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Pathology Flashcards

1
Q

What is the role of an autopsy?

A

Who was deceased?
When did they die?
Where did they die?
Cause of death

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2
Q

How is an autopsy done?

A 
History 
External examination 
Evisceration 
Internal examination 
Reconstruction
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3
Q

What deaths are referred to a coroner?

A

Presumed natural - death unknown
Presumed iatrogenic - peri/postoperative deaths
Presumed unnatural - accidents, unlawful killing

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4
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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5
Q

Causes of acute inflammation

A 
Microbial infections 
Hypersensitivity reactions 
Physical agents  
Chemicals
Tissue necrosis
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6
Q

Clinical features of acute inflammation

A 
Redness (rubor)
Heat (calor) 
Swelling (tumor)
Pain (dolor)
Loss of function
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7
Q

What makes up the cellular exudate for acute inflammation?

A

Neutrophil polymorphs
Macrophages
Lymphocytes

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8
Q

Features of Neutrophil polymorphs

A

Short lived, pus cells
First on the scene of acute inflammation
Attract other inflammatory cells
Cytoplasmic granules full of enzymes that kill bacteria
Diagnostic histological feature

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9
Q

Features of lymphocytes

A

Long lived cells
Produce chemicals that attract other inflammatory cells
Immunological memory

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10
Q

Features of macrophages

A

Long lived cells
Phagocytic properties
may present antigen to lymphocyte

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11
Q

Features of endothelial cells

A

Become sticky in areas of inflammation so inflammatory cells adhere to them
Become porous to allow inflammatory cells to pass into tissues

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12
Q

Give an example of acute inflammation

A

Acute appendicitis

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13
Q

What are the benefits of inflammation?

A

Destruction of invading microorganisms and wailing off of an abscess cavity preventing infection spread

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14
Q

What are the outcomes of acute inflammation?

A

Resolution
Suppuration
Organisation (fibrosis)
Progression to chronic inflammation

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15
Q

What are the negatives of inflammation?

A

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

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16
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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17
Q

Causes of chronic inflammation

A

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

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18
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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19
Q

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

A

Lymphocytes
Plasma cells
Macrophages
Fibroblasts

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20
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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21
Q

Where are granulomas seen?

A

Tuberculosis
Leprosy
Sarcoidosis

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22
Q

How can you treat inflammation?

A

Aspirin, ibuprofen (NSAIDs)

Corticosteroids

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23
Q

What is resolution?

A

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

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24
Q

What is repair?

A

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

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25
Q

Which organ is a good example for resolution?

A

Liver

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26
Q

What affects resolution of the liver?

A

Cirrhosis (ongoing damage resulting in abnormal architecture)

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27
Q

What cells can regenerate?

A 
Hepatocytes 
Pneumocytes 
All blood cells
Gut epithelium 
Skin epithelium 
Osteocytes
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28
Q

What cells can’t regenerate?

A

Myocardial cells

Neurones

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29
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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30
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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31
Q

When does 1st intention healing occur?

A

Incision wound

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32
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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33
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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34
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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35
Q

What is organisation?

A

Repair of specialised tissue by the formation of a fibrous scar

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36
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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37
Q

What produces collagen?

A

Fibroblasts

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38
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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39
Q

What is a thrombosis?

A

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

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40
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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41
Q

What does Virchow’s triad do?

A

Predisposes to thrombosis

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42
Q

When does an arterial thrombosis normally occur?

A

When superimposed on atheroma

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43
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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44
Q

What is a vein thombus most commonly due to?

A

Stasis

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45
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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46
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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47
Q

What does an occlusion of a coronary artery result in?

A

Myocardial infarction

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48
Q

What does occlusion of a cerebral artery result in?

A

Cerebral infarction (stroke)

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49
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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50
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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51
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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52
Q

What is the most common occurrence of an embolus?

A

Pulmonary embolism from deep leg vein thrombosis

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53
Q

What is Ischaemia?

