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Phase 2a pre clinical > general pathology > Flashcards

general pathology Flashcards

1
Q

hospital autopsies

A

<10% of autopsies in the UK

Requires Medical Certificate cause of Death (MCCD)

Audit, teaching, governance, research

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2
Q

medico-legal autopsies

A

> 90% of autopsies in the UK

Coronial

forensic

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3
Q

presumed natural death

A

Cause of death not known

not seen by doctor within days of death

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4
Q

presumed iatrogenic deaths

A

peri/post operative deaths

anaesthetic deaths

abortion

complications of therapy

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5
Q

presumed unnatural deaths

A

accidents

custody deaths

war/industrial pensions

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6
Q

doctor referral for autopsy

A

No statutory duty to refer

common law duty

GMC guidance

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7
Q

registrar of BDM referral for autopsy

A

statutory duty to refer

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8
Q

other referrals for autopsy

A

Relatives

the police

anatomical pathology technicians

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9
Q

histopathologists

A

Hospital autopsies

coronial autopsies
(Natural deaths, drowning, suicide, accidents, road traffic deaths, fire deaths, industrial deaths, peri/post operative deaths)
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10
Q

forensic pathologists

A 
Coronial autopsies
(homicide, death in custody, neglect and any done by histopathologists due to the action of a third party)
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11
Q

inflammation

A

local and physiological response to tissue injury

not a disease but a manifestation of disease

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12
Q

outcomes and harmful effects of inflammation

A

Benefits=
resolution
suppuration
organisation

Diseases=
Digestion of normal tissue
Swelling
Compressing brain tissue
Fibrosis from chronic inflammation 
Autoimmunity
Over reaction to stimulus
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13
Q

acute inflammation

A

initial and often transient series of tissue reactions to injury

sudden onset

short duration

usually resolves

cell type= neutrophil polymorphs

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14
Q

chronic inflammation

A

Subsequent of often prolonged tissue reactions following the initial response

slow onset or sequel to acute

long duration

may never resolve

cell type= macrophages

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15
Q

cells involved in inflammation

A 
neutrophil polymorphs
macrophages
lymphocytes
endothelial cells
fibroblasts
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16
Q

neutrophil polymorphs (inflammation)

A

short lived

first on the scene of acute

cytoplasmic granules full of enzymes that kill bacteria

usually die at the scene of inflammation

release chemicals that attract other inflammatory cells such as macrophages

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17
Q

macrophages (inflammation)

A

long lived cells- weeks to months

phagocytic properties

ingest bacteria and debris

carry debris away

present antigens to lymphocytes

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18
Q

lymphocytes (inflammation)

A

long lived cells- years

produce chemicals that attract other inflammatory cells

immunological memory

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19
Q

endothelial cells (inflammation)

A

line capillaries

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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20
Q

fibroblasts (inflammation)

A

long lived cells

form collagen in areas of chronic inflammation

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21
Q

causes of acute inflammation

A

microbial infections (bacterial, viruses)

hypersensitivity (parasites, allergic reactions)

physical agents (trauma, ionising radiation, heat)

chemicals (corrosives, acids, alkalis)

bacterial toxins

tissue necrosis

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22
Q

microbial infections (inflammation)

A

most common cause of acute inflammation

viruses lead to death of cells by intracellular multiplication

bacteria release exotoxins

parasitic infections and TB inflammation are examples of where hypersensitivity is important

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23
Q

hypersensitivity inflammation

A

altered state of immunological responsiveness causes inappropriate or excessive immune reaction

damages tissues

has cellular or chemical mediators

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24
Q

physical agents in inflammation

A

tissue damage leading to inflammation may occur through physical trauma, UV or other ionising radiation, burns or frostbite

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25
Q

chemicals in inflammation

A

corrosive chemicals provoke inflammation through gross tissue damage

infecting agents may release specific chemical irritants that lead directly to inflammation

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26
Q

tissue necrosis (inflammation)

