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Semester Two > Pathological Processes > Flashcards

Pathological Processes Flashcards

1
Q

What are the common causes of cell injury?

A

Hypoxia
Physical agents
Chemical agents
Micro-organisms
Immune mechanisms
Dietary insufficiency and deficiencies and dietary excess
Genetic abnormalities (inborn errors of metabolism)

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2
Q

What is the mechanism of hypoxic cell injury?

A

Cell is deprived of oxygen, mitochondrial
ATP production stops. ATP-driven membrane ionic pump runs down. Sodium and water seep into the cell. Cell swells, and membrane is stretched.
Glycolysis allows cell to survive for a little longer. Cell initiates a heat-shock response, won’t be able to cope if hypoxia persists.
pH drops due to glycolysis and lactic acid accumulation. Calcium enters cell - activates phospholipases (membrane lose phospholipid), proteases (cytoskeleton is damaged and membrane proteins attacked), ATPase (causing further loss of ATP), endonucleases (nuclear chromatin clump)
ER and other organelles swell.
Enzymes leak out of lysosomes - these attack cytoplasmic components
All cell membranes are damaged and show blebbing.
Cell dies - possibly killed by bleb bursting.

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3
Q

How do the different mechanisms of cell injury target different components of the cell?

A

Cell membranes
Nucleus
Proteins - structural proteins and enzymes
Mitochondria

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4
Q

Define hypoxia

A

Oxygen deprivation

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5
Q

Define hypoxaemic hypoxia

A

Low level of oxygen in the blood

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6
Q

Define anaemic hypoxia

A

The oxygen carrying ability of the blood decreased

Cyanide poisoning, CO poisoning

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7
Q

Define ischaemic hypoxia

A

Insufficient blood flow to provide adequate oxygenation

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8
Q

Define histiocytic hypoxia

A

Cells can’t utilise the oxygen

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9
Q

Name some examples of physical agents that cause cell injury

A 
Direct trauma
Extreme temperatures (burns and severe cold)
Sudden changes in atmospheric pressure
Electric currents
Radiation
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10
Q

Name some examples of chemical agents that cause cell injury

A 
Glucose or salt in hypertonic solutions
Oxygen in high concentrations
Poisons
Insecticides
Herbicides
Asbestos
Alcohol
Illicit drugs
Therapeutic drugs
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11
Q

What is the mechanism of ischaemia-reperfusion cell injury?

A

Blood flow returned to a tissue subject to ischaemia but not yet necrotic. The damage to the tissue can be worse than if blood flow was not restored.
May be due to increased production of oxygen free radicals with reoxygenation - due to burst of mitochondrial activity; may be due to increased number of neutrophils following blood supply (more inflammation and increased tissue injury); may be due to delivery of complement proteins and activation of the complement pathway

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12
Q

How do free radicals cause cellular damage?

A

Attack lipids in cell membranes and cause lipid peroxidation
Damage proteins, carbohydrates and nucleic acids
Cause mutations (mutagenic)

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13
Q

What does the anti-oxidant system consist of?

A

Enzymes (superoxide dismutase), catalases, peroxidases)
Free radical scavengers
Storage proteins

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14
Q

How do free radical scavengers form part of the anti-oxidant system?

A

They neutralise free radicals

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15
Q

Name examples of free radical scavengers

A

Vitamins A, C, and E

Glutathione

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16
Q

How do storage proteins form part of the anti-oxidant system?

A

Sequester “hide away/isolate” transition metals in the extracellular matrix.
Transferrin and ceruloplasmin sequester iron and copper, which catalyse the formation of free radicals.

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17
Q

Name some heat shock proteins

A

Stress proteins
Unfoldases
Chaperonins
Ubiquitin

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18
Q

What is the heat shock response?

A

All cells from any organism turn down their usual protein synthesis and turn up synthesis of HSPs in response to stress

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19
Q

Why are HSPs important in cell injury?

A

Heat shock response plays a key role in maintaining protein viability and thus maximising cell survival

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20
Q

Describe the appearance of injured cells in a light microscope

A

Cytoplasmic
Nuclear changes
Abnormal intracellular accumulations

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21
Q

What are the reversible changes observed in injured cells in an electron microscope?

A

Swelling - cell and organelles due to Na+/K+ pump failure
Cytoplasmic blebs - symptomatic of cell swelling
Clumped chromatin due to reduced pH
Ribosome separation from ER due to failure of energy-dependant process of maintaining ribosomes in the correct location

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22
Q

What are the irreversible changes observed in injured cells in an electron microscope?

A

Increased cell swelling
Nuclear changes - pyknosis, karyolysis, or karyorrhexis
Swelling and rupture of lysosomes - reflects membrane damage
Membrane defects
Appearance of myelin figures (damaged membranes)
Lysis of the endoplasmic reticulum due to membrane defects
Amorphous densities in swollen mitochondria

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23
Q

Define oncosis

A

Cell death with swelling; the spectrum of changes that occur prior in cells injured by hypoxia and some other agents

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24
Q

Define apotosis

A

Cell death with shrinkage; cell death induced by a regulated intracellular program where a cell activates enzymes that degrade its own nuclear DNA and proteins

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25
Q

Define necrosis

A

In a living organism the morphological changes that occur after a cell has been dead for some time (between 4 and 24 hours).
Necrosis describes morphological changes, not a type of cell death.
It is an appearance and not a process

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26
Q

What are the different types of necrosis?

A

Coagulative
Liquifactive (colliquitive)
Caseous
Fat

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27
Q

What happens in coagulative necrosis?

A

Proteins undergo denaturation, and then coagulate

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28
Q

What happens in liquifactive necrosis?

A

Proteins undergo dissolution by the cells own enzymes

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29
Q

What is gangrene?

A

Clinical term to describe necrosis that is visible to the naked eye

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30
Q

What are the different types of gangrene?

A

Wet and dry gangrene

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31
Q

How does dry gangrene come about?

A

Necrosis is modified by exposure to are resulting in drying

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32
Q

How does wet gangrene come about?

A

Necrosis is modified by by infection with a mixed bacterial culture.

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33
Q

What is the underlying process in dry gangrene?

A

Coagulative necrosis

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34
Q

What is the underlying process in wet gangrene?

A

Liquifactive necrosis

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35
Q

What is gas gangrene?

A

Wet gangrene where the tissue has become infected with anaerobic bacteria that produce visible and palpable bubbles of gas within the tissues

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36
Q

What is infarction in relation to necrosis?

A

Infarction is a cause of necrosis - ischaemia (reduced blood supply)

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37
Q

What are the classifications of infarcts?

A

Red or white

- indicates how much haemorrhage there is into the infarct

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38
Q

What is a white infacrt?

A

Anaemic
Occurs in ‘solid’ organs (those with good stromal support) after occlusion of an “end” artery - any artery that is the sole support of arterial blood to a segment of an organ

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39
Q

What is a red infarct?

A

Haemorrhagic

Occurs where there is extensive haemorrhage into dead tissue

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40
Q

What molecules are released by injured, dying and dead cells?

A

Potassium
Enzymes (can indicate the organ involved and the extent, timing and evolution of the tissue damage)
Myoglobin (this is released from dead myocardium and striated muscle)

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41
Q

What are the consequences of dead/dying cells leaking molecules?

A

Can cause local irritation and local inflammation
May have general toxic effects on the body
May appear in high concentrations in the blood and can be measured and thus aid in diagnosis

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42
Q

What is apoptosis?

A

The death of a single cell (or small cluster of cells) due to activation of an internally controlled suicide programme

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43
Q

What is the appearance of apoptotic cells under a light microscope?

A

They are shrunken, intensely eosinophilic

Chromatin condensation, pyknosis and karyorrhexis

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44
Q

What is the appearance of apoptotic cells under an electron microscope?

