102 - Swollen Finger Flashcards
(124 cards)
1
Q
5 signs of acute inflammation
A
Redness Swelling Pain Heat Loss of function
2
Q
3 components of the immune system
A
- External barriers
- Innate response
- Adaptive response
3
Q
Role of external barriers in the immune system. Examples
A
Prevent pathogens entering body e.g. Skin, mucous membranes.
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.
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.
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.
7
Q
What is an abscess
A
Localised formation of pus
8
Q
What is pus?
A
Living/dead leukocytes, bacteria and damaged cells.
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.
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.
11
Q
IgM
A
Secreted early in immune response
12
Q
IgE
A
Involved in allergy and parasitic reactions
13
Q
IgG
A
Can cross placenta
14
Q
IgA
A
Secreted in breast milk and tears
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
16
Q
When do neutrophils appear?
A
In large numbers at the start of infection. First on scene.
17
Q
When do eosinophils appear?
A
Parasitic infection
18
Q
When do basophils appear
A
In inflammation - release histamine
19
Q
What do B lymphocytes do?
A
Produce antibodies
20
Q
What does penicillin act on?
A
Destruction of microbial cell wall
21
Q
How does trimethoprim act?
A
Prevents folate synthesis
22
Q
How do quinolones work?
A
Inhibit DNA gyrase - prevent DNA supercoiling
23
Q
How does Rifampicin work?
A
Inhibits RNA polymerase. Both start with R
24
Q
How do macrolides work?
A
Affect the microbial 50S subunit to prevent protein synthesis.
25
How do tetracyclines work?
Affect the microbial 30S subunit to prevent protein synthesis
26
What is the role of Interleukin-1 in the body
Pyrogen. Increases body temperature
27
How does the immune system recognise pathogens?
Recognition - molecules/receptors on immune system cells bind to molecular receptors on pathogen that are not present on self cells.
28
What are PRR's?
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
29
What are PAMPS?
Pathogen associated recognition receptors. Molecules on pathogen that can be recognised by PRRs.
30
What are DAMPS?
Damage associated recognition proteins. Self patterns that PRRs can recognise. Are present only on damaged self cells that need to be removed.
31
How to treat autoimmune disorders
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).
32
4 stages of phagocytosis.
Attachment of phagocyte to cell for destruction. Ingestion - membrane proteins engulph and take into phagocyte. Killing. Degradation - various enzymes responsible for breakdown.
33
How do neutrophils reach the site of infection?
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.
34
Aims and 4 stages of the inflammatory response
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.
35
What is systemic inflammation?
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.
36
What are opsonins?
Sugars that coat pathogens to promote removal by the immune system. 1 end binds pathogen, other binds phagocyte and stimulates phagocytosis.
37
What are interferons?
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.
38
Role of inflammation
Aims to remove pathogens before can proliferate and cause a problem. Helps transport effector cells to site of infection. Also involved in tissue repair.
39
What are RAMPS?
Resolution associated molecular patterns. Switch off inflammatory response. Chronic inflammation occurs if this fails.
40
How is inflammation initiated?
PRRs recognise PAMPs - initiate signal transduction pathways - pro-inflammatory gene expression - inflammation.
41
Chain of infection. What is it? Why important?
* 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.
42
Outline the immune response
Damage/Pathogen invasion. Innate response - cytokines, phagocytes, antigen presenting cells. Adaptive response Resolution/death
43
What is autoimmunity?
Immune response against self. Tolerance fails. Common but can be life threatening. Generally multifactorial.
44
What is TNF-A
Tumor Necrosis Factor alpha.
Involved in regulation of immune cells. Endogenous pyrogen.
45
How did vancomycin resistance develop
Appears to be spontaneous. Possible major clinical implications.
46
Differences between bacteria and eukaryotes
Bacteria: Have a peptidoglycan cell wall No nucleus/nuclear membrane - chromosome free in cytoplasm No mitochondria
47
Classes of potential antimicrobial targets
Class I - Targets reactions producing ATP Class II - Targets pathways making small molecules Class III - Targets pathways converting small molecules into macromolecules.
