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Phase 2a > ICS - Pathology > Flashcards

ICS - Pathology Flashcards

1
Q

Define inflamation

A

a local physiological response to tissue injury

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2
Q

give a benefit and negative of inflamation

A

+destroys microorganisms, can stop teh spread of infection
-it can produce disease and leade to distorted tissues

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3
Q

define exudate

A

a protien rich fluid tha leaks out of vessel walls

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4
Q

what do neutrophils do

A

phagocytose debris and bacteria, they contain enzymose in lysosomes. they are the first to arrive at the sight of infection

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5
Q

what do fibroblasts do

A

produce connective tissue

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6
Q

how long do macrophages, lymphocytes and then neuropills live for

A

Macrophages - montsh to years
neurotphils - 2-3 days
lymphocytes - years

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7
Q

what do macrophages do

A

phagocytosis, and transport material to teh lymph nodes and cause a secondary immune reaction

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8
Q

what are three specalised macrophages

A

kuppffer cells in liver
osteoclasts in bone
microglial in breain

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9
Q

what are lymphocytes

A

produce chemicals whihc crontrol inflamaion and antibodies, they also have memory cells

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10
Q

what is the sequance of inflamation

A

injury/infection
neutrophills arrive and phagocytose
macrophages arrive and phagocytose
resolution or progression to chronic

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11
Q

what are examples of acute (neutrophil mediated) inflamation

A

microbial infections - bactera and viruses
hypersensitivity reactions parasites
physical agents - trauma, heat, cold (frostbite)
chemicals - corrosives and acids
bacterail toxis
tissue necrosis - ischemic

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12
Q

what is a granuloma

A

are collections of macrophges surronded by lymphocytes seen in chronic inflamation

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13
Q

when can granulomas be found

A

myobacterial infection like TB or leprosy

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14
Q

how does chronic inflamation work

A

few neutrophils, macrophagesm lymphocytes and then fibroblasts, often scar tissue formed

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15
Q

what is resolution

A

everything goinf back to normal and te tissue fully regenerating

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16
Q

what is repair

A

the initiating factor is still present and teh tissue cant regenerate, it is teh repplacement of damaged tissues by fiberous tissues

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17
Q

what is fibrosis

A

teh thickening and scarring of tissues

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18
Q

name 5 cells that regenerate

A

hepatocytes, pneumocytes, blood cells, gut epithelium, skin epithelium, osteocytes

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19
Q

what are teh two types of autopsy

A

hospitlal - medical certification and used for teaching and research
medicolegal - 90% of autopsies, sorted into coronial and fronnsic. conronical means death is not due to unlawful action

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20
Q

what is teh role of the coronial autopsy

A

who dies, when, where, how did their deat come about

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21
Q

when are 3 times deaths reffered to the coroner

A

natureal - its uncertain how they dies and they havent seen a doctor within 14 days
iantrogenic - caused by medical miustreatent such as illigal abortions and anastheic deaths
unatural - accidents, industrial deaths, suicide, murder

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22
Q

who refeerres to teh coroner

A

doctors, registrar of birth and death, poilce, relatives

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23
Q

who perfoerms autopsies?

A

histophalologists - hospital, coronial, natural deaths and accidents
forensic pathologists - homicide and neglect

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24
Q

what are the three main stages of autopsy

A

external, evisceration (y shaped inscision t exaine organs and brain) internal examination (heart and vessles, lungs, liver spleen, CNS<, endocrine)

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25
Q

what is _acute_inflamation

A

the initial and transient tissue reaction to injury

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26
Q

what are the 3 steps of inflamation

A

vascular - dialation of vessles
exudative component - vascular leakage
neutrophil polymorph - neutrophills are recruited

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27
Q

what are the 4 outcomes of inflamation

A

resolution - all heals like normal
suppuration - pus formation in a pyogenic membrane and an abcess
organisation - fibrosis, dead tissues removed, granulation tissues is formed in the space, then this fibrosis
preogression - causative agent isnt removed and chronic inflamation starts

