is formed of monocytes of the blood, macrophages in connective tissue, lymphoid organs, bone marrow, liver and lung.

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25
Q

What is amyloidosis?

A

The build-up of amyloid (abnormal protein) in organs and tissues.

This can make it difficult for the organs and tissues to work properly.

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26
Q

What are the 5 cardinal signs of acute inflammation?

A
  • Rudor
  • Calor
  • Tumor
  • Dolor
  • Loss of function (movement inhibited by pain or swelling immobilising tissues)
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27
Q

What is rubor?

A

Redness
- due to dilation of small blood vessels
- eg. sunburn, cellulitis, acute conjunctivitis

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28
Q

What is calor?

A

Heat
- seen in peripheral areas of the body due to vascular dilation increasing blood flow through the region (hyperaemia)
- systemic fever may contribute to local temperature rise

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29
Q

What is tumor?

A

Swelling
- results from oedema and the physical mass of inflammatory cells migrating to the area
- formation of connective tissue contributes to swelling as the response progresses

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30
Q

What is dolor?

A

Pain
- stretching and distortion of tissues due to inflammatory oedema
- some chemical mediators of acute inflammation induce pain (bradykinin, prostaglandins and serotonin)

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31
Q

Name 3 endogenous chemical mediators of acute inflammation.

A

Bradykinin, histamine, nitric oxide.

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32
Q

What 5 processes are caused by endogenous chemical mediators?

A
  1. Vasodilation
  2. Recruitment of neutrophils
  3. Chemotaxis
  4. ↑ vascular permeability
  5. Itching and pain
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33
Q

What are the 3 processes involved in the acute inflammatory response?

A
  1. Changes in vessel caliber
    • Vasodilation brings blood and cells into the
      site of inflammation
  2. ↑ vascular permeability and formation of fluid exudate (pus)
  3. Formation of cellular exudate
    • Accumulation of neutrophil polymorphs within extracellular space
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34
Q

Following injury, what are the first 2 chemical mediators released?

A
  1. Histamine
  2. Thrombin
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35
Q

Name 5 terms used to describe types of inflammation.

A
  1. Serous (presence of protein-poor fluid eg. blisters)
  2. Suppurative (production of large amounts of pus eg. abscess)
  3. Membranous (formation of a membrane eg. candidiasis)
  4. Pseudomembranous (formation of a false membrane composed of necrotic epithelium and leukocytes)
  5. Necrotising (tissue death)
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36
Q

Describe the 4 potential outcomes of acute inflammation.

A
  1. Resolution (complete restoration of tissue)
  2. Suppuration (formation of pus)
  3. Organisation (replacement of tissue with granulation tissue as part of the healing process)
  4. Progression to chronic inflammation
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37
Q

Describe the difference between resolution vs. repair.

A

Resolution
- when the initiating factor is removed and the tissue is able to regenerate

Repair
- the initiation factor is still present and the tissue is unable to regenerate

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38
Q

What types of cells are able to regenerate?

A
  • Hepatocytes
  • Osteocytes
  • Pneumocytes
  • Blood cells
  • Gut and skin epithelial cells
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39
Q

What types of cells are unable to regenerate?

A
  • Myocardial cells
  • Neuronal cells
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40
Q

What are the 3 main cell types involved in chronic inflammation?

A
  1. Macrophages
    • M1 (promote inflammation)
    • M2 (inhibit inflammation and promote repair)
  2. Lymphocytes
    • B (differentiate into plasma cells)
    • T (cell-mediated immunity)
  3. Plasma cells (produce antibodies)
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41
Q

What cell forms when several macrophages fuse together?

A

Multi-nucleated giant cell.

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42
Q

Give 4 causes of chronic inflammation.

A
  1. Primary chronic inflammation
  2. Transplant rejection
  3. Recurrent acute inflammation
  4. Progression from acute inflammation
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43
Q

Give 5 examples of primary chronic inflammation.

A
  1. Infective substances having resistance to phagocytosis (eg. TB, leprosy)
  2. Endogenous materials (eg. uric acid crystals)
  3. Exogenous materials (eg.asbestos)
  4. Autoimmune diseases (eg. chronic gastritis, rheumatoid arthritis)
  5. Other chronic inflammatory diseases (eg. chronic inflammatory bowel disease)
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44
Q

What is granulation tissue composed of?