48
Most important class of potential antimicrobial targets
Class III - Targets pathways converting small molecules into macromolecules.
49
Main ways antibiotics target microbes (4) Why do these target microbes specifically?
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.
50
What is antibiotic resistance?
The ability of bacteria to adapt to resist antibiotics.
51
How can antibiotic resistance be spread?
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
How do mutations generate antibiotic resistance?
Spontaneous mutation rate in bacteria very low but Short bacterial generation time allows rapid evolution.
53
How does gene amplification help generate antibiotic resistance?
Theory that antibiotic use can induce an increase in number of copies of pre-existing resistance genes.
54
How do plasmids help generate antibiotic resistance?
Extrachromosomal genetic elements that can replicate independently, can contain resistance genes. Not sure how develop.
55
What are the 2 clinically relevant methods of transfer of resistance genes between bacteria?
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
What are T cells? Name 2 main types.
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
What are cytokines?
Small, soluble proteins involved in cell signalling that bind to specific receptors.
58
What do autocrine cytokines work on?
Work on the cell that produces them
59
What do Paracrine cytokines work on?
Can work on adjacent cells
60
What do endocrine cytokines work on?
Can work on distant cells via bloodstream. Very rare - usually travel short distances.
61
What are chemokines
Subgroup of cytokines that recruit phagocytes.
62
What do bactericidal antibiotics do?
Cause bacterial cell death
63
What do bacteriostatic antibiotics do?
Stop growth/development of bacteria cells. Immune system can then destroy.
64
What is the MIC?
Minimum inhibitory concentration - lowest concentration of an antimicrobial agent that stops visible growth of that microbe.
65
How do time dependent agents work?
Drug is most effective when present in sufficient doses over a long time period. Multiple doses a day.
66
How do concentration dependent agents work?
Drug is most effective when present at a high concentration. Single dose/day.
67
How to activate complement pathway?
3 diff ways. Classical, lectin or alternative.
68
What is the lectin pathway of complement
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
What is the alternative pathway of complement
Starts due to spontaneous generation. C3 unstable and can split on own. If pathogen present, binds and pathway activated.
70
What is the Classical pathway of complement?
Antibody binds microbe antigen
71
What is the membrane attack complex?
Part of complement. Generated by C5b and forms on surface of pathogen.
72
How does the membrane attack complex work?
Lipophillic so inserts into pathogen membrane. Inserts poly-C9 tube through pathogen membrane to cause lysis in susceptible bacteria.
73
Main aim of 3 pathways of complement activation
Form C3 convertase.
74
Role of C3 convertase act in complement?
C3 convertase splits into C3a and C3b. C3 convertase + C3b bind to form C5 convertase
75
Role of C5 convertase in complement
Splits into C5a and C5b. C5a and C3a recruit phagocytes to source of infection. Inflammatory mediators.
76
Role of C3b in complement?
Opinisation - coats pathogen to trigger phagocytosis
77
What is paronychia?
Localised infection of the skin folds surrounding the nail.
78
Cellular components of the innate immune system
Phagocytes, degranulating cells & NK cells.
79
Soluble components of the innate immune system
Complement, cytokines, anti-microbial proteins, Acute Phase proteins.
80
Cellular components of the adaptive immune system
B & T Cells.
81
Soluble components of the adaptive immune system
Antibodies
82
How does the innate immune system recognise pathogens?
Molecules/receptors on cells of immune system bind to molecules/receptors on pathogens that are not present on self cells.
83
Apart from phagocytosis - how else can the innate immune system respond?
Synthesis or secretion of new products. Can either directly kill pathogens or recruit other cells responsible for pathogen killing.
84
What does the inflammatory response aim to do?
Recruit more phagocystes and other proteins into the site of infection from the blood.
85
What is cell migration?
What are the 2 important factors in control of cell migration?
Movement of cells around the body. Carefully controlled.
Control where cells go in organ.
If they can enter the bloodstream.
86
What are leukocytes?
What is their unique property?
White blood cells
Can move through the body - able to both travel in the bloodstream and enter tissues.
87
What are adhesion molecules?
What do they do?
