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4TH YEAR > CSIM2- mechanisms and investigations of disease > Flashcards

CSIM2- mechanisms and investigations of disease Flashcards

1
Q

2 types of imaging that use NON-ionising radiation

A

US

MRI

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2
Q

3 pros of US

A

no radiation
patient centred
can be focussed

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3
Q

3 cons of US

A

hard to interpret
needs specialist operator
may give false reassurance

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4
Q

4 cons of MRI

A

slow
needs IV contrast to be effective (anaphalaxis, NSF)
needs a specific question
accessibility

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5
Q

contraindications for MRI

A 
any metal:
pacemaker
insulin pumps 
hearing aids
metal clips
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6
Q

4 uses of interventional radiology

A

biopsies
drainage
angioplasty
tumour ablation

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7
Q

two groups particularly at risk from radiation

A

pregnant
children

however clinical need outweighs risk

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8
Q

1 CT scan is equal to what life time risk of cancer

A

1/1000

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9
Q

what are 2 potential risks of using IV contrast?

A 
anaphylaxis 
contrast nephropathy (tell the radiologist about any renal impairment)
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10
Q

what are the RED FLAGS in sepsis according to the sepsis trust?

A 
Pulse > 130
resp. >25
lactate >2
purpuric rash
less than A on AVPU
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11
Q

define secondary brain injury

A

damage due to hypoxic insult some time after the initial injury

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12
Q

how to calculate the cerebral perfusion pressure?

A

CPP = MAP - ICP

mean arterial pressure - intracranial pressure

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13
Q

when ICP increases how does the body compensate?

A

squeeze out some of the CSF and venous blood

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14
Q

what happens in the skull when the brain can no longer compensate for an increase in pressure?

A 
uncal herniation (transtentorial herniation)
blood vessels kink
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15
Q

4 signs of increased ICP

A

decreased level of consciousness
pressor response
projectile vomiting
CN 6 palsy

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16
Q

what is another name for the pressor response and what are the characteristic triad?

A

cushing’s response:
irregular breathing
increased BP
reduction in HR

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17
Q

4 signs of brainstem herniation

A

CN 3 palsy
motor posturing
lower extremity rigidity
hyperventilation

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18
Q

what is the normal range of ICP? when to treat?

A

5-15mmHg , treat above 20

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19
Q

how can the ICP be lowered artificially?

A

remove mass/ lesion
drain CSF
reduce parenchymal volume
reduce cerebral blood flow

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20
Q

how can we reduce the parenchymal vol. in raised ICP?

A

osmotic therapy

sometimes resection

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21
Q

how can the arterial blood flow to the brain be reduced in raised ICP?

A

sedation
mechanical ventilation
avoid fever
treat seizures

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22
Q

how can cerebral blood in the veins be reduced in raised ICP?

A

head up

avoid jugular pressure

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23
Q

how does sedation and controlled ventilation reduce ICP?

A

if o2 decreases then there will be vasodilation in the brain -> increased blood flow
same with high co2

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24
Q

what is the main imaging tool in major trauma and why?

A

CT because it shows where the bleeding is coming from

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25
Q

5 reasons for a trauma call and an example for each?

A

physiological- ABC approach
anatomical- 2 or more proximal long bone fractures/ head penetration etc.
high risk mechanism of injury- car crash
multiple trauma victims
discretionary-consider age, co-morbidities

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26
Q

what is the bodies response to reduced MAP due to haemorrhage? (3)

A

baroreceptor response : increase SNS and decrease PNS
endocrine response : catecholamine and steroid release
reduced renal perfusion ->RAA axis activation -> Na and hence water retention

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27
Q

where does blood go in major trauma?

A

blood on the floor and 4 more:

  1. long bones
  2. pelvis
  3. abdomine
  4. thorax
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28
Q

what would you expect an ABG to look like in major trauma?

A 
pH: decreased
pCO2: decreased
pO2: variable
lactate: increased
bicarb: decreased
base excess: decreased

i.e. metabolic (lactic) acidosis with resp. compensation where possible

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29
Q

what is likely to happen to Hb immediately after major trauma?

A

stay the same: it is a conc. so blood loss will not reduce the conc. of Hb immediately. in the following hours fluid will be sucked in from surrounding tissue (or given IV) so the Hb will DECREASE

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30
Q

how should the circulating blood volume be restored?

