introduction to clinical sciences Flashcards
(156 cards)
1
Q
autopsy types
A
hospital <10%
medico-legal >90%
2
Q
acute vs chronic inflammation cells
A
acute – neutrophil polymoprhs
chronic – macrophages + lymphocytes
3
Q
lifespan of neutrophils, macrophages and lymphocyes
A
neutrophils- hours
macrophages - weeks - months
lymphocytes - weeks-years
4
Q
endothelial cells’ reaction when inflammed
A
sticky- other cells stick to it
gaps- increased vascular permeability – protein leaves– swelling
5
Q
granuloma =
A
occurs in chronic inflammation
macrophages (endotheloid cells) surrounded by lymphocytes
harmful stuff walled off
6
Q
options for damaged tissue
A
RESOLUTION = damaging factor removed. the tissue is undamaged or able to regenerate
REPAIR = damaging factor remains. the tissue is damaged and can not regenerate
– fibrous tissue replaces damaged tissue. fibroblasts –> collagen
REGENERATION. - healed
7
Q
which cells are able to regenerate
A
pneumocytes
hepatocytes (but contined damage leads to cirrhosis - much fibrosis)
osteocytes
skin epithelium (but collagen causes scar)
gut epithelium
8
Q
which cells are unable to regenerate
A
neurones - brain + spine
myocardial cells
cilia in organ of corti
these are non-dividing tissues
9
Q
laminar flow
is this in arteries or vein
A
in centre of vessel
arteries . in veins, the speed is slower so blood drops with gravity
10
Q
reperfusion injury
A
ischaemia
cells = :/
blood flow increases
cells dont readjust/cope. they produce damaging chemicals
so sometimes patients are kept cold/in coma until adjusted to avoid this
11
Q
Which organs have multiple blood supply
what does this prevent
A
infarction (hopefully)
lungs
liver
circle of willis
12
Q
apoptosis mechanism
A
enzymes released
cell shrinkage inc nucleus shrinkage
macrophage engulfs
the effectors are capases (these are switched on or off by proteins)
13
Q
what triggers apoptosis
A
cosmic rays, UV —-> DNA damage
DNA damage
- strands broken
- base alteration
- cross linkage
this damage is detected by p53 gene
14
Q
name 2 examples in physiology where apoptosis is seen
A
1 developement : trim down webbed digits to elegant fingers
2 high cell turnover areas - eg villi
15
Q
name 2 examples in pathology where apoptosis is seen
A
1 too much apoptosis – HIV
2 not enough apoptosis – cacner
16
Q
name 4 causes of necrosis
A
(traumatic cell death)
infarction
venom
frost bite
pancreatitis
17
Q
what are the 3 types of necrosis
A
coagulative necrosis – more viscous
liquifactive necrosis – more runny
caseous necrosis – looks like soft cheese (TB)
18
Q
hypertrophy
A
increased size of tissue due to increase SIZE of cells
- body builders skeletal muscle
19
Q
hyperplasia
A
increased size of tissue due to increase NUMBER of cells
- smooth muscle
- endometrium
20
Q
does pregnancy involve hypertrophy or hyperplasia
A
both
21
Q
atrophy
A
decreased size of tissue due to increase NUMBER OR SIZE of cells
(joint term)
22
Q
metaplasia
A
change in differentation of a cell from one fully differentaited cell type to a different fully differentiated cell type
ciliated columnar epithelium –> squamous (smokers)
squamous –> glandular columnar (barrets oesoph)
23
Q
dysplasia
A
imprecise term - morphological changes in cells in progression to becoming cancer
- lose maturity
24
Q
homeobox genes
A
a group of genes that direct developement . they each code for a different part of the body
25
which tissues divide more: old or young
young
26
telomeres
at end of chromosome
dont code for anything
get shorter as you get older, each time DNA replicates
27
name 3 pathologies of ageing
- senile dementia- - atrophy of brain
- dermal elastosis = wrinkles - collagen cross links protein in skin due to UVB light
- osteoporesis
- cataracts - the lens is foggy due to protein cross-linked due to UVB light
- deafness - cilia in the organ of Corti nonreplaceable
- sarcopenia -skeletal mass and strength declines (decreased testosterone and growth hormone)
28
carcinogenesis
normal cells to neoplastic cells (malignant) through multiple permanetnt genetic alterations/mutations on DNA
29
carcinogen classes
```
chemical (UVA ,UVB light)
viral
hormones (steroids, oestrogen)
parasites
mycotoxins (aflatoxin b1)
ionizing, nonionizing( x rays ionising radiation)
miscellaneous (asbestos, arsenic)
host factors (race, gender, age, diet, smoking etc)
```
30
neoplasm contains
neoplastic cells
- normally monoclonal
stroma
- support mechanically + nutririon, growth factos, framework
- avascular until 2mm
31
how to classify a neoplasm
behavioural - benign/malignant/ bordeline
histogenic - cell of origin
32
behviousal classification of neoplasm
benign vs malignant
```
benign =
localised (no metastases/invasion)
non invasive- doesnt infiltrate surroundings, just pushes
low mitotic activity, slow growth
necrosis and ulceration = rare
well defined border
```
33
innate vs adaptive immunity
innate
- non specific
- no lymphocytes (no memory). think non-lymphocyte leukocytes!
