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EMS - JL > 17,18,19 > Flashcards

17,18,19 Flashcards

1
Q

What do patterns recognition receptors recognise

A

Recognise antigens and have diversity of type

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2
Q

what are the 2 themes of PRRs

A

Recognsiing PAMPS and DAMPS

Recognise foreign cells accordingly but not the exact type

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3
Q

What does the TLR-4 receptor recognise

A

LPS

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4
Q

What does the TLR-5 receptor recognise

A

Flagellin

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5
Q

What does the TLR-9 receptor recognise

A

DNA fragments (intracelluar)

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6
Q

What does NLRP3 and RLRs recogneis

A

IL-1 the first pro-inflammatory cytokine produced in infection

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7
Q

What do collections recorgnise

A

Complex carbohydrates in microbes

e.g. MBL, surfactant protein A & B

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8
Q

How to the carbohydrates bind to the callectns in the C-type Lectin family

A

Via Carbohydrate Recognition Domains

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9
Q

Role of the C-typle Lectin familias

A

Neutrilisng pathogen in recruitment of adaptive response

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10
Q

Antimicrobial peptide examples

A

Defensins, cathelins, protegrins, probiotics

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11
Q

What do plasmocytoid dendritic cells produce

A

IFN –> an anti tumour and antibviral

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12
Q

what do mast cells and basophils release in response to PAMPS

A

Il-6, TNF and IFN

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13
Q

What do epithelial cells produce

A

Antibmicrobial peptides and local mediation of innate immunity

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14
Q

What does surfactant protein in the lungs bind

A

Microbes and promote their clearance

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15
Q

What IL causes muscle ache and drowsiness

A

IL-1

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16
Q

What cytokines are classically produced initially and important for the adaptive immune response to occur

A

IL-1, IL-6 and TNF

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17
Q

What is IL-23 used for

A

By macrophages and dendritic cells to target T lymphocytes

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18
Q

What happens when a lymphocyte encounters an antigen

A

Undergoes clonal expansion!

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19
Q

Where t and B cells first meet infection

A

In the lymph nodes

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20
Q

How is the diversity of antigen receptors increased

A

By the VJD recombination of genes

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21
Q

Why is there still some auto-reactivity of T cells

A

Although we delete T cells that recognise our own cells there are still similar structures in pathogens and human cells (but this amount is small)

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22
Q

What happens in antigen presentation

A 
Antigen internalised and broken down by proteasome
Peptides associated with newly synhtesised class II molecules and brought to the surface
Foreign peptides recognised by T helper cells and these are activated and produce cytokines needed by B cells
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23
Q

What are histocompatibility NTIGENS

A

Glycoproteins on the surface of mammalian cells

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24
Q

What are class 1 HLA

A

HLA-A,B.C

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25
Q

What are class 2 HLA’s

A

HLA-DQ,DP,DR

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26
Q

What do MHC1 present to

A

Cytotoxic T cells

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27
Q

What do MHC2 present to

A

Helper T cells

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28
Q

How is a T cell activated

A

B cell presents antigen to it, needs a signal from a T cell receptor and a second signal from another CD protein to go any further

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29
Q

What are the roles of antigens

A

Neutrilisation, agglutination and precipitation of dissolved antigens
Enhances phagocytosis

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30
Q

What does activation of the complement system cause

A

Cell lysis

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31
Q

How do cytotoxic T lymphocytes kill cells

A

Bind to infected cells
Perforin makes hole in cell membrane
Enzyme enters promoting apoptosis

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32
Q

What are the targets of HIV

A

CD4 cells

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33
Q

What do suppressor T lymphocytes do?

A

Dampen down the immune response

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34
Q

What is the significance of IL-17

A

Produced by t-lymphocytes and plays an important role in autoimmune conditions

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35
Q

What is immunodefeciency

A

lack of an efficient immune system –> susceptible to infection

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36
Q

What disease are you susceptible to if PRRs aren’t working

A

Pneumococcus and HSV (don’t get an inflammatory response)

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37
Q

What disease are you susceptible to if Effector T cells aren’t working

A

SCID and opportunistic infections

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38
Q

What disease are you susceptible to if complement proteins aren’t working

A

meningococcus

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39
Q

What disease are you susceptible to if macrophages/neutrophils aren’t working

A

GCD, aspergillus, staphylococcus

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40
Q

What disease are you susceptible to if cytokines aren’t working

A

Mycobacterium

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41
Q

What disease are you susceptible to if B cells aren’t working

A

recurrent sino-pulmonary infections

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42
Q

What is hypersensitivity

A

Undesirable reactions produced by normal immune system against innocuous antigens in a pre-sensitised (immune host_

