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BDS stage 2 > IAH theme 2 > Flashcards

IAH theme 2 Flashcards

1
Q

What are the immediate defences ?

A

Physical and chemical barriers
complement
phagocytosis

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2
Q

What are the induced defences ?

A

neutrophil chemotaxis
cytokines
interferon response

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3
Q

What are the adaptive defences ?

A

antibodies
cell mediated immunity
memory

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4
Q

What is the role of the adaptive immune response in an infection ?

A

to clear the infection

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5
Q

Describe the course of an infection ?

A 
establishment of infection 
threshold reached to activate adaptive response 
induction of adaptive response 
adaptive response
memory cells
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6
Q

What are the charactersitics of the immune response to an infection ?

A

dynamic- intensity changes with time
organised-in time and location- multiple secondary lymphoid locations
improved- increased affinity of BCRs, isotype switch

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7
Q

What is the isotype switch ?

A

IgM to IgA

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8
Q

What does the success of an infection depend on ?

A

properties of pathogen
dose of innoculation
route and mode of transmission
host properties

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9
Q

How do pathogen properties influence success of an infection ?

A

method of infection

extracellular/intracellular

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10
Q

How does the dose of innoculation influence the success of an infection ?

A

large dose needs to overcome innate immunity

multiple exposures mean more likely to get infected

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11
Q

How does the route and mode of transmission infleuce the success of an infection ?

A

mucosal surfaces more likely to get infected

dirty injection

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12
Q

How do host properties influence the success of an infection ?

A

health, age, chornic conditions
chronic disease mean immune system is already burdened
smoking and drugs can effect CNS and host defences

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13
Q

Describe the stages of the immune response after a skin breach ?

A

skin breach
complement, AMP and phagocytosis try to eradicate
dendritic cells migrate to lymoh nodes to present antigen
NK cells made
cytokines
chemokines made
adaptive immunity initiated
via efferent lymphatics- T, B and antibodies transported to site
infection cleared by antibodies, activated macrophages and CD8 cells

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14
Q

What is a primary infection ?

A

pathogen estbalishes at an initial site

adhere, colonise and penetrate

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15
Q

What is the job of the innate immunity in an infection ?

A

contain the infection

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16
Q

What are obligate intracellular pathogens ?

A

spread from cell to cell

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17
Q

How do extracellular bacteria sprea ?

A

blood

lymphatics

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18
Q

How do pathogens that dont enter tissues causes disease ?

A

toxin activity

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19
Q

Which bacteria produce neurotoxins ?

A

clostridium botulinum
clostridium tetani
cholera

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20
Q

What happens without innate immunity ?

A

high duration of infection

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21
Q

What is SCID ?

A

no RAG enzyme
no T/B cell development - no adaptive response
innate immunity still present so lower number of microorganisms
infection contained but cant be cleared by adaptive

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22
Q

What is TLR3 ?

A

viral PRR in innate system

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23
Q

What to TLR3 mutations lead to ?

A

lead to HSV induced encephalitits
HSV Is normally just cold sores
highlights importance of innate immuntiy

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24
Q

What is SCID ?

A

Severe combined immunodeficiency
RAG mutation in T cell development
lack of cell mediated and antibody immunity- no activated macrophages or B cells
susceptible to wide range of infections

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25
Q

What does establishment of a bacterial infection trigger ?

A

complement activation
activation of dendritic cells
innate signalling by macrophages for neutrophils

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26
Q

What happens in a cytokine milieu ?

A

cytokines made by T cells
specific TFs amde
differentiation of CD4 into effector cells

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27
Q

What are the different types of CD4 cells ?

A 
Th17
Treg
Th1
Th2
Tfh
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28
Q

What are the features of the cytokine milieu that allow T cell differnetiation into effector T cells?

A

mutual regualtion- positive/negative feedback

phenotypic plasticitiy- can change into different types

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29
Q

What is the role of the Th17 cell ?

A

reinforce innate immunity

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30
Q

What is the role of the Treg cell ?

A

supression of the immune system

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31
Q

What is the role of the Th1 cell ?

A

macrophage activation

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32
Q

What is the role of the Th2 cell ?

A

B cell activation

Mast cell activation

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33
Q

What is the role of the Tfh cell ?

A

B cell activation in lymph nodes

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34
Q

What does HIV do ?

A

take out CD4 cells

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35
Q

How are pathogen destruction mechnanisms tailored ?

A

tailored to the type of pathogen and its mechanism of pathogenicity

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36
Q

Bacteria that produce toxins require what type of destruction ?

A

antibodies to neutralise the toxin

eg. C.tetani

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37
Q

What type of destruction mechanism do extracellular bacteria require ?

A

antibodies

eg. strep pneumoniae in pneumonia

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38
Q

What type of destruction mechanism do intracellular bacteria require ?

A 
cant be reached by antibodies
infected cell has to die 
use macrophages activated by Th1 cells
CD8 cells 
eg. Mycobacterium
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39
Q

How does Mycobacterium Tb infect ?

A

infects macrophages - intracellular
macrophages present antigen via MHC Class II to Th1 cell
co receptor recognition too - CD40 on macrophage and CD40 receptor on Th1 cell
Th1 cell activates macrophage
signal 3- IFN gamma released by macrophages- type II interferon- activates macrophages
Fas ligand pathway for death if bacteria are resistant to digestion
Th1 cells also recruit macrophages from monocytes in blood

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40
Q

What happens if Myco TB resists macrophage digestion ?

A

chronic inflammation develops

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41
Q

What are the 2 types of infections manifested by Mycobacterium leprae ?

A

tuberculoid leprosy

lepromatous leprosy

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42
Q

What are the characteristics of tuberculoid leprosy ?

A

low infectivity
local inflammation and peripheral nerve damage
normal serium Immunoglobulin levels
Normal T cell responsiveness allowing macrophage activation via Th1 and IFN gamma

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43
Q

What are the characteristics of lepromatous leprosy ?

A 
high infectivity
boen, cartilage and nerve damage 
hypergammaglobuminemia 
low or absent T cell responsiveness to antigens 
failed Th1 response 
Th2 respone activated instead
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44
Q

What is the consequence of activating the Th2 resposne instead of Th1 in lepromatous leprosy ?

A

Th2 response triggered
trigger B cell activation
produces antibodies
no effect on intracellular mycobacterium

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45
Q

Why is there no Th1 response in lepromatous leprosy ?

A

Th2 response activated
IL4/IL10 reciprocal inhibition means Th1 cells are supressed
no activation of macrophages to clear infection

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46
Q

What causes an imbalance between the Th1.Th2 resposne ?

A

peptide amount
MHC dnesitiy
cytokine milieu

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47
Q

What does an abundance of peptide lead to ?

