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Phase 2a > Introduction To Clinical Sciences > Flashcards

Introduction To Clinical Sciences Flashcards

1
Q

What is inflammation?

A
  • local response to cellular injury
  • capillary dilation, leukocytic infiltration, redness, heat, pain
  • serves to initiate elimination of noxious agents and damaged tissue
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2
Q

When is inflammation good / bad?

A

Good - infection & injury

Bad - autoimmunity / over-reaction to stimulus

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3
Q

What causes acute inflammation?

A

Tissue damage (e.g. by noxious compounds, trauma, microbial invasion).

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4
Q

Which cells are predominantly involved in acute inflammation?

A

Neutrophils

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5
Q

Features of acute inflammation?

A
  • sudden onset
  • short duration
  • usually resolves
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6
Q

What causes chronic inflammation?

A
  • some viral infections
  • hypersensitivity reactions
  • persistent causal agent
  • sometimes resolution of acute inflammation results in tissue fibrosis & ongoing damage
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7
Q

Which cells are predominantly involved in chronic inflammation?

A

Macrophages and lymphocytes

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8
Q

Features of chronic inflammation?

A
  • slow onset / sequel to acute
  • long duration
  • may never resolve
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9
Q

Lifespan of neutrophils?

A

Short lived, usually die at scene of inflammation (pus).

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10
Q

What is the role of lymphocytes in inflammation?

A
  • first responders to acute inflammation (respond to agent causing tissue damage)
  • have cytoplasmic granules containing bacteria-killing enzymes
  • release chemicals to attract other inflammatory cells (e.g. macrophages)
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11
Q

Lifespan of macrophages?

A

Weeks - months

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12
Q

What is the role of macrophages in inflammation?

A
  • phagocytosis of bacteria and debris
  • carry debris away
  • present antigens to lymphocytes
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13
Q

Lifespan of lymphocytes?

A

Years

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14
Q

Role of lymphocytes in inflammation?

A
  • produce chemicals to attract other inflammatory cells

- immunological memory for past infections

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15
Q

What is the role of endothelial cells in inflammation?

A
  • become sticky in areas of inflammation so inflammatory cells adhere to them
  • become porous to allow passage of inflammatory cells into tissues
  • grow into areas of damage to form new capillaries
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16
Q

How do capillaries dilate in acute inflammation?

A

Arteriole dilates and precapillary sphincter opens, allowing capillaries to fill.

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17
Q

What happens if capillaries all dilate at once?

A

Haemodynamic shock - blood pressure falls rapidly. Occurs in sepsis, for example.

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18
Q

What is the role of fibroblasts in inflammation?

A

Long lived, spindle shaped cells.

Form collagen in areas of chronic inflammation and repair.

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19
Q

What is a granuloma?

A

An aggregation of immune cells seen in some conditions involving inflammation.

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20
Q

When might a granuloma form?

A
  • TB
  • leprosy
  • Crohn’s disease
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21
Q

How do antihistamines treat inflammation?

A

Block histamine, a mediator of inflammation.

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22
Q

How do corticosteroids treat inflammation?

A

Interact with DNA to suppress inflammatory genes - interact with the transcription complex.

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23
Q

How does ibuprofen treat inflammation?

A

Inhibits prostaglandin synthetase, therefore inhibiting prostaglandin synthesis. Prostaglandins are mediators of inflammation.

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24
Q

When is damage resolved vs repaired?

A

Resolution - when initiating factor removed, tissue is undamaged or able to regenerate.
Repair - when initiating factor is still present, or tissue is damaged and unable to regenerate.

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25
Q

Which cell populations can regenerate?

A

Labile and stable cells.

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26
Q

What is meant by organisation in tissue repair?

A
  • repair of specialised tissue by the formation of a fibrous scar
  • dead tissue is removed by phagocytosis and granulation tissue is produced on a fibrin scaffold
  • granulation tissue accumulates collagen and the scar forms
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27
Q

What does granulation tissue consist of?

A

Capillary loops and myofibroblasts.

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28
Q

What is the role of myofibroblasts in organisation?

A

They contract to bring surrounding tissues together.

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29
Q

What can be a damaging effect of scar contraction in organisation?

A

May result in a stricture, causing stenosis or obstruction of a lumen.
May result in a muscle contracture.

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30
Q

What happens in the event of persistent liver damage?

A

Liver cirrhosis, then fibrosis.

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31
Q

Why is resolution of an abrasion possible (in most cases)?

A

The bottom skin layer remains so the epidermis can regenerate.

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32
Q

What is healing by 1st intention?

A
  • skin edges are close
  • a weak fibrin join forms between them
  • fibrin join is replaced by a strong collagen join
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33
Q

What is healing by 2nd intention?

A
  • gaping loss of tissue
  • organisation: granulation tissue fills gap to provide a framework for epithelial cells, then collagen accumulates in it
  • epithelial cells grow over the top of the gap
  • contraction of fibrous (collagen) scar
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34
Q

Which cells produce collagen (e.g. when it accumulates in granulation tissue / in fibrosis)?

A

Fibroblasts

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35
Q

What does gliosis mean?

A

Fibrosis occurring in the brain.

