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Year 1 SBA revision > 102 - Swollen Finger > Flashcards

102 - Swollen Finger Flashcards

1
Q

5 signs of acute inflammation

A

Redness Swelling Pain Heat Loss of function

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2
Q

3 components of the immune system

A
  • External barriers
  • Innate response
  • Adaptive response
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3
Q

Role of external barriers in the immune system. Examples

A

Prevent pathogens entering body e.g. Skin, mucous membranes.

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4
Q
  • Describe the innate immune response:
    • How does it develop?
    • Is it specific?
    • How does it improve?
    • How does it destroy pathogens
A
  • Born with,
  • Doesn’t change in response to pathogens so is fast.
  • Non-antigen specific,
  • Doesn’t improve after repeat exposure.
  • Causes Inflammation resulting in phagocytosis and microbe killing
  • Critical, immediate line of defence.
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5
Q

Describe the adaptive immune response:

  • How does it develop?
  • Is it specific?
  • How does it improve?
  • How does it destroy pathogens
A
  • Antigen specific,
  • Slower as needs to develop.
  • Generates memory and responds quicker to subsequent infections.
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6
Q

Comparison of adaptive and innate immunity.

A
  • Innate - rapid set response.
  • Adaptive - Slower, antigen specific response.
  • Integrated, both interact with each other.
  • Finding more overlap. Innate no longer thought simple.
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7
Q

What is an abscess

A

Localised formation of pus

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8
Q

What is pus?

A

Living/dead leukocytes, bacteria and damaged cells.

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9
Q

Abscess formation - 4 stages

A
  • Pathogen deposited in tissue.
  • Blood vessels dilate - get more blood/leukocytes to site of infection.
  • Pus formation - surrounding blood vessels clot to prevent spread.
  • Pressure builds up - abscess expands in direction of least resistance and can erupt and discharge at body surface.
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10
Q

5 stages of response to infection

A
  • Awareness - pathogen detected.
  • Immediate response - Innate immune cells migrate to site of infection and activate.
  • Delayed response - Adaptive immune cells migrate to site of infection.
  • Destruction of pathogen
  • Immunity - ongoing response to pathogen.
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11
Q

IgM

A

Secreted early in immune response

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12
Q

IgE

A

Involved in allergy and parasitic reactions

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13
Q

IgG

A

Can cross placenta

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14
Q

IgA

A

Secreted in breast milk and tears

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15
Q

What can trigger hypersensitivity reactions?

A
  • ACID
    • A - Allergic - bee sting
    • C - Cytotoxic - Myasthenia gravis
    • I - Immune complex - Rheumatoid arthritis
    • D - Delayed - Contact dermatitis.

Hypersensitivity types 1-4

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16
Q

When do neutrophils appear?

A

In large numbers at the start of infection. First on scene.

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17
Q

When do eosinophils appear?

A

Parasitic infection

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18
Q

When do basophils appear

A

In inflammation - release histamine

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19
Q

What do B lymphocytes do?

A

Produce antibodies

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20
Q

What does penicillin act on?

A

Destruction of microbial cell wall

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21
Q

How does trimethoprim act?

A

Prevents folate synthesis

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22
Q

How do quinolones work?

A

Inhibit DNA gyrase - prevent DNA supercoiling

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23
Q

How does Rifampicin work?

A

Inhibits RNA polymerase. Both start with R

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24
Q

How do macrolides work?

A

Affect the microbial 50S subunit to prevent protein synthesis.

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25
Q

How do tetracyclines work?

A

Affect the microbial 30S subunit to prevent protein synthesis

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26
Q

What is the role of Interleukin-1 in the body

A

Pyrogen. Increases body temperature

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27
Q

How does the immune system recognise pathogens?

A

Recognition - molecules/receptors on immune system cells bind to molecular receptors on pathogen that are not present on self cells.

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28
Q

What are PRR’s?

A

Pattern Recognition Receptors - on cells of innate immune system that are able to recognise molecular patterns on pathogens that aren’t present on self-cells

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29
Q

What are PAMPS?

