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FOM sem 1 > immune system > Flashcards

immune system Flashcards

1
Q

describe viruses

A

obligate intracellular parasites

hijacks host machinery to propogate themselves

ability to evade our immune defences (virulence factor)

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2
Q

describe bacteria

A

singe cell prokaryotes

extracellular/intracellular

virulence is factors they produce e.g toxins, enzymes, motility etc

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3
Q

what are the two types of immunity

A

innate and adaptive

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4
Q

what are the three components of innate immunity

A

static/anatomical barriers
soluble barriers
cellular barriers

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5
Q

what are examples of static barriers

A

skin
mucosa
stomach acid
tears
microbiome

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6
Q

what are examples of soluble barriers

A

antimicrobial peptides
complement proteins
cytokines
opsonins

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7
Q

what are examples of cellular barriers

A

macrophages
neutrophils
NKC
basophil/mast cell
dendritic cells

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8
Q

what are examples of the cells in the adaptive immunity

A

t cells (CD4 and CD8)
b cells

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9
Q

what do NKC do

A

kills by apoptosis

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10
Q

what do neutrophils do

A

phagocytose bacteria and viruses

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11
Q

what do basophilss/mast cells do

A

inflammatory response

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12
Q

what do macrophages do

A

phagocytose bacteria and viruses

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13
Q

what do dendritic cells do

A

links to adaptive immunity by presenting antigens on surface to activate t cells

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14
Q

what do CD4 t cells do

A

secrete cytokines to help other cells (t helper cell)

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15
Q

what do CD8 t cells do

A

kills by apoptosis

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16
Q

what do B cells do

A

divide and differentiate into plasma cells which secrete antibodies

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17
Q

contrast the innate and adaptive immune responses

A

innate is non specific whereas adaptive is specific

innate has already formed barriers to combat pathogens whereas the adaptive takes time to build up defence

innate recognises common components of pathogens whereas adaptive recognises any pathogen

innate has no memory whereas adaptive does

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18
Q

what is the intugementary system comprised of

A

skin and accessory organs

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19
Q

what is the function of the integumentary system

A

protection
immunity
sensation
thermoregulation
water balance
waste excretion
vit D production

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20
Q

what are the 3 layers of the skin

A

epidermis (outermost layer/epithelial tissue)

dermis (CT)

hypodermis (adipose tissue)

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21
Q

describe the epidermis

A

stratified squamous keratinised epithelium that is avascular and contains a basement membrane that attaches to CT and is semipermeable

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22
Q

what are the 5 layers of the epidermis

A

stratum corneum
stratum lucidum
stratum granulosum
stratum spinosum
stratum basal

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23
Q

what is the stratum basal

A

bottom most layer of epidermis containing single layer of epithelial cells

germinating layer (i.e stem cells where keratinocytes start to grow)

constantly dividing

tightly bound to underlying CT

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24
Q

what is the stratum spinosum

A

has spiny projections of desmosome microfilaments > maintenance and structural integrity which assist in holding the cells tightly together and giving the skin strength, resilience and flexibility

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25
Q

what is the stratum granulosum

A

thin granular layer

keratinocytes accumulate granules of keratin as they migrate towards the surface > secrete keratin into extracellular space

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26
Q

what is the stratum lucidum

A

thin clear layer of cells

starting to die

filled w intermediate form of keratin

only seen in thick skin (palms and soles)

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27
Q

what is the stratum corneum

A

outermost layer > multiple layers of dead cells embedded in keratin

waterproof barrier

desquamation > cells shed

very thick in thick skin

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28
Q

what are the four cell types in the epidermis

A

keratinocytes
langerhan cells/dendritic cells
melanocytes
merkel cells

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29
Q

what are keratinocytes

A

provide protection by producing keratin

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30
Q

what are langerhan cells

A

cells of the immune system
antigen presenting cells
derived from bone marrow
mostly in stratum spinosum

bone marrow > in blood as monocyte > differentiate into langerhan cell > ingest > digest > present antigen > lymph node > warn others