A

MHC complexes drive Th1 response

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48
Q

What does a limited amount of peptide lead to ?

A

MHC complexes drive Th2 response

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49
Q

What are the characteristics of mucosal surfaces ?

A

thin and permeable
route of infection
no keratin

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50
Q

What is present on each mucosal surface ?

A

natural, commensal, non pathogenic commensal microbiota

disticnt immune defences like peyers patches

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51
Q

What are the anatomical features of the mucosal immune system ?

A

comaprtments of lymphoid tissue- tonsils and peyers

specialised antigen uptake cells- M cell

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52
Q

What are the effector mechanisms of the mucosal immune system ?

A

Memory T cell
regulatory T cell
secretory igA
microbiotia

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53
Q

What are the immunoregulatory features of the mucosal immune system ?

A

down regulate immune responses to food/non harmful antigens

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54
Q

What is the micorbiotia like across different mucosal surface ?

A

varies in composition and diversity

different phyla

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55
Q

What can the composition of the microbiotia influence ?

A

immune system development and disease susceptibiliity

success of immumotherapy

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56
Q

What is the role of the microbiota on mucosal surfaces ?

A

synthesis AMPs
stimulate epithelial cells to make AMPs
compete with pathgoens for niches

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57
Q

What are the signs of inflammtion ?

A

heat due to increased blood flow
Redness due to increased blood flow- vasodialtion
Swelling due to neutrophil influx and tissue fluid influx
pain due to oedema, pressure, pus and chemical pain mediators like bradykinin and prostaglandind
loss of function due to chronic inflammation

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58
Q

What does “itis” refer to ?

A

inflamamtion

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59
Q

What is acute inflammation ?

A

the initial tissue response to a number of inflammatory agents

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60
Q

What are agents of acute inflammation ?

A 
infections 
physical agents - trauma 
chemicals 
tissue necrosis 
immunological disease
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61
Q

How does tissue necrosis lead to inflammation ?

A

ischaemic infarction - blockage in blood vessel leads to death of blood vessel- cells burst open stimulating inflammation

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62
Q

What are the vascular changes in the early stages of inflammation ?

A

oedema, neutrophil and fibrin accumualtion in extracellualr spaces
increased vascular permeability to allow proteins to enter

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63
Q

How is neutrophil chemotaxis stimulated ?

A

IL8 release from macrophages

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64
Q

What are the benefits of acute inflamamtion ?

A

toxin dilution due to tissue fluid accumulation
entry of immune system elements- neutrophils and monocytes
transport of drugs
fibrin accumulation- blood clotting
delivery of oxygen and nutrients for neutrophils - high metabolic activity - divert energy to specific site

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65
Q

What are the 2 types of acute inflammation ?

A

membranous

suppurative

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66
Q

What is suppurative inflamamtion ?

A

production of pus
can be walled off by fibrotic tissue in repair forming an abscess
pus formed by pyogenic bacteria

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67
Q

What is an example of pyogenic bacteria ?

A

Staph aureus

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68
Q

What is it called when pus accumulates in a lumen ?

A

empyma

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69
Q

What is membranous inflammation ?

A

of mucosal surfaces

neutrophil chemotaxis, epithelium is coated in fibrin, desquamted

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70
Q

What are the consequences of untreated dental abscess ?

A

spread to fascial layers and spaces
cellulitis
press on carotid artery
septicaemia

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71
Q

What is the objective of acute inflammation ?

A

reduction in infection

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72
Q

What is fibrosis ?

A

due to chronic inflammation

attempt to repair damaged tissue

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73
Q

What does persistence of the causal agent lead to ?

A

chronic inflammation

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74
Q

What are the diseases Mycobacterium can cause by infecting macrophages ?

A

tuberculosis

leprosy

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75
Q

How do Th1 cells attempt to activate macrophages ?

A

Th1 cells are presented with antigen on class II
Th1 cells are activated and recognise
release IFN gamma
this activates macrophages to try to digest the infected cells

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76
Q

What happens in TB ?

A

pathogen persists
activated macrophages dont work
infection is contained but not cleared
leads to granuloma formation

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77
Q

What are granulomas ?

A

macrophages fuse into multinuclear giant cells
surrounded by epithelioid cells
surrounded by Th1 cells - CD4

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78
Q

What is the structure of granulomas ?

A

middle has few cells- large macrophages
outside has specs- densely stained - H&E stained T cells
Pink as middle is necrotic due to lack of oxygen

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79
Q

When are granulomas formed ?

A

bacteria resist the microbicidal effects of activated macrophages

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80
Q

How do Th1 cells activate macrophages ?

A

macrophage presents antogen via MHC class II
engagement with Th1 cell
Th1 cell proliferates via IL2
Th1 cell release IFN gamma to activate macrophages

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81
Q

What happens when the centre of the granuloma is cut off from oxygen ?

A

cut off from blood supply

cells die by anoxia and lytic macrophage enzymes

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82
Q

How does a necrotic granuloma manifest ?

A

caseation necrosis leads to caesation

cottage cheese appearance

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83
Q

What does caeseation of adrenal gland lead to ?

A

due to TB

lead to adrenal insufficirncy

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84
Q

What are the other manifestations of caeseation necrosis ?

A

confluent granulomas- pulmonary TB
lymoh node caeseation
miliary TB
Ghon complex

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85
Q

What is associated with the Ghon complex ?

A

anthracasis

tissue blackening

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86
Q

What can inflammation lead to ?

A

diseases with a loss of function

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87
Q

What happens in arthritis ?

A

loss of joint function

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88
Q

What happens in periodontal disease ?

A

loss of tooth function

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89
Q

What are the systemic effects of inflammation ?

A

fever
acute phase response
shock

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90
Q

What happens in fever ?

A

raising of temperature - not preferable for microbes

adaptive immunity becomes more potent

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91
Q

How does the body raise temperature ?

A

act on hypothalamus temperature control sites

physiologic response is to act on muscle and fat- altering metabolism to generate heat

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92
Q

How is the systemic fever effect triggered ?

A

pro inflammatory cytokines

IL6 IL1 TNF- alpha

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93
Q

What is the acute phase response ?

A

bacteria induce macrophages to produce IL6
acts on hepatocytes
induce synthesis of acute phase proteins- C reactive protein, fibrinogen and mannose binding lectin

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94
Q

What is the role of CRP ?

A

binds to phosphocholine on bacterial surfaces and opsinises bacteria to activate complement

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95
Q

What is the role of mannose binding lectin ?

A

binds to carbohydrates on bacteria

opsinisation

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96
Q

What can CRP be used in ?

A

CRP assay for suspected fever

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97
Q

What is septicaemia

A

infection of blood

might be via an endoxtoxin from gram negative bacteria like in a dental abscess untreatd

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98
Q

What happens in septic shock ?