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43
Q

What type is type 1 hypersensitivity

A

anaphylactic - IgE mediated

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44
Q

Common antigens in type 1 hypersensitivity

A

pollen, bee venom, anaimal danader

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45
Q

Onset of type 1 hypersensitivity

A

15-30 munutes

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46
Q

What happens in type 1 hypersensitivity

A

IgE mediated mast cell and basophil deranulation

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47
Q

What is IgE produced under

A

By B cells under the control of Il-4 and CD40-L-CD40 interaction

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48
Q

What receptor does IgE attach to

A

FC13 receptor on mast cells has a high affinity for it

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49
Q

How do mast cells activate

A

Fc3R1 receptor in high densities on the surface binds IgE, crss linking by he allergen activates the mast cell

Causese degranulation of synthesis of lipid mediators

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50
Q

What mediators are pre formed

A

histamine
Kallikrin
Tryptase

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51
Q

What does histamine do

A

increases vascular permeability (vasodilation), smooth muscle contraction and stimulates irritant nerve receptors

52
Q

What does kallikrein do

A

activates bradykinin (similar role to histamines)

53
Q

What are the lipid mediators and how are they formed

A

Formed from arachidonic acid
Leukotrienes (formed due to 5lipooxygenase enzyme)
Prostaglandins (formed due to COX enzyme)

Takes 4-6 hours to produce these lipid mediators

54
Q

What causes the late phase repose and what is their role

A

Basophils - similar role to mast cells but longer term
Eosinophils - Make granules containing cytotoxic proteins –> release granule content in tissues causing tissue damage. Also make cheekiness to attract cells to site of inflammation
T cells - in early and late response –> produce cytokines –> cause inflammmation

55
Q

What is the type 2 hypersensitivity reaction

A

Antibodiy mediate cytotoxic reaction

56
Q

how does type 2 hypersensitivity occur

A

Antigen binds to antibody on cell membrane
Complement cascade activated
Fc protions of Immunoglobulin/C3b aggregate with FcR5/C3Rb resulting in opposition, phagocytsosis and destruction

57
Q

Antibodies in type 2 hypersensitivity

A

IgG (and IgM)

58
Q

What type of reactions usually occur in type 2 hypersensitivity

A

usually haemopoietic cells

Blood group incompatibilities, autoimmune haemolysis

59
Q

What is hypersensitivity type 3 reactions

A

Immune complex reactions

60
Q

What happens in hypersensitivity type 3 reactions

A

Antigen antibody complex formed –> deposited around body causing inflammation
FCR in complex binds to C1q –> activates the complement cascade

61
Q

What happens in hypersensitivity type 3 reactions when the complement cascade is activated

A

C5a attracts neutrophils
C3b binds opsonin
Attempted phagocytosis of these complexes –> releases enzymes and oxygen free radicals –> consequence is tissue damage

62
Q

Types of reactions in hypersensitivity type 3

A

Vasculitis, nephritis, Arturhs reaction, farmers lung, glomerular nephritis

63
Q

What is hypersensitivity type 4 reactions

A

T cell mediated CD4+ reaction

Delayed type reaction

64
Q

Examples of delayed type reactions

A

Tuberculin skin test

65
Q

What happens in hypersensitivity type 4 reaction

A

Perivascular infiltration of lymphocytes and monocytes
Langerhans cells present antigens to T cells
T cells release cytokines
Cytokines activate macrophages
Macrophages cause tissue damage

66
Q

What are haptens

A

small chemicals causing changes to innate proteins

67
Q

What are Type V Hypersensitivity reactions

A

Inactivation e.g.

1) Direct –> intrinsic factor B-12 deficiency
2) Indirect –> binding to hormone resulting in clearance antigen antibody complex
3) Receptor blockade –> e.g. inappropriate response to ACHR Receptor in myasthenia gravis

68
Q

What is T cell mediated cytotoxicity CD8+ T cells

A

Contact dermatitis
Nickel acts as a happen with epidermal proteins
Keratinocytes may present this to CTL precursors!