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31
Q

what are melanocytes

A

produce melanin
stratum basal

ingested by keratinocytes > moved to apex to protect nucleus > protects DNA from photo damage

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32
Q

what are merkel cells

A

mechanoreceptors > respond to stretch or torque
in highly sensitive skin
long processes that interact w cells across different layers
reside in stratum basal

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33
Q

describe keratinisation

A

as keratinocytes move towards surface of skin > increased keratin production > cells flatten + nuclei disappear > layers or keratinised cells form stratum corneum

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34
Q

how long does it take for skin to regenerate completely

A

approx 28 days

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35
Q

contrast thin and thick skin

A

thin skin covers most of the body whereas thick is palms and soles

thin skin has a thin stratum corneum whereas thick skin has a thick stratum corneum

thin skin has no stratum lucidum whereas thick does

thin skin has hair follicles whereas thick does not

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36
Q

why is there a corrugated interface in the junction b/w epidermis and dermis

A

increase SA > adds strength > ensures integrity of the joining of the two layers

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37
Q

describe the dermis

A

two layers: papillary dermis and reticular dermis

papillary dermis - loose CT

reticular dermis - dense CT w thick collagen fibres > provides strength

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38
Q

describe the hypodermis

A

layer of adipose tissue that underlines the skin

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39
Q

what is the function of the hypodermis

A

insulation
energy storage
cushioning

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40
Q

what are the ancillary structures in the integumentary system

A

nerves
sweat glands
hair/hair follicles

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41
Q

describe the role of nerves in the integumentary system

A

sensing temp, touch, pain and pressure

high density of nerve endings

each sense has its own nerve fibre

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42
Q

what are the two types of sweat glands in the integumentary system

A

merocrine (eccrine)
apocrine

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43
Q

describe merocrine sweat glands

A

widely distributed
secrete sweat directly onto skin surface

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44
Q

describe apocrine sweat glands

A

areas of hair e.g under arms
connected to hair follicles so that hair shaft can move secretions onto surface

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45
Q

what are the two portions of the sweat glands and what do they do

A

secretory portion which make and release sweat

duct portion which sweat travels along

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46
Q

what is the function of sweat glands in the integumentary system

A

thermoregulation
waste removal

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47
Q

what do hair and hair follicles do in the integumentary system

A

involved in touch sensation and thermoregulation

has sebaceous glands and arrector pilli muscles

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48
Q

describe thermoregulation in cold environments

A

cold
> vasoconstriction > blood away from surface of skin
> arrector pilli muscles contract > trap heat

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49
Q

describe thermoregulation in hot environments

A

heat
> vasodilation > blood towards surface of skin
> swear glands > sweat > evaporation
> arrector pilli muscles relax > heat escape

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50
Q

what is the function of barriers to infection

A

prevents pathogens from crossing epithelia and colonising tissues

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51
Q

describe the anatomical barrier mucous membranes

A

has mucus which is produced by goblet cells > it is highly viscous so it traps microbes

has cilia which are hair like projections > propel microbes out of tracts

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52
Q

describe the anatomical barrier commensal microbes

A

digest dietary fibres > produce metabolites, vitamins, short chain fatty acids > maintain healthy colon

competes w pathogenic microbes for nutrients and space

release antimicrobial substances (lactic acid and bacteriocins)

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53
Q

can commensal microbes causes disease

A

yes under some circumstances
for example, when the body is immunocompromised the commensal bacteria becomes opportunistic and takes over

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54
Q

describe the soluble barrier antimicrobial peptides (AMPs)

A

cationic proteins that disrupt membrane integrity or cell anabolism

e.g Defensins

produced by keratinocytes, mucosa, neutrophils, macrophages

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55
Q

do AMPs bind and destroy eukaryotic membranes

A

no
since they are cationic and bacterial membranes have a negative charge, they are more drawn to that

mammalian membranes have cholesterol which makes the membrane not have a negative charge so it doesn’t attract AMPs