A

death of tissues to due lack of oxygen or nutrients

usually from inadequate blood flow

acute inflammatory response due to peptides released from dead tissue

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27
Q

macroscopic appearance of inflammation

A

Top Cars Require Driving Licences

Tumor, Calor, Rubor, Dolor, Loss of function

Some Hoes Read Porn Lots

Swelling, Heat, Red, Pain, Loss of function

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28
Q

Rubor

A

Redness

acutely inflamed tissue appears red
caused by dilation of small blood vessels in damaged area

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29
Q

Calor

A

Heat

only in peripheral parts of the body- skin

caused by increased blood flow- hyperaemia
vascular dilation to deliver blood to area

systemic fever from chemical mediators, contributes

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30
Q

tumor

A

Swelling

oedema- accumulation of fluid in extravascular space as part of fluid exudate

physical mass of inflammatory cells migrating into the area

formation of connective tissue

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31
Q

dolor

A

Pain

partly stretching of tissues due to oedema and pus under pressure in abscess cavity

chemical mediators- bradykinin and prostaglandins and serotonin- induce pain

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32
Q

loss of function

A

movement of inflamed area is consciously and reflexly inhibited by pain

severe swelling may immobilise tissues

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33
Q

Acute inflammation response has 3 processes

A

changes in vessel diameter and flow

increased vascular permeability and formation of the fluid exudate

formation of the cellular exudate- emigration of neutrophil polymorphs into extravascular space

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34
Q

stages in neutrophil polymorph emigration (inflammation)

A

margination of neutrophils

pavementing of neutrophils

pass between endothelial cells

pass through basal lamina and migrate into adventitia

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35
Q

endogenous chemical mediators cause:

inflammation

A

vasodilation

emigration of neutrophils

chemotaxis

increased vascular permeability

itching and pain

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36
Q

chemical mediators released from cells

inflammation

A

histamine

lysosomal compounds

chemokines

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37
Q

plasma factors

inflammation

A

enzymatic cascade systems, which are unrelated and produce various inflammatory mediators

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38
Q

systemic effects of inflammation

A

pyrexia
constitutional symptoms
weight loss
amyloidosis

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39
Q

causes of chronic inflammation

A

transplant rejection
progression from acute
primary chronic
recurrent episodes of acute

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40
Q

macroscopic appearance of chronic inflammation

A

chronic ulcer

chronic abscess cavity

thickening of the wall of a hollow viscus

granulomatous inflammation

fibrosis

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41
Q

microscopic features of chronic inflammation

A

The cellular infiltrate consists characteristically of lymphocytes plasma cells and
macrophages
A few eosinophil polymorphs may be present, but neutrophil polymorphs are scarce
Some of the macrophages may form multinucleate giant cells
There may be evidence of continuing destruction of tissue at the same time as tissue
regeneration and repair
Tissue necrosis may be a prominent feature, especially in granulomatous conditions such as tuberculosis

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42
Q

granulomas

A

aggregate of epitheliod histiocytes (activated macrophages)

may contain other cells such as lymphocytes and histiocytic giant cells

granulomatous inflammation is a specific type- such as tuberculosis and leprosy

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43
Q

epitheliod histiocytes

A

resemble epithelial cells

activated macrophages

arranged in clusters

little phagocytic activity but adapted to secretory function

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44
Q

appearance of granulomas

A

may be augmented by presence of caseous necrosis or by conversion of some of the histiocytes into multinucleate giant cells

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45
Q

histiocytic giant cells

A

form where particulate matter, that is indigestible by macrophages, accumulates

form when foreign particles are too large to be ingested by just one macrophage

multinucleate giant cells w/ 100+ nuclei

little phagocytic activity

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46
Q

types of histiocytic multinucleate cells

A

langhans giant cells- horse shoe arrangement of peripheral nuclei at one pole

foreign body giant cells- large with nuclei randomly scattered throughout

touton giant cells- central ring of nuclei, peripheral to which there is lipid material

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47
Q

treating inflammation

A

aspirin

ibuprofen- inhibit prostaglandin synthase

steroids- bind to DNA up regulate inhibitors of inflammation and down regulate chemical mediators of inflammation