A

Granulation tissue is composed of small blood vessels in a connective tissue matrix with myofibroblasts.

It is important in healing and repair.

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45
Q

Give 4 macroscopic features of chronic inflammation.

A
  1. Chronic ulcer
  2. Chronic abscess cavity
  3. Granulomatous inflammation
  4. Fibrosis
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46
Q

Define resolution.

A
  • Tissue restored to normal, preinjury state.
  • Tissue architecture undamaged (able to regenerate)
  • The initiating factor is removed
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47
Q

Define repair.

A
  • Tissue repaired, however unable to regenerate to pre-injury state (replaced with scar/fibrotic tissue)
  • Tissue architecture is damaged (unable to regenerate)
  • Initiating factor is still present (eg. repeated alcohol damage to the liver)
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48
Q

Give 3 examples of repair.

A
  • Myocardial cell after MI
  • Neurones in the brain after a cerebral infarction
  • Neurones of the spinal cord after trauma
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49
Q

What is special about the liver? (resolution)

A

Provided damage/loss isn’t repeated hepatocytes can fully regenerate.

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50
Q

What happens to the liver if damage is repeated?

A

If the initiating factor is not removed (alcoholism or result of hepatitis) then resolution will not occur.

Instead, repair will take place, leading to fibrous scarring, regenerative nodules and eventually cirrhosis (nodular/fibrotic liver).

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51
Q

Describe liver fibrosis.

A

Inflammation and injury cause fibrosis, the medical term for scarring.

As it progresses from one stage to the next, scar tissue slowly replaces normal functioning tissue.

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52
Q

Describe liver cirrhosis.

A

Defined as stage 4 fibrosis, accompanied by non-functional regenerative nodules.
- Liver function diminishes
- Blood flow alteration
- Inability to synthesise proteins
- Inability to process drugs and toxins
- Decreased immune function

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53
Q

What is lobar pneumonia?

A

Bacterial infection caused by strep pneumonia. One lobe of the lungs fills with pus and neutrophil polymorphs fill alveoli of the lungs.

Resolution can occur in the walls of alveoli but only if architecture remains intact.

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54
Q

What happens to the lungs as a result of covid-19?

A

Interstitial pneumonia affecting more than just one lobe.

Interstitium and connective tissue of the lungs fill with fluid (presents with a patchy round glass appearance).

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55
Q

Will skin abrasions resolve or repair?

A

Repair (as long as skin is scraped but no hole has been made).

Top layer of stratified squamous epithelial cells are scraped off, exposing stem cells underneath (regenerate the skin underneath the scab).

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56
Q

Describe healing by first intention.

A

Surgical incisions

  1. Edges of incision brought together using stitches
  2. The incision wound fills with blood forming thrombus
  3. Exudation of fibrinogen causes formation of a weak fibrin
  4. Epidermal growth and collagen synthesis leads to strong collagenous join
  5. Epidermis grows over the top
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57
Q

Describe healing by second intention.

A

Instances when edges cannot be brought together (eg. trauma)

  1. Small BVs move in from the edges of the gap
  2. Fibroblasts enter the site of trauma and make collagen (granulation of tissue)
  3. Fibroblasts organise tissue to form organised collagen fibrils
  4. Early thrombus scar forms before skin contracts
  5. Epidermis will grow across the top (leaving white scar)
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58
Q

Which 2 factors stop blood clotting? (under normal circumstances)

A
  1. Laminar blood flow
  2. Endothelial cells are not sticky when healthy
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59
Q

Define a thrombus.

A

A solid mass formed from blood constituents in an intact vessel in a living person.

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60
Q

What are the constituents of a thrombus?

A
  • Platelets
  • RBCs
  • Fibrin (active form of fibrinogen)
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61
Q

What are the stages of thrombosis?

A
  1. Platelet aggregation
  2. Clotting cascade
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62
Q

What stimulates platelet aggregation?

A

Endothelial damage changes localised blood flow from laminar to turbulent.

Platelets come into contact with the endothelium and stick

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63
Q

What drug inhibits platelet aggregation?

A

Aspirin

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64
Q

What stimulates the clotting cascade?

A

Chemicals released from the platelets

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65
Q

What protein is made at the end of the clotting cascade?

A

Fibrin (from polymerisation of the protein fibrinogen)

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66
Q

Describe the feedback mechanism of thrombosis.