A

Cytoplasmic budding
Fragmentation
Membrane-bound apoptotic bodies which contain cytoplasm, organelles and often nuclear fragments

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45
Q

What is the fate of apoptotic cells?

A

Eventually removed by macrophage phagocytosis

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46
Q

Why does apoptosis not induce inflammation?

A

There is no leakage of cell contents so does not induce inflammation

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47
Q

What are the three phases of apoptosis?

A

Initiation
Execution
Degradation/phagocytosis

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48
Q

What are abnormal cellular accumulations?

A

If the cell is unable to metabolise something it will remain in the cell as one of these

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49
Q

When are abnormal cellular accumulations seen?

A

When metabolic processes become deranged

Often occur with sublethal or chronic injury

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50
Q

Are all abnormal cellular accumulations dangerous?

A

No, they can be reversible, harmless or toxic

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51
Q

What can abnormal cellular accumulations derive from?

A

Cell’s own metabolism
Extracellular space, e.g. spilled blood
Outer environment, e.g. dust

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52
Q

What are the five main groups of intracellular accumulations?

A 
Water and electrolytes
Lipids - triglycerides and cholesterol
Proteins - e.g. Mallory's hyaline, alpha-1 antitrypsin
'Pigments' - exogenous and endogenous
Carbohydrates
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53
Q

What are the different types of calcification?

A

Dystrophic and metastatic

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54
Q

What is pathological calcification?

A

Abnormal deposition of calcium salts within tissues

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55
Q

Where does dystrophic calcification occur?

A 
Areas of dying tissue
Atherosclerotic plaques
Some neoplastic growths
Aging or damaged heart valves
Tuberculous lymph nodews
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56
Q

Describe dystrophic calcification

A

No abnormality in calcium metabolism or serum calcium or phosphate concentrations
A local change of disturbance in the tissue favours the nucleation of hydroxyapatite crystals

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57
Q

Describe metastatic calcification

A

Disturbance is body-wide
Hydroxyapatite crystals are deposited in normal tissues throughout the body when there is hypercalcaemia secondary to disturbances in calcium metabolism.
Usually asymptomatic but it can be lethal

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58
Q

What happens when a cell ages?

A

It accumulates damage to cellular constituents and DNA.

Decline in the ability to replicate.

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59
Q

Why are older cells unable to replicate?

A

Replicative senescence
The ends of chromosomes are called telomeres and with every replication the telomere is shortened.
When the telomeres reach a critical length, the cell can no longer divide

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60
Q

What are the common causes of acute inflammation?

A

Microbial infections (bacterial, viral, parasitic and microbial toxins)
Hypersensitivity reactions
Physical and chemical agents (thermal injury - burns or frostbite; irradiation, environmental chemicals)
Tissue necrosis (any cause)
Foreign bodies (splinters, dirt, sutures)

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61
Q

What is acute inflammation?

A

Short term process occurring in response to tissue injury, usually appearing within minutes or hours

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62
Q

What are the clinical signs of inflammation?

A 
Rubor
Calor
Tumor
Dolor
Loss of function
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63
Q

What is rubor?

A

Redness

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64
Q

What is calor?

A

Heat

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65
Q

What is tumor?

A

Swelling

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66
Q

What is dolor?

A

Pain

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67
Q

What causes rubor?

A

Caused by increased blood circulation

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68
Q

What causes calor?

A

Increased blood circulation leads to a rise of body temperature at the site of inflammation

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69
Q

What causes tumor?

A

Fluid leaks into the tissues

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70
Q

What causes dolor?

A

Some of the released mediators such as bradykinin increase the sensitivity to pain

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71
Q

What tissue changes occur in acute inflammation?

A

Vascular phase

Cellular phase

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72
Q

What occurs during the vascular phase?

A

Changes in blood flow

Accumulation of exudate

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73
Q

What occurs during the cellular phase?

A

Delivery of neutrophils

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74
Q

Describe the changes in blood flow in the vascular phase of acute inflammation

A

Vasoconstriction in seconds
Vasodilatation in minutes (causing heat and redness)
Increased permeability - fluids and cells can escape

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75
Q

Describe the movement of fluid in the vascular phase of acute inflammation

A

Vasodilatation - increased capillary hydrostatic pressure
Increased vessel permeability - plasma proteins move into interstitium, increased interstitial oncotic pressure
Fluid movement - out of vessel into interstitium, causing oedema (tumor)

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76
Q

What changes to blood are there in acute inflammation?

A

Movement of fluid out of vessel - increased viscosity of blood
Reduced flow through the vessel - stasis

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77
Q

What is a fluid exudate?

A

Fluid that filters from the circulatory system into areas of inflammation

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78
Q

What is in a fluid exudate?

A

High protein content

Many contain some white and red cells

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79
Q

What is a neutrophil?

A

Primary type of leucocyte involved in acute inflammation

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80
Q

Why are neutrophils important in mediating acute inflammation?

A

Each neutrophil contains about 2,000 granules containing bactericidal substances
Must:
1- chemotaxis (summoned to place of injury)
2- activation (switch to higher metabolic level)
3- margination (stick to the endothelial surface)
4- diapedesis (crawl through the endothelium)
5- recognition-attachment (recognise the bacterium and attach to it)
6- phagocytosis (engulf the bacterium)

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81
Q

What are some of the key chemical mediators involved in acute inflammation?

A 
Vasoactive amines
Vasoactive peptides
Complement components
Clotting and fibrinolytic cascades
Mediators derived from phospholipids
Cytokines and chemokines
Exogenous mediators of inflammation
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82
Q

Describe vasoactive amines

A

Histamine and serotonin

cause vasodilatation, increased vascular permeability

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83
Q

Describe vasoactive peptides

A

Bradykinin
circulates in blood as part of kininogen
effects are: increased vascular permeability, vasodilatation and burning pain

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84
Q

Describe mediators derived from phospholipids

A

Prostaglandins, thromboxanes and leukotrienes
leukotriene B4 - powerful chemotaxis agent
cause vasodilatation and prostaglandins cause pain

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85
Q

Describe complement components

A

C3a, C5a
function is to form a tube which punches holes in bacteria - causing them to die
circulates in the blood as a number of disassembled proteins

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86
Q

Describe cytokines and chemokines

A

Interleukins, tumour necrosis factor (TNF), interferons
polypeptides that act as messengers between cells
Chemokines - cytokines involved in chemotaxis
Cytokines are produced by macrophages, appear in hours following injury
Local and systemic effects - TNF causes cachexia

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87
Q

Describe exogenous mediators

A

Endotoxin produced by gram negative bacteria
when released, causes inflammation - but if released into blood activates numerous inflammatory mechanisms at once - results in septic shock

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88
Q

What are the local and systemic short and long term consequences of acute inflammation

A

Local - damage to normal tissue, obstruction of tubes (i.e. intestine or Fallopian tubes), loss of fluid (due to oedema), pain and loss of function

Systemic - fever, leucocytosis, acute phase response, shock

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89
Q

What are the effects of acute inflammation on organs?

A

Can lose function

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90
Q

What are some features of acute inflammation seen in lobar pneumonia?

A

jk

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91
Q

What are some features of acute inflammation seen in acute appendicitis?

A

ki

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92
Q

What are some features of acute inflammation seen in bacterial meningitis?

A

jk

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93
Q

What are some features of acute inflammation seen in ascending cholangitis?

A

k

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94
Q

What are some features of acute inflammation seen in liver abscesses?

