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Phase 2a Introductory Clinical Science > Pathology > Flashcards

Pathology Flashcards

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1
Q

What is inflammation?

A

Inflammation is the local physiological response to tissue injury that involves inflammatory cells.

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2
Q

What is the likely cause of inflammation that is red? What about if it is red and there is pus?

A
  1. Virus

2. Bacteria

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3
Q

How can inflammation be good? Give two answers.

A

Fight infections

Repair injuries

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4
Q

How can inflammation be bad? Give three answers.

A

Autoimmune response
Over-reaction to stimulus
Can cause disease e.g. fibrosis (from chronic) can cause distortion to tissue and alter function

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5
Q

What are the classifications of inflammation?

A

Acute and Chronic

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6
Q

How would you classify acute inflammation? (3 options)

A

Sudden onset

Short duration

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7
Q

What can happen after an acute inflammation? (give 4 options and why they occur)

A

Resolution
Chronic inflammation (caused by persistent causal agent)
Suppuration (e.g. pus forming) form excessive exudate
Organisation and repair (from excessive necrosis)

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8
Q

How would you classify chronic inflammation? (4 options)

A

Slow onset (can occur after acute inflammation or on its own without acute)
Long duration
May never resolve

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9
Q

What are the inflammatory cells?

A 
Neutrophil polymorph
Macrophages
Lymphocytes
Endothelial cells
Fibroblasts
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10
Q

Describe Neutrophils

A

Short lived, first at scene of acute inflammation, phagocytose bacteria, die at scene of inflammation, release chemicals to attract other inflammatory cells

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11
Q

Describe Macrophages

A

Long lived (weeks to months), phagocytic properties, ingest bacteria and debris, carry debris away, if bacterial can’t be ingested they hold it inside them, present antigens of bacteria to lymphocytes

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12
Q

Describe lymphocytes

A

Long lived cells (years), produce chemicals to attract other inflammatory cells, immunological memory

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13
Q

Describe endothelial cells

A

Line capillaries, grow into areas of inflammation to form new vessels, become more porous to allow more inflammatory cells to leave vessel, become sticky to cause inflammatory cells to stay at site of inflammation and not flow past

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14
Q

Describe fibroblasts

A

long lived cells, form collagen to repair

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15
Q

Which cells are most prominent in acute vs chronic inflammation?

A

Acute- neutrophil

Chronic- macrophages and lymphocytes

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16
Q

List the causes of acute inflammation

A 
Microbial infections
hypersensitivity
physical agents e.g. trauma
chemicals
bacterial toxins
tissue necrosis
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17
Q

List the causes of chronic inflammation

A

Primary chronic inflammation
transplant rejection
progression from acute inflammation
recurrent episodes of acute inflammation

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18
Q

Describe the appearance of acute inflammation

A 
Redness,
heat,
swelling,
pain,
loss of function
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19
Q

Describe the macroscopic appearance of chronic inflammation

A 
Chronic ulcers,
chronic abscess cavity,
thickening of wall of hollow viscus
granulomatous inflammation
fibrosis
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20
Q

What is an autopsy?

A 
History/ scene
external examination
evisceration
internal examination
reconstruction
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21
Q

What are the types of autopsies?

A

Hospital and medico-legal

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22
Q

Describe hospital autopsy

A

occurs at the request of clinician to find out more about cause of death.
have to have consent from family and death certificate

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23
Q

Describe medico-legal autopsy

A

occur at request of persona of medical or legal background

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24
Q

What are the types of death

A

Presumed natural deaths
presumed iatrogenic deaths
Presumed unnatural deaths

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25
Q

Describe a presumed natural death

A

cause of death not known and/or deceased has not seen doctor in last illness or in last 2 weeks of life

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26
Q

describe a presumed iatrogenic death

A

postoperative, anaesthetic, abortion death, complication of therapy

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27
Q

Describe a presumed unnatural death

A

accidents, industrial deaths, suicide, unlawful killing, neglect, custody deaths, war/industrial pensioners’ death

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28
Q

Who make referrals?

