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Phase 2a > Pathology > Flashcards

Pathology Flashcards

1
Q

What is acute inflammation?

A

Initial response of tissue to injury

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2
Q

Describe the onset of acute inflammation.

A

Early onset (seconds to minutes)

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3
Q

How long does acute inflammation last?

A

Short duration (hours to days)

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4
Q

What cells are involved in acute inflammation?

A

Neutrophils and monocytes

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5
Q

What steps are involved in acute inflammation?

A

Vascular and exudative component and recruitment of neutrophil polymorphs

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6
Q

What is the vascular component of acute inflammation?

A

Dilation of vessels

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7
Q

What is the exudative component of acute inflammation?

A

Vascular leakage of protein-rich fluid

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8
Q

What are the causes of acute inflammation?

A

Microbial infections, hypersensitivity reactions, physical agents, chemicals, bacterial toxins and tissue necrosis

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9
Q

What are some causes of microbial infections?

A

Bacteria, viruses

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10
Q

What are some causes of hypersensitivity reactions?

A

Parasites

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11
Q

What physical agents can cause acute inflammation?

A

Trauma, heat, cold

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12
Q

What chemicals can cause acute inflammation?

A

Corrosives, acids

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13
Q

Give a cause of tissue necrosis.

A

Ischaemic infarction

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14
Q

What are the 5 characteristics of acute inflammation?

A

Rubor (redness), calor (heat), tumor (swelling), dolor (pain) and loss of function

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15
Q

What is rubor?

A

Redness

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16
Q

What is calor?

A

Heat (only peripheral in acute inflammation)

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17
Q

What is tumor?

A

Swelling

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18
Q

What is dolor?

A

Pain

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19
Q

What causes redness in acute inflammation?

A

Dilation of small vessels

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20
Q

What causes swelling in acute inflammation?

A

Oedema or a physical mass

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21
Q

How are vessels affected in the acute inflammatory response process?

A

Changes in vessel calibre (gets wider) which increases vessel flow

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22
Q

How is vascular permeability affected in the acute inflammatory response process?

A

Increased vascular permeability which leads to formation of fluid exudate

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23
Q

How do neutrophil polymorphs reach the site of acute inflammation?

A

Increased vascular permeability which allows for the formation of cellular exudate

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24
Q

What are the stages of neutrophil polymorph emigration?

A
  1. Migration of neutrophils
  2. Adhesion of neutrophils
  3. Neutrophil emigration
  4. Diapedesis
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25
Q

Why do neutrophils migrate in acute inflammation?

A

Due to increase in plasma viscosity and slowing of flow due to injury

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26
Q

Where do neutrophils first migrate to in acute inflammation?

A

Plasmatic zone

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27
Q

What happens once neutrophils have migrated to the plasmatic zone in acute inflammation?

A

Adhesion to the vascular endothelium occurs in venules (pavementing)

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28
Q

What happens after pavementing during acute inflammation?

A

Neutrophils pass through endothelial cells, onto the basal lamina and then the vessel wall

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29
Q

What happens in diapedesis in acute inflammation?

A

RBCs may also escape from vessels. This is a passive process and indicates severe vascular injury

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30
Q

What are the outcomes of acute inflammation?

A
  1. Resolution
  2. Suppuration
  3. Organisation
  4. Progression
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31
Q

What is resolution in terms of acute inflammation?

A
  • The complete restoration of tissues to normal

- There is minimal cell death and rapid destruction of the causal agent

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32
Q

Give an example of a disease where resolution is seen after acute inflammation.

A

Acute lobar pneumonia

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33
Q

What is suppuration?

A
  • Formation of pus

- This becomes surrounded by a pyogenic membrane, which is the start of healing

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34
Q

What does suppuration lead to?

A

Scarring

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35
Q

What is organisation in terms of acute inflammation?

A
  • Replacement by granulation tissue

- New capillaries grow into the inflammatory exudate, macrophages migrate and fibrosis occurs

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36
Q

What is progression in terms of acute inflammation?

A

Causative agent is not removed so there is progression to chronic inflammation

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37
Q

What is chronic inflammation?

