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Antibacterials Flashcards

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1
Q

Anti-microbial

A

Inhibits growths of micro-organisms

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2
Q

Anti-bacterial

A

Inhibits growth of bacteria

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3
Q

Antibiotic

A
  • Inhibits growth of micro-organisms
  • Made by other micro-organisms
  • Extended to include synthetic drugs
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4
Q

MOA of Anti-bacterials

A
  1. Cell wall synthesis inhibitors
  2. Protein synthesis inhibitors
  3. Drugs that affect nucleic acid synthesis
  4. Urinary antiseptics
  5. Miscellaneous
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5
Q

Bacteriostatic vs Bactericidal

A

Bacteriostatic = Reversible inhibition of growth
Bactericidal = Irreversible inhibition of growth
- Immunocompromised pts
- Life-threatening situations

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6
Q

Selective toxicity

A

Ability to injure/kill an invading microorganism w/o harming host cell
- Inc selective toxicity = Dec AE

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7
Q

Post-antibiotic effect

A

When the killing action continues once drug plasma levels are below measurable levels

  • lag time required for synthesis of new enzymes or cellular components
  • persistence of agent at target site
  • enhanced susceptibility of bacteria to phagocytic/ defense mechanism
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8
Q

Antibacterial spectrum

A

Broad spectrum - against several group of micro-organism
Narrow spectrum- against few groups of micro-organisms
Extended spectrum - against gram +ve + some gram -ve micro-organisms

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9
Q

Broad spectrum Antibiotic uses

A
  • Empiric therapy

- Mixed infection (multiple bacteria present)

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10
Q

Disadvantages of Broad Spectrum Antibiotics

A
  • Selection of multi-drug resistant

- Disruption of normal flora

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11
Q

Uses of Narrow Spectrum Antibiotics

A
  • Treating infections of known origin
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12
Q

Disadvantages of Narrow- Spectrum Antibiotics

A
  • Must know causative organism

- Not useful for empiric therapy

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13
Q

Uses of Extended Spectrum

A
  • Empiric therapy

- Mixed infection

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14
Q

Disadvantages of Extended Spectrum drugs

A
  • Selection of multi-drug resistant bacteria

- Disruption of normal flora

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15
Q

Minimum effective dose/ Minimun inhibitory Conc

A

Lowest conc. of antibiotic that prevents visible growth

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16
Q

Minimal Bactericidal Concentration (MBC)

A

Lowest concentration of antibiotic that results in a 99.9% decline in colony count after overnight broth dilation incubation.

MBC (truly bactericidal agent) =/just slightly > MIC

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17
Q

Factors for selecting the right agent

A
  1. Organism identity
  2. Organism susceptibility to agent
  3. Necessity of empiric therapy
  4. Site of infection
  5. Pharmacological factors
  6. Patient factors
  7. Cost of therapy
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18
Q

Actions in Gram +ve & Gram -ve organisms based on Cell wall

A

Gram +ve- Will NOT block some substances so they will easy pass through
- Thick mesh-like cell wall made of peptidoglycan

Gram -ve - Will block passage of some substances to cell membrane due to the Lipopolysaccharide layer

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19
Q

Development of Antibiotic resistance

A

Antibiotic kill sensitive bacteria but not the rare resistant bacteria– > Resistant bacteria multiplies & passes on the resistance

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20
Q

Mechanisms of Resistance

A
  1. Altered uptake of Antibiotic
    - Dec permeability or uptake mechanisms. Inc in multi-drug resistance pumps
  2. Altered target
    - change in receptor site affinity or modification of targeted metabolic pathways
  3. Drug inactivation
    - Bacteria produce enzymes that inactivate drug
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21
Q

Types of Resistance

A
  1. ## Primary
  2. ## Acquired
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22
Q

Empiric therapy

A 
Given when immediate therapy is requires
 CHoice of drug is influenced by:
- Site of infection
- Pt. Hx
Broad spectrum may be required
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23
Q

Site of Infection

A

Penetration of BBB

  1. Lipid solubility
  2. Molecular weight - Larger = Less likely to penetrate
  3. Protein binding of the drug = Inc binding = Dec free drug conc available for penetration
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24
Q