A

Pathogen associated recognition receptors. Molecules on pathogen that can be recognised by PRRs.

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30
Q

What are DAMPS?

A

Damage associated recognition proteins. Self patterns that PRRs can recognise. Are present only on damaged self cells that need to be removed.

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31
Q

How to treat autoimmune disorders

A

Normally easier to replace what is missing than fight back but not always possible. Need to suppress immune system either with generic treatments (usually chemical - steroids) or targeted treatments for specific molecules (usually proteins).

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32
Q

4 stages of phagocytosis.

A

Attachment of phagocyte to cell for destruction. Ingestion - membrane proteins engulph and take into phagocyte. Killing. Degradation - various enzymes responsible for breakdown.

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33
Q

How do neutrophils reach the site of infection?

A

Chemokine IL-8 is generated by inflammation and spreads out forming a concentration gradient that is closest at the centre of infection. Neutrophils can move along this to reach infection site.

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34
Q

Aims and 4 stages of the inflammatory response

A

Aims to recruit cells and soluble factors from blood to site of infection.

4 stages.

Vasodilation - increased blood flow increases supply of cells and soluble factors.

Activation of endothelial cells - become stickier for leukocyte adhesion.

Increased vascular permeability - Easier for cells/proteins to pass through blood vessels.

Chemotactic factors - Attract cells from blood into tissue.

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35
Q

What is systemic inflammation?

A

Acute inflammatory response - to eliminate pathogen, confined to one area. If not stopped then macrophage derived cytokines can build up in the blood and affect other organs.

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36
Q

What are opsonins?

A

Sugars that coat pathogens to promote removal by the immune system. 1 end binds pathogen, other binds phagocyte and stimulates phagocytosis.

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37
Q

What are interferons?

A

Cytokines that inhibit viral replication in infected cells. Can act within cell or can be secreted. Alert immune response to infection and amplify immune response.

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38
Q

Role of inflammation

A

Aims to remove pathogens before can proliferate and cause a problem. Helps transport effector cells to site of infection. Also involved in tissue repair.

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39
Q

What are RAMPS?

A

Resolution associated molecular patterns. Switch off inflammatory response. Chronic inflammation occurs if this fails.

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40
Q

How is inflammation initiated?

A

PRRs recognise PAMPs - initiate signal transduction pathways - pro-inflammatory gene expression - inflammation.

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41
Q

Chain of infection. What is it? Why important?

A
  • Infectious organism
  • Reservoir
  • Means of exit
  • Route of transmission
  • Means of entry
  • Susceptible host.

All needs to be in place for transmission. Break chain - break infection.

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42
Q

Outline the immune response

A

Damage/Pathogen invasion. Innate response - cytokines, phagocytes, antigen presenting cells. Adaptive response Resolution/death

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43
Q

What is autoimmunity?

A

Immune response against self. Tolerance fails. Common but can be life threatening. Generally multifactorial.

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44
Q

What is TNF-A

A

Tumor Necrosis Factor alpha.

Involved in regulation of immune cells. Endogenous pyrogen.

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45
Q

How did vancomycin resistance develop

A

Appears to be spontaneous. Possible major clinical implications.

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46
Q

Differences between bacteria and eukaryotes

A

Bacteria: Have a peptidoglycan cell wall No nucleus/nuclear membrane - chromosome free in cytoplasm No mitochondria

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47
Q

Classes of potential antimicrobial targets

A

Class I - Targets reactions producing ATP Class II - Targets pathways making small molecules Class III - Targets pathways converting small molecules into macromolecules.

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48
Q

Most important class of potential antimicrobial targets

A

Class III - Targets pathways converting small molecules into macromolecules.

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49
Q

Main ways antibiotics target microbes (4) Why do these target microbes specifically?

