immune system Flashcards

(215 cards)

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
what is the stratum granulosum
thin granular layer keratinocytes accumulate granules of keratin as they migrate towards the surface > secrete keratin into extracellular space
26
what is the stratum lucidum
thin clear layer of cells starting to die filled w intermediate form of keratin only seen in thick skin (palms and soles)
27
what is the stratum corneum
outermost layer > multiple layers of dead cells embedded in keratin waterproof barrier desquamation > cells shed very thick in thick skin
28
what are the four cell types in the epidermis
keratinocytes langerhan cells/dendritic cells melanocytes merkel cells
29
what are keratinocytes
provide protection by producing keratin
30
what are langerhan cells
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
31
what are melanocytes
produce melanin stratum basal ingested by keratinocytes > moved to apex to protect nucleus > protects DNA from photo damage
32
what are merkel cells
mechanoreceptors > respond to stretch or torque in highly sensitive skin long processes that interact w cells across different layers reside in stratum basal
33
describe keratinisation
as keratinocytes move towards surface of skin > increased keratin production > cells flatten + nuclei disappear > layers or keratinised cells form stratum corneum
34
how long does it take for skin to regenerate completely
approx 28 days
35
contrast thin and thick skin
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
36
why is there a corrugated interface in the junction b/w epidermis and dermis
increase SA > adds strength > ensures integrity of the joining of the two layers
37
describe the dermis
two layers: papillary dermis and reticular dermis papillary dermis - loose CT reticular dermis - dense CT w thick collagen fibres > provides strength
38
describe the hypodermis
layer of adipose tissue that underlines the skin
39
what is the function of the hypodermis
insulation energy storage cushioning
40
what are the ancillary structures in the integumentary system
nerves sweat glands hair/hair follicles
41
describe the role of nerves in the integumentary system
sensing temp, touch, pain and pressure high density of nerve endings each sense has its own nerve fibre
42
what are the two types of sweat glands in the integumentary system
merocrine (eccrine) apocrine
43
describe merocrine sweat glands
widely distributed secrete sweat directly onto skin surface
44
describe apocrine sweat glands
areas of hair e.g under arms connected to hair follicles so that hair shaft can move secretions onto surface
45
what are the two portions of the sweat glands and what do they do
secretory portion which make and release sweat duct portion which sweat travels along
46
what is the function of sweat glands in the integumentary system
thermoregulation waste removal
47
what do hair and hair follicles do in the integumentary system
involved in touch sensation and thermoregulation has sebaceous glands and arrector pilli muscles
48
describe thermoregulation in cold environments
cold > vasoconstriction > blood away from surface of skin > arrector pilli muscles contract > trap heat
49
describe thermoregulation in hot environments
heat > vasodilation > blood towards surface of skin > swear glands > sweat > evaporation > arrector pilli muscles relax > heat escape
50
what is the function of barriers to infection
prevents pathogens from crossing epithelia and colonising tissues
51
describe the anatomical barrier mucous membranes
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
52
describe the anatomical barrier commensal microbes
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)
53
can commensal microbes causes disease
yes under some circumstances for example, when the body is immunocompromised the commensal bacteria becomes opportunistic and takes over
54
describe the soluble barrier antimicrobial peptides (AMPs)
cationic proteins that disrupt membrane integrity or cell anabolism e.g Defensins produced by keratinocytes, mucosa, neutrophils, macrophages
55
do AMPs bind and destroy eukaryotic membranes
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
56
describe the soluble barrier complement system
complement activation > cascade activation of complement proteins > opsonisation, initiation of inflammatory response, punching of hole in cell membranes
57
what are the 3 types of complement activation
classical pathway alternative pathway lectin pathway
58
what happens in the classical pathway of complement activation
complement component recognises antibody-antigen complex
59
what happens in the alternative pathway of complement activation
complement component binds generally on to microbe surface
60
what happens in the lectin pathway of complement activation