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36
Q

Which cell types can regenerate?

A
  • hepatocytes
  • pneumocytes
  • all blood cells
  • gut and skin epithelium
  • osteocytes
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37
Q

Which cell types don’t regenerate?

A
  • myocardial cells

- central neurones (peripheral can repair but rarely regain full functionality)

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38
Q

What is meant by laminar flow?

A

Normal blood flow through the middle of the vessel.

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39
Q

Why does endothelial cell injury result in platelet aggregation?

A

Collagen is exposed which causes platelet adherence & aggregation.

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40
Q

What are the features of platelets?

A
  • no nucleus
  • alpha granules (involved in platelet adhesion)
  • dense granules (involved in platelet aggregation)
  • derived from megakaryocytes in bone marrow
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41
Q

What is a thrombus formed from?

A

Layers of aggregated platelets and red blood cells within a fibrin mesh framework.

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42
Q

What is meant by thrombosis?

A

A solid mass of blood constituents formed within an intact vascular system (during life).

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43
Q

What are the three components of Virchow’s triad?

A
  • change in the vessel wall (e.g. endothelial injury)
  • change in blood flow (e.g. stasis, turbulence)
  • change in blood constituents (causing hypercoaguability)
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44
Q

Which components of Virchow’s triad are involved when an atheroma forms?

A
  • change in blood flow (turbulence)

- change in vessel wall

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45
Q

What is the most common cause of arterial thrombosis?

A

Atheroma

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46
Q

What is the most common cause of venous thrombosis?

A

Stasis (most thrombi begin at valves where there is turbulence).

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47
Q

What are the 4 possible outcomes for a thrombus?

A

1) degradation = resolution
2) organisation into a scar (may narrow vessel lumen)
3) recanalisation - when capillaries grow into the thrombus and fuse to form larger vessels, vessel becomes patent again
4) embolism

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48
Q

Why is aspirin used to prevent thrombus formation?

A

Aspirin inhibits platelet aggregation.

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49
Q

What is an embolus?

A

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

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50
Q

What is the most common form of embolism?

A

Pulmonary embolism due to deep vein thrombosis.

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51
Q

What is a systemic embolus?

A

An embolus which arises in the arterial system. E.g. from the heart due to AF, or from an arterial atheroma.

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52
Q

What is meant by gangrene?

A

An infarction of mixed tissues in bulk (e.g. part of a limb).

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53
Q

Examples of organs with dual blood supply?

A
  • lungs
  • liver
  • some parts of brain
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54
Q

What is meant by shock?

A

Profound circulatory failure causing hypoperfusion of organs.

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55
Q

What are the two types of shock?

A

Cardiogenic: reduced stroke volume as a result of an acute MI.
Hypovolaemic: loss of effective circulating blood volume.

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56
Q

What are the clinical effects of arterial thrombosis?

A
  • loss of pulses distal to thrombus
  • area is cold, pale, painful
  • tissue death = gangrene
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57
Q

What are the clinical effects of venous thrombosis?

A
  • 95% of the time it occurs in leg veins

- area is tender, swollen and reddened

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58
Q

Why doesn’t atherosclerosis occur in pulmonary arteries?

A

They are a low pressure system so there is no endothelial damage from shearing forces.

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59
Q

Why is atherosclerosis common in the aorta and systemic arteries?

A

High pressure system so the endothelium is subject to shearing forces (particularly at branching points).

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60
Q

Examples of agents causing endothelial damage?

A
  • free radicals
  • nicotine
  • carbon monoxide
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61
Q

What is the result of haemorrhage within an atherosclerotic plaque?

A

Causes plaque expansion.

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62
Q

What is meant by elastic and muscular arteries?

A

Elastic - most major arteries surrounding the heart.

Muscular - continue from elastic arteries, distributing blood to regions of the body.

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63
Q

What is the structure of the artery wall?

A

Tunica intima: endothelial cells with subendothelium of connective and elastic tissue.
Tunica media:
- elastic arteries: 40-70 fenestrated elastic membranes with smooth muscle cells and collagen between them.
- muscular arteries: ~40 layers of smooth muscle, connected by gap junctions.
Tunica adventitia: connective tissue containing lymphatics, nerves, and vasa vasorum.

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64
Q

What are the vasa vasorum?

A

Blood vessels which supply arteries.

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65
Q

What is the structure of an arteriole?

A
  • 3 layers of smooth muscle cells
  • no internal elastic lamina
  • external elastic lamina present in larger arterioles only
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66
Q

What are metarterioles?

A
  • supply capillary beds
  • have precapillary sphincters (rings of smooth muscle) to control blood flow to the capillary bed
  • no continuous smooth muscle layer (just endothelium)
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67
Q

What is the early development stage of an atherosclerotic plaque?

A

Fatty streak lesion.

  • yellow elevation of intimal liming
  • composed of lipid-laden macrophages
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68
Q

What is the composition of an atherosclerotic plaque?

A
  • central lipid core
  • cap of fibrous tissue covered by endothelium
  • fibrous cap contains collagen and inflammatory cells
  • foam cells present (macrophages what have phagocytosis lipoproteins)
  • plaque beck was calcified in later stages
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69
Q

What are some risk factors for atherosclerosis?

