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Phase 2A revision > PATHOLOGY > Flashcards

PATHOLOGY Flashcards

1
Q

What is acute inflammation?

A

Initial and often transient series of tissue reactions to injury, it’s got a sudden onset, short lived and usually resolves on its own

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2
Q

Causes of acute inflammation

A 
Microbial infections 
Hypersensitivity reactions 
Physical agents  
Chemicals
Tissue necrosis
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3
Q

Clinical features of acute inflammation

A 
Redness (rubor)
Heat (calor) 
Swelling (tumor)
Pain (dolor)
Loss of function
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4
Q

What makes up the cellular exudate for acute inflammation?

A

Neutrophil polymorphs
Macrophages
Lymphocytes

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5
Q

Give an example of acute inflammation

A

Acute appendicitis

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6
Q

Give a benefit of inflammation.

A

Inflammation can destroy invading micro-organisms and can prevent the spread of infection.

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7
Q

What are the outcomes of acute inflammation?

A

Resolution
Suppuration
Organisation (fibrosis)
Progression to chronic inflammation

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8
Q

What are the negatives of acute inflammation?

A

Autoimmunity
When it’s an over-reaction to the stimulus
Fibrosis resulting from chronic inflammation

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9
Q

What is chronic inflammation?

A

Subsequent and often prolonged tissue reactions following the initial response, it has a slow onset, long duration and may never resolve

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10
Q

Causes of chronic inflammation

A

Primary chronic inflammation
Transplant rejection
Progressing from acute inflammation
Recurrent episodes of acute inflammation

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11
Q

Causes of primary chronic inflammation

A

Exogenous materials
Endogenous materials
Resistance of infective agent to phagocytosis and intracellular killing – TB
Autoimmune diseases – rheumatoid arthritis
Primary granulomatous diseases – Crohn’s

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12
Q

What is the cellular exudate in chronic inflammation mainly made of?

A

Lymphocytes
Plasma cells
Macrophages
Fibroblasts

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13
Q

What is a granuloma?

A

Group of epitheloid histiocytes which can contain lymphocytes and histolytic giant cells
Can cause caseous necrosis

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14
Q

Give an example of a granulomatous disease.

A

Tuberculosis
Leprosy
Sarcoidosis

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15
Q

How can you treat inflammation?

A

Aspirin, ibuprofen (NSAIDs)

Corticosteroids

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16
Q

What is resolution?

A

Initiating factor removed, and tissue is undamaged or able to regenerate

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17
Q

What is repair?

A

Initiating factor is still present, and tissue is damaged and unable to regenerate

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18
Q

Which organ is a good example for resolution?

A

Liver

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19
Q

What affects resolution of the liver?

A

Cirrhosis (ongoing damage resulting in abnormal architecture)

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20
Q

Name 5 types of cells capable of regeneration.

A 
Hepatocytes 
Pneumocytes 
All blood cells
Gut epithelium 
Skin epithelium 
Osteocytes
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21
Q

Name 2 types of cells that are incapable of regeneration.

A

Myocardial cells

Neurones

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22
Q

What happens after a skin abrasion?

A

Only top cell layer is removed, leaving the bottom layer/follicles/glands for scab to form and for the epidermis to eventually be regenerated

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23
Q

What are the 2 types of skin wound healing?

A

Healing by 1st intention (+ve)

Healing by 2nd intention (-ve)

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24
Q

When does 1st intention healing occur?

A

Incision wound

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25
Q

How does healing by 1st intention work?

A

Edge to edge healing (heals w/ reasonable scar)
Fibrinogen exudation
Both ends are sealed together, the slight gap is filled with blood, fibrin etc which holds together a little with stitches
Epidermis regrows, fibroblasts produce collagen
Small scar forms

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26
Q

When does 2nd intention healing occur?

A

When tissue loss has occurred (2 edges can’t be brought together nicely)

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27
Q

How does 2nd intention healing work?

A

Infection or haemorrhage prevent healing by first intention
Loss of tissue, granulation tissue forms and organisation occurs (phagocytosis of any debris)
Epithelial regeneration and early fibrous scar
Scar contradiction

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28
Q

What is organisation?

A

Repair of specialised tissue by the formation of a fibrous scar

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29
Q

How does organisation occur?

A

Granulation tissue is formed and dead tissue is removed by phagocytosis
Granulation tissue contracts and accumulated collagen to form a scar

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30
Q

What produces collagen?