complement component binds onto sugar residues on bacteria surface
61
what is opsonisation
complement protein coats surface w C3b proteins to promote phagocytosis
62
what happens to initiate inflammatory response
release of anaphylatoxins > binds to immune cells to trigger inflammatory response / chemoattractants to phagocytes
63
what happens in the punching of holes in cell membranes
formation of membrane attack complex (MAC) on surface of target cells
64
describe the soluble barrier opsonins
they are soluble proteins tag microbes so that it is easier fro phagocytes to eliminate
65
what are the professional phagocytes
neutrophils and macrophages
66
what is the difference b/w apoptosis and phagocytosis
apoptosis is of infected/tumour cells by NK cells phagocytosis is of extracellular bacteria by professional phagocytes
67
what are the 2 major mechanisms of endocytosis
pinocytosis (non specific) receptor-mediated (specific)
68
explain the process of phagocytosis
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
69
what triggers phagocytosis
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
70
explain the role of NK cells
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
71
how are NK cells made in haematopoiesis
haematopoietic stem cell > common lymphoid progenitor > NK cells made in bone marrow, mature in thymus
72
how are CD4 and CD8 t cells made in haematopoiesis
haematopoietic stem cell > common lymphoid progenitor > T pre cursor > CD4 and CD8 made in bone marrow, mature in thymus
73
how are B cells made in haematopoiesis
haematopoietic stem cell > common lymphoid progenitor > B precursor > B cell made in bone marrow, mature in bone marrow
74
how are granulocytes made in haematopoiesis
haematopoietic stem cell > common myeloid progenitor > granulocytes (neutrophils, eosinophils, basophils) made in bone marrow, mature in bone marrow
75
how are platelets made in haematopoiesis
haematopoietic stem cell > common myeloid progenitor > megakaryocyte > platelets made in bone marrow
76
how are erythrocytes made in haematopoiesis
haematopoietic stem cell > common myeloid progenitor > erythroblast > erythrocytes made in bone marrow
77
how are macrophages made in haematopoiesis
haematopoietic stem cell > common myeloid progenitor > monocyte > macrophage made in bone marrow, mature in tissue
78
how are dendritic cells made in haematopoiesis
haematopoietic stem cell > common myeloid progenitor > monocyte > dendritic cell made in bone marrow, mature in tissue
79
what are primary lymphoid organs
where lymphocytes undergo ontogeny that is, they develop into mature B and T cells ie in bone marrow and thymus
80
what happens during lymphocyte ontogeny
B and T cells develop receptors to recognise non self antigens
81
what occurs at secondary lymphoid organs
mature lymphocytes encounter antigen and differentiate into effector cells (t helper cell, cytotoxic t cell, plasma cell)
82
what are the two secondary lymphoid organs
lymph nodes spleen
83
function of the lymph node
filters tissue borne antigens lymph enters via the afferent lymphatic vessel, filters through the parenchyma, leaves via efferent lymphatic vessel
84
function of the spleen
organ that filters blood-borne antigen
85
function of mucosal-associated lymphoid tissue (MALT)
filters mucosa-borne antigens
86
what are the lymph node vessels
afferent and efferent lymphatic vessels lymphatic artery lymphatic vein
87
what is the functional tissue of the lymph node known as
parenchyma
88
what are the major regions of the parenchyma
cortex - predominant B cells arranged in primary and secondary follicles paracortex - predominantly T cells medulla - populated by both B and T cells
89
how does lymphocyte trafficking occur
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
what are cytokines
intercellular communicators > secreted to communicate w another cell (receiver cell must have corresponding receptor)
91
what are the 3 cytokine actions
autocrine (self) paracrine (neighbour cell) endocrine (distant via blood)
92
what are actions of interleukins (IL)
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
what are interferons (IFN)
fight against virus infection IFN alpha and IFN beta inhibits viral replication in neighbouring cells
94
what are chemokine
chemotactic cytokine > recruitment of cells IL-8 released by macrophage > 'trail' that extravasated neutrophil follows
95
what MHC marker do CD8 t cells recognise peptides on
MHC 1
96
what MHC marker do CD4 t cells recognise peptides on
MHC 2
97
does MHC 1 present endogenous or exogenous peptides
endogenous
98
does MHC 2 present endogenous of exogenous peptides
exogenous
99
where are MHC 1 markers found
all nucleated cells
100
where are MHC 2 markers found
antigen presenting cells (dendritic cells, macrophage, B cells)
101
describe the process of antigen processing w MHC 1