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48
Q

regeneration/resolution

A

initiating factor is removed

tissue is undamaged or able to regenerate

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49
Q

examples of regeneration

A

liver after surgery to remove a lobe

lobar pneumonia- pneumocytes can regenerate

skin abrasions

skin wounds- healing by first intention

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50
Q

repair

A

initiating factor is still present

tissue is damaged and unable to regenerate

replacement of damaged tissue by fibrous tissue

collagen produced by fibroblasts

brain fibrosis= gliosis

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51
Q

examples of repair

A

heart after myocardial infarction

brain after cerebral infarction

liver cirrhosis

skin wounds- healing by second intention

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52
Q

cells that regenerate

A 
hepatocytes
pneumocytes
blood cells
gut epithelium
skin epithelium
osteocytes
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53
Q

cells that dont regenerate

A

myocardial cells

neurones

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54
Q

regeneration example

A

healing by first intention-

sutured edge to edge
two edges fill gap with blood and fibrin
epidermis regrows
fibroblasts form collagen
scar forms, stronger than normal skin
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55
Q

repair example

A

healing by seconds intention

large amount of tissue loss- normally trauma
can’t be sutured together
gap present so no epithelial cells to regenerate
gap filled by capillaries and collaged until two edges can grow
large scar formed

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56
Q

Ways our healthy body prevents thrombosis occurring spontaneously

A

Laminar flow- cells travel in the centre of arterial vessels and don’t touch the side

endothelial are not sticky when they are healthy

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57
Q

thrombosis definition

A

the formation of a solid mass from blood constituents in an intact vessel of a living person

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58
Q

formation of a thrombus

A

platelet aggregation

platelets release chemicals when they aggregate causing them to start the cascade of clotting proteins in the blood

both of these reactions involve positive feedback loops; therefore difficult to stop

once clotting cascade has started there is a formation of insoluble fibrin

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59
Q

causes of thrombosis

A

change in vessel wall
change in blood flow
change in blood constituents

usually a combination of two or three

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60
Q

drugs preventing thrombosis

A

aspirin
heparin
warfarin

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61
Q

embolus definition

A

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

formed when a solid mass in the blood is carried through the circulatory system to a place where it gets stuck and blocks it

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62
Q

cause of embolism

A

thrombus

air

other- cholesterol crystals, tumours, amniotic fluid, fat

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63
Q

embolism location

A

in venous system then- vena cava -> right side of heart -> lodge in pulmonary arteries (location depends on size) -> can lodge as lungs split into capillaries (lungs act as a filter for venous emboli

in arterial system it can travel anywhere downstream

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64
Q

ischaemia

A

reduction in blood blow to a tissue without any other implications

inadequate blood supply

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65
Q

infarction

A

reduction in blood flow to a tissue with subsequent local cell death
macroscopic event usually caused by thrombus blockage

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66
Q

atheroma

A

aka atherosclerosis

pathology of arteries when there is deposition of lipids in the arterial wall with surrounding fibrosis and chronic inflammation

the plaques can enlarge to occlude the lumen of vessels

endothelium overlying a plaque may rupture and initiate thrombosis within the vessel

plaques are predominant cause of myocardial or cerebral infarction

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67
Q

plaques contain:

A

fibrous tissue

lipids- cholesterol

lymphocytes

68
Q

atherosclerosis distribution in arteries

A

never low pressure systems- pulmonary arteries

high pressure systems=common e.g. aorta

69
Q

epidemiology of atherosclerosis

A

increases with age

more common in lower socioeconomic populations due to risk factors

70
Q

risk factors of atherosclerosis

A

raised serum lipids- hyper lipidaemia

hypertension

diabetes mellitus

cigarette smoking

71
Q

endothelial damage theory

A

 Any factor that causes endothelial damage in arteries will lead eventually, by repeated small
amounts of damage, to the formation of atherosclerotic plaques
 The major process after endothelial damage is chronic inflammation with macrophages and
fibroblasts
 The lipids within plaques probably derive from the breakdown of inflammatory cells in the
plaque
 Understanding pathogenesis of atheroma enables prevention or to stop progression