Pharmacological factors

A
  1. Route of administration
  2. Route of elimination
  3. Half life affected by diseases & other drugs
  4. Drug interaction
  5. Dosing schedule
  6. AEs & Idiosyncratic responces
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25
Route of Administration
Mild infection = Oral Serious infection - Parenteral * Drugs w/ poor absorption from GI tract = Parenteral
26
Complications of Antibiotic therapy
1. Hypersensitivity (Urticaria --> Anaphylactic shock) 2. Direct toxicity (affect hosts cellular processes) 3. Superinfection (new or secondary infection that occurs during antimicrobial use ) BENEFITS > RISKS
27
Patient factors
1. Immune state 2. Renal or Hepatic dysfunction 3. Poor perfusion 4. Age 5. Pregnancy 6. Lactation
28
Advantages of Combination Therapy
- Achieve synergistic effects - Emergency situation - Delay resistance - Treat mixed infection - Treat immunosuppressed
29
Mechanism of Synergism
1. Sequential blockade 2. Blockade of drug-inactivating enzymes 3. Enhanced drug uptake
30
Disadvantages of Combination Therapy
- Can select for multi-drug resistant bacteria - Some agents only act on multiplying bacteria & if combined w/ another agent that causes bacteriostasis they will be less effective
31
Antimicrobial Chemoprophylaxis
- Should always be directed toward a specific pathogen - No resistance should develop - Should be used for a limited duration - Conventional therapeutic doses should be employed - Should only be used in situations of documented drug efficacy
32
Inhibitors of Cell Wall Synthesis (classes & names)
1. B-lactam Antibiotics - Penicillin - Cephalosporins - Carbapenems - Monobactams 2. Vancomycin 3. Daptomycin 4. Bacitracin
33
Features of Cell wall Synthesis Inhibitors
- Selective toxicity- Mammalian cell do NOT have cell wall - Inactive against organisms w/o Peptidoglycan cell wall (mycoplasma, protozoa, fungi, viruses) - Require actively proliferating bacteria
34
Peptidoglycan
Chains of Polysaccharides & polypeptides that cross-link to form cell wall
35
Penicillin-binding proteins (PBPs)
- Transpeptidases involved in cell wall synthesis are target site for B-lactam antibiotics - Resistance can develop w/ PBP mutation (S. aureus)
36
Structure of B-lactams
1. B-lactam ring = Responsible for antibiotic effect | 2. Nitrogen - Attached to b-carbon relative to the Carbonyl ring
37
MOA of B-Lactams
Inhibit last step in Peptidoglycan synthesis by binding to PBPs --> Activates autolytic enzymes --> Cell death - Bactericidal
38
B- Lactamases
Bacterial enzymes that hydrolyze & break B-lactam ring - Penicillinase - Cephalosporinase
39
B-Lactamase Inhibitors MOA
Protects penicillin from inactivation - Contain B-lactam ring that has higher affinity for B-lactamase - No antibiotic activity - Used in fixed combination
40
B-lactamase Inhibitors (names)
- Clavulanic acid - Sulbactam - Tazobactam - Avibactam
41
B-lactamase Inhibitors (names)
- Clavulanic acid - Sulbactam - Tazobactam - Avibactam
42
Synergistic Combinations
Cell wall synthesis inhibitors + Protein Synthesis inhibitors - CWSI breaks the cell wall to allow easy entry of PSI into cell * Should NEVER be placed in same infusion fluid bc it will form inactive compound
43
Penicillin
44
Penicillin Spectrum
Gram +ve bacteria & Gram -ve (porin permit easy transmembrane entry) Ability to reach PBPs is determined by size, charge & hydrophobicity
45
Penicillin Resistance Mechanism
1. Inactivation by B-lactamase 2. Modification of target PBPs (MRSA) 3. Impaired penetration of drug to target PBOs 4. Inc efflux
46
Types of Penicillin
1. Natural - Penicillin G/ Benzylpenicillin - Penicillin V 2. Repository - Penicillin G Procaine - Penicillin G Benzathine
47
Spectrum of Natural Penicillin/ Penicillin G
- Gram +ve cocci - Gram +ve rods - Gram -ve cocci - Most anaerobes
48
Penicillin G Resistance
Susceptible to inactivation by B-lactamase
49
Clinical Applications of Penicillin G
``` Gram +ve organism DOC for: 1. Syphilis (Benzathine penicillin G) 2. Strep infections 3. Susceptible pneumococci ```
50
Repository Penicillin (names)
- Penicillin G Procaine | - Penicillin G Benzathine
51
Pharmacokinetics of Repository Penicillin
52
Clinical application Of Penicillin G Benzathine
DOC for: 1. Syphilis 2. Rheumatic fever prophylaxis
53
Spectrum of Penicillin V
Similar to Penicillin G but LESS active against Gram -ve bacteria - More acid stable than G so can be give orally
54
Clinical Application of Penicillin V
DOC for: - Strep throat (Mostly for mild-moderate infections - Pharyngitis, tonsilitis & skin infections)
55
Anti-staphylococcal Penicillin (Names) &
- Nafcillin - Oxacillin - Dicloxacillin
56
Clinical Applications of Anti-staphylococcal Penicillin
B-lactamase-producing Staphylococci - Inactive against MRSA - B-lactamase resistant
57
Extended- Spectrum Penicillins (Names)
1. Ampicillin 2. Amoxicillin (highest oral bioavailability for penicillin) - Mostly used in children & pregnancy
58
Clinical applications of Amoxicillin
1. Acute otitis media, Streptococcal pharyngitis, Pneumonia, Skin infections, UTIs, etc. 2. URTI 3. Prophylaxis for susceptible infections 4. Prophylactic treatment for cats, dogs & human bite (Amoxicillin + Clavulanic acid)
59
Clinical applications of Ampicillin
- Acute otitis media, Strep pharyngitis, Pneumonia, Skin infections, UTIs, etc. - Treatment of dogs, cats & huma bite (Ampicillin + Sulbactam)
60
Anti-pseudomonal Penicillins (names)
1. Ticarcillin | 2. Piperacillin
61
Spectrum of Anti-pseudomonal penicillins
Gram -ve & Gram +ve Bacilli | - Active against P. aeruginosa
62
Clinical application of Anti-pseudomonal Penicilin
1. Treat P. aeruginosa 2. Treat mod-severe infections of susceptible organisms (Uncomplicated & complicated skin, gynecologic & intra-abdominal infection, Febrile neutropenia)
63
Pharmacokinetics of Penicillins
64
AEs of Penicillins
1. Hypersensitivity | 2.

Pharmacology (16 decks)

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