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Phase 2a > ICS > Flashcards

ICS Flashcards

1
Q

Define inflammation

A

Increased vascular permability accompanied by infiltration of inflammatory cells

Response to injury or infection

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2
Q

When is inflammation beneficial?

A

Destruction of invading microorganisms
Walling off abscess cavity to prevent spread of infection

Good in injury and infection

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3
Q

When is inflammation bad?

A

Autoimmune reactions
Overreaction

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4
Q

What is the sequence of acute inflammation?

A
  1. injury or infection
  2. neutrophils arrive and phagocytose and release enzymes
  3. macrophages arrive and phagocytose
  4. either resolution with clearance of inflammation or progression to chronic inflammation
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5
Q

What is acute inflammation + example?

A

Initial reaction of tissue to injury
e.g. acute appendicitis, strep throat, frostbite

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6
Q

What are the 5 principal causes of acute inflammation?

A

Microbial infections
Hypersensitivity reactions
Physical agents
Chemicals
Tissue necrosis

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7
Q

Example of acute inflammation by microbial infection

A

Pyogenic bacteria
Viruses

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8
Q

Examples of acute inflammation by physical agents

A

Trauma
Ionising radiation
Heat
Cold

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9
Q

Examples of acute inflammation by chemicals

A

Corrosives
Acids and alkalis
Reducing agents
Bacterial toxins

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10
Q

Example of acute inflammation by tissue necrosis

A

Ischaemic infarction

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11
Q

What are the essential macroscopic appearances of acute inflammation?

5 cardinal signs

A

Redness from dilation
Increase in temp in peripheral parts from increased blood flow
Swelling from oedema
Pain
Loss of function

rubor, calor, tumor, dolor

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12
Q

What cells are involved in inflammation?

A

Neutrophil polymorphs
Macrophages
Lymphocytes
Endothelial cells
Fibroblasts

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13
Q

What do neutrophil polymorphs do?

A

First cells to arrive in acute inflammation
Adhesion to microorganisms
Phagocytosis and intracellulara killing of microorganisms
Release lysosomal products

Short lived and die on scene

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14
Q

What accumulates in the early stages of acute inflammation?

A

Oedema, fibrin and neutrophil polymorphs accumulate in extracellular space

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15
Q

What are the 5 cardinal signs in inflammation?

A

Rubor
Dolor
Calor in extremeties
Tumour
Loss of function

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16
Q

What are the early stages of acute inflammation?

A

Changes in vessel calibre and flow
Increased vascular permeability
Formation of fluid exudate
Formation of cellular exudate and emigration of neutrophil polymorphs into extracellular space
Diapedesis
Chemotaxis of neutrophils

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17
Q

What is diapedesis?

in acute inflammation

A

red cells being passively forced out of vessels by hydrostatic pressure
Lots of RBCs in extravascular space implies severe vascular injury

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18
Q

What is chemotaxis?

of neutrophils in acute inflammation

A

neutrophil polymorphs attracted to certain chemical substances in solution

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19
Q

What do histamine and thrombin cause in acute inflammation?

A

upregulation of adhesion molecules on surface of endothelial cells leading to firm neutrophil adhesion to endothelial surface

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20
Q

What do endogenous chemical mediators cause?

A

Vasodilation
Emigration of neutrophils
Chemotaxis
Increased vascular permeability
Itching and pain

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21
Q

What does histamine cause in acute inflammation?

A

Vascular dilation and immediate increased vascular permeability

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22
Q

What is the most important source of histamine in humans?

A

Mast cells

also present in basophil , eosinophil leucocytes and platelets

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23
Q

What is the diagnostic histological feature of acute inflammation?

A

Accumulation of neutrophil polymorphs in extracellular space

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24
Q

What is in the fluid exudate?

acute inflammation

A

high protein content
immunoglobulins
coagulation factors (fibrinogen)

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25
Q

What does resolution mean?

A

Complete restoration of the tissues to normal after acute inflammation

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26
Q

What conditions favour resolution?