A

jk

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95
Q

Name a few inherited disorders of the acute inflammatory process

A

Hereditary angio-oedema
Alpha-1 antitrypsin deficiency
Chronic granulomatous disease

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96
Q

Describe hereditary angio-oedema

A

Extremely rare, autosomal dominant
Deficiency of C1-esterase inhibitor
Patients have attacks of non-itchy cutaneous angio-oedema (rapid oedema of the dermis, subcutaneous tissue, mucosa and submucosal tissues)
Can also experience recurrent abdominal pain due to intestinal oedema.
Family history of sudden death due to laryngeal involvement

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97
Q

Describe alpha-1 antitrypsin deficiency

A

Autosomal recessive disorder - varying levels of severity
alpha-1 antitrypsin deactivates enzymes released from neutrophils
Patients with this disorder develop emphysema because enzymes destroy normal parenchymal tissue
Liver disease can occur as the hepatocytes produce an abnormal version of the protein - polymerises and can’t be exported from the ER. Causes hepatocyte damage and eventually cirrhosis

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98
Q

Describe chronic granulomatous disease

A

Phagocytes are unable to generate superoxide - bacteria are phagocytised by cannot be killed because phagocytes can’t generate an oxygen burst
Results in many chronic infections in the first year of life
Numerous granulomas and abscesses affecting skin, lymph nodes, sometimes the lung, liver and bones occur

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99
Q

What is the aetiology of chronic inflammation?

A

Exposure - sometimes, long-term, low-level exposure to an irritant can result in chronic inflammation
Autoimmune disorders - immune system mistakenly attacks normal healthy tissue, as in psoriasis
Hypersensitivity
Autoinflammatory diseases
Persistent acute inflammation

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100
Q

Define chronic inflammation

A

Inflammation of prolonged duration in which active inflammation, tissue injury, and the healing proceed simultaneously

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101
Q

What are the actions of macrophages in chronic inflammation?

A

“big eater”

They phagocytose, secrete numerous substances that summon and activate other cells, present antigens to the immune system and initiate an immune response, stimulate angiogenesis (formation of new blood vessels), induce fibrosis, fever, acute phase reaction and cachexia

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102
Q

What are the actions of giant cells in chronic inflammation?

A

Multiple macrophages fused together

Can clear up larger molecules via phagocytosis

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103
Q

What are the actions of lymphocytes in chronic inflammation?

A

Process antigens
Secrete antibodies
Secrete cytokines that influence other inflammatory cells
Kill cells (done by natural killer cells which attack virus-infected cells and sometimes cancer cells)

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104
Q

What are the actions of eosinophils in chronic inflammation?

A

They attack large parasites such as worms and they are present in high numbers in some immune responses (i.e. in the bronchi in asthma, and in some tumours)

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105
Q

What are the actions of fibroblasts in chronic inflammation?

A

Can respond to chemotactic stimuli and move to sites where they are needed
Produce connective tissue substances such as collagen, elastin and glycosaminoglycans

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106
Q

What are the actions of myofibroblasts in chronic inflammation?

A

Specialised fibroblasts with contractile activity

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107
Q

What are the complications of chronic inflammation?

A

Fibrosis
Impaired function
Involvement inappropriate immune response

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108
Q

How will tissue destruction after chronic inflammation affect organs?

A

If the tissue is worn away, then organs won’t be able to function properly

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109
Q

How will excessive fibrosis after chronic inflammation affect organs?

A

Can impair the function

If there are enough myofibroblasts - can slowly contract and cause more problems

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110
Q

How will atrophy after chronic inflammation affect organs?

A

If enough of the tissue is atrophied, then the organ will not be able to function and will fail

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111
Q

What features of chronic inflammation are seen in rheumatoid arthritis?

A

The immune system attacks the body’s normal tissues - the resulting chronic inflammation becomes a disease process

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112
Q

What features of chronic inflammation are seen in ulcerative colitis?

A

kj

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113
Q

What features of chronic inflammation are seen in Crohn’s disease?

A

jk

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114
Q

What features of chronic inflammation are seen in chronic cholecystitis?

A

jk

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115
Q

What features of chronic inflammation are seen in chronic gastritis?

A

jk

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116
Q

What features of chronic inflammation are seen in liver cirrhosis?

A

jkbgfv

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117
Q

What are the different types of giant cell?

A

gdgd

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118
Q

What are the actions of Langhan giant cells?

A

Found in granulomatous conditions

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119
Q

What are the actions of foreign body giant cells?

A

Involved in the foreign body reaction, phagocytosis, and degradation
Often seen when a hard to digest foreign body is present
If the foreign body is small - phagocytised by the giant cell and can be seen within it
If the foreign body is large - giant cell sticks to its surface

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120
Q

What are the actions of Touton giant cells?

A

Form in lesions where there is a high lipid content - fat necrosis and xanthomas

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121
Q

What do Langhan giant cells look like?

A

Nuclei are arranged around the periphery of the giant cell

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122
Q

What do foreign body giant cells look like?

A

Nuclei are arranged randomly in the cell

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123
Q

What do Touton giant cells look like?

A

Nuclei are arranged in a ring towards the centre of the cell

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124
Q

Describe a granuloma

A

Aggregation of macrophages that forms in response to chronic inflammation
Occurs when the immune system attempts to isolate foreign substances which it is unable to eliminate

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125
Q

Describe granulomatous inflammation

A

A type of chronic inflammation in which granulomas are seen

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126
Q

What is the aetiology of granulomatous inflammation?

A

Body’s way of dealing with particles that are poorly soluble or difficult to eliminate
This includes foreign bodies such as thorns, splinters, ‘tough’ bacteria (Mycobacterium tuberculosis) and (Mycobacterium leprae)

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127
Q

What is labile tissue?

A

Continuously dividing tissues

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128
Q

What is stable tissue?

A 
Quiescent tissues
(quiescent = in a state or period of inactivity or dormancy)
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129
Q

What is permanent tissue?

A

Non-dividing tissues

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130
Q

What are the differences between labile, stable and permanent tissues?

A

They all have different proliferative activity

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131
Q

Give examples of labile tissue

A

Surface epithelia
Lining mucosa of secretory ducts of the glands of the body
Columnar epithelia of GI tract and uterus
Transitional epithelium of urinary tract
Cells of bone marrow and haematopoietic tissues

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132
Q

Give examples of stable tissue

A

Parenchymal cells of the liver, kidneys and pancreas
Mesenchymal cells such as fibroblasts, bone osteoclasts and smooth muscle cells
Vascular endothelial cells
Resting lymphocytes
Other white blood cells

133
Q

Give examples of permanent tissue

A

Neurones

Skeletal and cardiac muscle cells

134
Q

What is the role of stem cells in regeneration and repair?

A

In order for tissues to regenerate, cells must be replaced.

In tissues where regeneration is possible differentiated cells are very often replaced by cells derived from stem cells

135
Q

What does the term ‘unipotent’ mean?

A

Stem cells that can usually only give rise to one type of adult - they are lioneage specific

136
Q

What does the term ‘multipotent’ mean?

A

Stem cells that can produce several types of differentiated cell
e.g. haematopoietic stem cells

137
Q

What does the term ‘totipotent’ mean?

A

Cells that have the ability to self-renew by dividing and the ability to develop into the three primary germ cell layers of the embryo and into extra-embryonic tissues such as placenta

138
Q

What are the different types of communication between cells?

A 
Autocrine
Paracrine
Endocrine
Epidermal growth factor
Vascular endothelial growth factor
Platelet-derived growth factor
Tumour necrosis factor
139
Q

How does autocrine signalling work?

A

Cells respond to the signalling molecules that they themselves produce

140
Q

How does paracrine signalling work?

A

A cell produces the signalling molecules, this acts on adjacent cells
Responding cells are close to the secreting cell and are often a different type

141
Q

How does endocrine signalling work?

A

Hormones are synthesised by cells in an endocrine organ, they are then conveyed in the blood stream to target cells to effect physiological activity

142
Q

How do growth factors help cells to communicate?