A

Reduction in blood flow

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54
Q

What is Infarction?

A

Death of cells due to reduction in blood supply

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55
Q

What is infarction normally caused by?

A

Thrombosis of an artery

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56
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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57
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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58
Q

What areas are most susceptible to infarction?

A

Watershed territories

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59
Q

What are the functions of histamine?

A 
Vasodilation
Emigration of neutrophils (chemotaxis) 
Increase vascular permeability
Pain 
Itching
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60
Q

Role of plasma factors

A

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

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61
Q

What is the microscopic appearance of chronic inflammation?

A

Chronic ulcer
Abscess cavity
Granulatomous inflammation
Fibrosis

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62
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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63
Q

Causes of an embolus

A 
Air injected 
Thrombus/atheroma
Amniotic fluid
Fat 
Tumour
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64
Q

What happens in a venous system embolism?

A

Goes to RHS heart
Pulmonary system
Pulmonary embolism

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65
Q

What happens in an arterial system embolism?

A

Goes to LHS heart
Systemic system
Embolism anywhere

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66
Q

What is end arterial supply?

A

Single artery supplies organ - more susceptible to infarction

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67
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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68
Q

What is an atherosclerosis?

A

Build up of plague in arteries , narrows arteries

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69
Q

Where are atherosclerosis’ found?

A

Systemic arterial system - high pressure systems

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70
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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71
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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72
Q

What do the risk factors for atherosclerosis do?

A

Damage the endothelial cells

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73
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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74
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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75
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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76
Q

Define apoptosis

A

Programmed cell death

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77
Q

Define necrosis

A

Traumatic cell death

78
Q

What types of DNA damage cause apoptosis to occur?

A

Single/double stand break
Base alteration
Cross linking

79
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
80
Q

Example of normal apoptosis

A

Removal of finger webbing during development

81
Q

What can a lack of apoptosis cause?

A

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

82
Q

In what is excess apoptosis present?

A

HIV mediated T cell destruction

83
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

84
Q

Define hypertrophy

A

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

85
Q

Define hyperplasia

A

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

86
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)

87
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)

88
Q

Define dysplasia

A

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

89
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

90
Q

What are other examples of developmental conditions?

A

Cleft lip/palate - cells fail to migrate and join

Ventricular septal defect (VSD)

91
Q

What are the signs of a VSD

A

Strong heart murmur

Left ventricular hypertrophy

92
Q

Name 3 types of development

A

Congenital
Inherited
Acquired

93
Q

What is congenital development?

A

Present at birth - can be inherited or acquired

94
Q

What is inherited development?

A

Genetic abnormality

95
Q

What is acquired development?

A

Caused by external/environmental factors

96
Q

Give an example of a chromosomal condition

A

Down’s syndrome - trisomy 21

97
Q

What occurs in Down’s syndrome?

A

Increased beta amyloid production

Causes early dementia and increase cataract risk

98
Q

Why do growth disorders occur?

A

Growth hormone deficiency or excess caused by pituitary adenoma

99
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

100
Q

What is a telomere?

A

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

101
Q

What happens to a telomere as you age?

A

Telomeres get shorter

102
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

103
Q

Explain dermal elastosis

A

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

104
Q

Explain osteoporosis

A

Decrease in normal bone matrix caused by lack of oestrogen

Increase bone resorption and decreased bone formation

105
Q

Why does cataracts occur?

A

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

106
Q

Why does senile dementia occur?

A

Cortical atrophy

Plague and neurofibrillary tangle formation

107
Q

What is sarcopenia?

A

Skeletal muscle atrophy

Caused by decreased GH, decreased testosterone and increased catabolic cytokines

108
Q

How does deafness occur?

A

Damage and subsequent loss of cochlear hair cells

109
Q

Does apoptosis or necrosis cause an inflammatory response?