- present from birth
adaptive
- specific to antigen
- lymphocytes required
- aquired, learnt (memory)§
34
complements
=?
when activated, they?
which immune system are they part of
they are proteins
```
1 direct lysis (cell death by breaking cell membrane)
2 increase chemotaxis ( attract more wbc)
3 osponisation (coat/surrounding organism by binding to it, easier to phagocytose)
```
they are part of the innate immune system only
35
different T lymphocyte cells
Th - clocks antigen, cytokines released -- activate macrophages. and natural killer cells. and activate B cells --> memory + plasma
Tc - target damaged/ infected cells --> apoptosis
Ts- inhibits Th to suppress immune response
36
poly/mononuclear lymphocytes
which are which!
poly
- neutrophil
- eosinophil
- basophil (-> mast cell)
mono
- monocyte (-> macrophage)
- T cell
- B cell
37
cytokines
made of
types
= proteins
interferons (IFN) - antiviral resistance in unaffected cells
interleukins (IL) - pro/anti inflammatory (secreted by leukocytes, act on leukocutes to divide, differentiate, secrete)
colony stimulating factors - direct division and differentation of bone marrow stem cells (--> blood cells)
tumour necrosis factors - mediate inflammation and cytoxic reactions
chemokines - direct leukocytes where to go
38
leukocytes vs lymphocytes
leukocyte = wbc
lymphocyte = type of leukocyte. they are mononuclear . they are either B or T
39
what happens in innate response
- coagulation
- increased blood supply
- increased vascular permeability
- endothelium --> sticky --> wbc recruited to tissue out of vessel
- these then kill pathogens and dead cells and neutrolise -toxins
- cells proliferate to repair damage
- clot removed
- normal fucntion reestablished
40
types of adaptive response
cell mediated -- kill infected cell with intracellular , intrinsic pathogen (cellular response)
MHC1, CD8(Tc)
humoral -- for an extracellular, extrinsic pathogen (antibody response)
MHC2, CD4 (Th)
41
what is a MHC?
types
which immune response to they relate to? how?
major histocompatibility complex- on cell surface, like receptor. it displays antigens
MHC1 is on all nucleated cells
MHC2 is on APC only
cell mediated adaptive response -- intrinsic (intracellular) = MHC1
extrinsic (extracellular)= MHC2
they are on the outside of infected cells, and fit together with antigens on CD8/4 cells. this activates them to become T lymphocytes
42
what are CD4 and CD8 cells?
CD4 is precursor to Th cell (then goes on to activate macrophages and natural killer cells, and causes B cells to differenetiate)
CD8 is precursor to Tc cell (then goes on to kill infected phagocytes and damaged cells)
they are activated to become these by MHC on APC infected pathogen
CD4 activated by MHC2 (extrinsic-)
CD8 activated by MHC1 (intrinsic)
43
what are natural killer cells
```
the 3rd type of lymphocyte (not T or B)
large granular lymphocyte
they kill cells (virus and tumours) by secreting stuff - apoptosis
also attract more immune cells
found in spleen and tissues
```
44
Humoral (extra cellular) adaptive immune response
how is the pathogen presented
effect
naiive B lymphocyte encounters a pathogen that is complementary to its receptor
pathogen presented on MHC2
this activates CD4 --> Th (which then goes on to activate macrophages and natural killer cells, and causes B cells to differentiate)
and also activates B cell -- clonal expansion and differentiation (to plasma/memory. cells)
45
antibodies role in adaptive immune response
how do they work
antibodies are specific to the encountered pathogen
1 opsonisation - surround to enhance phagocytosis (helps guide phagocytosis)
2 neutralise - bind to and neutralise bacteria + toxins
3 activate complements
46
types of pattern recognition receptor (PRR)
these can circulate freely (activate complements) and these are on immune cells:
nod like receptors (NLR) - for bacteria
rig like receptors (RLR) - for viruses
toll like receptors (TLR) - for lots of things
can initiate tissue repair?