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28
Q

what are the 5 main signs of inflamation

A

redness - rubour
swelling - tumours
heat - calor
pain - dolor
loss of function

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29
Q

what factors increase vascular permeability

A

histamine, bradykinine, NO, platelet activating factor

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30
Q

what are the stages of neutrophil emigration

A

margination - they move to the side of teh vessels due to the slowing of flow
adhesion - they begin to stick to the sides, this is called pavementting
emigtation - move out og teh wall of venules and viens
diapedesis - some red blood cells may also leak out which indicates significant injury

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31
Q

what are chemical mediators involved in inflamation

A

histamine is released fro mast cells and up regulaes teh inflamation
lysosomal compounds
seratonin
chemokine

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32
Q

6 causes of chronic inflamation

A
  • resistance of infecive agens - TB leprosy
  • endogenous materals - necrotic tissues
    exogenous materials - asbestos, silica
    autoimmune conditions - rhumatoid arthiritus
    primary granulation diseases - chrons
    transplant rejection
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33
Q

which cells are involved in chronic inflamation

A

lymphocytesm macrophagesm plasma cells

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34
Q

macrospcpic features of chronic inflamation

A

ulcer, abcess cavity, granulomatous inflamation, fibeosis

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35
Q

microscopic appearance of chronic inflamation

A

tissue necrossis, lymphocyes, plasma cells and macrophages, continuing destruction

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36
Q

whhat are the cellular components of chronic inflamation

A

b lymphocytes - turn into plasma cells and produce antibodies
t lymphocytes - cell mediated immunity
macrophages - respond to chemotactic stimuli

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37
Q

what is a granuloma

A

an aggragate of epithelioid histocytes,

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38
Q

when do granulomas develop

A

tb, leprosy, chrons, TB, Sarcoidossi

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39
Q

how would you look for a TB stain

A

ziehl-neeleson stain

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40
Q

what indicates a parasite

A

granuloma and eosinophil

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41
Q

define laminar flow

A

cells travelling in the middle and not touching the sides

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42
Q

defien thrombus

A

solid mass of blood consituents formed within intact vascular systems during life

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43
Q

define embolus

A

a mass of material in the vascular system which lodges in the vessel and block it - this can be a thrombus whihc has broken off

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44
Q

define ischemia

A

reduction in blood flow to a tissue

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45
Q

define infarction

A

a reduction of blood flow leading to cell death

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46
Q

what two factors prevent blood clots

A

laminar flow, endothelial cells releaseing chemicals

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47
Q

what are the most commen factors of thrmbosis and what do these make up

A

reduced blood flow, blood vessle injury, increased coaguility
thsi is called virchows traingle

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48
Q

what are 4 causes of embolism

A

thrombus, air, cholesterol, tumous, fat

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49
Q

what is it called when an organ is ony supplied by one vlood supply

A

end artery supply

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50
Q

what are platelets

A

no nucleus, they come from megacaryocytes, they are activated when they ome into contact with collagen

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51
Q

what are teh two granules in plateletS

A

ALPHA - platelet adhesion
dense - platele aggragation

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52
Q

how does a theombus plaque from athelosclarosis

A

a plaque causes a chnage in teh vessle wall
this creates turbulance
fibrin and platelets accumulate and start clumping
thsi causes more turbulance and causes positive feedback

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53
Q

what is venous thrombosis

A

low blood pressure causes the blood to sit
thrombi begins at valves, produces a turbulance
whne blood pressure falls, the flow through the vwins slows

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54
Q

what are clinical theatures of venous, then arteral thrimbus

A

arterial - loss of pulse distally, area is cold, possible gangrene
venous - tender, area is red and swollen