A

Fibroblasts

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31
Q

Name 3 places where repair occurs and after what

A

Heart after an MI
Brain after a cerebral infarction
Spinal cord after trauma

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32
Q

What is a thrombosis?

A

Solid mass of blood constituents formed within intact vascular system during life

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33
Q

What is Virchow’s triad?

A

Factors that can lead to thrombosis formation:

  1. Change in vessel wall
  2. Change in blood flow (laminar –> turbulent)
  3. Change in constituents of blood
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34
Q

What does Virchow’s triad do?

A

Predisposes to thrombosis

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35
Q

When does an arterial thrombosis normally occur?

A

When superimposed on atheroma

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36
Q

How does an arterial thrombus occur?

A

Vessel wall damage
Laminar flow disruption
Collagen exposed
Platelets stick to collagen and aggregate - positive feedback
Rbc’s can get trapped - thrombus formation and fibrin deposition (fibrinogen –> fibrin by platelet factors)
Fibrin mesh holds it all together
Thrombus can then build up and occlude artery

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37
Q

What is a vein thombus most commonly due to?

A

Stasis

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38
Q

What are the outcomes of a thrombus?

A
  1. Lysis and resolution
  2. Organisation – into a scar
  3. Recanalisation – scar and residual thrombus
  4. Embolism – breaks off
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39
Q

How can you prevent a thrombus?

A

Exercise
Compression stockings
Aspirin – anti platelet drug, makes endothelial cells less sticky, not a full-blown thrombus occurs

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40
Q

What does an occlusion of a coronary artery result in?

A

Myocardial infarction

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41
Q

What does occlusion of a cerebral artery result in?

A

Cerebral infarction (stroke)

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42
Q

What is laminar flow? and why is it important?

A

Cells travel in the centre of arterial vessels and don’t touch arteries - this is important in reducing risk of blood clots

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43
Q

What is an Embolus?

A

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

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44
Q

What is the most common cause of an embolus?

A

Piece of thrombus breaking off and getting lodged in a smaller vessel

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45
Q

What is the most common occurrence of an embolus?

A

Pulmonary embolism from deep leg vein thrombosis

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46
Q

What is Ischaemia?

A

Reduction in blood flow

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47
Q

What is Infarction?

A

Death of cells due to reduction in blood supply

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48
Q

What is infarction normally caused by?

A

Thrombosis of an artery

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49
Q

Explain a reperfusion injury

A

Occurs after ischaemia
Blood supply severely limited but cells don’t actually die
Blood flow re-established (reactive hyperaemia - cells overwhelmed with O2)
ROS production that cause damage to tissue and inflammatory response

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50
Q

Name organs with 2 blood supplies

A

Lungs - bronchial arteries and pulmonary arteries
Liver - portal vein and hepatic artery
Some parts of the brain

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51
Q

What areas are most susceptible to infarction?

A

Watershed territories

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52
Q

What are the functions of histamine?

A 
Vasodilation
Emigration of neutrophils (chemotaxis) 
Increase vascular permeability
Pain 
Itching
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53
Q

Role of plasma factors

A

Complement system
Kinin system
Coagulation cascade (pro-clotting)
Fibrinolytic system (anti-clotting)

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54
Q

What is the microscopic appearance of chronic inflammation?

A

Chronic ulcer
Abscess cavity
Granulatomous inflammation
Fibrosis

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55
Q

What is a histiocytic giant cell?

A

Indeigestible foreign material causes macrophages to fuse together - multinucleate giant cells
Can collect and form granulomas

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56
Q

Causes of an embolus

A 
Air injected 
Thrombus/atheroma
Amniotic fluid
Fat 
Tumour
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57
Q

What happens in a venous system embolism?

A

Goes to RHS heart
Pulmonary system
Pulmonary embolism

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58
Q

What happens in an arterial system embolism?

A

Goes to LHS heart
Systemic system
Embolism anywhere

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59
Q

What is end arterial supply?

A

Single artery supplies organ - more susceptible to infarction

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60
Q

What are watershed territories?

A

Parts of the brain the have a dual blood supply, but low BP can cause ischaemia

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61
Q

What is an atherosclerosis?

A

Build up of plague in arteries , narrows arteries

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62
Q

Where are atherosclerosis’ found?

A

Systemic arterial system - high pressure systems

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63
Q

What are the components of an atheroma?

A

Fibrous cap
Cholesterol and lipid core
Smooth muscle cells surrounded by foam cells
Macrophages

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64
Q

Risk factors for atherosclerosis

A

Smoking - free radicals, nicotine, CO
Hypertension - increased shearing forces
Diabetes - superoxide anions and glycosylation products
Hyperlipidaemia - lipids
Increasing age
Male gender

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65
Q

What do the risk factors for atherosclerosis do?