A
  • hypercholesterolaemia
  • smoking
  • hypertension
  • poorly controlled diabetes
  • male
  • increasing age
  • obesity
  • sedentary lifestyle
  • low socioeconomic status
  • some infections (e.g. influenza)
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70
Q

How might certain infections contribute to atherosclerosis?

A

By switching on inflammation pathways.

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71
Q

What main stages are involved in plaque development?

A

Chronic occurrence of:

1) endothelial injury
2) tissue response of vascular wall to injury (inflammation and repair)

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72
Q

What is the cellular response to endothelial injury?

A
  • endothelial cells have increased thrombogenicity, enhanced expression of adhesion molecules for monocytes and increased permeability to LDLs.
    X
  • thrombus forms, and inflammatory cells and lipids enter the intima and form plaques.
  • macrophages and T lymphocytes also accumulate in plaque tissue.
  • foam cells die and deposit lipid into the plaque core
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73
Q

How do tissue repair processes assist plaque formation?

A
  • growth factors stimulate proliferation of smooth muscle cells
  • smooth muscle cells produce collagen to enclose the lipid core in a fibrous cap
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74
Q

What are 4 potential clinical manifestations of atherosclerosis?

A

1) reversible tissue ischaemia (when 50-75% vessel stenosis has occured)
2) acute atherothrombotic occlusion due to plaque rupture
3) embolism (may lead to infarction)
4) ruptured abdominal atherosclerotic aneurysm

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75
Q

Which risk factors for atherosclerosis are non-modifiable?

A
  • age
  • gender
  • family history (genetics & shared environment)
  • ethnicity (South Asian / sub-Saharan African - increased risk compared to European)
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76
Q

Which risk factors for atherosclerosis are modifiable?

A
  • smoking
  • hyperlipidaemia
  • sedentary lifestyle
  • unhealthy diet
  • obesity
  • excessive alcohol
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77
Q

What are some examples of co-morbidities which have an increased risk of atherosclerosis?

A
  • hypertension
  • diabetes (poorly controlled)
  • CKD
  • dyslipidaemia
  • atrial fibrillation
  • systemic inflammatory disorders (e.g. rheumatoid arthritis)
  • influenza
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78
Q

What is meant by apoptosis?

A

Programmed cell death - individual cell deletion in physiological growth control and in disease.

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79
Q

What can happen if apoptosis is reduced?

A

Neoplasia

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80
Q

What can happen if apoptosis is increased?

A

Atrophy

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81
Q

What happens during apoptosis?

A
  • enzymatic digestion of the nucleus and cytoplasmic contents
  • phagocytosis of breakdown products (contained in membrane-bound bodies) by neighbouring cells
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82
Q

What are some inducers of apoptosis?

A
  • growth factor withdrawal
  • loss of matrix attachment
  • glucocorticoids
  • some viruses
  • free radicals
  • ionising radiation
  • DNA damage
  • ligand binding at ‘death receptors’
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83
Q

What are some inhibitors of apoptosis?

A
  • growth factors
  • extracellular matrix
  • sex steroids
  • some viral proteins
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84
Q

What pathway leads to apoptosis?

A

Activation of caspases (by the Bcl2 protein, or by the binding of the Fas ligand to the Fas receptor).

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85
Q

What is the role of apoptosis in HIV

A

The HIV virus induced apoptosis in T lymphocytes.

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86
Q

What is meant by necrosis?

A

Traumatic cell death - death of tissues following bioenergetic failure and loss of plasma membrane integrity. Induces inflammation and repair.

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87
Q

What is coagulative necrosis?

A

Most common form of necrosis. Cells retain their outlines so tissue texture is initially normal / firm, and then layer may become soft.

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88
Q

What is liquifactive necrosis?

A

When necrotic tissue liquefies (e.g. cerebral necrosis).

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89
Q

What is caseous necrosis?

A

Seen in TB - where the dead tissue is structureless.

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90
Q

What is gangrene? (In terms of necrosis).

A

Necrosis with putrefaction (decay) of tissues (due to bacteria).

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91
Q

What is fat necrosis?

A

Trauma to adipose tissue, leading to an inflammatory response (fat phagocytosis) resulting in fibrosis.

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92
Q

What are homeobox genes?

A

Genes that regulate gene expression and control aspects of morphogenesis and differentiation.

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93
Q

What does congenital mean?

A

Present at birth (condition may be inherited or acquired during embryogenesis).

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94
Q

What are the three most common chromosomal abnormalities?

A
  • trisomy 21 (Down’s syndrome) 1 in 1000 births
  • trisomy 18 (Edwards’ syndrome) 1 in 5000 births
  • trisomy 13 (Patau’s syndrome) 1 in 6000 births
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95
Q

Why does Alzheimer’s occur in people with Down’s syndrome?

A

Increased beta amyloid deposition in the brain - gene for beta amyloid is located on chromosome 21.

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96
Q

What are the three categories of single gene disorder?

A
  • enzyme defects
  • defects in receptors or cellular transport
  • non-enzyme protein defects
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97
Q

What is meant by polygenic inheritance?