A

give blood ideally , or FFP (fresh frozen plasma)/ platelet

dont give crystalloids/ colloids much anymore due to hypotermia

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31
Q

explain the trauma TRIAD OF DEATH

A

patient becomes acidotic due to vasocontriction, hypotension (and hypoperfusion) causing anaerobic respiration.
this leads to decreased heart performance
this leads to hypothermia (also due to cold fluid admin. and exposure)
hypothermia causes decreased coagulation
this has the effect of exacerbating the acidosis

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32
Q

what is an immunoassay?

A

biochemical test that measures the conc. or presence of proteins (or other macro molecules) with antibodies

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33
Q

advantages of monoclonal immunoassay?

A

recognizes single epitote (foreign target antigen)
little batch variability
high specificity

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34
Q

pros and cons of immunoassay

A

pros:
automated therefore fast
sensitive
widely applicable e.g. BNP

cons:
cross-reactive: hard to produce an antibody that only reacts to the epitote you want
some are manual
heterophilic antibodies screw results

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35
Q

clinical application for immunoassay?

A

cancer diagnosis and prognosis

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36
Q

microarrays advantages

A

can look at 1000s of antigens at the same time so cost effective

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37
Q

microarray diadvantages

A

imprecise

not yet robust enough for clinical practice

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38
Q

define proteomics

A

study of the full set of proteins encoded by the human genome (30,000 genes)

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39
Q

which lab tests are used in proteomics

A 
2D electrophoresis (protein material in disease sample is compared to non-diseased sample
mass spec (produces peptide finger print)
microarrays
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40
Q

which lab tests are used in metabolomics?

A

mass spec

NMR

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41
Q

what are the limiting factors in the -omics?

A

huge amount of data with complex interpretation

statistical significance not proven yet

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42
Q

define genomic test

A

test nucleic acid to answer a diagnostic / prognostic question

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43
Q

diagnostic genetic testing is what? and what are the practical problems

A

finding the gene mutation to confirm the diagnosis (usually 100% sensitive)

multiple genes cause same phenotype
different phenotypes
unknown genes

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44
Q

what is it that causes degenerative disorders of the CNS?

A

aggregates of misfolded proteins

where these deposit determines what kind of problem you get

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45
Q

on post-mortem what are you able to see in Alzheimers?

A

senile plaques: short amino acid called amyloid Beta. this comes from a much bigger pre-cursor protein

Tau protein (particularly in FTLD): these cause nerve cells to die off

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46
Q

how can we slow the accumulation of amyloid beta in alzheimers

A

inhibit the enzyme that is breaking down the large protein precursor into amyloid beta

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47
Q

why do tau proteins aggregate in dementia?

A

enzymes cause phosphorylation of tau which reduces micro tubule biding and promotes aggregation (because they’re hydrophobic)

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48
Q

what is seen on microscopy in PD?

A

lewy bodies

neural loss

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49
Q

what could be a diagnostic biomarker in PD?

A

alpha-synclein

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50
Q

how could vaccination work as a therapy in degenerative disorders?

A

infusion of antibodies into patients could reduce symptoms

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51
Q

how do lysosomal storage disorders lead to symptoms?

A

loss of function of an enzyme leads to progressive accumulation of metabolite within lysosomes leads to organ disfunction

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52
Q

in which cells is the pathology in Gaucher’s disease?

A

accumulation of metabolites in macrophages -> skeletal problems and anaemia. also spleen and liver problems

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53
Q

treatment for Gaucher’s disease?

A

replace defective enzymes (B-glucosidase)

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54
Q

what is hunter syndrome?

A

enzyme deficiency that causes skeletal deformities, developmental delay and recession, cardiac and lung abnormalities and hepatosplenomagaly

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55
Q

how do pharmacological chaperones treat lysosomal storage defects?

A

stabilizes proteins in the endoplasmic reticulum to prevent protein misfolding

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56
Q

define iron deficiency anaemia and symptoms

A
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57
Q

effects of iron overlaod

A

liver cirrhosis
diabetes
cardiomyopathy
endocrine dysfunction

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58
Q

how does iron enter a cell?

A

transferrin

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59
Q

what is haemachromotosis?

A

elevated transferrin iron saturation and elevated ferritin leads to complications of high iron (cariomyopathy, diabetes, cirrhosis, arthritis) and hypogonadotrop ic hypogonadism

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60
Q

treatment for haemachromotsis?

