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Foundations of Medicine > Week 10 Science and Scholarship: Immune System > Flashcards

Week 10 Science and Scholarship: Immune System Flashcards

1
Q

name the 4 layers of immunity

A

static barriers
soluble barriers
cellular barriers
adaptive immunity

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2
Q

what are static barriers

A

-continous barrier
-first layer of defence that consists of skin, mucosa, stomach acid, tears and microbiome

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3
Q

what are soluble barriers

A

-work minutes/hours after exposure
-second layer of defence, consist of antimicrobial peptides, complements, opsonins and cytokines

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4
Q

what are cellular barriers

A

-work minutes/hours after exposure
-third layer of defence, consist of macrophages, neutrophils, NKC’s, basophils and dendritic cells

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5
Q

what is adaptive immunity

A

-works hours/days after exposure
-fourth layer of defence that consists of B and T cells

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6
Q

Contrast innate vs adaptive immunity

A

-innate people are born with, adaptive people acquire
-innate is front line defence, adaptive develops later
-innate recognises common pathogens, adaptive recognises all pathogens
-innate has no memory, adaptive has memory

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7
Q

name all the functions of the integumentary system

A

protection
immunity
sensation
thermoregulation
osmoregulation
Vitamin D production

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8
Q

how does the integumentary system ‘protect’

A

protects the body from UV radiation, infection and physical injury

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9
Q

how is the integumentary system involved with ‘immunity’

A

houses immune cells that help defend against pathogens and initiate immune responses

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10
Q

how is the integumentary system involved with ‘sensation’

A

contains sensory receptors that allow us to detect temperature, touch, pressure and pain

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11
Q

how is the integumentary system involved with ‘thermoregulation’

A

regulates body temperature via various mechanisms; sweating, vasodilation, vasoconstriction, shivering and

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12
Q

how is the integumentary system involved with ‘osmoregulation’

A

helps maintain the balance of electrolytes and water in the body preventing dehydration or fluid overload

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13
Q

how is the integumentary system involved with ‘Vitamin D production’

A

synthesis vitamin D when exposed to sunlight, aiding bone health and calcium absorption

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14
Q

name components of integumentary system

A

skin
hair
sudoriferous and sebaceous glands
nails

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15
Q

function of sweat and oil glands

A

-regulate body temperature
-antibacterial effects
-moisturise skin

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16
Q

name the layers of skin

A

epidermis
dermis
hypodermis

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17
Q

describe the epidermis

A

outermost layer that provides protection
-avascular
-renewed via epidermal turnover/desquamation

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18
Q

describe the dermis

A

middle layer, contains CT and other structures (nerves, blood vessels, glands)

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19
Q

describe the hypodermis

A

deepest layer, made of mainly fat tissue, proving insulation, connecting skin to underlying tissues and energy storage

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20
Q

name the stratum of the epidermis

A

corneum
lucidium
granulosum
spinosum
basale

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21
Q

describe corneum of epidermis

A

-ouermost layer
composed of dead keratinocytes

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22
Q

describe lucidium of epidermis

A

thin, translucent layer that is only found in thick, hairless area eg palm

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23
Q

describe the granulosum in epidermis

A

layer where keratinocytes begin to flatten and produce keratin

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24
Q

describe spinosum in epidermis

A

layer in which keratinocytes increase in size and provide strength

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25
Q

describe basale in epidemris

A

deepest layer, site of rapid cell division

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26
Q

name the key cells of the epidermis

A

keratinocytes
langerhan cells
melanocytes
merkel cells

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27
Q

function of keratinocytes

A

epidermal cells that produces the protein keratin, which contribute to strength and water proofing skin

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28
Q

function of langerhan cells

A

specialised immune cells in the epidermis that play a role in antigen presentation and immune response activation

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29
Q

function of melanocytes

A

cells in the epidermis that produce the pigment melanin, responsible for skin, hair and eye colour as well as UV protection

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30
Q

function of merkel cells

A

specialised cells in epidermis that are involved in sensation, especially touch and pressure