47
what are lectins
| what do lectins do
they are carb contating protein
| they bind the proteins and lipids in microbe wall. this activates complements
48
toll like receptors (TLR) types
TLR4
- - detects gram + bacteria
- - regulates neutrophil level in the blood
- - increase levels of cytokines so CD4 and CD8 activation to T cells
TLR5
-- detects flagella
TLR3
-- detects double-stranded RNA (virus)
TL7/8
-- detects single stranded RNA (virus)
49
PRR and PAMP. which is where?
| they stand for...
PRR is on immune cell - pattern recognition receptor
| PAMP is on pathogen- pattern associated molecular patterns
50
what is a phagolysosome
this is created when lysosome vesicle binds with vacuole (phagocyte engulfed pathogen)
51
APC presents antigen how?
after phagocytosis, the antigen is presented on MHC
52
how are pathogens destroyed within the cell
oxygen dependant - ROI
- - o2* --> h2o2 --> *OH (kills bacteria)
- - NO increases vasodilation (wbc into area)
oxygen independent
- enzymes
- pH
- defensin protein
53
symptoms of allergic reaction
eczema
itching
red
bloating
vom
diarr
bronchoconstriction
excess mucous
54
atopy
inherited tendency to have exaggerated IgE response
| -- hayfever, asthma, eczema
55
gel and coombs classification of hypersensitivity reactions
1. allergy, atopy, anaphylaxis
igE binds to mast cells so they release histamine
regulated by antihistamine (eosinophils)
2 ig G mediated
bound to cell surface antigens
transfusion reactions
drug/metablite combines with protein and body considers it foreign so creates antibodies
3 immune complexes = antibody + target
cause immune response --> tissue damage--> inflammation
SLE
hay barely compost droppings
4 T cell mediated, no ig
TB, contact dermatitis
granulomas
56
barriers to infection=
which immune response are they
physical (skin, cilia, mucous membranes)
physiological (cough,sneeze, vom, diar)
chemical (pH of stomach, vagina, skin, saliva, tears)
biological (nonpathogenic microbes compete for resources)
innate
57
how does penicillin work
halt cell wall synthesis
58
each antibody characteristics
IgM- beginning . large molecule (many connected)
IgG- v specific (target single epitopes). most abundant. single complex
IgE - allergies. single complex
IgA- on mucosal surface double complex
59
desensitisation to anaphylaxis
not possible
60
treatment for type 1 allergy reactions
cause/avoid exposure to allergen
antihistamine
steroid --> decrease inflammation
desensitisation
61
pros and cons of live attenuated organism vaccination
full natural response
one dose required only
b+t cell response
natural mutation - resistant
immunocomprimised patients cannot have
correct preparation vital
side effects of immune response- fever
62
pros and cons of inactivated organism vaccination
no risk of infection
full immune response triggered
easy storage
booster required (patient compliance)
only B cell repsponse, not T
immune response side effects eg fever
63
example of live organism vaccination
MMR
BCG
varicella
64
example of inactivated organism vaccination
cholera
polio
hep a
rabies
65
example of subunit vaccination
hib
| tetanus
66
pros and cons of subunit vaccination
no risk of infection
easy storage
weak immune response
booster required (compliance)
immune response side effects eg fever
67
pros and cons of pathogen DNA vaccinations
safe - no risk of infection
easy to store
easy to deliver
cheap
weak immune response
68
what is a vaccine agonist
something added to vaccine to increase immune response eg receptor agonist (more cytokines etc)
69
phsyicochemical drug interactions
molecules react regardless of body
70
pharmacodynamic drug interactions
+types
drugs effect on body
summation (1+1=2)
synergism (1+1 >2)
antagonism (1+1=0)
potentialism (1+1=1+1.5)
71
pharmacokinetic drug interaction
body's effect on drug
```
ADME
absorption
distribution
metabolism
excretion
```
72
absoprtion pharmacokinetics
- bioavailability- not all absorbed orally
- motility of gut - higher motility = quicker and fuller absopriton
- acidity: increases unionised proportion in equilibrium(which can cross the membrane)
73
what drug molecules can cross membrane (absorption)
unionised
as these are lipophilic
-- so can cross tissues/cell membranes INC GUT and placenta and brain!