A

circulatroy collapse causing hypoperfusion of organs

systemic inflammation means blood leaves circulation to enter tissues

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99
Q

What can lead to septic shock ?

A

haemorrhage
generalised vascular permeability
dilution

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100
Q

What does localised TNF lead to ?

A

macrophages are activated to release TNF alpha
release of plasma proteins into tissue
increased phaocyte/lymphocyte migration to tissue
phagocytosis of bacteria - contains infection

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101
Q

What does systemic TNF lead to ?

A 
macrophages in liver/spleen activated 
secrete TNF alpha into blood 
systemic oedema 
reduced blood volume 
collapse of vessels 
multiple organ failure as hypoperfused 
septic shock
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102
Q

What are the pathways to inflamamtion ?

A 
hypersenstivity
immunodeficneciy 
autoimmunity 
infecton 
metabolic disroders
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103
Q

Different classes of viral pathogen require what ?

A

different effector mechanisms

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104
Q

What type of immunity do viruses require ?

A

cell mediated

humoral

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105
Q

What are the role of CD8 cells in viral infections ?

A

clear infection
recognise infected cells
antigen specific

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106
Q

What is the role of antibodies in viral infections ?

A

contain infection

stop spreading

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107
Q

Are NK cells antigen specific ?

A

no

they are innate lymphoid cells

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108
Q

How are NK cells activated ?

A

IFN alpha and beta
type one IFN
released from virally infected cells
IL-12

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109
Q

How do NK cells ensure the cell is virally infected ?

A

have complex array of receptors

KIR receptor

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110
Q

What does the KIR receptor detect ?

A 
increased MHC class I expression 
infected cells make more MHC class I
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111
Q

What are KIR genes like ?

A

highly polymorphic

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112
Q

What do NK cells release ?

A

IFN gamma
type II IFN
activates macrophages, this leads to CD8 activation

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113
Q

How are cytotoxic CD8 cells activated ?

A

Naive T cell stimulated to proliferate by APC
Naive T cell releases IL2 - growth factor allows T cell proliferation
naive differnetiate into cytotoxic
Effector T cell kill virally infected cell

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114
Q

How do cytotoxic CD8 cells kill ?

A

CD8 cells recognise virally infected cells via TCR
and MHC class I
signal 2 and 3 not needed
CD8 induces apoptosus

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115
Q

How do CD8 cells carry out apoptosis ?

A

infected cells are killed by action of lytic grnaules that contain cyttoxic molecules such as perforin and granzymes

IFN gamma secreted by CD8 cells promotes antigen presentation and dead cell scavenging

successively kill others and jump to other cells

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116
Q

How do IgA protect against viral infections ?

A

bind to virus and prevent it entering cells

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117
Q

How do CD4 cells help CD8 cell sin viral infections ?

A

CD4 helps CD8 to fully funtion

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118
Q

What happens to CD4 cells in HIV ?

A

massive depletion

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119
Q

What happens to cellular immunity in AIDS ?

A

no CD4 cells to help CD8 cells in viral infections

no B cell help- no antibodies

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120
Q

What are the characteristics of AIDS ?

A

severe reduction in CD4 cells
severe infections by pathogens that dont normally infect healthy people
aggressive forms of karposis sarcoma and B cell lymphoma
fatal

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121
Q

What causes AIDS ?

A

HIV-1/HIV-2

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122
Q

How is HIV spread ?

A

from primates

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123
Q

How does HIV enter cells ?

A

CD4 receptor

CCR5 coreceptor

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124
Q

What is the CCR5 receptor ?

A

a chemokine receptor on memory T cells

HIV blocks out the receptor so memory to infection is wiped out

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125
Q

Which other cells is the CCR5 Co receptor also present on ?

A

macrophaes
dendritic cells
virus switches between cell types

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126
Q

What are the first cells to be infected with HIV ?

A

T cells

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127
Q

How does HIV affect T cells ?

A

virus swithces to T cells later on in the infection

causing a rapid decline in T cell numbers and progression to AIDS

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128
Q

What are the phases of a HIV infection ?

A

flu like symptoms
asymptomatic
symptomatic
AIDS

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129
Q

Describe the immune response to HIV ?

A

initial infection is asymomatic or might have like flu like symptoms
acute viraemia abundant virus circulates after infection and leads to depletion in CD4 T cells
activation of anti-HIV specific response - cytotoxic T cells and seroconversion antibodies
Virus load decreases and CD4 cells recover
Asymptomatic phase starts as CD4 cells recover - clinical latency od 2-15 years
high mutation rates in HIV- evasion from immune system
persistent infection and replication of HIV in T cells
rate of decline overtakes the rate of haematopoietic cells
immunodeficnecy ensures
AIDS progression

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130
Q

Which region do fungal infections target ?

A

oropharyngeal area

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131
Q

What are some predisposing conditions to fungal infections ?

A

immunodeficiency from HIV, chemotherapy, haematological malignancies

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132
Q

How many species of candida are there in the mouth ?

A

12

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133
Q

What can aspergillus cause ?

A

aspergillosis

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134
Q

What is 80% of oral candida ?

A

is candida albicans

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135
Q

What type of pathogen is candida ?

A

commensal

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136
Q

What are the candida morphologies ?

A

budding yeast
hypahe
pseudohyphae

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137
Q

What are the immune responses to candida ?

A

inhibition of adhesion and growth by IgA and lactoferrin
AMPs
neutrophils and macrophages
mucosal dendritic cells uptake yeast

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138
Q

How is candida recognised ?

A

TLR 2
TLR4
TLR9
on myeloid cells

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139
Q

What is the cell mediated immunity response to candid a?

A

IL-12

IFN gamma from NK cells which favours differentiation of Th1 cells

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140
Q

What are some predisposing factors to candidiasis ?

A

broad spectrum antibiotics - lead to thrush
corticosteroid inhalers in asthma
salivary abnromalities
smoking
chemotherapy can lead to xerostomia and neutropenia
HIV
ill fiting dentures

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141
Q

What is pseudomembranous candidiases characterised ?

A

plaques can be scraped off

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142
Q

How is chronic hyperplastic candidiasis characterised ?

A

plaques cant be scraped off

has penetrated tissues

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143
Q

What is erythematous candidiasis ?

A

poorly fitted dentures

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144
Q

What is pneumocystis jirovecii ?

A

opportunistic fungal pathogen
common in environment
causes pneumonia in AIDS and other immunosupressed
lack of CD4 Th1 cells leads to impaired alveolar macrophage function (not activated by IFN gamma) and infection

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145
Q

What is the evolution of pathogens like ?

A

in parallel to evolution of the human immune system

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146
Q

Which part of the immune system has evolved ?