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55
Q

what are teh 4 fates if a thromvus

A

resolution
organised - becies a scar causing a slight narrowing of teh vessel
recanalisation - intimal cells proliferate and capilleries grow into teh thrombus and fuse to make larger vessles
embolis - parts break off and lodegg elsewhere

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56
Q

arterial thrombus: causes, pressure, risks, constituents, treatments

A

atheroma
high oressure
MI and stroke
platelets
Tx - anti platelets such as asprin

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57
Q

venous thrombus: causes, pressure, risks, constituents, treatments

A

stasis
low pressure
DVT/PE
red blood cells
anticoagulents such as warfrin

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58
Q

what are the three main arterial embolisms and where can they travel

A

arterial - anywhere down stream
mural (from inside left ventricle) - anywhere
cholesteril crystals - in teh descending aorta can go to lower limbs or renal arterys

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59
Q

which three organs have multiple blood supplys are are less susptable to ischemia

A

liver brain, lungs

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60
Q

what is a reperfusion injury

A

damage to tissue dutring re oxeygenation, due to build up of wast materials it can flood bakc in

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61
Q

what is atherleroscarosis

A

accuulation of fibrolipid plaques in systemic arrteries

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62
Q

what diseases are characterized by atherlosclarosis

A

MI, aortic anyerisms, gangrene, carotid atheroma, peripheral vascular disease

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63
Q

how do altehrosclarosis form

A

endotherlial disfunction
hight levels of LDL accumulate
macrophages surround it
formation of fatty streak
realse of cytokines
smooth muscle proliferation around lipid core

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64
Q

risk factors of atherlosclarosis

A

smoking
hypertension
diabetoes
male
increased age

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65
Q

define apoptosis

A

programmed cell death, happnes in single cells and prevemts cells with damage from dividing

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66
Q

how does a cell decide to apoptose

A

DNA damage within the cell, p35 is a protien whihc can detect DNA changes and trigger i

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67
Q

how does a cell apoptose

A

triggers a series of protiens whihc lead to enzyme release which autodigests teh cell

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68
Q

what enzymes are used in apoptosis

A

caspases, they work in a cascade

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69
Q

what are two reasons why cells may apoptose in health

A

deelopment - removal if cells during groth and development
cell turnover - removal of cells during normal turnover for example teh top layer of skin being shawn off o teh cells at teh topi of villu being replaces

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70
Q

apoptosisin disease 2 examples

A

cancer - cells with damaged DNA
HIV - causes apoptosis of CD4 helper cells

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71
Q

define necrosis

A

wholesale destruction of large numbers of cells by some external factor

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72
Q

give examples of clincal necrosis

A

infacrciton due to loss of blood supply,
frostbite
venom and toxis
pancreatisis

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73
Q

what is caseous necrosis

A

like soft cheese, due to tuberculosis

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74
Q

what factors regulate apoptosis (inducers and inhibitors)

A

inhibitors:
growth factor
extracellualr matrix
sex steriods
INDUCERS:
glucocortacoids
free radicals
ionising radiation
DNA damage

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75
Q

what is the intrinsic pathway for apoptosis

A

pro and anti apoptopic of bic -2
bax form bax-bax dimers whihc enchance stimuli
responds to growth factos and biochemical stress
p53 gene incuces cell cycles arrent and intitaes DNA repair or apoptoais

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76
Q

what is teh extrinsic pathway fo apoptosis

A

ligand binding death receptors are on the cell surface
FAS ligand binding receptors result in teh clustering of receptor molecuels onteh cell surface
caspes are activated triggereing teh process
teh pathway is used by teh immune system to eleiminate lymphocytes

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77
Q

what are eh 4 types of necrosis

A

coagulative - caused by ischemia
liquefactive - occurs in brain due to lack of soma
caseous - cheese cause by TB
gangrene - necrosis with rotting of eh tissue - smells bad eh