A

Minimal cell death and tissue damage
Organ regenerative capacity
Rapid destruction of causal agent
Rapid removal of fluid and debris

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27
Q

Example of acute inflammatory condition that usually resolves completely

A

Acute lobar pneumonia

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28
Q

What does excessive exudate lead to in acute inflammation?

A

Suppuration (formation of pus)

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29
Q

What does excessive necrosis in acute inflammation lead to?

A

Repair and organisation of tissue
Fibrosis

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30
Q

What does a persistent causal agent in acute inflammation lead to?

A

Chronic inflammation
Fibrosis

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31
Q

What circumstances favour organisation in acute inflammation?

A

Large amounts of fibrin formed which can’t be removed
Lots of necrotic tissue
Dead tissue not easily digested
Exudate and debris can’t be removed

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32
Q

What is organisation of tissue in inflammation?

A

Replacement of tissue by granulation tissue as part of the repair process

New capillaries grow into exudate
Macrophages migrate into area and fibroblasts proliferate
Fibrosis and scar formation

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33
Q

Example of acute inflammation recurring and leading to chronic

A

Chronic cholecystitis

normally due to presence of gallstones

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34
Q

What are the main cells in chronic inflammation?

A

Lymphocytes
Plasma celss
Macrophages

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35
Q

What is a granuloma?

A

an aggregate of epithelioid histiocytes

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36
Q

What are the systemic effects of inflammation?

A

Pyrexia
Malaise
Anorexia and nausea
Weight loss
Reactive hyperplasia (lymph node enlargement)
Haematological changes
Amyloidosis

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37
Q

What do fibroblasts do?

(inflammation)

A

Produce collagenous connective tissue in scarring following
some types of inflammation

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38
Q

What are some conditions associated with granuloma formation?

A

Sarcoidosis
Crohns
TB
Wegener’s granulomatosis

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39
Q

What specific infections can cause granulomas?

A

Mycobacterial: TB, leprosy

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40
Q

What is the sequence of chronic inflammation?

A

either progression from acute inflammation or starts as
‘chronic’ inflammation
no or very few neutrophils
macrophages and lymphocytes, then usually fibroblasts
can resolve if no tissue damage (e.g. viral infection like
glandular fever)
often ends up with repair and formation of scar tissue

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41
Q

What cancers commonly
spread to bone?

A

breast, lung,
thyroid, kidney, prostate

BLT KP

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42
Q

How can carcinomas spread?

A

spread to the lymph nodes that drain the site of the carcinoma
spread to bone via blood

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43
Q

What type of carcinoma can’t spread?

A

Basal cell carcinoma

complete excision = cure

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44
Q

What are carcinogens?

A

Agents known or suspected to cause tumours

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45
Q

What does carcinogenic mean?

A

Cancer causing

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46
Q

What does oncogenic mean?

A

Tumour causing

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47
Q

What % of cancer risk is environmental?

A

85%

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48
Q

What are the classes of carcinogens?

A

Chemical
Viral
Ionising and non-ionising radiation
Hormones, parasites and mycotoxins
Miscellaneous

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49
Q

What % of cancers do viruses cause?

A

10-15%

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50
Q

Examples of chemical carcinogens

A

Polycyclic aromatic hydrocarbons
Aromatic amines
Nitrosamines
Alkylating agents

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51
Q

What are examples of DNA viral carcinogens?

and what cancers can they cause?

A

Human herpes virus 8 (causing kaposi sarcoma)
Epstein barr virus (nasopharyngeal carcinoma)
Hep B virus (hepatocellulara carcinoma)
Human papillomavrius (squamous cell carcinomas)
Merkle cell polyomavrius (merkle cell carcinoma)

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52
Q

What are some examples of viral RNA carcinogens?

A

Human T-lymphotrophic virus (adult T cell leukaemia)
Hep C virus (hepatocellular carcinoma)

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53
Q

What are biological agents that might increase risk of cancer?

A

Increased oestrogen
Anabolic steroids
Aflatoxin B1 (mycotoxin)
Chlonorchis sinensis (parasites)

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54
Q

Example of radiant energy that might cause cancer?