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
describe the process of antigen processing w MHC 2
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
what is MHC 1 used for
intracellular pathogen or tumour > initiate apoptosis CD8 T cells activate via MHC 1 > produce effector t cytotoxic cell > kill infected cell
104
what is MHC 2 used for
extracellular pathogens > produce antibody and phagocytosis CD4 T cells activate via MHC 2 > production of t helper cells
105
immunoglobulin vs antibody
Ig = structure Ab = function
106
describe IgM
pentametric 10 antigen binding sites binds to antigen in blood and tissue first Ig to be secreted
107
describe IgG
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
describe secretory IgA
dimeric 4 antigen binding sites binds to antigen in mucosa protected from enzymatic degradation by secretory component
109
where are Ig produced
By B cells in bone marrow
110
what are Ig expressed on surface of B cell called
B cell receptor
111
what do antibodies bind to
epitopes (antigenic determinants) on antigens > forms Ab-Ag complex (no covalent bonding)
112
what is the structure of Ig
4 polypeptides joined by disulphide bonds y shaped 2 light chains 2 heavy chains
113
what is the function of Ig
binds specifically to antigen base of molecule mediates biological activity
114
what are the 5 Ig isotypes
IgG IgA IgM IgE IgD
115
what are the roles of Ab
neutralisation - blocks binding to host cell agglutination - prevents colonisation opsonisation - enhances phagocytosis complement activation - leads to cell death
116
what is Ab affinity
strength of binding of Ab to antigen
117
why is a higher affinity better
higher affinity means an AbAg complex can form for longer so that biological functions can take place
118
how does the humeral response begin
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
describe the process of clonal selection
activated B cell proliferates to make clones of itself > differentiates into plasma (effector) cells and memory B cells expressing IgG
120
what do Plasma cells do
secrete IgM Ab into circulation to neutralise antigen
121
what do memory B cells do
remain in circulation in case of secondary exposure so that it can repeat the clonal proliferation process again
122
Do IgG also get secreted
yes they are secreted by plasma cells in the second encounter
123
describe the primary antibody response
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
why is there a large lag period at the start of the primary immune response
time for B cells to meet antigen, proliferate, make plasma cells that secrete antibodies
125
describe the secondary antibody response
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
why does the secondary response have a shorter lag phase
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
describe the activation of naive CD4 t cells into t helper cells
naive CD4 meets processed Ag on MHC 2 marker on antigen presenting cell > activates > clonal expansion > differentiates > T helper cell formed
128
describe the activation of naive CD8 t cells into cytotoxic t cells
naive CD8 meets processed Ag on MHC 1 marker AND receives cytokines from t helper > clonal expansion > differentiates > cytotoxic t cells formed
129
describe the role of T helper cells
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
what are the local vascular changes during an inflammatory response
vasodilation increased membrane permeability
131
describe the role of T cytotoxic cells
recognises peptide presented on MHC 1 on self cell > initiates apoptosis
132
describe the mechanism behind apoptosis
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
how do other immune cells contribute to cell mediated immunity
Antibody dependent cell cytotoxicity here immune cells detects antibodies binding onto target cell > things like apoptosis, phagocytosis and lytic enzymes
134
what is vaccination
process of getting a vaccine
135
what is immunisation
process of getting a vaccine and becoming immune to the disease
136
what is a vaccine
a weak (attenuated) form or part of an infections agent
137
what does immunisation do
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
vaccination of what leads to just humoral immunity
inactivated whole organism purified or recombinant subunit > do not enter the cell
139
vaccination of what leads to both humoral and cell mediated immunity
live attenuated mRNA > enters cell
140
what are the 4 types of vaccines
live attenuated inactivated vaccines = whole organism purified subunit cloned = part of organism
141
how does vaccination stimulate antibody production
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
describe formation of live attenuated vaccines
virus passed on from one culture to another > accumulates genetic mutations > acclimatises to new environment > becomes attenuated
