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Year 5 Pathology - Week 1 > Antimicrobial agents - 1 > Flashcards

Antimicrobial agents - 1 Flashcards

1
Q

Differentiate between gram positive and gram negative bacteria

A

Gram positive - stain PURPLE because they retain dye
- they only have one layer of peptidoglycan cell wall, filled with LPS, Lipid A etc

Gram Negative bacteria - stain piNk, do not retain as much dye as they have a double cell membranes with a thin sandwich filling of peptidoglycan in the middle

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2
Q

What do you call the structures either side of the peptidoglycan filling in a gram negative bacterium?

A

Outer membrane and cell membrane

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3
Q

What is a key structural unit of peptidoglycan cell walls?

A

The NAM-NAG peptide cross link

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4
Q

Which enzyme is important for this cross-link?

A

Transpeptidases

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5
Q

Which classes of antibiotics inhibit cell wall synthesis?

A

Beta lactams and glycopeptides

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6
Q

What is the target of beta lactam antibiotics?

A

Transpeptidases so that they can inhibit the peptide cross linking of NAM-NAG, this causes weak cell walls and the bacteria to lyse and dye

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7
Q

When can beta lactam antibiotics work?

A

When the bacteria are dividing and trying to form new cell walls.

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8
Q

Name four classes of beta lactam antibiotics

A

Penecillins
Cefalosporins
Carbapenems
Monobactams

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9
Q

Name four classes of beta lactam antibiotics

A

Penecillins
Cefalosporins
Carbapenems
Monobactams

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10
Q

Name four types of penecilins

A

Penicilin
Amoxicillin
Flucloxicillin
Pippercilin

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11
Q

What does penicillin cover?

A

Gram positive only

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12
Q

What does amox cover?

A

Gram positive AND gram negative, hence it’s called BROAD SPECTRUM
Also enterococci

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13
Q

What’s the problem with amox and what was created to cover it?

A

Amox is targeted by beta lactamases, so flucloxacillin was created instead

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14
Q

What is the benefit of fluclox over amox?

A

Fluclox is resistant to staph aureus which produces beta lactamases

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15
Q

Name two drugs which have been created to overcome beta lactamase resistance to penicillin-based antibiotics

A

Clavulanic acid and TAZOBACTAM

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16
Q

What do you call clavulanic acid + amox

A

Co-amoxiclav

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17
Q

What do you call tazobactam + a particular penicillin (what penicillin is it?)

A

Tazocin - piperacillin

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18
Q

What does piperacillin cover?

A

Like amox - g -ve and g+ve
Also covers Pseudoamonas aeuroginosa and other non-enteric gram negatives

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19
Q

What class of drugs were created after beta lactamase producing bacteria were discovered?

A

Cephalosporins

20
Q

Briefly describe the efficacy of cephalosporins

A

First generation - more effective against gram positive
As you go down e.g. second/third gen - more effective against gram negatives

21
Q

Name a first gen cephalosporin

A

CephaLEXin

22
Q

Name a second gen cephalosporin

A

CefuROXime

23
Q

Name two third gen cephalosporins

A

CefoTAXime
CefTAZIDime
CefTRIAXone

24
Q

What was the advantage of cephalosporins?

A

They were stable against beta lactamases

25
Q

How did bacteria evolve against cephalosporins?

A

They started producing EXTENDED SPECTRUM BETA LACTAMASES (ESBL)

26
Q

What class of antibiotics were developed in response to ESBL cephalosporin resistance?

A

Carbapenems

27
Q

How did bacteria evolve against carbapenems?

A

They started producing carabepenemases

28
Q

Name two bacteria which produced carbapenemases

A

Acinobacter baumannii (gram negative)
Klebsiella pneumoniae (gram negative)

29
Q

What are some of the advantages of penicillin based drugs?

A

They are relatively non-toxic, short half life, renally excreted, and do not cross an intact blood brain barrier

30
Q

Name another cell wall synthesis inhibitor besides beta lactams

A

Glycopeptides

31
Q

How do glycopeptides work?

A

They prevent transpeptidase and transglycosidase from forming peptide bonds

32
Q

Which type of bacteria do glycopeptides work on and why?

A

Only gram positive, because they are large molecules are can’t get through gram negative outer membranes.

33
Q

Name two glycopeptides

A

Vancomycin
Teicoplanin

34
Q

Name a key infection that vancomycin is used against

A

Serious C. difficile infections

35
Q

What other key infection can be treated with glycopeptides?

A

MRSA

36
Q

What is a key side effect of glycopeptides that you have to be aware of?

A

Nephrotoxicity

37
Q

List five classes of bacterial protein synthesis inhibitors

A

Tetracyclines
Oxazolidinones

Macrolides
Aminoglycosides
Chloramphenicol

Protein->chicken->two big macs

38
Q

Chloramphenicol is used as the alternative when?

A

For patients with meningitis who are resistant to ceph and penicillin

39
Q

How do aminoglycosides work?

A

Bind to the amino-acyl site of the 30s ribosomal subunit

40
Q

How quickly do aminoglycosides work?

A

VERY quickly - they’re rapidly bactericidal depending on concentration

41
Q

How do you give aminoglycosides and why?

A

One big dose, then smaller doses depending on trust guidelines. This is because the bactericidal nature depends on the concentration of bacteria-aminoglycoside binding.

Concentration-dependent killing.

42
Q

Key side effects of aminoglycosides

A

Ototoxic and nephrotoxic.

43
Q

Name two aminoglycosides which are particularly active against pseudomonas aeuroginosa

A

Gentamicin and tobramycin

44
Q

Which patients often get hit with pseudomonas? Which antibiotic is used

A

Cystic fibrosis patients - tobramycin is used

45
Q

Explain the pathophysiology of cystic fibrosis - genetics, epidemiology, mechanism, symptoms etc.

A

This is an autosomal recessive condition (chromosome 7), whereby there is a defective cystic fibrosis transmembrane regulator (CFTR) channel.

Normally, a functional CFTR would allow chloride from inside the cell to go out into the mucus. Sodium would follow, and later water by osmosis. This would make the mucus liquidy. However in cystic fibrosis, chloride can’t escape, and sodium ends up coming into the cell from the mucus. Water follows sodium, so the mucus becomes thick and the cilia become unable to beat away infections.

You end up with very thick mucus which is unable to clear infections and sadly people pass way before the age of 40…

Mainly affects Caucasian people.

Symptoms:

Malnutrition (from defective CFTR in gut?)
Infections (bronchiectasis = widening of airway, filled with mucus)
Salty sweat (due to the opposite direction of CFTR - chloride can’t get out into the cell from the sweat, so electrolytes are lost and salt and water follow.

Year 5 Pathology - Week 1 (26 decks)

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