A

Multiple genes involved.

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98
Q

What is the difference between acromegaly and gigantism?

A

Acromegaly is caused by growth hormone excess post-puberty. Causes abnormally large hands and feet, etc.

Gigantism is caused by growth hormone excess pre-puberty. Causes tall stature.

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99
Q

What are three types of foetal development anomaly? Examples?

A

Embryo division abnormalities: e.g. conjoined twins.
Teratogen exposure: e.g. thalidomide
Failure of cell and organ migration: e.g. undescended testis

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100
Q

What are 6 anomalies of organogenesis?

A
  • agenesis/aplasia: organ fails to develop
  • atresia: lumen fails to develop
  • hypoplasia: organ fails to develop its normal size
  • maldifferentiation
  • ectopia & heterotopia: small areas of mature tissue from one organ are present within another tissue.
  • choristoma: one or more mature differentiated tissues aggregate as a tumour-like mass at an inappropriate site.
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101
Q

What is hypertrophy?

A

An increase in the size of a tissue caused by an increase in the size of the constituent cells.
E.g. skeletal muscle

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102
Q

What happens in cardiac hypertrophy?

A
  • after an MI, scar tissue replaces myocardial tissue.
  • the remaining myocardium undergoes compensatory hypertrophy
  • therefore right ventricular hypertrophy may result from left ventricular failure, leading to pulmonary hypertension
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103
Q

What is hyperplasia?

A

Increase in the size of a tissue, caused by an increase in the number of the constituent cells.
E.g. in individuals living at high altitude, hyperplasia occurs in red blood cell-producing bone marrow cells (stimulated by erythropoietin).

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104
Q

What causes an enlarged prostate?

A

Hyperplasia of smooth muscle.

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105
Q

How does hyperplasia aid tissue repair?

A
  • proliferation of capillary endothelial cells (angiogenesis) and myofibroblasts in scar tissue.
  • regeneration of specialised cells within a tissue.
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106
Q

What is meant by atrophy?

A

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

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107
Q

What is an example of physiological atrophy?

A

Involution of Wollfian / Müllerian ducts.

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108
Q

What are 7 causes of pathological atrophy?

A
  • decreased function & disuse
  • loss of innervation
  • loss of blood supply
  • pressure atrophy
  • lack of nutrition
  • loss of endocrine stimulation
  • hormone-induced atrophy
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109
Q

What is meant by metaplasia?

A

When a cell changes from one fully-differentiated type to another, due to an altered cellular environment.

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110
Q

What types of cells does metaplasia affect?

A

Epithelial and mesenchymal cells.

E.g. ciliated columnar epithelium in bronchi becomes squamous as a result of smoking.

111
Q

What can metaplasia give rise to?

A

Dysplasia and carcinoma.

112
Q

What is meant by dysplasia?

A

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

113
Q

What is the difference between metaplasia and dysplasia?

A

Metaplastic cells have normal architecture and arrangement, whereas this is abnormal in dysplastic cells.

114
Q

What is meant by senescence?

A

The process by which cells irreversibly stop dividing and enter a state of permanent growth arrest without undergoing apoptosis.

115
Q

What is meant by frailty syndrome?

A

A gradual deterioration in health, leading to death (where there is no single cause / combination of causes).

116
Q

What are some characteristics of frailty syndrome?

A
  • sarcopenia
  • reduced activity
  • poor appetite
  • osteoporosis
  • frequent falls
117
Q

What is the role of the telomere of a chromosome?

A

Telomere shortens with every cell division, limiting the number of mitotic divisions that a cell can perform.

118
Q

What are some causes of ageing and death in cells, other than telomere shortening?

A
  • cross-linking or mutations of DNA
  • loss of calcium influx controls
  • damage to mitochondrial DNA
  • loss of DNA repair mechanism
  • free radicals generation
  • accumulation of toxic by-products of metabolism
  • activation of ageing and death genes
119
Q

What causes dermal elastosis in old age?

A

Exposure to UV-B light causes protein cross-linking. Therefore the skin contains less collagen and elastin, and the remainder is abnormal.

120
Q

Why is immunity impaired in old age?

A
  • increased memory cells but decreased naive cells, so reduced capacity to respond to novel antigens.
  • thymus (source of T cells) atrophies.
121
Q

What implications does impaired immunity have in old age?

A
  • recurrence of dormant previous infections (e.g. chicken pox virus as shingles).
122
Q

What cardiovascular changes are seen in old age?

A
  • accumulated atherosclerotic lesions

- loss of elasticity in arteries = increased systolic BP

123
Q

What is osteoporosis? What implications does it have?

A

Loss of bone matrix (normal mineralisation but thinned trabeculae) due to increased bone resorption and decreased bone formation. Linked to a lack of oestrogen.
Causes fractures of vertebral bodies, leading to stooped posture and loss of height. Increased risk of fragility fractures.

124
Q

What causes cataracts?

A

Exposure to UV-B light causes protein cross-linking, damaging the lens.

125
Q

What is meant by sarcopenia? Why does it occur?

A

Loss of muscle due to decreased growth hormone, decreased testosterone, and increased catabolic cytokines.

126
Q

What causes deafness in old age?