A

Subsequent and prolonged response to tissue injury

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38
Q

What cells are involved in chronic inflammation?

A

Lymphocytes, macrophages and plasma cells

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39
Q

When does chronic inflammation occur?

A

Longer onset

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40
Q

How long does chronic inflammation last?

A

Long last effects

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41
Q

What are the causes of primary chronic inflammation?

A
  • Resistance of infective agent
  • Endogenous materials
  • Exogenous materials
  • Autoimmune conditions
  • Primary granulomatous diseases
  • Transplant rejection
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42
Q

What infective agents could cause chronic inflammation?

A

TB, leprosy

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43
Q

What endogenous materials could cause chronic inflammation?

A

Necrotic tissue

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44
Q

What exogenous materials could cause chronic inflammation?

A

Asbestos, silica

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45
Q

What autoimmune conditions could cause chronic inflammation?

A

Hashimoto’s, rheumatoid arthritis

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46
Q

What primary granulomatous diseases could cause chronic inflammation?

A

Crohn’s, sarcoidosis

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47
Q

What is the macroscopic appearance of chronic inflammation?

A
  • Chronic ulcer
  • Chronic abscess cavity
  • Granulomatous inflammation
  • Fibrosis
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48
Q

What is the microscopic appearance of chronic inflammation?

A
  • Characteristically lymphocytes, plasma cells and macrophages
  • Evidence of continuing destruction
  • Possible tissue necrosis
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49
Q

What microscopic feature of acute inflammation is not seen in chronic inflammation?

A

Exudation (are others but cba lol)

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50
Q

What do macrophages do?

A

Respond to chemotactic stimuli

Produce cytokines

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51
Q

What cytokines do macrophages produce?

A

Interferon alpha and beta, IL1, 6, 8, TNF-alpha

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52
Q

In what type of inflammation are granulomas seen?

A

Chronic

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53
Q

What are granulomas?

A

Aggregate of epithelioid histocytes (clump of macrophages surrounded by lymphocytes)

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54
Q

What conditions can cause granulomas?

A

TB, leprosy, Crohn’s and sarcoidosis

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55
Q

What is the most common condition to cause granulomas?

A

TB

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56
Q

What stain can be used to identify TB granulomas?

A

Ziehl-Neelsen stain

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57
Q

What does the combination of granulomas and eosinophils indicate?

A

A parasite

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58
Q

What happens to the cells involved in acute inflammation?

A

Neutrophil extravasation

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59
Q

What happens to the cells involved in chronic inflammation?

A
  • Cellular infiltrate of lymphocytes, macrophages and plasma cells
  • Possible granulomas
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60
Q

What is thrombosis?

A

The solidification of blood contents that forms within the vascular system during life

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61
Q

What are the features of platelets?

A
  • No nucleus

- Alpha granules and dense granules

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62
Q

What are platelets derived from?

A

Megakaryocytes

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63
Q

What do alpha granules do?

A

Involved in platelet adhesion e.g. fibrinogen

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64
Q

What do dense granules do?

A

Cause platelets to aggregate e.g. ADP

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65
Q

What do platelets do once activated?

A

Release their granules when they come into contact with collagen

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66
Q

What happens if platelets are activated within an intact vessel?

A

A thrombus is formed

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67
Q

What is the result of chronic inflammation?

A

Fibrosis and scar tissue

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68
Q

What is the first stage of thrombosis?

A

Platelet aggregation (starts the clotting cascade)

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69
Q

Why are platelet aggregation and the clotting cascade hard to stop?

A

Both have positive feedback loops

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70
Q

What factors contribute to thrombosis?

A

Virchow’s triad:

  1. Reduced blood flow
  2. Increased coagulability
  3. Blood vessel injury
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71
Q

Give some examples of causes of reduced blood flow.

A 
Atrial fibrillation
Long distance travel
Varicose veins
Venous obstruction (e.g. pregnancy)
Immobility
Ventricular/venous insufficiency
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72
Q

Give some examples of causes of increased coagulability.

A

Sepsis
Smoking
Coagulation disorders
Malignancy (e.g. cancer)

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73
Q

Give some examples of causes of blood vessel injury.