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31
Q

whats keratinisation

A

-as keratinocytes migrate towards surface, keratin production increases, cells flatten and nuclei disappear
-this layer of keratinised cells forms the corneum
-keratin accumulates in cytoplasm and ‘leaks’ out surrounding corneum and providing protection

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32
Q

how long is the skin regeneration cycle

A

28 days

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33
Q

thick vs thin skin

A

-thick skin is found in areas of high friction and mechanical stress whereas thin skin is found everywhere else (more flexible)
-thick skin is has five epidermal layers (and a prominent lucidium) whereas thin skin has 4 layers (no lucidium)
-thick skin is hairless, thin is hairy

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34
Q

name the two layers of the dermis

A

papillary dermis
reticular dermis

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35
Q

describe papillary dermis

A

loose CT, allows for movement of molecules and exchange of waste/gases

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36
Q

describe reticular dermis

A

dense CT, thick collagen fibres and aids strength

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37
Q

name the accessory structures of the skin

A

nerves
hair follicles
sweat glands (merocrine)
sweat glands (apocrine)

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38
Q

function of nerves in skin

A

perceive stimuli and communicate with NS to maintain homeostasis

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39
Q

function of sweat glands (merocrine) in skin

A

secrete sweat onto body , glands are widely distributed

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40
Q

function of sweat glands (apocrine) in skin

A

secrete and move sweat through hair follicles (under armpits)

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41
Q

dermal blood vessels ___ to thermo (up) regulate

A

constrict

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42
Q

dermal blood vessels ___ to thermo (down) regulate

A

dilate

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43
Q

describe blood flow to achieve thermo (up) regulation

A

directed to deep regions

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44
Q

describe blood flow to achieve thermo (down) regulation

A

directed to superficial regions

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45
Q

arrestor pili muscle ___ to achieve thermo (up) regulation

A

contract (goosebumps)

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46
Q

arrestor pili muscle ___ to achieve thermo (down) regulation

A

expand/relax

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47
Q

how do antimicrobial peptides work

A

-for example defensins, are cationic proteins that disrupt bacterial cell membrane integrity or cell anabolism
-their positive charge allows them to bind to the negatively charged membranes of bacteria
-do not bind to mammalian membranes t/f ensuring they only target microbial invaders

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48
Q

what are complement pathways

A

a group of soluble factors that play a vital role in the immune response ; eliminate pathogens, enhance inflammation, promote clearance of cellular debris

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49
Q

name the different complement pathways

A

classical pathway
lectin pathway
alternative pathway

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50
Q

how does the classical complement pathway work

A

-initiated when antibodies bind to antigens on surface of pathogens
-leads to a series of enzymatic reactions, forming C3 convertase enzyme
-this enzyme cleaves the C3 protein to C3a and C3b fragments, initiating downstream complement events
-C3b acts as an opsonin, tagging pathogens for for recognition and phagocytosis
-also the membrane attack complex (MAC) lyses the pathogen

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51
Q

how does the alternative complement pathway work

A

-inititated when C3 is hydrolysed in the absence of specific antibodies or lectins
-C3 enzyme converts forms , initiating downstream complement events
-opsonisation, inflammation and pathogen lysis occurs

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52
Q

how does lectin complement pathway get initiated

A

lectin binds mannose (sugar) on pathogen

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53
Q

whats haematopoisesis

A

-the making of blood cells
-two lineages: myeloid and lymphoid

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54
Q

name the cells that a haematopoietic stem cell can differentiate into

A

B naive cell
CD8+ T cell
CD4+ T cell
natural killer cell

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55
Q

what is a B naive cell

A

differentiates in the bone marrow and expresses a B surface cell receptor

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56
Q

whats a CD8+ T cell

A

differentiates in the thymus and expresses a T surface cell receptor

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57
Q

whats a CD4+ T cell

A

differentiates in the thymus and expresses a T surface cell receptor

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58
Q

whats a natural killer cell

A

differentiates in the thymus, expresses no surface cell receptor, contains granules that enable cellular death against viral cells or tumours