A

Damage the endothelial cells

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66
Q

Explain the pathogenesis of atherosclerosis

A
  1. Endothelial cell damage – see risk factors
  2. Repeated endothelial damage -> multiple thrombi -> aggregation -> atheroma formation
  3. Vascularised plaque can haemorrhage – propagates atheroma formation
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67
Q

What are the complications of atherosclerosis?

A

Cerebral/myocardial infarct
AAA –> weakens aorta and leads to aortic rupture
Peripheral vascular disease - gangrene

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68
Q

How can you treat atheroma?

A

Aspirin - anti platelet drug
Statins - lower cholesterol
Diet, exercise, control of blood pressure, smoking cessation, weight loss

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69
Q

Define apoptosis

A

Programmed cell death

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70
Q

Define necrosis

A

Traumatic cell death

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71
Q

What types of DNA damage cause apoptosis to occur?

A

Single/double stand break
Base alteration
Cross linking

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72
Q

Explain mechanism of apoptosis

A
  1. P53 (gatekeeper of genome) detects DNA damage -> acts as switch for apoptosis
  2. Bcl2 and Fas ligand receptor signal for capsases -> apoptosis
  3. Membrane bound cell fragments engulfed by macrophages
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73
Q

Example of normal apoptosis

A

Removal of finger webbing during development

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74
Q

What can a lack of apoptosis cause?

A

Cancer - mutation in p53 means cell damage isn’t detected

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75
Q

In what is excess apoptosis present?

A

HIV mediated T cell destruction

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76
Q

Give examples of necrosis

A

Myocardial/cerebral infarction
Avascular necrosis of bone - scaphoid or head of femur break
Caseous necrosis - pathological sign of TB

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77
Q

Define hypertrophy

A

Increase in size of a tissue caused by an increase in size of the constituent cells (eg skeletal muscle)

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78
Q

Define hyperplasia

A

Increase in size of a tissue caused by an increase in number of the constituent cells (eg. enlarged prostate)

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79
Q

Define atrophy

A

Decrease in size of tissue caused by a decrease in number of the constituent cells or a decrease in their size (eg. underuse of muscle, Alzheimers)

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80
Q

Define metaplasia

A

Change in differentiation of a cells from one fully differentiated type to a different fully differentiated type (eg. lung cancer - ciliated columnar –> squamous epithelium)

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81
Q

Define dysplasia

A

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

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82
Q

Explain spina bifida

A

Lack of vertebrae formation - spinal cord is exposed

Myelomeningocele is the most severe - nerves and meninges bulge out of the back

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83
Q

What are other examples of developmental conditions?

A

Cleft lip/palate - cells fail to migrate and join

Ventricular septal defect (VSD)

84
Q

Name 3 types of development

A

Congenital
Inherited
Acquired

85
Q

What is congenital development?

A

Present at birth - can be inherited or acquired

86
Q

What is inherited development?

A

Genetic abnormality

87
Q

What is acquired development?

A

Caused by external/environmental factors

88
Q

Give an example of a chromosomal condition

A

Down’s syndrome - trisomy 21

89
Q

What occurs in Down’s syndrome?

A

Increased beta amyloid production

Causes early dementia and increase cataract risk

90
Q

Why do growth disorders occur?

A

Growth hormone deficiency or excess caused by pituitary adenoma

91
Q

Give an example of a growth disorder due to a:

  1. Deficiency in GH
  2. Excess of GH
A
  1. Dwarfism

2. Acromegaly - increased extremity size

92
Q

What is a telomere?

A

Regions at the end of a chromosome that count the number of cell replication

93
Q

What happens to a telomere as you age?

A

Telomeres get shorter

94
Q

How can age-related cell damage happen?

A

Free radical generation and peroxidation of cell membrane
Cross linking of DNA/proteins
Loss of Ca influx control –> mitochondrial damage
accumulation of toxic by-products

95
Q

Explain dermal elastosis

A

UVB lights causes cross linking of protein (collagen) so damages cells
low elastic properties of skin = wrinkles

96
Q

Explain osteoporosis

A

Decrease in normal bone matrix caused by lack of oestrogen

Increase bone resorption and decreased bone formation

97
Q

Why does cataracts occur?

A

UVB light causes lens protein cross linkage –> crystallin production –> clouding of lens

98
Q

Why does senile dementia occur?