A

doctors, registrar at BDM, relatives, police, other properly interested parties

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29
Q

Who performs autopsies?

A

doctors: histopathologists and forensic pathologists

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30
Q

what is the role of the coronal autopsy?

A

to find out who was deceased, when they died, where they died, how they came about their death.

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31
Q

What are the systemic effects of inflammation? (5 options)

A

Weight loss, fever, amyloidosis, constitutional symptoms e.g. anorexia, enlargement of lymph nodes

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32
Q

Describe the microscopic appearance of chronic inflammation

A

lots of macrophages and lymphocytes, almost no neutrophils, not a lot of exudate (fluid with proteins), lots of granulation tissue, tissue necrosis

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33
Q

What is a granulomatous inflammation?

A

type of chronic inflammation, a granuloma it is an aggregate of epithelioid histiocytes with sometimes other cells like lymphocytes

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34
Q

Describe epithelioid histiocytes

A

types of macrophages, little phagocytic activities

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35
Q

what can cause granulomatous inflammation

A

necrosis, histiocytes becoming giant cells. in-digestibility of matter by macrophages, beryllium drug traces

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36
Q

Describe healing of inflammation (5 things)

A 
regeneration of cells
angiogenesis starts
fibroblast proliferate
collagen synthesis
leads to granulation tissue (different from granuloma)
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37
Q

When does resolution happen?

A

if the initiating factor is removed

if the tissue is undamaged or can regenerate

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38
Q

what is angiogenesis?

A

new blood vessels forming

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39
Q

when does repair happen?

A

when the initiating factor is not removed

when the tissue is damaged and can’t regenerate

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40
Q

what is repair?

A

replacement of damaged tissue by fibrous tissue made of collagen.

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41
Q

what is regeneration?

A

process of replacing injured or dead cells.

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42
Q

which cells can regenerate? (6 options)

A 
hepatocytes
pneumocytes
all blood cells
gut epithelium
skin epithelium
osteocytes
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43
Q

which cells cannot regenerate? (2 options)

A

myocardial cells

neurons

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44
Q

what is 1st intention healing?

A

The incision has caused a gap between two surfaces of skin. If you keep the two surfaces together the gap will be filled by fibrin which over time is turned into collagen by fibroblasts. Squamous epithelium will cover the collagen.

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45
Q

what is 2nd intention healing?

A

The incision has created a gap between two surfaces of skin so large that the two surfaces cannot be brought together. Therefore, repair occurs from bottom up which leaves us with granulation tissue with lots of capillary loops.

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46
Q

why does the blood not always clot inside vessels?

A

Laminar flow

endothelial cells aren’t usually sticky

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47
Q

What is a thrombosis?

A

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

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48
Q

what three factors can lead to a thrombosis?

A

change in vessel wall, blood flow and/or blood constituents

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49
Q

what can occur to a thrombus? (4 things)

A

resolved by drugs, turn to scar tissue, re-canalised, embolise.

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50
Q

What is embolism?

A

the process of a solid mass in blood being carried through circulation to a place where it gets stuck and blocks a vessel

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51
Q

What is ischaemia?

A

reduction in blood flow

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52
Q

what is reperfusion injury?

A

blood given too quickly after ischaemia so lots of oxygen and lots of radical oxygen species that can kill cells.

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53
Q

what is an infarction?

A

reduction in blood flow that leads to cell death

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54
Q

what is a watershed area?

A

an area with two supplies of blood but both weak, there can be cell death here if there is a drop in blood pressure.

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55
Q

What is atheroma?

A

the condition characterised by the accumulation of lipid in the intima of arteries causing their lumen to narrow, their walls to weaken and predisposing them to thrombosis

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56
Q

what is atherosclerosis?