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59
Q

what are the primary lymphoid organs

A

-it is where lymphocytes undergo synthesis
-the thymus and bone marrow

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60
Q

where does B cell ontogeny occur

A

bone marrow

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61
Q

where does T cell ontogeny occur

A

begins in bone marrow but concludes in thymus

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62
Q

where does fluid transfer from blood into tissue

A

capillaries and post capillary section

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63
Q

name secondary lymphoid organs

A

spleen and lymph nodes

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64
Q

function of bone marrow

A

production of B cells and T cells
-educates B cells and neutrophils, monocytes, eosinophils, and NKC’s

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65
Q

function of thymus

A

maturation and education of T cells

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66
Q

function of lymph nodes

A

-filters lymph fluid,
-detects and eliminates foreign substances, filters tissue-borne antigens
-stores immune cells (B,T etc) for surveillance

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67
Q

function of spleen

A

-filters blood
-removes old or damaged RBC’s
-reservoir for immune cells eg lymphocytes
-filters tissue-borne antigens

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68
Q

name the structural features that comprise the lymph node

A

-cortex and paracortex
-follicles
-medulla
-sinus
-antibodies
-afferent vessel
-efferent vessel
-trabecula

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69
Q

function of cortex and paracortex in lymph node

A

-cortex contains B cells and paracortex contains T cells
-facilitating the interaction between immune cells and the initiation of immune responses within the lymph nodes

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70
Q

function of follicles in lymph node

A

-areas in the cortex where B cells proliferate and produce antibodies as part of adaptive immune system

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71
Q

function of medulla in lymph node

A

-contains plasma cells that produce antibodies
-contains macrophages that phagocytose pathogens and cellular debris

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72
Q

function of sinus in lymph node

A

-spaces in lymph node where lymph circulates and immune cells meet antigens carried by lymph
-allows for immune surveillance and response

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73
Q

function of antibodies in lymph node

A

-produces by B cells, specifically target and neutralise pathogens, aiding immune response

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74
Q

function of afferent vessel in lymph node

A

bring lymph (along with pathogens and antigens) to lymph node for filtration and initiation of immune response

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75
Q

function of efferent vessel in lymph node

A

carry filtered lymph (along with immune cells and antibodies) to other parts of body

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76
Q

function of trabecula in lymph node

A

-fibrous CT partitions within lymph nodes
-provide structural support and contain blood vessels that supply nutrients to lymph node

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77
Q

what are cytokines

A

intercellular communicators,
-small proteins that are secreted to communicate with cells.

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78
Q

name the effects of cytokines

A

autocrine, paracrine, endocrine

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79
Q

name the cytokine classes

A

interleukins
interferons
chemokines
tumour necrosis factors

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80
Q

describe role of interleukins

A

-proteins produced by cells in response to viral infection or other immune stimuli
-involved in inhibiting viral replication and modulating immune response

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81
Q

describe role of interferons

A

-group of cytokines produced by various immune cells
-act as signalling molecules to regulate immune responses and allow communication between cells

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82
Q

describe role off chemokines

A

-small proteins that help recruit and guide immune cells to specific locations by attracting and directing their movement

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83
Q

describe role of tumour necrosis factors

A

-pro inflammatory cytokine that is involved in inflammation, cell death, immune system regulation in response to tumour development and infections

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84
Q

foul tasting/smelly mucous is indicative of

A

bronchiectasis

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85
Q

pink/frothy mucous is indicative of

A

pulmonary oedema

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86
Q

haemoptysis is indicative of

A

TB
lung cancer
pulmonary embolism

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87
Q

chest pain (irritation of parietal pleura) indicates

A

lobar pneumonia
pneumothorax
pulmonary embolism

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88
Q

voice hoarseness is indicative of

A

upper airway problems eg laryngitis, vocal cord tumours

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89
Q

fever is indicative of

A

viral/ bacterial infection

90
Q

weight loss/ night sweats are indicative of

A

cancer/ infection

91
Q

smoking is indicative of

A

COPD, emphysema, lung cancer

92
Q

asthma can be indicative of

A

atopic triad (eczema, hay fever-allergic rhinitis)

