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phase 2a mine > introduction to clinical sciences > Flashcards

introduction to clinical sciences Flashcards

1
Q

autopsy types

A

hospital <10%

medico-legal >90%

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2
Q

acute vs chronic inflammation cells

A

acute – neutrophil polymoprhs

chronic – macrophages + lymphocytes

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3
Q

lifespan of neutrophils, macrophages and lymphocyes

A

neutrophils- hours
macrophages - weeks - months
lymphocytes - weeks-years

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4
Q

endothelial cells’ reaction when inflammed

A

sticky- other cells stick to it

gaps- increased vascular permeability – protein leaves– swelling

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5
Q

granuloma =

A

occurs in chronic inflammation

macrophages (endotheloid cells) surrounded by lymphocytes

harmful stuff walled off

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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

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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

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8
Q

which cells are unable to regenerate

A

neurones - brain + spine
myocardial cells
cilia in organ of corti

these are non-dividing tissues

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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

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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

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11
Q

Which organs have multiple blood supply

what does this prevent

A

infarction (hopefully)

lungs
liver
circle of willis

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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)

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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

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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

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15
Q

name 2 examples in pathology where apoptosis is seen

A

1 too much apoptosis – HIV

2 not enough apoptosis – cacner

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16
Q

name 4 causes of necrosis

A

(traumatic cell death)

infarction
venom
frost bite
pancreatitis

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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)

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18
Q

hypertrophy

A

increased size of tissue due to increase SIZE of cells

  • body builders skeletal muscle
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19
Q

hyperplasia

A

increased size of tissue due to increase NUMBER of cells

  • smooth muscle
  • endometrium
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20
Q

does pregnancy involve hypertrophy or hyperplasia

A

both

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21
Q

atrophy

A

decreased size of tissue due to increase NUMBER OR SIZE of cells

(joint term)

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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)

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23
Q

dysplasia

A

imprecise term - morphological changes in cells in progression to becoming cancer
- lose maturity

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24
Q

homeobox genes

A

a group of genes that direct developement . they each code for a different part of the body

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25
Q

which tissues divide more: old or young

A

young

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26
Q

telomeres

A

at end of chromosome
dont code for anything
get shorter as you get older, each time DNA replicates

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27
Q

name 3 pathologies of ageing

A
  • 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)
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28
Q

carcinogenesis

A

normal cells to neoplastic cells (malignant) through multiple permanetnt genetic alterations/mutations on DNA

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29
Q

carcinogen classes

A 
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)
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30
Q

neoplasm contains

A

neoplastic cells
- normally monoclonal

stroma

  • support mechanically + nutririon, growth factos, framework
  • avascular until 2mm
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31
Q

how to classify a neoplasm

A

behavioural - benign/malignant/ bordeline

histogenic - cell of origin

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32
Q

behviousal classification of neoplasm

A

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
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33
Q

innate vs adaptive immunity

A

innate

  • non specific
  • no lymphocytes (no memory). think non-lymphocyte leukocytes!
  • present from birth

adaptive

  • specific to antigen
  • lymphocytes required
  • aquired, learnt (memory)§
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34
Q

complements

=?
when activated, they?

which immune system are they part of

A

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

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35
Q

different T lymphocyte cells

A

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

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36
Q

poly/mononuclear lymphocytes

which are which!

A

poly

  • neutrophil
  • eosinophil
  • basophil (-> mast cell)

mono

  • monocyte (-> macrophage)
  • T cell
  • B cell
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37
Q

cytokines

made of

types

A

= 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

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38
Q

leukocytes vs lymphocytes

A

leukocyte = wbc

lymphocyte = type of leukocyte. they are mononuclear . they are either B or T

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39
Q

what happens in innate response

A
  • 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
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40
Q

types of adaptive response

A

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)

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41
Q

what is a MHC?

types

which immune response to they relate to? how?

A

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

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42
Q

what are CD4 and CD8 cells?