143
what are the pros and cons of live attenuated vaccine
pros single dose only imparts life long humoral and CMI cons reversion to wild type
144
describe formation of inactivated vaccines
virus injected into chicken egg > viral replication > harvest virus > inactivate w beta-propiolactone
145
what are the pros and cons of inactivated vaccines
pros stimulates humoral immunity no reversion to wild type cons little to no CMI more than one dose required contains egg product
146
describe formation of purified subunit vaccines
break up bacteria > isolate capsular polysaccharides > conjugate to protein > vaccine stimulates production of IgM and IgG and B memory cells
147
pros and cons of purified subunit vaccines
pros stimulates humoral immunity no chance of reverting to wild type cons little to no CMI more than one dose required
148
describe formation of cloned vaccines
isolate genetic material and produce recombinant products
149
pros and cons of cloned vaccines
pros stimulates humoral immunity no reversion to wild type cons multiple doses required
150
what is an adjuvant
substance that enhances immune response
151
why are vaccines sometimes administered w an adjuvant
slow release of vaccine > prevents it from being cleared too quickly > greater antibody response
152
what is passive immunity
transfer of ready made antibodies from one person to another > short lived and no memory e.g breastfeeding
153
what is inflammation
protective response designed to rid the organism of both the cause of injury and the consequences of the injury linked to healing/repair
154
what are the key components of inflammation
blood components blood vessels and endothelium chemical mediators cellular and extracellular components of CT
155
what are the type types of inflammation
acute and chronic
156
what is acute inflammation
occurs directly after injury lats for minutes, hours or days immediate vasodilation and increased vessel permeability
157
what are causes of acute inflammation
infections trauma infarction
158
what are aims of acute inflammation
deliver nutrients and defence cells destroy any infective agents remove debris
159
what are clinical effects and causes of acute inflammation
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
what are systemic effects of acute inflammation
malaise myalgia arthralgia decreased appetite leukocytosis fever
161
what are features of acute inflammation
vascular and cellular response chemical mediators exudate variable tissue necrosis
162
explain vascular and cellular response in acute inflammation
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
what is the main cell type in acute inflammation
neutrophils
164
what is neutrophilia
increase in neutrophil count in blood
165
what are some chemical mediators of acute inflammation and what do they do
histamine - vasodilation, increase vascular permeability serotonin - vasodilation, increase vascular permeability prostaglandins - vasodilation, pain, fever
166
what is exudate
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
what is the function of exudate
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
what are the 4 types of acute inflammatory exudate
serous fibrinous purulent hemorrhagic
169
describe serous exudate
generally less serious thin fluid e.g blister
170
describe fibrinous exudate
large amounts of fibrin common in membrane lined cavities e.g pericarditis
171
describe purulent exudate
large quantities of pus e.g brain meningitis
172
describe hemorrhagic exudate
many red blood cells due to ruptured blood vessels
173
what are the 3 outcomes of acute inflammation
resolution repair chronic inflammation
174
describe the resolution outcome of acute inflammation
return of damaged tissue to normal minimal damage
175
describe the repair outcome of acute inflammation
damaged tissue must undergo repair scar tissue formation healed tissue may differ from original tissue
176
describe the chronic inflammation outcome of acute inflammation
damaged tissue unable to repair itself bc persisting damage stimulus
177
what is chronic inflammation
inflammation of prolonged duration persists until damaging stimulus is eradicated tissue cannot undergo resolution
178
causes of chronic inflammation
unresolved acute inflammation prolonged exposure to potentially toxic endogenous/exogenous agents immune-mediated
179
explain unresolved acute inflammation causing chronic inflammation
e.g osteomyelitis persistent infection in bone
180
explain exposure to potentially toxic agents causing chronic inflammation
e.g wear particles in prosthetic implant degradation over time > release toxic exogenous agents > granulomatous inflammation
181
explain immune-mediated cause of chronic inflammation
e.g rheumatoid arthritis autoimmune > destruction of articular cartilage