high polarization decreases absorption (ionised is water soluble due to charges)
74
enzyme induction/inhibition in regard to pharmacokinetic metabolism
enzyme induction- enzyme effect improved so more metabolism so more potency (where metabolite is active)
enzyme inhibition- enzyme abilities reduced so less metabolism so less potency
75
excretion pharmacokinetics
neutralisation of acid increases excretion speed
this doesnt happen for alkali neutralisation though
76
is warfarin highly protein bound or highly unbound
protein bound -- less effect
77
ligandability
drugability
the ability of protein target to bind small molecules (ie drug) with high affinity
this then modifies protein function
drug target= receptor, enzymes, transporters, ion channels
78
types of drug target
rreceptor,
enzymes,
transporters,
ion channels
79
types of receptor
- ligand-gated ion channels
- g protein-coupled receptors- secondary intracellular messenger
- kinase linked receptors-- enzymatic activity intracellularly
- cytosolic/ nuclear receptors -- intracellular!! transcription switched on
80
what type of drug target do beta adrenoreceptors work on
g protein coupled receptors (receptor)
81
what type of drug target do nicotinic ACh work on
ligand gated ion channels (receptor)
82
what type of drug target do growth hormones work on
kinase linked receptors
83
what type of drug target do steroid hormones work on
nuclear receptors
they can go intracellular!
84
G proteins swithed on/off when...
```
on= bound to GDP
off= bound to GTP
```
so GDP/GTP regulate this receptor activity
85
what type of drug target does histamine work on
g protein coupled receptors (receptor)
86
affinity
how well ligand binds to receptor
Applies to agonist and antagonist
87
efficacy
how well ligand activates a receptor
Applies to agonists only
88
receptor reserve
this is when an agonist only needs to activate a small fraction of receptors to get the full response (so there are spare receptors - in reserve)
There is no receptor reserve for partial agonists as they are unable to get the full response even using all the receptors!!
89
how do statins work
block rate limiting step in cholesterol synthesis
enzyme inhibition
90
autonomic ganglia pathways - receptors and neurotransmitter and length of fibres eg to affect on heart
```
PARASYMP
= cholinergic system
-- long ganglion
-- synapse: ACh at nicotinic receptor
--short fibre
-- ACh at muscarinic receptor in effector tissue
```
```
SYMP
= adrenergic system
-- short ganglion
-- synapse: ACh in nictonic receptor
-- long ganglion
-- Noradrenaline at alpha/beta receptor
```
91
types of muscarinic receptors
M1- brain
M2- heart
M3 - glandular and smooth muscle
M4/5- CNS
92
what are each of these (drug types):
pilocarpine
atropine
hyoscine
muscarinic agonist
pilocarpine
muscarinic antagonist
atropine
hyoscine
93
treatment of bronchoconstriction
block M3 - anticholinergics or antimuscarinics
94
parasympathetic effect on salivary glands/sweating
stimulates salivary gland
no effect on sweat glands (these are triggered with symp)
95
name 3 catecholamines
noradrenaline
adrenaline
dopamine (this is the precursor! to nor/adrenaline)
96
what manages (Regulates):
- anaphylactic
- shock
- adrenaline
| - noradrenaline
97
types of adrenergic receptors
```
alpha 1 - smooth muscle contraction
alpha 2 - smooth muscle mixed effects
beta 1 - heart (chon and inotropic)
beta2 - smooth muscle relaxation
beta 3 - lipolysis stimulation and relaxation of detrusor
```
98
example of alpha muscarinic receptor agonist
```
shock treatment
(vasoconstriction)
```
think adrenaline is correct!
