Week 102 - Swollen finger Flashcards

1
Q

What are the three functions of the complement system?

A

1) Destroys pathogens through membrane-attack-complexes.
2) Inflammatory mediation (C3a and C5a attract immune cells)
3) Opsonise pathogens (C3b)

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2
Q

What are the three pathways of the complement cascade?

A

1) Classical pathway
2) Lectin pathway
3) Alternative pathway

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3
Q

What is the classical pathway of the complement system?

A
  • C1 binds to antibodies on the pathogen surface

* C1 catalyses breakdown of C2 and C4 to form C3 convertase.

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4
Q

What is the lectin pathway of the complement system?

A
  • ‘Mannose binding lectin’-MASP protein complex binds to mannose on the pathogen surface.
  • This complex acts as C3 convertase.
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5
Q

What is the alternative pathway of the complement system?

A
  • This is spontaneous cleaving of C3 in the circulation.

* C3b then binds to the pathogen and acts as a C3 convertase.

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6
Q

What are the three main stages of the complement cascade?

A
• C3 splits 
- C3a Inflammatory mediator
- C3b opsonises and acts as C5 convertase and C3 convertase.
• C5 splits
- C5a Inflammatory mediator
- C5b - Catalyst of further cascade
• Membrane attack complex forms
- C6, C7, C8 and 5xC9
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7
Q

What are the three safeguards of the complement system to prevent self-attack?

A
  • C3 inactivated by blood proteins unless bound to a pathogen.
  • C3 convertase inactivation is accelerated by human cell surface proteins.
  • MAC is kicked off human cell surfaces by surface proteins.
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8
Q

What are the two methods of chemokine action?

A
  • Autocrine - Feedback loop, to amplify response.

* Paracrine - Act on other cells, communication.

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9
Q

Which interleukin is responsible for activation of T-cells?

A

IL-12

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10
Q

What are the four main mechanisms of action of antibiotics?

A
  • Disruption of the cell wall.
  • Inhibition of nucleic acid synthesis.
  • Inhibition of protein synthesis.
  • Antimetabolite activity.
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11
Q

What is the difference in the structure of the bacterial wall between gram +ve / -ve?

A

Gram -ve have a membrane on the outside of the peptidoglycan, whilst in gram +ve the peptidoglycan is the most outerly layer.

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12
Q

Give some examples of Beta-lactams and describe their mechanism of action.

A
  • Penicillins, cephalosporins, carbapenems.

* Form covalent bonds with proteins in the cell wall preventing final cross-linking, thus disrupting the wall.

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13
Q

Give some examples of Glycopeptides and describe their mechanism of action.

A
  • Vancomycin, Teicoplanin
  • They inhibit the release of the building block part of the membrane, they prevent addition to the growing end of the peptidoglycan.
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14
Q

Give three antibiotics that work by inhibiting the production of nucleic acids in antibiotics.

A
  • Quinolones.
  • Metronidazole
  • Rifampicin
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15
Q

Give some examples of Quinolones, and describe their mechanism of action.

A
  • Ciprofloxacin, levofloxacin.

* They inhibit the DNA gyrase enzyme, which stops supercoiling of bacterial DNA.

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16
Q

What is the mechanism of action of metronidazole?

A

Damages DNA, which prevents DNA synthesis.

17
Q

What is the mechanism of action of Rifampicin?

A

Inhibits the action of RNA polymerase.

18
Q

Which three families of antibiotics work by inhibiting protein synthesis? Give the stand-alone antibiotic which also acts in this way.

A
  • Tetracyclines
  • Aminoglycosides
  • Chloramphenicol
  • Macrolides
19
Q

What is the mechanism of Tetracyclines? Give some examples.

A

• Inhibits protein synthesis by binding to the 30s subunit of the ribosome.

20
Q

Give some examples of Aminoglycosides, and describe their mechanism of action.

A
  • Gentamicin, Amikacin.

* Binds to the 30s subunit of the ribosome, leading to misreading of codon on mRNA.

21
Q

Give some examples of macrolides, and describe their mechanism of action.

A
  • Clarithromycin, Erythromycin.

* Binds to the 50s subunit of the ribosome and prevents translocation. (Where tRNA is moved along ribosome).

22
Q

What are the two most likely bacteria found on the skin? Give an antibiotic for the treatment of each.

A
  • Steptococcus - Penicillin V

* Staphylococcus - Flucloxacillin

23
Q

What type of bacteria is most likely to be found within an abscess? Give an antibiotic that will treat it.

A

Anaerobes - Metronidazole

24
Q

How do anti-Beta-lactamases work?

A

• They widen the spectrum of the drug, by adding to the molecule a subunit that will irreversibly bind to the beta-lactamases.

25
Q

Give two examples of what can be added to an anti-biotic to add beta-lactamase resistance, give an example antibiotic for each.

A
  • Clavulanic Acid - Co-Amoxiclav (Augmentin)

* Tazobactam - Tazocin

26
Q

Week 102 - Swollen Finger: Which cytokine is responsible for T-cell activation?

A

IL-12

27
Q

Week 102 - Swollen Finger: Which cytokines (four) are responsible for vasodilation, vascular permeability, fever, macrophage and lymphocyte activation?

A
  • Il-1ß
  • TNF-å
  • IL-6
  • IL-8
28
Q

Week 102 - Swollen Finger: What are the four main mechanisms through which antibiotics work?

A
  • Disruption of cell wall
  • Inhibition of nucleic acid synthesis
  • Inhibition of protein synthesis
  • Antimetabolite activity
29
Q

Week 102 - Swollen Finger: What is the difference between gram-negative and gram-positive bacteria in terms of cell wall composition?

A

The gram -ve bacteria have an outer membrane that covers the peptidoglycan layer, whilst gram +ve bacteria have the peptidoglycan layer exposed.

30
Q

Week 102 - Swollen Finger: Give examples of some Beta-lactams and describe their mechanism of action.

A
  • Penicillins, cephalosporins, carbapenems.

* Form covalent bonds with penicillin-binding proteins to inhibit final formation of cross-links.

31
Q

Week 102 - Swollen Finger: Give examples of glycopeptides and describe their mechanism of action.

A
  • Vancomycin, Teicoplanin.
  • Inhibits the release of the building block unit from the cell membrane. Prevent addition to growing end of peptidoglycan.