69
Q

What are granulomas

A

Focal collection of inflammatory cells in tissue

70
Q

What Th1 cells sectere

A

IFN and Il-2

IL-2 also released by macrophages crucial for granulomatous response

71
Q

What are the 2 types of reaction in leprosy

A

Th1 - protective

Th-2 non-protective

72
Q

Examples of granulomatous reactions

A

Mycobacterium: TB, leprosy

Also crowns, sarcoidosis and Wegeners granulomatosis

73
Q

Features of acute inflammation

A 
Fast onset
Neutrophils
Prominent signs
Mild, self-limiting tissue injury
Vessels dilate and leak --> protein rich exudate
74
Q

Features of chronic inflammation

A 
Slow onset: days to years
Macrophages, lymphocytes, plasma cells
Subtle signs
Severe and progressive
Granulation and scar tissue abundant
Usually primary but can be sequential from acute
75
Q

Causes of acute to chronic inflammation

A

Most common is suppurative acute infection
Pus forms an abscess –> if deep enough the walls thicken
Granulation and fibrous tissue forms

Recurrent acute can lead to chronic e.g. cholecystitis –> gall bladder inflammation due to stones

76
Q

Macroscopic features of chronic inflammation

A

Chronic abscess cavity
Granulomatours e.g. Crohns –> non caseating granulomatous
Fibrosis prominent once inflammatory infiltrate has stopped

77
Q

What is osteomyelitis

A

Chronic abscess in the bone marrow

78
Q

Microscopic features of chronic inflammation

A

Cellular infiltration of mononuclear cells
Exudation of fluid is not prominent
Fibrous tissue produced from granulation tissue

79
Q

The roll of cytokines in chornic inflammation

A

Attract macrophages
Attract neutrophils and facts to increase vascular permeability
Perforin kills invading cells
Produceds interferons to activate NK cells and macrophages
Basophils release prostaglandins to increase blood flow

80
Q

What traps macrophages in the tissue in chronic inflammatoin

A

Macrophage inhibition factor

81
Q

What cell is important in chronic inflammation

A

Macrophages –> they releasee cytokines causing monocytes to enter the endothelium of blood vessels
Macrophages proliferate in tissues and become immobilised

82
Q

Role of macrophages in chronic inflammation

A

Attracted by cytokines, phagocyte bacteria and damaged tissue
Proteases released after they debris damaged tissue

83
Q

What do macrophages do in low oxygen

A

Released factors to cause angiogenesis

Induces cells to re-epitheliase the wound and create granulation tissue

84
Q

What is granulation tissue

A

New connective tissue and blood vessels
It grows from the base of the wound
Aims to replace injured cells by fibrous tissue (appears light red/dark punk due to capillaries)

85
Q

Where does granulation tissue form from

A

Forms from the base of the wound

86
Q

What happens in fibrosis

A

formation of fibrous connective tissue during repair of damaged tissue
Scarring, macrophage induced lying down of connective tissue

87
Q

When is it called a fibroma

A

If it develops from 1 cell line

88
Q

What is a granuloma

A

Aggregate of epithelium histiocytes and other cells, lymphocytes and histolytic giant cells

89
Q

When do histolytic giant cells form

A

Material is indigestable to macrophages

90
Q

When do giant multinucleate cells from

A

Form when 2 or m ore macrophages try to engulf the same particle
No known function!

91
Q

What is epitheliod histiocyte

A

Large vesicular nuclei and esoninophilic cytoplasm

92
Q

Granulomatous bacteria disease

A

TB - lungs, miliary, cough, haemoptysis and night sweats

Leprosy - nerve granulomas, rest, skin, eyes, loss of pain sensation and injury. No autoamputation

93
Q

Granulomatours parasitic disease

A

Schistosomiasis

94
Q

Granulomatous fungal disease

A

Cryptococcus - risk in immunocompromised

95
Q

Granulomatous synthetic disease

A

Silicosis - occupational disease causing scarring and granulations in the lung

96
Q

Unknown granulomatous diseases

A

Sarcoidosis and Crohns

97
Q

Stages of Granuloma formation in TB

A

Stage 1 - 1 week: Inhale TB, invades alveolar macrophages via mannose receptor. TB multiplies inside macrophage

Stage 2 - 2-3 weeks: exponential TB proliferation - can’t be contained in a single macrophage

Stage 3: After 3 weeks: Phagocytosis and proliferation balanced. 90% of patients stop here and are asymptomatic
Round complex formed macrophages with TB in centre and new macrophages surround it –> TB can survive here for years and immune system may destroy it leaving scar