A

TNF - induces fibroblast migration, fibroblast proliferation and collagenase secretion

143
Q

How do adhesion molecules help cells to communicate?

A

Bind cells to each other - cadherins

Bind cells to the extracellular matrix - integrins

144
Q

How does the concept of contact inhibition help cells to communicate?

A

After becoming isolated, normal cells will replicate until they have cells touching them and then stop - form a monolayer sheet of cells with no overlap

145
Q

What processes are involved in regeneration?

A

The capacity to regrow parts of an organ or tissue after damage

146
Q

What processes are involved in resolution?

A

Pathogens and damaged tissue are removed by macrophages

147
Q

What processes are involved in fibrous repair/organisation?

A

1- phagocytosis of necrotic tissue debris
2- proliferation of endothelial cells which results in small capillaries that grow into the area (angiogenesis)
3- proliferation of fibroblasts and myofibroblasts that synthesise collagen and cause wound contraction
4- granulation tissue becomes less vascular and matures into a fibrous scar
5- scar matures and shrinks due to contractions of fibrils within myofibroblasts

148
Q

How does regeneration, resolution, fibrous repair/organisation affect different tissues?

A

Some tissues are capable of regenerating, some aren’t capable of any at all

149
Q

What are the histological components of granulation tissue?

A

Presence and proliferation of fibroblasts, keratinocytes, endothelial cells, new thin-walled capillaries, and inflammatory cell infiltration of the extracellular matric

150
Q

Describe the synthesis of collagen

A

Collagen consists of a triple helix of three polypeptide alpha chains with gly-x-y repeating sequence
Synthesised by fibroblasts and myofibroblasts:
1- preprocollagen is produced
2- modified to procollagen, takes on the triple helix form and secreted
3- procollagen is cleaved to make fibrillar collagen

151
Q

What are the different types of collagen?

A

Type I (fibrillar) - most common type, present in hard and soft tissues
Type II - part of cartilage, bone and vitreous humour
Type III - found in loose connective tissues and in the muscle

152
Q

What are some defects of collagen synthesis?

A

Scurvy
Ehlers-Danlos syndrome
Osteogenesis imperfecta
Alport syndrome

153
Q

Describe how scurvy affects collagen synthesis

A

Vitamin C is required for hydroxylation of procollagen

Patients with scurvy cannot heal wounds adequately, and have a tendency to bleed as capillaries are fragile

154
Q

Describe how Ehlers-Danlos syndrome affects collagen synthesis

A

Heterogenous group of 6 inherited disorders where collagen fibres lack adequate tensile strength
Skin is hyperextensible, fragile and susceptible to injury. Joints are hypermobile

155
Q

Describe how osteogenesis affects collagen synthesis

A

Patients have too little bone tissue and hence extreme skeletal fragility
Too little collagen in the sclera of the eye - making it look blue

156
Q

Describe how Alport syndrome affects collagen synthesis

A

X-linked disease
Type IV collagen is abnormal, results in dysfunction of the glomerular basement membrane, the cochlea of the ear and the lens of the eye

157
Q

What is primary intention?

A

Would healing occurring in incisional, closed, non-infected and sutured wounds
There is disruption of epithelial basement membrane continuity but death of only a limited number of epithelial and connective tissue cells

158
Q

What is secondary intention?

A

Seen in excisional wounds or wounds with tissue loss and separated edges. Seen in infected wounds
The wound is filled with granulation tissues, which grows in from the wound margins

159
Q

How can you distinguish between primary and secondary intention?

A

Can be primary or secondary intention depending on the size of the wound and the amount of tissue that has been lost

160
Q

What is the healing process of bone fractures?

A

1- haematoma fills the gap and surrounds the bone injury; provides a foundation for the subsequent cell growth
2- fibrin mesh and granulation tissue is formed; platelets and inflammatory cells release cytokines - these activate osteoprogenitor cells to osteoclastic and osteoblastic activity
3- soft callus forms
4- hard callus forms, is laid down by osteoblasts - initially is woven bone (is weaker and less organised but can be formed quickly)
5- lamellar bone is more organised
6- remodelling of the bone occurs

161
Q

How does size, location and type of wound influence the efficacy of healing and repair?

A

Foreign bodies - produces persistent inflammation and favours infection
Haematoma - if large, can slow healing
Necrotic tissue - needs clearing, if there’s a lot will take longer
Mechanical stress - can pull delicate tissue apart
Protection - keeps wound clean and free from infection
Surgical techniques - good techniques promote rapid healing and minimise scarring

162
Q

What are the systemic factors influencing the efficacy of healing and repair?

A

Malignancy - due to cachexia seen with malignant tumours
Genetic disorders - affect collagen synthesis
Drugs - steroids (immunosuppressive, inhibit collagen synthesis), cytotoxics (anti-mitogenic, impair cells proliferation and healing), antibiotics (treat bacterial infections, reduce inflammation)
Vitamin deficiency - vit C deficiency inhibits collagen synthesis
Malnutrition or protein loss - can’t synthesise protein

163
Q

What are the complications of fibrous repair?

A

Can form fibrous adhesions compromising organ function or blocking tubes
Can lose function due to replacement of specialised functional cells by non-functioning collagenous scar tissue
Can disrupt complex tissue relationships within an organ
Can overproduce fibrous scar tissue
Can have excessive scar contraction causing obstruction of tubes, disfiguring scars following burns or joint contractures

164
Q

Describe insufficient fibrosis

A

Insufficient fibrosis would mean the wound would remain open - leaving it susceptible to infection etc

165
Q

Describe excessive fibrosis

A

Keloid scars can form
A keloid scar is an overgrowth of fibrous tissue, due to an overproduction of collagen, that exceeds the borders of the scar
They don’t regress - excision just creates another one

166
Q

Describe excessive contraction

A

This can lead to deformity characterised by skin constriction and functional limitations
The skin is “contracted” - pulled too tight

167
Q

What are some of the special aspects of regeneration and repair in cardiac muscle?

A

Has very limited/no regenerative capacity
Myocardial infarction is followed by scar formation
This can compromised cardiac function

168
Q

What are some of the special aspects of regeneration and repair in the liver?

A

Has remarkable capacity to regenerate
If part is removed, compensatory growth of liver tissue occurs and there is liver restoration of liver mass by enlargement of the lobes that remain
Hepatocytes regenerate first

169
Q

What are some of the special aspects of regeneration and repair in peripheral nerves?

A

When a nerve is severed, the axons degenerate
Proximal stumps of degenerated axons sprout and elongate
Use Schwann cells vacated by distal degenerated axons to guide them back to tissue that the nerve innervates

170
Q

What are some of the special aspects of regeneration and repair in cartilage?

A

Doesn’t heal well due to lack of blood supply, lymphatic drainage and innervation

171
Q

What are some of the special aspects of regeneration and repair in central nervous system?

A

Neural tissue is a permanent tissue

When damage occurs, the neural tissue is replaced by proliferation of CNS supportive elements (glial cells) = gliosis

172
Q

What is haemostasis?