110
Q

Name 5 types of necrosis

A 
Caseous necrosis 
Coagulative necrosis 
Colliquative necrosis 
Fibrinoid necrosis 
Fat necrosis
111
Q

Where is caseous necrosis seen?

A

It is a pathological sign of tuberculosis

112
Q

What is coagulative necrosis?

A

Cells become firm and pale

Seen in most tissues

113
Q

What is colliquative necrosis?

A

Dead area is liquefied

Seen in brain

114
Q

What is fibrinoid necrosis a microscopic feature of?

A

Malignant hypertension - in arterioles

115
Q

What can cause necrosis?

A

Ischaemia
Metabolic
Trauma

116
Q

What is the hayflick phenomenon?

A

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

117
Q

What is a BCC caused by?

118
Q

Does a BCC metastasise?

A

BCC only invade locally

119
Q

How can you treat a BCC

A

Complete local excision = cure

120
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)

121
Q

What is leukaemia?

A

Tumour of WBC, circulates around the body

122
Q

Name 5 cancers that commonly spread to bone

A
  1. Breast
  2. Thyroid
  3. Kidney
  4. Lung
  5. Prostate
123
Q

Give symptoms of leukaemia

A 
Weight loss
Fever 
Frequent infections
Fatigue and loss of appetite 
Easy SOB 
Night sweats 
Easy bleeding and bruising
124
Q

How can you confirm a breast cancer diagnosis?

A

Mammogram or a needle core biopsy

125
Q

Treatment for breast cancer that has NOT spread

A

Remove tumour –> mastectomy

126
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

127
Q

What treatment is used if breast cancer has metastasised?

A

Chemo and radiotherapy

128
Q

What is adjuvant therapy?

A

Extra treatment given after surgical excision

129
Q

What is the purpose of adjuvant therapy?

A

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

130
Q

Give examples of breast cancer adjuvants

A

Radiotherapy after lumpectomy

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

131
Q

Define carcinogenesis

A

Transformation of normal cells to neoplastic cells through permanent genetic changes

132
Q

Features of carcinogenesis

A

Applies to malignant neoplasms

Multistep process

133
Q

What does oncogenesis refer to?

A

Benign and malignant tumours

134
Q

Define carcinogen

A

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

135
Q

What is the difference between carcinogenic and oncogenic?

A 
Carcinogenic = cancer causing 
Oncogenic = tumour causing
136
Q

Name the carcinogen classes

A

Chemical
Radiation
Biological organisms
Miscellaneous

137
Q

Give examples of chemical carcinogens

A

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

138
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)

139
Q

Give an example of a hormone carcinogen

A

Increased oestrogen –> mammary and endometrial cancer

140
Q

Give an example of a mycotoxin carcinogen

A

Mycotoxin (Aflatoxin B1) –> hepatocellular cancer

141
Q

Give an example of a parasite carcinogen

A

Parasites –> cholangiocarcinoma and bladder cancer

142
Q

Give an example of a viral carcinogen

A

HPV –> cervical cancer

143
Q

Give an example of a misscellaneous carcinogen

A

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

144
Q

Name host factors for carcinogenesis

A

Race
Constitutional
Premalignant conditions
Transplacental exposure

145
Q

Give examples of race as a host factor

A

Increased melanin in black skin –> decreased skin cancer incidence
Reverse smoking/betal nut chewing –> increase oral cancer in India, SE Asia

146
Q

Give examples of constitutional host factors

A

Inherited predisposition – familial adenomatous polyposis (chr 5), retinoblastoma (chr 13)
Age – increased incidence of all cancers
Gender – breast cancer 200x more likely in females

147
Q

Give examples of premalignant conditions as host factors

A

Local abnormality associated with increased risk of malignancy at that site
Colonic polyps, ulcerative colitis (bowel cancer), cervical dysplasia, undescended testes (testicular cancer)

148
Q

Define tumour

A

Any abnormal swelling

Neoplasm, inflammation, hypertrophy and hyperplasia

149
Q

Define Neoplasm

A

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

150
Q

What is the structure of a neoplasm?