93
Q

wheezing indicative of

A

asthma,COPD

94
Q

what can recent travel be indicative of

A

long flights/ immobilisation be indicative of pulmonary embolism, infections eg TB

95
Q

chronic cough, chest pain radiating to throat and burning indicates

A

acid reflux

96
Q

voice hoarseness, throat clearing cough and sore throat indicative of

A

post nasal drip

97
Q

painful, persistent acute cough with voice hoarseness indicates

A

laryngitis

98
Q

painful, persistent intense cough with stridor indicates

A

pertussis

99
Q

cough, wheeze and rapid dyspnoea indicates

A

asthma

100
Q

cough, wheeze and moderate dyspnoea indicates

A

tracheatis

101
Q

cough, wheeze and long term dyspnoea that worsens in morning indicates

A

COPD

102
Q

cough, wheeze and long term dyspnoea that has massive bleeding indicates

A

bronchial malignancy

103
Q

cough with purulent (green sputum) and recent onset indicates

A

pneumonia

104
Q

cough with purulent (green sputum), blood and fever indicates indicates

A

TB

105
Q

cough with purulent (green sputum), blood and dyspnoea indicates

A

bronchiectasis

106
Q

pink frothy sputum and cough indicates

A

pulmonary oedema

107
Q

taking ACE inhibitors can be indicative of

A

dry scratchy, persistent and chronic cough
-normally has hypertension

108
Q

worsening chronic cough and worsening dyspnoea indicates

A

interstitial lung disease

109
Q

chest pain under breastbone indicates

A

pulmonary embolism

110
Q

chest pain radiating on ipsilateral side indicates

A

pneumothorax

111
Q

what is the significance of MHC markers

A

-T cells cannot recognise antigens in their natural form
-natural antigens are in the form of folded polypeptides, these are cleaved into shorter peptides, the peptides are presented on MHC molecules
t/f T cells can recognise the antigen

112
Q

CD8 cells recognise which MHC marker

A

MHC class 1

113
Q

CD4 cells recognise which MHC marker

A

MHC class 2

114
Q

how do MHC class I present

A

presents endogenous peptides

115
Q

how do MHC class II present

A

presents exogenous peptides

116
Q

Describe antigen processing (MHC I)

A

-endogenous protein is synthesised within the body
-protein is digested into short peptides (8-10 AA)
-peptides enter the rough ER
-peptides are loaded onto MHC I
-MHC I are exported to surface via vesicular transport
-MHC I is expressed on a nucleated cell

117
Q

Describe antigen processing (MHC II)

A

-exogenous proteins are taken up via pinocytosis, endocytosis or phagocytosis
-exogenous antigen is digested in the endosome by lysosomes
-MHC II travels from rough ER into endosome
-peptide loaded onto MHC II
-MHC II expressed on APC

118
Q

How are intracellular pathogens/tumours managed by MHC

A

-CD8+ T cells are activated
-MHC I is activated
-T cytotoxic cell (Tc) is produced and apoptosis occurs

119
Q

How are extracellular pathogens managed by MHC

A

-CD4+ T cells are activated
-MHC II is activated
-T helper (Th) is produced and phagocytosis occurs

120
Q

what is immunoglobulin (Ig)

A

refers to the structure of a molecule
-Ig has a heavy and light chain
-Y shaped glycoproteins
-4 PP chains held by 4 disulphide bonds
-A.B.S

121
Q

what does antibody (Ab) mean

A

refers to the function of a molecule

122
Q

name the Ig isotopes

A

IgM,IgA,IgD,IgG,IgE (MADGE)