A

Trauma (especially orthopaedic)
Orthopaedic or major surgery
Hypertension
Invasive procedures (e.g. cannulation

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74
Q

Referring to Virchow’s triad, what causes thrombosis?

A

2 factors from Virchow’s triad

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75
Q

What is the first stage of arterial thrombosis?

A

An atheromatous plaque that results in a change in the vessel wall

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76
Q

What might atheromatous plaques have?

A

A fatty streak - yellow streaks on arterial wall

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77
Q

What happens after the formation of the atheromatous plaque and consequent change in the arterial wall?

A

Over time, the plaque grows and protrudes into the lumen which causes a degree of turbulence in blood flow

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78
Q

Describe normal blood flow.

A

Laminar flow - red blood cells flow through the middle of the vessel and do not collide with the endothelium

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79
Q

What does turbulent blood flow cause?

A

Loss of intimal/endothelial cells which exposes collagen

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80
Q

What happens after intimal cells are lost as a result of turbulent blood flow?

A

Fibrin deposition and platelet clumping occurs. Platelets adhere to exposed collagen and activate

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81
Q

What happens once platelet aggregation has commenced on the arterial endothelium?

A

Formation of the platelet layer (first layer of thrombus)

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82
Q

What does the first layer of thrombus allow for?

A

Precipitation of a fibrin meshwork in which RBCs get trapped

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83
Q

What happens to the fibrin meshwork formed during thrombosis?

A

The structure protrudes further into the lumen causing more turbulence and more platelet deposition

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84
Q

In what direction do thrombi grow?

A

In the direction of blood flow - propagation

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85
Q

Do atheroma form in veins?

A

No - there is lower blood pressure in veins

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86
Q

Where do thrombi begin in veins?

A

Valves

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87
Q

How can veins become damaged and cause thrombosis?

A

Valves produce a degree of turbulence and can be damaged e.g. trauma, stasis

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88
Q

What happens in the veins if blood pressure falls?

A

Flow through the veins slows, allowing for a thrombus to form

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89
Q

What are the clinical features of arterial thrombi?

A

Loss of pulse distal to thrombus
Area becomes cold, pale and painful
Possible gangrene

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90
Q

What are the clinical features of venous thrombi?

A

Tender

Area becomes reddened and swollen

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91
Q

What can happen after thrombus formation?

A

Resolution
Organisation
Recanalisation
Embolus

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92
Q

What happens in the resolution of a thrombus?

A

Body dissolves and clears it

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93
Q

What happens in the organisation of a thrombus?

A

Becomes a scar - results in slight narrowing of the vessel lumen

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94
Q

What happens in recanalisation of a thrombus?

A

Intimal cells may proliferate

Capillaries may grow into the thrombus and fuse to form larger vessels

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95
Q

How does a thrombus turn into an embolus?

A

Fragments of the thrombus break off into the circulation

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96
Q

What is an arterial thrombus most commonly caused by?

A

Atheroma

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97
Q

What is a venous thrombus most commonly caused by?

A

Stasis

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98
Q

What type of blood pressure causes arterial thrombi?

A

High

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99
Q

What type of blood pressure causes venous thrombi?

A

Low

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100
Q

What are arterial thrombi mainly made of?

A

Platelets

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101
Q

What are venous thrombi mainly made of?

A

RBCs

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102
Q

What conditions can arterial thrombi lead to?

A

MI/stroke

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103
Q

What can venous thrombi lead to?

A

DVT/PE

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104
Q

How are arterial thrombi treated?

A

Anti-platelets e.g. aspirin

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105
Q

How are venous thrombi treated?

A

Anti-coagulants e.g. warfarin

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106
Q

What is an embolism?

A

A mass of material in the vascular system able to lodge in a vessel and block its lumen

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107
Q

What type of embolism do arterial embolisms cause?

A

Systemic embolism

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108
Q

Where can arterial emboli travel to?

A

Anywhere downstream of its entry point

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109
Q

Where can mural thrombi in the left ventricle go?