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56
Q

describe the soluble barrier complement system

A

complement activation > cascade activation of complement proteins > opsonisation, initiation of inflammatory response, punching of hole in cell membranes

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57
Q

what are the 3 types of complement activation

A

classical pathway
alternative pathway
lectin pathway

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58
Q

what happens in the classical pathway of complement activation

A

complement component recognises antibody-antigen complex

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59
Q

what happens in the alternative pathway of complement activation

A

complement component binds generally on to microbe surface

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60
Q

what happens in the lectin pathway of complement activation

A

complement component binds onto sugar residues on bacteria surface

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61
Q

what is opsonisation

A

complement protein coats surface w C3b proteins to promote phagocytosis

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62
Q

what happens to initiate inflammatory response

A

release of anaphylatoxins > binds to immune cells to trigger inflammatory response / chemoattractants to phagocytes

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63
Q

what happens in the punching of holes in cell membranes

A

formation of membrane attack complex (MAC) on surface of target cells

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64
Q

describe the soluble barrier opsonins

A

they are soluble proteins

tag microbes so that it is easier fro phagocytes to eliminate

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65
Q

what are the professional phagocytes

A

neutrophils and macrophages

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66
Q

what is the difference b/w apoptosis and phagocytosis

A

apoptosis is of infected/tumour cells by NK cells

phagocytosis is of extracellular bacteria by professional phagocytes

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67
Q

what are the 2 major mechanisms of endocytosis

A

pinocytosis (non specific)
receptor-mediated (specific)

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68
Q

explain the process of phagocytosis

A
  1. plasma membrane expands to form pseudopods
  2. pseudopods retract and seal off to form phagosome
  3. phagosome fuse w lysosome
  4. lysosome release lysozymes which break down the foreign material
  5. broken down material excreted by exocytosis
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69
Q

what triggers phagocytosis

A

recognition of microbes directly > pattern recognition receptors (PRRs) which sense common patterns like lipopolysaccharide

recognition of microbes indirectly > opsonin receptors e.g C3bR which detects the complement protein C3b

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70
Q

explain the role of NK cells

A
  1. recognises tumour/infected cell
  2. degranulation occurs ie NK cells release cytotoxic chemical
  3. infected cell self destructs into apoptotic bodies
  4. apoptotic bodies are detected and phagocytosed by professional phagocytes
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71
Q

how are NK cells made in haematopoiesis

A

haematopoietic stem cell > common lymphoid progenitor > NK cells

made in bone marrow, mature in thymus

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72
Q

how are CD4 and CD8 t cells made in haematopoiesis

A

haematopoietic stem cell > common lymphoid progenitor > T pre cursor > CD4 and CD8

made in bone marrow, mature in thymus

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73
Q

how are B cells made in haematopoiesis

A

haematopoietic stem cell > common lymphoid progenitor > B precursor > B cell

made in bone marrow, mature in bone marrow

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74
Q

how are granulocytes made in haematopoiesis

A

haematopoietic stem cell > common myeloid progenitor > granulocytes (neutrophils, eosinophils, basophils)

made in bone marrow, mature in bone marrow

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75
Q

how are platelets made in haematopoiesis

A

haematopoietic stem cell > common myeloid progenitor > megakaryocyte > platelets

made in bone marrow

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76
Q

how are erythrocytes made in haematopoiesis

A

haematopoietic stem cell > common myeloid progenitor > erythroblast > erythrocytes

made in bone marrow

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77
Q

how are macrophages made in haematopoiesis

A

haematopoietic stem cell > common myeloid progenitor > monocyte > macrophage

made in bone marrow, mature in tissue

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78
Q

how are dendritic cells made in haematopoiesis

A

haematopoietic stem cell > common myeloid progenitor > monocyte > dendritic cell

made in bone marrow, mature in tissue

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79
Q

what are primary lymphoid organs

A

where lymphocytes undergo ontogeny
that is, they develop into mature B and T cells ie in bone marrow and thymus