A

regular phlebotomy and reduced iron diet

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61
Q

acute and chronic effects of copper overload?

A

acute : GI spasm, kidnet damage, rhabdomyolysis, haematemesis

Chronic : cirrhosis, diabetes, renal damage, neurophsychiatric problems

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62
Q

Wilsons disease is a problem of…

A

copper retention: due to failure of the copper to get into the bile it isnt excreted

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63
Q

symptoms/ signs of Wilsons

A

cirrhosis, extra-pyramidal symptoms, cardiomyopathy and nephocalcinosis

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64
Q

name a copper deficiency disorder

A

Menke’s disease

severe developmental delay and hair/ skin/ nail defects

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65
Q

sensitivity = …

A

true positives / (true positives + false negatives)

i.e. who has the disease

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66
Q

specificity = …

A

true negs / (true negs + false positives)

i.e. who hasnt got the diease

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67
Q

define positive predictive value and give equation

A

% of people who actually have the disease out of those who tested positive
positive predictive value = true pos. / (true pos. + false pos.)

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68
Q

define likelihood ratio

A

likelihood of the result meaning there is disease vs. there being no disease

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69
Q

equation for positive likelihood ratio

A

LR+ = sensitivity / (1- specificity)

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70
Q

equation for negative likelihood ratio

A

LR- = ( 1 - sensitivity) / specificity

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71
Q

roughly what LR+ is considered useful ?

A

> 10

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72
Q

roughly what LR- is considered useful?

A

the lower the better , 1 is USELESS

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73
Q

describe endocrine signalling

A

uses hormones which are secreted into the blood so they can be carried to their site of action. they are present at very low levels.
act via receptors on or in target cells
the same hormone can have a heterogeneous response depending on the cell

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74
Q

what is paracrine signalling?

A

the chemical acts on the adjacent cell

75
Q

what is autocrine signalling? e.g.?

A

target site is on the same cell - amplification process

T-cell lymphocytes

76
Q

what is juxtacrine signalling?

A

contact-dependent signalling

i.e. grow when not touching, stop on contact (cancer doesnt have this)

77
Q

define ligand

A

extra-cellular signalling molecule

78
Q

what is a third messenger system and what is another name for it?

A

molecule that transmit messages from outside the nucleus to inside or visa verse
also called DNA binding molecules

79
Q

why do most signal transduction therapies target the beginning of a pathway?

A

the higher up the pathway the more specific and the less unpredictable outcomes

80
Q

define second messenger

A

small molecules synthesised in cells in response to an external signal which are responsible for intracellular signal transduction e.g. Ca2+

81
Q

4 ways specificity of biosignalling can be influenced

A
  1. different interactions between ligand and receptor
  2. cell- specific expression of receptors (only some cells will express the correct receptor)
  3. cell- specific expression of signal transduction proteins (so the same signal - receptor combination can have different effects in the cell)
  4. cell-specific expression of effector proteins - there can be a varied response depending on what the cell does in response to the signal
82
Q

how does a direct ligand-gated channel work?

A

a signal, acting as a ligand, binds to a receptor changing its shape such that a specific ions can now flow through

83
Q

around 40% of medical drugs use what kind of signal transduction?

A

G-protein coupled type

84
Q

which type of signal transduction is used in most of our senses? (smell, sight, taste)

A

GPCR

85
Q

explain how a mutation in the V2R gene on the X chromosome results in congenital diabetes insipidus in males

A

normally AVP (anti-diuretic hormone) binds to the V2 vasopressin receptor (GPCR) and stimulates water reabsorption. if the V2R gene is inactivated then this cannot happen so cannot generate appropriately concentrated urine

86
Q

what area are tyrosine kinase-linked signals important

A

cell growth, differentiation and survival

87
Q

how could the inhibition of EGFR have therapeutic effects in cancer patients?

A

EGFR is expressed to varying degrees in a variety of cancers e.g. colorectal, pancreatic, head and neck, renal, breast. by introducing an anti-body to bind to extracellular domain of EGFR , growth factor can be blocked

88
Q

what are the 4 types of receptor in signal transduction?

A
  1. direct ligand gated channel
  2. G protein coupled receptor
  3. tyrosine kinase- linked
  4. intracellular steroid / thyroid type
89
Q

where are intracellular receptor proteins found?

A

in the cytosol or nucleus

90
Q

what type of molecules can reach intracellular receptors?

A

small or hydrophobic

91
Q

two examples of hormones that work on intracellular receptors?