A

Positive feedback (no stopping the reaction once it’s started)

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67
Q

Give 3 factors that lead to thrombus formation.

A
  1. Change in vessel wall (eg. trauma)
  2. Change in blood constituents (eg. high levels of platelets)
  3. Change in blood flow (eg. veins in legs)
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68
Q

What is stasis?

A

Very slow or no blood flow.

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69
Q

Give 2 risk factors for thrombosis.

A
  1. Smoking
  2. Atheroma
70
Q

Define an embolism.

A

A solid mass in the blood which causes a blockage in the vasculature.

71
Q

Give 6 causes of embolism.

A
  1. Thrombus (most common)
  2. Air
  3. Cholesterol crystals
  4. Tumour
  5. Amniotic fluid
  6. Fat
72
Q

What happens to an embolus if it enters the venous system?

A

Filtered by the lungs.

Travels through the vena cava, through the right-hand side of the heart and lodges somewhere in the lungs depending on size.

Blood vessels in the lung split down to capillary size (act as sieve).

73
Q

What happens if an embolus enters the arterial system?

A

It will travel anywhere downstream of its entry point.

74
Q

Define ischaemia.

A

The reduction of blood flow in tissues.

Does not result in any further complications by itself.

75
Q

Define an infarct.

A

Reduction in blood flow that leads to cell death due to an inadequate oxygen supply to sustain metabolic demand.

76
Q

What is the usual cause of an infarct?

A

Thrombosis of an artery.

77
Q

Where might an infarct have a reduced impact?

A

Organs with dual blood supply.

78
Q

Which organs have a dual blood supply?

A
  • Liver (portal venous and hepatic artery supply)
  • Lung (pulmonary venous and bronchial artery supplies)
  • Areas of the brain (circle of willis)
79
Q

What is an atheroma?

A

Focal thickening of the tunica intima of arteries, produced through the movement of LDLs from the lumen.

80
Q

How is an atheroma formed?

A

The LDLs cause a cascade of events which leads to the development of obstructive fibrolipid plaque.

Mediated through inflammatory response and smooth muscle cell proliferation.

81
Q

Define atherosclerosis.

A

The condition caused by atheromas, marked by arteries narrowed with and hardened by plaque, causing CV complications (eg. angina, myocardial/ cerebral infarction).

82
Q

What is atherosclerotic plaque made up of?

A
  • Fibrous tissue
  • Lipid component (cholesterol)
  • Lymphocytes
83
Q

Give 6 non-modifiable risk factors for atherosclerosis.

A
  1. Age
  2. Gender
  3. Ethnicity
  4. Family history (1st degree)
  5. Diabetes mellitus
  6. Hypertension (genetic)
84
Q

Give 6 modifiable risk factors for atherosclerosis.

A
  1. Smoking
  2. Lack of exercise
  3. Obesity
  4. Type 2 diabetes
  5. High cholesterol
  6. Hypertension (lifestyle)
85
Q

Give 5 complications of atherosclerosis.

A
  1. Cerebral infarction
  2. Myocardial infarction
  3. Peripheral vascular disease (gangrene)
  4. Increased renin release (increased BP)
  5. Aortic aneurysm (rupture may result in sudden death)
86
Q

Why may a patient with atherosclerosis be advised to take aspirin?

A

Aspirin inhibits platelet aggregation, therefore reducing plaque formation.

87
Q

Define apoptosis.

A

Programmed cell death.

88
Q

Describe the steps for apoptosis.

A
  1. Pyknosis (nucleus condenses)
  2. Blebs form (the cell membrane becomes irregular)
  3. Apoptotic bodies from (cell membrane breaks off into separate compartments, containing vesicles)
  4. Phagocytosis of the cell debris
89
Q

When does apoptosis occur?

A
  1. Fully differentiated cells
  2. In development (separating fingers in embryo)
  3. In normal function (villi in the GIT)
  4. In disease processes
    - Cancer (lack of apoptosis)
    - HIV (too much apoptosis)
90
Q

Why does apoptosis occur in fully differentiated cells?

A
  • Cells are continuously monitoring for DNA damage
  • If damage is detected, apoptosis is triggered
  • Cell cycle is regulated by p53 protein
91
Q

What mediates apoptosis?

A

Caspases (enzymes)

Regulated by the Bcl2 gene and FasL binding to Fas receptors.

92
Q

Define necrosis.