A

adaptive immunity

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147
Q

How do we know pathgoens evade the immune system ?

A

from genomics

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148
Q

Why is evasion of the immune system necessary for pathogens ?

A

exploit habitat and compete in it

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149
Q

What is immune system evasion aided by ?

A

short life cycles

rapid mutation rate

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150
Q

What are social factors affecting spread of infectious diseases ?

A

poverty
agricultural techniques have lead to increased malaria incidence
migration
global circulation of blood and tissues

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151
Q

How do the large number of serotypes of Strep pneumoniae differ ?

A

in their capsular polysaccharide

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152
Q

What does each different serotype do ?

A

elicit a different serotype antibody response

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153
Q

Protective immunity is ?

A

serotype specific

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154
Q

What does serotype variety allow ?

A

bacteria to prosper

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155
Q

How is genetic variation defined ?

A

different serotypes require different serotype specific antibodies

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156
Q

Having specifc antibodies to one serotype does not ensure…..

A

immunity and antibodies to other different serotypes

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157
Q

How many serotypes does Strep Pneumoniae have ?

A

90

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158
Q

How many serotypes does the gneus salmonella have ?

A

2500 types

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159
Q

How are serotypes discovered ?

A

with assays

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160
Q

What can a species with a high serotype variety do ?

A

evade the immune system

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161
Q

Give an example of antigenic drift ?

A

neutralising antibodies can usually bind to infleunza antigen haemaglutinin
prevent cellular invasion
mutation occurs in haemaglutinin to produce a new version
neutralising antibodies can no longer bind- cellular invasion

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162
Q

What is antigenic drift ?

A

gradual change in genome due to point mutation in genes
different strains are prodcued
subtle changes in genes and vaccines

163
Q

Which genes in the influenza virus undergo antigenic drift ?

A

genes for viral envelope proteins

haemaglutinin and neuraminidase

164
Q

How do individuals become effected with antigenic drift variations ?

A

based on previous exposure to straisn
different degress of immunity
can be used to predict specific vaccines

165
Q

Does antigenic drift diseases cause epifemics ?

A

no - limited epidemics

166
Q

What is the characteristic of small pox ?

A

small pox has no antigenic variability

eradicated successfully with vaccine

167
Q

Give an example of antigenic shift ?

A

human infected with human virus and avian virus strains
recombination of viral RNA in human host produces new novel haemaglutinin
no existing immunity to novel haemaglutinin

168
Q

What does antigenic shift lead to ?

A

acute radical change in virus and new strain not ever seen before
radically different strain appears suddenly

169
Q

What is the infectivity like of antigenic shit pathogens ?

A

infects large numbers of people

severe disease and pandemics

170
Q

What are the genetic chnanges in antigenic shift ?

A

recombiantion of genomes between avian and human virus

171
Q

Why do avain viruses infect humans ?

A

culture of animal husbandry

172
Q

Viruses dividing rapidly allows what ?

A 
large numbers of MHC class I expression with antigen by cell 
activate CD8
173
Q

What type of state can viruses adopt ?

A

a quiescent state
low replication rates
doesnt produce enough antigen for presentation
no recognition

174
Q

How do viruses also evade the immune system ?

A

immunosurveillance

175
Q

What happens to viruses in the quiscent state ?

A

they are reactivated and causes disease

176
Q

Where does herpes simplex live ?

A

nervous system- trigeminal tract - persists

manifests as cold spores

177
Q

Where does HSV infect ?

A

epithelial cells

leading to pathology

178
Q

Why does HSV persist in Nervous system ?

A 
immune system has small amount of MHC class I expression 
avoid immune attack as it cant be activated
179
Q

How is HSV reactivated ?

A 
times of stress
sunlight
bacterial infection
hormonal changes
HSV reactivated and infects epithelial cells causing spores
180
Q

What are examples of latent viral infections ?

A

Lentivirus group- HIV

EBV

181
Q

How does EBV cause glandular fever ?

A

infecting B cells
remaining dormant in a small number in B cells
swollen lymph nodes

182
Q

Which individuals are likely to be reinfected with EBV ?

A

immunosupressed individuals

183
Q

Reactivated EBV can lead to what ?

A

disseminated EBV and infected B cells can become malignant - B cell lymphoma

184
Q

What does reactivation of varicella zoster lead to ?

A

shingles in adult life

185
Q

Why is sabotage and subversion of the immune system the greatest in viruses ?

A

greatest variety of mechanisms in their life cycle

life cycle depends on interactions with host cell metabolic and synthetic processes

186
Q

What are the mechanisms of Herpes simplex ?

A 
blocks normal antigen presntation by MHC class I 
lives in nervous system where there isnt much MHC class I anyway
187
Q

What are the consequences of no MHC class I expression ?

A

no recognition of virally infected cells by cytotoxic cells

mechanism of herpes simplex and cytomegalovirus

188
Q

How does treponema pallidium evade antibody recognition ?

A

coats in fibronectine- evade antibody recognition

189
Q

What does P.gingivalis do to digest antibodies ?

A

secrete proteases

190
Q

How does Mycobacterium TB evade phagocytosis ?

A

prevents fusion of lysosome and phagosome

191
Q

What are bacteria superantigens ?

A

staphylococcal enterotoxins

192
Q

What do bacterial superantigens do ?

A 
link TCRs and MHC class I independent of the antigen
stimualtes excessive polyclonal response of T cells
193
Q

What is the consequence of excessive T cell cytokine release ?

A

toxic shock syndrome

194
Q

What is an example of toxic shock syndrome ?

A

staph aureus contaminated vaccines

195
Q

What happens to T cells in toxic shock after being overstimualted ?

A

undergo apoptosis

leaves few clones in circualtion

196
Q

What happen in toxic shock syndrome ?

A 
toxin shock 
dissemianted infection
systemic inflamamtion 
loss of blood loss to the tissue 
organ hypoperfusion
197
Q

What are the causes of Primary immunodeficiencies ?

A

affect immune cell development

gene mutation

198
Q

What are the consequences of primary immunodeficienciencies ?

A

innate/adaptive immune deficiency manifesting as recurrent infections

199
Q

What do T cell deficincies lead to ?

A

candida infections
viral infections
intracellular pathogens as no CD8

200
Q

What do complement, B cell and phagocyte deficiencies lead to ?

A

extracellular pathogen infections

pyogenic infections

201
Q

What are examples of Primary immunodeficincies ?

A

SCID
XLA
CVIDs

202
Q

What are many primary immunodeficnecies due to ?

A

x linked recessive mutations

203
Q

What happens in SCID ?

A

T cell deficnecy
leads to severe immunodeficnecy
no T cells, no help for B cells and no memory cells as no T cell cytokines mase

204
Q

What is X linked SCID caused by ?

