AntimicroChemo Flashcards

1
Q

MIC

A
  • Minimal inhibitory concentration

- Minimum concentration of antimicrobial needed to inhibit visible growth of a given organism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

MBC

A
  • Minimal bactericidal concentration

- Minimum concentration of the antimicrobial needed to kill a given organism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Sensitive

A

Organism inhibited or killed by levels of the antimicrobial that are available at the site of infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Resistant

A
  • Organism that is not killed or inhibited by levels of the antimicrobial that are available at the site of infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Bactericidal

A

An antimicrobial that kills bacteria -> penicillins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Bacteriostatic

A

Antimicrobial that inhibits growth of bacteria -> erythromycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Routes of administration

A

Topical: on surface, skin or mucous membranes

Systemic: Internal, oral or parenteral (IV or IM, occasionally subcutaneously)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Three different areas of metabolic activity to inhibit or kill bacteria

A
  1. Inhibition of cell wall synthesis
  2. Inhibition of protein synthesis
  3. Inhibition of nucleic acid synthesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Inhibition of cell wall synthesis and examples

A
  • Human cells don’t have cell walls which means that these antibiotics don’t inhibit their synthesis
  • Penicillins and cephalosporins (β-lactams)
  • Vancomycin, teicoplanin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Penicillins and cephalosporins mechanism

A

β-lactams inhibit cell wall synthesis, they disrupt peptidoglycan synthesis by inhibiting enzymes that crosslink C-chains

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Vancomycin and teicoplanin

A
  • Act on cell wall synthesis and stage prior to β-lactams. Inhibit assembly of peptidoglycan precursor.
  • Can only act on Gram positive since they cannot penetrate Gram negative cell wall
  • Given parenterally
  • Vancomycin is toxic, needs monitoring
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Inhibition of protein synthesis and examples

A
  • Involves translation of mRNA at the ribosome
  • Gentamicin (Aminoglycosides)
  • Erythromycin, clarithromycin and tetracyclines
  • Linezolid
  • Daptomycin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Gentamicin

A
  • Gram -ve antimicrobial
  • Also, most staphylococci are sensitive to them
  • Injectable rather than oral abx
  • Toxicity needs to be monitored -> hearing and renal function loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Erythromycin, clarithromycin and tetracyclines

A
  • E and C are macrolides, a good alternative to penicillin in Gram +ve infections -> allergy to penicillin
  • Some resistance: Staph aureus, Strep. Pyogenes and Strep. Pneumoniae
  • C has better penetration into tissue -> lower MIC. Good for Haemophilus influenza
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Linezolid

A
  • Good against MRSA
  • Can be given orally
  • Reserved for serious infections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Daptomycin

A
  • Active against Gram positives in general and MRSA especially.
  • Serious infections, specialist advice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Inhibition of nucleic acid synthesis and examples

A
  • Inhibit DNA synthesis either directly or indirectly by interrupting the supply of DNA precursors
  • Trimethoprim and sulphamethoxazole
  • Ciprofloxacin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Trimethoprim and sulphamethoxazole

A
  • Can be used in a combined form called co-trimoxazole as they inhibit different steps in purine sythesis
  • Less likely to cause C.diff
  • Trimethoprim commonly used in UTIs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Ciprofloxacin

A
  • Particularly effective against Gram negative organisms including Pseudomonas
  • Fluoroquinolones
  • Inhibits DNA synthesis more directly
  • Can be used orally as well as parenterally
  • Can’t use on children as it interferes with cartilage growth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Antifungal drugs

A
  • Polyenes
  • Azoles
  • Allylamines
  • Echinocandins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Polyenes

A
  • Bind to ergosterol in fungal cell wall
  • Also bind to sterols e.g. cholesterol -> toxicity: renal, cardiac and hepatic toxicity
  • Examples: amphotericin B (IV) only given for serious yeast infections, Nystatin (only give topically)
22
Q

Azoles

A
  • Inhibit ergosterol synthesis
  • Examples: fluconazole, used parenterally and orally to treat yeast infections, not all yeasts sensitive to fluconazole.
    Voriconazole and itracoazole used to treat filamentous fungi, aspergillosis spp.
23
Q

Allylamines

A
  • Suppress ergosterol synthesis, act at different stage in pathway from azoles
  • Example: Terbinafine is used to treat skin (dermatophytes) and nail (oncycohmycosis) infections either orally or topically
24
Q

Echinocandins

A
  • Inhibit synthesis of glucan polysaccharides in several types of fungi
  • Fungicidal against Candida spp. and several Aspergillus spp. for serious infections on specialist advice
25
Q

Anti-Viral Drugs and examples of viruses you can treat

A
  • Only virustatic
  • Antiherpes
  • Anti-HIV
  • Chronic Hep B and Hep C
  • Viral Respiratory Infections
26
Q

Antiherpes

A
  • Nucleoside analogue

- Aciclovir, used against VZV and Herpes Simplex

27
Q

Anti-HIV

A
  • Nucleoside analogue interferes with the action of reverse transcriptase
  • Slows replication of virus
  • Zidovudine (AZT)
28
Q

Chronic Hep B and C

A
  • Pegylated interferon-α is manufactured (usually in body as part of host immune response) given as subcutaneous injection
29
Q