A

Traumatic cell death.

93
Q

Define genetic disease.

A

A disease that occurs primarily from a genetic abnormality.

94
Q

Define congenital disease.

A

A disease with symptoms present at birth.

95
Q

Define inherited disease.

A

A disease caused by an inherited genetic abnormality. It may not manifest until later in life.

(Inherited does not mean congenital)

96
Q

Define acquired disease.

A

A disease caused by non-genetic environmental factors that usually occurs at birth.

(Acquired diseases can also be congenital eg. fetal alcohol syndrome)

97
Q

Define atrophy.

A

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

98
Q

Give examples of the 2 types of atrophy.

A
  1. Physiological atrophy - thymus atrophy after puberty.
  2. Pathological atrophy - skeletal muscle atrophy (an adaption to skeletal muscle disease)

Skeletal muscle, cardiac muscle, secondary sex organs and the brain are all especially susceptible to atrophy.

99
Q

Define hypertrophy.

A

Increase in tissue size caused by an increase in the size of constituent cells.

100
Q

Describe the mechanism of hypertrophy.

A

Increase in intracellular protein, cytosol or other cytoplasmic components.

101
Q

Give 2 causes of hypertrophy.

A
  1. Mechanical signals (eg. stretch)
  2. Trophic signals (eg. growth factors)
102
Q

Give examples of the 2 types of hypertrophy.

A
  1. Physiological hypertrophy - skeletal muscle cells hypertrophy with sustained weight-bearing exercise.
  2. Pathological hypertrophy - cardiac muscle cells hypertrophy as a result of hypertension.
103
Q

Define hyperplasia.

A

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

104
Q

What is compensatory hyperplasia?

A

Permits tissue and organ regeneration.

Common in epithelial cells of the epidermis and intestine, liver hepatocytes, bone marrow cells and fibroblasts.

105
Q

What is hormonal hyperplasia?

A

Occurs mainly in organs that depend on oestrogen (eg. oestrogen-dependant uterine cells undergo hyperplasia and hypertrophy following pregnancy).

106
Q

What is pathological hyperplasia?

A

Abnormal increase in cell division.

Occurs in the endometrium (endometriosis).

107
Q

Define metaplasia.

A

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

108
Q

Describe the mechanism of metaplasia.

A

A reversible process thought to be caused by stem cell reprogramming.

109
Q

Give 3 examples of metaplasia in the respiratory tract in response to irritants eg. smoke.

A
  1. Bronchial cells convert from mucus-secreting, ciliated, columnar epithelium to non-ciliated, squamous epithelium incapable of secreting mucus.
  2. Barrett’s oesophagus (non-keratinising squamous epithelium becomes mucinous columnar cells)
  3. If stress persists, metaplasia can progress to dysplasia and eventually carcinoma
110
Q

Define dysplasia.

A

Morphological changes seen in cells in the progression to becoming cancer.

Can involve changes to the shape, size and organisation of cells.

111
Q

Give an example of dysplasia.

A

Tissues prone to dysplasia include cervical and respiratory epithelium, where it is strongly associated with the development of cancer.

112
Q

Define carcinogenesis.

A

The multi-step process of the transformation of normal cells to neoplastic cells through permanent genetic alterations to mutations.

113
Q

What is a carcinogen?

A

Mutagenic agents known to cause cancer.

Carcinogenic = cancer causing
Oncogenic = tumour causing

114
Q

Define oncogenesis.

A

The process by which normal cells transform into benign neoplasms.

115
Q

What percentage of cancer risk is due to environmental factors?

A

85% = Environmental
15% = Genetic

116
Q

Give 5 host factors that can affect cancer risk.

A
  1. Race
  2. Diet
  3. Constitutional factors
  4. Premalignant conditions
  5. Transplacental exposure
117
Q

Why do constitutional factors affect cancer risk?

A
  1. Sex - breast cancer 200x more likely in women
  2. Age - cancer incidence increases with age
  3. Inherited genes:
    - Gene on Ch5 = ↑ risk of bowel cancer
    - Gene on Ch13 = ↑ risk of retinoblastoma
118
Q

Which premalignant conditions affect cancer risk?

A
  • Colonic polyps = ↑ risk of colorectal cancer
  • Cervical intraepithelial neoplasia (CIN) = ↑ risk of
    cervical cancer
  • Ulcerative colitis = ↑ risk of bowel cancer
  • Undescended testis = ↑ risk of testicular cancer
118
Q

Give the 5 categories of carcinogens.