A

Anywhere

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110
Q

Where can cholesterol crystals from an atheromatous plaque in the descending aorta go to?

A

Any lower limb or the renal artery

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111
Q

What conditions can thrombi in the left ventricle cause if they form emboli?

A

Cerebral infarct (stroke)
Renal infarct
Ischaemic bowel
Ischaemic foot (dry gangrene)

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112
Q

What type of embolism do venous embolisms cause?

A

Pulmonary emboli

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113
Q

Where do emboli travel to in the venous system?

A

The vena cava and lodge in the pulmonary arteries (pulmonary embolism)

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114
Q

What conditions can small pulmonary emboli cause?

A

Idiopathic pulmonary hypertension

115
Q

Why might small pulmonary emboli go untreated?

A

May occur unnoticed

116
Q

What conditions can large pulmonary emboli cause?

A

Acute respiratory or cardiac problems

117
Q

What symptoms do large pulmonary emboli cause?

A

Chest pain and shortness of breath

118
Q

How quickly do large pulmonary emboli resolve?

A

Slowly

119
Q

What can massive pulmonary emboli result in?

A

Sudden death

120
Q

Where are massive pulmonary emboli often impacted?

A

Across the bifurcation of one of the pulmonary arteries

121
Q

What do massive pulmonary emboli tend to be?

A

Long thrombi derived from the leg veins

122
Q

What is ischaemia?

A

The reduction in blood flow to a tissue or part of the body

123
Q

What causes ischaemia?

A

Constriction or blockage of the blood vessels supplying the tissue

124
Q

What is infarction?

A

Necrosis of part of the whole of an organ that occurs when the artery supplying it becomes obstructed

125
Q

Can the effects of ischaemia be reversed?

A

Yes

126
Q

How long do ischaemia attacks last?

A

Briefly

127
Q

What cells are most vulnerable to ischaemic attacks?

A

Cardiomyocytes and cerebral neurons

128
Q

Why are most organs susceptible to infarcts?

A

They only have a single artery supplying them

129
Q

Which organs are less susceptible to infarcts and why?

A

Liver, brain and lungs because they have a dual supply

130
Q

What is a reperfusion injury?

A

Damage to tissue during reoxygenation

131
Q

What is atherosclerosis?

A

Disease characterised by the formation of atherosclerotic plaques in the intima of large and medium sized arteries e.g. coronary arteries

132
Q

How does atherosclerosis present?

A

Often asymptomatic

133
Q

What accumulates in the intimal atherosclerotic plaques?

A

Lipids, macrophages and smooth muscle cells

134
Q

How can atherosclerosis cause life threatening damage?

A

If a thrombus forms on a disrupted plaque

135
Q

What conditions can atherosclerosis cause?

A 
Cerebral infarction
Carotid atheroma, leading to TIAs
MI
Aortic aneurysm (can cause sudden death)
Peripheral vascular disease
Gangrene
136
Q

What is the first stage of atherosclerosis?

A

Endothelial cell dysfunction (lots of cholesterol damages wall)

137
Q

What happens once the arterial wall has been damaged by cholesterol?

A

High levels of LDL in the blood will begin to accumulate in the arterial wall

138
Q

How does the site of atherosclerosis become inflamed?

A

Macrophages are attracted to the site of damage and take up liquid to form foam cells (inflammatory response)

139
Q

What is formed after the recruitment of macrophages in atherosclerosis?

A

A fatty streak

140
Q

What is the earliest stage in the formation of a plaque?

A

Fatty streaks

141
Q

What do the activated macrophages in atherosclerosis release?

A

Cytokines and growth factors

142
Q

What is the final stage of atherosclerosis?

A

Smooth muscle proliferation (to intima) around the lipid core and formation of a fibrous cap (collagen)

143
Q

What are the risk factors for atherosclerosis?

A 
Hypercholesterolaemia (most important risk factor)
Smoking
Hypertension
Diabetes
Male sex
Increasing age
144
Q

How can you prevent atherosclerosis?

A 
Smoking cessation
Blood pressure control
Weight reduction
Low dose aspirin
Statins
145
Q

Why should aspirin be used to prevent atherosclerosis?