A

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)

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43
Q

what are natural killer cells

A 
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
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44
Q

Humoral (extra cellular) adaptive immune response

how is the pathogen presented

effect

A

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)

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45
Q

antibodies role in adaptive immune response

how do they work

A

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

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46
Q

types of pattern recognition receptor (PRR)

A

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?

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47
Q

what are lectins

what do lectins do

A

they are carb contating protein

they bind the proteins and lipids in microbe wall. this activates complements

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48
Q

toll like receptors (TLR) types

A

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)

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49
Q

PRR and PAMP. which is where?

they stand for…

A

PRR is on immune cell - pattern recognition receptor

PAMP is on pathogen- pattern associated molecular patterns

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50
Q

what is a phagolysosome

A

this is created when lysosome vesicle binds with vacuole (phagocyte engulfed pathogen)

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51
Q

APC presents antigen how?

A

after phagocytosis, the antigen is presented on MHC

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52
Q

how are pathogens destroyed within the cell

A

oxygen dependant - ROI

    • o2* –> h2o2 –> *OH (kills bacteria)
    • NO increases vasodilation (wbc into area)

oxygen independent

  • enzymes
  • pH
  • defensin protein
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53
Q

symptoms of allergic reaction

A

eczema
itching
red

bloating
vom
diarr

bronchoconstriction
excess mucous

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54
Q

atopy

A

inherited tendency to have exaggerated IgE response

– hayfever, asthma, eczema

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55
Q

gel and coombs classification of hypersensitivity reactions

A
  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

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56
Q

barriers to infection=

which immune response are they

A

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

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57
Q

how does penicillin work

A

halt cell wall synthesis

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58
Q

each antibody characteristics

A

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

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59
Q

desensitisation to anaphylaxis

A

not possible

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60
Q

treatment for type 1 allergy reactions

A

cause/avoid exposure to allergen
antihistamine
steroid –> decrease inflammation
desensitisation

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61
Q

pros and cons of live attenuated organism vaccination

A

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

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62
Q

pros and cons of inactivated organism vaccination

A

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

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63
Q

example of live organism vaccination

A

MMR
BCG
varicella

64
Q

example of inactivated organism vaccination

A

cholera
polio
hep a
rabies

65
Q

example of subunit vaccination

A

hib

tetanus

66
Q

pros and cons of subunit vaccination

A

no risk of infection
easy storage

weak immune response
booster required (compliance)
immune response side effects eg fever

67
Q

pros and cons of pathogen DNA vaccinations

A

safe - no risk of infection
easy to store
easy to deliver
cheap

weak immune response

68
Q

what is a vaccine agonist

A

something added to vaccine to increase immune response eg receptor agonist (more cytokines etc)

69
Q

phsyicochemical drug interactions

A

molecules react regardless of body

70
Q

pharmacodynamic drug interactions

+types

A

drugs effect on body

summation (1+1=2)
synergism (1+1 >2)
antagonism (1+1=0)
potentialism (1+1=1+1.5)

71
Q

pharmacokinetic drug interaction

A

body’s effect on drug

ADME
absorption
distribution
metabolism
excretion
72
Q

absoprtion pharmacokinetics

A
  • 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
Q

what drug molecules can cross membrane (absorption)

A

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
Q

enzyme induction/inhibition in regard to pharmacokinetic metabolism

A

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
Q

excretion pharmacokinetics

A

neutralisation of acid increases excretion speed

this doesnt happen for alkali neutralisation though

76
Q

is warfarin highly protein bound or highly unbound

A

protein bound – less effect

77
Q

ligandability

A

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
Q

types of drug target

A

rreceptor,
enzymes,
transporters,
ion channels

79
Q

types of receptor

A
  • 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
Q

what type of drug target do beta adrenoreceptors work on

A

g protein coupled receptors (receptor)

81
Q

what type of drug target do nicotinic ACh work on

A

ligand gated ion channels (receptor)

82
Q

what type of drug target do growth hormones work on

A

kinase linked receptors

83
Q

what type of drug target do steroid hormones work on

A

nuclear receptors

they can go intracellular!