Stage 4: Reactivation –> Proliferation away from immune cells. Active symptomatic infection, contagious and more likely in immune compromised

98
Q

What histological features are you likely to see in granulomas

A

Langerhans giant cells
Caseous necrosis
Epithelioid macrophages

99
Q

Describe inflammation in CV system post MI

A

Involved in atheroma formation –> macrophages adhere to epithelium and recuit other cells, process lipids that accumulate in plaques

100
Q

Describe inflammation in Multiple Sclerosis

A

Plasma cells and T lymphocytes seen in white matter where macrophages break down myelin

101
Q

How does H. Pylori produce gastritis

A

Produces gastritis that damage the intestinal linig

102
Q

What happens rheumatoid arthritis

A

Inappropriate immune response

Immune cells accumulate in the joints

103
Q

What happens in a prolonged exposure to toxic agents (liver)

A

Cytochrome P450-E1 metabolises ETOH –> oxidation of NADPH produces free radicals
ETOH activates macrophages –> Produces TNF-alpha. Mitochondria produce reactive oxygen species. Both of these mechanisms cause apoptosis and necrosis

104
Q

What are the mechanisms of healing damaged cells

A

Healing by regeneration or healing by repair

105
Q

Types of cell population

A

Lable
Stable (Quiescent)
Permanent

106
Q

Describe lable cell populations

A

High cell turnover
Active stem cell population in the basal zone - proliferation
Excellent regenerative capacity
E.g. epithelia

107
Q

Describe stable cell population

A

Low physiological turnover BUT turnover can massively increased if needed
Good regenerative capacity
E.g. liver and renal tubules

108
Q

Describe permanent cell populations

A

No physiological turnover
Long life cells
No regenerative capacity –> lost the capacity divided due to their very specialised function

109
Q

What is essential for the regeneration of cells

A

The survival of the connective tissue framework –> i.e. in the glomeruli and the lungs
In liver cirrhosis cells can proliferate but can’t rebuild normal tissue architecture

110
Q

What are reservoirs of stem cells in adult tissues called

A

Adult stem cell niches

111
Q

When can stem cell niches be destroyed

A

Full thickness burn

Radiation

112
Q

What controls regeneration

A

Covering defect
Contact inhibition
Complex control by growth factors, cell-cell and cell-matrix interactions

113
Q

Repair of cells

A

Healing of cells by non-specialised fibrous tissue scar

114
Q

basic pathological process of scar formation

A

Organisation and granulation tissue fundamental for scar formation

115
Q

3 components of granulation tissue

A

1) New capillary loops
2) Phagocytic cells - macrophages and neutrophils
3) Myofibroblasts - lays down matrix/connective tissue and can become contractily

116
Q

What happens as granulation tissue matures

A

Vascularity and cellularity decreases

Collagen, ECM and wound strength all increase

117
Q

Factors inhibiting healing: Local

A

Infection, haematoma, blood supply, foreign okies and mechanical stress

118
Q

Factors inhibiting healing: Systemic

A 
Age, drugs (steroids), anaemia, diabetes due to the restricted blood supply and metabolic deficit
Malnutrtion
Catabolic state
Vitamin C Defeciency
Trace metal defeciency
119
Q

What are the two types of healing

A

Healing by first intention

Healing by second intention

120
Q

What is healing by first intention

A

Edges of wound opposed
No infection
Clot forms in between edges and phagocytes remove the clot
Healing by process of organisation and granulation converts it to scar

121
Q

What is healing by second intention

A

Wound edges not opposed –> extensive tissue loss

Not functionally different to first intention but much more granulation tissue and more extensive scarring

122
Q

Describe wound strength by day

A

Day 7 - 10% strength allows sutures to be removed

Week 4 - 70-80% strength

123
Q

How do bone fractures heal

A

Haematoma becomes organised
Nectrotic fragments removed
Osteoblasts lay down woven bone - forms a swollen area
Remodelling according to mechanical stress
Replacement by lameallar bone

124
Q

How does healing in the brain occur

A

Neutrons are terminally differentiated hence can’t regenerate
Supporting tissue is glial cells NOT collagen/fibroblasts hence no scar tissue forms

INSTEAD

Damage tissue removed leaving a cyst!
Proliferation of astrocytes to form glial cells which line the cysts GLIOSIS OCCURS

125
Q

Where does gliosis occur

A

during healing in the brain

EMS - JL (10 decks)

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