123
Q

IgM
*structure
*# binding sites
*binding location

A

pentameric
10 binding sites
blood; tissue

124
Q

IgA
*structure
*# binding sites
*binding location

A

Dimeric
4 binding sites
mucosa

125
Q

IgD
*structure
*# binding sites
*binding location

A

monomeric
2 binding sites
blood; tissue

126
Q

IgG
*structure
*# binding sites
*binding location

A

monomeric
2 binding sites
blood (neutrophil); tissue

127
Q

IgE
*structure
*# binding sites
*binding location

A

monomeric/dimeric
2 binding sites
mucosa, GI tract and respiratory tract

128
Q

whats an antigen

A

substance, usually a protein or carbohydrate that is capable of stimulating an immune response in the body

129
Q

name the ways antibodies can act

A

neutralisation
agglutination
opsonisation
complement protein activation
(ACON)

130
Q

how do antibodies ‘neutralise’

A

antibody binds to the antigen, prevents antigen binding to body cells

131
Q

how do antibodies ‘agglutinate’

A

arms of antibodies bind to antigens, prevents colonisation

132
Q

how do antibodies ‘opsonise’

A

antigen recognises opsonin receptor and enhances phagocytosis

133
Q

why do antibodies activate complement proteins

A

works in classical pathway, C3b deposition, forms membrane attack complex and cell death occurs

134
Q

Describe humoral antibody response

A

-naive B cell sitting in secondary lymphoid tissue (lymph node)
-when antigen drains into lymph node it recognises a s+c naive B cell
-naive B cell is activated and proliferates to create a clone of itself
-proliferated B cell divides into plasma and memory cells
-plasma cells secrete IgM and memory cells secrete IgG

135
Q

list the cells produced to ultimately form B memory cells

A

naive B cells -recognise
mature B cell-activate
mature B cells-proliferate
Plasma cells or memory cells-differentiate

136
Q

Outline steps of primary immune response

A

1.lag period:first B cell must find its antigen after exposure
2.initial spike of IgM antibodies:plasma cell (IgM) production increases
3.following rise in IgG antibodies: memory B cell (IgG) production increases
4.IgM and IgG antibodies have achieved their function t/f concentrations decrease

137
Q

Outline steps of secondary immune response

A

1.reduced lag period due to more cloned B memory cells to recognise antigen
2.initial spike of IgG due to B memory cells
3.spike of IgM due to plasma cells (immune response)
4.more B memory cells for priming future exposures

138
Q

list the clinical relevances of B cells

A

-autoimmune disorders
-allergies
-B cell malignancies

139
Q

how are autoimmune disorders linked to the clinical relevance of B cells

A

B cells can produce autoantibodies that mistakenly target and attack the body’s own tissues leading to autoimmune disorders. eg RA, MS

140
Q

how are allergies linked to the clinical relevance of B cells

A

B cells can be activated by allergens, leading to production of IgE antibodies, histamine is released and allergic symptoms occur

141
Q

how are B cell malignancies linked to the clinical relevance of B cells

A

abnormal proliferation or dysfunction of B cells can lead to development of B cell lymphomas

142
Q

name the ways B cells can be modulated

A

stem cell transplantation
therapeutic vaccines

143
Q

how can stem cell transplantation be used to modulate B cells

A

in some cases, stem cells transplantation can be used to replace abnormal or dysfunctional immune cells with healthy cells

144
Q

how can therapeutic vaccines be used to modulate B cells

A

vaccines can be designed to target specific antigens associated with diseases involving B cells, such as cancers, vaccines aim to stimulate an immune response against diseased cells

145
Q

Outline the development of T cells

A

-early phase in the thymus
-production in bone marrow
-completion of development in thymus
-CD4+ and CD8+ T cells produced + migrate to lymph nodes

146
Q

how are T cells activated

A

-T cells meet processed antigens (via MHC II) in lymphoid tissue
-naive T cells activated and differentiate
-MHC II allows for the antigen recognition by T cells
-clonal selection and expansion occurs
-T helper (CD4+)/T cytotoxic(CD8+) and T memory produced