Viral Respiratory Infections

A
  • Treat influenza A and B within 48 hours of the onset of symptoms and post-exposure prophylaxis
  • Zanamavir and Oseltamivir
30
Q

2 basic mechanisms of bacterial resistance

A
  • Inherent resistance

- Acquired resistance

31
Q

Inherent resistance

A
  • All strains of given species are naturally resistant to an antibiotic. Usually due to inability of the drug to penetrate the bacterial cell wall
32
Q

Acquired resistance - 2 basic ways resistance is acquired

A
  1. Target may have changed. Spontaneous mutation during multiplication of bacterial DNA can result in a change in structure of function which no longer allows the antibiotic to work.
  2. Genes that code for resistance can spread from organism to organism or species to species. Commonest
33
Q

2 mechanisms of resistance to β-lactam antibiotics

A
  1. β-lactamase production

2. Alteration of penicillin binding protein (PBP)

34
Q

β-lactamase production

A
  • Cleaves β-lactam ring of the antibiotic. Inactivated
  • Resistant to penicillins or cephalosporins
  • Most strains of Staph. aureus produve β-lactamase
  • Common in Gram negative bacilli
35
Q

Combating β-lactamase

A
  1. Introduce second component to the antibiotic that protects enzyme degradation. E.g. co-amoxiclav has β-lactamase inhibitor clavulanic acid
  2. Modify antibiotic side chain to produce an antibiotic resistant to actions of β-lactamase e.g. flucloxacillin
36
Q

Alteration of penicillin binding protein

A
  • β-lactams can no longer bind as PBP genes have mutated
  • These are resistant to all β-lactams
  • Example: Staph aureus, MRSA strain
37
Q

Glycopeptide resistance

A
  • Vancomycin and teicoplanin resistance, unusual in Gram positive organisms
  • Vancomycin resistant enterococci is a new one: peptidoglycan precursor has altered structure, vancomycin can’t bind
38
Q

2 Factors that affect side effects

A
  1. Dose
  2. Length of treatment.

Too much of one of these and you can get a side effect

39
Q

Side effects

A
  • Immediate hypersensitivity
  • Delayed hypersensitivity
  • Gastro intestinal
  • Thrush
  • Liver toxicity
  • Renal toxicity
  • Neurological toxicity
  • Haematological toxicity
40
Q

Immediate hypersensitivity

A
  • Anaphlactic
  • IgE mediated and occurs within minutes of administration
  • Itching, urticaria, nausea, vomiting ,wheezing and shock
  • Laryngeal oedema may prove fatal
41
Q

Delayed hypersensitivity

A
  • Hours or days
  • Immune complex or cell mediated mechanism
  • Drug rashes are most common manifestation
  • Drug fever - serum sickness and erythema nodosum may also occur
42
Q

Gastro Intestinal side effects

A
  • Nausea and vomiting are common
  • Diarrhoea can come from toxin production by C. diff -> anaerobic gram positive bacillus carried asymptomatically in GI tract -> appears to overgrow -> CDAD, associated diarrhoea or CDI, infection -> pseudomembranous colitis
  • This is why broad spectrum antibiotics are restricted
43
Q

Thrush

A
  • Broad spectrum antimicrobials also suppress normal flora and there can be overgrowth of resistant organisms
44
Q

Liver toxicity

A
  • Transient elevation of enzymes or severe hepatitis can occur
  • More common in people with pre-existing liver disease and in pregnancy
  • Associated drugs: tetracycline, anti-TB drugs and rifampicin, flucloxacillin
45
Q

Renal toxicity

A
  • Kidney is most important route of drug excretion
  • Nephrotoxicity is more common in patients with pre-existing renal disease
  • Most commonly seen with aminoglycosides or vancomycin
46
Q

Neurological toxicity

A
  • Ototoxicity -> aminoglycoside or vancomycin
  • Optic neuropathy -> ethambutol (anti-TB drug) with dose related optic nerve damage
  • Encephalopathy and convulsions -> may result from high dose β-lactams or aciclovir, needs to be reduced in the presence of renal impairment
  • Peripheral neuropathy -> metronidazole and nitrofurantoin can cause this. Anti-TB drug, isoniazid can also induce neuropathy
47
Q

Haematological toxicity

A
  • Toxic effect -> selective depression of one cell line or unselective depression of all bone marrow elements
48
Q

Prevention of adverse reactions

A
  • Antimicrobials should be used only when indicated
  • Minimum dose
  • Minimum duration necessary to achieve efficacy
  • Be aware of who could be affected by adverse effects from kidney and liver
  • Never underestimate side effects of antibiotics, always report any side effects
49
Q

Prophylaxis

A
  • Prevent future infection
  • If patient has been exposed to other patients with highly communicable disease
  • Following surgical procedure associated with high post-operative infection rate
50
Q

Monotherapy vs combination

A
  • Additive 1+1=2
  • or antagonistic 1+1=0
  • or synergistic 1+1=4
  • 2 cidal and 2 static drugs are additive or synergistic
  • 1 static and 1 cidal are antagonistic
51
Q

Penetration to site of infection

A

Antimicrobial needs to reach site of infection

52
Q

Role of lab

A
  • Monitoring efficacy: can measure that therapeutic levels have been achieved, make sure they’ve not gone toxic. Measure with serum
  • Susceptibility: automated (computers), E test (simple, measure one antibiotic against one organism)