A

Inhibits aggregation of platelets

146
Q

Why should statins be used to prevent atherosclerosis?

A

Cholesterol reducing drug

147
Q

What is apoptosis?

A

A cellular process in which a defined and programmed sequence of intracellular events leads to the removal of a cell without the release of products harmful to surrounding cells

148
Q

What inhibits apoptosis?

A

Growth factors
Extracellular cell matrix
Sex steroids

149
Q

What induces apoptosis?

A 
Glucocorticoids
Free radicals
Ionising radiation
DNA
damage
150
Q

What does the intrinsic apoptosis pathway use?

A

Pro/anti-apoptotic members of the Blc-2 family:
Bax
p53

151
Q

What happens in the intrinsic apoptosis pathway?

A

Bax forms Bax-Bax dimers which enhance apoptotic stimuli

152
Q

What determines the cell’s susceptibility to apoptotic stimuli?

A

Bcl-2:Bax ratio

153
Q

What does the intrinsic apoptosis pathway respond to?

A

Growth factors and biochemical stress

154
Q

What is the role of the p53 gene in intrinsic apoptosis?

A

Induces cell cycle arrest and initiates DNA damage repair

155
Q

What induces apoptosis if DNA damage is difficult to repair?

A

p53 gene

156
Q

What happens in extrinsic apoptosis?

A

Ligand-binding at death receptors on the cell surface

157
Q

Give some examples of death receptors involved in extrinsic apoptosis.

A

TNFR1 and CD95

158
Q

What does ligand-binding in extrinsic apoptosis result in?

A

Clustering of receptor molecules on the cell surface and the initiation of signal transduction cascade

159
Q

What molecules trigger extrinsic apoptosis?

A

Caspases once activated

160
Q

What is the purpose of extrinsic apoptosis?

A

Used by the immune system to eliminate lymphocytes

161
Q

What is necrosis?

A

Traumatic cell death which induces inflammation and repair

162
Q

What is necrosis characterised by?

A

Bioenergetic failure and loss of plasma membrane integrity

163
Q

What is the most common type of necrosis?

A

Coagulative necrosis

164
Q

Where can coagulative necrosis occur?

A

Most organs

165
Q

What is coagulative necrosis caused by?

A

Ischaemia

166
Q

Where does liquefactive necrosis occur?

A

In the brain due to its lack of substantial supporting stroma

167
Q

What does caseous necrosis cause?

A

A ‘cheese’ pattern

168
Q

What disease is characterised by caseous necrosis?

A

TB

169
Q

What is gangrene?

A

Necrosis with rotting of the tissue

170
Q

How does gangrene present?

A

Affected tissue appears black due to deposition of iron sulphide (from degraded haemoglobin)

171
Q

What is hypertrophy?

A

Increase in cell size without cell division

172
Q

Where is muscle hypertrophy commonly seen?

A

In athletes due to increased muscle activity

173
Q

Where is uterine hypertrophy seen?

A

Pregnancy

174
Q

What is hyperplasia?

A

Increase in cell number by mitosis

175
Q

In what cells can hyperplasia occur?

A

Only in cells that divide - can’t happen in myocardial cells or nerve cells

176
Q

Where is hyperplasia of bone marrow cells seen?

A

In those living at high altitudes

177
Q

What is atrophy?

A

The decrease in the size of an organ or cell either by reduction in cell size and/or number

178
Q

Where does atrophy occur naturally?

A

During the development of the GU tract

179
Q

Give an example of a disease where atrophy occurs.

A

Muscle atrophy in ALS

180
Q

What is metaplasia?

A

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

181
Q

When does metaplasia occur?

A

In response to alterations in the cellular environment

182
Q

Give some examples of metaplasia.

A
  • Ciliated columnar cells in epithelium of bronchi in smokers become simple squamous
  • Squamous epithelium of oesophagus can become columnar epithelium in response to stomach acid (Barrett’s oesophagus)
183
Q

What is dysplasia?

A

Morphological changes seen in cells in the progression to becoming cancer (not cancer but could become cancer)

184
Q

What is carcinogenesis?