A

Cortical atrophy

Plague and neurofibrillary tangle formation

99
Q

What is sarcopenia?

A

Skeletal muscle atrophy

Caused by decreased GH, decreased testosterone and increased catabolic cytokines

100
Q

How does deafness occur?

A

Damage and subsequent loss of cochlear hair cells

101
Q

Does apoptosis or necrosis cause an inflammatory response?

A

Necrosis

102
Q

Name 5 types of necrosis

A 
Caseous necrosis 
Coagulative necrosis 
Colliquative necrosis 
Fibrinoid necrosis 
Fat necrosis
103
Q

Where is caseous necrosis seen?

A

It is a pathological sign of tuberculosis

104
Q

What is coagulative necrosis?

A

Cells become firm and pale

Seen in most tissues

105
Q

What is colliquative necrosis?

A

Dead area is liquefied

Seen in brain

106
Q

What is fibrinoid necrosis a microscopic feature of?

A

Malignant hypertension - in arterioles

107
Q

What can cause necrosis?

A

Ischaemia
Metabolic
Trauma

108
Q

What is the hayflick phenomenon?

A

Number of times a normal human cell population will divide before cell division stops

109
Q

What is a BCC caused by?

A

UVB light

110
Q

Does a BCC metastasise?

A

BCC only invade locally

111
Q

How can you treat a BCC

A

Complete local excision = cure

112
Q

What lymph nodes to carcinomas spread to?

A

The lymph nodes that drain the site of the carcinoma (e.g. breast cancer –> ancillary lymph nodes)

113
Q

What is leukaemia?

A

Tumour of WBC, circulates around the body

114
Q

Name 5 cancers that commonly spread to bone

A
  1. Breast
  2. Thyroid
  3. Kidney
  4. Lung
  5. Prostate
115
Q

Give symptoms of leukaemia

A 
Weight loss
Fever 
Frequent infections
Fatigue and loss of appetite 
Easy SOB 
Night sweats 
Easy bleeding and bruising
116
Q

How can you confirm a breast cancer diagnosis?

A

Mammogram or a needle core biopsy

117
Q

Treatment for breast cancer that has NOT spread

A

Remove tumour –> mastectomy

118
Q

If axillary nodes are affected, how do you know and what treatment should be done?

A

Confirm by ultrasound and needle core biopsy and then remove any affected axillary nodes

119
Q

What treatment is used if breast cancer has metastasised?

A

Chemo and radiotherapy

120
Q

What is adjuvant therapy?

A

Extra treatment given after surgical excision

121
Q

What is the purpose of adjuvant therapy?

A

Tries to remove micro-metastases that could be present even if tumour is completed excised

122
Q

Give examples of breast cancer adjuvants

A

Radiotherapy after lumpectomy

Anti-oestrogen therapy (tamoxifen) - if oestrogen receptor positive

123
Q

Define carcinogenesis

A

Transformation of normal cells to neoplastic cells through permanent genetic changes

124
Q

Features of carcinogenesis

A

Applies to malignant neoplasms

Multistep process

125
Q

What does oncogenesis refer to?

A

Benign and malignant tumours

126
Q

Define carcinogen

A

Mutagenic (act on DNA) agents that cause (or are suspected to cause) tumours

127
Q

What is the difference between carcinogenic and oncogenic?

A 
Carcinogenic = cancer causing 
Oncogenic = tumour causing
128
Q

Name the carcinogen classes

A

Chemical
Radiation
Biological organisms
Miscellaneous

129
Q

Give examples of chemical carcinogens

A

Polycyclic aromatic hydrocarbons (smoking, mineral oils) –> lung and skin cancer

130
Q

Give examples of radiation carcinogens

A

UVA and B –> BCC, melanoma
Ionising radiation –> skin (radiographers – thorium), lung (uranium miners), thyroid cancer (Ukrainian children - Chernobyl nuclear explosion)

131
Q

Give an example of a hormone carcinogen

A

Increased oestrogen –> mammary and endometrial cancer

132
Q

Give an example of a mycotoxin carcinogen

A

Mycotoxin (Aflatoxin B1) –> hepatocellular cancer

133
Q

Give an example of a parasite carcinogen

A

Parasites –> cholangiocarcinoma and bladder cancer

134
Q

Give an example of a viral carcinogen

A

HPV –> cervical cancer

135
Q

Give an example of a misscellaneous carcinogen

A

Asbestos –> lung cancer, asbestosis (unknown mechanism of action)

136
Q

Name host factors for carcinogenesis

A

Race
Constitutional
Premalignant conditions
Transplacental exposure

137
Q

Define tumour

A

Any abnormal swelling

Neoplasm, inflammation, hypertrophy and hyperplasia

138
Q

Define Neoplasm

A

A lesion resulting from the NEW AUTONOMOUS ABNORMAL growth of cells that PERSISTS after removal of initiating stimulus

139
Q

What is the structure of a neoplasm?