84
Q

G proteins swithed on/off when…

A 
on= bound to GDP
off= bound to GTP

so GDP/GTP regulate this receptor activity

85
Q

what type of drug target does histamine work on

A

g protein coupled receptors (receptor)

86
Q

affinity

A

how well ligand binds to receptor

Applies to agonist and antagonist

87
Q

efficacy

A

how well ligand activates a receptor

Applies to agonists only

88
Q

receptor reserve

A

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
Q

how do statins work

A

block rate limiting step in cholesterol synthesis

enzyme inhibition

90
Q

autonomic ganglia pathways - receptors and neurotransmitter and length of fibres eg to affect on heart

A 
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
Q

types of muscarinic receptors

A

M1- brain
M2- heart
M3 - glandular and smooth muscle
M4/5- CNS

92
Q

what are each of these (drug types):
pilocarpine
atropine
hyoscine

A

muscarinic agonist
pilocarpine

muscarinic antagonist
atropine
hyoscine

93
Q

treatment of bronchoconstriction

A

block M3 - anticholinergics or antimuscarinics

94
Q

parasympathetic effect on salivary glands/sweating

A

stimulates salivary gland

no effect on sweat glands (these are triggered with symp)

95
Q

name 3 catecholamines

A

noradrenaline
adrenaline
dopamine (this is the precursor! to nor/adrenaline)

96
Q

what manages (Regulates):

  • anaphylactic
  • shock
A
  • adrenaline

- noradrenaline

97
Q

types of adrenergic receptors

A 
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
Q

example of alpha muscarinic receptor agonist

A 
shock treatment
(vasoconstriction)

think adrenaline is correct!

99
Q

example of alpha muscarinic receptor antagonist

A

decrease prostate hypertrophy
lower BP
(vasodilation)

100
Q

example of beta muscarinic receptor agonist

A

asthma treatment (relaxation)
overactive bladder treatment
but- s/e high HR

101
Q

example of beta muscarinic receptor antagonist

A

beta blockers

- but side effect = bronchoconstriction

102
Q

codeine the drug

A

= prodrug

metabolised in liver to morphine

103
Q

antagonist to opioids

104
Q

morphine orally

when is morphine dangerous to give

A

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
Q

what type of drug target do opioids work on

A

g protein coupled receptors

106
Q

opioid action of opioids

A

g protein coupled receptors (MOP, KOP, DOP, NOP receptors)

inhibit release of pain transmitter in CNS

107
Q

stomach and intestines - they absorb what pH of drugs

A 
stomach = weak acidic drugs
intestine= weak base drugs
108
Q

ATP binding cassette (ABC)

A

this is a carrier that moves drugs across membranes

109
Q

liver metabolism of drug

A

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
Q

advantage of drug routes:

transcutaneous
intradermal/subcut 
intramuscular
intranasal
inhalational
A
  • 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
Q

urine excretion equation

A

urine excretion = glomerular filtration + tubular secretion - reabsorption

112
Q

first order kinetics

zero order kinetics

A

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
Q

HALF LIFE
definition
and symbol
and equation

A

time taken for drug conc in plasma to half

T1/2
= 0.693 / K

114
Q

BIOAVAILABILITY
symbol
of IV
of oral

A

f = 1 (100% reaches circulation)

f> 1 (incomplete absorption)

115
Q 
DISTRIBUTION
defintion
symbol
calculation : 50 ml drug given and now there is 2mg/L plasma conc
depends on
A

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
Q 
CLEARANCE
definition
symbol
equation
x2
A

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
Q

STEADY STATE
definition
symbol
equation

A

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
Q

loading dose vs maintaing dose

equations

A

loading dose = Css x Vd

maintainind dose. = Css x t/f x Cl

119
Q

what determines how long a drug will take to reach Css (steady state)

A

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
Q

adverse drug reaction
definition
types

A

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
Q

are side effects the same as adverse drug reaction?