A

Loss of hair cells in the cochlea.

127
Q

Does basal cell carcinoma metastasise?

A

No, it only invades locally (but it is malignant).

128
Q

How is basal cell carcinoma treated?

A

Complete local excision. Skin graft may be required for healing.

129
Q

Where do carcinomas commonly spread?

A

To lymph nodes draining the site of the carcinoma.

130
Q

Lymph nodes where breast cancer spreads to?

A

Axillary lymph nodes.

131
Q

Which cancers commonly spread to bone?

A
  • breast
  • prostate
  • lung
  • thyroid
  • kidney
132
Q

How is a breast cancer diagnosis confirmed?

A
  • mammogram & ultrasound scan

- biopsy

133
Q

How is it determined whether breast cancer has spread to the axilla?

A

Biopsy of lymph nodes / scan.

134
Q

How is it determined whether breast cancer has metastasised?

A
  • bone scan

- CT scan (e.g. liver)

135
Q

Why can a tumour reoccur if it has been completely excised?

A

Micro metastases could be present.

136
Q

What is adjuvant therapy?

A

Extra treatment given after surgical excision of a tumour (e.g. chemotherapy, radiotherapy) to destroy micro metastases.

137
Q

What crystals are deposited in tissues in gout?

A

Uric acid crystals.

138
Q

What is calcification in diseased tissues called?

A

Dystrophic calcification.

139
Q

How does vinblastine work?

A

Antimicrotubule agent so inhibits metaphase.

140
Q

How does etoposide work?

A

Inhibits topoisomerase (unwinds DNA helix) so inhibits DNA replication.

141
Q

How does ifosamide work?

A

Binds directly to DNA causing cross-linking, inhibits DNA synthesis.

142
Q

How does cisplatin work?

A

Binds directly to DNA, causing cross linking. Inhibits DNA synthesis.

143
Q

What are the drawbacks of conventional chemotherapy?

A 
Not selective for tumour cells.
Damages healthy dividing cells, causing:
- myelosuppression (damages bone marrow cells, resulting in low white blood cell count and anaemia).
- hair loss
- diarrhoea
144
Q

What is choriocarcinoma?

A

Malignant tumour of the placenta.

145
Q

How are differences between cancer cells and healthy cells studied?

A
  • gene arrays
  • proteomics
  • tissue microarrays
146
Q

Which alterations to growth factor receptors might appear in tumour cells?

A
  • over-expression = more cell proliferation

- constitutive activation of receptor (always switched on) = more cell proliferation

147
Q

How can alterations to growth factor receptors be exploited in targeted cancer therapy?

A
  • monoclonal antibody against growth factor receptor

- small molecular inhibitor of growth factor receptor

148
Q

How does cetuximab work?

A

Monoclonal antibody binds competitively to external domain of EGFR.

149
Q

What is EGFR?

A

epidermal growth factor receptor

150
Q

How are patients selected for Cetuximab therapy?

A

Immunohistochemistry - stain for EGFR.

151
Q

How does herceptin work?

A

Monoclonal antibody against Her-2 (human epidermal growth factor receptor 2).
Promotes endocytosis of Her-2.
Flags cancer cells for lymphocyte recognition.

152
Q

What is the her-2 gene associated with in terms of breast cancer characteristic?

A
  • large size
  • high grade
  • aneuploidy
  • negative oestrogen receptor status
  • poor prognosis
153
Q

How is her-2 amplification detected?

A
  • fluorescent in situ hybridisation (FISH)

- immunohistochemistry

154
Q

What is meant by carcinoma in situ?

A

An epithelial neoplasm exhibiting all the cellular features associated with malignancy, but which has not yet invaded through the epithelial basement membrane separating it from potential routes of metastasis.

155
Q

What is meant by micro-invasive carcinoma?

A

Carcinoma has invaded through the basement membrane but has not spread far. There is a low chance of metastasis and it can still be treated locally.

156
Q

How do neoplastic cells invade the basement membrane?

A
  • cell motility (due to gene activation)

- proteases - matrix metalloproteinases

157
Q

How do neoplastic cells invade the extracellular matrix?

A
  • cell motility

- proteases - matrix metalloproteinases

158
Q

How do tumour cells become motile?

A

Motility factors:

  • tumour cell derived motility factors
  • breakdown products of extracellular matrix
159
Q

What is the name for the process by which tumour cells invade the capillary endothelium? How do tumour cells achieve this?

A

Intravasation

  • collagenases
  • cell motility
160
Q

How do tumour cells evade the host immune defence in the blood stream?

A
  • aggregation with platelets
  • shedding of surface antigens
  • adhesion to other tumour cells
161
Q

How do neoplastic cells leave blood vessels and enter tissues? What is the name for this process?

A

Extravasation

  • adhesion receptors
  • collagenases
  • cell motility
162
Q

How does the neoplasm develop at the metastatic site?

A
  • growth factors (often neoplastic cells produce their own)

- angiogenesis promotors: e.g. vascular endothelial growth factor (VEGF)

163
Q

How does avastin inhibit angiogenesis? What is its current use?