A

Neoplastic cells

Stroma - connettive tissue framework

140
Q

What does the stroma provide of the neoplasm?

A

Mechanical support
Nutrition
Intracellular signalling
Contains blood vessels which perfuse the tumour

141
Q

A tumour <2mm is known as a …?

A

Avascular nodule

142
Q

How big is a vascularised nodule?

A

> 2mm

143
Q

What happens when there is increased growth in tumour angiogenesis?

A

Increased growth = central necrosis

144
Q

How can neoplasms be classified?

A 
Behavioural = being, malignant 
Histogenetic = cell of origin
145
Q

Features of benign neoplasms

A

Localised and on-invasive
Slow growth rate - out and up
Close resemblance to normal tissue

146
Q

Problems with benign neoplasms

A 
Pressure on adjacent structures
Flow obstruction
Hormone production
Transformation to a malignant neoplasm 
Anxiety
147
Q

Features of malignant neoplasms

A

Invasive and metastases
Rapid growth rate - down and in
Poorly defined and irregular borders

148
Q

Problems with malignant neoplasms

A 
Tissue destruction
Paraneoplastic effects (symptoms not just due to cancer at the site) - weight loss
Metastasise 
Pressure on adjacent structures
Flow obstruction
Hormone production
Anxiety and pain
149
Q

What is the suffix for neoplasms?

A

-oma

150
Q

What neoplasms do epithelial cells form?

A

Carcinomas

151
Q

What neoplasms do connective tissues form?

A

Sarcomas

152
Q

What neoplasms do lymphoid/haemopoietic organs form?

A

Lymphomas or leukaemia

153
Q

What is a papilloma?

A

A benign non glandular epithelial neoplasm

154
Q

What is an adenoma?

A

A benign glandular epithelial neoplasm

155
Q

What is a carcinoma?

A

A malignant non glandular epithelial neoplasm

156
Q

What is a adenocarcinoma?

A

A malignant glandular epithelial neoplasm

157
Q

Name some benign connective tissue neoplasms

A 
Lipoma = adipocytes 
Chondroma = cartilage 
Osteoma = bone 
Angioma = vascular 
Rhabdomyoma = striated muscle
Leiomyoma = smooth muscle 
Neuroma = nerves
158
Q

What is the suffix for malignant connective tissue neoplasms?

A

-sarcoma

159
Q

Name some malignant connective tissue neoplasms

A 
Liposarcoma = adipose tissue 
Chondrosarcoma = cartilage 
Osteosarcoma = bone 
Angiosarcoma = vascular 
Rhabdomyosarcoma = striated muscle 
Leiomyosarcoma = smooth muscle
160
Q

What is graded malignancy?

A

Carcinomas and sarcomas are further classified according to degree of differentiation (how much it resembles normal tissue)

161
Q

What are the types of grade of malignancy?

A

Low grade – looks like parent tissue (well differentiated)
High grade – doesn’t look like parent tissue (poorly differentiated)
Anaplastic – unknown origin cell type

162
Q

Name some exceptions to -oma rule

A

Granuloma
Melanoma - malignant
Lymphoma - malignant
Treatoma

163
Q

What is a carcinoma in situ?

A

Carcinoma fills cavity but has not invaded any other tissue

164
Q

What are the 8 stages of metastasis?

A
  1. Detachment
  2. Invasion
  3. Intravasation
  4. Evasion
  5. Adherence
  6. Extravasation
  7. Growth
  8. Angiogenesis
165
Q

Explain invasion

A

Some cells go through the basement membrane into the extracellular matrix using enzymes (proteases, collagenase, cathepsin D, urokinase-like plasminogen activator)

166
Q

What is intravasation?

A

Tumour cells move from ECM to blood/lymph vessels

167
Q

What is evasion?

A

Aggregate with platelets, shed surface antigens and stick to other tumour cells

168
Q

Explain adherence

A

Adherence of ells to endothelium at a remote location

169
Q

Explain extravasation

A

Tumour cells move from vessels to new tissue area

170
Q

What is angiogenesis?