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80
Q

what happens during lymphocyte ontogeny

A

B and T cells develop receptors to recognise non self antigens

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81
Q

what occurs at secondary lymphoid organs

A

mature lymphocytes encounter antigen and differentiate into effector cells (t helper cell, cytotoxic t cell, plasma cell)

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82
Q

what are the two secondary lymphoid organs

A

lymph nodes
spleen

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83
Q

function of the lymph node

A

filters tissue borne antigens

lymph enters via the afferent lymphatic vessel, filters through the parenchyma, leaves via efferent lymphatic vessel

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84
Q

function of the spleen

A

organ that filters blood-borne antigen

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85
Q

function of mucosal-associated lymphoid tissue (MALT)

A

filters mucosa-borne antigens

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86
Q

what are the lymph node vessels

A

afferent and efferent lymphatic vessels
lymphatic artery
lymphatic vein

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87
Q

what is the functional tissue of the lymph node known as

A

parenchyma

88
Q

what are the major regions of the parenchyma

A

cortex - predominant B cells arranged in primary and secondary follicles

paracortex - predominantly T cells

medulla - populated by both B and T cells

89
Q

how does lymphocyte trafficking occur

A

lymphocytes enter node via artery > through high endothelial venue into paracortex > T cells stay in paracortex while B cells migrate into cortex > B cells meet antigens > when it is time to leave, both B and T cells leave via efferent vessel

90
Q

what are cytokines

A

intercellular communicators > secreted to communicate w another cell (receiver cell must have corresponding receptor)

91
Q

what are the 3 cytokine actions

A

autocrine (self)
paracrine (neighbour cell)
endocrine (distant via blood)

92
Q

what are actions of interleukins (IL)

A

inflammatory response
> macrophage releases TNF-alpha and IL-1 beta > binds to receptor > neutrophil binds to homing receptor > extravasates

proliferation
> CD4 releases IL-2 > autocrine > CD4 proliferates

93
Q

what are interferons (IFN)

A

fight against virus infection

IFN alpha and IFN beta inhibits viral replication in neighbouring cells

94
Q

what are chemokine

A

chemotactic cytokine > recruitment of cells

IL-8 released by macrophage > ‘trail’ that extravasated neutrophil follows

95
Q

what MHC marker do CD8 t cells recognise peptides on

A

MHC 1

96
Q

what MHC marker do CD4 t cells recognise peptides on

A

MHC 2

97
Q

does MHC 1 present endogenous or exogenous peptides

A

endogenous

98
Q

does MHC 2 present endogenous of exogenous peptides

A

exogenous

99
Q

where are MHC 1 markers found

A

all nucleated cells

100
Q

where are MHC 2 markers found

A

antigen presenting cells (dendritic cells, macrophage, B cells)

101
Q

describe the process of antigen processing w MHC 1

A

endogenous protein > digested into short peptides > peptides taken into ER > loaded onto MHC 1 marker > MHC 1 exported to surface > MHC 1 expressed on surface of nucleated cell

102
Q

describe the process of antigen processing w MHC 2

A

uptake of exogenous antigen > digested in endoscope > MHC 2 enters endoscope > peptide loaded onto MHC 2 > MHC 2 expressed on surface of antigen presenting cell

103
Q

what is MHC 1 used for

A

intracellular pathogen or tumour > initiate apoptosis

CD8 T cells activate via MHC 1 > produce effector t cytotoxic cell > kill infected cell

104
Q

what is MHC 2 used for

A

extracellular pathogens > produce antibody and phagocytosis

CD4 T cells activate via MHC 2 > production of t helper cells

105
Q

immunoglobulin vs antibody

A

Ig = structure
Ab = function

106
Q

describe IgM

A

pentametric
10 antigen binding sites
binds to antigen in blood and tissue
first Ig to be secreted

107
Q

describe IgG

A

monomeric
2 antigen binding sites
binds to antigen in blood and tissue
high affinity
secreted on 2nd encounter w antigen
binds to Fc receptors on macrophage and neutrophils

108
Q

describe secretory IgA

A

dimeric
4 antigen binding sites
binds to antigen in mucosa
protected from enzymatic degradation by secretory component