A

no. side effects can be adverse drug reactions but are not always noxious

122
Q

rawlins thompson classification of adverse drug reaction

A

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
Q

DoTS of adverse drug reactions

A

dose relatedness
timing
susceptibility of patient

124
Q

risk factors for adverse drug reactions

A 
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
Q

ADR (adverse drug reaction) yellow card

A

used to report ADRs
by doctor
spot trends early so can be monitored for safety

126
Q

non-immunological allergic reaction

A

mast cell degranulation caused by drugs (allergen)

no prior exposure

127
Q

are all allergic reactions immediate like anaphylaxis

A

no

eg hepatitis, some rashes

128
Q

types of anaphylaxis

A

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
Q

urticaria =

A

rash
itchy
red bumps

aka hives

130
Q

types of death (as referred to coroners)

A

presumed natural (cause of death not known) – majoirty

presumed iatrogenic (complications of therapy inc surgery, anaesthetic)

presumed unnatural (accidents, neglect, murder)

131
Q

how do fibroblasts respond to chronic inflammation and repair

A

form collagen (fibrosis)

132
Q

how do vessels respond to acute inflammation

133
Q

outcomes of acute inflammation

A

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
Q

why dont clots form normally

A

laminar flow

endothelial cells are not sticky when healthy

135
Q

thrombus formation steps

A
  • 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
Q

venous embolism will lodge?

A

pulmonary arteries

vena cava –>lung, acts as a filter (vessels split to capillary size)

137
Q

end artery supply =

A

an organ that only receives blood supply from one artery

thrombosis more problematic

138
Q

name an example of a disease with a single gene disorder

name an example of a polygenic disorder

A

sickle cell anaemia

breast cancer

139
Q

carcinogenic
oncogenic
mutagenic

A 
cancer causing (malignant)
tumour causing (benign and malignant)
mutation causing
140
Q

in situ neoplasia only applies to what kind of neoplasms

A

epithelial

141
Q

stages of metastasis

A 
detachment
invasion (through basement membrane)
evasion of host defences
arrest
extravasation
vascularisation
142
Q

mechanisms of evading host defences

A

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

143
Q

herceptin action

A

this binds to Her2 protein so reduces the growth factor produced to slow growth in breast cancer

144
Q

describe a monocyte nucleus

A

Kidney shaped

145
Q

do these play a part in innate or adaptive immunity?

  • monocytes (macrophages)
  • neutophils
  • t lymphocytes
  • b lymphocytes
A

innate and adaptive

innate

adaptive

adaptive

146
Q

list the immunoglobulins in order of majority

147
Q

what are immunoglobulins made of

A

glycoproteins

148
Q

epitope=

A

part of antigen that binds to antibody/receptor binding site

149
Q

sebum=

A

skin secretions. these are part of innate immunity

150
Q

name 3 pathogens lacking vaccine

A

herpes simplex virus
malaria
HIV

151
Q

how are tumours recognised as foreign?

A

they express foreign antigens

TSA = tumour specific antigens (only on tumours)
TAA = tumour associated antigens (over-expressed on cancer cells)
152
Q

cancer immuno-surveilence

A

= elimination stage of immunoediting

attacks tumour with immune system to protect tissue, to return it to normal tissue

153
Q

cancer immunoediting

3 phases

A

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
Q

potency=

A

conc of agonist that gives half Emax (theoretical maximum response of agonist ie infinity high agonist conc)

155
Q

gene therapy

A

recombinant (multisourced) nucleic acid used to regulate /replace/ add /delete a genetic sequence

156
Q

irreversible drug binding- is this good or bad

A

equivalent to elimination! bad! cannot re-enter circulation

phase 2a mine (38 decks)

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