147
Q

Explain the processes involved in cell-mediated immunity in the adaptive immune response

A

1.APC’s ingest pathogens and present them on cell via MHC
2.naive T cells recognise MHC via TCR’s and co-stimulatory signals (become activated)
3.T cell undergoes clonal expansion
4.T cells differentiate into Tc cells, Th cells, Treg cells
5.effector T cells migrate to site of infection via chemotaxis guided by chemokine
6.Tc cells recognise and bind to infected cells that display antigen on MHC I
7.Tc cells release cytotoxic chemical eg perforins that lead to apoptosis of infected cell
8.Th cells release cytokines to amplify immune response, attract macrophages, activate B cells
9.some T cells divide into T memory cells for long term immunity
10. Tregs suppress excessive immune response, prevent autoimmunity and maintain homeostasis

148
Q

list the clinical relevances of T cells

A

autoimmune disease
infectious diseases
transplant rejection

149
Q

how are autoimmune diseases linked to the clinical relevancies of T cells

A

T cells mistakenly recognise self cells as foreign leading to responses against body cells

150
Q

how are infectious diseases linked to the clinical relevancies of T cells

A

T cells are essential in responding to viral, fungal and bacterial infections, understanding them can aid drug and vaccine development

151
Q

how are transplant rejections linked to the clinical relevancies of T cells

A

T cells are involved in allograft rejection, where the recipients immune system recognises organ as foreign and rejects it

152
Q

name the way T cells can be modulated

A

cytokine therapies
T cell engineering
immune checkpoint inhibitors

153
Q

how can cytokine therapies be used to modulate T cells

A

administration of cytokines eg interferons or interleukins modulates T cells and enhances there immunity against specific diseases

154
Q

how can T cell engineering be used to modulate T cells

A

techniques like CAR T cell therapy, involves modifying patients T cells to express specific receptors against tumour antigens, enhancing anti cancer activity

155
Q

how can immune checkpoint inhibitors be used to modulate T cells

A

drugs that block inhibitory receptors on T cells unleash their anti tumour responses by relieving immune suppression t/f enhance T cell activity against cancer cells

156
Q

what is vaccination

A

the uptake of injection (orally or injection)

157
Q

what is immunisation

A

process of getting the vaccine and subsequently getting immune to the disease

158
Q

whats a vaccine

A

weak form (attenuated) or part of (protein or nucleic acid) an infectious agent

159
Q

describe vaccination action

A

-they must activate CD4+ cells in the adaptive immune system by first passing the static, soluble and cellular barriers of innate system

160
Q

function of MALT

A

filters mucosa-borne antigens

161
Q

is natural immunity or vaccination preferred

A

natural immunity

162
Q

name the vaccine types

A

live
inactivated
purified subunit
cloned

163
Q

define live vaccine and give an example

A

antigen microbes are grown repeatedly in cell culture eg.mumps

164
Q

define inactivated vaccine and give an example

A

antigen microbes are inactivated, exposed to heat, chemicals or radiation eg influenza
-HI only

165
Q

define purified subunits vaccine and give an example

A

components of the microbe are isolated and proteins (+polysaccharide) are administered eg tetanus
-HI only

166
Q

define cloned vaccine and give an example

A

genetic material of antigen is isolated and recombinant DNA is administered eg COVID 19
-HI only

167
Q

attenuated and mRNA vaccines differ to other vaccines because

A

they can enter the host cell t/f stimulates cell mediated and humoral response
-can undergo reversion
-only need one dose

168
Q

Describe vaccination action
-first exposure

A

1.the vaccine is introduced to the body and injected under the skin
2.the vaccine is taken up and digested by DC, Toll-like receptors on surface of DC facilitate relocation to secondary lymphoid organs
3.vaccine is processed and presented on MHC II to naive CD4+ cell
4.”line up” of CD4+ cells to find a complementary match
5.activation, proliferation and differentiation into Th cell
6.Th cells activate a B cell that recognises the vaccine
7.B cell activates, proliferates and differentiates, into IgM plasma cell, IgG memory cells
8.clones of B memory cells that can recognise infectious agents