A

Formation of blood vessels

171
Q

Name 3 routes of metastasis

A

Haematogenous - by blood stream
Lymphatic
Transoelomic - in pleural, pericardial and peritoneal cavities

172
Q

What tumours commonly metastasise to the lungs?

A

Most carcinomas and sarcomas (venous –> pulmonary system)

173
Q

What tumours commonly metastasise to the liver?

A

Colon, stomach, pancreas, intestine (portal system)

174
Q

What tumour never metastasises?

A

Basal cell carcinoma

175
Q

What term describes a cancer that has not invaded through the basement membrane?

A

Carcinoma in situ

176
Q

Give 2 promoters of tumour angiogenesis

A
  1. Vascular endothelial growth factors

2. Fibroblast growth factors

177
Q

Give 3 inhibitors of tumour angiogenesis

A
  1. Angiostatin
  2. Endostatin
  3. Vasculostatin
178
Q

Define exudate

A

A protein rich fluid that leaks out of vessel walls due to increased vascular permeability

179
Q

Give 3 endogenous chemical mediators of acute inflammation

A
  1. Bradykinin
  2. Histamine
  3. Nitric Oxide
180
Q

The activity of what enzyme in the blood can act as a marker for granulomatous disease?

A

Angiotensin converting enzyme

181
Q

Define abscess

A

Acute inflammation with a fibrotic wall

182
Q

what are the steps of acute inflammation?

A
  • Initial reaction of tissue to injury
  • Vascular component: dilation of vessels
  • Exudative component: vascular leakage of protein-rich fluid
183
Q

what is a rhabdomyoma?

A

Benign striated muscle neoplasm.

184
Q

what is a sarcoma?

A

Malignant connective tissue neoplasm.

185
Q

what is a leiomyoma?

A

A benign smooth muscle neoplasm.

186
Q

what is a neuroma?

A

A benign neoplasm of nerves.

187
Q

what is a chondrosarcoma?

A

A malignant neoplasm of cartilage.

188
Q

what is a liposarcoma?

A

A malignant neoplasm of adipose tissue.

189
Q

what is a melanoma?

A

A malignant neoplasm of melanocytes.

190
Q

what is a lymphoma?

A

A malignant neoplasm of lymphoid cells.

191
Q

what is a mesothelioma?

A

A malignant neoplasm of mesothelial cells.

192
Q

what is the role of p53 protein?

A

p53 protein looks for DNA damage, if damage is present p53 switches on apoptosis.

193
Q

What protein can switch on apoptosis if DNA damage is present?

A

p53 protein

194
Q

Activation of which family of protease enzymes can turn on apoptosis?

A

Caspases.

195
Q

Activation of what receptor can activate caspase and therefore apoptosis?

A

FAS receptor.

196
Q

What is required for a tumour to enter the blood stream (intravasation)?

A
  1. Collagenases.

2. Cell motility.

197
Q

What is required for a tumour to exit the blood stream (extravasation)?

A
  1. Adhesion receptors.
  2. Collagenases.
  3. Cell motility.
198
Q

What causes the pain associated with acute inflammation?

A
  1. Stretching and distortion of tissues due to oedema and pus under high pressure in an abscess cavity.
  2. Chemical mediators e.g. bradykinin and prostaglandins, are also known to induce pain.
199
Q

Describe the process of neutrophil polymorph migration into tissues as seen in acute inflammation.

A
  1. Margination of neutrophils.
  2. Pavementing of neutrophils.
  3. Neutrophils pass between endothelial cells.
  4. Neutrophils pass through basal lamina and migrate into adventitia.
200
Q

Chemical carcinogens: what types of cancer do polycyclic aromatic hydrocarbons cause?

A

Lung cancer and skin cancer.

201
Q

Chemical carcinogens: what can expose people to polycyclic aromatic hydrocarbons?

A

Smoking cigarettes and mineral oils.

202
Q

Chemical carcinogens: what types of cancer do aromatic amines cause?

A

Bladder cancer.

203
Q

Chemical carcinogens: what types of people are more susceptible to bladder cancer caused by aromatic amine exposure?

A

People who work in the rubber/dye industry.

204
Q

Chemical carcinogens: what type of cancer do nitrosamines cause?

A

Gut cancer.

205
Q

Chemical carcinogens: what type of cancer do alkylating agents cause?

A

Leukaemia; the risk is small in humans.

206
Q

Why can cigarette smoking lead to atherosclerosis?

A

Cigarette smoking releases free radicals, nicotine and CO into the body. These all damage endothelial cells.

Phase 2A revision (38 decks)

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