A

Neoplastic cells

Stroma - connettive tissue framework

151
Q

What does the stroma provide of the neoplasm?

A

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

152
Q

A tumour <2mm is known as a …?

A

Avascular nodule

153
Q

How big is a vascularised nodule?

154
Q

What happens when there is increased growth in tumour angiogenesis?

A

Increased growth = central necrosis

155
Q

How can neoplasms be classified?

A 
Behavioural = being, malignant 
Histogenetic = cell of origin
156
Q

Features of benign neoplasms

A

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

157
Q

Problems with benign neoplasms

A 
Pressure on adjacent structures
Flow obstruction
Hormone production
Transformation to a malignant neoplasm 
Anxiety
158
Q

Features of malignant neoplasms

A

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

159
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
160
Q

What is the suffix for neoplasms?

161
Q

What neoplasms do epithelial cells form?

A

Carcinomas

162
Q

What neoplasms do connective tissues form?

163
Q

What neoplasms do lymphoid/haemopoietic organs form?

A

Lymphomas or leukaemia

164
Q

What is a papilloma?

A

A benign non glandular epithelial neoplasm

165
Q

What is an adenoma?

A

A benign glandular epithelial neoplasm

166
Q

What is a carcinoma?

A

A malignant non glandular epithelial neoplasm

167
Q

What is a adenocarcinoma?

A

A malignant glandular epithelial neoplasm

168
Q

Name some benign connective tissue neoplasms

A 
Lipoma = adipocytes 
Chondroma = cartilage 
Osteoma = bone 
Angioma = vascular 
Rhabdomyoma = striated muscle
Leiomyoma = smooth muscle 
Neuroma = nerves
169
Q

What is the suffix for malignant connective tissue neoplasms?

170
Q

Name some malignant connective tissue neoplasms

A 
Liposarcoma = adipose tissue 
Chondrosarcoma = cartilage 
Osteosarcoma = bone 
Angiosarcoma = vascular 
Rhabdomyosarcoma = striated muscle 
Leiomyosarcoma = smooth muscle
171
Q

What is graded malignancy?

A

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

172
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

173
Q

Name some exceptions to -oma rule

A

Granuloma
Melanoma - malignant
Lymphoma - malignant
Treatoma

174
Q

What is a carcinoma in situ?

A

Carcinoma fills cavity but has not invaded any other tissue

175
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
176
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)

177
Q

What is intravasation?

A

Tumour cells move from ECM to blood/lymph vessels

178
Q

What is evasion?

A

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

179
Q

Explain adherence

A

Adherence of ells to endothelium at a remote location

180
Q

Explain extravasation

A

Tumour cells move from vessels to new tissue area

181
Q

What is angiogenesis?

A

Formation of blood vessels

182
Q

Name 3 routes of metastasis

A

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

183
Q

What tumours commonly metastasise to the lungs?

A

Most carcinomas and sarcomas (venous –> pulmonary system)

184
Q

What tumours commonly metastasise to the liver?

A

Colon, stomach, pancreas, intestine (portal system)

185
Q

What tumour never metastasises?

A

Basal cell carcinoma

186
Q

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

A

Carcinoma in situ

187
Q

Give 2 promoters of tumour angiogenesis

A
  1. Vascular endothelial growth factors

2. Fibroblast growth factors

188
Q

Give 3 inhibitors of tumour angiogenesis

A
  1. Angiostatin
  2. Endostatin
  3. Vasculostatin
189
Q

Define exudate

A

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

190
Q

Give 3 endogenous chemical mediators of acute inflammation

A
  1. Bradykinin
  2. Histamine
  3. Nitric Oxide
191
Q

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

A

Angiotensin converting enzyme

192
Q

Define abscess

A

Acute inflammation with a fibrotic wall

PHASE 2A (16 decks)

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