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Semester 3 > Infection Session 2 > Flashcards

Infection Session 2 Flashcards

1
Q

Why is physiological state relevant in gestational diabetes?

A

During pregnancy bacteria in the large bowel can cause gestational diabetes

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2
Q

What is the difference in calendar and relative time when considering a patient with a suspected infection?

A

Calendar time considers seasonal diseases e.g. Flu or chickenpox
Relative considers time since a potential exposure

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3
Q

By what 7 mechanisms can infection occur?

A 
Contiguous spread
Inoculation
Haematogenous
Ingestion
Inhalation
Vector
Vertical transmission
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4
Q

How do aerosols form?

A

Around a ‘seed’ e.g. a dust particle

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5
Q

Why is chickenpox so contagious?

A

Virus rapidly multiplies in lungs and is transmitted via inhalation

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6
Q

What sequence does management of infection usually take?

A

History –> examination –> diagnosis –> specific+/- supportive Tx –> infection prevention in hospital and community

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7
Q

How are the vast majority of infection diagnoses made?

A

History alone

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8
Q

Why is debridement of tissue sometimes used to treat infection?

A

Dead tissue has a low redox potential and bloodflow so is a perfect environment for anaerobic bacteria

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9
Q

Why does the dead space left following debridement often need packing?

A

Blood/serosa can accumulate here and promote microbial growth

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10
Q

What outcomes are possible following an infection?

A

Resolution
Chronic infection –> potential disability
Death

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11
Q

What is an antibiotic?

A

Antimicrobial produced by a living organism

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12
Q

What are the four main types of antimicrobials?

A

Antibacterial
Antiviral
Antiprotozoal
Antifungal

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13
Q

What is the difference between a bactericidal and bacteriostatic antibacterial agent?

A

Bactericidals kill, bacteriostatics inhibit

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14
Q

What are the ideal features of antimicrobial agents?

A 
Selectively toxic
Few adverse effects
Reach site of infection
Oral/IV formulation
Long half-life for infrequent dosing
No interference w/other drugs
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15
Q

How do beta-lactams act as antibacterials?

A

Inhibit cell wall regeneration by binding to penicillin binding protein so new X-links cannot be formed

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16
Q

How do glycopeptides act as antibacterials?

A

Bind to peptidoglycan thus blocking cell wall X-linking enzyme

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17
Q

What mechanisms can bacteria use to be resistant to beta-lactams?

A

Decrease their permeability to them
Express beta-lactamases to inactivate drug
Alter target enzyme so it has a lower affinity

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18
Q

Which classes of antibacterials inhibit protein synthesis by blocking a variety of enzymes?

A

Tetracyclines
Aminoglycosides
Macrolides

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19
Q

How can bacteria be resistant to tetracyclines?

A

Increase efflux to actively pump out before it takes effect

Alter target enzyme

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20
Q

Which class of antibacterials do trimethoprim and rifampicin belong to and how do they act?

A

Quinolones (floroquinolones clinically)

Bind to DNA gyrase to interfere with DNA supercoiling

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21
Q

What are polymixins?

A

Antibacterials that inhibit cell membrane function

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22
Q

Will a bacterium only ever have one mechanism of resistance to one particular drug?

A

No, might have different mechanisms for same class as well as multiple mechanisms for different classes

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23
Q

Does there need to be a high level of antibiotic exposure for a chromosomal gene mutation resulting in antibiotic resistance to occur?

A

No

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24
Q

What two methods form the basis of antibiotic resistance?

A

Chromosomal gene mutation

Horizontal gene transfer

25
Q

What is the qualitative method of measuring antibiotic activity?

A

Disc sensitivity to examine zone of inhibition around disc

26
Q

What is the quantitative measure of antibiotic sensitivity?

A

Minimum inhibitory concentration

27
Q

How is minimum inhibitory concentration measured?

A

Bacterial broth is cultured in a serial dilution of antibiotic

28
Q

Are carbapenems broad or narrow spectrum?

A

Broad - including anaerobes and most G-ve

29
Q

What are penicillins mainly active against?

A

Streptococci

30
Q

What is flucoxacillin active against?

A

Staph and streptococci

31
Q

Give an example of a commonly used beta-lactamase inhibitor combination therapy.

A

Co-amoxiclav

32
Q

How do new generation of cephalosporins compare to old generations?

A

Increased G-ve spectrum and decreased G+ve activity

33
Q

Are cephalosporins active against anaerobes?

A

No

34
Q

What is the relevance of cephalosporins to C.diff infection?

A

Broad spectrum so widespread use –> resistant C.diff strains

35
Q

How does the activity of vancomycin against G+ve bacteria compare to its activity against G-ve?

A

Active against most G+ve but not G-ve

36
Q

Why is vancomycin given orally for intestinal infections?

A

Not normally absorbed into the blood

37
Q

Why must care be taken with vancomycin use?

A

It has a narrow therapeutic window

38
Q

What class of antimicrobials does vancomycin belong to?

A

Glycopeptides

39
Q

Why are tetracyclines not widely used in hospitals?

A

Broad spectrum

40
Q

In what common situation might carbapenems, tetracyclines or macrolides be used?

A

Penicillin allergy

41
Q

What are tetracyclines active against?

A

Chlamydia
Some protozoa
Atypical pneumonia pathogens

42
Q

Why are tetracyclines not given to children under 12 y.o.?

A

Stain bones and teeth yellow

43
Q

Which antimicrobial is reserved for severe G-ve sepsis?

A

Gentamicin

44
Q

Why is gentamicin reserved as a last resort for severe G-ve sepsis?

A

Profound activity against G-ve but is potentially nephrotoxic

45
Q

What is used in primary care as an alternative to penicillin for mild G+ve infections?

A

Macrolides

46
Q

Why are macrolides used in combination with drugs for typical respiratory pathogens?

A

They are active against atypical respiratory pathogens

47
Q

Name two macrolides.

A

Erythromycin

Clarithromycin

48
Q

What activity do quinolones have?

A

Very active against G-ve and atypical pathogens

49
Q

Why is there a concern with quinolones and C.diff infection?

A

Rapidly increasing resistance

50
Q

What action do trimethoprim and sulphonamides have?

A

Inhibit folic acid synthesis

51
Q

What is trimethoprim most commonly used for in the UK?

A

UTI

52
Q

When might you use a combination of trimethoprim and sulphonamides?

A

In a specific and unusual infection

53
Q

What class of antifungals acts by inhibiting cell-membrane synthesis?

A

Azoles

54
Q

What is an over-the-counter antifungal used to treat Candida?

A

Fluconazole

55
Q

How does the activity of Azoles and Polyenes differ even though their mechanism of action is the same?

A

Azoles active against yeasts +/- moulds

Polyenes active against more complicated moulds

56
Q

Why can aciclovir be used against Herpes simplex and Varicella Zoster viruses?

A

Upon phosphorylation it inhibits viral DNA polymerase

57
Q

How does Tamiflu work?

A

Inhibits viral neuraminidase

58
Q

What is metronidazole active against?

A

Anaerobic bacteria and several protozoa

59
Q

What are the 7 patient factors which can affect disease?

A 
Age
Gender
Physiological state
Pathological state
Social factors
Time
Place

Semester 3 (50 decks)

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