99
example of alpha muscarinic receptor antagonist
decrease prostate hypertrophy
lower BP
(vasodilation)
100
example of beta muscarinic receptor agonist
asthma treatment (relaxation)
overactive bladder treatment
but- s/e high HR
101
example of beta muscarinic receptor antagonist
beta blockers
| - but side effect = bronchoconstriction
102
codeine the drug
= prodrug
| metabolised in liver to morphine
103
antagonist to opioids
naloxone
104
morphine orally
when is morphine dangerous to give
due to bioavailability, only half metabolised by liver
so dose x2
with poor renal function - not excreted enough so builds up (especially the metabolite which is even more potent. this is quickly excreted with normal renal function)
105
what type of drug target do opioids work on
g protein coupled receptors
106
opioid action of opioids
g protein coupled receptors (MOP, KOP, DOP, NOP receptors)
| inhibit release of pain transmitter in CNS
107
stomach and intestines - they absorb what pH of drugs
```
stomach = weak acidic drugs
intestine= weak base drugs
```
108
ATP binding cassette (ABC)
this is a carrier that moves drugs across membranes
109
liver metabolism of drug
phase 1 -- functionalisation
makes more polar (add functional groups -OH, -NH2, -SH) eg oxidation.
uses CYP450 enzyme in SER of hepatocytes
more hydrophilic so more easily excreted
phase 2 -- conjugation:
covalent bond between it and endogenous substance (eg glucuronic acid)
readily excreted -- much more water soluble, large, polar, inactive
110
advantage of drug routes:
```
transcutaneous
intradermal/subcut
intramuscular
intranasal
inhalational
```
- transcutaneous slow and continuous
- intradermal/subcut local effect + slow release
- intramuscular quick due to blood flow
- intranasal high surface area
- inhalational high surface area
111
urine excretion equation
urine excretion = glomerular filtration + tubular secretion - reabsorption
112
first order kinetics
zero order kinetics
1 --decline in drug conc in plasma decreases exponentially as drug is distributed (think curly L shape)
0 -- decline in drug conc in plasma is constant, due to enzymes becoming saturated
113
HALF LIFE
definition
and symbol
and equation
time taken for drug conc in plasma to half
T1/2
= 0.693 / K
114
BIOAVAILABILITY
symbol
of IV
of oral
f = 1 (100% reaches circulation)
f> 1 (incomplete absorption)
115
```
DISTRIBUTION
defintion
symbol
calculation : 50 ml drug given and now there is 2mg/L plasma conc
depends on
```
rate of movement in and out of tissues. low distribution = high proportion at target site
Vd (volume of distribution).
50/2/L =25L
depends on blood flow to tissues and rate of movement across membranes (latter applies to water soluble NOT lipid soluble drugs)
116
```
CLEARANCE
definition
symbol
equation
x2
```
volume of plasma cleared of drug per unit time
CL = (dose of drug x f) / area under curve (blood conc/ time curve)
f= bioavailability and =1 if IV so then for IV just = dose of drug/ area under curve
CL = k x Vd
117
STEADY STATE
definition
symbol
equation
balance between drug input and drug elimination. when equal = steady state . this allows constant therapeutic effect to be maintained
Css
= D x f/t %CL
(d = initial dose. f = bioavailability. t=time. Cl= clearance)
rate of infusion / cL
so rate of infusion = d x f/t
118
loading dose vs maintaing dose
| equations
loading dose = Css x Vd
maintainind dose. = Css x t/f x Cl
119
what determines how long a drug will take to reach Css (steady state)
half life -- slow elimation will take longer
distribution -- high distribution --> longer to reach Css
high initiial dose -- increases rate of diffusion so shortens time to css
120
adverse drug reaction
definition
types
unintended effects that are noxious (painful)
(dont have to be unpredictable)
toxic effects = above therapeutic range (does too high / excretion reduced)
collateral effects= within therapeutic range (drug affects more than just target site)
hypersusceptitbility effects = below the therapeutic range (hypersensitive)
121
are side effects the same as adverse drug reaction?
no. side effects can be adverse drug reactions but are not always noxious
122
rawlins thompson classification of adverse drug reaction
A- augmented pharmacological.