A

mutations in genes for cyotkine signalling molecules
genes for IL-2 receptor and Jak3
lack of cells that need these cytokines for development- T cells, NK cells and B cells

205
Q

What is Jak3 ?

A

protein kinase

206
Q

What are other causes of SCID ?

A

RAG 1/2 mutation

ADA mutations

207
Q

What is ADA ?

A

adenosine deaminase

208
Q

What is the treatment for SCID ?

A

bone marrow transplantation

209
Q

What is the most common primary immunodefcinecy ?

A

CVID

210
Q

What are the characteristics of CVID ?

A

mild immunodeficiency
heterogeneous clinically
defects in immunoglobulin production- limited to one type
can cause recurrent infections but many people dont have symptoms

211
Q

What are the forms of IgA deficiency ?

A

familial and sporadic

212
Q

What is hyper IgE deficiency syndrome ?

A

high IgE levels

autosomal dominant

213
Q

How does hyper IgE deficinecy syndrome manifest ?

A

recurrent infection with fungi and pyogenic bacteria

214
Q

What is the cause of hyper IgE deficinecy syndrome ?

A

mutation in STAT TF pathway for Th17 regulation - depleted Th17

215
Q

What are the dental abormalities in hyper IgE deficnecy syndrome ?

A

supernumerary teeth
fusion of primary teeth
retention of primary
delayed/ectopic eruption of permenant teeth

216
Q

What is the technique used to assess Th17 cell deficinecy ?

A

flow cytometry

217
Q

What is XLA ?

A

brutons x linked agammaglobulinemia

218
Q

What happens in XLA ?

A

failure of BCR signalling
B cells are arrested at pre B Cell stage
leads to B cell deficiency
lack of antibodies

219
Q

What is the consequence of XLA ?

A

recurrent infections with extracellular pyogenic bactiera like strep pneumoniae
chronic infections with poliovirus,Hep B and Hep C

220
Q

What is the treatment for XLA ?

A

immunoglobulin infusion

antibiotics for bacterial infections

221
Q

What do complement deficiencies lead to ?

A

recurrent infections with extracellular bacteria

222
Q

What does C3 deficiency lead to ?

A

recurrent strep pneumoniae

pnuemococcus infection

223
Q

What does C5 deficiency lead to ?

A

susceptibility to neissera menigitides

leads to meningococcus infectious

224
Q

What other disroders can complement deficinecy lead to ?

A

congenital neutropenia

leukocyte adhesion deficiencies

225
Q

Why do complement and Ig deficiencies overlap ?

A

they both work together

226
Q

What are the causes of secondary acquired immunodeficinecies ?

A 
immune senescnece- ageing and poor nutrition 
Burns- remove skin and vasculature 
immunosupressants 
tumours 
HIV
227
Q

What is chronic lymphocytic leukaemia ?

A

make only one type of cell
die from infections
vaccines also become ineffective

228
Q

Where is HIV prevalent ?

A

sub sahran africa

229
Q

What was the HIV prevalence in 2018?

A

37.9 million

230
Q

What was the daily HIV incidence in 2018 ?

A

5000 new cases a day

231
Q

What are the properties of HIV ?

A

genetic variability is high due to high mutation rate
classified into 3 groups based on nucloetide sequencing -
M,O and N

232
Q

What are the factors that influence AIDS progression ?

A

viral load when innoculated - high viral loads can lead to faster progression
Age
genetic host variation- some genotypes confer resistnace to AIDS progression
antiviral drug treatment- prolongs T cell recovery periof

233
Q

What is the evidence of resistanct to AIDS progression ?

A

progression resistance in seroconverted individuals with low viral load
HIV negative individuals with high exposure dont get virus

234
Q

What is the effect of age on AIDS preogression ?

A

younger HIV+ people are less likely to succumb to AIDS- slow progression

235
Q

What are the host genetic variants that influence AIDS progression ?

A

KIR
HLA
CCR5

236
Q

What do polymorphisms in HLA ans KIR do ?

A

different polymorphisms make some people more resistant and some more susceptible to AIDS

237
Q

What is CCR5 ?

A

chemoline receptor on memory cells

238
Q

What does HIV do to CCR5 ?

A

binds to it and blocks it

239
Q

What happens in a CCR5 mutation ?

A 
frameshift 
producing a truncated protein 
HIV no longer binds 
hetero- slow progression
homo- progression halted
240
Q

What does HIV do with reverse transcriptase ?

A

HIV converts RNA to cDNA

via reverse transcriptase

241
Q

Why is reverse transcriptase targeted in HIV therapy ?

A

stops viral replication

242
Q

How is Reverse transcriptase targeted

A

with nuceloside analogues and non-nucleoside analogues

243
Q

What is the role of protease in HIV ?

A

cuts large proteins into smaller ones

uses this for viral assembly

244
Q

How can protease be targeted in HIV therapy ?

A

protease inhibitors

245
Q

What is the problem with HIV therapy ?

A

resistance to therapy is conferred in HIV quickly due to high mutation rate

246
Q

How does drug resistance happen in HIV ?

A

drug initially given and RNA decreases, CD4 cells recover

mutation happens again and virus appears with resistance and CD4 cells deplete

247
Q

How can HIV drug resistance be avoided ?

A

combinatorial drug therapy

248
Q

What is HAART ?

A

highly active antiretroviral therapy

249
Q

What does HAART do ?

A

reduces viral load

reducing morbidity and mortalit

250
Q

What has an increase in HAART lead to ?

A

decrease in deaths

251
Q

What are the disadvantages of HAART ?

A

Doesnt fully clear virus
lifelong treatment necessary
expensive
severe side effects

252
Q

What is the definition of autoimmunity ?

A

responses to self antigen/commensal flora leading to tissue damage

253
Q

What is the normal state of self tolerance ?

A

lymphocytes which react to self antigen are eliminated

254
Q

What is autoimmuniy characterised by ?

A

breakdown in self tolerance

255
Q

What is autoimmunity mediated by ?

A

autoreactive antibodies

autoreactive T cells

256
Q

What is psoriasis ?

A

autoreactive T cells against skin antigens
skin inflammation
formation of scaly patches and plaques

257
Q

What is rheumatoid arthritis ?

A

autoreactive T cells against joint synovium

joint destruction and inflammation

258
Q

What is graves disease ?

A

autoantibodies agaisnt TSH receptor

leads to hyperthyroidism and overproduction of thyroid hormones

259
Q

What is hashimoitos thyroiditis ?

A

Autoantibodes and autoreactive T cells to thyroid antigens
destruction of thyroid tissue
hypothyroidism
underproduction of thyroid hormones

260
Q

What is Systemic lupus erythematosus ?