A
  1. Viral
  2. Chemical
  3. Radiation
  4. Hormones, parasites and mycotoxins
  5. Miscellaneous (eg. asbestos and arsenic)
119
Q

Which viruses are carcinogenic?

A
  • Hepatitis B and C
  • Human Herpes Virus 8 (HHV-8) → Kaposi sarcoma
  • HPV → squamous cell carcinoma (cervix, mouth and
    oesophagus)
  • Epstein- Barr virus (EBV) → glandular fever (lymphoma)
  • HIV → increased risk of cerebral lymphoma
120
Q

What are the features of chemical carcinogens?

A
  1. No common structural features
  2. Most do not act directly (require metabolic
    conversion)
  3. Enzymes required for conversion may be ubiquitous or confined to certain organs
121
Q

What is the difference between ionising and non-ionising radiation?

A

Non-ionising:
- UV light - ↑ exposure to UVA or UVB = ↑ basal cell
carcinoma, squamous cell carcinoma and melanoma

Ionising:
- Skin cancer in radiographers
- Lung cancer in uranium miners and people living in
areas with granite bedrock
- Thyroid cancer in Ukrainian children (Chernobyl)

122
Q

Which hormones can be carcinogenic?

A
  • Increased exposure to oestrogen = ↑ risk of
    breast/endometrial cancer
  • Anabolic steroids = ↑ risk of hepatocellular carcinoma
123
Q

Give an example of a carcinogenic mycotoxin.

A

Aflatoxin B1 increases risk of hepatocellular carcinoma.

124
Q

Give an example of a carcinogenic parasite.

A

Schistosoma (blood-flukes) increases risk of bladder cancer.

125
Q

Which types of cancer can be caused by polycyclic aromatic hydrocarbons?

A

Lung and skin cancer.

126
Q

What can expose people to polycyclic aromatic hydrocarbons?

A

Smoking cigarettes and mineral oils.

127
Q

What type of cancer can be caused by aromatic amines and who may be exposed to them?

A

Bladder cancer.

People who work in the rubber/dye industry.

128
Q

What type of cancer can be caused by nitrosamines?

A

Cancer of the gut.

129
Q

What type of cancer can be caused by alkylating agents?

A

Leukaemia.

130
Q

What is a neoplasm?

A

A lesion resulting from a new and abnormal tissue growth which persists independent of its initiating stimulus.

131
Q

What causes a neoplasm?

A
  1. Tissue growth (new + abnormal + autonomous)
  2. Persists after initiating stimulus has been removed
132
Q

What are the features of a benign neoplasm?

A
  1. Slow growing - have a low mitotic growth of division
  2. Well circumscribed - no invasion to surrounding
    lymph/tissue
  3. Resemble cell origin - rarely necrotic
  4. Often exophytic - grow outwards
133
Q

What are the long-term effects of a benign neoplasm?

A
  • Pressure on adjacent tissues
  • Obstruction of ducts/hollow organs
  • Produce hormones
  • Can be pre-malignant
134
Q

What are the features of a malignant neoplasm?

A
  1. Fast-growing:
    • High mitotic rate of division
    • Hyperchromatic nuclei
    • Pleomorphic nuclei
  2. Poorly defined, irregular, infiltrative borders:
    • Invasion of surrounding lymph/tissue (can
      metastasise to other areas)
  3. Variable resemblance to cell of origin
    • Commonly necrotic, commonly ulcerate
  4. Often endophytic (grow invasively inwards)
135
Q

Describe the structure of neoplasms.

A
  • Neoplastic cells
  • Stroma
136
Q

What are the features of neoplastic cells?

A
  1. Always derived from nucleated cells
  2. Usually monoclonal
  3. Growth pattern related to parent cell
  4. Synthetic activity related to parent cell (collagen,
    mucin, keratin, hormones secretion)
137
Q

What is the function of the stroma?

A
  • Connective tissue framework supporting the
    neoplasm
  • Provides mechanical and nutritional support
138
Q

Give 2 factors that promote blood vessel growth.

A
  1. VEGF (important for tumour angiogenesis)
  2. Fibroblast growth factors
139
Q

What are the 2 classifications of neoplasms?