-- extension of primary effects. they are predictable, common, dose dependant
B- bizarre
--unpredictable, not dose dependant, not readily reversed
eg allergy
C- chronic/continuous
-- long term drug treatment
D- delayed
-- effect is late, follows after treatment
E- end of treatment
-- following abrupt drug withdrawal
F- failure of therapy
123
DoTS of adverse drug reactions
dose relatedness
timing
susceptibility of patient
124
risk factors for adverse drug reactions
```
PATIENT
women
old
young
polypharmacy
allergies/hypersensitivity
hepatic/renal impairment
genetic predisposition
adherence problems
```
DRUG
steep dose-response curve
low therapeutic index (= narrow range between effective and toxic)
PRESCRIBER
low understanding
busy/ tired / overwhelmed
125
ADR (adverse drug reaction) yellow card
used to report ADRs
by doctor
spot trends early so can be monitored for safety
126
non-immunological allergic reaction
mast cell degranulation caused by drugs (allergen)
| no prior exposure
127
are all allergic reactions immediate like anaphylaxis
no
| eg hepatitis, some rashes
128
types of anaphylaxis
1 vasodilation, vascular permeability -- swelling and shock (hypotension), so organ perfusion decreases (unconscious), bronchoconstriction, urticaria
2 drug combines with protein, antibodies, cell damage
3 small vessels damaged/blocked, inflammation
4 local allergic reaction
129
urticaria =
rash
itchy
red bumps
aka hives
130
types of death (as referred to coroners)
presumed natural (cause of death not known) -- majoirty
presumed iatrogenic (complications of therapy inc surgery, anaesthetic)
presumed unnatural (accidents, neglect, murder)
131
how do fibroblasts respond to chronic inflammation and repair
form collagen (fibrosis)
132
how do vessels respond to acute inflammation
dilation
133
outcomes of acute inflammation
resolution (complete restoration of tissues to normal)
suppuration (formation of pus)
organistation (tissue is replaced by granulation tissue (fibrovascular connective tissue) as part of repair process)
progression to chronic inflammation
134
why dont clots form normally
laminar flow
| endothelial cells are not sticky when healthy
135
thrombus formation steps
- damage to endothelium cause some endothelial cells to lift away
- collagen exposed (endothelin 1 released --> vasoconstriction)
- platelets stick to exposed collagen (via von willeband factor (at glycoprotein b)
- platelets release chemicals which causes amplification, activation and aggrevation
- rbc get trapped within aggregating platelets
- clotting factors join (--> clotting cascade) so large protein molecule fibrin is formed
- positive feedback loop
136
venous embolism will lodge?
pulmonary arteries
| vena cava -->lung, acts as a filter (vessels split to capillary size)
137
end artery supply =
an organ that only receives blood supply from one artery
thrombosis more problematic
138
name an example of a disease with a single gene disorder
name an example of a polygenic disorder
sickle cell anaemia
breast cancer
139
carcinogenic
oncogenic
mutagenic
```
cancer causing (malignant)
tumour causing (benign and malignant)
mutation causing
```
140
in situ neoplasia only applies to what kind of neoplasms
epithelial
141
stages of metastasis
```
detachment
invasion (through basement membrane)
evasion of host defences
arrest
extravasation
vascularisation
```
142
mechanisms of evading host defences
aggregation with platelets
shedding of surface antigens
adhesion to other tumour cells
143
herceptin action
this binds to Her2 protein so reduces the growth factor produced to slow growth in breast cancer
144
describe a monocyte nucleus
Kidney shaped
145
do these play a part in innate or adaptive immunity?
- monocytes (macrophages)
- neutophils
- t lymphocytes
- b lymphocytes
innate and adaptive
innate
adaptive
adaptive
146
list the immunoglobulins in order of majority
G A M D E
147
what are immunoglobulins made of
glycoproteins
148
epitope=
part of antigen that binds to antibody/receptor binding site
149
sebum=
skin secretions. these are part of innate immunity
150
name 3 pathogens lacking vaccine
herpes simplex virus
malaria
HIV
151
how are tumours recognised as foreign?
they express foreign antigens
```
TSA = tumour specific antigens (only on tumours)
TAA = tumour associated antigens (over-expressed on cancer cells)
```
152
cancer immuno-surveilence
= elimination stage of immunoediting
attacks tumour with immune system to protect tissue, to return it to normal tissue
153
cancer immunoediting
3 phases
elimination (cancer immuno-survelience) --attacks tumour with immune system to protect tissue to return it to normal tissue
equilibrium - immune system constantly fighting tumour to keep it at bay (stays same size, pre-malignant)
escape- immune system insufficient to control tumour, and it escapes and spreads and the immune burden increases
154
potency=
conc of agonist that gives half Emax (theoretical maximum response of agonist ie infinity high agonist conc)
155
gene therapy
recombinant (multisourced) nucleic acid used to regulate /replace/ add /delete a genetic sequence
156
irreversible drug binding- is this good or bad
equivalent to elimination! bad! cannot re-enter circulation