182
what are some common systemic effects of chronic inflammation
arthralgia myalgia fever chronic fatigue depression, anxiety
183
what are features of chronic inflammation
mononuclear cell infiltration tissue destruction attempts at healing via fibrosis and angiogenesis
184
what are the main cells involved in chronic inflammation
macrophage lymphocytes plasma cells
185
what are pros and cons of activated macrophages
positives increased lysosomal enzymes production of cytokines, growth factors, and other mediators negatives responsible for much of the tissue injury
186
what is a granulomatous inflammation
focal collections of macrophages, epitheloid cells, and multinucleate giant cells that have a amassed substance they cannot digest
187
how does a granulomatous inflammation occur
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
what are other cells involved in chronic inflammation
fibroblast endothelial cells eosinophils
189
what are the two outcomes of chronic inflammation
organisation and repair - fibrosis / healed tissue will differ from original tissue / loss of function co morbidities - poor prognosis
190
chronic inflammation is a contributor to diseases such as...
cancer Alzheimers CVD CKD
191
what are the aims of wound healing
remove damaged tissue fill a gap caused by tissue destruction restore structural continuity restore function
192
what are the two types of wound healing
regenerative - tissue replaced w functional tissue non regenerative - replacement of tissue w CT (scar)
193
which cells can undergo regenerative healing
labile cells stable cells
194
what are the phases of wound healing
reactive phase reparative phase remodelling phase
195
describe the reactive phase of healing
haemostasis - platelet aggregation and clot formation inflammation - eliminate pathogens and limit damage
196
describe the reparative phase of healing
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
describe the remodelling phase of healing
scar formation realignment of tissue
198
what is primary intention healing
occurs in wounds w dermal edges that are close together closer occurs fast (approx a week) complete return to function w minimal scarring
199
secondary intention healing
sides of wound are not opposed healing occurs from bottom of wound upwards much larger amounts of granulation tissue > scarring
200
what is the function of granulation tissue
protects wound surface fills wound from its base w new tissue and vasculature replaces necrotic tissue
201
what are components of granulation tissue
new, thin walled blood vessels fibroblasts keratinocytes endothelial cells inflammatory cell infiltration of ECM
202
describe the sequential change in granulation tissue
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
what are the four stages of fracture healing
formation of a haematoma and granulation tissue formation of a soft callus conversion to a hard callus remodelling
204
what are factors that influence wound healing
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
what is a hypersensitivity reaction
inappropriate and/or exaggerated response to an antigen
206
what is the consequence of a hypersensitivity reaction
over reacting inflammatory response and destruction of innocent cells
207
what are the 4 types of hypersensitivity reactions
type 1 - immediate type 2 - cytotoxic type 3 - immune complex type 4 - delayed type hypersensitivity
208
describe type 1 hypersensitivity reactions
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
describe asthma as a type 1 hypersensitive reaction
deep in lung eosinophils play major role chronic inflammation
210
what are treatment options for type 1 HS reactions
avoidance histamine receptor blocking puffer monoclonal antibody therapy desensitisation
211
describe type 4 hypersensitivity reactions
cell mediated (no antibody) symptoms develop days after exposure e.g contact dermatitis , granulomatous disease
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how does screening/central tolerance of T cells occur
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
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how does screening/central tolerance of B cells occur
in bone marrow cells w BCRs against self are apoptosed while cells w BCRs against non self become mature/naive B cells
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how do autoimmune diseases occur
some T and B cells escape the screening process during central tolerance > self reactive lymphocytes
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what are some examples of autoimmune diseases and their self antigen and immune effector
T1 diabetes - pancreatic beta cells - autoantibodies and Th cells MS - brain white matter - Th, Tc and autoantibodies rheumatoid arthritis - CT, IgG - autoantibodies