A

thyroid

steriod

92
Q

how do intracellular signals have an effect on the body?

A

act as transcription factors, turning on specific genes

93
Q

what are the 5 components of the innate immune system?

A
  1. physical / chemical barriers
  2. phagocytic leukocytes
  3. dendritic cells
  4. natural killer T cells
  5. plasma proteins (complement)
94
Q

2 components of adaptive immunity

A
  1. humoral (B cells which mature into antibody secreting plasma cells)
  2. cell mediated (T cells that mature into effector helper T and cytotoxic T cells)
95
Q

how are specific antibodies made?

A

randomly through recombination of regions of the immunoglobulin genes.
B cells that make antibodies against foreign molecules AND self are allowed to be made.
there is then a process of negative selection where the B cells making self antibodies are DESTROYED

96
Q

how can the process of antibody production lead to autoimmune disease

A

the negative selection process doesnt always destroy the B cells that produce antibodies with a low affinity to self

97
Q

what makes autoimmunity pathogenic?

A

it is normal for there to be autoantibodies in individuals. it is pathogenic when:

  1. there is activation of T/B cells and amplification of autoantibody responses
  2. there is increased or novel exposure of ‘self’ antigen
98
Q

4 functions of antibodies

A
  1. opsonisation -> phagocytosis
  2. cytotoxicity
  3. immune complex formation
  4. mediate inflammation
99
Q

pathophys of Goodpastures syndrome

A

AKA anti-GBM disease
anti-GBM antibodies bind to the basement membrane of capillaries causing the WBC to attack it.
leads to inflammation of the vessels -> glomerulonephritis and alveolar capillartitis

100
Q

anti-body mediated AID is what type of hyper-sensitivity?

A

type II

101
Q

how do streptococcal cell wall antigens cause acute rheumatic fever?

A

they cross react with cardiac heart muscle

102
Q

what antigens are present in Goodpastures syndrome?

A

collagen type IV basement membrane

103
Q

type III hypersensitivity is mediated by what?

A

immune complexes:

ineffective clearance of immune complexes by the innate immune cells leads to an inflammatory response

104
Q

what are the two general ways the immune system can be over active?

A

failure to switch off

wrong target

105
Q

allergy is what kind of hypersensitivity?

A

type I

106
Q

describe sensitisation in a type I hypersensitivity reaction

A

antigen comes into contact with a B cell
it is presented to a T helper cell
IgE is produced for that antigen
a mast cell is coated in this IgE

107
Q

what is it that causes the inflammatory response in type I hypersensitivity?

A

degranulation of the mast cell on re-rexposure

108
Q

what dose of adrenaline do you give in anaphylaxis? 3 other things?

A

0.5ml of 1 in 1000 IM
fluid bolus
chlorphenamine 10mg IV
hydrocortisone 200mg IV (for the late phase)

109
Q

when would you do a mast cell tryptase test and why?

A

1hr after onset of anaphylaxis

to monitor progress

110
Q

3 medications to give on discharger following anaphylaxis?

A

oral prednisolone
antihistamine (10/ 20mg PRN)
CONSIDER adrenaline autoinjector x2

111
Q

4 tests available for allergy follow up?

A

RAST testing for specific IgE
skin prick
oral challenges
intradermal testing

112
Q

what is Bayes theorem ?

A

the pre-test characteristics of a patient must be considered along with the test result to work out the post test probability of having a disease

113
Q

if the likelihood ratio of a test is 10, what is the approx. change in probability with a positive result?

A

add on 45%

114
Q

if the likelihood ratio of a test is 2, what is the approx. change in probability with a positive result?

A

add on 15%

115
Q

with what pre-test probability might you not want to do the test and why?

A

very low- would you treat even if positive?

very high- just treat anyway

116
Q

why is there increased lactate in sepsis?

A
  1. macrophage activity
  2. decreased clearance of lactate
  3. increased anaerobic respiration
117
Q

what is adult respiratory distress syndrome? what does it look like on CXR?

A

injury to the basement membrane of the alveoli causes them to fill with fluid
diffuse opacity

118
Q

when and why would you do a tryptase test?

A

24 hrs after anaphylaxis to rule out mastocytosis (excess mast cells)

119
Q

what is von willebrand factor and where is it stored?

A

blood glycoprotein involved in haemostasis

stored in the endothelial cells

120
Q

how does von williebrand factor work?