A

autoantibodies and autoreactive T cells against DNA and chromatin leads to glomerulonephritis

261
Q

What is sjorgens syndrome ?

A

autoanitobodies and autoreactive T cells against ribonucleoprotein antigens
lymphocyte infiltrate of exocrine glands

262
Q

What is crohns disease ?

A

Autoreactive T cells against intestinal Flora antigens

intestinal epithelium inflammation and scarring

263
Q

What is multiple sclerosis ?

A

autotoreactive T cells against brain antigens
formation of sclerotic plaues in brain and destruction of myelin sheath
leading to muscle weakness

264
Q

What is type one DM ?

A

autoreactie T cells against pancreatic Beta cells
destruction of pancreatic beta cells
non production of insulin

265
Q

What are the mechanisms of self tolerance ?

A

central tolerance

antigen segregation

266
Q

What is central tolerance ?

A

deletion and editing of T cells that react to self antigen
happens in thymus gland
breakdown leads to autoimmunity

267
Q

What is antigen segregation ?

A

physical barrier to self antigen and lymphoid system

in peripheral organs like pancreas

268
Q

Is breakdown in self tolerance enough to trigger autimmunity ?

A

not sufficient

environmental triggers like infection and genetic triggers will also be needed

269
Q

Can autoimmune cells that escape central tolerance be destroyed ?

A

yes- peripheral tolerance- Treg cells

270
Q

What is the aetiology of autoimmunity ?

A

unknown

271
Q

What is the effector mechanism of autoimmunity ?

A

autoreactive T cells

autoantibodies

272
Q

What is the aim of the normal immune system ?

A

remove non self antigen

273
Q

Can self antigen be eliminated ? What is the implication of this ?

A

self antigen cannot be destroyed hence a chronic infection ensues

274
Q

What are the exceptions to the destruction of self antigen rule ?

A

hashimotos thyroiditis and type one DM - actually destroy the tissue

275
Q

What are the ways in which autoimmune disease can be classified ?

A

organ specific
non specific- many tissues effected
inflammatory bowels disease
clustering in families

276
Q

What are examples of organ specific autoimmune diseases ?

A

type one DM
goodpastures syndrome
crohns disease
graves diseasse

277
Q

What is an examples of a sytemic autoimmune disease ?

A

rheumatoid arthritis
primary shorjens syndrome
systemic leupus erythematosus

278
Q

What is the progress of autoimmune diseases ?

A

activation phase leads to a chronic phase

279
Q

How are the chronic effects of autoimmune diseases mediated ?

A

autoantibodies

autoimmune T cells

280
Q

What mediates the effects of myasthenia gravis ?

A

autoreactive antibodies

281
Q

What is tissue breakdown mediated by in autoimmune diseases and what is the result ?

A

tissue breakdown mediated b integrated immune response
loss of tissue function
tissue breakdown replenishes self antigen

282
Q

What is a type II autoimmune disease ?

A

antibodies against cell surface

283
Q

What are examples of type II autoimmune diseases ?

A

goodpastures syndrome
pemphigus vulgaris
bullous pemphigoid

284
Q

What is goodpastures syndrome ?

A

antibodies against collagen type IV in basement membrane

manifests as pulomonary haemorrhage and glomerulonephritis

285
Q

What is pemphigus vulgaris ?

A

autoantibodies agaisnt epidermal cadherin joins epithelial cells
mainfests as skin blistering and heamorrhage

286
Q

How can we identify pemphigus vulgaris ?

A

create antibodies complementary to antibodies that are autoimmune to cadherin
tag first antibody with fluorsence

287
Q

What is bullous pemphigoid ?

A

autoimmune antibodies to basement membrane

288
Q

What is a type III autoimmune disease ?

A

immune complex- complex of antigen an antibodies causing effects- large molecules that depsoit in tissue recruiting neutrophils leading to inflammation

289
Q

What are the 2 examples of type III autoimmune disease ?

A

mixed essential cryoglobulinemia

rheumatoid arthritis

290
Q

What is the complex in mixed essential cryoglobulinemia ?

A

rheumatoid facto igG complexes- systemic vasculitis

291
Q

What is the complex in rheumatoid arthritis ?

A

rheumatoid factor IgG complexes

292
Q

What is a type IV autoimmune disease ?

A

T cell mediated

293
Q

What are examples of type IV autoimmune diseases ?

A

Type I DM

multiple sclerosis

294
Q

What is type one DM ?

A

T cells cluster around B islets of langerhans and destroy - leading to non production of insulin
antigen is pancreatic beta cell

295
Q

What is multiple sclerosis ?

A

myelin protein
destruction of myelin sheath by T cells
brain invasion by CD4 cells
muscle weakness

296
Q

What are the cells of the pancreas ?

A

alpha cells- glucagon
beta cells- insulin
gamma cells- somatostatin- GHIH

297
Q

How does type one DM selectively target beta cells ony ?

A

effector cytotoxic T cells recognise peptides of a beta cell specific protein- kill B cell- no insulin made

298
Q

What classification is Rheumatoid arthritis ?

A

type III and IV

299
Q

Myasthenia gravis and graves disease are examples of what ?

A

autoantibodies against cell surface receptors

300
Q

What happens in myasthenia gravis ?

A

affects NMJ
antibodies to acetylcholine receptors which are degraded
no signalling between neurones and muscles

301
Q

What is graves disease ?

A

autoimmune B cell makes antibodies against TSH receptor on thyroid gland, the antibodies also stimulate thyroid hormone production
autoimmune antibodies shut down TSH via negative feedback and thyroid hormone
trigger thyroid production- hyperthyroidism

302
Q

What is SLE ?

A

antibodies to common antigens like DNA
widespread butterfly red patches
systemic
detected in immunofluoresence

303
Q

What is the evidence for the genetic component of autoimmune diseases ?

A

family studies- it is in families
nearly 100% concordance in identical twins
mice clones have different susceptibility

304
Q

What is the evidence for the environmental component of autoimmune diseases ?

A

lack of 100% concordance in identical twins

different age of onset in identical mice

305
Q

What is the difficulty of analysing genes for autoimmune diseases ?

A

outbred popualtion

interindividual variation is great

306
Q

What are the ways in which we can analyse genes to look at gene association ?

A

candidate gene studies look at association and linkage
GWAS
knock out genes to see if needed in pathogenesis

307
Q

What is the conclusion from study of genes and autoimmune diseases ?

A

autoimmune diseases are polygenic being influenced by multiple alleles on numerous different gene loci

308
Q

What is a gene loci ?

A

area of a chromosome

309
Q

Which gene variants are associated with Autoimmune diseases ?

A

HLA variants- they are highly polymorphic

310
Q

What do HLA genes do ?