A

atheroma causes the hardening of the arteries i.e. when the atheroma forms a plaque

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57
Q

What is the atherosclerosis plaque made of?

A

fatty streaks, fibro-lipid plaques, lymphocytes

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58
Q

Why do atherosclerosis plaques occur?

A

endothelial damage theory

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59
Q

What are the risk factors for atherosclerosis? (4 things)

A

cigarette smoking
hypertension
poorly controlled diabetes
hyperlipidaemia

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60
Q

How do the risk factors relate to the Endothelial damage theory?

A

Cigarette smoke has nicotine, free radicals, CO which damage the endothelial cells
hypertension puts pressure on the cells
poorly controlled diabetes causes an increase in superoxide anions and glycosylation products which damage endothelial cells
hyperlipidaemia directly damages the endothelial cells

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61
Q

in what type of arteries do atherosclerosis plaques form?

A

large and middle arteries (with high pressure)

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62
Q

Describe the development of an atherosclerosis plaque in a young person compared to an old person

A

young person- fatty streaks
older person- plaques (asymptomatic until thrombus causes full blockage or until sudden event e.g. low blood pressure from bleeding)

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63
Q

Greater/ lower depravity = greater/lower cases of ischaemic heart disease= greater/lower cases of atherosclerosis plaque

A

Greater depravity = greater cases of ischaemic heart disease= greater cases of atherosclerosis plaque

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64
Q

what are the complications of atherosclerosis plaques? (6 things)

A 
cerebral infarction
carotid atheroma
myocardial infarction
aortic aneurysm
peripheral vascular disease
gangrene
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65
Q

What is apoptosis?

A

the physiological cellular process in which a programmed sequence of intracellular events leads to the death of a cell without the release of products harmful to surrounding cells. (programmed cell death)

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66
Q

how does apoptosis occur?

A

by activating non-lysosomal endogenous endonuclease which digest nuclear DNA into smaller DNA fragments. The death of scattered single cells which form membrane-bound bodies which are eventually phagocytosed by the surrounding cells including macrophages.

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67
Q

What can lead to apoptosis? (3 things)

A

DNA damage (detected by p53 protein)
ionising radiation
free radicals

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68
Q

What are caspases?

A

enzymes that carry out apoptosis

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69
Q

What enzyme will carry out apoptosis?

A

Caspase

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70
Q

what is necrosis?

A

traumatic dell death where large qualities of cells die unexpectedly i.e. not programmed

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71
Q

what are the characteristics of necrosis?

A

bioenergetics failure

loss of plasma membrane integrity

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72
Q

what can cause necrosis? (3)

A

ischaemia, metabolic problems, trauma

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73
Q

Give 4 examples of necrosis

A

frostbite necrosis
cerebral infarction
avascular necrosis of bone
caseous necrosis

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74
Q

what is caseous necrosis as strong indication of?

A

TB

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75
Q

What are chromosomal abnormalities?

A

missing, extra, irregular portion of chromosomal DNA.

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76
Q

Describe congenital defects

A

abnormalities present at birth, can be inherited or acquired

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77
Q

What causes an inherited abnormality?

A

caused by inherited genetic abnormality

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78
Q

what causes an acquired abnormality?

A

non-genetic environmental factors

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79
Q

What is hypertrophy?

A

increase in size of tissue caused by an increase in size of constituent cells, increase of cell size without cell division

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80
Q

to grow larger, what would a non-dividing cell do?

A

hypertrophy

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81
Q

what is ploidy?

A

increase in DNA content

82
Q

give two examples of hypertrophy

A

muscle hypertrophy in athletes where skeletal muscle of limb increase in size.
hypertrophy of arterial smooth muscles in arterial walls in hypertension

83
Q

what is hyperplasia?

A

Increase in size of tissue caused by increase in number of constituent cells, increase in cell number by mitosis without increase in cell size. decrease in cell loss by apoptosis is a component.