169
Q

Describe vaccination action
-second exposure

A

1.antigen is presented on MHC II, proliferation of B cell begins
2.surplus of B cells differentiate into IgM secreting plasma cells and IgG secreting memory cells (tops up memory)

170
Q

whats an adjuvant

A

substance that enhances immune response in non living vaccines, act like a depot for slow vaccine release to prime immune response

171
Q

what is passive immunity

A

transfer of ready made antibodies From one person to another

172
Q

name the general steps of inflammation

A

initial insult
inflammation
inflammatory mediators
demolition, repair and result

173
Q

name the types of inflammation

A

chronic and acute

174
Q

Contrast acute vs chronic inflammation

A

-acute is an early response vs chronic is a later response
-acute inflammation is short vs chronic is long
-acute inflammation involves neutrophil, fibrin and oedematous exudate vs chronic involves macrophages, lymphocytes, plasma cells and fibrosis/scars
-acute is non specific vs chronic can be specific or non specific

175
Q

what is acute inflammation

A

-occurs directly following insult/injury
-aims to deliver nutrients, defence cells, remove debris and destroy infections

176
Q

what can acute inflammation lead to

A

resolution, repair or chronic inflammation

177
Q

name the effects of acute inflammation

A

redness
heat
pain
swelling
loss of function
malaise
myalgia
leukocytosis

178
Q

describe redness in inflammation

A

vasodilation and increased blood flow (hyperaemia)

179
Q

describe heat in inflammation

A

heat released by hyperaemia

180
Q

describe pain in inflammation

A

pressure effects on nerve endings and chemical factors eg prostaglandin

181
Q

describe swelling in inflammation

A

accumulation of exudate and hyperaemia

182
Q

describe function loss in inflammation

A

direct local damage and various factors eg swelling

183
Q

describe malaise in inflammation

A

general feeling of unwellness

184
Q

describe myalgia in inflammation

A

muscle aches and pains particularly in joints (arthralgia)

185
Q

describe leukocytosis (WBC+) in inflammation

A

neutrophils in acute inflammation and macrophages in viral infection.

186
Q

Outline sytsematic steps in acute inflammation

A
  1. break in skin/injury introduces bacteria
  2. macrophages engulf the pathogen and release chemotaxins (cytokine)
  3. mast cells activated, release histamine
  4. histamine dilates local blood vessels and widens capillary pores, some cytokines cause neutrophils and monocytes to stick to blood vessel wall
  5. chemotaxins attract neutrophils and monocytes, increased leakiness moves exudate to site of injury
  6. macrophages and neutrophils destroy bacteria

pain and swelling occur due to exudate itself

187
Q

role of neutrophils

A

-respond most to bacterial infection
-phagocytotic
-destroy bacteria
-release free radicals
-release lysosomal digestive enzymes

188
Q

role of monocytes

A

-leave circulation at site of inflammation
-phagocytose tissue debris and pathogens
-initiate immune response

189
Q

role of macrophages

A

specialised functions eg dust cells, osteoclasts
-long living

190
Q

whats exudate

A

-protein rich mixture of fluid and cellular debris that has escaped from blood vessels due to increased permeability of blood vessels

191
Q

name the components of exudate

A

-plasma proteins
-inflammatory cells
-fluid/electrolytes
-cytokines
-enzymes

192
Q

role of plasma proteins in inflammation

A

-eg fibrinogens, complements and immunoglobulins
involved in immune response

193
Q

role of inflammatory cells in inflammation

A

-neutrophils, monocytes and macrophages
-involved in immune response

194
Q

role of fluid/electrolytes in inflammation

A

provides nutrients for inflammation eg water, potassium, sodium and chloride

195
Q

role of cytokines in inflammation

A

mediate inflammatory responses eg chemokine, interleukins, TNF

196
Q

role of enzymes in inflammation

A

catalyse tissue repair and remodelling

197
Q

name the systemic effects of chronic inflammation

A

arthralgia,myalgia
anxiety
depression
fever
mood disorders
leukopenia
chronic fatigue/insomnia
GI complications
weight gain/loss
frequent injections