109
Q

where are Ig produced

A

By B cells in bone marrow

110
Q

what are Ig expressed on surface of B cell called

A

B cell receptor

111
Q

what do antibodies bind to

A

epitopes (antigenic determinants) on antigens

> forms Ab-Ag complex (no covalent bonding)

112
Q

what is the structure of Ig

A

4 polypeptides joined by disulphide bonds
y shaped
2 light chains
2 heavy chains

113
Q

what is the function of Ig

A

binds specifically to antigen
base of molecule mediates biological activity

114
Q

what are the 5 Ig isotypes

A

IgG
IgA
IgM
IgE
IgD

115
Q

what are the roles of Ab

A

neutralisation - blocks binding to host cell

agglutination - prevents colonisation

opsonisation - enhances phagocytosis

complement activation - leads to cell death

116
Q

what is Ab affinity

A

strength of binding of Ab to antigen

117
Q

why is a higher affinity better

A

higher affinity means an AbAg complex can form for longer so that biological functions can take place

118
Q

how does the humeral response begin

A

B cells made in bone marrow > circulation > moves to secondary lymphoid tissue > here, there is a B cell repertoire waiting to meet an antigen

antigen > lymph node > recognised by appropriate (specific BCR) B cell

119
Q

describe the process of clonal selection

A

activated B cell proliferates to make clones of itself > differentiates into plasma (effector) cells and memory B cells expressing IgG

120
Q

what do Plasma cells do

A

secrete IgM Ab into circulation to neutralise antigen

121
Q

what do memory B cells do

A

remain in circulation in case of secondary exposure so that it can repeat the clonal proliferation process again

122
Q

Do IgG also get secreted

A

yes they are secreted by plasma cells in the second encounter

123
Q

describe the primary antibody response

A

1- lag period
2- initial spike of IgM
3- followed by rise in IgG
4- at the end, many B memory cels expressing IgGs are formed > primed against antigen

124
Q

why is there a large lag period at the start of the primary immune response

A

time for B cells to meet antigen, proliferate, make plasma cells that secrete antibodies

125
Q

describe the secondary antibody response

A

1- reduced lag period
2- initial spike of IgG 9much higher than the primary response)
3- followed by spike of IgM (similar to primary response)
4- at the end, more B memory cells expressing IgG are formed

126
Q

why does the secondary response have a shorter lag phase

A

there are already many B memory cells present, so it takes less time for the antigens to be recognised and for antibody secreting plasma cells to be produced

127
Q

describe the activation of naive CD4 t cells into t helper cells

A

naive CD4 meets processed Ag on MHC 2 marker on antigen presenting cell > activates > clonal expansion > differentiates > T helper cell formed

128
Q

describe the activation of naive CD8 t cells into cytotoxic t cells

A

naive CD8 meets processed Ag on MHC 1 marker AND receives cytokines from t helper > clonal expansion > differentiates > cytotoxic t cells formed

129
Q

describe the role of T helper cells

A

recognise peptide on MHC 2 marker on naive b cell > release cytokines > b cell activated > differentiate/proliferate > antibody production

release cytokines > activate macrophage > increased phagocytotic activity and increase expression of MHC 2

130
Q

what are the local vascular changes during an inflammatory response

A

vasodilation
increased membrane permeability

131
Q

describe the role of T cytotoxic cells

A

recognises peptide presented on MHC 1 on self cell > initiates apoptosis

132
Q

describe the mechanism behind apoptosis

A

immune cell recognises self cell > forms seal with a gap > immune cell releases perforins and granzymes which go towards the self cell through the gap > perforins attach to self cell to form pores > grazymes travel through pores > initiate apoptosis

133
Q

how do other immune cells contribute to cell mediated immunity

A

Antibody dependent cell cytotoxicity

here immune cells detects antibodies binding onto target cell > things like apoptosis, phagocytosis and lytic enzymes