A

Stopping of haemorrhage

“halting the blood” - literal definition

173
Q

Describe the principles of haemostasis

A

1- severed artery contracts to decrease pressure downstream
2- primary haemostatic plug of activated platelets forms - forms in seconds to minutes
3- secondary haemostatic plug forms as fibrin filaments stabilise the platelet plug into a blood clot - forms in 30 minutes

174
Q

Describe the role of the vessel wall in haemostasis

A

Arterial media contracts when artery is damaged
Subendothelium traps platelets
Endothelium performs a balancing act between opposing and favouring clotting

175
Q

Describe the role of platelets and the platelet plug in haemostasis

A

Platelets are activated by collagen surfaces, ADP, thromboxane, thrombin
They stick to exposed subendothelium (specifically to von Willebrand factor), then aggregate with other platelets. They then swell and change shape into sticky, spiny spheres. They secrete factors from platelet granules that help platelet plug to grow and aid clotting

176
Q

Describe the role of the coagulation system in haemostasis

A

This is the whole system of cells, proteins and processes that mediate blood clotting
It is vital

177
Q

Describe the role of the fibrinolytic system and plasmin in haemostasis

A

Side effect of tPA - bleeding, commonly from the gums or nose, but can occur in the brain
The clotting cascade sets fibrinolysis in motion
After surgery fibrinolytic activity drops and remains low for 7-10 days, the time period that is associated with the increased risk of postoperative thrombosis

178
Q

Describe the role of the production of thrombin and fibrin in haemostasis

A

In order for blood to clot fibrin has to be produced - thrombin cleaves fibrinogen into fibrin
Can’t have fibrin without thrombin
Thrombin can’t circulate in the blood otherwise blood would be solid - it is activated by a number of clotting factors
Clotting factors need vitamin K for their synthesis

179
Q

Describe the role of thrombin inhibitors in haemostasis

A

Natural anticoagulants
They oppose the formation of fibrin - the main natural anticoagulants are antithrombin III, protein C and protein S.
Fibrin degradation products inhibit clotting

180
Q

What are the common tests in a coagulation screen?

A

Platelet count
Bleeding time
PT (Prothrombin time) - measure of the time taken for blood to clot via the extrinsic pathway
APTT (Activated partial thromboplastin time) - measure of the time taken for blood to clot via the intrinsic pathway

Play Tennis OUTSIDE (PT - extrinsic)
Play Table Tennis INSIDE (APTT - intrinsic)

181
Q

Interpret the common tests in a coagulation screen

A

PT = 12-13 seconds
APTT = 35-45 seconds
Bleeding time = 1 to 6 minutes
Thrombin time = 10-15 seconds

182
Q

What are some common inherited bleeding disorders?

A

Haemophilia A and B

Von Willebrand Disease

183
Q

What is haemophilia A?

A 
Factor VIII (8) deficiency (either decreased amounts of decreased activity)
X-linked recessive disease, affects males
184
Q

What is haemophilia B?

A

Factor IX (9) deficiency
Clinically indistinguishable from haemophilia A
X-linked recessive disease with variable clinical severity
Normal platelet count, bleeding time and PT, but prolonged APTT
Treated with recombinant factor IX

185
Q

What is thrombophilia?

A

Inherited or acquired defects of haemostasis resulting in a predisposition to thrombosis
More likely to get a deep vein thrombosis, for example

186
Q

What is von-Willebrand disease?

A

Most common inherited bleeding disorder
Due to a deficiency or abnormality in von Willebrand factor
Bleeding time and APTT can be raised in the condition
Common presentation of mucosal bleeding reflects the inadequate platelet function and adhesion

187
Q

What is the pathophysiology of disseminated intravascular coagulation?

A

Secondary complication in a variety of conditions
An activator of clotting gets into the blood and microthrombi are formed throughout the circulation
Uses platelets, fibrin and coagulation factors and activates fibrinolysis - patient may then experience haemorrhage

188
Q

What is the treatment of disseminated intravascular coagulation?

A

Treat the underlying cause of DIC
Transfusions of platelets, fresh frozen plasma (FFP), cryoprecipitates (contains factor VIII, fibrinogen, von Willebrand factor and factor XIII), red blood cells
Occasionally may require an anticoagulant such as heparin

189
Q

What are some of the complications associated with disseminated intravascular coagulation?

A

Conditions such as neurological impairment, gangrene of the skin, renal failure, respiratory distress and gastrointestinal ulceration
Haemorrhagic component results in conditions such as intracerebral bleeding, petechiae, haematuria, epistaxis and GI bleeding

190
Q

What is the mode of action of commonly used anticoagulants?

A

Suppress the synthesis or function of various clotting factors that are normally present in the blood

191
Q

How are commonly used anticoagulants monitored?

A

APTT test

192
Q

What are the complications of anticoagulants?

A 
Blood in urine
Blood in stool
Severe bruising
Prolonged nosebleeds
Bleeding gums
Vomiting/coughing up blood
Heavy periods in women
193
Q

What are the principles of thrombosis?

A

Changes in the vascular wall (endothelial damage) - platelets will adhere to von Willebrand factor, if there is also stasis then a thrombus will form
Changes in the blood flow (slow or turbulent flow) - thrombosis is more frequent in veins due to slower blood flow. Turbulent flow can itself produce endothelial damage. Abnormal flow allows thrombi to grow more easily
Changes in the blood (hypercoagulability) - increased circulating levels of fibrinogen and factor VIII so blood is hypercoagulable
(appears that only two out of the three are required for a thrombus to form)

194
Q

What are the principles of embolism?

A

Sudden blocking of an artery by a thrombus or foreign material which has been brought to its site of lodgement by the blood current
Can’t have embolization in veins because the blood flow is from smaller to larger vessels

195
Q

What are the different types of embolism?

A

Thromboemboli - emboli arisen from thrombi
Pulmonary emboli
Paradoxical emboli - thromboemboli from systemic veins embolising in systemic arteries - have to bypass the lungs
Emboli from Atheroma
Fat and Bone Marrow emboli - complication of bone fractures, can occur after liposuction
Gas emboli
Amniotic fluid emboli - complication of labour and C-section
Talcum emboli - microscopic foreign bodies with which drugs have been ‘cut’, found in lungs of intravenous drug abusers

196
Q

What are the outcomes of thrombosis?

A

Resolution - dissolved
Propagation - grows
Organisation - undergoes fibrous repair and forms a fibrous scar on the wall of the vessel
Recanalisation - of an occluding thrombus, new channels lined with endothelium run through the occlusion and restore blood flow
Embolisation - part of the thrombus breaks off and embolises

197
Q

What are the outcomes of embolism?

A

Can die
Chronic damage to lungs (pulmonary hypertension
Can recur

198
Q

What are the complications of thrombosis?

A

Occlusion of an artery at the site, resulting in ischaemia and infarction
Embolisation of part of the thrombus resulting in occlusion of an artery distant to the site of the thrombus
Congestion and oedema in the venous bed resulting in pain and sometimes skin ulceration
Repeated miscarriages due to thrombosis of the uteroplacental vasculature which often seen in inherited thrombophilias

199
Q

What are the complications of embolism?

A

gh

200
Q

What are the preventative methods available for thromboembolic disease?

A

General prophylaxis - preventing venous stasis (mobilise early after operation or illness; during + after surgery, legs can be elevated; compression stockings, calf muscle stimulation and passive calf muscle exercises) or preventing hypercoagulability (anticoagulants)
Aspirin - platelets can’t produce thromboxane A2 (a powerful platelet aggregator)
Heparin - activates antithrombin III
Warfarin - interferes with vitamin K metabolism
Filters - pulmonary emboli prevented by putting umbrella-shaped filter in the inferior vena cava

201
Q

What are the treatments for thromboembolic disease?

A

Aspirin - platelets can’t produce thromboxane A2 (a powerful platelet aggregator)
Heparin - activates antithrombin III
Warfarin - interferes with vitamin K metabolism

202
Q

What is meant by the term ‘ateriosclerosis’?

A

Hardening of the arteries

The walls of arteries are thickened and lose their elasticity

203
Q

What is meant by the term ‘atherosclerosis’?

A

A disease of large and medium sized arteries that begins in the intima
Plaques are formed in the arterial wall and these are filled with atheroma - plaques often calcify

204
Q

What us meant by the term ‘atheroma’?

A

The necrotic core of the atherosclerotic plaque

Consists of dead cells, debris and cholesterol crystals

205
Q

What are the cellular events that lead to the formation of atherosclerotic lesions?