A
  • binds to VEGF, stopping it from binding to its receptor

- was ineffective in cancer trials, but has a use in treating wet macular degeneration

164
Q

Which tumours commonly metastasise to the liver?

A
  • colon
  • stomach
  • pancreas
  • neuroendocrine (carcinoid) tumours of the small intestine
165
Q

How do metastases reach the liver?

A

Via the portal circulation.

166
Q

What are the two types of bone metastasis?

A

Lytic - causes bone breakdown.

Sclerotic - causes new bone formation.

167
Q

What is the definition of neoplasm?

A

A lesion resulting from the autonomous (or relatively autonomous) growth of cells, which persists after the initiating stimulus has been removed.

168
Q

3 most common cancers in males?

A
  • prostate
  • lung
  • bowel
169
Q

3 most common cancers in females?

A
  • breast
  • lung
  • bowel
170
Q

True or false: neoplastic cells can derive from non-nucleated cells (e.g. red blood cells).

A

False: they derive from nucleated cells only.

171
Q

True or false: neoplastic cells are usually monoclonal.

A

True

172
Q

What is the neoplastic stroma?

A
  • connective tissue framework

- provides mechanical support and nutrition

173
Q

What cells and tissue types are found in the neoplastic stroma?

A
  • fibroblasts (produce collagen)

- blood vessels

174
Q

What is meant by a benign neoplasm?

A

A localised, non-invasive neoplasm.

175
Q

Growth rate and mitotic activity of a benign neoplasm?

A
  • slow growth

- low mitotic activity

176
Q

Does a benign neoplasm resemble normal tissue?

A

Close resemblance.

177
Q

How are benign neoplasms localised?

A

They are circumscribed or encapsulated.

178
Q

What is the nuclear morphometry of a benign neoplasm?

A

Often normal.

179
Q

Does necrosis / ulceration often occur in a benign neoplasm?

A

Necrosis and ulceration are rare because benign neoplasms don’t usually outgrow their blood supply.

180
Q

Are benign neoplasms exophytic or endophytic?

A

Exophytic - they can’t invade underlying tissues so grow upwards and outwards.

181
Q

How do benign neoplasms cause morbidity and mortality?

A
  • pressure on adjacent structures
  • obstruct flow
  • production of hormones
  • become a malignant neoplasm
  • cause anxiety
182
Q

What is meant by a malignant neoplasm?

A

Malignant neoplasms are invasive and commonly metastasise.

183
Q

What is the growth rate and mitotic index for a malignant neoplasm?

A
  • rapid growth rate

- high mitotic index

184
Q

Does a malignant neoplasm resemble normal tissue?

A

Variable resemblance:

  • good resemblance (well-differentiated) = low grade
  • poor resemblance (poorly-differentiated) = high grade
185
Q

What characteristics do nuclei have in malignant neoplasms?

A
  • hyperchromatic nuclei

- pleomorphic nuclei

186
Q

Does necrosis / ulceration occur in malignant neoplasms?

A

Necrosis and ulceration is common as the neoplasm often outgrows its blood supply.

187
Q

Is the growth of a malignant neoplasm exophytic or endophytic?

A

Often endophytic due to invasion of underlying tissues.

188
Q

Morbidity and mortality caused by malignant neoplasms?

A
  • destruction of adjacent tissue
  • metastases
  • blood loss from ulcers
  • obstruction of flow
  • hormone production
  • paraneoplastic effects
  • anxiety and pain
189
Q

What is meant by paraneoplastic effects?

A

Metabolic effects due to tumour secretion of chemical signalling molecules, or the immune response to the tumour.

190
Q

What is a papilloma?

A

Benign tumour of non-glandular, non-secretory epithelium.

191
Q

What is an adenoma?

A

Benign tumour of glandular or secretory epithelium.

192
Q

What is a carcinoma?

A

Malignant epithelial neoplasm.

193
Q

What is an adenocarcinoma?

A

Malignant tumour of glandular epithelium.

194
Q

What is a lipoma?

A

Benign neoplasm from adipocytes.

195
Q

What is a chondroma?

A

Benign neoplasm from cartilage.

196
Q

What is an osteoma?

A

Benign neoplasm from bone.

197
Q

What is an angioma?

A

Benign vascular neoplasm.

198
Q

What is a rhabdomyoma?

A

Benign neoplasm of striated muscle.

199
Q

What is a leiomyoma?

A

Benign neoplasm of smooth muscle.

200
Q

What is a neuroma?

A

Benign neoplasm from nerves.

201
Q

How are malignant connective tissue neoplasms named?

A

‘sarcoma’ prefixed by cell type of origin:

  • liposarcoma
  • rhabdomyosarcoma
  • osteosarcoma
202
Q

What is meant by an anaplastic tumour?

A

A tumour where the cell-type of origin is unknown - malignant with a poor prognosis.

203
Q

What is a melanoma?

A

Malignant neoplasm of melanocytes.

204
Q

What is a mesothelioma?

A

Malignant neoplasm of mesothelial cells (e.g. pleura).

205
Q

What is a lymphoma?

A

Malignant neoplasm of lymphoid cells.

206
Q

What is a leukaemia?

A

Malignant neoplasm of haemopoeitic organs.