A

Target peptidoglycan synthesis - affects cell wall - no cell wall in eukaryotes. Target folate synthesis - stops DNA synthesis - humans get from diet and don’t synthesise. Target Protein synthesis - human/bacteria have diff ribosomes. Target Nucleic acid synthesis - bacterial nucleus is free in cytoplasm.

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50
Q

What is antibiotic resistance?

A

The ability of bacteria to adapt to resist antibiotics.

51
Q

How can antibiotic resistance be spread?

A

Transfer of resistance bacteria between people Plasmid transfer of resistance genes between bacteria Transfer of resistance genes between genetic elements within bacteria on transposons.

52
Q

How do mutations generate antibiotic resistance?

A

Spontaneous mutation rate in bacteria very low but Short bacterial generation time allows rapid evolution.

53
Q

How does gene amplification help generate antibiotic resistance?

A

Theory that antibiotic use can induce an increase in number of copies of pre-existing resistance genes.

54
Q

How do plasmids help generate antibiotic resistance?

A

Extrachromosomal genetic elements that can replicate independently, can contain resistance genes. Not sure how develop.

55
Q

What are the 2 clinically relevant methods of transfer of resistance genes between bacteria?

A

Bacterial conjugation - Cell-cell contact transfers resistance between bacteria. Key method. Transduction - Plasmid DNA enclosed in a bacterial virus transfers resistance between bacterium of same species.

56
Q

What are T cells? Name 2 main types.

A

Cells capable of recognising diff antigens that are presented to it by antigen presenting cells. 2 types: T Helper - CD4 - Help B cells produce antibodies T Cytotoxic - CD8 - Directly kill infected cells.

57
Q

What are cytokines?

A

Small, soluble proteins involved in cell signalling that bind to specific receptors.

58
Q

What do autocrine cytokines work on?

A

Work on the cell that produces them

59
Q

What do Paracrine cytokines work on?

A

Can work on adjacent cells

60
Q

What do endocrine cytokines work on?

A

Can work on distant cells via bloodstream. Very rare - usually travel short distances.

61
Q

What are chemokines

A

Subgroup of cytokines that recruit phagocytes.

62
Q

What do bactericidal antibiotics do?

A

Cause bacterial cell death

63
Q

What do bacteriostatic antibiotics do?

A

Stop growth/development of bacteria cells. Immune system can then destroy.

64
Q

What is the MIC?

A

Minimum inhibitory concentration - lowest concentration of an antimicrobial agent that stops visible growth of that microbe.

65
Q

How do time dependent agents work?

A

Drug is most effective when present in sufficient doses over a long time period. Multiple doses a day.

66
Q

How do concentration dependent agents work?

A

Drug is most effective when present at a high concentration. Single dose/day.

67
Q

How to activate complement pathway?

A

3 diff ways. Classical, lectin or alternative.

68
Q

What is the lectin pathway of complement

A

Immune system recognises bacteria as coated in mannose but absent in humans. C4 cleaved by mannose binding lectin binding to pathogen to start pathway.

69
Q

What is the alternative pathway of complement

A

Starts due to spontaneous generation. C3 unstable and can split on own. If pathogen present, binds and pathway activated.

70
Q

What is the Classical pathway of complement?

A

Antibody binds microbe antigen

71
Q

What is the membrane attack complex?

A

Part of complement. Generated by C5b and forms on surface of pathogen.

72
Q

How does the membrane attack complex work?

A

Lipophillic so inserts into pathogen membrane. Inserts poly-C9 tube through pathogen membrane to cause lysis in susceptible bacteria.

73
Q

Main aim of 3 pathways of complement activation

A

Form C3 convertase.

74
Q

Role of C3 convertase act in complement?

A

C3 convertase splits into C3a and C3b. C3 convertase + C3b bind to form C5 convertase

75
Q

Role of C5 convertase in complement

A

Splits into C5a and C5b. C5a and C3a recruit phagocytes to source of infection. Inflammatory mediators.

76
Q

Role of C3b in complement?

A

Opinisation - coats pathogen to trigger phagocytosis

77
Q

What is paronychia?