A

1- chronic endothelial damage
2- lipid droplets cross the endothelium and accumulate in the intima. Lipids oxidise and macrophages ingest - they are then called foam cells
3- foam cells cause the endothelium to bulge, smooth muscle moves to the lesion and starts to proliferate - then called a fatty streak
4- plaque grows as number of foam cells and smooth muscle cells increases. Some smooth muscle cells will lie over the plaque but underneath the endothelium, forming a roof - this is reinforced by collagen, elastin and other matrix proteins and results in a fibrous cap
5- cells in the centre die and necrosis develops, dead cells release cholesterol and crystals appear in the plaque. Plaque may undergo calcification

206
Q

What cells are involved in the formation of an atherosclerotic plaque?

A

Macrophages - become foam cells

Smooth muscle cells

207
Q

What is the role of endothelial cells in the formation of an atherosclerotic plaque?

A

hj

208
Q

What is the role of platelets in the formation of an atherosclerotic plaque?

A

As the endothelium stretches over the plaque, gaps appear between the endothelial cells - platelets adhere to these gaps

209
Q

What is the role of smooth muscle cells in the formation of an atherosclerotic plaque?

A

Some smooth muscle cells take up lipid and appear foamy

Some smooth muscle cells will lie over the plaque but beneath the endothelium forming a “roof”

210
Q

What is the role of macrophages in the formation of an atherosclerotic plaque?

A

They ingest the oxidised lipids to become foam cells

211
Q

What are the variable macroscopic appearances of athersclerosis?

A

White to yellow in colour

Impinge on the lumen of the artery

212
Q

What are the various microscopic appearances of atherosclerosis?

A

Intimal foam cells
Smooth muscle cells
Some extracellular lipid
Fibrosis, necrosis, cholesterol clefts, disruption of the internal elastic lamina, extension into the media and ingrowth of small vessels from the adventitia

213
Q

Where are the common sites of atherosclerosis?

A 
Heart
Brain
Kidneys
Legs
Bowel
214
Q

What are the complications of atheroma in the heart?

A

Myocardial infarction, chronic ischaemic heart disease, arrhythmias, cardiac failure and sudden cardiac death

215
Q

What are the complications of atheroma in the brain?

A

Transient ischaemic attacks (TIAs), cerebral infarction, multi-infarct dementia

216
Q

What are the possible complications of atherosclerotic plaques in general?

A 
Ulceration
Thrombosis on the plaque
Spasm at the site of the plaque
Embolisation
Calcification
Haemorrhage
Aneurysm formation
Rupture of the atherosclerotic artery
217
Q

What are the complications of atheroma in the legs?

A

Peripheral vascular disease, gangrene

218
Q

What are the complications of atheroma in the bowel?

A

Ischaemic colitis, malabsorption, bowel infarction

219
Q

What are the modifiable risk factors for the development of atherosclerosis?

A 
Hyperlipidaemia
Hypertension
Cigarette smoking
Geography
Obesity - hypertension, diabetes mellitus, hypertriglyceridemia, reduced HDL
Infection - Chlamydia pneumoniae or CMV
220
Q

What are the non-modifiable risk factors for the development of atherosclerosis?

A

Increasing age
Male gender
Genetic predisposition

221
Q

What are some of the interventions involved in preventing atherosclerotic disease?

A 
Decreasing total and LDL cholesterol and increasing HDL
Stop smoking
Controlling hypertension
Controlling weight and regular exercise
Sensible alcohol intake
Treating diabetes mellitus
Anti-oxidants
222
Q

What are some of the interventions involved in managing atherosclerotic disease?

A

Lipid-lowering drugs

Thrombolysis, angioplasty, stents, and coronary artery bypass grafts (CABG)

223
Q

What are the principles of the cell cycle?

A

G1 -> S -> G2 -> M

After completion, either re-starts from G1 or exits (G0) until further growth signals occur

224
Q

Define ‘hyperplasia’

A

Increase in tissue or organ size due to increased cell numbers

225
Q

Define ‘hypertrophy’

A

Increase in tissue or organ size due to an increase in cell size without an increase in cell numbers

226
Q

Define ‘atrophy’

A

Shrinkage of a tissue or organ due to an acquired decrease in size and/or number of cells

227
Q

Define ‘metaplasia’

A

Reversible replacement of one adult differentiation cell type by another or a different type

228
Q

Define ‘aplasia’

A

A complete failure of a specific tissue or organ to develop

229
Q

Define ‘hypoplasia’

A

The congenital underdevelopment or incomplete development of a tissue or organ

230
Q

Define ‘involution’

A

Overlaps with atrophy

Normal programmed shrinkage of an organ

231
Q

Define ‘atresia’

A

‘No orifice’ - the congenital imperforation of an opening

232
Q

Define ‘reconstitution’

A

Replacement of a lost part of the body rather than a small group of cells

233
Q

Define ‘dysplasia’

A

Abnormal maturation of cells within a tissue

234
Q

Explain hyperplasia

A

A response to increased functional demand and/or external stimulation
Can only occur in labile or stable cell populations - remains under physiological control, is reversible.
Either hormonal (result is an increase in functional capacity) or compensatory (increase after tissue damage) or pathological (secondary to excessive hormonal stimulation or growth factor production)
A risk of neoplasia in hyperplastic tissue

235
Q

Explain hypertrophy

A

Can occur in many tissues but seen especially in permanent cell populations - they have little to no replicative potential
It is a response to increased functional demand and/or hormonal stimulation
They synthesise more cytoplasm

236
Q

Explain atrophy

A

A reduced supply of growth factors and/or nutrients will result in atrophy
Cellular atrophy - decrease in cell size to a size at which survival is still possible
Organ/tissue atrophy - due to combination of cellular atrophy and apoptosis
Atrophy is associated with disease, and senescence
Is reversible up to a point
Best treated by removal of the cause

237
Q

Explain metaplasia

A

The change from one type of cell to another - may be part of a normal maturation process, or caused by some sort of abnormal stimulus

238
Q

Explain aplasia

A

Embryonic developmental disorder

Also is used to describe an organ whose cells have ceased to proliferate

239
Q

Explain hypoplasia

A

An adequate number of cells within the tissue which is present
It is an embryonic developmental disorder and is in a spectrum with aplasia

240
Q

Explain involution

A

Programmed shrinkage of an organ

241
Q

Explain atresia

A

An orifice or passage in the body is closed or absent

242
Q

Explain reconstitution

A

Requires the coordinated regeneration of several types of cells
Very minimal in a mammal - most mammals can’t even reconstitute a lose nail bed or the root of a hair

243
Q

Explain dysplasia

A

Abnormal maturation of cells within a tissue - potentially reversible but is often a pre-cancerous condition

244
Q

Give examples of hyperplasia

A

Physiological - increased bone marrow production of erythrocytes in response to hypoxia and the resulting erythropoietin, and the proliferation of the endometrium under the influence of oestrogen
Pathological - epidermal thickening in chronic eczema or psoriasis and enlargement of the thyroid gland in response to iodine deficiency

245
Q

Give examples of hypertrophy

A

Physiological - skeletal muscle hypertrophy of a bodybuilder and the smooth muscle hypertrophy of a pregnant uterus
Pathological - ventricular cardiac muscle hypertrophy in response to hypertension or valvular disease, smooth muscle hypertrophy above an intestinal stenosis due to extra work and demand required, bladder smooth muscle hypertrophy with bladder obstruction due to enlarged prostate gland

246
Q

Give examples of atrophy

A

Physiological - ovarian atrophy in post-menopausal woman, and the decrease in the size of the uterus after parturition
Pathological - muscle atrophy after disuse due to immobilisation, tissues around an enlarging brain tumour atrophy, wasting of muscles with malnutrition