207
Q

What is a teratoma?

A

Neoplasm containing elements of each layer of the trilaminar disk.

208
Q

Where do teratomas occur most often?

A

The gonads, where germ cells are abundant.

209
Q

What is a blastoma?

A

Neoplasm with a histological resemblance to the embryonic form of the organ in which they arise.

210
Q

What is meant by a mixed tumour?

A

Tumour consisting of a combination of cell types.

211
Q

What is meant by an endocrine tumour?

A

Tumour consisting of peptide hormone-secreting cells in epithelial tissues, often functionally active.

212
Q

What is meant by a carcinoid tumour?

A

An endocrine tumour that doesn’t produce any known peptide hormones, or produces a mixture of peptide hormones.

213
Q

What is meant by a carcinosarcoma?

A

A mixture of carcinoma and sarcoma, malignant.

214
Q

What is a hamartoma?

A

A benign tumour-like lesion. Consists of two or more mature cell types normally found in the organ in which it arises. Growth of a hamartoma is related to overall body growth. May be mistaken for a malignant neoplasm.

215
Q

What is a cyst?

A

Fluid-filled space lined by epithelium. Some are neoplasms, some aren’t - may have local effects similar to those produced by the true tumour.

216
Q

What are some challenges when trying to identify carcinogens?

A
  • latent interval may be decades
  • environment is complex
  • ethical constraints
217
Q

Where is hepatocellular carcinoma common?

A
  • areas with hepatitis B/C

- areas with mycotoxins

218
Q

What types of laboratory evidence for carcinogens are there?

A
  • incidence of tumours in laboratory animals
  • cell/tissue cultures
  • mutagenicity testing in bacterial cultures
219
Q

What are the drawbacks to laboratory evidence for carcinogens?

A
  • animals / cultures may metabolise agents differently to humans
  • bacterial mutation may not = carcinogenicity
220
Q

What is meant by a pro-carcinogen?

A

A chemical carcinogen that requires metabolic conversion to become an ultimate carcinogen.

221
Q

What cancers can polycyclic aromatic hydrocarbons causes?

A
  • lung cancer

- skin cancer

222
Q

What are two sources of polycyclic aromatic hydrocarbons?

A
  • smoking

- mineral oils

223
Q

What type of cancer can aromatic amines cause?

A

Bladder cancer

224
Q

Which occupation(s) involve contact with aromatic amines?

A

Rubber / dye workers

225
Q

Which cancers are associated with alcohol?

A
  • oropharynx
  • larynx
  • oesophagus
  • liver
  • breast
  • colorectal
226
Q

What are the processes by which alcohol causes cancer?

A
  • ethanol affects mucous membranes, making it easier for cells in the oropharynx to absorb other carcinogens
  • ethanol increases oestrogen levels
  • acetaldehyde (metabolite of ethanol) is a mutagen
227
Q

Which disease is caused by the Epstein-Barr virus?

A

Infectious mononucleosis (glandular fever).

228
Q

Which cancers can be caused by the Epstein-Barr virus?

A
  • nasopharyngeal carcinoma
  • Burkitt’s lymphoma
  • Hodgkin’s lymphoma
  • B- and T-cell lymphomas
  • leiomyosarcoma
229
Q

Which cancers can be caused by HPV?

A

Squamous cell carcinomas of the:

  • oropharynx
  • cervix
  • vulva
  • vagina
  • penis
  • anus
230
Q

Which cancer can be caused by the hep B virus?

A

Hepatocellular carcinoma

231
Q

Which cancers can be caused by human herpes virus 8?

A
  • Kaposi’s sarcoma

- primary effusion lymphoma

232
Q

What is a primary effusion lymphoma?

A

An HIV-associated lymphoma that arises in body cavities such as the pleural space, pericardium and peritoneum.

233
Q

Which cancers can be caused by human T lymphotrophic virus 1?

A

Adult T-cell leukaemia / lymphoma

234
Q

Which cancers can be caused by the hep C virus?

A
  • hepatocellular carcinoma
  • non-Hodgkin’s lymphoma
  • potentially pancreatic cancer and cholangiocarcinoma (bile duct cancer)
235
Q

Which cancers can be caused by exposure to UV light?

A
  • basal cell carcinoma
  • melanoma
  • squamous cell carcinoma
236
Q

Which condition increases risk of cancer due to UV light exposure?

A

Xeroderma pigmentosum - extreme sensitivity to UV light.

237
Q

Which cancers are associated with increased oestrogen levels?

A
  • breast cancer

- endometrial cancer (type of uterine cancer)

238
Q

Which cancer is associated with anabolic steroid use?

A

Hepatocellular carcinoma

239
Q

What is an example of a mycotoxin and it’s associated cancer?

A

Aflatoxin B (found in contaminated food) - hepatocellular carcinoma

240
Q

What is cholangiocarcinoma?

A

Bile duct cancer

241
Q

What are two examples of cancers that can be caused by parasites?

A
  • cholangiocarcinoma: can be caused by chlonorchis sinesis, a parasite that lives within bile ducts
  • bladder cancer: can be caused by shistosoma
242
Q

Which cancers can asbestos cause?