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78
Q

what is hypertrophy

A

increased cell size witout division

79
Q

what is hyperplasia

A

increased cell number by mitosis

80
Q

what is atrophy

A

decrease in the size of an organ or cell be reduction in number or size of cell

81
Q

what is metaplasia

A

teh change in differentiation from one cell type to another

82
Q

give an example of metplasia

A

barretts eosophogus

83
Q

what is dysplasia

A

morphological changes seen in cells in eyh progression to becoming cancer

84
Q

what is carciogenesis

A

the transformaiton of cells into neoplastci cells though permenant genetic alteraltions

85
Q

what is a neoplasm

A

a lesion resulting frm the automomous of relitavly automonous abnormal cell growth

86
Q

define tumour

A

any abnormal cell growth

87
Q

name 5 carciogens

A

HPV
UV
Smoking
asbestos
b- naphthylamine from dies (bladder cancer)

88
Q

what is teh role of macrophages in accute inflamation

A

secrete chemical mediators
cytokines interluikin 1 and tumour necrossi factor alpha
these attract neutophil polymorpjs
thye clear away teh dead cells and tissues

89
Q

role of teh lymphatic in acute inflamation

A

terminal lymphatics are blind-ended
they help drain away eh odema of teh inflamitory exudate
antigens are carried in teh lymph syestems to the lymphocytes

90
Q

how does adhesion to teh microorganisms work

A

opsonisation by either imunoglobbulin or complemetn components

91
Q

what is spinla bifida occulta

A

there is no back process of teh vertebreal body

92
Q

what s a systolic murmur

A

when teh foramen ovale doesnt close up and blood leale through

93
Q

what genes code for parts of teh body

A

homeobox gnes - they account for teh migration of cells

94
Q

what is an example of enviromental condenital birth defects

A

cleft foot - bent feet

95
Q

what are three risks of down syndroe

A

early cataracts, early altziemers, heart problems

96
Q

what is autosomal inheritance

A

all inheritance of paired chrmoseomes of tehsame size (just excludes sex chromosomes)

97
Q

what is co dominant alleles

A

where two are dominatn, such as a b blood grouops

98
Q

what are three sypmtomsof fetal alcohol syndrome

A

small eye opsnings, smooth philestrum, thin upper lip

99
Q

what bones can grow after pubity

A

hands, feet and jaw

100
Q

what is mixed hypertrophy and hyperplasia

A

increase in teh size of teh organ due to increase in number and size of cells

101
Q

what is teh limit of human cell division called

A

the hayflick limit

102
Q

why is there a limit on the number of times cells can divide

A

the telomere get shorter each time

103
Q

what is progeria

A

where ageing is accelerates due to mutations in cell membranes

104
Q

what are factors that will lead to cell apoptosis

A

cross linking of protines, loss of calcium ion controll, telomere shorteing, free radicla generation , loss of DNS repait mechanism

105
Q

what is eh one way show to slow down aging

A

calorie restriction

106
Q

what are 6 effects if aging on teh body

A

skin - wrinliking caused by collagen cross links caused by UV
eyes- protien cross links in the lens caused by UV
osteoporosis - lack of oestrogen in women
dementia - atherlosclarosis and genetics, not being obese
sarcopeia ( loss of muscle ) reduced growth hormone and testosterone
deafness - heor cells dont divide and are damaged by loud noises

107
Q

are basal cell carcinomas invasive?

A

it only invades locally and doesnt spread

108
Q

how do you treat a basal cell carcinoma

A

cut it out

109
Q

wha are the nearset lymph nodes to teh breast?