A

encode MHC proteins - MHC has peptide groove where antigen sits
changing amino acid composition of peptide binding groove changes interaction between antigen and MHC

311
Q

Variations in HLA genes can confer what ?

A

resistance to breakdown in self tolerance

suscpetibility

312
Q

What is the role of MHC ?

A

antigen presentation

T cell development in thymus gland

313
Q

Which polymorphism effects CD4 cells ?

A

DR class II

314
Q

Which polymorphism effects CD8 cells ?

A

B27 class I

315
Q

What is the odds ratio ?

A

ratio of the chance of a disease developing in members of the population exposed to a certain factor compared to members who are not exposed

316
Q

Which polymorphism is present in most AD diseases ?

A

DR polymorphism- class II

317
Q

Which gender is more at risk for AD diseases ?

A

females

318
Q

What is the role of infection in AD diseases ?

A

infection can trigger autoimmunity in hosts with the right genetic make up

319
Q

Why does infection play a role in AD diseases ?

A

infection triggers MHC presentation and APC activation and cytokines - bystander effect of autoimmune cells
adaptive resposne more likely to be triggered
adjuvant effect demonstrated in animal models

320
Q

What is molecular mimicry ?

A

cross reaction between microbial antigens and own antigens

stimulate autoimmune reaction to self antigens

321
Q

Give an example of molecular mimicry ?

A

rheumatic fever
infection with strep antigen
cross react with cardiac muscle
degenerate cardiac muscle

322
Q

What is an allergic response ?

A

hypersensitivity reaction to an otherwise harmless extrinsic antigen

323
Q

What is the classification of allergic responses ?

A

same as autoimmune- type II.III and IV

but also have type I not seen in autoimmune

324
Q

What are the shared effects of autoimmune and allergic responses ?

A

inflammation and tissue destruction

325
Q

What are the environmental antigens in hypersensitivity ?

A

inhaled- plant pollen and dust mice faeces
injected- drugs and insect venom
ingested- peanuts and shellfish
contacted materials- plant oil and metal

326
Q

What is a type I hypersensitive reaction ?

A

immediate type

327
Q

What is the range of consequences in a type I hypersensitive reaction ?

A

mild attrition to anaphylaxis

328
Q

What is atopy ?

A

an allergy with a genetic predisposition like hayfever

329
Q

What are examples of atopic disorders ?

A

10-40% caucasians have one

asthma, eczema and uticaria

330
Q

What is uticaria ?

A

hives

331
Q

What mediates type I hypersensitivity reactions ?

A

IgE and mast cells

332
Q

When do type I hypersensitivity reactions occur ?

A

immediately after exposure to allergen

333
Q

What do mast cells do in hypersensitivity reactions ?

A

release inflamamatory mediators

cause pathological effects

334
Q

What does the hygeine hypothesis state ?

A

early childhood exposure to particular micoorganisms like gut flora and helminth parasites protect against allergic diseases by contributing to immune development
explains why allergies are increasing as children are getting less exposure to these microbes

335
Q

What is Der P I ?

A

common respiratroy allergen found in foecal pellets of house dust mite

336
Q

What are the 2 phases that lead to type I hypersensiticity ?

A

sensitisation and reaction

337
Q

What happens in the sensitisation phase of type I hypersensitivity ?

A

susceptible individuals present antigen to get a Th2 response
activates B cells and mast cells
plasma cells made which made IgE to the allergen

338
Q

What happens in the reaction phase of type I hypersensitivity ?

A

allergen is encountered again
IgE binds to mast cells via Fc receptrors
releasing inflamamtory mediators
cause hypersensitivity

339
Q

What does cross linking of IgE on mast cell surfaces lead to ?

A

on second exposure leads to release of mast cell granules containing inflammatory mediators
like histamine

340
Q

What types of molecules can be released by mast cells in granules ?

A

histamine, heparin

TNF-alpha

341
Q

What do histamine and heparin do ?

A

toxic to parasites
increase vascular permebaility
smooth muscle contraction
anticoagualant

342
Q

What does TNF-alpha do ?

A

promotes inflamamtion via cytokines leads to swelling

343
Q

What are the IgE mediated reactions to extrinsic antigens ?

A

systemic anaphlyaxis

acute uticaria

344
Q

What happens in systemic anaphylaxis ?

A

stimuli- drugs, venom and peanutes
allergens enter via IV or after absorption
edema, increased vascular permeability, circulatory collapse and death

345
Q

What is acute uticaria ?

A

animal hair, bee stings and allergy resting
allergens enter through skin
leads to wheal and flare
local increase in blood flow , vascular permeability and eedema

346
Q

What are the phases of an allergic reaction ?

A

imemdiate reaction and late reaction

347
Q

What is usually an imemdiate reaction in allergic situations ?

A

Wheal- raised area

flare- redness

348
Q

What is a late reaction to allergic reactions ?

A

swelling spreads from site of injection

swelling leads to increased blood flow and tissue fluid to area.

349
Q

What is systemic anaphylaxis ?

A

allergens reaching the bloodstream activating mast cells throughout the body
mast cell degranulation throughout the body

350
Q

What are some of the systemic effects of systemic anaphylaxis ?

A

increased capillary permeability
smooth muscle contraction
wheezing
stomach cramps

351
Q

Why has IgE evolved ?

A

to get rid of metazoan parasites
eg. ascaris and schistosoma - worms

conventional immune systems are not effective to get rid of

352
Q

What are the effects of IgE ?

A

eject pathogen by physical force - coughing, sneezing and vomiting
invovles Th2 response- help B cells to produce IgE

353
Q

What does IgE arm ?

A

arms mast cells, eosinophils and basophils to respond to parasite antigens by binding to Fc receptors on the cells

354
Q

What are the other roles of mast cells ?

A

at mucosal surfaces express Fc receptors and TLRs

355
Q

What is a type I hypersensitive reaction ?

A

Immune response at the cell surface

356
Q

What is an example of a type II hypersensitive reaction ?

A

haemolytic anaemia

357
Q

What are the causes of heamolytic anaemia ?

A

penicillin allergy
blood group incompatibility
autoimmune haemolytic anaemia

358
Q

What happens in haemolytic anaemia ?

A

autoimmune Antibodies bind to RBCs
the antibodies also bind to Fc receptors on phagocytes leading to phagocytosis
complement fixation- RBC destruction and intravascular haemolysis

359
Q

What happens in type III hypersensitivity ?

A

antigen.antibody complex deposition leads to inflammation

360
Q

What is an example of type III hypersensitive reactions ?

A

serum sickness
in response to injected therapeutic antibody such as mouse antibody
in susceptible individuals the albumin proteins in serum also lead to an immune response - deposition of complexes in skin leads to rash

361
Q

What is another cause of type III hypersensitivity ?