A

UV

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55
Q

Examples of miscallenous carcinogens

A

Metals
Asbestos

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56
Q

What host factors can affect carcinoma risk?

A

Ethnicity
Diet / Lifestyle
Constitutional factors - age, gender etc.
Premalignant lesions
Transplacental exposure

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57
Q

What are premalignant conditions?

A

Identifiable local abnormality associated with increase risk of malignancy at that site

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58
Q

What does hyperplasia mean?

A

Increase in cell number by mitosis (causing increase in tissue size)

e.g. 4 cells become 8

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59
Q

What does hypertrophy mean?

A

Increase in cell size without cell division (causing increase in tissue size)

e.g. 4 little cells become 4 big cells

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60
Q

What does atrophy mean?

A

Decrease in size of an organ or cell

may be physiological (uterus after menopause) or pathological (injury)

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61
Q

What does hypoplasia mean?

A

Failure of development of an organ
e.g. failure of development of the legs in adult spina bifida patients

failure of morphogenesis, similar to atrophy

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62
Q

What does metaplasia mean?

A

An acquired form of altered differentiation
Transformation of one mature differentiated cell into another
Affects epithelia or mesenchymal cells
Often increased risk of malignancy

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63
Q

What does dysplasia mean?

A

Increased cell proliferation
Pre-malignant
Presence of atypical morphology

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64
Q

What does ischaemia mean?

A

Inadequate blood supply to part of or all of an organ

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65
Q

What does neoplasia mean?

A

‘new growth’
characterised by abnormal, unco-ordinated and excessive cell proliferation

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66
Q

What is a neoplasm?

A

An abnormal tissue mass
the excessive growth of which is uncoordinated with normal tissues
persists after the removal of the neoplasm-inducing stimulus

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67
Q

What does infarction mean?

A

death of tissue due to insufficient blood supply

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68
Q

What is a tumour?

A

Abnormal swelling

synonymous with neoplasm

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69
Q

What is apoptosis?

A

A form of normal or pathological individual cell death characterised by activation of endogenous endonucleases

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70
Q

What is necrosis?

A

Pathological cellular or tissue death in a living organism, irrespective of caurse

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71
Q

Difference between apoptosis and necrosis

A

Both models of cell death
Apoptosis: active process involving single-cell death, normal and abnormal, cell membrane intact, no inflammatory reaction
Necrosis: response to injury, almost always a group and pathological, cell membrane integrity lost, inflammatory response and repair common

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72
Q

What can activate the intrinsic pathway of apoptosis?

A

intracellular signals: DNA damage, failure to conduct cell division

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73
Q

What genes regulate the final common pathway of apoptosis?

A

bcl-2 protein family

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74
Q

What do the bcl-2 protein family do?

A

Inhibit or activate the death pathway in apoptosis

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75
Q

What inhibits apoptosis?

A

Growth factors, cell matrix, sex steroids, some viral proteins

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76
Q

What are some apoptosis inducers?

A

Growth factor withdrawal, loss of matrix attachment, glucocorticoids, some viruses, free radicals, ionising radiation, DNA damage, Fas ligand

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77
Q

What do caspase enzymes do?

A

Effector molecules for apoptosis
Switched on by internal and external signals (bcl-2 inhibit, bax proteins switch on, Fas ligand binds to fas receptor = switches on)

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78
Q

What diseases are associated with increased apoptosis?

A

AIDS
Neurodegenerative disorders

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79
Q

What diseases are associated with decreased apoptosis?

A

Cancer
Autoimmune disease

80
Q

What tumours commonly metastasise to the lungs?

A

Sarcomas
Any common cancers

81
Q

What tumours commonly metastasise to the liver?

A

colon
stomach
pancreas
carcinoid tumours of intestine

82
Q

What makes up neoplasms?

A

Neoplastic cells
Stroma (framework)

83
Q

What are features of neoplastic cells?

A

Derived from nucleated cells
Usually monoclonal
Growth pattern and synthetic activity related to parent cells

84
Q

What does the stroma provide in the neoplasm?

A

Connective tissue framework
Mechanical support anda nutrition

85
Q

Why is it important to classify neoplasms?