A

Localised infection of the skin folds surrounding the nail.

78
Q

Cellular components of the innate immune system

A

Phagocytes, degranulating cells & NK cells.

79
Q

Soluble components of the innate immune system

A

Complement, cytokines, anti-microbial proteins, Acute Phase proteins.

80
Q

Cellular components of the adaptive immune system

A

B & T Cells.

81
Q

Soluble components of the adaptive immune system

A

Antibodies

82
Q

How does the innate immune system recognise pathogens?

A

Molecules/receptors on cells of immune system bind to molecules/receptors on pathogens that are not present on self cells.

83
Q

Apart from phagocytosis - how else can the innate immune system respond?

A

Synthesis or secretion of new products. Can either directly kill pathogens or recruit other cells responsible for pathogen killing.

84
Q

What does the inflammatory response aim to do?

A

Recruit more phagocystes and other proteins into the site of infection from the blood.

85
Q

What is cell migration?

What are the 2 important factors in control of cell migration?

A

Movement of cells around the body. Carefully controlled.

Control where cells go in organ.

If they can enter the bloodstream.

86
Q

What are leukocytes?

What is their unique property?

A

White blood cells

Can move through the body - able to both travel in the bloodstream and enter tissues.

87
Q

What are adhesion molecules?

What do they do?

A

Found on leukocytes and endothelial cells. Interactions allow migration of leukocytes across the endothelium and into the blood.

88
Q

What do chemotactic factors do?

A

Act directly on cells and cause movement in a particular direction

OR

Act indirectly by altering expression or binding activity of adhesion molecules.

89
Q

Why is the innate system important if there is an adaptive system?

A

Early response to pathogens.

Might not be able to stop all infections but can limit proliferation of infection before the adaptive immune system can respond.

90
Q

How do cells migrate from the blood into tissue?

What is this process called and what are the 3 general stages.

A

Extravasation -

* Rolling

* Activation and firm attachment (chemokine aided)

* Transendothelial migration.

91
Q

What is the pattern recognition strategy?

A

Technique used by the innate immune system. Recognises patterns of highly conserved receptors on pathogens.

92
Q

What can the immune system respond to?

A
  • Pathogens
  • Damaged self.
93
Q

What are the 2 key classes of PRRs?

A
  • Receptors mediating phagocytosis.
  • Receptors mediating the inflammatory response.
94
Q

What are RAMPs?

Why are they important?

What happens if they go wrong?

A

Resolution associated molecular patterns.

Act to switch off inflammatory response caused by PAMPs and DAMPs.

If they do not work, chronic inflammation occurs e.g. Rhematoid arthritis.

95
Q

4 causes of inflammation

A
  • Infection
  • Tissue damage
  • Trauma
  • Irritants (inc allergy)
96
Q

What causes swelling in inflammation?

A

Extra fluid reaching site

97
Q

What causes redness and heat in inflammation?

A

Vasodilation of capillaries

98
Q

What causes pain in inflammation?

A

Inflammatory factors - destroy the cells and make patient aware of infection

99
Q

How are T Cells activated?

A

Antigen presenting cells present antigen to T cells

100
Q

What are the 2 types of T cells and what are their roles?

A
  • TH - THelper - CD4 - Help B cells produce antibodies
  • TC - TCytotoxic - CD8 - Directly kills infected cells
101
Q

How do activated Tc cells work.

A
  • Binds to antigen
  • Mitosis and differentiation
  • Destroys cells
102
Q

How do activated TH cells work?

A
  • TH receptor binds to antigen
  • Virgin or memory B cell recruited
  • Mitosis and differentiation
  • Effector B cells - produce antibodies.
  • Memory B cells - remember response for future infections
103
Q

Hand hygiene:

What are the three levels and when are they used.

A
  • Level 1 - Liquid soap and warm water.
    • Social/direct contact
  • Level 2 - Alcohol gel
    • Clean proceedures
  • Level 3 - Antibacterial solutions
    • Surgery/Aseptic proceedures
104
Q

How to treat autoimmune disease

A

Either replace missing factors destroyed by the autoimmunity or supress the immune system.