247
Q

Give examples of metaplasia

A

Bone marrow is destroyed by disease, splenic tissue undergoes metaplasia to bone marrow
Bronchial pseudostratified ciliated columnar epithelium to stratified squamous epithelium due to the effect of cigarette smoke

248
Q

Give examples of aplasia

A

Thymic aplasia which results in infections and auto-immune problems
Aplasia of a kidney
Aplasia of the bone marrow in aplastic anaemia

249
Q

Give examples of hypoplasia

A

Renal hypoplasia
Breast hypoplasia
Testicular hypoplasia in Klinefelter’s syndrome
Hypoplasia of the chambers of the heart

250
Q

Give examples of involution

A

Uterus after childbirth shrinks
Thymus in early life
Temporary foetal organs such as the pro- and mesonephros

251
Q

Give examples of atresia

A

Atresia of the anus or vagina

Aural atresia is a congenital deformity where the ear canal is underdeveloped

252
Q

Give examples of reconstitution

A

Lizards can regrow their tails
Deer can regrow their antlers
Most mammals cannot regrow a nail bed or the root of the hair

253
Q

Give examples of dysplasia

A

Epithelial dysplasia

Hip dysplasia

254
Q

Define ‘neoplasm’

A

An abnormal growth of cells that persists after the initial stimulus is removed

255
Q

Define ‘dysplasia’

A

A pre-neoplastic alteration in which cells show disordered tissue organisation

256
Q

Define ‘tumour’

A

Any clinically detectable lump or swelling

257
Q

Define ‘cancer’

A

Any malignant neoplasm

258
Q

Define ‘metastasis’

A

A malignant neoplasm that has spread from its original site to a new non-contiguous site

259
Q

Define ‘anaplasia’

A

The loss of the mature or specialised features of a cell or tissue
Cells with no resemblance to any tissue are called anaplastic

260
Q

Define ‘pleomorphism’

A

Cells in a tumour have more than one distinct form - increasing variation in size and shape of cells and nuclei

261
Q

Define ‘progression’

A

A neoplasm emerges from the monoclonal population through a process called progression - the accumulation of yet more mutations

262
Q

Define ‘in situ’

A

No invasion through epithelial basement membrane

263
Q

What is the difference between benign and malignant tumours?

A

Benign - confined to their site or origin and do not produce metastases
Malignant - neoplasm with the potential to metastasise

264
Q

What are the macro- and microscopic features of benign tumours?

A

Macro - they are in confined local area and so have a pushing outer margin
Micro - cells closely resemble the parent tissue, they are well differentiated

265
Q

What are the macro- and microscopic features of malignant tumours?

A

Macro - Irregular outer margin and shape and may show areas of necrosis and ulceration
Micro - range from well to poorly differentiated cells
- increasing nuclear size
- increasing nuclear to cytoplasmic ratio
- more mitotic figures

266
Q

What is the biological behaviour of benign tumours?

A

They remain confined to their site or origin and do not produce metastases

267
Q

What is the biological behaviour of malignant tumours?

A

They have the potential to metastasise

268
Q

What is the difference between in-situ and invasive malignancy?

A 
In-situ = no invasion through epithelial basement membrane
Invasive = penetrated through basement membrane
269
Q

How are proto-oncogenes involved in the development of neoplasms?

A

They become abnormally activated (then called oncogenes), and favour neoplasm formation

270
Q

How are tumour suppressor genes involved in the development of neoplasms?

A

They can become inactive and stop suppressing neoplasm formation

271
Q

What is the concept of clonality?

A

c

272
Q

What is the reasoning behind the nomenclature given to benign and malignant neoplasms?

A

Organised system - takes site into account, benign or malignant, tissue the tumour forms and sometimes gross morphology
Benign neoplasms end in -oma
Malignant ones end in -carcinoma if it is an epithelial malignant neoplasm
Malignant ones end in -sarcoma if it is a stromal malignant neoplasm

273
Q

What are the histological characteristics of a squamous cell carcinoma?

A

Nests of squamous epithelial cells arising from the epidermis and extending into the dermis
Malignant cells are often large with abundant eosinophilic cytoplasm and a large, often vesicular, nucleus.
Variable keratinisation is present

274
Q

What are the histological characteristics of an adenocarcinoma?

A

Dark staining, eosinophilic cytoplasm
In lungs:
Lepidic - lacks architectural complexity; no lymphovascular or perineural invasion
Acinar - gland forming, round/oval glands invading the stroma
Papillary - malignant cuboidal/columnar cells replace alveolar lining
Micropapillary - ill defined projection that lacks fibrovascular cores
Solid - sheets of neoplastic cells

275
Q

What the histological characteristics of a malignant melanoma?

A

Pleomorphic and have hyperchromatic nuclei with prominent nucleoli
Melanin pigment is present as fine granules
Frequent mitosis

276
Q

What is the most common cancer of the bladder?

A

Transitional cell carcinoma

277
Q

What is the most common cancer of the oesophagus?

A

Squamous cell carcinoma

Adenocarcinoma

278
Q

What is the most common cancer of the stomach/bowel?

A

Adenocarcinoma

279
Q

What are the most common cancers of the skin?

A

Squamous cell carcinoma
Malignant melanoma
Basal cell carcinoma

280
Q

What are the most common cancers of the lungs?

A

Adenocarcinoma
Squamous cell carcinoma
Small cell carcinoma

281
Q

What is the most common cancer of the breast/prostate?

A

Adenocarcinoma

282
Q

What is the most common cancer of the brain?

A

Astrocytoma

283
Q

What is the most common cancer of the thyroid/pancreas/uterus?

A

Adenocarcinoma

284
Q

What is the most common cancer of the cervix?

A

Squamous cell carcinoma

285
Q

What is the process of invasion and metastasis?

A

1- grow and invade at the primary site
2- enter a transport system and lodge at a secondary site
3- grow at the secondary site to form a new tumour (colonisation)

286
Q

What are the cellular alterations that are required for invasion to occur?

A

Altered adhesion
Stromal proteolysis
Motility
These three allow a carcinoma cell to appear like a mesenchymal cell rather than an epithelial cell - it is called epithelial-to-mesenchymal transition (EMT)

287
Q

What processes determine the site of a metastasis?

A

Depends on
1- regional drainage of blood, lymph or coelomic fluid
- lymphatic metastasis is to lymph nodes
- transcoelomic spread is to other areas in the space or to adjacent organs
- blood-borne metastasis is sometimes to the next capillary bed that the cells encounter
2- the “seed and soil” phenomenon is due to interactions between malignant cells and the local tumour environment at the secondary site

288
Q

What processes determine the transportation routes for malignant cells?

A

Blood vessels via capillaries and venules
Lymphatic vessels
Fluid in body cavities (pleura, peritoneal, pericardial and brain ventricles) - this is known as transcoelomic spread

Carcinomas typically spread via lymphatics first
Sarcomas tend to spread via blood stream

289
Q

Which neoplasms most frequently spread to the bones?

A

Breast, bronchus, kidney, thyroid and prostate

290
Q

What are lytic lesions?

A

AKA bone lesions or osteolytic lesions - areas where bone has been destroyed, leaving a hole in the bone as a result of cancerous plasma cells building up in your bone marrow

291
Q

What are sclerotic lesions?

A

An unusual hardening or thickening of the bone

Can be benign or malignant

292
Q

What are the differences between lytic and sclerotic lesions?

A

Lytic - holes

Sclerotic - excess build up/thickening

293
Q

What are the local effects of neoplasms?

A
  • destroys normal tissue
  • ulceration at a surface, leading to bleeding
  • compression of adjacent structures
  • blocking tubes and orifices
294
Q

What are the systemic effects of neoplasms?