134
Q

what is vaccination

A

process of getting a vaccine

135
Q

what is immunisation

A

process of getting a vaccine and becoming immune to the disease

136
Q

what is a vaccine

A

a weak (attenuated) form or part of an infections agent

137
Q

what does immunisation do

A

primes the immune system before a natural infection

lower chance of falling ill and lessens the severity due to the presence of more memory B cells and IgG

138
Q

vaccination of what leads to just humoral immunity

A

inactivated whole organism
purified or recombinant subunit

> do not enter the cell

139
Q

vaccination of what leads to both humoral and cell mediated immunity

A

live attenuated
mRNA

> enters cell

140
Q

what are the 4 types of vaccines

A

live attenuated
inactivated vaccines
= whole organism

purified subunit
cloned
= part of organism

141
Q

how does vaccination stimulate antibody production

A

vaccine > dendritic cell takes it up > presented on MHC2 to naive CD4 cells > CD4 activates and differentiates into T helper cells

B cell independently recognises vaccine > present on MHC2 > B cell also receive cytokines from t helper > B cell proliferate and differentiate into IgM producing plasma cells and IgG expressing memory B cells

142
Q

describe formation of live attenuated vaccines

A

virus passed on from one culture to another > accumulates genetic mutations > acclimatises to new environment > becomes attenuated

143
Q

what are the pros and cons of live attenuated vaccine

A

pros
single dose only
imparts life long humoral and CMI

cons
reversion to wild type

144
Q

describe formation of inactivated vaccines

A

virus injected into chicken egg > viral replication > harvest virus > inactivate w beta-propiolactone

145
Q

what are the pros and cons of inactivated vaccines

A

pros
stimulates humoral immunity
no reversion to wild type

cons
little to no CMI
more than one dose required
contains egg product

146
Q

describe formation of purified subunit vaccines

A

break up bacteria > isolate capsular polysaccharides > conjugate to protein > vaccine stimulates production of IgM and IgG and B memory cells

147
Q

pros and cons of purified subunit vaccines

A

pros
stimulates humoral immunity
no chance of reverting to wild type

cons
little to no CMI
more than one dose required

148
Q

describe formation of cloned vaccines

A

isolate genetic material and produce recombinant products

149
Q

pros and cons of cloned vaccines

A

pros
stimulates humoral immunity
no reversion to wild type

cons
multiple doses required

150
Q

what is an adjuvant

A

substance that enhances immune response

151
Q

why are vaccines sometimes administered w an adjuvant

A

slow release of vaccine > prevents it from being cleared too quickly > greater antibody response

152
Q

what is passive immunity

A

transfer of ready made antibodies from one person to another > short lived and no memory

e.g breastfeeding

153
Q

what is inflammation

A

protective response designed to rid the organism of both the cause of injury and the consequences of the injury

linked to healing/repair

154
Q

what are the key components of inflammation

A

blood components
blood vessels and endothelium
chemical mediators
cellular and extracellular components of CT

155
Q

what are the type types of inflammation

A

acute and chronic

156
Q

what is acute inflammation

A

occurs directly after injury
lats for minutes, hours or days
immediate vasodilation and increased vessel permeability

157
Q

what are causes of acute inflammation

A

infections
trauma
infarction

158
Q

what are aims of acute inflammation

A

deliver nutrients and defence cells
destroy any infective agents
remove debris

159
Q

what are clinical effects and causes of acute inflammation

A

redness - vasodilation and increase blood flow (hyperaemia)

heat - hyperaemia

pain - pressure on nerve endings

swelling - accumulation of exudate and hyperaemia

loss of function - direct local damage + combined effects of above

160
Q

what are systemic effects of acute inflammation

A

malaise
myalgia
arthralgia
decreased appetite
leukocytosis
fever

161
Q

what are features of acute inflammation

A

vascular and cellular response
chemical mediators
exudate
variable tissue necrosis

162
Q

explain vascular and cellular response in acute inflammation

A

vasodilation and increase blood flow which then slows down > vessels become leaky and permeable > exudation > neutrophils attracts to damaged area > macrophage and lymphocytes migrate to damaged area