198
Q

whats chronic inflammation

A

-mononuclear cell infiltration (macrophages, lymphocytes and plasma cells
-tissue destruction
-fibrosis and angiogenesis to replace damaged CT

199
Q

name the cells in chronic inflammation

A

-lymphocytes
-plasma cells
-fibroblasts
-endothelial cells
-eosinophils

200
Q

lymphocyte role in chronic inflammation

A

release cytokines to activate macrophages, persistent + feedback loop until homeostasis

201
Q

plasma cells role in chronic inflammation

A

B cells mediated by Th cells release antibodies

202
Q

fibroblast role in chronic inflammation

A

produce and secrete components of the ECM, for immune response and healing

203
Q

endothelial cells role in chronic inflammation

A

angiogenesis

204
Q

eosinophil role in chronic inflammation

A

abundant in IgE responses (allergies); granules contain toxic components (they mediate them)

205
Q

name stages of wound healing

A

reactive
reparative
remodeling

206
Q

what happens in reactive stage of wound healing

A

-haemostasis
-inflammation:redness, heat, pain, swelling
-immune cell action

207
Q

what happens in reparative stage of wound healing

A

-Granulation tissue formation
-angiogenesis
-epithelialisation
-contraction

208
Q

what happens in remodelling stage of wound healing

A

-maturation of scar tissue
-scar formation
-continual vascular and cellular changes

209
Q

primary vs secondary intention healing

A

-primary occurs in clean, well edged wounds vs secondary occurs in large, deep wounds
-primary the gap can be closed vs secondary has larger gap
-primary heals sequentially and systemically vs secondary heals bottom to top
-primary has smaller inflammatory response vs second has large and profound one
-primary is less complex and easy to manage vs secondary is complex and hard to manage

210
Q

name the components of granulation tissue

A

fibroblasts
capillaries
ECM
inflammatory cells
myofibroblasts

211
Q

what is hypersensitivity

A

reactions that are exaggerated/inappropriate response to antigens that leads to over inflammation and destruction of innocent cells

212
Q

how many hypersensitivity reactions is there

A

4

213
Q

Outline type I hypersensitivity

A

-‘immediate’
-2 to 30 minute symptom onset
-allergen is the antigen
-IgE isotope
-effector is mast cell
-pathology eg is asthma

214
Q

Outline type IV hypersensitivity

A

-‘delayed type’
-more than 72h symptom onset
-antigen is haptens;bacteria
-no Ig isotope
-effector is T cell; macrophage
-pathology eg is dementia

215
Q

Explain the concept of immunological tolerance

A

Each T cell receptor and B cell receptor is unique in that the portion that recognises the shape of the antigen is different, the shape to recognise the antigen is randomly generated because of this some TCR and BCR can be complementary and bind to self antigens

216
Q

what is caused by a breach of tolerance to self

A

autoimmune diseases

217
Q

what is the self antigen and immune effector for type 1 diabetes

A

self antigen=beta pancreatic cells
immune effector=auto antibodies and Th cells

218
Q

what is the self antigen and immune effector for myasthenia gravis

A

self antigen=Ach receptors
immune effector=blocking auto antibodies

219
Q

what is the self antigen and immune effector for multiple sclerosis

A

self antigen=brain white matter
immune effector=Th cells, Tc cells, auto antibodies

220
Q

what is the self antigen and immune effector for rheumatoid arthritis

A

self antigen=CT,IgG
immune effector=auto antibodies

221
Q

what is the self antigen and immune effector for sytemic lupus erythmatosus

A

self antigen=DNA, erythrocytes
immune effector=auto antibodies

222
Q
A

Foundations of Medicine (18 decks)

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