72
Q

atherosclerosis formation

A

endothelial cells dysfunction- cholesterol damages wall
high levels of LDL begins to accumulate in arterial wall
macrophages attracted to site of damage and take up lipid to form foam cells- inflammatory response
formation of a fatty streak= earliest stage of a plaque
activated macrophages release their own products- cytokines and growth factors
smooth muscle proliferation around lipid core and formation of a fibrous cap of collagen

73
Q

complications of atherosclerosis

A

cerebral infarction

carotid atheroma- emboli causing transient ischemic attacks

myocardial infarction

aortic aneurysms

peripheral vascular disease

gangrene

74
Q

prevention of atherosclerosis

A

reduce lipids- reduces epithelial damage

reduce BP- reduces epithelial damage

stop smoking- reduces epithelia damage

low dose aspirin reduces platelet aggregation at site of damage

75
Q

apoptosis definition

A

programmed cell death of a single cell

76
Q

necrosis definition

A

unprogrammed death of a large number of cells due to an adverse event

77
Q

apoptosis uses

A

turnover of cells- stem cells divide to produce new cells which mature and differentiate and eventually die by the process of apoptosis

embryogenesis- apoptosis removes cells no longer needed as organs develop

DNA damage- cells can detect DNA damage (p53 protein)

78
Q

initiation and control of apoptosis

A

apoptosis is implemented by caspases and Bcl2 protein

decision as to whether a cell should activate this process or not is less well understood

alternatives to apoptosis can be used

cells with a lot of DNA damage prefer apoptosis

abnormal apoptosis can occur in a variety of situations including drugs, graft versus host disease and neurodegeneration

p53 is involved in detection of DNA damage

breakdown in control of apoptosis can cause Cancer (lack of) or HIV (too much)

79
Q

necrosis

A

catastrophic event that physically causes death of a large number of cells and resolved or is repaired by basic inflammatory processes

80
Q

examples of necrosis

A 
infarction
burn
frostbite
toxic spider venom
avascular necrosis of bone
pancreatitis
81
Q

types of necrosis

A

coagulative necrosis- sticks together

liquefactive necrosis- liquid

caseous necrosis- resembles soft cheese e.g. TB

82
Q

genetic disease

A

one that occurs primarily from a genetic abnormality

some diseases that are pure genetic diseases

83
Q

inherited diseases

A

caused by inherited genetic abnormality

may not manifest until later in life

84
Q

types of inherited disease

A

chromosome abnormalities e.g. Down syndrome

Mendelian inheritance e.g. single gene disorders

85
Q

single gene disorder

A

abnormality of a single gene causes the disease

dominant or recessive

86
Q

dominant definition

A

will be present where there is only one copy of the abnormal gene

e.g. Huntington’s

87
Q

Recessive definition

A

only expressed if both copies of the gene are abnormal

e.g. cystic fibrosis

88
Q

co-dominant definition

A

both alleles are expressed

e.g. AB blood group

89
Q

autosomal definition

A

occurring on the non-sex chromosomes

90
Q

sex-linked definition

A

occurs on the sex chromosomes

regions which dont have a corresponding region on the opposing chromosome

mostly x-linked as men only have one Y and women have none

more common in males as they only have one X

91
Q

polygenic inheritance

A

interaction of several genes usually on different chromosomes

e.g. breast cancer

many diseases have strong genetic component still need the appropriate environment to be expressed as disease

92
Q

congenital diseases

A

present at birth

mostly genetic but can be acquired- rhesus haemolytic disease or foetal alcohol syndrome

93
Q

acquired diseases

A

disease or condition developed after birth

caused by non-genetic environmental factors but may have strong genetic background

94
Q

disorders of development

A

neural tube defect

cleft palate

spina bifida

ventricular septal defect

95
Q

disorders of growth

A

GH deficiency

GH excess

mutation in the COL2A1- type II collagen

mutation in fibroblast growth factor receptor 3 gene

96
Q

hypertrophy

A

increase in size of tissue caused by an INCREASE IN SIZE of cells without an increase in number