163
Q

what is the main cell type in acute inflammation

A

neutrophils

164
Q

what is neutrophilia

A

increase in neutrophil count in blood

165
Q

what are some chemical mediators of acute inflammation and what do they do

A

histamine - vasodilation, increase vascular permeability

serotonin - vasodilation, increase vascular permeability

prostaglandins - vasodilation, pain, fever

166
Q

what is exudate

A

protein rich fluid and cells that have escaped from blood vessels due to increase vascular permeability

contains fluid, fibrin, many neutrophils and few macrophages

167
Q

what is the function of exudate

A

carries proteins, fluids and cells from local blood vessels into the damaged area to mediate local defences

destroy infective causative agent

breakdown and remove damaged tissue

168
Q

what are the 4 types of acute inflammatory exudate

A

serous
fibrinous
purulent
hemorrhagic

169
Q

describe serous exudate

A

generally less serious
thin fluid
e.g blister

170
Q

describe fibrinous exudate

A

large amounts of fibrin
common in membrane lined cavities
e.g pericarditis

171
Q

describe purulent exudate

A

large quantities of pus
e.g brain meningitis

172
Q

describe hemorrhagic exudate

A

many red blood cells due to ruptured blood vessels

173
Q

what are the 3 outcomes of acute inflammation

A

resolution
repair
chronic inflammation

174
Q

describe the resolution outcome of acute inflammation

A

return of damaged tissue to normal
minimal damage

175
Q

describe the repair outcome of acute inflammation

A

damaged tissue must undergo repair
scar tissue formation
healed tissue may differ from original tissue

176
Q

describe the chronic inflammation outcome of acute inflammation

A

damaged tissue unable to repair itself bc persisting damage stimulus

177
Q

what is chronic inflammation

A

inflammation of prolonged duration
persists until damaging stimulus is eradicated
tissue cannot undergo resolution

178
Q

causes of chronic inflammation

A

unresolved acute inflammation
prolonged exposure to potentially toxic endogenous/exogenous agents
immune-mediated

179
Q

explain unresolved acute inflammation causing chronic inflammation

A

e.g osteomyelitis
persistent infection in bone

180
Q

explain exposure to potentially toxic agents causing chronic inflammation

A

e.g wear particles in prosthetic implant
degradation over time > release toxic exogenous agents > granulomatous inflammation

181
Q

explain immune-mediated cause of chronic inflammation

A

e.g rheumatoid arthritis
autoimmune > destruction of articular cartilage

182
Q

what are some common systemic effects of chronic inflammation

A

arthralgia
myalgia
fever
chronic fatigue
depression, anxiety

183
Q

what are features of chronic inflammation

A

mononuclear cell infiltration
tissue destruction
attempts at healing via fibrosis and angiogenesis

184
Q

what are the main cells involved in chronic inflammation

A

macrophage
lymphocytes
plasma cells

185
Q

what are pros and cons of activated macrophages

A

positives
increased lysosomal enzymes
production of cytokines, growth factors, and other mediators

negatives
responsible for much of the tissue injury

186
Q

what is a granulomatous inflammation

A

focal collections of macrophages, epitheloid cells, and multinucleate giant cells that have a amassed substance they cannot digest

187
Q

how does a granulomatous inflammation occur

A

injury > inability to digest inciting agent > failure of acute inflammatory response > persistence of injurious agent > recruitment of macrophages w epitheloid and giant cell formation > granuloma

188
Q

what are other cells involved in chronic inflammation

A

fibroblast
endothelial cells
eosinophils

189
Q

what are the two outcomes of chronic inflammation

A

organisation and repair - fibrosis / healed tissue will differ from original tissue / loss of function

co morbidities - poor prognosis

190
Q

chronic inflammation is a contributor to diseases such as…

A

cancer
Alzheimers
CVD
CKD

191
Q

what are the aims of wound healing

A

remove damaged tissue
fill a gap caused by tissue destruction
restore structural continuity
restore function