84
Q

give three examples of hyperplasia

A

bone marrow cell hyperplasia in people living in high altitude leads to increase in number of red blood cells
hyperplasia of breast tissue in puberty
endometrial of uterus hyperplasia due to too much oestrogen compared to progesterone

85
Q

can hyperplasia and hypertrophy occur together?

A

yes

86
Q

give an example of co-existence of hyperplasia and hypertrophy

A

enlargement of uterine smooth muscle in pregnancy

87
Q

what is atrophy?

A

decrease in size of tissue/organ/cell caused by decrease in number of constituent cells and/or decrease in cell size, not just a cessation of growth

88
Q

what causes atrophy generally?

A

decreased requirement of body for the function of a particular cell or organ

89
Q

what is used to cause atrophy to occur?

A

apoptosis

90
Q

give three examples of atrophy

A

atrophy of muscle in disused limb
tissue hypoxia leads to atrophy
in Alzheimer’s dementia there is brain atrophy

91
Q

what is metaplasia?

A

change in differentiation of a cell from one fully differentiated type to a different fully differentiated type

92
Q

why does metaplasia occur?

A

change in cellular environment, the new cells can better withstand the new environment

93
Q

what risk does metaplasia increase?

A

risk of cancer

94
Q

give two examples of metaplasia

A
  1. metaplasia in smoker’s bronchus from ciliated respiratory epithelial cells to non-ciliated squamous cells
  2. in vitamin A deficiency transitional and columnar epithelium are replaced by squamous epithelial cells
95
Q

what is dysplasia

A

morphological changes seen in cells in the progression to becoming cancerous

96
Q

what are the characteristics of dysplasia? (3)

A

increased cell proliferation
presence of atypical morphology
reduction in differentiation

97
Q

what can cause dysplasia?

A

chronic physical or chemical damage, if not removed then early dysplasia cannot be reversed

98
Q

What stops dividing cells from living forever?

A

telomeres limit number of divisions

99
Q

what are telomeres

A

found at the end of chromosome DNA and start replication, get shorter with every replication so limit number of divisions

100
Q

the length of the telomere is passed down genetically from mother or father?

A

father

101
Q

Whats stops non-dividing cells from living forever?

A

accumulation of damage (e.g. DNA damage, free radicals)

102
Q

what is dermal elastosis?

A

the accumulation of abnormal elastin in the skin

103
Q

how does dermal elastosis occur?

A

UV-B light strikes proteins in skin and causes them to cross link

104
Q

what is a cataract?

A

clouding of lens in the eye reducing vision

105
Q

what causes cataracts?

A

UV-B light striking proteins in eye causing them to cross link

106
Q

what is sarcopaenia?

A

loss of muscle

107
Q

Define carcinogenesis

A

transformation of normal cells to neoplastic cells via permanent genetic alterations or mutations

108
Q

What type of neoplasm does carcinogenesis refer to?

A

Malignant neoplasms

109
Q

What type of neoplasm does oncogenesis refer to?

A

Benign and malignant neoplasms

110
Q

How many steps is carcinogenesis?

A

multi step, minimum two mutations to same cell

111
Q

What are carcinogens?

A

agents known or suspected to cause neoplasms, to cause carcinogenesis.

112
Q

What type of of neoplasms do carcinogens cause?

A

malignant

113
Q

what type of agent causes any neoplasm?

A

oncogenic agent

114
Q

what do carcinogens act on to cause carcinogenesis?

A

DNA, they are mutagenic

115
Q

x% of cancer are due to environment and y% is inheritance

A 
x= 85
y= 15
116
Q

why is it difficult to identify carcinogens?

A

long latent interval
complex environment
ethical issues of testing directly on humans

117
Q

how can we identify carcinogens through experiments? (4)

A
  1. tests on mice, bacteria, cells
  2. epidemiological evidence
  3. occupational risk factors
  4. direct evidence from accidents
118
Q

how many classes of carcinogens are there? List them.