A

Increasing tumour burden leads to a parasitic effect on the host, paired with secreted factors such as cytokines:

  • reduced appetite
  • weight loss (cachexia)
  • malaise
  • immunosuppression
  • thrombosis
  • can secrete hormones
  • can have neuropathic effects
  • skin problems
  • fever
  • finger clubbing
  • myositis (inflammation in the muscles)
  • hypercalcaemia
  • anaemia
  • DIC
295
Q

What is the multifactorial nature of neoplasia pathogenesis?

A

A combination of intrinsic host factors and extrinsic factors related to the environment and behaviour account for cancer risk

296
Q

What are the intrinsic factors of neoplasia pathogenesis?

A

Hereditary
Age
Gender (especially hormonal)

297
Q

What are the extrinsic factors of neoplasia pathogenesis?

A 
High body mass index
Low fruit and vegetable intake
Lack of physical activity
Tobacco use
Alcohol use
Three main categories: (1) chemicals, (2) radiation, and (3) infections
298
Q

List extrinsic carcinogenic agents

A

(1) chemicals
- asbestos
- polycyclic hydrocarbons
- aromatic amines (e.g 2-napthylamine)
- nitrosamines

(2) radiation
- ultraviolet radiation
- ionising radiation

(3) infections
- human papilloma virus
- Epstein Barr virus
- hepatitis B and C viruses
- human immunodeficiency virus
- Helicobacter pylori
- parasites

299
Q

What is the mechanism of action for carcinogenic chemicals?

A

Some are initiators, some are promoters - have to have I followed by P
Some chemicals are pro-carcinogens, are activated by enzymes in the liver
Some chemicals are both initiators and promoters - these are called complete carcinogens

300
Q

What is the mechanism of action for carcinogenic radiation?

A

UV doesn’t penetrate deeper than the skin - but we come across it everyday from sunlight, so it is very dangerous
Radiation can damage DNA directly and indirectly by producing free radicals

301
Q

What is the mechanism of action for carcinogenic infections?

A

Some infections directly affect genes that control cell growth
Others cause chronic tissue injury where regeneration acts as a promoter for pre-existing mutations or can cause new mutations
HPV is a direct carcinogen because it expresses E6 and 7 protein which inhibit proteins important in cell proliferation
Hepatitis B and C cause chronic liver cell injury and regeneration - indirect carcinogen

302
Q

What are functions of proto-oncogenes in neoplasia?

A

The genes that enhance neoplastic growth are known as oncogenes - they are abnormally activated versions of proto-oncogenes
Only one allele of each proto-oncogene needs to be activated to favour neoplastic growth

303
Q

What are the functions of tumour suppressor genes in neoplasia?

A

Genes that inhibit neoplastic growth are known as tumour suppressor genes
Both alleles must be inactivated because they act like brakes on tumour growth

304
Q

What are the functions of caretaker genes in neoplasia?

A

Genes that maintain genetic stability - a class of tumour suppressor genes

305
Q

What are the stages of carcinogenesis?

A

Initiation - a mutagen that causes mutations to DNA that increase cancer risk
Promotion - this is prolonged proliferation in target tissues
Progression - steady accumulation of multiple mutations

306
Q

What alterations in growth control are required to achieve carcinogenesis?

A

1- self sufficiency in growth signals
2- resistance to growth stops signals
3- no limit on the number of times a cell can divide (cell immortalisation)
4- sustained ability to induce new blood vessels (angiogenesis)
5- resistance to apoptosis
6- the ability to invade and produce metastases

307
Q

Which medical conditions are associated with an increased risk of malignancy?

A

Ulcerative colitis

Cirrhosis

308
Q

What tumours can be inherited?

A

BRCA1 and BRCA2 genes are inherited and carry an increased lifetime risk of ovarian and breast cancers in women
Germline mutations as well as somatic mutations
Familial adenomatous polyposis and colorectal cancer
Hereditary non-polyposis colon cancer syndrome
Familial breast cancer
Retinoblastoma

309
Q

What are the most common types of cancer in adults?

A

Breast, lung, prostate and bowel carcinomas - accounted for over half of all new cancers in the UK

310
Q

What are the most common types of cancer in children?

A

Younger than 14 - leukaemias, central nervous system tumours and lymphomas are most common

311
Q

What is the leading causes of cancer-related death?

A

Lung cancer is the biggest cause of cancer-related deaths in the UK

312
Q

What is meant by tumour stage?

A

A measure of the malignant neoplasm’s overall burden
T refers to the size of the primary tumour (T1 to T4)
N describes the extent of regional node metastasis (N0 to N3)
M describes the distant metastatic spread (M0 or M1)

Stage I - early local disease (M0)
Stage II - advanced local disease (any T, N1 or more, M0)
Stage III - regional metastasis
Stage IV - advanced disease with distant metastasis (any T, any N, M1

313
Q

What is meant by tumour grade?

A 
Describes the degree of differentiation of a neoplasm
G1 - well-differentiated
G2 - moderately differentiated
G3 - poorly differentiated
G4 - undifferentiated or anaplastic
314
Q

What is the significance of the stage and grade of a tumour?

A

Staging is a powerful predictor of survival
Grade is important for planning treatment and estimating prognosis in certain types of malignancy (soft tissue sarcoma, primary brain tumours, lymphomas, breast + prostate cancer)

315
Q

What are the principles behind surgery to treat cancer?

A

The mainstay of treatment for most cancers

316
Q

What are the principles behind radiotherapy to treat cancer?

A

Kills proliferating cells by triggering apoptosis or interfering with mitosis
Focused on the tumour with shielding of surrounding healthy tissue
Given in fractionated doses to minimise damage
Kills rapidly dividing cells - especially in G2 of the cell cycle - causes either direct or indirect DNA damage, triggering apoptosis

317
Q

What are the principles behind chemotherapy to treat cancer?

A

Affects proliferating cells
Antimetabolites mimic normal substrates involved in DNA replication
Cisplatin cross-links the two strands of DNA helix
Antibiotics act in different ways - could inhibit enzymes needed for DNA synthesis, or could cause double-stranded DNA breaks

318
Q

What are the principles behind hormone therapy to treat cancer?

A

Selective oestrogen receptor modulators bind to oestrogen receptors, preventing oestrogen from binding. They are used to treat hormone receptor-positive breast cancer
Androgen blockade is used for prostate cancer

319
Q

What are the principles behind targeted molecular therapies to treat cancer?

A

Can identify specific mutations in the cancer cells to help target and attack only those cells
New therapies are always emerging

320
Q

What is meant by the term ‘adjuvant treatment’?

A

Treatment that is given in addition to the primary treatment

Usually refers to surgery followed by chemo- or radiotherapy

321
Q

What is meant by the term ‘neoadjuvant treatment’?

A

The administration of therapeutic agents before a main treatment
Neoadjuvant hormone therapy prior to radical radiotherapy for adenocarcinoma of the prostate

322
Q

Why is adjuvant treatment used?

A

Additional cancer treatment given after the primary treatment will lower the risk that the cancer will come back
To destroy the remaining cancer cells

323
Q

Why is neoadjuvant treatment used?

A

To help reduce the size of a tumour or kill cancer cells that have spread

324
Q

How are tumour markers used in diagnosis of disease?

A

Some tumour markers are released only by certain tumours - could help to identify what tumour is present

325
Q

How are tumour markers used in the monitoring of disease?

A

Most useful for monitoring tumour burden during treatment and follow up

326
Q

What are the principles behind the UK cervical cancer screening program?

A

Attempts to detect cancers as early as possible when the chance of cure is highest

327
Q

What are the principles behind the UK breast cancer screening program?

A

Attempts to detect cancers as early as possible when the chance of cure is highest

328
Q

What are the principles behind the UK colorectal cancer screening program?

A

Attempts to detect cancers as early as possible when the chance of cure is highest

Semester Two (3 decks)

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