A
  • mesothelioma
  • lung cancer
  • laryngeal cancer
  • ovarian cancer
243
Q

What is a premalignant condition?

A

Local abnormality associated with increased risk of malignancy at that site.

244
Q

What are some examples of premalignant conditions?

A
  • colonic polyps
  • cervical dysplasia
  • ulcerative colitis
  • undescended testis
245
Q

What are the three main stages in the process of carcinogenesis?

A

Initiation - carcinogen induces genetic alterations that give the cell its neoplastic potential.
Promotion - stimulation of clinal proliferation of the initiated cell.
Progression - process leading to malignant behaviour.

246
Q

What genetic alterations are needed for a cell to become neoplastic?

A
  • expression of telomerase
  • inactivation of both copies of a tumour suppressor gene
  • activation of oncogenes
247
Q

What causes increased genomic instability?

A
  • ageing

- some genetic conditions

248
Q

What are the two types of tumour suppressor gene?

A

Caretaker genes: repair DNA damage

Gatekeeper genes: stop proliferation of cells with DNA damage

249
Q

Where is the p53 gene located?

A

p arm of chromosome 17

250
Q

What is the function of the p53 gene?

A
  • repairs DNA damage by arresting the cell cycle in G1 until damage is repaired
  • stimulates apoptotic cell death if there is extensive DNA damage
251
Q

How can p53 lose its function?

A
  • DNA mutations
  • complexes form of normal and mutant p53 proteins (this inactivâtes the normal protein)
  • binding of normal p53 protein to proteins encoded by oncogenic DNA viruses (e.g. HPV)
252
Q

What is Li-Fraumeni syndrome?

A

Inherited germline mutation in the p53 gene (heterozygous).

253
Q

What are the 5 classifications of oncogenes?

A
  • growth factors
  • growth factor receptors
  • signalling mediator with tyrosine kinase activity
  • signalling mediator with nucleotide binding activity (disrupts intracellular signalling)
  • nuclear-binding transcription factor onco-proteins (regulate cell proliferation)
254
Q

What is tyrosine kinase?

A

Enzyme - functions as an ‘on’ or ‘off’ switch in many cellular functions. Transfers a phosphate group from ATP to the tyrosine residues of proteins within a cell.

255
Q

How are oncogenes activated?

A
  • mutation resulting in an excessively active onco protein molecule
  • gene amplification / enhanced transcription resulting in excessive oncoprotein production
256
Q

How does epigenetics contribute to genetic alterations in neoplastic cells?

A
  • hypermethylation of promoter DNA sequences = gene silencing
  • histone modifications can up- or down-regulate genes (methylation, acetylation, phosphorylation)
  • miRNA degrades mRNA, leading to reduced expression
  • changes to the number of copies of enhancer and silencer DNA sequences
257
Q

What is the structure of a neoplasm?

A
  • neoplastic cells

- stroma

258
Q

What is the neoplastic stroma?

A

Connective tissue framework for mechanical support, intercellular signalling and nutrition.

259
Q

How is the neoplastic stroma formed?

A

Tumour cells produce growth factors, inducing connective tissue fibroblast proliferation.

260
Q

Why do some cancers have abundant myofibroblasts?

A

Provide contractility to retract adjacent structures.

261
Q

Example of a factor that limits the growth of a tumour?

A

Blood supply - the ability of nutrients to diffuse into the neoplastic cells.

262
Q

How is angiogenesis induced?

A

Factors secreted by tumour cells - e.g. vascular endothelial growth factor (VEGF).

263
Q

Why might some tumours have a lymphocytic infiltrate? What impact does this have on prognosis?

A

A lymphocytic infiltrate likely reflects a host immune reaction to the tumour. These tumours generally have a better prognosis.

264
Q

What can be seen on histological images of neoplastic cells?

A
  • loss of differentiation
  • loss of cellular cohesion
  • nuclear enlargement, hyperchromasia & pleomorphism
  • increased mitotic activity
265
Q

Which tumour shapes are usually benign?

A
  • sessile
  • pedunculated polyp
  • papillary
266
Q

Which tumour shapes are usually malignant?

A
  • exophytic / fungating
  • ulcerated
  • annular
267
Q

Where are annular tumours found?

A

Common in large bowel, often cause intestinal obstruction.

268
Q

Does sarcoma have an in situ phase?

A

No, only carcinoma has an in situ phase?

269
Q

What is the route of metastasis in carcinoma vs sarcoma?

A

Carcinoma - lymph

Sarcoma - blood

270
Q

How do neoplastic cells achieve proliferation and immortalisation?

A
  • autocrine growth stimulation (expression of oncogenes for growth factors, etc)
  • inactivation of tumour suppressor genes
  • reduced apoptosis (apoptosis inhibiting genes)
  • telomerase
271
Q

What is nuclear hyperchromasia?

A

More DNA per cell than in the normal population.

272
Q

What is aneuploidy / polyploidy?

A

Abnormal / increase number of chromosomes. Associated with increased tumour aggressiveness and nuclear pleomorphism.

273
Q

Why might neoplastic cells synthesise unexpected substances?

A

Some genes are de-repressed in neoplastic cells.

Phase 2a (10 decks)

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