97
Q

physiological uses of hypertrophy

A

skeletal muscle cells exposed to an increased workload cannot divide and respond by hypertrophing

98
Q

pathological hypertrophy

A

myocardium undergoes hypertrophy with high BP

99
Q

hyperplasia

A

increased growth caused by an INCREASE IN NUMBER of cells

can be accompanies by increase of cell size

100
Q

physiological use of hyperplasia

A

during pregnancy and lactation, breast epithelial cells respond to increase in demands by increasing in number

101
Q

pathological hyperplasia

A

prostate undergoes hyperplasia with age in response to excess of oestrogen stimulation

102
Q

atrophy

A

decrease in size of tissue caused by DECREASE IN NUMBER of constituent cells or by DECREASE IN THEIR SIZE

103
Q

physiological use of atrophy

A

various embryological structures undergo atrophy during foetal life

thymus atrophies in early adult life

104
Q

pathological atrophy

A

occurs as a result of loss of blood supply, loss of innervation, loss of pressure, lack of nutrition, lack of or result of hormonal stimulation

105
Q

metaplasia

A

reversible transformation of one mature cell type into another fully differentiated cell type

adaptive response to injurious stimuli

e.g. transformation of normal pseudostratified columnar epithelium of bronchi intro squamous epithelium following repeated exposure to cigarette smoke

106
Q

dysplasia

A

premalignant condition characterised by increased growth, cellular atypia and decreased differentiation

imprecise term for morphological changes seen in cells in progression into cancer

107
Q

ageing

A

progressive loss of various functions and accumulation of diseases

108
Q

mechanisms of ageing

A

many organs do not have cells that regenerate so if they die there will be a loss of function in that organ

acquired cancers may occur because of accumulated DNA damage over a lifetime of cell divisions

109
Q

manifestations of ageing

A

development of acquired cancers

neurodegeneration- dementia, parkinsons

dermal elastosis

osteoporosis

osteoarthritis

vision loss

deafness- loss of hair cells

reduced immunity

110
Q

cancer

A

generic term for malignant tumour

111
Q

metastasis

A

the development of secondary malignant growths at a distance from a primary site of cancer

112
Q

metastatic tumours

A

arise from cells that naturally move around the body- lymphocytes

tumours from these cells will never stay in one site so the treatment for these must always be for the whole body

113
Q

non- metastatic tumour

A

only spread locally and do not metastasise to other regions

tumours can be treated by local excision

114
Q

mixture of non-metastatic and metastatic

A

most common tumours e.g. breast cancer

tumour staging is important

if it hasnt spread it can be excised

but if it has spread then it requires excision and systemic treatment

115
Q

useful cancer treating facts

A

basal cell carcinoma of the skin invades locally- so can be locally excised

carcinomas spread to lymph nodes that drain the primary site and so can spread through the blood to bone

most common carcinomas to do so are breast, prostate, lung, thyroid and kidney

116
Q

carcinogenesis

A

the transformation of normal cells to neoplastic cells through permanent genetic alterations or mutations

applies only to malignant tumours

117
Q

carcinogens

A

agents known or suspected to cause cancer

118
Q

oncogens

A

cause tumours

119
Q

environmental agents and cancer

A

account for 85% of cancer risk factors

chemical
viruses
radiation
biological agents (hormones, parasites, mycotoxins)
miscellaneous
120
Q

host factors and cancer

A 
race
diet
age
gender
premalignant lesions
transplacental exposure
121
Q

chemicals and cancer

A

no common structural features

some act directly

most require metabolic conversion from pro-carcinogens to ultimate carcinogens

122
Q

radiant energy and cancer

A

ionising radiation

long term effect

skin cancer and sunlight

lung cancer in uranium miners

123
Q

biological agents and cancer

A

hormones- oestrogen increases risk of mammary cancer

mycotoxins- aflatoxin B2= hepatocellular carcinoma

parasites- shistosoma= bladder cancer

124
Q

miscellaneous carcinogens

A

asbestos

125
Q

conventional chemotherapy mechanism of action

A

vinblastine= antimicrotubule agent- prevents anaphase

etoposide= prevents topoisomerase II- prevents DNA replication

cisplatin and ifosamide= bind directly to DNA- inhibits DNA synthesis by cross linking