A

teh axillery

110
Q

what are the 5 cancers that most commenly spread to bone

A

breaast, prostate, lung, thyroid kidney

111
Q

what is adjuvant therapy

A

treatment given alongside surgical exciscion

112
Q

what is the name of the main cell in inflamation

A

neutrohil polymorphs

113
Q

what is teh name of ye cells tthat produce collagen in scarring

A

fibroblasts

114
Q

what is an example of accute inflamation

A

appendicitus

115
Q

where is an example of where granulomas will form

A

chrons disease

116
Q

what is an example of hyperplasia

A

benign prostate enlargement

117
Q

what is an example of a chronic inflamation at the start

A

infection mononucleousus

118
Q

what is an example of necrosis

A

renal infaon

119
Q

what is an example of necrosis

A

renal infaon

120
Q

what is the process of a solid ass formed by blood constituents called

A

thrombosis

121
Q

is a drug what is a drug whihc inhbits platelet aggragation

A

asprin

122
Q

what is teh pattern of differntiation of metaplasmic cells lining the bronchi of ciggy smokers

A

cilliated - squamous

123
Q

what are carcinogens

A

cancer causing agents

124
Q

what does oncogenic mean

A

tumour causing

125
Q

what % of cancer risk is enviromental

A

85%

126
Q

what is an occupation risk and an example

A

a risk for cancer that comes from your work, such as bladder cancer from analine dye and rubber, this is caused by the beta-naphthylamine

127
Q

give tw examples of chemical carcinogens

A

polycyclic aromatic hydrocarbons - lung cancer
aromatic amines - bladder cancer - rubber/dye workers

128
Q

what are the 5 classes of carciogens

A

chemical
viral
inoising and non ionising
hormonaes, parasites and mycotoxins
miscalaneous

129
Q

what percentage of all cancers do viral carcinogens caus

A

10-15%

130
Q

give two examples of DNA viruses that are carcinogens

A

Hep B, epstien barr virus

131
Q

give two examples of RNA viiruses

A

Hep c, human t lymphotrophic virus

132
Q

what is an example of radating carconoma

A

UVA and UVB radiation

133
Q

what are two examples of biologica agents

A

hormons - oestrogen causeing breast and endometrial
Chlonorchis sinensis → cholangiocarcinoma
Shistosoma → bladder cancer

134
Q

what are two miscalaneous causes of cancer

A

asbestos and metals such as arsnic

135
Q

what are host factors

A

factors of the person whihc can increase or decrease teh risk of developing cancer

136
Q

what are 5 host factors of cancer

A

ethnicity, diet, age and gender, transplacental exposure

137
Q

what is a premalignant condition?

A

identifiable local abnormality associated with increased risk of malignancy at that sight

138
Q

what are some examples of pre malignent conditions

A

colonic polyps, cervial dysplpasia, ulcerative colitis, undescended testes

139
Q

what is carciogenesis

A

the transformation of normal cells into neoplasmic cells through permenant genetic alteraltion or mustations

140
Q

what is teh defornition of a tumour

A

any abnormal swelling

141
Q

what are the behavioura lclassificationsn of benign tumours

A

dont invade basement membrane,
exophyic (grows out)
low mitotic activity
circumcised
necrosis and ulceration rare

142
Q

whaat are behavioral classification of malignant tumours

A

invade basement membrane, endophytic (grows inwards), highly mitotic, poorly circumcised, necorsis and ulceration commen

143
Q

what is teh histogenetic classification of tumours

A

based on specific cell origin of the tumour

144
Q

what are three histogenetic classification of tumours

A

epithelial cell - carcinomas
connective tissues - sarcomas
lymphoid - lymphomas or leukemia

145
Q

what is the histologiacal grading of tumours

A

grade based on te hextent to which teh tumour resembles its original
histology
there are three grades -
1 - well differentiated to be like normal tissue
2 - moderatly differentialted
3 - poorly differentiated (this is teh worst one)

146
Q

define metastasis

A

teh process where malignant tuours spread to from tuours at other sights

147
Q

what is a cancer that nerver metastasises

A

basal cell carcinoma

148
Q

what is teh process of metastasis

A

Detachment of tumour cells from their neighbours
Invasion of the surrounding connective tissue to reach conduits of metastasis
Intravasation into the lumen of vessels
Evasion of host defence mechanisms, such as NK cells
Adherence to endothelium at a remote location
Extravasation of the cells from the vessel lumen into the surrounding tissue
Tumour cells proliferate in the new environment