A
  1. Based on the behaviour of the tumour
  2. Based on the histological cell of origin
140
Q

Give the 3 behaviour categories of neoplasm.

A
  1. Benign
  2. Borderline
  3. Malignant
141
Q

Give the 4 main histological categories of neoplasm.

A
  1. Epithelial
  2. Connective tissue
  3. Lymphoid
  4. Haemopoietic
142
Q

What is the suffix given to all neoplasms?

A

“-oma”

143
Q

What is a papilloma?

A

A benign non-glandular/secretory epithelial neoplasm.

144
Q

What is an adenoma?

A

A benign glandular/secretory epithelial neoplasm.

145
Q

What is a carcinoma?

A

A malignant epithelial neoplasm.

146
Q

What is a Lipoma?

A

A benign neoplasm of adipocytes.

147
Q

What is a chondroma?

A

A benign neoplasm of cartilage.

148
Q

What is an osteoma?

A

A benign neoplasm of bone.

149
Q

What is an angioma?

A

A benign neoplasm of the vascular system.

150
Q

What is a rhabdomyoma?

A

A benign neoplasm of striated muscle.

151
Q

What is a leiomyoma?

A

A benign neoplasm of smooth muscle.

152
Q

What is a neuroma?

A

A benign neoplasm of nerves.

153
Q

What suffix is used for the malignant form of connective tissue neoplasms?

A

Take the prefix and add it to the suffix ‘sarcoma’.

154
Q

What is meant by ‘well-differentiated’?

A

A neoplasm that closely resembles normal tissue.

Usually has a lower grade and a better prognosis.

155
Q

What is meant by ‘poorly differentiated’?

A

A neoplasm that doesn’t resemble normal tissue.

Usually has a higher grade and a worse prognosis.

156
Q

What is meant by ‘anapaestic’?

A

When the cell-type of origin is unknown, the tumour of origin is said to be anaplastic.

157
Q

Give 3 exceptions to the “-oma” suffix that are not neoplasms.

A
  1. Granuloma (type of inflammation)
  2. Mycetoma (ball of fungus)
  3. Tuberculoma (inflammation due to TB)
158
Q

Which 3 malignant neoplasms do not have the suffix “carcinoma/sarcoma”?

A
  1. Melanoma (melanocytes)
  2. Mesothelioma (mesothelial cells)
  3. Lymphoma (lymphoid cells)
159
Q

Give 2 eponymously named neoplasms.

A
  1. Ewing’s sarcoma
  2. Kaposi’s sarcoma
160
Q

Give the 5 other exceptions to neoplasm nomenclature.

A
  1. Teratoma
  2. Embryonal tumour (blastoma)
  3. Mixed tumours
  4. Carcinosarcomas
  5. APUDomas (amine content and/or precursor uptake and decarboxylation)
160
Q

When is a neoplasm considered ‘in situ’?

A

The neoplasm has proliferated but has not broken through the basement membrane to other tissues.

(only applies to epithelial neoplasms)

161
Q

When is a cancer considered to be invasive?

A

It has breached its own tissue type into another area - i.e. it will have broken through the basement membrane into connective tissue.

162
Q

What is a micro-invasive carcinoma?

A

A carcinoma that has only just broken through the basement membrane.

162
Q

What is invasion dependant on?

A
  1. Decreased cellular adhesion
  2. Increased cellular motility
  3. Production of lytic enzymes to breakdown surrounding tissues (eg. proteases)
163
Q

Define metastasis.

A

The process by which a malignant neoplasm spreads from its primary site to produce secondary neoplasms at distant sites.

164
Q

Through which mediums can metastasis occur?

A
  • Via blood vessels
  • Via lymphatics
  • Across body cavities
  • Along nerves
  • Direct implantation during surgery
165
Q

What are the 8 steps of the metastatic cascade?

A
  1. Detachment
  2. Invasion
  3. Intravasion
  4. Evasion of host defences
  5. Arrest
  6. Extravasion
  7. Growth at metastatic site
  8. Vascularisation
166
Q

Give 2 angiogenesis promotors for neoplastic blood vessels.

A
  1. Vascular endothelial growth factor
  2. Basic fibroblast growth factor
167
Q

Give 3 endogenous inhibitors of neoplastic angiogenesis.

A
  1. Angiostatin
  2. Endostatin
  3. Vasculostatin

phase 2a (11 decks)

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