126
Q

Conventional chemotherapy issues

A

not selective for tumour cells

usually affects normal cells that also divide fast- myelosuppression, hair loss, diarrhoea

not good treatment for slow dividing tumours

127
Q

conventional chemotherapy tumours

A

fast dividing tumours

germ cell tumours of testis
acute leukaemias
lymphomas
embryonal paediatric tumours

128
Q

targeted chemotherapy

A

more effective with fewer side effects

recognises differences between normal cells and cancer cells

129
Q

detecting differences between normal and cancer cells

A

gene arrays- different expression of genes (overexpression of growth factor receptor due to mutation in this gene)

proteomics- different proteins

tissue microarrays

130
Q

Cetuximab (Erbitux)

A

monoclonal antibody against epidermal growth factor receptor

chimeric IgG humanised monoclonal antibody,
binds competitively to extracellular domain of EGFR,
antitumour activity in xenograft models,
blocks production of VEGF, interleukin 8 and bFGF

131
Q

programmed cell death protein I

A

immune checkpoint
inhibits t cell response
prevents auto-immunity in normal physiology

132
Q

treating breast cancer using oestrogen receptors

A

epithelial cells respond to oestrogen as a growth factor, giving a drug that blocks oestrogen receptors on the cancer cells should inhibit their growth

only effective if the breast cancer has oestrogen receptors on the surface of its cells

133
Q

treating breast cancer using HER2 protein

A

some tumours overexpress a growth factor on the cell surface (HER2 protein) (coded for by (HER2 gene)

20% of breast cancer have amplified number of copies of this gene

use herceptin and lapatinib

134
Q

neoplasm

A

a lesion resulting from the autonomous or relatively autonomous abnormal growth of cells which persists after the initiating stimulus has been removed

Neoplasia is:
o Autonomous
o Abnormal
o Persistent
o New growth
135
Q

neoplasm and tumour difference

A

tumour is any abnormal swelling, including:

neoplasm,
inflammation,
hypertrophy,
hyperplasia

136
Q

neoplastic cells

A

derive from nucleated cells

usually monoclonal

growth pattern related to parent cell

synthetic activity related to parent cell (collagen, keratin, hormones etc. )

137
Q

tumour angiogenesis

A

benign neoplasms are slow growing therefore dont outgrow blood supply

malignant neoplasms are fast growing so outgrow blood supply- forms central necrosis

138
Q

classification of neoplasms

A

classification occurs to determine treatment and prognosis

methods of classification= behavioural (benign/malignant)
histogenetic (cell of origin)

139
Q

behavioural classification

A

classified as benign, borderline, malignant

Borderline tumours defy precise classification

140
Q

benign neoplasms

A
  • localised, non-invasive
  • slow growth rate
  • low mitotic activity
  • close resemblance to normal tissue
  • circumscribed or encapsulate
  • nuclear morphometry often normal
  • necrosis and ulceration are rare
141
Q

morbidity and mortality of benign neoplasm

A 
pressure on adjacent structures
obstruct flow
produce hormone
transform into malignant
anxiety
142
Q

malignant neoplasm

A
  • invasive
  • metastasise
  • rapid growth
  • variable resemblance to normal tissue
  • poorly defined or irregular border
  • hyperchromatic and pleomorphic nuclei
  • increased mitotic activity
  • necrosis and ulceration= common
  • encroach upon and dectroy surrounding tissue
  • have ‘crab like’ cut surface (cancer= latin for crab)
143
Q

morbidity and mortality of malignant neoplasms

A 
destruction of adjacent tissue
metastases
blood loss from ulcers
obstruction of flow
hormone production
anxiety and pain
144
Q

histogenetic classification

A

histogenesis= specific cell of origin of tumour

145
Q

nomenclature of neoplasia

A

have suffix -oma

prefix defends on behavioural and histogenesis

146
Q

benign epithelial neoplasms

A

papillomas:

  • benign tumour of non-glandular, non secretory epithelium
  • prefix with cell type of origin, e.g. squamous cell papilloma

adenomas:

  • benign tumour of glandular or secretory epithelium
  • prefix with cell type of origin e.g. colonic adenoma
147
Q

malignant epithelial neoplasms

A

carcinomas:

  • malignant tumour of epithelial cells
  • prefixed with cell type e.g. transitional cell carcinoma

adenocarcinomas:

  • carcinomas of glandular epithelium
    e. g. adenocarinoma of colon
148
Q

benign connective tissue neoplasms

A

prefix of cell of origin

  • lipoma=adipocytes
  • chondroma=cartilage
  • osteoma=bone
  • angioma=vascular
  • rhabdomyoma=striated muscle
  • leimyoma=smooth muscle
149
Q

malignant connective tissue neoplasms

A
  • liposarcoma=adipose tissue
  • chondrosarcoma=cartilage
  • osteosarcoma=bone
  • angiosarcoma=blood vessels
  • rhabdomyosarcoma=striated muscle
  • leiomyosarcoma=smooth muscle
150
Q

further malignant classification

A

anaplastic= cell type of origin is unknown

carcinomas and sarcomas are further classified according to degree of differentiation (low grade is more differentiated)

151
Q

exceptions to neoplasm classification

A
  • not all omas are neoplasms (granuloma= inflammation)
  • not all malignant tumours are carcinoma or sarcoma (melanoma= malignant melanocytes, lymphoma=malignant lymphoid cells)
  • some tumours are named after people (burkitt’s lymphoma, kaposi’s sarcoma, grawitz tumour)
152
Q

in situ neoplasia

A

applies only to epithelia neoplasms

the lesion has the cytological features of a malignant neoplasms

may progress to invasive disease

screening may allow detection and treatment of the disease before the development of carcinoma

153
Q

invasion of neoplasia

A

defining feature of a malignant neoplasm

enables neoplastic cells to spread directly through tissues and gain access to blood vessels and lymphatic channels

dependent upon- decreased cellular adhesion, abnormal cellular motility, production of enzymes with a lytic effect on the surrounding tissues

154
Q

metastasis

A

process by which a malignant tumour spreads from its primary site to produce secondary tumours at distant sites

may occur via blood vessels (haematogenous), lymphatics, across body cavities (transcoelomic), along nerves or as a result of direct implantation during surgery (iatrogenic)

155
Q

metastasis cascade

A

detachment

invasion

intravasation

evasion of host defences

arrest

extravasation

vascularisation

156
Q

mechanism for neoplasia invasion of basement membrane

A

invasion of a basement membrane then invasion of extracellular matrix

proteases- matrix metalloproteinases (collagenase, cathepsin D, urokinase-type plasminogen activator)

cell motility

157
Q

tumour cell motility

A

tumour cell derived motility factors

breakdown products of extracellular matrix

158
Q

intravasation of neoplasm

A

collagenases

cell motility

159
Q

neoplasm evasion of host immune defence

A

aggregation with platelets

shedding of surface antigens

adhesion to other tumour cells

160
Q

extravasation of neoplasm

A

adhesion receptors

collagenases

cell motility

161
Q

growth at metastatic site

A

growth factors

tend to be autocrine, positive feedback

162
Q

angiogenesis of new metastases

A

angiogenesis promoters- vascular endothelial growth factors, basic fibroblast growth factor

angiogenesis inhibitors- angiostatin, endostatin, vasculostatin

163
Q

Routes of metastasis (lungs)

A

tumours invade veins and lymphatics as arteries have thick walls, so tumours travel to lungs via right side of heart

sarcomas and any common (non-colonic) cancers tend to metastasise in the lung

164
Q

Routes of metastasis (Liver)

A

tumours from colon travel via portal vein to liver where the capillaries act as a filter

colon, stomach, pancreas, carcinoid tumours of the intestine

165
Q

Routes of metastasis (Bone)

A 
Prostate
breast
thyroid
lung
kidney

Phase 2a pre clinical (6 decks)

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