A

5

chemical, viral, radiation, biological agents, miscellaneous

119
Q

do chemical carcinogens act directly or indirectly?

A

Both!
Directly (doesn’t matter where contact is, will cause mutation)
Indirectly (procarcinogens need to be activated into ultimate carcinogens)

120
Q

How does the type of enzyme affect where a cancer occurs in relation to a chemical carcinogen

A

pro-carcinogens need an enzyme to activate them to ultimate carcinogens. If the enzyme is universal then mutation will occur at contact, but if enzyme is in a specific organ, mutation will occur at organ

121
Q

give four examples of chemical carcinogens and what cancer they cause

A
  1. polycyclic aromatic hydrocarbons in tar cause skin cancer and if absorbed lung cancer
  2. aromatic amines cause bladder cancer
  3. nitrosamines cause gut cancer
  4. alkylating agents cause leukaemia (small risk)
122
Q

give two examples of viral carcinogens and what cancer they cause

A
  1. human papillomavirus causes cervical cancer

2. Hep B and C cause hepatocellular cancer

123
Q

Give four examples of how radiation can cause cancer

A
  1. UVA and UVB lead to skin cancer (basal cell carcinoma, squamous cell carcinoma, melanoma)
  2. radiographers - skin cancer
  3. uranium miners - lung cancer
  4. Ukrainian children - thyroid cancer
124
Q

give the four types of biological carcinogens

A

hormones
mycotoxins (from fungi)
parasites
bacteria

125
Q

Give two examples of hormone carcinogens and the cancer they cause

A
  1. oestrogen increase leads to mammary or endometrial cancer

2. anabolic steroid increase leads to hepatocellular carcinoma

126
Q

give an examples of a mycotoxin carcinoma

A

aflatoxin b1 causing hepatocellular carcinoma

127
Q

give two examples of parasites that cause cancer

A
  1. chlonorchis sinensis causing cholangiocarcinoma

2. shistosoma causing bladder cancer

128
Q

Give an example of a bacterial infection that can cause cancer

A

helicobacter pylori that can cause gastric lymphomas

129
Q

What do we mean by miscellaneous carcinogens?

A

those that we don’t understand their method of action

130
Q

give two examples of miscellaneous carcinogens

A
  1. asbestos - lung and pleura cancer

2. nickel- cancer of mucosal lining of nose and lungs

131
Q

What host factors can increase risk of cancer (5)

A

race, diet, constitutional, premalignant lesions, trans-placental exposure

132
Q

give two examples of a race host factor that could affect risk of cancer

A
  1. black people have more melanin so protected against skin cancer
  2. SE asia and India they do reverse smoking so more oral cancer
133
Q

why do dietary factors affect carcinogenesis?

A

may have a lot of carcinogens
may lack protective factors
may affect intestinal transit time

134
Q

what are the three constitutional factors that affect risk of cancer and give some examples

A
  1. inherited predisposition (BRCA1 and BRCA2 on chromosome 17 and 13 increase risk of breast cancer)
  2. age (increase age more cancer)
  3. gender (female increase risk of breast cancer)
135
Q

what are premalignant lesions?

A

identifiable abnormalities that are associated with increased risk of cancer at that site

136
Q

give four examples of premalignant lesions

A

cervical dysplasia
colonic polyps
ulcerative colitis
un-descended testis

137
Q

what is trans-placental exposure?

A

carcinogen give to mother but affect seen in fetus when it becomes baby/child/adult

138
Q

give an example of a trans-placental exposure

A

diethylstiboestrol to mother increases risk of child having vaginal adenocarcinoma

139
Q

What is a lesion?

A

A local abnormality

140
Q

Define a neoplasm

A

a lesion resulting from autonomous abnormal growth of cells which persists after the initiating stimulus has been removed. it is a new growth.