To supress the immune system - can either use a generic treatment (usually chemicals) or a targetted, specific treatment (usually proteins, antibodies, receptors).

105
Q

What does methotrexate do?

A

Inhibits folic acid synthesis so inhibits all dividing cells including T cells. Used to treat autoimmunity.

106
Q

What does azathioprine do?

A

Inhibits DNA synthesis so affects dividing B & T cells (all dividing cells).

Used to treat autoimmunity.

107
Q

How do glucocorticoids work?

A

Inhibit innate immune system effects to reduce inflammation. Inhibits B, T and antibody production.

108
Q

Where do the cells of the immune system form?

A

From pluripotent stem cells found in the bone marrow (spleen & liver in the foetus.

109
Q

What 2 types of cell do pluripotent haematopoetic stem cells form?

A
  • Common lymphoid progenitor cells
  • Common myeloid progenitor cells
110
Q

What are the lymphoid cells (form from common lymphoid progenitor)

A

Cells of the innate immune system

111
Q

What are myeloid cells

A

Cells of the adaptive immune response as well as NK and dendritic cells.

112
Q

What 3 types of cells form from the common myeloid progenitor?

A
  • Immature dendritic cells
  • Megakaryocyte/Erythrocyte progenitor
  • Granulocyte/Macrophage progenitor
113
Q

What granulocytes are found in blood?

A
  • Neutrophils
  • Eosiophils
  • Basophils
114
Q

What granulocytes are found in tissues?

A
  • Mast cells
  • Macrophages - only their precursors circulate in the blood.
115
Q

What do neutrophils do

A

1st cell at site of inflammation.

Phagocytic

Green colour of pus is mostly due to dead neutrophils

116
Q

3 key functions of the lymphatic system

A
  • Tissue drainage
  • Antigen trapping
  • Fat transport
117
Q

What do macrophages do?

A

Phagocytic cells.

Found in almost all tissues, induces inflammation, secretes signalling proteins to recruit other cells and has a role in antigen presentation.

118
Q

What do dendritic cells do and where are they found?

A

Mostly found at potential points of pathogen entry.

Take up pathogens by phagocytosis - continously ingesting fluids and surveying environment.

Antigen presenting cells - links innate and adaptive immune response.

119
Q

What are Natural Killer cells?

A

Lymphoid cells but part of the innate immune response.

Specialised to recognise abnormal cells - have a role in immunoregulation.

Contain cytotoxic mediators that damage cell membranes - Perforin - punches holes into the membranes.

2 types of receptors - activating and inhibitory.

120
Q

What is the complement system?

A

A group of blood based proteins that work together to remove microbes.

Generally circulate as inactive ‘zymogens’ in the blood. Activate in the presence of infection.

Sequential activation - causes enzyme cascade which results in microbial death.

121
Q

Primary lymphatic organs - What are they & what do they do?

A

Make lymphocytes - atrophy with age.

Thymus and bone marrow.

122
Q

Secondary lymphoid organs - What are they and what do they do?

A

Store lymphocytes.

  • Spleen
  • Lymph nodes
  • Tonsils
  • Peyers patches (modified gut lymphoid tissue)
123
Q

First step of complement

A
  • Triggered in 3 different ways.
  • Initial zymogen activated by proteolytic cleavage which starts an enzyme cascase.
  • Each activated zymogen proteolytically cleaves another complement protein causing a conformational change.
  • Small amounts of pathogen detected - rapid amplification of response.
124
Q

Describe the common complement pathway

A
  • All 3 complement pathways result in the formation of C3 convertase.
  • C3 splits into C3a and C3b
  • C3 convertase and C3b bind to form C5 convertase.
  • C5 splits into C5a and C5b
  • C3b - binds to pathogen - opinosises.
  • C3a/C5a - inflammatory mediators - recruit phagocytes

Year 1 SBA revision (37 decks)

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