A

released into plasma when endothemilum is damaged

traps passing platelets

121
Q

how does the endothelium regulate vWf to prevent clots?

A

releases nitrous oxide to prevent adhesion (can i bind here please? NO!)

122
Q

how is vasculitis classified?

A

small, medium and large

123
Q

what is the most common vasculitis?

A

GCA

124
Q

how is vision lost in GCA?

A

occultion of the blood supply to the eye

125
Q

how is GCA diagnosed? and treated?

A

biopsy

steroids

126
Q

what is Bechet’s disease?

A

small vessel inflammation in veins and arteries that causes mouth ulcers, genital sores, eye inflammation , rashes

127
Q

what changes are associated with endothelial dysfunction?

A 
reduced NO bioavailability
pro-vaso-constriction
pro-coagulopathy
pro-inflammation
pro-oxidative stress
128
Q

what type of vascular disease is anti-neutrophil cytoplasic antibdies (ANCA) associated with?

A

small vessel vasculitis

129
Q

what are the systemic symptoms of small vessel vasculitis?

A

ENT- saddle bridge nose
lungs- wheeze, breathlessness, dry cough, haemoptysis
skin- ulcers, rash, necrosis
eys- dry, red gritty, painful eyes with or w/o vision loss
nerves- loss of sensation
bowels- bleedins, diarrhoea, abdo. pain

130
Q

how are macrophages primed?

A

NK cells and T cells release IFN-gamma when a barier has been penetrated
this upregulates the expression of MHCII

131
Q

how do marophages kill bacteria?

A

recognise PAMP: increase reactive o2 molecules and lysosome number

132
Q

other than phagcytosis, what do macrophages do when primed?

A

release cytokine that have the following affect:

  1. active compliment cascade
  2. active vascular endothelium
  3. increase anti-bodie production
  4. recruits other cells
133
Q

where are NK cells made?

A

bone marrow

134
Q

what can NK cells do?

A

kill tumour and virally infected cells

135
Q

how do macrophages and NK cells have an amplification effect?

A

macrophages activate NK cells and NK cells release IFN-gamma which activates macrophages

136
Q

where are neutrophils made and what attracts them?

A

bone marrow

TNF-a

137
Q

what is the ‘bridge’ between innate and adaptive immune systems?

A

dendritic cells:

awaits sampling by t cells at lymph nodes

138
Q

what is meant by ‘contexualised’ discrimination? (immune system)

A

our bodies will allow the retention of harmless ‘non-self’ e.g. in the gut

139
Q

how is peripheral tolerance achieved?

A

Tregs made in the peripheries and tolerogenic DCs can turn off self reactive T-lyphocytes by cell- cell inhibition

140
Q

what are t-regs and what ar the types?

A 
CD4+ T lymphocytes which suppress potentially deleterious activities of T lymhocytes
thymic tregs (central tolerance)
peripheral tregs- induced in peripheries `
141
Q

AIRE deficency is an example of what mechanism of auto-immunity?

A

failure of central tolerance: non-expression of self antigen -> organ specific auto-immunity and chronic mucocutaneous candidiasis

142
Q

give an example of a disorder of Treg cells?

A

IPEX syndrome

143
Q

define primary immundeficincy

A

loss OR GAIN in function

144
Q

what type of infection are neutrophils, compliment and antibodies responible for clearing?

A

EXTRAcellular

145
Q

Tx for anti-body, compliment , neutrophil deficiency?

A

abx prophylaxis
anti fungal prophylaxis (particularly in compliment)
replacement Ig

146
Q

what could be a non-congenital cause of neutrophil deficiency

A

chemo/ radio therapy

bone marrow failure

147
Q

how are t cells involved in extra cellular infection clearing?

A

B cell actvation

148
Q

how do t cell deficient patients present/

A

persistent viral infection (t cells clear intracelluar infections)
protazoal infections +/- bacterial infections

149
Q

tx for t lymphocyte deficiency ?

A

abx prophylaxis
anti fungal prophylaxis (particularly in compliment)
replacement Ig
haematopoietic stem cell transplant

150
Q

how can phagocyte deficiency lead to non-infectious resp. failure?

A

cells arent cleared so get a build up surfactant

151
Q

3 types of rejection, their time periods and what mediates it?

A

hyper-acute: straight away- anti-bodies (pre-existing)

acute: days/ weeks - T-cells and anti-bodies
chronic: months/ years - compliment, ab, adhesion molecules

152
Q

what does chronic rejection cause?