192
Q

what are the two types of wound healing

A

regenerative - tissue replaced w functional tissue

non regenerative - replacement of tissue w CT (scar)

193
Q

which cells can undergo regenerative healing

A

labile cells
stable cells

194
Q

what are the phases of wound healing

A

reactive phase
reparative phase
remodelling phase

195
Q

describe the reactive phase of healing

A

haemostasis - platelet aggregation and clot formation

inflammation - eliminate pathogens and limit damage

196
Q

describe the reparative phase of healing

A

epithelialisation - epithelial layer begins to grow under clot

granulation tissue forms

myofibroblasts which have contractile properties contract the wound by drawing in edges of it

197
Q

describe the remodelling phase of healing

A

scar formation
realignment of tissue

198
Q

what is primary intention healing

A

occurs in wounds w dermal edges that are close together

closer occurs fast (approx a week)

complete return to function w minimal scarring

199
Q

secondary intention healing

A

sides of wound are not opposed

healing occurs from bottom of wound upwards

much larger amounts of granulation tissue > scarring

200
Q

what is the function of granulation tissue

A

protects wound surface
fills wound from its base w new tissue and vasculature
replaces necrotic tissue

201
Q

what are components of granulation tissue

A

new, thin walled blood vessels
fibroblasts
keratinocytes
endothelial cells
inflammatory cell infiltration of ECM

202
Q

describe the sequential change in granulation tissue

A
  1. vascular granulation tissue = newly formed capillaries, macrophages and support cells
  2. fibrovascular granulation tissue = proliferating fibroblasts, capillaries and macrophages
  3. fibrous granulation tissue = fibroblasts synthesise collagen and align themselves, contraction frequently occurs
203
Q

what are the four stages of fracture healing

A

formation of a haematoma and granulation tissue

formation of a soft callus

conversion to a hard callus

remodelling

204
Q

what are factors that influence wound healing

A

local factors
e.g infection, mechanical factors, foreign bodies, vascular supply, size, location

systemic factors
e.g poor nutrient supply, metabolic status, circulatory status, drug therapies, age-reduced collagen and fibroblast synthesis

205
Q

what is a hypersensitivity reaction

A

inappropriate and/or exaggerated response to an antigen

206
Q

what is the consequence of a hypersensitivity reaction

A

over reacting inflammatory response and destruction of innocent cells

207
Q

what are the 4 types of hypersensitivity reactions

A

type 1 - immediate
type 2 - cytotoxic
type 3 - immune complex
type 4 - delayed type hypersensitivity

208
Q

describe type 1 hypersensitivity reactions

A

IgE mediated (anaphylaxis)
allergens
atopic patients predisposed to producing high levels of IgE > produce IL4 and IL5 in response to allergens
degranulation (of histamine and serotonin) occurs very quickly

209
Q

describe asthma as a type 1 hypersensitive reaction

A

deep in lung
eosinophils play major role
chronic inflammation

210
Q

what are treatment options for type 1 HS reactions

A

avoidance
histamine receptor blocking
puffer
monoclonal antibody therapy
desensitisation

211
Q

describe type 4 hypersensitivity reactions

A

cell mediated (no antibody)
symptoms develop days after exposure

e.g contact dermatitis , granulomatous disease

212
Q

how does screening/central tolerance of T cells occur

A

in the thymus
TCRs generated in thymocytes > screen > cells w TCRs against self are apoptosed while cells w TCRs against non self become mature/naive t cells

213
Q

how does screening/central tolerance of B cells occur

A

in bone marrow
cells w BCRs against self are apoptosed while cells w BCRs against non self become mature/naive B cells

214
Q

how do autoimmune diseases occur

A

some T and B cells escape the screening process during central tolerance > self reactive lymphocytes

215
Q

what are some examples of autoimmune diseases and their self antigen and immune effector

A

T1 diabetes - pancreatic beta cells - autoantibodies and Th cells

MS - brain white matter - Th, Tc and autoantibodies

rheumatoid arthritis - CT, IgG - autoantibodies

FOM sem 1 (10 decks)

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