A

The transformation of normal cells into neoplastic cells through permanent genetic alterations or mutations

185
Q

What is a neoplasm?

A

A lesion resulting from the autonomous or relatively autonomous abnormal growth of cells

186
Q

In what cells can neoplasms not occur?

A

RBCs because they don’t have nuclei

187
Q

What is a tumour?

A

Any abnormal swelling

188
Q

What is a carcinogen?

A

An environmental agent participating in the causation of tumours

189
Q

What can cause lung tumours?

A

Smoking

190
Q

What can cause bladder cancer?

A

B-naphthylamine (dyes and rubber industry)

191
Q

What can cause scrotal cancer?

A

Polycyclic aromatic hydrocarbons (soot exposure)

192
Q

What can cause Burkitt’s lymphoma?

A

EBV

193
Q

What can cause cervical cancer?

A

HPV

194
Q

What can cause skin cancer?

A

UV radiation

195
Q

What can cause hepatocellular carcinoma?

A

Aflatoxins (mycotoxins)

196
Q

What can cause mesothelioma?

A

Asbestos

197
Q

Describe the growth of benign tumours.

A

Don’t invade basement membrane and exophytic (grows outwards)

198
Q

Describe the mitotic activity of benign tumours.

A

Low mitotic activity

199
Q

What type of tumour is circumscribed?

A

Benign - malignant are poorly circumscribed

200
Q

In what type of tumour is necrosis and ulceration common?

A

Malignant - they are rare in benign

201
Q

Describe the growth of malignant tumours.

A

Invades the basement membrane and endophytic (grows inwards)

202
Q

How are tumours classified?

A

Behaviour and histogenesis

203
Q

What are cancers of epithelial cells called?

A

Carcinomas

204
Q

What are cancers of connective tissues called?

A

Sarcomas

205
Q

What are cancers of lymphoid called?

A

Lymphomas or leukaemia

206
Q

What is a grade 1 cancer?

A

Well differentiated (most closely resembles parent tissue)

207
Q

What is a grade 2 cancer?

A

Moderately differentiated

208
Q

What is a grade 3 cancer?

A

Poorly differentiated

209
Q

What is the suffix of epithelial tumours?

A

-oma

210
Q

What is a papilloma?

A

Benign tumour of non-glandular tissue

211
Q

What is an adenoma?

A

Benign tumour of secretory tissue

212
Q

What is a carcinoma?

A

Malignant tumour of epithelial cells

213
Q

What is an adenocarcinoma?

A

Malignant tumour of glandular epithelium

214
Q

What connective tissues can be affected by cancer?

A 
Adipocytes
Striated muscle
Smooth muscle
Cartilage
Bone
215
Q

What is a lipoma?

A

Benign tumour of adipocytes

216
Q

What is a rhabdomyoma?

A

Benign tumour of striated muscle

217
Q

What is a leiomyoma?

A

Benign tumour of smooth muscle cells

218
Q

What is a chondroma?

A

Benign tumour of cartilage

219
Q

What is an osteoma?

A

Benign tumour of bone

220
Q

What is a liposarcoma?

A

Malignant tumour of adipocytes

221
Q

What is a rhabdomyosarcoma?

A

Malignant tumour of striated muscle

222
Q

What is a leiomyosarcoma?

A

Malignant tumour of smooth muscle

223
Q

What is a chondrosarcoma?

A

Malignant tumour of cartilage

224
Q

What is an osteosarcoma?

A

Malignant tumour of bone

225
Q

What is metastasis?

A

The process whereby malignant tumours spread from their site of origin to form other tumours at distant sites

226
Q

What type of cancer never metastasises?

A

Basal cell carcinoma

227
Q

What is the first stage of metastasis?

A

Detachment of tumour cells from their neighbours

228
Q

What happens in metastasis once tumour cells have detached from their neighbours?

A

Invasion of the surrounding connective tissue to reach conduits of metastasis

229
Q

What happens once tumour cells have invaded surrounding connective tissue?

A

Intravasation into the lumen of vessels

230
Q

What happens in metastasis after intravasation?