A

To determine appropriate treatment
To provide prognostic information
To aid communication

86
Q

What can neoplasms be classified as?

A

Benign
Borderline
Malignant

87
Q

Features of benign neoplasms

A

Localised, non-invasive
Slow growth rate
Low mitotic activity
Close resemblance to normal tissue
Circumscribed or encapsulated

88
Q

Why worry about benign neoplasms?

A

Pressure on adjacent structures
Obstruct flow
Produce hormones
Transform to malignant neoplasm
Anxiety

89
Q

Features of malignant neoplasms

A

Invasive
Metastases
Rapid growth rate
Variable resemblance to normal tissue
Poorly defined or irregular border

90
Q

Histological features of malignant neoplasms

A

Hyperchromatic nuclei
Pleomorphic nuclei
Increased mitotic activity
Necrosis and ulceration common
Growth on mucosal surfaces and skin often endophytic

91
Q

Histological features of benign neoplasms?

A

Nuclear morphometry often normal
Necrosis rare
Ulceration rare
Growth on mucosal surfaces usually exophytic

92
Q

Why worry about malignant neoplasms?

A

Destruction of adjacent tissue
Metastases
Blood loss from ulcers
Obstruct flow
Produce hormones
Paraneoplastic effects
Anxiety and pain

93
Q

Where might neoplasms arise from?

A

Epithelial cells
Connective tissues
Lymphoid/haematopoietic organs

94
Q

What is a papilloma?

A

Benign neoplasm of non-glandular non-secretory epithelium

95
Q

What is an adenoma?

A

Benign neoplasm of glandular or secretory epithelium

96
Q

What is a carcinoma?

A

Malignant epithelial neoplasm

97
Q

What are adenocarcinomas?

A

Carcinomas of glandular epithelium

98
Q

When is a neoplasm described as anaplastic?

A

cell type of origin cannot be determined

99
Q

Example of an inherited predisposition for cancer

A

Familial adenomatous polyposis risk for colorectal cancer

100
Q

When is the suffix -oma used + exceptions

A

Benign connective tissue neoplasms
not neoplasm: granuloma
malignant: melanoma, mesothelioma, teratoma

101
Q

When is the suffix sarcoma used + exceptions?

A

Malignant connective tissue neoplasms
melanoma and mesothelioma also malignant

102
Q

What are the different aetiologies of cancer?

A

Transformation of germline cells: inheritable cancers (<10%, Rb, BRCA1, 2)
Transformation of somatic cells: noninheritable cancers (>90%)
Environmental factors

103
Q

What are some hallmarks of cancer?

A

Growth self-sufficiency
Evade apoptosis
Ignore anti-proliferative signals
Limitless replication potential
Sustained angiogenesis
Invade tissues
Escape immune surveillance

104
Q

What is cancer immunosurveillance?

A

Immune system can recognize and destroy nascent transformed cells, normal control

105
Q

What is cancer immunoediting?

A

Tumours tend to be genetically unstable; thus immune system can kill and also induce changes in the tumour resulting in tumour escape and recurrence

106
Q

What are tumour specific antigens?

A

Are only found on tumours
As a result of point mutations or gene rearrangement
Derive from viral antigens

107
Q

What are tumour associated antigens?

A

Found on both normal and tumour cells, but are overexpressed on cancer cells
Developmental antigens which become derepressed. (CEA)
Differentiation antigens are tissue specific
Altered modification of a protein could be an antigen

108
Q
A
109
Q

What is the main purpose of the immune system?

A

Discriminate between self and non self

110
Q

What are the different types of immunity?

A

Innate
Adaptive

both made up of cells and soluble factors

111
Q

What is innate immunity?

A

Instinctive
non-specific
does not depend on lymphocytes
present from birth

112
Q

What is adaptive immunity?

A

Specific ‘Acquired/learned’ immunity
requires lymphocytes
antibodies

113
Q

What is haematopoesis?

A

The commitment and differentiation processes that leads to the formation of all blood cells from pluripotent haematopoietic stem cells

starts in bone marrow

114
Q

What are the polymorphonuclear leukocytes?