149
Q

what are he routes of metastasis

A

Bone metastasises from lung, breast, kidney, thyroid, prostate
Lymphatic metastasis is common (secondary tumours in lymph nodes)
Carcinomas prefer lymphatic spread

150
Q

what does TNM staging stand for

A

t - priamry tumour
n - lymphatic node status
m - metastatic status

151
Q

what do cacers need to invade teh basement bembrane

A

enzymes such as collegenase, thepsin D

151
Q

what has to happen to a tumour after its bigger than 1 mm

A

it ha sto form its own blood supply

152
Q

how do cancer cells evade host immune defense

A

aggregation with platelets
shedding of surface antigens
adhesion to other tumour cells

153
Q

what is angiogenesis

A

the productino of new blood vessles

154
Q

what cancers most commently metastasise to lung

A

sarcomas and any other commen cancers as they travel move int teh venous system and get loged in teh lung whihc is teh next small capiller system thye g though

155
Q

where is cholerectal cancer most likely to spread to

A

the liver as it drains though teh hepatic portalvein

156
Q

what cancers most commenly spread to the liver

A

colon , stomach, pancreass

157
Q

what does a neoplasm release in order to initaitae angiogenesis

A

vascular endothelial growth factors

158
Q

whta is teh prescens og granulomas and eosinophils indicatibve of

A

parasitic infection such as worms

159
Q

what is teh difference between a thrombois and a clot

A

clot - coagulated outside g teh vascular system
thrombosis - solidification of blood constituents within teh vascual system

160
Q

what are two reasons thrombuses dont form at all times

A

laminar flow - cells trave in eh middle and dont touch teh sides
endothelial cells
endothlial cells - arent sticky when healthy

161
Q

what is a neoplasia

A

a lesion resulting from teh autonomus or relitavly autonomus abnormal groth of cells whihc persists after teh inititing stimulus has been removed
it means a new growth in greek

162
Q

what are teh two constituent parts of a neoplasm

A

neoplasmic cells - deived of nucluated cells and growth patter related to parent cell
stroma - the connective tissue framework whihc provides mechanical support and nutrition

163
Q

why shold you classify neoplasms

A

to determine apropriate treatment
to provide prognostic information

164
Q

what are teh two methods of classification

A

behavioural - benign/malignant
histogenic - cell of origin

165
Q

what are teh problems with benign neoplasma

A

pressure on structure, obstruct flow, release hormones, transform into malignant, patient anxietys

166
Q

A transitional cell carcinoma of the bladder is a malignant tumour true or false?

A

true - and carcinoma is malignant

167
Q

Which tumour has the shortest median survival?

A

Anaplastic carcinoma of the thyroid

168
Q

what does the term adenoma mean

A

benign tumour of teh glandular or secretory epithelium

169
Q

what is an angioma

A

vascular neoplasm

170
Q

ehat is teh diffecne between wet and dry gangrene

A

dry - teh tissue is mumified around it and it is kind of isolated and falls off
wet - bacterial and it speads (worse)

171
Q

what are teh nomenclature rules about namng tumours

A

-oma is benign for example lipoma
-sarcoma is malignant connective tissue for example liposarcoma
-carcenoma is malignnt epithlium tissue, basal cell carcinoma,

172
Q

what are the exceptions to teh naming of tumours

A
  • not all omas are neoplasms: granuloma is chrominc inflamation, mycetoma is fungus in teh bofy and tuberculoma is a mass of TB
    -Not all malignant sumours are carcinomas or sarcomas: melanoma, mesotheioma, lymphoma
    -teratoma - neoplasm of germ cells whihc has all three germ layers of the embryo
173
Q

what are the stages of neutropills entering the tissues in inflamation

A

margination - migrate to teh edges (margins)
adhesion - selectins bind to teh neutrophills and cause rolling
emigration and diapedesis - they move through teh gaps into tissue
chemotaxis - move to teh sight of inflamation by being called by chemokines