A

pencillin allergy

362
Q

What happens in penicillin allergy ?

A

penicllin modifies protein on RBC
creates foreign epitopes
creates antibodies to penicillin modified proteins leading to other hypersensitivies

type I- anaphylaxis
type II- haemolytic anaemia
type III- serum sickness

363
Q

What is a type IV hypersensitive reaction ?

A

delayed type T cell mediated

364
Q

What happens in type IV hypersensitive reactions ?

A

activation of macrophages by Th1 cells
secretions lead to tissue necrosis

activation of CD8 cells - cytotoxic to cells

365
Q

Where can type IV hypersensitivty be seen ?

A

allergic contact dermititis
graft rejection
poison ivy and nickel allergy

366
Q

What happens in allergic contact dermititis ?

A

antigen is injected into subcutaenous tissue
processed by local APCs
Th1 cell recognises antigen
releases cytokines that act on vascular endothelium, recruit neutrophils casuing a visible lesion

367
Q

How does allergic contact dermititis manifest ?

A

blisterng skin lesions

368
Q

What happens in nickel allergy ?

A

T cell mediated response to foreign antigens or modified self antigens
nickel modifies peptides in allergy leading to a CD4 response

369
Q

What happens in poison ivy allergy ?

A

chemical in ivy called pentadecatechol modfies self antigens leading to CD8 response

370
Q

Why is type IV hypersensitivity delayed ?

A

requires development of T cells

unlike immediate type I- already sensitised

371
Q

What considerations should be made with allergic rhinitis ?

A

mouthbreather and develop mild gingival hyperplasia

372
Q

What considerations should be made with antihistamines ?

A

cause dry mouth

373
Q

What is angiodema ?

A

rapid swelling of dermis and mucosa in response to allergen

374
Q

What is oral allergy syndrome ?

A

food allergy from fruit and veg

leading to allergic reactions in the mouth

375
Q

Where can latex allergies be found ?

A

gloves. dental dams and tubing

376
Q

What are the histological features of coeliac disease ?

A

inflammatory filtrate
tissue damage
lengthening crypts
increased epithalial cell division

377
Q

What are the clinical consequences of coeliac disease ?

A 
abdmoinal distention 
malabsorption 
diarrhoea 
anaemia 
intestinal cancer
378
Q

What is coeliac disease ?

A

inflamamtion of the jejunum due to a response to gluten

379
Q

What is gluten ?

A

complex of proteins found in wheat, barley and oats

380
Q

What is the management of coeliac disease ?

A

elimination from the diet

381
Q

Why is the incidence of coeliac disease increasing in china and india ?

A

western diet increasing

382
Q

What is the molecular basis of coeliac disease ?

A

normally gluten peptides dont bind to MHC class II
in coelaic disease, enzyme called trandglutaminase modifes peptides allowing them to be presented MHC class II - activates CD4 cells
activated CD4 cells kill mucosal epithelial cells via Fas pathway
activated T cells also secrete IFN gaamma to activate other inflamamtory cells like macrophages

383
Q

is transglutaminase active in non coeliacs ?

A

no it is inactive in non coeliacs

384
Q

What is the genetic predisposition to coeliac disease ?

A

95% of coeliacs have HLA-DQ2 allele
but this does not lead to coeliac disease, just more suscpetible to coeliac disease

80% concordance in identical twins
6x higher in downs syndrome

strong genetical element but also an environmental interaction

385
Q

What are inflammatory bowel diseases ?

A

chronic inflammatory diseases with features of autoimmune disease
immune response to commensal gut flora
crohns disease and ulcerative colitis
antigens are from gut microflora

386
Q

What are the manifestations of crohns disease ?

A

transmural inflammatory lesions - involve epithelium and lamina propia
chronic and episodic
thickened/fissured bowel
fistulation

387
Q

What happens in normal immune gut regulation ?

A 
mucus present in mucosal layers 
paneth cells make AMPs
IgA also present 
M cell samples environment for antigen and presents to peyers patch 
activate T/B cells make IgA
388
Q

What happens in crohns disease ?

A

cant secrete AMPs- cant tolerate normal microflora

389
Q

What are the oral manifestations of crohns disease ?

A

cheilitis
oral ulceration
fissuring
glossitis

390
Q

What are the genetic variants associated with crohns disease ?

A

NOD2
ARGM
IL23R

391
Q

What happens to NOD2 in crohns disease ?

A

NOD2 is intracellular PRR
detects peptidoglycan and muramyl dipeptides

mutations means cells cant recognise bacteria
mutations in all mucosal cells- includig mouth
Immune dysfucntion means imparied AMP secretion
sustained bacterial exposure

392
Q

What happens to IRGM in crohns disease ?

A

IRGM usually used in autophagy - tag with ubiquitin to recycle

immune dysfucntion means mutation leads to sustained cytokine secretion and inflammation

393
Q

What happens to IL23R in crohns disease ?

A

usually IL23R activates Th17 cells and inhibits Treg cells

immune dysfucntion leads to sustained inflamamtions and supression of T reg cells

394
Q

What is the pathogenesis of crohns disease ?

A

Failure of immunoregulatory mechanisms to toelrate commensal bacteria
failure of innate immunity- no AMPs leading to failure of the adaptive immunity- CD4 cells
microbial dysbiosis

395
Q

Which metabolic disorders are involved with inflammation ?

A

gout and T2DM

396
Q

Are gout and T2DM genetic ?

A

no- theyre acquired

mainly environmental

397
Q

What other conditions can gout and diabetes be involved with ?

A

obesity and CVD

398
Q

What is gout ?

A

inflammation of the digits, toes and joints

EG. metatarsal joint

399
Q

What leads to gout ?

A

uric acid crystal deposition
leads to inflamamtion
activates the inflamamsome

400
Q

What is the inflammasome ?

A

complex of proteins which drive IL-1 secretion
more inflamamtion
use anti IL-1 therapy

401
Q

What are the forms of gout ?

A

primary gout- may be genetic

secodnary gout- due to chemotherapy/drugs

402
Q

What is the pathway for gout ?

A 
primary/secondary gout 
hyperuricemia 
crystal formation in periphery 
crystal depostion 
gout flares
403
Q

What factors can exacerbate crystal deposition in gout ?

A

western diet
obesity
age

404
Q

What is the link between diabetes type 2 and inflammation ?

A

hyperglycaemia
advanced glycation end products and oxidative stress
immune dysfucntion- cytokine imbalance- TNF alpha, IL-6 and IL-1
exacerbated by adipokines
inflamamtroy state
enhanced tissue destruction leading to rheumatoid arthritis, impaired tissue repair leading to CVD and periodontitis , pancreatic Beta cell destruction

BDS stage 2 (28 decks)

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