A

Neutrophils
Eosinophil
Basophil

115
Q

What are the mononuclear leukocytes?

A

Monocytes
B cells
T cells
Mast cells
Natural killer cells (type of T)
Dendritic cells (kupffer in liver, langerhans in skin)

116
Q

What are the different T cells?

A

T-regs
T-helpers (CD4,Th1,Th2)
Cytotoxic (CD8)

117
Q

What do B cells become when they differentiate?

A

Plasma cells

118
Q

What are the soluble factors of the immune system?

A

Complement
Antibodies
Cytokines
Chemokines

119
Q

What is complement?

in the immune system

A

Group of 20 serum proteins secreted by teh liver that need to be activated to be functional
Activated as part of the immune response

120
Q

What are the main modes of action for complement?

A

Direct lysis
Attract more Leukocytes to site of infection
Coat invading organisms

121
Q

What do antibodies do?

can also be called immunoglobulins

A

Bind specifically to antigens

soluble
secreted
bound to B cells as part of B-cell antigen receptor
glycoproteins

122
Q

What are the 5 distinct classes of immunoglobulins?

A

IgG (IgG1-4)
IgA (IgA1 & 2)
IgM
IgD
IgE

123
Q

Which parts of IgG bind to what?

A

Fc binds to receptors
Fab bind to non self

Y shape, fab at top, fc at bottom

124
Q

What does IgM do?

A

Responsible for primary immune response
Initial contact with the antigen

125
Q

What is the structure of IgM?

A

Pentamer
J chain
Mainly found in blood
10% of serum Igs

126
Q

What is the structure of IgA?

A

Monomer or dimer
15% of Igs in serum
Held together with J chain

127
Q

What is the structure of IgD?

A

Accounts for 1% of Ig in serum
A transmembrane monomeric form (mIgD) is present on mature B cells

128
Q

What is the structure of antibodies?

A

Y shape
Fab region at top with antigen binding site
Antigen binding site binds to specific epitope
Fc region and receptor at bottome

129
Q

What is IgE associated with?

A

Associated with hypersensitivity allergic response and defence against parasitic infections

130
Q

What does IgE bind to?

A

Receptors on basophils and mast cells triggering histamine release

131
Q

What are cytokines?

A

Proteins secreted by immune and non-immune cells

132
Q

What are the different cytokines?

A

Interferons
Interleukins
Colony stimulating factors
Tumour necrosis factors

133
Q

What do interferons do?

(cytokines)

A

induce a state of antiviral resistance in uninfected cells & limit he spread of viral infection

134
Q

What are chemokines?

A

Group of approx 40 proteins that direct movement of leukocytes (and other cells) from the bloodstream into the tissues or lymph organs by binding to specific receptors on cells

135
Q

What do interleukins do?

(cytokines)

A

produced by many cells, over 30 types
Can be pro-inflammatory (IL1) or anti-inflammatory (IL-10)
Can cause cells to divide, to differentiate and to secrete factors

136
Q

What do colony stimulating factors do?

(cytokines)

A

Involved in directing the division and differentiation on bone marrow stem cells – precursors of leukocytes

137
Q
A
138
Q

What do Tumour Necrosis Factors do?

(cytokines)

A

Mediate inflammation and cytotoxic reactions

139
Q

Features of the innate immune response

A

1st line of defence
Provides barrier to antigen
Instinctive
Present from birth
Slow response
No memory

140
Q

Features of the adaptive immune response

A

Response specific to antigen
Learnt behaviour
Memory to specific antigen
Quicker response

141
Q

What are some physical barriers in the innate immune response?

A

Skin
Lysozyme in tears
Mucus and cilia
Acid in the gut
commensals

142
Q

What is the process of inflammatory response to tissue damage?

A

Stop bleeding (coagulation)
Acute inflammation (leukocyte recruitment)
Kill pathogens, neutralise toxins, limit pathogen spread
Clear pathogens/dead cells (phagocytosis)
Proliferation of cells to repair damage
Remove blood clot – remodel extracellular matrix
Re-establish normal structure/function of tissue

143
Q

What are the main chemokines?