141
Q

Define a tumour

A

any abnormal swelling

142
Q

Give 4 examples of tumours

A

neoplasm, inflammation, hypertrophy, hyperplasia

143
Q

What is a neoplasm made off?

A

Neoplastic cells

stroma

144
Q

What type of cells are neoplastic cells derived from?

A

nucleated cells

145
Q

describe the growth pattern and synthetic activity of a neoplastic cell

A

the growth pattern will to a variable extent relate to the parent cell. the synthetic activity will also to a variable extent related to that of the parent cell.

146
Q

What is the stroma?

A

a connective tissue framework that the neoplastic cells are embedded in. Mechanical and nutritional support is offered by the stroma

147
Q

How does a stroma form?

A

desmoplastic reaction: the induction of connective tissue proliferation by growth factors in immediate tumour environment

148
Q

what does the stroma contain?

A

blood vessels, fibroblasts, myofibroblasts, lymphocytes

149
Q

How will a carcinoma in situ first appear?

A

single neoplastic cell will appear, cell grows faster than healthy cells so takes over the area. remains surrounded by basement membrane

150
Q

What is a carcinoma in situ?

A

a carcinoma, a neoplasm that is surrounded by basement membrane i.e. the basement membrane has not been breached

151
Q

What can happen to a carcinoma in situ?

A

completely removed surgically or destroyed by body
stays there for long time
turns into micro-invasive carcinoma

152
Q

What is invasion?

A

if the carcinoma breaches the basement membrane

153
Q

How (and what does it need) does a neoplasm invade past the basement membrane?

A

digest basement membrane (needs metalloproteinases)
un-attaches from other cells (loss of surface adhesion)
move past basement membrane (needs more cellular motility)

154
Q

what is the difference between a micro-invasive carcinoma and an invasive carcinoma?

A

micro-invasive: the length of the total cells that have left the basement membrane is less than 1mm
invasive: more than 1mm, need angiogenesis

155
Q

What is metastasis?

A

process where malignant neoplasm spreads from site of origin to form other tumours at distant site.

156
Q

what does carcinomatosis mean?

A

extensive metastatic disease

157
Q

describe the steps of metastasis (7)

A 
detachment
invasion
intravasion
evasion
arrest
extravasation
growth
158
Q

describe intravasion

A

neoplastic cells enter vessel lumen by using metalloproteinases and motility.

159
Q

Describe evasion

A

neoplastic cells evade host’s defences by
aggregation with platelets
shedding surface antigens
adhesion to other tumour cells

160
Q

describe arrest

A

neoplasm arrest their movement by adhering to endothelium of vessel at remove location

161
Q

describe extravasion

A

neoplastic cells leave vessel lumen and enter surrounding tissues, cell motility and metalloproteinases are used

162
Q

what are the routes of metastasis? (4)

A

haematogenous (blood stream)
lymphatics
transcoelomic (into pleura, pericardia, peritoneal cavities)
implantation routes (surgical accident spilling neoplastic cells)

163
Q

what methods of classification do we use to classify neoplasms?

A

behavioural and histogenetic

164
Q

What are the options for behavioural classification?

A

benign, borderline, malignant (spectrum)

165
Q

Describe benign neoplasms (5)

A 
localised
non-invasive
clear borders
slow growth rate
resemble normal tissue with nuclear morphometry
166
Q

which type of tumour would you see a lot of necrosis and ulceration?

A

malignant NOT benign

167
Q

which type of tumour grows in an exophytic manner on mucosal surfaces?

A

benign

168
Q

how do benign and malignant differ in the way they grow on mucous surfaces?