Found on leukocytes and endothelial cells. Interactions allow migration of leukocytes across the endothelium and into the blood.
88
What do chemotactic factors do?
Act directly on cells and cause movement in a particular direction
OR
Act indirectly by altering expression or binding activity of adhesion molecules.
89
Why is the innate system important if there is an adaptive system?
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
How do cells migrate from the blood into tissue?
What is this process called and what are the 3 general stages.
Extravasation -
## Footnote
\* Rolling
\* Activation and firm attachment (chemokine aided)
\* Transendothelial migration.
91
What is the pattern recognition strategy?
Technique used by the innate immune system. Recognises patterns of highly conserved receptors on pathogens.
92
What can the immune system respond to?
* Pathogens
* Damaged self.
93
What are the 2 key classes of PRRs?
* Receptors mediating phagocytosis.
* Receptors mediating the inflammatory response.
94
What are RAMPs?
Why are they important?
What happens if they go wrong?
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
4 causes of inflammation
* Infection
* Tissue damage
* Trauma
* Irritants (inc allergy)
96
What causes swelling in inflammation?
Extra fluid reaching site
97
What causes redness and heat in inflammation?
Vasodilation of capillaries
98
What causes pain in inflammation?
Inflammatory factors - destroy the cells and make patient aware of infection
99
How are T Cells activated?
Antigen presenting cells present antigen to T cells
100
What are the 2 types of T cells and what are their roles?
* TH - THelper - CD4 - Help B cells produce antibodies
* TC - TCytotoxic - CD8 - Directly kills infected cells
101
How do activated Tc cells work.
* Binds to antigen
* Mitosis and differentiation
* Destroys cells
102
How do activated TH cells work?
* 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
Hand hygiene:
What are the three levels and when are they used.
* Level 1 - Liquid soap and warm water.
* Social/direct contact
* Level 2 - Alcohol gel
* Clean proceedures
* Level 3 - Antibacterial solutions
* Surgery/Aseptic proceedures
104
How to treat autoimmune disease
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
What does methotrexate do?
Inhibits folic acid synthesis so inhibits all dividing cells including T cells. Used to treat autoimmunity.
106
What does azathioprine do?
Inhibits DNA synthesis so affects dividing B & T cells (all dividing cells).
Used to treat autoimmunity.
107
How do glucocorticoids work?
Inhibit innate immune system effects to reduce inflammation. Inhibits B, T and antibody production.
108
Where do the cells of the immune system form?
From pluripotent stem cells found in the bone marrow (spleen & liver in the foetus.
109
What 2 types of cell do pluripotent haematopoetic stem cells form?
* Common lymphoid progenitor cells
* Common myeloid progenitor cells
110
What are the lymphoid cells (form from common lymphoid progenitor)
Cells of the innate immune system
111
What are myeloid cells
Cells of the adaptive immune response as well as NK and dendritic cells.
112
What 3 types of cells form from the common myeloid progenitor?
* Immature dendritic cells
* Megakaryocyte/Erythrocyte progenitor
* Granulocyte/Macrophage progenitor
113
What granulocytes are found in blood?
* Neutrophils
* Eosiophils
* Basophils
114
What granulocytes are found in tissues?
* Mast cells
* Macrophages - only their precursors circulate in the blood.
115
What do neutrophils do
1st cell at site of inflammation.
Phagocytic
Green colour of pus is mostly due to dead neutrophils
116
3 key functions of the lymphatic system
* Tissue drainage
* Antigen trapping
* Fat transport
117
What do macrophages do?
Phagocytic cells.
Found in almost all tissues, induces inflammation, secretes signalling proteins to recruit other cells and has a role in antigen presentation.
118
What do dendritic cells do and where are they found?
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
What are Natural Killer cells?
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
What is the complement system?
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
Primary lymphatic organs - What are they & what do they do?
Make lymphocytes - atrophy with age.
Thymus and bone marrow.
122
Secondary lymphoid organs - What are they and what do they do?
Store lymphocytes.
* Spleen
* Lymph nodes
* Tonsils
* Peyers patches (modified gut lymphoid tissue)
123
First step of complement
* 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
Describe the common complement pathway
* 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