A

Evasion of host defence mechanisms, such as NK cells

231
Q

What happens in metastasis after the evasion of host defence mechanisms?

A

Adherence to endothelium at remote location

232
Q

What happens in metastasis after tumour cells have adhered to endothelium elsewhere?

A

Extravasation of the cells from the vessel lumen into the surrounding tissue

233
Q

What happens after extravasation in metastasis?

A

Tumour cells proliferate in the new environment and grow their own blood supply

234
Q

What cancers metastasise to bone?

A

Lung, breast, kidney, thyroid, prostate

235
Q

Which secondary cancer is common?

A

Secondary tumours in lymph nodes - lymphatic metastasis

236
Q

How do carcinomas tend to spread?

A

Lymphatic spread

237
Q

How do sarcomas tend to spread?

A

Haematogenous spread

238
Q

How are tumours staged?

A

TMN staging

239
Q

What is the ‘T’ in TMN staging?

A

Primary tumour size

240
Q

What is the ‘M’ in TMN staging?

A

Metastatic status - extent of distant metastases

241
Q

What is the ‘N’ in TMN staging?

A

Lymph node status - degree of lymph node involvement

242
Q

What does exudate contain?

A

Leukocytes and high in protein and lactate dehydrogenase (LDH)

243
Q

Why causes formation of exudate?

A

Occurs due to inflammation and increased capillary permeability

244
Q

In what conditions is exudate found?

A

Pneumonia, cancer, TB, viral infection, PE, autoimmune conditions

245
Q

What is transudate?

A

Transudates accumulate due to increased hydrostatic pressure or low plasma oncotic pressure

246
Q

What does transudate contain?

A

Low in protein and lactate dehydrogenase (LDH)

247
Q

In what conditions is transudate found?

A

Congestive heart failure (CHF), cirrhosis, nephrotic syndrome, PE, hypoalbuminaemia

248
Q

When does hyperacute transplant rejection take place?

A

Occurs minutes to hours following revascularisation of the graft

249
Q

Why does hyperacute transplant rejection occur?

A

Due to performed circulating cytotoxic antibody which reacts with MHC class I antigens in the donor organ

250
Q

What does hyperacute transplant rejection cause?

A

Complement mediated endothelial injury

251
Q

How is hyperacute transplant rejection resolved?

A

In most cases the graft will have to be removed as it is usually damaged too much by the recipient immune system

252
Q

When does acute transplant rejection occur?

A

Occurs a few days or weeks following transplantation

253
Q

What percentage of all transplants result in acute rejection?

A

Up to 20% of all transplants

254
Q

What is acute transplant rejection associated with?

A

Increased expression of MHC class I and class II antigens in inflamed grafts, and with early infiltration of CD8+ T lymphocytes

255
Q

When does chronic transplant rejection occur?

A

Seen after months or years

256
Q

How is chronic transplant rejection resolved?

A

Not thought to be immunologically mediated, and doesn’t respond to immunosuppressive therapy

257
Q

Which cells play a central role in organ rejection?

A

CD4+ T lymphocytes

258
Q

What are the two phases of organ rejection?

A
  • An afferent phase (initiation or sensitising component)

- An efferent phase (effector component)

259
Q

What happens in the afferent phase of organ rejection?

A

Donor MHC molecules within the graft are recognised by the recipient CD4+ T cells - this is known as allorecognition

260
Q

What happens in the effector phase of organ rejection?

A

The effector phase of rejection is orchestrated by CD4+ T cells which enter the graft and recruit effector cells responsible for the tissue damage of rejection

261
Q

What are the effector cells involved in organ rejection??

A
  • Macrohages
  • CD8+ T cells
  • Natural killer cells
  • B lymphocytes
262
Q

What are the most important cytokines in graft rejection?

A

Interleukin-2 and interferon-gamma

263
Q

What are the critical targets of graft rejection?

A

Microvasculature and the specialised parenchymal cells or the organ, such as renal tubules, pancreatic islets of Langerhans and cardiac myocytes

264
Q

What do the endogenous chemical mediators cause in acute inflammation?

