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Pharmacology > Antibacterials > Flashcards

Antibacterials Flashcards

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
Q

Route of Administration

A

Mild infection = Oral
Serious infection - Parenteral

  • Drugs w/ poor absorption from GI tract = Parenteral
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26
Q

Complications of Antibiotic therapy

A
  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
Q

Patient factors

A
  1. Immune state
  2. Renal or Hepatic dysfunction
  3. Poor perfusion
  4. Age
  5. Pregnancy
  6. Lactation
28
Q

Advantages of Combination Therapy

A
  • Achieve synergistic effects
  • Emergency situation
  • Delay resistance
  • Treat mixed infection
  • Treat immunosuppressed
29
Q

Mechanism of Synergism

A
  1. Sequential blockade
  2. Blockade of drug-inactivating enzymes
  3. Enhanced drug uptake
30
Q

Disadvantages of Combination Therapy

A
  • 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
Q

Antimicrobial Chemoprophylaxis

A
  • 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
Q

Inhibitors of Cell Wall Synthesis (classes & names)

A
  1. B-lactam Antibiotics
    - Penicillin
    - Cephalosporins
    - Carbapenems
    - Monobactams
  2. Vancomycin
  3. Daptomycin
  4. Bacitracin
33
Q

Features of Cell wall Synthesis Inhibitors

A
  • 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
Q

Peptidoglycan

A

Chains of Polysaccharides & polypeptides that cross-link to form cell wall

35
Q

Penicillin-binding proteins (PBPs)

A
  • Transpeptidases involved in cell wall synthesis are target site for B-lactam antibiotics
  • Resistance can develop w/ PBP mutation (S. aureus)
36
Q

Structure of B-lactams

A
  1. B-lactam ring = Responsible for antibiotic effect

2. Nitrogen - Attached to b-carbon relative to the Carbonyl ring

37
Q

MOA of B-Lactams

A

Inhibit last step in Peptidoglycan synthesis by binding to PBPs –> Activates autolytic enzymes –> Cell death

  • Bactericidal
38
Q

B- Lactamases

A

Bacterial enzymes that hydrolyze & break B-lactam ring

  • Penicillinase
  • Cephalosporinase
39
Q

B-Lactamase Inhibitors MOA

A

Protects penicillin from inactivation

  • Contain B-lactam ring that has higher affinity for B-lactamase
  • No antibiotic activity
  • Used in fixed combination
40
Q

B-lactamase Inhibitors (names)

A
  • Clavulanic acid
  • Sulbactam
  • Tazobactam
  • Avibactam
41
Q

B-lactamase Inhibitors (names)

A
  • Clavulanic acid
  • Sulbactam
  • Tazobactam
  • Avibactam
42
Q

Synergistic Combinations

A

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
Q

Penicillin

44
Q

Penicillin Spectrum

A

Gram +ve bacteria & Gram -ve (porin permit easy transmembrane entry)

Ability to reach PBPs is determined by size, charge & hydrophobicity

45
Q

Penicillin Resistance Mechanism

A
  1. Inactivation by B-lactamase
  2. Modification of target PBPs (MRSA)
  3. Impaired penetration of drug to target PBOs
  4. Inc efflux
46
Q

Types of Penicillin

A
  1. Natural
    - Penicillin G/ Benzylpenicillin
    - Penicillin V
  2. Repository
    - Penicillin G Procaine
    - Penicillin G Benzathine
47
Q

Spectrum of Natural Penicillin/ Penicillin G

A
  • Gram +ve cocci
  • Gram +ve rods
  • Gram -ve cocci
  • Most anaerobes
48
Q

Penicillin G Resistance

A

Susceptible to inactivation by B-lactamase

49
Q

Clinical Applications of Penicillin G

A 
Gram +ve organism
DOC for:
1. Syphilis (Benzathine penicillin G)
2. Strep infections
3. Susceptible pneumococci
50
Q

Repository Penicillin (names)

A
  • Penicillin G Procaine

- Penicillin G Benzathine

51
Q

Pharmacokinetics of Repository Penicillin

52
Q

Clinical application Of Penicillin G Benzathine

A

DOC for:

  1. Syphilis
  2. Rheumatic fever prophylaxis
53
Q

Spectrum of Penicillin V

A

Similar to Penicillin G but LESS active against Gram -ve bacteria

  • More acid stable than G so can be give orally
54
Q

Clinical Application of Penicillin V

A

DOC for:
- Strep throat
(Mostly for mild-moderate infections - Pharyngitis, tonsilitis & skin infections)

55
Q

Anti-staphylococcal Penicillin (Names) &

A
  • Nafcillin
  • Oxacillin
  • Dicloxacillin
56
Q

Clinical Applications of Anti-staphylococcal Penicillin

A

B-lactamase-producing Staphylococci

  • Inactive against MRSA
  • B-lactamase resistant
57
Q

Extended- Spectrum Penicillins (Names)

A
  1. Ampicillin
  2. Amoxicillin (highest oral bioavailability for penicillin)
    - Mostly used in children & pregnancy
58
Q

Clinical applications of Amoxicillin

A
  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
Q

Clinical applications of Ampicillin

A
  • Acute otitis media, Strep pharyngitis, Pneumonia, Skin infections, UTIs, etc.
  • Treatment of dogs, cats & huma bite (Ampicillin + Sulbactam)
60
Q

Anti-pseudomonal Penicillins (names)

A
  1. Ticarcillin

2. Piperacillin

61
Q

Spectrum of Anti-pseudomonal penicillins

A

Gram -ve & Gram +ve Bacilli

- Active against P. aeruginosa

62
Q

Clinical application of Anti-pseudomonal Penicilin

A
  1. Treat P. aeruginosa
  2. Treat mod-severe infections of susceptible organisms (Uncomplicated & complicated skin, gynecologic & intra-abdominal infection, Febrile neutropenia)
63
Q

Pharmacokinetics of Penicillins

64
Q

AEs of Penicillins

A
  1. Hypersensitivity

2.

Pharmacology (16 decks)

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