A

CXCL – mainly neutrophils
CCL –monocytes, lymphocytes, eosinophils, basophils
CX3CL – mainly T lymphocytes & NK Cells
XCL – mainly T lymphocytes

chemokine - attracted cell

144
Q

Where are pathogen-associated molecular patterns?

A

On surface of bacteria/microbe
Bind to PRR

145
Q

What receptors are on cells in our body that bind to PAMPs?

A

Pattern recognition receptors

146
Q

Where are the cells that sense microbes?

A

In blood – Monocytes, Neutrophils
In tissues – Macrophages, Dendritic cells

147
Q

What are C-type lectin receptors?

A

Expressed by Macrophages and DC
bind to carbohydrates in a Ca2+-dependent manner
The receptors have a carbohydrate-recognition domain/s (CRD)

bind to foreign carbs

148
Q

What do scavenger receptords bind to?

A

Bind to a variety of ligands including endogenous lipids and lipoproteins
in particular bacterial cell wall components of both Gram-negative and Gram-positive bacteria.

they are membrane bound

149
Q

What do toll-like receptors do?

A

Bind to different foreign molecules

150
Q

What is the function of scavenger receptors in homeostasis?

A

bind and internalize lipid containing molecules such as modified low-density lipoprotein (LDL) and oxidised LDL (oxLDL) from the plasma
when this is dysregulated it can lead to atherosclerosis

151
Q

What different receptors are there in the immune response?

A

CLR
TLR
Scavenger

152
Q

What are the different activation pathways for complement?

A

Classical - Ab bound to microbe
Alternative – C’ binds to microbe
Lectin – activated by mannose binding lectin bound to microbe

153
Q

What is phagocytosis?

A
154
Q

What are the stages of phagocytosis?

A

Binding
Engulfment
Phagosome formation
Phagolysosome
Membrane disruption/fusion
antigen presentation

155
Q

What mediates phagocytosis?

A

opsonic receptors

156
Q

What are the 2 mechanisms of microbial killing?

A

oxygen dependent
oxygen independent

157
Q

How does O2 dependent killing pathway work?

A

Reactive Oxygen Intermediates (ROI)
Superoxides (O2-) are converted to H2O2 then ·OH (free radical)
Nitric Oxide (NO) – vasodilation (Viagra) increase extravasation but also anti-microbial

158
Q

What is involved in the O2 independent killing pathway?

A

Enzymes: (eg lysozyme)
Proteins: defensins (insert into membranes), TNF
pH

159
Q

How does the neutrophil get from circulation to the site of infection?

extravasation

A

Neutrophil moving very fast in circulation
Rolls and tethers onto endothelium
Remains static (adhesion) and passes through gaps in endothelium walls
Travels through chemokine gradient (transmigration)
Reaches site of infection

160
Q

What cells are in adaptive immunity?

A

T cells
B cells
Anitgen presenting cells

161
Q

Where are T cells?

A

Start in thymus
Circulation
Lymphoid tissues (spleen, lymph nodes, MALT)

162
Q

Where do adaptive immune cells gather?

A

Secondary lymphoid tissues
(spleen, lymph nodes, MALT)

163
Q

Where do B cells and APCs start?

A

Bone marrow

164
Q

Why does cell-mediated immunity require cell to cell contact?

A

to control Ab responses via contact with B cells
to directly recognise and kill viral infected cells

165
Q

What is T cell selection?

A

T cells that recognise self are killed in the foetal thymus as they mature

166
Q

What does cell-mediated immunity require?

A

Major Histocompatibility Complex (MHC)
Intrinsic/Endogenous (intracellular) antigens
Extrinsic/Exogenous (extracellular) antigens
Cell to cell contact

167
Q

What is the purpose of cell mediated immunity?

A

Recognise self or non-self
Interlay between APCs and T cells

168
Q

What does a major histocompatibility complex do?

A

Displays peptides from self or non-self proteins
MHC 1 glycoproteins on all nucleated cells
MHC 2 glycoproteins only on APCs

169
Q

What do T cells do?