A
  • Vasodilation
  • Emigration of neutrophils
  • Chemotaxis (the attraction of neutrophil polymorphs towards certain chemicals e.g at the site of inflammation)
  • Increased vascular permeability
  • Itching & pain
265
Q

What are the endogenous chemical mediators of acute inflammation?

A 
Histamine and thrombin
Lysosomal compounds
-  Eicosanoids - type of prostaglandin 
- 5-hydroxytryptamine (serotonin)
- Chemokine (chemotactic cytokines)
266
Q

Which cells can regenerate?

A
  • Hepatocytes
  • Pneumocytes
  • All blood cells
  • Gut epithelium
  • Skin epithelium
  • Osteocytes
267
Q

Which cells can’t regenerate?

A
  • Myocardial cells

- Neurones

268
Q

What is the difference between a thrombus and a clot?

A 
Thrombus = the solidification of blood contents that forms within the vascular system during life
Clot = blood coagulated outside of the vascular system or after death
269
Q

What is gangrene?

A

When whole areas of a limb or a region of the gut have their arterial supply cut off and large areas of mixed tissue die in bulk

270
Q

What can ischaemic damage cause?

A
  • Cerebral infarction
  • Carotid atheroma - emboli causing transient
    ischaemic attacks or cerebral infarcts
  • Myocardial infarction
  • Aortic aneurysm - rupture causes certain death
  • Peripheral vascular disease
  • Gangrene
271
Q

What is an aneurysm?

A

A localised permanent dilation of part of the vascular tree

272
Q

What are some apoptosis inhibitors?

A
  • Growth factors
  • Extracellular cell matrix
  • Sex steroids
  • Some viral proteins
273
Q

What are some apoptosis inducers?

A
  • Growth factor withdrawal
  • Loss of matrix attachment
  • Glucocorticoids
  • Some viruses
  • Free radicals
  • Ionising radiation
  • DNA damage
  • Ligand-binding at ‘death receptors’
274
Q

How do benign tumours cause morbidity and mortality?

A

Pressure on adjacent structures (e.g. bening meningeal tumour causing epilepsy)
Obstruction to the flow of fluid (e.g. benign epithelial tumour blocking duct)
Production of a hormone (e.g. benign thyroid tumour causing thyrotoxicosis (excessive thyroid hormone)
Transformation into a malignant neoplasm
Anxiety & stress since patient thinks the lesions may be something more sinister

275
Q

How do malignant tumours cause morbidity and mortality?

A

Pressure on and destruction of adjacent tissue
Formation of secondary tumours (metastases)
Blood loss from ulcerated surfaces
Obstruction of flow (e.g. malignant tumour of the colon causing intestinal obstruction)
Hormone production
Paraneoplastic effects resulting in weight loss and debility
Anxiety and pain - many cancers cause no pain until quite late into the disease

276
Q

What are the 3 major families of proteinases in neoplastic invasion?

A
  • Interstitial collagenases; degrade types I,II & III collagen
  • Gelatinases; degrade type IV collagen and gelatin
  • Stromelysins; degrade type IV collagen and proteoglycans
277
Q

What do proteinases do in neoplastic invasion?

A

These enzymes are secreted by malignant neoplastic cells, enabling them to digest the surrounding connect tissue

278
Q

What cancers are there screening programmes for in the UK?

A
  • Cervical cancer
  • Breast cancer
  • Colorectal cancer
279
Q

What is lead time bias?

A

Earlier detection does not affect the inevitable fatal outcome, but prolongs the apparent survival time

280
Q

What is length bias?

A

Preferential detection of slow growing tumours with intrinsically better prognosis

281
Q

What is overdiagnosis bias?

A

Diagnosis of lesions that, although histologically malignant, are
clinically relatively harmless

282
Q

What is selection bias?

A

Volunteers for screening are more at risk of good-prognosis tumours

283
Q

What is atopy?

A

Inherited tendency for overproduction of IgE antibodies to common environmental antigens

284
Q

What do you find within a granuloma?

A
  • Multinucleate giant cells
  • Lymphocytes
  • Epithelioid histocytes

Phase 2a (25 decks)

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