A

malignant: endophytic
benign: exophytic

169
Q

how do benign neoplasms cause morbidity and mortality? (5)

A 
pressure on adjacent structures
block of flow
production of hormones
transform into malignant tumours
anxiety
170
Q

give an example of a borderline tumour

A

some ovarian lesion

171
Q

describe malignant tumours (5)

A 
invasive
irregular border
can metastasise
rapid growth rate-increase mitosis
variable resemblance to normal tissue
nucleus hyperchromatic and pleomorphic
172
Q

how can malignant neoplasms cause morbidity and mortality? (7)

A 
destruction of adjacent tissues
metastasis
blood loss from ulcers
obstruction of flow
hormone production
anxiety and pain
paraneoplastic effects
173
Q

what does histogenetic classification refer to?

A

the cell of origin of the neoplasm

174
Q

what can we learn from histogenesis?

A

degree of resemblance to original cell allows grading of tumour (good resemblance low grade so good prognosis)

175
Q

what is the suffix of an epithelial non-glandular neoplasm benign?

A

papilloma

176
Q

what is the suffix of an epithelial non-glandular neoplasm malignant?

A

carcinoma

177
Q

what is the suffix of an epithelial glandular neoplasm benign?

A

adenoma

178
Q

what is the suffix of an epithelial glandular neoplasm malignant?

A

adenocarcinoma

179
Q

what is the suffix for a benign adipocyte neoplasm?

A

lipoma

180
Q

what is the suffix for a malignant adipocyte neoplasm?

A

liposarcoma

181
Q

what is the suffix for a benign cartilage neoplasm?

A

chondroma

182
Q

what is the suffix for a malignant cartilage neoplasm?

A

chondrosarcoma

183
Q

what is the suffix for a benign bone neoplasm?

A

osteoma

184
Q

what is the suffix for a malignant bone neoplasm?

A

osteosarcoma

185
Q

what is the suffix for a benign vascular neoplasm?

A

angioma

186
Q

what is the suffix for a malignant vascular neoplasm?

A

angiosarcoma

187
Q

what is the suffix for a benign nerve neoplasm?

A

neuoma

188
Q

what is the suffix for a benign straited muscle neoplasm?

A

rhabdomyoma

189
Q

what is the suffix for a malignant straited muscle neoplasm?

A

rhabdomyosarcoma

190
Q

what is the suffix for a benign smooth muscle neoplasm?

A

leiomyoma

191
Q

what is the suffix for a malignant smooth muscle neoplasm?

A

leiomyosarcoma

192
Q

how do you describe a tumour of unknown cell type?

A

anaplastic

193
Q

EXCEPTIONS: give 3 tumours that end with “oma” but are not neoplasms

A

granuloma
mycetoma
tuberculoma

194
Q

EXCEPTIONS: give 3 malignant tumours that don’t end with sarcoma or carcinoma

A

melanoma
mesothelioma
lymphoma

195
Q

EXCEPTIONS: give 4 neoplasms that are named after a person

A

burkitt’s lymphoma
ewings’s sarcoma (osteosarcoma)
grawitz tumour (renal cell carcinoma)
kaposi sarcoma (angiosarcoma)

196
Q

EXCEPTIONS: give 4 examples of miscellaneous tumours

A

teratoma
embryonal tumour (blastoma)
mixed tumour
APUDomas

197
Q

what is grade 0 in duke’s staging of cancer?

A

carcinoma in situ

198
Q

what is grade 1 in duke’s staging of cancer and what is the survival rate?

A 
no nodal involvment (N0)
no metastases (M0)
tumour invades submucosa (T1)
tumour invades muscularis propria (T2)
90-100%
199
Q

what is grade 2 in duke’s staging of cancer and what is the survival rate?

A

N0, M0
tumour invades subserosa (T3)
tumour invades other organs (T4)
75-85%

200
Q

what is grade 3 in duke’s staging of cancer and what is the survival rate?

A

M0, any T
regional lymph nodes involved (N1)
30-40%

201
Q

what is grade 4 in duke’s staging of cancer and what is the survival rate?

A

distant metastases (M1)
any N and any T
less than 5%

Phase 2a Introductory Clinical Science (7 decks)

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