174
Q

defien granuloma

A

aggragtes of epitheioid histocytes (macrophages)

form a horseshoe shape

175
Q

what do granulomas secrete and hat does this mean

A

ACE - its a blood marker, increased levels inficate granulomatas disease

176
Q

what are three histologially distuinguishable types of granuloma

A

central necrosis (caseating, it looks loke cottage cheese) - means its TB

NO nectosis - sarcoidosis, leprosy, vasculitis, chronns

granuloma and eosinophil indicate a parasite

177
Q

causes, constituents an tratments for venous, and arterial throbi

A

venous - venous stasis, RBC and fibrin, anticoagulents (warfrin)

arterial - arthrogenesis, platelets and fibrin, antiplatelets (warfrin)

178
Q

what are teh symptoms of a venous thrombi and an example

A

tender, swollen red,

deep vein thrombosis

179
Q

what are teh symptoms of an arterial thrombi and an example

A

cold, pale, loss of pulse

MI, Strokem peripheral vascular disease

180
Q

what is teh defornitino for apoptosis

A

non inflairoy controlled cell death

teh cells shrink, teh organelles are retained and its fragmented for a macrophge to phagosytose

181
Q

what are the three mehcanisms of apoptosis

A
  • Intrinsic- Bax acts on mitochondial membrane to produce cytrochrome c release
    • Extrinsic - Fas Ligend or TNF-ligand beind to receptos and acivates caspase enzymes
    • Cytotoxic T cells - CD8 injext perforin which breaks down te hcell membrane

they all lead to caspases being released

182
Q

define hypertrophy and hyperplasia

A

hypertrophy - cell gets bigger
hyperplasia - number of cell increases because of mitosis

183
Q

define atrophy and etaplasia

A

atrophy - number of cells or size of cells decreases
metaplasia- one cell types changes into another cell type (barretts oesophogus)

184
Q

define dysplasia

A

growth of abnormal cell types whihc can be poorly differentiated and be precencerous, the cell hasnt fully differnetiated properly says haroon

185
Q

define ischemia and infarciotion

A

ischemia- perfusion is decreased with no cell death
infarction - tissue death due to lack of perfusion

186
Q

what are teh cells in barretts oesophogus

A

stratified squamous non keratanising epitheloium of the eosophogus become simple columnar of the stomach

187
Q

what are teh 5 classes of carcinogen

A
  • Classes of carcinogens - chemical, virus, ionising, hormone, miscalanious (asbestos)
188
Q

what s teh pathwa of spread throuht the body

A
  • How they spread through the body - detatchement, invasion of other tissue, invasion of bastment membrane, evasion of host defence and extravasiion to distant site
189
Q

what are teh three main ways that cancers are spread

A
  • Three main wats of spread - heamtogenis, lymphatic, transcolemic (through effusinos)
190
Q

what are teh 5 mian metastasis to bone

A

BLTKP

breast, lung, thyroid, kidnry, prostate

191
Q

how do sarcomas and carcinomas typically travel, and what are the 4 exceptions

A

Sarcomas - often spread by blood, carcinomas often lymphatically (the exceptions to this are follicular thyroid, chonocarcinoma, Rcc and HCC)

192
Q

what are teh two Gentetic mutation involved in colorectal cancer

A

Gentetic mutation involved in colorectal cancer -

-FAP (familial adenomis polypsis) - gene mutation cuaing thousands of precancerous polyps, this is autosomal dominant
-HNPCC (lynch syndrome) - autosomas dominant, there is mutation in the gene involved in renewal and care of teh colerectal cells

193
Q

what type of prevention in screening and what are teh three ones screened in teh UK

A

secondary

cervical, breast, cholerectal

Phase 2a (18 decks)

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