A

FIBROSIS
atherosclerosis
inflammation/ scarring

153
Q

what are the three criteria for graft v host disease?

A

graft has immunologically competent cells
host appears foreign to the graft, i.e. it has alloantigens that stimulate the graft
host is unable to mount an effective immune response to the graft

154
Q

3 ways to prevent rejection?

A

ABO matching (prevents hyper acute)
HLA matching e.g. with family members
immunosuppression: destroy T cells with serotherapy, prednisolone

155
Q

what is graft v host disease?

A

when bone marrow/ stem cells rejects host

RARE: liver transplant (there are lots of immune cells here)

156
Q

who is at risk of GVHD?

A

neonates

immunocompetent

157
Q

which organs does acute GVHD effect?

A

skin (painful rash, blisters)
liver (raised LFTs and possibly jaundice)
gut (anorexia, dyspepsia, bleeding, diarrhoea)

158
Q

what factors increase risk of GVHD?

A

sex mismatch
previous pregnancies
peripheral cells worse than core cells
age

159
Q

what investigation is used to determine extent of liver fibrosis?

A

biopsy is the gold standard

160
Q

what can LFTs tell you about fibrosis?

A

AST/ALT ratio

161
Q

why do blockages form in the liver in cirrhosis?

A

regeneration leads to nodule formation

162
Q

which cells cause pulmonary fibrosis?

A

abnormal activation of fibroblasts

163
Q

what will the U&Es look like in chronic renal failure?

A 
high phosphate  (kidneys cant clear it)
 low calcium
164
Q

two main causes of high calcium

A

malignancy (boney mets or ectopic parathyroid tissue)

hyperparathyroidism

165
Q

define carcinogenesis

A

process of a normal cell becoming a cancer cell

166
Q

what is the smallest detectable tumour?

A

1cm

167
Q

why do cells not normally metastasize to other parts of the body? e.g. why no liver cells on skin?

A

cellular proteins and surface glycoproteins have a contact inhibition system

168
Q

define hypertrophy

A

increase in size of tissue due to increase in size of cells

169
Q

define hyperplasia

A

increase in size of tissue due to increase in number of cells

170
Q

define metaplasia

A

replacement of one fully differentiated tissue with another due to persistant injury. when this stimulus is removed it will return to initial state

171
Q

define dysplasia

A

archetectual and cytological changes similar to malignancy.

some features of cancer but not cancer yet- can also return to normal if stimulus removed

172
Q

3 steps in chemical carcinogenesis

A
  1. initiation- chemical damage to DNA and repair had failed before replication
  2. Promotion- reversible process that requires multiple exposure. if a promotor is removed the cancer could stabilise
  3. Progression- irreversible process that involves multiple complex DNA changes
173
Q

2 types of non-ionising radiation that could cause cancer?

A

radio-waves

UV

174
Q

which tissue is particularly sensitive to ionising radiation?

A

breast, thyroid, bone marrow

175
Q

why are male pilots more likely to have daughters than sons?

A

exposure to radiation

y chromosome is more susceptible to it

176
Q

which UV type has the most effect on DNA and which is the most clinically relevant?

A

UVC is the most potent but us mostly absorbed by the air so is negligible.
UVB is the most important in cancer

177
Q

how does non-ionising radiation cause changes in DNA?

and how do cells normally stop this?

A

electron excitation

nucleotide excision repair pathway

178
Q

what % of cancers are thought to be due to infection globally?

A

15%

179
Q

what does EBV increase risk of?

A

Hodgkins and burkett’s lymphoma

180
Q

example of exogenous hormones causing cancer

A

HRT, COCP*- over exposure to oestrogen linked with breast cancer

only if this is used after oestrogen would normally be lowered

181
Q

whats the difference between somatic and germline mutation

A

germline- error in every bit of DNA. can be hereditary but not always
somatic- in the tumour there is a mutation but this is not present in the other cells (unless present in the germline cells). this cannot be passed on

somatic mutations and germline mutations can affect the same genes

182
Q

how can mutations occur in normal cell division?

A

mis-segregation

mitotic recombination

183
Q

how many cancers are familial?

A

10%

184
Q

why is it dificult to get chemo to cancer cells?

A

they are very hypoxic so arent well supplied by our blood vessels. only about 20% of cells can be reached

4TH YEAR (12 decks)

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