A

recognise antigen in association with MHC
DO NOT respond to soluble antigens only intracellular presented antigens

170
Q

How do T cells become functional?

A

inactive naive T cell
activated, e.g. into CD4 or CD8
CD4: IL-12lo —> ab production, IL-12hi —> IFNy helps kill pathogens intracellularly
CD8: kill intracellular pathogens directly

171
Q

How are B cells activated?

A

th2 cells are primed and bind to specific B cell
Th2 secretes cytokines
B cells divide (clonal expansion) and differentiate into plasma cells and memory B cells

Make 1 antibody that bind to 1 specific receptor

172
Q

What are the primary lymphoid organs?

A

thymus
bone marrow

173
Q

What are the secondary lymphoid organs and tissues?

A

tonsils and adenoids
bronchus associated lymphoid tissue
lymph nodes
bone marrow
spleen
peyers patach

174
Q

How do B cells activate and differentiate?

A

Binds antigen and becomes activated
Activated B cells go to lymph nodes where they proliferate (clonal expansion)
differentiate into plasma cells.
These plasma cells secrete antibodies of same specificity but are generally IgM – these later turn into IgG but still have same specificity to the same antigen (class switching)
Some B cells recalculate for years (Memory B cells)

175
Q

What is the restimulation of memory B cells?

A

Very quick secondary response

176
Q

What can specific secreted antibodies do?

A

Neutralise toxin by binding to it
Increase opsonisation – phagocytosis
Activate complement

177
Q

What are damage associated molecular patterns?

A

Endogenous molecules created to alert the host to tissue injury and initiate repair

178
Q

What are secreted and circulating PRRs?

A

Antimicrobial peptides secreted into lining fluids (from epithelia and phagocytes)

179
Q

What are pentraxins?

A

Proteins like CRP
react with the C-polysaccharide of pneumococci, some antimicrobial actions
activates complement, promotes phagocytosis

e.g. of secreted and circulating PRR

180
Q

Examples of secreted and circulating PRRs

A

Pentraxins
Lectins and collectins

181
Q

What are lectins and collectins?

A

carbohydrate-containing proteins that bind carbohydrates or lipids in microbe walls.
Activate complement, improve phagocytosis.
Mannose binding lectin
Surfactant proteins A and D

182
Q

What are cell-associated PRRs?

A

Receptors that are present on the cell membrane or on organelles within the cytosol of cells
TLRs are the main family
Recognise a broad range of molecular patterns

183
Q

What do TLR2 and 4 bind to?

A

bacteria, viruses and self

184
Q

What does TLR5 bind to?

A

Bacteria flagellin

185
Q

What are some examples of membrane bound PRRs?

A

Mannose receptor - on macrophages (fungi)
Dectin-1 - widespread on phagocytes (beta glucans in fungal walls)
Scavenger receptors - on macrophages (wide variety of lipid-related ligands from pathogens or from host cells that are damaged, apoptotic or senescent)

186
Q

What are nod-like receptors involved in?

A

sensing cytoplasmic bacterial pathogens and DAMPS
regulation of inflammatory & cell death responses

187
Q

What characterised NOD like receptors?

A

presence of a conserved nucleotide-binding and oligomerisation domain

188
Q

What does NOD1 do?

A

recognizesmeso-diaminopimelic acid (meso-DAP)-containing PGN fragments (mainly Gram-negative) in the periplasmic space

189
Q

What does NOD2 do?

A

senses muramyl dipeptide (MDP) a breakdown product of PG in the cell wall, found in the PGN of nearly all Gram-positive and Gram-negative organisms

190
Q

What is type 1 hypersensitivity?

A

an immediate reaction to
environmental antigens mediated via IgE

191
Q

What is atopy?

A

an inherited trait for Type I hypersensitivity

192
Q

What are allergens?

A

antigens that trigger allergic
reactions

193
Q
A
194
Q

What diseases are associated with ageing?

A

Cardiovascular
Neurodegenerative
Cancer
COVID-19
Autoimmune

195
Q
A

Phase 2a (14 decks)

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